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Tami Hendriksz, D.O.

Touro University-California Joint MSPAS/MPH Program

Objectives Part 1
y Recognize the pathophysiology of heart failure. y Identify and recognize the compensatory mechanisms of heart failure. y Differentiate the following:
y y y y y

High-output versus low-output heart failure (including common causes of each) Systolic vs diastolic heart failure Acute vs. chronic heart failure Right-sided vs. Left-sided heart failure Backward versus forward heart failure

y Recognize risk factors for heart failure. y Identify the etiologies of heart failure.

Objectives Part 2
y Identify and recognize modes of prevention of CHF. y Recognize the prognosis of heart failure. y Recognize the common symptoms and physical exam findings of y y y y y

CHF. Recognize the diagnostic work-up of CHF and identify lab results and findings seen on EKG and CXR that are consistent with CHF. Recognize the role of echocardiography in the diagnosis and management of CHF. Recognize the pharmacologic and non-pharmacologic treatments in the management of chronic CHF. Identify the stages of heart failure. Recognize the presentation, work-up and mainstays of treatment of acute heart failure and pulmonary edema.

Case Presentation
y Chief Complaint: 74-year-old woman with shortness of breath and

swelling.

y History: Martha Wilmington, a 74-year-old woman with a history of

rheumatic fever while in her twenties, presented to her physician with complaints of increasing shortness of breath ("dyspnea") upon exertion. She also noted that the typical swelling she's had in her ankles for years has started to get worse over the past two months, making it especially difficult to get her shoes on toward the end of the day. In the past week, she's had a decreased appetite, some nausea and vomiting, and tenderness in the right upper quadrant of the abdomen. distended. Auscultation of the heart revealed a low-pitched, rumbling systolic murmur, heard best over the left upper sternal border. In addition, she had an extra, "S3" heart sound.

y On physical examination, Martha's jugular veins were noticeably

Heart Failure
y The inability of the heart to pump sufficient blood

to meet the metabolic demands of the body

y or

y The ability to do so only if the cardiac filling

pressures are abnormally high

y or both y =impaired ability of the ventricle to fill with or eject

blood

Epidemiology
y y y y y y y y

Prevalence: estimated at 5-million Americans (75% > 65 yo) Increases steeply with age Incidence is increasing (3-4 fold increase from 1971 to 1999) 1/5 of hospital admissions in >65yo are due to HF (most common dx) More Medicare $ on HF Dx and Tx than any other Dx Lifetime risk of developing HF after age 40 is 20% Incidence doubles with each successive decade 6-9x greater risk of sudden death in patients with HF

Risk Factors for Heart Failure


y Any condition that causes myocardial necrosis or produces chronic pressure or volume overload can induce myocardial dysfunction and heart failure y y y y y y

Valvular heart disease Coronary heart disease HTN DM Dyslipidemia Metabolic syndrome (abd obesity, dyslipidemia, elevated BP, glucose intolerance)

Some Review
y Heart normally accepts blood at low filling pressures during diastole y Propels it forward at higher pressures in systole y In a healthy person, cardiac output is matched to the body s total metabolic need y The ability to increase cardiac output during increased activity is called cardiac reserve y Cardiac output (CO)=volume of blood ejected from the ventricle per minute. CO=SV x HR y Ejection Fraction (EF)= the fraction of end-diastolic volume ejected from the ventricle during each systolic contraction
y

The fraction of blood pumped out of ventricles with each heart beat

y EF=SV/EDV Normal=____

Some Review
y CO=SV x HR y SV is determined by preload, afterload and myocardial contractility y Preload=the stretch on the myocardial fibers before systole y Volume stretching the heart at the end of diastole (end-diastolic volume, EDV) y Largely determined by the venous return to the heart y Afterload=the force the contracting heart must generate to eject blood from the filled heart y Affected by systemic (peripheral) vascular resistance, and ventricular wall tension

y LVEDV=the amount of blood returned to the heart by the

venous system

Pathophysiology
y There is no single, simple model that effectively explains

the syndrome of HF y Currently the consensus view integrates multiple pathophysiologic models to explain the cascade of events leading to this clinical syndrome
y Structural y Functional y Biological y Hemodynamic

Compensatory Mechanisms
Fall in cardiac output recruits mechanisms to maintain sufficient BP and perfuse the organs. 1. Frank-Starling Mechanism 2. Neurohormonal alterations 3. Development of ventricular hypertrophy and remodeling

Frank-Starling Mechanism
"Within physiological limits, the force of contraction is directly proportional to the initial length of the muscle fiber".

y Impaired LV function, causes SV, incomplete chamber emptying, and LVEDV, increase stretch y contractile force/ SV of next contraction to a point y Long term compensation leads to LVEDV

Frank-Starling Mechanism

Neurohormonal Alterations
BP=CO x TPR (total peripheral resistance) 1. Adrenergic nervous system
y

y y

Decreased perfusion to baroreceptors realease of norepinephrine oSympathetic qParasympathetic oHR, ocontractility, ovasoconstriction (E) A-II constricts arterioles (oTPR), stimulates thirst, increases aldosterone Promotes water retention, opreload

2.

Renin-Angiotensin-Aldosterone system
y

3.

Increased production of ADH


y

Ventricular Hypertrophy and Remodeling


y Develops over time in response to hemodynamic burdens y Sustained wall stress (dilitation or pressure) stimulates hypertrophy and stiffness y Eccentric hypertrophy= synthesis of new sarcomeres in series, elongation of myocytes, chamber enlarges in proportion to increase in wall thickness. Due to VOLUME overload (MR or AR) y Concentric hypertrophy= synthesis of sarcomeres in parallel with old, myocytes thicken. Wall thickness increases without proportional chamber dilitation. Due to PRESSURE overload (AS, HTN)

A sarcomere is the basic unit of a muscle's cross-striated myofibril

High-output HF vs Low-output HF
y High-output HF=normal myocardial function but

increased demand
y Severe anemia, hyperthyroidism, AV shunting,

pregnancy y Tends to be specifically treatable

y Low-output HF=impaired pumping ability of the heart y Ischemic heart disease, cardiomyopathy, myocarditis, arrhythmia

Systolic HF vs Diastolic HF
y Systolic HF= decreased pump function and decreased

EF y Diastolic HF= impaired ventricular filling from stiff chamber with normal EF

Forward HF vs Backward HF
y Forward Heart Failure - The inability of the heart to

pump blood at a sufficient rate to meet the oxygen demands of the body at rest or at exercise
y Inadequate discharge of blood into the arterial system

y Backward Heart Failure - The ability of the heart to

pump blood at a sufficient rate ONLY when heart filling pressures are abnormally high
y Back-up of blood in the venous and atrial system behind the

failing ventricle

y These are hypotheses to describe the clinical

manifestations of HF

Right HF vs Left HF
y Right Heart Failure - The inability of the right side of the heart to adequately pump venous blood into the pulmonary circulation
Causes a back-up of fluid in the body, resulting in swelling and edema (peripheral edema & engorged liver and spleen) y Causes = left heart failure, pulmonary HTN, PV stenosis, P embolism
y

y Left Heart Failure - The inability of the left side of the heart to pump into the systemic circulation
y

Causes accumulation of fluid in the lungs (pulmonary edema)

y Causes= MI, cardiomyopathy, AS, MR

y Usually if failure has existed for years it affects both sides

(biventricular failure)

Left HF

Right HF

Acute HF vs Chronic HF
y Acute HF= Sudden onset of HF y Often due to massive MI, rupture of cardiac valve leaflet y Symptoms = hypotension and flash pulmonary edema y Usually largely systolic and the sudden reduction in cardiac output often results in systemic hypotension without peripheral edema y Chronic HF= HF that develops or progresses slowly over

time

y Dilated Cardiomyopathy or multi-valvular HD y Arterial pressure tends to be well maintained until very late

in the course, but there is often accumulation of peripheral edema

Causes of HF
Systolic Dysfunction
y Impaired contractility
y MI y Transient myocardial ischemia y Chronic volume overload y Mitral Regurge or Aortic Regurge y Dilated cardiomyopathy

y Increased Afterload (pressure overload)


y Aortic Stenosis y Uncontrolled HTN

Causes of HF
Diastolic Dysfunction
y Impaired Ventricular Relaxation
y LV hypertrophy y Hypertrophic cardiomyopathy y Restrictive cardiomyopathy y Transient myocardial ischemia

y Obstruction of LV filling
y Mitral Stenosis y Pericardial constriction/tamponade

Most Common Underlying Causes of HF


y Ischemic Heart Disease (75%) y Cardiomyopathies y Valvular diseases y HTN y Congenital heart disease

Precipitating Causes
Acute disturbance that places an additional load on a myocardium that is chronically excessively burdened
y y y y y y y y y y y

Infection Arrhythmias Physical, dietary, fluid, environmental, emotional excesses MI Pulmonary Embolism Anemia Thyrotoxicosis Pregnancy Aggravation of HTN Rheumatic and viral myocarditis Infective endocarditis

Clinical Presentation Left-Sided HF


y Dyspnea (DOE or at rest) y Dulled Mental Status y Nocturia y Fatigue/weakness y Orthopnea y Paroxysmal Nocturnal Dyspnea y Nocturnal cough y Hemoptysis

Clinical Presentation Right-sided failure


y Abdominal discomfort (RUQ) y Nausea, anorexia y Peripheral edema y Unexpected weight gain

Left HF

Right HF

Directed History
y Onset, Progression, Provoking, Palliative, Quality,

Timing y PMH: pulmonary dz (copd, asthma), DM, lipids, CAD/PVD, RF, MI, HTN, congenital, valvular disease y FH: MI, strokes, PAD, sudden cardiac death, myopathy, need for pacemaker, cardiomyopathy y SH: Exercise, smoke, drink, diet, stress y Meds: CARDIOTOXINS

Directed Physical
y Vitals: BP(sitting and standing), Wt, BMI,

oRR, oHR y Gen: cachexia (if severe), dusky, diaphoretic y Neck: JVD y Lungs: pulmonary rales, coarse rhonchi and wheezing. Pleural effusions (both R and L) y Heart: PMI, louder P2, S3, S4, MR. Right ventricular heave, TR y Abdomen: Hepatomegaly, RUQ tenderness y PV: pulsus alternans, peripheral edema

Clinical Presentation
Symptoms
Left-Sided Dyspnea (DOE) Orthopnea PND Fatigue

Physical Findings
Diaphoresis Tachycardia Tachypnea Pulmonary rales Loud P2 S3 gallop (+/- S4) JVD Hepatomegaly Peripheral edema

Right-Sided

Peripheral edema RUQ pain

Laboratory Testing
y CBC y UA y CMP (Mg and Ca) y Liver Enzymes y Fasting Glucose, HgAIC y Lipids y TSH y (BNP)

Diagnostic Studies
y ECG: LAE, LVH, ST-T changes, RVH, active

ischemia, old MI, arrhythmias (AF, VT) y CXR: Cardiomegaly, cephalization, pleural effusions, Kerley B lines, batwing or butterfly pattern y Echocardiogram with Doppler: to determine LVEF, wall motion abnormalities, chamber size, & valve fxn. Differentiates systolic from diastolic HF. y Stress testing/Cardiac Cath: in selected pts. Can assess wall abnormalities, valve fxn and EF

cardiomegaly

cephalization

Kerley B lines (septal lines)

Pleural Effusion

http://www.mypacs.net/cgi-bin/repos/mpv3_repo/wrm/repoview.pl?cx_subject=1666444&cx_image_only_mode=off&cx_repo=mpv4_repo

Echocardiogram
http://www.heartfailure.org/eng_site/hf_test_ecg.asp

Two-dimensional echocardiogram showing a fourchambers view of the heart in a patient with systolic dysfunction. Note dilated LV. (LV = left ventricle; RV = right ventricle; RA = right atrium; LA = left atrium)

Two-dimensional echocardiogram showing a fourchambers view of the heart in a patient with diastolic dysfunction. Note the normal LV size with hypertrophy.

Framingham Criteria for Diagnosis of Congestive Heart Failure


To establish a clinical diagnosis of congestive heart failure by these criteria, at least one major and two minor criteria are required.
MAJOR CRITERIA y Paroxysmal nocturnal dyspnea y Neck vein distention y Rales y Cardiomegaly y Acute pulmonary edema y S3 gallop y Increased venous pressure (>16 cmH2O) y Positive hepatojugular reflux MINOR CRITERIA y Extremity edema y Night cough y Dyspnea on exertion y Hepatomegaly y Pleural effusion y Vital capacity reduced by onethird from normal y Tachycardia ( 120 bpm) MAJOR OR MINOR y Weight loss 4.5 kg over 5 days' treatment

Stages of Heart Failure

Acute Cardiogenic Pulmonary Edema


y Results from severe L-sided HF y Elevated capillary hydrostatic pressure

leads to rapid accumulation of fluid within the interstitium and alveolar spaces of the lung y Often with hypoxemia y Due to sudden insult to previously Asx pt OR precipitating event in chronic compensated HF

Acute Cardiogenic Pulmonary Edema


y Severe dyspnea y Anxiety y Hypoxemia y Tachycardia y Tachypnea y Cold, clammy skin y Coughing frothy sputum y Rales +/- wheezing y Tx: lasix, morphine, nitrates, oxygen, position

Goals of Therapy
1. 2. 3. 4. 5.

Identification and correction of the underlying condition causing HF Elimination of the precipitating cause of symptoms Management of HF symptoms
a) b)

Treatment of pulmonary and systemic vascular congestion Measures to increase CO

Modulation of the neurohormonal response Improvement of long-term survival

A Winning Hand
y The Hand You re Dealt - Know your type of heart failure y An ACE Up Your Sleeve - Take your medicine y Playing Your Cards Right - Eat a healthy diet y The High Stakes - Record a log of daily weights y Don t Gamble With Your Health - Report early signs of worsening y Stack the Deck - Keep regular doctor visits

http://www.afmc.org/HTML/consumer/health_info/hfailures.aspx

Diastolic HF Management
y Estimated 1/2 of patients with HF have preserved

LVEF y Correct underlying cause y Reduce volume overload (cautious diuretics) y Slow HR y Reduce afterload

Non-Pharmacologic Management
y Lifestyle Modification
y Weight reduction y Smoking cessation y ETOH avoidance y Cardiotoxin avoidance y Exercise y Na/Fluid restriction

y Daily Weights y Control metabolic syndrome

Medications to Avoid in HF
y Most antiarrhythmics (save amiodarone) y NSAIDS and COX-2 inhibitors y Can increase blood pressure and interfere with blood-pressurelowering drugs y Antacids with added sodium y Thiazolidinediones (glitazones) y Can result in dangerous levels of fluid retention y Certain Chemo agents y Cardiotoxic y Hormone replacement therapy & OCPs y Can raise blood pressure y Stimulants (Adderall, methylphenidate, cocaine, meth) y Elevate blood pressure and increase heart rate y Sildenafil (Viagra) y Can increase blood to heart and increase exercise tolerance y Caution when using it with other medications (such as nitrates)

Pharmacologic Management
y ACE-Inhibitors y ARBs y Beta-blockers y Diuretics y Hydralazine y Nitrates y Inotropic agents y Aldosterone Antagonists

y Implantable Cardioverter-Defibrillators (ICDs):

Advanced Nonpharmacologic Interventions

osurvival in LVEF <35% y Cardiac Resynchronization Therapy (CRT) via Biventricular Pacemaker: symptomatic HF with widened QRS complex y Ventricular assist devices: short but significant prolongation of survival in patients who had end-stage heart failure and were ineligible for transplantation y Percutaneous coronary intervention y Coronary artery bypass grafting (CABG) y Cardiac Transplantation: severe LV dysfunction, refractory to maximal medical mgmt. y Hospice

Biventricular Pacemaker

Implantable CardioverterDefibrillator Ventricular Assist Devices

Prognosis
y Symptomatic HF confers a 1-year mortality of 45% y <50 % of patients are living 5 yrs after their initial

dx & <25 % are alive at 10 years y Worse prognosis than the majority of cancers

Prognosis

Prevention
y Treatment of HTN (with focus on systolic pressure)

reduces incidence of HF by 50%


y Effective even in pts >75 yrs old

y Reduce risk of first or recurrent MIs y Control DM, hypertension, dyslipidemia y In post-MI patients and/or those with reduced LVEF y Add beta blockers and ACEI delays progression of LV dysfunction & HF

Case Presentation
y Chief Complaint: 74-year-old woman with shortness of breath and

swelling.

y History: Martha Wilmington, a 74-year-old woman with a history of

rheumatic fever while in her twenties, presented to her physician with complaints of increasing shortness of breath ("dyspnea") upon exertion. She also noted that the typical swelling she's had in her ankles for years has started to get worse over the past two months, making it especially difficult to get her shoes on toward the end of the day. In the past week, she's had a decreased appetite, some nausea and vomiting, and tenderness in the right upper quadrant of the abdomen. distended. Auscultation of the heart revealed a low-pitched, rumbling systolic murmur, heard best over the left upper sternal border. In addition, she had an extra, "S3" heart sound.

y On physical examination, Martha's jugular veins were noticeably

Case Questions
y 1. What is causing this murmur? y A low-pitched, rumbling murmur is usually due to a stenotic (i.e. narrowed) valve. The left, upper

sternal border is where the closing sound of the pulmonic valve is heard the best. Since Martha's murmur is heard best in this area, it is most likely due to pulmonic valve stenosis.

y 2. What is causing her "S3" heart sound? y The "S3" heart sound is an extra sound heard early in ventricular diastole in individuals with

congestive heart failure, corresponding to the time when there is rapid filling of the ventricle with blood. One theory regarding its cause is that ventricular wall tension is increased in congestive heart failure, causing atrial blood to be forced against a relatively non-compliant ventricular wall during diastole, creating the "S3" heart sound.

y 3. Is her history of rheumatic fever relevant to her current symptoms? Explain. y Her history of rheumatic fever may or may not be relevant to her current symptoms. Rheumatic

fever is thought to be caused by a hypersensitivity response to an infection by Streptococcus pyogenes. Certain bacterial antigens appear to be cross-reactive with antigens from human heart tissue. Hence, an immune response to the bacterium may cause unwanted destruction of human heart tissue, including the pericardium, myocardium, and endocardium. Destruction of the myocardium can, itself, lead to congestive heart failure. Destruction of the endocardium can involve the valves, though by far the most commonly affected are the valves in the left side of the heart (i.e. the mitral and / or aortic valves). Since it is Martha's pulmonic valve that is stenotic, it may be unrelated to her prior history of rheumatic fever.

Case Questions
y y

4. A chest X-ray reveals a cardiac silhouette that is normal in diameter. Does this rule out a possible problem with Martha's heart? Explain. A "normal" cardiac silhouette does not rule out a problem with Martha's heart. Her pulmonic stenosis creates more resistance to the outflow of blood from the right ventricle into the pulmonary artery. Over time, the right ventricle will undergo concentric hypertrophy in an attempt to generate stronger contractions to overcome this resistance to flow. In concentric hypertrophy, the thickness of the wall increases, but the overall diameter of the ventricle does not change much. Since Martha's ventricular diameter hasn't changed much, the silhouette appearance of her heart on a chest X-ray will not be enlarged. 5. You examine Martha's abdomen and find that she has an enlarged liver ("hepatomegaly") and a moderate degree of ascites (water in the peritoneal cavity). Explain these findings. Martha's hepatomegaly and moderate ascites are caused by increased systemic venous pressure. Since there is resistance to the flow of blood out of the right ventricle into the pulmonary artery, hydrostatic pressure rises in Martha's right ventricle, right atrium, and central systemic veins (this is why her jugular veins appear distended). This build-up of hydrostatic pressure is reflected backwards into her more peripheral systemic veins - - thus pressure rises in the inferior vena cava and hepatic vein of the liver. Elevated venous pressure in the hepatic sinusoids forces water from the bloodstream into the interstitial spaces of the liver, causing the liver to become swollen. A similar build-up of systemic venous pressure forces water from the bloodstream out into the peritoneal cavity, causing "ascites." 6. Examination of her ankles reveals significant "pitting edema." Explain this finding. The pitting edema in Martha's ankles is also caused by an elevated systemic venous pressure. Fluid escaping from the peripheral capillaries into the interstitial spaces of her legs causes them to become edematous. This condition is aggravated when Martha spends several hours of the day standing, and is alleviated to some extent when Martha lies down with her feet above heart level.

y y

y y

Case Questions
y 7. She is advised to wear support stockings. Why would this help her? y Support stockings will place an external pressure on Martha's lower legs,

forcing some of the excess interstitial fluid into the lymphatic and blood vessels. One must be careful, however, when advising patients to wear support stockings. The stockings should place even pressure around the entire lower legs, and should not have restrictive bands of elastic at the top. Furthermore, if the patient has atherosclerosis and blockage of arteries supplying the legs, such support stockings may actually limit arterial blood flow into the legs, and thus should not be used.

y 8. Which term more accurately describes the stress placed upon Martha's heart

-- increased pre-load or increased afterload? y Increased afterload

y 9. What is the general term describing Martha's condition? y Right-sided congestive heart failure, which classically causes systemic

edema. Compare this with left-sided congestive heart failure, which causes pulmonary edema.

Case Questions
y y

10. How might Martha's body compensate for the above condition? The increased afterload placed upon Martha's right ventricle decreases her right ventricular stroke volume (i.e. decreases the volume of blood pumped out of the ventricles per contraction). To maintain an adequate cardiac output (i.e. volume of blood pumped out of the heart in one minute) to meet Martha's metabolic needs, she must either (A) increase the strength of contraction (i.e. increased contractility), and / or (B) increase the heart rate (i.e. the number of contractions per minute). In either case, Martha's sympathetic nervous system coordinates the response via the baroreceptor reflex. Furthermore, since Martha's cardiac output is likely to be below that required to meet her metabolic needs, the sympathetic nervous system stimulates systemic arteriolar vasoconstriction to the "less vital" organs (e.g. those of digestion and urination) while more blood is preferentially diverted to the "more vital" organs (e.g. the heart and brain). Over the long term, Martha's right ventricle will undergo concentric hypertrophy as mentioned in #4. This will allow the right ventricle to increase its strength of contraction, but there are limits to how well this mechanism works. For example, as Martha's right ventricular wall thickens, the innermost portion of it receives relatively less blood, limiting its contractile strength. Reduced cardiac output will diminish blood flow to the kidneys, triggering the renin-angiotensin-aldosterone (R-A-A) axis. During this response, the hormone renin is released from the juxtaglomerular ("granular") cells of the nephrons and enzymatically converts the liver protein angiotensinogen into angiotensin I. Angiotensin I, in turn, is converted into angiotensin II by ACE (i.e. angiotensin-converting enzyme). Angiotensin II has multiple effects, most of which serve to increase the systemic arterial pressure. Angiotensin II directly causes widespread systemic arteriolar vasoconstriction (hence, its name), which increases the total peripheral resistance to blood flow, and thus also the blood pressure. It also triggers the hypothalamic release of ADH (antidiuretic hormone), a hormone that stimulates the kidneys to conserve water and produce smaller volumes of very concentrated urine, ultimately increasing total blood volume and blood pressure. Perhaps most importantly, angiotensin II stimulates the release of the hormone aldosterone from the adrenal cortex. Aldosterone stimulates tubular reabsorption of sodium ions (in exchange for hydrogen and potassium ions) in the distal renal tubules of the kidneys. The movement of sodium ions from the renal tubules back into the bloodstream is followed by the osmotic movement of water, thus increasing the systemic blood volume and blood pressure. As can be seen, the R-A-A axis increases total blood volume and thus increases the pre-load placed upon Martha's right ventricle. This increase in pre-load will increase the strength of right ventricular contraction via the Frank-Starling relationship in the heart, though there are limits to the effectiveness of this heightened R-A-A axis (see answer #12).

CaseQuestions
y 11. Martha is started on a medication called digoxin. Why was she given this

medication, and how does it work?

y Digoxin is a digitalis derivative that slows the heart rate (i.e. it is a negative

chronotropic drug) and increases the contractility (i.e. it is a positive inotropic drug) of Martha's failing right ventricle, making it a more efficient pump. By blocking the Na+/K+ ATPase pump in the cardiac contractile cell membrane, digoxin increases intracellular Na+ concentration. This, in turn, decreases the tendency of the cell membrane Na+/Ca+2 ion exchanger to move Na+ ions into the contractile cell and Ca+2 ions out of the contractile cell. The net effect of digoxin is thus to increase the concentration of Ca+2 ions in contractile cells. Cytoplasmic Ca+2 directly and indirectly helps to initiate the sliding filament mechanism of muscle contraction in contractile cells. It directly does so by binding to troponin C and uncovering the myosin globular head binding sites on actin proteins. It indirectly does so by stimulating release of additional Ca+2 ions from the sarcoplasmic reticulum into the cytoplasm. In the end, the higher the cytoplasmic Ca+2 ion concentration, the stronger and more long-lasting the ventricular contraction.

CaseQuestions
y 12. Two weeks after starting digoxin, Martha returns to the physician's office for a follow-

up visit. On physical examination, she still has significant hepatomegaly and pitting edema, and is significantly hypertensive (i.e. she has high blood pressure). Her physician prescribes a diuretic called furosemide (or "Lasix"). Why was she given this medication, and how does it work?

y The activation of the R-A-A axis (as described in #10 above) may initially be a useful

response, helping to increase the pre-load and thus the stroke volume of the right ventricle via the Frank-Starling relationship of the heart. However, continued increases in pre-load will only increase the stroke volume up to a certain point, beyond which any further increase in blood volume can exacerbate the systemic edema and congestive heart failure. At this point, it is useful to treat Martha's systemic edema with furosemide ("Lasix"), a loop diuretic which blocks the active transport of sodium ions from the loop of Henle back into the bloodstream. Since less sodium is reabsorbed, less water follows by osmosis. This will increase Martha's urinary output and help her to excrete some of the excess sodium and water from her interstitial fluid. Martha's high blood pressure places an increased workload ("afterload") on her heart. Her physician may prescribe an "ACE inhibitor" medication (e.g. captopril, enalopril) to block the conversion of angiotensin I to angiotensin II. This will effectively slow down the R-A-A axis and significantly reduce her systemic arterial blood pressure, allowing her ventricles to function more efficiently.

References
SA Hunt, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society. Circulation. 2005;112:e154-e235. http://circ.ahajournals.org/cgi/content/full/112/12/e154 L Goldman & DA Ausiello. Cecil Textbook of Medicine, 23rd ed. Saunders, 2007. Chapters 57 & 58. National Institutes of Health Website on Heart Failure. http://www.nhlbi.nih.gov/health/dci/Diseases/Hf/HF_WhatIs.html. Accessed May 11, 2010. I Dumetru. Heart Failure. Emedicine article. Updated January 22, 2010. http://emedicine.medscape.com/article/163062-overview. Accessed May 12, 2010. McGraw Hill. Anatomy & Physiology Case Studies. http://www.mhhe.com/biosci/ap/ap_casestudies/cases/ap_case16.html. Accessed May 10, 2011.