Acute Respiratory Distress Syndrome (ARDS) – Flashcards

A form of respiratory failure that follows a number of respiratory insults; underlying problem of alveolar-capillary membrane damage; non-cardiac pulmonary edema; Refractory hypoxemia is key feature; ARDS is when the lungs are unable to exchange oxygen and CO2 between the alveoli and capillaries therefore results in the body getting unoxygenated blood; the alveoli cannot transfer its oxygen to the capillaries and the capillaries cannot dump off the CO2 to the alveoli

no matter what you do, hypoxia will NOT reverse

cause of ARDS; 2 types Direct - pneumonia, aspiration Indirect - sepsis, severe trauma, MSOF Chemical mediators released - damage to capillary wall Alveoli wall becomes permeable -allows fluid to accumulate causing pulmonary edema -reduction in surfactant causing alveolar collapse

Decreased lung compliance -low PO2, high PCO2 Hyalin membrane forms when fluid is in the interstitial spaces (scar like tissue) resulting in -increase in dead space -increased work of breathing -Shunting (occurs due to arterial blood that is not getting oxygen) Refractory hypoxemia that doesn't improve with O2

Shock states - hemorrhagic and septic Inhalation injury - aspiration of gastric contents, smoke, toxins, near drowning, O2 toxicity Infection - gram-negative sepsis, viral pneumonia Drug overdose- heroine, methadone, propoxyphene, ASA, TCA's Trauma - burns, head injury, lung injury/contusion, fat emboli Other- DIC, pancreatitis, uremia, massive transfusions, CABG

Acute exudative phase Proliferative phase Fibrotic phase *goal is to try and stop the process so it stops damaging the alveoli

Dyspnea, tachypnea, tachycardia, increased BP, cool pale clammy skin, cyanosis (late sign/poor indicator by itself), restless - altered LOC - lethargy

Dyspnea, altered respiratory rate, disorientation (quickly changes to CNS depression), CO2 vasodilating (headache, warm flushed skin, bounding pulse)

earliest sign is increased respiratory rate Progressive respiratory distress 3 classic s/s - dyspnea -Hypoxemia (PaO240) refractory to high O2 administration -Diffuse bilateral infiltrated on xray (white out) signs of respiratory failure diffuse fine crackles, coarse rhonchi and wheezes PINK FROTHY SPUTUM (membrane RBC and protein transfer into the lungs) X-ray will have white out look (fluid) Change in LOC - confusion, agitation, anxiety leading to lethargy Hypotension, decreased cardiac output tachycardia decreased urinary output body can reduce blood flow to nonessential organs and deliver to essential ones

Intubation often required - keep PaO2>60 with lowest FiO2 as possible to keep ABG greater 60 (barotrauma) Prevent air trapping with ventilation use 5ml/kg of tidal volume and PEEP use 1:1 ratio for I/E on vent instead of 1:2 Prone position or frequent changes -increases blood flow to anterior lungs -shift fluid/edema out of posterior lungs -helps expand lungs -labor intensive, patients may not be able to tolerate it

surfactant replacement therapy -instilled via bronchoscopy -may improve immediate O2 demands -studies did not show a change in overall outcome Oxygenation/ventilation - liquefy secretions, humidified O2 -adequate IV fluids (use PA cath to avoid over hydration, hypotension) -bronchodilation - steroids can help reduce swelling but can also increase blood glucose levels which impairs healing - nutrition (increase protein/fat, decrease CHO3, enteral feedings, need >2000 cal)

Antibiotics - culture first then treat infection if one is present Surfactant replacement - increase alveolar surface tension Diuretic - eliminate atelectasis and fluid restriction Possible nebulizer tx - to dilate pulmonary vasculature H2 blockers or proton pump inhibitors - to prevent stress ulcers Anticoagulants - prevent DVT

Chest xray - ground glass appearance or white out look Sputum and blood cultures to determine if infection ABG respiratory acidosis r/t CO2 retention metabolic acidosis r/t lactic acid production Electrolyte imbalances r/t fluid shift; watch cardiac markers Increased WBC r/t infection Increased BUN and creatinine r/t diminished perfusion to kidneys Increased liver function tests r/t diminished perfusion to kidneys Increased glucose r/t stress response and steroids Hgb/Hct r/t low concentration and blood loss

Perfusion - IV fluid therapy and inotropic meds Positioning - rotation therapy, prone to improve oxygenation, ventilation, and perfusion to lung fields Protective lung ventilation - use least invasive method of oxygen delivery possible to maintain PaO2 >60 Protocol weaning - start weaning as soon as patient stable to avoid oxygen toxicity Prevent complications - ventilator assisted pneumonia, DVT, decreased nutritional status, and ventilator induced lung injury