Chapter 34

Focus on Coronary Artery Disease and Acute Coronary Syndrome
(Relates to Chapter 34, Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome, in the textbook)
Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Coronary Artery Disease and Acute Coronary Syndrome

A type of blood vessel disorder that is included in the general category of atherosclerosis Begins as soft deposits of fat that harden with age Referred to as hardening of arteries

Atherosclerosis (contd)
Can occur in any artery in the body Atheromas (fatty deposits) Preference for the coronary arteries

Cardiovascular diseases are the major cause of death in the United States Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general
Progression of Atherosclerosis
Fig. 34-2
Coronary Artery Disease Etiology and Pathophysiology

Fatty streaks . Fibrous plaque: show the progressive changes in endothelium Result = narrowing of vessel lumen Complicated lesion Continued inflammation can result in plaque instability, ulceration, and rupture.Artery inner wall compromise. Platelets accumulate and thrombus forms Increased narrowing or total occlusion of lumen
Reflect the end organ involved : Heart myocardial infarct Legs gangrene Aorta atherosclerotic aneurysm Viscera infarcts
patho
Inflammation and endothelial injury play role to develop atherosclerosis. Endothelial wall can injury as result of tabaco,lipds,HTN,diabetics,infection(clamydia,pn eumonie ,herps)casuing inflammation. C reactive protein (CPR): marker of systemic inflammation. it rise in pet with CAD. It indicate unstable plaques andoxidation of ldl.
Risk Factors for CAD

Risk factors can be categorized as
Nonmodifiable risk factors Age Gender Ethnicity Family history Genetic predisposition
Risk Factors for CAD

Risk factors can be categorized as
Modifiable risk factors Elevated serum lipids Hypertension Tobacco use Physical inactivity Obesity Diabetes
Metabolic syndrome Psychologic states Homocysteine level
Lipoprotein:
Lipprotein:Elevated serum lipid levels is one of the most firmly established risk factors for CAD. There are three different types. High-density lipoproteins (HDLs) carry lipids away from arteries and to the liver for metabolism. High serum HDL levels are desirable. HDL levels are increased by physical activity, moderate alcohol consumption, and estrogen administration. Elevated low-density lipoprotein (LDL) levels correlate most closely with an increased incidence of atherosclerosis and CAD. *Increased HDL and decreased triglycerides is good Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
HTN and tabacco use:

Nictotine cause catechlamine(epnephrine,norepinephrine) realse,which increased HR,pheripheral vasoconstrduction,and rise B.P. these change incread cardiac workload,and gret mycordial oxygen consumption.
Risk Factors for CAD Health Promotion

Identification of people at high risk
Health history, including use of prescription/nonprescription medications Presence of cardiovascular symptoms Environmental patterns: diet, activity Values and beliefs about health and illness

Health-promoting behaviors
Physical fitness
30 minutes >5 days/week Regular physical activity contributes to: Weight reduction Reduction of BP increase in HDL cholesterol

Nutritional therapy
Therapeutic Lifestyle Changes Omega-3 fatty acids

Cholesterol-lowering drug therapy
Drugs that restrict lipoprotein production: Statins, niacin Drugs that increase lipoprotein removal: Bile acid sequestrants Drugs that decrease cholesterol absorption: Ezetimibe (Zetia)

Antiplatelet therapy ASA Clopidogrel (Plavix) if aspirn is intolerant.
Clinical Manifestations of CAD Chronic Stable Angina

Etiology and Pathophysiology
Reversible (temporary) myocardial ischemia = angina (chest pain) O2 demand > O2 supply

Etiology and Pathophysiology
Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis For ischemia to occur, the artery is usually 75% or more stenosed

Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms

Pain usually lasts minutes
Subsides when the precipitating factor is relieved Pain at rest is unusual ECG may reveal ST segment depression
Location of Chest Pain (Angina)
Fig. 34-7
Chronic Stable Angina Types of Angina

Prinzmetals (variant) angina
Occurs at rest usually in response to spasm of major coronary artery Seen in patients with a history of migraine headaches and Raynauds phenomenon Spasm may occur in the absence of CAD
Chronic Stable Angina Types of Angina

Prinzmetals (variant) angina When spasm occurs
Chest pain Marked, transient ST segment elevation
May occur during REM sleep May be relieved by moderate exercise

Chronic Stable Angina

Nursing and Collaborative Management Drug therapy: Goal: and/or O2 supply O2 demand
Short-acting nitrates: Sublingual Long-acting nitrates Nitroglycerin ointment Transdermal controlled-release nitroglycerin

Nursing and Collaborative Management
Drug therapy: Goal: O2 demand and/or O2 supply
-Adrenergic blockers Calcium channel blockers
If -adrenergic blockers are poorly tolerated, contraindicated, or do not control anginal symptoms Used to manage Prinzmetals angina
Angiotensin-converting enzyme inhibitors


Diagnostic Studies Health history/physical examination Laboratory studies 12-lead ECG Chest x-ray Echocardiogram Exercise stress test

Diagnostic Studies Cardiac catheterization

Diagnostic Coronary revascularization: Percutaneous coronary intervention Balloon angioplasty Stent
Placement of a Coronary Artery Stent
Fig. 34-9
Pre- and Post-PCI with Stent Placement
Fig. 34-10
Acute Coronary Syndrome

When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops ACS encompasses:
Unstable angina (UA) NonST-segment-elevation myocardial infarction (NSTEMI) ST-segment-elevation (STEMI)
Relationship Between CAD, Chronic Stable Angina, and ACS
Fig. 34-11
Acute Coronary Syndrome Etiology and Pathophysiology

Deterioration of a once stable plaque Rapture, expose the intima to blood and stimulating platelt aggregation and local vasoconstriction and thrombus formation.
Result
Partial occlusion of coronary artery: UA or NSTEMI Total occlusion of coronary artery: STEMI
Coronary Thrombogenesis Secondary to Plaque Deterioration
Clinical Manifestations of ACS Unstable Angina

Unstable angina
New in onset Occurs at rest Has a worsening pattern
UA is unpredictable and represents a medical emergency
Symptom : Woman develop UA before CAD daignised. Fatique,(most prominent) shortness of breath,indigestion, anexity.
Clinical Manifestations of ACS Myocardial Infarction (MI)

Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis) Necrosis of entire thickness of myocardium takes 4 to 6 hours
Acute Myocardial Infarction

Myocardial infarction (MI) occurs as a result of sustained ischemia, causing irreversible myocardial cell death. Contractile function of the heart stops in the infarcted area(s). The acute MI process takes time, evolving over a period of up to 12 hours. Infarctions are described based on the location of damage. Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. The pain is usually described as a heaviness, pressure, tightness, burning, constriction, Fig. 34-13 or crushing.
Complications after MI Dysrhythmias are the most common complication and the most common cause of death in patients in the prehospital period. Other complications include heart failure, cardiogenic shock, papillary muscle dysfunction or rupture, ventricular aneurysm, and pericarditis. Primary diagnostic studies used to determine whether a person has UA or an MI includes an ECG and serum cardiac markers.
Clinical Manifestations of ACS Myocardial Infarction

The degree of altered function depends on the area of the heart involved and the size of the infarct
Contractile function of the heart is disrupted in areas of myocardial necrosis)
Occlusion of the Left Anterior Descending Coronary Artery, Resulting in MI
Fig. 34-12
Clinical Manifestations of ACS Myocardial Infarction Pain

Total occlusion anaerobic metabolism and lactic acid accumulation
Clinical Manifestations of ACS Myocardial Infarction Pain

Described as heaviness, constriction, tightness, burning, pressure, or crushing Common locations: substernal, retrosternal, or epigastric areas; pain may radiate

During the initial phase of MI ,ischemic myocardial cell release catecholamines: Sympathetic nervous system stimulation results in Release of glycogen Diaphoresis Vasoconstriction of peripheral blood vessels Skin: ashen, clammy, and/or cool to touch

Cardiovascular:in response to realse catecholamine, HR and BP, later BP (secondary to in CO). Crackles if present for several days (suggest left ventricular dysfunction) Hepatic engorgement and peripheral edema and Jugular venous distention(R v DYSF) Abnormal heart sounds S3 or S 4 New murmur ,a loud holosytolic murmur ,may indicate septal defect or mitral value dysfunction.

Nausea and vomiting
Can result from reflex stimulation of the vomiting center by the severe pain
Fever
Systemic manifestation of the inflammatory process caused by cell death
Myocardial Infarction Healing Process

Development of collateral circulation improves areas of poor perfusion
Necrotic zone identifiable by ECG changes and nuclear scanning 10 to 14 days after MI, scar tissue is still weak and vulnerable to stress
Complications of Myocardial Infarction

Dysrhythmias
Most common complication Present in 80% of MI patients
Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock

Heart failure
A complication that occurs when the pumping power of the heart has diminished Pulmonary congestion on X rays,carackle on auscultation, JVD.

Cardiogenic shock
Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure Requires aggressive management e.g control of dysthymias,intraaortic ballon pump.GOAL: max 02 and reduce the demand of 02 and prevent complication like renal failure.

Papillary muscle dysfunction
Causes mitral valve regurgitation Condition aggravates an already compromised LV
Ventricular aneurysm
Results when the infarcted myocardial wall becomes thinned and bulges out during contraction

Acute pericarditis
An inflammation of visceral and/or parietal pericardium May result in cardiac compression, LV filling and emptying, heart failure
Pericardial friction rub may be heard on auscultation

Diagnostic Studies
Unstable Angina and Myocardial Infarction
Detailed health history and physical 12-lead ECG: Changes in QRS complex, ST segment, and T wave can rule out or confirm UA or MI Serum cardiac markers Coronary angiography Others: Exercise stress testing, echocardiogram
Serum Cardiac Markers After MI
Fig. 34-15
Collaborative Care Acute Coronary Syndrome

Emergency management
Initial interventions Ongoing monitoring
Emergent PCI
Treatment of choice for confirmed MI Balloon angioplasty + drug-eluting stent(s) Ambulatory 24 hours after the procedure

Fibrinolytic therapy
Indications and contraindications Marker of reperfusion: Return of ST segment to baseline Rescue PCI if thrombolysis fails Major complication: Bleeding

Drug therapy
IV nitroglycerin Morphine sulfate -adrenergic blockers Angiotensin-converting enzyme inhibitors Antidysrhythmia drugs Cholesterol-lowering drugs Stool softeners

Nutritional therapy Progress to low-salt, low saturated fat, low-cholesterol diet

Coronary surgical revascularization
Fail medical management Presence of left main coronary artery or three-vessel disease Not a candidate for PCI (e.g., lesions are long or difficult to access) Failed PCI with ongoing chest pain

Coronary surgical revascularization
Coronary artery bypass graft (CABG) surgery Requires cardiopulmonary bypass Uses arteries and veins for grafts
CABG Surgery
Fig. 34-16
Nursing Management Chronic Stable Angina and ACS

Nursing Assessment Subjective Data Health history Functional health patterns Objective Data

Nursing Diagnoses Acute pain Ineffective tissue perfusion (cardiac) Anxiety Activity intolerance

Planning: Overall goals
Relief of pain Preservation of myocardium Immediate and appropriate treatment Effective coping with illness-associated anxiety Participation in a rehabilitation plan Reduction of risk factors
Nursing Management Chronic Stable Angina

Health Promotion
Therapeutic lifestyle changes to reduce cardiac risk factors

Acute Interventions for anginal attack
Rest Administration of supplemental oxygen 12-lead ECG Prompt pain relief first with a nitrate followed by an opioid analgesic if needed Auscultation of heart sounds Comfortable positioning of the patient

Ambulatory and Home Care
Patient teaching CAD and angina Precipitating factors for angina Risk factor reduction Medications
Definition: a spectrum of clinical presentations: Unstable angina: angina of recent onset (<2 months), worsening or angina at rest. Non ST elevation myocardial infarction: incomplete occlusion of coronary vessels leading to ischemia and mild necrosis of myocardium (Troponin-I raised only) ST elevation myocardial infarction: complete occlusion of coronary vessels leading to necrosis of the myocardium
ACS
History & Exam Central crushing chest pain, that may radiate to the arm, neck or jaw, brought on by exercise, cold weather, following a big meal, or stress. The pain is associated with nausea +/- vomiting, diaphoresis, pallor, syncope or pre syncope, palpitations and dyspnoea
Investigations: the diagnosis is clinical

Bloods: FBC:haemoglobin (anaemia?), leucocytosis (infection?) U&E: electrolyte disturbances establish a baseline for the patient and assess their renal function. LFTs:deranged in case of right heart failure. Coags: bleeding disorder, this patient may undergo thrombolysis. Glucose: Diabetes mellitus, hypoglycaemia/hyperglycaemia Fasting serum lipids: hyperlipidemia BNP: heart failure? & Cardiac enzymes:
ECG: Unstable angina: Normal, there may be ST Depression/T wave inversion Non-STEMI: ST depression/T wave inversion (ischemia) STEMI: ST elevation for >1mm in 2 contiguous chest leads New onset LBBB
ACS
On examination: Tachycardia, tachypnoea, hypo/hypertension, pallor, anxiety, signs of left or right heart failure, a 4 heart sound, pansystolic murmur.
Nursing Management ACS

Acute Intervention
Pain: Nitroglycerin, morphine, oxygen Continuous monitoring
ECG VS, pulse oximetry Heart and lung sounds
Rest and comfort

Balance rest and activity Begin cardiac rehabilitation

Acute Intervention
Anxiety Emotional and behavioral reaction
Maximize patients social support systems Consider open visitation

Coronary revascularization: ICU for first 24 to 36 hours
Pulmonary artery catheter for measuring CO, other hemodynamic parameters Intraarterial line for continuous BP monitoring Pleural/mediastinal chest tubes for chest drainage Continuous ECG monitoring to detect dysrhythmias (esp. atrial dysrhythmias)

Coronary revascularization: ICU for first 24 to 36 hours
Endotracheal tube connected to mechanical ventilation Extubation within 12 hours Epicardial pacing wires for emergency pacing of the heart Urinary catheter to monitor urine output NG tube for gastric decompression

Coronary revascularization: Care is focused on
Assessing the patient for bleeding (e.g., chest tube drainage, incision sites) Monitoring fluid status Replacing electrolytes PRN Restoring temperature (e.g., warming blankets)

Ambulatory and Home Care
Patient teaching Physical exercise Resumption of sexual activity Emotional readiness of patient and partner Physical expenditure

Evaluation
Relief of pain Preservation of myocardium Immediate and appropriate treatment Effective coping with illness-associated anxiety Participation in a rehabilitation plan Reduction of risk factors
Sudden Cardiac Death (SCD)

Unexpected death from cardiac causes
Most deaths occur outside of hospital CAD accounts for about 80% of all SCDs

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Chapter 34

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Focus on Coronary Artery Disease and Acute Coronary Syndrome

Coronary Artery Disease and Acute Coronary Syndrome

Coronary Artery Disease and Acute Coronary Syndrome

Coronary Artery Disease and Acute Coronary Syndrome

Coronary Artery Disease Etiology and Pathophysiology

Risk Factors for CAD

Risk Factors for CAD

Metabolic syndrome Psychologic states Homocysteine level

HTN and tabacco use:

Risk Factors for CAD Health Promotion

Risk Factors for CAD Health Promotion

Risk Factors for CAD Health Promotion

Therapeutic Lifestyle Changes Omega-3 fatty acids

Risk Factors for CAD Health Promotion

Risk Factors for CAD Health Promotion

Clinical Manifestations of CAD Chronic Stable Angina

Clinical Manifestations of CAD Chronic Stable Angina

Clinical Manifestations of CAD Chronic Stable Angina

Clinical Manifestations of CAD Chronic Stable Angina

Location of Chest Pain (Angina)

Chronic Stable Angina Types of Angina

Chronic Stable Angina Types of Angina

May occur during REM sleep May be relieved by moderate exercise

Chronic Stable Angina

Chronic Stable Angina

Angiotensin-converting enzyme inhibitors

Chronic Stable Angina

Chronic Stable Angina

Diagnostic Studies Cardiac catheterization

Placement of a Coronary Artery Stent

Pre- and Post-PCI with Stent Placement

Acute Coronary Syndrome

Relationship Between CAD, Chronic Stable Angina, and ACS

Acute Coronary Syndrome Etiology and Pathophysiology

Coronary Thrombogenesis Secondary to Plaque Deterioration

Clinical Manifestations of ACS Unstable Angina

UA is unpredictable and represents a medical emergency

Clinical Manifestations of ACS Myocardial Infarction (MI)

Acute Myocardial Infarction

Clinical Manifestations of ACS Myocardial Infarction

Occlusion of the Left Anterior Descending Coronary Artery, Resulting in MI

Clinical Manifestations of ACS Myocardial Infarction Pain

Clinical Manifestations of ACS Myocardial Infarction Pain

Clinical Manifestations of ACS Myocardial Infarction

Clinical Manifestations of ACS Myocardial Infarction

Clinical Manifestations of ACS Myocardial Infarction

Myocardial Infarction Healing Process

Complications of Myocardial Infarction

Complications of Myocardial Infarction

Complications of Myocardial Infarction

Complications of Myocardial Infarction

Complications of Myocardial Infarction

Pericardial friction rub may be heard on auscultation

Serum Cardiac Markers After MI

Collaborative Care Acute Coronary Syndrome

Collaborative Care Acute Coronary Syndrome

Collaborative Care Acute Coronary Syndrome

Collaborative Care Acute Coronary Syndrome

Collaborative Care Acute Coronary Syndrome

Collaborative Care Acute Coronary Syndrome

Nursing Management Chronic Stable Angina and ACS

Nursing Management Chronic Stable Angina and ACS

Nursing Management Chronic Stable Angina and ACS

Nursing Management Chronic Stable Angina