Role of airway receptors in altitude-induced dyspnea

Mansoor, Jim K.; Eldridge, Marlowe W.; Yoneda, Ken Y.; Schelegle, Ed S.; Wood, Steve

doi:10.1097/00005768-200109000-00005

Cited by 8 publications

(7 citation statements)

References 15 publications

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“…One might imagine that aerosolized local anesthesia could be used to temporarily denervate the lung, but it is difficult to anesthetize pulmonary stretch receptors using safe doses of aerosol local anesthetics (59,128,140). A positive result (diminution or elimination of mechanoreceptor relief) would support the SAPSR theory, but a negative result could be ascribed to failure of anesthesia.…”

Section: Evidence From Pharmacological Interventionmentioning

confidence: 99%

Air Hunger: A Primal Sensation and a Primary Element of Dyspnea

Banzett

Lansing

Binks

2021

Comprehensive Physiology

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The sensation that develops as a long breath hold continues is what this chapter is about. We term this sensation of an urge to breathe "air hunger". Air hunger is a primal sensation that alerts us to a failure to meet an urgent homeostatic need -to maintain gas exchange. Anxiety, frustration, and fear evoked by air hunger motivate behavioral actions to address the failure. Air hunger can be reliably quantified by most experimental subjects using rating scales, i.e., there is a consistent relationship between stimulus and rating. Stimuli that increase air hunger include hypercapnia, hypoxia, exercise, and acidosis, while tidal expansion of the lungs reduces air hunger. As such, the defining experimental paradigm to evoke air hunger is to elevate the drive to breath while mechanically restricting ventilation. Functional brain imaging studies have shown that air hunger activates the insular cortex (an integration center for perceptions related to homeostasis, including pain, food hunger and thirst), as well as limbic structures involved with anxiety and fear. The unpleasantness and emotional consequences of air hunger make it the most debilitating component of dyspnea, a symptom commonly associated with respiratory, cardiovascular and metabolic diseases. Although much has been learned about air hunger in the past few decades, much remains to be discovered, such as an accepted method to quantify air hunger in non-human animals, fundamental questions about neural mechanisms, and adequate and safe methods to mitigate air hunger in clinical situations. DIDACTIC SYNOPSIS Air hunger is the conscious appreciation of an uncomfortable urge to breathe.  Air hunger can be reliably scaled by most people using various psychophysical rating scales.Although non-human vertebrates presumably sense air hunger, there is currently no accepted experimental model to scale air hunger in animals.  Air hunger is a primal sensation, alerting the animal to a threat to homeostasis that requires a behavioral response more complex than increasing respiratory muscle output or cardiac output.  Air hunger activates limbic and paralimbic regions in the brain giving rise to anxiety and fear.  Air hunger arises when minute ventilation is less than desired minute ventilation. Current understanding is that a copy of motor activity in medullary respiratory centers ('corollary discharge') projects to sensory cortex, and is compared to signals of tidal lung inflation arising mainly in pulmonary stretch receptors.  Air hunger is the most uncomfortable and most prominent of the sensations comprising clinical dyspnea.

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Section: Evidence From Pharmacological Interventionmentioning

confidence: 99%

Air Hunger: A Primal Sensation and a Primary Element of Dyspnea

Banzett

Lansing

Binks

2021

Comprehensive Physiology

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“…Conversely, pulmonary afferents sensing lung inflation relieve air hunger (12,13,16,20). [This would also account for the absence of breathlessness and increase in sense of rapid breathing on ascent to altitude (21).] Thus it is not surprising to us that, in the study by Chonan et al (9), the peak level of difficulty of breathing averaged Ͻ15% of the visual analog scale.…”

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confidence: 97%

Time course of air hunger mirrors the biphasic ventilatory response to hypoxia

Moosavi¹,

Banzett²,

Butler³

2004

Journal of Applied Physiology

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Determining response dynamics of hypoxic air hunger may provide information of use in clinical practice and will improve understanding of basic dyspnea mechanisms. It is hypothesized that air hunger arises from projection of reflex brain stem ventilatory drive ("corollary discharge") to forebrain centers. If perceptual response dynamics are unmodified by events between brain stem and cortical awareness, this hypothesis predicts that air hunger will exactly track ventilatory response. Thus, during sustained hypoxia, initial increase in air hunger would be followed by a progressive decline reflecting biphasic reflex ventilatory drive. To test this prediction, we applied a sharp-onset 20-min step of normocapnic hypoxia and compared dynamic response characteristics of air hunger with that of ventilation in 10 healthy subjects. Air hunger was measured during mechanical ventilation (minute ventilation = 9 +/- 1.4 l/min; end-tidal Pco(2) = 37 +/- 2 Torr; end-tidal Po(2) = 45 +/- 7 Torr); ventilatory response was measured during separate free-breathing trials in the same subjects. Discomfort caused by "urge to breathe" was rated every 30 s on a visual analog scale. Both ventilatory and air hunger responses were modeled as delayed double exponentials corresponding to a simple linear first-order response but with a separate first-order adaptation. These models provided adequate fits to both ventilatory and air hunger data (r(2) = 0.88 and 0.66). Mean time constant and time-to-peak response for the average perceptual response (0.36 min(-1) and 3.3 min, respectively) closely matched corresponding values for the average ventilatory response (0.39 min(-1) and 3.1 min). Air hunger response to sustained hypoxia tracked ventilatory drive with a delay of approximately 30 s. Our data provide further support for the corollary discharge hypothesis for air hunger.

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“…In such conditions, human exercise capacity is limited. Other limiting factors are ambient temperature, humidity, degree of activity, and stress (19). Consequences of altitude ascent are often symptoms of high-altitude illness and infection.…”

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confidence: 99%