ARDS Flashcards
ARDS (acute respiratory distress syndrome)
diffuse lung injury with non-cardiogenic pulmonary edema; disruption of alveolar-capillary membrane (alveoli filling with fluid)
4 hallmark features of ARDS
- bilateral patchy infiltrates on chest XR
- no s/s of HF (PAWP 18 or less)
- no improvement in PaO2 despite increasing O2 delivery
- acute onset
PaO2/FiO2 ratio
look at PaO2 on ABGs and divide by % of O2 pt is receiving; ex: PaO2 83 and 45% FiO2 = 83/0.45 = 184.4
Berlin criteria: timing
within a week of clinical insult/worsening symptoms
Berlin criteria: chest x-ray
bilateral opacities not explained by effusions, lobar collapse, or nodules
Berlin criteria: origin of edema
respiratory failure not fully explained by HF or fluid overload; need echocardiography
Berlin criteria: mild ARDS
2005
Berlin criteria: moderate ARDS
1005
Berlin criteria: severe ARDS
PaO2/FiO2 with PEEP >5
risk factors for ARDS
sepsis, pneumonia, trauma, aspiration, multiple transfusions, fat embolism, or pancreatitis
direct lung injury
lung epithelium sustains a direct insult
indirect lung injury
insult occurs elsewhere in body and mediators are transmitted via bloodstream to lungs
examples of direct injury
aspiration, pulmonary infections, pulmonary contusions, toxic inhalation, drug overdose, burns, near drowning
examples of indirect injury
sepsis, hyper-transfusion of blood, trauma, pancreatitis, cardiopulmonary bypass, shock, DIC
ARDS pathology
injury –> inflammatory response –> damage to alveolar-capillary membrane –> increased vascular permeability –> protein rich fluid –> decreased gas exchange –> respiratory failure
exudative phase
within 72 hr, capillary membranes begin to leak - protein rich fluid fills the alveoli - hyaline membrane formed -disrupts gas exchange
fibroproliferative phase
day 7-10 after onset until 1 mo, alveolar cells damaged and surfactant production declines, VQ mismatch, hypoxemia, pulmonary htn develops and increase in R vent afterload and R sided HF
resolution phase
after around 21 days, altered healing process - development of fibrotic tissue in the ACM, structural and vascular remodeling takes place to reest. the ACM
complications of ARDS
right to left shunting, ineffective surfactant activity, increased pulmonary vascular resistance, altered lung compliance (increased work of breathing)
physical assessment
Restlessness, disorientation, change in LOC, CXR normal in early stage and infiltrates develop in about 24hr, resp. distress with dyspnea, tachycardia and hypoxia that doesnt respond to O2 therapy and PEEP, crackles/rhonchi, refractory hypoxemia, develops into metabolic acidosis and increased lactate levels, hypotension
A-a gradient
PAO2 minus PaO2, should be less than 15, greater than 15 is hypoxia
PAO2
alveolar oxygen tension; normal is 104 mmHg
PaO2
arterial oxygen tension; normal is 95 mmHg
what does an increased A-a gradient indicate?
shunting
histology with ARDS
alveolar inflammation, thickened septum from protein leakage, congestion and decreased alveolar volume
reducing ventilator related lung injury
low tidal volume and setting PEEP higher
appropriate vent tidal volume for ARDS
4-6ml/kg
appropriate FiO2 for ARDS
less than 60 to minimize O2 toxicity
appropriate PEEP for ARDS
5-15 cm H2O to prevent alveolar collapse
permissive hypercapnea
PaCO2 60-100 (lower respiratory rates), this protects lungs from ventilator related injury
high frequency oscillatory ventilation (HFOV)
when pt doesnt respond to AC or PRVC; uses very low tidal volumes at very high rates, constant airway pressure and prevents complete alveolar closure
inhaled nitric oxide
controversial, vasodilator with no systemic effects that reduces pulmonary arterial pressure
inverse-ratio ventilation (IRV)
prolonging inspiration time to prevent complete exhalation (I:E on vent)
ECMO/bypass
allows lungs to rest by providing complete pulmonary and cardiac support; bleeding is a common complication
goal of ARDS therapy
treatment of the underlying cause, cardio-pulmonary support, specific therapy targeted at lung injury and supportive therapy
additional support options
bronchodilators, administer exogenous surfactant, sedationi/neuromuscular blocking agents, nutritional support, monitor vials and UOP
sepsis treatment
empirical antibiotics, c&s and change antibiotics as needed, avoid nephrotoxic drugs, enteral feedings preferred
when is prone positioning most beneficial?
the first 36hr
when would you consider prone positioning?
low TV and PEEP not successful, PaO2/FiO2 below 100 (severe ARDS), would want to maintain for 18-20 consecutive hours
