In decompensated right ventricular (RV) failure, the right ventricular wall is weak and cannot handle the pressure put upon it as easily as the left ventricle. A cautious approach to fluid management is paramount as a large fluid bolus will only increase the strain on the weakened RV, further compromising hemodynamics.
In circumstances of hypovolemia, cardiac output may benefit from small aliquots of crystalloids (250 mL) but we must be very careful to monitor the patient closely for further drops in hemodynamics [1].
Alternatively, performance of a passive leg raise with an associated increase in cardiac output measured via ETCO2 or bedside ultrasound may identify a patient as fluid responsive and can guide volume resuscitation.
Read more: Identifying right ventricular failure
Vasopressors and inotropes
So, if the administration of large fluid boluses are detrimental to the patient with acute RV failure, what are we to do? Remember that the RV is perfused in systole and diastole over the pressure gradient between the systemic blood pressure (SBP) and the RV chamber pressure (RVP).
To prevent RV ischemia, systemic hypotension must be avoided so that this pressure gradient is maintained. This creates a conundrum. How are we to increase systemic pressure without further contributing more to RV insult? The answer lies in the administration of vasopressors.
Unfortunately, many of the common vasoactive agents used to decrease systemic hypotension can non-selectively cause vasoconstriction, increasing the pulmonary vascular resistance and RV pressure. Having a thorough understanding of the different types of vasoactive agents is vitally important. Phenylephrine is a pure alpha-1 agonist, which acts on the pulmonary vasculature and increases RV afterload, so this is not a wise choice. Norepinephrine, in contrast, has been demonstrated to increase the pulmonary vascular resistance less than phenylephrine, while augmenting inotropy. Vasopressin is a good choice for use in RV failure as it is a systemic vasoconstrictor but has little effect on the pulmonary vasculature.
Inotropes like dobutamine will augment RV contractility and can have a role when other agents have failed. However, dobutamine can drop systemic vascular resistance and generally require concurrent use of another vasopressor. Epinephrine offers both beta-1 and beta-2 effects as well as alpha-1 effects, balancing inotropy with vasoconstriction and providing a standalone agent that increases cardiac output without concern for vasodilation and hypotension [2].
Airway management considerations
Respiratory failure in right ventricular failure is particularly difficult to manage; and intubation should be avoided if possible. Patients in RV failure are very prone to peri-intubation hemodynamic collapse due to an increase in RV afterload with positive pressure ventilation and the decrease in systemic vascular resistance with induction. An ideal strategy for airway management involves optimizing hemodynamics prior to intubation with vasopressors, choosing an appropriately dosed induction agent with a good hemodynamic profile, and using a low-tidal-volume strategy with the avoidance of hypercapnia, hypoxemia and excessive PEEP.
Non-invasive ventilation is an attractive alternative, but CPAP, which is commonly employed in the prehospital setting, can also cause an increase in RV afterload and decreased preload. High-flow nasal cannula may be a better option along with a non-rebreather. Commercial high-flow cannulas that can offer up to 60 Lpm are not commonplace in the prehospital setting, but using a regular nasal cannula set at flush rate underneath a non-rebreather may provide enough FIO2 to mitigate hypoxia. Just remember that any switch from negative pressure ventilation to positive pressure ventilation will increase intrathoracic pressure, causing further drops in preload.
RV dysfunction treatments
Now that we understand the pathophysiology of RV failure, we can see that increases in PVR, coupled with hypoxia and acidosis, are detrimental.
In the crashing patient with RV failure, inhaled nitric oxide should be considered if available. Nitric oxide will selectively dilate the pulmonary vasculature, causing decreased pulmonary vascular resistance and improving ventilation perfusion mismatch by increasing perfusion to well-ventilated parts of the lung.
In a pinch, and if available, 5 mg of nebulized nitroglycerin can be administered. This will cause decreased pulmonary vascular resistance and decrease the workload the RV must pump against. If you have access to a center that has extracorporeal membrane oxygenation (ECMO) transport, this should be considered, as ECMO can be used as salvage therapy in decompensated RV failure [3].
As you can see the management of right ventricular failure and massive pulmonary embolism can be challenging. Having a firm grasp of physiology, coupled with a tailored approach to your treatment modalities will assist you better in managing these complex patients.
References
- Matthews JC, McLaughlin V. Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: A detailed review of the pathophysiology, diagnosis, and management. Current cardiology reviews. 2008;4(1):49-59.
- Kwak Y, Lee C, Park Y, Hong Y. The effect of phenylephrine and norepinephrine in patients with chronic pulmonary hypertension. Anesthesia. 2002;57(1):9-14.
- Belohlavek J, Rohn V, Jansa P, et al. Veno-arterial ECMO in severe acute right ventricular failure with pulmonary obstructive hemodynamic pattern. J Invasive Cardiol. 2010;22(8):365.
