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Best Practice & Research Clinical Anaesthesiology 26 (2012) 217229

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Best Practice & Research Clinical


Anaesthesiology
journal homepage: www.elsevier.com/locate/bean

Right ventricular failure after LVAD implantation:


Prevention and treatment
Massimiliano Meineri, MD, Assistant Professor of Anaesthesia a, d,
Adriaan E. Van Rensburg, MB.ChB, MMED, FCA[SA], FRCPC, Assistant
Professor of Anaesthesia b, e, Annette Vegas, MD, FRCPC, Associate Professor
of Anaesthesia c, *
a

University of Toronto, Staff Anaesthesiologist, Toronto General Hospital, Department of Anaesthesia and Pain Management, 200
Elizabeth Street, EN 3-442, Toronto, ON, Canada M5G 2C4
b
University of Toronto, Staff Anaesthesiologist, Toronto General Hospital, Department of Anaesthesia and Pain Management, 200
Elizabeth Street, EN 3-443, Toronto, ON, Canada M5G 2C4
c
University of Toronto, Staff Anaesthesiologist, Toronto General Hospital, Department of Anesthesia and Pain Management, 200
Elizabeth Street, EN 3, Toronto, ON, Canada M5G 2C4

Keywords:
heart Failure/physiopathology/*therapy
heart-assist devices/*adverse effects
haemodynamics
risk assessment
risk factors
treatment outcome
ventricular dysfunction
right/*aetiology/physiopathology/therapy
*ventricular function, left
*ventricular function, right

Right ventricular failure (RVF) complicates 2050% of left


ventricular assist device (LVAD) implantation cases and contributes to increased postoperative morbidity and mortality. Normal
LVAD function alters the highly compliant right ventricular (RV)
physiology, which may unmask RVF. Risk scores for predicting RVF
post-LVAD incorporate multiple risk factors but have not been
prospectively validated. Prevention of RVF consists of optimising
RV function by modifying RV preload and afterload, providing
adequate intra-operative RV protection and minimising blood
transfusions. Treatment of RVF relies on inotropic support,
decreasing pulmonary vascular resistance and adjusting LVAD
ows to minimise distortion of RV geometry. RVAD insertion is
a last recourse when RVF is refractory to medical treatment.
2012 Elsevier Ltd. All rights reserved.

* Corresponding author. Tel.: 1 416 340 4800x6443; Fax: 1 416 340 3698.
E-mail addresses: massimiliano.meineri@uhn.ca (M. Meineri), adriaan.vanrensburg@uhn.ca (A.E. Van Rensburg), annette.
vegas@uhn.ca (A. Vegas).
d
Tel.: 416 340 4800x5877; Fax: 416 340 3698.
e
Tel.: 416 340 4800x8727; Fax: 416 340 3698.
1521-6896/$ see front matter 2012 Elsevier Ltd. All rights reserved.
doi:10.1016/j.bpa.2012.03.006

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M. Meineri et al. / Best Practice & Research Clinical Anaesthesiology 26 (2012) 217229

Introduction
The treatment of refractory heart failure with ventricular assist devices (VADs) has become an
established practice with acceptable results as either a destination therapy (DT) or a bridge-totransplant (BTT) therapy. Technological developments have led to the use of non-pulsatile continuous-ow devices with superior overall results compared with the original pulsatile devices.13
Some degree of right ventricular dysfunction (RVD) is common in patients presenting for left
ventricular assist device (LVAD) surgery. The incidence of overt right ventricular failure (RVF) postLVAD implantation has been reported between 20% and 50%18 and remains unchanged despite an
improved immediate postoperative mortality9 with newer generations of LVADs.6,10,11 Early RVF postLVAD is associated with increased operative mortality, postoperative morbidity, mortality, intensive
care unit (ICU) and hospital length of stay.4,7,12 The development of RVF shortens survival even after
successful heart transplantation in BTT LVAD patients.13
The diagnosis of RVF post-LVAD implantation is complex. Most studies46,14,15 have used a combination of management criteria to dene RVF, confounding comparisons between trials. This article
reviews basic right ventricular physiology and pathophysiology before and after LVAD implantation, as
well as management strategies for RVF in this complex clinical situation.
Physiology and pathophysiology of RV function
Normal
The right ventricle (RV) is structurally and mechanically distinct from the left ventricle (LV) and
responds differently to diseased states (Table 1). Anatomically the RV is a complex three-dimensional
structure that forms the most anterior part of the heart lying directly beneath the sternum.16 In sagittal
section it appears triangular and is crescent shaped in cross section with the interventricular septum
(IVS) concave towards the LV (Fig. 1). RV shape and function are signicantly inuenced by the position
of the IVS, which becomes a prominent factor when either ventricle is affected by abnormal loading
conditions. The RV and LV are connected in series: the output of one ventricle is the input for the other.
Contraction of the highly compliant thin-walled RV is a sequential process starting at the inlet, then
free wall and ending at the infundibulum (or RV outow tract). Under normal conditions, the RV is
coupled to the highly compliant pulmonary vascular system, which renders it a volume pump (low
pressure) rather than a pressure pump. During the cardiac cycle, the RV pumps an equal stroke volume
(SV) as the LV, but at 25% of the stroke work.17 The RV has a greater end-diastolic volume than the LV, so
the RV ejection fraction is less (RVEF 4045%) than the LV (LVEF 5055%).18 There is an inverse relationship between RVEF and pulmonary artery pressure (PAP). The RV is more sensitive to an afterload
change compared to the LV. A similar increase in afterload to the RV (PAP) and LV (aortic pressure) leads
to a signicantly greater decrease in SV for the RV compared to the LV.19 In contrast, the RV tolerates
and adapts more easily to volume (diastolic) overload.
Normal RV perfusion occurs during both systole and diastole. Lower stroke work and wall stress
ensure that the RV has lower resting coronary blood ow (0.40.7 ml min1 g1 of myocardium) and
oxygen extraction (50% vs. 75%) compared with the LV.19 This ow and extraction reserve make the RV
more resilient to ischaemia.
Table 1
Normal RV and LV parameters.

EDV, ml/m2
Mass, g/m2
Wall thickness, mm
Ventricular pressure, mmHg
Ventricular elastance, mmHg/ml
PVR versus SVR, dyn s cm5
Ejection fraction, %

Right ventricle

Left ventricle

75  13 [49100]
26  5 [1734]
25
25/4 [[1530]/[17]]
1.30  0.84
70 [20130]
4045

65  12 [4490]
87  12 [64110]
711
130/8 [[90140]/[512]]
5.48  1.23
1100 [7001600]
5055

EDV, end-diastolic volume; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance.

M. Meineri et al. / Best Practice & Research Clinical Anaesthesiology 26 (2012) 217229

219

Fig. 1. RV size and Function. Two perpendicular sections of a 3D TEE reconstruction of the right ventricle from tricuspid valve [TV] to
pulmonary [PV] valve are shown. The cross section [A] demonstrates the crescent shape and the sagittal section [B] the triangular
shape of the RV. Ventricular interdependence between the left ventricle [LV] and RV during systole relies on interventricular septum
position as shown in cross section for different clinical scenarios.

Ventricular interdependence implies that the shape, size and compliance of one ventricle affect the
size, shape and pressurevolume relationship of the other through direct mechanical interactions.16,19
Systolic interdependence is mediated primarily through the IVS, while diastolic interdependence
occurs mainly via the pericardium. Ventricular interdependence becomes an important factor when
one of the ventricles is exposed to altered loading conditions (Fig. 1).
Heart failure
Left heart failure can affect the RV through multiple mechanisms. Pulmonary hypertension is a common
complication of both systolic and diastolic left heart failure, which incites the initial adaptive response of
RV hypertrophy.15 Over a short time, progressive contractile dysfunction is followed by RV dilatation to
increase preload and maintain cardiac output (CO). Clinically this manifests as rising lling pressures,
decrease in CO and worsening tricuspid regurgitation (TR) from poor leaet coaptation. RVF causes hepatic
venous hypertension, which contributes to hepatic hypoxia and persisting liver dysfunction.
In heart failure patients, an elevated PAP >39 mmHg and the presence of RV dysfunction are
powerful independent predictors of mortality. As the RV fails, the typical inverse relationship of RVEF
and PAP is lost. Low PAPs in the setting of RVF are in fact associated with reduced patient survival.
The same cardiomyopathic process that affects the LV can also involve the RV. Interventricular septal
dysfunction and coronary ischaemia from either coronary artery disease or decreased perfusion by a failing
LV may negatively affect the RV. Diastolic RV function can be impaired by a dilated LV in a limited pericardial
space.17 Preoperative LV dysfunction may mask underlying RV dysfunction as RV preload is limited.
Post-LVAD implantation
LVAD function has an unpredictable effect on RV function (Fig. 2). Successful lling of the LVAD
requires the native RV to increase its output to match LVAD ow. Augmentation of CO and systemic

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M. Meineri et al. / Best Practice & Research Clinical Anaesthesiology 26 (2012) 217229

Fig. 2. Heart failure and LVAD Physiology. Ao, aorta; CO cardiac output; CVP, central venous pressure; LAP, left atrial pressure; LVAD,
left ventricular assist device; LVEDP, left ventricular end diastolic pressure; LVEDV, left ventricular end diastolic volume; MR, mitral
regurgitation; TR, tricuspid regurgitation; PA, pulmonary artery; PCWP, pulmonary capillary wedge pressure; RAP, right atrial
pressure; RVEDP, right ventricular end diastolic pressure; RVEDV, right ventricular end diastolic volume.

blood ow by the LVAD increase venous return to the RV. To cope with the increased preload, RV
diastolic compliance improves through decreased RV afterload and leftward IVS shift as the LVAD
reduces LV pressure. RV efciency is maintained as the unloaded RV does not need to contract as
vigorously to eject the increased RV preload.6,15,20,21 Clinically, this shows as a decrease in pulmonary
capillary wedge pressure (PCWP), PAP and peak RV systolic pressure (RVSP), which are conrmed by
LVAD experimental models (Fig. 2).
Despite the favourable effects of reduced RV afterload, the RV may become mechanically disadvantaged. RV pressure is related to free wall contraction and the position of the IVS. Global RV
contractility may be impaired during LVAD support from changes in the IVS position and motion
(Fig. 1). When the LV is severely unloaded, the IVS will bulge signicantly into the LV, jeopardising
efcient RV contraction. The RV free wall must work harder and cannot compensate for the loss of
septal function causing fatigue, which further exhausts the RV. Maintaining normal septal position and
function can compensate for the loss of RV free wall function.
A concern with continuous LV unloading by newer non-pulsatile devices is their potential negative
effect on RV function by consistently altering IVS position. However, Patel et al.6 found no difference in
RVD between pulsatile and continuous-ow LVADs.
LVAD implantation produces an inconsistent change in perioperative TR. Worsening of TR may
result from a leftward shift in the IVS, increased pulmonary vascular resistance (PVR) from cardiopulmonary bypass (CPB), systemic inammatory response syndrome (SIRS), transfusion and increased
preload. High LVAD ows may distort the tricuspid valve (TV) annulus.
Interestingly, explanted pulsatile LVAD-supported hearts have shown less RV structural remodelling than the LV unless the RV was also supported by an RVAD.22
Assessment of RV function
Structure and function
Right heart assessment denes RV structure, determines function and identies potential reversible
causes of dysfunction. Evaluation of the RV is challenging due to its anterior retrosternal position,
complex geometry, poor endocardial border denition and the marked load dependence of haemodynamic indices.

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221

Echocardiography is the most commonly used modality for RV evaluation, although cardiac
magnetic resonance imaging (MRI) has become the gold standard. There is good correlation between
cardiac MRI and computed tomography (CT) providing alternative modalities for RV evaluation23
during workup for LVAD insertion.
Assessment of RV structure includes an evaluation of RV shape, size, volume and wall thickness.24
Three-dimensional echocardiography (Fig. 1) is a promising modality that could lead to a more
accurate evaluation; however, MRI is still considered the most reliable method for measuring RV
volume.25,26 RVEF (normal 4076%)16 and RV fractional area change (RVFAC) (normal >40%) can be
calculated from size and volume measurements obtained by any of these modalities.
Tricuspid valve annular plane systolic excursion (TAPSE) is an echocardiographic MMode
measurement of the lateral TV annulus longitudinal displacement during systole. A value of >15 mm
displacement is a normal quantitative measure of RV systolic function. It is, however, less reliable in
patients with regional RV dysfunction since it only measures the lateral free wall longitudinal movement. Assessment of the TV annulus size, the presence and severity of TR, inferior vena cava size and
hepatic venous blood ow pattern should also be part of routine RV evaluation. Despite relatively good
correlation among TAPSE, RVFAC and RVEF,16 most echocardiographers use a subjective eyeball
assessment classifying global RV function as good, mild, moderate or severely reduced.
Post-LVAD implantation
Echocardiography remains the primary imaging modality for monitoring cardiac function in LVAD
patients,26 as MRI is no longer an option but cardiac CT is a reliable alternative to MRI.27 Relative change
in RV size and the degree of TR from an established baseline is serially followed with worsening RV
function suggested by increased RV size and TR.
A decrease in TAPSE has been described15 post-LVAD placement from reduced RV afterload and the
RV contractile requirement to sustain CO. However, a low TAPSE in conjunction with increasing RV size
and TR supports worsening RV function.28
A key structural feature to evaluate is the IVS position, as abnormal motion towards one side or the
other determines LV and RV shape. Septal changes might be suggestive of RV dysfunction, abnormal
loading conditions, incorrect LVAD settings/placement or LVAD device failure. The pericardial space
should be examined for possible right heart compression by uid collections or thrombus.
During continuous-ow LVAD support, pre-existing RVD does not worsen in the intermediate
median follow-up of 4.5 months. Moreover, the dimensions of the right-sided cardiac chambers were
reduced in parallel with changes in the left-sided chambers. The RV response, however, appeared to be
variable.
Denition and predictors of RV failure
Denition RVF
Patients presenting for LVAD surgery may demonstrate a broad clinical spectrum of preoperative RV
dysfunction from being relatively asymptomatic to fulminant RVF. In this patient population, RVF is
dened as a clinical syndrome that impairs the ability of the right heart to ll and eject appropriately or
the inability of the RV to provide adequate blood ow through the pulmonary circulation at a normal
central venous pressure (CVP).29
Due to the retrospective nature of most studies, there is a lack of a universal denition for RVF postLVAD among authors. RVF occurs when transpulmonary ow is unable to ll the LVAD despite maximal
medical therapy. RVAD implant is unequivocally accepted as an extreme sign of RVF. Nevertheless, RVF
not requiring RVAD is variously dened, directly as haemodynamic derangement, indirectly as a need
for pharmacological support (inotropes or pulmonary vasodilators for >14 days) or as a combination of
the two (Table 2).47,12,14,30
Potapov et al.11 used more specic haemodynamic and inotropic support criteria to institute inhaled
nitric oxide (iNO) to manage RVF (Table 3). This proposed haemodynamic denition of RVF has only
been used by a few authors.10,11

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Table 2
General criteria for RVF post-LVAD.





RVAD implantation or RV mechanical support [ECMO]


Inotropic support for > 14 days, and/or started 14 days after LVAD implantation
Pulmonary vasodilators [iNO] administered for > 214 days post-LVAD implantation
Hospital discharge on inotropes

ECMO, extra-corporeal membrane oxygenator; iNO, inhaled nitric oxide; LVAD, left ventricular assist device; RVAD, right
ventricular assist device; RV, right ventricle.

Table 3
Criteria for iNO to manage RVF.
 Inability to wean from cardiopulmonary bypass (CPB)
 Any 2 of the following sustained for > 15 min after separation from CPB:
B Mean arterial pressure  55 mmHg
B Central venous pressure  16 mmHg
B Mixed venous saturation  55%
 Administration of more than 20 inotropic equivalents (IE)
B
B
B
B

10 mg/kg/min dopamine, dobutamine, enoximone or amrinone 10 IE


0.1 mg/kg/min epinephrine or norepinephrine 15 IE
1.0 mg/kg/min milrinone 15 IE
0.1U/min vasopressin 10 IE

 LVAD pump ow rate index  2.0 l/min2 calculated as LVAD ow divided by body surface area.

Risk factors
Many authors have attempted to identify preoperative risk factors and develop risk scores to better
identify LVAD candidates at risk for postoperative RVF and plan treatment. These at-risk patients may
benet from preoperative optimisation of right heart function or planned biventricular assist device
(BiVAD) support. However, because of its multifactorial nature postoperative RV dysfunction remains
difcult to predict in individual potential LVAD candidates.
Studies have identied both patient characteristics and haemodynamic parameters as altering risk.
However, most studies are limited by small sample size, single institution, retrospective nature and the
use of different VADs within the same study.
Preoperative risk factors for post-LVAD RVF include patients characteristics (female gender and
non-ischaemic cardiomyopathy33), preoperative need for support (mechanical ventilation,4,5,13,30
mechanical circulatory support5,30 or intra-aortic balloon pump (IABP)6) haemodynamic parameters,
biochemical markers and echocardiographic measurements (Table 4).
Haemodynamic parameters that may identify a vulnerable RV include increased preoperative4 or
intra-operative12 CVP and a decreased RV stroke work index4,5,31 (RVSWI <300 mmHg ml1 m2).
While the severity of PAP is an easily measured parameter, RV function remains the most important
determinant of survival. Patients without pulmonary hypertension are more likely to develop RVF and
die after LVAD surgery. This likely reects poor RV contractility that is unable to overcome an elevated
PVR. Low preoperative RV performance (low PAP or RVSWI) should suggest the need for RVAD/BiVAD
support. Fixed pulmonary hypertension associated with concomitant pulmonary disease requires
preoperative assessment with pulmonary vasodilators.
Signs of end-organ damage and hepatic congestion, possibly as surrogates of impaired preoperative
RV function, have also correlated to increased risk of RVF and the need for BiVAD support. These
include increased serum creatinine (Cr),5,31 blood urea nitrogen4,13 and aspartate aminotransferase
(AST) and bilirubin.5 Elevated preoperative non-specic neurohumoral markers of heart failure, such as
N-terminal pro-brain natriuretic peptide and neopterin, and the inammatory markers procalcitonin
and big endothelin-1 were found in patients developing RVF post-LVAD.11

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Table 4
Risk factors for RVF post-LVAD studies.
Author, year

Ochiai,30 2002

245 HM I
Novacor
108 HM I
54 Novacor

Dang, 2005
Santambrogio,13
2006

LVAD

Patel,6 2008

77 HM I
HM II
266 Multiple
Fitzpatrick,8
2008
devices
Matthews,5 2008 197 Multiple
devices
35 HM XVE
Puwanant,28
2008
HM II
Thoratec
Baumwol,7 2010 40 Multiple
devices
Kormos,4 2010 484 HM II

RVF denition

Risk factors

RVAD

Mechanical Support, Female Gender

Inotropes >14 days, RVAD


MAP <80 mmHg, Severe TR,
Inotropes
iNO
Inotropes/vasodilators >14 days,
RVAD
RVAD

Intraop [ CVP, Y PAP, Y MAP, Reoperation


Mech Ventilation

Inotropes/vasodilators >14 days,


RVAD
Inotropes/vasodilators >14 days,
RVAD
Inotropes >14 days, iNO > 48 h,
Sildenal post iNO, RVAD
Inotropes/vasodilators >14 days,
RVAD

[ AST, ALT, Cr, BUN


IABP
CI < 2.2 l/min/m2, RVSWI < 250, [ Cr, Previous
heart surgery
Mech Ventilation, Mechanical Support, Preop
Inotropes, Y CI, Y RVSWI, [ Cr, [ AST
Tricuspid annular motion < 7.5 mm

Severe TR
CVP/PCWP > 0.64, BUN > 39 ng/dL, Mech
Ventilation

Patient characteristics

Laboratory

Haemodynamics

Female gender
Small BSA
Non-ischemic
Previous heart surgery
Preoperative inotropes
Mechanical ventilation
Mechanical circulatory assist

[ AST, ALT, bilirubin [2.0 mg/dL]


Y albumin
[ Cr [1.9 mg/dL], BUN
[ C-reactive protein, NT-proBNP
Severe TR
Tricuspid annular motion < 7.5 mm
RV SAX/LAX > 0.6
RV dysfunction: [ RVEDV, RVESV

CI < 2.2 l/min/m2


RVSWI < 250
CVP/PCWP > 0.64
Intraop [ CVP
Intraop Y PAP/MAP

BSA, Body surface area; BUN, blood urea nitrogen; CI, cardiac index; Cr, creatinine; CVP, central venous pressure; HM, Heart
Mate; IABP, intra-aortic balloon pump; iNO, inhaled nitric oxide; MAP, mean arterial pressure; PAP, pulmonary arterial pressure;
PCWP, pulmonary capillary wedge pressure; RVAD, right ventricular assist device; RVEDV, right ventricular end diastolic
volume; RVESV, right ventricular end systolic volume; RV SAX/LAX, right ventricle short to long axis ratio; RVSWI, right
ventricular stroke work index; TR, tricuspid regurgitation.

Preoperative presence of severe TR and RV short/long axis ratio >0.6 have a high specicity (87%
and 97%, respectively) and good sensitivity (66% and 37%) in identifying patients at risk of post-LVAD
RVF. Increasing severity of TR also directly correlates with the odds of occurrence of post-LVAD RVF.7 In
a small study by Puwanant et al.11 preoperative TAPSE <7.5 mm better predicted post-LVAD RVF than
RVFAC with a specicity of 91% and a sensitivity of 46%.28
Risk scores
Risk scoring systems have been proposed to quantify the risk of RVF post-LVAD, though none has
been prospectively validated on heart failure patient populations.
Drakos et al.14 included seven preoperative variables found to correlate with postoperative RVF after
multivariate regression analysis (Table 5). The incidence of RVF was 44% in this retrospective study of
175 patients implanted with various pulsatile and continuous-ow LVADs. RVF was dened as the need
for inotropic support for >14 days, iNO for >48 h or RVAD implant. The sum of all points assigned to
each variable generated a prediction model, which stratied patients into four different risk groups.
The incidence of RVF was 11% in the lowest risk group versus 83% for the highest group. Destination
therapy was identied as a strong independent predictor in addition to increased PVR and the use of
a preoperative IABP.
Matthews et al.5 retrospectively looked at 197 LVAD recipients, 35% were complicated by RVF.
Independent preoperative risk factors for RVF were identied (vasopressor use, AST, bilirubin and Cr)
and a risk score developed (Table 5).

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Table 5
Risk scores for RVF post-LVAD.
Matthews5 [2008]

Fitzpatrick31 [2009]

Drakos14 [2010]

Preoperative variables

Points

Preoperative variables

Preoperative variables

Points

Vasopressor use
Cr  2.3 mg/dl
Bilirubin  2 mg/dl
AST  80 IU/L

4
3
2.5
2

Cardiac index  2.2 L/min/m2


RVSWI  0.25 mmHg L/m2
Severe RV dysfunction
Cr  1.9 mg/dl
Previous cardiac surgery
SBP  96 mmHg

Destination therapy
IABP
PVR
1.7
1.82.7
2.84.2
>4.3
Inotrope dependency
Obesity
ACE or ARB
B-Blocker

3.5
4

Risk score

1
2
3
4
2.5
2
2.5
2

Risk score

Risk score

Total points

Odds ratio

Each variable valued:

Total points

Risk RVF [%]

3.0
4.05.0

0.49
2.8

5.5

7.6

1 [abnormal] or 0 [normal] use


These cut offs for abnormal
Dichotomic variable yes 1
Risk Score [ 18 * [CI] 18 * [RVSWI] 17 *
[Cr] 16 * [Previous Cardiac Surgery] 16 *
[RV dysfunction] 13 * [SBP]
Score < 50 predicts need for BiVAD

<5
5.58.0
8.512
>12.5

11
37
56
83

ACE, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; B-Blocker, beta blocker; Cr, Creatinine; CI,
Cardiac Index; IABP, Intra-aortic balloon pump; RVSWI, right ventricular stroke work index; SBP, systolic blood pressure.

A similar risk score was developed by Fitzpatrick31 in a slightly larger population of 266 patients
also receiving different types of LVADs. In this retrospective study, RVF was dened as the need for
RVAD, which was used in 34% of cases. An RVAD risk score was developed using the preoperative risk
factors correlated to postoperative need for RVAD after LVAD implantation following multivariate
logistic regression analysis (Table 5). Using a formula, a score >50 was predictive of need for BiVAD
with good sensitivity (83%) and specicity (80%).
The National Institutes of Health-sponsored Interagency Registry for Mechanical Assisted Circulatory Support (INTERMACS) provided systematic data collection in the largest LVAD database in the US.
A recent study comparing INTERMACS level I and II (sicker decompensating) to level III and IV patients
did predict a higher risk of postoperative complications and mortality but did not sensitively predict
postoperative RVF or need for RVAD.32
Prevention and treatment of RV dysfunction
Meticulous attention to optimising preload, afterload and contractility in the perioperative period is
crucial to prevent RVF in patients with pre-existing RVD (Fig. 3). This includes simple measures such as
maintenance of normal sinus rhythm or AV synchronicity, adequate ventilation, temperature, acid
base balance and prevention of coagulopathy. There have been no studies to date that assess the impact
of preoperative management on RVF post-LVAD.

Preoperative prevention
Van Meter et al.33 proposed a management algorithm that includes preoperative RV optimisation to
maintain a CVP <16 mmHg and a PA systolic pressure <65 mmHg. They considered using an RVAD in
the presence of liver dysfunction with elevated bilirubin. However, their retrospective analysis of 35
pulsatile LVAD patients using this algorithm could not eliminate postoperative RVF.
The optimal preoperative CVP is undened, though a value > 15 mmHg correlates to postoperative
RVF4 and warrants treatment according to some authors.33 Aggressive preoperative diuresis and, if

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Cardioversion
MgSO
Digoxin

fast

HR
80-100bpm

Rhythm
Normal Sinus

Diuresis
Dialysis
Decrease
LVAD flow

high

high

abnormal

Mg SO
Lidocaine
Amiodarone

low

Volume bolus

Contractility
CI > 2.0-4.0

low

PDI
Epinephrine
Dobutamine

TEE/TTE

iNO
Flolan
Lung
protective
ventilation

DDD Pacing
Epinephrine
Isoproterenol

slow

Preload
CVP 10-15 mmHg

Interventricular
septum position

RV Afterload
PVR 40-100
dynes.s.cm

Leftward
bulge

LV Afterload
SVR 800-1200
dynes.s.cm

225

low

MAP < 50mmHg


Low LVAD flow
Peripheral hypoperfusion

Decrease LVAD
flow

Phenylephrine
Norepinephrine
Vasopressin
Methylene Blue

Consider RVAD

CI, cardiac index; CVP, central venous pressure; HR, heart rate; iNO, nitric oxide; LVAD, left
ventricular assist device; MAP, mean arterial pressure; Mg SO , magnesium sulphate; PDI,
phosphodiesterase inhibitor; RVAD, right ventricular assist device; TEE, transesoephageal
echocardiography

Fig. 3. Management algorithm for RVF.

ineffective, continuous veno-venous haemodialysis (CVVHD) are effective measures CVP and relieve RV
distension.15
Preoperative treatment of an elevated PVR is suggested33 but unsupported by any studies to date.
The use of pulmonary artery catheters may be useful, as it allows continuous assessment of PAP and
careful titration of pulmonary vasodilators.
Preoperative coagulopathy predisposes to increased intra-operative bleeding. Intra-operative blood
transfusions in this setting are particularly detrimental since these risk RV volume overload, increase PVR
and worsen SIRS. Preoperative administration of vitamin K15,34 and intra-operative use of aprotinin35,36
are common practices to reduce bleeding that are validated by studies on rst-generation LVADs.
Pharmacological support of LV function is key to maintaining adequate end-organ perfusion,
minimising hypotension and avoiding the vicious cycle of ischaemia further exacerbating heart failure.
This may require the use of an IABP or temporary mechanical support devices37 when pharmacological
therapy is unsuccessful. Preoperative use of IABP is a risk factor for postoperative RVF6; nevertheless,
some authors have a low trigger to use an IABP38 to ultimately preserve RV function.
Pharmacological management
LV dysfunction therapy such as beta blockade or angiotensin-converting enzyme inhibitors is not
necessarily ideal for RV dysfunction. Instead, consider supporting the RV with inotropes that allow
some pulmonary vasodilatation (dobutamine or milrinone) while maintaining adequate systolic blood
pressure (epinephrine) for coronary perfusion. Alpha-adrenergic stimulation of the RV may have an

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overall negative inotropic effect. Differential contraction of the RV outow tract (RVOT) may predispose
to low RV CO from RVOT obstruction, particularly if the RV is underlled.
Specic pulmonary vasodilators (iNO and Flolan) may be required to reduce PVR and manage RVF.
In a methodologically awed prospective study by Potapov et al., perioperative administration of iNO
did not signicantly reduce RV dysfunction.39 The authors admitted that it might be difcult to perform
a prospective study using this drug.
Mortality directly correlates with the duration of inotrope support and remains high even after the
inotropes are stopped. Patients who tolerated early weaning of drugs (postoperative day 1) had a better
6-month survival than those who did not.40
Surgical management
TR is considered a run off mechanism for the failing RV and thus has not been aggressively treated
even in patients at risk of RVF. Functional TR may worsen post-LVAD from a leftward septal shift with
a consequent tethering of the TV septal leaet. Thus, the amount of residual TR should be carefully
assessed post-CPB by varying the LVAD pump ow. Correction of TR may indirectly contribute to
improved RV function by decreasing venous congestion and improving renal perfusion.
Different criteria have been proposed to proceed with TV repair during LVAD implant: TV annulus
>40 mm,41 moderate42,43 or severe TR.44 In these small single-centre studies TV repair or replacement
has had a neutral impact reducing neither RVF nor morbidity and mortality post-LVAD.
Surgical consideration should be given to myocardial revascularisation45 to salvage hibernating RV
myocardium.
Modications to CPB technique consisting of an RA to LA bypass46 and PA to aorta bypass47 may be
necessary to minimise RV overload and LVAD inow. Off-pump LVAD implant is becoming progressively popular as it has the obvious advantage of reducing blood loss and CPB-induced SIRS.48 Alternative minimally invasive surgical approaches49 have been proposed to further minimise surgical
stress and postoperative morbidity.
Weaning from CPB may unmask acute RVF. Shortening CPB time, continuing ventilation during CPB
and minimising transfusion-related lung injury are strategies that may avoid undesirable increases in
PVR. Careful deairing of the heart under trans-oesophageal echocardiogram (TEE) guidance, before CPB
weaning, is crucial to avoid systemic and right coronary air embolism. Alternatively, in-eld CO2
insufation has been used to reduce air emboli.50 Successful CPB weaning involves gradually reducing
CPB ows with an increase of LVAD ows as TEE monitors RV function, LV volume and IVS septal shift
(Fig. 1). Maintaining the IVS midline requires an adequate LV volume. If the LV is underlled it would be
hazardous to increase the pump speed to improve CO as this shifts the IVS leftward further impairing
RV function (suction cascade).
After separation from CPB, low PVR should be maintained by choosing a protective mechanical
ventilation strategy with low PEEP, avoiding hypoxia, hypercarbia and acidosis. Protamine administration, as a trigger for an acute PVR increase, should be deferred until stable haemodynamic has been
established.
Mechanical support
Intra-operative RVF may preclude weaning from CPB and necessitate alternative forms of
mechanical support. Given the lack of long-term RVADs, they are used as a rescue treatment when
conventional RVF therapy fails. No publication denes the criteria for RVAD implantation. In the largest
series reported to date, RVAD use occurred in 8% of patients post-LVAD implantation and correlated
with poor outcome.9
In a small retrospective analysis by Fitzpatrick et al. elective BiVAD implantation correlated with
a better 1 year, long-term and transplantation survival compared to emergent RVAD implant for acute
RVF post-VAD.8 Patients with severe RVF requiring BiVAD support were more severely ill, with
signicantly higher preoperative Cr and total bilirubin levels, IABP support, lower RVSWI, higher CVP
and CVP/PCWP ratio.

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Early RVAD implantation at the time of LVAD surgery improved survival to transplant (70% vs. 52%)
compared to RVAD insertion >24 h post-LVAD surgery.51 The use of an RVAD however reduced survival
after transplantation at 1, 5 and 10 years compared to those not requiring RVADs. RVAD implantation is
an independent predictor of mortality in LVAD patients as a BTT.4
To summarise, RVF post-LVAD implant is a frequent serious problem, which worsens morbidity,
mortality and hospital length of stay. LVAD support with the new continuous-ow devices modies RV
geometry by septal displacement and increasing RV preload. These changes may lead to RVF in
a patient with pre-existing RVD. RVF post-LVAD is multifactorial; risk factors include patient characteristics, biomarkers, haemodynamic and echocardiographic parameters of RV dysfunction. Several
risk scores to predict the risk of RVF have been developed but none has been prospectively validated.
Prevention of RVF relies on treatment of modiable preoperative risk factors and optimisation of RV
function. This consists of decreasing RV preload and afterload while maintaining adequate end-organ
perfusion. Intra-operative management minimises blood transfusion and CPB time to avoid worsening
PVR. Surgical correction of TR may also improve postoperative morbidity.
There are no specic guidelines for treating RVF post-LVAD implant. RVAD insertion is a last
recourse when RVF is refractory to medical treatment. There is some evidence that earlier institution of
RVAD or elective BiVAD is benecial.

Practice points
The RV is anatomically and functionally distinct from the LV and more sensitive to changes in
afterload (PVR).
Management of RVF in the LVAD patient relies on maintaining sinus rhythm and contractility,
optimising preload and reducing PVR.
Correction of preoperative coagulopathy, use of off-pump technique and attention to surgical
haemostasis may minimise the need for transfusions and benet postoperative RV function.
Adequate RV protection, careful deairing and slow progressive increase of LVAD ow are key for
successful weaning from CPB.
For newer-generation continuous-ow LVADs maintaining the interventricular septum in
a neutral position is crucial to optimising RV function.

Research agenda
Further research is needed to prospectively study the impact of risk scores in identifying heart
failure patients at risk for RVF.
Development and validation of standardised algorithms to manage RVF may improve outcome
in these patients.
Dening guidelines for BiVAD implantation would benet patients likely to experience RVF postLVAD implantation and provide the institution of more timely mechanical support.

Conict of interest
None declared.
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