Conv. ventilation physi

Physiology of positive pressure ventilation

SAMIR EL ANSARY

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Mechanical ventilation –

Supports / replaces the normal ventilatorypump moving air in & out of the lungs.

Primary indications –

a.apnea

b.Ac. ventilation failure

c. Impending ventilation failure

d.Severe oxygenation failure

Goals

Manipulate gas exchange

↑ lung vol – FRC, end insp / exp lung inflation

Manipulate work of breathing (WOB)

Minimize CVS effects

ARTIFICIAL VENTILATION

- Creates a transairway P gradient by ↓ alveolar P to a level below airway opening P- Creates – P around thorax

e.g. iron lungchest cuirass / shell

- Achieved by applying + P at airway opening producing a transairwayP gradient

Negative pressure ventilation Positive pressure

ventilation

ventilation without artificial airway-Nasal , face mask

adv.1.Avoid intubation / c/c2.Preserve natural airway defences3.Comfort4.Speech/ swallowing + 5.Less sedation needed6.Intermittent use

Noninvasive

Disadv1.Cooperation2.Mask discomfort3.Air leaks4.Facial ulcers, eye irritation, dry nose5.Aerophagia6.Limited P supporte.g. BiPAP, CPAP

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)

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

Pressure gradients

Distending pressure of lungs

Elastance load

Resistance load

Distending

pressure

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).

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)

Trans pulmonary pressure (pressure at airway opening minus pleural pressure) [= Transrespiratory pressure?]Transpulmonary pressure is the distending force of the

lungThe airway-pressure gauge on a positive-pressure

ventilator displays transrespiratory pressure

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.

Elastance(measure of stiffness) is the inverse of compliance(measure

of stretchiness)

An increase in elastance implies that the system is becoming stiffer.

Mean airway pressure Paw = Transrespiratorypressure

Mean alveolar pressure Palv = Transthoracicpressure

Transpulmonary pressure is the distending pressure in a spontaneously(negative)

breathing patient Transrespiratory pressure is the distending

pressure in positive pressure ventilation

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

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 H2OR = 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

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

How -End inspiratory hold

• Pendelluft phenomenon• Visco-elastic properties of lung

End-inspiratory pause

Ppeak < 50 cm H2OPplat < 30 cm H2O

Ppeak = Pplat + Paw

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

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).

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.

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

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

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

Ppeak < 50 cm H2O; Pplat < 35 cm H2O – to avoid

barotrauma

• 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

Why

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 < MAP ACV

• Hemodynamic consequences

Factors

1. Mandatory breath modes

2. ↑insp time , ↓ exp time

3. ↑ PEEP

4. ↑ Resistance, ↓compliance

5. Insp flow pattern

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

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

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

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

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

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

Inadequate expiratory time - Air trapping

iPEEP

Flow curve FV loop

1. Allow more time for expiration2. Increase inspiratory flow rate3. Provide ePEEP

Disadv1. Barotrauma / volutrauma2. ↑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 effects4. May ↑ PVR

Minimising Auto PEEP1. ↓airflow res – secretion management, bronchodilation,

large ETT2. ↓Insp time ( ↑insp flow, sq flow waveform, low TV)3. ↑ exp time (low resp rate )4. Apply PEEP to balance AutoPEEP

Cardiovascular effects of PPV

Spontaneous ventilation PPV

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

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

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 afterload1. emptying of thoracic aorta during insp2. Compression of heart by + P during systole 3. ↓ transmural P across LV during systole

PPV

↓ preload, ventricular filling

↓ afterload , ↑ventricular

emptying

CO –1. INCREASE2. DECREASE

1. Intravascular fluid status

2. Compensation – HR, vasoconstriction

3. Sepsis,

4. PEEP, MAP

5. LV function

Effect on other body systems

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

What is a ‘ mode of ventilation’ ?

A ventilator mode is delivery a sequence of

breath types & timing of breath

Breath characteristics

A= what initiates a breath -

TRIGGER

B = what controls / limits it –

LIMIT

C= What ends a breath -

CYCLING

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

CONTROL/ LIMIT

Variable not allowed to rise above a preset value

Does not terminate a breath

Pressure

Volume

Pressure Controlled

• Pressure targeted, pressure limited - Ppeakset

• Volume Variable

Volume Controlled

• Volume targeted, volume limited - VT set

• Pressure Variable

Dual Controlled

• volume targeted (guaranteed) and pressure limited

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

Breath types

SpontaneousBoth triggered and cycled by the patient

Control/Mandatory Machine triggered and machine cycled

AssistedPatient triggered but machine cycled

Waveforms

1. Volume -time

2. Flow - time

3. Pressure - time

a) Volume – time graphs

1. Air leaks

2. Calibrate flow transducers

b) Flow waveforms

1. Inspiratory flow waveforms

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

Inspiratory and expiratory flow waveforms

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)

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)

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

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

Volume controlled Pressure controlled

Advantages1. Guaranteed TV2. Less atelectasis3. TV increases linearly with MV

Advantages1. Limits excessive airway P2. ↑ MAP by constant insp P – better

oxygenation3. 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

Disadvantages1. Limited flow may not meet

patients desired insp flow rate-flow hunger

2. May cause high Paw ( barotrauma)

Disadvantages1. Variable TV

↑TV as compliance ↑↓TV as resistance ↑

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)

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

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 – MANDATORYASSISTED

• Trigger – PATIENTTIME

• Limit - VOLUME• Cycle – VOLUME / TIME

Once patient initiates the breath the ventilator takes over the WOBIf he fails to initiate, then the ventilator does the entire WOB

3. Intermittent mandatory ventilation (IMV)

Breath stackingSpontaneous breath immediately after acontrolled breath without allowing timefor 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 – MANDATORYSPONTANEOUS

• Trigger – PATIENTVENTILATOR

• Limit - VOLUME• Cycle - VOLUME

4.Synchronized Intermittent Mandatory Ventilation (SIMV)

• Breath –SPONTANEOUS

ASSISTEDMANDATORY

• Trigger – PATIENTTIME

• Limit - VOLUME• Cycle – VOLUME/ TIME

• 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 inspiratoryeffort

• Weaning

Adv Allows patients to exercise their respiratory muscles in

between – avoids atrophy

Avoids breath stacking – ‘Synchronisation window’

5.Pressure controlled ventilation (PCV)

• Breath – MANDATORY• Trigger – TIME• Limit - PRESSURE• Cycle – TIME/ FLOW

Rise timeTime taken for airway pressure to rise from baseline to maximum

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

Newer modes of ventilation

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

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

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

Dual control – breath to breath

P limited + FLOW cycled

Vol support /

variable P

support

P limited + TIME cycled

PRVC

Volume supportAllows automatic weaning of P support as

compliance alters.OPERATION –

C = VP

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

Pressure regulated volume controlled (PRVC)

• Autoflow / variable P control

• Similar to VS except that it is a modification of PCV rather than PSV

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

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

Pitfalls :

During the switch from time-cycled to flow cycled ventilation

Mean airway pressure

hypoxemia may occur

Automode

Compensates for the resistance of ETT

Facilitates “ electronic weaning “ i.e pt during ATC mimic their breathing pattern as if extubated ( provided upper airway contorlprovided)

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

Static conditionSingle P support level can eliminate ETT

resistance

Dynamic conditionVariable flow e.g. tachypnoea & in different

phases of resp.

P.support needs to be continously altered to eliminate dynamically changing WOB.

1. Feed resistive coefof ETT

2. Feed % compensation desired

3. Measuresinstantaneous flow

Calculates P support proportional to resistance throughout respiratory cycle

Limitation

Resistive coef changes in vivo ( kinks, temp,molding,

secretions) Under/ overcompensation may result.

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

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

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

Proportional Assist Ventilation

• Targets fixed portion of patient’s work during “spontaneous” breaths

• Automatically adjusts flow, volume and pressure needed each breath

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)

Biphasic positive airway pressure (BiPAP)

PCV & a variant of APRVTime 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

BiPAP

Bi- vent

Advantages

1. Allows unrestricted spontaneous breathing

2. Continuous weaning without need to change ventilatory mode – universal ventilatorymode

3. Synchronization with pt’s breathing from exp. to insp. P level & vice versa

4. Less sedation needed

Neurally Adjusted Ventilatory Assist (NAVA)

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512

9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY

GOOD LUCK

SAMIR EL ANSARYICU PROFESSOR

AIN SHAMSCAIRO

elansarysamir@yahoo.com