Early in the course of AMI, patients frequently exhibit evidence of increased autonomic nervous system activity. Sinus bradycardia, atrioventricular block, and hypotension may occur from increased vagal tone. Activation of atrial and ventricular receptors in the myocardium may result in enhanced efferent sympathetic activity, increased circulating catecholamines, and increased local catecholamine release. These increased catecholamines in the setting of a sensitive myocardium form the substrate for the generation of tachyarrhythmias. Electrical instability during acute myocardial infarction results in ventricular premature beats, ventricular tachycardia, ventricular fibrillation, accelerated idioventricular rhythms, and some AV junctional tachycardias.
The hemodynamic consequences of dysrhythmias are dependent on ventricular function. Patients with left ventricular dysfunction have a relatively fixed stroke volume. They depend upon changes in heart rate to alter cardiac output. The range of heart rate that is optimal becomes narrowed with increasing dysfunction. Slower or faster heart rates may further depress cardiac output.
Additionally, maintenance of the atrial kick is important for patients with AMI. Patients with normal hearts have a loss of 15 to 20 percent of left ventricular output when the atrial kick is eliminated. Patients with reduced left ventricular compliance, as occurs from AMI, have a 35 percent reduction in stroke volume when the atrial systole is eliminated.
"Pump" failure with resultant increased sympathetic stimulation results in sinus tachycardia, atrial fibrillation/flutter, and supraventricular tachycardias. Conduction disturbances result in bradydysrhythmias such as sinus bradycardia, junctional escape rhythms, and atrioventricular and idioventricular blocks.
The significance of cardiac dysrhythmias during acute myocardial infarction is the subject of some debate. Sinus bradycardia during the early phases of AMI may predispose to hypotension and repetitive ventricular dysrhythmias. On the other hand, it appears to be protective because it reduces the myocardial oxygen requirement. The net effect is that the presence of sinus bradycardia does not appear to increase mortality during AMI.
Almost all patients with first-degree AV block have infranodal disturbances above the His bundle and will not progress to higher degrees of AV block. Mobitz I (Wenckebach) accounts for 90 percent of second-degree AV block. It generally occurs within the AV node, is associated with narrow QRS complexes, and results from ischemic injury. It is more common with inferior than anterior AMI, is intermittent usually during the first 72 h after infarction, and rarely progresses to complete heart block or other pathologic rhythm. Conversely, Mobitz 2 second-degree heart block originates from conduction lesions below the His bundle, is associated with a wide QRS complex, is usually associated with anterior AMI, and does progress to complete heart block.
Complete heart block can occur in patients with both anterior and inferior AMI. This is because the atrioventricular conduction system receives blood supply from both the AV branch of the right coronary artery and the septal perforating branch of the left anterior descending coronary artery. Complete heart block occurs in the setting of inferior myocardial infarction; it usually progresses from lesser forms of AV block. This form of third degree block is usually stable and should resolve. In the absence of right ventricular involvement, the mortality is approximately 15 percent. It rises to greater than 30 percent when right ventricular involvement is present. In contrast, complete heart block in the setting of an anterior MI is seldom benign and portends a grave prognosis. Junctional rhythms are usually transient and occur within 48 h of infarction. Whether they affect long-term prognosis is not clear.
Sinus tachycardia is quite prominent in patients with anterior wall AMI. Because of increased myocardial oxygen utilization, persistent sinus tachycardia is associated with a poor prognosis. The etiology of the sinus tachycardia should be determined. It may include anxiety, pain, left ventricular failure, fever, pericarditis, hypovolemia, atrial infarction, pulmonary emboli, or use of medications that accelerate heart rate. Similarly, paroxysmal supraventricular tachycardia, atrial fibrillation, and atrial flutter are associated with an increased mortality. Atrial premature contractions are common. They occur in up to 50 percent of AMI patients, and are not associated with an increased mortality related to the acute event.
Ventricular premature contractions are common in patients with AMI. They do not appear to have much prognostic ability. Accelerated idioventricular rhythms in patients with AMI have not been shown to have an effect on prognosis. Ventricular tachycardia shortly after AMI is often transient and does not portend a poor prognosis. When ventricular tachycardia occurs late in the course of AMI, it is usually associated with transmural Q-wave infarction and left ventricular dysfunction, induces hemodynamic deterioration, and is associated with a mortality rate approaching 50 percent. Primary ventricular fibrillation, occurring shortly after symptom onset does not appear to have a large effect on mortality and prognosis. Delayed or secondary ventricular fibrillation during hospitalization is associated with severe ventricular dysfunction and a 75 percent in-hospital mortality.
Intraventricular conduction disturbances occur in 10 to 20 percent of patients with AMI. Approximately half of these disturbances are already present at the time of ED presentation and may not represent a new finding. Blood supply to the left anterior division comes from septal perforators of the left anterior descending coronary artery. Both the right bundle branch and the left posterior division obtain a dual blood flow from both the left anterior descending and right coronary arteries. For this reason, left anterior hemiblock is more common.
New right bundle branch block occur in approximately 2 percent of AMI patients, most commonly anteroseptal AMI, and is associated with an increased mortality because it often leads to complete AV block. New left bundle branch block occurs in 5 percent of patients with AMI and is associated with a high mortality. The left posterior fascicle is larger than the left anterior fascicle. Thus, left posterior hemiblock is associated with a higher mortality than isolated left anterior hemiblock because it represents a larger area of infarction. Bifascicular block (right bundle branch block and a left hemiblock) is associated with an increased likelihood of progression to complete heart block; it represents a large infarction and is associated with an increased likelihood of pump failure and mortality. Other combinations of heart block and their treatment are discussed in Ch,a£ ,48,.
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