This allows breath-by-breath quantification of the volume of lung units that are ventilated but not perfused and measurement of alveolar VD. In this technique expired CO 2 is plotted against exhaled lung volume.
Separation of the components requires simultaneous measurement of volume and CO 2 by what is called volumetric capnography (Vcap). Īlthough simple to apply, standard time-based capnography does not allow identification of the volume components of the signal, which is necessary for determination of the anatomical source of CO 2 and understanding the pathological processes. This creates a slight delay between collection and gas analysis.
In the side-stream technique gas is continuously aspirated from the primary airway through a sampling line that is placed between the patient and the Y-piece of the ventilator. In the mainstream approach the infrared light source and sensor are placed in the primary airflow tube so that expired gas is sampled directly during expiration and the CO 2 signal is in-phase with the air-flow and pressure signals. Expired CO 2 can be obtained by sampling either mainstream or side-stream expiratory flow. Time-based capnography refers to the elimination of CO 2 over time and gives an indication of ventilation inefficiency. Capnography is the measurement of expired PCO 2. When CO 2 production and total ventilation (VE) are constant, arterial PCO 2 (partial pressure of carbon dioxide) increases in proportion to the increase in VD. But neither index was altered by exercise or vasodilation the latter improves the hypoxemia by increasing the PVO2 from an increase in the cardiac output.Ventilation dead space (VD) refers to the parts of the lung and airways that do not partake in the clearance of carbon dioxide (CO 2) and indicates the inefficient portion of ventilation. We conclude that ventilation-perfusion imbalance as shown by increased Vd/Vt and Qs/Qt, contributes significantly to the abnormal gas exchange in pulmonary hypertension. Intravenous prostacyclin increased the cardiac index and raised the PVO2 and the PaO2 but again with no significant changes in Vd/Vt and Qs/Qt. Exercise produced an increase in cardiac index, a fall in PVO2, no significant change in PaO2 and also no appreciable changes in the Vd/Vt and Qs/Qt. The physiological shunt, Qs/Qt (15 +/- 17%) and the dead space, Vd/Vt (0.47 +/- 0.11) were elevated above normal. At rest arterial oxygen tension, PaO2 (mean 8.1 +/- 1.7 kPa) and mixed venous oxygen tension, PVO2 (3.6 +/- 0.4) were reduced. This enabled an assessment of the contribution of V/Q imbalance to the abnormal gas exchange on the condition. Haemodynamic and gas exchange measurements were made at rest, on supine exercise and on acute vasodilatation with intravenous prostacyclin in eight patients with pulmonary hypertension.
0 kommentar(er)
