Not having the normal use of mental faculties by reason of the introduction of cocaine is defined drug intoxication by the laws in America, Europe, and most of the rest of the World, and it is a serious crime in specific contexts (e.g., in drug-impaired driving).

[5] Chronic intranasal usage can degrade the cartilage separating the nostrils (the nasal septum), which can eventually lead to its complete disappearance, a condition known as Cocaine-Induced Midline Destructive Lesions (CIMDL).

Individuals with cocaine overdose should be transported immediately to the nearest emergency department, preferably by ambulance in case cardiac arrest occurs en route.

According to the National Institute on Drug Abuse, approximately 14,600 deaths occurred in the US in 2017 due to an overdose where cocaine was somehow involved in any capacity, defined or undefined.

[10] Because of the increase in heart rate, cocaine users can be prone to elevated body temperatures, tremors, chest pains, and subject to nausea and vomiting.

Physiological changes caused by cocaine withdrawal include vivid and unpleasant dreams, insomnia, hypersomnia, anger, increased appetite, weight gain, psychomotor retardation, agitation, depression, and anxiety.

Cocaine's acute effect in the central nervous system is to raise the amount of dopamine and serotonin in the nucleus accumbens (the pleasure center in the brain).

Cocaine acts like a class I antiarrhythmic agent by blocking sodium and potassium channels, in a similar way of local anesthetics such as lidocaine and interferes with action potential propagation.

[29] The alpha-2 agonist dexmedetomidine may also be useful for agitation, but effects on heart rate and blood pressure are variable based on several studies and case reports.

[29] Nitric-oxide mediated vasodilators, such as nitroglycerin and nitroprusside, are effective at lowering blood pressure and reversing coronary arterial vasoconstriction, but not heart rate.

The phenomenon of "unopposed alpha-stimulation," in which blood pressure increases or coronary artery vasoconstriction worsens after blockade of beta-2 vasodilation in people using cocaine, is controversial.

[36][37] This rarely-encountered and unpredictable adverse effect has resulted in some clinicians advocating for an absolute contraindication of all beta-blockers, including specific, non-specific, and mixed.

[38] Many clinicians have disregarded this dogma and administer beta-blockers for cocaine-related chest pain and acute coronary syndrome, especially when there is demand ischemia from uncontrolled tachycardia.

[39][40][41][42][43] Of the 1,744 people in the aforementioned systematic review,[29] only 7 adverse events were from putative cases of "unopposed alpha-stimulation" due to propranolol (n=3), esmolol (n=3), and metoprolol (n=1).

[44][45][46][47][48] Some detractors of beta-blockers for cocaine-induced chest pain have cited minimal acute mortality and the short half-life of the medication, making it unnecessary to aggressively treat any associated tachycardia and hypertension.

[38][49] However, the long-term effect of cocaine use and development of heart failure, with early mortality, high morbidity, and tremendous demand on hospital utilization should be taken under consideration.

[50][51][52] Calcium channel blockers may also be used to treat hypertension and coronary arterial vasoconstriction,[53] but fail to lower tachycardia based on all cocaine-related studies.