Accurate measurements of arterial P CO 2 (P a,CO 2 ) currently require blood sampling because the end-tidal P CO 2 (P ET,CO 2 ) of the expired gas often does not accurately reflect the mean alveolar P CO 2 and P a,CO 2 . Differences between P ET,CO 2 and P a,CO 2 result from regional inhomogeneities in perfusion and gas exchange. We hypothesized that breathing via a sequential gas delivery circuit would reduce these inhomogeneities sufficiently to allow accurate prediction of P a,CO 2 from P ET,CO 2 . We tested this hypothesis in five healthy middle-aged men by comparing their P ET,CO 2 values with P a,CO 2 values at various combinations of P ET,CO 2 (between 35 and 50 mmHg), P O 2 (between 70 and 300 mmHg), and breathing frequencies (f ; between 6 and 24 breaths min −1 ). Once each individual was in a steady state, P a,CO 2 was collected in duplicate by consecutive blood samples to assess its repeatability. The difference between P ET,CO 2 and average P a,CO 2 was 0.5 ± 1.7 mmHg (P = 0.53; 95% CI −2.8, 3.8 mmHg) whereas the mean difference between the two measurements of P a,CO 2 was −0.1 ± 1.6 mmHg (95% CI −3.7, 2.6 mmHg). Repeated measures ANOVAs revealed no significant differences between P ET,CO 2 and P a,CO 2 over the ranges of P O 2 , f and target P ET,CO 2 . We conclude that when breathing via a sequential gas delivery circuit, P ET,CO 2 provides as accurate a measurement of P a,CO 2 as the actual analysis of arterial blood. Accurate measurement of arterial P CO 2 (P a,CO 2 ) is important for the clinical assessment of patients and, in physiological studies, for the assessment of control of breathing and cerebral blood flow. Currently, the reference standard for measuring P a,CO 2 is analysis of arterial blood via direct arterial puncture. This invasive approach has a number of disadvantages for both the subject (discomfort and potential arterial wall damage) and investigator (restricted mobility of the catheter insertion site, cost, time delay for blood analysis, and limited temporal resolution of changes in P a,CO 2 ). As a result, investigators have long sought a suitable non-invasive method to measure P a,CO 2 .Non-invasive methods of predicting P a,CO 2 from alveolar P CO 2 (P A,CO 2 ) consider the lung to be a tonometer in which CO 2 equilibrates between alveolar gas and capillary blood. In reality, however, the lung is not a single homogeneous time-invariant gas exchange compartment. Rather, P CO 2 varies in different regions of the lung as a result of differences in ventilation-to-perfusion matching (V A /Q ) throughout the lung and, in each lung region, throughout the respiratory cycle (Dubois et al. 1952;Lenfant, 1967). The contribution to the P a,CO 2 of blood passing each alveolus reflects the average P CO 2 in that alveolus during the respiratory cycle (Jones et al. 1979;Robbins et al. 1990). P a,CO 2 , then, reflects the timeand flow-weighted averages of all alveolar ventilatory fluctuations in allV A /Q regions throughout the lung, i.e. the mean P A,CO 2 (Lenfant, 1967). As a result, the r...
COVID-19 has caused great devastation in the past year. Multi-organ point-of-care ultrasound (PoCUS) including lung ultrasound (LUS) and focused cardiac ultrasound (FoCUS) as a clinical adjunct has played a significant role in triaging, diagnosis and medical management of COVID-19 patients. The expert panel from 27 countries and 6 continents with considerable experience of direct application of PoCUS on COVID-19 patients presents evidence-based consensus using GRADE methodology for the quality of evidence and an expedited, modified-Delphi process for the strength of expert consensus. The use of ultrasound is suggested in many clinical situations related to respiratory, cardiovascular and thromboembolic aspects of COVID-19, comparing well with other imaging modalities. The limitations due to insufficient data are highlighted as opportunities for future research.
Both hypoxia and carbon dioxide increase cerebral blood flow (CBF), and their effective interaction is currently thought to be additive. Our objective was to test this hypothesis. Eight healthy subjects breathed a series of progressively hypoxic gases at three levels of carbon dioxide. Middle cerebral artery velocity, as an index of CBF; partial pressures of carbon dioxide and oxygen and concentration of oxygen in arterial blood; and mean arterial blood pressure were monitored. The product of middle cerebral artery velocity and arterial concentration of oxygen was used as an index of cerebral oxygen delivery. Two-way repeated measures analyses of variance (rmANOVA) found a significant interaction of carbon dioxide and hypoxia factors for both CBF and cerebral oxygen delivery. Regression models using sigmoidal dependence on carbon dioxide and a rectangular hyperbolic dependence on hypoxia were fitted to the data to illustrate this interaction. We concluded that carbon dioxide and hypoxia act synergistically in their control of CBF so that the delivery of oxygen to the brain is enhanced during hypoxic hypercapnia and, although reduced during normoxic hypocapnia, can be restored to normal levels with progressive hypoxia.
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