Advanced Hemodynamic and Cardiopulmonary Ultrasound for Critically Ill Patients in the Emergency Department

Mitral Valve Inflow Velocity

Assessment of the MV inflow is performed by placing the pulse-wave Doppler gate between the tips of the MV leaflets in the AP4 view. Early diastolic filling produces the E-wave, and LA contraction produces the late diastolic A-wave (Figure 8a).

The interpretation of these waves can be categorized in four patterns: (1) normal; (2) abnormal relaxation; (3) pseudonormalization; and (4) restrictive. The mitral inflow pattern for normal and pseudonormalization are very similar, and other techniques are used to differentiate them, such as the E-wave/A-wave (E/A) ratio, deceleration time, or alternatively, using either tissue Doppler imaging or pulmonary vein Doppler analysis. 

Tissue Doppler Imaging

Tissue Doppler imaging enables the clinician to measure myocardial velocities such as the speed of relaxation to evaluate if LV relaxation is due to a drop in LV pressure below LA pressure after systole, pulling the MV open; or if increased LA pressure is required to push open the MV and fill the LV. 

For this study, the tissue Doppler sampling gate is placed at the septal or lateral annulus of the MV in the AP4 view to visualize early diastolic mitral annulus velocity (e’) (Figure 8b). The E/e’ ratio can be helpful for estimating LV filling pressures. An E/e’ of less than 8 is associated with normal LV filling pressure whereas an E/e’ >15 is associated with an elevated LV filling pressure.28,29 When the E/e’ is 8 to 10, other indices such as the E/A ratio and deceleration time, as well as the clinical picture, can provide insight into the presence of hemodynamically significant diastolic dysfunction.

Learning and applying the assessment of diastolic parameters can be challenging; however, these parameters can be used to help predict LV filling pressures in patients with findings of pulmonary edema on chest radiograph. Limitations of these techniques are inter-rater variability, as well as the ability of the operator to acquire the required AP4 view. In addition, these techniques are unreliable in patients with irregular cardiac rhythms, severe mitral disease, and in hypertrophic cardiomyopathy. 

Right Ventricular Assessment

The right ventricle (RV) is a small, thin-walled ventricle with only two layers of muscle, as opposed to the three layers of the LV. In contrast to the rocking motion of LV contraction, the orientation of the two muscle layers of the RV permits mostly longitudinal contraction. The circumferential muscle fibers are shared at the base and apex with the LV, which can provide some of the contractile strength of the RV.³⁰ Because of this orientation, RV strain, which can manifest as decreased longitudinal contraction, speed of contraction, septal movement, and tethering abnormalities through ventricular interdependence, can be measured easily using bedside echocardiography. 

In healthy individuals, the RV is a low-pressure chamber that acts as a conduit for propelling venous return into the pulmonary circulation without much effect on systemic hemodynamics. However, in critical illness, RV abnormalities can have profound effects on hemodynamics, and  the efforts typically used to improve LV performance will worsen a failing RV. 

While RV dysfunction is most commonly due to chronic LV disease, acute RV dysfunction is commonly encountered in critical illness,³¹ including many septic patients with ARDS,^32,33 PE, or decompensated chronic pulmonary hypertension.³⁴ The examinations that follow, allow the EP to assess for the presence of RV dysfunction and to guide resuscitation appropriately to avoid the untoward hemodynamic effects of conventional resuscitation strategies in these patients. 

When evaluating the RV, the clinician must determine (1) if the patient’s RV strain is due to pressure or volume overload; and (2) if the patient’s RV is responsive or nonresponsive to a preload challenge, prompting an alteration in the resuscitation plan in nonresponsive cases. 

Right Ventricular Pressure/Volume Overload

While inferior vena cava (IVC) ultrasound has been shown to be a pre-heart/lung assessment of cardiopulmonary interactions that predicts volume responsiveness, the IVC is also a good predictor of right atrial (RA) pressure.³⁵ If the IVC is dilated and lacks respiratory variation, the patient likely has an elevated RA pressure, which is most likely transmitted from an elevated RV pressure (Figure 9a). However, compliance of the RA, RA pressure and, by extension, IVC prediction of that RA pressure, may underestimate the degree of RV pressure or afterload. 

In the presence of pressure overload of the RV, septal motion will be toward the LV and flatten during systole (Figure 9b). Despite movement of the septum toward the LV on systole, the LV is still able to fill in diastole and maintain an adequate cardiac output (often with concomitant tachycardia). When the RV is volume-overloaded, the septum flattens on diastole, which has a more deleterious effect on cardiac output (Figure 9c). Due to pericardial restraint on the free wall of the LV, the LV is unable to fill during diastole and thus cardiac output drops.^30,36 The well-known “D-sign” occurs when the RV is both pressure- and volume-overloaded, which often occurs when a hypotensive patient with a pressure-overloaded RV receives a bolus of fluid. McConnell’s sign occurs when the pressure and volume-overloaded RV has apical “blinking” caused by tethering of the shared muscle fibers with the LV.³⁷ 

Right Ventricular Strain and Contractile Reserve 

The longitudinal contraction of the RV can be easily measured on bedside ultrasound. In the apical view, M-mode imaging through the lateral annulus of the tricuspid valve will provide a measurement of the systolic movement of the RV. Increased strain on the RV will lead to decreased tricuspid annular plane systolic excursion (Figure 10a).³⁸