Break on Through to The Other Side: On Management of Acute Right Heart Failure
Clinical Scenario: You are working in TCC when EMS brings in a patient with respiratory distress. She is a middle aged-female breathing 40 times per minute, with bilateral crackles, and edema from her legs all the way up her anterior chest. You think to yourself, "acute heart failure" and place the patient on BiPAP. You are about to order the nitro drip when you see a subcutaneous infusion device anchored to the patient's abdomen. As you examine it more closely, you realize that it is a infusion of not insulin as you first thought, but Treprostinil, a pulmonary vasodilator. You look the patient up and find that she has a history of severe pulmonary hypertension secondary to interstitial lung disease. Shortly after being put on BiPAP, the patient's blood pressure tanks from a SBP of 150 to 70. You realize, in a panic, that this patient does not have bread and butter left heart dysfunction but acute right heart failure. What do you do now?
Clinical question: What is the pathophysiology of right ventricular failure? Given this pathophysiology, what are the treatment goals and therapeutic options when managing acute right ventricular failure?
Literature Review:
Just like the left ventricle is adapted to be the work horse of systemic perfusion, the right ventricle has an anatomy and physiology uniquely suited to its function of optimizing venous return and providing sustained low-pressure perfusion through the lungs [1]. Unlike the left ventricle which generates high pressure pulsatile flow, the right ventricle (RV) ejects blood quasi-continuously from the right atria to the lungs. This sustained low pressure perfusion is possible because of the low resistance of the pulmonary vascular bed, intimately coupling RV output with pulmonary vascular resistance.
RV failure (RVF) [defined as reduced cardiac output and an elevated right ventricular filling pressure] has many underlying etiologies [2]. As emergency medicine residents, we can think of acute right heart failure in two situations that have specific and reversible causes: acute inferior MI and massive PE. While these certainly are important etiologies for RVF, it is also important to realize that RV failure is the most common cause of death in patients with preexisting pulmonary hypertension [2]. Indeed, in most cases, acute RV failure is a combination of established pulmonary vascular disease complicated by an acute derangement such as pneumonia, sepsis or ARDS [3]. Unlike the relatively reversible causes of acute RV failure such as MI or PE, management of RV failure in the face of underlying pulmonary arterial hypertension (PAH) is a much more complicated business. Indeed, pulmonary hypertension patients experiencing acute heart failure necessitating inotropic or vasoactive drugs have a documented mortality of 40-60% [4].
When it comes to management of acute right heart failure in the emergency department, there are couple things to acknowledge right off the bat:
a. Alleviate Congestion and Manage Preload: As discussed above, fluid balance is tricky in patients with RVF because you want just enough preload to promote an efficient fill but not too much which will cause the RV to stretch further and impede LV function. This is where physical exam and bedside cardiac US can help you. Peripheral edema > consider diuresis.
b. Decrease Right Ventricular Afterload: RV afterload is determined by the pulmonary vascular resistance (PVR), which may be altered chronically in pulmonary hypertension (such as interstitial lung disease or COPD) or acutely in conditions such as pulmonary embolism or ARDS. Because it is adapted to sustained perfusion in a low pressure system, the RV is poorly adapted to acute increases in PVR. The first line treatment for decreasing pulmonary vascular resistance is to correct hypoxia, hypercarbia and acidosis by treating the underlying exacerbating condition (i.e. pneumonia, sepsis). If these measures have failed, you can consider pulmonary vasodilators such as NO or prostacyclin. In the ED, the most commonly inhaled pulmonary vasodilators such as nitric oxide and flolan (esoprostenol) can be initiated. NO is significantly more expensive and can only be used in ventilated patients. Flolan can be used with a mask temporarily but only a small amount is reaching the pulmonary vasculature.
c. Optimize cardiac output: Restoration of right ventricular contractility is one of the mainstays of treatment of acute right heart failure. According to several recent reviews, low dose dobutamine (in the realm of 5-10 mcg/kg/min) is the treatment of choice[1,2,3,4]. There are not any large clinical studies in patients with acute right side heart failure secondary to pulmonary hypertension. However, in a dog model of RV failure secondary to acute rise in pulmonary artery pressures, dobutamine restored cardiac output, increased heart rate and restored arterial pressure better than norepinephrine [5].
d. Optimize Right Ventricular Perfusion: Other than inferior MI, where restoration of coronary perfusion requires PCI or lysis, maintaining right ventricular perfusion is accomplished through support of the systemic blood pressure. The ideal vasoactive medication would increase systemic arterial pressure and RV contractility without increasing pulmonary vascular resistance. Norepinephrine seems to be the agent of choice for this purpose. In one small study of 10 ICU patients with right ventricular dysfunction in context of septic shock, norepinephrine infusion was associated with increased myocardial oxygen delivery by maintaining systemic perfusion pressure, although pulmonary vascular resistance was also slightly increased [6]. Low dose vasopressin has also been considered an alternative agent for this purpose [3]. Vasopressin use does make some physiologic sense, as there are no V1 receptors in the lung, so PVR will not increase.
So what if you gave the nitroglycerin? Nitroglycerin is very useful in management of left heart dysfunction/hypertensive urgency because it functions to reduce afterload and preload, thus improving pulmonary edema and promoting forward-flow through the system. But what is the effect of this intervention on the right heart? In right heart dysfunction in acute MI, nitroglycerin is contraindicated because forward flow is preload dependent and nitro administration can lead to significant hypotension. If there is a right heart afterload problem, multiple studies of patients with stable pulmonary hypertension have demonstrated that at low doses (30 mcg/min), nitroglycerin can have a beneficial vasodilatory effects on the pulmonary vasculature [7,8,9]. However, given the risk of increased hypotension and decreased right ventricular perfusion during acute RVF, some may argue that nitroglycerin is relatively contraindicated and has the potential for harm.
Clinical Takehome: The right ventricle reacts poorly to acute rises in pulmonary vascular resistance. RVF may be seen in a wide-variety of critically ill patients in the ED, including those with prexisting pulmonary hypertension, PE, sepsis, ARDS, and acute MI. Acute management of most right heart failure involves optimizing preload, maximizing RV perfusion and contractility, and decreasing afterload. You should probably throw the cardiac US probe on these patients to evaluate the cause of their hypotension and the effectiveness of your interventions. Even with aggressive intervention, acute RV failure carries a poor prognosis.
Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty Reviewed by Enyo Ablordeppy and Brian Fuller
References:
1. Mebazaa, A., Karpati, P., Renaud, E., & Algotsson, L. (2009). Acute right ventricular failure—from pathophysiology to new treatments. In Applied Physiology in Intensive Care Medicine (pp. 261-272). Springer Berlin Heidelberg.
2. Hoeper, M. M., & Granton, J. (2011). Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. American journal of respiratory and critical care medicine, 184(10), 1114-1124.
3. Green, E. M., & Givertz, M. M. (2012). Management of acute right ventricular failure in the intensive care unit. Current heart failure reports, 9(3), 228-235.
4. Sztrymf, B., Günther, S., O’Callaghan, D. S., & Humbert, M. (2014). Acute Right Heart Failure in Pulmonary Hypertension. In The Right Heart (pp. 261-275). Springer London.
5. Kerbaul, F., Rondelet, B., Motte, S., Fesler, P., Hubloue, I., Ewalenko, P., ... & Brimioulle, S. (2004). Effects of norepinephrine and dobutamine on pressure load-induced right ventricular failure*. Critical care medicine, 32(4), 1035-1040.
6. Schreuder, W. O., Schneider, A. J., Groeneveld, A. B., & Thijs, L. G. (1989). Effect of dopamine vs norepinephrine on hemodynamics in septic shock. Emphasis on right ventricular performance. CHEST Journal, 95(6), 1282-1288.
7.Cockrill, B. A., Kacmarek, R. M., Fifer, M. A., Bigatello, L. M., Ginns, L. C., Zapol, W. M., & Semigran, M. J. (2001). Comparison of the Effects of Nitric Oxide, Nitroprusside, and Nifedipine on Hemodynamics and Right Ventricular Contractility in Patients With Chronic Pulmonary Hypertension*. CHEST Journal, 119(1), 128-136.
8.Morley, T. F., Zappasodi, S. J., Belli, A., & Giudice, J. C. (1987). Pulmonary vasodilator therapy for chronic obstructive pulmonary disease and cor pulmonale. Treatment with nifedipine, nitroglycerin, and oxygen. CHEST Journal, 92(1), 71-76.
9. Brent, B. N., Berger, H. J., Matthay, R. A., Mahler, D., Pytlik, L., & Zaret, B. L. (1983). Contrasting acute effects of vasodilators (nitroglycerin, nitroprusside, and hydralazine) on right ventricular performance in patients with chronic obstructive pulmonary disease and pulmonary hypertension: a combined radionuclide-hemodynamic study. The American journal of cardiology, 51(10), 1682-1689.
Clinical question: What is the pathophysiology of right ventricular failure? Given this pathophysiology, what are the treatment goals and therapeutic options when managing acute right ventricular failure?
Literature Review:
Just like the left ventricle is adapted to be the work horse of systemic perfusion, the right ventricle has an anatomy and physiology uniquely suited to its function of optimizing venous return and providing sustained low-pressure perfusion through the lungs [1]. Unlike the left ventricle which generates high pressure pulsatile flow, the right ventricle (RV) ejects blood quasi-continuously from the right atria to the lungs. This sustained low pressure perfusion is possible because of the low resistance of the pulmonary vascular bed, intimately coupling RV output with pulmonary vascular resistance.
RV failure (RVF) [defined as reduced cardiac output and an elevated right ventricular filling pressure] has many underlying etiologies [2]. As emergency medicine residents, we can think of acute right heart failure in two situations that have specific and reversible causes: acute inferior MI and massive PE. While these certainly are important etiologies for RVF, it is also important to realize that RV failure is the most common cause of death in patients with preexisting pulmonary hypertension [2]. Indeed, in most cases, acute RV failure is a combination of established pulmonary vascular disease complicated by an acute derangement such as pneumonia, sepsis or ARDS [3]. Unlike the relatively reversible causes of acute RV failure such as MI or PE, management of RV failure in the face of underlying pulmonary arterial hypertension (PAH) is a much more complicated business. Indeed, pulmonary hypertension patients experiencing acute heart failure necessitating inotropic or vasoactive drugs have a documented mortality of 40-60% [4].
When it comes to management of acute right heart failure in the emergency department, there are couple things to acknowledge right off the bat:
1. Right ventricular failure is pathophysiologically different from left ventricular failure: In the ED, we are comfortable taking care of left ventricular failure or fluid overload in the emergency department. Acute volume overload? BiPAP, nitro, diurese. Cardiogenic shock? Pick your inotrope. While severe left ventricular failure leads to back-up and subsequent right heart dysfunction because of pulmonary congestion, the cause and management of respiratory distress in this patient population is different. Remember, right ventricular failure causes peripheral but not pulmonary edema and fluid balance is a lot trickier to discern.
2. Not all Right Ventricular Failure is the same, and treatment depends largely on whether there is an afterload problem: Primary RV failure is usually due to a problem with the lungs. Across a broad cohort of critically ill patients, pulmonary hypertension and RV dysfunction are going to occur in the setting of 1) PE; 2) pre-existing pulmonary hypertension; 3) ARDS; 4) sepsis. In the instance that RV failure is primarily cardiac (i.e. acute MI), there is no impedance to forward flow in the system and so fluid management is more straightforward in that usually increased RV preload is necessary to maintain systemic perfusion [3]. However, in the setting of an acute increase pulmonary vascular resistance/right ventricular afterload, increased fluid resuscitation leads to RV dilation with nowhere for the fluid to go (i.e. not able to get through the pulmonary vasculature to the left atrium and improve stroke volume in the left ventricle). This not only leads to increased free wall tension in the RV and resultant ischemia, RV dilation can lead to impingement of LV filling because of dynamic septal bulging and further drop in systemic blood flow. The further drop in systemic blood flow leads a decreased RV perfusion and worsening RV failure. The end of this viscous cycle? Death.
With these thoughts in mind, the management of acute right heart failure depends on the underlying etiology, but generally can be broken down into four main treatment goals [1,2,3]:
With these thoughts in mind, the management of acute right heart failure depends on the underlying etiology, but generally can be broken down into four main treatment goals [1,2,3]:
a. Alleviate Congestion and Manage Preload: As discussed above, fluid balance is tricky in patients with RVF because you want just enough preload to promote an efficient fill but not too much which will cause the RV to stretch further and impede LV function. This is where physical exam and bedside cardiac US can help you. Peripheral edema > consider diuresis.
b. Decrease Right Ventricular Afterload: RV afterload is determined by the pulmonary vascular resistance (PVR), which may be altered chronically in pulmonary hypertension (such as interstitial lung disease or COPD) or acutely in conditions such as pulmonary embolism or ARDS. Because it is adapted to sustained perfusion in a low pressure system, the RV is poorly adapted to acute increases in PVR. The first line treatment for decreasing pulmonary vascular resistance is to correct hypoxia, hypercarbia and acidosis by treating the underlying exacerbating condition (i.e. pneumonia, sepsis). If these measures have failed, you can consider pulmonary vasodilators such as NO or prostacyclin. In the ED, the most commonly inhaled pulmonary vasodilators such as nitric oxide and flolan (esoprostenol) can be initiated. NO is significantly more expensive and can only be used in ventilated patients. Flolan can be used with a mask temporarily but only a small amount is reaching the pulmonary vasculature.
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| Image source: Reference 3 |
d. Optimize Right Ventricular Perfusion: Other than inferior MI, where restoration of coronary perfusion requires PCI or lysis, maintaining right ventricular perfusion is accomplished through support of the systemic blood pressure. The ideal vasoactive medication would increase systemic arterial pressure and RV contractility without increasing pulmonary vascular resistance. Norepinephrine seems to be the agent of choice for this purpose. In one small study of 10 ICU patients with right ventricular dysfunction in context of septic shock, norepinephrine infusion was associated with increased myocardial oxygen delivery by maintaining systemic perfusion pressure, although pulmonary vascular resistance was also slightly increased [6]. Low dose vasopressin has also been considered an alternative agent for this purpose [3]. Vasopressin use does make some physiologic sense, as there are no V1 receptors in the lung, so PVR will not increase.
So what if you gave the nitroglycerin? Nitroglycerin is very useful in management of left heart dysfunction/hypertensive urgency because it functions to reduce afterload and preload, thus improving pulmonary edema and promoting forward-flow through the system. But what is the effect of this intervention on the right heart? In right heart dysfunction in acute MI, nitroglycerin is contraindicated because forward flow is preload dependent and nitro administration can lead to significant hypotension. If there is a right heart afterload problem, multiple studies of patients with stable pulmonary hypertension have demonstrated that at low doses (30 mcg/min), nitroglycerin can have a beneficial vasodilatory effects on the pulmonary vasculature [7,8,9]. However, given the risk of increased hypotension and decreased right ventricular perfusion during acute RVF, some may argue that nitroglycerin is relatively contraindicated and has the potential for harm.
Clinical Takehome: The right ventricle reacts poorly to acute rises in pulmonary vascular resistance. RVF may be seen in a wide-variety of critically ill patients in the ED, including those with prexisting pulmonary hypertension, PE, sepsis, ARDS, and acute MI. Acute management of most right heart failure involves optimizing preload, maximizing RV perfusion and contractility, and decreasing afterload. You should probably throw the cardiac US probe on these patients to evaluate the cause of their hypotension and the effectiveness of your interventions. Even with aggressive intervention, acute RV failure carries a poor prognosis.
Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty Reviewed by Enyo Ablordeppy and Brian Fuller
References:
1. Mebazaa, A., Karpati, P., Renaud, E., & Algotsson, L. (2009). Acute right ventricular failure—from pathophysiology to new treatments. In Applied Physiology in Intensive Care Medicine (pp. 261-272). Springer Berlin Heidelberg.
2. Hoeper, M. M., & Granton, J. (2011). Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. American journal of respiratory and critical care medicine, 184(10), 1114-1124.
3. Green, E. M., & Givertz, M. M. (2012). Management of acute right ventricular failure in the intensive care unit. Current heart failure reports, 9(3), 228-235.
4. Sztrymf, B., Günther, S., O’Callaghan, D. S., & Humbert, M. (2014). Acute Right Heart Failure in Pulmonary Hypertension. In The Right Heart (pp. 261-275). Springer London.
5. Kerbaul, F., Rondelet, B., Motte, S., Fesler, P., Hubloue, I., Ewalenko, P., ... & Brimioulle, S. (2004). Effects of norepinephrine and dobutamine on pressure load-induced right ventricular failure*. Critical care medicine, 32(4), 1035-1040.
6. Schreuder, W. O., Schneider, A. J., Groeneveld, A. B., & Thijs, L. G. (1989). Effect of dopamine vs norepinephrine on hemodynamics in septic shock. Emphasis on right ventricular performance. CHEST Journal, 95(6), 1282-1288.
7.Cockrill, B. A., Kacmarek, R. M., Fifer, M. A., Bigatello, L. M., Ginns, L. C., Zapol, W. M., & Semigran, M. J. (2001). Comparison of the Effects of Nitric Oxide, Nitroprusside, and Nifedipine on Hemodynamics and Right Ventricular Contractility in Patients With Chronic Pulmonary Hypertension*. CHEST Journal, 119(1), 128-136.
8.Morley, T. F., Zappasodi, S. J., Belli, A., & Giudice, J. C. (1987). Pulmonary vasodilator therapy for chronic obstructive pulmonary disease and cor pulmonale. Treatment with nifedipine, nitroglycerin, and oxygen. CHEST Journal, 92(1), 71-76.
9. Brent, B. N., Berger, H. J., Matthay, R. A., Mahler, D., Pytlik, L., & Zaret, B. L. (1983). Contrasting acute effects of vasodilators (nitroglycerin, nitroprusside, and hydralazine) on right ventricular performance in patients with chronic obstructive pulmonary disease and pulmonary hypertension: a combined radionuclide-hemodynamic study. The American journal of cardiology, 51(10), 1682-1689.