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Biomedical subjects

K B Saunders

Publications and source records attributed to K B Saunders.

At least 19 recordsLinked to original sources
PubMed1992

Estimates of mean alveolar PCO2 during steady-state exercise in man: a theoretical study.

The partial pressure of carbon dioxide in arterial blood is an important operator in the control of breathing, by actions on peripheral and central chemoreceptors. In experiments on man we must often assume that lung alveolar PCO2 equals arterial PCO2 and obtain estimates of the former derived from measurements in expired gas sampled at the mouth. This paper explores the potential errors of such estimates, which are magnified during exercise. We used a published model of the cardiopulmonary system to simulate various levels of exercise up to 300 W. We tested three methods of estimating mean alveolar PCO2 (PACO2) against the true value derived from a time average of the within-breath oscillation in steady-state exercise. We used both sinusoidal and square-wave ventilatory flow wave forms. Over the range 33-133 W end-tidal PCO2 (P(et)CO2) overestimated PACO2 progressively with increasing workload, by about 4 mmHg at 133 W with normal respiratory rate for that load. PCO2 by a graphical approximation technique (PgCO2; "graphical method") underestimated PACO2 by 1-2 mmHg. PCO2 from an experimentally obtained empirical equation (PnjCO2; "empirical method") overestimated PACO2 by 0.5-1.0 mmHg. Graphical and empirical methods were insensitive to alterations in cardiac output or respiratory rate. End-tidal PCO2 was markedly affected by respiratory rate during exercise, the overestimate of PACO2 increasing if respiratory rate was slowed. An increase in anatomical dead space with exercise tends to decrease the error in P(et)CO2 and increase the error in the graphical method. Changes in the proportion of each breath taken up by inspiration make no important difference, and changes in functional residual capacity, while important in principle, are too small to have any major effect on the estimates. Changes in overall alveolar ventilation which alter steady-state PACO2 over a range of 30-50 mmHg have no important effect. At heavy work loads (200-300 W), P(et)CO2 grossly overestimates by 6-9 mmHg. The graphical method progressively underestimates, by about 5 mmHg at 300 W. A simulated CO2 response (the relation between ventilation and increasing PCO2) performed at 100 W suggests that a response slope close to the true one can be obtained by using any of the three methods. The graphical method gave results closest to the true absolute values. Either graphical or empirical methods should be satisfactory for detecting experimentally produced changes in PACO2 during steady-state exercise, to make comparisons between different steady-state exercise loads, and to assess CO2 response in exercise.(ABSTRACT TRUNCATED AT 400 WORDS)

Arteries↗
PubMed1992

Ventilatory responsiveness to carbon dioxide below the normal control point in conscious normoxic humans.

A recently developed CO2 pulse technique was used to test for ventilatory sensitivity to CO2 in four normal men following 2 min voluntary hyperventilation down to an end-tidal CO2 tension (PETCO2) of 20 mmHg (2.7 kPa). Pure CO2 was injected into the inspiratory limb of a breathing circuit at 0.4 l.min-1 for 30 s and any small ventilatory response was detected against background noise by ensemble-averaging of multiple runs. Following hyperventilation, ventilation was initially often above control and apnoea was not seen. In one subject, the ventilatory response to the CO2 pulse was barely detectable either before or after hyperventilation. In another subject, there was a response to pulses given before hyperventilation and 3 and 5.5 min after hyperventilation but not 30 s after hyperventilation when PETCO2 was about 25 mmHg (3.3 kPa) and rising. In the two remaining subjects ventilatory responses were seen to CO2 pulses started 30 s after hyperventilation, although PETCO2 following the pulse remained some 5 mmHg (0.7 kPa) below baseline. We conclude that in some subjects the PETCO2 threshold lies well below the normal PETCO2. The technique is tedious for the experimental subject because of the large number of repetitions required and, therefore, unsuitable for a study on a large number of subjects.

Adult↗
PubMed1991

Hypoxia following voluntary hyperventilation during exercise in man.

The importance of carbon dioxide in the control of ventilation during exercise was tested by emptying CO2 stores by voluntary hyperventilation. Healthy subjects were studied after 3 min hyperventilation down to an end-tidal PCO2 of about 20 mmHg on a background of steady exercise at 75 W. Control runs were performed when the hyperventilation was made isocapnic by the addition of CO2. Following hypocapnic hyperventilation, there was a period when ventilation fell below control and this was accompanied by a fall in end-tidal PO2 (minimum 48 mmHg) and oximeter reading (minimum 73%). Ventilation rapidly returned to baseline following isocapnic hyperventilation and hypoxia was not seen. A mathematical simulation suggested that brain PCO2 recovered more slowly than arterial PCO2 and that at the times that ventilation was depressed central chemoreceptor PCO2 would have been low. We conclude that CO2 provides a crucial drive for maintaining adequate ventilation during steady exercise and that the central chemoreceptor may be involved.

Adolescent↗
PubMed1990

Timing of deep breaths during rest and light exercise in man.

1. We used digital filtering techniques and segmental analysis to dissect a series of respiratory variables into three components: (a) outlying values, including deep breaths or sighs; (b) random variation; (c) non-stationary baseline variation. 2. Records of about 30 min breathing were obtained from normal adults at rest and at 50 W exercise. 3. Deep breaths were defined as having a tidal volume greater than 2.5 sd above the mean. 4. We related these deep breaths to preceding trends in tidal volume and end-tidal partial pressure of CO2. 5. At rest, there was no relation between deep breaths and tidal volume, but the deep breaths were significantly clustered around the troughs in end-tidal partial pressure of CO2. 6. At 50 W exercise, there was no relation between deep breaths and end-tidal partial pressure of CO2, but the deep breaths were significantly clustered around tidal volume troughs. 7. Results obtained by pneumography were concordant with those obtained by using a mouthpiece to measure ventilation.

Adult↗
PubMed1990

The effect of almitrine on the steady-state ventilatory response to carbon dioxide at rest and during exercise in man.

Almitrine has potential as a tool for testing the physiological role of the peripheral chemoreceptor. The effects of almitrine on CO2 chemosensitivity were studied at rest and during light exercise using a constant inflow technique that avoids the hyperoxia of rebreathing methods. The steady-state ventilatory response to CO2 was measured in two groups of six normal men before and 150 min after 100 mg oral almitrine bismesylate or placebo. One group was studied at rest, the other while pedalling at 50 W. The resting group showed a significant increase in CO2 response slope after almitrine when compared with placebo but there was no significant change in the response intercept. During exercise the individual results were very variable and after almitrine no significant change was seen in either the response slope or intercept. Control ventilation was not affected by almitrine in either group. Even in the absence of marked hyperoxia the effect of almitrine on CO2 sensitivity at rest in small. The lack of effect at 50 W is against any important role for the peripheral chemoreceptor during light exercise but other interpretations are possible.

Adult↗
PubMed1979

Changes in arterial blood gases during and after a period of oxygen breathing in patients with chronic hypercapnic respiratory failure and in patients with asthma.

1. Ten patients with chronic hypercapnic respiratory failure (group 1) and eight patients with asthma (group 2) breathed pure O2 from an MC mask for 60 min. Blood gases were measured during this period and for the subsequent 45 min. 2. In mine of ten patients in group 1 and in all eight patients in group 2 arterial O2 tension (Pa,O2) fell to values lower than had been obtained before O2 was given. 3. These undershoots in Pa,O2 are unrelated to changing CO2 stores or to hypoventilation, and are more likely due to persistence of altered ventilation-perfusion ratios associated with O2 breathing. 4. Magnitude of the undershoots is usually small, and periods of less than 15 min of O2 are unlikely to be harmful.

Adolescent↗
PubMed1979

Effect of an inhaled antihistamine (clemastine) as a bronchodilator and as a maintenance treatment in asthma.

Although intravenous chlorpheniramine can cause bronchodilatation, oral and parenteral antihistamines have not proved useful in treating asthma. Inhaled antihistamines may cause throat irritation, but a recent study of the antihistamine, clemastine, showed it to be an effective bronchodilator without irritant effects. We have extended these studies to determine the site of action of inhaled clemastine and to assess its potential usefulness both as a bronchodilator and as a maintenance treatment. Eleven stable asthmatic patients received inhaled clemastine and placebo and the effect was assessed by serial maximum expiratory flow volume (MEFV) curves breathing air and a helium/oxygen (He/O2) mixture. There was no significant improvement in peak flow rates during air breathing after clemastine and no significant difference between the responses to drug and placebo. Minor but significant changes were seen in some flow measurements on the downslope of the MEFV curve during air and He/O2 breathing, and these are tentatively ascribed to a dilating effect of clemastine on peripheral airways where flow is laminar. Subsequent administration of inhaled isoprenaline showed the patients to be still capable of significant bronchodilatation. The addition of clemastine, from a pressurised aerosol, to the patients' therapeutic regimen for two weeks was no more effective than placebo in controlling airflow obstruction, and did not reduce the need for standard bronchodilators. In our patients clemastine was not a clinically useful bronchodilator either acutely or as a maintenance treatment for asthma.

Adult↗
PubMed1978

Depression of central respiratory drive by nitrazepam.

In a group of patients with chronic bronchitis, repeated night sedation with 10 mg nitrazepam produced a fall in central respiratory drive and a steady rise in arterial carbon dioxide tension. The changes produced over a five-day period were not clinically important, except in two patients who were already hypercapnic before receiving nitrazepam. The use of this drug in patients with carbon dioxide retention should be avoided.

Aged↗
PubMed1978

Sensitivity of the carotid body to within-breath changes in arterial PCO2.

Respiration, sinus nerve chemoreceptor discharge, and carotid arterial pH were monitored in cats. Chemoreceptor discharge frequency showed oscillations that had a respiratory period when averaged over many respiratory cycles. These oscillations disappeared when pH oscillations of respiratory period were eliminated from the carotid arterial blood. The maximum sinus nerve discharge was associated with the most acid point of the recorded pH oscillation. Briefly increasing PCO2 by giving CO2-rich saline into the aortic root resulted in brief reduction in carotid arterial pH, and when this reduction occurred during inspiration tidal volume increased, even with a pH change no larger than the pH oscillations. However, increased chemoreceptor discharge could only be demonstrated when each pH change had twice the amplitude of the pH oscillations. Injections of fixed acid mixed with free carbonic anhydrase transiently increased chemoreceptor frequency, whereas injections of fixed acid alone had no effect. The carotid body is therefore sensitive to small rapid changes in arterial PCO2, and the pH electrode record indicates the size of the stimulus except when fixed acid changes are produced too closely upstream.

Animals↗
PubMed1978

Central airways obstruction in carcinoma of the bronchus treated by radiotherapy: a study of pulmonary function.

A battery of lung function tests was performed on 28 patients with carcinoma of the bronchus, before radiotherapy, six weeks later, and at three months. Twenty-five had evidence of ariways obstruction, though only five had a forced expiratory ratio of less than 50%. Nine were shown to have obstruction to a main or lobar bronchus, while 11 definitely did not, but the only significant difference in lung function between groups was in the residual volume calculated from single breath helium dilution. Eight of ten cases of squamous cell carcinoma were central, and seven of these obstructive. Of seven cases with undifferentiated cells only two were central (p less than 0.05) and one obstructive. Breathlessness on presentation was significantly more common in patients with central tumours (6/12) than those with peripheral lesions (1/8), and all six breathless patients with central tumours claimed that this symptom improved after radiotherapy. Radiotherapy may have a palliative effect for breathlessness in patients with central airways obstruction due to tumour.

Aged↗
PubMed1978

Bromhexine in severe asthma.

Fourteen patients with acute severe asthma necessitating hospital admission were all treated with a standard therapeutic regimen, and in addition received either bromhexine or placebo (initially intravenously and subsequently orally) double-blind. We were unable to show any significant improvement in the rate of recovery of the bromhexine-treated group, in terms of either arterial blood gases or change in peak expiratory flow rates.

Acute Disease↗
PubMed1976

80% of patients with intrinsic asthma are homozygous for HLA W6. Is intrinsic asthma a recessive disease?

Of 26 patients with intrinsic asthma, 21 (81%) were homozygous for the histocompatibility antigen HLA-W6. Also, half the patients had complement defects, in particular low levels of C2. This is the first indication of a strong genetic component in intrinsic asthma, apart from that already known from family studies. These findings suggest that intrinsic asthma may be a recessive disease.

Asthma↗