Dr.

KANNAN NAIR
Jr.CONSULTANT
APOLLO HOSPITALS
Overview
Intro
NIV
Basic Modes
Settings
Specific Conditions
Ventilators
Other modes
Acute respiratory failure
 Hypoxia (PO2 < 60mmHg)
 Low inspired O2
 Hypoventilation – CNS, peripheral neuro, muscles, chest wall
 V/Q mismatch
 Shunt – pneumonia, APO, collapse, contusions
 Alveoli perfused but not ventilated
 Venous admixture
 Anatomical shunt – cardiac anomaly
 Increased dead space (hypercapnia) – hypovolaemia, PE, poor cardiac function
 Diffusion abnormality – severe destructive disease of the lung – fibrosis,
severe APO, ARDS
 Hypercapnia (PCO2 >50mmHg)
 Hypoventilation
 Dead space ventilation
 Increased CO2 production
Shunt
450 0
mmHg mmHg

100% 70%
70
% %
70 85%
Mechanical Ventilation
Pump gas in and letting it flow out
Function
 Gas exchange
 Manage work of breathing
 Avoid lung injury
Physics
 Flow needs a pressure gradient
 Pressure to overcome airway resistance and inflate lung
 Pressure (to overcome resistance) = Flow x Resistance
 Alveolar pressure = (Volume/Compliance) + PEEP
 Airway pressure = (Flow x Resistance) + (V/C) + PEEP
Gas Exchange
Oxygenation – get O2 in
 FiO2
 Ventilation (minor effect) – alveolar gas equation, CO2 effect
 Mean alveolar pressure
 Mean airway pressure – surrogate marker, affected by airway resistance
 Pressure over inspiration + expiration
 Set Vt or inspiratory pressure
 Inspiratory time
 PEEP
 Reduce shunt
 Re-open alveoli – PEEP
 Prolonging inspiration – improve ventilation of less compliant alveoli
Ventilation – get CO2 out
 Alveolar ventilation = RR x (Tidal volume – Dead space)
Adverse Effects
 Barotrauma
 High alveolar pressure
 High tidal volume
 Shear injury –
 Repetitive collapse + re-expansion of alveoli
 Tension at interface between open + collapsed alveoli
 Pneumothorax, pneumomediastinum, surgical emphysema, acute lung injury
 Gas trapping
 Insufficient time for alveoli to empty
 Increase risk
 Airflow obstruction – asthma, COPD
 Long inspiratory time
 High respiratory rate
 Progressive
 Hyperinflation
 Rise in end-expiratory pressure – intrinsic-PEEP, auto-PEEP
 Result – Barotrauma, Cardiovascular compromise (high intrathoracic pressure)
 Oxygen toxicity
 Acute lung injury due to high O2 concentrations
 Cardiovascular effects
 Preload – positive intrathoracic pressure reduces venous return
 Afterload - positive intrathoracic pressure reduces afterload
 Cardiac Output – depends on LV contractility
 Normal – IPPV decreases CO
 Reduced – IPPV increases CO
 Myocardial O2 consumption - reduced
NIV
CPAP
Similar to PEEP
Splint alveoli open – reduce shunt
Spontaneous breathing at elevated baseline pressure
BiPAP
Ventilatory assistance without invasive artificial airway
Fitted face/nasal mask
Initial settings 10/5
NIV
NIV
 Indicator of success  Contraindications
 Known benefits  Cardiac/Resp arrest
 Younger age  Non-respiratory organ failure
 Lower APACHE score  Encephalopathy GCS <10
 Cooperative  GIH
 Intact dentition  Haemodynamically unstable
 Moderate hypercarbia (pH<7.35,  Facial or neurological surgery,
>7.10) trauma or deformity
 Improvement within first 2 hrs  High aspiration risk
 Prolonged ventilation
anticipated
 Recent oesophageal
anastamosis
NIV Benefits
General
COPD
Cardiogenic pulmonary oedema
Hypoxaemic respiratory failure
Asthma
Post-extubation
Immunocompromised
Other diseases
What is a Mode?
3 components
Control variable
Pressure or volume
Breath sequence
Continuous mandatory
Intermittent mandatory
Continuous spontaneous
Targeting scheme (settings)
Vt, inspiratory time, frequency, FiO2, PEEP, flow
trigger
Volume Control Ventilation
Set tidal volume
Minimum respiratory rate
Assist mode – both ventilator and patient can initiate
breaths
Advantage
 Simple, guaranteed ventilation, rests respiratory muscle
Disadvantages
 Not synchronised – ventilator breath on top of patient breath
 Inadequate flow – patient sucks gas out of ventilator
 Inappropriate triggering
 Decreased compliance – high airway pressure
 Requires sedation for synchrony
Pressure Control Ventilation
Set inspiratory pressure
Constant pressure during inspiration
High initial flow
Inspiratory pause – built in
Advantages
Simple, avoids high inspiratory pressures, improved
oxygenation
Disadvantages
Not synchronised
Inappropriate triggers
Decreased compliance – reduced tidal volume
PCV
Pressure Support
Set inspiratory pressure
Patient initiates breath
Back-up mode – apnoea
Cycle from inspiration to expiration
Inspiratory flow falls below set proportion of peak
inspiratory flow
Advantages
Simple, avoids high inspiratory pressure, synchrony,
less sedation, better haemodynamics
Disadvantages
Dependent on patient breaths
Affected by changes in lung compliance
PS
Synchronised Intermittent Mandatory
Ventilation
Mandatory breaths – VCV, PCV
Patient breaths – depends on SIMV cycle
Synchronised mandatory breath
Pressure support breath
Advantages
Synchrony, guaranteed minute ventilation
Disadvantages
Sometimes complicated to set
SIMV
VCV vs PCV
VCV vs PCV - Advantages
PCV + PS • VCV
Variable flow – Consistent TV
Reduced WOB • changing
Max Palveolar = Max impedance
Pairway (or less) • Auto-PEEP
Palveolar controlled – Minimum min. vent.
Variable I-time & (f x TV) set
pattern (PS) – Variety of flow waves
Better with leaks
VCV vs PCV - Disadvantages
PCV + PS • VCV
Variable tidal volume – Variable pressures
• airway
 Too large or too small
 No alarm/limit for
• alveolar

excessive TV (except – Fixed flow pattern

some new gen. vents) – Variable effort = variable
Some variablity in work/breath
– Compressible vol.
max pressures (PC,
– Leaks = vol. loss
expir. effort)
Settings
 FiO2 – start at 1.0
 RR – average 12, higher for those with sepsis/acidosis
 Tidal volume – 500ml, 8ml/kg, smaller volumes in ARDS
 Inspiratory pressure - <30cmH2O, sum of PEEP + Pinsp
 Inspiratory time
 I:E – normally 1:2, simulates normal breathing – synchrony
 PCV – easy to set
 VCV – complicated, Time = Volume/Flow
 PEEP
 Start at 5cmH2O
 Higher – APO, ARDS
 Lower – asthma, COPD
 Triggering
 Flow triggering – more sensitive, synchrony, -2cmH2O
 Pressure triggering
 Inappropriate triggering – triggering when no patient effort
 Oxygenation
 FiO2, PEEP, Insp Time, InspP, Insp pause
 Problems – CVS effects, gas trapping, barotrauma
 Ventilation
 Tidal volume, RR, eliminate dead space
 Problems – barotrauma, gas trapping (reduced minute ventilation)
Troubleshooting

 Airway pressure
 Ventilator – settings, malfunction
 Circuit – kinking, water pooling, wet filter
 ETT – kinked, obstructed, endobronchial intubation
 Patient – bronchospasm, compliance (lungm, pleura, chest wall), dysynchrony, coughing
 Inspiratory pause pressure - Estimate of alveolar pressure
 Tidal volume
 Reduced – respiratory acidosis
 Monitor in PCV/PS
 Changes in compliance – anywhere in system
 Expired Vt – more accurate
 Minute ventilation – determined by RR + Vt
 Apnoea – important in PS
Total PEEP

Pressure
 Intrinsic PEEP (gas trapping)
 Expiratory pause hold

PEEPe
 Hypotension – after initiating IPPV
 Hypovolaemia/Reduced VR PEEPi
 Drugs
 Gas trapping – disconnect

Time
Tension pneumothorax
 Dysynchrony
 Patient factors
 Ventilator – settings, eg I:E
 PS > SIMV > PCV/VCV
Troubleshooting
Desaturation
Patient causes
 All causes of hypoxic respiratory failure
 Endobronchial intubation, PTx, collapse, APO, bronchospasm,
PE
Equipment causes
FIO2 1.0
Sat O2 waveform
Chest moving?
 Yes – Examine patient, treat cause
 No – Manually ventilate
 No – ETT/Patient problem
 Yes – Ventilator problem – setting, failure, O2 failure
Ventilators
Maquet Evita
VCV PS
PCV PCV+
PRVC SIMV
PS/CPAP PCV+A
SIMV (VC) + PS Autoflow
SIMV (PC) + PS
SIMV (PRVC) + PS
MMV
NAVA
Adaptive Modes - PRVC
PCV unable to deliver guaranteed minimum
minute ventilation
Changing lung mechanics + patient effort
Pressure controlled breaths with target tidal
volume
Inspiratory pressure adjusted to deliver minimum
target volume
Not VCV - average minimum tidal volume
guaranteed
Like PCV – constant airway pressure, variable
flow (flow as demanded by patient)
Adaptive Modes - PRVC
Consistent tidal volumes
Promotes inspiratory flow synchrony
Automatic weaning
Inappropriate – increased respiratory drive, eg severe
metabolic acidosis
Evidence – lower peak inspiratory pressures
VCV vs PRVC
Adaptive Modes - Autoflow
First breath uses set TV & I-time
 Pplateau measured
Pplateau then used
V/P measured each breath
Press. changed if needed (+/- 3)
Dual mode similar to PRVC
 Targets vol., applies variable press. based on mechanics
measurements
 Allows highly variable inspiratory flows
 Time ends mandatory breaths
Adds ability to freely exhale during mandatory inspiration
(maintains pressure)
PCV + Assist
Like PCV, flow varies automatically to varying patient
demands
Constant press. during each breath - variable press.
from breath to breath
Mandatory + patient breaths the same
Inverse Ratio Ventilation
Increased mean airway pressure
Prolonged I:E ratio
Improved oxygenation
Reduced shunting
Improved V/Q matching
Decreased dead space
Heavy sedation, paralysis
Preferred PCV
Benefit – no effect in mortality in ARDS
Other Modes
Adaptive support ventilation
Mandatory minute ventilation
Adaptive pressure control
Proportional assist ventilation
Pressure support (spontaneous breaths)
Pressure applied function of patient effort
Automatic tube compensation
adjusts its pressure output in accordance with flow,
theoretically giving an appropriate amount of pressure
support
Airway Pressure-Release
Ventilation
High constant PEEP + intermittent releases
Unrestricted spontaneous breaths – reduced sedation
Extreme form of inverse ratio ventilation
E:I – 1:4
Spontaneous breaths – 10-40% total minute
ventilation
APRV
Settings – 2 pressure levels, 2 time durations
Uses – ALI, ARDS
Caution – COPD, increased respiratory drive
APRV
Increase mean airway pressure
Alveolar recruitment, improve oxygenation
Promote spontaneous breathing
Improved V/Q match, haemodynamics
Improved synchrony
Evidence – no difference in mortality, decreased
duration of ventilation
High-Frequency Ventilation
4 types
High frequency jet ventilation
 Ventilation by jet of gas
 14-16G cannula, specialised ventilator
 35 psi, RR100-150, Insp 40%

High frequency oscillatory ventilation

High frequency percussive ventilation
 HFV + PCV
 HFOV – oscillating around 2 pressure levels
 Less sedation, better clearance of secretions

High frequency positive pressure ventilation

 Conventional ventilation at setting limits
High Frequency Oscillatory Ventilation
Ventilator delivers a constant flow (bias flow)
Valve creates resistance – maintain airway
pressure
Piston pump oscillates 3-15Hz (RR160-900)
“Chest wiggle” – assess amplitude
Tidal volumes – less than dead space
Ventilation – achieved by laminar flow
Deep sedation, paralysis
HFOV
CO2 clearance
Decrease oscillation frequency, increase amplitude,
increase inspiratory time, increase bias flow (with ETT
cuff leak)
Oxygenation
Mean airway pressure, FiO2
Settings
Airway pressure amplitude
Mean airway pressure
% inspiration
Inspiratory bias flow
FiO2
HFOV
Applications
 ARDS
 Lung protection – highest mean airway pressure + lowest tidal
volumes
 Ventilatory failure – FiO2>0.7, PEEP>14, pH <7.25, Vt >6ml/kg,
plateau pressure >30)
Contraindicated
 Severe airflow obstruction
 Intracranial hypertension
Evidence
 Animal models – less histologic damage + lung inflammation
 Better oxygenation as rescure therapy in ARDS
 No difference in mortality
Mean Airway Pressure
Main factor in recruitment and oxygenation
Increased surface area for O2 diffusion
Problems
Barotrauma
Haemodynamic instability
Contraindicated patients
Deep sedation, paralysis
Specific Conditions
 ARDS
 Definition
 Diffuse bilateral pulmonary infiltrates
 No clinical evidence of Left Atrial Hypertension (CWP<18mmHg)
 PaO2/FiO2 of 300 or less
 Exclusions
 Unilateral lung disease
 Children (wt less than 25kg)
 Severe obstructive lung disease (asthma, COPD)
 Raised intracranial pressure
 High PEEP, low volumes + pressure
 SIMV(PRVC) + PS
 Vt 6ml/gk – check plateau pressure
 Pins >30cmH2O – reduce Vt
 Lowest plateau pressure possible
 RR 6-35, aim pH 7.3-7.45
 Evidence – improved mortality

FiO2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0

PEEP 5 5-8 8-10 10 10-14 14 14-18 18-22
Ventilator Induced Lung Injury
Excessive inflation pressure
Mechanical tissue damage
Inflammation – mechano-signaling due to tensile
forces
Overstretching of lung units
Shear force at junction of open and collapsed tissue
Repeated opening and closing of small airways under
high pressure
 End-Expiration Pathways to VILI

Extreme Stress/Strain Tidal Forces Moderate Stress/Strain

(Transpulmonary and
Microvascular
Pressures)

Rupture Signaling

Mechano signaling via

integrins, cytoskeleton, ion channels

inflammatory cascade

Cellular Infiltration and Inflammation

Marini / Gattinoni CCM 2004

Spectrum of Regional Opening Pressures
(Supine Position)
Opening
Pressure
Superimposed
Pressure Inflated 0

Small Airway 10-20 cmH2O

Collapse

Alveolar Collapse
(Reabsorption) 20-60 cmH2O

Consolidation 
= Lung Units at Risk for Tidal
Opening & Closure
Lung Protection Strategies
Heterogenous lung units
PEEP
Tidal volume
Keep the lung as open as possible without generating
excessive regional tissue stresses is a major goal of
modern practice
Prone Ventilation
Homogenise transpleural pressure
Compression – reduced compression from heart +
abdomen
Improved recruitment
Increase in FRC
Decreased shunt
Benefit
Improved oxygenation in 60-80% patient, even on
return to supine position
No change mortality
Recruitment Manoeuvres
Open collapsed lung tissue so it can remain open during
tidal ventilation with lower pressures and PEEP, thereby
improving gas exchange and helping to eliminate high
stress interfaces
Although applying high pressure is fundamental to
recruitment, sustaining high pressure is also important
Methods of performing a recruiting maneuver include
single sustained inflations and ventilation with high PEEP
Three Types of Recruitment Maneuvers
Specific Conditions
 Unilateral lung disease
 Similar approach to ARDS
 Increase Insp time – improve gas distribution
 Lateral position – normal lung down
 Reduce shunt
 Reduce normal lung compliance
 Risk of contamination
 Independent lung ventilator
 Asthma
 Maximise expiratory time, low RR – permissive hypercarbia
 Short inspiratory time
 High airway pressure - ?significance
 Expiratory hold
 Aim – PEEPi < 10cmH20, Pplat <20cmH2O
 COPD
 Similar to asthma
 Bronchospasm not as great, reduced lung compliance
Airway Obstruction
Aim – relieve work of breathing, minimise auto-PEEP
Gas trapping
 Increases work of breathing
 Haemodynamic compromise
 Predisposes to barotrauma
 Decreases ventilation
PEEP
 Effects Depend on Type and Severity of Airflow Obstruction
 Generally Helpful if PEEP  Original Auto-PEEP
 Potential Benefits
 Decreased Work of Breathing
 Increased VT
 Improved Distribution of Ventilation
NAVA
Neurally adjusted ventilatory assist
Controls ventilator output by measuring the neural
traffic to the diaphragm
NAVA senses the desired assist using an array of
esophageal EMG electrodes positioned to detect the
diaphragm’s contraction signal
Flexible response to effort
Improves synchrony and weaning
 Ideal
Central Nervous System
Neuro-Ventilatory Coupling

Technology

Phrenic Nerve

New
Diaphragm Excitation Ventilator
 Technology Unit
Diaphragm Contraction

Chest Wall and Lung
Expansion
 Current
Airway Pressure, Flow and Technology
Volume