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

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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.

Figure 9.

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

Figure 10.

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

From the same apical view, tissue Doppler at the lateral tricuspid annulus will give a tricuspid annular peak velocity, a measure of the isovolumetric contraction velocity. This measurement will provide a measure of the contractile reserve of the RV (Figure 10b). A measure of less than 10 cm/sec indicates that further volume and inotropic challenges to the RV will not be effective, and the focus should be to decrease RV afterload with pulmonary vasodilators. 34,39,40

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