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All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. History: This is a 12 year old male who was transferred to our institution in a comatose state after being treated for a closed head injury at an outlying hospital.
Findings: Non-infused computed tomography of the brain revealed ventricular enlargement of the lateral, third, and probably fourth ventricles.
Discussion: Neurogenic pulmonary edema (NPE) is a form of noncardiogenic pulmonary edema which occurs rapidly following an acute CNS injury. Studies of the effects of chronic hypoxemia can be performed in the laboratory by decreasing either the concentration of inspired oxygen or the barometric pressure in a hypobaric chamber.
Thus, studies of high-altitude physiologists are of interest not only to mountaineers and aviators but also to physicians.
High altitude has generally been defined as an elevation above 3000 m (approximately 10,000 ft). Mountaineers and aviators have experimented with humansa€™ ability to function and survive at extreme altitudes. Changes in healthy individuals at high or extreme altitude may be exaggerated; in patients with chronic cardiopulmonary disease, changes may occur at modest elevations. At sea level (barometric pressure, 760 mm Hg), the PO2 of ambient air is 159 mm Hg (ie, 760 mm Hg A— 0.2093).
Humans have shown an ability to adapt for short periods to a barometric pressure one third that of sea level on Mount Everest without supplemental oxygen. At sea level, the PO2 available in the atmosphere and the oxygen demands of mitochondria are large. At high altitudes, the decrease in barometric pressure reduces the amount of oxygen initially available in the environment, making the slope of the cascade considerably less steep than it otherwise is. Changes occur at all levels of the oxygen transport system, namely, ventilation, pulmonary diffusion, circulation, and tissue diffusion.
An increased hypoxic ventilatory response is an important means of acclimatization for a sea-level resident who aspires to participate in activities at high altitude. In contrast, the native high-altitude resident has a blunted hypoxic ventilatory response (ie, is desensitized) to hypoxia.
After desensitization to hypoxia has occurred in the high-altitude resident, it persists for years, even if the person returns to sea level. Therefore, native high-altitude residents can perform a given physical activity with a relatively small ventilatory requirement; hence, they have less dyspnea than others do. A patient with cyanotic congenital heart disease also has a blunted hypoxic ventilatory response. This outcome is unlike that observed in the native highlander, whose response remains blunted for years. Configurational changes of the chest, anatomic changes of the lungs to increase the surface area of the alveoli, and an improved ventilation-perfusion ratio owing to pulmonary hypertension have been offered as possible explanations for this finding. A 32% decrease in coronary blood flow has been observed after 10 days at 3100 m (10,200 ft).[5] However, no evidence of myocardial ischemia is observed.
In general, systemic blood pressure is slightly lower at high altitude than it is at sea level. The final step in the oxygen cascade is the diffusion of oxygen from the capillaries to the mitochondria. The Mount Everest Medical Expedition revealed a progressive leftward shift at high altitudes as the respiratory alkalosis increased. In summary, at each stage of the oxygen transport system, considerable changes occur to facilitate oxygen delivery. No less important than the transport system is the transport vehiclea€”namely, the red blood cell (RBC). The degree of polycythemia is directly related to the altitude, up to an elevation of 3660 m (12,000 ft). The platelet count decreases by 7% after 2 days at 2990 m (9800 ft) and by 25% after 2 days at 5370 m (17,600 ft). Increased fibrinogen levels and a decreased clot lysis time were noted in 38 soldiers living at high altitude for 2 years, as compared with control subjects at sea level.[8] Soldiers with clinical evidence of pulmonary arterial hypertension had somewhat low levels of fibrinogen, high levels of platelet factor III, and increased platelet adhesiveness. Similar studies of the coagulation status of patients with cyanotic congenital heart disease have been conducted. Most visitors to high altitude notice initial weight loss, which has been attributed to reduced dietary intake, enhanced water loss, and loss of stored body fat. Because the retina of the eye has a great requirement for oxygen, vision is the first sense altered with the lack of oxygen. In acute hypoxia, reduction of arterial oxygen saturation to 85% decreases a persona€™s capacity for mental concentration and abolishes fine motor coordination.
One year after the American Medical Research Expedition to Everest, reductions in finger-tapping speed persisted. On initial exposure to altitude, cerebral blood flow (CBF) decreases because of vasoconstriction associated with hypocarbia.
A surprising observation is that the climbers with a high ventilatory response to hypoxia have the most impairment. Pulmonary arterial pressure is inversely dependent on a persona€™s age and on the environment.
In one study, right-heart catheterizations were performed in 32 healthy children aged 1-14 years and living permanently above 4240 m (14,000 ft).[10] For children aged 1-5 years, the mean pulmonary arterial pressure was 45 mm Hg (normal at sea level, 12-15 mm Hg).
In anatomic terms, the delayed decrease in the pulmonary arterial pressure is associated with persistence of the fetal elastic fibril pattern and with medial hypertrophy in the pulmonary arterioles.
In Leadville, Colorado (3100 m [10,200 ft]), mean pulmonary arterial pressure was 25 mm Hg in healthy high school students and 54 mm Hg after exercise.[11] a€”values surprisingly similar to those in adults during Operation Everest II at a simulated altitude of 8840 m [29,000 ft] in a hypobaric chamber. Data from newborn calves suggest that pulmonary vascular resistance at a normal pH increases when the partial pressure of oxygen (PO2) falls below 65 mm Hg.[13, 14] These data are supported by the clinical observation in humans that increases in pulmonary arterial pressure are not seen until the PAO2 decreases below 60-65 mm Hg, which corresponds to altitudes higher than 3000 m (about 9840 ft). Noninvasive and invasive methods of evaluating pulmonary arterial pressure were compared in a separate study from Kyrgyzstan et al.[15] A combination of ECG and Doppler measurements was found to correlate with cardiac catheterization data.
Among adults from high-altitude areas who move to sea level, pulmonary arterial pressures return to normal in 2 years.
Some residents of newly settled high-altitude communities in the United States may be at increased risk for problems in adapting to high-altitude living.
The patient continued to live at high altitude for 2 years and then moved to sea level for 11 months, where she was reexamined. People from the mountainous regions of North America represent a genetically mixed community.
The selection processes reflected in these differences can allow permanent inhabitation at altitudes as high as 5100 m (16,700 ft). Elite mountaineers who climb Everest without oxygen, as well as some native populations, have an allelic skew, with an excess of the I allele and the II genotype in intron 16 of the human angiotensin-converting enzyme (ACE) gene.
Chronic hypoxia, pulmonary venous hypertension, and increased pulmonary blood flow can markedly increase pulmonary pressures in many genetically susceptible individuals; these factors may be additive. The 20-25% of individuals who respond in this fashion at sea level are known as hyperreactors.
High-altitude pulmonary edema (HAPE) is an unusual form of noncardiogenic pulmonary edema that typically develops in healthy individuals after a rapid ascent to altitudes above 2500 m (8200 ft), though the author and others have seen it at lower altitudes (see the images below). Sustained exposure to high altitude for 24 hours or longer is usually required for HAPE to develop. A reduced concentration of exhaled nitric oxide, increased plasma endothelin-1 levels, augmented sympathetic activation, and high pulmonary arterial pressures suggest a possible defect in pulmonary nitric oxide synthesis and excessive sympathetically induced hypoxic pulmonary constriction.
HAPE has been described in patients with a congenital absence of the right or left pulmonary artery. Overperfusion edema during uneven vasoconstriction induced by high-altitude hypoxia has been suggested as a possible underlying cause.
At sea level, the pulmonary vascular pressor response to local pulmonary hypoxia diverts blood to relatively well ventilated areas, improving ventilation-perfusion matching and oxygenation. As noted (see above), pulmonary arterial pressure increases with altitude, and in some patients (ie, hyperreactors), this response is marked. In addition to heightened pulmonary vasoreactivity, a reduced hypoxic ventilatory response has been described in patients who have had HAPE. Acetazolamide, a potent carbonic anhydrase inhibitor and mild diuretic, is also a respiratory stimulant. Treatment with nifedipine has been reported, and this agent has been used prophylactically with some success. Each winter, millions of people ski at altitudes of 2500-3500 m (8200-11,500 ft) in Colorado. However, within 6-96 hours of arrival, many individuals have headache, insomnia, anorexia, nausea, vomiting, dizziness, dyspnea, and loss of coordination. The development of acute mountain sickness is directly related to the speed and height of ascent and inversely related to age. Ginkgo 60 mg given 3 times a day before ascent, aspirin, ibuprofen, and acetaminophen have also been effective in susceptible individuals. Oliguria and the retention and redistribution of bodily water into the intravascular and extravascular spaces of the cerebral and pulmonary circulations appear to occur during episodes of acute mountain sickness. Although several hypotheses regarding the cause of HAPE have been offered, the etiology of acute mountain sickness and HACE remains to be elucidated. Acute mountain sickness that progresses to confusion and neurologic symptoms has been defined as HACE. An increase in red blood cell (RBC) production and resulting polycythemia are normal responses to high altitude. Symptoms of Monge disease range from diminished mental and physical capacity to headaches, personality changes, unconsciousness, and coma. Periods of hypoventilation and arterial desaturation during sleep, as well as small tidal volumes, were described in residents of Leadville, Colorado, with excessive polycythemia.
Blood viscosity increases with the hematocrit, which in turn decreases cerebral blood flow. Similar increases in erythropoietin values, hematocrits, and blood viscosity have been described in patients with cyanotic congenital heart disease.
Travel by pregnant women from low to high altitudes or from high to low altitudes can induce premature labor because of the effect of changing barometric pressures on the amniotic sac.
Compared with mothers who deliver large babies, mothers of low-birth-weight infants hypoventilate and have decreased oxygen saturations from early to late gestation.
Pregnant women at high altitude who have an increased ventilatory response to hypoxia augment the normal increase in maternal ventilation associated with pregnancy; thus, they improve their arterial saturations and produce heavier babies than they otherwise would. Healthy full-term infants born in Cerro de Pasco, Peru (4340 m [14,200 ft]), had mean saturation values of 43%, 72%, and 88% (maximal) at 1 minute, 15 minutes, and 30 minutes of life, respectively.[26] By comparison, a control group in Lima, Peru (150 m [500 ft]), achieved near-maximal oxygen saturations by 15 minutes of life.
The lowered oxygen levels are associated with an elevated incidence of periodic breathing and apnea. The data regarding a potentially increased incidence of sudden infant death syndrome at altitude are conflicting. The fall in the pulmonary arterial pressure from systemic fetal levels to adult levels can be delayed in newborns at high altitude.[29] At high and moderate altitudes, a few infants have a delayed transition from fetal hemodynamics.
Examination findings in these infants are generally unremarkable, aside from moderate cyanosis (peripheral saturation, 80-90%), slight tachypnea, and a single loud second heart sound. The response of these patients to exercise at high altitude when they are older has not been established. In a few infants, the pulmonary hypertension does not resolve or else redevelops after subsequent exposure to altitude; these infants may experience failure to thrive and cor pulmonale. Human and animal data suggest that perinatal exposure to hypoxia may manifest as lifelong exaggerated hypoxic pulmonary vasoconstriction.
Oxygen saturations in healthy infants residing in or traveling to Summit County, Colorado, a popular ski resort with an altitude of 2800 m (9200 ft), are 88-97% (mean, 91.7%). Patent ductus arteriosus, atrial septal defect, and anomalies of the branchial arch are all more common at altitude.
In the authora€™s experience, the incidence of patent ductus arteriosus at moderate altitude is only minimally elevated.
The reactivity of the pulmonary vascular bed is known to vary widely from one person to another. In Denver, 34 infants with a ventricular septal defect and pulmonary hypertension were compared with 54 infants at sea level at Texas Childrena€™s Hospital.[13, 14] Despite similar pulmonary arterial pressures, the infants at sea level had half the vascular resistance that the infants from Denver had. The hypoxic banding of the pulmonary artery is responsible for the relative infrequency with which infants with refractory congestive failure from left-to-right shunts at moderate altitude are encountered. Consequently, examination of the right ventricular precordial impulse, assessment of the second heart sound, and electrocardiography (ECG) are extremely important. Because of anecdotal reports of irreversible pulmonary vascular obstructive disease in children younger than 2 years living at moderate altitude, early repair is recommended for children who have clinically significant pulmonary arterial hypertension in infancy.
Administration of oxygen or nitric oxide in the catheterization laboratory may help document a decrease in pulmonary vascular resistance. In addition, reversible causes of chronic hypoventilation (eg, tonsil or adenoid hypertrophy) are corrected before any decision is made regarding a patienta€™s suitability for surgery. For pulmonary vasodilation, administering oxygen by conventional means is evidently not as effective as raising the barometric pressure. Recommendations regarding travel to high altitude for patients with cyanosis are based on whether the cyanosis is associated with increased or decreased pulmonary blood flow, on the systemic saturation, and on the patienta€™s hematocrit at moderate altitude.
Because mild chronic hypoxia stimulates pulmonary vascular hyperreactivity, the progression of pulmonary vascular obstructive disease is thought to be accelerated at moderate or high altitude.
Case reports describe children from Leadville, Colorado, who had primary pulmonary hypertension.
Patients undergoing the Fontan procedure are uniquely sensitive to the effects of an increased pulmonary vascular resistance. The postoperative course at sea level has been typical for children undergoing this operation.
Chronic hypoxia associated with cystic fibrosis may contribute to the development of retinopathy at a relatively low altitude, in comparison with that seen in high-altitude hikers.
Splenic sequestration syndrome in patients with sicklea€“hemoglobin C disease has been described both during air travel in unpressurized cabins and at moderate altitude.[34] In patients with the sickle cell trait, altitude-induced splenic syndrome (acute left upper quadrant pain and tender splenic enlargement) appeared to be less common in African Americans than in people of other races. Air travel is a common mode of transportation for patients with congenital heart disease or chronic pulmonary disease who are traveling to and from major medical centers. All aircraft with pressurized cabins can maintain a certain pressure differential with respect to the outside atmosphere, but they do not maintain a sea-level pressure of 760 mm Hg. At cabin pressures equivalent to an altitude as high as 8915 ft (2700 m), alveolar oxygen tension (PAO2) is 59 mm Hg and arterial oxygen tension (PaO2) 55 mm Hg in a healthy individual.
Anecdotal reports describe deterioration in patients with unrepaired total anomalous venous connection during air travel.[36] Patients with Eisenmenger syndrome may have exaggerated decreases in saturations with minimal exertion while in flight.
All patients with cystic fibrosis, chronic emphysema, cyanotic congenital heart disease, severe chronic asthma, coronary insufficiency, fibrotic pulmonary changes, or a PaO2 higher than 50 mm Hg should receive supplemental oxygen during flights above 22,500 ft (6900 m). Adults with stable cyanotic congenital heart disease or irreversible pulmonary hypertension have traveled on commercial airlines without consequence. Commercial airlines do not carry therapeutic oxygen systems sufficient to sustain a patient on anything more than an emergency basis. Patients on stretchers can be accommodated in the first-class section by having the airline staff remove seats. The reduction in cabin pressure associated with air flight allows gas volumes to expand (Boyle law).
A Tozzo Frios conta com uma vasta gama de produtos como: frios, laticA­nios, embutidos, enlatados, congelados e produtos a granel.
Topics are richly illustrated with more than 40,000 clinical photos, videos, diagrams, and radiographic images.
The articles assist in the understanding of the anatomy involved in treating specific conditions and performing procedures. Check mild interactions to serious contraindications for up to 30 drugs, herbals, and supplements at a time. Plus, more than 600 drug monographs in our drug reference include integrated dosing calculators. 2: CT scan of posterior fossa reveals a left cerebellar hematoma and blood in fourth ventricle. 3: CT scan through cerebral hemispheres shows blood in dilated lateral ventricles and blood in third ventricle. Nature has provided a third option, high altitude, which allows examination of the effects of chronic hypoxemia in individuals under varying conditions.

Knowledge gained on mountain peaks may give insight into the pathophysiology of patients with cyanotic heart disease or chronic lung disease. In healthy persons, clinically significant changes are difficult to demonstrate at elevations lower than this. The conquests of Mount Everest (8884 m [about 29,140 ft]) without supplemental oxygen were a stringent test of survival ability in a severely hypoxemic environment. As air passes through the respiratory tract, it is saturated with water vapor, which makes the inspired PO2 149 mm Hg (ie, [760 a€“ 47 mm Hg] A— 0.2093). At that elevation, the calculated PAO2 is 35 mm Hg, and the arterial PO2 (PaO2) is 28 mm Hg. At each stage of the oxygen transport system, PO2 decreases; this disease is figuratively called the oxygen cascade. Mechanisms that compensate for the decreased availability of oxygen in the environment include changes in the intracellular enzyme systems to allow them to function at low levels of oxygen and changes in the oxygen transport system to increase the amount of oxygen delivered.
Mountain climbers with an increased hypoxic ventilatory response are better able to climb to great heights, presumably because of the increased availability of alveolar oxygen; this capacity may also have a downside.
The hypoxic ventilatory response persists for the sea-level resident who remains at high altitude. Improved oxygen usage in the peripheral tissues with decreased ventilatory effort has been postulated as an explanation for this phenomenon.
Offspring of lowlanders born and raised at high altitude have the same phenomenon as that of native highlanders. An important distinction between the native highlander and the patient with cyanotic heart disease may be that although they both have arterial hypoxemia, the highlander has a lowered PAO2, whereas the patient with cyanosis has a normal PAO2. This gradient may limit exercise by the newcomer to high altitude even if he or she hyperventilates.
Animal studies in chronically hypoxic newborn rats have shown structural changes that appear to optimize the structure and function of the lungs.
On initial ascent, sympathetic activity markedly increases, resulting in an initial increase in heart rate and cardiac output. This finding is presumably due to increased extraction of oxygen from coronary arterial blood and reduced oxygen requirements secondary to decreased cardiac work. The decreased cardiac output, stroke volume, and exercise capacity noted at high altitude may be due to decreased preload secondary to a reduction in plasma volume associated with arrival at high altitude. Right-axis deviation, right precordial T-wave inversion from a normally upright adult T wave, and T-wave changes in the left precordial leads have been described in mountaineers. This difference is thought to be secondary to the vasodilatory effects of hypoxia on the systemic vascular smooth muscle. As might be expected at high altitude, a PAO2 of 40-70 mm Hg is associated with rapid unloading of oxygen for small changes in oxygen tension.
Therefore, the actual PO2 for 50% oxygen saturation (P50) at altitude is not significantly different from that at sea level.
The extent to which the patient with cyanosis makes use of these or similar mechanisms can be a focus of future research.
This evidence suggests that conversion to fibrin, and possibly platelet deposition, were occurring in these subjects. The Operation Everest II project performed in a hypobaric chamber showed no changes in coagulation factors. This phenomenon is demonstrated by diminished night vision even at altitudes below 3000 m (about 9600 ft). Also observed were declines in visual long-term memory and verbal learning, along with increased aphasic errors during neuropsychological testing after climbs to high altitude.
The hypocapnia associated with hyperventilation possibly causes a marked decrease in CBF that offsets any beneficial effects of increased oxygenation. At sea level, pulmonary arterial pressure rapidly decreases from the systemic level of the fetus to near-adult levels in the first hours or days after birth. Electrocardiography (ECG) demonstrates persistence of fetal right ventricular (RV) dominance. Pulmonary arterial pressures at lower altitudes, such as Denver, Colorado (1610 m [about 5280 ft]), are near sea-level values. Pulmonary flow acceleration time was found to be a good predictor of pulmonary hypertension. Unlike natives of older communities in the Andes or in Tibet, they have not been genetically selected for high-altitude living. In comparison with Andean or Tibetan populations, differences in the adaptation to altitude are demonstrable. Tibetan teenagers living at high altitude have saturations similar to those of their newly arrived Han counterparts, but they have increased maximal oxygen uptake and increased cardiac output with exercise. Genetic susceptibility to high-altitude pulmonary edema (HAPE) has been attributed to variants of the endothelial nitric oxide synthetase gene (NOS3). At sea level, 25-30% of adults with critical mitral stenosis and 19% of those with a congenital absence of the pulmonary artery and increased flow to the other lung develop severe pulmonary hypertension. In such patients, the minimal chronic hypoxia found at even moderate altitude may prime the pulmonary vascular bed and provoke a hyperreactive response that causes a further increase in hypoxia, increased pulmonary blood flow, or pulmonary venous hypertension. Individuals with Down syndrome, obesity, or chronic lung disease may be at an increased risk when they travel to even moderate altitude.
Some individuals tolerate high altitude at first but become ill if they attempt to climb to higher altitudes. The edema fluid is protein-rich, but the primary problem is a hydrostatically induced permeability leak with mild alveolar hemorrhage, which is followed by inflammation. In these patients, HAPE develops at moderate altitudes (2000-3000 m [approximately 6500-9800 ft]). In addition to focusing on genetic susceptibility, speculation concerning the genesis of HAPE has centered on the role of alveolar hypoxia and overperfusion caused by an uneven hypoxic pulmonary vasoconstriction during periods of exercise at high altitude. However, at high altitude, where alveolar hypoxia is global, such a diversion through a universally constricted pulmonary vascular bed is of little benefit. This response can result in severe pulmonary arterial hypertension at rest or with exercise. In such individuals, failure to increase the tidal volume and respiratory rate at high altitude further lowers their alveolar oxygen tension (PAO2) and further increases their pulmonary vascular resistance.
Some assert that the high pressure resulting from the increased pulmonary arteriolar resistance distends the endothelial pores, yielding an exudate of plasma-rich fluid. It has been helpful in preventing acute mountain sickness, which may be part of the spectrum of high-altitude pulmonary hypertension.
Its vasodilatory effects effectively counteract the hypoxia-induced increase in pulmonary arterial pressure. These symptoms represent acute mountain sickness, a spectrum that in its severest form can manifest itself as HAPE or high-altitude cerebral edema (HACE). Acetazolamide 250-500 mg given at bedtime, with or without theophylline 500 mg, is also helpful in relieving the headaches and insomnia in mild cases.
Persons who have recovered from any degree of acute mountain sickness can usually reascend at a slow rate.
A low acute hypoxic ventilatory response and hypoxic depression of ventilation have been described in mountain climbers with a history of acute mountain sickness. However, some high-altitude residents become severely symptomatic as a result of excessive polycythemia. In theory, this desaturation further decreases both alveolar and systemic oxygen tensions and stimulates RBC production. The worsened hypoxemia due to hypoventilation and the reduced cerebral blood flow combine to cause symptoms. Changes in the placenta occur in response to lowered maternal arterial oxygen concentrations, and the incidence of preeclampsia is heightened.
Maternal smoking at high altitude is associated with a 2- to 3-fold reduction in the babya€™s birth weight in comparison with maternal smoking at sea level. Of interest, these same women, when they were not pregnant, have the typical blunted hypoxic ventilatory response observed in long-term residents. In Denver (1610 m [5300 ft]), the mean saturation is 92-93% at rest, decreasing to 85% during sleeping and feeding. High incidences of hyperbilirubinemia at 3100 m (10,200 ft)[27] and elevated neutrophil counts in the neonate at various altitudes have been reported.[28] In older children, mean oxygen saturations are 92% at 2800 m (9200 ft) and 87% at 4018 m (13,200 ft). Many of these infants are at risk for pulmonary vascular hyperreactivity (eg, Down syndrome) or were subjected to perinatal stress. In that time, findings on clinical examination usually suggest a decrease in the pulmonary arterial pressure. The infantsa€™ conditions may reflect a benign spectrum of the more serious and persistent fetal circulation syndrome or, as is more likely, may represent an exaggeration of the normal delayed fall in pulmonary vascular resistance observed at high altitude.
This condition has been referred to as symptomatic HAPE (SHAPE) or subacute infantile mountain sickness (SIMS). Therefore, the author follows patients with such findings during the first years of their lives and cautions their parents to avoid taking their infants to the summit of Pikes Peak (4303 m [14,100 ft]). In Bolivia, near La Paz, at an altitude of 4018 m (13,200 ft), the mean saturation is 87.3%.
In school-aged children living at high altitude, the incidence of patent ductus arteriosus is 18-30 times that noted at sea level.
However, closure of the ductus, as assessed with Doppler echocardiography, is often delayed for 7-10 days among infants in the neonatal intensive care unit. In healthy people, pulmonary arterial pressure does not substantially increase until alveolar oxygen tension (PAO2) exceeds 65 mm Hg.
The author has heard a loud murmur in a patient at a relatively low altitude that could not be heard during an examination at a higher elevation.
However, the decrease, as indicated by an increase in the intensity of a murmur and by clinical signs of an increasing left-to-right shunt, sometimes does not occur until after several days of oxygenation. Several patients for whom surgery was deemed inappropriate at moderate altitude, even after oxygenation, had decreased pulmonary vascular resistance when they were transferred to sea level, and their condition was successfully repaired. After returning to moderate altitude, patients often have persistent hyperreactivity to hypoxia and exercise. The size of the patent foramen ovale seems to be clinically significant.[30] It is plausible that right-to-left shunting occurs across a large patent foramen ovale in the setting of increased pulmonary arterial pressure and that this shunt contributes to relatively severe hypoxemia and worsening HAPE. The incidence of symptomatic polycythemia and the frequency of phlebotomies do not appear to be higher at moderate altitude than at sea level.
Ideal candidates for the Fontan procedure have the same survival rates at moderate altitude that they do at sea level.
After a return to moderate altitude, however, many of these patientsa€™ conditions deteriorate acutely. Survival data for patients with chronic diseases (eg, cystic fibrosis) who live at altitude are lacking. Rimsza et al described hemorrhagic retinopathy and symptoms similar to those of acute mountain sickness at 3049 m (10,000 ft).[31] They speculated that other individuals with chronic hypoxia may be at a similar risk. This finding was in contrast to the generally benign nature of sickle cell trait in African Americans at moderate altitude. Factors unique to this mode of transportation include the cabin pressure at altitude, the acceleration-deceleration forces, and the increases in gas volumes associated with reduced cabin pressure.
Most commercial aircraft are designed to keep their cabin pressure at no lower than 565 mm Hg (equivalent to an altitude of 8000 ft [2400 m]) at maximum operating altitude. In a patient with a resting PaO2 of 50 mm Hg at sea level, PaO2 may decrease to 30 mm Hg during air travel. However, if a patient resides at 6200 ft (1900 m) and tolerates that altitude well, little change occurs during flight, as the cabin pressure varies little from the local ambient barometric pressure. Many, but not all, airlines allow patients to carry on oxygen supplies if they arrange for this well in advance.
Patients with polycythemia may be at an increased risk from the effects of dehydration associated with air travel.
In commercial aircraft, acceleration and climb angle have little effect on healthy sitting passengers. For this reason, a pneumothorax or congenital cyst of the lung may enlarge and complicate air travel; therefore, commercial air travel is not recommended for patients with such conditions. The heart and pulmonary circulation at high altitudes: healthy highlanders and chronic mountain sickness. Higher pulmonary artery pressure in children than in adults upon fast ascent to high altitude. Acute changes in pulmonary artery pressures due to exercise and exposure to high altitude do not cause left ventricular diastolic dysfunction. Changes of cardiac structure and function in pediatric patients with high altitude pulmonary hypertension in Tibet.
Effects of mild chronic hypoxia on the pulmonary circulation in calves with reactive pulmonary hypertension.
Role of hypoxia in determining pulmonary vascular resistance in infants with ventricular septal defects.
Respiratory nitric oxide and pulmonary artery pressure in children of aymara and European ancestry at high altitude. Children at high altitude: an international consensus statement by an ad hoc committee of the International Society for Mountain Medicine, March 12, 2001. Arterial oxygen saturation in healthy newborns delivered at term in Cerro de Pasco (4340 m) and Lima (150 m). Venha conhecer nossa loja pessoalmente ou acesse a pA?gina de produtos e confira alguns dos nossos itens. Welders, firefighters, military and aerospace personnel, individuals working with explosives, traffic personnel, and farmers generally have higher risk of short-term exposure than those in other occupations. Customize your Medscape account with the health plans you accept, so that the information you need is saved and ready every time you look up a drug on our site or in the Medscape app.
Finally, physicians caring for patients who already have hypoxemia should understand the alterations provoked by changes in altitude that may affect these patients while they are living in or visiting mountainous regions or traveling by air. The changing position of the sun in relation to the equator affects barometric pressure, producing a seasonal atmospheric tide. Humans can permanently live at 5100 m (16,700 ft), where the barometric pressure is approximately one half that of sea level.
A low hypoxic ventilatory response has been implicated in acute mountain sickness, excessive polycythemia, and low birth weight.
At extreme altitudes, marked respiratory alkalosis develops to maintain a PAO2 of more than 35 mm Hg. Studies of high-altitude residents showed that for desensitization to occur, exposure to high altitude must occur in early childhood and last several years.
The native highlander hyperventilates compared with the lowlander, and the high-altitude resident hypoventilates compared with the newcomer to altitude. The most blunted ventilatory responses have been noted in patients with the highest degree of desaturation. The development of notable arterial desaturation during exercise suggests this possibility. However, after prolonged exposure, maximal oxygen uptake decreases, stroke volume is lowered, and cardiac output falls below sea-level values. Left ventricular (LV) dysfunction has been suggested; however, echocardiographic indices of LV contractility are normal and chamber sizes are reduced at altitude.
ECGs of immigrants to high altitude demonstrate an increase in RV hypertrophy with increased duration of high-altitude residence. The incidence of hypertension at high altitude has been reported to be less than that the rate at sea level. Increases in the capillary density and decreases in the size of muscle fibers combine to shorten the distance over which oxygen must diffuse. Some suggest that increased oxygen affinity or left-shifting of the oxygen-hemoglobin dissociation curve may be beneficial at high altitude. In addition, within hours of exposure to altitude, RBC production increases because production of erythropoietin is heightened. However, if the systemic arterial saturation falls below 60%, erythropoietic activity decreases. At altitude, climbers with polycythemia exhibit reduced maximal oxygen consumption, even on 100% oxygen. At high altitude, appetite and caloric intake decrease dramatically in unacclimatized persons, who generally find fat distasteful and prefer sweets. At 3048 m (10,000 ft), people require more time to learn a new task than they do at low elevations. This finding prompted some to surmise whether climbs to extreme altitude cause brain damage. Blood flow appears to be regionally uneven, increasing at the brainstem level at the expense of cortical flow.
In infants born at high altitude, however, the decrease is both slower and smaller than the decline just described.
Thus, a critical alveolar oxygen tension (PAO2) appears to mark the level of hypoxia necessary to maintain pulmonary vasoconstriction.
Inhalation of oxygen at high altitude achieves only modest reductions in pulmonary arterial pressure in comparison with the reductions induced by a permanent change of residence to sea level. More remote and longer inhabiting populations perform better than the newly arriving lowlanders.
Inability to adapt (ie, a deficient ventilatory response to hypoxia and hypercapnia) has been described in a family.
Individuals with a genetic risk for increased thrombosis may be at increased risk for HAPE. Although pulmonary arterial pressures are elevated, this change does not necessarily cause pulmonary vascular disease. In such cases, the authora€™s practice is to correct clinically significant cardiac lesions at an early age to allow the pulmonary arterial pressures to regress if continued residence at altitude is contemplated. HAPE has been reported in both previously healthy high-altitude residents and visitors from lowlands.

The initial or return ascent to altitude is usually rapid and accomplished via either automobile or aircraft. Fatigue, dyspnea, nausea, and sleeplessness may progress to visible cyanosis, tachypnea, and a productive cough with copious production of pink sputum. The author has treated patients with saturations higher than 60% and severe pulmonary edema on chest radiographs who rapidly improved during a 30-minute ambulance descent from 8000-6000 ft (about 2400-1800 m).
Cardiac catheterization during the acute phase of HAPE reveals pulmonary hypertension with normal wedge or left atrial pressures but increased capillary pressure. Although this is an uncommon defect, the risk of HAPE in these individuals seems to be extremely high. An increase in pulmonary vasoreactivity has been documented in children and adults in whom HAPE was diagnosed.
Elevated plasma levels of atrial natriuretic factor and vasopressin have been reported in patients with HAPE.
Early recognition, rest, and immediate descent may yield rapid improvement, usually in 24-48 hours.
The respiratory stimulant effect of the drug is presumably the reason for its beneficial effect. Potent diuretics (eg, furosemide) have the theoretical disadvantage of further depleting the already decreased intravascular volume. Upon arriving at high altitude, most individuals note a sensation of breathlessness due to the hypoxia-induced hyperventilation and palpitations from the increased heart rate. Obese patients and those with chronic lung disease are at particular risk, even at moderate altitudes. Symptoms observed in preverbal children include increased fussiness, decreased appetite, poor sleep patterns, and decreased playfulness. Additional symptoms include headaches, nausea, and vomiting that progress to ataxia, confusion, hallucinations, disorientation, focal neurologic findings, coma, and death.
In affected individuals, magnetic resonance imaging (MRI) shows reversible white matter edema, especially in the splenium of the corpus callosum, without abnormalities of the gray matter.
Normal arterial saturation at that altitude (ie, 81%) may fall as low as 60% in affected individuals.
Phlebotomy improves symptoms and oxygen saturations, and it lowers pulmonary arterial pressure.
Gestational age at the time of delivery is not affected; this finding implies intrauterine growth retardation. In Leadville, Colorado (3100 m [10,200 ft]), the highest saturation was 87-90% during the first 48 hours.
Many infants are discharged from the authora€™s nursery with oxygen supplementation during the first few months of life to manage clinically significant apneic episodes.
However, RV dominance on the electrocardiogram (ECG) usually resolves more slowly than the clinical abnormalities do. Accordingly, the author does not recommend immediate medical or surgical intervention to close the ductus in infants, except in those with signs of clinically significant volume overload.
However, in people with reactive pulmonary vasculature and a chronic stimulus to maintain reactivity (eg, increased pulmonary blood flow or pulmonary venous hypertension), even the minimal hypoxia due to a moderate increase in elevation may be enough to stimulate a substantial increase in pulmonary vascular resistance. A thriving infant may have a clinically significant defect with severe pulmonary arterial hypertension. Therefore, for appropriate individuals, oxygen is administered at home 1 week before the planned catheterization procedure to achieve maximal reduction of pulmonary vascular resistance. Recommendations regarding high-altitude exercise (eg, skiing) for this group of patients are lacking.
Exercise is undoubtedly more limited at high altitude than it is at sea level, but objective data are lacking.
Overnight stays increase the patienta€™s risk because of the potential increase in desaturation associated with hypoventilation during sleep. If social circumstances are favorable, patients with this condition are encouraged to move to lower altitudes. Whether patients whose cardiac output is sensitive to pulmonary vascular resistance should live or even visit regions at moderate altitude is questionable. The incidence of bronchopulmonary dysplasia among infants does not appear to be significantly increased at moderate altitudes, though long-term care of these patients usually involves prolonged oxygen therapy to maintain adequate saturations. However, on flights above 22,500 ft (6860 m) altitude, the cabin pressure may be equivalent to that encountered at altitudes as high as 8915 ft (2700 m). In patients with reactive pulmonary hypertension, pulmonary arterial pressures may substantially decrease during a flight, and hypoxemia may increase. The Federal Aviation Administration (FAA) has strict rules regarding the type of systems allowed on an aircraft.
A prone or supine patient whose head is toward the front of the aircraft can experience considerable venous pooling and decreased cardiac output during takeoff. Additionally, individuals living in particular urban areas or near congested highways may have increased risk of long-term low-level exposure.
Easily compare tier status for drugs in the same class when considering an alternative drug for your patient. Although cold, low humidity, increased solar radiation, and poor economic conditions limit the ability to survive at high altitude, hypoxia is the most important factor. However, after 4 days of exposure to even modest increases in altitude, ventilation is consistently greater than normal ventilation at sea level. In a decompression chamber with conditions equal to those at Mount Everest, PaCO2 is 8 mm Hg.
After arterial saturations are surgically corrected and normalized, the ventilatory response to hypoxia returns to normal.
The native high-altitude resident has a pulmonary diffusion capacity 20-30% higher than that of a sea-level resident. The reduction in stroke volume is thought to be secondary to decreased ventricular filling.
Loss of normal circadian rhythm and QTc prolongation have been described in both infants and adults. In several species of animals, this response appears to help them adapt to high altitude, but it does not appear in humans after 40 days of marked hypobaric exposure. As with fetal hemoglobin, a leftward shift facilitates oxygen loading in a hypoxic environment.
This observation suggests that peripheral extraction of oxygen from blood is limited by its reduced flow. Fluid losses result from the insensible water losses associated with hyperventilation and low humidity, as well as diuresis induced by hypoxia and the cold environment. During these episodes, electrocardiography (ECG) usually shows evidence of right ventricular (RV) hypertrophy or strain. This finding supports the concept that HAPE is not related to left ventricular (LV) dysfunction. Administration of oxygen and inhaled nitric oxide is beneficial but cannot replace rapid descent. With serious forms, symptoms include headache, vomiting, ataxia, lassitude, and reduced urination. They are less symptomatic at sea level than at altitude, but whether the disease process is altered is unknown. In the authora€™s experience, several patients who did not meet the hemodynamic criteria for surgery at moderate altitude were treated with recatheterization at sea level. As always, patients with the best operative results have the most flexibility in this regard. If connecting flights at moderate-altitude airports are to be taken, planning for additional oxygen supplies and a wheelchair to reduce the patienta€™s exertion may be indicated. NO2 is a mucous membrane irritant commonly associated with other toxic products of combustion.
Exercise markedly reduces maximum cardiac output; this effect is more pronounced in visitors than in natives. Others suggest that a rightward shift may increase the ability of the blood to unload oxygen at the tissue level. Phlebotomy and hemodilution experiments in mountain climbers and autologous RBC transfusions in athletes have not yielded information about the ideal hematocrit for any given altitude.
Prolonged postural drainage in the head-down position, assisted by steady compression of the upper abdomen, was helpful in a person who had HAPE in a remote setting.[19] Also helpful is a recompression chamber (Gamow bag). Rales, peripheral edema (often periorbital), and retinal hemorrhages are sometimes found in affected hikers in Nepal or skiers in Colorado. During the first 4 months of life at 3000 m (9800 ft), mean arterial oxygen saturations are 80-91%. Therefore, the patienta€™s head is positioned toward the rear of the aircraft (except if he or she has cerebral edema). Symptoms most commonly range from mild cough and mucous membrane irritation to severe exacerbations of underlying pulmonary diseases like COPD or asthma and, in extreme cases, death. The hypoxia-induced increase in minute ventilation occurs shortly after arrival at altitude and increases during week 1. The initial absence of significant symptoms does not exclude a subsequent development of serious disease. In an era founded largely on the success and availability of fossil fuels, the realization of the harmful effects of fossil fuel byproducts has become an increasing public health concern. Clean air is recognized as a basic requirement for human health and well-being, alongside access to clean water and sanitation.[1] NO2 in particular is among the most commonly recognized components of air pollution. NO2 and the other pollutants it consorts with are increasingly associated with worsening lung function, increased risk of ischemic heart disease and stroke, increased rates of hospital admissions, and even increased rates of mortality.[2, 3, 4] NO2 is a reddish-brown gas that has a sharp, harsh odor at higher concentrations, but it may be clear and odorless at lower, but still harmful, concentrations. When farm silos are filled with fresh organic material (eg, corn, other grains), anaerobic fermentation of the crops results in NO2 production. This may also occur with silage bags, but this risk is lower given natural outdoor ventilation. In either case, farmers who enter silos, work with silage bags, or remain near open silo hatches during the first 10 days after filling may experience NO2 toxicity in a phenomenon known as silo fillera€™s disease. As a result, when inhaled, it easily bypasses the moist oral mucosa and upper airways and penetrates deep into the lower respiratory tract. Toxicity depends largely on the concentration and duration of exposure, as well as an individuala€™s baseline pulmonary function. Elderly individuals or individuals with COPD or asthma are at much higher risk of adverse events, are more susceptible to developing infections, and may experience more severe symptoms than healthy individuals with normal pulmonary function. These values are based on using NO2 as a general marker for the complex mixture of pollutants generated by combustion. Some studies suggest that chronic exposure to NO2 may predispose individuals to the development of chronic lung diseases, including infection and COPD, and particularly asthma in children. Because NO2 is poorly water soluble, it hydrolyzes more slowly than other water-soluble gases, resulting in deep lung injury in the bronchioles and alveoli. Type I pneumocytes and ciliated airway cells are primarily affected, but damage also occurs from free radical generation, which results in protein oxidation, lipid peroxidation, and cell membrane damage.
A proposed pathway involves oxidation of mitochondrial cytochrome c,[15] which can result in electron transport chain decoupling and cellular apoptosis. The chemical irritation of the alveoli and bronchioles results in rapid destruction of the epithelial cells and breakdown of the pulmonary capillary bed. Nitrogen oxides can alter immune function and macrophage activity, leading to an impaired resistance to infection. NO2 binds to hemoglobin with great affinity, forming nitrosyl hemoglobin, which is readily oxidized to methemoglobin. Methemoglobin results in a leftward shift of the oxygen disassociation curve, which impairs the oxygen delivery and compounds the already present hypoxia.
In untreated cases, fibrous granulation tissue may develop within small airways and alveolar ducts resulting in bronchiolitis obliterans.
As its name suggests, bronchiolitis obliterans refers to an inflammatory process that results in the progressive partial or complete obliteration of the small airways. Proliferative bronchiolitis is more common and is characterized by the development of steroid-reversible intraluminal polyps that obstruct the small airways. By contrast, constrictive bronchiolitis is a more diffuse and chronic process characterized by concentric thickening and destruction of bronchioli. While fumes containing sulfur or ammonia have been associated with constrictive bronchiolitis, proliferative bronchiolitis is more common with nitrogen dioxide toxicity.
Gas- and kerosene-fired household appliances and motor vehicle exhaust all pose significant risk of exposure. For example, there are multiple reports of nitrogen dioxide exposure occurring in ice skating rinks secondary to poor ventilation and exhaust from ice resurfacing machines[16] and exposures in mines where poor ventilation results in exposure to fumes from diesel engine equipment or explosives.
Silo fillera€™s diseaseSilos filled with freshly cut corn, oats, grass, alfalfa, or other plant material generates oxides of nitrogen within hours. Maximum concentrations of NO2 are reached within 1-2 days, and then the levels begin to fall after 10-14 days. Silage that is heavily fertilized, has experienced drought, or is derived from immature plants produces much higher concentrations of nitrogen oxides within the silo. The same phenomenon occurs with silage bags, but because of better natural ventilation, the hazard is lower.
During storage, NO2, which is 1.5 times heavier than air, can remain in deep depressions of the silage material. Exposure can develop while attempting to level the silage without proper ventilation or breathing apparatus. One documented case occurred in an individual who traversed the ladder at the opening of a silo. The heavier-than-air NO2 flowed down the side of the silo, exposing the worker to toxic levels of gas. The US Environmental Protection Agency (EPA) has regulations for monitoring nitrogen dioxide (NO2) concentrations and has historically found outdoor ambient air concentrations highest in large urban regions such as the New York metropolitan area, Chicago, and Los Angeles.[8] In the 2006 World Health Organization (WHO) air quality global update, it was estimated that more than 2 million premature deaths occur each year secondary to the effects of both indoor and outdoor air pollution.
While more than half of this disease burden was in developing countries, the effect in developed countries in not negligible.[1] In the United States, the EPA estimates that 16% of US housing units are located within 100 yards of a major highway, railroad, or airport. In addition, this population likely includes an increased proportion of lower-income individuals and minorities.[4] Individuals at increased risk of adverse effects include those with underlying asthma or COPD, those with other pulmonary diseases with poor pulmonary function (eg, interstitial lung disease, pulmonary fibrosis, pulmonary hypertension), and those with existing cardiovascular disease and low oxygen reserve. Elderly persons and children are also at increased risk of respiratory infections or asthma exacerbations, respectively. An estimated annual incidence of 5 cases per 100,000 silo-associated farm workers per year was reported in New York.[17, 18] Silo filler's disease is likely significantly underreported. The long-term prognosis for an individual patient can be determined by conducting follow-up pulmonary function tests. In patients with lung damage from NO2, improvement in pulmonary function may take weeks or months.
Infection (eg, pneumonia) is possible because of the mucosal injury caused by pulmonary edema and the inhibition of immune function by NO2.
Bronchiolitis obliterans consists of fibrous granulation tissue that develops within small airways and alveolar ducts. Death can result from bronchiolar spasm, laryngeal spasm, reflex respiratory arrest, or asphyxia.
They should wear appropriate personal protective equipment in the workplace.Advise patients that delayed symptoms, including life-threatening pulmonary edema and dyspnea caused by bronchiolitis obliterans, may result.
Therefore, patients should be followed for a minimum of 2-3 months after exposure to monitor possible development of bronchiolitis obliterans. Fred Harchelroad, MD, FACMT, FAAEM, FACEP Director of Medical Toxicology, Allegheny General HospitalDisclosure: Nothing to disclose.
WHO Air quality guidelines for particulate matter, ozone, nitrogen dioxide and sulfur dioxide.
Stroke and long-term exposure to outdoor air pollution from nitrogen dioxide: a cohort study. Associations between short-term exposure to nitrogen dioxide and mortality in 17 Chinese cities: the China Air Pollution and Health Effects Study (CAPES). Air pollution and emergency department visits for cardiac and respiratory conditions: a multi-city time-series analysis. Association of indoor nitrogen dioxide exposure with respiratory symptoms in children with asthma. Chronic cough and dyspnea in ice hockey players after an acute exposure to combustion products of a faulty ice resurfacer.
Critical review of the human data on short-term nitrogen dioxide (NO2) exposures: evidence for NO2 no-effect levels. Seasonal and diurnal analysis of NO2 concentrations from a long-duration study conducted in Las Vegas, Nevada. Traffic and meteorological impacts on near-road air quality: summary of methods and trends from the Raleigh Near-Road Study. Genetic polymorphism of GSTM1 and antioxidant supplementation influence lung function in relation to ozone exposure in asthmatic children in Mexico City.
Outdoor air pollution, genetic susceptibility, and asthma management: opportunities for intervention to reduce the burden of asthma. Adhesion of Streptococcus pneumoniae to human airway epithelial cells exposed to urban particulate matter. Long-term exposure to ambient air pollution and risk of hospitalization with community-acquired pneumonia in older adults.
FDA Drug Safety Communication: Serious CNS reactions possible when methylene blue is given to patients taking certain psychiatric medications.

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