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Restrictive Lung Diseases Flashcards

1
Q

What are the four types of RLD?

A
  • Acute intrinsic
  • Chronic intrinsic
  • Chronic extrinsic
  • Other (obesity)
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2
Q

Define RLD

A

anything that interferes with normal lung expansion during inspiration

  • affects both lung expansion & compliance*
  • cannot increase lung volume in proportion to increased alveolar pressure*
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3
Q

Principle features of RLD (4)

A

reduction in TLC
decrease in all lung volumes & capacities
NORMAL FEV1/FVC RATIO
reduced DLCO

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4
Q

Classification of RLD by TLC

A

65-80 % = mild
50 - 65% = moderate
< 50% = severe

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5
Q

Vt

A

500 mL

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6
Q

IRV

A

3000 mL

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7
Q

IC

A

3500 mL

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8
Q

ERV

A

1100 mL

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9
Q

RV

A

1200 mL

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10
Q

FRC

A

2300 mL

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11
Q

VC

A

4600 mL

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12
Q

TLC

A

5800 mL

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13
Q

Acute intrinsic (define; anesthesia considerations)

A

abnormal movement of intravascular fluid

  • lung volume:
  • anesthetic considerations: not relieved by oxygen, HTN, tachycardia, diaphoresis
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14
Q

Chronic intrinsic

A

pulmonary fibrosis

  • lung volume:
  • anesthetic considerations:
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15
Q

Chronic extrinsic

A

traumatic vs non-traumatic

  • lung volume:
  • anesthetic considerations:
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16
Q

Pulmonary edema

A

ACUTE INTRINSIC

  • cardiogenic pulmonary edema = butterfly pattern on CXR; hydrostatic
  • non-cardiogenic pulmonary edema = hydrostatic, permeability
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17
Q

Starling’s Law

A

Q = K(Pc - Pi) - ( πc - πi)

flow = fluid filtration coefficient
capillary hydrostatic - ISF hydrostatic
oncotic pressure capillary - oncotic pressure ISF

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18
Q

S/S Cardiogenic PUlmonary edema

A

rapid, shallow breathing not relieved by oxygen.

htn, tachycardia, diaphoresis

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19
Q

Non-cardiogenic pulmonary edema

A

Elevated Pc
K changed

causes: neurogenic, uremic, high-altitude, upper airway obstruction

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20
Q

Negative pressure pulmonary edema

A

Caused by an obstructed upper airway with a prolonged, forceful inspiratory effort against an obstructed upper airway in spontaneously breathing pt

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21
Q

S/S NPPE

A

SNS stimulation - increased afterload, HTN, central volume displacement (increased CVP, JVD, gallops)

  • bradycardia b/c hypoxic
  • seesaw breathing, tachypnea
  • hypoxemia
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22
Q

NPPE RF

A

male, young, overzealous fluid admin, hx cardiac or pulmonary dx

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23
Q

NPPE onset

A

minutes - hours

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24
Q

Treatment of NPPE

A

oxygen will not help (but we still give it)
PEEP or CPAP
vasodilator to decrease preload
optimize fluids

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25
Q

Non-cardiogenic pulmonary edema examples (4)

A

aspiration pneumonitis
pneumonia
ARDS
TRALI

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26
Q

What are the three aspiration syndromes?

A

chemical pneumonitis (mendelson’s syndrome), mechanical obstruction, bacterial infection

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27
Q

What is mendelson’s syndrome?

A

pneumonitis from perioperative aspiration producing an asthma-like syndrome
pharmacologic prophylaxis doesn’t change outcome

greatest frequency during intubation or emergence

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28
Q

RF for mendelson’s syndrome

A 
abdominal pathology, obesity, hiatal hernia
DM, neuro deficit
lithotomy, c-section
difficult intubation
GERD
inadequate anesthesia
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29
Q

Pathophys of mendelson’s syndrome

A

aspirated substance –> lung parenchyma injury –> inflammation –> secondary injury in 24h

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30
Q

Clinical features of mendelson’s syndrome

A

arterial hypoxemia give CPAP

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31
Q

anesthetic considerations for mendelson’s syndrome

A

RF, NPO standards, pharm prophylaxis, cricoid pressure, awake intubation, regional

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32
Q

Mendelson Treatment

A
  1. tilt head down or turn
  2. rapid suction of mouth/pharynx
  3. supplemental O2
  4. PEEP (APL valve)
  5. Abx not recommended
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33
Q

Acute Respiratory Failure

A

PaO2 < 60 mmHg despite O2 supplementation
PaCO2 > 50 mmHg in absence of respiratory compensation

most common cause –> ARDS

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34
Q

ARDS goals (3)

A

patent upper airway
correct hypoxia
remove CO2

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35
Q

ARDS physiology

A

insult to A/C membrane causing increased capillary permeability and subsequent interstitial and alveolar edema

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36
Q

ARDS RF

A

sepsis, pneumonia, trauma, aspiration

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37
Q

S/S ARDS (4)

A

dyspnea, hypoxia, hypovolemia, lung stiffness

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38
Q

ARDS definition

A

-lung injury of acute onset w/one-week of apparent clinical insult and progression of pulmonary symptoms
-bilateral opacities on imaging
-resp failure not explained by cardiac or volume overload
-PaO2/FiO2
mild 200 - 300
moderate 100-200
severe < 100

39
Q

TRALI

A
  • acute lung injury d/t blood tx (usually plt)
  • occurs secondary to the interaction btw transfused blood & the recipients WBCs
  • neutrophils become trapped in pulmonary vasculature, leading to non-cardiogenic pulmonary edema
40
Q

TRALI RF

A

sx, malignancy, sepsis, alcoholism, liver dx

41
Q

TRALI management

A
  1. stop tx
  2. r/o incompatibility reaction/TACO
  3. IV fluids
  4. diuretics
  5. vent support
  6. lab findings
42
Q

Neurogenic pulmonary edema

A

severe head injury causing massive sympathetic outflow

43
Q

Chronic Intrinsic RLD (5)

A
  • autoimmune (sarcoidosis)
  • cytotoxic and non-cytotoxic drug exposure
  • oxygen toxicity
  • idiopathic pulmonary fibrosis
  • radiation injury
44
Q

Lung Parenchyma (4 cell types)

A
  • Type I: epithelial (structural, not metabolically active)
  • Type II: globular cell, surfactant producer, rapidly reproduce in response to injury
  • Alveolar macrophage: scavenger lysosome guy
  • Fibroblast: collagen and elastin synthesis cell (chronic insult results in fibrosis)
45
Q

Interstitium Thin Side

A

fused basement of epithelial and endothelial layers

responsible for gas exchange

46
Q

Interstitium Thick side

A

type I collagen

responsible for fluid exchange

47
Q

Idiopathic Pulmonary Fibrosis pathophys (3)

A

principle feature: thickening of the interstitium of the alveolar wall leading to

  1. infiltration of lymphocytes
  2. fibroblasts increasing collagen bundles
  3. cellular exudate w/i alveoli (desquamation)

all resulting in alveolar architecture destroyed & scarred

48
Q

Clinical features of idiopathic pulmonary fibrosis

A

not common - affects adults at age 50 - 70

  • dyspnea, shallow breathing
  • crackles
  • clubbing
  • CXR w/reticulonodular pattern; patchy shadows @ base
  • cor pulmonale in advanced stages
49
Q

Lab values w/idiopathic pulmonary fibrosis

A

arterial PO2 and PCO2 are reduced, but pH is normal
hypoxemia mild at rest
PO2 falls drastically with exercise
V/Q mismatch - diffusion capacity of CO is 5 mL/m

50
Q

normal diffusion capacity of CO

A

25 - 30 mL/m

51
Q

Idiopathic pulmonary fibrosis PFTs

A

FVC: decreased
FEV1/FVC: normal
FEF 25 - 75: normal

52
Q

Idiopathic pulmonary fibrosis pressure-volume curve

A

flattened and displaced downward

53
Q

Drug induced pulmonary dx

A

cytotoxic (CA drugs)

non-cytotoxic (amiodarone)

54
Q

Amiodarone

A

etiology: direct toxicity, immunologic mechanisms, activates RAS
* takes form of chronic interstitial pneumonitis, pneumonia, ARDS or fibrosis mass

55
Q

Amiodarone non-cytotoxic injury diagnosis

A

2 or more of the following

  • new onset pulm s/s
  • new x-ray abnormalities
  • decrease in DLCO
  • abnormal gallium 67 uptake (w/e that is lol)
  • histological changes

others: tachypnea, hypoxia, dry non-productive cough

56
Q

Treatment of amio induced pulmonary dx

A

stop drug - half-life 40 - 70 days

if fibrosis occurs, it is IRREVERSIBLE

57
Q

Bleomycin

A

antitumor abx that causes cytotoxic injury directly –> inflammatory response

chronic pneumonitis and fibrosis
acute hypersensitivity
non-cardiogenic pulmonary edema

58
Q

Clinical diagnosis of bleomycin induced lung injury

A 
dyspnea
dry cough
low grade fever
fatigue
malaise
^all of these develop over weeks to months

XRAY w/diffuse interstitial infiltrates

59
Q

Bleomycin treatment

A

stop it duh and give steroids

60
Q

Anesthesia management of bleomycin

A 
monitor O2
ABG
pre-oxygenate 3-4 minutes
use minimum O2 to target PaO2
PEEP +
judicious use of fluids

*low volumes, high RR (this will increase deadspace tho)

61
Q

Methotrexate (RA drug)

A

causes cytotoxic injury
acute pulmonary toxicity is more common
s/s: dry cough, dyspnea, hypoxemia, infiltrates

62
Q

Oxygen toxicity

A

-advanced age, prolonged exposure, radiation, chemo

63
Q

Clinical features of oxygen toxicity

A
  • may begin w/i 6 hours, chest pain on inspiration, tachypnea non-productive
  • by 24h, paresthesia, anorexia, nausea, and headache
  • decreased tracheal mucus, decreased VC & pulmonary compliance, and diffusing capacity and increased A-a
64
Q

Anesthetic management of oxygen toxicity

A

judicious use of O2, PEEP, corticoid steroids

65
Q

Sarcoidosis RF

A

age 20 - 40, african americans

66
Q

Pathophysiology of sarcoidosis

A

Unclear cause; characterized by the presence of epithelioid-cell granulomata

67
Q

How do you manage sarcoidosis?

A

corticosteroids

68
Q

Chronic extrinsic

A

non-traumatic (obesity, pregnancy, sk/nm d/o)

traumatic (flail chest, pneumothorax, pleural effusion)

69
Q

Pectus excavatum

A

most common chest wall deformity (nuss procedure)

higher incidence (CHD, asthma)

70
Q

Pectus carinatum

A

longitudinal protrusion of the sternum

increased risk of incidence of CHD

71
Q

Scoliosis

A

most common spinal deformity

  • 25% of patients have concomitant congenital abnormalities (MV prolapse most common)
  • VC and FEV1 < 50% suggest postoperative complications
72
Q

Cobb Angle

A

What determines the severity of scoliosis

> 60 degrees (diminished pulmonary function)
70 degrees (pulmonary symptoms develop)
110 degrees (significant gas exchange impairment)

73
Q

Ankylosing Spondylitis

A

Marie-Strumpell disease - chronic inflammatory disorder of the spine

etiology: unclear

74
Q

Ankylosing spondylitis is most common

75
Q

s/s ankylosing spondylitis

A

pain, stiffness, fatigue

76
Q

cardiac complications of ankylosing spondylitis (4)

A

aortic valve dx
conduction disturbence
ischemia heart disease
cardiomyopathies

77
Q

pulmonary complications of ankylosing spondylitis

A 
apical fibrosis
interstitial lung dx
chest wall restriction
sleep apnea
spontaneous pneumothorax
70% 
*cricoarytenoid involvement*
78
Q

cervical spondylosis

A

can entrap nerves and affect the diaphragm

79
Q

Anesthetic management of ankylosing spondylitis

A

most are asymptomatic

  • upper airway management
  • limited cervical ROM
  • regional?
  • CV complications
  • positioning
80
Q

flail chest

A

paradoxical movement of the chest wall at the site of the fracture leads to limited alveolar ventilation and subsequent

  • hypoventilation
  • hypercapnia
  • alveolar collapse
81
Q

flail chest anesthetic considerations

A

pain control (block?)

82
Q

pneumothorax

A

simple: no communication w/atmosphere
communicating: air in pleural cavity exchanges w/atmospheric air
tension: air progressively accumulates under pressure with the pleural cavity

83
Q

pneumothorax treatment

A

simple: just observe
communicating: dressing, oxygen, thoracotomy tube, intubate & ventilate ?
nitrous oxide???

84
Q

tension pneumothorax (3)

A

true medical emergency
compression of contralateral lung & great vessels
decreased VR, CO, BP
shunting of blood to non-ventilated areas

85
Q

tension pneumo hallmark signs

A

hypotension
tachycardia
increased CVP
increased airway pressure

86
Q

atelectasis patho (3)

A

blockage of airways
loss of diaphragmatic tone under GA
maldistribution of ventilation on PPV

87
Q

pleural effusion types (4)

A 
abnormal collection of fluid in pleural space
hydrothorax
empyema (infection)
hemothorax (blood)
chylothorax (lipids)
88
Q

name 3 types of hydrothorax

A

blockage of lymphatic drainage
cardiac failure
reduction in plasma colloid osmotic pressure

89
Q

obesity

A

direct weight added to the rib cage

indirect by abdominal panniculus

90
Q

clinical features obesity & respiration

A

shallow, rapid breathing –> hypercapnia

91
Q

treatment for obese resp. distress pt

A

cpap

weight management….

92
Q

anesthetic management of obese pt

A

I:E (1:1)
adjust Ve to accomodate higher RR
Maintain PIP

93
Q

pregnancy leads to RLD through (3) mechanisms

A
  1. changes in thorax (increase subcostal angle & circumference, cranial displacement of diaphragm)
  2. decrease in FRC
  3. RV is increased
94
Q

neurogenic

A

characterized by expiratory muscle weakness; inefficient diaphragm; weak swallowing muscles

Physiology (5 decks)

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