Hemodynamics 1 PDF Notes

Hemodynamics 1 Debra Hazen-Martin, PhD Office: 792-2906 Email: [email protected] Hemodynamic Disorders 1: Edema, Hyperemia, Congestion and Hemorrhage Outline: I. Overview of Homeostasis A. Terms B. Normal Fluid Movement II. Edema – Causes and Consequences A. Increased Hydrostatic Pressure 1) Loca...

Hemodynamics 1 Debra Hazen-Martin, PhD Office: 792-2906 Email: [email protected] Hemodynamic Disorders 1: Edema, Hyperemia, Congestion and Hemorrhage Outline: I. Overview of Homeostasis A. Terms B. Normal Fluid Movement II. Edema – Causes and Consequences A. Increased Hydrostatic Pressure 1) Local 2) Systemic 3) Reduced Plasma Oncotic Pressure B. Lymphatic Obstruction C. Sodium and Water Retention III. Hyperemia and Congestion A. Hyperemia B. Congestion 1) Acute 2) Chronic Passive IV. Hemorrhage A. Classification of Types and Location B. Examples Suggested Reading: Robbins Basic Pathology by Kumar, Abbas and Aster, Chapter 4 (97-105) Objectives: 1) Define homeostasis, hemostasis, edema, anasarca, hydrothorax, hydropericardium, ascites, transudate, exudate, hyperemia, congestion, hemorrhage, hematoma, petechial, purpura, and ecchymosis 2) Describe mechanisms that alter normal fluid dynamics to cause edema. 3) Differentiate the causes of local vs. systemic edema. 4) Describe the differences in hyperemia and congestions with regard to oxygen supply to tissues affected. 5) Contrast the features of acute and chronic passive congestion in the lung and liver. 6) Describe the different forms of hemorrhage and their possible causes. 1 Hemodynamics 1 I. Overview: Homeostasis is a state of equilibrium in the body with respect to the chemical composition of fluids and tissues. In the body, and important element is the maintenance of the proper ration and composition of intra-vascular and extra-vascular fluid. Three factors are responsible for maintenance of homeostasis: 1) maintenance of an intact vessel wall 2) normal intra-vascular pressures and osmolarity 3) balancing the fluid vs. clotted state of blood (hemostasis) Alterations in vessel wall and or hemostasis will lead to thrombosis or hemorrhage. Alterations in normal intra-vascular pressure or osmolarity of the blood may lead to the formation of edema and/or congestion. Water comprises 60% of the total body weight. Of that amount, 2/3 will be contained within cells (intracellular) while 1/3 is found in the extracellular environment. 75% of the extracellular water is found within the interstitial tissue spaces while only 25% contributes to the water of plasma within the vascular system. The balance between interstitial water and that in plasma is crucial and alterations may lead to edema. A. Terms you must know: 1. 2. 3. 4. 5. 6. 7. Edema - a condition of excess fluid in the interstitial tissue space. Anasarca - extreme generalized edema of subcutaneous tissues, cavities, and organs. Hydrothorax - collection of fluid in the pleural cavity. Hydropericardium - collection of fluid in the pericardial cavity. Hydro-peritoneum or ascites - collection of fluid in the peritoneal cavity. Transudate - a protein poor edematous fluid with specific gravity under 1.012 resulting from non-inflammatory mechanism. Exudate - a protein rich edematous fluid with specific gravity over 1.012 resulting from increases in vascular permeability during inflammation. 2 Hemodynamics 1 B. Normal Fluid Movement Between Compartments: Interstitial fluid is generated at the capillary bed. Hydrostatic pressure is normally 32 mm Hg at the arteriolar side, forcing fluid from the blood to the interstitial space at a rate of 14 ml/min. The venous end of the capillary bed has a reduced hydrostatic pressure, but the plasma colloid osmotic pressure contributes for a final pressure of 26 mm Hg causing a return of interstitial fluid to blood of 12 ml/min. The difference in pressures results in a net loss of fluid and accumulation in the interstitial space (2ml/min). It is the job of the lymphatic system to remove the excess fluid and deliver it back to the venous system. Failure to do so results in edema. II. Edema Causes and Consequences: It is fairly simple to understand how edema occurs if you simply consider a failure in any part of the system illustrated in the previous slide. The 4 causes of edema include an increased arterial hydrostatic pressure, a decrease in the venous osmotic pressure, failure of the lymphatic drainage or conditions that cause Na / H20 retention either directly or indirectly. A. Increased hydrostatic pressure: Increases in hydrostatic pressure may be local or systemic. 1. Local - One way to increase hydrostatic pressure is to block the venous outflow. A blood clot in the vein will stop flow and back up blood at the arterial side of the system to increase pressure. The increase in pressure causes excess movement of fluid out of the vessel and this exceeds the capacity of fluid retrieval by the lymphatic system. An example of this situation is deep vein thrombosis of the lower limb. Edema forms in tissues that are distal to the occlusion and obviously this would affect only that limb. 3 Hemodynamics 1 2. Systemic - Increases in hydrostatic pressure may be systemic due to cardiac failure resulting in generalized edema. When the heart fails, there is a decrease in cardiac output leading to decreased arterial flow to the kidney. This initiates the renin - angiotensin response. Renin is secreted by the J-G cells and converts angiotensinogen to angiotensin I which causes secretion of aldosterone by the adrenal cortex. Circulating aldosterone stimulates reabsorption of Na+ by the distal tubule of the kidney and water follows to result in an overall increase in blood volume. The increased blood volume does not increase cardiac output or kidney arterial pressure because the failing heart cannot respond. Therefore the physiologic response only increases venous pressure and forces fluid into the interstitial tissues. In left ventricular failure, blood backs up into the left atrium impairing venous return from the lungs. Pulmonary edema is profound and the lungs may be 2-3X their normal weight. Microscopically, the alveolar spaces are filled with edematous fluid and small hemorrhages of the capillaries may result from congestion so that RBC’s are found within the space as well. The presence of fluid impairs ventilation. Right ventricular failure seldom occurs in the absence of left ventricular failure. Here venous return to the right atrium is impaired so tributaries to the SVC and IVC are congested. This essentially increases systemic venous pressures and portal vein pressure indirectly. The result is generalized tissue and organ edema. Dependent portions of the body are more susceptible, resulting in pitting edema. 4 Hemodynamics 1 B. Reduced plasma osmotic pressure: Osmotic pressure drops with an absence of protein in the blood. Albumin is the major protein in the plasma. So, reductions in synthesis of albumin due to liver disease and/or malnutrition or loss of albumin at the glomerulus (nephrotic syndrome) have similar impact. When protein content of plasma falls, osmotic pressure at the venous end of the capillary bed is insufficient to retrieve the lost interstitial fluid formed at the arterial end. Blood volume drops and cardiac output decreases. The body’s response is activation of the renin-angiotensin response which ultimately results in reabsorption of sodium and water to increase overall volume. The resulting increased blood volume only further reduces the osmotic pressure when the protein deficiency persists. Inadequate levels of circulating protein results in systemic edema. Peri-orbital edema, organ edema and ascites are prominent in situations of decreased protein synthesis due to liver failure, malnutrition or protein loss due to renal failure. 5 Hemodynamics 1 C. Lymphatic Obstruction: When the lymphatic system fails to remove interstitial fluid at the same rate is produced (2ml/min) edema results. Lymphatic failure is frequently due to blockage of the lymphatic channels. Blockage may occur as a result of parasite infection and fibrosis (filarial worms) and produces a local edema termed elephantitis. Although you will seldom see this disease, it illustrates the importance and effectiveness of the lymphatic system. More commonly lymphatic channels are blocked by primary or metaplastic neoplasms. In addition, removal of lymph nodes (ex: axillary dissection for breast cancer treatment) will result in localized edema distal to the removal. D. Sodium and Water Retention: This process may be a secondary response to aldosterone secretion initiated by cardiac failure and/or loss of blood volume as described above and in both cases the resulting fluid retention only further exacerbates the original problem. However, sodium and water retention may occur when the primary event is an acute reduction of kidney function resulting in lack of urine production. You will learn more about these kidney diseases in the future. 6 Hemodynamics 1 Conclusion: The forms of edema considered today result largely through non-inflammatory events and therefore result in an edema that is protein poor (transudate) as opposed to the protein rich (exudate) edema of inflammation. The consequences of edema are site dependent and vary from trivial to lethal. Chronic collection of edema in dependent portions of the body (lower limb) coupled with congestion of blood may result in secondary infection and complications in wound healing. Pulmonary edema interferes with ventilation and may cause death or lead to infection. Edema of tissues within closed spaces such as the brain is of major concern and often fatal. In this slide, the edematous brain has herniated through the foramen magnum and the impression of the foramen is seen on the cerebellum. III. Hyperemia and Congestion: Both hyperemia and congestion involve an increase of blood within the vessels of a tissue or organ. 7 Hemodynamics 1 A. Hyperemia: The increased volume of blood in hyperemia is an active physiologic response to a functional demand (exercising muscle), hormonal or neurogenic trigger (blushing), or inflammation. All involve arteriolar dilation and an increase of oxygenated RBC’s to an area. The increased transport of oxygenated blood through the areas causes a transient redness. B. Congestion: Congestion is the passive back-up of blood due to venous obstruction. Congestion may be local or systemic and often accompanies development of edema. The venous back up causes a sluggish flow of oxygenated blood to tissues so tissues appear blue-red (cyanotic) and hypoxia leads to capillary damage with the potential for hemorrhage or loss of blood from the vessel. Long-standing (chronic) congestion leads to cell death. As an example consider acute and chronic congestion of the lung. Acute pulmonary congestion typically involves collection of edematous fluid within the alveolar spaces. Note that the alveolar capillaries are engorged with red blood cells making the septa appear thicker than those of the normal lung. Even in acute congestion transient hypoxia may cause small hemorrhages of the capillaries and RBC’s may be seen within the alveolar space. The presence of fluid within the alveolar sac complicates gas exchange (ventilation). 8 Hemodynamics 1 In chronic pulmonary congestion, as one would see in individuals suffering from cardiac failure, RBC’s continue to fill the capillaries and alveolar septa are thickened due to fibrosis. Macrophages have entered the picture to phagocytose and digest the RBC’s resulting from hemorrhage. They become filled with hemosiderin (iron micelles) and appear yellow-brown. These are called “heart failure cells”. Chronic passive congestion in the liver gives a unique gross morphology termed “nutmeg liver.” Remember that portal and arterial blood flow from the periphery of the liver lobule to the central vein. If venous blood “backs up” it occurs from the central vein outward. Central areas are therefore most congested and subject to hypoxia. Grossly, the central areas appear red while the periphery of the lobule is a normal color and this creates the nutmeg appearance. Microscopically, the central areas are congested with red blood cells and at high powers centri-lobular necrosis (cell death) is apparent with hemosiderin laden macrophages and lipofuscin loaded hepatocytes. In long standing congestion due to heart failure, fibrosis (cardiac cirrhosis) may occur. 9 Hemodynamics 1 IV. Hemorrhage: Extravasation of blood occurs due the rupture of blood vessels. Capillary damage occurs during chronic congestion and many other disorders. Rupture of larger arteries and veins may occur due to trauma, atherosclerotic damage, and inflammatory or neoplastic invasion of the vessel wall. Hemorrhage may occur to external and internal surfaces of the body or within a body cavity or tissue. A collection of blood within the body is called a hematoma. A. Types of hemorrhage: As you can see in the table hemorrhage can be classified and given specific names according to the size and site of the hemorrhage. The common causes of each type of hemorrhage are included in the table. B. Examples: 1. Petechial hemorrhage: These are pinpoint lesions (1-2 mm) which occur on serosal surfaces and skin. They are frequently a result of a local increase in intra-vascular pressure or alterations in blood clotting such as decreases in platelet numbers (thrombocytopenia) or clotting factors. 10 Hemodynamics 1 2. Purpura: These lesions are slightly larger (3-5mm) and occur in many of the same conditions as petechia. They commonly accompany diseases involving vasculitis or any condition where vessels are fragile. 3. Ecchymosis (bruise): These lesions are larger than 1cm and occur in subcutaneous tissues and are commonly called bruises. They occur in the conditions described for the smaller lesions in addition to trauma. The color changes noted as a bruise resolves reflects the step wise breakdown of red blood cells by macrophages. The initial bruise is blue-red (Hg) followed by bluegreen (bilirubin) and finally the yellowbrown color of the remnant iron (hemosiderin). 4. Hematoma: A large collection of blood may form in any area of the body and we frequently name them according to the specific site as indicated in the diagram above. The clinical significance of the hemorrhage is not always directly proportional to volume. Clearly, a rapid loss of 20% on one’s blood volume can lead to hypovolemic shock. Slower chronic losses of blood which leave the body (ulcer, menstrual) may lead to iron deficiency anemia. Yet even small hemorrhages may be fatal when they involve the cerebral arteries. 11