Right Ventricle

Right ventricle is made up of trabeculae carneae but also contains the crista supraventricularis, which divides the inflow (from the atrium) and the outflow (to the PA). The crista is also attached to the anterior tricuspid valve, controlling it via the anterior papillary muscle (APM). Internal diameter is ~ 3.5 cm (as compared to 4.5 cm for the LV). Also obey’s Starling’s law, although according to Barash the RV Frank-Starling curve is shifted upwards and leftward as compared to the LV [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 875, 2006)], i.e. initially the RV is very fluid responsive but reaches a plateau at lower preload than the LV, primarily due to restraint imposed by the pericardium. Normal RVEF is 40%.

“The Forgotten Ventricle,” for a variety of reasons (less well understood, PA pressures not always available) is often neglected when considering the physiology of the cardiovascular system. In relatively healthy patient, this may be acceptable because in the setting of normal pulmonary vascular resistance the right ventricle does not impact hemodynamics significantly, and can sometimes behave as a passive conduit for systemic venous blood flow. PVR is about 10% of SVR, and the energetic requirements of the RV are about 20% of those of the LV.

The RV has a complex contractile mechanism (spiral contraction causing downward movement of the TCV, followed by contraction of the free wall, and then contraction of the LV, which acts as a “wringer”) [Kaplan JA, ed. Essentials of Cardiac Anesthesia. Saunders, 2008 p 64)]. When volume overloaded, the RV loses a significant amount of mechanical strength, in what is commonly referred to as acute cor pulmonale (note that when the RV does hypertrophy in the face of chronic pulmonary hypertension, the adaptive changes are not entirely favorable and a supply:demand mismatch often arises). During normal functioning, the RV produces a triangular flow waveform, and continues to eject after maximal pressures are reached (unlike the LV, which produces a square-wave). In the setting of RV failure, the shape of the RV outflow waveform approaches that of the LV.

Importantly, the RV is highly dependent on both the interventricular septum as well as the LV. Compared to the LV, the RV appears to be less preload sensitive and more afterload sensitive [Stein PD et al. Am J Cardiol 44: 1050, 1979] (function begins to deteriorate with mean PA pressures > 40 mm Hg [McIntyre KM and Sasahara AA. Am J Cardiol 28:288, 1971; Redington AN et al. Br Heart J 59:23, 1988]). Patients at increased risk for RV dysfunction include those with pulmonary hypertension, COPD, ARDS, pulmonary hypertension, and RV ischemia/infarction. RV function is difficult to quantify, and RVEF, when measured, is extremely load-dependent (particularly afterload dependent).

Right Ventricular “Downward Spiral”

When vascular resistance becomes excessive, the RV fails more readily than the LV. RVEF falls rapidly, and RV end-systolic and end-diastolic pressures rise. Concurrently, decreased RV outflow and bulging of the IV septum into the LV (both of which conspire to reduce inflow into the LV) leads to systemic hypotension, which leads to tachycardia – this, in addition to raised filling pressures and increased outflow impedance, increase myocardial oxygen consumption despite the fact that RV oxygen delivery has fallen significantly (systemic hypotension and high RV pressures). This worsens RV function and a spiral ensues. Consider vasopressin in this setting, as it will preferentially increase SVR, thus increasing RV perfusion pressure with a less substantial increase in resistance to RV outflow.

Right Ventricular Ischemia as a Major Component of RV Failure

There is some evidence that ischemia may play a prominent role in the pathophysiology of RV failure in the face of increased PVR. Increased aortic pressures seem to improve the RV’s ability to tolerate afterload – in animal experiments, Scharf et al. found that increasing SVR via descending aortic occlusion improved the RV’s ability to tolerate increases in PVR, however this mechanism did not improve cardiac output, presumably because the effects on the systemic circulation counteracted the improvements in RV function [Scharf S et al. J Crit Care 1:163, 1986]. Data from animal studies suggest that norepineprine improves RV function (as compared to volume and isoproterenol) in the setting of acute pulmonary embolism [Molloy WD et al. Am Rev Respir Dis 130:870, 1984]. Lastly, experiments with intentional PA constriction show that initiation of phenylephrine can reduce biochemical and functional evidence of ischemia [Vlahakes GJ et al. Circulation 63:87, 1981; FREE Full-text at Circulation]. Keep in mind, however, the pulmonary vascular bed does have a significant concentration of alpha receptors [Rudner XL et al. Circulation 100: 2336, 1999; FREE Full-text at Circulation], and by comparison a relative dearth of vasopressin receptors.

Right Ventricular Ionotropy

When increased RV ionotropy is required, the major drugs to be considered are low dose epinephrine (no alpha activity at 0.005 – 0.02 ug/kg/min, significant alpha activity begins at 0.02 ug/kg/min), dobutamine (some alpha activity), and isoproterenol (no alpha activity).