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N932 Pathophysiology > Restrictive Lung Disease > Flashcards

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

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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

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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
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4
Q

cardiogenic pulmonary edema clinical signs

A

rapid shallow breathing not relieved by O2

SNS stimulation including HTN, tachycardia, diaphoresis

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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

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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.

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7
Q

most common cause of negative pressure pulmonary edema?

A

laryngospasm

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8
Q

signs/symptoms of negative pressure pulmonary edema

A 
intense SNS stimulation
increase in afterload
hypertension
central volume displacement
rapid/shallow breathing
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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
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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

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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
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12
Q

anesthetic management of pulmonary edema

A

O2
PEEP or CPAP
pharmacologic therapy (decrease preload with vasodilator maybe)
fluid balance (ex diuretic)

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13
Q

3 aspiration syndromes

A 
chemical pneumonitis (mendelsons)
mechanical obstruction
bacterial infection
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14
Q

normal amount of clear liquid in stomach of humans

A

1.5ml/kg

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15
Q

how does mendelsons syndrome present

A

produces asthma like syndrome

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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

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17
Q

greatest frequency of occurrence for mendelsons syndrome

A

intubation

emergence

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18
Q

mendelsons syndrome pathophysiology

A

aspirated substance causes lung parenchyma injury, inflammatory reaction, secondary injury in 24 hours

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19
Q

clinical feature of mendelsons syndrome

A

arterial hypoxemia

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20
Q

anesthetic considerations regarding mendelsons syndrome

A

risk factors, NPO standards, pharmacologic prophylaxis, carotid pressure, awake intubation, regional anesthetic

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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
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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)

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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

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24
Q

ARDS pathophysiology

A

severe damage and inflammation at the alveolar capillary membrane. increased capillary permeability and subsequent interstitial and alveolar edema

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25
Q

ARDS risk factors (4)

A

sepsis, pneumonia, trauma, aspiration pneumonitis. factors are additive, high mortality rate.

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26
Q

clinical features of ARDS

A

resembles pedema and aspiration pneumonitis: dyspnea, hypoxia, hypovolemia, lung stiffness

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27
Q

ARDS tx

A

supportive care, no definitive treatment

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28
Q

ARDS: Berlin Definition

A

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

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29
Q

ARDS Classification based on PaO2/FiO2 ratio

A

mild: 201-300
moderate: 101-200
severe: <101

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30
Q

ARDS anesthetic considerations

A

patient evaluation is key including current vent settings
protective ventilation including open lung strategy
permissive hypercapnea
PEEP
prone positioning increases SA for gas exchange

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31
Q

TRALI pathophysiology

A

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.

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32
Q

predisposing factors (6) and greatest incidence of TRALI

A

greatest incidence after platelet transfusions

predisposing factors: surgery, malignancy, sepsis, alcoholism, liver disease, donor risk factors

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33
Q

TRALI clinical feature

A

acute onset and hypoxemia

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34
Q

treatment of TRALI

A

supportive, includes lung protective ventilation strategies

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35
Q

anesthetic management of TRALI

A 
stop transfusion immediately
R/O incompatibility reaction, TACO
IV fluids
diuretics
ventilation support
lab findings
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36
Q

neurogenic acute intrinsic restrictive pulmonary problem: think head injury

A

increase in SNS outflow, increased after load, pulmonary edema ensues

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37
Q

high altitude acute intrinsic restrictive pulmonary problem

A

decreased partial pressure at high altitudes exacerbates pulmonary edema

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38
Q

type 1 epithelial cells in lung parenchyma

A

structural cell: mechanical support, not active metabolically

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39
Q

type 2 epithelial cells in lung parenchyma

A

globular cell: little support, metabolically active surfactant producers, rapidly reproduce in response to injury

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40
Q

alveolar macrophages in lung parenchyma

A

scavenger cell: contains lysosomes that digest engulfed matter

41
Q

fibroblasts in lung parenchyma

A

collagen and elastin synthesizing cell. chronic insult to these result in fibrosis, since its responsible for structural support

42
Q

thin side of interstitium

A

fused basement of alveolar epithelial and capillary endothelial layers, responsible for gas exchange

43
Q

thick side of interstitium

A

includes type 1 collagen, responsible for fluid exchange

44
Q

principle feature of pulmonary fibrosis

A

thickening of interstitium of alveolar wall

45
Q

other pathophysiological changes related to pulmonary fibrosis

A

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
Q

clinical features of pulmonary fibrosis

A

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
Q

idiopathic pulmonary fibrosis usually affects which age range

A

50-70’s

48
Q

Idiopathic Pulmonary Fibrosis related to:
arterial PO2
arterial PCO2
pH

A

arterial PO2 and PCO2 are reduced but pH is normal, therefore hypoxemia is mild at rest but PO2 falls drastically with exercise

49
Q

how to diagnose pulmonary fibrosis

A

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
Q

Idiopathic Pulmonary Fibrosis: what to expect on pulmonary function studies

A

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
Q

non cytotoxic injury: amiodarone etiology

A

direct toxicity, immunologic mechanisms, activation of RAAS. takes form of chronic interstitial pneumonitis, pneumonia, ARDS, or fibrosis mass.

52
Q

non cytotoxic injury: amiodarone clinical diagnosis

A

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
Q

non cytotoxic injury: amiodarone treatment

A 
stop drug (t1/2 40-70 days)
if fibrosis occurs, it is irreversible
54
Q

cytotoxic injury: bleomycin etiology

A

direct toxicity, inflammatory response. chronic pneumonitis and fibrosis, acute hypersensitivity, non cardiogenic pulmonary edema

55
Q

cytotoxic injury: bleomycin clinical diagnosis

A

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
Q

cytotoxic injury: bleomycin treatment

A 
discontinue agent (if early enough, patient will recover)
corticosteroid therapy
57
Q

cytotoxic injury: bleomycin anesthetic management

A 
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
Q

cytotoxic injury: methotrexate use and pulmonary sequelae

A

used for RA, acute pulmonary toxicity more common

59
Q

cytotoxic injury: methotrexate clinical signs

A

dry cough, dyspnea, hypoxemia, infiltrates on CXR

60
Q

cytotoxic injury: methotrexate treatment

A

discontinue agent

61
Q

oxygen toxicity predisposing factors

A

advanced age
prolonged exposure
radiation therapy
chemotherapy agents

62
Q

oxygen toxicity pathophysiology

A

excessive production of free oxygen radicals causes damage to cells

63
Q

oxygen toxicity clinical features:
at 6 hours
at 24 hours
physiologic changes

A

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
Q

oxygen toxicity anesthetic management

A

judicious use of O2
PEEP
corticosteroid therapy

65
Q

Sarcoidosis pathophysiology

A

cause is unclear, disease is characterized by presence of epithelioid cell granulomata. is a systemic problem.

66
Q

sarcoidosis predisposing factors

A

ages 20-40, AA

67
Q

sarcoidosis management

A

corticosteroids. sometimes it resolves spontaneously, sometimes it doesnt.

68
Q

sarcoidosis signs/symptoms

A

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
Q

Pectus Excavatum
sx
tx

A

most common chest wall deformity
can be corrected with NUSS procedure
increased incidence of congenital heat disease, asthma
surgery is only effective tx

70
Q

pectus carinatum

A

longitudinal protrusion of sternum
associated with increased incidence of congenital heart disease
surgery is only effective treatment

71
Q

kyphosis

A

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
Q

scoliosis
sx
VC/FEV1

A

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
Q

Cobb angle

A

> 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
Q

Ankylosing Spondylitis cause and most common patient population

A

cause is unclear, most common in white males under 40

75
Q

clinical signs of ankylosing spondylitis

A

pain, stiffness, fatigue

76
Q

cardiac complications related to ankylosing spondylitis

A

aortic valve disease, conduction disturbance, ischemic heart disease, cardiomyopathy

77
Q

pulmonary complications (~70%) of ankylosing spondylitits

A 
apical fibrosis (distinguishing feature that shows up on CXR's)
interstitial lung disease
chest wall restriction
sleep apnea
spontaneous pneumothorax
78
Q

ankylosing spondylitis anesthetic considerations

A

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
Q

Flail Chest signs/symptoms

A

hypoventilation, hypercapnia, progressive alveolar collapse. they dont want to breathe because its painful

80
Q

flail chest anesthetic considerations

A

pain control: intercostal nerve block, epidural catheter, erector spinae block

81
Q

pneumothorax types (3)

A

simple, communicating, tension

82
Q

simple pneumothorax definition and treatment

A

no communication with the atmosphere. no shift in mediating or diaphragm
-tx- observation is key. aspiration or thoracotomy tube

83
Q

communicating pneumothorax definition and tx

A

air in pleural cavity exchanges with atmospheric air

-tx: 3 sided dressing, O2, thoracotomy tube, intubation/ventilation

84
Q

tension pneumothorax definition

A

true medical emergency. air progressively accumulates under pressure with the pleural cavity

85
Q

increased intrathoracic pressure from tension pneumothorax causes:

A

compression of contralateral lung and great vessels, decreased venous return, decreased CO, decreased BP, shunting of blood to non ventilated areas

86
Q

hallmark signs of tension pneumothorax

A

hypotension, tachycardia, increased CVP and increased airway pressure, JVD

87
Q

treatment of tension pneumothorax

A

needle decompression with large bore 16g IV in 2-3rd ICS

88
Q

hemothorax etiology and anesthetic considerations

A

result of trauma or disease process
anesthetic considerations include airway management, restoration of circulating volume, evacuation of accumulated blood, maybe thoracotomy

89
Q

atelectasis incidence, pathophysiology

A

occurs universally under GA, pathophysiology includes blockage of airways, loss of diaphragmatic tone under GA, maldistribution of ventilation on PPV

90
Q

pleural effusion types (4), s/sx

A

hydrothorax, empyema, hemothorax, chylothorax

can’t hear tympany

91
Q

hydrothorax

A

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

92
Q

empyema

A

infection

93
Q

chylothorax

A

lipids

94
Q

pleural effusion treatment

A

thoracotomy tube, thoracentesis, pleurodesis

95
Q

obesity clinical features and treatment

A

shallow rapid breathing results in hypercapnia

treatment: weight management, CPAP

96
Q

obesity anesthetic management

A

ventilation strategies, I:E ratio with BMI cutoff 40
adjust MV to accommodate higher RR
maintain PIP
bring CPAP if OSA

97
Q

pregnancy

A

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
Q

neurogenic RLD r/t GB/MG

A

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
Q

surgical reasons for RLD

A

anesthetic medications
patient positioning
pneumoperitoneum

N932 Pathophysiology (4 decks)

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