JULIEN MAIZEL, SHARI EL-DASH and MICHEL SLAMA

Overview

Left ventricular (LV) diastolic dysfunction is a clinical entity that remains poorly understood and identified in the intensive care unit (ICU) setting. It is essential to clarify the difference between diastolic heart failure, LV diastolic dysfunction, and increased LV filling pressure. Diastolic heart failure is a clinical syndrome defined by the presence of symptoms of congestive heart failure in the setting of diastolic dysfunction (and preserved systolic function).¹ This syndrome is also called heart failure with a normal LV ejection fraction and, in cardiology, accounts for more than 50% of all cases of acute heart failure. The proportion may be even higher in the ICU setting, although no precise statistics are available.

Diastolic dysfunction is an alteration in LV properties marked by degradation in LV relaxation or an increase in LV stiffness (or both). Some evidence indicates that diastolic dysfunction increases the risk for death in patients with septic shock.² In addition, evaluation of diastolic function can provide the intensivist with important hemodynamic information concerning patients’ fluid responsiveness. In patients with a steep LV pressure-volume relationship, infusion of small amounts of fluid may significantly increase LV diastolic pressure and precipitate acute pulmonary edema. Diastolic dysfunction may coexist with systolic dysfunction in patients with congestive heart failure. Furthermore, in the absence of congestive heart failure, LV filling pressure or LV end-diastolic pressure is not necessarily increased in patients with diastolic (or even systolic) dysfunction. Both diastolic function and LV filling pressure can be explored with echocardiography.

Diastole is classically split into three different physiologic events: LV relaxation, LV passive filling, and left atrial (LA) contraction. Impairment in each of these events may lead to congestive heart failure. Impairment of LV relaxation is mainly due to failure of calcium recapture in the sarcoplasmic reticulum, whereas myocardial infiltration or fibrosis increases LV stiffness.³

Recently, Nagueh et al described a practical approach for classifying diastolic function with transthoracic echocardiography (TTE) that involves taking several parameters into account: mitral inflow, early septal and lateral mitral annular systolic velocity with tissue Doppler, LA volume, pulmonary venous return flow, and even the response to a Valsalva maneuver.⁴ In ICU patients, obtaining some of these parameters (e.g., the response to a Valsalva maneuver) can pose quite a challenge.⁵ Detection of other parameters (e.g., pulmonary venous flow [PVF]) may require the application of transesophageal echocardiography (TEE).

Mitral flow: Left ventricular filling

Mitral inflow can be recorded (with both TTE and TEE) by placing the pulsed wave Doppler sample volume at the tip of the mitral leaflets (Figure 32-1). Color flow imaging can help optimize alignment of the Doppler beam, particularly if the left ventricle is dilated. Two waves are described in mitral inflow: the E wave (early filling velocity), which corresponds to the early LV/LA pressure gradient and is affected mainly by LV relaxation and preload, and the A wave, which is due to atrial contraction, reflects the LA/LV pressure gradient during late diastole, and is affected by LV compliance and LA contractile function (and thus disappears in atrial fibrillation) (see Figure 32-1).

Parameters of mitral inflow include measurements of E and A peak systolic velocity, the E/A ratio, and the deceleration time (DT) of E. The E/A ratio has three main patterns. In the normal pattern, E has a higher peak velocity than A does and therefore E/A is greater than 1 (Figure 32-1A). The second pattern has a small E wave with an E/A ratio of less than 1 and increased DT. This pattern usually corresponds to impairment of LV relaxation, yet with low atrial pressure (Figure 32-1B). The third pattern consists of very high E velocity with an E/A ratio higher than 2 and a short DT. It is associated with severe impairment of LV compliance and with high LV diastolic and pulmonary arterial occlusion pressure (Figure 32-1C).⁶ Mitral flow is affected by many factors, such as heart rate, preload, afterload, and LA and LV contractility. Nonetheless, since many of these factors are frequently altered in critically ill patients, diastolic function should not be assessed by the mitral flow pattern alone but rather by a global interpretation of all the available information.

Pulmonary venous flow

To record PVF, the pulsed wave Doppler sample volume is placed in the pulmonary vein just distal to its entry point. Although good alignment can be achieved with TTE in some patients (Figure 32-2), measurement of PVF usually requires performance of TEE. The pulmonary venous waveform consists of a peak systolic (S) velocity, which is usually divided into two peaks, S1 and S2, and a peak diastolic (D) velocity. Following these antegrade waves is a retrograde reverse A wave (Ar) caused by atrial contraction (see Figure 32-2). Further information can be obtained by analyzing ensuing parameters such as the S/D ratio, systolic filling fraction (integral of S/[S + D]), peak Ar (reverse A) velocity in late diastole, duration of Ar velocity, and its difference from the mitral A-wave duration. The velocity of the S1 component is primarily defined by variation in LA pressure, as well as by both LA contractility and relaxation.⁷ The S2 component is instead related to stroke volume and propagation of the pulse wave along the branches of the pulmonary artery. D-wave velocity, on the other hand, is a function of LV filling and compliance and thus accompanies the changes observed in mitral E velocity. Pulmonary venous Ar velocity and duration are influenced by late diastolic LV pressure, atrial preload, and LA contractility. Decreasing LA compliance with increasing LA pressure decreases S velocity and increases D velocity, respectively, thereby reducing the S/D ratio to less than 1.^8–10 This situation is also characterized by a drop of less than 40% in the systolic filling fraction⁸ and shortening of the DT of D velocity, usually less than 150 msec.