Restrictive Lung Disease Flashcards
1
Q
Principle Features of RLD
A
reduction in total lung capacity
decrease in all lung volumes and capacities
normal FEV1/FVC ratio (ability to exhale unchanged)
reduced diffusing capacity of carbon monoxide (DLCO), which also means decrease in O2 diffusion capacity
2
Q
Classification of RLD by TLC
mild
moderate
severe
A
Mild 65-80% of predicted TLC
moderate 50-65% of predicted TLC
severe less than 50% of predicted TLC
3
Q
cardiogenic pulmonary edema pathophysiology
A
left sided incompetence or failure increases pulmonary capillary pressure until rate of fluid transudation exceeds lymphatic drainage resulting in alveolar flooding.
- excessive arterial pressure, hydrostatic issue
- more (+) than usual NFP
4
Q
cardiogenic pulmonary edema clinical signs
A
rapid shallow breathing not relieved by O2
SNS stimulation including HTN, tachycardia, diaphoresis
5
Q
non cardiogenic pulmonary edema primary pathophysiological etiology and reasons it can occur
A
primarily a filtration issue. “flooded lymph”
neurogenic, uremic, high altitude, upper airway obstruction- causes
6
Q
negative pressure pulmonary edema cause
A
caused by upper airway obstruction with a prolonged, forceful inspiratory effort against an obstructed upper airway in spontaneously breathing patients.
7
Q
most common cause of negative pressure pulmonary edema?
A
laryngospasm
8
Q
signs/symptoms of negative pressure pulmonary edema
A
intense SNS stimulation increase in afterload hypertension central volume displacement rapid/shallow breathing
9
Q
predisposing factors to negative pressure pulmonary edema (6)
A
male young long period of obstruction overzealous fluid administration hx cardiac disease hx pulmonary disease
10
Q
onset of negative pressure pulmonary edema. is pedema a medical emergency?
A
a few minutes to several hours. yes it is a medical emergency and requires immediate intervention
11
Q
early recognition of pulmonary edema includes
A
tachypnea sympathetic stress stimulation hypoxemia with low PaCO2 initially increased CVP, JVD, gallop lung auscultation CXR most reliable and expedient tool
12
Q
anesthetic management of pulmonary edema
A
O2
PEEP or CPAP
pharmacologic therapy (decrease preload with vasodilator maybe)
fluid balance (ex diuretic)
13
Q
3 aspiration syndromes
A
chemical pneumonitis (mendelsons) mechanical obstruction bacterial infection
14
Q
normal amount of clear liquid in stomach of humans
A
1.5ml/kg
15
Q
how does mendelsons syndrome present
A
produces asthma like syndrome
16
Q
predisposing factors to mendelsons syndrome
A
abdominal pathology, obesity, diabetes, neurologic deficit, lithotomy position, difficult intubation, reflux disease, hiatal hernia, inadequate anesthesia, c section, GB, diseases that impair surgery, laparotomy aka type of surgery
17
Q
greatest frequency of occurrence for mendelsons syndrome
A
intubation
emergence
18
Q
mendelsons syndrome pathophysiology
A
aspirated substance causes lung parenchyma injury, inflammatory reaction, secondary injury in 24 hours
19
Q
clinical feature of mendelsons syndrome
A
arterial hypoxemia
20
Q
anesthetic considerations regarding mendelsons syndrome
A
risk factors, NPO standards, pharmacologic prophylaxis, carotid pressure, awake intubation, regional anesthetic
21
Q
treatment of mendelsons syndrome
A
tilt head down or turn rapid suction of mouth or pharynx (tracheal suction NOT indicated) supplemental O2 PEEP abx possibly discharge appropriateness
22
Q
acute respiratory failure PaO2 and PaCO2
A
PaO2 < 60mmHg despite O2 supplementation (absence of R to L cardiac shunt)
PaCO2 >50mmHg in absence of respiratory compensation (abrupt change with corresponding decrease in pH)
23
Q
treatment of acute respiratory failure and 3 principle goals
A
directed at supporting oxygenation and ventilation
three principle goals: patent upper airway, correction of hypoxia, removal of excess CO2
24
Q
ARDS pathophysiology
A
severe damage and inflammation at the alveolar capillary membrane. increased capillary permeability and subsequent interstitial and alveolar edema
25
ARDS risk factors (4)
sepsis, pneumonia, trauma, aspiration pneumonitis. factors are additive, high mortality rate.
26
clinical features of ARDS
resembles pedema and aspiration pneumonitis: dyspnea, hypoxia, hypovolemia, lung stiffness
27
ARDS tx
supportive care, no definitive treatment
28
ARDS: Berlin Definition
lung injury of acute onset with one week of apparent clinical insult and progression of pulmonary symptoms. bilateral opacities on imaging not explainable by other pathology. resp failure also cannot be explained by cardiac volume or overload. also characterized by decreased PaO2/FiO2 ratio
29
ARDS Classification based on PaO2/FiO2 ratio
mild: 201-300
moderate: 101-200
severe: <101
30
ARDS anesthetic considerations
patient evaluation is key including current vent settings
protective ventilation including open lung strategy
permissive hypercapnea
PEEP
prone positioning increases SA for gas exchange
31
TRALI pathophysiology
acute lung injury associated with blood transfusion. secondary to interaction between transfusion and WBC's. activated neutrophils become trapped within pulmonary microvsculature, leading to non cardiogenic pedema.
32
predisposing factors (6) and greatest incidence of TRALI
greatest incidence after platelet transfusions
| predisposing factors: surgery, malignancy, sepsis, alcoholism, liver disease, donor risk factors
33
TRALI clinical feature
acute onset and hypoxemia
34
treatment of TRALI
supportive, includes lung protective ventilation strategies
35
anesthetic management of TRALI
```
stop transfusion immediately
R/O incompatibility reaction, TACO
IV fluids
diuretics
ventilation support
lab findings
```
36
neurogenic acute intrinsic restrictive pulmonary problem: think head injury
increase in SNS outflow, increased after load, pulmonary edema ensues
37
high altitude acute intrinsic restrictive pulmonary problem
decreased partial pressure at high altitudes exacerbates pulmonary edema
38
type 1 epithelial cells in lung parenchyma
structural cell: mechanical support, not active metabolically
39
type 2 epithelial cells in lung parenchyma
globular cell: little support, metabolically active surfactant producers, rapidly reproduce in response to injury
40
alveolar macrophages in lung parenchyma
scavenger cell: contains lysosomes that digest engulfed matter
41
fibroblasts in lung parenchyma
collagen and elastin synthesizing cell. chronic insult to these result in fibrosis, since its responsible for structural support
42
thin side of interstitium
fused basement of alveolar epithelial and capillary endothelial layers, responsible for gas exchange
43
thick side of interstitium
includes type 1 collagen, responsible for fluid exchange
44
principle feature of pulmonary fibrosis
thickening of interstitium of alveolar wall
45
other pathophysiological changes related to pulmonary fibrosis
infiltration of lymphocytes
fibroblasts increase collagen bundles
cellular exudate seen within alveoli- "desquamation"
thickening of interstitium leads to decreased O2 diffusion
-alveolar architecture destroyed and scarring results
46
clinical features of pulmonary fibrosis
dyspnea
rapid shallow breathing that worsens with exercise
crackles on lung auscultation bilaterally
finger clubbing
CXR: reticulonodular pattern, patchy shadows at base
cor pulmonale in advanced stages
47
idiopathic pulmonary fibrosis usually affects which age range
50-70's
48
Idiopathic Pulmonary Fibrosis related to:
arterial PO2
arterial PCO2
pH
arterial PO2 and PCO2 are reduced but pH is normal, therefore hypoxemia is mild at rest but PO2 falls drastically with exercise
49
how to diagnose pulmonary fibrosis
DLCO. diffusion capacity of carbon monoxide will be very low.
closer to 5ml/min/mmHg when normal 25-30
-this means VQ mismatch expected
50
Idiopathic Pulmonary Fibrosis: what to expect on pulmonary function studies
decreased FVC with normal FEV1/FVC
normal FEF25-75%
flow volume curve is smaller and shifted to the right
pressure volume curve flattened and displaced downward
51
non cytotoxic injury: amiodarone etiology
direct toxicity, immunologic mechanisms, activation of RAAS. takes form of chronic interstitial pneumonitis, pneumonia, ARDS, or fibrosis mass.
52
non cytotoxic injury: amiodarone clinical diagnosis
two or more of the following: new onset pulmonary symptoms, new X-ray abnormalities, decrease in DLCO, abnormal gallium 67 uptake, histologic changes note in lung biopsy
53
non cytotoxic injury: amiodarone treatment
```
stop drug (t1/2 40-70 days)
if fibrosis occurs, it is irreversible
```
54
cytotoxic injury: bleomycin etiology
direct toxicity, inflammatory response. chronic pneumonitis and fibrosis, acute hypersensitivity, non cardiogenic pulmonary edema
55
cytotoxic injury: bleomycin clinical diagnosis
dyspnea, dry cough, low grade fever, fatigue, malaise developing over weeks to months, tachypnea. X-ray with diffuse interstitial infiltrates
-if caught early enough, patient will recover
56
cytotoxic injury: bleomycin treatment
```
discontinue agent (if early enough, patient will recover)
corticosteroid therapy
```
57
cytotoxic injury: bleomycin anesthetic management
```
monitor oxygen saturation
ABG analysis
preoxygenate 3-4 minutes
pre determine target PaO2, then use minimum FiO2 to achieve it
PEEP
judicious use of fluids
```
58
cytotoxic injury: methotrexate use and pulmonary sequelae
used for RA, acute pulmonary toxicity more common
59
cytotoxic injury: methotrexate clinical signs
dry cough, dyspnea, hypoxemia, infiltrates on CXR
60
cytotoxic injury: methotrexate treatment
discontinue agent
61
oxygen toxicity predisposing factors
advanced age
prolonged exposure
radiation therapy
chemotherapy agents
62
oxygen toxicity pathophysiology
excessive production of free oxygen radicals causes damage to cells
63
oxygen toxicity clinical features:
at 6 hours
at 24 hours
physiologic changes
may begin within 6 hours of exposure, chest pain on inspiration, tachypnea, non productive cough
by 24 hours, paresthesia, anorexia, nausea, headache
physiologic changes include decreased tracheal mucous, VC, pulmonary compliance, diffusing capacity. increased PAO2-PaO2 gradient
64
oxygen toxicity anesthetic management
judicious use of O2
PEEP
corticosteroid therapy
65
Sarcoidosis pathophysiology
cause is unclear, disease is characterized by presence of epithelioid cell granulomata. is a systemic problem.
66
sarcoidosis predisposing factors
ages 20-40, AA
67
sarcoidosis management
corticosteroids. sometimes it resolves spontaneously, sometimes it doesnt.
68
sarcoidosis signs/symptoms
dry eyes, blurry vision, enlarged lymph nodes, hacking cough, cough up blood, cardiac complications, liver and spleen enlargement, joint pain/arthritis/swelling of knees, rashes, lupus permit, erythema nodosum, skin lesions on back, SQ nodules
69
Pectus Excavatum
sx
tx
most common chest wall deformity
can be corrected with NUSS procedure
increased incidence of congenital heat disease, asthma
surgery is only effective tx
70
pectus carinatum
longitudinal protrusion of sternum
associated with increased incidence of congenital heart disease
surgery is only effective treatment
71
kyphosis
accentuated posterior curvature of the spine
unless the deformity is severe, patients usually able to maintain normal respiratory function
anesthetic considerations: supportive positioning with pillows
72
scoliosis
sx
VC/FEV1
deformity of the spinal column resulting in lateral curvature and rotation of spine and rib cage. most common spine deformity. 25% of patients have concomitant congenital abnormalities, mitral valve prolapse most common.
VC and FEV1<50% suggest postop pulmonary complications
severity determined by cobb angle
73
Cobb angle
>60 degrees, diminished pulmonary function
>70 degrees, pulmonary symptoms develop
>110 degrees, significant gas exchange impairment
the greater the curvature, the greater the loss of pulmonary function. this is how the surgeon decides when surgery is necessary. is respiratory compromise is severe, they will likely stay intubated postoperatively
74
Ankylosing Spondylitis cause and most common patient population
cause is unclear, most common in white males under 40
75
clinical signs of ankylosing spondylitis
pain, stiffness, fatigue
76
cardiac complications related to ankylosing spondylitis
aortic valve disease, conduction disturbance, ischemic heart disease, cardiomyopathy
77
pulmonary complications (~70%) of ankylosing spondylitits
```
apical fibrosis (distinguishing feature that shows up on CXR's)
interstitial lung disease
chest wall restriction
sleep apnea
spontaneous pneumothorax
```
78
ankylosing spondylitis anesthetic considerations
cervical spondylosis can entrap nerves and affect diaphragm
can cause cricoaretynoid involvement. manifests as weak, hoarse voice
c-spine and airway issues can happen
consider regional and no intubation if possible
upper airway management huge
also consider positioning (at risk for neuropathies, pressure ulcers, brachial plexus stretch)
CV complications can be precipitated
let them position themselves since usually theyre in pain
79
Flail Chest signs/symptoms
hypoventilation, hypercapnia, progressive alveolar collapse. they dont want to breathe because its painful
80
flail chest anesthetic considerations
pain control: intercostal nerve block, epidural catheter, erector spinae block
81
pneumothorax types (3)
simple, communicating, tension
82
simple pneumothorax definition and treatment
no communication with the atmosphere. no shift in mediating or diaphragm
-tx- observation is key. aspiration or thoracotomy tube
83
communicating pneumothorax definition and tx
air in pleural cavity exchanges with atmospheric air
| -tx: 3 sided dressing, O2, thoracotomy tube, intubation/ventilation
84
tension pneumothorax definition
true medical emergency. air progressively accumulates under pressure with the pleural cavity
85
increased intrathoracic pressure from tension pneumothorax causes:
compression of contralateral lung and great vessels, decreased venous return, decreased CO, decreased BP, shunting of blood to non ventilated areas
86
hallmark signs of tension pneumothorax
hypotension, tachycardia, increased CVP and increased airway pressure, JVD
87
treatment of tension pneumothorax
needle decompression with large bore 16g IV in 2-3rd ICS
88
hemothorax etiology and anesthetic considerations
result of trauma or disease process
anesthetic considerations include airway management, restoration of circulating volume, evacuation of accumulated blood, maybe thoracotomy
89
atelectasis incidence, pathophysiology
occurs universally under GA, pathophysiology includes blockage of airways, loss of diaphragmatic tone under GA, maldistribution of ventilation on PPV
90
pleural effusion types (4), s/sx
hydrothorax, empyema, hemothorax, chylothorax
| can't hear tympany
91
hydrothorax
blockage of lymphatic drainage, cardiac failure, reduction in plasma colloid osmotic pressure
92
empyema
infection
93
chylothorax
lipids
94
pleural effusion treatment
thoracotomy tube, thoracentesis, pleurodesis
95
obesity clinical features and treatment
shallow rapid breathing results in hypercapnia
| treatment: weight management, CPAP
96
obesity anesthetic management
ventilation strategies, I:E ratio with BMI cutoff 40
adjust MV to accommodate higher RR
maintain PIP
bring CPAP if OSA
97
pregnancy
RLD r/t changes in thorax, increases in subcostal angle and circumference, cranial displacement of diaphragm, decrease in FRC, increase in RV
-denitrogenate the shit out of mom, because if you're putting her to sleep, shit probably isn't going great. also, she will have an edematous airway and a full stomach
98
neurogenic RLD r/t GB/MG
expiratory muscle weakness, inability to cough forcefully, absence of abdominal tone leads to inefficient diaphragm, weakness of swallowing muscles may lead to aspiration. decreased FRC also seen.
99
surgical reasons for RLD
anesthetic medications
patient positioning
pneumoperitoneum
