Patho Exam 2: Respiratory Distress & ARDS (Lecture 2)

Question 1

What is the primary function of the lungs?

Answer 1

oxygenate blood and remove CO2

Question 2

What is Acute Respiratory Failure?

Answer 2

Lung cannot perform their primary role in gas exchange.

End-result in longstanding respiratory disease or complication of another disorder.

Question 3

How do you define respiratory failure in values of paO2 and paCO2?

Answer 3

paO2 <50-60 mmHg

paCO2 can be high or low (= 50 mmHg)

Question 4

Define hypoxemic (normocapnic) in terms of paO2 and paCO2

Hint: “cap” = CO2

Answer 4

Low paO2

Normal paCO2

Question 5

Define hypercapnic (ventilatory respiratory failure) in terms of paO2 and paCO2

Hint: “cap” = CO2

Answer 5

Low paO2
High paCO2 (pt is retaining to CO2 in their body)

Question 6

Intrinsic & Obstructive respiratory failure is related to…

Hint: COPD

Answer 6

Hypercapnic

• issue with taking CO2 out
• COPD builds up in blood

Question 7

Intrinsic & Restrictive respiratory failure is related to…

Answer 7

Hypoxemic

-restricts proper O2 intake

Question 8

Extrinsic respiratory failure is…

Hint: Trauma, narcotic

Answer 8

Hypercapnic

Question 9

What is the general rule for PCO2 and PO2

Hint: Inverse relationship

Answer 9

PCO2 increase; PO2 decrease

PCO2 decrease; PO2 increase

Question 10

Increase affinity to Hgb means…

Answer 10

Easy to bind but Harder to take O2 off of Hgb; Left shift

Question 11

Decrease affinity to Hgb means…

Answer 11

Harder to bind but Easier to take O2 off of Hgb; Right shift

i.e: Exercising

Question 12

If there is an increase in CO2, what affects does it have on pH and affinity?

Answer 12

Increase CO2 = acidosis (more acidic) = decrease in O2-Hgb affinity

Increase in temperature; febrile

Question 13

A decrease in CO2 would affect the pH and affinity in what way…

Answer 13

Decrease CO2 = alkalosis (more basic) = increase in O2-Hgb affinity

Decrease in temperature

Question 14

What are the s/s of hypoxemia? What are the PO2 levels during hypoxemia?

Answer 14

Hypoxemia begins when PO2 drops is 40-50mmg.

• Pts will express confusion, motor impairment, slurring of speech.
• Initially, tachycardic and hypertensive but will become bradycardic and hypotensive later.
• Pulmonary blood vessels constrict (helps increase BP in surrounding tissues)

Question 15

What are the s/s of hypercapnia?

Answer 15

Always associated w/ hypoxemia

• CNS depression (CO2 narcosis)
• Cerebral vasodilation (give all O2 to brain)
• Pulmonary vasoconstriction
• Respiratory acidosis (due to high levels of CO2)

Question 16

Why wouldn’t sx’s concerning increase in PCO2 be presented in a pt w/ h/o COPD.

Answer 16

Body adapts to chronic high levels of PCO2. Pts w/ h/o COPD, having higher chronic levels of PCO2, may not present w/ sx’s unless there is a markedly elevated level of PCO2 if susceptible.

Question 17

The hypercapnia range of PCO2 is > 50 mmHg, distinguish the ranges of further hypercapnia and their associated sx’s.

Answer 17

PCO2 60-75mmHg = air hunger, rapid breathing (to breath off CO2)

PCO2 80-100mmHg= disorientation, lethary, semi-comatose

PCO2 >100mmHg = comatose, anesthesia, death.

Question 18

The ranges in ABG to diagnose respiratory failure are…

Answer 18

ABG ranges:

PO2 = 50-60 mmHg or less

PCO2 = 50 mmHg or more

Question 19

Respiratory acidosis is…

Answer 19

Hypercapnia (Increase in CO2)

Alveolar HYPOventilation

Question 20

Respiratory alkalosis is…

Answer 20

Hypocapnia (Decrease in CO2/acidity)

Alveolar HYPERventilation

Question 21

What are the systems responsible to maintain acid-base balance

Answer 21

1. Hematologic (RBCs)
2. Lungs (blowing off CO2 to decrease acidity
3. Kidneys (excretion and retention)

Question 22

Define and describe ARDS?

Answer 22

ARDS: Acute/Adult Respiratory Distress Syndrome

“Acute lung injury” with high mortality (50-60% mortality)
- alveoli are diffusely injured, decrease massive amount of gas exchange

Question 23

Why is ARDS so severe?

Answer 23

Due to the untreatable infiltrates and severe hypoxemia.

Damage to diffuse alveoli w/ no response to treatment = no gas exchange.

Question 24

Pathophysiology behind ARDS

Answer 24

AC-membrane is severely damaged (direct or non-direct)

This causes massive inflammatory = capillaries expand and leak = increase capillary permeability

Cause WBC response; neutrophils, macrophages and platelets

Question 25

What are the 3 phases of ARDS?

Answer 25

1. Hemorrhagic/exudative (24-48 hours)
2. Fibrotic (7 days)
3. Body-wide (10-14 days)

Question 26

Elaborate on the Hemorrhagic/Exudative phase of ARDs

Answer 26

24-48 hours

• excessive immune response
• increase in fluid, protein and inflammatory cells into capillaries = alveolar are not dry

Question 27

Describe the Fibrotic phase of ARDS.

Answer 27

7 days

• “disordered healing”
• connective tissue in lungs proliferate

Question 28

Describe the Body-wide phase of ARDS.

Answer 28

10-14 days (rare for pt to survive to this duration)

• sepsis/systemic infection
• organs shut down

Question 29

List the clinical course of ARDs.

Answer 29

Hyperventilation (compensatory mechanism)

Respiratory Alkalosis ( breathing too much CO2 off)

Dyspnea and hypoxemia (O2 decrease intake)

Metabolic acidosis

Respiratory acidosis

Further hypoxemia (worsens)

Hypotension

Decrease in cardiac output

Death