Biomedical subjects
W N Gardner
Publications and source records attributed to W N Gardner.
Relation of hypocapnic symptoms to rate of fall of end-tidal PCO2 in normal subjects.
Hyperventilation is of little clinical relevance unless it causes symptoms. These are often non-specific. Their threshold for onset and relation to steady level of arterial (or its equivalent, end-tidal PCO2; PETCO2) are uncertain, and it has been suggested that they may relate better to the rate of fall of PCO2 than to the absolute level. We investigated this in nine normal subjects, who breathed to and fro through a pneumotachograph into an open circuit in which the concentration of CO2 could be varied. Tidal volume, respiratory frequency and ventilation was measured on-line by a Compaq computer, and PETCO2 at the mouth was measured by capnograph. Subjects overbreathed at a fixed rate and depth until symptoms consisting of dizziness, paraesthesiae and light headedness occurred. Then, without their knowledge and while they continued to overbreathe, inspired CO2 was increased to restore PETCO2 to normal and abolish symptoms, and was then withdrawn again over either approximately 0.1, 2.5 or 5 min until symptoms were again reported. The PETCO2 at this point was noted. The three protocols were performed in each subject in a random order and the same symptoms were reported each time. When averaged across all subjects, symptoms occurred at mean PETCO2 values of 20.3, 19.2 and 18.6 mmHg (2.71, 2.56 and 2.48 kPa), respectively. These were not significantly different, and it can be concluded that there was no influence of rate of fall of PCO2 on threshold for symptoms. Chest pain only occurred in one subject and may have a different mechanism.
Recurrent hyperventilation tetany due to mild asthma.
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Hyperventilation provocation in patients with chest pain and a negative treadmill exercise test.
Seventeen (39%) of 44 patients with chest pain but without significant ST depression on treadmill exercise had their usual chest pain reproduced during or after 3 min of voluntary hyperventilation (VHV) at rest. These patients with hyperventilation positive tests had not only significantly more hyperventilation-related symptoms and respiratory complaints but also shorter breath-holding times, lower mean resting end-tidal pCO2 and higher mean respiratory rates than those with negative tests and normal controls. Of the psychological variables, only phobic avoidance scores for agoraphobia were higher in patients with positive tests. These findings suggest that in two fifths of patients with exercise tests negative for ischaemia, chest pain is associated with HV, but abnormalities of breath control and relative hypocapnia are present even in the absence of chest pain. It is possible that a chronic abnormality of respiratory control may interact with attitudinal factors in the experience of non-cardiac chest pain.
Respiration during exercise in conscious laryngectomized humans.
We compared respiratory patterning at rest and during steady cycle exercise at work rates of 30, 60, and 90 W in 7 male chronically laryngectomized subjects and 13 normal controls. Breathing was measured with a pneumotachograph and end-tidal PCO2 by mass spectrometer. Inspired air was humidified and enriched to 35% O2. Peak flow, volume, and times for the inspiratory and expiratory half cycles, time for expiratory flow, minute ventilation, and mean inspiratory flow were computer averaged over at least 40 breaths at rest and during the last 2 min of 5-min periods at each work rate. During the transition from rest to exercise and with increasing work rate in both groups, there was an increase in respiratory rate and depth with selective and progressive shortening of expiratory time; these responses were not significantly different between the two groups, but there was a suggestion that respiratory "drive" as quantitated by mean inspiratory flow may limit in the laryngectomized subjects at high work rates. Time for expiratory flow increased on transition from rest to exercise and then decreased in both groups as the work rate increased; it was shorter in the laryngectomy than control group at all levels. In the laryngectomized subjects there was significantly more breath-by-breath scatter in some variables at rest, but there was no difference during exercise. It is concluded that chronic removal of the larynx and upper airways in mildly hyperoxic conscious humans has only subtle and, therefore, functionally insignificant effects on breathing during moderate exercise. Evidence is provided that the upper airways can modulate expiratory flow but not expiratory time during exercise.
Hyperventilation clinical practice.
There is uncertainty about the diagnosis and definition of the hyperventilation syndrome. We prefer to regard hyperventilation (or hypocapnia with which it is synonymous) as a physiological response to abnormally increased respiratory "drive", which can be caused by a wide range of organic, psychiatric and physiological disorders, or a combination of these. This review outlines a clinical scheme for the diagnosis and assessment of hyperventilation and its causes.
Value of measuring end tidal partial pressure of carbon dioxide as an adjunct to treadmill exercise testing.
The end tidal partial pressure of carbon dioxide (PCO2) was measured during treadmill exercise in 30 normal controls and 113 patients referred for assessment of chest pain. Among the 92 patients without significant ST depression hypocapnia occurred more often in those reporting "typical" than "atypical" chest pain (17 of 22 patients compared with 29 of 70; p less than 0.01). Hypocapnia was uncommon in patients with significant ST depression whether reporting typical or atypical chest pain (one of 10 patients and two of 11, respectively). Hypocapnia at rest (PCO2 less than 4 kPa) occurred in 16 (14%) patients but in only one control. Hypocapnia occurred during or after exercise in only one control and three of the 21 patients with significant ST depression on exercise (group 1). The remaining 92 patients were divided into those with a history suggestive of hyperventilation (group 2; n = 30) and those without (group 3; n = 62). Hypocapnia developed significantly more often in both these groups (21 and 25 patients respectively) than in controls or patients with significant ST depression. An abnormal response of the PCO2 to exercise provided objective data to support a clinical suspicion of chest pain induced by hyperventilation in 24 cases, suggested a cause for equivocal ST depression other than coronary stenosis in five patients, and led to the diagnosis of previously unsuspected respiratory disease in 14 patients. Measurement of end tidal PCO2 gives additional valuable diagnostic information during the conventional treadmill exercise test in patients with both typical and atypical chest pain.
Panic anxiety and hyperventilation in patients with chest pain: a controlled study.
We studied the relation between mood disorder and hyperventilation (hypocapnia) before and during exercise treadmill testing in 113 chest pain patients attending a cardiac clinic and 30 healthy controls. In most patients end-tidal PCO2 (PCO2) rose in the normal way on exercise but in a subset of 24 (21 per cent) there was no rise: these patients with initial hyperventilation had significantly higher anxiety scores than those with a normal exercise-induced rise in PCO2. Two of the 24 had ischaemic heart disease and 10 (42 per cent) complained of recent panic anxiety compared with 12 (13 per cent) of the 89 with normal rise in PCO2 (p less than 0.05). Rates of psychiatric morbidity were similar in patients with 'typical' and 'atypical' chest pain. Resting hypocapnia occurred more often in patients with panic anxiety than in either anxious or non-anxious patients without panic. Panic patients also reported more symptoms of breathlessness and hyperventilation-related complaints than those without panic. Our findings confirm the important association between panic and hyperventilation in patients with chest pain. Furthermore, patients with exercise-induced hyperventilation are more likely to have a psychiatric than a cardiac disorder. Early detection and treatment of these patients may reduce the potential morbidity associated with unnecessary invasive investigations.
Exertional gastroesophageal reflux.
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Hyperventilation syndromes in medicine and psychiatry.
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Laser photodynamic therapy for inoperable bronchogenic squamous carcinoma.
Fifteen consecutive patients with advanced squamous bronchogenic carcinoma, most of whom had had radiotherapy, were given palliative photodynamic therapy, using either haematoporphyrin derivative or dihaematoporphyrin ether to light sensitize their tumour. All tumours responded to treatment by subsequent light at 630 nm and in the 12 patients where adequate tumour illumination was achieved there was complete clearing of the bronchus in three and partial (more than 50 per cent clearing) in the remaining nine, with relief of haemoptysis and/or breathing obstruction. One patient with recurrent tumour in a pneumonectomy stump after radiotherapy has remained disease-free for over two years since photodynamic therapy. The main complications were temporary skin light sensitization reaction in three, infection after reaeration of lung tissue in two, and transient but severe worsening of breathing obstruction in two.
Breathing in Parkinson's disease.
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Controlled study of respiratory responses during prolonged measurement in patients with chronic hyperventilation.
The respiratory responses of 17 patients with chronic hyperventilation but without demonstrable organic disease (group H) to various manoeuvres were compared with those of 21 healthy controls (group C). The responses were tested according to a 60 min protocol in which periods of rest were replaced by exercise, voluntary hyperventilation (VHV), reading, and CO2 inhalation. 5 patients with severe resting hypocapnia were investigated overnight during sleep. Chronic hyperventilation was of two types--persistent or provoked by exercise or VHV. It was due to modest increases in tidal volume and respiratory frequency but was generally not conspicuous. End-tidal PCO2 levels were gradually corrected to near normal during sleep but not by inhalation of CO2.
Abnormal breathing patterns associated with angina-like chest pain.
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Respiratory and psychiatric abnormalities in chronic symptomatic hyperventilation.
Many physicians believe that the hyperventilation syndrome is invariably associated with anxiety or undiagnosed organic disease such as asthma and pulmonary embolus, or both. Twenty one patients referred by specialist physicians with unexplained somatic symptoms and unequivocal chronic hypocapnia (resting end tidal Pco2 less than or equal to 4 kPa (30 mm Hg) on repeated occasions during prolonged measurement) were investigated. All but one complained of inability to take a satisfying breath. Standard lung function test results and chest radiographs were normal in all patients, but histamine challenge showed bronchial hyper-reactivity in two of 20 patients tested, and skin tests to common allergens were positive in three of 18. Ventilation-perfusion scanning was abnormal in a further three of 15 patients studied, with unmatched perfusion defects in two and isolated ventilation defects in one. None of the 21 had thyrotoxicosis, severe coronary heart disease, or other relevant cardiovascular abnormalities. Ten of the 21 patients were neurotic and suffered from chronic psychiatric disturbance characterised by anxiety, panic, and phobic symptoms. The remainder had no detectable psychiatric disorders but reported proportionately more somatic than anxiety symptoms. Severe hyperventilation can occur in the absence of formal psychiatric or detectable respiratory or other organic abnormalities. Asthma and pulmonary embolus must be specifically excluded.
The pattern of the human respiratory response to step change of PA,O2 [proceedings].
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Very small, very short-latency changes in human breathing induced by step changes of alveolar gas composition.
1. Three healthy young males were maintained for sessions of about 1 hr in a state of mild asphyxia (PA,O2 approximately 55, PA,CO2 approximately 45 torr), i.e. with moderately strong drives from both arterial and intracranial chemoreceptors. Tidal volume (VT), breath duration (TT) and duration of inspiration (TI) were recorded, and ventilation (VE) and duration of expiration (TE) were derived breath by breath. 2. The arterial chemoreceptor component of the drive was briefly and abruptly reduced, perhaps silenced, by three separate procedures: the inspiratory pathway was connected for two breaths to a second gas supply line containing, B, hypoxia with Pi,CO2 zero (removal of hypercapnia with maintained hypoxia); C, pure oxygen (removal of asphyxia); and D, oxygen with 40 torr added PCO2 (removal of hypoxia with maintained hypercapnia). In controls, A, the second inspiratory line contained the maintenance mixture so that the switch involved no change of inspiratory gas composition. Each type of test was repeated twenty-four times on each subject. 3. Responses attributable to silencing of arterial chemoreceptors (i.e. with 1 1/2--3 breath latencies about equal to the lung-to-ear circulation time) are reported elsewhere. 4. Very small responses, occurring only half a respiratory cycle after first inhalation of the test mixture, were detected by pooling all responses of each kind from all subjects. When hypoxia was withdrawn, with (C) or without (D) simultaneous withdrawal of hypercapnia, VT and VE were reduced by 3 and 2% respectively, probably because gas mixtures containing high oxygen concentrations are appreciably more viscous than hypoxic mixtures and so require more effort to breathe in and out. When hypercapnia was withdrawn with (C) or without (B) simultaneous withdrawal of hypoxia, TE was significantly lengthened (mean, + 65 +/- 18 msec), 5. The change of TE was discussed in relation to known effects of CO2 on airway receptors in the dog.
The relation between tidal volume and inspiratory and expiratory times during steady-state carbon dioxide inhalation in man.
1. Ambiguities and discrepancies in the published descriptions of the patterns of breathing in man have been re-investigated.Steady-state hyperpnoea during rest was induced in normal subjects of both sexes by means of CO(2) inhalation, usually in high O(2), but sometimes in low (P(A, O2) approximately 200 and 55 torr respectively).2. The relations between mean tidal volume V(T) and mean times for inspiration T(I) and expiration T(E) were satisfactorily divided into lower and upper parts (ranges 1 and 2) in nineteen out of thirty-three experiments using an objective least-squares method, and polynomials were fitted separately to each of the following pairs of variables V(T,lower), T(I); V(T,lower), T(E); V(T,upper), T(I); V(T,upper), T(E).3. The breakpoints occurred when V(T) was about one third of vital capacity, but there was much variation between subjects.4. In range 2, V(T) was inversely related to both T(I) and T(E) and there appeared to be linkage between T(I) and T(E), all as described by Clark & Euler (1972). The relation suggested by Hey, Lloyd, Cunningham, Jukes & Bolton (1966) over range 2 was not confirmed.5. The main part of the relation described by Hey et al. (1966) is concerned with range 1. Here the relation between V(T) and T(I) was variable; slight, but significant negative correlation predominated. V(T) was, on the other hand, strongly and inversely related to T(E), and plots of (T(E) - T(I)) against V(T) over both ranges showed even less scatter. Hence (a) T(E) is probably related to V(T) through two mechanisms, one involving a link with T(I) and another prominent one being quite independent of T(I), (b) most changes of respiratory frequency in normal man are brought about by change of T(E) rather than of T(I), and (c) there is no region of constant frequency as implied by Clark & Euler (1972).