Calcium channel antagonists (CCAs) are commonly used medications, prescribed for a myriad of disorders, including hypertension, angina, pulmonary hypertension, migraine prophylaxis, and diffuse esophageal spasm [1,2]. The therapeutic mechanism of CCAs involves inhibition of calcium ion influx through voltage-gated L-type calcium channels in both cardiac and vascular smooth muscle cells [4]. Dihydropyridine CCAs primarily target vascular channels, whereas non-dihydropyridines are more selective to myocardial calcium channels [4]. Clinical signs and symptoms from CCA toxicity are a direct effect of their therapeutic effects on the cardiovascular system, with hypotension being the most frequent sign. In addition, sinus bradycardia, reflex tachycardia, and varying degrees of atrioventricular (AV) block can manifest [4]. In severe cases, both non-dihydropyridine and dihydropyridine CCAs lose their selectivity and may present with a combination of profound distributive and cardiogenic shock [4]. This pathophysiology can ultimately result in cardiovascular collapse and cardiac arrest [4,5].

Treatment of CCA toxicity is complex, with therapies having significant adverse effects. Hyperinsulinemia euglycemia (HIE) therapy acts as an inotrope through proposed improved energy utilization, but can also induce hypoglycemia, hypokalemia, volume overload, arterial dilation, and worsening distributive shock [4]. Other therapies include nitric oxide scavengers and ECMO [6,7]. As CCA poisoning can produce multiple shock phenotypes, identifying the predominant form is essential to guide therapy selection. This assessment is particularly important, as each intervention carries distinct risks and potential adverse effects, and treatment directed at one shock type, such as fluids for distributive shock, may in fact be detrimental if applied to another, such as cardiogenic shock. Ultrasound can be a useful tool in assessing shock states in cardiovascular drug overdose.

Point-of-care ultrasound (POCUS) plays a crucial role in diagnosing and treating critically ill patients, providing real-time assessment of interventions. POCUS can be easily adapted to the management of CCA overdose by its rapid assessment of myocardial function [8]. Measurement of left ventricular outflow tract velocity time integral (VTI) and mitral valve end-point septal separation (EPSS) offer objective surrogate markers of cardiac output and ejection fraction (EF) [9]. These variables allow POCUS to quantify the improvement, or lack thereof, in cardiac function following therapeutic interventions. POCUS can also be used to estimate the inferior vena cava collapsibility index, a surrogate intravascular volume status and central venous pressure [10]. The American College of Cardiology, American Heart Association, and the Heart Rhythm Society guidelines support the use of hemodynamic monitoring, such as point-of-care echocardiography, in the management of calcium channel antagonist overdoses [11]. We report three cases of CCA overdose in which POCUS-guided hemodynamic assessment enabled precise characterization of shock type and facilitated accurate evaluation of patient responsiveness to antidotal and vasopressor interventions.