Challenging Ventilation Dogma (for ED)
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Challenging Ventilation Dogma (for ED)
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Challenging Ventilation Dogma (for ED)
- 1. CHALLENGING VENTILATION DOGMAA/PROF LUKE TORRE INTENSIVIST SCGH ANAESTHETIST JHC AUGUST 2015
- 2. OBJECTIVES โข YES โข challenge ventilation strategy โข link ventilation to mechanisms of pathology โข insight into the future and invite your own discussions โข NO โข Bore you to death with complex respiratory physiology โข Tell you all how to do your job
- 3. DR NADER HABASHI SHOCK TRAUMA CENTRE BALTIMORE USA
- 4. DOGMAS OF THE PAST โข cricoid pressure is an essential part of RSI โข optimal positioning for a lumbar spinal/epidural requires the patient to put their chin on their chest โข chest compressions to ventilation ratio is 15:2 โข we should pre oxygenate all patients with 2 minutes of 100% oxygen
- 5. WE NEED TO BREAK THE RULES
- 6. THE ORIGINS OF MECHANICAL VENTILATION DENMARK 1952-53
- 7. HOW SHOULD WE VENTILATE SOMEONE? โข normal tidal volume (7-12ml/kg LBW) โข normal respiratory rate (10-20) โข normal I:E ratio (1:2) โข normal PEEP (3-5cm H2O) โข FiO2 <60% โข limit peak and plateau pressures
- 8. WHY MIGHT AN ICU PATIENT NEED DIFFERENT SETTINGS TO NORMAL?
- 9. DIFFERENCESโฆ. โข we donโt lie flat on our backs all day long โข we use our muscles to breath โข we make negative pressure in our chest and pull air in โข we cough โข we donโt have complex life threatening organ system injuries โข we donโt have acute lung injury
- 10. APO DO I BREATHE NORMALLY WITH A CXR LIKE THIS?
- 11. VENTILATOR ASSOCIATED LUNG INJURY โข barotrauma โข volutrauma โข atelectotrauma โข biotrauma โข (oxygen toxicity)
- 13. VOLUTRAUMA OVERDISTENTION OF THE BABY LUNG
- 14. ARDSNET VENTILATION WITH REGIONAL OVER DISTENTION
- 15. ATELECTRAUMA WHAT WE HAVE FORGOTTEN ABOUT
- 16. BIOTRAUMA
- 17. BIOTRAUMA METHOD NORMAL TV NORMAL PEEP HIGH TV NORMAL PEEP โVolutraumaโ NORMAL TV NO PEEP โAtelectraumaโ HIGH TV NO PEEP โVolutrauma and Atelectraumaโ TNF ALPHA RELATIVE INCREASE IN LEVELS 1 3 6 56
- 18. CURRENT VENTILATION DOGMA โข BAROTRAUMA โข KEEP PLATEAU PRESSURE <30CM H2O โข VOLUTRAUMA โข KEEP TV 4-6ML/KG โข ATELECTRAUMA โข KEEP PEEP TITRATED TO FIO2 โข BIOTRAUMA โข DO THE ABOVE WELL TO STOP THIS HAPPENING
- 20. CPAP
- 22. A NEW METHOD OF VENTILATING โข Start with a lung constantly pressurised to a safe pressure (<30cm H2O) โข occasionally let it deflate for a moment (0.5sec) and then immediately reinflate (CO2 control) โข reduce sedation and allow the patient to breathe on top of the open lung โข the more spontaneous breathing they do the less often you need to deflate the lung
- 25. WHY SHOULD APRV BE A GOOD THING? โข VOLUTRAUMA โข Ph = Pplateau then over distention unlikely โข Although Tv is not controlled, the entire lung alveoli take the volume they can at that pressure, there is no baby lung anymore and a fully inflated lung can take 10ml/kg easily, โข Spontaneous breathing better distributed ventilation โข ATELECTRAUMA โข By having a short expiratory phase and I:E ratios about 9:1, atelectasis is prevented altogether
- 28. DOES IT WORK? CAN APRV PREVENT VALI
- 30. THE RESEARCH โข 3 groups: โข sham: ventilated with 10ml/kg, PEEP 5cm H2O, โopen closeโ laparotomy โข ARDSnet: ventilated with 6ml/kg, titrated PEEP, plateau pressure <30mmHg, laparotomy with septic shock induced 48 hours โข APRV: ventilated with APRV, Ph=Pplat, Pl=0, Th 4-6s, Tl 75% PEFR, (Tv 10ml/kg) laparotomy with septic shock induced 48 hours
- 33. AND UNDER THE MICROSCOPE ARDSNET VENTILATION
- 34. AND UNDER THE MICROSCOPEโฆ APRV
- 35. AND UNDER THE MICROSCOPE ARDSNET VENTILATION
- 36. AND UNDER THE MICROSCOPEโฆ APRV
- 38. WHEN SHOULD WE USE APRV IN ICU? โข As a rescue therapy for Type 1 Respiratory Failure โข As a primary therapy for those at risk of T1RF โข shock states, multi-trauma, burns, predicted prolonged ventilation โข For everyone!
- 39. THE MAGIC BULLET? VENTILATION DURATION SECRETION CLEARANCE SEDATION REDUCTION VALI LOS ICU LOS HOSPITAL ECMO USAGE MORTALITY
- 40. V-V ECMO APRV, PRONE POSITIONING AND NITRIC OXIDE MAY MAKE V-V ECMO OBSOLETE FOR ACUTE TYPE 1 RESPIRATORY FAILURE A RESCUE THERAPY ONLY IF THE ABOVE FAIL!!
- 43. HOW DOES THIS AFFECT ME IN ED โข most days it doesnโt, but bad habits are hard to break! โข think about your I:E ratio more โข PEEP is your friend โข let your patients breathe if you can โข what if your patient is severely hypoxic in ED post intubation?????????
- 44. HOW DO I DO APRV ON A SHITTY OXYLOG? โข paralyse the patient โข PCV+ โข inverse ratio (2-4:1) โข moderate PEEP (10-15) โข Pinsp <30cm H2O โข normal resp rate โข minimise derecruitment โข suctioning, disconnections โข recruitment manoeuvres โข 40 at 40, PHARLAP
- 45. HYPOTENSION FAR LESS OF A PROBLEM THAN YOU WOULD BELIEVE
- 47. WEST ZONES OF THE LUNG! PARADOXICAL HYPOXIA WITH APRV IN THE SETTING OF HYPOVOLAEMIA
- 48. SUMMARY โข Conventional ventilation settings for short term in healthy lungs is safe, but not ideal โข Conventional ventilation settings in sick lungs, sick patients and for long term ICU patients is not safe because of atelectrauma, volutrauma and biotrauma โข Barotrauma does not exist in a ventilated lung, high plateau pressures are a indicator of potential volutrauma only! โข There is growing evidence that ideal positive pressure ventilation strategies require a constantly pressurised lung and, where possible, spontaneous ventilation to prevent VALI and manage T1RF
- 49. THANKS
Editor's Notes
- Thanks to Dr Habashi who has done a lot of research in this area. The videos you are going to see today are research that was done by his group at the STC in Baltimore
- to break the rules we need to understand how the rules came to beโฆ. so we need to go back to the origins of PPV
- Most people will be familiar with this picture from medical history. cuirass ventilators or iron lungs have been available since the early 1800s and essentially augmented natural negative pressure ventilation. they were largely replaced in the 1950s during the polio epidemics. In 1952 in Denmark, 5700 new cases of polio emerged, they had 6 cuirass ventilators! Positive pressure methods of ventilation had been developed about 10 years earlier and with improvements in placement of tracheostomy tubes, they quickly took over as the preferred mode of ventilation. Positive pressure ventilation also provided the advantages over the iron lung in the care of the unwell patient by allowing access to their body. Mortality dropped from 90% at the start of the epidemic to 25% largely due to the increased number of people able to receive ventilation. This also saw the enlistment of medical students and families to act as mechanical ventilators and indeed the first automated ventilator was designed by Engstrom and advances on his work and his company have continued to this day in the way of GE
- the question that would have confronted the medical students and families of these patients, squeezing the ventilation bags would have been how should I ventilate the patient? I imagine if any of us were the treating respiratory specialists at the time the answer we would have given would be simply this: โreproduce normalityโ give a normal TV, RR, I:E ratio, PEEP that makes sense and that right there was the foundation of ventilation dogma that still persists today. Everyday each of us sets our ventilator with these same settings, and most ventilators now preset the values for us based on the age weight and height of the patient depending on the machine!
- But the question really is; do we need to ventilate ICU patients differently than a normal human being? Are their differences???
- I think there areโฆ. so do people need to be ventilated differently when they have these problems?
- take APO as an example. How does a person in APO breathe when they present to ED. bolt upright, rapid high breathing with short expiration to stop lung derecruitment, attempted gas trapping. they try to the best of their ability to change their ventilation method, so clearly we need to do the same in patients. and more importantly, as PPV is so different to NPV, and just because we are reproducing the same numbers doesnโt man they do the same thing.
- We have also learnt over the decades that indeed conventional ventilation itself can cause lung injury, and these are the ways current knowledge has identified. so we need to understand a bit about the various injuries that a ventilator can do to lungsโฆ.. this is where things can get boring and so Iโll keep it briefโฆ
- I would challenge all of you with the following statement. There is no such thing as lung barotrauma! Now lets think about this. why does a scuba diverโs lungs get air leak when they ascend too rapidlyโฆ. volume overdistention of their lung and a bleb bursts. the high pressure in the lung is not why it bursts, it is simply a warning that volume overdistention is occurring. give a demonstration of squeezing a medium balloon and watch where it bursts. the pressure must be the same everywhere in the balloon and perhaps slightly less at the point where it bursts as that is still expanding and gas flows to the area of lowest pressure! football bladder blown up โdeflategate" joke with Tom Brady of the New England Patriots. Then cut the seam and continue to inflate and watch it explode. this is why we donโt care about high Paw in asthma as the lung units are not over distended this is why we care about plateau pressures, because they represent alveolar pressure and if alveolar pressure is <30cm H2O its unlikely that there is overdistention. Impossible no, there can be regional overdistention which I will show you shortly. If plateaus are above 30, the risk of over distension is increasing and therefore lung injury rabbits in casts are a good example of why barotrauma doesnโt exist. Could describe that here also what we are learning is that its not high pressures that are the determinates of damage, but rather than over distension of lung, and high pressure may be an indicator of this. TREMBLAY SAID IT WELL IN AN ARTICLE IN 1997 EVIDENCE AGAINST BAROTRAUMA IN THE LITERATURE
- there is something wrong with this picture and I canโt quite put my finger on it. overdistension of alveoli causes stretch of basement membranes with leak and pulmonary oedema. This affects surfactant production production and quality and cell function. neutrophils are also leaked into the area and inflammation ensues. Volumtrauma on the other hand is becoming more and more important. This is over distension of regional lung units in the absence of high pressure. This was shown in animal models where rabbits were ventilated with high pressures of 45CM H2O for 1 hour had gross injury. The same rabbits encased in a plaster cast and ventilated to the same pressure of 45 CM H2O but much lower tidal volumes, had no lung injury. So it isn the pressure causing lung injury but alveolar stretch by high volumes, particularly when the distribution of ventilation is not equal.
- This video shows volutrauma beautifullyโฆ. these are surfactant depleted rats lungs which have acquired ARDS and are being ventilated with an ardsnet strategy. You can see why LTV is important and the concept of the baby lung being all that is left behind and why therefore you only use 4-6ml/kg. This is what gattinoni talks about in the concept of baby lung.
- these are microscopy videos of rat lungs with ARDS on SIMV LTV. atelectrauma has 2 components: the repeated alveolar collapse and expansion results in inflammatory mediators, overstretch and surfactcant loss leading to inflammation. second, the opening and closing of alveoli next to collapse segments of lung that donโt move cause high shear forces and shear injury further inciting inflammation. This may actually be the MOST important factor in the pathogenesis of lung injury
- coined to describe the cytokines and inflammatory mediators released from the lung on a ventilator due to volutrauma and atelectrauma, that are released into the blood stream and result in end organ damage not only in the remaining lung tissue but on other end organs (eg kidneys, vasculature and even other areas of lung)
- A study by Tremblay in 1997 measured TNFalpha levels in bronchial lavage fluid in rat lungs with normal ventilation parameters, high tidal volumes normal PEEP and low PEEP normal tidal volume. In all of these groups levels were elevated suggesting BOTH volutrauma and atelectrauma are very important and the combination is extremely important. but we do nothing proactive about atelectrauma.
- SO THIS IS WHAT WE DO TODAY. WHAT IโD SAY ABOUT THIS IS THAT barotrauma doesnโt exist so this is just dumb although we protect volumes to prevent volutrauma, we donโt control distribution, so we can still get overdistention in the most compliant areas of lung WE ARE NOT TREATING THE UNDERLYING PROBLEM OF LUNG COLLAPSE AND ATELECTRAUMA. WE ARE REACTIVE WITH OUR PEEP TO COMBAT THE SHUNT THAT WE ALLOW TO OCCUR! AND BY PROTECTING VOLUMES WITH ONLY 4-6ML/KG WE ONLY FURTHER INHIBIT OUR ABILITY TO RECRUIT LUNG UNITS WE ARE NOT AGRRESSIVE IN RECRUITING LUNG WE GIVE NO IMPORTANCE TO THE I:E RATIO
- so why could mechanical ventilators, even when we control conventional settings so perfectly, still be bad for lungs??? The answer is in this MRI video which is actually a pair of HEALTHY LUNGS: dependant collapse canโt be overcome distribution of gas canโt be controlled
- and this video shows why spontaneous ventilation is so superior to mechanical ventilation diaphragm is doing all the work there is no collapse there is equal volume distribution and no over distension the tidal volume is what the lungs can take for that pressure
- the next concept is about recruitment. We think that just putting peep up or having an I:E ratio of 1:1 will solve atelectasis and oxygenation. but what we need to understand is that collapse lung units take a sustained and constant pressure to be recruited and once recruited, are so deplete of surfactant that they are easy to collapse again. This rat lung is being insufflated with 30cm H2O and watch how long it takes to recruit
- although really this is nothing new, but rather breathing on high CPAP with occasional brief pauses for CO2 control our tidal volume is achieved in deflation not inflation
- key points pressure is controlled you arenโt raising the pressure to breathe you are dropping the pressure to breath (exhale) the patient can breathe in any part of the cycle settings: Ph 28 Pl 0 Th 6 Tl about 0.8
- key points the deflation is only to allow peak expiratory flow to reduce 25% does this cause gas trappingโฆ..YES does it cause breath stackingโฆ NO because you are using pressure control not volume control
- Now this is microscopy of lungs in APRV mode. The key points are: there is fantastic recruitment of alveoli there is minimal atelectasis of alveoli there is small pulsations of all alveoli during the release and reinflation phase, showing how there is minimal overdistention of alveoli despite what the tidal volume may be.
- so to induce septic shock hereโs what they didโฆ the pigs got a laparotomy and their SMA was clamped for 30 mins. They got a cecotomy and a faecolith was placed free in the abdomen. The clamp was release, the caecum closed and the the abdomen closed. This is known to induce septic shock and MOF with ARDS in 100% of pigs with conventional ventilation from previous studies. explain HOW SICK THE PIGS GOT!!
- these are the LTV lungs. You can see dense areas of hemorrhagic aletectasis and inflammation, particularly in the dependant zones of the lungs.
- APRV lungs as a butchers son this is sheer beauty to my eyes! good enough to eat.
- importantly there is heavy alveolar infiltration with inflammatory cells and oedema and smaller alveolar spaces and small lymphatic channels
- lymphatic channels are full of fluid, there is peri-arteriolar oedema and relatively little inflammatory infiltrate
- the key is the amount of neutrophils that have entered the alveolar space compared to APRV
- And in case you still arenโt sure what biotrauma isโฆ. note the noradrenaline dose, MAP, lactate registered as the study progressed was far higher in the Ardsnet group due to not just the septic shock but the progressive lung inflammation and SIRS response this caused to the body, promoting MODS
- what we donโt know yet is how this mode will affect real patient outcomes. There are many potential benefits touted for this and we really need studies on patients in ICUs to ascertain its benefit if anyโฆ
- I personally have seen that for T1RF, my recipe is now much simplerโฆ. APRV, prone positioning (as proven by the PROSEVA trial) +/- inhaled nitric oxide is the ultimate management you can give patients. Only if they fail this, and I have yet to see someone fail this should they go onto ECMO. Habahsiโs group in Baltimore have not used ECMO in over 10 years. Now Chris Nickson has just actually hired someone to kill me after hearing this statement
- this is an example of APRV in action. This lady would otherwise be on ECMO. She has dense bilateral pneumonia and was on 100% FiO2 when intubated on SIMV. We turned her prone 12-16 hours a day, put her on APRV and this is her CXR 24 hours later. What is so impressive is the open lung areas at her bases which usually are the first to go in these patients. She was on 40% oxygen 72 hours later. secretion clearance
- same patient, next day!!! this is an example of APRV in action. This lady would otherwise be on ECMO. She has dense bilateral pneumonia and was on 100% FiO2 when intubated on SIMV. We turned her prone 12-16 hours a day, put her on APRV and this is her CXR 24 hours later. What is so impressive is the open lung areas at her bases which usually are the first to go in these patients. She was on 40% oxygen 72 hours later. secretion clearance
- I would be the first to acknowledge that for 95% of anaesthesia, none of this is important and there is no real demonstrable problem by ventilating people conventionally for elective and emergency anaesthesia, Operations are short and patients are extubated at the end and return to normal ventilation. But i would say thatโฆ. bad habits are hard to break
- the main limitation is the high flow valve that allows the patient to spontaneously breathe at any part of the respiratory cycle. without this spontaneous ventilation is not possible so if you donโt have it youโre better to use PCV+ in a paralysed patient as above.
- Now I know what you are all thinking. As I trained in ANZCA also i know of the dreaded hypotension you get with high intrathoracic pressures. I would argue this is not a problem. There is a transient hypotension on escalating pressures, but not once equilibrium is reached as pressures equilibrate all over the body. also the pressure is transmitted through a relatively non-compliant lung who needs that pressure just to return to a better part of the compliance curve. So the whole pressure isnโt exerted on the CVS system.
- aprv turns zone 2 into zone 1 and thus all blood flow that participates in gas exchange goes to the lower zones. The problem there is that initially they are the collapsed segments of lung where shunt is occurring and now the shunt fraction greatly increases, so hypoxia worsens!