Effects of different dosages and modes of sodium bicarbonate administration during cardiopulmonary resuscitation

Department of Pharmacy, Hartford Hospital, CT.
American Journal of Emergency Medicine (Impact Factor: 1.27). 12/1992; 10(6):525-32. DOI: 10.1016/0735-6757(92)90176-X
Source: PubMed


Systemic acidosis occurs during cardiac arrest and cardiopulmonary resuscitation (CPR). The present study investigated the effect of different modes of sodium bicarbonate administration on blood gas parameters during CPR. Arterial and venous blood gases were obtained during 10 minutes of CPR which was preceded by 3 minutes of unassisted ventricular fibrillation in 36 dogs. Following 1 minute of CPR, the animals received one of four treatments in a randomized and blinded manner: normal saline (NS), sodium bicarbonate bolus dose 1 mEq/kg (B), sodium bicarbonate continuous infusion 0.1 mEq/kg/min (I), and sodium bicarbonate bolus dose (0.5 mEq/kg) plus continuous infusion 0.1 mEq/kg/min (L+I). Eleven dogs completed NS, 8 B, 8 I, and 9 L+I protocol. Following NS infusion, both arterial and venous pH declined consistently over time. Significant differences compared with NS treatment in venous pH were observed at 12 minutes of ventricular fibrillation (L+I, 7.27 +/- 0.05; NS, 7.15 +/- 0.05; B, 7.20 +/- 0.05; I, 7.24 +/- 0.04, each bicarbonate treatment versus NS, and L+I versus B, (P < .05). The B group had an elevated venous PCO2 (mm Hg) concentration following 6 minutes of ventricular fibrillation compared with NS, L+I, and I groups (81 +/- 14 versus 69 +/- 10 versus 68 +/- 10 versus 71 +/- 8, respectively, (P = .07). Arterial pH and PCO2 values showed a similar trend as the venous data with the L+I group demonstrating arterial alkalosis (pH > 7.45) at 12 minutes of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

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    ABSTRACT: The routine use of sodium bicarbonate in patients with cardiac arrest has been discouraged, with the benefit of outcome evaluation. Current recommendations include an elaborate stratification of circumstances in which bicarbonate is to be used. The physiological and clinical aspects of bicarbonate administration during cardiopulmonary resuscitation in animal and human studies were reviewed. The onset of significant acidemia or alkalemia is associated with adverse system specific effects. The administration of bicarbonate may mitigate the adverse physiological effects of acidemia, improve response to exogenously administered vasopressor agents, or simply increase venous return due to an osmolar effect, resulting in increased coronary perfusion pressure. Likewise, bicarbonate may have adverse effects in each of these areas. The preponderance of evidence suggests that bicarbonate is not detrimental and may be helpful to outcome from cardiac arrest. An objective reappraisal of the empirical use of bicarbonate or other buffer agents in the appropriate "therapeutic window" for cardiac patients may be warranted.
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    ABSTRACT: The use of bicarbonate is rooted in three decades of clinical experience and observational studies. For many years, bicarbonate passed the tried and true test for clinical therapies; however, administration of sodium bicarbonate during cardiac arrest and hypoxic acidosis has become increasingly controversial. The controversy provides an excellent opportunity to evaluate the impact an evidence-based approach might have on a common clinical practice. Is bicarbonate efficacious in the treatment of the severe acidosis that accompanies cardiac arrest during cardiopulmonary resuscitation (CPR)? Are the deleterious effects of bicarbonate clinically relevant? What is the evidence upon which a rational decision may be based? This review evaluates and ranks the evidence supporting the use of sodium bicarbonate in the therapy of acidosis associated with cardiac arrest during CPR.
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    ABSTRACT: Buffer therapy, especially sodium bicarbonate (SB), is still one of the most controversial issues in cardiopulmonary resuscitation. This critical review focuses around four issues: 1) the necessity of buffer therapy, 2) evidence for its beneficial effects, 3) evidence for its detrimental effects, and 4) differences among the various available buffers. The major conclusions of this review are: 1) significant, deleterious metabolic acidosis often exists at the time that drugs (epinephrine) are initiated during cardiopulmonary resuscitation. 2) Although clinical evidence is lacking, buffer therapy is probably beneficial when used in conjunction with effective ventilation and measures to optimize tissue perfusion. 3) No substantial evidence shows a detrimental effect of buffer therapy, specifically sodium bicarbonate; if appropriately used, sodium bicarbonate does not increase serum sodium and osmolarity, does not interfere with oxygen release, does not increase tissue carbon dioxide concentrations, and does not paradoxically worsen intracellular acidosis. 4) Despite theoretic differences, there is not enough factual basis to favor the use of other buffers over sodium bicarbonate. Prospective clinical trials and more laboratory research using relevant experimental models are badly needed to resolve the important controversy over buffer therapy in cardiopulmonary resuscitation.
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