Authors Accepted Manuscript

Markers of Right Ventricular Dysfunction in Adult

Cardiac Surgical Patients

Vasileios Zochios, Aristotle D. Protopapas, Ken

Parhar

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PII: S1053-0770(17)30545-1
DOI: http://dx.doi.org/10.1053/j.jvca.2017.06.019
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To appear in: Journal of Cardiothoracic and Vascular Anesthesia
Cite this article as: Vasileios Zochios, Aristotle D. Protopapas and Ken Parhar,
Markers of Right Ventricular Dysfunction in Adult Cardiac Surgical Patients,
Journal of Cardiothoracic and Vascular Anesthesia,
http://dx.doi.org/10.1053/j.jvca.2017.06.019
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Type of contribution: Editorial

Markers of Right Ventricular Dysfunction in Adult Cardiac Surgical patients

1
Vasileios Zochios MD MRCP, 1, 2Aristotle D Protopapas FRCS, 3Ken Parhar MD FRCPC

1
University Hospitals Birmingham NHS Foundation Trust
Department of Critical Care Medicine, Queen Elizabeth Hospital, Edgbaston, Mindelsohn Way,
Birmingham, B15 2GW, UK

2
Imperial College London

3
Department of Critical Care Medicine, University of Calgary, Foothills Medical Center, 3134
Hospital Drive NW, Calgary, Alberta, Canada T2N 2T9

Source of support: Nil

Conflicts of interest: Nil

Corresponding author:

Dr Vasileios Zochios MD MRCP (UK)

University Hospitals Birmingham NHS Foundation Trust
Department of Critical Care Medicine, Queen Elizabeth Hospital, Edgbaston, Birmingham, B15
2WB, UK
Perioperative Critical Care and Trauma Trials Group, Institute of Inflammation and Ageing
Centre of Translational Inflammation Research
University of Birmingham, Birmingham, UK
Email: vasileioszochios@doctors.org.uk

Keywords: right ventricular dysfunction, right ventricular failure, echocardiography, cardiac surgery

1
The Right Ventricle (RV) is responsible for directing blood flow to the low resistance pulmonary

circulation, and subsequently onwards to the left ventricle. Given the complex anatomy,

interventricular interactions, coronary blood supply, and challenges with cardioprotection, a thorough

understanding of the RV is crucial for perioperative management in order to limit the risk of acute RV

dysfunction (RVD) which may lead to RV failure (RVF).1

RVF can be defined as the inability of the RV to provide adequate blood flow through the pulmonary

circulation at normal central venous pressure (CVP).2, 3

RVD definitions vary in the literature.
2, 4, 5
According to the American Society of Echocardiography , RVD is present when the parameters

used to quantify RV function are less than the lower or greater than the higher reference value of the

normal range (mean + SD): tricuspid annular plane systolic excursion (TAPSE) (mm) <17 (24 + 3.5);

pulsed Doppler systolic myocardial velocity (S) (cm/sec) <9.5 (14.1 + 2.3); color doppler S wave

(cm/sec) < 6 (9.7 + 1.85); right ventricular fractional area change (RVFAC) (%) < 35 (49 + 7); RV

three-dimensional (3D) ejection fraction (EF) (%) <45% (58 + 6.5); pulsed doppler RV index of

myocardial performance (RIMP) > 0.43 (0.26 + 0.085). 2-5 RVFAC has been used to grade the degree

of systolic RVD as mild, moderate or severe for RVFAC values of 25 to 35%, 18 to 25% and less

than or equal to 18% respectively. 4-7

Hemodynamic parameters obtained from the pulmonary artery catheter (PAC) such us CVP,

pulmonary capillary wedge pressure (PCWP), cardiac index (CI) and mixed venous oxygen saturation

(SvO2) have been used to characterize RVD. PAC indices suggestive of RVD include: CVP>

20mmHg, CVP>PCWP, CI < 2.l L/min/m2, mixed venous oxygen saturation < 55%.8, 9 Although PAC

has fallen out of favor and PAC-derived data are not utilized routinely to guide therapy in the

intensive care unit (ICU) or operating room, PAC still has a role in the perioperative management and

monitoring of patients with known pulmonary vascular dysfunction and RVD.

2
In the context of left ventricular assist device (LVAD) placement, acute RVF is described by the

Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) as documented

elevated right atrial pressure (> 16 cm H2O) or dilated inferior vena cava (absence of inspiratory

variation) on echocardiography and associated features of venous congestion (peripheral edema,

ascites, deranged liver function and palpable hepatomegaly).10 Patients with the aforementioned

features who require positive inotropes, pulmonary vasodilators or RV mechanical support (RVAD)

post-implantation meet the definition for severe RVF.10

RVF in the context of cardiac surgery confers high perioperative mortality rate (up to 75%).11-13 The

reported incidence of refractory RVF varies from 0.1% (post-cardiotomy) to 30% (post-left

ventricular assist device (LVAD) insertion).11-13 Patients with chronic thromboembolic pulmonary

hypertension (CTEPH) undergoing pulmonary endarterectomy (PEA) are at risk of RVF as they may

have pre-existing RVD (despite normal hemodynamics) due to chronic increase in RV afterload

which sometimes fails to completely recover postoperatively. 14

Causes of RVD in Cardiac Surgery

Perioperative factors that increase the risk of RVD/RVF include:

long cardiopulmonary bypass (CPB) time (>150min) and acute pulmonary hypertension;15, 16

suboptimal intraoperative myocardial protection (stunning);15, 17

coronary embolism or graft occlusion causing RV ischemia; 15, 18, 19

donor heart ischemia and pre-existing pulmonary vascular dysfunction (in heart transplant

patients)15, 20, 21

Injurious perioperative mechanical ventilation leading to ventilator induced lung injury

(VILI) and acute respiratory distress syndrome (ARDS)22, 23

3
ARDS after cardiac surgery can adversely affect RV function usually due to an increase in RV

afterload.3 Gajic et al showed that the generic risk of ARDS post cardiac surgery is approximately

10%.24 A retrospective analysis of 3,434 cardiac surgical patients showed that in the era of low-tidal

volume protective mechanical ventilation 45.6% (1,567) of the patients received tidal volumes

between 10 and 12 ml/kg predicted body weight (PBW) and 33.3% (1,143) received tidal volumes

greater than 12ml/kg PBW.25 Intraoperative high tidal volume ventilation causes collapse of alveolar

vessels due to tension of the alveolar wall leading to an increase in pulmonary vascular resistance and

RVD.22 Specifically, ventilation with high tidal volumes and/or high driving pressure (difference

between plateau pressure and total positive-end expiratory pressure) may result in increased alveolar

stress and strain, VILI and RVD.23

Recent data on perioperative RVD

The impact of RVD on clinically important outcomes has been studied in pre- and postoperative

cardiac surgery settings. However, very few studies are adequately powered to address the research

questions posed. In a recent pragmatic cohort study of 400 cardiac patients undergoing surgery

(52.5% coronary artery bypass graft surgery (CABG), 57% valve replacement, 7.5% valve repair,

11.5% abdominal aortic aneurysm repair), Peyrou et al demonstrated that preoperative RVD assessed

by echocardiography predicts postoperative mortality.26 The strongest echocardiographic

prognosticator in multivariate regression analysis was RV fractional area change (RVFAC) < 35% for

both overall (three-year) and cardiovascular mortality [hazard ratios (HR) 3.0 (95% confidence

interval (CI) 1.56.1) and 10.5 (95% CI 4.319.9) respectively].26 Garatti et al, undertook a

retrospective case-control study of 324 patients with ischemic left ventricular (LV) failure undergoing

surgical ventricular reconstruction and found that preoperative RVD (defined as TAPSE<16mm) was

associated with increased five and eight- year mortality compared with controls (39 vs 17% and 52 vs

23% respectively).27 Although this was a very specific patient population the study raised awareness

of the potential adverse effect of RVD on clinical outcomes. In a prospective randomized trial,

patients with ischemic cardiomyopathy and moderate to severe RVD (defined as RVFAC 20-30% and

4
RVFAC< 20% respectively) undergoing surgical ventricular reconstruction in addition to CABG have

higher short and long term mortality compared with controls (CABG).28 This data highlight the

complex interactions between LV and RV and need for diligent preoperative assessment and risk

stratification in this subset of cardiac surgical patients.

Bootsma et al examined the prognostic impact of postoperative RVD in a large heterogenous cohort

(n =1,109) of cardiac surgical patients (coronary artery bypass grafting, valve surgery, combination of

graft and valve surgery, aortic surgery).29 The authors tested the hypothesis that RVD in cardiac

surgical patients (not selected for RV-related risk factors) is a predictor of long term mortality. 29 All

patients enrolled had a pulmonary artery catheter (PAC) placed (protocol mandated approach) and

continuous PAC-derived RV ejection fraction (RVEF) monitoring. The authors utilized RVEF to

characterize RV function and define RVD and found that all-cause two-year mortality in patients with

postoperative RVEF < 20% was 16.7% (p<0.001).29 RVEF assessed by PAC or echocardiography

does not have established prognostic value and thus it cannot reliably predict RVD and provide a

causal link between RVD and mortality in cardiac surgical patients. 2-7 In addition, it has been shown

that thermodilution technique systematically underestimates RVEF and therefore the results of this

study may not be generalizable.30

In post-heart transplant patients, Hosenpud et al found a linear relationship between pulmonary

vascular resistance and mortality and RVF accounting for up to 20% of early deaths. 31 In patients with

LVAD implant, preoperative RVD and postoperative RVF result in significant post-LVAD morbidity

and mortality.32 In terms of predicting RVF in LVAD patients, PAC-derived indices have been used

and in the Heart Mate II Bridge-to-Transplant Pivotal Trial a ratio of CVP to PCWP of greater than

0.63 was found to be an independent predictor of early RVF risk.33 Single echocardiography markers
34
such as TAPSE (< 7.5mm) and RV to LV diameter ratio (thought to be analogous to CVP/PCWP

ratio)35 have been shown to predict RVF in post-LVAD patients. Early diagnosis and management of

RVD is paramount in the VAD patient population and guides further decision making (need for right

VAD or transplantation). Table 1 summarizes echocardiographic and hemodynamic markers of RVD

5
that could potentially serve as RVF predictors in LVAD and non-LVAD cardiac surgical patients.4-7, 8,
9, 33, 36-40, 41, 43

The aforementioned studies highlight the need for early diagnosis of RVD in the perioperative period.

The question remains that if RVD is quickly identified, will implementation of RV-protective

strategies (eg lung protective ventilation, pulmonary vasodilatation, normoxia /normocapnia,

extracorporeal life support) prevent further progression to RVF?

Risk-prediction models such as EURO-score II and the American Society of Thoracic Surgeons (STS)

score are used in cardiac surgery to aid risk stratification and decision making. 44-47 The validity of

EURO-score II and STS risk models has not been assessed in the setting of RVD and it is possible

that in patients with preoperative RVD, morbidity and mortality are significantly underestimated. Of
44
note, pulmonary hypertension (PH) is incorporated in EURO-score II; however, the model

underestimates the risk for patients with isolated RVD without PH (eg ischemic RVD). Addition of

ASE RVD criteria to EURO-score II and STS risk prediction tools should be considered and

validated.

Bedside diagnostic modalities - Identifying patients at risk

Invasive hemodynamic monitoring

Use of arterial and CVP monitoring is standard practice in cardiac surgery. Apart from real-time

blood pressure monitoring, arterial line monitoring detects pulse-pressure variation (PPV), the

dynamic changes in arterial pulse pressure induced by positive pressure ventilation. PPV is thought to

predict fluid responsiveness provided there is no spontaneous breathing effort, heart rhythm is regular

and the patient is receiving appropriate controlled tidal volume.48 PPV in the early postoperative

period may be due to reduced RV preload or increased RV afterload. RVD due to elevated RV

afterload should be suspected and investigated promptly (echocardiography) in fluid unresponsive

patients as further volume loading can be deleterious to a dysfunctional RV.48, 49 Although CVP is a

6
poor guide of volume status, very low CVP may reflect hypovolemia. In contrast a rapidly rising CVP

in response to a fluid challenge may indicate impeding RVD.8, 9

Pulmonary artery catheter (PAC)

Due to its invasive nature, unproven benefits and the increasing availability of non-invasive

diagnostic modalities, perioperative use of PAC is uncommon in non-cardiac surgical setting.

However, as evidenced by an international survey of the members of the society of cardiovascular

anesthesiologists (SCA) the majority of SCA responders still prefer to use PAC in most cardiac

surgeries.50 A thermal filament placed into the RV enables continuous RVEF monitoring: this has not

been validated so far in large prospective studies as an independent predictor of outcomes. 29 Because

of the risks associated with PAC use (placement, measurement of PCWP), PACs should probably be

reserved for:

patients with known preoperative RVD;

those who require escalation of vasoactive medications and appear to be fluid unresponsive

in the immediate postoperative period;

heart transplant or LVAD recipients (where PAC can also be utilized to estimate

transpulmonary gradient a marker of pulmonary vascular dysfunction) and

patients with CTEPH undergoing pulmonary endarterectomy as they usually have pre-

existing RVD whereby perioperative pulmonary arterial pressure (PAP) and pulmonary

vascular resistance (PVR) monitoring is paramount.

In cardiac surgical patients with a PAC in place and features of RVD, the rate of change in PVR could

potentially serve as a novel parameter for monitoring the natural history of RVD/RVF due to

abnormal pulmonary vasculature and response to therapy.

7
Echocardiography

Perioperative echocardiography (transesophageal or transthoracic) can be used to assess RV function.

In particular, intraoperative transesophageal echocardiography (TEE) is the imaging modality of

choice in cardiac anesthesiology practice and usually complements the PAC measurements listed

above.8, 9, 50
Transthoracic echocardiography (TTE) plays an important role in the postoperative

period, but the TTE image quality after cardiac surgery can be challenging. It may also be used

intraoperatively in congenital heart disease by way of some simple sterile precautions and

preparations, especially in pediatric operations through sternotomy.

Patients with clinically suspected RVD assessed by echocardiography may have RV dilatation

(volume overload) and/or septal dyskinesia during end-systole (pressure overload).2, 51 Assessment of

RV function is based on qualitative and quantitative parameters. Due to its complex geometry

(crescent shape) measurements by 2D echocardiography can be challenging.4, 5, 7 In the RV-focused

view, RV diameter >41mm at the base and >35mm at the mid-level indicates RV dilatation. 4, 5, 7

RV systolic function is commonly assessed using TAPSE; however it is known to have some

limitations such as being angle dependent and representative of global RV function instead only

assessing the RV free wall. 4, 5, 7

RIMP, RVFAC, three-dimensional (3D) RV ejection fraction, S,

longitudinal strain and strain rate by doppler tissue imaging (DTI) can be used to assess global RV

function but none of these indices have been reproduced as early predictors of RVD in cardiac

surgery. 4, 5, 7 RVFAC and 3D RV volumes and EF have been found to correlate well with cardiac

magnetic resonance (CMR)-derived RVEF (gold standard for evaluation of RV function) but their

predictive value in cardiac surgical patients with suspected RVD has not been tested in adequately

powered prospective studies. 52-55

10,
Indices of RV diastolic function such as ratio of early tricuspid inflow to annular diastolic velocity
13
have not been assessed in the context of cardiac surgery and the impact of RV diastolic dysfunction

on outcomes remains unknown.

8
Final thoughts

We acknowledge the urgent need for a consensual RVD definition for cardiac surgical patients which

should encompass hemodynamic (PAC-derived) and echocardiographic criteria to enable the clinician

to identify patients with RVD without clinical features of end-organ hypoperfusion in order to provide

the opportunity to intervene prior to progression of RVD. Single hemodynamic or echocardiographic

parameters have not been proven reliable in predicting perioperative RVD and therefore a validated

multiparametric risk prediction model may help in the prompt diagnosis of RVF/RVD and allow for

the implementation of strategies to prevent progression to RVF and reduce mortality in the cardiac

surgical patient population.14

9
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15
Table 1. Markers of RVD (RVF predictors)

MARKERS OF RVD Non-LVAD Cardiac Surgery LVAD Cardiac Surgery

ECHOCARDIOGRAPHY TAPSE < 17mm 4-7 TAPSE < 7.5mm 36

Pulsed Doppler systolic RV short/long axis ratio >0.6
myocardial velocity (S) < 9.5
(OR 4.4) 37
cm/sec4-7

RVFAC < 35% 4-7 Grade III/IV tricuspid

regurgitation (OR 4.7) 37

RVEF (3D) < 45% 4-7 RV to LV end-diastolic

diameter ratio >0.72 (OR 11.4)
38

RIMP > 0.43 4-7 RV peak longitudinal Strain >

-9.6% 39
E/A < 0.8 or > 2 4-7 LVEDD > 74mm (OR 0.6) 40

Depressed free wall RV

longitudinal strain 41
HEMODYNAMICS
CVP> 20 mmHg 8, 9 CVP>15 mmHg 42

CVP>PCWP 8, 9 CVP/PCWP >0.63 33

CI < 2.l L/min/m2 8, 9 CI < 2.2 L/min/m2 (OR 5.7)

RVSWI < 0.25 mmHg/L/m2
(OR 5.1) 43

Abbreviations: CI, cardiac index; CVP, central venous pressure; E/A, ratio of peak velocity flow in
early (E wave) to late (A wave) diastole; LV, left ventricular; LVEDD, left ventricular end-diastolic
diameter; OR, odds ratio; PCWP, pulmonary capillary wedge pressure; RIMP, pulsed doppler right
ventricular index of myocardial performance; RV, right ventricular; RVD, right ventricular
dysfunction; RVEF, right ventricular ejection fraction; RVF, right ventricular failure; RVFAC, right
ventricular fractional area change; RVSWI, right ventricular stroke work index; TAPSE, tricuspid
annular plane systolic excursion

16