Effect of verapamil on acute anaphylactic shock in Guinea pigs

Effect of verapamil on acute anaphylactic shock in Guinea pigs

and intubation delay of 5 m i n u t e s or longer (6). Inadequate docum e n t a t i o n of neurologic examination prior to blockade was noted in 6 of ...

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and intubation delay of 5 m i n u t e s or longer (6). Inadequate docum e n t a t i o n of neurologic examination prior to blockade was noted in 6 of 25 succinylcholine and 9 of 94 p a n c u r o n i u m cases. Failure to sedate patients who might be aware of paralysis occurred in 3 of 25 succinylcholine and 8 of 94 p a n c u r o n i u m uses. Neuromuscular blocking agents facilitate expeditious m a n a g e m e n t of selected critical patients in the ED. Their prudent use requires anticipation of potential complications, preparation for surgical airway should intubation fail, documentation of physical examination before paralysis and prior sedation w h e n patient responds to pain.

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Effect of Verapamil on Acute Anaphylactic Shock in Guinea Pigs

WA Jacobs, MC Gunderson, SP Holt, BC White, JN Love / Department of Emergency Medicine, Butterworth Hospital, Grand Rapids, Michigan; Section of Emergency Medicine, College of Human Medicine, Michigan State University, East Lansing It is well k n o w n t h a t calcium ion influx across the plasma m e m b r a n e is a necessary step in mast cell degranulation. Mast cells will not degranulate in vitro in the absence of calcium. This has led to a proposed role for calcium channel blockers, such as verapamil, in the t r e a t m e n t of acute anaphylaxis. The effect of verapamil on anaphylaxis was studied in 16 albino guinea pigs. The animals were sensitized to ovalbumin (OA), later challenged with an IV injection of OA to induce anaphylaxis, and were observed for 1 hour. The guinea pigs were divided into 4 groups of 4 each w i t h Group 1 being a control group and receiving no treatment. Group 2 received 0.2 cc of 1:2,000 epinephrine IV 2 minutes after the OA injection. Group 3 received 5 m g / k g of ver a p a m i l i n t r a p e r i t o n e a l l y 20 m i n u t e s prior to OA injection. Group 4 received 1 mg/kg of verapamil IV 2 m i n u t e s after OA injection. The m e a n times of death, in seconds, after OA injection for the different groups were as follows: Group 1, 557 _+ 141; Group 2, 3098 + 1005~ Group 3, 429 + 37; and Group IV, 713 -+ 486. T h e data were a n a l y z e d by t h e Kruskal-Wallis one-way ANOVA. The use of epinephrine significantly improved survival time in anaphylaxis (P < .02). There was no significant protective effect of verapamil on anaphylaxis in guinea pigs at the doses used in this study (P > .05).

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Hemodynamic Effects of Naloxone in Anaphylactic Shock

WG Barsan, JR Hedges, S Syverud / Department of Emergency Medicine, University of Cincinnati Medical Center, Cincinnati Recent reports suggest that endorphins may contribute to hemodynamic depression in septic and hemorrhagic shock. There is also evidence that reversal of endorphin effects w i t h high-dose naloxone may improve h e m o d y n a m i c function and improve survival in shock states. The purpose of this study was to examine the effects of naloxone on h e m o d y n a m i c parameters and survival in anaphylactic shock. A rabbit model of anaphylactic shock was used. Briefly, anaphylactic shock was induced in sensitized rabbits with horse serum. Three m i n u t e s after the onset of shock, rabbits were treated w i t h a 3 mg/kg bolus of naloxone followed by a 3 mg/kg/hr infusion (group 1, n=8), or by injection with an equal v o l u m e of saline (group 2, n = 7). Cardiac output, blood pressure, heart rate, and body temperature were monitored continuously for 60 minutes, and the experiment was terminated. Survival in group 1 and group 2 was not significantly different. There was a significant increase in cardiac index in group 1 animals at 10 m i n u t e s (P < .001) and 15 m i n u t e s (P < .01). Stroke volume index was also higher at 10 m i n u t e s and 15 m i n u t e s (P < .05). Although m e a n blood pressure was higher in group 1 animals at all time intervals after naloxone was begun, the difference was statistically significant only at 60 m i n u t e s (P < .05). Peripheral vascular r e s i s t a n c e was n o t s i g n i f i c a n t l y different. A l t h o u g h

14:5 May 1985

naloxone t r e a t m e n t does appear to improve h e m o d y n a m i c function in anaphylactic shock, there is no apparent beneficial effect on survival in this model.

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Central and Peripheral Catheter Flow Rates in "Pediatric" Dogs

D Hedge, G Fleisher, C Delgado-Paredes / Emergency Department, The Children's Hospital of Philadelphia, Philadelphia Several authors have reported flow rates for various catheters in vitro, but these studies may not reflect differences in vivo because of venous pressure, valves, and/or venous tortuosity, particularly in the small vessels of the child. We studied flow rates of 4 small-gauge catheters in a "pediatric" dog model to determine the following: 1) whether there is a difference between in vitro and in vivo flow rates; 2) w h e t h e r there is a difference between flow rates of the same catheters placed in central or peripheral veins in the n o r m o t e n s i v e patient; and 3) w h e t h e r h y p o t e n s i o n affects flow through the same catheter placed in a central vs a peripheral vein. Catheters were inserted into an ear vein (peripheral) and the femoral vein (central); infusions were measured in triplicate over a 60-second interval. We found significant differences between in vivo and in vitro flow rates for 2 of the larger (20-gauge) catheters. These differences were greatest w h e n fluid was delivered under 300 m m Hg of pressure. There was a significant difference in flow rates for one of the catheters designed for central vein use w h e n delivered through 300 m m Hg pressure (P < .05). There were, however, no significant differences between the flow rates of the same catheters placed either in the central or peripheral vein w h e n delivered by use of gravity. In hypotensive dogs there were no significant differences in flow for the same catheter in central vs peripheral veins with gravity (4 cc/min), but under 300 m m Hg pressure the difference increased significantly (17 cc/min, P < .05). Our data indicate that the results of in vitro studies cannot be e x t r a p o l a t e d directly to predict achievable flow rates in clinical practice. In particular, a small-diameter catheter in the central circulation may allow delivery of fluid under pressure at a faster rate than a catheter of larger diameter in a peripheral vein. Thus decisions as to site, type, and size of catheter for fluid resuscitation should be based on data obtained in vivo.

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Efficacy of Current Recommendations for Bicarbonate Therapy in a Pediatric Animal Model for CPR

G Caputo, G Fleisher, C Delgado-Paredes/Emergency Department, The Chlidren's Hospital of Philadelphia, Philiadelphia This study assessed the adequacy of the recommended dose of bicarbonate (2 mEq/kg initially, then 1 mEq/kg every 10 min) for CPR in children in an animal model for pediatric CPR using 6-12 wk old, 3-10 kg dogs. Animals were anesthetized with fentanyl/ droperidol, paralyzed with pancuronium, intubated orotracheally, and ventilated. Femoral venous and arterial catheters were inserted, and p e n t o b a r b i t a l 10 m g / k g was given for m a i n t e n a n c e of a n e s t h e s i a . S t a n d a r d m o n i t o r i n g was p e r f o r m e d . A f t e r pH, PaCO2, and PaO2 stabilized in the physiologic range, the endotracheal tube was occluded, leading to cardiac arrest. Five m i n after cardiac arrest, CPR was b e g u n w i t h a m e c h a n i c a l resuscitator at a rate of 80/min, and supplemental oxygen was delivered by a volume ventilator at a rate of 20/min. All animals received a bolus of epinephrine initially, followed by an infusion of 1 ~g/kg/min. They were assigned consecutively to receive no NaHCO 3 (Grp 0) or a dose of 2 mEq/kg (Grp 2), half being repeated after 10 and 20 min. ABGs and lactate levels were obtained at the time of cardiac arrest (-5), ! m i n prior to resuscitation (-1), and 3, 6, 9, 12, 15, 20, 25, 30, 35, and 40 m i n after the start of CPR. Grp 0 and Grp 2 did not differ significantly in terms of weight (6.19 vs 5.37 kg); mean blood pressure prior to arrest (88 vs 76 m m Hg); onset of arrest after anoxia (252 vs 248 see); or blood pressure achieved during CPR (20 vs 17 m m Hg). There was no

Annals of Emergency Medicine

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