7/4/2015. diffuse lung injury resulting in noncardiogenic pulmonary edema due to increase in capillary permeability

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1 Leanna R. Miller, RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, CMSRN, NP Education Specialist LRM Consulting Nashville, TN Objectives Identify the 5 criteria for the diagnosis of ARDS. Discuss the common etiologies that lead to ARDS. Describe the priorities in the management of patients with ARDS. diffuse lung injury resulting in noncardiogenic pulmonary edema due to increase in capillary permeability 1

2 refractory hypoxemia diminished compliance diffuse infiltrates on chest x-ray normal PAOP PaO 2 / FiO 2 ratio < 200 2

3 Etiology shock trauma infections inhaled toxins 3

4 Etiology aspiration near-drowning massive blood transfusions fat or amniotic fluid emboli pancreatitis Phase I & II subclinical respiratory distress ABGs (respiratory alkalosis) hyperventilating Phase III established respiratory distress pulmonary shunt > 10% above baseline chest x-ray shows infiltrates crackles in lung bases 4

5 Phase IV severe respiratory failure rising pco 2 rising physiologic shunt white-out on chest x-ray Diagnosis history signs/symptoms labs (ABGs) x-ray hemodynamics Treatment establish patent airway restore arterial O 2 level 5

6 Mechanical Ventilation conventional with PEEP PC / IRV HFJV APRV Goals of mechanical ventilation in ARDS are to: maintain oxygenation avoiding oxygen toxicity and the complications of mechanical ventilation maintain oxygen saturation in the range of 85-90% aim of reducing the fraction of inspired oxygen (FIO 2 ) to less than 60% within the first hours usually requires the use of moderate-to-high levels of PEEP 6

7 experimental studies have shown that mechanical ventilation may promote a type of acute lung injury (ALI) termed ventilatorassociated lung injury protective ventilation strategies using low tidal volumes and limited plateau pressures improves survival when compared with conventional tidal volumes and pressures ARDS Network study patients with ALI and ARDS were randomized to mechanical ventilation tidal volume of 12 ml/kg of predicted body weight and an inspiratory pressure of 50 cm water or less tidal volume of 6 ml/kg and an inspiratory pressure of 30 cm water or less the study was stopped early after interim analysis of 861 patients demonstrated that subjects in the low-tidal-volume group had a significantly lower mortality rate (31% versus 39.8%) 7

8 mechanical ventilation with a tidal volume of 6 ml/kg predicted body weight is recommended, with adjustment of the tidal volume to as low as 4 ml/kg if needed to limit the inspiratory plateau pressure to 30 cm water or less increase the ventilator rate and administer bicarbonate as needed to maintain the ph at a near normal level (7.3) High-frequency ventilation uses low tidal volumes and high respiratory rates. diminishes alveolar distention compared to conventional ventilation in adults demonstrates early improvement in oxygenation but no improvement in survival. 8

9 Fluid Management maintain adequate perfusion isotonic solutions fluid restriction consider diuretics* *Seeley (2013) Updates in the management of acute lung injury: A focus on the overlap between AKI and ARDS. Advances in Chronic Kidney Disease, 20(1): primary ARDS due to aspiration, pneumonia, or inhalational injury treated with fluid restriction secondary ARDS due to remote infection or inflammation requires initial fluid and potential vasoactive drug therapy essential in directing initial treatments to stabilize the patient Improve systemic O 2 Delivery modest volume expansion vasopressors/vasodilators 9

10 Sedation control anxiety & physical activity may require addition of neuromuscular blocker suggestions: propofol versed Positioning good lung in dependent position both lungs are equally injured beneficial positions include: prone right lung down 60-75% of patients with ARDS have significantly improved oxygenation when turned from the supine to the prone position improvement in oxygenation is rapid and often substantial enough to allow reductions in FiO 2 or level of CPAP 10

11 Possible mechanisms for improvement are: recruitment of dependent lung zones increased functional residual capacity (FRC) improved diaphragmatic excursion increased cardiac output improved ventilation-perfusion matching despite improved oxygenation with the prone position, randomized controlled trials of the prone position in ARDS have not demonstrated improved survival Pharmacologic Therapy corticosteroids antimicrobials non - steroidal anti - inflammatory agents anti pyretic Star Trek Meds 11

12 No drug has proved beneficial in the prevention or management of acute respiratory distress syndrome (ARDS). Hemoglobin 12 to 15 gm / dl factors decreasing offloading: hypophosphatemia alkalosis hypothermia Nutritional Support often overlooked in ARDS ingredients required: stress amino acid trace elements omega 3 / omega 6 Oxepa or Impact 12

13 patients who required mechanical ventilation within 48 hours of developing acute lung injury received either trophic or full enteral feeding for the first 6 days Initial lower-volume trophic enteral feeding did not improve ventilator-free days 60-day mortality infectious complications it was associated with less gastrointestinal intolerance Other Therapeutics nitric oxide surfactant ECMO a partial liquid ventilation a Michaels, et al (2013) Adult refractory hypoxemic ARDS treated with ECMO, American Journal of Surgery. 205(5):

14 Extracorporeal Membrane Oxygenation (ECMO) Description type of cardiopulmonary bypass CO 2 removal; O 2 replacement ventilated (lower V T, FiO 2, & PEEP) Extracorporeal Membrane Oxygenation (ECMO) Complications technical difficulties cannula malposition hemorrhage sepsis ECMO appeared to improve survival in patients with H1N1-associated ARDS who could not be oxygenated with conventional mechanical ventilation 14

15 randomized controlled trial that compared partial liquid with conventional mechanical ventilation partial liquid ventilation resulted in increased morbidity pneumothoraces hypotension hypoxemic episodes trend toward higher mortality 48 - year old alcoholic with GI bleed & pancreatitis severe epigastric pain, acute abdomen ultrasound confirms enlarged, edematous pancreas hemodynamically unstable refractory hypoxemia HR 130 BP 80 / 50 / 62 15

16 HR 130 BP 80 / 50 / 62 CI 2.2 PAP 15 / 8 / 10 PAOP / CVP 2 / 1 PVRI 290 SVRI 2218 SVI 28 LVSWI/RVSWI 22.8 / 2.6 ABGs (.70 FiO 2 ) ph 7.38 pco 2 45 po 2 50 SaO 2.83 HCO 3 27 SvO 2 60% 16

17 PaO 2 / FiO 2 Ratio (P/F) 50 / Normal = > 300 ALI = < 250 ARDS = < 200 Laboratory Values Na 150 Cl 96 Hgb / Hct 12.1 / 36.3 CO 2 26 Anion Gap Na (CO 2 + Cl) 150 ( ) 28 (Normal = 12 15) 17

18 PEEP can DOI 2 WOB VOI 2 triggers inflammatory response maldistributed blood flow VOI 2 ideal Hgb is 12 DOI 2 until VOI 2 plateaus DOI 2 = CI ( 1.38 x Hgb x SaO 2 ) X 1.38 X 12.1 X 0.83 x ml/min/m 2 (normal = ml/min/m 2 ) 18

19 VOI 2 = CI X 1.38 X Hgb X (SaO 2 - SvO 2 ) X x 1.38 x 12.1 x ( ) x ml/min/m 2 (Normal ml/min/m 2 ) In Summary 6 P s of ARDS Management Pathophysiology Prevention Positive Pressure Ventilation Perfusion Pharmacology Positioning 19

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