VENTILATION FOR THE SURGICAL RESIDENT

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VENTILATION FOR THE SURGICAL RESIDENT

• POS review lecture 2008-2009
• Heather Whittingham

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OBJECTIVES

• Respiratory physiology
• oxygen delivery
• abnormalities of gas exchange
• review of lung volumes
• chest wall and respiratory mechanics
• Mechanical Ventilation
• indications
• nomenclature
• ventilation modes invasive and non-invasive
• special circumstances ARDS, refractory hypoxemia
  and BPF
• complications High pressures, VILI, Auto-PEEP,
  VAP
• weaning

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RESPIRATORY PHYSIOLOGY REVIEW
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OXYGEN DELIVERY

• oxygen is carried in the blood in two forms
• bound to Hb (SpO2)
• dissolved in plasma (PaO2)
• oxygen content (CaO2) is the sum of both
• oxygen delivery is a product of both the arterial
  O2 content and cardiac output

harder to unload O2
Hb x SpO2 x (1.36)

easier to unload O2
(PaO2) x (0.003)
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OXYGENATION

• Hypoxia is a state of tissue oxygen deprivation
• anaerobic metabolism ? lactic acidosis
• can lead to cellular, tissue and organ death
• Hypoxia can result from
• low PaO2
• anemia or abnormal Hb
• low cardiac output states/ impaired perfusion
• inability to utilize O2 (eg. cyanide)
• Hypoxemia refers to low PaO2 in the blood

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ABNORMAL GAS EXCHANGE

• Efficiency of gas exchange the a-a gradient
• P(A-a)O2 PAO2 PaO2
• PAO2 713 x FiO2 1.25 x PaCO2
• cumbersome, normal values not known for
  supplemental O2
• Often use P/F ratio instead PaO2/FiO2
• normal on FiO2 0.21 is 450-500 range
• tells us nothing about alveolar ventilation
  (PCO2)
• will be dependent on level of PEEP/ CPAP

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ABNORMAL GAS EXCHANGE
Physiologic Mechanism of Hypoxia Description
Low PiO2 altitude, disconnection of tubing
Hypoventilation displaces O2 from alveolus masked by supplemental O2
V/Q mismatch inappropriately low ventilation for degree of perfusion usu responds to O2
Shunt alveoli that are perfused are not ventilated with true shunt, minimal effect of O2 healthy alveoli cant compensate for sick ones
Low mv PaO2 low CO or high consumption can decrease PaO2 in presence of large shunt
Diffusion abnormality theoretic abnormality, not clinically relevant
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INTRAPULMONARY SHUNT
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VENTILATION

• Ventilation refers to CO2 clearance
• Alveolar ventilation
• air that meets perfused alveoli and participates
  in gas exchange
• Dead space ventilation
• air doesnt contact perfused alveoli to
  participate in gas exchange
• anatomic alveolar equipment
• wasted ventilation
• Minute Ventilation (MV)
• RR x VT
• total gas (L/min) of ventilation
• normal 6-8 L/min

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ABNORMAL GAS EXCHANGE

• HYPERCAPNIA
• Mechanisms
• Increased CO2 production
• malignant hyperthermia
• thyroid storm
• Decreased CO2 clearance
• low minute ventilation (RR x VT)
• high dead space ventilation

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LUNG VOLUMES

• TLC amount of gas in lungs after maximal
  inspiration
• RV amount of gas in lungs after maximal
  expiration
• VC volume of gas expired going from TLC to RV
• FRC volume of gas in lungs at the resting state
  (end-expiration)
• TV amount of gas inhaled in a normal inspiration

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PULMONARY COMPLIANCE

• Defined as the ability of the lung to stretch
  (change in volume) relative to an applied
  pressure
• Factors affecting compliance
• lung volume (overdistention vs. atelectasis)
• interstitial pathology (CHF, ILD)
• alveolar pathology (pneumonia, CHF, blood)
• pleural pathology (pleural effusion, fibrosis)
• chest wall mechanics
• diaphragm mobility
• chest wall deformities
• abdominal pressures

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RESPIRATORY FAILURE
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RESPIRATORY FAILURE

• Acute respiratory failure
• any impairment of O2 uptake or CO2 elimination
  or both that is severe enough to be a threat to
  life
• The signs and symptoms of respiratory failure are
  non-specific and often non-respiratory
• reflect end-organ dysfunction of neurologic and
  cardiovascular systems

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RESPIRATORY FAILURE

• Clinical signs and Symptoms
• hypoxia is relatively easily identified on
  clinical examination
• hypercapnia can be more subtle in its
  presentation
• may not be in respiratory distress (central
  failure)

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MECHANICAL VENTILATION
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MV INDICATIONS

• Hypoventilation
• arterial pH more important than absolute pCO2
• can result from central or mechanical failure
• respiratory acidosis with pH lt7.25 and pCO2 gt50
• Hypoxemia
• hypoxemia refractory to conservative measures
• pO2 lt 60 with FiO2 gt60
• Respiratory Fatigue
• excessive work of breathing suggestive of
  impending respiratory failure
• Airway Protection

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MV INDICATIONS
the patient looked like they need to be placed
on a ventilator

• most absolute criteria for initiation of
  mechanical ventilation are arbitrary and reflect
  a line drawn in the sand
• fail to account for a spectrum of disease
• a PaO2 of 61 is acceptable and 59 is not?
• chronic vs acute derangements
• fail to account for co-morbid disease management
• precise control of PaCO2 in a patient with a head
  injury
• assisted hyperventilation to compensate for a
  metabolic acidosis
• airway maintenance with nasal airway or surgical
  airway

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NOMENCLATURE

• A mode is a pattern of breaths delivered by the
  ventilator
• pressure support
• pressure control
• volume control
• To understand the differences, must understand
  the phases of ventilation
• expiratory passive phase, PEEP applied
• triggering change from expiration to inspiration
• inspiratory assisted inspiratory flow
• cycling end of inspiration and change to
  expiration

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PHASES OF VENTILATION

• Triggering
• patient triggered (flow, pressure)
• machine triggered (time)
• Inspiration-assisted
• Cycling
• time (PCV)
• volume (VCV)
• flow (PSV)
• Expiration- passive

C
INSP
B
A
EXP
D
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VOLUME CONTROL (VCV)

• Set tidal volume, cycles into exhalation when
  target volume has been reached airway pressure
  dependent on lung compliance
• guarantees a minimum minute ventilation (MV RR x
  Vt)
• useful for patients with a decreased respiratory
  drive
• post-operative, head-injured, narcotic overdose
• Variables
• Trigger patient or machine controlled
• Inspiratory phase set inspiratory flow rate
• Cycling SET
• Expiratory phase set amount of PEEP
• Alarms high pressure (default into PCV and
  cycle), high RR

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PRESSURE CONTROL (PCV)

• Inspiratory pressure and inspiratory time are
  set tidal volume is dependent on lung compliance
• allows for control of peak airway pressures
  (ARDS)
• a longer inspiratory time can allow for better
  recruitment and oxygenation
• Variables
• Trigger patient or machine controlled
• Inspiratory phase SET- target pressure,
  generated quickly and maintained throughout high
  initial flow rate
• Cycling time
• Expiratory phase set amount of PEEP
• Alarms high and low tidal volumes, high RR

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PRESSURE SUPPORT (PSV)

• Spontaneous mode of ventilation patient
  generates each breath and a set amount of
  pressure is delivered with each breath to
  support the breath
• comfortable determine own RR, inspiratory flow
  and time
• Vt depends on level of pressure support set, lung
  compliance and patient effort
• Variables
• Trigger patient controlled must initiate breath
• Inspiratory phase SET support pressure
• Cycling flow cycled (when falls to 25 of peak)
• Expiratory phase set amount of PEEP
• Alarms apnea and high RR

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NOMENCLATURE

• CMV (Controlled Mechanical Ventilation)
• minute ventilation entirely determined by set RR
  and Vt
• patient efforts do not contribute to minute
  ventilation
• AC (Assist/Control)
• combination of mandatory (set rate) and patient
  triggered breaths
• patient triggered breaths deliver same Vt or
  pressure as mandatory breaths
• SIMV (Synchronized Intermittent Mandatory
  Ventilation)
• combination of mandatory and patient-triggered
  breaths
• pure SIMV, patient not assisted on additional
  breaths
• can combine SIMV with PSV, so additional breaths
  are supported

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NOMENCLATURE

• Comparison of respiratory pattern using different
  modes

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PEEP

• Positive End-Expiratory Pressure (PEEP)
• constant baseline pressure delivered throughout
  cycle
• by convention called CPAP if breathing
  spontaneously and PEEP if receiving positive
  pressure ventilation
• 3-5cm H20 PEEP provided to all intubated patients
  to overcome the decrease in FRC caused by bypass
  of glottis
• Advantages
• Improve oxygenation by preventing end-expiratory
  collapse of alveoli and help recruit new alveoli
• may prevent barotrauma caused by repetitive
  opening and closing of alveoli
• creates hydrostatic forces to fluid from alveoli
  into interstitium

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PEEP- COMPLICATIONS

• Potential complications
• may overdistend alveoli
• causing barotrauma
• can worsen oxygenation by increasing dead space
• decreases venous return (high intrathoracic
  pressures)
• decreasing cardiac output
• increases RV afterload
• can contribute to RV strain and/or failure
  associated with severe respiratory failure
• lung heterogeneous
• some areas may be getting too much, while others
  not enough

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PEEP- CONTRAINDICATIONS

• Relative contraindications to high PEEP
• circumstances where risk may outweigh benefit

RELATIVE CONTRAINDIATIONS MECHANISM OF HARM
Hypotension Decreased venous return
Right Heart Failure High RV afterload ? worsened RV failure
Right to Left Intracardiac Shunts High RV afterload ? worsened shunt
Increased ICP Can increase CVP, decreasing cerebral venous drainage and further increasing ICP
Hyperinflation Worsening gas trapping
Asymmetric or Focal lung disease High pressure preferrentially directed to normal lung
Bronchopleural Fistula Increased air leak ? prevent healing
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NON-INVASIVE VENTILATION

• The delivery of PPV without an ETT
• avoids complications of intubation, including VAP
• Two fundamental types CPAP and bi-level or BiPAP
• CPAP delivers continuous positive pressure
  throughout respiratory cycle
• useful for hypoxemic respiratory failure
• BiPAP delivers pressure support during
  inspiration (IPAP), coupled with PEEP during
  expiration (EPAP)
• useful for hypercapneic or combined respiratory
  failure

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NIV INDICATIONS

• Has been shown to decrease need for intubation
  and decrease morbidity mortality in certain
  patients
• Acute cardiogenic pulmonary edema (ACPE)
• COPD exacerbation
• May decrease re-intubation rate after extubation
  in COPD
• Fundamental requirements
• spontaneously breathing patient who can protect
  airway
• potentially reversible condition
• ability to improve within a few hours
• cooperative patient
• no hemodynamic instability, no cardiac ischemia

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NIV CONTRAINDICATIONS

• Hemodynamic instability or shock
• Decreased LOC and inability to protect airway
• Inadequate respiratory drive
• High risk of aspiration (SBO, UGI bleed)
• Facial trauma or craniofacial abnormality
• Upper airway obstruction
• Uncooperative patient
• Inability to clear secretions or excessive
  secretions

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NIV MONITORING

• NIV has been successful if the patients work of
  breathing has decreased and blood gas
  abnormalities are starting to resolve
• Clinical improvement is usually evident within
  the 1st hour
• Biochemical improvement usually evident within
  2-4 hours of initiation

If ongoing evidence of respiratory failure
despite NIV within a few hours of
initiation CONSIDER INTUBATION
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SPECIAL CIRCUMSTANCES
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ARDS

• Definition
• bilateral pulmonary infiltrates
• absence of LA hypertension
• severe hypoxemia (PaO2/FiO2 ratio lt200)
• Heterogeneous lung involvement
• dependent atelectatic, consolidated
• non-dependent relatively preserved
• Concept of the baby lung
• high inflation pressures/ volumes used for
  hypoxemia can damage normal lung (volutrauma,
  barotrauma)
• repetitive opening/closing of marginal areas
  causes additional trauma (atelectrauma)

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ARDS VENTILATION

• Important to understand principles of ARDS to
  minimize ventilator-induced lung injury
• Lung protective ventilation (ARDSnet)
• compared tidal volume of 12ml/kg (840) and
  plateau lt50 cm H2O vs 6ml/kg (420) and plateau
  lt30 cm H2O
• stopped early for benefit
• mortality 31 vs 39 (p0.007)
• more vent free days
• Mild permissive hypercapneia ok
• May require sedation to maintain

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REFRACTORY HYPOXIA

• Some additional modes of ventilation can be tried
  for hypoxia refractory to conventional
  ventilation
• recruitment maneuvers
• inverse ratio ventilation (IgtE)
• prone ventilation
• airway pressure release ventilation (APRV)
• high frequency oscillation ventilation (HFOV)
• None to date have shown an increased mortality,
  but can improve oxygenation

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APR VENTILATION

• APRV ventilates by time-cycled switching between
  two pressure levels (Phigh and Plow)
• degree of ventilator support is determined by the
  duration of the two pressure levels and the tidal
  volume delivered
• tidal volume determined by ? P and respiratory
  compliance
• permits spontaneous breathing in any phase
• better ventilation of posterior, dependent lung
  regions after 24h
• improves recruitment
• lower sedation required
• C/I if deep sedation needed, COPD?

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HFO VENTILATION

• HFOV achieves gas transport by rapidly
  oscillating a small Vt (anatomic dead space)
  achieving rapid gas mixing in the lung
• gas transport occurs along partial-pressure
  gradients
• oscillates around a constant high mean airway
  pressure (mPaw) to maintain alveolar recruitment,
  avoiding big ? P
• risk of barotrauma and hemodynamic compromise
  limilar to conventional ventilation
• O2 mPaw and FiO2
• CO2 frequency and ?P

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BRONCHOPLEURAL FISTULA

• Presence of a persistent air-leak gt24h after
  insertion of a CT is highly suggestive of a
  bronchopleural fistula
• after exclusion of an external leak
• Weaning from PPV entirely is optimal
• When not possible, select strategy to minimize
  minute ventilation and intrathoracic pressure

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BPF- MANAGEMENT

• Wean ventilatory support as much as tolerates
• PSV may be preferable to full ventilation
• limit mean airway pressure and number of high
  pressure breaths
• avoid alkalosis consider permissive hypercapnia
• minimize PEEP (intrinsic and extrinsic) treat
  bronchospasm
• Limit VT to 6-8 ml/kg
• Minimize inspiratory time (keep IE ratio low,
  use high flows)
• Use lowest CT suction that maintains lung
  inflation
• Explore positional differences that minimize leak

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BPF- MANAGEMENT

• Consider specific or unconventional measures for
  physiologically significant leaks
• independent lung ventilation
• endobronchial approach to sealing leak
• surgical closure
• Treat underlying cause of respiratory failure

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BPF in ARDS

• Usually a measure of severity of underlying
  disease will -- -often doesnt improve until
  ARDS improves
• BPF nearly always improves without specific
  therapy
• BPF usually not physiologically significant
  (lt10), even in presence of hypercapnia
• Reducing the size of the leak has minimal effect
  on gas exchange
• No specific measures have been shown to affect
  outcome
• Patients almost never die of BPF they die with
  BPF

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COMPLICATIONS OF VENTILATION
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HIGH AIRWAY PRESSURES

• Decreased Compliance
• pneumothorax
• mainstem intubation
• dynamic hyperinflation
• CHF
• ARDS
• consolidation
• pneumonectomy
• pleural effusion
• abdominal distention
• chest wall deformity

• Increased Resistance
• bronchospasm
• secretions
• small ETT
• mucosal edema
• biting ETT

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VILI

• VENTILATOR-INDUCED LUNG INJURY
• multiple recognized forms
• barotrauma
• high ventilation pressures result in global or
  regional overdistention ? can result in alveolar
  rupture
• may be gross (PTX, BPF, subcut emphysema) or
  microscopic
• volutrauma/atelectrauma
• ventilation at low lung volumes causes repetitive
  opening and closing of alveoli
• may lead to shear stress, disruption of
  surfactant and epithelium
• biotrauma
• mechanical stretch or shear injury lead to
  inflammatory mediator release and cellular
  activation

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VILI

• Prevention
• low VT ventilatory strategies
• minimize peak and plateau pressures
• PEEP for recruitment and minimize end-expiratory
  collapse
• tolerate mild to moderate permissive hypercapnia
  to achieve above goals
• allowing PCO2 to rise into high 40s to 50s to
  reduce driving and plateau pressures
• generally considered safe at low levels
• contraindications increased ICP, acute or
  chronic cardiac ischemia, severe PH, RV failure,
  uncorrected severe metabolic acidosis, TCA
  overdose, pregnancy

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AUTO-PEEP

• aka intrinsic PEEP or dynamic hyperinflation
• Seen when a patient has failed to expire full VT
  and subsequent breaths delivered result in
  increasing hyperinflation

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AUTO-PEEP

• Making the diagnosis
• inspection continuous inward movement of chest
  until start of next breath
• auscultation persistence of breath sounds until
  start of next ventilator breath
• failure to return to baseline on waveform before
  delivery of next breath

Auto-PEEP
normal
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AUTO-PEEP
COMPLICATIONS OF AUTO-PEEP
Hypotension from increased intrathoracic pressure with decreased venous return
Decreased efficiency of diaphragm and force generated
May be unable to generate sufficient pressure to trigger breaths
Increased work of breathing, and respiratory muscle fatigue
Increased agitation, ventilator asynchrony
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AUTO-PEEP MANAGEMENT

• Lengthen time for exhalation
• slow controlled rate on ventilator
• lengthen IE ratio (shorten I time)
• may require patient sedation if patient-driven
• Treat bronchospasm
• bronchodilators
• corticosteroids if asthma or AECOPD
• Match intrinsic PEEP to minimize gas trapping by
  dynamic collapse

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VAP

• Nosocomial infection of lung that develops gt48h
  after ETT
• 9-27 of mechanically ventilated patients
• 2nd most common nosocomial infection (UTI 1st)
• Risk of VAP highest early in course, but
  incidence increases with duration of mechanical
  ventilation
• 3/day (1-5), 2/day (5-10), 1/day (gt10)
• overall mortality 27
• microbiology
• 60 GNB E coli, P aeruginosa, Klebsiella or
  Acinetobacter sp.
• GPC incidence is increasing (esp common in TBI,
  DM)
• 20-40 are polymicrobial

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VAP

• Mechanism
• Aspiration of oropharyngeal pathogens or leakage
  of secretions around ETT primary routes into LRT
• Infected biofilm on ETT with embolization during
  suctioning
• Risk factors

mechanical ventilation COPD longer duration of MV
age gt60 ARDS re-intubation
male sinusitis supine position
trauma aspiration paralytics
NG tube low ETT cuff pressure post-surgical patient
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VAP

• DIAGNOSIS suspect if MV gt48h -and-
• fever
• WBC
• purulent sputum
• new or progressive infiltrate on CXR
• increased O2 requirements
• Prevention
• VAP bundle HOB gt30, sedation vacations, DVT
  prophylaxis, stress ulcer prophylaxis
• oral decontamination with antiseptic
• handwashing

• Problem
• no gold standard
• broad DDx
• significant overlap with infectious
  tracheobronchitis
• colonization ? infection

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WEANING
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WEANING

• Weaning refers to gradual withdrawal of
  ventilatory support
• Most patients (75) do not require weaning and
  rather require liberation from mechanical
  ventilation
• if no respiratory muscle weakness or abnormal
  lung mechanics have developed during illness
• Initial task is to determine if the initial
  reason for intubation and mechanical ventilation
  have resolved
• pneumonia or other pulmonary process treated and
  improving
• oxygenation, RR, VT, minute ventilation, RSBI
  (f/VT) adequate
• hemodynamically stable
• level of consciousness improved or airway
  protection resolved

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WEANING

• Next is to determine if the patient can breathe
  without the ventilator
• Spontaneous Breathing Trial (SBT) most common
  method
• must be HD stable, no cardiac ischemia,
  oxygenation should be adequate and PaO2/FiO2
  ratio gt120 at PEEP 5
• sedatives and narcotics should be discontinued in
  advance
• 30 m- 2h trial of reduced support t-piece, PSV
  (lt8/5) on FiO2 0.5
• if RR lt35, ?HR lt20 bpm, ?BP lt20mmHg, ABG w/o
  acidosis -and-
• cough PF gt60L/min, ETT suction ltq2h and cuff leak
• ? consider trial of extubation

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WEANING

• If fails SBT, attempt to identify contributing
  treatable factors
• hypoxemia- consider diuresis and afterload
  reduction
• excessive secretions- treat infections
• bronchospasm- bronchodilation, steroids
• hypercapnia- less sedation, treat cause if
  identified
• if suspect strength-load imbalance, may need
  weaning
• Many weaning strategies have been tried for
  patients that fail their 1st SBT
• once daily t-piece trial gt/ PSV gt SIMV (most
  patients 5d)
• does not account for patients with respiratory
  muscle weakness or underlying weaning failure

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QUESTIONS?