Dr. Babai Halder

Assistant Professor,MMC

Hemodynamics:

Hyperemia,Congestion &

Haemorrhage

Haemodynamic Disorders

Oedema

Increased volume of fluid in the interstitial (extravascular, extracellular) space in a tissue

Hyperaemia & congestion

Increased volume of blood (within blood vessels) in a particular tissue/organ

Haemorrhage

Extravasation of blood because of vessel rupture

ARTERIOLE VENULECAPILLARY BED

Arteriolar dilation engorgement with oxygenated blood

Hyperaemia

Normal

Impaired outflow accumulation of deoxygenated blood (cyanosis)

ARTERIOLE VENULECAPILLARY BED

Congestion

Normal

IMPAIRED VENOUS

OUTFLOW

Hyperemia and Congestion

Both indicate a local increased volume of blood in

a particular tissue.

There is increased vascular volume

• Hyperemia is an active process – arteriolar

dilation – arterial side

• Congestion is a passive process -impaired

outflow – venous side - may be systemic / local

Hydrostatic pressure is increased in both the

conditions, hence, Hyperemia and congestion are

always associated with edema.

Hyperaemia vs Congestion

Hyperaemia vs Congestion

Hyperaemia

active process

arteriolar dilation

Affected organ-

pink/Red

e.g. skeletal muscle

during exercise

(physiologic),

inflammation

(pathologic)

Usually local

Congestion

passive process

impaired venous

outflow

Affected organ- bluish

e.g. cardiac failure

(systemic), venous

obstruction (local)

Local / systemic

Both = Increased volume of blood in

tissue

Hyperaemia

Sympathetic Neurogenic Mechanisms

Examples –

1. Inflammation

2. Blushing

3. Menopausal flush

4. Muscular Exercise

5. High grade Fever

Congestion

Local- Portal Venous Obstruction,

Outside Pressure, intraluminal

Occlusion

Systemic - Heart Faailure

Heart Failure

Right- Sided

Back Pressure

Systemic Congestion

Cvc Liver, Spleen, Kidney & Leg veins

Left-Sided

Back Pressure

CVC Lung

Consequences of Impaired

Venous Outflow

Increased intravascular

pressure

Stasis

HAEMORRHAGE

NECROSIS

CONGESTION

OEDEMA

HYPOXIA

FIBROSIS

Capillary rupture

Acute /Chronic

CVC liver

Chronic venous congestion of the liver occurs in

right heart failure and sometimes due to occlusion

of inferior vena cava and hepatic vein.

Gross-

the liver is enlarged and tender and the capsule is

tense.

C/S- the central regions of the hepatic lobules are

grossly red-brown and slightly depressed (owing

to a loss of cells) due to congestion and are

accentuated against the surrounding/ peripheral

zones of uncongested tan to yellow liver due to

fatty changes (nutmeg liver).

CVC liver -- microscopy

In acute hepatic congestion:

• Central vein and sinusoids are distended with

blood

• Central hepatocyte degeneration

• The periportal hepatocytes - may only develop

fatty change.

In chronic hepatic congestion:

Centrilobular necrosis with loss of hepatocytes

dropout

Hemorrhage, including hemosiderin-laden

macrophages

Hepatic fibrosis [In severe, long-standing hepatic

congestion there may even be grossly evident

Centrilobular necrosis - causes

NOTE: Because the central portion of the hepatic

lobule is the last to receive blood, centrilobular

necrosis can also occur whenever there is

reduced hepatic blood flow (including shock from

any cause); there need not be previous hepatic

congestion.

CVC Lung -

Chronic venous congestion of the lung occurs in

left heart failure, especially in rheumatic mitral

stenosis so that there is consequent rise in

pulmonary venous pressure.

Gross:

The lungs are heavy and firm in consistency.

The sectioned surface is dark. The sectioned

surface is rusty brown in colour referred to as

brown induration of the lungs.

Cvc lung

CVC Lung - MicroscopicAcute pulmonary congestion:

alveolar capillaries engorged with blood

alveolar septal edema and/or

focal intraalveolar hemorrhage

Chronic pulmonary congestion:

the septa are thickened and fibrotic

Rupture of dilated and congested capillaries may result in minute intra-alveolar haemorrhages. The breakdown of erythrocytes liberates haemosiderinpigment which is taken up by alveolar macrophages, so called heart failure cells, seen in the alveolar lumina.

CVC Spleen

Chronic venous congestion of the spleen occurs

in right heart

failure and in portal hypertension from cirrhosis of

liver.

Grossly, the spleen in early stage is slightly to

moderately enlarged (up to 250 g as compared to

normal 150 g), while in long-standing cases there

is progressive enlargement and may weigh up to

500 to 1000 g.

The organ is deeply congested, tense and

cyanotic. Capsule is thickend. Sectioned surface

is deep red to gray tan(depending on the degree

of fibrosis).

CVC spleen (Congestive splenomegaly). Sectioned surface shows that the spleen is

heavy and enlarged in size. The colour of sectioned surface is grey-tan.

Microscopically, the features are as under:

i) Red pulp is enlarged due to congestion and marked sinusoidal dilatation and there are areas of recent and old haemorrhages. Sinusoids may get converted into capillaries (capillarisation of sinusoids).

ii) There is hyperplasia of reticuloendothelial cells in the red pulp of the spleen (splenic macrophages).

iii) White pulp is hyperplastic first then becomes atrophied due to pressure & hemorrhage.

iv) There is fibrous thickening of the capsule and of the trabeculae.

v) Some of haemorrhages overlying fibrous tissue, get deposits of haemosiderin pigment and calcium salts; these organised structures are termed as Gamna-Gandy bodies or siderofibrotic nodules.

vi) Firmness of the spleen in advanced stage is seen more commonly in hepatic cirrhosis (congestive splenomegaly) and is the commonest cause of hypersplenism.

CVC spleen. The sinuses are dilated and congested. There is increased fibrosis in

the red pulp, capsule and the trabeculae. Gamna-Gandy body is also seen.

CVC Spleen

Gamna- Gandy Bodies/ Siderofibrotic nodules

CVC Kidney

Grossly, the kidneys are slightly enlarged and

the medulla is congested.

Microscopically, the changes are rather mild.

The tubules may show degenerative changes like

cloudy swelling and fatty change. The glomeruli

may show mesangial proliferation.

HAEMORRHAGE Haemorrhage is the escape of blood from a blood

vessel. The bleeding may occur externally, or internally into the serous cavities (e.g. haemothorax, haemoperitoneum, haemopericardium),or into a hollow viscus.

Extravasation of blood into the tissues with resultant swelling is known as haematoma.

Large extravasations of blood into the skin and mucous membranes are called ecchymoses.

Purpuras are small areas of haemorrhages (upto 1 cm) into the skin and mucous membrane, whereas petechiae are minute pinhead-sized haemorrhages.

Microscopic escape of erythrocytes into loose tissues may occur following marked congestion and is known as diapedesis.

ETIOLOGY

The blood loss may be large and sudden (acute),

or small repeated bleeds may occur over a period

of time (chronic). The various causes of

haemorrhage are as under:

1. Trauma to the vessel wall e.g. penetrating wound

in the heart or great vessels, during labour etc.

2. Spontaneous haemorrhage e.g. rupture of an

aneurysm, septicaemia, bleeding diathesis (such

as purpura), acute leukaemias, pernicious

anaemia, scurvy.

3. Inflammatory lesions of the vessel wall e.g. bleeding from chronic peptic ulcer, typhoid ulcers, blood vessels traversing a tuberculous cavity in the lung, syphilitic involvement of the aorta, polyarteritis nodosa.

4. Neoplastic invasion e.g. haemorrhage following vascular invasion in carcinoma of the tongue.

5. Vascular diseases e.g. atherosclerosis.

6. Elevated pressure within the vessels e.g. cerebral and retinal haemorrhage in systemic hypertension, severe haemorrhage from varicose veins due to high pressure in the veins of legs or oesophagus.

THANK YOU……