OBJECTIVES
 Respiratory physiology
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oxygen delivery
abnormalities of gas exchange
review of lung volumes
chest wall and respiratory mechanics
 Mechanical Ventilation
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indications
nomenclature
ventilation modes: invasive and non-invasive
special circumstances: ARDS, refractory hypoxemia and BPF
complications: High pressures, VILI, Auto-PEEP, VAP
weaning
RESPIRATORY
PHYSIOLOGY REVIEW
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:
[Hb] x SpO2 x (1.36)
+
(PaO2) x (0.003)
 oxygen delivery is a product of
both the arterial O2 content
and cardiac output
harder to
unload O2
easier to
unload O2
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:
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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
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
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 can’t 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
INTRAPULMONARY SHUNT
VENTILATION
 Ventilation refers to CO2 clearance
 Alveolar ventilation
 air that meets perfused alveoli and participates in gas exchange
 Dead space ventilation
 air doesn’t 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
ABNORMAL GAS EXCHANGE
HYPERCAPNIA
 Mechanisms:
• rarely causes hypercapnia in
absence of other ventilatory
defect
 Increased CO2 production
 malignant hyperthermia
 thyroid storm
 Decreased CO2 clearance
 low minute ventilation (RR x VT)
 high dead space ventilation
• low respiratory drive
• CNS depression
• drugs
• OHS/ CSA
• respiratory mechanical failure
• fatigue
• neuromuscular disease
• chest wall abnormality
• underlying lung pathology
• COPD
• ILD
• pulmonary embolism
• pulmonary vascular disease
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 (endexpiration)
 TV: amount of gas inhaled in a
normal inspiration
PULMONARY COMPLIANCE
 Defined as the ability of the lung to stretch (change in
volume) relative to an applied pressure
 Factors affecting compliance:
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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
RESPIRATORY FAILURE
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 nonspecific and often nonrespiratory
 reflect end-organ dysfunction
of neurologic and
cardiovascular systems
RESPIRATORY FAILURE
HYPOXEMIC
HYPERCAPNIC
Won’t breathe
Can’t breathe
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)
General
• tachypnea
• dyspnea
• diaphoresis
• central
cyanosis (late)
Respiratory
• wheeze
• dyspnea
• cough
• accessory
muscle use
•abdominal
paradox
Cardiovascular
• tachycardia
• dysrhythmias
• hypertension
• hypotension
Neurologic
• restlessness
• headache
• confusion
• delirium
• tremor
• asterixis
• seizures
• coma
MECHANICAL
VENTILATION
MV: INDICATIONS
 Hypoventilation
 arterial pH more important than absolute pCO2
 can result from central or mechanical failure
 respiratory acidosis with pH <7.25 and pCO2 >50
 Hypoxemia
 hypoxemia refractory to conservative measures
 pO2 < 60 with FiO2 >60%
 Respiratory Fatigue
 excessive work of breathing suggestive of impending
respiratory failure
 Airway Protection
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
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
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expiratory: passive phase, PEEP applied
triggering: change from expiration to inspiration
inspiratory: assisted inspiratory flow
cycling: end of inspiration and change to expiration
PHASES OF VENTILATION
A. Triggering:
patient triggered (flow, pressure)
machine triggered (time)
B. Inspiration-assisted
INSP
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time (PCV)
volume (VCV)
flow (PSV)
D. Expiration- passive
EXP
C. Cycling
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:
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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
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
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:
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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
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
NOMENCLATURE
 Comparison of respiratory pattern using different modes:
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
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
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
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
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:
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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
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
NIV: MONITORING
 NIV has been successful if the patient’s 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
SPECIAL CIRCUMSTANCES
ARDS
 Definition:
 bilateral pulmonary infiltrates
 absence of LA hypertension
 severe hypoxemia (PaO2/FiO2 ratio <200)
 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)
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 <50 cm
H2O vs 6ml/kg (420) and plateau <30 cm H2O
 stopped early for benefit
 mortality 31 vs 39% (p=0.007)
 more vent free days
 Mild permissive hypercapneia ok
 May require sedation to maintain
REFRACTORY HYPOXIA
 Some additional modes of ventilation can be tried for
hypoxia refractory to conventional ventilation:
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recruitment maneuvers
inverse ratio ventilation (I>E)
prone ventilation
airway pressure release ventilation (APRV)
high frequency oscillation ventilation (HFOV)
 None to date have shown an increased mortality, but can
improve oxygenation
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 Δ 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?
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 Δ P
 risk of barotrauma and hemodynamic compromise limilar to
conventional ventilation
 O2: mPaw and FiO2
 CO2: frequency and ΔP
BRONCHOPLEURAL FISTULA
 Presence of a persistent air-leak >24h
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
BPF- MANAGEMENT
 Wean ventilatory support as much as tolerates
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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 I:E ratio low, use high flows)
 Use lowest CT suction that maintains lung inflation
 Explore positional differences that minimize leak
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
BPF in ARDS
 Usually a measure of severity of underlying disease will --often doesn’t improve until ARDS improves
 BPF nearly always improves without specific therapy
 BPF usually not physiologically significant (<10%), 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
COMPLICATIONS OF
VENTILATION
HIGH AIRWAY PRESSURES
 Decreased Compliance
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pneumothorax
mainstem intubation
dynamic hyperinflation
CHF
ARDS
consolidation
pneumonectomy
pleural effusion
abdominal distention
chest wall deformity
 Increased Resistance
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bronchospasm
secretions
small ETT
mucosal edema
biting ETT
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
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 40’s to 50’s 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
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
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”
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
AUTO-PEEP: MANAGEMENT
 Lengthen time for exhalation
 slow controlled rate on ventilator
 lengthen I:E 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
VAP
 Nosocomial infection of lung that develops >48h 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 (>10)
 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
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 >60
ARDS
re-intubation
male
sinusitis
supine position
trauma
aspiration
paralytics
NG tube
low ETT cuff pressure
post-surgical patient
VAP
 DIAGNOSIS: suspect if MV >48h -and
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fever
WBC
purulent sputum
new or progressive infiltrate on CXR
increased O2 requirements
Problem:
• no gold standard
• broad DDx
• significant overlap with
infectious tracheobronchitis
• colonization ≠ infection
 Prevention:
 VAP bundle: HOB >30°, sedation vacations, DVT prophylaxis,
stress ulcer prophylaxis
 oral decontamination with antiseptic
 handwashing
WEANING
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
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 >120 at PEEP ~5
 sedatives and narcotics should be discontinued in advance
 30 m- 2h trial of reduced support: t-piece, PSV (<8/5) on FiO2 0.5
 if RR <35, ΔHR <20 bpm, ΔBP <20mmHg, ABG w/o acidosis -and cough PF >60L/min, ETT suction <q2h and cuff leak

consider trial of extubation
WEANING
 If fails SBT, attempt to identify contributing treatable factors:
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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 >/≈ PSV > SIMV (most patients ≤ 5d)
 does not account for patients with respiratory muscle weakness
or underlying weaning ‘failure’
QUESTIONS?