Comprehensive Physiology Wiley Online Library

Ventilatory Responses to Acute and Chronic Hypoxia

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Abstract

The sections in this article are:

1 Ventilatory Responses to Acute Hypoxia
1.1 Mechanisms of Ventilatory Changes during Acute Hypoxia
2 Ventilatory Acclimatization to Short‐Term Hypoxia
2.1 Historical Perspective
2.2 Time Course
2.3 Variation
3 Mechanisms of Short‐Term Accumatization to Hypoxia
3.1 Role of Medullary Chemoreceptors
3.2 Role of Peripheral Chemoreceptors
3.3 Possible Mechanisms for Increased Carotid Body Sensitivity during Short‐Term Acclimatization
3.4 Role of the Central Nervous System
3.5 Ventilation, Metabolic Rate, and Lung Mechanics
4 Deacclimatization Following Acclimatization to Short‐Term Hypoxia
5 Ventilation and Ventilatory Control in Long‐Term Hypoxia
5.1 Mechanisms of Acclimatization to Long‐term Hypoxia
6 Effects of Hypoxia on Breathing During Sleep
6.1 Sleep at Sea Level
6.2 Sleep during Hypoxia
6.3 Changes in Breathing during Sleep at Sea Level
6.4 Changes in Breathing during Sleep at High Altitude
7 Benefits and Shortcomings of Breathing Changes During Hypoxia
Figure 1. Figure 1.

Schematic of the temporal pattern of pulmonary ventilation (), partial pressure of carbon dioxide in arterial blood (Paco2, and partial pressure of oxygen in arterial blood (Pao2 during exposure of humans to an altitude of approximately 4,300 m.

Figure 2. Figure 2.

Schematic of some of the structures involved in ventilatory changes caused by hypoxia (upper portion) and a listing of the postulated mechanism for the ventilatory changes during each phase of hypoxia.

Figure 3. Figure 3.

O2–CO2 diagram indicating mean values of alveolar Paco2 after completion of ventilatory acclimatization to various levels of prolonged hypoxia according to Rahn and Otis . Triangle values were added by West et al. for extreme altitudes.

From West et al.
Figure 4. Figure 4.

Mean (± SE) changes in arterial Po2 and acid‐base status in five human subjects during 10–11 days' sojourn at 4,300 m.

From Forster et al.
Figure 5. Figure 5.

Mean (± SE) changes in arterial Pco2 (Paco2 and arterial Po2 (Pao2 during exposure of carotid body intact (circles) and carotid body–denervated (triangles) goats to two levels of hypobaric hypoxia (moderate, left; severe, right). C indicates control normoxia values; open symbols indicate acute return to normoxia. Asterisks indicate significant difference from control normoxia value.

From Smith et al.
Figure 6. Figure 6.

Left panel: Mean (± SE) changes in systemic arterial Po2, Pco2, and pH in six awake goats during 6 h of isolated perfusion of the carotid body with blood controlled at a Po2 of 40 torr by an extracorporeal circuit. Open symbols indicate normoxic conditions at the carotid body. The time‐dependent fall in Paco2 from 0.5 h to 4 h is indicative of acclimatization in the absence of brain hypoxia. Right panel: Mean (± SE) changes in systemic arterial Po2, Pco2, and pH in six awake goats during 4 h of isolated perfusion of the carotid body with blood controlled at a mean normoxic Pco2 of 78 torr by an extracorporeal circuit. Open symbols indicate normocapnic conditions at the carotid body. There was no evidence of acclimatization (no time‐dependent fall in Paco2 with hypercapnic stimulation of the carotid body. Arrows indicate significant differences between means (P < 0.05).

From Bisgard et al.
Figure 7. Figure 7.

Left panel: Data from chloralose‐anesthetized goats illustrating the time course of single fiber carotid body afferent discharge frequency up to 4 h of arterial hypoxia (Pao2 = 40 torr, n = 13). Right panel: Data from control normoxic goats (n = 5).

From Nielsen et al.
Figure 8. Figure 8.

Integrated electromyogram of the crural diaphragm and the transversus abdominis muscles and the transthoracic impedance measurement of pulmonary ventilation in one carotid body‐denervated pony during sea‐level control, after 5 and 20 min and 3 and 48 h of hypoxia (Pao2 ≈ 45 torr) and after 10 min of return to sea level. Numbers in parentheses are Paco2 in torr. Note the constant waxing and waning (Cheynes‐Stokes) of breathing throughout hypoxia, which was alleviated within 10 min of return to sea level.



Figure 1.

Schematic of the temporal pattern of pulmonary ventilation (), partial pressure of carbon dioxide in arterial blood (Paco2, and partial pressure of oxygen in arterial blood (Pao2 during exposure of humans to an altitude of approximately 4,300 m.



Figure 2.

Schematic of some of the structures involved in ventilatory changes caused by hypoxia (upper portion) and a listing of the postulated mechanism for the ventilatory changes during each phase of hypoxia.



Figure 3.

O2–CO2 diagram indicating mean values of alveolar Paco2 after completion of ventilatory acclimatization to various levels of prolonged hypoxia according to Rahn and Otis . Triangle values were added by West et al. for extreme altitudes.

From West et al.


Figure 4.

Mean (± SE) changes in arterial Po2 and acid‐base status in five human subjects during 10–11 days' sojourn at 4,300 m.

From Forster et al.


Figure 5.

Mean (± SE) changes in arterial Pco2 (Paco2 and arterial Po2 (Pao2 during exposure of carotid body intact (circles) and carotid body–denervated (triangles) goats to two levels of hypobaric hypoxia (moderate, left; severe, right). C indicates control normoxia values; open symbols indicate acute return to normoxia. Asterisks indicate significant difference from control normoxia value.

From Smith et al.


Figure 6.

Left panel: Mean (± SE) changes in systemic arterial Po2, Pco2, and pH in six awake goats during 6 h of isolated perfusion of the carotid body with blood controlled at a Po2 of 40 torr by an extracorporeal circuit. Open symbols indicate normoxic conditions at the carotid body. The time‐dependent fall in Paco2 from 0.5 h to 4 h is indicative of acclimatization in the absence of brain hypoxia. Right panel: Mean (± SE) changes in systemic arterial Po2, Pco2, and pH in six awake goats during 4 h of isolated perfusion of the carotid body with blood controlled at a mean normoxic Pco2 of 78 torr by an extracorporeal circuit. Open symbols indicate normocapnic conditions at the carotid body. There was no evidence of acclimatization (no time‐dependent fall in Paco2 with hypercapnic stimulation of the carotid body. Arrows indicate significant differences between means (P < 0.05).

From Bisgard et al.


Figure 7.

Left panel: Data from chloralose‐anesthetized goats illustrating the time course of single fiber carotid body afferent discharge frequency up to 4 h of arterial hypoxia (Pao2 = 40 torr, n = 13). Right panel: Data from control normoxic goats (n = 5).

From Nielsen et al.


Figure 8.

Integrated electromyogram of the crural diaphragm and the transversus abdominis muscles and the transthoracic impedance measurement of pulmonary ventilation in one carotid body‐denervated pony during sea‐level control, after 5 and 20 min and 3 and 48 h of hypoxia (Pao2 ≈ 45 torr) and after 10 min of return to sea level. Numbers in parentheses are Paco2 in torr. Note the constant waxing and waning (Cheynes‐Stokes) of breathing throughout hypoxia, which was alleviated within 10 min of return to sea level.

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Gerald E. Bisgard, Hubert V. Forster. Ventilatory Responses to Acute and Chronic Hypoxia. Compr Physiol 2011, Supplement 14: Handbook of Physiology, Environmental Physiology: 1207-1239. First published in print 1996. doi: 10.1002/cphy.cp040252