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juan carlos vidal

Permissive hypercapnia and Volume-targeted

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Hi all. I would like your experience in ventilation with guaranteed volume in premature babies under 750 grams.
In my ucin I have a drager vn500 ventilator and a sle5000.

Which one looks better ventilator  for this function?

What pco2 values do they tolerate?

How to manage hypercapnia with this strategy?

What maximum pressures do you tolerate at these weights before going into vafo?

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Great question, Juan Carlos.

I am partial to the VN500, but I'm sure both devices can deliver VG quite well. The problem is that babies don't like to be acidotic. Consequently, there is a problem with permissive hypercapnea in the first days of life in small preemies, because their kidneys are not able to compensate for respiratory acidosis. Therefore, the baby will try to generate a tidal volume sufficient to bring the PCO2 down and normalize the pH. As you know when the tidal volume exceeds the target value, PIP will come down and pretty soon, your baby may be on endotracheal CPAP with rising oxygen requirement (due to the drop in MAP), tachypnea and increased work of breathing. You would have to sedate the baby sufficiently to suppress their respiratory drive, which is a bad idea. People find all kinds of ways to reduce the support for the baby's effort, for example changing from AC to SIMV at a low rate, so the baby is unable to generate adequate minute ventilation and correct the acidosis. So, the baby is struggling, but the doctor is happy, because the PCO2 is where he or she wants it. If you can buffer the acidosis by adding some acetate to your TPN and get the pH up to near normal, you might be able to let the CO2 rise gradually. 

The focus needs to be on pH, not PCO2, because it's the pH that is the primary stimulus for respiratory drive.  Basically it is better to support the baby's effort to maintain normal pH and avoid the mistake of looking only at the PCO2. Ultimately, it is the perivascular pH that controls cerebral circulation, but unfortunately all studies keep focusing on PCO2 and ignoring pH. What we know is that rapid fluctuations in PCO2 confer the greatest risk of IVH. 

Once the baby is a bit older and the kidneys are more mature, it'a s lot easier to allow permissive hypercapnia if they still need mechanical ventilation.

I hope this helps, 

MK

 

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On 12/10/2019 at 1:37 PM, Martin.Keszler said:

Great question, Juan Carlos.

I am partial to the VN500, but I'm sure both devices can deliver VG quite well. The problem is that babies don't like to be acidotic. Consequently, there is a problem with permissive hypercapnea in the first days of life in small preemies, because their kidneys are not able to compensate for respiratory acidosis. Therefore, the baby will try to generate a tidal volume sufficient to bring the PCO2 down and normalize the pH. As you know when the tidal volume exceeds the target value, PIP will come down and pretty soon, your baby may be on endotracheal CPAP with rising oxygen requirement (due to the drop in MAP), tachypnea and increased work of breathing. You would have to sedate the baby sufficiently to suppress their respiratory drive, which is a bad idea. People find all kinds of ways to reduce the support for the baby's effort, for example changing from AC to SIMV at a low rate, so the baby is unable to generate adequate minute ventilation and correct the acidosis. So, the baby is struggling, but the doctor is happy, because the PCO2 is where he or she wants it. If you can buffer the acidosis by adding some acetate to your TPN and get the pH up to near normal, you might be able to let the CO2 rise gradually. 

The focus needs to be on pH, not PCO2, because it's the pH that is the primary stimulus for respiratory drive.  Basically it is better to support the baby's effort to maintain normal pH and avoid the mistake of looking only at the PCO2. Ultimately, it is the perivascular pH that controls cerebral circulation, but unfortunately all studies keep focusing on PCO2 and ignoring pH. What we know is that rapid fluctuations in PCO2 confer the greatest risk of IVH. 

Once the baby is a bit older and the kidneys are more mature, it'a s lot easier to allow permissive hypercapnia if they still need mechanical ventilation.

I hope this helps, 

MK

 

thank you very much for your reply
and in the narrow range of weight and gestational age, which values of ph make reference as the minimum objective

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I agree with Martin

And regarding the values for a ventilated baby... Usually a minimum of 7.25 with a pco2 of 45-55 and not to exceed 75 as it is associated with a poor neurodevelopmental outcome. 

 

These values are independent of gestational age and weight.

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In our unit our concern with the permissive hypercapnea is the higher risk of IVH. We do practice the IVH bundle that main role is to minimally handle the baby. The point of adding acetate is part of our practice , as if the baby - and this usually the case - is in TPN , it’s considered. If there is a UAC - in babies who need close eye in hemodynamic monitoring - the UAC fluid running is Na acetate at a rate of not lower than 0.8ml - 1 ml / hour. We do start with PEEP of no less than 6 . And the Vt that allows to ventilate and oxygenate within targets . PH is the main point we look at in then blood gas as we allow for no lower than 7.25 , and PCO2 of no more than 75. 
we have for some time used VIVE as addition mode to the current main mode of AC + VG, but it’s role doesn’t really work with all ( meant to eliminate the CO2) but no strong evidence . 
once kidneys ability of concentration matures within the DOL 6-9 we do recognize a sudden change in the PCO2, which is now been compensated by the kidneys . I do concur that sedation sedation sedation is a core management point with it , some ventilation issues are solved , in our unit, we do use fentanyl as infusion , midazolam as scheduled doses and dexmedetomidine if needed as infusion especially when baby is extubatable and we plan for use of CPAP immediately post extubation . Hope this helps 

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This is an older abstract we did years ago when little was understood on vg

Evaluation of Volume Guarantee (VG) Ventilation Strategy utilizing the Drager 8000 Plus on babies most likely to develop Bronchopulmonary Dysplasia (BPD).

John Minski R.R.T., Lewis Rempel S.R.T., Ron Heese R.R.T., Mary Seshia MBChB., Univ. of Manitoba, Canada.

Background: As part of the Evidence-based Practice Implementation and Change (EPIC) Collaboration in Canada, we examined our current ventilatory strategies in those babies most likely to develop BPD (<32 weeks GA) from birth and continuing through 36 weeks post menstrual age (PMA). Health Science Centre, Winnipeg (HSC), began using the Babylog ventilator in 1995; by 1997 all ventilators used were upgraded to version 5.0 allowing us to incorporate VG with pulmonary graphics; all ventilators were mounted with a laptop computer to allow for continuous monitoring of pulmonary graphics. To reduce ventilator-induced lung injury we aimed to reduce volutrauma by using the VG option.

This strategy begins in the resuscitation room (RR) where babies have either no or <1min. hand ventilation, are placed directly to VG, and administered surfactant via the closed system. VG continues through the transport and ventilator management in the NICU, with no interruption (i.e. no hand ventilation, or pressure limited ventilation). One early evaluation (1997) of a limited implementation of this strategy and reported by the Canadian Neonatal Network demonstrated a favourable outcome for babies <32wks GA. As a result of this evaluation we standardized the following ventilation strategies. To minimize potential hand ventilation, in the RR the Babylog is fully operational  (except for the set VG) prior to intubation. Once the newborn is determined to need mechanical ventilation(MV), and the weight obtained, the VG is set with standard settings of 3.5 -5.0 ml/kg on  Assist Control (AC)+ VG, set rate of 50 breaths per min., PEEP 5-7cmH2O, Ti 0.25-0.35sec, and FiO2 1.0. Surfactant is mostly given on the AC+ VG mode with Ti and PEEP optimized utilizing pulmonary graphics, and FiO2 adjusted to maintain O2 Sats. between 88 and 94%. We have an exit strategy to HFV if at any VG the required PIP is >25 or MAP ³12 cmH2O regardless of oxygen requirements. Once some recovery is demonstrated and there is adequate respiratory drive, the baby is switched to Pressure Support Ventilation (PSV) +VG mode. This is continued to extubation. Criteria for extubation include PSV+VG, PIP £14 and PEEP 5- 6 cmH2O. All babies transition to NCPAP 6-8 cmH2O and then progress to low flow O2 (0.3-0.5 lpm) by nasal cannula via a blender if continued 02 therapy is required.

Objective: For babies most likely to develop BPD, to evaluate our current ventilator strategies, which include the exclusive use of a targeted tidal volumes (AC+VG and PSV+VG) for those babies on conventional ventilation (Babylog 8000 Plus).

Design: A retrospective chart audit at HSC of babies <32 weeks GA, born between July 03 and May 04 who received MV and/or CPAP. The audit included outcome (death, BPD{O2 dependence at 36 weeks PMA}, pneumothorax),  mode of ventilation, ventilator parameters and all blood gases in the RR , days 1,2,3 ,7,14,28 and 36 weeks PMA.

Results: Forty nine charts were audited. 44 babies received MV, 5 required only CPAP. Mean GA was 28wks, BWt 1193g.  five babies died and 4 developed BPD. None developed a pneumothorax. Mode, ventilatory parameters (medians), and all pCO2 values (median and interquartile range) from birth until death or extubation are shown in the table.

Conclusion: Our 10% rate of BPD in this sample of babies <32 weeks GA requiring MV and or CPAP compares favourably to that reported by others. Our strategy of  early surfactant,  minimal hand ventilation and avoidance of volutrauma through the utilization of VG with  low tidal volumes contributes to this.

Day of life

Mode(n)

Set VG

(ml/kg)

Set Rate (bpm)

Spont.

Rate (bpm)

pCO2(mmHg)

Median (1st,3rd  quartile)

PIP

(cmH2O)

PEEP

(cmH2O)

MAP

(cmH2O)

FiO2

(%)

RR

AC (36)

4

42

60

52 (46,63)

20

6

8.5

40

1

AC (30)

PSV(6)

JET (1)

HFO (2)

4.1

3.9

48

15

360

450

59

48

42 (39,48)

44  (37,45)

53  (53,54)

51  (45,57)

19

11

21

28 (DP)

6

6

9

8.4

7.3

12

12

27

22

63

29

2       

AC (21)

PSV(6)

JET (2)

HFO (2)

4.0

3.9

40

15

360

450

50

60

45 (42,48)

43 (42,46)

46 (38,50)

43  (38,58)

15

11

21

26.5 (DP)

6

6

9

8.4

6.5

10.5

27

21

63

29

3

AC(19)

PSV(6)

JET  (2)

HFO (1)

4.0

3.9

41

15

270

420

50

45

48 (44,50)

41 (36,48)

44 (40,51)

43 (43,43)

16

11

21

23 (DP)

6

6

6

7.3

6.9

7.9

11.5

21

21

61

31

7

AC(12)

PSV(3)

JET (1)

HFO (2)

4.5

4.2

50

15

270

420

55

58

54 (52,54)

54 (54,56)

41 (40,51)

53 (52,53)

17

 

20

24 (DP)

6

6

7

 

8

8.4

9.9

12.5

27

26

76

40

14

AC (6)

JET (6)

3.9

40

360

50

55 (53,56)

53 (45,53)

15

19

6

8

7.9

9.5

25

38

28

AC (5)

PSV (1)

Jet (2)

4.2

3.9

30

15

310

55

56

56 (53,63)

38 (38,38)

50 (48,53)

13

9

26

6

5

8

7.4

5.8

10.3

23

24

50

36wks PMA

PSV (1)

3.9

15

56

38 (38,38)

9

5

5.8

22

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On 12/10/2019 at 5:37 PM, Martin.Keszler said:

Great question, Juan Carlos.

I am partial to the VN500, but I'm sure both devices can deliver VG quite well. The problem is that babies don't like to be acidotic. Consequently, there is a problem with permissive hypercapnea in the first days of life in small preemies, because their kidneys are not able to compensate for respiratory acidosis. Therefore, the baby will try to generate a tidal volume sufficient to bring the PCO2 down and normalize the pH. As you know when the tidal volume exceeds the target value, PIP will come down and pretty soon, your baby may be on endotracheal CPAP with rising oxygen requirement (due to the drop in MAP), tachypnea and increased work of breathing. You would have to sedate the baby sufficiently to suppress their respiratory drive, which is a bad idea. People find all kinds of ways to reduce the support for the baby's effort, for example changing from AC to SIMV at a low rate, so the baby is unable to generate adequate minute ventilation and correct the acidosis. So, the baby is struggling, but the doctor is happy, because the PCO2 is where he or she wants it. If you can buffer the acidosis by adding some acetate to your TPN and get the pH up to near normal, you might be able to let the CO2 rise gradually. 

The focus needs to be on pH, not PCO2, because it's the pH that is the primary stimulus for respiratory drive.  Basically it is better to support the baby's effort to maintain normal pH and avoid the mistake of looking only at the PCO2. Ultimately, it is the perivascular pH that controls cerebral circulation, but unfortunately all studies keep focusing on PCO2 and ignoring pH. What we know is that rapid fluctuations in PCO2 confer the greatest risk of IVH. 

Once the baby is a bit older and the kidneys are more mature, it'a s lot easier to allow permissive hypercapnia if they still need mechanical ventilation.

I hope this helps, 

MK

 

Dr Keszler @Martin.Keszler

- If a neonate is trying to compensate acidosis and we increase VG to aviod endotracheal CPAP  you think we should worry about pH, but low pCO2 is associated with PVL. So what can we do to balance both issues? 
- What is the lowest PIP you feel comfortable with while using VG? Patient with PEEP 5, would you feel OK if he is using PIP of 9-10? Or in that case you would consider he is approaching ET CPAP and you would increase VG?

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