Hemodinamic disorder

C.Murtono Pathology Dept Atma Jaya Med.Faculty

HEMODINAMIC DISORDERS
OXIGEN DISTRIBUTION IS VERY IMPORTANT 60% OF BODY WEIGHT AN ADULT IS WATER ( 40% INTRA- AND 20% EXTRACELLULAIR ) MANY DISEASES AND MORTALITY ARE BASED ON HEMODINAMIC DISORDER

EDEMA
ACCUMULATION OF ABNORMAL AMOUNT OF FLUID IN THE INTERCELLULER TISSUE SPACES OR BODY CAVITY. CLASSIFICATION OF EDEMA : I. GENERALIZED OR LOCALIZED II. INFLAMMATORY AND NON INFLAMMATORY

CAUSE OF EDEMA
1. INCREASE IN INTRAVASCULAIR HYDROSTATIS PRESSURE 2. A FALL OF OSMOTIC PRESSURE OF THE PLASMA 3. LYMPHATIC OBSTRUCTION 4. RENAL RETENTION OF SALT

1.INCREASE OF INTRAVASCULAR HYDROSTATIC PRESSURE

LOCAL INCREASE, e.c. trombosis of lower leg. The result is edema of lower leg
GENERALIZED EDEMA, e.c.systemic edema caused by increased systemic venous pressure, as seen by congestive heart failure.

2. REDUCED PLASMA OSMOTIC

PRESSURE
THE LOSS OF ALBUMIN, like in nephrotic syndrome, a kidney disorder with leaky of glomerular basement membrane and generelized edema. THE REDUCED SYNTHESIS OF SERUM PROTEIN, due diffuse disease of the lever, such as cirrhosis. Also in malnutrition ( protein deffensiasi ). Fluid move from intravascular to interstitial tissue.

3. LYMPHATIC OBSTRUCTION
FROM THE LUMEN, like filariasis cause fibrosis of lymph channel in inguinal region. Resulting edema of external genital and lower limb ( elephantiasis ) FROM THE WALL, like tumour of the wall ( myoma, fibroma cs ) FROM OUTSIDE, ,fibrosis of perilymphatic tissue ( ec .due radiation in mamma Ca )

4. SODIUM AND WATER RETENTION

SALT RETENTION BY ACUTE REDUCTION OF RENAL FUNCTION CAUSED EDEMA.
RETAINED SALT AND WATER EXPANSION OF INTRAVASCULAR FLUID VOLUME INCREASED HYDROSTATIC PRESSUREEDEMA.

MORPHOLOGY
SUBCUTANEOUS EDEMA , prominent manifestation of cardiac failure, particularly right ventricel. Distribution of edema influenced by gravity. RENAL DYSFUNCTION AND NEPHROTIC SYNDROME ,initially periorbital edema, but later generalized edema ( anasarca ). FINGER PRESSURE caused pitting edema.

MORPHOLOGY
PULMONARY EDEMA, mostly in the lower lobe. On sectioning, frothy ,sanguinous fluid. Microscopic, wide septal capillair with proteinous fluid in alveoli. BRAIN EDEMA, could be localized ( localized process like abscess or neoplasma). If generalized , like encephalitis, hypertensive crisis, or venous obstruction. Brain is heavier than normal, gyri flattened with narrowed sulci. Peri vascular spaces widened.

HYPEREMIA-CONGESTION
HYPEREMIA, OR ACTIVE HYPEREMIA, an arterial dilatation caused an increased blood flow. Excessive body heat, as exercise or febrile. Blushing , due neurogenic mechanism. CONGESTION, OR PASSIVE HYPEREMIA, an venous dilatation. Congestion could be classified as localized or generalized. Also acute or chronic.

CONGESTION
Closely related with edema, commonly occur together. Localized congestion ec venous return of blood obstructed or portal hypertension by cirrhosis Systemic congestion ec decompensatio cordis right or left.

MORPHOLOGY congestion of the lung

ALVEOLAR CAPILLARIES CONGESTED , RUPTURED, ALVEOLI FILLED WITH BLOOD. EDEMA FLUID COLLECTS IN THE ALVEOLAIR SEPTA. RUPTURED ERITROCYTES INGESTED BY MACROPHAGE ( HEART FAILURE CELL ) SEPTA FIBROUS ( BROWN INDURATION )

MORPHOLOGY congestion of the liver

Causa : right sided heart failure , obstruction of vena cava inferior , or hepatic vein. Around v.centralis is red blue , surrounded uncongested lever cells ( nutmeg liver ) V. centralis distended wiwh blood, the cells are atrophic due chronic hypoxia. Periferi : fatty changes. Advance : hemorrhagic necrosis

MORPHOLOGY congestion of the spleen

Spleen enlarged : congestive splenomegali Causa : obstruction of v splenica ( trombus ), intrahepatic (cirrhosis ), or systemic ( heart failure ) Spleen enlarged ( until 5000 gram), firm, capsul thickened, hemorrhage with organization ( Gamna Gandhi , fibrosis+ iron+ calcium )

HEMORRHAGE
IMPLIES RUPTURE OF BLOOD VESSEL. CAN BE EXTERNAL OR HEMATOMA IN THE CAVITY : HEMOTHORAX , HEMOPERICARDIUM , HEMARTHROSIS , HEMOPERITONEUM . MINUTE: PETECHIAE, SLIGHTLY LARGER : PURPURA, SUBCUTANE HEMATOMA 1 - 2cm : ECCHYMOSES

HEMORRHAGE
RELEASED HEMOGLOBIN BILIRUBIN HEMOSIDERIN SO THE PATIENT WITH LARGE HEMORRHAGE BECOMES JAUNDICE. CLINICAL : DEPEND ON VOLUME OF THE BLOOD, RATE OF LOSS , SITE OF HEMORRHAGE.. SLOW LOSSES : - , LARGER/ ACUTE : SCHOK , VERY LARGE : DEATH. REPEATED : IRON DEFFICIENCY.

THROMBOSIS

FORMATION OF CLOTTED MASS OF BLOOD WITHIN THE NON INTERUPTED VASCULAR SYSTEM CAUSES : 1. ENDOTHELIAL INJURY 2. ALTERATIONS IN NORMAL BLOOD FLOW 3. HYPERCOAGULABILITY

ENDOTHELIAL INJURY
MOST THROMBI IN THE HEART AND ULCERATED PLAQUES OF ATHEROSCLEROTIC ARTERI EXOGEN INJURY:CHEMICALS ( SMOKING ), ENDOGEN INJURY : HYPERCHOLESTEROLEMI, BACTERIAL TOXINS, IMMUNOLOGIC INJURY ( TRANSPLANT )

ALTERATIONS OF BLOOD FLOW

TURBULENCE - ARTERIAL THROMBI SLUGGISH / STASIS - VENOUS THROMBI

HYPERCOAGULABILITY
PRIMARY : antithrombin defficiency, protein c defficiency, Fibrinolysis deffect SECUNDAIR : prolonged bed rest , myocard infarct, leukemia, cancer diss intrav ,coagul,thromb. thromboc.pur, oral contrasepsi sickle cell anemia,smoking late pregnancy

Morphology of thrombus
ARTERIIL THROMBUS : ENDOTHELIAL INJURY, TURBULENCE, BIFURCATIO, OT BRANCH. INTERSPERSE BETWEEN DARKER LINES (AGGREGATED PLATELETS ) WITH PALER LAYER (COAGULATED FIBRIN ) LINES OF ZAHN. ON SURFACE MURAL THROMBI , IN SMALLER ARTERI : OCCLUSIVE THROMBI , ON HEART VALVE ( WITH BACTERI )VEGETATION , IN BRANCHSADDLE THROMBUS

VENOUS THROMBUS ( PHLEBOTHROMBOSIS )

MOSTLY IN LOWER EXTREMITIES : v.femoralis , poplitea , deep calf , iliac veins ATTACHED TO UNDERLYING VESSEL the tail fragmented EMBOLUS Diff Diagnosis with post mortal clot. Clot is rubbery , or gelatinous. Clot not attached to the underlying tissue.

WHAT HAPPENS WITH THROMBUS

may propagate , cause obstruction May embolize Removed by fibrinolytic activity Organized , fibroblast and endothelial cells ingrowth vascularized connective tissue ( recanalization

CLINICAL CORRELATION
CAUSE OBSTRUCTION, cause myocardial infarction , encephalomalacia ( strokes PROVIDE SOURCE OF EMBOLI superficial, cause local swelling, pain, tenderness DEEP VEIN THROMBOSIS, cause edema foot, ankle , Homan sign. MULTIPEL THROMBOSIS : phlebitis migrans : Ca pancreas.

DISSEMENATED INTRAVASCULAR COAGULATION ( D.I.C. )

MINUTE THROMBI FORMED IN MICROCIRCULATION, ESPECIALLY CAPILLAIR, AND VENULE COMPLICATION OF UNDERLYING DISEASE . CIRCULATORY INSUFFISIENCY,lung, brain,heart, kidney. SIMPTOM: HEMORRHAGIC DIATHESE AND OCCLUSION IN MICROCIRCULATION

Morphology of thrombus
THROMBUS ARTERIIL : ENDOTHELIAL INJURY, TURBULENCE, BIFURCATIO, OT BRANCH. INTERSPERSE BETWEEN DARKER LINESM (AGGREGATED PLATELETS ) WITH PALER LAYER ( COAGULATED FIBRIN ) LINES OF ZAHN. ON SURFACE MURAL THROMBI ,

EMBOLISM
OCCLUSION OF SOME PART OF CARDIOVASCULAIRE SYSTEM BY EMBOLUS TRANSPORTED TO THE SITE THROUGH THE BLOODSTREAM. 95% ARISE FROM THROMBUS, THE REST ARISE FROM: BAT, BUBBLE OF GAS , ATHEROSCLEROTIC DEBRIS , BONE MARROW FRAGMENTS, TUMOUR CELLS.

PULMONARY EMBOLISM
64% OF AUTOPSIES , SOME ASIMPTOMATIC 15% DEATH OF HOSPITALIZED PATIENT. SMALLER EMBOLIES CAUSE PULMONARY HEMORRHAGE AND INFARCTION. LARGE EMBOLIES CAUSE ACUTE COR PULMONALE WITH SUDDEN , SEVERE HYPOXEMIA. AMONG THE SURVIVER: RAPID FIBRINOLYSIS

SYSTEMIC EMBOLI
Mostly ( 85% ) due the heart thrombus, secondary to myocardial infarction. Also arrythmia , like atrial fibrillation. Atrial emboli cause infarction, in lower extremities ( 70%) that cause gangren , brain ( 10%) that fatal, viscera (10%).

AMNIOTIC FLUID EMBOLISM

UNCOMMON :( 1 : 50.000 labor) with fatality rate 86%. Suddenly, respiratory difficulty with cyanosis, cardiovascular shock, convul sion, coma, pulmonary edema. Tear of placenta membrane, amniotic fluid into maternal circulation ( epitel, lanugo fat, muconium). Death due anaphylaxis.

Air embolism ( Caisson )

Gas obstructs vascular flow. Causa: gas breathing under pressure, during delivery/abortion during pneumothorax injury to chest wall. Lead to multiple foci ischemic necrosis.

FAT EMBOLI
Following fracture of the shaft long bone Sudden onset of tachypeu ,dyspneu and tachycardia. Accompanied by rest less, delirium, coma.

INFARCTION
AREA OF ISCHEMIC NECROSIS produced by occlusion ( by either arteri al supply or venous drainage). Nearly 99% caused by thromboembolic event , and mostly by arterial occlusion. Ovary, testis have single venous outflow chance for venous thrombosis.

TYPES OF INFARCT ( I )
1. White vs hemorrhagic 2. Presence vs absance of bacterial infection. White infarct : arterial occlusion in solid organ , ec kidney , heart , spleen. Blood from anastomosis initial hemorrhage lyses hemoglobine hemosiderin

TYPES OF INFARCT ( II )
HEMORRHAGIC INFARCT: - with venous occlusion - in loose tissue - tissue with double circulation - tissues previously congested. In lung , small intestine

MORPHOLOGY OF INFARCT
WEDGE shaped, apex the focus of vascular occlusion. The next 24 hours , the sharp define , with hyperemia and inflammatory infiltration Fibroblastic reparative response from periphery and replaced the infarct area with scar tissue. Exception : brain liquefaction. Septic convert to abscess

MAJOR DETERMINANTS OF INFARCT

1. The nature of vascular supply, ec 2 arte ries in lung, liver , hand ( not end arteri). 2. Rate of development of occlusion, slowly development of occlusion less likely to infarction 3. Vulnerability of the tissue to hypoxia ,ec brain,neuron, myocard is sensitif.

CLINICAL SIGNIFICANT
CORONARY heart disease : 33% of all. Cerebral infarction. Pulmonary infarction Ischemic necrosis ( + gangren in DM ) Kidney infarction Gut hemorrhagic infarction.

SHOCK ( I )
Hypoperfusion of tissue due to reduction of blood volume or cardiac output or redistribution of blood, resulting in an adequate effective circulating volume. Defficiency in oxygen deliveryaerobic to anerobic metabif worsenirreversibel injury / cell death.

SHOCK ( II )
3 types: 1. Cardiogenic, failure of myocardial pump due myocardial damage, arryth mia,or pulmonary embolism 2. Hemorrhagic,due fluid loss 3. Septic shock, most commonly gram negative / or endotoxin

SHOCK ( III )
RARELY : 1. neurogenic shock due anaesthetic accident or spinal cord injury massive peripheral dilatation.
2. Anaphylactic shock : initiated by type 1 hypersensitivity reaction.

MORPHOLOGY OF SHOCK
Hypoxic failure of multiple organ system Brain : hypoxic encephalopathy Heart: subendocardial necrosis/hemorrh Kidney:acute tubular necrosis Lung: shock lung Adrenal : stress response Intestinal: hemorrhagic enteropathy

The End of Lecture