This is an international consensus statement of an ad hoc committee formed by the International Society for Mountain Medicine (ISMM) at the VI World Congress on Mountain Medicine and High Altitude Physiology (Xining, China; 2004) and represents the committee's interpretation of the current knowledge with regard to the most common chronic and subacute high altitude diseases. It has been developed by medical and scientific authorities from the committee experienced in the recognition and prevention of high altitude diseases and is based mainly on published, peer-reviewed articles. It is intended to include all legitimate criteria for choosing to use a specific method or procedure to diagnose or manage high altitude diseases. However, the ISMM recognizes that specific patient care decisions depend on the different geographic circumstances involved in the development of each chronic high altitude disease. These guidelines are established to inform the medical services on site who are directed to solve high altitude health problems about the definition, diagnosis, treatment, and prevention of the most common chronic high altitude diseases. The health problems associated with life at high altitude are well documented, but health policies and procedures often do not reflect current state-of-the-art knowledge. Most of the cases of high altitude diseases are preventable if on-site personnel identify the condition and implement appropriate care.
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...
Eleven healthy young men native to high altitude underwent haemodynamic studies at their original place of residence and after two years' residence at sea level. The investigation sought to determine the long-term effects of the suppression of the hypoxic stimulus upon heart rate, cardiac output, and pulmonary artery pressure of highlanders. For comparative purposes the influence of oxygen inhalation at high altitude was also studied.The heart rate fell at sea level and bradycardia was seen in most of the cases. The fall in heart rate is probably related to an increase in the predominance of the parasympathetic nervous system of highlanders after the relief of hypoxia. Oxygen inhalation at high altitude produced a smaller reduction in heart rate than after descending to sea level. The increase in heart rate during exercise was similar in both environments.Cardiac output increased moderately with the descent to sea level. This change was not associated with changes in oxygen uptake, but with a reduction in the values of haemoglobin, arterial oxygen content, and arteriovenous difference of oxygen. Stroke index increased significantly on descent to sea level, mainly as a consequence of the reduction in heart rate. At both altitudes exertion caused a similar increase in cardiac output which was related to the increase in heart rate rather than to stroke index which did not show significant variations. Oxygen inhalation at high altitude did not alter cardiac output and stroke index.Mean resting pulmonary arterial pressure fell to normal after two years' residence at sea level, but the pressure response to exercise was similar to that observed at high altitude and greater than that seen in healthy lowlanders. Oxygen inhalation at high altitude produced only a partial reduction in pulmonary hypertension. A recurrence ofpulmonary hypertension was observed on return to high altitude. These observations emphasize the importance of the structural characteristics of t the pulmonary vessels of highlanders in the mechanism of high altitude pulmonary hypertension.
The response elicited by exercise on pulmonary pressure, cardiac output, and arterial oxygen saturation in 35 lifetime residents of high altitude has been studied at high altitude (14,900 feet above sea level), and 22 residents of low altitude have been studied at sea level. A procedure combining cardiac catheterization, arterial cannulation, and spirometry was carried out. The exercise was moderate and was performed in supine position using a bicycle ergometer, the work load being 300 kg-m/min/m, 2 and the average increase of the oxygen uptake being 4.7 times at sea level and 4.8 times at high altitude. Both at sea level and at high altitude the cardiac output augmented during exercise proportionally to the increase in oxygen uptake, and thus followed the pattern of response described by other authors. The cardiac output as well as the oxygen intake, for the magnitude of exertion performed in this study, was almost the same at sea level and at high altitude. The cardiac output rose during exercise almost exclusively as a result of an increase in the heart rate, with the stroke volume remaining practically constant. Despite similar increase in cardiac output, the response of pulmonary pressure was smaller for sea-level subjects than for the high-altitude subjects. Increments of mean pulmonary pressure of nearly 50% and 100% were observed on exercise at sea level and at high altitude, respectively. During exercise the arterial oxygen saturation did not change in the sea-level studies, but decreased significantly in the high-altitude studies. The decrement observed in high-altitude residents is related to a fall in arterial pO 2 which at resting conditions is placed on the steep part of the oxygen dissociation curve.
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