hemodynamics congestion & hyperemia
TRANSCRIPT
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……