T4 - Restrictive Lung Disease Flashcards
Restrictive lung disease affects these two things…
Lung expansion and compliance
RLD is typically r/t connective tissue diseases, environmental factors, pulmonary fibrosis, conditions that increase alveolar or interstitial fluid, and diseases that limit excursion of the chest/diaphragm
What is the hallmark of RLD?
Inability to increase lung volume in proportion to an increase in alveolar pressure
…these disorders lead to reduced surface area for gas diffusion, causing V/Q mismatching and hypoxia
As lung elasticity is destroyed, pts become symptomatic d/t
Hypoxia
Inability to clear secretions
Effects of RLD on FEV, FEV1, and FEV1:FVC ratio
↓FEV
↓FVC
↔/↑FEV1:FVC ratio
…also, a reduced diffusion capacity for carbon monoxide (DLCO)
Effects of RLD on lung volumes
All lung volumes are decreased, especially total lung capacity (TLC)
Expected changes in the volume flow loop
What is the principal feature of RLD, represented in spirometry
TLC
TLC is used to classify RLD as mild, moderate, or severe. What are the % of predicted value ranges?
Mild: TLC 65-80%
Moderate: TLC 50-65%
Severe: TLC <50%
List of RLD causes
What is the cause of pulmonary edema? Acute pulmonary edema?
Interstitial fluid leakage into the interstitium & alveolar space
Acute pulmonary edema can be c/b increased capillary pressure or by increased capillary permeability
…both lead to “capillary stress failure”
What characteristics does a CXR showing pulmonary edema have?
Bilateral, symmetric perihilar opacities
…butterfly fluid pattern, more commonly seen w/increased capillary pressure than increased capillary permeability
Diffuse alveolar damage, typically present with increased-permeability pulmonary edema, is associated with _______
ARDS
Pulmonary edema c/b increased capillary permeability is characterized by ↑ or ↓ concentration of protein and secretory products in the edema fluid.
↑
With what kinds of heart failure (2) can cardiogenic pulmonary edema be present?
Acute & decompensated
What are the characteristics of cardiogenic pulmonary edema? (4)
Dyspnea
Tachypnea
Elevated cardiac pressures
SNS activation
What conditions increase the risk of cardiogenic pulmonary edema? (vague answer)
Conditions that acutely increase preload s/a acute aortic regurgitation and acute mitral regurgitation
Conditions that increase afterload or SVR s/a LV outflow tract obstruction, mitral stenosis, and reno-vascular HTN
Negative pressure pulmonary edema (post-obstructive pulmonary edema) results after the relief of an acute upper airway obstruction; what are the causes? (6)
Laryngospasm
Epiglottitis
Tumors
Obesity
Hiccups
OSA
…onset after relief of obstruction ranges from a few minutes to 2-3hrs
Treatment for negative pressure pulmonary edema
Supplemental O2 and maintenance of a patent upper airway, this form of pulmonary edema is typically self-limited
Mechanical ventilation may occasionally be needed for a brief period
Common signs of negative pressure pulmonary edema
Tachypnea
Cough
Failure to maintain SpO2 >95%
….can be confused with aspiration or pulmonary embolism
Pathogenesis of negative pressure pulmonary edema
Spontaneous ventilation is necessary to create negative pressure, drawing in fluid. High negative intrapleural pressure is developed against an obstructed upper airway, and negative intrapleural pressure decreases interstitial hydrostatic pressure, increases venous return, and increases left ventricular afterload. These factors produce acute pulmonary edema by increasing the transcapillary pressure gradient.
Pathogenesis of neurogenic pulmonary edema
- Develops in a small fraction of acute brain injury patients
- Occurs minutes-hours after CNS injury
- Massive outpouring of SNS impulses from the injured CNS that results in generalized vasoconstriction and blood volume shift into the pulmonary circulation.
- leads to the transfer of fluid into the interstitium and alveoli.
Pathogenesis of re-expansion pulmonary edema (REPE)
The rapid expansion of a collapsed lung may lead to REPE
The risk of REPE after relief of a pneumothorax or pleural effusion is related to:
- amount of air/liquid that was in the pleural space (>1 increases risk)
- the duration of collapse (>24 hrs increases the risk)
- speed of re-expansion
Treatment for REPE
Supportive care
What two drugs are especially risky for causing drug-induced pulmonary edema?
Opioids (heroin)
Cocaine - causes pulmonary vasoconstriction, acute myocardial ischemia, and myocardial infarction
A _____ protein concentration of pulmonary edema fluid suggests a ______ permeability pulmonary edema
high
high
Can naloxone be used to treat opioid-induced pulmonary edema?
There is no evidence to support this
If pulmonary edema on chest x-ray does not respond to diuretics, what other condition might be present?
Diffuse alveolar hemorrhage (DAH)
Treatment of drug-induced pulmonary edema
Supportive
Intubation and mechanical ventilation
Heights causing high-altitude pulmonary edema (HAPE) and influencing factors
2500-5000m
Influenced by the rate of ascent to that altitude
Onset of high-altitude pulmonary edema (HAPE)
Onset is often gradual but typically occurs within 48-72 hours at high altitude
Sudden pulmonary edema may be preceded by less severe symptoms of acute mountain sickness
Treatment of high-altitude pulmonary edema (HAPE)
O2 administration and quick descent to lower altitude
Inhalation of nitric oxide may improve oxygenation
Anesthetic implications w/pulmonary edema
Elective surgery should be delayed
Optimize cardiorespiratory function before surgery
Anesthetic implications w/pleural effusion
Large pleural effusions may need to be drained
Anesthetic implications w/hypoxemia
- Mechanical ventilation and PEEP
- Current evidence shows benefit from ventilation using low TV & RR of 14-18 while attempting to keep end-inspiratory plateau pressure <30 cmH2O
- Careful titration of PEEP in conjunction with inspiratory pause is recommended to optimize lung compliance
Breathing patterns with restrictive lung disease
- Rapid, shallow breathing
- Tachypnea should not be used as the sole criteria for delaying extubation if gas exchange and other assessments are satisfactory
Chemical pneumonitis sx:
Abrupt onset dyspnea, tachycardia, and decreased SP02
Pathogenesis of aspiration pneumonitis
- Pts w/ decreased airway reflexes are at risk for aspiration
- When gastric fluid is aspirated, it distributes throughout the lungs and destroys surfactant-producing cells and pulmonary capillary endothelium
- As a result, there is atelectasis and leakage of intravascular fluid into the lungs, producing capillary-permeability pulmonary edema
Evidence of aspiration pneumonitis
- CXR may not demonstrate evidence of aspiration pneumonitis for 6-12 hrs
- Evidence of aspiration is most likely in the superior segment of the RLL if the pt aspirated in the supine position
Interventions for chemical pneumonitis
- Many CRNA’s recommend keeping the HOB elevated for intubation & extubation to decrease aspiration risk
- If aspiration noted, the oropharynx should be suctioned and the pt turned to the side
- T-burg position will not stop gastric reflux, but can prevent aspiration once gastric contents are in the pharynx
- After an episode, pts may need to be monitored for 24-48 hrs
Measurement of gastric fluid pH is useful, since it reflects the pH of the aspirated fluid - The aspirated gastric fluid is also rapidly redistributed to peripheral lung regions, so lavage is not useful unless there has been an aspiration of particulate material
- Aspiration pneumonitis is best treated w/ supplemental 02 & PEEP
- Bronchodilation may be needed to relieve bronchospasm
- There is no evidence that abx decreases the incidence of pulmonary infection or alter outcomes
- Abx may be considered if a pt symptomatic after 48 hrs and + culture results
Tx for E-Cigarette (vaping) –associated lung injury (EVALI)
Antibiotics, systemic steroids, and supportive care are the mainstays of therapy
Sx for E-Cigarette (vaping) –associated lung injury (EVALI)
Dyspnea, cough, N/V/D, abd pain, and pleuritic or nonpleuritic chest pain
Pt may be febrile, tachycardia, tachypnea, and hypoxic
What is the most commonly reported finding and it directly r/t the severity of initial disease process in COVID-19
A drop in diffusion capacity
Who is at the highest risk for long-term pulmonary complications r/t COVID-19?
Pts who need mechanical ventilation
What is acute respiratory failure?
When the Pa02 is <60 mmHg despite 02 supplementation and in the absence of a right-to-left intracardiac shunt
What change occurs with PaCO2 in ARF?
- PaC02 can be increased, unchanged, or decreased d/o the relationship of alveolar ventilation to C02
- A production PaC0 >50 mmHg in the absence of respiratory-compensated metabolic alkalosis is consistent with the diagnosis of ARF
- ARF is distinguished from chronic respiratory failure based on the relationship of PaC02 to arterial pH, ARF is typically accompanied by abrupt increases in PaC02 and decreases in pH
3 tx goals of ARF:
1) a patent airway 2) hypoxemia correction 3) removal of excess C02
What PaO2 level corresponds with an adequate PsO2 of >90%?
> 60 mmHg
What is volume-cycled ventilation (VCV):
Fixed TV w/inflation pressure as dependent variable
What are the primary modes of VCV? (2)
Assisted/controlled ventilation (A/C) and synchronized intermittent mandatory ventilation (SIMV)
What vent mode has a set RR ensuring the number of breaths even if there is no inspiratory effort? If negative pressure is sensed, a tidal volume will be delivered.
A/C ventilation
What vent mode allows SV, while providing a predefined minute ventilation? The circuit provides sufficient gas flow and periodic mandatory breaths that are synchronous with the pt’s inspiratory efforts
SIMV