Oxygen therapy and toxicity

16,807 views 63 slides Jun 18, 2019
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About This Presentation

Oxygen therapy


Slide Content

Oxygen Therapy and Toxicity PRESENTER Dr Krishna Dhakal Second year Resident Department of Anesthesiology and Intensive Care NAMS MODERATOR Dr. Santosh Parajuli Department of Anesthesiology Shahid Gangalal National H eart Centre

Learning Objectives To Define oxygen therapy To Explain the indication of oxygen therapy To know briefly about oxygen cascade To List the sources of oxygen To Classify and explain the sources of oxygen delivery devices To Explain the hazards of oxygen

Introduction Oxygen therapy It is the administration of oxygen at concentrations greater than that in ambient air (20.9%) with the intent of treating or preventing the symptoms and manifestations of hypoxemia or tissue hypoxia .

Goals of Oxygen Therapy Correct documented or suspected hypoxemia Decrease the symptoms associated with chronic hypoxemia Decrease the workload hypoxemia imposes on the cardiopulmonary system Removal of entrapped gas from the body cavities and vessels.

Indication Documented Hypoxemia Adults, children and infants > 1 month of age. Pao2< 60mm Hg Sao2 < or Spo2 < 92% at rest breathing room air Neonates Pao2< 50mm Hg Sao2 < or Spo2 < 88% at rest in room air COPD, Myocardial Infarction, pulmonary edema, ALI, ARDS, pulmonary fibrosis, cyanide poisoning, carbon monoxide poisoning. Perioperative and postoperative period with general anaesthesia Prior to tracheal suctioning or bronchoscopy Severe Trauma Any clinical suspicion of hypoxemia or hypoxia

Oxygen Cascade The process of declining oxygen tension from atmosphere to mitochondria Atmosphere air (dry) (159 mm Hg ) [ PIO2=PB x FIO2] ↓ humidification Lower resp tract (moist) ( 150 mm Hg ) [ PIO2=(PB-PH2O) x FIO2 ] ↓ O2 consumption and alveolar ventilation Alveoli PAO2 (104 mm Hg) [ PAO2= PIO2- PaCO2/RQ] ↓ venous admixture Arterial blood PaO2 (100 mm Hg) ↓ tissue extraction Venous blood PV O2 (40 mm Hg) ↓ Mitochondria PO2 (7 – 37 mmHg)

The Alveolar arterial gradient PAO2=104 mmHg PaO2=100mmHg Venous admixture A-a = 4 -25 mm Hg PaO 2 = 120 − Age/3 Alveolar Air Arterial Blood

The A-a Gradient The alveolar-to-arterial O2 partial pressure gradient (A–a gradient) is normally less than 15 mm Hg PaO2 = 120 − Age/3 The A–a gradient for O2 depends on the amount of right-to-left shunting, the amount of V/Q mismatch, and mixed venous O2 tension The A–a gradient for O2 is directly proportional to shunt

How Does Oxygen Therapy Work? Oxygen Transport Oxygen content Oxygen flux Oxygen uptake O2 extraction ratio

Oxygen cascade Venous Admixture ( physiological shunt) V/Q mismatch Normal True shunt Bronchial vein Thebesian vein Normal : upto 5 % of the cardiac output

Oxygen Cascade P a O 2 = 97mm Hg (Sat. > 95 %) P V O 2 = 40mm Hg Sat. 75% Arterial blood Mixed venous blood Cell mitochondria PO2= 7-37mmHg Tissue utilization

Oxygen Content (Co 2 ) Amount of O2 carried by 100 ml of blood Co2 = Dissolved O2 + O2 Bound to hemoglobin Co2 = Po2 × 0.0031 + So2 × Hb × 1.34 (Normal Cao2 = 20 ml/100ml blood Normal Cvo2 = 15 ml/100ml blood) C(a-v)o2 = 5 ml/100ml blood Co2 = arterial oxygen content ( vol %) Hb = hemoglobin (g%) 1.34 = oxygen-carrying capacity of hemoglobin Po2 = arterial partial pressure of oxygen (mmHg) 0.0031 = solubility coefficient of oxygen in plasma

O 2 Hb dissociation curve

Oxygen Flux Amount of of O2 leaving left ventricle per minute. Do2 =CO x Cao2 = CO × SaO2 x Hb conc x 1.34 = 5000 x 0.97 x 15.4 x 1.34 /100 = 1000 ml/min CO = cardiac output in ml per minute. Do2 = oxygen flux

Oxygen Uptake (VO2) When blood reaches the systemic capillaries, oxygen dissociates from hemoglobin and moves into the tissues. The rate at which this occurs is called the oxygen uptake (Vo2). VO2 = CO X ( CaO2 – CvO2 ) = CO X 1.34 X Hb X ( SaO2 – SvO2 ) Normal VO2 = 200–300 mL /min or 110–160 mL /min/m2

The fraction of the oxygen delivered to the capillaries that is taken up into the tissue . An index of the efficiency of oxygen transport. O2ER = VO2 / DO2 = CO x C(a-v)o2 CO x Cao2 = SaO2 - SvO2 / SaO2 Normal - 0.25 (range = 0.2–0.3) Oxygen-Extraction Ratio ( O 2 ER )

Oxygen Cascade

Sources of oxygen Atmosphere Compressed Oxygen cylinders : gaseous, liquid (cryogenic container) Oxygen concentrators

Oxygen cylinders Medical gas distribution systems Central supply(G and H type cylinders) Patients transport, resuscitation, anesthesia machine ( E type)

Different type of cylinders

Oxygen Source Central supply system : Located outdoors, restricted area Cylinder banks connected to a common manifold Primary and secondary supply Reserve supply away from main supply

Oxygen concentrators Based on Pressure swing adsorber technology (adsorbs nitrogen onto the molecular seive made of zeolite ) Deliver 90-96% oxygen Remote location , Domiciliary use

Advantages: Cost effective, simple to use, portable Not affected by altitude changes Compatible with anaesthesia machine, vaporisers , ventilators Disadvantages: Maintanence : regular servicing of compressor, filters Device malfuntion : excessive noise, overheating, shut down Argon accumulation

O2 Delivery System Classification DESIGNS Low- flow system Reservoir systems High flow system Enclosures PERFORMANCES (Based on predictability and consistency of FiO2 provided) Fixed Variable

Oxygen flow rate and concentration Respiratory Distress Non respiratory Distress Minute vol (RR x TV) 20 l/min (40bpm x 500ml) 5 l/min (10bpm x 500ml) O 2 flow rate 2 l/min 2 l/min Oxygen concentration 2 l/min of 100% oxygen + 18 l/min air drawn into mask (21%) = 20 l/min minute volume FiO 2 = (1.0x2) + (0.21x18) / 20 = 0.38 (38.8%) 2 l/min of 100% oxygen + 3 l/min air drawn into mask (21%) = 5 l/min FiO 2 = (1.0x2) + (0.21x3) / 5 = 0.53 (53%)

Low flow system The gas flow is insufficient to meet patient’s peak inspiratory and minute ventilatory requirement O2 provided is always diluted with air FiO2 varies with the patient’s ventilatory pattern Deliver low and variable FiO2 → Variable performance device

High flow system The gas flow is sufficient to meet patient’s peak inspiratory and minute ventilatory requirement. FiO2 is independent of the the patient’s ventilatory pattern Deliver low- moderate and fixed FiO2 → Fixed performance device

Low Flow or Variable performance equipment Nasal cannula Nasal mask Simple Oxygen mask Oxygen tent Mask with gas reserviour Partial rebreathing Non- rebreathing High flow or fixed performance equipment Anaesthesia bag (Bag mask valve system) Venturi mask (with or without nebulliser )

Nasal cannula A plastic disposable device consisting of two tips or prongs 1 cm long, connected to oxygen tubing Inserted into the vestibule of the nose FiO2 – 24-40% Flow – 1-6 L/min

Nasal Cannula Advantages Easy to use, well tolerated by most patients Patients can eat, drink and talk. May be used in patients with COPD requiring long term oxygen therapy. Disadvantages May cause pressure sores around ears and nose. May dry and irritate nasal mucosa. Not able to achieve high concentrations of inhaled O2 in patients who have a high minute ventilation. Most of the oxygen wasted. May not be good for mouth breather

Reservoir systems Reservoir system stores a reserve volume of O2, that equals or exceeds the patient’s tidal volume Delivers mod- high FiO2 Variable performance device To provide a fixed FiO2, the reservoir volume must exceed the patient’s tidal volume Examples: Reservoir cannula Simple face mask Partial rebreathing mask Non rebreathing mask Tracheostomy mask

Reservoir masks Commonly used reservoir system Three types Simple face mask Partial rebreathing masks Non rebreathing masks

Simple face masks Reservoir - 100-200 ml Variable performance device FiO2 varies with O2 input flow, mask volume, extent of air leakage patient’s breathing pattern FiO2: 40 – 60% Input flow range is 5-8 L/min Minimum flow – 5L/min to prevent CO2 rebreathing

Simple Face Mask Merits Moderate but variable FiO2. Good for patients with blocked nasal passages and mouth breathers Easy to apply Demerits Uncomfortable Interfere with further airway care Proper fitting is required Rebreathing (if input flow is less than 5 L/min ) Oxygen Flow Rate(L/Min) FiO2 5-6 0.4 6-7 0.5 7-8 0.6

Partial rebreathing face mask During inspiration : Draws air from the mask, from the bag, holes in the side of the mask. During expiration : First one third of exhaled gases (from anatomical dead space) will flow back into the reservoir bag High enough O2 flow to keep the bag from deflating more than one third its volume during inspiration, then exhaled CO2 will not accumulate in the reservoir bag. Maximum FiO2 of 0.7 to 0.8 FGF > 8L/min

Nonrebreathing Face Mask Has 2 unidirectional valves Expiratory valves prevents air entrainment Inspiratory valve prevents exhaled gas flow into reservoir bag FiO 2 : 0.80 – 0.90 FGF : 10 – 15L/min To deliver ~100% O 2 , bag should remain inflated Factors affecting FiO 2 Air leakage and Pt’s breathing pattern

Tracheostomy Collar/ Mask Inserted directed into trachea Is indicated for chronic o2 therapy O2 flow rate 8 to 10L Provides good humidity Comfortable ,more efficient Less expensive

High flow systems The gas flow is sufficient to meet patient’s peak inspiratory and minute ventilatory requirement. FiO2 is independent of the the patient’s ventilatory pattern Deliver low- moderate and fixed FiO2 → Fixed performance device Examples: Air entrainment devices

Principle : Based on Bernoulli principle – A rapid velocity of gas exiting from a restricted orifice will create subatmospheric lateral pressures, resulting in atmospheric air being entrained into the mainstream. Entrainment Ratio: Air = 100 - %O2 O2 %O2 - 21

fi02 Flow Rate (L/min) Air :02entrapment ratio Total Gas flow(L/min) 24% 4 25:1 104 28% 6 10:1 66 35% 8 5:1 48 40% 10 3:1 32 60% 15 1:1 Twice O2 flow

Complications of Oxygen therapy

Complications of Oxygen therapy 1. Oxygen toxicity 2. Depression of ventilation 3. Retinopathy of Prematurity 4. Absorption atelectasis 5. Fire hazard

Oxygen Toxicity O xygen toxicity is a condition resulting from the harmful effects of breathing molecular  oxygen  ( O 2 ) at increased  partial pressures. The metabolites of oxygen are more damaging than the parent molecule itself. These are formed in the process of conversion of O2 to water in the ETC (electron transport chain) in mitochondria. The superoxide and hydroxyl radicals are free radicals → very active chemically

Oxygen toxicity

CNS effects Also known as Paul Bert effect Central nervous system toxicity - caused by short exposure to high partial pressures of oxygen at greater than atmospheric pressure(> 1 atm pressure) Symptoms may include disorientation, brief periods of rigidity→ convulsions and unconsciousness, and seizures. Visual changes esp. tunnel vision, tinnitus, etc. are also common Oxygen toxicity,JIACM 2003; 4(3): 234

Pulmonary effects Also known as Lorraine Smith’s effect First organ to be exposed to high concentration of O2 Pulmonary toxicity occurs only with exposure to partial pressures of oxygen greater than 0.5 bar (50  kPa ) ARDS like features

Tracheobronchitis, or inflammation of the upper airways most common findings, Others: cough, substernal chest pain, ARDS like features Preterm newborns are known to be at higher risk for bronchopulmonary dysplasia with extended exposure to high concentrations

How much O2 is safe? 100% - not more than 12hrs 80% - not more than 24hrs 60% - not more than 36hrs Goal should be to use lowest possible FiO2 compatible with adequate tissue oxygenation

P. Del Portillo et al

Hypoventilation COPD patients with chronic CO2 retention. Altered respiratory drive dependent on relative hypoxemia. Correction of hypoxemia leads to loss of respiratory drive. Increase oxygen concentration by 4-7% (i.e. Fio2 0.32-0.36) with a goal of achieving Spo2 by 90-93%. Venturi mask when possible

Retinopathy of prematurity (ROP) Premature or low-birth-weight infants who receive supplemental O 2 ↑PaO 2 ↓ retinal vasoconstriction ↓ necrosis of blood vessels ↓ new vessels formation ↓ Hemorrhage → retinal detachment and blindness To minimize the risk of ROP - PaO 2 below 80 m mHg

Absorption atelectasis Large volume of nitrogen in the lungs is replaced with oxygen, Oxygen is subsequently absorbed into the blood, The effect is reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis

Risks of fire I mproper use of oxygen Incorrect design of oxygen systems Incorrect operation and maintenance of oxygen system

Summary Oxygen therapy is administration of oxygen in concentration greater than that of environment (>20.9%). Oxygen can be obtained from different sources including environment employing several industrial/non-industrial techniques. It is very important to be aware the varying FiO2 with variable performance devices and it is important to choose devices appropriate for the patient. Oxygen in concentrations higher than required to maintain normal PaO2 is associated with toxicity . The potential hazards of oxygen therapy are: absorpotion atelectasis, CNS/Respiratory problems, depression of ventilation, ROP, and fire hazards . Goal should be to use lowest possible FiO2 compatible with adequate tissue oxygenation

Bibliography Marinos , The ICU Book, 4th Edition Barash , Paul G Cullen’s Clinical Anesthesia, 7th edition Mikhail & Morgan’s Clinical Anesthesiology, 5th edition Carvalho M, Soares M, Machado HS. Paradigms of Oxygen Therapy in Critically Ill patients. J Intensive & Crit Care 2017,3:1 Internet : Wikipedia.org , Uptodate BTS Guidelines for oxygen use in adults in healthcare and emergency settings -2017
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