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

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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

FIO20.3

0.4

0.4

0.5

0.5

0.6

0.7

0.7

0.7

0.8

0.9

0.9

0.9

1.0PEEP

5 5 8 8 10 10 10 12 14 14 14 16 1820-24

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)1301-1308New 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 12

Pplateau <30 <50

PEEP Protocol Protocol

Actual PEEP 8.1 9.1

Result (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 1.0

PEEP 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 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

0

5

10

15

20

25

30

35

40

Oct

-06

No

v-06

Dec

-06

Jan

-07

Feb

-07

Mar

-07

Ap

r-07

May

-07

Jun

-07

Jul-

07

Au

g-0

7

Sep

-07

Oct

-07

No

v-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

NHSN 50th Percentile 4.1

Complications of Mechanical Ventilation