Hemodynamic Disturbances PDF

Summary

This document provides an overview of hemodynamic disorders, focusing on edema and hemorrhage. It details the definitions, causes, mechanisms, and types of each. The material includes diagrams and classifications of the different conditions.

Full Transcript

HEMODYNAMIC DISTURBANCES Disorders of blood flow Edema Definition - Pathological accumulation of excess fluids in the interstitial tissue spaces and serous sacs. - Edema fluid may be either transudate or exudate. -Approximately 60% of body weight is w...

HEMODYNAMIC DISTURBANCES Disorders of blood flow Edema Definition - Pathological accumulation of excess fluids in the interstitial tissue spaces and serous sacs. - Edema fluid may be either transudate or exudate. -Approximately 60% of body weight is water, two thirds of which is intracellular with the remainder is in the extracellular compartments (the interstitial tissue & plasma). Exudate Transudate Occurs in cases of Caused by conditions inflammation. other than inflammation High protein content Low protein content (4-8 gm%). (below 3 gm%). Specific gravity above 1018. Specific gravity below 1015. Clots on standing Does not clot on standing. (presence of fibrinogen) (no fibrinogen) Contains inflammatory cells. No inflammatory cells. Filtration out Reabsorption in 15 mmHg 45 mmHg HP HP Mechanism of edema formation Rates of filtration & reabsorption across the capillary wall depend on ❑ Capillary hydrostatic pressure (n: 45-15 ) mmHg ❑ Plasma osmotic pressure (n: 30 ) mmHg - Normally, capillary hydrostatic & osmotic forces are balanced, so that the amount of Interstitial fluid remains constant. - At arterial end: H.P. > O.P.→ filtration of tissue fluid At venous end: H.P. < O.P.→ withdrawal of tissue fluid Normal homeostasis ARTERIOLE VENULE CAPILLARY BED H: 45 O: 30 H: 15 O: 30 Net flow out No net flow Net flow in hydrostatic P Excess fluid LYMPHATICS osmotic P Increased hydrostatic pressure ARTERIOLE CAPILLARY BED VENULE H: 60 O: 30 H: 15 O: 30 Net flow out Net flow No net flow out hydrostatic P Overall excess flow out osmotic P Decreased osmotic pressure ARTERIOLE VENULE CAPILLARY BED H: 45 O: 20 H: 15 O: 20 No net flow Net flow out Net flow out hydrostatic P Overall excess flow out Osmotic P Lymphatic obstruction ARTERIOLE CAPILLARY BED VENULE Net flow No net flow Net flow out in LYMPHATIC hydrostatic P Excess fluid osmotic P Excess fluid collects Causes of Oedema (1) Increased capillary hydrostatic pressure: A rise in the venous pressure is followed by a rise in the capillary pressure, increased transudation fluids into the tissue spaces. (2) Decrease colloid osmotic pressure of the plasma: When the plasma proteins falls below 2.5 gm% the colloid osmotic pressure of the blood diminishes an excess fluid passes into the tissue spaces and serous sacs i.e. generalized oedema. (3) Increased capillary permeability: Caused by toxins, chemicals histamine and serotonin in acute inflammation and hypoxia. The plasma escapes into the tissue spaces and withdraw more fluids from the vessels by its osmotic pressure. (4) Lymphatic obstruction: Is especially important in the production of local oedema. (5) Sodium and water retention: Retention of sodium occurs when excretion in the urine is less than the intake. This occurs in congestive heart failure, liver cirrhosis, nephrotic syndrome. Oedema is classified into (1) Localized oedema: Localized in a part of the body. The total amount of fluids in the body is within normal but its distribution is wrong and abnormal amount accumulates in the affected area e.g. obstructive and inflammatory oedema. (2) Generalized oedema (anasarca): The process involves the whole body. The total amount of fluids in the body is increased e.g. cardiac, renal and nutritional oedema. Oedema is also classified into: (1) Soft oedema (pitting): The accumulated fluid is present free in the tissue spaces and can be moved by pressure, so the affected part pits on pressure e.g. cardiac, renal and nutritional oedema. (2) Hard oedema (non-pitting): The oedema fluid is in excess or is united with the tissue elements, so the oedematous part does not pit on pressure, e.g. lymphatic oedema. LOCALIZED OEDEMA (1) Inflammatory Oedema: Occurs in acute inflammation. The oedema fluid is an exudate. (2) Obstructive Oedema: (A) Venous obstruction: This leads to oedema in the area drained by the obstructed vein. Common examples of oedema due to venous obstruction are: (a) Liver cirrhosis and bilharzial hepatic fibrosis cause intestinal oedema (b) Acute left sided heart failure causes acute pulmonary oedema. (c) The pregnant uterus compresses the iliac veins causing oedema in the lower limbs. (B) Lymphatic obstruction: Causes lymphatic oedema (lymphoedema). (a) Acute lymphangitis and lymphadenitis. (b) Filarial lymphangitis and lymphadenitis. (c) Post-inflammatory and post-irradiation fibrosis in the lymph vessels and lymph nodes. (d) Mechanical compression of the lymph vessels e.g. by tumors. (e) Tumor emboli and cords in the lymph vessels and tumor metastases in the lymph nodes. GENERALIZED OEDEMA (1) Cardiac oedema: Occurs in congestive heart failure. Muscular edema (2) Renal oedema: Occurs in renal diseases It starts at the eyelids and ankle and later becomes generalized. (3) Nutritional oedema: Caused by hypoproteinaemia due to: (a) Inadequate protein intake. (b) Interference with the intake, passage, digestion or absorption of food in the alimentary tract. (c) Decrease plasma protein formation as in chronic liver diseases or blood sucking parasites (parasitic edema) Pathological Features of Oedema All tissues except bone may be the seat of oedema. Common sites are the subcutaneous tissue, connective tissue, mucous membranes, lungs, brain and serous cavities. Subcutaneous tissue: The affected area appears swollen. Lung: Becomes heavy and its cut surface oozes frothy sanguineous fluid. Microscopically a pale red homogenous coagulum of protein appears in the alveolar spaces. Brain: It becomes heavy. The intracranial tension is increased. Serous cavities: A transudate accumulates, HEMORRHAGE 1 Definition 2 Causes and Mechanism 3 Types 4 Effect and Fate HEMORRHAGE Definition: Escape of blood outside the blood vessels or cardiac chambers. Causes of Hemorrhage: ‘Mechanism’ (1)Traumatic hemorrhage “Rhexis”= the rupture of blood vessel caused by mechanical injury to the vascular wall either accidental or surgical. (2) Spontaneous hemorrhage “DIAPEDESIS”= the passage of blood cells through capillary walls into the tissues’ (a) Diseases of the vascular wall e.g. atheroma and aneurysm. (b) Inflammatory injury to the vascular wall as in phlebitis. (c)Increased intravascular tension e.g. chronic venous congestion and hypertension. (d) Hemorrhagic blood diseases as hemophilia(impairs the body's ability to make blood clots) and purpura. (e) Vitamin C and K deficiency. Types of Hemorrhage (1) External Hemorrhage: Escape of blood outside the body. (a) Epistaxis. Bleeding from the nose. (b) Haemoptysis: Coughing of blood. The source of blood is the lung or the bronchi. The blood is red, frothy and alkaline. (c) Hematemesis: Vomiting of blood. The source of blood is the esophagus, stomach and duodenum. The blood is digested, brown in colour, acidic and mixed with food particles. (d) Melena: Presence of dark digested blood in the stools. (e) Hematuria: Blood in urine. (2) Internal Hemorrhage Escape of blood inside the body cavities (a) Hemothorax: Haemorrhage into the pleura. (b) Hemopericardium: Haemorrhage into the pericardium. (c) Hemoperitoneum: Haemorrhage into the peritoneum. (d) Hematocele: Haemorrhage into the tunica vaginalis. (e) Hemoarthrosis: Haemorrhage into a joint cavity. (3) Interstitial Hemorrhage Escape of blood into the interstitial tissue spaces, it may be:= ‘Classification according to size of Hemorrhage” (a) Petechial haemorrhage: Small amount of blood “Pinpoint” (b) Ecchymosis: Moderate amount of blood. (c) Suffusions: Diffuse flat irregular areas of bleeding (c)Hematoma: Large amount of blood causing a swelling. Petechiae Ecchymoses Hematoma Microscopic picture Presence of free RBCs in between tissue elements with liberation of golden yellow to brown pigment of hemosiderin. Effect of Hemorrhage “Depends on amount of blood lost” (1) Small amount: No effect. (2) Small amount repeatedly (chronic haemorrhage):, e.g. peptic ulcers leading to anemia. (3) Moderate amount: (less than 750 cc.). Is compensated by: (a) Immediate fall in the blood pressure stimulates the aortic arch and carotid sinus reflexes which increase the heart rate. (b) Proteins are added from the liver (c) Red cells and white cells are added by the hyperplastic bone marrow. (4) Massive amount: Causes hemorrhagic shock. cardiac output decreases and blood pressure falls causing hemorrhagic shock and death. Thanks Any questions?

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