Right ventricular (RV) dysfunction is common in critically ill patients.1–3 It is associated with multiple clinical scenarios frequently encountered by the intensivist, including acute cor pulmonale, acute RV dysfunction of sepsis, and acute RV infarction. In addition, the assessment of RV function is essential to determination of a patient's preload responsiveness. Echocardiography is the best available method to diagnose and monitor RV function at the bedside and provides the critically ill patient a prompt, accurate, noninvasive, and serial method to monitor the function of the right heart and its responsiveness to different clinical interventions. This chapter describes a variety of echocardiographic methods to assess RV function that are particularly relevant to critical care practice for both the novice and experienced echocardiographer. While the assessment of RV function in the noncritically ill patient is beyond the purview of this chapter, the techniques described here are also applicable to the assessment of RV function in the ambulatory patient.
The RV comprises two anatomically and functionally different cavities separated by the crista supraventricularis: an inflow region (the sinus) and an outflow tract (the cone or infundibulum). The tricuspid valve (TV) and its apparatus plus heavily trabeculated myocardium form the sinus. Smooth myocardium and the pulmonic valve form the infundibulum. The sinus generates pressure during systole while the infundibulum modulates this pressure and prolongs its duration. Right ventricular contraction occurs serially in three different phases: (a) contraction of the sinus along its longitudinal axis, (b) radial contraction of the RV free wall toward the interventricular septum (IVS), and (c) torsion of the left ventricle (LV) (clockwise rotation of the LV base with counterclockwise rotation of apex) pulling the RV in similar manner. Overall, LV contraction contributes 25% of its own stroke work to the generation of RV stroke work via the IVS. In pulmonary hypertension, this contribution increases to 35%.4
The normal RV is less muscular than the LV and has a free wall thickness 3.3 millimeters (mm). As a consequence, it is easily affected by its surroundings and the effects of increased afterload. Unlike the LV, it is able to acutely dilate. Relative to the LV, the RV is a lower pressure chamber, with normal pressures of approximately 30/10 centimeters of water (cm/H2O) with the patient in the resting state. When afterload increases acutely, the RV is unable to correspondingly generate higher pressures. However, when subjected to chronic loading conditions, the RV compensates with a hypertrophic response that is suggested by a thickened RV free wall on echocardiography. In this situation, the RV can generate up to systemic-level pressures, such as is seen with advanced pulmonary arterial hypertension.
Acute cor pulmonale (ACP) is defined as the clinical setting in which the RV experiences a sudden increase in afterload.5 This may occur in the context of previously normal RV function or in the RV that is already impaired. Sudden increases ...