BRANT: Chapter 12 - PULMONARY VASCULAR DISEASE Flashcards
Most common mechanism that results to pulmonary edema
Increased capillary hydrostatic pressure
(Hydrostatic pulmonary edema)
Thickening of the following structures results to what radiologic finding/s:
a. Axial interstitium
b. Peribronchovascular interstitium
c. Central connective tissue septa
d. Peripheral interlobular septa
e. Interlobar fissures
a. Loss of definition on the intrapulmonary vascular shadows
b. Peribronchial cuffing and tram tracking
c. Kerley A lines
b. Kerley B lines
e. Subpleural edema
Most common form of pulmonary edema which is usually caused by an elevation in the pulmonary venous pressure (pulmonary venous hypertension [PVH])
Hydrostatic pulmonary edema (normal capillary permeability)
Give the PCWP with the following findings:
a. Normal chest
b. Alveolar following with radiographic findings of bilateral airspace opacities in the perihilar and lower lung zones
c. Interstitial edema: loss of vascular definition, peribronchial cuffing and Kerley lines
d. Constriction of lower lobe vessels and enlargement of upper lobe vessels
a. 8 to 12 mm Hg
b. >25 mm Hg
c. 19 to 25 mm Hg
d. 12 to 18 mm Hg
Cephalization first before interstitial edema and then alveolar edema
Unilateral pulmonary edema may develop in the lung that is reexpanded by the rapid evacuation of a large pleural fluid collection or pneumothorax. This is known as ____
Reexpansion pulmonary edema
The following are causes of unilateral pulmonary edema, except:
a. Position
b. Central pulmonary embolism
c. Bronchogenic carcinoma
d. Fibrosing mediastinitis
e. All of the above can cause unilateral pulmonary edema
e. All of the above can cause unilateral pulmonary edema
In severe mitral regurgitation, which lobe is the resulting alveolar pulmonary edema most expected?
Right upper lobe
Alveolar pulmonary edema localized to the right upper lung may be seen in patients with severe mitral regurgitation, likely as a result of preferential regurgitant flow of blood into the right upper lobe pulmonary vein across the superiorly and posteriorly oriented mitral valve.
Edema associated with ALI or ARDS is called
Lung injury or increased capillary permeability edema
The following are causes of pulmonary venous hypertension and pulmonary edema:
a. Systemic overload
b. Mitral regurgitation
c. Mitral valve stenosis
d. All of the above
d. All of the above
The following are etiiologies of increased permeability pulmonary edema, except:
a. Aspiration of fluid
b. Narcotics
c. Fat embolism
d. All of the above
d. All of the above
Stage of ARDS:
Within 12 to 24 hours following the initial insult, damage to capillary endothelium produces engorged capillaries and proteinaceous interstitial edema.
Stage 1: Exudative ARDS
Stage of ARDS:
Within the first week, the injury to type 1 pneumocytes leads to the flooding of alveoli with edema fluid and proteinaceous and cellular debris, which form hyaline membranes lining the distal airways and alveoli.
Stage 2 or proliferative ARDS
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 airspaces. This fibroblastic tissue may resolve and leave minimal scarring or, particularly in those with severe disease and long-standing oxygen requirements, result in extensive interstitial fibrosis.
Stage 3 or fibrotic ARDS
Widened vascular pedical on PA view
> 53 mm
Vascular pedicle represents the mediastinal width at the level of the SVC and left subclavian artery
The following can sometimes distinguish capillary permeability edema from hydrostatic edema:
a. Nondependent or peripheral distribution of edema
b. Absence of other signs such as interlobular septal thickening and subpleural edema
c. Lack of short-term change
d. All of the above
d. All of the above
Pulmonary edema following head trauma, seizure, or increased intracranial pressure. It is a complex phenomenon that appears to involve both hydrostatic and increased permeability mechanisms.
Neurogenic pulmonary edeama
Massive sympathetic discharge from the brain in these conditions produces systemic vasoconstriction and increased venous return, with resultant increase in LV diastolic pressure and hydrostatic pulmonary edema.
This develops in certain individuals after rapid ascent to altitudes above 3,500 m. Edema typically develops within 48 to 72 hours of ascent and appears to reflect a varied individual response to hypoxemia, in which scattered areas of pulmonary arterial spasm result in transient pulmonary arterial hypertension (PAH).
High-altitude pulmonary edema
A severe and often fatal form of pulmonary edema may develop in a pregnant woman when amniotic fluid gains access to the systemic circulation during labor.
Amniotic fluid embolism
Embolic obstruction of the pulmonary vasculature by mucin and fetal squames within the amniotic fluid leads to sudden PAH and cor pulmonale with decreased cardiac output and pulmonary edema.
The embolization of marrow fat to the lung is a common complication occurring 24 to 72 hours after the fracture of a long bone such as the femur.
Fat embolism
Within the lung, the fat is hydrolyzed to its component fatty acids, causing increased pulmonary capillary permeability and hemorrhagic pulmonary edema.
25/M, CKD, with hemoptysis. Diagnosis
Goodpasture syndrome
Goodpasture syndrome is an autoimmune disease characterized by damage to the alveolar and renal glomerular basement membranes by a cytotoxic antibody. The antibody is directed primarily against renal glomerular basement membrane and cross reacts with alveolar basement membrane to produce the renal injury and pulmonary hemorrhage characteristic of this disorder
CT scans demonstrate ground-glass and airspace opacities without interlobular septal thickening acutely. Within several days, the airspace opacities resolve, giving rise to reticular opacities in the same distribution owing to resorption of blood products into the pulmonary interstitium. This results in the so-called CRAZY PAVING PATTERN
DDX: Idiopathic Pulmonary Hemorrhage: children, F=M, normal renal function
T/F: The most common radiographic findings in PE without infarction are cardiac enlargement, or more precisely right heart enlargement
False
Peripheral airspace opacities and linear atelectasis.
Signs of pulmonary embolism:
a. Localized peripheral oligemia with or without distended proximal vessel
b. Pleura-based, homogenenous, wedge-shaped opacity without air bronchograms, typically found in the posterior or lateral costophrenic sulcus of the lung
c. Enlarged pulmonary artery
d. Abrupt tapering or cutoff of a pulmonary artery
e. Enlarged right descending pulmonary artery
f. Dilated right descending pulmonary artery with sudden cut-off
a. Westermark sign
b. Hampton hump
c. Fleischner sign
d. Knuckle sign
e. Palla sign
f. Chang sign
Sign and diagnosis.
Hampton hump of PE
T/F: In embolism without infarction, the airspace opacities should resolve completely within 7 to 10 days, whereas infarcts resolve over the course of several weeks or months and usually leave a residual linear parenchymal scar and/or localized pleural thickening.
True
First imaging study in pregnant women with a normal chest radiograph suspected to have pulmonary embolism
V/Q scanning
Because the radiation dose to the breast is less with V/Q scanning than with CT angiography
T/F: Contiguous or overlapping 1- to 2-mm scans through the entire thorax during injection of 80 to 120 mL of 300 to 350 mg I(iodine)/mL nonionic contrast injected through an 18-gauge or larger IV catheter at 10 mL/s allow routine dense opacification of second- and third-order subsegmental pulmonary arteries.
False
Contiguous or overlapping 1- to 2-mm scans through the entire thorax during injection of 80 to 120 mL of 300 to 350 mg I(iodine)/mL nonionic contrast injected through an 18-gauge or larger IV catheter at 5 mL/s allow routine dense opacification of second- and third-order subsegmental pulmonary arteries.
Chronic vs Acute thrombus in PE:
a. Intraluminal filling defect or nonopacified vessels with a convex filling toward the proximal lumen
b. Filling defect is adherent to the vessel wall rather than in the center of the lumen or when a web is present
a. Acute
b. Chronic
Acute or Chronic PE
Acute
Acute or Chronic PE
Chronic
It was traditionally considered to be the gold standard in the diagnosis of PE, but has been almost entirely supplanted by CTA.
Pulmonary angiography
PE is diagnosed on pulmonary angiography when an intraluminal filling defect or the trailing end of an occluding thrombus is outlined by contrast. Secondary signs, including a prolonged arterial phase, diminished peripheral perfusion, and delay in the venous phase, are nonspecific and are not used to diagnose PE.
Most common source of PE
DVT in the LE
PAH is defined as a systolic pressure in the pulmonary artery exceeding ____ either measured directly by right heart catheterization or as estimated by echocardiography.
30 mm Hg
A useful measurement for enlargement of the central pulmonary arteries, usually indicating PAH in the absence of a left-to-right shunt, is a transverse diameter of the proximal interlobar pulmonary artery on posteroanterior chest radiograph that exceeds ____.
16 mm
In patients younger than 50 years, a ratio of the diameter of the main pulmonary artery (measured at the level of the main right pulmonary artery) to the transverse diameter of the ascending aorta at the same level greater than 1 strongly correlates with a mean pulmonary artery pressure greater than ____
20 mm Hg
Because the aorta normally enlarges with advancing age, in patients older than 50 years, a maximum transverse measurement of the main pulmonary artery greater than ____ correlates better
29 mm
Most common causes of PAH. Give 2
Parenchymal lung disease and obesity hypoventilation syndrome
Parenchymal lung disease, particularly emphysema and diffuse interstitial fibrosis, are common causes of PAH.
The following comprise the three diseases that comprise idiopathic or primary pulmonary hypertension, except:
a. Plexogenic pulmonary arteriopathy
b. Recurrent microscopic PE
c. Pulmonary venoocclusive disease
d. All of the above
d. All of the above
It is characterized by the proliferation of capillaries throughout the pulmonary interstitium, resulting in venular obstruction.
Pulmonary capillary hemangiomatosis (PCH)
The combination of pulmonary edema with a normal heart size, absent findings for PVH, normal PCWP, and the insidious onset of dyspnea should suggest this diagnosis rather than left heart failure, mitral valve disease, or large vessel pulmonary venous occlusion.
PVOD/PCH
