Acute Respiratory Distress Syndrome (ARDS)

Question 1

ARDS

Answer 1

• “wet lung” or “post traumatic lung”
• severe, acute onset and progressive alveolar + capillary damage
• 35-60% mortality

Question 2

etiology

Answer 2

near drowning 
aspiration gastric contents 
increased smoke inhalation 
radiation 
septicemia
burns
fat embolism 
drugs 
chest trauma

Question 3

patho

Answer 3

• trauma to lung tissue and cells that make up lung wall results in increased cap permb (inflmtn also increases cap permb)
• diffuse consolidation
• inactivation of surfactant -> atelectasis
• hyaline membrane forms d/t buildup of cellular debris and exudate that is rich in protein and thick

Question 4

describe the patho of trauma to lung tissue

Answer 4

• lung trauma -> influx of inflm cells, release of free radicals, phospholipids and proteases -> alveolar and capillary damage -> increased permb -> proteins, cells, and fluids enter IS and alveoli from capillaries
• pulm edema d/t compromised compliance and limited alveoli expansion, causing decreased gas exchange
• activated neutrophils release a variety of products that damage alveolar cells

Question 5

describe the patho of inactivation of surfactant

Answer 5

free radicals, increased movement of proteins into alveolus and proteases causes l/o surfactant

Question 6

hyaline membrane

Answer 6

hyaline refers to glossy hard appearance/structure (not an actual membrane)
- lining is impervious (: nothing can move across it) therefore gas exchange can’t occur -> profound hypoxemia

Question 7

manifestations

Answer 7

• appear abruptly
• acute resp distress
• tachypnea (compensatory response to hypoxia)
• dyspnea
• profound hypoxemia

Question 8

complications

Answer 8

• pulmonary HTN (compensatory vasoconstriction d/t hypoxemia)
• early resp alkalosis
• late metabolic acidosis
• multi-organ failure (kidneys, liver, brain, heart)

Question 9

why does early resp alkalosis occur?

Answer 9

• occurs with tachypnea as excess CO2 is exhaled
• decreased ability to form carbonic acid and increased pH (= respiratory)
• volatile acid, so its respiratory

Question 10

why does late metabolic acidosis occur?

Answer 10

• tachypnea causes increased workload of resp muscles, increasing demand for ATP
• w/ decreased gas exchange, O2 is in low supply to complete the ETC, so anaerobic metabolism occurs
• buildup of lactic acid = acidosis, fixed acid = metabolic

Question 11

diagnosis

Answer 11

CXR - shows lung consolidation

Question 12

treatment

Answer 12

• stat detection and intervention (if gas exchange is not completely impaired, admin O2)
• resp support
• address the cause
• deal w/ complx (ABGs for blood pH, treat w/ meds)