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Complications of Mechanical Ventilation. Ventilator-Induced lung injury (VILI) Overdistention Volutrauma Repeated recruitment and collapse Atelectetrauma.

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Presentation on theme: "Complications of Mechanical Ventilation. Ventilator-Induced lung injury (VILI) Overdistention Volutrauma Repeated recruitment and collapse Atelectetrauma."— Presentation transcript:

1 Complications of Mechanical Ventilation

2 Ventilator-Induced lung injury (VILI) Overdistention Volutrauma Repeated recruitment and collapse Atelectetrauma Inflammatory mediators Bio trauma High-pressure induced lung damage Barotrauma FiO2 Oxygen toxic effect

3 The Problem of Heterogeneity in ARDS

4 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

5 Ventilator-induced Lung Injury (VILI) OverDistension Collapse

6 Pinsp = 40 mbar

7 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

8 Spectrum of Regional Opening Pressures (Supine Position) Superimposed Pressure Inflated 0 Alveolar Collapse (Reabsorption) cmH 2 O Small Airway Collapse cmH 2 O Consolidation  ) (from Gattinoni) Lung Units at Risk for Tidal Opening & Closure = Opening Pressure

9 How Much Collapse Is Dangerous Depends on the Plateau R = 100% Pressure [cmH 2 O] Total Lung Capacity [%] R = 22% R = 81% R = 93% 0 0 R = 0% R = 59% Some potentially recruitable units open only at high pressure More Extensive Collapse But Lower P PLAT Less Extensive Collapse But Greater P PLAT From Pelosi et al AJRCCM 2001

10 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.

11 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

12 Histopathology of VILI Belperio et al, J Clin Invest Dec 2002; 110(11):

13 Mechanisms of Airspace Injury “Stretch” “Shear” Airway Trauma

14 ARDS

15 ARDS after PEEP preventing atelectotrauma

16 Atelectetrauma

17 The PEEP Effect NEJM 2006;354:

18 Avoiding Atelectotrauma :How much PEEP is enough? ARDSnet protocol: PEEP - FiO2 Combinations FIO PEEP GOAL: PaO mm Hg or SpO % Use these FiO 2 /PEEP combinations to achieve oxygenation goal. New Eng J Med. 2000;342(18)

19 Zone of ↑ Risk

20 Biotrauma Biophysical biochemical Injury due to MV High volume & Low PEEP Cytokines, complement, prostanoids, leukotrienes, O 2 - Proteases Organ dysfucntion

21 Lung-Protective Ventilation ARDS Network, 2000: Multicenter randomized,861Pts Lung-protective ventilationConventional ventilation Tidal Volume (ml/kg) 612 P plateau <30<50 PEEP Protocol Actual PEEP Result (p<0.001) 31.0%39.8% Principle for FiO2 and PEEP Adjustment FiO PEEP NEJM 2000; 342:

22 Lung-Protective Ventilation Low VT Low Plateau pressure Result: –22% reduction in mortality (31% vs 39.8%) –Increase ventilator-free days NEJM 2000; 342:

23 Volume Pressure Zone of Overdistention “Safe” Window Zone of Derecruitment and Atelectasis 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

24 Dependent to Non-dependent Progression of Injury

25 Links Between VILI and MSOF Biotrauma and Mediator De-compartmentalization Slutsky, Chest 116(1):9S-16S

26 Effect of 45 cmH2O PIP Control 5 min 20 min

27 Baro-trauma Etiology :Directly related to airway pressures/PEEP Incidence –4% - 15% –Highest in ARDS –Incidence now decreased secondary to lung protective ventilation

28 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.

29 Barotrauma-Complications Pneumothorax Interstitial emphysema Pneumomediastinum- leads to PTX in 42% of patients in one study Pneumopericardium Subcutaneous emphysema Pneumoperitoneum

30 Gas Extravasation

31 Barotrauma

32

33 Oxygen Toxicity : FIO2 > 60 % for > 24h Absorptive atelectasis –O2/ N2 = 21/ 79 >>>>>> 50/ 50 Carbon dioxide Water vapour Oxygen Nitrogen

34 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.

35 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

36

37 Infectious complications of Mechanical ventilation

38 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

39 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

40 Organism Entry for VAP

41 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

42 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

43 VAP prevention :VAP Bundle Elevation of the head of the bed o Use o for neonates and small infants, otherwise o 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

44 HOB o decrease risk of aspiration 45 o head-up tilt is the goal in all patients unless contraindicated No benefit of semi- recumbency ~30 o over standard care ~10 o Supine position is harmful

45 HOB Elevation Leads to Significant reduction in VAP Dravulovic et al. Lancet 1999;354:

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47 Handwashing Strict handwashing before and after handling patient or patient’s equipment or supplies

48 Does the VAP bundle work in real life NHSN 50 th Percentile 4.1

49 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


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