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Complications of Mechanical Ventilation. Ventilator-Induced lung injury (VILI). The Problem of Heterogeneity in ARDS. -10. 0. 10. The Problem of Heterogeneity Especially in ARDS. Some lung units may be overstretched while others remain collapsed at the same airway pressure. - PowerPoint PPT Presentation
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Complications of Mechanical Ventilation
Ventilator-Induced lung injury (VILI)
-10 0 10
The Problem of Heterogeneity in ARDS
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)
OverOverDistensionDistension
CollapseCollapse
Pinsp = 40 mbar
Ventilator-Induced Lung Injury Atelectotrauma Vs Volutrauma
Atelectrauma: Repetitive alveolar collapse and reopening of the under-recruited alveoli
Volutrauma:Over-distension of normally aerated alveoli due to excessive volume delivery
Dreyfuss: J Appl Physiol 1992
Spectrum of Regional Opening Pressures (Supine Position)
Superimposed Pressure Inflated 0
Alveolar Collapse(Reabsorption) 20-60 cmH2O
Small AirwayCollapse
10-20 cmH2O
Consolidation
(from Gattinoni))Lung Units at Risk for Tidal Opening & Closure
=
OpeningPressure
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
“Stretch”
“Shear”
Airway Trauma
-10 0 10
ARDS
ARDS after PEEPpreventing atelectotrauma
Atelectetrauma
The PEEP Effect
NEJM 2006;354:1839-1841
Avoiding Atelectotrauma :How much PEEP is enough? ARDSnet protocol:
PEEP - FiO2 Combinations
FIO2 0.3
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
PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 20-
24
GOAL: PaO2 55-80 mm Hg or SpO2 88-95%
Use these FiO2/PEEP combinations to achieve oxygenation goal.
New Eng J Med. 2000;342(18)1301-1308New Eng J Med. 2000;342(18)1301-1308
Zone of↑ Risk
Biotrauma
Biophysical biochemical Injury due to MVHigh volume & Low PEEP
Cytokines, complement, prostanoids, leukotrienes, O2
- Proteases
Organ dysfucntion
Lung-Protective VentilationARDS Network, 2000: Multicenter randomized,861Pts
Lung-protective ventilation Conventional ventilation
Tidal Volume (ml/kg) 6 12Pplateau <30 <50PEEP Protocol ProtocolActual PEEP 8.1 9.1Result (p<0.001) 31.0% 39.8%
Principle for FiO2 and PEEP AdjustmentFiO2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0PEEP 5 5-8 8-10 10 10-14 14 14-18 18-24
NEJM 2000; 342: 1301-1308
Lung-Protective VentilationLow VT Low Plateau pressure
• Result:– 22% reduction in mortality (31% vs 39.8%)– Increase ventilator-free days
NEJM 2000; 342: 1301-1308
Volume
Pressure
Zone ofOverdistention
“Safe”Window
Zone ofDerecruitment
and Atelectasis
Injury
Injury
Optimized Lung Volume “Safe Window”
• Overdistension – Edema fluid accumulation– Surfactant degradation– High oxygen exposure– Mechanical disruption
• Derecruitment, Atelectasis– Repeated closure / re-expansion– Stimulation inflammatory
response– Inhibition surfactant– Local hypoxemia– Compensatory overexpansion
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• Pneumomediastinum-leads
to PTX in 42% of patients in one study
• Pneumopericardium• Subcutaneous emphysema• Pneumoperitoneum
Gas Extravasation
Barotrauma
Oxygen Toxicity : FIO2 > 60 % for > 24h
• Absorptive atelectasis– O2/N2 = 21/79
>>>>>> 50/50 Carbon dioxide
Water vapour
Oxygen
Nitrogen
2A2A2A2A NPOHPC OPOPp re s s u reA lv e o la r
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 (45-71% 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 semi-recumbency ~30o over standard care ~10o
• Supine position is harmful
HOB Elevation Leads to Significant reduction in VAP
Dravulovic et al. Lancet 1999;354:1851-1858
0
5
10
15
20
25%
VA
P
Supine HOB Elevation
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
05
10152025303540
Oct
-06
Nov
-06
Dec
-06
Jan-
07
Feb-
07
Mar
-07
Apr
-07
May
-07
Jun-
07
Jul-0
7
Aug
-07
Sep-
07
Oct
-07
Nov
-07
Dec
-07
Jan-
08
Feb-
08
0%
20%
40%
60%
80%
100%
VAP Infection Rate VAP Bundle Compliance%Linear (VAP Infection Rate) Linear (VAP Bundle Compliance%)
NHSN 50th Percentile 4.1
Complications of Mechanical Ventilation