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MECHANICAL

VENTILATION

Dr.lakshmi phani nadella


qA mechanical ventilator is a complex
system consisting of a power supply,
compressed air and oxygen, a drive
mechanism to provide motive force to
push oxygen into the patient’s lungs
and a control mechanism to manage
the gas flow, volume, pressure and
timing.
qIt is connected to the patient’s lungs
through breathing hoses and a special
tube inserted into the patient’s
airway.

qPatients of all ages, from newborns to
geriatrics, routinely receive mechanical
ventilation in practically every hospital in
the country.
qIn the vast majority of these patients,
mechanical ventilation is a temporizing
measure and the patients are expected
to be removed (weaned) from the
ventilator when appropriate
indications
 Respiratory failure
 Apnoea / respiratory arrest
 Inadequate ventilation(acute vs chronic)
 Inadequate oxygenation
 Chronic respiratory insufficiency with FTT
 Cardiac insufficiency
 Eliminate the work of breathing
 To reduce the oxygen consumption
 Neurologic dysfunction
 Central hypoventilation and frequent apnoea
 Comatose patient with GCS < 8
 Inability to protect the airway

PHYSIOLOGICAL OBJECTS OF
MECHANICAL VENTILATION:


1. SUPPORT OR MANIPULATE
PULMONARY GAS EXCHANGE.
 ALVEOLAR VENTILATION – to achieve
normocapnia

ALVEOLAR OXYGENATION – to maintain
normal Po2


2.INCREASE LUNG VOLUME.


3.REDUCE THE WORK OF BREATHING.
CLINICAL OBJECTIVES:

1.REVERSE ACTUE RESPIRATORY FAILURE.

2.REVERSE RESPIRATORY DISTRESS.

3.REVERSE HYPOXEMIA.

4.PREVENT or REVERSE ATELECTASIS and
maintain FRC.

5.REVERSE RESPIRATORY MUSCLE FATIGUE.

6.PERMIT SEDATION or PARALYSIS or BOTH

7.REDUCE SYSTEMIC or MYOCARDIAL O2
CONSUMTION.

8.MINIMIZE ASSOCIATED COMPLICATIONS and
REDUCE MORTALITY.

ARF is diagnosed and managed
with arterial blood gases ...
q↑ PaCO2 accompanies ↓ PaO2.
ARF is 2º to acute alveolar hypoventilation.
q
qWith severe ↓ PaO2 alone, there is a marked
ventilation / perfusion (V/Q) impairment.
q
qHowever, ↓VA and ↓ V/Q frequently co-exist!


PaO2 < 50 mm Hg

PaCO2 > 50 - 60 mm Hg

and / or

Significant respiratory acidemia

Causes of respiratory failure
qRespiratory Center in Brain Brain
qNeuromuscular Connections
qThoracic Bellows Nerves
qAirways (upper & lower)
qLung parenchyma (alveoli)
Bellows
respiratory failure !
Airways
Alveoli
disrupted “link” to cause
It only requires one
 Assesment
Look for the of need
signs of for mechanical
respiratory ventilation:
failure / distress:

1. increase in respiratory rate
2.decrease in respiratory rate accompanied by increasing

effort or increasing retractions


3. prolonged apnoea with cyanosis or bradycardia or both


4.cyanosis not relieved by administration of O2

5.hypotension, pallor and a decrease in peripheral perfusion

6.tachycardia(leading to bradycardia

7.periodic breathing with prolonged respiratory pauses
8.gasping and the use of accessory muscles
Basic Physiology
 Negative pressure circuit
Gradient between mouth and
pleural space is the driving
pressure
need to overcome resistance
maintain alveolus open
overcome elastic recoil forces
Balance between elastic recoil of
chest wall and the lung=FRC
Basic Physiology

http://www.biology.eku.edu/RITCHISO/301notes6.ht
RESPIRATORY PHYSIOLOGY
Normal pressure-volume
relationship in the lung

http://physioweb.med.uvm.edu/pulmonary_phy
siology
Ventilation
Carbon Dioxide

PaCO2= k * metabolic production
alveolar minute ventilation


Alveolar MV = resp. rate * effective tidal vol.

Effective TV = TV - dead space

Dead Space = anatomic + physiologic
Oxygenation
Oxygen:
 Minute ventilation is the amount of fresh
gas delivered to the alveolus
 Partial pressure of oxygen in alveolus
(PAO2) is the driving pressure for gas
exchange across the alveolar-capillary
barrier
 PAO2 = ({Atmospheric pressure - water
vapor}*FiO2) - PaCO2 / RQ
 Match perfusion to alveoli that are well
ventilated
 Hemoglobin is fully saturated 1/3 of the
way thru the capillary
Oxygenation

http://www.biology.eku.edu/RITCHISO/301notes6
.htm
 The sigmoidal shape of the oxygen disassociation
curve is of critical importance. Hemoglobin can
only carry so much oxygen (1.34 ml per gram of
hemoglobin) regardless of high the PaO2 may
be. Furthermore, dissolved oxygen contributes
very little to oxygen content (0.003 ml
oxygen/dL/mmHg PaO2 ).
 As a result, increasing the PaO2 oxygen in
oxygenated blood cannot overcome the effect
of shunted blood that is deoxygenated and the
patient will be desaturated to a degree
proportional to the magnitude of the shunt
CO2 vs. Oxygen
 The disassociation curve for carbon dioxide is far
more linear and is steeper. As a result, there is
much less of a limit on how much carbon
dioxide can be carried by hemoglobin and
exchanged at the alveolar-capillary barrier.
 Since carbon dioxide is also far more soluble than
oxygen (by a factor of 20), dissolved CO2
contributes significantly -about 10% - to the
amount that is exchanged at the alveolus.
 For these reasons, PaCO2is not affected by shunt
or diffusion barriers as is oxygen (and explains
why a child with cyanotic heart disease is
hypoxemic but not hypercarbic).

Abnormal Gas Exchange
 Hypoxemia can be  Hypercarbia can be
due to: due to:
hypoventilation hypoventilation
V/Q mismatch V/Q mismatch
shunt
diffusion
impairments

Due to differences between oxygen and CO2 in their


solubility and respective disassociation curves,
shunt and diffusion impairments do not result in
hypercarbia
Gas Exchange
 Hypoventilation and V/Q mismatch are the
most common causes of abnormal gas
exchange in the PICU
 Can correct hypoventilation by increasing
minute ventilation
 Can correct V/Q mismatch by increasing
amount of lung that is ventilated or by
improving perfusion to those areas that are
ventilated
Mechanical Ventilation
Ventilators deliver gas to the

lungs using positive pressure


at a certain rate. The amount
of gas delivered can be
limited by time, pressure or
volume. The duration can be
cycled by time, pressure or
flow.
PHASES OF VENTILATORY CYCLES:
1. INITIATION OF INSPIRATION (triggering)

2.INSPIRATORY PHASE

3.CHANGE OVER FROM INSPIRATION TO


EXPIRATION (cycling)

4.EXPIRATORY PHASE

CYCLING
 How the machine switches from inspiration to
expiration .
 TIME CYCLING : phase ends after a preset time .

 This is seen in pressure controlled ventilation.


 The volume and flow vary.


Cycling
 FLOW CYCLING: the machine cycles into
expiration once flow changes

 Volume, pressure and time vary


 Cycling mechanism in pressure support ventilation


 Inspiratory flow ends at 25% of the peak flow



CYCLING
 Volume cycling :used in volume controlled
ventilation

 The ventilator cycles once the set volume is


delivered

 The pressure and the flow rates of gas will vary


 With an inspiratory pause the breath is volume


limited and time cycled
TRIGGERING
 This is how inspiration is initiated in association
with patients breath

 It can be by changes in pressure, flow or time


 Pressure triggering :breath delivered with↓ ι ν


β ασε λ ι ν ε π ρ ε σσυ ρ ε .

Υ συ αλ λ ψ σ ε τ ατ −1χ µ Η 2ο

Τ ηε λ ο ωε ρ τ ηε π ρ ε σσ υ ρ ε
τ η ε µ ο ρ ε σ ε ν σ ι τ ι ϖε τ η ε
µ αχ ηι ν ε

TRIGGERING
 TIME TRIGGERING : This is determined by the
respiratory rate or I:E ratio.

 The rate of breathing is controlled by the


ventilator.

 The breath is controlled or mandatory.


 The patient cannot obtain air from the machine.


 Generally used on apneic patients.


TRIGGERING
 FLOW TRIGGERING:The ventilator delivers a
constant background flow (flow by).

 Any change caused by patient effort is sensed by


the flow sensor

A breath is delivered to the patient


 This requires less work of breathing when


compared to pressure triggering

Typical vent settings
qFIO2
qRate
qVolume
qPIP and PEEP
qFlowrate, I-time, I:E Ratio
qSighs, inspiratory pause
qMode ???
q
 Different
Different brands
brands of
of ventilators
ventilators have
have different
different
control
control layouts,
layouts, but
but they
they all
all accomplish
accomplish
essentially
essentially the
the same
same functions.
functions.
Ventilator Settings
qTidal Volume (VT)
§ amount of gas delivered with each preset breath
§ in mechanically ventilated patients it’s usually set at 6 - 8 ml/kg
q
qRespiratory Rate (RR)
§ the frequency of breaths delivered by the ventilator
q
qFraction of Inspired Oxygen (FIO2)
§ the fraction of inspired oxygen delivered to the patient by the
ventilator
§ change by ABG and O2 saturation

qVentilatory Mode
 CMV, IMV, SIMV, A/C, PCV

Ventilator Settings
qSigh
 may be included as part of the ventilator settings
 a breath that has a greater volume than the preset
VT , usually 1.5 to 2.0 times the VT
 No longer routinely used

 Sensitivity
 used to determine the patient’s effort to initiate
an assisted breath (inspiration)

qInspiratory : Expiratory Ratio (I : E Ratio)
 usually set at 1 :2, may be manipulated to
facilitate gas exchange
Ventilator Settings
qPeak Inspiratory Pressure (PIP)
 peak pressure registered in the airway during
normal ventilation
 value used to set high and low pressure alarm
limits
 Not to be confused with Peak Flow which measures
the velocity of air flow per unit of time (L/min)

qAdjuncts to Mechanical Ventilation
 PEEP, CPAP, PSV

qPressure Limits
 high pressure limit is the maximum pressure the
ventilator can generate to deliver the preset VT
 usually set 10 - 20 cm H2O above the PIP
Ventilator Settings
qAlarms
VENTILATOR ALARMS MUST NEVER BE IGNORED OR DISARMED!!!!

qLoss of Power
ELECTRICAL FAILURE ALARMS ARE A MUST FOR ALL VENTILATORS

 Most ICU ventilators do not have battery back up like at home


 Know back up system (special emergency outlets)
 Check that power cord plug not accidentally disconnected

 Frequency
 Alarms if RR goes above or below set levels

qVolume
 Volumes go above or below preset levels (ie. VT or minute volume)



Ventilator Settings
q Pressure
 Change in inspiratory or peak airway pressure above or below
preset limits

Low Pressure Alarms High Pressure Alarms

Disconnection  Compliance: secretions
 Loss of VT pneumothorax
 Leaks ARDS/Pulmonary

edema

Extubation bronchospasm
 ETT in R mainstem
“bucking” coughing
 pt. biting on tube
 tubing kinked
 H2O in tubing
Monitored parameters
qSpontaneous VT

qVital Capacity (VC)


qNegative Inspiratory Force (NIF)

qCompliance

qMinute Volume (MV)


 determines alveolar ventilation (RR x VT = MV)

qAirway Placement / Patency


qABGs
COMMON MODES OF VENTILATION
 Volume targeted ventilation

(flow controlled, volume cycled)
 AC
 Pressure targeted ventilation
 PCV (pressure controlled, time cycled)
 PS
 Combination modes
 SIMV
with PS and either volume or pressure-targeted
mandatory cycles

Control Ventilation
The ventilator delivers a pre-determined VT (volume or pressure
targeted) at a preset frequency

qAdvantages
§Guaranteed minute ventilation or peak pressure

qDisadvantages
§No patient interaction. The patient can not initiate a
breath
Assist/Control Ventilation
The ventilator delivers a pre-determined VT (volume or pressure
targeted) with each inspiratory effort generated by the patient. A back-
up frequency is set to insure a minimum VE

qAdvantages
§Patient can increase VE by increasing respiratory
rate

qDisadvantages
§Dys-synchrony
§Respiratory alkalosis
§Dynamic hyperinflation
Ø
Ø

Synchronized Intermittent Mandatory
Ventilation (SIMV)
The ventilator delivers a pre-determined VT (volume or pressure
targeted) at a preset frequency and allows the patient to take
spontaneous breaths between ventilator breaths. Spontaneous
breaths may be augmented with pressure support.
qAdvantages
§Decreased mean airway pressure
§Improved venous return

qDisadvantages
§Increased oxygen consumption
§Increased work of breathing
Pressure Control Ventilation
(PCV)
The practitioner sets the maximal pressure obtained by the ventilator
(preset Pressure), frequency and time the pressure is sustained
(inspiratory time). Inspiratory time is set as a percent of the total cycle
or absolute time in seconds.
qAdvantages
§Tidal volume variable with constant peak airway pressure
§Full ventilatory support
§Decreased mean airway pressure
§Control frequency

qDisadvantages
§Requires sedation or paralysis
§Ventilation does not change in response to clinical changing
needs
High Frequency Ventilation
High frequency ventilation is broadly defined as ventilatorysupport using small
tidal volumes with high respiratory rates. Initially used in children, now used in
adults who cannot be effectively ventilated with conventional methods.
qAdvantages
§Use small tidal volumes at very lower peak inspiratory pressures
§May be associated with lower incidence of pneumothorax
§Improves gas exchange in infants with RDS at lower airway pressures
than conventional ventilation
§Can reduce flow through a bronchopleural fistula and may promote its
healing

qDisadvantages
§Gas trapping
§Necrotizing tracheobronchitis when used in the absence of adequate
humidification
Pressure Support Ventilation (PSV)
The ventilator delivers a predetermined level of positive pressure
each time the patient initiates a breath. A plateau pressure is
maintained until inspiratory flow rate decreases to a specified level
(e.g. 25% of the peak flow value).
qAdvantages
§The flow rate, inspiratory time, and frequency are
variable and determined by the patient
§Decreased inspiratory work
§Enhanced muscle reconditioning
§

qDisadvantages
§Requires spontaneous respiratory effort
§Delivered volumes affected by changes in
compliance
Positive End Expiratory Pressure (PEEP)
PEEP is the application of positive pressure to change baseline
variable during CMV, SIMV, IMV and PCV. PEEP is primarily used
to improve oxygenation in patients with severe hypoxemia.

qAdvantages
§Improves oxygenation by increasing FRC
§Decreases physiological shunting
§Improved oxygenation will allow the FIO2 to be lowered
§Increased lung compliance
§
qDisadvantages
§Increased incidence of pulmonary brotrauma
§Potential decrease in venous return
§Increased work of breathing
§Increased intracranial pressure
§
Continuous Positive Airway pressure
(CPAP)
Continuous Positive Airway Pressure is simply a spontaneous
breath mode, with the baseline pressure elevated above zero.
qAdvantages
§Improves oxygenation by increasing FRC
§Decreases physiological shunting
§Improved oxygenation will allow the FIO2 to be
lowered
§Increased lung compliance
§
qDisadvantages
§Increased incidence of pulmonary brotrauma
§Potential decrease in venous return
§Increased work of breathing
§Increased intracranial pressure
§
Inverse Ratio Ventilation (IRV)
qThe ventilator delivers a prolonged inspiration with a
proportionately shorter expiratory time. The I:E ratio of each
respiratory cycle is  1:1.
qIRV ventilation may be accomplished in a pressure controlled,
time cycled mode (PCV-IRV) or a volume cycled mode (VCV-IRV)
q

§PCV-IRV
•Peak pressure and I-time or I:E ratio are
set
•Flow is decelerating
•Tidal volume is variable

§VCV-IRV
•Achieved by applying an inspiratory
pause, decreasing the flow rate or applying
a decelerating flow pattern
Inverse Ratio Ventilation (IRV)
qAdvantages qDisadvantages
§ Maintains elevated § Auto - PEEP
mean airway § Exacerbation of hemo-
pressure, while dynamic instability
maintaining safe § Barotrauma
peak alveolar § Requires deep sedation
pressures and paralysis
§ Recruitment of lung § Changes in lung
units with decreased compliance result in
compliance changes in delivered
VT (PCV - IRV)
Ø
Airway Pressure Release
Ventilation (APRV)
The ventilator cycles through a high and low CPAP level while the
patient breathes spontaneously

APRV was developed to provide ventilatory support to


spontaneously breathing patients with acute lung injury.

qAPRV uses intermittent decreases (rather than increases) in


airway pressure
§VT varies depending upon pulmonary
compliance, airway resistance, and the duration
of the airway pressure release
§Alveolar ventilation is augmented by the brief
releases in the higher CPAP level to the lower
CPAP level
Airway Pressure Release
Ventilation (APRV)
q Advantages
§ Lower peak airway q Disadvantages
pressures § Tidal volume varies with
§ Recruitment and changes in the resistance
stabilization of and compliance
collapsed properties of the lung
alveoli(intrinsic PEEP § Synchrony  airway
due to short pressure release is not
expiratory phase) synchronized with
§ Reduced deadspace spontaneous breathing
ventilation 

§ Allows spontaneous
breathing
Complications
 Ventilator Induced Lung Injury
Oxygen toxicity
Barotrauma / Volutrauma
Peak Pressure

Plateau Pressure

Shear Injury (tidal volume)

PEEP


Complications
 Cardiovascular Complications
Impaired venous return to RH
Bowing of the Interventricular Septum
Decreased left sided afterload (good)
Altered right sided afterload
Sum Effect…..decreased cardiac output
(usually, not always and often we don’t
even notice)
Complications
Other Complications
Ventilator Associated Pneumonia
Sinusitis
Sedation
Risks from associated devices (CVLs,
A-lines)
Unplanned Extubation
Complications of Mechanical
Ventilation

qVentilator Acquired Pneumonia Issues


 Circuit Change frequency



 Closed system suction change frequency

 Elevate head of bed

 Limit the number of disconnects

Complications of Mechanical
Ventilation
qEmergency Response / Procedure

 Disconnect ventilator circuit from patient


 Provide
manual ventilation with self-inflating
manual resuscitation bag

 Callimmediately for Respiratory Care


Practitioner
Heated Humidification
Extubation
Weaning
Is the cause of respiratory failure
gone or getting better ?
Is the patient well oxygenated and
ventilated ?
Can the heart tolerate the
increased work of breathing ?
 In truth, you are always weaning a patient in the
sense that you are always trying to minimize
the ventilator settings.
 “True” weaning implies a different expectation -
that the patient is improving and will soon not
need mechanical ventilation.
 This usually happens when the disease process is
improving or resolved and the patient has
acceptable parameters.
 It is important to assess the ability of the heart
to handle the increased demands that
extubation may place upon it (e.g.,
pneumonia/ARDS has resolved but significant
septic shock with cardiovascular collapse is
present).

PARAMETERS FOR WEANING
 RR < 25/min
 TIDAL VOLUME > 5mL/kg
 VITAL CAPACITY > 10mL/kg
 MINUTE VENTILATION < 10L/MIN
 PaO2/FiO2 > 200
 SHUNT < 20%
 NEGATIVE INSP FORCE < 25cm of H2O
 SHALLOW BREATHING INDEX (RR/Vt) < 105
Extubation
Weaning (cont.)
decrease the PEEP (4-5)
decrease the rate
decrease the PIP (as needed)
What you want to do is decrease
what the vent does and see if the
patient can make up the
difference….
Weaning is really the Transfer of
demands from ventilator to the
patient
Extubation
Extubation
Control of airway reflexes
Patent upper airway (air leak around
tube?)
Minimal oxygen requirement
Minimal rate
Minimize pressure support (0-10)
“Awake ” patient
BASIC VENTILATOR SETTINGS
 Tidal volume--10 to 15ml/kg (std = 12 ml/kg)
 Respiratory rate--initially 10 to 16/minute
 FiO2--0.21 to 1.0 depending on disease
process
 100% causes oxygen toxicity and atelectasis in
less than 24 hours
 40% is safe indefinitely
 PEEP can be added to stay below 40%
 Goal is to achieve a PaO2 >60
 I:E Ratio--1:2 is good starting point
 Obstructive disease requires longer expirations
 Restrictive disease requires longer inspirations

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