Harrison’s Manual of Medicine



Ventricular Tachycardia
Secondary Prevention
Early recognition and immediate treatment of acute MI are essential; diagnosis is based on characteristic history, ECG, and evolution of cardiac enzymes.
SYMPTOMS   Chest pain similar to angina (Chap. 2) but more intense and persistent (>30 min); not fully relieved by rest or nitroglycerin, often accompanied by nausea, sweating, apprehension. However, 25% of MIs are clinically silent.
PHYSICAL EXAMINATION   Pallor, diaphoresis, tachycardia, S4, dyskinetic cardiac impulse may be present. If CHF exists: rales, S3. Jugular venous distention is common in right ventricular infarction.
ECG   Q-wave MI   ST elevation, followed by T-wave inversion, then Q- wave development (Chap. 113) over several hours.
Non-Q-wave MI   ST depression followed by persistent ST-T-wave changes without Q-wave development. Comparison with old ECG helpful.
CARDIAC ENZYMES   Time course is important for diagnosis; creatine phosphokinase (CK) level should be checked every 8 h for first day: CK rises within 4–8 h, peaks at 24 h, returns to normal by 48–72 h. CK-MB isoenzyme is more specific for MI but may also be elevated with myocarditis or after electrical cardioversion. Total CK (but not CK-MB) rises (two- to threefold) after IM injection, vigorous exercise, or other skeletal muscle trauma. A ratio of CK-MB mass: CK activity ³2.5 suggests acute MI. CK-MB peaks earlier (about 8 h) following acute reperfusion therapy (see below). Cardiac-specific troponin T and troponin I are highly specific for myocardial injury and are the preferred biochemical markers for acute MI. They remain elevated for 1–2 weeks.
NONINVASIVE IMAGING TECHNIQUES   Useful when diagnosis of MI is not clear. Echocardiography detects infarct-associated regional wall motion abnormalities (but cannot distinguish acute MI from a previous myocardial scar). Echo is also useful in detecting RV infarction, LV aneurysm, and LV thrombus. Myocardial perfusion imaging (thallium 201 or technetium 99m- sestamibi) is sensitive for regions of decreased perfusion but is not specific for acute MI.

Initial Therapy
Goal is to relieve pain, minimize extent of infarcted tissue, and prevent/treat arrhythmias and mechanical complications. Aspirin (160–325 mg chewed at presentation, then 160–325 mg po qd) should be administered immediately. For Q-wave MI (ST-segment elevation MI), early thrombolytic therapy with streptokinase, reteplase (rPA), or tissue plasminogen activator (tPA) can reduce infarct size and mortality and limit LV dysfunction. In appropriate candidates (Fig. 121-1 and Fig. 121-2), thrombolysis should be initiated as quickly as possible (ideally within 30 min) in the emergency room or coronary care unit (CCU); pts treated within 3 h of initial symptoms benefit the most. Complications include bleeding, reperfusion arrhythmias, and, in the case of streptokinase, allergic reactions. Anticoagulation with heparin [60 U/kg, then 12 (U/kg)/h] is begun concurrently with the thrombolytic agent (Fig. 121-1). Subsequent coronary arteriography is reserved for pts with recurrent angina or positive exercise test prior to discharge. In pts with contraindications to thrombolytic therapy (Fig. 121-1), primary percutaneous transluminal coronary angioplasty (PTCA) and/or stenting can be undertaken to restore coronary flow. Primary PTCA may be preferred over thrombolytic therapy in cardiogenic shock, in pts of advanced age (>70), and in some highly experienced centers, especially if delay can be minimized.

FIGURE 121-1. Approach to thrombolytic therapy of pts with acute MI.

FIGURE 121-2. Management strategy for pts suspected of having an ST-segment elevation. Acute MI pts should receive aspirin (ASA), beta blockers (in the absence of contraindications), and an antithrombin (particularly if a relatively fibrin-specific thrombolytic agent is used). Adjunctive antithrombin therapy is probably not required for pts receiving streptokinase. Pts treated within 12 h who are eligible for thrombolytic therapy should expeditiously receive such treatment or be considered for primary percutaneous transluminal coronary angioplasty (PCI). Immediate, primary PCI is also to be considered when lytic therapy is contraindicated. An intravenous glycoprotein IIb/IIIa (GPIIb/IIIa) inhibitor may be helpful for reducing thrombotic complications during primary PCI. Pts treated after 12 h should receive the initial medical therapy noted above and, on an individual basis, may be candidates for ACE inhibitors (particularly if LV function is impaired).

The initial management of non-ST-segment elevation MI (non-Q MI) is different (Fig. 121-3). Thrombolytic therapy should not be administered. Begin aspirin and antithrombin therapy: either low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC q12h) or IV heparin [60 U/kg followed by 12(U/ kg)/h, then adjust to maintain PTT at 2 × control). Begin beta blocker and IV nitroglycerin (Table 121-1) for control of ischemic pain. In high-risk patients, add IV glycoprotein IIb/IIIa inhibitor [e.g., tirofiban, 0.4 (µg/kg)/min × 30 min then 0.1 (µg/kg)/min, or eptifibatide, 180 µg/kg then 2 (µg/kg)/ min] and consider cardiac catheterization/revascularization.

FIGURE 121-3. Management strategy for pts with unstable angina and acute MI without ST- segment elevation. These pts should be treated with an antithrombin and aspirin. Nitrates should be administered for recurrent episodes of angina. The risk of death and cardiac ischemic events may be reduced in high-risk pts if an intravenous GPIIb/IIIa inhibitor is administered. Adequate beta blockade should be established; when that is not possible or contraindications exist, a calcium antagonist can be considered. Pts at high risk should be triaged to cardiac catheterization with plans for revascularization if clinically suitable; pts who are clinically stable can be treated more conservatively with continued observation in the hospital and consideration of a stress test to screen for any provocable myocardial ischemia. CABG, coronary artery bypass grafting; LV, left ventricular. [Modified from EM Antman, in RM Califf (ed): Acute Myocardial Infarction and Other Acute Ischemic Syndromes, in E Braunwald (Series ed): Atlas of Heart Diseases, vol. 8. Philadelphia, Current Medicine 1996.]

Table 121-1 Intravenous Vasodilators and Inotropic Drugs Used in Acute MI

Additional Standard Treatment
(Whether or not thrombolytic therapy is administered):

Hospitalize in CCU with continuous ECG monitoring.

IV line for emergency arrhythmia treatment.

Pain control: (a) Morphine sulfate 2–4 mg IV q5–10 min until pain is relieved or side effects develop [nausea, vomiting, respiratory depression (treat with naloxone 0.4–1.2 mg IV), hypotension (if bradycardic, treat with atropine 0.5 mg IV; otherwise use careful volume infusion)]; (b) nitroglycerin 0.3 mg SL if systolic bp >100 mmHg; for refractory pain: IV nitroglycerin (begin at 10 µg/min, titrate upward to maximum of 200 µg/min, monitoring bp closely); (c) b-adrenergic antagonists (see below).

Oxygen 2–4 L/min by nasal cannula (maintain O2 saturation >90%).

Mild sedation (e.g., diazepam 5 mg PO qid).

Soft diet and stool softeners (e.g., docusate sodium 100–200 mg/d).

b-Adrenergic blockers (Chap. 124) reduce myocardial O2 consumption, limit infarct size, and reduce mortality. Especially useful in pts with hypertension, tachycardia, or persistent ischemic pain; contraindications include CHF, systolic bp <95 mmHg, heart rate <50 beats/min, AV block, or history of bronchospasm. Administer IV (e.g., metoprolol 5 mg q5–10 min to total dose of 15 mg), followed by PO regimen (e.g., metoprolol 25–100 mg bid).

Anticoagulation/antiplatelet agents: Pts who receive thrombolytic therapy are begun on heparin and aspirin. In absence of thrombolytic therapy, administer aspirin 160–325 mg qd and low-dose heparin (5000 U SC q12h). Full-dose IV heparin (PTT 2 × control) or low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC q12h) followed by oral anticoagulants is recommended for pts with severe CHF, presence of ventricular thrombus by echocardiogram, or large dyskinetic region in anterior MI. Oral anticoagulants are continued for 3 to 6 months, then replaced by aspirin.

ACE inhibitors reduce mortality in pts following acute MI and should be prescribed within 24 h of hospitalization for pts with CHF and those who are hemodynamically stable with ST-segment elevation MI or left bundle branch block—e.g., captopril (6.25 mg PO test dose) advanced to 50 mg PO tid. ACE inhibitors should be continued indefinitely in pts with CHF or those with asymptomatic LV dysfunction [ejection fraction (EF) £40%].

Serum magnesium level should be measured and repleted if necessary to reduce risk of arrhythmias.

VENTRICULAR ARRHYTHMIAS   Isolated ventricular premature beats (VPBs) occur frequently. Precipitating factors should be corrected [hypoxemia, acidosis, hypokalemia (maintain serum K+ ~ 4.5 mmol/L), hypercalcemia, 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). If hemodynamically tolerated, use IV lidocaine [bolus of 1.0–1.5 mg/kg, infusion of 20–50 (µg/kg)/min; use lower infusion rate (» 1 mg/min) in pts of advanced age or those with CHF or liver disease], IV procainamide (bolus of 15 mg/kg over 20–30 min; infusion of 1–4 mg/min) or IV amiodarone (bolus of 75–150 mg over 10–15 min; infusion of 1.0 mg/min for 6 h, then 0.5 mg/min).
VENTRICULAR FIBRILLATION   VF requires immediate defibrillation (200–400 J). If unsuccessful, initiate CPR and standard resuscitative measures (Chap. 29). Ventricular arrhythmias that appear several days or weeks following MI often reflect pump failure and may warrant invasive electrophysiologic study.
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.
SUPRAVENTRICULAR ARRHYTHMIAS   Sinus tachycardia may result from CHF, hypoxemia, pain, fever, pericarditis, hypovolemia, administered drugs. If no cause is identified, may treat with beta blocker (Table 124-1). For persistent sinus tachycardia (>120), use Swan-Ganz catheter to differentiate CHF from decreased intravascular volume (Table 121-2). Other supraventricular arrhythmias (paroxysmal supraventricular tachycardia, atrial flutter, and fibrillation) are often secondary to CHF, in which digoxin (Chap. 116) is treatment of choice. In absence of CHF, may also use verapamil or beta blocker (Chap. 115). If hemodynamically unstable, proceed with electrical cardioversion.

Table 121-2 Indications for Swan-Ganz Catheter in Acute Myocardial Infarction

BRADYARRHYTHMIAS AND AV BLOCK   (See Chap. 115) 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. 115), (3) new bifascicular block (LBBB, RBBB + left anterior hemiblock, RBBB + left posterior hemiblock), (4) any bradyarrhythmia associated with hypotension or CHF.
CONGESTIVE HEART FAILURE   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) have developed.

(See Chap. 32 and Chap. 116) Initial therapy includes diuretics (begin with furosemide 10–20 mg IV), inhaled O2, and vasodilators, particularly nitrates [PO, topical, or IV (Chap. 116) unless pt is hypotensive (systolic bp <100 mmHg)]; digitalis is usually of little benefit in acute MI unless supraventricular arrhythmias are present. Diuretic, vasodilator, and inotropic therapy (Table 121-1) best guided by invasive hemodynamic monitoring (Swan-Ganz pulmonary artery catheter, arterial line) particularly in pts with accompanying hypotension (Table 121-2 and Table 121-3; Fig. 121-4). In acute MI, optimal pulmonary capillary wedge pressure (PCW) 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).

Table 121-3 Hemodynamic Complications in Acute MI

FIGURE 121-4. Approach to hypotension in pts with acute myocardial infarction; PCW, pulmonary capillary wedge pressure.

Normal SVR = 900 – 1350 dyn · s/cm5. If PCW > 20 mmHg and pt is hypotensive (Table 121-3 and Fig. 121-4), evaluate for VSD or acute mitral regurgitation, add 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.
If CHF improves on parenteral vasodilator therapy, oral therapy follows with ACE inhibitor (e.g., captopril, enalapril, or lisinopril–Chap. 124) or the combination of nitrates plus hydralazine (Chap. 116).

CARDIOGENIC SHOCK   Severe LV failure with hypotension (bp <80 mmHg) and elevated PCW (>20 mmHg), accompanied by oliguria (<20 mL/ h), peripheral vasoconstriction, dulled sensorium, and metabolic acidosis.

(See Chap. 30) Swan-Ganz catheter and intraarterial bp monitoring are essential; aim for mean PCW of 18–20 mmHg with adjustment of volume (diuretics or infusion) as needed. Intraaortic balloon counterpulsation may be necessary to maintain bp and reduce PCW. Administer high concentration of O2 by mask; if pulmonary edema coexists, intubation and mechanical ventilation should be considered. Acute mechanical complications (see below) should be sought and promptly treated.
If cardiogenic shock develops within 4 h of first MI symptoms, acute reperfusion by PTCA may markedly improve LV function.

Hypotension may also result from RV MI, which should be suspected in the setting of 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, gauged by PCW and arterial pressure. 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 with Doppler 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 RA to RV 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. Surgical correction is postponed for 4–6 weeks after acute MI if pt is stable; surgery should not be deferred if pt is unstable. Acute ventricular free-wall rupture presents with sudden loss of bp, pulse, and consciousness, while ECG shows an intact rhythm; emergent surgical repair is crucial, and mortality is high.
PERICARDITIS   Characterized by pleuritic, positional pain and pericardial rub (Chap. 120); atrial arrhythmias are common; must be distinguished from recurrent angina. Often responds to aspirin 650 mg PO qid. Anticoagulants should be withheld when pericarditis is suspected to avoid development of tamponade.
VENTRICULAR ANEURYSM   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, ECG shows persistent ST-segment elevation, >2 weeks after initial infarct; aneurysm is confirmed by echocardiography and by left ventriculography. The presence of thrombus within the aneurysm, or a large aneurysmal segment due to anterior MI, warrants oral anticoagulation with warfarin for 3–6 months.
In contrast, 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.
RECURRENT ANGINA   Usually associated with transient ST-T wave changes; signals high incidence of reinfarction; when it occurs in early post-MI period (2 weeks), proceed directly to coronary arteriography in most pts, to identify those who would benefit from percutaneous coronary intervention or coronary artery bypass surgery.
DRESSLER’S SYNDROME   Syndrome of fever, pleuritic chest pain, pericardial effusion, which may develop 2–6 weeks following acute MI; pain and ECG characteristic of pericarditis (Chap. 120); usually responds to aspirin or NSAIDs. Reserve glucocorticoid therapy (prednisone 1 mg/kg PO qd) for those with severe, refractory pain.
Submaximal exercise testing should be performed prior to or soon after discharge. A positive test (Chap. 122) in certain subgroups (angina at a low workload, a large region of provocable ischemia, or provocable ischemia with a reduced LVEF) suggests need for cardiac catheterization to evaluate myocardium at risk of recurrent infarction. Beta blockers (e.g., timolol, 10 mg bid; metoprolol, 25–100 mg bid) should be prescribed routinely for at least 2 years following acute MI (Table 124-1), unless contraindications present (asthma, CHF, bradycardia, “brittle” diabetes). Aspirin (80–325 mg/d) is administered to reduce incidence of subsequent infarction, unless contraindicated (e.g., active peptic ulcer, allergy). If the LVEF £40%, an ACE inhibitor (e.g., captopril 6.25 mg PO tid, advanced to target dose of 50 mg PO tid) should be used indefinitely.
Modification of cardiac risk factors must be encouraged: discontinue smoking; control hypertension, diabetes, and serum lipids (target LDL £100 mg/dL) (Chap. 178); and pursue graduated exercise.

For a more detailed discussion, see Antman EM, Braunwald E: Acute Myocardial Infarction, Chap. 243, p. 1386, in HPIM-15.

About these ads


  1. nice information, many thanks to the author. it is incomprehensible to me now, but in general, the usefulness and significance is overwhelming. thanks again and good luck!http://www.comodesbloquearcelular.net

  2. Nice blog over here! I’ll just wanna say thnx for that. If you like to visit my website cherk out: sexdate thanks for visiting!

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s


Get every new post delivered to your Inbox.

Join 371 other followers

%d bloggers like this: