Sinus Arrest after - NCBI

Brief Communication

Sinus Arrest after Nimodipine Treatment for a Head Injury

Stephen D. Nash, MD Mitchell V. Patt, MD

erebral vasospasm is a potentially catastrophic consequence of severe head injury.' Calcium influx across damaged cell membranes contributes to vasospasm. Calcium antagonists block the pathological calcium influx, thus reducing traumatic vasospasm, and may limit the secondary damage caused by ischemia. The dihydropyridine class of calcium antagonists has been well studied and found to be beneficial in reducing cerebral vasospasm.2 Two animal studies published in 19793- showved that nifedipine couldl reduce cerebral artery spasm. The calcium channel blocker nimodipine has been shown to be a more potent cerebral vasodilator than nifedipine. Nimodipine, compared with a placebo, has been shown to improve survival in patients with a variety of head injuries and subarachnoid bleeding.'"2- We describe a case of nimodipine-induced sinus arrest in a patient with traumatic subarachnoid hemorrhage.

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Case Report

Key words: Calcium channel blockers; nimodipinel adverse effects; subarachnoid hemorrhage; sinus arrest

From: State University of New York (Dr. Nash), Syracuse, New York 13202, and State University of New York, Health Science CenterSyracuse, New York Heart Center (Dr. Patt), Syracuse, New York 13210 Address for reprints: Stephen D. Nash, MD, 600 East Genesee Street, Suite 204, Syracuse, NY 13202 Texas Heart InstititteJournal

A previously healthy 37-year-old man slipped on a patch of ice and struck the back of his head. He remained conscious and did not see a physician until approximately 24 hours later when a persistent headache caused him to seek medical attention. Neurologic examination was nonfocal except for the severe posterior headache. Funduscopic examination did not suggest increased intracranial pressure. The remainder of his examination, which included the cardiovascular system, yielded normal results. An initial electrocardiogram. complete blood count. and screening blood chemistry profile were normal. Computerized tomography (CT) of the head revealed subarachnoid hemorrhage, which extended from the superior aspect of the left tentorium cerebelli anteriorly to the falx with no midline shift. The patient was placed on nimodipine (60 mg orally every 4 hr) and was monitored continuously in the intensive care unit. Approximately 18 hours after receiving the 1st dose of nimodipine, he developed sinus arrest with a slow ventricular escape rhythm (Fig. 1). Atropine (0.5 m1g) was administered intravenously with prompt return to sinus rhythm (Fig. 2). The nimodipine was discontinued. Physical examination revealed no change, and a repeat CT scan was identical, showing no cerebral edema, mass effect, or shift of midline structures. The patient had 2 similar episodes of brief sinus arrest during the next 5 hours. After the 3rd episode, a temporary pacemaker was placed, but his cardiac rhythm stabilized and he remained in normal sinus rhythm without conduction disturbance for the remainder of his hospitalization. The hemorrhage slowly resolved, and the patient showed sufficient clinical improvement to be discharged from the hospital 5 days later. It should be noted that the half-life of nimodipine is 8 hours, which, in our patient, approximated the time it took for the dysrhythmia to resolve.

Discussion Sinus arrest is the abrupt loss of atrial activity, usually followeld by an escape rhythm. Normal sinus node function requires the movement of extracellular calcium into cells through slow channels; therefore, sinus node function may be inhibited by calcium channel blockers. Although sinus node depression is more Sinus Arrest after Nimodipine Treatment for Head Injury

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Acknowledgments

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The authors wish to extend special thanks to Samuel Goldhaber, MD, Dominick C. Adonato, Jr., MD, and Ms. Cathy Basic for their assistance in the preparation of this manuscript.

References 1. ~~~~~~~~~~.

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juryxvith the calciuii-i infILIx blocker nimodipine. NeLirochir_.

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Lirgia 1985;28:103-9.

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fig. 2 Recovery of sinus rhythm following

2.

atropine

admlnlstratlon.

3.

4.

verapamil and diltiazem, use of the dihydropyridine nifedipine has been ii-nplicated in a number of conduction abnormalities, including

common

with

sinus arrest.' To our knowledge, this is tl-ie Ist docuii-iented case of nimodipine-induced sinus arrest, although chance association cannot be excluded. One i-najor application of nimodipine is in the reduction of cerebral vasospasm in patients with subarachnoid hemorrhage. Sinus arrest should be recognized as a possible complication, heretofore Linrecognized in such patients. Accordingly, treatment in an intensive care unit or another setting with close monitoring capabilities is advised for patients with head injuries

who

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Kostron H. RLliiipf E, Stampfl G, Russegger L, GrLinert V. Treatment of cerebral vasospasm following severe head in-

being given nimodipine.

Sinus Arrest after Nimodipine Treatment for Head In'ury

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BNtj 1989:298:636-42. Pliilippon J, Grot) R, DegreOLi F, GLIggiari M,

Rivierez M, Viars P. Prevention of vasospasm in subaraci-inoid haemorrhage. A controlled studyxith niiiiodipine. Acta NeLirochir

1986:82:110-4. 8.

Satoh H, Hashiiiioto K. Comparative effects of a new calcium cliannel antagonist, iiiepirodipine, on rabbit spontaneously heating sino-atrial node cells. ELir j Pharii-iacol 1991;193: 9-13.

l'olunie 21, Number 2, 1994