1 / 55

ARDS - Management

ARDS - Management. By H P Shum Sept 2005. ARDS - Definition. Bilateral acute lung infiltration Hypoxemia No clinical evidence of elevated left atrial pressure or PAWP <=18mmHg Differentiated from Acute lung injury by PaO2/FiO2 <300mmHg. ARDS - pathophysiology.

joaquin
Download Presentation

ARDS - Management

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. ARDS - Management By H P Shum Sept 2005

  2. ARDS - Definition • Bilateral acute lung infiltration • Hypoxemia • No clinical evidence of elevated left atrial pressure or PAWP <=18mmHg • Differentiated from Acute lung injury by PaO2/FiO2 <300mmHg

  3. ARDS - pathophysiology • Formation of protein-rich alveolar edema after damage to the integrity of the lung’s alveolar-capillary barrier • Can be initiated by physical or chemical injury or by extensive activation of innate inflammatory responses

  4. ARDS - Causes • Sepsis or SIRS • Severe traumatic injury • Massive transfusion • Near drowning • Smoke inhalation • Drug overdose (commonly TCA)

  5. ARDS – physiological derangement • Ventilation-perfusion mismatch • Intrapulmonary shunt • Surfactant inactivation leading to atelectasis • Decreases lung compliance (stiff lung)

  6. ARDS - imaging

  7. ARDS – ventilator setting • Tidal volume • PEEP • Use of specific ventilation modalities

  8. ARDS – ventilator setting • Low tidal volume • Mortality benefit mainly based on two studies

  9. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome • Amato MB et al. N Engl J Med. 1998 Feb 5;338(6):347-54 • N=53 • Conventionalventilation • Lowest possible PEEP • TV 12ml/kg • Aim normal PaCO2 • Protective ventilation • PEEP above the lowerinflection point on the static pressure–volume curve • TV <6ml/kg • driving pressures< 20 cm of water above the PEEP value • permissivehypercapnia   

  10. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network N Engl J Med 2000 May 4;342(18):1301-8 • N=861 • Traditional gp • TV 12ml/kg • plateau pressure <=50mmH2O • Low TV gp • TV 6ml/kg • plateau pressure <=30mmH2O   

  11. But …. Not all studies using low TV ventilation give rise to good outcome compare with conventional ventilation methods

  12. Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. Pressure- and Volume-Limited Ventilation Strategy Group Stewart TE et al. N Engl J Med 1998 Feb 5;338(6):355-61 • N =120 • Limited ventilation gp • TV 8ml/min • Plateau pressure <30mmH2O • Conventional gp • TV 10-15ml/kg • Plateau pressure <50mmH2O

  13. Recommendation • Important to avoid over-distension of alveoli in the relatively normal parts of lung • start at 6-7 ml/kg predicted BW (to maintain plateau pressure <30 cm H2O) • allow PCO2 to rise slowly (i.e. giving kidneys time to compensate for respiratory acidosis), aim to keep pH > 7.25 (instead of aiming for a target PCO2, but advisable not to allow Pco2 to rise above 20 kPa) • Allow upper limit of RR to 35 bpm • Use sedation if needed

  14. Positive end-expiratory pressure (PEEP) • Insufficient PEEP may result in: • alveolar derecruitment • cyclical atelectasis • progressive lung injury • refractory hypoxemia

  15. Excessive PEEP, particularly in combination with hypovolemia, can decrease cardiac output and oxygen delivery, and increase the risk of barotrauma Am J Respir Crit Care Med 2002 Apr 1;165(7):978-82

  16. Continuous diaphragm sign

  17. What PEEP level is good for ARDS? High vs low …. • Amato study using low TV 6ml/kg with high PEEP (average >16mmH2O) showed improved mortality • However …

  18. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome Brower RG et al. N Engl J Med 2004 Jul 22;351(4):327-36 • N=549 • low PEEP gp • 8.3mmH2O • High PEEP gp • 13mmH2O   

  19. PEEP setting • Optimal PEEP will change from patient to patient, based in different pathophysiology and depending upon the stage and severity of the disease • no optimal way to assess "best PEEP" • PEEP is added in increments of 2-5 cm until the "best/optimal PEEP" is obtained, choose the level which provides the highest static compliance and the lowest airway plateau pressure • PEEP above lower inflection point on static P-V curve • PEEP > 20 cmH2O is rarely beneficial and usually results in additional pressure-induced lung injury • Level of PEEP used in ARDS still controversial

  20. Recruitment maneuvers • utilizing a CPAP of 35 to 40 cmH20 for 40 seconds • can improve oxygenation and alveolar recruitment, but are relatively less effective than a continuous high PEEP level Intensive Care Med 2000 May;26(5):501-7 Am J Respir Crit Care Med 2002 Jan 15;165(2):165-70

  21. Ventilator modes • fully supported modes of ventilation are favored over partially-supported modes

  22. Inverse ratio ventilation (IRV) • I:E ratio > 1 may be able to improve oxygenation in patients who remain hypoxic despite PEEP • But … • A lot of negative studies a/v showed that IRV do not had survival benefit Anesthesiology. 2001 Nov;95(5):1182-8 Anesthesiology. 1998 Jan;88(1):35-42 Am J Respir Crit Care Med 1997 May;155(5):1637-42 • increases the risk of air trapping, barotrauma, hemodynamic instability • require significant sedation and possibly neuromuscular blockade which may increase ICU stay and risk of critical illness neuromyopathy

  23. Prone ventilation • routine use of prone positioning in all patients with ALI / ARDS cannot be currently recommended due to a lack of clinical data support • Indications: • as an adjunctive therapy to improve oxygenation in established ALI and ARDS • considered in patients who require PEEP >12 cmH2O and a FiO2 >0.60 • should better used early within 36 hours of the onset of ARDS • optimum duration unknown

  24. Effect of prone positioning on the survival of patients with acute respiratory failure Gattinoni Let al. N Engl J Med 2001 Aug 23;345(8):568-73 • N =304 • Multicenter RCT • tx gp • prone >=6h/d 10d • control gp • supine  

  25. Effects of systematic prone positioning in hypoxemic acute respiratory failure: a randomized controlled trial Guerin Cet al. JAMA 2004 Nov 17;292(19):2379-87 • N=791 • propective, unblinded, multicenter RCT • prone gp • > = 8hr /d • control gp • supine  

  26. Airway pressure release ventilation (APRV) • lung volume and hence oxygenation is maintained by continuous positive airway pressure • CO2 clearance is achieved by the transient release of circuit pressure allowing gas to escape and lung volume to fall • CPAP is then re-established to the previous level, allowing the entry of fresh gas into the system

  27. Also resulted in significant improvement in the cardiac index, systemic haemodynamic, O2 delivery, and vasopressor requirement and renal perfusion Crit Care 2001 Aug;5(4):221-6 Intensive Care Med 2002 Oct;28(10):1426-33

  28. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury Putensen C et al. Am J Respir Crit Care Med 2001 Jul 1;164(1):43-9 • determine whether use of APRV with spontaneous breathing better prevents deterioration of cardiopulmonary function • N = 30, MV trauma pt at risk of ARDS • PCV vs APRV for 72 hr, cross over study

  29.   

  30. High frequency ventilation • proposed as an alternate form of lung protective ventilation that could theoretically prevent overdistension and cyclical atelectasis • lung inflated and kept open with very low tidal volumes and low airway pressure, aimed to produce minimal shear injury

  31. However … Risks of barotrauma and hemodynamic compromise with high frequency ventilation can approximate those of conventional ventilation Chest 1993 May;103(5):1413-20

  32. High-frequency ventilation versus conventional ventilation for treatment of acute lung injury and acute respiratory distress syndrome Wunsch H et al. Cochrane Database Syst Rev 2004;(1):CD004085 • only include RCT =2 • one recruit children, n =58 • other recruit adult, n =148 insufficient evidence to support the broad application of HFV to all patient with ALI / ARDS

  33. Inhaled vasodilator • Nitric oxide vs prostacyclin • Act locally and short half life • Minimal systemic effect • Rarely cause hypotension

  34. Effects of inhaled nitric oxide in patients with acute respiratory distress syndrome: results of a randomized phase II trial. Inhaled Nitric Oxide in ARDS Study Group Dellinger RP et al. Crit Care Med 1998 Jan;26(1):15-23 • Prospective, multicenter, randomized, double-blind, placebo-controlled study • N = 177 • placebo vs NO at 1.25, 5, 20, 40, or 80 ppm • responsive if PaO2 >=20% PaO2 improved on first 4 hrs of tx Percentage of pt who alive and off MV at D28  

  35. Low-dose inhaled nitric oxide in patients with acute lung injury: a randomized controlled trial Taylor RW et al. JAMA 2004 Apr 7;291(13):1603-9 • Multicenter, randomized, placebo-controlled study, triple blinded • n = 385 • placebo vs NO 5ppm to 28d

  36. nitric oxide • produce toxic radicals • NO2 and methemoglobin concentrations may increase • immunosuppressant properties that theoretically could increase the risk of nosocomial infection • cause DNA strand breakage and base alterations that are potentially mutagenic

  37. Prostacyclin (PG I2) improve PaO2 and decrease PAP • No study shown improvement of mortality associated with prostacyclin use in ARDS inhaled vasodilators, if used at all, should be reserved for patients with intractable, life-threatening hypoxemia despite conventional management

  38. Function of endogenous surfactant • modulate alveolar surface tension • prevent atelectasis • facilitates mucous clearance • scavenges oxygen radicals • suppresses inflammation • Surfactant dysfx occur in ARDS and in theory exogenous surfactant can offer helps

  39. Treatment of acute respiratory distress syndrome with recombinant surfactant protein C surfactant Spragg RG et al. Am J Respir Crit Care Med 2003 Jun 1;167(11):1562-6 • N=40 • high dose (1ml 4x in 24 hr) • low dose (0.5ml 4x in 24 hr) • control

  40. Effect of recombinant surfactant protein C-based surfactant on the acute respiratory distress syndrome Spragg RG et al. N Engl J Med 2004 Aug 26;351(9):884-92 • multicenter, randomized, double-blind trials • N = 448 • 1ml 4x in 24hr for tx gp Improvement of PaO2/FiO2 but no survival benefit was detected

  41. Partial liquid ventilation • involves filling the lungs with a fluid (perfluorocarbon, also called Liquivent or Perflubron) which has • very low surface tension, similar to surfactant • high density, oxygen readily diffuses through it • may have some anti-inflammatory properties • The lungs are filled with the liquid, the patient is then ventilated with a conventional ventilator using a protective lung ventilation strategy. • Liquid will help the transport of oxygen to parts of the lung that are flooded and filled with debris, help remove this debris and open up more alveoli improving lung function. 

  42. All of them are case report, some indicate beneficial outcome in true of improved survival and oxygenation but negative reports present as well Larger studies are needed to determine what role, if any, PLV will play in the treatment of ARDS

More Related