Serial changes in nasal potential difference and lung  electrical impedance tomography at high altitude

Mason, Nicholas; Petersen, Morten Krogh; Mélot, Christian; Imanow, Bakyt; Matveykine, Olga; Gautier, Marie-Therese; Sarybaev, Akpay; Aldashev, Almaz; Миррахимов, М М; Brown, Brian; Leathard, A D; Naeije, Robert

doi:10.1152/japplphysiol.00777.2002

Cited by 48 publications

(35 citation statements)

References 46 publications

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“…This is in keeping with previous hemodynamic and echocardiographic measurements, indicating an enhanced LV systolic function in hypoxic healthy volunteers (2,6,19,24,29). In contrast, hypoxia did not affect RV area SF, TAPSE, nor any of the pulsed TDI indexes of systolic RV function, all of which were increased by dobutamine.…”

Section: Discussionsupporting

confidence: 91%

“…keeping with previous reports of hypoxic exposure-induced LV diastolic dysfunction on the basis of transmitral flow (2,6,19) and recently of mitral annulus pulsed TDI increased A wave in high-altitude newcomers (2). The authors of this last study suggested that increased atrial contraction may prevent the appearance of LV diastolic dysfunction in healthy subjects.…”

Section: Discussionsupporting

confidence: 90%

“…Recent hypobaric chamber experiments confirmed the preservation of LV systolic function but showed an alteration of mitral inflow pattern with a decrease of the E/A ratio, suggestive of an alteration of diastolic function (6). This observation was confirmed in high-altitude newcomers (2,19), with mitral annulus pulsed TDI measurements in one of these studies (2).…”

Section: Discussionmentioning

confidence: 63%

“…The mechanisms accounting for this limitation of maximal cardiac output remain unclear. Echocardiographic studies in hypoxic healthy volunteers have shown a preservation of left ventricular (LV) contractility but reported altered mitral flow patterns, suggestive of LV diastolic dysfunction (2,6,19). Hypoxic pulmonary vasoconstriction would be expected to induce major right ventricle (RV) function changes in response to increased afterload (21).…”

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confidence: 99%

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Right and left ventricular adaptation to hypoxia: a tissue Doppler imaging study

Huez¹,

Retailleau²,

Unger³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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107

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Hypoxia has been reported to alter left ventricular (LV) diastolic function, but associated changes in right ventricular (RV) systolic and diastolic function remain incompletely documented. We used echocardiography and tissue Doppler imaging to investigate the effects on RV and LV function of 90 min of hypoxic breathing (fraction of inspired O 2 of 0.12) compared with those of dobutamine to reproduce the same heart rate effects without change in pulmonary vascular tone in 25 healthy volunteers. Hypoxia and dobutamine increased cardiac output and tricuspid regurgitation velocity. Hypoxia and dobutamine increased LV ejection fraction, isovolumic contraction wave velocity (ICV), acceleration (ICA), and systolic ejection wave velocity (S) at the mitral annulus, indicating increased LV systolic function. Dobutamine had similar effects on RV indexes of systolic function. Hypoxia did not change RV area shortening fraction, tricuspid annular plane systolic excursion, ICV, ICA, and S at the tricuspid annulus. Regional longitudinal wall motion analysis revealed that S, systolic strain, and strain rate were not affected by hypoxia and increased by dobutamine on the RV free wall and interventricular septum but increased by both dobutamine and hypoxia on the LV lateral wall. Hypoxia increased the isovolumic relaxation time related to RR interval (IRT/RR) at both annuli, delayed the onset of the E wave at the tricuspid annulus, and decreased the mitral and tricuspid inflow and annuli E/A ratio. We conclude that hypoxia in normal subjects is associated with altered diastolic function of both ventricles, improved LV systolic function, and preserved RV systolic function. dobutamine; right ventricle; left ventricle; echocardiography EXPOSURE TO HYPOXIA in humans is associated with a preserved cardiac output at rest but limited cardiac output during exercise (26). The mechanisms accounting for this limitation of maximal cardiac output remain unclear. Echocardiographic studies in hypoxic healthy volunteers have shown a preservation of left ventricular (LV) contractility but reported altered mitral flow patterns, suggestive of LV diastolic dysfunction (2,6,19). Hypoxic pulmonary vasoconstriction would be expected to induce major right ventricle (RV) function changes in response to increased afterload (21). It has been recently suggested that inhibition of the hypoxic pressor response by sildenafil improves exercise capacity at high altitude by allowing for increased cardiac output and O 2 delivery to the tissues (10).How hypoxia and hypoxic pulmonary vasoconstriction-related increase in afterload affect RV function is not exactly known.Standard Doppler echocardiography to evaluate RV function is limited by its complex geometry and nonconcentric contraction patterns (3, 4, 16). We wondered whether tissue Doppler imaging (TDI) could provide a more exact assessment of RV function. This recently introduced approach allows the noninvasive determination of myocardial velocity in the human heart and has the potential of shape-independent a...

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 63%

mentioning

confidence: 99%

See 2 more Smart Citations

Right and left ventricular adaptation to hypoxia: a tissue Doppler imaging study

Huez¹,

Retailleau²,

Unger³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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107

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“…Two recent studies reported an altitude-induced increase in nasal PD in healthy subjects [34,35]. This finding, which is in contrast with the current data and all the available in vitro and in vivo data on the effects of hypoxia on respiratory sodium transport [5,15], has been attributed to nasal epithelial dryness-induced increase in chloride secretion [35], a phenomenon that has never been shown to occur at the alveolar level.…”

Section: Discussioncontrasting

confidence: 89%

High altitude impairs nasal transepithelial sodium transport in HAPE-prone subjects

Sartori¹,

Duplain²,

Lepori³

et al. 2004

Eur Respir J

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High-altitude pulmonary oedema (HAPE) occurs in predisposed individuals at altitudes w2,500 m. Defective alveolar fluid clearance secondary to a constitutive impairment of the respiratory transepithelial sodium transport contributes to its pathogenesis. Hypoxia impairs the transepithelial sodium transport in alveolar epithelial type II cells in vitro. If this impairment is also present in vivo, high-altitude exposure could aggravate the constitutive defect in sodium transport in HAPE-prone subjects, and thereby further facilitate pulmonary oedema.Therefore, the aim of the current study was to measure the nasal potential difference (PD) in 21 HAPE-prone and 29 HAPE-resistant subjects at low altitude and 30 h after arrival at high altitude (4,559 m).High-altitude exposure significantly decreased the mean¡SD nasal PD in HAPEprone (18.0¡6.2 versus 12.5¡6.8 mV) but not in HAPE-resistant subjects (25.6¡9.4 versus 22.9¡9.2 mV). This altitude-induced decrease was not associated with an altered amiloride-sensitive fraction, but was associated with a significantly lower amilorideinsensitive fraction of the nasal PD.These findings provide evidence in vivo that an environmental factor may impair respiratory transepithelial sodium transport in humans. They are consistent with the concept that in high-altitude pulmonary oedema-susceptible subjects, the combination of a constitutive and an acquired defect in this transport mechanism facilitates the development of pulmonary oedema during high-altitude exposure. High-altitude pulmonary oedema (HAPE) is a lifethreatening condition that occurs in predisposed but otherwise healthy individuals at altitudes w2,500 m. Augmented alveolar fluid flooding related to exaggerated hypoxic pulmonary vasoconstriction plays an important role in its pathogenesis, secondary to endothelial dysfunction and sympathetic overactivity [1][2][3]. However, recent observations indicate that this mechanism may not be sufficient to cause high-altitude pulmonary oedema [4].Active sodium transport across the alveolar epithelium plays an important role in keeping the lungs free of fluid [5,6]. In alveolar epithelial cells, sodium enters the apical membrane primarily through the amiloride-sensitive cation channels (mainly ENaC), and is then transported across the basolateral membrane into the interstitium by the ouabain-inhibitable Na-K-ATPase [5][6][7][8].A genetic impairment of the transepithelial sodium transport mechanism facilitates pulmonary oedema in transgenic mice [9,10] and possibly also in humans, as suggested by HAPE-prone subjects who have a smaller nasal potential difference (PD) (an indirect marker of vectorial sodium transport in the distal airways) [11] than mountaineers resistant to this condition [12]. Consistent with this concept, prophylactic stimulation of this transport mechanism with the b 2 -adrenergic agonist salmeterol, at a dose that stimulates respiratory sodium transport in vitro [8] and increases alveolar fluid clearance in vivo [13], decreased the incidence of HAPE in h...

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High‐Altitude Pulmonary Edema

Swenson

Bärtsch²

2012

Comprehensive Physiology

138

123

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High-altitude pulmonary edema (HAPE), a not uncommon form of acute altitude illness, can occur within days of ascent above 2500 to 3000 m. Although life-threatening, it is avoidable by slow ascent to permit acclimatization or with drug prophylaxis. The critical pathophysiology is an excessive rise in pulmonary vascular resistance or hypoxic pulmonary vasoconstriction (HPV) leading to increased microvascular pressures. The resultant hydrostatic stress causes dynamic changes in the permeability of the alveolar capillary barrier and mechanical injurious damage leading to leakage of large proteins and erythrocytes into the alveolar space in the absence of inflammation. Bronchoalveolar lavage and hemodynamic pressure measurements in humans confirm that elevated capillary pressure induces a high-permeability noninflammatory lung edema. Reduced nitric oxide availability and increased endothelin in hypoxia are the major determinants of excessive HPV in HAPE-susceptible individuals. Other hypoxia-dependent differences in ventilatory control, sympathetic nervous system activation, endothelial function, and alveolar epithelial active fluid reabsorption likely contribute additionally to HAPE susceptibility. Recent studies strongly suggest nonuniform regional hypoxic arteriolar vasoconstriction as an explanation for how HPV occurring predominantly at the arteriolar level causes leakage. In areas of high blood flow due to lesser HPV, edema develops due to pressures that exceed the dynamic and structural capacity of the alveolar capillary barrier to maintain normal fluid balance. This article will review the pathophysiology of the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung at high altitude, as well as therapeutic and prophylactic strategies to reduce the morbidity and mortality of HAPE.

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Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude

Cited by 48 publications

References 46 publications

Right and left ventricular adaptation to hypoxia: a tissue Doppler imaging study

Right and left ventricular adaptation to hypoxia: a tissue Doppler imaging study

High altitude impairs nasal transepithelial sodium transport in HAPE-prone subjects

High‐Altitude Pulmonary Edema

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