objectives respiratory physiology oxygen delivery abnormalities of gas exchange review of lung...
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OBJECTIVESRespiratory 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 DELIVERYoxygen 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
[Hb] x SpO2 x (1.36)
(PaO2) x (0.003) + easier to
unload O2
harder to unload O2
OXYGENATIONHypoxia 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 EXCHANGEEfficiency 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 EXCHANGEPhysiologic Mechanism of Hypoxia
Description
Low PiO2 altitude, disconnection of tubing
Hypoventilation displaces O2 from alveolusmasked by supplemental O2
V/Q mismatch inappropriately low ventilation for degree of perfusion; usu responds to O2
Shunt alveoli that are perfused are not ventilatedwith true shunt, minimal effect of O2healthy 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
VENTILATIONVentilation 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 EXCHANGEHYPERCAPNIA
Mechanisms: Increased CO2 production
malignant hyperthermiathyroid 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
• rarely causes hypercapnia in absence of other ventilatory defect
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
PULMONARY COMPLIANCEDefined 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 FAILUREAcute 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
HYPOXEMIC
HYPERCAPNIC
Won’t breathe
Can’t breathe
RESPIRATORY FAILURE
RESPIRATORY FAILUREClinical signs and Symptoms
hypoxia is relatively easily identified on clinical examination
hypercapnia can be more subtle in its presentationmay not be in respiratory distress (central failure)
• tachypnea• dyspnea• diaphoresis• central cyanosis (late)
• tachycardia• dysrhythmias• hypertension• hypotension
• restlessness• headache• confusion• delirium• tremor• asterixis• seizures• coma
• wheeze• dyspnea• cough• accessory muscle use•abdominal paradox
MECHANICAL VENTILATION
MV: INDICATIONSHypoventilation
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
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
“the patient looked like they need to be placed on a ventilator”
NOMENCLATUREA “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 VENTILATIONA. Triggering:
patient triggered (flow, pressure)
machine triggered (time)
B. Inspiration-assisted
C. Cycling time (PCV) volume (VCV) flow (PSV)
D. Expiration- passive
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
NOMENCLATURECMV (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
NOMENCLATUREComparison of respiratory pattern using
different modes:
PEEPPositive 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- COMPLICATIONSPotential complications:
may overdistend alveoli:causing barotraumacan worsen oxygenation by increasing dead space
decreases venous return (high intrathoracic pressures)decreasing cardiac output
increases RV afterloadcan 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- CONTRAINDICATIONSRelative 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: INDICATIONSHas 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: CONTRAINDICATIONSHemodynamic 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: MONITORINGNIV 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 NIVwithin a few hours of initiation…
CONSIDER INTUBATION
SPECIAL CIRCUMSTANCES
ARDSDefinition:
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 benefitmortality 31 vs 39% (p=0.007)more vent free days
Mild permissive hypercapneia ok
May require sedation to maintain
REFRACTORY HYPOXIASome 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 VENTILATIONAPRV 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 VENTILATIONHFOV 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- MANAGEMENTWean 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- MANAGEMENTConsider 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 ARDSUsually 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 PRESSURESDecreased 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
VILIVENTILATOR-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 alveolimay lead to shear stress, disruption of surfactant and
epithelium biotrauma:
mechanical stretch or shear injury lead to inflammatory mediator release and cellular activation
VILIPrevention:
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-PEEPaka: intrinsic PEEP or dynamic hyperinflation
Seen when a patient has failed to expire full VT and subsequent breaths delivered result in increasing hyperinflation
AUTO-PEEPMaking 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
“normal”
“Auto-PEEP”
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: MANAGEMENTLengthen 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
VAPNosocomial 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
VAPMechanism:
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
VAPDIAGNOSIS: suspect if MV >48h -and-
feverWBCpurulent sputumnew or progressive infiltrate on CXR increased O2 requirements
Prevention: VAP bundle: HOB >30°, sedation vacations, DVT
prophylaxis, stress ulcer prophylaxis oral decontamination with antiseptic handwashing
WEANING
WEANINGWeaning 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
improvingoxygenation, RR, VT, minute ventilation, RSBI (f/VT) adequate
hemodynamically stable level of consciousness improved or airway protection
resolved
WEANINGNext 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?