From the FDA Drug Label
Desglymidodrine does not stimulate cardiac beta-adrenergic receptors Midodrine has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.
Midodrine does not directly increase cardiac demand as it does not stimulate cardiac beta-adrenergic receptors and has no significant effect on pulse rates in patients with autonomic failure 1.
From the Research
No, midodrine does not increase cardiac demand. Midodrine is an alpha-1 adrenergic receptor agonist that primarily causes peripheral vasoconstriction, which increases blood pressure by constricting blood vessels. Unlike medications that stimulate beta receptors (such as dobutamine or epinephrine), midodrine does not directly increase heart rate, contractility, or cardiac output. In fact, through a reflex mechanism called the baroreceptor reflex, the increase in blood pressure from midodrine often leads to a slight decrease in heart rate. This makes midodrine particularly useful for conditions like orthostatic hypotension, where patients need blood pressure support without adding cardiac stress. The medication is typically dosed at 2.5-10 mg three times daily, with the last dose taken at least 4 hours before bedtime to avoid supine hypertension. Midodrine works by converting to its active metabolite, desglymidodrine, which provides the alpha-1 agonist effects that increase vascular tone without directly affecting the workload of the heart 2.
Key Points
- Midodrine is an alpha-1 adrenergic receptor agonist that increases blood pressure through peripheral vasoconstriction
- It does not directly increase heart rate, contractility, or cardiac output
- Midodrine is useful for conditions like orthostatic hypotension, where patients need blood pressure support without adding cardiac stress
- The medication is typically dosed at 2.5-10 mg three times daily, with the last dose taken at least 4 hours before bedtime to avoid supine hypertension
- Midodrine works by converting to its active metabolite, desglymidodrine, which provides the alpha-1 agonist effects that increase vascular tone without directly affecting the workload of the heart 2
Clinical Considerations
- Midodrine may be used off-label in patients with heart failure with reduced ejection fraction (HFrEF) and symptomatic hypotension to allow optimization of medical therapy 2
- Increasing the dosing frequency of midodrine to every 6 hours may optimize its pharmacokinetic profile without compromising safety 3
- Midodrine is well tolerated, with the most commonly reported adverse events being piloerection, pruritus, paraesthesias, urinary retention, and chills 4