Myocardial (from the Latin. Infarcire - stuff, fill) - necrosis in a tissue or organ
resulting from the termination or significant reduction of arterial inflow, at least - venous outflow.
Myocardial - dying areas organ or tissue due to disturbances in blood supply it with the
development of severe hypoxia.
Myocardial - a vascular (circulatory) necrosis.
The causes are heart attack, thrombosis, embolism, prolonged spasm of the artery or functional body strain in low blood supply (the latter only occurs in myocardial infarction).
Form a heart attack depends on the structural features of the vascular system of a body, the presence of anastomoses, collateral blood supply (angioarchitectonics). Thus, in the bodies of the main vessel having a triangular (conical, wedge-shaped) heart attacks, whereas the loose or a mixed type of branching vessels observed irregular shape of a heart attack. For color(appearance) isolated white, white with red hemorrhagic rim and heart attacks. For consistency heart attacks are tight and the City "are.
Kidney. Wedge-infarct cortex. The numbers "2" marked hemorahiynyy whisk.
1). White (ischemic, bloodless) resulting from myocardial lesions corresponding artery. These heart attacks occur in the spleen, brain, heart, kidneys and are in most cases kolikvatsiynyy coagulation or less (in the brain) necrosis. After about 24 hours from the start of myocardial necrosis zone is well visible, clearly contrasting his pale yellow or pale brown with a zone of preserved tissue. Between them lies the demarcation zone, represented by inflammatory leukocyte and macrophage infiltration and vessels flushed with formennyh diapedesis of blood up to the formation of small hemorrhages. In the myocardium and the kidneys due to a large number of vascular anastomoses and collaterals demarcation zone occupies a large area. In this regard, those of heart attack called ischemic with hemorrhagic rim.
2). The red (hemorrhagic) heart attack develops when arteries clogged and (rarely) veins and usually occurs in the lungs, intestines, ovaries, brain. Of great importance in the genesis of myocardial red is mixed type of blood supply and the presence of venous stasis. For example, thromboembolic obstruction or thrombus branch pulmonary artery anastomosis is on blood flow in the area of low pressure systems bronchial arteries with subsequent rupture of capillaries mezhalveolyarnyh partitions. In very rare cases, blocking these anastomoses (possibly in the presence of pneumonia the same location) in the lungs may develop white heart attack. Also extremely rare splenic vein thrombosis is not formed the white and red (venous) infarction of the spleen. The zone of necrosis seeping blood, giving diseased tissue dark red or black. Demarcation zone with myocardial not pronounced as it takes a small area.
Lung. At the bottom of the image necrotic tissue that is impregnated with blood "yu - hemorahiynyy heart attack.
Within days of segmented neutrophils and macrophages rezorbuyut partially necrotic tissue. 7-10 Day is celebrated with growing demarcation zone of granulation tissue that gradually covers the entire area of necrosis. There myocardial organization, its scarring. There is another favorable result - the formation of cysts on the site necrosis (oral, sometimes filled with fluid), which often occurs in the brain.
When small amounts of ischemic stroke (cerebral infarction) may be replacing its glial tissue with the formation of glial scar. Adverse outcomes of heart attack is his festering.
Stasis (stasis - stop) is arrest of blood flow in the vessels of microcirculatory system (capillaries). The capillaries and veins are dilated paralytically and filled with blood. In the lumen of some capillaries the homogenous eosinophilic masses can be seen. They are columns of erythrocytes sticked together, which is called prestasis. Sludge syndrome (phenomenon) is regarded as a type of stasis. It is characterized by sticking of erythrocytes, leukocytes and thrombocytes to each other, which is accompanied by blood viscosity increase. Stasis may be discirculatory as a result of venous hyperemia or ischemia. Causes of stasis: • Physical factors (temperature elevation, cold). • Chemical factors. • Infection. • Infectious-allergic factors. • Autoimmune factors. Short stasis is reversible, long one causes hyaline thrombi formation, vascular permeability increase, edema, bleeding. Isolated vein spasm may cause leukostasis, accumulation of erythrocytes within venules (small veins) and capillaries. It is observed in hypoxia. In shock, leukostasis may be generalized, but as a rule it is localized in the venules. Microcirculation disturbances. There are four links in microcirculation: 1. The link of inflow and distribution of the blood (arterioles and precapillaries). 2. Intermediate (exchange) link (capillaries). 3. Depot link (postcapillaries and venules). 4. Drainage link (lymphatic capillaries and postcapillaries). The function of microcirculation is exchange between the blood and tissue. Pathology of microcirculatory system is formed of vascular, intravascular and extravascular changes. Vascular changes are those in the thickness and shape of the vessels, angiopathies with disturbance of vascular permeability as a result of hypoxia. Intravascular changes manifest as different disturbances of blood rheology (sludge, prestasis, stasis). They are observed in shock of different origin. Extravascular changes are perivascular edema, hemorrhage, lymphostasis on the lymph vessels. Ukrainian kosnpekt translated
stasis
Stasis (from the Latin. Stasis - Stop) - stop blood flow in the vessels
microvasculature (especially in the capillaries, at least - in venules). Stop
the blood is usually preceded its motion (prestaz).
The causes of stasis are:
1). Infections;
2). intoxication;
3). Shock;
4). Long-term artificial blood circulation;
5). Effects of physical factors (cold stasis with frostbite).
In stasis pathogenesis of primary importance is the change in the
rheological properties of blood microvessels until the development of
sludge syndrome (from the English. Sludge - swamp), which is
characterized formennyh adhesion of blood cells, especially red blood cells,
causing significant hemodynamic disturbances. Sludge red blood cells,
white blood cells, platelets is possible not only in the microvasculature, but
in large vessels. It leads to increased erythrocyte sedimentation rate
(ESR).
Stopping blood flow leads to increased vascular permeability of capillaries
(and venules), edema, and rise plazmorrahiyi ischemia.
Value stasis determined by its localization and duration. Thus, most of the
acute stasis leads to reversible changes in the tissues, but in the brain
contributes to the development of severe, sometimes fatal swelling of
dislocation syndrome, which noted with coma. Where there are multiple
Shock is defined as a clinical state of cardiovascular collapse characterized by (1) an acute reduction of effective circulating blood volume and (2) an inadequate perfusion of cells and tissues
The final result is hypotension and cellular hypoxia and, if uncompensated, may lead to impaired cellular metabolism and death.
Primary or initial shok. It is transient and usually a benign vasovagal attack resulting from sudden reduction of venous return to the heart caused by peripheral pooling of blood. It can occur immediately following trauma, severe pain or emotional over-reaction such as due to fear, sorrow or surprise. The attack usually lasts for a few seconds or minutes
Secondary of true shok. This is the form of shock, which occurs due to hemodynamic derangements with hypoperfusion of the cells. This type of shock is the true shock, which is commonly referred to as “shock” if not specified, and is the type described below.
According to etiology and pathogenesis shock is classified as:
1. Hypovolemic. Reduction in blood volume induces hypovolemic shock. The causes of hypovolemia include: a) Severe hemorrhage (external or internal) e. g. in trauma, surgery, b) Fluid loss e. g. in severe burns, crush injury to a limb, persistent vomitings and severe diarrhea causing dehydration.
2. Cardiogenic. Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart without actual reduction of blood volume (normovolemia) results in cardiogenic shock. The causes include:
•Deficient emptying (myocardial infarction, rupture of the heart, cardiac arrhythmias).
•Deficient filling (cardiac tamponade from hemopericardium).
•Obstruction to the outflow (pulmonary embolism, ball valve thrombus).
3. Septic. Severe bacterial infections or septicemia induce septic shock:
•Gram-negative septicemia (endotoxic shock,) e.g. infection with E. coli, Proteus Klebsiella, Pseudomonas and bacteroides. Endotoxins of gram-negative bacilli have been implicated as the most important mediator of septic shock
•Gram-positive septicemia (exotoxic shock) is less common e.g. infection with streptococci, pneumococci caused by endotoxins).
4. Anaphylactic (immediate reaction of hypersensitivity).
5. Neurogenic (in intoxication with hypnotic preparations, ganglioblockers, narcotics).
Stages of Shock. Deterioration of the circulation in shock is a progressive phenomenon and can be divided arbitrarily into 3 stages:
1. Non-progressive (initial compensated reversible) shock. In the early stage of shock, an attempt is made to maintain adequate cerebral and coronary blood supply by redistribution of blood. This is achieved by activation of various neurohormonal mechanisms causing widespread vasoconstriction and by fluid conservation by the kidney.
2. Progressive decompensated shock. This is a stage when the patient suffers from some other stress or risk factors besides persistence of the shock so that there is progressive deterioration.
3. Decompensated (irreversible) shock. When the shock is so severe that in spite of compensatory mechanisms and despite therapy and control of etiologic agent, which caused the shock, no recovery takes place it is called decompensated or irreversible shock.
Shock morphology
Three main pathological processes are observed in shock:
Microscopically, it is characterized by generalized spasms of the vessels, microthrombosis, signs of increased vascular permeability in microcirculatory system, hemorrhages, degenerations, necroses connected with hypoxia and damaging effect of endotoxins.
Morphologic features of complications in Shock
•Shock kidney: degeneration and necrosis in proximal canals with development of necrotic nephrosis (or symmetrical cortical necroses are possible), which results in acute renal insufficiency.
•Shock liver: glycogen amount in the hepatocytes decreases, hydropic degeneration and centrolobular necroses resulting in acute hepatic insufficiency develop. Combination of renal and hepatic insufficiency is called hepatorenal syndrome.
•Shock lung: atelectasis foci, serous-hemorrhagic edema, stases and thromboses in the microcirculatory bed resulting in acute respiratory insufficiency.
•Shock heart: degeneration and necrosis in cardiomyocytes, reduction in glycogen amount, fat degeneration, and necrotic foci.
•Shock gastrointestinal: the hypoperfusion of alimentary tract may result in mucosal and mural infarction called hemorrhagic gastroenteropathy.
•Shock brain: Hypoxic changes in the brain. Ischemic neurons appear shrunken and have eosinophilic cytoplasm. The pericellular spaces are dilated because of edema. Rarification of brain tissue presents.
•Similar changes occur in nervous, endocrine systems, and immune organs.
Shock morphology depends not only on the cause of the shock but also on its stage. At the early stage, disturbances of hemodynamic and DIC syndrome are noted. At the last stages degenerative and necrotic process occurs.
Intensive transfusion therapy of shock masks clinicomorphological picture. But the constant features are liquid cadaver blood irrespective of the composition of transfused fluids. Blood clots in the cardiac cavities and vessels are characteristic for terminal states of nonshock origin. So blood composition is a criterion for differential diagnosis.
Clinical Features
The classical features of decompensated shock are characterized by depression of 4 vital processes:
•Very low blood pressure.
•Subnormal temperature.
•Feeble and irregular pulse.
•Shallow and sighing respiration.
Renal dysfunction in shock is clinically characterized by a phase of oliguria due to ATN and a later phase of diuresis due to regeneration of tubular epithelium. With progression of the condition the patient may develop stupor, coma and death.
Side Lesson from university Moodle Website
Shock - severe pathological condition characterized by circulatory collapse (acute heart failure) after a super impact on hemostasis . There are hypovolemic, cardiogenic, septic shock and vascular types. Hypovolemic shock caused by rapid decrease of 20% or more blood volume that is observed in acute blood loss, dehydration. The loss of fluids and electrolytes is possible with extensive burns (due to the release of plasma damaged microcirculatory blood vessels), severe vomiting, profuse diarrhea. Cardiogenic shock occurs in response to a decrease in stroke volume of the heart is damaged, there is a myocardial infarction, severe myocarditis, acute mitral or aortic insufficiency, thrombosis valve prosthesis, interventricular septum rupture, cardiac hemotamponadi shirt. The marked drop in blood pressure leads to a significant reduction in blood supply tissue similar to hypovolemic changes. Septic (toxic - infectious) shock occurs when the infection is caused by gram - negative ( E . Coli , Proteus , Klebsiella ) less gram - positive (stafilo-, streto-, pneumococci) microflora. Toxins released (mainly endotoxins) activate the complement system, coagulation, fibrinolysis and platelets and neutrophils. As a result, stimulated the formation of nitric oxide (powerful vasodilator), tumor necrosis factor α, interleukin that cause acute circulatory failure. Vascular shock may be neurogenic (traumatic, pain at the spinal cord injury as a complication of anesthesia) or anaphylactic that caused generalized hypersensitivity reactions. Due to severe vasodilation, increased permeability of capillaries and arteriovenous reset redistribution of intravascular blood volume, accompanied by a significant decrease in total peripheral vascular resistance. Shock goes through three stages: Non- progressive (early) stage of shock is characterized by a decrease in blood pressure and cardiac output volume while maintaining relatively normal blood supply to vital organs. This is due to compensatory vasoconstriction of blood vessels, especially the skin and intestines. After depletion of adaptive mechanisms of shock moves to the next stage. Progressive stage of shock expressed by different clinical symptoms, deep collapse, which is caused by reduced blood supply of all organs and tissues (tissue hypoperfusion due to arterial dilatation), the development of metabolic and circulatory disorders. During the irreversible stage of shock, there is a pronounced lack of blood flow at the microcirculation in violation of the integrity of the vascular wall, multiple organ failure, a rapidly growing, ends in death of the patient. When morphological study noted generalized degenerative and necrotic changes, the phenomenon of DIC (petechial haemorrhages, stasis, blood clots in the microvasculature). In addition, due to the peculiarities of the structure and functioning of various organs, there are typical changes - the shock bodies . Thus, for shock kidney characterized by the development of necrotic nephrosis (necrosis convoluted tubule epithelium). Shock lung appears foci atelectasis, sero-hemorrhagic edema, sometimes with deposition of fibrin strands ( hyaline membrane ). In the brain there is ischemic encephalopathy , manifested by edema, hemorrhage point and focal necrosis. In the heart of the small watch, mainly subendokardialni foci of hemorrhage and necrosis infarction, fatty cardiomyocytes. In cortical layer of the adrenal gland decreases until the complete disappearance of lipid used for the synthesis of steroid hormones. In the gastrointestinal tract are hemorrhage, severe erosion and ulcers in the lining. ShockLiver different fatty hepatocytes, and in some cases even their tsentrolobulyarnym necrosis. Forecast shock depends on the type, severity, stage at which treatment was started, presence of complications . Currently, in severe cardiogenic or septic shock mortality is 50% higher.
You've probably heard the word 'hemorrhage', but what does it actually mean? In this lesson, we will define this medical term and take a look at the different hemorrhage classifications, and symptoms of each.
Hemorrhage Defined
Bill is a bloody mess as he is brought into the emergency room. He was using a chainsaw that kicked back while cutting a fallen tree branch in his backyard, and now has a deep cut across his torso. The ER team has seen far worse and can save his life, but his injury is a good example of a hemorrhage. In simplest terms, ahemorrhage is when blood vessels rupture, often due to an injury, resulting in excessive bleeding. A hemorrhage can be either external or internal (which is harder to detect). Let's take a look at the Advanced Trauma Life Support (ATLS) classification of hemorrhage, along with the symptoms present in each class.
Hemorrhage Classes
ATLS classes divide hemorrhage into four classes, based on the amount of blood lost. These four classes increase in severity, with Class 1 the least severe and Class 4 the most dangerous.
Class 1
The adult human body contains roughly five liters of blood. In the Class 1, or minimal stage of hemorrhage, there is less than 15%, or approximately 750ml, of blood loss. Patients still tend to have normal pulse rates and blood pressure. They are unlikely to have any further major medical problems because of the blood loss. Consider that a blood donation is about 450-500ml, and has very few side effects.
Class 2
Class 2, or mild hemorrhage, is defined as a 15-30% blood loss amount. In an adult, this would be equivalent to losing 750 to 1500 ml, which is about the equivalent of one or two bottles of wine.
Symptoms include a rapid heart rate, decreased pulse in the arms and legs, and an increased respiratory rate. The patient might be irritable or mentally altered and combative. His skin might be cooler to the touch and have delayed capillary refill. Urine production may be decreased, and have a higher concentration of other substances than normal. Thankfully for Bill, quick medical treatment means that his bleeding didn't progress beyond this class.
Class 3
Moderate blood loss of 30-40% of total volume is considered Class 3 hemorrhage. This would be like losing a 2-liter soda bottle worth of blood. At this stage, blood pressure will drop, and heart and respiration rates will rise. The patient's mental status may shift to a lethargic or irritable state, and he may experience a diminished pain response. The skin will not only feel cool but begin to lose color.
Class 4
Severe blood loss, or Class 4 hemorrhage, is defined as blood loss greater than than 40%. This class is characterized by severely high heart and respiration rates, along with dangerously low blood pressure. A lethargic state may progress to a coma. The skin and extremities will feel cold and begin turning blue, a condition known as cyanosis. Patients with Class 4 hemorrhage will be unable to produce or pass urine.
Lesson Summary
A hemorrhage is the term for when blood vessels rupture, often due to an injury, resulting in excessive bleeding. They are classified according to Advanced Trauma Life Support (ATLS) standards. The degree of severity places it into one of four classes, with Class 4 being the most dangerous.
Class 1 is less than 15% of blood volume loss, and is comparable to a blood donation. Class 2 is blood loss of between 15% and 30%, and can involve additional medical complications such as increased heart and respiration rates, mental status changes, and impaired urine production. Class 3 blood loss of 30-40% shows an advancement of the Class 2 symptoms. In Class 4, the patient loses more than 40% of blood volume and risks coma, experiences major skin and temperature changes, and can no longer produce urine.
Side Lesson from university Moodle website
Hemorrhage (i.e. bleeding) is a discharge of blood from the vascular compairtment to the exterior of the body or into nonvascular body spaces. Mechanisms of hemorrhages 1. By destruction of the blood vessel’s wall (f.e. trauma, rupture of aneurysm). 2. By diapedesis of erythrocytes because of the increased permeability of the vascular wall (f.e. intoxication, hypoxia). 3. By ulceration of the vessel’s wall (f.e. ulcer of stomach, necrosis of tumor, pulmonary tuberculosis). Thus a severe decrease in the number of platelets (thrombocytopenia) or a deficiency of a coagulation factor (e.g., factor VIII in hemophylia) is assosiated with spontaneous hemorrhages unrelated to any apparent trauma. Types of hemorrhages according to the site of origin 1. Cardiac, as following a penetrating heart wound. 2. Arterial, due to trauma and rupture of a dissecting aneurysm. 3. Capillary, which is usually due to trauma, inherent vessel wall weakness, or a coagulation defect. 4. Venous, which is usually caused by trauma or surgical operation, from esophageal varices. Types of internal hemorrhages • Petechia – a small mucosal or serosal hemorrhage or minute punctate hemorrhage usually in the skin or conjunctiva. • Purpura or hemorrhagic infiltration - the accumulation of some erythrocytes in tissue between cells. • Ecchymoses or bruise - the superficial large extravasations of blood into the skin and mucous membranes. Following a bruise in association with coagulation defect, an initially purple discoloration of the skin turns green and then yellow before resolving, a sequence that reflects the progressive oxidation of bilirubin released from the hemoglobin of degraded of red blood cells. A good example of an eccxymosis is a “black eye”. • Hematoma - a grossly visible localized accumulation of the blood in the soft tissue. Types of hemorrhages in body cavities • Hemothorax – hemorrhage in the pleural cavity. • Hemopericardium – hemorrhage in the pericardium cavity. • Hemoperitoneum – hemorrhage in the abdomen cavity. • Hemoarthrosis – hemorrhage in the joint cavity. External hemorrhages may be such as: • Melena is deposition of the blood in the faces (excrement or stool) due to hemorrhage from ulcer of stomach, polip or ulcer of intestines. • Hemoptyesis is hemorrhage from lungs. • Metrorrhagia is hemorrhage from uterus. Outcomes of hemorrhages • Coagulation of the blood. • Organization and incapsulation of the hematoma. • Brown cystic formatiom (in cerebral hematoma due to accumulation of hemosiderin). • Purulent fusion of the hematoma. In cases of death from acute massive hemorrhage, the most significant postmorten changes are gross rather then microscopic and consists in generalized pallor of tissue, collapse of the great veins, and a flabby, shrunken, gray spleen. A sudden loss of 33% of blood volume may cause death, while loss of upto 50% of blood volume over a period of 24 hours may not be necessarily fatal. However chronic blood loss generally produces an iron deficiency anemia, whereas acute hemorrhage may lead to serious immediate consequences such as hypovolemic shock.
Ischemia is yet another term that refers to a condition of the heart, but what does it mean? What is ischemia? Read this lesson to learn what it is, what causes it, what the symptoms are, and how to treat it.
What is Ischemia?
The heart is a complicated organ, and just like any pop song on the radio will tell you, there are lots of ways for it to get hurt. Heartbreak aside, it sometimes seems like there are more medical terms that refer to heart conditions than one can keep track of. Ischemia is one such condition. But what makes this one stand out?
Ischemia is the medical term for a condition where your heart does not get enough oxygen. Typically this is caused by a blockage that prevents adequate blood flow from reaching the heart. Blood carries oxygen around the body, so if the blood stops moving, oxygen stops being delivered.
Causes of Ischemia
What causes these blockages that prevent blood from reaching the heart properly? They usually occur when the blood vessels (specifically the coronary arteries) narrow due to the buildup of plaque (composed of cholesterol and other waste products). Over time, the plaque accumulates, and this prevents blood from properly flowing; this is called coronary artery disease. (When this process causes pain, it's called angina.)
A second possible cause of ischemia is the presence of a blood clot. Sometimes the plaques that form as part of coronary artery disease rupture, and a piece breaks off that then lodges somewhere else in the body, blocking blood flow. Typically this scenario would result in a full on heart attack. A final cause of ischemia is what's called a coronary artery spasm. In this scenario, the muscles briefly contract, causing the artery to narrow, temporarily preventing blood from reaching the heart.
Additionally, while these aren't considered causes of ischemia, there are risk factors associated with the probability of developing ischemia. These include smoking, high blood pressure, high levels of 'bad' cholesterols, low physical activity or obesity, a family history of heart disease, and other diseases such as diabetes.
Ischemia is caused by a blockage in the arteries leading to the heart. As a result, the heart does not get enough oxygenated blood.
Symptoms of Ischemia
Some cases of ischemia have no symptoms at all -- this is called silent ischemia. (Silent ischemia is more common in women, the elderly, and those who have diabetes.) However, when symptoms are present, they usually include pain or pressure in the chest, pain in the neck, shoulder, jaw, or arm, irregular heart beat, difficulty breathing, and nausea or vomiting. Symptoms may be present all the time, or they may only be present during times of physical exertion or emotional stress. Other situations, such as laying down, drug use, and extremely cold temperatures may also trigger ischemia symptoms.
Treatment Options
How can ischemia be treated? The primary goal of treatment is to increase the amount of blood that flows to the heart. Thus, there are two primary treatment techniques: medication and surgery.
There are a number of different medication options, depending on the severity of the specific case, and I'll mention a few of them here. One option is aspirin. Aspirin reduces the clotting capability of blood, lessening the chance of a clot forming. Another medication is nitroglycerin, a drug that causes the temporary widening of arteries. Then there is a class of medication called beta blockers. These work by slowing down the heart rate and decreasing blood pressure, allowing blood to move with less force throughout the vessels. Cholesterol-lowering drugs may also be used to help prevent plaque from forming.
The other treatment option is surgery, of which there are two main types. The first is called an angioplasty, in which a small metal device (a stent) is fed through the artery and placed in the area where the blockage exists. The stent remains there to keep the artery open. The second option is a coronary artery bypass surgery. This is a more serious operation and involves taking a vessel from another part of the body and grafting it into the heart region to provide another route for blood around the blockage. Coronary artery bypass surgery is much more invasive than an angioplasty and it has a much longer recovery period.
Lesson Summary
Ischemia is a condition where the heart is not receiving adequate oxygenated blood. This is usually due to a blockage somewhere in the vessels leading to the heart caused by coronary artery disease, a blood clot, or a coronary artery spasm. In some instances, the person may feel no symptoms (called silent ischemia), but in others, symptoms may include chest pains or pressures, pain felt elsewhere in the body, difficulty breathing, or nausea and vomiting. There are two primary treatment types for ischemia: medication and surgery. There are a number of different medication options, depending on the cause of the ischemia, and surgery may involve a less-invasive procedure where a metal stent is placed in the artery to keep it open or a more serious surgery where a new blood vessel is created to bypass the blockage.
In this lesson we will explore the phenomenon of reactive hyperemia including the natural purpose it serves as well as how it is used as a diagnostic tool for Peripheral Vascular Disease.
Reactive Hyperemia
I'm sure you've had your blood pressure taken before. The nurse had you roll up your sleeve and put an inflatable cuff around your arm that she inflated until it felt really tight. You probably started to notice that your hand may have felt a little cool, like it was starting to get a little numb, or maybe it throbbed. Then, as she slowly deflated the cuff, you felt the blood surge back to your hand. Voila! That was reactive hyperemia in action. Ok, so what why did you feel that surging rush of blood? Well, let's take a closer look at why we experience reactive hyperemia.
What is Reactive Hyperemia
Reactive hyperemia refers to the temporary increase ('hyper') of blood flow ('emia') to an area as a result of (or reaction to) ischemia, or an arterial blockage ('isch', meaning to stop or block, 'emia', meaning blood flow). This occlusion (blockage) can take the form of any outside force, like a tourniquet wrapped around the arm during a blood draw or a clamp placed on a vessel during surgery, or internal, like a buildup of plaque or a blood clot within the vessel that impedes or interrupts blood flow.
Blood Flow to Tissue Prior to Occlusion and Post Occlusion Reactive Hyperemia (PORH)
Ok, so reactive hyperemia might sound like a pretty obvious phenomenon- not so special, you occlude blood flow to an area, the blood pressure builds behind the point of the blockage and then, when you remove the occlusion, blood rushes to the area, temporarily increasing blood flow. Ok, that makes perfect sense but, what purpose does it serve? Well, it's actually a really important process that reduces further damage to the occluded tissue. During occlusion, cells are deprived of vital oxygen and metabolic wastes buildup; normally these wastes would've been washed away by the constant flow of blood. Now, this temporarily high surge of blood actually ensures that all cells receive enough oxygen immediately and that any dead cells and metabolic wastes are swiftly flushed from the area to reduce continued damage.
What's interesting is that this temporary surge of blood isn't just because blood flow builds up behind the clot but because your body actually responds to the reduced blood flow by secreting chemicals, calledvasodilators, that dilate (open) the deprived vessels. This dilation increases the size of the vessels thereby enabling a higher volume of blood to rush to the deprived area once the clot or blockage is cleared. In turn, this increased flow flushes the area of the vasodilators, causing the vessels to return to their normal size, thus reestablishing normal blood flow to the area.
Ok, so now that we understand what reactive hyperemia does, let's take at how it can be used to diagnose vascular diseases.
Peripheral Vascular Disease (PVD)
_Peripheral Vascular Disease (PVD) is actually a general term used to describe a progressive and chronic narrowing of your veins, lymph vessels, or arteries although, in the case of arterial damage the disease is referred to as Peripheral Arterial Disease (PAD). Now, PVD and PAD may not sound like a big deal, but they can be life threatening. Consider for a moment that your blood brings oxygen and nutrients to every cell and tissue of your body and, in the process, flushes away normal metabolic wastes. Now, consider interrupting or impeding that blood supply, thereby essentially starving, suffocating, and poisoning your tissues in one fall swoop. Yikes!
Now, PVD and PAD aren't actually primary disorders; they're known as secondary diseases, meaning that they're caused by some other disease affecting either the muscle of your heart or the vessels of your body. In actuality, the primary cause of PVD/PAD could really be any of a host of other disease like blood clotting within veins (known as deep vein thrombosis) or an enlargement of venous vessel (known as varicose veins) in the case of PVD, while atherosclerosis (hardening of the arteries due to plaque buildup) is the most common cause of PAD. Both PVD and PAD have associated risks of stroke and heart attack so they're certainly no laughing matter.
So, how is reactive hyperemia used to diagnose PVD/PAD you ask? Well, since PVD and PAD both result in reduced blood flow either to the limbs (in other words arterial) or from the limbs (venous), a reactive hyperemia test, can be used to essentially compare blood pressures between the legs to identify any differences that might indicate vessel narrowing.
Reactive Hyperemia & Diagnostic Testing
Ankle Brachial Index Evaluation (ABI)
The naturally occurring phenomenon of reactive hyperemia is utilized in various ways to diagnose the restriction of blow flow to particular limbs. In the case of PVD and PAD a test called an Ankle Brachial Index Evaluation (ABI) is utilized to compare the flow of blood between the lower limbs. An ABI evaluation is conducted by placing blood pressure cuffs around both of the patient's arms and legs while an ultrasound device measures and tracks the pulse in all four regions. The systolic pressure (or the blood pressure when the heart is contracting) is calculated for all four limbs and, since healthy individuals have higher systolic pressures in their legs than their arms, a simple calculation (dividing the systolic pressure of each ankle by the higher of the two found in the arms) can provide a quick assessment. ABIs above 0.90 are considered normal, anything in the 0.70-0.90 range indicates mild PVD, 0.50-0.70 indicates moderate PVD, and anything less than 0.50 indicates severe PVD.
Lesson Summary
Reactive hyperemia refers to a temporary increase in blood flow to an area after a period of arterial occlusion. Vasodilators secreted by blood deprived cells dilate deprived vessels ensuring that, post occlusion, blood will experience minimal resistance when resupplying the area. Reactive hyperemia ensures that, post occlusion, all cells will receive enough oxygen quickly and any dead cells and/or metabolic wastes will be swiftly flushed from the area to reduce continued damage. This phenomenon can be used to test for _Peripheral Vascular Disease (PVD) (a progressive narrowing of veins or lymph vessels) as well as Peripheral Arterial Disease (PAD) (narrowing of arteries) by way of a Ankle Brachial Index Evaluation (ABI). ABI values greater than 0.90 are normal, while values below that indicate some degree of PVD.
Side Lesson from the University Moodle Website
Hyperemia and congestion are the terms used for increased volume of blood within dilated vessels of an organ or tissue the increased volume from arterial and arteriolar dilatation being referred to as hyperemia or active hyperemia, whereas the impaired venous drainage is called venous congestion or passive hyperemia. The capillaries and veins are dilated paralytically and filled with blood. Arterial or active hyperemia is caused by an increased supply of blood from arterial system. The affected tissue or organ is pink or red in appearance (erythema). I. Common arterial or active hyperemia is a result • Of increasing volume of circulating blood (pletora). • Of increasing of amount of erythrocytes. • Vacatic (lat. – vacuum) because of decreased atmospheric pressure. II. Local arterial hyperemia can be • Angioneurotic – because of dilatation of arteries and arterioles. • Collateral. • Hyperemia after anemia. • Vacatic. • Inflammatory. • In arterio-venous fistula. Venous, or passive hyperemia, or congestion is caused by impediment to the exit of blood through venous pathway. The dilatation of veins and capillaries due to impaired venous drainage results in passive hyperemia or venous congestion, commonly referred to as congestion. Congestion may be acute or chronic, the latter being more common and called chronic venous congestion. I. Common congestion or Systemic (General) venous congestion is engorgement of systemic veins. It can be a result of • left-sided and right-sided heart failure • diseases of the lungs which interfere with pulmonary blood flow, like pulmonary fibrosis, emphysema, etc. • cardiac decompensation. II. Local congestion can be a result of • venous obstruction because of its thrombosis, • compression of venous vessel with tumor or ingrowth of connective tissue, • development of collateral blood circulation. Morphology of congestion Because of the increase in venous blood, organs become swollen and purplish. With long continued over-distension, the wall of the venules shows reactive thickening and there is mild intestinal fibrosis of the organs, giving them a very firm consistency. These changes are seen typically in the kidney and spleen. Important additional changes are found in the lungs and liver. Lungs. The lungs are burcly, congested and brownish in color. Pulmonary venous engorgement leads to alveolar hemorrhage. Hemoglobin from intra-alveolar blood is transformed into hemosiderin, which is then phagocytized by macrophages. These macrophages are known as heart failure cells. Phagocytes full of brown pigment migrate into intestinal tissue and to the lymph nodus. The sectioned surface is dark brown. It process in lungs is named as “brown induration” of the lungs. Spleen. Chronic venous congestion of the spleen occurs in right heart failure and in portal hypertension from cirrhosis of liver. The spleen in early stage is moderately enlarged while in long-standing cases there is progressive enlargement and may weigh up to 500 g to 1000 g. The organ is deeply congested, tense and cyanotic (“cyanotic induration of the spleen”). Sectioned surface is gray tan. The red pulp shows congestion and marked sinusoidal dilatation with areas of recent and old hemorrhages. These hemorrhages may get organized. This advanced stage seen more commonly in hepatic cirrhosis is called congestive splenomegaly and is the commonest cause of hypersplenism. Liver. Chronic venous congestion of the liver occurs in right heart failure and sometimes due to occlusion of inferior vena cava and hepatic vein. The liver is enlarged and tender and the capsule is tense. Cut surface shows characteristic “nutmeg liver” due to red and yellow mottled appearance. The changes of congestion are more marked in the centrolobular zone due to severe hypoxia than in the peripheral zone. The centrolobular hepatocytes undergo degenerative changes, and eventually centrolobular hemorrhagic necrosis may be seen. The peripheral zone of the lobule is less severely affected by chronic hypoxia and shows some fatty change in the hepatocytes. If the patient has periods of remission, the remaining liver cells may undergo compensatory hyperplasia. This results in small, irregular, pale nodules alternating with areas of fibrosis – so-called cardiac cirrhosis. It’s not true cirrhosis and does not causes hepatic failure. Outcomes of congestion: • Edema. • Stasis. • Hemorrhage. • Thrombosis. • Induration of organs. • Atrophy of organs.
No less than 6% of medical students won't turn into a specialist inside of seven years, as indicated by a study by the Association of American Medical Colleges. In any case, what number of the 94% who do complete medical school will really flourish amid those years? Our estimate is not very many. Below are the top 4 practices that each and every medical student should have in order to survive, maintain and ultimately flourish with classes in a medical college.
1- Time management
This is presumably the ability most critical to med school achievement. Keeping your life sorted out will make it conceivable to handle the expansion in scholarly workload med school brings. Abstain from working amid this first year. Numerous college students, myself included, would work 15-20 hours a week while as yet winning high evaluations. It is enticing to keep up that way of life in medical school, yet the normal med student is putting in 50-60 hours of work every week.
Spreading yourself too thin in first year can prompt disappointment. You should organize among your own, familial, and outside commitments. It might take a couple of weeks for you to make sense of what parity of extracurricular exercises you can deal with yet coursework must be a need.
2- Know how you learn
Numerous students traverse student using only maybe a couple study methods, or packed finally to succeed. Going to address was generally a given. The sheer volume of data you will learn in medical school implies you should distinguish your best and proficient study strategies to succeed. It is troublesome (if not inconceivable) to make up for lost time in med school once you fall behind.
Going to lectures in the main month can offer you some assistance with deciding on the off chance that they are successful for you. Regardless of whether you go to address, taking in a little measure of material every day will permit you to coordinate the greater part of the data all the more viably and permit you to recall that it long haul.
3- Search out and identify with upperclassmen
These are students who have experienced precisely what you are going to encounter. They can give profitable data about how they learned/concentrated viably and what their style was. Ask them what books or assets were useful. They know which speakers are the most useful, how exams are organized, and how every first year class is sorted out. Abstain from listening to companions or relatives who went to medical school quite a while prior. The present techniques and objectives of medical instruction are vastly different than they were only 10-15 years prior. Every school does things a little diversely so these students are your best asset for comprehending what will work your first year.
4- Participate in social exercises with your schoolmates
There is a typical saying that med school is a great deal like secondary school, and it's really exact. These are individuals you will put in the following 4 years with, all in the same classes for a long time. Right on time in first year, you will hear the same inquiries again and again: "Where did you go to student?" and "What was your major?" Eventually you will develop to appreciate these individuals through shared admiration and common enduring. Having a solid social network can keep you propelled and be another extraordinary study asset.
There is no single most ideal approach to traverse your first year, and you might discover you have to change amid your initial couple of weeks, however in the event that you take your late spring before first year to RELAX and consider what has permitted you to succeed previously, and what you need to enhance, you will both appreciate and profit by your first year of medical school. So don't stress excessively! We're certain that in the event that you concentrate on med school that you'll do fine.
