The Diagnosis and Treatment of Postoperative Right Heart Failure

Background: Acute right heart failure is a life-threatening condition that can arise postoperatively. The options for symptomatic treatment have been markedly expanded in recent years through the introduction of percutaneously implantable mechanical cardiac support systems.

Methods: This review is based on publications retrieved by a selective literature search in PubMed as well as on guidelines from Germany and abroad.

Results: The diagnostic evaluation of right heart failure is chiefly based on echocardiography and pulmonary arterial catheterization and is intended to lead to immediate treatment. Alongside treatment of the cause of the condition, supportive management is crucial to patient survival. A variety of ventilation strategies depending on the situation, catecholamine therapies, inhaled selective pulmonary vasodilators, and cardiac support systems are available for this purpose. The in-hospital mortality of postoperative right heart failure is 5–17 %. The results of the use of cardiac support systems reported in case series are disappointing, but nonetheless good compared to what these critically ill patients would face without such treatment. In one observational study, the 30-day survival rate was 73.3%.

Conclusion: Survival is aided by the rapid recognition of right heart failure, targeted multidisciplinary treatment, and contact with an extracorporeal life support (ECLS) center for additional supportive treatment measures. Further studies on the use of pharmacological and mechanical cardiac support systems must be carried out to provide stronger evidence on which treatment recommendations can be based.

The increase in surgery performed in patients of advanced age, combined with numerous comorbidities and the increasing complexity of surgical procedures, brings with it challenges in postoperative intensive care (1). Acute right heart failure causing cardiorespiratory instability is a serious complication seen disproportionately often in certain patient groups, and can result within hours to days in acute decompensated heart failure with multiple organ failure (2). Targeted diagnostic investigations centered on echocardiography and the initiation of causal treatment are critical to the prognosis (1, 2, 3, 4). Concomitant symptomatic treatment based around carefully tailored ventilation and catecholamine therapy, inhaled selective vasodilators, and mechanical circulatory support systems can ensure the patient survives when the natural prognosis would otherwise have been poor.

Hospital mortality rates are 5% to 17%, depending on the underlying disease, the severity of the acute right heart failure, the presence of concomitant biventricular failure, and any comorbidities (4). Results from case series and small observational studies of temporary mechanical circulatory support (MCS) in acute right heart failure are sobering, but nevertheless good in terms of this critically ill patient group (1, 2, 3). Observational studies on the use of venoarterial extracorporeal circulatory support (VA-ECMO) show a hospital mortality rate of 38.6% (5), while the rate shown in a THRIVE study using a “tandem heart system” was 57% (6). In a case series that included 30 patients with right ventricular failure of various etiologies, the Impella assist device was implanted. The 30-day survival rate was 73.3% (7). The present review article provides information on diagnosis, monitoring, and general options for medication and mechanical cardiac support as well as options available at specialist centers.

Figure 4

Patient with temporary right heart strain with a large extracorporeal system

Learning goals

After reading this article, the reader should:

• Be able to list the risk groups and the symptoms of acute postoperative right heart failure;
• Know the basic pathological mechanisms, diagnostic steps, and treatment options for postoperative right heart failure;
• Know the options for further treatment available at specialist centers and be able to refer patients accordingly.

Method

A selective literature search of PubMed was carried out that included current guidelines and recommendations from professional bodies (German Society of Anesthesiology and Intensive Care Medicine [Deutsche Gesellschaft für Anästhesiologie und Intensivmedizin], European Society of Cardiology, German Cardiac Society [Deutsche Gesellschaft für Kardiologie], German Society for Thoracic and Cardiovascular Surgery [Deutsche Gesellschaft für Thorax-, Herz- und Gefäßchirurgie]), and expert opinions (review articles).

Definition of acute right heart failure

Acute right heart failure is a rapidly progressive syndrome characterized by combined forward and backward failure due to impaired right ventricular filling and/or reduced right ventricular stroke volume, often with associated subsequent right ventricular (RV) dilatation and tricuspid regurgitation (5). An increase in central venous pressure (CVP) and in the ratio of CVP to pulmonary arterial wedge pressure (PAWP), and a clinical triad of hypotension, absence of pulmonary congestion, and raised CVP, are also characteristic (8) (Figure 1).

Figure 1

Etiology and pathogenesis of acute postoperative right heart failure

Incidence

The exact incidence of postoperative right ventricular failure is difficult to determine; it varies depending on the patient group and the surgical procedure in question. Approximately 10% of noncardiac surgical patients over the age of 70 present with right ventricular failure preoperatively and are at increased risk of postoperative right heart decompensation (2). Patients undergoing cardiothoracic surgery occupy a special position. For example, the incidence of postoperative right heart failure after implantation of a left ventricular assist device (LVAD) is reported to be 10% to 20% (9).

Pathophysiology and causes

The pathophysiologic causes of postoperative right heart failure, although they end in the same condition, are diverse in origin; they can basically be divided into disorders of preload, afterload, and contractility (Figure 1).

The reduced right ventricular stroke volume that ensues leads via reduced left ventricular preload to reduced left ventricular stroke volume, with resultant cardiogenic shock (serial interdependence). The main symptoms of the systemic hypoperfusion that follows are microvascular dysfunction with lactic acidosis and organ hypoperfusion with multiple organ failure, usually accompanied by acute tricuspid regurgitation with corresponding congestive symptoms (3, 4).

Preload pathologies

In a patient with preexisting heart failure, reduced cardiac preload – e.g., due to postoperative acute bleeding or, if there is atrial fibrillation or flutter, to loss of active atrial filling – can lead to a critical drop in cardiac output. By contrast, an excessive rise in right ventricular preload can cause RV dilatation with interventricular septal shift and compression of the left ventricle, associated with decreasing stroke volume. In addition, overstretching of the right ventricle leads to acute loss of contractility. Incautious fluid replacement, especially in a patient with raised afterload and impaired contractility, can trigger acute right heart decompensation (Figure 1).

Afterload pathologies

If the pulmonary circulation changes, right ventricular stroke volume falls due to increased pulmonary vascular resistance (PVR). Postoperative causes include hypoxia, hypercapnia, reduced functional residual capacity, pulmonary infection, and direct influences on the pulmonary circulation such as edema, hemorrhage, or surgical trauma, or systemic inflammatory response (9).

A special form is acute pulmonary artery embolism, the overall annual incidence of which is from 39 to 115 per 100 000 persons. Patients who have undergone surgery, especially orthopedic or trauma surgery or abdominal or cancer surgery, are at increased risk. Obstruction of the pulmonary circulation by thrombotic material, endothelial cell swelling, and released pulmonary vasoconstrictors such as thromboxane, acutely increase right ventricular afterload.

Pulmonary microthromboses, which in the intensive care setting are frequently seen in patients with disseminated intravascular coagulopathy or, more recently, in patients with COVID-19-related pneumonia, can also trigger acute right heart failure (10, 11).

In addition, acute respiratory failure of any etiology, cardiogenic shock, and septic events can lead to an acute increase in right ventricular afterload (10, 12, 13, 14).

To complicate matters further, intensive care itself causes critical right ventricular stresses (9):

• Ventilation with positive pressures and overstretching of the alveoli;
• Catecholamine therapy, primarily with norepinephrine;
• Aggressive fluid resuscitation.

If arrhythmias increase in frequency perioperatively, that will increase myocardial oxygen consumption. Tachycardia also shortens diastolic time, resulting in coronary hypoperfusion (15).

Pathologies of contractility

Another pathophysiologic mechanism is the reduction in RV contractility in a patient with acute myocardial ischemia. It is rare for this to occur in the right ventricle alone (right heart infarction rates in infarct-related cardiogenic shock are reported to be from 5% to 16%) (8). More commonly, right heart failure occurs after acute inferior-posterior (19% to 51%) or anterior myocardial infarction (10%) (8). Where hypotension or a rise in right ventricular pressure occurs perioperatively, a coronary stenosis that previously was without hemodynamic consequences can significantly reduce myocardial perfusion and result in ischemia (9).

Cardiothoracic surgery patients as a risk group

Patients undergoing cardiothoracic surgery are a high-risk population for postoperative right heart failure. Loss of pulmonary vascular luminal cross-sectional area, such as occurs in pneumonectomy, the use of extracorporeal circulation, or use of the heparin antagonist protamine, can give rise to an acute increase in resistance in the pulmonary circulation (9).

Cardioplegic arrest, like postresuscitation cardiac arrest, may likewise lead to contractile dysfunction. When the heart is opened, an air embolism, which particularly affects the right coronary artery (RCA) because it lies uppermost, can trigger acute right heart failure (16). Mitral valve surgery and implantation of a LVAD are high-risk procedures (17).

Other entities that can cause acute right heart failure are secondary pathologies in which increased intrathoracic pressures occur, such as hemothorax or pneumothorax or extensive pleural effusion. Acute external compression, such as is caused by pericardial effusion, can lead to a clinical picture of acute right heart failure with an otherwise normal right ventricular ejection fraction (16).

Diagnosis of right heart failure

Apart from the initial clinical examination and history taking, the key diagnostic tool is bedside echocardiography, supplemented by blood tests, electrocardiography (ECG), and diagnostic imaging, coupled with monitoring via a pulmonary artery catheter. Figure 2 gives an overview of the comparative value of the various diagnostic procedures, including the recommendation grades stated in clinical guidelines. The diagnosis is made based on a synoptic overview of all the findings (4, 5).

Figure 2

ECLS, extracorporal life support

Clinical signs

The clinical presentation depends primarily on the disease. Forward failure of the right ventricle causes secondary left heart failure with reduced cardiac output. Symptoms of centralization, microvascular dysfunction, and end-organ hypoperfusion predominate: altered level of consciousness, cold and clammy skin, oligo-/anuria, and hypoxemia. Forward and backward failure results in gastrointestinal and liver failure, the latter indicating a poor prognosis. Acute backward failure also causes hepatojugular reflux, jugular vein distension, hepatic pulsations, tricuspid regurgitation, and paradoxical pulse. With time, ascites, anasarca, and peripheral edema develop (2, 3, 4, 5).

Electrocardiography

Various ECG abnormalities, although limited by their low sensitivity, are indications of acute right heart failure: sinus tachycardia, atrial fibrillation and flutter, right axis deviation, SI-QIII pattern, right bundle branch block, T-wave inversion in leads II, III, avF, and V_1–4, tall T-waves, and P pulmonale (3, 18). ST-segment elevations in the right precordial leads are diagnostic of right heart infarction (sensitivity and specificity 70% to 100%) (8).

Blood tests

There are currently no right-heart-specific biomarkers. B-type natriuretic peptide (BNP), N-terminal (NT)-pro-BNP, and cardiac troponin have a high sensitivity for acute heart failure and right heart strain in patients with pulmonary artery embolism (5, 18) (BNP: sensitivity 95%, specificity 35%). Other blood values are abnormal in line with hypoperfusion of organs (8).

Echocardiography

Postoperative echocardiographic assessment of the right heart concentrates on visualizing RV size and assessing systolic function, systolic pulmonary artery pressure (PAP), and fluid status. Bedside focused transthoracic echocardiography is primarily used to evaluate the right heart function. Imaging of the right heart after cardiothoracic surgery is often restricted by the presence of drains and trapped air. For this reason, all available scanning planes should be used, supplemented if necessary by transesophageal echocardiography.

The size of the right ventricle is determined by measuring the longitudinal and transverse diameters in the base and the middle regions plus the proximal external diameter of the right ventricle. If in the parasternal short axis the interventricular septum shows a D-shaped configuration, this indicates increased right ventricular pressure.

RV function is quantified by measuring the tricuspid annular plane systolic excursion (TAPSE; normal >20 mm, pathological <16 mm), tricuspid annular systolic velocity (TASV; normal >9.5 cm/s), and RV fractional area change (RV-FAC; normal >35%). In addition, an assessment of the overall function of the RV should be carried out, including evaluating the kinetics of the septal and apical segments and the free wall of the right ventricle. In some cases, determining RV thickness may be helpful.

To estimate systolic PAP, continuous-wave (CW) Doppler is used to measure the maximum velocity of the tricuspid regurgitant jet. The estimated right atrial pressure or measured CVP is then added (19, 20).

Pulmonary artery catheter

In patients with complex, refractory right heart failure, invasive continuous monitoring is required for diagnosis and to guide treatment (3). The S3 guideline on intensive care of patients undergoing heart surgery gives a detailed overview of the strength of the evidence, indications, and available studies relating to the use of pulmonary artery catheterization (Figure 2). So long as the physiological relationships involved and the limitations on interpretation of the findings are kept in mind, a pulmonary artery catheter does, by directly measuring pulmonary arterial pressure, provide valuable information about pressures in both the right and left atria, cardiac output, PVR, and tissue perfusion (21). As in the systemic circulation, PAP is the product of PVR and cardiac output. A rise may be an expression either of increased resistance or of improved RV function with increased cardiac output (22). Factors affecting LV function and LV backward failure also lead to higher pressures in the pulmonary circulation and can be detected in the ratio between mean PAP and PAWP in the form of postcapillary pulmonary hypertension (23).

Less invasively, transpulmonary thermodilation using pulse contour cardiac output (PiCCO) is available to monitor fluid responsiveness markers and cardiac output but does not provide information about the pulmonary circulation (22).

Treatment

Treatment for acute right heart failure is multidisciplinary; the primary aim is causal treatment that will improve the prognosis. Concomitant symptomatic treatment in the intensive care unit is required and is based on the principles of ensuring appropriate preload, reducing PVR, increasing contractility, and maintaining adequate coronary perfusion. Overall, the strength of the evidence-based recommendations is classified as moderate to weak, and the recommendations are supplemented by others from other guidelines (3, 4) (Figure 2).

Fluid management

In patients with acute right heart failure, optimizing preload through administering or, more frequently, volume deprivation is essential (3, 4). Variables marking fluid responsiveness that are assessed in the clinical context include the evolution of CVP, echocardiography including determining the diameter of the inferior vena cava and its variation over the respiratory cycle, and pulse contour analysis. Raised CVP may be due to hypervolemia, restricted atrial contraction due to atrial fibrillation, decreasing right ventricular contractility as an efficiency-related variable, or pericardial tamponade, pneumothorax, increased intraabdominal pressure, or increased ventilatory pressure. In evaluating CVP, it is important to take into account any limitations or possible misinterpretations. Of particular relevance is tricuspid regurgitation, a frequently concomitant pathology (9).

Fluids can be given with caution if there are signs of reduced preload, e.g., CVD of 8–10 mm Hg or PAWP/CVP ratio ≥1, according to the guideline on fluid therapy in adults (24). Fluid responsiveness in the individual patient can be further tested by passive leg raising (autotransfusion). In case of RV volume overload, the right ventricle should be quickly relieved by giving vasodilators, inodilators, or loop diuretics, or even a kidney transplant (3, 4).

Stabilization of heart rhythm

Optimal atrial filling and contraction are key in the treatment of heart failure (4). Maintaining or restoring sinus rhythm and rate control are fundamental (15). In addition, a heart rate of 90 to 100 beats/min increases cardiac output. A temporary pacemaker is often necessary in intensive care after heart surgery in order to ensure constant atrial stimulation at an optimized rate (9).

Ventilation strategy

According to the S3 guideline on invasive ventilation and the use of extracorporeal techniques in acute respiratory failure, priority should be given to noninvasive ventilation or respiratory support by means of high-flow nasal oxygen therapy (25). Should invasive ventilation become necessary, the following basic principles should be followed: high ventilation pressure, hypercapnia, and acidosis should be avoided because of their pulmonary vasoconstrictor effects (3). By compressing thoracic blood vessels, ventilation leads to a drop in preload and a rise in afterload of the right heart, while the left heart afterload is reduced. Insufficient oxygenation results in hypoxic pulmonary vasoconstriction (HPV) and may cause the patient’s condition to deteriorate. Positive end-expiratory pressure (PEEP) should always be employed. In addition to protecting the lungs, improving oxygenation, re-opening atelectasis, and reducing HPV, it results in reduced cardiac preload and afterload. Overstretching of the alveoli with vascular compression and hyperinflammation must be avoided (9). Overall, except for permissive hypercapnia, the staged protocol of the Acute Respiratory Distress Syndrome (ARDS) Network study should be used and protective ventilation strategies applied (25).

Reducing elevated pulmonary vascular resistance

For acute drug therapy, nitroglycerin is available. Given intravenously it lowers PVR, but its vasodilator effect is nonselective. Systemic hypotension and intrapulmonary right-to-left shunts leading to reduced oxygenation are adverse effects, so it is not a first-choice drug (9).

Inhaled selective pulmonary vasodilators are better options. Inhaled nitric oxide (iNO) leads to relaxation of pulmonary vascular smooth muscle, right ventricular afterload falls, cardiac output rises, and the redistribution of perfusion leads to improved oxygenation. Because it is rapidly metabolized, no significant hypotension occurs. Prolonged bleeding times due to impaired platelet function and the occurrence of potentially toxic substances have been described as side effects, but do not occur at therapeutic doses (26). In patients with fixed pulmonary hypertension due to fibrotic remodeling, pulmonary vasodilators have minimal effect (9). Observational studies after cardiac surgery support this approach. For instance, in a retrospective study by Maxey et al. , iNO lead to a significant drop in mean PAP (35.3 mm Hg before iNO, 22.7 mm Hg after iNO, P <0.001) followed by a rise in cardiac index (2.3 L × min^-1 × m^-2 before iNO, 3.1 L × min^-1 × m^-2 after iNO), as well as improved oxygenation (Pao₂/Fio₂ 183 before iNO, 254 after iNO) (26).

The prostaglandin I₂ (PGI₂) analog iloprost, with its more potent pulmonary vasodilation and superior ease of application via ultrasonic nebulizer, is a favorable option available for intermittent use. It can also be used in nonintubated patients and has a longer duration of action. Systemic effects are detectable but are very small. PGI₂ is regarded as a potent platelet aggregation inhibitor. However, no negative effects of inhaled iloprost on coagulation have been demonstrated (27, 28). This approach is based on a comprehensive prospective study which showed that inhaled iloprost reduced mean PAP (36 ± 9 mm Hg iloprost, 30 ± 8 mm Hg after iloprost, P <0.001) and improved oxygenation (Pao₂/Fio₂ 95 ± 36 before iloprost, 186 ± 111 after iloprost, P = 0.001) (27).

Receptor-independent inotropes such as phosphodiesterase 3 (PDE3) inhibitors (enoximone, milrinone) are also available. These increase contractility and reduce systemic and pulmonary resistance (9).

Coronary perfusion pressure

Sufficient systemic perfusion pressure is required for adequate coronary and organ perfusion. Coronary perfusion is negatively affected by arterial hypotension, raised PVR, and right ventricular dilatation, as well as by shortened diastole against a background of tachycardia (15).

The aim of carefully nuanced catecholamine therapy is to increase systemic resistance while maintaining a reduced right ventricular afterload. Potent vasoconstrictors include norepinephrine at moderate dosages and vasopressin, which has less effect on the pulmonary circulation and almost no proarrhythmic effects (29, 30).

Increasing contractility

Myocardial RV function can be maximized by rhythm management, rate control, and increasing contractility (3, 4).

All available inotropes affect both ventricles, with the response being less in the right ventricle because of its lower myocardial strength, contractile reserve, and β₁-receptor density. Except for levosimendan, all of them are proarrhythmogenic, increase myocardial oxygen consumption, and trigger cardiotoxic events.

Norepinephrine with its balance of α- and β₁-adrenergic effects is the first choice (9); with this drug dose-dependent pulmonary vasoconstriction limits the increase in contractility. Next, the β-mimetic dobutamine may be added. At low dosages, dobutamine causes systemic and pulmonary vasodilation with reduction of afterload; at higher dosages, peripheral vasoconstriction rises (8, 9). Its efficacy is limited by down-regulation of β₁-receptors in patients with chronic heart failure and in those on long-term β-blockers (9).

The treatment may be supplemented with PDE3 inhibitors, which increase myocardial contractility while at the same time promoting diastolic relaxation.

In the S3 guideline on infarct-related cardiogenic shock, the calcium sensitizer levosimendan received the recommendation “may be used” when the hemodynamic effect of catecholamines is inadequate, and in this situation it was preferred over PDE3 inhibitors (8). Its favorable effect profile includes reducing PAWP and pulmonary artery and central venous pressures while at the same time increasing right ventricular function (stroke volume and TAPSE) (3, 4, 31, 32, 33). Peripheral vasodilation caused by inodilators may necessitate the use of vasopressors.

Epinephrine, as a reserve drug, is a potent inotrope with dose-dependent α- and β-mimetic effects. At low dosages, contractility enhancement predominates, whereas at higher dosages, peripheral vasoconstriction predominates, with the adverse effects of increased afterload (9).

Mechanical circulatory support in right heart failure

Venoarterial ECMO can support all forms of acute circulatory or pulmonary failure. It is regularly used in patients in cardiogenic shock due to acute left or acute decompensated heart failure (34). The data supporting its use in cases of isolated right heart failure are poor but it is used nonetheless on a theoretical basis because it takes over the entire heart and lung function (5). Direct RV bypass as a temporary RV assist device (RVAD) is a variant of venoarterial ECMO. In this system, venous blood is drained through a cannula placed in the right atrium and fed from there into the pulmonary artery (Figure 3a). Surgical access via a partial or full sternotomy is usually required. If respiratory failure is also present, an oxygenator may be connected into the bypass system (5, 35, 36).

Figure 3

Chest radiographs of a patient with a left ventricular assist device (LVAD) (*) and a temporary right ventricular assist device

Percutaneous solutions available include the “tandem heart system” in combination with the Protek Duo cannula (Liva Nova PLC, London, UK) and the Impella RP (37). The raised assisted RV output leads to a secondary rise in total cardiac output. The key element of the “tandem heart” is the Protek Duo cannula, which is implanted via the right jugular vein in a similar way to pulmonary artery catheterization. Blood flow is generated via an inflow in the right atrium and an outflow in the pulmonary artery. If the patient is also in respiratory failure, an oxygenator can be added in (36, 38). The Impella RP, working as an axial pump, is implanted via the femoral vein; blood is drained via an inflow in the right atrium and fed in via an outflow above the pulmonary valve (Figure 3b). With this device, adding in oxygenation is not possible (39, 40).

Reported in-hospital mortality rates from acute right heart failure ranging from 38.6% (VA-ECMO) to 57% (“tandem heart system”) in small observational studies appear sobering, but in relation to the very poor natural outcome in this critically ill patient group they are good (6, 7). However, the available data are only descriptive. As with resuscitation—which the use of mechanical circulatory support per se equates to – the ability to generate evidence is limited by ethical concerns. Ultimately, the clinical decision regarding mechanical circulatory support is always to be taken on a case-by-case basis, weighing the individual patient’s assessed risk against the assessed prognosis.

Conflict of interest statement
The authors declare that no conflict of interest exists.

Manuscript received on 30 June 2021, revised version accepted on 14 April 2022.

Translated from the original German by Kersti Wagstaff, MA.

Corresponding author
Dr. med. Juliane Ende

Klinik und Poliklinik für Anästhesiologie und Intensivtherapie

Universitätsklinikum Carl Gustav Carus an der Technischen Universität Dresden

Fetscherstr. 74, 01307 Dresden, Germany

Cite this as:
Ende J, Wilbring M, Ende G, Koch T: The diagnosis and treatment of postoperative right heart failure. Dtsch Arztebl Int 2022; 119: 514–24. DOI: 10.3238/arztebl.m2022.0207

►Supplementary material

Case Report:
www.aerzteblatt-international.de/m2022.0207

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