Key result
Intravenous propranolol (2 mg) reduced cardiac output by 13% in uncomplicated thyrotoxicosis and by 30% to subnormal levels in thyrotoxic cardiac failure, demonstrating deleterious effects.
Why the study?
Does intravenous propranolol alter haemodynamics in hyperthyroid patients with and without heart failure?
Does intravenous propranolol alter haemodynamics in hyperthyroid patients with and without heart failure?
Intravenous propranolol significantly depresses cardiac function in patients with thyrotoxic heart failure, indicating that beta-blockers are contraindicated in this specific population.
Haemodynamic studies were performed in 10 patients with uncomplicated thyrotoxicosis and seven with thyrotoxic cardiac failure. The cardiac output of those with uncomplicated hyperthyroidism was higher than normal at rest. After 2 mg of intravenous propranolol there was a 13% fall but the level was still higher than normal. In patients with thyrotoxic cardiac failure the resting cardiac output was normal, but it fell after propranolol by 30% to subnormal levels. In both groups there was an increase in right heart pressures and fall in the rate of increase in arterial pressure, which indicated a decrease in myocardial contractility. These results indicate that increased autonomic activity is a compensatory phenomenon in hyperthyroid heart failure and that its abolition by beta-blocking drugs has a deleterious effect on cardiac function. They are therefore contraindicated in patients with thyrotoxic heart failure.
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Hamid Ikram (1977) studied Hyperthyroidism with and without heart failure (n=17). Intravenous propranolol vs. Baseline was evaluated on Cardiac output. Intravenous propranolol (2 mg) reduced cardiac output by 13% in uncomplicated thyrotoxicosis and by 30% to subnormal levels in thyrotoxic cardiac failure, demonstrating deleterious effects.
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