Cocaine is a potent stimulant that can create a sense of intense excitement, enhance mental alertness, and produce hyperactivity, all while reducing the desire to eat or rest. Cocaine toxicity is one of the leading causes of drug-related death recorded by medical examiners in the United States.1 The cardiovascular complications the drug produces have been linked to death in younger, healthy individuals who likely would not have, under normal circumstances, died without its usage.1
The 2015 National Survey on Drug Use and Health estimated that 968,000 individuals at least 12 years of age had used cocaine.2 Cocaine abuse is a significant risk factor for the development of acute myocardial infarction, especially for individuals who abuse it at a younger age.
An alkaloid, cocaine comes primarily from South America, where it is extracted from the leaves of the Erythroxylum coca bush. It is typically consumed in two forms: freebase or hydrochloride salt (powder).
Cocaine is well absorbed through mucous membranes, making it usable orally, nasally, or rectally. The freebase form is processed by adding baking soda, which removes the hydrochloride. This form can be heated until it melts, allowing it to be smoked, and is known as crack cocaine.
Crack cocaine is the most potent and addictive form of the drug, producing its effects within 3–5 seconds of inhalation, and each hit lasting from 5–15 minutes. Cocaine used intravenously usually takes between 10 seconds to a minute for onset, with lasting effects of about one hour. Cocaine used intranasally can take anywhere from 1–5 minutes for effects to occur but can last between 1–2 hours.3
One of the most addictive characteristics of cocaine is that when used for the first time, it produces an intense high that is nearly impossible to replicate. The user keeps trying to obtain this high again, but will never reach quite that same pinnacle. Continued chasing of this high is what causes the lasting detrimental myocardial effects that lead many young users to early deaths. Even once use stops, the damage to the heart tissue cannot be reversed.
Effects on the Heart
Cocaine directly affects cardiac action potential by blocking potassium channels, increasing the long-opening calcium channel flow and stopping entrance of sodium during the depolarization phase.1 Along with stimulation of the sympathetic nervous system, this is considered a primary mechanism that causes the arrhythmias cocaine can produce.
Stimulation of the sympathetic nervous system increases blood pressure as well as heart rate. Patients with existing myocardial abnormalities take medications to prevent such increases in their heart rate and blood pressure, placing them at increased risk for developing lethal arrhythmias when they use cocaine.3 These same effects are produced by medication therapy used in the treatment of arrhythmias, such as sodium, potassium, and calcium channel blockers today. However, cocaine toxicity-produced arrhythmias are not treated in the clinical setting with this same approach due to this mechanism.
Another frequently abused illegal drug, methamphetamine, results in similar stimulant effects on the nervous system. Stimulation of the autonomic nervous system results in the release of norepinephrine, dopamine, and serotonin. Unlike cocaine, however, amphetamines do not contain the same ion channel-blocking properties.4
Cocaine’s effects on the myocardium can result in infarct or ischemia due to several mechanisms. Coronary vessel constriction will decrease myocardial oxygen supply along with increasing myocardial oxygen demand from increasing heart rate, blood pressure and contractility. Cocaine-induced hypertension is the result of the vasopressor effects of norepinephrine stimulating the alpha-adrenergic receptors in the heart’s vasculature.1
Coronary vessel constriction occurs with the increase in alpha stimulation, increasing production of endothelin, then decreasing the production of nitric oxide. Exacerbating atherosclerosis and thrombus formation occurs from the increased plasminogen-activation inhibitor, and platelet activation is increased, as well as aggregability and endothelial permeability.3 Cocaine use thus produces myocardial structural damage, resulting in heart failure and exacerbating underlying cardiomyopathies, and can result in sudden cardiac death.1
Prolonged use of cocaine can result in inflammation within the myocardium, the middle layer representing the bulk of the heart’s muscle mass. Enlarging of the heart will result in a damaged and stretched myocardium, as it can cause geometric changes in the mass size of the left ventricle.
Any of these will impair myocardial function, potentially producing heart failure and ultimately leading to sudden premature death. Around 5%–20% of sudden deaths in young adults reveal an underlying undiagnosed cardiomyopathy.5
Any time a younger, otherwise-healthy individual presents with chest pain accompanied by unexplained tachycardia, tachypnea, agitation, paranoia, tunnel vision-type focus, profound diaphoresis, and bruxism, consider a stimulant such as cocaine in your differential diagnosis.
Scene and Transport Considerations
Patients who consume cocaine are at risk for development of excited delirium. Excited delirium patients present with symptoms of paranoia, disorientation, hyperaggression, hallucinations, incoherent speech, shouting, and increased strength and endurance, as well as hyperthermia. These patients pose a safety concern for EMS crews, law enforcement, themselves, and others involved, such as family members. When restrained these patients present a higher risk of cardiac arrest.
It is imperative that EMS and all first responders preserve their own safety when treating and transporting these patients. Keep them as calm as possible, using a nonjudgmental approach along with calming reassurance that you are there to help. Avoid stimuli such as loud noises, bright or flashing lights, volatile family members, and defensive posturing. Stimulating them will only exacerbate the problem.
Everyone involved in the care of these patients should understand this potential problem. Cooperation will be needed from law enforcement, other responding EMS personnel, and any family and friends present.
Use caution during transport and know these patients are unpredictable. Stay relaxed and make sure safety belts are properly placed in case of an accident, but not so tight the patient feels trapped. Avoid sirens if possible, as well as erratic driving and any loud stimuli that could agitate their behavior.
Benzodiazepines can be used for their sedative effects, which will help manage anxiety, agitation, and tachyarrhythmias.1 Benzodiazepines, however, do not always result in decreasing tachycardia, hypertension, and vessel spasms when given alone. When combined with nitroglycerin they can result in better relief of chest pain, blood pressure, and heart rate.6
Nitroglycerin combined with calcium channel blockers can assist in alleviating cocaine-induced hypertensive crisis.3 Calcium channel blockers given alone can alleviate cocaine-induced hypertension along with chest pain resulting from coronary vessel spasms but are not likely to lower heart rate.
Morphine can be beneficial in reducing blood pressure and relieving chest pain but will not lower the heart rate and in some cases may increase it.6 Fentanyl can help with control of chest pain and is possibly beneficial for lowering heart rate and blood pressure.
Labetalol and carvedilol, which are both combined alpha and beta blockers, are effective in the treatment of hypertension and tachycardia induced by cocaine.6 Labetalol is recommended by the ACC/AHA for the management of cocaine-associated chest pain.
Administration of beta blockers, specifically those that target beta-1 receptors, remains somewhat controversial in the setting of cocaine toxicity. This controversy comes from a phenomenon known as unopposed alpha stimulation, which causes increases in blood pressure or vasoconstriction of the coronary arteries.
Although this occurs rarely, it has caused some systems to not utilize beta blockers in the prehospital setting.6 Evidence has shown that beta blocker administration in cocaine toxicity can, in certain cases, be beneficial for the patient and not as harmful as once suspected.7
Use 0.9% sodium chloride boluses of 20 mL/kg for body temperature reduction. Patients with cocaine toxicity can become dehydrated from constant sympathetic nervous system stimulation, uncontrolled thermoregulation, and fluid loss from sweating, as well as decreased oral intake. EMS crews should obtain a glucose measurement when possible and treat accordingly.
Administration of lidocaine along with sodium bicarbonate 8.4% is indicated in the event the patient suffers cardiac arrest due to cocaine toxicity. Procainamide is not recommended in ventricular tachycardia, as it can further prolong the QT intervals and widen the QRS complex.3
Aside from the insidious myocardial changes brought on by repeated cocaine use, the patient under the effects of stimulant drugs can prove complex to treat in the prehospital setting. Understanding the pathophysiological changes and how medications interact will help the provider deliver the best possible care.
1. Phillips K, Luk A, Soor GS, et al. Cocaine cardiotoxicity: A review of the pathophysiology, pathology, and treatment options. Am J Cardiovasc Drugs, 2009; 9(3): 177–96.
2. John WS, Wu LT. Trends and correlates of cocaine use and cocaine use disorder in the United States from 2011 to 2015. Drug Alcohol Depend, 2017 Nov 1; 180: 376–84.
3. Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med, 2001 Aug 2; 345(5): 351–8.
4. Fischbach P. The role of illicit drug use in sudden death in the young. Cardiol Young, 2017 Jan; 27(S1): S75–S79.
5. Cooper LT Jr., ElAmm C. Giant cell myocarditis: Diagnosis and treatment. Herz, 2012 Sep; 37(6): 632–6.
6. Richards JR, Garber D, Laurin EG, et al. Treatment of cocaine cardiovascular toxicity: A systematic review. Clin Toxicol (Phila), 2016 Jun; 54(5): 345–64.
7. Finkel J, Marhefka G. Time for reassessment: A review of beta-blockers in the setting of cocaine associated chest pain and acute coronary syndrome. The Medicine Forum, 2010; 12(1): 7.
Sidebar: Cocaine—Points to Remember
Cocaine is a powerfully addictive stimulant drug made from the leaves of the coca plant native to South America.
Street dealers often mix it with cornstarch, talcum powder, or flour to increase profits.
They may also mix it with other drugs, such as amphetamine or fentanyl.
People snort cocaine powder through the nose or rub it into their gums. Others dissolve the powder and inject it into the bloodstream or inject a combination of cocaine and heroin (speedball). Another method is to smoke crack cocaine.
Cocaine increases levels of the natural chemical messenger dopamine in brain circuits related to the control of movement and reward.
Cocaine use will increase the chances of premature death.
Behavioral therapy may be used to treat cocaine addiction.
While no government-approved medicines are currently available to treat cocaine addiction, researchers are testing some treatments that have been used against other disorders.
—Source: National Institute on Drug Abuse
Roger L. Layell, FP-C, CCP-C, CCEMT-P, NRP, is a flight and critical care paramedic at Wake Forest Baptist Health AirCare in Winston-Salem, N.C. He has 15 years of experience in the field as a paramedic and 10 of critical care experience in the HEMS environment.