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PathoPhysiology Respiratory - CP > Restrictive Lung Disease > Flashcards

Restrictive Lung Disease Flashcards

1
Q

Which of the following is the most appropriate treatment for acute cardiogenic pulmonary edema?

a. albuterol breathing treatment
b. PEEP
c. colloids to increase oncotic pressure
d. surgical intervention

A

b. PEEP

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2
Q

Definition of restrictive lung disease

A

any condition that interferes with normal lung expansion during inspiration

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3
Q

Principle feature of RLD

A

reduction in total lung capacity

normal FEV1/FVC ratio

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4
Q

the limit in lung expansion and chest excursion results in a

A

limited area for gas diffusion

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5
Q

increase in hypoxemia leads to changes in

A

pulmonary vasculature

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6
Q

Mild classification of RLD by TLC

A

65-80% of predicted TLC

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7
Q

Moderate classification of RLD by TLC

A

50-65% of predicted TLC

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8
Q

Severe classification of RLD by TLC

A

<50% of TLC

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9
Q

normal tidal volume

A

500 mL

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10
Q

normal IRV

A

3000mL

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11
Q

normal ERV

A

1100 mL

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12
Q

normal RV

A

1200 mL

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13
Q

TLC = ___ + ____

A

VC + RV

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14
Q

RV = ____ - _____

A

FRC - ERV

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15
Q

VC = ___ + ____ + ____

A

IRV + Vt + ERV

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16
Q

FRC = ____ + ____

A

ERV + RV

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17
Q

Acute intrinsic RLD

A

abnormal movement of intravascular fluid

ex. pulmonary edema

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18
Q

Chronic intrinsic RLD

A

pulmonary fibrosis

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19
Q

Chronic extrinsic RLD

A

traumatic vs non traumatic

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20
Q

Other classifications of RLD

A

Obesity, pregnancy

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21
Q

Cardiogenic pulmonary edema

A

acute intrinsic RLD
pump failure
“butterfly” pattern on cxray
issue with hydrostatic pressure

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22
Q

Noncardiogenic pulmonary edema

A

acute intrinsic RLD
from aspiration, altitude changes, head trauma, chest trauma, poor anesthesia techniques
issue with hydrostatic pressure, permeability of capillary

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23
Q

Starling’s Law

A

Flow = K [(Pc - Pi) - o(nc - ni)]
net flow is out!
explains the flow of fluid and filtrates in and out of capillaries

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24
Q

Arterial end per starling’s law

A

net filtration pressure POSITIVE

water, oxygen, nutrients pushed OUT

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25
Q

Venous end per starling’s law

A

net filtration pressure NEGATIVE

veins pick up excess water, carbon dioxide, and wastes from ISF and excess enters the lymph

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26
Q

Cardiogenic pulmonary edema patho and S/S

A

Hydrostatic issue, pressure on arterial end excessive
left sided incompetence or failure = increased pulmonary capillary pressure until rate of transudation exceeds lymph drainage = alveolar flooding

S/S: rapid shallow breathing NOT relieved by O2, sympathetic stimulation (HTN, Tachycardia, diaphoresis)

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27
Q

Noncardiogenic pulmonary edema patho

A

Filtration issue
caused by upper airway obstruction with a prolonged forceful inspiratory effort against an obstructed upper airway in spontaneously breathing patients
negative pressure = sympathetic stimulation = increase afterload = HTN = central volume displacement
commonly caused by laryngospasm following extubation

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28
Q

negative pressure pulmonary edema

A

predisposing factors: young males, long period of obstruction, overzealous fluid administration, hx of cardiac or pulmonary disease
onset: few minutes - hours
S/S: rapid shallow breathing

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29
Q

respiration deals with

A

gas exchange

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30
Q

ventilation deals with

A

the mechanics of breathing, movement of air

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31
Q

anesthestic management of pulmonary edema

A

oxygen, PEEP or CPAP, meds to decrease preload (vasodilators), fluid balance (diuretic)

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32
Q

non cardiogenic permeability issues

A

aspiration pneumonitis, pneumonia, ARDS, TRALI

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33
Q

3 aspiration syndromes

A

chemical pneumonitis, mechanical obstruction, bacterial infection

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34
Q

mendelson’s syndrome

A

pneumonitis from perioperative aspiration
produces asthma like syndrome
pH and volume of gastric material (1.5mL/kg for humans, pH <2.5)

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35
Q

predisposing factors for mendelson’s syndrome

A

abdominal pathology, obesity, diabetes, neuro deficit, lithotomy position, difficult intubation, reflux, hiatal hernia, inadequate anesthesia, c-section
greatest frequency is during intubation or emergence

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36
Q

mendelson’s syndrome patho and anesthestic considerations

A

patho: aspirated substance causes lung parenchyma injury, inflammatory reaction (2nd injury w/in 24 hours)
anesthetic considerations: risk factors, NPO, pharm prophylaxis, cricoid pressure, awake intubation, regional

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37
Q

Treatment of mendelson’s syndrome

A

tilt head down or turn, rapid suction of mouth, supplemental O2, PEEP

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38
Q

Acute respiratory failure

A

inability to provide adequate O2 and eliminate CO2
PaO2 < 60 despite O2 supplementation
PaCO2 >50 in absence of respiratory compensation
ARDS common cause

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39
Q

three principal goals of acute respiratory failure

A

patent upper airway, correction of hypoxia, removal of excess CO2

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40
Q

ARDS definition and risk factors

A

insult to the alveolar capillary membrane causing increased capillary permeability and subsequent interstitial and alveolar edema

risk factors: sepsis, pneumonia, trauma, aspiration pneumonitis

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41
Q

ARDS patho, clinical features, treatment

A

patho: severe damage and inflammation at the alveolar capillary membrane
clinical features: dyspnea, hyoxia, hypovolemia, lung stiffness
treatment: no definitive treatment, supportive care

42
Q

Berlin definition of ARDS

A

lung injury of acute onset with one week of apparent clinical insult and progression of pulmonary symptoms
respiratory failure not explained by cardiac or volume overload

43
Q

decreased arterial PaO2/FiO2 ratio

A

mild 201-300
moderate 101-200
severe <101

ex. 100/1.0 = <101 = severe

44
Q

anesthetic considerations for ARDS

A

eval the pt

protective ventilation - open lung strategy, PEEP

45
Q

TRALI definition, predisposing factors

A

acute lung injury associated with blood transfusion
secondary to interaction between the transfused blood and the recipients WBCs
greatest incidence platelet transfusion
predisposing factors: surgery, malignancy, sepsis, alcoholism, liver disease

46
Q

TRALI patho, clinical features, treatment

A

patho: activated neutrophils become trapped w/in the pulmonary microvasculature = noncardiogenci pulmonary edema
clinical features: acute onset and hypoxemia
treat: supportive, LPV strategy

47
Q

anesthetic management of TRALI

A

stop transfusion, r/o incompatibility reaction, IV fluids, possible diuretics, vent support

48
Q

chronic intrinsic RLD examples

A

idiopathic pulmonary fibrosis, radiation injury, cytotoxic and noncytotoxic drug exposure, o2 toxicity, autoimmune diseases (sarcoidosis)

49
Q

type 1 epithelial cells

A

structural, mechanical support, not active metabolically

50
Q

type 2 epithelial cells

A

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

51
Q

alveolar macrophage

A

scavenger cell, contains lysosomes that digest debris

52
Q

fibroblast

A

collagen and elastin synthesis cell, chronic insult = fibrosis

53
Q

thin vs thick side of interstitium

A

thin - fused basement of epithelial and endothelial layers, gas exchange
thick - type 1 collagen, fluid exchange

54
Q

layers that O2 must pass through

A

layer of surfactant, alveolar epithelium, interstitium, capillary endothelium, plasma, erythrocyte

55
Q

idiopathic pulmonary fibrosis

A

thickening of the interstitium of the alveolar wall
infiltration of lymphocytes
fibroblasts increase collagen bundles
exudate in alveoli

56
Q

clinical features of idiopathic pulmonary fibrosis

A

elderly
dyspnea - rapid shallow, worse with exercise, increased dead space ventilation
crackles, finger clubbing
arterial Po2 and Pco2 reduced, pH normal
diffusion capacity of carbon monoxide low - 5mL/min/mmHg

57
Q

pulmonary function studies of idiopathic pulmonary fibrosis

A

decreased FVC w/ normal FEV1/FVC
normal FEF25-75%
smaller and right shift on flow volume curve

58
Q

pressure volume curve for fibrosis

A

flattened and displaced downward

higher pressure, smaller volumes

59
Q

non-cytotoxic injury

A

amiodarone

direct toxicity, immunologic mechanisms, activation of RAAS

60
Q

amiodarone non-cytotoxic injury diagnosis and treatment

A

diagnosis: 2 or more - new onset pulmonary symptoms, new xray abnormalities, decrease in DLCO, abnormal gallium 67 uptake, histologic changes from lung biopsy

treatment: Stop (half life 40-70 days)
if fibrosis occurs it is irreversible!

61
Q

Bleomycin cytotoxic injury

A

direct toxicity, inflammatory response

diagnosis: dyspnea, dry cough, low grade fever, fatigue, malaise, xray w/ diffuse interstitial infiltrates
treat: d/c, corticosteroids

62
Q

bleomycin anesthetic management

A

monitor o2 sat, abg, preoxygenate, predetermine targey PaO2, PEEP, judicious use of fluids

63
Q

methotrexate cytotoxic injury

A

acute pulmonary toxicity
dry cough, dyspnea, hypoxemia, infiltrates
d/c agent

64
Q

oxygen toxicity predisposing factors and patho

A

advanced age, prolonged exposure, radiation therapy, chemo

patho: excessive production of free O2 radicals causes damage to cells

65
Q

clinical features of oxygen toxicity

A

w/in 6 hours of exposure, chest pain on inspiration, tachypnea, nonproductive cough
by 24 hours - paresthesia, anorexia, nausea, HA
decreased tracheal mucous, vital capacity, pulmonary compliance, diffusing capacity
increased PAO2- PaO2

66
Q

anesthetic management of oxygen toxicity

A

judicious use of O2, PEEP, corticosteroids

67
Q

autoimmune pulmonary fibrosis

A

multiple organ involvement and dysfunction

68
Q

sarcoidosis

A

age 20-40, african americans
cause unclear, characterized by the presence of epithelioid-cell granulomata
treat with corticosteroids

69
Q

nontraumatic chronic extrinsic causes

A

skeletal and neuromuscular disorders

70
Q

traumatic chronic extrinsic causes

A

flail chest, pneumothorax, pleural effusion

71
Q

pectus excavatum

A

most common deformity of the chest
nuss procedure to fix it
increased incidence with congenital heart disease and asthma

72
Q

pectus carinatum

A

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

73
Q

kyphosis

A

accentuated posterior curvature of the spine
usually able to maintain normal respiratory function unless severe
can’t lay flat

74
Q

scoliosis

A

deformity of the spinal column = lateral curvature and rotation of the spine and rib cage
common to have mitral valve prolapse
VC and FEV1 <50%= postop complications
severity determined by Cobb angle

75
Q

Cobb angle

A

> 60 - diminished
70 - symptoms develop
110 - significant gas exchange impairment
the greater the curvature, the greater the loss of pulmonary function

76
Q

ankylosing spondylitis

A 
marie - strumpell disease
chronic inflammatory disorder of the spine
cause unclear
common in white, males <40
pain, stiff, fatigue
77
Q

cardiac complications with ankylosing spondylitis

A

aortic valve diseae, conduction disturbence, ischemic heart disese, cardiomyopathy

78
Q

pulmonary compications with ankylosing spondylitis

A

apical fibrosis, interestitial lung disease, chest wall restriction, sleep apnea, spontaneous pneumothorax

79
Q

cervical spondylosis can

A

entrap nerves and affect diaphragm

can cause cricoarytenoid involvement

80
Q

anesthetic management of ankylosing spondylitis

A

upper airway management priority
limited cervical spine movement
regional
positioning

81
Q

flail chest

A

multiple rib fractures = paradoxical movement of the chest wall at the site of fracture
insufficient breathing limits alveolar ventilation = hypoventilation, hypercapnia, progressive alveolar collapse

82
Q

flail chest anesthetic considerations

A

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

83
Q

pneumothorax

A

simple, communicating, or tension

84
Q

simple pneumo

A

no communication w/ atmosphere, no shift of mediastinum

85
Q

communicating pneumo

A

air in the pleural cavity exchanges with atmospheric air

86
Q

tension pneumo

A

air progressively accumulates under pressure with the pleural cavity

87
Q

increased intrathoracic pressure from tension pneumo causes

A

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

88
Q

hallmark signs of tension pneumo

A

hypotension, tachycardia, increased CVP/JVD, airway pressure

89
Q

treatment for tension pneumo

A

needle decompression

chest tube

90
Q

patho of atelectasis

A

blockage of airways
loss of diaphragmatic tone under GA
maldistribution of ventilation on PPV

91
Q

pleural effusion

A

abnormal collection of fluid in the pleural space

hydro, empyema, hemo, chylo - thorax

92
Q

hydrothorax

A

blockage of lympathetic drainage
cardiac failure
reduction in plasma colloid osmotic pressure
probably have CA

93
Q

empyema

A

infection

94
Q

hemothorax

A

blood

95
Q

chylothorax

A

lipids

96
Q

treatment for pleural effusion

A

thoracostomy tube, thoracentesis, pleurodesis

97
Q

obesity considerations

A

imposes a restrictive load on rib cage
directly by weight and indirectly by abdominal panniculus
shallow rapid breathing

98
Q

ventilation strategies with obesity

A 
BMI >40 1:1 ratio, <40 1:1.5 ratio
adjust minute ventilation to accommodate higher respiratory rate
maintain PIP
driving pressure <15 
do they have OSA and CPAP with them?
99
Q

pregnancy considerations

A

changes in thorax - increases subcostal angle and circumference, cranial displacement of diaphragm
decrease FRC, increase RV

100
Q

neurogenic causes

A

expiratory muscle weakness, inability to cough forcefully
absence of abdominal muscle tone = inefficient diaphgram
weakness of swallowing muscles = aspiration

PathoPhysiology Respiratory - CP (4 decks)

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