Hemodynamic Disorders

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Hemodynamic Disorders

• Dr. Raid Jastania

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Intended Learning Outcomes

• Students should be able to define edema,
  congestion, hemorrhage, thrombosis and embolism.
• Students should know the common causes of
  hemodynamic disorders and the consequences of
  them.
• Students should understand the mechanisms of
  thrombosis.
• Students should understand the types of shock.

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Edema

• Edema is defined as increased fluid in
  interstitial tissue space.
• Hydrothorax is edema in the thoracic cavity.
  Hydropericardium is edema in the pericardial
  cavity, and hydroperitoneum is edema in the
  peritoneum.

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Edema

• Mechanisms and Causes
• Increased hydrostatic pressure
• Decreased osmotic pressure
• Lymphatic obstruction
• Sodium retention
• Inflammation

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Edema

• Mechanisms and Causes
• Increased hydrostatic pressure
• Can be localized as in limbs eg. Deep vein
  thrombosis DVT
• Can be generalized as in heart failure.
• Decreased osmotic pressure
• Common causes liver cirrhosis, nephritic
  syndrome and malnutrition

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Edema

• Mechanisms and Causes
• Lymphatic obstruction
• As in elephantiasis or obstruction by malignancy
  or following surgery and radiation therapy.
• Sodium retention
• As in excessive salt intake in renal
  insufficiency, or increased rennin-angiotensin-ald
  osterone system.
• Inflammation

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Edema

• Common sites of edema
• Subcutaneous edema occurs in heart failure in
  the dependent part of the body eg. Legs and
  sacral area (dependent edema, or pitting edema)
• Pulmonary edema is accumulation of fluid in the
  alveolar space. It occurs in heart failure (Left
  side failure). It can occur with renal failure or
  pulmonary infection.
• Brain edema
• Localized in abscess or around tumors
• Generalized in encephalitis, hypertensive
  crisis.

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Hyperemia and Congestion

• It is local increase in the volume of blood in
  tissues.
• Hyperemia is an active process eg. Increase blood
  to skeletal muscle during exercise
• Congestion is passive eg. Heart failure.
• Congestion Edema - tissue hypoxia.

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Hyperemia and Congestion

• Common sites of congestion
• Pulmonary congestion
• Acute alveolar capillary congestion with edema
  and focal hemorrhage
• Chronic like acute with fibrosis of alveolar
  walls and hemosiderin.
• Liver congestion
• Acute congestion of central veins and sinusoids
• Chronic like acute with necrosis of the central
  region and fibrosis (nutmeg liver, and Cardiac
  cirrhosis).

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Hemorrhage

• Hemorrhage is extravasation of blood due to
  rupture of blood vessel.
• Causes
• Trauma
• Atherosclerosis
• Inflammation
• Erosion by tumor

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Hemorrhage

• Hemorrhage can be external or internal
  (hematoma).
• Hemothorax, themopericardium, hemoperitoneum,
  hemarthrosis.
• It can be minimal or fatal.
• Clinical significance depend on the site,
  amount, chronicity.

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Hemorrhage

• Petechiae minute hemorrhage (1-2mm) of skin and
  mucosa. Occur due to thrombocytopenia, clotting
  factor deficiency, or increased pressure in
  capillaries.
• Purpura small hemorrhage (3-5mm), usually due to
  trauma or vasculitis.
• Bruises is subcutaneous hematoma. Change in
  color red blue green yellow brown due to
  metabolism of hemoglobin to bilirubin and
  hemosiderin.

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Shock

• Shock is systemic hypoperfusion due to reduction
  in cardiac output or in effective circulation.
• Features Hypotension, hypoperfusion, cellular
  hypoxia.

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Shock

• Types
• Cardiogenic shock
• Hypovolemic Shock
• Septic shock
• Neurogenic shock
• Anaphylactic shock

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Shock

• Cardiogenic shock
• failure of the heart to pump sufficient blood.
• Causes myocardial damage eg. Myocardial
  infarction, arrhythmia, pulmonary embolism with
  outflow obstruction.
• Hypovolemic Shock
• Loss of blood or plasma eg. Hemorrhage or severe
  burn

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Shock

• 3. Septic shock
• Systemic infection, commonly due to gram negative
  bacteria
• 4. Neurogenic shock
• As in spinal cord injury
• 5. Anaphylactic shock

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Septic Shock

• 25-50 mortality
• Common cause of death in ICU
• 70 due to endotoxin-producing gram negative
  bacilli
• Endotoxins are bacterial wall lipopolysaccharides
  (LPS)
• LPS binds to protein in plasma

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Septic Shock

• LPS activate WBC by the interaction with the
  receptor CD14 on macrophages and neutrophils.
• Stimulates the release of IL-1 and TNF
• Activates endothelial cells, and complement system

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Septic Shock

• With high level of LPS
• Systemic vasodilatation (hypotension)
• Decreased myocardial contraction
• Wide-spread endothelial activation
• Activation of coagulation system

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Stages of shock

1. Initial non-progressive stage
2. Progressive stage
3. Irreversible stage

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Stages of shock

• Initial non-progressive stage
• There is compensation and perfusion of vital
  organs
• By the action of baroreceptors, neurohormonal
  action, catecholamines, Renin-angiotensin-aldoster
  one system
• Tachycardia, peripheral vasoconstriction

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Stages of shock

• 2. Progressive stage
• Tissue hypoxia
• Anaerobic glycolysis
• Lactic acidosis
• Arteriolar dilatation
• 3. Irreversible stage
• Tissue injury, necrosis, infarction
• Common organs affected heart, kidney, brain,
  lungs, adrenal and GI tract