Pulmonary hypertension is the hallmark of pulmonary microvascular occlusion. Hence pulmonary artery pressure (PAP) provides a rough measure of disease severity. It is not ideal as it will not distinguish between micro- and macrovascular occlusion. Furthermore, PAP does not rise unless more than 50 per cent of pulmonary vessels are occluded and hence may fail to detect significant microvascular occlusion. In addition, it is affected passively by intrathoracic pressure, pulmonary blood flow, and pulmonary downstream pressure, all of which may change unpredictably.
These drawbacks are partially overcome by calculating pulmonary vascular resistance (PVR) as where PAOP is the pulmonary artery occluded pressure and CO is cardiac output. Unfortunately, PVR overestimates the true vascular resistance and fails to reflect changes over time when the critical closing pressure of pulmonary vessels (which ideally is equal to PAOP) greatly exceeds PAOP ('vascular waterfall' phenomenon). However, this is precisely what happens in severe microvascular occlusion, thereby limiting the diagnostic value of PVR.
The problem can be solved by directly assessing the pulmonary vascular closing pressure (CP) by measuring PAP at different pulmonary blood flows ( Fig..2). CP is then obtained by extrapolating the pressure-flow curve to a pulmonary blood flow of zero. PVR is now calculated more correctly as
Fig. 2 Pressure-flow plots and critical closing pressure (CP) of the lung. Pressure-flow plots and CP values are shown both at baseline and after induction of experimental pulmonary hypertension by infusion of thromboxane in dogs. See text for further explanation.
The slope of the pressure-flow relationship reflects the incremental resistance upstream of vascular closure. Hence, any shift of the pressure-flow curve to the left reflects increased vascular resistance (Fig 2). Clearly, CP and pressure-flow plots are the optimal tools for evaluating pulmonary vascular pathophysiology, but unfortunately they are difficult to obtain in patients.
In contrast, the gradient between end-diastolic pulmonary artery pressure (PA ed) and PAOP can be assessed easily and may distinguish postcapillary from a (pre)capillary origin of pulmonary hypertension. Physiologically there should be no major gradient. If (pre)capillary resistance rises, PA ed will markedly exceed PAOP. Conversely, if pulmonary hypertension is caused by left ventricular failure and pulmonary venous congestion, PA ed and PAOP will both rise with no gradient.
Pulmonary capillary pressure (PCP) is the major determinant of transvascular filtration in the lung ( Fig 3). PCP provides information on the risk of pulmonary edema formation and the efficacy of vasodilator therapy, and it also allows identification of the relative contributions of arterial resistance (PVR art) and venous resistance (PVRven) to total PVR:
Fig. 3 Pulmonary capillary pressure (PCP). The vascular pressure transient after pulmonary artery occlusion is analyzed at end-expiration and the inflection point between the rapid and slow components is identified by visual inspection (arrow). See text for further explanation.
An example is shown in Fig. 2 and Fig, 3. Microvascular occlusion was induced by infusion of the potent pulmonary vasoconstrictor thromboxane. Mean PAP rose from 16 to 27 mmHg while CO remained stable at 4 l/min. Based on PAOP values of 8 mmHg and 9 mmHg respectively, 'conventional' PVR can be calculated as 160
dyn s/cm5 at baseline and 360 dyn s/cm5 with thromboxane. The assumption of an increased PVR is confirmed by a steepening of the pressure-flow plot (Fig, 2) and an increase in the PAed-PAOP gradient from 6 to 17 mmHg; CP increased from 8 to 12.5 mmHg. Using CP instead of PAOP for calculation of PVR does not change baseline resistance but results in a PVR value of 290 dyn s/cm5 with thromboxane. This analysis demonstrates that 'conventional' PVR overestimates 'true' PVR by 24
per cent in this situation. PCP rose from 10 to 15 mmHg with thromboxane (Fig 3). Baseline PVRart and PVRven values were 120 dyn s/cm5 and 40 dyn s/cm5
respectively, and 246 dyn s/cm5 and 123 dyn s/cm5 respectively with thromboxane. These data suggest that the relative venous contribution to total PVR was 25 per cent at baseline and 33 per cent during infusion of thromboxane.
Finally, the vasoconstrictor component of pulmonary hypertension can be quantified by testing pulmonary vascular reactivity. Inhalation of oxygen or nitric oxide and infusion of the prostaglandin I2 analog epoprostenol have been used for this purpose. A reduction of pulmonary vascular resistance with 'therapy' suggests that vascular occlusion is partly due to active pulmonary vasoconstriction, responds to pharmacological therapy, has occurred recently (in chronic disease vascular reactivity is almost lost), and affects micro- rather than macrovessels.
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