Hemodynamic

disturbance

DR. USHA.M
HEMODYNAMICS
 Literally means “Blood movement” is the
study of blood flow.
Hemodynamic disturbance

1. Edema
2. Hyperemia & congestion
3. Hemorrhage
4. Thrombosis
5. Infarction
6. 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

 Isaccumulation of excessive fluid

in the interstitial spaces.
Classification of edema according to
distribution of fluid

1. 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
Pathogenesis of edema:-

1. Increased hydrostatic pressure

2. Increased permeability of the vessel
wall
3. Decreased oncotic pressure
4. Sodium retention in the kidneys
5. Obstruction of lymph flow
1. Hydrostatic edema

 Resultsfrom increased intra

vascular pressure (hydrostatic
pressure).
Causes :-
1. Impaired venous return
congestive cardiac failure
constrictive pericarditis,
ascitis (liver disease)
2. Venous obstruction
thrombi, tumor
3. 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
 Sodium Retention
 Excessive salt intake with renal
insufficiency
 Increased tubular reabsorption of
sodium
 Renal hypoperfusion

 Increased renin-angiotensin-
aldosterone secretion
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 Edema of

plasma inflamed tissue

Endothelial No changes endothelial

changes permeability

Character Non inflammatory Inflammatory

edema edema
Feature Transudate Exudate
Protein Low(<1g/dl) High
(>2.5g/dl)
Glucose Same as Low(,60mg/d
plasma l)
Specific Low(1.015) High(>1.018)
gravity
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 decreased plasma

Angiotensin oncotic pressure
Mechanism

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 renal hypoperfusion

Pressure
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
Pitting Edema
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

 Indicatesextravasation 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

 Is appearance of blood in urine.

1. Microscopic – detectable by
microscopic examination of urine.
2. 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

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© 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 right heart failure

Pressure into pressure into the

Pulmonary vein systemic venous system

CVC LUNGS 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).