Physiology of Hypoxia part 3
1.Part 1 Causes of hypoxia.
2.Part 2 Altitude illnesses
Venous to arterial shunts
•Cyanotic congenital heart disease, septal defects with shunt reversal
•“right-to-left shunts”
•Large amounts of unoxygenated venous blood bypass the lungs and dilute the oxygenated blood Administration of 100% O2 – has little eff
Ventilation – perfusion imbalance
•Patchy V/Q imbalance – commonest cause of hypoxic hypoxia clinically
•Some diseases – prevent ventilation of some alveoli
•Unoxygenated blood reaching those alveoli – sent to the left side of the heart unoxygenated! •Nonventilated but perfused alveoli – act as a right to left shunt!
Lung collapse
•When a bronchus is obstructed, the gas in the alveoli beyond the obstruction is absorbed
•The lung segment collapses
•This is known as atelectasis
•Causes:
–Obstruction of airways
–Absence of surfactant
–Pnuemothorax
•Air enters the pleural space, through a rupture of lung or hole in chest wall
•The lung collapses and the mediastinum shifts to the opposite side.
•Marked dyspnea
•Presence of a flap of tissue, that functions as a one-way (inward) valve, over the opening – Tension pneumothorax (Potentially fatal!)
Asthma
•An acute obstructive lung disease
•Characterized by:
–Airway obstruction
•Due to bronchoconstriction and mucus hypersecretion
–Airway inflammation
–Airway hyperresponsiveness
•The patient must avoid the extrinsic allergens
Emphysema
•A chronic obstructive lung disease
•Enlargement of the air spaces and destruction of the lung tissue distal to the terminal bronchiol
•Elasticity of the lung reduced
•Increased V/Q
•Physiological dead space – greatly increases
•Severe hypoxia with polycythaemia develops
2. Causes of anaemic hypoxia
1. Anaemia
2. Carbon monoxide poisoning
Anaemic hypoxia
•Anaemia = Abnormally low Hb level for age and sex
•In anaemia – red blood cell 2,3-BPG increases
•Therefore, hypoxia due to mild – moderate anemia is not severe at rest
•But anemic patients may have considerable difficulty during exercise
•This is because of the limited ability to increase O2 delivery to the active tissues
Carbon monoxide poisoning
•CO – A gas formed in the body; Functions as a chemical messenger in the brain
•In larger amounts – poisonous!
•Exhaust of gasoline engines – contain > 6% CO
•CO reacts with hemoglobin to form carbonmonoxyhemoglobin (carboxyhemoglobin, COHb)
•COHb cannot take up O2
•CO poisoning – considered a form of anaemic hypoxia because the amount of Hb that can carry O2 is reduced
•The affinity of hemoglobin for CO is 210 times its affinity for O2
•Therefore, COHb liberates CO very slowly
•Also, when COHb is present the dissociation curve of the remaining HbO2 shifts to the left.
• Therefore, if two people with CO poisoning and anaemia have the same level of HbO2, the person with CO poisoning will be much more seriously incapacitated
•Symptoms of CO poisoning – similar to other types of hypoxia
•In arterial blood PO2 remains normal. Carotid and aortic chemoreceptors are not stimulated.
•Therefore, no stimulation of respiration.
•COHb – cherry red in colour. Visible in skin, nail beds, and mucous membranes.
•When 70 – 80% of circulating Hb is converted to COHb – Death!
Treatment of CO poisoning
•Immediate termination of the exposure.
•Adequate ventilation, by artificial respiration if necessary.
•Ventilation with O2 is better than ventilation with fresh air (O2 hastens the dissociation of COHb). Hyperbaric oxygenation is also useful
3. Causes of stagnant hypoxia
•Due to slow circulation
•General or local circulatory deficiency
•Seen in:
–Shock
•Kidneys, heart affected
–Congestive cardiac failure
•Liver, brain affected
–Prolonged hypotension Acute respiratory distress syndrome may result
4. Causes of histotoxic hypoxia
•Due to inhibition of tissue oxidative processes
•Due to:
–Cyanide poisoning
•Cyanide inhibits cytochrome oxidase
–Vitamin deficiency
Oxygen Treatment
•Administration of O2 rich gas mixture is of great benefit in many forms of hypoxia:
–High altitudes
–Asthma
–CO poisoning
–Hypoventilation
•However, not useful in hypoxic hypoxia due to shunting of unoxygenated venous blood past the lungs
•It is also of very limited value in stagnant, anemic and histotoxic hypoxia
•That is because in these instances all that can happen is an increase in the amount of dissolved O2 in the arterial blood.
•Treatment regimes that deliver less than 100% O2 are of value both acutely and chronically
Hypercapnic patients with severe pulmonary failure (i.e. Emphysema):
•CO2 level may be extremely high so that it depresses rather than stimulates respiration.
•Some of these patients keep breathing only because of the hypoxic stimulation of carotid and aortic chemoreceptors drive the respiratory center.
•If the hypoxic drive is withdrawn by administering O2, breathing may stop.
•During the resultant apnea, the arterial PO2 drops but breathing may not start again.
•This is because the increase in PCO2 further depresses the respiratory center.
•Therefore, O2 therapy in this situation must be started with care.
Oxygen Toxicity
•O2 toxicity may develop due to prolonged administration of 100% oxygen.
•This is to the production of the superoxide anion (O2–), which is a free radical, and H2O2. When 80–100% O2 is administered for 8 hours or more, the respiratory passages become irritated, causing substernal distress, nasal congestion, sore throat, and coughing
•Infants treated with O2 for respiratory distress may develop:
–Bronchopulmonary dysplasia
•Chronic condition, lung cysts & densities
–Retinopathy of prematurity (retrolental fibroplasia)
•Opaque vascular tissue in the eyes, may lead to serious visual defects
•These are considered to be manifestations of O2 toxicity.