Restrictive Lung Diseases Flashcards
(94 cards)
1
Q
What are the four types of RLD?
A
- Acute intrinsic
- Chronic intrinsic
- Chronic extrinsic
- Other (obesity)
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*
3
Q
Principle features of RLD (4)
A
reduction in TLC
decrease in all lung volumes & capacities
NORMAL FEV1/FVC RATIO
reduced DLCO
4
Q
Classification of RLD by TLC
A
65-80 % = mild
50 - 65% = moderate
< 50% = severe
5
Q
Vt
A
500 mL
6
Q
IRV
A
3000 mL
7
Q
IC
A
3500 mL
8
Q
ERV
A
1100 mL
9
Q
RV
A
1200 mL
10
Q
FRC
A
2300 mL
11
Q
VC
A
4600 mL
12
Q
TLC
A
5800 mL
13
Q
Acute intrinsic (define; anesthesia considerations)
A
abnormal movement of intravascular fluid
- lung volume:
- anesthetic considerations: not relieved by oxygen, HTN, tachycardia, diaphoresis
14
Q
Chronic intrinsic
A
pulmonary fibrosis
- lung volume:
- anesthetic considerations:
15
Q
Chronic extrinsic
A
traumatic vs non-traumatic
- lung volume:
- anesthetic considerations:
16
Q
Pulmonary edema
A
ACUTE INTRINSIC
- cardiogenic pulmonary edema = butterfly pattern on CXR; hydrostatic
- non-cardiogenic pulmonary edema = hydrostatic, permeability
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
18
Q
S/S Cardiogenic PUlmonary edema
A
rapid, shallow breathing not relieved by oxygen.
htn, tachycardia, diaphoresis
19
Q
Non-cardiogenic pulmonary edema
A
Elevated Pc
K changed
causes: neurogenic, uremic, high-altitude, upper airway obstruction
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
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
22
Q
NPPE RF
A
male, young, overzealous fluid admin, hx cardiac or pulmonary dx
23
Q
NPPE onset
A
minutes - hours
24
Q
Treatment of NPPE
A
oxygen will not help (but we still give it)
PEEP or CPAP
vasodilator to decrease preload
optimize fluids
25
Non-cardiogenic pulmonary edema examples (4)
aspiration pneumonitis
pneumonia
ARDS
TRALI
26
What are the three aspiration syndromes?
chemical pneumonitis (mendelson's syndrome), mechanical obstruction, bacterial infection
27
What is mendelson's syndrome?
pneumonitis from perioperative aspiration producing an asthma-like syndrome
*pharmacologic prophylaxis doesn't change outcome*
greatest frequency during intubation or emergence
28
RF for mendelson's syndrome
```
abdominal pathology, obesity, hiatal hernia
DM, neuro deficit
lithotomy, c-section
difficult intubation
GERD
inadequate anesthesia
```
29
Pathophys of mendelson's syndrome
aspirated substance --> lung parenchyma injury --> inflammation --> secondary injury in 24h
30
Clinical features of mendelson's syndrome
arterial hypoxemia *give CPAP*
31
anesthetic considerations for mendelson's syndrome
RF, NPO standards, pharm prophylaxis, cricoid pressure, awake intubation, regional
32
Mendelson Treatment
1. tilt head down or turn
2. rapid suction of mouth/pharynx
3. supplemental O2
4. PEEP (APL valve)
5. Abx not recommended
33
Acute Respiratory Failure
PaO2 < 60 mmHg despite O2 supplementation
PaCO2 > 50 mmHg in absence of respiratory compensation
most common cause --> ARDS
34
ARDS goals (3)
patent upper airway
correct hypoxia
remove CO2
35
ARDS physiology
insult to A/C membrane causing increased capillary permeability and subsequent interstitial and alveolar edema
36
ARDS RF
sepsis, pneumonia, trauma, aspiration
37
S/S ARDS (4)
dyspnea, hypoxia, hypovolemia, lung stiffness
38
ARDS definition
-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
TRALI
- 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
TRALI RF
sx, malignancy, sepsis, alcoholism, liver dx
41
TRALI management
1. stop tx
2. r/o incompatibility reaction/TACO
3. IV fluids
4. diuretics
5. vent support
6. lab findings
42
Neurogenic pulmonary edema
severe head injury causing massive sympathetic outflow
43
Chronic Intrinsic RLD (5)
- autoimmune (sarcoidosis)
- cytotoxic and non-cytotoxic drug exposure
- oxygen toxicity
- idiopathic pulmonary fibrosis
- radiation injury
44
Lung Parenchyma (4 cell types)
- 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
Interstitium Thin Side
fused basement of epithelial and endothelial layers
responsible for gas exchange
46
Interstitium Thick side
type I collagen
| responsible for fluid exchange
47
Idiopathic Pulmonary Fibrosis pathophys (3)
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
Clinical features of idiopathic pulmonary fibrosis
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
Lab values w/idiopathic pulmonary fibrosis
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
normal diffusion capacity of CO
25 - 30 mL/m
51
Idiopathic pulmonary fibrosis PFTs
FVC: decreased
FEV1/FVC: normal
FEF 25 - 75: normal
52
Idiopathic pulmonary fibrosis pressure-volume curve
flattened and displaced downward
53
Drug induced pulmonary dx
cytotoxic (CA drugs)
| non-cytotoxic (amiodarone)
54
Amiodarone
etiology: direct toxicity, immunologic mechanisms, activates RAS
* takes form of chronic interstitial pneumonitis, pneumonia, ARDS or fibrosis mass
55
Amiodarone non-cytotoxic injury diagnosis
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
Treatment of amio induced pulmonary dx
stop drug - half-life 40 - 70 days
| if fibrosis occurs, it is IRREVERSIBLE
57
Bleomycin
antitumor abx that causes cytotoxic injury directly --> inflammatory response
chronic pneumonitis and fibrosis
acute hypersensitivity
non-cardiogenic pulmonary edema
58
Clinical diagnosis of bleomycin induced lung injury
```
dyspnea
dry cough
low grade fever
fatigue
malaise
^all of these develop over weeks to months
```
XRAY w/diffuse interstitial infiltrates
59
Bleomycin treatment
stop it duh and give steroids
60
Anesthesia management of bleomycin
```
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
Methotrexate (RA drug)
causes cytotoxic injury
acute pulmonary toxicity is more common
s/s: dry cough, dyspnea, hypoxemia, infiltrates
62
Oxygen toxicity
-advanced age, prolonged exposure, radiation, chemo
63
Clinical features of oxygen toxicity
- 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
Anesthetic management of oxygen toxicity
judicious use of O2, PEEP, corticoid steroids
65
Sarcoidosis RF
age 20 - 40, african americans
66
Pathophysiology of sarcoidosis
Unclear cause; characterized by the presence of epithelioid-cell granulomata
67
How do you manage sarcoidosis?
corticosteroids
68
Chronic extrinsic
non-traumatic (obesity, pregnancy, sk/nm d/o)
| traumatic (flail chest, pneumothorax, pleural effusion)
69
Pectus excavatum
most common chest wall deformity (nuss procedure)
higher incidence (CHD, asthma)
70
Pectus carinatum
longitudinal protrusion of the sternum
*increased risk of incidence of CHD*
71
Scoliosis
most common spinal deformity
- 25% of patients have concomitant congenital abnormalities (MV prolapse most common)
- VC and FEV1 < 50% suggest postoperative complications
72
Cobb Angle
What determines the severity of scoliosis
> 60 degrees (diminished pulmonary function)
> 70 degrees (pulmonary symptoms develop)
> 110 degrees (significant gas exchange impairment)
73
Ankylosing Spondylitis
Marie-Strumpell disease - chronic inflammatory disorder of the spine
etiology: unclear
74
Ankylosing spondylitis is most common
men < 40
75
s/s ankylosing spondylitis
pain, stiffness, fatigue
76
cardiac complications of ankylosing spondylitis (4)
aortic valve dx
conduction disturbence
ischemia heart disease
cardiomyopathies
77
pulmonary complications of ankylosing spondylitis
```
apical fibrosis
interstitial lung dx
chest wall restriction
sleep apnea
spontaneous pneumothorax
70%
*cricoarytenoid involvement*
```
78
cervical spondylosis
can entrap nerves and affect the diaphragm
79
Anesthetic management of ankylosing spondylitis
most are asymptomatic
* upper airway management
* limited cervical ROM
* regional?
* CV complications
* positioning
80
flail chest
paradoxical movement of the chest wall at the site of the fracture leads to limited alveolar ventilation and subsequent
- hypoventilation
- hypercapnia
- alveolar collapse
81
flail chest anesthetic considerations
pain control (block?)
82
pneumothorax
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
pneumothorax treatment
simple: just observe
communicating: dressing, oxygen, thoracotomy tube, intubate & ventilate ?
nitrous oxide???
84
tension pneumothorax (3)
true medical emergency
compression of contralateral lung & great vessels
decreased VR, CO, BP
shunting of blood to non-ventilated areas
85
tension pneumo hallmark signs
hypotension
tachycardia
increased CVP
increased airway pressure
86
atelectasis patho (3)
blockage of airways
loss of diaphragmatic tone under GA
maldistribution of ventilation on PPV
87
pleural effusion types (4)
```
abnormal collection of fluid in pleural space
hydrothorax
empyema (infection)
hemothorax (blood)
chylothorax (lipids)
```
88
name 3 types of hydrothorax
blockage of lymphatic drainage
cardiac failure
reduction in plasma colloid osmotic pressure
89
obesity
direct weight added to the rib cage
| indirect by abdominal panniculus
90
clinical features obesity & respiration
shallow, rapid breathing --> hypercapnia
91
treatment for obese resp. distress pt
cpap
| weight management....
92
anesthetic management of obese pt
I:E (1:1)
adjust Ve to accomodate higher RR
Maintain PIP
93
pregnancy leads to RLD through (3) mechanisms
1. changes in thorax (increase subcostal angle & circumference, cranial displacement of diaphragm)
2. decrease in FRC
3. RV is increased
94
neurogenic
characterized by expiratory muscle weakness; inefficient diaphragm; weak swallowing muscles
