Operation Everest II: Elevated high-altitude pulmonary resistance unresponsive to oxygen

B. M. Groves, J. T. Reeves, J. R. Sutton, P. D. Wagner, A. Cymerman, M. K. Malconian, Paul Rock, P. M. Young, C. S. Houston

Research output: Contribution to journalArticle

192 Citations (Scopus)

Abstract

High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347, (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 ± 0.9 to 34 ± 3.0 mmHg and from 1.2 ± 0.1 to 4.3 ± 0.3 mmHg·l-1·min, respectively. During near maximal exercise PAP increased from 33 ± 1 mmHg at sea level to 54 ± 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.

Original languageEnglish
Pages (from-to)521-530
Number of pages10
JournalJournal of Applied Physiology
Volume63
Issue number2
StatePublished - 1 Dec 1987

Fingerprint

Oxygen
Arterial Pressure
Lung
Oceans and Seas
Respiration
Vascular Resistance
Pulmonary Wedge Pressure
Atrial Pressure
Cardiac Output
Sports
Volunteers
Heart Failure
Hemodynamics
Exercise
Pressure

Cite this

Groves, B. M., Reeves, J. T., Sutton, J. R., Wagner, P. D., Cymerman, A., Malconian, M. K., ... Houston, C. S. (1987). Operation Everest II: Elevated high-altitude pulmonary resistance unresponsive to oxygen. Journal of Applied Physiology, 63(2), 521-530.
Groves, B. M. ; Reeves, J. T. ; Sutton, J. R. ; Wagner, P. D. ; Cymerman, A. ; Malconian, M. K. ; Rock, Paul ; Young, P. M. ; Houston, C. S. / Operation Everest II : Elevated high-altitude pulmonary resistance unresponsive to oxygen. In: Journal of Applied Physiology. 1987 ; Vol. 63, No. 2. pp. 521-530.
@article{41f92fa0dcf04612948ef3e0c1b11d6b,
title = "Operation Everest II: Elevated high-altitude pulmonary resistance unresponsive to oxygen",
abstract = "High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347, (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 ± 0.9 to 34 ± 3.0 mmHg and from 1.2 ± 0.1 to 4.3 ± 0.3 mmHg·l-1·min, respectively. During near maximal exercise PAP increased from 33 ± 1 mmHg at sea level to 54 ± 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100{\%} O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.",
author = "Groves, {B. M.} and Reeves, {J. T.} and Sutton, {J. R.} and Wagner, {P. D.} and A. Cymerman and Malconian, {M. K.} and Paul Rock and Young, {P. M.} and Houston, {C. S.}",
year = "1987",
month = "12",
day = "1",
language = "English",
volume = "63",
pages = "521--530",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "2",

}

Groves, BM, Reeves, JT, Sutton, JR, Wagner, PD, Cymerman, A, Malconian, MK, Rock, P, Young, PM & Houston, CS 1987, 'Operation Everest II: Elevated high-altitude pulmonary resistance unresponsive to oxygen', Journal of Applied Physiology, vol. 63, no. 2, pp. 521-530.

Operation Everest II : Elevated high-altitude pulmonary resistance unresponsive to oxygen. / Groves, B. M.; Reeves, J. T.; Sutton, J. R.; Wagner, P. D.; Cymerman, A.; Malconian, M. K.; Rock, Paul; Young, P. M.; Houston, C. S.

In: Journal of Applied Physiology, Vol. 63, No. 2, 01.12.1987, p. 521-530.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Operation Everest II

T2 - Elevated high-altitude pulmonary resistance unresponsive to oxygen

AU - Groves, B. M.

AU - Reeves, J. T.

AU - Sutton, J. R.

AU - Wagner, P. D.

AU - Cymerman, A.

AU - Malconian, M. K.

AU - Rock, Paul

AU - Young, P. M.

AU - Houston, C. S.

PY - 1987/12/1

Y1 - 1987/12/1

N2 - High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347, (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 ± 0.9 to 34 ± 3.0 mmHg and from 1.2 ± 0.1 to 4.3 ± 0.3 mmHg·l-1·min, respectively. During near maximal exercise PAP increased from 33 ± 1 mmHg at sea level to 54 ± 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.

AB - High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347, (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 ± 0.9 to 34 ± 3.0 mmHg and from 1.2 ± 0.1 to 4.3 ± 0.3 mmHg·l-1·min, respectively. During near maximal exercise PAP increased from 33 ± 1 mmHg at sea level to 54 ± 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.

UR - http://www.scopus.com/inward/record.url?scp=0023639981&partnerID=8YFLogxK

M3 - Article

C2 - 3654410

AN - SCOPUS:0023639981

VL - 63

SP - 521

EP - 530

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 2

ER -

Groves BM, Reeves JT, Sutton JR, Wagner PD, Cymerman A, Malconian MK et al. Operation Everest II: Elevated high-altitude pulmonary resistance unresponsive to oxygen. Journal of Applied Physiology. 1987 Dec 1;63(2):521-530.