Lung Transplant, Respiratory Failure, ARDS, and ABGs

Question 1

general indications for lung transplant

Answer 1

*pt’s lungs are damaged to the point of disability, with life expectancy < 5 years:
-FEV1 < 25% predicted and falling
-FVC < 30% predicted and falling
-DLCO < 30% predicted and falling
*pt otherwise has good function of other organs
*typical diseases: IPF, COPD, CF, NSIP, scleroderma, A1AT deficiency, PAH

Question 2

indications to NOT do a lung transplant

Answer 2

*other organs are too damaged to withstand major surgery and rehab
*disease affecting the lungs is uncontrolled and likely to recur
*BMI is too high
*uncontrolled acid reflux (GERD)
*process not acceptable to patient or lungs are not available

Question 3

after lung transplant: immune rejection

Answer 3

*a persistent and unending battle
*acute rejection = immediate and highly inflammatory
*chronic rejection = slow and progressive
*medications are use to reduce cell-mediated immunity (prednisone, mTOR inhibitors, mycophenolate mofetil)
*sine qua non feature of chronic rejection: progressive airflow obstruction on PFTS; aka bronchiolitis obliterans syndrome (BOS):
-biopsy demonstrates constrictive/obliterative bronchiolitis

Question 4

3 types of respiratory failure

Answer 4

1. Hypoxemic Respiratory Failure (Type 1)
2. Hypercapnic Respiratory Failure (Type 2)
3. Mixed (Hypoxemic & Hypercapnic) Respiratory Failure (Type 1 & 2)

Question 5

arterial blood gas (ABG) reports what?

Answer 5

-pH
-PaCO2
-PaO2
-HCO3-
-base excess
-O2 saturation

Question 6

hypoxia vs. hypoxemia

Answer 6

*hypoxia = low oxygen gas pressure (ex. tissue hypoxia, alveolar hypoxia)

*hypoxemia = low blood oxygen CONTENT
-usually due to low oxyhemoglobin
-most common: low oxyhemoglobin percentage (saturation)
-sometimes due to severe anemia or hemoglobinopathies

Question 7

5 mechanisms of hypoxemia

Answer 7

1. decreased inspired PO2
2. hypoventilation or increased dead space
3. diffusion limitation
4. V/Q mismatching
5. shunt

Question 8

mechanisms of hypoxemia: decreased inspirated PO2

Answer 8

*due to decreased inspired oxygen
*examples: high altitudes (climbing to the top of Mt. Everest); low concentrations of oxygen in the inspired air
*not commonly seen in medical practice

Question 9

mechanisms of hypoxemia: hypoventilation

Answer 9

*increased PCO2 (failure to eliminate CO2)
*can be due to diaphragm dysfunction, medications (ex. opioids or benzodiazepines), or brainstem stroke

Question 10

mechanisms of hypoxemia: increased dead space

Answer 10

*air spaces that are ventilated but not perfused
*dead space first creates hypercapnia (increased PCO2) and consequently causes hypoxemia
*normal dead space in trachea and conducting airways
*abnormal increases in dead space: severe emphysema, pulmonary embolism, increased zone 1 physiology

Question 11

mechanisms of hypoxemia: diffusion limitation

Answer 11

*decreased diffusion as a result of alveolar thickening or loss of area
*alveolar problems include emphysema and loss of alveolar units (COPD)
*interstitial problems include: pulmonary edema, pulmonary fibrosis

Question 12

mechanisms of hypoxemia: V/Q mismatching

Answer 12

*things that decrease the “V” (ventilation):
-alveolar filling/airway obstruction (edema, pus, blood, atelectasis, mucus plugging)
*things that decrease the “Q” (perfusion):
-perfusion defects (pulmonary arterial hypertension, pulmonary embolism)

Question 13

acute respiratory distress syndrome (ARDS) - overview

Answer 13

*a special case of V/Q mismatch
*constellation of findings with different underlying causes
*recognized in patients with infiltrates on both sides of the lung that are acute

Question 14

acute respiratory distress syndrome (ARDS) - diagnostic criteria

Answer 14

*diagnosed by “Berlin criteria”:
-timing: onset less than 1 week
-imaging: bilateral opacities not fully explained by effusions, lung collapse, or nodules
-cause: not fully explained by hydrostatic edema (such as cardiac failure or other fluid overload)

Question 15

acute respiratory distress syndrome (ARDS) - classification of severity

Answer 15

*severity is classified by PaO2/FiO2 ratio (P/F ratio), measured with > 5 cmH20 of PEEP:
-mild: between 300 and 200
-moderate: between 200 and 100
-severe: less than 100

note: normal P/F ratio is ~500

Question 16

acute respiratory distress syndrome (ARDS) - pathophysiology

Answer 16

*increased alveolar capillary permeability and surfactant dysfunction
*non-cardiogenic pulmonary edema can result from inflammation and cytokine release in many conditions (esp. pneumonia, sepsis)

Question 17

acute respiratory distress syndrome (ARDS) - causes

Answer 17

*pneumonia
*sepsis
*major trauma
*pancreatitis

Question 18

acute respiratory distress syndrome (ARDS) - management

Answer 18

*LOW TIDAL VOLUME mechanical ventilation:
-maintain tidal volume at 6mL/kg of ideal body weight
-maintain mean airway pressure as low as possible
-“permissive hypercapnia”: tolerate some hypercapnia to keep the tidal volume low

*other management principles:
-conservative fluid management
-prone positioning (on stomach)
-corticosteroids

Question 19

mechanisms of hypoxemia: shunt

Answer 19

*blood passing form right to left heart without seeing a functional alveolus (the blood has no opportunity to participate in gas exchange)
*normal shunts: bronchial circulation and thebesian veins (1-3% of CO)
*ABNORMAL:
-patent foramen ovale
-complete fill of airway (edema, blood, pus)
-atelectasis, mucus plugging, foreign body

Question 20

mechanisms of hypoxemia: which one(s) correct with 100% oxygen?

Answer 20

all of them EXCEPT SHUNTS

i.e. decreased inspirated PO2, hypoventilation/increased dead space, diffusion limitation, and V/Q mismatching all can be corrected by placing the patient on 100% oxygen

Question 21

hypercapnic respiratory failure - causes

Answer 21

*caused by an imbalance in the normal PaCO2 homeostasis, resulting from any of:
1. increased CO2 production (fever or poising)
2. decreased minute ventilation (CNS injury, depressants, obesity, hypoventilation syndrome)
3. increased dead space (severe COPD)

Question 22

hypercapnic respiratory failure - clinical presentation

Answer 22

*somnolence
*lethargy
*asterixis
*the acutely ill respiratory patient that’s “tiring out”

*note - thing of CO2 narcolepsy

Question 23

causes of respiratory acidosis

Answer 23

*common causes:
-airway obstruction (COPD)
-depression of respiratory control centers (sedatives, opiates)

*recall: primary disturbance = ELEVATED PCO2

Question 24

causes of metabolic acidosis

Answer 24

*common causes:
-ingested toxins (ethylene glycol)
-lactic acidosis (shock, severe sepsis)
-diarrhea

*recall: primary disturbance = DECREASED [HCO3-]

Question 25

causes of respiratory alkalosis

Answer 25

*common causes:
-hyperventilation
-CNS tumors
-drugs (salicylates such as ASPIRIN)
-acute pulmonary embolism

*recall: primary disturbance = DECREASED PCO2

Question 26

causes of metabolic alkalosis

Answer 26

*common causes:
-vomiting
-ingestion of antacids

*recall: primary disturbance = INCREASED [HCO3-]

Question 27

arterial blood gas (ABGs) - normal values and reporting format

Answer 27

pH | PaCO2 | PaO2 | HCO3-
7.40 | 40 | 100 | 24

Question 28

ABG interpretation - stepwise approach

Answer 28

1. look at the pH (acidosis or alkalosis?)
2. a) look at the PaCO2 (respiratory or metabolic?)
3. b) does the [HCO3-] confirm your suspicion?
4. check to see if COMPENSATION has occurred

Question 29

interpret this ABG: 7.34 | 48 | 98 | 25

Answer 29

*respiratory acidosis (acute/uncompensated)

Question 30

interpret this ABG: 7.49 | 30 | 104 | 22

Answer 30

*respiratory alkalosis (acute/uncompensated)

Question 31

interpret this ABG: 7.35 | 30 | 102 | 16

Answer 31

*metabolic acidosis (with respiratory compensation)

Question 32

interpret this ABG: 7.50 | 48 | 98 | 36

Answer 32

*metabolic alkalosis (with respiratory compensation)

Question 33

rules for checking if compensation has occurred in RESPIRATORY ACIDOSIS

Answer 33

*for PaCO2 increases of 10 mmHg:

-acute (uncompensated; change due to buffering): bicarb increases by 1.0

-chronic (COMPENSATION): bicarb increases by 4.0

note - there is acute and chronic in the respiratory ones because it takes time for the kidney to compensate

Question 34

rules for checking if compensation has occurred in RESPIRATORY ALKALOSIS

Answer 34

*for PaCO2 decreases of 10 mmHg:

-acute (uncompensated; change due to buffering): bicarb decreases by 2.0

-chronic (COMPENSATION): bicarb decreases by 5.0

note - there is acute and chronic in the respiratory ones because it takes time for the kidney to compensate

Question 35

rules for checking if compensation has occurred in METABOLIC ACIDOSIS

Answer 35

*for [HCO3-] decreases of 1.0:

-PaCO2 decreases by 1.2

note - respiratory changes are very rapid (no acute vs. chronic changes)

Question 36

rules for checking if compensation has occurred in METABOLIC ALKALOSIS

Answer 36

*for [HCO3-] increases of 1.0:

-PaCO2 increases by 0.7

note - respiratory changes are very rapid (no acute vs. chronic changes)

Question 37

interpret this ABG: 7.23 | 60 | 93 | 24

Answer 37

note: appropriate compensation has NOT occurred (because the bicarb should be 4 points higher due to the the 20 points increase in PaCO2)

we call this a MIXED ACID-BASE DISORDER (respiratory acidosis AND metabolic acidosis)

Question 38

tips on mixed acid-base disorders

Answer 38

*if 2 disorders are present, you will pick up on this when you check for expected changes (so remember to check)
*you CANNOT have respiratory acidosis and respiratory alkalosis at the same time