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Andy Pybus St George Private Hospital Sydney

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1 Andy Pybus St George Private Hospital Sydney
Simulating ECMO. Andy Pybus St George Private Hospital Sydney

2 MSE (Aust) PL www.ecmosimulation.com
Conflict of interest: MSE (Aust) PL Before I start, I need to declare a conflict of interest in that: Much of the data used in this talk was prepared using this ECMO simulator in which I have a significant commercial interest.

3 Presentation plan: Rationale for simulation.
Components of a simulator. Interactive scenarios.

4 Rationale for simulation.
Why simulate? Education. Training. Competency assessment. Therapeutic / contingency planning. (What will happen if ??)

5 Components of a simulator:
Physiological models. Pharmacological models. Equipment models.

6 Model Myocardial Contractility Chronotropy Inotropy ECG
Hb Dissociation Blood Gases Mechanical Pumps Cannula Flow Respiratory Mechanics PK Models Model CO2 Sensitivity BIS Baro - Reception Fluid Spaces NM Transmission Hypoxic Responses Starling Behaviour V:Q Relationship Vascular Pressures Thermal Behaviour

7 VV ECMO Paradigm: Aims:
To ‘arterialise’ as great a proportion of the venous return as is possible. To ‘rest’ the native lung.

8 VA ECMO Paradigm: Aims: Circulatory Support. (Respiratory Support.)

9

10 Your Resources:

11 The Patient: The patient is a 24 year-old man, weighing 75 kgs, who has been admitted to your Intensive Care Unit for ongoing care. When he came in, he gave a 4 day history of increasing respiratory distress, fever and a productive cough. He deteriorated rapidly and required intubation and ventilation shortly after admission. Sputum cultures grew a sensitive staphylococcus aureus. Despite treatment with appropriate antibiotics, the use of prone ventilation, permissive hypercarbia and inhaled nitric oxide, his condition has not improved… During this talk, I’m going to ask you to imagine that you’re treating this patient... He’s an otherwise fit young man who presents with a short history of pneumonia. Despite the best of care, he continues to deteriorate…

12 The clinical picture: His blood gases on 100% oxygen are: PaO2 45 mm Hg PaCO2 58 mm Hg pH 7.18 SaO2 74% Hb 85 g/L You calculate his Total Static Lung Compliance as: 10 ml/cm H2O You calculate his ‘Shunt’ and ‘Deadspace’ as: Qs/Qt 0.70 Vd/Vt 0.80 You estimate his oxygen consumption to be: 200 ml/min. This is his clinical picture now, as you can see: his gases are horrible, and… he has very stiff lungs...

13 The clinical picture: His blood gases on 100% oxygen are: PaO2 45 mm Hg PaCO2 58 mm Hg pH 7.18 SaO2 74% Hb 85 g/L You calculate his Total Static Lung Compliance as: 10 ml/cm H2O You calculate his ‘Shunt’ and ‘Deadspace’ as: Qs/Qt 0.70 Vd/Vt 0.80 You estimate his oxygen consumption to be: 200 ml/min. This is his clinical picture now, as you can see: his gases are horrible, and… he has very stiff lungs...

14 Subsequently… The decision is made to put the patient on VV ECMO. This is successfully implemented using a ‘Quadrox’ hollow-fibre lung and a dual-cannula drainage system. The patient is sedated, heparinised and ventilated on 70% oxygen with a PEEP of 10 cms H2O, a tidal volume of 350 mls and a rate of 8 bpm. The artificial lung is ventilated with 100% oxygen at a gas flow rate of 2.0 lpm. and ECMO blood flow rate of 3.5 lpm.

15 Dual drainage Cannula system:
SVC drainage IVC drainage Atrial return

16 After 10 minutes on ECMO, you do some blood gases…
PaO2: 55 mm Hg, PaCO2: 55 mm Hg You'd like to see the PCO2 a bit lower and ask your registrar what he thinks you should do. He suggests increasing the patient’s tidal volume to 600 mls and upping the rate to 15 bpm. Is this appropriate?

17 The clinical picture: His blood gases on 100% oxygen are: PaO2 45 mm Hg PaCO2 58 mm Hg pH 7.18 SaO2 74% Hb 85 g/L You calculate his Total Static Lung Compliance as: 10 ml/cm H2O You calculate his ‘Shunt’ and ‘Deadspace’ as: Qs/Qt 0.70 Vd/Vt 0.80 You estimate his oxygen consumption to be: 200 ml/min. This is his clinical picture now, as you can see: his gases are horrible, and… he has very stiff lungs...

18

19 VV ECMO: PaCO2 and Gas Flow:
If we look at this graphically…. In the left hand graph, I’ve put our patient on VV ECMO at a constant blood flow of five lpm and explored the effect of changing the gas flow to the device. As you can see, as the gas flow is increased from two to ten lpm, so the patient’s PaCO2 falls steadily. The right hand graph summarises the same data after a ten minute equilibration period at each gas flow rate. This gives us our first law of ECMO that “PaCO2 is controlled by adjustment of gas flow through the artificial lung.” Blood Flow: 5.0 lpm Blood Flow: 5.0 lpm

20 You also think that you'd like the patient’s SaO2 a bit higher and ask your registrar what he thinks you should do. He suggests increasing the blood flow through the ECMO system. Could he be right (this time)?

21 PaO2 and Blood Flow: Again, if we look at this graphically…. In the left hand graph, I’ve put our patient on VV ECMO and explored the effect of changing the blood flow through the device. As you can see, as the blood flow is increased from zero to five lpm, so the patient’s PaO2 rises steadily. The right hand graph summarises the same data after a ten minute equilibration period at each blood flow rate. This gives us our second law of ECMO that “PaO2 is controlled by adjustment of blood flow through the artificial lung.”

22 You contemplate cooling the patient to 35Oc in order to further improve oxygenation.
You discuss this plan with the registrar (who has a lot of experience with these kind of cases). He tells you that reducing the patient’s temperature will have no effect on his SaO2. Is he right?

23 ECMO and Temperature: Blood Flow: 5.0 lpm
So let’s examine this graphically… On the right I’ve shown you the effect of changing the patient’s temperature on the metabolic rate. As you can see, a change in temperature of about seven degrees more or less doubles the metabolic rate. In the left-hand graph, I’ve shown you the effect of cooling our patient by only three degrees on the patient’s PaO2. Throughout the cooling period I’ve maintained the ECMO flow steady at 5 lpm. As a result of the reduction in metabolic rate, PaO2 rises from about 69 mm Hg to about 78 mm Hg. This leads us to our eighth law that we can improve oxygenation by cooling.

24 VV ECMO: Basic Manipulations:
“A simple technique for use in a complex environment.” Adjusting Gas Flow will affect the PaCO2. Adjusting Blood Flow will affect the PaO2. Adjusting Temperature will affect the SvO2. Gas Flow Blood Flow Let’s first consider the basic manipulations which we can make using a VV ECMO system… As I’ve said here, ECMO is essentially: “A simple technique for use in a complex system.” The system is so simple, that when all is said and done, there are only 3 things you can do with it. Adjust the Gas Flow which will affect the patient’s PaCO2. Adjust the Blood Flow which will affect the patient’s PaO2. Using the system’s heat exchanger adjust the patient’s temperature which will: Initially affect their metabolic rate Then their SvO2. Finally their arterial PO2. Temperature (VO2)

25 VV ECMO: The Effect Of Gas Flow:
Blood Flow Gas flow is analogous to minute ventilation PaCO2 is ≅ to 1/gas flow PaCO2 is easily controlled CO2 ‘Dissociation’ curve So let’s start by examining the effect of changing gas flow through the device. The first thing that we can say is that Gas flow through the artificial lung is analogous to the minute ventilation of the patient’s normal lung. As with the normal lung, there is an inverse relationship between PaCO2 and ventilation. “The more we ventilate, the lower the PaCO2 .” Finally, as we’ll see, during VV ECMO, PaCO2 is almost always easily controlled. This is largely because the whole blood CO2 dissociation curve is essentially linear over the clinical range and.. This is importantly different from the shape of the Oxygen dissociation curve. Temperature (VO2)

26 VV ECMO: The Effect Of Blood Flow:
Gas Flow Blood Flow PaO2  to blood flow Blood flow as a fraction of cardiac output Limits of achievable PaO2 Effect of cardiac output Effect of Hb dissociation curve Now let’s examine the effect of changing blood flow through the device. The first thing we can say is that as blood flow through the device is increased, so the PaO2 tends to rise. “The more blood flow we put through the artificial lung, the higher the patient’s PaO2 .” However, we shouldn’t forget that what’s really important is blood flow as a fraction of the patient’s total cardiac output. If we’re able to capture the patient’s entire venous return and fully arterialise it, then there will be no need for the patient’s own lungs to participate in gas exchange at all. On the other hand, if we can only capture half the return, then we’ll leave the patient’s lungs with plenty of work to do. Failure to capture the entire venous return coupled with the non-linearity of Hb dissociation curve limit the achievable PaO2 . Temperature (VO2)

27 VV ECMO: The Effect Of Temperature:
Gas Flow Blood Flow As Temperature falls: VO2↓ ↓ ↓ ↓ SvO2 ↑↑ ↑↑ PaO2 ↑↑ ↑↑ Oxygenator Efficiency ↑↑↑ But: SvO2 is also importantly affected by Hct and CO. Finally, let’s examine the effect of heating or cooling the patient. As the temperature falls, various things happen: Metabolic rate will fall, Mixed venous saturation will rise and this will lead to a secondary increase in PaO2 As we’ll see, the artificial lung itself will tend to become more efficient. However, we shouldn’t forget that SvO2 is also importantly affected by haematocrit and Cardiac Output. Temperature (VO2)

28 You’re still worried about the patient’s saturation.
Your registrar tells you that further increasing the gas flow through the artificial lung will increase the SaO2. Is he right?

29

30 You’ve now been a bit worried about hypoxia all day and you notice that the patient has a haematocrit of 25% The registrar (who has a lot of experience with these kind of cases) suggests that you transfuse the patient.

31

32 The registrar (who’s now beginning to get on your nerves) also points out that the patient’s last known cardiac output was over 9 lpm. He suggests that reducing the patient’s output will increase his arterial PO2. Could he be right??

33 VV ECMO: The Effect of ↑ Cardiac Output:
Competing influences: PaO2 tends to rise because: As CO ↑, so SvO2 ↑. As SvO2 ↑↑, so SaO2 ↑↑.

34 VV ECMO: The Effect of Cardiac Output:
Competing Influences: PaO2 tends to fall because: As CO ↑, so fraction of CO passing through the oxygenator ↓. As CO ↑, so Qs/Qt ↑.↑ Lynch JP, Mhyre JG, Dantzker DR. Influence of cardiac output on intrapulmonary shunt. J Appl Physiol Feb;46(2):

35 VV ECMO: The Effect of ↑ Cardiac Output:
Net Effect: As CO ↑, so PaO2 ↓.

36 You want to go home after a long day, but need to know that the registrar can change the oxygenator if he really has to. You ask him how long it will take him. He tells you “30 seconds”. You then ask him how long it will take before the patient desaturates profoundly. He tells you “Five minutes or so”… Is his confidence well-founded?

37

38 On the ward round the following day, you’re discussing the concept of ‘Resting’ the lung.
The registrar asserts that: “If VV ECMO is working very well, there’s no requirement for tidal ventilation.” Could he be right?

39 VV ECMO: Resting the lung:
Parameter Before After ECMO Blood Flow (lpm) 5.0 ECMO Gas Flow (lpm) 2.5 Ventilator Tidal Volume (mls) 500 200 Ventilator Frequency (bpm) 15 4 Ventilator PEEP (cm H2O) 10 Ventilator FiO2 1.0 0.6 PaO2 PaCO2 In this slide I’ve explored the effect of ‘resting the lung’ on gas exchange. At the start of the experiment, The patient is on ECMO at 5 lpm, but is fully ventilated. At the black arrow, the ventilator is turned right down, and the gas flow through the oxygenator is increased. As you can see, there is a small fall in PaO2, but PaCO2 remains virtually unchanged. Oxygen transfer through the natural lung is occurring by means of ‘Apnoeic Oxygenation’. This gives us our tenth law of ECMO which is to ‘Rest the Lung’.

40 The registrar then goes on to say:
“Even at low blood flow rates, VV ECMO can usually control arterial PCO2.” Surely, he’s not right again?

41

42 You’re now getting pretty exasperated with the registrar
You’re now getting pretty exasperated with the registrar. He’s getting far too many answers right!! In desperation, you ask him how he thinks the patient would respond to VA ECMO. You’re not sure what size of arterial return cannula should be used. The registrar tells you a 15F cannula will be fine. Is he right?

43 Return (Arterial) Cannula:
Basis for recommendation: ? Blood Flow: 5.0 lpm

44 So here I’ve started the patient on VA ECMO at a blood flow rate of over two lpm.
I do a blood gas and note that the PaO2 is only ~ 70 mm Hg. The registrar tells me that the oxygenator is probably failing. Could he be right?

45 VA ECMO: Differential Circulation:
If peripheral arterial cannulation is used, then in the ‘proximal’ circulation: PaO2 is set by adjusting FiO2 / PEEP to native lung. PaCO2 is set by adjusting oxygenator settings. Requirement for tidal ventilation reduced.

46 VA ECMO: Special problems:
The ‘unclamped’ circuit. Pump flow : Pre-load nexus. Differential circulation. Afterload dependence. Left heart stasis. Limb ischaemia.

47 Presentation available at:
‘Downloads’ section.


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