Therapeutic Gases - Oxygen

Therapeutic Gases - Oxygen

OxygenOxygen, 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 OxygenationOxygen 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 OxygenationBlood 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

FIGURE 2-1 Anchor Points of the Oxygen Dissociation Curve. The curve is shifted to the right by an increase in temperature, PCO2, H+, and 2,3-DPG. The oxygen concentration scale is based on a hemoglobin concentration of 14.5 g/100 ml.

FIGURE 9-3 Response of the Arterial PO2 to Increased Inspired Oxygen Concentrations in a Lung With Various Amounts of Shunt. Note that the PO2 remains far below the normal level for 100% oxygen. Nevertheless, useful gains in oxygenation occur even with severe degrees of shunting. (This diagram shows typical values only; changes in cardiac output, oxygen uptake, etc., affect the position of the lines.)

Oxygen DeprivationHypoxia is the term used to denote insufficient oxygenation of the tissues.

Causes of HypoxiaPrepulmonary 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 HypoxiaPulmonary 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 HypoxiaPostpulmonary 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 HypoxiaRespiration

Cardiovascular System

Central Nervous System

Cellular and Metabolic Effects

RespirationVentilatory 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 SystemCardiac 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.

CNSThe 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 (130 Pa), 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 sicknessa 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 InhalationThe 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.

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

Therapeutic Uses

Correction of Hypoxia

Reduction of the Partial Pressure of an Inert Gas

Oxygen as a Diluent

Hyperbaric Oxygen Therapy

CCONSERVATIVE MANAGEMENTOXYGEN THERAPYClear benefit of long term o 2 TRIALS- N O T T ( Nocturnal O2 Ttherapy trial ) M R C ( Medical Rsearch Council, UK )

Continuous O2 (24 hrs/day) better than nocturnal O2 (12 hrs/day) which is better than no O2

OXYGEN THERAPY

MODES OF OXYGEN DELIVERY

APPARATUS O2 FLOW CONC.(L / MIN) %

NASAL CATHETER 2 6 25 40 SEMI RIGID MASK 4 15 35 - 70VENTURI MASK 6 12 24, 28, 35,40, 50, 60SOFT PLASTIC MASK4 15 40 80VENTILATORS VARYING 21 100CPAP CIRCUITSVARYING 21 100OXYGEN TENT 7 10 60 - 80

Nasal kanul1liter/mt --- FiO2 = 24%2 l/mt --- FiO2 = 28%3 l/mt --- FiO2 = 32%4 l/mt --- FiO2 = 36%5 l/mt --- FiO2 = 40%6 l/mt --- FiO2 = 44%

mask5 6 l/mt --- FiO2 = 40%6 7 l/mt --- FiO2 = 50%7 8 l/mt --- FiO2 = 60%

PATIENTS FOR HOME OXYGEN THERAPY STABLE COURSE OF DISEASE 2 ABGs AT ROOM AIR AT REST FOR 20 MNTS * RESTING PaO2 < 55 FOR > 3 WKS OR PaO2 55 59 + CLINICALLY COR PULMONALE AND / OR HAEMATOCRIT > 55 % * NOCTURNAL HYPOXEMIA OR HAEMATOCRIT > 55 % OR CLINICAL PULMONARY HYPERTENSION * NORMOXIC PATIENT WITH LESS DYSPNOEA + INCREASING EXERCISE CAPABILITY WITH O2

OXYGEN DOSE

# CONTINUOUS O2 FLOW 1 2 L/MIN WITH SINGLE / DOUBLE NASAL CANNULA WITH ADEQUATE SaO2# LOWEST FLOW TO RAISE PaO2 TO 60-65 mm OR SaO2 88-94 %# INCREASE BASE -LINE FLOW BY 1 L / MIN DURING SLEEP AND EXERCISE

CONTROLLED O2 THERAPYMODERATE TO SEVERE HYPOXIA (PaO2 7.25SEVERITY OF ACIDOSIS IS A BETTER PROGNOSTIC GUIDE THAN ABSOLUTE pCO2 LEVELS. contd

CONTROLLED OXYGEN THERAPY contdNORMALLY 24% - 26% INSPIRED OXYGEN UPTO 30% IF HYPOXIA UNRELIEVED.RESPONSE --- 1. RELIEF OF HYPOXIA + REDUC. IN PCO2 + CLINICAL IMPROVEMENT 2. RELIEF OF HYPOXIA + INITIAL RISE IN PCO2 AND pH /< 7.25 LATER CHANGING TO NORMAL WITH FALL IN PCO2 3. IF UNCONTROLLED OXYGEN THEN RAPID RISE IN PCO2 AND DROP IN pH