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Hypovolemia explains the reduced stroke volume at altitude
During acute altitude exposure tachycardia increases cardiac output (Q) thus preserving systemic O(2) delivery. Within days of acclimatization, however, Q normalizes following an unexplained reduction in stroke volume (SV). To investigate whether the altitude-mediated reduction in plasma volume (PV)...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3841030/ https://www.ncbi.nlm.nih.gov/pubmed/24303166 http://dx.doi.org/10.1002/phy2.94 |
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author | Siebenmann, Christoph Hug, Mike Keiser, Stefanie Müller, Andrea van Lieshout, Johannes Rasmussen, Peter Lundby, Carsten |
author_facet | Siebenmann, Christoph Hug, Mike Keiser, Stefanie Müller, Andrea van Lieshout, Johannes Rasmussen, Peter Lundby, Carsten |
author_sort | Siebenmann, Christoph |
collection | PubMed |
description | During acute altitude exposure tachycardia increases cardiac output (Q) thus preserving systemic O(2) delivery. Within days of acclimatization, however, Q normalizes following an unexplained reduction in stroke volume (SV). To investigate whether the altitude-mediated reduction in plasma volume (PV) and hence central blood volume (CBV) is the underlying mechanism we increased/decreased CBV by means of passive whole body head-down (HDT) and head-up (HUT) tilting in seven lowlanders at sea level (SL) and after 25/26 days of residence at 3454 m. Prior to the experiment on day 26, PV was normalized by infusions of a PV expander. Cardiovascular responses to whole body tilting were monitored by pulse contour analysis. After 25/26 days at 3454 m PV and blood volume decreased by 9 ± 4% and 6 ± 2%, respectively (P < 0.001 for both). SV was reduced compared to SL for each HUT angle (P < 0.0005). However, the expected increase in SV from HUT to HDT persisted and ended in the same plateau as at SL, albeit this was shifted 18 ± 20° toward HDT (P = 0.019). PV expansion restored SV to SL during HUT and to an ∼8% higher level during HDT (P = 0.003). The parallel increase in SV from HUT to HDT at altitude and SL to a similar plateau demonstrates an unchanged dependence of SV on CBV, indicating that the reduced SV during HUT was related to an attenuated CBV for a given tilt angle. Restoration of SV by PV expansion rules out a significant contribution of other mechanisms, supporting that resting SV at altitude becomes reduced due to a hypovolemia. |
format | Online Article Text |
id | pubmed-3841030 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-38410302013-12-03 Hypovolemia explains the reduced stroke volume at altitude Siebenmann, Christoph Hug, Mike Keiser, Stefanie Müller, Andrea van Lieshout, Johannes Rasmussen, Peter Lundby, Carsten Physiol Rep Original Research During acute altitude exposure tachycardia increases cardiac output (Q) thus preserving systemic O(2) delivery. Within days of acclimatization, however, Q normalizes following an unexplained reduction in stroke volume (SV). To investigate whether the altitude-mediated reduction in plasma volume (PV) and hence central blood volume (CBV) is the underlying mechanism we increased/decreased CBV by means of passive whole body head-down (HDT) and head-up (HUT) tilting in seven lowlanders at sea level (SL) and after 25/26 days of residence at 3454 m. Prior to the experiment on day 26, PV was normalized by infusions of a PV expander. Cardiovascular responses to whole body tilting were monitored by pulse contour analysis. After 25/26 days at 3454 m PV and blood volume decreased by 9 ± 4% and 6 ± 2%, respectively (P < 0.001 for both). SV was reduced compared to SL for each HUT angle (P < 0.0005). However, the expected increase in SV from HUT to HDT persisted and ended in the same plateau as at SL, albeit this was shifted 18 ± 20° toward HDT (P = 0.019). PV expansion restored SV to SL during HUT and to an ∼8% higher level during HDT (P = 0.003). The parallel increase in SV from HUT to HDT at altitude and SL to a similar plateau demonstrates an unchanged dependence of SV on CBV, indicating that the reduced SV during HUT was related to an attenuated CBV for a given tilt angle. Restoration of SV by PV expansion rules out a significant contribution of other mechanisms, supporting that resting SV at altitude becomes reduced due to a hypovolemia. Blackwell Publishing Ltd 2013-10 2013-10-02 /pmc/articles/PMC3841030/ /pubmed/24303166 http://dx.doi.org/10.1002/phy2.94 Text en © 2013 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society http://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation. |
spellingShingle | Original Research Siebenmann, Christoph Hug, Mike Keiser, Stefanie Müller, Andrea van Lieshout, Johannes Rasmussen, Peter Lundby, Carsten Hypovolemia explains the reduced stroke volume at altitude |
title | Hypovolemia explains the reduced stroke volume at altitude |
title_full | Hypovolemia explains the reduced stroke volume at altitude |
title_fullStr | Hypovolemia explains the reduced stroke volume at altitude |
title_full_unstemmed | Hypovolemia explains the reduced stroke volume at altitude |
title_short | Hypovolemia explains the reduced stroke volume at altitude |
title_sort | hypovolemia explains the reduced stroke volume at altitude |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3841030/ https://www.ncbi.nlm.nih.gov/pubmed/24303166 http://dx.doi.org/10.1002/phy2.94 |
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