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PowerPoint Presentation:

Air is everywhere but you need a fan to feel it , similarly Oxygen is in the atmosphere but you need devices to deliver it in purest form during necessity

Topics :

Topics Introduction Historical aspects Tissue oxygenation Recognition of hypoxia Indications STOT LTOT Oxygen delivering devices Techniques of administration monitoring Oxygen toxicity prevention management


INTRODUCTION Oxygen is widely available and commonly prescribed by medical and paramedical staff. Administered correctly it may be life saving Often given without careful evaluation of its potential benefits and side effects.

Introduction :

Introduction Like any drug there are clear indications for treatment with oxygen and appropriate methods of delivery. Inappropriate dose and failure to monitor treatment can have serious consequences Vigilant monitoring to detect and correct adverse effects swiftly is essential.


INTRODUCTION In a recent hospital survey 21% of oxygen prescriptions were inappropriate 85% of patients were inadequately supervised Similar studies report that oxygen is prescribed inappropriately in general practice. To ensure safe and effective treatment prescriptions should cover the flow rate, delivery system, duration, and monitoring of treatment. SOURCE:BMJ

History :

History Joseph priestly discovered oxygen in eighteenth century Lavoisier demonstrated respiratory gas exchange In 1899 Lorrain- smith confirmed the potential toxicity of inhaled oxygen.

Tissue oxygenation:

Tissue oxygenation Average adult – O2 consumption 225-250 ml/min Increase in 10 fold during exercise Oxygen reserve is very small in the body Can stand for only 4-6 min after cessation of spontaneous ventilation

O2 delivery and utilization :

O2 delivery and utilization Transport of O2 from atmosphere to mitochondria involve integration of * pulmonary * cardiovascular and * hematological system Under normal condition pronounced drop in Po2 b/n atmosphere & tissue is seen.

Oxygen delivery :

Oxygen delivery Oxygen delivery to the periphery determined by * oxygen content of the arterial blood(CaO2) * cardiac output( CO) D o2 = (CO )x ( CaO2 )x 10 Do2 is O2 delivery /min

Oxygen delivery:

Oxygen delivery Oxygen content of arterial blood(Ca O2) is determined by * hemoglobin concentration( Hb ) * saturation of hemoglobin( Sa O2) * oxygen tension in the arterial blood(pa O2) Ca O2 = {( Hb )x 1.34x SaO2)+Pa O2 x 0.0031)

Hypoxia - mechanisms:

Hypoxia - mechanisms Aerobic metabolism – balance between DO2 (delivery of oxygen) & vO2 (oxygen utilization) should exist. O2 delivery to tissue exceeds O 2 utilization under normal conditions O2 delivered to the tissue per unit time defines upper limit of O2 available. When Do2 falls below critical levels or when O2 consumption increases -anaerobic metabolism ensues.

Mechanisms of hypoxia :

Mechanisms of hypoxia

Causes of tissue hypoxia :

Causes of tissue hypoxia Three broad categories Arterial hypoxemia Reduced tissue delivery Excessive or dysfunctional tissue utilization

Causes of Arterial Hypoxemia:

Causes of Arterial Hypoxemia Cause Clinical examples Effect of O2 therapy Decreased oxygen intake Altitude Rapid increase in Pao2 Ventilation-perfusion imbalance Chronic obstructive pulmonary disease Moderately rapid increase in Pao2 Shunt Atrial septal defect Pulmonary arteriovenous fistula Rapid but variable increase in Pao2 depending on size of shunt Diffusion defect Interstitial pneumonitis Moderately rapid increase in Pao2 Alveolar hypoventilation Chronic obstructive pulmonary disease Initial response: Increase in Pao2 Late response: Variable depending upon whether supplemental O2 depresses minute ventilation

Causes of tissue hypoxia:

Causes of tissue hypoxia category Clinical examples IMPAIRED DELIVERY Circulatory (forward flow) Hypovolemia ; heart failure Distributive Sepsis; arterial insufficiency Defective Blood-O2Transport Inherited abnormal hemoglobins Acquired abnormal hemoglobin (Carbon monoxide poisoning) Anemia


Hypoxia-Clinical. Correct use of O2 therapy requires clinical recognition of tissue hypoxia. Evaluation of patho physiological basis of hypoxia. Understanding of factors that predict those hypoxic patients likely to receive benefit. Continued assessment of the optimal dosage.

Clinical manifestations:

Clinical manifestations Highly variable and nonspecific Depends on the duration of hypoxia( acute /chronic) The individual’s fitness Cyanosis the hallmark of hypoxia occurs only when conc. of reduced Hb is 1.5 g/dl or more. Cyanosis is not a reliable sign as it is absent in anemia and during periods of poor peripheral circulation.

Signs and symptoms of acute hypoxia:

Signs and symptoms of acute hypoxia System Signs and symptoms Respiratory Tachypnea , breathlessness, dyspnea cyanosis Cardiovascular Increased cardiac output palpitations Tachycardia arrhythmias Hypotension angina vasodilatation, Diaphoresis shock

PowerPoint Presentation:

system Signs and symptoms Central nervous Headache, confusion impaired judgment, inappropriate behavior, euphoria, delierium , restlessness, seizures, obtundation , Coma papilledema , Neuromuscular Weakness tremor, asterixis , hyper- reflexia , incoordination Metabolic Sodium and water retention, lactic acidosis

Laboratory &other assessments:

Laboratory &other assessments Lab assessment is desirable because of variability of presentation and nonspecificity of signs & symptoms Quantification of degree of oxygenation of individual tissue is difficult. SpO2 is mandatory in all the cases

Lab :

Lab VO2 –mean pulmonary artery pressure -requires pulmonary artery catheterization -represents mean tissue PO2 -levels of less than 30mm hg indicate tissue hypoxia SpO2 ,Pa O2 & serum lactate levels are surrogate markers for tissue hypoxia.

Lab :

Lab SpO2 is measured by infrared pulse oximetry . PaO2 is determined by ABG analysis via arterial puncture/ indwelling arterial catheter. Both useful in excluding arterial hypoxemia, neither directly measures tissue Po2 Inadequate tissue O2 delivery-inferred by moderate decrease in PaO2 Inference warranted-acute ill patient + PaO2 < 50 mm hg + high blood lactate levels

Treatment I:

Treatment I Empiric oxygen treatment Cardiac/ respiratory arrest Hypotension Respiratory Distress Trauma GCS decrease from any cause Postoperative

Treatment II:

Treatment II Verify hypoxemia Pulse oximetry ABG’s Start Oxygen treatment. Treatment goal ( set level) Administration mode, flow, when to stop

Indications of O2 therapy:

Indications of O2 therapy There are two types of oxygen administration techniques Hyperbaric oxygen therapy Normobaric oxygen therapy * STOT short-term oxygen therapy *LTOT long- term oxygen therapy

Indications of STOT:

Indications of STOT Accepted Indications Acute hypoxemia (Pao2 < 60 mmHg; Sao2 < 90%) Cardiac and respiratory arrest Hypotension (systolic blood pressure < 100 mmHg) Low cardiac output and metabolic acidosis (bicarbonate < 18 mmol /L) Respiratory distress (respiratory rate > 24/min) the ACCP,the national heart lung and blood institute& other organisations

Indications of STOT:

Indications of STOT Questionable Indications Uncomplicated myocardial infarction Dyspnea without hypoxemia Sickle cell crisis Angina the ACCP,the national heart, lung& blood institute

Indications of STOT:

Indications of STOT Others Carbon monoxide poisoning- if hyperbaric oxygen not available t1/2-circulating CO 80 min v/s 320 min Dyspnea without hypoxemia Accelerating resorption of pneumothorax

Guidelines for initial oxygen dose :

Guidelines for initial oxygen dose Clinical setting Fraction of oxygen in inspired air (%) Cardiac or respiratory arrest 100 Hypoxaemia with Paco2 < 5.3 kPa 40­60 Hypoxaemia with Paco2 > 5.3 kPa 24 initially


LTOT Two trials NOTT and BMRCD study support LTOT Studies reported a decreased mortality in patients receiving LTOT Study showed nocturnal oxygen 15h/day ,better than no oxygen therapy Continuous oxygen therapy imparts most benefit

LTOT -indications:

LTOT -indications Continuous Oxygen Resting Pao2 < 55 mmHg or oxygen saturation < 88% Resting Pao2 of 56–59 mmHg or oxygen saturation of 89% in the presence of any of the following indicative of cor pulmonale: a. Dependent edema suggesting congestive heart failure b. P pulmonale on the electrocardiogram (P wave > 3 mm in standard leads II, III, or aVF)

LTOT -indications:

LTOT -indications Continuous Oxygen Polycythemia (hematocrit > 56%) Resting Pao2 > 59 mmHg or oxygen saturation > 89% reimbursable only with additional documentation justifying the oxygen prescription and a summary of more conservative therapy that has failed

LTOT -indications:

LTOT -indications Noncontinuous Oxygen During exercise: Pao2 < 55 mmHg or oxygen saturation < 88% with a low level of exertion During sleep Pao2 < 55 mmHg or oxygen saturation 88% with associated complications *pulmonary hypertension, daytime somnolence, and *cardiac arrhythmias

Techniques/devices :

Techniques/devices To delivery O2 to the patient –requirements Oxygen supply sources system compressed gas cylinders liquid oxygen oxygen concentrators Oxygen delivery equipment devices high flow devices low flow devices

oxygen supply sources-system compressed cylinders:

oxygen supply sources-system compressed cylinders Advantages disadvantages Provides highest flow Heavy weight Moderate cost Refilling difficult& required frequently Wide availability Must be secured to prevent injury Small cylinders available for travel Low maintenence

Liquid oxygen:

Liquid oxygen Advantage Disadvantage Provides moderate flow High cost Light weight Incompatibility of parts among vendors Excellent portability Waste of unused O2 coz of pressure venting Ease of filling Risk of thermal burns Limited availability+ maintanence available

Oxygen concentrators:

Oxygen concentrators Advantages Disadvantages Unlimited gas volume Limited flow rates available Low cost Heavy weight Good availability Poor portability Ease of use Regular maintenance needed

Oxygen delivery systems:

Oxygen delivery systems Two types High flow system- * venturi & reservoir *nebulizer blender Low flow system- *Nasal cannula *oxygen masks *oxygen tents *mask with reservoir bags

Low flow devices:

Low flow devices Provide fraction of minute voluntary ventilation as pure O2 Remainder of ventilatory requirement is fulfilled by entrained room air Flow supplied through these devices are low Cannot deliver constant inspired O2 conc.- small fluctuations in tidal volume alters amount of entrained room air

Low flow devices:

Low flow devices Shallow breathing-entrains less air into mask - high conc of inspired O2 Deep hyrepneic breathing -entrains more room air Changes in respiratory frequency-affects exhalation time-variable filling of device’s inspiratory reservoir.

Nasal cannulae:

Nasal cannulae

Nasal cannulae:

Nasal cannulae Most widely used for delivering low flow O2 Advantages Simple , inexpensive Easy to use Disadvantages Variable fio2 High flows may cause drying of mucus membranes

Nasal cannulae:

Nasal cannulae Delivers O2 at flows 1 – 6 l/min Fio2 ranges from 0.24-0.44 Above 6 l/min ,Fio2 is not significantly increased above 0.44

Nasal cannulae:

Nasal cannulae 100 % O2 flow/min Fio2 (%) 1 24 2 28 3 32 4 36 5 40 6 44

Oxygen masks:

Oxygen masks

simple Oxygen masks:

simple Oxygen masks Can deliver fio2 of 50-60% requires a flow of 5 to 6 l/min to avoid accumulation of CO2 within the mask Disadvantages Impair with eating,drinking &expectorating Can get displaced Increased risk of aspiration by concealment of vomitus

Simple oxygen masks:

Simple oxygen masks 100 % O2 flow/min Fio2 (%) 5-6 40 6-7 50 7-8 60

Masks with reservoir bags:

Masks with reservoir bags To deliver an Fio2 >60% to patients who do not have artificial airways. A reservoir bag 600-1000ml can be attached to the simple face mask Source of O2 at 5-8 L/min ,continuous-for adequate distension of the bag & to flush CO2 out. Partial non rebreathing -no one way valves The true non rebreathing mask has one way valve between mask & the reservoir

PowerPoint Presentation:

Masks with reservoir bags o2 L/min fio2 6 60 7 70 8 80 9 90 10 >99 Non rebreathing masks 4-10l/min 60-100

High flow oxygen delivery:

High flow oxygen delivery Useful In treatment of hypoxic patients who depend on their hypoxic drive to breathe but who require controlled increments in Fio2 young, vigorous patients with hypoxemia who have an abnormal ventilatory pattern and whose ventilatory requirements may exceed the delivery capabilities of low-flow system

High flow oxygen delivery:

High flow oxygen delivery Two types of devices: jet mixing venturi masks Reservoir nebulizers and humidifiers

Venturi mask:

Venturi mask

Venturi mask-priciple:

Venturi mask- priciple Works on the venturi modification of bernoulli principle A jet of 100 percent oxygen flows through a fixed constrictive orifice, past open side ports, thereby entraining room air.

Venturi principle-Oxygen mask. Venturi..flv:

Venturi principle- Oxygen mask. Venturi .. flv

Venturi v/s simple mask:

Venturi v/s simple mask

Venturi mask:

Venturi mask Flow of O2 100% FiO2 3(80) 0.24 6(68) 0.28 9 (50) 0.35 12(50) 0.40 15(41) 0.50

Venturi mask -advantages:

Venturi mask -advantages Reliably provides an Fio2 up to 0.50 It is an ideal device for Rx of hypoxemia in patients with COPD & chronic respiratory failure with blunted hypercarbic respiratory drive

Other high flow systems:

Other high flow systems Reservoir nebulizers & Humidifiers used to provide supplemental oxygen or highly humidified gas high humidification-adjuvant in decreasing secretions Air –oxygen blenders converts high pressure wall sources of compressed air & oxygen( 50-70 psi) to usable ,predictable flows upto 100 L/min

Devices for LTOT:

Devices for LTOT Oxygen supply sources for LTOT O2 concentrators. Compressed gas source. Liquid oxygen source.


LTOT Delivery devices includes the one similar to STOT Most patients use nasal cannulae @ O2 rate of 2-4 L/min

O2 is costly-save it!:

O2 is costly-save it! There are devices to conserve o2 Reservoir Nasal cannulae Electronic conserver devices 1.Pulse devices 2.Demand devices Transtracheal catheters.

PowerPoint Presentation:

Reservoir nasal cannula -stores 20 ml extra O2 during expiration and delivers it as bolus in next inspiration Pulse devices –deliver a fixed volume during each inspiration. Demand devices-deliver a fixed bolus at beginning and extra O2 depending upon inspiration time.

Transtracheal catheter:

Transtracheal catheter Newer modality Bypasses anatomical dead space Delivers O2 directly into trachea Decrease o2 consumption by 50-70% Techniques-Delivered directly through hollow catheter inserted surgically under LA or - percutaneously through seldingers technique

Transtracheal catheter:

Transtracheal catheter Advantages lack of nasal/facial irritation infrequent catheter displacement during sleep Disadvantages infection development of potentially fatal mucus balls catheter breakages high cost

Humidification of oxygen:

Humidification of oxygen When oxygen is delivered at a flow rate of 1­4 l/min by mask or nasal prongs the oropharynx or nasopharynx provides adequate humidification. At higher flow rates or when oxygen is delivered directly to the trachea humidification is necessary.

Recommendation for monitoring:

Recommendation for monitoring Arterial blood gas analysis should be performed before oxygen therapy if possible Arterial blood gases should be measured or oximetry done within 2 hours of starting oxygen therapy and Fio2 adjusted accordingly. (An adequate response is defined as Pao2 > 7.8 kPa or Sao2 > 90%) Hypoxaemic patients at risk of arrhythmias or respiratory failure should be monitored continuously by oximetry

PowerPoint Presentation:

In patients at risk of type II respiratory failure, arterial blood gases should be measured more frequently to assess Pao2 and Sao2 should be monitored continuously by oximetry In the acute stage response should be assessed daily by arterial blood gas analysis or oximetry and Fio2 adjusted accordingly

Stopping oxygen treatment:

Stopping oxygen treatment arterial oxygenation is adequate with the patient breathing room air (Pao2 >8 kPa,Sao2 > 90%). In patients without arterial hypoxaemia but at risk of tissue hypoxia, oxygen should be stopped when the acid­base state and clinical assessment of vital organ function are consistent with resolution of tissue hypoxia.

Oxygen adverse effects:

Oxygen adverse effects Pulmonary Depression of hypoxic ventilatory drive Pulmonary vasodilation Absorption atelectasis Cytoxic damage .


AE-oxygen Extrapulmonary Depression of erythropoiesis Systemic vasoconstriction Depression of CO

Oxygen toxicity:

Oxygen toxicity Breathing O2 at Sea level(1 atm ) -80% O2 5000 ft(0.8 atm ) -100% O2 Hyperbaric chambers(2 atm )-40% O2 produces same toxic profile for same duration of O2 consumption

Mechanism :

Mechanism Due to excess O2 supply-free radicals are generated by various metabolic pathways The free radicals generated are superoxide anion(O2-), H2O2, hydroxyl radical (OH-), peroxy nitrites(ONOO-)

PowerPoint Presentation:

Free radicals cross react with the lipids , proteins & nucleic acids to produce cellular damage. Cellular defense – against free radicals * enzymatic system-SOD *enzyme cofactor system-GSH Peroxidase *Non enzymatic- vit A, vita E, vita C

Pathology of O2 toxicity on lungs:

Pathology of O2 toxicity on lungs Four phases Initiation phase Inflammatory phase-ARDS Destructive phase-apoptosis + necrosis Proliferation & fibrosis phase Secondary changes decreased lung compliance Dlco decreased increased alv -art O2 gradient

Pulmonary changes:

Pulmonary changes O2 @ 1 atm Exposure duration manifestations 100% >12h Decreased tracheobronchial clearance; decreased forced vital capacity; cough; chest pain >24h Altered endothelial function >36h Increased alveolar-arterial oxygen gradient; decreased carbon monoxide diffusing capacity >48h Increasing alveolar permeability; Pulmonary edema; surfactantinactivation >60 h Acute respiratory distress syndrome

PowerPoint Presentation:

60% oxygen 7 days Mild chest discomfort without changes in lung mechanics; possible changes in morphometry 24-28% oxygen months Subclinical pathological changes; no clinical toxicity documented

O2 toxicity-clinical syndromes:

O2 toxicity-clinical syndromes ACUTE –TRACHEOBRONCHITIS & ARDS after exposure of 12 hours c/o substernal chest pain+ non productive cough tracheobronchial function –decreased mucus clearance systemic symptoms-malaise ,nausea ,anorexia & headache may be seen

O2 toxicity:

O2 toxicity CHRONIC PULMONARY SYNDROMES Neonatal respiratory distress syndrome Persistent morphologic change- bronchopulmonary dysplasia data in adults not available

Diagnosis of oxygen toxicity:

Diagnosis of oxygen toxicity Depends on nonspecific symptoms and PFT Symptoms & signs chest pain , tachypnea , cough Presence of cracles -interstitial/alveolar edema PFT- decreased VC , pulmonary compliance& decreased Dlco widening of alveolar arterial O2 gradient

PowerPoint Presentation:

CXR changes increased interstitial markings alveolar filling

O2toxicity potentiation:

O2toxicity potentiation Bleomycin Disulfiram Nitrofurantoin Paraquet Protein malnutrition Vitamin A,C &E deficiency

O2 toxicity-prevention and Mx:

O2 toxicity-prevention and Mx Administer O2 judiciously- achievehigh effect less toxicity Early detection very difficult and no specific therapy Measure response to O2 with SpO2,pO2,VO2

PowerPoint Presentation:

Follow the guideline 100% O2 –transport & early mx of critically ill pt monitor evidence of respiratory depression-if not on mechanical ventilation if needed Fio2 1.0 –given for 24 hours , improve pulmonary exchange , optimize O2 delivery and limit tissue metabolic demands

Dangers of oxygen treatment:

Dangers of oxygen treatment Fire: Oxygen promotes combustion. Facial burns and deaths of patients who smoke when using oxygen are well documented Pulmonary oxygen toxicity: Paul­Bert effect: Breathing hyperbaric oxygen (for example, when diving) can cause severe cerebral vasoconstriction and epileptic fits


summary Oxygen is a life saving treatment. It should be treated like any other drug; It should be prescribed in writing, with the required flow rate and the method of delivery clearly specified.

PowerPoint Presentation:

Failure to correct hypoxaemia (Pao2 > 8 kPa ) for fear of causing hypoventilation and carbon dioxide retention is unacceptable clinical practice. Careful monitoring of treatment is essential and will detect those patients at risk of carbon dioxideretention

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