Download Mechanical Ventilation

Mechanical Ventilation & Strategies
for Oxygenation
Dawn Oddie
1
What are we going to talk about?
 Physiology
 Ventilation
classifications
 Types of Ventilation
 Optimising Oxygenation
 Complications of Ventilation
 Weaning from Ventilation
2
Physiology
3
Where it all happens!
4
Physiology of normal breathing
I:E ratio times
Negative pressure
Active inspiration
Passive expiration
How do we breathe?
Respiratory rate
High lung volume (Inhalation)
Low lung volume (Exhalation) /
Functional residual capacity
Tidal volumes
5
How is normal breathing
controlled
How do you know,
 Rate - How fast / slow to breathe?
 Tidal volume - How big a breathe to
take in?
 I:E ratio – How long to breath in /
out for?
 When to cough / sneeze?
6
Nervous Control / Chemical







Respiratory centre. Reticular formation – brain stem
– Medullary rhythmicity area
– Pneumotaxic area / Apneustic area (transition from I to E)
Inflation (Hering-Breuer) reflex - Stretch receptors
Cortical influences – cerebral cortex giving some voluntary
control eg hold breath underwater
Central chemosensitive area (pH / H+) – Medulla
Peripheral chemoreceptors (CO2 / O2 / H+) – carotid bodies
Proprioceptors – joints / muscles
Other influences – Baroreceptors / Temp / Pain / stretching
the anal sphincter muscle / Irritation of the air passages
7
Lung Volumes
8
Respiratory Mechanics- Compliance




Compliance is ΔV/ΔP (Change in Volume / change in pressure)
– Total lung is made up of thoracic and lung compliance
Pulmonary compliance (or lung compliance) is the ability of the lungs
to stretch during a change in volume relative to an applied change in
pressure.
Compliance is greatest at moderate lung volumes, and much lower
at volumes which are very low or very high. LIP and UIP can be
good guides
Pulmonary Surfactant increases compliance by decreasing the
surface tension of water. The internal surface of the alveolus is
covered with a thin coat of fluid. The water in this fluid has a high
surface tension, and provides a force that could collapse the
alveolus. The presence of surfactant in this fluid breaks up the
surface tension of water, making it less likely that the alveolus can
collapse inward. If the alveolus were to collapse, a great force would
be required to open it, meaning that compliance would decrease
drastically.
9
Respiratory MechanicsCompliance


Low compliance indicates a stiff lung and means extra
work is required to bring in a normal volume of air. This
occurs as the lungs in this case become fibrotic, lose
their distensibility and become stiffer.
In a highly compliant lung, as in emphysema, the elastic
tissue has been damaged, usually due to their being
overstretched by chronic coughing. Patients with
emphysema have a very high lung compliance due to
the poor elastic recoil, they have no problem inflating the
lungs but have extreme difficulty exhaling air. In this
condition extra work is required to get air out of the
lungs.
10
Causes of Decreased Intrathoracic
Compliance
Decreased Chest Wall
Compliance
Decreased Lung Compliance
Obesity
Ascites
Neuromuscular weakness
Flail Chest
Kyphoscoliosis
Paralysis
Scleroderma
Pectus Excavatum
Tension Pneumothorax
Intubation
Pulmonary oedema
ARDS
Connective tissue disease
Sarcoidosis
Dynamic Hyperinflation
Lymphangitis Carcinomatosis
11
Some Important Physiology
 V/Q
Mismatch
 Oxygen Cascade
 Oxyhaemoglobin Dissociation Curve
 Spirometry Trace
12
Supply and demand

V/Q mismatch
– V = Ventilation
– P = Perfusion
– Hypoxic Pulmonary Vasoconstriction
Functional alveoli
 Permeable membranes
 Circulating volume – with

–
–
–
–
Adequate haemoglobin levels
Oxygen saturation of haemoglobin (affinity)
Oxygen dissociation
Perfusion pressure
13
When room air just isn’t
enough…..
Increased
metabolic demand
 V/Q mismatch

– Damaged alveoli /
airways
– Blocked alveoli
– Inadequate
circulation
14
Some indications to increase O2












Acute respiratory failure eg pneumonia, asthma, pulmonary
oedema, pulmonary embolus
Acute myocardial infarction
Cardiac Failure
Shock
Hypermetabolic states eg major trauma, sepsis, burns
Anaemia
Carbon monoxide poisoning
Cardio respiratory resuscitation
During / post anaesthesia
Pre-suction
Suppressant drug eg narcotics
Pyrexia (Oxygen consumption increases by 10% for each
degree rise)
15
Effect of insufficient oxygen
Reduced oxygen supply leads to cellular
shift from aerobic to anaerobic
metabolism
 Production of lactic acid
 Increasing metabolic acidosis

– Low pH
– Low HCO3
– Negative base excess

Cell death / system wide failure
16
What is oxygen

What percentage of oxygen is in
atmospheric air?
In normal circumstances with a average
respiratory rate sufficient to meet
metabolic demands

Oxygen delivery (mls O2/min) = Cardiac output
(litres/min) x Hb concentration (g/litre) x 1.31
(mls O2/g Hb) x % saturation
Oxygen Consumption = 200 - 250 mls / min
17
Haemoglobin
18
Haemoglobin




Intracellular protein contained within
erythrocytes (red blood cells)
Made up of 2 pairs of polypeptide chains (2Alpha,
2 Beta), each bound to a haem group that
contains iron. Each molecule of haemoglobin can
combine with 4 molecules of oxygen
Primary vehicle for oxygen transportation in the
blood (small amount in plasma Approx 1.5-3%)
Each haemoglobin molecule has a limited
capacity for holding oxygen molecules. How
much of that capacity that is filled by oxygen
bound to the haemoglobin at any time is the
oxygen saturation (SaO2)
19
Haemoglobin
Average 70Kg Adult = 900g of circulating
haemoglobin (Hb 14-18g/dl)
 1g Haemoglobin can carry 1.34ml oxygen
Example,
10g/dl with an average 5l circulating volume
= 500g total body haemoglobin
If fully saturated 500 x 1.34 = 670ml of
oxygen
(Only approx 25% unloads leaving venous
sats (SvO2) 70-75% - useful in times of
higher metabolic demand etc

20
The transfusion debate…
Risks of
transfusion
vs
Reduced oxygen
carrying capacity
21
Factors affecting carriage
 Timing
of haemoglobin uptake and
release of oxygen affected by,
– Partial pressure of oxygen (PaO2)
– Temperature
– Blood pH
– Partial Pressure of Carbon dioxide
(PaCO2)
22
Partial Pressure - effect of Altitude

At sea level we live under
a layer of air that is several
miles deep – the
atmosphere. The pressure
on our bodies is about the
same as 10 metres of sea
water pressing down on us
all the time. At sea level,
because air is
compressible, the weight
of the air around us
compresses making it
denser. As you go up a
mountain, the air becomes
less compressed and
therefore thinner.
23
Partial Pressure - effect of Altitude
The important effect of this
decrease in pressure is: in a
given volume of air, there are
fewer molecules present. The
percentage of those molecules
that are oxygen is exactly the
same: 21%.
The problem is that there are
fewer molecules of everything
present, including oxygen.
So why is this an issue?
24
Partial Pressure of gases

In a mixture of ideal gases, each gas has a
partial pressure which is the pressure which the
gas would have if it alone occupied the volume.
The total pressure of a gas mixture is the sum of
the partial pressures of each individual gas in the
mixture.
Dalton's law (also called Dalton's law of partial
pressures) states that the total pressure exerted
by a gaseous mixture is equal to the sum of the
partial pressures of each individual component in
a gas mixture.
25
Partial Pressure



Partial pressure (PP) is a way of describing how much of a
gas is present. All gases exert pressure on the walls of
their container as gas molecules bounce constantly of the
walls
PP is also used to describe dissolved gases. In this case,
the PP of a gas dissolved in blood is the PP that the gas
would have, if the blood were allowed to equilibrate with a
volume of gas. When blood is exposed to fresh air in the
lungs, it equilibrates almost completely so that the PP of
oxygen in the air spaces in the lungs is equal to the partial
pressure of oxygen in the blood.
PP of arterial blood is slightly less than PP of oxygen in
lungs – due to physiological shunt (some blood passing
through lungs without encountering an air space)
26
Partial Pressure of gases


The partial pressure of a gas dissolved in a liquid
is the partial pressure of that gas which would be
generated in a gas phase in equilibrium with the
liquid at the same temperature. The partial
pressure of a gas is a measure of thermodynamic
activity of the gas's molecules. Gases will always
flow from a region of higher partial pressure to
one of lower pressure; the larger this difference,
the faster the flow.
Gases dissolve, diffuse, and react according to
their partial pressures, and not necessarily
according to their concentrations in a gas
mixture.
27
Oxygen dissociation curve
Dissociation curve relates oxygen saturation of
Haemoglobin (Y axis) and partial pressure of
arterial oxygen (X axis) in the blood
28
Dissociation curve explained
Extent of oxygen binding to haemoglobin
depends on PaO2 of blood, but relationship
not precisely linear
 Slope steeply progressive between 1.5 –
7kPa (area of most rapid uptake and
delivery of oxygen to and from
haemoglobin), then plateaus out between
9 – 13.5kPa
 Haemoglobin almost completely saturated
at 9kPa – further increases in partial
pressure of oxygen will result in only slight
rises in oxygen binding

29
Oxygen dissociation curve



The partial pressure of
oxygen in the blood at
which haemoglobin is
50% saturated
(26.6mmHg) is known
as the P50
P50 is conventional
measure of haemoglobin
affinity for oxygen
Increased P50 indicates a
right shift of the
standard curve –
meaning larger partial
pressure necessary to
maintain a 50% oxygen
saturation
30
Oxygen dissociation curve
Increased affinity
Reduced Affinity
31
Factors influencing the position of oxygen
dissociation curve
To the right,
 Hyperthermia
 Acidosis (pH)
 Increased pCO2
 Endocrine
disorders
Curve shifts to left,
 Hypothermia
 Alkalosis
 Decreased pCO2
 Carbon monoxide
Generally a shift to the,
Right will favour unloading of oxygen to the tissues
Left will favour reduced tissue oxygenation
32
Factors influencing the position of
oxygen dissociation curve - explained
To the right
 As pH declines
(acidosis) the
affinity of
haemoglobin for
oxygen reduces.
Result – less
oxygen is bound
while more oxygen
is unloaded
Bohr effect
To the left
 Temperature – as
body temp falls the
affinity of
haemoglobin for
oxygen increases.
Result – more
oxygen is bound
while less oxygen
is unloaded
33
mmHg vs. kPa

Both measures commonly in use
The kiloPascal: A pressure of one thousand
pascals (1 kPa) is about 10.2 cm H2O or about
7.75 mmHg.
 Atmospheric pressure is about 1034 cmH2O or
101.9 kPa. The useful approximations are 1000
cm H2O or 100 kPa.
 mmHg to kPa: To convert pressure in mmHg to
kPa, divide the value in mmHg by 7.5.
Eg.

– 60mmHg = 8.0kPa
– 30mmHg = 4.0kPa
34
The oxygen cascade

Transport has three stages (steps),
– By gas exchange in the lungs
 Partial
pressure gradient of oxygen (PaO2) in alveoli
13.7kPa
 Partial pressure gradient of oxygen (PaO2) in
pulmonary capillaries 5.3kPa
– Transport of gases in the blood
 Partial
pressure gradient of oxygen (PaO2) in arterial
blood 13.3kPa
– Movement from blood into the tissues
 Partial
pressure gradient of oxygen (PaO2) in tissues
2.7kPa
 Mitochondrial pressure 0.13-1.3kPa
35
Oxygen delivery to tissues….



The amount of oxygen bound to the haemoglobin
at any time is related to the partial pressure of
oxygen to which the haemoglobin is exposed.
Eg in lungs at the alveolar-capillary interface,
partial pressure of oxygen is high so oxygen
readily binds. As the blood circulates to other
body tissue in which the partial pressure of
oxygen is less the haemoglobin releases the
oxygen into the tissues.
Haemoglobin cannot maintain its full bound
capacity in the presence of lower oxygen partial
pressures.
36
Supplementing Oxygen










Nasal cannula
Fixed performance mask
Variable performance mask
Non rebreathe reservoir
Tracheostomy mask
Tents / head boxes
Bag valve mask
CPAP – nasal / facial or hood
BiPAP – IPAP / EPAP
Intubation and mechanical ventilation
37
Indicators for initiating
mechanical ventilation?
38
Types of positive pressure
ventilation
 Non
invasive
 Invasive
39
CPAP / PEEP / EPAP


Pressure applied at end of expiration to maintain
alveolar recruitment
Airway pressure kept positive
Beware of gas trapping (autoPEEP) in non
compliant lungs
40
CPAP
41
NIV - BiPAP
 IPAP
/ PS / ASB
– Inspiratory assistance with each
spontaneous breath
 EPAP
– Expiratory resistance
42
The science of mechanical ventilation
is to optimise pulmonary gas
exchange; the art is to achieve this
without damaging the lungs
43
What is a Mechanical Ventilator?
Generates a
controlled flow of
gas in and out of a
patient
 Inhalation
replenishes
alveolar gas
 Balance needed
between O2
replenishment and
CO2 removal

44
Ventilators – What do they need
to do…
 Mechanical
ventilators are flow
generators
 Must be able to,
– Control
– Cycling
– Triggering
– Breaths
– Flow pattern
– Mode or breath pattern
45
Ventilator strategy
 Aim
to achieve adequate minute
volume with the lowest possible
airway pressure
46
Ventilator Classification
Control
– How the ventilator knows how much
flow to deliver
 Can
be,
– Volume controlled
(volume limited, volume
targeted) & pressure variable
– Pressure controlled
(pressure limited, pressure
targeted) & volume variable
– Dual controlled
pressure limited
(volume targeted (guaranteed)
47
Ventilator Classification
Cycling
 How the ventilator switches from
inspiration to expiration (the flow has
been delivered – how long does it stay there?)
– Time cycled e.g. pressure controlled ventilation
– Flow cycled e.g. pressure support
– Volume cycled. The ventilator cycles to expiration
once a set tidal volume has been delivered.
48
Ventilator Classification
Triggering

What causes the ventilator to cycle to
inspiration. Ventilators may be……
– Time triggered
 Cycles
at set frequency as determined by the rate
– Pressure triggered
 Ventilator
senses the patients inspiratory effort by
sensing a decrease in baseline pressure
– Flow triggered
 Constant
flow through circuit – flow-by. Ventilator
detects a deflection or change in this flow. Requires
less work from the patient than pressure triggered
49
Ventilator Classification
Breaths
– Mandatory
 (controlled)
rate
– determined by the respiratory
– Assisted
 E.g.
synchronised intermittent mandatory
ventilation (SIMV)
– Spontaneous
 No
additional assistance during inspiration
e.g. CPAP
50
Ventilator Classification
Flow pattern
– Sinusoidal (normal breathing)
– Decelerating (inspiration slows as alveolar pressure
increases)
– Constant
(flow continues at a constant rate until set
tidal volume is delivered)
– Accelerating
(not used in clinical practice)
51
Ventilator Classification
Mode or Breath Pattern
– CMV
– Volume Assist-Control
(caution with sensitivity)
– Synchronised Intermittent
Mandatory Ventilation – SIMV
– Pressure support
– High frequency ventilation
–BiPAP/BILEVEL – airway
pressure release ventilation
–Proportional assist
ventilation
Enhance patient interactivity
–Automatic tube
compensation
52
Methods of Ventilation
 Synchronised
Intermittent Mandatory
Ventilation – SIMV
 Pressure Control
 Volume control
 Pressure regulated volume control
 Pressure support
 Continuous positive airway pressure
(CPAP)
53
Waveforms
54
So the problem is this
If the patient is hypoxic then they need O2
 If still hypoxic then they need +ve
pressure
 If still hypoxic then you need to increase
the Ti time (at the expense of the Te time)
 Adjustment of the I:E ratio (did) mean
increased sedation as it was impossible to
breath with the flipped ratio.
 New modes have now been developed to
allow spontaneous ventilation on adjusted
I:E ratios e.g. BIPAP and APRV

55
Biphasic Positive Airway
Pressure
56
BIPAP / APRV (Airway pressure release ventilation)
57
Why is mechanical ventilation
bad for you?
58
Problems with Mechanical
Ventilation
Mechanical Ventilation
Intubation
Prolonged
Ventilation
Ventilator Induced Lung Injury
59
Problems with Intubation
60
Problems with Intubation
 Bypass
natural protective
mechanisms – moisten, filter, warm
 Plastic tubing – airway trauma, vocal
cord damage
 Pressure sores – oral or from cuff
 Mouth care!
 Need sedation
61
Sedation and Ventilation

Good Points
–
–
–
–
–
Reduced pain
Reduced stress
Easier to nurse
Better for relatives
Less chance of lines
falling out

Bad Points
– Increased
pneumonia risk
– Venous thrombosis
– Pressure area
problems
– Hypotension
– Prolonged ICU stay
– Better for relatives
– Increased
barotrauma
62
Problems with Prolonged
Ventilation
 Barotrauma
 Volutrauma
 Oxygen
Toxicity
 Pneumonia (VAP)
 Sheer Stress – flow delivery
63
Barotrauma – pressure



Air leak from alveoli
situated near
respiratory
bronchioles
10 – 20% of
ventilated patients
Predisposing factors
– Frequent +ve pressure
breaths
– Infection
– ARDS
– Hypovolaemia
64
Volutrauma - volume



Excessive stretch in the
absence of excessive
airway pressure.
If alveoli cannot over
distend they are less
likely to be damaged
Not just a mechanical
problem but also a local
and generalised
inflammatory response.
– C.f. IL-6 levels in
ARDS Net lung
protection study.
65
Volutrauma
66
Ventilators
 Aim
to achieve adequate minute
volume with the lowest possible
airway pressure
– High PEEP levels 10 – 20 (open lung)
– Permissive hypercapnia
– Patient specific tidal volume 6 – 7ml/Kg
– Improved inverse ratio capabilities
67
Oxygen – the risks








Highly flammable
Compressed
Dry gas – Think humidification!
Blindness in neonates (overgrowth of blood
vessels)
Drying of mucus membranes / secretions
COPD – respiratory drive
Toxic – inflammation / scarring after 40hrs with
100%
Dry eyes
68
Oxygen toxicity
 Central
nervous system
– Visual changes, ringing in ears, nausea,
twitching, irritability, dizziness,
convulsions
 Pulmonary
– Lungs show inflammation / scarring
(ARDS) and pulmonary oedema
 Retinopathic
– Retinal damage
69
Other Complications




Decreased cardiac
output
Pneumonia (VAP)
Psychological
problems
Endotracheal tube
complications
–
–
–
–
Laryngeal injury
Tracheal stenosis
Tracheomalacia
Endobronchial
intubation
– Sinusitis
70
Suctioning and Mechanical
Ventilation
 Causes
Lung de-recruitment due to
– Disconnection from the ventilator
 Loss
of PEEP
 Worse V/Q mismatch
– Suctioning procedure itself
 High
negative pressure decreases lung
volume
 Worse if the suction is open
Suction only when clinically indicated / Pre oxygenate /
Minimal suction pressure / limit suction time
71
Prone Positioning
What a nightmare!
 Can dramatically
alter oxygenation
 Also

– Induces a uniform
V/Q distribution
– Promotes alveolar
recruitment
– Promotes secretion
drainage
72
Prone Positioning
 Debate
about outcome in the most
hypoxic
 Complications,
– Manual Handling
– Accidental Extubation
– Pressure sores
– Facial Oedema
– Line disconnection
73
Gattinoni et al (2001)
NEJM 345 (8): 568
Oxygenation
Survival
Improved oxygenation, but not overall survival rate
74
High-Frequency Oscillatory
Ventilation in Adults





Seems a nice idea
3 – 10 Hz oscillation
‘Tidal volume’ less
than normal
Less opening and
closing of lungs
Well established in
neonatal and
paediatric population
Issues,
 Patients need heavy
sedation / NMJ
blockade
 Drop in preload
 Transport not possible
 Clinical Ex difficult
 Little research until
now
75
HFOV for ARDS in Adults
Derdak et al (2002) Am J Resp & Crit Care Med Vol 166.
pp. 801 – 808
 Multi-centre
randomised control trial
 148
patients
 HFOV n = 75
 Conventional Ventilation n = 73
 Outcome measure was survival
without mechanical ventilation at 30
days
76
HFOV for ARDS in Adults
Derdak et al (2002) Am J Resp & Crit Care Med Vol 166.
pp. 801 – 808
Non significant
trend towards
higher survival
 37% versus 52%
 P = 0.102
 Big improvement in
PaO2/FiO2 (p =
0.008) in HFOV.

77
HFOV for ARDS in Adults
Derdak et al (2002) Am J Resp & Crit Care Med Vol 166.
pp. 801 – 808
 Unanswered
Questions
– Ideal timing of the intervention
– Prone position
– Nitric Oxide
– When do you discontinue
– Long term effects on lung function
– Use of volume recruitment methods
78
ECMO




It involves connecting the
internal circulation to an
external blood pump and
artificial lung.
A catheter placed in the
right side of the heart
carries blood to a pump,
then to a membrane
oxygenator, where gas
exchange of O2 and CO2
takes place.
The blood then passes
through tubing back into
the patient's veins or
arteries.
Patients are
anticoagulated
79
CESAR Trial (recruited 2001 – 2006)
(reported 2008)
Conventional
Ventilation or
ECMO for Severe
Adult Respiratory
Failure
 180 patients
 Use of ECMO
results in 1 extra
survivor for every
6 patients treated

80
Your Patient is Hypoxic So What
Do You Do
 Remember
– “Air goes in and out and blood goes
round and round”
– That just getting air into the lungs may
not be enough
81
Your Patient is Hypoxic So What
Do You Do
 Decide
– How much time to you have?
– What resources are available
– Is escalation appropriate
82
Your Patient is Hypoxic - What Do You
Do?
– Increase the supply of Oxygen
– Drive it into the lungs
– Get the lungs in the best shape possible
– Make sure blood is getting to the lungs
– Reduce the metabolic demand for
oxygen
83
Scenarios
84
Case
44 year old lady
11/7 post
intubation for
pneumonia.
 Trachy. FiO2 .3, PO2
11
 Sudden SOB
 FiO2 1.0, Sats 80%

– Increase the supply
of Oxygen
– Drive it into the
lungs
– Get the lungs in the
best shape possible
– Make sure blood is
getting to the lungs
– Reduce the demand
for oxygen
85
Case
70 year old
gentleman
 Sudden SOB
 HR 150 bpm
 RR 50
 FiO2 0.21

– Increase the supply
of Oxygen
– Drive it into the
lungs
– Get the lungs in the
best shape possible
– Make sure blood is
getting to the lungs
– Reduce the demand
for oxygen
86
Case
55 year old
 Rescued from
smoke filled room
 PaO2 7 on FiO2
85%

– Increase the supply
of Oxygen
– Drive it into the
lungs
– Get the lungs in the
best shape possible
– Make sure blood is
getting to the lungs
– Reduce the demand
for oxygen
87
THE END
88