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Re: Is Higher Blood Pressure always better for Patients With Post-MI Cardiogenic Shock ?

Dear Editor

Cardiogenic shock is an ominous complication of myocardial infarction (MI), occurring in 4 to 7%of cases. The majority of patients have an ST elevation (Q wave) MI, but cardiogenic shock can occur, although less frequently after a non-ST elevation (non-Q wave) MI.[1,4]

The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Hemodynamic criteria for cardiogenic shock are hypotension (systolic blood pressure < 90 mm Hg) and a reduced cardiac index (CI< 2.2 L/min/m²) in the presence of elevated pulmonary capillary wedge pressure (PCWP > 15 mm Hg). Cardiogenic shock, like other types of shock, is characterized by systemic hypoperfusion, with consequent tissue hypoxia and vital organ dysfunction. It must be emphasized that hypotension is not synonymous with shock. Patients with low blood pressure may have normal tissue perfusion if systemic vascular resistance (SVR) is also decreased.

On the other hand, tissue perfusion may be impaired despite normal blood pressure in the presence of severe sympathetically – mediated peripheral vasoconstriction. Most patients with acute MI and cardiogenic shock have severe and extensive coronary artery disease, often involving all the three major coronary arteries. Fixed coronary stenoses limit coronary blood flow despite maximal coronary arteriolar dilatation. Coronary perfusion pressure then becomes the major determinant of coronary blood flow.

Accordingly, any mild drop in blood pressure can significantly reduce coronary perfusion pressure and hence coronary blood flow. The combination of severe diffuse coronary artery disease and prolonged hypotension are particularly detrimental to patients with cardiogenic shock. The apparently limited efficacy of thrombolysis in patients with acute MI complicated by cardiogenic shock may be due to failure to improve coronary perfusion pressure during administration of thrombolytic agents. The rate of coronary thrombolysis can be restored to normal levels if the blood pressure is raised by aggressive use of vasopressors or insertion of intra-aortic balloon pump.[28,29]

Historically, mortality rate of cardiogenic shock complicating acute MI is 80 to 90 percent.[5] However, lower values for in-hospital mortality have been noted in more recent studies ranging from 56 to 74%.[1,4] This significant reduction in mortality of cardiogenic shock may be attributed to the increased use of intra-aortic balloon pump (IABP) and coronary reperfusion strategies which, by restoring patency of the infarct-related artery, can limit the infarct size.[2,3] There are promising data on the use of percutaneous coronary intervention (PCI) for cardiogenic shock complicating acute MI. The long-term outcome of patients with cardiogenic shock appears to be improved with early revascularization using either PCI or CABG as illustrated by the 1-year survival rate from the SHOCK trial.[2] Until coronary revascularization can be performed, the circulation must be supported either pharmacologically -by inotropics and vasopressors- or mechanically by intra-aortic balloon pump. Sympathomimetic inotropic and vasopressor agents remain the first-line therapy to reverse hypotension and maintain vital organ perfusion. A second goal of therapy is to maintain coronary perfusion pressure as high as possible during the administration of thrombolytic agents to facilitate coronary reperfusion. Dopamine is often used in cardiogenic shock as it increases myocardial contractility and supports the blood pressure. Norepinephrine is a potent vasopressor and is often used when dopamine is inadequate.

In spite of its potent inotropic effect, dobutamine is less often used in cardiogenic shock because it produces mild vasodilatation that may increase hypotension. On the other hand, dopamine and Norepinephrine have several deleterious effects in the setting of acute MI complicated by cardiogenic shock. Excessive vasoconstriction in response to vasopressors increase afterload and may further depress LV function and decrease cardiac output. Systemic hypoperfusion may occur as a result of decreased cardiac output and high SVR in spite of the relatively preserved blood pressure. Furthermore, cardiac work and myocardial oxygen demand are increased because of vasopressor – induced increase in afterload and heart rate that may worsen myocardial ischemia. Hence, the potential beneficial effect of vasopressors on coronary perfusion pressure and myocardial oxygen supply may be offset by increased demand.

Finally, dopamine may increase whole- body oxygen uptake - because of its calorigenic effect -and exacerbate tissue hypoxia. Dobutamine may be particularly useful in cardiogenic shock if improved tissue oxygenation rather than hemodynamic stability will be the goal of therapy. In contrast to dopamine and norepinephrine, dobutamine increases cardiac output, lowers afterload and SVR and improves tissue perfusion with only minimal increase in myocardial oxygen demand and whole-body oxygen uptake. We can hypothesize that maintaining adequate perfusion and oxygenation to the heart, brain and other vital organs may be more important than simply increasing the blood pressure - by excessive vasoconstriction - even at the expense of cardiac output, myocardial oxygen demand and tissue oxygenation. Tissue oxygenation can be monitored directly by measuring whole-body oxygen uptake (by calorimetery) or indirectly by calculating oxygen extraction ratio (O₂ ER = SaO₂ –SvO₂/ SaO₂) where SaO₂ is arterial O₂ saturation and SvO₂ is mixed venous O₂ saturation – of blood taken from pulmonary artery with Swan-Ganz catheter.

Other parameters of tissue oxygenation include arterial blood lactate and gastric mucosal pH. Similarly, cerebral perfusion and oxygenation can be evaluated by calculating cerebral O2 extraction ratio (cerebral O₂ ER = SaO₂ – SvjO₂/ SaO₂) where SvjO₂ is O₂ saturation of blood taken from internal jugular vein. Maintaining adequate coronary perfusion - while preventing significant increase in myocardial O₂ demand - is of critical importance during pharmacologic and mechanical therapy of cardiogenic shock. Myocardial oxygenation (reflecting the balance between O₂ supply and demand) can be evaluated directly by measuring myocardial blood lactate, oxygen extraction ratio, regional pH, PCO₂ and base deficit during transvenous catheterization of the coronary sinus (that drains most of the cardiac veins and opens into the right atrium). Adequacy of coronary blood flow can be assessed indirectly by repeated echocardiography to demonstrate any significant changes in ejection fraction and regional wall-motion abnormalities. Serial ECGs can also be used to detect early ST segment -T wave changes suggestive of increased size of infarct or ischemic area. Mechanical ventilation may be particularly important in cardiogenic shock - regardless of the blood gases – as it significantly reduces oxygen uptake (VO₂) - by allowing adequate sedation, analgesia and muscle paralysis – in a clinical setting of decreased oxygen delivery to the tissues (DO₂). Furthermore, mechanical ventilation can improve arterial oxygenation and increase myocardial O₂ supply.

In conclusion, it may be more appropriate to titrate the pharmacologic therapy of cardiogenic shock according to the parameters of myocardial and tissue oxygenation rather than to the hemodynamic parameters alone, while waiting for coronary revascularization.

References

1. Hochman, js, Boland, j, Sleeper, et al .and the SHOCK Registry Investigators. Current spectrum of cardiogenic shock and effect of early revascularization on mortality: Results of an international registry. Circulation 1995; 91: 873.

2. Holmes, DR Jr, Bates, ER, Kleinman, NS, et al. Contemporary reperfusion therapy for cardiogenic shock: The GUSTO-1 trial experience. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.J Am Coll Cardiol 1995; 26:668.

3. Goldberg, RJ, Samad, NA, Yarzebski, J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl j Med1999; 340:1162.

4. Holmes, DR Jr, Berger, PB, Hochman, Js, et al. cardiogenic shock in patients with acute ischemic syndromes with and without ST- segment elevation. Circulation 1999; 100:2067.