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Hemodynamic Disorders
Blood flow ensures the transportation of nutrients, hormones, metabolic wastes, O 2 and CO 2 throughout the body to maintain cell level metabolism, the regulation of the pH, osmotic pressure and temperature of the whole body, and the protection from microbial and mechanical harms. The study of the blood flow is called hemodynamics. Thus hemodynamics deals with the dynamics of blood flow. Hemodynamic response continuously monitors and adjusts to conditions in the body and its environment. Hemodynamic explains the physical laws that govern the flow of blood in the blood vessels. Hemodynamic Disorders Edema (Increased EC fluid) Hyperemia (Increased blood flow in arteries) Congestion (Impaired flow of venous blood) Hemorrhage (Extravasation-the leakage of a fluid out of its container into the surrounding area) Hemostasis (The arrest of bleeding or the interruption of blood flow through a vessel) Thrombosis (When blood clots block veins or arteries) Embolism (Blocked artery caused by a foreign body, such as a blood clot or an air bubble) Infarction (tissue death or necrosis due to inadequate blood supply to the affected area) Shock (Circulatory failure - when the body is not getting enough blood flow)
1. Edema When normal fluid homeostasis cannot be maintained within physiologic range, changes in vascular volume, pressure, protein content etc. all effect the net movement of water across the vascular wall. Such water extravasation into the interstitial spaces is called edema. Edema causes swelling. For example: Edema in the lungs causes water to fill alveoli. It leads to difficulty in breathing. Approximately 60% of lean body weight is water, two thirds of which is intracellular. Most of the remaining water is found in extracellular compartments in the form of interstitial fluid; only 7% of the body’s water is in blood plasma. Under normal circumstances, the tendency of vascular hydrostatic pressure to push water and salts out of capillaries into the interstitial space is nearly balanced by the tendency of plasma colloid osmotic pressure to pull water and salts back into vessels. There is usually a small net movement of fluid into the interstitial, but this drains into lymphatic vessels and ultimately returns to the bloodstream via the thoracic duct , keeping the tissues dry. Elevated hydrostatic pressure or diminished colloid osmotic pressure disrupts this balance and results in increased movement of fluid out of vessels. ShockEmbolism Haemostasis (^) Edema s O o o
If the net rate of fluid movement exceeds the rate of lymphatic drainage, fluid accumulates. Within tissues the result is edema , and if fluid accumulate within any adjacent body cavity it is termed as an effusion. Edema fluids and effusions may be inflammatory or non-inflammatory. In inflammatory edema protein rich exudates accumulate due to increases in vascular permeability caused by inflammatory mediators. Usually, inflammation associated edema is localized to one or a few tissues, but in systemic inflammatory states, such as sepsis generalized edema may appear, often with severe consequences. In contrast, non-inflammatory edema and effusions are protein poor fluids called transudates. Non-inflammatory edema and effusions are common in many diseases, including heart failure, liver failure, renal disease, and severe nutritional disorders. tissues (^) edema netrateoffluid movement (^) rateof lymphatic body cavity effusion drainage d eat onto
e) Inflammation Immediately following an injury, the traumatized area becomes red, warm, and painful, and it begins to swell. The swelling process, also known as edema, is the result of acute inflammation, a response triggered by damage to living tissues. In the case of injury, the purpose of the inflammatory response is to remove components of damaged tissue in order to allow the body to begin to heal. Example - acute inflammation, chronic inflammation, angiogenesis.
2. Hyperemia Hyperemia and congestion both are caused by increased blood volumes within tissues, but have different underlying mechanisms and consequences. Hyperemia is an active process in which arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow. Affected tissues turn red (erythema) because of increased delivery of oxygenated blood. 3. Congestion Congestion is a passive process resulting from reduced outflow of blood from a tissue. It can be systemic, as in cardiac failure, or localized, as in isolated venous obstruction.
Acute pulmonary congestion is marked by blood-engorged alveolar capillaries and variable degrees of alveolar septal edema and intra-alveolar hemorrhage. In chronic pulmonary congestion, the septa become thickened and fibrotic, and the alveolar spaces contain numerous macrophages laden with hemosiderin (“heart failure cells”) derived from phagocytosed red cells. In acute hepatic congestion, the central vein and sinusoids are distended with blood, and there may even be central hepatocyte dropout due to necrosis. The periportal hepatocytes, better oxygenated because of their proximity to hepatic arterioles, experience less severe hypoxia and may develop only reversible fatty change. In chronic passive congestion of the liver, the central regions of the hepatic lobules, viewed on gross examination, are red-brown and slightly depressed (owing to cell loss) and are accentuated against the surrounding zones of uncongested tan, sometimes fatty, liver (nutmeg liver) (Fig. A). Microscopic findings include centrilobular hepatocyte necrosis, hemorrhage, and hemosiderin- laden macrophages (Fig. B). In long-standing, severe hepatic congestion (most commonly associated with heart failure), hepatic fibrosis (“cardiac cirrhosis”) can develop. Because the central portion of the hepatic lobule is the last to receive blood, centrilobular necrosis also can occur in any setting of reduced hepatic blood flow (including shock from any cause); there need not be previous hepatic congestion. Figure: Liver with chronic passive congestion and hemorrhagic necrosis. A, In this autopsy specimen, central areas are red and slightly depressed compared with the surrounding tan viable parenchyma, creating “nutmeg liver” (so called because it resembles the cut surface of a nutmeg). B, Microscopic preparation shows centrilobular hepatic necrosis with hemorrhage and scattered inflammatory cells.
Within minutes the secreted products recruit additional platelets, which undergo aggregation to form a primary hemostatic plug. c) Secondary hemostasis: deposition of fibrin Tissue factor is also exposed at the site of injury. Tissue factor binds and activates factor VII , setting in motion a cascade of reactions that results in thrombin generation. Thrombin cleaves circulating fibrinogen into insoluble fibrin , creating a fibrin mesh work, and also is a potent activator of platelets, leading to additional platelet aggregation at the site of injury. This sequence, referred to as secondary hemostasis, consolidates the initial platelet plug
d) Clot stabilization and resorption Polymerized fibrin and platelet aggregates undergo contraction to form a solid, permanent plug that prevents further hemorrhage. At this stage, counter regulatory mechanisms (e.g., tissue plasminogen activator , t- PA) are set into motion that limit clotting to the site of injury and eventually lead to clot resorption and tissue repair.
5. Hemorrhage Hemorrhage is an acute loss of blood from a damaged blood vessel. The bleeding can be minor, such as when the superficial vessels in the skin are damaged, leading to petechiae and ecchymosis. It can also be significant, leading to a more life threatening symptoms and altered mental status. Hemorrhaging can be either external or internal. Hemorrhage is a leading cause of potentially preventable death. Rapid loss of up to 20% of the blood volume or slow losses of even larger amounts may have little impact in healthy adults; greater losses, however, may result in hypovolemic shock. Fatal intracerebral bleed (Hemorrhage) Ecchymoses (^) Purpura EPA
7. Embolism An embolism is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin, where it can cause infarction. It is a clot that travels from the site where it is formed to another location in the body. The vast majority of emboli are dislodged thrombi, hence the term thromboembolism. Other rare emboli are composed of fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or even foreign bodies. Emboli travel through the blood until they encounter vessels too small to permit further passage, causing partial or complete vascular blockage. The clinical consequences vary widely depending on the size and the position of the lodged embolus, as well as the vascular bed that is impacted. Different types of embolism include: 1. Pulmonary embolism: Originate from deep venous thromboses and are the most common form of thromboembolic disease. Most pulmonary emboli (60% to 80%) are clinically silent because they are small. Sudden death, right heart failure, or cardiovascular collapse occurs when emboli obstruct 60% or more of the pulmonary circulation. 2. Systemic Thromboembolism: It refers to emboli that travel through the arterial circulation. These emboli originate in the left heart, aorta, or large arteries and are carried by the arterial blood into various organs such as brain, spleen, and kidney. 3. Fat and Marrow Embolism: Occurs when fat and marrow elements are embolized into the bloodstream during acute long bone fractures. 4. Air Embolism: Gas bubbles within the circulation can coalesce to form frothy masses that obstruct vascular flow and cause distal ischemic injury. A particular form of gas embolism, called decompression sickness, occurs when individuals experience sudden decreases in atmospheric pressure. E.g Scuba and deep sea divers during rapid ascend. 5. Amniotic Fluid Embolism: Amniotic fluid embolism is the fifth most common cause of maternal mortality worldwide. It is a rare but serious condition that occurs when amniotic fluid — the fluid that surrounds a baby in the uterus during pregnancy — or fetal material, such as fetal cells, enters the mother's bloodstream. Amniotic fluid embolism is most likely to occur during delivery or in the immediate postpartum period.
