(For arrhythmias, see also Chaps. 122 and 123)
Isolated ventricular premature beats (VPBs) occur frequently. Precipitating factors should be corrected (hypoxemia, acidosis, hypokalemia, hypomagnesemia, CHF, arrhythmogenic drugs). Routine beta blocker administration (see above) diminishes ventricular ectopy. Other in-hospital antiarrhythmic therapy should be reserved for pts with sustained ventricular arrhythmias.
If hemodynamically unstable, perform immediate electrical countershock (unsynchronized discharge of 200–300 J or 50% less if using biphasic device). If hemodynamically tolerated, use IV amiodarone (bolus of 150 mg over 10 min, then infusion of 1.0 mg/min for 6 h, then 0.5 mg/min).
VF requires immediate defibrillation (200–400 J). If unsuccessful, initiate cardiopulmonary resuscitation (CPR) and standard resuscitative measures (Chap. 10). Ventricular arrhythmias that appear several days or weeks following MI often reflect pump failure and may warrant invasive electrophysiologic study and implantation of a cardioverter defibrillator (ICD).
Accelerated Idioventricular Rhythm
Wide QRS complex, regular rhythm, rate 60–100 beats/min, is common and usually benign; if it causes hypotension, treat with atropine 0.6 mg IV.
Sinus tachycardia may result from heart failure, hypoxemia, pain, fever, pericarditis, hypovolemia, administered drugs. If no cause is identified, suppressive beta blocker therapy may be beneficial to reduce myocardial oxygen demand. Other supraventricular arrhythmias (paroxysmal supraventricular tachycardia, atrial flutter, and fibrillation) are often secondary to heart failure. If hemodynamically unstable, proceed with electrical cardioversion. In absence of acute heart failure, suppressive alternatives include beta blockers, verapamil, or diltiazem (Chap. 123).
Bradyarrhythmias and AV Block
(See Chap. 122) In inferior MI, usually represent heightened vagal tone or discrete AV nodal ischemia. If hemodynamically compromised (CHF, hypotension, emergence of ventricular arrhythmias), treat with atropine 0.5 mg IV q5min (up to 2 mg). If no response, use temporary external or transvenous pacemaker. Isoproterenol should be avoided. In anterior MI, AV conduction defects usually reflect extensive tissue necrosis. Consider temporary external or transvenous pacemaker for (1) complete heart block, (2) Mobitz type II block (Chap. 122), (3) new bifascicular block (LBBB, RBBB + left anterior hemiblock, RBBB + left posterior hemiblock), (4) any bradyarrhythmia associated with hypotension or CHF.
CHF may result from systolic “pump” dysfunction, increased LV diastolic “stiffness,” and/or acute mechanical complications.
Symptoms Dyspnea, orthopnea, tachycardia.
Examination Jugular venous distention, S3 and S4 gallop, pulmonary rales; systolic murmur if acute mitral regurgitation or ventricular septal defect (VSD) has developed.
TREATMENT: HEART FAILURE
Initial therapy includes diuretics (begin with furosemide 10–20 mg IV), inhaled O2, and vasodilators, particularly nitrates (PO, topical, or IV [Chap. 124] unless pt is hypotensive [systolic bp <100 mmHg]); digitalis is usually of little benefit in acute MI (See Chaps. 13 and 124). Diuretic, vasodilator, and inotropic therapy (Table 119-1) may be guided by invasive hemodynamic monitoring (Swan-Ganz pulmonary artery catheter, arterial line), particularly in pts with accompanying hypotension (Table 119-2; Fig. 119-3). In acute MI, an acceptable pulmonary capillary wedge (PCW) pressure is 15–20 mmHg; in the absence of hypotension, PCW >20 mmHg is treated with diuretic plus vasodilator therapy (IV nitroglycerin [begin at 10 μg/min] or nitroprusside [begin at 0.5 μg/kg per min]) and titrated to optimize bp, PCW, and systemic vascular resistance (SVR).
Normal SVR = 900 − 1350 dyne • s/cm5. If PCW >20 mmHg and pt is hypotensive (Table 119-2 and Fig. 119-3), evaluate for VSD or acute mitral regurgitation, consider dobutamine (begin at 1–2 [μg/kg]/min), titrate upward to maximum of 10 (μg/kg)/min; beware of drug-induced tachycardia or ventricular ectopy.
After stabilization on parenteral vasodilator therapy, oral therapy follows with an ACE inhibitor or an ARB (Chap. 124). Consider addition of long-term aldosterone antagonist (spironolactone 25–50 mg daily or eplerenone 25–50 mg daily) to ACE inhibitor if LVEF ≤40% or symptomatic heart failure or diabetes are present—do not use if renal insufficiency or hyperkalemia are present.
TABLE 119-1IV VASODILATORS AND INOTROPIC DRUGS USED IN ACUTE MI ||Download (.pdf) TABLE 119-1IV VASODILATORS AND INOTROPIC DRUGS USED IN ACUTE MI
|Drug ||Usual Dosage Range ||Comment |
|Nitroglycerin ||5–100 μg/min ||May improve coronary blood flow to ischemic myocardium |
|Nitroprusside ||0.5–10 (μg/kg)/min ||More potent vasodilator, but improves coronary blood flow less than nitroglycerin |
| || ||With therapy >24 h or in renal failure, watch for thiocyanate toxicity (blurred vision, tinnitus, delirium) |
|Dobutamine ||2–20 (μg/kg)/min ||Results in ↑ cardiac output, ↓ PCW, but does not raise bp |
|Dopamine ||2–20 (μg/kg)/min ||More appropriate than dobutamine if hypotensive |
| || ||Hemodynamic effect depends on dose: (μg/kg)/min |
| || || <5: ↑ renal blood flow |
| || || 2.5–10: positive inotrope |
| || || >10: vasoconstriction |
|Norepinephrine ||0.5–30 μg/min ||Less likely than dopamine to cause arrhythmias in cardiogenic shock |
TABLE 119-2HEMODYNAMIC COMPLICATIONS IN ACUTE MI ||Download (.pdf) TABLE 119-2HEMODYNAMIC COMPLICATIONS IN ACUTE MI
|Condition ||Cardiac Index, (L/min)/m2 ||PCW, mmHg ||Systolic bp, mmHg ||Treatment |
|Uncomplicated ||>2.5 ||≤18 ||>100 ||— |
|Hypovolemia ||<2.5 ||<15 ||<100 ||Successive boluses of normal saline |
| || || || ||In setting of inferior wall MI, consider RV infarction (esp. if RA pressure >10) |
|Volume overload ||>2.5 ||>20 ||>100 ||Diuretic (e.g., furosemide 10–20 mg IV) |
| || || || ||Nitroglycerin, topical paste or IV (Table 119-1) |
|LV failure ||<2.5 ||>20 ||>100 ||Diuretic (e.g., furosemide 10–20 mg IV) |
| || || || ||IV nitroglycerin (or if hypertensive, use IV nitroprusside) |
|Severe LV failure ||<2.5 ||>20 ||<100 ||If bp ≥90: IV dobutamine ± IV nitroglycerin or sodium nitroprusside |
| || || || ||If bp <90: IV dopamine |
| || || || ||If accompanied by pulmonary edema: attempt diuresis with IV furosemide; may be limited by hypotension |
| || || || ||If new systolic murmur present, consider acute VSD or mitral regurgitation |
|Cardiogenic shock ||<2.2 ||>20 ||<90 with oliguria and confusion || |
IV norepinephrine or dopamine
Intraaortic balloon pump
Reperfusion by PCI or CABG may be life-saving
Emergency management of cardiogenic shock and pulmonary edema. (Modified from Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 7: The era of reperfusion: Section 1: Acute coronary syndromes [acute myocardial infarction]. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 102:1172, 2000.)
(See Chap. 11) Severe LV failure with hypotension (bp <90 mmHg), elevated PCW (>20 mmHg), cardiac index <2.2 L/min/m2, accompanied by oliguria, peripheral vasoconstriction, dulled sensorium, and metabolic acidosis.
TREATMENT: CARDIOGENIC SHOCK
Swan-Ganz catheter and intraarterial bp monitoring are not always essential but may be helpful; aim for mean PCW of 18–20 mmHg with adjustment of volume (diuretics or infusion) as needed (Fig. 119-3). Vasopressors (e.g., norepinephrine or dopamine [Table 119-1]) and/or intraaortic balloon counterpulsation may be necessary to maintain systolic bp >90 mmHg and reduce PCW. Administer high concentration of O2 by mask; if pulmonary edema coexists, consider bilateral positive airway pressure (BiPAP) or intubation and mechanical ventilation. Acute mechanical complications (see below) should be sought and promptly treated.
If cardiogenic shock develops within 36 h of acute STEMI, reperfusion by PCI or coronary artery bypass grafting (CABG) may markedly improve LV function.
May also result from right ventricular MI, which should be suspected in inferior or posterior MI, if jugular venous distention and elevation of right-heart pressures predominate (rales are typically absent and PCW may be normal); right-sided ECG leads typically show ST elevation, and echocardiography may confirm diagnosis. Treatment consists of volume infusion. Noncardiac causes of hypotension should be considered: hypovolemia, acute arrhythmia, or sepsis.
Acute Mechanical Complications
Ventricular septal rupture and acute mitral regurgitation due to papillary muscle ischemia/infarct develop during the first week following MI and are characterized by sudden onset of CHF and new systolic murmur. Echocardiography and Doppler interrogation can confirm presence of these complications. PCW tracings may show large v waves in either condition, but an oxygen “step-up” as the catheter is advanced from right atrium to right ventricle suggests septal rupture.
Acute medical therapy of these conditions includes vasodilator therapy (IV nitroprusside: begin at 10 μg/min and titrate to maintain systolic bp ~100 mmHg); intraaortic balloon pump may be required to maintain cardiac output. Mechanical correction is the definitive therapy. Acute ventricular free-wall rupture presents with sudden loss of bp, pulse, and consciousness, while ECG shows an intact rhythm (pulseless electrical activity); emergent surgical repair is crucial, and mortality is high.
Characterized by pleuritic, positional pain, and pericardial rub (Chap. 116); atrial arrhythmias are common; must be distinguished from recurrent angina. Often responds to aspirin, 650 mg PO qid. Anticoagulants should be avoided when pericarditis is suspected to avoid development of pericardial bleeding/tamponade.
Localized “bulge” of LV chamber due to infarcted myocardium. True aneurysms consist of scar tissue and do not rupture. However, complications include CHF, ventricular arrhythmias, and thrombus formation. Typically an aneurysm is confirmed by echocardiography or by left ventriculography. The presence of thrombus within the aneurysm, or a large aneurysmal segment due to anterior MI, warrants consideration of oral anticoagulation with warfarin for 3–6 months.
Pseudoaneurysm is a form of cardiac rupture contained by a local area of pericardium and organized thrombus; direct communication with the LV cavity is present; surgical repair usually necessary to prevent rupture.
Usually associated with transient ST-T wave changes; signals high incidence of reinfarction; when it occurs in early post-MI period, proceed directly to coronary arteriography, to identify those who would benefit from revascularization.