Pulmonary vascular disease Flashcards
Under normal conditions, interstitial spaces of the lung is kept dry by
Pulmonary lymphatics located within the axial and peripheral interstitium of the lung
Because there are no lymphatic structures immediately within the alveolar walls (parenchymal interstitium), filtered interstitial fluid is drawn to lymphatics by a
Pressure gradient from alveolar interstitium to the axial and peripheral interstitium
When the rate of fluid accumulation in the interstitium exceeds the lymphatic drainage capabilities of the lung, fluid accumulates first within the
Interstitial spaces
Most common mechanism of pulmonary edema
Change in the normal starling forces that govern fluid movement in the lung
Imbalance of starling forces in pulmonary edema is most commonly the result of
Increase capillary hydrostatic pressure, and less commonly diminished plasma oncotic or interstitial hydrostatic pressure
Other mechanisms in pulmonary edema aside from imbalance in starling forces
- obstruction or absence of the normal pulmonary lymphatics, which leads to the excess accumulation of interstitial fluid.
- disorders can injure the epithelium of the capillaries and alveoli, causing an increase in capillary permeability that allows protein-rich fluid to escape from the capillaries into the pulmonary interstitium
Thickening of axial interstitium results in what imaging findings
Loss of definition of intrapulmonary shadows and thickening of peribronchovascular interstitium causing peribronchial cuffing and tram tracking
Involvement of peripheral and subpleural interstitial structures in pulmonary edema produces
Kerley lines and subpleural edema
Represents thickening of central connective tissue septa and peripheral interlobular septa, respectively
Kerley A and B lines
Kerley C lines represent a network of thickened interlobular septa
It is the accumulation of fluid within the innermost (interstitial) layer of the visceral pleura
subpleural edema
subpleural edema are is best seen in ____ and appears as smooth thickening of the interlobular fissures
lateral radiographs
Develops when fluid in the interstitial spaces extends into the alveoli
Airspace pulmonary edema
Most common form of pulmonary edema
Hydrostatic pulmonary edema
Hydrostatic pulmonary edema is usually caused by
elevation in pulmonary venous pressure (pulmonary venous hypertension)
Causes of pulmonary venous hypertension may be divided into four major categories
- obstruction to left ventricular inflow,
- left ventricular systolic dysfunction (LV failure),
- mitral valve regurgitation and
- systemic or pulmonary volume overload
classic cause of obstruction to left ventricular inflow is
mitral stenosis
more common causes of LV inflow obstruction
poor left ventricular compliance (diastolic dysfunction), such as caused by hypertrophy or chronic ischemic subendocardial fibrosis
3 Common causes of LV failure include
- ischemic heart disease,
- aortic valve stenosis and regurgitation, and
- nonischemic cardiomyopathy
Normal pcwp
8-12 mmHg
Pcwp level that leads to findings of interstitial pulmonary edema such as loss of vascular definition, peribronchial cuffing and Kerley lines
19-25 mmHg
- Mild elevation of PCWP (12 to 18 mm Hg) produces constriction of lower lobe vessels and enlargement of upper lobe vessels.
- Progressive elevation of PCWP (19 to 25 mm Hg) leads to the findings of interstitial pulmonary edema:
• loss of vascular definition,
• peribronchial cuffing, and
• Kerley lines.
Pcwp level that produces alveolar filling with radiographic findings of bilateral airspace opacities in the perihilar and lower lung zones
More than 25 mmHg
classic radiographic findings of Pulmonary Venous Hypertension
enlargement of pulmonary veins and redistribution of pulmonary blood flow to the nondependent lung zones
True or false: with PVH in the upright patient with normal lung parenchyma, the upper zone vessels are frequently as large as or larger in diameter than the lower zone vessels
true
alveolar pulmonary edema localized to the right upper lung may be seen in patients with
severe mitral regurgitation
When respiratory failure develops as a result of this condition, and is associated with increased lung stiffness (noncompliance) it is termed
acute lung injury or when severe, ARDS
6 most common causes of increased permeability edema
shock, severe trauma, burns, sepsis, narcotic overdose and pancreatitis
key factors in the development of capillary endothelial damage
recruitment and activation of neutrophils in the lung, with release of enzymes and oxygen radicals
Stage of ARDS: happens within 12-24 hours following initial insult, damage to capillary endothelium produces engorged capillaries and proteinaceous interstitial edema
Stage 1: exudative
Stage of ARDS: within the first week, injury to type 1 pneumocytes leads to flooding of alveoli with edema fluid and proteinaceous and cellular debris, which form hyaline membranes lining the distal airways and alveoli
Stage 2: proliferative
Stage of ARDS: occurring 10 to 14 days following the initial insult, type 2 pneumocytes proliferate in an attempt to reline the denuded alveolar surfaces and fibroblastic tissue proliferates within the interspaces
Stage 3: fibrotic
Radiographic pattern of ARDS
patchy peripheral airspace opacities by 12-24 hours, with minimal or absent interlobular septal thickening, coalesce over the next days to produce confluent bilateral airspace opacities with air bronchograms, after a week becomes coarse reticulonodular, if unchanged, honeycombing
in pulmonary edema associated with chronic cardiac failure, the vascular pedicle, which represents the mediastinal width at the level of SVC and left subclavian artery measures
> 53 mm on PA radiograph
90% of all primary tracheal tumors in adults are malignant or benign?
Malignant