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RADIOLOGY

HEARD FAILURE

PULMONARY EDEMA

Year 5 Group 5, 2011/2012

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CONGESTIVE HEART FAILURE

Introduction

Congestive heart failure (CHF) is the result ofinsufficient output because ofcardiac failure,high resistance in the circulation or fluid

overload. Causes of CHF Coronary artery disease

Hypertension

Cardiomyopathy

Cardiac valvular lesions Arrhythmias

Hyperthyroidism

Severe anemia

Left to right shunts

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CONGESTIVE HEART FAILURE

Introduction

Left ventricle (LV) failure

Most common and results in decreased cardiacoutput and increased pulmonary venous

pressure.In the lungs, LV failure will lead to dilatation ofpulmonary vessels, leakage of fluid into theinterstitium and the pleural space and finallyinto the alveoli resulting in pulmonary edema.

Right ventricle (RV) failureUsually the result of long standing LV failure or

pulmonary disease and causes increasedsystemic venous pressure resulting in edema independent tissues and abdominal viscera.

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CONGESTIVE HEART FAILURE

Clinical Features1. Left Heart Failure

Shortness of breath

Paroxysmal nocturnal dypsnea

Orthopnea

Cough

2. Right Heart Failure

Edema

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CONGESTIVE HEART FAILURE

Illustration of features in CHF

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CONGESTIVE HEART FAILURE

Pathophysiology of CHF

Left Ventricular Failure

CO decreases and pulmonary venous pressure increases

Pulmonary capillary pressure exceeds the oncotic pressure of plasma proteins

Fluid accumulates in and around the capillaries in the interlobular septa

Further accumulation occurs in interstitial tissues of the lungs

Finally with increasing fluids alveolar fill with edema fluid

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CONGESTIVE HEART FAILURE

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Stage I : Redistribution

1. Redistribution of pulmonary blood flow

2. Increase in width of the vascular pedicle

3. Increased artery-to-bronchus ratio in the

upper and middle lobes

4. Cardiomegaly

5. Dilatation of azygos vein

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Stage I Redistribution

Redistribution of pulmonary blood flow

Views of the upper lobe vessels of a patient in good condition

(left) and during a period of CHF (right). Notice also the increased

width of the vascular pedicle (red arrows).

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Bordered on the right by the superior vena

cava and on the left by the left subclavian

artery origin

Indicator of the intravascular volume

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Stage I Redistribution

Increased artery-to-bronchus ratio in the upper and middle

lobes (normal 0.85)

On the left a patient with cardiomegaly and redistribution.

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

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

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Stage I Redistribution

Cardiomegaly (Cardiothoracic ratio, CTR)

Ratio of the transverse diameter of the heart to the

internal diameter of the chest at its widest point just

above the dome of the diaphragm

Cardiomegaly CTR is > 50%

a

bc

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Stage I Redistribution

Dilatation of azygos vein (Sign of increased right atrial pressure )

Standing position - > 7 mm is most likely abnormal & a

diameter > 10 mm is definitely abnormal.

Supine patient > 15 mm is abnormal

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Stage II: Pulmonary interstitial edema

4 key radiographic signs

a) Thickening of the interlobular septa

(Kerley-B, Kerley-A)

b) Peribronchial cuffing

c) Fluid in the fissures

d) Pleural effusions

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a) Thickening of the interlobular

septa: The Kerley B line

B = distended interlobular septa

Location and appearance

Bases 1-2 cm long

Horizontal in direction

Perpendicular to pleural surface

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Kerley A line

A = connective tissue near bronchoarterial

bundle distends

Location and appearance

Near hilum

Run obliquely

Longer than B lines

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Kerley B lines (red arrows)

Kerley A lines (yellow arrows)

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Kerley B lines (red arrows)

Kerley A lines (yellow arrows)

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Kerley C = reticular network of lines

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b) Peribronchial cuffing

Interstitial fluid accumulates

around bronchi

Causes thickening of bronchial wall

When seen on end, looks like little

doughnuts

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Peribronchialcuffing appears

as numerous,

small, ringlike

shadows that

look like little

doughnut

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c) Fluid in the fissures

Fluid may collects in the subpleural space

which is between visceral pleura and lung

parenchyma

Normal fissure is thickness of a sharpened

pencil line

Fluid may collect in any fissure including

major(horizontal), minor(oblique),

accessory fissures, azygous fissure

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d) Pleural effusion

As a result of either increasedproduction or decreased absorptionof pleural fluid, fluid in excess of 2-5ml can collect in the pleural space,

typically at a pulmonary capillarywedge pressure of 20 mmHg.

Features of pleural effusion: Subpulmonic effusion

Blunting of costophrenic angles Meniscal sign

Opacified hemithorax

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Subpulmonic effusion

Fluid is first collected in area beneath the lung btw theparietal pleura lining the sup. surface of diaphragm andthe visceral pleura under the lower lobe

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Stage III: Pulmonary alveolar

edema

When pulmonary venous pressure

is sufficiently elevated (about 25mmHg), fluid spills out of the

interstitial tissues of the lung into

the airspaces.

This results in pulmonary edema

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Fluffy, indistinct,patchy airspacedensities that are

usually centrallylocated.

Outer third of thelung is usuallyspared, and the LZ> UZ, giving rise tobat-wing, angelwing or butterflyconfiguration of

pulmonary edema Presence of pleural

effusion(cardiogenic)

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Classification

Pulmonaryedema

Cardiogenic

Pulmonaryinterstitialedema

Pulmonaryalveolaredema

Non-cardiogenic

- ARDS

- V. Overload

- Malignancy

PULMONARY EDEMA

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NON-CARDIOGENIC

PULMONARY EDEMA

1. Increase capillary permeability Acute Respiratory Distress Syndrome (ARDS)

Sepsis

Uremia

DIC

Smoke inhalation

Near drowning

2. Volume overload

3. Lymphangitic spread of malignancy

4. Others High-altitude pulmonary edema

Neurogenic pulmonary edema

Reexpansion pulmonary edema

Heroin or other overdose

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NON-CARDIOGENIC

PULMONARY EDEMA

The vascular pedicle width (VPW) can help in differentiatingthese different forms of pulmonary edema (6):

Normal VPW: most common in capillary permeability or

acute cardiac failure.

Widened VPW: most common in overhydration/renal failure

and chronic cardiac failure.

Narrowed VPW: most common in capillary permeability.

Other features

less demonstrate pleural effusion and Kerley B line

normal heart sizemore patchy and peripheral

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NON-CARDIOGENIC

PULMONARY EDEMA

On the left a patient with

ARDS.

There is alveolar edema inboth lungs.

Notice that the VPW is

normal.

The vessels in the upper

lobes are not dilated and nocardiomegaly.

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Chest radiograph

shows bilateral

perihilar airspace

shadowing with

normal heart size

and no pleural

effusion.

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