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Dive into the research topics where Gary L. Swart is active.

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Featured researches published by Gary L. Swart.


Resuscitation | 1999

The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations

William J. Brady; Gary L. Swart; Daniel J. DeBehnke; O. John Ma; Tom P. Aufderheide

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.


Resuscitation | 1995

The hemodynamic and arterial blood gas response to asphyxiation: a canine model of pulseless electrical activity

Daniel J. DeBehnke; Swen J. Hilander; Daniel W. Dobler; Laurie L. Wickman; Gary L. Swart

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 laboratorys 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.


American Journal of Emergency Medicine | 1999

Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: prehospital and ED treatment with atropine.

Gary L. Swart; William J. Brady; Daniel J. DeBehnke; O John; Tom P. Aufderheide

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


Wilderness & Environmental Medicine | 1995

Serum potassium concentration as a predictor of resuscitation outcome in hypothermic cardiac arrest

Paul R. Bender; Daniel J. DeBehnke; Gary L. Swart; Kent N. Hall

The purpose of this study was to determine whether serum potassium concentration (SK) can predict resuscitation outcome in a canine model of severe hypothermic cardiac arrest. Fifteen adult mongrel anesthetized dogs were immersed to the neck in a 4 degrees C water bath and ventilated with room air, with ventilation halved at 45 min and stopped at 90 min. After cardiac arrest, 14 of the dogs were kept in the water bath for periods of 2-7 h, and another was held in arrest for 13 h. Following 10 min of closed chest cardiopulmonary resuscitation (CPR) (simulating a short transport time to a hospital), animals were placed on cardiopulmonary bypass and rapidly rewarmed. With appearance of ventricular fibrillation, animals were defibrillated up to three times. Standard advanced cardiac life support was initiated at a core temperature (Tc) of 30 degrees C. Eight of the 15 dogs had return of spontaneous circulation (ROSC), at Tc ranging from 30.4 to 36.5 degrees C. The eight dogs with ROSC did not differ from the seven without ROSC in time to arrest (128 +/- 48 versus 128 +/- 23 min) (mean +/- SD) or Tc at arrest (18.1 +/- 2.2 versus 17.9 +/- 3.1 degrees C), but had higher Tc at the end of the arrest period (9.7 +/- 3.0 versus 5.2 +/- 2.0 degrees C), reflecting a shorter arrest period in the dogs with ROSC (225 +/- 95 versus 420 +/- 193 min). SK (mEq liter(-1)) did not differ between dogs with and without ROSC at baseline (3.5 +/- 0.4 versus 3.7 +/- 0.4) or at arrest (3.4 +/- 0.7 versus 4.3 +/- 2.2), but there was a trend toward higher SK at the end of arrest in the group without ROSC (4.6 +/- 1.5 versus 9.4 +/- 6.3; range 3.2-7.8 versus 3.5-21.4; p = .053). SK was similar after 10 min of CPR in the groups with and without ROSC (6.6 +/- 2.9 versus 9.0 +/- 2.4; range 2.5-11.1 versus 4.5-11.0; p = .107). SK after 10 min of CPR was higher in some animals with ROSC (9.6 and 11.1) than in others which did not have ROSC (4.5 and 7.9). We conclude that very high SK following prolonged hypothermic cardiac arrest may be suggestive of an inability to resuscitate. However, SK after both prolonged hypothermic cardiac arrest and a brief period of CPR is not a good predictor of resuscitation using cardiopulmonary bypass rewarming in an animal model.


Prehospital and Disaster Medicine | 1994

The Efficacy of Atropine in the Prehospital Treatment of Unstable Bradycardia and Atrioventricular Block

Gary L. Swart; William J. Brady; Daniel J. DeBehnke

Purpose: To determine if public expectations about the survival rate from prehospital cardiac arrest (PCA) is consistent with actual EMS system performance, and if knowledge of actual resuscitation rates influences an individuals desire to be resuscitated from PCA. Methods: A questionnaire was administered to a convenience sample of individuals presenting to an urban teaching hospital emergency department. The questionnaire captured demographic data and an estimate of the probability of surviving a PCA in the local area. Individuals then were asked, before and after being informed of the actual local resuscitation rate, whether they would wish resuscitation from PCA. The actual resuscitation rate was calculated retrospectively from three years of ambulance run data and review of hospital records. Data were analyzed using the paired Mest and logistic regression.


Academic Emergency Medicine | 1999

A Standardized Letter of Recommendation for Residency Application

Samuel M. Keim; Judith A. Rein; Carey D. Chisholm; Pamela L Dyne; Gregory W. Hendey; Nicholas J. Jouriles; Randall W. King; Walter Schrading; Joseph A Salomone; Gary L. Swart; John M. Wightman


Academic Emergency Medicine | 2000

Emergency Medicine Resident Errors Identification and Educational Utilization

Cherri Hobgood; O. John Ma; Gary L. Swart


Academic Emergency Medicine | 2008

The Effect of Compression Duration on Hemodynamics during Mechanical High‐impulse CPR

Gary L. Swart; James R Mateer; Daniel J. DeBehnke; Stephen J. Jameson; Jeffrey L. Osborn


Academic Emergency Medicine | 1995

Standard and Higher Doses of Atropine in a Canine Model of Pulse less Electrical Activity

Daniel J. De Behnke; Gary L. Swart; David Spreng; Tom P. Aufderheide


Critical Care Medicine | 1995

EFFECTS OF ATROPINE ON RESUSCITATION FROM PULSELESS ELECTRICAL ACTIVITY

Daniel J. DeBehnke; Gary L. Swart; David Spreng; Tom P. Aufderheide

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Daniel J. DeBehnke

Medical College of Wisconsin

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Tom P. Aufderheide

Medical College of Wisconsin

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William J. Brady

University of Virginia Health System

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O John

University of North Carolina at Chapel Hill

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O. John Ma

University of North Carolina at Chapel Hill

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Daniel J. De Behnke

Medical College of Wisconsin

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Daniel W. Dobler

Medical College of Wisconsin

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