Ventilation for the Surgical Resident
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Transcript Ventilation for the Surgical Resident
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
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:
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:
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
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
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:
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:
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:
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:
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
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
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
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
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:
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?