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Blood flow redistribution and ventilation-perfusion mismatch during embolic A model of oxygen transfer from air to blood was included to assess the impact of. Hypoventilation (ventilation/perfusion ratio Oxygen responsive. Neurogenic. Anesthesia, head trauma, central nervous system neoplasia, edema. The ventilation-perfusion ratio is exactly what you think it should be - the ratio oxygen in to /removing CO2 from the alveoli) and the perfusion (removing O2.
Ventilation/perfusion ratio - Wikipedia
To summarize, this model includes the following. Diameters were defined using a Strahler-diameter ratio.Lung Anatomy and Physiology - Gas Exchange in the Lungs Respiration Transport Alveoli Nursing
Third, it includes a model of parenchymal tissue deformation under gravity,[ 19 ] to which the vascular networks are tethered. These values were used for all simulations unless otherwise stated. By solving equations for Poiseuille resistance including gravity, conservation of mass, vessel elasticity, and a microcirculatory model see Multiscale Model and Clark et al. Emboli vary in size and shape, and an embolus traveling into the lung via the pulmonary trunk could deposit in numerous locations.
Studying the relationship between embolic arterial obstruction, PAP, and hemodynamics therefore first requires assessment of the likely distribution of emboli.
All potential sites and their probability of occlusion were calculated for three sizes of emboli 5, 7, or 10 mm radius. The probability of occlusion was assumed to be proportional to the baseline flow rate to the occluded vessel i. The emboli were assumed to occlude the first vessel that they encountered that was smaller in radius than the embolus, and they did not deform within the artery. Flow distribution was simulated for each site of occlusion.
To quantify the relationship between volume of obstructed tissue and hemodynamic outcomes in the model, emboli of a single size either 5, 7, or 10 mm radius were added cumulatively in random order and flow distribution re-calculated, until there were emboli in blood vessels that feed nearly all capillary beds.
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The number of acini distal to the occlusion and PAP were recorded. Lung occlusion was defined as the percentage of acinar units distal to occlusions relative to total number of acini. To assess the impact of obstruction on microcirculatory flow in the unobstructed tissue, for the 10 mm simulations the capillary sheet flow-rate, capillary pressures, and capillary recruitment were calculated.
To quantify the relationship between PAP and cardiac output in the PE model, simulations were repeated for increased cardiac output. Oxygen transfer from air to blood was estimated using a simple model based on Kapitan and Hempleman[ 26 ] describing oxygen O2 partial pressure balance in each acinus.
For post-occlusion simulations retaining PvO2 at 40 mmHg assumes that oxygen uptake in the systemic circulation adapts reduces and so this will likely overestimate oxygen partial pressures. More likely, oxygen consumption by the body remains close to baseline levels and PvO2 reduces; therefore, lower values of 30 mmHg and 20 mmHg were also considered in simulations.
This assumption is likely to be valid except at very high levels of occlusion as discussed later. The ventilation-weighted sum of PAO2 was calculated as an estimate of expired O2 partial pressures from the full lung.
As most capillary O2 is bound to Hemoglobin, to calculate arterial pulmonary venous O2 partial pressures PCO2 was converted to O2 content CCO2 and an acinar perfusion-weighted sum of CCO2 was calculated before conversion back to partial pressure units. The lowest part of the lung in relation to gravity is called the dependent region.
In the dependent region smaller alveolar volumes mean the alveoli are more compliant more distensible and so capable of more oxygen exchange. The apex, though showing a higher oxygen partial pressure, ventilates less efficiently since its compliance is lower and so smaller volumes are exchanged. Perfusion[ edit ] The impact of gravity on pulmonary perfusion expresses itself as the hydrostatic pressure of the blood passing through the branches of the pulmonary artery in order to reach the apical and basal areas of the lungs, acting respectively against or synergistically with the pressure developed by the right ventricle.
Thus at the apex of the lung the resulting pressure can be insufficient for developing a flow which can be sustained only by the negative pressure generated by venous flow towards the left atrium or even for preventing the collapse of the vascular structures surrounding the alveoli, while the base of the lung shows an intense flow due to the higher resulting pressure. Excretion of carbon dioxide is also impaired, but a rise in the arterial partial pressure of carbon dioxide paCO2 is very uncommon because this leads to respiratory stimulation and the resultant increase in alveolar ventilation returns paCO2 to within the normal range.
These abnormal phenomena are usually seen in chronic bronchitisasthmahepatopulmonary syndromeand acute pulmonary edema. Because of the increased dead space ventilation, the PaO2 is reduced and thus also the peripheral oxygen saturation is lower than normal, leading to tachypnea and dyspnea. This finding is typically associated with pulmonary embolism where blood circulation is impaired by an embolus. Ventilation is wasted, as it fails to oxygenate any blood.