Introduction to

Haemodynamic disorder
Dr Nicholas TITILOYE
 n= equal fluid
gain and loss
inflammation =
excess fluid
loss
hydrostatic
pressure- red
arrow n=
arterial end=
32, venous
end= 12
inflammation
arterial end=
50, venous end
30
mean oncotic
pressure-
green arrows
 CAUSES OF OEDEMA
Increased hydrostatic pressure
Heart failures and venous return obstruction
Reduced plasma oncotic pressure
Nephrotic syndrome, liver cirrhosis,
malnutrition
Sodium and water retention
Increased intake, renal hypoperfusion
Lymphatic obstruction
Inflammatory, neoplastic, post radiation &
surgical
 Morphology of oedema
Subcutaneous oedema – pitting
oedema, dependent oedema, anasarca
oedema
Renal dysfunction oedema – periorbital
oedema
Pulmonary oedema
Brain oedema
Effusions – seen in body cavities –
hydrothorax, hydropericardium and
hydroperitonium (Ascitis)
Hyperaemia and congestion
Both arises as a result of increased
blood volume within tissues
Hyperaemia
This is an active process in which
arteriolar dilatation leads to blood flow
Causes of arteriolar dilatation is
inflammation and exercise
Affected tissue appears red, erythema
Hyperaemia and congestion
Congestion
Congestion is a passive process
arising from reduced outflow of blood
from tissue
Systemic congestion - from cardiac
failure
Localized congestion – from isolated
venous obstruction
The tissue appears cyanosed
 Thrombosis
Definition : – Formation of a clotted mass of
blood within the non – interrupted vascular
system.
A thrombus is a mass formed from the blood
constituents within a vessel or heart during
life.
Thrombosis may be likened to haemostasis
occurring in the wrong place & at the wrong
time.
It is harmful rather than beneficial.
 PATHOGENESIS
Rudolf Virchow suggested 3 main
pathogenesis of oedema
Virchow triads
1. Injury to endothelium.
2. Alteration in normal blood flow.
3. Hypercoagulability .
 Antithrombotic properties of
normal endothelium
a. Antiplatelet properties
- Inhibition of platelet aggregation
PGI2, NO, Adenosine Diphosphatase.
b. Anticoagulant properties
Antithrombin III activity
Thrombomodulin activation of protein C/S
and inhibition of Va & VIIIa
c. Fibrinolysis
Production of t- PA(tissue plasminogen
activator) by normal endothelium
 Prothrombotic functions.
a. Stimulation of platelet aggregation &
adhesion
VWF(Von Willebrand factor)
PAF(Platelet Activation Factor)
b . Procoagulant factors
c .Inhibition of fibrinolysis
t-PA inhibitor
 1. Endothelial injury

[Link] of prothrombotic properties.

e.g; myocardial infarction
◼ atherosderosis.(Plaque build up in coronary artery)
◼ Valvulitis (inflammation of heart valve caused by
rheumatic fever)
◼ Prosthetic valves
◼ Haemodynamic stress e.g hypertension
◼ Others - …. smoking
Hypercholesterolemia, homocystinuria
- endotoxins
Chemical injury to vessels :sclerosing agents-
varicose veins.
[Link] in normal blood flow

turbulence due to deformity of vessel …

(arterial) –loss of the normal laminar
pattern
slowing of blood flow (stasis). (Venous
thrombosis).
 3. Hypercoagulability
Def. Alteration of blood coagulation
mechanism that in some way predisposes
to thrombosis
Primary – genetic defect affecting
coagulation proteins
ATIII def.
Protein C/S.
 Secondary factors

Prolonged bed rest,

MI
tissue damage
cardiac failure
DIC, (Disseminated Intravascular Coagulation)
Acute leukaemia,
Myeloproliferative disorders
Cancer. Eg. mucinous carcinoma of pancreas
 Morphology
a thrombus can occur anywhere in circulatory
system.
cardiac chambers, arteries, veins or capillaries
May have apparent laminations (lines of Zahn).
Produced by alternating layers of paler platelets
admixed with some fibrin, separated by darker
layers containing more red cells.
 Arterial thrombi
Common sites: coronary, cerebral, femoral
arteries.
usually occlusive; almost always
superimposed on atheromatous plaque.
Usually grey, white, friable, composed of
tangled strands and layers of fibrin and
platelets enmeshed in clot .Firmly attached
to the wall.
 Venous Thrombosis.
Usually starts in valve pockets
Produce a long cast of the lumen of the
vein.
red thrombi,
90% lower extremities (deep veins and
superficial veins)
PM CLOT(Particulate Matter)

rubbery, gelatinous
forms a cast of vessels.
Chicken fat supernatant & dark red
dependent portion.
Not attached to the wall of the vessels.
 Fate of thrombus
Propagation
Dissolution – by Fibrinolytic activity
Organization and incorporation into the wall
Recanalization
Calcification
Embolization
 EMBOLISM
An embolus is a detached intravascular
solid, liquid or gaseous mass that is
carried by the blood to a distant site.
 Emboli may arise in
thrombi (thromboembolism)
fragment of bone/bone marrow
atheromatous debris.
Droplets of fat
Air/nitrogen
Fluid – amniotic fluid.
Source and destination of emboli
systemic veins ( Venous emboli) –
pulmonary arteries (pulmonary embolism)
left side of heart (Arterial emboli) –
systemic circulation (systemic embolism)
e.g. in brain, kidney spleen, intestine.
PULMONARY EMBOLUS.
Arterial emboli almost always cause
infarction. Major sites of lodgement are
Lower extremities
Brain
Viscera
Upper limb
 Air embolism
Tubal insufflation
Head & neck surgery
Mismanaged blood transfusion
The clinical features that develops mimics
closely that of massive pulmonary
embolism.
 Nitrogen embolism
“caisson” diseases, decompression
sickness
Occurs in people that work in high
atmospheric pressure.
Divers, tunnellers
Nitrogen dissolves in plasma at high
pressures
In rapid ascent ------the bends.
 Fat embolism
Fracture of long bones,
Hyperlipidemia
Ischaemic bone necrosis
Acute pancreatitis

Fat globules in lungs( oil red O)

 Amniotic fluid embolism
Occurs during labour &immediate post-
partum period
Occurs following tear in the placental
membrane &/or rupture of uterine veins
Epithelial squames from fetal skin are
seen in the microvasculature of
pulmonarry vessels at autopsy
 Ischaemia & infarction.
Ischaemia : loss or reduced blood supply to an
organ or tissue due to obstruction to blood flow.
[Link], thrombi.
The blood supply is insufficient to cater for the
metabolic need of the organ.
The end result is infarction.
An infarct is an area of ischaemic necrosis within
a tissue or organ produced by occlusion of
either its arterial supply or venous drainage.
 Types of infarct
White (anaemic) infact.
Occurs with arterial occlusion and in solid
tissues
Occlusion, initial haemorrhagic
appearance due to seepage of blood,
lyses of red cells ,haemosiderin
deposition,palor of organ
Coagulative necrosis : (kidney spleen,
heart)
 Red infant are encountered in
◼ venous occlusion
◼ loose tissue
◼ tissue with double circulation
◼ and tissue previously congested.
e.g. Lung – double circulation
- Small intestine
 MORPHOLOGY
all infarcts tend to be Wedge – shape with
the apex of the wedge pointing towards
the focus of vascular occlusion
a few hours: Poorly defined.
24hrs – demarcation becomes defined.
Colour change is intense.
Several Days – pale infarct becomes
yellow – white and sharply demarcated.
Border - rim of hypereamia
 Microscopy
Coagulative necrosis of affected organ.
Inflamm. Exudates – a few hrs – few days
– fibroblastic reparative response
beginning in the preserved margin.
Brain – liquefactive necrosis.
Septic infarction – abscess formation.
MYOCARDIAL INFARCTION.
SHOCK
 THE NATURE OF SHOCK
Shock or cardiovascular collapse is a
clinico-pathological syndrome
characterized by widespread tissue
hypoperfusion and hypoxia.

If not quickly reversed, shock may

culminate in multi-organ failure.
It is the final common pathway for a
number of potentially lethal clinical
events, including severe
haemorrhage, extensive trauma or
burns, large myocardial infarction,
massive pulmonary embolism, and
microbial sepsis.
Systemic hypoperfusion is caused by
reduction either in cardiac output or in
the effective circulating blood volume.
Hypoperfusion -- reversible cellular
injury,
persistence -- irreversible tissue
injury and can cause death.
 The principal varieties of
shock
• Hypovolaemic shock- which may
result from haemorrhage,
gastroenteritis or burns.

• Cardiogenic shock- acute

myocardial infarction, valvular
insufficiency or cardiac tamponade.
• Septic shock- such as occurs in
gram-negative or gram-positive
bacterial septicaemia, or less
commonly, viral (dengue) or fungal
(systemic candidiasis) infection.
• Anaphylactic shock – which results
from IgE-mediated hypersensitivity
reaction.
Neurogenic shock – such as
occurs in spinal anaesthetic
accidents or spinal cord
trauma, owing to loss of
vascular tone and peripheral
pooling of blood.
 PATHOPHYSIOLOGY
HYPOVOLAEMIC SHOCK
Inadequate blood or plasma volume
stroke volume and cardiac output reduction
result in reflex tachycardia.
Arterial hypotension occurs if fluid loss
continues unabated,
 PATHOPHYSIOLOGY-CTD
CARDIOGENIC SHOCK
-Failure of myocardial pump owing to
intrinsic myocardial damage, extrinsic
pressure, or obstruction to outflow
stroke volume and cardiac output
reduction
B.P.= C.O X PR
C.O = S.V X H.R.
PR =1/r4 (total peripheral
resistance)
B.P = SV XH.RX1/r4
 PATHOPHYSIOLOGY-CTD

SEPTIC SHOCK
- Overwhelming microbial infections
Peripheral vasodilation and pooling of
blood; endothelial activation/injury;
leukocyte-induced damage; disseminated
intravascular coagulation; activation of
cytokine cascades
 ANAPHYLACTIC SHOCK
Initiated by a generalized IgE-mediated
hypersensitivity response, is associated
with systemic vasodilation and increased
vascular permeability
NEUROGENIC SHOCK
-owing to loss of vascular tone and
baroreceptor reflexes with consequent
peripheral pooling of blood.
 PATHOPHYSIOLOGY-CTD
STAGES OF SHOCK
1. Non progressive phase- reflex
compensatory mechanism
failure-baroreceptor reflexes;
cathecolamines; renin-angiotensin
aldost. axis, ADH; generalized
sympathetic stimulation →
vasoconstriction, renal conservation of
fluid.
2. Progressive stage - worsening
circulatory and metab. Changes-resultant
metabolic lactic acidosis lowers the tissue
pH and blunts the vasomotor response;
arterioles dilate, and blood begins to pool
in the microcirculation.
3. Irreversible stage: irreversible cellular
and tissue injury → endo. Injury + DIC &
→ Multi-organ failure
THE ORGAN PATHOLOGY OF
SHOCK:
1. Microthrombi- especially frequent in the brain
and intestines, which is the basis of DIC.
[Link]- on mucocutaneous surfaces,
serosal membranes and in parenchymal organs.
[Link] –ischaemic (micro-) infarcts due to
tissues hypoperfusion constitute the major
complications of shock.
Specific organ changes include:
 LUNGS

Adult respiratory distress syndrome occurs in

about 50% of cases of shock,
Often in traumatic & septic & less often in
hypovolaemic shock.
Diffuse alveolar damage -shock lung.
Loss of type 1 alveolar pneumocytes and
capillary endothelial cells
Resulting in fluid exudation and hyaline
membrane formation.
The damage is mediated by toxic oxygen
derived free radicals, neutrophil enzymes and
complement activation.
 HEART

1. Cardiac involvement occurs in 36.6% of

fatal cases of shock, most often in
cardiogenic and hypovolaemic shock and not as
often in septic shock.
Petechial subepicardial and subendocardial
haemorrhages and sub-endocardial myocardial
necrosis.
Histologically -coagulative necrosis, contraction
band necrosis (coagulative myocytolysis) may
occur.
 KIDNEYS

Acute tubular necrosis is the principal renal

lesion in shock occurring in 21.1% of cases.
Extensive loss of the periodic acid-schiff
positive brush border of the proximal tubules is
usually observed.
The distal tubules are usually dilated, lined by
flattened cells and contain pigmented, granular
or hyaline casts.
A rarer complication of shock is bilateral renal
cortical necrosis
 BRAIN

Cerebral lesions are observed in only 6.8% of

fatal cases of shock,
Since the brain is well able to autoregulate its
blood flow within an arterial pressure range of
65-140mmHg.
The brain shows selective vulnerability of
various cells and anatomic regions to hypoxia.
(a) Neurons, followed by oligodendrocytes,
astrocytes, microglial cells and vascular
endothelium are progressively more resistant
to hypoxia.
 BRAIN CTD.
(b) Among cortical neurous, pyramidal cells are most
sensitive to hypoxia (layers 3 and 5).- Pseudolaminar
necrosis
(a) Phylogenetically newer cortical neurons are more
sensitive than brainstem and spinal cord neurons. The
end-folium (CA4) and Sommer’s sector (CA1) of the
hippocampus and Purkinje cells of the cerebellum are
exquisitively sensitive to hypoxia.
(b) Watershed (border) zones between the arterial
territories of major cerebral and cerebellar arteries may
show hypoxic damage.
The histologic lesion observed in hypoxic neuron
damage is loss of Nissl substance (red neuron).
 OTHER ORGANS
Hypoxic brain damage is believed to involve
neurotoxicity of glutamate and other excitatory amino
acids.

Liver
Centrizonal hepatic necrosis is found in 56% of
cardiogenic,46% of hypovolaemic and 32% of septic
shock. In septic shock additional cholestasis with bile
concretions in small ducts are found.
Pancreas
Only 6.4% of fatal shock cases show pancreatic lesions,
ranging from focal necrosis to extensive haemorrhagic
pancreatitis.
 OTHER ORGANS
Gastrointestinal tract (GIT)
GIT lesions are observed in 26% of septic 16.2%
of cardiogenic and 8.8% of hypovolaemic shock.
These lesions are produced not only by
hypotension, but also by rennin-angiotensin –
mediated splanchic vasospasm.
Petechial haemorrhages, erosion and acute
ulcers are the most frequent gastroduodenal
lesions.
Ischaemic enteritis, colitis or enterocolitis may
also occur, sometimes complicated by
perforation and peritonitis.
 OTHER ORGANS
[Link]
Pituitary hemorrhagic necrosis occurs in 1-
8% of cases of shock, exemplified in its full-
blown stage by Sheehan’s syndrome.
9. Adrenals
Adrenal lesions are observed in 14.1% of
cases of shock, including lipid depletion and
adrenal haemorrhage, with or without necrosis.
 OTHER ORGANS
Thrombosis of the adrenal sinusoids or
central vein may also occur. Lesions
occur from zona reticularis towards zona
glomerulosa
Thank you