Introduction

• Congestive heart failure (CHF) is the result of insufficient output

because of cardiac failure, high resistance in the circulation or fluid
overload.

• Left ventricle (LV) failure is the most common and results in

decreased cardiac output and increased pulmonary venous
pressure.

• In the lungs LV failure will lead to dilatation of pulmonary vessels,

leakage of fluid into the interstitium and the pleural space and
finally into the alveoli resulting in pulmonary edema.

• Right ventricle (RV) failure is usually the result of long standing LV

failure or pulmonary disease and causes increased systemic
venous pressure resulting in edema in dependent tissues and
abdominal viscera.
In the illustration: patient with CHF.

• Increased pulmonary venous

pressure is related to the
pulmonary capillary wedge
pressure (PCWP) and can be
graded into stages
Stage I: Redistribution

• In a normal chest
film with the patient
standing erect, the
pulmonary vessels
supplying the upper
lung fields are
smaller and fewer in
number than those
supplying the lung
bases.

• The pulmonary vascular bed has a significant reserve capacity and recruitment may open
previously non-perfused vessels and causes distension of already perfused vessels.

• This results in redistribution of pulmonary blood flow.

• The upper lobe vessels have a diameter > 3 mm (normal 1-2 mm).

• Notice the increased artery-to-bronchus ratio at hilar level (arrows)

 Stage II - Interstitial edema

• Stage II of CHF is characterized by fluid leakage into the interlobular and

peribronchial interstitium as a result of the increased pressure in the capillaries.
• When fluid leaks into the peribronchovascular interstitium it is seen as
thickening of the bronchial walls (peribronchial cuffing) and as loss of definition
of these vessels (perihilar haze)
Stage III - Alveolar edema

• This stage is
characterized by
continued fluid leakage
into the interstitium,
which cannot be
compensated by
lymphatic drainage.

• This eventually leads to

fluid leakage in the
alveoli (alveolar
edema) and to leakage
into the pleural space
(pleural effusion).
Introduction

• Pulmonary edema is defined as an abnormal accumulation of

fluid in the extravascular compartments of the lung.

• The relative amounts of intravascular and extravascular fluid in

the lung are mostly controlled by the permeability of the
capillary membrane & the oncotic pressure
Introduction

• Cardiogenic and non-cardiogenic.

• Pulmonary edema can be divided into 4 categories on the

basis of pathophysiology:
(a) increased hydrostatic pressure edema,
(b) permeability edema with diffuse alveolar damage (DAD),
(c) permeability edema without DAD,
(d) mixed edema due to simultaneous increased hydrostatic
pressure and permeability changes
Cardiogenic pulmonary edema.
• Heart failure
• Coronary artery disease with
left ventricular failure.
• Cardiac arrhythmias
• Fluid overload -- for
example, kidney failure.
• Cardiomyopathy
• Obstructing valvular lesions
-- for example, mitral
stenosis
• Myocarditis and infectious
endocarditis
Non-cardiogenic pulmonary edema.
• Smoke inhalation.
• Head trauma
• Overwhelming sepsis.
• Hypovolemia shock
• Re-expansion
• High altitude pulmonary edema
• Disseminated intravascular coagulopathy
(DIC)
• Near-drowning
• Overwhelming aspiration
• Heroin overdose
 INCREASED HYDROSTATIC PRESSURE EDEMA

Increased hydrostatic pressure edema in a 33-year-old man with acute myelocytic leukemia who
was admitted for fluid overload with renal and cardiac failure. Successive chest radiographs
demon- strate progressive lobar vessel enlargement, peribronchial cuffing (arrows in b), bilateral
Kerley lines (ar- rowheads in c), and late alveolar edema with nodular areas of increased opacity.
The fluid overload is con- firmed by the increasing size of the azygos vein.
Bat Wing Edema
• Bat wing edema refers to a
central, nongravitational
distribution of alveolar
edema.
• It is seen in less than 10%
of cases of pulmonary
edema and generally occurs
with rapidly developing
severe cardiac failure as seen
in acute mitral insufficiency
(associated with papillary
muscle rupture, massive
myocardial infarct, and valve (3) Bat wing edema in a 71-year-old woman with fluid
leaflet destruction due to overload and cardiac failure. Chest radiograph
septic endocarditis) or renal demonstrate bat wing alveolar edema with a central
distribution and sparing of the lung cortex. The
failure. infiltrates resolved within 32 hours.
(4) Bat wing edema in a 66-
year-old woman with fluid
overload of renal origin who
was undergoing hemodialysis
for hypertensive
nephroangiosclerosis. The
patient was found
unconscious after lying on
her right side for several
hours. Chest radiograph
shows un- usual recumbent
bat wing pulmonary edema
with associated right-sided
pleural effusion.
 kesimpulan

Pulmonary hypertension, tanda: pelebaran pembuluh darah

paru
- inverted coma: bendungan arteri pulmonalis
- kranialisasi/inverted mustache: bendungan vena
pulmonalis di daerah suprahilar

- Septal lines (kerley B lines)

- Effusi pleura
- Bat’s wings pattern (edema alveolar)
“Thank you.”