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Myocardial Infarction
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Relationships Among CAD, Stable Angina, and MI
Fig. 33-8
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Relationships Among Stable Angina, Unstable Angina, ACS, and MI
Myocardial demand > myocardial supply Ischemia is reversible No intimal disruption; no thrombus** Unstable angina Partially occlusive thrombus that stabilize, lyse, or progress to total occlusion**
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Relationships Among Stable Angina, Unstable Angina, ACS, and MI
Myocardial Infarction Myocardial demand > myocardial supply Non-reversible ischemia leading to cell death Intimal disruption → arterial spasm & thrombosis Acute coronary syndrome Includes both unstable angina and MI because both tend to be caused by intimal disruption and thrombosis Disruption is oxygen supply is prolonged and not immediately reversible
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Myocardial Infarction: Etiology and Pathophysiology
Primary reason is disruption of atherosclerotic plaque → platelet aggregation and thrombus formation Myocardial cyanosis occurs within the 1st 10 seconds of occlusion ECG changes Total occlusion anaerobic metabolism and lactic acid accumulation
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Fig. 33-9
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Myocardial Infarction: Etiology and Pathophysiology
Occurs as a result of sustained ischemia, causing irreversible cellular death Myocardial function is altered Degree of alteration depends on location and size of infarct
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Myocardial Infarction: Etiology and Pathophysiology
Contractile function of the heart stops in the areas of myocardial necrosis Most MIs involve the left ventricle (LV) Described by the area of occurrence Lateral, inferior, posterior, anterior, right ventricular, etc.
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Etiology and Pathophysiology Healing Process
Scar tissue is present by day 10 – 14, but is weak Healed by 6 weeks post MI Ventricular remodeling In attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate
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Myocardial Infarction “Typical” Symptoms
Pain Chest pain not relieved by rest, position change, or nitrates Pressure, aching, burning, crushing, squeezing, swelling, or heavy in quality The hallmark of an MI Dyspnea, diaphoreses, N & V
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Myocardial Infarction “Atypical” Symptoms
Up to 1/3 of patients do not experience chest pain Dyspnea, nausea/ vomiting, feeling faint or light-headed, and sweating or “fever” Those without chest pain delay longer in seeking Rx Up to 10% of MIs are totally asymptomatic (i.e., “silent MI”)
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Atypical symptoms more likely to occur among
Women Elderly Diabetics CHF African Americans
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Other Clinical Manifestations Myocardial Infarction
Fever May within 1st 24 hours up to 100.4° May last as long as 1 week Systemic manifestation of the inflammatory process caused by cell death
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Clinical Manifestations Myocardial Infarction
Cardiovascular manifestations indicating complication of CHF BP and heart rate initially Later the BP may drop from CO urine output Crackles Hepatic engorgement Peripheral edema
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Complications of Myocardial Infarction
Dysrhythmias Most common complication Present in 80% of MI patients Most common cause of death in the prehospital period
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Complications of Myocardial Infarction
Congestive heart failure A complication that occurs when the pumping power of the heart has diminished
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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
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Complications of Myocardial Infarction
Papillary muscle dysfunction Causes mitral valve regurgitation Condition aggravates an already compromised LV
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Complications of Myocardial Infarction
Ventricular aneurysm Results when the infarcted myocardial wall becomes thinned and bulges out during contraction
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Complications of Myocardial Infarction
Pericarditis Inflammation of the pericardium May result in cardiac compression, LV filling and emptying, and cardiac failure (cardiac tamponade)
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Complications of Myocardial Infarction
Dressler syndrome Characterized by pericarditis with effusion and fever that develops 1 to 4 weeks after MI
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Diagnostic Studies Myocardial Infarction
History of pain Risk factors Health history ECG – characteristic changes of MI Serum cardiac markers (troponin, CK MB)
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Cardiac Markers Troponin CK MB
Muscle protein released into blood after MI Rises in 3 – 12 hrs; peak at 24 – 48 hrs, returns to baseline in 5 – 14 days CK MB Enzymes released into blood after MI Rises hrs, peaks 24 hr, returns to baseline in 2 – 3 days
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Collaborative Care Myocardial Infarction
Fibrinolytic therapy Percutaneous coronary intervention (PCI), more commonly called PTCA (percutaneous transluminal coronary angioplasty)
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PTCA with Stent
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Fibrinolytic Therapy Lyses thrombi (cardiac and others), thus halting progression of MI Ideally, treatment should occur within 6 hr of onset of MI Contra-indications Conditions that put patient at high risk of hemorrhage (Table 33-14) Prevent and monitor for bleeding
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Collaborative Care Myocardial Infarction
Drug Therapy IV nitroglycerin Antiarrhythmic drugs Morphine
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Collaborative Care Myocardial Infarction
Drug Therapy -Adrenergic blockers ACE inhibitors Stool softeners
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Collaborative Care Myocardial Infarction
Nutritional Therapy Diet restricted in saturated fats and cholesterol Low sodium
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Nursing Management Angina and Myocardial Infarction Nursing Diagnoses
Acute pain Ineffective tissue perfusion Anxiety Activity intolerance Ineffective therapeutic regimen management
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Nursing Management Angina and Myocardial Infarction Planning
Overall goals: Relief of pain No progression of MI Immediate and appropriate treatment
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Nursing Management Angina and Myocardial Infarction Planning
Overall goals: Cope effectively with associated anxiety Cooperation of rehabilitation plan Modify or alter risk factors
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Nursing Management Angina and Myocardial Infarction Nursing Implementation: Angina
Acute Intervention Administration of oxygen Vital signs ECG Pain relief
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Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Acute Intervention Morphine Continuous ECG Frequent vital signs Rest and comfort
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Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Acute Intervention Anxiety Emotional and behavioral reactions Communicate with family Provide support
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Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Ambulatory and Home Care Rehabilitation Cardiac rehabilitation Physical exercise
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Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Ambulatory and Home Care Resumption of sexual activity Emotional readiness Physical training
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Sudden Cardiac Death Unexpected death from cardiac causes
Disruption in cardiac function Abrupt loss of cerebral blood flow
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Sudden Cardiac Death Usually occurs within 1 hour of onset of symptoms
Occurs secondary to natural causes Accounts for about 50% of all deaths from cardiovascular causes Mostly caused by ventricular arrhythmias
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Sudden Cardiac Death Nursing and Collaborative Management
Implantable cardioverter-defibrillator (ICD)
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