A Rare Case of Amitriptyline-Induced Third-Degree Atrioventricular Block
Location
Moultrie, GA
Start Date
17-4-2026 12:00 PM
End Date
17-4-2026 1:00 PM
Description
Introduction: Cardiotoxicity, including orthostatic hypotension and cardiac conduction abnormalities, are a major concern with tricyclic antidepressants (TCA). TCAs have significant activity as antagonists at α1-, H1-, H2-, and M-receptors and block fast sodium channels in the myocardium, resulting in cardiac conduction abnormalities and potentially atrioventricular node block. Profound bradycardia is another toxic effect of tricyclic antidepressants, owing to their anticholinergic effects. TCA toxicity can result in life-threatening complications from complete heart block and prolonged QTc interval. While TCA-induced heart blocks are common, third-degree heart block is rare, with an incidence of about 0.02% to 0.04%. We present a case of amitriptyline toxicity causing complete heart block, also known as third-degree heart block, which led to profound bradycardia and acute respiratory failure.
Objective: We report the case of a 60-year-old Black male with a history of myocardial infarction, status post CABG on two occasions, and aortic valve replacement, who presented with dyspnea and bradycardia in the 30s. On exam, he was in moderate distress with labored breathing, coarse breath sounds, and sporadic crackles. Labs showed WBC of 12.8 K with left shift, hemoglobin of 11, and platelets of 149. The metabolic panel showed sodium 128 mEq/L, potassium 5.2 mEq/L, and ProBNP 5198 pg/mL, with normal kidney and liver functions and a negative troponin. Chest x-ray was negative for acute processes. EKG on admission showed a new third-degree heart block. Transthoracic echocardiogram showed a left ventricular ejection fraction of 60%.
Methods: He received 1 g of calcium gluconate, IV Lasix, glucagon, and bicarbonate, but his heart rate did not improve. A dobutamine drip was initiated, and transcutaneous pacing was started after the patient continued to be bradycardic. Amitriptyline was determined to be the cause of QT prolongation leading to third-degree heart block, and was discontinued.
Results: After the heart rate stabilized and the third-degree heart block resolved, transcutaneous pacing was discontinued. Carvedilol was started, and he was discharged with an event monitor. A permanent pacer was not inserted as the offending agent was discontinued.
Discussion: Clinicians need to examine a patient’s medication list and look for drug interactions that can increase the risk of TCA toxicity. Patients who have a history of liver failure should not be on TCA due to primary clearance through the liver. Patients who have a prior history of cardiovascular disease should be monitored carefully, as prior cardiac insult can result in an increased risk for cardiac toxicity. In addition, cocaine causes arrhythmias through its inhibition of cardiac sodium potassium channels, which can result in a prolonged QT interval. Treating tricyclic antidepressant toxicity requires sodium bicarbonate, which alkalinizes the serum, dilutes the active free tricyclic antidepressant, and corrects cardiac arrhythmias. This case highlights the importance of monitoring patients taking TCAs. Awareness of the risk factors of TCA toxicity and appropriate treatment is necessary to prevent increased mortality.
Embargo Period
5-29-2026
A Rare Case of Amitriptyline-Induced Third-Degree Atrioventricular Block
Moultrie, GA
Introduction: Cardiotoxicity, including orthostatic hypotension and cardiac conduction abnormalities, are a major concern with tricyclic antidepressants (TCA). TCAs have significant activity as antagonists at α1-, H1-, H2-, and M-receptors and block fast sodium channels in the myocardium, resulting in cardiac conduction abnormalities and potentially atrioventricular node block. Profound bradycardia is another toxic effect of tricyclic antidepressants, owing to their anticholinergic effects. TCA toxicity can result in life-threatening complications from complete heart block and prolonged QTc interval. While TCA-induced heart blocks are common, third-degree heart block is rare, with an incidence of about 0.02% to 0.04%. We present a case of amitriptyline toxicity causing complete heart block, also known as third-degree heart block, which led to profound bradycardia and acute respiratory failure.
Objective: We report the case of a 60-year-old Black male with a history of myocardial infarction, status post CABG on two occasions, and aortic valve replacement, who presented with dyspnea and bradycardia in the 30s. On exam, he was in moderate distress with labored breathing, coarse breath sounds, and sporadic crackles. Labs showed WBC of 12.8 K with left shift, hemoglobin of 11, and platelets of 149. The metabolic panel showed sodium 128 mEq/L, potassium 5.2 mEq/L, and ProBNP 5198 pg/mL, with normal kidney and liver functions and a negative troponin. Chest x-ray was negative for acute processes. EKG on admission showed a new third-degree heart block. Transthoracic echocardiogram showed a left ventricular ejection fraction of 60%.
Methods: He received 1 g of calcium gluconate, IV Lasix, glucagon, and bicarbonate, but his heart rate did not improve. A dobutamine drip was initiated, and transcutaneous pacing was started after the patient continued to be bradycardic. Amitriptyline was determined to be the cause of QT prolongation leading to third-degree heart block, and was discontinued.
Results: After the heart rate stabilized and the third-degree heart block resolved, transcutaneous pacing was discontinued. Carvedilol was started, and he was discharged with an event monitor. A permanent pacer was not inserted as the offending agent was discontinued.
Discussion: Clinicians need to examine a patient’s medication list and look for drug interactions that can increase the risk of TCA toxicity. Patients who have a history of liver failure should not be on TCA due to primary clearance through the liver. Patients who have a prior history of cardiovascular disease should be monitored carefully, as prior cardiac insult can result in an increased risk for cardiac toxicity. In addition, cocaine causes arrhythmias through its inhibition of cardiac sodium potassium channels, which can result in a prolonged QT interval. Treating tricyclic antidepressant toxicity requires sodium bicarbonate, which alkalinizes the serum, dilutes the active free tricyclic antidepressant, and corrects cardiac arrhythmias. This case highlights the importance of monitoring patients taking TCAs. Awareness of the risk factors of TCA toxicity and appropriate treatment is necessary to prevent increased mortality.