Anatomically, the ventricle is a thin-walled, low-pressure structure which, unlike the left ventricle, receives most of its blood supply during systole (Figure 1). It has a complex, crescentic shape in contrast to the left ventricle which has a simple 'ellipsoid' form. As a result, calculation of right ventricular volume, by any means other than thermodilution, is difficult.

Functionally, the important differences between the right and left ventricle are:

Firstly, that the RV is extremely sensitive to changes in afterload (PVR) ^{1, 2} and, in this respect, more resembles the behaviour of a 'sick' as opposed to a 'healthy' left ventricle (Figure 2). It is possibly for this reason, that the 'inodilators' such as milrinone seem particularly effective in the treatment of right ventricular failure.

Secondly, at typical filling volumes, the RV is a highly compliant chamber and as such, is relatively insensitive to changes in preload. However, at high inflow volumes, pericardial constraint interferes with ventricular filling and compliance falls quite markedly ³.

Finally, that the ventricle has an 'intricate' pattern of activity in that the contraction and relaxation phases of the outflow tract are delayed in comparison to those of the inflow tract. This is in contrast to left ventricle which has a 'simple' pattern of unified coaxial shortening.

Because the ventricle is thin-walled, any increase in afterload can lead to pronounced increases in wall-tension and therefore oxygen utilisation. Again, this is a powerful argument for the use of inodilators such as amrinone or milrinone in the management of acute right ventricular failure.

Measurement of ventricular function.
The introduction of rapid response time thermistors into clinical practice allowed for the development of thermal dilution techniques which permitted the estimation of right ventricular end-diastolic volume, end-systolic volume and ejection fraction.

The method was based on the observation that if a thermal indicator was introduced into the ventricle during the diastolic interval, then fractional washout of the indicator occurred in a stepwise fashion with each subsequent beat of the heart. This thermal washout could be detected as a series of temperature plateaux in the main pulmonary artery (Figure 3).

It was established that each plateau reflected the intraventricular temperature during the previous beat of the heart and that the ratio of succeeding plateaux could be used to calculate the end-diastolic volume of the ventricle when suitable correction factors were applied. Because of the exponential nature of the decrease in temperature plateaux, the ratio of any plateau to that of the preceding beat equaled the end-systolic volume (ESV) of the ventricle divided by the end-diastolic volume (EDV). By definition, ESV is the difference between EDV and stroke volume (SV). If SV is measured as thermodilution output divided by heart rate and beat-to-beat temperature plateaux are also recorded, EDV is the only unknown variable in the equation and can be calculated.

The technique has been used to examine the performance of the right ventricle during separation from cardiopulmonary bypass and has been found to be of some use. - For example, right ventricular myocardial protection is often relatively poor if retrograde cardioplegia is used during cross-clamping and sudden increases in pulmonary vascular resistance can occur shortly after separation from bypass when protamine is administered.

Under either of these circumstances, the ability to quantify right ventricular dysfunction may be particularly useful because specific therapy (notably inodilators such as amrinone or milrinone) targeted at improving right ventricular function is now available. However, the accuracy of the technique is still in question and it remains to be seen whether right ventricular ejection fraction measurement offers patients any clear benefit or whether it is still a technique in search of a role.

1. Weber K, Janicki J, Shroff S et al: The right ventricle: Physiologic and pathophysiologic considerations. Crit Care Med 11:323, 1983

2. Abel FC, Waldhausen JA Effects of alterations in pulmonary vascular resistance on right ventricular function. J Thorac Cardiovasc Surg 54(6): 886 (1967)

3. Burger W; Straube M; Behne M et al Role of pericardial constraint for right ventricular function in humans. Chest, 107:46-9, 1995 Jan

Last edited on: 13/11/2000