Cardiac
Chest pain: Chest pain is the most frequent cocaine-related symptom and constitutes approximately 40% of cocaine-related emergency department visits. Chest pain following cocaine use may be due to a number of causes, including those directly attributable to the effects of cocaine, such as myocardial infarction and aortic dissection, and causes due to complications of the route of administration. For example, inhalation of cocaine, resulting in pneumomediastinum and pneumothorax, and intravenous injection, resulting in septic emboli, may all manifest as chest pain and other cardiopulmonary symptoms.
The incidence of cocaine-associated myocardial infarction has been found to range from 0-31% in retrospective studies of patients who present to the emergency department with chest pain following cocaine use. The Cocaine Associated Chest Pain (COCHPA) trial has been the largest prospective multicenter study. That study determined the incidence to be 6%. The pain is frequently described as substernal pressurelike discomfort and is associated with shortness of breath and diaphoresis. Patients who are affected are usually young males (aged 19-40 y) who smoke cigarettes and repetitively use cocaine. Most commonly, the chest pain occurs 60 minutes after use and persists for about 120 minutes, but the period of cocaine-ischemia may persist for as long as 2 weeks following cessation of cocaine use. Atypical presentations of myocardial infarction are also very common in the cocaine-using population.
Respiratory: Shortness of breath, like chest pain, is a frequent symptom that brings patients who use cocaine to the emergency department and may be due to a number of cardiopulmonary processes. Cocaine smoking is associated with acute exacerbations of asthma, bronchiolitis obliterans, cardiogenic and noncardiogenic pulmonary edema, interstitial pneumonitis, pulmonary vascular hypertension, pulmonary hemorrhage, thermal injury to the airway, pneumothorax, and significant impairment of the diffusing capacity of the lung. Shortness of breath may also be due to cocaine-induced laryngospasm. Inhalation of cocaine may result in pneumomediastinum and pneumothorax.
Gastrointestinal: Abdominal pain following cocaine use should raise suspicion of ischemic bowel; bowel perforation; and, in the smuggler, bowel obstruction. Abdominal pain may also be caused by hepatic necrosis due to cocaine use, which is similar to the necrosis commonly observed with acetaminophen. Renal infarction may also manifest as abdominal pain.
Skeletal muscle: Cocaine use can lead to rhabdomyolysis, which may be associated with hyperthermia, seizures, or agitation. Rhabdomyolysis associated with cocaine use is usually severe, leading to renal failure and acidosis. Asymptomatic rhabdomyolysis may be observed in patients who chronically use cocaine and may be attributed to the effects of cocaine on the dopaminergic system.
Back pain may be a symptom of rhabdomyolysis, renal infarction, or aortic dissection.
...
On the use of benzos for coke use in medicine:
Medical Care: Patients with cocaine poisoning may exhibit severe CNS and cardiovascular dysfunction, leading to a loss of airway protective reflexes, cardiovascular collapse, and mortality.
Admit all patients with major adrenergic symptoms, severe hyperthermia, severe agitation, recurrent convulsions, persistent arrhythmias and dysrhythmias, severe hypertension, and complications (eg, respiratory failure, cardiogenic and noncardiogenic pulmonary edema, altered mental status, myocardial ischemia and infarction, hypotension and shock, severe rhabdomyolysis, severe acidosis) to the intensive care unit. Complications such as aortic dissection, intracerebral bleeding, and subarachnoid bleeding require surgical intensive care. Also, admit asymptomatic body packers and body stuffers to the ICU.
...
Psychomotor agitation: The immediate control of psychomotor agitation is critical in preventing the lethality of cocaine poisoning. Psychomotor agitation is managed in the standard fashion. Benzodiazepines, such as diazepam and lorazepam, are the mainstay of therapy and may be used generously until sedation is accomplished. Avoid physical restraints in patients with psychomotor agitation because they may interfere with heat dissipation. Likewise, avoid neuroleptic agents because they interfere with heat dissipation and, perhaps, lower the seizure threshold.
Convulsions: Aggressively treat recurrent seizures because they may worsen hyperthermia, rhabdomyolysis, hypoxia, and acidosis. Seizures may also be a manifestation of an acute intracerebral complication. Imaging studies and, when indicated, cerebrospinal fluid (CSF) analysis should follow immediate seizure control.
In the setting of cocaine toxicity, seizures are treated in the standard manner, except that phenytoin may be ineffective in this circumstance and may be part of the street additives to cocaine bulk. Incremental doses of benzodiazepines, such as diazepam (0.1-0.3 mg/kg, intravenously) and lorazepam, are the preferred initial anticonvulsants because they are quick acting, effective, and titratable. When a total dose of 8 mg of lorazepam fails to control seizures, barbiturates, which have traditionally been effective anticonvulsants in toxic ingestions, may be effective in controlling seizures because they may act synergistically with the benzodiazepines.
Because phenobarbital acts slowly, a short-acting barbiturate, such as pentobarbital or amobarbital, may be considered. If these agents are not rapidly effective in controlling the seizures, consider barbiturate anesthesia with ventilatory support and neuromuscular blockade. In these cases, electroencephalographic monitoring is required to monitor the presence or absence of seizure activity.
Neuromuscular blockade is indicated to control muscle activity and the subsequent development of acidosis. Neuromuscular blockade may be accomplished with nondepolarizing agents, such as vecuronium. Continue the neuromuscular blockade until the electroencephalogram results are normal for 2 or more hours.
Hypertension: Hypertension is common in patients intoxicated with cocaine and is due to alpha-mediated vasoconstriction, which is secondary to norepinephrine generated by the CNS. Cocaine-induced hypertension commonly responds to benzodiazepines. Benzodiazepines have been shown to be effective in the treatment of cocaine-induced hypertension, with or without chest pain or tachycardia.
When benzodiazepines fail to control hypertension, vasodilators, such as nitroprusside and nitroglycerin, are effective in controlling the blood pressure. If a contraindication to nitrate therapy exists, alpha-blockers, such as phentolamine, which block the vasomotor effect of norepinephrine, may be used.
Beta-blockers, in general, are best avoided in the setting of cocaine toxicity because they may result in unopposed alpha effects of cocaine. Beta-blockers have been reported to increase the blood pressure, reduce coronary blood flow, reduce left ventricular function, and reduce the cardiac output and tissue perfusion in patients with cocaine toxicity. Furthermore, in animal models of cocaine toxicity, beta-blockers have been associated with an increased risk of seizures and an increased mortality.
Beta-blocker toxicity (acute rises in blood pressure) in the setting of cocaine poisoning also extends to the short-acting, beta1 selective antagonists, such as esmolol, and to labetalol, which has both alpha-blockade and beta-blockade activity (in a 1:3 ratio when used intravenously and a 1:7 ratio when used orally).
Nifedipine may potentiate the incidence of seizures and death after cocaine administration and should be avoided in the treatment of cocaine-induced hypertension. In addition, calcium channel blockers are also thought to dilate splanchnic vessels, thereby increasing absorption of ingested cocaine from the gastrointestinal tract, which may become disastrous in body packers and body stuffers.
Myocardial ischemia and infarction: The administration of oxygen, nitrates, and aspirin are recommended in all patients with cocaine-induced myocardial ischemia. Benzodiazepines (diazepam, lorazepam) may be used to control cocaine-induced sympathetic tone. Phentolamine may relieve cocaine-induced coronary artery vasoconstriction and ameliorate myocardial ischemia. Likewise, verapamil and diltiazem (Cardizem) may ameliorate coronary vasoconstriction. If signs of a transmural myocardial infarction are present on the electrocardiogram, thrombolytic therapy may be beneficial in the absence of any contraindications; however, percutaneous transluminal coronary angioplasty (PTCA) may be as beneficial and safer. Again, beta-adrenergic blockade may be harmful in a patient with cocaine-induced myocardial ischemia because the unopposed alpha effects of cocaine result in coronary vasoconstriction.
Supraventricular tachycardias: Consider electrical cardioversion in all unstable patients. Correct hypoxia, acidosis, and myocardial ischemia. Cocaine-induced atrial tachyarrhythmias that are stable commonly respond to benzodiazepines, which reduce CNS sympathetic effects of cocaine. If sedative-hypnotics fail to control the arrhythmia, diltiazem and verapamil may be effective. Adenosine generally is ineffective in cocaine-induced supraventricular tachycardias.
...
Ventricular arrhythmias: When ventricular arrhythmias occur shortly after cocaine use, they are thought to be due to the effects of cocaine on the sodium channels. These arrhythmias may respond to sodium bicarbonate, the general antidote for sodium channel blockers. Sodium bicarbonate may be considered in patients with tachycardias associated with QRS durations greater than 100 milliseconds. As in tricyclic antidepressant (TCA) toxicity, maintain the pH at a range of 7.50-7.55.
These dysrhythmias also respond to lidocaine, especially when used in combination with benzodiazepines. Initial concerns about the use of lidocaine in the setting of cocaine poisoning have proven unfounded because of major differences in kinetics between the 2 compounds, which actually result in reduced effects of cocaine when lidocaine is present. No adverse effects from the use of lidocaine in the setting of cocaine poisoning have yet been reported.
Magnesium may also be considered in the treatment of ventricular dysrhythmias, especially in torsades.
[same cite as above]
Please Scroll Down to See Forums Below 
