Approach Considerations

Tests to order in patients with suspected calcium channel blocker toxicity include glucose, potassium, bicarbonate, lactate, and calcium levels and an electrocardiogram (ECG). Measurement of arterial blood gases should be considered in patients with significant toxicity, to determine the acid-base status and respiratory function. Lactate levels should be considered in all hypotensive patients.

Abnormal findings may include hyperglycemia, hypokalemia, and a decreased serum bicarbonate level secondary to lactic acidosis. The calcium level is used as a baseline before administering intravenous calcium; however, patients with severe poisoning may require calcium therapy before the value becomes available.

Foley catheter placement may be indicated to monitor urine output in severely poisoned patients.

In patients who present to the emergency department (ED) after a suicide attempt, as well as those with a history of co-ingestion, laboratory tests should also include the following:

Serum aspirin level
Serum acetaminophen level
Urine toxicology - Results may suggest significant co-ingestants such as opiates
Cardiac biomarkers, such as troponin I, may help differentiate drug-induced bradycardia from ischemic causes

Glucose levels

Calcium channel blocker (CCB) overdose can result in hyperglycemia from impaired insulin release. Hyperglycemia can help distinguish CCB toxicity from beta-blocker toxicity, which produces a very similar clinical picture but often lowers the glucose level.

Levine et al retrospectively analyzed 40 nondihydropyridine overdoses and found that the severity of toxicity correlated directly with the degree of hyperglycemia. For patients requiring temporary pacemaker placement or vasopressor support compared with those who did not, median initial serum glucose concentrations were 188 mg/dL and 129 mg/dL, respectively. The median peak serum glucose concentrations for those 2 groups were 364 mg/dL and 145 mg/dL, respectively.^[22]

Electrocardiography

An ECG should be performed in all patients who present to the ED who may have ingested any cardiac medication. Toxicity from calcium channel blockers may manifest as any of the following:

Bradycardia
Tachycardia, reflex secondary to vasodilation
First-, second-, or third-degree atrioventricular (AV) block
Any type of bundle-branch block
Nonspecific ST-T wave changes

The ECG can also be used to evaluate for signs of digitalis toxicity and tricyclic antidepressant (TCA) toxicity. Blockade of cardiac myocyte fast sodium channels by TCAs results in a widened QRS complex and a positive deflection in the augmented voltage unipolar right arm lead (aVR) in the terminal 40 microseconds of the complex, noted as an positive R wave in aVR greater than 3 mm. Sodium channel blockade can rapidly progress to malignant dysrhythmias if left untreated.

Imaging Studies

A chest radiograph may be helpful to determine heart size and the presence or absence of congestive heart failure. In patients with congestive heart failure, aggressive fluid boluses to treat hypotension may exacerbate heart failure or cause acute pulmonary edema.

Cardiac echocardiography may be needed to help distinguish causes of refractory hypotension from vasodilation versus cardiac pump failure.

If bowel obstruction is suspected, abdominal radiography is recommended. Color-flow vascular ultrasonography of the intra-abdominal arterial supply may confirm bowel infarction.

Treatment & Management

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Media Gallery

Calcium channel blocker; diltiazem.

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Author

B Zane Horowitz, MD, FACMT Professor, Department of Emergency Medicine, Oregon Health and Sciences University School of Medicine; Medical Director, Oregon Poison Center; Medical Director, Alaska Poison Control System

B Zane Horowitz, MD, FACMT is a member of the following medical societies: American College of Medical Toxicology

Disclosure: Nothing to disclose.

Coauthor(s)

Derrick Lung, MD, MPH, FACEP, FACMT Physician, Department of Emergency Medicine, San Mateo Medical Center

Derrick Lung, MD, MPH, FACEP, FACMT is a member of the following medical societies: American College of Emergency Physicians, American College of Medical Toxicology

Disclosure: Nothing to disclose.

Chief Editor

Michael A Miller, MD Clinical Professor of Emergency Medicine, Medical Toxicologist, Department of Emergency Medicine, Texas A&M Health Sciences Center; CHRISTUS Spohn Emergency Medicine Residency Program

Michael A Miller, MD is a member of the following medical societies: American College of Medical Toxicology

Disclosure: Nothing to disclose.

Acknowledgements

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society