Presentation on theme: "Hemodynamic Disorders Dr. Raid Jastania. Intended Learning Outcomes 1.Students should be able to define edema, congestion, hemorrhage, thrombosis and."— Presentation transcript:
Hemodynamic Disorders Dr. Raid Jastania
Intended Learning Outcomes 1.Students should be able to define edema, congestion, hemorrhage, thrombosis and embolism. 2.Students should know the common causes of hemodynamic disorders and the consequences of them. 3.Students should understand the mechanisms of thrombosis. 4.Students should understand the types of shock.
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.
Edema Mechanisms and Causes: –Increased hydrostatic pressure oCan be localized as in limbs eg. Deep vein thrombosis DVT oCan be generalized as in heart failure. –Decreased osmotic pressure oCommon causes: liver cirrhosis, nephritic syndrome and malnutrition
Edema Mechanisms and Causes: –Lymphatic obstruction oAs in elephantiasis or obstruction by malignancy or following surgery and radiation therapy. –Sodium retention oAs in excessive salt intake in renal insufficiency, or increased rennin- angiotensin-aldosterone system. –Inflammation
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: oLocalized: in abscess or around tumors oGeneralized: in encephalitis, hypertensive crisis.
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.
Hyperemia and Congestion Common sites of congestion: –Pulmonary congestion: oAcute: alveolar capillary congestion with edema and focal hemorrhage oChronic: like acute with fibrosis of alveolar walls and hemosiderin. –Liver congestion: oAcute: congestion of central veins and sinusoids oChronic: like acute with necrosis of the central region and fibrosis (nutmeg liver, and Cardiac cirrhosis).
Hemorrhage Hemorrhage is extravasation of blood due to rupture of blood vessel. Causes: –Trauma –Atherosclerosis –Inflammation –Erosion by tumor
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.
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.
Shock Shock is systemic hypoperfusion due to reduction in cardiac output or in effective circulation. Features: Hypotension, hypoperfusion, cellular hypoxia.
Shock 1.Cardiogenic shock: a.failure of the heart to pump sufficient blood. b.Causes: myocardial damage eg. Myocardial infarction, arrhythmia, pulmonary embolism with outflow obstruction. 2.Hypovolemic Shock: a.Loss of blood or plasma eg. Hemorrhage or severe burn
Shock 3. Septic shock: a.Systemic infection, commonly due to gram negative bacteria 4. Neurogenic shock: a.As in spinal cord injury 5. Anaphylactic shock
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
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
Septic Shock With high level of LPS: oSystemic vasodilatation (hypotension) oDecreased myocardial contraction oWide-spread endothelial activation oActivation of coagulation system
Stages of shock 1.Initial non-progressive stage a.There is compensation and perfusion of vital organs b.By the action of baroreceptors, neurohormonal action, catecholamines, Renin-angiotensin-aldosterone system c.Tachycardia, peripheral vasoconstriction