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• The altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema.
  olivier castagna, david mac Iver
  Published on: 18 April 2017

• Published on: 18 April 2017

  The altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema.

  • olivier castagna, Scuba doctor Underwater research team (ERRSO) from the Military biomedical research institute (IRBA) Toulon, France
  • Other Contributors:
    • david mac Iver, Visiting Professor & Consultant Cardiologist

  To the editor,
  The postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
  In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
  It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of...

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  To the editor,
  The postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
  In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
  It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of increase in pulmonary vascular pressure in IPE occurrence. They, furthermore, proposed several possible explanations for IPE and SIPE: 1) transient impairment of left ventricular (LV) systolic function, 2) reduced diastolic LV compliance. They suggested that redistribution from the periphery into the thorax combined with a less compliant LV would lead to a higher LV end-diastolic pressure and pulmonary artery pressure and pulmonary artery wedge pressure in SIPE-susceptible individuals. The authors proposed that, with augmented preload attributable to immersion in cold water, a greater LV wall stiffness in SIPE-susceptible individuals could be the cause of higher LV filling pressure during exercise in cold water.
  We recently investigated the relationship between altered cardiac function and the development interstitial pulmonary edema in SCUBA divers. Fifteen healthy males performed a 30-min SCUBA dive in open sea. Echocardiography and lung ultrasound were performed before and immediately after immersion. We observed an increased preload and a right-left heart imbalance. Immediately following the dive the diameter of the inferior vena cava increased by 47 ± 5.2%, systolic pulmonary artery pressure increased by 105 ± 8.6%, left atrial volume increased by 18.0 ± 3.3% and left ventricle end-diastolic volume increased by 10.1 ± 2.4% suggesting both right and left ventricular filling pressures were elevated. Doppler studies showed an increased mitral E peak (+2.5 ± 0.3%) and E/A ratio (+22.5 ± 3.4%) with a decreased mitral A peak (-16.4 ± 2.7%), E peak deceleration time decreased (-14.5 ± 2.4%) consistent with rapid early left ventricular filling but there was no change in left ventricular stroke volume. There was an increase in right/left ventricle diameter ratio (+33.6 ± 4.8%) suggesting a relative increase in right heart output compared to the left.
  We suggest the changes probably reflect rapid early LV filling driven by the higher pulmonary artery pressures secondary to increased work done by the right ventricle.3 It is unlikely our subjects had reduced left ventricular compliance due to an abnormality interstitial collagen or changes in intracellular titin (in the absence of known heart disease or hypertension). It is, however, plausible that the subjects reached the left ventricular/pericardial elastic limit towards the end of diastole, required higher end-diastolic pressures to achieve greater end-diastolic volumes in the presence of thick walled ventricle or developed abnormal intracellular calcium homeostasis during effort.4
  Energy needs to be either added to the fluid or converted (say from kinetic energy) to create a higher pressure. A higher left ventricle end-diastolic pressure cannot be directly caused by diastolic dysfunction as the latter is not a form of energy. We think that the changes in left ventricle (LV) filling patterns are the result of an increased pulmonary venous pressure causing a rapid early diastolic filling due to the higher initial atrio-ventricular pressure gradient. The reduced A-wave velocity is a consequence of the higher end-diastolic pressure as the LV is already well filled. The “blood shift” induced by immersion will, sequentially, increases the right ventricular filling pressure, increasing right ventricle end-diastolic volume triggering the Frank-Starling mechanism, RV contraction and sequentially increasing pulmonary artery pressure, capillary pressure and, finally, LV filling pressure.3 At the same time, dilatation of the right heart might hamper filling of the left ventricle (ventricular interdependence) because of the limited distensibility of the pericardium and, so, may inhibit LV stroke volume.
  We observed that increased preload and a right-left heart imbalance were correlated with the accumulation of extravascular lung water (EVLW). We showed that it was the changes in right ventricular physiology rather than changes in left ventricular indices that correlated with the development of interstitial pulmonary edema. The severity of interstitial pulmonary edema, was significantly correlated with measures of increased cardiac preload, right ventricular area change (a surrogate of right ventricle ejection fraction) and pulmonary artery pressure, but not left ventricle ejection fraction (LVEF) or left ventricle stroke volume (LVSV). Furthermore, the lung comet score correlated significantly with IVC diameter, systolic pulmonary artery pressure, right/left ventricle diameter ratio and E-wave deceleration time.
  We have previously suggested acute pulmonary edema resulted from a mismatch or imbalance between the right and left ventricular stroke volume (SV)5. Although the pathophysiology of pulmonary (alveolar) edema (APE) is generally described in terms of a failing left ventricle, in reality, for APE to occur, there must be a mismatch between the right and left ventricular SV as fluid is lost from the circulation into the airspaces. The augmentation of right ventricular contractility increases stroke volume (and pulmonary pressures) relative to left ventricular SV which could then cause an increase in capillary hydrostatic pressure leading to transudation of fluid into the lung interstitium.5 A failure to increase LV stroke volume (relative to the RV stroke volume) due to a higher peripheral vascular resistance brought about by conditions such as systemic hypertension or cold water may increase the likelihood of occurrence of SIPE and IPE. The extravasation of fluid into the lung interstitium due to the RV/LV stroke volume mismatch is further exacerbated by higher heart rates explains interstitial pulmonary edema during exercise in divers.6
  We provide a greater understanding to the pathophysiological mechanisms proposed by Moon and colleagues.1, 2 The altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema. Our findings may have implications for the pathogenesis of immersion pulmonary edema and could help reduce the deaths in swimming induced pulmonary edema.
  We would be pleased to answer any request for further information.

  Yours respectfully,
  Olivier Castagna, M.D., Ph.D.

  1. Moon RE, Martina SD, Peacher DF and Kraus WE. Deaths in triathletes: immersion pulmonary oedema as a possible cause. BMJ Open Sport Exerc Med. 2016;2:e000146.
  2. Moon RE, Martina SD, Peacher DF, Potter JF, Wester TE, Cherry AD, Natoli MJ, Otteni CE, Kernagis DN, White WD and Freiberger JJ. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil. Circulation. 2016;133:988-96.
  3. MacIver DH, Adeniran I, MacIver IR, Revell A and Zhang H. Physiological mechanisms of pulmonary hypertension. Am Heart J. 2016;180:1-11.
  4. Adeniran I, MacIver DH, Hancox JC and Zhang H. Abnormal calcium homeostasis in heart failure with preserved ejection fraction is related to both reduced contractile function and incomplete relaxation: An electromechanically detailed biophysical modelling study. Frontiers Physiology. 2015;6:1-14.
  5. MacIver DH and Clark AL. The vital role of the right ventricle in the pathogenesis of acute pulmonary edema. The American journal of cardiology. 2015;115:992-1000.
  6. Castagna O, Gempp E, Poyet R, Schmid B, Desruelle AV, Crunel V, Maurin A, Choppard R and MacIver DH. Cardiovascular Mechanisms of Extravascular Lung Water Accumulation in Divers. Am J Cardiol. 2017;119:929-932.

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  Conflict of Interest:
  None declared.

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