Restrictive Lung Disease Flashcards
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
b. PEEP
Definition of restrictive lung disease
any condition that interferes with normal lung expansion during inspiration
Principle feature of RLD
reduction in total lung capacity
normal FEV1/FVC ratio
the limit in lung expansion and chest excursion results in a
limited area for gas diffusion
increase in hypoxemia leads to changes in
pulmonary vasculature
Mild classification of RLD by TLC
65-80% of predicted TLC
Moderate classification of RLD by TLC
50-65% of predicted TLC
Severe classification of RLD by TLC
<50% of TLC
normal tidal volume
500 mL
normal IRV
3000mL
normal ERV
1100 mL
normal RV
1200 mL
TLC = ___ + ____
VC + RV
RV = ____ - _____
FRC - ERV
VC = ___ + ____ + ____
IRV + Vt + ERV
FRC = ____ + ____
ERV + RV
Acute intrinsic RLD
abnormal movement of intravascular fluid
ex. pulmonary edema
Chronic intrinsic RLD
pulmonary fibrosis
Chronic extrinsic RLD
traumatic vs non traumatic
Other classifications of RLD
Obesity, pregnancy
Cardiogenic pulmonary edema
acute intrinsic RLD
pump failure
“butterfly” pattern on cxray
issue with hydrostatic pressure
Noncardiogenic pulmonary edema
acute intrinsic RLD
from aspiration, altitude changes, head trauma, chest trauma, poor anesthesia techniques
issue with hydrostatic pressure, permeability of capillary
Starling’s Law
Flow = K [(Pc - Pi) - o(nc - ni)]
net flow is out!
explains the flow of fluid and filtrates in and out of capillaries
Arterial end per starling’s law
net filtration pressure POSITIVE
water, oxygen, nutrients pushed OUT
Venous end per starling’s law
net filtration pressure NEGATIVE
veins pick up excess water, carbon dioxide, and wastes from ISF and excess enters the lymph
Cardiogenic pulmonary edema patho and S/S
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)
Noncardiogenic pulmonary edema patho
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
negative pressure pulmonary edema
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
respiration deals with
gas exchange
ventilation deals with
the mechanics of breathing, movement of air
anesthestic management of pulmonary edema
oxygen, PEEP or CPAP, meds to decrease preload (vasodilators), fluid balance (diuretic)
non cardiogenic permeability issues
aspiration pneumonitis, pneumonia, ARDS, TRALI
3 aspiration syndromes
chemical pneumonitis, mechanical obstruction, bacterial infection
mendelson’s syndrome
pneumonitis from perioperative aspiration
produces asthma like syndrome
pH and volume of gastric material (1.5mL/kg for humans, pH <2.5)
predisposing factors for mendelson’s syndrome
abdominal pathology, obesity, diabetes, neuro deficit, lithotomy position, difficult intubation, reflux, hiatal hernia, inadequate anesthesia, c-section
greatest frequency is during intubation or emergence
mendelson’s syndrome patho and anesthestic considerations
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
Treatment of mendelson’s syndrome
tilt head down or turn, rapid suction of mouth, supplemental O2, PEEP
Acute respiratory failure
inability to provide adequate O2 and eliminate CO2
PaO2 < 60 despite O2 supplementation
PaCO2 >50 in absence of respiratory compensation
ARDS common cause
three principal goals of acute respiratory failure
patent upper airway, correction of hypoxia, removal of excess CO2
ARDS definition and risk factors
insult to the alveolar capillary membrane causing increased capillary permeability and subsequent interstitial and alveolar edema
risk factors: sepsis, pneumonia, trauma, aspiration pneumonitis
ARDS patho, clinical features, treatment
patho: severe damage and inflammation at the alveolar capillary membrane
clinical features: dyspnea, hyoxia, hypovolemia, lung stiffness
treatment: no definitive treatment, supportive care
Berlin definition of ARDS
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
decreased arterial PaO2/FiO2 ratio
mild 201-300
moderate 101-200
severe <101
ex. 100/1.0 = <101 = severe
anesthetic considerations for ARDS
eval the pt
protective ventilation - open lung strategy, PEEP
TRALI definition, predisposing factors
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
TRALI patho, clinical features, treatment
patho: activated neutrophils become trapped w/in the pulmonary microvasculature = noncardiogenci pulmonary edema
clinical features: acute onset and hypoxemia
treat: supportive, LPV strategy
anesthetic management of TRALI
stop transfusion, r/o incompatibility reaction, IV fluids, possible diuretics, vent support
chronic intrinsic RLD examples
idiopathic pulmonary fibrosis, radiation injury, cytotoxic and noncytotoxic drug exposure, o2 toxicity, autoimmune diseases (sarcoidosis)
type 1 epithelial cells
structural, mechanical support, not active metabolically
type 2 epithelial cells
globular cells, little support, metabolically active, surfactant producers, rapidly reproduce in response to injury
alveolar macrophage
scavenger cell, contains lysosomes that digest debris
fibroblast
collagen and elastin synthesis cell, chronic insult = fibrosis
thin vs thick side of interstitium
thin - fused basement of epithelial and endothelial layers, gas exchange
thick - type 1 collagen, fluid exchange
layers that O2 must pass through
layer of surfactant, alveolar epithelium, interstitium, capillary endothelium, plasma, erythrocyte
idiopathic pulmonary fibrosis
thickening of the interstitium of the alveolar wall
infiltration of lymphocytes
fibroblasts increase collagen bundles
exudate in alveoli
clinical features of idiopathic pulmonary fibrosis
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
pulmonary function studies of idiopathic pulmonary fibrosis
decreased FVC w/ normal FEV1/FVC
normal FEF25-75%
smaller and right shift on flow volume curve
pressure volume curve for fibrosis
flattened and displaced downward
higher pressure, smaller volumes
non-cytotoxic injury
amiodarone
direct toxicity, immunologic mechanisms, activation of RAAS
amiodarone non-cytotoxic injury diagnosis and treatment
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!
Bleomycin cytotoxic injury
direct toxicity, inflammatory response
diagnosis: dyspnea, dry cough, low grade fever, fatigue, malaise, xray w/ diffuse interstitial infiltrates
treat: d/c, corticosteroids
bleomycin anesthetic management
monitor o2 sat, abg, preoxygenate, predetermine targey PaO2, PEEP, judicious use of fluids
methotrexate cytotoxic injury
acute pulmonary toxicity
dry cough, dyspnea, hypoxemia, infiltrates
d/c agent
oxygen toxicity predisposing factors and patho
advanced age, prolonged exposure, radiation therapy, chemo
patho: excessive production of free O2 radicals causes damage to cells
clinical features of oxygen toxicity
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
anesthetic management of oxygen toxicity
judicious use of O2, PEEP, corticosteroids
autoimmune pulmonary fibrosis
multiple organ involvement and dysfunction
sarcoidosis
age 20-40, african americans
cause unclear, characterized by the presence of epithelioid-cell granulomata
treat with corticosteroids
nontraumatic chronic extrinsic causes
skeletal and neuromuscular disorders
traumatic chronic extrinsic causes
flail chest, pneumothorax, pleural effusion
pectus excavatum
most common deformity of the chest
nuss procedure to fix it
increased incidence with congenital heart disease and asthma
pectus carinatum
longitudinal protrusion of sternum
associated with increased incidence of congenital heart disease
surgery only effective treatment
kyphosis
accentuated posterior curvature of the spine
usually able to maintain normal respiratory function unless severe
can’t lay flat
scoliosis
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
Cobb angle
> 60 - diminished
70 - symptoms develop
110 - significant gas exchange impairment
the greater the curvature, the greater the loss of pulmonary function
ankylosing spondylitis
marie - strumpell disease chronic inflammatory disorder of the spine cause unclear common in white, males <40 pain, stiff, fatigue
cardiac complications with ankylosing spondylitis
aortic valve diseae, conduction disturbence, ischemic heart disese, cardiomyopathy
pulmonary compications with ankylosing spondylitis
apical fibrosis, interestitial lung disease, chest wall restriction, sleep apnea, spontaneous pneumothorax
cervical spondylosis can
entrap nerves and affect diaphragm
can cause cricoarytenoid involvement
anesthetic management of ankylosing spondylitis
upper airway management priority
limited cervical spine movement
regional
positioning
flail chest
multiple rib fractures = paradoxical movement of the chest wall at the site of fracture
insufficient breathing limits alveolar ventilation = hypoventilation, hypercapnia, progressive alveolar collapse
flail chest anesthetic considerations
pain control! intercostal nerve block, epidural catheter, erector spinae block
pneumothorax
simple, communicating, or tension
simple pneumo
no communication w/ atmosphere, no shift of mediastinum
communicating pneumo
air in the pleural cavity exchanges with atmospheric air
tension pneumo
air progressively accumulates under pressure with the pleural cavity
increased intrathoracic pressure from tension pneumo causes
compression of contralateral lung and great vessels, decreased venous return, CO, and BP, shunting of blood to nonventilated areas
hallmark signs of tension pneumo
hypotension, tachycardia, increased CVP/JVD, airway pressure
treatment for tension pneumo
needle decompression
chest tube
patho of atelectasis
blockage of airways
loss of diaphragmatic tone under GA
maldistribution of ventilation on PPV
pleural effusion
abnormal collection of fluid in the pleural space
hydro, empyema, hemo, chylo - thorax
hydrothorax
blockage of lympathetic drainage
cardiac failure
reduction in plasma colloid osmotic pressure
probably have CA
empyema
infection
hemothorax
blood
chylothorax
lipids
treatment for pleural effusion
thoracostomy tube, thoracentesis, pleurodesis
obesity considerations
imposes a restrictive load on rib cage
directly by weight and indirectly by abdominal panniculus
shallow rapid breathing
ventilation strategies with obesity
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?
pregnancy considerations
changes in thorax - increases subcostal angle and circumference, cranial displacement of diaphragm
decrease FRC, increase RV
neurogenic causes
expiratory muscle weakness, inability to cough forcefully
absence of abdominal muscle tone = inefficient diaphgram
weakness of swallowing muscles = aspiration
