Altitude illness is a relevant threat to the life and health of participants in mountaineering expeditions.
To determine if impedance cardiography (ICG) can be used in noninvasive monitoring of ...haemodynamic disturbances at high altitude.
The study was performed in a group of 13 participants of two mountaineering expeditions in the Himalayas. The ICG examination was performed before the expedition and again at high altitude (4,300-5,700 m) with concurrent estimates of clinical symptoms of acute mountain sickness (AMS) and those suggesting an increased risk of high altitude pulmonary oedema (HAPO).
High altitude influenced the haemodynamic profile of the subjects. Significant changes were observed for: stroke index (baseline vs. high altitude: 51.2 ± 10.3 vs. 35.5 ± 11.3 mL/m(2); p = 0.0007), cardiac index (3.24 ± 0.49 vs. 2.63 ± 0.66 L/min/m(2); p = 0.013), Heather index (16.6 ± 4.3 vs. 12.8 ± 4.45 Ohm/s(2); p = 0.006), heart rate (64.1 ± 11.7 vs. 75.4 ± 15.4 1/min; p = 0.045) and systemic vascular resistance index (2,051.3 ± 438.9 vs. 2,668.4 ± 856.2 dyn × s × cm(-5) × m(2); p = 0.027). AMS was observed in six subjects (mild: n = 5, severe: n = 1). Three of them revealed symptoms suggesting an increased risk of HAPO and this subgroup (vs. subgroup without such symptoms) was characterised by higher thoracic fluid content index (baseline: 19.2 ± 0.9 vs. 17.9 ± 2.0 1/kOhm x m(2); p = 0.176, at high altitude: 20.8 ± 1.4 vs. 17.7 ± 1.6 1/kOhm x m(2); p = 0.018) and lower Heather index (baseline: 11.4 ± 2.0 vs. 18.2 ± 3.5 Ohm/s(2); p = 0.028, at high altitude: 9.2 ± 2.1 vs. 13.9 ± 4.4 Ohm/s2; p = 0.028).
ICG may be a helpful, noninvasive tool in monitoring cardiovascular dysfunction occurring at high altitude, especially with breathing disorders.
Summary This case highlights the difficulties associated with the differential diagnosis of pulmonary symptoms in patients with pre-existing diseases in extreme environmental conditions. A ...58-year-old man with child-onset allergic asthma developed dyspnoea and an acute non-productive cough during a trekking expedition on Mt. Kilimanjaro (5895 m) in Tanzania. The symptoms were believed initially to be linked to the high altitude exposure (high altitude pulmonary oedema (HAPE) or high altitude cough) or his pre-existing asthma. However, he was later diagnosed correctly with a reinfection of Bordetella pertussis . Pertussis is a highly communicable disease with potentially serious medical consequences that could have affected all of the expedition members. The effectiveness of a pertussis vaccine declines 4–12 years after the vaccination. Thus, it is suggested that the status of immunisation against pertussis should be checked along with those of other infections prior to travel.
The ongoing Covid-19 is a contagious disease, and it is characterised by different symptoms such as fever, cough, and shortness of breath. Rising concerns about Covid-19 have severely affected the ...healthcare system in all countries as the Covid-19 outbreak has developed at a rapid rate all around the globe. Intriguing, a clinically used drug, acetazolamide (a specific inhibitor of carbonic anhydrase, CA, EC 4.2.1.1), is used to treat high-altitude pulmonary oedema (HAPE), showing a high degree of clinical similarities with the pulmonary disease caused by Covid-19. In this context, this preliminary study aims to provide insights into some factors affecting the Covid-19 patients, such as hypoxaemia, hypoxia as well as the blood CA activity. We hypothesise that patients with Covid-19 problems could show a dysregulated acid-base status influenced by CA activity. These preliminary results suggest that the use of CA inhibitors as a pharmacological treatment for Covid-19 may be beneficial.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Pulmonary oedema (PO) can emerge from mechanical disorders in pulmonary circulation leading to elevated fluid filtration in the lung, or from increased vascular permeability due to inflammatory or ...toxic injury of the alveolar-capillary barrier. A number of these disorders causing PO is associated with increased catecholamine (CA) levels in plasma and lung tissue and/or increased sympathetic activation such as neurogenic PO, high-altitude PO or PO in patients with phaeochromocytoma. Experimental CA stimulation in animals induced PO after less than one hour of infusion. Both alpha- and beta-adrenergic mechanisms are involved in the pathogenesis but also in the resolution of PO. CAs increase pulmonary capillary pressure and thus, enhance fluid filtration into the pulmonary interstitium. Additionally, by activation of proinflammatory cytokines, they induce pulmonary inflammation that may lead to capillary leak. Finally, they play an important role in the regulation of alveolar fluid clearance. The present paper considers the pathways by which CAs contribute to the development of PO of various origin.
BACKGROUND: The precise mechanism of high altitude pulmonary oedema (HAPE) remains unclear. The purpose of this study was to evaluate the role of cytokines and P-selectin in the development of HAPE ...which occurred at moderate altitude in Japan. METHODS: The following cellular and biochemical markers and chemotactic cytokines were measured in the bronchoalveolar (BAL) fluid from four patients with HAPE at 2857-3180 m in the Japanese Alps: total proteins, albumin, lactate dehydrogenase (LDH), and interleukin (IL)-1 alpha, IL-1 beta, IL-1 receptor antagonist (ra), IL-6, IL-8, IL-10, tumour necrosis factor (TNF)-alpha, and the soluble form of P-selectin. RESULTS: At admission there were significant increases in the levels of total cells, especially macrophages and neutrophils, total protein, albumin and LDH when compared with 13 healthy individuals. Furthermore, the levels of IL-1 beta, IL-6, IL-8, and TNF-alpha were also considerably increased but returned quickly to the normal ranges or were not detected after recovery. The levels of IL-1 alpha, IL-10, and P-selectin did not change. CONCLUSIONS: These results suggest that an inflammatory process almost identical with acute respiratory distress syndrome (ARDS) may occur in HAPE, but that these changes are transient and are not associated with any increase in P-selectin levels in the BAL fluid.
(Keeping in view the importance of High Altitude Pulmonary Oedema (HAPO) as well as the absence of published evidence as regards recurrence rate of this disease, a cohort study was undertaken, based ...on data available with the Central Diseases Registry. The inception cohort consisted of all cases of HAPO occurring over a one year period. This cohort was followed up for another 12 months, to observe any recurrence. The study revealed that the recurrence rate of HAPO in terms of incidence density was 1.83 per 1000 person-months of those who had an initial episode (95% confidence limit 0.53 to 3.13 per 1000 person-months). The cumulative incidence was 32.9 per 1000, over an average follow up of 18 months (95% confidence limit 4.55 to 61.25 per 1000). The time gap between the initial episode and recurrence was 115 to 208 days. All recurrent cases had their initial as well as recurrent episode at the first stage of high altitude (9000 to 12000 feet), with the onset being within 48 hours of entry into high altitude. Based on the findings, some recommendations for prevention of recurrence of HAPO have been submitted.)
Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound ...of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and during 15-min periods of either hypoxic (F(I)O2 0.125) or hyperoxic (F(I)O2 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000 m and 8150 m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm x s(-1) (P<0.001) in the controls, from 63 (3) to 75 (3) cm x s(-1) (P<0.001) in the high-altitude pulmonary-oedema-susceptible subjects, and from 58 (4) to 70 (4) cm x s(-1) (P<0.001) in the successful high-altitude climbers. Hyperoxia decreased mean middle cerebral flow velocity to 60 (3) cm x s(-1) (P<0.001), 53 (3) cm x s(-1) (P<0.01), and 49 (3) cm x s(-1) (P<0.01) in the controls, high-altitude pulmonary-oedema-susceptible, and high-altitude climbers, respectively. We conclude that a transcranial Doppler-based estimate of cerebral blood flow is affected by hypoxic and hyperoxic breathing, and that it is not predictive of tolerance to high altitude.
BACKGROUND--Subjects with previous high altitude pulmonary oedema may have stronger than normal hypoxic pulmonary vasoconstriction. Susceptibility to high altitude pulmonary oedema may be detectable ...by echo Doppler assessment of the pulmonary vascular reactivity to breathing a hypoxic gas mixture at sea level. METHODS--The study included 20 healthy controls, seven subjects with a previous episode of high altitude pulmonary oedema, and nine who had successfully climbed to altitudes of 6000-8842 m during the 40th anniversary British expedition to Mount Everest. Echo Doppler measurements of pulmonary blood flow acceleration time (AT) and ejection time (ET), and of the peak velocity of the tricuspid regurgitation jet (TR), were obtained under normobaric conditions of normoxia (fraction of inspired oxygen, FIO2, 0.21), of hyperoxia (FIO2 1.0), and of hypoxia (FIO2 0.125). RESULTS--Hypoxia decreased AT/ET by mean (SE) 0.06 (0.01) in the control subjects, by 0.11 (0.01) in those susceptible to high altitude pulmonary oedema, and by 0.02 (0.02) in the successful high altitude climbers. Hypoxia increased TR in the three groups by 0.22 (0.06) (n = 14), 0.56 (0.13) (n = 5), and 0.18 (0.1) (n = 7) m/s, respectively. However, AT/ET and/or TR measurements outside the normal range, defined as mean +/- 2 SD of measurements obtained in the controls under hypoxia, were observed in only two of the subjects susceptible to high altitude pulmonary oedema and in five of the successful high altitude climbers. CONCLUSIONS--Pulmonary vascular reactivity to hypoxia is enhanced in subjects with previous high altitude pulmonary oedema and decreased in successful high altitude climbers. However, echo Doppler estimates of hypoxic pulmonary vaso-constriction at sea level cannot reliably identify subjects susceptible to high altitude pulmonary oedema or successful high altitude climbers from a normal control population.
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