Pulmonary- Restrictive disease Flashcards
1
Q
What are the differences between obstructive and restrictive diseases regarding the FEV1 and FEV1/FVC?
(chart)
A
2
Q
Restrictive lung disease is a reduction in:
No change in:
A
- Reduction in:
- TLC
- FRC
- RV
- VC (nml >70 ml/kg)
- FEV1
- FVC
- Total volume exhaled
- No change in:
- Expiratory flow rates
- FEV1/FVC ratio
3
Q
What are the components of restrictive lung disease?
A
- Inspiration is limited due to reduced compliance or the lung or chest wall (“stiff lungs”)
- Reduction in lung compliance leads to increased work of breathing and dyspnea
- Rapid, shallow breathing pattern
- increased dead space ventilation
- Normal gas exchange
- advanced disease will have increased PaCO2 and decreased PaO2 with pulmonary HTN and cor pulmonale
4
Q
What are the different classifications of RLD?
A
- Acute Intrinsic- pulmonary edema
- Chronic intrinsic- diseased lung parenchyma
- Chronic extrinsic- chest wall, intra-abdominal and neuromuscular diseases
- Disorders of the pleura and mediastinum
5
Q
What is Pulmonary edema?
What will a CXR show?
A
- Fluid leakage from the intravascular space into the lung interstitium and alveoli
- Caused by
- increased capillary/hydrostatic pressure (Cardiogenic)
- increased capillary permeability (inflammatory process)
- CXR will show bilateral symmetrical opacities
6
Q
What is acute respiratory distress syndrome?
A
- Diffuse pulmonary endothelial injury
- H2O, solutes, and macromolecules diffuse from intravascular space/capillaries into lung parenchyma and alveoli
- Sepsis often co-exists producing further inflammatory mediators and lung injury
- Often ARDS signals the beginning of multiple organ system failure
7
Q
What is aspiration pneumonitis?
What will patient demonstrate clinically?
A
- Acidic gastric secretions destroy surfactant producing cells and damage the pulmonary capillary endothelium
- Causes increased permeability and pulmonary edema with atelectasis (similar to ARDS)
- Clinically:
- hypoxia
- tachypnea
- bronchospasm
- pulmonary vascular constriction (HPV) can develop into pulmonary HTN
- CXR changes 6-12 hours later, usually in RLL
8
Q
How is aspiration pneumonitis treated?
A
- # 1 treatment is delivery of increased FiO2
- PEEP- may need to reintubate
- B2 agonist for bronchospasm
- +/- lavage with 5 ml NS
- fiberoptic bronchoscopy- if solid material aspiration is suspected
- ABX, steroids- some use them, some dont
9
Q
What is cardiogenic pulmonary edema?
symptoms?
A
- Left ventricular failure with increased pulmonary vascular hydrostatic pressures
- SNS activation more dramatic than with increased capillary permeability edema
- Symptoms
- extreme dyspnea
- tachypnea
- hypertension
- tachycardia
- diaphoresis
10
Q
What is neurogenic pulmonary edema?
A
- Occurs minutes to hours following as acute brain injury (especially the medulla)
- Secondary to massive SNS discharge in response to CNS insult
- Generalized vasoconstriction with large shift of blood volume into pulmonary vessels
- causes vessel injury and fluid leaks into lung parenchyma and alveoli
- *similar to cardiogenic
11
Q
What is treatment for Neurogenic (and cardiogenic) pulmonary edema?
A
- Supportive treatment
- control ICP elevations
- increased FiO2
- positive pressure ventilation, PEEP
- diuretics NOT indicated
- resolution of edema occurs within a few days
12
Q
What drugs cause drug-induced pulmonary edema?
How is it treated?
A
- Heroin- high permeability type
- Cocaine- pulmonary vasoconsriction or MI can result in edema
- Treatment is supportive
13
Q
What is High altitude pulmonary edema?
Treatment
A
- Thought to be caused by intense HPV after 48-96 hours at 2,500-5,000 m altitude with rapid ascent
- Increased pulmonary vascular pressures results in high permeability pulmonary edema
- treatment:
- O2
- prompt descent
- NO
14
Q
What is re-expansion pulmonary edema?
Treatment?
A
- Enhanced capillary membrane permeability
- occasionally occurs following evacuation of pneumothorax or pleural effusion
- more common if >1L fluid/air was in the pleural space for >24 hours and if re-expansion occurs rapidly
- Treatment:
- supportive
- NO diuretics
15
Q
What is negative pressure pulmonary edema?
A
- Occurs minutes to 3 hours after acute upper airway obstruction in a spontaneously breathing person
- Causes:
- post-extubation laryngospasm
- OSA
- epiglottitis
- tumors
- obesity
- hiccups
- Highly negative pressure against the closed upper airway
- decreased interstitial hydrostatic pressure
- increased venous return
- increased afterload on left ventricle
- increased SNS outflow
- hypoxemia with further SNS activation
18
Q
What is the pathology of pumlonary hypertension?
(chart)
A
25
Q
What is flail chest?
A
- Caused by rib fractures or sternotomy dehiscence; paradoxical inward movement of a part of the rib cage during inspiration
- lung will decrease in volume during inhalation and increase in volume during exhalation
- decreased PaO2 and increased PaCO2 secondary to alveolar hypoventilation
- positive pressure ventilation required until thoracic cage can be stabilized
