You are on page 1of 4

HIGH ALTITUDE PHYSIOLOGY The Barometric Pressure, and Therefore, the Ambient PO2 @ the Peak of Mount Everest

Are Each About 1/3 of Their Respective Values @ Sea Level Column of Water Relatively noncompressible has a uniform density Column of Air Does not have the same density at all altitudes

Column of air in the atmosphere does not have the same density at all altitudes Density of air: decreases exponentially ascending from the sea level of the mass of the earths atmosphere is contained in the lowest 5500m The next of the mass of the earths atmosphere is contained in the next 5500m @higher & higher altitudes: o # of gas molecules pressing down on a mountain climber falls exponentially o PB falls by half for each ~5500m of ascent Peak of mount Everest o Highest point of land on the earths surface o 8,848 m above sea level o PB = 255mmHg (1/3 of PB of sea level) o Ambient PO2 = ~53mmHg A climber at the peak of Mt. Everest: o The PO2 of the humidified inspired air entering the alveoli is even lower, because of the effects of water vapor so that the inspired PO2 = 21% x (25547) = 44mmHg compared with 149mmHg @ sea level HYPOXIA! @ base camp at Mt. Everest: For every 5500m, the barometric pressure falls by half o Arterial O2 delivery [arterialblood O2 content x CO] can still

meet O2 demands in most healthy, active persons o However, body compensatory responses to reduced ambient O2 @ high altitude are different in different people Thus, exposure to an altitude of 5500 m is problematic for a significant portion of the popn Up to an Altitude of ~3100 m, Arterial O2 Content Falls More Slowly Than Does PB Because of the Shape of the Hb-O2 dissociation cure - Reason: @ this altitude, arterial PO2 is 60-70 mm Hg, w/c corresponds to the relatively flat portion of the O2-Hb dissociation curve, where almost all of the O2 in blood is bound to Hb - Decreasing arterial PO2 has relatively little effect on arterial O2 content until arterial PO2 falls below this flat portion - Thus, the characteristics of Hb protect the arterial O2 content, despite modest reductions of PO2 - Uptake of O2 that the systemic tissues take up o The product of CO and the arteriovenous (a-v) difference in O2 content - @ sea level: o arterial PO2 = 100mm Hg Hb saturation = ~ 97.5% o mixed venous PO2 = 40mm Hg Hb saturation = ~ 75% o difference of arterial & venous O2 contents = ~ 25% of Hbs maximal carrying capacity for O2 - @ an altitude of 3,100 m: o arterial PO2 = ~ 60mm Hg Hb saturation = ~ 88% o mixed venous PO2 = 33 mm Hg Hb saturation = ~ 88% 22.5% = 65.5% - as a result, the a-v difference of PO2 is much larger at sea level (100 40 = 60 mm Hg) than at 3,100 m (60 33 = 27 mm Hg), even though the a-v differenc in O2 content is the same o reason: O2 Hb dissociation curve is steeper in region covered by PO2 values at high altitude

@ very high altitudes o Uptake of O2 by pulmonarycapillary blood slows Smaller O2 gradient from alveolus to blood O2 may no longer reach diffusion elquilibrium between alveolar air and pulmonary-capillary blood alveolar PO2, maximal attainable arterial PO2, actual arterial PO2 because of a failure of pulmonary capillary blood to equilibrate with alveolar air Hypoxemia - reduction in blood O2 content at different altitudes During the First Few Days, Compensatory Adjustments to Hypoxemia Include TACHYCARDIA & HYPERVENTILATION Reduction in arterial PO2 Stimulates peripheral chemoreceptors Immediate increase in ventilation 2 effects Brings alveolar PO2 (thus blows off CO2 Arterial PO2) closer to the Ambient PO2 respiratory alkalosis Inhibits the peripheral but especially the central chemoreceptors Decrease in ventilator drive total ventilation during an acute exposure to 4500m is only about twice that at sea level accompanying the hyperventilation during acute altitude exposure is an increase in heart rate (tachycardia)

probably due to the increased sympathetic drive that accompanies acute hypoxemia

increased CO Enhances O2 delivery during the next few days to weeks at an elevation of 4500m acclimatization ventilation to increase progressively by about the same amount as acute response PO2 continues to improve & PCO2 falls 2 mechanisms for this slower phase of increased ventilation -

1. pH of CSF decreases counteracting the respiratory alkalosis induced by the increase in ventilation Offsetting the inhibition of central chemoreceptors

*long term hypoxia appears to increase the sensitivity of the peripheral chemoreceptors to hypoxia This effect may better account for acclimization 2. the kidneys respond over a period of several days to respiratory alkalosis by decreasing their rte of acid secretion So that blood pH spillage of HCO3into decreases toward normal the urine Osmotic dieresis & alkaline urine *the consequence of reducing both CSF and plasma pH is to remove part of the inhibition caused by alkaline pH, allowing hypoxia to drive ventilation to higher values

Long-Term Adaptations to Altitude Include (1) increases in Hct, (2) Pulmonary Diffusing Capacity, (3) Capillarity, & (4) Oxidative Enzymes although increases in ventilation and CO help to maintain O2 delivery during acute hypoxia, they are costly from an energy standpoint and cannot be sustained for extended periods many of these adaptations are mediated by an increase in hypoxiainducible factor 1 (HIF-1) o a transcription factor that activates genes involved in erythropoiesis angiogenesis other processes

2- to 3-fold increase in pulmonary diffusing capacity 3. Capillary Density Hypoxia Tissues release growth factors that hypoxic tissue release (VEGF, FGF, and angiogenin) Tissue angiogenesis occurs within days of exposure to hypoxia 4. Oxidative Enzymes Hypoxia Promotes expression of oxidative enzymes in the mitochondria Enhance the tissues ability to extract O2 from the blood Thus, accilimatization to high altitude not only increases O2 delivery to the periphery, but also increase O2 uptake by the tissues

1. Hematocrit (Hct) o Prolonged hypoxemia slow increase in RBC mass o @ sea level: [Hb] = 14-15g/dL to more than 18g/dL Hct increases from 4045% to more than 55% o Prolonged hypoxemia, renal hypoxia, Norepinephrine Stimulates the production of EPO from fibroblast-like cells in the kidney Increased production of RBC precursors in bone marrow 2. Pulmonary Diffusing Capacity Acclimatization to high altitude Increase in blood volume of pulmonary capillaries to the associated increase in capillary surface area available for diffusion Surface area expands even further Because hypoxia stimulates an increase in depth of inspiration

Ascent to Altitude Leads to Fatigue, Nausea, and Decreased Cognition in Most People and to Acute or Chronic Mountain Sickness in Susceptible Individuals A rapid ascent may precipitate a constellation of relatively mild symptoms o Drowsiness o Fatigue o Headache o Nausea o A gradual decline in cognition These effects of hypoxia are progressive with increasing altitude Initially, these symptoms reflect an inadequate compensatory response to hypoxemia resulting in reduced O2 delivery to the brain In longer term, symptoms may stem from mild cerebral edema, which probably results from dilation of

cerebral arterioles, leading to increased capillary filtration pressure and enhanced transudation People who ascend rapidly to altitudes as seemingly moderate as 3,000m to 3,500m develop acute mountain sickness (AMS) o Symptoms: headache Fatigue Dizziness Dyspnea Sleep disturbance Peripheral edema Nausea Vomiting o Symptoms usually develop within the first day and last for 3 to 5 days o Primary problem: hypoxia o Symptoms probably have 2 causes: Progressive, more severe case of cerebral edema Pulmonary edema, w/c occurs as hypoxia leads to hypoxic pulmonary vasoconstriction Increases total pulmonary resistance, pulmonary pressure and transudation o Cerebral or pulmonary edema can be fatal if the exposure is not rapidly reversed Providing supplemental O2 Removing the individual from the high altitude Those least likely to develop symptoms ventilate more in response to hypoxia, and therefore, tend to have a higher PO2 and lower PCO2 Less cerebral vasodilation and minimizes pulmonary vasoconstriction

Etiology: overproduction of RBCs (an exaggerated response to hypoxia) Hct can exceed 60% increase blood viscosity & vascular resistance increasing the risk of vascular thrombosis

Chronic mountain sickness - Occurs after prolonged residence at high altitude

You might also like