Bench to bedside: resuscitation from prolonged ventricular fibrillation.

Ventricular fibrillation (VF) remains the most common cardiac arrest heart rhythm. Defibrillation is the primary treatment and is very effective if delivered early within a few minutes of onset of VF. However, successful treatment of VF becomes increasingly more difficult when the duration of VF exceeds 4 minutes. Classically, successful cardiac arrest resuscitation has been thought of as simply achieving restoration of spontaneous circulation (ROSC). However, this traditional approach fails to consider the high early post-cardiac arrest mortality and morbidity and ignores the reperfusion injuries, which are manifest in the heart and brain. More recently, resuscitation from cardiac arrest has been divided into two phases; phase I, achieving ROSC, and phase II, treatment of reperfusion injury. The focus in both phases of resuscitation remains the heart and brain, as prolonged VF remains primarily a two-organ disease. These two organs are most sensitive to oxygen and substrate deprivation and account for the vast majority of early post-resuscitation mortality and morbidity. This review focuses first on the initial resuscitation (achieving ROSC) and then on the reperfusion issues affecting the heart and brain.

Left ventricular myocardial adenosine triphosphate changes during reperfusion of ventricular fibrillation: the influence of flow and epinephrine.

OBJECTIVE: To determine whether epinephrine in combination with high flow worsens left ventricular (LV) myocardial high-energy phosphate stores during reperfusion of ischemic ventricular fibrillation (VF). DESIGN: Blinded, prospective block randomized, placebo controlled study. SETTING: University medical center research laboratory. SUBJECTS: A total of 22 mixed breed swine weighing 22.0+/-3.3 kg (SD). INTERVENTIONS: Open-chest swine, anesthetized with alpha-chloralose, underwent 10 mins of nonperfused VF followed by reperfusion with cardiopulmonary bypass for 90 mins and then defibrillation. Animals were block randomized to four groups for reperfusion: Group 1 (n = 5), high flow (100 mL/kg/min) and epinephrine (2.5 microg/kg/min); Group 2 (n = 5), high flow and placebo; Group 3 (n = 6), low flow (30 mL/kg/min) and epinephrine; and Group 4 (n = 6), low flow and placebo. MEASUREMENTS AND MAIN RESULTS: In vivo LV creatine phosphate (CP) and adenosine triphosphate (ATP) were determined using whole wall and spatially localized 31P NMR spectroscopy at 4.7 Tesla. During perfusion of the fibrillating myocardium, epinephrine significantly increased aortic pressure (p < .05) and improved defibrillation rates (p < .01). ATP levels during reperfusion were significantly decreased within all groups compared with baseline. There were no differences in ATP levels between groups. High flow, independent of epinephrine, was associated with increased preservation of ATP (p < .05), increased CP/ATP ratios (p < .02) in all layers of the LV wall, and decreased aortic and cardiac vein lactates (p < .001). CONCLUSIONS: Epinephrine, in combination with flow higher than standard cardiopulmonary resuscitation flows, increased perfusion pressure and defibrillation rates, but did not significantly alter myocardial ATP during VF reperfusion in the in vivo heart Reperfusion flow, independent of epinephrine, is a critical determinant of myocardial ATP preservation.

Flow requirements in ventricular fibrillation: An in vivo nuclear magnetic resonance analysis of the left ventricular high-energy phosphate pool.

STUDY OBJECTIVE: We sought to determine whether flow rates of approximately 60% of normal values are sufficient to preserve the left ventricular myocardial high-energy phosphate pool during ventricular fibrillation (VF). METHODS: Mixed-breed swine (weight 22. 4+/-2.5 kg) were anesthetized with alpha-chloralose, placed in a state of VF, and perfused with extracorporeal circulation at a target flow of 50 mL.kg(-1).min(-1). In vivo whole-wall (average of left ventricular wall) and spatially localized phosphorous-31 nuclear magnetic resonance (NMR) spectra were acquired at baseline and during VF. RESULTS: Mean flow during VF was 58+/-20 mL.kg(-1). min(-1) (+/-SD; 95% confidence interval, 44 to 71) or about 60% of baseline cardiac output (n=13). Whole-wall adenosine triphosphate (ATP) decreased during perfused VF (P <.05), whereas creatine phosphate (CP) remained unchanged from baseline. With spatially localized NMR, the ratios of CP/ATP were similar at baseline in all layers (endocardium --> epicardium) of the left ventricular wall. However, during perfused VF, subepicardial CP/ATP ratios increased by 14% to 40% compared with baseline values, whereas subendocardial CP/ATP ratios remained unchanged (1% to 3% increase). An additional 4 animals perfused at 72+/-10 mL.kg(-1).min(-1) (+/-SD; 95% confidence interval, 56 to 92) during VF had preservation of CP and ATP levels. CONCLUSION: Flow levels equivalent to 60% of baseline cardiac output were insufficient to maintain normal high-energy phosphate levels in the in vivo fibrillating myocardium. At this level of flow, myocardial high-energy phosphate loss is nonhomogeneous within the left ventricular wall.

In-vivo myocardial substrate alteration during perfused ventricular fibrillation.

OBJECTIVES: Earlier work suggests the in-vivo heart alters its substrate utilization as a function of cardiac work. Previous work has also demonstrated the high oxygen requirements of the heart during ventricular fibrillation (VF). The authors hypothesized that myocardial substrate utilization during VF with perfusion is similar to the normal beating heart under conditions of increased workload. METHODS: Myocardial substrate selection was studied in the in-vivo porcine myocardium using 13carbon nuclear magnetic resonance (13C NMR) under conditions of increased cardiac work (dobutamine group) and VF with extracorporeal perfusion (VF group). Once the animal preparation was completed, metabolic steady state was achieved with the infusion of unlabeled acetate into the left anterior descending (LAD) coronary artery. The infused substrate was then changed to [2-13C] acetate and glutamate pool labeling was monitored by 13C NMR. The glutamate C4 resonance areas at baseline and after intervention of either increased workload (dobutamine group) or perfused VF (VF group) were compared within groups using paired t-tests. RESULTS: Baseline aortic and great cardiac vein lactates, glucose levels, blood gases, hemoglobin levels, and temperatures were similar between groups. In both groups, there was a significant decrease from baseline in the labeling of C4 glutamate peaks (dobutamine group: 20.2+/-14.9 vs 84.7+/-32.7, p = 0.002; and VF group: 49.8+/-24.4 vs 83.9+/-24.4, p = 0.02), indicating selection against acetate oxidation in favor of other endogenous substrates. CONCLUSIONS: In the in-vivo heart, despite the absence of functional contractions, changes in substrate utilization during perfused VF are similar to changes that occur with increased workload in the normal beating heart.

Epinephrine and high-flow reperfusion after cardiac arrest in a canine model.

STUDY OBJECTIVES: Epinephrine has been used in cardiac arrest to increase the low blood flow generated by standard CPR methods. Reperfusion with high flow such as that obtained with cardiopulmonary bypass (CPB) may obviate the need for or alter the dose of epinephrine after cardiac arrest. The objective of this study was to evaluate the effect of high-flow reperfusion after cardiac arrest with and without epinephrine on coronary perfusion pressure, defibrillation energy, restoration of spontaneous circulation (ROSC), and 2-hour survival after prolonged cardiac arrest. DESIGN: Prospective, randomized, double-blind, placebo-controlled study using a canine model. INTERVENTIONS: Thirty mongrel dogs were randomized to receive, after ventricular fibrillation cardiac arrest of 12 minutes' duration without CPR, placebo (n = 10), standard-dose epinephrine (.02 mg/kg) (n = 10), or high-dose epinephrine (.2 mg/kg) (n = 10) during reperfusion with CPB. Epinephrine or placebo was given with the start of CPB and then every 5 minutes, followed by countershock until ROSC or crossover at the fourth dose to high-dose epinephrine. RESULTS: ROSC was achieved in the first 15 minutes of bypass in 10 of 10 dogs given high-dose epinephrine, in 9 of 10 given standard-dose epinephrine, and in 1 of 10 given placebo. After the crossover to high-dose epinephrine, ROSC was achieved in 8 of 10 dogs originally given placebo and the remaining animal given the standard dose of epinephrine. During early reperfusion, the high-dose group had a higher mean coronary perfusion pressure (high dose, 153 + 62 mm Hg; standard dose, 81 +/- 18 mm Hg; placebo, 51 +/- 15 mm Hg; P < .002) and a shorter mean ROSC time (high dose, 16.2 +/- 8 minutes; standard dose, 20.3 +/- 3.6 minutes; placebo, 27.9 +/- 3.2; P < .02) and required less defibrillation energy. CPB flow during ventricular fibrillation was 63% of baseline cardiac output in all three groups. Two-hour survival was 5 of 10 in the high-dose group, 8 of 10 in the standard-dose group, and 5 of 10 in the placebo group. CONCLUSION: Restoration of high blood flow alone is insufficient to restore spontaneous circulation after prolonged cardiac arrest. Epinephrine, when administered early under high-flow conditions, increases coronary perfusion pressure, decreases defibrillation energy, and decreases time elapsed before ROSC. Higher doses of epinephrine under conditions of high-flow reperfusion do not improve 2-hour survival compared with standard-dose epinephrine.

Epinephrine-mediated changes in carbon dioxide tension during reperfusion of ventricular fibrillation in a canine model.

OBJECTIVE: Previous studies suggest that epinephrine may alter the correlation of perfusion with measures of PCO2 during cardiopulmonary resuscitation. This study investigated the effects of epinephrine on PaCO2 and mixed venous PCO2 in a high-flow reperfusion model of cardiac arrest. DESIGN: Prospective, block randomized, blinded, placebo-controlled, laboratory study. SUBJECTS: Thirty mixed breed canines. INTERVENTIONS: After a 12-min ventricular fibrillation cardiac arrest, 30 mixed breed canines were reperfused with standardized (3200 revolutions/min) cardiopulmonary bypass and were given placebo (n = 10), standard dose epinephrine (0.02 mg/kg; n = 10), or high-dose epinephrine (0.2 mg/kg; n = 10). Arterial and mixed venous blood gases, coronary perfusion pressure, pump flow and peripheral vascular resistance were compared between groups during the early reperfusion period using analysis of variance with a post hoc Tukey's multiple comparison test. MEASUREMENTS AND MAIN RESULTS: Baseline variables were similar between groups. With reperfusion, the high-dose epinephrine group had higher coronary perfusion pressures (p < .002), lower systemic pump flow (p < .01), and higher peripheral vascular resistance (p < .001). In the high-dose epinephrine group, both PaCO2 (high-dose epinephrine, 40 +/- 6 torr [5.3 +/- 0.8 kPa]; standard dose epinephrine, 45 +/- 7 torr [6.0 +/- 0.9 kPa]; placebo, 54 +/- 4 torr [7.2 +/- 0.5 kPa]; p < .01) and mixed venous PCO2 (high-dose epinephrine, 55 +/- 10 torr [7.3 +/- 1.3 kPa]; standard dose epinephrine, 57 +/- 9 torr [7.6 +/- 1.2 kPa]; placebo, 67 +/- 4 torr [8.9 +/- 0.5 kPa]; p < .05) were significantly decreased, and arterial pH, PaO2, and mixed venous PO2 were significantly increased compared with the placebo group. CONCLUSION: In this model, when ventilation and CO2 production are constant, the decrease in PaCO2 with epinephrine is due to decreased pulmonary blood flow (flow to membrane oxygenator) and peripheral shunting.

Myocardial metabolic changes during reperfusion of ventricular fibrillation: a 31P nuclear magnetic resonance study in swine.

OBJECTIVE: Myocardial metabolic requirements during reperfusion of ventricular fibrillation are poorly understood. The objective of this study was to determine if controlled reperfusion after a clinically relevant global ischemia period of 10 mins was sufficient to prevent or reverse myocardial ischemia as indicated by changes in myocardial high energy phosphates, myocardial intracellular pH, and great cardiac vein lactate. DESIGN: Prospective laboratory study with controlled reperfusion. SETTING: Research laboratory at a university medical center. SUBJECTS: Five swine weighing 19 +/- 3 kg. INTERVENTIONS: Ten minutes of nonperfused ventricular fibrillation followed by reperfusion with cardiopulmonary bypass (flow 30 mL/kg/min) for 50 mins. MEASUREMENTS AND MAIN RESULTS: Myocardial adenosine triphosphate (ATP), phosphocreatine, and intracellular pH were determined using in vivo 31P nuclear magnetic resonance. Myocardial blood flow, measured by 15-mu radiolabeled microspheres, was significantly increased above baseline during reperfusion. Phosphocreatine was depleted during the 10 mins of nonperfused ventricular fibrillation, but recovered to 122 +/- 18% of baseline with reperfusion and was 112 +/- 18% at 60 mins (p < .005). ATP concentrations decreased to 51 +/- 16% of baseline after 10 mins of nonperfused ventricular fibrillation, improved to 67 +/- 9% of baseline with early reperfusion, and were 65 +/- 9% of baseline at 60 mins (p < .02). Myocardial intracellular pH improved from 6.11 +/- 0.18 after 10 mins of nonperfused ventricular fibrillation, to 6.89 +/- 0.20 with early reperfusion, and then decreased to 6.85 +/- 0.35 at 60 mins ventricular fibrillation (p < .001). Despite myocardial blood flows higher than baseline during the reperfusion period, great cardiac vein/aortic lactate gradient increased over the reperfusion period. CONCLUSION: Prolonged reperfusion with supranormal myocardial blood flow does not restore normal myocardial aerobic metabolism in the fibrillating myocardium after a 10-min nonperfused ventricular fibrillation period.

Norepinephrine-induced hypertension following cardiac arrest: effects on myocardial oxygen use in a swine model.

STUDY OBJECTIVE: Recent studies suggest that norepinephrine-induced hypertension early after cardiac arrest ameliorates cerebral hypoperfusion and improves neurologic outcome. The purpose of this study was to evaluate the effects of early norepinephrine-induced hypertension on postresuscitation myocardial blood flow and oxygen use. DESIGN: Prospective, controlled laboratory study. PARTICIPANTS: Ten swine. INTERVENTIONS: All animals underwent 10 minutes of ventricular fibrillation cardiac arrest followed by 5 minutes of low-flow cardiopulmonary bypass (10 mL/kg.min), norepinephrine (0.12 mg/kg), and defibrillation. Animals then were assigned to a hypertension group (mean aortic pressure, 95 mm Hg) or a control group (mean aortic pressure, 75 mm Hg) by titrating a norepinephrine infusion to attain the prescribed aortic pressure. RESULTS: Myocardial blood flow, perfusion pressure, and oxygen metabolism were compared between groups at different times using analysis of variance with a post-hoc Tukey test. Groups had similar myocardial blood flow during ventricular fibrillation, total defibrillation energy, and time to restoration of spontaneous circulation. Fifteen minutes after restoration of spontaneous circulation, the hypertension group had significantly elevated myocardial blood flow, 965 +/- 314 mL/min.100 g versus 325 +/- 67 mL/min.100 g in the control group (P < .001), myocardial oxygen consumption of 51.2 +/- 26.9 mL O2/min.100 g versus 6.4 +/- 3.4 mL O2/min.100 g (P < .001), and myocardial oxygen extraction of 46% +/- 20% versus 14% +/- 4% (P < .01). CONCLUSION: In the early resuscitation period, increasing the norepinephrine dose to induce mild hypertension significantly increases oxygen use in the postischemic myocardium.

Organ blood flow following cardiac arrest in a swine low-flow cardiopulmonary bypass model.

STUDY OBJECTIVE: To determine organ blood flow changes, relative to baseline, following cardiac arrest and resuscitation in a closed-chest cardiac arrest swine model using cardiopulmonary bypass to achieve reproducible return of spontaneous circulation (ROSC). INTERVENTIONS: Following 10 min of ventricular fibrillation (VF), animals (n = 10) received low-flow cardiopulmonary bypass at 10 ml/kg/min from 10-15 min. At 15 min of VF, norepinephrine (0.12 mg/kg) was given and bypass flow increased to 50 ml/kg/min, followed by countershocks at 16 min. Following ROSC, cardiopulmonary bypass was immediately weaned off with norepinephrine support. Organ blood flows were determined during normal sinus rhythm, during reperfusion of VF and during the early post-ROSC period while off cardiopulmonary bypass support. Organ blood flows during the early ROSC period were compared with organ blood flow at baseline and during VF. RESULTS: During early reperfusion of VF prior to any drug therapy, myocardial, cerebral and abdominal organ blood flows were all low. All animals achieved ROSC at 16.9 +/- 0.7 min and were weaned from bypass in < 5 min following ROSC. During the early post-ROSC period, blood flow to the myocardial, cerebral and adrenal vascular beds was significantly elevated relative to baseline. Simultaneously, blood flow to the kidneys, liver, spleen and lungs was reduced relative to baseline. CONCLUSIONS: This low-flow bypass model produces reproducible high resuscitation rates and ROSC times. Early post-resuscitation organ blood flow is characterized by a selective hyperemia involving the cerebral, myocardial and adrenal vascular beds, in contrast to hypoperfusion of the pulmonary and mesenteric vascular beds.

Early detection of myocardial infarction with magnetic resonance imaging in a canine model.

STUDY OBJECTIVE: To determine the effectiveness of magnetic resonance imaging in detecting early myocardial infarction in vivo after coronary artery occlusion. DESIGN: A prospective, controlled canine study using a left anterior descending coronary artery ligation model. INTERVENTIONS: After thiopental anesthesia, nine mongrel dogs underwent cardiac-gated magnetic resonance imaging with a 2.35-T magnet with a 40-cm bore before and four hours after ligation of the left anterior descending coronary artery. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and left ventricular blood flow changes were determined. The mean image intensity ratio of the suspected infarct region to the normal myocardium was determined in the four-hour postocclusion images and compared with the ratio from the same anatomic region obtained at baseline. The area of necrotic and ischemic myocardium was determined using fluorescein and triphenyl tetrazolium chloride staining immediately after four-hour images. All animals were noted to have necrotic (range, 1.8% to 20.4% of ventricles) and ischemic (range, 9.2% to 36.6% of ventricles) myocardium with histochemical staining. The mean intensity ratio of infarcted myocardium four hours after left anterior descending coronary artery occlusion was significantly higher than baseline (four hours, 2.31 +/- 0.82; baseline, 1.02 +/- 0.09; P < .002). CONCLUSION: Magnetic resonance imaging can distinguish myocardial edema associated with acute infarcting myocardium in vivo as early as four hours after left anterior descending coronary artery occlusion. Magnetic resonance imaging may be clinically useful in identifying thrombolytic therapy candidates among acute myocardial infarction patients presenting with atypical symptoms.

Fructose-1,6-diphosphate fails to limit early myocardial infarction size in a canine model.

STUDY OBJECTIVE: Fructose-1,6-diphosphate (FDP) appears to improve early post-myocardial infarction hemodynamics and limit early myocardial infarct size in previous canine studies. However, these studies did not account for the effect of collateral blood flow on infarct size. Our objective was to determine the effect of FDP on early infarct size and hemodynamics while measuring regional myocardial blood flow. DESIGN: A prospective, blinded, placebo-controlled laboratory study using a canine open-chest left anterior descending coronary artery (LAD) occlusion model. INTERVENTIONS: Twenty-two mongrel dogs were assigned randomly to receive either FDP (175 mg/kg, then 2 mg/kg/min for two hours) or placebo, beginning five minutes after LAD occlusion. MEASUREMENTS AND MAIN RESULTS: Regional myocardial blood flow, hemodynamics, and myocardial infarct size were determined. Infarct size was assessed using magnetic resonance imaging in a subset of animals. Three of the 22 dogs had no infarct and significantly higher collateral blood flow than the 19 animals with myocardial infarction (P < .001). Four hours after LAD occlusion, cardiac index, dP/dtmax, heart rate, and systolic and mean aortic pressures were not statistically different between groups. Infarct size expressed as area of necrosis/area at risk was similar between groups (FDP, 0.55 +/- 0.28; controls, 0.59 +/- 0.31). CONCLUSION: FDP given after occlusion of the LAD in this canine model did not limit early myocardial infarct size.

Arterial pH and carbon dioxide tension as indicators of tissue perfusion during cardiac arrest in a canine model.

BACKGROUND AND METHODS: Previous studies have shown that Paco2 and end-tidal CO2 reflect coronary artery perfusion pressures during cardiac arrest. We investigated the relationship of coronary artery perfusion pressure to central arterial pH and Paco2 values during resuscitation from cardiac arrest in a canine model. Twenty-four mongrel dogs were block randomized to three different resuscitation groups after induction of ventricular fibrillation and cardiac arrest: a) standard cardiopulmonary resuscitation (CPR) and advanced life support (n = 8); b) cardiopulmonary bypass (n = 8); or c) open-chest CPR (n = 8). Central arterial blood gases and perfusion pressures were monitored during cardiac arrest and during resuscitation. RESULTS: Prearrest blood gases and hemodynamic values were similar between groups. Sixteen dogs from all three groups were successfully resuscitated. Survivors had significantly higher coronary artery perfusion pressure (p = .03), Paco2 (p = .015), and lower pH (p = .01) values than nonsurvivors. There was no correlation of pH and Paco2 during mechanical external CPR. However, after institution of the different resuscitation techniques, pH and Paco2 each showed a statistically significant correlation (r2 = .50 and .33, respectively) with coronary artery perfusion pressure. CONCLUSIONS: Central arterial pH and Paco2 monitoring during cardiac arrest may reflect the adequacy of tissue perfusion during resuscitation and may predict resuscitation outcome from ventricular fibrillation.

Use of cardiopulmonary bypass, high-dose epinephrine, and standard-dose epinephrine in resuscitation from post-countershock electromechanical dissociation.

STUDY OBJECTIVE: To determine the effects of cardiopulmonary bypass with standard-dose epinephrine, high-dose epinephrine, and standard-dose epinephrine on perfusion pressures, myocardial blood flow, and resuscitation from post-countershock electromechanical dissociation. DESIGN: Prospective, controlled laboratory investigation using a canine cardiac arrest model randomized to receive one of three resuscitation therapies. INTERVENTIONS: After the production of post-countershock electromechanical dissociation, 25 animals received ten minutes of basic CPR and were randomized to receive cardiopulmonary bypass with standard-dose epinephrine, high-dose epinephrine, or standard-dose epinephrine. MEASUREMENTS AND MAIN RESULTS: Myocardial blood flow was measured using a colored microsphere technique at baseline, during basic CPR, and after intervention. Immediate and two-hour resuscitation rates were determined for each group. Return of spontaneous circulation was achieved in eight of eight cardiopulmonary bypass with standard-dose epinephrine compared with four of eight high-dose epinephrine and three of eight standard-dose epinephrine animals (P less than .04). One animal was resuscitated with CPR alone and was excluded. Survival to two hours was achieved in five of eight cardiopulmonary bypass with standard-dose epinephrine, four of eight high-dose epinephrine, and three of eight standard-dose epinephrine animals (NS). Coronary perfusion pressure increased significantly in the cardiopulmonary bypass with standard-dose epinephrine group when compared with the other groups (cardiopulmonary bypass with standard-dose epinephrine, 76 +/- 45 mm Hg; high-dose epinephrine, 24 +/- 12 mm Hg; standard-dose epinephrine, 3 +/- 14 mm Hg; P less than .005). Myocardial blood flow was higher in cardiopulmonary bypass with standard-dose epinephrine and high-dose epinephrine animals compared with standard-dose epinephrine animals but did not reach statistical significance. Cardiac output increased during cardiopulmonary bypass with standard-dose epinephrine (P = .001) and standard-dose epinephrine (NS) compared with basic CPR but decreased after epinephrine administration in the high-dose epinephrine group (NS). CONCLUSION: Resuscitation from electromechanical dissociation was improved with cardiopulmonary bypass and epinephrine compared with high-dose epinephrine or standard-dose epinephrine alone. However, there was no difference in survival between groups. Cardiopulmonary bypass with standard-dose epinephrine resulted in higher cardiac output, coronary perfusion pressure, and a trend toward higher myocardial blood flow. A short period of cardiopulmonary bypass with epinephrine after prolonged post-countershock electromechanical dissociation cardiac arrest can re-establish sufficient circulation to effect successful early resuscitation.

Objectives to direct the training of emergency medicine residents on off-service rotations: research.

This is the 16th in a series of objectives to direct resident training in Emergency Medicine. Research is recognized as an important component of physician training, yet it is often neglected in medical school and residency curricula. We offer here an objective-based program for resident physicians' exposure to research design and methodology.

Arterial blood gases during cardiac arrest: markers of blood flow in a canine model.

Measures of CO2 have been shown to correlate with coronary perfusion pressure and cardiac output during cardiac arrest. We evaluated arterial pH (pHa) relative to blood flow during cardiac arrest in a canine electromechanical dissociation (EMD) model of cardiac arrest using different resuscitation techniques. Following 15 min of cardiac arrest, 24 mongrel dogs received epinephrine with continued CPR or closed-chest cardiopulmonary bypass. Central arterial blood gases, end-tidal carbon dioxide (PetCO2), coronary perfusion pressure and cardiac output were measured. During CPR, prior to epinephrine or bypass, there was no correlation of pHa, PACO2 and PetCO2, with cardiac output or coronary perfusion pressure. Immediately after instituting the resuscitation techniques, both pHa and PaCO2 showed a significant correlation with cardiac output (pHa; R = -0.78, P less than 0.001 and PaCO2; R = 0.87, P less than 0.001) and with coronary perfusion pressure (pHa; R = -0.75, P less than 0.001 and PaCO2; R = 0.75, P less than 0.001). Eventual survivors (n = 15) had an early significant decrease in pHa, base excess and a significant increase in PaCO2 which was not present in non-survivors (n = 9). Neither pHa nor PaCO2 correlate with blood flow under low flow conditions of CPR. However, with effective circulatory assistance, pHa and PaCO2 reflect systemic blood flow and reperfusion washout.

Comparison of standard external CPR, open-chest CPR, and cardiopulmonary bypass in a canine myocardial infarct model.

STUDY OBJECTIVES: After cardiac arrest, open-chest CPR (OCCPR) and cardiopulmonary bypass (CPB) have demonstrated higher resuscitation rates when compared individually with standard external CPR (SECPR). We compared all three techniques in a canine myocardial infarct ventricular fibrillation model. TYPE OF PARTICIPANTS: Twenty-six mongrel dogs were block-randomized to receive SECPR and advanced life support (nine), CPB (nine), or OCCPR (eight). DESIGN AND INTERVENTIONS: All dogs received left anterior descending coronary artery occlusion followed by four minutes of ventricular fibrillation without CPR and eight minutes of Thumper CPR. At 12 minutes, dogs received one of three resuscitation techniques. After resuscitation, all animals received four hours of intensive care. Animals that were resuscitated had histochemical determination of ischemic and necrotic myocardial areas. MEASUREMENTS: Intravascular pressures were measured and coronary perfusion pressure was calculated during baseline, cardiac arrest, resuscitation, and postresuscitation periods. Percent necrotic myocardium, percent ischemic myocardium, and necrotic-to-ischemic ratios were determined for resuscitated animals. Epinephrine dosage and number of countershocks were determined for each group. MAIN RESULTS: Nine of nine CPB and six of nine OCCPR, compared with two of eight SECPR animals, were resuscitated (P less than .01). Three of nine CPB and OCCPR and two of eight SECPR dogs survived to four hours (P = NS). Coronary perfusion pressure two minutes after institution of technique was significantly higher with CPB (75 +/- 37 mm Hg) and OCCPR (56 +/- 31 mm Hg) than in SECPR animals (16 +/- 16 mm Hg, P less than .04). Epinephrine required for resuscitation was significantly less with CPB (0.10 +/- 0.02 mg/kg) than for SECPR (0.28 +/- 0.11 mg/kg, P less than .002). The ratio of necrotic to ischemic myocardium at four hours was significantly lower with CPB (0.15 +/- 0.31) and OCCPR (0.39 +/- 0.25) than for SECPR (1.16 +/- 0.31, P less than .02). CONCLUSION: OCCPR and CPB produce higher coronary perfusion pressures and improved resuscitation rates from ventricular fibrillation when compared with SECPR in this canine myocardial infarct cardiac arrest model. CPB and OCCPR yielded similar resuscitation results, although less epinephrine was required with CPB.

Objectives to direct the training of emergency medicine residents on off-service rotations: critical care medicine, Part 2.

This article is the second of two parts outlining the objectives for resident rotations in intensive care units. It is part of a larger continuing series on the goals and objectives to direct the training of emergency medicine residents on off-service rotations. The critical care unit allows the resident an opportunity to provide continuing care for critically ill patients, many of whom enter the health care system through the emergency department. Critical care medicine is a natural continuum of emergency medicine, and provides the resident with the ability to follow the natural progression of seriously ill patients, as well as build confidence and experience in caring for the critically ill and injured. These objectives are designed to help focus the resident's reading and study during the rotation.

Objectives to direct the training of emergency medicine residents on off-service rotations: critical care medicine, Part 1.

This article is the first of two parts outlining the objectives for a resident rotating in the intensive care unit (ICU). It is part of a larger continuing series on the goals and objectives to direct the training of emergency medicine residents on off-service rotations. The critical care unit is a valuable rotation that allows the resident to see and care for critically ill patients, many of whom present initially to the emergency department. Critical care is a logical continuum for the sick and injured patient as he moves from the prehospital and emergency department (ED) settings to the ICU. These objectives are designed to focus the resident's reading and study during a critical care rotation.