Transcript No Slide Title

Complications of
Mechanical Ventilation
Ventilator-Induced lung injury
(VILI)
Volutrauma
Atelectetrauma
• Overdistention
• Repeated recruitment and collapse
Bio trauma
• Inflammatory mediators
Barotrauma
• High-pressure induced lung damage
Oxygen toxic effect • FiO2
The Problem of Heterogeneity in
ARDS
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0
10
The Problem of Heterogeneity
Especially in ARDS
• Some lung units may be overstretched while
others remain collapsed at the same airway
pressure.
• Finding the right balance of TV and PEEP to
keep the lung open without generating high
pressures is the goal.
• This presents major difficulty for the clinician,
who must apply only a single pressure to
ventilate patients
Ventilator-induced Lung Injury
(VILI)
Collapse
Over
Distension
Pinsp = 40 mbar
Ventilator-Induced Lung Injury
Atelectotrauma Vs Volutrauma
Atelectrauma:
Repetitive alveolar
collapse and reopening
of the under-recruited
alveoli
Dreyfuss: J Appl Physiol 1992
Volutrauma:
Over-distension of normally
aerated alveoli due to
excessive volume delivery
Spectrum of Regional Opening Pressures
(Supine Position)
Opening
Pressure
Superimposed
Pressure
Inflated
0
Small Airway
Collapse
10-20 cmH2O
Alveolar Collapse
(Reabsorption)
20-60 cmH2O
Consolidation
=
Lung Units at Risk for Tidal
Opening & Closure
(from Gattinoni)

Effect of lung expansion on pulmonary vasculature. Capillaries that are
embedded in the alveolar walls undergo compression even as interstitial
vessels dilate. The net result is usually an increase in pulmonary
vascular resistance, unless recruitment of collapsed units occurs.
VALI vs VILI
• Ventilator-associated lung injury (VALI)
– Acute lung injury that resembles ARDS in
patients receiving MV
– VALI may be associated with pre-existing
lung pathology
– VALI is associated only with MV
• Ventilator induced lung injury (VILI)
– Acute lung injury directly induced by MV in
animal models
Histopathology of VILI
Belperio et al, J Clin Invest Dec 2002; 110(11):1703-1716
Mechanisms of Airspace Injury
Airway Trauma
“Stretch”
“Shear”
ARDS
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10
ARDS after PEEP
preventing atelectotrauma
Atelectetrauma
The PEEP Effect
NEJM 2006;354:1839-1841
Avoiding Atelectotrauma :How much PEEP is
enough? ARDSnet protocol:
PEEP - FiO2 Combinations
GOAL: PaO2 55-80 mm Hg or SpO2 88-95%
Use these FiO2/PEEP combinations to achieve
oxygenation goal.
FIO2
0.3
PEEP 5
0.4
0.4
0.5
0.5
0.6
0.7
0.7
0.7
0.8
0.9
0.9
0.9
1.0
5
8
8
10
10
10
12
14
14
14
16
18
20-24
New Eng J Med. 2000;342(18)1301-1308
Zone of
↑ Risk
Biotrauma
Cytokines,
complement,
prostanoids,
leukotrienes,
O2- Proteases
Organ
dysfucntion
Biophysical biochemical Injury due to MV
High volume & Low PEEP
Lung-Protective Ventilation
ARDS Network, 2000: Multicenter randomized,861Pts
Lung-protective ventilation
6
12
<30
Protocol
8.1
31.0%
<50
Protocol
9.1
39.8%
Tidal Volume (ml/kg)
Pplateau
PEEP
Actual PEEP
Result (p<0.001)
Conventional
ventilation
Principle for FiO2 and PEEP Adjustment
FiO2
PEEP
0.3
5
0.4
5-8
0.5
8-10
0.6
10
0.7
10-14
0.8
14
0.9
14-18
1.0
18-24
NEJM 2000; 342: 1301-1308
Lung-Protective Ventilation
Low VT Low Plateau pressure
• Result:
– 22% reduction in mortality (31% vs 39.8%)
– Increase ventilator-free days
NEJM 2000; 342: 1301-1308
Optimized Lung Volume “Safe
Window”
•
Overdistension
–
–
–
–
Edema fluid accumulation
Surfactant degradation
High oxygen exposure
Mechanical disruption
Zone of
Overdistention
Injury
“Safe”
Window
•
Derecruitment, Atelectasis
– Repeated closure / re-expansion
– Stimulation inflammatory
response
– Inhibition surfactant
– Local hypoxemia
– Compensatory overexpansion
Volume
Zone of
Derecruitment
and Atelectasis
Injury
Pressure
Dependent to Non-dependent
Progression of Injury
Effect of 45 cmH2O PIP
Control
5 min
20 min
Baro-trauma
• Etiology :Directly related to airway
pressures/PEEP
• Incidence
– 4% - 15%
– Highest in ARDS
– Incidence now decreased secondary to lung
protective ventilation
Barotrauma-Pathophysiology
• Some alveoli become more distended than
others. Alveolar pressure increases and
forms a pressure gradient between the alveoli
and adjacent perivascular sheath.
• Air dissects into the perivascular sheath
leading to perivascular interstitial
emphysema (PIE) and further moves into
areas of least resistance including
subcutaneous tissue and tissue planes.
Barotrauma-Complications
• Pneumothorax
• Interstitial emphysema
• Pneumomediastinumleads to PTX in 42% of
patients in one study
• Pneumopericardium
• Subcutaneous
emphysema
• Pneumoperitoneum
Gas Extravasation
Barotrauma
Oxygen Toxicity : FIO2 > 60 % for >
24h
A lve o la r p re ssure  P A O 2  P A C O 2  P A H 2 O  P A N 2
• Absorptive
atelectasis
– O2/N2 = 21/79
>>>>>> 50/50
Oxygen
Carbon
dioxide
Water
vapour
Nitrogen
Hyperoxia toxicity: mechanism
• Free radicals: lipid peroxidations, especially
in the cell membranes, inhibit nucleic acids
and protein synthesis, and inactivate cellular
enzymes.
• Explosive free radical production leading to
swamping of the anti-oxidant enzyme
systems and as a result free radicals escape
inactivation.
Oxygen Toxicity
• Absorptive atelectasis
– O2/N2 = 21/79 >>>>
50/50
• Accentuation of
hypercapnia
– Chronic respiratory failure:
PCO2 with PO2
• Damage to airways
– Bronchopulmonary
dysplasia
• Diffuse alveolar damage
Infectious complications of
Mechanical ventilation
Maxillary Sinus and Middle Ear
Effusion
• Maxillary effusion
– 20% in patients intubated for > 7 days.
– 47% when the gastric tube is placed nasally
– 95%
• Secondarily infected maxillary effusion (4571% of effusions)
• Middle ear effusion (29%) with 22% of them
become infected
• Hearing impairment that may contribute to the
confusion and delirium in elderly population
VAP: Definitions
• VAP – ventilator associated pneumonia
– >48 hours on vent
– Combination of:
•
•
•
•
CXR changes
Sputum changes
Fever, ↑ WBC
positive sputum culture
• Occurs secondary to micro-aspiration of
upper airway secretions
Organism Entry for VAP
Risk Factors for VAP
• No 1 risk factor is endotracheal intubation
• Factors that enhance colonization of the oropharynx
&/or stomach:
– Poor oral hygiene
• Conditions favoring aspiration into the respiratory
tract or reflux from GI tract:
–
–
–
–
–
–
Supine position
NGT placement
Re-Intubation and self-extubation
Surgery of head/neck/thorax/upper abdomen
GERD
Coma/ depressed Glascow coma scale
Significance of VAP
• Mortality 20-70%(Leading cause of mortality
from nosocomial infections in hospitals)
• Increases mechanical ventilation days
• Increases ICU stay by 4.3 days
• Increases hospital LOS by 4-9 days
• Increases cost -Excess costs of
approximately 11,000 -$40,000/patient
VAP prevention :VAP Bundle
• Elevation of the head of the bed 30-45o
• Use 15-30o for neonates and small infants,
otherwise 30-45o
• Daily sedation vacations (minimize duration
of intubation
• Daily assessment of readiness to extubate
• Peptic ulcer disease (PUD) prophylaxis
• Oral care protocol (chorhexidine)
• DVT prophylaxis option
HOB 30-45o decrease risk of
aspiration
• 45o head-up tilt is the
goal in all patients
unless contraindicated
• No benefit of semirecumbency ~30o over
standard care ~10o
• Supine position is
harmful
HOB Elevation Leads to Significant
reduction in VAP
25
% VAP
20
15
10
5
0
Supine
HOB Elevation
Dravulovic et al. Lancet 1999;354:1851-1858
Handwashing
• Strict handwashing
before and after
handling patient or
patient’s equipment
or supplies
Does the VAP bundle work in
real life
CCU VAP Bundle Compliance Vs Infection Rate
VAP Infection Rate
Linear (VAP Infection Rate)
VAP Bundle Com pliance%
Linear (VAP Bundle Com pliance%)
40
100%
35
80%
30
25
60%
20
40%
15
10
20%
Feb-08
Jan-08
0%
Dec-07
Nov-07
Oct-07
Sep-07
Aug-07
Jul-07
Jun-07
May-07
Apr-07
Mar-07
Feb-07
Jan-07
Dec-06
Nov-06
0
Oct-06
5
NHSN 50th
Percentile 4.1
Complications of Mechanical
Ventilation
Complications
related to
Intubation
Mechanical
complications
related to
presence of
ETT
Ventilator
induced lung
injury
Complications
related to
Oxygen
Infectious
complications
of mechanical
ventilation