Clinical supervision in the emergency department: a costly inefficiency for academic medical centers.
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Academic Medical Centers↗
Biomedical subjects
D J DeBehnke
Publications and source records attributed to D J DeBehnke.
Research fundamentals: choosing an appropriate journal, manuscript preparation, and interactions with editors.
This article, the last in a series on research methodology prepared by the Research Committee of the Society for Academic Emergency Medicine (SAEM), describes the process of journal selection, manuscript preparation, manuscript submission, and responding to editorial and reviewer comments. Methods for completing each step of this process are described. Following these methods will increase the chance of publishing one's work in the highest-quality and most appropriate journal.
Humans↗
Effects of endothelin-1 on resuscitation rate during cardiac arrest.
OBJECTIVES: Endothelin-1 (ET-1) is a potent peripheral and coronary artery vasoconstrictor and has been shown to improve coronary perfusion pressure (CPP) during cardiac arrest. The effect of ET-1 on return of spontaneous circulation (ROSC) following cardiac arrest has not been studied. Our hypothesis was that ET-1 does not improve ROSC from cardiac arrest when compared to placebo. METHODS: A total of 11 immature swine were used in this laboratory study. Animals were randomized to receive 300 microg ET-1 and standard dose epinephrine (SDE) or placebo and SDE during arrest. After a 10-min period of no-flow ventricular fibrillation (VF), CPR was performed for 3 min followed by ET-1/SDE or placebo/SDE administration. Following drug administration, standard ACLS was followed with SDE given every 3 min. Aortic pressure was monitored during resuscitation. ROSC was defined as any perfusing rhythm with a systolic pressure greater than 60 mmHg for 60 s. Animals received post-ROSC care as needed for 2 h post-ROSC. CPP and ROSC were analyzed using repeated measures ANOVA and Fischer's exact test respectively. P<0.05 was considered significant. RESULTS: Pre-arrest variables and CPP prior to ET-1 administration were not different between groups. Following ET-1 administration, CPP was significantly increased at all time points in ET-1/SDE versus placebo/SDE animals. ROSC was achieved in 1/5 (20%) ET-1/SDE versus 1/6 (16.7%) placebo/SDE animals (P>0.05). The resuscitated ET-1/SDE animal survived 6.5 min compared to 120 min for the resuscitated placebo/SDE animal. CONCLUSIONS: In our study, ET-1 administration during cardiac arrest increases CPP but does not improve ROSC.
Animals↗
The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations.
OBJECTIVE: To determine the efficacy of atropine therapy in patients with hemodynamically compromising bradycardia or atrioventricular block (AVB) in the prehospital and emergency department settings. METHODS DESIGN: Retrospective review of prehospital, emergency department, and hospital records. PARTICIPANTS: Prehospital patients with hemodynamically compromising bradycardia or AVB with evidence of spontaneous circulation who received atropine as delivered by emergency medical services personnel (advanced life support level). SETTING: Urban/suburban fire department-based emergency medical service system with on-line medical control serving a population of approximately 1.6 million persons. DEFINITIONS: Hemodynamic instability was defined as the presence of any of the following: ischemic chest pain, dyspnea, syncope, altered mental status, and systolic blood pressure less than 90 mmHg. Bradycardia was defined as sinus bradycardia, junctional bradycardia, or idioventricular bradycardia (grouped as bradycardia) while AVB included first-, second- (types I and II), or third-degree (grouped as AVB). The response that occurred within one minute following each dose of atropine was defined as none, partial, complete, or adverse. MAIN RESULTS: Of 172 patients meeting entry criterion complete data was available for 131 (76.1%) and constitutes the study population. The mean age was 71 years. Fifty-one percent were female. Forty-five patients had AVB and 86 bradycardia. Patients with AVB were more likely to have a presenting systolic blood pressure less than 90 mmHg than those with bradycardia. In the 131 patients, responses to atropine were as follows: 26 (19.8%) = partial, 36 (27.5%) = complete, 65 (49.6%) = none, and 4 (2.3%) = adverse. Patients presenting with bradycardia (compared to AVB) more commonly: (1) received a single dose of atropine; (2) a lower total dose of atropine in the prehospital interval; (3) were more likely to arrive in the ED with a normal sinus rhythm; and (4) were less likely to receive additional atropine or isoproterenol in the ED. Those patients who achieved normal sinus rhythm over the total course of care were likely to have achieved that rhythm during the prehospital interval. There was no difference between groups in the likelihood of leaving the ED with a normal sinus rhythm achieved during the ED interval. Acute myocardial infarction was more common in patients presenting with AVB (55.5%) than with bradycardia (23.2%, P = 0.001). CONCLUSIONS: Approximately one-half of patients who received atropine in the prehospital setting for compromising rhythms had either a partial or complete response to therapy. Adverse responses were uncommon. Those patients who presented with hemodynamically unstable bradycardia to EMS personnel responded more commonly to a single dose and a lower total dose of atropine compared to similar patients with AVB. Those patients who achieve normal sinus rhythm by ED discharge were likely to have achieved it during the prehospital interval.
Aged↗
Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: prehospital and ED treatment with atropine.
The purpose of this study was to investigate the therapeutic response to atropine of patients experiencing hemodynamically compromising bradyarrhythmia related to acute myocardial infarction (AMI) in the prehospital (PH) setting and the therapeutic impact of the PH response to atropine on further Emergency Department (ED) care. In addition, the prevalence of AMI in patients presenting with atrioventricular block (AVB) is noted. Retrospective review of PH, emergency department (ED), and hospital records. PH patients, with hemodynamically compromising bradycardia or AVB with evidence of spontaneous circulation, who received atropine as delivered by emergency medical services (EMS) personnel, were used. Urban/suburban fire department-based emergency medical services (EMS) system with on-line medical control serving a population of approximately 1.6 million persons. Hemodynamic instability was defined as the presence of any of the following: ischemic chest pain, dyspnea, syncope, altered mental status, and systolic blood pressure less than 90 mm Hg. Bradycardia was defined as sinus bradycardia, junctional bradycardia, or idioventricular bradycardia (grouped as bradycardia), whereas AVB included first-, second- (types I and II), or third-degree (grouped as AVB). The response that occurred within 1 minute of atropine dosing was recorded as none, partial, complete, or adverse. Comparisons were made between patients with AMI and non-AMI hospital discharge diagnoses. The diagnosis of AMI was confirmed by abnormal elevations in creatinine phosphokinase MB fraction. One hundred seventy-two patients meeting entry criteria were identified. Of these, 131 (76.1%) had complete PH, ED, and hospital records and were used for data analysis. Forty-five patients (34.3%) had a primary hospital discharge diagnosis of AMI; the remaining patients had a non-AMI discharge diagnosis. AMI patients were significantly younger (67 +/- 12 v 73 +/- 13 years, P = .025), were less likely to have a history of heart disease (35.5% v54.7%, P = .038), and were more likely to present with chest pain (68.9% v24.4%, P < .001) or hypotension (60% v37.2%, P = .013) compared with non-AMI patients. Forty-five of 131 patients presented with AVB, of which 25 had a hospital discharge diagnosis of AMI (55.6%). The mean time from first dose of atropine to ED arrival and the total dose of atropine received in the PH setting did not differ between AMI and non-AMI groups (15.2 +/- 7.7 v 16.2 +/- 8.7 minutes, P= .5; and 0.9 +/- 0.49 v 1.0 +/- 0.58 mg, P = .25). The likelihood of achieving normal sinus rhythm in the PH setting did not differ between AMI and non-AMI groups (40% v 18.6%, P = .07). No differences were found between AMI and non-AMI groups in the amount of additional atropine given (1.2 +/- 0.58 v 1.3 +/- 1.1 mg, P = .58) or the use of other resuscitative therapies after ED arrival (isoproterenol, 13.3% v12.8%, P = .93; dopamine, 28.9% v26.7% P = .79; transcutaneous pacing, 26.7% v26.7%, P = .99; transvenous pacing, 8.9% v5.8%, P = .51), with the exception of thrombolytic therapy (24.4% v 0%, P< .001) and cardiac catheterization (22.2% v3.4%, P = .001). Despite a lack of significant difference in achieving a normal sinus rhythm in the prehospital or ED setting, AMI patients were more likely to achieve a normal sinus rhythm over the total course of PH and ED care than non-AMI patients (44.4% v24.4%, P = .019). Hemodynamically unstable (by ACLS criterion) AVB presenting in the PH setting is associated with a hospital diagnosis of AMI in most (55.6%) patients in this study. AMI patients with hemodynamically unstable AVB or bradycardia are no more likely to respond to atropine therapy in the PH setting than patients with non-AMI hospital diagnoses. Finally, although there is no difference in the treatment of compromising AVB or bradycardia received by AMI versus non-AMI patients in the PH or ED setting, AMI patients are more likely to achieve a normal sinus rhythm over the t
Age Distribution↗
Prevalence, therapeutic response, and outcome of ventricular tachycardia in the out-of-hospital setting: a comparison of monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and torsades de pointes.
OBJECTIVE: To investigate out-of-hospital ventricular tachycardia (VT) cardiac arrest patients, comparing the prevalences and outcomes of the following VT subtypes among this population: monomorphic VT (MVT), polymorphic VT (PVT), and torsades de pointes (TdP, PVT with a prolonged QT interval). METHODS: This was a retrospective review from a fire department-based paramedic system of nontraumatic VT cardiac arrest patients (January 1991 to December 1994) with a supraventricular perfusing rhythm (SVPR) at some time during out-of-hospital care, with a measurable QT interval. QT interval was measured from an SVPR, and corrected QT interval (QTc) was calculated and considered prolonged if > 0.45 sec. VT was classified as polymorphic or monomorphic. TdP was defined as PVT with a prolonged QT interval. RESULTS: 196 patients were identified; six were excluded due to incomplete medical records, leaving 190 who met inclusion criteria and were used for data analysis. 117 (62%) patients had MVT, while 73 (38%) patients had PVT; of the 73 patients with PVT, 37 (51%) had normal QTc (non-TdP PVT) and 36 (49%) had prolonged QTc (TdP PVT). 97 (51%) patients had prolonged QTc (PQTc). Regardless of VT type (i.e., MVT vs PVT), 97 (51%) patients had prolonged QTc, with a mean QTc of 0.476+/-0.15 seconds prearrest and 0.464+/-12 seconds postarrest. Patients with PQTc were not more likely to have PVT (70 [37%] vs 76 [40%]; p = 0.705). No significant difference with respect to paramedic-witnessed arrests in each VT morphology group and each QT group was found. The overall hospital discharge rate was 28.4%. Regardless of VT type, patients had similar rates of out-of-hospital return of spontaneous circulation (ROSC) and hospital discharge; patients with PQTc were less likely to be discharged from the hospital (19.6% vs 37.6%; p = 0.01). 27.8% of TdP and 26.8% of non-TdP patients were discharged (p = 0.912). CONCLUSIONS: In this population of out-of-hospital VT arrest patients, MVT is the most common form of VT encountered; PVT and the subtype TdP are also seen in this population with approximately equal frequencies. All three rhythm types demonstrate similar responses to standard Advanced Cardiac Life Support therapy with equal rates of out-of-hospital ROSC and hospital discharge. PQTc may be a marker of poor clinical outcome in patients with out-of-hospital VT arrest.
Aged↗
The importance of being earnest--and student-centered.
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Career Choice↗
Undergraduate curriculum. SAEM Undergraduate Education Committee, Society for Academic Emergency Medicine.
The specialty of emergency medicine (EM) is becoming more and more involved in medical school education. The previous article discusses the integration of EM in medical school curricula. This outline was developed by the SAEM Undergraduate Education Committee to offer specific goals and objectives as well as suggestions for implementation of EM concepts into medical school curricula.
Curriculum↗
Cocaine-associated dystonic reaction.
Dystonic reactions are extrapyramidal motor dysfunctions that result from an insufficient activity of nigrostriatal dopamine and present clinically as spasms of the various muscle groups. Neuroleptic drugs are a known cause of dystonia and are the most frequently encountered trigger. Cocaine use has been associated with dystonias, though much less often. When reported in the setting of a dystonic reaction, cocaine has been described as a predisposing factor for the patient already using neuroleptic agents. Fewer reports of dystonia as a direct result of cocaine use, independent of neuroleptics, are found in the literature. The cases of two acute dystonic reactions secondary to cocaine use are presented, with a discussion of the pathophysiology and treatment alternatives.
Adult↗
What's new in ... emergency medicine.
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Emergency Medical Services↗
Cardiac arrest.
This article reviews the critical resuscitations necessary during prehospital and emergency department treatment of cardiac arrest. Standard therapy for cardiac arrest rhythms is presented. Novel pharmacologic agents, types of cardiopulmonary resuscitation, and circulatory-assist devices are discussed.
Adult↗
Use of ultrasonography for the evaluation of pregnant trauma patients.
The expeditious diagnosis and management of the pregnant trauma patient is essential for the survival of both the mother and fetus. The rapid trauma ultrasound examination, which has been accurately utilized by trauma surgeons and emergency physicians, may have a tremendous impact on the timely identification of acute intraperitoneal injuries and, potentially, on the evaluation of fetal viability in the pregnant trauma patient. This report describes our experience with the rapid trauma ultrasound examination in the management of three pregnant trauma patients and outlines the potential advantages and limitations of the procedure.
Adolescent↗
The effects of endothelin-1 on coronary perfusion pressure during cardiopulmonary resuscitation in a canine model.
OBJECTIVE: To study the hemodynamic effects of exogenously administered endothelin-1 (ET-1), a peptide produced by endothelial cells with potent non-adrenergically mediated vasoconstrictor properties. METHODS: A prospective drug intervention study was carried out in a resuscitation research laboratory. Fifteen mixed-breed dogs were anesthetized and instrumented for hemodynamic monitoring. Asphyxia arrest was produced by clamping the endotracheal tube. Hemodynamic data were collected continuously. Following loss of aortic fluctuations monitored by thoracic aortic catheter, the animals remained in pulseless electrical activity (PEA) for 10 minutes. After 10 minutes of no-flow PEA, closed-chest CPR was begun and the animals were randomized to one of three treatment groups (EPI, 0.02 mg/kg epinephrine IV every 3 minutes; ENDO, 100 micrograms ET-1 IV at 0 minutes; and EPI/ENDO, a combination of the EPI and ENDO treatments). RESULTS: ENDO and EPI alone produced similar coronary perfusion pressures (CPPs). The EPI/ENDO combination produced significantly improved CPP compared with that of either EPI or ENDO alone. In the EPI group, the best mean CPP was 16 +/- 14 mm Hg and occurred 7 minutes after drug administration. In the ENDO group, the best mean CPP was 28 +/- 7 mm Hg and occurred 13 minutes after drug administration. In the EPI/ENDO combination group, the best mean CPP was 61 +/- 37 mm Hg and occurred 7 minutes after drug administration (p < 0.05 compared with the EPI and ENDO groups alone). CONCLUSION: ET-1 is a potent vasoconstrictor. The combination of EPI and ENDO significantly improved CPP compared with that for either agent alone. ET-1 should be investigated further as a vasoconstrictor in cardiac arrest.
Animals↗
Treatment of out-of-hospital supraventricular tachycardia: adenosine vs verapamil.
OBJECTIVE: To compare the use of adenosine and the use of verapamil as out-of-hospital therapy for supraventricular tachycardia (SVT). METHODS: A period of prospective adenosine use (March 1993 to February 1994) was compared with a historical control period of verapamil use (March 1990 to February 1991) for SVT. Data were obtained for SVT patients treated in a metropolitan, fire-department-based paramedic system serving a population of approximately 1 million persons. Standard drug protocols were used and patient outcomes (i.e., conversion rates, complications, and recurrences) were monitored. RESULTS: During the adenosine treatment period, 105 patients had SVT; 87 (83%) received adenosine, of whom 60 (69%) converted to a sinus rhythm (SR). Vagal maneuvers (VM) resulted in restoration of SR in 8 patients (7.6%). Some patients received adenosine for non-SVT rhythms: 7 sinus tachycardia, 18 atrial fibrilation, 7 wide-complex tachycardia (WCT), and 2 ventricular tachycardia; no non-SVT rhythm converted to SR and none of these patients experienced an adverse effect. Twenty-five patients were hemodynamically unstable (systolic blood pressure < 90 mm Hg), with 20 receiving drug and 13 converting to SR; 8 patients required electrical cardioversion. Four patients experienced adverse effects related to adenosine (chest pain dyspnea, prolonged bradycardia, and ventricular tachycardia). In the verapamil period, 106 patients had SVT: 52 (49%) received verapamil (p < 0.001, compared with the adenosine period), of whom 43 (88%) converted to SR (p = 0.11). Two patients received verapamil for WCT; neither converted to SR and both experienced cardiovascular collapse. VM resulted in restoration of SR in 12 patients (11.0%) (p = 0.52). Sixteen patients were hemodynamically unstable, with 5 receiving drug (p = 0.005) and 5 converting to SR; 9 patients required electrical cardioversion (p = 0.48). Four patients experienced adverse effects related to verapamil (hypotension ventricular tachycardia, ventricular fibrillation). Recurrence of SVT was noted in 2 adenosine patients and 2 verapamil patients in the out-of-hospital setting and in 23 adenosine patients and 15 verapamil patients after ED arrival, necessitating additional therapy (p = 0.48 and 0.88, for recurrence rates and types of additional therapies, respectively). Hospital diagnoses, outcomes, and ED dispositions were similar for the 2 groups. CONCLUSION: Adenosine and verapamil were equally successful in converting out-of-hospital SVT in patients with similar etiologies responsible for the SVT. Recurrence of SVT occurred at similar rates for the 2 medications. Rhythm misidentification remains a common issue in out-of-hospital cardiac care in this emergency medical services system.
Adenosine↗
Evaluation of an esophageal Doppler probe for the identification of experimental pseudo-electromechanical dissociation: a preliminary study.
STUDY OBJECTIVE: To determine the effectiveness of an esophageal doppler device to non-invasively detect experimental pseudo-electromechanical dissociation (pseudo-EMD). DESIGN: Prospective, controlled, laboratory investigation using an asphyxial canine cardiac arrest model and a newly-developed esophageal flat-flow probe doppler unit. INTERVENTIONS: Mongrel dogs (20) were instrumented for hemodynamic monitoring. The esophageal doppler probe was placed in the distal esophagus of each animal. Electromechanical dissociation (EMD) was induced by clamping the endotracheal tube. MEASUREMENTS AND MAIN RESULTS: A period of pseudo-EMD was defined as the time where cardiac contractility was present, measured by a micromanometer tipped thoracic aortic catheter, without concurrent femoral pulses by palpation. The pseudo-EMD period could be produced consistently in all 20 animals. The characteristic doppler flow sounds were easily heard using the esophageal device in all animals. The time from endotracheal tube clamping until loss of femoral pulses was 622 +/- 96 s; until loss of radial artery doppler signals was 616 +/- 92 s; until loss of esophageal doppler signals was 728 +/- 88 s; and until loss of aortic fluctuations by thoracic aortic catheter was 728 +/- 82 s. The times to loss of esophageal doppler sounds and loss of aortic fluctuations were not significantly different. However, they were significantly longer than the time to loss of femoral pulses (P < 0.02). CONCLUSIONS: The canine asphyxial EMD model can be used for short experimental studies of pseudo-EMD. Pseudo-EMD can be consistently and non-invasively detected with this esophageal doppler device. The device is as reliable as a micromanometer tipped aortic arch catheter in detecting pseudo-EMD. The doppler device could potentially be useful in improving recognition of near cardiac arrest in pre-hospital and emergency department settings. Further research on the utility of this device in other models of low-flow states should be performed.
Animals↗
The hemodynamic and arterial blood gas response to asphyxiation: a canine model of pulseless electrical activity.
OBJECTIVE: Asphyxiation is a time-honored animal model for producing pulseless electrical activity cardiac arrest. To date, there has not been a detailed description of the hemodynamic and arterial blood gas response to asphyxiation in a large number of animals. Our objective was to describe a single laboratory's experience with a standardized canine model of asphyxial pulseless electrical activity arrest. METHOD: Design--Data from 4 separate research protocols using a standardized asphyxial model were retrospectively reviewed. Setting--Resuscitation research laboratory. Participants--169 mixed-breed dogs. Interventions--Each animal was anesthetized and instrumented for hemodynamic monitoring. The endotracheal tube was clamped and hemodynamic data was monitored. Following loss of aortic fluctuations by thoracic aortic catheter, animals remained in pulseless electrical activity for up to 20 min. Hemodynamic data was measured continuously and arterial blood gases were sampled intermittently. RESULTS: Following endotracheal tube clamping, there was a characteristic increase in heart rate and systolic blood pressure. The heart rate peaked at 2-3 min following clamping, while the systolic blood pressure peaked at 7 min. Both heart rate and systolic blood pressure then steadily decreased until loss of aortic fluctuations. Loss of aortic fluctuations occurred 11.4 +/- 2.4 min following clamping. Following loss of aortic fluctuations, the heart rate steadily decreased. Arterial blood gases during asphyxiation and pulseless electrical activity arrest showed profound hypoxemia with hypercarbia (pH 7.03 +/- 0.07; Pco2 93 +/- 19; Po2 12 +/- 7 at loss of aortic fluctuation). CONCLUSIONS: In this canine asphyxial model of pulseless electrical activity, a characteristic hemodynamic pattern of mild tachycardia-hypertension-bradycardia-hypotension was produced. Arterial blood gases reflect a profound hypoxemia and respiratory acidosis.
Animals↗
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.
Animals↗
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.
Animals↗