Cardio-Respiratory Studies in Chronic Mountain Sickness (Monge’s Syndrome)

Ergueta, J. C.; Spielvogel, Hilde; Cudkowicz, Leon

doi:10.1159/000192835

Cited by 47 publications

(26 citation statements)

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“…A similar and more exaggerated mechanism, yielding very large VDS, was found in patients at high altitude who suffered from chronic mountain sickness (Monge's syndrome) and who were hypercapnic in the presence of a VE/m2/BTPS which exceeded that of controls. Expressing their minute ventilation as VA = V E -V D S demonstrated, however, a crit ical reduction in VA which was well below that of controls [12]. During steady-state exercise, A at both altitudes continued to have lower VE/m2/ BTPS than C. B showed larger VE/m2/BTPS at La Paz than D, but not at 5,200 m. At both altitudes, D had slower f than C and the two female groups and they delivered the largest VT.…”

Section: Discussionmentioning

confidence: 77%

“…Studies on Monge's syndrome suggest that pulmonary blood flow is principally directed towards the lower lung zones, the presence of severe pulmonary hypertension notwithstanding. Surprisingly, Monge's syndrome in females seems less prevalent than in males; only one female with chronic mountain sickness was observed in a series of 20 pa tients from La Paz [12]. The ability to moderate hypoxic drive through hypercapnia by changing VDS during moderate effort characterizes the fe male at altitude, and an adaptive mechanism emerges that differs from that extant in C. It is well established that ventilatory responses to hypoxia are mediated through peripheral chemoreceptors; in man, these responses are markedly decreased after vagal and glossopharyngeal nerve block [30] and following denervation of the glomus by carotid endarterectomy [31].…”

Section: Discussionmentioning

confidence: 96%

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Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

1972

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At two altitudes (3,600 and 5,200 m), resident native women (A) showed higher PAco₂ and Paco₂, lower PAO₂ and PaO₂, as well as lower arterial pH, than native males (C) of similar age. Resting minute ventilation (VE/m²), tidal volume (VT) and respiratory frequency (f) were similar. The differences in the alveolar-arterial gas tensions in A stem from larger dead space (VDS), VDS/VT and reduced alveolar ventilation (VA). Newcomer females (B) at both altitudes differed from new- comer males (D) in regard to larger resting VA, f and smaller VT. No differences were demonstrated in size of VDS, VDS/VT or VO₂/BSA; but PAco₂ and PacO₂ were lower, PAO₂ and Pa higher and VE/VO2 and VA/VO₂ (ventilatory equivalents) above those for resting newcomer males. A contrasted with resting B at 3,600 m (12,200 ft), showing higher PAco₂ and Paco₂, lower Pao₂ and arterial pH, reduction in VA and larger VDS/VT. Both C and D at 3,600 and 5,200 m during steady-state 60-W (367 kg/m/min) exercise showed lower PAco₂ and Paco₂, higher arterial pH, smaller VDS and higher VE/VO₂ than exercising A. The latter differed from C exercising at the same work load in that VE/m² and VA were reduced, PAco₂ and Paco₂ were higher, Pa-ao₂ gradients were wider, pH was lower and VDS as well as VDS/VT were larger. Contrasted with B during steady-state 60-W exercise at both altitudes, D showed consistently smaller VDS and larger VA. While both C and A had higher resting f than D, f of newcomer females at La Paz was higher than that of A. Control of ventilation by relating VE to Pao₂ and Paco₂ at rest and exercise at both altitudes showed marked attenuation of hypoxic and hypercapnic drives, particularly in the native resident female, suggesting diminished peripheral chemoreceptor function.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 96%

Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

1972

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“…The normal value of [Hb] at 3,600 m is 160±20 g·L -1 [11]. Subjects were included in the normocythaemic (LHb) group when [Hb] was ð180 g·L -1 , and in the H-Hb group when [Hb] was >180 g·L -1 .…”

Section: Methodsmentioning

confidence: 99%

Pulmonary hypertension in high-altitude chronic hypoxia: response to nifedipine

Antezana

Antezana²,

Aparicio³

et al. 1998

Eur Respir J

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The vasoconstrictive effect of hypoxia upon pulmonary artery vessels is well known in most mammalian species, including humans. A pure form of hypoxic pulmonary artery hypertension can be seen in high-altitude residents. A loss of adaptation to chronic hypoxia, known as chronic mountain sickness (CMS), is observed in 5-10% of people sojourning above 3,000 m and is characterized by excessive polycythaemia (H-Hb), pulmonary hypertension and nonspecific neurological symptoms [1]. Ongoing pulmonary vasoconstriction leads to increased vascular resistance and pulmonary artery pressure (Ppa), which are probable maladaptive responses to high altitude since they result in minimal improvement in ventilation-perfusion matching and increased workload for the right ventricle.In addition to vasoconstriction, chronic alveolar hypoxia is associated with structural changes in the media of terminal portions of pulmonary arterioles [2], such as smooth muscle cell proliferation, thickening of the media, proliferation and turgescence of endothelial cells. Recently, this vascular remodelling has been found in only a few residents at high altitude [3], but it is admitted that sustained hypoxia is able to increase muscularization of the small pulmonary vessels and to increase even further the pulmonary vascular resistance.A reduction in Ppa, under hypoxic conditions, has been obtained by the calcium channel-blocker nifedipine in healthy humans exposed to acute normobaric hypoxia [4] or in subjects suffering from high-altitude pulmonary oedema in hypobaric hypoxia [5]. In other aetiologies of pulmonary hypertension, such as primary pulmonary hypertension [6] or secondary to obstructive pulmonary disease [7,8], nifedipine and felodipine were efficient in decreasing Ppa. Calcium antagonists have also been shown to be efficient in experimental hypoxic pulmonary vasoconstriction [9,10].Reversal of hypoxic pulmonary hypertension with calcium channel-blockers has not been evaluated in a population chronically exposed to high altitude. Venesection has been used to treat CMS, but no modification of pulmonary haemodynamics has been reported.The objectives of this study were to assess pulmonary hypertension in native residents at high-altitude by echocardiography, to analyse the relationship between Ppa and H-Hb, and to study the effect of acute administration of nifedipine on pulmonary pressure. In the presence of reversible vascular changes in altitude-induced pulmonary hypertension, a nifedipine-induced vasodilatation could be anticipated. Materials and methods SubjectsThirty males and one females, native residents of La Paz (3,500-4,100 m), Bolivia, were included in this nonrandomized study. Asymptomatic subjects were recruited Systolic pulmonary arterial pressure (Ppa) was studied by Doppler echocardiography, at rest and after sublingual nifedipine, in 31 asymptomatic residents at 3,600 m. Individuals were separated into two groups according to resting Ppa: a group with low Ppa (ð4.7 kPa, n=17) and a group with high Ppa (>4.7 kPa, n=14). Ind...

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“…28,54 Afterward, Bolivian investigators reported 2 studies. 55,56 Further cardiac catheterization studies on CMS have not been performed in the Andean region. Chinese and Kyrgyz investigators have also published interesting observations on CMS and related diseases, as discussed in the following sections.…”

Section: Chronic Mountain Sicknessmentioning

confidence: 99%

“…Ergueta et al found average values of Hb 26 g/dL, PPA 51 mm Hg, and SaO 2 84% in 2 patients studied in La Paz. 55 Manier et al reported Hb 21Ϯ1 g/dL and PPA 56 Chinese investigators have made important clinical and epidemiological studies in the last 2 decades. There are limited observations of pulmonary hemodynamics, however.…”

Section: Cardiac Catheterization and Pulmonary Hemodynamics In Cmsmentioning

confidence: 99%

The Heart and Pulmonary Circulation at High Altitudes

2007

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Abstract-More than 140 million people worldwide live Ͼ2500 m above sea level. Of them, 80 million live in Asia, and 35 million live in the Andean mountains. This latter region has its major population density living above 3500 m. The primary objective of the present study is to review the physiology, pathology, pathogenesis, and clinical features of the heart and pulmonary circulation in healthy highlanders and patients with chronic mountain sickness. A systematic review of worldwide literature was undertaken, beginning with the pioneering work done in the Andes several decades ago. Original articles were analyzed in most cases and English abstracts or translations of articles written in Chinese were reviewed. Pulmonary hypertension in healthy highlanders is related to a delayed postnatal remodeling of the distal pulmonary arterial branches. The magnitude of pulmonary hypertension increases with the altitude level and the degree of exercise. There is reversal of pulmonary hypertension after prolonged residence at sea level. Chronic mountain sickness develops when the capacity for altitude adaptation is lost. These patients have moderate to severe pulmonary hypertension with accentuated hypoxemia and exaggerated polycythemia. The clinical picture of chronic mountain sickness differs from subacute mountain sickness and resembles other chronic altitude diseases described in China and Kyrgyzstan. The heart and pulmonary circulation in healthy highlanders have distinct features in comparison with residents at sea level. Chronic mountain sickness is a public health problem in the Andean mountains and other mountainous regions around the world. Therefore, dissemination of preventive and therapeutic measures is essential. Key Words: altitude Ⅲ altitude sickness Ⅲ hypertension, pulmonary P eople native to high altitude (HA) environments live in an environment of hypobaric hypoxia with low ambient partial pressure of oxygen. As a consequence, they develop alveolar hypoxia, hypoxemia, and polycythemia. Despite this, healthy highlanders are able to perform physical activities similar to and often even more strenuous than those of people living at sea level (SL). This phenomenon has been ascribed to adaptive mechanisms that occur at sequential steps of the oxygen transport system with the main purpose of decreasing the total pO 2 gradient from ambient hypoxic air to mixed venous blood at the tissue level.The heart and pulmonary circulation in healthy people living at HA exhibit important physiological and anatomic characteristics, which resemble those that occur in chronic clinical conditions associated with alveolar hypoxia, hypoxemia, and polycythemia. Healthy HA natives have pulmonary hypertension (PH), right ventricular hypertrophy (RVH) and increased amount of smooth muscle cells (SMCs) in the distal pulmonary arterial branches. All these findings become exaggerated when healthy highlanders lose their capacity for adaptation and develop chronic mountain sickness (CMS). The physiological, pathological, pathogenic, and cl...

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Cardio-Respiratory Studies in Chronic Mountain Sickness (Monge’s Syndrome)

Cited by 47 publications

References 34 publications

Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

Respiratory Studies in Women at High Altitude (3,600 m or 12,200 ft and 5,200 m or 17,200 ft)

Pulmonary hypertension in high-altitude chronic hypoxia: response to nifedipine

The Heart and Pulmonary Circulation at High Altitudes

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