Restrictive Lung Disease Flashcards
restrictive lung disease affects the lung’s
expansion and compliance
hallmark of restrictive lung disease
inability to increase lung volume in proportion to an increase in alveolar pressure
restrictive lung disease is typically related to (5)
connective tissue disease, environmental factors, pulmonary fibrosis, conditions that increase alveolar or institial fluid, and diseases that limit excursion of the chest/diaphragm
with restrictive lung disease there is reduced surface area for gas diffusion causing
VQ mismatching and hypoxia
as the lung elasticity worsens, patients become symptomatic due to
hypoxia, inability to clear secretions, and hypoventilation
PFT results in RLD
FEV1?
FVC?
FEV1:FVC ratio
Diffusing Capacity?
reduced FEV1
reduced FVC
normal/increased FEV1/FVC ratio
reduced diffusing capacity
which volumes are decreased with RLD
all of them! Especially TLC
TLC is used to classify restrictive lung disease
whats the difference in mild, moderate, severe disease
MILD: TLC 65-80% predicted value
MODERATE: TLC 50-65% predicted value
SEVERE: TLC < 50% predicted value
pulmonary edema is caused by
intravascular fluid leakage into the interstitium and alveolar space
acute pulmonary edema can be caused by an increased
capillary pressure or increased capillary permeability
T/F on CXR, pulmonary edema appears as unilateral perihilar opacities
false - bilateral, symmetric peihilar opacities
the butterfly pattern on CXR with pulmonary edema is more commonly seen with
increased capillary pressure > capillary permeability
pulmonary edema caused by increased capillary permeability is characterized by a high concentration of
protein and secretory products in the edema fluid
diffuse alevolar damage is present with increased permeability pulmonary edema - and associated with what syndrome
ARDS
cardiogenic pulmonary edema is seen in
acute decompensated HF
characteristics of cardiogenic pulmonary edema
dyspnea
tachypnea
elevated cardiac pressures
SNS activation
when would you suspect cardiogenic pulmonary edema
pt has a decreased systolic or diastolic cardiac function
what increases risk of cardiogenic pulmonary edema
acute increases in preload
* acute aortic regurg and acute mitral regurg
increase afterload or SVR
* LV outflow tract obstruction - mitral stenosis and reno-vascular HTN
what can cause negative pressure pulmonary edema
laryngospasm, epiglottis tumors, obesity, hiccups, OSA
results after the relief of acute upper airway obstruction
T/F a paralyzed/mechanically ventilated patient is capable of creating a negative pressure to draw in fluid
false, spontaneous ventilation is necessary
how long after relief of airway obstructoion will the onset of pulmonary edema be seen
few minutes to 2-3 hours
what pathogenesis is related to the development of negative pressure pulm edema
hella negative intrapleural pressure against an obstructed upper airway
what is the body’s response to the negative pressure from spontaneously breathing against a closed airway
SNS activation, HTN, and central displacement of blood volume
treatment of negative pressure pulmonary edema
supplemental O2 and maintenance of patent upper aiway is usually suffiecint
this form of pulm edema is typically self-limited
mechanical ventilation may be needed for a brief period
how long does it take for negative pressure pulmonary edema to resolve
12-24 hours
neurogenic pulmonary edema develops in which patients
acute brain injury
how long does it take for neurogenic pulmonary edema to occur after CNS inijury
minutes to hours
and may mainfest during the periop period
why does neurogenic pulmonary edema occur
massive outpouring of SNS impulses from the injured CNS resulting in generalized vasoconstriction and blood volume shift into the pulmonary circulation
the increased pulmonary capillary caused by translocation of blood volume leads to transfer of fluid into the ______ & ________
what can occur to the blood vessels
intersitium and alveoli
pulmonary HTN and hypervolemia can injure the blood vessels in the lungs
what predisposes someone to re-expansion pulmonary edema
relief of a pneumothorax or pleural effusion
rapid expansion of collapsed lung
risk of re-expansion pulmonary edema is related to the duration of the collaspse… what time period increases the risk
greater than 24 hour
risk of re-expansion pulmonary edema is related to the amount of air/liquid in the plueral space…. how much air/fluid increases the risk
greater than 1L
what is a risk associated with re-expansion pulmonary edema when managing a patient with a pleural/pneumothorax
rate of re-expansion
what is the factor for development of re-expansion pulmonary edema
high protein content of pulmonary edema fluid suggests enhanced permability as a factor
drug induced pulmonary edema can occur following the administration of what drugs
heroin and cocaine
what causes the pulmonary edema in drug-induced
high permeability pulmonary edema
high protein concentration of pulmonary edema
why might cocaine not be ur best friend
alt Q: what can cocaine cause
causes pulmonary vascoconstriction
acute myocardial ischemia/infarction
T/F a patient that develops opioid induced pulmonary edema can be reversed quickly with Naloxone
false - no evidence shows that naloxone increases the resolution speed
if the pulmonary edema evident on CXR doesnt respond to diuretics what is the differential diagnosis
diffuse alveolar hemorrhage
high altitude pulmonary edema occurs at what heights
2500-5000 m and influenced by rate of ascent to the altitude
what is the time period for development of HAPE
gradual onset within 48-72 at high altitude
what precedes sudden pulmonary edema
acute mountain sickness
cause of edema in HAPE is presumed to be
hypoxic pulmonary vasoconstriction which increases pulmonary vascular pressure
treatment for HAPE
O2 & descent from high altitude
inhaled nitric oxide may improve oxygenation
elective surgey should be ______ in patiets with pulmonary edema
delayed
efforts to optimize cardioresp function before surgery
persistent hypoxemia may warrant
Mechanical ventilation and PEEP
youre about to extubate your abestoses patient, they’re tachypneic pulling low VT with a normal ABG.
pull the tube or wait
patients with restrictive lung disease typically have rapid, shallow breathing
tachypnea should be used as the sole criteria for delaying extubation if gas exchange and other assessments are satisfactory
what patients are at increased risk for apiration
patients with decreased airway reflexes
recommendations for intubation/expiration to decreased aspiration risk
elevated HOB
chemical pneumonitis symptoms
abrupt onset dyspnea, tachycardia, decreased SpO2
what happens when gastric fluid is aspirated
it distributes throughout the lungs and destroys surfactant producing cells and pulmonary capillary endothelium
as a result atelactasis and leakage of fluid into the lungs occurs
chemical pneumonitis may present with Acute lung injury and have what symtoms
tachypnea, bronchospasm, acute pulmonary HTN, arterial hypoxemia
if you note aspiration what steps do you do next
suction the oropharynx
turn patient on the side
t/f trendelenburg will stop gastric reflux
no - trendelburg will not stop gastric reflux but can precent aspirations once contents are in the pharynx
when might a patient need lavage of the lungs
aspiration of particulate material
aspirated gastric fluid is rapidly redistributed to peripheral lung regions
aspiration pneumonitis is treated by
supplemental O2 and PEEP
bronchodilation to relieve bronchospasm
do you give ABX immediately after aspiration
if pt is symptomatic after 48 hours and positve culture results
no evidence that ABX decrease the pulmonary infection or alter outcomes
what is EVALI (E-cigarette (vaping) - associated lung injury)
form of ALI and is associated with pneumonia, diffuse alvoelar damage and broncholitis
THC/Vitamin E Acetate/nicotine/CBD/oils are assocaited with EVALI
symptoms of EVALI
dyspnea, cough, N/V/D, abominal pain, and pleuritc or nonplueritic pain
may be febrile, tachycardic, tachypnea, hypoxic
radiology of EVALI
diffuse alveolar damage similar to ARDS
treatment of EVALI
antibiotics, systemic steriods, supportive care
COVID-19 Induced Restrive Lung Disease have perisistent _______ ________ lung disease
inflammatory interstitial lung disease
pulmonary symptoms with COVID lungs
dyspnea to ventilator dependence and pulmonary fibrosis
what is the most commonly reported finding with COVID lungs and is directly related to the serverity of inital disease process
drop in diffusion capacity
survivors of COVID have what 3 things
decreased exercise capacity
hypoxia
opacities on CT
COVID lung patients requiring mechanical ventilation are at high risk of
pulm complications
acute respiraory failure is present when
PaO2 < 60 mmhg despite supplemental O2 and in absence of right to left intracardiac shunt
what is the PaCO2 in acute lung failure
incrased, unchanged, decreased
depends on the relaionship of alveolar ventilation to CO2 production
for diagnosis of Acute Lung Failure what is the PaCO2 in the absence of respiratory compensation metabolic alkaolosis
PaCO2 > 50 mmHg
how to distinguish ARF from chronic respiratory failure
pH- PaCO2
acute: increased PaCO2 and low pH
chronic: pH is normal with elevated PaCO2
why is the pH normal with chronic respiratory failure
metabolic compensation of the kidneys for respiratory acidosis
3 treatment goals of acute respiratory failure
patent airway
hypoxemia correction
removal of excess CO2
O2 via NC, venturi mask, nonrebreather, or T peiece can correct
hyopxemia caused by mild-moderate VQ mismatch
these devices seldomly provide O2 concnetrations > 50%
when NC, venturi mask, or T piece fail to maintain PaO2 > 60 mmHg then what is initiated
CPAP - continuous positive airway presure
CPAP may increase lung volumes by
opening collapsed alveoli and decreasing right to left intrapulmonary shunting
maintaining a PaO2 > 60 mmHg is adequate as
SpO2 > 90%
ARDS is caused by
inflammatory injury to the lung and manifests as hypoxemic respiratory failure
what is the highest risk factor for ARDS
sepsis
hallmark of ARDS
rapid onset respiratory failure, arterial hypoxemia, and CXR findings similar to cardiogenic pulmonary edema
what causes increased alveoalr capillary membrane permeability and alveolar edema
proinflammatory cytokienes
acute ARDS will resolve completely but may progress to
fibrosiing alveolitis with perisitent arterial hypoxemia and decreased pulmonary compliance
ARDS management consists of
supportive care consists of ventiliation, antibiotics,stress ulcer prophlayxis, DVT prophlyxais, and early enteral feedings
for refractory hypopxemia in ARDS what are 2 proposed therapies
proning
ECMO
why proning?
exploits gravity and respositioning the heart in the thorax to recriut lung units and improve VQ matching
when is ECMO indicated for rescue therapy
severe hypoxemic and or alveolar hypercapnic respiratory failuer and possible rescue therapy
rest the lungs unil servere hypoxemia and acidosis resolve
additional supportive therapy for ARDS
optimal fluid management, NMB, inhaled nitric oxide, prostacylcins, recruitment manuevers, surfactant replacement, glucocorticoids, ketoconazole
intrinsic restrictive lung disease
sarcoidosis
hypersenstivity PNE
pulmonary langerhans cell histiocytosis
pulmonary alevoalr proteinosis
lymphangioleiomyomatosis
pts with chronic intrinisic RLD present with
dyspnea and nonproductive cough
what can occur due to chronic intrinisc RLD
pulmonary HTN and cor pulmonale due loss of pulm vasculature
digit clubbing is common in some ILDs such as
abestosis and idopathic pulmonary fibrosis
sarcoidosis is systemic granulomatous disorder that most commonly involves the lungs and intrathroci lymh nodes going unnoticed until incidental findings on CXR
what symptoms might be present
dyspnea and cough
wheezing - if theres bronchiole involvement
crackles are uncommon
laryngeal sarcodosis occurs up to 5% of patietns and can interfere with
intubation
what test is used to detect sarcoidosis
Kveim test
what is used to supress symptoms of sarcoidosis
corticosteroids
