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Dive into the research topics where John M. Schoffstall is active.

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Featured researches published by John M. Schoffstall.


Annals of Emergency Medicine | 1985

Comparison of intraosseous, central, and peripheral routes of sodium bicarbonate administration during CPR in pigs

William H. Spivey; Claire M. Lathers; Daniel R. Malone; Henry D. Unger; Sheela Bhat; Robert N McNamara; John M. Schoffstall; Nihal Turner

Obtaining venous access continues to be one of the most difficult problems faced by a physician caring for the pediatric patient in cardiac arrest. Our study examined the use of the intraosseous route (through the bone) to obtain venous access for sodium bicarbonate administration in a cardiac arrest model. Ventricular fibrillation was induced in 23 domestic swine. Cardiopulmonary resuscitation was performed for five minutes and sodium bicarbonate (1 mEq/kg) was administered through a peripheral IV line (n = 6), a central IV line (n = 5), or intraosseously (n = 6). Controls (n = 6) did not receive bicarbonate. Blood pH was sampled every two minutes for 30 minutes from the right ventricle, left ventricle, and femoral artery. An analysis of variance revealed that the central and intraosseous routes were significantly different (P less than .05) from the peripheral group, and that all three groups were significantly different (P less than .05) from the control. Pathology studies revealed only minor damage to bone when sodium bicarbonate was administered intraosseously. These data demonstrate that the intraosseous route is a rapid and effective alternative for venous access in a cardiac arrest model.


Annals of Emergency Medicine | 1993

Comparison of intermittent and continuously nebulized albuterol for treatment of asthma in an urban emergency department

Gail Rudnitsky; Robert S Eberlein; John M. Schoffstall; Janice E Mazur; William H. Spivey

STUDY OBJECTIVE To compare continuously nebulized albuterol with intermittent bolus nebulization of albuterol. DESIGN Consecutive block enrollment in groups of ten to continuous or intermittent therapy. SETTING Urban emergency department. TYPE OF PARTICIPANTS Patients who presented to the ED with moderate to severe asthma and did not improve after one treatment with nebulized albuterol. INTERVENTIONS All patients received an initial nebulized treatment with 2.5 mg albuterol followed by 125 mg solumedrol. Patients in the intermittent group received 2.5 mg nebulized albuterol at 30, 60, 90, and 120 minutes after the initial treatment. Patients in the continuous group received 10 mg albuterol nebulized in 70 mL over two hours. RESULTS There was no difference between groups in age, sex, or initial peak expiratory flow rate (PEFR). Ninety-nine patients were included in the study (47 continuous and 52 intermittent). There was no statistically significant difference in PEFRs or admission rate between groups over the two-hour study period. One subgroup analysis was performed on patients with PEFRs on presentation to the ED of 200 L/min or less. Mean +/- SD baseline PEFR at presentation to the ED was 135 +/- 35 in the 35 patients in the continuous group and 137 +/- 45 in the 34 patients in the intermittent group). At 120 minutes, PEFR was 296 +/- 98 in the continuous group and 244 +/- 81 in the intermittent group (P = .01). Admission: discharge ratios for this subgroup analysis were 11:24 in the continuous group and 19:14 in the intermittent group (P = .03). Mean +/- SD heart rate in the subgroup analysis was 102 +/- 21 at baseline for the continuous group and 109 +/- 22 at baseline in the intermittent group. At 120 minutes, heart rate was 90 +/- 18 in the continuous group and 104 +/- 16 in the intermittent group (P = .002). CONCLUSIONS Continuous nebulization offers no benefit over intermittent therapy in patients with an initial PEFR of more than 200 L/min. In PEFRs of 200 or less, continuous nebulization may decrease admission rate and improve PEFRs when compared with standard therapy.


Annals of Emergency Medicine | 1991

Comparison of two doses of endotracheal epinephrine in a cardiac arrest model

Steven G Crespo; John M. Schoffstall; Leanne R Fuhs; William H. Spivey

STUDY OBJECTIVE The objective of this study was to measure plasma catecholamine levels and the cardiovascular response before and after endotracheal administration of epinephrine in a swine cardiac arrest model. DESIGN Prospective, controlled laboratory investigation. TYPE OF PARTICIPANTS Twenty-one swine weighing 10 to 12 kg, anesthetized with ketamine and alpha-chloralose and ventilated with room air. INTERVENTIONS Ventricular fibrillation was induced with 90 V of 60 Hz current delivered to the right ventricle by transvenous pacemaker. Blood samples for epinephrine were drawn before arrest and every two minutes thereafter. At five minutes, external mechanical cardiac compressions were initiated. Nine animals received no further therapy and served as controls. Two groups of six animals received either 0.01 mg/kg or 0.1 mg/kg of epinephrine through the endotracheal tube at ten and 20 minutes. Blood samples were assayed for epinephrine. MEASUREMENTS Arterial blood pressure, lead II ECG, and plasma epinephrine. MAIN RESULTS Swine receiving epinephrine 0.01 mg/kg had an increase in epinephrine levels after drug administration, but these were not significantly different from control levels. The 0.1-mg/kg dose group had a significant increase in plasma epinephrine levels compared with controls and the 0.01-mg/kg dose group after receiving epinephrine at ten and 20 minutes. These increases were from 14 +/- 3 to 215 +/- 40 ng/mL (+/- SEM) at 12 minutes after arrest and from 151 +/- 56 to 402 +/- 80 ng/mL at 22 minutes after arrest. CONCLUSION These data suggest that standard dosing of epinephrine through the endotracheal tube during arrest does not produce significant increases in plasma catecholamines or blood pressure. Epinephrine 0.1 mg/kg produces a significant increase in plasma epinephrine levels, but it is not sufficient to produce a significant change in blood pressure.


Annals of Emergency Medicine | 1991

Effects of calcium channel blocker overdose-induced toxicity in the conscious dog

John M. Schoffstall; William H. Spivey; Linda M Gambone; Ronald Shaw; Siu P Sit

STUDY OBJECTIVE To evaluate the effects of nifedipine, diltiazem, and verapamil overdose on systemic hemodynamics and blood flows to the coronary, superior mesenteric, renal, and iliac arteries in the unanesthetized dog. DESIGN Nonblinded, controlled animal study. SETTING Research laboratory of a large pharmaceutical company. TYPE OF PARTICIPANTS Nineteen healthy mongrel dogs obtained from a commercial supplier. INTERVENTIONS Under general anesthesia, flow probes were placed about the ascending aorta, circumflex coronary, superior mesenteric, renal, and iliac arteries; a micromanometer was implanted into the tip of the left ventricle; and a catheter was inserted into the descending aorta. Experiments were performed after a recovery period of at least two weeks. MEASUREMENTS AND MAIN RESULTS Arterial blood pressure, heart rate, cardiac output, left ventricular pressure, and regional blood flows were measured prior to drug administration, and after 0.03, 0.1, 0.3, 1.0, and 3.0 mg/kg IV administration of the study drugs. Dogs receiving diltiazem or verapamil also received a dose of 10.0 mg/kg. When the blood pressure had been reduced from baseline by 30%, 1.43 mg/kg nifedipine IV (six dogs) decreased total peripheral resistance by 51%, increased cardiac output by 35%, and increased heart rate by 132%. Coronary blood flow and iliac blood flow increased 93% and 45%, respectively, but mesenteric blood flow and renal blood flow were not significantly altered. Diltiazem (eight) and verapamil (seven) at equivasodepressor doses (1.43 to 4.43 mg/kg) caused less peripheral vasodilation and reflex tachycardia. At severely toxic levels when arterial blood pressure fell by 50%, all three drugs decreased cardiac output. Nifedipine still increased heart rate. Diltiazem and verapamil caused high-grade atrioventricular block, resulting in bradycardia. All three drugs caused a redistribution of cardiac output favoring the coronary bed over the other beds. CONCLUSIONS In the conscious dog, calcium channel blocker-induced hypotension at the moderate level is associated with disparate effects on systemic hemodynamics, probably resulting from differential reflex sympathetic activation. However, at a more severe level, their toxic effects are similar and manifested predominantly by their actions on the slow calcium channel.


Resuscitation | 1990

Endogenous and exogenous plasma catecholamine levels in cardiac arrest in swine.

John M. Schoffstall; William H. Spivey; Sharon Davidheiser; Leanne R Fuhs; Richard Kirkpatrick

The use of epinephrine in cardiac arrest remains an area of continuing controversy. This study was undertaken to characterize the effect of endogenous and exogenous epinephrine on plasma epinephrine levels, and the relationship between plasma epinephrine and norepinephrine and mean arterial pressure and diastolic arterial pressure. Nineteen young swine were anesthetized with ketamine and alpha-chloralose and instrumented with arterial and central venous lines. Ventricular fibrillation was induced by pacemaker. At 5 min post arrest cardiopulmonary resuscitation (CPR) was begun with a mechanical resuscitator. Animals were randomized to receive either saline placebo (n = 9), 0.01 mg/kg epinephrine (n = 5) or 0.1 mg/kg epinephrine (n = 5) via the central venous line. Plasma was drawn for high pressure liquid chromatographic analysis of catecholamines every 2 min. The resuscitation was carried on for 30 min after the arrest. Plasma epinephrine levels differed significantly between treated subjects and controls, as did mean arterial pressure and diastolic arterial pressure. There was a correlation between both mean arterial pressure and diastolic arterial pressure with plasma epinephrine and log epinephrine, but no correlation with plasma norepinephrine. The two doses of epinephrine did not differ in the degree to which they elevated the mean arterial pressure and diastolic pressure. We conclude that the endogenous catecholamine response to cardiac arrest while producing norepinephrine and epinephrine levels many times greater than those in the resting animal, is not sufficient to maintain blood pressure. There is a strong correlation between blood pressure and the log of the plasma epinephrine concentration, but epinephrine concentration alone does not solely account for changes in blood pressure during arrest.


Annals of Emergency Medicine | 1992

Plasma catecholamine levels after intraosseous epinephrine administration in a cardiac arrest model

William H. Spivey; Steven G Crespo; Leanne R Fuhs; John M. Schoffstall

STUDY OBJECTIVE To measure plasma catecholamine levels and the cardiovascular response after administering epinephrine by the intraosseous (IO) route in an animal cardiac arrest model. MODEL Eighteen anesthetized swine (weight, 12 to 15 kg) subjected to five minutes of electrically induced ventricular fibrillation followed by 25 minutes of chest compression and ventilation. INTERVENTIONS Animals were anesthetized with 30 mg/kg IM ketamine and 75 mg/kg IV a-chloralose, intubated, placed on a respirator, and surgically instrumented. Ventricular fibrillation was induced. After five minutes of cardiac arrest, mechanical chest compressions were initiated and continued until the end of the experiment. Animals received 0.01 mg/kg IO epinephrine (five) or 0.1 mg/kg IO epinephrine (five) at ten and 20 minutes. The eight controls did not receive epinephrine. MEASUREMENTS AND MAIN RESULTS Plasma epinephrine levels increased from 1.0 to approximately 40 to 85 ng/mL with the initiation of CPR. Epinephrine (0.01 mg/kg) increased plasma epinephrine levels to 222 +/- 72 ng/mL at 12 minutes after arrest but did not increase diastolic or mean blood pressure. Epinephrine (0.1 mg/kg) increased plasma epinephrine levels to 1,103 +/- 157 ng/mL at 12 minutes after arrest and increased diastolic and mean arterial blood pressures. CONCLUSION IO epinephrine is rapidly transported to the central circulation but requires larger than currently recommended doses to produce a significant change in blood pressure.


Resuscitation | 1989

Plasma catecholamines, pH, and blood pressure during cardiac arrest in pigs.

Claire M. Lathers; N. Tumer; John M. Schoffstall

This study examined plasma epinephrine (E) and norepinephrine (NE) concentrations, pH, and mean arterial blood pressure (MAP) in a cardiac arrest model. Twenty-three domestic swine (15-26 kg) were anesthetized with ketamine 20 mg/kg, i.m. and alpha-chloralose 25 mg/kg, i.v. and ventilated with a respirator. Catheters were placed in the right ventricle, left ventricle and femoral arteries for MAP recordings and blood pH sampling every 2 min. Catecholamine samples were taken from the femoral artery every 2 min. Cardiac arrest was induced by endocardial stimulation with a Grass S88 stimulator. Five minute post arrest resuscitation was initiated with a mechanical resuscitator. Ten minute post arrest NaHCO3 1 mEq/kg was administered by the peripheral i.v. (P; n = 6), central (CE; n = 5), or intraosseous, via the tibia, (I; n = 6), route. Controls (C; n = 6) did not receive NaHCO3. MAP (mean +/- S.D.) prior to arrest was: C 144 +/- 16, P 139 +/- 11, CE 137 +/- 13 and I 133 +/- 11 mmHg. Five and 25 min post arrest it was: C 21 +/- 5 and 17 +/- 6, P 34 +/- 8 and 23 +/- 7, CE 17 +/- 7 and 14 +/- 10 and I 26 +/- 6 and 11 +/- 3 mmHg, respectively. A 2-way analysis of variance did not reveal any difference in MAP values in the four groups. In all groups the blood pH from the femoral artery demonstrated a respiratory alkalosis that peaked at approximately 7.48 5 min after initiation of mechanical resuscitation. In the groups receiving NaHCO3, it peaked at 7.77 +/- 0.09 CE and 7.65 +/- 0.06 P 2 min post infusion and at 7.71 +/- 0.06 I 8 min post infusion. An analysis of variance revealed that the CE and I routes were significantly different (P less than 0.05) from the P group and that all three groups were different (P less than 0.05) from the C. Plasma E and NE concentrations at 0, 6, 10, 12, 20 and 30 min post arrest in the C group were, respectively: 3 and 10, 94 and 327, 119 and 329, 92 and 234, 33 and 135, and 127 and 62 ng/ml, respectively. All 3 groups receiving NaHCO3 demonstrated similar patterns and were not significantly different from C when compared with a 2-way analysis of variance.(ABSTRACT TRUNCATED AT 400 WORDS)


Journal of Emergency Medicine | 1999

Thyrotoxic periodic paralysis in a Jamaican male

William Walters; Sang Woo Han; John M. Schoffstall

Thyrotoxic periodic paralysis is a rare endocrine disorder most prevalent among individuals of Asian descent that presents as proximal muscle weakness, hypokalemia, and signs of hyperthyroidism. We present the case report of a patient with previously undiagnosed hyperthyroidism, protracted muscle weakness with transient exacerbations, and nocturnal onset of periodic paralysis affecting the upper and lower limbs.


Pediatric Emergency Care | 1993

Inefficacy of intraperitoneal fluid administration in a shock model.

Robert M. McNamara; John M. Schoffstall; Ron S. Fuerst

Intraperitoneal (IP) fluid administration has been previously used to treat dehydrated children. The relative ease and reported safety of this route suggests its potential utility for volume resuscitation in the acutely ill child. Previous research regarding IP fluid infusion has not examined its use in shock states. This experiment sought to examine the efficacy of an IP fluid infusion in a shock model. Ten immature swine were randomized to receive either no treatment (n=5) or 30 ml/ kg of warmed lactated Ringers solution (n=5) IP 20 minutes after a graded 40% hemorrhage. Mean arterial pressure (MAP), heart rate (HR), hematocrit (Hct), pH, and Pco2 were determined serially, and the experiment concluded 60 minutes after intervention. A mean of 89.5% of the administered fluid load was recovered from the peritoneal cavity, and the IP infusion had no ameliorative effect on MAP or HR. The lack of clinically significant absorption of an administered isotonic intraperitoneal fluid infusion in this model suggests that this route should not


Annals of Emergency Medicine | 1991

Serum glucose after intraperitoneal infusion of 5% dextrose solution.

Robert M. McNamara; John M. Schoffstall; Ronnie S Fuerst

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.

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