Immersion Pulmonary Edema in Special Forces Combat Swimmers

Mahon, Richard T.; Kerr, Stewart; Amundson, Dennis E.; Parrish, John S.

doi:10.1378/chest.122.1.383-a

Cited by 38 publications

(28 citation statements)

References 5 publications

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“…The diver ascends to the surface with severe dyspnoea and commonly describes a cough producing blood-tinged sputum. Similar findings can occur in swimmers related to exercise while immersed [11][12][13][14][15][16]. Auscultation reveals bibasilar rales and the chest radiograph shows a typical pulmonary oedema pattern.…”

Section: Immersion Pulmonary Oedemasupporting

confidence: 61%

Lung injury related to extreme environments

Adir

Bové

2014

Eur Respir Rev

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@ERSpublications Lung injury is a well understood and preventable consequence of water immersion while swimming and diving http://ow.ly/AOdvgAs extreme sports become more popular, related respiratory injury may compromise the athlete's performance and result in morbidity and even mortality. In this article we will discuss different lung injuries in relation to performing different activities in an extreme environment. Hydrostatic lung injuriesThe evolution of fish to amphibians, reptiles to endothermic birds and mammals has been accompanied by a progressively thinner pulmonary blood gas barrier, to accommodate the constraint of increased oxygen uptake and carbon dioxide output [1]. Accordingly, pulmonary circulation has evolved as a separate high flow-low pressure system. In humans, mean pulmonary artery pressures (PAP) are 8-20 mmHg, pulmonary wedge pressures are 5-14 mmHg and pulmonary capillary pressures are 8-12 mmHg [2]. A low-pressure regimen preserves the integrity of an alveolar capillary membrane only 0.3 mm thick. However, this structure is vulnerable to increased pressures during strenuous exercise or environmental hypoxic exposure as a cause of stress failure of the pulmonary capillaries and accumulation of extravascular lung water [3]. Reports of lung injury related to extremes of exercise and variations in ambient pressure and altitude confirm this vulnerability. The resulting lung injury takes the form of noncardiogenic pulmonary oedema.The occurrence of noncardiogenic pulmonary oedema and pulmonary haemorrhage has been described in relation to a variety of disorders related to auto-and exogenous immunological reactions, infections and certain inhalants. However, numerous reports of lung injury manifesting as pulmonary oedema with associated haemorrhage have been described more recently in relation to immersion underwater, swimming, extreme exercise and exposure to altitude. In addition, pulmonary oedema resulting from negative intra-alveolar pressure has been described in the anaesthesia literature and may play a role in exercise-and immersion-induced pulmonary oedema. Haemodynamically induced pulmonary oedemaA single mechanism responsible for production of noncardiogenic pulmonary oedema related to immersion, altitude and exercise has not been identified. However, a combination of haemodynamically related factors, alterations in capillary integrity, increased blood volume and increased cardiac output may all contribute to the syndrome. WEST et al.[4] described exercise-induced pulmonary haemorrhage in race For editorial comments see page 401.

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Section: Immersion Pulmonary Oedemasupporting

confidence: 61%

Lung injury related to extreme environments

Adir

Bové

2014

Eur Respir Rev

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“…Immersion pulmonary edema (IPE) is a condition in which cough, hemoptysis, dyspnea, and hypoxemia develop after surface swimming or diving, often in young, healthy individuals (34,45,57,64,96,123), including exceptionally fit military divers (59,64,95,121). It occurs predominantly in males.…”

Section: Pathological Effects Of Divingmentioning

confidence: 99%

Pulmonary gas exchange in diving

Moon

Cherry²,

Stolp³

et al. 2009

Journal of Applied Physiology

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Moon RE, Cherry AD, Stolp BW, Camporesi EM. Pulmonary gas exchange in diving. J Appl Physiol 106: 668 -677, 2009. First published November 13, 2008 doi:10.1152/japplphysiol.91104.2008.-Diving-related pulmonary effects are due mostly to increased gas density, immersion-related increase in pulmonary blood volume, and (usually) a higher inspired PO 2. Higher gas density produces an increase in airways resistance and work of breathing, and a reduced maximum breathing capacity. An additional mechanical load is due to immersion, which can impose a static transrespiratory pressure load as well as a decrease in pulmonary compliance. The combination of resistive and elastic loads is largely responsible for the reduction in ventilation during underwater exercise. Additionally, there is a density-related increase in dead space/tidal volume ratio (VD/VT), possibly due to impairment of intrapulmonary gas phase diffusion and distribution of ventilation. The net result of relative hypoventilation and increased VD/VT is hypercapnia. The effect of high inspired PO 2 and inert gas narcosis on respiratory drive appear to be minimal. Exchange of oxygen by the lung is not impaired, at least up to a gas density of 25 g/l. There are few effects of pressure per se, other than a reduction in the P50 of hemoglobin, probably due to either a conformational change or an effect of inert gas binding. respiratory dead space; ventilation-perfusion ratio; respiratory mechanics DESPITE HAVING EVOLVED in and adapted to an atmosphere with gas density close to 1 g/l, the performance of the human lung in the diving environment is remarkable. Adequate ventilation and gas exchange have been achieved at an ambient pressure up to 71 atmospheres absolute (ATA) [701 m of sea water (msw); 2,310 ft of sea water (fsw)] with an ambient PO 2 of 0.39 ATA (49), and with a PO 2 of 0.2 ATA up to a gas density of 25 g/l (50). Adequate exchange of oxygen and carbon dioxide while diving requires the ability to maintain ventilation in the face of significantly increased resistive and elastic loads. Resistance is increased primarily by the increase in breathing gas density. Elastic load is enhanced primarily by changes in transrespiratory pressure (P TR ). Inertial mechanical load is also increased, although this has a minimal effect on the diver. Added challenges include blunted respiratory drive due to elevated partial pressures of inert gas and oxygen, and possibly impaired diffusion within the alveolus (7). While in most dives the breathing gas is hyperoxic, thus precluding hypoxemia, hypercapnia is common. Hyperoxia, particularly in the venous blood, can induce a small reduction in CO 2 solubility, and hence an increase in venous PCO 2 via the Haldane effect (27,122). Arterial PCO 2 (Pa CO 2 ) is not affected by the Haldane effect because of regulation of breathing via the chemoreceptors, although hypercapnia does occur for other reasons as discussed below.Studies of pulmonary gas exchange under hyperbaric conditions designed to simulate diving have been performed...

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“…Symptoms may manifest early in dives, with reports of dyspnea as early as 7 min after reaching depth (13). Other cases have been reported after prolonged periods of exercise and immersion (1,29,30,34). The cause for this phenomenon is unknown.…”

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confidence: 96%

“…Pulmonary edema has been described in the dependent lung of special forces combat swimmers swimming in the lateral decubitus position (29,30). One study reported that subjects who have experienced IPE have an exaggerated vasoconstrictive response to applications of cold to the head and neck (40).…”

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confidence: 99%

Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA

Wester¹,

Cherry²,

Pollock³

et al. 2009

Journal of Applied Physiology

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Immersion pulmonary edema (IPE) is a condition with sudden onset in divers and swimmers suspected to be due to pulmonary arterial or venous hypertension induced by exercise in cold water, although it does occur even with adequate thermal protection. We tested the hypothesis that cold head immersion could facilitate IPE via a reflex rise in pulmonary vascular pressure due solely to cooling of the head. Ten volunteers were instrumented with ECG and radial and pulmonary artery catheters and studied at 1 atm absolute (ATA) during dry and immersed rest and exercise in thermoneutral (29 -31°C) and cold (18 -20°C) water. A head tent varied the temperature of the water surrounding the head independently of the trunk and limbs. Heart rate, Fick cardiac output (CO), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) were measured. MPAP, PAWP, and CO were significantly higher in cold pool water (P Յ 0.004). Resting MPAP and PAWP values (means Ϯ SD) were 20 Ϯ 2.9/13 Ϯ 3.9 (cold body/cold head), 21 Ϯ 3.1/14 Ϯ 5.2 (cold/warm), 14 Ϯ 1.5/10 Ϯ 2.2 (warm/warm), and 15 Ϯ 1.6/10 Ϯ 2.6 mmHg (warm/cold). Exercise values were higher; cold body immersion augmented the rise in MPAP during exercise. MAP increased during immersion, especially in cold water (P Ͻ 0.0001). Except for a transient additive effect on MAP and MPAP during rapid head cooling, cold water on the head had no effect on vascular pressures. The results support a hemodynamic cause for IPE mediated in part by cooling of the trunk and extremities. This does not support the use of increased head insulation to prevent IPE. diving; immersion; pulmonary edema; pulmonary circulation IMMERSION PULMONARY EDEMA (IPE) occurs sporadically in healthy divers and swimmers and is characterized by cough, shortness of breath, decreased blood oxygen levels (17,24,29,35,39), and sometimes death (13). Symptoms may manifest early in dives, with reports of dyspnea as early as 7 min after reaching depth (13). Other cases have been reported after prolonged periods of exercise and immersion (1,29,30,34). The cause for this phenomenon is unknown. Risk factors seem to include heavy exertion and cold water (24), although IPE has been reported in water close to thermoneutral temperatures without exertion (17,24). Studies of individuals who have recovered from IPE have not identified chronic pulmonary function abnormalities or pulmonary hypertension (28). Ventricular function (24) and resting pulmonary artery systolic pressures (28) are generally normal.

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Immersion Pulmonary Edema in Special Forces Combat Swimmers

Cited by 38 publications

References 5 publications

Lung injury related to extreme environments

Lung injury related to extreme environments

Pulmonary gas exchange in diving

Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA

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