Thanks to Ben Taylor for his Grand Rounds talk which looks at the problems that may result from whacking on a bit of oxygen.

Transcription

1 EMERGENCY MEDICINE Liverpool Hospital The Weekly Probe 4 th July, 2012 Volume 15, Issue 20 THIS WEEK: 1. Hyperoxia and the perils of oxygen therapy 2. Next week s case 3. Joke of the Week Hyperoxia The Silent Killer of the Critically Ill? Thanks to Ben Taylor for his Grand Rounds talk which looks at the problems that may result from whacking on a bit of oxygen. A 65 year-old female presents with shortness of breath. She has a history of hypertension, IHD, CCF, morbid obesity and type 2 diabetes. She has been given high flow oxygen therapy by the paramedics en-route to the emergency department. On arrival to the ED, her pulse oximetry is 98%, RR 30, BP 110/ What do you think about her oxygen therapy? 2. What should you do? 3. What are the pros and cons of oxygen therapy? Love is like oxygen You get too much you get too high Not enough and you're gonna die Love gets you high Sweet Love is Like Oxygen 1978

2 Uses of Oxygen in the ED Supplemental Oxygen has been part of standard therapy for ACS/AMI, stroke, cardiac arrest, acute respiratory failure and resuscitation of the critically ill for many years. Dangers of hypoxia well known. 100% O2 saturation has been seen as a goal for resuscitation of patients in ED. But more is better oxygen culture may ignore the dangers of hyperoxia. The problem is, that despite oxygen therapy becoming the accepted norm, there is little evidence to support its routine use Subsequently there is a need for large well controlled trial to clarify the situation. Oxygen Transport Apologies to those who have recently completed their primary exams but just some important physiology to cover; key concepts to understand are oxygen carriage and the oxygen dissociation curve. Oxygen Carriage Dissolved Oxygen Small proportion of oxygen carriage Directly proportional to partial pressure 100 ml blood at PO 2 100mmHg carries 0.3 ml oxygen Strenuous exercise, you require 3L/min of oxygen This means you would need a cardiac output of 1000 L/ min using this mechanism alone. Haemoglobin Major mechanism for oxygen carriage. Oxygen binds to haemoglobin after dissolving in the blood. This process follows the oxygen dissociation curve. There is a rapid increase in oxygen carriage to a PO 2 of 60 mmhg, and then the curve flattens off. Oxygen capacity is the maximum amount of oxygen that can be carried by haemoglobin. One gram of haemoglobin combine with up to 1.39 ml oxygen. On the flat part of the curve, 100% saturation can equate to a PO 2 anywhere from 100 to in excess 500 mmhg depending on the situation and V/Q mismatch. (See graph below) Oxygen Saturation Amount O 2 combined with Hb/ O 2 capacity x 100 Arterial Saturation with PO mmhg is 97.5% Venous Saturation with PO 2 40 mmhg is 75% Oxygen Content Maximum amount of oxygen that blood can carry (1.39 Hb x Saturation/100) PO 2 Increasing the PO 2 will only make tiny differences in oxygen content.

3 Why is Hyperoxia Bad? Prolonged supra-normal O 2 tension causes long-term damage to tissues, particularly lungs. Hyperoxia increases oxygen free radicals - damage cells & cell membranes. Reperfusing tissues are particularly susceptible to oxidative stress. Hyperoxia causes widespread vasoconstriction cerebral & coronary vessels. Increased SVR with reduced cardiac output. Increased V/Q mismatch, absorption atelectasis. Evidence of potential harm in the following conditions: Neonatal resuscitation COPD Post cardiac arrest AMI/ACS Stroke Traumatic Brain Injury ARDS /Acute Lung Injury Neonatal Resuscitation. Several neonatal resuscitation studies: 100% O 2 vs. room air. Cochrane review 2005: pooled results of 5 trials, >1300 neonates. Reduced mortality, no evidence of harm in air group. AHA/ARC recommendations: start with room air (21%O 2 ), increase FiO 2 only if hypoxia with appropriate ventilation. ACS/ AMI. Rawles et al. BMJ 1976, 157 patients with uncomplicated AMI. Randomised to supplemental O 2 or air for 1 st 24 hours. Non-significant trend toward increased mortality in O 2 group. Cochrane review 2010 (3 trials, 387 pts) Conclusion: limited evidence available showed no benefit, but potential harm from O 2 use in uncomplicated MI. Large RCT is needed. McNulty et al. Effects of supplemental oxygen administration on coronary blood flow in patients undergoing cardiac catheterisation. Am J Physiology Heart Circ Physiology. 2005:288: H Reduced blood flow due to vasospasm In stable patients with IHD, administration of high flow oxygen reduces coronary artery blood flow.

4 American Heart Association Recommendations September Routine use of supplemental oxygen is not recommended. Oxygen therapy is indicated in patients with hypoxia (O 2 Saturation less than 93%) and where there is evidence of shock. COPD Our drive to breathe is altered based on the input to multiple sensors; the main ones are the chemoreceptor s. Central chemoreceptor s detect changes in CSF ph and thus the CO 2 levels however there is buffering and transport in the blood-brain barrier, so that over time there is compensation and thus normalisation of the ph, resetting the sensor allowing chronic hypercarbia without the respiratory compensation. Peripheral receptors (carotid and aortic bodies) respond to decreases in arterial oxygen (and increases in CO 2 ). This is faster yet less important than the central receptors. The most common issue with hypercarbia is the chronic CO2 retainers. As mentioned due to long standing compensatory CSF ph changes, they have lost their CO2 & ph related stimulus to ventilation. Thus arterial hypoxia becomes the chief stimulus to ventilation. Give them oxygen and the ventilation is depressed further. Common cause of hypercarbia is the use of non-rebreather devices and high flow masks. Published in EMA Hobart study, RCT 405 patients with presumed COPD Randomised to high flow O 2 (8-10L NRM) vs. titrated O 2 nasal prongs (SpO %) Primary outcome was in-hospital mortality Overall mortality 9% in high flow O 2, 4% in titrated O 2 Significant reduction in respiratory acidosis & hypercapnoea Average duration of pre-hospital O 2 therapy was only 45mins Average PO 2 in titrated O 2 group was 80mmHg this still may be too high. 56% pts in titrated O 2 group were actually given high-flow by paramedics. So for the CO2 retainers (as would be expected in the case example given at the start of the discussion) Get the high flow mask off (controlled oxygen therapy nasal prongs or venturi mask) Aim for SpO 2 of 88-92%. Make sure nebulisers are given on air with nasal prong oxygen simultaneously. Correct precipitants- CCF, infection, sedation / drugs, electrolytes. Maximise ventilation sit them up, wake them up. Consider BiPAP for type 2 respiratory failure.

5 Post-Cardiac Arrest Commonly 100% oxygen is provided following ROSC in cardiac arrest. Should we be doing this? JAMA, June 2010: 303 (21) Multicentre cohort study, >6000 pts Retrospective review of cardiac arrests resuscitated with ROSC (ICU database over 5 yrs) Primary outcome was survival to hospital discharge PaO 2 on ABG within 24hrs of admission to ICU Stratified into hypoxia (PaO 2 <60), normoxia (60-300) & hyperoxia (>300) Hyperoxia - a significant independent risk factor for in-patient mortality (OR for death 1.8) Hyperoxia even worse than hypoxia! (Mortality 69% vs. 57% hypoxia vs. 50% normoxia) How should we oxygenate patients post cardiac arrest? Current AHA/ARC guidelines advocate ongoing use of 100% oxygen during resuscitation phase (maximum likelihood of achieving ROSC) Post ROSC controlled reoxygenation strategy ILCOR consensus status 2008: SpO % ARC recommendation: SpO %. Targets based solely on pre-clinical data Need for trials of controlled reoxygenation post arrest Stroke Supplemental O 2 was part of standard emergency care for patients with acute stroke. Scandinavian study, Stroke pts, ischaemic stroke, randomised to O 2 3l nasal prongs or air for 1 st 24hrs Non- significant trend to reduction in survival in O 2 group. Sub group analysis; patients with severe stroke had a significant reduction in survival compared to O 2 group (82% v 91%) Australian National Stroke Foundation Guidelines: 2010 Patients who are hypoxic (SpO 2 < 95%) should be given supplemental oxygen. Traumatic Brain Injury Davis et al. Both Hyperoxia and Extreme Hyperoxaemia may be detrimental in patients with severe TBI. J Neurotrauma Retrospective review 3420 TBI patients Stratified by PO 2 on ABG on arrival to ED TSS/ISS used to calculate predicted survival for each patient Mean observed vs. predicted survival differential was determined for each PO 2 stratification Demonstrated reduced survival in both the hypoxic and hyperoxic groups.

6 Graph of survival differential v PO 2 group When is high flow oxygen still appropriate? During resuscitation of a cardio-respiratory arrest (AHA/ARC) Pre-oxygenation prior to emergency RSI (increases oxygen reserve/frc, nitrogen washout, increased safe apnoea time) Shock, severe sepsis, major trauma (but scanty evidence for these) Near-drowning CO poisoning (reduction in the elimination t 1/2 carboxyhaemoglobin) Conclusion No evidence to support indiscriminate use of high flow O 2 in all critically ill patients. High flow oxygen therapy causes hyperoxia, and in many situations this is potentially harmful. In some specific situations- high flow O 2 is still appropriate (pre-rsi, during cardiac arrest). All others - Goldilocks approach (not too much, not too little, just right) COPD with risk of hypercapnoeic respiratory failure: SpO 2 88% - 92% Everyone else aim for normoxia (93-95%) i.e. if not hypoxic don t give any extra O 2! We need more evidence / trials to definitively clarify the indications / contraindications with these major presentation groups and in specific subgroups.

7 NEXT WEEKS CASE 42 year-old female with a history of Down s Syndrome presents with 1 month of lethargy, anorexia, sleepiness and generalised oedema. There are no other medical problems, and she is on no regular medications. On examination:temp = 33 C, PR 60 bpm, BP 80/- There is decreased AE bilaterally at both bases, and she has generalised pitting oedema. There is a non-tender pustular rash on her left breast. ECG; Sinus bradycardia with low voltage. CXR; Cardiomegaly with large bilateral effusions. What is your differential diagnosis and subsequent management? JOKE / QUOTE OF THE WEEK