Hemodynamic Disorders PDF

a edema  EDEMA Def: EXCESS ACCUMULATION OF FLUID IN EXTRACELLULAR OR INTRACELLULAR LOCATIONS. TYPES: Localized: involving one organ or part of the body; Lung edema and Ascites. Acmmulation canito of thisintentional Gen...

a edema  EDEMA Def: EXCESS ACCUMULATION OF FLUID IN EXTRACELLULAR OR INTRACELLULAR LOCATIONS. TYPES: Localized: involving one organ or part of the body; Lung edema and Ascites. Acmmulation canito of thisintentional Generalized: involving the entire body (Anasarca) Special Types: Pulmonary & Cerebral edema  WATER I 60 II as 03.024 4 60% of body 2/3 of body water is INTRA-cellular The rest is INTERSTITIAL between cells Extracellular rafascularinterstitial Only 5% is INTRA-vascular EDEMA is SHIFT of fluid to the INTERSTITIAL SPACE HYDRO-THORAX, I IT PERICARDIAL EFFUSIONS, ASCITES, & ANASARCA Generalized  Edema: Pathogenesis (Development) causes ofedema 1 increase hydrostatic pressure 2 decrease osmotic pressure 3 lymphatic obstruction 4 Nat retention Prof AdelOsman Musalam2019  INCREASED HYDROSTATIC PRESSURE Nrj Impaired venous return Congestive heart failure Ascites (liver cirrhosis) oooo Venous obstruction or compression Thrombosis External pressure (e.g., mass) Lower extremity inactivity with prolonged dependency Prof AdelOsman Musalam2019  REDUCED PLASMA OSMOTIC o PRESSURE (HYPOPROTEINEMIA) Protein-losing nephropathies I 23 24 (nephrotic syndrome) ht.mg 4m a fffffff Liver cirrhosis (ascites) Albumin.ie IW4 I 21 SI it Malnutrition Malabsorbtion Prof AdelOsman Musalam2019 LYMPHATIC OBSTRUCTION (LYMPHEDEMA) C Parasite s.JO Inflammatory no Ama I Neoplastic Postsurgical as in breast cancer Prof AdelOsman Musalam2019  Na+ RETENTION Renal hypoperfusionIncreased renin-angiotensin-aldosterone secretion Aidesterone Prof AdelOsman Musalam2019  INFLAMMATION lead to a  ↑ ↑ Capillary permeability e.g.: Acute inflammation  Areas of increased vascular permeability or areas of increased blood vessels will appear “edematous”Localized  CAUSES & TYPES OF DIET EDEMA 1 2 INCREASED DECREASED HYDROSTATIC ONCOTIC osmotic PRESSURE PRESSURE Congestive Heart Nephrotic Syndrome Failure Ascites Cirrhosis (Ascites) Venous Obstruction Protein Malnutrition 3 INCREASED 4 LYMPHATIC PERMEABILITY OBSTRUCTION Acute Inflammation Inflammatory Types Neoplastic A) Generalized edema: as Cardiac, Hepatic, Renal, Nutritional edema B) Localized edema: as inflammatory, neoplastic, local venous obstruction, Ascites  MORPHOLOGY OF Edema I JLQi EDEMA Pleural effusion (hydrothorax) Pericardial effusion (hydropericardium) Peritoneal Ascites (edema in peritoneal cavity) Cerebral edema (in brain, intra- and extracellular)Special Type Anasarca (widespread edema in many organs)Generalized Prof AdelOsman Musalam2019  Edema: Morphology Dependent Edema is a prominent feature of Renal, Hepatic, Congestive Heart Failure & Nutrional. if there is edema first thing we think about is congestive hear and second is renal disease Facial edema (around Eyes) is often the initial manifestation of Nephrotic Syndrome …… Renin-angiotensin-Aldsteron axis stim……..salt & water retention in S.C. tissue periorbital at first. Icatenus Edema of the Brain is due to:Trauma, Abscess, Neoplasm, Infection (Encephalitis) Prof AdelOsman Musalam2019  MORPHOLOGY OF EDEMA – Swelling and wetness of the tissues; – Can show "pitting" when pressed against (Pitting edema). increased hydrostatic pressure Pitting edema decreased osmotic pressure non pitting edema lymphatic obstruction inflammation Morphology of Edema: Pitting edema Pitting edema 0 0 Prof AdelOsman Musalam2019 Morphology of Edema ASCITES PERIORBITAL (RENAL) Prof AdelOsman Musalam2019  Morphology of Edema Pulmonary Edema is most frequently seen in Congestive Heart Failure – May also be present in Renal failure The Lungs are typically 2-3 times normal weight outflow Cross sectioning causes an outpouring of frothy, sometimes blood-tinged fluid Prof AdelOsman Musalam2019 Gross Picture of Pulmonary Edema Prof AdelOsman Musalam2019 Normal Lung ME: Pulmonary Edema Prof AdelOsman Musalam2019  Lymph-Edema Lymphatic Obstruction Impaired lymphatic drainage with resultant lymphedema, usually localized Usually due to INFLAMMATION or NEOPLASTIC OBSTRUCTION Filariasis - A parasitic infection affecting inguinal lymphatics resulting in elephantiasis idle s Prof AdelOsman Musalam2019 Elephantiasis (Rt. Limb) non pitting Prof AdelOsman Musalam2019  Lymphatic Obstruction Neoplasia Resection and/or radiation to axillary lymphatics can lead to arm edema Carcinoma of breast with obstruction of superficial lymphatics can lead to an unusual appearance of the breast - “peau d’orange” (orange peel) Ii Prof AdelOsman Musalam2019  THROMBOSIS Prof AdelOsman Musalam2019  THROMBOSIS platelet fibrin RBCs Def:FORMATION OF A SOLID MASS OF BLOOD ELEMENTS WITHIN A BLOOD VESSELE OR CARDIAC CHAMBER IN A LIVING mm BODY EXAMPLE: CORONARY THROMBUS Prof AdelOsman Musalam2019  Hemostasis & Thrombosis Hemostasis: is the normal, rapid formation of a localized “plug” at the site of vascular injury 1 Couglation factors what keep it normal Smooth blood vessels 2 Thrombosis: Abnormal activation of the normal hemostatic process Thrombosis is Pathologic Prof AdelOsman Musalam2019 CAUSES & PATHOGENESIS OF THROMBOSIS (Predisposing Factors) Virchow’s Triad 3 hypertention – Endothelial injury Smooking hypercholestremia – Stasis or turbulence of blood flow – Blood hypercoagulability Primary Congenintal Secondary weight Prof AdelOsman Musalam2019 VIRCHOWS TRIAD Prof AdelOsman Musalam2019  Thrombosis Thrombosis Anti-thrombotic Regulation Release of Thrombomodulin TPA and t-PA = tissue type Plasminogen Activator = Fibrinolysis Prof AdelOsman Musalam2019  Lc COMPOSITION OF THROMBUS Fibrin, Platelets, RBC's LOCATION OF THROMBI Arteries, veins, heart chambers, heart valves TYPES OF THROMBI 1According site: arterial, venous, capillary, in cardiac chambers (Mural), or on cardiac valves (vegetations). 2 According color: a. Pale thrombus: formed of platelets b. Red thrombus: formed mainly of blood clot C- Mixed thrombus: Lines of zahn and blood clots 3- According the presence of microorganism: a- septic thrombus: containing microorganism (bacteria) b- Aseptic thrombus: absence of organism  MORPHOLOGY OF THROMBI Thrombi Develop IN THE CARDIOVASCULAR SYSTEM M/E: Lines of Zahn –Alternating Pale Layers of Platelets & Fibrin With Darker Layers of RBs (seen in heart, aorta & large arteries) Prof AdelOsman Musalam2019  FATE OF THE THROMBUS E Propagation: Enlarge by additional platelets and fibrin Embolization: Part of the thrombus of_ dislodges and get transported in the vasculature Dissolution: If newly formed can be its dissolved by fibrinolytic factors but later due to fibrin polymerization become resistant to fibrinolytic agents am Organization and recanalization 5 4 ELI was iI ii Jit I Thrombus Thrombus Prof AdelOsman Musalam2019 Cardiac Mural Thrombus Prof AdelOsman Musalam2019 Thrombus Propagated into the Inferior Vena Cava Prof AdelOsman Musalam2019  F DVT, Thrombo-Embolism Deep Vein Thrombosis Prof AdelOsman Musalam2019 Pulmonary Thrombo-Embolism (Gross) Prof AdelOsman Musalam2019 EMBOLISM Prof AdelOsman Musalam2019  EMBOLISM Def: AN EMBOLUS IS AN INSOLUABLE SOLID, LIQUID OR GASEOUS MASS THAT IS CIRCULATING IN THE BLOOD TO A SITE DISTANT FROM ITS POINT OF ORIGIN. (Intravascular foreign material carried in the blood stream to a point distant from its origin) it Thrombus Is Is III I Iil Li put it.G If I slit of Thrombus I 4 ir Thrombus Thromboembolism t.it Embolism embolism IE Wiss Is Prof AdelOsman Musalam2019  TYPES OF EMBOLI 30 50 ml will do embolism Gas (as in surgery, chest wall injury, or decompression sickness) o.TL AIW Liquid (amniotic fluid, radiographic contrast material, fat after soft tissue trauma or bone fracture )fatty liver Solid (Thrombus-- most common, Atheroma, Bone marrow (yellow marrow)& Foreign Body e.g. bullet) S IF  ORIGINS & SITES OF EMBOLIZATION Venous (systemic veins e.g. deep venous throbosis (DVT) to pulmonary arteries Saddle Pulmonary Embolus ) Arterial (heart or aorta to systemic circulation) Paradoxic RT. Lt. side of the heart (systemic venous, through Septal Defect in heart, to systemic arterial circulation) Pulmonary Embolus Saddle Pulmonary Embolus  death of area gtain INFARCTION Is formation of an infarct deadtissue result from failure of blood Sypply  INFARCTION Def: AN INFARCT IS A LOCALIZED AREA OF ISCHEMIC NECROSIS CAUSED BY OCCLUSION OF THE vascular (MAINLY ARTERIAL) SUPPLY. Block 85-90% of all infarcts due to arterial Thrombotic or Embolic events  INFARCTION Other less common causes:  Vasospasm constriction of Blood vessle  Expansion of atheroma due to intraplaque Hemorrhage degenarationofwall of artery  External compression as tumor  Traumatic vascular rupture  Vessel twisting as testicular torsion or bowel twisting  Venous thrombosis in organs with single efferent vein as testis and ovary (usually cause congestion rarely cause infarction due to opening of bypass channels)  Infarcted Colon Remaining Colon  MORPHOLOGY OF INFARCTS It differs with different tissues and durations anemic white p Pale (white): often roughly wedge-shaped, in solid organs with single blood supply (ex: kidneys, spleen, heart) Hemorrhagic (Red): in organs which are soft and have dual blood supply or collaterals (ex: Lungs, Bowel, Liver). With healing they are converted to fibrous tissue.  MORPHOLOGY OF INFARCTS Microscopically:  Coagulative necrosis in most tissues except CNS liquefactive necrosis to  Early inflammatory response along the infarction  Later, repair by fibrosis and scar formation  Factors affecting infarct development  Anatomy of the vascular supply: presence or absence of alternative blood supply if it supply by on or two  Rate of occlusion: slowly developing occlusion less likely to cause infarction rate infarction  Tissue vulnerability to hypoxia: neurons 3-4 minutes, cardiac muscles 20-30 minutes, fibroblast many hours Lung: Red Infarct & Spleen: Pale Infarct Gg orihiteff Hyperemia & Congestion  Hyperemia & Congestion Increased blood in an area compared to normal. i5Tpys blood in artier adobe.de Hyperemia: Hyperemia is an Active process resulting from augmented tissue inflow due to arteriolar dilation (e.g. acute inflammation), occurs in inflammation and muscle exercise. Congestion Congestion is a Passive process resulting from impaired outflows from a tissue (e.g. cardiac failure or venous obstruction- DVT) Dincrease blood in organ  Hyperemia in Pneumonia Hyperemia Infection (Pneumonia) Chronic Passive congestion (Lung) Heart failure cells are alveolar macrophages containing hemosiderin in chronic venous congestion of the lung  “Nutmeg” Liver Isis “Nutmeg” Liver Cross Section of a Nutmeg Chronic passive congestion (Liver)  Hemorrhage  Hemorrhage Def: Extravasation of blood due to rupture of blood vessels escape blood outside blood vessels AE: – Rupture of a large vessel: Trauma, Atherosclerosis, Inflammatory or Neoplastic Erosion – Rupture of small vessels: hemorrhagic diathesis  CAUSES OF HEMORRHAGE – Vascular diseases with rupture (atherosclerosis, arteritis, aneurysms, etc.). ICII – Low platelets (below 10,000 -15,000/cu mm); – Coagulopathy (factors less than 10% activity); peptic ulcer espicaly – Ulcers, tumors, coagulation factors, infarcts, trauma  Types of Hemorrhage May be external, into a body cavity, or into a tissue Petechiae: minute hemorrhages into skin or lining surface (pin heads) Purpura (slightly larger hemorrhages than petechia) Ecchymoses (over 1-2 cm subcutaneous hematoma =‘bruise’) we Hematoma: accumulation of blood enclosed or confined within tissue  TYPES OF HEMORRHAGE – Hemoptysis: coughing up of blood – Hematemesis: vomiting up of blood – Melena: dark black blood per rectum – Hematochezia: bright red blood per rectum – Hematuria: blood, gross or microscopic, in urine – Hemopericardium:blood into pericardium – Hemothorax: blood into thoracic cavity – Hemoperitoneum: blood into peritoneal cavity Petechial hemorrhage (Pericardium) Ecchymoses Hematoma (Toenail)  Hemorrhage Why do bruises change color as they Resolve? a The RBC’s in a hemorrhage are broken down: – hemoglobin (red) bilirubin (blue- green) hemosiderin (golden-brown)  Clinical Effects of Hemorrhage 20% blood loss, hemorrhagic shock Bleeding into the brainstem is fatal Chronic recurrent bleeding iron deficiency anemia! SHOCK  SHOCK f WI Systemic Hypoperfusion due to Reduction in: Cardiac Output (CARDIOVASCULAR COLLAPSE) causes greha burns vomiting heavy sweat The End Results are: Hypotension, followed by Impaired Tissue Perfusion and Cellular Hypoxia  SHOCK Types: 1.Cardiogenic, III Wil 2.Neurogenic, LA Will Nerve or CNS 3. Hypovolemic, IN E 4. Septic, andInfection 5. Anaphylactic Shock E I Hypersensevity  TYPES of SHOCK CARDIOGENIC: (Acute, Chronic Heart Failure) HYPOVOLEMIC: (Hemorrhage or Leakage) SEPTIC: (“ENDOTOXIC” shock, #1 killer in ICU) NEUROGENIC: (loss of vascular tone) ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased vascular permeability) CARDIOGENIC shock MI (Myocardial infarction) VENTRICULAR RUPTURE ARRHYTHMIA Abnormal heart beat accumulation of fluid CARDIAC TAMPONADE in Pericardial Sac PULMONARY EMBOLISM (acute RIGHT heart failure or “cor pulmonale”)  HYPOVOLEMIC shock HEMORRHAGE, Vasc. compartmentH2O VOMITING, Vasc. compartmentH2O DIARRHEA, Vasc. compartmentH2O BURNS, Vasc. compartmentH2O  SEPTIC shock events* (overwhelming infection) Peripheral vasodilation Pooling Endothelial Activation Disseminated intravascular coagulation (DIC): sepsis favors procoagulant state in the body leading to thrombi in small vessels throughout the body. * Think of this as a TOTAL BODY inflammatory response  STAGES of SHOCK Non-Progressive: Reflex compensatory mechanisms are activated and vital organ perfusion is maintained. Progressive: Tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis. HE w̅ Irreversible: Cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possible last  GOOD LUCK