Hemodynamic & Shock 2024 PDF

HEMODYNAMIC DISORDERS, THROMBOEMBOLISM & SHOCK TANYA WRIGHT, DDS CU SCHOOL OF DENTAL MEDICINE [email protected] TOPICS OF DISCUSSION HYPEREMIA CONGESTION EDEMA HEMORRHAGE HEMOSTASIS THROMBOSIS EMBOLISM INFARCTION SHOCK OBJECTIVES Define the terms hyperemia, congestion, edema, embolism, inf...

HEMODYNAMIC DISORDERS, THROMBOEMBOLISM & SHOCK TANYA WRIGHT, DDS CU SCHOOL OF DENTAL MEDICINE [email protected] TOPICS OF DISCUSSION HYPEREMIA CONGESTION EDEMA HEMORRHAGE HEMOSTASIS THROMBOSIS EMBOLISM INFARCTION SHOCK OBJECTIVES Define the terms hyperemia, congestion, edema, embolism, infarction, thrombosis, thromboembolism and shock Understand and list the causes and examples of edema List the predisposing factors for thrombosis and its complications Explain the role of thrombin and platelets in hemostasis List the types of emboli List the types of shock and explain how organs are affected HYPEREMIA & CONGESTION Hyperemia Increase in blood volume within tissues Active process Increase in blood volume (arteriolar dilation & increased blood inflow), oxygenated blood Ex. Inflammation or exercising skeletal muscle Congestion Increase in blood volume within tissues Passive process Impaired venous outflow Tissue is cyanotic (blue-red color) due to accumulation of deoxygenated hemoglobin Can be acute or chronic, involved with cardiac failure Ex. Liver has “nutmeg appearance” due to right-sided heart failure Lung-thick, fibrotic septa, alveolar spaces have macrophages containing hemosiderin NORMAL LIVER “NUTMEG LIVER” https://peir.path.uab.edu/library/_data/i/upload/2013/08/01/20130801105539-36f0b7ceme.jpg Courtesy of Robbins Basic Pathology, 10th ed Courtesy of Normal Liver Histology 101 Courtesy of Fortea, J et al. International Journal of Molecular Sciences 2020 HYPEREMIA CONGESTION ACTIVE PASSIVE RED TISSUE (OXYGENATED BLOOD) BLUE TISSUE (DEOXYGENATED BLOOD) CYANOTIC ARTERIOLAR DILATION IMPAIRED VENOUS FLOW SEEN WITH INFLAMMATION SKELETAL MUSCLE CARDIAC FAILURE EDEMA Accumulation of fluid in tissues due to water in extravascular spaces Can impair wound healing & clearance of infections Body weight is 60% water 2/3 intracellular, 5% blood plasma, rest is interstitial fluid Effusion- edema in body cavity Hydrothorax (pleural cavity) Hydropericardium (pericardial cavity) Hydroperitoneum-known as ascites (peritoneal cavity) Anasarca-generalized and severe form of edema Causes Increase in hydrostatic pressure Reduced plasma osmotic pressure Lymphatic obstruction Sodium (salt) retention Inflammation EDEMA Increased hydrostatic pressure Caused by impaired venous flow/return Transudate-protein poor; result of increased hydrostatic pressure or reduced colloid pressure Exudate-protein rich with high specific gravity; caused by increased vascular permeability Ex. Congestive heart failure (*Refer to Complete Anatomy link in Canvas*) Reduced plasma osmotic pressure Caused by and leads to reduction in plasma albumin & loss of fluid from circulation Ex. Nephrotic syndrome affecting the renal (kidney) system Protein malnutrition Cirrhosis of liver EDEMA Lymphatic obstruction Compromises resorption of fluid from interstitial spaces Localized obstruction by inflammatory or neoplastic condition or complication of therapy Ex. Removal of axillary lymph nodes in patients w/ breast cancer (lymphedema of arm) *Refer to Complete Anatomy link in Canvas* for lymphedema Sodium retention (Salt retention) Causes increase in hydrostatic pressure & reduced plasma osmotic pressure due to excessive salt retention Ex. Acute renal failure LYMPHATIC SYSTEM Courtesy of Complete Anatomy App Ramachandran, Savitha & Chew, Khong-Yik & Tan, Bien-Keem & Kuo, Yur-Ren. (2020). Current operative management and therapeutic algorithm of lymphedema in the lower extremities. Asian journal of surgery. 44. 10.1016/j.asjsur.2020.08.010. LYMPHEDEMA FLUID MOVEMENT & CAUSES OF EDEMA Courtesy of Robbins Basic Pathology, 11th ed CAUSES OF EDEMA EXAMPLES INCREASED HYDROSTATIC PRESSURE IMPAIRED VENOUS RETURN ARTERIOLAR DILATION REDUCED PLASMA OSMOTIC PRESSURE (HYPOPROTEINEMIA) CONGESTIVE HEART FAILURE CONSTRICTIVE PERICARDITIS LIVER CIRRHOSIS VENOUS OBSTRUCTION/COMPRESSION (THROMBOSIS, PRESSURE) LOWER EXTREMITY INACTIVITY HEAT NEUROHUMORAL DYSREGULATION NEPHROTIC SYNDROME REDUCED PROTEIN SYNTHESIS (ADVANCED LIVER DISEASE) MALNUTRITION PROTEIN-LOSING GASTROENTEROPATHY LYMPHATIC OBSTRUCTION INFLAMMATORY NEOPLASTIC POSTSURGICAL/POSTIRRADIATION SODIUM RETENTION EXCESSIVE SALT INTAKE W/RENAL INSUFFICIENCY DECREASED RENAL EXCRETION OF SODIUM (INCREASED RENIN-ANGIOTENSIN-ALDOSTERONE SECRETION) INFLAMMATION ACUTE/CHRONIC INFLAMMATION ANGIOGENESIS EDEMA Common in subcutaneous tissues, lungs, brain Subcutaneous edema Diffuse Found in body parts greatest distance below heart esp. legs Represents underlying heart or kidney disease Pitting edema Finger pressure displaces interstitial fluid (leaves depression) https://upload.wikimedia.org/wikipedia/commons/thumb/8/84/Combinpedal.jpg/611pxCombinpedal.jpg?20101015085945 PITTING EDEMA EDEMA Pulmonary edema Lungs weigh two to three times normal weight Can be seen with left ventricular failure, renal failure or lung injury (acute) https://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/2005/nejm_2005.353.issue26/nejmcp052699/production/images/img_medium/nejmcp052699_f1.jpeg EDEMA Brain edema Can be localized (due to abscess or tumor) Can be generalized (due to pathology or injury) Life threatening Dental complications include Cellulitis Cavernous sinus thrombosis (*Refer to Complete Anatomy link in Canvas*) CAVERNOUS SINUS THROMBOSIS Form of cellulitis and presents as acute and edematous spread usually unilateral Can result from dental infection (10% cases) or thrombosis Cavernous sinus location Lateral to sella turcica and medial to temporal bone Comprised of thin-walled veins Various nerves can be found (abducens, trochlear, oculomotor, branches of trigeminal) Internal carotid artery found Infection spread Anterior teeth-perforation of facial maxillary bone and spread to canine space Posterior teeth-involve buccal/infratemporal space and spread by emissary veins Clinical presentation Enlargement of eyelids and conjunctiva, swelling of forehead and nose Canine space-swelling on lateral border of nose extend to eye and periorbital area CAVERNOUS SINUS THROMBOSIS CAVERNOUS SINUS DIAGRAM Courtesy of Complete Anatomy App Courtesy of Color Atlas of Common Oral Diseases 5th Ed, Langlais et al Courtesy of Robbins Basic Pathology, 10th ed PATHWAYS TO EDEMA HEMORRHAGE Leakage of blood from vessels Damage to vessels or defective clot formation Can be caused by Trauma Atherosclerosis Erosion of vessel due to inflammation or neoplasm Can present in various forms Petechiae-pinpoint dots (1-2 mm) Purpura-larger (3-5 mm) Ecchymosis-described as bruise (1-2 cm) Hematoma-larger than ecchymoses, can be elevated/raised Dependent on Volume of blood lost Rate of bleeding Location of bleed Health of person affected PETECHIAL HEMORRHAGE Courtesy of Color Atlas of Oral and Maxillofacial Diseases, Neville et al ECCHYMOSIS Courtesy of Color Atlas of Oral and Maxillofacial Diseases, Neville et al HEMATOMA Courtesy of Color Atlas of Oral and Maxillofacial Diseases, Neville et al BRAIN HEMATOMA Courtesy of Robbins Basic Pathology, 10th ed HEMOSTASIS Clot formation caused by traumatic vessel injury Involves platelets, clotting factors, endothelium at site of vascular injury Limits and prevents extent of bleeding Steps include Arteriolar vasoconstriction Form platelet plug (primary hemostasis) Deposition of fibrin (secondary hemostasis) Clot stable & resorption Endothelial cells are central regulators Determine if clot forms, propagate, or dissolve Can inhibit platelet aggregation/coagulation Can promote fibrinolysis NORMAL HEMOSTASIS STEPS Courtesy of Robbins Basic Pathology, 11th ed HEMOSTASIS Platelets Disc-shaped fragments shed from megakaryocytes; enter bloodstream Form primary plug, seal vascular defect, and provide surface to bind to coagulation factors Adhesion- work with von Willebrand factor Activation-change shape to spiky appearance to activate and release granule contents Thrombin and ADP help with activation Recruitment-platelets and ADP released to produce additional rounds of platelets production of thromboxane A2 (prostaglandin) occurs Aspirin can inhibit platelet aggregation and cause mild bleeding defect Inhibits cyclooxygenase (required for thromboxane A2 synthesis) Aggregation-bind to fibrinogen to form bridges between platelets and plug is formed thrombin stabilizes plug and converts fibrinogen into fibrin PLATELET COMPONENTS https://www.mdpi.com/membranes/membranes-12-00182/article_deploy/html/images/membranes-12-00182-g001.png HEMOSTASIS Role of Thrombin Controls parts of hemostasis; links clotting to inflammation and repair Converts fibrinogen into fibrin-activates factors V, VIII, and XI Stabilizes clots by activating factor XIII Activates platelets Contributes to tissue repair by activating PARs (protease-activated receptors) (PARs expressed on endothelium inflammatory cells) Prevents clots from moving past site of injury-becomes anticoagulant ROLE OF THROMBIN IN HEMOSTASIS Courtesy of Robbins Basic Pathology, 11th ed HEMOSTASIS Coagulation involves extrinsic or intrinsic factors which leads to fibrin clot deposition Prothrombin time (PT) Measures the amount of time for a fibrin clot to form (9-12 seconds normal) Involves extrinsic pathway (Factors II (prothrombin), V, VII, X, fibrinogen) Used for patients taking warfarin (Coumadin) Partial thromboplastin time (PTT) Measures the amount of time for a fibrin clot to form (25-37 seconds normal) Involves intrinsic pathway (Factors II (prothrombin), V, VIII, IX, X, XI, XII, fibrinogen) Used for patients taking Heparin INR (International normalized ratio) Measures how long it takes for blood to clot Normal- 1.1 or below for immunocompetent patients Used for patients taking warfarin (Coumadin) (Normal range is 2-3) https://upload.wikimedia.org/wikipedia/commons/3/32/1909_Blood_Clotting.jpg INTRINSIC VS EXTRINSIC CLOTTING PATHWAYS HEMOSTASIS Factors limiting coagulation Dilution-coagulation factors washed out and removed by liver Need of negatively-charged phospholipids-provided by activated platelets Factors expressed by intact endothelium next to injury site Fibrinolysis occurs with fibrin breakdown due to plasmin Results from activation of coagulation cascade Plasmin-formed from plasminogen, degrades fibrin and becomes inactive Plasminogen activator-tissue plasminogen activator (t-PA)-most important one t-PA-synthesized by endothelium, binds to fibrin (activity confined to site of clot) may be used in patients with transient ischemic attacks or cerebral infarction (stroke) THROMBOSIS Abnormal clot formation; pathologic counterpart to hemostasis; can cause embolus Underlies serious and common form of cardiovascular disease Can result from Virchow triad Endothelial injury Abnormal blood flow (stasis or turbulent blood flow) Stasis-blood flow is slow Turbulent-blood flow is chaotic, may result from narrowed vessel (stenotic) or widened vessel (aneurysm)involve with arterial/cardiac thrombi Hypercoagulability of blood (genetic or acquired) Courtesy of Robbins Basic Pathology, 10th ed THROMBOSIS-VIRCHOW TRIAD Endothelial injury Causes platelets to be activated Need platelets to activate and adhere for thrombus formation Cardiac and arterial clots rich in platelets Aspirin & platelet inhibitors used with coronary artery disease and myocardial infarction Limit fibrinolysis by increasing plasminogen activator inhibitors (affects t-PA) Abnormal blood flow Turbulent-can help cause endothelial injury and form pockets of stasis, promote endothelial cell activation Stasis-major factor in developing venous thrombi can impede inflow of clotting factor inhibitors slows washout of activated clotting factors Seen in aneurysms (dilated arteries), myocardial infarction, polycythemia vera, atrial fibrillation (cause turbulent flow) Hypercoagulability Blood to clot at an abnormal tendency; caused by changes in coagulation factors Important risk factor for venous thrombosis HYPERCOAGULABLE STATES CAUSES EXAMPLES PRIMARY (GENETIC) COMMON FACTOR V MUTATION PROTHROMBIN MUTATION INCREASED LEVELS OF FACTOR VIII, IX, XI, OR FIBRINOGEN PRIMARY (GENETIC) RARE ANTITHROMBIN DEFICIENCY PROTEIN C DEFICIENCY PROTEIN S DEFICIENCY PRIMARY (GENETIC) VERY RARE FIBRINOLYSIS DEFECTS HOMOZYGOUS HOMOCYSTINURIA SECONDARY (ACQUIRED) HIGH RISK FOR THROMBOSIS SECONDARY (ACQUIRED) ELEVATED RISK FOR THROMBOSIS PROLONGED BED REST/IMMOBILIZATION MYOCARDIAL INFARCTION ATRIAL FIBRILLATION TISSUE INJURY CANCER PROSTHETIC HEART VALVES DIC HEPARIN-INDUCED THROMBOCYTOPENIA ANTIPHOSPHOLIPID ANTIBODY SYNDROME CARDIOMYOPATHY NEPHROTIC SYNDROME PREGANCY/POSTPARTUM BIRTH CONTROL USE SICKLE CELL ANEMIA SMOKING VIRCHOW TRIAD Courtesy of Robbins Basic Pathology, 10th ed THROMBOSIS Can cause tissue infarction and block vessels Examples include cerebrovascular accident “stroke” or myocardial infarction “heart attack” Can develop in the cardiovascular system Mural thrombi-occur in heart chambers or aortic lumen; myocardial infarction a cause Aortic thrombi-found in aneurysmal dilation & atherosclerotic plaques Arterial thrombi-rich in platelets and occlusive; atherosclerosis major cause Venous thrombi- rich in red blood cells and occlusive Heart vegetations-thrombi on heart valves may result in infective endocarditis Sterile, verrucous endocarditis (Libman-Sacks endocarditis) in patients with lupus LIBMAN-SACKS ENDOCARDITIS VEGETATIONS (ARROWS) Courtesy of Robbins Basic Pathology, 11th ed Evolution of thrombus THROMBOSIS Propagation-enlarges Embolization-dislodges and moves somewhere else Dissolution-can shrink rapidly with activation of fibrinolytic factors Organization & Recanalization-organized due to growth of endothelial cells, smooth muscle cells fibroblasts Histology Composed of red blood cells (RBCs), platelets and fibrin Alternation of fibrin/platelets and RBCs known as lines of Zahn Seen in thrombi in flowing blood (helps to distinguish from postmortem clots) Trousseau syndrome Known as migratory thrombophlebitis Inflammation of vein due to blood clot (recurrent and appears in different locations) Associated with undiagnosed malignancy THROMBOSIS ORGANIZED THROMBUS Courtesy of Robbins Basic Pathology, 11th ed THROMBOSIS PULMONARY THROMBOEMBOLUS-LINES OF ZAHN RBCs Platelets/ Fibrin Courtesy of Wikimedia Commons, Dr. Yale Rosen THROMBOSIS Deep vein thrombosis Occurs in deep veins of legs at or above knee (popliteal, femoral, iliac) Can result in embolism and travel to lungs Asymptomatic (50%) Predisposing factors include congestive heart failure, bed rest, pregnancy, immobilization *Refer to Complete Anatomy link in Canvas* Disseminated intravascular coagulation Widespread thrombosis Can be sudden or gradual, subtle onset Can occur in obstetric complications (eclampsia) or malignancies Excessive clotting and bleeding can occur at same time (due to consumption of platelets & coagulation proteins) DEEP VEIN THROMBOSIS EMBOLISM Detached mass (solid, liquid, or gas) carried by blood from point of origin to a distant site Majority result from dislodged thrombus (can be called thromboembolism) Can cause infarction, hypoxia, hypotension, right-sided heart failure Most common type is pulmonary Arise from deep vein thrombosis and can cause death Block main pulmonary artery, occur at bifurcation of pulmonary arteries, enter arterioles *Refer to Complete Anatomy link in Canvas* Various types of emboli include Systemic Fat Amniotic fluid Air PULMONARY EMBOLISM Courtesy of www.britannica.com Courtesy of Robbins Basic Pathology, 10th ed EMBOLISM Systemic Arise from cardiac mural thrombi (80%) Can occur from aortic aneurysms, thrombi, valve vegetations, venous system (paradoxical emboli) Paradoxical-venous embolus goes through atrial/ventricular heart defect & enter systemic circulation Arterial-can migrate to lower extremities or central nervous system *Refer to Complete Anatomy link in Canvas* Venous-migrate to lungs Fat Caused by soft tissue crush injury or rupture of marrow vascular channels Common with severe skeletal injuries (90%) EMBOLISM Amniotic fluid Grave complication of labor; can result in death Survivors may have some form of permanent neurologic deficit Present with severe dyspnea, cyanosis, hypotensive shock, seizures, coma, pulmonary edema may occur Results from tears in placental membrane or uterine vein rupture-contents enter maternal circulation Air/Gas Trapped air/gas bubbles can obstruct vascular flow and cause ischemic injury Decompression sickness-sudden change in atmospheric pressure/undergoing rapid ascent nitrogen expands in tissues and gets into blood stream affects scuba divers, unpressurized aircraft treat by placing in high pressure chamber (hyperbaric chamber) INFARCTION Area of ischemic necrosis caused by occlusion of blood supply to tissue Arterial thrombus or embolism typically responsible Common in heart (myocardial) and brain (cerebral) Gangrene-necrosis of extremities; usually associated with diabetes Based on color and if microbial infection present Red (hemorrhagic) or white (anemic) Septic (infection present) or bland (no infection present) Wedge-shaped (occluded vessel at apex, organ periphery form base) INFARCTION Red Result of venous occlusion Be in tissues with dual circulations (lungs, small intestines) Be in previous congested tissues Occur in areas where flow is reestablished after infarction White Found in solid organs with end arterial circulations (heart, spleen, kidney) For septic, cardiac valve vegetations embolize or microbes plant in necrotic tissue; abscess is formed RED INFARCT WHITE INFARCT Courtesy of Robbins Basic Pathology, 10th ed INFARCTION Factors of influence Anatomy of vascular supply Rate of occlusion Tissue vulnerability to hypoxia Anatomy of vascular supply Alternative blood supply can help with infarction not forming Rate of occlusion If occlusion develops slowly, allows for development of collateral blood supplies Ex. Coronary artery occludes, collateral circulation can increase to prevent infarction Tissue vulnerability to hypoxia Neurons (irreversible damage in 3-4 minutes) Myocardial cells (irreversible damage in 20-30 minutes) Fibroblasts can survive hours after ischemia SHOCK Result of diminished cardiac output or reduced effective circulating blood volume Impairs tissue perfusion results in cellular hypoxia Can be reversible or irreversible depending if prolonged or not Can be fatal Three types Cardiogenic Hypovolemic Septic Cardiogenic (*Refer to Complete Anatomy link in Canvas*) Low cardiac output due to myocardial(heart) pump failure Ex. Myocardial infarction Hypovolemic Low cardiac output due to blood or plasma volume loss Ex. Result of severe burns SHOCK Septic Caused by bacterial or fungal infections (usually gram-positive bacteria) Associated with severe systemic inflammatory response syndrome (SIRS) Can also be caused by burns, trauma, pancreatitis Caused by massive outpour of inflammatory mediators of innate & adaptive immune cells Vasodilation Vascular leakage Venous blood pooling (skin feels warm and be flushed) Result in tissue hypoperfusion, cell hypoxia, organ dysfunction Organ failure can occur which can result in death SEPTIC SHOCK Pathogenesis Bacterial/fungal infection activate innate immune system (complement) involves Macrophages Neutrophils Dendritic cells Endothelial cells Innate system produce cytokines (TNF, IL-1, IL-12, IL-18) Cause elevated levels of acute inflammation Coagulation activated by Factor XII Thrombin increases inflammation by activation of PARs Patient experiences inflammatory and immunosuppressive states (innate and adaptive immune cells involved) SEPTIC SHOCK PATHWAYS Courtesy of Robbins Basic Pathology, 11th ed SHOCK Outcome for septic shock Dependent on infection (extent and virulence) Immune status If comorbid condition exist Pattern and level of mediator production Treatment for septic shock Antibiotics and fluids, supplemental oxygen, treat underlying cause Stages of shock (based on hypovolemic type) Initial (nonprogressive)-cardiac output and blood pressure maintained to keep vital organs Progressive-widespread tissue hypoxia occurs if underlying causes not corrected, vital organs begin to fail Irreversible-widespread cell injury, ischemic bowel, renal failure, myocardial function decreases SHOCK Anaphylactic Severe allergic reaction Caused by IgE-mediated hypersensitivity reaction Increased vascular permeability and systemic vasodilation Patient presentation for cardiogenic and hypovolemic Pale with clammy, cyanotic skin Weak pulse, hypotension, tachypnea Prognosis Varies with duration and origin of shock Hypovolemic-young and healthy patients, 90% survival Septic-mortality rate 20-30% ANAPHYLACTIC SHOCK BEE STING REACTION NORMAL https://metro.co.uk/wp-content/uploads/2019/08/comp-1567142908.png?crop=0px%2C0px%2C1200px%2C630px&resize=1200%2C630 MECHANISM OF ACTION TYPE OF SHOCK CLINICAL EXAMPLES CARDIOGENIC MYOCARDIAL INFARCTION VENTRICULAR RUPTURE ARRHYTHMIA CARDIAC TAMPONADE PULMONARY EMBOLISM MYOCARDIAL PUMP FAILURE HYPOVOLEMIC HEMORRHAGE WATER LOSS (VOMITING, DIARRHEA, BURNS) INADEQUATE BLOOD OR PLASMA VOLUME SEPTIC BACTERIAL/FUNGAL SEPSIS TOXIC SHOCK SYNDROME Courtesy of Robbins Basic Pathology, 11th ed PERIPHERAL VASODILATION, BLOOD POOLING; ENDOTHELIAL INJURY; LEUKOCYTE DAMAGE; CYTOKINE CASCADE ACTIVATION SUMMARY OVERVIEW EDEMA: Accumulation of fluid in tissues Result in water into extravascular spaces HEMOSTASIS: Process of blood clot to prevent excessive bleeding after blood vessel damage (involves platelets/thrombin) HEMORRHAGE: Excessive bleeding THROMBOSIS: Inappropriate clot Can cause myocardial infarction, pulmonary embolism, cerebrovascular accident EMBOLISM: Movement of clot (most common type-pulmonary embolism) INFARCTION: Area of necrosis to tissue caused by occluded blood vessel SHOCK: Diminished cardiac output or reduced circulating blood volume that can lead to cell hypoxia Three types (septic, hypovolemic, cardiogenic) ANY QUESTIONS!! Courtesy of CBR