Browsing by Author "Lewis, C. M."
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- ItemKoronere bloedvloei en miokardiale energiemetabolisme by geisoleerde linker en regter ventrikulere hipertrofie(Stellenbosch : Stellenbosch University, 1967) Lewis, C. M.; Stellenbosch University. Faculty of . Dept. of .
- Item'n Nie-indringende benadering tot pulmonere hemodinamika(HMPG, 1981-08) Lewis, C. M.; Stewart, R. I.Currently available investigative methods employed in the evaluation of the pulmonary circulation involve cardiac catheterization and, in respect of exercise determinations, only supine data have been recorded. Consequent upon a 3-year study of pulmonary haemodynamics and gas exchange at rest and during exercise on the treadmill in patients with chronic hypoxaemic lung disease, correlations have been established which accurately characterize the venous admixture (Q(VA)/Q(t), the quantitative expression of hypoxaemia), cardiac output and pulmonary artery pressure (PA), permitting the prediction of these variables in the erect posture. The employment of fibre-optic oximetry obviates the need for arterial cannulation. The relevant regression formulae are as follows: Q(VA/Q(t) = 8,85 x In (Hb (100 - SaO2) x heart rate/VO2 - 3,66 (r = 0.97; SEE = 2,43) PA(m) (resting) = 0,4516 (Q(VA/Q(t)) + 8,2 (r = 0,90; SEE = 2,7) PA(m) (exercise) = 1,453 (Q(VA)/Q(t)) + 3,8 (r = 0,96; SEE = 4,0) Cardiac output may be derived directly from VO2 and the known components of Q(VA)/Q(t), and total pulmonary vascular resistance in turn from Qt and PAm. Direct comparison of the predicted values derived by this means with actual determinations yielded no systematic differences. The clinical application of these principles ensures reliable estimates of haemodynamic variables, without resort to invasive techniques, during free movement and graded exercise testing.
- ItemVentilation during steady-state exercise in patients with chronic obstructive pulmonary disease : a preliminary study(Health & Medical Publishing Group, 1985) Stewart, R. I.; Lewis, C. M.In this preliminary study 20 patients with chronic obstructive pulmonary disease (COPD) walked on the treadmill until symptoms limited further exercise. When minute volume exceeded 60% of the predicted maximum breathing capacity the arterial carbon dioxide partial pressure was frequently low, thus indicating hyperventilation; the arterial oxygen partial pressure also declined on exercise. In only 2 patients was there alveolar hypoventilation. Although other factors may be operative, the hyperventilation in some patients with COPD may be induced by an exertional decline in alveolar oxygen partial pressure. In 4 patients the exercise tidal volume exceeded the resting inspiratory capacity, indicating a decline in functional residual capacity and increased work of breathing. It is concluded that there is a need further to assess patients with COPD in respect of the association between exertional dyspnoea, alveolar ventilation and lung mechanics.