Maggiorini Marco
Intensive Care Unit, DIM University Hospital, Zurich, Switzerland.
Adv Exp Med Biol. 2003;543:177-89. doi: 10.1007/978-1-4419-8997-0_13.
The purpose of this review is to find the evidence that a disproportionate pulmonary vasoconstriction persisting for days, weeks and years during residence at high altitude is the common pathophysiologic mechanism of high altitude pulmonary edema (HAPE), subacute mountain sickness and chronic mountain sickness. A recent finding in early HAPE suggests that transmission of excessively elevated pulmonary artery pressure to the pulmonary capillaries leading to alveolar hemorrhage as the pathophysiologic mechanism of HAPE. The elevated incidence of HAPE in Indian soldiers led the Indian Army to extend the acclimatization period from a few days to 5 weeks. Using this protocol, HAPE was prevented, but after several weeks of residence at an altitude of 6000m dyspnea, anasarca and pleuro-pericardial effusion developed. Clinical examination revealed severe congestive right heart failure. This condition has been previously described in long-term high altitude residents of the Himalaya and the Andes. In rats, smooth muscle cells appear in normally non-muscular arterioles within days of simulated altitude. Rapid remodeling of the small precapillary arteries may prevent HAPE but increase pulmonary vascular resistance leading to pulmonary hypertension in long-term high altitude residents. Symptoms and signs of HAPE, subacute mountain sickness and chronic mountain sickness reverse completely after residents are transfered to low altitude. In conclusion, these findings strongly suggest that pulmonary hypertension at high altitude, which could be named "high altitude pulmonary hypertension", is the principal and common pathogenic factor of all three cardio-pulmonary manifestations of high altitude illness. Accordingly, subacute mountain sickness and chronic mountain sickness could be renamed in "acute-" and "chronic right heart failure of high altitude", respectively.
本综述的目的是寻找证据，证明在高海拔地区居住期间持续数天、数周和数年的不成比例的肺血管收缩是高原肺水肿（HAPE）、亚急性高山病和慢性高山病的常见病理生理机制。HAPE早期的一项最新发现表明，肺动脉压力过度升高传递至肺毛细血管导致肺泡出血是HAPE的病理生理机制。印度士兵中HAPE的高发病率促使印度军队将适应期从几天延长至5周。采用该方案可预防HAPE，但在海拔6000米居住数周后，出现了呼吸困难、全身性水肿和胸膜心包积液。临床检查显示严重的充血性右心衰竭。这种情况此前在喜马拉雅山和安第斯山脉的长期高海拔居民中已有描述。在大鼠中，模拟海拔数天内，正常无肌性的小动脉内会出现平滑肌细胞。小的毛细血管前动脉的快速重塑可能预防HAPE，但会增加肺血管阻力，导致长期高海拔居民出现肺动脉高压。将居民转移至低海拔后，HAPE、亚急性高山病和慢性高山病的症状和体征会完全消失。总之，这些发现强烈表明，高海拔地区的肺动脉高压，可称为“高原肺动脉高压”，是高原病所有三种心肺表现的主要和常见致病因素。因此，亚急性高山病和慢性高山病可分别重新命名为“急性高原右心衰竭”和“慢性高原右心衰竭”。
