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Dr. T.R.Chandrashekar
Prof and H.O.D Department of Critical Care Medicine
Institute of Gastrointestinal diseases and organ Transplant
(IGOT), Bangalore.
How do I safely ventilate my patient in OT ?
Some facts about respiratory system
Base has more alveoli and has more super imposed pressure due to alveoli
above it, become more if lung weight due to Interstitial edema increases
Superimposed pressure
chestwall
Lung and chestwall are
in a series
In OT
Why do we ventilate patients undergoing surgery?
Patients choice Surgery warrant GA Normal Lungs?
GA in supine position
Cephalad movement of Diaphragm-
basal atelectasis
Laparoscopy –Pneumoperitoneum
Reverse Trendelenburg position
Large hernia surgeries
Do patients always have normal lungs?
40 yr old farmer with 4 day old small bowel perforation,
peritonitis with sepsis on noradrenaline, abdomen tense, SPO2
95% of 15L O2 NRM with bag, RR 29/min HR 110/min,
BP100/60mm Hg, lactate 1.8mmol/L, restless posted for
emergency laparotomy and procedure. UO adequate.
Abruptio placenta 25 yr old primi taken for emergency surgery,
LSCS on GA after baby extraction uterus atony, PPH not
responding to drugs, plan for hysterectomy, requires lot of fluids and
noradrenaline till blood is organized, requires massive transfusion
Is this patient more prone to PPC?
How do we ventilate this patient?
Mechanical ventilation is a lung support system
Is not a treatment for any disease
Mechanical ventilation causes harm - VALI or
Physician associated Lung injury
Permissible atelectasis - close the Lung and allow it to rest
Lung collapse is not always detrimental.
Recent data suggest -“partial recruitment” better protects the
lung from VILI compared to “full recruitment”.
Reset Physiological Goal posts in your head
Open Just enough lung- to have Adequate OXYGEN in
blood for the patient to survive- SPO2 of 86% to 92%
Pursuit ofbetteroxygenation atthecostofVILIleadsto
GoodABG andaDeadpatient?
The goal in any sick patient is to optimise Oxygen
delivery into Microcirculation and use in cell Mitochondria
O2
CO
2
Intra thoracic
pressure
Decreased Preload
Cardiac compression
Decreased Cardiac output
Do2= Oxygen content X CO
O2 delivery to mitochondria
is a Cardio-Respiratory function
There is evidence that
large VT, low PEEP and
High FIo2 lead to post
op Complications
•Postoperative pulmonary complications (PPCs) are pulmonary abnormalities that result in identifiable
disease or dysfunction and adversely affect the patient's clinical outcome.
••PPCs play a significant role in patient morbidity, mortality, and length of stay in hospital.
•Perioperative strategies for prevention and management could improve patient outcomes. Anaesthetists are
well placed to implement these.
••Preoperative strategies include optimizing cardiorespiratory disease, early smoking cessation, and
prehabilitation exercise programmes.
••Intraoperative strategies include shorter duration of surgery, judicious and monitored use of neuromuscular
blocking agents, and lung protective ventilation.
••Postoperative strategies include effective analgesia, early mobilization, and lung expansion techniques.
What are the problems encountered in MV under GA?
Postoperative pulmonary complications (PPCs)
What are PPCs?
Definition / incidence
How doe recognize them pre-operatively? Management?
Intra-operative management—Including induction/Emergence
Postoperative management
Intraoperative risk factors
Changes in pulmonary physiology
GA in supine position
Cephalad movement of Diaphragm- basal atelectasis
Laparoscopy –Pneumoperitoneum
Reverse Trendelenburg position
Large hernia surgeries
Anaesthetic agents diminish respiratory drive and the response to hypoxia and hypercapnia, resulting in hypoventilation
ventilation–perfusion mismatching and increased shunt fraction. Prolonged periods of 100% oxygen may produce
absorption atelectasis as all the oxygen is absorbed and the splinting effect of nitrogen in the alveoli is lost.
Following surgery, particularly abdominal and thoracic, pain may limit respiratory excursion and cause splinting of the
diaphragm, further reducing FRC and vital capacity
The effects of anaesthesia, bed rest, and opioids inhibit the cough reflex and impair respiratory tract ciliary activity, while
dry gases result in mucus plugging.
These physiological effects contribute to the development of PPCs.
Anaesthetic factors
NMB- inadequate reversal/sedation
surgical factors
The surgical site and the duration of surgery (>3 h) influence the risk of developing PPCs.1
Prolonged surgery and anaesthesia alters immune defence and gas exchange capacity by depressing
alveolar macrophage function, interfering with surfactant production, slowing mucociliary clearance, and
increasing the permeability of the alveolar–capillary barrier.
Abdominal and thoracic and head and neck surgeries are the most likely to interfere with respiratory
function and are strongly linked to PPCs, particularly in the context of tissue trauma, fluid shifts, and blood
transfusion.
Other types of surgery associated with increased risk of PPCs include neurosurgery, with a likely reason
being reduced conscious level and the associated risk of aspiration.
Vascular and emergency surgeries are also associated, perhaps because of the higher risk patient cohort.
Peripheral and orthopaedic procedures are considered to be lower risk for PPCs.
Definition of PPCs
Jammer I et al. Eur J Anaesthesiol. 2015;32:88-105
Mazo V et al. Anesthesiology. 2014Aug;121(2):219-31
Canet J et al. Eur J Anaesthesiol. 2015; 32:1–13 [Epub ahead of
print]
 Primary outcome (composite)
 Respiratory insufficiency
 Bronchospasm
 Pleural effusion
 Respiratory infection
 Atelectasis
 Aspiration pneumonitis
 Pneumothorax
Strategies to prevent postoperative pulmonary complications
Guldner A, Pelosi P,de Abreu GM Curr Opin Anesthesiol 2013,26:141–151
Preoperatively
• Assess general physical status and identify risk
factors
- Risk Scores
– Preoperative SpO2
• Preoperative “optimization”
– Cessation of smoking
– Treat pre-op infection and/or bronchospasm
– Alleviate anemia (< 10 g/dL) (?)
• Education regarding physiotherapy
Intraoperativel
y
• Anaesthetic/surgical plan
– Consider regional anesthesia for pain control
– Choose short-acting drugs/avoid PORC
(monitoring)
– Limit duration of surgery and fluids - GDT
– If feasible, use laparoscopic techniques
– Reduce emergent surgery
• Ventilatory strategies
– Protective ventilation (Low tidal volume 6-8 ml/kg
IBW)
Strategies to prevent postoperative pulmonary complications
Guldner A, Pelosi P,de Abreu GM Curr Opin Anesthesiol 2013,26:141–151
Strategies to prevent postoperative pulmonary complications
Guldner A, Pelosi P,de Abreu GM Curr Opin Anesthesiol 2013,26:141–151
Postoperatively
• Selective use of nasogastric tube
- If PONV
- Inability to oral feeding
- Abdominal distension
• Effective pain management and minimize
respiratory depression
• Post-op Physiotherapy and/or NRS
- Early ambulation
- Mobilization of secretions
- Deep breathing (Incentive spirometry?)
- CPAP/NPPV
Ventilator-Induced Lung Injury
Slutsky AS & Ranieri VM N Engl J Med 2013;369:2126-36
Perioperative Positive Pressure
Ventilation An Integrated Approach
to Improve Pulmonary Care
Futier E., Marret E., Jaber S. Anesthesiology 2014;121:400–8
LAS VEGAS –
Intraoperative Ventilation Settings
9,682 patients - 38 countries - 146 centers
• VT = 500 [455–557]ml
• VT = 8.1 [7.3–9.1] ml/kg PBW
• PEEP = 3.5 [0–5] cm H2O
• < 2 cm H2O – 32%
• 2–5 cm H2O – 60%
• < 10% RM
LOW VT – LOW PEEP – NO RMs !
Schultz M, Hemmes S, Abreu GM , Pelosi P for the PROVEnet and LAS VEGAS investigators
Some facts about respiratory system
Base has more alveoli and has more super imposed pressure due to alveoli
above it, become more if lung weight due to Interstitial edema increases
Superimposed pressure
chestwall
Lung and chestwall are
in a series
Understanding Stress and Strain
Clinical equivalents
Stress  PL transpulmonary pressure
Strain  VT / FRC
The linkage is the specific elastance
VT
PL = *
Elspec
Barotrauma
FRC
Volotrauma
Gastric balloon
Measured in some ventilators
Set by clinician
Compliance-Volume
change for a given pressure
change
Which pressures to Monitor?
Which Volumes to Monitor?
Functional Reserve Capacity
Total Lung Capacity
End Inspiratory Lung Volume
Lung and Chest wall
Pv= 30 cm H2O
25
5 for chest wall 20 for chest wall
10
The pressure to which alveoli is exposed!
Alveolar pressure
Pleural pressure
Transpulmonary
pressure- PL
Esophageal balloon
Main determinant of VILI
Pv= 30 cm H2O
Edema
Obesity
IAH
VT
PL = X
Elspec
FRC
Stress Strain
Intensity property
Capacitance property
PEEP Intensive
property =10
1500ml
500ml
Understanding stress & strain
Transpulmonary pressure -PL
(Pplat-Pleural pressure)
PL
PL
PL
Tidal volume
Tidal volume
Tidal volume
FRC
FRC
Stress
VT
FRC
Volotrauma
Strain
FRC
Compliance = % of baby lung
What can we use to provide LPV?
Use surrogates
Pplat < 28 to 30 cm H2O
Driving pressure < 15 cm H2O
Compliance FRC and TLC deduction
PL, FRC estimation
Pplat estimation in normal conditions
Lung and chest wall contribute 50% each
In ARDS lung may contribute 20% to 80%
Obesity BMI>28
Chest wall edema
Pplat> 30 cmH2O
Clinical equivalents
Stress  PL transpulmonary pressure
Strain  VT / FRC
The linkage is the specific elastance
VT
PL *
Elspec
Barotrauma
FRC
Volotrauma
12 to 13 cm H2O for human lung
=
500ml
500ml
Stress
750ml
MV in OT and in Normal Lungs
Tidal volume setting
6 to 8ml IBW
Height in cm - 100 in Male
Height in cm - 110 in female
I:E ratio
PEEP =5 cm H2O
Can be personalised looking at
Pplat and driving pressure
( Should be checked in every patient in OT)
Same tidal volume
7 to 12 PEEP
Pplat of less than 17
Driving pressure < 13
Recruitment Maneuver can be
done if required - BP
Ambu Bag RM not to be done
Use of NIV or HFNO before
intubation can be considered
High FiO2 without PEEP may not prevent Atelectasis
1
3
2
4
Volume in a cul-de-sac
(Alveoli)
Pressure changes
P Pplat
Pplat
End-inspiratory
Alveolar pressure
PIP
Inspiratory hold
PEEP
P Pplat- PEEP
Driving pressure Plateau pressure
(ΔP) =(Pplat – PEEP)
Most important button on your Ventilator
Start
breath
O2
breaths
Exp.
hold
Insp.
hold
!
Volume controlled mode
Passive patient
Inspiratory hold 1 to 2 seconds
Start
breath
O2
breaths
Exp.
hold
Insp.
hold
Main
screen
Menu
Quick
start
Alarm
profile
Save Trends
i
!
12-25 15:32
Mode
Volume Control
Automode
Admit
patient
Nebulizer Status
Additional
values
Set ventilation mode
Volume control V
Tidal volume
500
Resp. Rate
15
PEEP
8
O2 conc.
50
I:E
1:2.0
T. Pause
T. Insp. Rise
Trigger s.ensitivity
V
Cancel Accept
Ppeak
Pplat
30
24
RR 15
O2 50
Vee
I:E
0
1:2.0
MVe 7.0
MVi 7.5
VTi 501
VTe 471
PEEP
PIP
Pplat
resistance
flow
compliance
tidal volume
No active breathing
Treats lung as single unit
Chest wall???
End-inspiratory
Alveolar pressure
Transairway pressure
PIP-Pplat
D
R
I
V
I
N
G
P
R
E
S
S
U
R
E
Pplat
P= Pplt- PEEP
Vt / CRS
Insp
Hold
1-2 sec
Inspiratory hold 2-3sec
No flow state
Reflects End-inspiratory
Alveolar pressure
Plateau pressure should be < 30cm H20
Alveolar
pressure
Alveolar
pressure
Surrogates for LPV instead of PL and FRC
Pplat
PEEP
P= Pplat- PEEP
Maximum stress
Static stress
Stress Amplitude
Pplat=DP+ PEEP
DP= Pplat-PEEP
Compliance=VT/DP
P= is a surrogate for cyclical lung strain and parenchymal
deformation of the functional lung units ( BABY Lung)
Plateau pressure is the maximum static stain
DP is pressure applied for tidal volume delivery
Vt/ Crs-Is tidal volume appropriate for the Lung size
PEEP 5 cm H20 PEEP 10 cm H20
1
5
3
0
2
0
2
5
3
5
Pplat
27
Pplat
33
Pplat
23
Plateau pressure
Responders
Non-Responders
Over-distending alveolus
TNF,
IL-6
IL-6
Responders
Non-Responders
D
P
D
P
D
P
PIP vs Pplat
Normal High Raw
Low Compliance
Time (sec)
Paw
(cm
H
2
O)
PIP
PIP
PIP
PPlat
PPlat
PPlat
Normal compliance 100cm H2O
Ventilated patient 60 to 70 cm H20
50 to 40cm H20 mild lung injury
Less than 40 cm H20 moderate ARDS
Less than 30 cm H2O severe ARDS
Compliance numbers
Questions
How do we estimate Pplat?
What does it signify?
How do we calculate DP?
What does it mean to you?
How do you estimate compliance?
What does it tell you?
Volume controlled mode
Passive patient
Inspiratory hold 1 to 2 seconds
End inspiratory alveolar pressure
Pplat-PEEP
Pressure generated for
tidal volume generation
Tidal volume/ DP
Is lung compliant or stiff
Questions
C
R
Peak pressure – Pplat= Transairway
pressure will be increased
Pplat and DP
will be normal
Peak pressure – Pplat= Transairway
pressure will be normal
Pplat and DP will be raised
Case scenario-1
• Asthmatic for hemicolectomy after induction
• Peak pressure starts showing 42cm H2O
• Patient not getting ventilated desaturating?
• How do you proceed?
Pressure Relief (safety) valve- vents gas out once this pressure is
reached-10cm above PIP (usually set at 40 cm H2O)
DP 11
Insp Hold
1 To 2 seconds
Pplat
15
Ppeak
42
PEEP 4 cm H2O
Trans airway pressure?
42-15=27cm H2O
Bronchospasm
How do you manage?
after 2 hrs Ppeak
32 cm H2O
Ppeak
21 cm H2O
After 3 hrs
Case scenario-2
• DM,HT,IHD for amputation in the middle of the
surgery HR120/mt, EF 40%
• Peak pressures go up
• How do you evaluate the patient?
DP
Insp Hold
1 To 2 seconds
Pplat 28
Ppeak
32
PEEP 6 cm H2O
DP=28-6=22
Bilateral crepts
Pink frothy secretions
What is your diagnosis
Management?
TEE
Lasix
PEEP 12 cm H2O
After 2 hrs Pplat 18
Ppeak
25
Abruptio placenta 25 yr old primi taken for emergency surgery,
LSCS on GA after baby extraction uterus atony, PPH not
responding to drugs, plan for hysterectomy, requires lot of fluids and
noradrenaline till blood is organized, requires massive transfusion
DP
Insp Hold
1 To 2 seconds
Pplat 26
Ppeak
30
PEEP 10 cm H2O
DP=28-16
FIO2
I:E
VC/AVC Mode
VT
7ml/kg
PEEP
RR
50%
450ml
6
cmH2O
18/min
1:2
Ppeak
21
Fluid over load?
BP100/60mmHg
Lactate 2.5
How do we proceed
Case scenario-4
• 45 yr old obese lady with large incisional hernia under GA mesh repair
done
• Before abdomen closure After
• Peak Pressure 24cm H2O
• Pplat 18cm H20
• Compliance 65 cm H20
32cm H2O
27cm H20
45cm H2O
What do you do now before extubation?
Post extubation?
Increase PEEP
Increase FIO2
RM before extubation
Post extubation- HFNC/NIV
Spirometry / LMWH/ Close observation
ARDS PATIENT on ventilator
VT 7ml/kg, PEEP 14, FIO2 100%, I:E 1:2, RR 20
PEAK PRESSURE 38 cm H2O
Pplat- 32cm H2O, ABG pH7.29, pco2 58
PEEP 14
38 cm H2O
Insp
Hold
1-2sec
Pplat is 32 cm H2O
DP 32-14=18 cmH2O
Reduce Vt 6 to 5 ml/kg
watch Pplat 30 and DP 15
SPO2 90%
PCO2 55
pH 7.29
Next day morning
PEAK PRESSURE 33, Pplat 28cmH2O
you don't require ABG or a X-RAY
you know pco2 would be down, x-ray would be better
DP 18 cmH2O
Pplat=32 cmH2O
Minutes
SPO2/ ETCO2
Clinical examination
Ventilator parameters
See the chest
Hear the chest
VT / Ve /
RR
PIP
Pplat
U/S, X-ray, ABG
Plateau pressure in
Pressure control Modes
Start
breath
O2
breaths
Exp.
hold
Insp.
hold
Main
screen
Menu
Quick
start
Alarm
profile
Save Trends
i
!
12-25 15:32
Mode
Volume Control
Automode
Admit
patient
Nebulizer Status
Additional
values
Set ventilation mode
Pressure control P Ti =1.33 s (33%)
PC above PEEP
18
Resp. Rate
15
PEEP
5
O2 conc.
40
I:E
1:2.0
T. Insp. rise
5
Basic
I:E
Trigger
Trigger s.ensitivity
V
Cancel Accept
Pmax at
30 cm H2O
PC+ PEEP= Pplat
18+5= 23 cm H20
VC to PC mode
FIO2
I:E
PC/APC Mode
PC over
PEEP
PEEP
RR
50%
12
cmH2O
6
cmH2O
18/min
1:2
DP
Insp
Hold
Cs
Pplat Pplat
PC + PEEP=Pplat
PC-PEEP=DP
VT/ DP= 450/6= 75 cm H2O
FIO2
I:E
VC/AVC Mode
VT
7ml/kg
PEEP
RR
50%
450ml
6
cmH2O
18/min
1:2
DP 12
Insp
Hold
Cs 37.5
Pplat
24 18
12-6=6cm H2O
450 ml VT
It is important to understand
That no mode of MV is
Inherently Safer than
another,
as all can be provided
safely or not, -depends on
Which Mode is better?
Vigilance with which the
Caregiver Makes appropriate
adjustments in response to the
changing nature of the problem.
The alarms that place limits on
the process
Settings that the clinician selects
Pick the correct statements
1.Plateau pressure is estimated with a inspiratory hold
of 2 seconds in a passive patient with constant flow.
2. Pplat is a surrogate of end inspiratory alveolar
pressure.
3.Driving pressure is the difference between Pplat and
PEEP
4. Pplat also includes the chest wall component
5. In PCM Pplat= PC level + PEEP
Questions
How do we estimate Pplat?
What does it signify?
How do we calculate DP?
What does it mean to you?
How do you estimate compliance?
What does it tell you?
Volume controlled mode
Passive patient
Inspiratory hold 1 to 2 seconds
End inspiratory alveolar pressure
Pplat-PEEP
Pressure generated for
tidal volume generation
Tidal volume/ DP
Is lung compliant or stiff
The underlying Patho-physiology of respiratory diseases is
Dynamic - so should be the clinician and settings.
Alveoli is a cul-de-sac (closed space)
Pressure
Volume change for change in pressure is compliance
Which pressure should we monitor?
If volume is placed in a closed space what increases?
Which Alveoli will have more pressure
A
B
Peak pressures- both resistance and compliance
Plateau pressure < 30 cm H2O- End Insp Alveolar pressure
Driving pressure <15 cm H2O
Surrogates for LPV instead of PL and FRC
Pplat
PEEP
P= Pplat- PEEP
Maximum stress
Static stress
Stress Amplitude
Pplat=DP+ PEEP
DP= Pplat-PEEP
Compliance=VT/DP
P= is a surrogate for cyclical lung strain and parenchymal
deformation of the functional lung units ( BABY Lung)
Plateau pressure is the maximum static stain
DP is pressure applied for tidal volume delivery
Vt/ Crs-Is tidal volume appropriate for the Lung size
Air always travels in the path of least resistance……
AIR
Normal alveoli-over
distended-Volutrauma
Increased time constants
Stiff alveoli
May fill slowly & take less volume
What tidal volume ?
TNF, IL-6
Some facts about respiratory system
Base has more alveoli and has more super imposed pressure due to alveoli above it,
become more if lung weight due to Interstitial edema increases
Superimposed pressure
chestwall
Lung and chestwall are
in a series
Clinical equivalents
Stress  PL transpulmonary pressure
Strain  VT / FRC
The linkage is the specific elastance
VT
PL = *
Elspec
Barotrauma
FRC
Volotrauma
Gastric balloon
Measured in some ventilators
Set by clinician
Compliance-Volume
change for a given pressure
change
Which pressures to Monitor?
Which Volumes to Monitor?
Functional Reserve Capacity
Total Lung Capacity
End Inspiratory Lung Volume
Lung and Chest wall
Pv= 30 cm H2O
25
5 for chest wall 20 for chest wall
10
The pressure to which alveoli is exposed!
Alveolar pressure
Pleural pressure
Transpulmonary
pressure- PL
Esophageal balloon
Main determinant of VILI
Pv= 30 cm H2O
Edema
Obesity
IAH
The pressure to which alveoli is exposed!
Alveolar pressure
Pleural pressure
Transpulmonary
pressure- PL
Esophageal balloon
20 30
30
5
-15
20
PL= 20-5=15
PL= 30-(-15)=45
PL= 30-20=10
Stress and strain in the lung during
Mechanical ventilation
Pressure
Stress= Pressure(force) /Surface area
Pressure
In the context of MV- Pressure and Surface area
what should we consider?
PL
FRC
VT
PL = X
Elspec
FRC
Stress Strain
Intensity property
Capacitance property
PEEP Intensive
property =10
1500ml
500ml
VT
PL = X
Elspec
FRC
Stress
Strain
Intensity property
Capacitance property
PEEP
Intensive
property =10
Baby
lung
=1500
ml
Baby
lung
=500ml
PL Intensive property
Recruitment is a capacitive property
12cm
H2O
Understanding stress & strain
Transpulmonary pressure -PL
(Pplat-Pleural pressure)
PL
PL
PL
Tidal volume
Tidal volume
Tidal volume
FRC
FRC
Stress
VT
FRC
Volotrauma
Strain
F
R
C
F
R
C
F
R
C
FRC
DP
DP
DP
Baby lung size-Small
Compliance <30cm H20
Baby lung size-Medium
Compliance =50cm H20
Baby lung size-normal
Compliance =70cm H20
Force
Area-baby lung
Force
Force
Understanding stress & strain
Transpulmonary pressure -PL
(Pplat-Pleural pressure)
PL
PL
PL
Tidal volume
Tidal volume
Tidal volume
FRC
FRC
Stress
VT
FRC
Volotrauma
Strain
FRC
Relationship between stress and strain
Normal Lung
ARDS Lung
VT
FRC
VT
FRC
500ml
2000ml
500ml
500ml
=
=
0.25
=
=
1
If compliance is 20 cm
H2O
Add PEEP volume
with 15 PEEP=325ml
2.5 X FRC=
TLC
Relevant lung volumes
V
FRC
= Strain
TLC = 2.5 x FRC
VT
PEE
P
FRC
EELV
EILV
VT>
FRC
Volutrau
ma
Gattinoni.
Estimate compliance
Insp
Hold
1-2 sec
TIDAL VOLUME
P-plat-PEEP
Compliance %= % Lung FRC
Compliance 25 cm H2O Compliance 40 cm H2O
Baby lung will be 25% of
FRC
Normal FRC 2000ml
25% of 2000ml= 500ml
TLC=2 times FRC
TLC=2 x 500ml=1000
PEEP15 ,VT 400ml
Inspiratory Lung volume
FRC + PEEP volume + VT
500 +375ml +400ml= 1275ml
1275/1000= 1.275 strain
Baby lung will be 40% of
FRC
Normal FRC 2000ml
40% of 2000ml= 800ml
TLC=2 times FRC
TLC=2 x 800ml=1600
PEEP 12, VT 400ml
Inspiratory Lung volume
FRC + PEEP volume +
VT
800 +480ml +400ml=
1200ml
1680/1600= 1.05 strain
The underlying Patho-physiology of respiratory diseases is
Dynamic - so should be the clinician and settings.
Preoperative patient assessment
PPCs are a major cause of increased morbidity, length of stay, mortality, and
economic burden after surgical procedures, and are the most frequent
complication that has to be handled by the anaesthesiologist.1,2,6 For this reason,
it is useful to implement clinical scores in clinical practice, with the purpose of
stratifying risk, selecting patients that might benefit from a planned admission to
the ICU, and to identify potentially modifiable risk factors. There is still no single
universally accepted score able to predict the occurrence of PPCs, although several
have been recently proposed and validated. The Assess Respiratory Risk in Surgical
Patients in Catalonia (ARISCAT)3,7 and those proposed by Gupta et al.8 and
Arozullah et al.9 are the most used scores
Integrated multidisciplinary protocols applied before or after
surgery, based on early mobilization, chest physiotherapy,
semi-recumbent position, and coughing and deep breathing
exercises, seem to have advantages in terms of PPC
prevention.23
The panel agreed that the intraoperative ventilation strategy
should be guided by an awareness of the factors that pose the
greatest risk: age >50 yr, BMI >40 kg m2 , ASA physical status
>2, obstructive sleep apnoea, preoperative anaemia,
preoperative hypoxaemia, emergency or urgent surgery, and
ventilation duration >2 h
Intraoperative atelectasis, related changes in lung mechanics,
and postoperative pulmonary complications Atelectasis occurs
in roughly 90% of all patients undergoing general anaesthesia
and can persist for weeks after operation.18,19 Intraoperative
atelectasis results in decreased functional residual capacity
(FRC), increased heterogeneity of lung expansion, cyclic lung
overstress, and increased DP. DP is the pressure difference that
generates VT, and can be expressed as the ratio between VT
and respiratory system compliance (CRS).20 Lower
intraoperative DP values have been associated with a reduction
in PPCs,21,22 and high DP is considered a key mediator of lung
injury during positive-pressure ventilation.23 Therefore,
intraoperative ventilation that avoids derecruitment without
causing over-distension of alveoli may decrease postoperative
pulmonary risk by improving perioperative oxygenation and
respiratory mechanics,3,24,25 and reducing oxidative stress,
inflammatory response, and lung injury.26,2
A dedicated score should be used for risk evaluation. The greatest risk factors for PPCs include age >50 yr, BMI >40 kg m2 , AS
>2, OSA, preoperative anaemia, preoperative hypoxaemia, emergency or urgent surgery, ventilation duration >2 h, and
intraoperative factors (such as haemodynamic impairment and low oxyhaemoglobin saturation)
Use a low-tidal-volume protective-ventilation strategy (6-8 ml kg PBW). ZEEP is not recommended. Appropriate PEEP and
recruitment manoeuvres may improve intraoperative Respiratory function and prevent PPCs.
The formation of perioperative clinically significant atelectasis may be an important risk factor for the development of PPC
Individualised mechanical ventilation should be used and may improve intraoperative respiratory function, but the beneficia
effects are likely to disappear after extubation
The ventilator should initially be set to deliver VT LESS THAN EQUAL TO 6-8 ml/ kg PBW
and PEEP=5 cm H2O. Evidence regarding I:E ratio settings is lacking.
EEP should be individualised to the patient in order to avoid
increases in driving pressure (PplatePEEP) whilst maintaining a
low VT. To optimise intraoperative respiratory function in obese
patients, during pneumoperitoneum insufflation, and during
prone or Trendelenburg positioning, PEEP adjustment may be
required
Before induction of anaesthesia, position the patient with the
HOB elevated 30 deg (i.e. ‘beach chair’); avoid flat supine
position. If not contraindicated, before the loss of spontaneous
ventilation, use NIPPV or CPAP to attenuate anaesthesia-
induced respiratory changes
During induction, monitor for an obstructive breathing pattern
and use a combination of appropriate techniques, including
positioning, application of NIPPV or CPAP, or placement of a
nasopharyngeal airway to avoid upper airway obstruction
After intubation, FIO2 should be set to <0.4. Thereafter, use the
lowest possible FIO2 to achieve SpO2 >94%
No specific mode of controlled mechanical ventilation is
recommended
In addition to standard monitoring (ASA/ESA), dynamic
compliance, driving pressure (PplatePEEP), and Pplat should be
monitored on all controlled mechanically ventilated patients.
Decreasing compliance caused by surgical/ anaesthesia factors
(i.e. pneumoperitoneum, positioning, and circuit disconnect)
should be treated by appropriate interventions. Individualised
PEEP can prevent progressive alveolar collapse. Recruitment
manoeuvres can reverse alveolar collapse, but have limited
benefit without sufficient PEEP. Statement: Increasing FIO2 may
be effective in increasing the oxygenation, but is not an
effective intervention to improve dynamic compliance of the
respiratory system. The effectiveness of interventions aimed at
optimising respiratory system mechanics should be evaluated
by measuring an improvement of the respiratory system
compliance under a constant tidal volume
High-quality supportive evidence is lacking to recommend a
routine ARM for all patients after tracheal intubation. However,
an ARM may be considered according to an individual
riskebenefit assessment
The bag-squeezing ARM should be avoided in favour of a
ventilator-driven ARM
ARMs should be performed using the lowest effective Pplat (30
-40 cm H2O in non-obese; 40-50 cm H2O in obese) and
shortest effective time or fewest number of breaths
Continuous haemodynamic and oxygen saturation monitoring
is recommended before and during an ARM. Ensure adequate
haemodynamic stability before performing an ARM. Avoid
ARMs when contraindicated
PEEP should be individualised after an ARM to avoid both
alveolar overdistention and collapse.
Optimise patient positioning and avoid ZEEP during emergence.
Avoid tracheal tube suctioning immediately before tracheal
extubation.
Avoid apnoea with ZEEP before extubation
Prophylactic NIPPV/CPAP should be considered after operation
for patients with prior routine use of NIPPV/ CPAP
Administration of postoperative supplemental oxygen is
recommended when room air SpO2 decreases below 94%.
Avoid routine application of supplemental oxygen without
investigating and treating the underlying cause.
When high FIO2 (>0.8) is used during emergence, the use of low FIO2 (,0.4 WITH
CPAP P immediately after tracheal extubation may reduce the risk of resorption
atelectasis.
In the appropriate clinical scenario, the use of low FIO2 (<0.4) during emergence from general anaesthesia
can improve pulmonary function in the postoperative period
Moderate- to high-quality recommendations with strong expert support: The ventilator should
initially be set to deliver VT 6e8 ml kge1 PBW and PEEP>5 cm H2O. ZEEP is not recommended.
Appropriate PEEP and recruitment manoeuvres may improve intraoperative respiratory function
and prevent PPCs. Before the induction of anaesthesia, position the patient with the HOB
elevated 30 deg (i.e. ‘beach chair’); avoid flat supine position. If not contraindicated, before the
loss of spontaneous ventilation, use NIPPV or CPAP to attenuate anaesthesiainduced respiratory
changes. In addition to standard monitoring (ASA/ESA), dynamic compliance, driving pressure
(PplatePEEP), and Pplat should be monitored on all controlled mechanically ventilated patients.
Continuous haemodynamic and oxygen saturation monitoring is recommended before and
during an ARM. Ensure adequate haemodynamic stability before performing an ARM. Avoid
ARMs when contraindicated. Moderate- to high-quality statements with strong expert support:
The formation of perioperative clinically significant atelectasis may be an important risk factor
for the development of PPCs. Decreasing compliance caused by surgical/anaesthesia factors
(i.e. pneumoperitoneum, positioning, and circuit disconnect) should be treated by appropriate
interventions. Individualised PEEP can prevent progressive alveolar collapse. Recruitment
manoeuvres can reverse alveolar collapse, but have limited benefit without sufficient PEEP.
Increasing FIO2 may be effective in increasing the oxygenation, but is not an effective
intervention to improve dynamic compliance of the respiratory system
More than 230 million major surgical procedures are undertaken each year worldwide [1] and postoperative
complications imposed a significant clinical and economic burden to surgical patients as well as the public health
systems [2, 3]. Postoperative pulmonary complications (PPCs) are common postoperative complications that
occur in 2% to 40% of patients and are associated with increased morbidity, mortality, and length of stay (LOS)
[3–9]. In noncardiac patients, PPCs occur more frequently than cardiac complications [10]. Though it came to
wide attention in recent years, the literature investigating the incidence and outcome of PPCs in Chinese
inpatients remains scarce.
It is known that PPCs have a multifactorial etiology and had been defined broadly, including respiratory tract
infection, pneumonia, respiratory failure, atelectasis, pleural effusion, pneumothorax, bronchospasm, and
aspiration pneumonitis [11]. Previous studies demonstrated that PPCs were associated with a series of
perioperative risk factors, such as age, smoking, chronic obstructive pulmonary disease (COPD), type of surgery,
and serum albumin [4, 6, 7, 11–14]. A majority of these risk factors can be intervened and improved [15–17].
Therefore, identifying perioperative risk factors of PPCs is an important step toward improving quality of care in
surgical patients, which has been already explored in several studies [11, 12, 18].
Development and validation of a score to predict postoperati
respiratory failure in
a multicentre European cohort
Canet J et al. Eur J Anaesthesio.l 2015; 32:1–13 [Epub ahead of print]
POST-OPERATIVE RESPIRATORY FAILURE
New-onset hypoxaemia appearing within 5
postoperative days at three levels of severity:
- Mild (PaO2 < 60 mmHg or SpO2 < 90% on room
air but responding to mask/nasal supplemental
oxygen);
- Moderate (noninvasive or invasive mechanical
ventilation to treat a PaO2 < 60 mmHg or SpO2 <
90%);
- Severe (invasive MV to manage a PaO /FiO 200
Severgnini and colleagues (2013)65 Initial setting: 7 ml kg1 IBW,
RR 6 min1 , PEEP 10 cm H2O, I:E ratio 3:1 VT increased in steps
of 4 ml kg1 IBW until plateau pressure 30 cm H2O for three
breaths Settings returned to original, with PEEP maintained at
10 cm H2O Futier and colleagues (2013)66 CPAP 30 cm H2O for
30 s Treschan and colleagues (2012)108 Three manual bag
ventilations with a maximal pressure of 40 cm H2O before
extubation Weingarten and colleagues (2010)109 Three-step
increase in PEEP: 4–10 cm H2O for three breaths 10–15 cm
H2O for three breaths 15–20 cm H2O for 10 breaths PEEP
reduced and maintained at 12 cm H2O Repeated 30 and 60 min
after the first RM and hourly thereafter
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How do I safely ventilate my patient inOT.pptx

  • 1. Dr. T.R.Chandrashekar Prof and H.O.D Department of Critical Care Medicine Institute of Gastrointestinal diseases and organ Transplant (IGOT), Bangalore. How do I safely ventilate my patient in OT ?
  • 2. Some facts about respiratory system Base has more alveoli and has more super imposed pressure due to alveoli above it, become more if lung weight due to Interstitial edema increases Superimposed pressure chestwall Lung and chestwall are in a series
  • 3. In OT Why do we ventilate patients undergoing surgery? Patients choice Surgery warrant GA Normal Lungs? GA in supine position Cephalad movement of Diaphragm- basal atelectasis Laparoscopy –Pneumoperitoneum Reverse Trendelenburg position Large hernia surgeries
  • 4. Do patients always have normal lungs? 40 yr old farmer with 4 day old small bowel perforation, peritonitis with sepsis on noradrenaline, abdomen tense, SPO2 95% of 15L O2 NRM with bag, RR 29/min HR 110/min, BP100/60mm Hg, lactate 1.8mmol/L, restless posted for emergency laparotomy and procedure. UO adequate. Abruptio placenta 25 yr old primi taken for emergency surgery, LSCS on GA after baby extraction uterus atony, PPH not responding to drugs, plan for hysterectomy, requires lot of fluids and noradrenaline till blood is organized, requires massive transfusion Is this patient more prone to PPC? How do we ventilate this patient?
  • 5. Mechanical ventilation is a lung support system Is not a treatment for any disease Mechanical ventilation causes harm - VALI or Physician associated Lung injury Permissible atelectasis - close the Lung and allow it to rest Lung collapse is not always detrimental. Recent data suggest -“partial recruitment” better protects the lung from VILI compared to “full recruitment”. Reset Physiological Goal posts in your head Open Just enough lung- to have Adequate OXYGEN in blood for the patient to survive- SPO2 of 86% to 92% Pursuit ofbetteroxygenation atthecostofVILIleadsto GoodABG andaDeadpatient?
  • 6. The goal in any sick patient is to optimise Oxygen delivery into Microcirculation and use in cell Mitochondria O2 CO 2 Intra thoracic pressure Decreased Preload Cardiac compression Decreased Cardiac output Do2= Oxygen content X CO O2 delivery to mitochondria is a Cardio-Respiratory function
  • 7. There is evidence that large VT, low PEEP and High FIo2 lead to post op Complications
  • 8. •Postoperative pulmonary complications (PPCs) are pulmonary abnormalities that result in identifiable disease or dysfunction and adversely affect the patient's clinical outcome. ••PPCs play a significant role in patient morbidity, mortality, and length of stay in hospital. •Perioperative strategies for prevention and management could improve patient outcomes. Anaesthetists are well placed to implement these. ••Preoperative strategies include optimizing cardiorespiratory disease, early smoking cessation, and prehabilitation exercise programmes. ••Intraoperative strategies include shorter duration of surgery, judicious and monitored use of neuromuscular blocking agents, and lung protective ventilation. ••Postoperative strategies include effective analgesia, early mobilization, and lung expansion techniques.
  • 9. What are the problems encountered in MV under GA? Postoperative pulmonary complications (PPCs) What are PPCs? Definition / incidence How doe recognize them pre-operatively? Management? Intra-operative management—Including induction/Emergence Postoperative management
  • 10. Intraoperative risk factors Changes in pulmonary physiology GA in supine position Cephalad movement of Diaphragm- basal atelectasis Laparoscopy –Pneumoperitoneum Reverse Trendelenburg position Large hernia surgeries Anaesthetic agents diminish respiratory drive and the response to hypoxia and hypercapnia, resulting in hypoventilation ventilation–perfusion mismatching and increased shunt fraction. Prolonged periods of 100% oxygen may produce absorption atelectasis as all the oxygen is absorbed and the splinting effect of nitrogen in the alveoli is lost. Following surgery, particularly abdominal and thoracic, pain may limit respiratory excursion and cause splinting of the diaphragm, further reducing FRC and vital capacity The effects of anaesthesia, bed rest, and opioids inhibit the cough reflex and impair respiratory tract ciliary activity, while dry gases result in mucus plugging. These physiological effects contribute to the development of PPCs. Anaesthetic factors NMB- inadequate reversal/sedation
  • 11. surgical factors The surgical site and the duration of surgery (>3 h) influence the risk of developing PPCs.1 Prolonged surgery and anaesthesia alters immune defence and gas exchange capacity by depressing alveolar macrophage function, interfering with surfactant production, slowing mucociliary clearance, and increasing the permeability of the alveolar–capillary barrier. Abdominal and thoracic and head and neck surgeries are the most likely to interfere with respiratory function and are strongly linked to PPCs, particularly in the context of tissue trauma, fluid shifts, and blood transfusion. Other types of surgery associated with increased risk of PPCs include neurosurgery, with a likely reason being reduced conscious level and the associated risk of aspiration. Vascular and emergency surgeries are also associated, perhaps because of the higher risk patient cohort. Peripheral and orthopaedic procedures are considered to be lower risk for PPCs.
  • 12. Definition of PPCs Jammer I et al. Eur J Anaesthesiol. 2015;32:88-105 Mazo V et al. Anesthesiology. 2014Aug;121(2):219-31 Canet J et al. Eur J Anaesthesiol. 2015; 32:1–13 [Epub ahead of print]  Primary outcome (composite)  Respiratory insufficiency  Bronchospasm  Pleural effusion  Respiratory infection  Atelectasis  Aspiration pneumonitis  Pneumothorax
  • 13. Strategies to prevent postoperative pulmonary complications Guldner A, Pelosi P,de Abreu GM Curr Opin Anesthesiol 2013,26:141–151 Preoperatively • Assess general physical status and identify risk factors - Risk Scores – Preoperative SpO2 • Preoperative “optimization” – Cessation of smoking – Treat pre-op infection and/or bronchospasm – Alleviate anemia (< 10 g/dL) (?) • Education regarding physiotherapy
  • 14. Intraoperativel y • Anaesthetic/surgical plan – Consider regional anesthesia for pain control – Choose short-acting drugs/avoid PORC (monitoring) – Limit duration of surgery and fluids - GDT – If feasible, use laparoscopic techniques – Reduce emergent surgery • Ventilatory strategies – Protective ventilation (Low tidal volume 6-8 ml/kg IBW) Strategies to prevent postoperative pulmonary complications Guldner A, Pelosi P,de Abreu GM Curr Opin Anesthesiol 2013,26:141–151
  • 15. Strategies to prevent postoperative pulmonary complications Guldner A, Pelosi P,de Abreu GM Curr Opin Anesthesiol 2013,26:141–151 Postoperatively • Selective use of nasogastric tube - If PONV - Inability to oral feeding - Abdominal distension • Effective pain management and minimize respiratory depression • Post-op Physiotherapy and/or NRS - Early ambulation - Mobilization of secretions - Deep breathing (Incentive spirometry?) - CPAP/NPPV
  • 16. Ventilator-Induced Lung Injury Slutsky AS & Ranieri VM N Engl J Med 2013;369:2126-36
  • 17. Perioperative Positive Pressure Ventilation An Integrated Approach to Improve Pulmonary Care Futier E., Marret E., Jaber S. Anesthesiology 2014;121:400–8
  • 18. LAS VEGAS – Intraoperative Ventilation Settings 9,682 patients - 38 countries - 146 centers • VT = 500 [455–557]ml • VT = 8.1 [7.3–9.1] ml/kg PBW • PEEP = 3.5 [0–5] cm H2O • < 2 cm H2O – 32% • 2–5 cm H2O – 60% • < 10% RM LOW VT – LOW PEEP – NO RMs ! Schultz M, Hemmes S, Abreu GM , Pelosi P for the PROVEnet and LAS VEGAS investigators
  • 19. Some facts about respiratory system Base has more alveoli and has more super imposed pressure due to alveoli above it, become more if lung weight due to Interstitial edema increases Superimposed pressure chestwall Lung and chestwall are in a series
  • 21. Clinical equivalents Stress  PL transpulmonary pressure Strain  VT / FRC The linkage is the specific elastance VT PL = * Elspec Barotrauma FRC Volotrauma Gastric balloon Measured in some ventilators Set by clinician
  • 22. Compliance-Volume change for a given pressure change Which pressures to Monitor? Which Volumes to Monitor? Functional Reserve Capacity Total Lung Capacity End Inspiratory Lung Volume
  • 23. Lung and Chest wall Pv= 30 cm H2O 25 5 for chest wall 20 for chest wall 10 The pressure to which alveoli is exposed! Alveolar pressure Pleural pressure Transpulmonary pressure- PL Esophageal balloon Main determinant of VILI Pv= 30 cm H2O Edema Obesity IAH
  • 24. VT PL = X Elspec FRC Stress Strain Intensity property Capacitance property PEEP Intensive property =10 1500ml 500ml
  • 25. Understanding stress & strain Transpulmonary pressure -PL (Pplat-Pleural pressure) PL PL PL Tidal volume Tidal volume Tidal volume FRC FRC Stress VT FRC Volotrauma Strain FRC
  • 26. Compliance = % of baby lung
  • 27. What can we use to provide LPV? Use surrogates Pplat < 28 to 30 cm H2O Driving pressure < 15 cm H2O Compliance FRC and TLC deduction PL, FRC estimation Pplat estimation in normal conditions Lung and chest wall contribute 50% each In ARDS lung may contribute 20% to 80% Obesity BMI>28 Chest wall edema Pplat> 30 cmH2O
  • 28. Clinical equivalents Stress  PL transpulmonary pressure Strain  VT / FRC The linkage is the specific elastance VT PL * Elspec Barotrauma FRC Volotrauma 12 to 13 cm H2O for human lung = 500ml 500ml Stress 750ml
  • 29.
  • 30. MV in OT and in Normal Lungs Tidal volume setting 6 to 8ml IBW Height in cm - 100 in Male Height in cm - 110 in female I:E ratio PEEP =5 cm H2O Can be personalised looking at Pplat and driving pressure ( Should be checked in every patient in OT) Same tidal volume 7 to 12 PEEP Pplat of less than 17 Driving pressure < 13 Recruitment Maneuver can be done if required - BP Ambu Bag RM not to be done Use of NIV or HFNO before intubation can be considered High FiO2 without PEEP may not prevent Atelectasis 1 3 2 4
  • 31. Volume in a cul-de-sac (Alveoli) Pressure changes P Pplat Pplat End-inspiratory Alveolar pressure PIP Inspiratory hold PEEP P Pplat- PEEP Driving pressure Plateau pressure (ΔP) =(Pplat – PEEP)
  • 32. Most important button on your Ventilator Start breath O2 breaths Exp. hold Insp. hold ! Volume controlled mode Passive patient Inspiratory hold 1 to 2 seconds
  • 33. Start breath O2 breaths Exp. hold Insp. hold Main screen Menu Quick start Alarm profile Save Trends i ! 12-25 15:32 Mode Volume Control Automode Admit patient Nebulizer Status Additional values Set ventilation mode Volume control V Tidal volume 500 Resp. Rate 15 PEEP 8 O2 conc. 50 I:E 1:2.0 T. Pause T. Insp. Rise Trigger s.ensitivity V Cancel Accept Ppeak Pplat 30 24 RR 15 O2 50 Vee I:E 0 1:2.0 MVe 7.0 MVi 7.5 VTi 501 VTe 471
  • 34. PEEP PIP Pplat resistance flow compliance tidal volume No active breathing Treats lung as single unit Chest wall??? End-inspiratory Alveolar pressure Transairway pressure PIP-Pplat D R I V I N G P R E S S U R E Pplat P= Pplt- PEEP Vt / CRS Insp Hold 1-2 sec
  • 35. Inspiratory hold 2-3sec No flow state Reflects End-inspiratory Alveolar pressure Plateau pressure should be < 30cm H20 Alveolar pressure Alveolar pressure
  • 36. Surrogates for LPV instead of PL and FRC Pplat PEEP P= Pplat- PEEP Maximum stress Static stress Stress Amplitude Pplat=DP+ PEEP DP= Pplat-PEEP Compliance=VT/DP P= is a surrogate for cyclical lung strain and parenchymal deformation of the functional lung units ( BABY Lung) Plateau pressure is the maximum static stain DP is pressure applied for tidal volume delivery Vt/ Crs-Is tidal volume appropriate for the Lung size
  • 37. PEEP 5 cm H20 PEEP 10 cm H20 1 5 3 0 2 0 2 5 3 5 Pplat 27 Pplat 33 Pplat 23 Plateau pressure Responders Non-Responders Over-distending alveolus TNF, IL-6 IL-6 Responders Non-Responders D P D P D P
  • 38. PIP vs Pplat Normal High Raw Low Compliance Time (sec) Paw (cm H 2 O) PIP PIP PIP PPlat PPlat PPlat
  • 39. Normal compliance 100cm H2O Ventilated patient 60 to 70 cm H20 50 to 40cm H20 mild lung injury Less than 40 cm H20 moderate ARDS Less than 30 cm H2O severe ARDS Compliance numbers
  • 40. Questions How do we estimate Pplat? What does it signify? How do we calculate DP? What does it mean to you? How do you estimate compliance? What does it tell you? Volume controlled mode Passive patient Inspiratory hold 1 to 2 seconds End inspiratory alveolar pressure Pplat-PEEP Pressure generated for tidal volume generation Tidal volume/ DP Is lung compliant or stiff
  • 41. Questions C R Peak pressure – Pplat= Transairway pressure will be increased Pplat and DP will be normal Peak pressure – Pplat= Transairway pressure will be normal Pplat and DP will be raised
  • 42. Case scenario-1 • Asthmatic for hemicolectomy after induction • Peak pressure starts showing 42cm H2O • Patient not getting ventilated desaturating? • How do you proceed? Pressure Relief (safety) valve- vents gas out once this pressure is reached-10cm above PIP (usually set at 40 cm H2O) DP 11 Insp Hold 1 To 2 seconds Pplat 15 Ppeak 42 PEEP 4 cm H2O Trans airway pressure? 42-15=27cm H2O Bronchospasm How do you manage? after 2 hrs Ppeak 32 cm H2O Ppeak 21 cm H2O After 3 hrs
  • 43. Case scenario-2 • DM,HT,IHD for amputation in the middle of the surgery HR120/mt, EF 40% • Peak pressures go up • How do you evaluate the patient? DP Insp Hold 1 To 2 seconds Pplat 28 Ppeak 32 PEEP 6 cm H2O DP=28-6=22 Bilateral crepts Pink frothy secretions What is your diagnosis Management? TEE Lasix PEEP 12 cm H2O After 2 hrs Pplat 18 Ppeak 25
  • 44. Abruptio placenta 25 yr old primi taken for emergency surgery, LSCS on GA after baby extraction uterus atony, PPH not responding to drugs, plan for hysterectomy, requires lot of fluids and noradrenaline till blood is organized, requires massive transfusion DP Insp Hold 1 To 2 seconds Pplat 26 Ppeak 30 PEEP 10 cm H2O DP=28-16 FIO2 I:E VC/AVC Mode VT 7ml/kg PEEP RR 50% 450ml 6 cmH2O 18/min 1:2 Ppeak 21 Fluid over load? BP100/60mmHg Lactate 2.5 How do we proceed
  • 45. Case scenario-4 • 45 yr old obese lady with large incisional hernia under GA mesh repair done • Before abdomen closure After • Peak Pressure 24cm H2O • Pplat 18cm H20 • Compliance 65 cm H20 32cm H2O 27cm H20 45cm H2O What do you do now before extubation? Post extubation? Increase PEEP Increase FIO2 RM before extubation Post extubation- HFNC/NIV Spirometry / LMWH/ Close observation
  • 46. ARDS PATIENT on ventilator VT 7ml/kg, PEEP 14, FIO2 100%, I:E 1:2, RR 20 PEAK PRESSURE 38 cm H2O Pplat- 32cm H2O, ABG pH7.29, pco2 58 PEEP 14 38 cm H2O Insp Hold 1-2sec Pplat is 32 cm H2O DP 32-14=18 cmH2O Reduce Vt 6 to 5 ml/kg watch Pplat 30 and DP 15 SPO2 90% PCO2 55 pH 7.29 Next day morning PEAK PRESSURE 33, Pplat 28cmH2O you don't require ABG or a X-RAY you know pco2 would be down, x-ray would be better DP 18 cmH2O Pplat=32 cmH2O
  • 47. Minutes SPO2/ ETCO2 Clinical examination Ventilator parameters See the chest Hear the chest VT / Ve / RR PIP Pplat U/S, X-ray, ABG
  • 49. Start breath O2 breaths Exp. hold Insp. hold Main screen Menu Quick start Alarm profile Save Trends i ! 12-25 15:32 Mode Volume Control Automode Admit patient Nebulizer Status Additional values Set ventilation mode Pressure control P Ti =1.33 s (33%) PC above PEEP 18 Resp. Rate 15 PEEP 5 O2 conc. 40 I:E 1:2.0 T. Insp. rise 5 Basic I:E Trigger Trigger s.ensitivity V Cancel Accept Pmax at 30 cm H2O PC+ PEEP= Pplat 18+5= 23 cm H20
  • 50. VC to PC mode FIO2 I:E PC/APC Mode PC over PEEP PEEP RR 50% 12 cmH2O 6 cmH2O 18/min 1:2 DP Insp Hold Cs Pplat Pplat PC + PEEP=Pplat PC-PEEP=DP VT/ DP= 450/6= 75 cm H2O FIO2 I:E VC/AVC Mode VT 7ml/kg PEEP RR 50% 450ml 6 cmH2O 18/min 1:2 DP 12 Insp Hold Cs 37.5 Pplat 24 18 12-6=6cm H2O 450 ml VT
  • 51. It is important to understand That no mode of MV is Inherently Safer than another, as all can be provided safely or not, -depends on Which Mode is better? Vigilance with which the Caregiver Makes appropriate adjustments in response to the changing nature of the problem. The alarms that place limits on the process Settings that the clinician selects
  • 52. Pick the correct statements 1.Plateau pressure is estimated with a inspiratory hold of 2 seconds in a passive patient with constant flow. 2. Pplat is a surrogate of end inspiratory alveolar pressure. 3.Driving pressure is the difference between Pplat and PEEP 4. Pplat also includes the chest wall component 5. In PCM Pplat= PC level + PEEP
  • 53. Questions How do we estimate Pplat? What does it signify? How do we calculate DP? What does it mean to you? How do you estimate compliance? What does it tell you? Volume controlled mode Passive patient Inspiratory hold 1 to 2 seconds End inspiratory alveolar pressure Pplat-PEEP Pressure generated for tidal volume generation Tidal volume/ DP Is lung compliant or stiff
  • 54. The underlying Patho-physiology of respiratory diseases is Dynamic - so should be the clinician and settings.
  • 55. Alveoli is a cul-de-sac (closed space) Pressure Volume change for change in pressure is compliance Which pressure should we monitor? If volume is placed in a closed space what increases? Which Alveoli will have more pressure A B Peak pressures- both resistance and compliance Plateau pressure < 30 cm H2O- End Insp Alveolar pressure Driving pressure <15 cm H2O
  • 56. Surrogates for LPV instead of PL and FRC Pplat PEEP P= Pplat- PEEP Maximum stress Static stress Stress Amplitude Pplat=DP+ PEEP DP= Pplat-PEEP Compliance=VT/DP P= is a surrogate for cyclical lung strain and parenchymal deformation of the functional lung units ( BABY Lung) Plateau pressure is the maximum static stain DP is pressure applied for tidal volume delivery Vt/ Crs-Is tidal volume appropriate for the Lung size
  • 57. Air always travels in the path of least resistance…… AIR Normal alveoli-over distended-Volutrauma Increased time constants Stiff alveoli May fill slowly & take less volume What tidal volume ? TNF, IL-6
  • 58. Some facts about respiratory system Base has more alveoli and has more super imposed pressure due to alveoli above it, become more if lung weight due to Interstitial edema increases Superimposed pressure chestwall Lung and chestwall are in a series
  • 59. Clinical equivalents Stress  PL transpulmonary pressure Strain  VT / FRC The linkage is the specific elastance VT PL = * Elspec Barotrauma FRC Volotrauma Gastric balloon Measured in some ventilators Set by clinician
  • 60. Compliance-Volume change for a given pressure change Which pressures to Monitor? Which Volumes to Monitor? Functional Reserve Capacity Total Lung Capacity End Inspiratory Lung Volume
  • 61. Lung and Chest wall Pv= 30 cm H2O 25 5 for chest wall 20 for chest wall 10 The pressure to which alveoli is exposed! Alveolar pressure Pleural pressure Transpulmonary pressure- PL Esophageal balloon Main determinant of VILI Pv= 30 cm H2O Edema Obesity IAH
  • 62. The pressure to which alveoli is exposed! Alveolar pressure Pleural pressure Transpulmonary pressure- PL Esophageal balloon 20 30 30 5 -15 20 PL= 20-5=15 PL= 30-(-15)=45 PL= 30-20=10
  • 63. Stress and strain in the lung during Mechanical ventilation Pressure Stress= Pressure(force) /Surface area Pressure In the context of MV- Pressure and Surface area what should we consider? PL FRC
  • 64. VT PL = X Elspec FRC Stress Strain Intensity property Capacitance property PEEP Intensive property =10 1500ml 500ml
  • 65. VT PL = X Elspec FRC Stress Strain Intensity property Capacitance property PEEP Intensive property =10 Baby lung =1500 ml Baby lung =500ml PL Intensive property Recruitment is a capacitive property 12cm H2O
  • 66. Understanding stress & strain Transpulmonary pressure -PL (Pplat-Pleural pressure) PL PL PL Tidal volume Tidal volume Tidal volume FRC FRC Stress VT FRC Volotrauma Strain F R C F R C F R C FRC DP DP DP Baby lung size-Small Compliance <30cm H20 Baby lung size-Medium Compliance =50cm H20 Baby lung size-normal Compliance =70cm H20 Force Area-baby lung Force Force
  • 67. Understanding stress & strain Transpulmonary pressure -PL (Pplat-Pleural pressure) PL PL PL Tidal volume Tidal volume Tidal volume FRC FRC Stress VT FRC Volotrauma Strain FRC
  • 68. Relationship between stress and strain Normal Lung ARDS Lung VT FRC VT FRC 500ml 2000ml 500ml 500ml = = 0.25 = = 1 If compliance is 20 cm H2O Add PEEP volume with 15 PEEP=325ml 2.5 X FRC= TLC
  • 69. Relevant lung volumes V FRC = Strain TLC = 2.5 x FRC VT PEE P FRC EELV EILV VT> FRC Volutrau ma Gattinoni.
  • 70. Estimate compliance Insp Hold 1-2 sec TIDAL VOLUME P-plat-PEEP Compliance %= % Lung FRC Compliance 25 cm H2O Compliance 40 cm H2O Baby lung will be 25% of FRC Normal FRC 2000ml 25% of 2000ml= 500ml TLC=2 times FRC TLC=2 x 500ml=1000 PEEP15 ,VT 400ml Inspiratory Lung volume FRC + PEEP volume + VT 500 +375ml +400ml= 1275ml 1275/1000= 1.275 strain Baby lung will be 40% of FRC Normal FRC 2000ml 40% of 2000ml= 800ml TLC=2 times FRC TLC=2 x 800ml=1600 PEEP 12, VT 400ml Inspiratory Lung volume FRC + PEEP volume + VT 800 +480ml +400ml= 1200ml 1680/1600= 1.05 strain
  • 71. The underlying Patho-physiology of respiratory diseases is Dynamic - so should be the clinician and settings.
  • 72.
  • 73.
  • 74. Preoperative patient assessment PPCs are a major cause of increased morbidity, length of stay, mortality, and economic burden after surgical procedures, and are the most frequent complication that has to be handled by the anaesthesiologist.1,2,6 For this reason, it is useful to implement clinical scores in clinical practice, with the purpose of stratifying risk, selecting patients that might benefit from a planned admission to the ICU, and to identify potentially modifiable risk factors. There is still no single universally accepted score able to predict the occurrence of PPCs, although several have been recently proposed and validated. The Assess Respiratory Risk in Surgical Patients in Catalonia (ARISCAT)3,7 and those proposed by Gupta et al.8 and Arozullah et al.9 are the most used scores
  • 75. Integrated multidisciplinary protocols applied before or after surgery, based on early mobilization, chest physiotherapy, semi-recumbent position, and coughing and deep breathing exercises, seem to have advantages in terms of PPC prevention.23
  • 76. The panel agreed that the intraoperative ventilation strategy should be guided by an awareness of the factors that pose the greatest risk: age >50 yr, BMI >40 kg m2 , ASA physical status >2, obstructive sleep apnoea, preoperative anaemia, preoperative hypoxaemia, emergency or urgent surgery, and ventilation duration >2 h
  • 77. Intraoperative atelectasis, related changes in lung mechanics, and postoperative pulmonary complications Atelectasis occurs in roughly 90% of all patients undergoing general anaesthesia and can persist for weeks after operation.18,19 Intraoperative atelectasis results in decreased functional residual capacity (FRC), increased heterogeneity of lung expansion, cyclic lung overstress, and increased DP. DP is the pressure difference that generates VT, and can be expressed as the ratio between VT and respiratory system compliance (CRS).20 Lower intraoperative DP values have been associated with a reduction in PPCs,21,22 and high DP is considered a key mediator of lung injury during positive-pressure ventilation.23 Therefore, intraoperative ventilation that avoids derecruitment without causing over-distension of alveoli may decrease postoperative pulmonary risk by improving perioperative oxygenation and respiratory mechanics,3,24,25 and reducing oxidative stress, inflammatory response, and lung injury.26,2
  • 78. A dedicated score should be used for risk evaluation. The greatest risk factors for PPCs include age >50 yr, BMI >40 kg m2 , AS >2, OSA, preoperative anaemia, preoperative hypoxaemia, emergency or urgent surgery, ventilation duration >2 h, and intraoperative factors (such as haemodynamic impairment and low oxyhaemoglobin saturation) Use a low-tidal-volume protective-ventilation strategy (6-8 ml kg PBW). ZEEP is not recommended. Appropriate PEEP and recruitment manoeuvres may improve intraoperative Respiratory function and prevent PPCs. The formation of perioperative clinically significant atelectasis may be an important risk factor for the development of PPC Individualised mechanical ventilation should be used and may improve intraoperative respiratory function, but the beneficia effects are likely to disappear after extubation The ventilator should initially be set to deliver VT LESS THAN EQUAL TO 6-8 ml/ kg PBW and PEEP=5 cm H2O. Evidence regarding I:E ratio settings is lacking. EEP should be individualised to the patient in order to avoid increases in driving pressure (PplatePEEP) whilst maintaining a low VT. To optimise intraoperative respiratory function in obese patients, during pneumoperitoneum insufflation, and during prone or Trendelenburg positioning, PEEP adjustment may be required Before induction of anaesthesia, position the patient with the HOB elevated 30 deg (i.e. ‘beach chair’); avoid flat supine position. If not contraindicated, before the loss of spontaneous ventilation, use NIPPV or CPAP to attenuate anaesthesia- induced respiratory changes
  • 79. During induction, monitor for an obstructive breathing pattern and use a combination of appropriate techniques, including positioning, application of NIPPV or CPAP, or placement of a nasopharyngeal airway to avoid upper airway obstruction After intubation, FIO2 should be set to <0.4. Thereafter, use the lowest possible FIO2 to achieve SpO2 >94% No specific mode of controlled mechanical ventilation is recommended
  • 80. In addition to standard monitoring (ASA/ESA), dynamic compliance, driving pressure (PplatePEEP), and Pplat should be monitored on all controlled mechanically ventilated patients. Decreasing compliance caused by surgical/ anaesthesia factors (i.e. pneumoperitoneum, positioning, and circuit disconnect) should be treated by appropriate interventions. Individualised PEEP can prevent progressive alveolar collapse. Recruitment manoeuvres can reverse alveolar collapse, but have limited benefit without sufficient PEEP. Statement: Increasing FIO2 may be effective in increasing the oxygenation, but is not an effective intervention to improve dynamic compliance of the respiratory system. The effectiveness of interventions aimed at optimising respiratory system mechanics should be evaluated by measuring an improvement of the respiratory system compliance under a constant tidal volume
  • 81. High-quality supportive evidence is lacking to recommend a routine ARM for all patients after tracheal intubation. However, an ARM may be considered according to an individual riskebenefit assessment The bag-squeezing ARM should be avoided in favour of a ventilator-driven ARM ARMs should be performed using the lowest effective Pplat (30 -40 cm H2O in non-obese; 40-50 cm H2O in obese) and shortest effective time or fewest number of breaths Continuous haemodynamic and oxygen saturation monitoring is recommended before and during an ARM. Ensure adequate haemodynamic stability before performing an ARM. Avoid ARMs when contraindicated PEEP should be individualised after an ARM to avoid both alveolar overdistention and collapse. Optimise patient positioning and avoid ZEEP during emergence. Avoid tracheal tube suctioning immediately before tracheal extubation.
  • 82. Avoid apnoea with ZEEP before extubation Prophylactic NIPPV/CPAP should be considered after operation for patients with prior routine use of NIPPV/ CPAP Administration of postoperative supplemental oxygen is recommended when room air SpO2 decreases below 94%. Avoid routine application of supplemental oxygen without investigating and treating the underlying cause. When high FIO2 (>0.8) is used during emergence, the use of low FIO2 (,0.4 WITH CPAP P immediately after tracheal extubation may reduce the risk of resorption atelectasis. In the appropriate clinical scenario, the use of low FIO2 (<0.4) during emergence from general anaesthesia can improve pulmonary function in the postoperative period
  • 83. Moderate- to high-quality recommendations with strong expert support: The ventilator should initially be set to deliver VT 6e8 ml kge1 PBW and PEEP>5 cm H2O. ZEEP is not recommended. Appropriate PEEP and recruitment manoeuvres may improve intraoperative respiratory function and prevent PPCs. Before the induction of anaesthesia, position the patient with the HOB elevated 30 deg (i.e. ‘beach chair’); avoid flat supine position. If not contraindicated, before the loss of spontaneous ventilation, use NIPPV or CPAP to attenuate anaesthesiainduced respiratory changes. In addition to standard monitoring (ASA/ESA), dynamic compliance, driving pressure (PplatePEEP), and Pplat should be monitored on all controlled mechanically ventilated patients. Continuous haemodynamic and oxygen saturation monitoring is recommended before and during an ARM. Ensure adequate haemodynamic stability before performing an ARM. Avoid ARMs when contraindicated. Moderate- to high-quality statements with strong expert support: The formation of perioperative clinically significant atelectasis may be an important risk factor for the development of PPCs. Decreasing compliance caused by surgical/anaesthesia factors (i.e. pneumoperitoneum, positioning, and circuit disconnect) should be treated by appropriate interventions. Individualised PEEP can prevent progressive alveolar collapse. Recruitment manoeuvres can reverse alveolar collapse, but have limited benefit without sufficient PEEP. Increasing FIO2 may be effective in increasing the oxygenation, but is not an effective intervention to improve dynamic compliance of the respiratory system
  • 84.
  • 85. More than 230 million major surgical procedures are undertaken each year worldwide [1] and postoperative complications imposed a significant clinical and economic burden to surgical patients as well as the public health systems [2, 3]. Postoperative pulmonary complications (PPCs) are common postoperative complications that occur in 2% to 40% of patients and are associated with increased morbidity, mortality, and length of stay (LOS) [3–9]. In noncardiac patients, PPCs occur more frequently than cardiac complications [10]. Though it came to wide attention in recent years, the literature investigating the incidence and outcome of PPCs in Chinese inpatients remains scarce. It is known that PPCs have a multifactorial etiology and had been defined broadly, including respiratory tract infection, pneumonia, respiratory failure, atelectasis, pleural effusion, pneumothorax, bronchospasm, and aspiration pneumonitis [11]. Previous studies demonstrated that PPCs were associated with a series of perioperative risk factors, such as age, smoking, chronic obstructive pulmonary disease (COPD), type of surgery, and serum albumin [4, 6, 7, 11–14]. A majority of these risk factors can be intervened and improved [15–17]. Therefore, identifying perioperative risk factors of PPCs is an important step toward improving quality of care in surgical patients, which has been already explored in several studies [11, 12, 18].
  • 86. Development and validation of a score to predict postoperati respiratory failure in a multicentre European cohort Canet J et al. Eur J Anaesthesio.l 2015; 32:1–13 [Epub ahead of print] POST-OPERATIVE RESPIRATORY FAILURE New-onset hypoxaemia appearing within 5 postoperative days at three levels of severity: - Mild (PaO2 < 60 mmHg or SpO2 < 90% on room air but responding to mask/nasal supplemental oxygen); - Moderate (noninvasive or invasive mechanical ventilation to treat a PaO2 < 60 mmHg or SpO2 < 90%); - Severe (invasive MV to manage a PaO /FiO 200
  • 87. Severgnini and colleagues (2013)65 Initial setting: 7 ml kg1 IBW, RR 6 min1 , PEEP 10 cm H2O, I:E ratio 3:1 VT increased in steps of 4 ml kg1 IBW until plateau pressure 30 cm H2O for three breaths Settings returned to original, with PEEP maintained at 10 cm H2O Futier and colleagues (2013)66 CPAP 30 cm H2O for 30 s Treschan and colleagues (2012)108 Three manual bag ventilations with a maximal pressure of 40 cm H2O before extubation Weingarten and colleagues (2010)109 Three-step increase in PEEP: 4–10 cm H2O for three breaths 10–15 cm H2O for three breaths 15–20 cm H2O for 10 breaths PEEP reduced and maintained at 12 cm H2O Repeated 30 and 60 min after the first RM and hourly thereafter