Do steroids cause tachycardia?

Do Steroids Increase Heart Rate?

Steroids have paradoxical effects on heart rate: while oral and intravenous corticosteroids commonly cause bradycardia (slowing of heart rate) rather than tachycardia, they significantly increase the risk of atrial fibrillation (which presents with rapid irregular heart rate), and beta-2 agonist bronchodilators cause tachycardia. 1

Corticosteroids and Bradycardia

The most common acute cardiac effect of corticosteroids is bradycardia, not tachycardia:

• Bradycardia occurs with both intravenous pulse-dose steroids and standard oral doses of prednisone 2, 3, 4, 5
• This effect is dose-dependent and can occur even with standard oral prednisone doses (as low as 52 mg daily) 5
• Bradycardia typically resolves after discontinuing or reducing the steroid dose 2, 4, 5
• The mechanism involves direct increase in cellular potassium efflux, which shortens action potential duration 6

Corticosteroids and Atrial Fibrillation (Tachycardia)

While acute administration causes bradycardia, corticosteroids significantly increase the risk of atrial fibrillation, which presents with rapid heart rate:

• Current oral corticosteroid users have an odds ratio of 2.7 (1.9-3.8) for developing atrial fibrillation compared to non-users 1
• High-dose corticosteroids (≥7.5 mg prednisone equivalents) carry an odds ratio of 6.07 (3.90-9.42) for atrial fibrillation 1
• Risk is particularly elevated in patients with rheumatic, allergic, or malignant hematologic diseases (OR 7.90; 4.47-13.98) 1
• The relative risk is greatest at the beginning of therapy and with short-term use 1

Mechanisms of Atrial Fibrillation

Three primary pathways explain corticosteroid-induced atrial fibrillation 1:

1. Direct cellular effects: Increased cellular K+ efflux 1
2. Mineralocorticoid-like effects: Elevation of atrial pressures 6
3. Long-term cardiovascular damage: Promotion of atherosclerosis, diabetes mellitus, hypertension, heart failure, and ischemic heart disease 1

Beta-2 Agonist Bronchodilators and Tachycardia

Beta-2 agonists used for asthma/COPD DO cause tachycardia:

• A single dose of β2 agonists increases mean heart rate by 9.1 (5.3–12.9) beats/min 7
• The relative risk for adverse cardiovascular events, including atrial fibrillation, is 2.54 (1.59–4.05) 7
• These medications have low rates of tremor, palpitations, or tachycardia due to their specificity for β-adrenergic receptors 7

Inhaled Corticosteroids

Inhaled corticosteroids can cause tachycardia, but this is less common than with systemic steroids:

• Tachycardia and anxiety symptoms can occur, particularly at moderate to high doses 6
• Inhaled corticosteroids do not increase arrhythmia risk to the same degree as oral/IV steroids 1
• Using spacers with metered dose inhalers reduces systemic absorption and associated side effects 6

Clinical Management Recommendations

For Patients Requiring Corticosteroids:

• Use the lowest dose for the shortest period possible to minimize cardiovascular risk 1
• Target doses <7.5 mg prednisone daily when feasible 1
• Monitor heart rate and blood pressure during infusion in older patients with active cardiac conditions 4
• Young patients free of cardiac conditions can safely receive pulse-dose steroids without continuous monitoring 4

Monitoring Strategy:

• Screen for and aggressively manage hypertension, dyslipidemia, and hyperglycemia 1
• Consider cardiovascular risk assessment before initiating therapy, particularly in patients with pre-existing risk factors 1
• Hemodynamic monitoring is recommended for patients receiving more than one dose of intravenous steroid therapy, especially those with cardiac/hepatic comorbidities or taking medications with negative chronotropic effects 3

Important Caveats

• Former corticosteroid use is not associated with increased atrial fibrillation risk - the risk is present only during active use 1
• Bradycardia is self-limiting and resolves after discontinuing steroid infusion, requiring no specific treatment 4
• The cardiovascular effects must be balanced against the therapeutic benefits of controlling underlying inflammatory conditions 1