A 29-year-old man is brought to the emergency department by his friend due to retrosternal chest pain for the past hour. The patient is agitated and restless. Temperature is 38.1 C (100.6 F), blood pressure is 180/106 mm Hg in the right arm and 182/104 mm Hg in the left arm, pulse is 110/min, and respirations are 20/min. Physical examination shows bilaterally dilated pupils, normal heart and lung sounds, and a nontender abdomen. ECG shows sinus tachycardia with ST-segment depression in the precordial leads. Chest x-ray reveals no parenchymal opacities or pleural effusion and a normal mediastinum and cardiac silhouette. Cardiac enzymes are normal. Sublingual nitroglycerin and benzodiazepine therapy relieve the symptoms. Which of the following is the most likely cause of this patient's chest pain?
Cardiovascular effects of cocaine intoxication | |
Physiologic effects |
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Clinical manifestations |
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Treatment |
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This patient is agitated and restless and has dilated pupils, tachycardia, and hypertension, suggesting increased sympathetic activity from cocaine intoxication. Cocaine use commonly leads to adverse cardiovascular effects that result from inhibition of the presynaptic reuptake of norepinephrine.
Overstimulation of adrenergic receptors (eg, alpha-1, beta-1) causes an increase in heart rate, blood pressure, and myocardial contractility, leading to an increase in myocardial oxygen demand. Arterial vasoconstriction, including coronary vasoconstriction, is also enhanced (alpha-1 effect), leading to a decrease in myocardial oxygen supply. This myocardial oxygen supply-demand mismatch often causes myocardial ischemia, evidenced in this patient by retrosternal chest pain and ST-segment depression on ECG. Peripheral vasoconstriction may also impair heat loss, causing low-grade fever.
Patients with suspected cocaine-induced chest pain are frequently treated with nitroglycerin (reduces cardiac preload) and benzodiazepines (reduces sympathetic outflow to alleviate tachycardia/hypertension) in order to improve myocardial ischemia. Benzodiazepines also calm cocaine-induced psychomotor agitation, which helps further decrease myocardial oxygen demand.
(Choice A) Acute pericarditis causes sharp, pleuritic chest pain and sometimes fever and may lead to widespread ST-segment elevation (but not depression) on ECG. The chest pain typically requires anti-inflammatory medication (eg, ibuprofen) to resolve.
(Choice B) Acute aortic dissection commonly presents with abrupt-onset, tearing chest pain in the setting of hypertension, and cocaine use increases the risk. However, a widened mediastinum is expected on chest x-ray, and blood pressure asymmetry is often present in the upper extremities. In addition, the chest pain is unlikely to resolve without pain medication.
(Choice C) Coronary artery thrombosis causes myocardial infarction associated with atherosclerotic plaque rupture, which is unlikely in this relatively young patient. Cocaine use rarely causes coronary artery thrombosis; associated chest pain is usually from myocardial ischemia due to myocardial oxygen supply-demand mismatch.
(Choice E) Acute pulmonary embolism may cause pulmonary infarction, leading to pleuritic chest pain. An associated pleural effusion is usually expected on chest x-ray, and the pain is unlikely to resolve without pain medication.
Educational objective:
Cocaine intoxication causes increased sympathetic activity, which may be recognized by agitation, dilated pupils, tachycardia, and hypertension. Cocaine-induced chest pain typically results from myocardial oxygen supply-demand mismatch (ie, myocardial ischemia) in the setting of coronary artery vasoconstriction. Sublingual nitroglycerin and benzodiazepines help improve the myocardial ischemia and relieve the chest pain.