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Biomedical subjects

A C Powles

Publications and source records attributed to A C Powles.

36 records · Page 2Linked to original sources
PubMed1981

The effect of drugs on the cardiovascular response to exercise.

Anti-hypertensives, diuretics, digitalis, beta-blockers, nitrates, anti-arrhythmics, and psychiatric drugs are reviewed for their effects on the cardiovascular response to exercise, in particular work capacity, heart rate, blood pressure, anginal threshold, and exertional arrhythmias. The limitations of these measurements to assess changes in the various aspects of cardiovascular performance in the presence of drugs becomes evident, emphasizing the need for an understanding of the relationship between drug effects on specific target organs and the altered integrated exercise response. The variable response of individuals to drug therapy, depending on the pathophysiological effects of their disease, demonstrates the value of exercise testing in selecting optimal drug regimens.

Adrenergic beta-Antagonists↗
PubMed1980

Retinal studies at 446 torr in a hypobaric chamber.

This study was designed to see if retinal haemorrhage occurred after 24 h of decompression to a pressure of 446 torr. Four subjects were studied after 24 h of decompression and had retinal photography and fluorescein angiography performed at rest and following maximum exercise. No haemorrhages or fluorescein leakage was noted, even though the subjects experienced typical symptoms of acute mountain sickness and showed an increase in lung density-consistent with subclinical pulmonary edema. We conclude that 24 h exposure to 446 torr with a period of maximal exercise is an inadequate stress, either in time and/or degree, of hypoxia to produce retinal haemorrhage or leakage, as measured by flourescein.

Adult↗
PubMed1979

How to be less invasive.

Unless cardiac output is reduced, alveolar ventilation can be monitored without arterial blood gas analysis by estimating arterial carbon dioxide tension (PaO2) from rebreathing measurement of mixed venous carbon dioxide tension (PvCO2) (PaCO2 = 0.8 PvCO2). If cardiac output is reduced, the PvCO2 - PaCO2 difference increases, reflecting the increased venoarterial carbon dioxide (CO2) content difference (Fick principle). A reduction in cardiac output can thus be quantified without catheterization of the central circulation by measuring both PaCO2 and PvCO2. The significance of such a reduction in cardiac output for oxygen (O2) delivery to tissues is determined by calculation of mixed venous O2 saturation (SvO2), using the inter-relationship of CO2 production to O2 consumption. With normal arterial oxygenation (SaO2) and hemoglobin concentration, PaCO2 less than 0.8 PvCO2 - 12 implies a reduction in cardiac output such that SvO2 is less than 33 per cent, which indicates inadequate O2 delivery to tissues. Ear oximetry and rebreathing measurement of PvCO2 are simple, noninvasive, bedside techniques.

Carbon Dioxide↗
PubMed1979

Reduced heart rate response to exercise in ischemic heart disease: the fallacy of the target heart rate in exercise testing.

When exercise testing 159 patients with prior myocardial infarction, we identified 39 who were limited by fatigue. This group was all in sinus rhythm; none were taking drugs likely to impair the chronotropic response of the heart; none experienced chest pain or developed ischemic ECG changes. In 18 of this group, maximal heart rate achieved with exercise was 2SD or more below the age predicted value, and their heart rate response to exercise was reduced compared to that of the other 21 whose maximal exercise heart rates were within 2SD of age predicted values. A subgroup of 8 subjects with reduced exercise heart rates was studied before and after vagal blockade. In the 4 subjects whose infarction was inferior, the reduction in heart rate response was more profound and persisted after vagal blockade, suggesting either reduced pacemaker responsivness, due to ischemia or infarction, or autonomic imbalance as possible mechanisms. All 8 showed alinear increases in ventilation at higher power outputs and mean blood lactate postexercise was 7.5 mM/I without vagal blockade. Our findings suggest that a reduced heart rate response to exercise, already shown to imply added coronary risk, may be subdivided aetiologically and possibly prognostically. The use of a "Target Heart Rate" in such patients offers no safety margin, and maximal exercise capacity will be grossly over-estimated if extrapolated from the submaximal heart rate response. A cardiovascular limitation to exercise may be detected by an alinear increase in ventilation.

Adult↗
PubMed1979

Interpretation of blood gas analysis by physicians in a community teaching hospital.

Forty-two interns and residents on the staff of a community teaching hospital were questioned to assess their understanding of blood gas abnormalities. Misunderstandings were such that 24% of the residents and interns might have given inadequate care had their interpretations dictated practice. Few therapeutic misadventures in fact occurred, largely because of supervision. Even without supervision, it is unlikely that much harm would have come about, partly because pattern recognition and rules of thumb provided adequate guidance and partly because no notice was taken of the results of the blood gas analysis anyway. Those who wish to promote rational practice should direct their educational efforts to improved understanding of the mechanisms of hypoxaemia and of the chemical, physiological and pathophysiological interactions of PCO2, bicarbonate and pH in the various acid-base disorders.

Blood Gas Analysis↗
PubMed1978

An improved rebreathing method for measuring mixed venous carbon dioxide tension and its clinical application.

The mixed venous carbon dioxide tension (PVCO2) can be measured at the bedside by a rebreathing equilibrium technique that is quick, simple and noninvasive. Only one brief period of rebreathing is required. The technique is accurate even when the lungs are not normal, and gives a graphic record that allows verification of the accuracy of the estimate. The PVCO2 is affected mainly by changes in alveolar ventilation and cardiac output. It can be measured instead of the arterial carbon dioxide tension (PACO2) to follow changes in alveolar ventilation when the cardiac output is normal (PaCO2 = 0.8 PVCO2). When the cardiac output is abnormal, measurement of both PaCO2 and PvCO2 is useful in determining how much the cardiac output is reduced. Consideration of the relation between oxygen consumption and carbon dioxide production suggests that the equation PaCO2 = 0.8 PVCO2 - 12 indicates a reduction in cardiac output that may impair the oxygen supply to tissues. Simple corrections can be applied to allow for variations in arterial oxygen saturation and hemoglobin concentration that will affect this relationship.

Blood Gas Analysis↗
PubMed1978

Primary alveolar hypoventilation treated with nocturnal electrophrenic respiration.

A case of primary alveolar hypoventilation is described. Despite characteristic clinical findings, the diagnosis was delayed for 4 years. Alleviation of nocturnal hypoxemia and hypercapnia initially by a rocking bed and subsequently by phrenic nerve stimulation was accompanied by reversal of cor pulmonale and polycythemia. Electrophrenic respiration is an effective form of long-term management in primary alveolar hypoventilation.

Carbon Dioxide↗
PubMed1976

Arterial oxygenation and carbon dioxide tensions in the production of hypoxic electroencephalographic changes in man.

1. To investigate the interaction of hypoxaemia and blood PCO2 in the production of cerebral hypoxia, we studied six healthy men in whom acute progressive hypoxia was induced by using a rebreathing technique, while the PCO2 was kept constant. 2. At least two blood PCO2 tensions were studied in each subject. Arterial oxygen saturation was monitored continuously by ear oximetry, calibrated for each subject with arterialized blood. The onset of cerebral hypoxia was identified by the appearance of frontal slow waves (less than 5 Hz) in the electroencephalogram (EEG), which was recorded continuously with the bipolar 10-20 electrode placement system. 3. All subjects developed frontal slow waves during at least one experiment: the EEG changes were similar both within and among subjects, irrespective of the blood PCO2 value. 4. The arterial oxygen saturation at which slow-wave activity first occurred showed a significant inverse linear relationship to the PCO2 value at which hypoxia was induced. 5. The results imply that more profound levels of hypoxia are tolerated with high PCO2 values than with normal or low PCO2 values before hypoxic EEG changes become evident. Thus if eucapnia is maintained, EEG changes suggestive of cerebral hypoxia are unlikely to occur if arterial oxygen saturation remains above 75%.

Adult↗
PubMed1976

Ear oximetry: accuracy and practicability in the assessment of arterial oxygenation.

The accuracy of three ear oximeters (Waters XP-350, Waters 0-1100, Hewlett-Packard 47201A) was evaluated on 52 subjects during acute progressive and steady-state hypoxia. Ear oximeter readings were compared with measured arterial saturation (SAO2) in arterial or "arterialized" capillary blood samples. Hewlett-Packard (HP) 47201A ear oximeter readings most closely approximated measured Sao2 (y=0.99x - 1.52, r=0.97), although both the HP 47201A and Waters 0-1100 oximeters provided similarly accurate estimates of SAO2 once the characteristics of the individual oximeters were known (standard error of estimate; 2.52 and 2.98 per cent SAO2, respectively). The HP 47201A ear oximeter was relatively insensitive to changes in ear-piece position and differences in skin pigmentation, and offered the added advantages of comfort, simplicity of operation, and stability of characteristics.

Arteries↗
PubMed1975

The bronchodilator effect of fenoterol (Berotec).

The efficacy of the selective beta 2 sympathomimetic fenoterol (Berotec) in aerosol and tablet forms was studied in 15 subjects with reversible airways obstruction. The maximal bronchodilator effect of fenoterol by aerosol (0.4mg) was found to equal that of isoprenaline, and to be maintained at that level over the three hour period studied. When given orally, neither one tablet (2.5 mg) nor two tablets (5 mg) of fenoterol increased the FEV1 to the same extent as isoprenaline, and the larger oral dose (5 mg) produced troublesome side effects in several subjects. It is concluded that fenoterol by aerosol is an effective bronchodilator with a duration of action of at least three hours, without significant side effects.

Adolescent↗