Abstract
Acute failure of the right ventricle is a common challenge in the intensive care unit that is associated with significant morbidity and mortality. Although often a complication of left ventricular failure, right ventricular failure is a distinct clinical entity, both in terms of its hemodynamic abnormalities and response to treatment. Effective management of right ventricular failure must consider the unique properties of the right ventricle and the pulmonary circulation, and their response to common pharmacologic and mechanical interventions. In this review, we present a contemporary approach to patients with acute failure of the right ventricle including strategies for mechanical ventilation, hemodynamic management, and mechanical circulatory support.
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Introduction
Management of the patient with cardiogenic shock typically focuses on optimizing the function of the left ventricle. Indeed, early animal experiments in open pericardial models suggested that even severe compromise of the right ventricle had little impact on systemic cardiac output [1]. As more relevant animal models have been studied, and as data from patients has accumulated, it has become clear that dysfunction of the right ventricle portends a worse prognosis and alters the response to conventional therapies [2, 3]. Still, understanding of the pathophysiology and management of right ventricular failure remains far behind that of the left ventricle. In this review, we describe the pathophysiology of right ventricular failure and present current pharmacologic and mechanical management strategies for treatment.
Principles and Pathophysiology
Failure of the right ventricle is a vicious cycle (Fig. 1). After an initial insult increases pulmonary vascular resistance (eg, pulmonary embolus) or decreases right ventricular function (eg, right ventricular infarct), the right ventricle adapts in an attempt to maintain stroke volume. However, the primary responses of the right ventricle to volume and pressure overload (dilatation and hypertrophy, respectively) ultimately diminish cardiac output.
Pathophysiology of right ventricular (RV) failure. An initial increase in pulmonary vascular resistance (PVR) or decrease in RV function leads to RV dilation and increased RV wall stress. These result in volume and pressure overload of the right ventricle, which contribute to ventricular interdependence and decreased cardiac output. Low cardiac output worsens right coronary artery (RCA) ischemia, which in turn further worsens RV function
Chamber dilation can increase the stroke volume of the right ventricle by increasing preload and thus moving to a more favorable position on the Frank-Starling curve. However, this dilation also can produce functional or secondary tricuspid regurgitation. Particularly when combined with high pulmonary vascular resistance, the increased tricuspid insufficiency worsens systemic congestion in spite of the larger stroke volume and is associated with worsening renal function [4••].
Hypertrophy of the right ventricle allows for the generation of higher pressures to overcome increased pulmonary vascular resistance. However, elevated pressure in the right ventricle compromises filling of the right coronary artery by decreasing the pressure gradient between the aorta and the right ventricle. Under normal conditions, the right coronary artery fills primarily during systole. Elevated right ventricular pressure lessens the pressure gradient during systole and restricts filling of the right coronary artery to diastole. Furthermore, when elevated pressures in the right ventricle result in high right atrial pressures, blood can flow across a previously insignificant patent foramen ovale, thus compromising both the output of the right ventricle and blood oxygenation. In sum, the right ventricle is particularly sensitive to changes in afterload and is prone to failure with acute elevations in pulmonary artery pressure [5, 6].
Pressure and volume overload of the right ventricle also worsen cardiac output by compromising function of the left ventricle. One important mechanism for this effect is ventricular interdependence [7]. Increased volume and pressure in the right ventricle displace the interventricular septum toward the left ventricle. At the same time, this dilation exacerbates the constraining effect of the pericardium. Together, these factors compromise filling of the left ventricle and distort its geometry resulting in decreased stroke volume.
Ultimately, the effects of right ventricular remodeling on the right and left ventricles can compound each other and result in marked hemodynamic decline. As the right ventricle continues to remodel, function of the left ventricle, and hypotension, worsen. With lower aortic pressure, perfusion of the right coronary artery is reduced and perpetuates right ventricular ischemia and dysfunction (Fig. 1). The interventions discussed below will target different components of this progression with the aim of attenuating or reversing the vicious cycle.
Treatment of Underlying Disease
Right ventricular failure can result from direct injury to the right ventricle, or as a consequence of another cardiopulmonary disease process. Right ventricular infarct or cardiomyopathies affecting the right ventricle decrease right ventricular output by impairing contractility. Other disease processes may impair right ventricular output by increasing afterload (eg, pulmonary embolism, acute respiratory distress syndrome [ARDS]) or increasing preload (eg, acute mitral regurgitation). Indeed, the most common cause of right ventricular dysfunction is failure of the left ventricle, which can combine these mechanisms by distorting the geometry of the right ventricle, elevating filling pressures, and increasing pulmonary afterload.
Management of acute right ventricular failure combines pharmacologic and mechanical supportive care with treatments directed at the underlying disease process. Major causes of acute right ventricular failure and their specific treatments are listed in Table 1, and reviewed more fully elsewhere [8, 9]. Ultimately, the goal of the supportive measures described below is to preserve end-organ perfusion until targeted therapies can be delivered and take effect, or in some cases until the natural history of the disease resolves.
Ventilator Management
Careful management of oxygenation and ventilation is essential to the treatment of right ventricular failure, particularly in those patients that require mechanical ventilation. Both hypoxia and hypercapnia promote pulmonary vasoconstriction and increase the afterload of the right ventricle [10, 11]. However, large tidal volumes, high plateau pressures, and high positive end expiratory pressures all can increase the pulmonary resistance and afterload of the right ventricle as well. To balance these competing concerns, the ventilator strategy should prioritize achieving normoxia and hypocarbia, but should do so with moderate tidal volumes (~8 cc/kg) and lower levels of positive end expiratory pressure (<12 cm H2O) to maintain moderate plateau pressures (<30 mmHg) [12]. This approach may require a relatively higher respiratory rate and concentration of inspired oxygen. Less common ventilator techniques, such as high frequency oscillatory mode and prone positioning, have shown some suggestions of improved right ventricular function in small studies of patients with right ventricular failure and ARDS [13, 14].
Hemodynamic Management
Preload Optimization
Classic studies in the dog demonstrate that the right ventricle responds more favorably to increases in preload than does the left ventricle [15, 16]. Volume loading of the canine right ventricle increases both the stroke work of the right ventricle and systemic cardiac output. These data provided the physiologic rationale for the traditional practice of aggressively volume loading the failing right ventricle.
However, later clinical studies on the failing human heart suggest a more tempered approach to volume resuscitation. These studies support volume loading only in patients with low central venous pressures and satisfactory mean arterial pressures [17, 18]. Volume loading can be beneficial for the collapsed right ventricle, but once the right ventricle is adequately filled, excess volume can become detrimental. Moreover, in patients with low mean arterial pressure, particular caution should be taken to avoid raising right ventricular filling pressures relative to systemic pressures. The physiology behind these recommendations is mediated by several features: ventricular interdependence (lessened left ventricular filling with increasing right ventricular volume), worsened tricuspid regurgitation with increased right ventricular volume, and hypoperfusion of the right ventricle, particularly in patients with systemic hypotension or right ventricular ischemia. In sum, these studies call for fluid loading to a goal central venous pressure of 10–12 mmHg taking care to avoid excessive volume loading (more than 2 l of fluid), especially in patients with mean arterial pressure less than 60 mmHg.
Vasopressors and Positive Inotropic Support
After ensuring adequate right ventricular filling pressures, inotropic support can further augment the cardiac output of the right ventricle. A number of intravenous medications increase inotropy, and selection of the optimal agent depends on the desired effects on systemic and pulmonary vascular tone. In most cases, patients with right ventricular failure requiring inotropic support will have invasive hemodynamic monitors in place, and medications will be titrated to optimal hemodynamic parameters. Relevant properties of commonly used agents are summarized in Table 2.
Dobutamine is a catecholamine that increases cardiac contractility without substantial increases in vascular resistance. This profile arises from its strong agonism of both the β1- and β2- adrenergic receptors and mild affinity for the α1-adrenergic receptor. This mixture modestly reduces or does not change systemic and pulmonary vascular tone. In patients with right ventricular failure, the addition of dobutamine can improve hemodynamics when compared with volume loading alone [19], pure vasodilation with nitroprusside [20], or an inopressor such as norepinephrine [21]. Because of its predominant effect on contractility, dobutamine is the first-line inotrope in primary right ventricular dysfunction, such as right ventricular myocardial infarction.
Milrinone is a positive inotrope that also dilates both the systemic and pulmonary vasculature. It is a phosphodiesterase (PDE) 3 inhibitor that acts on both the myocardium and vascular smooth muscle to increase contractility and vasodilation. In patients with acute or chronic pulmonary hypertension, milrinone improves cardiac output and decreases pulmonary pressures [22]. Milrinone similarly lowers pulmonary pressures and improves cardiac output in patients with depressed right ventricular function following cardiac surgery and cardiopulmonary bypass [23]. Because of its combined effect on contractility and pulmonary vascular resistance, milrinone is the first-line inotrope in patients with preserved mean arterial pressures and right ventricular failure secondary to high pulmonary afterload (eg, pulmonary embolism or following cardiac transplantation).
Systemic hypotension in right ventricular failure plays a pernicious role in reducing right coronary artery perfusion and should be treated with vasopressors. The ideal vasopressor should increase systemic pressure more strongly than pulmonary arterial pressure. Arginine vasopressin (vasopressin) fits this profile and may even lead to a decrease in pulmonary vascular resistance [24]. Based on studies in the rat, vasopressin achieves selective pulmonary vasodilation via the release of nitric oxide [25, 26]. Vasopressin is a particularly effective medicine in the postoperative setting, where patients may be relatively refractory to catecholamines given either alone or in combination. It is often used in combination with inotropic agents as a first-line pressor in patients with depressed right ventricular function and systemic hypotension.
The catecholamine vasopressors (epinephrine, norepinephrine, dopamine) increase cardiac index and systemic vascular resistance, while likely also increasing pulmonary vascular resistance. In animal models and case reports of acute right ventricular failure, norepinephrine has been most successful in increasing systemic vascular resistance more than pulmonary vascular resistance [27–29]. In patients with severely diminished contractility of the right ventricle, such as following right ventricular infarct or cardiopulmonary bypass, epinephrine is the preferred agent because of its greater stimulation of α-adrenergic receptors [30]. As with all of the aforementioned inotropes, at higher doses these agents may cause unwanted tachycardia and myocardial ischemia. In patients who do not tolerate inodilators because of hypotension, the combination of vasopressin and a catecholamine is the recommended treatment.
Pulmonary Vasodilators
The right ventricle is exquisitely sensitive to increases in afterload and its performance can be impaired with even minimal increases in afterload (pulmonary pressures of 30–40 mmHg) [6]. Selective pulmonary vasodilation is an attractive strategy to improve right ventricular function by relieving increased afterload without causing systemic hypotension. Two classes of agents exist for this purpose: 1) intravenous medications with selective effects on the pulmonary vasculature; and 2) inhaled agents that are delivered directly to the lungs. Delivery of vasodilators by inhalation may improve ventilation/perfusion (V/Q) mismatch by directing blood flow to ventilated areas of the lung.
The most extensively used inhaled vasodilator is nitric oxide, which dilates pulmonary vasculature by increasing the production of cyclic guanosine monophosphate. Nitric oxide may also improve outcomes in right ventricular failure by reducing inflammatory cytokine production in the lung [31]. Small studies have demonstrated hemodynamic improvements with inhaled nitric oxide in patients following right ventricular myocardial infarction, left ventricular assist device implantation, or cardiac transplant [32, 33]. Inhaled nitric oxide may act synergistically with systemic inodilators [34–36]. The application of inhaled nitric oxide may be limited by methemoglobinemia, reactive nitrogen species, and rebound pulmonary hypertension after discontinuation [37]. In addition, in patients with advanced biventricular heart failure, inhaled nitric oxide may increase pulmonary capillary wedge pressure and worsen pulmonary edema [38, 39].
An alternative to nitric oxide is the prostacyclin family of molecules, which promotes vasodilation through the activation of cyclic adenosine monophosphate. Although published experience with prostacyclins in the intensive care setting is limited, epoprostenol is the preferred agent because of its potency and short half-life (~5 min). In patients with right ventricular failure following cardiac transplant or cardiopulmonary bypass, treatment with inhaled epoprostenol improves hemodynamics as well as inhaled nitric oxide [40, 41]. Because of the comparable efficacy with reduced side effects and cost, prostacyclin has become a first-line pulmonary vasodilator at many centers. The use of inhaled epoprostenol, however, may be limited by the development of hypotension, bradycardia, headache, or flushing.
PDE type 5 (PDE5) inhibitors promote vasodilation by blocking the degradation of cyclic guanosine monophosphate. These agents can improve symptoms and hemodynamics in patients with chronic pulmonary arterial hypertension but their role in the acute setting has not been adequately tested [42]. Small studies suggest that following treatment with inhaled vasodilators, PDE5 inhibitors may protect against rebound pulmonary hypertension [43]. PDE5 inhibitors also have been used to reduce pulmonary vascular resistance following left ventricular assist device implantation, and to improve symptoms and exercise capacity in patients with advanced heart failure and secondary pulmonary hypertension [44••, 45]. In addition to direct vasodilator effects, there is in vitro data suggesting that PDE5 inhibition can increase right ventricular contractility [46]. Whether this contributes to reversal of right ventricular failure in patients remains unknown.
Rhythm Control
The sensitivity of right ventricular performance to preload suggests that optimal filling by synchronized atrial and ventricular contraction may be critical for right ventricular cardiac output. Indeed, studies with isolated rat right ventricles demonstrate that augmented right atrial contraction is an important adaptation to decreased right ventricular function [3]. In patients with right ventricular infarcts requiring temporary electronic pacemaker placement, atrioventricular synchrony significantly improves cardiac output over dissociated rhythms and can sometimes reverse hypotension and shock [47, 48]. In patients with right ventricular dysfunction and a right bundle branch block, pacing in a location that restores synchronous right ventricular contraction may further enhance the benefits of ventricular pacing [49]. Our current practice is to aggressively attempt to maintain sinus rhythm in patients with right ventricular failure and atrial tachyarrhythmias, and to implant temporary pacemakers in patients (particularly following right ventricular infarct) with high-degree atrioventricular nodal block.
Mechanical Rescue Therapies
Patients with right ventricular failure that is refractory to medical therapy may be candidates for interventional treatment or mechanical circulatory support. Currently available devices for right ventricular support provide temporary relief, either until native heart function can recover or as a bridge to heart (or heart-lung) transplant or another procedure (eg, pulmonary embolectomy).
Right Ventricular Assist Device
A right ventricular assist device drains blood from the vena cava or right atrium and returns it to the pulmonary artery, thus unburdening the failing right ventricle. These devices have been used successfully in the treatment of right heart failure following right ventricular infarct [50], cardiopulmonary bypass [51, 52], left ventricular assist device implantation [53], and cardiac transplant [54]. In patients with severe biventricular failure, bilateral percutaneous ventricular assist devices may be used as a bridge to durable mechanical circulatory support (so-called, “bridge to bridge”) or as a bridge to recovery (eg, in the setting of fulminant myocarditis).
Extracorporeal Membrane Oxygenation
In right ventricular failure caused by high pulmonary pressures, a right ventricular assist device, which pumps blood into the pulmonary circulation, may not restore adequate blood flow to the left ventricle. Veno-arterial extracorporeal membrane oxygenation (ECMO) drains deoxygenated blood from the venous circulation and returns oxygenated blood to the arterial circulation. Veno-arterial ECMO can thus provide biventricular cardiac support as well as respiratory support. For this reason, veno-arterial ECMO would seem to be the preferred mechanical support for patients with right ventricular failure in the setting of pulmonary hypertension or acute pulmonary emboli [55, 56••]. However, current experience with ECMO in adults with cardiac failure remains limited without clear data to support its efficacy [57]. Other limitations of veno-arterial ECMO include the need for an experienced perfusionist and risks of bleeding, thromboembolism, pulmonary hemorrhage, and cannulation-induced vessel injury.
Balloon Atrial Septostomy
Early observational data in patients with pulmonary hypertension demonstrated improved survival in the presence of a patent foramen ovale [58, 59]. This led to the hypothesis that creation of an interatrial shunt by balloon atrial septostomy could improve hemodynamics in patients with right ventricular failure by unloading the right ventricle and perhaps prolong survival. In patients with advanced pulmonary hypertension, balloon atrial septostomy may have a role in symptom palliation or in bridging patients to lung transplant [60]. However, current data indicate that patients with severe right ventricular failure and cardiogenic shock respond poorly to balloon atrial septostomy [61]. A possible alternative method to relieve pulmonary hypertension is the creation of a shunt between the pulmonary artery and descending aorta, the Potts shunt. In an intriguing case report, children who developed pulmonary hypertension following an arterial switch procedure for transposition of the great arteries had improvements in functional status and right ventricular function following this procedure [62]. Further validation will be necessary before considering wider application of this technique.
Conclusions
Failure of the right ventricle is a common challenge in the intensive care unit that worsens prognosis and complicates the approach to treatment. This review presents a comprehensive approach to patients with right ventricular failure in the intensive care unit (Fig. 2). Although these recommendations represent current clinical practice, there remains minimal data from large-scale or randomized clinical trials to guide them. As a result, many questions remain for future investigation. Can prophylactic use of these treatments prevent failure of the right ventricle? What role will PDE5 inhibitors play in the acute setting of right ventricular failure? What is the optimal timing and patient selection for mechanical circulatory support? Future studies may clarify these questions and provide novel therapies to treat this challenging patient population.
Management of acute right ventricular (RV) failure. An algorithm for the management of patients with acute right ventricular failure in the intensive care unit. AV atrioventricular; CVP central venous pressure; MAP mean arterial pressure; PEEP positive end expiratory pressure; RVAD right ventricular assist device; VA-ECMO veno-arterial extracorporeal membrane oxygenation
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Green, E.M., Givertz, M.M. Management of Acute Right Ventricular Failure in the Intensive Care Unit. Curr Heart Fail Rep 9, 228–235 (2012). https://doi.org/10.1007/s11897-012-0104-x
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DOI: https://doi.org/10.1007/s11897-012-0104-x