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AS - N932 Advanced Pathology > Restrictive Lung Diseases > Flashcards

Restrictive Lung Diseases Flashcards

1
Q

Restrictive Lung Disease

A

RLD
Any condition that interferes w/ normal lung expansion during inspiration
↓total lung capacity (TLC)
↓ALL lung volumes & capacities
Normal FEV1/FVC ratio
Reduced diffusing capacity of carbon monoxide

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2
Q

TLC % in RLD

A

Mild 65-80% TLC
Moderate 50-65% TLC
Severe <50% TLC

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3
Q

Acute INtrinsic Causes

A

Pulmonary edema

  • Cardiogenic
  • Non-cardiogenic
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4
Q

Starling’s Law

A

Capillary hydrostatic pressure
Interstitial fluid hydrostatic pressure
Blood colloid osmotic pressure
Interstitial fluid colloid osmotic pressure

Arterial - net positive outflow
Venous - net negative inflow
Excess enters lymphatic system

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5
Q

Cardiogenic Pulmonary Edema

A

Acute INtrinsic RLD
L-sided heart incompetence or failure ↑pulmonary capillary pressure until fluid transudation exceeds lymph drainage → alveolar flooding

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6
Q

Cardiogenic Pulmonary Edema S/S

A 
Rapid, shallow breathing not relieved by O2
Sympathetic stimulation S/S
- Hypertension
- Tachycardia
- Diaphoresis
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7
Q

NON-Cardiogenic Pulmonary Edema

A 
Acute INtrinsic RLD
↑capillary hydrostatic pressure w/ change in fluid filtration coefficient
Causes:
- Neurogenic
- Uremic
- High altitude
- Upper airway obstruction
Lymph system overload → alveoli
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8
Q

Negative Pressure Pulmonary Edema

A

Acute INtrinsic RLD
Caused by prolonged, forceful inspiratory effort against an obstructed upper airway in spontaneously breathing patients
*Most common cause = laryngospasm

Intense sympathetic stimulation
↑afterload
Hypertension
Central volume displacement

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9
Q

Negative Pressure Pulmonary Edema

Risk Factors

A 
Male
Young age
Long obstruction period
Over zealous fluid admin
History cardiac or pulmonary disease
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10
Q

Negative Pressure Pulmonary Edema

Onset

A

Minutes to several hours

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11
Q

Negative Pressure Pulmonary Edema

S/S

A

Rapid and shallow breathing

See-saw breathing

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12
Q

Pulmonary Edema Management

A

Medical emergency
Early recognition = key

  • Oxygen
  • PEEP or CPAP
  • Pharmacologic therapy (vasodilator to ↓preload)
  • Fluid balance (goal-directed fluid therapy)
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13
Q

Pulmonary Edema S/S

A 
Tachypnea - sympathetic stress stimulation
Hypoxemia (low PaCO2 initially)
↑CVP
Jugular vein distension 
Lung auscultation
CXR = most reliable
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14
Q

NON-Cardiogenic Pulmonary Edema

Causes

A

Aspiration pneumonitis
Pneumonia
ARDS
TRALI

*Not typically anesthesia patients

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15
Q

Aspiration Pneumonitis

A 
NON-cardiogenic acute INtrinsic RLD
Three syndromes:
- Chemical (Mendelson's syndrome)
- Mechanical obstruction
- Bacterial infection
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16
Q

Mendelson’s Syndrome

A 
NON-cardiogenic acute INtrinsic RLD
*Anesthesia caused
Pneumonitis from periop aspiration
Produces an asthma-like syndrome
pH <2.5
Volume 25mL
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17
Q

Mendelson’s Risk Factors

A

Abdominal pathology, obesity, diabetes, neurologic deficit, lithotomy position, difficult intubation, reflux, hiatal hernia, inadequate anesthesia, cesarean section
→ Pharmacologic prophylaxis minimal impact
→ Most frequently occurs during induction/intubation & emergence

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18
Q

Mendelson’s Pathophysiology

A

Aspirated substance (acidic gastric contents) causes lung parenchyma injury, inflammatory reaction, & secondary injury in 24hr

→ Arterial hypoxemia

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19
Q

Mendelson’s Considerations

A 
Risk factors
NPO standards
Pharmacologic prophylaxis
Cricoid pressure (?)
Awake intubation
Regional anesthetic
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20
Q

Mendelson’s Treatment

A

Head down or lateral
Suction mouth or pharynx (tracheal suction NOT indicated)
Minimal supplemental O2
PEEP or bag-mask w/ APL
Antibiotics (not recommended)
Discharge dependent on patient disposition - potentially longer PACU stay or admit overnight depending on severity

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21
Q

Acute Respiratory Failure

A

NON-cardiogenic acute INtrinsic RLD
Inability to provide adequate O2 & eliminate CO2
PaO2 <60mmHg despite supplemental O2
PaCO2 >50mmHg w/o respiratory compensation
ARDS → acute respiratory failure

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22
Q

Acute Respiratory Failure

Treatment

A

GOAL = support oxygenation & ventilation

  1. Patent upper airway
  2. Correct hypoxia
  3. Remove excess CO2
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23
Q

ARDS

A

NON-cardiogenic acute INtrinsic RLD
Insult to the alveolar-capillary membrane causing ↑capillary permeability → interstitial & alveolar edema
Severe damage & inflammation at alveolar-capillary membrane

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24
Q

ARDS Risk Factors

A

Sepsis
Pneumonia
Trauma
Aspiration pneumonitis

Factors are additive
HIGH mortality rate

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25
Q

ARDS Clinical S/S

A

Resembles pulmonary edema & aspiration pneumonitis
Dyspnea, hypoxia, hypovolemia, ↓lung compliance

NO definitive treatment
Identify & treat cause
Supportive care

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26
Q

ARDS Berlin Definition

A

Acute onset lung injury
Apparent clinical insult & progression pulmonary S/S
Bilateral opacities on imaging (not explained by other pathology)
Respiratory failure not explained by cardiac or volume overload
↓arterial PaO2/FiO2 ratio

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27
Q

PaO2/FiO2 Ratio

A

P:F ratio
Arterial PO2 / FiO2 (fraction inspired)

MILD 201-300
MODERATE 101-200
SEVERE <100

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28
Q

ARDS Anesthetic Implications

A

Protective lung ventilation
“Open lung” strategy + pressure to prevent atelectasis
Permissive hypercapnia (?)
+PEEP
Prone positioning ↑surface area available for gas exchange

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29
Q

Transfusion Related Acute Lung Injury

A

TRALI
NON-cardiogenic acute INtrinsic RLD
Acute lung injury associated w/ blood transfusion
Occurs 2° to interaction b/w transfused blood & patient WBCs
*Highest incidence after platelet transfusion

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30
Q

TRALI Risk Factors

A 
Surgery
Malignancy
Sepsis
Alcoholism
Liver disease
Donor risk factors
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31
Q

TRALI Pathophysiology

A

Activated neutrophils become trapped w/in pulmonary vasculature → non-cardiogenic pulmonary edema

Associated w/ blood transfusion r/o transfusion associated circulatory overload (TACO)
Acute onset hypoxemia
Supportive treatment w/ LPV

32
Q

TRALI Anesthetic Implications

A 
STOP transfusion immediately
R/O incompatibility reaction or TACO
IV fluids
Diuretics (?)
Ventilation support
Lab findings
33
Q

Chronic INtrinsic RLD

A

Disease characterized by pulmonary fibrosis (stiff rubber band)

  • Idiopathic pulmonary fibrosis
  • Radiation injury
  • Cytotoxic & non-cytotoxic drug exposure
  • O2 toxicity
  • Autoimmune diseases (sarcoidosis)
34
Q

Type 1 Epithelial Cell

A

Lung parenchyma

Structural - mechanical support, not active metabolically

35
Q

Type 2 Epithelial Cell

A

Lung parenchyma
Globular cell - minimal support
Metabolically active - produce surfactant
Rapidly reproduce in response to injury

36
Q

Alveolar Macrophage

A

Lung parenchyma

Scavenger cell - contains lysosomes that digest engulfed matter

37
Q

Fibroblast

A

Lung parenchyma

Collagen & elastin synthesis cell

38
Q

Interstitium

A

Thin - fused basement epithelial & endothelial layers
→ Gas exchange

Thick - includes type 1 collagen
→ Fluid exchange

Continuous w/ perivascular space
Route fluid drains from capillaries to lymph

39
Q

Idiopathic Pulmonary Fibrosis

A

Chronic INtrinsic RLD
Presents as thickened alveolar wall interstitium
- Lymphocytes infiltration
- Fibroblasts ↑collagen bundles
- Cellular exudate w/in alveoli “desquamation”
Alveolar architecture destroyed & scarring results

40
Q

Idiopathic Pulmonary Fibrosis S/S

A 
Dyspnea:
- Rapid, shallow breathing
- Worsens w/ exercise
Mild hypoxemia at rest
Crackles bilaterally to auscultation
Finger clubbing
CXR:
- Reticulonodular pattern
- Patchy shadows at base
Cor pulmonale in advanced stages
↓arterial PO2 & PCO2
Normal pH
↓PO2 drastically w/ exercise
Oxygen diffusion limited d/t interstitium thickness
V/Q mismatch
↓diffusion capacity carbon monoxide 5mL/min/mmHg (normal 25-30mL/min/mmHg)
↓FVC (forced vital capacity)
Normal FEV1/FVC
Flow-volume curve shift to the R
Pressure-volume curve flattened & displaced downward
41
Q

Drug-Induced Pulmonary Disease

A 
Chronic INtrinsic RLD
Direct - toxic effects
Indirect - inflammation or immune process enhancement
Cytotoxic (cancer)
Non-cytotoxic
42
Q

Non-Cytotoxic Injury

A 
Chronic INtrinsic RLD
Amiodarone → ventricular dysrhythmic
Etiology - direct toxicity, immunologic mechanisms, RAAS activation → chronic interstitial pneumonitis, pneumonia, ARDS, or fibrosis
Clinical diagnosis (2+) 
- New onset pulmonary S/S, CXR abnormalities, ↓DLCO, abnormal gallium-67 uptake, histologic changes noted in lung biopsy
Treatment - discontinue 
Half-life 40-70 days
Fibrosis = irreversible
43
Q

Bleomycin

A

Chronic INtrinsic RLD - cytotoxic injury
Bleomycin → anti-tumor antibiotic
Etiology - direct toxicity & inflammatory response → chronic pneumonitis & fibrosis, acute hypersensitivity, non-cardiogenic pulmonary edema
Clinical diagnosis
- Dyspnea, dry cough, low-grade fever, fatigue, & malaise developing over weeks to months
- CXR w/ diffuse interstitial infiltrates
Treatment - discontinue & corticosteroid therapy

44
Q

Bleomycin Anesthesia Implications

A 
Monitor O2 saturation
ABG analysis
Pre-oxygenation 3-4min
Determine target PaO2 & utilize minimum FiO2 to achieve
\+PEEP
IV fluid management
45
Q

Methotrexate

A

Chronic INtrinsic RLD - cytotoxic injury
Used to treat rheumatoid arthritis
Acute pulmonary toxicity common → dry cough, dyspnea, hypoxemia, infiltrates
Treatment - discontinue

46
Q

Oxygen Toxicity

A

Chronic INtrinsic RLD
*Anesthesia caused
Risk factors - advanced age, prolonged exposure, radiation therapy, chemotherapy agents
Patho - excessive O2 free radicals production → damage to cells

47
Q

Oxygen Toxicity S/S

A

Begins w/in 6hr exposure
Chest pain on inspiration, tachypnea, non-productive cough
24hr paresthesia, anorexia, nausea, headache

Physiological changes ↓tracheal mucus, vital capacity, pulmonary compliance, & diffusion capacity, & ↑PAO2/PaO2

48
Q

Oxygen Toxicity

Anesthesia Management

A

Minimal FiO2
PEEP to maintain “open lung” (alveoli open & prevent atelectasis)
Corticosteroid therapy

49
Q

Autoimmune Disorders

A

Chronic INtrinsic RLD
→ Sarcoidosis
Characterized by multiple organ involvement & dysfunction

50
Q

Sarcoidosis

A

Chronic INtrinsic RLD
Predisposing factors: 20-40yo African Americans
Cause unclear - genetic component (?)
Patho - epithelioid-cell granulomata present → enlarged lymph nodes, scarring & granulomas, cough, liver/spleen enlargement, joint pain/swelling
Management - corticosteroids

51
Q

Chronic EXtrinsic RLD

A 
Non-traumatic
- Obesity
- Pregnancy
- Skeletal & neuromuscular disorders (1° kyphosis)
Traumatic
- Flail chest
- Pneumothorax
- Pleural effusion
52
Q

Skeletal Disorders

A 
NON-traumatic 
Chronic EXtrinsic RLD
- Pectus excavatum
- Pectus carinatum
- Kyphosis
- Scoliosis
53
Q

Pectus Excavatum

A

NON-traumatic chronic EXtrinsic RLD

  • Most common chest wall deformity
  • Nuss procedure
  • ↑incidence CHD & asthma
  • Only effective treatment = surgery
54
Q

Pectus Carinatum

A

NON-traumatic chronic EXtrinsic RLD

  • Longitudinal sternum protrusion
  • Associated w/ ↑incidence CHD
  • Only effective treatment = surgery
55
Q

Kyphosis

A

Most common skeletal disorder
NON-traumatic chronic EXtrinsic RLD
- Posterior spine curvature accentuated
- Patients able to maintain normal respiratory function unless severe deformity

56
Q

Scoliosis

A

NON-traumatic chronic EXtrinsic RLD

  • Spinal column deformity resulting in lateral curvature & rotation of the spin & rib cage
  • Most common spine deformity
  • 25% patients also have concomitant congenital abnormalities (mitral valve prolapse most common)
  • VC & FEV1 <50% → postop pulmonary complications
  • Severity determined by Cobb angle
57
Q

Cobb Angle

A

> 60 degrees = diminished pulmonary function
70 degrees = pulmonary symptoms develop
110 degrees = significant gas exchange impairment
↑curvature ↑pulmonary function LOSS

58
Q

Ankylosing Spondylitis

A

Marie-Strumpell disease (rheumatoid spondylitis)
Chronic spine/joint inflammatory disorder
Etiology unclear
Most common in white males <40yo
Clinical S/S
- Pain, stiffness, & fatigue
Most patients are asymptomatic

59
Q

Ankylosing Spondylitis Complications

A 
Cardiac 
- Aortic valve disease, conduction disturbance, ischemic heart disease, & cardiomyopathy
Pulmonary up to 70%
- Apical fibrosis
- Interstitial lung disease
- Chest wall restriction
- Sleep apnea
- Spontaneous pneumothorax

Limited cervical ROM & extension
Cricoarytenoid involvement → weak, hoarse voice

60
Q

Ankylosing Spondylitis

Anesthesia Implications

A 
1° upper airway management
Limited cervical spine movement
Consider regional anesthetic
Avoid intubation when possible
Patient self-position prior to induction
CV complications
61
Q

Chest Trauma

A

Traumatic chronic EXtrinsic RLD

  • Flail chest
  • Pneumothorax
  • Tension pneumothorax
  • Hemothorax
62
Q

Flail Chest

A

Traumatic chronic EXtrinsic RLD
Multiple 2+ rib fractures → paradoxical chest wall movement at the fracture site
Insufficient breathing limits alveolar ventilation → hypoventilation, hypercapnia, & progression alveolar collapse
Anesthetic considerations:
- Pain control w/ intercostal nerve block, epidural catheter, or erector spinae block
- ↓pain w/ breathing d/t patient unable to feel rib cage → more effective ventilation

63
Q

Pneumothorax

A

Traumatic chronic EXtrinsic RLD
SIMPLE
- No communication w/ atmosphere
- No mediastinum or diaphragm shift
- Observation (treatment not always required, may potentially self-resolve)
- Aspiration or thoracotomy tube
COMMUNICATING
- Air in pleural cavity exchanges w/ atmospheric
- Dressing, FiO2, thoracotomy tube, intubation & ventilation
TENSION

64
Q

Tension Pneumo

A

Traumatic chronic EXtrinsic RLD
Air progressively accumulates under pressure w/in pleural cavity = medical emergency
↑intra-thoracic pressure → contralateral lung & great vessels compression ↓VR ↓CO/BP
Shunt blood to non-ventilated areas
S/S:
- Hypotension, tachycardia, ↑CVP, ↑airway pressure

NEEDLE DECOMPRESSION 16G
*Ideally place chest tube

65
Q

Hemothorax

A 
Traumatic chronic EXtrinsic RLD
Rapid collection blood w/in intra-thoracic cavity d/t trauma
Chronic disease process or condition → blood builds-up over time
Anesthetic considerations:
- Airway management
- Restore circulating blood volume
- Evacuate blood accumulated
- Potential thoracotomy
66
Q

Atelectasis

A

General anesthesia → supine → induction

Patho - airways blocked ↓gas exchange, loss diaphragmatic tone, PPV maldistribution

67
Q

Pleural Effusion

A

Abnormal fluid collection w/in pleural space

  • Hydrothorax
  • Empyema
  • Hemothorax
  • Chylothorax
68
Q

Hydrothorax

A

Abnormal fluid collection w/in pleural space

  • Lymph system blocked & unable to drain fluid
  • Cardiac failure
  • ↓plasma colloid osmotic pressure
69
Q

Empyema

A

Abnormal fluid collection w/in pleural space
Pyothorax or purulent pleuritis
- Infection (pus)

70
Q

Chylothorax

A

Abnormal fluid collection w/in pleural space

- Lipids

71
Q

Pleural Effusion Treatment

A

Thoracostomy (chest) tube
Thoracentesis
Pleurodesis

72
Q

Other RLD

A

Obesity
Pregnancy
Neurogenic
Surgical

73
Q

Obesity

A

Restrictive load (direct weight & indirect abdominal panniculus) ↑pressure ↓FRC
Shallow rapid breathing → hypercapnia
Treatment - weight management & CPAP
Anesthetic considerations:
- I:E ratio BMI <40 1:1.5 or >40 1:1
- Adjust minute ventilation to accommodate ↑RR
- Maintain PIP (patient individualized)

74
Q

Pregnancy

A 
↑subcostal angle & circumference
Upward diaphragm displacement
↓FRC (ensure fully de-nitrogenated)
↑RV (unable to utilize)
Airway Δ after laboring hours
75
Q

Neurogenic

A

Guillain-Barre or Myasthenia Gravis
Characterized by expiratory muscle weakness - inability to cough forcefully = aspiration risk
Absence abdominal muscle tone → inefficient diaphragm (unable to fully expand)
Weak swallowing muscles/reflex → aspiration

76
Q

Surgical

A

Anesthetic medications
↓reflexes ↓tone
Patient positioning - supine, reverse Trendelenburg, lithotomy, etc.
Pneumoperitoneum (laparoscopic procedure w/ insufflation)

AS - N932 Advanced Pathology (8 decks)

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