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?