CIRCULATORY DISTURBANCES

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CIRCULATORY DISTURBANCES

• BY
• DR.SOHEIR SAAD

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CIRCULATURY DISTURBANCES
In circulatory disturbances, the amount of blood
in the tissues may be increased or it may be
decreased.
Hyperemia It means active dilatation of
the arterioles and capillaries in response to
increased metabolic activity.
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Increased Blood Content

• Hyperaemia
• Active dilation of arterioles and capillaries
• arterial hyperaemia
• Physiological ---- muscular Ex.
• Pathological ------acute inflammation

• Congestion
• Passive dilation of veins and
• capillaries
• Venous Congestion
• General
• acute as acute heart failure chronic (
  gradual) e.g. RT sided HF.
• Local
• Acute sudden complete venous obstruction due
  to thrombosis
• chronic gradual incomplete venous obstruction
  e.g. venous compression

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Congestion It means passive dilatation of the
veins and capillaries in consequence to
obstruction of the venous outflow from part.

• General Venous Congestion
• A) Acute occurs in acute cardiac failure.

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• B) Chronic venous congestion
• affecting the whole venous system.
• It is associated with cardiac or pulmonary
  diseases since the entire circulating blood pass
  through them.
• - Cardiac diseases e.g. mitral stenosis, or
  those which produce left-sided heart failure e.g.
  aortic valve diseases and hypertension,.
• - Lung diseases which reduce the pulmonary
  vascular bed e.g. fibrosis, tuberculosis and
  emphysema.
• In most cardiac diseases, chronic venous
  congestion C.V.C is preceded or associated with
  pulmonary chronic venous congestion. When
  pulmonary disease is the primary cause, passive
  congestion of the lung does not occur and back
  pressure affect the right side of the heart and
  cause chronic venous congestion.

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Manifestations of Chronic Venous Congestion I.
Physical examination of the patient shows -
Congested pulsating neck veins. - Enlarged tender
liver. - Generalized cardiac oedema. - Mild
cyanosis due to hypoxia (deficient oxygenation of
blood). II. All internal organs are affected,
they are congested, slightly enlarged and there
may be little impairment of function.
1. Changes in the Lung Occur in cases of
mitral and left sided heart failure. The end
result is brown induration.
2. Changes in the Liver Result in Nut Meg liver
Cardiac Cirrhosis
Changes in the Spleen
Changes in the Kidney
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Chronic venous congestion of the lung
1.Alveolar wall thick 2.Alveolar capillary are
congested 3.Alveolar lumen filled with
R.B.Cshemosidrin
(Macrophage engulphing R.B.Cs)
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Chronic venous congestion of the lung
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ISCHAEMIA

• Decrease blood supply to a part of tissue due to
  occlusion of its artery
• 1-Sudden Ischemia (Acute ischemia)
• Sudden complete arterial occlusion by
• Thrombosis or embolism
• Surgical ligature of the artery
• Twisting of the pedicle of the movable organ
• Arterial spasm e.g. ergot poisoning
• EFFECTS
• A-sudden occlusion----- infarction and gangrene
  (inefficient collaterals)
• B-Efficient collaterals may not cause tissue
  damage
• 2-Gradual Ischemia (Chronic ischemia)
• Gradual incomplete occlusion
• Atherosclerosis
• End arteritis as in syphilis
• Pressure on the artery
• EFFECTS
• A With inefficient collaterals---- cellular
  degeneration, atrophy and replacement fibrosis
• B-With efficient collaterals no tissue damage
  occurs

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INFARCTION

• Is an area of coagulative necrosis (liquefactive
  in the brain) due to sudden occlusion of either
  arterial or venous supply (ischemia)
• Gross Picture
• Is pyramidal shaped as the arteries have a fan
  like distribution. The base is directed
  towards the surface of the organ.
• Is sub capsular, early raised due to edema,
  late depressed due to healed by fibrosis.
• It is surrounded by a red zone ( congestion)
• Firm in consistency, size depends on the size
  of the occluded vessel.

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TYPES OF INFARCTION

• RED INFARCTION (Hemorrhagic)
• Its occur in soft and vascular organs as lung,
  liver and intestine, early red due to
  hemorrhage and late pale in color
• PALE INFARCTION
• Are more common and occur in firm and less
  vascular organs as kidney, heart and spleen
• Microscopically, the structural outline of the
  affected tissue is preserved but the cellular
  details are lost.

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Microscopically, the structural outline of the
affected tissue is preserved but the cellular
details are lost.
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THROMBOSIS
Def.of thrombus Formation of a compact mass
composed of the elements of the circulating blood
inside a vessel or a heart during life.
CAUSES 1-Damage to the vascular endothelium
2- Slowing of blood stream(stasis)
3-Disorders of blood stream
4-Changes in the blood composition
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Causes 1-Damage to the vascular endothelium
( Indothelial Enjury) -Mechanical e.g. trauma
,pressure and ligature -Inflammatory e.g.
phlebitis, arteritis and endocarditis
-Degenerative e.g. atheroma and myocardial
infarction The platelet adhere to the
damaged endothelium 2- Slowing of blood
stream (stasis) -In heart failure e.g. in leg
veins -Valvular diseases e.g. in the auricles of
the heart -Varicose veins and in the portal
veins secondary to liver cirrhosis showing acute
inflammation
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• 3-Disorders of blood stream
• Aneurysm, atheroma, varicose veins (changes
  vascular lumen)
• Compression of the vessel wall from outside
• 4-Changes in the blood composition
• Platelets e.g. after operation increases in
  number and become more sticky----- lysis and
  release thromboplastin
• Fibrinogen e.g. increases during pregnancy and in
  lobar pneumonia
• Red cells e.g. in polycythemia
• WBCs e.g. in leukemia
• Plasma e.g. decreases in dehydration

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Classification of Thrombusaccording to

• COLOR
• Pale, formed of platelets and fibrin, small,
  grayish white, firm and adherent
• Red, formed of red cells and fibrin, dark soft
  and loosely attached to the vessel
• Mixed, common and has pale and red components

• Presence or absence of bacteria
• Infected or septic
• Non infected or aseptic

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Sites of Thrombus Formation

• 1.Thrombus in veins
• More common because of thin wall and slow blood
  flow
• Thrombophlebitis ----Septic
• Phlebothrombosis---- occurs in the veins of the
  calf Ms and femoral ,iliac veins------ pulmonary
  emboli
• In the varicose veins

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• 2.Thrombosis in Arteries
• less common than veins because of rapid flow
  and thick elastic wall but occur in arteries
  affected by
• Atheroma, polyarteritis nodosa and thromboangitis
  obliterans (roughness of the intima)
• Aneurysm due to stasis
• Lead to ischaemia

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• 3.Thrombosis in the heart
• more common in the the left side
• Mural---- occur over infarction
• Vegetations---- pale over the valve
• Auricular--- adherent to valve, if detach called
  ball thrombus
• Agonal--- red thrombi occurring in Rt. V at the
  time of death specially lobar pneumonia
• 4.Thrombosis in capillaries (very rare)
• occur in acute inflammation ,sever cold and
  frost bite

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Mechanism of Thrombosis 1. Endothelial cell
injury releases thrombotic tissue factors (factor
VIII) and platelets adhesive factors. The exposed
collagen in the subendothelium also stimulates
platelets adhesion and clotting events. 2. The
aggregated platelets release both a) ADP (strong
promotor of thrombogenesis) which induce more
platelets aggregation and synthesis of
thromboxane A2 which causes vaso-constriction. b)
Thrombin which changes fibrinogen to fibrin. - So
platelet aggregation is induced by ADP, TX A2 and
thrombin. 3. This platelet aggregation is
reversible by many thrombotic inhibitory factors
e.g. prostaglandins called prostacyclin (PG I2)
secreted by endothelial cells. 4. With the
increasing in amount of ADP-TX A2, the platelets
contract forming irreversible aggregated
platelets. 5. Thrombin transforms fibrinogen into
fibrin mesh entangling platelets and other blood
cells forming thrombus. - The adherent platelets
release more adenosine diphospharte ADP which
promotes further aggregation and adhesion of
platelets in lines called lines of Zahn more
fibrin is formed, the thrombus enlarge and
finally occludes the lumen of the vessel
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Fate of the Thrombus

• 1-septic thrombus----- fragmented by the
  proteolytic enzymes into septic emboli causes
  pyaemic abscesses
• 2-Aseptic thrombus--- its element disintegrate
  and form a pale red structure less mass
• If mass is small it dissolves by fibrinolysis
• If mass is large it undergoes

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If mass is large it undergoes

• Organization the thrombus is invaded by
  capillaries and fibroblast --- change to fibrous
  mass lead to permanent vascular occlusion
• Organization and Canalization some time
  capillaries dilated and allow Passage of blood
  through the thrombus
• Incorporation the fibrosed thrombus shrinks
  from the vascular wall leaving a space which gets
  lined by endothelium
• Dystrophic calcification----- phlebolith
• Detachment--- aseptic emboli--- infarctions
• Propagating thrombus--- due to spread of venous
  thrombosis

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CLOT

• A mass of blood elements formed in stagnant
  blood, is soft ,red, smooth surface, and not
  adherent to the vessel wall
• Post-mortem clots( occur in cardiac chambers
  after death) there are two types
• 1-Red or current jelly clot occurs with
  rapid blood clotting, formed of fibrin ,red and
  white blood cells
• 2-Yellow or chicken fat clot occurs
  with slow blood clotting, which allow
  sedimentation of red cells with plasma, fibrin
  and white cells above.

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Difference Between Thrombus And Clot

• THROMBUS
• Occur in circulatory blood
• Firmly attached
• Friable and dry
• Pale, pale red or red
• Shows lines of Zhan's

• CLOT
• In stagnant blood
• Loosely attached
• Soft and moist
• Red and yellow
• No line of Zhan's

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EMBOLISM

• Embolus An insoluble solid, liquid or gaseous
  mass circulating in blood stream
• Embolism Is the process of impaction of the
  embolus in a narrow vessel
• Sites of Emboli
• Systemic arteries
• Pulmonary arteries
• Intrahepatic branches of the portal vein
• TYPES of Emboli
• 1-Detached thrombi and vegetation
• 2-Tumor emboli
• 3-Parasitic (e.g. bilharzias ova)
• 4-Air emboli
• 5-Fat emboli
• 6-Clumps of bacteria
• 7-Amniotic fluid emboli
• EFFECT of EMBOLI of Thrombotic origin depends
  upon
• Size and nature (septic or aseptic)
• State of the collateral circulation in affected
  organ
• Aseptic produces transient ischemia if it has
  good collateral circulation and infarction if
  poor
• Septic produces pyaemic abscess at site of
  impaction

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HEMORRHAGE

• Escape of blood outside the blood vessels or
  cardiac chambers
• TYPES
• EXTERNAL Hemorrhage
• Epistaxis bleeding from the nose
• Hemoptysis coughing of blood, red frothy and
  alkaline
• Hematemesis vomiting of blood. From
  esophagus, stomach and duodenum, brown in
  color, digested, acidic, and mixed with food.
• Melena dark digested blood in stools
• Hematuria blood in urine
• Menorrhagia prolonged menstrual bleeding
• Metrorrhagia Irregular uterine bleeding not
  related to menstruation

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• INTERNAL Hemorrhage
• Escape of blood inside the body cavities
• Hemothorax hemorrhage into the pleura
• Hemopericardium hemorrhage into the
  pericardium
• Hemoperitoneum hemorrhage into the peritoneum
• Hematocele hemorrhage into tunica vaginalis
• Hemoarthrosis hemorrhage into joint cavity
• INTERSTITIAL Hemorrhage
• Petechial pointed blood from capillary
  origin
• Ecchymosis Moderate amount of blood
• Hematoma Large amount of blood causing
  swelling
• Interstitial hemorrhage first dark red --- green
  (biliverdin)----brown (hemosiderin)---- yellow
  gradually fades

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• EFFECT OF HEMORRHAGE
• Small amount no effect
• Small amount (repeatedly)chronic causes
  microcytic hypochromic anemia
• Moderate amount less than (750cc) is
  compensated by
• Immediate fall in blood pressure stimulates
  the aortic arch and carotid sinus reflexes which
  increase the heart rate
• Reflex vasoconstriction in the skin, muscle
  and splanchnic area to maintain the blood
  pressure and release of adrenaline elevates the
  blood pressure
• The decreased hydrostatic pressure inside
  the vessels allow the colloid osmotic pressure to
  withdraw tissue fluids into the blood
• Proteins are added from the liver and
  reticulo-endothelial system
• Red and white cells are added by the bone
  marrow.
• Massive amount
• Causes hemorrhagic shock and death
• The venous return decreases, cardiac output
  decreases and blood pressure falls

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• OEDEMA
• Definition
• It is an abnormal accumulation of fluid in
  tissue spaces and serous cavities. This fluid may
  be in the form of transudate or exudate.
• There is a continuous interchange of fluid
  between blood and the tissues. Some fluid enters
  the lymphatics before eventually returning to the
  blood stream.
• In order to maintain, this normal condition, two
  main forces operate a pressure gradient which
  controls the rate and direction of fluid
  movement.
• A) Forces that drive fluid outside the vessels
• - Hydrostatic pressure of the blood.
• Osmolarity of interstitial fluid.
• B) Forces retaining fluid inside the vessels
• - Protein osmotic pressure.
• - Interstitial tissue pressure.

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• CAUSES Of Oedema
• Increased capillary hydrostatic pressure
• A rise in the venous pressure is followed by
  a rise in the capillary pressure, increased
  transudation of fluid into the tissue spaces and
  decrease reabsorption at the venous end of the
  capillaries, so edema occurs.
• Decrease colloid osmotic pressure of the plasma
• When the total plasma proteins drops below
  2.5gm
• lead to excess fluid passes into the tissue
  spaces
• Increased capillary permeability
• Caused by toxins or chemicals as serotonin and
  histamine in acute inflammation and hypoxia
• The plasma escapes into the tissue spaces and
  withdraw- more fluids from the vessels by its
  osmotic pressure
• Lymphatic obstruction local edema
• Sodium and water retention
• due to renal or increased aldosterone occurs
  in CHF, liver cirrhosis, nephrotic syndrome and
  acute glomerulonehpritis

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Classification Of Oedema

• Localized
• Obstructive
• Acute Inflammation
• Allergic
• Hard (Non-Pitting)

• Generalized
• (Anasarca)
• Cardiac, Renal
• Nutritional
• Soft (Pitting)

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LOCALIZED EDEMAObstructive

• Venous Obstruction
• Liver cirrhosis-- ascitis
• Acute left sided heart failure---- pulmonary
  edema
• The pregnant uterus edema lower limbs
• Pressure on a large vein

• Lymphatic Obstruction
• Acute lymphangitis and lymphadenitis( Filarial)
• Post-inflammatory and post-irradiation
• Tumor emboli in lymph vessels and tumor
  metastases in the lymph nodes

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• Generalized Edema
• Cardiac In congestive heart failure
• Renal in renal diseases
• 1.Nephretic syndrom
• 2.Nephrotic syndrom
• Nutritional caused by hypo-proteinemia
• Inadequate protein intake
• Interference with the intake, passage, digestion
  or absorption of food in GIT.
• Decrease plasma protein formation as in chronic
  liver diseases

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• Clinically
• Oedema can be classified according to its nature
  into
• Pitting (Soft Oedema)
• The oedema fluid is free in the tissue spaces
  and can be moved by pressure from one area to
  another, so it pits on pressure by the examining
  finger. Occurs in cardiac, renal and hepatic
  oedema as the fluid is a transudate (low protein
  content).
• B) Non-Pitting (Hard Oedema)
• Oedema fluid unites with tissue elements, cannot
  be moved or pit on pressure, e.g. lymphatic
  oedema.
• 1. In case of filariasis.
• 2. Infiltration of lymphatics by malignant cells.
• 3. Surgical removal of lymph nodes.
• 4. Fibrosis of lymphatics after radiotherapy.

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• Pathological Feature of Edema
• All tissue except bone may be seated of edema
• Common sites are
• Subcutaneous Tissue
• Gross Affected area appears swollen, covering
  skin is stretched, inelastic and pitting. When
  skin is incised a clear fluid oozes out.
• Microscopic Connective tissue fibers separated
  from each other and its protein content
  coagulates to form homogenous pink substance.
• LUNG
• Gross Heavy, cut surface oozes frothy fluid
• MIC. Alveolar spaces filled with pale red
  homogenous protein
• BRAIN
• Gross Heavy, suilci narrow and gyri are swollen
  and increase intracranial pressure
• SEROUS CAVITIES
• A transudate accumulates with a specific gravity
  below 1015

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SHOCK

• Definition
• Shock means acute circulatory failure due to
  marked acute reduction in the cardiac output
• CLINICAL PICTURE
• The patient is usually quiet or restless
• The skin is cold, pale, and covered with sweat
• The pulse is weak and rapid, blood pressure low,
  respiration shallow and rapid
• The urine volume is decreased ( oliguria)

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TYPES OF SHOCK

• Normovolmic shock
• The blood volume is normal
• Example
• 1.Cardiogenic shock
• 2.Neurogenic shock
• 3.Anaphylactic shock
• 4.Endotoxin shock

• HYPOVOLEMIC SHOCK
• Due to decreased blood volume
• Example
• 1.Hemorrhge(loss of whole blood)
• 2.Losse of plasma(sever burnsperitonitis)
• 3.Losse of fluidelectorolyt
• (diarrheavomiting)

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CARDIOGENIC SHOCK

• Myocardial infarction
• Major pulmonary emboli
• Following cardiac surgery
• Myocarditis
• Other causes of acut ht. faliure

Pathogenesis if compensatory vasoconstriction
does not correct the shock, tissue anoxia will
cause more dilation of the blood vessels and the
shock becomes irreversible
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NEUROGENIC SHOCK

• IN sever pain or fear v.c of arterioles
  venules
• In spinal injury
• Pathogenesis
• Reflex vasodilatation venous return decreases
  cardiac output decreases blood pressure falls
  cerebral anoxia loss of consciousness (
  transient)
• N.B
• Shock can be reversible if the cause cane be
• adequately treated.
• However shock cane be irreversable and dost
• respond to therapy
  prolonged tissue anoxia
• and acidosis.

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EFFECTS OF SHOCKThese vary according to severity
and duration of the condatio,the effects are
secondary to

• 1.Hypxia