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Clinical Guide (Chapters 11 (A, B, C, D) & 12)please check out for resources on understanding ECG/EKG readings!!!Anemia: low level concentrations of erythrocyte or hemoglobin, most commonly due to a deficiency in one of three conversion factors for converting Reticulocytes into Erythrocytes. Aplastic Anemia: An abnormality in the bone marrow due to chemical or radiation damage results in the inability to synthesize erythrocytes. Normocytic Anemia: anemia due to blood loss (blood volume loss, not specifically erythrocytes) as a direct result of trauma.Microcytic Anemia: anemia due to Iron (Fe2+) deficiency, resulting in a decrease in erythrocytes specifically.Macrocytic Anemia: anemia due to Vitamin B12 or Folic Acid (Folate) deficiency, resulting in a decrease in erythrocytes specifically. >If only B12 is deficient, the condition is also called “Pernicious Anemia”Polycythemia: “Polyvera”, an abnormal excess in Erythrocyte concentration resulting from two causes: >Primary Polycythemia: caused by an abnormality in bone marrow due to a tumorous growth, genetic condition, or a congenital condition. >Secondary Polycythemia: caused by an excessive production of the Erythropoietin hormone signal, which can be induced artificially by intravenous “blood-doping”.-symptoms: increased levels of erythrocytes, leukocytes, platelets, and increased Hematocrit, resulting in headaches, hypertension, vomiting, and difficulties sleeping.Thrombosis: blood clot formation as a result of abnormal coagulation, resulting in increased risk for myocardial infarctions and stroke in the cerebral arteries.Thrombocytopenia: an abnormally low concentration of platelets, which inhibits sufficient blood clot formation, resulting in easy bruising, prolonged bleeding from injuries, fatigue, easy bleeding from mucous membrane tissues (in the nose, mouth and gums).Leukemia: a form of cancer affecting bone marrow, resulting in abnormal leukocyte production. >Acute: rapid production of excess immature leukocytes, most common in children. >Chronic: excessive buildup of immature but abnormal leukocytes >Lymphoblastic: “Lymphocytic”, characterized by excessive production of mature Lymphocytes which affects the immune system >Myeloblastic: “Myelogenous”, characterized by excessive production of both mature and immature myelocytes (a precursor cell to the granulocytes)-Immature or abnormal leukocytes are not functional and compromise immune system function, increasing the risk of infection.-Symptoms include inflammation, fever, weight loss, weakness, headaches, bone &/or joint pain, bleeding easily, swollen lymph nodes in the throat and armpits.-Treatments depend on type, stage of progression, and severity of the leukemia. >Chemotherapy: kills leukemic cells >Interferon-α (INFa): a growth factor that controls leukemic cell proliferation by slowing it down and by increasing the immune system’s response for anti-leukemic activity. >Radiation Therapy: controls cancerous leukemic cell growth via high-energy radiation exposure >Stem-cell transplantation (SCT): Bone marrow transplant induces synthesis of new, mature and healthy leukocytes. Allows the patient to continue radiation and chemotherapy treatment to get rid of remaining leukemic cells.Sickle Cell Disease: A group of genetic blood diseases, most common is Sickle Cell Anemia. Results in the production of an abnormal form of hemoglobin called “hemoglobin-S” (but abnormal hemoglobin-C is also seen). Normal red blood cells contain A-type hemoglobins. Abnormalities in the folding of hemoglobin-S inhibit its ability of pick up and carry oxygen. Buildup of hemoglobin-S in red blood cells causes them to take a “sickle” shape, resulting in an inability to pass through smaller blood vessels and capillaries. Hemoglobin-S can also form aggregates (clusters) in the blood stream. While normal erythrocytes have a life span of ~120 days, sickle cells are destroyed more rapidly. -Symptoms: Hypoxemia (irritates sensory nerves & affects cellular respiration), pain (associated with inflammation and antibody accumulation in joints and abdominal cavity), headaches, fatigue, fever, increased risk of bacterial infection, increased heart rate (tachycardic palpitation due to heart compensating for O2 deficiency), jaundice (damage to erythrocytes causes excessive production of Bilirubin)-Treatment: supplemental Iron, B12 and Folate, antibiotics for bacterial infectionsAtherosclerosis: the accumulation of cholesterol/fat/lipids (with connective tissue composed of collagen and elastic fibers, smooth muscle cells, Calcium deposits, and some inflammatory cells like Macrophages and T-cells) as “intimal plaques” or “atheroma” under the endothelial layer of blood vessel walls of the medium and large arteries, which can attract and accumulate Ca2+, causing calcification (hardening) of the blood vessel walls. Calcification can weaken blood vessels, making them susceptible to rupture, resulting in localized internal bleeding. If it doesn’t rupture, it may obstruct the blood vessel over time. Hypercholesterolemia, smoking & drinking can increase the risk of developing Atherosclerosis, which increases the risk of Myocardial Infarction or stroke. Thyroid issues can also cause Atherosclerosis, as the Parathyroid can secrete Parathyroid Hormone (PTH) in excess, causing Hypercalcemia (which puts large amounts of Ca2+ in contact with any developing plaque formations). The accumulation of fatty plaque under the endothelial lay activates growth factors involved in cell proliferation & cell growth, attracts white blood cells (like Neutrophils) that cause local inflammation, and creates an accumulation site for Ca2+. Common arteries affected include the coronary arteries, carotid artery, cerebral arteries, the aorta and its branches, and the major arteries located in the limbs. If condition worsens it may result in Stroke, muscle damage, blood vessel damage, organ damage-Causes: Diabetes, chronic cigarette use, familial predisposition, Hypercholesterolemia or Hyperlipidemia (also known as Dyslipidemia), sedentary lifestyle, obesity, and hypertension.-Symptoms: “tight” feeling chest pains, and shortness of breath. The obstruction of arteries can cause Angina, a deficiency in blood flow and supply, which can also cause pain.Heart Murmurs: can be benign or caused by any sort of defect in the Atrioventricular valves (Tricuspid or Mitral), like an insufficiency (backflow of blood), or stenosis (restricted opening of valve), that causes blood to rush violently through the heart or outside the heart in its major vessels. Glomerulonephritis: “Nephritic Syndrome”, a disorder characterized by localized edema and inflammation of the glomeruli, high blood pressure, and blood in the urine. Glomerulonephritis has two degrees of severity: -Primary Glomerulonephritis: only affects the kidneys with more localized symptoms -Secondary Glomerulonephritis: cause is more widespread and affects multiple areas in the body, causing many additional disorders.-Causes of Glomerulonephritis differ, depending of if the condition is Acute or Chronic, but both can damage the glomerulus of the nephron, decreasing the Glomerular Filtration Rate (GFR).>Acute: Often the result of post-infection complications of the skin or throat via bacterial, parasitic, or viral pathogen (such as bacterial Streptococcus, Staphylococcus, Pneumococcus, viral Chicken pox, and parasitic Malaria). If the cause is Acute but non-infectious, it may be due to Membranoproliferative glomerulonephritis (overactive cell membrane proliferation thickens the porous tissue of the glomerular vessels, decreasing and inhibiting filtrate outflow), or due to auto-immune disorders such as Systemic Lupus Erythematosus (Lupus, inflammatory condition in which the immune system attacks the patient’s own tissue) or Immunoglobulin A Nephropathy (IgA Nephropathy, “Berger’s Disease”, the most common cause of glomerulonephritis characterized by deposits of IgA antibody in the glomerulus)>Chronic: Usually the result of a form of a genetic disorder, Hereditary Nephritis, but in other forms of chronic glomerulonephritis the cause is unknown.-Symptoms: Edema (seen early on) which can result in vasculitis of the glomerulus capillaries (damage that decreases their filtration rate) which decreases urine production and can result in an obstruction to blood-flow, and fluid retention in other areas of the body. Periorbital Edema is a typical result of kidney problems where fluid is retained in the face and around the eyes (“puffy” face and eyes), edema may later progress to the legs. High blood pressure, Hypertension and all the typical symptoms associated (headache, vomiting, nausea, vertigo, nosebleeds). Additional symptoms include visual impairment, fever, weakness and fatigue, and malaise. If the cause is auto-immune, leukocytes may infiltrate abdominal tissues and cause inflammation and irritation in the GI, joints, and other visceral organs, resulting in joint pain, abdominal pain, and loss of appetite associated with GI irritation. Advanced cases may result in a coma.-Treatment: Bloodwork and urinalysis is done to determine severity and cause (auto-immune cause is detected by antibody count in bloodwork, and blood +other solutes in the blood can indicate severity of the condition). A low-protein, low-sodium diet may be recommended if the case is less severe to see if the condition resolves itself. Diuretics can be used to increase urine production and flush out some of the retained fluid and solute (most notably sodium), medications (like Angiotensin-converting enzyme (ACE) inhibitors, and Angiotensin II receptor blockers (ARBs)) for controlling Hypertension and high blood pressure can also be administered simultaneously. Prescribe antibiotics if the cause is bacterial, or antivirals/antiparasitic if the cause is viral/parasitic. If the conditioned has advanced to end-stage Renal failure, dialysis is recommended while the patient waits for organ transplant.Pyelonephritis: a condition involving bacterial infection (most commonly Escherichia coli/E. coli, 90%) in one or both kidneys due to two possible causes: an advanced or untreated urinary tract infection (UTI) that has spread up the ureters and into the Renal system, or an infection in the circulatory system that has entered the Renal system thought the Renal artery. -Symptoms: fever, back pain, severe abdominal pain, nausea, vomiting, changes in color or scent of urine, fresh blood in the urine (may appear pink)-Treatment: After urinalysis and bloodwork is one to confirm diagnosis, a one-month course of antibiotics is prescribed.Kidney Stones: “Calculi”, hard masses formed within the urinary tract as a result of highly concentrated urine saturated with salts that accumulate together over time, or due to a deficiency of inhibitory factors (Citrate) that prevent mass formation. The majority of stone composition (~80%) is Calcium (Ca2+) due to calcium salt formation and aggregation, along with varied amounts of uric acid, cysteine amino acid, and other waste solute. Stone formation is more common in those with Hyperparathyroidism, a condition of the Parathyroid glands resulting in excessive secretion of Parathyroid Hormone (PTH), which controls the secretion of Ca2+ into the blood (results in Hypercalcemia which ends up in the urine in such large amounts it is not all reabsorbed and ends up aggregating into calcified masses in the urinary tracts, ureter, urethra, and even inside the kidney). Stone formation can obstruct urinary tracts and cause a decrease in urination, an increase in waste fluid retention, and damage to the tissues which causes pain. This also makes the urinary tract and kidneys susceptible to bacterial infection.-Treatment: If the stones are small enough and detected early (have not yet caused infection, major symptoms, or obstruction) they may be passed on their own without treatment, though this process can be painful. Since long-term dehydration may increase the likelihood of stone formation (due to concentrated amounts of solute building up over time), an increase in the amount and frequency of water consumption is recommended but there is no definitive proof that increased hydration breaks apart already formed stones or makes passing them any easier. Drugs may be prescribed if the stone is too large to pass on its own and is causing problems. Verapamil acts as a calcium ion channel blocker to inhibit the passage of calcium from tissues into the blood stream. Potassium citrate is a supplemental citrate salt that dissociate from potassium in the body and attaches to calcium to inhibit stone formation via calcification. Tamsulosin is an α-adrenergic receptor blocker which targets cells with this receptor type in the neck of the bladder leading to the urethra, resulting in smooth muscle relaxation of the bladder neck so urine (and the stone) can pass more easily. Procedures like laser-targeted breakdown of the stone, and surgery can also be employed if the stone is too large. The pain associated with passing the stone can be alleviated with non-steroidal anti-inflammatory drugs (NSAIDs) or opioid medications like morphine.Metabolic Acidosis: acidity of the blood as a result of: a loss in base products, excessive metabolic “fixed acid” by-product, or excessive ingestion of “fixed acid” sources from diet (includes H2SO4 sulfuric acid as a by-product of protein catabolism, H3PO4 phosphoric acid as a result of phospholipid catabolism, ketoacids, lactic acid, salicylic acids, and others not mentioned). While these acids are classified as “non-volatile” and are expected in the circulatory at a production rate of 40-60 mmoles/day, excessive amounts can have adverse effects:-Arterial blood becomes acidic with the increase of [H+], called “acidemia”-As a result, bicarbonate HCO3- acts as a buffer to relieve the blood of excess fixed acid (takes H+, becomes H2SO3, and dissociates into CO2 and H2O) which decreases [HCO3- ] in the blood.-With the loss of buffer acidemia continues and the respiratory system attempts to compensate by increasing the respiratory rate (increased gas exchange), which results in hyperventilation (“Kussmaul breathing”).-The Renal system attempts to compensate for the acidemia as well by excreting increased amounts of fixed acids in titratable forms and NH4+ ammonium by-product, and by reabsorbing more newly formed HCO3- bicarbonate into the blood, so it can continue buffering the acid in the blood. *Chorionic Metabolic Acidosis: a condition of metabolic acidosis in the Chorion of a developing embryo. This is usually compensated for by increasing ammonia NH3 synthesis to titrate fixed acids (by removing an H+ from the fixed acids, becoming NH4+ ammonium) so they are excreted instead of building up in the embryonic Chorion.Metabolic Alkalosis: alkalinity of the blood, “alkalemia”, due to excessive loss of fixed acid, or an increase in alkaline by-product. This may be due to Hyperaldosteronism, where excess Aldosterone increases absorption of HCO3- bicarbonate into the blood, or it may be caused by Hypoaldosteronism, where a deficiency of Aldosterone results in increased absorption on H+ into the blood.-Arterial [HCO3- ] (bicarbonate concentration) increases-Alkalemia causes a compensatory decrease in respiratory rate-The Renal system compensates by increasing urine excretion of bicarbonate HCO3- due to excessive concentrations in the filtration tubule that cannot be completely reabsorbed into the blood.*If vomiting occurs it results in a loss of H+ and causes an increase in the reabsorption of bicarbonate HCO3-, which increases blood alkalinity and worsens the patient’s condition.Hypertension: -Primary Hypertension: “Essential Hypertension”, has an unknown cause, but some factors are known to increase blood pressure. Environmental factors including excessive dietary Na+, obesity and stress have been attributed to Primary Hypertension. Other factors include hormonal imbalances, renal dysfunction, cardiovascular issues, obstruction or destruction of blood vessels, mechanisms of the Sympathetic Nervous System, and the Renin-Angiotensin-Aldosterone mechanism. Any of these factors result in an increase in cardiac output (CO) and/or an increase in total peripheral resistance (TPR). >Na+: increased intracellular [Na+] results in increased intracellular [Ca2+] due to open channels in blood vessel wall cells, resulting in contractions of the smooth muscle of blood vessel walls, increasing the blood pressure.>Stress can affect hormone levels: increased Cortisol (stress hormone) raises blood pressure, increased Norepinephrine causes vasoconstriction, decreased vasodilation hormones like Prostaglandins and/or Bradykinins result in prolonged vasoconstriction. -Secondary Hypertension: Can affect multiple organ systems even during pregnancy; cause is known and can be treated.Causes:1-Adrenal gland disorders: Adrenal Cortex secretes Aldosterone, Cortisol and Androgen while Adrenal Medulla is the central lobe that secrete Adrenaline & Noradrenaline. Excess secretions of Cortisol, Noradrenaline (Norepinephrine), and Aldosterone can be caused by a tumor, infection, or autoimmune disorder and results in increased blood pressure via interactions with the Renal system: >excess secretion of Renin: kidney tumor can affect cells that secrete Renin enzyme, must be removed >excess secretion of ACE: “Angiotensin Converting Enzyme” cell of the lung tissues secreting ACE in excess must be treated with an ACE-inhibitor such as Captopril >excess secretion of Angiotensin II (Ag II): treated with an Ag II-blocker such as Valsartan >excess secretion of Aldosterone: treated with Aldosterone receptor/channel-blocker such as Spironolactone >Hypercalcemia: treated with Calcium channel blockers such as Barnidipine >excess secretion of Norepinephrine: treated by blocking the affected receptor (β1) with β1-blockers such as Propranolol or Atenolol (preferred for those with respiratory issues) >Diuretics: if Renal failure progresses to ~50% functionality urination must be accelerated with the use of diuretics to help decrease blood volume and pressure, and to increase filtration rate.2-Cushing’s Syndrome: a tumor, infection or auto-immune disorder in the Adrenal Cortex results in the excess secretion of Aldosterone, Androgen, and more specifically Cortisol. >Symptoms: increased [Na+] in the blood, decreased [K+] in the blood, increased blood pressure, headache, vomiting, nausea, sleep disorder, nose bleeds, anxiety. Increased Cortisol levels cause increased Systolic/Diastolic blood pressure and TPR (total peripheral vascular resistance), increased blood glucose (eventual Hyperglycemia called “Steroid Diabetes”), obesity/weight gain in the face and belly while limbs stay thin due to Cortisol degrading proteins in the limb muscles. Increased Androgen results in abnormal facial hair growth in females, decreases in Estrogen and Progesterone, irregular menstrual cycle and ovulation, possible infertility. >Treatment: If the cause in a tumor, surgical removal is required. If cause is infectious, antibiotics are prescribed. Additional medications are given to control symptoms.3-Hyperaldosteronism: “Conn’s Disease” tumors on cells specific for Aldosterone secretion in Adrenal Cortex cause excess secretions. >Symptoms: Hypertension, headache, vomiting, nausea, sleep disorder, nose bleeds, Hypernatremia, Hypokalemia. >Treatment: surgical removal of tumor and medications for controlling symptoms4-Pheochromocytoma: a tumor of the Adrenal Medulla >Symptoms: excess secretion of Adrenaline and Noradrenaline, Hypertension, headache, vomiting, nausea, sleep disorder, sweating, muscles spasms, palpitations, tachycardia, heart disease5-Kidney Disease: cysts of the kidneys (Polycystic Kidney Disease), tumors, Renal failure, or obstructed Renal artery can cause a decrease in Renal filtration rate, resulting in fluid retention and build-up, causing Edema and increased blood pressure. 6-Steroidal Drugs: long term use of Synthetic Cortisols (anti-inflammatory Corticosteroids like Prednisone) which are typically used to treat inflammatory auto-immune conditions like Dermatitis or Chron’s disease, can lead to increases in total peripheral vascular resistance (TPR), increases in Systolic/Diastolic pressures, and increased arterial resistance7-Non-steroidal Drugs: Prolonged use of non-steroid anti-inflammatory drugs (NSAIDs) such as Motrin or Aleve (over the counter Ibuprofen), and weight-loss drugs (like Meridia) cause salt (NaCl) and water retention into the blood, increased Sympathetic activity and increased blood pressure due to their effect on the endothelial layer of blood vessel walls. Some birth control/contraceptives use a combination of Progesterone and Estrogen, which increases appetite and increases the absorption of NaCl and fluid, resulting in Edema, high blood pressure, weight gain, and water weight gain.8-Coarctation of Aorta: a birth defect of congenital heart condition in which a portion of the Aortic artery walls are narrowed. >Symptoms: Hypertension, tension in the head and neck, damage or rupture of cerebral arteries can occur, resulting in intracranial hemorrhage, increased pulse in the carotid artery, low pulse in the femoral artery (if the patient has Turner’s Syndrome, an XO chromosomal monosomy) >Treatment: surgical removal of the narrowed portion of the aorta9-Preeclampsia: Hypertension during pregnancy due to malformed or dysfunctional endothelial layer in maternal blood vessels (those developed to supply maternal blood to the placenta and developing fetus). Changes in maternal hormone levels during pregnancy can cause this, resulting in damaged blood vessels and increased blood pressure which may be life-threatening to the mother and child.10-Thyroid and Parathyroid conditions: increased secretions of T3-T4 can result in increased sensitivity of Sympathetic receptors α1 & β1 to Norepinephrine. Overstimulation of these receptors, especially α1, causes Hypertension. >Symptoms: severe headaches, vomiting, nausea, sleep disorders, nose bleeds, problems with vision, anxiety, vertigo, weakness and fatigue, heart palpitations, increased heart rate and contractility in the myocardium-More general symptoms of Hypertension: may be asymptomatic (no symptoms), headache, fatigue, vertigo/dizziness, shortness of breath or difficulty catching breath after mild activity, convulsions, blurry vision or seeing double, nausea and vomiting, anxiety and sweating, nose bleeds, tinnitus, heart palpitations, malaise, frequent urination, red or flushed face, pallid or pale skin except for face.-Common treatments for High Blood Pressure: >Angiotensin-converting enzyme inhibitors (ACE inhibitors): Captopril and Ramipril >Angiotensin II receptor blockers (ARBs): Valsartan >Diuretics: Thiazide based drugs such as Hydrochlorothiazide >Calcium channel blockers: Felodipine or Barnidipine (“Benidipine”) >β1 adrenergic blockers: Propranolol or Atenolol -Arrhythmias: a change from normal sinus rhythm (impulses coming rhythmically from the sinus (SA) node) due to abnormal conduction impulses or impulse disturbances, although these arrhythmias still maintain their own consistent rhythm outside the normal rhythm. Arrythmias can arise from acute environmental factors or from underlying pathological conditions. >Sinus Tachycardia: occurs if the sinus impulse frequency causes the heart rate to rise above 100 beats per minute. Tachycardia is normal if all other ECG patterns are normal and if the rise in heart rate occurs concurrently with a stressor (exercise, stress, fear, illness). Tachycardia is abnormal if the resting heart rate is 100-180. Tachycardia rhythm is regular on an ECG. >Sinus Bradycardia: occurs if the sinus impulse frequency drops the heart rate below 50 to 60 beats per minute. Can occur in athletes, can be caused by hypothyroidism, low blood sugar, or injury to the brainstem. On ECG readouts, the P-waves are normal, and the rhythm is regular.-Supraventricular arrhythmia (Atrial or Nodal Extrasystole): an “atrial arrhythmia” that occurs when ectopic (abnormal) impulses come from the Atria or Atrioventricular Nodal cells (the AV node) and transmit those ectopic impulses to the ventricles to disrupt normal sinus rhythm. Atrial (or Nodal) “Extrasystole” can be thought of as an “extra” systolic impulse being conducted abnormally from ectopic atrial tissue or from the AV node. ECG readouts typically show an abnormal or negative P-wave; if the ectopic impulses are coming from atrial tissue then the QRS should be normal, but if the ectopic impulses are coming from the AV node (Nodal) then the P-wave may be merged with the QRS or appear after the QRS. The ECG rhythm is irregular.-Atrial Tachycardia: heart rate presents within a range of 100-250 bpm. A disruption in normal sinus rhythm as a result of ectopic impulses coming from the Atria rather than the Sinoatrial (SA) node. The atrial rhythm is regular although it diverges from a normal sinus rhythm. On an ECG readout the P-waves occur before every QRS and can appear flat, and irregular, or the P-wave may be lost within the QRS because of the rapid rate of atrial-to-ventricular depolarization. -Ventricular Tachycardia: occurs when multiple successive ventricular ectopic impulses result in a heart rate greater than 120-250 BPM. This can develop from Ventricular Extrasystole and can result in incomplete or “twitchy” chamber contractions, which leads to a decreased amount of blood filling the ventricular chambers, thus decreasing cardiac output. -AV node block (1, 2 & 3 degrees): damage to the Atrioventricular (AV) node can disrupt or “block” Nodal conduction impulses; the severity of impulse disruption results in different degrees of AV node block. >1st degree AV node block: Atrioventricular conduction is partially blocked, a P-wave occurs before each QRS but the PR-interval lasts longer than 0.2 seconds. >2nd degree AV node block: Atrioventricular conduction is inhibited by severe damage to the AV node so that only one out of a few conductive impulses are able to stimulate the ventricles. On an ECG, every other P-wave may present without a QRS complex following it. >3rd degree AV node block: a complete block of Atrioventricular conduction, where none of the impulses coming from the atria are conducted through the AV node, so none of the impulses reach the ventricles, this results in a decreased heart rate characteristic of Bradycardia (50-60 bpm). ECG may have a negative T-wave after intermittent QRS.-Atrial Fibrillations & Atrial Flutter: supraventricular arrhythmias characterized by abnormal and rapid atrial waves that are out of rhythm with ventricular waves. >Atrial Fibrillation: contractions in atrial and ventricular chambers are irregular, though atrial chambers contract more rapidly than the ventricles, resulting in a rapid heartbeat that is out of sync. Because of the rapid contractions, the chambers do not pump out an adequate stroke volume, which can result in blood pooling and possibly clotting within the chambers. >Atrial Flutter: regular but increased rate of atrial contractions that occur more quickly than ventricular contractions, which results in a rapid but regular heart rate. -Myocardial Infarction: occurs when blood flow to the myocardial tissue is compromised (typically due to atherosclerosis), resulting in a lack of oxygen being supplied to the cells, causing tissue damage (or death) and a decreased capacity for cells to generate ATP in order to fuel sufficiently regular and strong myocardial muscle contractions. Decreased contractility of the myocardium then results in a decreased or absent stroke volume released as cardiac output. Common risk factors for myocardial infarction include atherosclerosis, chronically high stress, diabetes, coronary artery disease, high blood pressure, alcoholism, smoking, hypercholesterolemia, hypercalcemia, and kidney disease. >Symptoms: retrosternal pain lasting longer than 20 minutes, with radiating pain up to the left shoulder, down the left arm to the left ring and pinky finger, radiating pain in the submandibular region, a feeling of “impending doom”, a feeling of intense squeezing pressure in the chest, indigestion, anxiety and palpitations, Dyspnea (trouble breathing), vertigo, nausea, and sweating. >Diagnostics: check patient and/or family history for records of similar episodes of chest pain or infarctions, ECG readout should show an elevated or depressed ST-segment as an indicator of infarction as well as an elevated positive R-wave, and wider negative Q-waves. Post myocardial-infarction the ECG should be monitored to ensure the readout returns to normal and stays normal within a couple days or else the patient is at risk for an additional infarction. Blood tests can be drawn to test for elevated levels of lactic acid and lactate dehydrogenase enzyme, which indicates cellular anaerobic respiration (which is the result of a lack of oxygenation to the myocardial tissue). Blood tests may also reveal increased levels of Troponin-I (which inhibits Actin & Myosin binding), increased levels of Troponin-T (binds Actin to Tropomyosin, inhibiting Actin & Myosin binding), and increased levels of Myoglobin (a protein similar to Hemoglobin that binds oxygen tightly and acts as back-up storage in muscle cells to store and release oxygen when cells are deoxygenated). -Endocarditis: the inflammation of the endocardium, typically as a result of post-surgical bacterial infection but can also develop due to a congenital heart disease (such as atrial septal defect or patent ductus arteriosus), auto-immune condition, valve replacement surgery, or prior rheumatic heart disease (damage to valves as a result of rheumatic fever). Bacterial endocarditis comes with the risk of developing clots of infected blood that can break off and spread the infection to other organs. ................
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