Acute Respiratory Distress Syndrome (ARDS)

Question 1

ARDS

Answer 1

severe, acute onset and progressive alveolar and capillary damage that results in pt losing all resp Fx and will die w/o Tx in mins

Question 2

mortality rate

Answer 2

36-60% (high unless there’s prompt intervention)

Question 3

etiology

Answer 3

• inhaling excessive amounts of smoke (caught in fire, NOT smoking)
• near-drowning, inhaling water
• alcohol abuse
• drugs (cocaine & heroin if inhaled)
• burns

Question 4

patho

Answer 4

• trauma to lung tissue & cells that make up lung wall –> inc cap permb –> results in influx of inflm, plasma proteins & exudate from capillaries into IS & alveoli –> pulmonary edema –> fluid inside alveoli –> l/o compliance & alveoli expansion limited
• cells that enter target injured cells –> cellular debris
• activated neutrophils release products that damage alveolar cells
• damage to T2 alveolar cells –> inability to produce surfactant
• damaged cells release free radials and inflm cells release proteases –> injure capillaries & alveoli
• build-up of cellular debris & exudate form protein-risk, thick “hyaline membrane”

Question 5

the inability to produce surfactant results in what

Answer 5

surface tension within alveoli dec and widespread atelectasis throughout alveoli in lungs

Question 6

hyaline membrane is impervious, what does that mean

Answer 6

nothing can move across it so gas exchange cannot occur –> hypoxia

Question 7

mnfts

Answer 7

• very severe acute respiratory distress
• tachypnea (compensatory)
• dyspnea
• excessive hypoxemia
• lung consolidation (CXR)

Question 8

lung consolidation

Answer 8

solidification of exudate & inflm debris

Question 9

cmplx

Answer 9

• pulmonary HTN
• early respiratory alkalosis
• late metabolic acidosis
• multi-organ failure

Question 10

how does early respiratory alkalosis occur

Answer 10

Occurs w/ tachypnea as excess CO2 is exhaled, dec ability to form carbonic acid and inc pH

Question 11

how does late metabolic acidosis

Answer 11

Tachypnea causes inc in workload of resp muscles, inc their demand for ATP. With dec gas exchange, O2 is in low supply to complete ETC, so anaerobic metb occurs (glycolysis, which produces an excess of lactic acid)

Question 12

Tx

Answer 12

• early intervention = good prognosis
• supplemental O2 (if gas exchange isn’t fully impaired)
• advanced respiratory support
• reverse the cause (ex. address fluid-buildup)
• anti-inflm drugs (ex. steroids)
• cmplx –> ABGs for blood pH