Gangguan Hemodinamika PDF

Gangguan Hemodinamika Yanti Ivana S. 1 Tujuan Pembelajaran Mahasiswa memahami dan mampu menjelaskan kembali dasar- dasar Edema dan efusi Hiperemia dan kongesti Hemostasis & thrombosis Embolisme Iskemia, infark, syok...

Gangguan Hemodinamika Yanti Ivana S. 1 Tujuan Pembelajaran Mahasiswa memahami dan mampu menjelaskan kembali dasar- dasar Edema dan efusi Hiperemia dan kongesti Hemostasis & thrombosis Embolisme Iskemia, infark, syok 2 1. Tekanan hidrostatik menarik cairan masuk ke dalam pembuluh darah 2. Edema adalah pengumpulan cairan dalam ruang tertentu seperti cavum pleura, ruang sinovial. 3. Kongesti terjadi ketika terjadi vasodilatasi venula. 4. Hemostasis adalah peristiwa normal yang terjadi ketika terjadi perdarahan 5. Pada kondisi Syok terjadi hipoperfusi jaringan 3 Edema: Swelling of tissues as a result of excess interstitial fluid Effusion: The escape of fluid from the blood vessels or lymphatics into the tissues or a cavity Hyperemia: an excess of blood in a part Congestion: abnormal accumulation of fluid, usually blood, in a body part, organ, or area Hemostasis: arrest of the escape of blood by either natural means (clot formation or vessel spasm) or artificial means (compression or ligation) Thrombosis: formation, development, or presence of a thrombus (Thrombus: a stationary blood clot along the wall of a blood vessel, frequently causing vascular obstruction. 4 Embolism: An embolism is an obstruction in a blood vessel due to a blood clot or other foreign matter that gets stuck while traveling through the bloodstream Ischemia: is an insufficient supply of blood to an organ, usually due to a blocked artery. Infarct: a localized area of ischemic necrosis produced by anoxia following occlusion of the arterial supply or the venous drainage of the tissue, organ, or part. Shock: Shock is a medical emergency in which the organs and tissues of the body are not receiving an adequate flow of blood. This deprives the organs and tissues of oxygen 5 EDEMA & EFUSI 6 Cardiovascular Digestive Limphatic system Immune Limphatic Functions: returning fluid and proteins filtered out of the capillaries to the circulatory system picking up fat absorbed at the small intestine and transferring it to the circulatory system, serving as a filter to help capture and destroy foreign pathogens 7 Sistem Limfatik 8 Pertukaran cairan di kapiler 9 Lymph movement The lymphatic system has no single pump like the heart. Lymph flow depends primarily on waves of contraction of smooth muscle in the walls of the larger lymph vessels. Flow is aided by: contractile fibers in the endothelial cells the one-way valves external compression created by skeletal muscles. 10 1. Tekanan hidrostatik menarik cairan masuk ke dalam pembuluh darah 11 Edema Edema occurs when too much interstitial fluid accumulates Reduced concentration of plasma protein Causes of edema Increased permeability of capillary walls Increased venous pressure Blockage of lymph vessels 12 Reduced concentration of plasma protein Decreases plasma-colloid osmotic pressure Cause: Excessive loss of plasma protein in the urine → kidney disease Reduced synthesis of plasma protein → liver disease Diet deficient in protein Significant loss of plasma protein → large burned surface 13 Increased permeability of the capillary wall More plasma protein pass from plasma Cause ex: Histamine induced widening capillary pores → tissue injury / allergic reaction 14 Increased venous pressure elevation in outward pressure across the capillary walls → congestive heart failure localized restriction of venous return → pregnancy 15 Blockage of the lymph vessel Excess filtered fluid is retained in the interstitial fluid rather than returned to the blood through the lymphatics. obstruction of the lymphatic system, particularly at the lymph nodes. Parasites, cancer, or fibrotic tissue growth caused by therapeutic radiation can block the movement of lymph through the system. Ex: elephantiasis is a chronic condition marked by gross enlargement of the legs and lower appendages when parasites block the lymph vessels. removed during surgery, a common procedure in the diagnosis and treatment of cancer. 16 17 EFUSI Akumulasi cairan pada jaringan/rongga tertentu Misal: Efusi pleura Efusi perikardia Efusi sendi 18 2. Edema adalah pengumpulan cairan dalam ruang tertentu seperti cavum pleura, ruang sinovial. 19 HIPEREMIA & KONGESTI 20  Hyperemia & Congestion → a local increased volume of blood in a particular tissue. Hyperemia Congestion is an active process is a passive process resulting from augmented resulting from impaired tissue inflow because of outflow from a tissue. arteriolar dilation, as in It may occur systemically, as skeletal muscle during in cardiac failure, or it may exercise or at sites of be local, resulting from an inflammation. isolated venous The affected tissue is redder obstruction. (Erythema) because of the The tissue has a blue-red engorgement of vessels with color (cyanosis), oxygenated blood particularly as worsening congestion leads to accumulation of deoxygenated hemoglobin in the affected tissues 21  Congestion and edema commonly occur together, primarily since capillary bed congestion can result in edema due to increased fluid transudation. In long-standing congestion (chronic passive congestion), the stasis of poorly oxygenated blood also causes chronic hypoxia → parenchymal cell degeneration or death (sometimes with microscopic scarring). Capillary rupture at these sites of chronic congestion may also cause small foci of hemorrhage; breakdown and phagocytosis of the red cell debris can eventually result in small clusters of hemosiderin-laden macrophages. 22 3. Kongesti terjadi ketika terjadi vasodilatasi venula. 23 HEMOSTASIS & TROMBOSIS 24 Hemorrhage Hemorrhage generally indicates extravasation of blood due to vessel rupture. Rupture of a large artery or vein is almost always due to vascular injury (trauma, atherosclerosis, or inflammatory or neoplastic erosion of the vessel wall). Hemorrhage may be manifested in a variety of patterns, depending on the size, extent, and location of bleeding 25 Hematoma → accumulation of blood within tissue Petechiae → minute 1- to 2-mm hemorrhages into skin, mucous membranes, or serosal surfaces Purpura → Slightly larger (≥3 mm) hemorrhages Ecchymoses → Larger (>1 to 2 cm) subcutaneous hematomas (i.e., bruises) Hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis (in joints) → Large accumulations of blood in one or another of the body cavities 26 Hemostasis & Thrombosis Normal hemostasis is the result of a set of well-regulated processes that accomplish two important functions maintain blood in a fluid, clot-free state in normal vessels induce a rapid and localized hemostatic plug at a site of vascular injury Thrombosis → an inappropriate activation of normal hemostatic processes, such as the formation of a blood clot (thrombus) in uninjured vasculature or thrombotic occlusion of a vessel after relatively minor injury 27 Regulation of hemostasis & thrombosis Hemostasis and thrombosis are regulated by: vascular wall - Platelets endothelium coagulation cascade 28 Hemostasis Injury Vasoconstriction (neurogenic mechanism) & secretion local factor (ex: endothelin) – vascular wall Primary hemostasis - Platelet Secondary hemostasis - Coagulation Solid, permanent plug (& Antithrombotic counter – regulation) 29 1. Arteriolar Vasoconstriction Reflex neurogenic mechanism Local secretion of endothelin 30 2. Primary Hemostasis – PLATELET Platelet respond to exposure of subendothelial ECM by: Adhesion Shape change Granule release Recruitment Platelet aggregation (1° hemostatic plug) Platelets adhere to exposed extracellular matrix (ECM) via von Willebrand factor (vWF) and are activated, undergoing a shape change and granule release; released adenosine diphosphate (ADP) and thromboxane A2 (TxA2) lead to further platelet aggregation to form the primary hemostatic plug. 31 3. Secondary Hemostasis – COAGULATION Tissue factor release Phospholipid complex expression Thrombin activation Fibrin polymerization (2° hemostatic plug) Local activation of the coagulation cascade (involving tissue factor and platelet phospholipids) results in fibrin polymerization, "cementing" the platelets into a definitive secondary hemostatic plug. 32 4. Antithrombotic Counter- Regulation Factors released to limit the size of the hemostatic plug Counter-regulatory mechanisms, such as release of tissue type plasminogen activator (t-PA) (fibrinolytic) and thrombomodulin (interfering with the coagulation cascade), limit the hemostatic process to the site of injury. 33 Thrombosis Three primary influences predispose to thrombus formation, the so-called Virchow triad: endothelial injury stasis or turbulence of blood flow blood hypercoagulability 34  Thrombi may develop anywhere in the cardiovascular system: within the cardiac chambers on valve cusps in arteries, veins, or capillaries. They are of variable size and shape, depending on the site of origin and the circumstances leading to their development. 35 Embolism An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin. Almost all emboli represent some part of a dislodged thrombus, hence the commonly used term thromboembolism. Rare forms of emboli include droplets of fat, bubbles of air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, or even foreign bodies such as bullets. Unless otherwise specified, an embolism should be considered to be thrombotic in origin. 36  Inevitably, emboli lodge in vessels too small to permit further passage, resulting in partial or complete vascular occlusion. The potential consequence of such thromboembolic events is the ischemic necrosis of distal tissue, known as infarction. Depending on the site of origin, emboli may lodge anywhere in the vascular tree; the clinical outcomes are best understood from the standpoint of whether emboli lodge in the pulmonary or systemic circulations 37 Types Location Pulmonary thromboembolism Systemic thromboembolism Type of substances Fat thromboembolism Air thromboembolism Amniotic fluid thromboembolism 38 ISKEMIA, INFARK, SYOK 39 Ischemia & infarct An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Infarction involving different organs is a common and extremely important cause of clinical illness. In the United States, more than half of all deaths are caused by cardiovascular disease, and most of these are attributable to myocardial or cerebral infarction. Pulmonary infarction is a common complication in a number of clinical settings, bowel infarction is frequently fatal, and ischemic necrosis of the extremities (gangrene) is a serious problem in the diabetic population. 40 Cause thrombotic or embolic events, and almost all result from arterial occlusion local vasospasm expansion of an atheroma owing to hemorrhage within a plaque extrinsic compression of a vessel (e.g., by tumor). twisting of the vessels (e.g., in testicular torsion or bowel volvulus), compression of the blood supply by edema or by entrapment in a hernia sac traumatic rupture of the blood supply. 41 Venous Thrombosis Although venous thrombosis may cause infarction, it more often merely induces venous obstruction and congestion. Usually, bypass channels rapidly open after the thrombosis, providing some outflow from the area, which, in turn, improves the arterial inflow. Infarcts caused by venous thrombosis are more likely in organs with a single venous outflow channel, such as the testis and ovary. 42 4. Hemostasis adalah peristiwa normal yang terjadi ketika terjadi perdarahan 43 Shock Shock, or cardiovascular collapse, is the final common pathway for a number of potentially lethal clinical events, including severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis. Regardless of the underlying pathology, shock gives rise to systemic hypoperfusion caused by reduction either in cardiac output or in the effective circulating blood volume. The end results are hypotension, followed by impaired tissue perfusion and cellular hypoxia. Although the hypoxic and metabolic effects of hypoperfusion initially cause only reversible cellular injury, persistence of shock eventually causes irreversible tissue injury and can culminate in the death of the patient. 44 45 Types Cardiogenic shock results from myocardial pump failure. This may be caused by intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade), or outflow obstruction (e.g., pulmonary embolism). Hypovolemic shock results from loss of blood or plasma volume. This may be caused by hemorrhage, fluid loss from severe burns, or trauma. Septic shock is caused by systemic microbial infection. Most commonly, this occurs in the setting of gram-negative infections (endotoxic shock), but it can also occur with gram-positive and fungal infections. 46 47 Stages of Shock An initial nonprogressive phase during which reflex compensatory mechanisms are activated and perfusion of vital organs is maintained A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances, including acidosis An irreversible stage that sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible. 48 5. Pada kondisi Syok terjadi hipoperfusi jaringan 49  TERIMA KASIH SEMOGA BERMANFAAT 50 Pustaka Kumar, Abbas, Fausto, et al, 2015, Robbins and Cotran’s Pathologic Basis of Disease, 9th ed, Saunders Sherwood, L., 2016, Human Physiology: From Cells to Systems, 9th ed, Cengage Learning, Boston 51