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Hemodynamic
disturbance
DR. USHA.M
HEMODYNAMICS

Literally means “Blood movement” is the
study of blood flow.
Hemodynamic disturbance
1.
2.
3.
4.
5.
6.
Edema
Hyperemia & congestion
Hemorrhage
Thrombosis
Infarction
Shock
Edema
Normal body water distribution:Two compartments:
1. Intracellular – comprising of two- thirds of
total body fluid.
2. Extracellular – comprising of one- third of
total body fluid.
1. Interstitial compartment- 75%
2. Intra vascular compartment – 25%
Normal fluid exchange
There are two ends for a capillary
1. Arteriolar end
2. Venous end
The pressure is high in the arteriolar end
then the venous end.Normally the fluid
moves out from the vessel in arteriolar
end into interstitial tissue. From
interstitial tissue same fluid moves back
into vessel at venous end.The small
amount of fluid which is left in interstitial
space is cleared by lymphatics.

Starling forces
Normal fluid pressures
1. Osmotic pressure
Is exerted by the chemical constituents of the
body fluids
Eg. Electrolytes – crystalloid osmotic
pressure
proteins (albumin)- oncotic osmotic
pressure.
2. Hydrostatic pressure
Pressure within the blood vessel.
Edema
 Is
accumulation of excessive fluid
in the interstitial spaces.
Classification of edema according to
distribution of fluid
Localized edema
involving one organ or part of the body.
eg-pleural effusion,ascitis,pericardial
effusion ,etc.
2. Generalized edema
Involving the entire body- ANSARCA
1.
Pathogenesis of edema:1.
2.
3.
4.
5.
Increased hydrostatic pressure
Increased permeability of the vessel
wall
Decreased oncotic pressure
Sodium retention in the kidneys
Obstruction of lymph flow
1. Hydrostatic edema
 Results
from increased intra
vascular pressure (hydrostatic
pressure).
Causes :1.
2.
3.
Impaired venous return
congestive cardiac failure
constrictive pericarditis,
ascitis (liver disease)
Venous obstruction
thrombi, tumor
Arteriolar dilatation
heat, inflammation
2. Increased vascular
permeability
Commonest cause is
inflammation.Release of inflammatory
mediators like histamine, bradykinin,
PAF & others leads to increased
permeability.
 Other causes: Injury,

3.Decreased plasma oncotic
pressure
1.Decresed synthesis in the liver – end
stage liver disease.
2.Incresed loss in urine(nephrotic
syndrome) or stool (protein losing
enteropathy)
3.Inadequte intake-kwashiokar
Lymphatic obstruction
Elephantiasis
 Edema of the arm following surgical
resection of axillary lymph nodes
 Edema of hand following post irradiation
fibrosis.

TRANSUDATE & EXUDATE
Feature
Transudate
Exudate
Definition
Ultra filtrate of
plasma
Edema of
inflamed tissue
Endothelial No changes
changes
Character
 endothelial
permeability
Non inflammatory Inflammatory
edema
edema
Feature
Transudate
Exudate
Protein
Low(<1g/dl)
High
(>2.5g/dl)
Glucose
Same as
plasma
Low(,60mg/d
l)
Specific
gravity
Low(1.015)
High(>1.018)
PH
>7.3
<7.3
LDH
low
High
Cells
Few
Many
Example
CCF
Infections
Volume Repletion Reaction
Goldman: Cecil Textbook of Medicine, 22nd ed.
Renal edema
Causes:1. Nephorotic syndrome
2. Glomerulonephritis
3. Acute tubular injury
Nephorotic edema
Heavy proteinuria
hypoproteinemia
Activation of renin
Angiotensin
Mechanism
decreased plasma
oncotic pressure
Retention of Na &water
edema
Nephritic edema
Glomerulonephritis
glomerular lesion
I
decreased filtration followed by
increased absoption of Na & water by tubules
Na & water retention
edema
Acute tubular injury
Toxins , drugs
ATN
Fails to excrete Na & water
edema
Cardiac edema
congestive cardiac failure
↓ cardiac output
↑ central venous
Pressure
renal hypoperfusion
activation of renin angiotensin
↑ capillary hydrostatic
aldosterone mechanism
pressure
Na & water retention
edema
Pulmonary edema
causes :1. Left heart failure
2. ARDS
3. Shock
4. Infections - pneumonia
left ventricular failure
↑ hydroastatic pressure
↑ pressure in pulmonary veins
↑ pressure in pulmonary capillaries
interstitial edema
pressure on alveolar wall &breaks alveolar
linning
alveolar edema
Hepatic Oedema
hepatic pathology
(e.g. cirrhosis)
↓
obstruction of portal venous system
↓
increased hydrostatic pressure
&
↓albumin synthesis d.t. hepatocyte damge
↓
hypoproteinaemia
↓
transudate oedema (ascitis).
Ascites
Cerebral edema
Causes:1. Infection - encephalitis,meningitis
2. Brain infarct, hemorrhage
3. Trauma
4. Tumors
Localised Oedema:

acute inflammatory oedema
- ↑ vascular permeability exudate
- ↑ hydrostatic pressure of capillaries 
hyperaemia
- ↑ osmotic pressure of interstitial fluid
- ↑ fluidity of ground substance

allergic (hypersensitivity) oedema
- histamine release  ↑ vascular
permeability  exudate (e.g. allergic
rhinitis)
Pitting & non pitting edema
is clinical terms for subcutaneous edema
of leg.
Pitting Oedema
Clinical Features of Oedema








Considerable quantities must accumulate before clinically
apparent (oedema can be assessed by weighing the
patient
approx. 5 litres)
Generalised
Cardiac Oedema
- gravitational distribution
- pitting oedema  holds depression for a few minutes
Renal Oedema
- fluid retention
- generally distributed in C.T.  puffy face/eyelids
Serous Cavities
- e.g. hydrothorax/ascites
Brain Oedema
- swollen; narrow sulci & flattened gyri
Pulmonary Oedema
- exudate
- prone to infection  e.g. bronchopneumonia
- rales
Hemorrhage
 Indicates
extravasation of blood
due to rupture of vessel.
Classification based on origin
1. Cardiac- penetrating wound
rupture of ventricles in MI
2. Arterial – trauma
rupture of aneurysm
3. Capillary – trauma, surgery
4. Venous – trauma, surgery
Petechiae, Pupura, Ecchymoses
Refers to the hemorrhage into the skin
& mucosae.
Petechiae- pinpoint hemorrhage ( < 1mm)
Purpura- 1mm- 1cm in diameter
Echymoses- >1cm

Petechiae
Purpura
Ecchymosis
Hematoma
Is grossly visible accumulation of
extravasted blood in tissue.
 First it is red, then as the blood is
deoxygenated it becomes dusky &
bluish red.

Body cavity hemorrhage
Hemothorax – accumulation of blood in
pleural cavity
Hemopericardium – in pericardial cavity
Hemoperitonium – in peritonial cavity
Hemoarthrosis – in intra – articular space
Hematocephalus – in ventricles of brain
Hematuria

1.
2.
Is appearance of blood in urine.
Microscopic – detectable by
microscopic examination of urine.
Macroscopic – visible to naked eye
Hematuria signifies disease of kidney or
urinary tract
Hematemesis
Is vomiting of blood.
 Sign of esophageal & gastric
hemorrhage like rupture of esophageal
varices & peptic ulcer bleeding.

Hematochezia
Bleeding through rectem.
 Sign of diseases in large intestine.

Melena
Black colored blood in stools.
 Indicates bleeding in upper GIT.
 Blood is partialy digested by HCLof
gastric juice & transformed into a black
pigment called hematein.This pigmentis
not digested in the intestines & is
passed in the feces.

Epistaxis & Hemoptysis
Epistaxis is bleeding from the nose.
 Hemoptysis is bleeding from lungs.

Menorrhagia & Metrorrahagia
Menorrhagia is heavy menstrual
bleeding.
 Metrorrhagia occurs at any time & is
not related to menstrual cycle.

Effects of Hemorrhage

Site of hemorrhage
– brain, pericardium, pleural spac

Rate of blood loss
– acute
• loss of > 20% of blood volume may cause
hypotension or hypovolemic shock
• hemoglobin concentration not altered
– non-acute
• volume loss compensated by shift of fluid from
extravascular to intravascular compartment
• hemoglobin concentration decreased
HYPEREMIA &
CONGESTION
Is increase in volume of blood in a
particular tissue.
 Hyperemia is an “active process” , the
increased blood influx results from
arteriolar dilatation.
 Congestion, also known as “passive
hyperemia”, results due to stagnation of
blood because of venous obstruction.

Normal
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM)
© 2005 Elsevier
Hyperemia
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM)
© 2005 Elsevier
Congestion
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June 2005 07:26 PM)
© 2005 Elsevier
Examples:Hyperemia:1. Inflammation
2. Blushing – adrenergic stimulation
3. Exercise – incresed blood flow to the
muscle.
Congestion:Obstruction of veins due to thrombi or
backward pressure due to heart failure.
Color of hyperemic & congested
tissue:Hyperemic tissue contains increased
amounts of oxygenated blood &
therefore the tissue appears bright red.
 Congested tissue contains increased
amounts of deoxygenated blood &
appears blue.
 Hyperemic tissue is warm, while
congested blood is cold & clammy.

Chronic venous congestion
(CVC):
In CVC there is long standing there is
accumulation of deoxygenated blood &
hence there is damage to the tissue.
Mechanism

heart failure
left heart failure
Pressure into
Pulmonary vein
CVC LUNGS
right heart failure
pressure into the
systemic venous system
CVC LIVER SPLEEN KIDNEY
CVC Lung
Causes:Left heart failure
Gross :The lungs are heavy. Lungs appear
brown- BROWN INDURATION OF
LUNGS.
CVC Lungs
Micro:Rupture of congested vessel results in
edema & hemorrhage. Lysis of RBC’s
releases hemosiderin pigment which is
taken up by macrophages – HEART
FAILURE CELLS.
CVC Liver
Causes:1. Right heart failure
2. Occlusion of inferior vena cava or
portal vein.
GROSS APPEARANCE:NUTMEG APPEARANCE – Alternate
areas of red & yellow .
CVC Liver
Micro:Periportal zone
midzonal
Centrilobular
CVC Liver (MICRO)
Blood fills up the central vein & sinusoids
around it. Followed by centrilobular
hepatocytes necrosis.
 In the long standing cases the necrotic
area is replaced by fibrous tissue.
 The areas with blood appears red &
areas with fibrosis appears whitish
yellow- NUTMEG APPEARANCE.
CVC Spleen
Causes:1. Right heart failure
2. Portal hypertension
GROSS:Spleen is enlarged & congested.
CVC Spleen (micro)
Red pulp appears congested.
GAMMA GANDY BODIES OR
SIDEROFIBROTIC NODULES:Deposits of hemosiderin & calcium salts
on fibrous tissue.
Gamma gandy bodies
CVC Kidney
Cause:1. Right heart failure
2. Obstruction of renal vein
Gross:Kidney is congested.
CVC Kidney (micro)
Glomeruli – shows mesangial
proliferation.
 Tubules – shows degenerative changes
(cloudy swelling).
