Coronary Artery Disease and Acute Coronary Syndrome Myocardial Infarction

I. Description Cardiovascular diseases are the major cause of death in Canada, US, Europe. Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general II. Etiology and Pathophysiology Developmental Stages Complicated lesion Final stage in development The most dangerous Plaque consists of a core of lipid materials within an area of dead tissue With the incorporation of lipids, thrombi, damaged tissue, and accumulation of calcium, the growing lesion becomes complex Collateral Circulation Normally some arterial branching, termed collateral circulation, exists within the coronary circulation Growth of collateral circulation is attributed to two factors: The inherited predisposition to develop new vessels The presence of chronic ischemia When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation to develop III. Clinical Manifestations of CAD Angina Pectoris Acute Coronary Syndrome Sudden Cardiac Death Stable Angina Results when the lack of oxygen supply is temporary and reversible Acute Coronary Syndrome (ACS) Develops when the oxygen supply is prolonged and not immediately reversible ACS encompasses: Unstable angina Non-ST-segment-elevation myocardial infarction (NSTEMI) ST-segment-elevation (STEMI) Relationships among CAD, Stable Angina, and MI

Myocardial ischemia: O2 demand > O2 supply Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis In CAD the coronary arteries are unable to dilate to meet increased metabolic needs because they are already chronically dilated beyond the obstructed area For ischemia to occur, the artery is usually 75% or more stenosed In addition, the diseased heart has difficulty increasing the rate of blood flow Coronary spasm The constriction is transient and reversible Causes either subtotal or total narrowing Myocardial cyanosis occurs within the 1st 10 seconds of coronary occlusion ECG changes Total occlusion anaerobic metabolism and lactic acid accumulation Myocardial Infarction Occurs as a result of sustained ischemia, causing irreversible cellular death The degree of altered function depends on the area of the heart involved and the size of the infarct Contractile function of the heart stops in the areas of myocardial necrosis Most involve the left ventricle (LV) Transmural MI Subendocardial MI Infarctions are described by the area of occurrence IV. Healing Process Within 24 hours, leukocytes infiltrate the area of cell death Enzymes are released from the dead cardiac cells (important indicators of MI) Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by 2nd or 3rd day 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

By 6 weeks after MI, scar tissue has replaced necrotic tissue Area is said to be healed Ventricular remodeling In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate

Dressler syndrome Pulmonary embolism

Types of Angina Silent Ischemia Up to 80% of patients with myocardial ischemia are asymptomatic Associated with diabetes mellitus and hypertension Prinzmetals Angina When spasm occurs: Pain Marked, transient ST segment elevation with angina (unlike with AMI; ST = MI) May occur during REM sleep Clinical Manifestations Myocardial Infarction Pain -The hallmark of an MI Location of Chest Pain

Nausea and vomiting Sympathetic nervous system stimulation Fever Cardiovascular manifestations Later the BP may drop from CO urine output Crackles Hepatic engorgement Peripheral edema Complications of Myocardial Infarction Arrhythmias Congestive heart failure Cardiogenic shock Papillary muscle dysfunction Ventricular aneurysm Pericarditis

Diagnostic Studies Myocardial Infarction History of pain Risk factors Health history ECG: ST elevation, greater than 1 mm above PR Interval; T Wave inversion (flipped T Waves); Pathological Q-wave (Q wave greater than size of R wave) Serum cardiac markers: CK-MB: indicates muscle damage (rises 312 hours post AMI returns to normal 2-3 days) Triponen: is a myocardial muscle protein (rises as quickly as CK; remains elevated for 2 weeks) Myoglobin: rises 3 hours after AMI; lacks cardiac specificity Collaborative Care Angina Percutaneous coronary intervention Stent placement Atherectomy Laser angioplasty Myocardial revascularization (CABG) MIDCABG procedure Myocardial Infarction Fibrinolytic therapy Cardiac catheterization Percutaneous coronary intervention Drug Therapy IV nitroglycerin Antiarrhythmic drugs Morphine -Adrenergic blockers Angiotensin-converting enzyme inhibitors Stool softeners Nutritional Therapy Diet restricted in saturated fats and cholesterol Low sodium Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI Acute Intervention Morphine Continuous ECG Frequent vital signs Rest and comfort Anxiety Emotional and behavioral reactions Communicate with family Provide support Ambulatory and Home Care Rehabilitation Cardiac rehabilitation Physical exercise

Resumption of sexual activity Emotional readiness Physical training Nursing Management Angina and Myocardial Infarction Evaluation Pain level Cardiac pump effectiveness Anxiety control Energy conservation Health orientation