Case #10: A Case of Chest Pain
Author: Christian Marcelo, MD
Peer Reviewer: Jill Theobold, MD, PhD
A 33 year old male with no past medical history presents with chest pain that began 30 minutes prior to arrival, lasted 10 minutes, and has now completely resolved. On exam, he appears slightly agitated, diaphoretic, and his pupils are dilated. The remainder of his exam (including cardiac and pulmonary) is unremarkable. His ECG demonstrates sinus tachycardia and his cardiac enzymes are within normal limits. The paramedics state that they picked him up from a house party.
Vitals: Temp: 98.2, HR: 128, RR: 10, BP: 184/102, O2 sat: 95% on RA
What toxidrome is this patient currently displaying?
This patient presents with the classic
sympathomimetic toxidrome (diaphoresis, mydriasis, tachycardia, hypertension, and hyperthermia).
This should not be confused with the anticholinergic toxidrome (which also presents with mydriasis, tachycardia, hypertension, and hyperthermia), as the anticholinergic syndrome is associated with dry and flushed skin, rather than diaphoresis as noted in this case.
In fact, on further prompting, one of his friends mentions that he had experimented with cocaine earlier that night.
How is cocaine used? What are the onsets and durations associated with each manner?
IV: Onset is <1 min and duration is 60 min
Nasal: Onset is 5 min and duration is 120 min
Inhalation: Onset is <1 min and duration is 60 min
What is the mechanism of action of cocaine?
1. Stimulates alpha-1, alpha-2, beta-1, and beta-2 receptors. Significant effects are noted on cardiac and peripheral vasculature alpha receptors. This is why beta-blockers are relatively contraindicated.
2. Blocks sodium channels. This can cause QRS prolongation and Torsades de Pointes.
3. Increases glutamate and aspartate in the brain, causing diffuse CNS excitation.
What other signs and symptoms can be observed in cocaine toxicity?
General: Hyperthermia, Agitation
HEENT: Mydriasis, Angioedema, Inhalational burns
Cardiovascular: Tachycardia, Hypertension, Arrhythmias, MI
Pulmonary: Bronchospasm, Pneumothorax, Alveolar hemorrhage
GI: Mesenteric ischemia/infarction
Neuro: Agitation, Seizures, Coma, Headache, Focal neurologic deficits
What is the clinical utility of a urine toxicology screen that is positive for cocaine?
The urine toxicologic screen will demonstrate the presence of cocaine if used within the prior 2-3 days. However, this does not imply that cocaine is associated with the patient’s current presentation.
What is the management of these patients?
-General treatment is
symptomatic, starting with ABCs. If a patient needs to be intubated, succinylcholine should be
avoided as it shares the plasma cholinesterase enzymatic breakdown pathway, which can lead to prolonged accumulation of either or both medications.
–Benzodiazepines can be used as needed for hypertension, tachycardia, and agitation.
-If hyperthermia develops, patients should be rapidly cooled, as hyperthermia is directly correlated with mortality. Acetaminophen does not work for thermoregulation in cocaine toxicity.
-Consider Bicarbonate therapy for wide QRS complexes, as cocaine can cause Na channel blockade (similar to TCA overdose). (Note: IV Bicarbonate should be given as an IV PUSH, NOT drip).
–Avoid beta blockers due to the theoretical risk of unopposed alpha stimulation with resultant end-organ ischemia.
How does cocaine use affect the evaluation of chest pain patients?
Patients should be evaluated and treated the same as non-cocaine users. Moreover, the increased degree of atherosclerosis associated with chronic cocaine use should lower the threshold for a full cardiac evaluation.
References
Levis JT, Garmel GM. Cocaine-associated chest pain. Emerg Med Clin North Am. 2005 Nov;23(4):1083-103.
Muirhead TT, Eide MJ. Images in clinical medicine. Toxic effects of levamisole in a cocaine user. N Engl J Med. 2011 Jun 16;364(24):e52.
Pozner CN, Levine M, Zane R. The cardiovascular effects of cocaine. J Emerg Med. 2005 Aug;29(2):173-8.
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