Fluid and Hemodynamic Derrangements


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By: Dr. Pamela Fabie

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Fluid and Hemodynamic Derrangements

  1. 1. By: Dr. Pamela Josefina T. Fabie
  2. 2.  The abnormal accumulation of fluid in the intercellular tissue of body cavities.  It may be localized or systemic
  3. 3. • ANASARCA – when edema is sever and generalized; with diffused swelling of all tissues and organs in the body• ASCITES – collection of edema fluid in the peritoneal cavity
  4. 4. • HYDROTHORAX – collection of edema fluid in the thoracic (pleural cavity) • PERICARDIAL EFFUSION – collection of edema fluid in the pericardial sac
  5. 5. FACTORS CONTRIBUTING TO EDEMA FORMATIONI. Arteriolar Dilatation – inflammation, heat, toxins, neurohumoral excess or deficitII. Reduced Effective Osmotic Pressure I. Hypoproteinemia – malnutrition, cirrhosis, nephrotic syndrome, protein-osing gastroenteropathy II. Leaky Vascular Endothelium – inflammation, burns, trauma, allergy III. Lymphatic Obstruction
  6. 6. III. Increased Venous Pressure – congestive heart failure, thrombophlebitis, liver cirrhosisIV. Sodium Retention – excessive salt intake, increased tubular reabsorption of sodium
  7. 7. MORPHOLOGY OF EDEMAA. In Cardiac Failure – edema is most severe in the dependent parts of the body (“dependent edema”)B. In Renal Failure – generalized, most manifested in loose tissues like the face, particularly the eyelids
  8. 8. “Pitting Edema” – fingerpressure over the edematoussubcutaneous tissue displace theinterstitial fluid from the skin toleave pitted depressionsEdema of the brain and the lungsare most life-threatening forms;edema of the brain is encounteredwith trauma, infections (meningitis,brain abscess, encephalitis)hypertensive crises, etc.
  9. 9. Pulmonary Edema – major manifestation of leftventricular failure; also found in renal disease, shock, infectionwithin the lungs, hypersensitivity states
  10. 10. • HYPEREMIA – occurs when arterial and arteriolar dilatation produces an increased flow of blood into capillary beds, with opening of inactive capillaries• Causes redness in the affected part;• Active hyperemia of the skin is seen whenever excess body heat must be dissipated like in muscular exercise and high fever. “Blushing”
  11. 11. • CONGESTION (Passive Hyperemia)• Results from impaired venous drainage• Causes an intensified blue-red colored, accentuated when there is an increase of deoxygenated blood – “Cyanosis”• Closely related with edema
  12. 12. Indicates exravasation of blood due to rupture of blood vessels
  13. 13. • HEMATOMA – significant amount of released blood accumulating within a tissue forming a massive clot; it may be relatively insignificant (as in bruise)or life-threatening
  14. 14. PETECHIAE – Minute (1-2mm), typically assoc. withlocalized intravascualr pressure, low plateletcounts(thrombocytopenia), defective platelet function, orclotting factor deficienciesPURPURA – Slightly larger (3-5mm), typically assoc. with many ofthe same disorders that causepetechiae, as well intrauma, vascular inflammation(vasculitis) or increased vascularfragility
  15. 15. ECCHYMOSES – Larger (1-2cm), theseare subcutaneous hematomas (bruises)The erythrocytes in these local hemorrhages aredegraded and phagocytosed by macrophages; theHemoglobin (red-blue color) is then enzymaticallyconverted to Bilirunin (blue-green) and eventually intoHemosidirin (golden-brown) accounting for acharateristic color changes in a hematoma
  16. 16. Formation of a solid mass in living blood vessels or in the heart from theconstituents of the blood; resultant mass is called “Thrombus”. A blood clot is formed by coagulation of extravascular blood
  17. 17. DANGERS OF THROMBOSIS 1. Diminished or obstructed blood flow  ischemia to tissue/organ 2. Becomes dislodged  EmbolusEMBOLUS – intravascular solid, liquid, or gaseousmass carried in the bloodstream to some siteremoved from its origin, or from its point of entry inthe CVS
  18. 18. INFARCTS – ischemic necrosis of tissuesArterial Thrombi – dry, friable grey massescomposed of almost regularly arrangedalternating layers of fibrin and platelets with scantamount of darker red coagulated blood resultingto laminations known as “Lines of Zhan”.
  19. 19. Venous Thrombi – more gelatinous moistappearance; called “Stasis or Red Coagulation” or“Phlebothrombosis” (90% in in veins)Post-Mortem Clot – cyanotic dark red “CurrantJelly” or with supernatant portion of coagulatedclear plasma “chicken fat” overlying a portion ofdarker hue where the red cells have settled
  20. 20. Detached intravascular solid, liquid orgaseous mass that is carried by the blood to a site distant from its point of origin
  21. 21. SYSTEMIC EMBOLISM – travel through the arterialcirculation; thrombi from the left side of the heart;affects the heart, lower extremity. Kidneys and spleen.Almost always cause infarction of the affected partsPULMONARY EMBOLISM – most common formand one of the most lethal; 95% arise from the thrombiwithing the veins of the legs – SADDLE EMBOLUS – large thrombus lodged in the bifurcation of the main pulmonary artery
  22. 22. • AIR OR GAS EMBOLISM– sometimes happen after delivery or abortion when it is forced into ruptured uterine venous sinuses by the powerful contractions of the uterus – “Caisson Disease” or decompression sickness, bends, chokes – occurs in sudden changes in atmospheric pressure and deep-sea divers
  23. 23. • FAT EMBOLISM (Circulating fat Microglobules) – caused by severe trauma to fat-laden tissues such as fractures of bone containing fatty marrows or fat depots• AMNIOTIC EMBOLISM (Amniotic Fluid Infusion) – fatal maternal obstetric complication; trauma in Labor
  24. 24. A localized area of ischemic necrosis in an organ or tissueresulting from occlusion of either its arterial supply or venous drainage, either by thrombosis and/or embolism
  25. 25. TYPES OF INFARCT1. ANEMIC (white) – encountered witharterial occlusion and in solid tissues;common in heart. Spleen and kidneys2. HEMORRHAGIC (red) – with venousocclusions in loose tissues, in tissues withdouble circulation and in tissue withpreviously congested; common inlungs, ovarian pedicles, intestine and brain
  26. 26. Infarcts may either be “Septic” or “Bland” • Presence or absence of bacterial infection In the area of necrosisIschemic Coagulative Necrosis – characteristiccytologic change in all infarcts
  27. 27. A constellation of syndromes, all characterized by low-perfusion circulatory insufficiency leading to imbalance in the metabolic needs of vital organs and the available blood flow; as aresult, oxygen and nutrient delivery to cells and removal of waste products are decreased
  28. 28. Signs and Symptoms:Hypotension, weak thready pulses, cool clammyskin, tachycardia, alterations inrespiration, sensorium, peripheral cyanosis andoliguria
  29. 29. CLASSIFICATION OF SHOCK1. HYPOVOLEMIC – reduction of bloodvolume from external loss of blood plasma orwater; reduction in blood volume from internalloss (internal haemorrhage); heart unable topump enough blood to the body 2. CARDIOGENIC – inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively
  30. 30. 3. SEPTIC– overwhelming gram-negatve infections (endotoxemia);overwhelming gram-positive infections(endotoxic shock) 4. NEUROGENIC – occurs in anaesthetic accident or spinal cord injury due to vascular tone and peripheral pooling of blood
  31. 31. 5. ANAPHYLACTIC – initiated by a generalizedimmunoglobulin E-mediated hypersensitivityresponse; associated with systemic vasodilation andincreased vascular permeability
  32. 32. 3 Most Causes of Shock1. Loss of blood volume – hypovolemic shock2. Pump Failure – cardiogenic shock3. Action of Toxins on peripheral vessels – Septic and neurogenic shock