Journal of Critical Care 29 (2014) 184.e1–184.e8

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Echocardiography in the use of noninvasive hemodynamic monitoring☆ Roy Beigel, MD, Bojan Cercek, MD, PhD, Reza Arsanjani, MD, Robert J. Siegel, MD ⁎ The Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA

a r t i c l e

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Keywords: Hemodynamics Noninvasive monitoring Echocardiography Pulmonary artery catheter

a b s t r a c t Invasive pulmonary artery catheter measurements are the standard method for assessment of hemodynamic evaluation at the present time. However, this invasive approach is associated with an increase in patient morbidity and without evidence of a reduction in mortality. Doppler echocardiography is a noninvasive method that provides robust data regarding patients' hemodynamic indices. Several parameters are available for noninvasive hemodynamic evaluation using Doppler echocardiography. Most of these measurements are easily obtained and provide a safe alternative to invasive hemodynamic assessment. As Doppler echocardiography is able to provide additional valuable information, such as cardiac systolic and diastolic function, and the presence of pericardial and pleural effusions, which can play a significant role in the patients’ hemodynamic status, using this noninvasive modality in the daily practice for hemodynamic assessment can prove an alternative to invasive measures in selected patients as well as a complementary tool for those still in need of invasive monitoring. © 2014 Elsevier Inc. All rights reserved.

Although pulmonary artery (PA) catheter measurements remain the criterion standard for hemodynamic evaluation at the present time, its routine use is controversial [1-3], as it has been associated with an increase in patient morbidity [4,5]. Echocardiography is an excellent diagnostic tool, which is readily available and can provide important information regarding several hemodynamic parameters. Various methods and parameters are available for noninvasive hemodynamic evaluation using Doppler echocardiography (Table 1). These measurements, discussed in this review, are easily obtained in most patients, providing a safe alternative to invasive assessment. 1. Central venous pressure Accurate evaluation of the central venous pressure (CVP), which is equivalent to the right atrial pressure (RAP), is an essential component in the hemodynamic assessment of patients and a requisite for the noninvasive estimation of the PA pressures (Fig. 1). 1.1. Inferior vena cava parameters The most commonly used echocardiographic method uses the inferior vena cava (IVC) size and its respiratory variation for the evaluation of RAP. The IVC is a highly compliant vessel; therefore, its size and flow dynamics vary with changes in CVP and volume. As

☆ There are no conflicts of interest to declare. ⁎ Corresponding author. The Heart Institute Cedars Sinai Medical Center 8700 Beverly Boulevard Los Angeles, CA. Tel.: +310 423 3849; fax: +310 423 8571. E-mail address: [email protected] (R.J. Siegel). 0883-9441/$ – see front matter © 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcrc.2013.09.003

shown in Fig. 1, during inspiration (which produces negative intrathoracic pressure), vena cava pressure decreases and flow increases [6,7]. At low or normal RAP, there is systolic predominance in IVC flow, such that the systolic flow is greater than the diastolic flow. As RAP increases, it is transmitted to the IVC, resulting in blunting of the forward systolic flow, reduced IVC collapse with inspiration, and eventually IVC dilatation. For RAP assessment, an IVC with a diameter less than 2.1 cm and collapse greater than 50% correlates with a normal RAP of 0 to 5 mm Hg. An IVC less than 2.1 cm with less than 50% collapse and an IVC greater than 2.1 cm with greater than 50% collapse correspond to an intermediate RAP of 5 to 10 mm Hg. An IVC greater than 2.1 cm with less than 50% collapse suggests a high RAP of 15 mm Hg [8] (Table 1). Using midrange values of 3 mm Hg for normal and 8 mm Hg for intermediate RAP is recommended. However, if there is minimal collapse of the IVC (b35%) and/or secondary indices of elevated RAP are present (such as bulging of the interatrial septum toward the left ventricle (LV), increased right atrial [RA] dimensions, other indices suggestive of elevated RAP—see next) upgrading to the higher pressure limit (ie, 5 and 10 mm Hg in case of normal and intermediate RAP, respectively) should be done. Patients should be supine during assessment of the IVC as other positions may lead to either under or overestimation of IVC diameter and/or collapsibility [9]. Patients with low compliance with deep inspiration may have a diminished IVC collapse. In these cases, a “sniff” maneuver, which causes a sudden decrease in intrathoracic pressure hence accentuating the normal inspiratory response, can differentiate those with normal IVC collapsibility from those with a diminished IVC collapsibility. The IVC can also be dilated in individuals with a normal RAP. A dilated IVC in the setting of normal RAP is commonly seen in athletes and in patients on mechanical ventilator support [10,11] as

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Table 1 Various methods used for the echocardiographic hemodynamic evaluation Method CVP/RAP IVC parameters—using subcostal imaging of the IVC

Venous flow pattern using Doppler estimation of flow in the vena cava, jugular, or hepatic veins

Tricuspid inflow using Doppler and TDI of the tricuspid annulus

SPAP Bernoulli equation with the TR maximal jet velocity (V)

Pulmonary flow acceleration time

Criteria used

Comments

IVC dimensions: enlarged N2.1 cm IVCCI: Diminished b50% CVP/RAP categorized to: • Normal RAP ~3 mm Hg (IVC b2.1 cm; IVCCI N50%) • Intermediate RAP ~8* • Elevated RAP ~N15 mm Hg (IVC N2.1 cm, IVCCI b50%) —see also comments *In cases where the IVC diameter and collapse do not fit the normal or elevated criteria, the use of additional methods might allow for better estimation. Vs N Vd – normal CVP/RAP Vs b Vd – elevated CVP/RAP (N8 mm Hg)

Most widely used method for evaluation of CVP/RAP Problematic in mechanically ventilated patients In situations of high RAP, the IVC may be fully dilated and not collapsing making estimation above a certain point difficult and unreliable

E/e' N 6: CVP/RAP N10 mm Hg

4 × V2 = ΔP; ΔP + CVP = SPAP

b100 milliseconds indicates elevated SPAP

Not applicable in cases where there is severe TR, as this alters the systolic venous flow pattern Atrial fibrillation or past cardiac surgery can cause the hepatic vein systolic flow to be diminished regardless of RAP Found to be adequate in mechanically ventilated patients where IVC parameters might not be applicable May not be an accurate method in patients who have undergone cardiac surgery Widely validated and simple method Easy to obtain in most patients Underestimation/overestimation of CVP can cause inaccuracies • Not widely studied • Validated only in patients with chronic heart failure Measurements can be affected by extremes of heart rate (60N and N100)

DPAP Bernoulli equation with the PR end diastolic jet velocity (V)

4 × V2 = ΔP; ΔP + CVP = DPAP

Not widely validated PR jet not always acquirable Underestimation/overestimation of CVP can cause inaccuracies

MPAP Bernoulli equation with the PR maximal jet velocity (V)

4 × V2 = ΔP; ΔP + CVP = MPAP

Not widely validated PR jet not always acquirable Underestimation/overestimation of CVP can cause inaccuracies Easy to obtain in most patients Underestimation/overestimation of CVP can cause inaccuracies Validated only invasively Validated using echocardiography in a single study

Tracing of the TR jet

Mean pressure gradient + CVP = MPAP

Empirical formulas

MPAP = 0.61 SPAP + 2 mm Hg MPAP = DPAP + 1/3 (SPAP-DPAP)

PVR Using empirical formulas

LA filling pressures/PCWP Mitral inflow parameters: E wave, A wave, DT, E/A ratio

PVR (WU) = 10 × TR velocity/RVOT VTI + 0.16 PVRI = 1.97 + 190 × [SPAP/(HR × RVOT VTI)] SPAP/(HR × RVOT VTI) N 0.076 correlated with severe pulmonary vascular disease with PVRI N 15 WU/m2

Not widely validated Evaluated in 1 study in patients with pulmonary hypertension

Impaired LV relaxation: E/A b 1 or E/A N 2 DT prolonged N240 milliseconds Pseudonormal: 1bE/Ab2, 160 b DT b 240 milliseconds Restrictive filling: E/A N 2, DT short b 160 milliseconds

* In young, healthy subjects some parameters can be similar as in those with disease. * Poor correlation in patients with coronary artery disease and those with hypertrophic cardiomyopathy with EF ≥ 50% é Lateral values higher than septal ones *In patients with normal LVEF (≥50) has low sensitivity and high specificity. *In patients with mitral annular calcification, severe MR, or constrictive pericarditis might not give an adequate estimate of filling pressures. *Might not be valid for patients with acute decompensated heart failure Influenced by age (D dominant in young individuals b40 years)

TDI combined with mitral inflow parameters

é, á E/é ratio b 8 – normal LV filling pressures ≥15 (for septal é) or N 12 (for lateral é) – elevated LV filling pressures

Pulmonary vein flow

S N D – normal S b D – elevated LA pressure or normal in young (b40) individuals

CO Doppler measurements using the LVOT VTI and LVOT diameter (2R)

SV = π × R2 × (LVOT VTI); CO = SV × HR

IVCCI indicates IVC collapsibility index; HR, heart rate; LVEF, LV ejection fraction; MR, mitral regurgitation.

LVOT VTI normal values: 18-20 cm; b12 cm suggestive of shock. Significant aortic regurgitation can lead to overestimation of the SV and consequently CO In the absence of pulmonic shunting the RVOT and RVOT VTI can be used as an alternate

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Fig. 1. Evaluation of the CVP/RAP. The upper images demonstrate normal CVP of 4 mm Hg. A, Subcostal image of the IVC during inspiration showing its collapse (arrow). B, This is also demonstrated in M mode showing full collapse of the IVC during inspiration (collapsibility index of 100), which is consistent with a low CVP. C, Flow in the SVC of the same patient showing that the systolic flow (S) is more dominant than the diastolic flow (D) again consistent with normal RAP. The lower images demonstrate an elevated CVP of 18 mm Hg. D, Subcostal image of the IVC, which is dilated measuring 2.3 cm, without any respiratory collapse, consistent with an elevated CVP of greater than 15 mm Hg. Tricuspid inflow velocities (E) and TDI (F) of the tricuspid annulus are also consistent with an elevated CVP as the ratio E/e’ is 13.5 (see text for more details).

well as in those with a prominent Eustachian valve or a narrowing of the IVC-RA junction. 1.2. Vena cava dynamics for the assessment of fluid responsiveness Only a limited number of studies comprising a small number of patients have evaluated the use of echocardiography in the critical care setting for evaluation of volume responsiveness, which was defined as an increase in the cardiac output (CO) following administration of 7 to 10 mL/kg of colloid solutions. Using transthoracic echocardiography in septic, mechanically ventilated patients, the IVC distensibilty index ([maximal diameter − minimal diameter]/ minimal diameter) was found to be a good predictor of response to volume expansion, as opposed to the CVP, which was a poor predictor by itself. A distensibilty index of N12% [12] to 18% [13] was a found to be a good predictor in favor of volume expansion. In addition, in septic, mechanically ventilated patients, the superior vena cava (SVC) collapsibility index ([maximal SVC diameter − minimal SVC diameter]/maximal SVC diameter) on transesophageal echocardiogram has been proposed as method for evaluation of volume status [14]. Patients with an index less than 30% were never fluid responsive, whereas patients with an index greater than 60% were consistently fluid responsive. Muller et al examined 40 nonventilated, acute circulatory failure patients and showed that an IVC distensibilty index greater than 40% was associated with fluid responsiveness, which was defined as an increase of greater than 15% of the LV outflow tract (LVOT) velocity time integral (VTI) after a bolus of 500 mL of colloid solution. Lower levels (b40%), however, did not exclude fluid responsiveness [15]. Conversely, Kumar et al found that even with direct hemodynamic measurement, neither CVP nor PA occlusion pressure appeared to be predictors of ventricular preload with respect to optimizing cardiac performance in normal volunteers [16]. 1.3. Systemic venous flow The central venous Doppler flow pattern seen in the vena cava, jugular, and hepatic veins is characterized as seen mainly by 2

generally distinct waveforms [17]. The first is the systolic wave (Vs) caused by RA relaxation and descent of the tricuspid ring associated with right ventricular (RV) systole. The second is the diastolic wave (Vd), which occurs during rapid ventricular filling when the tricuspid valve is open. When the RA pressure is low normal, there is a systolic predominant venous flow, with the velocity of Vs greater than of Vd (Fig. 1C). With elevation of the RA pressure, Vs is substantially decreased and Vs/Vd is less than 1 [18-21]. 1.4. Tricuspid valve inflow and tissue Doppler imaging Doppler and tissue Doppler imaging (TDI) provide an alternative method for RAP evaluation when subcostal views cannot be obtained and when there is inability to assess the IVC and hepatic indices. Using the pulse wave (PW) Doppler in the apical 4-chamber view, the tricuspid inflow pattern consisting of the early (E wave) and late atrial (A wave) filling of the RV can be recorded. The use of TDI allows recording of myocardial and annular velocities as well as measurement of the velocity of tissue relaxation of the lateral tricuspid annulus in diastole (e’ wave) (Fig. 1E and F). A high E velocity combined with a low e’ with an E/e' ratio of greater than 6 is predictive of an RAP greater than 10 mm Hg [22,23]. This correlation was also found to be accurate in patients on mechanical ventilation. A prior study evaluating these parameters demonstrated that the RAP correlated significantly with the E/e’: RAP = 1.62 (E/E’) − 2.13. However, it should be noted that the tricuspid valve E/e’ is less accurate in patients who have undergone prior cardiac surgery [23]. Using the 2010 American Society of Echocardiography criteria [8], which is based on IVC parameters, RAP can be categorized as low (05), normal (6-10), or elevated (11-20). A multiparameter approach using different indices may yield a more accurate estimation of RAP as the combination of these measurements assessing the dynamic changes (IVC collapsibility), flow (IVC, central veins, tricuspid inflow), and dimensions (IVC, RA) should provide the best noninvasive assessment of the RAP/CVP.

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2. Pulmonary artery hemodynamics Current echocardiography Doppler modalities allow evaluation and estimation of numerous parameters from the pulmonary vasculature: systolic PA pressure (SPAP), diastolic PA pressure (DPAP), and mean PA pressure (MPAP) as well as indirect estimation of other parameters such as pulmonary vascular resistance (PVR) (Fig. 2). 2.1. Systolic PA pressure The echocardiographic SPAP value equals the systolic pressure gradient between the PA and the RV plus the RAP (in the absence of pulmonic stenosis). This pressure gradient (ΔP) can be calculated using the simplified Bernoulli equation: ΔP = 4 × V 2, where V is the velocity of the tricuspid regurgitation (TR) jet in centimeters per second. An alternate, less widely used, method for screening patients for the presence of pulmonary hypertension is the pulmonary flow acceleration time, which is the interval between the onset of the forward flow in the PA to its peak velocity. Values of less than 100 milliseconds have been found to be highly correlated with pulmonary hypertension [24,25]. Although the Bernoulli equation has been widely validated [26,27], it can be imprecise in patients with hyperinflation and severe lung disease [28,29], possibly as a result of obscure visualization of the heart due to hyperinflation resulting in improper alignment and difficulty in obtaining a clear TR signal in a large number of patients [28]. To reduce the false-negative results, multiple imaging planes and color Doppler signals should be used for optimal alignment with the regurgitant jet. Injection of agitated saline can also enhance the Doppler flow velocity tracing and give a better signal, therefore reducing the false-negative results. Echocardiographic underestimation of the SPAP can be due to variations in Doppler angle of interrogation, underestimation of RAP, the presence of severe TR, or a poor TR signal [8,30]. Overestimation is less common and is often due to overestimation of the RAP and overestimation of the TR signal peak velocity as well as mistakenly using the tricuspid valve closing spike, due to tricuspid valve closure, for the tricuspid maximal velocity. 2.2. Diastolic PA pressure Doppler echocardiography can also estimate the DPAP[8] using the simplified Bernoulli equation, with the pulmonic regurgitation (PR) jet velocity during end diastole providing the end-diastolic PA-RV gradient. The DPAP can be estimated by adding the end-diastolic PARV gradient to the RAP [31]. Similar to SPAP, the most common errors

in DPAP estimation have been attributed to inaccurate estimation of RAP [32]. However, the PR jet is not always detected; however, again similar to TR, agitated saline can be used to enhance the Doppler signal as well. 2.3. Mean PA pressure The peak PR jet identifies the diastolic pressure gradient between the RV and the PA. Application of the Bernoulli equation to the peak PR jet velocity provides an estimation of the MPAP [32]. Furthermore, the addition of the RAP improves the accuracy of this estimate [33]. Another simple method to evaluate MPAP is by adding the RAP to the RA-RV mean systolic gradient, which can be derived from the TR profile [34]. Alternatively, several empirical formulas (Table 1) have been suggested for the estimation of the MPAP [35,36]. However, these calculations were derived from invasive studies and have not been validated by Doppler echocardiography [36]. 2.4. Pulmonary vascular resistance Using the maximal TR velocity and the RV outflow tract (RVOT) VTI correlates well with the transpulmonary pressure gradient and transpulmonary flow, respectively. Pulmonary vascular resistance can be calculated easily using the simple equation: PVR [woods units (WU)] = 10 × TR velocity/RVOT VTI + 0.16 [37]. Previously, it has been shown that, in patients with a ratio of less than 0.175, there is a low likelihood to have a PVR greater than 2 WU, practically excluding pulmonary vascular disease [37]. Although this ratio has been validated in several studies, its reliability in patients with a very high PVR (N8 WU) is poor [38]. 3. Left-sided filling pressures Invasive measurements for left-sided filling pressures include the pulmonary capillary wedge pressures (PCWPs), which reflect the left atrial (LA) pressure, which in absence of mitral stenosis reflects LV end-diastolic pressure (LVEDP), which is the pressure at the onset of the QRS complex on electrocardiogram (Fig. 3). Mitral stenosis can cause an overestimation of PCWP, whereas aortic insufficiency and a noncompliant LV result in underestimation of PCWP. Left-sided filling pressures are considered elevated when the PCWP is greater than 12 mm Hg or the LVEDP is greater than 16 mm Hg [39], with elevated filling pressures being the main physiologic consequence of diastolic dysfunction [40]. Noninvasive assessment of left-sided filling pressures (LA and LV) is done using the diastolic function parameters, which will be further discussed and are also listed in Table 1.

Fig. 2. Evaluation of PA pressure. A, Using Doppler imaging of the TR jet, a maximal velocity is obtained (268 cm/s). Using the Bernoulli equation: ΔP = 4 × v2, a maximal systolic pressure gradient (Max PG) of 29 mm Hg between the RV and atrium is calculated, which when added to the RAP estimates the SPAP (assuming lack of pulmonic stenosis). Tracing of the TR jet provides the mean pressure gradient (Mean PG) of 17, which when added to the RAP, estimates the MPAP. B, Doppler tracing of the pulmonary regurgitation jet. Using the Bernoulli equation, we can estimate the MPAP using the peak velocity (asterisk, 217 cm/s), which equals 19 mm Hg + the RAP. The PR jet also allows for the calculation of the end diastolic PA pressure by using the end-diastolic pressure gradient (arrow), which, in this case, is 2 mm Hg added to the RAP. C, Pulmonary artery acceleration time, which is the time interval between the onset of the forward flow in the PA to its peak velocity, is an additional method for evaluation of elevated PA pressure. Values of less than 100 milliseconds have been found to be highly correlated with pulmonary hypertension.

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Fig. 3. Evaluation of left heart filling pattern and estimation of LA filling pressure. A, Mitral valve inflow Doppler. Primary measurements include the early (E) and late (A) diastolic atrial filling velocities, DT (yellow line) of the E wave. B, Evaluation of left-sided filling pressures. ENA with a restrictive filling pattern (DT, 129 milliseconds). B, Tissue Doppler imaging from the lateral mitral annulus. The early diastolic velocity is expressed as é. In this patient, the E/é is elevated and equals – 133/7.2 = 18.4. C, Doppler flow in the pulmonary vein from the same patient demonstrating blunted systolic (S) flow and an S/D ratio less than 1. D, In the 4-chamber view, LA area is moderately enlarged (31.2 cm2). All of these finding are consistent with elevated left-sided filling pressures.

3.1. Mitral inflow parameters The mitral inflow velocities can be obtained in most patients using the PW Doppler in the apical 4-chamber view low velocities can be obtained. The primary measurements include the peak diastolic early filling (E wave) and the diastolic late atrial filling (A wave) velocities, the ratio between these (E/A), and the peak velocity deceleration time (DT). Normal values of the mitral inflow parameters vary with age, with the E wave velocity decreasing and the DT and A wave increasing in amplitude with age (N60 years), resulting in a decrease in the E/A ratio (b1). Heart rate and rhythm, PR interval, CO, mitral annular size, and LA function [39] can affect the mitral inflow. It is well established that the mitral E-wave velocity primarily reflects the LA-LV pressure gradient during the early stage of diastole and is thus amenable to changes in the preload and alterations in LV relaxation [39,41]. The mitral A-wave velocity reflects the LA-LV pressure gradient during the late stage of diastole, which is affected by LV compliance and the LA contractile function. The DT of the mitral E-wave is influenced by the LV relaxation, LV diastolic pressure after mitral valve opening, and the LV compliance. Alterations in the LV end-systolic and/or end-diastolic volumes, LV elastic recoil, and/or LV diastolic pressures directly affect the mitral inflow velocities (E-wave) and the time intervals (DT) [39]. The use of these parameters, especially the E/A ratio and the DT, the echocardiographic filling pattern can be classified to either normal (ENA, E/A N1 but b2, DT N 160 milliseconds), impaired LV relaxation (EbA, DT N 240 milliseconds), pseudonormal LV filling (ENA, DT N 160 milliseconds), or restrictive LV filling (ENNA, E/AN2, DTb140 milliseconds).

However, in patients with an LV ejection fraction greater than 50% [42-44], mitral inflow variables do not correlate as well with hemodynamic measurements (such as LA pressure, and LVEDP). In these patients, it is more appropriate to use TDI. 3.2. Tissue Doppler annular early and late diastolic velocities Tissue Doppler imaging measurements include both systolic (S) and diastolic velocities. The early diastolic velocities are expressed as Ea, Em, É, or é, and the late diastolic velocity as Aa, Am, Á, or á, with most commonly used terms being é and á. Tissue Doppler imaging is acquired using PW Doppler from the apical views to acquire the mitral annular velocities [45]. American Society of Echocardiography guidelines [39] recommend acquiring and measuring TDI signals from both the septal and lateral sides of the mitral valve annulus. The normal values of these parameters, like other indices of LV diastolic function, are influenced by age, with a decrease in é and an increase in á and the E/é ratio noted with increasing age [46]. The hemodynamic determinants of the é velocity include LV relaxation, preload, systolic function, and LV minimal pressure [39]. A significant association between é and LV relaxation has been shown in several studies [47,48]. Furthermore, although preload has minimal effect on é in the presence of LV impaired relaxation [49,50], it increases é in patients with normal or enhanced LV relaxation [49-52]. Consequently, in patients with cardiac disease, é velocity can be used to correct for the effect of LV relaxation on mitral E velocity, and the E/é ratio can be applied for the prediction of LV filling pressures [39]. Once acquired, it is also possible to calculate additional time intervals and ratios using a combination of TDI and mitral inflow parameters such as the E

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velocity to é ratio (E/é), which plays an important role in the estimation of LV filling pressures, especially in patients with preserved cardiac function. Although the combination of TDI and mitral inflow velocities allows for prediction of LV filling pressures, it is important to take these parameters into context of the clinical situation to make a reliable assessment (ie, age, presence of cardiovascular disease, other echocardiographic abnormalities). Furthermore, it should be kept in mind that these criteria are somewhat limited in their accuracy for LV filling pressures. The septal é is usually lower than the lateral é velocity, so the E/é ratio from the septal signal is usually higher than the lateral é. In the context of regional myocardial dysfunction, American Society of Echocardiography recommends to use the average é velocity, whereas in patients with atrial fibrillation, an average measurement from 10 cardiac cycles should be used. An E/é ratio of less than 8 (for either septal or lateral) is usually associated with normal LV filling pressures. Conversely, a ratio of greater than or equal to 15 for septal or greater than or equal to 12 for lateral é is associated with increased LV filling pressures [39]. When the value is midrange (between 8 and 15), other indices should be used to assess LV filling pressures. More recent studies have shown that, in those with normal ejection fraction, the lateral é has the best correlation with LV filling pressures and invasive parameters of LV stiffness [53,54]; however, the validity of E/e' in patients with acute decompensated heart failure E/é remains controversial [55-57]. 3.3. Pulmonary venous flow Pulmonary venous flow provides important information for the assessment of LV diastolic function and LA filling pressure. In most patients, the best Doppler recordings are obtained from the apical 4chamber view, with the pulmonary venous flow being obtainable in

approximately 90% of adult patients [58]. As shown in Fig. 3C, variables including the peak systolic velocity (S), peak anterograde diastolic velocity (D), and the S/D ratio are obtained. The “S” wave is primarily influenced by changes in the LA pressure, contraction, and relaxation and by the stroke volume (SV) and pulsewave propagation in the PA vasculature tree [59,60]. The “D” wave is influenced by the same factors that influence the mitral E velocity [61]. With an increase in LA pressure, there is a decrease in “S” and increase in “D” velocities resulting in an S/D ratio of less than 1. Normal values of pulmonary venous inflow are strongly related to age. In young normal subjects, there is usually prominent D velocity, reflecting their mitral E wave; however, this gradually declines (age N40 years) with age resulting in an increase in the S/D ratio. 3.4. Left atrial dimensions Chronic elevation of left-sided filling pressures leads to LA enlargement. There is a significant association between LA dimensions and elevated left-sided filling pressures; hence, evaluation of LA dimensions is an important adjunct to the echocardiographic evaluation of the left-sided filling pressures [62]. Left atrial measurements are usually obtained most accurately from the apical views [63]. However, it should be noted that LA enlargement is not a specific sign for elevated filling pressures, as it can accompany other situations where the left-sided filling pressures are not elevated and diastolic dysfunction is not present, such as in trained athletes, patients with chronic atrial fibrillation or flutter, bradycardia, high output states, and certain mitral valvular diseases. In these cases, mitral inflow pattern, pulmonary vein flow, and TDI can serve as useful tools for evaluation and estimation of left-sided filling pressures. Unlike patients with impaired myocardial function where the primary tool for evaluation of left-sided filling pressures is based on the E/A ratio and DT, these estimations can be more challenging in those with

Fig. 4. Calculation of the SV and CO. A, Using Doppler, the LVOT VTI is measured (18.3 cm) and when multiplied by the cross-sectional area through which the stroke distance moves provides the SV. B, The LVOT diameter is 1.9 cm, and the cross-sectional area is πx (1.9/2)2 = 2.83. The SV is thus 52 mL, and the CO equals the SV times heart rate, which in this case is 5.4 L/min. C and D, In the absence of pulmonic shunting, the pulmonic outflow tract can be used instead of the LVOT using the similar principles.

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normal LV function, who should be primarily assessed using the E/é ratio, preferably with the use of other parameters. It has previously been shown that using a simplified approach of 3 echocardiographic parameters provides an accurate and practical approach for the routine estimation of the elevated left-sided filling pressures [62]. 4. Cardiac output It is possible to measure the stroke distance using Doppler imaging, which refers to the distance traveled by a column of blood during a fixed time (the cardiac cycle) (Fig. 4). Multiplying the stroke distance with the cross sectional area through which the column moves gives the SV. This can be obtained at several sites, with the most common and accurate being the LVOT [64,65]. It is necessary that Doppler velocities be obtained parallel to the direction of flow as well as obtaining the cross-sectional area through which the flow is occurring. The SV = π × R 2 × (LVOT VTI), where R is the radius of the LVOT measured in midsystole using the parasternal long-axis view. The CO is defined as SV times the heart rate. Based on the fact that the LVOT diameter is subject to variability (as it is not a truly circular structure but rather ellipsoid in nature) as well as significant source of error especially because this value is squared, the LVOT VTI is the most important parameter in evaluation of SV. Normal values of the LVOT VTI are within the range of 18 to 20 cm with values of less than 12 cm suggestive of shock. Significant aortic regurgitation will lead to overestimation of the SV and, consequently, the CO. Assuming there is no pulmonic shunting and able to be visualized, the pulmonic outflow tract can be used for assessment of SV instead of the LVOT [66]. 5. Conclusions Prior studies have assessed the use of Doppler echocardiography for hemodynamic monitoring, mainly in the heart failure population [67,68]. These have shown a good correlation between measurements obtained noninvasively by Doppler echocardiography and invasively using the PA catheter, therefore demonstrating that hemodynamic monitoring can be adequately achieved noninvasively. However, taking into account the spectrum of data available, the limits of agreement are less robust indicating that noninvasive measurements are generally reflective of the hemodynamic values but precision for an individual measurement may be suboptimal. As Doppler echocardiography is able to provide additional valuable information, such as cardiac function and the presence of pericardial and pleural effusions, which can play a significant role in the patients' hemodynamic status, using this noninvasive modality in the daily practice for hemodynamic assessment can prove an alternative to invasive measures in selected patients as well as a complementary tool for those still in need of invasive monitoring. Acknowledgments Dr Beigel is a recipient of a fellowship grant from the American Physicians' Fellowship for Medicine in Israel. References [1] Gore JM, Goldberg RJ, Spodick DH, Alpert JS, Dalen JE. A community-wide assessment of the use of pulmonary artery catheters in patients with acute myocardial infarction. Chest 1987;92:721–7. [2] Harvey S, Harrison DA, Singer M, et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet 2005;366:472–7. [3] Ivanov RI, Allen J, Sandham JD, Calvin JE. Pulmonary artery catheterization: a narrative and systematic critique of randomized controlled trials and recommendations for the future. New Horiz 1997;5:268–76.

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[4] Connors Jr AF, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996;276:889–97. [5] Shah MR, Hasselblad V, Stevenson LW, et al. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA 2005;294:1664–70. [6] Wexler L, Bergel DH, Gabe IT, Makin GS, Mills CJ. Velocity of blood flow in normal human venae cavae. Circ Res 1968;23:349–59. [7] Gabe IT, Gault JH, Ross Jr J, et al. Measurement of instantaneous blood flow velocity and pressure in conscious man with a catheter-tip velocity probe. Circulation 1969;40:603–14. [8] Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr 2010;23:685–713 quiz 786–788. [9] Nakao S, Come PC, McKay RG, Ransil BJ. Effects of positional changes on inferior vena caval size and dynamics and correlations with right-sided cardiac pressure. Am J Cardiol 1987;59:125–32. [10] Jue J, Chung W, Schiller NB. Does inferior vena cava size predict right atrial pressures in patients receiving mechanical ventilation? J Am Soc Echocardiogr 1992;5:613–9. [11] Goldhammer E, Mesnick N, Abinader EG, Sagiv M. Dilated inferior vena cava: a common echocardiographic finding in highly trained elite athletes. J Am Soc Echocardiogr 1999;12:988–93. [12] Feissel M, Michard F, Faller J-P, Teboul J-L. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care Med 2004;30:1834–7. [13] Barbier C, Loubières Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med 2004;30:1740–6. [14] Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med 2004;30: 1734–9. [15] Muller L, Bobbia X, Toumi M, et al. Respiratory variations of inferior vena cava diameter to predict fluid responsiveness in spontaneously breathing patients with acute circulatory failure: need for a cautious use. Crit Care 2012;16:R188. [16] Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med 2004;32:691–9. [17] Reynolds T, Appleton CP. Doppler flow velocity patterns of the superior vena cava, inferior vena cava, hepatic vein, coronary sinus, and atrial septal defect: a guide for the echocardiographer. J Am Soc Echocardiogr 1991;4:503–12. [18] Sivaciyan V, Ranganathan N. Transcutaneous doppler jugular venous flow velocity recording. Circulation 1978;57:930–9. [19] Appleton CP, Hatle LK, Popp RL. Superior vena cava and hepatic vein Doppler echocardiography in healthy adults. J Am Coll Cardiol 1987;10:1032–9. [20] Appleton CP, Hatle LK, Popp RL. Demonstration of restrictive ventricular physiology by Doppler echocardiography. J Am Coll Cardiol 1988;11:757–68. [21] Ghio S, Recusani F, Sebastiani R, et al. Doppler velocimetry in superior vena cava provides useful information on the right circulatory function in patients with congestive heart failure. Echocardiography 2001;18:469–77. [22] Nageh MF, Kopelen HA, Zoghbi WA, Quiñones MA, Nagueh SF. Estimation of mean right atrial pressure using tissue Doppler imaging. Am. J. Cardiol. 1999;84:1448– 1451, A8. [23] Elif Sade L, Gulmez O, Eroglu S, Sezgin A, Muderrisoglu H. Noninvasive estimation of right ventricular filling pressure by ratio of early tricuspid inflow to annular diastolic velocity in patients with and without recent cardiac surgery. J Am Soc Echocardiogr 2007;20:982–8. [24] Lanzarini L, Fontana A, Campana C, Klersy C. Two simple echo-Doppler measurements can accurately identify pulmonary hypertension in the large majority of patients with chronic heart failure. J Heart Lung Transplant 2005;24:745–54. [25] Dabestani A, Mahan G, Gardin JM, et al. Evaluation of pulmonary artery pressure and resistance by pulsed Doppler echocardiography. Am J Cardiol 1987;59:662–8. [26] Currie PJ, Seward JB, Chan KL, et al. Continuous wave Doppler determination of right ventricular pressure: a simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750–6. [27] Berger M, Haimowitz A, Van Tosh A, Berdoff RL, Goldberg E. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound. J Am Coll Cardiol 1985;6:359–65. [28] Fisher MR, Criner GJ, Fishman AP, et al. Estimating pulmonary artery pressures by echocardiography in patients with emphysema. Eur Respir J 2007;30:914–21. [29] Arcasoy SM, Christie JD, Ferrari VA, et al. Echocardiographic assessment of pulmonary hypertension in patients with advanced lung disease. Am J Respir Crit Care Med 2003;167:735–40. [30] Horton KD, Meece RW, Hill JC. Assessment of the right ventricle by echocardiography: a primer for cardiac sonographers. J Am Soc Echocardiogr 2009;22:776–92 quiz 861–2. [31] Lee RT, Lord CP, Plappert T, Sutton MS. Prospective Doppler echocardiographic evaluation of pulmonary artery diastolic pressure in the medical intensive care unit. Am J Cardiol 1989;64:1366–70. [32] Masuyama T, Kodama K, Kitabatake A, Sato H, Nanto S, Inoue M. Continuous-wave Doppler echocardiographic detection of pulmonary regurgitation and its application to noninvasive estimation of pulmonary artery pressure. Circulation 1986;74: 484–92. [33] Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. Echocardiographic determination of mean pulmonary artery pressure. Am J Cardiol 2003;92:1373–6.

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R. Beigel et al. / Journal of Critical Care 29 (2014) 184.e1–184.e8

[34] Aduen JF, Castello R, Lozano MM, et al. An alternative echocardiographic method to estimate mean pulmonary artery pressure: diagnostic and clinical implications. J Am Soc Echocardiogr 2009;22:814–9. [35] Dini FL, Traversi E, Franchini M, Micheli G, Cobelli F, Pozzoli M. Contrast-enhanced Doppler hemodynamics for noninvasive assessment of patients with chronic heart failure and left ventricular systolic dysfunction. J Am Soc Echocardiogr 2003;16:124–31. [36] Chemla D, Castelain V, Humbert M, et al. New formula for predicting mean pulmonary artery pressure using systolic pulmonary artery pressure. Chest 2004;126:1313–7. [37] Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol 2003;41:1021–7. [38] Rajagopalan N, Simon MA, Suffoletto MS, et al. Noninvasive estimation of pulmonary vascular resistance in pulmonary hypertension. Echocardiography 2009;26:489–94. [39] Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr 2009;22:107–33. [40] Brutsaert DL, Sys SU, Gillebert TC. Diastolic failure: pathophysiology and therapeutic implications. J Am Coll Cardiol 1993;22:318–25. [41] Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988;12:426–40. [42] Nishimura RA, Appleton CP, Redfield MM, Ilstrup DM, Holmes Jr DR, Tajik AJ. Noninvasive Doppler echocardiographic evaluation of left ventricular filling pressures in patients with cardiomyopathies: a simultaneous Doppler echocardiographic and cardiac catheterization study. J Am Coll Cardiol 1996;28:1226–33. [43] Yamamoto K, Nishimura RA, Chaliki HP, Appleton CP, Holmes Jr DR, Redfield MM. Determination of left ventricular filling pressure by Doppler echocardiography in patients with coronary artery disease: critical role of left ventricular systolic function. J Am Coll Cardiol 1997;30:1819–26. [44] Nagueh SF, Lakkis NM, Middleton KJ, Spencer 3rd WH, Zoghbi WA, Quiñones MA. Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy. Circulation 1999;99:254–61. [45] Waggoner AD, Bierig SM. Tissue Doppler imaging: a useful echocardiographic method for the cardiac sonographer to assess systolic and diastolic ventricular function. J Am Soc Echocardiogr 2001;14:1143–52. [46] De Sutter J, De Backer J, Van de Veire N, Velghe A, De Buyzere M, Gillebert TC. Effects of age, gender, and left ventricular mass on septal mitral annulus velocity (E’) and the ratio of transmitral early peak velocity to E’ (E/E’). Am J Cardiol 2005;95:1020–3. [47] Sohn DW, Chai IH, Lee DJ, et al. Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol 1997;30:474–80. [48] Ommen SR, Nishimura RA, Appleton CP, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneous Doppler-catheterization study. Circulation 2000;102:1788–94. [49] Nagueh SF, Sun H, Kopelen HA, Middleton KJ, Khoury DS. Hemodynamic determinants of the mitral annulus diastolic velocities by tissue Doppler. J Am Coll Cardiol 2001;37:278–85. [50] Hasegawa H, Little WC, Ohno M, et al. Diastolic mitral annular velocity during the development of heart failure. J Am Coll Cardiol 2003;41:1590–7. [51] Firstenberg MS, Levine BD, Garcia MJ, et al. Relationship of echocardiographic indices to pulmonary capillary wedge pressures in healthy volunteers. J Am Coll Cardiol 2000;36:1664–9.

[52] Caiani EG, Weinert L, Takeuchi M, et al. Evaluation of alterations on mitral annulus velocities, strain, and strain rates due to abrupt changes in preload elicited by parabolic flight. J Appl Physiol 2007;103:80–7. [53] Rivas-Gotz C, Manolios M, Thohan V, Nagueh SF. Impact of left ventricular ejection fraction on estimation of left ventricular filling pressures using tissue Doppler and flow propagation velocity. Am J Cardiol 2003;91:780–4. [54] Kasner M, Westermann D, Steendijk P, et al. Utility of Doppler echocardiography and tissue Doppler imaging in the estimation of diastolic function in heart failure with normal ejection fraction: a comparative Doppler-conductance catheterization study. Circulation 2007;116:637–47. [55] Mullens W, Borowski AG, Curtin RJ, Thomas JD, Tang WHW. Tissue Doppler imaging in the estimation of intracardiac filling pressure in decompensated patients with advanced systolic heart failure. Circulation 2009;119:62–70. [56] Nagueh SF. Letter by Nagueh et al regarding article, “Tissue Doppler imaging in the estimation of intracardiac filling pressure in decompensated patients with advanced systolic heart failure”. Circulation 2009;120:e44. [57] Galderisi M, Esposito R. Letter by Galderisi and Esposito regarding article, “Tissue Doppler imaging in the estimation of intracardiac filling pressure in decompensated patients with advanced systolic heart failure”. Circulation 2009;120: e46. [58] Jensen JL, Williams FE, Beilby BJ, et al. Feasibility of obtaining pulmonary venous flow velocity in cardiac patients using transthoracic pulsed wave Doppler technique. J Am Soc Echocardiogr 1997;10:60–6. [59] Appleton CP. Hemodynamic determinants of Doppler pulmonary venous flow velocity components: new insights from studies in lightly sedated normal dogs. J Am Coll Cardiol 1997;30:1562–74. [60] Smiseth OA, Thompson CR, Lohavanichbutr K, et al. The pulmonary venous systolic flow pulse—its origin and relationship to left atrial pressure. J Am Coll Cardiol 1999;34:802–9. [61] Nishimura RA, Abel MD, Hatle LK, Tajik AJ. Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography. Effect of different loading conditions. Circulation 1990;81:1488–97. [62] Rafique AM, Phan A, Tehrani F, Biner S, Siegel RJ. Transthoracic echocardiographic parameters in the estimation of pulmonary capillary wedge pressure in patients with present or previous heart failure. Am J Cardiol 2012;110:689–94. [63] Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:1440–63. [64] Lewis JF, Kuo LC, Nelson JG, Limacher MC, Quinones MA. Pulsed Doppler echocardiographic determination of stroke volume and cardiac output: clinical validation of two new methods using the apical window. Circulation 1984;70: 425–31. [65] Dubin J, Wallerson DC, Cody RJ, Devereux RB. Comparative accuracy of Doppler echocardiographic methods for clinical stroke volume determination. Am Heart J 1990;120:116–23. [66] Kirkpatrick JN, Lang RM. Heart failure: hemodynamic assessment using echocardiography. Curr Cardiol Rep 2008;10:240–6. [67] Stein JH, Neumann A, Preston LM, et al. Echocardiography for hemodynamic assessment of patients with advanced heart failure and potential heart transplant recipients. J Am Coll Cardiol 1997;30:1765–72. [68] Temporelli PL, Scapellato F, Eleuteri E, Imparato A, Giannuzzi P. Doppler echocardiography in advanced systolic heart failure: a noninvasive alternative to Swan-Ganz catheter. Circ Heart Fail 2010;3:387–94.