PubMed Health⌕ Search

Biomedical subjects

G L Swart

Publications and source records attributed to G L Swart.

8 recordsLinked to original sources

Emergency medicine resident errors: identification and educational utilization.

OBJECTIVES: To evaluate the error management systems emergency medicine residency directors (EMRDs) use to identify and report clinical errors made by emergency medicine residents and their satisfaction with error-based teaching as an educational tool. METHODS: All 112 EMRDs listed by the Accreditation Council for Graduate Medical Education in 1996 were sent a 15-item survey. Five areas of error evaluation and management were assessed: 1) systems for tracking and reporting clinical errors; 2) resident participation in the systems; 3) resident remediation; 4) EMRD-perceived satisfaction with current error-reporting mechanisms, their educational value, and their ability to identify and prevent errors; and 5) EMRDs' perceptions of faculty and resident satisfaction with the systems. RESULTS: The response rate was 86%. All EMRDs indicated that methods are in place to track and report errors at their institutions. These include morbidity and mortality conference (94%), quality assurance case review conference (76%), and continuous quality improvement audits (60%). A majority of programs (58%) present resident cases anonymously in order to enhance teaching (39%), to avoid embarrassment (28%), and to avoid individual blame (24%). While mandated resident remediation is not required at 48% of the programs, 24% require lectures, 17% require written reports, and 6% require extra clinical shifts. The EMRDs rated the educational value of morbidity and mortality conference as outstanding (11%) or excellent (53%), and rated their systems for identifying key resident errors as outstanding (0%), excellent (14%), or good (47%). CONCLUSIONS: All emergency medicine residency programs have systems to track and report resident errors. Resident participation varies widely, as does resident remediation processes. Most EMRDs are satisfied with their systems but few EMRDs rate them as excellent in the detection or prevention of clinical errors.

Adult↗

Left ventricular aneurysm and peripheral embolism as cause of atypical foot pain.

Sudden occlusion of a peripheral artery by embolization or acute thrombosis results in acute ischemia. This is most commonly associated with sudden onset of severe pain, numbness and pallor. Chronic ischemia from peripheral vascular disease results in intermittent claudication. We present a case of peripheral embolization from a left ventricular aneurysm in a previously asymptomatic male who presented to the emergency department complaining of two weeks of pain in his left great toe. Included in the discussion are important diagnostic tests for peripheral thromboembolism and ventricular aneurysm as well as suggestions for emergency department management.

Adult↗

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↗

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↗

Standard and higher doses of atropine in a canine model of pulseless electrical activity.

OBJECTIVE: To determine whether standard or increased doses of atropine improve the return of spontaneous circulation (ROSC) rate in a canine model of pulseless electrical activity (PEA). METHODS: A prospective, controlled, blinded laboratory investigation was performed using an asphyxial canine cardiac arrest model. After the production of asphyxial PEA, 75 dogs remained in untreated PEA for 10 minutes and then were randomized to receive placebo (group 1) or one of four doses of atropine (group 2, 0.04 mg/kg; group 3, 0.1 mg/kg; group 4, 0.2 mg/kg; group 5, 0.4 mg/kg). All the animals received mechanical external CPR and epinephrine (0.02 mg/kg every 3 minutes) throughout resuscitation. RESULTS: The ROSC rates were not significantly different between the groups (group 1, 73%; group 2, 67%; group 3, 40%; group 4, 47%; group 5, 27%; p = 0.06). The heart rates and hemodynamics during resuscitation were not significantly different between the groups. CONCLUSION: In this canine model of asphyxial PEA cardiac arrest, standard-dose atropine did not improve ROSC rates, compared with placebo. Increasing doses of atropine tended to decrease ROSC rates, compared with placebo and standard-dose atropine.

Analysis of Variance↗

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

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.

Animals↗

The effect of compression duration on hemodynamics during mechanical high-impulse CPR.

OBJECTIVE: To determine whether shorter compression durations combined with fixed increased compression velocity during mechanical high-impulse CPR (HI-CPR) improve resuscitation hemodynamics, compared with mechanical standard CPR (SCPR). METHODS: A porcine model of ventricular fibrillation was used, with each animal serving as its own control. Twelve anesthetized swine (20-25 kg each) were instrumented for hemodynamic monitoring. Ventricular fibrillation was induced and followed, after 3 minutes, by mechanical SCPR (50% duty cycle) for 10 minutes. Mechanical HI-CPR was then applied, with compression durations varied randomly at 2-minute intervals for 20% (COM20), 30% (COM30), and 40% (COM40) of the CPR cycle. A 2-minute mechanical SCPR control phase completed the experiment. RESULTS: Hemodynamic measurements were significantly better for COM20 and COM30 vs SCPR, including, respectively: mean arterial pressure (MAP), 45 +/- 8 and 43 +/- 7 vs 36 +/- 7 torr; coronary perfusion pressure (CPP), 21 +/- 6 and 21 +/- 8 vs 16 +/- 6 torr; and end-tidal CO2 (ETCO2), 7 +/- 2 and 6.6 +/- 2 vs 5 +/- 1.4 torr. MAP, CPP, and ETCO2 during COM40 were not significantly different from those during SCPR, and there was no difference between COM20 and COM30 for any hemodynamic parameter. Aortic flow velocity was significantly better in COM20, COM30, and COM40 vs SCPR: 2.3 +/- 0.7, 2.1 +/- 0.9, and 1.95 +/- 0.9 vs 1.3 +/- 0.5 cm/sec, respectively. CONCLUSION: In a swine model of mechanical HI-CPR, shorter compression durations combined with fixed increased compression velocity significantly improve resuscitation hemodynamics, compared with those afforded by mechanical SCPR.

Animals↗