Immersion Pulmonary Edema

FOR RELATED ARTICLE, SEE PAGE 1934Immersion pulmonary edema (IPE) occurs in swimmers and divers.1Wilmshurst P.T. Nuri M. Crowther A. Webb-Peploe M.M. Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension.Lancet. 1989; 333: 62-65Abstract Scopus (148) Google Scholar In this issue of CHEST, Volk et al2Volk C. Spiro J. Boswell G. et al.Incidence and impact of swimming-induced pulmonary edema on Navy SEAL candidates.Chest. 2021; 159: 1934-1941Abstract Full Text Full Text PDF Scopus (7) Google Scholar report that, in fit and healthy young men having US Navy SEAL training, 106 of 2117 men (5%) experienced swimming-induced pulmonary edema (SIPE). High incidence rates were also reported in young recruits to the Israeli Defense Force and during competitive river races in Sweden.3Adir Y. Shupak A. Gil A. et al.Swimming-induced pulmonary edema: clinical presentation and serial lung function.Chest. 2004; 126: 394-399Abstract Full Text Full Text PDF PubMed Scopus (106) Google Scholar,4Hardstedt M. Seiler C. Kristiansson I. Lundeqvist D. Klingberg C. Eriksson A.B. Swimming-induced pulmonary edema: diagnostic criteria validated by lung ultrasound.Chest. 2020; 58: 1586-1595Abstract Full Text Full Text PDF Scopus (13) Google Scholar The precise incidence rates differed, which may be because of differences in duration and intensity of exposure, but there is no doubt that SIPE is common, even in healthy individuals. FOR RELATED ARTICLE, SEE PAGE 1934 If a person suddenly is immersed up to their neck in water that is warm, so that cooling does not occur, the hydrostatic effects of water compression immediately pushes as much as 700 mL of blood centrally. Heart size increases, and cardiac filling pressures increase considerably.5Arborelius M. Balldin U.I. Lilja B. Lundgren C.E.G. Hemodynamic changes in man during immersion with the head above water.Aerosp Med. 1972; 43: 592-598PubMed Google Scholar This triggers immersion natriuresis and secondary diuresis that gradually return the filling pressures to usual levels for that individual. In cold water, vasoconstriction increases pulmonary capillary pressure further. In addition, the immersed person breathes with continuous negative airway pressure equal to the vertical distance between the water surface and the lung centroid. The raised pulmonary capillary pressures and negative airway pressures set the stage for fluid transudation into the alveoli; however, usually additional factors are required to precipitate frank pulmonary edema. Using invasive measurement, Moon et al6Moon R.E. Martina S.D. Peacher D.F. et al.Swimming-induced pulmonary edema: pathophysiology and risk reduction with sildenafil.Circulation. 2016; 133: 988-996Crossref PubMed Scopus (51) Google Scholar showed that people who had IPE have higher pulmonary capillary wedge pressures than control subjects when performing exercise while submerged in water at 20°C. In older people, left heart disease or hypertension may elevate preimmersion pulmonary capillary pressure, so that small increases cause the critical pressure differential between pulmonary capillary and alveoli to be exceeded. In fit young people, the additional factor is often strenuous swimming, but excessive fluid intake before swimming is also implicated.7Weiler-Ravell D. Shupak A. Goldenberg I. et al.Pulmonary oedema and haemoptysis induced by strenuous swimming.BMJ. 1995; 311: 361-362Crossref PubMed Scopus (103) Google Scholar Volk et al2Volk C. Spiro J. Boswell G. et al.Incidence and impact of swimming-induced pulmonary edema on Navy SEAL candidates.Chest. 2021; 159: 1934-1941Abstract Full Text Full Text PDF Scopus (7) Google Scholar report that 10 episodes of SIPE were in trainees who had had previous episodes. Recurrence of IPE is well-described, including separate episodes when swimming and when diving in the same individuals.1Wilmshurst P.T. Nuri M. Crowther A. Webb-Peploe M.M. Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension.Lancet. 1989; 333: 62-65Abstract Scopus (148) Google Scholar,6Moon R.E. Martina S.D. Peacher D.F. et al.Swimming-induced pulmonary edema: pathophysiology and risk reduction with sildenafil.Circulation. 2016; 133: 988-996Crossref PubMed Scopus (51) Google Scholar,7Weiler-Ravell D. Shupak A. Goldenberg I. et al.Pulmonary oedema and haemoptysis induced by strenuous swimming.BMJ. 1995; 311: 361-362Crossref PubMed Scopus (103) Google Scholar This suggests individual susceptibility, which is explained easily in those individuals with heart disease. It is less explicable in fit young individuals. Recurrent episodes of IPE are more frequent in those individuals with hypertension.8Gempp E. Demaistre S. Louge P. Hypertension is predictive of recurrent immersion pulmonary edema in scuba divers.Int J Cardiol. 2014; 172: 528-529Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar Some individuals who were normotensive at presentation with recurrent IPE became hypertensive when followed for ≥8 years.1Wilmshurst P.T. Nuri M. Crowther A. Webb-Peploe M.M. Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension.Lancet. 1989; 333: 62-65Abstract Scopus (148) Google Scholar These individuals have exaggerated vasoconstrictor responses to cold and other physiologic stimuli that predate onset of hypertension. Indeed, some of them got cardiac decompensation or even pulmonary edema out of the water during extreme cold exposure when lying supine.1Wilmshurst P.T. Nuri M. Crowther A. Webb-Peploe M.M. Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension.Lancet. 1989; 333: 62-65Abstract Scopus (148) Google Scholar They have increased susceptibility to pulmonary edema without the addition of negative airway pressure breathing from immersion. During immersion, the magnitude of negative airway pressure varies. When an individual is swimming, the lung centroid is nearer the surface than when the individual is standing vertically in the water. So, when one is swimming, inspiration involves less negative airway pressure than when standing. Many swimmers, when doing front crawl or breast-stroke, breathe out with their head underwater, so their mouth is at about the same level as the lung centroid, and the airway pressures are relatively normal during expiration. In scuba divers the situation is more complicated and affected by the type of equipment used, breathing gas, and depth. Open-circuit scuba delivers the breathing gas, commonly air, at the diver’s mouth at ambient pressure. Therefore, during head-first descent with the mouth below the lung centroid, the scuba diver breathes with CPAP. At depth, when an individual is swimming horizontally, the mouth is at about the level of the lung centroid. So airway pressures will be near normal, but the air will be denser in proportion to the absolute pressure, and maximum voluntary ventilation is inversely proportional to square root of density. At 30 m in seawater, the pressure is 4 bar. So air is four times denser than at the surface, and maximum voluntary ventilation is halved. At 30 m, a diver breathing air has an inspired Po2 of 0.84 bar, which produces additional vasoconstriction. If the diver experiences IPE at depth, during his ascent, his head is above his lung centroid, and respiration is with continuous negative airway pressure. This tends to worsen the IPE. In addition, the ascent causes a rapid reduction in inspired Po2 from 0.84 to 0.21 bar, so that some affected divers become unconscious during the ascent and drown. Scuba divers also use rebreathers, which are analogous to ultra-low flow in an anesthetic circle circuit. The diver breathes via a closed circuit from a gas reservoir, termed a counter-lung. CO2 is removed chemically from the expired gas, and the decrease in oxygen partial pressure is measured by oxygen sensors and corrected from an oxygen cylinder. The vertical distance between the counter-lung and the diver’s lung centroid determines whether the diver is breathing with a negative or positive airway pressure. Castagna et al9Castagna O. Regnard J. Gempp E. et al.The key roles of negative pressure breathing and exercise in the development of interstitial pulmonary edema in professional male SCUBA divers.Sports Med Open. 2018; 4: 1Crossref PubMed Scopus (16) Google Scholar assessed interstitial pulmonary edema using ultrasound-detected lung comet score in professional divers, who had not had IPE, after four interventions in random order. They used rebreathers underwater in the prone position at rest and on exercise, with the counter-lung mounted anteriorly or posteriorly. The lung comet score was zero at rest, irrespective of the counter-lung position. When the divers exercised, the lung comet score was 4.2 with the counter-lung mounted anteriorly so that there was positive pressure breathing and 15.1 with negative pressure breathing with a back-mounted counter-lung. Pulmonary artery pressure that was measured in the water with the use of echocardiography increased by approximately 6 mm Hg between the start and end of immersion at rest whether positive or negative pressure breathing, by 13 mm Hg during exercise with positive pressure breathing, and by 17 mm Hg during exercise with negative pressure breathing. Our present understanding suggests that episodes of IPE are the result of the interplay between individual predisposition and environmental circumstance, including equipment used in the case of divers. But there is more to understand, including why women appear more susceptible to IPE than men.4Hardstedt M. Seiler C. Kristiansson I. Lundeqvist D. Klingberg C. Eriksson A.B. Swimming-induced pulmonary edema: diagnostic criteria validated by lung ultrasound.Chest. 2020; 58: 1586-1595Abstract Full Text Full Text PDF Scopus (13) Google Scholar /cms/asset/106170cd-365d-44f6-a4ee-371395af98f6/mmc1.mp3Loading ... Download .mp3 (31.17 MB) Help with .mp3 files Audio Incidence and Impact of Swimming-Induced Pulmonary Edema on Navy SEAL CandidatesCHESTVol. 159Issue 5PreviewThe burden of SIPE in NSW training was greater than anticipated. Clinical symptoms and physical examination assisted by imaging were able to differentiate SIPE from pneumonia. ECG was not a useful diagnostic or screening tool, and height and weight did not affect risk of SIPE. Full-Text PDF