Smoking and chronic respiratory disease: finding in surveys carried out in 1957 and 1966 in Staveley in Derbyshire, England.

نویسندگان

  • I T Higgins
  • M W Higgins
  • J C Gilson
  • H Campbell
  • W E Waters
  • B G Ferris
چکیده

either group. In 8 of the 32 individuals (4 with COPD and 4 without) the changes in V/Q were of sufficient magnitude to cause a significant decrease in PaOz, averaging 10.4 mm Hg decrease immediately after smoking; there were no changes in PaCO:! or pH. In six of these eight, the response was primarily in the airways as indicated by increased A-a, Q S / Q ~ and alveolar shunting. In two of the eight, the response was primarily vascular as judged by an increase in physiologic dead space, wasted ventilation, alveolar dead space and a decrease in the effective gas exchange compartment of the lungs. An additional six patients with COPD were studied to determine the effect of cigarette smoking on levels of carboxyhemoglobin and cardiac output. Smoking one cigarette increased the carboxyhemoglobin from an average of 4.26 percent to 5.36 percent. Three of the subjects had a mean decrease of 1.1 L/minute in cardiac output and three a mean increase of 2.21 L/minute as a result of smoking. If we assume an individual with a presmoking Pa02 of 70 mm and 14 grams of hemoglobin he will sustain a decrease of 7 ml/L in 0 2 if his Pa02 drops by 10 mm Hg as seen in our eight hypoxia responding patients, an additional loss of 16.13 ml/L due to carboxy hemoglobin and 4.2 ml/liter due to leftward displacement of the oxyhemoglobin dissociation curve. This is a net loss of 27.33 ml of O2/L of blood or 15 percent. A mean decrease of 1.1 L/minute in cardiac output will further decrease oxygen delivery by 161 ml Oz/minute. In some instances, significant decrease in 0 2 delivery for cellular metabolism can result from smoking.

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عنوان ژورنال:
  • Chest

دوره 59  شماره 

صفحات  -

تاریخ انتشار 1971