CASE REPORT epicardial pacing, blunt trauma
Successful Epicardial Pacing in Blunt Trauma Resuscitation Epicardial pacing wires were used successfully in the resuscitation of a moribund victim of blunt trauma after fluid resuscitation and chemical measures had failed. Application of these wires to treat the bradycardia of shock should be considered in selected patients when standard measures fail. [Lick S, Rappaport WD, Mclntyre KE: Successful epicardial pacing in blunt trauma resuscitation. Ann Emerg Med August 1991;20:908-909.] INTRODUCTION Bradycardia during hypovolemic shock is a well-documented but underappreciated phenomenon. ~ Millikan et al reported the successful use of temporary epicardial pacing wires in the resuscitation of two victims of penetrating trauma. 2 We present what appears to be the first reported case of the successful use of these wires in a blunt trauma victim.
CASE REPORT A 44-year-old man was involved in a head-on automobile accident and intubated in the field. On transport, his heart rate temporarily dropped from 120 to 50. He arrived in the emergency department with a palpable blood pressure of 60 mm Hg and pulse of 100. Diagnostic peritoneal lavage was negative. The patient remained hypotensive despite wide-open IV fluid; he became bradycardic, with his heart rate dropping below 20, refractory to atropine. Emergency thoracotomy disclosed a distended pericardium, which was opened, releasing fresh clot and relieving the tamponade. Cardiac arrest followed immediately. With intracardiac epinephrine and cardiac massage, electrical activity of the heart as well as palpable femoral pulses returned. The patient was taken immediately to the operating room; however, bradycardia and hypotension again supervened. Epicardial pacing wires were placed on the left ventricle, and a temporary pacemaker generator set at 20 mA captured the ventricle wall at a rate of 100. Blood pressure returned to normal. Further exploration revealed a 1-cm tear in the left atrium, which was repaired. The patient resumed sinus rhythm at a rate of 110, and he needed no further pacing during his hospital stay. Postoperatively, the patient had a prolonged ICU course and was discharged on postoperative day 30, by which time he had recovered neurologic function to the level of following simple commands. At six months, he was able to care for himself at home with assistance.
Scott Lick, MD William D Rappaport, MD Kenneth E Mclntyre, MD Tucson, Arizona From the Department of Surgery, University of Arizona Medical Center, Tucson. Received for publication December 11, 1990. Revision received March 26, 1991. Accepted for publication April 12, 1991. Address for reprints: William D Rappaport, MD, Department of Surgery, University of Arizona Medical Center, 1501 North Campbell Avenue, Tucson, Arizona 85724.
DISCUSSION Bradycardia associated with decompensated shock is well reported in both animals and human beings.~ Although the initial response to shock is tachycardia, once hypotension occurs a slowing of the heart soon follows. Two mechanisms have been postulated to explain this phenomena. The first is that of a protective vagal reflex. Mazor and Rogel noted that the bradycardia induced by hypovolemic shock was accompanied by an increase in stroke volume and stroke work, resulting in increased perfusion compared with the tachycardic state, a In addition, Gauer and Henry showed that when a heart beats vigorously in a hypovolemic state, subendocardial hemorrhage and inefficient pump filling occur. 4 This bradycardic response could be a protective mechanism, presumably through ventricu-
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Annals of Emergency Medicine
EPICARDIAL PACING Lick, Rappaport & Mclntyre
lar afferents and vagal efferents, to allow for more efficient heart function and to prevent endocardial damage. Animal experiments show that intrap e r i c a r d i a l i n j e c t i o n of n i c o t i n e (stimulating receptors) resulted in bradycardia in a hemorrhagic shock model. 5 Cutting of the vagi inhibited this response. The other mechanism proposed is that of metabolic depression of the pacemakers and conduction system. Studies of h y p o v o l e m i c shock in dogs show a biphasic bradycardic response. 6 A pacemaker shift occurs from the sinoarterial node to a lower area in the atrium, resulting in a mild bradycardia. This slowing is blunted but not eliminated by vagotomy. The mechanism is presumed to be one of ischernia to the sinoatrial node. Later, a second, more profound bradycardia develops, leading to heart block and terminal ventricular arrhythmias. This is not affected by vagotomy, but is probably due to the Purkinje fibers being more sensitive to anoxia and hyperkalemia than the atrial conduction system. 7,s Thus, low cardiac-output shock begins as a compensated state consisting of mild tachycardia, increased vascular resistance, and normoten-
sion. It progresses to a decompensated state, comprising hypotension, bradycardia, and decreased vascular r e s i s t a n c e . This d e c r e a s e in resistance is proposed to be due to increased vascular endothelial tension, causing the release of prostaglandin E¢, which inhibits the release of norepinephrine at the presynaptic level. 9 Anoxia and hyperkalemia then contribute to the suppression of the conducting system of the ventricle. Both mechanisms may have contributed to the refractory bradycardia seen in our patient. Millikan et al reported the successful use of epicardial pacing in two cases of penetrating chest trauma. 2 Both cases i n v o l v e d p e n e t r a t i n g chest injuries with one case of cardiac tamponade. In both patients, severe bradycardia u n r e s p o n s i v e to fluids and attempts at chemical conversion occurred. Epicardial pacing wires were successful in returning the heart rate to normal, and both patients were eventually discharged neurologically intact.
SUMMARY Epicardial pacing wires and external pacemakers are readily available at trauma centers, EDs, and operating
Annals of Emergency Medicine
rooms. In selected patients they appear to be effective in breaking the h y p o p e r f u s i o n - b r a d y c a r d i a cycle. Their use should be considered in cases of trauma-associated bradycardia when volume and chemical measures have failed.
REFERENCES 1. Secher NH, Bie P: Bradycardia during reversible hemorrhagic shoek-A forgotten observation? C]in Physiol 1985;5:315-32;B 2. Millikan JS, Moore EE, Dunn EL, et al: Temporary cardiac pacing in traumatic arrest victims. Allll Enlerg Med 1980;9:591 593 3. Mazor A, Rogel S: Cardiac aspects of shock: Effects of an iscbcmic body on a non ischemic heart. Anti Sure 1972; 178:128. 4. Gaucr OH, Henry IP: Negative ( Gz) acceleration in relation tl) arterial oxygen saturation, subendocardia] hemorrhage and venous pressure in the forehead. Aerospacc Med 1964;35:533 545. 5. Oberg B, Thoren P: Increased activity in vagal cardiac affercnts correlated to the appearance of reflux bradycardia during severe hemorrhage in cats. Act~I Physio] Scan 1970;80:22a-23a. 6. Knstreva DR, Castancr A, Pedcrsen DH, et al: Nonvagally mediated bradycardia during cardiac tamponade or severe hemorrhage Cordio]o,gy 1981;68:65-79. 7. Vassallc M: On the mechanisms underlying cardiac seandstill: Factors determining the success or failure of escape pacemakers in the heart I A m (21dl Cardio] 1985;5:35b-42b. 8. Vassalle M, Greenspan K, Iomain S, et al: Effect of potassium on automaticity and conduction of canine hearts. Am / Phy.~io] 1964;207:334-340 9. Bond RF: A review of the skin and muscle hemodynamics during hemorrhagic hypntension and shock Adv Sh(l~k Res 1982;8:53 71).
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