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Definitions

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  1. Definitions • The 1994 North American-European Consensus Conference (NAECC) criteria: • Onset - Acute and persistent • Radiographic criteria - Bilateral pulmonary infiltrates consistent with the presence of oedema • Oxygenation criteria - Impaired oxygenation regardless of the PEEP concentration, with a Pao2/Fio2 ratio  300 mmHg (40 kPa) for ALI and  200 mmHg (27 kPa) for ARDS • Exclusion criteria - Clinical evidence of left atrial hypertension or a pulmonary-artery catheter occlusion pressure of  18 mm Hg. Bernard GR et al., Am J Respir Crit Care Med 1994

  2. Mortality from ARDS • ARDS mortality rates - 31% to 74% • The variability in the rates quoted is related to differences in the populations studied and in the precise definitions used. • The main causes of death are nonrespiratory causes (i.e., die with, rather than of, ARDS). • Respiratory failure has been reported as the cause of death in 9% to 16% of patients with ARDS. • Early deaths (within 72 hours) are caused by the underlying illness or injury, whereas late deaths are caused by sepsis or multiorgan dysfunction. • There is a controversy about the role of hypoxemia as a prognostic factor in adults. Nevertheless, in some studies, both Pao2/Fio2 ratio and Fio2 were variables independently associated to mortality. Frutos-Vivar F, et al. Curr Opin Crit Care. 2004. Vincent JL, et al. Crit Care Med. 2003. Ware LB. Crit Care Med. 2005.

  3. Clinical Disorders Associated with the Development of ALI/ARDS • Direct insult • Common • Aspiration pneumonia • Pneumonia • Less common • Inhalation injury • Pulmonary contusions • Fat emboli • Near drowning • Reperfusion injury • Indirect insult • Common • Sepsis • Severe trauma • Shock • Less common • Acute pancreatitis • Cardiopulmonary bypass • Transfusion-related TRALI • Disseminated intravascular • coagulation • Burns • Head injury • Drug overdose Atabai K, Matthay MA. Thorax. 2000. Frutos-Vivar F, et al. Curr Opin Crit Care. 2004.

  4. Epidemiology • NIH, 1972 - Incidence of ARDS in the United States: 75 cases per 105 person.years population (approximately 150,000 cases per year) • International multi-center ALI/ARDS cohort studies, 1989 - 2002 • Incidence estimates of ALI/ARDS = 1.3 to 22 cases per 105 person.years • ARDS Network Study (NAECC definitions), 2003 - Incidence of ALI/ARDS in the United States: 32 cases per 105 person.years (range 16 - 64) • ARDS Network Study (NAECC definitions), 2003 - The average number of cases of ALI per ICU bed per year (2.2) varied significantly from site to site (range 0.7 - 5.8)

  5. The ARDS Lungs Vt • External forces applied on the lower lobes at end inspiration and end expiration in a patient in the supine position and mechanically ventilated with positive end-expiratory pressure. • Large blue arrows: Forces resulting from • tidal ventilation • Small blue arrows: Forces resulting from • positive end-expiratory pressure (PEEP) • Green arrows: forces exerted by the • abdominal content and the heart on the • lung aerated lung Vt consolidated lung PEEP Rouby JJ, et al. Anesthesiology. 2004.

  6. Ventilator induced lung injury Positive pressure ventilation may injure the lung via several different mechanisms Alveolar distension “VOLUTRAUMA” Repeated closing and opening of collapsed alveolar units “ATELECTRAUMA” Oxygen toxicity Lung inflammation “BIOTRAUMA” VILI Multiple organ dysfunction syndrome

  7. Ventilator-induced Lung InjuryConceptual Framework • Lung injury from: • Overdistension/shear - > physical injury • Mechanotransduction - > “biotrauma” • Repetitive opening/closing • Shear at open/collapsed lung interface • Systemic inflammation and death from: • Systemic release of cytokines, endotoxin, bacteria, proteases “volutrauma” “atelectrauma”

  8. Less Extensive Collapse But Greater PPLAT 100 R = 100% R = 93% Total Lung Capacity [%] Some potentially recruitable units open only at high pressure R = 81% More Extensive Collapse But Lower PPLAT 60 R = 59% From Pelosi et al AJRCCM 2001 20 R = 22% 0 0 60 20 40 Pressure [cmH2O] R = 0% How Much Collapse Depends on the Plateau

  9. Denver Health · · · · · TLC Ventral Alveoli · · · · · · · · · · · · · FRC · · · · · Dorsal Alveoli · · · · PV Relationships(ARDS, Supine) VL (% TLC) -20 -15 -10 -5 0 5 10 15 20 25 30 Ptp (cm H2O)

  10. ARDS Network Low VT Trial • Patients with ALI/ARDS (NAECC definitions)of < 36 hours • Ventilator procedures • Volume-assist-control mode • RCT of 6 vs. 12 ml/kg of predicted body weight PBW Tidal Volume (PBW/Measured body weight = 0.83) • Plateau pressure  30 vs.  50 cmH2O • Ventilator rate setting 6-35 (breaths/min) to achieve a pH goal of 7.3 to 7.45 • I/E ratio:1.1 to 1.3 • Oxygenation goal: PaO2 55 - 80 mmHg/SpO2 88 - 95% • Allowable combination of FiO2 and PEEP: 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 1.0 1.0 1.0 PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 18 20 22 24 • The trial was stopped early after the fourth interim analysis (n = 861 for efficacy; p = 0.005 for the difference in mortality between groups) ARDS Network. N Engl J Med. 2000.

  11. 1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.0 0 20 40 60 80 100 120 140 160 180 ARDS Network: Improved Survival with Low VT Proportion of Patients Lower tidal volumes Survival Discharge Traditional tidal values Survival Discharge Days after Randomization ARDS Network. N Engl J Med. 2000.

  12. ARDS Network: Additional Findings In ALI and ARDS patients, 6 ml/kg PBW tidal volume ventilation strategy was associated with: • PaO2/FiO2 lower in 6 ml/kg low VT group • High RR prevented hypercapnia with minimal auto-PEEP (difference of median intrinsic PEEP between the groups was < 1 cm H2O) • No difference in their supportive care requirements (vasopressors-IV fluids-fluid balance-diuretics-sedation) • ~10% mortality reduction • Less organ failures • Lower blood IL-6 and IL-8 levels ARDS Network. N Engl J Med. 2000. Parsons PE, et al. Crit Care Med. 2005. Hough CL, et al. Crit Care Med. 2005. Cheng IW, et al. Crit Care Med. 2005.

  13. Open lung concept exp insp

  14. 40 Opening pressure 30 Closing pressure 20 From Crotti et al AJRCCM 2001. 10 0 0 5 10 15 20 25 30 35 40 45 50 Paw [cmH2O] Opening and Closing Pressures in ARDS High pressures may be needed to open some lung units, but once open, many units stay open at lower pressure. 50 %

  15. Recruitment Maneuvers (RMs) • Proposed for improving arterial oxygenation and enhancing alveolar recruitment • All consisting of short-lasting increases in intrathoracic pressures • Vital capacity maneuver (inflation of the lungs up to 40 cm H2O, maintained for 15 - 26 seconds) (Rothen HU. BJA. 1999; BJA 1993.) • Intermittent sighs (Pelosi P. Am J Respir Crit Care Med. 2003.) • Extended sighs(Lim CM. Crit Care Med. 2001.) • Intermittent increase of PEEP (Foti G. Intensive Care Med. 2000.) • Continuous positive airway pressure (CPAP) (Lapinsky SE. Intensive Care Med. 1999. Amato MB. N Engl J Med. 1998.) • Increasing the ventilatory pressures to a plateau pressure of 50 cm H2O for 1-2 minutes (Marini JJ. Crit Care Med. 2004. Maggiore SM. Am J Respir Crit Care Med. 2003.) Lapinsky SE and Mehta S, Critical Care 2005

  16. Other manoeuvres • Prone positioning ventilation • Prolonged inspiration • Inverse ratio ventilation

  17. Limit of open lung strategy • To minimise VILI to the less damaged alveoli • need to minimise individual alveolar volume – cannot measure this hence use pressure as surrogate • i.e max insp pressure (plateau pressure 30-32cm H20) • as PEEP increases and max pressure remains unchanged ,TV will decrease • Alveolar ventilation will decrease • alv V: dead space vent ratio will decrease PaCO2 increases - Resp acidosis

  18. Increasing PaCO2 • Management options Increase resp rate Anatomical dead space 150ml

  19. Increasing PaCO2 • Permissive hypercapnia • Tracheal gas insufflation – attempting to reduce dead space Accompanying as alveolar ventilation decreases will require increasing FIO2 and eventually will result in alveloar hypoxia and arterial hypoxaemia

  20. High frequency ventilation • High frequency Jet ventilation • Delivers very short high pressure jets of air and relies on passive exhalation • High frequency flow interrupter: • eg infant star – relies on high frequency interruption of flow , passive exhalation – normal circuit • High frequency oscillatory ventilation • pressurised circuit , uses a diaphragm piston unit to actively move gas in and out of the lungs – requires special non-compliant circuit , active expiration

  21. High-frequency Oscillatory Ventilation 3100B HFOV

  22. High-frequency Oscillatory Ventilation Characterized by rapid oscillations of a reciprocating diaphragm, leading to high-respiratory cycle frequencies, usually between 3 and 9 Hz in adults(180 -600breaths per min), and very low VT (0.1-3ml/kg). Ventilation in HFOV is primarily achieved by oscillations of the air around the set mean airway pressure mPaw (35cm -45cm H2O).

  23. High-frequency Oscillatory Ventilation • Active expiration Pressurised circuit

  24. High-frequency Oscillatory Ventilation 0.1-3ml/kg 3-9 hz 35cm H20 90 cm

  25. Pressure attenuation during HFOV

  26. Pressure attenuation during HFOV Distal airways Increase the frequency: What happens to TV: decreases What happens to VILI: Decreases and hence wish to maximise this What happens to PaCO2: Increases – alveolar MV decreases

  27. Further questions If PaCO2 is rising and pH is < 7.25: What adjustments may be required? • Increase alveolar ventilation – how? • Increase amplitude • Decrease frequency • Remove ETT suction elbow 2. Decrease dead space • Introduce cuff leak • Tracheal gas insufflation

  28. Further Questions: What effect does this ventilation have on RV function: Increase after load Decrease preload In which conditions would HFOV be contraindicated: • Severe obstructive airways disease • Intractable shock - must not be hypovolaemic (CVP at least 8mmHg) • Intracranial hypertension

  29. Recruitment Manoeuvre prior to connection to HFOV • May cause barotrauma , volutrauma and haemodynamic compromise • Hence these manoeuvres should not be attempted without a senior member of the intensive care medical team being present • recommended manoeuvre: • Perform endotracheal toilet bfore manoeuvre • Patient requires to be heavily sedated +/- paralysed • should not be hypovolaemic or intractable shock • Ventilator mode PCV • High pressure alarm increased • PEEP gradually increased to 25 cm H2O whilst observing haemodynamics • Measure lung compliance and gradually reduce peep to level just above point that results in a loss in lung compliance

  30. Final Questions Diagnosis of pneumothorax: • high index of suscpician • Desaturation • haemodynamic change • Chest sounds difficult • mPaw and ∆P may not change • Decrease chest wiggle on side of pneumothorax Abrupt rise in paCo2 and increase in ∆P - . Airway obstruction Change in resistance

  31. High-frequency Oscillatory Ventilation • Characterized by rapid oscillations of a reciprocating diaphragm, leading to high-respiratory cycle frequencies, usually between 3 and 9 Hz in adults, and very low VT. Ventilation in HFOV is primarily achieved by oscillations of the air around the set mean airway pressure mPaw. • HFOV is conceptually very attractive, as it achieves many of the goal of lung-protective ventilation. • Constant mPaws: Maintains an “open lung” and optimizes lung recruitment • Lower VT than those achieved with controlled ventilation (CV), thus theoretically avoiding alveolar distension. • Expiration is active during HFOV: Prevents gas trapping • Higher mPaws (compared to CV): Leads to higher end-expiratory lung volumes and recruitment, then theoretically to improvements in oxygenation and, in turn, a reduction of FiO2. Chan KPW and Stewart TE, Crit Care Med 2005