Determinants of Aortic Pressure Variation During Positive-Pressure Ventilation in Man: Discussion

8 Sep
2014

We observed that changes in SAP during positive-pressure ventilation in humans cannot be explained by proportional changes in LV volume. The effects of positive-pressure ventilation on LV volume and SAP are complex and not interpretable by a single mechanism. If SAP increases relative to apneic values during ventilation, it does so during the inspiratory phase, whereas if SAP decreases, it does so during the expiratory phase. These changes in SAP are inconsistently associated with changes in SA, EDA, or ESA, suggesting that coupled changes in LV performance are not primary determinants of SAP variations during ventilation. Although the decrease in SAP after a positive-pressure breath appears to be accentuated during hypovolemic states, the mechanism for these changes does not appear to relate to coupled changes in LV preload. Because the changes in SAP during positive-pressure ventilation are in phase with the change in the airway pressure, we favor the hypothesis that positive-pressure, ventilation-induced changes in SAP may reflect concomitant changes in ITP similar to those in phase 3 of a Valsalva maneuver. inhalers for asthma

Consistent with a direct effect of ITP on SAP variations, the decrease in SAP was more pronounced in the closed (p < 0.05) than in the open chest condition for the same Vt. If the observed decrease in SAP was secondary to a decrease in venous return, then we would expect to see a decrease in SA and EDA. This was not the case. Although SA decreased in 56% of our subjects and EDA decreased in 80% of our subjects (Fig 3), this decrease occurred during the time that SAP was increasing. Furthermore, the relation between the degree of decrease in SAP and the corresponding decrease in SA and EDA (Fig 3) was variable. From the Fourier analysis, we saw that in the closed chest condition, the SAP signal always preceded the change in LV area. These data are consistent with the hypothesis that the increase in ITP from positive-pressure ventilation directly alters the SAP. Finally, if the decrease in SAP represents a deficit in LV output secondary to the positive-pressure breath, we would expect that SAP would decrease in proportion to the SA deficit preceding it during the breath. The data show that was also not the case (Fig 7), and it implies that a decrease in SAP during positive-pressure ventilation is not necessarily secondary to a decrease in LV stroke volume.

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