Alveolar-Capillary Oxygen Disequilibrium in Hepatic Cirrhosis

doi:10.1378/chest.73.4.507

Chest

Volume 73, Issue 4, April 1978, Pages 507-511

https://doi.org/10.1378/chest.73.4.507 Get rights and content

Hypoxemia is a frequent occurrence in patients with severe hepatic disease. Multiple mechanisms have been implicated in the production of such hypoxemia. The case of a 35-year-old man with cyanosis, clubbing, and cirrhosis is presented. Physiologic data from this patient revealed normal pulmonary function, except for a low diffusing capacity and a 28 percent shunt while the patient was breathing 100 percent oxygen. A perfusion scan with radioactive ^99mtechnetium-labelled macroaggregated albumin revealed 67 percent of the labelled macroaggregated albumin in the systemic circulation. Postmortem examination demonstrated normal pulmonary parenchyma, markedly dilated intraparenchymal capillaries and arterioles, subpleural angiomata, and cirrhosis. No anatomic arteriovenous connections were demonstrated before or after death. We conclude that the arterial hypoxemia of some patients with hepatic cirrhosis results from dilated gas-exchanging blood vessels. These widened vessels prevent end pulmonary capillary oxygen tension from reaching equilibrium with alveolar gas, perhaps because of the widened distance for diffusion.

Section snippets

CASE REPORT

A 35-year-old white man first came to medical attention in August 1966, when he was admitted to the Jewish Hospital of St. Louis with fatigability, bruisability, petechiae, and splenomegaly. A chest x-ray film and the results of routine laboratory examinations were within normal limits. The only abnormal laboratory data noted were a white blood cell count (WBC) of 1,450/cu mm, a platelet count of 10,000/cu mm, and a prothrombin time of 16 seconds (40 percent of control). A splenectomy was

DISCUSSION

Although hypoxemia is not uncommon in cirrhosis, it appears to us that patients with cirrhosis and hypoxemia may be separated into two types, depending upon the clinical presentation and the severity of the hypoxemia. The majority of patients with hepatic disease who have mild arterial hypoxemia constitute type 1. They develop a minimal decrease in arterial oxygen saturation (SaO₂), which causes little, if any, symptoms. The hypoxemia is probably best explained by the proposal of Ruff et al,²

ACKNOWLEDGMENT

We are grateful to Burton A. Shatz. M.D., for allowing us to study and report the findings from his patient, and to Mr. David A. Sinks for his technical assistance.

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: Manuscript received May 27; revision accepted July 27.

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Chest

Alveolar-Capillary Oxygen Disequilibrium in Hepatic Cirrhosis

Section snippets

CASE REPORT

DISCUSSION

ACKNOWLEDGMENT

J Pediatr

Am Heart J

The cause of hyperventilation and arterial hypoxia in patients with cirrhosis of the liver

Am J Med Sci

Regional lung function in patients with hepatic cirrhosis

J Clin Invest

Hypoxaemia and cirrhosis of the liver

Thorax

Lung perfusion scanning in hepatic cirrhosis

Br Med J

Systemic circulatory adjustments in hepatic disease

Med Clin North Am

Multiple pulmonary arteriovenous fistulas in juvenile cirrhosis

Am J Med

Arterial changes in the lungs in cirrhosis of the liver: Lung spider nevi

N Engl J Med