C53-36 Amphetamine Induced Severe Hypokalemia Leading to Recurrent Cardiac Arrest: Clinical Challenges in Critical Care Management

Introduction While the cardiac complications of hypokalemia are well documented, there is limited literature specifically addressing hypokalemia induced by stimulant use, particularly amphetamines. We present a unique case of amphetamine-induced hypokalemia (AIH) causing recurrent cardiac arrests despite aggressive potassium repletion and intensive supportive care, highlighting the challenges in recognition and management of this life-threatening condition. Case presentation A 54-year-old male with a history of hypertension, bilateral internal carotid artery aneurysms, multiple cerebral aneurysms, and nicotine dependence presented with altered mental status. Shortly after, he suffered two episodes of cardiac arrest within minutes, requiring advanced cardiac life support to achieve return of spontaneous circulation. Following this, he developed stage C cardiogenic shock along with an idioventricular rhythm, causing severe bradycardia (20-30 beats per minute). Transcutaneous pacing was initiated, followed by transvenous pacing due to persistent instability. Lab work revealed a critically low potassium level of < 1.5 mEq/L. Urine toxicology was positive for amphetamines, supporting AIH as a likely contributor to arrhythmia and cardiac arrest. He was admitted to the intensive care unit, where he received aggressive potassium repletion, gradually increasing his serum potassium to 3.2 mEq/L over two days. Despite potassium correction and maximal vasopressor support, the patient experienced a third cardiac arrest and could not be resuscitated. Discussion AIH poses distinct management challenges compared with hypokalemia from renal or gastrointestinal losses. Because AIH results from a β2-adrenergic–mediated intracellular shift rather than total body depletion, potassium repletion may appear refractory until sympathomimetic activity subsides. Ongoing adrenergic stimulation drives potassium into cells via activation of the sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) pump, so aggressive replacement can lead to undercorrection initially and rebound hyperkalemia once adrenergic tone resolves. Notably, patients remain at risk for arrhythmias even after serum potassium improves, as hypokalemia induces persistent cellular and electrophysiological disturbances, including calcium overload, triggered activity, and altered Na+/K+-ATPase function, that may not immediately normalize with correction.Effective management also depends on controlling the underlying hyperadrenergic state. Benzodiazepines are first-line to blunt catecholamine excess, reduce agitation, and facilitate potassium normalization. In refractory cases, mixed α/β-blockers such as labetalol may be considered, while pure β-blockers are avoided to prevent unopposed α-stimulation. Because current guidelines do not specifically address stimulant-induced electrolyte disturbances, clinicians must recognize these dynamic transcellular shifts and adjust therapy accordingly. This case highlights the need for vigilance, careful titration, and adrenergic control to prevent fatal arrhythmias in amphetamine-associated hypokalemia.