Transcript Ventilation - Dr. Mehdi Hasan Mumtaz

VENTILATION
CMV
SPONTANEOUS
LFPPV
HFPPV
Disadvantages
1. Pulmonary
2 Cardiac
3. Renal
4. Brain
5. Other Organs
- TC
- Barotrauma
VENTILATION
Prof. Mehdi Hasan Mumtaz
- VIQ Mismatch
- BaroNelufltsma
VARYING TC
Compliance
Modes of Ventilation
- IMV
- VMMV
- SIMV
- SIMV
- PEEP
- PSV
Resistance
VENTILATION
Partial Ventilatory
Support
Full Ventilatory
Support
Conventional
Support To
modulate
inspiration & VT
-PSV
-PAV
-IRV
Non-Conventional
Modulation of
minute
ventilation
-IMV
-SIMV
-MMV
-BIPAP
-APRV
-ECMO
-ECCO2R
-IVOX
-LIQID LUNG
VENTILATION
CONCEPT OF “LUNG REST”
1.
Acceptable blood gases.
(permissive hypercapnoea)
2.
Alteration of ventilatory
pattern to reduce lung
stress. (low peak, mean end
expiratory pressure low
minute volumes).
Use of artificial membrans
or
Artificial lung assist (ALA).
1. ECMO.
2. ECCO2R.
3. IVOX.
ASSISTED VENTILATION
“Incorporation of Spontaneous Breaths”
Paw
VT
Pulmonary Circulation
Organ Perfusion
Harmonious relationship between patient
& Ventilator.
ASSISTED VENTILATION
Advantages of Spontaneous
Ventilatory Effects
lnspiratorv assist
Mechanical ventilation
Peak airway pressure
Venous return
Less effect on return renal function
Less sedation.
Muscle Relaxation



Muscle weakness
Impaired gut motility
Suppression of cough reflex.
PROPORTION ASSIST
VENTILATION (PAV)
Younes 1992 First Described & Used
Pattern of Operation
Advantages
Greater Comfort
 No fighting with machine
 Less Sedation
 Less ParalysIs
 Preservation respiratory control
 Less airway pressure

VENTILATION
Volume Controlled (VC)
Vs
Pressure Controlled (PC)
1. VOLUME CONTROLLED
VT
F
MV
= Preset or constant
= Preset
= constant
Mechanics change
- airway pressure change
- monitor carefully
VENTILATION
Volume Controlled (VC)
Vs
Pressure Controlled (PC)
2. PRESSURE CONTROLLED
- lnspiratory pressure
- Inspiratory flow
- VT&MV
= Preset or constant
= High initially - decelerate rapidly
= Monitor on time constant
= Monitor volumes carefully
PC-IRV = Recommended in ARDS
VARYING I:E RATIO
Collapsable Alveoli Kept Open
External PEEP
Internal PEEP (Auto PEEP)



VT.
 ET.
TC.
Compliance
Resistannce
VARYING I:E RATIO
Regional
Whole resp system
Ventilator system
Narrow tube
Ventilator System
Slow PEEP valve
Slow alveolar compartment = auto PEEP.
Fast alveolar Compartment = need ext. PEEP
INVERSE RATIO
VENTILATION (IRV)
1871
Reynolds - First Proposed- Neonates
1980
1983
1984
1989
1992
Baun et al
Ravizza etal
Cole et al
Abraham Yoshihama
Barbas etal
Advocated for
ARDS
INVERSE RATIO
VENTILATION (IRV)
ADVANTAGES:
More homogenous ventilation
Opens CoIIapsible alveoli
Intrinsic PEEP
-Regional



-Individual
Slow compartment
Faster compartment
(Prepondrance in ARDS)
Improvement in gas exchange.
Contra-indication = obstructive lung disease
BIPAP
“PC-ventilation with unrestricted
spontaneous breathing at anymoment
of ventilatory cycle”
Baum et al 1989 first described (Evita).
Rouby et al 1992 intermittent mandatory
pressure release ventilation (IMPRV).
Sydow et al 1993 BIPAP + APRV.
SUBDIVISION
CMV – BIPAP
IMV – BIPAP
No spontaneous breathing
APRV – BIPAP
Spontaneous breathing at
high pressure level
GENUINE - BIPAP
Spontaneous breathing at
both CPAP level.
Spontaneous breathing at
low pressure
VC-IRV
VT=8-12ml/KG
I:E=2:1-3:1
PEEP=5cmH2O
F=10-15min
BIPAP-APRV
CPAP = 15-30CM FOR 2-4 S
PRESSURE TO
RELEASE = 5 cmH2O for
0.5-0.78
RESULT:
No significant
change from VC
conventional ventilation
Peak airway pressure -low
Peak & mean pressure low in
24 hrs.
Progressive alveolar
recruitment.
ADVANTAGES
Less MV
Partial Spontaneous Breathing.
Low peak airway pressure.
Less impairment of P. circulation.
Improved O2 delivery.
Effective alveolar recruitment.
AIRWAY PRESSURE RELEASE
VENTILATION (APRV)
1987 - Down & Group (Stock etal 1987)
“Spontaneous breathing at preset (CPAP)
interrupted by short (1-1.5S) releases of
pressure plateau for further expiration”
AIRWAY PRESSURE RELEASE
VENTILATION (APRV)
Useful features:
• Reduces lung volume.
• High airway pressure.
• Intrinsic PEEP in slow alveoli.
• Preservation of Spontaneous breathing.
• Less baro/voluntrauma.
• Reduction in circulatory compromise.
• Better ventilation/perfusion.
Application of APRV
• BIPAP.
• IMPRV.
PERMISSIVE HYPERCAPNOEA
VT
 PIP.
PCO2.
“1990 - Hickling”
Extrinsic PEEP
Maintain PaW
Intrinsic PEEP
ADVANTAGES



 Barotrauma
 Volutrauma
 Physiological effect
DISADVANTAGES = Hypercarbia
Compensation
- HCO3 & Kidney
- HCO infusion
Selection Criteria
OI =
Mean airway P x FIO2%
-------------------------------Post-ductal Pa02
Complications
Bleeding
Intracranial
Pulmonary
Nasal
UmbIicaI artery
Chest tube site
NeurologicaI Handicap
Septic
Procedure:
Warning



Clinical assessment.
Radiological assessment.
Lung compliance.
Criteria
A. Fast Selection criteria
-
PaO2<6.6
PaCO2=3.9-5.9
F102= 1.0
PEEP> 5cmH2O for 5min
B. Slow Selection Criteria
48hrs assessment with conventional therapy
-
PaO2<6.6
PaCO2=3.9-5.9
F102= 0.6
PEEP> 5cmH2O for 15min
QS/QT> 30% at FIO2 1.0&PEEP =5cmH20
ECCO2R
“VENTILATION SPARING MANOEUVRE”
CO2 - Remove by circuit.
O2
- Transfer by lung.
1978 Gattinoni.
 Oxygenation by entrainment
C PAP.
FRC-kept normal.
L FPPV+PEEP
CO2- Removed – Veno –Venous circuit.
Less ventilatory P- less barotrauma.
More lung rest.
ECCO2R
Less circuit as compared to ECMO.
Less flow 1-1.5L/min=2.5L/m2/min.
Less heparinisation.
Modification – hemofilteration.
>85% HCO3  metabolic acidosis.
Direct base = THAM, NaoH.
Indirect = acetate & lactate.
Complications.
Bleeding.
Platelet consumption.
IVOX
“Gas exchange without
Extracorporeal circuit”
Hollow fibre gas transfer membranes.
Gas exchange.




Surface area-fibre bundles.
(0.21-0.52m2) Ext. diameter = 7-10mm.
Gas flow.
Venacava blood flow.
HB.
IVOX
Gas transfer=100mIO2 and 75ml CO2/min.
Indications.






Reversible pathology.
Patient waiting for lung transplant.
Shunt fraction >25% <35%.
IVC>15 mm.
NO-systemic bacteraemia.
NO-coagulopathy.
VENTILATION IN LIQUID PHASE
“Hysteresis” phenomenon observed during Insuflation
of lungs is due to surface “tension” effect, which
can be eliminated by substituting saline to the air.
CHARACTERISTICS OF LIQUID:
Stable
Absence of toxicity
High Solubility for O2 & CO2
Low Surface tension
Should not locally suplant surfactant
Should not be absorbed capillans/Lymph
Expelled by lungs.
VENTILATION IN LIQUID PHASE
Example:
- “Fluorocarbon”
- Density 1.76 mg/ml
- Surface tension -15 dynes/cm
ADVANTAGES:



Uniform expansion.
Uniform Gas exchange.
Improvement of compliance
HIGH FREQUENCY
VENTILATION
Adverse effects of LFPPV
1. Time constant = C o< R
Barotrauma
2. CO
O2 delivery
Tissue perfusion
Use of modes
Definition
“Ventilation above 4 times the normal rate for the
subject”
Adult =15x4=60 (1Hz/min).
Neonate=30x4=120 (2Hz/min)
HIGH FREQUENCY
VENTILATION
GOALS
“Reduction in transpulmonary
pressure difference”
Smaller Vt   Peak & Mean airway pressure

 Barotrauma.
 Reduction of Co.
MODE OF HIGH FREQUENCY
VENTILATION
HFPPV - Oberg & Sjostrand
HFJV - Klain & Smith
HFO - Lunken Heimer
Mode
HFPPV
HFJV
HFO
Frequency min-1
60-120 (1-2 Hz)
60-240 (1-4 Hz)
180-1200 (3-20Hz)
VT
ml/kg.
3-5
2-5
1-3
PHYSIOLOGICAL EFFECTS
1. GAS EXCHANGE
VD/VT  efficiency (Large min v.)
ARTERIAL OXYGENATION



F102
VA (Alveolar Ventilation)
Lung Volume
2. AIRWAY PRESSURES
VT airway  airway P. Transpulmonary P.
I:E Ratio
Normocapnoea + F 
airway P
depends
PHYSIOLOGICAL EFFECTS
1. Pressure generator - mean P.
Constant.
FVT peak airway P.
Intrinsic PEEP,
V.Mode
airway pressure
PEEPimprove oxygenation
2. Flow generator  peak mean
ENP P. & F above Initial FPPV
3. VENTILATION
Lung volume (intrinsic PEEP).
Thoracic compl.
3. Factors
Intrinsic.
T. Compliance.
Even distribution (Time constant)
4. VENTILATORY DRIVE
Reflex suppression
1. Vagal afferents.
2. non -vagal afferents.
Cause = Lung Volume
frequency
Advantage = less sedation required
5. CIRCULATION
BP.
Unchanged
Pulmonary P.
CVP
Intra-Pulmonary shunt
Fluctuations in P.
Fluctuations in ICP.
Urine flow.
PHYSIOLOGICAL BASIS OF
GAS TRANSPORT
Across alveolar capillary membrane independent
of mode of ventilation.
From alveoli to mouth.
 Low F. large V. -VT>VD no problem.
 High F. low volume.
1. VT>VD=if normocpnic
(F=15-75)
VT(70%)VD (50%)
VD/VT Ratio (0.6-0.8)
Necessitate MV o< Freq needed.
PHYSIOLOGICAL BASIS OF
GAS TRANSPORT
2. VT=VD
(120-300)
Effective VD<VD anat.
VT exceeds VD anat by 1.2
 Conductive G. trans P.
VT 0.8-1.2 VD anat.
Eff. VD<VD anat.
VT < VD
(F300-2400) (VD:VT = 1.2-2.0)
4- additional Gas Transport Mechanisms
1.
2.
3.
4.
Direct alveolar ventilation.
Pendeluft.
Convective Streaming.
Augmented (Taylorian) dispersion.
VT < VD
BEST FREQUENCY 60-1201 min
• Anaesthesia - airway surgery
- lung surgery
• Management of high compliance
conditions
- Broncho - P. Fistula
- Bullous emphysenia
• Weaning from ventilation
CLINICAL APPLICATIONS
1. ANAESTHESIA
a. Surgery on Conducting airways & Lungs
b. Laryngoscopy, microsurgery, Laser surgery on
larynx
c. Tracheal resection & tracheostomy
d. Bronchoscopy.
2. RESUSCITATION
Percutaneous Trannstracheal Jet Ventilation
with 100% O2.
- Direct delivery of 02 below cords.
- Intrinsic PEEP.
- Pulsatile Expired gas flow prevent
aspiration.
CLINICAL APPLICATIONS
3. ICU
Broncho-pleural fistula.
4. OTHER ADVANTAGES
- Weaning
- Endobronchial Sunction
DIFFERENTIAL LUNG V
WHOLE – L.V.
LOBAR – V.
WHY DLV - NEEDED?
Variable Time Constant
 TC = R o< C

APPROACHES TO IMPROVE
SURVIVAL IN SEVERE ARDS
1. Improvement of basic ventilatory regimen
PCV+PEEP +Permisive hypercapnoea.
2. Adjunctive supportive measures.
- Body position changes.
- Reduction of pulmonary oedema.
3. Sophisticated ventilatory measures.
- DLV.
- HFJV.
4. Future therapeutic approaches.
- Selective manipulation of pul blood flow e.g. inhalation
of nitric oxide.
- Artificial surfactant.
- Intravascularr oxygenation (IVOX).
INDICATIONS FOR
VENTILATORY SUPPORT
PCO2
DEAD
SPACE
mmHg
VD/VT
NORMAL
VALUE
30 40
03 04
VENT. SUGG.
45 50
0.5 0.6
ASSIST
MUST
>55
>.6
OXYGENATION
PO2mmHg
FIO2 21%
PO2mmHg
FIO2 100%
P(A-aDO2)
FIO2 21%
P(A-ADO2)
FIO2-100
Qs/qt (%)
80-90
50-60
<50
550-630
200-300
<200
5-20
55-59
>60
20-60
350-450
>450
3%-8%
30%-40%
12-16
6-8
50-60
30-35
3.5-4.0
10.0-15.0
MECHANISM
OF
VENTILATION
RESP. RATE
TIDAL VOLUME
MI/KG
VITAL CAPACITY
MI/KG
>35
<3.5
<10
HEAD INJURY
Coma – GCS<8

NOT



Obeying
Speaking.
Eye opening.
Loss of protective laryngeal reflexes.
Ventilatory in-sufficiency.


Hypoxaemia
(PaO2 <9KPa on air.
<13KPa on O2.
Hypercarbia PaCO2>6kPa.
Spontaneous hyperventilation

PaCO2<3.5Kpa.
Respiratory arrhythmias.
HEAD INJURY - INIDCATIONS
BEFORE TRANSFER
Deteriorating conscious level.
Bilateral fracture mandible.
Copious bleeding in mouth.
Seizures.
IPPV Indications
COPD-Failure
“Failure of conservative treatment”
Hypoxia
Acidosis
Worsening
Respiratory m fatique.
Non-arousable somnohance
PaO2<50 with O2 therapy but
PH not<7.26
CMV INITIATION
Mode of ventilation.
Inflation volume.
Respiratory rate.
Inspired O2 level.
HOW TO INITIATE CMV
Choose suitable ventilator mode.
Adjust FIO2=1.0 target SPO2.
Adjust VT 8-10 ml/kg – avoid high PIP.
Choose respiratory rate.
Target PH not PCO2
Mi ventilation.
Use PEEP in diffuse lung disease.
High PIP>60cm H2O. Concern
High Palv >35cm H2O.
Maintain DO2.



Flow rate
VT
HB.
CO.
SaO2.
Consider – sedation, analgesia, change of position.
GOALS
Ensure-optimum O2 delivery.
Effective & appropriate ventilation.
Decrease work of breathing.
PEEP
Improve oxygenation.
Improve gas exchange.


Recruiting atelactasis.
Recrutig non-functioning alveoli.
Improve compliance.
Improve FRC.
Decrease shunt fraction.
Decreases pulmonary oedema.
ADVERSE EFFECT-PEEP
Non-uniform lung injury.

Worsen oxygenation PO2.

Worsen ventilation PCO2.
Hypotension.
Barotrauma.
INITIATION OF PEEP
Initiation at 5cmH2O.
Increments 2-3 cmH2O.
Maximum 15cmH2O.
Monitor.



BP.
HR.
PaO2.
SPECIFIC CLINICAL
SITUATIONS
A. Respiratory Distress Syndrome.
Adequate oxygenation
Adequate DO2.
Goals
Work of breathing.
Avoid excessive PIP.
Avoid high FIO2.
Settings
PCMV
PCMV+PEEP
PCMV+IRV
SPECIFIC CLINICAL
SITUATIONS
B. Obstruction airway disease.
Support oxygenation.
Goals
Assist ventilation
Approximate PH.
Settings





VT-initial 8-10ml/kg
I:E ratio-avoid-PEEPI.
Barotrauma-caution.
Reduce RR&VT expiratory time.
Aggressive obstruction management.
SPECIFIC CLINICAL
SITUATIONS
C. Asymmetric Lung Disease.
Time constant


Mechanical effect.
V/Q ratio.
Standard principals.
Result dependent change.
Less involved lung.

Dependent position.
DLV.
SPECIFIC CLINICAL
SITUATIONS
D. congestive Heart Failure.
 Work of breathing.
 Load on heart
Goals
 Oxygenation
 Pul. Oedema.
Strategy.



IPPV.
SQUARE WAVE PATTERN
PEEP.
SPECIFIC CLINICAL
SITUATIONS
E. Myocardial Ischaemia.
Work of breathing.
Goals
DO2
Strategy

As for CHF
SPECIFIC CLINICAL
SITUATIONS
F. Neuromuscular disease.
“Intact respiratory drive”
Higher VT:


Avoid air hunger.
Dyspnea sensation.
10-12ml/kg
Ventilate
- Normal PH.
MONITORING CMV
Chest radiograph.


Post intubation.
Deterioration.
Blood gases.
Vital signs.
Inspiratory pressures.
Pulse oxymetry.
Ventilator alarms.
ACUTE HYPOTENTION
CMV
Negative to positive intrathoracic
pressure.
Tension pneumothroax


Clinical
X-ray
Auto-PEEP.




Hypotension.
Intrathoracic P.
Manometer dial.
condition.
Acute myocardial ischaemia/infarction.

ECG