1. The cardiovascular effects of cocaine are biphasic.An initial increase in blood pressure and a tachycardia, secondary to sympathetic stimulation, precedes the pronounced depression of the CNS. Sweating, vomiting and restlessness may occur. Sympathetic vasoconstriction can be intense, with increased metabolism, hyperthermia, hypoxia, and convulsions. Ventricular fibrillation or asystole has occurred with doses as low as 30mg.Tachycardia and hypertension occurred during anaesthesia, when a patient injected two speedballs into his infusion just before surgery (Samuels et al 1991).
2. ECG abnormalities may be misinterpreted. Tachycardia, chest pain and large inferior Q waves on ECG in a young cocaine user led to the incorrect diagnosis of myocardial infarction (Lustik et al 1999). In the event she had WPW syndrome and successful ablation of the accessory pathway was accompanied by return to normal of the short PR interval and disappearance of the Q wave.
3. Toxic doses produce an initial tachypnoea and increased depth of respiration.This may be rapidly followed by central respiratory depression.
4. When taken nasally, the vasoconstrictor effects on the mucosa may eventually lead to nasal ulceration and septal perforation.
5. Anaesthetics may interact with cocaine when toxic levels exist. An animal study of a cocaine infusion in the presence of 0.75—1.5 MAC isoflurane showed reduction in cerebral and spinal cord blood flow and increased systemic vascular resistance, diastolic pressure, and coronary perfusion pressure (Boylan et al 1996).Arrhythmias and altered ventricular conduction also occurred. Ketamine potentiates strongly the cardiovascular toxicity of cocaine.
6. Vasoconstrictors, such as phenylephrine and felypressin, can precipitate hypertensive crises, ventricular tachycardia, and myocardial ischaemia during acute cocaine toxicity.
7. Intraoperative pulmonary oedema occurred after instillation of phenylephrine (0.5 ml 0.25%) into the nose of a 24-year-old man (Singh et al 1994). Echocardiography, whilst he received IPPV, showed right ventricular hypokinesia and an ejection fraction of 30%. When he had recovered, his echocardiogram became normal. Pulmonary oedema has also being reported after ketamine 50 mg, given for traction pain during tubal ligation under spinal anaesthesia (Murphy 1993). In both of these cases, a history of cocaine use was later obtained. The mechanism of the oedema is unclear. Contributing factors may be damaged pulmonary endothelium, or transient left ventricular dysfunction secondary to myocardial ischaemia or pulmonary vasocontriction.
8. There have been a number of reports of chronic rhabdomyolysis in association with cocaine abuse, and acute renal failure has occurred (Singhal et al 1989). In a study of cocaine users presenting to an emergency department, 24% had evidence of rhabdomyolysis (Welch et al 1991). One developed multiorgan failure and died.
9. A greatly increased risk of endocarditis in iv cocaine users (Chambers et al 1987).
10. Intravenous users are at risk of contracting hepatitis B, sexually transmitted diseases, and AIDS.
11. Hot cocaine fumes, when smoked or inhaled, may cause pulmonary damage, as may the chemicals used in the processing (Gossop 1987).Two patients presented with acute respiratory distress for which they eventually required tracheal intubation and IPPV In both patients, superficial white plaques, mucosal ulceration, and severe supraglottic oedema had been found on fibreoptic laryngoscopy. Each patient finally admitted to aspirating hot fragments while smoking crack (Reino & Lawson 1993).A third patient had sudden airway obstruction whilst smoking crack. Following a CT scan for a confusional state, he developed stridor and upper airway obstruction. Numerous polyps, oedema, and a narrowed aperture were o
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