Hemodynamic Disorders
Hemodynamic Disorders
Introduction
• Organs and cells need intact circulatory system
for delivery of :
– oxygen, nutrients,
– hormones,
– electrolytes, water ; and
for removal of:
– metabolic waste and
– carbon dioxide
• For their normal function cells and tissues
need
• intact circulation
• normal fluid homeostasis including:
– Intact vessel wall integrity
– maintenance of intravascular pressure
• 60% of body weight is water
• Intracellular fluid compartment – 40%
• Extracellular fluid compartment – 20%
– Interstitial fluid including lymph fluid
– Intravascular fluid or blood plasma
– Transcellular fluid
Edema
• Edema is an increased fluid collection in the
interstitial tissue spaces.
• The fluid can be collected in different body
cavities:
– Hydrothorax
– Hydropericardium or
– Hydroperitoneum(ascites)
• Anasarca is a severe and generalized edema
with profound subcutaneous tissue swelling
There are two types of edema fluid:
1. Transudate
– It is a protein-poor fluid
– occur when there is
• under conditions of reduced plasma protein
2. Exudate (inflammatory edema)
– is a protein-rich
– Occurs because of increased vascular
permeability following inflammation
Pathophysiology of edema
➢Conditions that result in edema are:
• Increased Hydrostatic Pressure
• Reduced Plasma Osmotic Pressure
(Hypoproteinemia)
• Lymphatic Obstruction
• Inflammation
• Sodium and water retention
Increased Hydrostatic Pressure
➢Conditions that increase hydrostatic pressure:
A. Impaired venous return
– congestive heart failure
– constrictive pericarditis
– ascites (liver cirrhosis)
B. Venous obstruction or compression
– Thrombosis
– external pressure (e.g., mass)
Reduced Plasma Osmotic Pressure
(Hypoproteinemia)
➢Causes:-
• Protein-losing glomerulopathies (nephrotic
syndrome)
• Liver cirrhosis
• Malnutrition
• Protein-losing gastroenteropathy
Lymphatic Obstruction
• Inflammatory
• Neoplastic
• Postsurgical
• Postirradiation
Edema can involve any body part but most
common sites includes:
• subcutaneous tissues,
• lungs, and
• brain
• Subcutaneous edema can be diffuse (anasarca)
or more prominent in regions with high
hydrostatic pressure
• dependent edema is an edema which is more
prominent in certain body areas with higher
effects e.g. Lower extremities
– It is a prominent feature of cardiac failure
• Edema due to renal dysfunction is generally
more severe than cardiac edema and affects all
parts of the body equally.
Subcutaneous edema can be pitting or
nonpitting
• Pitting edema – is when a finger pressure over
edematous tissue displaces the interstitial
fluid and leaves a finger-shaped depression
• None pitting edema – when finger pressure
leaves no depression
Effects of edema
• Depends on site of occurrence
• Can be minor or sever.
– pulmonary edema can cause death by interfering
with normal ventilatory function.
– Brain edema is serious and can be rapidly fatal.
HEMORRHAGE
• it is extravasation of blood from vessels into the
extravascular space
• The extravasation can be either to the exterior of the body
or into non vascular body spaces
Causes
• Trauma – the most common cause
• Atherosclerosis
• inflammatory erosion of the vessel wall
• Neoplasm
• Congestion
• Aneurysm
• Vitamin C deficiency
• spontaneous haemorrhage
➢Terminologies
• Hematoma: accumulation of blood in tissues.
• Petechiae :Minute (1- to 2-mm) hemorrhages
into skin, mucous membranes.
• Purpura :Slightly larger (up to 1 cm) superficial
hemorrhages in the skin
• Ecchymosis: A larger superficial hemorrhage in
the skin
• Hemothorax, Hemoperitoneum,Hemarthrosis,…
– Accumulation of blood at the respective tissue spaces
• Consequence of haemorrhage depends on
• The volume of blood lost
– Greater losses can cause haemorrhagic (hypovolemic)
shock.
• The rate of blood loss – much blood losses can be
tolerated if they appear in long period of time
• The site of haemorrhage is also important
– bleeding in subcutaneous tissues can be insignificant
– if bleeding located in the brain it may cause death
HYPEREMIA AND CONGESTION
• both indicate a local increased volume of
blood in a particular tissue.
• Hyperemia is an active process resulting from
augmented blood flow due to arteriolar
dilation.
– The affected tissue is more red than normal
➢Congestion is a passive process resulting from
impaired venous return out of a tissue.
• It can be
– local, resulting from an isolated venous
obstruction or
– systemically, as in cardiac failure, or it may be.
• The tissue has a blue-red color (cyanosis)
• congestion and edema commonly occur
together.
1. Acute passive congestion
• occurs in shock, acute inflammation, or sudden right-sided
heart failure.
2. Chronic passive congestion
• In long-standing congestion → poorly oxygenated
blood causes hypoxia → results in parenchyma cell
degeneration, fibrosis or cell death.
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❑Pulmonary congestion:
– 1. Acute pulmonary congestion:
• Alveolar capillaries engorged with blood
• Septal edema
• capillary rupture and passage of red cells into the
alveoli.
– 2. Chronic passive congestion
• left-sided heart failure
• Thickened & fibrotic septa
• Phagocytosis and degradation of red cells result in
intra-alveolar hemosiderin laden macrophages called
heart failure cells➔ brown indurations
• Can result in pulmonary hypertension
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❑Hepatic congestion:
A. Acute hepatic congestion:
– central hepatocyte degeneration.
– Peripheral hepatocytes better oxygenated & develop only
fatty changes.
B. Chronic passive congestion of the liver and lower
extremities is most often caused by right-sided heart failure.
• Nutmeg liver, Central lobules grossly depressed
because of loss of cells & appear red brown
• the surrounding brownish-yellow, often fatty, liver
cells.
• cardiac cirrhosis
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Hemostasis
• Hemostasis a collective term which involves:
• 1. maintenance of blood in a fluid, clot-free
state in normal vessels
• 2 prevent blood loss by inducing the rapid
formation of a localized hemostatic plug at the
site of vascular injury.
Normal Hemostasis
• sequence of events in hemostasis at a site of vascular
injury :
A. Local vasoconstriction
– This effect is transient and reduce blood flow
B. Primary hemostasis
– Characterized by platelets aggregation
C. Secondary hemostasis
– Involves activation of the coagulation cascade →clot
formation
D. Counter-regulation (fibrinolysis)
– to limit the hemostatic plug to the site of injury
Thrombosis
• It is blood clot (thrombus) formation in
uninjured vessels or thrombotic occlusion of a
vessel after relatively minor injury
• Both hemostasis and thrombosis involve three
components:
– the vascular wall
– platelets, and
– the coagulation cascade
Pathogenesis
• There are three factors that predispose to
thrombus formation.
They are called Virchow's triad
• (1) endothelial injury
• (2) stasis or turbulence of blood flow, and
• (3) blood hypercoagulability
Endothelial Injury
• An intact dry and smooth endothelium is anti
thrombotic (prevent adhesion of platelet and
other blood cells)
• Endothelial injury by itself can lead to
thrombosis
• Physical loss or functional disruption of
endothelium → exposure of sub endothelial
ECM, adhesion of platelets→ thrombosis
Endothelial dysfunction in the absence of
endothelial cell loss may occur with:
• hypertension,
• turbulent flow over scarred valves, or
• the action of bacterial endotoxins.
• Hypercholesterolemia
• products absorbed from cigarette smoke
• radiation
Alterations in Normal Blood Flow
• Turbulence contributes to arterial and cardiac
thrombosis by causing endothelial injury or
dysfunction.
• stasis is a major contributor to the
development of venous thrombi.
• Normal blood flow is laminar.
• Stasis and turbulence :
– Disrupt laminar flow and bring platelets into
contact with the endothelium
➢ Conditions that alter blood flow
Turbulence
• Ulcerated atherosclerotic plaques
• Stenosed valves,…
Stasis
• Aneurysms, abnormal aortic and arterial dilations
• Myocardial infarction
• Atrial fibrillation,…
Hypercoagulability
• Contributes less frequently to thrombotic
states
• Is defined as any alteration of the coagulation
pathways that predisposes to thrombosis.
• Can be primary (genetic) or secondary
(acquired) disorders .
• Of the inherited causes of hypercoagulability,
mutations in the factor V gene and the
prothrombin gene are the most common
Secondary (Acquired) Hypercoagulable States :-
• oral contraceptive use
• Pregnancy
• Cancers
• Smoking and obesity
• Prolonged bed rest or immobilization
• Advanced age,….
Types of thrombus
Arterial thrombi Venous thrombi
– Arise at the site of – Arise at area of stasis
endothelial injury – Grow in the direction
and turbulence of blood flow from
– Grow in a retrograde its site of
fashion, against attachment.
blood flow from its – Has loose
site of attachment. attachment
– Has firm attachment – Almost invariably
– They are usually occlusive
occlusive – 90% of occur in
lower extremities.
• Mural thrombi: thrombi occurring in heart
chambers or in the aortic lumen.
• Vegetations: thrombi on heart valves .
– E.g. infections can cause valve damage,
subsequently leading to large thrombotic masses
(infective endocarditis)
– Sterile vegetations can also develop on
noninfected valves in hypercoagulable states.
Fate of the Thrombus
• Propagation: the thrombus may accumulate
more platelets and fibrin, eventually causing
vessel obstruction.
• Embolization: thrombi may dislodges or fragment
and travel to other sites in the vasculature.
• Dissolution: removal of thrombi by fibrinolytic
activity
• Organization and recanalization: Thrombi induce
inflammation and fibrosis ,and there will be
formation of capillary channels across the
thrombus, re establishing lumen continuity.
EMBOLISM
• An embolus is a detached intravascular mass that
is carried by the blood to a site distant from its
point of origin
➢ Causes of embolism:
– Thromboembolism – 99%
– Fat droplets
– Air embolism
– Atherosclerotic debris (cholesterol emboli),
– Tumor fragments,
– Foreign bodies,…
Thromboembolism
• Emboli lodge in vessels resulting in partial or
complete vascular occlusion → ischemic
necrosis (infarction) of downstream tissue
• The site of impaction of an embolus depends
on the source of the emboli
• Embolism in the pulumonary arteries & their
branches derive from thrombus in systemic
veins or the right side of the heart.
• systemic emboli arise from the left side of the
heart or arteries.
Thromboembolism
• a) Pulmonary thromboembolism (PTE)
• b) Systemic thromboembolism
• c) Crossed embolism
Pulmonary thromboembolism
• > 95% of venous emboli originate from deep leg
vein thrombi.
• Reach to right side of the heart before entering
the pulmonary vasculature.
• The effect of pulmonary embolism depends on
the size of the embolus and on the state of
pulmonary circulation.
• Depending on the size of the embolus, it may
occlude the main pulmonary artery, impact
across the bifurcation (saddle embolus), or pass
out into the smaller, branching arterioles .
• Most pulmonary emboli (60% to 80%) are
clinically silent because they are small.
• Sudden death, right ventricular failure (cor
pulmonale), or cardiovascular collapse occurs
when 60% or more of the pulmonary
circulation is obstructed with emboli.
• patient who has had one pulmonary embolus
is at high risk of having more.
Systemic Thromboembolism
• refers to emboli in the arterial circulation
Origins of systemic Thromboembolism :
• intracardiac mural thrombi-80%
– two-thirds of which are associated with left
ventricular wall infarcts and dilated left atria
• aortic aneurysms
• thrombi on ulcerated atherosclerotic plaques,
• fragmentation of valvular vegetations
• In contrast to venous emboli, which tend to
lodge primarily in one vascular bed (the lung),
arterial emboli can travel to a wide variety of
sites.
• The major sites for arteriolar embolization are:
– the lower extremities (75%)
– brain (10%)
– intestines, kidneys, and spleen affected to a lesser
extent
The consequences of embolization depend on:
• vulnerability to ischemia,
• caliber of the occluded vessel, and
• the collateral blood supply
Crossed embolism
• or paradoxical embolism
• occurs in the presence of interventricular
defect when an embolus transferred from the
right to the left side of the heart, then to
systemic circulation.
Fat Embolism
• It is due to entry of fat globules in the
circulation.
• It usually follows fracture of bones
• it is asymptomatic in most cases and fat is
removed.
The pathogenesis includes :
• mechanical vascular obstruction by fat emboli
• biochemical injury.
– free fatty acid from fat globules cause local toxic
injury to endothelium.
• Fat embolism occur due to inflammation
induced raised tissue pressure at the site of
injury that forces fat in to marrow sinsosoid &
veins
• The features of this syndrome are a sudden
onset of dyspnea, blood stained sputum,
taccycardia, change in mental status
Air embolism
• Entry of gas bubbles within the circulation that
can obstruct vascular flow
• Clinical effect seen if >100cc air enter in to
circulation
• Air may enter the circulates during:
– Obstetric procedures
– Chest wall injury
– In deep see divers & under water construction
workers.
– Neck wounds penetrating the large veins
– Cardio thoracic surgery.
– Arterial catheterisation& intra venous infusion. Etc.
Amniotic fluid embolism
• It is a grave but uncommon complication of
labour
• It had mortality rate over 80%.
• The amniotic fluid containing fetal material
enters via the placental bed, the ruptured
uterine veins.
• The onset is characterized by sudden sever
dyspnea,cyanosis, hypotensive shock followed
by seizure & coma of the labouring mother.
• 50% cases they will develop DIC due to fetal
material activation of the coagulation cascade.
Infarction
• An infract is an area of ischemic necrosis caused
by occlusion of either the arterial supply or
venous drainage in a particular tissue.
• 99% of all infarcts result from arterial
thromboembolism
• Mechanism include:
– Local vasospasm
– Expansion of atheroma
– External compression of the vessels. e.g trauma
– Entrapment of vessels at hernial sacks etc.
Factors that determine the size & development
of an infract:
A. The nature of vascular supply
• The presence of dual blood supply in the Lung
, Liver, Hand & fore arm offset the occurrence
of infraction rapidly unlike renal & spleenic
circulation, which have end arterial supply.
• B: Rate of development occlusion:
– slowly developing occlusions → provide time for
collaterals dev’t →infraction are less likely
• C: Vulnerability or susceptibility to hypoxia
– Death of cells after ischemia varies
• Neurons after 3 to 4 minutes
• Myocardial cells die after 20-30min of ischemia
• D: Oxygen content of blood
– in an anaemic patients even partial obstruction may
lead to tissue infarction
• E: The severity & duration of ischemia.
Types of infarcts
• Infarcts are classified deepening on:
• A) The basis of their colour (reflecting the
amount hemorrhages)
– Hemorrhagic (red)
– white(anemic)
• B) The presence or absence of microbial
infection
– Septic
– Bland
A. Red infarcts
• It occurs:
– Venous occlusions as in ovarian torsion
– In loose tissues such as lung which allow blood to
collect in infarcts zone
– Tissues with dual circulations (eg. lung), permitting
flow of blood from unobstructed vessel in to necrotic
zone
– In tissues that were previously congested because of
sluggish out flow
– When flow is re established to a site of previous
arterial occlusion & necrosis
B. White infarcts
• It occurs in arterial occlusion or in solid organs
such as heart, spleen, kidney, where the
solidity of the tissue limits the amount of
hemorrage that can percolate
Morphology
• Gross
• All infarcts tend to be wedge shaped, with the
occluded vessel at the apex and the periphery
of the organ forming the base.
• Microscopy
• ischemic coagulative necrosis.
• The brain is an exception to this
generalization, where liquifactive
• necrosis is common.
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.
Disseminated intravascular
coagulation (DIC)
Definition: -
• - It is an acute, or chronic thrombohemorrhagic
disorder
• occurring as a result of progressive activation of
• coagulation pathway beyond physiologic set point
• secondary to a variety of diseases resulting in
failure of
• all components of hemostasis, hence the other
term for
• DIC is consumption coagoulopathy.
Etiology and Pathogenesis