Cardiac changes induced by immersion and breath-hold diving in humans

Marabotti, C; Scalzini, Alessandro; Cialoni, Danilo; Passera, Mirko; LʼAbbate, Antonio; Bedini, Remo

doi:10.1152/japplphysiol.00126.2008

Cited by 45 publications

(51 citation statements)

References 25 publications

(26 reference statements)

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“…The decrease in cardiac output was associated with Doppler-echocardiographic signs of diastolic left ventricular dysfunction (prevalence of early diastolic Wlling associated to shortened early Wlling deceleration time) no diVerently than those clinically observed in advanced hypertensive heart disease or in constrictive/restrictive heart diseases (Nishimura and Tajik 1997;Oh et al 2006), conWrming previous results (Marabotti et al , 2009.…”

Section: Discussionsupporting

confidence: 85%

“…The negative Wnding of changes in right ventricular diastolic dimension both during breath-hold diving, as in previous studies (Marabotti et al , 2009, and after underwater chest re-expansion also deserves a comment which concerns the relative inaccuracy of echocardiography in studying right ventricular cavity. In fact, owing to the complex three-dimensional shape of the right ventricle, only linear dimensions (mm) can be obtained in comparison to 3D (mL) of the left ventricle; this limitation may prevent the detection of small changes in right ventricular volume.…”

Section: Discussionmentioning

confidence: 57%

“…As a matter of fact, a cardiac diving response similar to that of marine mammals (reduction in stroke volume and cardiac output) was observed in humans only during immersion at depth, as compared to conditions, such as head-out surface immersion and full-body surface immersion, while breathing and breath-holding (Marabotti et al 2009), suggesting a possible role of chest squeeze in the induction of cardiovascular changes. On the other hand, reduction of chest volume, as occurring during breath-hold diving at residual lung volume, was able to induce hemoptysis and lower airways edema even at shallow depth (Lindholm et al 2008).…”

Section: Discussionmentioning

confidence: 93%

“…Beyond pointing out the integrated eVect of the diving reXex and of the body immersion during shallow diving, this approach has also highlighted the mechanical eVect of increased hydrostatic pressure and chest squeeze on cardiac function as a critical issue. In fact, a previous study on breath-hold diving has documented Doppler-echocardiographic changes consistent with a constrictive/restrictive pattern (Marabotti et al 2009). On the basis of this observation, we hypothesized that chest volume reduction, associated with a simultaneous increase of pulmonary blood content (pulmonary blood shift) (Arborelius et al 1972;Hong et al 1969), exerts a constraint on the heart that can induce a relative reduction of cardiac Wlling and output.…”

Section: Introductionmentioning

confidence: 91%

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Effects of depth and chest volume on cardiac function during breath-hold diving

Marabotti

Scalzini²,

Cialoni

et al. 2009

Eur J Appl Physiol

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Cardiac response to breath-hold diving in human beings is primarily characterized by the reduction of both heart rate and stroke volume. By underwater Doppler-echocardiography we observed a "restrictive/constrictive" left ventricular filling pattern compatible with the idea of chest squeeze and heart compression during diving. We hypothesized that underwater re-expansion of the chest would release heart constriction and normalize cardiac function. To this aim, 10 healthy male subjects (age 34.2 +/- 10.4) were evaluated by Doppler-echocardiography during breath-hold immersion at a depth of 10 m, before and after a single maximal inspiration from a SCUBA device. During the same session, all subjects were also studied at surface (full-body immersion) and at 5-m depth in order to better characterize the relationship of echo-Doppler pattern with depth. In comparison to surface immersion, 5-m deep diving was sufficient to reduce cardiac output (P = 0.042) and increase transmitral E-peak velocity (P < 0.001). These changes remained unaltered at a 10-m depth. Chest expansion at 10 m decreased left ventricular end-systolic volume (P = 0.024) and increased left ventricular stroke volume (P = 0.024). In addition, it decreased transmitral E-peak velocity (P = 0.012) and increased deceleration time of E-peak (P = 0.021). In conclusion the diving response, already evident during shallow diving (5 m) did not progress during deeper dives (10 m). The rapid improvement in systolic and diastolic function observed after lung volume expansion is congruous with the idea of a constrictive effect on the heart exerted by chest squeeze.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 91%

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Effects of depth and chest volume on cardiac function during breath-hold diving

Marabotti

Scalzini²,

Cialoni

et al. 2009

Eur J Appl Physiol

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“…Hair coat is wet, damp, 60 or hair if dried may be aggregated in spikes Froth emanating from nostrils or oral cavity 26,43,48,60,79,80 Froth in larynx or airways 26,43,48,60,79,80 Lungs distended and fail to collapse 49,60 Pulmonary congestion and edema 2,26,34,43,60,70,84 Pulmonary hemorrhages 2,26,35,79,80 Pulmonary emphysema 26,43,60 Right ventricular distension 2,43 Water and or foreign material in stomach 2,43 Aspirated stomach contents or other foreign material in larynx or airways 2,12,26,60 Mucus at the base of the tongue or in larynx 26 Fluid in the frontal or paranasal sinuses 49 Contusions or bruising in skin or subcutis if forcible submersion 49,60 Other traumatic lesions such as fractures 57 examination and determination of the cause of death even more challenging. Early changes are skin maceration, lividity, rigor mortis, and algor mortis, and late changes include initial putrefaction, advanced putrefaction including adipocere formation, and skeletonization.…”

Section: Lesionmentioning

confidence: 99%

Veterinary Forensic Pathology

McEwen

Gerdin²

2016

Vet Pathol

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Determining the cause of death in animals recovered from bodies of water, swimming pools, or other water-containing vessels is challenging. Animals recovered from water may or may not have drowned. The diagnosis of drowning is usually one of exclusion, requiring information from the crime scene, recovery scene, the medical history or reliable witness accounts. While there are characteristic macroscopic and microscopic lesions of drowning, none are specific and are dependent on the volume and tonicity of the drowning medium. Beyond interpreting the postmortem findings, the court may ask pathologists to comment on the behavioral and welfare implications of drowning. This requires an understanding of the drowning process, which is a complex series of sequential, concurrent, and overlapping cardiorespiratory reflexes, electrolyte and blood gas abnormalities, aspiration, physical exhaustion, and breathlessness eventually culminating in death. This review addresses the mechanisms, lesions, and diagnostic issues associated with drowning in nonaquatic companion animals.

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Saturation Diving; Physiology and Pathophysiology

Brubakk

Ross

Thom

2014

Comprehensive Physiology

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In saturation diving, divers stay under pressure until most of their tissues are saturated with breathing gas. Divers spend a long time in isolation exposed to increased partial pressure of oxygen, potentially toxic gases, bacteria, and bubble formation during decompression combined with shift work and long periods of relative inactivity. Hyperoxia may lead to the production of reactive oxygen species (ROS) that interact with cell structures, causing damage to proteins, lipids, and nucleic acid. Vascular gas-bubble formation and hyperoxia may lead to dysfunction of the endothelium. The antioxidant status of the diver is an important mechanism in the protection against injury and is influenced both by diet and genetic factors. The factors mentioned above may lead to production of heat shock proteins (HSP) that also may have a negative effect on endothelial function. On the other hand, there is a great deal of evidence that HSPs may also have a "conditioning" effect, thus protecting against injury. As people age, their ability to produce antioxidants decreases. We do not currently know the capacity for antioxidant defense, but it is reasonable to assume that it has a limit. Many studies have linked ROS to disease states such as cancer, insulin resistance, diabetes mellitus, cardiovascular diseases, and atherosclerosis as well as to old age. However, ROS are also involved in a number of protective mechanisms, for instance immune defense, antibacterial action, vascular tone, and signal transduction. Low-grade oxidative stress can increase antioxidant production. While under pressure, divers change depth frequently. After such changes and at the end of the dive, divers must follow procedures to decompress safely. Decompression sickness (DCS) used to be one of the major causes of injury in saturation diving. Improved decompression procedures have significantly reduced the number of reported incidents; however, data indicate considerable underreporting of injuries. Furthermore, divers who are required to return to the surface quickly are under higher risk of serious injury as no adequate decompression procedures for such situations are available. Decompression also leads to the production of endothelial microparticles that may reduce endothelial function. As good endothelial function is a documented indicator of health that can be influenced by regular exercise, regular physical exercise is recommended for saturation divers. Nowadays, saturation diving is a reasonably safe and well controlled method for working under water. Until now, no long-term impact on health due to diving has been documented. However, we still have limited knowledge about the pathophysiologic mechanisms involved. In particular we know little about the effect of long exposure to hyperoxia and microparticles on the endothelium.

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Cardiac changes induced by immersion and breath-hold diving in humans

Cited by 45 publications

References 25 publications

Effects of depth and chest volume on cardiac function during breath-hold diving

Effects of depth and chest volume on cardiac function during breath-hold diving

Veterinary Forensic Pathology

Saturation Diving; Physiology and Pathophysiology

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