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. Administration of colloids to increase oncotic pressure
D. Surgical Intervention
B. PEEP
What is restrictive lung disease?
Any condition that interferes with normal lung expansion during inspiration
- it will affect both lung expansion and lung compliance (delta V/delta P)
- it is an inability to increase lung volume in proportion to an increase in alveolar pressure
The principle feature of restrictive lung disease is
a reduction in total lung capacity (TLC)
RLD causes a decrease in ____ and normal ______
all lung volumes and capacities; and normal FEV1/FVC ratio
Restrictive lung disease can create higher
pressures to get the same volume
Restrictive lung disease results in
reduced diffusing capacity of carbon monoxide (DLCO)
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
stimulation of peripheral chemoreceptors (pulmonary and carotid)
RLD is classified based upon
TLC
Mild RLD is defined as
65-80% of predicted TLC
Moderate RLD is defined as
50-65% of predicted TLC
Severe RLD is defined as
less than 50% of TLC
In RLD if lungs don’t expand it results in
atelectasis leading to hypoxemia leading to changes in pulmonary vasculature leading to pHTN leading to HF if left unchecked
RLD can be classified as:
acute intrinsic
Chronic intrinsic
Chronic extrinsic
and other
Within the RLD classification system, acute intrinsic is due to
abnormal movement of intravascular fluid
Within the RLD classification system, chronic intrinsic is due to
pulmonary fibrosis
Within the RLD classification system, chronic extrinsic is due to
traumatic vs. non-traumatic
Within the RLD classification system, the other factors include
obesity or pregnancy
Acute intrinsic RLD is due to
pulmonary edema and can be from cardiogenic pulmonary edema or non-cardiogenic pulmonary edema
Cardiogenic pulmonary edema can show up as
a “butterfly” pattern in the chest x-ray; tends to be bilateral and uniform
hydrostatic
Non-cardiogenic pulmonary edema is a result of
a hydrostatic & permeability issue
Starling’s law is responsible for explaining the
flow of fluid and filtrates in and out of capillaries
On the arterial end of the capillary,
net filtration pressure is POSITIVE; water, oxygen and nutrients are pushed out
On the venous end of the capillary,
net filtration pressure is NEGATIVE; veins pick up excess water, carbon dioxide and wastes from interstitial fluid
excess enters lymph
In a healthy individual, the net flow of fluid is typically
out
Cardiogenic pulmonary edema is considered to be a
hydrostatic issue
Explain the pathophysiology of cardiogenic pulmonary edema
left-sided incompetence or failure increases pulmonary capillary pressure until the rate of fluid transudation exceeds lymphatic drainage resulting in alveolar flooding
pressure on the arterial side is excessive and exceeds what lymph can take care of
Clinical signs of cardiogenic pulmonary edema include:
rapid shallow breathing not relieved by O2
signs of sympathetic stimulation- HTN, tachycardia, and diaphoresis
Non-cardiogenic pulmonary edema is due to
a disease process that has created leakiness leading to fluid in the air filled sac
Filtration issue
Non-cardiogenic pulmonary edema is considered to be
perfusion without ventilation
Non-cardiogenic pulmonary edema can be due to
neurogenic, uremic, high-altitude, or upper airway obstruction
Negative pressure pulmonary edema is caused by
upper airway obstruction with a prolonged, forceful inspiratory effort against an obstructed upper airway in spontaneously breathing patients
Negative pressure in the intrathoracic cavity from negative pressure pulmonary edema leads to
intense sympathetic stimulation nervous stimulation and increase in afterload
hypertension
central volume displacement
The most common cause of negative pressure pulmonary edema is
laryngospasm following extubation
Negative pressure pulmonary edema should never occur in
a patient with an ETT
Signs and symptoms of negative pressure pulmonary edema include
rapid and shallow breathing
see-saw breathing
dropping saturation
Negative pressure pulmonary edema onset:
a few minutes to several hours
Predisposing factors for negative pressure pulmonary edema include
male, young age, long period of obstruction, overzealous fluid administration, history of cardiac or pulmonary disease
Pulmonary edema is a
medical emergency requiring immediate intervention
Early recognition of pulmonary edema is key and includes
tachypnea, sympathetic stress stimulation
hypoxemia with low PaCO2 initially
increased CVP, jugular vein distension, gallops
lung auscultation
chest XR is most reliable and expedient tool
Negative pressure pulmonary edema is a ______ issue
respiration-gas exchange issue not a ventilatory issue
Management of pulmonary edema includes
oxygen, PEEP or CPAP, fluid balance, pharmacologic therapy- decreased preload
Non-cardiogenic permeability can be due to
aspiration pneumonitis, pneumonia, ARDs, and TRALI
Aspiration pneumonitis consists of
three aspiration syndromes: chemical pneumonitis (Mendelson's syndrome), mechanical obstruction, or bacterial infection
Mendelson’s syndrome is
pneumonitis from perioperative aspiration
it produces an asthma-like syndrome
The pH and volume of gastric material that causes damage to the lungs during aspiration is
25 mL and pH <2.5
Predisposing factors for Mendelson’s syndrome include:
abdominal pathology, obesity, diabetes, neurologic deficit, lithotomy position, difficult intubation, reflux disease, hiatal hernia, inadequate anesthesia, C-section
The greatest frequency of Mendelson’s syndrome occurs during
intubation or emergence
anytime the airway is manipulated
Giving ______ will not change the outcome for Mendelson’s syndrome
pharmacologic prophylaxis
The pathophysiology of Mendelson’s syndrome is
aspirated substance causes lung parenchyma injury, inflammatory reaction, secondary injury in 24 hours
Clinical features of Mendelson’s syndrome includes
arterial hypoxemia
Anesthetic considerations for Mendelson’s syndrome include
Risk factors, NPO standards, pharmacologic prophylaxis, cricoid pressure, awake intubation, and regional anesthetic
The treatment for Mendelson’s syndrome is
tilt head down or turn head
rapid suction of the mouth or pharynx- tracheal suction not indicated
Supplemental O2 (minimal)
PEEP
antibiotics are generally not recommended
discharge is dependent on how the patient is doing
The treatment of acute respiratory failure includes:
directed at supporting oxygenation and ventilation
three principle goals include: patent upper airway, correction of hypoxia, removal of excess CO2
Acute respiratory failure is defined as
inability to provide adequate O2 and eliminate CO2
- PaO2 < 60 mmHg despite oxygen supplementation- absence of R to L cardiac shunt
- PaCO2 >50 mmHg in absence of respiratory compensation- abrupt PaCO2 changes with corresponding decreases in pH
A common cause of acute respiratory failure is
acute respiratory distress syndrome (ARDS)
ARDS is an insult to the
alveolar-capillary membrane causing increased capillary permeability and subsequent interstitial and alveolar edema
Risk factors for ARDS include
sepsis, pneumonia, trauma, and aspiration pneumonitis
- factors are additive
- high mortality rate exists
The pathophysiology of ARDs is
severe damage and inflammation at the alveolar-capillary membrane–> lung tissue becomes stiff
not pulmonary edema but it is very similar
Clinical features of ARDs include
resembles pulmonary edema and aspiration pneumonitis
-dyspnea, hypoxia, hypovolemia, lung stiffness
Treatment for ARDs include
no definitive treatment; care is supportive
Anesthetic considerations for ARDS include
patient evaluation is key (what are current vent settings)
protective ventilation- PEEP, permissive hypercapnia, open lung strategy to maintain balance between alveolar recruitment and fluid balance
prone positioning
The Berlin definition is
lung injury of acute onset with one- week of apparent clinical insult and progression of pulmonary symptoms
bilateral opacities on imaging not explainable by other pathology
respiratory failure is not explained by cardiac or volume overload
A characteristic of ARDS is
decreased PaO2/FiO2 ratio
Mildly decreased P:F ratio is
201-300
Moderately decreased P:F ratio is
101-200
Severely decreased P:F ratio is
<101
The pathophysiology of a TRALI is
activated neutrophils become trapped within the pulmonary microvasculature leading to non-cardiogenic pulmonary edema
Clinical features of TRALI include
associated with blood transfusion (r/o TACO)
acute onset and hypoxemia
Treatment for TRALI includes:
supportive, with lung protective ventilation strategy
Predisposing factors to TRALI include:
surgery, malignancy, sepsis, alcoholism and liver disease, donor risk factors
TRALI is an
acute lung injury associated with blood transfusion
-occurs secondary to an interaction between the transfused blood and the recipients white blood cells
The greatest incidence of TRALI is following a
platelet transfusion
Anesthetic management of a TRALI includes
stop transfusion immediately R/O incompatibility reaction, TACO IV fluids diuretics? Ventilation support lab findings
Diseases characterized by pulmonary fibrosis include:
idiopathic pulmonary fibrosis, radiation injury, cytotoxic and non-cytotoxic drug exposure, O2 toxicity, autoimmune diseases-sarcoidosis
The lung parenchyma is composed of
various cell types with specific functions Type 1 epithelial type 2 epithelial Alveolar macrophage fibroblast
Type 1 epithelial cells are
structural cells providing mechanical support, not active metabolically
Type 2 epithelial cells are
globular cells- little support, metabolically active surfactant producers. Rapidly reproduce in response to injury
Alveolar macrophages are
scavenger cells- contain lysosomes that digest engulfed matter
Fibroblast are
collagen and elastic synthesis cells- chronic insult results in fibrosis
The interstitium is
between the alveolar epithelium and capillary endothelium
consists of “thin side” and “thick side”
The thin side is
mostly gas and is fused basement of epithelial and endothelial layers
responsible for gas exchange
The thick side is
mostly fluid and includes type 1 collagen and is responsible for fluid exchange
The interstitium is continuous with
perivascular spaces
-it is the route by which fluid drains from the capillaries to the lymphatics
Oxygen must pass through various structures on its way from alveolar gas to the hemoglobin of a red blood cell including
layer of surfactant, alveolar epithelium, interstitium, capillary endothelium, plasma, and erythrocyte
Idiopathic pulmonary fibrosis is also known as
diffuse interstitial pulmonary fibrosis, interstitial pneumonia, and cryptogenic fibrosing alveolitis
The principle feature of idiopathic pulmonary fibrosis is
thickening of the interstitium of the alveolar wall
- infiltration of lymphocytes
- fibroblasts increase collagen bundles
- cellular exudate seen within the alveoli- “desquamation”
Alveolar architecture is _____ in idiopathic pulmonary fibrosis
destroyed and scarring results
Clinical features of idiopathic pulmonary fibrosis include
Not common… affects adults in the fifth to seventh decade of life
dyspnea- rapid shallow breathing worsens with exercise
crackles on lung auscultation bilaterally
finger clubbing
chest XR- reticulonodular pattern, “patchy” shadows at base
Cor pulmonale in advance stages
With idiopathic pulmonary fibrosis, arterial
PO2 and PCO2 are reduced but pH is normal; hypoxemia is mild at rest
With idiopathic pulmonary fibrosis, PO2 falls drastically with
exercise; diffusion of oxygen limited by thickness of the interstitium
With idiopathic pulmonary fibrosis, ventilation
perfusion mismatches
diffusion capacity of carbon monoxide is very low
5 mL min/ mmHg (normal is 25-30 mL/min/mmHg)
Pulmonary function studies with idiopathic pulmonary fibrosis demonstrate
decreased FVC with normal FEV1/FVC
Normal FEF 25-75%
the flow volume curve is not “scooped out”
The pressure volume curve with idiopathic pulmonary fibrosis
is flattened and displaced downward (reduced TLC)
as compared to normal
There are over _____ agents that produce adverse effects on the lung parenchyma
100 pharmacologic agents
The mechanism of drug-induced pulmonary disease is due to
not well-defined
direct- toxic effects
indirect- enhancement inflammation or immune process
Drug induced pulmonary disease can be
cytotoxic (drugs that we give that are meant to kill cells) and non-cytotoxic (drugs that happen to kill cells)
Non-cytotoxic injury is typically a result of
amiodarone which is used to treat ventricular dysrythmias
The etiology of amiodarone injury is
direct toxicity, immunologic mechanisms, activation of renin-angiotensin system
The clinical diagnosis of amiodarone induce lung fibrosis:
two or more of the following- new onset pulmonary symptoms, new x-ray abnormalities, decrease in DLCO, abnormal gallium 67 uptake, histologic changes noted in lung biopsy
Amiodarone induced lung fibrosis takes the form of
chronic interstitial pneumonitis, pneumonia, ARDs, or fibrosis mass
The treatment for includes
stop drug (half-life is 40 to 70 days) if fibrosis occurs, it is irreversible
Bleomycin is an
antitumor antibiotic that causes direct toxicity and inflammatory response
Bleomycin causes
chronic pneumonitis and fibrosis, acute hypersensitivity, non-cardiogenic pulmonary edema
The clinical diagnosis of lung injury from bleomycin is from these symptoms:
dyspnea, dry cough, low-grade fever, fatigue, and malaise developing over weeks to months
XR with diffuse interstitial infiltrates
The treatment for bleomycin cytotoxic injury is
discontinuation of agent
corticosteroid therapy
Anesthetic management for patients taking bleomycin includes
monitor O2 saturation, ABG analysis, pre-oxygenation 3-4 minutes, pre-determinate target PaO2, then use minimum fiO2 to achieve it; positive PEEP, judicious use of fluids
Methotrexate is
a drug used to treat rheumatoid arthritis that can result in cytotoxic injury
acute pulmonary toxicity is more common
Clinical signs of methotrexate lung injury includes
dry cough, dyspnea, hypoxemia, and infiltrates
Treatment for cytotoxic injury from methotrexate includes
discontinuation of the agent
Pre-disposing factors for oxygen toxicity include
advanced age, prolonged exposure, radiation therapy, & chemotherapy agents
The pathophysiology of oxygen toxicity includes
excessive production of free O2 radicals causing damage to cells
The symptoms that all restrictive patients have in common is
tachypnea
Clinical features of oxygen toxicity includes
May begin within 6 hours of exposure, chest pain on inspiration, tachypnea, non-productive cough
by 24 hours, paresthesia, anorexia, nausea, and headache
Physiologic changes of oxygen toxicity include:
decreased tracheal mucous, vital capacity, pulmonary compliance, and diffusing capacity, and an increased PAO2-PaO2
Anesthetic management for oxygen toxicity includes:
judicious use of O2, PEEP, corticosteroid therapy
Autoimmune issues are characterized by
multiple organ involvement and dysfunction
Chronic extrinsic fibrosis can be
non-traumatic- skeletal and neuromuscular disorder
Traumatic- flail chest, pneumothorax, or pleural effusion
Predisposing factors to sarcoidosis include
ages 20-40, African Americans
Pathophysiology of sarcoidosis includes
cause is unclear; disease is characterized by the presence of epitheliod-cell granulomata
Management of sarcoidosis includes
corticosteroids
sometimes it resolves spontaneously and other times it doesn’t making it a very difficult course
Skeletal disorders include
pectus excavatum
pectus carinatum
kyphosis
scoliosis
Pectus excavatum is
the most common chest wall deformity
concave chest
____ _______ can be performed to correct pectus excavatum
Nuss procedures; if it causes cardiac impingement they will do procedure
Surgery is the only effective treatment
Pectus excavatum results in an increased incidence of
congenital heart disease and asthma
Pectus carinatum is the
longitudinal protrusion of the sternum
Pectus carinatum is associated with
an increased incidence of congenital heart disease
The only effective treatment for pectus carinatum is
surgery
Kyphosis is the
accentuated posterior curvature of the spine
With kyphosis, unless the deformity is severe, patients are usually
able to maintain normal respiratory function
The Cobb angle is used to determine
the loss of pulmonary function
the greater the curvature, the greater the loss of pulmonary function
A Cobb angle of >60 degrees results in
diminished pulmonary function
A Cobb angle of >70 degrees results in
pulmonary symptoms
A Cobb angle >110 degrees results in
significant gas change impairment
Scoliosis is the
deformity of the spinal column resulting in lateral curvature and rotation of the spine and rib cage
The most common spine deformity is
scoliosis
25% of patients with scoliosis have
concomitant congenital abnormalities
mitral valve prolapse is most common
The severity of scoliosis is determined by the
Cobb angle
a VC and FEV1 <50% is suggestive of
postoperative pulmonary complications
Ankylosing spondylitis is also known as
Marie-Strumpell disease (rheumatoid spondylitis)– chronic inflammatory disorder of the spine
The etiology of ankylosing spondylitis is
unclear
most common in white males under 40
Clinical signs of ankylosing spondylitis include
pain, stiffness, and fatigue
Cardiac complications associated with ankylosing spondylitis include
aortic valve disease, conduction disturbance, ischemic heart disease, and cardiomyopathy
Pulmonary complications associated with ankylosing spondylitis include
apical fibrosis*- will show up on chest XR, interstitial lung disease, chest wall restriction, sleep apnea, and spontaneous pneumothorax
The functional impairment related to ankylosing spondylitis is seen with
coexisting CV and respiratory disease
Cervical spondylosis can
entrap nerves and affect the diaphragm
Ankylosing spondylitis can result in
cricoarytenoid involvement which manifests as a weak, hoarse voice
Most patients with ankylosing spondylitis are
asymptomatic
The anesthetic management of patients with ankylosing spondylitis includes
upper airway management is a priority - limited cervical spine movement - regional anesthetic CV complications positioning
Chest trauma includes
flail chest, pneumothorax, tension pneumothorax, and hemothorax
Flail chest is
when multiple rib fractures causing paradoxical movement of the chest wall at the site of the fracture
Flail chest results in
insufficient breathing limiting alveolar ventilation and leading to hypoventilation, hypercapnia, and progressive alveolar collapse
Anesthetic considerations for flail chest include
pain control–> intercostal nerve block, epidural catheter, erector spinae block
Pneumothorax types include
simple, communicating, and tension
A tension pneumothorax is when
air progressively accumulates under pressure with the pleural cavity
A communicating pneumothorax is when
air in the pleural cavity exchanges with atmospheric air
A simple pneumothorax is
no communication with the atmosphere
no shift of the mediastinum or diaphragm
The treatment for a simple pneumothorax is
observation, aspiration, or thoracotomy tube
The treatment for a communicating pneumothorax is
dressing, O2, thoracotomy tube, intubation, and ventilation
A tension pneumothorax is a
true medical emergency
results in increased intra thoracic pressure
The increased intra thoracic pressure that is from a tension pneumothorax causes:
compression of contralateral lung and great vessels
decreased venous return, CO and BP
shunting of blood to non-ventilated areas
The hallmark signs of tension pneumothorax include
hypotension, tachycardia, increased CVP and increased airway pressure
The treatment for a tension pneumothorax in the OR is
needle decompression
ideally we want a chest tube when possible
A hemothorax is the result of
trauma
or can be from disease processes
Anesthetic considerations for a hemothorax includes
airway management, restore circulating volume, evacuation of accumulated blood, thoracotomy
The pathophysiology of atelectasis is
blockage of airways
loss of diaphragmatic tone under GA
Maldistribution of ventilation on PPV
Atelectasis occurs universally under
general anesthesia
A pleural effusion is the
abnormal collection of fluid in the pleural space
can be hydrothorax, empyema, hemothorax, chylothorax
Empyema is the result of
infection
Hemothorax is the accumulation of
blood
Chylothorax is the accumulation of
lipids
Hydrothorax is the result of
blockage of lymphatic drainage
reduction in plasma colloid osmotic pressure
cardiac failure
Treatment for pleural effusion is
thoracostomy tube, thoracentesis, pleurodesis
Other factors that can cause restrictive lung disease include
obesity, pregnancy, neurogenic, and surgical
Obesity imposes a
restrictive load on the rib cage
directly by weight added to the rib cage
indirectly by the abdominal panniculus
Clinical features of obesity include
shallow rapid breathing resulting in hypercapnia
The treatment of obesity related restrictive lung disease includes
weight management
CPAP
The anesthetic management of the obese patient includes
ventilation strategies- I:E ratio of 1:1
adjust minute ventilation to accommodate higher respiratory rate
maintain PIP- based on what patient can tolerate
Pregnancy leads to restrictive lung disease through
changes in thorax- increases in subcostal angle and circumference, cranial displacement of the diaphragm
-decrease in FRC
RV is increased- can’t do anything with this though
Neurogenic restrictive lung disease is characterized by
expiratory muscle weakness-> inability to cough forcefully
The absence of _______ leads to inefficient diaphragm in the neurogenic patient
abdominal muscle tone
Weakness of ____ muscles may lead to _____ in the neurogenic patient
swallowing muscles; aspiration
Surgical effects that result in a restricted lung include
anesthetic medications, patient positioning, pneumoperitoneum
All of the following factors place this patient at risk for acute intrinsic cardiac pulmonary edema except: A. Hypertension B. CAD C. DM II D. Ejection fraction <40% E. All of the above are factors
C
Which of the following factors may have contributed to this potential aspiration? A. DM II B. hyperlipidemia C. BMI 32 D. CAD
A & C
Following the induction of anesthesia, you notice a moderate amount of gastric secretions in the oropharynx. Which of the following actions is the least appropriate?
A. Tilting the patient’s head down or to the side
B. suctioning the oropharynx
C. Intubation
D. Tracheal and bronchial suction
E. All are appropriate actions
D.
Which of the following statements best describes the intraoperative management of aspiration pneumonitis:
A. routine administration of a broad spectrum antibiotic
B. increasing PIP to maintain a TV of 10-12 mL/kg
C. improving V/Q with the addition of PEEP
D. ventilating with 100% supplemental oxygen
C.
Which of the following ventilation strategies best would optimize V/Q matching during surgery?
A. spontaneous ventilation using a 50% nitrous oxide/oxygen mixture to maximize preload
B. Pressure control ventilation with a ventilation rate of 12 and the peak inspiratory pressure (PIP adjust to maintain a tidal volume 6-8 mL/kg and a PEEP of 10 cmH2O
C. assist control ventilation with a ventilation rate of 8 bpm and tidal volume of 8-10 mL/kg
D. intermittent mandatory ventilation (IMV) with a ventilation rate of 12 and a tidal volume of 6-8 mL/kg
B.
