Bad Request (Invalid Hostname)

	More NurseWeek Features   Smoke-Free Zone   Nurses and patients tackle nicotine addiction   Bloodless Survival     Surgical techniques to use when transfusion drops out of the equation
Substance abuse and athletes is a costly and potentially deadly combination.

Substance abuse among athletes is a recognized problem in sports and the abuse of drugs has been implicated at every level of competition. Athletes, coaches, trainers, and health professionals must be alert to the possibility of drug use in athletes and the catastrophic effects many of these substances have on the cardiovascular system.

Athletes might use drugs for therapeutic, recreational or social reasons, as performance-enhancing (ergogenic) aids, or to mask the presence of other drugs during drug testing.¹ The American College of Sports Medicine reported in 2000 that the abuse of recreational drugs, such as cocaine, among athletes far outweighs the abuse of ergogenic drugs.

Athletes are thought to be vulnerable to recreational substance abuse because of some combination of the following variables: fame, fortune, free time, and a feeling of invincibility.² Recreational drugs are largely performance-impairing (ergolytic) drugs.

Ergolytic drugs

Cocaine is an alkaloid extracted from the leaves of the Erythroxylum coca bush grown in South America. Its therapeutic use is that of a local anesthetic. It is available as a hydrochloride salt, which can be taken orally, intravenously, intranasally, and as the “free base” or “crack” form, which can be smoked. Cocaine is metabolized by the plasma and liver cholinesterases into water-soluble metabolites, which are excreted in the urine.³ Individuals with hereditary cholinesterase deficiency may have a fatal reaction to even small doses of cocaine.⁴

Myocardial infarction (MI) has been reported in first-time and chronic cocaine users with and without risk factors for coronary artery disease. Acute MI has occurred with all routes of administration and is not dose dependent.

The pathophysiology of cocaine induced MI remains unclear, but probably includes an increase in myocardial oxygen demand, coronary vasospasm, and increased thrombotic potential.¹ Cocaine causes an increase in heart rate, systemic blood pressure, and left ventricular contractility. It induces marked constriction of coronary arteries. Even small amounts of the drug cause vasoconstriction of epicardial coronary arteries so that myocardial oxygen supply decreases, even as demand increases.

Cocaine enhances platelet activity, which may cause clot formation in coronary arteries, increase production of endothelin (a potent vasoconstrictor), and decrease production of nitric oxide (a potent vasodilator). When taken systemically, cocaine blocks the presynaptic uptake of norepinephrine and dopamine, and acts as a powerful sympathomimetic agent.³

The occurrence of an acute MI in a young athlete without cardiovascular risk factors should raise suspicion of occult cocaine use.

Cocaine also has been associated with aortic dissection, endocarditis, dilated cardiomyopathy, deep vein thrombosis, cardiac dysrhythmia, and stroke.^1,3

Alcohol: the often-forgotten drug

Alcohol abuse has been implicated in the development of heart disease for more than a century. Adverse consequences of alcohol abuse are hypertension, stroke, coronary events, lipid abnormalities, cardiac arrhythmias, systolic dysfunction, and dilated cardiomyopathy.^1,4 The precise mechanism by which alcohol produces hypertension is unknown.¹

Excessive alcohol ingestion may increase the risk of stroke threefold in young athletes. The highest incidence of stroke occurs in nonalcoholic men who drink more than 300 grams on weekends. (12 ounces of beer = 13 grams).¹ Alcohol abuse should be considered in athletes with new-onset hypertension or with unexplained stroke.¹

Marijuana, diuretics, and tobacco

Marijuana is derived from the Cannabis sativa plant and can be smoked or eaten. Its use decreases exercise performance, stroke volume, and increases heart rate.^1,4

Athletes misuse diuretics before competition in an attempt to dilute urinary concentration of other prohibited drugs and sometimes to lose weight quickly to make a certain weight class. Diuretics can deplete potassium and cause cardiac dysrhythmias and death.¹

Athletes use smokeless tobacco for its nicotine properties. Nicotine is a central stimulant that relaxes skeletal muscles, constricts blood vessels, and increases heart rate and blood pressure. Nicotine can cause coronary artery spasm and lower the threshold for ventricular fibrillation, and death has been reported in athletes using smokeless tobacco following vigorous exercise.¹

Ergogenic drugs

Athletes use stimulants in an effort to increase time to exhaustion by masking the physiologic response to fatigue.¹ Amphetamines are sympathomimetic agents, which increase heart rate, respiration, and blood pressure.