Mikhail Podlog, DO
Editor: Anna Van Tuyl, MD
The left ventricle (LV) is widely studied and much is known about its normal function, how it performs under stress, and the causes, sequelae, and treatments of LV failure. On the other hand, much less is understood about the right ventricle (RV), including right ventricular failure (1,3). There are many causes of right ventricular failure, the most common being failure of the left ventricle, but one important condition to always consider is pulmonary hypertension (PH), defined as a mean pulmonary artery pressure of 25 mm Hg or higher (1). As pulmonary pressures rise, the increase in afterload on the RV decreases right ventricular stroke volume and output, increasing RV volume. Since the RV cannot adapt as rapidly as the LV to increases in afterload, this has several detrimental effects on the cardiovascular system.
First, the increased volumes and pressures in the RV causes bulging of the interventricular septum into to LV, decreasing left ventricular preload. This results in a decrease in cardiac output, leading to hypotension and cardiac ischemia (1,3). Second, increased pressures in the RV cause a rise wall tension, decreasing right coronary artery perfusion, which leads to further ischemia. (1,3) Finally, increased pressures in the RV cause tricuspid regurgitation leading to decreased cardiac output (2). All of these processes ultimately cause what is referred to as the right ventricular spiral of death.
World Health Organization (WHO) Classifications of Pulmonary Hypertension
As always, the first step is considering the diagnosis. The most common presenting complaint is exertional dyspnea and pulmonary hypertension should always be thought about if an alternative diagnosis does not explain the patient’s presentation (1). Although a definitive diagnosis of PH requires right heart catheterization, there are several ways ED providers can assess for its presence.
1. Apical 4 (A4) chamber – RV greater than 2/3rd-1x the size of LV (1,4)
2. Parasternal short – flattening of interventricular septum, D-shaped LV (1,2)
3. TAPSE (Tricuspid Annular Plane Systolic Excursion)- M mode through tricuspid annulus in A4 view, >1.6 nml, <1.0 severe dysfunction (7)
CTA Chest - If RV is greater than 9/10ths of LV, that correlates with increased risk of adverse events and death. (1,4)
Definitive treatment of pulmonary hypertension usually involves treating the underlying causes. This includes diuretics for left heart failure, bronchodilators and steroids for lung diseases, thrombolysis for pulmonary emboli, etc. Appropriate consultations with cardiologists, pulmonologists and other specialists is also emergently indicated for further management. (1,2,3) In the meantime, there are certain things that emergency department providers must do to resuscitate and stabilize the patient in front of them.
Optimize Volume Status
Volume status in these patients is difficult to assess, as the physical exam as well as ultrasound visualization of the IVC is often unreliable. Overloading these patients can lead to further increase in RV volume causing decreased cardiac output and an accelerated path down the spiral of death. Overly diuresing these patients may also lead to a decreased cardiac output if the patient is preload dependent. Here are some tips one can use to assess these patients. (2)
1. Assume the patient is fluid overloaded and avoid large boluses of fluids -> negative balance is usually key for these patients. (1,2,6)
2. If there is clear volume loss (diarrhea, blood loss) -> low volume boluses of 250cc of isotonic solution and monitor for effects on blood pressure, heart rate, and urine output. (1)
a. If patient is anemic transfuse blood as decreased Hgb and iron has been associated with increased mortality (3,4)
3. Use passive leg raise maneuver and assess for changes in blood pressure and heart rate (this stimulates giving a bolus and can be rapidly reversed by lowering the legs).
4. Consider expedited admission to the ICU where a pulmonary artery catheter can be used to obtain accurate central pressures and guide further fluid management, although the efficacy of this is highly debated. (2)
Consider early pressor support
Systemic vasopressors can help prevent the downward spiral of RV failure several ways. Increasing left ventricular afterload can decrease interventricular septum bowing into the LV, increasing cardiac output. Vasopressors also assist in maintaining coronary perfusion to the right ventricle, decreasing effects of ischemia. Although literature is very scant comparing the variety of pressors available, certain pressors have advantages over others in treating pulmonary hypertension.
1. Norepinephrine – proven benefits in several types of shock; helps maintain coronary perfusion of right ventricle; may increase pulmonary vascular resistance (1,4)
2. Vasopressin – peripheral vasopressor just like norepinephrine, may actually decrease pulmonary vascular resistance through a NO-induced mechanism (1,2)
3. Phenylephrine – avoid due to increase in pulmonary vascular resistance when compared to other pressors available (1,5)
4. Dobutamine – augments myocardial contractility and reduces RV and LV afterload -> increased CO; but disadvantages include decreased SVR and tachycardia so may need to combine with a vasopressor (1,2,3,4)
5. Milrinone – Unlike dobutamine, PDE3 inhibitors are inotropic and augment cardiac output without chronotropic effects, but disadvantages include decreased SVR as well so may need to combine with a vasopressor; may consider inhaled milrinone if available (2,3,4)
Treat atrial arrhythmias
Patient with pulmonary hypertension are predisposed to atrial tachyarrhythmias. These patients do not tolerate atrial arrhythmias as cardiac output is preload dependent and any minor change can have drastic effects. Calcium channel blockers and beta blockers should be avoided as they may further impair cardiac function. Cardioversion should always be strongly considered as first line especially for unstable patients (1). Amiodarone can be tried if the patient is stable, and can also be used to pretreat the patient prior to cardioversion. (2,3)
Pulmonary vasodilators are the only medications that directly reverse the symptom-causing pathology. These are very useful in patients with idiopathic pulmonary hypertension (Category 1) and must be quickly given if a patient is on an IV pump of these medications that has malfunctioned. Inhaled preparations of these medications are also very effective at delivery the medication to highly ventilated portions of the lung, causing local vasodilation and improving V/Q mismatch. Below is a table that lists the categories of pulmonary vasodilators and their potential uses in emergencies.
Airway and ventilation management
Maintaining tight control of ventilation and oxygenation is crucial in these patients. Hypoxemia as well as hypercarbic respiratory acidosis can lead to increased pulmonary vasoconstriction, further exacerbating the underlying pathology. Therefore oxygen saturations and carbon dioxide levels in the blood must be maintained in the normal range. (1,4)
If a patient is in respiratory failure, intubation should be avoided at all costs. Intubating these patients can lead to a fatal hemodynamic collapse for two main reasons:
1. Sedation -> Loss of native catecholamines -> decreased SVR/vasodilation -> decreased venous return -> cardiovascular collapse (1)
2. Positive pressure ventilation -> increase RV and LV afterload and decreased RV preload -> decreased CO -> cardiovascular collapse (1)
Therefore try to avoid intubating these patients. If respiratory support is needed, first try NIPPV. This avoids the adverse effect of eliminating the patient’s innate catecholamine surge. In addition, the NIPPV can be removed rapidly if the patient begins to deteriorate. (1) If a patient needs to be intubated, following these guidelines can increase your chance of success.
1. Place an arterial line prior to intubation in order to quickly assess any hemodynamic changes and respond appropriately.
2. Avoid hypoxia -> preoxygenate the patient and utilize apneic oxygenation during the intubation
3. Avoid hypercarbia -> induce respiratory alkalosis prior to intubation (4). Hypercarbia worsens pulmonary vasoconstriction.
4. Consider performing awake intubation.
a. Induce with etomidate -> cardiovascular neutral (2)
b. Paralyze the patient -> increases chances of first pass success
c. Push dose pressors -> Have ready at the bedside along with your induction/paralytics (1)
d. Have norepinephrine drip ready -> Have the pump primed and connected; just having the medication in the room is not good enough (1)
6. Vent settings -> keep intrathoracic pressures low (similar to ARDS protocol) -> low TV, PEEP, low plateau pressures (2,3)
LVAD, ECMO, atrial septostomy, lung transplant, PH referral center (1,2,3)
1. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine, Wilcox
2. Hoeper MM, Granton J. Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. Am J Respir Crit Care Med. 2011;184:1114-1124
3. Acute Right Ventricular Failure in the Setting of Acute Pulmonary Embolism or Chronic Pulmonary Hypertension: A Detailed Review of the Pathophysiology, Diagnosis, and Management
4. Lahm T, McCaslin CA, Wozniak TC, et al. Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol. 2010;56:1435-1446.
5. Kwak YL, Lee CS, Park YH, et al. The effect of phenylephrine and norepinephrine in patients with chronic pulmonary hypertension. Anaesthesia. 2002;57:9-14
6. Ternacle J, Gallet R, Mekontso-Dessap A et al. Diuretics in normotensive patients with acute pulmonary embolism and right ventricular dilatation. Circ J 2013;77:2612–2618.
7. Schmid E, Hilberath JN, Blumenstock G, Shekar PS, Kling S, Shernan SK, Rosenberge P, Nowak-Machen M. Tricuspid annular plane systolic excursion (TAPSE) predicts poor outcome in patients undergoing acute pulmonary embolectomy. Heart, Lung and Vessels. 2015; 7(2): 151-158