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CHAPTER 34 Overdose of Cardiotoxic Drugs 363
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Cocaine is metabolized by nonenzymatic hydrolysis and liver esterases, including plasma cholinesterase. The two major metabolites include benzoylecgonine and ecgonine methyl ester, neither of which crosses the blood-brain barrier. Both compounds are water soluble and are excreted in the urine. Cocaine metabo­lites may be detected in the urine up to 72 hours after an exposure, although heavy users may have positive urine screens for up to 3 weeks.
158
When a user of cocaine also coingests ethanol, hepatic transesterification will create another pharmacologically active metabolite, cocaethylene. Cocaethylene is not on the routine urine screens for cocaine metabolites.
Pathophysiology. The pharmacologic effects of cocaine in
humans include the ability to stabilize membranes and block nerve conduction. The resulting effects on myocardial tissue cause blockade of fast sodium channels leading to widening of the QRS complex with subsequent arrhythmias. The sympatho­mimetic effects of cocaine are caused by impaired catecholamine reuptake and enhanced catecholamine release at nerve terminals.
157
The increased synaptic concentrations of neurotransmitters stimulate α- and β-receptors throughout the autonomic nervous system, resulting in a cascade of clinical effects. Cocaine may also enhance the release of norepinephrine and dopamine in the CNS.
159
The unique ability of cocaine to inhibit nerve conduc­tion while enhancing vasoconstriction is primarily responsible for its cardiovascular toxicity.
157
Cocaethylene is also a potent sodium channel blocking agent and appears to prolong the recovery time for the channel compared with cocaine.
160
In animal models, cocaine plus ethanol
depressed myocardial contractility more than either agent given
161,162
alone.
Once formed, cocaethylene has a longer half-life than
cocaine.
The mechanism of cocaine-induced myocardial ischemia is thought to be multifactorial. Cocaine increases myocardial oxygen demand while increasing heart rate and blood pressure. Usually, myocardial oxygen demand results in coronary vasodilatation; however, cocaine taken by some routes can induce coronary vasospasm.
163
Coronary artery thrombus formation has also been implicated as a cause of cocaine-induced myocardial ischemia. Thrombus formation leading to myocardial infarction (MI) has been associated with coronary artery vasospasm.
164
The vasospasm may damage the endothelium and cause release of vasoactive substances, precipitating platelet aggregation. Cocaine may enhance this effect because in vitro studies have demonstrated that cocaine alone may directly stimulate platelet aggregation
165
and platelet thromboxane production.
Cocaine activates platelets
in whole blood by inducing the release of platelet α-granule contents and by promoting the binding of fibrinogen to the surface of the platelet.
165
Clinical Manifestations. The clinical effects of cocaine result
from diffuse hyperadrenergic stimulation both centrally and peripherally. The peripheral sympathomimetic effects include tremor, mydriasis, urinary retention, and ileus. Adrenergic stimulation of the CNS leads to agitation, hallucinations, sei­zures, and coma. and anxiety due to increased dopaminergic transmission.
166
Patients may experience psychosis, paranoia,
167
Cerebrovascular complications from cocaine-induced vaso­spasm and a hyperadrenergic state include cerebral infarctions, transient ischemic attacks, and subarachnoid and intracranial hemorrhages.
166,167
Myocardial ischemia and MI are well-documented complica­tions of cocaine use. Ischemia of the myocardium does not require a massive exposure to cocaine and occurs commonly in the young adult with no history of cardiac risk factors. Symptoms of chest pain may be typical, atypical, or absent. A delay of several hours in the onset of chest discomfort may occur after exposure to the
168–170
drug.
ECGs from patients with cocaine-associated chest pain may demonstrate a variety of abnormalities, including classic findings of myocardial injury, such as ST segment elevation. However, they may also be normal or have only nonspecific findings. A study of 42 cocaine users with chest pain and normal or nondiagnostic ECGs documented 8 of these patients as having acute MI, defined by total creatinine kinase and myocardial isoenzyme levels. useful in ruling out cocaine-induced ischemia.
171
Thus single or even serial ECGs may not be
Cocaine has been associated with a variety of arrhythmias. Sinus tachycardia is common owing to the sympathomimetic effects. Atrial fibrillation, premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation have all been described.
172
Arrhythmias may occur with or without underlying ischemia. Cocaine can cause sodium channel blockade, widening of the QRS complex, and associated arrhythmias. Toxicity related to sodium channel blockade should be treated with sodium bicarbonate, as previously discussed.
Hypertension is also common with cocaine poisoning. The elevation in blood pressure combined with tachycardia may increase shear forces on the great vessels, resulting in aortic or coronary artery dissection.
174
The intestinal vasculature is
susceptible to α-stimulating effects of catecholamines; ischemic colitis has been described in adults in utero exposure to cocaine.
175
as well as in neonates after
176
The uteroplacental vasculature may also respond to cocaine exposure with diminished uterine blood flow after maternal cocaine use.
177
Extreme hyperthermia is often documented in cocaine overdose. Temperatures are frequently reported in excess of 106°F and are thought to result from a disturbance in thermoregulation due to extensive dopaminergic stimulation combined with excessive musculoskeletal activity and agitation.
178,179
Although cocaine-induced hyperthermia may occur independent of seizure activity, it can be exacerbated by concomitant convulsions. An acute rise in the central body temperature has also occurred after rupture of bags of cocaine ingested by body packers (individuals who conceal illicit drugs in their bodies for smuggling purposes).
181
Rhabdomyolysis also contributes to the morbidity and mortal­ity of cocaine poisoning. All routes of cocaine exposure have been associated with a rise in serum creatinine phosphokinase level from direct myotoxicity.
181–183
An association has been made between drug-induced hyperthermia and rhabdomyolysis, but observations suggest that cocaine can also induce rhabdomyolysis independently of hyperthermia. olysis is associated with myoglobinuric renal failure. is not known to be directly toxic to the renal tubules; however,
181
Cocaine-induced rhabdomy-
183
173
180
Cocaine
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the effects of cocaine on renal blood flow may exacerbate the effects of myoglobinuria.
Novel Psychoactive Substances
Novel psychoactive substances (NPSs) come in many forms and are very popular owing to their wide availability. They can be classified based on their chemical families, which include phenylethylamines, amphetamines, cathinones, piperazines, pipradrols/piperidines, aminoindanes, benzofurans, and trypt­amines (Table 34.1). effects based on their actions on dopamine, serotonin, and norepinephrine. Most of these have no approved uses in the United States but some of the phenylethylamines are used for treatment of narcolepsy, attention deficit disorder, and weight loss. Synthetic cannabinoids are commonly included in the NPSs but will be discussed separately owing to their differing mechanisms. Amphetamines are described as the prototypi­cal agent of this class, as they all have similar mechanisms of action.
Amphetamines have been recognized for their stimulant properties for centuries and continue to be abused by various routes, including intravenous and oral administration. “Ice” is a pure preparation of methamphetamine and is marketed in a solid form, hence its nickname. This preparation is volatile and can be smoked, resulting in rapid absorption and effect. This form of methamphetamine rapidly became one of the leading
TABLE 34.1 Novel Psychoactive
Substances
Chemical Name Nickname
Synthetic Cathinones
4-Methyl-N-ethyl cathinone 4-MEC, Shrimp α-Pyrrolidinovalerophenone Alpha PVP, Flakka, Gravel
Benzofurans
5-(2-Aminopropyl)benzofuran 5-APB, Benzo Fury 6-(2-Aminopropyl)benzofuran 6-APB, Benzo Fury
Piperazines
3-Chlorophenylpiperazine mCPP, Legal X Methoxypiperamide MeOP, MEXP
Pipradrols/Piperidines
N-Methyl-3-piperidyl benzilate JB-336, BZ (RS)-2-benzhydrylpiperdine 2-DPMP, Ivory Wave
184
They have varying intoxicating and toxic
drugs of abuse in Hawaii and California in the 1980s.
185,186
Illicit laboratories can produce large quantities of methamphetamines because of the ease of availability of most reagents. In recent years, advances and simplification of synthesis techniques have led to many new psychoactive substances being produced and distributed as “legal highs” before legislation could be initiated to make them illegal.
184
Abuse of amphetamines results in euphoria, with increased self-confidence and well-being. Persistent use with repetitive doses over several days is common. During this “speed run,” the user may not sleep or eat owing to the stimulant and anorectic effects of the drug. Chronic use of amphetamines can rapidly lead to tolerance; increasing doses are usually required to maintain euphoria.
Pharmacology. The volume of distribution of amphetamines
tends to be large and the half-life ranges from 8 to 30 hours.
187
Elimination is primarily through hepatic transformation, but renal excretion results in significant elimination of certain members of the amphetamine family, such as methamphet-
188
amine.
Although acidification of the urine may enhance the excretion of some amphetamine derivatives, it may also exacerbate renal toxicity in the presence of rhabdomyolysis and is therefore not recommended.
189
Pathophysiology. The pharmacologic mechanisms of action
of amphetamines are diverse but are thought to rely on indirect effects on catecholamine receptors. These compounds act by entering presynaptic neurons and stimulating the release of endogenous catecholamines, such as norepinephrine and dopa­mine. Amphetamines also inhibit the reuptake of catecholamines and their breakdown by the monoamine oxidase enzyme system. These effects may last for hours, whereas those of cocaine may resolve within several minutes.
187
Increased catecholamine release results in stimulation of α- and
β-receptors both peripherally and centrally. Dopaminergic and serotonergic receptor stimulation may contribute to the behavioral disturbances and hyperthermic effects that are common with these poisonings.
190
The release of dopamine may be responsible for the pleasurable effects reported with these drugs. Although all members of the amphetamine family may produce a general­ized hyperadrenergic state, the pattern of effects with these compounds differs with modification of the parent molecule, resulting in different anorectic, cardiovascular, and hallucinogenic properties.
191
Aminoindanes
5,6-methylenedioxy-2-aminoindane MDAI, Woof-Woof, MDog 5-Methoxy-6-methyl-2-aminoindane MMAI
Tryptamine
N,N-Dimethyltryptamine DMT, Fantasia
Phenethylamines/Amphetamines
3, 4-Methylenedioxymethamphetamine MDMA, Adam, Ecstasy, XTC 3, 4-Methylenedioxymethamphetamine MDEA, Eve 3, 4-Methylenedioxyamphetamine MDA, Love Drug 4-Methyl-2, 5-dimethoxyamphetamine DOM/STP, Serenity, Tranquility
Clinical Manifestations. Physical findings in amphetamine
poisoning are similar to those seen with other sympathomimetic drugs. The cardiovascular toxicity of amphetamines manifests most commonly as tachycardia and hypertension. Arrhythmias are a common cause of death and can include ventricular tachycardia and ventricular fibrillation.
192
Hypertensive emergen­cies with intracranial hemorrhages and cerebrovascular accidents may be more common with amphetamine and methamphetamine than cocaine abuse.
193
Acute myocardial ischemia, MI, aortic dissection, and dilated cardiomyopathy are also known to occur in the setting of amphetamine use.
194
Diffuse vascular spasm
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has also been reported with amphetamine poisoning and may result in death.
195,196
CNS toxicity is the most common reason for amphetamine­poisoned patients to present to a hospital. Most victims are agitated, anxious, and can become volatile and violent. Tactile and visual hallucinations may contribute to patient agitation, and psychoses similar to paranoid schizophrenia are frequently observed in these patients. Mydriasis and diaphoresis are common. Seizures often complicate amphetamine poisoning.
184,196
As in acute cocaine intoxication, hyperthermia is well docu­mented in amphetamine poisoning and is associated with increased morbidity and mortality. Hyperthermia may occur independent of seizures and has been associated with rhabdo­myolysis, coagulopathy, renal failure, and death.
184,196–198
Synthetic Cannabinoids
Marijuana has a long history of recreational and medicinal use and is the most widely produced and consumed illicit substance. Synthetic cannabinoids were developed initially in an attempt to provide the therapeutic benefits claimed by botanical cannabis while limiting the psychoactive effects. Around 2004, these synthetic cannabinoids started being produced for use as legal alternatives to marijuana.
199,200
These chemicals were marketed under names such as “K2” or “Spice” and were packaged with statements such as “not for human consumption” or “for aro­matherapy use only.” Many different compounds have been produced and distributed. It was rapidly recognized by toxicolo­gists that these products had greater effects or potency at smaller doses than standard marijuana. They also seemed to have effects not commonly seen with marijuana use, including tachycardia, arrhythmias, seizures, and delirium.
Pharmacology. The synthetic cannabinoids would be expected
to have a large volume of distribution based on their lipophilic-
200
it y.
These compounds are mostly glucuronidated or hydroxyl­ated in the liver and then excreted in the urine. Some of their metabolites are active at cannabinoid receptors, which may increase the length of perceived effects.
199
Pathophysiology. Synthetic cannabinoids act by stimulating
cannabinoid receptors found throughout the body. Two can­nabinoid receptors have been identified so far: CB1 and CB2. These receptors are G-protein coupled receptors that cause down-regulation of adenylyl cyclase and decrease cellular cyclic adenosine monophosphate (cAMP) levels when activated. This leads to changes in cellular signaling and neurotransmitter release, including acetylcholine, dopamine, norepinephrine, glutamine, and GABA. CB
receptors are predominantly in the brain;
1
increased activation leads to modulation of GABA and glutamate neurotransmission. CB2 is primarily expressed in peripheral tissues of the immune system including the spleen, tonsils, thymus, and gastrointestinal system; activation leads to changes in immunomodulation.
199,200
Synthetic cannabinoids generally have a much higher potency and affinity for these receptors than delta-9-tetrahydrocannabinol (delta 9-THC) found in marijuana. The changes in GABA and glutamate in the brain are the probable cause leading to the
199
psychosis, seizures, and other central nervous effects often reported with these chemicals, although the exact mechanisms are unclear at this time. The arrhythmias, tachycardia, and hypertension seen with these agents are likely the result of increased release of excitatory neurotransmitters, but this too has not been fully elucidated.
199,200
Clinical Manifestations. The clinical findings from synthetic
cannabinoid overdose are like those seen with the other sym­pathomimetic drugs. The most commonly reported cardiovascular symptoms are tachycardia, hypertension, chest pain, and arrhythmias. There have been reports of sudden cardiac death after synthetic cannabinoid use. The cause of cardiac death seems to be cardiovascular vasospasm like that described with other sympathomimetic drugs. Acute myocardial ischemia has also been theorized to be caused by increased myocardial oxygen demand resulting from tachycardia and hypertension. A final possible factor for the increased cardiac deaths is the fact that synthetic cannabinoids lead to increased platelet activation that may amplify plaque rupture induced by increased shear forces in the coronary arteries.
200
In most cases, patients present to medical facilities due to the CNS effects of these agents with psychomotor agitation, psychosis, anxiety, confusion, and changes in memory. Seizures are some of the most severe CNS effects noted from these chemicals but are generally easily controlled with benzodiazepines.
200
Unlike other sympathomimetic agents, synthetic cannabinoids have not been associated with significant hyperthermia. Other physical signs include dilated pupils, reddened conjunctivae, nausea, vomiting, and shortness of breath. In severe cases, can­nabinoids have been associated with ischemic strokes and acute kidney injury requiring hemodialysis.
199,200
Management. Successful treatment of sympathomimetic
poisoning begins with aggressive supportive care. Management of airway, breathing, and circulation are initial priorities. Place­ment of the patient in a quiet setting may reduce the amount of stimulation and reduce patient agitation; however, the victim must be continuously monitored for potential complications. Vital signs should be obtained frequently and body temperature verified by rectal thermometer if hyperthermia is suspected. Rapid cooling measures should be instituted as soon as hyperthermia is detected; neuromuscular paralysis may be required in severe cases of hyperthermia.
Decontamination of the patient who ingested sympathomimet­ics or bags containing these drugs begins with the administration of activated charcoal, as described earlier. Whole-bowel irrigation with an isosmotic, isoelectric lavage solution (e.g., Go-Lytely) may enhance the removal of bags from the gastrointestinal tract. Due to the large volume of distribution of these agents, hemo­dialysis and hemoperfusion are not effective in their removal; however, hemodialysis may be required if acute renal failure develops as a complication of rhabdomyolysis.
Rapid and effective control of hypertension from sympatho­mimetic poisoning is imperative. The use of β-blockers to control the hypertension associated with sympathomimetics is contro­versial because these drugs may theoretically potentiate both
201
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coronary and peripheral vasoconstriction due to unopposed α-agonist activity. labetalol as an alternative to nonselective β-blocking agents,
202,203
Case reports have suggested the use of
204
but labetalol is a more potent β- than α-antagonist. One study of patients given intranasal cocaine while undergoing angiography demonstrated that labetalol reduced the mean arterial pressure but had no effect on coronary artery vasoconstriction.
205
The
current literature supports the use of β-blocking agents in sympathomimetic overdose to control hypertension, with labetalol being the most supported. nitroprusside, or phentolamine—can be considered.
206
Vasodilators—such as nitroglycerin,
207,208
Cocaine-, NPS-, or cannabinoid-related chest pain must be considered to represent active myocardial ischemia. Therapy should initially include the application of oxygen and the reduc­tion of central sympathomimetic effects with the liberal use of benzodiazepines. Nitroglycerin has been demonstrated to be effective in alleviating cocaine-induced vasoconstriction in diseased and nondiseased coronary arteries.
208
An antiplatelet drug, such as aspirin, may be administered because platelets are activated by cocaine. Heparin may be considered when ischemia is refractory to more conservative management.
Treatment of sympathomimetic-induced arrhythmias begins with the administration of benzodiazepines to sedate the patient and reduce catecholamine release.
209
Wide complex tachycardias from cocaine have been effectively treated with intravenous sodium bicarbonate.
210
Lidocaine may be considered for treatment
of arrhythmias secondary to ischemia or refractory to sodium
bicarbonate but should be used with caution because it has potentiated cocaine-induced seizures and death in rats.
Benzodiazepines are the mainstay of treatment for the CNS effects of sympathomimetic poisonings. These sedative-hypnotics have been demonstrated to reduce the lethality of both cocaine and amphetamines.
209,212
Butyrophenones have also been effective in reducing the dopaminergic-based delirium associated with amphetamine use.
213
Butyrophenones must be administered cautiously to patients with either cocaine, NPS, or cannabinoid toxicity because most antipsychotic medications may lower seizure thresholds, alter temperature regulation, and cause acute dystonias.
CONCLUSION
Many drugs possess the ability to cause life-threatening cardio­toxicity in overdose. In this chapter, we have outlined some of the most significant and most common agents in this regard, with emphasis on clinical presentation and management. Although primary resuscitative efforts in all disease states should focus on airway and circulation, the varied mechanisms of action of cardiotoxic compounds may require specific therapeutic interven­tions. Early consultation with a certified regional poison control center or a medical toxicologist may assist in the care of these patients.
The full reference list for this chapter is available at
ExpertConsult.com.
211
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