TABLE 1702 Key Diagnostic Features of Calcium Channel Antagonist Overdose

Other clinical manifestations of CCB toxicity stem from multiorgan hypoperfusion and inhibition of metabolic processes and may indicate impending severe shock. Physical examination (and intuition) may provide the best initial evidence of incipient severe toxicity. Most patients with significant toxicity are drowsy and asthenic. However, muscular weakness does not occur from a direct effect of CCBs on skeletal muscle excitation contraction even with massive overdoses. Mydriasis is not a key feature of CCB poisoning, although some patients do exhibit dilated pupils. Mental function is often altered, with behavior ranging from agitation to coma. Noncardiogenic pulmonary edema is sometimes seen. Hypoxemia also has been reported, presumably from intrapulmonary ventilation-perfusion mismatch. Metabolic (lactic) acidosis with hyperglycemia is described in multiple case reports and in laboratory reports. Hypokalemia is observed frequently but carries little prognostic meaning. However, hyperkalemia is an ominous finding, suggesting severe poisoning. Hypercalcemia is not caused by CCB overdose, although hypocalcemia has been reported.10

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