Thoracic blood shift
Thoracic blood shift, commonly shortened to blood shift in freediving, is the redistribution of blood from the peripheral circulation into the thorax and pulmonary circulation during immersion and diving. It increases central and pulmonary blood volume and becomes particularly important during deep breath-hold diving, when increasing ambient pressure compresses the gas in the lungs.[1][2]
The shift begins with immersion itself and is augmented during descent by hydrostatic compression and changes in intrathoracic pressure. It is related to, but is not synonymous with, the diving response: peripheral vasoconstriction during apnea can contribute to centralisation of blood, while immersion and pressure also produce mechanical redistribution of venous blood independently of the autonomic response.[1][3]
Mechanism
[edit]During immersion, hydrostatic pressure on the body and reduction of the gravitational pooling of blood in the limbs increase venous return and central blood volume. During descent, increasing ambient pressure progressively compresses pulmonary gas according approximately to Boyle's law. As lung volume decreases, blood is displaced into the vessels of the chest and lungs, occupying part of the thoracic volume previously occupied by gas.[2]
The effect becomes increasingly important at low lung volumes. Falling intrathoracic pressure and peripheral vasoconstriction can further increase the movement of blood into the thoracic circulation. The pulmonary vascular bed becomes engorged, increasing the volume of blood contained within and around the lungs.[2][3]
Role in deep breath-hold diving
[edit]
Thoracic blood shift is important in explaining why the surface residual volume (RV) of the lungs does not represent a rigid depth limit for breath-hold divers. A simple application of Boyle's law predicts that, once a lung initially near total lung capacity has been compressed to its surface RV, further descent would require compression below the minimum lung volume measured at the surface. Redistribution of blood into the thorax partially replaces the volume lost by the compressed pulmonary gas, allowing the chest and lungs to accommodate further reduction in gas volume.[2][3]
Historical measurements using impedance plethysmography demonstrated substantial blood redistribution during breath-hold dives. Schaefer and colleagues reported shifts of approximately 1,047 mL at 27 m (90 ft) and 850 mL at 40 m (130 ft).[4] Later observations during simulated dives have also demonstrated large increases in thoracoabdominal blood volume.[3]
The blood shift does not completely prevent airway or alveolar collapse. At extreme depths, regional airway closure and atelectasis may occur and pulmonary gas exchange can become impaired. Other adaptations used by elite freedivers, including glossopharyngeal insufflation ("lung packing") and exsufflation, can further alter the lung volumes at which these effects occur.[2]
Pathophysiology
[edit]The same pulmonary vascular engorgement that helps accommodate lung compression may contribute to injury when sufficiently pronounced. Increased pulmonary blood volume, negative intrathoracic pressure and elevated pulmonary capillary pressure can increase mechanical stress on the alveolar–capillary membrane.[2]
At extreme compression this has been associated with pulmonary edema and hemorrhage, including hemoptysis, within the spectrum commonly called lung squeeze by freedivers. Thoracic blood shift is therefore regarded as a protective physiological response to compression, but its capacity is finite and the associated vascular changes may contribute to pulmonary pathology at extreme depths.[2][5]
Research history
[edit]The ability of human breath-hold divers to descend substantially deeper than predicted from the ratio of total lung capacity to residual volume led physiologists to investigate changes in thoracic blood volume during descent. Experiments in the 1960s demonstrated pressure-dependent movement of blood into the thorax and helped establish blood shift as an explanation for human tolerance of lung compression below the predicted surface-RV limit.[4][1]
Subsequent research has incorporated measurements of pulmonary gas exchange, thoracic blood volume, cardiovascular function and lung mechanics. Modern reviews regard thoracic blood shift as one of the principal pulmonary and circulatory responses enabling deep human breath-hold diving, while also recognising its relationship to pulmonary vascular stress and diving-related lung injury.[3][2][6]
See also
[edit]References
[edit]- 1 2 3 Fitz-Clarke, John R. (2018). "Breath-Hold Diving". Comprehensive Physiology. 8 (2): 585–630. doi:10.1002/cphy.c160008. ISBN 978-0-470-65071-4. PMID 29687909.
{{cite journal}}: CS1 maint: periodical has ISBN (link) - 1 2 3 4 5 6 7 8 Tetzlaff K, Lemaitre F, Burgstahler C, Luetkens JA, Eichhorn L (2021). "Going to Extremes of Lung Physiology—Deep Breath-Hold Diving". Frontiers in Physiology. 12 710429. doi:10.3389/fphys.2021.710429. PMC 8299524. PMID 34305657.
- 1 2 3 4 5 Patrician A, Dujić Ž, Spajić B, Drviš I, Ainslie PN (2021). "Breath-Hold Diving – The Physiology of Diving Deep and Returning". Frontiers in Physiology. 12 639377. doi:10.3389/fphys.2021.639377. PMC 8176094. PMID 34093221.
- 1 2 Schaefer KE, Allison RD, Dougherty JH, Carey CR, Walker R, Yost F, Parker D (1968). "Pulmonary and circulatory adjustments determining the limits of depths in breathhold diving". Science. 162 (3857): 1020–1023. doi:10.1126/science.162.3857.1020. PMID 5725383.
- ↑ Schipke JD, Lemaitre F, Cleveland S, Tetzlaff K (2019). "Effects of Breath-Hold Deep Diving on the Pulmonary System". Respiration. 97 (5): 476–483. doi:10.1159/000495757. PMID 30783070.
- ↑ Paganini M, Moon RE, Camporesi EM, Bosco G (2026). "Advances in breath-hold diving research: a state-of-the-art review". European Journal of Applied Physiology. 126 (3): 1223–1243. doi:10.1007/s00421-025-06093-6. PMC 13013280. PMID 41417060.