This document discusses the physiology of positive pressure ventilation. It covers: - The goals and types of mechanical ventilation including positive and negative pressure ventilation. - Key concepts including pressure gradients, time constants, airway pressures, and the effects of PEEP. - How mechanical ventilation supports gas exchange and manipulates work of breathing while minimizing cardiovascular effects. - Different pressure, volume, and flow waveforms and how they impact ventilation. - Common ventilator modes like volume control, pressure control, and how they are classified based on triggers, limits, and cycling variables.

1. Physiology of positive
pressure ventilation
SAMIR EL ANSARY

2. Global Critical Care
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3. Mechanical ventilation –
Supports / replaces the normal ventilatory
pump moving air in & out of the lungs.
Primary indications –
a.apnea
b.Ac. ventilation failure
c. Impending ventilation failure
d.Severe oxygenation failure

4. Goals
 Manipulate gas exchange
↑ lung vol – FRC, end insp / exp lung
inflation
Manipulate work of breathing (WOB)
Minimize CVS effects

5. ARTIFICIAL
VENTILATION
- Creates a transairway P
gradient by ↓ alveolar P
to a level below airway
opening P
- Creates – P around
thorax
e.g. iron lung
chest cuirass / shell
- Achieved by applying +
P at airway opening
producing a transairway
P gradient
Negative pressure
ventilation Positive pressure
ventilation

6. ventilation without artificial airway
-Nasal , face mask
adv.
1.Avoid intubation / c/c
2.Preserve natural airway defences
3.Comfort
4.Speech/ swallowing +
5.Less sedation needed
6.Intermittent use
Noninvasive
Disadv
1.Cooperation
2.Mask discomfort
3.Air leaks
4.Facial ulcers, eye irritation, dry
nose
5.Aerophagia
6.Limited P support
e.g. BiPAP, CPAP

7. Ventilatory support
FULL PARTIAL
All energy provided by ventilator
e.g. ACV / full support SIMV ( RR
= 12-26 & TV = 8-10 ml/kg)
Pt provides a portion of energy
needed for effective ventilation
e.g. SIMV (RR < 10)
Used for weaning
WOB total = WOB ventilator (forces gas into lungs)+ WOB patient (msls draw gas into
lungs)

8. Understanding physiology of PPV
1) Different P gradients
2) Time constant
3) Airway P ( peak, plateau, mean )
4) PEEP and Auto PEEP
5) Types of waveforms

9. Pressure gradients

11. Distending pressure of lungs
Elastance load
Resistance load
Distending
pressure

12. Flow through the airways is generated by
Transairway pressure (pressure at the airway
opening minus pressure in the lungs).
Expansion of the elastic chamber is generated
by Transthoracic pressure (pressure in the lungs
minus pressure on the body surface).

13. Transrespiratory pressure (pressure at the airway
opening minus pressure on the body surface) is the
sum of these two pressures and is the total pressure
required to generate inspiration.
Transrespiratory pressure can have two components,
one secondary to the ventilator (pvent) and one
secondary to the respiratory muscles (Pmusc)

14. Trans pulmonary pressure (pressure at airway opening
minus pleural pressure) [= Transrespiratory pressure?]
Transpulmonary pressure is the distending force of the
lung
The airway-pressure gauge on a positive-pressure
ventilator displays transrespiratory pressure

15. Pressure, volume, and flow are functions of time
and are called variables. They are all measured
relative to their values at end expiration.
Elastance and resistance are assumed to
remain constant and are called parameters.

16. Elastance(measure of stiffness) is
the inverse of compliance(measure
of stretchiness)
An increase in elastance implies
that the system is becoming stiffer.

17. Mean airway pressure Paw = Transrespiratory
pressure
Mean alveolar pressure Palv = Transthoracic
pressure

18. Transpulmonary pressure is the distending
pressure in a spontaneously(negative)
breathing patient
Transrespiratory pressure is the distending
pressure in positive pressure ventilation

20. Airway pressures
Peak insp P (PIP)
• Highest P produced
during insp.
• PRESISTANCE + P INFLATE
ALVEOLI
• Dynamic compliance
• Barotrauma
Plateau P
• Observed during end insp
pause
•P INFLATE ALVEOLI
•Static compliance
•Effect of flow resistance
negated

21. Time constant
• Defined for variables that undergo exponential
decay
• Time for passive inflation / deflation of lung / unit
t = compliance X resistance
= VT .
peak exp flow
Normal lung C = 0.1 L/cm H2O
R = 1cm H2O/L/s
COAD – resistance to exp increases → time constant increases → exp time to be
increased lest incomplete exp ( auto PEEP generates).
ARDS - inhomogenous time constants

22. Why and how to separate dynamic
& static components ?
• Why – to find cause for altered airway
pressures
• How – adding end insp pause
- no airflow, lung expanded, no
expiration

23. How -End inspiratory hold
• Pendelluft phenomenon
• Visco-elastic properties of lung
End-inspiratory pause
Ppeak < 50 cm H2O
Pplat < 30 cm H2O
Ppeak = Pplat + Paw

24. At the start of inflation, the airway pressure
immediately rises because of the resistance to gas flow
(A), and at the end of inspiratory gas flow the airway
pressure immediately falls by the same pressure (A) to
an inflexion point.
Thereafter, the airway pressure more gradually declines
to the plateau pressure.
The loss of airway pressure after the inflexion (B) is
due to gas redistribution (Pendelluft) and the visco-
plasto-elastic lung and thorax behaviour

25. P2(Pplat) is the static pressure of the respiratory
system, which in the absence of flow equals the
alveolar pressure, which reflects the elastic retraction
of the entire respiratory system.
The pressure drop from PIP to P1 represents the
pressure required to move the inspiratory flow along
the airways without alveolar interference, thus
representing the pressure dissipated by the flow-
dependent resistances(airway resistance).

26. The slow post-occlusion decay from P1 to P2 depends
on the viscoelastic properties of the system and on the
pendulum-like movement of the air (pendelluft).
During the post-inspiratory occlusion period there is a
dynamic elastic rearrangement of lung volume, which
allows the different pressures in alveoli at different
time constants to equalize, and depends on the
inhomogeneity of the lung parenchyma.

27. The lung regions that have a low time constant (ie,
rapid zones), where the alveolar pressure rises rapidly,
are emptied in the lung regions that have higher time
constants (ie, slow zones), where the pressure rises
more slowly because of higher resistance or lower
compliance

28. The static compliance of the respiratory
system mirrors the elastic features of the respiratory
system, whereas
The dynamic compliance also includes the
resistive (flow-dependent) component of the airways
and the endotracheal tube

29. When the inspiratory pause is shorter than 2 seconds,
P2 does not always reflect the alveolar pressure.
The compliance value thus measured is called quasi-
static compliance.
In healthy subjects the difference between static
compliance and quasi-static compliance is minimal,
whereas it is markedly higher in patients who have
acute respiratory distress syndrome or chronic
obstructive pulmonary disease

30. Ppeak < 50 cm H2O; Pplat
< 35 cm H2O – to avoid
barotrauma

31. • Pendulum like movement of air between lung units
• Reflects inhomogeneity of lung units
• More in ARDS and COPD
• Can lead to falsely measured high Pplat if the end-
inspiratory occlusion duration is not long enough

32. Why

33. Mean airway P (MAP)
• average P across total cycle time (TCT)
• MAP = 0.5(PIP-PEEP)X Ti/TCT + PEEP
• Decreases as spontaneous breaths increase
• MAPSIMV < MAPACV
• Hemodynamic consequences
Factors
1. Mandatory breath modes
2. ↑insp time , ↓ exp time
3. ↑ PEEP
4. ↑ Resistance, ↓compliance
5. Insp flow pattern

34. PEEP
BENEFITS
1. Restore FRC/
Alveolar recruitment
2. ↓ shunt fraction
3. ↑Lung compliance
4. ↓WOB
5. ↑PaO2 for given FiO2
DETRIMENTAL EFFECTS
1. Barotrauma
2. ↓ VR/ CO
3. ↑ WOB (if overdistention)
4. ↑ PVR
5. ↑ MAP
6. ↓ Renal / portal bld flow
PEEP prevents complete collapse of the alveoli and keep them
partially inflated and thus provide protection against the development
of shear forces during mechanical inflation

35. How much PEEP to apply?
Lower inflection point – transition from flat to steep part
- ↑compliance
- recruitment begins (pt. above closing vol)
Upper inflection point – transition from steep to flat part
- ↓compliance
- over distension

36. Set PEEP above LIP – Prevent end expiratory airway collapse
Set TV so that total P < UIP – prevent overdistention
Limitation – lung is inhomogenous
- LIP / UIP differ for different lung units

37. Auto-PEEP or Intrinsic PEEP
• What is Auto-PEEP?
– Normally, at end expiration, the lung volume is
equal to the FRC
– When PEEPi occurs, the lung volume at end
expiration is greater then the FRC

38. Auto-PEEP or Intrinsic PEEP
• Why does hyperinflation occur?
– Airflow limitation because of dynamic collapse
– No time to expire all the lung volume (high RR or
Vt)
– Lesions that increase expiratory resistance
Function of-
Ventilator settings – TV, Exp time
Lung func – resistance,
compliance

39. Auto-PEEP or Intrinsic PEEP
• Auto-PEEP is measured in a relaxed pt with an
end-expiratory hold maneuver on a mechanical
ventilator immediately before the onset of the
next breath

40. Inadequate expiratory time - Air trapping
iPEEP
Flow curve FV loop
1. Allow more time for expiration
2. Increase inspiratory flow rate
3. Provide ePEEP

41. Disadv
1. Barotrauma / volutrauma
2. ↑WOB a) lung overstretching ↓contractility of diaphragm
b) alters effective trigger sensitivity as autoPEEP must be
overcome before P falls enough to trigger breath
3. ↑ MAP – CVS side effects
4. May ↑ PVR
Minimising Auto PEEP
1. ↓airflow res – secretion management, bronchodilation,
large ETT
2. ↓Insp time ( ↑insp flow, sq flow waveform, low TV)
3. ↑ exp time (low resp rate )
4. Apply PEEP to balance AutoPEEP

42. Cardiovascular effects of PPV
Spontaneous ventilation PPV

43. Determinants of hemodynamic effects
due to – change in ITP, lung volumes, pericardial
P
severity – lung compliance, chest wall
compliance, rate & type of ventilation, airway
resistance

44. Low lung compliance – more P spent in lung expansion & less change in ITP
less hemodynamic effects (DAMPNING EFFECT OF LUNG)
Low chest wall compliance – higher change in ITP needed for effective ventilation
more hemodynamic effects

45. Effect on CO ( preload , afterload )
Decreased PRELOAD
1.compression of intrathoracic veins (↓ CVP, RA
filling P)
2.Increased PVR due to compression by alveolar
vol (decreased RV preload)
3.Interventricular dependence - ↑ RV vol
pushes septum to left & ↓ LV vol & LV output
Decreased afterload
1. emptying of thoracic aorta during insp
2. Compression of heart by + P during systole
3. ↓ transmural P across LV during systole

46. PPV
↓ preload,
ventricular filling
↓ afterload ,
↑ventricular
emptying
CO –
1. INCREASE
2. DECREASE
1. Intravascular fluid status
2. Compensation – HR, vasoconstriction
3. Sepsis,
4. PEEP, MAP
5. LV function

47. Effect on other body systems

48. Overview
1. Mode of ventilation – definition
2. Breath – characteristics
3. Breath types
4. Waveforms – pressure- time, volume –time, flow-
time
5. Modes - Volume & pressure limited
6. Conventional modes of ventilation
7. Newer modes of ventilation

49. What is a ‘ mode of ventilation’ ?
A ventilator mode is delivery a sequence of
breath types & timing of breath

50. Breath characteristics
A= what initiates a breath -
TRIGGER
B = what controls / limits it –
LIMIT
C= What ends a breath -
CYCLING

51. TRIGGER
What the ventilator
senses to initiate a
breath
Patient
• Pressure
• Flow
Machine
• Time based
Recently – EMG monitoring of phrenic
Nerve via esophageal transducer
Pressure triggering
-1 to -3 cm H2O
Flow triggering
-1 to -3 L/min

52. CONTROL/ LIMIT
Variable not allowed to
rise above a preset
value
Does not terminate a
breath
 Pressure
 Volume
 Pressure Controlled
• Pressure targeted,
pressure limited - Ppeak
set
• Volume Variable
 Volume Controlled
• Volume targeted,
volume limited - VT set
• Pressure Variable
 Dual Controlled
• volume targeted
(guaranteed) and
pressure limited

53. CYCLING VARIABLE
Determines the end of
inspiration and the
switch to expiration
 Machine cycling
• Time
• Pressure
• Volume
 Patient cycling
• Flow
May be multiple but
activated in hierarchy as
per preset algorithm

54. Breath types
Spontaneous
Both triggered and
cycled by the patient
Control/Mandatory
Machine triggered
and machine cycled
Assisted
Patient triggered but
machine cycled

55. Waveforms
1. Volume -time
2. Flow - time
3. Pressure - time

56. a) Volume – time graphs
1. Air leaks
2. Calibrate flow transducers

57. b) Flow waveforms
1. Inspiratory flow waveforms

58. Sine
Square
Decelerating
• Resembles normal
inspiration
• More physiological
• Maintains constant flow
• high flow with ↓ Ti &
improved I:E
• Flow slows down as
alveolar pressure increases
• meets high initial flow
demand in spont breathing
patient - ↓WOB
Accelerating
• Produces highest PIP as
airflow is highest towards
end of inflation when
alveoli are less compliant
Square- volume
limited modes
Decelerating –
pressure limited
modes
Not used

59. Inspiratory and expiratory flow waveforms

60. 2. Expiratory flow waveform
 Expiratory flow is not driven by ventilator and is passive
 Is negative by convention
 Similar in all modes
 Determined by Airway resistance & exp time (Te)
Use
1.Airtrapping & generation of AutoPEEP
2.Exp flow resistance (↓PEFR + short Te) & response
bronchodilators (↑PEFR)

61. c) Pressure waveform
1. Spontaneous/ mandatory breaths
2. Patient ventilator synchrony
3. Calculation of compliance & resistance
4. Work done against elastic and resistive
forces
5. AutoPEEP ( by adding end exp pause)

62. Classification of modes of ventilation
Volume controlled Pressure controlled
TV & inspiratory flow are
preset
Airway P is preset
Airway P depends on above
& lung elastance &
compliance TV
& insp flow depend on
above & lung elastance &
compliance

64. Volume controlled Pressure controlled
Trigger - patient /
machine
Patient / machine
Limit Flow Pressure
Cycle Volume / time time / flow
TV Constant variable
Peak P Variable constant
Modes ACV, SIMV PCV, PSV

65. Volume controlled Pressure controlled
Advantages
1. Guaranteed TV
2. Less atelectasis
3. TV increases linearly with MV
Advantages
1. Limits excessive airway P
2. ↑ MAP by constant insp P – better
oxygenation
3. Better gas distribution – high insp flow
↓Ti & ↑Te ,thereby, preventing
airtrapping
4. Lower WOB – high initial flow rates
meet high initial flow demands
5. Lower PIP – as flow rates higher when
lung compliance high i.e early insp.
phase
Disadvantages
1. Limited flow may not meet
patients desired insp flow rate-
flow hunger
2. May cause high Paw (
Disadvantages
1. Variable TV
↑TV as compliance ↑
↓TV as resistance ↑

66. Conventional modes of ventilation
1. Control mandatory ventilation (CMV / VCV)
2. Assist Control Mandatory Ventilation (ACMV)
3. Intermittent mandatory ventilation (IMV)
4. Synchronized Intermittent Mandatory
Ventilation (SIMV)
5. Pressure controlled ventilation (PCV)
6. Pressure support ventilation (PSV)
7. Continuous positive airway pressure (CPAP)

67. 1. Control mandatory ventilation (CMV / VCV)
• Breath - MANDATORY
• Trigger – TIME
• Limit - VOLUME
• Cycle – VOL / TIME
• Patient has no control
over respiration
• Requires sedation and
paralysis of patient

68. 2. Assist Control Mandatory Ventilation
(ACMV)
• Patient has partial control over his respiration – Better Pt ventilator synchrony
• Ventilator rate determined by patient or backup rate (whichever is higher) – risk of
respiratory alkalosis if tachypnoea
• PASSIVE Pt – acts like CMV
• ACTIVE pt – ALL spontaneous breaths assisted to preset volume
• Breath – MANDATORY
ASSISTED
• Trigger – PATIENT
TIME
• Limit - VOLUME
• Cycle – VOLUME / TIME
Once patient initiates
the breath the
ventilator takes over
the WOB
If he fails to initiate,
then the ventilator
does the entire WOB

69. 3. Intermittent mandatory ventilation (IMV)
Breath stacking
Spontaneous breath immediately after a
controlled breath without allowing time
for expiration ( SUPERIMPOSED BREATHS)
 Basically CMV which allows
spontaneous breaths in
between
 Disadvantage
 In tachypnea can lead to
breath stacking - leading to
dynamic hyperinflation
 Not used now – has been
replaced by SIMV
• Breath – MANDATORY
SPONTANEOUS
• Trigger – PATIENT
VENTILATOR
• Limit - VOLUME
• Cycle - VOLUME

70. 4.Synchronized Intermittent Mandatory
Ventilation (SIMV)
• Breath –
SPONTANEOUS
ASSISTED
MANDATORY
• Trigger – PATIENT
TIME
• Limit - VOLUME
• Cycle – VOLUME/ TIME

71. • Basically, ACMV with spontaneous breaths (which
may be pressure supported) allowed in between
• Synchronisation window – Time interval from the
previous mandatory breath to just prior to the next
time triggering, during which ventilator is
responsive to patients spontaneous inspiratory
effort
• Weaning
Adv
 Allows patients to exercise their respiratory muscles in
between – avoids atrophy
 Avoids breath stacking – ‘Synchronisation window’

72. 5.Pressure controlled ventilation (PCV)
• Breath – MANDATORY
• Trigger – TIME
• Limit - PRESSURE
• Cycle – TIME/ FLOW
Rise time
Time taken for airway
pressure to rise from
baseline to maximum

73. 6.Pressure support ventilation (PSV)
• Breath – SPONTANEOUS
• Trigger – PATIENT
• Limit - PRESSURE
• Cycle – FLOW
( 5-25% OF PIFR)
After the trigger, ventilator generates a flow sufficient to raise and then maintain
airway pressure at a preset level for the duration of the patient’s spontaneous
respiratory effort

75. Newer modes of ventilation

77. Dual modes of ventilation
Devised to overcome the limitations of both V &
P controlled modes
Dual control within a
breath
Switches from P to V
control during the same
breath
e.g. VAPS
PA
Dual control from breath
to breath
P limit ↑ or ↓ to maintain a
clinician set TV
ANALOGOUS to a resp
therapist who ↑ or ↓ P limit
of each breath based on
TV delivered in last breath

78. Dual control within a breath
Combined adv –
1. High & variable initial flow rate of P controlled
breath ( thereby - ↑ pt – vent synchrony,
↓WOB, ↓sense of breathlessness)
2. Assured TV & MV as in V controlled breaths
Starts as P limited breaths but change over to V
limited breath by converting decelerating flow
to constant flow if minimum preset TV not
delivered

79. 1. Breath triggered (pt/ time) –
2. P support level reached quickly –
3. ventilator compares delivered and desired/ set TV
4. Delivered = set TV -------- Breath is FLOW cycled as in P controlled modes
5. Delivered < set TV -------- Changeover from P to V limited ( flow kept constant + Ti ↑)
P rises above set P support level
till set TV delivered

80. Dual control – breath to breath
P limited +
FLOW cycled
Vol support /
variable P
support
P limited +
TIME cycled
PRVC

81. Volume support
Allows automatic weaning of P support as
compliance alters.
OPERATION –
C = V
P
changes during
weaning & guides
P support level
Preset & constant
P support dependent
on C
compliance
↑ - P support ↓
↓ - P support ↑
By
3 cm H2O /
breath
Deliver
desired
TV

83. Pressure regulated volume controlled
(PRVC)
• Autoflow / variable P control
• Similar to VS except that it is a
modification of PCV rather than PSV

84. 1. Conventional V controlled mode – very high P would have resulted in an
attempt to deliver set TV -------- BAROTRAUMA
2. Conventional P controlled mode – inadequate TV would have been
delivered

85. Shifts between P support (flow cycled)& P
control (time cycled) mode with pt efforts
Combines VS & PRVC
If no efforts : PRVC (time cycled)
As spontaneous breathing begins : VS (flow
cycled)
Automode

86. Pitfalls :
During the switch from time-cycled
to flow cycled ventilation
Mean airway pressure
hypoxemia may occur
Automode

87.  Compensates for the resistance of ETT
 Facilitates “ electronic weaning “ i.e pt during ATC mimic their
breathing pattern as if extubated ( provided upper airway contorl
provided)
 Operation
As the flow ↑ / ETT dia ↓, the P support needs
to be ↑to ↓WOB
∆P (P support) α (L / r4 ) α flow α WOB
Automatic Tube Compensation

88. Static condition
Single P support level can eliminate ETT
resistance
Dynamic condition
Variable flow e.g. tachypnoea & in different
phases of resp.
P.support needs to be continously altered
to eliminate dynamically changing WOB.

89. 1. Feed resistive coef
of ETT
2. Feed %
compensation
desired
3. Measures
instantaneous flow
Calculates P support
proportional to
resistance throughout
respiratory cycle
Limitation
Resistive coef changes in vivo ( kinks, temp,molding,
secretions) Under/ overcompensation may result.

90. Airway pressure release ventilation
(APRV)
• High level of CPAP with brief intermittent
releases to a lower level
Conventional modes – begin at low P & elevate
P to accomplish TV
APRV – commences at elevated P & releases P
to accomplish TV

91. Higher plateau P – improves oxygenation
Release phase – alveolar ventilation & removal of CO2
Active patient – spontaneous breathing at both P levels
Passive patient – complete ventilation by P release

92. Settings
1.Phigh (15 – 30 cmH2O )
2.Plow (3-10 cmH2O ) == PEEP
3. F = 8-15 / min
4. Thigh /Tlow = 8:1 to 10:1
If ↑ PaCO2 -↑ Phigh or ↓ Plow
- ↑ f
If ↓ PaO2 - ↑ Plow or FiO2

94. Proportional Assist Ventilation
• Targets fixed portion of patient’s
work during “spontaneous”
breaths
• Automatically adjusts flow, volume
and pressure needed each breath

95. WOB
Ventilator measures – elastance & resistance
Clinician sets -“Vol. assist %” reduces work of elastance
“Flow assist%” reduces work of resistance's
Increased patient effort (WOB) causes increased applied
pressure (and flow & volume)
ELASTANCE
(TV)
RESISTANCE
(Flow)

97. Biphasic positive airway pressure
(BiPAP)
PCV & a variant of APRV
Time cycled alteration between 2 levels of CPAP
BiPAP – P support for spontaneous level only at low CPAP level
Bi-vent - P support for spontaneous level at both low & high
CPAP
 Spontaneous breathing at both levels
 Changeover between 2 levels of CPAP synchronized with exp & insp

99. BiPAP
Bi- vent

100. Advantages
1. Allows unrestricted spontaneous breathing
2. Continuous weaning without need to change
ventilatory mode – universal ventilatory
mode
3. Synchronization with pt’s breathing from exp.
to insp. P level & vice versa
4. Less sedation needed

101. Neurally Adjusted Ventilatory Assist
(NAVA)

102. Global Critical Care
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9555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY

103. GOOD LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com