MECHANISMS OF GAS EXCHANGE IMPAIRMENT IN PATIENTS WITH LIVER CIRRHOSIS
Section snippets
GAS EXCHANGE AT REST
A wide variety of diseases can interfere with resting pulmonary gas exchange and cause arterial hypoxemia in patients with cirrhosis.3, 68, 76 First, these patients often smoke, so airway disease is not rare.3, 68, 76 Second, patients with alcoholic cirrhosis may develop repeated episodes of pneumonia, which may damage the pulmonary parenchyma significantly.3, 68, 76 Third, ascites and, less frequently, pleural effusion can restrict alveolar ventilation and interfere with gas exchange.1, 35, 135
GAS EXCHANGE DURING EXERCISE
The analysis of the pulmonary circulation and gas exchange during exercise in patients with cirrhosis also has contributed to our understanding of the mechanisms underlying HPS. In 1989, Agusti et al6 used the MIGET to study six patients with cirrhosis and mild hypoxemia, both at rest and during steady state, submaximal (70% maximal O2 uptake [Vo 2]) exercise. The more conspicuous findings of this study6 were: (1) During exercise, Vo 2 is similar to that seen in healthy subjects cycling at a
PATHOGENESIS OF THE GAS EXCHANGE ABNORMALITY IN CIRRHOSIS
Whether the precise mechanisms that underlie the vascular systemic and pulmonary disturbances in HPS are related to failure of metabolism, insufficiency of production of one or several circulating vasoactive substances by the damaged liver cells, or altered metabolism of some of the recently discovered paracrine factors synthesized by endothelial cells152 remains elusive. To date a large body of potential circulating humoral vasodilators, including glucagon and prostacyclin, has been detected,
Medical Strategies
The hypothesis that abnormal pulmonary gas exchange in patients with HPS is related to underlying vascular abnormalities in the lung111 has prompted numerous experimental trials using either vasoactive drugs or different medical treatments aiming to increase the pulmonary vascular tone. Although anecdotal beneficial effects on arterial oxygenation have been described, overall therapeutic consequences cannot be derived from these studies.
Almitrine bismesylate has been reported to enhance hypoxic
SUMMARY
This article reviews the basic pathophysiologic mechanisms underlying the abnormal pulmonary gas exchange often seen in patients with cirrhosis. To summarize, the following keypoints seem appropriate: (1) Patients with cirrhosis have a low pulmonary vascular tone characterized by a poor or absent hypoxic pressor response. This results in a marked dilation of the pulmonary vasculature. (2) This abnormal pulmonary vascular tone, independently of airway disease, causes Va /Q mismatch and mild to
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2019, Clinics in Liver DiseaseCitation Excerpt :ET-1 may also play a role in human disease, as it was shown in a single study in which blood levels of ET-1 in the hepatic vein were higher in patients with cirrhosis with IPVD and HPS compared with those without IPVD, and blood ET-1 levels correlated with the degree of bile duct proliferation in the corresponding liver biopsy specimens.136 The pulmonary vasculature in patients with cirrhosis has been demonstrated to have decreased pulmonary vascular tone with a poor or absent hypoxemic vasoconstrictor response.137–139 The capillary network is the choke point in the pulmonary circulation, with a normal diameter of between 8 and 15 μm.
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2016, Anesthesiology ClinicsCitation Excerpt :Therefore, hypoxemia evolves with liver disease progression from a principally restrictive process to a combination of restrictive as well as obstructive processes.6 Although the physiology of portal hypertension has been widely recognized, the physiologic changes induced on pulmonary vascular tone through hepatic vasoactive mediators are increasingly recognized as a significant contribution to VQ imbalance.5 As cardiac output and circulating blood volumes increase, systemic venodilation increases blood flow through the pulmonary circulation.
Recumbent deoxygenation in mild/moderate liver cirrhosis: The "clinodeoxia". The ortho-clino paradigm
2014, Respiratory MedicineCitation Excerpt :In any case, to correctly frame the extent of the hypoxemia, we highlight that the study population was recruited in Bisaccia village, which is elevated 2820 feet above sea level. As demonstrated by multiple inert gas elimination techniques [27–29], the three main mechanisms leading to hypoxemia in liver cirrhosis are ventilation-perfusion mismatch, alveolar capillary limitation of oxygen diffusion (so called “diffusion-perfusion defect”) and, rarely, true intrapulmonary shunts. At least two of this mechanisms are operating in our study population.
Abnormal hyperventilation in patients with hepatic cirrhosis: Role of enhanced chemosensitivity to carbon dioxide
2012, International Journal of Cardiology
Address reprint requests to, Alvar GN Agusti, MD, Servei Pneumologia, Hospital Universitari Son Dureta, c/ Andrea Doria 55, 07014 Palma Mallorca, Spain
This article is supported in part by ABEMAR, the Comissio de Universitats i Recerca de la Generalitat (GRQ 94-9103) and grants 94/986, 95/544, and 95/752 from the Fondo de Investigacion Sanitaria (FIS).
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From the Pulmonary Service, Hospital Universitari Son Dureta; Department of Fundamental Biology and Health Sciences, Universitat Illes Balears, Mallorca (AGNA); and Servei Pneumologia i Al.lergia Respiratoria, Department of Medicine, Hospital Clinic, Barcelona University, Barcelona (JR, RR-R), Spain