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Complications of Mechanical Ventilation

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.

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Complications of Mechanical Ventilation

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  1. Complications of Mechanical Ventilation

  2. Ventilator-Induced lung injury (VILI)

  3. The Problem of Heterogeneity in ARDS -10 0 10

  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) Over Distension 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) Opening Pressure 0 Inflated Small Airway 10-20 cmH2O Collapse Alveolar Collapse 20-60 cmH2O (Reabsorption)  Consolidation Superimposed Pressure = Lung Units at Risk for Tidal Opening & Closure (from Gattinoni)

  9. 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.

  10. 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

  11. Histopathology of VILI Belperio et al, J Clin Invest Dec 2002; 110(11):1703-1716

  12. Mechanisms of Airspace Injury Airway Trauma “Stretch” “Shear”

  13. ARDS -10 0 10

  14. ARDS after PEEPpreventing atelectotrauma

  15. Atelectetrauma

  16. The PEEP Effect NEJM 2006;354:1839-1841

  17. 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)1301-1308

  18. Zone of ↑ Risk

  19. Biotrauma Cytokines, complement, prostanoids, leukotrienes, O2- Proteases Organ dysfucntion Biophysical biochemical Injury due to MV High volume & Low PEEP

  20. Lung-Protective Ventilation ARDS Network, 2000: Multicenter randomized,861Pts NEJM 2000; 342: 1301-1308

  21. 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

  22. 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 Zoneof Overdistention Injury “Safe” Window Zone of Derecruitment and Atelectasis Volume Injury Pressure

  23. Dependent to Non-dependent Progression of Injury

  24. Effect of 45 cmH2O PIP Control 5 min 20 min

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

  26. 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.

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

  28. Gas Extravasation

  29. Barotrauma

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

  31. 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.

  32. 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

  33. Infectious complications of Mechanical ventilation

  34. 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

  35. 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

  36. Organism Entry for VAP

  37. 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

  38. 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

  39. 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

  40. 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

  41. HOB Elevation Leads to Significant reduction in VAP Dravulovic et al. Lancet 1999;354:1851-1858

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

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

  44. Complications of Mechanical Ventilation

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