Cardiac output as a controller of ventilation through changes in right ventricular load

Jones, P. W.; Huszczuk, A; Wasserman, K.

doi:10.1152/jappl.1982.53.1.218

Cited by 77 publications

(47 citation statements)

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“…Usually, Pa,CO 2 is low at rest and does not fall further during exercise. This is thought to reflect hypoxaemic stimulation of carotid chemoreceptors and possibly also vagal reflex activation via stretch receptors in the pulmonary circulation [132].…”

Section: Ventilatory and Gas-exchange Abnormalitiesmentioning

confidence: 99%

“…V9E at any given V9CO 2 is typically increased. Contributory factors include: premature metabolic acidaemia (reflecting reduced O 2 delivery and/or utilisation) [146,147]; increased physiological dead space [4]; increased sympathetic system activation via mechano-or pressor-receptor stimulation in the exercising muscles [148][149][150][151][152] and, possibly, contributions from cardiopulmonary vagal and sympathetic reflexes [132,153,154]. Several studies have shown that breathing pattern in CHF is more rapid and shallow than in healthy controls at any given V9E [4,155,156].…”

Section: Ventilatory Abnormalitiesmentioning

confidence: 99%

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Recommendations on the use of exercise testing in clinical practice

Palange¹,

Ward²,

Carlsen³

et al. 2006

Eur Respir J

562

390

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Evidence-based recommendations on the clinical use of cardiopulmonary exercise testing (CPET) in lung and heart disease are presented, with reference to the assessment of exercise intolerance, prognostic assessment and the evaluation of therapeutic interventions (e.g. drugs, supplemental oxygen, exercise training). A commonly used grading system for recommendations in evidence-based guidelines was applied, with the grade of recommendation ranging from A, the highest, to D, the lowest.For symptom-limited incremental exercise, CPET indices, such as peak O 2 uptake (V9O 2 ), V9O 2 at lactate threshold, the slope of the ventilation-CO 2 output relationship and the presence of arterial O 2 desaturation, have all been shown to have power in prognostic evaluation. In addition, for assessment of interventions, the tolerable duration of symptom-limited high-intensity constant-load exercise often provides greater sensitivity to discriminate change than the classical incremental test. Field-testing paradigms (e.g. timed and shuttle walking tests) also prove valuable.In turn, these considerations allow the resolution of practical questions that often confront the clinician, such as: 1) ''When should an evaluation of exercise intolerance be sought?''; 2) ''Which particular form of test should be asked for?''; and 3) ''What cluster of variables should be selected when evaluating prognosis for a particular disease or the effect of a particular intervention?''

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Section: Ventilatory and Gas-exchange Abnormalitiesmentioning

confidence: 99%

Section: Ventilatory Abnormalitiesmentioning

confidence: 99%

Recommendations on the use of exercise testing in clinical practice

Palange¹,

Ward²,

Carlsen³

et al. 2006

Eur Respir J

562

390

View full text Add to dashboard Cite

show abstract

“…If preventing the rise in pulmonary gas exchange per se prevents the rise in during occlusion by reducing the stimulation of 'receptors' located in the central circulation, it remains unclear why V, is always markedly depressed for a given level of 0, uptake, CO, output and PET,C02, during total obstruction and not during partial occlusion. This implies that factors unrelated to the consequences of the reduction in venous flow to the central circulation, which includes the involvement of arterial chemoreceptors (Dejours et al 1955;Yamamoto & Edward, 1960;Sylvester et al 1973) and receptors located in the right heart (Jones et al 1982) or in the pulmonary circulation (Lloyd, 1984), contribute to the changes in ventilation during the occlusion procedures.…”

Section: Effect Of Vascular Occlusionmentioning

confidence: 99%

“…However, if factors more directly related to venous return were involved, the exercise-induced hyperpnoea should be attenuated in similar proportion during partial or total occlusion (Yamamoto & Edwards, 1960;Sylvester et nl. 1973;Ponte & Purves, 1978;Jones et a/. 1982;Huszczuk et al 1986).…”

mentioning

confidence: 99%

Control of breathing and muscle perfusion in humans

Haouzi

Chenuel

Chalon

2001

Experimental Physiology

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Very brief and intense exercise triggers a biphasic metabolic and respiratory response with a second phase that occurs after the cessation of the muscular activity. The effects on minute ventilation (VE) produced by manipulation of the peripheral circulation in metabolically active muscles could thus be studied without the confounding effects of painful contractions. The second phase of breath-by-breath ft and pulmonary gas exchange responses to a brief change in work rate (400 W for 12 s) were studied in six healthy male subjects on four occasions (24 tests). An upper thigh cuff inflation was randomly applied either above or below the systolic blood pressure (200 or 90 Torr, respectively) for 90 s just after the cessation of the contractions prior to the delayed rise in pulmonary gas exchange (eight tests in each subject). Total occlusion produced a significant reduction in the delayed rise in T & (-29 ? 3 %) which normally occurred 20-25 s after the cessation of the contractions. In contrast, cuff inflation at a level predominantly impeding venous return while partially maintaining the arterial supply reduced the rise in pulmonary gas exchange in similar proportion to that during total obstruction but with a slight but not significant reduction in ventilation (-9 f 5%). ft during partial occlusion was if anything higher than in control tests with similar oxygen uptake (280 W), despite a higher blood pressure (BP) during occlusion (+7 Torr). It is concluded that the factors resulting from a reduction in venous return or from the involvement of the arterial baroreflex are not responsible for the changes in ft produced by the obstruction of the circulation to and from metabolically active muscles. It is proposed that factors related to the level of the perfusion pressure in hyperaemic muscles, possibly located at the venular end of the microcirculation, could account for the changes in J& observed.

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“…JONES et al (1982) found in dogs that right atrium strain caused by an increase in Q correlated linearly with VE. It has been assumed that the mechanoreceptors involved in these organs are activated by the sudden increase of venous return at the onset of exercise, and the reflex therefrom may provide a direct link between Q and VE without the mediation of any humoral factors, i.e., a physically mediated cardiodynamic process.…”

Section: Discussionmentioning

confidence: 91%

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man.

et al. 1989

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In order to know the role of cardiodynamic factors for exercise hyperpnea, ventilation and several cardiorespiratory variables were measured simultaneously in human subjects during exercise. Cardiac output (Q) and mixed venous C02 content (Cv~o2) were determined by a rebreathing method. The correlation coefficients (r) for the relationships between minute expiratory ventilation (VE) and each of end-tidal C02 tension (PETCo2), Q, Cv~o2, Cot flow into the lung (QC02, the product of Q and Cv~o2), oxygen consumption (Vo2), and C02 output (V02) were determined during the steady-state exercise up to 90 W. The correlation was highly significant (r = 0.840.99, p <0.001) in each case except for PETCo2 (r = 0.13, N. S.). The highest correlation was observed in the VE-Va 2 relationship. It was assume that V02 released from the pulmonary capillaries into the alveoli is the most likely stimulus leading to exercise hyperpnea. Arterial C02 oscillation may be regarded as a potential linkage between V02 and VE.Key words : exercise hyperpnea, cardiac output, rebreathing method.Among a number of hypotheses concerning the mechanism of inducing exercise hyperpnea, the cardiodynamic hypothesis proposed by Wasserman and his associates (WASSERMAN et al., 1974(WASSERMAN et al., , 1986 has attracted many investigators during the last decade. C02 flow from venous blood to the lung, i.e., the product of cardiac output (Q) and mixed venous C02 content (Cv~o2) causes an increase in ventilation during excercise by means of some unidentified mechanisms. More recently, MIYAMOTO et al. (1981MIYAMOTO et al. ( , 1982 have determined the kinetics of Q by adopting an ensemble-averaging technique to impedance cardiography, evidently showing that the change in Q precedes that in ventilation during the unsteady-state of step exercise. However, the mechanism linking C02 flow to ventilation has remained unsettled.

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Cardiac output as a controller of ventilation through changes in right ventricular load

Cited by 77 publications

References 0 publications

Recommendations on the use of exercise testing in clinical practice

Recommendations on the use of exercise testing in clinical practice

Control of breathing and muscle perfusion in humans

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man.

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