Sympathomimetics That Cause Tachycardia
Epinephrine, dobutamine, dopamine, and cocaine are the sympathomimetic drugs most strongly associated with tachycardia due to their β-adrenergic stimulating effects. 1
Mechanism of Tachycardia
Sympathomimetic drugs cause tachycardia through several mechanisms:
Direct β-adrenergic receptor stimulation:
- β1-receptors in the heart increase heart rate and contractility
- β2-receptors cause peripheral vasodilation (which can reflexively increase heart rate)
Indirect effects:
- Inhibition of catecholamine reuptake
- Stimulation of endogenous norepinephrine release
- Reflex tachycardia from peripheral vasodilation
Specific Sympathomimetics and Their Tachycardic Effects
Catecholamines
Epinephrine: Potent cardiac stimulant with significant β-adrenergic effects that accelerates heart rate, improves cardiac conduction, and increases cardiac output. Can cause significant tachycardia and arrhythmias, particularly at higher doses. 1, 2
Dobutamine: Relatively selective β1-adrenergic agonist that increases myocardial contractility and can decrease peripheral vascular resistance, commonly causing tachycardia. 1
Dopamine: At infusion rates of 2-15 μg/kg/min, stimulates β1-receptors causing increased myocardial contractility with significant risk of tachycardia and arrhythmias. 1
Non-Catecholamine Sympathomimetics
Cocaine: Produces sympathomimetic toxidrome marked by tachycardia through catecholamine reuptake inhibition and postsynaptic β-adrenergic receptor agonism. 1
Phenylephrine: Primarily an α1-selective adrenergic agonist with minimal β-adrenergic effects, making it the adrenergic agent least likely to produce tachycardia. 1
β2-agonists (salbutamol, terbutaline): Commonly used bronchodilators that can cause tachycardia, especially at higher doses. 1
Comparative Tachycardic Effects
| Sympathomimetic | Tachycardia Risk | Primary Mechanism |
|---|---|---|
| Epinephrine | High | Mixed α and β effects, stronger β at lower doses |
| Dobutamine | High | Predominantly β1 effects |
| Dopamine | High | Dose-dependent β1 effects at moderate doses |
| Cocaine | High | Catecholamine reuptake inhibition |
| Norepinephrine | Moderate | Predominantly α effects with some β1 |
| Phenylephrine | Low | Almost pure α-adrenergic effects |
Clinical Implications
Cardiac patients: Sympathomimetics significantly increase risk of arrhythmias in patients with congestive heart failure (odds ratio 4.0) 3
Monitoring requirements: During administration of sympathomimetics, patients should be monitored for:
- Tachycardia
- Hypertension
- Cardiac arrhythmias
- ECG changes 1
Overdose concerns: Sympathomimetic overdose can cause extreme tachycardia progressing to potentially fatal arrhythmias, including:
Special Considerations
Pregnancy: Over-the-counter sympathomimetics have been reported to cause arrhythmias during pregnancy 5
Pediatric patients: Children may be particularly sensitive to sympathomimetic effects, with reports of persistent arrhythmias following overdose 4
Priapism management: When using phenylephrine (a sympathomimetic with lower tachycardia risk) for priapism, monitoring for cardiovascular side effects including tachycardia is essential 1, 6
Pitfalls and Caveats
Reflex tachycardia: Even vasopressors like phenylephrine that don't directly stimulate β-receptors can cause reflex tachycardia through baroreceptor activation
Indirect sympathomimetics: Drugs that release endogenous catecholamines may have delayed or prolonged effects compared to direct-acting agents
Drug interactions: β-blockers may mask tachycardia from sympathomimetics but won't necessarily prevent other adverse effects
Tolerance development: Tachyphylaxis to the chronotropic effects can develop with prolonged use of some sympathomimetics
Remember that the tachycardic effects of sympathomimetics must be weighed against their therapeutic benefits in specific clinical scenarios, with appropriate monitoring and dose adjustments to minimize adverse cardiovascular effects.