Medicina Intensiva 48 (2024) 528---542

http://www.medintensiva.org/en/

UPDATE IN INTENSIVE CARE MEDICINE: ULTRASOUND IN THE CRITICALLY ILL PATIENT. CLINICAL
APPLICATIONS

Right ventricular dysfunction in the critically ill.

Echocardiographic evaluation
Virginia Fraile-Gutiérrez a,∗ , Lluis Zapata-Fenor b , Aaron Blandino-Ortiz c ,
Manuel Guerrero-Mier d , Ana Ochagavia-Calvo e

a
Department of Intensive Care Medicine, Hospital Universitario Río Hortega, Valladolid, Spain
b
Department of Intensive Care Medicine, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
c
Department of Intensive Care Medicine, Hospital Universitario Ramón y Cajal, Madrid, Spain
d
Department of Intensive Care Medicine, Hospital Universitario Virgen de Valme, Seville, Spain
e
Department of Intensive Care Medicine, Hospital Universitario de Bellvitge de L’Hospitalet de Llobregat, Barcelona, Spain

Received 12 February 2024; accepted 20 May 2024

Available online 29 July 2024

KEYWORDS Abstract Right ventricular dysfunction is common in critically ill patients, and is associated
Right ventricle; with increased mortality. Its diagnosis moreover remains challenging. In this review, we aim to
Echocardiography; outline the potential mechanisms underlying abnormal biomechanics of the right ventricle and
Right ventricular the different injury phenotypes. A comprehensive understanding of the pathophysiology and
dysfunction; natural history of right ventricular injury can be informative for the intensivist in the diagnosis
Cor pulmonale and management of this condition, and may serve to guide individualized treatment strategies.
We describe the main recommended parameters for assessing right ventricular systolic and
diastolic function. We also define how to evaluate cardiac output and pulmonary circulation
pressures with echocardiography, with a focus on the diagnosis of acute cor pulmonale and
relevant applications in critical disorders such as distress, septic shock, and right ventricular
infarction.
© 2024 Elsevier Espa?a, S.L.U. and SEMICYUC. All rights are reserved, including those for text
and data mining, AI training, and similar technologies.

PALABRAS CLAVE Disfunción del ventrículo derecho en el paciente crítico. Evaluación ecocardiográfica
Ventrículo derecho;
Ecocardiografía; Resumen La alteración del ventrículo derecho (VD) es frecuente en los pacientes críticos y
Disfunción ventricular su disfunción se asocia a mayor mortalidad, lo que plantea un reto clínico en su diagnóstico.
derecha; En esta revisión, pretendemos describir los posibles mecanismos de la biomecánica anormal
Cor pulmonale del VD y los distintos fenotipos de su lesión. La comprensión de la fisiopatología y la historia

DOI of original article: https://doi.org/10.1016/j.medin.2024.05.008

∗ Corresponding author.
E-mail address: vicky uvi@yahoo.es (V. Fraile-Gutiérrez).

https://doi.org/10.1016/j.medine.2024.06.019
2173-5727/© 2024 Elsevier Espa?a, S.L.U. and SEMICYUC. All rights are reserved, including those for text and data mining, AI training, and
similar technologies.
 Medicina Intensiva 48 (2024) 528---542

natural de la lesión del VD puede informar al intensivista sobre el enfoque del diagnóstico y
la monitorización de este, así como sobre la aplicación de intervenciones personalizadas con
relevancia terapéutica.
Se realiza una descripción de los parámetros de evaluación de la función sistólica y diastólica
del VD, junto con la estimación del gasto cardiaco y las presiones del circuito pulmonar mediante
ecocardiografía, con énfasis en el diagnóstico del cor pulmonale agudo junto con aplicaciones
clínicas en el paciente crítico como en el distrés, shock séptico e infarto de VD.
© 2024 Elsevier Espa?a, S.L.U. y SEMICYUC. Se reservan todos los derechos, incluidos los de
miner?a de texto y datos, entrenamiento de IA y tecnolog?as similares.

Many disease conditions in critically ill patients have an as the ratio between the anteroposterior and septolateral
impact on the function of the right ventricle (RV), and dys- diameters of the LV (Fig. 1A).13 When the RV experiences
function of the latter is associated with increased patient volume overload, it undergoes dilatation accompanied by
mortality.1 This disorder may result from contractility alter- flattening of the IVS, with EI > 1 during diastole (Fig. 1B).
ations secondary to coronary ischemia or sepsis, or increased Excessive preload may cause impaired contractility and a
afterload as in acute respiratory distress syndrome (ARDS) or decrease in coronary perfusion pressure.1 However, in the
pulmonary thromboembolism (PTE) --- though it may also be presence of pressure overload, the RV experiences dilata-
a consequence of the treatments used, such as vasoactive tion with septal deviation towards the LV and EI > 1 during
drugs, mechanical ventilation (MV) or water overload.1---4 both systole and diastole, with a ‘‘D’’-shaped LV, indicative14
Understanding the pathophysiology and natural history of of a poor patient prognosis (Fig. 1C).15 This finding is known
RV injury and adequate on-site monitoring can help the as the reverse Bernheim effect.9,12
intensivist establish a diagnosis and prescribe treatment to There is no universally accepted definition of RV
optimize RV function.1,5 failure.4,5 Recently, three different phenotypes have been
Ultrasound is a noninvasive and widely available tech- identified in patients with ARDS (normal RV function, RV
nique that has become a key tool for routine clinical dilatation, and dilatation of the RV with impaired systolic
evaluation purposes.6---8 Right ventricle alterations are com- function), associated with different clinical outcomes16,17
mon in the critical patient, though their diagnosis may (Fig. 2). Dilatation of the RV causes expansion of the
prove challenging and requires physiological knowledge tricuspid valve annulus and the appearance of tricuspid
of cardiorespiratory diseases in order to offer adequate insufficiency (TI), which produces venous congestion and
treatment.5 associated renal and/or hepatic damage, with an increase
in mortality.18 Congestion should be evaluated based on the
size of the inferior vena cava (IVC) and its variation during
Pathophysiology of RV dysfunction, its the breathing cycle, together with the hepatic venous flow
importance in intensive care, and ventricular pattern.
interdependence The interaction between the RV and the pulmonary
artery (PA) circulation under different loading conditions
is referred to as right ventricle --- pulmonary artery (RV-PA)
The RV is semilunar in shape and envelops the left ventricle
coupling and determines the relationship between RV con-
(LV). It consists of three segments: inflow tract, body and
tractility, measured by end-systolic elastance (Ees), and PA
outflow tract. The end-diastolic volume of the RV is slightly
afterload, measured by pulmonary artery elastance (Ea)1,18
greater than that of the LV, and as a result, it has a slightly
(Fig. 2). The system is considered to be coupled when
lesser ejection fraction (RVEF). The helicoid distribution of
Ees/Ea > 1.19,20 Acute pulmonary vascular dysfunction due
its muscle fibers generates a mainly longitudinal contractile
to multiple causes such as thrombosis, lung edema, MV
pattern, due to the lesser amount of circumferential fibers.
and vasoconstriction (secondary to hypoxemia, hypercapnia,
The RV wall is also comparatively thinner (under 5 mm) and
and acidosis) leads to acute PHT, which in turn induces an
is characterized by great distensibility and poor tolerance of
increase in the intrinsic contractile force of the RV to com-
increased pressure in the pulmonary circuit.9---11 The chronic
pensate the increase in afterload (homeometric adaptation
increase in RV afterload generated by pulmonary hyperten-
or Anrep effect).21 This should be reported as a hyperdy-
sion (PHT) produces an increase in the thickness of the RV
namic RV, though in critically ill patients it may be limited by
wall as a compensatory mechanism.
systemic infection and hypotension.22 Another mechanism
Both ventricles are anatomically and physiologically inte-
is RV dilatation to preserve blood flow (heterometric adap-
grated through the interventricular septum. Ventricular
tation or Starling mechanism)5,23 and reduction of Ees/Ea
interdependence is defined as the changes produced in one
to < 1, caused by the increase in Ea, which can lead to RV-PA
ventricle secondary to an increase in pressure or volume
decoupling and a negative diastolic interventricular interac-
in the other, and is evaluated along the short axis of the
tion, with a RV end-diastolic pressure (EDP) higher than that
parasternal plane.12 Under normal conditions, the IVS is
of the LV --- which negatively affects LV filling and cardiac
concave towards the LV throughout the cardiac cycle, and
output.5,18
the eccentricity index (EI) of the LV is 1. This index is defined

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Figure 1 Ventricular interdependence. RV: right ventricle; LV: left ventricle; EI: eccentricity index; A: normal eccentricity pattern
of the LV; B: volume overload with flattening of the septum only in diastole; C: pressure overload with flattening of the septum in
systole and diastole; D2: anteroposterior diameter of the LV; D1: septo-lateral diameter of the LV.

Quantification of the right ventricle chambers Table 1 Basic echocardiographic parameters in the study
of the right ventricle.
Because of its anatomy, the RV must be examined using
multiple acoustic windows, including the long paraster- Ratio between area of RV and area of LV
nal axis, short parasternal axis (inflow tract and outflow IVS motion
tract of the RV), apical four-chamber (4C) window, the RV wall thickness in subcostal plane
modified apical window for the RV, and the subcostal win- TAPSE
dow, using transthoracic echocardiography (TTE).24,25 The IVC size and collapse
report should present an evaluation based on qualitative Vmax TI
and quantitative parameters,24 though in immediate patient RV: right ventricle; LV: left ventricle; IVS: interventricular sep-
life-threatening situations, there are protocols guided by tum; TAPSE: tricuspid annular plane systolic excursion; IVC:
qualitative parameters of great reproducibility and corre- inferior vena cava; Vmax TI: maximum velocity of tricuspid insuf-
lation versus other cardiac assessment techniques such as ficiency.
magnetic resonance imaging (MRI) and three-dimensional
(3D) echocardiography,26,27 provided the exploration is per-
The quantification parameters are described in Table 2 and
formed by an expert operator.28 Table 1 describes the
Fig. 3.
echocardiographic parameters for the basic study of the RV.

Systolic evaluation of the right ventricle

Structural evaluation of the right ventricle - M mode
Although the plane corresponding to the short parasternal o TAPSE (tricuspid annular plane systolic excursion). This
axis is the best option for evaluating ventricular interde- parameter represents a measure of longitudinal function.
pendence, the apical 4C plane is the projection indicated It is determined in the apical 4C plane with the cursor
for performing measurements of the size of the right atrium optimally aligned in the lateral tricuspid annulus, and
(RA) and the RV. Dilatation of the RV is based on the ratio measures the degree of longitudinal displacement of the
between its transverse diameter or end-diastolic area (EDA) annular segment of the RV from end-diastole to the sys-
concerning the LV, measured in end-diastole. The normal tolic peak. It is not particularly dependent upon good
ratio is RV/LV < 0.6, while 0.6---1 is indicative of moderate image quality. The TAPSE has a prognostic value in PHT,31
dilatation, and > 1 corresponds to severe dilatation.5,29,30 and a value of < 17 mm suggests systolic dysfunction of the

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Figure 2 RV phenotypes. RV: right ventricle; LV: left ventricle; RV/LV: right and left ventricle end-diastolic area ratio; TAPSE:
tricuspid annular plane systolic excursion; PA: pulmonary artery; IVS: interventricular septum; Tac: pulmonary artery acceleration
time; PAPs: pulmonary artery systolic pressure; CVP: central venous pressure; IVC: inferior vena cava; CVVH: continuous venous-
venous hemodiafiltration.

Figure 3 A. TAPSE. B. FAC. C. Tissue Doppler. The arrow indicates the systolic wave and the star indicates the velocity of the e
wave. D. TEI index: measures the ratio between the isovolumetric contraction and relaxation times in relation to systolic ejection.
It can be quantified with pulsed Doppler or from the tissue Doppler registry. The advantage of tissue Doppler is that it can record
all the information of the cardiac cycle in the same beat, and improves the reproducibility of the technique. Measurement is made
of the isovolumetric contraction time (ICT), the isovolumetric relaxation time (IRT) and the ejection time (ET) in the pulsed tissue
Doppler spectrum of the lateral tricuspid annulus. E. Strain.

RV.24 The parameter has limitations in post-heart surgery plane through tracing of the end-diastolic (EDA) and end-
patients (Fig. 3A). systolic area (ESA) of the RV, taking care to include the
- Two-dimensional (2D) mode trabeculae in the cavity. Formula: (EDA-ESA)/EDA x 100,
o FAC (fractional area change). This parameter estimates values < 35% indicate systolic dysfunction.24 The FAC is
global ventricular function. It is quantified in the apical 4C an independent predictor of heart failure, sudden death,

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Table 2 Echocardiographic parameters for quantification of the size and systolic function of the right ventricle.
Parameter Normal value Characteristics
Wall thickness (mm) <5 The lateral wall of the RV is measured in the subcostal plane
Thickness > 5 mm indicates RV hypertrophy and suggests pressure
overload in the absence of other disease
RV/LV ratio < 0.6 0.6---1 moderate RV dilatation
>1 severe RV dilatation
Eccentricity index =1 >1 in diastole suggests volume overload and >1 in systole and
diastole indicates pressure overload
TAPSE (mm) > 17 Reproducible, easy to obtain
Good correlation of RVEF with MRI, FAC and ECO 2D
Limitation: angle dependent
FAC (%) > 35 Less reproducible, requires good 2D image
Good correlation with MRI
Limitation: quantification difficulty
Sẃave with TDI (cm/s) > 9.5 Reproducible, easy to obtain
Good correlation with ECO 2D, MRI
Limitation: angle dependent
TEI index RIMP > 0.43 via PW Limitation: with PW, measurement cannot be made in one same
and > 0.54 via DTI beat, with DTI measurement of IVRT and IVCT is made in the
same beat
RV free wall strain (%) > −20% Requires high 2D image quality, avoid angulations of apical 4C
window
Limitation: requires offline software for calculation
Medium quantification difficulty
RV ejection fraction in > 45% Precise measurement of volumes and EF
3D (%) Good correlation with MRI, with slightly lesser volumes
Limitation: few studies in critical patients
Speckle-tracking Independent of Doppler angle
Requires good 2D image quality, affected by cardiac motion
artifacts in plane
Limitation: quantification difficulty
Requires software not readily available in critical care
RV: right ventricle; LV: left ventricle; TAPSE: tricuspid annular plane systolic excursion; FAC: fractional area change; DTI: Doppler tissue
imaging; PW: pulsed wave Doppler; MRI: magnetic resonance imaging; IVRT: isovolumetric relaxation time; IVCT: isovolumetric contraction
time.

stroke and mortality in patients with PTE.32 Compared A RIMP > 0.43 via PW and > 0.54 via DTI indicates dys-
with TAPSE, the FAC is more precise in estimating systolic function of the RV24 (Fig. 3D).
function, taking MRI as reference33 (Fig. 3B). o Strain/strain rate tissue deformation image. The data
- Doppler obtained from the DTI study can be used to deter-
o Doppler tissue imaging (DTI). Systolic pulse wave veloc- mine the degree of myocardial deformation of the free
ity (S′ ). This parameter is obtained in the apical 4C wall (strain) and the velocity of myocardial deforma-
plane using DTI, placing the cursor of the pulsed-wave tion (strain rate). Strain and strain rate estimate the
(PW) Doppler at the middle portion of the basal segment global and regional systolic function of the RV, respec-
of the lateral tricuspid annulus. It measures the longi- tively. Strain is defined as the percentage of systolic
tudinal velocity. Although the parameter physiologically shortening of the free wall of the RV from the base to
decreases with age, a value < 9.5 cm/s is considered to the apex, while strain rate is the velocity with which
be abnormal24 (Fig. 3C). such shortening takes place.24 Both parameters offer a
o Right ventricle index of myocardial performance (RIMP) good correlation with myocardial contractility,34 though
or Tei index. This is an index of the global performance strain is less influenced by heart motion and is therefore
of the RV. The isovolumetric contraction time (IVCT), considered to be more reliable --- though it is depen-
isovolumetric relaxation time (IVRT) and ejection time dent upon the loading conditions. The strain values
(ET) should be measured from the same heartbeat using should be measured from the apical 4C window without
PW or DTI in the lateral tricuspid annulus. It is important angulation and with high-quality imaging since rever-
to ensure that the non-consecutive beats have similar beration and artifacts can affect the placement of the
RR intervals. The index may be underestimated under reference points and cause their quantification to be
conditions of high RA pressures, which will shorten IVRT. underestimated. The reference points should be limited

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Table 3 Right ventricle diastolic function grades.

Parameters Normal Abnormal Restrictive
• 2D
RV wall ≤ 5 mm > 5 mm
IVC diameter and collapse Dmax IVC ≤ 21 mm and Dmax IVC > 21 mm and ICIVC
ICIVC > 50% > 50%
• Pulsed Doppler
E/A tricuspid flow 0.8---2.1 < 0.8 > 2.1
Tricuspid EDT (ms) 120---229 > 229 < 120
• Tissue Doppler
Tricuspid e′ /a′ ≥1 <1
Tricuspid E/e′ ≤6 >6
IVRT of RV (ms) ≤ 73 > 73
• Hepatic venous flow
S wave / D wave ≥1 <1 < 1 and reverse
wave
ICIVC: Index of respiratory collapse of the IVC; Dmax : maximum diameter; IVC: inferior vena cava; E/A: tricuspid filling waves; EDT: E
wave deceleration time; ms: millisecond; E/e′ : ratio between tricuspid flow E wave and lateral e′ wave of TDI in the lateral tricuspid
annulus; IVRT: isovolumetric relaxation time; RV: right ventricle; S wave: systolic wave of hepatic venous flow; D wave: diastolic wave
of hepatic venous flow.

to the myocardial free wall excluding the pericardium, • Quantification via PW of the tricuspid inlet flow in the
which may prove difficult since the free wall of the RV zone of maximum tricuspid leaflet opening. Determina-
is usually thin. A value > ---20% is considered normal24 tion is made of the E wave, A wave, E/A ratio and E wave
(Fig. 3E). deceleration time (EDT). This flow is strongly dependent
upon preload, postload and the respiratory phase, and
A pathological value has prognostic implications in determination of the mean of 5 cycles is advised. On the
patients with normal LV function.35 It is also associated with other hand, the coexistence of moderate or severe TI,
greater mortality in septic shock (SS),2,36 PHT,37 patients or atrial fibrillation, underestimates the measurements
with LV circulatory assist measures38 and COVID-19 cases.39 obtained.
• DTI at the lateral tricuspid annulus. This is less dependent
- Speckle-tracking echocardiography. An analysis is made upon preload and postload than PW. We obtain the isovol-
of speckle motion in the two-dimensional image; it is umetric relaxation time (IVRT), e′ wave, a′ wave and the
independent of the Doppler angle, with the possibility of e′ / a′ ratio (Fig. 3C and D).
quantifying the dynamics of thickening, shortening and • PW in the suprahepatic vein. This is strongly depen-
rotation of cardiac function.24,40---42 Few studies on critical dent upon the respiratory cycle, MV and positive
patients have been published, however. end-expiratory pressure (PEEP), and determination of the
- Three-dimensional echocardiography (ECO-3D). This tech- mean of 5 cycles is advised. Three waves are obtained: an
nique offers a more precise measure of the volumes and anterograde systolic wave (S), caused by relaxation of the
RVEF, though the quantified volumes are slightly inferior RA; an anterograde diastolic wave (D), during rapid ven-
to those recorded with MRI.43,44 Availability in critical tricular filling; and a reverse flow wave (AR) during the
patients is limited. atrial systole.

Evaluation of diastolic dysfunction of the right ventricle As in the LV, there is no echocardiographic parameter
During their evolutive course, a great variety of cardiological capable of isolatedly indicating the existence or grade of
disorders (both primary and secondary) are characterized by diastolic dysfunction of the RV. Instead, we must integrate
diastolic alterations of the RV (myocardiopathies, LV valve all the determinations, and the guides recommend classify-
diseases, congenital heart disorders, rheumatoid arthritis, ing the situation as normal or abnormal, with an evolution
vasculitis, ARDS), though there is currently no consensus towards restriction in some disease conditions.
regarding their evaluation and quantification, and they do
not form part of standard clinical echocardiographic assess- Hemodynamic monitoring
ment.
Recently, guidelines have been published13 for their eval- It should be mentioned that for the quantification of car-
uation based on four parameters (Table 3): diac output (CO) and pulmonary pressures or central venous
pressure (CVP), we need to place a pulmonary artery
• Two-dimensional (2D) imaging. Increase in volume of the catheter or central venous catheter, respectively. However,
RA, dilatation of the IVC with a decrease in inspiratory col- transthoracic echocardiography (TTE) allows us to estimate
lapsibility index (CI) of the IVC and myocardial thickening these parameters on a noninvasive basis, since due to the
of the RV. anatomy and retrosternal position involved, a poorer analy-

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 V. Fraile-Gutiérrez, L. Zapata-Fenor, A. Blandino-Ortiz et al.

Figure 4 A. Variation of the inferior vena cava. The 2D inspiration and expiration image is shown in M mode. B. Continuous Doppler
recording of tricuspid insufficiency. The red arrow indicates tricuspid insufficiency maximum velocity. C. Isovolumetric relaxation
time (IRT). D. Pulmonary artery acceleration time (Tac). E. Pulsed Doppler recording of pulmonary insufficiency. The arrows indicate

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 Medicina Intensiva 48 (2024) 528---542

Table 4 Echocardiographic parameters for hemodynamic quantification of the right-side cavities.

Estimated parameter and Quantification Characteristics
echocardiographic parameter
Right atrial pressure (RAP) • Dmax IVC > 21 mm and
• ICIVC < 50% (RAP > 15)
• Dmax IVC > 21 mm and
• IVC ICIVC = (Dmax IVC --- Dmin IVC/Dmax IVC) x 100 • ICIVC > 50% (RAP 5---10)
• Dmax IVC ≤ 21 mm and
• ICIVC < 50% (RAP 5---10)
• Dmax IVC ≤ 21 mm and
ICIVC > 50% (RAP 0---5)

RAP = 1.62 E/e′ + 2.13

• Tricuspid E/e ′
E/e′ > 6 estimates RAP > 10 mmHg
D wave > S wave
Absence of systolic flow wave RAP > 20 mmHg
• Hepatic flow wave

Systolic pulmonary artery pressure (PAPs)

• TI PAPs = 4x (Vmax TI)2 + RAP IVRT > 59 ms predicts PAPs > 40 mmHg

IVRT < 40 ms excludes PAPs < 40 mmHg

IVRT (PPV 100%)
• DTI Tac > 120 ms is normal
Tac < 100 ms suggests PHT
60/60 sign is Tac < 60 ms with Vmax
TI ≤ 60 mmHg associated with PAPs
> 60 mmHg

• PA Tac

Diastolic pulmonary artery pressure (PAPd) PAPd = 4x (VPIed )2 + RAP

Mean pulmonary artery pressure (PAPm)

• IP PAPm = 4x(VPIpd )2 + RAP

PAPm = 0.61x (VmaxTI)2 + 2 mmHg
If Tac < 120 ms, PAPm = 90 --- (0.62 x Tac)
• TI
• PA Tac Tac < 100 ms predicts PAPm
> 25 mmHg
Pulmonary vascular resistance (PVR) PVR = 10 x (VmaxTI/VTIRVOT ) + 0.16.
RAP: right atrial pressure; IVC: inferior vena cava; ICIVC : Index of collapse of the IVC; Dmax : maximum diameter; Dmin : minimum diameter;
D wave: diastolic wave; S wave: systolic wave; PAPs: systolic pulmonary artery pressure; PAPd: diastolic pulmonary artery pressure; PAPm:
mean pulmonary artery pressure; TI: tricuspid insufficiency; PI: pulmonary insufficiency; Tac: pulmonary artery acceleration time; Vmax TI:
Maximum velocity of tricuspid insufficiency; DTI: tissue Doppler imaging; IVRT: isovolumetric relaxation time; VPIpd protodiastolic velocity
of the pulmonary artery; VPIed : end-diastolic velocity of the pulmonary artery; VTIRVOT: velocity-time integral of the right ventricle outflow
tract.

the protodiastolic maximum velocity of the pulmonary insufficiency flow (VPIed ) and the end-diastolic maximum velocity of the
pulmonary insufficiency flow (VPIed ). F. Normal type I pulmonary artery flow with symmetrical ascent and descent. G. Type I pulmonary
artery flow with symmetrical triangular follow, normal flow. H. Type II pulmonary artery flow with asymmetrical triangular follow,
suggestive of increased pulmonary pressure. I. Type III pulmonary artery flow with an arrow indicating the mesosystolic notch due
to early closure of the pulmonary valve.

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 V. Fraile-Gutiérrez, L. Zapata-Fenor, A. Blandino-Ortiz et al.

sis is afforded by transesophageal echocardiography (TEE).25 • TI. Based on the calculation of Vmax TI (Table 4).
The echocardiographic parameters are shown in Fig. 4 and • PI. Based on quantification of the maximum diastolic
Table 4. velocity of PI in protodiastole (Fig. 4E).
• Tac (Fig. 4D---G).
Right atrial pressure (RAP)
Right atrial pressure is determined from CVP, and it can be Pulmonary vascular resistance (PVR)
estimated using the following parameters: Quantitative measurement of pulmonary vascular resistance
(PVR) requires us to relate two measurements: Vmax TI via
• Collapsibility index (CI) of the inferior vena cava (IVC). CW Doppler and the velocity-time integral of the right
The IVC is measured in the subcostal plane at 1---2 cm from ventricle outflow tract (VTIRVOT ) via PW (image). Quantifi-
its access to the RA, behind the hepatic vein, with the cation is made in Woods units. Formula: PVR = Vmax TI /
patient in the supine position and at the end of expiration. VTIRVOT x 10 + 0.16.
Formula: CI = [Dmax IVC - Dmin IVC]/Dmax IVC). In critically We can also evaluate PVR in a semi-quantitative manner
ill patients there are situations where dilatation of the IVC observing the presence of ‘‘notches’’ in the PW spectrum
without respiratory collapse does not predict the response of the flow velocity in the right ventricle outflow tract
to crystalloid administration45 (Fig. 4A). (Fig. 4F---H). A mesosystolic notch is indicative of severe PHT
• Tricuspid E/e′ ratio. Registry via PW is made of the pro- (Fig. 4I).
todiastolic filling velocity at tricuspid valve level (wave
E), and DTI is used to record the relaxation rate of the Clinical applications in intensive care
lateral wall of the tricuspid annulus in protodiastole (e′
wave). An E/e′ ratio > 6 has been shown to be associated to Acute dysfunction of the RV is a heterogeneous syndrome
high RAP: > 10 mmHg.25 It has been validated in ventilated resulting from RV-PA decoupling secondary to disorders that
patients.13 have a high incidence in critically ill patients.4 Such decou-
• Hepatic vein flow pattern: An S < D wave ratio is associated pling is generally seen in cases characterized by a rapid
with high RAP.13,25 increase in PAP, in situations of end-stage PHT and in patients
• Interatrial septum. Displacement towards the left atrium with mild PAP presenting inflammatory conditions such as
(LA) is associated with high RAP values. ARDS, sepsis and left ventricular failure --- all these disor-
ders also being associated with negative inotropic effects.
Pulmonary artery pressure (PAP) Furthermore, in many of these scenarios, the patients are
Systolic, diastolic and mean PAP can be estimated from subjected to MV, which in itself may intensify or even
TI or pulmonary insufficiency (PI) flow using the simplified cause RV failure by inducing an increase in PVR. When
Bernoulli equation in the absence of pulmonary stenosis, and MV is applied in patients without cardiorespiratory disease,
RAP is added to the calculated gradient. the tidal volume has no deleterious hemodynamic conse-
quences. However, in the presence of lung injury, the rise in
Systolic pulmonary artery pressure (PAPs) transpulmonary pressure increases RV afterload and reduces
Color Doppler is used to record TI, placing the continuous Tac (Fig. 4G).
wave (CW) Doppler cursor with good alignment to calculate
the maximum velocity of TI (Vmax TI), which is equivalent to Precapillary vs postcapillary pulmonary
the pressure gradient between the RA and RV. In situations hypertension
of massive TI, the formula is not applicable, since the iner-
tial component is not negligible. PAPs = 4 x Vmax TI2 + RAP
The most common cause of RV failure is PHT, defined as
(Fig. 4B).
PAPm ≥ 25 mmHg.29 The analysis of TI allows us to estimate
In patients without detectable TI, estimation can be
PHT, with Vmax TI ≤ 2.8 m/s being associated with a low prob-
made via:
ability of PHT, while Vmax TI > 3.4 m/s is associated with a high
probability of PHT (Fig. 5).
• IVRT. We position DTI at the level of the free wall of the
Diagnosing the cause of PHT is crucial to define the
RV in the tricuspid valve (Fig. 4C).
appropriate treatment. In this regard, a first step is to
• Pulmonary artery acceleration time (Tac), which is the
determine whether the underlying cause is precapillary,
interval from the start of ejection of the RV to the peak
with pulmonary capillary pressure (PCP) (wedge pressure)
flow velocity through the pulmonary valve (Fig. 4D---G).
≤ 15 mmHg, or postcapillary due to pathology of the LV,
The 60/60 sign is associated to Tac < 60 with a tricuspid
with PCP ≥ 15 mmHg. The echocardiographic findings sug-
systolic gradient > 30, but < 60 mmHg.
gestive of a pre- or postcapillary etiology are described in
Fig. 6.29 The calculation of PVR contributes to establishing
Diastolic pulmonary artery pressure (PAPd) the differentiation.30
Calculation is made of the peak velocity of PI in end-diastole An invasive parameter that has been shown to be use-
(VPIed ) in the short parasternal axis plane at the large vessel ful in differentiating between pre- and postcapillary PHT
level (Fig. 4E). This method is imprecise in the presence of is the transpulmonary gradient, defined as the difference
massive TI. between PAPm and the pressure of the LA, estimated from
the PCP.46 A value of > 12 mmHg is indicative of a precapillary
Mean pulmonary artery pressure (PAPm) origin. Recently, a surrogate indicator of the transpulmonary
Several methods have been described for estimating PAPm: gradient has been proposed in the form of the echographic

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Figure 5 Algorithm to determine the probability of pulmonary hypertension based on echocardiography. A the presence of signs of
at least 2 categories must be present. b Collapse < 50% with forced inspiration, < 20% with normal inspiration. **RV: Right ventricle;
LV: Left ventricle; TAPSE: tricuspid annular plane systolic excursion; PAPs: pulmonary artery systolic pressure; RVOT: right ventricle
outflow tract; PA: pulmonary artery; RA: right atrium; IVC: inferior vena cava; PHT: pulmonary hypertension.

pulmonary to left atrial ratio (ePLAR) measured from the whether echocardiography alone can differentiate between
relationship between Vmax TI, as an estimate of pulmonary the two conditions, and the existing evidence is scarce and
pressure, and the mitral E/e′ ratio, as an estimate of the sometimes contradictory.
pressure of the LA. In this regard, ePLAR > 0.30 m/s would In general, when the RV afterload experiences an acute
be indicative of precapillary PHT, while < 0.25 m/s would be increase, the consequences are dilatation and impaired
indicative of postcapillary PHT.46 function, while if the pressure increase is gradual, the RV
has time to adapt, and remodeling and hypertrophy are more
likely to occur.49 However, the thickness of the free wall of
Acute and chronic cor pulmonale
the RV can double in 48 hours after the increase in afterload,
and so the above is not entirely specific.49
Precapillary PHT secondary to lung disease, hypoxia or pul- Several specific patterns may help in establishing a dis-
monary vascular occlusion is classically referred to as cor tinction, as in the case of acute PTE, where a clot in transit
pulmonale. Depending on the evolution of the increase may be observed in the RA or RV, and even in the main
in RV afterload, a distinction is made between acute and trunk of the pulmonary artery. In general, the RV is unable
chronic cor pulmonale. In this respect, acute cor pulmonale to generate high pressure against acute increases in after-
(ACP) can be secondary to ARDS or PTE, and is defined load; consequently, PAPs > 60 mmHg are more suggestive of
by the presence of dilatation of the RV quantified by an a chronic process. The 60/60 sign and the McConnell sign,
EDA RV/ EDA LV ratio > 0.6 accompanied by paradoxical described as a relatively hyperkinetic RV vertex versus a
motion of the IVS.47 The chronic form of cor pulmonale hypokinetic or akinetic RV free wall, have a high positive
(CCP) in turn is mainly due to chronic obstructive pulmonary predictive value (PPV) in the diagnosis of acute PTE.50
disease (COPD), lung fibrosis or chronic PTE. All of these The global longitudinal strain of the LV can help dis-
conditions induce chronic hypoxemia and/or remodeling of tinguish between the chronic and the acute form of cor
the pulmonary circulation,48 requiring the RV to adapt in pulmonale.51,52 In the acute context, it is altered mainly
compensation because of the increase in mechanical effort due to regional impairment of the septal, apical and lat-
involved. eral segments, while in the chronic presentation, the global
Distinguishing ACP from CCP is a challenge in critical longitudinal strain of the LV is preserved, with only minimal
patients, and is mainly based on the clinical history and the septal involvement.
findings of the clinical examination. It is difficult to know

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Figure 6 Echocardiographic signs suggestive of pre- and postcapillary pulmonary hypertension. The blue arrow indicates the inter-
atrial septum bulging towards the left atrium. LA: left atrium; ePLAR: echographic pulmonary to left atrial ratio = [VmaxTI/(E/e′ )
mitral]; PHT: pulmonary hypertension; RVOT: right ventricle outflow tract; LV: left ventricle.

Acute respiratory distress syndrome (ARDS) Septic shock

It is estimated that 21% of all patients with moderate to Right ventricle dysfunction affects 35% of all patients with
severe ARDS will present ACP,52 and this in turn is associated septic shock (SS), and its underlying etiology is multifac-
with increased mortality.53 Taking into account that pneu- torial, since it may be caused by an increase in preload
monia as a cause of ARDS, a driving pressure ≥ 18 cmH2 O, due to excessive fluid therapy, direct myocardial involve-
a PaO2 /FiO2 < 150 mmHg and a PaCO2 ≥ 48 mmHg have all ment, or an increase in afterload secondary to hypoxemia,
been identified as risk factors for the development of ACP in hypercapnia or the application of MV.
patients with non-COVID-19 ARDS (N-ARDS), a score has been Right ventricle dysfunction is correlated to mortal-
developed allowing the early identification of those patients ity, with a more than two-fold increase in mortality risk
at risk of presenting ACP and who should be subjected to over both the short and long term.59 Such patients have
echocardiographic follow-up.8,52 lower CO and SvO2 values than patients without dysfunc-
In patients with ARDS secondary to COVID-19 (C-ARDS), tion, requiring higher doses of vasoactive drugs and fluid
the incidence of ACP is estimated to be 18---38%.54,55 therapy.60 It should be noted that the latter may be a
However, the published studies indicate that in COVID-19 cause or consequence of the situation since the pres-
patients, the ACP risk score lacks validity, since in the con- ence of RV dysfunction induces false-positive results in the
text of C-ARDS the main mechanism associated with the volume response tests such as the variability of systolic
development of ACP is the presence of thromboembolic phe- (stroke) volume or pulse pressure, leading to the erroneous
nomena in the pulmonary blood vessels. Thus, the finding administration of fluid therapy and hence a positive fluid
of ACP in C-ARDS patients is an indication for performing balance.61
computed tomography to discard the presence of PTE. Although there are validated cut-off points for RV
In ACP, the RV, before undergoing dilatation via dysfunction,25 their applicability is limited in patients
homeometric adaptation to the afterload, increases its con- with SS, since these parameters must be contextualized
tractility to preserve ventricular-atrial coupling. Although under the conditions of pre- and afterload that can be
the measurement gold standard is Ees/Ea, echocardio- dynamically altered due to the use of vasopressors, MV
graphic assessment based on the TAPSE/PAPs ratio has and eventually ARDS. Table 5 shows the main echocar-
been shown to be a clinically relevant and reliable surro- diographic studies and the parameters used to define RV
gate parameter of invasive Ees/Ea measurements56 (Fig. 2). dysfunction.
Recent studies have shown that in both C-ARDS and N-ARDS, A recent meta-analysis of RV dysfunction and mortality in
early RV-PA decoupling takes place and could be related to patients with SS found only TAPSE < 16 mm to be associated
the posterior development of ACP and patient mortality.57,58 with increased mortality.62

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Table 5 Studies on the relationship between right ventricular dysfunction and mortality in sepsis/septic shock.
Author/year Inclusion criterion N Echography Right ventricular Incidence
time dysfunction criterion
Cirulis,20 2018 Severe sepsis/septic shock 146 48 h EDD RV/LV > 0.9 55.5%
Furian,21 2012 Severe sepsis/septic shock 45 24 h RV-S′ < 12 cm/s 31.1%
Geri,22 2019 Post hoc analysis of hemosepsis 360 12 h EDA RV/LV > 0.8 22.5%
and HemoPred
Mokart,23 2007 Septic shock 45 1 day EDD RV > 30 mm + septal 37.8%
dyskinesia, visual
RV > LV + PAPs > 45 mmHg
Ordre,24 2014 Severe sepsis/septic shock 60 24 h ASE criteriaa 71.6%
Pulido,25 2012 Severe sepsis/septic shock with 71 24 h RV-S′ < 15 cm/s, RV/LV 46.5%
TTE < 24 h ratio, regional
contractility alterations,
expert opinion
Vallabhajosyula,26 Severe sepsis/septic shock with 388 72 h ASE criteriaa 55.1%
2017 TTE < 72 h
N: number of patients; EDD: end-diastolic diameter; RV: right ventricle; LV: left ventricle; S′ : tissue Doppler systolic wave; EDA:
end-diastolic area; PAPs: systolic pulmonary artery pressure; ASE: American Society of Echocardiography; TTE: transthoracic echocar-
diography.
a Criteria of the American Society of Echocardiography for the diagnosis of right ventricular dysfunction: semi-quantitative criteria

of size and function, tricuspid annular plane systolic excursion (TAPSE) < 16 mm, right ventricular S′ < 15 cm/s, and right ventricular
fractional area change < 35%.

Right ventricle ischemia Table 6 Characteristics of the right ventricle that deter-
mine its greater ischemic resistance.
The coronary circulation of the RV presents features that
distinguish it from that of the LV, with flow in systole and LESS OXYGEN CONSUMPTION, due to lesser thickness of the
diastole. The outflow tract and anterior wall are irrigated myocardial wall and contraction against a system of
by branches of the right coronary artery (RC) and anterior lesser pressure.
descending artery (AD), while the inferior wall is irrigated by INCREASED OXYGEN EXTRACTION UNDER ISCHEMIC
the posterior descending artery, and the lateral wall by the CONDITIONS, with 50% extraction under resting
RC. Up to one-third of all patients with acute myocardial conditions.
infarction (AMI) secondary to AD lesions can present asso- GREATER OXYGEN SUPPLY DURING CARDIAC CYCLE, due to
ciated RV dysfunction due to a decrease in flow from the homogeneous blood supply from the right coronary artery
branches of the AD to the anterior wall of the RV and/or during systole and diastole.
involvement of the interventricular septum.13 Right ventri- RAPID DEVELOPMENT OF COLLATERALS after occlusion of
cle AMI is usually caused by proximal occlusion of the RC, the right coronary artery, particularly from the
generally in association with AMI of the lower LV.42 Isolated moderator band artery - a branch of the anterior
necrosis of the RV occurs in < 3% of the cases, due either to descending artery.
left-side dominance or to isolated occlusion of branches of PRESERVATION OF THE INFUNDIBULUM FROM ISCHEMIA, with
the RC.63 11---30% of its perfusion being derived from an
In the absence of hypertrophy and/or PHT, the RV is independent artery with its own ostium.
less vulnerable to ischemia than the LV, conditioned by the
factors25 described in Table 6. The severity of dysfunction
depends on the location of the occlusion of the RC. Con-
sidering the aforementioned characteristics of resistance to
ischemia, spontaneous recovery from dysfunction is com- • Color Doppler identifies mechanical complications such as
mon. Thus, the term AMI of the RV includes a spectrum wall rupture, right-to-left shunting through the foramen
of conditions associated with transient ischemia, ischemic ovale, or secondary TI due to annular dilatation and/or
damage or myocardial necrosis. papillary muscle ischemia.
The following echocardiographic parameters of AMI of • S′ /RIMP. This is a new index that combines the peak of the
the RV have been described: S′ wave measured by DTI in the tricuspid annulus with the
right ventricle index of myocardial performance (RIMP),
with good sensitivity and specificity in identifying AMI of
• TAPSE <10 mm has a positive predictive value (PPV) of 75% the RV in patients presenting inferior AMI.64 Specifically,
in diagnosing AMI of the RV (Fig. 3); in the presence of S′ /RIMP < 17 is associated with RV dysfunction due to prox-
dilatation of the RV this value is not reliable, however, imal lesions of the RC in the context of inferior AMI, with
since there is an increase in the radial component. a sensitivity of 85% and a specificity of 87%.

539
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