From the Guidelines
In patients with severe pulmonary hypertension and low ejection fraction, vasopressin (AVP) is a valuable adjunctive agent to norepinephrine, which is generally considered the preferred first-line vasopressor. The selection of inotropes and vasopressors in these patients is challenging, and the goal is to maintain systemic vascular resistance (SVR) greater than pulmonary vascular resistance (PVR) to avoid right ventricular ischemia 1. Key considerations for vasopressor therapy in this context include:
- Starting norepinephrine at 0.01-0.03 mcg/kg/min and titrating to maintain adequate systemic perfusion while minimizing pulmonary vascular resistance
- Adding vasopressin at 0.01-0.04 units/min when norepinephrine alone is insufficient or to reduce norepinephrine requirements
- Considering dobutamine (2.5-10 mcg/kg/min) for inotropic support if needed
- Avoiding epinephrine and high-dose dopamine due to their potential to significantly increase pulmonary vascular resistance Careful hemodynamic monitoring is essential during vasopressor therapy, with attention to maintaining adequate right ventricular perfusion pressure while avoiding excessive pulmonary vasoconstriction that could worsen right heart failure 1. Inhaled nitric oxide (iNO) may also be beneficial in reducing PVR and improving cardiac output in these patients, particularly in those who are post-coronary bypass surgery or valve replacement 1. Overall, the management of patients with severe pulmonary hypertension and low ejection fraction requires a careful and individualized approach, taking into account the complex pathophysiology of these conditions and the potential risks and benefits of different therapeutic strategies 1.
From the FDA Drug Label
12 CLINICAL PHARMACOLOGY
12.1 Mechanism of Action Vasopressin causes vasoconstriction by binding to V1 receptors on vascular smooth muscle coupled to the Gq/11-phospholipase C-phosphatidyl-inositol-triphosphate pathway, resulting in the release of intracellular calcium.
- 2 Pharmacodynamics At therapeutic doses exogenous vasopressin elicits a vasoconstrictive effect in most vascular beds including the splanchnic, renal and cutaneous circulation.
The best vasopressor in patients with severe pulmonary hypertension and low ejection fraction (EF) is not explicitly stated in the provided drug label.
- Vasopressin tends to decrease heart rate and cardiac output, which may be a concern in patients with low EF.
- The label does not provide direct information on the use of vasopressin in patients with severe pulmonary hypertension and low EF. 2
From the Research
Vasopressor Options for Severe Pulmonary Hypertension with Low EF
- The choice of vasopressor in patients with severe pulmonary hypertension and low ejection fraction (EF) is crucial, as it can significantly impact patient outcomes 3, 4, 5, 6, 7.
- Arginine vasopressin (AVP) has been studied as a potential vasopressor in this context, with some studies suggesting its effectiveness in increasing systemic blood pressure while minimizing effects on pulmonary arterial pressure 3, 5, 7.
- However, other studies have raised concerns about the use of AVP in patients with compromised right ventricular function, as it may cause pulmonary vascular constriction and negative inotropic effects 4.
- Phenylephrine and epinephrine are alternative vasopressors that have been studied in patients with pulmonary hypertension, but their effects on systemic and pulmonary arterial pressure may vary 3, 4.
- The optimal dosing strategy for vasopressors in patients with severe pulmonary hypertension and low EF remains unclear and may require individualized approaches 3, 6.
Key Considerations
- The use of vasopressors in patients with severe pulmonary hypertension and low EF requires careful consideration of the underlying physiology and hemodynamics 6.
- A comprehensive understanding of the effects of different vasopressors on systemic and pulmonary arterial pressure is essential for making informed treatment decisions 3, 4, 5, 7.
- Further studies are needed to define the optimal use of vasopressors in this patient population and to identify the most effective treatment strategies 3, 6.