Because of its anatomy, the RV must be examined using multiple acoustic windows, including the long parasternal axis, short parasternal axis (inflow tract and outflow tract of the RV), apical four-chamber (4C) window, the modified apical window for the RV, and the subcostal window, using transthoracic echocardiography (TTE).24,25 The report should present an evaluation based on qualitative and quantitative parameters,24 though in immediate patient life-threatening situations, there are protocols guided by qualitative parameters of great reproducibility and correlation versus other cardiac assessment techniques such as magnetic resonance imaging (MRI) and three-dimensional (3D) echocardiography,26,27 provided the exploration is performed by an expert operator.28Table 1 describes the echocardiographic parameters for the basic study of the RV.

Structural evaluation of the right ventricle

Although the plane corresponding to the short parasternal axis is the best option for evaluating ventricular interdependence, the apical 4C plane is the projection indicated for performing measurements of the size of the right atrium (RA) and the RV. Dilatation of the RV is based on the ratio between its transverse diameter or end-diastolic area (EDA) concerning the LV, measured in end-diastole. The normal ratio is RV/LV < 0.6, while 0.6–1 is indicative of moderate dilatation, and > 1 corresponds to severe dilatation.5,29,30 The quantification parameters are described in Table 2 and Fig. 3.

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 planeThickness > 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 obtainGood correlation of RVEF with MRI, FAC and ECO 2DLimitation: angle dependent
FAC (%)	> 35	Less reproducible, requires good 2D imageGood correlation with MRILimitation: quantification difficulty
S´ wave with TDI (cm/s)	> 9.5	Reproducible, easy to obtainGood correlation with ECO 2D, MRILimitation: angle dependent
TEI index	RIMP > 0.43 via PW and > 0.54 via DTI	Limitation: with PW, measurement cannot be made in one same 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 windowLimitation: requires offline software for calculationMedium quantification difficulty
RV ejection fraction in 3D (%)	> 45%	Precise measurement of volumes and EFGood correlation with MRI, with slightly lesser volumesLimitation: few studies in critical patients
Speckle-tracking		Independent of Doppler angleRequires good 2D image quality, affected by cardiac motion artifacts in planeLimitation: quantification difficultyRequires 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.

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.

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It should be mentioned that for the quantification of cardiac output (CO) and pulmonary pressures or central venous pressure (CVP), we need to place a pulmonary artery catheter or central venous catheter, respectively. However, transthoracic echocardiography (TTE) allows us to estimate these parameters on a noninvasive basis, since due to the anatomy and retrosternal position involved, a poorer analysis is afforded by transesophageal echocardiography (TEE).25 The echocardiographic parameters are shown in Fig. 4 and Table 4.

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 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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The most common cause of RV failure is PHT, defined as PAPm ≥ 25 mmHg.29 The analysis of TI allows us to estimate PHT, with VmaxTI ≤ 2.8 m/s being associated with a low probability of PHT, while VmaxTI > 3.4 m/s is associated with a high probability of PHT (Fig. 5).

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.

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Diagnosing the cause of PHT is crucial to define the appropriate treatment. In this regard, a first step is to determine whether the underlying cause is precapillary, with pulmonary capillary pressure (PCP) (wedge pressure) ≤ 15 mmHg, or postcapillary due to pathology of the LV, with PCP ≥ 15 mmHg. The echocardiographic findings suggestive of a pre- or postcapillary etiology are described in Fig. 6.29 The calculation of PVR contributes to establishing the differentiation.30

Figure 6.

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

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An invasive parameter that has been shown to be useful in differentiating between pre- and postcapillary PHT is the transpulmonary gradient, defined as the difference between PAPm and the pressure of the LA, estimated from the PCP.46 A value of > 12 mmHg is indicative of a precapillary origin. Recently, a surrogate indicator of the transpulmonary gradient has been proposed in the form of the echographic pulmonary to left atrial ratio (ePLAR) measured from the relationship between VmaxTI, as an estimate of pulmonary pressure, and the mitral E/eʹ ratio, as an estimate of the pressure of the LA. In this regard, ePLAR > 0.30 m/s would be indicative of precapillary PHT, while < 0.25 m/s would be indicative of postcapillary PHT.46

Precapillary PHT secondary to lung disease, hypoxia or pulmonary vascular occlusion is classically referred to as cor pulmonale. Depending on the evolution of the increase in RV afterload, a distinction is made between acute and chronic cor pulmonale. In this respect, acute cor pulmonale (ACP) can be secondary to ARDS or PTE, and is defined by the presence of dilatation of the RV quantified by an EDA RV/ EDA LV ratio > 0.6 accompanied by paradoxical motion of the IVS.47 The chronic form of cor pulmonale (CCP) in turn is mainly due to chronic obstructive pulmonary disease (COPD), lung fibrosis or chronic PTE. All of these conditions induce chronic hypoxemia and/or remodeling of the pulmonary circulation,48 requiring the RV to adapt in compensation because of the increase in mechanical effort involved.

Distinguishing ACP from CCP is a challenge in critical patients, and is mainly based on the clinical history and the findings of the clinical examination. It is difficult to know whether echocardiography alone can differentiate between the two conditions, and the existing evidence is scarce and sometimes contradictory.

In general, when the RV afterload experiences an acute increase, the consequences are dilatation and impaired 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 the RV can double in 48 hours after the increase in afterload, and so the above is not entirely specific.49

Several specific patterns may help in establishing a distinction, as in the case of acute PTE, where a clot in transit may be observed in the RA or RV, and even in the main trunk of the pulmonary artery. In general, the RV is unable to generate high pressure against acute increases in afterload; consequently, PAPs > 60 mmHg are more suggestive of a chronic process. The 60/60 sign and the McConnell sign, described as a relatively hyperkinetic RV vertex versus a hypokinetic or akinetic RV free wall, have a high positive predictive value (PPV) in the diagnosis of acute PTE.50

The global longitudinal strain of the LV can help distinguish between the chronic and the acute form of cor pulmonale.51,52 In the acute context, it is altered mainly due to regional impairment of the septal, apical and lateral segments, while in the chronic presentation, the global longitudinal strain of the LV is preserved, with only minimal septal involvement.

It is estimated that 21% of all patients with moderate to severe ARDS will present ACP,52 and this in turn is associated with increased mortality.53 Taking into account that pneumonia as a cause of ARDS, a driving pressure ≥ 18 cmH2O, a PaO2/FiO2 < 150 mmHg and a PaCO2 ≥ 48 mmHg have all been identified as risk factors for the development of ACP in patients with non-COVID-19 ARDS (N-ARDS), a score has been developed allowing the early identification of those patients at risk of presenting ACP and who should be subjected to echocardiographic follow-up.8,52

In patients with ARDS secondary to COVID-19 (C-ARDS), the incidence of ACP is estimated to be 18–38%.54,55 However, the published studies indicate that in COVID-19 patients, the ACP risk score lacks validity, since in the context of C-ARDS the main mechanism associated with the development of ACP is the presence of thromboembolic phenomena in the pulmonary blood vessels. Thus, the finding of ACP in C-ARDS patients is an indication for performing computed tomography to discard the presence of PTE.

In ACP, the RV, before undergoing dilatation via homeometric adaptation to the afterload, increases its contractility to preserve ventricular-atrial coupling. Although the measurement gold standard is Ees/Ea, echocardiographic assessment based on the TAPSE/PAPs ratio has been shown to be a clinically relevant and reliable surrogate parameter of invasive Ees/Ea measurements56(Fig. 2). Recent studies have shown that in both C-ARDS and N-ARDS, early RV-PA decoupling takes place and could be related to the posterior development of ACP and patient mortality.57,58

Right ventricle dysfunction affects 35% of all patients with septic shock (SS), and its underlying etiology is multifactorial, since it may be caused by an increase in preload due to excessive fluid therapy, direct myocardial involvement, or an increase in afterload secondary to hypoxemia, hypercapnia or the application of MV.

Right ventricle dysfunction is correlated to mortality, with a more than two-fold increase in mortality risk over both the short and long term.59 Such patients have lower CO and SvO2 values than patients without dysfunction, requiring higher doses of vasoactive drugs and fluid therapy.60 It should be noted that the latter may be a cause or consequence of the situation since the presence of RV dysfunction induces false-positive results in the volume response tests such as the variability of systolic (stroke) volume or pulse pressure, leading to the erroneous administration of fluid therapy and hence a positive fluid balance.61

Although there are validated cut-off points for RV dysfunction,25 their applicability is limited in patients with SS, since these parameters must be contextualized under the conditions of pre- and afterload that can be dynamically altered due to the use of vasopressors, MV and eventually ARDS. Table 5 shows the main echocardiographic studies and the parameters used to define RV dysfunction.

A recent meta-analysis of RV dysfunction and mortality in patients with SS found only TAPSE < 16 mm to be associated with increased mortality.62

The coronary circulation of the RV presents features that distinguish it from that of the LV, with flow in systole and diastole. The outflow tract and anterior wall are irrigated by branches of the right coronary artery (RC) and anterior descending artery (AD), while the inferior wall is irrigated by the posterior descending artery, and the lateral wall by the RC. Up to one-third of all patients with acute myocardial infarction (AMI) secondary to AD lesions can present associated RV dysfunction due to a decrease in flow from the branches of the AD to the anterior wall of the RV and/or involvement of the interventricular septum.13 Right ventricle AMI is usually caused by proximal occlusion of the RC, generally in association with AMI of the lower LV.42 Isolated necrosis of the RV occurs in < 3% of the cases, due either to left-side dominance or to isolated occlusion of branches of the RC.63

In the absence of hypertrophy and/or PHT, the RV is 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. Considering the aforementioned characteristics of resistance to ischemia, spontaneous recovery from dysfunction is common. Thus, the term AMI of the RV includes a spectrum of conditions associated with transient ischemia, ischemic damage or myocardial necrosis.

The following echocardiographic parameters of AMI of the RV have been described:

• •

  TAPSE <10 mm has a positive predictive value (PPV) of 75% in diagnosing AMI of the RV (Fig. 3); in the presence of dilatation of the RV this value is not reliable, however, since there is an increase in the radial component.

• •

  Color Doppler identifies mechanical complications such as wall rupture, right-to-left shunting through the foramen ovale, or secondary TI due to annular dilatation and/or papillary muscle ischemia.

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  Sʹ/RIMP. This is a new index that combines the peak of the Sʹ 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 the RV in patients presenting inferior AMI.64 Specifically, Sʹ/RIMP < 17 is associated with RV dysfunction due to proximal lesions of the RC in the context of inferior AMI, with a sensitivity of 85% and a specificity of 87%.

• •

  Strain/strain rate.65 In patients with inferior AMI, the values in basal and middle segments of the RV are lower when associated with involvement of the RV.66

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  Three-dimensional echocardiography. A RVEF < 51% using ECO-3D in patients with inferior AMI of the LV is correlated to ischemic involvement of the RV.

Involvement of the RV upon admission is associated with a poorer prognosis in patients with AMI and with increased mortality in patients with cardiogenic shock.67 Its dysfunction in patients with inferior AMI increases the number of hospital readmissions when the parameter used is TAPSE < 15 mm,63 Sʹ wave < 8 cm/s68 or longitudinal strain of the RV > 22%.69