1. JJM Medical College ,Davangere Department of Anaesthesiology and Critical Care Seminar on ARDS- Acute Respiratory Distress Syndrome Chair Person: Dr. PRABHU M.D Presented By: Dr. TANMOY ROY 31st July 2009

3. HISTORY

4. EPIDEMIOLOGY

5. CAUSES

6. PATHOGENESIS AND PATHOLOGY

7. CLINICAL FEATURES

8. INVESTIGATIONS

9. MANAGEMENT

11. Known by many other names:Shock lung, Non-Cardiogenic pulmonary oedema, Adult respiratory distress syndrome, Acute lung injury etc.

12. It is actually defined as a disease complex presenting as:

13. severe arterial hypoxemia being resistant to treatment with supplemental O2 therapy

14. acute lung injury characterized by diffuse alveolar damage

16. EPIDEMIOLOGY Incidence of acute lung injury (ALI): 17.9-78.9 cases per 100,000 person-years Incidence of acute respiratory distress syndrome (ARDS): 13.5-58.7 cases per 100,000 person-years Approx 9% of ICU beds in US N Engl J Med. 2005;353:1685-93. Am J Respir Crit Care Med. 1999;159:1849-61

18. 3 diseases those are "common".

19. 1 disease that is "uncommon".

20. 8 diseases those are "rare".

22. Emphysema

24. Guillaine-Barre syndrome

25. Hantavirus

26. Muscular dystrophy

27. Myasthenia gravis

28. Pancreatitis

29. Pancreatitis, acute

32. ARDS can develop in neutropaenic patients also.

33. Variety of inflammatory mediators are produced also by alveolar macrophages.

36. Lasting for 1-6 days .

37. Alveolar oedema with a high protein content and large number of inflammatory cells indicating increased capillary permeability.

38. Collection of fluid, which is rich in protein along with cellular debris of destroyed alveolar cells, exudated RBCs and granular cells, lead to the formation of a coating over the denuded alveolar basement membrane called as the hyaline membrane.

40. Lasting for 6-10 days.

41. Characterized by infiltration of the interstitium by fibroblasts and collagen.

42. There is proliferation of the type 2 epithelial cells.

43. PEEP may not be effective in this stage.

45. From 10-14 days onwards.

46. There is large destruction resulting in emphysema and the dead space further increases.

47. Functionally the oxygenation improves, but there is pulmonary vascular obliteration due to fibrosis.

48. In survivors beyond 3-4 weeks, the lungs are completely remodeled by sparsely cellular collagenous tissue.

51. Stage1- Hyperventilation is the only clinical abnormality, No cyanosis. Chest X-ray is normal.

52. Stage2- Hyperventilation persists. Cyanosis ensures.

53. Stage3- Increasing respiratory distress with hyperventilation and cyanosis +chest x-ray showing diffuse consolidation.

54. Stage4- Hypercarbia, Metabolic acidosis and multiple organ failure manifest in this stage.

55. The multiple organ failure may be:

56. CVS- 10-23% cases, may be due to sepsis and depression of myocardium by TNF.

57. Renal- 40-55% cases, may be due to hypotension, nephrotoxic drugs and sepsis.

58. Liver- Fulminant hepatitis in 10% cases, while reversible enzyme changes in 95% cases.

59. Blood- DIC in 26% cases.

61. The PV curve consists of 2 sigmoid curves with the lower one representing inspiration and the upper one representing expiration.

62. Composed of 3 segments, the initial segment is flat representing low lung compliance due to collapse of peripheral airways and lung units. The next segment has a steeper slope representing improved lung compliance.

63. The lower inflection point marks the transition point between these first 2 segments. The steepness of the slope then decreases as compliance decreases with increasing lung volumes and pressures.

66. Similarity between ARDS and other causes of respiratory failure

69. The chest x-ray typically shows bilaterally fluffy involvementthat initially led clinicians to think that the pathology was homogenous.

70. But now with the advent of pulmonary imaging techniques, there has been convincing evidence that the involvement is segmental.

73. Contrary to the previous belief, the compliance of the lung in a patient with ARDS is normal for 1/3rd of the lung parenchyma and “stiff” for the rest. The healthy portion is frequently referred to as “baby lung”and is subject to injury because of injudicious assignment of tidal volume.

74. By selecting tidal volume on the basis of body weight (≥10 ml/kg), clinicians have overlooked the important fact that only a small fraction of the total lung in patients with ARDS participates in gas exchange. Therefore, a disproportionate share of tidal volume will travel to the better compliant baby lung, subjecting it to over distention and injury.

76. It is most reliable method for confirming or excluding the diagnosis of ARDS.

78. In normal subjects, the neutrophils make up less than 5% of the cells recovered in the lavage fluid, whereas in cases of ARDS, as many as 80% of the recovered cells are neutrophils.

79. A low neutrophil count in lavage fluid can be used to exclude diagnosis of ARDS, while a high neutrophil count can be considered as evidence of ARDS.

80. Total protein-

81. Because inflammatory exudates are rich in proteinaceous material, lung lavage fluid that is similarly rich in protein can be used as an evidence of lung inflammation.

82. When the protein concentration in lung lavage fluid is expressed as a fraction of the total protein concentration, the following criteria can be applied:

85. Nutritional support-

86. Fluid management-

87. Mainly aimed at reducing extra vascular lung water.

88. Urine output of 0.5-1 ml/kg/hr is consistent with an adequate cardiac output and intravascular fluid volume.

89. Normally a daily weight loss 0.2-0.4 kg is anticipated in adult patients receiving conventional intravenous fluid therapy.

91. Risk of hemodynamic compromise.

94. Adequate systemic hydration

95. Humidification of inspired gases

96. Chest physiotherapy

97. Tracheal suctioning

98. Bronchodilators-

99. This is to decrease airway resistance and airway reactivity.

100. Aerolised β-agonists are particularly helpful.

101. Sedation and Analgesia-

102. Sedation by Lorazepam 0.5-2 mg

103. Analgesia by Morphine 0.08-0.1 mg/kg.

104. Neuromuscular Blockers- In very high PEEP or inverse ratio ventilation, neuromuscular blockers may be required.

106. No effect on ARDS when given within 24hrs of onset.

107. During the fibro proliferative phase that begins 7-14 days after the onset of illness, there is definite survival benefit.

108. Methylprednisolone in the dose of 2-3 mg/kg/day can be used.

109. The strategy is low dose steroid; started early, and continued for a longer duration.

112. VILI, also known as ventilator induced lung injury, which is a complication of excessive inflation volumes leading to stress fractures in the alveolar capillary interface. These further progresses to infiltration of the distal airspaces with inflammatory cells and proteinaceous materials. This condition strikingly resembles the picture in ARDS.

113. Biotrauma- Bronchoalveolar lavage studies have shown that volutrauma is accompanied by the release of inflammatory cytokines from neutrophils that infiltrate the lungs. This effect is not explained by the mechanical forces and is called as biotaruma. These cytokines released into the circulation can enter distal organs to produce widespread inflammatory injury and multi organ failure.Now the concept has again reverted back to the favor of pressure support ventilation with a lower TV to maintain adequate oxygenation. This lowered TV, especially in the presence of increased dead space of ARDS, can lead to hypercapnia. But the current concept of permissive hypercapnia overrules this objection.

115. It is one of the consequences of low volume ventilation and is basically a decrease in CO2 elimination via lungs leading to hypercapnia and respiratory acidosis.

116. One of the most troublesome side effects of hypercapnia is brainstem respiratory stimulation with consequent hyperventilation, which often requires neuromuscular blockade to prevent ventilator asynchrony.

118. To mitigate the complications associated with the conventional high TV.

119. Aka “Open Lung Approach”or better known as “Lung Protective Ventilation”

120. The basic principles are:

121. Maintenance of lower inspiratory drive pressure

122. Acceptance of permissive hypercapnia over higher airway pressure

123. Providing liberal sedation to improve patient ventilator synchronization

124. Open collapsed lung units with recruitment maneuvers

125. Prevention of alveolar over distention by:

126. Plateau Airway Pressure ( Pplat) <30-35 cm H2O

127. TV<8ml/kg

128. Pressure Controlled Ventilation

130. Low volume ventilation was associated with collapse of the terminal airways at the end of expiration and reopening of airways during lung inflation. This repetitive cycle itself can be a source of lung injury.

131. PEEP was introduced to mitigate this problem by acting as a stent to keep small airways open at the end of expiration. Addition of low level PEEP (5-7 cm H2O) has become a standard practice during low volume ventilation.

132. PEEP acts as an aid to arterial oxygenation in ARDS.

133. Addition of PEEP often allows a reduction in FiO2to safer levels.

135. “CURRENT TREND OF VENTILATORY SETTINGS USED IN ards”

136. LUNG RECRUITMENT STRATEGIES: Patient to be put in prone position. Pillows are to be put beneath him; one beneath the upper chest and other beneath the pelvic area so that the abdomen hangs between them. Monitors are to be attached (pulse oximeter, EtCO2 monitor etc.) and a baseline ABG is to be taken. PEEP of 20 cm of H2O is to be kept for 90 sec. ABG is again repeated; if PaO2 is <300 mm Hg, PEEP to be increased to 30 cm H2O. To prevent derecruitment, maintain PEEP of 15 cm H2O with a tidal volume of 6 ml/kg.

139. Normal I: E ratio is 1:2.

140. When the TV of air gets into the respiratory tract with 1/3rd of the respiratory cycle, the peak airway pressure reaches high level. If the same TV is breathed over a more prolonged period, airway pressure rises gradually and the peak airway pressure reached is much less.

141. The incidence of barotrauma is much less.

142. During this prolonged inspiration, air gets into the atelectic alveoli and distends it and in the short expiration period, not whole of the air may be vented out; thus leaving a residual amount of air which acts as an auto PEEP and increases the FRC.

143. Responsible for improved oxygenation but at the same time has tendency to cause hypotension.

144. I: E ratios selected may vary from 1:1 to 1.2:1.

146. The lungs are partially filled with plerfluorocarbon (PFC) and ventilation is provided with a standard mechanical ventilator.

147. PFC is a clear inert liquid that improves gas exchange by:

148. recruiting dependent lung regions

149. clearing retained secretions

150. its anti-inflammatory properties

151. Least surface tension and high affinity for O2 and CO2. So it also causes a mass gas transfer.

153. NO cause vasodilatation of pulmonary vasculature, mostly the vessels perfusing the normal alveoli. The diseased alveoli are atelectic and do not get NO and so their corresponding vessels do not react to NO.

154. Thus blood supply is diverted to normally perfused alveoli thus reducing the shunt percentage. So oxygenation is increased without any increase in airway pressure.

155. The right ventricular performance is improved as the pulmonary artery pressure is decreased.

156. Disadvantage-

157. Combines with Hb and is immediately inactivated.

158. Formation of NO2 and methaemoglobin.

159. Formation of NO2 depends upon the % of O2 and the % of NO.

160. If kept within 5 ppm-40 ppm, the amount of NO2 produced is negligible.

161. Epithelial damage, pulmonary exudates, hemorrhage and death.

163. It is seen in CT scans that lower lobes are most affected and even within the same lobe, the disease is not homogeneous.

164. Ventilation in different postures may be beneficial.

165. Prone position ventilation may be advantageous (mean 17hrs/day).

167. The oxygenation and CO2 removal are taken care of by the membrane oxygenator.

168. This gives rest to the lung which is allowed to have time for recovery.

169. Intra Venous Oxygenation (IVOX):

170. Extra Pulmonary Intracorporeal membrane oxygenation.

171. Introduced into the central veins and does the oxygenation and CO2 removal.

172. Gives rest to the lungs for recovery.

174. Aim of this technique is to deliver the inspired volume of gas, bypassing the dead space, direct to the alveoli and/or to wash out the expired gases by a passive flow of fresh gas.

175. Three types of TGI-

176. Inspiratory bypass

177. expiratory washout

178. continuous catheter flow

179. Permissive Hypercapnia:

180. All efforts to decrease the PaCO2 are associated with problems of barotrauma or volutrauma or are associated with overshooting to hypocarbia.

181. Better to accept the Hypercarbia and to some extent respiratory acidosis.

182. Respiratory acidosis can be reduced by IV Carbicarb, which is an equimolar mixture of Na2CO3 and NaHCO3.

184. Ventilation at high rates (100-300breaths/min) with tidal volume less than dead space is found to maintain oxygenation without increasing the transtracheal pressure, thus avoiding barotrauma.

185. Types include:

186. High frequency PPV

187. High frequency jet ventilation

188. High frequency oscillation.

190. Oxygen exchange and arterial oxygenation-

191. Adequacy of oxygen exchange across alveolar capillary membranes is reflected by the PaO2.

192. This efficacy is paralleled by the differences between the calculated PaO2 and measured PaO2.

193. Calculation of A-a DO2 is useful for evaluating the gas exchange function of the lungs.

194. CO2 elimination-

195. The adequacy of alveolar ventilation relative to the metabolic production of carbon dioxide is reflected by the PaCO2.

196. The efficacy of carbon dioxide transfer across the alveolar capillary membrane is reflected by the VD/VT.

197. This ratio depicts areas in the lung that receive adequate ventilation but inadequate or no pulmonary blood flow.

199. Mixed PvO2 and the arterial to venous differences for oxygen (CaO2-CvO2) reflect the overall adequacy of the oxygen transport system relative to the extraction of oxygen by the tissues.

200. PvO2 less than 30 mmHg or a CaO2-CvO2 value more than 6ml/dl indicates need to increase cardiac output to facilitate tissue oxygenation.

201. Arterial pH-

202. Necessary to detect acidaemia or alkalaemia.

203. Intrapulmonary Shunting-

204. Right to left intrapulmonary shuntingof blood occurs when there is perfusion of alveoli that are not ventilated.

206. Assessment of weaning readiness-

207. Resolution of the cause of respiratory failure.

208. Central ventilatory drive must be adequate.

209. The patient must be able to maintain a patent airway, if extubation or decannulation is contemplated.

210. The patient must be able to cough and adequately clear secretions.

211. Airway resistance must be adequately low; airway edema or obstruction can preclude extubation.

212. The work of breathing must be adequately low; decreased lung compliance, increased airway resistance, and hyperinflation impose an increased load upon respiratory muscles.

213. Stable cardiovascular status.

215. Failure to adequately clear tracheobronchial secretions by coughing, and dynamic hyperinflation in patients with COPD or asthma are common causes.

216. Acute congestive heart failure and myocardial ischemia are common and significant causes of weaning difficulty, but can be difficult to detect.

217. Muscle weakness due to acute myopathy or polyneuropathy.

218. Occult muscle weakness can be due to inadequate rest following exhausting breathing trials.

219. Malnutrition and severe electrolyte imbalance also can contribute to weakness.

220. Auto-PEEP and hyperinflation.

221. Insufficiently treated pulmonary disease.

223. A parameter derived from measured respiratory rate and tidal volume, therapid shallow breathing index (RSBI), has been shown to be predictive of weaning success.

224. To calculate this parameter, the patient’s respiratory rate and minute ventilation are measured for one minute during spontaneous breathing. The measured respiratory rate is then divided by the tidal volume (expressed in liters).

225. A RSBI < 105 is reasonably predictive of weaning success.

226. Intubated with smaller diameter (<7 mm inner diameter) endotracheal tubes tend to have a higher RBSI.

227. If the patient meets criteria for weaning readiness and has a RSBI < 105, a spontaneous breathing trial can be performed.

229. Weaning can be accomplished by gradually reducing the set rate of the ventilator during SIMV (SIMV weaning); gradually reducing the level of pressure with PSV (pressure support weaning); or by providing for periodic trials of spontaneous breathing (T-piece weaning).

230. The disadvantage of SIMV may be that little adaptation by the patient’s effort to volume-cycled machine assistance appears to occur on a breath-by-breath basis during IMV.

231. Noninvasive mechanical ventilation can be an important adjunct to facilitate weaning in selected patients.

232. Noninvasive PSV weaning led to reduced weaning time, fewer ICU days, a decreased nosocomial pneumonia rate, and improved 60-day survival.

233. Long-term ventilatory requirements-

234. Some patients require a prolonged time (weeks or months) to wean.

235. A comprehensive focus on generalized rehabilitation, strength and endurance training, and adequate attention to nutrition may be successful.

238. PROGNOSIS The mortality rate in ARDS; though reduced now, still remains between 40-50% in well developed countries. Majority of the deaths occur in the first few days, either due to the original disease or due to the respiratory failure. This improvement in mortality is due to the better supportive care, that is being given and not due to any drugs. Those persons, who recover after prolonged ventilatory therapy, get back their normal lung functions within six months after the treatment.

240. CLINICAL ANAESTHESIA (PAUL G. BARASH) 4TH EDN.

241. A PRACTICE OF ANAESTHESIA (WYLIE AND DAVIDSON) 7TH EDN.

242. THE ICU BOOK (PAUL L. MARINO) 3RD EDITION.

243. CLINICAL APPLICATION OF MECHANICAL VENTILATION (DAVID W. CHANG) 3RD EDN.

244. INTERNATIONAL ANAESTHESIOLOGY CLINICS (VOL:47; NUMBER 1) WINTER 2009.

245. INTERNET.Thank You