VENTILATION STRATEGIES FOR THE CRITICALLY UNWELL Dr Nick Taylor Visiting Emergency Specialist Teaching Hospital Karapitiya Senior Specialist and Director ED Training Clinical Lecturer, Australian National University Canberra Hospital, Australia
CASE 1 19 yo with severe hypoxia Widespread B profile on USS lung Intubated with sucker through cords
HOW WILL YOU VENTILATE HIM?
CASE 2 25 yo female with severe asthma Intubated Sudden drop in sats, high pressures and low BP
HOW WILL YOU VENTILATE HER?
INTRO Traditional ventilation teaching is often complicated and difficult to understand There are only 2 main reasons for respiration
Supplying Oxygen Getting Rid of CO2
There are also essentially only two main types of lung pathology requiring ventilation
TWO TYPES OF VENTILATION LUNG INJURY (Oxygen Supply is the problem) LUNG OBSTRUCTION (Getting rid of CO2 is the problem)
Today we will learn to apply these principles to a critically unwell patient You can use these principles for NIV or IPPV
FIRST: VERY SIMPLE PULMONARY PHYSIOLOGY
HOW DO WE MEASURE VENTILATION? Minute Volume = Tidal Volume x Respiratory Rate
MINUTE VOLUME FOR A NORMAL CO2 Around 60mL/kg in spont breathing pt Because of dead space it s closer to 100-120mL/kg when intubated
How does our body control ventilation?
PRIMARY SERVO CONTROL OF MINUTE VENTILATION Respiratory centre in the medulla (brain stem) ph sensitive cells (dissolved CO2 changes ph in CSF) Responds to changes in arterial CO2, and adjusts minute volume accordingly As CO2 rises we ventilate more, if CO2 falls, we ventilate less
CO2 is inversely proportional to MV Thus when ventilating a patient, we guide ventilation adequacy with ETCO2
Note ETCO2 will differ from PaCO2 It is usually lower by 5-10 but varies substantially with different circuits and lung pathology This is because of non ventilated dead space or shunt
BACK UP PLAN Hypoxic respiratory drive Need PO2 < 50 Clearly not your day to day ventilation controller!
OTHER VARIABLES What is the inevitable 3 rd major variable which goes along with TV and RR? Pressure
HOW DOES PRESSURE VARY WITH MV? Lung dynamics (particularly compliance) and coexisting pathology play a major role in how the lung will respond to a given RR and TV
COMPLIANCE Change in pressure for a given volume Low compliance = high elastic recoil and difficult to expand - a thick balloon (hard to inflate, easy to deflate) High compliance = low elastic recoil, Easy to expand - a plastic bag (easy to inflate, hard to deflate)
PRESSURES PIP (Peak inspiratory pressure) and EEP (end expiratory pressure) PIP is less useful as a measure of barotrauma than Alevolar pressure Plateau pressures (alveolar pressures) can be measured using an inspiratory breath hold Plateau pressures should be kept <30mmHg
Notice oxygen hasn t been mentioned in regards to ventilation yet
OXYGENATION Depends on: FiO2 Quality and size of surface area available for gas exchange Perfusion of lungs Oxygen carrying capacity of blood Tissue perfusion at end-organ
Positive end expiratory pressure PEEP Use PEEP to prevent derecruitment of alveolar units (decrease shunt) Increase FRC (functional residual capacity) eg in the obese patient Also reduces venous return (Preload) as mean intrathoracic pressure rises Predominately helps oxygenation
PEEP CONTINUED PEEP of 3-5 cmh 2 O thought to be physiological when ETT insitu Thus all patients except those with extremely high auto PEEP (severe asthma) should have around 5 of PEEP
AUTO PEEP All lungs have a low amount of auto-peep which rises in disease states like asthma Measure with expiratory breath hold Difference between applied PEEP and Exp pressure is the auto PEEP
FLOW RATE Is the speed at which VT is delivered Normal setting 40-60 L/min Flow rate sets Tinsp and thus I:E ratio High flow > 60 L/min good for asthma (shorter Tinsp) but may increase Peak inspiratory Pressure (PiP) Low flow rates (20 to 50 L/min) = increase inspiratory time with improved distribution gases
I:E RATIOS Normal 1:2 Shorter insp times increase dead space ventilation Longer insp times improve oxygenation but increase haemodynamic instability Dependant on flow rate, inspiratory time and frequency
RISE TIME (RAMP) The amount of time it takes for set pressure to be reached from beginning inspiration Adjusts the peak inspiratory flow rate
LUNG INJURY VENTILATION
Injury ventilation is for basically everything except obstruction and thus includes ARDS, APO, pneumonia, contusions etc Oxygenation is the primary problem
NIV Mode CPAP PEEP start at 5-10 and increase by 2-3 every 5-10 minutes FiO2 depends on starting sats Aim to lower to <0.5 ASAP
IPPV MODE SIMV in Volume control mode
TV 6-8 ml/kg of ideal body weight This is a lung protective strategy For ARDS aim 6mL/kg
For ventilation Start at 18 Why 18? Dead space As a proportion of TV it s higher at lower TVs Need to compensate with rate to achieve MV RATE
PEEP/FIO2 For oxygenation Use PEEP tables No mortality diff high vs low PEEP but high PEEP may oxygenate better
IFR AND I:E Flow rates 50-80ml/min I:E ration 1:1.5-2
PERMISSIVE HYPERCAPNOEA Don t try and chase the CO2 unless acidosis (ph <7.15) becomes an issue
PLATEAU PRESSURES FOR INJURY Alveolar pressure Keep <30 cm H20 as associated with lower mortality
FIXING P PLAT Check P plat after changing TV /PEEP or q4h If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps (minimum = 4 ml/kg). If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT by 1 ml/kg until Pplat>25cmH2OorVT =6ml/kg. If Pplat < 30 and breath stacking or dys-synchrony occurs: increase VT in 1ml/kg increments to 7 or 8 ml/kg if Pplat remains < 30 cm H2O.
LUNG INJURY SALVAGE
RECRUITMENT Maybe useful when unable to achieve adequate oxygenation Multiple different methods described Pros/cons to doing it Simplest is PEEP 30-40cm/H2O for 1-2 minutes PRONING is another recruitment method which can decrease mortality on the very critically hypoxic
Volume mode Start at 8ml/kg TV SUMMARY INJURY VENTILATION Set initial rate for goal MV Reduce TV over 1-2 hours to 6ml/kg Adjust TV and RR for P plat and CO2 goals
OBSTRUCTION
Commonest causes are asthma and COPD Failure to expel CO2 A Ventilation problem
NIV Bi-Level mode Start at 10/4 Start with FiO2 0.4 or so Increase IPAP/PS by 2-3cm H20 every 10-15minutes using MV and CO2 goals to guide you
IPPV MODE SIMV VC (PC if you like, no real difference)
TV Start at 8mL/kg of ideal body weight
RATE Start at 10 bpm and be ready to lower it Time in expiration is important
I:E AND IFR Use high IFR of 80-100L/min Aim to get I:E 1:4-5
PERMISSIVE HYPERCAPNOEA ph >7.1 is OK
PEEP/FIO2 0 added PEEP Check auto PEEP with Expiratory Breath Hold FiO2 at 0.4 to start
Breath stacking DYNAMIC HYPERINFLATION Leads to High intrathoracic pressures and decreased venous return sometimes to arrest
OBSTRUCTION RESCUE STRATEGIES If BP drops profoundly or pressures rise dramatically think pneumothorax or dynamic hyperinflation Disconnect from ventilator Allow 10-20 sec apnoea Lung USS with slow RR for PTx May need chest compressions to reduce hyperinflation
OBSTRUCTION SUMMARY Low RR High IFR Long I:E ratio Moderate TVs Permissive hypercapnoea Watch out for dynamic hyperinflation
CASE 1 19 yo with severe hypoxia Widespread B profile on USS lung Intubated with sucker through cords
CASE CONTINUED Handbagged with PEEP valve no suction!!! When connected to ventilator: TV 60mL with PIP 50 What can you do??
Return to hand bagging CAN T VENTILATE LUNG INJURY Raise P limit of ventilator to 50 Set VC initially in CMV Rapid exchange back to vent circuit No suctioning!!! PEEP 30-40 for 1-2 minutes Ventilate with ARDS PEEP/FiO2 tables and injury strategy
CASE 2 25 yo female with severe asthma Intubated and ventilated with obstruction strategy Sudden drop in sats, high pressures and low BP
WHATS SHOULD YOU DO Hand bag at slow rate Pressures very high Lung USS done: Normal BP 50/25 Apnoea trialled no success 5 slow chest compressions with audible exhalation BP increased Return to ventilator at RR 6, I:E 1:5
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