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Coronary Artery Disease and Acute Coronary Syndrome Myocardial Infarction (relates to Chapter 33, “Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome,” in the textbook) Description • Cardiovascular diseases are the major cause of death in Canada • Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general 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 Etiology and Pathophysiology Developmental Stages • Complicated lesion – With the incorporation of lipids, thrombi, damaged tissue, and accumulation of calcium, the growing lesion becomes complex Etiology and Pathophysiology Collateral Circulation • Normally some arterial branching, termed collateral circulation, exists within the coronary circulation Etiology and Pathophysiology Collateral Circulation • Growth of collateral circulation is attributed to two factors: – The inherited predisposition to develop new vessels – The presence of chronic ischemia Etiology and Pathophysiology Collateral Circulation • When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing Collateral Circulation Fig. 33-5 Clinical Manifestations of CAD • Angina Pectoris • Acute Coronary Syndrome • Sudden Cardiac Death Clinical Manifestations • Stable Angina – Results when the lack of oxygen supply is temporary and reversible Clinical Manifestations • Acute Coronary Syndrome (ACS) – Develops when the oxygen supply is prolonged and not immediately reversible Clinical Manifestations • ACS encompasses: – Unstable angina – Non-ST-segment-elevation myocardial infarction (NSTEMI) – ST-segment-elevation (STEMI) Relationships Among CAD, Stable Angina, and MI Fig. 33-8 Etiology and Pathophysiology • Myocardial ischemia: – O2 demand > O2 supply • Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis Etiology and Pathophysiology • In CAD the coronary arteries are unable to dilate to meet increased metabolic needs because they are already chronically dilated beyond the obstructed area Etiology and Pathophysiology • 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 Etiology and Pathophysiology • Coronary spasm – The constriction is transient and reversible – Causes either subtotal or total narrowing Etiology and Pathophysiology • Myocardial cyanosis occurs within the 1st 10 seconds of coronary occlusion • ECG changes • Total occlusion anaerobic metabolism and lactic acid accumulation Etiology and Pathophysiology • Myocardial Infarction – Occurs as a result of sustained ischemia, causing irreversible cellular death Etiology and Pathophysiology • Myocardial Infarction – The degree of altered function depends on the area of the heart involved and the size of the infarct Etiology and Pathophysiology • Myocardial Infarction – Contractile function of the heart stops in the areas of myocardial necrosis – Most involve the left ventricle (LV) Etiology and Pathophysiology • Myocardial Infarction – Transmural MI • Involves the entire thickness of the myocardium Transmural MI Fig. 33-11 Etiology and Pathophysiology • Myocardial Infarction – Subendocardial MI • The damage has not penetrated through the entire thickness Etiology and Pathophysiology • Myocardial Infarction – Infarctions are described by the area of occurrence Etiology and Pathophysiology Healing Process • Within 24 hours, leukocytes infiltrate the area of cell death • Enzymes are released from the dead cardiac cells (important indicators of MI) Etiology and Pathophysiology Healing Process • Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by 2nd or 3rd day • Development of collateral circulation improves areas of poor perfusion Etiology and Pathophysiology Healing Process • Necrotic zone identifiable by ECG changes and nuclear scanning • 10 to 14 days after MI, scar tissue is still weak Etiology and Pathophysiology Healing Process • By 6 weeks after MI, scar tissue has replaced necrotic tissue – Area is said to be healed Etiology and Pathophysiology Healing Process • Ventricular remodeling – In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate Types of Angina Silent Ischemia • Up to 80% of patients with myocardial ischemia are asymptomatic • Associated with diabetes mellitus and hypertension Types of Angina Prinzmetal’s 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 – Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration • The hallmark of an MI Location of Chest Pain Fig. 33-12 Clinical Manifestations Myocardial Infarction • Nausea and vomiting – Can result from reflex stimulation of the vomiting center by the severe pain Clinical Manifestations Myocardial Infarction • Sympathetic nervous system stimulation – catecholamines released during initial phases of MI – Results in diaphoresis and vasoconstriction Clinical Manifestations Myocardial Infarction • Fever – May within 1st 24 hours up to 100.4° – May last as long as 1 week Clinical Manifestations Myocardial Infarction • Fever – Systemic manifestation of the inflammatory process caused by cell death Clinical Manifestations Myocardial Infarction • Cardiovascular manifestations – BP and heart rate initially – Later the BP may drop from CO Clinical Manifestations Myocardial Infarction • Cardiovascular manifestations – urine output – Crackles – Hepatic engorgement – Peripheral edema Complications of Myocardial Infarction • Arrhythmias – Most common complication – Present in 80% of MI patients – Most common cause of death in the prehospital period Complications of Myocardial Infarction • Congestive heart failure – A complication that occurs when the pumping power of the heart has diminished Complications of Myocardial Infarction • Cardiogenic shock – Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure – Requires aggressive management Complications of Myocardial Infarction • Papillary muscle dysfunction – Causes mitral valve regurgitation – Condition aggravates an already compromised LV Complications of Myocardial Infarction • Ventricular aneurysm – Results when the infarcted myocardial wall becomes thinned and bulges out during contraction Complications of Myocardial Infarction • Pericarditis – An inflammation of the visceral and/or parietal pericardium – May result in cardiac compression, LV filling and emptying, and cardiac failure Complications of Myocardial Infarction • Dressler syndrome – Characterized by pericarditis with effusion and fever that develops 1 to 4 weeks after MI Complications of Myocardial Infarction • Pulmonary embolism – Source of the thrombus may be the roughened endocardium or leg veins 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 ¼ size of R wave) Serum cardiac markers: CK-MB: indicates muscle damage (rises 3-12 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 – Surgical intervention alternative – Performed with local anesthesia – Ambulatory 24 hours after the procedure Collaborative Care Angina • Stent placement – Used to treat abrupt or threatened abrupt closure and restenosis following PCI Collaborative Care Angina • Atherectomy – The plaque is shaved off using a type of rotational blade – Decreases the incidence of abrupt closure as compared with PCI Collaborative Care Angina • Laser angioplasty – Performed with a catheter containing fibers that carry laser energy – Used to precisely dissolve the blockage Collaborative Care Angina • Myocardial revascularization (CABG) – Primary surgical treatment for CAD – Patient with CAD who has failed medical management or has advanced disease is considered a candidate Collaborative Care Angina • MIDCABG procedure – Minimally invasive direct coronary artery bypass grafting (MIDCABG) – Alternative to traditional CABG Collaborative Care Myocardial Infarction • Fibrinolytic therapy • Cardiac catheterization • Percutaneous coronary intervention Collaborative Care Myocardial Infarction • Drug Therapy – IV nitroglycerin – Antiarrhythmic drugs – Morphine Collaborative Care Myocardial Infarction • Drug Therapy – -Adrenergic blockers – Angiotensin-converting enzyme inhibitors – Stool softeners Collaborative Care Myocardial Infarction • 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 Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI • Acute Intervention – Anxiety – Emotional and behavioral reactions • Communicate with family • Provide support Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI • Ambulatory and Home Care – Rehabilitation – Cardiac rehabilitation – Physical exercise Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI • Ambulatory and Home Care – 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 Women and Coronary Artery Disease • About 500,000 deaths occur in women per year • Kills almost 10 times more women than breast cancer Women and Coronary Artery Disease • Manifest CAD 10 years later in life than men • Most have symptoms of angina rather than MI Women and Coronary Artery Disease • Diabetes mellitus found to be the single most powerful predictor of CAD in women