Lecture 6

1. Lecture 6 • Hypoxia • Hypocapnia • Hypercapnia • Asphyxia • Oxygen therapy • Drowning • Effects of increased barometric pressure • Nitrogen narcosis • Decompression sickness • Air embolism • Oxygen toxicity • Hyperbaric oxygen therapy • Acclimatization

2. Hypoxia • It is the deficiency of O2 at the tissue levels. It is also termed anoxia. • It is divided into 4 categories; • (1) Hypoxic Hypoxia: • - It is also termed anoxic anoxia & hypoxemia. • It is defined as an adequate PO2 in the arterial blood. • The primary causes of HH in diseases are hypoventilation, inadequate PO2 in the inspired air (such as altitude) or inadequate alveolar-capillary transfer (such as shunt or V/Q mismatch).

3. (2) Anemic hypoxia: • - It occurs in which the PaO2 is normal but the total O2 content of the blood is reduced because of inadequate No. of erythrocytes, deficient or abnormal Hb or competition for the Hb molecules by CO. • - It occurs due to lowering the O2-carrying capacity of the blood. • (3) Ischemic hypoxia: • - It is also termed stagnant hypoxia, circulatory hypoxia & hypoperfusion hyperoxia. • It occurs in which the BF to a tissue is too low that adequate O2, is not delivered to it despite a normal PO2 and Hb conc. • (4) Histotoxic hypoxia: • It occurs in which the quantity of O2 reaching the tissues is normal but the cell is unable to utilize the O2 because a toxic agent – cyanide, for example, has interfered with the cells metabolic.

4. Hypercapnia • It means excess CO2 in the body fluids. • It usually occurs in association with hypoxia only when the hypoxia is caused by hyperventilation or circulator deficiency. • Retention of CO2 in the body (hypercapnia) initially stimulates respiration. • Retention of larger amounts produces symptoms due to depression of the CNS; confusion, diminished sensory acuity, and eventually coma with respiratory depression and death. • CO2 is so much more soluble than O2 that hypercapnia is rarely a problem in patient with pulmonary fibrosis.

5. Hypocapnia • It is the result of hyperVE. • During voluntary hyperVE, the PaCO2 falls from 40 mmHg as low as 15 mmHg while the PAO2 rises to 120-140 mmHg. • The consequences of hypocapnia are due to the associated respiratory alkalosis, the blood pH being ↑ to 7.5 or 7.6. • Hypocapnia can cause cerebral vasoconstriction, cerebral hypoxia, dizziness, visual disturbances and anxiety.

6. Asphyxia • It is an inability to breath and suffocation. • The symptoms of Asphyxia includes; breathing difficulty, rapid pulse, high BP, convulsion, paralysis, coma and death. • The above symptoms of Asphyxia may vary on an individual basis for each patient. Only your doctor can provide adequate diagnosis of any signs or symptoms and whether they are indeed Asphyxia symptoms. • The possible causes of Asphyxia includes: choking, foreign body, suffocation, toxin fumes, CO poisoning, whooping cough, drowning, diphtheria, asthma, wound infection, heart failure and collapsed lung. • Treatment of Asphyxia includes; First aid to remove foreign body, Emergency resuscitation, Expired Air Resuscitation (EAR), and Cardio-Pulmonary Resuscitation (CPR)

7. Oxygen therapy • It is used in the treatment of patient with sever lung disease who increases the conc of inspired O2 or control VE by means of mechanical ventilator. • It is usually very effective in relieving hypoxemia, except when this is caused by a shunt (BF through unventilated alveoli). In this case the added O2 does not have access to the shunted blood. • O2 is now normally administered by small cannulas inserted into the nostrils or by means of a plastic oronasal mask. • Giving too much O2 may lead to Pulmonary edema

8. Drowning • It is suffocation by submersion, usually in water. • Studies of drowned or nearly drowned people show that the most important blood gas changes are severe hypoxemia combined with hypercapnia and respiratory acidosis. • In 10 % of drowning, the first gasp of water after losing struggle not to breathe triggers laryngospasm, and death results from asphyxia without any water in the lungs. In the remaining cases, the glottic muscles eventually relax and the lung are flooded. • The immediate goal in the treatment of drowning is resuscitation, but long-term treatment must take into account the circulatory effects of the water in the lungs.

9. Effects of increased barometric pressure • The ambient pressure increases by 1 atmos for every 10 m of depth in sea water and every 10.4 m of depth in fresh water. • Therefore, at a depth of 31 m (100ft) in the ocean, a diver is exposed to a pres of 4 atmos. • Those who dig underwater tunnels are also exposed to the same hazards because the press in the chambers in which they work is increased to keep out the water. • The hazards of exposure to ↑ barometric press used to be the concern largely of the specialists who cared for deep-sea divers and tunnel workers. • Examples of the ↑ barometric press includes; O2 toxicity, N2 narcosis, decompression sickness and air embolism (see the table).

11. Nitrogen narcosis • N2 narcosis is a condition that occurs in divers breathing compressed air. When divers go below depths of approx 100 ft, increase in the pp of N2 produces an altered mental state similar to alcohol intoxication. • N2 narcosis, commonly referred to as "rapture of the deep," typically becomes noticeable at 100 ft underwater and is incapacitating at 300 ft, causing stupor, blindness, unconsciousness, and even death. • N2 narcosis is caused by gases in the body acting in a manner described by Dalton's Law of pp. As the total gas press ↑ with ↑ dive depth, the pp of N2 increases and more N2 becomes dissolved in the blood. This high N2 conc impairs the conduction of nerve impulses and mimics the effects of alcohol or narcotics. • Symptoms of N2 narcosis include: giddiness; euphoria; disorientation; loss of balance; loss of manual dexterity; slowing of reaction time; fixation of ideas; and impairment of complex reasoning. • The problem of N2 narcosis can be avoided by breathing mixture of O2 and helium.

12. Decompression sickness • As a diver breathing 80% N2 ascends from a dive, the elevated PAN2 falls. N2 diffuses from the tissues into the lungs along the pp gradient. If the return to atmos press (decompression) is gradual, no harmful effects are observed; but if the ascent is rapid, N2 escapes from solution. Bubbles form in the tissues and blood, causing the ?“symptoms of decompression sickness. • Bubbles in the tissues cause sever pains, particularly around joints, and neurologic symptoms that include paresthesias and itching. • Bubbles in the bloodstream, which occure in more sever cases, obstruct the arteries to the brain, causing major paralysis and respiratory failure. • Bubbles in the pulmonary capillaries are apparently responsible for the dyspnea that divers call “the chokes”. This is characterized by serious shortness of breath, often followed by sever pulmonary edema and, occasionally, death. • Bubbles in the coronary artery may cause myocardial damage. • Treatment of this disease is prompt recompression in a press chamber, followed by slow decompression. Recompression is frequently life saving. Recovery is often complete, but there may be residual neurologic sequelae due to irreversible damage to the nervous sytstem.

13. Air embolism • An AE, or more generally gas embolism, is a medical condition caused by gas bubbles in the bloodstream. Small amounts of air often get into the blood circulation accidentally during surgery and other medical procedures, but AE which shows symptoms is relatively rare. Large emboli can be rapidly fatal. • AE can occur whenever a BV is open and a press gradient exists favoring entry of gas. Because the press in most arteries and veins is greater than atmospheric, an air embolus does not always happen when a BV is injured. In the veins above the heart, such as in the head and neck, the press is less than atmos and an injury may let air in. • Trauma to the lung can also cause an AE. This is often noticed after the patient is placed on a ventilator and air is forced into an injured vein causing sudden death.

14. Symptoms of an AE depend on where the bubbles lodge. They range from skin rashes, joint pain, visual disturbances, balance disturbances, breathing difficulties, extreme fatigue/lack of strength, numbness, paralysis, unconsciousness and death. If the embolism occurs in the coronary arteries of the heart, a heart attack will occur. If it lodges in the lungs, a pulmonary embolism will occur, resulting in shortness of breath and chest pain. • Gas embolism and decompression sickness are very difficult to distinguish, as they have very similar symptoms. The treatment for both is the same, because they are both the result of gas bubbles in the body. In a diving context, the two are often called decompression illness. • Recompression is the only lasting treatment of an AE. Normally this is carried out in a recmpression chamber.

15. Oxygen toxicity • OT or OT syndrome is severe hyperoxia caused by breathing O2 at elevated pp. The high conc of O2 damages cells. • Hyperoxia is excess O2 in body tissues or higher than normal pp of O2. Hyperoxia is caused by breathing air at pressures greater than normal atmos press or by breathing nitrox or O2 at normal atmos press for a prolonged period of time. • The OT syndrome may occur; - as a diving disorder, when divers breathe any breathing gas at the high press of depth, - as a potential complication of mechanical VE with pure O2, where it is called the respiratory lung syndrome. - OT is not a major factor in hyperVE, as some people believe. The problems caused by hyperVE are due to  CO2 within the blood. With or without hyperVE, it is impossible to develop OT breathing air at typical surface atmos press.

16. In humans, there are several types of O2 toxicity: • - CNS OT is manifested as convulsions, which although not lethal themselves, can cause drowning of divers or lethal pressure damage during a rapid ascent. • - The likelihood of this type of accident is directly proportional to the pp of O2in the breathing gas and to the duration of exposure. • - Pulmonary OT is caused by exposure over 16 hrs to pp of 0.5 bar or more. The damage to the lungs may be irreversible. This is rare complication in divers, but may be of concern in intensive care patients needing high-inspired oxygen concentrations. • - Rethinopathic OT causes damage to the retina. Oxygen may be a contributing factor for the disorder called retenopathy of prematurity.

17. Hyperbaric O2 therapy • The intense oxidizing properties of high-press O2 (hyperbaric O2) can have valuable therapeutic effects in several important clinical conditions. Therefore, large press tanks are now available in many medical centers into which patients can be placed and treated with hyperbaric O2. • The most useful use of hyperbaric O2 has been for treatment of gas gangrene, because the organism cannot live in a high PO2 environment. The organism is called clostridial, which best grow under anaerobic conditions. • A hyperbaric chamber is also useful for treating decompression sickness, arterial gas embolism, CO poisoning, osteomyelitis and myocardial infarction.

18. Major means of acclimatization • Mountain climbers have found that when they ascend a mountain slowly, over a period of days rather than the period of hours, they breathe much more deeply and therefore can withstand for lower atmos O2 conc than when they ascend rapidly. This is called acclimatization. • HyperVE is an ↑ in VE. • Figure show the changes in PAO2 and PACO2 that occur in acclimatized subjects and also in subjects acutely exposed to a low barometric press. • The cause of hyperVE is hypoxic stimulation of the peripheral chemoreceptors. The resulting low PaCO2 and alkalosis of the CSF and blood tend to inhibit this ↑ in VE activity. This is a suggestion, however, the cause of the sustained hyperVE is still not fully understood. • Polycythemia is another feature of acclimatization of high altitude is an ↑ in the RBC conc of the blood. The resulting rise in Hb conc and therefore O2-carrying capacity, means that, although the PaO2 and O2 saturation are diminished, the O2 content of the arterial blood may be normal or even above normal. • Polycythemia tends to maintain the PO2 of mixed venous blood as shown in the figure. • The stimulus for the ↑ production of RBCs is tissue hypoxia, which release erythropoiten from the kidney, which in turn stimulates the bone marrow. Polycythemia is also seen in many patients with chronic hypoxemia caused by lung or heart disease.

19. Other features of acclimatization includes; • - A shift to the right of the O2 dissociation curve, which result in a better unloading of O2 in the venous blood at a given PO2. • - ↑ the conc of capillaries in the peripheral muscles because the muscle fiber become smaller. There are also ↑ in some oxidative enzyme inside the cells. The maximum breathing capacity ↑ because the air is less dense and this makes possible the very high VE (upto 200 l/min) which occur on exercise. The maximum O2 uptake, however, declines rapidly above 4500m. • - Pulmonary vasoconstriction which occurs at high altitude as a result of alveolar hypoxia. • - Pulmonary hypertension which occasionally associated with high altitude pulmonary edema. Typically a climber or skier who has ascended to high altitude, perhaps without an adequate period of acclimatization, develops shortness of breath and may cough up pink, frothy sputum. The treatment is to move the patient to a lower altitude and to give O2 if this is available.