سشنات دكتور ظاهر

Oxygen Therapy

* Dr.Dhaher JS Al-habbo FRCP London UK Assistant Professor in Medicine DEPARTMENT OF MEDICINE

* Oxygen Therapy

Karl W.Scheelein 1772
* Joseph Priestly in1774

Oxygen Therapy

Joseph Priestley and Carl Wilhelm Scheele both independently discovered oxygen, but Priestly is usually given credit for the discovery. Priestley called the gas produced in his experiments 'dephlogisticated air' and Scheele called his 'fire air'. The name oxygen was created by Antoine Lavoisier who incorrectly believed that oxygen was necessary to form all acids.

The Element Oxygen

Oxygen is a drug
Colorless, odorless, tasteless gas, makes up 21% of room air .It is NOT flammable but does support combustion. should be regarded as a drug . Has a Drug Identification Number (DIN) Oxygen must be prescribed in all situations (except for the immediate management of critical illness). Oxygen should be prescribed to achieve a target saturation (Sp02), which should be written on the drug chart .
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Basic Concepts of Oxygen
Composition of Room Air Nitrogen 78.08% ~78% Oxygen 20.946% ~21% Trace gases ~1%Normal PO2 in arterial blood (PaO2) ≥ 95mmHg: decrease with age.PO2 in mitochondria ≥ 18 mmHg required to generate high energy phosphate bonds e.x ATPAt rest the average adult male consumes about 225-250 ml of O2/min.This can increase up to 10 folds during exercise.There’s very small O2 reserve that can be consumed within 4-6 minutes of cessation of spontaneous ventilation. *

Oxygen content of blood

The theoretical maximum oxygen carrying capacity is 1.39 ml O2/g Hb, but direct measurement gives a capacity of 1.34 ml O2/g Hb.1.34 is also known as Hьfner’s constant.The oxygen content of blood is the volume of oxygen carried in each 100 ml blood.It is calculated by: (O2 carried by Hb) + (O2 in solution) = (1.34 x Hb x SpO2 x 0.01) + (0.023 x PaO2) 10

Mechanisms of Hypoxia

* O2 Utilization
O2 Delivery
O2 Delivery
O2 Utilization
Shift from aerobic to anaerobic metabolism
Increase Lactic acid Progressive Acidosis
Cell Death

Basic Concepts of Oxygen

Oxygen Cascade:Inspired = 150 mmHg at Sea Level ↓ Alveolar PO2= 103 ↓ Arterial=100↓ Capillary= 51 ↓ Mitochondrial= 1-10(FiO2 expressed as 0.21-1.0 or 21- 100%) *

Clinical Conditions With Increased Risk of Hypoxia

Myocardial infarction Acute pulmonary disorders Sepsis Drug overdose Liver failure Head trauma CHF
Hypovolemic shock Blunt chest trauma Acute neuromuscular disease Acute abdomen (splinting) Acute pancreatitis Spinal cord injury

Indications for Oxygen Therapy

Tachypnea Cyanosis Restlessness Disorientation Cardiac arrhythmias Slow bounding pulse Tachycardia Hypertension
Dyspnea Coma Labored breathing (use of accessory muscles, nasal flaring) Lethargy Tremors/seizure activity

Oxygen Therapy

“Generally speaking”, a patient who is breathing less than 12 and more than 24 times a minute needs oxygen of some kind *

Oxygen therapy To ensure safe and effective treatment

Oxygen is required for the functioning and survival of all body tissues and deprivation for more than a few minutes is fatal. In immediately life threatening situations oxygen should be administered. Hypoxaemia. Acute hypotension. Breathing inadequacy. Trauma. Acute illness. CO poisoning. Severe anaemia. During the peri-operative period.

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Oxygen therapy

Oxygen therapy Humidification Is recommended if more than 4 litres/min is delivered. Helps prevent drying of mucous membranes. Helps prevent the formation of tenacious sputum. Oxygen concentrations will be affected with all delivery systems if not fitted correctly or tubing becomes kinked and ports obstructed.
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The oxyhaemoglobin dissociation curve showing the relation between partial pressure of oxygen and haemoglobin saturation
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Methods of Oxygen Delivery
Most common methods of oxygen delivery include Nasal Cannula Venturi Mask 100% Non-Rebreather Mask Mechanical Ventilation

Oxygen Delivery Methods

Nasal Cannula Comfortable, convenient, mouth breathing will not effect % of O2 delivered Liters/min = % 2 l/m = 24-28% 3 l/m = 28-30% 4 l/m = 32-36% 5 l/m = 36-40% 6 l/m = 40-44% Cannot administer > 6 liters/minute (44%)

Nasal Cannula

Provides limited oxygen concentration Used when patients cannot tolerate mask Prongs and other uses Concentration of 24 to 44% Flow rate set between 1 to 6 liters For every liter per minute of flow delivered, the oxygen concentration the patient inhales increases by 4%
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Venturi Mask

Provides precise concentrations of oxygen Entrainment valve to adjust oxygen delivery Mostly used in the hospital setting for COPD patients
* FiO2 Delivery Blue 24% Yellow 28% White 31% Green 35% Pink 40% Concerns Tight seal is a must Interferes with eating/drinking Condensation collection

Venturi Mask

* Red 40% 10/L/M
Blue 24% 2/L/M Yellow 35% 8/L/M White28% 4/L/M Green 60% 15/L/M Orange 31% 6/L/M

Oxygen Delivery Methods100% Non-Rebreather

Delivery percentages6 l/min = 55 – 60 %8 l/min = 60 – 80 %10 l/min = 80 – 90 %>12 l/min = 90 + % Benefit: Has a one way expiratory valve that prevents re-breathing expired gases Concern May lead to O2 toxicity


100% Non-Rebreather Mask
* partial rebreather Mask

Oxygen Delivery MethodsMechanical Ventilation

Allows administration of 100% oxygenControls breathing pattern for patients who are unable to maintain adequate ventilation Is a temporary support that “buys time” for correcting the primary pathologic process

Indications for Mechanical Ventilation

Mechanical Failure Ventilatory Failure Oxygenation Failure General Anesthesia Post-Cardiac Arrest

Mechanical Ventilation

Two categories of ventilators Negative pressure ventilators Iron lung Cuirass ventilator Positive pressure ventilators Two categories Volume-cycled (volume-preset) Pressure-cycled (pressure-preset)
Iron Lung

Mechanical Ventilation PEEP

Description Maintains a preset positive airway pressure at the end of expiration Increases PaO2 so that FiO2 can be decreased Increases DO2 (amt of delivered O2 to tissue) Maximizes pulmonary compliance Minimized pulmonary shunting Indications PaO2 < 60 on FiO2 > 60% by recruiting dysfunctional alveoli Increases intrapulmonary pressure after cardiac surgery to decrease intrathoracic bleeding (research does not support this idea)

Mechanical Ventilation PEEP 

Advantages Improves PaO2 and SaO2 while allowing FiO2 to be decreased Decreases the work of breathing Keeps airways from closing at end expiration (esp. in pts with surfactant deficiency) Disadvantages Increased functional residual capacity (increases risk for barotrauma) Can cause increased dead space and increased ICP In pts with increased ICP, must assure CO2 elimination Contraindicated: hypovolemia, drug induced low cardiac output, unilateral lung disease, COPD



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Mechanical Ventilation CPAP 

Description Constant positive pressure is applied throughout the respiratory cycle to keep alveoli open Indications To wean without having to remove the ventilator and having to connect to additional equipment


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Mechanical Ventilation CPAP

Advantages Takes advantage of the ventilator alarm systems providing psychological security of the ventilator being there Disadvantages Patient may sense resistance as he breathes through the ventilator tubing

Mechanical Ventilation Complications

Respiratory arrest from disconnection Respiratory infection (VAP) Acid-base imbalances Oxygen toxicity
Pneumothorax GI bleeding Barotrauma Decreased cardiac output

Ventilator Weaning

Vital Capacity at least 10 – 15 ml/kgTidal Volume > 5 ml/kgResting minute volume > 10 L per minuteABG’s adequate on < 40% FiO2Stable vital signsIntact airway protective reflexes (strong cough)Absence of dyspnea, neuromuscular fatigue, pain, diaphoresis, restlessness, use of accessory muscles


Primary Acid-base Disorders:Respiratory Alkalosis
Respiratory alkalosis - A primary disorder where the first change is a lowering of PaCO2, resulting in an elevated pH. Compensation (bringing the pH back down toward normal) is a secondary lowering of bicarbonate (HCO3) by the kidneys; this reduction in HCO3- is not metabolic acidosis, since it is not a primary process.Primary EventCompensatory Event HCO3- ↓HCO3- ↑ pH ~ ------- ↑ pH ~ --------↓ PaCO2 ↓ PaCO2

Primary Acid-base Disorders:Respiratory Acidosis

Respiratory acidosis - A primary disorder where the first change is an elevation of PaCO2, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary retention of bicarbonate by the kidneys; this elevation of HCO3- is not metabolic alkalosis since it is not a primary process.Primary EventCompensatory Event HCO3- ↑ HCO3- ↓ pH ~ --------- ↓ pH ~ ---------↑PaCO2 ↑ PaCO2

Primary Acid-base Disorders: Metabolic Acidosis

Metabolic acidosis - A primary acid-base disorder where the first change is a lowering of HCO3-, resulting in decreased pH. Compensation (bringing pH back up toward normal) is a secondary hyperventilation; this lowering of PaCO2 is not respiratory alkalosis since it is not a primary process.Primary EventCompensatory Event ↓ HCO3- ↓HCO3- ↓ pH ~ ------------ ↓ pH ~ ------------ PaCO2 ↓ PaCO2

Primary Acid-base Disorders: Metabolic Alkalosis

Metabolic alkalosis - A primary acid-base disorder where the first change is an elevation of HCO3-, resulting in increased pH. Compensation is a secondary hypoventilation (increased PaCO2), which is not respiratory acidosis since it is not a primary process. Compensation for metabolic alkalosis (attempting to bring pH back down toward normal) is less predictable than for the other three acid-base disorders.Primary Event Compensatory Event ↑ HCO3- ↑HCO3- ↑ pH ~------------ ↑ pH ~ --------- PaCO2 ↑PaCO2

Metabolic Acid-base Disorders: Some Clinical Causes

METABOLIC ACIDOSIS ↓HCO3- & ↓ pH -Increased anion gaplactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethylene glycol, methanol)-Normal anion gapdiarrhea; some kidney problems (e.g., renal tubular acidosis, interstitial nephritis) METABOLIC ALKALOSIS ↑ HCO3- & ↑ pH Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis, diuretics, corticosteroids, gastric suctioning, vomiting Chloride resistant: any hyperaldosterone state (e.g., Cushing’s syndrome, Bartter’s syndrome, severe K+ depletion)

RESPIRATORY ACIDOSIS ↑PaCO2 & ↓ pH Central nervous system depression (e.g., drug overdose)Chest bellows dysfunction (e.g., Guillain-Barrй syndrome, myasthenia gravis) Disease of lungs and/or upper airway (e.g., chronic obstructive lung disease, severe asthma attack, severe pulmonary edema)RESPIRATORY ALKALOSIS ↓PaCO2 & ↑ pH Hypoxemia (includes altitude)AnxietySepsisAny acute pulmonary insult (e.g., pneumonia, mild asthma attack, early pulmonary edema, pulmonary embolism) Respiratory Acid-base Disorders:Some Clinical Causes

Tamaulipas 10-2007

* PEGylated Multimeres
Polyme- risation
Surface Modification
Separation
Haemoglobin Multimeres
Monomeres Oligomeres
Haemo- globin
Hyper-polymeres
Production of the hemoglobin-hyerpolymers from pig blood
One-vessel- reaction