Effects of Epinephrine on PVR and SVR
Epinephrine has dose-dependent effects on pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR), with low doses decreasing SVR while higher doses increase both SVR and PVR. 1
Dose-Dependent Hemodynamic Effects
Low-Dose Epinephrine (<0.3 mcg/kg/min)
- Predominantly β-adrenergic effects 2:
- Decreased SVR due to β2-mediated vasodilation
- Increased cardiac output
- Minimal effect or slight decrease in PVR
- Positive inotropic and chronotropic effects
High-Dose Epinephrine (>0.3 mcg/kg/min)
- Predominantly α-adrenergic effects 2, 1:
- Increased SVR due to α1-mediated peripheral vasoconstriction
- Increased PVR
- Elevated systemic and pulmonary arterial pressures
Mechanism of Action
Epinephrine acts on both α- and β-adrenergic receptors throughout the vasculature 1:
β2 effects (predominant at low doses):
- Vasodilation in skeletal muscle beds
- Decreased peripheral resistance
- Increased venous return
α1 effects (predominant at higher doses):
- Vasoconstriction in most vascular beds including renal, splanchnic, mucosal, skin, and pulmonary circulation
- Increased arterial pressure
- Increased afterload on both ventricles
Clinical Implications
Pulmonary Hypertension Considerations
In patients with pulmonary hypertension, epinephrine can worsen pulmonary vascular resistance, especially at higher doses 2. The 2019 ESC guidelines note that PE-induced vasoconstriction is mediated by the release of thromboxane A2 and serotonin, which contributes to increased PVR 2. Epinephrine can exacerbate this effect.
Critical Care Applications
When managing critically ill pulmonary arterial hypertension (PAH) patients, a major guideline principle is to maintain SVR greater than PVR to prevent right ventricular ischemia 2. While epinephrine is listed among inotropes with "neutral or beneficial effects on PVR," this is likely true only at lower doses and in specific clinical contexts 2.
Vascular Supersensitivity
Research has demonstrated that in certain conditions, such as systemic hypertension, there may be pulmonary vascular supersensitivity to catecholamines, with epinephrine causing significant increases in PVR rather than the vasodilation seen in normotensive individuals 3.
Practical Recommendations
When using epinephrine in clinical practice:
Titrate carefully: Start with low doses (<0.3 mcg/kg/min) when increased cardiac output with minimal vasoconstriction is desired 2
Monitor both systemic and pulmonary hemodynamics: Particularly in patients with pre-existing pulmonary hypertension or right ventricular dysfunction 2
Consider alternatives: In patients with severe pulmonary hypertension, consider agents like inhaled nitric oxide that selectively decrease PVR without affecting SVR 2, 4
Be aware of combined effects: When epinephrine is used with other vasopressors or in hypoxic conditions, the effects on PVR may be additive 4
Conclusion
The effects of epinephrine on vascular resistance are dose-dependent and can vary based on the patient's underlying condition. At low doses, epinephrine primarily decreases SVR while at higher doses, it increases both SVR and PVR through α-adrenergic vasoconstriction.