BASED ON HEMODYNAMIC DISORDERS

1. HEMODYNAMIC
DISORDERS
LECTURE # 6
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2. HEMODYNAMIC DISORDERS
INTRODUCTION
 The study of the blood flow is called
hemodynamics.
 Thus hemodynamics deals with the
dynamics of blood flow.
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3. HEART, ARTERY, VEIN
GENERAL CIRCULATION
PULMONARY CIRCULATION
FUNCTIONS
DELIVER OXYGEN AND NUTRIENTS
CARRY AWAY METABOLIC WASTES
A HEALTHY CIRCULATING SYSTEM
1. Hemostasis
2. Normal Blood Volume
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5.  Edema (increased fluid in the ECF)
 Hyperemia (INCREASED flow)
 Congestion (INCREASED backup)
 Hemorrhage (extravasation)
 Thrombosis (clotting blood)
 Embolism (downstream travel of a clot)
 Infarction (death of tissues w/o blood)
 Shock (circulatory failure/collapse)
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DISORDERS

6. EDEMA (INCREASED FLUID IN THE
ECF)
 Increased hydrostatic pressure ( cardiac edema, etc.)
 Reduced plasma osmotic pressure (nephrotic, hepatic,
malnutrient edema, etc. )
 Lymphatic obstruction (filariasis infection — elephantiasis，
breast surgery, etc )
 Sodium and water retention (ARF, etc)
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elephantiasis Minimal Change Disease Pitting edema

8. HYPEREMIA (INCREASED FLOW)
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Arterial hyperemia (hyperemia)
An augmented blood flow inducing arteriolar and capillary dilation
Venous hyperemia (congestion)
Accumulation of Blood in Small Veins & capillaries result from
drainage difficulty of veins

9. Hyperemia
 Active process
 Red,
 raised temperature,
 increased volume ;
 Enhanced function;
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Congestion:
passive process;
Reddish blue color (cyanosis),
low temperature,
increased volume, edema;
Decreased function

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1. Systemic: general or pulmonary
Cardiac dysfunction (right or left)
2. Local: local venous compression or
obstruction
External Compression --- Tumor, Bandage
Thrombosis, Embolism Thickening of venous wall
Paralysis of neurogenic modulation –
Burn,
frostbite

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Acute pulmonary congestion Acute hepatic congestion

13. AN ESCAPE OF BLOOD FROM
A RUPTURED BLOOD VESSEL.
Hemorrhage
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14. HEMORRHAGE (EXTRAVASATION)
 Petechiae
 Purpuras
 Ecchymoses
 Hematoma
 Hemothorax
 Hemopericardium
Hemoperitoneum
The clinical
significance depends
on the volume, the rate
of loss and the site.
 Hemorrhagic shock
 Stroke
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—
—
hemoarthrosis

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Causes
1.Trauma
2.Peptic ulcer, aneurism, atherosclerosis
3.Enlarged interendothelial gap (basement
membrane injury).
4. The integrity of the vessels remains intact
5. Injury to vascular wall: sever infection,
anoxia, toxins

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6. Change in number and quality of platelets
uremia, leukemia,
7. idiopathic Disturbance of coagulation
mechanism
8. congenital disease,
9. DIC ,
10. deficiency of Vit. K

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Thrombosis
Blood clot (thrombus)
formation in cardiovascular
system of a living body

19. THROMBOSIS (CLOTTING BLOOD)
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Pathogenesis
 Endothelial injury
 Turbulence of blood flow
 Hypercoagulability

20. Clinical correlations
1. Venous thrombosis (phlebothrombosis)
Varicosities, embolism (sometimes fatal),
trauma, surgery, post partum
Cancer associated thrombosis
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21. CLINICAL CORRELATIONS
2. Cardiac and arterial thrombosis
 Mural thrombus
 cardiac infarction, rheumatic heart disease
 Embolize peripherally, brain, kidney, spleen, etc
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Mural thrombus Vegetation Hyaline thrombus

23. DIC (DISSEMINATED INTRAVASCULAR
COAGULATION)
 Usually happens in many severe disorders
 Coagulation System is Activated
 Consumption of coagulation substance and activation of
fibrinolytic system
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24. EMBOLISM (DOWNSTREAM TRAVEL
OF A CLOT)
Occlusion of cardiovascular system by some insoluble
mass.
 The mass is termed Embolus Solid, liquid, gaseous mass
 Thromboembolism 99%
 Fat, air, amniotic fluid, tumor fragment, etc
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25. PULMONARY THROMBO EMBOLISM
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26. TYPES
Systemic Thrombo-embolism
Fats Embolism
Gas Embolism
Amniotic Fluid Embolism
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27. FATS EMBOLISM
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28. ROUTE OF EMBOLI
Arterial emboli —— systemic embolism
Venous emboli —— pulmonary embolism
Portal vein emboli —— hepatic embolism
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29. INFARCTION (DEATH OF TISSUES)
Causes
 Occlusion of arterial supply or venous drainage
 Thrombosis, embolism, external compression
 Functional spasm of arteriole
Types
 White infarcts (anemic infarcts)
 Red infarcts (hemorrhagic infarcts) —
 Septic infarcts
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SPLEEN INFARCTION

31. FACTORS THAT INFLUENCE
DEVELOPMENT OF AN INFARCT
 Nature of the vascular supply
 Rate of development of occlusion
 Vulnerability to hypoxia
 Oxygen content of blood
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32. SHOCK (CIRCULATORY FAILURE/COLLAPSE)
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The typical signs of shock are low blood
pressure, rapid heart rate, signs of poor end-
organ perfusion (e.g., low urine output,
confusion, or loss of consciousness), and
weak pulses.
Circulatory shock is not related to the
emotional state of shock

33. SHOCK
 Shock is a life-threatening condition in
which delivery of oxygen to the organs is
low, causing organ damage and
sometimes death.
 Blood pressure is usually low.
 Shock has several causes: Low blood volume, inadequate
pumping action of the heart, or excessive widening (dilation)
ofblood vessels.
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