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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]
clinical definition of cardiogenic shock is decreased cardiac output and
evidence of tissue hypoxia in the presence of adequ...
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
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
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. 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. 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
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.
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
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.
5. Goldberg, RJ, Gore, JM, Alpert, JS, et al. Cardiogenic shock after
acute myocardial infarction.Incidence and mortality from a community wide
perspective, 1975 -1988. N Engl J Med 1991; 325: 1117.