Nonpulmonary Influences on Gas Exchange

Abstract

There are several determinants governing arterial and mixed venous blood PO2 and PCO2. Ventilation-perfusion imbalance, increased intrapulmonary shunt, and diffusion limitation to oxygen encompass the pulmonary factors. Alternatively, inspired oxygen concentration, overall ventilation, cardiac output, and oxygen consumption (uptake) are contemplated as the four most influential nonpulmonary determinants. All three pulmonary factors plus oxygen uptake cannot be directly modulated, but all the other remaining nonpulmonary determinants are. Inspired oxygen concentration, the amount and pattern of total ventilation, and cardiac output may be, at least in part, relatively well clinically controlled. Arterial PO2 (PaO2) may fall if inspired PO2, overall ventilation, and/or cardiac output decrease, and/or oxygen consumption increases, even though the pulmonary factors remain unchanged. Conversely, if inspired oxygen fraction, ventilation, and/or cardiac output increase, and/or oxygen consumption decreases, PaO2 may improve regardless of the changes operated at the level of the pulmonary determinants. Several pathophysiologic features deserve to be underlined. First, the importance of understanding the role played by mixed venous PO2 as a vital nonpulmonary determinant governing PaO2. Second, the response to 100% oxygen breathing repeatedly exhibits a consistent amount of agreement in the main findings. Third, there is always an interactive interplay between pulmonary and nonpulmonary determinants of PaO2 and arterial PCO2 (PaCO2) in any respiratory disease state following the use of pharmacologic or nonpharmacologic approaches. All in all both PaO2 and PaCO2 become the end-point outcomes of the complex interaction of pulmonary and nonpulmonary factors modulating pulmonary gas exchange. This needs to be unraveled to improve the understanding and management of most acute and chronic respiratory disease states.

Can the Lung be Obese? The Effects of Bariatric Surgery on Lung Function and Imaging

“…Importantly, the critical difference in the obese pulmonary vasculature response is plausibly related to the distinct effects of 100% oxygen breathing. In severe obesity, hypoxic pulmonary vasoconstriction is not reversed during BARCELONA RESPIRATORY NETWORK hyperoxic breathing, at variance with the usual release of hypoxic pulmonary vasoconstriction observed in chronic respiratory or liver disease states 49,54 . As alluded to above, this is likely due to the presence of increased perivascular adipose tissue, with changes in extra-vascular lung water (see below), related to the underlying low-grade chronic systemic and lung inflammation 41,55 .…”

“…acute lung conditions and those with chronic obstructive airway diseases. Like in individuals with extreme obesity, patients with acute respiratory state diseases always significantly increase intrapulmonary shunt during hyperoxic conditions, while the redistribution of pulmonary blood flow remains unaltered; by contrast, those affected by chronic obstructive airway disease (i.e., COPD) always increase the blood flow dispersion distribution, without accompanying changes in the intrapulmonary shunt component, usually discrete under basal conditions, as shown in numerous gas exchange studies 49 . In obese subjects there is an accumulation of adipose tissue in the vascular walls of the systemic circulation, and even perhaps in the pulmonary vascular bed.…”

“…Under conditions of hyperoxia, it has been consistently shown that low inspired ventilation-perfusion ratios, named "critical", become unstable and may ultimately collapse, thereby resulting in the development of reabsorption atelectasis 48 . Similarly, the simultaneous increases in mixed venous PO 2 also observed in morbid obese individuals during oxygen breathing facilitate the reduction of the pulmonary vascular tone 49 . Overall these findings may well reflect the presence of more rigid and fixed pulmonary vessels due to increased systemic (and perhaps pulmonary) inflammation in the context of an altered perivascular adipose tissue-induced endothelial dysfunction, already demonstrated in the cutaneous circulation 50 .…”

Ventilation–perfusion heterogeneity measured by the multiple inert gas elimination technique is minimally affected by intermittent breathing of 100% O 2

“…In COPD, it has been shown that the degree of collateral ventilation increases with disease severity (Hogg, Macklem, & Thurlbeck, 1969) and this increase in collateral flow potentially counteracts the development of absorption atelectasis and increase shunt (Barberà et al, 1996;Santos et al, 2000). In some COPD subjects, hyperoxia worsens V A ∕Q matching resulting in an increase in the number of low V A ∕Q units but with little or no increase in shunt (Barberà et al, 1996;Rodriguez-Roisin, 2014;Santos et al, 2000). This is the case for the majority of subjects in the present study, and the reversibility argues against atelectasis as a mechanism.…”

Padrão hemodinâmico tardio (> 2 anos) e vasodilatação intrapulmonar, antes e após tratamento cirúrgico da hipertensão portal secundária à forma hepatoesplênica da esquistossomose mansônica: análise comparativa entre desconexão ázigo-port

“…Este fato pode ser explicado pela utilização de diferentes métodos diagnósticos nos pacientes com hipertensão portal de origem cirrótica ou não. Alguns autores 64,65,66,67 utilizaram a cintilografia pulmonar com albumina marcada, cujo diâmetro das partículas é superior a 20 µm, enquanto outros adotaram a técnica de ecocardiografia contrastada, através da utilização de solução salina a 0,9% 60,62,63,68,69 60,61,63,64 , enquanto outros, do quarto ao sexto 68,71 . Alguns autores 72,73,74 identificaram em pessoas sadias o aparecimento de VIP durante esforço físico, com desaparecimento completo após repouso.…”