Manual of Stress, Heart Attacks and Cardiovascular Disease In Pennsylvania Workers Compensation Cases

Clifford A. Goldstein, Esquire The Chartwell Law Offices, LLP 2006

Copyright 2006 The Chartwell Law Offices, LLP.

About the Author

Clifford A. Goldstein, Esquire

Mr. Goldstein is a Senior Litigator in The Chartwell Law Offices, LLP, of Pennsylvania. Chartwell, designated by the Legal Intelligencer as the fastest growing law firm in Pennsylvania, defends employers and insurers in general and commercial litigation matters from four offices around the state. Mr. Goldstein is admitted to practice by Supreme Court of Pennsylvania, the Supreme Court of the United States, the United States District Court for the Eastern District of Pennsylvania and the United States Court of Appeals for the Third Circuit. A summa cum laude graduate of Temple University and its School of Law, Mr. Goldstein practices workers' compensation law under both the Pennsylvania Workers' Compensation Act and the Longshore and Harbor Workers' Compensation Act. He has lectured frequently on the topic of stress-related claims under both Acts and has litigated cases under both Acts at every level of trial and appeal, including cases appealed to the Supreme Court of the United States of America. Before joining Chartwell, Mr. Goldstein was the founder of the Weber Goldstein Greenberg & Gallagher law firm, and served as a partner at Americas oldest law firm, Rawle & Henderson. Mr. Goldstein began his legal career as an Assistant District Attorney under then D.A. Ed Rendell in Philadelphia, PA.

INTRODUCTION

Once relatively rare and only superficially analyzed, claims of disability allegedly attributable to job stress have become common. It has been estimated that approximately 15% of all workers' compensation claims nationally involve allegations of stress-related illness. As more and more jobs are converted from manual to mental, we are witnessing a dramatic change in the nature of workers' compensation claims. As the number of heavy industry and blue collar jobs declines, so too will the number of blunt trauma and mechanical injury claims encountered. Conversely, as the number of service-oriented and white collar jobs increases, there will be an increase in the number of claims alleging illness due to job stress. Claims of illness allegedly related to job stress are beginning to cause a serious economic impact on society in general, and on corporations and insurance carriers in particular. A recent estimate projected that the overall cost to the American economy of stress-related claims will soon top $150 billion per year. The cost to corporations is often decreased productivity, absenteeism, and staggering increases in medical costs. It is becoming commonplace for companies to spend millions of dollars a year on "stress management" programs for their employees, partly in an effort to stem the turbulent tide of claims of work-related stress illness. Claims of stress-related illness can be subdivided into three primary categories. The first category involves claims of psychiatric disability following a physical injury at work. An example of this "physical-mental" category of cases would be a worker who experiences a severe back injury on the job, subsequently develops chronic pain, and then develops a severe psychological depression as a result of the worker's inability to cope with the daily pain and the prospect of disability. The second category, referred to as "mental-physical", involves claims of physical illness or impairment flowing from a psychological stimulus at work. An example of this category of claim would be an individual who experiences overwhelming emotional stress on the job, triggering a heart attack, stroke, or other physical impairment.

The third category of stress-related claims involves the "mental-mental" case, in which an emotional or psychological stimulus at work produces psychiatric disability. In the "physical-mental" category of cases, claims adjusters, claims managers, risk managers, and attorneys are well equipped to differentiate between compensable and non-compensable cases using traditional investigation and litigation tools; however, because "mental-physical" and "mental-mental" claims are relatively new, involve evolving concepts of law, and new and highly technical issues, the need has arisen for workers' compensation practitioners to re-train and prepare for what will likely be one of the greatest challenges of the this decade. Under the Pennsylvania Workers' Compensation Act, the medical and legal issues in "mentalmental" cases, and perhaps in some mental-physical cases, differ dramatically from the issues in physical injury cases. Until 2000, most practitioners believed that mental-physical cases were governed by the same rules as other physical injuries. However, the Pennsylvania Supreme Court in the Davis v. WCAB (Swarthmore Borough), 751 A.2d 168 (Pa. 2000)decision, held that the same rules to mental-physical as to mental-mental claims, namely, that the claimant had to prove more than a subjective reaction to normal working conditions. This change caused the number of stress related heart attack claims to plummet. Claimants attorneys feared that the new burden of proof would make stress related heart attack claims as difficult to prove as mental-mental cases. In December of 2005, the Pennsylvania Supreme Court issued its decision in the Panyko v. WCAB (U.S. Airways) case, 888 A.2d 726 (Pa. 2005). The Court re-interpreted its holding in Davis, and reinstated the long standing law in Pennsylvania that stress-related heart attack claims would be no more difficult to prove than any other injury claims. Panyko did not expressly overrule Davis,

however, and it can be argued that Panyko created a new class of cases the mental-purely physical category. The Court ruled that such cases are not subject to the tougher abnormal working conditions burden. The Court was less than clear in its definition of and basis for establishing this new class of mental-purely physical claims. There is, as the dissent in Panyko pointed out, a conflict between Panyko and Davis, and if

Panyko is read broadly, the floodgates may now burst open with claims for stress-related cardiovascular disease and heart attack cases. To prepare for the anticipated onslaught of mental-physical and/or mental-purely physical claims, this article reviews the law, and more importantly, the medicine, that should guide consideration and litigation of stress-related heart disease claims. Claims in the "mental-physical" and mental-purely physical categories almost always involve injuries to or diseases of the cardiovascular system. Therefore, the scope of this article is expanded to include claims involving cardiovascular injury and disease, both allegedly resulting from mental stress and allegedly resulting from physical exertion on the job. The goal of this article is to provide the medical, legal and strategic knowledge necessary to allow proper evaluation and successful litigation of claims in which workers allege that their cardiovascular injuries or diseases are work-related. Too often in the past, claims involving work-related cardiovascular disease and injury have been handled by a simplistic review of the time and location of the cardiovascular events. This article is intended to assist you in understanding the role of "risk factors" and teach you to use medical articles, studies and texts to distinguish non-work-related illness from true compensable disability. Despite the urgency and dramatic economic impact of this topic, there are relatively few organized, understandable, and comprehensive guides to assist in separating compensable from non-compensable cases of cardiovascular injury or disease. We have therefore, prepared this article to highlight the data necessary for proper evaluation of these claims and to provide a useful guide for developing an effective claims handling and litigation strategy. This article is not intended to provide medical advice for the treatment, prevention or diagnosis of disease in any particular individual. Nor is this article intended to provide legal opinions or advice pertaining to any particular case. Rather, our attempt is to provide the basic education and resources necessary to allow each workers' compensation practitioner an opportunity to gain a

better understanding of the medical and legal issues presented and to develop a practical strategy for evaluating and litigating claims alleging work-related cardiovascular disease and injury.

CARDIOVASCULAR DISEASE THE MAGNITUDE OF THE PROBLEM

About one million Americans die of cardiovascular disease each year. Almost one out of two Americans die of cardiovascular deaths. To appreciate the impact of cardiovascular disease in the United States, consider the following: Heart and blood vessel disease kill more Americans per year than all

other causes of death combined. Contrary to popular belief, cardiovascular deaths affect more than

just the elderly. In fact, one fifth of cardiovascular deaths occur in people under the age 65. It has been estimated that 45% of all heart attacks occur in people under 65, and 5% of heart attacks occur in people under the age of 40. In addition to taking lives, cardiovascular disease affects almost one quarter of all Americans alive today. To gain a better understanding of the magnitude of the problem, review the following statistics: More than 60,000,000 Americans have high blood pressure; Over 2,000,000 Americans have survived a stroke; Over 4,900,000 Americans alive today, have a history of heart attack

or angina; This year 1,500,000 Americans will have heart attacks; and 5,300,000

Americans will have coronary artery bypass surgery this year. Not surprisingly, estimates of the amount of money expended by Americans for medical evaluation and treatment related to cardiovascular disease are staggering. The cost of

cardiovascular diseases and stroke in the United States for 2006 is estimated at $403.1 billion. This figure includes health expenditures (direct costs, which include the cost of physicians and other

professionals, hospital and nursing home services, the cost of medications, home health care and other medical durables) and lost productivity resulting from morbidity and mortality (indirect costs). By comparison, in 2004 the estimated cost of all cancers was $190 billion ($69 billion in direct costs, $17 billion in morbidity indirect costs and $104 billion in mortality indirect costs). In 1999, the estimated cost of HIV infections was $28.9 billion ($13.4 billion direct and $15.5 billion indirect). Measuring the number of cardiovascular disease cases that arise under the Pennsylvania Workers' Compensation Act or the amount expended for treatment of these diseases under the Act is difficult. No separate statistics are compiled by the Department of Labor charting the number of claims. However, according to the National Institute of Occupational Safety and Health, stress related claims account for 1 out of every 10 reports of work related illnesses. The American Institute of Stress has estimated that 75% of all doctor visits are for stress related complaints. When claims are made alleging work-related cardiovascular disease, the cases tend to have enormous exposure. There is of course no scheduled award available, and even if the initial period of disability is short, recurrences of disability are common. Many cardiovascular disease cases result in death and carry correspondingly high exposure for payment of benefits. Cases that do not result in death almost always result in claims of ongoing disability, either total or partial in nature. When stress related cardiovascular disease cases are encountered, they tend to be big cases. A great deal of media attention is directed to the topic of stress related illness. Virtually every day, any major newspaper will report on some alleged link between stress and illness, or reveal a story about the effect of "risk factors" on the development of cardiovascular disease. In one big city newspaper published in November, 2005, there were two separate front page articles discussing either the incidence of, causes of, or prevention of heart disease. The public clamor about stress and heart disease has resulted in a tremendous outpouring of money both in the public and private sector to develop "stress management" programs. Many major corporations are now expending millions, perhaps billions of dollars to educate workers about

the potential health effects of stress and to offer instruction on techniques for coping with, managing, or reducing stress. As claims of stress-related cardiovascular disease enter the limelight, the number of such claims under the Pennsylvania Workers' Compensation Act will increase significantly. Many of these claims are ill-defined, vague or baseless. It is therefore, increasingly important for all personnel involved in handling cases under the Pennsylvania Workers' Compensation Act to be able to distinguish compensable cases of stress-related cardiovascular disease from non-compensable cases. To do so, an understanding of the cardiovascular system, the risks of disease, and the provisions of the Act must be achieved. This seminar will facilitate such understanding and provide an outline for the reasonable and just evaluation and resolution of claims involving stress related cardiovascular disease under the Pennsylvania Workers' Compensation Act.

COMPENSABILITY OF HEART ATTACKS AND CARDIOVASCULAR DISEASE UNDER THE PENNSYLVANIA WORKERS' COMPENSATION ACT

Prior to the 1972 amendments to the Act, compensability in cardiovascular disease cases was triggered by the occurrence of an "accident". Although the term accident was not defined under the old version of the Act, the Pennsylvania courts defined "accident" as a sudden event that takes place without foresight or expectation. See Gilbert v. Aronimink Country Club, 214 Pa. Super. 70, 251 A.2d 724 (1969); Workmen's Compensation Appeal Board v. United Sheet Metal Co., 18 Pa. Cmwlth. 535, 336 A. 2d 896 (1975). Case law developed identifying four types of accidents: (1) a sudden, unexpected traumatic event such as a fall or blow; (2) unusual strain or exertion in the course of work causing an unexpected and sudden injury; (3) an unusual pathological result of an ordinary work condition; and (4) sudden and unexpected injury caused by the failure of an employer to furnish medical care to an employee. Under the old "accident" standard, most cardiovascular disease cases turned on whether the claimant had proven unusual strain or exertion. There could be no recovery unless the claimant proved that the death or injury resulted from overexertion or unusual strain encountered in the course of his employment. Whether the strain was unusual was determined in accordance with the individual work history of the claimant, and not with reference to the patterns or practices of the worker's profession generally. Borough of Throop v. Workmen's Compensation Appeal Board, 17 Pa. Cmwlth. 521, 333 A.2d 481 (1975); Muser v. I.B.M. Corp., 13 Pa. Cmwlth. 12, 317 A.2d 352 (1974). The requirement of an accidental injury was eliminated effective May 1, 1972. The term "accident" was replaced with the term "injury". Perhaps intentionally, the 1972 amendments filed to define the term "injury". The current version of the Act merely provides that: The term "injury" and "personal injury" as used in this act, shall be construed to mean an injury to an employee, regardless of his

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previous physical condition, arising in the course of employment and related thereto, and such disease or infection as naturally results from the injury or is aggravated, reactivated or accelerated by the injury; and wherever death is mentioned as a cause for compensation under this act, it shall mean only death resulting from such injury and its resultant effects, and occurring within three hundred weeks after the injury. Section 301 (C) (1); 77 P. S. 411 (1). Despite repeated opportunities to do so, the Pennsylvania courts have steadfastly refused to provide a definition of "injury". The Supreme Court of Pennsylvania has held that "injury" need not be given a technical meaning, and that a "standard" dictionary definition would suffice in determining whether an "injury" occurred under the Act. Workmen's Compensation Appeal Board v. Bernard S. Pincus Co., 479 Pa. 286, 388 A.2d 659 (1978). Unfortunately, there is no single or standard dictionary definition of injury. Some dictionaries define injury with specific reference to change or physical harm. Others more generally refer to the occurrence of symptoms such as pain. As more fully discussed in the section of these materials addressing claims of work related angina, the differing definitions of injury may influence the outcome of cases in which only symptoms and not change in physiology occur. As a result of the 1972 amendments to the Act, a claim can be deemed compensable even if the cardiovascular injury or disease results from regular or usual employment activities, and even if the worker had a history of pre-existing, non work-related cardiovascular disease. See Workmen's Compensation Appeal Board v. Pincus and Workmen's Compensation Appeal Board v. Ayers, 479 Pa. 286, 388 A.2d 659 (1978): Township of Haverford v. Workmen's Compensation Appeal Board, 118 Pa. Cmwlth. 476, 545 A.2d 971 (1988). Under current Pennsylvania law, cardiovascular related disabilities are compensable if it is proven that they a) arise during the course of employment and b) are causally related thereto. Haney v. Workmen's Compensation Appeal Board, 65 Pa. Cmwlth. 461, 463, 442 A.2d 1223, 1225 (1982); Ryan v. Workmen's Compensation Appeal Board, 82 Pa. Cmwlth. 643, 477 A.2d 16 (1984); Borough of Media v. Workmen's Compensation Appeal Board, 134 Pa. Cmwlth. 573, 577, 580 A.2d 431 (1990); Stanner v. Workmen's Compensation Appeal Board, 146 Pa. Cmwlth. 92, 98, 604 A.2d 1167, 1169 (1992), Farmery v. Workmen's Compensation Appeal Board, 767 A.2d 348, 354 (Pa.

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Cmwlth.. 2001); Acme Markets, Inc. v. Workers Compensation Appeal Board, 819 A.2d 143, 145 (Pa. Cmwlth.. 2003).

A. Arises During The Course Of Employment

A body of case law developed in the Commonwealth Court holding that to be compensable, an injury had to occur in the course of employment. See Paper Products Co., Inc., et al v. Workmen's Compensation Appeal Board, 67 Pa. Cmwlth. 577, 448 A.2d 652 (1982). It was believed that under the Commonwealth Court rule, if the injury or its manifestations occurred outside of the employment setting, benefits could not be awarded. In cardiovascular disease cases, however, the Supreme Court of Pennsylvania explicitly rejected the Commonwealth Court approach and held that an injury can be compensable even if it occurs outside of work. In Krawchuk v. Philadelphia Electric Co., 497 Pa. 115, 439 A. 2d 627 (1981), an electrical engineer had a heart attack at home and died. The referee found that during the few weeks preceding the decedent's death, the decedent was under great emotional stress as a result of the decedent's work on a special project for the employer, and the preparation of a treatise to be presented in California. The referee further found that for the five hours preceding his heart attack, the decedent was working at home on the treatise. The decedent's cardiologist testified that the decedent's death was causally related to the decedent's heavy work load, and relying upon this testimony, the referee awarded benefits. The employer appealed to the Workmen's Compensation Appeal Board, which reversed the award of benefits. Claimant appealed to the Commonwealth Court, which affirmed the decision of the Board. Claimant then appealed to the Supreme Court of Pennsylvania, seeking a

determination that the decedent's heart attack was compensable even though it occurred off the job. The Supreme Court of Pennsylvania reversed the Commonwealth Court, and held that the Act did not intend to create a dichotomy between injuries that manifest themselves on the employer's premises and those that manifest themselves outside of the normal work area. The court

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specifically rejected the proposition that in "off-premises" cases, in addition to proving that the injury arose in the course of employment and was related thereto, the claimant must also prove that the victim was actually engaged in the furtherance of his employer's business or affairs at the time of the cardiovascular event. The court ruled that the location of the cardiovascular event was merely a factor for the referee to consider in determining whether the injury arose in the course of employment and was related thereto. Soon after the Supreme Court of Pennsylvania's decision in Krawchuk, the Commonwealth Court decided Rizzo v. Workmen's Compensation Appeal Board, 69 Pa. Cmwlth. 92, 450 A.2d 291 (1982). In Rizzo, a school custodian had a heart attack at home and died. There was no suggestion that the decedent was performing any business activity for the employer at the time of his heart attack. The referee awarded benefits, choosing to believe the testimony of claimant's medical expert, and found that the decedent's heart attack was causally related to the decedent's employment since the decedent was suffering under the stress of managing several buildings during the energy crisis. The Board reversed the award, holding that the injury and death occurred at home at a time when the worker was not actually engaged in the furtherance of the business of his employer. The Commonwealth Court, following the holding in Krawchuk, reversed the Board and reinstated the award to the claimant. The case law since Krawchuk has been relatively clear that if the impetus of the cardiovascular disease occurred during employment, the location of the worker at the time of the cardiovascular event is merely one factor to be considered in determining whether the event arose in the course of employment. Stanner v. Workmen's Compensation Appeal Board, 146 Pa. Cmwlth. 92, 98, 604 A.2d 1167, 1169 (1992); Municipality of Bethel Park v. Workers Compensation Appeal Board, 161 Pa. Cmwlth. 274, 283, 636 A.2d 1254, 1259(1994); Acme Markets, Inc. v. Workers

Compensation Appeal Board, 819 A.2d 143, 147 (Pa. Cmwlth.. 2003). Another factor to be considered in determining whether a cardiovascular disease or injury

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arose in the course of employment is the time lag between the work stimulus and the cardiovascular result. In General Electric Co. v. Workmen's Compensation Appeal Board, 79 Pa. Cmwlth. 91, 468 A. 2d 885 (1982), a machinist worked twelve consecutive days. Thirty three hours after he completed his last shift, while at home, the worker had a heart attack and died. The decedent's widow filed a fatal claim petition, and in support thereof presented testimony from a pathologist. Claimant's medical expert opined that the stress of working twelve consecutive days aggravated the decedent's longstanding cardiovascular disease and played a significant role in the decedent's death. The referee awarded benefits, and the employer

appealed to the Board. After the Board affirmed the referee's order, the employer appealed to the Commonwealth Court, asserting that the thirty-three hour lag between the decedent's work and his heart attack, coupled with the fact that the heart attack occurred at the decedent's home, removed the decedent from the course of employment as a matter of law. The Commonwealth Court held that the passage of time, like the location of the attack, was merely a factor to be considered, and affirmed the award. Brody v. Workmen's Compensation Appeal Board, 138 Pa. Cmwlth. 456, 462; 588 A.2d 575, 578 (1991). The two most common fact patterns encountered in disputes over whether the cardiovascular disease or injury arose in the course of employment are: a) cases in which the injury occurs "off the clock" but on the employer's premises; ( See Penn Pad Co. v. Workmen's Compensation Appeal Board, 83 Pa. Cmwlth. 490, 478 A.2d 497 (1984); Port Authority of Allegheny County v. Workmen's Compensation Appeal Board, 66 Pa. Cmwlth. 393, 444 A. 2d 837 (1982); Babcock and Wilcox Construction Co., Inc. v. St. John, 48 Pa. Cmwlth. 1, 408 A. 2d 915 (1979) But See Good Shepherds Workshop v. Workmen's Compensation Appeal Board, 124 Pa. Cmwlth.. 262, 269; 555 A.2d 1374, 1378 (1989), But See Heverly v. Workmens Compensation Appeal Board, 134 Pa. Cmwlth.. 110, 578 A.2d 575 (1990)and b) cases in which the injury occurs off the employer's premises and "off the clock". See Township of Haverford v. Workmen's Compensation Appeal Board, 118 Pa. Cmwlth. 467, 545 A. 2d 971 (1988); distinguished; Rizzo v. Workmen's Compensation Appeal Board,

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Id. Id.?;But See Acme Markets, Inc. v. Workers Compensation Appeal Board, 819 A.2d 143 (Pa. Cmwlth. 2003)

B. Related To Employment
In addition to proving that the cardiovascular disease or injury arose in the course of employment, it must be proven that the cardiovascular disease or injury was causally related to the employment. It is axiomatic that in heart attack cases, where the causal connection between work and the injury is not an obvious one, the claimant bears the burden of establishing the link through unequivocal medical testimony. Dobash v. Workers Compensation Appeal Board, 836 A.2d 1085, 1088(Pa. Cmwlth. 2003); Haddon Craftsmen v. Workers Compensation Appeal Board, 809 A.2d 434, 439 (Pa. Cmwlth. 2003); Robert W. Borschell Painting v. Workmen's Compensation Appeal Board, 154 Pa. Cmwlth. 157, 161, 623 A.2d 394, 395 (1993); Harbison v. Workmen's Compensation Appeal

Board, 91 Pa. Cmwlth. 169, 496 A.2d 1306 (1985); Martino v. Workmen's Compensation Appeal Board, 87 Pa. Cmwlth. 154, 486 A.2d 1038 (1985); George v. Workmen's Compensation Appeal Board, 49 Pa. Cmwlth. 435, 411 A.2d 294 (1980); Lewis v. Workmen's Compensation Appeal Board, 91 Pa. Cmwlth. 91, 496 A.2d 1265 (1985); Haney v. Workmen's Compensation Appeal Board, 65 Pa. Cmwlth. 461, 442 A.2d 1223 (1982); Workmen's Compensation Appeal Board v. Bowen, 26 Pa. Cmwlth. 593, 364 A.2d 1387 (1976); Heffer v. GAF Corp., 29 Pa. Cmwlth. 365, 370 A.2d 1254 (1977).

C. Special requirement for cases in which the injury is not purely physical
In 2000, the Pennsylvania Supreme Court issued a Decision in the Davis v. WCAB (Swarthmore Borough), 561 Pa. 462, 751 A.2d 168 (2000). Davis, a police officer, asserted that repeated mental stress on the job resulted in post-traumatic stress syndrome, as well as shortness of breath, uncontrollable hand shaking, general muscle twitching, aches and pains. The Court explained that Davis suffered a psychic injury, which happened to be accompanied by physical symptoms. Therefore, the Court required Davis to meet the additional

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burden of proving that abnormal working conditions caused his disability. The Court reasoned that a psychic injury did not become a physical injury simply because it included physical symptoms. Most practitioners read Davis to require that in all mental-physical cases, the claimant had to prove abnormal working conditions; the same burden previously applied to only mental-mental cases. As a result, the number of claims for stress related heart attacks plummeted. In 2005, the Pennsylvania Supreme Court issued a decision in Panyko v. WCAB (U. S. Airways) 888 A. 2d 726 (Pa. 2005). Panyko was a baggage handler for U.S. Airways. He had a history of coronary artery disease including a prior heart attack and bypass surgery. Despite his bypass

procedure, he suffered additional periods of chest pain and disability in the years following surgery. Panykos boss called him in for a routine meeting to discuss his absences from work. Panyko

believed that the meeting was unjustified, and believed that the boss was unnecessarily threatening during the meeting. As for Panyko, he was angrily speakingwith his teeth clenched and his

hands were shaking. He turned red all over, and his entire body just clenched. As Panyko left the meeting, he felt neck, back and shoulder pain. He was taken to a hospital and diagnosed with a heart attack. Pankyo missed only 30 days from work. He filed a claim petition, and the case was litigated based solely on medical reports, without the benefit of testimony from any physician. An issue was raised concerning whether Panyko had given proper notice under Section 311 of the Act, but the issue was quickly swept aside so that the Court could address, head-on, the issue of whether the holding of the Davis case required Panyko to prove that the meeting with his boss constituted an abnormal working condition. In one of his last decisions before being unceremoniously removed from the Court by the voters of Pennsylvania, Justice Nigro authored an opinion that Panyko did not have to prove abnormal working conditions to prevail. Justice Nigro opined that Panykos heart attack constituted a purely physical injury, and hence, Davis did not control. Justice Nigro reasoned that Davis only requires proof of an abnormal working condition when the injury is psychic in nature, and merely

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accompanied by physical symptoms.

The Davis rule did not apply to Panyko, reasoned Justice

Nigro, because Panykos injury was purely physical. In a concurring opinion, Justice Saylor commented that the majority was, in effect, ruling that its earlier Davis decision was decided erroneously, and suggested that the majority should have simply admitted that the decision in Davis was a mistake, and that the Court never intended to require proof of an abnormal working condition in a mental-physical case. A dissenting opinion was authored by Justice Newman. She opined that the majority had unacceptably diluted the requirement of medical causation when it dispensed with the abnormal working condition requirement in a mental-physical case. Justice Newman warned that the majoritys decision would turn employers into general health insurers of their employees. Perhaps one of the most significant facts in Panyko is the fact that no medical testimony was elicited. Therefore, when Justice Nigro concluded that Panykos injury was purely physical, he

necessarily did so based upon his lay understanding of which, if any, symptoms suffered by Panyko were purely physical and which were psychic injuries accompanied by physical manifestations. As will be fully discussed in the medical sections of this article, it is not at all clear when symptoms, ranging from turning red to clenching teeth to chest pain, cross the line from mental to physical. If the parties had presented medical testimony, perhaps the Court could have provided more detail to support its conclusion that heart attacks, angina, and colitis constitute purely physical injuries, while shortness of breath, uncontrollable shaking and pain constitute only psychic injuries with accompanying physical manifestations, thus warranting a different standard of proof. Until additional guidance is developed by the courts, it appears that if a case is couched in terms of a purely physical injury, proof of an abnormal working condition is not required. If instead the case is framed as one involving physical symptoms of a psychic injury, the additional burden must be satisfied.

D. Is it necessary to present medical evidence at all?

It is interesting to note that very few cases are litigated without the presentation of medical

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evidence. Theoretically, a claimant could assert that the causal connection between the work and the cardiovascular disease or injury was obvious, and hence unequivocal medical evidence was unnecessary. Although this approach has been used in orthopedic injury cases, there are no

reported cardiovascular disease cases holding that the presentation of unequivocal medical evidence was unnecessary due to the obviousness of the causal relationship. In virtually all

cardiovascular disease cases, proof that the cardiovascular disease or injury was related to employment is attempted by the presentation of medical evidence. To survive an appeal, the medical evidence supporting causation must be unequivocal.

E. When is medical testimony unequivocal?

Medical testimony is unequivocal when it establishes that, in the professional opinion of the medical expert, the claimant's work experience was not a possible cause of the claimant's condition, but was in fact the cause of claimant's condition. Lewis v. Workmen's Compensation Appeal Board, 91 Pa. Cmwlth. 91, 496 A.2d 1265 (1985), citing Philadelphia College of Osteopathic Medicine v. Workmen's Compensation Appeal Board, 77 Pa. Cmwlth. 202, 465 A.2d 132 (1983). Unequivocal medical evidence has been described as medical testimony that establishes not that the injury or condition might have or even possibly did come from the assigned cause, but that in the expert's professional opinion; the result did come from the assigned cause. Dobash v. Workers Compensation Appeal Board, 836 A.2d 1085, 1088(Pa. Cmwlth. 2003); Haddon Craftsmen v. Workers Compensation Appeal Board, 809 A.2d 434, 439 (Pa. Cmwlth. 2003); Edwards v. Workmen's Compensation Appeal Board, 137 Pa. Cmwlth. 70,80; 585 A.2d 56, 63 (1990)(dissenting); Ryan v. Workmen's Compensation Appeal Board, 82 Pa. Cmwlth. 643, 477 A.2d 16 (1984); Gunther v. Workmen's Compensation Appeal Board, 66 Pa. Cmwlth. 487, 444 A.2d 1342 (1982). To be unequivocal, medical evidence must not be based on mere possibilities. Taulton v. Workers Compensation Appeal Board, 713 A.2d 142, 145 (Pa. Cmwlth. 142). Westmoreland Casualty Co. v. Workmen's Compensation Appeal Board, 36 Pa. Cmwlth. 307, 387 A.2d 683 (1978); Roeberg Enterprise, Inc v. Workmen's Compensation Appeal Board, 42 Pa. Cmwlth. 308, 400 A.2d

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911 (1979). While medical testimony must be unequivocal, it need not be stated with unqualified certainty. Cerro Metal Products, Inc. v. Workers Compensation Appeal Board, 855 A.2d 932, 937 (Pa. Cmwlth. 2004); Mitchell v. Workers Compensation Appeal Board, 796 A.2d 1015, 1018 (Pa. Cmwlth. 2002) Workmen's Compensation Appeal Board v. Bowen, 26 Pa. Cmwlth. 593, 364 A.2d 1387 (1976); Rosenberry Bros. Lumber Co. v. Workmen's Compensation Appeal Board, 36 Pa.

Cmwlth. 283, 387 A.2d 526 (1978). The mere absence of the magic words "his work caused his heart attack" should not necessarily preclude the recovery of benefits. Rosenberry, Id., at 387 A.2d 528. Even if the medical expert's testimony is equivocal with respect to the mechanism of death, his testimony will suffice to award benefits if unequivocal with respect to the cause of death. Latrobe Steel Co., v. Workmen's Compensation Appeal Board, 41 Pa. Cmwlth. 460, 399 A.2d 465 (1979). Frequently, during cross examination, a medical expert is unable, for example, to testify with any certainty as to whether a cardiovascular death was the result of spasm or occlusion. As long as the expert testifies unequivocally that the work caused the death, equivocation on the precise mechanism of death will be allowed. Penn Pad Company v. Workmen's Compensation Appeal Board, 83 Pa. Cmwlth. 490, 478 A.2d 497 (1984). The expert's testimony need not be without reservation, uncertainty or doubt, so long as the witness does not recant the opinion or belief first expressed. Lewis, Id. at 496 A.2d 1267; Philadelphia College of Osteopathic Medicine, Id., at 465 A.2d 135. Medical evidence which is less than positive is not legally sufficient to qualify as unequivocal evidence required by the Act. Yakemowicz v. Workmen's Compensation Appeal Board, 59 Pa. Cmwlth. 41, 428 A.2d 781 (1981). A fine description of the line separating unequivocal testimony from testimony based on uncertainty is found in Martino v. Workmen's Compensation Appeal Board, 87 Pa. Cmwlth. 154, 486 A. 2d 1038 (1985): Certainly it is not the law ... that every utterance which escapes the lips of a medical witness on a medical subject, must be certain, positive and without reservation, exception or peradventure of a doubt. (citations omitted) In addition, it is not absolutely essential that the medical expert use "magic words" such as " it is my

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professional opinion" (citations omitted). However, it is not sufficient for the medical witness to testify that the claimant's condition might have been or probably was the result of the claimant's work (citations omitted). Martino 87 Pa. Cmwlth. at 157; 486 A.2d at 1040. The testimony does not have to be absolute in medical terms; that is, the employment does not have to be the medical cause of the death or injury. Lamoreaux v. Workmen's

Compensation Appeal Board, 92 Pa. Cmwlth. 1, 497 A.2d 1388 (1985). The fact that other factors may have contributed to the injury does not render the medical testimony equivocal. New

Enterprise Stone and Lime v. Workmen's Compensation Appeal Board, 124 Pa. Cmwlth. 257, 555 A.2d 974 (1989). The question of whether a physician's testimony is equivocal must be decided from an examination of the entirety of the testimony. Bethlehem Steel Corp. v. Workmen's Compensation Appeal Board, 66 Pa. Cmwlth. 579, 445 A.2d 843 (1982); Bernardini v. Workmen's Compensation Appeal Board, 97 Pa. Cmwlth. 514, 510 A.2d 382 (1986). On review, the standard is whether, based upon a thorough review of the entire record, the medical testimony, taken as a whole, was sufficiently unequivocal to support a finding for the claimant. Harbison, Id., 496 A. 2d at 1307; Haney v. Workmen's Compensation Appeal Board, 65 Pa. Cmwlth. 461, 442 A.2d 1223 (1982). Whether medical evidence is equivocal requires a determination of its competency, not its credibility, and therefore, on appeal, the court must review the record to determine the propriety of the reliance on the evidence presented. Roeberg Enterprise, Inc v. Workmen's Compensation Appeal Board, 42 Pa. Cmwlth. 308, 400 A.2d 911 (1979). Although the above standards are easy to recite, they are often difficult to apply. There does not appear to be great consistency in determining when testimony is in fact, unequivocal. Weak opinions often suffice, especially if unrefuted or if there are no other known potential causes of the cardiovascular event. Consider the following examples: In Brennan v. Workmen's Compensation Appeal Board, 79 Pa. Cmwlth. 217, 468 A.2d 1193 (1983), the worker died while drinking beer and eating peanuts one full day after his last day of

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employment. The cause of death was aspiration of gastric contents. Simply put, the worker choked on peanuts, vomited, and died as a result of choking on his vomit. The widow filed a fatal claim, asserting that because of his history of working in the mines, the decedent had some sort of respiratory impairment that prevented the decedent from surviving the choking incident long enough to make it to a hospital. The medical evidence presented, established that without the underlying work-related lung condition, the decedent "could have possibly made it to the hospital". When asked for his opinion a second time, the expert opined that a causal relationship between the death and employment "could not be excluded with any certainty". Asked the same question for the third time, the expert testified that, within a reasonable degree of medical certainty, absent the underlying work-related condition, the decedent would have survived. The Commonwealth Court held that the above cited testimony was equivocal, and affirmed the denial of benefits to the widow. Had the factual circumstances not been so bizarre and attenuated, a different result could easily have followed. Frequently a claimant's expert is asked for an opinion on causation, and provides an equivocal answer. Most claimants attorneys respond by repeating or rephrasing the question in the hope of obtaining a clearer answer the second or third time around. Practitioners should be cautioned that while it is true that the referee has broad discretion concerning evidentiary rulings, "he cannot allow counsel to literally place the sought after answers into the witness's mouth". Blevins v. New Garden Township, 91 Pa. Cmwlth. 207, 496 A.2d 1309 (1985), citing Tomshuck v. Wallin Concrete Corp., 146 Pa. Super. 390, 395, 23 A. 2d 74, 77 (1941). On the other end of the spectrum is Workmen's Compensation Appeal Board v. Bowen, 26 Pa. Cmwlth. 593, 364 A. 2d 1387 (1976). In Bowen, claimant was performing strenuous labor, pulling heavy cable through a conduit. He experienced chest pain while doing so, and sought medical treatment. A heart attack was diagnosed. In support of his petition for benefits, claimant presented the testimony of his family

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physician. The claimant's medical witness testified that it was possible that extreme exertion could bring on a heart attack in any person who has coronary artery disease. The doctor was then asked if he had an opinion as to whether the claimant's exertion caused the claimant's heart attack. The doctor initially declined to answer, noting that he would rather answer a question as to whether the claimant's exertion could have caused the heart attack. The next time the

question was asked, the doctor testified that the claimant's activities possibly brought on the infarction. After being asked two more times the doctor finally and reluctantly answered "yes" to a leading question inquiring as to a causal relationship between the employment and the heart attack. The Commonwealth Court ruled that although the above cited testimony "seemed to lack unqualified certainty", the referee's award of benefits to the claimant was adequately supported by the doctor's testimony. The court's decision was no doubt influenced by the fact that the employer chose not to present any evidence in rebuttal to the testimony of claimant's doctor.

F. Use of Hypothetical Questions

The usual method of eliciting an opinion from an expert is to pose to the expert a hypothetical question based upon facts proven of record. Special care must be exercised in presenting and challenging hypothetical questions in cardiovascular disease cases. Hypothetical questions must be based on matters which appear of record and on facts which are warranted by the evidence. Borough of Morrisville v. Workmen's Compensation Appeal Board, 54 Pa. Cmwlth. 41, 419 A.2d 813 (1980). Where the medical evidence is based on assumed facts that were not in the record, the testimony is fatally flawed. Compensation Appeal Board, 92 Pa. Cmwlth. 1, 497 A.2d 1388 (1985). In order for a complaint concerning a hypothetical question to be valid, barring outright assumption of unsupported fact, there must be a timely objection and the specific elements of the question which are objectionable must be brought to the attention of the examiner. Pennsylvania State Oral School v. Workmen's Compensation Appeal Board, 82 Pa. Cmwlth. 323, 475 A.2d 175 Lamoreaux v. Workmen's

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(1984); Borough of Morrisville v. Workmen's Compensation Appeal Board, 54 Pa. Cmwlth. 41, 419 A.2d 813 (1980). Failure to raise a timely objection to an improper hypothetical question will preclude the appellate courts from passing on the propriety of the question. Workmen's

Compensation Appeal Board v. Jeddo Highland Coal Co., 19 Pa. Cmwlth. 90, 338 A.2d 744 (1975); Gordon v. State Farm LIfe Insurance Co., 415 Pa. 256, 203 A.2d 320 (1964). Moreover, the grounds upon which an objection to evidence is based must appear of record, and only those grounds for objection raised will be considered on appeal. Holy Family College v. Workmen's Compensation Appeal Board, 84 Pa. Cmwlth. 109, 479 A.2d 24 (1984).

G. Miscellaneous Rules
1. It is the claimant's burden to prove entitlement to benefits. Penn Pad Co. v. Workmen's Compensation Appeal Board, 83 Pa. Cmwlth. 490, 478 A.2d 497 (1984); Hinkle v. H. J. Heinz Co., 7 Pa. Cmwlth. 216, 298 A.2d 632 (1972). 2. Because of the remedial purposes of the Act, it must be liberally construed in favor of the claimant to effectuate its humanitarian objectives. Bley v. Commonwealth Dept. Of Labor and Industry, 484 Pa. 365, 399 A.2d 119 (1979); Krawchuk, Id. at 439 A.2d 630. 3. Medical evidence need not be presented by a Board-certified cardiologist to support an award of benefits. Workmen's Compensation Appeal Board v. Continental Meat Co., 22 Pa. Cmwlth. 51, 347 A. 2d 318 (1975). Generally, any licensed physician is legally competent to testify, even in fields of medicine in which the expert lacks special certification. Kocher v. Workmen's Compensation Appeal Board, 52 Pa. Cmwlth. 106, 415 A. 2d 162 (1980). Lack of Board-certification is merely an issue for consideration by the referee in weighing the evidence. 4. Mere presence of a pre-existing heart condition does not prevent recovery under the Act. See Babcock and Wilcox v. St. John, 48 Pa. Cmwlth. 1, 408 A.2d 915 (1979); Lanzarotta v. Workmen's Compensation Appeal Board, 42 Pa. Cmwlth. 284, 400 A.2d 697 (1979). 5. It is not necessary to identify and prove the precise work details that lead to the

cardiovascular disease or injury. Plumbers Contractors, Inc. v. Workmen's Compensation Appeal

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Board, 43 Pa. Cmwlth. 338, 402 A.2d 555 (1979); Pennsylvania State Oral School v. Workmen's Compensation Appeal Board, 82 Pa. Cmwlth. 323, 475 A.2d 175 (1984). 6. It is not necessary for an expert witness to examine the worker to offer an opinion on the issue of causation. Workmen's Compensation Appeal Board v. Continental Meat Company, 22 Pa. Cmwlth. 37, 347 A,2d 318 (1975). A medical witness can base an opinion in whole or in part on upon medical reports of others, if the reports are of a type customarily relied upon by the expert in the practice of his profession. Commonwealth v. Thomas, 444 Pa. 436, 282 A.2d 693 (1971). 7. Records of the medical or surgical care given to an employee by a hospital are

admissible for the medical and surgical facts contained therein. Section 422, 77 P. S. 835.

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ANATOMY OF THE HEART AND BLOOD VESSELS1

The Heart
The heart and blood vessels constitute the cardiovascular, or circulatory, system. The heart is a fist-sized muscular organ that lies in the front of the center and slightly to the left of center in the chest. The normal heart contains four chambers; two on the left and two on the right side. The

Most of the medical information in this article is the result of Cliff Goldsteins collaboration with one the worlds leading experts on stress and heart disease, David S. Goldstein M.D., Ph.D. Dr. Goldstein is an Attending Physician, Clinical Staff, The Clinical Center, NIH, Bethesda, MD and a Senior Investigator, National Institute of Neurological Disorders and Stroke, Bethesda, MD, 1990-date. He also serves as a Clinical Associate Professor of Medicine (Cardiology), Georgetown University School of Medicine, Washington, DC, and as a Visiting Professor of Medicine, the Johns Hopkins University School of Medicine, Baltimore, MD. Since 1999, he has served as the Chief, Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, Bethesda, MD. Dr. Goldstein is a graduate of Yale College, and he received his medical degree and Ph.D. in Behavioral Sciences from the Johns Hopkins School of Medicine. Dr. Goldstein is a Fellow of the American College of Physicians, and a Board-certified Internist. Author of more than 320 scholarly articles and 76 book chapters on the relationship of stress to cardiovascular disease, and is the author or 7 texts and treatises relating to this topic. He has lectured and presented his research findings throughout the United States and in dozens of foreign nations. Mr. Goldstein expresses his very deep gratitude for the materials and the education provided by Dr. Goldstein, who is also Mr. Goldsteins oldest brother.
1

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chambers of the right side receive blood that already has been through the various tissues of the body and so, has relatively low concentrations of oxygen and relatively high concentrations of carbon dioxide, which can be viewed as a waste product of body metabolism. The pumping chamber of the right side of the heart, called the right ventricle, pumps purplish, deoxygenated blood to the lungs at relatively low pressure via the pulmonary artery. In the lungs, oxygen that is breathed in enters the blood, and the bright red, oxygenated blood is delivered to the left side of the heart via the pulmonary veins. The pumping chamber of the left side of the heart, the left ventricle, pumps the oxygenated blood to the rest of the body at relatively high pressure via the aorta. Each day, the average heart beats 100,000 times, and pumps close to 2,000 gallons of blood. Over a 70 year lifetime, the heart beats about 2.5 billion times.

Blood Vessels
Arteries are large blood vessels that carry blood away from the heart. The aorta is the largest artery. Except for the pulmonary artery, all arteries contain oxygenated blood. Veins are blood vessels that carry blood toward the heart. Except for the pulmonary veins, all veins contain deoxygenated blood. The blood is carried to organs, tissues, and cells by progressively smaller blood vessels-arteries, arterioles, and capillaries. The blood is carried back to the heart by progressively larger blood vessels--capillaries, venules, and veins. The largest veins bringing deoxygenated blood from the rest of the body to the heart are the superior vena cava and the inferior vena cava. The superior vena cava drains the upper part of the body, the arms, and the head. The inferior vena cava drains the lower part of the body. Blood from both veins enters the right atrium, which empties into the right ventricle. Blood in the pulmonary veins enters the left atrium, which empties into the left ventricle. There are about 12,400 miles of arteries, veins, and capillaries in the human body.

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Coronary Arteries
The coronary arteries, like all arteries carrying oxygenated blood, are branches of the aorta. There usually are two coronary arteries, right and left. The origins of the coronary arteries are at the root of the aorta. The coronary arteries then travel along the surface of the heart, called the epicardium, and give off branches feeding the heart muscle. Typically, the left coronary artery divides into two arteries, the left anterior descending artery, which supplies the front of the heart, including much of the muscular left ventricle, and the circumflex artery, which courses around the heart to the left and posteriorly. The right coronary artery supplies the right side of the heart and courses around the heart to the right and posteriorly. In some people, the right coronary artery is the source of the posterior descending artery in the back of the heart; in others, the circumflex artery is the source of the posterior descending artery in the back of the heart.

Physiology of the Heart and Blood Vessels

Functions of the Cardiovascular System
All the cells of our bodies are bathed in a fluid environment, from which the nutrition of the cells is supplied, and through which cellular wastes are removed. The maintenance of this internal environment is one of the fundamental requirements of the life of all organisms, including humans. This internal environment is maintained to an important extent, by the cardiovascular system. The function of the heart and blood vessels is to deliver blood to the organs of the body. The blood in systemic arteries carries oxygen, vital fuels such as glucose, water, hormones, and electrolytes such as sodium, calcium, and potassium to all the cells of the body; and the blood delivers waste products to the sites where they are removed from the body--the kidneys, liver, and lungs.

Determinants of the Pulse

With each heartbeat, the left ventricle pumps blood forcefully and rapidly into the aorta

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and arterial tree, producing a pulsation that can be felt in all arteries. The pulse that is taken at the wrist is derived from the shock wave traveling from the aorta to the brachial artery of the upper arm to the radial artery at the wrist. The pulse in the ankle or upper surface of the foot is derived from the wave traveling from the aorta to the iliac artery to the femoral artery in the groin to the popliteal artery behind the knee to the dorsalis pedis and posterior tibial arteries of the foot. Just after the left ventricle pumps blood into the arterial system, the pressure inside all systemic arteries increases. The peak pressure associated with left ventricular ejection of blood is the systolic pressure. Between heartbeats, pressure in the arterial system rapidly falls. The lowest pressure during this relaxation phase is the diastolic pressure. The difference between the systolic pressure and the diastolic pressure is the pulse pressure, and this probably is what is felt as the pulse. Patients with large pulse pressures have full, bounding pulses, whereas patients with small pulse pressures have weak or thready pulses. The mean arterial pressure is usually defined as the diastolic pressure plus one-third of the pulse pressure. The pulse rate is the rate at which the pulse is felt over an artery such as the radial artery in the wrist, the femoral artery in the groin, or the carotid artery in the neck. A normal pulse rate in a person who is lying supine, i.e., on his back, is 60 to 90 beats per minute. Standing increases the pulse rate, and exercise and emotion increase pulse rate substantially. The pulse rate is normally identical to the heart rate, which is the rate at which the heart is beating. In pathologic situations such as some abnormal heart rhythms, called arrhythmias, the force of the heartbeat may be too small to produce a palpable pulse. The force of the heartbeat is determined complexly by several factors. These include the filling pressures of the right and left sides of the heart (preload), the resistance against which the heart is pumping (afterload), the actions of a variety of nervous and hormonal influences (such as activity of the sympathetic and vagus nerves in the heart and the blood concentration of adrenaline), heart rate, and intrinsic contractility.

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Cardiovascular Functional Nomenclature: Hemodynamic Parameters

The cardiac output is the total amount of blood pumped by the heart in one minute. A normal cardiac output is about 6 liters per minute. During exercise, the cardiac output increases markedly, in a manner usually related directly to the increase in oxygen consumption by the body. The cardiac output is determined by the heart rate and the volume of blood pumped per heartbeat, called the stroke volume. One can calculate that if the normal cardiac output is 6 liters, or 6000 milliliters, per minute, and the normal heart rate is 60 to 90 beats per minutes, then the normal stroke volume is from 6000/90 to 6000/60, or from about 70 to about 100 milliliters. Since there are about 30 milliliters in an ounce of volume, the stroke volume is about 2 to 3 ounces per heartbeat. During exercise, both the heart rate and stroke volume typically increase. Since the cardiac output is determined by the product of heart rate and stroke volume, cardiac output increases substantially during exercise. The mean arterial pressure is determined by the cardiac output and the total peripheral resistance, just as the pressure in a garden hose is determined by the rate of flow of water and the extent to which the nozzle is tightened. Total peripheral resistance, in turn, is determined by the resistances to blood flow in all the vascular regions of the body. The amount of oxygen used up by the heart is the myocardial oxygen consumption. This is determined mainly by the amount of work of the heart and can be estimated from the product of systolic blood pressure and heart rate, called the rate-pressure product. Normally, as myocardial oxygen consumption increases, coronary blood flow increases; however, in coronary artery disease, narrowing of the coronary arteries can limit the amount of blood flow. It is thought that the inability to increase coronary blood flow adequately when myocardial oxygen consumption is increased, is a determinant of coronary ischemia, also called myocardial ischemia, which is deficiency of delivery of blood to the heart. It has been proposed that spasmodic narrowing or closing of coronary arteries can also cause myocardial ischemia, even when myocardial oxygen

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consumption is not increased.

Electrical Conduction in the Heart and the Electrocardiogram

A heart removed from the body can beat by itself. This is due to spontaneous electrical changes in the membranes of the cells, called depolarization, that lead to sudden entry of electrolytes into the cells. The electrolytes are rapidly pumped out, and the cycle begins again. This situation can be unstable if the beating of the cells is not coordinated. Specialized heart cells transmit electrical signals from pacemaker cells in a region of the right atrium called the sinus node along conduction pathways in the septum separating the right and left ventricles. The electrical conduction in the heart can be detected, and this is the basis for the electrocardiogram. The electrocardiogram (also called the EKG or ECG) includes characteristic components that correspond to the sum of the coordinated activations of cells in the heart. The P wave corresponds to electrical activation of the left and right atrium. This is followed by the Q, R, and S waves, or the QRS complex, that corresponds to depolarization of the right and left ventricles. Finally, the T wave represents repolarization of the ventricles in preparation for the next heartbeat.

Heart Block and Arrhythmias

Normally, the heart is driven electrically by the sinus node activity, and the resulting heart rhythm is called normal sinus rhythm, abbreviated NSR. Other regions of the heart can drive the heartbeat when the usual electrical conduction pathways are blocked. This situation is called heart block. In the most severe form of heart block, the atria and ventricles are activated

independently. In this situation, complete heart block, the heart rate is the intrinsic spontaneous activation rate of the ventricles and can be too slow (30 beats per minute) to provide adequate blood to the brain. Complete heart block therefore is one cause of sudden loss of consciousness, or syncope. When the pattern of heartbeats is irregular, this is called an arrhythmia. Arrhythmias can be

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associated with some types of heart block, but other forms of heart block are associated with regular heart rhythms, and arrhythmias can occur without heart block. When the ventricular cells are activated haphazardly, there is no effective heart contraction. ceases. Blood flow to all organs

This is ventricular fibrillation, probably the main immediate cause of sudden death.

Asystole is the absence of electrical activation of the cells, and also causes sudden death.

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CARDIOVASCULAR DISEASES AND THEIR KNOWN AND SUSPECTED CAUSES

Of the many cardiovascular conditions, a few require discussion here because of their frequency and importance in terms of sickness and death.

Coronary Heart Disease

The coronary arteries supply all the fuels and nutrients used by the heart. When this blood supply is inadequate, the cells of the heart can malfunction or die. The lack of adequate blood supply to the cells of the heart is called myocardial ischemia. The ischemia usually is due to coronary narrowing by fatty deposits in the walls of the arteries (atherosclerosis); other causes include spasm of the coronary arteries, severe loss of blood (such as anemia due to hemorrhage), and conditions associated with severely increased metabolism (such as thyroid "storm"). Myocardial ischemia can be clinically silent, with the first manifestation being sudden death. Myocardial ischemia can also be manifested clinically in the form of a particular form of chest pain or pressure called angina pectoris, or angina. And myocardial ischemia can be

manifested clinically by the sudden death (necrosis) of heart cells. When heart muscle in a region supplied by a coronary artery dies, this is myocardial infarction, or heart attack.

Myocardial lnfarction Pathophysiology

Myocardial infarction is the death of heart muscle due to inadequate coronary blood flow. It is thought that most myocardial infarctions are due to the formation of clot inside a coronary artery that has been narrowed by atherosclerosis. Nevertheless, myocardial infarction can occur in the absence of clot formation, such as in the setting of coronary spasm. The high frequency of clot formation explains why drugs that dissolve clots often are effective in patients with acute myocardial infarction.

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Diagnosis
Myocardial infarction can be clinically unsuspected, or silent, and discovered on postmortem examination. Recognition of myocardial infarction during life depends on clinical signs and symptoms, clinical procedures such as EGG, echocardiography, or nuclear cardiology scanning, and biochemical assays for elevations in blood levels of specific enzymes. The typical symptoms of myocardial infarction are the development, over seconds to minutes, of crushing, constricting pain under the breastbone (sternum), with shortness of breath or rapid breathing, sweating, and a feeling of great distress. The pain can spread (radiate) to the upper chest, neck, or left arm. The pain can last for hours. Other conditions besides myocardial infarction can produce these symptoms. If the

clinical picture is suggestive enough (e.g., these symptoms in an adult man with a history of smoking, high blood pressure, and family history of premature cardiac death), the diagnosis of myocardial infarction can be made presumptively. On physical examination, patients with myocardial infarction may have only nonspecific findings (signs). If the infarction is extensive enough to decrease the effective pumping of the heart, the blood pressure is low, resulting in weakness, delirium, or declining level of consciousness, and simultaneous activation of the sympathoadrenal system results in a fast, thready pulse, sweating, and pallor. Sudden increases in fluid leaking from capillaries in the lungs can produce crackle-like breath sounds (rales) and distention of veins in the neck. Reflux of blood through incompetent heart valves can produce whooshing sounds, called murmurs, and abnormal changes in the stiffness of the ventricles can produce extra heart sounds (gallops) heard through the stethoscope. The EKG signs of myocardial infarction include acute elevations of the segment between the S and T waves (ST segment elevation), inversion of the T waves, the development of Q waves,

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or the loss of upright QRS complexes. The heart in myocardial infarction is highly susceptible to arrhythmias or heart block, including lethal ventricular fibrillation or asystole. The detection and rapid treatment of ventricular arrhythmias is one of the main reasons for admitting patients with heart attacks to coronary care units. In some patients with myocardial infarction, the EKG is either normal or has non-diagnostic changes. All the EKG changes in myocardial infarction can occur without there being an acute myocardial infarction at the time; however, the evolution of classic EKG changes, including the return of elevated ST segments towards normal and the development of large Q waves, is diagnostic. Nuclear medicine scans of the heart in patients with myocardial infarction can detect regions where the heart muscle is not contracting or not being perfused with blood, depending on the technique employed, and echocardiograms can be used to detect non-contracting regions and estimate the fraction of blood ejected by the heart during each beat (ejection fraction). Chest X-rays can detect enlargement of the heart and the increased fluid in the lungs (congestive heart failure and pulmonary edema) that occur in extensive myocardial infarctions. The mainstay of the diagnosis of myocardial infarction during life is the measurement of levels of enzymes that diffuse into the bloodstream by myocardial cells when they die. Blood levels of the enzyme creatine kinase, or creatine phosphokinase (CPK), typically increase 4-6 hours after the infarction, peak at 1 day, and then return to normal within 3 days. Levels of serum glutamic oxaloacetic transaminase (SGOT) increase and subsequently decrease more slowly, with the peak at about 2-3 days. Levels of lactic dehydrogenase (LDH-l) usually increase beginning about 12 hours after the infarction, peak at about 4 days, and return to normal after 1-2 weeks. If none of these enzyme changes occur, myocardial infarction is excluded clinically. Since all these enzymes are present in other organs besides the heart, high levels of the enzymes do not prove that a myocardial infarction has occurred. A subtype, or isozyme, of CPK, called CPK MB, is thought to be specific to the heart, and levels of CPK MB indicate the presence

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and severity of myocardial necrosis in patients with heart attacks. Levels of CPK MB increase slightly more rapidly than total CPK and decrease more rapidly to normal. Since even CPK MB levels do not increase immediately in patients with myocardial infarction, the enzyme results can be negative in patients dying suddenly of heart attacks.

Treatment
The treatment of myocardial infarction mainly is conservative. Anti-arrhythmic drugs, such as lidocaine, often are used to prevent or treat ventricular arrhythmias. Electrical shock is used to treat ventricular fibrillation or rapid ventricular rhythms such as ventricular tachycardia that can degenerate into ventricular fibrillation. Heart block that produces symptoms or low blood pressure can be treated with electrical cardiac pacing. Myocardial oxygen consumption can be decreased by sedation and by blocking adrenaline and noradrenaline receptors using various drugs. Heart failure can be treated with vasodilators that relax blood vessels, decreasing cardiac preload or afterload or both. Low blood pressure due to myocardial infarction (cardiogenic shock) may require administration of drugs that increase the force of heart contraction (inotropic drugs) or increase total peripheral resistance (vasoconstrictors). These drugs increase myocardial oxygen

consumption, and so, the infarct can extend. The use of anticoagulants such as heparin has been very controversial for many years. Anticoagulants do not dissolve clots so much as prevent new ones. In contrast, newer

thrombolytic drugs dissolve clots, and evidence has accumulated that rapid treatment of patients with myocardial infarction using thrombolytics can lessen the loss of functioning tissue.

Complications and Prognosis

Complications of myocardial infarction include post-infarction chest pain (angina pectoris); arrhythmias or heart block; heart failure; shock; myocardial rupture; ballooning out of a weakened portion of the left ventricle (left ventricular aneurysm); inflammation of the sac around

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the heart (pericarditis); and formation of a clot lining the inner wall of the ventricle (mural thrombus). Twenty percent of patients with myocardial infarction are dead on arrival at the hospital. In-hospital mortality is about 10% and determined mainly by the size of the infarcted area. The developments of congestive heart failure or low blood pressure are associated with worse prognosis. After discharge, the mortality rate is about 7% in the first year and about 4% per year thereafter.

Angina Pectoris
Angina pectoris is a disagreeable sensation of pressure or squeezing beneath the sternum that results from myocardial ischemia. The pressure-pain can radiate to the neck, jaw, or arm. Typically, angina pectoris is brought on during exercise, emotion, exposure to cold, or after a large meal and disappears within minutes of resting or taking nitroglycerine under the tongue. There can be sweating, pallor, or shortness of breath. In angina due to fixed narrowing of coronary arteries, the symptom develops reliably when myocardial oxygen consumption exceeds supply. In "dynamic" obstruction due to spasm,

ischemia may not be associated with increased myocardial oxygen consumption. In the setting of mild or moderate coronary atherosclerosis, relative ischemia due to increased metabolism or anemia can produce angina. Angina can be a chronic problem. There is an increased risk of myocardial infarction and sudden death, but the overall mortality is only a few percent per year. Attacks of angina pectoris probably do not produce any permanent myocardial damage per se.

Diagnosis
Angina pectoris is a symptom, not a disease. The diagnosis therefore is virtually entirely clinical--based especially on a carefully obtained medical history. Laboratory testing supporting the diagnosis of angina pectoris includes EGG, exercise stress

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testing, ambulatory EGG monitoring, tests of esophageal function, and cardiac catheterization with coronary angiography. Since the EKG at rest may be normal, exercise testing and

ambulatory monitoring are designed mainly to detect depression of the ST segment or alterations in the T wave, signs of myocardial ischemia that, if they disappear at rest, support the diagnosis of angina pectoris. Ambulatory monitoring can detect ischemic EKG changes or arrhythmias at particular times of day. Since inflammation or spasm of the esophagus can cause substernal chest pain that can mimic angina pectoris, tests of esophageal function can be performed in unclear cases. Coronary angiography involves injecting a radiologic contrast medium into the coronary arteries to detect sites of narrowing due to atherosclerosis. Provocative tests for coronary spasm also can be performed. Since atherosclerosis is common, the finding of atherosclerotic narrowing supports but does not prove the diagnosis. If the arteriogram is normal, ischemic heart disease is unlikely but still possible, such as in the microvascular angina due to limited coronary vasodilator reserve, coronary spasm, or diseases of heart muscle (cardiomyopathies). Two types of nuclear cardiology scans are used in the evaluation of patients with possible angina pectoris. Thallium-201 scanning shows areas of myocardial perfusion. During exerciseinduced angina or after administration of vasodilators that "steal" blood away from the involved coronary artery, ischemic regions have decreased uptake of the tracer. Radionuclide

angiography involves injection of a radioactive tracer that labels the pools of blood in the ventricles. The ejection fraction normally increases during exercise but can decrease in patients with angina. Areas of abnormal wall motion also can be seen.

Treatment
The treatment of choice for acute attacks of angina pectoris is sublingual nitroglycerine. Nitroglycerine and drugs similar to it dilate arterioles and veins, leading to decreased afterload and preload and decreased myocardial oxygen consumption.

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Attacks of angina can be prevented by several types of medication, including nitrates such as nitroglycerine, beta-adrenergic blockers such as propranolol and atenolol, and calcium channel blockers such as verapamil, diltiazem, and nifedipine. Platelet-inhibiting drugs such as small doses of aspirin also are commonly prescribed. When angina is disabling despite maximum drug therapy, or in the setting of certain types of coronary anatomy, coronary bypass grafting or coronary angioplasty are performed.

Hypertension (High Blood Pressure)

Hypertension is the chronic elevation of blood pressure. As blood pressure increases, longterm mortality increases. There is no definite threshold above which hypertension produces

decreased life span. A commonly used clinical criterion is a systolic blood pressure more than 140 millimeters of mercury (mm Hg) or a diastolic pressure more than 90. In the vast majority of cases, the cause of hypertension is unknown, and this is called primary or essential hypertension. Diseases that can cause secondary hypertension include kidney failure, narrowing of a renal artery (renal artery stenosis), and over stimulation or tumors of the adrenal cortex, adrenal medulla, or thyroid gland. Secondary hypertension also occurs in some women late in pregnancy or while taking birth control pills. Hypertension is a risk factor for atherosclerosis, kidney failure, heart failure, and strokes. There are several medical treatments for hypertension: diuretics, such as

hydrochlorothiazide; beta-adrenoceptor blockers, such as propranolol and atenolol; alphaadrenoceptor blockers such as prazosin; drugs that inhibit sympathetic nervous system activity, such as clonidine and alpha-methyldopa; drugs that inhibit release of norepinephrine from sympathetic nerve endings or deplete norepinephrine stores, such as guanethidine; drugs that block the formation of angiotensin II, such as captopril and enalapril; drugs that block calcium channels, such as nifedipine, verapamil, and diltiazem; and direct-acting vasodilators, such as minoxidil and hydralazine. These drugs all can have side effects.

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Non-pharmacological treatments for hypertension include restriction of dietary salt intake; supplementation of dietary calcium or potassium; weight loss; exercise training; and biofeedback or relaxation training. The efficacy of all these treatments varies widely among patients. Control of hypertension has been thought to be responsible for the decline of mortality due to stroke in recent years in the United States. Treatment with antihypertensive drugs has not, however, been found to decrease mortality due to coronary heart disease; the reason is unknown.

Sudden Death
Sudden death is defined as unexpected, non-traumatic death where the patient dies within 1 hour of the onset of symptoms. There is no breathing, pulse, consciousness, or

responsiveness. In the present discussion, sudden death and sudden cardiac death are used synonymously. The majority of patients suffering sudden death have severe coronary artery disease. Sudden death is the first manifestation of coronary disease in about 20% of patients. Sudden death is a common cause of mortality in patients with acute myocardial infarction.

Pathophysiology
Sudden cardiac death usually is due to uncoordinated beating of heart muscle cells (ventricular fibrillation) or lack of electrical activation of those cells (asystole).

Treatment
Ventricular fibrillation can be treated successfully by electrical shock (defibrillation). Asystole is thought to be unresponsive to defibrillation but can respond to intravenous or intracardiac injection of epinephrine (adrenaline). Drugs commonly used in support of patients with cardiac arrest include antiarrhythmics, such as lidocaine, bretylium, and procainamide; sodium bicarbonate to combat acidosis; and drugs that stimulate the force of the heartbeat or increase blood pressure, such as calcium, norepinephrine, epinephrine, dopamine, isoproterenol, and dobutamine.

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Long-Term Consequences
Cardiopulmonary resuscitation and advanced cardiac life support, including electrical defibrillation, result in the survival of a minority of patients with sudden death. The risk of recurrence is high.

Heart Failure Definition

Heart failure is not a disease, but a pathophysiologic state. It is not a heart attack. Heart failure is a condition where there is an inability of the heart to pump blood sufficiently to meet the demands of the body, or where those demands can be met only by increasing cardiac filling pressures. Rarely, the cardiac pumping function can be normal or even increased and yet still be inadequate when there are excessive metabolic demands, such as in severe anemia, abnormal shunts between an artery and a vein (arteriovenous fistulas), regurgitation of blood due to incompetent heart valves, and thyrotoxicosis. More typically, heart failure is due to decreased pumping ability. Often the abnormality becomes apparent clinically only during states of increased metabolic demand, such as exercise, emotion, blood loss, increased salt intake, or bloodstream infection. Failure of the right side of the heart can occur in chronic pulmonary disease and clot blocking the pulmonary arteries (pulmonary embolus).

Occurrence
Failure of the left side of the heart occurs in hypertension, myocardial infarction, arrhythmias, diseases of heart muscle (cardiomyopathies), abnormalities of heart valves, restriction of filling due inflamed or scarred membrane around the heart (pericarditis), and inflammation of the heart (myocarditis). Cardiomyopathies include overgrowth of heart muscle (hypertrophic cardiomyopathy), restriction of heart filling (restrictive cardiomyopathy), infiltration of the heart with

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non-contractile substances (infiltrative cardiomyopathy), and enlargement of the ventricular chamber (dilated cardiomyopathy).

Symptoms and Signs

In failure of the right side of the heart, increased pressure in systemic veins that empty into the right atrium results in enlargement of veins of the neck, engorgement and enlargement of the liver, and swelling of the dependent parts of the body (edema). In failure of the left side of the heart, increased pressure in the lungs results in shortness of breath (dyspnea) or coughing, especially when the patient lies down. In chronic left heart failure, however, all these clinical symptoms and signs can occur, due to retention of salt and water. Heart failure has been thought to result in salt and water retention for two general reasons: in "backward heart failure", increases in ventricular filling pressures result in backup of blood and increased systemic vein and capillary pressures, with transudation of fluid; in "forward heart failure" the decreased ejection of blood into the arterial system results in increased neuroendocrine activity that has the net effect of retaining salt and water. Hemodynamic, neural, and hormonal factors all contribute to the retention of salt and water in heart failure. When the kidney receives decreased blood flow, it filters less fluid.

Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system inhibits the ability of the kidney to excrete sodium. Increased levels of vasopressin, or anti-diuretic

hormone, result in the retention of water. The net effect of activation of these systems is to increase the filling pressures in the heart. This compensates for the decreased cardiac function and results in a relatively stable situation called compensated heart failure. Pulmonary edema is a severe increase in fluid in the interstitial space between cells in the lungs. The most common cardiac causes of pulmonary edema are acute myocardial infarction or acute overload of the left ventricle producing heart failure, and mitral stenosis, a valvular narrowing typically in patients with a history of rheumatic fever. Non-cardiac pulmonary edema

41

can result from conditions including severe systemic infections, blockade of draining lymphatic channels, some toxins, intra-thoracic suction by chest tubes, severe pancreatitis, exposure to high altitude, aspiration, and cardiopulmonary bypass.

Treatment
The treatment of heart failure includes specific and non-specific approaches. Reversible causes of heart failure include thyrotoxicosis, abnormal heart valves, shunting of blood inside the heart, high-output states such as severe anemia, and alcohol-and drug-induced cardiomyopathy. Patients with heart failure routinely are prescribed salt-restricted diets. The main forms of non-specific treatment for heart failure include: diuretics; digitalis glycosides such as digoxin; vasodilators to reduce preload, afterload, or both, such as nitrates, hydralazine, and prazosin; and drugs that inhibit the formation of angiotensin and aldosterone (angiotensin-converting enzyme, or ACE, inhibitors). Adjunctive treatment can include

anticoagulation, anti-arrhythmic drugs, and (in cases of dilated cardiomyopathy) low doses of beta-adrenoceptor blockers. Cardiac transplantation for heart failure is effective in some patients but is limited by cost and organ availability. The mortality in one year is about 10-20%. In pulmonary edema, treatment includes oxygen, morphine (to allay anxiety and decrease ventricular preload), rapidly-acting diuretics such as furosemide, nitrates, tourniquets applied in a rotating fashion on the limbs, blooddrawing (phlebotomy), and anti-asthmatic drugs such as aminophylline. In refractory pulmonary edema, hemodialysis can be done.

Prognosis
Although heart failure can be compensated for years, the long-term prognosis is poor, with annual mortality rates from 10 to 50% depending on the severity of the symptoms. About 1/2 of patients with heart failure die suddenly, presumably due to arrhythmias.

Stroke

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Stroke is the sudden occurrence of a neurologic deficit, with distinctive neurologic signs indicating the region of the brain that is involved. Despite a general decline in the frequency of stroke in recent years, it remains the third most common cause of death in the United States. There are several pathophysiologic mechanisms of stroke. They produce their effects by ischemia of a region of the brain or by increasing pressure inside the skull (intracranial pressure). Thrombosis (clot), the most common form, and embolism, the sudden movement of a piece of clot or other debris in arteries to the brain, result in blockage of an artery in the brain. Hemorrhage due to rupture of a blood vessel such as an aneurysm and hemorrhage into the subarachnoid space increase intracranial pressure. The treatment for a completed stroke generally is supportive. Anticoagulants are used in patients with clinical evidence of thrombosis. Thrombolytic drugs are being studied in clinical trials. When subarachnoid hemorrhage is due to rupture of an aneurysm or arteriovenous malformation, and the patient survives, neurosurgery is feasible.

Aneurysm
Aneurysm is a general term to describe a dilatation of a portion of the cardiovascular system. Arterial aneurysms can be located at sites along the aorta, the coronary arteries, and in the brain. They can be congenital; develop due to degenerative diseases of blood vessels, such as atherosclerosis and diseases of collagen, a structural protein; or can result from trauma. Ventricular aneurysms form in cases of extensive myocardial infarction where the muscular wall is thinned or does not contract. During systole, the aneurysm may balloon outward, compromising cardiac output. Ventricular aneurysms can fill with clot, increasing the risk of systemic emboli, and are associated with a high frequency of arrhythmias and heart failure. Aneurysms can be totally asymptomatic or can rupture or dissect. In dissection, the wall of the blood vessel is slit and the false channel fills with blood. This can produce arterial blockage. The dissection of an aortic aneurysm can extend back towards the heart or down the aorta

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towards the kidneys. Dissecting aortic aneurysms are surgical emergencies and can be corrected in some cases.

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DIAGNOSTIC TESTING IN CARDIOLOGY

1. Medical History
Symptoms are subjective manifestations of abnormal physiology. Their type, severity, onset, and evolution comprise the essential elements of a medical history. Eliciting a complete and accurate medical history is often a difficult task. Frequently, an acutely ill patient is unable to provide a full history. Patient histories can also be clouded by the effects of medication, underlying disease, lapses of memory, or intentional or unintentional misinformation. In compensation cases involving allegations of stress-related disease, the medical history may be distorted by a potential financial or secondary gain. The medical history ideally should include detailed information about the nature, extent and onset of the patient's symptoms. Information about current medications, other treatments received, and allergies, is routinely elicited. Critical to compensation claims is the taking of a social history from the patient. The social history should include questioning about cigarette smoking, alcohol consumption, coffee consumption, current or prior mental health problems, current or prior drug dependency, exercise habits, and changes in weight or diet. In cases involving allegations of stress-related disease, the social history should include questioning about marital status, the health of the patient's family, and sources of perceived stress other than stress on the job. It is not at all uncommon to discover that a claimant alleging disability due to job stress is simultaneously experiencing stressful personal problems such as divorce, death of a spouse or child, or provision of care to elderly or ill parents. When reviewing a case involving a claim of job stress induced cardiovascular disease, an effort should be made to examine the medical and social histories given by the worker to all medical providers. Frequently, the history given to an examining physician will differ from the history provided to emergency room personnel or prior family practitioners. A review of information

45

disclosed in pre-employment physicals and medical records from earlier non-work related conditions may also be of some benefit in determining the accuracy of the history given following the allegedly work-related event.

2. Physical Examination
Physical abnormalities are the objective signs of disease. The presence and form of

physical abnormalities is documented by physical examination. Physical examination includes observations of the patient and the recording of data following various testing performed. Although the examination of the heart is the most important part of the physical examination, a meticulous general physical exam is extremely important. The examination starts with the general appearance of the patient. Does the patient appear ill or well? Does the patient appear nourished or malnourished? Examination of the eyes, and in particular the fundi (eyegrounds) may be helpful in identifying patients with high blood pressure (hypertension) since chronic changes may be seen. Examination of the skin is very important and includes the mucous membranes (the lips and mouth). Cyanosis is a bluish color which may result from poor cardiac output (peripheral cyanosis involving the extremities, nailbeds and nose) or from diminished oxygen levels in the blood (central cyanosis involving the entire body). Clubbing of the fingers and toes is another manifestation of chronic central cyanosis. The soft tissue of the nail becomes enlarged and causes obliteration of the angle between the nail and the skin. Clubbing is usually seen with more chronic disease, and in particular chronic

cyanotic heart disease or severe pulmonary disease, but it can also be a normal variant. Palpation of the pulses gives a good estimation of the pulse pressure, indirectly related to the cardiac output. The best place to feel for pulses is the carotid artery, located on either side of the neck. A strong pulse indicates a wide pulse pressure. Other areas to feel for pulses are the elbow (brachial pulse), wrist (radial pulse), groin (femoral pulse), behind the knee (popliteal) and in

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the feet (posterior tibial and dorsalis pedis). A weak and thready pulse is an indication of a low pulse pressure, as occurs if there is poor blood supply to the extremities. Examination of the chest includes observations of respiratory rate, effort, and regularity. In the abdomen, painful enlargement of the liver, called hepatomegaly, occurs with congestive heart failure. In advanced congestive heart failure, the spleen may be palpable (splenomegaly). Jugular venous distension is a frequent finding in congestive heart failure. The jugular veins run along the neck and become distended when the heart fails. Fluid also backs up from the heart in congestive heart failure. When the left side backs up into the lungs it causes pulmonary edema. This may be heard by listening to the lungs with a stethoscope and hearing rales. These patients usually have an increased effort of breathing at rest and respond to oxygen and diuretics to remove this fluid from the lungs. Blood backing up from the right side of the heart causes jugular venous distension, hepatomegaly, fluid within the abdomen (ascites), and increased fluid in the legs. Fluid in the extremities is termed edema. Edema of the extremities can be seen either by swelling of the hands or feet or pushing on the skin to see if there is extra fluid there (pitting edema). This fluid can be decreased by the administration of diuretics. Measurement of blood pressure is done with a sphygmomanometer cuff. The cuff should fit snugly around the arm. The standard size cuff for an adult is 5 inches wide, but an 8 inch cuff is necessary in obese adults. In general, the width of the cuff selected should be at least 40% of the circumference of the limb to be used. If a cuff is used which is too small, blood pressure will be overestimated. The patient should be seated or lying comfortably and relaxed. The cuff is then inflated to a value approximately 30 mm Hg above the expected systolic value. A normal value of blood pressure in the adult is 120/80 mmHg, or 120 systolic and 80 diastolic.

Every blood pressure reading should have 2 numbers associated with it. A stethoscope is placed in the antecubital space (elbow) at the area where the brachial pulse can be felt. The

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cuff is then slowly deflated. The first appearance of clear tapping sounds represents the systolic pressure. The disappearance of the sounds is the diastolic pressure. Elevated blood pressure is termed hypertension. Multiple measurements at different times should be made before a patient is labeled as hypertensive. Sometimes even the anxiety of having the blood pressure taken can cause elevations. Low blood pressure is termed hypotension, and often is a sign of low cardiac output.

Examination of the Heart

There are three main points of the cardiac physical examination - inspection, palpation and auscultation. One should first visualize the chest and look for areas of abnormal

cardiovascular pulsations. The fingers are then used to palpate the heart. One can palpate the point of maximal impulse. If the point of maximum impulse is displaced, it can be a sign of enlargement of the heart. A sustained outward movement of an area of the heart is termed a heave or lift and can arise from enlargement of the right or the left ventricle. Auscultation of the heart is done with the stethoscope. There are 4 heart sounds. S1 is due to closure of the mitral and tricuspid valves, whereas S2 is due to closure of the aortic and pulmonic valves. S1 may be increased in various situations. S1 is normally split but the splitting may be wide in various conditions. Splitting and increased intensity of the second heart sound are equally important and may be abnormal in various situations. S3 and S4 are extra sounds not usually heard. They can however be normal. When they are abnormal they are called gallops or gallop rhythm. S3 can be heard in normal healthy children and young adults, whereas they are usually abnormal in older ages. Healthy older adults may have an S4 but it is usually abnormal in children. Also heard can be ejection clicks, either diastolic or systolic. The most common is an ejection click due to mitral valve prolapse. Clicks are always abnormal and usually indicate a problem with one of the cardiac valves. It is important also to listen for cardiac murmurs, which are whooshing sounds heard

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through the stethoscope. They are classified as systolic (between S1 and S2) or diastolic (between S2 and S1). They are also sub classified as early, mid, late or pan (throughout) systolic or diastolic. The intensity of a murmur is determined by the quantity and velocity of blood flow across the sound-producing area and its distance from the stethoscope. Murmurs are usually graded from 16, with a 1/6 murmur being the faintest and a 6/6 being the loudest. A thrill occurs when the murmur is felt on the chest and indicates at least a grade 4 murmur. Many murmurs may be innocent and do not signify pathology. The way a murmur sounds by auscultation can indicate whether it is innocent or pathologic. Dynamic auscultation uses a variety of physiologic and pharmacologic maneuvers to alter circulatory dynamics. These include respiration, postural changes, isometric exercise, and drugs. Using these maneuvers may help to classify murmurs and determine which ones require further investigation.

4. Electrocardiography (EKG or ECG)

An electrocardiogram is the major screening test in cardiology and provides a great deal of information regarding the status of the cardiovascular system. In general, an EKG is performed with 12 leads: 6 leads from the arms and legs - the limb leads, and 6 leads across the chest - the precordial leads. Sometimes 15 lead EKG's are done, which include 3 extra precordial leads, but these are not usually necessary for the interpretation. A rhythm strip of any lead may also be included. The limb leads are labeled I, II, III, AVR, AVL and AVF. The precordial leads are labeled V1V6. Each of these 12 leads is necessary for a full understanding of the cardiac status. Each cardiac beat should consist of a P wave, a QRS complex, and a T wave. There are also three intervals which are measured - the PR, the QRS, and the QT intervals. These intervals give an idea of conduction through the heart. If they are prolonged, there is often disease in the conduction system, but abnormal electrolyte levels and various drugs can also affect these intervals. The ST

49

segment is important in evaluating coronary artery disease. It is that portion of the EKG from the end of the QRS complex to the beginning of the T wave. Depression of the ST segment and inversion of T waves often indicate coronary ischemia. Interpretation of the EKG is divided into several parts. The heart rate and rhythm should first be established. The rhythm of the heart arises from the pacemaker of the heart, which is called the sinus node. This area is in the right atrium. From here, the impulses travel through the atria to the AV node, and then through the bundle branches to the ventricles. When the rhythm originates in this fashion it is called sinus rhythm. Normal sinus rhythm occurs at a rate of 60-100 beats/minute. When rates are faster than usual, they are called tachycardias. When they are slower than usual they are called bradycardias. Thus, a rhythm originating from the normal place in the heart at a faster than usual rate is called sinus tachycardia. There can be many reasons for sinus tachycardia and sinus bradycardia besides disease of the heart itself. When rhythms originate at areas other than the sinus node, they are termed arrhythmias. These other rhythms are called supraventricular tachycardia (SVT) or ventricular tachycardia (VT). Examples of SVT are atrial tachycardia, AV nodal reentry, atrial flutter, and atrial fibrillation. Ventricular tachycardia may degenerate to ventricular fibrillation. This is an unorganized, chaotic rhythm of the heart which provides no cardiac output. Ventricular fibrillation is a common cause of sudden death. The treatment of ventricular fibrillation is by defibrillation. This is accomplished by providing an electrical shock on the outside of the chest to try and resume a normal rhythm. The treatment of SVT or VT is either by drug therapy or by cardioversion (application of an electric shock synchronized to the patient's own rhythm). Heart block is another important EKG finding. If there is heart block, which can result from a heart attack, the rate generally is slow. There are three fascicles which supply conduction to the ventricles. Complete heart block occurs when all three fascicles are affected. Bifascicular block may be worrisome. Complete heart block generally results in a slow heart rate and requires

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insertion of either a temporary or permanent pacemaker. Although heart block is divided into first, second and third degree, only second and third degree may require pacemakers. Frequently, patients may also have extra beats of the heart during normal sinus rhythm. These are called ectopic beats or premature beats. They may be perceived as palpitations. If they come from the upper chambers of the heart, they are called PAC's (premature atrial contractions). If they come from the lower chambers, they are called PVC's (premature ventricular contractions). PAC's and PVC's may occur in normal individuals. Frequent PVC's are of concern in a patient with an abnormal heart, especially in the setting of acute myocardial infarction. PVC's can be uniform or unifocal, which means they come from one focus. This is generally more benign. If they occur from different focuses they are called multiform or multifocal. When two PVC's occur together, this is called a couplet or a pair. Three or more PVC's together is generally regarded as ventricular tachycardia. The EKG also can provide information about the status of the cardiac chambers and the flow through the coronary arteries. If the wall of a chamber is enlarged, this is called hypertrophy. There may be hypertrophy of the right atrium, left atrium, right ventricle or left ventricle. There are standard criteria that are generally used to evaluate for hypertrophy, but these may vary slightly among different published sources. Insufficient coronary blood flow, or coronary insufficiency, results in changes in the ST segments and T waves. These may be depressed or elevated, in one or several electrocardiographic leads. The leads which have changes can indicate which part of the heart is ischemic. If the ischemia resolves, the ST segments can return to normal. Prolonged, severe ischemia leads to a myocardial infarction. Cardiac muscle which loses its blood supply, dies, and is ineffective in providing contractile function is infarcted muscle. Q waves may develop on the surface cardiogram when a myocardial infarction occurs. Some Q waves may be normal. In addition, some ST segment changes may be nonspecific and may not be indicative of impending infarction. The term silent ischemia refers to changes in ST segments

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without chest pain. Some patients can have a silent myocardial infarction that can be diagnosed from the EKG.

5. Ambulatory Electrocardiogram

(Holter Monitor)

The ambulatory electrocardiogram, or Holter monitor, is a 24 or 48 hour recording of the heart rhythm. Leads are placed across the chest and the EKG is recorded by a tape recorder. This test can be performed either in a hospital or on an outpatient basis. In general, it is used to try and correlate symptoms with an abnormal heart rhythm. It may also be used as a guide to therapy in patients who may be having frequent rhythm problems. Many patients with coronary artery disease, and particularly those recovering from a myocardial infarction, have PVC's (premature ventricular contractions). This increases over the first several weeks and decreases at about 6 months. Although there is no agreement about the significance of individual properties of the PVC's, increased frequency and more complex forms of ventricular ectopy indicate an increased risk of sudden cardiac death in patients with a history of heart attack. Whether treatment of these extra beats will result in decreased mortality is unclear. In fact, certain drugs may exacerbate these abnormal rhythms. Newer scanners are able to evaluate ST segments as well. evaluating patients with silent ischemia. This may prove useful in

Not enough information regarding this technique is

currently available to draw conclusions about its validity.

6. Chest X-Ray
A chest x-ray (CXR) is an easy test that provides information about the heart size and the status of the lungs. Information is obtained both from the PA (anterior-posterior) and the lateral views. A chest x-ray can be done either in the x-ray department of a physician's office or hospital, or, in an emergency, can be performed on portable x-ray machines. The heart size may be normal or enlarged. An enlarged heart is termed cardiomegaly and can be mild, moderate or severe. When the heart fails, the heart size becomes enlarged. A build up of fluid in the lungs

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causes congestion in the lungs which, when severe, is called pulmonary edema. Congestive heart failure and pulmonary edema produce characteristic findings on a regular chest x-ray. One can also see accumulations of fluid around the lung itself, a phenomenon called a pleural effusion. Chest x-rays are frequently used serially to follow the cardiac size and the improvement or deterioration in the pattern of pulmonary edema.

7. Echocardiogram
An echocardiogram is a non-invasive way of looking at the internal chambers of the heart by a "sonar" type device. This is done by utilizing ultrasound to record information in the form of echoes. The ultrasonic transducer is placed on the surface of the chest and directed to the part of the heart to be examined. The technology of echocardiography has changed tremendously in the last 10 years. The first type, an M-mode, utilized only one dimension. These studies have now been almost replaced by two-dimensional echocardiography. "2-D" echos show movement of the heart in real time. The cardiac chamber sizes can be measured to see if they are enlarged. Heart function can also be determined. This is usually measured as the shortening fraction. A normal echocardiographic shortening fraction is 28-33%, which indicates that the heart is ejecting a normal amount of blood. In heart failure, the shortening fraction is diminished, sometimes markedly. This measurement is similar to the ejection fraction, which is measured during nuclear studies and catheterization. A normal ejection fraction is 60-70%. An echocardiogram can also allow visualization of the movement of the ventricular walls. Asymmetric movement of the wall or the ventricular septum may indicate an area of ischemia or infarction. There are other sophisticated measurements obtainable from the echocardiogram which are less useful clinically. Doppler echocardiography utilizes ultrasound to determine the velocity of blood. This is particularly helpful in evaluating flow across stenotic (narrowed) valves and regurgitant (leaky)

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valves. The severity of the obstruction or the regurgitation can be determined. Color flow Doppler has helped in identifying stenotic and regurgitant jets across abnormal valves. The coronary arteries are difficult to visualize by echocardiography. Although their origins may be seen, the resolution of the technique, to date, does not allow identification of occluded or narrowed coronary arteries.

8. Stress Testing
Exercise stress testing is used to aid in the evaluation of chest pain or arrhythmias. During exercise, both the electrocardiogram and blood pressure are continuously monitored. The EKG is monitored for changes in the ST segments, which may indicate ischemia (reduced blood flow). The maximal heart rate and blood pressure are measured. If the patient develops chest

discomfort, this can be correlated with any changes seen on the EKG. After baseline values are obtained, exercise is usually carried out on a motor-driven treadmill following a standard protocol. The patient is taken through different stages of exercise which are progressively more difficult. The EKG is continuously displayed, recorded once per minute. The blood pressure is usually recorded at the end of each stage of exercise. The test is continued until terminated by symptoms, exhaustion, the appearance of ST changes or arrhythmia. There are different protocols for evaluation of chest pain or rehabilitation following heart attack. The response of the patient to exercise may assist in the choice of therapy. Most controversial is the use of exercise stress testing as a screening test for coronary disease in the asymptomatic general public. In asymptomatic individuals, abnormal results are likely to be false positive results. It may though be useful in evaluating an individual's risk of

developing heart disease, when used in conjunction with lipid screening, high blood pressure, smoking history, age, sex, or a strong family history of coronary disease.

9. Nuclear studies

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Nuclear studies are also non-invasive and extremely useful. They can be conducted even in critically ill patients. They are also useful for serial measurements following myocardial infarction. The testing involves injection of a radioactive substance into a peripheral vein. The substances used are technetium-99m or thallium 201 and are relatively safe. The tests are performed by radiologists. The data obtained can be utilized to evaluate ventricular ejection fraction, regional wall motion abnormalities, and defects in distribution of the radionuclide in the heart muscle. The location of the defect on the radionuclide scan helps to identify which coronary vessel may be diseased. As mentioned earlier, the ejection fraction is a measure of how well the heart is pumping blood. The ejection fraction supplies prognostic information, since the ejection fraction is a

predictor of early mortality and the development of congestive heart failure or sudden death. Regional wall motion abnormalities may indicate areas of the heart that have been infarcted. These are best done using technetium-99m. This is frequently called a MUGA (multi-gated

acquisition) scan. This test can be done at rest or with exercise. The studies can also be performed as a first pass study or as an equilibrium study. During first pass, measurement of cardiac

performance is done from the initial transit of radiotracer through the heart. During equilibrium studies the radionuclide must reach equilibrium in the vascular space prior to imaging. To improve resolution, count acquisition is gated to a physiologic marker, such as the electrocardiogram (gated nuclear scan). Although both first pass and equilibrium studies provide accurate

information regarding cardiac performance, the gated equilibrium study is more widely used. This test can also be performed during exercise to see the response of the ejection fraction to exercise. Thallium-201 exercise testing provides a more reliable map of the pattern and location of a regional abnormalities of blood flow to heart muscle. Thallium is injected at the time of maximal exercise stress testing. Scanning is then performed looking for abnormalities in uptake of the

thallium in the heart. These are then compared to a resting study 3-4 hours later. This test is

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significantly more accurate than the exercise stress test alone in the detection of coronary heart disease. To maximize the accuracy of the test, a heart rate of at least 110 beats/minute should be achieved with exercise.

10. Cardiac Enzymes

Dying cells in the heart release a number of enzymes into the blood which can be measured. The three enzymes generally measured are creatine kinase (CK), glutamic oxaloacetic transferase (GOT), and lactic dehydrogenase (LDH). CK peaks the earliest, about 24 hours,

whereas GOT follows at 18-36 hours and LDH is the latest, rising and falling more slowly and peaking at about 3-6 days after the onset of pain. All of these enzymes are found in other organs of the body, but they can be fractionated into isozymes or isoenzymes, to tell if an elevated value is related to the heart or to another organ. For CK, CK-MB is found predominantly in heart, and CK-MM and CK-BB are found in brain and skeletal muscle. Thus elevation of CK-MB is indicative of myocardial damage. LDH may also be fractionated into 5 isoenzymes. The heart principally contains LDH 1. Patients suspected of having a myocardial infarction, with chest pain and

electrocardiographic changes virtually always undergo serial measurements of these enzymes. Persistently elevated levels help support the diagnosis of myocardial infarction, whereas normal levels exclude the diagnosis.

11. Cardiac Catheterization

When there is a strong suspicion that there is a problem with the coronary arteries, a cardiac catheterization is performed to actually look at the distribution of flow in the coronary arteries. Patients are usually sedated and, after administration of local anesthesia, a catheter is inserted into the femoral vein and femoral artery in the groin. A right heart catheterization via the femoral vein is then performed. This helps in assessing the degree of heart failure. Frequently recorded is a pulmonary arterial wedge pressure, which is the best indicator of left ventricular

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function from a right heart catheterization. The catheter in the femoral artery can then used for a left heart catheterization. This involves placement of the catheter through the aorta and into the left ventricle. Cardiac output, the amount of blood the heart ejects per minute, can be measured by various techniques using right or left approaches. The coronary arteries are visualized by performing angiograms. An angiogram is a movie done after injecting a radiographic dye into the vessel. Angiograms can be selective if done in an individual coronary artery. Since there is a right and a left coronary artery, these are generally the vessels that are visualized. A narrowing in a blood vessel it is called a stenosis. In general, a significant stenosis is when there is at least a 75% narrowing of the vessel. Sometimes, however, a lesser degree of narrowing may be significant. The major branches of the coronaries must be visualized - the right coronary and the left main coronary, which then divides to the left anterior descending and left circumflex. Other major branches can be large and have significant stenoses as well, such as diagonal and marginal branches. The incidence of complications of cardiac catheterization is low, although careful attention to detail and meticulous technique is required to achieve this standard of performance. Patients at increased risk include those over 65 years of age, those with severe congestive heart failure,and those with left main disease (10 times greater risk). Those patients also with other severe non-cardiac disease seem to be at increased risk of complications. Complications of cardiac catheterization include clots either on the catheters themselves or within the vessels. If a part of a clot breaks off, this is called an embolus. This can travel to various parts of the body and can be particularly serious if it goes to the brain, since this may result in a stroke. Perforation of the heart can occur. Contamination of catheters or fluids can result in infection. Arrhythmias and tears in coronary artery walls are also possible.

12. Treatment of Coronary Artery Disease 57

After the diagnosis of coronary artery disease has been made there are several therapeutic options. Following a myocardial infarction, one option is the use of thrombolytic therapy. Thrombolytic therapy involves the use of a drug to try to dissolve the clot (thrombus). If the infarction is very fresh, a substance such as streptokinase or TPA (tissue plasminogen activator) can be infused into a peripheral vein or directly into the coronary vessels to dissolve the clot within the coronary artery itself. Information regarding the superiority of thrombolytic therapy over other forms of therapy is currently being investigated. The major side effect of these drugs is the risk of serious bleeding. Percutaneous transluminal balloon angioplasty (PTCA) is a rather new procedure that can be done at the time of cardiac catheterization. A balloon catheter is placed across the This can be done either in lieu of

obstructed vessel to improve blood supply to the vessel.

thrombolytic therapy, after thrombolytic therapy has failed, or after successful thrombolysis when a significant severe residual obstruction remains. In general this is done when there is only single vessel disease but researchers have been investigating the role of balloon angioplasty for dilating multiple vessels. It is never done for disease of the left main coronary, because there is a high risk of myocardial infarction. The major problem with balloon angioplasty is that there appears to be a 30-40% restenosis rate. However, this is a procedure that can be done for patients with intractable or unstable angina without the need for surgery. Its current role and its risk/benefit ratio relative to surgery is under investigation. Coronary artery bypass grafting (CABG) is the usual surgical approach to the treatment of coronary artery disease. In this procedure, the saphenous vein, a superficial vein from the leg, or the internal mammary artery, an artery in the chest, is used to bypass the obstruction(s). This has become a relatively common form of treatment for coronary artery disease, particularly for multivessel disease. It can be performed relatively safely and with good results.

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Surgery is indicated when medical management of angina pectoris is unsatisfactory or in cases with particular types of coronary anatomy. The presence of coronary narrowing of itself in asymptomatic patients is not an indication for surgery, since, depending on the sites of the

narrowing, survival may not be increased by the surgery.

13. Blood Studies

Blood should be drawn and evaluated for glucose, cholesterol and triglyceride levels. As discussed in other chapters of this manual, elevated glucose levels can indicate diabetes, a risk factor in the development of cardiovascular disease. Cholesterol and triglyceride levels should also be reviewed to determine whether hyperlipidemia, another suspected risk factor for heart disease, is present. coronary risk. Analysis of lipoproteins or apo-lipoproteins also can be done to indicate

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RISK FACTORS FOR CARDIOVASCULAR DISEASE

Medical science has thus far failed to identify the exact pathophysiologic mechanisms of cardiovascular disease in humans. Considerable success has been achieved, however, in

identifying risk factors for cardiovascular disease. There is a virtual consensus among researchers that certain factors are clearly and strongly related to the development of cardiovascular disease. Many individuals with one or more risk factors for the development of cardiovascular disease never develop diagnosable disease. Conversely, many individuals die cardiovascular deaths or suffer cardiovascular disabilities without any indication of the presence of any of the recognized risk factors. During investigation and litigation of cardiovascular disease cases,

therefore, caution must be exercised to avoid confusing presence or absence of risk factors with the issue of causation. A great deal of time and effort will be spent in the litigation of a cardiovascular disease/injury case discussing the presence or absence of various risk factors. It is important to understand what the risk factors are, how they can affect the cardiovascular system, and how a determination can be made as to whether any one particular risk factor was present in the claimant/ decedent. This discussion of the recognized factors associated with an increased risk of cardiovascular disease will begin with characteristics over which individuals have no control.

A. Factors That Cannot Be Controlled 1. Age

Approximately seventy-five percent of all Americans who die cardiovascular deaths are over age sixty-five. As more and more Americans are living and working longer, cardiovascular disease allegedly attributed to work will of course increase proportionately.

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2. Sex
Until middle age, men are about five times more likely to have heart attacks as are women. It is believed that estrogen, a female sex hormone, somehow provides protection against arteriosclerosis and heart attacks. After menopause, when a woman's body stops making

estrogen, she loses this protection, and women in the middle-aged years and beyond, the risk of heart attack climbs. By age fifty-five, women are statistically as likely to develop cardiovascular disease as are men.

3. Heredity
Heart attacks, especially when they strike at a young age, seem to run in families. Although the particular genetic defects responsible for the tendency of heart disease to run in families have not yet been determined, there is strong evidence suggesting that a family history of cardiovascular disease is a predictor of an individual's likelihood of developing cardio- vascular disease. Careful investigation must be made in each case to determine the nature and extent of an individual's hereditary predisposition to cardiovascular disease. A detailed family history must be obtained, either through direct questioning of the claimant/widow or through investigation of collateral sources such as medical records. Whenever possible, an effort should be made to determine the age and cause of death of each of the decedent's/claimant's parents. The same information should be elicited with regard to each of the decedent's/claimant's siblings. Questions must be asked not only about the

occurrence of heart attacks, but the presence of hypertension, diabetes mellitus, vascular disease, stroke, angina, and heart failure. Frequently, difficulty is encountered in determining the cause of death of the claimants'/decedents' parents. Especially when the decedent's/claimant's parents die at an

advanced age, the precise cause of death may not been known to the claimant/widow.

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The above mentioned risk factors (age, sex, and heredity) are of course beyond individual control. But the list of risk factors that are controllable is considerably longer, and it is these

avoidable risk factors that attract the most interest during litigation.

B. The "Controllable" Risk Factors 1. Smoking

Doctors and researchers agree that one of the most important "controllable" risk factors for the development of cardiovascular disease is cigarette smoking. The report of the Workshop on Stress, Hyperactivity and Cardiovascular Disease of the National Institutes of Health concluded that cigarette smoking is one of the three most important risk factors for coronary artery disease and heart attack and that the degree of risk is proportional to the number of cigarettes smoked per day. With recent publicity concerning the connection between cigarette smoking and lung cancer, many people fail to realize that the risk of a cigarette smoker developing fatal cardiovascular disease is three times as great as the risk of a cigarette smoker dying of lung cancer. Studies have consistently shown that if all other factors were equal, a cigarette smoker would be at least twice as likely as a non-smoker to have a heart attack, and at least twice as likely to die from the attack if he had one. Cigarette smokers also have a fifty percent greater chance of having a stroke than do non-smokers. Nicotine can increase by 2 to 4 fold the amount of adrenaline in the circulation. Heavy smokers undergo this outpouring of adrenaline once every 20-30 minutes during working hours. Unlike alcohol, use of nicotine is almost always addictive. Because of the importance of cigarette smoking as a risk factor for heart disease, and the presence of cigarette smokers in the American work force, the importance of understanding the relationship between cigarette smoking and cardiovascular disease cannot be overemphasized.

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a. What Makes Cigarette Smoking So Dangerous?

Cigarette smoke contains thousands of chemicals. There are about a dozen gases that constitute ninety percent of cigarette smoke. Among these gases, carbon monoxide is the most important. Another component of cigarette smoke, nicotine, has been classified by some researchers as a poison, and it has been estimated that if the nicotine from five cigarettes were extracted and swallowed, it would cause death within a few minutes. Nicotine has a powerful and dramatic effect on the cardiovascular system. During the smoking of a cigarette, small blood vessels constrict, and there is an increase in blood pressure. Vascular resistance to the blood flow increases dramatically. Nicotine also increases the heart rate and increases the strength of heart contractions. Smoking cigarettes causes increased

demand for oxygen and has been linked to an increase in platelet aggregation, or the tendency of the blood to clot. Most or all of these effects of nicotine can be related to sympatho- adrenal stimulation and the release of adrenaline into the bloodstream. The carbon monoxide component of cigarette smoke has profound cardiovascular effects as well. Carbon monoxide interferes with the blood's oxygen-delivering capacity. When carbon monoxide is inhaled, the blood can lose as much as fifteen percent of its oxygen-carrying capacity. As a result, the heart and other parts of the body may not receive adequate

oxygenation. Heavy smokers can have up to 20 percent of their blood occupied by carbon monoxide. It must be noted that carbon monoxide levels are not lower when "low tar/low nicotine" cigarettes are consumed. In fact, whether "low tar/low nicotine" cigarettes or regular cigarettes are consumed, the carbon monoxide level in a smoker can be eight times higher than the maximum allowable level in the industrial work environment. increase the amount of carbon monoxide inhaled. Filtered cigarettes can actually

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It is not necessary for a cigarette smoker to have a two-or three-pack-per-day habit in order for the risk of cardiovascular disease to increase. Rather, it has been reported that the risk of cardiovascular disease increases significantly when consumption of cigarettes is more than fifteen cigarettes per day for a period of more than five years. As will be more fully discussed below, it has been theorized that higher concentrations of HDL ("good") cholesterol tend to reduce the risk of cardiovascular disease. Cigarette smoke

depresses HDL cholesterol concentrations. Therefore, in addition to its direct action through the effects of nicotine and carbon monoxide, cigarettes interplay with and intensify other risk factors. Nicotine stimulates the release of adrenaline and norepinephrine from the adrenal glands, and this increases arterial blood pressure. Even at low doses (less than one cigarette) nicotine frequently induces a fifteen beat per minute increase in heart rate. Additionally, even one

cigarette can induce up to a ten point increase in systolic and diastolic blood pressure. An additional effect of cigarette smoking is increased cardiac output. A larger volume of blood is ejected from the heart with each beat as a result of greater heart velocity and contraction. This increases myocardial oxygen consumption. It has also been demonstrated that cigarette smoking can cause abnormal heart rhythms that can cause sudden death. In an individual with pre-existing coronary heart disease, smoking can cause episodes of chest pain known as angina, which is due to an excess of myocardial oxygen consumption over supply. In summary, smoking cigarettes causes an increase in blood pressure, heart rate, cardiac output, any myocardial oxygen consumption. It constricts blood vessels, releases norepinephrine and epinephrine (adrenaline), and increases the blood's tendency to clot and form thrombosis. These profound cardiovascular effects of cigarette smoking mean that in individuals already experiencing impaired cardiac function, smoking can lead to the development of ischemia, heart attack, stroke, and death.

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It is therefore crucial in investigation and litigation of workmen's compensation cases involving cardiovascular disease to determine whether the subject was a cigarette smoker. Perhaps more importantly, it must be determined whether the subject was actually smoking cigarettes immediately before the onset of the cardiovascular event. Not infrequently, a claimant will give a history of having performed heavy exertional labor or having been subjected to emotional stress before the onset of a cardiovascular event. Upon further investigation and probing, it may be determined that the exertion or emotionally stressful event was separated from the cardiovascular event by several hours. If, during the interval the worker smoked one or more cigarettes, the employer may be able demonstrate that the cardiovascular event was precipitated by the cigarette smoking and not by the emotional or physical stress. For example, in a recently litigated case, the facts initially presented to the employer were that a thirty-four year old worker suffered a massive heart attack near the end of his twelve-hour shift. It was known that the worker's usual job duties were strenuous and manual in nature, and it was therefore theorized by the claimant's medical expert that the worker's heart attack was causally related to the physically stressful activities performed by the worker. Upon further investigation, it was learned that the last physically stressful effort put forth by the worker took place hours before his heart attack. During the hours before his heart attack, and particularly the thirty minutes before his heart attack, the worker was on a break, performing no physically stressful duties. Instead, the worker had smoked at least one cigarette and consumed at least one cup of coffee. When emergency resuscitation teams arrived on the scene, they specifically noted a lit cigarette on the ground within inches of the worker's mouth. Relying upon the objectively verifiable effect of cigarette smoking and the delay between the last physical exertion of the employee and his cardiovascular event, the employer was able to mount a substantial challenge to the work-relatedness of the claimant's heart attack. Since this

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particular worker had a documented family history of heart disease, pre-existing hyper- tension, pre-existing high cholesterol levels, and other risk factors for coronary heart disease, a credible argument was presented to the referee that the effects of the claimant's cigarette smoking, not his strenuous job duties, precipitated his heart attack. In addition to the acute effects of cigarette smoking, chronic cigarette smoking is linked to cardiovascular disease. Although the mechanism is less clear, it appears that cigarette smoking decreases HDL ("good") cholesterol levels therefore affects cholesterol deposits in the coronary arteries and the development of coronary artery disease. Although there is some agreement that cessation of cigarette smoking causes a reduction of cardiovascular risks, the precise nature and extent of the reduced risk is unknown. Often the decision to discontinue cigarette smoking is for health reasons, and the individual makes other life style choices which may affect cardiovascular risk, such as modifying diet, losing weight, treating high blood pressure, and discontinuing consumption of alcohol and coffee. It can be difficult to assess accurately the impact of reduced of cigarette smoking on overall cardio- vascular risk. Even two years after ceasing cigarette smoking, there is increased risk of cardiovascular death. By fifteen years after ending smoking, the chance of dying of a heart attack approaches that of nonsmokers. Again, the improvement may be due to modification of other risk factors. In addition to the chronic and acute direct effects of cigarette smoke, cigarette smoking interacts with other risk factors to compound the risk of coronary disease. For instance, smokers

often also are coffee drinkers. Caffeine itself affects cardiovascular function. When coupled with cigarette smoking, some of the effects are synergistic. There also is epidemiological evidence of an association between cigarette smoking and alcohol use. Alcohol consumption is another probable cardiac risk factor. When investigating cause of alleged work-related cardiovascular disease, it is imperative to elicit an accurate history of cigarette smoking, not only about whether the subject smoked, but

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also about the age at which the subject began smoking, the number of packs smoked per day, the types and brands smoked, and whether pipes, cigars, or chewing tobacco also were used. Because of the severe acute effects of cigarette smoking, every effort should be made to determine from every reasonable source whether the subject was smoking cigarettes immediately before the onset of the cardiovascular event. Cigar and pipe smokers have a smaller risk of heart disease than do cigarette smokers; however, the risk of heart disease for pipe and cigar smokers is still almost twice the risk for nonsmokers. Among those who inhale pipe or cigar smoke, the risk of heart disease is almost the same as for cigarette smokers.

2. Hypertension
The most prevalent cardiovascular disease is hypertension (chronic high blood pressure). Hypertension affects an estimated eight to eighteen percent of all adults in America. Hypertension is especially dangerous, because it usually strikes without symptoms. In combination with other cardiovascular diseases, it frequently threatens life and health. When blood pressure is regularly and substantially above normal, the heart must pump harder to circulate the blood. In addition to the increased work of the heart, hypertension

superimposed on weakened blood vessels in the brain can lead to stroke, and harmful effects on blood vessels in the kidneys and eyes can lead to kidney failure or blindness. The risk of stroke increases more than fourfold as blood pressure rises from normal through borderline to hypertensive. With blood pressures in the range of 140 over 90 to 159 over 94, there is a 1-1/2 times greater likelihood of having a stroke. When blood pressure readings enter the range of 160 over 95 and above, the likelihood of having a stroke is three times as great as in an individual with normal blood pressure.

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In addition to the risk of stroke, the heart muscle itself may eventually suffer from strain due to hypertension. High blood pressure also increases susceptibility to coronary narrowing, further denying the heart an adequate supply of blood. In the medical/legal context, there is often considerable debate over whether an individual was in fact hypertensive. A single high blood pressure reading does not justify a

diagnosis of hypertension; however, studies have indicated that even a single high blood pressure reading places an individual in a category at higher risk for development of cardiovascular disease than in an individual without that high reading. Medical records must be carefully reviewed to determine whether an individual claimant/decedent was hypertensive. Since blood pressure readings are common in office visits, an effort should be made to obtain records even from medical sources unrelated to the treatment of cardiovascular disease. For example, if immediately preceding a heart attack, a claimant had an office visit with his family physician, and the blood pressure was recorded at 145 over 90, not much could be said about whether the claimant was hypertensive at the time; however, if upon further investigation it was determined that the claimant saw a doctor for a sprained ankle one week earlier and had a blood pressure of 170/100, this reading in conjunction with the earlier equivocal reading would present firmer evidence of hypertension. If the claimant/decedent was ever treated by an ophthalmologist, this information may also be of critical importance. Hypertension can cause changes in the optic fundi, (eye grounds) which would probably be noted ophthalmological report. As age increases in Americans, so does the acceptable range of normal blood pressure. It is critical to determine whether the subject was compliant with therapeutic efforts to reduce blood pressure. For example, if medication was prescribed for a hypertensive individual, an effort might be made to consult with the treating physician or the claimant's/decedent's pharmacist, to discover whether prescriptions for anti-hypertensive medications had been

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renewed. Unfortunately, some individuals believe that after a brief period of taking their antihypertensive medication, they are "cured", and they cease further medication because they feel no symptoms. Abrupt discontinuation of anti-hypertensive medication may cause serious side effects including not only rebound hypertension but also coronary ischemia. In one recently litigated case, the decedent suffered a stroke during the night following a particularly stressful day at work. When the patient was admitted to the hospital, his wife stated that the decedent had been hypertensive for ten years and had been on medication until only a few days before the fatal stroke. The widow had advised emergency room officials that her husband had discontinued his anti-hypertensive medication abruptly, since he had felt that due to the lack of symptoms, it was senseless to keep taking the medication. One of the theories

presented by the employer's medical expert was that the abrupt discontinuation of antihypertensive medication, and not job stress, was the factor precipitating the employee's stroke. Workers' compensation practitioners should look beyond the simple question of whether an individual was hypertensive or not and attempt to obtain every available detail about the initial diagnosis of hypertension, the medication and/or regimen prescribed to combat the individual's hypertension, and the nature and extent of the individual's compliance with the prescribed measures. 3. Cholesterol/Triglycerides The role of cholesterol in cardiovascular disease has been widely debated for decades. Although there is a consensus that cholesterol plays a role, theories about the precise role of cholesterol in cardiovascular disease are constantly in flux. Initially, high total blood cholesterol levels were thought to be associated with high risk of coronary heart disease. A more modern theory is that cholesterol must be considered in two separate categories based on low density lipoproteins (LDL) and high density lipoproteins (HDL).

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HDL cholesterol is considered "good" cholesterol, because as HDL flow through the bloodstream, cholesterol is carried to the liver, where the cholesterol eventually is broken down. Although there is no consensus yet that high HDL cholesterol levels are helpful, there is a consensus that high HDL cholesterol levels do not cause an increased risk of heart disease. As noted

previously in this chapter, one unfortunate side effect of cigarette smoking is that it has tendency to reduce HDL levels and therefore to increase the risk of heart disease. In short, there is no increased risk posed by high HDL levels, and there is a great deal of evidence to suggest that higher HDL levels actually cause a lower chance of developing coronary artery disease. Some researchers have calculated that for every five points below average that HDL falls, there is a corresponding twenty-five percent increase in the risk of heart disease. LDL's on the other hand, have been linked to higher risk of heart disease. The higher the LDL level, the greater the risk of heart disease. Therefore, in considering whether an individual has a history of "high cholesterol levels," consideration should be given to the total serum level and especially to the ratio of HDL to LDL cholesterol. High triglyceride levels are not generally thought to increase the risk of coronary disease.

4. Diabetes Mellitus
Individuals suffering from diabetes mellitus fail to produce the amount of insulin needed by the body or have resistance to insulin effects. By mechanisms that are only partly understood, the resulting higher blood sugar levels are associated with increased cholesterol levels and atherosclerosis. Diabetics are well known to have an increased risk of developing coronary heart disease. Those who develop diabetes early in life are at greater risk of developing coronary heart disease than those who develop diabetes later. According to the World Health Organization, diabetics have a two times greater risk of suffering strokes; a ten times greater risk of blindness, and a two

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times greater risk of myocardial infarction. Overall, diabetics have a three times greater chance of dying of heart disease than do non-diabetics. Direct questioning of the claimant/survivor may reveal whether the patient was diabetic. Physicians' records or previous hospital records may also note the diagnosis of diabetes mellitus. Moreover, the inquiries should not end with simple answers to the question of whether or not diabetes mellitus was ever diagnosed. It is possible that from the medical records assembled evidence strongly indicative of diabetes mellitus can be cited, even though the diagnosis was never made. Blood levels of glucose above 200 mg/dl are themselves indicative of diabetes. For example, in a recently litigated case, blood glucose levels were obtained during four unrelated hospital visits by the decedent. On one additional visit to a hospital sugar was noted in the decedent's urine following routine urinalysis. Three of the blood glucose levels were

abnormally high. Upon probing, the decedent's widow admitted that both of the decedent's parents were diabetic. Although the decedent had never been told that he had diabetes and had never been medicated for diabetes, there was strong circumstantial evidence in apparently unrelated medical records to suggest that he was diabetic before his fatal heart attack. In addition to diabetes being a risk factor for the development of arteriosclerosis, poorly controlled diabetes can give rise to chemical and electrolyte imbalances which could interfere in complex ways with the normal electrical function of the heart, even to the extent of producing sudden death. Diabetics are also more likely to be obese, a separate risk factor for heart disease. More than one half of all diabetics are obese.

5. Obesity
Obesity is generally defined as body weight in excess of twenty percent of the range considered normal for a person's sex, body type, and height. The chart following this chapter offers guidelines for determining whether a claimant/decedent qualifies as obese.

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Extra weight increases the work of the heart. For every ten pounds of extra fat carried, the body must circulate blood through an additional mile of blood vessels. There is disagreement about whether obesity is a direct risk factor for cardiovascular disease; however, there is widespread agreement that obesity affects a variety of other risk factors. For example, overweight people are more likely to be hypertensive, tend to have lower levels of HDL and higher levels of LDL cholesterol, and often have diabetes. Obesity may also interfere with an individual's ability or desire to exercise, resulting in an increasingly sedentary lifestyle, considered by some to be in itself a risk factor for coronary heart disease.

6. Caffeine
Caffeine has a significant effect on the cardiovascular system. Acute caffeine ingestion by people not addicted to it causes an increase in blood pressure, especially in individuals with a family history of hypertension. Caffeine intake also causes an increase in heart rate. Coffee drinkers often also are cigarette smokers, and are subject to the combined effects of nicotine and caffeine. There is no evidence that chronic caffeine ingestion is a risk factor for any form of cardiovascular disease. There is some support for the view that caffeine in combination with cigarette smoking plays a role in cardiovascular disease. Because the effects of caffeine as an acute stimulant of the cardiovascular system are beyond dispute, it is important to determine whether the claimant/decedent2 was drinking coffee, tea, or caffeinated cola beverages at or before the onset of the cardiovascular event, especially if the worker was also a smoker. In a case involving a known history of hypertension and heavy cigarette smoking, it may be critical to determine whether, immediately before the onset of the cardiovascular event, the

It is unclear whether acute caffeine ingestion produces cardiovascular stimulation in caffeine addicted people.

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individual subjected his cardiovascular system to the additional strain produced by caffeine and nicotine in combination.

7. Decaffeinated Coffee
Recent research has suggested that drinking decaffeinated coffee may increase cholesterol levels, thus theoretically increasing the risk of coronary heart disease.

8. Alcohol
Alcohol has been implicated in a number of ways with heart disease. Acute alcohol intake can raise blood pressure and increase triglycerides. There is general agreement that long term abuse of alcohol can produce cardiomyopathy, a diffuse weakening of the heart muscle that in turn can induce heart failure or lethal arrhythmias. Until recently, some physicians theorized that one drink per day actually provided protection against heart disease. However, the most recent theory suggests that alcohol, even in moderation, causes ventricular hypertrophy, especially in individuals over 50.

9. Sedentary Lifestyle
It has been theorized that the risk of heart disease is greater among those who rarely exercise and live a sedentary life style than those who exercise regularly. Of course, this same population also tend to be overweight, and there is no agreement in the medical community about whether living a sedentary lifestyle is an independent risk factor for heart disease. There appears to be a consensus that regular exercise has a role in decreasing the risk of heart attack.

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STRESS AND CARDIOVASCULAR DISEASE

Definitions of "Stress"
The body maintains a constant, internal environment by myriad, continual compensatory reactions, tending to restore a state of equilibrium, thereby allowing independence from the external environment. The famous French physiologist, Claude Bernard, wrote: "It is the fixity of the 'milieu interieur' which is the condition of free and independent life. All the vital mechanisms, varied as they are, have only one object, that of preserving constant the conditions of life in the internal environment" (Bernard, 1878). Bernard's idea of the milieu interieur is the first and main guiding principle for the modern views about inter-relationships between the sympathoadrenal system, stress, and cardiovascular disease: All life forms possess means to preserve their integrity, by activation of compensatory systems to maintain the constancy of the internal environment. Walter B. Cannon (1871-1945) extended Bernard's concepts by showing that the maintenance of a stable internal environment depends on the sympathoadrenal system. The existence of the sympathoadrenal system can be traced to primordial, crucial challenges all higher organisms have faced as a direct consequence of their complex structure. Whereas single-celled organisms normally are surrounded by the nutrient medium they need, higher organisms must maintain their cellular temperature, take in and distribute oxygen, and ingest and deliver fuel and water, all by an internal system - mainly by the cardiovascular system. For the cardiovascular system to function efficiently in delivering water, oxygen, and fuel and in removing waste, there must be means to regulate and coordinate the blood supply to the various organs. This regulation depends on perceptions of the outside world and sensations from the inside. It is at this border between the external and internal environments that the sympathoadrenal system works. It consists of a nerve network--the sympathetic nervous system--

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and the medulla (from the Latin word for marrow) of the adrenal glands, which in humans are located just above the kidneys. The adrenal medulla releases the hormone adrenaline, or epinephrine, directly into the bloodstream. Adjustments in sympathoadrenal activity accompany virtually every human action and reaction and are the main means for acute regulation of cardiovascular function--from the subtle, unconscious shifts of the distribution of blood volume that occur each time we stand, to the desperate distress syndrome of shock (Goldstein, 1987). Cannon coined the term "homeostasis" to describe the "coordinated physiological processes which maintain most of the steady states in the organism". Cannon suggested that rapid activation of homeostatic systems-especially

adrenomedullary secretion--would preserve the internal milieu by producing compensatory and anticipatory adjustments which would enhance the survival of the organism and the species. In particular, he explained the emotional responses of rage and fear-which he called "fight or flight" responses--in these terms. From the work and ideas of Cannon we glean the following principles: Homeostatic systems maintain most of the steady states in the organism. The sympathoadrenal system is

prominent as a homeostatic system regulating cardiovascular performance during emergency reactions. Hans Selye popularized stress as a scientific and medical theory. He elaborated a theory of stress as a condition shared by all organisms in their interaction with the environment: Stress is the nonspecific response of the body to any demand upon it (Selye, 1974, p. 14). From the start, his theory claimed that stress and stress responses were nonspecific; that is, they were brought on regardless of the stimulus. According to Selye's theory, after specific

responses were removed from consideration, a nonspecific syndrome would remain. Although

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nonspecific with respect to the inciting agents, the stress response itself consisted of a stereotyped pattern. The stereotyped physiological pattern to which Selye referred consisted of three components: enlargement of the adrenal glands, involution of the thymus gland (associated with atrophy of lymph nodes and inhibition of inflammatory responses), and peptic ulceration of the stomach. These responses are elicitable by exogenous administration of glucocorticoids, which are steroids secreted by the rind, or cortex (from the Latin word for tree bark), of the adrenal gland. The stress response also was thought to have characteristic stages. Selye conceived of a triphasic "General Adaptation Syndrome" (G.A.S.). The first phase was a rapid "alarm" reaction. This stage was followed by a longer-lasting stage of "resistance", characterized by increased resistance to the particular stressor agent but decreased resistance to other stimuli (Selye, 1950). During this stage, most of the above morphological and biochemical changes were thought to disappear. The stage of resistance was dominated by a balanced effect of "syntoxic" and "catatoxic" hormones of the adrenal cortex. The adrenal corticosteroids (cortisol in humans, corticosterone in rats) were syntoxic in that they helped the body to put up with aggressors by acting as "tissue tranquilizers", inhibiting defensive reactions such as immune and inflammatory responses. Catatoxic agents were thought to pro-inflammatory, destroying aggressors by destructive enzymatic attack. The stage of resistance would end when stores of "adaptation energy" were spent. This would usher in the third stage of the G.A.S.: "exhaustion". There would be a resurgence of pituitaryadrenocortical hyperactivity, with attendant gastrointestinal ulcers and immunologic failure, and eventual death of the organism. According to Selye's theory, stress was not necessarily deleterious. He coined the term "eustress" to refer to stress that was not harmful and possibly was helpful to the body. "Distress" referred to damaging or unpleasant stress (Selye, 1974, p. 18). Excessive, repeated, or

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inappropriate stress responses were viewed as maladaptive, and Selye coined the phrase "diseases of adaptation" to refer to situations where the G.A.S. was "derailed" (Selye, 1956, p. 47). The contributions of stress to the diseases of adaptation were suggested mainly on the basis of effects of large doses of glucocorticoids or mineralocorticoids. If abnormal (hyper-, hypo-, or dysadaptive) responses did not directly cause these diseases, then they were thought to predispose the individual to develop these diseases, based on tendencies called "conditioning factors". The list of diseases proposed as diseases of adaptation was immense: Hyperfunctional and dysfunctional conditions included Cushing's disease, adrenal tumors, chromaffinomas, renal artery stenosis, hypertension, periarteritis nodosa, nephrosclerosis, nephritis, rheumatic and inflammatory diseases, gouty arthritis, peptic ulceration, eclampsia, diabetes, allergic and hypersensitivity disorders, and psychosomatic disorders. Hypofunctional conditions included Addison's disease, Waterhouse-Fredrichsen syndrome, cancer, and diseases of resistance in general (Selye, 1950, 1974). The most severely affected targets were thought to be the cardiovascular system, the joints, and metabolism. Selye's stress theory became and remains popular. Among other things, the theory

provided a ready explanation for how any distressing experience could lead to virtually any disease state. The theory also aroused intense interest and controversy. amplified the theory's controversiality. Although certainly helpful and thought-provoking, Selye's theory of stress has proven deficient in several important respects. The kernel of truth in Selye's theory was the recognition of the demand for activity. Whether in an otherwise healthy individual chronically repeated episodes of stress produce any disease--in particular, any cardiovascular disease--remains highly controversial. Stress is an unobservable condition that leads to adaptive responses. Prominent among responses to stress is adrenal release of glucocorticoids and catecholamines. Stress is a condition Bombastic publicity

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where expectations--whether genetically programmed, established by prior learning, or deduced from circumstances--do not match the current or anticipated perceptions of the internal or external environment, and this discrepancy between what is observed or sensed and what is expected or programmed elicits patterned, compensatory responses. Distress is a form of stress characterized by specific behavioral and autonomic communicated signs, pituitary-

adrenocortical and sympathoadrenomedullary activation, and a negative experience that motivates escape or avoidance. Physiological and psychological pathology could be produced if the responses, while compensatory in intent, actually turn out not to be so and are inappropriate or excessive. This would be particularly the case in individuals predisposed to exacerbation of underlying disease by the stressor. An example would be a large adrenaline response in a patient with coronary heart disease, producing excessive myocardial oxygen consumption, platelet aggregation, or coronary artery spasm and resulting in angina pectoris, myocardial infarction, or sudden death.

Stress Systems of the Body

Many systems are activated or inhibited during stress and contribute to stress responses. The activities of the sympathoneural, parasympathetic, and hormonal homeostatic systems are co-ordinated to serve adaptive purposes during stress. Activities of these systems are altered in primitively specific patterns regulated by physiological, biochemical, and psychological homeostats. Many of these patterns, which are at least partly inherited, can be understood teleologically on the basis of preservation of the internal environment and natural selection in evolution.

Sympathoneural
The sympathoadrenal (or sympathetic or sympathoadreno- medullary) system is probably the most sensitive, rapidly-acting, and powerful of the body's stress systems. As with the pituitary-

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adrenocortical system, it has been proposed that physiological stress can be defined by, and not just measured by, sympathetic activation. The sympathoneural system, the neuronal component of the sympathoadrenal system, consists of nerve networks. Most of the nerve endings are derived from nerve cells whose bodies are in ganglia (from the Latin and Greek words for swellings or tumors), accumulations of nervous tissue strung along each side the spinal column. Sympathoneural nerve endings are particularly concentrated in the outer layer (adventitial, from the Latin for "coming from abroad") and adventitial-medial layer of arterioles, the smallest and most numerous nutrient blood vessels; in heart muscle (myocardium); and in glands such as the salivary and sweats glands. Stimulation of sympathetic nerves results in almost instantaneous constriction of arterioles and therefore increased resistance to blood flow in that region. The blood is shifted to other regions with less resistance. Different patterns of sympathoneural activation in the kidneys, the gut (splanchnic) region, the heart, the skin, and skeletal muscle therefore result in rapid changes in the distribution of blood volume. Diffuse sympathetic stimulation invariably increases the total arteriolar resistance to blood flow, so that blood pressure increases, and stimulation of sympathetic nerves to the heart increases the force and rate of contraction. Stimulation of nerves to the salivary glands increases salivation, to the eye dates the pupil, to sweat glands increases sweating, to hair follicles causes goosebumps (piloerection), to the kidney inhibits excretion of sodium, and to skeletal muscle causes trembling. The chemical transmitter at sympathetic nerve endings is norepinephrine, or noradrenaline. During sympathetic stimulation, norepinephrine is released from the nerve endings and binds to specific receptors, such as on smooth muscle cells in blood vessel walls, causing the cells to contract. Norepinephrine therefore satisfies the three main defining criteria of a neurotransmitter: It is a chemical that is released from nerve terminals by electrical action potentials. It interacts with

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specific receptors on nearby structures. responses. Noradrenaline is a catecholamine.

And in so doing it produces specific physiological

Catecholamines are a class of chemicals with a

structure consisting of an organic, or benzene, ring, with two adjacent hydroxyl groups on the ring (making up a catechol) and a short organic tail ending in an amine group. Adrenaline and dopamine are also catecholamines.

Adrenomedullary
The adrenomedullary component of the sympathoadrenal system consists of nervous pathways leading to chromaffin cells of the inner portion, or medulla, of the adrenal gland. The word "chromaffin" is a histologic classification based on staining by chromium salts. The

adrenomedullary cells secrete catecholamines such as adrenaline directly into the bloodstream. The adrenomedullary component of the sympathoadrenal system therefore is hormonal. Almost all body systems are affected by adrenaline. It rapidly increases the rate and force of cardiac contraction, dilates bronchioles and increases the rate of breathing, redistributes blood volume toward the heart, brain, and skeletal muscle, stimulates the aggregability of platelets (thereby promoting the sealing of holes in blood vessels), relaxes smooth muscle of the uterus and gut, stimulates the release of white blood cells (neutrophils) from blood vessels, increases blood glucose, and decreases serum potassium concentrations. All these effects can be viewed as homeostatic during several types of emergency reactions, including traumatic hemorrhage, hypoglycemia, asphyxiation, cardiac collapse, and fight-or-flight responses.

Pituitary-Adrenocortical
The pituitary-adrenocortical system is the body's other main stress system, and activation of this system results in the secretion of hormones such as cortisol from the cortex of the adrenal glands into the bloodstream.

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Cortisol is a "glucocorticoid", so named because its actions tend to increase blood levels of glucose. Cortisol also inhibits delayed inflammatory responses, and as noted above the antiinflammatory effects of glucocorticoids figured prominently in the stress theory of Selye. Glucocorticoids are given at high dose to patients with inflammatory diseases and in shock. As with catecholamines, glucocorticoids affect virtually all body systems, although the effects are more delayed and the doses may not be physiologic. The glucocorticoid effect can result in diabetes and the anti-inflammatory effect in increased susceptibility to some infections, such as tuberculosis. Other effects include redistribution of body fat, leading to central, or truncal, obesity and a moon-faced appearance; retention of sodium and excretion of potassium by the kidney, leading to increased extracellular fluid volume, hypertension, and low serum potassium levels (hypokalemia); metabolic breakdown, or catabolism, or proteins, leading to muscle wasting; gastrointestinal bleeding, (one of the defining triad of signs in the General Adaptation Syndrome of Selye); and several forms of psychiatric disturbance. Release of adrenocortical glucocorticoids such as cortisol is predominantly under the control of corticotropin, or ACTH (an abbreviation for adrenocorticotropic hormone). ACTH is released mainly from the anterior lobe of the pituitary gland. The pituitary is a pea-sized gland that sits in a bony cavity, called the sea turcica from its shape being similar to that of Turkish saddle, at the end of a thin stalk (infundibulum) extending from the base of the brain. The pituitary gland is also known as the hypophysis, from the Greek words signifying its appearance as a growth beneath the brain. Release of ACTH from the anterior portion of the pituitary gland is, in turn, regulated especially by corticotropin releasing hormone (CRH). ACTH release is influenced not only by CRH but also by other central neuropeptides, such as vasopressin, by catecholamines in the brain, and by feedback inhibition from glucocorticoids in the circulation. CRH is released from sites in the hypothalamus, the region of the brainstem which gives rise to the pituitary gland, in response to

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several stressors. Factors regulating release of CRH are currently under active investigation and include feedback inhibition via circulating glucocorticoids.

Vasopressin
Water deprivation poses a different challenge to homeostasis, and another stress system, the vasopressin system, seems to have evolved with the main responsibility for maintaining the total body water content. The most potent selective stimulus for vasopressin release from the posterior pituitary gland is increased plasma osmolality (a property of solutions that depends on the concentration of solute particles), reflecting relatively inadequate plasma water. The other main known stimulus is decreased cardiac filling pressure, such as occurs during hemorrhagic hypotension. Vasopressin exerts an anti-diuretic effect--hence its other name, anti-diuretic hormone, or ADH. By forcing the kidney to excrete concentrated urine, its actions in the kidney result in the retention of "free water", so that excessive ADH release in pathologic states results in decreased serum osmolality and low serum sodium concentrations (hyponatremia). As the name implies, administration of vasopressin increases in blood pressure via vasoconstriction; however, it is unclear whether endogenous ADH participates importantly in tonic blood pressure regulation.

Renin-Angiotensin-Aldosterone
The body also has tremendously efficient means to preserve salt. During salt (sodium

chloride) restriction, the renin-angiotensin-aldosterone system forces the body to retain sodium. The main stimuli for release of renin in the kidneys are decreased renal perfusion pressure, decreased renal tubular concentrations of sodium, and decreased cardiac filling pressures. Renin catalyzes the conversion of angiotensin I to angiotensin II, the latter being a very potent vasoconstrictor. Angiotensin II (AII) also stimulates the adrenal cortex to release aldosterone,

which in humans is the main mineralocorticoid. Aldosterone augments renal sodium retention (hence the designation as a mineralocorticoid) by stimulating exchange of sodium for potassium,

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so that hyperaldosteronism is associated with a tendency to retain sodium and extracellular fluid volume, hypertension, and potassium wasting. Activation of the renin-angiotensin-aldosterone system therefore increases blood pressure both by angiotensin-induced vasoconstriction and aldosterone-induced sodium retention and expansion of extracellular fluid volume.

Parasympathetic
The parasympathetic nervous system mainly is involved with vegetative, conservative processes and so usually is shut down during most forms of stress. A general principle--to which there are exceptions--is that when sympathoadrenal activity is increased, parasympathetic activity is decreased. Thus, whereas the sympathoadrenal system rapidly uses up metabolic

energy in preserving homeostasis during several emergency conditions, the parasympathetic system tends to restore that energy during periods of quiescence. As would be predicted from this view, parasympathetic stimulation is thought to activate digestive processes, including release of gastrin and insulin, and to increase motility of the gut; whereas in the heart, parasympathetic stimulation decreases the force and rate of contraction. The main parasympathetic nerve is the vagus nerve, so named because of its wandering throughout the body, from the medulla of the brainstem, where it is the tenth cranial nerve, to the heart, bronchioles, stomach, skin, and gut. Unlike sympathetic nerve endings, where norepinephrine is the neurotransmitter, at parasympathetic nerve endings acetylcholine is released. Acetylcholine was the first

neurotransmitter to be identified, by Loewi in a series of brilliant experiments in the 1920's, and for this work he shared the Nobel Prize in Physiology of Medicine in 1936. Acetylcholine is broken down almost immediately after its release from parasympathetic nerve endings, and to this day there is no generally accepted method for measuring acetylcholine concentrations in blood. Acetylcholine or drugs like it stimulate digestive processes

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and gut motility; increase salivation; increase sweating; and decrease heart rate. Stimulation of parasympathetic activity (or possibly release of acetylcholine from sympathetic nerves in skeletal muscle) can induce vasodilation.

Endogenous 0pioids
The endogenous opioid system appears to be intimately connected physiologically with the corticotropin releasing hormone-pituitary adrenocortical and adrenomedullary systems and may contribute to the experience of pain and the occurrence of stress related analgesia. The discovery of this system was based on the hypothesis that the analgesic, morphine, works by binding to specific receptors in the brain. If there were receptors for morphine, which is derived from opium, then there could be endogenous morphine-like neurochemicals--opioids--in the brain that could inhibit the sensation of pain. The endogenous opioid, B-endorphin, is derived from a precursor, proopiomelanocortin (POMC), which also is a precursor of ACTH and of melanocyte stimulating-hormone (MSH). In the anterior pituitary, POMC gives rise to ACTH, as well as B-lipotropin, or B-LPH. In turn, B-LPH can be cleaved to form alpha-LPH and B-endorphin. As suggested by the name, B-endorphin, which contains 31 amino acids, is an endogenous opioid and acts as a neuro- transmitter in the central nervous system. And as would be predicted from its shared origin with that of ACTH, administration of CRH increases plasma levels of ACTH and B-endorphin in parallel. The highest concentrations of B-endorphin in the body are in the pituitary gland. Another class of endogenous opioids consists of the enkephalins, methionine-enkephalin and leucine-enkephalin. These are small peptides (5 amino acids each) with either methionine or leucine at the end. They, like B-endorphin, are derived from cleavage of larger precursor peptides that are not POMC. Enkephalins are packaged together with catecholamines in adrenomedullary cells and appear to be released with them. Enkephalins also are high in the dorsal columns of the spinal cord, involved in the transmission of sensory information to the brain.

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The physiologic role of endogenous opioids has been studied mainly by observing the effects administration of the opioids and by administration of naloxone, which blocks opioid actions. Endogenous opioids regulate the transmission of pain impulses and the experience of pain. In particular, enkephalins in the spinal cord inhibit transmission of pain impulses that would ascend in the lateral spinothalamic tract to the thalamus in the brain. Injection of B-endorphin into the cerebrospinal fluid space produces analgesia and has been used for pain in patients with terminal cancer. Release of B-endorphin in the brain may be the basis for analgesia produced by

acupuncture and placebos. In septic, hemorrhagic, or spinal shock, the hypotension appears to be the result partly of endogenous opioids, since naloxone can restore the blood pressure.

Physical Stress and Cardiovascular Disease Exercise

Any form of exercise, whether isometric (contraction against resistance without movement) or isotonic (contraction without resistance and with movement), can evoke symptoms in patients with underlying cardiovascular disease. In patients with atherosclerosis of arteries to the leg, walking produces a cramp-like pain called claudication. The pain disappears within a few minutes of resting. Walking programs can improve exercise tolerance. Sometimes vasodilators or pentoxyphyllin help. Buerger's disease is a form of severe atherosclerosis of arteries in smokers. In patients with angina pectoris, exercise often reliably brings on this symptom of myocardial ischemia. Judging from levels of cardiac enzymes, however, it is doubtful that angina pectoris is associated with appreciable cellular necrosis. Emotional distress, a large meal, or

exposure to cold also can precipitate an attack of angina. It has been suggested that isometric exercise, such as lifting and carrying heavy weights, increases cardiac afterload and blood pressure, and the increased myocardial oxygen consumption can precipitate angina.

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The increases in plasma levels of catecholamines, including adrenaline and noradrenaline, that occur during exercise return rapidly to baseline after the exercise ceases--usually within minutes. The same rapid return to baseline occurs after cessation of laboratory psychological stressors. There is little epidemiologic evidence that moderate exercise is hazardous in patients with coronary heart disease.

Temperature
Extremes of temperature can precipitate angina pectoris. High temperatures increase cardiac output and myocardial oxygen consumption. resistance and thereby increase ventricular afterload. Low temperatures increase peripheral

Hypoxia
Low inhaled oxygen tensions can precipitate angina pectoris in patients with coronary heart disease. This is due both to the direct effects of decreased oxygen supply to myocardial cells and due to indirect effects, by stimulation of receptors that lead to reflexive vasoconstriction and increases in ventricular afterload and by reflexive increases in adrenaline levels.

Hemorrhage
Severe anemia can precipitate angina pectoris. Chronic, unsuspected bleeding from the lower gastrointestinal tract can present clinically as angina pectoris, especially in elderly patients with cancer of the colon.

Hypoglycemia
Hypoglycemia, or a low blood glucose level, is a profound stimulator of release of adrenaline into the bloodstream. The released adrenaline is the main determinant of the

symptoms of hypoglycemia--sweating, fast pulse rate, trembling, hyperventilation, pallor, and a feeling of impending doom. In patients with insulin-dependent diabetes mellitus, beta-

adrenoceptor blockers are contraindicated, because these drugs mask the symptoms of

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hypoglycemia in the event of insulin overdose. Hypoglycemia can provoke angina pectoris both by the direct metabolic insult to myocardial cells and by the increased myocardial oxygen consumption caused by high circulating adrenaline levels.

Emotional Stress and Cardiovascular Disease

There is only indirect evidence that emotional stress is a primary causative factor in any cardiovascular disease. This has been a most difficult area in which to conduct meaningful

research. One problem is selection biases, where subjects in different job categories are compared. People self-select their occupations. Another problem is separation of other risk

factors, such as smoking, hypertension, and obesity. Results obtained in the laboratory may not be generalizable to real-life settings. There is no agreed-upon single biochemical index of emotional stress. Two reasonable candidates are corticotropin (ACTH) and adrenaline. In contrast with chronic stress, there is little doubt that acute stress can exacerbate underlying cardiovascular disease. A dramatic example of this phenomenon was the case of Dr. John Hunter. Hunter was one of the most renowned surgeons of the 18th century and is viewed as the father of scientific surgery. By all accounts an extraordinarily hard worker, he customarily rose before dawn. He was notoriously prone to argument, wrath, defensiveness, irrational outbursts, obstinateness, and impatience, i.e. he probably would fit the criteria for a "Type A" individual. In 1785 he began to experience angina pectoris, which had only recently been described by his friend, William Heberden. It appears, however, that Hunter either never recognized or never

admitted the condition for what it was and considered it instead to be due to rheumatism or dyspepsia, despite his having conducted the dissection of one of Heberden's cases! The relationship between emotional upset and his symptoms was, however, clear to him, and because argumentation frequently brought it on, he asserted: "My life is at the mercy of any rogue who chooses to provoke me" (Kobler, 1960).

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On October 16, 1793 Hunter became incensed at critical, insolent remarks against him at a meeting of the board of governors of St. George's Hospital. He left the room, collapsed and died. His A Treatise on the Blood, Inflammation, and Gun-Shot Wounds was published posthumously by his brother-in-law and colleague, Everard Home. Home's description of Hunter's condition and the circumstances of his death, published as a prefix, is itself a classic of cardiology (Willius & Keys, 1941). Here are a few excerpts: It is a curious circumstance that the first attack of these complaints was produced by an affection of the mind, and every future return of any consequence arose from the same cause; and although bodily exercise, or distention of the stomach, brought on slighter affections, it still required the mind to be affected to render them severe; and as his mind is irritated by trifles, these produced the most violent effects on the disease. His

coachman being beyond his times, or a servant not attending to his directions, brought on the spasms, while a real misfortune produced no effect. The affections above described were, in the beginning, readily

brought on by exercise, and he even conceived that if he had continued at rest, they would not have come on; but they at last seized him when laying in bed, and in his sleep, so as to awaken him, affections of the mind also brought them on; but cool thinking or reasoning did not appear to have that effect. While these complaints were upon him, his face was pale, and he had a contracted appearance, making him look thinner than ordinary; and after they went off his colour returned, and his face recovered its natural appearance. On October 16, 1793, when in his usual state of health, he went to St. George's Hospital, and meeting with some things which irritated his mind, and not being perfectly master of the

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circumstances, he withheld his sentiments, in which state of restraint he went into the next room, and turning around to Dr. Robertson, one of the physicians of the hospital, he gave a deep groan and dropped down dead. The muscular structure of the heart was paler and looser in its texture than the other muscles in the body....The coronary arteries had their branches which ramify through the substance of the heart in the state of bony tubes, which were with difficulty divided by the knife, and their transverse sections did not collapse, but remained open. After Hunter's death, Home plagiarized Hunter's work and burnt most of Hunter's manuscripts, which were in Home's possession. No action was taken against Home. One important point that Hunter's case illustrates is that it is difficult to predict from external circumstances whether a person will experience stress-induced angina. whereas major misfortunes did not. Acute stress probably can be additive to effects of nicotine and alcohol in precipitating ischemic episodes. Studies of laboratory animals have indicated that emotional stress, Trifles evoked rage,

superimposed on high blood cholesterol levels, also increases the severity of atherosclerosis. The theorizing that led to the concept of the Type A coronary prone behavior pattern reflects a somewhat different view about the effects of stress: the personality of the individual, more than the inherent noxiousness of the environmental situation, was thought to determine the magnitude of the stress response and the risk of coronary disease and death. The behavior pattern is thought to be a disorder based not on deleterious stressful aspects of the environment but on destructive stress responses. Although introduced and popularized by Friedman and Rosenman as described below, it was presaged by Osler in his famous statement that the coronary patient could be identified as

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"not the delicate neurotic but the robust, the vigorous in mind and body, the keen ambitious man, the indicator of whose engine is always full speed ahead" (Osler, 1910). The Type A coronary prone behavior pattern includes time urgency, competitiveness, and aggressiveness. The best evidence supporting the existence and significance of this pattern was the Western Collaborative Group Study of 3,524 men followed prospectively for 8-1/2 years (Rosenman et al., 1975). Subjects with the Type A behavior were twice as likely to develop

ischemic heart disease as those without Type A behavior, after taking into account all other known major risk factors. The findings from the Framingham study tended to agree (Haynes et al., 1978). After review of the highly provocative literature on the subject, a review panel of the National Heart, Lung, and Blood Institute concluded that "sufficient evidence exists to establish that behavioral factors powerfully influence cardiac vulnerability ...This means that pursuit of neural mechanisms by which psycho-social stressors regulate cardiac vulnerability will have a scientific payoff quite independent of results obtained from research on ischemic heart disease." The Multiple Risk Factor Intervention Trial (MRFlT) did not show significant differences in ischemic heart disease morbidity or mortality related to the Type A pattern (Shekelle et al., 1983). The classification was based not on structured interviews but questionnaire evaluations. Attempts to replicate the original findings of Friedman and Rosenman have occasionally failed, and so the status of the Type A pattern as a coronary risk factor continues to be debated. A recent study, for instance, found that in patients who had survived a myocardial infarction, Type A individuals were not at increased risk for sudden death or subsequent myocardial infarction. It is possible that some of the negative research findings in this area could have been obtained because only part of the constellation of components of the Type A pattern actually are related to the risk of ischemic heart disease. Exactly which components of the pattern are the cause of the increased coronary risk is unknown. In the reports of Rosenman, Friedman, and coworkers published in 1964 (Rosenman et al., 1964) and in follow-ups over the next decade

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(Rosenman et al., 1975), they emphasized a constellation of aggressiveness, time urgency, and competitiveness. The work of Williams and co-workers (e.g., Williams et al., 1980) has emphasized the component of hostility or anger. Some support has accrued that hostility itself may be a coronary risk factor independent of the Type A pattern (Barefoot et al., 1983; Shekelle et al., 1983). Another aspect emphasized by Wolf (1960) is joyless striving, which he termed the "Sysiphus Reaction", after the mythical King of Corinth who was condemned to Hades and forced to push a rock endlessly up the side of a mountain (Wolf, 1985). Syme (1985) has suggested that the relationship between the Type A personality and coronary risk may be mediated by the extent of social support: "...it is not difficult to imagine that persons with the Type-A behavior pattern have less supportive relationships because such relationships require substantial time and energy that may be regarded as "unproductive" type Type-A persons" (Syme, 1985, p. 65). In a study of Japanese men in California, the subpopulation of immigrants who became "acculturated" had coronary heart disease rates 2.5 to 5 times that of the subpopulation that retained its Japanese life style. Thus, the stress related to mobility and life change appear to be ameliorated in the setting of social support. Wolf (1985) drew about the same conclusion from a study of the citizens of Roseto, an Italian-American town in eastern Pennsylvania. This community, which retained its culture since

immigrating in 1882 until the 1960's, had relative freedom from heart attacks, despite similar consumption of animal fats, smoking, sedentary lifestyle, hypertension, and diabetes as inhabitants of nearby towns. Type A individuals respond to challenges that are perceived as personally threatening with excessive increases in plasma levels of catecholamines and in blood pressure (Glass et al., 1980). This would provide a simply mechanism for the increased coronary risk. Eliot, Buell, and co-workers have suggested that patterns of hemodynamic response during emotional stress, rather than the Type A pattern itself, may be the basis for the association

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between cardiovascular morbidity and stress in some patients (Eliot & Buell, 1985). Eliot and Buell emphasized that the pathologic consequences of emotional stress exceed by far those due to physical stress, and physical conditioning by exercise may or may not ameliorate the deleterious consequences of emotional stress. Physical stressors, however, have been viewed as much easier to study scientifically. Eliot & Buell (1985) have categorized patients as "hot reactors" or "cold reactors" based on excessive hemodynamic responses to a panel of tests, including mathematical problems, competitive video games, and the cold pressor test. Based on impedance cardiographic

estimates of cardiac output and mean arterial pressure by cuff, "hot reactors" are be subcategorized in terms of whether cardiac output or total peripheral resistance increases were the predominant cause of excessive pressor responses to the non-physical stressors. "Hot reactors" are not identified from the Type A interview, perhaps because the testing is designed so as not to be intimidating. Eliot & Buell (1985) reported that myocardial infarction patients with

inappropriately excessive hemodynamic responses had early reinfarction within 2 years, but no published references were cited or data presented. Individuals with pressor responses due to increased cardiac output were thought to have few cardiovascular complications. In contrast, several cases were cited where patients with large increases in total peripheral resistance (related to blunted increases in stroke volume during nonphysical stress) had new or pre-existing cardiovascular catastrophes. In one case, testing revealed alarming increases in total peripheral resistance 2 months before the patient was found dead at his desk (Eliot & Buell, 1985). Consistent with the general approach of Eliot and Buell, Manuck et al. (1983) reported that in cynomolgus monkeys subjected to psychosocial stress (the threat of capture and physical handling by the investigator while the animals were in their social groups), animals with relatively large heart rate responses also had more extensive coronary atherosclerosis than those that had

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relatively small heart rate responses. The changes in heart rate related to aggressive or submissive acts appeared to be unrelated to the extent of somatic activity. According to another theory, job-related stress is determined by the extent of challenge or threat and the extent of control over the situation, i.e., the perceived ability to cope. Threatening situations that the individual has no perceived control over are thought to be most stressful. Unfortunately, the topic of stress, personality, and coronary heart disease is viewed in the cardiologic research community as being so difficult and controversial, objective clinical experiments to support or refute the main hypotheses, such as that of the Type A pattern, may not be done. Perhaps the increasing interest in the medicolegal aspects of this topic will lead to funding of studies to settle these issues. In the meanwhile, it seems reasonable from the available research literature to conclude that acute episodes of emotional stress can precipitate angina pectoris, ventricular arrhythmias, or myocardial infarction by way of activation of the sympathoadrenal system. It is likely that chronically repeated episodes of emotional stress can accelerate the development of cardiovascular diseases in susceptible individuals. It is possible, but by no means proved, that stress causes cardiovascular disease in otherwise healthy people.

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References
Barefoot JC, Dahlstrom WG, Williams RB. Hostility, CHD incidence, and total mortality: a 25-year follow-up study of 255 physicians. Psychosom Med 1983;45:59-63. Bernard C. Lecons, sur les phenomenones de Ia vie communs aux animaux et aux vegetaux. Paris: alliere et fils, 1878. Eliot RS, Buell, JC. Utilization of a new objective, non-physical stress test. In Beamish RE, Singal PK, Dhalla NS (Eds). Stress and Heart Disease. Boston: Martinus Nijhoof Publishing, 1985, pp. 116-126. Glass DC, Krakoff LR, Contrada R, Hilton WF, Kehoe K Mannucci EG, Collins C, Snow B, Elting E. Effect of harassment and competition upon cardiovascular and plasma catecholamine responses in type A and type B individuals. Psychophysiology 17:453-463, 1980. Goldstein DS., Stress-induced activation of the sympathetic nervous system. In Grossman A (Ed). Neuroendocrinology of Stress. East Sussex, England: Bailliere Tindall, 1987, pp. 253-278. Haynes SG, Feinlieb M, Levine S, Scotch N, Kannel WB. The relationship of psychosocial factors to coronary heart disease in the Framingham Study. Il. Prevalence of coronary heart disease. Am J Epidemiol 1978; 107:384-402. Kobler J., The Reluctant Surgeon. A Biography of John Hunter. New York: Doubleday & Co., Inc., 1960. Manuck SB, Kaplan JR, Clarkson TB. Behaviorally-induced heart rate reactivity and atherosclerosis in cynomolgus monkeys. Psychosom Med 1983;45:95-108. Osler W., The Lumleian lectures on angina pectoris. Lancet 1910;1:697-699 and 839-844. Rosenman RH, Brand RJ, Jenkins CD, Friedman M, Straus R, Wurm M. Coronary heart disease in the Western Collaborative Group Study: Final follow-up experience of 8 1/2 years. J Am Med Assoc 1975;233:872-877. Rosenman RH, Friedman M, Straus R, Wurm M, Hahn R, Kositchek R, Werthessen N. A Predictive study of coronary heart disease. J Am Med Assoc 1964;1 89:15-22.

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Selye H., Stress without Distress. New YorkNew American Library, 1974. Selye H. The Physiology and Pathology of Exposure to Stress. A Treatise Based on the Concepts of the General-Adaptation Syndrome and the Diseases of Adaptation. Montreal, Canada:Acta, Inc., 1950. Selye H. The Stress of Life, New York: McGraw-Hill, 1956. Shekelle R, Hulley S, Neaton J. Type A behavior and risk of coronary death in MRFlT. Paper read at 23rd Annual Conference on Cardiovascular Disease and Epidemiology. San Diego, CA, 1983. Shekelle R, Gale M, Ostfeld A. Hostility, risk of coronary heart disease and mortality. Psychosom Med 1983;45:100-114. Syme SL., Socioenvironmental factors in heart disease. In Beamish RE, Singal PK, Dhalla NS (Eds). Stress and Heart Disease. Boston: Martinus Nijhoof Publishing, 1985, pp. 60-70. Williams RB Jr, Haney TL, Lee Kl, Kong YH, Blumenthal JA, Whalen RE. Type A behavior, hostility and coronary atherosclerosis. Psychosom Med 1980;42:539-549. Willius FA, Keys TE. Classics of Cardiology. New York:Dover Publications, Inc., 1961. Wolf SG., Stress and heart disease. Mod Concepts Cardiovasc Dis 1960;29:599-603. Wolf SG., Past present and future directions in the treatment of stress-related cardiovascular disorders. In Beamish RE, Singal PK, Dhalla NS (Eds). Stress and Heart Disease. Boston: Martinus Nijhoof Publishing, 1985, pp. 436-447.2

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OBTAINING, REVIEWING AND UNDERSTANDING MEDICAL RECORDS

I. Obtaining the necessary medical records
No aspect of case investigation, preparation, or litigation is more important than a comprehensive review of all pertinent past medical records. It is essential that adequate efforts be made to obtain medical records at the beginning of the case, to prevent later surprises, and to allow your expert a full opportunity to compare his findings to data previously collected. In fact, it has been said that the three cardinal rules in evaluating and litigating cardiovascular disease cases are: get the past records, get the past records, and get the past records. Only from a review of the past records can it be objectively determined which factors other than employment could have caused the cardiovascular disease or death. Obtaining the past medical records at the beginning of the case is important. Unless the past medical records are obtained early in the litigation, there is a significant chance that the records can never be obtained. Frequently witnesses forget the names of treating or evaluating doctors and hospitals; records are lost (especially when hospitals merge or close); and doctors fail to keep adequate records after selling their practices or retiring. Too frequently, it is believed that obtaining all the pertinent past medical records is only an important task for the defendant. However, obtaining all the necessary records has profound advantages for claimants' attorneys as well. Only after evaluation of all records can a claimants' lawyer realistically assess the likelihood of prevailing, the settlement value of a case, or the issues likely to be raised by the employer in opposition to the claim. Due to memory problems, lack of understanding of medical terms and conditions, and conscious or subconscious secondary gain, the necessary data cannot be collected solely from the claimant.

A. Sources of records 1. Records from the employer 96

A systematic search should be made for all past medical records from all sources. It is necessary to obtain records even from seemingly unrelated illnesses or accidents. For example, records from an earlier appendectomy should be obtained, since the pre-operative workup probably included a chest x-ray, blood work and an EKG. A visit to an orthopedic surgeon

following a back injury may be pertinent if an x-ray of the back was taken, since cardiovascular conditions such as calcification of the aorta can sometimes be seen. Obtain all records from all sources, and let your medical expert decide which information is relevant. The logical place to begin is with the employer. The claimant's employment application should be obtained in order to identify previous employers who may have additional medical information in their files, and to check for voluntary disclosure of pre-existing diseases by the worker. The claimant's complete personnel file should be obtained and searched for preemployment medical and social questionnaires. Often an applicant for a job is asked about cigarette smoking, alcohol consumption, or prescription or non-prescription drugs. Some

employers specifically ask questions about prior accidents and illnesses and about the family history of disease. Obviously, if a pre-employment physical was conducted, the records and results of the physical, including lab reports, x-rays and EKG's should be obtained. Similarly, records from annual or follow-up physical conducted by the employer should be obtained. The claimant's personnel file will probably also help to pinpoint the exact job title and duties of the claimant at the time of the cardiovascular event. Work logs, time cards, and daily reports may also be useful to prove or disprove the nature and extent of work performed before the cardiovascular event. If the employer maintains its own medical department or dispensary, these records should be separately and specifically requested. Often a request for a worker's personnel file will exclude such records unless they are specifically requested. If the employer contracts out to a health care facility for medical services, the medical facility's records should be subpoenaed.

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An effort should be made to obtain from the employer copies of all prior workers' compensation reports and claims made by the employee. Records of all prior claims for medical reimbursement under employer sponsored health plans should also be obtained. Miscellaneous records that should be obtained from the employer include life insurance questionnaires and reports of physicals, requests for prescription drug reimbursement, and nonwork related accident reports or requests for leaves of absence. Obviously, it will also be

necessary to obtain a statement from the employer of the employee's wages during the six calendar quarters preceding the date of injury, and a statement of wages and days worked during the 52 weeks preceding the cardiovascular event.

2. Records from claimant's medical providers

Do not settle for forms or copies of hospital discharge summaries. Obtain the entire file from each medical provider visited by the claimant. Sometimes the most helpful information is on a handwritten scratch pad or a casual note. Be sure also to obtain and review all

correspondence between the claimant's attorney and the practitioner. Records should be obtained from every doctor, hospital, clinic, rehabilitation facility, and therapist. Be certain to get the complete hospital file, including progress notes, nurses notes, consultation reports, and lab reports. The importance of reviewing the entire hospital file is demonstrated by the following true story. In a heart attack case, the hospital discharge summary, admissions history, and consultation reports were obtained initially. No particularly enlightening information was contained therein with regard to the personal stresses to which the claimant was subjected immediately before his heart attack. Subsequently, the nurse's progress notes were obtained. In these handwritten notes was a day by day log of all visitors to the claimant. The notes revealed that claimant's wheelchair-bound son visited, and that conversation between the claimant and his wife centered on whether to postpone bone marrow transplant surgery scheduled for the son a few days later in light of the

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claimant's heart attack. Progress notes and nurse's notes frequently contain useful information and should be reviewed carefully.

3. Records from prior medical providers

In addition to all records from treating or examining providers after the cardiovascular event, all records about treatment of any nature previously rendered to the claimant should be obtained. Particularly important are records from the claimant's family physicians. These records frequently include the results of blood studies and blood pressure readings. It is not at all

uncommon to see comments in the family doctor's records having profound impact on a case, such as comments about the claimant's need to lose weight, lower cholesterol levels, or admonitions to discontinue smoking. Even records from seemingly unrelated treatment should be obtained, since they may contain names of additional sources of information or provide useful personal and family history data. For example, records from the claimant's optometrist may contain information about

hypertension-related changes in the eye grounds. Records from a podiatrist may make reference to symptoms of intermittent claudication, a sign of cardiovascular disease. Records from a current or former psychiatrist or psychologist are particularly important, since they often catalog sources of stress in a individual's life other than employment.

4. Social Security records

If the claimant has applied for Social Security disability benefits, a subpoena should be issued to obtain the complete Social Security file. Since Social Security determinations are based upon occupational as well as non-occupational factors, it may be discovered that claimant reported non-work related maladies in an effort to obtain disability status. For example, a claimant may deny hypertension when questioned in his compensation case but may freely admit to hypertension to Social Security to enhance the chance of being deemed entitled to benefits.

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5. Unemployment Compensation records

Not infrequently, cardiovascular disease cases are filed only after a worker has been laid off due to lack of work. When applying for unemployment in most states, the worker must answer, under oath, whether he is capable of and available for employment. The unemployment file should be reviewed to determine whether any inconsistency exists between claimant's assertions concerning disability and assertions made in an effort to obtain unemployment.

6. Records from old employers

Particularly in cases in which the worker served for only a brief interval before the cardiovascular injury, an effort should be made to obtain dispensary, personnel, and medical records from the claimants previous employers.

7. Claimant's expert
The complete file should be obtained from the expert expected to testify on behalf of the claimant as soon as possible, and in all cases in advance of the expert's live or deposition testimony. An effort also should be made to obtain the expert's curriculum vitae.

8. "Index" reports
Consideration should be given to utilizing the services of a law suit or claims indexing service to determine whether the claimant has been involved in other litigation or compensation claims. If other cases are discovered, records should be obtained from all medical providers, insurance carriers and attorneys involved.

B. HOW TO OBTAIN THE RECORDS

A major advantage to obtaining records early in the investigation of a case is that the claimant may not yet be represented by an attorney and may agree to execute blanket authorizations for release of medical records. Even if represented, frequently the claimant will agree to sign an authorization, to avoid the expense and inconvenience of more formal measures.

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An effort should be made to interview the unrepresented claimant, with emphasis on location and identification of medical providers. Often the easiest way to obtain medical records is to get a written authorization from the claimant and write a friendly letter to the medical provider requesting the release of the records pursuant to the authorization and offering to reimburse promptly the provider for copying and mailing expenses incurred. Frequently overlooked is the simplest method of obtaining records - request them from your opponent! Pursuant to Section 422 of the Act, medical records and reports must be provided, but only if they are requested. If the claimant has been examined by a physician selected by the employer, claimant's attorney should request a copy of any reports generated, including copies of EKG's or other tests performed.

II. REVIEWING THE MEDICAL RECORDS

Many records obtained will be of poor photostatic quality. An effort should be made to obtain clearly legible copies, since referees are particularly annoyed by the submission of illegible copies. If the records are of reasonable photostatic quality, the next problem is usually deciphering the handwriting. Do not hesitate to call doctors and/or the hospital to ask for explanation of records made illegible due to sloppiness or poor penmanship. There is rarely an excuse for

rendering critical records useless as a result of poor habits. Hospital and doctor's records are simply too important to be jeopardized by such trivial problems. If the records are in particularly poor shape, and no cooperation is offered by the record keeper in deciphering them, consideration should be given to withholding payment to the provider until legible and coherent records are received.

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Assuming that the copies are clean and the handwriting legible, all records should be reviewed meticulously for three primary types of information: sources of additional medical records; evidence of pre-existing disease or factors pre-disposing to disease; and factual details concerning the circumstances surrounding the cardiovascular event. In reviewing the records, many abbreviations will be encountered. The chart following this chapter should be of some assistance in understanding the common medical abbreviations typically encountered in cardiovascular disease cases. Review of the records by a non-physician can usually find most medically, factually, and legally significant data; however, the records should be independently reviewed by a physician since lab reports, electro-diagnostic test results, and subtle findings may have little or no meaning to a layman and great significance to a medical expert. Obviously, review of the records should focus on finding facts about the worker's social and medical history, with emphasis on the risk factors usually associated with cardiovascular disease. If notations are made about medications, reference should be made to the Physician's Desk Reference to determine whether the drug was prescribed to treat a cardiovascular condition, or alternatively, whether the drug could have caused or aggravated a cardiovascular condition as a side effect. If records are discovered that help your case, they should be used during cross examination of your opponent's medical expert and an effort should be made to mark and submit the records into evidence. Recall that pursuant to Section 422 of the Act, medical and hospital records are admissible in cases involving less than 25 weeks of disability. In cases involving more significant disability, if your expert can testify that the records are of a type customarily relied upon by experts such as yours, and the records were reviewed by your expert to assist your expert in forming his own independent conclusions, the records may be admissible.

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ABBREVIATIONS COMMONLY ENCOUNTERED IN CARDIOVASCULAR DISEASE CASES

AP ASCVD AVM BP CA CABG CAD CC CCU CHD CHF Chol COPD CP CVA DM EKG ETOH FIb H/O HR HTN HX LVH MI NKDA NSR Ox3 P SOB SX TIA URI VF X

angina pectoris arteriosclerotic cardiovascular disease arteriovascular malformation blood pressure cancer coronary artery bypass graft coronary artery disease chief complaint coronary care unit coronary heart disease congestive heart failure cholesterol chronic obstructive pulmonary disease chest pain cerebral vascular accident (stroke) diabetes mellitus electrocardiogram alcohol fibrillation history of heart rate hypertension history left ventricular hypertrophy myocardial infarction no known drug allergies normal sinus rhythm oriented as to person, place and time pulse shortness of breath symptom transient ischemic attack upper respiratory infection ventricular fibrillation for

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THE ANGINA CONTROVERSY

There is a great deal of controversy over whether the occurrence of angina (angina pectoris) or other transient cardiovascular symptoms can form the basis for an award of benefits, and if so, the duration of any such award. Angina is an unpleasant sensation of pressure or squeezing beneath the sternum that results from myocardial ischemia. The pressure-like pain can radiate to the neck, jaw or arm. Typically, angina is brought on during exercise, emotional stress, exposure to cold, or eating a large meal. tongue. In angina due to fixed narrowing of coronary arteries, the symptom develops when myocardial oxygen consumption exceeds supply. Angina can also occur as a result of spasm. In "dynamic" obstruction due to spasm, ischemia may not be associated with increased myocardial oxygen consumption. Angina can be a chronic problem. There is an increased risk of myocardial infarction and sudden death, but the overall mortality is only a few percent per year. Most medical experts believe that attacks of angina do not produce any permanent damage to the heart. Angina is a symptom, not a disease. The diagnosis of angina is therefore based almost entirely on clinical examination and a carefully obtained history. Since angina is a symptom and not a disease, and in light of the fact that most medical experts believe that an attack of angina causes no worsening of the underlying condition of the heart, it is frequently argued that angina is not an "injury" under the Act. The term "injury" is not defined in the Act. The Act merely provides that: The term "injury" and "personal injury" as used in this act, shall be construed to mean an injury to an employee, regardless of his previous physical condition, arising in the course of employment and related thereto, and such disease or infection as naturally results from the injury or is aggravated, reactivated or Angina usually disappears within minutes of resting or taking nitroglycerine under the

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accelerated by the injury; and wherever death is mentioned as a cause for compensation resulting from such injury and its resultant effects, and occurring within three hundred weeks after the injury. Section 301 (c) (1); 77 P.S. 411 (1). Despite repeated opportunities to do so, the Supreme Court of Pennsylvania has refused to define the term "injury". Instead, the court has held that no technical definition of "injury" is

necessary, and that a "standard" dictionary definition suffices. Unfortunately, there is no single or standard dictionary definition of injury. Many dictionaries define injury with specific reference to change in physiology or physical harm. Others include in the definition the occurrence of pain. Dorland's Medical Dictionary, 26th Edition, defines injury as: harm or hurt; a wound or maim. Usually applied to damage inflicted to the body structure by an external force. The same medical dictionary defines "symptom" as: any subjective evidence of disease or of a patient's condition, i.e., such evidence as perceived by the patient; a change in a patient's condition indicative of some bodily or mental state. Applying the above definitions, it appears that angina is a symptom, and not an injury. Perhaps due to a lack of understanding of angina, the Commonwealth Court has issued a number of decisions holding that angina is an injury under the Act. In the one of the leading cardiovascular disease cases, Workmen's Compensation Appeal Board v. Pincus, 479 Pa. 286, 388 A.2d 659 (1978), the Commonwealth Court offered its analysis of the definition of injury in a cardiovascular disease case: Decedents' heart attacks caused physical damage to the internal tissues of the heart. Such damage to a bodily organ is no less an injury than a broken leg or a cut arm, and as such was intended by the legislature to be compensable if related to the decedent' employment. Id. at 388 A.2d 664. The court's holding was of course limited to the facts presented, and therefore addressed only the definition of "injury" in cases involving "physical damage to the internal tissues of the heart".

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However, this case has frequently and erroneously been cited as authority for the proposition that angina is an injury under the Act. In City of Altoona v. Workmen's Compensation Appeal Board, 50 Pa. Cmwlth 178, 411 A. 2d 1322, (1980), a fireman experienced severe chest pain on the job, but did not suffer a heart attack. Benefits were awarded, and on appeal to the Commonwealth Court, the issue of whether the worker's angina constituted an injury was addressed. The court held that claimant's angina constituted a compensable injury. It must be noted, however, that in City of Altoona, claimant's medical expert testified that claimant suffered a "heart injury", and that "something about the heart had to change" to initiate the onset of the worker's angina. This testimony, although perhaps incorrect as a matter of

medicine, fits within the "physical damage to the heart" definition provided in Pincus, Id. The court in City of Altoona did not address the issue of whether angina would still properly be classified as an injury absent medical testimony regarding change "about the heart". The issue of whether angina is an "injury" absent medical testimony that a physical change in the cardiovascular system took place was addressed in a footnote in Barnes and Tucker v. Workmen's Compensation Appeal Board, 40 Pa. Cmwlth. 152, 396 A.2d 900 (1979). In Barnes and Tucker, claimant had chest pain while lifting heavy wire at work. Ultimately, angina and coronary artery disease were diagnosed. Benefits were awarded, and an appeal followed on the issue of whether sufficient evidence was presented to allow the referee to find a causal relationship between the job and the angina. The issue of whether claimant's angina constituted an injury under the Act was not appealed, but the Commonwealth Court commented: We note that the only issue raised by the employer is the substantial evidence question discussed in the text. The employer has not raised the purely legal question of whether or not the claimant suffered an "injury" within the meaning of

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Section 301 (c) (1) of the Pennsylvania Workmen's Compensation Act. That section provides, inter alia, that " (t)he terms "injury" and "personal injury" as used in this act, shall be construed to mean an injury to an employee, regardless of his previous medical condition, arising in the course of his employment and related thereto, and such disease or infection as naturally results from the injury or is aggravated, reactivated or accelerated by the injury... Thus, the aggravation of a disease, the origin of which is not related to employment, is specifically included within the circular definition of "injury" only where the disease is aggravated by an "injury". It is difficult to see what "injury" has aggravated claimant's coronary heart disease... Since this issue has not been raised, our affirmance of the Board's grant of benefits should not be construed as resolving it. Barnes and Tucker, Id., at 396 A.2d 901. In Workmen's Compensation Appeal Board v. G.M. & W. Coal Co., 29 Pa. Cmwlth. 138, 370 A.2d 386 (1977), a maintenance man, while performing strenuous duties, fainted. After many examinations and test, a rare disease called sick sinus syndrome was diagnosed. The sinus node is a minute part of the heart that functions as the heart's natural pace maker. The claimant's medical expert testified, and the referee found that the sinus node was injured by the claimant's strenuous work duties. Clearly, this case involved physical damage to the heart, and not merely the occurrence of anginal symptoms. Relying on the four cases outlined above, the Commonwealth Court issued its first definitive (but arguably erroneous) decision holding that angina is compensable under the Act as an injury in Penn Cambria School District v. Workmen's Compensation Appeal Board, 52 Pa. Cmwlth. 244, 415 A.2d 943 (1980). It is difficult to understand how the Commonwealth Court found a basis in the four cases outlined above for this conclusion. Relying upon the arguably erroneous decision in Penn Cambria, the court again found angina to constitute a compensable injury in L.E. Smith Glass Company v. Workmen's Compensation Appeal Board, 102 Pa. Cmwlth. 268, 517 A.2d 1031 (1986).

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The medical testimony in an angina case should be carefully presented. If the medical evidence accepted by the referee establishes only the occurrence of a symptom, without any suggestion that a change in the physiology of the heart occurred, an argument can still be made that episode of angina did not constitute an injury under the Act, especially if the worker had angina both before and after the work incident. If an episode of angina is deemed to be an "injury", a controversy usually arises over the proper duration of compensation benefits. For example, if a worker with pre-existing coronary artery disease has an episode of angina on the job that lasts ten minutes, does entitlement to benefits extend beyond ten minutes? Does the answer change if resumption of employment is likely to cause further symptoms? In Schroeder v. Workmen's Compensation Appeal Board, 116 Pa. Cmwlth. 130, 541 A.2d 410 (1988), a fire fighter experienced angina as he drove a fire truck to a fire. The worker was intermittently hospitalized for diagnostic procedures relating to his angina. About five weeks after he left the hospital following the last of the diagnostic procedures, claimant returned to work. The referee found that the angina attack lasted only minutes, and because disability lasting less than seven days is not compensable pursuant to Section 306 (e) of the Act, the referee denied compensation benefits to the worker. The Commonwealth Court reversed the referee's decision and awarded benefits to the claimant, but only for the weeks that claimant was hospitalized for testing. The court did not award benefits for the five weeks after the hospitalization and before the worker returned to employment. The court reasoned that although the worker's chest pains lasted less than a day, the hospitalization was related to testing stemming from the angina episode, and therefore disability during the hospitalization was compensable. The court did not allow benefits to the claimant for the interval between the hospitalization and the claimant's return to employment, because

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"claimant presented no medical evidence showing that his failure to return to work until September 21, 1980 was the result of the work-related cardiac insufficiency (angina episode)". The most interesting aspect of the Schroeder case is that the referee determined that the claimant had an injury, and the Commonwealth Court determined that the injury resulted in compensable disability, but the court put the burden on claimant to prove entitlement to ongoing benefits until the claimant's return to employment. The opposite conclusion was reached by the Commonwealth Court in Steinle v. Workmen's Compensation Appeal Board, 38 Pa. Cmwlth. 241, 393 A.2d 503 (1978). In Steinle, a police officer had an episode of coronary insufficiency on the job as a result of emotional stress stemming from fear of ongoing racial disturbances in the borough. The employer argued that since claimant's symptoms had ceased, the worker's benefits should have stopped as well. The Commonwealth Court held that once claimant proved a compensable work-related injury, the burden shifted to the employer to prove that claimant was capable of returning to gainful employment. Another answer to the question of how long benefits should be paid following a brief episode of angina was provided in Roth v. Workmen's Compensation Appeal Board, ___ Pa. Cmwlth.___, 562 A.2d 952 (1989). The answer was that benefits are not awarded at all. In Roth, the medical testimony accepted by the referee established that the claimant had "nothing more than a transient episode of the type that the (worker) had before". The denial of benefits to the claimant was affirmed. In many cases, the employer will argue that an episode of angina is merely a transient symptom of underlying, non-work related disease, and that once the episode is over, entitlement to benefits ceases. This argument is particularly strong in cases in which the medical experts both testify that the occurrence of the anginal symptoms did not cause a change or worsening of the worker's overall cardiovascular condition. This argument is weakest in cases in which both experts agree that a resumption of employment will likely trigger further episodes of angina.

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CONTROLLABLE RISK FACTORS FOR CORONARY HEART DISEASE

CIGARETTE SMOKING HYPERTENSION DIABETES HIGH CHOLESTEROL LEVELS HIGH TRIGLYCERIDE LEVELS OBESITY ALCOHOLISM

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RISK FACTORS FOR CORONARY HEART DISEASE THAT CANNOT BE CONTROLLED

AGE MALE SEX FAMILY HISTORY RACE

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NON-ATHEROSCLEROTIC CARDIAC CAUSES OF CHEST PAIN

AORTIC VALVE DISEASE PULMONARY HYPERTENSION PERICARDITIS MITRAL VALVE PROLAPSE CARDIOMYOPATHY AORTIC ANEURYSM MITRAL STENOSIS

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DIAGNOSTIC EVALUATION FOR CARDIOVASCULAR DISEASE

HISTORY EKG (ELECTROCARDIOGRAM) CHEST X-RAY PHYSICAL EXAMINATION MUGA SCAN THALLIUM STRESS TESTING ANGIOGRAPHY CARDIAC CATHETERIZATION AUSCULTORY EXAMINATION GATED CARDIAC SCAN EXERCISE STRESS TESTING HOLTER MONITOR ECHOCARDIOGRAM CARDIAC ENZYMES

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SOME NON-CARDIAC CAUSES OF CHEST PAIN

MUSCLE ACHE GASTROINTESTINAL DISTRESS DIRECT TRAUMA TO THE CHEST HIATAL HERNIA ESOPHAGITIS ULCER BILIARY TRACT DISEASE HERPES ZOSTER THORACIC OUTLET SYNDROME ARTHRITIS RIB FRACTURE PULMONARY EMBOLISM PLEURISY HYPERVENTILATION CERVICAL RADICULOPATHY COSTOCHONDRITIS

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SOME CAUSES OF SUDDEN DEATH NOT RELATED TO CORONARY HEART DISEASE

TRAUMA ELECTROCUTION CEREBRAL HEMORRHAGE PULMONARY EMBOLISM GASTROINTESTINAL EMBOLISM AORTIC ANEURYSM OVERWHELMING INFECTION (SEPSIS) SHOCK HEAT STROKE ASPIRATION MEDICATION ERROR ANAPHYLAXIS DRUG OVERDOSE OR WITHDRAWAL

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FACTORS TENDING TO DISPROVE A CAUSAL LINK BETWEEN A CARDIOVASCULAR INJURY AND AN EMPLOYMENT EVENT

LONG TIME LAG BETWEEN EVENT AND INJURY DOCUMENTED PRE-EXISTING CARDIOVASCULAR DISEASE NO CHANGE IN SYMPTOMS OR FUNCTION FOLLOWING WORK EVENT INCONSISTENT OR UNVERIFIABLE HISTORY OF WORK EVENT PRESENCE OF ONE OR MORE RISK FACTORS NO CREDIBLE ARTICLES SUPPORTING CAUSATION UNDER SIMILAR CIRCUMSTANCES NON-WORK RELATED INTERVENING EVENT OR CONDITIONS EQUIVOCAL OPINION FROM THE WORKER'S TREATING PHYSICIAN

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FACTORS TENDING TO ESTABLISH A CAUSAL LINK BETWEEN CARDIOVASCULAR INJURY AND EMPLOYMENT EVENT

CLOSE TEMPORAL RELATIONSHIP LACK OF PRE-EXISTING PATHOLOGY LACK OF PRE-EXISTING SYMPTOMS SPECIFIC AND OBJECTIVELY VERIFIABLE EVENT AT WORK LACK OF INTERVENING EVENT OR CONDITION DRAMATIC CHANGE IN SYMPTOMS OR FUNCTION AFTER EVENT LACK OF TRADITIONAL RISK FACTORS UNEQUIVOCAL OPINION FROM AN ESTABLISHED EXPERT REPUTABLE ARTICLES SUPPORTING CAUSATION UNDER SIMILAR CIRCUMSTANCES

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CAUSES OF CARDIAC ARRHYTHMIAS NOT DUE TO HEART DISEASES

ACUTE EMOTIONAL STRESS PHYSICAL EXERTION NICOTINE CAFFEINE ALCOHOL ANESTHESIA ELECTRICAL SHOCK TRAUMA DIRECT CARDIAC INJURY HYPOGLYCEMIA MEDICATION HYPOXIA ABNORMAL ELECTROLYTES ENDOCRINE DISORDERS DRUG EFFECTS/WITHDRAWAL

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THE BODY'S RESPONSE TO CIGARETTE SMOKING

HEART RATE INCREASES TEN TO TWELVE BEATS PER MINUTE BLOOD PRESSURE INCREASES EIGHT TO TEN mm/MERCURY BLOOD VESSELS CONSTRICT THE HEART'S DEMAND FOR OXYGEN INCREASES BLOOD PLATELETS GET STICKIER AND AGGREGATION OR CLOTTING IS FACILITATED THE HEART BEATS FASTER AND HARDER CARDIAC OUTPUT IS INCREASED CARBON MONOXIDE LEVELS IN THE BLOOD INCREASE CIRCULATING LEVELS OF THE HORMONES CORTISOL AND EPINEPHRINE ARE INCREASED THE BLOOD'S OXYGEN CARRYING CAPACITY IS REDUCED

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