Page 12 - Assessing right ventricular function and the pulmonary circulation in pulmonary hypertension Onno Anthonius Spruijt

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An increase in the afterload of the RV leads to an increase in mPAP since the RV needs to build up more pressure to maintain an adequate CO. The load on the outflow of the RV can be divided into the resistance to steady state flow and the resistance to pulsatile flow from vascular impedance [4]. The resistance to steady state flow is known as the pulmonary vascular resistance (PVR) and is defined as PVR = (mPAP – PAWP) / CO. An increase in PVR can be due to a decrease in the pulmonary vessel radius or due to the loss of arterial surface [4]. A decrease in pulmonary arterial vessel radius is seen in group 1 and 4 PH patients and is due to thickening of the vascular wall, intravascular occlusions (either by exuberantly proliferating endothelial and smooth muscle cells or thrombosis and emboli) and loss of vessel number (rarefaction). Hypoxic vasoconstriction, also seen in group 3 PH patients can contribute to a decrease in the pulmonary arterial diameter. A decrease in arterial surface area is often observed in emphysema. Vascular rarefaction as the sole cause of an increased PVR is still a matter of debate, since even in severe emphysema, PH is rare. PVR can also be increased in conditions associated with an increased blood viscosity.
Resistance to pulsatile flow is mostly described by an inverse measure, the pulmonary arterial compliance. Pulmonary arterial compliance is assessed by stroke volume (SV) divided by the pulse pressure (PP) (SV/PP). It has been shown that in the pulmonary circulation PVR and compliance are inversely related [5]. The product of PVR and compliance, known as the RC time (Ƭ), can be calculated as Ƭ = PVR x compliance = ((mPAP – PAWP) / (SV x HR)) x (SV/PP) = T x ((mPAP – PAWP) / PP). Over a wide range of PVR, Ƭ remains relatively stable in healthy people and patients with precapillary PH [5-7].
mPAP can also be increased due to an increased PAWP. During RHC a balloon can be inflated to temporarily close a small pulmonary artery branch. The pressure proximal from the inflated balloon is the PAWP and is a surrogate measure of the pressure in the post-capillary system including the left atrial pressure. Left heart failure or left sided valvular disease results in an increase in PAWP, which can subsequently increase mPAP. A PAWP > 15mmHg is defined as abnormal and is due to left heart disease. Therefore, PH can be classified in pre- and postcapillary PH based on the PAWP [3]. The significance of a PAWP between 12 and 15mmHg is still unclear.
The degree to which an increase in CO could lead to an increase in mPAP depends on the degree to which lung vessels can distend and be recruited. The magnitude of vascular distention and lung vascular recruitment during exercise is still hotly debated. During exercise an increased demand for oxygen will increase CO, which is usually followed by at least some increase in the mPAP [8].