Adding to its complex toxicity, cocaine targets muscarinic acetylcholine, N-methyl-D-aspartate (NMDA), sigma, and kappa-opioid receptors. This Vaughn-Williams class IC effect increases the risk of conduction disturbance and tachyarrhythmias. Similar to local anesthetics such as lidocaine, cocaine blocks sodium channels and interferes with action potential propagation.
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Plasminogen activator inhibitor is also increased following cocaine use, thereby promoting thrombosis. Cocaine-induced platelet activation and thrombus formation are another deleterious effects caused by alpha-adrenergic- and adenosine diphosphate-mediated increase in platelet aggregation. Epicardial coronary arteries are especially vulnerable to these effects, leading to decreased myocardial oxygen supply. Cocaine and its metabolites may cause arterial vasoconstriction hours after use. The principal actions of cocaine on the cardiovascular system are from alpha- and beta-1-adrenoceptor stimulation resulting in increased heart rate, systemic arterial pressure, and myocardial contractility, which are major determinants of myocardial oxygen demand. Monoamines accumulate in the synaptic cleft resulting in enhanced and prolonged sympathetic effects. This drug binds and blocks monoamine (dopamine, norepinephrine, and serotonin) reuptake transporters with equal affinity. Its pharmacodynamics involves multiple complex mechanisms, although its half-life is short at about 1 hour. Hyperthermia is a marker for poor prognosis and is often associated with muscle breakdown, renal and liver injury, encephalopathy, disseminated intravascular coagulation (DIC), and metabolic acidosis.Ĭocaine can be snorted, swallowed, injected, or smoked. Individuals who develop excited delirium tend to be more sensitive to the elevated levels of catecholamines.Īnother feature of cocaine toxicity is hyperthermia, which may be as high as 45 C. Excited delirium is often associated with aggression, hyperactivity, extreme paranoia, hyperthermia, incoherent screaming, and unusual strength. These patients are often at risk for sudden death.
Chronic use of cocaine can lower the density of dopamine receptors leading to extrapyramidal symptoms, dystonia, bradykinesia, akinesia, and akathisia.Ī high risk of death is the ability of cocaine to induce delirium. Cocaine can also cause seizures by lowering the threshold for seizure initiation.
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In patients with even mild coronary disease, these hemodynamic changes plus its vasoconstriction ability can trigger an acute coronary syndrome.Īsides from the myocardium, cocaine can also increase the risk of ischemic stroke. Cocaine significantly increases myocardial oxygen requirements, heart rate, and cardiac output. Long-term use of cocaine can also alter cardiac histology leading to fibrosis, myocarditis, and contraction band necrosis. The increased catecholamine levels can induce life-threatening arrhythmias, and at the same time, the local anesthetic properties of cocaine further impair impulse conduction, leading to re-entry ventricular arrhythmias. The adverse effects on the heart are due to the direct actions of cocaine by inhibiting the reuptake of catecholamines into the nerve endings. Patients who abuse cocaine risk life-threatening consequences, including tachydysrhythmia, severe hypertension, acute coronary syndrome, stroke, acute myocardial and renal failure, seizure, hyperthermia, cocaine-induced rhabdomyolysis, and fetal/maternal morbidity and mortality.
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