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Acute Right Heart Failure

TSRA Primer - Critical Care

TSRA Content:


Authors: Stephanie N. Nguyen, MD, and Andrea N. Miltiades, MD, MS

This is a revision and update from the previous edition of the TSRA Primer in Cardiothoracic Surgery written by Walter Lech, MD, and David Odell, MD

Introduction

Historically, the left ventricle (LV) has been the main focus of heart failure studies given its perceived dominance in maintaining hemodynamic performance. The right ventricle (RV) was considered less essential and perhaps the ‘forgotten’ chamber, largely due to poor understanding of its complex physiology [1]. However, recent advances in imaging and monitoring techniques, as well as rigorous studies of right-sided hemodynamics have revealed unique RV structural geometry and function which make it a key component of the cardiopulmonary unit. The importance of the RV to overall hemodynamics is best exemplified in the setting of acute dysfunction.

Right heart failure (RHF) occurs when the RV fails to maintain a sufficient stroke volume through the pulmonary circulation to achieve adequate LV filling. This is caused by a variety of etiologies that are intrinsically unique to the RV, including differences in coronary perfusion, contractility, and afterload sensitivity. Overall, the result is a low cardiac output state and hemodynamic instability. Since RHF is an independent predictor of mortality and poor clinical outcomes [2], prompt recognition and treatment of the underlying etiology is critical. This section will cover key differences between the RV and LV, the pathophysiology of acute RHF, and review different management strategies for the failing RV.

Major differences between the RV and LV

Anatomy:
The RV is a thin-walled (3-5 mm), crescent-shaped structure that wraps around the LV with three anatomic segments, the inlet (tricuspid valve, chordae and papillary muscles), apex (trabeculated myocardium) and outlet (infundibulum and pulmonary valve) [3, 4]. The RV has only 2 layers of cardiomyocytes, a superficial circumferential layer which travels to the LV and a subendocardial longitudinal layer. The RV contracts in a peristaltic-like fashion, with three distinct motions: longitudinal shortening with the tricuspid valve moving towards the apex accounting for 70% of the right ventricular ejection fraction (RVEF), radial shortening from inward motion of the RV free wall (a lesser component of RVEF [20-30%]), and contraction of the interventricular septum bulging into the RV.

Normal septal position and twisting are essential for RV function. In contrast, the LV is a thick-walled conical chamber with 3 layers of cardiomyocytes, including helical fibers making up both the free wall and septum and transverse fibers at the base [3]. The significantly greater muscle mass and helical fiber orientation make the LV a superior pumping chamber with greater resistance to perturbations in pressure/volume. Both ventricles are separated by the interventricular septum (IVS), which may shift either rightward or leftward under certain loading conditions, ultimately affecting biventricular function. This phenomenon is known as ‘ventricular interdependence’ and will be discussed in further detail below.

Coronary perfusion:
Perfusion of the left coronary artery (LCA) primarily occurs during diastole due to impediment of coronary flow with systolic contraction. In contrast, the right coronary artery (RCA) is perfused throughout diastole and systole, owing to low RV systolic pressure. Therefore, increased RV afterload and prolonged isovolumetric contraction time increases oxygen demand and reduces systolic perfusion of the RCA. Moreover, elevated RV end-diastolic pressure increases free wall stress and intramural pressure, resulting in a decreased perfusion gradient and subendocardial ischemia [5].

Afterload sensitivity:
The LV pumps against a low-compliance, high-resistance systemic arterial circulation and is capable of adapting to changes in pressure. In contrast, the thin-walled RV is coupled to a high-compliance, low-resistance pulmonary circulation, therefore acute increases in afterload (i.e., pulmonary hypertension) are poorly tolerated and cause a dramatic decline in contractility and stroke volume [6]. In summary, this high sensitivity of the RV to afterload can trigger a number of sequelae, terminating in progressive cardiogenic shock:

Increased RV afterload à decreased contractility and stroke volume à RV dilation à tricuspid regurgitation (TR) à increased RV wall tension à decreased perfusion gradient à subendocardial ischemia à worsening RV function and distention à leftward shift of the IVS à decreased LV preload à decreased cardiac output and systemic hypotension à decreased RCA perfusion à ongoing RV ischemia à worsening RV function.

Etiology of RHF

Acute:

• Pulmonary embolism
• Myocardial ischemia
• Cardiac tamponade
• Post-cardiotomy
• Post left ventricular assist device (LVAD) implantation
• Pulmonary hypertensive crisis
• Intracardiac shunt
• Protamine reaction
• Acute Respiratory Distress Syndrome
• High-output heart failure (e.g., sepsis)
• Myocarditis

Chronic:

• Left heart failure
• Chronic thromboembolic pulmonary hypertension (CTEPH)
• Other causes of pulmonary hypertension
• Right-sided valvular disease
• Chronic lung disease and hypoxia
• Congenital heart disease
• Cardiomyopathy
• Constrictive pericardial disease

Diagnosis

A thorough history and physical examination can provide important clues to the presence of acute RHF, including a right-sided third heart sound, elevated jugular venous pressure, and peripheral edema, and clinical manifestations of a low cardiac output state, including low urine output, cool extremities. There will also be laboratory evidence of end-organ hypoperfusion, including transaminitis, coagulopathy, lactatemia, and renal insufficiency.

Imaging:
Two-dimensional (2D) echocardiography is a useful modality for assessment of RV function; however, it is limited by the complex geometry of the RV and its retrosternal position [7]. In the setting of acute decompensated RHF, qualitative assessment of RV function is performed by comparing its size to the LV at end-diastole in the apical 4-chamber view. Under normal conditions, the RV is 2/3 the size of the LV; however, if the RV is as large as the LV or comprises the apex, the RV is considered dilated. RV dilation with flattening of the interventricular septum (‘D sign’) in short-axis views signifies pressure and/or volume overload. Moreover, the presence of new TR is a sign of acute RV dysfunction and doppler measurement of the regurgitant jet allows for estimation of the pulmonary artery systolic pressure (PASP). Finally, presence of a pericardial effusion with right-sided compression during diastole represents cardiac tamponade.

Longitudinal shortening is the predominant contributor to RV systolic function and can be quantitatively assessed in the apical 4-chamber view using the following techniques: Tricuspid Annular Plane Systolic Excursion (TAPSE) and Tricuspid Annular Velocity (S’, “S Prime”). Both techniques measure the motion of the RV base towards the apex. TAPSE represents the maximum vertical motion of the tricuspid valve annulus, with a value of less than 1.7 cm indicating RV dysfunction [4]. Tricuspid Annular Velocity (S’, “S Prime”) uses tissue doppler to measure the peak velocity of the lateral tricuspid annulus with a velocity < 10 cm/s indicating RV systolic dysfunction. TAPSE and S’ may be reduced after cardiac surgery despite normal RV function, thus other methods of RV functional assessment should be used to correlate with clinical findings [8].

Right ventricular fractional area change (FAC) is a surrogate for ejection fraction and measures the longitudinal shortening, radial thickening and interventricular septum components of RV contraction. The endomyocardial border is traced at end-diastole and end-systole and applied to the equation: [(end-diastolic area − end-systolic area)/end-diastolic area] × 100. An FAC less than 35% indicates RV systolic dysfunction.

Invasive hemodynamic monitoring:
Right heart catheterization (RHC) is a critical component of RV assessment, particularly in patients with pulmonary hypertension. Measurement of the central venous pressure (CVP), right atrial pressure (RAP), PA pressure, pulmonary capillary wedge pressure (PCWP), pulmonary vascular resistance (PVR), and cardiac output (CO) can distinguish the etiology of RHF and ultimately guide therapy. A PA catheter may be helpful in the bedside diagnosis and management of RHF. An elevation in CVP or RAP alone (normal 8-12 mmHg) may be a marker of isolated RV dysfunction, whereas an elevated CVP in conjunction with a high PCWP (normal 4-12 mmHg) is suggestive of RHF secondary to LV dysfunction. Multiple formulas to quantify right-sided hemodynamics have been developed in recent years; however, no single formula definitively identifies RHF due to its complexity. Some commonly used formulas to assess RV function and values suggestive of RHF include [9]:


Kapur et al. Circulation (2017)

Medical Management

The initial approach to acute RHF relies on identifying and correcting the underlying etiology. In contrast to the LV, in which dysfunction is often irreversible, the RV is highly pliable, afterload dependent, and typically regains function once the underlying pathology is addressed [10]. The management of acute RHF requires an understanding of preload, afterload, and contractility.

Preload:
Fluid management is critical in the treatment of acute RHF and an assessment of the patient’s volume status should be made upon initial examination. Since the RV is coupled to a high-compliance, low-resistance pulmonary circulation, it is volume-responsive and preload-dependent. In the early postoperative period, intravascular volume may be depleted secondary to bleeding, increased vascular permeability, and insensible losses. In such cases of hypovolemia, it is reasonable to consider a small intravenous fluid bolus to optimize RV filling pressures. A PA catheter and echocardiography can be valuable if the there is any uncertainty regarding volume status.

Most cases of acute RHF are characterized by volume overload and RV distention. Elevations in RV preload are most commonly due to an elevation in intravascular volume or new TR. As previously discussed, this causes a leftward septal shift, impairing LV diastolic function and cardiac output. Concurrently, excessive RV preload causes ventricular distention and increased free wall stress, which decreases the coronary perfusion pressure, causing myocardial ischemia. As such, RV unloading is essential and may be achieved with aggressive diuresis or renal replacement therapy. Of note, volume removal should not be held in a hypotensive patient who is clearly volume-overloaded; vasopressor support should be added while attempting to improve systemic venous congestion.

Finally, sedatives and analgesics also limit sympathetic vasoconstriction of the systemic venous circulation, leading to decreased venous return and mechanical ventilation with high positive end-expiratory pressure (PEEP) also impedes RV preload by increasing intrathoracic pressure. Optimization of these factors is also important in improving hemodynamics, particularly in the early postoperative setting.

Afterload:
Excessive afterload plays a major role in nearly all cases of acute RHF, resulting in RV distention and its aforementioned downstream consequences. The simplest example is an acute massive PE, which occludes the pulmonary vasculature and causes an abrupt increase in RV afterload with significant hemodynamic instability. An important contributor to RV afterload is pulmonary hypertension (PH), which is characterized by aberrations in the pulmonary vascular bed, leading to increased PVR and RHF. PH is defined as a mean PAP ≥25 mm Hg and may be found in isolation or secondary to other pathology as defined by the World Health Organization classification for PH [11]. We will focus on Groups 1 and 2, which are most likely to trigger acute decompensated RHF.

Pulmonary arterial hypertension (Group 1) represents a group of disorders defined by the presence of precapillary PH with PCWP ≤ 15 mmHg and PVR > 3 Woods units [12]. This includes patients with idiopathic PAH and PAH associated with collagen vascular disease who have abnormal remodeling of the pulmonary vasculature. Acute decompensated PH is characterized by a sudden increase in PAP with resultant RV dysfunction. Treatment is multimodal and includes targeted management of the inciting event (e.g., hypoxia, hypercapnia, acidemia), aggressive diuresis to improve LV function and RV myocardial perfusion, and reduction of pulmonary vascular tone [10]. Several classes of pulmonary vasodilators have been developed for the treatment of elevated PA pressures and PVR. Inhaled nitric oxide (iNO) is a potent vasodilator with high pulmonary selectivity and rapid onset of action, making it an effective therapy in acute RHF [13]. Furthermore, it is also only active in well ventilated areas of the lung, reducing the potential for a V/Q mismatch. Prostacyclin analogs such as epoprostenol, and iloprost, and sildenafil (phosphodiesterase-5 inhibitor) are other pulmonary vasodilators that may be used to lower PA pressures in the setting of acute RHF, though the latter should be used with caution in the hypotensive patient due to systemic vasodilatory effects [14].

Pulmonary hypertension secondary to left heart disease (Group 2) is the most common cause of PH defined by the presence of postcapillary PH with PCWP > 15 mmHg, variable PVR and evidence of left-sided heart disease [15]. In this situation, LV diastolic and systolic dysfunction or significant left-sided valvular disease leads to increased left-sided filling pressures, increased hydrostatic back pressure, leading to pulmonary venous congestion, increased RV afterload and RHF. Specific causes of postcapillary PH secondary to left heart dysfunction include mitral stenosis and mitral regurgitation. Oftentimes, diuretics and timely repair of valvular lesions results in rapid reduction of PVR and improved biventricular function [16,17]; however, longstanding valvular pathology may result in irreversible remodeling of the pulmonary vascular bed and non-reactive PVR. Such patients are near prohibitive-risk surgical candidates and represent a challenging patient population since pulmonary vasodilators are ineffective and the optimal therapeutic strategy in this cohort remains unknown [11, 15].

Contractility:
Acute reductions in RV contractility result from an interplay between suboptimal RV mechanics and direct myocardial injury. In acute RHF, inotropic agents augment myocardial contractility and stroke volume to unload the RV and promote antegrade flow to maintain adequate cardiac output. Though inotropic support may be considered to support the RV and systemic perfusion until the underlying etiology is corrected, myocardial ischemia must first be ruled out since inotropes increase the risk of tachyarrhythmias and may exacerbate underlying ischemia via an oxygen supply/demand mismatch. In the event of an acute coronary syndrome, inotropes should be held and prompt revascularization performed.

Of the inotropic agents, milrinone (phosphodiesterase-3 inhibitor) is an appealing agent when there is concurrent PH due to its vasodilatory properties in the pulmonary vascular bed, but its use is limited in hypotensive patients given a similar vasodilatory effect on the systemic vasculature [18]. Given the long half-life of milrinone, concomitant vasopressor support may be necessary to manage vasoplegia. Dobutamine primarily acts on β1 adrenergic receptors to generate positive inotropy. Unlike milrinone, it has a short half-life and only a minor systemic vasodilatory effect. In cases of RHF with associated hypotension, drugs such as dopamine and epinephrine may be utilized given their inherent inotropic properties and additional dose-dependent vasopressor affect from α1 agonism [19].

Mechanical Circulatory Support

Invasive therapeutic options can be considered in cases of acute RHF that is refractory to medical therapy [9]. Mechanical circulatory support (MCS) is used to augment cardiac output and facilitate end-organ recovery in cardiogenic shock. The type of MCS employed for RHF is determined by the etiology of RHF – is it a primary RV insult or the result of pulmonary or left heart pathology? In cases of acute RHF secondary to left-sided heart failure, temporary devices such as venoarterial extracorporeal membrane oxygenation (VA-ECMO), intra-aortic balloon pump (IABP), and Impella 5.5 or CP (Abiomed, Danvers, MA) are widely utilized and target recovery of LV function. In contrast, there is much less experience with MCS devices for isolated RHF [9].

Surgical RVAD:
A temporary extracorporeal right ventricular assist device (RVAD) can be surgically implanted using a centrifugal continuous flow pump with the option to splice in an oxygenator. This approach requires a thoracotomy or sternotomy to facilitate right atrial and pulmonary artery cannulation [20].

Percutaneous RVAD:
Recent advances have been made in the development of percutaneous RVADs which provide direct RV bypass. The TandemHeart (CardiacAssist, Pittsburgh, PA) pump is an RVAD that utilizes RA-PA cannulation; however, mobility is limited by femoral venous cannulation [21]. The ProtekDuo (TandemLife, Pittsburgh, PA) is a dual-lumen cannula that is inserted via the internal jugular vein to the RA (outer inflow cannula) and positioned across the tricuspid valve to terminate in the PA (inner outflow cannula) [22]. This extracorporeal RVAD can be worn with a thoracic vest to enable early mobilization. The Impella RP (Abiomed, Danvers, MA) is an intracorporeal, catheter-based RVAD [23]. The device is a 22-F microaxial continuous-flow pump that is inserted via the femoral vein. The catheter sits across the tricuspid valve and RV, with the pump inflow positioned in the inferior vena cava and the outflow in the main PA to deliver up to 4L/min of flow.

Acute RHF post-LVAD implantation:
Acute RHF occurs in at least 20% of patients undergoing LVAD insertion and application of percutaneous RVADs is particularly effective [24]. Immediately after LVAD implantation, there is a marked improvement in LV unloading and venous return. This increased RV preload stress is exacerbated by perioperative intravenous fluids and blood products, as bleeding and coagulopathy are commonly encountered. As a result, RV work must increase significantly to maintain cardiac output. Additionally, a leftward septal shift can occur at high pump speeds, compromising RV geometry and function. Echocardiography is the primary assessment tool for monitoring patients early post-LVAD and any evidence of worsening RV function and TR, in combination with signs of systemic malperfusion, should warrant consideration of early RVAD support. Percutaneous devices are advantageous in this situation as they are easily implanted and explanted, minimally invasive, and provide direct bypass of the injured RV, allowing time for optimization of the patient and RV recovery.

Conclusion

Acute RHF remains a major cause of morbidity and mortality. A comprehensive understanding of the etiology, pathophysiology, and diagnosis of RV dysfunction informs the treatment strategy. While medical management is the initial mainstay of therapy, early surgical and catheter-based MCS can stabilize a critically ill patient and allow for RV recovery. Future efforts should focus on further understanding of the complex right-sided physiology, earlier detection of RHF, and continued development of minimally invasive RVAD technology.

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