Right Ventricular Dysfunction in Cardiac Anesthesia: Perioperative Assessment and Underlying Mechanisms

Abstract

The importance of right ventricular (RV) function has often been overlooked until recently; however, RV function is now recognized as a significant prognostic predictor in medically managing cardiovascular diseases and cardiac anesthesia. During cardiac surgery, the RV is often exposed to stressful conditions that could promote perioperative RV dysfunction, such as insufficient cardioplegia, volume overload, pressure overload, or pericardiotomy. Recent studies have shown that RV dysfunction during cardiac anesthesia could cause difficulty in weaning from cardiopulmonary bypass or even poor postoperative outcomes. Severe perioperative RV failure may be rare, with an incidence rate ranging from 0.1% to 3% in the surgical population; however, in patients who are hemodynamically unstable after cardiac surgery, almost half reportedly present with RV dysfunction. Notably, details of RV function, particularly during cardiac anesthesia, remain largely unclear since long-standing research has focused predominantly on the left ventricle (LV). Thus, this review aims to provide an overview of the current perspective on the perioperative assessment of RV dysfunction and its underlying mechanisms in adult cardiac surgery. This review provides an overview of the basic RV anatomy, physiology, and pathophysiology, facilitating an understanding of perioperative RV dysfunction; the most challenging aspect of studying perioperative RV is assessing its function accurately using the limited modalities available in cardiac surgery. We then summarize the currently available methods for evaluating perioperative RV function, focusing on echocardiography, which presently represents the most practical tool in perioperative management. Finally, we explain several perioperative factors affecting RV function and discuss the possible mechanisms underlying RV failure in cardiac surgery.

Graphical abstract

Keywords

right ventricular function / cardiac anesthesia / echocardiography / pulmonary artery catheters

1. Introduction

Importantly, the significance of the right ventricular (RV) function in medically managing cardiovascular diseases and cardiac anesthesia is now being recognized since, until recently, the RV function received much less attention than the left ventricular (LV) function [1, 2, 3, 4]. This overlooking of the RV may have originated from the Fontan procedure, whereby the circulatory system is established without a functional RV [5]. Yet, for whatever reason, cardiology research mainly focused on the LV, with the RV even noted as the “forgotten chamber” [6]. However, the important role of RV function has recently been shown in cardiovascular physiology [7, 8], and numerous studies have suggested the prognostic impact of the RV in cardiovascular diseases, even when LV global function is preserved [9, 10]. During cardiac surgery, the RV is often exposed to stressful conditions that could lead to perioperative RV dysfunction, such as insufficient cardioplegia, volume overload, pressure overload, or pericardiotomy. Recent studies have further shown that RV dysfunction during cardiac anesthesia could cause difficulty in weaning from cardiopulmonary bypass (CPB) or even poor postoperative outcomes [11, 12, 13, 14, 15]. Severe perioperative RV failure may be relatively rare, with an incidence rate ranging from 0.1% to 3% in the surgical population [3, 16]. However, in patients who are hemodynamically unstable after cardiac surgery, almost half reported RV dysfunction [17]. Moreover, in patients with advanced heart failure (HF) who underwent implantation of an LV assist device (LVAD), RV failure occurred in approximately 20–30% of patients [18].

Owing to the previous long-term focus on LV function, research on RV function remains relatively new, with limited clinical evidence regarding perioperative RV function. Therefore, this review aims to understand the current perspective on perioperative RV function in adult cardiac surgery to facilitate future research in this field. The review initially provides an overview of the basic RV anatomy, physiology, and pathophysiology, which will aid understanding of the perioperative RV function. The most challenging aspect of studying the RV in a perioperative setting is accurately assessing RV function using the limited modalities available in cardiac surgery. We then summarize the current methods for evaluating perioperative RV function, focusing on echocardiography, the most practical tool in cardiac anesthesia. Finally, we explain several perioperative factors affecting RV function and discuss the possible mechanisms underlying perioperative RV failure.

2. RV Anatomy, Physiology and Pathophysiology

The anatomy of the RV is more complicated than that of the LV, which makes accurately assessing its function more difficult; this is one of the main reasons why the RV function remains poorly understood. While the shape of the LV has been described as a rugby ball, the RV is more uniquely shaped, with the shape roughly described as triangular, although the shape could appear crescent-shaped when viewed in cross-section [19]. The volume of the RV is 10–15% greater than that of the LV; however, because the free wall in the RV is thinner, the weight of the RV is approximately 1/6 to 1/3 less than the LV [20, 21]. Thus, because of the larger (diastolic) volume of the RV, the ejection fraction (ejection volume/diastolic volume) would be lower in right ventricular ejection fraction (RVEF) than left ventricular ejection fraction (LVEF) [3]. In contrast, the compliance of the RV is higher than that of the LV because of its thinner wall, making the RV relatively more tolerant to volume overload than to pressure overload [22].

The outlet of the LV forms an acute angle with its inlet; thus, the LV contracts with twisting, causing a vortex in blood outflow to eject at a sharp angle [23]. In contrast, the RV outlet forms a more obtuse angle; therefore, the blood outflow is more streamlined, and RV contraction involves a peristalsis-like motion [24, 25]. Simply, the RV has three wall motions: (1) inward movement of the free wall, (2) shortening of the long axis, and (3) traction of the free wall due to LV contraction [19]. Long-axis shortening is the most important of these three motions in healthy adults, accounting for approximately 75% of the RV contractions [26, 27]. This is largely due to the unique myocardial layers in the RV. While the LV myocardium consists of three distinct layers, the RV has two layers, circumferential and longitudinal; the longitudinal layer accounts for approximately 75% of the RV myocardium thickness [26, 27]. For this reason, many echocardiographic parameters assess longitudinal RV contraction [28, 29]. However, in pathological conditions, such as in patients with pulmonary hypertension (PH), global RV function correlates more with transverse movement than longitudinal contraction [26, 27, 30]. Similar alterations in RV contraction reportedly occur after CPB during cardiac surgery, as described in detail in Section 3 [10, 12]. The final RV traction motion caused by LV contraction is also an important contraction pattern in the perioperative management of the RV. Since the LV and RV share the septum, the LV contractions contribute 20–40% of the RV cardiac output (CO) [8, 10]. This “ventricular interdependence” can be easily assessed and is often helpful in the hemodynamic management of the RV during cardiac anesthesia.

RV function can potentially be impaired in pathophysiological conditions, such as pressure overload, volume overload, or cardiomyopathy of the RV, with or without the patient’s symptoms [7]. In this point of view, RV “dysfunction” is defined by abnormal RV functional parameters, and “failure” is defined by hemodynamic decompensation with typical clinical signs or symptoms. The European Society of Cardiology proposed staging RV dysfunction and failure from Stage 1 to 4 in the position statement of HF with preserved LVEF (HFpEF) [9]. Stage 1 is defined as at risk for right HF (RHF) without RV dysfunction and signs/symptoms, and Stage 2 is RV dysfunction without signs/symptoms. Stage 3 is RV dysfunction with prior or current signs/symptoms, and Stage 4 is with refractory signs/symptoms requiring specialized interventions. RHF can occur acutely or chronically [10]. Acute RHF is typically caused by a sudden increase in RV afterload (e.g., pulmonary embolism, acute respiratory failure) or a decrease in RV contractility (e.g., RV ischemia, acute myocarditis). RV dilation due to decreased RV stroke volume can impair LV diastolic filling, worsening systemic hypoperfusion. This represents the aforementioned ventricular interdependence from the RV to the LV. Chronic RHF is commonly caused by gradually increased RV afterload, most frequently due to left HF (LHF). Pathologically, RV myocytes in chronic RHF show similar alterations to the remodeling in LHF [31].

3. Assessment of RV Function in Cardiac Surgery

Owing to the complex anatomy of the RV, as described in Section 2, assessing the RV function remains clinically challenging, particularly with the limited modalities available in the perioperative setting. Cardiac magnetic resonance imaging (MRI) is considered the gold standard measurement for accurately evaluating this complex anatomy [10]. However, MRI is not feasible during cardiac surgery, at least in the current clinical setting. From this perspective, there is no gold standard for assessing RV function during cardiac surgery; therefore, the most appropriate methods available in the clinical situation should be chosen. Due to the difficulty in determining RV function, establishing a perioperative treatment of RV failure remains limited; thus, the treatments recommended for managing RV failure during cardiac anesthesia should instead remain followed [8, 10]. This section discusses the current understanding of several methods for assessing perioperative RV function and summarizes their characteristics for appropriate use (Table 1, Ref. [8, 10, 12, 28, 29]).

3.1 Clinical Assessment

As the gold standard for assessing RV dysfunction during cardiac surgery is lacking, the first step in recognizing RV failure in current practice is often the usual clinical assessment of perioperative hemodynamic instability, with a quick estimation of RV dysfunction. For a quick echocardiographic assessment of the RV, eyeballing RV systolic function and dilatation, D-shaped septum, tricuspid regurgitation, or inferior vena cava diameter are useful parameters [14]. As mentioned above, in hemodynamically unstable patients after cardiac surgery, RV dysfunction was present in approximately half of the patients, which was simply assessed by right ventricular fractional area change (RVFAC) \le25% or severe RV dilation [17]. Jabagi et al. [32] suggested that either direct visual estimation of reduced RV contraction in the surgical field, a marked decrease in RV echocardiographic parameters, or poor hemodynamic parameters in pulmonary artery catheters could achieve clinical assessment of perioperative RV dysfunction. Visual RV assessment in the surgical field is a traditional method and is often clinically useful. However, it should be noted that the visual assessment is mostly of the RV anterior motion; thus, the assessment lacks an evaluation of the inferior or lateral wall of the RV. In addition, due to the complex anatomy of the RV, visual assessment of RV function is reportedly difficult with echocardiography [33], which is often accurate when assessing LVEF [34].

3.2 Echocardiographic Assessment

Transesophageal echocardiography (TEE) is often available during cardiac anesthesia, is minimally invasive, and is cost-effective; thus, TEE is one of the most practical methods for assessing perioperative cardiac function [35, 36]. However, TEE is reportedly much less accurate for assessing RV function than cardiac MRI, particularly with two-dimensional echocardiography [28, 29]. This is due to the unique shape of the RV, difficulty in visualizing the endocardial border with the developed trabeculae in the RV, or difficulty in aligning the RV away from the esophagus [12, 28, 29]. In addition, because the RV wall is thinner than the LV wall, the echocardiographic parameters of the RV function are more load-dependent; therefore, pressure- and volume-loaded conditions should always be considered during examinations [28].

There are two approaches for assessing RV systolic function by echocardiography: global and regional. With RVFAC as a representative example, global assessment is a conventional method for the echocardiographic assessment of systolic function. However, assessing the whole RV accurately is difficult because of its complex anatomy. Since long-axis contraction is the main component of RV systolic function in healthy adults, as mentioned above, echocardiographic regional assessment of longitudinal measures, such as tricuspid annular plane systolic excursion (TAPSE) or RV strain, is also commonly used. Fig. 1 summarizes the commonly used two-dimensional views and their measurement locations for assessing RV function in TEE.

3.2.1 Global RV Systolic Function

“D”-shaped ventricular septum in the transgastric short-axis view is a commonly observed clinical sign of RV ed fidysfunction, which is a qualitative RV assessment. As mentioned above, the RV crossed section is crescent in shape; thus, the ventricular septum in the short-axis view normally has a convex shape to the RV, and the LV forms a round “O” shape. However, in an RV-overloaded condition, the ventricular septum could change to a flattened shape, creating a “D” shape with a convex shape remaining on the LV lateral wall. A flattened septum during systole suggests pressure overload in the RV, while that during diastole suggests volume overload [12]. This is a convenient qualitative method, but it can also be evaluated quantitatively by measuring the ratio of the vertical to the horizontal diameter of the LV or the ratio of the horizontal diameter of the RV to that of the LV [37, 38].

RVFAC is the method conventionally used for assessing RV systolic function and is calculated as the percentage of the end-systolic to the end-diastolic area of the RV in a mid-esophageal 4-chamber view. Although similar to the commonly used two-dimensional LVEF calculated by Simpson’s biplane method, sagittal plane measurements are unsuitable for the RV due to its unique shape [28]. Thus, the RVFAC is measured only in a single plane, which is the main limitation of this method, as data from the anterior, infundibular, or inferior walls of the RV are missing. A RVFAC 35% is considered to indicate RV dysfunction, and several studies have shown that a reduced RVFAC is associated with higher morbidity and mortality after cardiac surgery [39, 40, 41].

The right ventricular index of myocardial performance (RIMP), also known as the Tei index or myocardial performance index (MPI), is a parameter of RV systolic and diastolic function, which is calculated as the sum of the isovolumetric contraction time and isovolumetric relaxation time, divided by the ejection time. The RIMP can be obtained by pulsed-wave or tissue Doppler. Using pulsed-wave Doppler, two separate images of the tricuspid inflow and right ventricular outflow tract (RVOT) should be obtained to measure the time interval from the closure to the opening of the tricuspid valve and the ejection time through the RVOT. Tissue Doppler is generally preferred because the RIMP can be measured using a single image of the tricuspid annulus in a 4-chamber view. However, a high-quality signal is required to calculate the above parameters accurately [29]. The normal upper limit of the RIMP is reportedly 0.4 by pulsed-wave Doppler and 0.55 by tissue Doppler [28].

Three-dimensional RVEF is currently the most accurate echocardiographic method for assessing RV systolic function and correlates well with the RVEF measured by cardiac MRI with high reproducibility. As it tends to underestimate RVEF slightly compared with MRI [19, 42], the lower limit of the three-dimensional RVEF is commonly set at 44% or 45% [28, 29]; comparatively, the lower limit of RVEF for cardiac MRI is 45%. Given the complex RV anatomy, it is reasonable that three-dimensional measurement is the most accurate. However, this measurement still has some technological issues, such as potential image dropout or software availability [12, 19, 42]. However, as technological issues are likely to improve in the near future, three-dimensional RVEF may become the gold standard in the perioperative assessment of RV systolic function, given that MRI is unavailable in the operating room.

3.2.2 Regional RV Systolic Function

Regional assessment of RV longitudinal contractions, such as TAPSE, RVIVA (right ventricular isovolumic acceleration), or RV strain, is clinically useful because longitudinal movement is easier to measure than assessing the global function of the RV by echocardiography, given its complex anatomy. However, the longitudinal RV measures are based on the principle that longitudinal contraction represents the major component of RV systolic function. This is true in healthy adults but may be incorrect in some pathological conditions, such as PH and cardiac surgery after CPB. Recent evidence has suggested that pericardiotomy and/or CPB during cardiac surgery often decrease RV longitudinal contraction, even when global function is preserved, with increased RV transverse shortening [43]. This alteration in RV contraction persists for approximately one week after surgery [44]. A similar reduction in longitudinal contractions is observed in patients with PH [26, 27, 30]. Although the clinical implications of changes in RV contraction remain unclear, the usefulness of regional RV assessment in cardiac surgery may be limited [10, 12].

3.2.3 RV Diastolic Function

Although RV systolic function remains unclear, RV diastolic function is even less studied, particularly in cardiac surgery. This is largely due to the acoustic angle dependence of TEE or positive pressure ventilation during surgery [12]. Using transthoracic echocardiography (TTE), the trans tricuspid E/A or E/e’ ratio is the parameter most commonly used to assess RV diastolic function [28, 29]; however, it may be difficult to measure accurately during cardiac anesthesia because of the angle-dependence of TEE. For the same reason, hepatic or splenic vein Doppler imaging may be unsuitable for perioperative assessment. RV diastolic dysfunction has been reported in many types of cardiovascular diseases and is a possible independent predictor of increased mortality [45, 46, 47]. Therefore, further studies are warranted to establish reliable echocardiographic parameters for perioperative assessment of RV diastolic function.

3.3 Hemodynamic Assessment by Pulmonary Artery Catheters

Pulmonary artery catheters (PACs) have been widely used in cardiac surgery since the 1970s; however, many recent studies have shown that PACs do not significantly improve patient outcomes and may even be harmful because of the potential complications associated with catheter use [48, 49, 50]. Therefore, PACs are currently used much less frequently during cardiac anesthesia but remain useful tools for detailed hemodynamic monitoring. Since right arterial pressure (RAP) is easily measured using central venous catheters during cardiac anesthesia, elevated RAP is one of the most common hemodynamic signals associated with perioperative RV dysfunction. However, the elevated RAP may be derived from increased left atrial pressure, which can be evaluated by measuring pulmonary capillary wedge pressure (PCWP). When PACs are used, the right atrium (RA)/PCWP ratio may be useful for assessing RV dysfunction. This ratio is usually about 0.5 but is higher in patients with RV dysfunction [51, 52]. In patients undergoing LVAD implantation, when the diagnosis of RV failure is sufficiently clear, with presumed normal LV function with the implanted devices, a preoperative RA/PCWP ratio >0.63 predicts RV failure after surgery [53]. In addition, PCWP is useful for estimating the causes of PH. Elevated PCWP suggests post-capillary PH, not pre-capillary PH [54]. The RV stroke work index (RVSWI) is another useful parameter, which is calculated as “RVSWI = 0.136 \times SVI \times(mPAP - RAP)” (SVI; stroke volume index, mPAP; mean pulmonary artery pressure). An RVSWI 4 suggests RV dysfunction and is reportedly associated with increased mortality [55, 56].

PACs provide many hemodynamic parameters, among which continuous CO, measured using the thermodilution technique, is one of the most useful parameters for perioperative hemodynamic management [54]. PACs can assess RV function specifically by estimating right ventricular end-diastolic volume (RVEDV) and RVEF using a rapid-response thermistor. In general, the thermodilution-derived RVEF underestimates the MRI-measured RVEF; thus, the lower limit of the RVEF by PACs is often set at 40%. RV physiology may explain this underestimation. An animal study revealed that the reduced temperature in the RA caused by cold fluid injection did not return to baseline within a single heartbeat [57]. In addition, MRI of the human heart demonstrated a recirculation of blood in the RV due to the phasic RV contraction pattern [25]. Although measuring the RVEF using PACs may be less accurate than MRI, it could be useful for trend monitoring, particularly in perioperative settings without reliable RV monitoring parameters.

3.4 Other Assessment Methods

Biochemical markers are frequently used in patients undergoing cardiac surgery, which are useful for the clinical management of HF but are not specific for RV failure [58, 59]. BNP (B-type natriuretic peptides) and cardiac troponin levels are reportedly elevated in patients with RV failure caused by acute pulmonary embolism (PE) and are associated with poor clinical outcomes [60, 61, 62]. However, both markers are also elevated in LV failure and are not sufficiently sensitive to assess the degree of dysfunction in each ventricle. Some studies have reported the development of specific biomarkers for RV dysfunction that may help evaluate and treat RV failure in the near future [10].

Electrocardiography (ECG) is often used for preoperative evaluation in cardiac surgery patients and may have diagnostic capabilities for RV dysfunction. On a 12-lead ECG, a qR pattern in V1 may indicate acute RV failure, and SI, QIII, TIII (deep S wave in I lead, and Q wave and negative T wave in III lead) is a famous pattern for pulmonary embolism [63, 64]. In addition, several studies have shown that QRS duration, particularly on the right-sided chest leads (V1, V2), correlates well with RV function and volume as evaluated using MRI [65]. Despite the potential utility of right-sided chest leads, because the chest leads are often unavailable during cardiac surgery, we recently investigated the usefulness of QRS duration on intracardiac right ventricular ECG obtained through a pacing catheter. Intravenous pacing is a useful tool in a small surgical site of minimally invasive cardiac surgery. Additionally, QRS duration in the RV has been shown to be useful for assessing RV function during cardiac surgery [66]. However, we need to be careful that ECG findings are often nonspecific, and even the famous “SI, QIII, T III” pattern is known to be seen in only about 20% of patients with pulmonary embolism [67]. Furthermore, the ECG waveform can be altered by many types of perioperative drugs and surgical stress [68, 69, 70].

4. RV Function in Cardiac Surgery

Although severe perioperative RV failure may be relatively rare, the incidence of mild-to-moderate RV failure remains unclear, which could have significant clinical implications. Many factors in cardiac surgery can cause perioperative RV failures, such as pre-existing RV dysfunction, pericardiotomy, CPB, mechanical ventilation, or RV volume and pressure overload. This section explains several factors affecting RV function in cardiac surgery and discusses the possible mechanisms underlying perioperative RV dysfunction.

Preoperative RV dysfunction is a possible cause of postoperative RV failure. Due to ventricular interdependence, patients with HF and reduced LVEF (HFrEF) often have RV dysfunction. In a meta-analysis, the prevalence of RV systolic dysfunction in HFrEF was as high as 48% [71]. Similar to patients with HFrEF, RV dysfunction is common in patients with HFpEF, with a prevalence of approximately 20%, as confirmed using MRI [72]. In patients with inferior wall myocardial infarction (MI), 30–50% are known to have MI in the RV [73, 74]. Hemodynamic compromise is less common in patients with right ventricular myocardial infarction (RVMI) than in those with LVMI but still occurs in 25–50% of patients with RVMI [75]. Valvular disease can also directly or indirectly affect RV function. In patients undergoing corrective surgery for isolated tricuspid regurgitation, the effective RVEF measured using MRI was reduced in more than half of the population [76]. In patients with left-sided valvular disease undergoing surgical treatment, preoperative RV dysfunction was observed in approximately 20% of the population [77]. Particularly, RV dysfunction was reportedly present in about 30% of mitral regurgitation cases [78]. PH, with or without valvular disease, is another well-known cause of RV failure. Since many factors in cardiac surgery could increase pulmonary vascular resistance, such as hypoxia, hypercapnia, acidosis, hypothermia, or anemia, we should carefully monitor RV function and optimize the perioperative factors to prevent perioperative RV failure [79, 80].

Intraoperative factors in cardiac surgery can directly reduce RV function, but among them, CPB appears to be the major cause of perioperative RV dysfunction. Several studies have shown that a long CPB duration strongly predicts RV failure during cardiac anesthesia [81, 82, 83]. Further, differences in cardioplegia can affect RV function after CPB. Warm cardioplegia (generally 34–35 °C) might yield better RV function than cold cardioplegia (less than 4 °C) after CPB [84, 85]. During CPB, many types of cytokines are induced, and endothelin-1, in particular, may play an important role in postoperative RV dysfunction through vasoconstriction of the pulmonary arterioles [86]. Coronary air embolism and acute graft occlusion are also well-known causes of RV failure during cardiac surgery. In addition to CPB, pericardiotomy itself, for example, could cause non-physiological patterns of RV filling, leading to possible RV dysfunction [87, 88, 89]. RV volume and pressure overload during cardiac surgery also potentially cause postoperative RV dysfunction [90, 91]. General anesthetics also appear to affect RV function negatively [92, 93, 94]. Although it is difficult to accurately evaluate the effects of anesthetics during general anesthesia because the above-mentioned intraoperative factors could also affect RV function, inhalational anesthetics, including sevoflurane and isoflurane, or propofol, have reportedly reduced echocardiographic RV parameters. Some studies compared the effects of inhalational and intravenous anesthetics on RV parameters; however, these results were inconsistent [95, 96, 97]. Although the specific mechanisms underlying postoperative RV dysfunction remain unclear, the above-mentioned perioperative factors might collectively affect RV function and cause RV failure during cardiac anesthesia.

5. Conclusions

Although much information on RV function, particularly during cardiac anesthesia, requires to be elucidated, this field is clearly developing, as summarized in this review. However, the major issue in this area is that the perioperative assessment of RV function has yet to be established without a gold standard that can replace cardiac MRI. Even if cardiac MRI were available in the operating room, it may not be useful for evaluating RV function during cardiac anesthesia. Currently, there are many parameters to assess perioperative RV function, yet we should understand their characteristics and choose the most suitable parameters in the perioperative setting to ensure their proper use. Hence, further technological progress and new ideas are needed to assess perioperative RV function accurately and practically. Real-time 3D RVEF or RV-specific biomarkers may be the most feasible methods. Once a gold standard for perioperative RV assessment has been established, more attention should be paid to the perioperative treatment of RV failure, which is being investigated in medical management but remains in its infancy. Elucidating the mechanisms through which perioperative RV dysfunction occurs may also help to improve its treatment and prevention. This review summarizes the current status and problems associated with perioperative RV function in cardiac anesthesia. Among these various issues, improving perioperative RV assessment is the most important, and we may be able to contribute to a better understanding and treatment of perioperative RV failure. Following an extended research period on LV function in cardiology and cardiac surgery, research should instead focus on the RV function.

References

[1] Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I: Anatomy, physiology, aging, and functional assessment of the right ventricle. Circulation. 2008; 117: 1436–1448. https://doi.org/10.1161/CIRCULATIONAHA.107.653576

[2] Haddad F, Doyle R, Murphy DJ, Hunt SA. Right ventricular function in cardiovascular disease, part II: pathophysiology, clinical importance, and management of right ventricular failure. Circulation. 2008; 117: 1717–1731. https://doi.org/10.1161/CIRCULATIONAHA.107.653584

[3] Haddad F, Couture P, Tousignant C, Denault AY. The right ventricle in cardiac surgery, a perioperative perspective: I. Anatomy, physiology, and assessment. Anesthesia and Analgesia. 2009; 108: 407–421. https://doi.org/10.1213/ane.0b013e31818f8623

[4] Haddad F, Couture P, Tousignant C, Denault AY. The right ventricle in cardiac surgery, a perioperative perspective: II. Pathophysiology, clinical importance, and management. Anesthesia and Analgesia. 2009; 108: 422–433. https://doi.org/10.1213/ane.0b013e31818d8b92

[5] Fontan F, Baudet E. Surgical repair of tricuspid atresia. Thorax. 1971; 26: 240–248. https://doi.org/10.1136/thx.26.3.240

[6] Rigolin VH, Robiolio PA, Wilson JS, Harrison JK, Bashore TM. The forgotten chamber: the importance of the right ventricle. Catheterization and Cardiovascular Diagnosis. 1995; 35: 18–28. https://doi.org/10.1002/ccd.1810350105

[7] Sanz J, Sánchez-Quintana D, Bossone E, Bogaard HJ, Naeije R. Anatomy, Function, and Dysfunction of the Right Ventricle: JACC State-of-the-Art Review. Journal of the American College of Cardiology. 2019; 73: 1463–1482. https://doi.org/10.1016/j.jacc.2018.12.076

[8] Harjola VP, Mebazaa A, Čelutkienė J, Bettex D, Bueno H, Chioncel O, et al. Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology. European Journal of Heart Failure. 2016; 18: 226–241. https://doi.org/10.1002/ejhf.478

[9] Gorter TM, van Veldhuisen DJ, Bauersachs J, Borlaug BA, Celutkiene J, Coats AJS, et al. Right heart dysfunction and failure in heart failure with preserved ejection fraction: mechanisms and management. Position statement on behalf of the Heart Failure Association of the European Society of Cardiology. European Journal of Heart Failure. 2018; 20: 16–37. https://doi.org/10.1002/ejhf.1029

[10] Konstam MA, Kiernan MS, Bernstein D, Bozkurt B, Jacob M, Kapur NK, et al. Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2018; 137: e578–e622. https://doi.org/10.1161/CIR.0000000000000560

[11] Mandoli GE, Cameli M, Novo G, Agricola E, Righini FM, Santoro C, et al. Right ventricular function after cardiac surgery: the diagnostic and prognostic role of echocardiography. Heart Failure Reviews. 2019; 24: 625–635. https://doi.org/10.1007/s10741-019-09785-2

[12] Silverton NA, Gebhardt BR, Maslow A. The Intraoperative Assessment of Right Ventricular Function During Cardiac Surgery. Journal of Cardiothoracic and Vascular Anesthesia. 2022; 36: 3904–3915. https://doi.org/10.1053/j.jvca.2022.05.028

[13] Merlo A, Cirelli C, Vizzardi E, Fiorendi L, Roncali F, Marino M, et al. Right Ventricular Dysfunction before and after Cardiac Surgery: Prognostic Implications. Journal of Clinical Medicine. 2024; 13: 1609. https://doi.org/10.3390/jcm13061609

[14] Varma PK, Jose RL, Krishna N, Srimurugan B, Valooran GJ, Jayant A. Perioperative right ventricular function and dysfunction in adult cardiac surgery-focused review (part 1-anatomy, pathophysiology, and diagnosis). Indian Journal of Thoracic and Cardiovascular Surgery. 2022; 38: 45–57. https://doi.org/10.1007/s12055-021-01240-y

[15] Varma PK, Srimurugan B, Jose RL, Krishna N, Valooran GJ, Jayant A. Perioperative right ventricular function and dysfunction in adult cardiac surgery-focused review (part 2-management of right ventricular failure). Indian Journal of Thoracic and Cardiovascular Surgery. 2022; 38: 157–166. https://doi.org/10.1007/s12055-021-01226-w

[16] Levy D, Laghlam D, Estagnasie P, Brusset A, Squara P, Nguyen LS. Post-operative Right Ventricular Failure After Cardiac Surgery: A Cohort Study. Frontiers in Cardiovascular Medicine. 2021; 8: 667328. https://doi.org/10.3389/fcvm.2021.667328

[17] Costachescu T, Denault A, Guimond JG, Couture P, Carignan S, Sheridan P, et al. The hemodynamically unstable patient in the intensive care unit: hemodynamic vs. transesophageal echocardiographic monitoring. Critical Care Medicine. 2002; 30: 1214–1223. https://doi.org/10.1097/00003246-200206000-00007

[18] Kaul TK, Fields BL. Postoperative acute refractory right ventricular failure: incidence, pathogenesis, management and prognosis. Cardiovascular Surgery. 2000; 8: 1–9. https://doi.org/10.1016/s0967-2109(99)00089-7

[19] Seo Y, Ishizu T, Ieda M, Ohte N. Right ventricular three-dimensional echocardiography: the current status and future perspectives. Journal of Echocardiography. 2020; 18: 149–159. https://doi.org/10.1007/s12574-020-00468-8

[20] Dell’Italia LJ. The right ventricle: anatomy, physiology, and clinical importance. Current Problems in Cardiology. 1991; 16: 653–720. https://doi.org/10.1016/0146-2806(91)90009-y

[21] Kawel-Boehm N, Maceira A, Valsangiacomo-Buechel ER, Vogel-Claussen J, Turkbey EB, Williams R, et al. Normal values for cardiovascular magnetic resonance in adults and children. Journal of Cardiovascular Magnetic Resonance. 2015; 17: 29. https://doi.org/10.1186/s12968-015-0111-7

[22] Woulfe KC, Walker LA. Physiology of the Right Ventricle Across the Lifespan. Frontiers in Physiology. 2021; 12: 642284. https://doi.org/10.3389/fphys.2021.642284

[23] Eriksson J, Carlhäll CJ, Dyverfeldt P, Engvall J, Bolger AF, Ebbers T. Semi-automatic quantification of 4D left ventricular blood flow. Journal of Cardiovascular Magnetic Resonance. 2010; 12: 9. https://doi.org/10.1186/1532-429X-12-9

[24] Sengupta PP, Narula J. RV form and function: a piston pump, vortex impeller, or hydraulic ram? JACC. Cardiovascular Imaging. 2013; 6: 636–639. https://doi.org/10.1016/j.jcmg.2013.04.003

[25] Fredriksson AG, Zajac J, Eriksson J, Dyverfeldt P, Bolger AF, Ebbers T, et al. 4-D blood flow in the human right ventricle. American Journal of Physiology. Heart and Circulatory Physiology. 2011; 301: H2344–H2350. https://doi.org/10.1152/ajpheart.00622.2011

[26] Brown SB, Raina A, Katz D, Szerlip M, Wiegers SE, Forfia PR. Longitudinal shortening accounts for the majority of right ventricular contraction and improves after pulmonary vasodilator therapy in normal subjects and patients with pulmonary arterial hypertension. Chest. 2011; 140: 27–33. https://doi.org/10.1378/chest.10-1136

[27] Kind T, Marcus JT, Westerhof N, Vonk-Noordegraaf A. Longitudinal and transverse movements of the right ventricle: both are important in pulmonary arterial hypertension. Chest. 2011; 140: 556–557. https://doi.org/10.1378/chest.10-3195

[28] Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. Journal of the American Society of Echocardiography. 2010; 23: 685–713; quiz 786–788. https://doi.org/10.1016/j.echo.2010.05.010

[29] Zaidi A, Knight DS, Augustine DX, Harkness A, Oxborough D, Pearce K, et al. Echocardiographic assessment of the right heart in adults: a practical guideline from the British Society of Echocardiography. Echo Research and Practice. 2020; 7: G19–G41. https://doi.org/10.1530/ERP-19-0051

[30] Kind T, Mauritz GJ, Marcus JT, van de Veerdonk M, Westerhof N, Vonk-Noordegraaf A. Right ventricular ejection fraction is better reflected by transverse rather than longitudinal wall motion in pulmonary hypertension. Journal of Cardiovascular Magnetic Resonance. 2010; 12: 35. https://doi.org/10.1186/1532-429X-12-35

[31] Ryan JJ, Huston J, Kutty S, Hatton ND, Bowman L, Tian L, et al. Right ventricular adaptation and failure in pulmonary arterial hypertension. The Canadian Journal of Cardiology. 2015; 31: 391–406. https://doi.org/10.1016/j.cjca.2015.01.023

[32] Jabagi H, Nantsios A, Ruel M, Mielniczuk LM, Denault AY, Sun LY. A standardized definition for right ventricular failure in cardiac surgery patients. ESC Heart Failure. 2022; 9: 1542–1552. https://doi.org/10.1002/ehf2.13870

[33] Schneider M, Ran H, Aschauer S, Binder C, Mascherbauer J, Lang I, et al. Visual assessment of right ventricular function by echocardiography: how good are we? The International Journal of Cardiovascular Imaging. 2019; 35: 2001–2008. https://doi.org/10.1007/s10554-019-01653-2

[34] Shahgaldi K, Gudmundsson P, Manouras A, Brodin LA, Winter R. Visually estimated ejection fraction by two dimensional and triplane echocardiography is closely correlated with quantitative ejection fraction by real-time three dimensional echocardiography. Cardiovascular Ultrasound. 2009; 7: 41. https://doi.org/10.1186/1476-7120-7-41

[35] Hahn RT, Abraham T, Adams MS, Bruce CJ, Glas KE, Lang RM, et al. Guidelines for performing a comprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. Anesthesia and Analgesia. 2014; 118: 21–68. https://doi.org/10.1213/ANE.0000000000000016

[36] Nicoara A, Skubas N, Ad N, Finley A, Hahn RT, Mahmood F, et al. Guidelines for the Use of Transesophageal Echocardiography to Assist with Surgical Decision-Making in the Operating Room: A Surgery-Based Approach: From the American Society of Echocardiography in Collaboration with the Society of Cardiovascular Anesthesiologists and the Society of Thoracic Surgeons. Journal of the American Society of Echocardiography. 2020; 33: 692–734. https://doi.org/10.1016/j.echo.2020.03.002

[37] Haddad F, Guihaire J, Skhiri M, Denault AY, Mercier O, Al-Halabi S, et al. Septal curvature is marker of hemodynamic, anatomical, and electromechanical ventricular interdependence in patients with pulmonary arterial hypertension. Echocardiography. 2014; 31: 699–707. https://doi.org/10.1111/echo.12468

[38] Kukucka M, Stepanenko A, Potapov E, Krabatsch T, Redlin M, Mladenow A, et al. Right-to-left ventricular end-diastolic diameter ratio and prediction of right ventricular failure with continuous-flow left ventricular assist devices. The Journal of Heart and Lung Transplantation. 2011; 30: 64–69. https://doi.org/10.1016/j.healun.2010.09.006

[39] Maslow AD, Regan MM, Panzica P, Heindel S, Mashikian J, Comunale ME. Precardiopulmonary bypass right ventricular function is associated with poor outcome after coronary artery bypass grafting in patients with severe left ventricular systolic dysfunction. Anesthesia and Analgesia. 2002; 95: 1507–1518, table of contents. https://doi.org/10.1097/00000539-200212000-00009

[40] Focardi M, Cameli M, Carbone SF, Massoni A, De Vito R, Lisi M, et al. Traditional and innovative echocardiographic parameters for the analysis of right ventricular performance in comparison with cardiac magnetic resonance. European Heart Journal. Cardiovascular Imaging. 2015; 16: 47–52. https://doi.org/10.1093/ehjci/jeu156

[41] Silverton NA, Lee JP, Morrissey CK, Tanner C, Zimmerman J. Regional Versus Global Measurements of Right Ventricular Strain Performed in the Operating Room With Transesophageal Echocardiography. Journal of Cardiothoracic and Vascular Anesthesia. 2020; 34: 48–57. https://doi.org/10.1053/j.jvca.2019.06.010

[42] Lang RM, Addetia K, Narang A, Mor-Avi V. 3-Dimensional Echocardiography: Latest Developments and Future Directions. JACC. Cardiovascular Imaging. 2018; 11: 1854–1878. https://doi.org/10.1016/j.jcmg.2018.06.024

[43] Raina A, Vaidya A, Gertz ZM, Susan Chambers, Forfia PR. Marked changes in right ventricular contractile pattern after cardiothoracic surgery: implications for post-surgical assessment of right ventricular function. The Journal of Heart and Lung Transplantation. 2013; 32: 777–783. https://doi.org/10.1016/j.healun.2013.05.004

[44] Diller GP, Wasan BS, Kyriacou A, Patel N, Casula RP, Athanasiou T, et al. Effect of coronary artery bypass surgery on myocardial function as assessed by tissue Doppler echocardiography. European Journal of Cardio-Thoracic Surgery. 2008; 34: 995–999. https://doi.org/10.1016/j.ejcts.2008.08.008

[45] Tei C, Dujardin KS, Hodge DO, Bailey KR, McGoon MD, Tajik AJ, et al. Doppler echocardiographic index for assessment of global right ventricular function. Journal of the American Society of Echocardiography. 1996; 9: 838–847. https://doi.org/10.1016/s0894-7317(96)90476-9

[46] Sade LE, Gulmez O, Eroglu S, Sezgin A, Muderrisoglu H. Noninvasive estimation of right ventricular filling pressure by ratio of early tricuspid inflow to annular diastolic velocity in patients with and without recent cardiac surgery. Journal of the American Society of Echocardiography. 2007; 20: 982–988. https://doi.org/10.1016/j.echo.2007.01.012

[47] Sallach JA, Tang WHW, Borowski AG, Tong W, Porter T, Martin MG, et al. Right atrial volume index in chronic systolic heart failure and prognosis. JACC. Cardiovascular Imaging. 2009; 2: 527–534. https://doi.org/10.1016/j.jcmg.2009.01.012

[48] Shah MR, Hasselblad V, Stevenson LW, Binanay C, O’Connor CM, Sopko G, et al. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA. 2005; 294: 1664–1670. https://doi.org/10.1001/jama.294.13.1664

[49] Binanay C, Califf RM, Hasselblad V, O’Connor CM, Shah MR, Sopko G, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. 2005; 294: 1625–1633. https://doi.org/10.1001/jama.294.13.1625

[50] National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wheeler AP, Bernard GR, Thompson BT, Schoenfeld D, Wiedemann HP, et al. Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. The New England Journal of Medicine. 2006; 354: 2213–2224. https://doi.org/10.1056/NEJMoa061895

[51] Drazner MH, Hamilton MA, Fonarow G, Creaser J, Flavell C, Stevenson LW. Relationship between right and left-sided filling pressures in 1000 patients with advanced heart failure. The Journal of Heart and Lung Transplantation. 1999; 18: 1126–1132. https://doi.org/10.1016/s1053-2498(99)00070-4

[52] Campbell P, Drazner MH, Kato M, Lakdawala N, Palardy M, Nohria A, et al. Mismatch of right- and left-sided filling pressures in chronic heart failure. Journal of Cardiac Failure. 2011; 17: 561–568. https://doi.org/10.1016/j.cardfail.2011.02.013

[53] Kormos RL, Teuteberg JJ, Pagani FD, Russell SD, John R, Miller LW, et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes. The Journal of Thoracic and Cardiovascular Surgery. 2010; 139: 1316–1324. https://doi.org/10.1016/j.jtcvs.2009.11.020

[54] Bootsma IT, Boerma EC, Scheeren TWL, de Lange F. The contemporary pulmonary artery catheter. Part 2: measurements, limitations, and clinical applications. Journal of Clinical Monitoring and Computing. 2022; 36: 17–31. https://doi.org/10.1007/s10877-021-00673-5

[55] Ochiai Y, McCarthy PM, Smedira NG, Banbury MK, Navia JL, Feng J, et al. Predictors of severe right ventricular failure after implantable left ventricular assist device insertion: analysis of 245 patients. Circulation. 2002; 106: I198–202.

[56] Kavarana MN, Pessin-Minsley MS, Urtecho J, Catanese KA, Flannery M, Oz MC, et al. Right ventricular dysfunction and organ failure in left ventricular assist device recipients: a continuing problem. The Annals of Thoracic Surgery. 2002; 73: 745–750. https://doi.org/10.1016/s0003-4975(01)03406-3

[57] Santamore WP, Gefen N, Avramovich A, Berger P, Kashem A, Barnea O. Right atrial effects on right ventricular ejection fraction derived from thermodilution measurements. Journal of Cardiothoracic and Vascular Anesthesia. 2007; 21: 644–649. https://doi.org/10.1053/j.jvca.2007.02.007

[58] Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022; 145: e895–e1032. https://doi.org/10.1161/CIR.0000000000001063

[59] McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. European Heart Journal. 2021; 42: 3599–3726. https://doi.org/10.1093/eurheartj/ehab368

[60] Maisel A, Mueller C, Adams K, Jr, Anker SD, Aspromonte N, Cleland JGF, et al. State of the art: using natriuretic peptide levels in clinical practice. European Journal of Heart Failure. 2008; 10: 824–839. https://doi.org/10.1016/j.ejheart.2008.07.014

[61] Januzzi JL, Jr, Filippatos G, Nieminen M, Gheorghiade M. Troponin elevation in patients with heart failure: on behalf of the third Universal Definition of Myocardial Infarction Global Task Force: Heart Failure Section. European Heart Journal. 2012; 33: 2265–2271. https://doi.org/10.1093/eurheartj/ehs191

[62] Lankeit M, Jiménez D, Kostrubiec M, Dellas C, Hasenfuss G, Pruszczyk P, et al. Predictive value of the high-sensitivity troponin T assay and the simplified Pulmonary Embolism Severity Index in hemodynamically stable patients with acute pulmonary embolism: a prospective validation study. Circulation. 2011; 124: 2716–2724. https://doi.org/10.1161/CIRCULATIONAHA.111.051177

[63] Murphy ML, Thenabadu PN, de Soyza N, Doherty JE, Meade J, Baker BJ, et al. Reevaluation of electrocardiographic criteria for left, right and combined cardiac ventricular hypertrophy. The American Journal of Cardiology. 1984; 53: 1140–1147. https://doi.org/10.1016/0002-9149(84)90651-9

[64] Kucher N, Walpoth N, Wustmann K, Noveanu M, Gertsch M. QR in V1–an ECG sign associated with right ventricular strain and adverse clinical outcome in pulmonary embolism. European Heart Journal. 2003; 24: 1113–1119. https://doi.org/10.1016/s0195-668x(03)00132-5

[65] Bassareo PP, Mercuro G. QRS Complex Enlargement as a Predictor of Ventricular Arrhythmias in Patients Affected by Surgically Treated Tetralogy of Fallot: A Comprehensive Literature Review and Historical Overview. ISRN Cardiology. 2013; 2013: 782508. https://doi.org/10.1155/2013/782508

[66] Watanabe R, Hori K, Ishihara K, Tsujikawa S, Hino H, Matsuura T, et al. Possible role of QRS duration in the right ventricle as a perioperative monitoring parameter for right ventricular function: a prospective cohort analysis in robotic mitral valve surgery. Frontiers in Cardiovascular Medicine. 2024; 11: 1418251. https://doi.org/10.3389/fcvm.2024.1418251

[67] Punukollu G, Gowda RM, Vasavada BC, Khan IA. Role of electrocardiography in identifying right ventricular dysfunction in acute pulmonary embolism. The American Journal of Cardiology. 2005; 96: 450–452. https://doi.org/10.1016/j.amjcard.2005.03.099

[68] Staikou C, Stamelos M, Stavroulakis E. Impact of anaesthetic drugs and adjuvants on ECG markers of torsadogenicity. British Journal of Anaesthesia. 2014; 112: 217–230. https://doi.org/10.1093/bja/aet412

[69] Nagele P, Pal S, Brown F, Blood J, Miller JP, Johnston J. Postoperative QT interval prolongation in patients undergoing noncardiac surgery under general anesthesia. Anesthesiology. 2012; 117: 321–328. https://doi.org/10.1097/ALN.0b013e31825e6eb3

[70] Hori K, Tsujikawa S, Egami M, Waki S, Watanabe R, Hino H, et al. Thoracic epidural analgesia prolongs postoperative QT interval on electrocardiogram in major non-cardiac surgery: a randomized comparison and a prospective cohort analysis. Frontiers in Pharmacology. 2023; 14: 936242. https://doi.org/10.3389/fphar.2023.936242

[71] Iglesias-Garriz I, Olalla-Gómez C, Garrote C, López-Benito M, Martín J, Alonso D, et al. Contribution of right ventricular dysfunction to heart failure mortality: a meta-analysis. Reviews in Cardiovascular Medicine. 2012; 13: e62–e69. https://doi.org/10.3909/ricm0602

[72] Aschauer S, Kammerlander AA, Zotter-Tufaro C, Ristl R, Pfaffenberger S, Bachmann A, et al. The right heart in heart failure with preserved ejection fraction: insights from cardiac magnetic resonance imaging and invasive haemodynamics. European Journal of Heart Failure. 2016; 18: 71–80. https://doi.org/10.1002/ejhf.418

[73] Kakouros N, Cokkinos DV. Right ventricular myocardial infarction: pathophysiology, diagnosis, and management. Postgraduate Medical Journal. 2010; 86: 719–728. https://doi.org/10.1136/pgmj.2010.103887

[74] Espinola-Zavaleta N, Gonzalez-Velasquez PJ, Gopar-Nieto R, Camacho-Camacho G, Solorzano-Pinot E, Fernández-Badillo V, et al. Right Atrial and Right Ventricular Function Assessed by Speckle Tracking in Patients with Inferior Myocardial Infarction. Reviews in Cardiovascular Medicine. 2022; 23: 123. https://doi.org/10.31083/j.rcm2304123

[75] Ondrus T, Kanovsky J, Novotny T, Andrsova I, Spinar J, Kala P. Right ventricular myocardial infarction: From pathophysiology to prognosis. Experimental and Clinical Cardiology. 2013; 18: 27–30.

[76] Seo MK, Park EA, Kim HK, Lee W, Kim YJ, Kim KH, et al. Electrocardiographic QRS duration reflects right ventricular remodeling in patients undergoing corrective surgery for isolated tricuspid regurgitation: a comparative study with cardiac magnetic resonance imaging. Clinical Cardiology. 2012; 35: 692–699. https://doi.org/10.1002/clc.22030

[77] Towheed A, Sabbagh E, Gupta R, Assiri S, Chowdhury MA, Moukarbel GV, et al. Right Ventricular Dysfunction and Short-Term Outcomes Following Left-Sided Valvular Surgery: An Echocardiographic Study. Journal of the American Heart Association. 2021; 10: e016283. https://doi.org/10.1161/JAHA.120.016283

[78] Le Tourneau T, Deswarte G, Lamblin N, Foucher-Hossein C, Fayad G, Richardson M, et al. Right ventricular systolic function in organic mitral regurgitation: impact of biventricular impairment. Circulation. 2013; 127: 1597–1608. https://doi.org/10.1161/CIRCULATIONAHA.112.000999

[79] Fayad FH, Sellke FW, Feng J. Pulmonary hypertension associated with cardiopulmonary bypass and cardiac surgery. Journal of Cardiac Surgery. 2022; 37: 5269–5287. https://doi.org/10.1111/jocs.17160

[80] Li YL, Zheng JB, Jin Y, Tang R, Li M, Xiu CH, et al. Acute right ventricular dysfunction in severe COVID-19 pneumonia. Reviews in Cardiovascular Medicine. 2020; 21: 635–641. https://doi.org/10.31083/j.rcm.2020.04.159

[81] Lang AL, Huang X, Alfirevic A, Blackstone E, Pettersson GB, Singh A, et al. Patient characteristics and surgical variables associated with intraoperative reduced right ventricular function. The Journal of Thoracic and Cardiovascular Surgery. 2022; 164: 585–595.e5. https://doi.org/10.1016/j.jtcvs.2020.11.075

[82] Schuuring MJ, van Gulik EC, Koolbergen DR, Hazekamp MG, Lagrand WK, Backx APCM, et al. Determinants of clinical right ventricular failure after congenital heart surgery in adults. Journal of Cardiothoracic and Vascular Anesthesia. 2013; 27: 723–727. https://doi.org/10.1053/j.jvca.2012.10.022

[83] Durand M, Chavanon O, Tessier Y, Casez M, Gardellin M, Blin D, et al. Right ventricular function after coronary surgery with or without bypass. Journal of Cardiac Surgery. 2006; 21: 11–16.

[84] Christakis GT, Buth KJ, Weisel RD, Rao V, Joy L, Fremes SE, et al. Randomized study of right ventricular function with intermittent warm or cold cardioplegia. The Annals of Thoracic Surgery. 1996; 61: 128–134. https://doi.org/10.1016/0003-4975(95)00933-7

[85] Honkonen EL, Kaukinen L, Pehkonen EJ, Kaukinen S. Right ventricle is protected better by warm continuous than by cold intermittent retrograde blood cardioplegia in patients with obstructed right coronary artery. The Thoracic and Cardiovascular Surgeon. 1997; 45: 182–189. https://doi.org/10.1055/s-2007-1013720

[86] Bond BR, Dorman BH, Clair MJ, Walker CA, Pinosky ML, Reeves ST, et al. Endothelin-1 during and after cardiopulmonary bypass: association to graft sensitivity and postoperative recovery. The Journal of Thoracic and Cardiovascular Surgery. 2001; 122: 358–364. https://doi.org/10.1067/mtc.2001.114936

[87] Cameli M, Lisi M, Righini FM, Focardi M, Lunghetti S, Bernazzali S, et al. Speckle tracking echocardiography as a new technique to evaluate right ventricular function in patients with left ventricular assist device therapy. The Journal of Heart and Lung Transplantation. 2013; 32: 424–430. https://doi.org/10.1016/j.healun.2012.12.010

[88] Dalén M, Oliveira Da Silva C, Sartipy U, Winter R, Franco-Cereceda A, Barimani J, et al. Comparison of right ventricular function after ministernotomy and full sternotomy aortic valve replacement: a randomized study. Interactive Cardiovascular and Thoracic Surgery. 2018; 26: 790–797. https://doi.org/10.1093/icvts/ivx422

[89] Zijderhand CF, Yalcin YC, Sjatskig J, Bos D, Constantinescu AA, Manintveld OC, et al. Pectus Excavatum and Risk of Right Ventricular Failure in Left Ventricular Assist Device Patients. Reviews in Cardiovascular Medicine. 2023; 24: 313. https://doi.org/10.31083/j.rcm2411313

[90] Guinot PG, Abou-Arab O, Longrois D, Dupont H. Right ventricular systolic dysfunction and vena cava dilatation precede alteration of renal function in adult patients undergoing cardiac surgery: An observational study. European Journal of Anaesthesiology. 2015; 32: 535–542. https://doi.org/10.1097/EJA.0000000000000149

[91] Li H, Ye T, Su L, Wang J, Jia Z, Wu Q, et al. Assessment of Right Ventricular-Arterial Coupling by Echocardiography in Patients with Right Ventricular Pressure and Volume Overload. Reviews in Cardiovascular Medicine. 2023; 24: 366. https://doi.org/10.31083/j.rcm2412366

[92] Martin C, Perrin G, Saux P, Papazian L, Albanese J, Gouin F. Right ventricular end-systolic pressure-volume relation during propofol infusion. Acta Anaesthesiologica Scandinavica. 1994; 38: 223–228. https://doi.org/10.1111/j.1399-6576.1994.tb03878.x

[93] Magunia H, Jordanow A, Keller M, Rosenberger P, Nowak-Machen M. The effects of anesthesia induction and positive pressure ventilation on right-ventricular function: an echocardiography-based prospective observational study. BMC Anesthesiology. 2019; 19: 199. https://doi.org/10.1186/s12871-019-0870-z

[94] Dalla K, Bech-Hanssen O, Ricksten SE. General anesthesia and positive pressure ventilation suppress left and right ventricular myocardial shortening in patients without myocardial disease - a strain echocardiography study. Cardiovascular Ultrasound. 2019; 17: 16. https://doi.org/10.1186/s12947-019-0165-z

[95] Boyd O, Murdoch LJ, Mackay CJ, Bennett ED, Grounds RM. The cardiovascular changes associated with equipotent anaesthesia with either propofol or isoflurane. Particular emphasis on right ventricular function. Acta Anaesthesiologica Scandinavica. 1994; 38: 357–362. https://doi.org/10.1111/j.1399-6576.1994.tb03907.x

[96] Kellow NH, Scott AD, White SA, Feneck RO. Comparison of the effects of propofol and isoflurane anaesthesia on right ventricular function and shunt fraction during thoracic surgery. British Journal of Anaesthesia. 1995; 75: 578–582. https://doi.org/10.1093/bja/75.5.578

[97] Xu WY, Wang N, Xu HT, Yuan HB, Sun HJ, Dun CL, et al. Effects of sevoflurane and propofol on right ventricular function and pulmonary circulation in patients undergone esophagectomy. International Journal of Clinical and Experimental Pathology. 2013; 7: 272–279.