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 and dangerous 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) in these patients due to 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 can cause cardiopulmonary collapse with little hope of adequate ventilation or regaining spontaneous circulation. The collapse is due to positive pressure ventilation causing an increase in intrathoracic pressure that reduce preload and therefore CO. Also, any transient hypoxemia that occurs during intubation will further constrict the pulmonary vasculature and worsen CO. And, as we all know, sedatives, narcotics, and anxiolytics can worsen respiratory drive and result in hypoventilation.
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. Diuretics may improve RV function that results from LV failure by reducing preload, but unfortunately in these patients, decreased preload also has the potential to worsen CO. In addition, diuresis may not the most effective treatment, because these effects may not occur for hours. (If you’ve stabilized your patient in the ED, you don’t want to potentially cause hemodynamic decompensation down the road.) When selecting vasopressors, consider the etiologies of pulmonary hypertension. Vasopressin may be the ideal pressor to use for group 1 patients. For groups 2-5, which encompass anything except primary pulmonary hypertension, norepinephrine is first-line.
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 reinitiated 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 these patients, this is a possible life-prolonging therapy until more definitive intervention is available.
- 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 may be a good choice for group 1.
- Norepinephrine is first line in groups 2-5. Its main benefits is that it helps maintain coronary perfusion, which may be compromised with RV dilatation. It can slightly increase inotropy but also unfortunately has slight alpha-receptor stimulation in the pulmonary vasculature. This will worsen the pulmonary hypertension.
- Phenylephrine should be avoided in pulmonary hypertension because it increases pulmonary vascular resistance.
- Dobutamine increases tachycardia and decreases systemic vascular resistance causing hypotension. It is a poor choice as a single agent.
- 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.
- 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 are useful for group 1, and maybe 4 and 5.
- 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 a first-line therapy for a patient with respiratory distress.
- 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.
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Wilcox, Susan R. et al. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine. Annals of Emergency Medicine. Volume 66, Issue 6, 619 – 628.
Edited by Dr. deSouza
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