Page 14 - Assessing right ventricular function and the pulmonary circulation in pulmonary hypertension Onno Anthonius Spruijt
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to be the result of an imbalance of the autonomic nervous system [22, 26-28]. The decrease in CO for a given workload results in insufficient oxygen delivery to peripheral tissues, anaerobic metabolism of glucose and muscle weakness due to acidosis [29]. Together these changes limit the maximal uptake of oxygen (VO2max) and result in early exercise termination. In PH, a reduced VO2max, O2 pulse and a reduced VO2 at the anaerobic threshold (VO2AT) result from a decreased blood flow and reflect RV dysfunction[30].
A second problem in PH is an increased ventilatory requirement, which is still poorly understood, but likely contributes to the patients’ sensation of dyspnea. In precapillary PH, dead space ventilation occurs because of hypoperfusion of normally ventilated alveoli due to loss of the pulmonary capillary bed. Dead space ventilation could lead to problems eliminating carbon dioxide, increasing minute ventilation (VE).
Figure 3: Comparison of VO2max, O2 pulse and VE/VCO2 between PAH patients and healthy controls. A: Decrease in AT- , B: decrease in VO2max- , C: decrease in O2 pulse- , D: increase in VE/CO2 slope- in PAH patients compared to healthy controls.
However, because PH patients are often hypocapnic at rest and during exercise, it is assumed that in addition to dead space ventilation, alveolar hyperventilation further contributes to the increased ventilatory requirement [31]. It is believed that exercise induced alveolar hyperventilation in PH is due to the summation of lactate acidosis, a hypoxemic ventilatory drive and a sympathetic nerve
 





























































































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