How to prevent volutrauma
during anaesthesia ?
New insights in
the bloodblood-gas barrier of the lung.
J P Mulier MD PhD
az St Jan av Brugge Belgium
JPMulier volutrauma Prague 19 02 2010
1
VILI: An aspect of Safety in
anesthesia ventilation?
• How to prevent volutrauma during anaesthesia ?
New insights in the bloodblood-gas barrier of the lung.
– J P Mulier MD PhD
– az St Jan av Brugge Belgium
JPMulier volutrauma Prague 19 02 2010
2
When disasters take place
• Why waiting for a disasters before action?
• Regulations and checklists are never 100%
safe.
• Why not using automatic safety issues?
JPMulier volutrauma Prague 19 02 2010
3
History
Lung trauma caused by mechanical ventilation
• Past baro trauma:
• high airway pressure rupture the alveolus to the pleura.
• Since 1992 focus on volutrauma:
• large tidal volume and not high airway pressure gives lung damage.
– “Dreyfuss 1992 barotrauma is volutrauma but which volume is the
responsible one?”
• Mechanical Ventilation is Bio trauma and gives multimultiorgan failure:
• release of mediators in the lung circulation due to lung damage
affecting other organs.
– Slusky ventilatorventilator-induced lung injury: from barotrauma to biotrauma.
• What is pathophysiology of volutrauma?
• Pulmonary capillary wall stress increases with rupture of alveolar,
endothelial or basal membrane.
– West J B Thoughts on the pulmonary bloodblood-gas barrier.
Am J Physiol Lung Cell Mol Physiol. 2003 Sep;285(3):L501Sep;285(3):L501-13.
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Old view: Alveolar anatomy
• One alveolus or a group of alveoli behaves as an
individual balloon.
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Old Physiologic view of the alveolus
• Alveolus = balloon
• Laplace law P=T/R
P = T/R
P/2 = T/2R
• Unequal balloon size gives collaps of smallest
•
•
alveoli.
Surfactant must change wall tension with a
factor 2 when radius halves.
Disruption of an alveolar wall always gives a
pneumothorax.
Impossible conclusions!
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Real alveolar anatomy
• Alveolus is part of one larger structure
– The lung is not an agglomerate of
independent balloons.
– The lung is one structure and no alveolus has
an independent wall.
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Artist impression of alveolus
at draeger
• High airway pressure does not increase
•
•
transmural pressure. Other side has same
pressure. Rupture or pneumothorax is not
possible.
if alveolar wall between alveoli would rupture it
gives no problems as the wall is full of holes.
Surfactant needed only to lower wall tension of
all alveoli.
• Why is volutrauma dangerous?
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Microscopic view of the alveolar wall
capillary rupture and not alveolar is dangerous
•
•
•
•
Small capillaries in the alveolar wall.
Wall is very thin at these locations.
Lungtrauma gives edema, protein and blood loss
When or why will a capillary bursts???.
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Electron Microscopy of the alveolar wall
• Thinnest wall at
– Capillary – alveoli:
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Lung trauma = Capillary wall rupture
• When do we have rupture?
• Pathophysiology of the pulm capillary
• High cardiac output gives high pulm cap
pressure and creates lung edema, lung bleeding
– Sport horse racing, running sport
– High altitude edema
– Extreme sport conditions = high cardiac output
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Very high wall stress in pulmonary capillaries
• R: 3,6 um
• Thickness: 0,34 um
• P: 52,5 cmH20
340 nm
T 5,5 N m2
• T: Wall stress approaches the ultimate tensile strength of collagen.
P 52,5 cmH20
• these extremely high values have not
previously been recognized:
• misled by the small radius of the
capillary, which reduces
circumferential tension . ( 25
dynes/cm [25 mN/m])
• the extreme thinness of the wall,
which follows directly from the
gas exchange function of the
blood--gas barrier was overlooked.
blood
•J West 1991
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Strength of the Capillary Wall
• the capillary endothelial layer, the alveolar epithelial layer, and the extra
cellular matrix (ECM) = the fused basement membranes
• the ECM ( type IV collagen ) has a central lamina densa with a lamina rara
on either side
• the great strength of the thin part of the bloodblood-gas barrier comes from an
extremely thin layer of type IV collagen ( 50 nm thick)
• 50 nm gives 38 Nm2
J West 1992
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Dilemma of the BloodBlood-Gas Barrier
• Efficient gas exchange needs an extremely thin blood
blood--gas barrier.
– it cannot be any thicker because human athletes show diffusion
limitation. J West 2003
– This is also true of thoroughbred racehorses. Fu 1992
– The extreme thinness of the barrier confers a survival advantage.
• Blood
Blood--gas barrier must be immensely strong because it forms the
walls of the pulmonary capillaries, and the stresses become
extremely high when the capillary pressure rises.
– the barrier has evolved to be as thin as possible for maximum efficiency
of gas exchange but to have just enough strength to maintain its
integrity under the most challenging normal physiological conditions.
– it is possible that the amount of type IV collagen in the capillary wall is
continuously being regulated, possibly by the level of pressure within
the capillary, and this explains why the extra cellular matrix increases in
disease such as mitral stenosis when the capillary pressure is raised.
– if the capillary transmural pressure rises to unphysiologically high levels,
or wall stress is greatly increased by over inflation, or the wall is
weakened by disease, alveolar edema, or hemorrhage, or both are
inevitable.
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Changes in Pulmonary Capillaries at
High Pressures
• a, Capillary endothelium is disrupted (arrow), but the alveolar epithelium and
•
•
•
the basement membranes are intact.
b, Alveolar epithelial layer (right) and capillary endothelial layer (left) are
disrupted.
c, Disruption of all layers of the capillary wall, with a red cell apparently passing
through the opening.
d, Scanning electron micrograph showing breaks in the alveolar epithelium.
J West 2003
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What determines acute changes in the
Pulmonary Capillary Pressure ?
•The pressure drop in the pulmonary circulation occurred
in the capillary bed, so in upstream capillaries the
pressure is close to pulmonary artery pressure.
•Pulmonary artery pressure is dependent on
•Cardiac output
•Stimulated by intropes, high filling and exercise
•Left atrial filling pressures and left ventricular
filling pressures
•Mitral stenosis and aortic or mitral regurgitation
•Left ventricular failure, ventricular hypertrophy
and ischemia
•Capillary position relative to the heart.
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Why is hyperinflation damaging the
capillary wall?
• Why is hyperinflation damaging the
capillary wall?
• Is volutrauma possible without pulmonary
hypertension?
• Is peep or high airway pressure not
protecting against high capillary pressure?
• Is peep not dropping the CO
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Three forces act on the bloodblood-gas barrier
•Pres cap
•Tens tmp
•Pres alv
•Tens el
•Vol alv
•Tens st
– Ttmp is the circumferential or hoop tension caused by the
capillary transmural pressure.
– Tel is the longitudinal tension in the alveolar wall elements
associated with lung inflation; this is transmitted to capillary
membrane.
– Tst is the surface tension of the alveolar lining layer; It exerts an
inward--acting force to support the capillary when the latter
inward
bulges into the alveolar space. J West 2003
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Hyperinflation increases wall stress
• Capillary is flattened
through increased alveolar
stretching
• Radius of ellips x 10 in flat
part -> T x 10
• With normal capillary
pressure capillary wall
ruptures
• Fu West 1992
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Some animals are protected against
hyperinflation
• Birds
• Mammalians
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Research studies
• Overinflation of the Lung increases the permeability
of pulmonary capillaries
– Respiratory failure treated with high levels of positive
end--expiratory pressure gives edema. Dreyfuss DAm
end
Rev Respir Dis. 1985;132:880
1985;132:880--884.
– High lung volume rather than the increased alveolar
pressure gives the increased permeability. Hernandez
LA. J Appl Physiol. 1989;66:2364
1989;66:2364--2368.
– If we increase lung volume while maintaining a
constant capillary transmural pressure, the number of
both endothelial and epithelial breaks is greatly
increased. Fu Z. J Appl Physiol. 1992;73:123
1992;73:123--133.
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lung trauma
• Each time the epithelial layers disrupt
– The basal membrane is stretched
– The basal membrane exposes to
• Blood (vascular endothelia)
• Air (alveolar endothelia)
– Spontaneous recovery exists
• Each time the basal membrane disrupts
– Leak of blood into the alveoli: red sputum
– Connection between two alveoli, no problem
– Connection between alveoli and interpleural
space: bulla and possible pneumothorax
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Clinical conditions at risk:
• Large tidal volume ventilation
• High peep
• Long bagsqeezing to open lungs
– No problem for collapsed lung but dramatic in healthy
lung
• Accidental over inflation:
– no manual ventilation with semisemi-closed pop valve
– Inflation over max lung vol
• Pressure above normal ventilation pressure
– Occluded expiratory tubing or valve
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Most common accident
is however a human error
• Manual system is outside electronic
ventilator and less protected
• Forgetting to switch from manual to
mechanical ventilation might happen
– with a closed APL valve
– with a high fresh gas flow
• Most of the time not reported !
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Manual system
• Manual system is outside electronic ventilator
– Anesthetists prefer a pure mechanical system, capable of giving high
pressures and large volumes
– only recently some alarms in Ohmeda, not in Drager
• Anesthesia Induction
– high fresh gas flow: 15 liter or more
– APL valve closed: different types
– Manual breathing bag
• Airway pressure rises very fast
• Airway pressure monitor
– High pressure alarm
– Apnoe alarm
– High peep alarm
• But if anesthetist does not react immediately,
risk for volutrauma exists
• The APL valve, a large manual balloon with a high compliance protects against
Prague 19 02 2010
high airway pressuresJPMulier
but notvolutrauma
against volutrauma.
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APL // Man – Mech switch
• APL (adjusted pressure limiting valve) valve
• Mechanical switch
• Electronic switch (older ventilators separated)
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Human risk
• the anesthetist assumes that he did start the correct mode while the
ventilator did not and remained in the manual mode.
– Verify ventilation mode
• two anesthetist: one connects the end tracheal tube to the
ventilator, assuming that the other starts the correct ventilation
mode
– The person who connects the tube always starts the ventilator
• after a difficult intubation or other distracting event, the anesthetist
finally relaxed, forget to change the ventilation mode
– Set the mobile phone off
– Stay alert, even when tube is finally in
• Drapes over the ventilator, anesthetist staying between patient and
ventilator, surgical procedures on the head requiring to turn the
ventilator in opposite direction makes the ventilator invisible for the
anesthetist.
– Have a separate induction room? But risk doubles?
– Request the place and position needed for the anesthetist
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How frequently happens this type of
human error ?
• 90 % of all anesthetist know a case in their
•
hospital of this type of human error.
50 % of all anesthetist tell that at least one case
a year happens in their hospital.
– Most of the time no barotrauma and therefore not
registered.
• Low blood pressure no time to measure
• Lung edema white lungs ?
• We are all afraid that it might happen with us
• We all assume that it is not traumatic !
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Definition of dangerous
• A ventilation mode is considered to be at risk
if the airway pressure stayed above 30 cmH20
for more than 5 seconds and dangerous if no
alarm did go off in that time.
• A ventilator is considered to be dangerous if
a dangerous ventilation mode could take place.
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Aestiva 5 DatexDatex-Ohmeda
pressure time relation in aestiva 5
balloon pressure in cmH2O
50
40
30
mode 1
mode2
20
mode 3
10
0
-10
0
5
10
15
20
25
30
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time in seconds
35
40
30
Juliana Dräger
pressure time relation in Juliana
balloon pressure in cmH2O
60
50
40
mode 1
mode2
30
mode 3
20
10
0
-10 0
5
10
15
20
25
30
time in seconds
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35
40
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Comparison of different
ventilators 1
ventilator
APL valve
alarm first alarm after
excel 210SE
30
30
high pressure
excel 210SE
75
30
high pressure 1 s
At risk
excel 210SE
75
100
sustained pressure 17 s
dangerous
excel 410
30
30
sustained pressure 15 s
excel 410
75
30
high pressure 3 s
At risk
excel 410
75
100
sustained pressure 18 s
dangerous
datex as3
30
30
high pressure
datex as3
80
30
high pressure 1 s
At risk
datex as3
80
80
high peep 5 s
At risk
aestiva5
30
30
apnoe
aestiva5
70
30
high pressure 2 s
At risk
aestiva5
70
99
apnoe 9 s
dangerous
JPMulier volutrauma Prague 19 02 2010
risk
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Comparison of different
ventilators 2
drager AV1
30
30
high pressure
drager AV1
106
30
high pressure 1 s
drager AV1
106
133
titus
30
30
titus
70
30
titus
70
99
cato
30
30
cato
70
30
cato
70
98
julian
30
30
julian
70
30
julian
70
98
At risk
dangerous
high pressure 1 s
At risk
dangerous
high pressure 1 s
At risk
dangerous
high pressure 1 s
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At risk
dangerous
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2 and 3 liter breathing bags
• US
EUR
old rubber
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Compliance of breathing bags
100
35 cmH20
60 cmH2O
2L USlatex free
2 L EURlatexfree
3 L EURlatex free
2 L black rubber
3 L black rubber
cmH2O
80
60
40
20
0
0
5
10
15
liter
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ANSI standard for anesthetic
equipment--reservoir bags Z79.4 1983
equipment
• Bag with volume greater than 1,5 l should
– not exceed a pressure of 35 cmH2O when at 2 times
its volume
– not exceed a pressure of 60 cmH2O when at 6 times
its volume
• 2 l EUR latex free at 2 x is 51 cmH20
• 3 l EUR latex free at 2 x is 45 cmH20
• 2 L US latex free at 2 x is 29 cmH20
– European anesthetic equipment does not comply with
the ansi standard of USA!
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How to choose a breathing bag?
• Never old black rubber balloons
• Use the largest possible balloon
– 2 liter or more
• Pediatric balloon with fingertip hole
– Contamination of room air
• not available anymore!
• Consider US type of balloons
– No volutrauma protection!
• Use VSV protection system
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Specifications of VSV 3 (safety frog)
• Alarm and valve open when:
– > 75 cmH2O
– > 20 CMH2O and >6 seconds
• VSV off
– Variation less than 2 cmH2O and >60 seconds
• VSV on
– > 10 cmH2O
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VSV 3 or safety frog effect
50
cmH2O
40
Euro 2l breathing
bag
Euro 2l breathing
bag with VSV
USA 2l breathing
bag
USA 2l breathing
bag with VSV
30
20
10
0
0
10
20
30
40
50
seconds
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How to use VSV
(safety frog) ?
• Connect VSV always in inspiratory limb of breathing circuit
– Inspiratory limb protects manual and automatic modes
– Manual bag position protects only manual mode
– Expiratory limb position does not solve risk for tubing occlusion
• No need to switch on or off
– Switches on automatically when pressure rises during normal ventilation
– Switches off when pressure stay zero longer than 1 minute
• Never have to worry about VSV function
– VSV is constant active during manual and mechanical ventilation
without interference
• VSV is working and protecting when you need it
• VSV is warning you with an alarm each time it opens the airway and
protects the patient
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Also useful when technical error
• APL valve closed or blocked during
spontaneous ventilation
• Not starting ventilator due to ventilator
failure or human error
• Blocked expiratory valve
• Defect peep valve ( higher or occlusion)
• Occluded expiratory tubing
– Accident in univ Zurich (Markus Weiss)
– No alarm is going off in Ohmeda ventilator !
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Safety frog
• Is produced Medec nv Benelux
• Prize of PGA New York for best
anesthesiology invention
• Prize of Bizidee for best product idea
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Insufficient research on volutrauma
• How to evaluate clinical damage ?
• Are only excessive volumes dangerous ?
• Should we limit tidal volumes ?
• Is pulmonary pressure important ?
• Is increasing cardiac output while lowering
ventilation volume safer ?
• Is Recovery of epithelial damage possible
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Effect of 40 cmH20 during 4 x 30 seconds
in rats preliminary data JPMulier 2008
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Effect of 40 cmH20 during 4 x 30 seconds
in rats preliminary data JPMulier 2008
Burkitt chamber count of BAL
• Without safety frog
11 RBC
With safety frog
0 RBC
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Effect of 40 cmH20 during 4 x 30 seconds
in rats preliminary data JPMulier 2008
total number of erythrocytes in BAL per ml
5.000.000
4.500.000
4.000.000
3.500.000
3.000.000
2.500.000
2.000.000
1.500.000
1.000.000
500.000
0
no safety frog
with safety frog
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Conclusion:What to do during anesthesia
• Prevent global hyperinflation or volutrauma
– Reduce tidal volume, increase frequency Allow mild hypercapnia
– No high peep. Allow mild hypoxia?
– Use safety frog to prevent ventilator and human error
• Prevent local hyperinflation
– keep lung open, use low peep
– Short time of bag sqeezing and look to lung during thoracotomy
• Volume controlled mode is safer than Pressure controlled
mode
• Good volume alarms
• Direct supervision
• No change in lung compliance by surgery, position,..
• Use assist ventilation, it is more physiologic, but today
still dangerous for hyperinflation
– Better to use volume assist mode
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?
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Obese patients are a challenge
Our new abdominal model
facilitates laparoscopy
and
prevents volutrauma
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Effect of VSV 2 on ventilation
• Interference only at freq of 4 breaths per minute
ventilation of non elastic test lung
C 11 ml/cmH2O
high R
60
cmH2O
50
40
12x 1/2 VSV on
30
6x 1/1 VSVon
20
4x 1/1 VSV on
4x 1/1 VSV off
10
0
0,00
10,00
20,00
time in sec
30,00
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40,00
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Prevent unequal alveolar distension
• Try spontaneous ventilation whenever possible.
• Use assist ventilation if tidal volume is to small
– due to morphine, muscle relaxants, deep anesthesia
or high work of breathing.
• Use mechanical ventilation only if frequency is
too low. Prevent volutrauma.
– High frequency, small tidal volume and low peep?
• Dead volume increases !
• Risk of atelectasis ! and hyperinflation of upper lung !
– Keep lung open with lowest peep possible !
– If airway pressure is high be alert !
– No recruitment maneuver: everyone does it although
everyone find it dangerous and useless.
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Prevent alveolar distension
• Pressure controlled is more dangerous than volume
•
controlled !
Prevent hyperinflation
– Lowest peep necessarily
– Never forget to switch from manual to mechanical ventilation
• Use safety frog to protect lung
• No large tidal volumes
– Accept hypercapnia, accept hypoxia ?
• High Airway pressure does not mean high alveolar
pressure.
– Airway, tubing resistance
• Danger of peep and long inspiratory times
• High alveolar pressure does not mean distension of
alveoli.
– Thorax compliance and lung compliance
• Danger in healthy lungs, thorax and in children
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Clinical conditions .
• Increased pulmonary capillary pressure causes
– a highhigh-permeability type of pulmonary edema
• Neurogenic Pulmonary Edema
– "sympathetic storm" raises pulmonary vascular pressures
intense peripheral vasoconstriction, which shifts blood to the
thorax; acute left ventricular failure caused by overwhelming
systemic hypertension; and reduced compliance of the left
ventricle, necessitating very high filling pressures. Minnear FL J
Appl Physiol. 1987;63:335
1987;63:335--341.
• HAPE (High
(High altitude pulmonary edema)
– hypoxic pulmonary vasoconstriction is uneven, with the result
that those capillaries not protected by arterial constriction are
exposed to a high pressure given the high cardiac output. West
JB. Eur Respir J. 1995;8:523
1995;8:523--529
• ARDS
– when ARDS follows trauma, a large release of catecholamines
gives a transient increase in pulmonary vascular pressures
combined with high peep ventilation leading to stress failure of
pulmonary capillaries. Bachofen M American Physiological
Society; 1979:2411979:241-252.
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World Health Organization
diagnostic classification of pulmonary hypertension
• 1 Pulmonary arterial hypertension
– 1.1 Primary pulmonary hypertension(a) Sporadic(b) Familial
– 1.2 Related to:(a) Collagen vascular disease(b) Congenital systemicsystemic-to
to--pulmonary
shunts(c) Portal hypertension(d) HIV infection(e) Drugs/toxins(1) Anorexigens(2)
Other(f) Persistent pulmonary hypertension of the newborn(g)
• 2 Pulmonary venous hypertension
– 2.1 Left
Left--sided atrial or ventricular heart disease
– 2.2 Left
Left--sided valvular heart disease
– 2.3 Extrinsic compression of central pulmonary veins(a) Fibrosing mediastinitis(b)
Adenopathy/tumours
– 2.4 Pulmonary venoveno-occlusive disease
• 3 Pulmonary hypertension associated with disorders of the respiratory
systemand/or hypoxaemia
–
–
–
–
3.1
3.3
3.5
3.7
Chronic obstructive pulmonary disease 3.2 Interstitial lung disease
Sleep disordered breathing
3.4 Alveolar hypoventilation disorders
Chronic exposure to high altitude
3.6 Neonatal lung disease
Alveolar–capillary dysplasia
Alveolar–
• 4 Pulmonary hypertension due to chronic thrombotic and/or embolic disease
– 4.1 Thromboembolic obstruction of proximal pulmonary arteries
– 4.2 Obstruction of distal pulmonary arteries(a) Pulmonary embolism (thrombus, tumour,
etc.)(b) In situ thrombosis(c) Sickle cell disease
• 5 Pulmonary hypertension due to disorders affecting the pulmonary
vasculaturedirectly
– 5.1 Inflammatory(a) Schistosomiasis(b)
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– 5.2 Pulmonary capillary haemangiomatosis
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Clinical conditions ..
– alveolar hemorrhage
• Exercise
Exercise--Induced Pulmonary Hemorrhage
– ExerciseExercise-induced pulmonary hemorrhage (EIPH) in racehorses is the
most dramatic example of such a condition West JB, J Appl Physiol.
1993;75:1097--1109
1993;75:1097
• Catastrophic Increase in Pulmonary Venous Pressure
– Occasionally, a catastrophic event such as rupture of the chordae
tendineae or a papillary muscle of the mitral valve causes alveolar
hemorrhage. Alveolar bleeding has also been described in patients with
very high left atrial pressures who are awaiting cardiac transplantation.
• Bleeding in Elite Human Athletes
– anecdotal accounts of hemoptysis after extreme exercise West JB. Am
Rev Respir Dis. 1991;143:A569.
– a combination of edema and hemorrhage
• Chronic Venous Hypertension
– mitral stenosis where hemoptysis occurs in approximately one half of
patients and the lungs contain large amounts of hemosiderin, alveolar
type II cells replace type I cells that were damaged Kay JM. J Pathol.
1973;111:239--245 Wood P. Br Med J. 1954;1:1051
1973;111:239
1954;1:1051--1063, 11131113-1124
• Hemorrhagic Pulmonary Edema in Elite Athletes
– prolonged intense exercise ex running the 9090-km Comrade's Marathon
in South Africa (McKechnie JK S Afr Med J. 1979;56:261
1979;56:261--265)
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