html xmlns=”http://www.w3.org/1999/xhtml” xml:lang=”en” style=”font-size:1.250rem;”> Laura D. Rosenthal DNP, ACNP, FAANP Myocardial infarction (MI), also known as heart attack, is defined as necrosis of the myocardium (heart muscle) resulting from local ischemia (deficient blood flow). The underlying cause is partial or complete blockage of a coronary artery. When blockage is complete, the area of infarction is much larger than when the blockage is partial. In this chapter, discussion is limited to acute MI caused by complete interruption of regional myocardial blood flow. This class of MI is called ST-segment elevation myocardial infarction (STEMI) because it causes elevation of the ST segment on the electrocardiogram (ECG). Management of STEMI differs from management of non–ST-elevation MI, which occurs when blockage of blood flow is only partial. In the United States STEMI strikes about 250,000 people each year and is the most common cause of death. Between 20% and 30% of STEMI victims die before reaching the hospital, another 5% to 6% die in the hospital, and 7% to 18% die within a year of hospital discharge. Risk factors for STEMI include advanced age, a family history of MI, sedentary lifestyle, high serum cholesterol, hypertension, smoking, and diabetes. The objectives of this chapter are to describe the pathophysiology of STEMI and to discuss interventions that can help reduce morbidity and mortality. Acute MI occurs when blood flow to a region of the myocardium is stopped owing to platelet plugging and thrombus formation in a coronary artery—almost always at the site of a fissured or ruptured atherosclerotic plaque. Myocardial injury is ultimately the result of an imbalance between oxygen demand and oxygen supply. In response to local ischemia, a dramatic redistribution of ions takes place. Hydrogen ions accumulate in the myocardium, and calcium ions become sequestered in mitochondria. The resultant acidosis and functional calcium deficiency alter the distensibility of cardiac muscle. Sodium ions accumulate in myocardial cells and promote edema. Potassium ions are lost from myocardial cells, setting the stage for dysrhythmias. Local metabolic changes begin rapidly after coronary arterial occlusion. Within seconds, metabolism shifts from aerobic to anaerobic. High-energy stores of adenosine triphosphate (ATP) and creatine phosphate become depleted. As a result, contraction ceases in the affected region. If blood flow is not restored, cell death begins within 20 minutes. Clear indices of cell death—myocyte disruption, coagulative necrosis, elevation of cardiac proteins in serum—are present by 24 hours. By 4 days, monocyte infiltration and removal of dead myocytes weaken the infarcted area, making it vulnerable to expansion and rupture. Structural integrity is partially restored with deposition of collagen, which begins in 10 to 12 days and ends with dense scar formation by 4 to 6 weeks. Myocardial injury also triggers ventricular remodeling, a process in which ventricular mass increases and the chambers change in volume and shape. Remodeling is driven in part by local production of angiotensin II. Ventricular remodeling increases the risk for heart failure and death. The degree of residual cardiac impairment depends on how much of the myocardium was damaged. With infarction of 10% of left ventricular (LV) mass, the ejection fraction is reduced. With 25% LV infarction, cardiac dilation and heart failure occur. With 40% LV infarction, cardiogenic shock and death are likely. The acute phase of management refers to the interval between the onset of symptoms and discharge from the hospital (usually 6–10 days). The goal is to bring cardiac oxygen supply back in balance with oxygen demand. This can be accomplished by reperfusion therapy, which restores blood flow to the myocardium, and by reducing myocardial oxygen demand. The first few hours of treatment are most critical. The major threats to life during acute STEMI are ventricular dysrhythmias, cardiogenic shock, and heart failure. To aid clinicians in the management of STEMI, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), and the Society for Cardiovascular Angiography and Interventions (SCAI) have updated a series of evidence-based guidelines, including the following: • 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines • 2015 ACC/AHA/SCAI Focused Update on Primary Percutaneous Coronary Intervention for Patients with ST-Elevation Myocardial Infarction: An Update of the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention and the 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction These guidelines are available at circ.ahajournals.org. The following discussion reflects recommendations in these documents. When a patient presents with suspected STEMI, several interventions should begin immediately. The objective is to minimize possible myocardial necrosis while waiting for a clear diagnosis. After STEMI has been diagnosed, more definitive therapy—reperfusion—can be implemented (see later). Supplemental oxygen, administered by nasal cannula, can increase arterial oxygen saturation and can thereby increase oxygen delivery to the ischemic myocardium. Accordingly, current guidelines recommend giving oxygen to all patients with reduced arterial oxygen saturation (below 90%). However, although oxygen is recommended, and using it seems to make sense, the practice is not evidence based. That is, we have no hard evidence to show that oxygen is beneficial. In fact there is some evidence that oxygen may actually be harmful, causing mortality to increase rather than decline. Aspirin suppresses platelet aggregation, producing an immediate antithrombotic effect. In the Second International Study of Infarct Survival (ISIS-2), aspirin caused a substantial reduction in mortality. Moreover, benefits were synergistic with fibrinolytic drugs: mortality was 13.2% with fibrinolytics alone, and dropped to 8% with the addition of aspirin. Because of these benefits, virtually all patients with evolving STEMI should get aspirin. Therapy should begin immediately after onset of symptoms and should continue indefinitely. The first dose (162–325 mg) should be chewed to allow rapid absorption across the buccal mucosa. Prolonged therapy (with 81–162 mg/day) reduces the risk for reinfarction, stroke, and death. According to the 2013 guideline updates, routine use of nonsteroidal antiinflammatory drugs (NSAIDs) other than aspirin should be discontinued. Unlike aspirin, these agents increase the risk for mortality, reinfarction, hypertension, heart failure, and myocardial rupture. Intravenous morphine is the treatment of choice for STEMI-associated pain. In addition to relieving pain, morphine can improve hemodynamics. By promoting venodilation, the drug reduces cardiac preload. By promoting modest arterial dilation, morphine may cause some reduction in afterload. The combined reductions in preload and afterload lower cardiac oxygen demand, helping preserve the ischemic myocardium. When given to patients undergoing acute STEMI, beta blockers (e.g., atenolol, metoprolol) reduce cardiac pain, infarct size, and short-term mortality. Recurrent ischemia and reinfarction are also decreased. Reduction in myocardial wall tension may decrease the risk for myocardial rupture. Continued use of an oral beta blocker increases long-term survival. Unfortunately, although nearly all patients can benefit from beta blockers, many don’t get them. Furthermore, among patients who do get a beta blocker, the dosage is often too low. Benefits result from several mechanisms. As STEMI evolves, traffic along sympathetic nerves to the heart increases greatly, as does the number of beta receptors in the heart. As a result, heart rate and force of contraction rise substantially, increasing cardiac oxygen demand. By preventing beta receptor activation, beta blockers reduce heart rate and contractility and thereby reduce oxygen demand. They reduce oxygen demand even more by lowering blood pressure. By prolonging diastolic filling time, beta blockers increase coronary blood flow and myocardial oxygen supply. Additional benefits derive from antidysrhythmic actions. Beta blockers should be used routinely in the absence of specific contraindications (e.g., bradycardia, significant LV dysfunction). The initial dose may be oral or IV; oral dosing is used thereafter. Treatment with an oral beta blocker should begin within 24 hours. Beta blockers are especially good for patients with reflex tachycardia, systolic hypertension, atrial fibrillation, and atrioventricular conduction abnormalities. Contraindications include overt severe heart failure, pronounced bradycardia, persistent hypotension, advanced heart block, and cardiogenic shock. The basic pharmacology of the beta blockers is presented in Chapter 14. In patients with STEMI, nitroglycerin has several beneficial effects: it can (1) reduce preload and thereby reduce oxygen demand; (2) increase collateral blood flow in the ischemic region of the heart; (3) control hypertension caused by STEMI-associated anxiety; and (4) limit infarct size and improve LV function. However, despite these useful effects, nitroglycerin does not reduce mortality. Nonetheless, because the drug is easily administered, offers hemodynamic benefits, and helps relieve ischemic chest pain, it continues to be used. According to the current guidelines, patients with ongoing ischemic discomfort should be given sublingual nitroglycerin (0.4 mg) every 5 minutes for a total of three doses, and then be assessed to determine whether IV nitroglycerin should be given. Indications for IV therapy include persisting ischemic discomfort, hypertension, and pulmonary congestion. Nitroglycerin should be avoided in patients with hypotension (systolic pressure below 90 mm Hg), severe bradycardia (heart rate below 50 beats/min), marked tachycardia (heart rate above 100 beats/min), or suspected right ventricular infarction. In addition, nitroglycerin should be avoided in patients who have taken sildenafil, avanafil, or vardenafil for erectile dysfunction or pulmonary hypertension within the last 24 hours, or tadalafil within the last 48 hours.
Management of ST-Segment Elevation Myocardial Infarction
Pathophysiology of STEMI
Management of STEMI
Routine Drug Therapy
Oxygen
Aspirin
Nonaspirin Nonsteroidal Antiinflammatory Drugs
Morphine
Beta Blockers
Nitroglycerin
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Management of ST-Segment Elevation Myocardial Infarction
Chapter 88
