Vasopressors and Pulmonary Vasoconstriction
Sympathomimetic vasopressors (norepinephrine, epinephrine, dopamine, phenylephrine) cause pulmonary vasoconstriction, while vasopressin does not affect pulmonary vascular resistance and is the preferred vasopressor in patients with pulmonary hypertension or right heart failure. 1
Differential Effects of Vasopressors on Pulmonary Circulation
Sympathomimetic Vasopressors
- Norepinephrine, epinephrine, phenylephrine, and metaraminol cause concentration-dependent vasoconstriction in both systemic and pulmonary arteries with similar potency 1
- These agents increase pulmonary artery pressure and pulmonary vascular resistance 2
- The pulmonary vasoconstriction occurs through:
- Direct α-adrenergic stimulation of pulmonary vascular smooth muscle
- Redistribution of blood volume from systemic to pulmonary circulation 3
Vasopressin
- Vasopressin is a potent vasoconstrictor in systemic circulation but has minimal to no effect on pulmonary vascular tone 1, 4
- It decreases the pulmonary-to-systemic vascular resistance ratio, unlike catecholamine vasopressors 5
- This selective effect makes vasopressin particularly valuable in patients with:
- Pulmonary hypertension
- Right ventricular failure
- Conditions requiring vasopressor support without worsening pulmonary pressures 2
Clinical Implications
Right Ventricular Dysfunction
- In right ventricular failure, excessive pulmonary vasoconstriction can worsen RV function by increasing afterload 2
- The traditional concept that "the RV is preload dependent" often leads to inappropriate volume loading, which may worsen RV dilation and tricuspid regurgitation 2
- For patients with RV dysfunction requiring vasopressor support:
Pulmonary Hypertension
- In pulmonary hypertension, sympathomimetic vasopressors can trigger pulmonary hypertensive crises 2
- These crises are accompanied by right-sided heart failure, systemic hypotension, and myocardial ischemia 2
- Management strategies include:
Mechanism of Vasopressor-Induced Pulmonary Hypertension
Recent research reveals that vasopressor-induced pulmonary hypertension occurs through two mechanisms:
Blood Volume Redistribution: Sympathomimetic vasopressors cause redistribution of blood from systemic to pulmonary circulation, increasing pulmonary blood volume and pressures 3
- This creates a hemodynamic pattern similar to left heart disease
- The trans-pulmonary gradient and pulmonary vascular resistance may remain stable despite increased pulmonary artery pressure
Direct Vasoconstriction: Sympathomimetics cause direct pulmonary vasoconstriction, though this effect is minimal compared to the volume redistribution effect 3
Clinical Recommendations
For patients with or at risk for pulmonary hypertension: Consider vasopressin as the first-choice vasopressor when hemodynamic support is needed 1, 5
For patients with right ventricular failure: Avoid excessive fluid administration and consider early use of vasopressin rather than catecholamine vasopressors 2
For septic shock with coexisting pulmonary hypertension: Consider adding vasopressin (up to 0.03 U/min) to norepinephrine to maintain mean arterial pressure while minimizing pulmonary vasoconstriction 6
For monitoring: When using sympathomimetic vasopressors in patients with pulmonary hypertension, closely monitor pulmonary artery pressures and right ventricular function, as worsening can occur rapidly 2
Common Pitfalls and Caveats
Avoid excessive fluid administration in patients with right ventricular dysfunction receiving vasopressors, as this can worsen RV dilation and function 2
Do not assume all vasopressors have similar effects on pulmonary circulation; their effects differ significantly 1
When using catecholamine vasopressors in patients with pulmonary hypertension, consider concurrent use of pulmonary vasodilators (inhaled nitric oxide, prostacyclins, sildenafil) to counteract pulmonary vasoconstriction 2
Remember that hypoxia and acidosis can potentiate pulmonary vasoconstriction induced by vasopressors, creating a vicious cycle 2