Arterial Blood Gases and Acid-Base Balance in Cyanotic Congenital Heart Disease 1

Morse, Minerva; Cassels, Donald E.

doi:10.1172/jci102800

Cited by 19 publications

(7 citation statements)

References 9 publications

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“…These findings are in keeping with those of Bing et al (1948) and Morse and Cassels (1953). (b) On exercise.…”

Section: Resultssupporting

confidence: 92%

“…The PC02 values found in the patients, as in those of Campbell, Hunt, and Poulton (1923), were lower than those usually seen under similar conditions in normal subjects and in others without central cyanosis. It would be tempting to relate this to the fact that there is in most of them a lowered arterial oxygen tension, since hypox'emia has been so widely held to be responsible for hyperventilation and consequent hypocapnia (Morse and Cassels, 1953). However, on examining the relation of the arterial oxygen to the CO2 levels, it is clear that the more cyanosed patients do not in fact have the lower values of PCo2 (Table III and Fig.…”

Section: Resultsmentioning

confidence: 99%

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Dyspnoea in Cyanotic Congenital Heart Disease

Davies¹,

Gazetopoulos²

1965

Heart

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“…These findings are in keeping with those of Bing et al (1948) and Morse and Cassels (1953). (b) On exercise.…”

Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

Dyspnoea in Cyanotic Congenital Heart Disease

Davies¹,

Gazetopoulos²

1965

Heart

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“…It would not be unexpected that the persistence of such hypoxia over a long period would lead to polycythemia. Finally, from the report of similar findings in a patient with diffuse disease of the central nervous system but without intrinsic pulmonary disease (24) would offer no explanation for the CO2 retention observed (11,25).…”

Section: Measurementsmentioning

confidence: 94%

Clinical and Physiological Aspects of a Case of Obesity, Polycythemia and Alveolar Hypoventilation

Jh¹,

Cook²,

Ad³

1955

J. Clin. Invest.

151

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The occurrence of arterial hypoxia with polycythemia usually results from some known type of pulmonary disease or from an abnormal communication between the right and left sides of the circulation. Although arterial oxygen unsaturation has been observed in patients with polycythemia vera (1)(2)(3)(4) Physical examination revealed an alert, cyanotic, slightly orthopneic man who weighed 290 pounds and was 67 inches in height. A few rales were heard at the right posterior lung base. The heart was in gallop rhythm, and the pulmonic second sound was accentuated. Mild edema of the abdominal wall and marked edema of the lower extremities was present.The significant laboratory findings were as follows: red blood cells 6.77 million per cu. mm.; hemoglobin 20 gm. per cent; hematocrit 69 per cent; white blood cells 6,000 per cu. mm. with a normal differential count and normal cellular morphology; platelets 150,000 per cu. mm. The bone marrow showed hyperplasia of the erythroid series, and reticulocytes were 1 per cent of the red blood cells. The blood uric acid was 9.6 mg. per cent. The urinary 17-ketosteroid excretion was 8 mg. in twenty-four hours (normal). X-ray of the chest showed cardiac enlargement and enlargement of the pulmonary vessels. Angiocardiography showed filling of the cardiac chambers in normal sequence. The sella turcica appeared normal by X-ray. An electrocardiogram showed evidence of right ventricular hypertrophy.

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“…These questions concerned the possibility that the increased viscosity of polycythemic blood might prevent proper diffusion of oxygen in the alveolarcapillary system, resulting in arterial oxygen unsaturation, the characteristics of the oxyhemoglobin dissociation curve in polycythemia vera, since this has been found shifted to the right in the blood of patients with cyanotic congenital heart disease (1), and the relation of a low CO2 content and combining power to polycythemia, since these were observed to be low in the secondary polycythemia of congenital heart disease (2)(3)(4).…”

mentioning

confidence: 99%