The shock state from CCB overdose is characterized by hypotension from profound vascular smooth muscle relaxation with decreased left ventricular contractility and bradycardia. Patients with severe CCB poisoning typically manifest heart rates of 45 to 55 beats per minute with no evidence of sinus node depolarization on surface ECG. The metabolic acidosis is caused by lactate accumulation. Each of these manifestations can be quantified at the bedside to help gauge the severity of overdose. Transthoracic echocardiography can be performed to estimate the left ventricular ejection fraction as an index of contractile function. Arterial blood gas analysis may reveal hypoxemia. Compensatory hypocarbia can be expected as the patient hyperventilates in an effort to offset CCB-induced metabolic acidosis. The arterial base deficit and the lactate concentration can provide indexes of overall toxicity with CCB overdose. Precise cause of the lactic acidosis remains to be elucidated but likely occurs as a combination of skeletal muscle hypoperfusion with impaired oxidative metabolism and reduced hepatic lactate uptake. Lactic acidosis may be important for diagnostic and therapeutic reasons. A lactate concentration greater than 2.0 mmol/L may portend a severe overdose that will lead to hemodynamic decompensation. Also, severe lactic acidosis can itself impair heart function and metabolism, thereby potentiating the negative inotropy of CCB poisoning. As mentioned earlier, hyperkalemia also can worsen the negative inotropy of severe CCB overdose. Hyperkalemia probably develops as a result of systemic insulin resistance and acidosis.
Was this article helpful?