Chapter 21 Marini Acute Coronary Syndromes

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SECTION II • Medical and Surgical Crises

a period of hours to days (“stunned myocardium”). Ischemia-induced decreases in LV compliance usu- ally require increased filling pressures to maintain stable cardiac output. Under most circumstances, a pulmonary capillary wedge pressure near 18 mm Hg is optimal. Pulmonary edema should be treated with oxy- gen, noninvasive or invasive mechanical ventila- tion, diuretics, and inotropic drugs, as dictated by hemodynamics, mental status, and ventilatory parameters. Coronary angiography with prompt revascularization by PCI or emergent coronary bypass surgery may be the only hope for most of these patients. Revascularization therapy may be particularly beneficial in those less than 75 years of age. Initial stabilization with IABP support is often helpful. IABP counterpulsations not only reduce afterload but also improve coronary blood flow. Because a substantial portion of the limited cardiac output must be diverted to the unsupported respiratory pump, mechanical ventilation can boost oxygen delivery to deprived vital organs and should be considered whenever respiratory distress becomes evident. Treatment of severe heart failure and cardiogenic shock is detailed in Chapter 3. Unfortunately, the prognosis for cardiogenic shock remains poor, with in-hospital mortality of 50% to 80%. Right Ventricular Infarction Some degree of right ventricular (RV) infarc- tion is seen in up to 30% to 40% of all inferior MIs. Hypotension, jugular venous distension, the Kussmaul sign, and clear lung fields are key diag- nostic characteristics. An important feature distin- guishing RV infarct from pulmonary embolism is the rarity of dyspnea in the former condition. RV infarction may be confirmed electrocardiographi- cally by ST segment elevation in right precordial leads (V 3 R and V 4 R). Pulmonary artery catheter- ization may be confirmatory when right atrial pres- sures are disproportionately elevated in relation to a wedge pressure. (Hemodynamic monitoring is also useful to exclude the presence of pericardial tamponade or constriction, which may have similar clinical appearance.) RV infarction, usually the result of RCA occlu- sion, rarely occurs as an isolated event. Inferior LV infarction almost always accompanies an RV infarct because the RV, posterior interventricular septum, and inferior LV wall share a common blood supply.

The physiologic derangements of RV infarction closely parallel those of constrictive pericarditis and tamponade. As the RV fails, it dilates, restricting LV filling. This combination of reduced RV sys- tolic function, RV dilation, and limited LV filling significantly reduces cardiac output. The present- ing symptom of RV infarction is hypotension—not pulmonary edema. Therefore, the treatment of the RV infarct differs in several important respects from symptomatic LV infarction. As a priority, the filling pressure of the RV must be optimized. Ultrasonic evaluation of RV filling status is usually helpful in making this determination. Effective filling may ini- tially require mean right atrial pressures higher than 20 mm Hg to maintain an acceptably high cardiac output. Once adequate RV filling has been ensured, cautious trials of inotropic drugs and/or afterload reduction also may prove helpful. Conduction disturbances are very common in RV infarction. Because of the difficulty in achiev- ing successful ventricular pacing and because of the substantial contribution of the atria to cardiac output during RV infarction, sequential AV pacing is often more successful than ventricular pacing alone. AF occurring during RV infarction is par- ticularly detrimental because of reduced ventricular compliance and should be treated aggressively with electrical or chemical cardioversion. Atrial infarction occurs rarely, usually in com- bination with infarction of the inferior wall of the LV. Fed by branches of the RCA, the right atrium is the most commonly affected chamber. Ischemia of the SA node and conduction pathways accounts for its most common manifestations: bradycardia, atrial arrhythmias, and heart block. Thrombi formed within the infarcted right atrium may embolize to the pulmonary artery. Acute Mitral Regurgitation Papillary muscle dysfunction or rupture is the most common mechanical complication of MI. In most cases, mild and transient MR is the result of papil- lary muscle ischemia or changes in LV geometry. MR has a wide range of presentations, however, ranging from minimal malfunction to frank rupture. MR most commonly results from malfunction of the pos- terior papillary muscle because it is fed by the single posterior descending artery, whereas the anterior papillary muscle is supplied by branches of both the LAD and circumflex arteries. Frank papillary muscle rupture is a rare but highly lethal event that carries