(Chest. 2005;128:3652-3663.)
© 2005
American College of Chest Physicians
Transesophageal Echocardiographic Evaluation of Diastolic Function*
Leanne Groban, MD and
Sylvia Y. Dolinski, MD, FCCP
* From the Department of Anesthesiology (Dr. Groban), Wake Forest University School of Medicine, Winston-Salem, NC; and the Medical College of Wisconsin (Dr. Dolinski), Milwaukee, WI.
Correspondence to: Leanne Groban, MD, Department of Anesthesiology, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1009; e-mail: lgroban{at}wfubmc.edu
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Abstract
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Diastolic dysfunction is increasingly recognized as a cause of hemodynamic instability in the perioperative setting. Difficulty weaning from cardiopulmonary bypass and an increased need for inotropic support can occur in the absence of systolic impairment. Diastolic dysfunction can also impede hemodynamic stabilization and weaning progress in the mechanically ventilated critically ill patient. The use of transesophageal echocardiography in the ICU can assist in diagnosing the presence and progression of diastolic impairment, which may help to target therapeutic interventions that lead to positive outcomes. This review summarizes the conventional and new echocardiographic modalities for evaluating diastolic function in the perioperative setting.
Key Words: diastolic function • echocardiography • heart failure • tissue Doppler
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Introduction
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Transesophageal echocardiography (TEE) is a useful technological advance in the assessment and management of the critically ill patient, particularly if cardiac or thoracic surgery is needed. This imaging modality can lead to rapid diagnoses and therapeutic interventions in patients suspected of having acute pulmonary vascular disease or cardiac causes of hemodynamic instability, such as acute coronary syndromes, infective endocarditis, and pericardial disease.12 Although commonly performed by sonographers (during transthoracic studies) and interpreted by cardiologists, Doppler echocardiographic evaluation of diastolic function can also be an important clinical tool in the armamentarium of the intensivist. The combination of mitral inflow velocity curves and tissue Doppler imaging (TDI) of the mitral annulus can be used to assess the severity of diastolic dysfunction as well as to estimate left ventricular (LV) compliance and filling pressures when a pulmonary artery catheter is not readily available.34 Additionally, in ICU patients, Doppler evaluation of diastolic function has been shown to be more accurate than B-type natriuretic peptide measurement for detecting pulmonary capillary wedge pressures of > 15 mm Hg.5 Doppler indexes of diastolic function can be used to predict mortality in patients with or without systolic impairment as well.6 Thus, in the setting of diastolic dysfunction, TEE can guide the ICU management of hemodynamic instability and vasoactive drug titration, can detect myocardial ischemia, and can aid the clinician in predicting prognosis.
Transthoracic imaging is often unsuccessful in the critically ill patient because of mechanical ventilation with high positive end-expiratory pressure (PEEP) [ie, > 15 cm H2O] or inaccessible imaging "windows" due to the presence of drains or dressings, or the inability to optimally position the patient.78 We advocate the use of examinations by TEE rather than by transthoracic echocardiography at the inception of hemodynamic instability. We recognize that when TEE is not available, two-dimensional transthoracic echocardiography image quality can be enhanced with the aid of a contrast injection9 or by the use of tissue harmonic imaging.10 The Society of Cardiovascular Anesthesiologists and the American College of Cardiologists recommend11 that at least 150 supervised examinations are necessary before a clinician is qualified to interpret independently comprehensive examination findings. The training of intensivists to perform a limited examination to evaluate LV function and volume status can be accomplished with didactic teaching and with a smaller number of supervised examinations. The exact number of such supervised examinations is likely learner- dependent.
Doppler echocardiographic evaluation of diastolic function also provides useful information that can guide the management of patients with known cardiac disease undergoing cardiac and noncardiac surgery. In cardiac surgical patients, diastolic dysfunction has been associated with difficult weaning from cardiopulmonary bypass, an increased need for inotropic drug support, and more frequent postoperative hemodynamic instability.1213 Many elderly patients (with or without cardiac disease) have diastolic dysfunction, and, if ignored, it may promote hemodynamic instability and make for more difficulty in weaning from mechanical ventilation.1415 This review presents examples, techniques, and strategies by which to assess left-ventricular diastolic function in patients with critical illnesses in the perioperative setting. To promote understanding of the clinical significance and interpretation of TEE measures of diastolic function, the phases of diastole, the determinants of diastolic function, and the mechanisms of diastolic dysfunction will be reviewed.
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Basic Physiology
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The physiology of diastole can be divided into cellular events and mechanical events. At the cellular level, diastole begins when adenosine triphosphate hydrolyzes and actin-myosin crossbridges unlink, leading to sarcomeric relaxation. This is related to decreases in cytoplasmic Ca2+ and the subsequent dissociation of Ca2+ from troponin.16 The majority of cytosolic Ca2+ is actively resequestered into the sarcoplasmic reticulum via the sarcoplasmic reticulum Ca2+-ATPase (SERCA2). The remaining cytosolic calcium is removed by the sarcolemmal sodium-calcium exchanger and other mechanisms.16
Phases of Diastole
At the mechanical level, diastole can be divided into the following four phases: (1) isovolumic relaxation; (2) rapid early filling; (3) slow filling (diastasis); and (4) atrial contraction (Fig 1 ). The isovolumic relaxation phase begins with aortic valve closure when the pressure within the LV begins to fall. The LV pressure will continue to fall even after the opening of the mitral valve. In fact, the LV pressure falls below the left atrial pressure (LAP) as a result of elastic recoil, creating a suction-like effect. Rapid filling of the LV occurs during this phase (Table 1
). Normally, LV relaxation ends in the first third of rapid filling so that the rest of the LV filling is dependent on such properties as LV compliance, ventricular interaction, and pericardial constraint. Finally, atrial systole contributes about 20% to the final LV volume.16
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Figure 1.. Electrical, pressure, flow (Doppler), TDI, and volume events during systole and diastole. IVR = isovolumic relaxation; MVVC = mitral valve closed; AVO = aortic valve open; AVC = aortic valve closed; MVO = mitral valve open. The figure was modified from Jaski.44
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Table 1.. Phases of Diastole, the Corresponding Physiologic Determinants, and the ECG and Echocardiographic Correlates*
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Mechanisms of Diastolic Dysfunction
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The evolution of diastolic dysfunction is complex. The pathophysiology is contingent on factors that are intrinsic and extrinsic to the myocardium that ultimately have an effect on one or more of the determinants of diastolic function (Table 2
).
Myocardial relaxation is an active process influencing the isovolumic relaxation phase and part of the early filling phase. Factors affecting myocardial relaxation include internal loading forces or the elastic recoil of the myocardium, which creates a "suction" or enhanced filling effect after systole; external loading forces, such as increased arterial impedance, which can impair relaxation; intracellular calcium overload (eg, ischemia), which can delay or prolong myocardial relaxation such that it impinges on the early filling phase of diastole; and nonuniformity or asynchrony between contraction and relaxation events (eg, intraventricular conduction defect [left bundle branch block]), resulting in the dissipation of myocardial energy, ultimately impairing ventricular relaxation.1718
Ventricular compliance is a passive process that influences all three filling phases of diastole.19 The intrinsic components that alter ventricular compliance include myocardial stiffness, resulting from diffuse fibrosis and/or infiltrative diseases, and chamber stiffness, resulting from increases in chamber size and/or thickness.1820 For instance, a dilated LV with impaired systolic function leads to higher end-systolic volumes, shifting the filling curve rightward. Diastolic filling occurs at a greater increase in pressure for a given increase in volume. The extrinsic factors that have a role in reducing ventricular compliance include the structures that surround the heart (ie, the pericardium, the right ventricle [RV], and the lungs).
The pulmonary veins (PVs), left atrium (LA), and mitral valve also play a role in diastolic function. The LA and PVs are the source for LV filling, thereby influencing all three filling phases. An increased pressure gradient between the LA and LV (eg, increased preload) enhances early diastolic filling. In contradistinction, reductions in preload (eg, provoked by nitroglycerin, Valsalva maneuver, or reverse trendelenburg position) attenuate early LV filling. Positive-pressure ventilation and increasing PEEP (eg, 5 to 20 cm H2O) can also lead to reductions in the rate of LV diastolic filling and LV compliance,2122 particularly in the hypovolemic patient. Likewise, LV filling can influence LAP. For example, a delay in relaxation may inhibit early filling, and this, in turn, leads to an increase in LAP. This increased LAP will help to return the early filling to normal (ie, the echo pattern is "pseudonormal" on transmitral pulsed Doppler). During diastasis, the LA and LV pressures are nearly equal. LV filling during this phase is determined by the rate of pulmonary venous return, which is a function of LV systolic function. During systole, the base of the heart stretches downward, resulting in a decrease in LAP and an acceleration of pulmonary venous return. Atrial systole has a major role in the late phase of diastolic filling. In the presence of a noncompliant LV, the atrium serves as a "booster" pump to compensate for a reduction in early diastolic filling.23 The importance of atrial contraction to LV filling is clearly demonstrated with advanced age. In young adults, LV relaxation is rapid, and there is an early diastolic suction effect that results in nearly 95% of filling during the early phase. By middle age, LV relaxation is slowed, early LV filling decreases, and the contribution of atrial contraction increases to about 30%. By age 65 years, further impairment of relaxation has occurred, and about 50% of flow may occur during atrial systole.24 Accordingly, the aggressive treatment of atrial fibrillation in the elderly reestablishes the late filling phase, and has a beneficial impact on stroke volume and cardiac output.25 Mitral valve abnormalities do not usually alter LV filling except in the presence of mitral stenosis. With mitral stenosis, the LV does not adequately fill during rapid, early filling or during diastasis (LA and LV pressures never equilibrate), thus is the reason for the chronically underfilled LV characteristic of mitral stenosis.
Heart rate (HR), an additional determinant of diastolic function, influences myocardial relaxation and all phases of LV filling. In the presence of bradycardia (ie, a HR of 
60 beats/min), most of the LV filling occurs before atrial contraction. In contrast, in the presence of tachycardia (ie, HR of 
90 beats/min), early filling is truncated and there is no diastasis phase. In this circumstance, atrial systole has an important role in maintaining cardiac output.
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Transesophageal Echocardiographic Evaluation of Diastolic Performance
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In conjunction with the anatomic and functional information provided by two-dimensional echocardiography (eg, systolic function or wall thickness) and color-flow Doppler imaging (eg, valvular regurgitant lesions), diastolic performance can be easily assessed perioperatively using conventional pulsed Doppler imaging of mitral inflow in combination with pulsed Doppler imaging of PV flow. Pulsed TDI can add to the diagnosis by its assessment of myocardial wall motion dynamics during diastole.3526 The physical principals, instrumentation, interpretation, and limitations of each methodology will be briefly discussed.
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Spectral Pulsed Doppler Imaging of Transmitral Flow and Pulmonary Venous Flow
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Mitral Inflow
The physical principles of conventional pulsed Doppler imaging focus on the low-intensity and high-velocity echoes of blood flow. The pulsed wave Doppler (PWD) imaging system uses short bursts of ultrasound energy that are transmitted and then recorded as the bursts are reflected from the target (namely, RBCs) and returned to the transducer. Given that the velocity of an ultrasound signal is constant in tissue at 1,540 m/s, the depth of penetration of the returning signal is known. The Doppler frequency shift resulting from the moving RBC is used to ascertain the direction and velocity of blood flow within the cardiovascular system. The Doppler equation depicted below is used to quantitate blood flow velocity. - V =
F/cos
x c/2FT
- F = Doppler frequency shift
- FT = transmitted frequency
- cos = angle of incidence between Doppler beam path and the scatter path (blood flow)
- c = velocity of sound in tissue (1540 m/s)
where F is Doppler frequency shift, FT is transmitted frequency, cos is the angle of incidence between the Doppler beam path and the scatter path (blood flow), and c is the velocity of sound in tissue (1,540 m/s).
When the angle of incidence is < 20° (cos > 0.94) the effects of the angle are usually minimal and can be ignored. When the angle of incidence exceeds 20°, blood flow velocity is underestimated. No Doppler frequency shift occurs when the angle approaches 90°.
With the imaging plane at the midesophageal four-chamber view, a sample volume of 2 to 5 mm is placed at the level of the open leaflets in diastole (Fig 2
, top, A). Color flow Doppler imaging can be used to help align the sample beam parallel to flow and to locate the point of maximal velocity. (A secondary control panel on most sector scanners allows the sonographer to adjust the sample angle to optimize parallel alignment.) The biphasic flow pattern is away from the probe and, thus, is displayed below the baseline. For optimal time measurements, the sweep speed is set at 50 to 100 mm/s.
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Figure 2.. Top, A: schematic of the midesophageal four-chamber view with PWD imaging sample volume at the level of the tips of the open mitral valve leaflets. The dotted line represents the Doppler beam. The insert at the upper right represents the sector scan angle (0 to 5°) of the phased-array transducer. Bottom, B: transmitral blood flow velocity profile obtained with PWD imaging at the midesophageal four-chamber view. The E wave represents early, rapid LV filling. The A wave represents late filling as a result of atrial systole. RA = right atrium.
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The primary limitation to PWD imaging is that it relies on the intermittent sampling of blood flow. That is, after pausing to receive the returning signal, the pulsed wave system emits another pulse. The rate of pulse emission is termed the pulse repetition frequency. The maximal blood flow velocity that can be quantified is restricted to half the pulse repetition frequency. When blood flow velocity exceeds this measuring limit, termed the Nyquist limit, the returning signal becomes distorted, making the velocity profile ambiguous. The distorted image signal wraps around the baseline, which is known as aliasing. Typically, aliasing begins to occur at a velocity of about 2 m/s.27
Clinically useful mitral inflow parameters include the following: early filling peak velocity (E); atrial peak velocity (A); E/A ratio; and deceleration time (DT) or the interval between the peak of the E wave to the zero baseline (reflects the mean LAP and LV compliance) [Fig 2, bottom, B]. The isovolumic relaxation time (IVRT), which is the period from the end of aortic systolic flow to the start of mitral inflow, can be measured (although with some difficulty) using continuous wave Doppler imaging between the aortic and mitral valves in the deep transgastric long-axis view (five-chamber view) or the transgastric long-axis two-chamber view rotating to 120°. The IVRT measurement is estimated from the cessation of the aortic flow and the onset of transmitral inflow. (To measure IVRT accurately, however, a simultaneous ECG and phonocardiogram are necessary to determine the timing of the aortic valve closing sound.)23
PV Flow
The open conduit of flow from the PVs into the LA (Fig 1) provides additional information with respect to diastolic function. The left upper PV is best suited for Doppler interrogation, as it lies nearly parallel to the ultrasound beam. Rotating the omni-probe from 0° and 90° in the midesophageal four-chamber view, the left upper PV can be visualized just lateral to the LA appendage. Color flow Doppler imaging is recommended to confirm its location and the presence of laminar flow. The sample volume is placed centrally, 1 to 2 cm from the vein orifice (Fig 3
, top, A).
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Figure 3.. Top, A: schematic of midesophageal two-chamber view at 90° with left upper PV visualized lateral to the LA appendage. Dotted line represents the PWD beam with the sample volume placed centrally, 1 to 2 cm from the vein orifice. The insert at the upper right represents the sector scan angle ranging between 60° and 90° for left upper pulmonary vein (LUPV) location. Bottom, B: pulmonary venous blood flow velocity profile obtained with PWD imaging at midesophageal level at 90°. PV systolic flow (S) represents LA relaxation, and the reduction in LAP at the base of the heart descends during systole. PV diastolic flow (D) represents the fall in atrial pressure as the ventricle fills in early diastole. The late diastolic retrograde velocity (AR) flow is due to atrial contraction. LAA = left atrial appendage.
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The PV systolic flow represents flow into the LA during ventricular systole. In the absence of mitral regurgitation (MR), the flow is toward the probe and the spectral display is above the baseline. The PV systolic component may appear to be biphasic. PVS1 represents LA relaxation and the reduction in LAP as the base of the heart descends during the early phase of ventricular systole. PVS2, the later systolic peak, reflects the RV stroke volume and atrial compliance. The antegrade PV diastolic wave represents the fall in atrial pressure as the ventricle fills in early diastole, thus maintaining forward flow from the PVs into the LA. The small retrograde flow during late diastole (which is away from the probe and toward the PV) is due to atrial contraction. It is referred to as PV atrial flow reversal (PVAR) [displayed below the baseline] (Fig 3, bottom, B).
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Pulsed Doppler Patterns of Diastolic Filling
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The four basic transmitral inflow patterns present a parabolic distribution with respect to the E/A ratio. That is, as the disease progresses from normal to severe diastolic dysfunction, the E-A relationship changes as follows: normal, E > A; abnormal filling relaxation, E < A; pseudonormal filling, E > A; and restrictive filling, E >> A.
A mitral inflow pattern of abnormal relaxation (E < A; prolonged IVRT; prolonged DT) commonly is associated with coronary artery disease, ischemic cardiomyopathy, hypertension, LV hypertrophy, and aging. Alterations in loading conditions (eg, reduced preload or increased afterload) can also change a normal filling pattern to an abnormal one (E < A) [Fig 4, 5
].2328
As relaxation becomes further delayed, it impinges on the early filling phase, resulting in an increase in LAP. This increased LAP causes the filling pattern to appear normal as the E/A ratio becomes > 1. This transition zone between abnormal relaxation and restrictive filling is termed pseudonormalization, and it is characterized by abnormal diastolic filling values. In order to differentiate between normal and "pseudonormal," evaluation of the transmitral flow at peak performance of a Valsalva maneuver (or any maneuver that reduces preload such as reverse Trendelenburg position, increasing PEEP [eg, 10 to 20 cm H2O], or nitroglycerin) and/or the evaluation of PV flow is advocated (Fig 6
). Likewise, findings from pulsed TDI can assist with the differentiation (vide infra). If the pseudonormal pattern is due to abnormal relaxation with elevated filling pressures, the PVAR wave will likely be > 25 cm/s and the transmitral E/A ratio during the Valsalva maneuver will be < 1. Incidentally, a Valsalva maneuver performed with a normal transmitral pattern will show proportional reductions in both E-wave and A-wave velocities, and the E/A ratio will remain > 1. A Valsalva maneuver superimposed on a restrictive pattern (ie, E >> A) may or may not "pseudonormalize" (E > A). That is, if diastolic dysfunction is at the far end of severity and it is irreversible, there will be no change with the Valsalva maneuver (Fig 4).
As diastolic dysfunction progresses, reductions in LV compliance coexist with impairments in myocardial relaxation, leading to large increases in LAP or LV end-diastolic pressure (ie, > 20 mm Hg). Elevations in LAP, in turn, increase the pressure gradient between the LA and LV, ultimately enhancing early filling, as manifested by high E-wave velocities (maximum E-wave velocity, > 1.2 m/s). The DT is shortened (< 140 ms) due to flow into the noncompliant ventricle. Correspondingly, the atrial contribution to filling is attenuated due to the early, rapid rise in LV pressure. This restrictive filling pattern, characterized by E >> A, decreased IVRT, and decreased DT, is seen with restrictive cardiomyopathies with LV ejection fractions (EFs) of > 40% (eg, infiltrative [sarcoidosis], noninfiltrative [idiopathic], and endomyocardial fibrosis), dilated cardiomyopathies with poor systolic function, and pericardial disease.23 The concomitant PV flow pattern shows blunting of the systolic wave (PV systolic wave less than the PV diastolic wave) as the gradient between the PV and LA is reduced due to elevated LAPs. The PVAR wave will be increased in amplitude (> 25 cm/s) as well as duration (longer than the transmitral A duration) [Fig 4, 5].23
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Limitations to Conventional Doppler
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- Load dependency: Increases in preload increase E-wave velocity, and shorten DT and IVRT. Correspondingly, reductions in preload (and increases in afterload) exhibit a transmitral pattern similar to impaired relaxation (ie, increase in IVRT, decrease maximum E-wave velocity, and increase DT). RV pressure overload (eg, from acute RV infarction or pulmonary embolus) also displays a mitral inflow pattern of abnormal relaxation.29
- HR and rhythm: With tachycardia (HR > 100 beats/min), the velocity of the A wave increases relative to that of the E wave. Eventually, the two waves merge, and transmitral Doppler imaging studies become difficult to interpret. In atrial fibrillation, there is loss of the A wave. The E wave and IVRT, however, remain useful. In heart block, the E-wave and A-wave velocities vary. A post-premature ventricular contraction beat may show an impaired relaxation pattern due to contraction and relaxation asynchrony. Variable velocities for E waves and A waves may be seen in a patient with normal sinus rhythm who is receiving ventricular inhibited backup pacing.
- MR: Depending on the severity of the regurgitation, both the mitral inflow and PV flow can be altered. As LAPs rise as a result of regurgitant flow, the mitral inflow pattern becomes restrictive (E >> A). The PV flow pattern during moderate MR may show an attenuated PV systolic wave and increased PVAR. With increasing severity, systolic pulmonary flow (ie, the PV systolic wave) is reversed (below the baseline).
- Aortic regurgitation: With severe aortic regurgitation, LV pressure rises quickly, and this is reflected in a restrictive mitral inflow pattern (increase in maximum E, decrease in DT, decrease in maximum A, and E >> A) and, in some instances, "diastolic" MR (eg, flow above the baseline during diastasis) can be seen on the spectral display.
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TDI
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Given the limitations of preload dependency, atrial fibrillation, tachycardia, and regurgitant valvular lesions, and the commonly observed pseudonormalization pattern, TDI has taken the "front-stage" in the transthoracic echocardiographic assessment of diastolic function and is now being used by the perioperative transesophageal echocardiographer. TDI focuses on the high-intensity, low-velocity echoes of the myocardium. It can be displayed either by PWD (ie, pulsed TDI) or color TDI. With the sample volume of 2 to 5 mm placed in the myocardial wall of interest (and preferably without wall motion abnormalities), myocardial velocity changes during systole and diastole can be assessed. Similar to conventional Doppler imaging, the TDI pattern of LV wall dynamics has a direct relationship with the physiologic aspects of the cardiac cycle (Fig 1). For optimal time measurements, sweep speed is usually set at 50 to 100 mm/s. Using the pulsed wave spectral mode, filters and baseline are adjusted to a low-velocity range (eg, –20 to 20 cm/s), with minimal gain settings (a TDI preset may be present on the newer machines).323
Since there are two different types of myocardial fibers within the wall (circumferential fibers are located in the middle portion of the myocardium, and longitudinal fibers are found along the subendocardium), TDI can be used to assess both transverse and longitudinal wall dynamics. Specifically, if one places the sample volume in the anterior wall imaged in the transgastric short axis (TG SAX) view, the spectral display represents transverse movement, whereas if the sample volume is placed within the mitral annular lateral wall in the midesophageal-chamber four (ME-4) chamber view, the spectral display represents the longitudinal movement of the myocardium. Because both circumferential and longitudinal fibers insert on the fibrous mitral annulus, a common position of the pulsed Doppler imaging sample using TEE is longitudinally along the lateral mitral annular wall (Fig 7 , top, A). The velocities along this wall are greater compared to the velocities from the corresponding septal wall.3031
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Figure 7.. Top, A: schematic of the midesophageal four-chamber view with pulsed Doppler imaging sample volume located at the lateral mitral annular wall for TDI assessment of diastolic function. Bottom, B: lateral mitral annular tissue Doppler waveforms for the assessment of LV diastolic function. S' or Sm refers to myocardial wall motion during systole. Note that E' or Em of > 8 cm/s is indicative of normal diastolic function. See the legend of Figure 2 for abbreviation not used in the text.
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Limitations to TDI
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- Sinus tachycardia (HR > 100 beats/min): If the mitral annular wall motion velocity during early filling (EM) and the mitral annular wall motion velocity during late filling (AM) fuse (as they do with mitral inflow Doppler imaging), the fused E wave and fused EM wave (fused E/fused EM) velocities can be used to predict filling pressures.3233
- Atrioventricular conduction disturbances: Asynchrony between contraction and relaxation events will manifest as impaired relaxation; thus, interpret with caution (eg, ventricular inhibited pacing will produce dissociated EM wave and AM wave, depending on the underlying rhythm; synchronous dual chamber pacing should have little affect on the TDI pattern).
- Local wall motion abnormalities: Because the EM wave represents only the net effect of myocardial relaxation, elastic properties, and the potential translational and tethering effects at the "sample" segment, the avoidance of sampling a wall affected by pronounced wall motion abnormalities is recommended. However, if regional wall motion abnormalities are widespread, averaging multiple segments will offer a good estimate of global ventricular relaxation.3435
- Mitral annular calcification: Severe mitral annular calcification may reduce the excursion of the mitral annulus, resulting in a marked underestimation of peak annular velocity, EM.36 Thus, those interpreting LAPs that were estimated by the E/EM ratio should proceed with caution.
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Pulsed Wave TDI Patterns of Diastolic Function in Health and Disease
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A normal pattern consists of three major signals. (Note that EM and E' are used interchangeably in textbooks and publications in order to distinguish them from conventional Doppler velocities. The authors will use EM exclusively here.)
A systolic signal and two distinct diastolic signals, early diastole (EM) and late diastole (AM), timed in relation to the onset of early inflow and atrial contraction, exist. (Fig 1, 7, bottom, B). The systolic waveform starts after the isovolumic contraction time and ends with the T wave of the ECG. The systolic contraction wave morphology may change depending on the wall segment analyzed. The peak velocity ranges between 8 and 18 cm/s. The EM wave registers after the T wave on the ECG. The EM wave may start either with or slightly before the E wave as it corresponds to the rapid filling period of the LV. The EM wave represents myocardial distension or elongation during early diastole, and its velocity relates to the velocity of relaxation. In fact, a strong relation between the EM wave and 
(the LV relaxation time constant) has been demonstrated, suggesting its value as an index of myocardial relaxation. After the EM wave, an intermediate period may be observed without evidence of myocardial wall motion, corresponding to diastasis. A second diastolic wave, the AM wave, registers after the P wave on the ECG. Little differences in timing occur between the AM wave and the transmitral "A" valve. The AM wave represents the passive myocardial distension caused by atrial contraction, either by retraction of the annular ring or due to the subsequent late ventricular filling. In patients with normal diastolic function, in all cardiac segments, the relationship between the diastolic waves (EM/AM) is always > 1.
With the normal aging process, the peak EM wave decreases, and the peak AM wave slightly increases as the atrial contribution to filling becomes relatively more important than the contribution from active myocardial relaxation, EM.3738 Likewise, with impaired relaxation, the EM wave is significantly reduced and the AM is mildly increased. An EM wave of 8 cm/s is indicative of impaired relaxation.39 As the severity of the disease progresses, the EM wave decreases further and the AM wave may also gradually decrease, indicating the irreversibility of restrictive filling.3940 Unlike the E/A ratios obtained with conventional Doppler imaging in the presence of restrictive filling (E >> A), EM/AM wave reversal persists with increased disease severity (Fig 4 , 5). Given that the EM wave remains reduced in all stages of diastolic dysfunction, it can be used to differentiate normal from pseudonormal mitral inflow patterns despite ensuing increases in LV filling pressures. This illustrates the value of the load independence of TDI.
Integration of conventional and TDI early filling parameters can be used to provide a good estimate of filling pressures (ie, the E/EM index).341 An E/EM ratio of 8 (5 to 12 mm Hg), in most circumstances, predicts normal filling pressures, and an E/EM ratio of >15 (at any annular site) predicts elevated filling pressures ( 15 mm Hg). Additional echocardiographic parameters (eg, LA size, use of the Valsalva maneuver with Doppler imaging, and/or pulmonary venous flow) are recommended to correctly classify diastolic function when the E/EM ratio is between 8 and 15, as there is considerable variability in filling pressure. In patients whose hearts are in sinus rhythm, pulmonary capillary wedge pressure (PCWP) can be estimated using the following formula: PCWP = 2 + 1.3 (E/EM) [lateral annular EM].32 TDI is also helpful in differentiating restrictive pericardial disease (eg, constrictive pericarditis) from restrictive myocardial disease (eg, amyloidosis).42 The EM wave may be preserved or significantly increased in the presence of constrictive pericarditis, whereas in restrictive myocardial disease, the EM wave is always 8 cm/s.
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An Echocardiographic Approach to Diastolic Assessment
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Based on the literature and personal experience, the authors recommend the integration of hemodynamic parameters (pulmonary artery occlusion pressures or pulmonary artery end-diastolic pressures), LA dimensions, and conventional Doppler imaging of mitral inflow in conjunction with TDI of the lateral mitral annular wall. When findings are equivocal, one may also consider a Doppler imaging evaluation at the peak of the Valsalva maneuver and Doppler imaging of PV flow. When one’s patient has nearly normal systolic function (EF 45%), the following algorithm can be used to aid in diastolic function assessment (Fig 8
). In patients with reduced EF (ie, < 45%), the evaluation of diastolic function can be approached in a similar manner. However, when estimating filling pressures using the Doppler E/EM ratio, a higher cutoff value is needed to detect elevated filling pressures than when using a lower ratio (E/EM > 15) in patients with normal EFs.43 TDI of the lateral mitral annular wall is useful, irrespective of systolic function. If regional wall motion abnormalities are present, both septal and lateral EMs should be used.
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Figure 8.. Algorithm for the assessment of diastolic function in the patient with a normal or near-normal EF (ie, 45%). E = early filling velocity with TDI. See the legend of Figure 3 for abbreviation not used in the text.
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In view of the fact that the majority of Doppler imaging parameters of diastolic function were acquired from patients who were neither intubated nor receiving mechanical ventilation, the figures found in the reference charts may vary slightly from the ICU patient.
In conclusion, diastolic dysfunction can impede hemodynamic stabilization and weaning progress in the mechanically ventilated critically ill patient. Transesophageal examination evaluates LV diastolic function best, especially with the addition of the use of TDI.
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Footnotes
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Abbreviations: A = A wave; AM = mitral annular wall motion velocity during late filling; DT = deceleration time; E = E wave; EF = ejection fraction; EM = mitral annular wall motion velocity during early filling; HR = heart rate; IVRT = isovolumic relaxation time; LA = left atrium atrial; LAP = left atrial pressure; LV = left ventricle ventricular; MR = mitral regurgitation; PEEP = positive end-expiratory pressure; PV = pulmonary vein; PVAR = pulmonary vein atrial flow reversal; PWD = pulsed wave Doppler; RV = right ventricle ventricular; TDI = tissue Doppler imaging; TEE = transesophageal echocardiography
This study was supported in part by the Dennis W. Jahnigen Career Development Scholar Award to Dr. Groban.
Received for publication April 4, 2005.
Accepted for publication July 16, 2005.
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References
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Abstract
Introduction
