Differences in systemic and myocardial blood acid-base status during cardiopulmonary resuscitation

Simultaneous arterial (aortic), mixed venous (pulmonary artery), and myocardial venous (great cardiac vein) blood gas and lactate concentrations were obtained in 12 dogs before and during cardiac arrest and CPR. We observed marked mixed venous and myocardial venous acidosis and increased PaCO2 but normal pHa and reduced PaCO2. Furthermore, the pH was significantly lower and the PCO2 significantly higher at the myocardial venous site compared to the mixed venous site, and marked myocardial lactate production occurred during CPR. Calculated bicarbonate and CO2 content (CCO2) did not increase during CPR from any site compared to control values and actually decreased significantly in arterial and myocardial venous samples. Changes in hydrogen ion concentration in both mixed venous and myocardial venous blood correlated with changes in lactate concentration but not total CCO2. Our results during CPR demonstrate a) a significant discrepancy between arterial and mixed venous blood gases but also a large and significant discrepancy between mixed venous and myocardial venous blood gases, b) significant anaerobic systemic and myocardial metabolism, and c) that mixed venous and myocardial venous acidosis is possibly a result of lactic acidosis.     

Selective acidosis in venous blood during human cardiopulmonary resuscitation: a preliminary report

During experimental CPR, a marked venoarterial gradient in PCO2 has been reported. This is accompanied by a disproportionate decrease in venous pH and a simultaneous increase in arterial pH. This study includes a case report of human CPR in which simultaneous arterial and mixed venous blood gases were obtained before and after cardiac arrest. Similar venoarterial PCO2 gradients were observed subsequently in six additional patients during arrest. These clinical data indicate that arterial blood gases fail to reflect striking increases in venous PCO2 and decreases in pH due to respiratory acidosis on the venous side of the circulation.     

Physiological variables during open chest cardiopulmonary resuscitation: results from a small series

OBJECTIVES: To evaluate the efficacy of open chest cardiac compressions for the resuscitation of pre-hospital cardiac arrest patients presenting with non-shockable rhythms on arrival at the emergency department. DESIGN: Prospective observational study of outcomes and physiological parameters during open chest cardiac compressions for non-traumatic pre-hospital cardiac arrest. SETTING: Large accident and emergency department receiving pre-hospital cardiac arrest patients with pre-hospital advanced life support provided by ambulance service paramedics. SUBJECTS: All patients in whom open chest cardiac compressions were performed by the author (JCC) during the period from January to May 1998 (seven patients). INTERVENTIONS: Assessment of artificial pulse and blood pressure generated by open chest cardiac compressions, measurement of arterial blood gases, recovery of spontaneous cardiac output, recovery of spontaneous ventilatory efforts and survival to admission and to discharge. RESULTS: Artificial pulse and recordable non-invasive blood pressures were generated in all patients; PO2 was physiological or supra-physiological in all patients; PCO2 was physiological or subphysiological in all patients; pH and base deficit were not corrected in the five patients with repeated samples (including two receiving 50 mEq sodium bicarbonate); three patients recovered spontaneous cardiac output (ROSC); two patients recovered spontaneous respiratory efforts (unrelated to ROSC); no patients survived to admission. CONCLUSIONS: Open chest cardiac compressions provide effective perfusion, enabling correction of ventilation parameters and showing clinical signs of adequate perfusion. However, acidosis was not corrected and the use of 50 mEq sodium bicarbonate was ineffective.     

Effects of sodium bicarbonate in canine hemorrhagic shock

We studied the use of sodium bicarbonate administration in a canine model of hemorrhagic shock to determine its effect on hemodynamics, arterial and venous blood gases, respiratory gases, and blood lactate levels. Thirteen dogs were anesthetized, paralyzed, mechanically ventilated, and hemodynamically monitored. Hypotension was induced and maintained at a mean arterial pressure of 40 to 45 mm Hg using controlled hemorrhage and reinfusion. After 2.5 h of shock, the dogs were randomized into two groups: one group (n = 6) received NaCl infusion; the other (n = 7) received sodium bicarbonate (1 mEq/kg followed by a continuous infusion of 2.5 mEq/kg.h for 2.5 h). CO2 production was increased in the alkali group, but there was no statistically significant difference between groups in any measured hemodynamic, blood gas, or respiratory gas variable. These included heart rate, BP, cardiac output, arterial and venous pH, CO2 production, and bicarbonate levels. Blood lactate levels, however, in the bicarbonate treated animals were significantly (p less than .01) higher than in the group treated with NaCl alone (10.1 +/- 3.2 vs. 5.1 +/- 1.2 mEq/L). These results are similar to the effects of bicarbonate found in other models of lactic acidosis, and suggest that bicarbonate therapy may have limited usefulness in the treatment of lactic acidosis.     

Acid base changes in arterial and central venous blood during cardiopulmonary resuscitation.

Twenty-seven patients in cardiopulmonary arrest had simultaneous measurements of arterial and central venous blood gases during cardiopulmonary resuscitation (CPR) with a pneumatic chest comparison and ventilation device. Mean central venous and arterial hydrogen ion concentrations, PCO2 and calculated bicarbonate concentrations were significantly different (P less than 0.01) at all sampling times (0, 10 and 20 min). Central venous blood samples predominantly showed a respiratory acidosis in contrast to a mixed disturbance in arterial samples inclined towards a metabolic acidosis. The mean difference between central venous PCO2 (pcv CO2) and arterial PCO2 (pa CO2) ranged from 5.18 to 5.83 kPa reflecting the low blood flow in patients undergoing CPR. Measurement of arterial Po2 indicated adequate oxygenation using the pneumatic device. Arterial blood gas analysis alone does not reflect tissue acid base status. Bicarbonate administration during CPR may have adverse effects and any decision as to its use should be based on central venous blood gas estimations.     

Effect of dichloroacetate in the treatment of anoxic lactic acidosis in dogs

Lactic acidosis is seen frequently after severe anoxia and circulatory failure. Because dichloroacetate (DCA) has been shown to be effective in the treatment of lactic acidosis, we studied its effect on lactate levels and pH in arterial and sagittal sinus blood specimens in a pediatric canine model of anoxic cardiac arrest followed by CPR. Lactate levels rose steadily in all puppies receiving DCA alone (group 1), DCA plus bicarbonate (group 2), bicarbonate alone (group 3), or neither drug (group 4). Arterial and sagittal-sinus lactate levels were in the range of 2 mmol/L during the baseline period, 6 mmol/L after anoxic arrest, and 10 mmol/L after 20 min of CPR. Bicarbonate, but not DCA, significantly raised arterial pH. Neither drug reversed the progression of acidosis in the sagittal sinus; mean pH ranged from 6.85 to 6.92 among the four groups after 20 min of CPR. We speculate that DCA did not decrease lactate levels or raise the pH in either the peripheral circulation or the CNS (sagittal sinus) because of poor perfusion achieved during closed-chest cardiac compression.     

Electroencephalographic consequences of alkalinization therapy during lactic acidosis: Different effects of sodium bicarbonate and carbicarb

To explore the differences between sodium bicarbonate and an experimental buffer, Carbicarb in the therapy of lactic acidosis, we performed the following studies. Rats were subjected to a combined respiratory and metabolic acidosis designed to simulate clinical lactic acidosis following cardiac arrest and resuscitation. The electroencephalogram (EEG) was monitored during induction and therapy of acidosis. The acidosis model was associated in a 22% fall in the amplitude of the EEG along with marked decreases in mean blood pressure, arterial PO₂, and pH, as well as increases in arterial PCO₂. Bicarbonate infusion was associated with a marked fall in mean blood pressure along with transient increases in arterial PCO₂, which were accompanied by significant and sustained decreases in the amplitude of the EEG. In contrast, Carbicarb did not lower blood pressure and had only transient effects on the amplitude of the EEG. These data suggested that bicarbonate therapy had deleterious effects on cerebral electric activity in this model of acidosis that were not shared by Carbicarb. if these data are confirmed in humans, Carbicarb may have advantages over bicarbonate in the clinical therapy of acute acidosis.     

Mixed venous blood gases are superior to arterial blood gases in assessing acid-base status and oxygenation during acute cardiac tamponade in dogs.

Recent reports using anesthetized ventilator-dependent animal models, have suggested that in certain shock states, a disparity exists between arterial and mixed venous blood gases with regard to acid-base status and oxygenation. In a chronically instrumented unanesthetized canine model of acute cardiac tamponade breathing room air, we studied the effect of a graded decline in cardiac output on arterial and mixed venous pH, PCO2, and PO2. Cardiac tamponade resulted in a profound arterial respiratory alkalosis, whereas mixed venous pH, PCO2, and calculated serum bicarbonate levels remained relatively unchanged. As intrapericardial pressure increased and cardiac output declined, the difference between arterial and mixed venous PCO2 progressively increased. Further, whereas arterial oxygenation improved as cardiac output declined, mixed venous oxygenation steadily worsened. This disparity began early in cardiac tamponade (reductions in cardiac output of 20-40%) long before arterial blood pressure began to fall and progressively worsened as hemodynamic deterioration and lactic acidosis developed. Our findings are consistent with the hypothesis that a reduction in blood flow, resulting in decreased CO2 delivery to the lungs, is the primary mechanism responsible for the difference in pH and PCO2 observed between arterial and mixed venous blood. In this conscious, spontaneously breathing animal model, mixed venous blood gases thus are superior to arterial blood gases in assessing acid-base status and oxygenation, even early in acute cardiac tamponade when the decline in cardiac output is in the range of 20 to 40% and arterial blood pressure has not changed significantly.     

Treatment of Lactic Acidosis with Dichloroacetate in Dogs

Lactic acidosis is a clinical condition due to accumulation of H(+) ions from lactic acid, characterized by blood lactate levels >5 mM and arterial pH <7.25. In addition to supportive care, treatment usually consists of intravenous NaHCO(3), with a resultant mortality >60%. Dichloroacetate (DCA) is a compound that lowers blood lactate levels under various conditions in both man and laboratory animals. It acts to increase pyruvate oxidation by activation of pyruvate dehydrogenase. We evaluated the effects of DCA in the treatment of two different models of type B experimental lactic acidosis in diabetic dogs: hepatectomy-lactic acidosis and phenformin-lactic acidosis. The metabolic and systemic effects examined included arterial blood pH and levels of bicarbonate and lactate; the intracellular pH (pHi) in liver and skeletal muscle; cardiac index, arterial blood pressure and liver blood flow; liver lactate uptake and extrahepatic splanchnic (gut) lactate production; and mortality. Effects of DCA were compared with those of either NaCl or NaHCO(3). The infusion of DCA and NaHCO(3), delivered equal amounts of volume and sodium, although the quantity of NaHCO(3) infused (2.5 meq/kg per h) was insufficient to normalize arterial pH.In phenformin-lactic acidosis, DCA-treated animals had a mortality of 22%, vs. 89% in those treated with NaHCO(3). DCA therapy increased arterial pH and bicarbonate, liver pHi and cardiac index, with increased liver lactate uptake and a fall in blood lactate. With NaHCO(3) therapy, there were decrements of cardiac index and liver pHi, with an increase in venous pCO(2) and gut production of lactate.Dogs with hepatectomy-lactic acidosis were either treated or pretreated with DCA. Treatment with DCA resulted in stabilization of cardiac index, a fall in blood lactate, and 17% mortality. NaHCO(3) was associated with a continuous decline of cardiac index, rise in blood lactate, and 67% mortality. In dogs pretreated with NaCl, mortality was 33%, but all dogs pretreated with DCA survived. Dogs pretreated with DCA also had lower blood lactate and higher arterial pH and bicarbonate than did those pretreated with NaCl.Thus, in either of two models of type B experimental lactic acidosis, treatment with DCA improves cardiac index, arterial pH, bicarbonate and lactate, and liver pHi. The mortality in dogs with type B lactic acidosis was significantly less in DCA-treated animals than in those treated with other modalities.     

Hypercarbic arterial acidemia following resuscitation from severe hemorrhagic shock

Arteriovenous pH and PCO2 gradients can develop during low cardiac output states. We have seen a transient rise in arterial PCO2 and a fall in arterial pH in humans receiving closed-chest cardiopulmonary resuscitation immediately following restoration of spontaneous circulation. Using a hemorrhagic shock model in sheep, serial arterial and mixed venous blood gases were sampled and CO2 elimination was measured. When cardiac output was less than 30% of the baseline value and the arteriovenous PCO2 difference was greater than 20 mmHg, the animals were rapidly resuscitated with intravenous 0.9% NaCl and dopamine. Following resuscitation, there was a transient arterial acidosis and hypercarbia due to passage of venous blood with a high CO2 content into arterial blood. The clinical implications in the setting of hemorrhagic shock are that (1) arterial blood gases are poor indicators of the systemic acid-base state, (2) arterial blood gases drawn immediately following volume resuscitation may be misinterpreted and should probably not be used to guide therapy and (3) there is a transient hypercarbic arterial acidosis following volume resuscitation that may have deleterious effects on cardiac and cerebral function in the early post-resuscitative period.     

Buffer administration during CPR promotes cerebral reperfusion after return of spontaneous circulation and mitigates post-resuscitation cerebral acidosis

To explore the effects of alkaline buffers on cerebral perfusion and cerebral acidosis during and after cardiopulmonary resuscitation (CPR), 45 anaesthetized piglets were studied. The animals were subjected to 5 min non-interventional circulatory arrest followed by 7 min closed chest CPR and received either 1 mmol/kg of sodium bicarbonate, 1 mmol/kg of tris buffer mixture, or the same volume of saline (n=15 in all groups), adrenaline (epinephrine) boluses and finally external defibrillatory shocks. Systemic haemodynamic variables, cerebral cortical blood flow, arterial, mixed venous, and internal jugular bulb blood acid-base status and blood gases as well as cerebral tissue pH and PCO(2) were monitored. Cerebral tissue acidosis was recorded much earlier than arterial acidaemia. After restoration of spontaneous circulation, during and after temporary arterial hypotension, pH in internal jugular bulb blood and in cerebral tissue as well as cerebral cortical blood flow was lower after saline than in animals receiving alkaline buffer. Buffer administration during CPR promoted cerebral cortical reperfusion and mitigated subsequent post-resuscitation cerebral acidosis during lower blood pressure and flow in the reperfusion phase. The arterial alkalosis often noticed during CPR after the administration of alkaline buffers was caused by low systemic blood flow, which also results in poor outcome.     

The sodium bicarbonate controversy

Sodium bicarbonate has been deleted from the advanced cardiac life support protocol. Sodium bicarbonate is no longer endorsed as the method of choice for the management of metabolic acidosis in the early rounds of cardiopulmonary resuscitation. This paper discusses mechanisms of acidosis occurring during cardiopulmonary arrest, past and present protocols for sodium bicarbonate administration and rationale for the deletion of sodium bicarbonate from resuscitation protocols.     

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

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)     

Physiological variables during open chest cardiopulmonary resuscitation: results from a small series

Objectives—To evaluate the efficacy of open chest cardiac compressions for the resuscitation of pre-hospital cardiac arrest patients presenting with non-shockable rhythms on arrival at the emergency department.

Design—Prospective observational study of outcomes and physiological parameters during open chest cardiac compressions for non-traumatic pre-hospital cardiac arrest.

Setting—Large accident and emergency department receiving pre-hospital cardiac arrest patients with pre-hospital advanced life support provided by ambulance service paramedics.

Subjects—All patients in whom open chest cardiac compressions were performed by the author (JCC) during the period from January to May 1998 (seven patients).

Interventions—Assessment of artificial pulse and blood pressure generated by open chest cardiac compressions, measurement of arterial blood gases, recovery of spontaneous cardiac output, recovery of spontaneous ventilatory efforts and survival to admission and to discharge.

Results—Artificial pulse and recordable non-invasive blood pressures were generated in all patients; PO₂ was physiological or supra-physiological in all patients; PCO₂ was physiological or subphysiological in all patients; pH and base deficit were not corrected in the five patients with repeated samples (including two receiving 50 mEq sodium bicarbonate); three patients recovered spontaneous cardiac output (ROSC); two patients recovered spontaneous respiratory efforts (unrelated to ROSC); no patients survived to admission.

Conclusions—Open chest cardiac compressions provide effective perfusion, enabling correction of ventilation parameters and showing clinical signs of adequate perfusion. However, acidosis was not corrected and the use of 50 mEq sodium bicarbonate was ineffective.

     

Interpretation of arterial blood gases: a clinical guide for nurses

Arterial blood gas analysis has become an essential skill for all healthcare practitioners. It provides important information with regard to adequacy of ventilation, oxygen delivery to the tissues and acid-base balance. Although each patient's clinical presentation will be judged individually, situations that warrant analysis of a blood gas sample include respiratory compromise, post-cardiorespiratory arrest, evaluation of interventions such as oxygen therapy, respiratory support and as a baseline before surgery. This article reviews the different parameters that are measured by various machines, with a focus on basic measurement of arterial blood gases. These include partial pressure of carbon dioxide in arterial blood (PaCO(2)), partial pressure of oxygen in arterial blood (PaO(2)), bicarbonate levels (HC0(3)(-)) in arterial blood and base excess/deficit. The physiology of acid-base balance is reviewed and the causes and presentation of the four acid-base disturbances is described. A systematic method to aid arterial blood interpretation is identified, together with discussion regarding the importance of interpreting PaO(2) readings in relation to the amount of inspired oxygen a patient is receiving (FiO(2)), the practice of temperate correction and the relationship between standardized and actual bicarbonate readings.     

pH homeostasis during cardiopulmonary resuscitation in critically ill patients.

We investigated the effect of repeated administration of sodium bicarbonate on acid-base balance and serum chemistry in a group of patients who developed cardiac arrest. A mixed acidosis persisted throughout the duration of resuscitation in the majority of patients in spite of the large ventilatory volume and multiple doses of bicarbonate they received. However, the repeated administration of bicarbonate prevented a severe fall in serum pH. Our study demonstrated the beneficial role of bicarbonate in the treatment of metabolic acidosis associated with cardiac arrest of prolonged duration. Analysis of our data strongly indicated that the primary factors which determine the serum pH during cardiopulmonary resuscitation are the duration of circulatory arrest, adequacy of ventilation and circulation, pH immediately before arrest, and quantity of bicarbonate administered and its volume of distribution in the various fluid and tissue compartments.     

Selected concepts and controversies in pediatric cardiopulmonary resuscitation

Although more than 80 years of research in cardiac resuscitation produced many important findings and greatly enhanced our understanding of the arrest state, outcome following pediatric cardiac arrest remains poor. Resuscitation guidelines have recently been published, but they may not reflect optimal therapy. Closed-chest compression-induced cardiac output may be higher in pediatric patients, particularly infants, than that previously reported in adults. To achieve higher cardiac outputs, direct cardiac compression is important; the recommended compression location has therefore been changed based on recent data. The optimal rate of compression, however, is uncertain, so further research is needed. Alternative vascular access sites, such as the endotracheal and intraosseous route for drug administration may permit more rapid drug delivery, but data suggest that a larger epinephrine dose than currently recommended should be used. It may also be helpful to dilute the drug in normal saline before endotracheal administration. Although experimental data suggest that a pure alpha-adrenergic agonist may be beneficial in a cardiac arrest, recent data show that epinephrine remains the drug of choice. Finally, the role of sodium bicarbonate in both the arrest and postarrest setting has become controversial. Recent data suggest that bicarbonate may be detrimental and that therapy of acidosis is best directed at improving perfusion, oxygenation, and ventilation. Alternative forms of therapy for acidosis, such as THAM and dichloroacetate may prove beneficial in the postarrest setting.     

A comparison of venous blood gases during cardiac arrest

Previous reports have advocated the use of mixed venous blood gases to estimate arterial pH and as a reflection of tissue acid-based balance. However, true mixed venous samples are difficult to obtain during cardiac arrest as they require a pulmonary artery catheter. The purpose of this study was to determine whether central or femoral venous samples could be used in place of pulmonary artery samples. Blood gases from these sites were drawn at intervals during experimental cardiac arrest in dogs. The PO2, PCO2, and pH from the pulmonary artery samples were strongly correlated with those from the central venous (r = .93, .99, and .99, respectively) and from the femoral venous samples (r = .73, .93, and .97, respectively). There were no significant differences in the pulmonary artery, central, or femoral venous gases. This animal model suggests that femoral and central venous samples mirror true mixed venous blood gases from the pulmonary artery and could be used in their place.     

Acid-base status of blood from intraosseous and mixed venous sites during prolonged cardiopulmonary resuscitation and drug infusions.

OBJECTIVES: a) To determine the relationship of acid-base balance (pH, PCO2) of blood samples from the intraosseous and the mixed venous route during prolonged cardiopulmonary resuscitation; b) to compare the effect of separate infusions of epinephrine, fluid boluses, or sodium bicarbonate through the intraosseous sites on the acid-base status of intraosseous and mixed venous blood during cardiopulmonary resuscitation; and c) to compare pH and Pco2 of intraosseous and mixed venous blood samples after sequential infusions of fluid, epinephrine, and sodium bicarbonate through a single intraosseous site. DESIGN: Prospective, randomized study. SETTING: Animal laboratory at a university center. SUBJECTS: Thirty-two mixed-breed piglets (mean weight, 30 kg). INTERVENTIONS: Piglets were anesthetized and prepared for blood sampling and cardiopulmonary resuscitation. After anoxic cardiac arrest, ventilation was resumed and chest compression was resumed. Blood gas samples from the pulmonary artery and both intraosseous sites were obtained simultaneously at baseline, at cardiac arrest, and at 5, 10, 15, 20, and 30 mins of cardiopulmonary resuscitation for group 1 (control group) and after drug (epinephrine and sodium bicarbonate) and saline infusions via one of the intraosseous cannulas in groups 2 through 5. MEASUREMENTS AND MAIN RESULTS: We found no differences between intraosseous and mixed venous pH and Pco2 during periods of <15 mins of cardiopulmonary resuscitation. However, this relationship was not maintained during prolonged cardiopulmonary resuscitation and after bicarbonate infusion. After large volume saline infusion, the pH and Pco2 of mixed venous and intraosseous blood were similar. During epinephrine infusion, the relationship between intraosseous and mixed venous pH and Pco2 was similar to that found in the control group. CONCLUSIONS: The intraosseous blood sample could be used to assess central acid-base balance in the early stage of arrest and cardiopulmonary resuscitation of <15 mins. However, during cardiopulmonary resuscitation of longer duration, drug infusions may render the intraosseous site inappropriate for judging central acidosis.     

Sodium bicarbonate improves the chance of resuscitation after 10 minutes of cardiac arrest in dogs.

The likelihood of successful defibrillation and resuscitation decreases as the duration of cardiac arrest increases. Prolonged cardiac arrest is also associated with the development of acidosis. These experiments were designed to determine whether administration of sodium bicarbonate and/or adrenaline in combination with a brief period of cardiopulmonary resuscitation (CPR) prior to defibrillation would improve the outcome of prolonged cardiac arrest in dogs. Ventricular fibrillation (VF) was induced by a.c. shock in anaesthetised dogs. After 10 min of VF, animals received either immediate defibrillation (followed by treatment with bicarbonate or control) or immediate treatment with bicarbonate or saline (followed by defibrillation). Treatment with bicarbonate was associated with increased rates of restoration of spontaneous circulation. This was achieved with fewer shocks and in a shorter time. Coronary perfusion pressure was significantly higher in NaHCO3-treated animals than in control animals. There were smaller decreases in venous pH in NaHCO3-treated animals than in controls. The best outcome in this study was achieved when defibrillation was delayed for approximately 2 min, during which time NaHCO3 and adrenaline were administered with CPR. The results of the present study indicate that in prolonged arrests bicarbonate therapy and a period of perfusion prior to defibrillation may increase survival.