When are pacemakers useful in acute myocardial infarction?

Abnormalities of atrioventricular (AV) conduction occur in as many as 25% of patients with myocardial infarction. Often these progress to third-degree heart block and are associated with a 50% increase in acute mortality. In general, patients with inferior myocardial infarction have block in the AV nodal area, and there is often a junctional escape rhythm with a rate of 40-60 beats per minute. These patients usually have an associated right ventricular infarction. In patients with anterior infarction, the block occurs in the His-Purkinje system, and there is often an unreliable ventricular escape rhythm with a rate of less than 40 beats per minute. Temporary pacing is required whenever any bradyarrhythmia or conduction disturbance results in significant symptoms, hypotension, or shock. In asymptomatic patients with inferior myocardial infarction, prophylactic pacing is rarely required. In asymptomatic patients with anterior myocardial infarction, indications for prophylactic pacing are controversial but generally include two or more of the following: first-degree AV block, new bundle branch block, or bifascicular bundle branch block.

The only absolute indication for permanent pacing in acute myocardial infarction is high-degree AV block that persists. In patients with acute inferior myocardial infarction, high-degree AV block almost always resolves within 2 weeks and permanent pacing is not indicated. There is controversy surrounding the use of prophylactic permanent pacing in patients with first-degree AV block combined with fascicular blocks in whom high-degree AV block has resolved.

Explain the potential mechanisms for hypotension in acute myocardial infarction.

The differential diagnosis for hypotension in the patient with myocardial infarction is important because treatment depends on the etiology.

Cardiogenic shock is categorized as hypotension (systolic blood pressure 90 mmHg) with a cardiac index of 1.8 L/min/m2 and elevation of left ventricular filling pressures (generally measured by the capillary wedge pressure). Clinical signs of hypoperfusion are also present, including oliguria, mental status changes, pulmonary edema, tachycardia, and pallor. Commonly, massive left ventricular myocardial damage ( 40% of left ventricular myocardium) is the etiology of shock in acute myocardial infarction. Another potential etiology of cardiogenic shock is right ventricular infarction which occurs in an inferior infarction. In this situation, the right ventricle may not be able to pump sufficient blood throligh the pulmonary circulation to support cardiac output. This should be suspected in patients with inferior infarction, hypotension, clear lung fields, and elevated neck veins with Kussmaul’s sign. The diagnosis can be confirmed with right-sided ECG leads or echocardiography. Right atrial pressures will be elevated out of proportion to pulmonary capillary wedge pressure in this situation, and invasive monitoring may be indicated. Hypovolemia should also be considered early in these patients, since fluid resuscitation alone may reverse the shock state. Pulmonary emboli, sepsis, aortic dissection, and tamponade must also be considered.

Symptomatic mechanical complications occur in 1% of patients with myocardial infarction and result from rupture of necrotic cardiac tissue. These complications usually occur from days 3-7 following acute infarction and include rupture of the ventricular free wall (often seen in first transmural anterior infarctions in hypertensive women), ventricular septal rupture, and acute papillary muscle rupture causing acute mitral regurgitation. Often presenting with hypotension and shock, patients with these complications approach 90% mortality if managed medically. Surgical repair of these mechanical complications is the only option if the patient can be stabilized using intraaortic balloon pumping and vigorous vasodilator therapy. The diagnosis can be established with the use of echocardiography and invasive hemodynamic monitoring. Mild to moderate mitral regurgitation is common in acute infarction and is managed medically.

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