Management of RV Failure and Pulmonary Hypertension

By Dr. C. Sterling M.D.

Pathophysiology of Right Ventricular Failure


The most common cause of pulmonary hypertension in the U.S. is left-sided heart failure, but many cases of pulmonary hypertension remain undocumented. Pulmonary arterial hypertension is a specific category of pulmonary hypertension and is a relatively rare disease. In the ED, we often do not consider this disease in the differential diagnosis of dyspnea. And, definitive diagnosis is often delayed as right-sided heart catheterization is required.


When resuscitating a patient in respiratory distress secondary to pulmonary hypertension, there must be a delicate balancing act to avoid right ventricle (RV) failure and hypotension. The most important concept to understand is that you cannot directly augment cardiac output (CO) due to the fixed pulmonary vascular resistance, so you must try to prevent further hypoxemia, pulmonary vascular constriction, and reductions in CO.


The approach to ventilation is complex. Our usual go-to therapies of non-invasive ventilation (NIV) and mechanical ventilation offers little hope of restoring adequate oxygenation and can cause cardiopulmonary collapse with then little chance of return of spontaneous circulation. The collapse is due to positive pressure ventilation causing an increase in intrathoracic pressure that further reduce preload and therefore CO. Also, any transient hypoxemia that occurs during intubation may further constrict the pulmonary vasculature, worsen LV filling, and reduce CO. And, as we all know, sedatives, narcotics, and anxiolytics can worsen respiratory drive and quickly result in hypoventilation.

Adapted from Wilcox et al.

Fluid resuscitation can also be tricky, because overloading the RV is the primary cause of RV failure. If you think your patient is hypovolemic, consider small fluid boluses of 250cc with careful reassessment of perfusion after each bolus. On the other hand, diuretics may improve RV function that results from LV failure, but unfortunately in these patients, decreased preload also has the potential to worsen CO. In addition, diuresis may not the most effective treatment, because the intended effects may not occur for hours. (If you’ve stabilized your patient in the ED, you don’t want to potentially cause volume depletion and further hemodynamic decompensation down the road.) When selecting vasopressors, consider the etiologies of pulmonary hypertension (Table 1). Vasopressin may be the ideal pressor to use for patients in group 1, and norepinephrine for groups 2-5 (Table 2) .

Adapted from WIlcox et al.

Most previously diagnosed patients will be on continuous pulmonary vasodilators. These should never be discontinued, because rebound pulmonary hypertension will occur. If a patient with history of pulmonary hypertension comes in with an infusion pump that has malfunctioned, this a life-threatening emergency. The infusion should restarted through new peripheral venous access, and the patient’s pulmonologist should be contacted. Finally, consider contacting the closest ECMO (extracorporeal membrane oxygenation) site early. If you can stabilize the patient for long enough, this is a possible life-prolonging therapy until more definitive intervention is available.



  1. Vasopressin may decrease pulmonary vascular resistance via nitric oxide-based mechanism; this will increase pulmonary vascular dilation and improve venous return to the heart. This would be a good choice for group 1.
  2. Norepinephrine (recommended for groups 2-5) helps maintain coronary perfusion, which may be compromised with RV dilatation. It can slightly increase inotropy but also unfortunately has some alpha-receptor stimulation in the pulmonary vasculature. This may worsen the pulmonary hypertension.
  3. Phenylephrine should be avoided in pulmonary hypertension because it increases pulmonary vascular resistance.
  4. Dobutamine increases tachycardia and decreases systemic vascular resistance, and this may result in hypotension. It is a poor choice as a single agent.


Other medications:

  1. Inhaled nitric oxide promotes vascular smooth muscle relaxation, and because it is inhaled, it is limited to ventilated regions of the lung. It decreases pulmonary artery pressure and pulmonary vascular resistance, and increases venous return to the heart. Consider this first-line therapy for a patient with pulmonary hypertension and respiratory distress.
  2. Beta blockers and calcium-channel blockers further impair right ventricular function. If patients arrive with new-onset atrial fibrillation, rhythm conversion should be strongly considered.
  3. Vasodilators can worsen ventilation-perfusion matching. Left ventricle (LV) dysfunction (group 2 patients) may have worsening pulmonary edema when the pulmonary arteries are dilated, but vasodilators may be useful for group 1, and maybe 4 and 5.
  4. Prostacyclins cause pulmonary vasodilation, decreases in pulmonary artery pressure, and pulmonary vascular resistance. Endothelin receptor antagonists increase cardiac output and decrease pulmonary artery pressure. And, phosphodiesterase-5 inhibitors block degradation of cyclic GMP, decrease pulmonary artery pressure, and increase cardiac output. This category of medications are common in outpatient regimens.


GERLACH, H., ROSSAINT, R., PAPPERT, D. and FALKE, K. J. (1993), Time-course and dose-response of nitric oxide inhalation for systemic oxygenation and pulmonary hypertension in patients with adult respiratory distress syndrome. European Journal of Clinical Investigation, 23: 499–502. doi: 10.1111/j.1365-2362.1993.tb00797.x

Krasuski RA, Warner JJ, Wang A, Harrison JK, Tapson VF, Bashore TM. Inhaled nitric oxide selectively dilates pulmonary vasculature in adult patients with pulmonary hypertension, irrespective of etiology. J Am Coll Cardiol 2000;36:2204-11.

Sim J-Y. Nitric oxide and pulmonary hypertension. Korean Journal of Anesthesiology. 2010;58(1):4-14. doi:10.4097/kjae.2010.58.1.4.

Wilcox, Susan R. et al. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine. Annals of Emergency Medicine. Volume 66, Issue 6, 619-28.

Edited by Dr. deSouza

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