Biomedical subjects

R S Fuerst

Publications and source records attributed to R S Fuerst.

8 recordsLinked to original sources

PubMed1995

Automatic mechanical device to standardize active compression-decompression CPR.

STUDY OBJECTIVE: To develop an automatic mechanical device capable of performing active compression-decompression (ACD) CPR in laboratory animals. DESIGN: A swine model was used to study standard and ACD CPR. One-minute periods of standard mechanical chest compressions were alternated with mechanical ACD CPR. SETTING: University hospital laboratory. INTERVENTIONS: A commercially available device that provided standard chest compressions only was modified to deliver ACD CPR. RESULTS: The absolute difference in intrapleural pressure and tidal volume almost doubled during ACD CPR compared with that with standard CPR. CONCLUSION: The presence of a greater negative change in intrapleural pressure confirmed that active decompression of the chest had occurred and that the device was capable of performing ACD CPR. The device provides consistent rate, depth, force, and duty cycle.

Animals↗

PubMed1994

Ventilation caused by external chest compression is unable to sustain effective gas exchange during CPR: a comparison with mechanical ventilation.

OBJECTIVE: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. DESIGN: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. INTERVENTIONS: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. RESULTS: During the first minute of chest compression, mean (+/- S.D.) minute ventilation was 11.2 +/- 5.9 l/min in the mechanically ventilated group and 4.5 +/- 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 +/- 1.4 l/min and 1.7 +/- 1.6 l/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 +/- 0.13 compared with 7.30 +/- 0.07 units) and PCO2 was higher (62 +/- 19 compared with 35 +/- 9 mmHg). Mixed venous PCO2 was also higher (76 +/- 15 compared with 61 +/- 8 mmHg). CONCLUSION: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.

Acid-Base Equilibrium↗

PubMed1994

Lack of uniform definitions and reporting in laboratory models of cardiac arrest: a review of the literature and a proposal for guidelines.

BACKGROUND: Researchers are interested in improved uniformity of definitions and standards of reporting data for human CPR studies, and international guidelines (Utstein style) have been developed. However, no guidelines exist for animal CPR investigations. OBJECTIVE: To assess published animal CPR studies for adequacy of reporting and uniformity of methods and definitions regarding such important factors as the interval from the onset of ventricular fibrillation to the start of CPR (the nonintervention interval), ventilation, chest compression, coronary perfusion pressure, and return of spontaneous circulation. DESIGN: A blinded review of the methodology described in 42 articles concerned with animal CPR research published during the last ten years. An article had to report cardiac arrest and CPR as part of the protocol and return of spontaneous circulation as one of the outcome variables in order to be included in this study. We excluded abstracts, nonresuscitation models, and human CPR studies. MEASUREMENTS AND MAIN RESULTS: There was wide variation in the experimental methods reported in the studies. The nonintervention interval ranged from 0 to 15 minutes. The majority of studies initiated CPR within three minutes after the onset of ventricular fibrillation. Twenty-two percent of studies reported tidal volume, and 18% reported minute ventilation. Of the 14 studies that used blood pressure or coronary perfusion pressure as a target for titration of chest compression force, 12 used different target blood pressure values. We found 29 different definitions of return of spontaneous circulation. The duration of return of spontaneous circulation ranged from 30 seconds to 60 minutes; however, 52% of studies did not report a duration. CONCLUSION: Important differences exist in animal CPR research methodology among laboratories. Failure to define or report minute ventilation, coronary perfusion pressure, and return of spontaneous circulation made it difficult to compare studies. In order to make valid comparisons of studies, blood flow and ventilation should be measured and controlled when they are not experimental variables. Uniform definitions and guidelines for reporting should be developed for laboratory CPR research.

Animals↗

PubMed1994

Pediatric analgesia and sedation.

Sedation and analgesia are essential components of the ED management of pediatric patients. Used appropriately, there are a number of medications and techniques that can be used safely in the emergency care of infants and children. Emergency physicians should be competent in the use of multiple sedatives and analgesics. Adequate equipment and monitoring, staff training, discharge instructions and continuous quality management should be an integral part of the ED use of these agents.

Analgesia↗

PubMed1994

Effect of ventilation on resuscitation in an animal model of cardiac arrest.

BACKGROUND: The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. METHODS AND RESULTS: Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of > 80 mm Hg for > 5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P < .05) lower mean arterial PO2 (38 +/- 17 mm Hg compared with 216 +/- 104 mm Hg) and higher PCO2 (62 +/- 16 mm Hg compared with 35 +/- 8 mm Hg), lower mixed venous PO2 (15 +/- 7 mm Hg compared with 60 +/- 7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P < .002). CONCLUSIONS: In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.

Animals↗

PubMed1994

The composition of gas given by mouth-to-mouth ventilation during CPR.

STUDY OBJECTIVE: To compare the concentration of a rescuer's exhaled O2 and CO2 during mouth-to-mouth ventilation with or without chest compression. DESIGN: Prospective repeated measures study. Simulated one- and two-rescuer cardiopulmonary resuscitation (CPR) was performed as recommended by the American Heart Association. SETTING: University laboratory. PARTICIPANTS: Fifty-five healthcare professionals certified in basic and advanced cardiac life support volunteered as rescuers in this study. MEASUREMENTS AND RESULTS: Thirty-three volunteers performed one-rescuer CPR, and 22 volunteers performed two-rescuer CPR. Minute ventilation for both groups increased 50% to 130% during CPR (p < 0.05). During the performance of CPR, the concentration of exhaled O2 increased from 16.4 +/- 0.7% to 16.9 +/- 0.5% in the one-rescuer CPR group and from 16.5 +/- 0.9% to 17.8 +/- 0.6% in the two-rescuer CPR group (p < 0.05). The concentration of exhaled CO2 in the one-rescuer CPR group did not change significantly throughout the entire experiment, but decreased in the two-rescuer CPR group from a baseline measurement of 4.0 +/- 0.6% to 3.5 +/- 0.4% (p < 0.05). During CPR, the concentration of exhaled CO2 was 4.0 +/- 0.4% in the one-rescuer CPR group compared with 3.5 +/- 0.4% in the two-rescuer CPR group (p < 0.05). CONCLUSIONS: The gas given by mouth-to-mouth ventilation is a hypercarbic and hypoxic mixture compared with room air. Mouth-to-mouth ventilation is the only circumstance in which a hypercarbic and hypoxic gas is given as therapy. Further laboratory and clinical studies are necessary to determine the effect of mouth-to-mouth ventilation during CPR.

Carbon Dioxide↗

PubMed1991

Serum glucose after intraperitoneal infusion of 5% dextrose solution.

STUDY OBJECTIVE: This study investigated the use of intraperitoneal (IP) glucose infusion as a therapy for hypoglycemia. DESIGN: Randomized, placebo-controlled, crossover design, with each animal serving as its own control. SETTING: Laboratory investigation. TYPE OF PARTICIPANTS: Seven female New Zealand White rabbits with a mean weight of 3.7 kg. INTERVENTIONS: Each animal was subjected to three experiments separated by a four-day period. After baseline measurements, the following interventions were undertaken: Control day, no treatment; placebo day, 10 mL/kg 0.9% normal saline solution IP; and treatment day, 10 mL/kg 5% dextrose solution IP. MEASUREMENTS AND MAIN RESULTS: Serial serum glucose levels were obtained. Compared with control and placebo, the mean absolute serum glucose value of the treatment group was significantly higher beginning at ten minutes after intervention and continuing until conclusion of the study at 30 minutes. For these time points, the mean increase in serum glucose levels (percent change) of the treatment group compared with the control group was as follows: ten minutes, 15.5 mg/dL (0.86 mmol/L) (11%), P less than .01; 15 minutes, 20.6 mg/dL (1.14 mmol/L) (14%), P less than .01; 20 minutes, 36.5 mg/dL (2.03 mmol/L) (26%), P less than .001; and 30 minutes, 34.7 mg/dL (1.93 mmol/L) (24%), P less than .001. CONCLUSION: Glucose instilled into the peritoneal cavity of rabbits is absorbed rapidly into the systemic circulation.

Absorption↗

PubMed1987

The role of aspartic and cysteine proteinases in albumin degradation by rat kidney cortical lysosomes.

We have investigated the degradation of 125I-labeled bovine serum albumin by lysates of rat kidney cortical lysosomes. Maximal degradation of albumin occurred at pH 3.5-4.2, with approximately 70% of the maximal rate occurring at pH 5.0. Degradation was proportional to lysosomal protein concentration (range 100-600 micrograms) and time of incubation (1-5 h). Dithioerythritol (2 mM) stimulated albumin degradation 5- to 10-fold. Albumin degradation was not inhibited by phenylmethanesulfonyl fluoride (1 mM) or EDTA (5 mM), indicating that neither serine nor metalloproteinases are involved to a significant extent. Pepstatin (5 micrograms/ml), an inhibitor of aspartic proteinases, inhibited albumin degradation by approximately 50%. Leupeptin (10 microM) and N-ethylmaleimide (10 mM), inhibitors of cysteine proteinases, decreased albumin degradation by 34 and 65%, respectively. Combinations of aspartic and cysteine proteinase inhibitors produced nearly complete inhibition of albumin degradation. Taken together, these data indicate that aspartic and cysteine proteinases are primarily responsible for albumin degradation by renal cortical lysosomes under these conditions. In keeping with the above data, we have measured high activities of the cysteine proteinases, cathepsins B, H, and L, in cortical tubules, the major site of renal protein degradation. Using the peptidyl 7-amino-4-methylcoumarin (NHMec) substrates (Z-Arg-Arg-NHMec, for cathepsin B; Arg-NHMec for cathepsin H; and Z-Phe-Phe-CHN2-inhibitable hydrolysis of Z-Phe-Arg-NHMec corrected for inhibition of cathepsin B activity for cathepsin L) values obtained were (means +/- SE, mU/mg protein, 1 mU = production of 1 nM product/min, n = 6): cathepsin B, 2.1 +/- 0.34; cathepsin H, 1.35 +/- 0.19; cathepsin L, 14.49 +/- 1.26. In comparison, the activities of cathepsins B, H, and L in liver were: 0.56 +/- 0.03, 0.28 +/- 0.04, and 1.27 +/- 0.16, respectively.

Animals↗