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Gas Exchange in the Lungs
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
When a subject is standing upright, both ventilation and perfusion increase from apex to base because of gravity. Because blood is denser than air, the effect on perfusion is greater than the effect on ventilation (Figure 17.4), At the apex of the lung, alveoli have a high ventilation–perfusion ratio of 3.3, and at the base of the lung, alveoli have a low ventilation–perfusion ratio of 0.6. The overall ventilation–perfusion ratio in normal lungs is 0.8.
Thromboembolism
Published in Daryl Dob, Griselda Cooper, Anita Holdcroft, Philip Steer, Gwyneth Lewis, Crises in Childbirth Why Mothers Survive, 2018
Arterial oxygenation is also decreased. Obstruction in the pulmonary vasculature causes redistribution of pulmonary blood flow and increases the perfusion in those regions of the lung that are unaffected. If ventilation is unchanged, and blood flow increases, this results in a low ventilation/perfusion ratio in these areas. Decreased cardiac output due to right heart failure leads to decreased mixed venous oxygen saturation, exaggerating the effects of ventilation/perfusion mismatch in the lungs. Furthermore, an acute increase in right heart pressure may cause right-to-left intracardiac shunting through an unsuspected patent foramen ovale.28
Mismatch and Shunt
Published in Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod, The Primary FRCA Structured Oral Examination Study Guide 1, 2017
Lara Wijayasiri, Kate McCombe, Paul Hatton, David Bogod
The ventilation–perfusion ratio is the ratio between the amount of air getting to the alveoli (the alveolar ventilation, VA, in L/min) and the amount of blood entering the lungs (the cardiac output, Q, in L/min).
Endothelialitis plays a central role in the pathophysiology of severe COVID-19 and its cardiovascular complications
Published in Acta Cardiologica, 2021
Christiaan J. M. Vrints, Konstantin A. Krychtiuk, Emeline M. Van Craenenbroeck, Vincent F. Segers, Susanna Price, Hein Heidbuchel
Although incompletely defined, it appears that initially pneumonic infiltrates are relatively small and confined most often to subpleural segments. Microscopic study shows in this phase, Infiltration of alveolar walls by numerous lymphocytes and interstitial edema, the typical lesions of a viral pneumonia [27,28]. When requiring mechanical ventilation these patients have near-normal pulmonary compliance, a low ventilation-perfusion ratio with normal pulmonary artery pressures, and low lung recruitability, requiring low expiratory pressure [26]. The marked hypoxaemia that patients with this L-phenotype may show may be related to impaired regional pulmonary vasoreactivity with loss of the normal hypoxic vasoconstrictor response leading to an increased shunt fraction [26]. Further, a thrombotic micro-angiopathy [29,30] contributes significantly to the pathophysiology of the COVID-19 pulmonary infection: fibrin thrombi are present both in capillaries and small arterioles; there also is activation of megakaryocytes, possibly native to the lung, with platelet aggregation and platelet-rich clot formation, in addition to fibrin deposition [31,32]. Entrapment of neutrophils in fibrin nets may additionally contribute to vascular obstruction.
Acute respiratory distress syndrome (ARDS) caused by the novel coronavirus disease (COVID-19): a practical comprehensive literature review
Published in Expert Review of Respiratory Medicine, 2021
Francisco Montenegro, Luis Unigarro, Gustavo Paredes, Tatiana Moya, Ana Romero, Liliana Torres, Juan Carlos López, Fernando Esteban Jara González, Gustavo Del Pozo, Andrés López-Cortés, Ana M Diaz, Eduardo Vasconez, Doménica Cevallos-Robalino, Alex Lister, Esteban Ortiz-Prado
This phenotype has an early stage characterized by a pneumonitis-like presentation, with a mild inflammation limited to the subpleural interstitium [13]. A non-homogeneous areas of the lung appear with different elastic properties, characterized by ground-glass opacification with occasional consolidation under radiographic imaging [14]. However, CT scans of the lung in these patients confirm that there are no significant areas to recruit, and indeed type L manifests low recruitment, low elastance, with nominal compliance and low lung weight [10,11,13,15,16]. As hypoxemia is secondary to the alteration of the ventilation/perfusion ratio (V/Q), rather than an intrinsic problem of the pulmonary alveoli, the deviation of the flow toward poorly oxygenated alveolar units is considered a pulmonary vascular dysregulation [8,10–12,15]. This is possibly attributed to the affinity of SARS-CoV-2 for the receptor for angiotensin-converting enzyme 2 (ACE2) located on the surface of endothelial cells and arterial smooth muscle cells [17]. Under normal conditions, these receptors are important for the natural ability of the pulmonary vasculature to produce selective vasoconstriction in response to hypoxia [18].
The effect of posture and exercise on blood CO kinetics during the optimized carbon monoxide rebreathing procedure
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2023
Walter F. J. Schmidt, Torben Hoffmeister, Nadine B. Wachsmuth, William C. Byrnes
In addition to the role of increased central blood volume, an improved ventilation perfusion ratio might also facilitate a faster mixing time in the supine position. A change in posture from standing to supine causes a redistribution of blood flow in the direction of gravity, resulting in a more even distribution of blood flow in the lungs. Thereby, blood flow in the apical parts of the lung increases and blood flow in the basal parts of the lung decreases [20]. As a result, more areas of the lung participate in gas exchange, which should lead to better diffusion of CO from the lungs to the blood. However, in this study, higher COHb% cannot be detected in arterialized blood in the supine position, so this effect is unlikely to be important for CO rebreathing.