10.10 Substance Use, Withdrawal and Cardiac Effects

Cocaine and Methamphetamine

Test-plan item II.G.1 is dominated by stimulants, because cocaine is a leading cause of drug-related chest pain in adults under 45 and because its management contradicts the reflexes of a cardiac nurse.

Mechanism — Four Simultaneous Insults

1. Blockade of norepinephrine, dopamine and serotonin reuptake at the presynaptic terminal, producing a catecholamine flood: tachycardia, hypertension, agitation, mydriasis, hyperthermia.
2. Alpha-1 mediated coronary vasoconstriction and vasospasm, reducing supply at the moment demand peaks. Spasm can occur in angiographically normal arteries.
3. Enhanced platelet aggregation and thromboxane production plus accelerated atherosclerosis — chronic users develop premature obstructive coronary disease and true thrombotic occlusion.
4. Direct sodium-channel blockade (a class I antiarrhythmic effect) widening the QRS, plus potassium-channel blockade prolonging the QT.

The risk of myocardial infarction is roughly 24 times baseline in the first hour after use and remains elevated for hours; cocaine's half-life is short (about 45–90 minutes) but the metabolites benzoylecgonine and cocaethylene (formed when cocaine and alcohol are combined) prolong vasospasm for many hours, which is why chest pain can present long after the high has faded.

Presentations to recognize: cocaine-associated chest pain (most patients have non-ischemic causes, but 5–6% are having a true MI), STEMI in a young patient, cocaine cardiomyopathy (dilated, from repeated catecholamine injury and tachycardia), aortic dissection from the acute pressure surge, ventricular arrhythmia, seizure, intracerebral hemorrhage, hyperthermia with rhabdomyolysis, and pneumomediastinum from crack inhalation. Levamisole, a common adulterant, causes agranulocytosis and a retiform purpuric vasculitis.

Management — The Single Highest-Yield Rule

Reperfusion for cocaine STEMI follows standard pathways with primary PCI preferred; thrombolysis carries added hemorrhagic risk in an uncontrolled hypertensive patient and does not address spasm.

Methamphetamine produces the same catecholamine syndrome with a much longer half-life (about 10–12 hours), so agitation, hypertension and hyperthermia persist far longer. It is a leading cause of methamphetamine-associated cardiomyopathy in young adults (often severely reduced EF with a real chance of recovery on abstinence) and of drug-induced pulmonary arterial hypertension. Management principles mirror cocaine: benzodiazepines, cooling, vasodilators, and hydration for rhabdomyolysis.

Alcohol

Chronic cardiac effects:

• Alcoholic cardiomyopathy — dilated cardiomyopathy after sustained heavy intake (classically more than about 80 g of ethanol daily for over 5 years). It can improve substantially with abstinence, which makes the conversation a therapeutic intervention.
• Holiday heart syndrome — new atrial fibrillation or other supraventricular arrhythmia after a binge, often in a structurally normal heart, typically converting spontaneously within 24 hours. Alcohol also drives recurrent AF in established patients, and reduction is a guideline-endorsed rhythm-control strategy.
• Hypertension — alcohol is one of the most common reversible contributors to resistant hypertension.
• Wet beriberi — thiamine deficiency causing high-output heart failure with warm extremities, wide pulse pressure, peripheral edema and lactic acidosis. Give thiamine 100–500 mg IV before or with any glucose load; giving dextrose first can precipitate Wernicke encephalopathy.

Withdrawal Timeline

Assessment and treatment. The CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol, revised) scores 10 items to a maximum of 67; treatment is generally triggered at 8–10 or above, with scores above 15–20 indicating severe withdrawal. Symptom-triggered dosing — reassess and dose only when the score exceeds threshold — reduces total benzodiazepine exposure and shortens withdrawal versus fixed schedules, and is the preferred approach in a patient who can be reliably assessed. The CIWA-Ar is invalid in an intubated, sedated or non-communicative patient; use a benzodiazepine-based protocol with an objective sedation scale instead.

• Benzodiazepines are the only class proven to prevent withdrawal seizures and delirium. Longer-acting agents (diazepam, chlordiazepoxide) give a smoother taper; lorazepam, oxazepam and temazepam are preferred in hepatic impairment and in the elderly because they undergo glucuronidation only, with no oxidative metabolism.
• Phenobarbital is an effective adjunct or alternative in benzodiazepine-refractory withdrawal.
• Dexmedetomidine blunts the sympathetic surge (useful when tachycardia and hypertension are threatening a fresh graft or stent) but is an adjunct only — it does not prevent seizures or delirium and must not replace benzodiazepines.
• Add thiamine, folate, magnesium and potassium; hypomagnesemia is nearly universal and lowers the seizure threshold.

Why this matters in a cardiac bed. Withdrawal typically peaks on hospital day 2–4, which is exactly when the patient is 48 hours post-PCI or post-CABG. The autonomic surge produces tachycardia and hypertension that increase myocardial oxygen demand, stress fresh anastomoses and suture lines, precipitate post-operative atrial fibrillation, raise bleeding risk, and cause the agitated patient to pull lines, chest tubes and pacing wires. Alcohol withdrawal is one of the leading contributors to post-cardiotomy delirium. Ask about alcohol on admission — before the elective case, not on day 3.

Opioids

Overdose recognition rests on the triad of miosis, respiratory depression and depressed level of consciousness, with bradypnea preceding hypoxemia. Cardiac consequences follow the hypoxemia: bradycardia, hypotension, arrhythmia and hypoxic arrest. Because opioid arrest is respiratory in origin, ventilation and oxygenation are the highest priority, before or alongside the antidote.

Naloxone dosing is a titration, not a bolus. In a patient with any likelihood of opioid dependence, give 0.04–0.4 mg IV and repeat every 2–3 minutes, titrating to adequate respirations and not to full alertness; the intranasal formulation is 2–4 mg per spray, and intramuscular dosing is used when no line is available. A full 2 mg push in a dependent patient produces precipitated withdrawal: a violent catecholamine surge with hypertension, tachycardia, vomiting and aspiration risk, agitation that is dangerous in a post-procedure patient, and — most importantly for a cardiac unit — flash (non-cardiogenic) pulmonary edema from a combination of catecholamine surge and negative intrathoracic pressure against a closed glottis. In a patient with active ischemia or a fresh stent, that surge can cause reinfarction.

Naloxone's half-life is 30–90 minutes, shorter than most opioids and far shorter than methadone or many illicit fentanyl analogs, so re-sedation is expected. Patients need continuous monitoring for at least 2–4 hours after the last dose, and repeat dosing or a continuous infusion (commonly two-thirds of the effective waking dose given hourly) for long-acting agents.

• Methadone causes dose-dependent QT prolongation and torsades through hERG potassium-channel blockade. Obtain a baseline ECG, monitor the QTc, correct potassium and magnesium, and review co-administered QT-prolonging drugs; a QTc above 500 ms should prompt discussion of dose reduction or a change of agent.
• Buprenorphine should generally be continued, not stopped, through a cardiac admission and through surgery; stopping it destabilizes the patient without improving analgesia. Because of its very high mu-receptor affinity and partial agonism, breakthrough pain requires higher doses of a full agonist and multimodal analgesia, and this needs to be planned rather than improvised.
• Fentanyl analogs dominate the illicit supply and may require repeated or larger naloxone doses, and xylazine, an alpha-2 agonist adulterant, causes sedation and necrotic wounds and is not reversed by naloxone — a patient who remains sedated with restored respirations after naloxone may have xylazine on board.

Other Cardiotoxic Agents

• Synthetic cannabinoids (K2, Spice) — far more cardiotoxic than cannabis; associated with myocardial infarction in young users, tachyarrhythmia, hyperthermia, seizures and acute kidney injury; not detected on routine toxicology screens.
• Energy drinks and high-dose caffeine — supraventricular and ventricular ectopy, hypertension, and QT effects, especially when combined with alcohol or stimulants.
• Anabolic-androgenic steroids — concentric left ventricular hypertrophy, reduced ejection fraction and diastolic dysfunction, premature coronary disease from a markedly lowered HDL, hypertension, polycythemia raising thrombotic risk, and increased arrhythmia. Ask young patients with unexplained cardiomyopathy about supplements.
• Injection drug use is the dominant driver of right-sided infective endocarditis — most often the tricuspid valve with Staphylococcus aureus — presenting with fever, a new tricuspid regurgitation murmur, and septic pulmonary emboli appearing as multiple peripheral nodular or cavitating lung lesions with pleuritic chest pain and hypoxemia rather than the systemic embolic phenomena of left-sided disease. It brings long-course IV antibiotics, which raises the difficult question of durable venous access in a person with active use, and it recurs when the underlying substance use disorder is untreated.
• Nicotine. Smoking cessation after myocardial infarction is one of the most powerful secondary prevention measures available, reducing mortality by roughly a third. Nicotine replacement therapy is safe in stable cardiovascular disease, and varenicline was shown in the EVITA trial to be effective and not to increase cardiovascular events when started in-hospital after acute coronary syndrome; bupropion is an alternative but is avoided in seizure risk. The historic reluctance to start cessation pharmacotherapy on a cardiac unit is not evidence-based, and the admission is the highest-yield teachable moment the patient will ever have.

Screening, Communication and Harm Reduction

CMC questions land on nursing judgment, so know the workflow:

• Screen everyone on admission, not selectively. Use validated tools — AUDIT-C for alcohol, a single-question screen for drug use, or an SBIRT (Screening, Brief Intervention, Referral to Treatment) framework — and document the last use, amount and route, which is what predicts the withdrawal clock.
• Anticipate withdrawal before it starts. Initiate a CIWA-Ar or COWS (Clinical Opiate Withdrawal Scale) protocol on admission for anyone at risk rather than reacting on day 3.
• Language matters and is testable. Use "person with a substance use disorder," "person who uses drugs," and "positive" or "negative" toxicology — not "addict," "abuser," "clean" or "dirty." Stigmatizing language measurably reduces the quality of care patients receive and makes them withhold the history you need to keep them safe.
• Treat pain. Undertreating pain in a patient with opioid use disorder is both a care failure and a driver of withdrawal-related sympathetic stress. Use multimodal analgesia and involve addiction medicine.
• Harm reduction at discharge: prescribe or dispense take-home naloxone and teach the patient and family to use it, offer medication for opioid use disorder (buprenorphine or methadone) or a warm handoff to a program, discuss never using alone, provide sterile-injection and wound-care education for people who will continue to inject, and offer hepatitis and HIV testing.
• Involve the patient in the plan. Abstinence-only framing at discharge from a cardiac unit predicts readmission; a realistic plan with an addiction consultation, medication, and follow-up predicts survival.