Myocardial perfusion and cardiac function affect blood flow to the entire body. As a result, any end organ can be damaged when cardiac pump function is decreased. In this section, discussion of the complications of ACS is limited to the direct effects on the heart. The systemic effects of cardiac function are discussed in organ-appropriate chapters of this book.
DYSRHYTHMIAS AND CONDUCTION DISTURBANCES
The genesis, diagnosis, and treatment of dysrhythmias are presented in chapter 18, "Cardiac Rhythm Disturbances." The effect dysrhythmias have in complicating the course of patients with ACS is the subject of this section.
Dysrhythmias occur in 72% to 100% of AMI patients treated in the coronary care unit. Table 49-12 shows the approximate frequency of the various dysrhythmias observed in patients with AMI. Many dysrhythmias occur in the prehospital and ED settings. The main consequences of dysrhythmias are impaired hemodynamic performance, compromised myocardial viability due to increased myocardial O2 requirements, and predisposition to even more serious rhythm disturbances due to diminished ventricular fibrillation threshold.
Early Dysrhythmias after Acute Myocardial Infarction
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Early Dysrhythmias after Acute Myocardial Infarction
|Dysrhythmia ||Frequency of Occurrence (%)|
|Sinus bradycardia ||35–40 |
|First-degree AV block ||4–15 |
|Second-degree AV block, type I ||4–10 |
|Second-degree AV block, type II ||0.5–1.0 |
|Third-degree AV block ||5–8 |
|Asystole ||1–5 |
|Sinus tachycardia ||30–35 |
|Atrial premature contractions ||50 |
|Supraventricular tachycardia ||2–9 |
|Atrial fibrillation ||4–10 |
|Atrial flutter ||1–2 |
|Ventricular premature beats ||99 |
|Accelerated idioventricular rhythm ||50–70 |
|Ventricular tachycardia, nonsustained ||60–69 |
|Ventricular tachycardia, sustained ||2–6 |
|Ventricular fibrillation ||4–7 |
The hemodynamic consequences of dysrhythmias are dependent on ventricular function. Patients with left ventricular dysfunction have a relatively fixed stroke volume. They depend on 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.
In addition, maintenance of the atrial filling of the ventricle (or "the atrial kick") is important for patients with AMI. Patients with normal hearts have a loss of 10% to 20% of left ventricular output when the atrial kick is eliminated. Patients with reduced left ventricular compliance, common in AMI, have up to 35% reduction in stroke volume when the atrial systole is eliminated. "Pump" failure with resultant increased sympathetic stimulation can also result in sinus tachycardia, atrial fibrillation or flutter, and supraventricular tachycardias.
Sinus tachycardia is quite prominent in patients with anterior wall AMI. Because of increased myocardial O2 use, persistent sinus tachycardia is associated with a poor prognosis in AMI; seek the cause and resolve it. Causes 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 fibrillation associated with AMI most typically occurs in the first 24 hours and is usually transient. It more often occurs in patients with excess catecholamine release, hypokalemia, hypomagnesemia, hypoxia, chronic lung disease, and sinus node or left circumflex ischemia. Patients with supraventricular tachycardia, atrial fibrillation, or atrial flutter who have hemodynamic compromise are best treated with direct current cardioversion (see chapter 18). Patients who are partially/fully compensated or who do not respond to cardioversion can receive amiodarone or-β-adrenergic antagonists to slow the ventricular rate65 absent any contraindications. Patients with ongoing ischemia but without hemodynamic compromise, clinical left ventricular dysfunction, reactive airway disease, or heart block should have rate control with β-adrenergic antagonists, such as atenolol (2.5 to 5.0 milligrams over 2 minutes to a total of 10 milligrams) or metoprolol (2.5 to 5.0 milligrams every 2 to 5 minutes to a total of 15 milligrams). Patients with contraindications to β-adrenergic antagonists can be treated with digoxin (0.3- to 0.5-milligram initial bolus with a repeat dose in 4 hours) or a calcium channel antagonist.5 Anticoagulate patients with atrial fibrillation and AMI to limit systemic embolization.
Sinus bradycardia without hypotension does not appear to increase mortality during AMI. Prognosis is related to the site of infarction, the site of the block (intranodal vs infranodal), the type of escape rhythm, and the hemodynamic response to the rhythm. Atropine is used for sinus bradycardia when it results in hypotension, ischemia, or ventricular escape rhythms and for treatment of symptomatic atrioventricular block occurring at the atrioventricular nodal level (such as second-degree type I). Atropine can improve heart rate, systemic vascular resistance, and blood pressure; use it with caution in the setting of AMI since the parasympathetic tone is protective against infarct extension, ventricular fibrillation, and excessive myocardial O2 demand.
Complete heart block can occur in patients with anterior and inferior AMI, because the AV conduction system receives blood supply from the atrioventricular branch of the right coronary artery and the septal perforating branch of the left anterior descending coronary artery. In the absence of right ventricular involvement, the mortality is approximately 15%. It rises to >30% when right ventricular involvement is present. Complete heart block in the setting of an anterior myocardial infarction portends a grave prognosis. Junctional rhythms are usually transient and occur within 48 hours of infarction.
The increased mortality in patients with heart block during AMI is related to more extensive myocardial damage and not to the heart block itself. As a result, pacing does not reduce mortality in patients with atrioventricular block or intraventricular conduction delay. Nonetheless, pacing is recommended to protect against sudden hypotension, acute ischemia, and precipitation of ventricular dysrhythmias in certain patients.
Use temporary transcutaneous pacers in patients at moderate to high risk of progression to atrioventricular block (see Table 49-13). Transvenous pacing follows for patients with a high likelihood (>30%) of requiring permanent pacing (Table 49-13). Patients with right ventricular infarction who are very dependent on atrial systole may require atrioventricular sequential pacing to maintain cardiac output.
Indications for Temporary Pacemaker Placement
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Indications for Temporary Pacemaker Placement
Temporary transcutaneous pacemaker indications
Unresponsive symptomatic bradycardia
Mobitz II or higher AV blocks
New LBBB and bifascicular blocks
RBBB or LBBB with first-degree block
Some cases with stable bradycardia and new or indeterminate-age RBBB
Temporary transvenous pacemaker indications
Unresponsive symptomatic bradycardia
Mobitz II or higher AV blocks
New or indeterminate-age LBBB
Alternating bundle-branch block
RBBB or LBBB with first-degree block
Consider in RBBB with left anterior or posterior hemiblocks
Overdrive pacing in unresponsive ventricular tachycardia
Unresponsive recurrent sinus pauses (>3 s)
Ventricular premature contractions are common in patients with AMI and are benign. Accelerated idioventricular rhythms in patients with AMI do not affect prognosis or require treatment. Ventricular tachycardia shortly after AMI is often transient and does not confer a poor prognosis. When ventricular tachycardia occurs late in the course of AMI, it is usually associated with transmural infarction and left ventricular dysfunction, induces hemodynamic deterioration, and is associated with a mortality rate approaching 50%. Primary ventricular fibrillation occurring shortly after symptom onset does not appear to have a large effect on mortality and prognosis, as long as it is quickly and effectively treated. Delayed or secondary ventricular fibrillation during hospitalization is associated with severe ventricular dysfunction and 75% in-hospital mortality.
New right bundle-branch block occurs in approximately 2% of AMI patients, most commonly with anteroseptal AMI; it is associated with an increased mortality and complete atrioventricular block. New left bundle-branch block occurs in <10% of patients with AMI and is also associated with a higher mortality than in patients without left bundle-branch block. Recognizing STEMI in the presence of left bundle-branch block is difficult,8 and due to this uncertainty and false catheterization lab activation, new or suspected new left bundle-branch block alone has been removed from the most recent recommendations for emergency perfusion.5 The left posterior fascicle is larger than the left anterior fascicle. Thus, left posterior hemiblock is associated with a higher mortality than is isolated left anterior hemiblock, because it represents a larger area of infarction. Bifascicular block (right bundle-branch block and a left hemiblock) has an increased likelihood of progression to complete heart block; it represents a large infarction and has more frequent pump failure and greater mortality.24 See chapter 18, "Cardiac Rhythm Disturbances" for more detail.
Some 15% to 20% of patients with AMI present with some degree of heart failure. One third of these patients have circulatory shock. In AMI, heart failure occurs from diastolic dysfunction alone or a combination of systolic and diastolic dysfunction. Left ventricular diastolic dysfunction leads to pulmonary congestion. Systolic dysfunction is responsible for decreased forward flow, reduced cardiac output, and reduced ejection fraction. In general, the more severe the degree of left ventricular dysfunction, the higher is the mortality. The degree of left ventricular dysfunction in any single patient depends on the net effect of prior myocardial dysfunction (prior myocardial infarction or cardiomyopathy), baseline myocardial hypertrophy, acute myocardial necrosis, and acute reversible myocardial dysfunction ("stunned myocardium"). For further discussion, see chapters 53, "Acute Heart Failure" and 50, "Cardiogenic Shock."
Mortality for patients with AMI increases as cardiac output decreases or pulmonary congestion increases, with mortality rates as follows: no heart failure, 10%; mild heart failure, 15% to 20%; frank pulmonary edema, 40%; and cardiogenic shock, 50% to 80%. Elevated levels of B-type natriuretic peptide or pro-B-type natriuretic peptide early in the hospital course portend a worse 30-day outcome.
The presence of shock in AMI results in a complex spiral relationship. Coronary obstruction leads to myocardial ischemia, which impairs myocardial contractility and ventricular outflow. The resulting reduction in arterial blood pressure leads to further decreases in coronary arterial perfusion, resulting in worsening myocardial ischemia and more severe myocardial necrosis. Interruption of this downward spiral requires careful attention to fluid management and the use of inotropic agents. Resolution of ischemia and preventing or minimizing the area of stunned myocardium that progresses to infarction are imperative; guidelines recommend that patients with STEMI and cardiogenic shock who are <75 years of age should be considered for PCI.5 For further discussion, see chapters 50 and 53.
Sudden decompensation of previously stable patients should raise concern for the mechanical complications of AMI. These complications usually involve the tearing or rupture of infarcted tissue, not seen in unstable angina. The clinical presentation of these entities depends on the site of rupture (papillary muscles, interventricular septum, or ventricular free wall).
Ventricular free wall rupture occurs in 10% of AMI fatalities, usually 1 to 5 days after infarction. Rupture of the left ventricular free wall usually leads to pericardial tamponade and death (in >90% of cases). Patients may complain of tearing pain or sudden onset of severe pain. They will be hypotensive and tachycardic and may have onset of confusion and agitation. Increased neck veins, decreased heart sounds, and pulsus paradoxus may be present. In the ED, echocardiography is the diagnostic test of choice. Near equalization of right atrial, right ventricular mid-diastolic, and right ventricular systolic pressures on pulmonary artery catheterization is also useful but seldom available in the ED. Treatment is surgical.
Rupture of the interventricular septum is more often detected clinically than rupture of the ventricular free wall. The size of the defect determines the degree of left-to-right shunt and the ultimate prognosis. Clinically, interventricular septal rupture presents with chest pain, dyspnea, and sudden appearance of a new holosystolic murmur. The murmur is usually accompanied by a palpable thrill and is heard best at the lower left sternal border. Doppler echocardiography is the diagnostic procedure of choice. Demonstration of left-to-right shunt by pulmonary catheter blood sampling may be useful. An O2 step-up of >10% from right atrial to right ventricular samples is diagnostic. Rupture of the interventricular septum is more common in patients with anterior wall myocardial infarction and patients with extensive (three-vessel) coronary artery disease. Treatment is surgical.
Papillary muscle rupture occurs in approximately 1% of patients with AMI, is more common with inferior myocardial infarction, and usually occurs 3 to 5 days after AMI. In contrast to rupture of the interventricular septum, papillary muscle rupture often occurs with a small- to modest-sized AMI. Patients present with acute onset of dyspnea, increasing heart failure and pulmonary edema, and a new holosystolic murmur consistent with mitral regurgitation. The posteromedial papillary muscle is most commonly ruptured, because it receives blood supply from one coronary artery, usually the right coronary artery. Echocardiography often can distinguish rupture of a portion of the papillary muscle from other etiologies of mitral regurgitation. Treatment is surgical.5,6
In the era of PCI intervention, early post-AMI pericarditis occurs in less than 5% of patients,66 a drop from 20% since the 1980s. It is more common in patients with transmural AMI and delayed initial presentations. Pericarditis results from inflammation adjacent on the epicardial surface of a transmural infarction, often 2 to 4 days after AMI. Pericardial friction rubs are detected more often with inferior wall and right ventricular infarction, because the right ventricle lies immediately beneath the chest wall. The pain of pericarditis can be confused with that of infarct extension or post-AMI angina. Classically, the discomfort of pericarditis becomes worse with a deep inspiration and may be relieved by sitting forward.
Echocardiography may demonstrate a pericardial effusion, but pericardial effusions are much more common than pericarditis and often are present in the absence of pericarditis. Similarly, pericarditis can be present in the absence of a pericardial effusion. The resorption rate of post-AMI pericardial effusions is slow, often taking several months. Treatment is symptomatic with aspirin, 650 milligrams PO every 4 to 6 hours, or colchicine, 0.6 mg twice daily. Ibuprofen is not recommended because it interferes with the antiplatelet effect of aspirin and can cause myocardial scar thinning and infarct expansion. Dressler's syndrome (late post-AMI syndrome) occurs 2 to 10 weeks after AMI and presents with chest pain, fever, and pleuropericarditis. Dressler's syndrome is treated with aspirin and colchicine.67
RIGHT VENTRICULAR INFARCTION
Isolated right ventricular infarction is extremely rare and is usually seen as a complication of an inferior infarction. The right ventricle most commonly receives its blood supply from the right coronary artery. In patients with left dominant systems, the blood supply may come from the left circumflex. The anterior portion of the right ventricle is supplied by branches of the left anterior diagonal artery. Approximately 30% of inferior wall myocardial infarction involves the right ventricle. The presence of right ventricular infarction is associated with a significant increase in mortality and cardiovascular complications. Right ventricular infarction can be diagnosed by the presence of ST-segment elevation in the precordial V4R lead in the setting of an inferior wall myocardial infarction (Figure 49-4). The presence of elevated neck veins or hypotension in response to nitroglycerin is also suggestive. Echocardiography or nuclear imaging can be diagnostic, but they are less readily available in the ED.
The most serious complication of right ventricular infarction is shock. The severity of the hemodynamic derangement in the setting of right ventricular infarction is related to the extent of right ventricular dysfunction, the interaction between the ventricles (the right and left ventricles share the interventricular septum), and the interaction between the pericardium and the right ventricle. Right ventricular infarction results in a reduction in right ventricular end-systolic pressure, left ventricular end-diastolic size, cardiac output, and aortic pressure as the right ventricle becomes more of a passive conduit to blood flow. Left ventricular contraction causes bulging of the interventricular septum into the right ventricle, with resultant ejection of blood into the pulmonary circulation. As a result, right ventricular infarction with concurrent left ventricular infarction has a particularly devastating effect on hemodynamic function. Fluid balance and maintenance of adequate preload are critical in the treatment of right ventricular infarction. Factors that reduce preload (volume depletion, diuretics, and nitrates) or decrease right atrial contraction (atrial infarction and loss of atrioventricular synchrony) and factors that increase right ventricular afterload (left ventricular failure) can lead to significant hemodynamic derangements.
Treatment of right ventricular infarction includes maintenance of preload, reduction of right ventricular afterload, and inotropic support of the ischemic right ventricle, in addition to early reperfusion. Patients with right ventricular infarction should not be treated with drugs, such as nitrates, that reduce preload. In the setting of right ventricular infarction, nitrates often will reduce cardiac output and produce hypotension. Instead, patients with marginal preload or hypotension should be treated with volume loading (normal saline). The increased preload will improve right ventricular cardiac output. If cardiac output is not improved after 1 to 2 L of normal saline, begin inotropic support with dobutamine.
High-degree heart block is very common in patients with right ventricular infarction. The loss of right atrial contraction can greatly compromise right ventricular cardiac output. Restitution of atrioventricular synchrony is important. Patients who do not attain hemodynamic improvement after placement of a ventricular pacer may still improve with atrioventricular sequential pacing.
When right ventricular infarction is accompanied by left ventricular dysfunction, the use of nitroprusside to reduce afterload or intra-aortic balloon counterpulsation may be of benefit. Reduction in left ventricular afterload may help passive movement of blood through the right ventricle.
Other complications of AMI that occur but are not usually seen in the ED include left ventricular thrombus formation, arterial embolization, venous thrombosis, pulmonary embolism, postinfarction angina, and infarct extension. With the more rapid discharge of uncomplicated AMI patients, keep these possibilities in mind for patients who return to the ED shortly after hospital discharge.
RECURRENT OR REFRACTORY ISCHEMIA
Patients unresponsive to medical management with continued ischemia require an individualized approach to treatment. Depending on the infarct distribution and coronary anatomy, decisions could be made regarding continued medical management, rescue angioplasty, or coronary artery bypass grafting. Refractory ischemia is investigated with coronary catheterization. Treat patients with ACS after stent placement with antithrombin and antiplatelet therapy, and these patients may require urgent coronary catheterization.
In situations where emergent catheterization is not available or the patient is hemodynamically unstable, an intra-aortic balloon pump may be used. Intra-aortic balloon counterpulsation delivers phased pulsations synchronized to the electrocardiograph, so that balloon inflation will occur at the time of aortic valve closure and deflation occurs just before onset of systole. The augmented coronary perfusion pressure during diastole enhances coronary blood flow. Balloon deflation during systole allows the left ventricle to eject blood against a lower resistance. The net effect of intra-aortic balloon counterpulsation is an increase in cardiac output, reduction in systolic arterial pressure, increase in diastolic arterial pressure, little change in mean arterial pressure, and reduction in heart rate. The reduction in left ventricular afterload leads to reduced myocardial O2 consumption, thereby decreasing the amount of myocardial ischemia. Intra-aortic balloon counterpulsation is recommended for patients with ACS who are refractory to aggressive medical management or are hemodynamically unstable as a means to bridge a patient's stability en route to definitive treatment.