Case Reports

Asystole Following Nitroglycerin: A Review of Two Cases

Case reports of a 54-year-old man with angina and a 69-year-old woman demonstrate an underreported, self-limiting side effect associated with nitroglycerin.

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Nitroglycerin (NTG), or glyceryl trinitrate, was first introduced into the medical community by Murrell,1,2 who reported on anecdotal observations of its antianginal properties by workers within manufacturing plants refining the product for its explosive properties. While the route of administration of NTG has changed from this incidental environmental exposure to the now formulated therapies available, its benefit as an outpatient, abortive treatment for stable angina has been validated beyond early subjective observations in the literature.1-3 In fact, its successful use over the years for angina has produced an expansive pharmacopeia, including its use for undifferentiated chest pain and exacerbation of congestive heart failure.3-5

Despite the extensive history of NTG as a proven vasodilator, emerging uses continue to be explored in equal measure with technological advances.2,6 Though morbidity and mortality reductions are dependent on its use within clinical practice, NTG is not an innocuous drug.5 Most of the reported side effects associated with NTG are well established and include hypotension, tachycardia, flushing, nausea, vomiting, and headache.3,6,7 An often forgotten side effect associated with NTG use is asystole. We present the following two cases to highlight both common uses of NTG as well as this underreported side effect.

Case 1: Nitroglycerin for Stable Anginal Chest Pain

A 54-year-old man with a history of hypertension (HTN), hyperlipidemia (HLP), and gastroesophageal reflux disease (GERD) presented to the ED for evaluation of a 3-hour history of intermittent, retrosternal, left-sided, nonradiating chest “pressure and tightness.” The patient stated that the chest discomfort began at rest but was exacerbated by exertion with episodes lasting 10 to 15 minutes. The patient rated the peak pain associated with these episodes as a “7” on a pain scale of 1 to 10. He further noted that his symptoms abated and he became “pain-free” when at rest.

The patient’s vital signs at presentation were: blood pressure (BP), 156/87 mm Hg; heart rate (HR), 68 beats/min; respiratory rate (RR), 18 beats/min; and temperature (T), 98.4°F. Oxygen saturation was 96% on room air.

The patient, who performed regular BP checks at home, noted that his recent BP readings had been very high. A review of the patient’s systems was positive for shortness of breath and diaphoresis; symptoms were otherwise negative, including any prior episodes. His social history was noncontributory and negative for tobacco, alcohol, or drug use. The patient did report that he had taken an uneventful 6-hour car ride the previous week.

On physical examination, the patient was nontoxic and resting comfortably, without signs of acute distress or pain. Cardiac and pulmonary examinations were normal, and radial pulses were 2+ and symmetric. The abdominal examination was benign and the neurological examination was nonfocal. There was no evidence of peripheral edema or asymmetry of the calves, which were nontender to palpation.

Figure 1.

The initial electrocardiogram (ECG) (Figure 1) showed a normal sinus rhythm of 65 beats/min, left axis deviation, and normal intervals; there was no acute ST-segment elevation or depression.

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