Page 437 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 37: Myocardial Ischemia 307

agonist, may be useful when tachyarrhythmias limit therapy with other and two small studies support the notion that vasopressor therapy
vasopressors. Vasopressor infusions need to be titrated carefully in to increase aortic pressure improves thrombolytic efficacy. 148,149 The use
patients with cardiogenic shock to maximize coronary perfusion pres- of intra-aortic balloon pumping to augment aortic diastolic pressure
sure with the least possible increase in myocardial oxygen demand. may increase the effectiveness of fibrinolytics as well.
Hemodynamic monitoring, with serial measurements of cardiac output, To date, emergency percutaneous revascularization is the only inter-
filling pressures, (and other parameters, such as mixed venous oxygen vention that has been shown to consistently reduce mortality rates in
saturation), allows for titration of the dosage of vasoactive agents to the patients with cardiogenic shock. An extensive body of observational and
minimum dosage required to achieve the chosen therapeutic goals. 140 registry studies has shown consistent benefits from revascularization.
Following initial stabilization and restoration of adequate blood pres- Notable among these is the GUSTO-1 trial, in which patients treated
sure, tissue perfusion should be assessed. If tissue perfusion remains with an “aggressive” strategy (coronary angiography performed within
inadequate, inotropic support or intra-aortic balloon pumping should 24 hours of shock onset with revascularization by PTCA or bypass
be initiated. If tissue perfusion is adequate but significant pulmonary surgery) had significantly lower mortality (38% compared with 62%).
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congestion remains, diuretics may be employed. Vasodilators can be The National Registry of Myocardial Infarction-2 (NRMI-2), which
considered as well, depending on the blood pressure. collected 26,280 shock patients with cardiogenic shock in the setting of
In patients with inadequate tissue perfusion and adequate intravas- MI between 1994 and 1997, similarly supported the association between
cular volume, cardiovascular support with inotropic agents should be revascularization and survival. Improved short-term mortality was
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initiated. Dobutamine, a selective β -adrenergic receptor agonist, can noted in those who then underwent revascularization during the refer-
1
improve myocardial contractility and increase cardiac output, and is ence hospitalization, either via PTCA (12.8% mortality vs 43.9%) or
the initial agent of choice in patients with systolic pressures greater than CABG (6.5% vs 23.9%). These data complement the GUSTO-1 sub-
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80 mm Hg. Dobutamine may exacerbate hypotension in some patients, study data and are important, not only because of the sheer number of
and can precipitate tachyarrhythmias. Use of dopamine may be prefer- patients from whom these values are derived, but also because NRMI-2
able if systolic pressure is less than 80 mm Hg, although tachycardia and was a national cross-sectional study which more closely represents
increased peripheral resistance may worsen myocardial ischemia. In general clinical practice than carefully selected trial populations.
some situations, a combination of dopamine and dobutamine can be The SHOCK study was a randomized, multicenter international
more effective than either agent used alone. Phosphodiesterase inhibi- trial that assigned patients with cardiogenic shock to receive optimal
tors such as milrinone are less arrhythmogenic than catecholamines, medical management—including IABP and thrombolytic therapy—or
but have the potential to cause hypotension, and should be used to undergo cardiac catheterization with revascularization using PTCA or
with caution in patients with tenuous clinical status. Levosimendan, a CABG. The primary end point, all-cause mortality at 30 days, was 46.7%
calcium sensitizer, has both inotropic and vasodilator properties and in the revascularization group, and 56% in the medical therapy group, a
does not increase myocardial oxygen consumption. Several relatively difference that did not reach statistical significance (p = 0.11). Planned
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small studies have shown hemodynamic benefits with levosimendan in follow-up, however, revealed a significant benefit from early revascular-
cardiogenic shock after MI. 141,142 Survival benefits have not been shown ization at 6 months and at 1 year (p < 0.03). Subgroup analyses also
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either in cardiogenic shock or acute heart failure. This drug is not revealed benefit in patients younger than 75, those with prior MI, and
143
available in the United States. those randomized less than 6 hours from onset of infarction. 152,153
Intra-aortic balloon counterpulsation (IABP) reduces systolic afterload The SMASH trial was similarly design, but enrolled sicker patients.
154
and augments diastolic perfusion pressure, increasing cardiac output and The trial was terminated early due to difficulties in patient recruit-
improving coronary blood flow. These beneficial effects, in contrast to ment, and enrolled only 55 patients, but showed a reduction in 30-day
144
those of inotropic or vasopressor agents, occur without an increase in absolute mortality reduction similar to that in the SHOCK trial (69%
oxygen demand. IABP does not, however, produce a significant improve- mortality in the invasive group vs 78% in the medically managed group,
ment in blood flow distal to a critical coronary stenosis, and has not p = NS), and this benefit was also maintained at 1 year.
154
been shown to improve mortality when used alone without reperfusion When the results of both the SHOCK and SMASH trials are put into
therapy or revascularization. In patients with cardiogenic shock and com- perspective with results from other randomized, controlled trials of
promised tissue perfusion, IABP can be an essential support mechanism patients with acute myocardial infarction, an important point emerges:
to stabilize patients and allow time for definitive therapeutic measures to despite the moderate relative risk reduction (for the SHOCK trial 0.72,
be undertaken. 144,145 In appropriate settings, more intensive support with CI 0.54-0.95, for the SMASH trial, 0.88, CI, 0.60-1.20) the absolute ben-
mechanical assist devices may also be implemented. efit is important, with 9 lives saved for 100 patients treated at 30 days in
both trials, and 13.2 lives saved for 100 patients treated at one year in the
Reperfusion Therapy: Although fibrinolytic therapy reduces the likeli- SHOCK trial. This latter figure corresponds to a number needed to treat
138
hood of subsequent development of shock after initial presentation, (NNT) of 7.6, one of the lowest figures ever observed in a randomized,
its role in the management of patients who have already developed controlled trial of cardiovascular disease.
shock is less certain. The available randomized trials 43,46,59,146 have not On the basis of these randomized trials, the presence of cardiogenic
demonstrated that fibrinolytic therapy reduces mortality in patients shock in the setting of acute MI is a class I indication for emergency
with established cardiogenic shock. On the other hand, in the SHOCK revascularization, either by percutaneous intervention or CABG. 41
Registry, patients treated with fibrinolytic therapy had a lower
147
p = 0.005), even after adjustment for age and revascularization status ■ INDICATIONS FOR TEMPORARY PACING
in-hospital mortality rate than those who were not (54% vs 64%,

(OR 0.70, p = 0.027). IN ACUTE MYOCARDIAL INFARCTION
Fibrinolytic therapy is clearly less effective in patients with car- Damage to the impulse formation and conduction system of the heart
diogenic shock than in those without. The explanation for this lack from MI can result in bradyarrhythmias and conduction disturbances
of efficacy appears to be the low reperfusion rate achieved in this that do not respond reliably to conventional pharmacologic agents such
subset of patients. The reasons for decreased thrombolytic efficacy in as atropine or isoproterenol. These disturbances may lead to further
patients with cardiogenic probably include hemodynamic, mechani- hemodynamic compromise and coronary hypoperfusion. Disturbances of
cal, and metabolic factors that prevent achievement and maintenance conduction distal to the AV node and the bundle of His are particularly
of infarct-related artery patency. Attempts to increase reperfusion worrisome, even if they are tolerated well hemodynamically. Ventricular
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rates by increasing blood pressure with aggressive inotropic and pressor escape rhythms in the setting of acute MI are unstable and unreliable; their
therapy and intra-aortic balloon counterpulsation make theoretic sense, discharge rate may vary widely, with abrupt acceleration to ventricular

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