Therapeutic gases

Therapeutic Gases - Oxygen

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Oxygen

Oxygen, water, and food are of fundamental importance to the animal organism. Of these three basic essentials for the maintenance of life, the deprivation of oxygen leads to death most rapidly. Therapy with oxygen is useful or necessary for life in several diseases and intoxications that interfere with normal oxygenation of the blood or tissues.


Normal Oxygenation

Oxygen moves down a stepwise series of partial pressure gradients from the inspired air to the body's cells and their mitochondria. Air normally contains 20.9% oxygen, equivalent (at normal barometric pressure) to a partial pressure of 159 mm Hg


Normal Oxygenation

Blood Oxygen ContentOxygen in blood is carried primarily in

chemical combination with hemoglobin and to a small extent in physical solution in plasma.

When fully saturated, each gram of hemoglobin binds about 1.3 ml of oxygen.

Hemoglobin is about 98% saturated when air is breathed under normal circumstances


Oxygen Deprivation

Hypoxia is the term used to denote insufficient oxygenation of the tissues.


Causes of Hypoxia

Prepulmonary Hypoxia. Hypoxia can be caused by inadequate delivery of oxygen to the lung. results from inadequate ventilation brought about

by airway obstruction (laryngospasm, bronchospasm), muscular weakness (disease or neuromuscular-blocking drugs), or impaired respiratory drive [central nervous system (CNS) disease, opioids, anesthetics].


Causes of Hypoxia

Pulmonary Hypoxia - abnormal pulmonary function can impair oxygenation of the blood.mismatch between ventilation and

perfusion- (e.g., adult respiratory distress syndrome, asthma, emphysema).

thickened barrier to diffusion and intrapulmonary shunting of venous blood (fibrosis, pulmonary edema).


Causes of Hypoxia

Postpulmonary Hypoxia – inadequate delivery of oxygen to tissues

may be the result of low cardiac output (shock), maldistribution of cardiac output (sepsis, vascular occlusion)

an inadequate concentration of oxygen in arterial blood (anemia, hemoglobinopathies, carbon monoxide poisoning).


the tissues may be unable to extract or utilize sufficient oxygen. This may result from an unusually high metabolic demand (thyrotoxicosis, hyperpyrexia) or to malfunction of cellular enzyme systems (cyanide poisoning).


Effects of Hypoxia

Respiration

Cardiovascular System

Central Nervous System

Cellular and Metabolic Effects


Respiration

Ventilatory rate and depth progressively increase during hypoxia as a result of stimulation of carotid and aortic chemoreceptors; minute ventilation almost doubles when normal individuals inspire gas with a PO2 of 50 mm Hg


Cardiovascular System

Cardiac output increases with hypoxia as a result of increased heart rate and decreased peripheral vascular resistance.

Severe hypoxia, however, can produce bradycardia and, ultimately, circulatory failure.


CNS

The CNS is least able to tolerate hypoxia. Hypoxia is accompanied initially by decreased intellectual capacity and impaired judgment and psychomotor ability; this state progresses to confusion and restlessness and ultimately to stupor, coma, and death as the PaO2 decreases below 30 to 40 mm Hg.


Cellular and Metabolic EffectsDelivery of oxygen to mitochondria slows as the partial pressure gradient from capillaries to tissues decreases.

At a mitochondrial PO2 of less than about 1 mm Hg, aerobic metabolism stops, and the less efficient anaerobic pathways of glycolysis become responsible for the production of cellular energy.

The cellular concentrations of Na+, Ca2+, and H+ increase, leading to cell death.


Adaptation to Hypoxia

Long-term hypoxia results in adaptive physiological changes increased numbers of pulmonary alveoli,

increased concentrations of hemoglobin in blood and myoglobin in muscle, and a decreased ventilatory response to hypoxia

Short-term exposure to altitude produces similar adaptive changes


Acute exposure - "mountain sickness“ a syndrome characterized initially by headache,

nausea, dyspnea, and impaired judgment, progressing to pulmonary and cerebral edema

Mountain sickness is treated by inhalation of oxygen, descent to lower altitude, or by an increase in ambient pressure. Treatment with diuretics (carbonic anhydrase inhibitors) and steroids also may be helpful.


Effects of Oxygen Inhalation

The primary use for inhalation of oxygen is to reverse the effects of hypoxia; other consequences usually are minor. However, when oxygen is breathed in excessive amounts, toxic effects can occur


Respiration Inhalation of oxygen at 1 atmosphere or above causes a small degree of respiratory depression in normal subjects, presumably as a result of loss of tonic chemoreceptor activity.

Within a few minutes, ventilation increases because of a paradoxical increase in the tension of carbon dioxide in tissues.


Carbon dioxide is carried by blood in the form of bicarbonate. This mechanism of carbon dioxide transfer operates more readily when a hydrogen ion acceptor, such as deoxyhemoglobin (a stronger base than oxyhemoglobin), is available.

Oxygen at a high PO2, (e.g., during hyperbaric oxygenation), the amount of physically dissolved oxygen may be sufficient to satisfy the requirements of tissue. little or no oxygen is extracted from oxyhemoglobin, and deoxyhemoglobin is not formed.

Carbon dioxide is then buffered less efficiently, and the PCO2 of the tissues rises by several mm Hg.


Oxygen Toxicity

Oxygen toxicity probably results from an increased production of reactive species such as superoxide anion, singlet oxygen, hydroxyl radical, and hydrogen peroxide. The oxidative damage initiated by these substances is propagated by lipid peroxidation and ultimately involves all components of the cell. Cell injury and death are presumed to result from loss of membrane integrity.


Effects on CNS

Central Nervous System. CNS oxygen toxicity does not occur when the partial pressure of inspired oxygen is less than 2 atmospheres; its occurrence is thus limited to a small number of hyperbaric applications. CNS toxicity is observed before pulmonary toxicity when oxygen is administered at partial pressures above 2.5 atmospherescharacterized by convulsions, which may be preceded by visual symptoms or muscular twitching


The effect on the central nervous system :muscle twitching and spasm nausea and vomiting dizziness vision (tunnel vision) and hearing difficulties (tinnitus) twitching of facial muscles irritability, confusion and a sense of impending doom trouble breathing, anxiety unusual fatigue incoordination convulsion.


Respiratory Tract

Pulmonary system first to exhibit toxicity; Symptoms of pulmonary oxygen poisoning begin slowly as a substernal irritation that becomes progressively more intense and widespread along with with increased coughing. Uncontrollable coughing occurs in severe cases, symptoms originating in the trachea and major bronchi associated with a constant burning sensation, which is worsened by inspiration.


Pulmonary function changes to hyperoxic O2 exposures include: 1. decreases in inspiratory and expiratory lung volumes 2. decreases in flow rates 3. decreases in carbon monoxide diffusing capacity 4. decrease in lung compliance.


Effects on Eye

At increased atmospheric pressures, vision may be affected. Symptoms may include photophobia, amblyopia, mydriasis, bilateral progressive constriction of visual acuity was found after breathing pure oxygen for four and one-half hours at normal atmospheric pressures.


Therapeutic Uses

Correction of Hypoxia

Reduction of the Partial Pressure of an Inert Gas

Oxygen as a Diluent

Hyperbaric Oxygen Therapy


Therapeutic gases

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