Oxygen Therapy 2024 (PDF)

Oxygen Therapy Foundations of Critical Care 2024 D.Freer Learning Objectives Understand the properties of oxygen Safety aspects related to oxygen Physiological effects of high oxygen administration CO2 retainers Oxygen delivery equipment available and how to de...

Oxygen Therapy Foundations of Critical Care 2024 D.Freer Learning Objectives Understand the properties of oxygen Safety aspects related to oxygen Physiological effects of high oxygen administration CO2 retainers Oxygen delivery equipment available and how to determine delivery method When would you administer oxygen and when wouldn’t you?  CHECK IT! At the beginning of every shift! And after a critical transport  What is all the fuss about Oxygen? Delivery of oxygen is dependent on 4 variables: CO, Hb, SaO2, and PaO2 1. What changes Cardiac Output? HR SV Preload Contractility Afterload 2. What changes functional Hb – oxygen carrying capacity? Blood loss – acute / chronic Haematological conditions, e.g. sickle cell anaemia Iron levels 3. What changes SaO2 – our functional oxygen? Shifting of the oxy-haemaglobin dissociation curve – pH, CO2, Temperature, 2-3 DPG Diffusion across alveolar-capillary membrane FiO2 3. What Changes PaO2 – our oxygen reserve? Diffusion across alveolar-capillary membrane FiO2 Oxygen administration changes FiO2 and only affects two of oxygen delivery variables: SaO2 & PaO2 The Oxygen Cascade from Atmosphere to Mitochondria Atmosphere to Alveoli Atmospheric air: 21% oxygen = PaO2 of 159 mmHg Airway gas mixture: Diluted by water vapour = PaO2 of 149 mmHg Alveolar gas mixture: Diluted by CO2 = PaO2 of 99 mmHg Also, some oxygen is taken up by the capillaries, which decreases the alveolar PaO2 Capillary to Mitochondria Pulmonary endcapillary blood Essentially the same as alveolar gas, in health PaO2 approx. 99mmHg Arterial blood Diluted by venous admixture= PaO2 of 92 mmHg The difference between alveolar and arterial gas is the A-a gradient Normal A-a gradient is 7mmHg in the young, and 14mmHg in the old Tissue oxygen tension Drops due to diffusion distance Varies from tissue to tissue, but is usually around 10-30 mmHg Mitochondrial oxygen tension Drops due to diffusion distance Usually between 1-10 mmHg At sea level Atmospheric pressure = 760mmHg Oxygen makes up 21% of this Therefore, the partial pressure of oxygen at sea level is 760 x 0.21 = 159mmHg That’s why the oxygen cascade start with a PaO2 of 159mmHg (often rounded to 160mmHg) Change in Altitude Higher altitude Decrease in atmospheric PaO2 Affects the whole oxygen cascade Decrease in oxygen dissolved in blood (PaO2) Lower altitude (below sea level & hyperbaric) Increase in atmospheric PaO2 and oxygen dissolved in blood. Does the FiO2 change? No, the molecules are just further apart… Effect of atmospheric pressure Atmospheric pressure ATA (mmHg) FiO2 PatmO2 PAlvO2 0.5atm 18000 ft 380mmHg 0.21 80mmHg ~50mmHg 1 atm Sea Level 760mmHg 0.21 160mmHg ~100mmHg 2 atm 10mbsw 1520mmHg 0.21 320mmHg ~200mmHg Change in Altitude The higher up a mountain we go, the further apart the oxygen molecules are. High altitude places stress on people with underlying cardio / respiratory conditions. If we live in higher areas for long times, develop compensatory mechanisms Increased RBC Increased lung capacity Reason for high altitude training What about in an aeroplane? Oxygen Discovered in 18th Century (1772-1780) Named from the Greek (oxy gene – “acid former”) Oxygen reacts to produce oxides (e.g. sulphur, carbon, aluminium, and phosphorous) Earth’s most plentiful element by weight (46%) Properties of Oxygen Colourless, odourless, tasteless Soluble in solution Essential for life – aerobic metabolism Liquefies at -183 degrees Celsius Vigorously supports combusion Oxygen Cylinders Manufactured in accordance with Australian Standards Colour coded White Body / white shoulder Labelled “Oxygen” No agreed international standard for O2 cylinders Filled to 16,300kPa at 15o Celcius In most critical care areas have plumbed oxygen Care of oxygen cylinders Store in a cool well ventilated area Keep away from ignition sources Heat, flammable liquids & gases Patient’s going for a ciggie Keep free from oil or grease Secure upright with restraints Should be refilled if below 5,000 kPa Know how to replace cylinder Open the valve slowly Indications for Oxygen Administration Correction or prevention of hypoxemia SaO2< 90% & PaO2 < 60mmHg Respiratory Failure Cardio-respiratory arrest Shock Severe Trauma Acute myocardial infarction with low SpO2 Anaesthesia / procedural sedation Indications in the absence of hypoxemia Decreased oxygen carrying capacity Carbon monoxide poisoning Severe anaemia / sickle cell disease Debatable – Promote reabsorption of air in body cavities Air embolism, pneumothorax Decompression sickness Explanation is decrease the partial pressure of nitrogen in the lungs and create a diffusion gradient for nitrogen to be exhaled. Goals of oxygen therapy Reduce or correct hypoxemia Reduce the bodies compensatory mechanisms Patient will be less SOB, reduce the work of breathing Increased WOB can account for up to 40% of total oxygen consumption Reduce tachycardia Reducing myocardial oxygen demand Effectiveness of Oxygen Therapy Depends on the cause of hypoxemia and hypoxia Shunt (VQ) Ventilation is ok Issue with perfusion Physiological in the trachea Pathological – PE Oxygen administration generally more effective as ventilation is ok Oxygen Delivery Systems Low flow / Variable performance systems Oxygen flow rate is less than the patient’s inspiratory flow Do not provide all the gas necessary to meet inspiratory demand Room air entrained to make up the difference Oxygen diluted with room air resulting in variable FiO2 Higher minute ventilation = more entrained room air = lower FiO2 with same O2 flow rate Peak inspiratory Oxygen Entrained air flow flow rate 30 L/min 10 L/min 20 L/min 60 L/min 10 L/min 50 L/min Oxygen Delivery Systems High flow / Fixed performance systems Gas flow rate > patient’s inspiratory flow rate Gas flow sufficient to meet patient’s demand Delivers a fixed FiO2 not affected by the patients ventilatory pattern Low-flow / variable performance systems Nasal specs Hudson mask Tracheostomy mask Reservoir bag masks Manual resuscitators Nasal Cannula Inexpensive, comfortable FiO2 will be less in patients who Oxygen flow rate FiO2 1 L/min 0.24 are SOB 2 L/min 0.28 FiO2 may be reduced in mouth 3 L/min 0.32 breathers 4 L/min 0.36 Simple face mask (Hudson mask) Provides 100-200ml reservoir Higher concentration of oxygen Some rebreathing of CO2 A minimum of 6LPM is required for all face masks to flush expired Oxygen flow rate FiO2 CO2 6 L/min 0.50 FiO2 reduced with increased 8 L/min 0.55 WOB, poor seal, tolerance 10 L/min 0.60 12 L/min 0.65 Unable to eat, dries mucosa 15 L/min 0.70 Tracheostomy mask Similar to a simple face mask Delivery is dependent on the status of the cuff Why? Requires humidification Why? Non-rebreather face mask Contain a 750 ml reservoir bag that stores O2 during expiration On inspiration Valves on the exhalation port seal against the mask The patient draws pure O2 from the reservoir bag Increases O2 concentration On exhalation Valve between mask & reservoir bag prevents expired gases entering the reservoir bag Expired gas exits through exhalation ports One or two valves on exhalation ports of the face mask Non-rebreather masks Theoretically can deliver up to FiO2 1.0 In reality, the FiO2 is nearer 0.6-0.8 Room air entrained as no tight seal Adjust flow rate so reservoir bag does not collapse Temporising measure – reserved for critical care areas / pre-hospital / procedural sedation / anaesthesia Manual resuscitation bag Self-refilling, non-rebreathing resuscitators Normally disposable Can deliver very close to FiO2 of 1.0 Different sizes for adults and children Only inflate approx. 1/3 volume of the ventilation bag If cannot intubate, try at least to ventilate What do you do if you cannot intubate & cannot ventilate? Pocket Mask Expired air – FiO2 16% O2 @ 10l/min – FiO2 0.5 High flow / fixed performance systems Venturi mask Nasal high-flow NIV IPPV These will be discussed more in subsequent presentations Venturi Mask Uses the venturi principle O2 flow rate is supplemented by entraining room air O2 flow rate @ 6-8 l/min  total flow 40-60 l/min Delivers a fixed FiO2 How a venturi mask works O2 is forced through a constriction The velocity of gas flow increases This creates a sudden drop in pressure beyond the constriction Air is entrained via holes in the bottom of the mask The size of the orifice & flow rate determine the concentration O2 FiO2 O2 flow Total gas flow 0.24 4 L/min 104 L/min 0.28 6 L/min 66 L/min 0.35 8 L/min 48 L/min 0.40 8 L/min 32 L/min 0.60 12 L/min 24 L/min Benefits of Venturi Mask Accurately delivers a prescribed FiO2 Gas flow is high enough to meet peak inspiratory demands High flow rates eliminate rebreathing of CO2 Since room air is entrained humidification is not essential Best means of managing patients with chronic COPD Delivers predictable FiO2 Minimises rebreathing CO2 Flow & Concentration Flow is not the same as concentration Low-flow masks can deliver high FiO2 (e.g. resuscitation bag) High-flow masks can deliver low FiO2 (e.g. venturi mask) Which Device? Nasal cannula Normal vital signs, slightly low SpO2, long-term O2 therapy Face masks & non-rebreather masks Higher concentration required / acutely ill patients Delivering an accurate FiO2 not necessary High flow devices Controlled O2 therapy required Exacerbation of COPD (Venturi) Humidification o Room air is 20 C with a relative humidity of 50% Medical oxygen is both cold & dry 10-15 º Celsius Relative humidity is zero Potential for? Under humidification Mucus thickens Reduction in Cilia movement Leads to bacterial colonisation / increased risk of infection Atelectasis from mucus plugging small airways Reduced lung compliance and increased work of breathing Respiratory failure Patients at risk Thick tenacious sputum – bronchitis Difficulty expectorating Neuromuscular dysfunction Chest wall abnormalities Smokers Chronic lung disease Dehydration Elderly High FiO2 Humidification & risk infection  Humidification Hot water humidifiers – e.g Fisher & Paykel “gold standard” Humidifies air with water vapour The airway naturally uses water vapour Water vapour does not transport bacteria or viruses into the lungs Reduces the likelihood of pathogens entering the lungs More efficient Inspired relative humidity of 100% at 37oC (bypassed airway) Inspired relative humidity of 85% at 34oC (mask) Heat & Moisture Exchangers Exhaled gases pass through HME Nursing Care of HME Change every 24 hrs Heat & moisture retained Care with nebulised Heat & moisture added with next inspired breath medications Less efficient than hot water humidifiers Can saturate with nebulised medication No risk of thermal injury or overhydration Reduction in Small increase in airway resistance & dead space effectiveness Becomes a barrier to Contra-indications gas exchange Copious secretions Small tidal volumes Dead space may compromise ventilation  CO2 Large tidal volumes Ability to humidify gases may be compromised Unwelcome effects of oxygen Arterial spasm Oxygen toxicity Pulmonary oxygen toxicity CNS oxygen toxicity Retrolental fibroplasia (blind) Absorption atelectasis Worsening CO2 retention Under humidification Fire hazard… Pulmonary oxygen toxicity Low dose prolonged administration of O2 FiO2 >0.6 for > 24 hours Believed to be due to toxic O2 free radicals Causes Mucociliary function depressed Endothelial cell damage causes interstitial oedema Decreased macrophage activity Reduced surfactant – reduced surface tension & collapse Decreased compliance Decreased diffusion capacity Pulmonary Oxygen toxicity Signs & Symptoms Shortness of breath Substernal pain Deteriorating gas eschange Poor lung compliance Chest x-ray changes Sound familiar? Difficult to differentiate between pulmonary oxygen toxicity and a deterioration in a pre- existing lung condition Absorption Atelectasis Develops in patients with high FiO2 N2 is the most abundant gas in the alveoli The pressure exerted by N2 splints the alveoli open FiO2 1.0 “washes out” all the N2 Leaves only O2 which is rapidly absorbed  alveolar collapse Develops in < 1 hr  worsening hypoxemia THINK ABOUT THIS IN THE ED!!! Oxygen and CO2 retention The traditional theory is that oxygen administration to CO2 retainers causes loss of hypoxic drive, resulting in hypoventilation and type 2 respiratory failure. This is a myth. Patients suffering from COPD exacerbations, regardless of whether they have CO2 retention, generally have HIGH respiratory drive (unless there is impending hypercapnic coma) The real explanation involves: Increased V/Q mismatch (most important) The Haldane effect How oxygen causes CO2 retention V/Q mismatch In COPD, over time patients optimise their gas exchange by hypoxic vasoconstriction (i.e. they reduce blood supply to areas where gas exchange does not occur well). Administering a high level of oxygen will increase oxygen tension, reducing hypoxic pulmonary vasoconstriction. Results in increased perfusion to areas where ventilation is poor Increased dead space ventilation (V>Q) and higher PaCO2 due to overall lack of gas exchange at the alveolar level How oxygen causes CO2 retention The Haldane effect: Describes the difference in the quantity of carbon dioxide carried in oxygenated and deoxygenated blood. CO2 has a higher affinity for deoxygenated Hb than oxygenated Hb Giving a patient high levels of oxygen will decrease the affinity of CO2 for Hb. Carbon dioxide will be displaced by oxygen, resulting in a higher PaCO2. For patients who cannot increase their minute ventilation and blow off this CO2 (i.e. those with COPD), the Haldane effect accounts for about 25% of their total PaCO2 increase. What do we do? In patients with COPD, hypoxic pulmonary vasoconstriction is the most efficient way to optimise the V/Q ratio to improve gas exchange. This physiological mechanism is counteracted by oxygen therapy and accounts for the largest increase of oxygen-induced hypercapnia. A titrated oxygen therapy to achieve saturations of 88%-92% is recommended in patients with an acute exacerbation of COPD. “permissive hypoxemia” to avoid hypercarbia In extremist, always give oxygen Hypoxia kills faster than hypercarbia Oxygen delivery O2 delivery depends on more than just O2 therapy Ventilation Diffusion of O2 into the blood Binding with haemoglobin (Enough carriers, ability to bind) Adequate cardiac output (HR, preload, contractility, & afterload) Diffusion into the cell Nursing Care Mouth care/ nasal care Pressure area care – observe ears and nares Ensure treatment/ medication order unless it is an emergency Oxygen after all is a medication….. And just like other medications has positive and negative effects. Take home messages Overall goal of oxygen therapy is to avoid tissue hypoxia The devices are different and terms are used interchangeably Faced with a hypoxic patient ALWAYS think Oxygen first Long term oxygen therapy is not without side effects Consider different approaches for the chronic CO2 retainer when planning oxygen therapy Questions?