Hypoxic ventilatory drive in normal man

Weil, John V.; Byrne-Quinn, Edward; Sodal, I. E.; Friesen, W O; Underhill, B. Kevin; Filley, Giles F.; Grover, Robert F.

doi:10.1172/jci106322

Cited by 382 publications

(188 citation statements)

References 32 publications

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“…Next, hypoxaemia was induced by the method of Well, et al 5 Inhaled oxygen was gradually replaced with air and then with a mixture of air and nitrogen, so that end-tidal oxygen decreased to 5.3-6.0 kPa (40-45 tort) over an 8-10 minute period. End-tidal carbon dioxide concentration was monitored continuously and carbon dioxide was added directly to inhaled gas if necessary to maintain end-tidal isocapnia.…”

Section: Methodsmentioning

confidence: 99%

Variable effects of anaesthetics on the ventilatory response to hypoxaemia in man

Knill

Clement

1982

Canad. Anaesth. Soc. J.

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We compared the ventilatory response to isocapnic hypoxaemia with a standard response to hyperoxic hypercarbia in human subjects sedated with methoxyflurane, diethyl ether or nitrous oxide, or anaesthetized with methoxyflurane. Compared to the awake state, methoxyflurane 0.1 MAC sedation did not alter either response significantly; methoxyflurane 1.1 MAC anaesthesia depressed both, with a somewhat greater effect on the hypoxaemic response. Diethyl ether 0.1 MAC sedation reduced only the hypoxaemic response. Nitrous oxide 0.1 MAC reduced both hypoxaemic and carbon dioxide responses in parallel. The evidence suggests that all three agents -like thiopentone, halothane and enflurane -can impair the ventilatory response to isocapnic hypoxaemia in man, but that in relation to the carbon dioxide responses, the magnitude of this depressive effect varies. Halothane and enflurane are the most depressant, nitrous oxide and thiopentone the least, with methoxyflurane and diethyl ether appearing to be intermediate in effect. to isocapnic hypoxaemia in man, -with halothane and enflurane being particularly potent in this effect, depressing the hypoxic reflex out of proportion to their other ventilatory effects. These observations suggest that, rather than being resistant, the response to hypoxaemia may be relatively sensitive to depression by certain anaesthetics in man. The purpose of the present study was to determine how three other anaesthetic agentsmethoxyflurane, diethyl ether and nitrous oxide

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Section: Methodsmentioning

confidence: 99%

Variable effects of anaesthetics on the ventilatory response to hypoxaemia in man

Knill

Clement

1982

Canad. Anaesth. Soc. J.

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“…It has also been established that respiratory drive derives from detection of high carbon dioxide levels by peripheral chemoreceptors and receptors in the medulla [10]. There is also the theory of hypoxic drive, a form of respiratory drive, in which the medulla detects low levels of oxygen rather than high levels of carbon dioxide, resulting in the drive to breathe [11]. Hypoxic drive was thought to occur in patients with chronically elevated levels of CO 2 , such as patients with chronic obstructive pulmonary disease (COPD), but recent studies have shown that patients with COPD do not rely on hypoxic drive to breathe [12].…”

Section: Respiratory Drivementioning

confidence: 99%

Widespread depolarization during expiration: A source of respiratory drive?

Jerath¹,

Crawford²,

Barnes

et al. 2015

Medical Hypotheses

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a b s t r a c tRespiration influences various pacemakers and rhythms of the body during inspiration and expiration but the underlying mechanisms are relatively unknown. Understanding this phenomenon is important, as breathing disorders, breath holding, and hyperventilation can lead to significant medical conditions. We discuss the physiological modulation of heart rhythm, blood pressure, sympathetic nerve activity, EEG, and other changes observed during inspiration and expiration. We also correlate the intracellular mitochondrial respiratory metabolic processes with real-time breathing and correlate membrane potential changes with inspiration and expiration. We propose that widespread minor hyperpolarization occurs during inspiration and widespread minor depolarization occurs during expiration. This depolarization is likely a source of respiratory drive. Further knowledge of intracellular and extracellular ionic changes associated with respiration will enhance our understanding of respiration and its role as a modulator of cellular membrane potential. This could expand treatment options for a wide range of health conditions, such as breathing disorders, stress-related disorders, and further our understanding of the Hering-Breuer reflex and respiratory sinus arrhythmia.Ó 2014 Elsevier Ltd. All rights reserved. IntroductionIn addition to gas exchange and oxygenation of the blood, respiration in the lungs can regulate multiple physiological processes throughout the body. Studies of the cardiovascular system, the peripheral nervous system, and the central nervous system provide evidence that respiratory patterns can exert a significant and immediate influence on a wide range of bodily functions, including changes in blood pressure and sympathovagal balance. Patterned respiration can regulate blood pressure and heart rate [1], as well as regulate rhythmic centers of the brain that control cardiovascular output [2,3]. While the majority of these findings have demonstrated the impact of respiration on cardiac output and other processes in isolated preparations, little work has focused on respiration's direct influence on membrane potential.This article reviews the current understanding of respiration as a regulator of cardiovascular physiology and nervous system function. More specifically, we discuss the role of respiratory rhythm and rate on both systemic and local control of these systems. We describe the role of pulmonary stretch receptors (with a focus on slowly adapting receptors) in converting breathing patterns into a functional, multi-faceted, mechanism that allows respiration to communicate with, and direct various aspects of cardiovascular and nervous system physiology. We propose a hypothesis in which inspiration and expiration are associated with transient increases and decreases in membrane potential that may underlie these widespread changes and how these membrane potential changes may underlie the chaotic dynamics of rhythmic breathing.Many studies focus on the brainstem as the primary modulator of resp...

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“…Early methods (Richardson et al, 1966;Weil et al, 1970) (Slessarev et al, 2007). Prospective end-tidal targeting makes use of a gas-blending device, called the RespirAct™, in combination with a modified sequential gas delivery system.…”

Section: Using Prospective End-tidal Targeting To Measure the Odc In mentioning

confidence: 99%

The in-vivo oxyhaemoglobin dissociation curve at sea level and high altitude

Balaban

Duffin

Preiss

et al. 2013

Respiratory Physiology & Neurobiology

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Some animals have adapted to hypoxia by increasing their haemoglobin affinity for oxygen, but in vitro studies have not shown any change of haemoglobin affinity for oxygen in human high altitude natives or lowlanders acutely acclimatized to high altitude. We conducted the first in vivo study of the oxyhaemoglobin dissociation curve by progressively reducing arterial PO 2 while maintaining normocapnia in lowlanders at sea level, lowlanders sojourning at 3600m for two weeks and native Andeans at the same altitude. We found that the in vivo PO 2 at which haemoglobin is half-saturated (P 50 ) is higher in lowlanders at sea level (32 mmHg) than that measured in vitro (27 mmHg) and that lowlanders and highlanders do significantly increase the in vivo affinity of their haemoglobin for oxygen with exposure to high altitude. These results indicate the value of an in vivo approach for studying the oxyhaemoglobin dissociation curve.iii

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Hypoxic ventilatory drive in normal man

Cited by 382 publications

References 32 publications

Variable effects of anaesthetics on the ventilatory response to hypoxaemia in man

Variable effects of anaesthetics on the ventilatory response to hypoxaemia in man

Widespread depolarization during expiration: A source of respiratory drive?

The in-vivo oxyhaemoglobin dissociation curve at sea level and high altitude

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