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elevation or LBBB who develop shock within 36 hours of MI and who are suitable for revascularization that can be performed within 18 hours of shock. Patients with good prior functional status who agree to inva- sive care may be selected for such an invasive strate- gy. (Level of Evidence: B)

Cardiogenic shock in patients with STEMI is most com- monly (75% of cases) caused by extensive LV dysfunction, but important other causes include mechanical complications (acute severe MR, VSR, and subacute free-wall rupture with tamponade). Important conditions that may mimic cardio- genic shock include aortic dissection and hemorrhagic shock. Echocardiography with color flow Doppler is extremely use- only in patients with associated hypervolemia (see above).

Low doses should be used unless there is renal insufficiency, chronic diuretic use, or the presence of chronic CHF and hypervolemia as described above. Typical furosemide doses range from 20 to 80 mg IV (0.5 to 1.0 mg/kg).

Angiotensin converting enzyme inhibitors are indicated for patients with pulmonary congestion. Oral ACE inhibitors, preferably a short-acting agent such as captopril, beginning with 1 to 6.25 mg, should be instituted early in normotensive or hypertensive patients. The dosage may be doubled with each subsequent dose as tolerated up to 25 to 50 mg every 8 hours, then changed to a long-acting agent. Although the risk of hypotension and shock after vasodilator or diuretic admin- istration during the acute phase of MI is substantial for those without a hypertensive response to pulmonary edema, the risk is lower in the late phase after MI. Hence, most patients can tolerate ACE inhibitors before discharge. For patients who presented with CHF complicating MI, ramipril adminis- tration between days 3 and 10 significantly reduced 30-day mortality (relative hazard 0.73; 95% CI 0.602 to 0.89; p greater than 0.002) in 2006 patients in the Acute Infarction Ramipril Efficacy Study (767). Given the good tolerability of ACE inhibition within 24 hours of MI in the ISIS-4 and GISSI-3 (lisinopril) studies and the beneficial effects on early infarct expansion, it is recommended that ACE inhibitors be initiated early for those who have pulmonary congestion. However, hypotension should be avoided, par- ticularly during and immediately after reperfusion therapy (767,768). Routine intravenous enalapril is not recommend- ed (769) unless severe hypertension is present. ACE inhibitors are the only adjunctive medication (beyond aspirin and reperfusion therapy) demonstrated to reduce 30-day mortality when CHF complicates STEMI. Therefore, if blood pressure limits use of vasodilators, ACE inhibitors are preferred. Intravenous sodium nitroprusside substantially reduces afterload and preload; however, its use has been associated with coronary steal. Digitalis has no role in the management of pulmonary edema complicating STEMI unless rapid AF is present. Nesiritide (synthetic natriuretic brain peptide) is a new vasodilator agent that promotes diure- sis in patients with volume overload and decompensated chronic CHF (class 3 to 4) (770). It has not been investigat- ed in STEMI and is not indicated for treatment of pulmonary edema in these patients. Nesiritide is a potent vasodilator and may result in hypotension, particularly in patients with STEMI, in whom CHF usually is not due to volume over- load.

An aldosterone antagonist, eplerenone, was found to be effective for secondary prevention of death and recurrent hospitalization in patients 3 to 14 days after MI with CHF and LVEF less than 0.40. Spironolactone has been demon- strated to improve survival in a population of patients with chronic CHF, which includes those with remote MI (722) (see Section 7.12.6). In contrast to the recommendation to avoid initiation of beta-blockade during pulmonary edema, beta-blockers are strongly recommended before hospital dis- charge for secondary prevention of cardiac events (273). The

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0.03, 12 months) (184,494). The prespecified subgroup analysis of patients less than 75 years old showed a 15.4% absolute reduction in the primary end point at 30 days (initial medical stabilization group 56.8% versus emergency revas- cularization group 41.4%, p less than 0.01), whereas no treat- ment benefit was apparent for the 56 patients greater than 75 years old. Intra-aortic balloon pump support was used in 86% of both groups; 63% of the initial medical stabilization group received thrombolytic agents, and 25% underwent delayed revascularization (Figure 29) (184). The (S)MASH study [(Swiss) Multicenter Trial of Angioplasty for Shock] randomly assigned 55 refractory shock patients to either PCI or conventional care. The mortality rate in the PCI group was 9 absolute percentage points lower at 30 days (69% versus 78%) than in the conventional therapy group but did not reach statistical significance (495). The group difference was similar to that observed at 30 days in the SHOCK trial (494). Given the large overall treatment benefit of 13 lives saved per 100 patients treated, emergency revascularization is rec- ommended for those less than 75 years who are suitable for revascularization. Patients with life-shortening illnesses, no vascular access, previously defined coronary anatomy that was unsuitable for revascularization, anoxic brain damage, and prior cardiomyopathy were excluded from the trial. For those enrolled, the treatment benefit was similar for all other subgroups examined: diabetics, women, prior MI or hyper- tension, and early or late developing shock. The elderly pose a special problem. There were only 56 patients 75 years of age or older in the SHOCK trial, and firm conclusions can- not be drawn. The mortality rate for the elderly patients assigned to initial medical stabilization was similar to younger patients assigned to initial medical stabilization and was therefore unexpectedly low (53.1%). Imbalances in ful to assess the cause of shock. (See Section 7.6.1 for dis-

cussion on hemodynamic assessment.)

Nonrandomized studies have suggested that mechanical reperfusion of occluded coronary arteries by PCI or CABG may improve survival in patients with MI and cardiogenic shock. In large clinical trials, such patients have an in-hospital survival rate that ranges from 20% to 50% when treated with intravenous fibrinolytic therapy (482,483,772,773). In other case series, mechanical reperfusion with PCI has been report- ed to result in hospital survival rates as high as 70%, but selection bias influenced these findings. However, a multi- center, prospective, randomized study confirmed this gener- al approach (184). The SHOCK trial tested the hypothesis that emergency revascularization for cardiogenic shock due to an ST-elevation/Q-wave or new LBBB MI would result in reduction in all-cause 30-day mortality compared with initial medical stabilization and delayed revascularization as clini- cally determined. In the SHOCK trial, cardiogenic shock was defined as clinical evidence of systemic hypoperfusion with systolic blood pressure less than 90 mm Hg for at least 30 minutes (or the need for supportive measures to maintain systolic blood pressure greater than 90 mm Hg), cardiac

index of no more than 2.2 L/min/m2_{and PCWP of at least 15}

mm Hg.

In the SHOCK trial, 152 patients were randomly assigned to the emergency revascularization strategy, and 150 patients were assigned to a strategy of initial medical stabilization. The 30-day mortality rate for emergency revascularization patients was 46.7% versus 56.0% for initial medical stabi- lization patients (95% CI minus 20.5 to plus 1.9%, p equals 0.11). However, the mortality rate at 6 and 12 months (sec- ondary end points) was significantly lower in the emergency revascularization group (53.3% versus 66.4%, p less than

Figure 29.Kaplan-Meier survival of cardiogenic shock after early revascularization curve 1-year postrandomization. Survival estimates for early revascularization (n=152) and initial medical stabilization (n=149) groups. Log-rank test P = 0.04. Reprinted with permission from Hochman et al. JAMA 2001;285:190-2. Copyrighted © 2001, American Medical Association. All rights reserved (184).

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fit). If skilled personnel are available, IABP placement before transport will help stabilize the patient. If the patient presents in shock within 3 to 6 hours of MI onset and delays in transport and intervention are anticipated, fibrinolytic therapy and IABP may be initiated. Nonrandomized studies suggest that this combination is beneficial (778), and a small randomized trial observed a trend toward benefit for those in classic shock, with acceptable complication rates. Fibrinolytic therapy should be administered to those patients who are not candidates for early revascularization and who do not have a contraindication to fibrinolysis.

When shock has resolved, ACE inhibitors and beta-block- ers, initiated in low doses with progressive increases as rec- ommended in the ACC/AHA Guidelines for the Evaluation and Management of Heart Failure, should be administered before discharge (771). (See Section 7.6.7.6 for discussion of mechanical support for the failing heart.)

7.6.6. Right Ventricular Infarction

1. Patients with inferior STEMI and hemodynamic com-