Respiration

High altitude Changes Atmosph. Pressure at sea level=760mmHg and PO2=160mmHg As one ascends – Atmosph pressure keeps on decreasing Composition or percentage of constituent gases remains same At 10,000 feet = 523 mmHg PO2=110mmHg At 50,000 feet = 87 mmHg PO2=18mmHg Acclimatization – try to be normal at high altitude.

BAROMETRIC PRESSURE CHANGES IN HIGH ALTITUDE As the altitude increases above the sea level, the corresponding atmospheric pressure decreases. The partial pressure of Oxygen also decreases. The arterial Oxygen saturation levels also decrease with increase in the altitude.

PARTIAL PRESSURES OF OXYGEN

ACCLIMATIZATION “Getting used to…” People remaining at high altitudes for days, weeks or years become more and more acclimatized to low PO2. This causes the hypoxia to cause fewer deleterious effects on their bodies. They can thus work harder at higher altitudes without hypoxic effects.

Acclimatization At 10,000 feet, atmosph pressure = 523 and alveolar PO2 = 110mmHg The changes in response to hypoxia if somebody stays at high altitude for sometime by Great increase in pulmonary ventilation Increases RBCs no Increased diffusion capacity of lung Increased vascularity of the tissue Increased ability of tissue cells to use oxygen despite low PO2

Increased Pulmonary Ventilation Hypoxic stimulation of resp. center by periph. Chemoreceptors Immediate compensation to ↓PO2 by ↑ alveolar ventilation to →↑ CO2 exhaling →↑ PCO2 → inhibitory effect as resp. center opposes ↓ PO2 stimulatory effect After a few days stimulatory effect overwhelms inhibitory effect b/c ↓ HCO3 ions in brain

Increased RBCs Count Hypoxia → erythropoietin →↑ RBC production Hct from normal (40-45) to 60-65 Hb from normal (15mg/dl) to 20-22G/dl

Increased Diffusing Capacity ↑ Pulmonary capillary blood vol. → capillaries expanding → ↑ surface area Also inc in air vol → ↑ surface area Inc in pulm art blood pressure– more perfusion So diffusing capacity for O2 from normal (21 ml/mmHg/mint) to 65 ml/mmHg/mint

Increased Vascularity of Tissue (Circulatory Changes) Initially ↑ cardiac out by 30% approx. As Hct ↑ - C.O. becomes normal ↑ in capillaries in non-pulmonary areas – called increased capillarity (angiogenesis) Hypoxia → pulmonary vasoconstriction → Retrograde pressure on Rt heart → Rt ventricular hypertrophy Pulmonary vasoconstriction → pulmonary hypertension

Cellular Acclimatization More capillary formation in tissue → ↑ vascularity Also ↑ Mitochondria, ↑ Myoglobin & Cytochromes oxidase enzyme

Acute Mountain Sickness May be nausea, vomitting, headache, Irritability, Dyspnoea, at 1200ft At 18000 ft - twitching, seizures At 23000 ft – coma leading to death Cerebral vasodilatation in response to hypoxia →fluid leakage into cerebral tissue → cerebral edema → Disorientation & other cerebral dysfunction Pulmonary edema – exact cause not known

Vasocosntriction in pulmonary capillaries leads to increased blood pressure in open capillaries leading to edema Breathing oxygen, especially under pressure, can reverse symptoms

Chronic Mountain Sickness RBC count ↑ - so Hct ↑ Pulmonary arterial pressure ↑ Rt heart – hypertrophy ↑ Hct → ↑ blood viscosity → sluggish circulation → ↑ O2 supply Natives at high altitude – Chest barrel shaped – chest longer Aortic & carotid bodies of bigger size Pulmonary hypertension & Rt ventricular hypertrophy ↑ RBC count with ↑ Hct

Seen in people who reside for long at high altitudes. Red cell number and mass increases exceptionally. Pulmonary arterial pressure becomes very high. The heart becomes enlarged in the right side. The peripheral arterial pressure begins to fall Congestive Cardiac failure & death follows They need to be taken to low altitudes as soon as possible. They recover in low altitudes within days or weeks.