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Biomedical subjects

M Maggiorini

Publications and source records attributed to M Maggiorini.

At least 55 records · Page 3Linked to original sources
PubMed1995

Pulmonary vascular impedance response to hypoxia in dogs and minipigs: effects of inhaled nitric oxide.

The pig has been reported to present with a stronger hypoxic pulmonary vasoconstriction (HPV) than many other species, including dogs. We investigated [pulmonary arterial pressure (Ppa)-pulmonary arterial occluded pressure (Ppao)] vs. pulmonary blood flow (Q) relationships and pulmonary vascular impedance (PVZ) spectra in nine minipigs and nine weight-matched dogs. The animals were anesthetized and ventilated in hyperoxia [inspired O2 fraction 0.4] or hypoxia (inspired O2 fraction 0.12). PVZ was computed from the Fourier series for Ppa and Q. In hyperoxia, the pigs had a higher Ppa (26 +/- 1 vs. 16 +/- 1 mmHg), a higher first-harmonic impedance (Z1), and a more negative low-frequency phase angle but no different characteristic impedance (Zc) compared with the dogs at the same Q. Hypoxia in the dogs increased (Ppa-Ppao) at all levels of Q studied by an average of 2 mmHg but did not affect Z1 or Zc. Hypoxia in the pigs increased (Ppa-Ppao) at all levels of Q by an average of 13 mmHg and increased Z1 and Zc. Inhaled NO (150 ppm) reversed the hypoxia-induced changes in (Ppa-Ppao)/Q plots and PVZ in the dogs and pigs. However, differences in (Ppa-Ppao)/Q plots and PVZ between the dogs and pigs in hyperoxia and hypoxia were not affected by inhaled NO. We conclude 1) that minipigs present with an elevated pulmonary vascular resistance and impedance in hypoxia more than in hyperoxia and 2) that baseline differences in pulmonary hemodynamics between dogs and minipigs are structural rather than functional.

Administration, Inhalation↗
PubMed1995

Effects of dexfenfluramine on hypoxic pulmonary vasoconstriction and embolic pulmonary hypertension in dogs.

There has been suggestion of a possible relationship between the intake of the appetite suppressant dexfenfluramine and the development of primary pulmonary hypertension. We investigated the pulmonary vascular effects of acute intravenous dexfenfluramine in pentobarbital-anesthetized dogs ventilated in hyperoxia (fraction of inspired oxygen, FIO2, 0.4) and either challenged with a FIO2 of 0.1 to induce hypoxic pulmonary hypertension (n = 20) or given autologous blood clots to induce embolic pulmonary hypertension (n = 6). Pulmonary vascular tone was evaluated by multipoint (mean pulmonary artery pressure [Ppa] - pulmonary artery occluded pressure [Ppao])/cardiac output (Q) plots. Hypoxia increased Ppa - Ppao over the entire range of Q studied, from 1.5 to 4.0 L/min/m2, in 12 dogs (responders) and had no significant effect on (Ppa - Ppao)/Q plots in 8 other dogs (nonresponders). Dexfenfluramine did not affect (Ppa - Ppao)/Q plots in 6 responders but shifted (Ppa - Ppao)/Q plots to higher pressures in hypoxia in 6 nonresponders (p < 0.001). Dexfenfluramine had no effect on (Ppa - Ppao)/Q plots in the 6 dogs with embolic pulmonary hypertension. Because dexfenfluramine has serotoninergic properties, we compared the effects of ketanserin, a serotonin (5-hydroxytryptamine, 5-HT) S2 receptor antagonist, on naturally present versus dexfenfluramine-restored hypoxic pulmonary vasoconstriction. Ketanserin did not affect hyperoxic or hypoxic pulmonary vascular tone, neither in 6 responders nor in 2 nonresponders with dexfenfluramine-restored hypoxic vasoconstriction. We conclude that dexfenfluramine restores hypoxic pulmonary vasoconstriction in dogs with weak or absent hypoxic pressor response and that this effect is unlikely to be mediated by activation of 5-HT S2 receptors.

Animals↗
PubMed1994

Infectious complications in 100 consecutive heart transplant recipients.

Clinical and laboratory data on infectious complications in 100 consecutive heart transplant recipients were analyzed retrospectively. The mean length of follow-up was 651 +/- 466 days. All patients received a basic immunosuppressive regimen including cyclosporine (whole blood target trough level 400-600 micrograms/l), azathioprine (1 mg/kg/day) and prednisone (0.15 mg/kg/day). Early rejection prophylaxis consisted of polyclonal rabbit antithymocyte globulin (ATG) (4 mg/kg/day for 4 days) in the first 57 patients and monoclonal murine OKT-3 (5 mg/day for 14 days) in the remaining patients. The primary cause of death was infection in three patients and rejection in 16 (p < 0.001). The incidence of infection was 0.96/patient/year (n = 179); 95 infections were nosocomial (53%), 47 community-acquired (26%) and 37 opportunistic (21%). The number of hospitalizations due to infections was fewer than that due to rejection (53 versus 246 respectively, p < 0.0001), but the mean length of hospital stay was longer in the first group (13.85 +/- 10.92 days versus 3.48 +/- 2.28 days, p < 0.001). Previous early rejection prophylaxis with OKT-3 was associated with a greater number of opportunistic and nosocomial infections compared to prophylaxis with ATG (p < 0.05), as was treatment with ATG and steroid pulses compared to steroid pulses alone in cases of opportunistic infection (p < 0.05).

Adult↗
PubMed1994

Should cardiac transplantation for congenital heart disease be delayed until adult age?

The number of pediatric heart transplantations for complex congenital heart disease has increased over the last years, but little experience has been reported in adolescent and adult populations. Between 1987 and 1992, 14 patients (mean age 33.2 years, range 14 to 51 years) were transplanted in our institution because of structural congenital heart disease (n = 9) or other rare disorders of the endomyocardial morphogenesis (n = 5). The main diagnosis included transposition of the great arteries, congenitally corrected transposition of the great vessels, left superior vena cava, tricuspid atresia with right ventricular hypoplasia, double outlet right ventricle with transposition, left ventricular sinusoidal malformation and right ventricular dysplasia. In several cases there were additional intracardiac malformations, including ventricular septum defect, atrial septum defect as well as different forms of pulmonary stenosis. Seven patients had undergone one or more palliative repairs that consisted of modified Blalock-Taussig shunts, Glenn's cavopulmonary anastomosis, Waterstone shunt, Blalock-Hanlon atrioseptectomy and Brock pulmonary valvotomy. Two patients had undergone Senning procedure for transposition of the great arteries. The donor cardiectomy was modified in order to include complete inflow and outflow tissue in the explant and transplantation could be performed without prosthetic material in all patients; deep hypothermic cardiac arrest was never necessary in this series. There was no early or late mortality after a mean follow-up of 37 months (range 4 to 74 months); postoperative echocardiography and cardiac catheterization demonstrated perfect anatomical and functional results in all patients. Adolescent and adult patients with complex congenital cardiac diseases can be transplanted with a very low perioperative risk, even after several prior operative procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Anesthetic depth defined using multiple noxious stimuli during isoflurane/oxygen anesthesia. I. Motor reactions.

BACKGROUND: Potency of inhaled anesthetics usually is defined by determining the minimal alveolar concentration (MAC) that prevents movement in 50% of patients in response to skin incision. Skin incision, however, is usually only a single event and, thus, determination of potency cannot be repeated in one patient. Traditional MACskin incision cannot be used to predict response to other noxious stimuli. The aim of this study was to investigate the effects of other noxious stimulation patterns and then compare these to MACskin incision measuring the end-tidal isoflurane concentrations with the corresponding arterial concentrations. METHODS: In 26 patients, the end-tidal and corresponding arterial isoflurane concentrations needed to suppress eye opening to verbal command and motor response after trapezius squeeze, 50 Hz electric tetanic stimulation, laryngoscopy, skin incision, and tracheal intubation in 50% of all patients were determined. RESULTS: The end-tidal (equivalent arterial) isoflurane concentrations (mean +/- SE, adjusted to sea level) expressed in vol% (to allow comparison) increased in the following order (mean +/- SE): vocal command 0.37 +/- 0.09 (0.36 +/- 0.09); trapezius squeeze 0.84 +/- 0.07 (0.65 +/- 0.07); laryngoscopy 1.00 +/- 0.12 (0.78 +/- 0.09); tetanic stimulation 1.03 +/- 0.09 (0.80 +/- 0.06); skin incision 1.16 +/- 0.10 (0.97 +/- 0.17); and intubation 1.76 +/- 0.13 (1.32 +/- 0.11). CONCLUSIONS: Different stimuli require different isoflurane concentrations to suppress motor responses. Tetanic stimulation and, to some extent, trapezius squeeze are reproducible and noninvasive stimulation patterns that can be used as an alternative to skin incision when evaluating potency of an anesthetic agent. In contrast to skin incision, they can be repeated.

Adult↗
PubMed1994

Enhanced cerebral blood flow in acute mountain sickness.

Mean blood flow velocity (v) of both middle cerebral arteries (MCA) was assessed by transcranial Doppler sonography (TCD) in 23 subjects at an altitude of 490 m, as well as after a rapid ascent to a high altitude research laboratory at 4559 m, and daily during a continued 72-h stay at this altitude. Relative changes of mean blood flow velocities (v) of both MCA at high altitude were expressed as percentages of low altitude values and correlated with the development of signs and symptoms of acute mountain sickness (AMS) and changes of arterial PO2, PCO2, and hemoglobin. After ascent to 4559 m, overall MCA-v (mean of all measurements obtained in each subject at high altitude) increased significantly to 148 +/- 16% of baseline values in the subjects with AMS (AMS+) and to 127 +/- 24% in the subjects without AMS (AMS-) (mean +/- SD). This v increase was higher in subjects with AMS and reached statistical significance on day 1 (+50 +/- 19%) and on day 2 (+48 +/- 23%) as compared to the healthy subjects (+27 +/- 24% and +21 +/- 26% on days 1 and 2, respectively). The rise of MCA-v correlated inversely with arterial PO2 on days 2 (r = -0.62, p < 0.005), 3 (r = -0.67, p < 0.025) and 4 (r = -0.69, p < 0.025) and from days 1 to 4 (r = -0.51, p < 0.001). MCA-v did not correlate with blood pressure, arterial PCO2 or hemoglobin. Our results suggest that subjects with AMS have a higher MCA-v increase due to a lower arterial PO2 than healthy subjects.

Acute Disease↗
PubMed1993

[Role of heart transplantation in the treatment of complex congenital malformations in adolescents and adults].

The number of pediatric heart transplants for complex congenital heart disease has increased in recent years, but little experience has been reported in the adolescent and adult population. Between 1987 and 1992, 6 patients (mean age 24 years, range 14 to 42) underwent transplant in our institution because of structural congenital heart disease with or without prior palliative operation or definitive repair. The diagnose covered: congenitally corrected transposition of the great vessels, late systemic ventricular failure after surgically corrected transposition of the great arteries, left superior vena cava, and tricuspid atresia with right ventricular hypoplasia. The palliative repairs included modified Blalock-Taussig shunt, cavo-pulmonary Glenn shunt, two aorto-pulmonary Waterstone shunts, two Blalock-Hanlon atrioseptectomies and one pulmonary valvotomy by the method of Brock. One patient had undergone pulmonary artery banding, in two patients atrial repair by Senning's technique had been performed for definitive repair of transposition of the great arteries. Donor cardiectomy was modified to remove complete inflow and outflow tissue and transplantation was performed without prosthetic material in all patients, in no case was deep hypothermic arrest necessary. There was no early or late mortality after a mean follow-up of 28 months. Postoperative echocardiography and cardiac catheterization demonstrated perfect anatomical and functional results. There was no early or late mortality after a mean follow-up of 28 months. Postoperative echocardiography and cardiac catheterization demonstrated perfect anatomical and functional results. Adult patients with complex congenital cardiac diseases can be transplanted with a very low perioperative risk, even after several prior operative procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Treatment of acute mountain sickness by simulated descent: a randomised controlled trial.

OBJECTIVE: To evaluate the therapeutic efficacy of a portable hyperbaric chamber for treatment of acute mountain sickness. DESIGN: Controlled randomised trial over two mountaineering seasons. SETTING: High altitude research laboratory at 4559 m above sea level. SUBJECTS: 64 climbers with acute mountain sickness randomly allocated to different treatments. INTERVENTIONS: One hour of treatment in the hyperbaric chamber at a pressure of 193 mbar or 20 mbar as control or bed rest. MAIN OUTCOME MEASURES: Symptoms of acute mountain sickness before, immediately after, and 12 hours after treatment. Permitted intake of analgesic and antiemetic drugs in the follow up period. RESULTS: Treatment with 193 mbar caused greater relief of symptoms than did control treatment or bed rest. During the 12 hour follow up period intake of analgesics was similar (58-80% of subjects in each group). Symptom scores had improved in all subjects after 12 hours with no significant differences between groups. CONCLUSIONS: One hour of treatment with 193 mbar in a portable hyperbaric chamber, corresponding to a descent of 2250 m, leads to a short term improvement in symptoms of acute mountain sickness but has no beneficial long term effects attributable to pressurisation.

Acute Disease↗
PubMed1993

Hemodynamic effects and concentration-effect relationship of a graded infusion of piroximone in patients with severe heart failure.

Piroximone is a new phosphodiesterase III inhibitor that combines inotropic and vasodilator properties. To elucidate the optimal dose regimen and the dose-concentration-effect relationships, we studied eight patients with congestive heart failure of New York Heart Association class IV during a continuous multistage infusion over a 24-h period followed by a 4-h washout. After a bolus of 0.5 mg/kg, infusions at a rate of 2.5, 5.0, and 10.0 micrograms/kg/min for 8 h each were given to determine the maintenance dose of piroximone required to achieve an increase in cardiac index > or = 30%. Serial assessment of hemodynamics, plasma piroximone levels, and ventricular ectopic beats was performed. Following the loading dose and at higher infusion rates (5 and 10 micrograms/kg/min) Piroximone produced significant hemodynamic changes compared to baseline, i.e., a maximum increase in cardiac index from 2.2 +/- 0.4 to 3.6 +/- 0.8 L/min/m2 (67 +/- 21%), decreases in right atrial pressure from 14 +/- 3 to 9 +/- 3 mm Hg (40 +/- 16%), pulmonary capillary wedge pressure from 29 +/- 5 to 23 +/- 7 mm Hg (28 +/- 18%), pulmonary vascular resistance from 249 +/- 93 to 151 +/- 59 (45 +/- 19%), and systemic vascular resistance from 1,330 +/- 442 to 752 +/- 272 dyn s/cm5 (44 +/- 19%). Piroximone increased the heart rate by 10% at the highest dose and produced a decrease in mean arterial pressure by 13%. There was a slight increase in ventricular ectopy in two patients (2.2 and 3 VPBs/min) and no change in the remaining six.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Indications for heart transplantation, preoperative assessment and treatment].

Heart transplantation [HTx] is a therapeutic option for an end-stage congestive cardiomyopathy. At the present time five and ten years' survival results after cardiac transplantation can be compared to those of coronary bypass surgery in patients with a three-vessel disease. Ten-year survival after coronary surgery in patients with a three-vessel disease and impaired left-ventricular function is 64%, without decreased left-ventricular function 72%, and after HTx between 60 and 70%. In spite of good results HTx remains a therapeutic possibility only for well-selected candidates with an expected survival of less than twelve months. Symptoms and signs for a poor prognosis are: functional NYHA-class III-IV, cardiothoracic ratio > 0.55, walking distance of less than 300 m in the 6-minute walk test, VO2 max. of < 14 ml/kg, cardiac index < 2.25 l/min/m2, pulmonary capillary wedge pressure > 16 mmHg. A syncope of any origin is, in patients with functional class III-IV, associated with a 1-year sudden-death incidence of 45%. Because of a high daily variability, ventricular ectopy alone is of limited prognostic value. Secondary pulmonary hypertension is a common finding in end-stage congestive heart failure. A mean pulmonary artery pressure above 55 mmHg and a transpulmonary gradient of > 12 mmHg are associated with a poor prognosis. If pulmonary vascular resistance exceeds 4 Wood units (320 dyn.sec.cm-5), reversibility has to be proved, using sodium nitroprussid or prostaglandine E1. An irreversible pulmonary vascular resistance above 8-Wood units (640 dyn.sec.cm-5) is an absolute contraindication for HTx; lung or heart-lung transplantation are the only

Heart Failure↗
PubMed1993

[Prevention and therapy of altitude sickness].

Climbing in the Alps and trekking in the Andes or in the Himalayas became more and more popular in the last years. This is the reason why more and more tourists develop symptoms of acute mountain sickness (AMS) at an altitude higher than 2500 m a.s.l. To avoid an unpleasant stay at altitude, an accurate acclimatization is necessary. This can be achieved by a slow ascent at a climbing rate of 300 to 600 m in one day. If that is not possible, climbers should spend at least nine or more nights at an altitude higher than 2500 m a.s.l. in the last 30 days before ascent. This would improve performance at high altitude and significantly decrease symptoms of AMS. If acclimatization for one or another reason may not be possible or if somebody is still susceptible to AMS, pharmacological prophylaxis and treatment can be used. Drug of first choice for AMS prophylaxis is acetazolamide, a carboanhydrase inhibitor who increases ventilation. Acetazolamide has been used in a dosage of 250 to 500 mg 12 to 24 h. before ascent. If climbers have a history of high-altitude pulmonary edema (HAPE), nifedipine, a potent vasodilator which decreases pulmonary artery pressure, is the drug of the first choice and should be taken in a dosage of 3 x 20 mg, beginning one day before climbing and continuing during climbing. Prophylactic administration of nifedipine has no effect on symptoms of AMS in subjects who are not susceptible to HAPE.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1992

[Pathophysiology, prevention and therapy of altitude pulmonary edema].

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.

Aldosterone↗
PubMed1992

Prevention and treatment of high altitude pulmonary edema by a calcium channel blocker.

High altitude pulmonary edema (HAPE) is characterized by marked pulmonary hypertension. Treatment of 6 subjects suffering from radiographically documented HAPE with the calcium channel blocker nifedipine, lowered pulmonary artery pressure and resulted in clinical improvement, better oxygenation, reduction of alveolar-arterial oxygen gradient and a progressive clearing of alveolar edema on chest x-ray. This amelioration occurred despite continued exercise at an altitude above 4000 m and without supplementary oxygen. Prophylactic application of nifedipine slow release preparation, 20 mg every 8 hours, prevented HAPE in 9 out of 10 subjects with a history of radiographically documented HAPE upon rapid ascent and subsequent stay to an altitude of 4559 m. Seven of 11 comparable subjects who received placebo developed pulmonary edema at 4559 m. As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean systolic pulmonary artery pressure, alveolar-arterial pressure gradient of oxygen and symptom score of acute mountain sickness at 4559 m. Thus nifedipine offers a potential emergency treatment of HAPE when descent or evacuation is impossible and oxygen is not available. Prophylactic administration of nifedipine prevents HAPE in susceptible subjects. High pulmonary artery pressure has an important role in the pathogenesis of HAPE.

Acute Disease↗
PubMed1991

Prevention of high-altitude pulmonary edema by nifedipine.

BACKGROUND: Exaggerated pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in high-altitude pulmonary edema. We previously found that nifedipine lowered pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with high-altitude pulmonary edema. We therefore hypothesized that the prophylactic administration of nifedipine would prevent its recurrence. METHODS: Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented high-altitude pulmonary edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment. The diagnosis of pulmonary edema was based on chest radiography. Pulmonary-artery pressure was measured by Doppler echocardiography and the difference between alveolar and arterial oxygen pressure was measured in simultaneously sampled arterial blood and end-expiratory air. RESULTS: Seven of the 11 subjects who received placebo but only 1 of the 10 subjects who received nifedipine had pulmonary edema at 4559 m (P = 0.01). As compared with the subjects who received placebo, those who received nifedipine had a significantly lower mean (+/- SD) systolic pulmonary-artery pressure (41 +/- 8 vs. 53 +/- 16 mm Hg, P = 0.01), alveolar-arterial pressure gradient (6.6 +/- 3.8 vs. 11.8 +/- 4.4 mm Hg, P less than 0.001), and symptom score of acute mountain sickness (2.0 +/- 0.7 vs. 3.9 +/- 1.9, P less than 0.01) at 4559 m. CONCLUSIONS: The prophylactic administration of nifedipine is effective in lowering pulmonary-artery pressure and preventing high-altitude pulmonary edema in susceptible subjects. These findings support the concept that high pulmonary-artery pressure has an important role in the development of high-altitude pulmonary edema.

Adult↗
PubMed1991

Enhanced exercise-induced rise of aldosterone and vasopressin preceding mountain sickness.

A possible contribution of exercise to the fluid retention associated with acute mountain sickness (AMS) was investigated in 17 mountaineers who underwent an exercise test for 30 min on a bicycle ergometer with a constant work load of 148 +/- 9 (SE) W at low altitude (LA) and with 103 +/- 6 W 4-7 h after arrival at 4,559 m or high altitude (HA). Mean heart rates during exercise at both altitudes and during active ascent to HA were similar. Exercise-induced changes at LA did not differ significantly between the eight subjects who stayed well and the nine subjects who developed AMS during a 3-day sojourn at 4,559 m. At HA, O2 saturation before (71 +/- 2 vs. 83 +/- 2%, P less than 0.01) and during exercise (67 +/- 2 vs. 72 +/- 1%, P less than 0.025) was lower and exercise-induced increase of plasma aldosterone (617 +/- 116 vs. 233 +/- 42 pmol/l, P less than 0.025) and plasma antidiuretic hormone (23.8 +/- 14.4 vs. 3.4 +/- 1.8 pmol/l, P less than 0.05) was greater in the AMS group, whereas exercise-induced rise of plasma atrial natriuretic factor and changes of hematocrit, potassium, and osmolality in plasma were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1991

Cognitive changes at high altitude in healthy climbers and in climbers developing acute mountain sickness.

We report the cognitive functions of 17 non-acclimatized mountaineers who ascended from low lands to an altitude of 4,559 m in 24 h and were studied there within 6 h. We found that this rapid ascent to high altitude had small, but differential effects upon cognitive performance depending upon the later development of acute mountain sickness (AMS). Subjects who developed AMS within a 24-48-h stay at high altitude were mildly impaired in short term memory, but improved in conceptual tasks, while subjects who remained healthy had a better short term memory performance but no improvement in cognitive flexibility. Possible explanations for these unexpected effects of high altitude are discussed.

Adult↗
PubMed1990

Prevalence of acute mountain sickness in the Swiss Alps.

OBJECTIVE: To assess the prevalence of symptoms and signs of acute mountain sickness of the Swiss Alps. DESIGN: A study using an interview and clinical examination in a representative population of mountaineers. Positive symptoms and signs were assigned scores to quantify the severity of acute mountain sickness. SETTING: Four huts in the Swiss Alps at 2850 m, 3050 m, 3650 m, and 4559 m. SUBJECTS: 466 Climbers, mostly recreational: 47 at 2850 m, 128 at 3050 m, 82 at 3650, and 209 at 4559 m. RESULTS: In all, 117 of the subjects were entirely free of symptoms and clinical signs of acute mountain sickness; 191 had one or two symptoms and signs; and 158 had more than two. Those with more than two symptoms and signs were defined as suffering from acute mountain sickness. At 4559 m 11 climbers presented with high altitude pulmonary oedema or cerebral oedema, or both. Men and women were equally affected. The prevalence of acute mountain sickness correlated with altitude: it was 9% at 2850 m, 13% at 3050 m, 34% at 3650 m, and 53% at 4559 m. The most frequent symptoms and signs were insomnia, headache, peripheral oedema, and scanty pulmonary rales. Severe headache, vomiting, dizziness, tachypnoea, and pronounced pulmonary rales were associated with other symptoms and signs and therefore characteristic of acute mountain sickness. CONCLUSION: Acute mountain sickness is not an uncommon disease at moderately high altitude--that is, above 2800 m. Severe headache, vomiting, dizziness, tachypnoea, and pronounced pulmonary rales indicate severe acute mountain sickness, and subjects who suffer these should immediately descend to lower altitudes.

Acute Disease↗