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Published on: April 28, 2020
Severe carvedilol toxicity without overdose - caution in cirrhosis
Satish Maharaj1, Karan Seegobin1, Julio Perez-Downes1
1Department of Internal Medicine, University of Florida College of Medicine, 4th Fl. LRC Building, 653 W 8th St, Jacksonville, Fl 32209 USA.
Insights
Patients with cirrhosis may experience carvedilol toxicity even at standard doses. Early recognition of this beta blocker toxicity and prompt treatment with glucagon are crucial for improved outcomes in this at-risk population.
Area of Science:
- Cardiology
- Hepatology
- Clinical Pharmacology
Background:
- Carvedilol is increasingly prescribed for portal hypertension in patients with cirrhosis.
- Despite hepatic metabolism, no specific dosage adjustments exist for mild to moderate hepatic impairment.
- Carvedilol offers improved outcomes in variceal bleeding and hepatic decompensation compared to other treatments.
Observation:
- A case of cardiogenic shock occurred in a patient with cirrhosis after a 25 mg oral dose of carvedilol.
- The event was diagnosed as carvedilol toxicity based on clinical toxidrome recognition, not overdose.
- The patient recovered after treatment with a glucagon bolus and infusion.
Findings:
- Patients with cirrhosis are a high-risk group for beta blocker toxicity.
- The standard carvedilol toxicity threshold of 50 mg is not applicable to patients with cirrhosis.
- Glucagon is an effective antidote for carvedilol-induced toxicity.
Implications:
- Healthcare providers must recognize the clinical toxidrome of carvedilol toxicity in cirrhotic patients.
- Hospitals should ensure glucagon is available for treating carvedilol toxicity in this population.
- Dose adjustment and slow titration of carvedilol are recommended for patients with cirrhosis.
Background:
Carvedilol is used in the management of hypertension, ischemic heart disease, heart failure and most recently, portal hypertension. It has been associated with improved outcomes regarding variceal bleeding, hepatic decompensation and death when compared to propranolol and endoscopic band ligation. The main cause of portal hypertension is cirrhosis and therefore carvedilol is increasingly used in these patients. Due to its extensive hepatic metabolism, carvedilol is contraindicated in severe hepatic impairment. However, there are no dosage adjustments in the manufacturer's labelling for mild to moderate hepatic impairment.
Case Presentation:
We present a case of cardiogenic shock that occurred after carvedilol 25 mg orally was administered to a patient with cirrhosis. As there was no overdose, the diagnosis was based on clinical recognition of the toxidrome. The patient was successfully treated with glucagon 5 mg bolus followed by infusion.
Conclusions:
Patients with cirrhosis represent a special at-risk group for beta blocker toxicity. The typical threshold for carvedilol toxicity in overdose is 50 mg but in patients with cirrhosis this is not applicable. Nurses and physicians need to recognize the toxidrome early. Hospitals where carvedilol is used in patients with cirrhosis should have glucagon in formulary at doses to treat toxicity (bolus and infusion). Finally, dose adjustment and slow uptitration of carvedilol in cirrhosis is recommended.
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