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Vol. 291, Issue 2, 773-777, November 1999
The Institute of Critical Care Medicine, Palm Springs, California
(S.S., M.H.W., W.T., H.P.P., E.M.); and The University of
Southern California School of Medicine, Los Angeles, California (S.S.,
M.H.W., W.T.)
Although buffer agents alone have failed to improve the success of
resuscitation, we now examine the widely held concept that it is the
combined effect of alkaline buffer and adrenergic agents that improves
outcomes of cardiopulmonary resuscitation. In the present report, the
effects of both CO2-consuming and
CO2-generating buffer agents in combination with adrenergic
vasopressor drugs were investigated. Ventricular fibrillation was
electrically induced in Sprague-Dawley rats weighing between 450 and
550 g. Precordial compression and mechanical ventilation were
initiated after 8 min of untreated ventricular fibrillation.
Animals were then randomized to receive bolus injections of either
inorganic sodium bicarbonate buffer, organic tromethamine buffer, or
saline placebo. The
1 adrenergic effects of epinephrine
were blocked with esmolol. The vasopressor amine was injected 2 min
after injection of the buffer agent. Electrical defibrillation was
attempted at the end of 8 min of precordial compression. In 15 additional animals, the sequence of administration of the adrenergic
vasopressor and buffer agents was reversed such that the adrenergic
vasopressor was injected before the buffer agents. All animals were
restored to spontaneous circulation. Both bicarbonate and tromethamine
significantly decreased coronary perfusion pressure from 26 to 15 mm Hg
and reduced the magnitude of the vasopressor effect of the adrenergic
vasopressor. When the vasopressor preceded the buffer, declines in
coronary perfusion pressure after administration of buffer agents
were prevented. In each instance, however, greater impairment of
postresuscitation myocardial function and decreased
postresuscitation survival were observed after treatment with
buffer agents.
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