Lung Transplant, Respiratory Failure, ARDS, and ABGs Flashcards

1
Q

general indications for lung transplant

A

*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

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2
Q

indications to NOT do a lung transplant

A

*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

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3
Q

after lung transplant: immune rejection

A

*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

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4
Q

3 types of respiratory failure

A
  1. Hypoxemic Respiratory Failure (Type 1)
  2. Hypercapnic Respiratory Failure (Type 2)
  3. Mixed (Hypoxemic & Hypercapnic) Respiratory Failure (Type 1 & 2)
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5
Q

arterial blood gas (ABG) reports what?

A

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

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6
Q

hypoxia vs. hypoxemia

A

*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

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7
Q

5 mechanisms of hypoxemia

A
  1. decreased inspired PO2
  2. hypoventilation or increased dead space
  3. diffusion limitation
  4. V/Q mismatching
  5. shunt
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8
Q

mechanisms of hypoxemia: decreased inspirated PO2

A

*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

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9
Q

mechanisms of hypoxemia: hypoventilation

A

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

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10
Q

mechanisms of hypoxemia: increased dead space

A

*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

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11
Q

mechanisms of hypoxemia: diffusion limitation

A

*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

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12
Q

mechanisms of hypoxemia: V/Q mismatching

A

*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)

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13
Q

acute respiratory distress syndrome (ARDS) - overview

A

*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

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14
Q

acute respiratory distress syndrome (ARDS) - diagnostic criteria

A

*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)

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15
Q

acute respiratory distress syndrome (ARDS) - classification of severity

A

*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

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16
Q

acute respiratory distress syndrome (ARDS) - pathophysiology

A

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

17
Q

acute respiratory distress syndrome (ARDS) - causes

A

*pneumonia
*sepsis
*major trauma
*pancreatitis

18
Q

acute respiratory distress syndrome (ARDS) - management

A

*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

19
Q

mechanisms of hypoxemia: shunt

A

*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

20
Q

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

A

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

21
Q

hypercapnic respiratory failure - causes

A

*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)

22
Q

hypercapnic respiratory failure - clinical presentation

A

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

*note - thing of CO2 narcolepsy

23
Q

causes of respiratory acidosis

A

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

*recall: primary disturbance = ELEVATED PCO2

24
Q

causes of metabolic acidosis

A

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

*recall: primary disturbance = DECREASED [HCO3-]

25
Q

causes of respiratory alkalosis

A

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

*recall: primary disturbance = DECREASED PCO2

26
Q

causes of metabolic alkalosis

A

*common causes:
-vomiting
-ingestion of antacids

*recall: primary disturbance = INCREASED [HCO3-]

27
Q

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

A

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

28
Q

ABG interpretation - stepwise approach

A
  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
29
Q

interpret this ABG: 7.34 | 48 | 98 | 25

A

*respiratory acidosis (acute/uncompensated)

30
Q

interpret this ABG: 7.49 | 30 | 104 | 22

A

*respiratory alkalosis (acute/uncompensated)

31
Q

interpret this ABG: 7.35 | 30 | 102 | 16

A

*metabolic acidosis (with respiratory compensation)

32
Q

interpret this ABG: 7.50 | 48 | 98 | 36

A

*metabolic alkalosis (with respiratory compensation)

33
Q

rules for checking if compensation has occurred in RESPIRATORY ACIDOSIS

A

*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

34
Q

rules for checking if compensation has occurred in RESPIRATORY ALKALOSIS

A

*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

35
Q

rules for checking if compensation has occurred in METABOLIC ACIDOSIS

A

*for [HCO3-] decreases of 1.0:

-PaCO2 decreases by 1.2

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

36
Q

rules for checking if compensation has occurred in METABOLIC ALKALOSIS

A

*for [HCO3-] increases of 1.0:

-PaCO2 increases by 0.7

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

37
Q

interpret this ABG: 7.23 | 60 | 93 | 24

A

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)

38
Q

tips on mixed acid-base disorders

A

*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