As you pick up your supplies and equipment from your Fourth of July standby assignment, your dispatcher sends you to a young man experiencing chest pain after the fireworks display. As you approach, you see the 24-year-old man is in obvious distress, breathing heavily and perspiring profusely. It’s a warm evening, and the patient appears to have been running for the past half hour. He complains of “stabbing chest pain.” He rates the pain as 7 on a scale of 10 and says it started during the fireworks.
The patient denies allergies, any medical history and takes no medicines regularly. The patient, who is a cigarette smoker, admits to drinking “two beers” but is in an overly agitated state and has difficulty sitting still for a provider to take his vitals, which are as follows:
HR: 140 (with a wide complex tachycardia determined by a later ECG), and
The 12-lead ECG reveals ST elevation in V1, V2, and V3 with T-wave inversion. Upon further interview, the patient’s friends stated he may have snorted some cocaine about three hours ago.
Typical chest pain, associated with acute myocardial infarction, is not usually “sharp” or “stabbing.” However, this may be the presentation in cocaine-related chest pain. Additionally, whereas 12-lead ECGs are the single best clinical predictor of AMI, specific in roughly 50% of AMI, they aren’t as reliable in the evaluation of cases of cocaine-induced chest pain. Some patients experiencing cocaine-related chest pain may have early repolarization syndromes.(1) These may be normal variants in the age/ethnic cohort of the specific patient, creating the appearance of AMI in patients who aren’t suffering an acute myocardial infarction.(2,3)
The Office of National Drug Control Policy states that more than 3 million people in the U.S. are considered long-term cocaine users. According to data from the Drug Abuse Warning Network (DAWN), more than 4,000 deaths occurred in 2000 from cocaine, which affects the central nervous and cardiovascular systems.
Symptoms of cocaine’s effects on the Central Nervous System (CNS) include excited delirium, paranoia and agitation. The CNS may become toxic, and this toxicity could cause seizures along with the previously mentioned symptoms.
The cardiovascular effects may include dysrhythmias, and myocardial ischemia and infarction. In some cases, aortic dissection may occur. Frequent users will likely develop cardiac hypertrophy and atherosclerosis. The effects of cocaine on the body are the result of blockage of the reuptake of epinephrine and norepinephrine in combination with increased presynaptic release of these excitatory neurotransmitters.
The sympathomimetic effects that follow — tachycardia and hypertension — are going to increase myocardial oxygen needs.(4) At the same time, they will decrease bloodflow by inducing the constriction of the coronary vasculature and encourage the creation of new platelet aggregation.(5,6) Cocaine will also bring on early atherosclerotic disease states in patients, which is a danger from the underlying disease, but also cocaine’s effects enhance vasoconstriction in those areas of atherosclerosis.(7,8)
Field treatment for patients experiencing AMI-type chest pain is normally focused on oxygenation, aspirin, nitrates and morphine. Occasionally, some EMS systems will use beta blockers and/or prehospital fibrinolytics in those cases where the patient is field diagnosed as having an active STEMI. For more on this, read the MarchJEMSarticle Prehospital Fibrinolysis in Concert with Rapid PCI.For patients with cocaine-induced chest pain, it will be important to maintain airway control and respiratory support with oxygen and waveform capnography guiding the respiratory assessment.
Additionally, large bore IV access should be obtained in the arm or antecubital vein, as in all cardiac cases, for administration of fluids and medicines. Acquisition of a 12-lead is also important and time sensitive, because the patient who has ingested cocaine may be experiencing vasospastic episodes. This constriction caused by the cocaine will deprive the myocardium of oxygen and may create ST elevation.
Serial 12-leads done directly prior to treatment, during oxygenation and pharmacologic support, during transport, and at the emergency department (ED) may show your efforts created a better oxygenated heart and thereby reduced ST elevation. The crew with multiple 12-leads in hand will be able to better demonstrate the success of the field therapy.
From a pharmacologic standpoint, oxygen remains a mainstay in chest pain treatment, as is aspirin. Oxygen will feed the oxygen-starved heart while aspirin will help prevent further clot aggregation. Nitrates will be useful in reducing preload on the heart by creating peripheral vasodilation. Morphine may also be useful from a peripheral vasodilation perspective. Many protocols use benzodiazepines for cocaine-induced seizure activity and for sedation which in turn decreases sympathetic tone thereby reducing cardio-spasm and myocardial O2 consumption. Morphine might be contraindicated in cases where benzodiazapines have been used.
For those systems using beta blockers in the field, an increasing body of data shows beta blockage in the cocaine-induced chest pain patient may lead to unopposed alpha stimulation and exacerbate the negative effects of cocaine, particularly vasospasm. Because of this, many EDs don’t treat cocaine-induced chest pain patients with beta blockers. Additionally cocaine has been known to cause dissection, so lytics may not be appropriate.(9)
Patients that have gone to the cardiac catheterization lab with suspected cocaine induced AMI, have sometimes been found to have no coronary blockage. These patients had appeared on a 12-lead ECG to have major AMI. This syndrome many times occurs because of severe cocaine induced vasospasm. Field responders should focus on controlling the vasoconstrictive effects of cocaine on the heart and continuing to oxygenate the myocardial tissue.
1. Hollander JE, Lozano M, Fairweather P, et al: “‘Abnormal’ electrocardiograms in patients with cocaine-associated chest pain are due to ‘normal’ variants.”Journal of Emergency Medicine.12(2):199-205, 1994.
2. Amin M, Gabelman G, Karpel J, et al: “Acute myocardial infarction and chest pain syndromes after cocaine use.”The American Journal of Cardiology.66(20):1434-7, 1990.
3. Gitter MJ, Goldsmith SR, Dunbar DN, et al: “Cocaine and chest pain: clinical features and outcome of patients hospitalized to rule out myocardial infarction.”Annals of Internal Medicine.115:277-82, 1991.
4. Boehrer JD, Moliterno DJ, Willard JE, et al: “Hemodynamic effects of intranasal cocaine in humans.”Journal of the American College of Cardiology.20(1):90-3, 1992.
5. Kugelmass AD, Oda A, Monahan K, et al: “Activation of human platelets by cocaine.”Circulation.88(3):876-83, 1993.
6. Moliterno DJ, Lange RA, Gerard RD, et al: “Influence of intranasal cocaine on plasma constituents associated with endogenous thrombosis and thrombolysis.”The American Journal of Medicine.96(6):492-6, 1994.
7. Dressler FA, Malekzadeh S, Roberts WC: “Quantitative analysis of amounts of coronary arterial narrowing in cocaine addicts.”The American Journal of Cardiology.65(5):303-8, 1990.
8. Flores ED, Lange RA, Cigarroa RG, et al: “Effect of cocaine on coronary artery dimensions in atherosclerotic coronary artery disease: Enhanced vasoconstriction at sites of significant stenoses.”Journal of the American College of Cardiology.16(1):74-9, 1990.
9. Baumann BM, Perrone J, Hornig SE, et al. “Cardiac and hemodynamic assessment of patients with cocaine-associated chest pain syndromes.”Journal of Toxicology. Clinical toxicology.38(3):283-90, 2000.