Restrictive Lung Diseases Flashcards Preview

AS - N932 Advanced Pathology > Restrictive Lung Diseases > Flashcards

Flashcards in Restrictive Lung Diseases Deck (76)
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1

Restrictive Lung Disease

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

2

TLC % in RLD

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

3

Acute INtrinsic Causes

Pulmonary edema
- Cardiogenic
- Non-cardiogenic

4

Starling's Law

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

5

Cardiogenic Pulmonary Edema

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

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Cardiogenic Pulmonary Edema S/S

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

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NON-Cardiogenic Pulmonary Edema

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

8

Negative Pressure Pulmonary Edema

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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Negative Pressure Pulmonary Edema
Risk Factors

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

10

Negative Pressure Pulmonary Edema
Onset

Minutes to several hours

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Negative Pressure Pulmonary Edema
S/S

Rapid and shallow breathing
See-saw breathing

12

Pulmonary Edema Management

Medical emergency
Early recognition = key

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

13

Pulmonary Edema S/S

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

14

NON-Cardiogenic Pulmonary Edema
Causes

Aspiration pneumonitis
Pneumonia
ARDS
TRALI

*Not typically anesthesia patients

15

Aspiration Pneumonitis

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

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Mendelson's Syndrome

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

17

Mendelson's Risk Factors

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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Mendelson's Pathophysiology

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

→ Arterial hypoxemia

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Mendelson's Considerations

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

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Mendelson's Treatment

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

21

Acute Respiratory Failure

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

22

Acute Respiratory Failure
Treatment

GOAL = support oxygenation & ventilation
1. Patent upper airway
2. Correct hypoxia
3. Remove excess CO2

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ARDS

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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ARDS Risk Factors

Sepsis
Pneumonia
Trauma
Aspiration pneumonitis

Factors are additive
HIGH mortality rate

25

ARDS Clinical S/S

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

NO definitive treatment
Identify & treat cause
Supportive care

26

ARDS Berlin Definition

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

27

PaO2/FiO2 Ratio

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

MILD 201-300
MODERATE 101-200
SEVERE <100

28

ARDS Anesthetic Implications

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

29

Transfusion Related Acute Lung Injury

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

30

TRALI Risk Factors

Surgery
Malignancy
Sepsis
Alcoholism
Liver disease
Donor risk factors