HOSA Circulatory Diseases and Conditions

Circulatory System

Primary function to circulate blood to organs/tissues of body; heart at center of it all, pumping 5 quarts of blood per minute in adult in cardiac cycle; comprised of networks of vessels (arteries, veins, capillaries)

Cardiac Cycle

Consists of two side-by-side pumps, each divided into two chambers; upper chambers are atria, lower chambers are ventricles; venous blood enters heart from body, enters RA, passes tricuspid valve, w/ atrial contraction enters RV; blood pumped thru pulmonary valve, w/ ventricular contraction, into pulmonary arteries into lungs; in lungs, CO2 removed and O2 added into blood; freshly oxygenated blood returns into heart via pulmonary veins, entering LA, moving through mitral (bicuspid) valve w/ atrial contraction, entering LV; as LV contracts, blood is forced through aortic valve into aorta and rest of body

Cardiac Cycle Steps

(1) Diastole, atria fill, all valves close (2) Diastole, inc atrial P, opens AV valve, ventricles fill (3) Systole Begins, Atria contract and empty, ventricles are full (4) Systole, Ventricles begin contraction, P closes AV valves, Atria relaxes (5) Systole, Ventricles contract, inv P in ventricles, aortic/pulmonary valves open, blood ejected into aorta and pulmonary artery (6) Ventricles empty, ventricles relax, aortic pulmonary valves close

Heart Valves

Prevents blood from flowing backwards

Pericardium

Double-layered enclosing heart, composed of inner serous layer (visceral pericardium or epicardium) and outer fibrous layer (parietal pericardium); between layers is pericardial cavity, a small amount of serous fluid reducing friction during cardiac movements

Tachycardia

Heartbeat is abnormally fast

Bradycardia

Heartbeat is abnormally slow

Arrhythmias

Disorders of cardiac rhythm, dysrhythmias

Palpitations

Rapid fluttering of the heart

Syncope

Fainting

Coronary Artery Disease (CAD)

 arteries supplying myocardium (heart muscle) become narrowed by atherosclerotic deposits over time, causing temporary cardiac ischemia, eventually MI (heart attack); OG asymptomatic, w/ first symptoms pain of angina pectoris; when advanced, MI described as burning, squeezing, crushing, radiating to arm, neck, or jaw; Nausea, vomiting, weakness, changes in ECG often; can be sudden death event; sudden chest pain is medical emergency; plaque in lumen (opening) of coronary arteries results in atherosclerosis and subsequent narrowing of lumen of arteries; myocardium needs adequate blood to function, w/o blood becomes constricted by atherosclerosis; arteriosclerosis associated w/ elderly, diabetics; arteries lose elasticity, become hard, narrow, resulting in cardiac ischemia, where cells in myocardium weaken and die; replacement scar tissue forms hindering heart ability to pump, causing heart failure; genetic predisposition, those older than 40, more men, postmenopausal women, history of smoking, residence in urban society, hypertension, diabetes, obesity risk factors; elevated cholesterol or HDL levels, lack of exercise, stress can induce; often no chest pain until 75% of coronary arteries occluded; collateral circulation often develops to supply tissue w/ needed O2, nutrients; ECG shows ischemia, arrhythmias; treadmill testing, thallium, cardiolite scan, CT, stress echocardiograms, cardiac catheterization, angiograms grounds diagnosis; Vasodilators, other meds prescribed; angioplasty w/ balloon or stenting attempted to open constricted arteries; reduction of plaque buildup w/ hypolipidemic drugs work sometimes; beta-blockers, anticoagulants prevent blood clots and breaking off and lodging of cerebral arteries; if blockage severe or drugs don’t work, coronary artery bypass surgery may be req; experimental gene therapy w/ injections of DNA directly into cardiac muscle to stimulate growth being tried; prognosis varies w/ response to treatment and Y/N smoking; diet low in salt, fat, cholesterol, exercise, low stress, no smoking prevents

Angina Pectoris

Chest pain after exertion, result of low O2 supply to myocardium; sudden onset of left sided chest pain after exertion, can radiate to left arm or back; dyspnea; pain relieved by ceasing strenuous activity and placing nitroglycerin tablets or spray sublingually (under tongue); BP can inc during attack, arrhythmias; 1st time req immediate assessment, could be life-threatening; if already diagnosed and cessation of activity/vasodilating meds no relief within 20 min, medical emergency; atherosclerosis narrows coronary arteries, compromises blood flow to myocardium, causing no O2 for exertion as vessels cannot supply it; spasms of coronary arteries can cause; severe prolonged tachycardia, anemias, respiratory disease can cause ischemia; ECG during anginal episodes shows ischemia; many diagnosis tests for CAD also performed; cessation of strenuous activity, placing nitroglycerin under tongue helps; prognosis varies w/ extent of arterial involvement, often disappearing after stopping activity and taking meds; lifestyle modifications, diet of low fat, cholesterol, salt can prevent

Myocardial infarction (Heart Attack)

Death of myocardial tissue from ischemia; occlusion of coronary artery leads to ischemia and infarct (death) of myocardium causing sudden, severe substernal and left-sided chest pain that is crushing, feeling of massive constriction of chest, sometimes burning, could be mild discomfort; pain radiates btwn left/right arms, back, jaw, not relieved by rest or nitroglycerin; irregular heartbeat, dyspnea, diaphoresis, usually w/ denial and anxiety; esp in diabetics; early intervention improves survival and avoids irreversible damage; calling 911 for entrance, chewing a 5 grain/325 mg aspirin tablet, w/ emergency intervention immediately; primary ventricular fibrillation contributes to most deaths caused by MI; results from insufficient O2 supply; pain is from ischemia, and if unreversed in six hours, cardiac muscle dies; coronary thrombosis most common cause ; History, ECG, chest radiographs, lab tests for cardiac enzyme levels; changes in enzyme levels indicate death of cardiac tissue; enzymes CPK, troponin, lactic dehydrogenase (LDH), aspartate aminotransferase (AST); ECG changes in PR, QRS complexes in ST segment corresponds to ischemic areas; O2 administered, morphine for pain, aspirin ASAP to reduce risk of additional damage, vasodilation attempted by nitroglycerin drip; lidocaine or amiodarone by intravenous drip after loading bolus for arrhythmias; thrombolytic drugs (TPA, streptokinase, Activase) administered ASAP w/ diagnosis unless contraindications; attempt to open occlusion and restore blood flow w/ angioplasty done in 6-hour window before permanent damage, a coronary bypass surgery; current standard care is attempt to open artery w/ stent 60-90 minutes after arrival, being more effective than thrombolytic drugs; oftentimes, 65% of deaths within first hour; prognosis determined by immediate defibrillation for ventricular fibrillation; late mortality depends on extent to damage to heart muscle and complications, w/ late cardiac death sudden by fatal arrhythmia; lifestyle mods, w/ appropriate exercise, diet low in fat, cholesterol, salt, control of hypertension, weight loss, and smoking cessation can prevent

Cardiac Arrest

Sudden, unexpected cessation of cardiac activity; patient unresponsive, no respiratory effort, no palpable pulse; true life-threatening emergency; immediate CPR and defibrillation may restore heart contractions; due to anoxia (no O2 to tissue), or interruption of E stimuli to heart; respiratory arrest, arrhythmia, MI, electrocution, drowning, severe trauma, massive hemorrhage, drug overdose can cause; ECG shows ventricular fibrillation or asystole; CPR within 4-6 min req, defibrillation attempted by trained life-support personnel; epinephrine, isoproterenol, dobutamine drugs to stimulate heart; antiarrhythmic drugs (lidocaine, amiodarone) can be administered; prognosis varies w/ duration of cardiac arrest, how early CPR is, how long respiratory efforts cease; at 10 min of cardiac arrest, full brain death inevitable; complete intervention req for successful resuscitation; health, age can affect; lifestyle mods can reduce risk

Therapeutic Hypothermia

Patients w/ cardiac arrest, CPR, sometimes report falling into lakes/cold climates resuscitating them; studies show this can improve neurologic outcome and dec mortality; cooling to 90 F, 32/33C, immediately following cardiac arrest, by cooling blankets, ice to cardiopulmonary bypass, can be uncomfortable due to shivering; patients must be heavily sedated and placed on mechanical ventilation; done for 18-24 hours, afterward rewarming process; rapid rewarming can be disastrous, must be done slowly, using arctic sun, int devices (innercool catheter)

Essential Hypertension

Abnormally high BP in arterial system, insidious onset, w/ few symptoms until permanent damage; headaches, epistaxis, lightheadedness, syncope, but often no symptoms; detected during BP tests in phys exam; if accompanied by hyperlipidemia, leads to atherosclerosis; Unknown etiology, but stress, age, heredity, smoking, obesity, sedentary lifestyle, poor diet, hyperactive personality or type A personality causative factors; systolic >140 mmHg, diastolic >90 mm Hg indicates; systolic 120-140 mm hG borderline hypertension; diuretics to reduce circulating blood volume, beta-adrenergic blocked to slow heartbeat dilate vessels, vasodilators, Ca channel blocked to slow heartbeat, reduce conduction irritability, dilate vessels, ACE inhibitors to vasodilate and inc renal blood flow, ARBs; drugs can be prescribed singly/combo; drug fit to patient; limiting Na intake, diet management, weight reduction, exercise, reducing stress, no smoking can help; prognosis varies w/ response to drugs, lifestyle; no prevention, but lowering risk factors can help

Malignant Hypertension

Life-threatening, severe form of hypertension; severe headache, blurred vision, dyspnea suggests onset; many unaware, found in elevated BP reading at physical; req prompt assessment and intervention to avoid risk of cerebral vascular accident; etiology unknown, but extreme stress contributes; systole >200 mm Hg, diastole > 120 mm Hg; aggressive intervention of intravenous vasodilators (Hyperstat), sodium nitroprusside administered; BP must be monitored an drug therapy for rest of life; prognosis varies w/ response to therapy, due to risk of CVA, stroke, irreversible renal damage; if drug therapy unsuccessful, death likely; prevention unknown, dec risk factors best

Congestive Heart Failure (CHF)

acute/chronic inability for heart to pump enough blood throughout body for homeostasis; insidious onset w/ gradually inc dyspnea; cardiac, respiratory rates inc, patient becomes anxious; w/ progression veins distant, edema in ankles; if right heart fails, liver/spleen enlarge, peripheral edema prominent; if left fails, pulmonary congestion, pronounced respiratory difficulty; key symptoms req prompt med assessment; underlying condition and compromise heart, commonly MI, hypertension, CAD, COPD, cardiac valve damage, arrhythmias, cardiomyopathy; history phys exam, diminished breath sounds, radiographs shows fluid in lungs grounds diagnosis; ECG discovers underlying cause, evaluating cardiac chamber size, ventricular function, disease of myocardium/valves/cardiac structures/pericardium, catheterization to monitor pressures of circulation; digitalis preps to strengthen and slow heartbeat, beta-blockers and ACE inhibitors to treat CHF by inc blood flow, diuretics to reduce volume of fluid, vasodilators to reduce vascular P, restricted fluid/Na intake, sometimes pacemakers, defibrillators, or heart transplant; prognosis varies, w/ acute responding well to meds, chronic vulnerable to major organ impairment; controlling BP esp in men, early med intervention best to prevent

Cor Pulmonale

Right-sided heart disease, w/ enlargement of right ventricle as sequela to primary lung disease; dyspnea, distended neck veins, edema of extremities, enlarged tender liver; chest discomfort, shortness of breath, limb swelling req prompt med assessment; from acute/chronic pulmonary disease and pulmonary hypertension; diseased pulmonary blood vessels impair flow of blood to pulmonary tissue, inc pulmonary BP and workload of right side of heart, causing right ventricle hypertrophy and less effective pumping; chronic conditions cause include emphysema, fibrotic pulmonary lesions; primary acute causative factor is pulmonary emboli; chronic hypoxemia stimulates bone marrow in adaptive response to prod inc RBC to carry more O2, leading to polycythemia, inc blood viscosity; diagnosis based on history of hypoxia and pulmonary disease; radiographs of chest, echocardiography reveal pulmonary congestion, right-sided heart enlargement, ECG shows freq arrhythmias; bronchodilators, supplemental O2, bed rest, digitalis preps to strengthen, slow heartbeat, diuretics for edema if present, anticoagulants to avoid thromboembolisms, phlebotomy if polycythemia problematic, low-salt diet encouraged; prognosis varies w/ response to treatment; prevention not known

Pulmonary Edema

Fluid shift into extravascular spaces of lungs; dyspnea, coughing, orthopnea, inc cardiac/respiratory rates, bloody frothy sputum; BP may fall, skin becomes cold, clammy, symptoms often at night after laying down; shortness of breath, esp when lying down, should seek emergency care; caused by left-sided heart failure, mitral valve disease, pulmonary embolus, systemic hypertension, arrhythmias, renal failure; head trauma, drug overdose, exposure to high altitudes can cause; pulmonary circulation is overloaded w/ excessive volume of blood; diminished breath sounds w/ presence of rales, rhonchi, wheezing, arterial blood gas shows low O2 saturation inc CO2 retention of bicarb dec pH of blood, chest radiographs shows inc opacity of pulmonary tissue, enlarged heart, prominent pulmonary vessels; patient placed in Fowler’s position (sitting), O2 therapy, diuretics for fluid excretion, intravenous vasodilators (nitroglycerine, nitroprusside), morphine sulfate to induce venous dilation, B2-adrenergic drugs to dilate bronchioles and control bronchial spasms; severe cases req mechanical ventilation; is a life-threatening med emergency, prognosis varies w/ severity and response to treatment; avoidance of risk factors, viz drug overdose, prevents

Cardiomyopathy

Noninfla disease of cardiac muscle which enlargens myocardium, ventricular dysfunction; symptoms of CHF, dyspnea, fatigue, tachycardia, palpitations, chest pain; peripheral edema, hepatic congestion sometimes present; syncope, cardiac murmurs sometimes, w/ symptoms and signs vary w/ type/cause; symptoms req prompt med assessment; primary causes unknown; Dilated version from chronic alcoholism, autoimmune process, viral infection, resulting in diffuse degeneration of myocardial fibers followed by dec contractile effort; hypertrophic version thought to be genetic, considered idiopathic; left ventricular wall, ventricular septum hypertrophies causing small elongated LV, obstruction of aortic valve; Restrictive version when infiltrative process of heart causes fibrosis, thickening of myocardium; history, phys exam, chest radiographs show cardiomegaly, ECG shows rhythm abnormalities grounds diagnosis; Dilated treated w/ control of CHF, e.g. antiarrhythmic agents, digitalis, anticoagulants, limited activities w/ some patients restricted to bed rest; Hypertrophic version aimed to reduce workload of heart, e.g. Beta-adrenergic blockers (propranolol hydrochloride) to reduce myocardial contractility, heart rate, conductivity, preventing arrhythmias, Ca channel blockers to reduce BP, relax heart, ACE inhibitors to relax blood vessels, reduce heart’s workload; Restrictive treated same as hypertrophic, but changes caused are irreversible and poorer prognosis; meds improves survival rate, but some conditions are fatal; many times idiopathic, so prevention is nonspecific and based on cause

Pericarditis

Acute/chronic infla of pericardium (serosa); normally, epicardium filled w/ small amount of thin lubricating serous fluid; when blood or infla exudate released into pericardial sac/space, friction, irritation btwn layers results in this; fever, malaise, chest pain fluctuating w/ inspiration/heartbeat; anxious feeling, report of a “pounding heart;” a detectable friction rub/grating sound in phase w/ heartbeat heard on auscultation w/ stethoscope; tachycardia sometimes, can be benign or isolated or from 2ndary infection; idiopathic or consequence of infla or infection elsewhere in body; bacteria, viruses, trauma, rheutamic fever, malignant neoplastic disease cause; can be 2ndary to MI; acute infla of pericardium can cause adhesions to form btwn pericardium/heart causing loss of elasticity, constrictive version; chronic version can incite fibrous calcification of visceral membrane, which come in direct contact w/ myocardium; scarred/rigid pericardium interferes w/ heart contraction, dropping cardiac output; elevated WBC, erythrocyte, ESR, cardiac enzyme levels, ECG changes, echocardiograph shows pericardial fluid and thickened pericardium to ground diagnosis; constrictive version has catheterization show elevated P in cardiac chambers; if infectious cause, antibiotics and possible surgical drainage/aspiration; bed rest, analgesics, antipyretics, NSAIDs, corticosteroids prescribed; acute often resolves completely, chronic adhesions or calcifications may necessitate resection of pericardium

Myocarditis

Infla of muscular walls of heart; damage to myocardium by pathogenic invasion or toxic insult; acute/chronic, small/diffuse, any age; palpitations, fatigue, dyspnea, fever, arrhythmia, tenderness to chest; freq a viral, bacterial, fungal, protozoal infection or complication of influenza, diphtheria, mumps, rheumatic fever; occasionally idiopathic; associated w/ MI; Li, cocaine, chronic alcoholism, radiation, chem poisoning can cause; can be complication of collagen disease; elevated WBC, ESR, cardiac enzyme levels; ventricular enlargement on chest radiographs, myocardial biopsy confirms diagnosis; if infection is cause, antiinfective agents given, rest, reduce heart workload; quinidine, procainamide to stabilize arrhythmia; analgesics, antiinfla agents, O2 prescribed; prognosis for full recovery favorable unless chronic and damages cardiac muscle; prevention not possible based on underlying cause, but early antimicrobial agents can

Endocarditis

Infla of lining of valves of heart; often 2ndary to infection elsewhere in body, results of preexisting heart disease, or consequence of abnormal immunologic reaction; vague symptoms of infection, fever, chills, night sweats, weakness, anorexia, fatigue; charact by vegetative growths on cardiac valves which may be released into bloodstream as emboli, lodging into vessels, inducing ischemia in heart, lungs, brain, extremities; dysfunction of valves not closing disrupts/obstructs blood flow thru chambers, prod cardiac murmur heard on auscultation; bacteremia, presence of infectious agents in bloodstream, can cause, commonly S. aureus, group A beta-hemolytic streptococci, E. coli; intravenous drug users at high risk for fungal version; septic emboli carried by arterial circulation can result in infarcts and new places for bacterial infection; urinary tract infection, skin infection, dental infection can cause; complete blood count shows leukocytosis, elevated ESR; blood cultures show causative organism; echocardiograph shows valve involvement w/ vegetation or abscesses; ECG shows arrhythmia and conduction defects, grounds diagnosis; causative organism dictates antiinfective therapy, often intravenous antibiotics, for several weeks; antipyretics, anticoagulants, drugs for complications; bed rest in acute phase, damage to cardiac valves may need surgical repair; early diagnosis w/ antibiotics often yields full recovery

Rheumatic Fever

Systemic infla and autoimmune disease involving joints, cardiac tissue; follows a sore throat from group A beta-hemolytic streptococcus; often children, experiences fever, polyarthritis, joint pain, edema, redness, limited ROM; joints (finger, knee, ankle) w/ infla transient; carditis, cardiac murmurs, cardiomegaly, CHF, weakness, malaise, anorexia, weight loss, rash on trunk, ab pain, small nodules on tendon sheaths; often 1-5 weeks after upper respiratory tract infection; antibodies after sore throat cross-react w/ normal tissue, causing antibody to attack body’s own cells; antibodies migrate to endocardium where mitral/aortic valves see vegetations form on tissue; history of upper tract infections in preceding weeks suggests, presence of carditis, polyarthritis adds to diagnosis; streptococcal antibody level, antistreptolysin O titer, elevated in tests; inc cardiac enzyme levels, WBC count, ESR aid; antibiotics to prevent onset of fever, penicillin req to eradicate infection; antipyretics for fever, antiinfla agents for relief of arthritic symptoms; bed rest; prognosis good w/ treatment; antibiotics for strep throat prevents

Rheumatic Heart Disease

Cardiac manifestations following rheumatic fever; acute endocarditis leads to chronic cardiac involvement, valvular damage due to vegetations causing stenosis of valves, viz. mitral/aortic; congestive heart failure leads to dyspnea, tachycardia, edema, nonproductive cough, cardiac murmurs; after rheumatic fever, vegetations enlarge, valves may scar, causing stenosis of opening; diagnosis based on history of rheumatic fever, cardiac murmurs, echocardiogram shows vegetations; surgery to relieve stenosis or replace valves, good dental hygiene important for no gingival infection, prophylactic antibodies before dental procedures; prognosis varies w/ extent of damage, recurrences likely; prevention is prophylactic administration of antibiotics for strep throat

Valvular Heart Disease

acquired/congenital disorder of any of four valves, from insufficiency or stenosis; insufficiency, where valves fail to close properly, allows blood back into previous chambers during contraction; stenosis, hardening of cusps preventing complete opening, causes blood flow into next chambed impeded; mitral valve most often; diagnosis req ECG, radiograph chest, echocardiogram, catheterization, digitalis/quinidine treatments for arrhythmias, antibiotic prophylaxis

Mitral Stenosis

Blood from LA to LV impeded; mitral/bicuspid valve affected; dyspnea, fatigue, sometimes cough, palpitation w/ hemoptysis, cyanotic look; rheumatic heart disease most common cause, group A beta-hemolytic streptococcus stimulates antibody prod which attacks body tissue in autoimmune response; often insidious, acute onset; cardiac murmur heard (diastolic), echocardiogram confirms diagnosis; limiting Na intake, diuretics, low workload on heart, anticoagulants for no thrombi; if atrial fibrillation from stenosis, digoxin to slow rapid heart rate; surgery as commissurotomy to free valve for blood flow possibly, or balloon valvuloplasty nonsurgically; valve replacement last resort; prognosis improves w/ treatment, prevention of rheumatic fever key

Mitral Insufficiency

Blood from LV flows back to LA; dyspnea, fatigue, heart murmur as blood leaks back; difficulty breathing warrants screening; scar tissue from infla/vegetations, rheumatic fever, mitral valve prolapse, CAD, MI, cardiac dilation causes; patient history of sore throat, rheumatic fever, pys exam for murmur, echocardiogram grounds diagnosis; bed rest, O2 therapy, antibiotics for infection; if severe, surgery or replacement of valve may be req; prognosis generally good, but can lead to CHF; preventing rheumatic fever, or scarring of mitral valve helps prevent

Mitral Valve Prolapse

Often benign, where 1+ cusps of mitral protrudes back into LA during ventricular contraction; cusps do not close completely; oftentimes asymptomatic, found during routine exam; chest pain, dyspnea, dizziness, fatigue, syncope, anxiety, all ages; abnormally long/short chordae tendineae can be cause; malfunctioning papillary muscles inc severity; regurgitation of blood during LV systole resulting in rushing, gurgling cardiac murmur is charact; typical click-murmur syndrome heard on auscultation, echocardiogram confirms failure valve closure; premature ventricular contractions  detected on ECG are not harmful; treatment not req if no symptoms; discomfort/anxiety treated w/ beta-blockers, advised to avoid caffeine, smoking, large heavy meals; prognosis good, prevention unknown

Arrhythmias

Deviation from normal heartbeat; occurs w/ interference w/ conduction system of heart; palpitations, tachycardia, skipped heartbeats, bradycardia, syncope, fatigue; pacemaker (sinoatrial SA node), atrioventricular (AV) node, bundle branches, Purkinje fibers defects; ischemia, drugs can cause; failure of SA node responsible; heart block occurs when impulses from SA node are slow or irregular or below AV node; diagnosis made from 12-lead ECG; treatment varies w/ cause; drug-induced resolve w/ cessation of drug; anticoagulants (Coumadin) prevent thromboembolism; ischemia cause responds to O2 therapy and inc blood flow to tissues; if not too unstable/serious, cardioversion w/ electric shock to heart can restore, resetting heart rhythm and discontinuing antiarrhythmic meds; sometimes fatal; sometimes treated w/ ablation tech w/ catheters; if bradycardic, pacemaker to maintain rate > 60 bpm req; implantable cardioverter defibrillators possible for tachycardic heart rates; prognosis varies depending on type of arrhythmia (listed below from normal sinus to ventricular fibrillation); preventing drug-induced and avoiding known causes can prevent

Normal Sinus Rhythms

60-100 bpm, regular, P wave uniform; impulse originated in SA node, conduction normal; normal diagnosis, no treatment needed

Sinus Tachycardia

Rate > 100 bpm; regular, P wave uniform; rapid impulse in SA node, conduction normal; diagnosis rapid rate; Beta blockers, Ca channel blockers, possible ICD treats

Sinus Bradycardia

Rate < 60 bpm, regular, P wave uniform; slow impulses from SA node, conduction normal; Slow diagnosis; Atropine treats

Premature Atrial Contraction

Rate depends on underlying rhythm; usually normal P wave, diff morphology from other P waves; irritable atrium, single ectopic beat arising prematurely, conduction through ventricle normal; irregular heartbeat from ECG grounds diagnosis; treatment often unnecessary, antiarrhythmic drugs Rx

Atrial Tachycardia

150-250 bpm, normal rhythm, sudden onset; irritable atrium, firing at rapid rates, normal conduction; rapid rate w/ atrial/ventricular rates identical diagnosed by ECG; reflex vagal stimulation, Ca channel-blocking drugs (verapamil), cardioversion; may be ICD candidate

Atrial Fibrillation

Atrial Rate >350 bpm, ventricular rate <100 bpm (controlled) or > 100 bpm (rapid ventricular response) Atrial ectopic foci discharging too rapid and chaotic rate for muscles to respond and contract, causing quivering of atrium; AV node blocks some impulses and ventricle responds irregularly; ECG shows no P waves, grossly irregular ventricular rates; IV verapamil, if unsuccessful procainamide, if unsuccessful cardioversion; may be ICD candidate

1st-Degree Heart Block

Rate depends on rate of underlying rhythm; PR interval > 0.20 seconds; Delay at AV node, impulse eventually conducted; ECG shows PR interval > 0.2 seconds; Atropine, if unsuccessful, artificial pacemaker insertion req

2nd Degree Heart Block

= Wenckbach Heart Block; Intermittent block w/ progressively longer delay in conduction until one beat is blocked; atrial rate normal, ventricular rate slower than normal, irregular rhythm; SA node initiates impulse, conduction thru AV node blocked intermittently; ECG shows normal P waves, some P waves not followed by QRS complex; PR interval progressively longer, followed by block of impulse; mild forms, no treatment; severe forms req artificial pacemaker

Classic 2nd-Degree Heart Block

Ventricular rate slow (½, ⅓, ¼ of atrial rate) rhythms; regular P waves, QRS complex dropped every second, third, fourth beat; SA node initiates impulse, conduction through AV node blocked; ECG shows P waves present, QRS complex blocked every second, third, fourth impulse; req artificial pacemaker

3rd-Degree Heart Block

Atrial rate normal, ventricular rate 20-40, 40-60 bpm; no relationship btwn P wave and QRS complex; SA node initiates impulse, which is completely blocked from conduction, causing atria and ventricles to beat independently; ECG shows P waves, QRS complexes w/ no relationship to each other, rhythms regular but independent; req artificial pacemaker

Premature Ventricular Contraction (Single Focus)

Single ectopic beat, arising from ventricle, followed by compensatory pause; ectopic beat originates in irritable ventricle; ECG shows bizarre QRS complex > 0.12 second usually followed by compensatory pause; often no treatment if < 6/minute and single focus; candidate for ICD

Multifocal Arrhythmia

Coupling, two in a row (bigeminy), every other beat, (trigeminy) every third beat, (quadrigeminy) every fourth beat; rate depends on underlying rhythm; rhythm (ir)regular; P wave absent before ectopic beat; same as single focus etiology, diagnosis, treatment; candidate for ICD

Ventricular Tachycardia

Rate of 150-250 bpm, rhythm often regular; focus on pacemaker normally single, patient experiencing palpitations, dyspnea, anxiety following chest pain; 4+ consecutive PVC’s at rapid rate due to advanced irritability of myocardium, indicating ventricular common of heart rate; ECG shows runs of 4+ PVCs, P wave buried in QRS complex; Often forerunner of ventricular fibrillation; immediate intervention necessary, IV lidocaine, if unsuccessful, cardioversion, procainamide, bretylium may be used; candidate for ICD

Ventricular Fibrillation

Lethal Arrhythmia; patient loses consciousness right after onset; no peripheral pulses palpable, no heart sounds, no BP; Ventricular fibers twitch rather than contract, reason unknown; pulseless, unconscious patient, ECG shows rapid repetitive chaotic waves from ventricle to ground diagnosis; recognizing terminate rhythm, precordial shock (defibrillation); survivors candidates for ICD

Shock

Collapse of cardiovascular system, including vasodilation, fluid shift w/ inefficient cardiac output; causes inadequate perfusion of organs/tissues; pale, cold, clammy skin; weak thready pulse, rapid breathing, altered level of consciousness, tachypnea; BP drops, patient anxious irritable restless, feeling of impending doom; dizziness, extreme thirst, profuse sweating; late stages see pupil dilation, eyes dull and lusterless, shaking, trembling; life-threatening, req emergency med assistance; caused by anaphylaxis, hemorrhage, sepsis, respiratory distress, heart failure, neurologic failure, emotional catastrophe, severe metabolic insult; regardless of cause, amount of blood effectively circulating reduced, causing vital organs not enough O2/nutrients to support life; failure of heart to pump can cause, vascular collapse w/ massive dilation, constriction of vessels, insufficient O2 can cause; history of precipitating events grounds diagnosis; altered level of consciousness, respiratory distress suggests shock; aggressive intervention w/  ABCs (airway, breathing, circulation) of emergency care done; establishing ventilation for O2 to vital organs, control of visible bleeding, surgery to halt int bleeding; patient should be in supine position, feet/legs elevated, kept warm, not overheated; vital signs monitored, volume replacement w/ IV fluids, use supplemental O2 if available; intervention improves prognosis, but if untreated, can result in irreversible damage; most onset not preventable, but immediate intervention req

Cardiogenic Shock

Inadequate output of blood by heart; Myocardium fails to pump effectively, many previous symptoms of shock; often preceded by MI, severe heart failure, arrhythmias, acute valve failure; life-threatening condition; any insult disturbing heart’s ability to pump blood can cause; valve failure e.g.; clinical picture, history can lead to suspicion; ECG, radiograph of chest showing hypotensive state indicates diagnosis; treatment is general measures for shock, including meds to inc efficiency of myocardium, blood vessels; blood supply to vital organs improved, O2 demands of myocardial tissue must be reduced; blood volume assessment determines what drugs to dilate/constrict cardiac vessels; sometimes intraaortic balloon pump may be inserted; prognosis varies, often unfavorable; prevention unlikely in most cases, but can avoid being fatal w/ immediate intervention

Cardiac Tamponade

Compression of heart muscles, restriction of heart movement by blood/fluid trapped in pericardial sac; when coronary, epicardial, or pericardial vessel breaks and blood is trapped in pericardial sac; myocardium may rupture, sending blood into pericardial sac; blood constricts the heart restricting movement, less blood can enter heart chambers per beat; sudden severe dyspnea, rapidly falling BP, weak pulse, patient is in shock, becomes cyanotic above nipple line, level of consciousness falls; life-threatening emergency; may result from insult to integrity of vessel in pericardium, allowing blood to fill in pericardial space; P of blood causes heart to beat inappropriately, leading to cardiac arrest; may occur in patients w/ certain cancers, chronic kidney failure, other med conditions e.g. hypothyroidism, lupus; diagnosis based on clinical picture and history of trauma; heart sounds muffled/distant, but breath sounds normal; treatment of insertion of needle into pericardial space and withdrawing offending blood, surgery usually to repair leak done; prognosis varies and depends on causative factor, success of intervention, and health status of patient; often positive w/ surgery; prevention not possible

Blood Vessel Anatomy

Composed of three layers, besides one-cell walled capillaries; tunica intima, tunica media, tunica externa; lining of vessel lumen (tunica intima) is smooth, thin endothelium allowing min friction w/ blood; middle portion (tunic media) composed of smooth muscle, elastic tissue, under control of sympathetic NS, allowing constriction/dilation of vessel walls, changing B; connective tissue makes up tunica externa for support, protection; arterial walls thicker than venous walls, tunica media heavier in arteries to compensate heavier BP; veins have valves to prevent backflow and assist blood return to the heart

Emboli

Clots of aggravated material, often blood, lodging in vessel inhibiting flow; symptoms vary w/ location, magnitude of area of tissue affected; severe pain in area; if lodged in extremities, are becomes pale, numb, cold to touch; if large artery, nausea, vomiting, fainting, eventually shock; if symptoms w/ extreme pain, req immediate entrance to ER; often blood clots, but also air bubbles, fat globules, bacterial clumps, pieces of tissue (placenta); often venous thrombosis in legs from venous stasis; portions of thrombus can break from clot, traveling until it lodges in a smaller vessels; arrhythmias can cause formation in heart in coronary arteries; clinical picture, history of any condition putting P on or dec flow of veins, pain in calf/leg can ground; treatment depends on area; if pulmonary embolism, MI, CVA, aggressive treatment for survival; if arterial embolus, to prevent death of tissue/gangrene aggressive treatment; blood flow reestablished by lowering limb, wrapping, heating area, treating constriction of vessels; Heparin, Lovenox to deter clot formation, antispasmodic drugs for vascular spasms; if therapy no work, surgery to remove obstruction; urokinase can be administered w/ catheter to spot; prognosis varies w/ location and treatment; reduced phys activity req to prevent

Arteriosclerosis

Hardening of arteries; three forms (1) atherosclerosis (2) Monckeberg’s (3) arteriolosclerosis

Atherosclerosis

Plaques of fatty deposits form within tunica intima; Responsible for most MI, cerebral infarction; often asymptomatic, w/ first symptoms angina pectoris, dizziness, elevated BP, shortness of breath; etiology complicated, but risk factors of heredity, sedentary life, diet rich w/ lipids, cholesterol-producing foods, smoking, diabetes mellitus, hypertension, obesity; lipids and cholesterol in blood form thick, stiff, lesions in medium size to large arteries; lesions spread and expand to occlude artery, forming fatty streaks on wall migrating to tunica intima; plaque forms and thickens arterial wall; sequela ulceration in plaque can aggravate thrombosis; ischemia from reduced blood can cause pain; infarct when advanced occlusion; routine phys exam grounds diagnosis, as blood shows elevated cholesterol, triglyceride, lipid levels; Doppler studies show reduced blood flow to major vessels; dietary changes to avoid saturated fats, cholesterol, lipids, no smoking, hypertension, diabetes mellitus controlled; Hyperlipidemic drugs (Mevacor, Zocor), niacin, Advicor and Zetia to stop cholesterol absorption by intestine; prognosis varies based on compliance w/ drugs, exercise, diet changes; prevention important by altering life

Monckeberg’s

Arteriosclerosis caused by medical calcific sclerosis, involving arterial tunica media, destruction of muscle, elastic fibers w/ Ca deposits there

Arteriolosclerosis

Walls of arterioles thicken, losing elasticity, contractility

Aneurysms

Weakening and resulting local dilation of wall of artery; either insidious or sudden acute onset; symptoms vary w/ size and extent of dilation; abdominal aortic aneurysm most common form; asymptomatic aneurysm of aorta often found in routine phys exam w/ abdomen palpated or from radiographs; as aneurysm enlarges, ab/back pain, pulsating mass in abdomen; complication of leakage in artery wall or sudden rupture of weak area causing hemorrhagic shock; rupture of cerebral aneurysm mimics CVA w/ unilateral neurologic deficits noted; if rupture, med emergency; buildup of atherosclerotic plaque to weaken vessel primary cause; trauma, infection, infla, congenital causative factors; Aortic ass noted in midabdomen w/ pulsating observed; bruit heard on auscultation another sign; cerebral aneurysms found during rupture w/ catastrophic consequences; radiographs, ultrasonography, CT, MRI all help confirm diagnosis; treatment varies w/ size, location, likelihood of rupture of defect; aortic treated w/ surgical repair; catheter based stent grafts alternative to surgery; if aorta wall breached, immediate surgery req; prognosis varies w/ location; surgery makes prognosis better before rupture; speed of intervention affects prognosis; prevention unlikely

Phlebitis

Infla of vein, often lower leg, including cranial veins; pain, tenderness of affected area more severe w/ progression; swelling, redness, warmth noted, w/ tender cordlike mass under skin; deep venous infla affects tunica intima, allowing formation of clots; req prompt assessment; cause uncertain, possibly no reason; venous stasis, obesity, blood disorders, injury, surgery possible causes; clinical picture and history ground diagnosis; superficial version symptomatic treatment w/ analgesics; no massaging of tender area to not stimulate clot formation; prognosis positive w/ treatment; prevention not possible

Thrombophlebitis

Result of infla of vein forming thrombus on vessel wall; interferes w/ blood flow causing edema; pain, swelling, heaviness, warmth of affected area w/ chills, fever, tender to palpation; req prompt assessment; venous stasis, blood disorders causing hypercoagulable state, injury to venous wall w/ important roles causes; deep venous infla of phlebitis affects tunica intima, allowing clot formation; clinical picture off gross edema in one leg w/ measurable difference in leg circumference suggests; tender to palpation area, radiographic venography, ultrasonography confirms diagnosis; immediate intervention req, immobilizing to prevent spreading of thrombus and dislodging into embolus; Heparin to prevent clot, antibiotics for information; prompt intervention pos outcome; often resolves w/o further treatment req; if no resolve, surgery needed to ligate affected vessel; collateral circulation develops; preventing formation during periods of immobilization or reduced phys activity essential

Varicose Veins

Swollen, tortuous, knotted veins in lower leg; symptoms develop gradually, w/ feeling of fatigue in legs, cont dull ache; leg cramps at night, swelling ankles; w/ progression, vein thickens and feels hard to touch, pain worsen can can dull or feel stabbing; no clear cause, but defective or absent valves suspected; prolonged standing or sitting puts pressure on valves, gravity pushed blood down, putting inc P on valves; w/o normal contractions, venous walls distend to point at which valves are no longer competent; stasis of blood swells veins; enlarged uterus during pregnancy inc P on leg veins, pelvic veins; presence of twisted, swollen, knotted veins of lower leg on clinical inspection and history of prolonged standing/sitting or pregnancy can make diagnosis; advanced varicosities cause skin of affected area to have brown discoloration; rest throughout day while lying down, elevating feet higher than heart can relieve; exercise, legs in warm water to inc flow of blood, support stockings to encourage return flow of blood; if must stand for long, moving legs a must; painful twisted veins which have progressed beyond other treatments req surgery in vein ligation and stripping/injection of sclerosing solutions that harden and atrophy; collateral circulation develops to augment blood flow to heart; treatment often resolves conditions; wearing support stockings, moving legs can prevent; weight loss can help

Buerger’s Disease

= Thromboangiitis Obliterans; infla of peripheral arteries and veins in extremities w/ clots; intense pain of affected areas, often legs at instep of food, aggravated by exercise relieved by rest; if not resolved and circulation not restored, atrophy, ulcers, gangrene can develop; esp males; long-term smoking/tobacco causes; infla and clots cause vessels to obliterate and compromise circulation; ischemic tissue dies, gangrene follows; most often Jewish; diagnosis follows reports of pain in legs, arteriogram, ultrasonogram can identify site of clot; ulcers of skin can indicate severity; long-term smoking history suggests diagnosis; cessation of smoking, Plavix improves circulation, Buerger-Allen exercises improve circulation where feet and legs elevated 45-90 degrees until they blanch and lower to rest of body reddened; rest in supine position; if these don’t help, surgery req to establish detours or to bore pathway through clot itself; amputation of gangrenous tissue imperative; no cure known, but stopping smoking can relieve; if treatment fails, amputation req; prevention by avoiding smoking

Raynaud’s Disease

Vasospastic condition of fingers, hands, feet, causing pain, numbness, discoloration of areas; bilateral, precipitated by cold, causing blanching (white) discoloration, followed by blue as venous blood remains, and finally red/purple when circulation restored; attacks precipitated by stress; more women; disease = primary, phenomenon = secondary; when severe, digits ulcerate and painful; oftentimes prognosis good; small peripheral arteries, arterioles supplying fingers, hands, feet spasm and constrict, compromising circulation; spasms follow cold or stress; made worse by smoking tobacco; clinical picture, history of numbness to area, normal arterial pulses present; women in puberty or 40, esp those who smoke grounds diagnosis; treatment of episodes by applying warmth to area, stop smoking, avoid cold, avoid stress; drug therapy to dilate vessels includes vasodilators, alpha-adrenergic blockers, Ca channel blockers, but can worsen condition; Recurs but treatment prognosis good; wearing globes, shoes for cold, stopping smoking prevents, lowers recurrence

Blood Dyscrasias

Red = Erythrocytes, White = Leukocytes, Platelets = Thrombocytes, and plasma makes up blood; blood transports O2, nutrients, hormones, and rids waste in infla response, maintains homeostasis, A/B balance, fluid balance, body temp; blood synthesized by hematopoietic system in bone marrow (myeloid) and lymphoid tissue in lymph nodes, spleen, thymus, bone marrow, GI tract; reticulo-endothelial system found in spleen, liver, lymph nodes, bone marrow, removes worn-out blood cells from bloodstream, breaking them down for components, recycling to body; stem cells in bone marrow form blast cells (erythroblasts (rubriblasts)) which become RBC, and myeloblasts which become WBC; malfunctioning of this systems causes dyscrasias, impairment of blood formation

Anemias

Reduction in quantity of RBCs or hemoglobin in measured volume of blood, reducing ability to carry O2; symptoms vary w/ severity, pallor, fatigue, dizziness, shortness of breath, irregular heartbeats; treatments vary w/ cause, from acute/chronic blood loss, impaired RBC prod, inherited or acquired hemolytic conditions, anorexia nervosa, and hemolytic-hemoglobin disorders; types include iron deficiency, folic acid deficiency, pernicious aplastic, sickle cell, hemorrhagic, hemolytic; fatigue, pale, w/ progression more pronounced symptoms, dyspnea, tachycardia, pounding heart, pallor on hands and nail beds, conjunctiva, mucus membranes of mouth; often diagnosed incidentally in phys exam; anemias classified by color/size of RBC, as hypo/normo/hyperchromic spherocytosis, or microcytic, normocytic, macrocytic; also classified by causative factors; low RBC in blood studies, low hemoglobin, hematocrit, changes in morphology of corpuscles can ground diagnosis; bone marrow studies can show aberrations; treatment directed at cause; dietary/supplements of iron if cause, treatment of slow insidious bleed, folic acid replacement, vitamin B12 for pernicious; causative factor for hemolytic, aplastic eliminated; sickle cell no cure; treatments often symptomatic, bed rest, inc fluids, analgesics helpful; if condition exacerbates, hospitalization, O2 administration, IV therapy, narcotic analgesics, packed RBC transfusion; prognosis varies based on cause and type; prevention depends on type and cause, often unpreventable

Iron-Deficiency Anemia

2ndary to blood loss through hemorrhage, slow insidious bleed, or heavy menstrual flow due to insufficient iron in diet

Folic Acid Deficiency Anemia

Low folic acid for DNA synthesis, preventing maturation of blood cells; consequence of dietary deficiency, similar clinical picture to pernicious anemia

Pernicious Anemia

Considered macrocytic anemia, where immature RBCs larger than normal; hemoglobin volume reduced, w/ subsequent reduction in O2-carrying capacity; considered an autoimmune response

Aplastic Anemia

Results from insult to hematopoietic cells (stem cells) of bone marrow; all blood cell type prod reduced due to exposure of myelotoxins, e.g. benzene, alkylating agents, antimetabolites, insecticides, radiations, certain drugs

Sickle Cell Anemia

Chronic hereditary hemolytic form; mainly black race; presence of hemoglobin S w/ hemoglobin A in RCB causes sickle/elongated shape, deoxygenation; rigid, misshapen cells obstruct capillary flow, inducing tissue hypoxia, further sickling, leading to further obstruction, infarction; when sickled cells reoxygenated, resume natural round disk shape of a normal RBC; hemoglobin S reduces O2 carrying capacity

Hemorrhagic Anemia

Results from large amount of blood volume loss (hypovolemia) in short duration

Hemolytic Anemia

Caused by abnormal destruction of RBCs; heredity plays some role, but exposure to chem toxins and certain bacterias or autoimmunity may be caused

Agranulocytosis (Neutropenia)

blood dyscrasia where leukocytes very low; can be rapid onset; severe fatigue, weakness, followed by sore throat, ulcerations of oral mucosa, dysphagia, elevated body temp, weak, rapid pulse, chills; req prompt assessment; often caused by drug toxicity, hypersensitivity, e.g chemo, benzene; is acute insult to body’s immune system reducing body response to bacterial infection; infectious agents invading in oral or pharyngeal mucosa often present or no longer held in check by absent granulocytes; chlorpromazine, propylthiouracil, phenytoin, chloramphenicol sensitivity can cause; can accompany aplastic or megaloblastic anemia, tuberculosis, uremia, malaria; more women; dec number of polymorphonuclear cells in blood studies, bone marrow studies show lack of granulocytes and developing WBCs not maturing, history shows exposure to offending agents, blood, urine, oral cultures may be positive for bacteria or toxins; antimicrobial therapy to eliminate offending microorganism, cultures done to monitor growth of microbes; if cause is toxicity of drug, exposure to agent halted; aggressive therapy as can be fatal within week if untreated;  prognosis varies on etiology, but cessation of exposure to toxin improvement seen; prevention is avoiding toxin

Polycythemia

Abnormal inc in amount of hemoglobin, RBC count, or hematocrit, causing absolute inc in RBC mass; symptoms related to how much inc mass; headaches, dyspnea, irritability, mental sluggishness, dizziness, syncope, night sweats, weight loss; circulatory stagnation, thrombus, inc blood viscosity sometimes; splenomegaly, clubbing of fingers, cyanosis observed; req prompt assessment; unknown etiology; relative version when plasma volume is reduced by dehydration, plasma loss, fluid/electrolyte imbalances, or burns; reduced O2 supply to tissues results in compensation of body to manufacture more hemoglobin to carry additional O2, which occurs when chronic pulmonary and cardiac disease or live at high altitudes where O2 concentration reduced; symptoms suggest diagnosis; periodic phlebotomy to reduce blood count, relative polycythemia often subsides when reducing causative factors; periodic phlebotomies for life can resolve or have positive prognosis; prevention unknown

Thrombocytopenia

Idiopathic purpura considered an autoimmune response; involves reduced clotting capability of blood

Leukemias

Malignant neoplasms of blood-forming organs (bone marrow, spleen, lymph nodes) prod abnormal, uncontrolled, clonal proliferation of one type of blood cell in lymphoid or myeloid cell lines; large number of leukemic leads to bone marrow overcrowding, reduced prod of normal blood cells; reduced number of functional neutrophils, RBCs, platelets results in freq infections, anemia, clotting problems; classified by cell type, degree of differentiation of neoplastic cells; acute composed of immature-appearing, large hematopoietic cells (blasts); chronic version prod more mature-appearing, yet hypofunctional cells; acute disease rapid progression, quickly fatal; chronic leukemias slower progression, measured in years; leukemic cell type refers to whether neoplastic cell derive from lymphoid or myeloid lineage

Acute Lymphocytic Leukemia (ALL)

charact by overprod of immature lymphoblasts in bone marrow and lymph nodes; pale look, bone pain, weight loss, sore throat, fatigue, night sweats, weakness; bleeding of gingiva may be noted; tendency inc to bruising, recurrent infections; as leukemic cells infiltrate spleen, liver, lymph nodes, NS, they interfere w/ organ function; lymphadenopathy, splenomegaly common; headache, blurred vision, nausea, vomiting, cranial nerve palsies; symptoms req prompt assessment; more children; exact cause unknown, but prolonged exposure to radiation, certain chemicals, drugs, viruses, smoking, genetic factors (Downs) can contribute; peripheral blood smear shows inc number immature lymphocytes and reduced number RBC, platelets; microscopic exam of bone marrow aspiration or biopsy req for definitive diagnosis; blast cells make up 30% of all nucleated cells to diagnose; CSF may be withdrawn; karyotype for abnormalities can help; aggressive chemo for 2-3 years, CNS prophylactically w/ intrathecally administered methotrexate and intracranial radiation therapy as CNS invasion common; if Philadelphia chromosome present, treated w/ imatinib mesylate; allogenic bone marrow transplant for patients w/ relapse; 5-year survival 78-85%; adults w/ cytogenetic abnormalities worse prognosis; children can tolerate higher doses of drugs than adults can; CNS invasion or Philadelphia chromosome, failure to achieve remission has chemo treatment; no prevention unknown

Chronic Lymphocyte Leukemia (CLL)

neoplasm involving lymphocytes, slow progressing, results in accumulation of mature-appearing but hypofunctional lymphocytes; often no symptoms until CBC reveals lymphocytosis, thrombocytopenia, anemia; weight loss, fever, night sweats, extreme fatigue, splenomegaly, hepatomegaly, painless swelling of cervical, supraclavicular, or axillary lymph nodes that spontaneously waxes and wanes; susceptibility to frequent viral, fungal infections; certain patterns of chromosomal changes (trisomy of 12, 3, 16, deletion of 13) can be seen; median diagnosis 60 yo, mostly males; performance during terminal phases often poor; freq death from systemic infection, bleeding, cachexia; 95% cases found incidentally during routine bloodwork; peripheral blood smear, bone marrow studies show lymphocytes, > 10000/microliter, bone marrow hypercellular; smudge cells (broken lymphocytes) may be seen; Rai system stages in US; (0) patient has lymphocytosis and bone marrow infiltration >30% blasts, median survival 12 years (I) Patients have lymphadenopathy, median survival time 9 years (II) Splenomegaly or hepatomegaly, 6 years (III) anemia, 1 year (IV) thrombocytopenia, 1 year; treatment withheld until symptomatic and evidence of hemolytic anemia, painful lymphadenopathy, or symptoms; chemo (fludarabine), radiation therapy, monoclonal antibodies against B lymphocyte surface antigens, Rituxan against CD20, Campath against CD52; bone marrow transplant not generally available; nonmyeloablative transplants show promise; 5-year survival 73%, poorer prognosis for low platelet or hemoglobin; prevention unknown

Acute Myelogenous Leukemia

rapid, progressive neoplasm of cells committed to myeloid line of development; leukemic cells accumulate in bone marrow, peripheral blood, other tissues; rapid accumulation of myeloblasts leads to pancytopenia, anemia, easy bleeding/bruising, inc risk of infection; gingival bleeding, epistaxis, menorrhagic, weight loss, fatigue, pallor; lymphadenopathy, organomegaly rare; most common adult leukemia; positive family history of AML or other leukemias, prior theory w/ ionizing radiation, prior chemo for Hodgkin’s disease, non-Hodgkin’s lymphoma, ovarian/breast cancer, chronic exposure to benzene, smoking can cause; many cases during atomic bomb of Japan; clinical picture and peripheral blood smear grounds diagnosis; 50% patients have Auer rod visible in leukemic cells, diagnostic; bone marrow aspiration biopsy needed for definitive, showing hypercellular >20-30% myeloblasts; AML divided into seven subtypes using FAB classification based on predominant morphologic cell type; routine lab testing, chest x-rays, ECG, HSV, CMV serology to find treatment; chemo first, often cytarabine, daunorubicin to induce remission; bone marrow transplant after first remission can improve survival; complete remission defined as normal peripheral blood, <5% blasts in cels; APL M3 distinct form w/ translocation btwn long arms of chromosomes 15/17, creating fusion gene, impairing differentiation, apoptosis of promyelocytes; all-trans retinoic acid, a derivative of vitamin A, w/ cytotoxic chemo can treat; high 5-year survival, ranging 15-70%; advanced age, history of prior hematologic disorder, poor performance status, some cytogenetic abnormalities make prognosis worse; prevention unknown

Chronic Myelogenous Leukemia (CML)

Slowly progressing neoplasm in hematopoietic stem cells or early progenitor cells, resulting in excess of mature-appearing hypofunctional neutrophils; 50% patients asymptomatic, w/ disease suggested from abnormalities leukocytosis, thrombocytosis on routine blood tests; weight loss, fatigue, excessive sweating, bleeding episodes, upper left quadrant pain, acute gouty arthritis, tenderness to lower sternum; anemia, splenomegaly; often adults >40; exposure to ionizing radiation only known risk factor; invariably associated w/ abnormal chromosome 22 (Philadelphia Chromo); has triphasic course (1) chronic phase (2) accelerated phase (3) blast phase; most in chronic phase, where abnormal proliferation of WBC begun, splenomegaly common, but mild symptoms; accelerated has inc leukocytosis, neutrophil differentiation impaired, bone pain, fever, night sweats; blast crisis resembles AML, >30% blasts in peripheral blood flow, after 3-5 years after diagnosis; diagnosis by clinical picture, blood, bone marrow studies; CBC reveals anemia, leukocytosis, thrombocytosis; bone marrow biopsy shows hyperplastic, w/ more mature leukemic cells; definitive diagnosis req demonstrating presence of Philadelphia Chromosome or Bcr/Abl fusion gene product by cytogenetic analysis, FISH, or PCR; presence of Philadelphia distinguishes CML from others; Bone marrow transplant only chance for full cure, however, only viable for 25% patients; if unable to undergo immediate transplant, drug inhibiting Bcr/Abl tyrosine kinase, Gleevec, developed to induce remission of all phases; complete remission is ablation of Philadelphia chromosome and its gene products; 5-year survival 35%, w/ poorer prognosis w/ larger spleen size, older age, higher % blast cells, platelet count >700,000 microliters; prevention unknown

Autologous Transplant

BMT in which patient serves as his or her own donor for stem cells

Allogeneic Transplant

BMT in which donor is HLA-identical to patient, often a sibling

Syngeneic Transplant

BMT in which the patients identical twin serves as stem cell donor

HLA Type

Identity of leukocyte surface antigens, human leukocyte antigens, which is determined for patient and donor to determine the degree of compatibility; closer the match is, lower risk of transplant related complications

Unrelated Donor / Mismatched Transplant

Transplant in which donor does not match all of the key HLA antigens; associated w/ greatest risk of complications

Lymphatic Disease

Lymphatic system composed of lymphatic vessels, tissues, nodes, tonsils, thymus, and spleen, and lymph; lymphatic vessels originate at capillary level, along venous system, progress and empty to R/L subclavian veins; system has no pump; lymph nodes are collections of tissue, filtering foreign material (bacteria, viruses) from lymphatic circulation; Lymphocytes are prod mainly in lymph nodes as part of body’s defense mechanisms; lymphatic vessels are thin walled, larger vessels contain valves; muscles exert intermittent pressure on vessels, causing lymph to flow by milking action; smooth muscle in vessel walls contracts to aid return of lymph to cardiovascular system

Lymphedema

Abnormal collection of lymph, often in extremities; results in swelling of extremity; No pain; extremity can be grossly distended; unilateral limb swelling req prompt assessment; obstruction of lymph vessel/node may be infla or mechanical; if untreated, connective tissues lose elasticity, edema becomes permanent; lymphatic circulation may be compromised by infections, neoplasms, thrombus; allergic rxns can cause, trauma, surgery to affected part; tight clothes that constricts can cause temporary version, removing constriction resolves; women w/ mastectomies may experience in adjacent arms; prolonged lymphedema rarely is associated w/ development of lymphosarcoma; painless swelling grounds diagnosis; imaging, radioactive isotope studies, lymphangiography confirms; affected limb elevated above heart for drainage, elastic bandages or stocking applied to affected part to compress for drainage, diuretics for lower volume, surgery to relieve mechanical obstruction sometimes, antibiotics for infection cause; prognosis varies w/ cause and patient response to therapy; surgery req if conservative measures fail; not life threatening, but carries danger of uncontrolled infection easily developing; stagnant interstitial fluids are breeding group for infections, local defenses become overwhelmed; most cases not preventable, but less tight clothing helps

Lymphangitis

Infla of lymph vessels; Often manifests as red streak at site of entry of infective organism, spreading to regional lymph node that is swollen, tender; cellulitis around surrounding tissue, fever, chills, malaise; symptoms req prompt assessment; bacterial invasion of lymph vessels at site of local trauma/ulceration freq cause; oftentimes no portal of entry detectable; bacteria travels to regional lymph nodes to stimulate infla; visual inspection of area sufficient for diagnosis; final confirmation by cultures of infected tissue; systemic antibiotics, affected area elevated rest and warm wet dressings applied; surgical drainage of purulent material indicated; prognosis varies w/ amount of tissue involved and nature of causative organism, i.e. response to antibiotics; surgery more positive outcome; condition cannot be prevented, good hand washing helps

Lymphoma

Malignant neoplasms from uncontrolled proliferation of cellular components of lymphatic system; dysfunctional cells either B, T, or rarely both cells; neoplastic lymphocytes migratory and found not only in lymph structures, also bloodstream, bone marrow, in later disease liver, lungs, other organs; lymphomas two categories (1) Hodgkin’s Disease (2) non-Hodgkin’s Lymphomas; treatment based on stage of disease, staged by Ann Arbor-Cotwold's staging system; staging based on affected lymph structures, extranodal tumor sites, presence/absence of systemic B symptoms of lymphoma, i.e. weight loss >10% body weight in 6 months, persistent fevers >38 C, night sweats; (I) Single lymph structure involved (II) 2+ lymph structures, w/ involvement on same side of diaphragm (III) Lymph regions both sides of diaphragm involved (IV)  Widespread involvement of extranodal tissues both sides of diaphragm, w/ A/B to indicate if B symptoms are there or not

Hodgkin’s Disease

Cancer of lymphatic system; tumors in tissue of lymph nodes spread to other nodes, spleen, liver, bone marrow; painless enlargement of lymph nodes in neck or mediastinum, fatigue, alcohol-induced pain, pruritus; w/ progression, systemic B symptoms; Hodgkin’s differentiated from other lymphomas by presence of Reed-Sternberg cell, a large cell w/ 2+ mirror-image nuclei, each w/ one nucleolus; symptoms req prompt assessment; 15% of all lymphomas, either in 20s or 50+; risk factors previous history of malignancy, prior chemo, family history of Hodgkin’s, other immunosuppressions, Epstein-Barr Virus; painless lymphadenopathy and typical symptoms leads, excisional lymph node biopsy definitive for diagnosis, showing Reed-Sternberg cells; blood studies show mild normochromic, normocytic anemia, neutrophilic leukocytosis, lymphopenia, eosinophilia, elevated ESR and serum alkaline phosphatase; bone marrow biopsy sometimes; chest CT, ultrasonography of spleen, liver and kidney tests; I/II stage good prognosis w/ radiation alone, sometimes chemo; IIIB/IV w/ chemo treatment, ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) therapy; relapses treated w/ more chemo; bone marrow transplant for many relapses; one of the most treatable cancers, 5-year survival 90%; death from disease itself, other cancers secondary, or cardiovascular disease; poorer prognosis from B symptoms, low serum albumin/hemoglobin, male gender, 45+, anemia, of high ESR; prevention impossible

Non-Hodgkin’s Lymphoma

# of heterogeneous neoplasms of lymphoid cells, wide signs and symptoms from slow, indolent growth to rapidly fatal progression; some treatable, others not good prognosis; painless lymphadenopathy, fatigue, pruritus, bone pain, GI symptoms; tonsils, adenoids enlarged, B symptoms potentially; symptoms req prompt assessment; incidence of NHL peak in preadolescents, drops, then inc w/ inc age; risk factors of family history of prior malignancy, previous radiation therapy, immunotherapy, chemo, HIV infection, HTLV, Epstein-Barr virus, Hep C virus, immunosuppression, connective tissue disorders, Crohn’s, celiac, H. pylori infection; grouped into 3 categories based on neoplasm behavior (1) indolent lymphomas w/ subtypes (1) follicular lymphoma (2) small lymphocytic lymphoma (3) mantle cell lymphoma (4) marginal zone lymphomas, from B/T-cell or NK-cell line (2) Aggressive lymphomas w/ subtypes diffuse large B-cell lymphomas, peripheral T-cell lymphomas (3) Highly aggressive version rarer, including Burkitt’s, adult T-cell lymphoma; patient evaluation must include determination of histologic subtype, extent of disease, performance status of patient; all involved lymphoid sites phys examined;excisional biopsy of intact lymph node necessary for histopathologic identification of disease; immunologic, cytogenetic, molecular studies can further aid; bone marrow aspiration and biopsy determines extent of disease, w/ marrow involved stage IV; CBC, peripheral blood smear, studies of renal/liver functions, chest radiographs, CT of abdomen and pelvis to show extent, ground diagnosis; indolent treated by waiting for symptoms until chemo or radiation necessary, not curable w/ conventional therapies; more aggressive lymphomas have rapid progression, req CHOP chemo (cyclophosphamide, doxorubicin, vincristine, prednisone), w/(o) rituximab and w/(o) radiation; relapses treated w/ high dose chemo and BMt; 5-year survival 53%, w/ prognosis affected by age, presence of extranodal disease, B-symptoms, stage at time of diagnosis; indolent have better survival even if untreated, but generally not curable; aggressive version rapidly fatal if unresponsive to therapy; no prevention known

Transfusion Incompatibility reaction

Blood transfused has antibodies to recipient RBCs or recipient has antibodies to donor RBCs; hypersensitivity reaction ranges from mild to fatal; hemolysis, agglutination, bacterial, allergic, circulatory overload transfusion reactions; severity depends on amount of incompatible blood transfused; chills, fever, tachycardia; more severe rxn back pain, vomiting, diarrhea, hives, rash, substernal tightness, dyspnea, becoming hypotensive, progress to state of circulatory collapse; w/ worsening, bleeding from puncture site, blood in urine, renal failure; if allergic rxn, hives, itching, anaphylaxis; will be observed immediately in hospital setting if rxn; ABO- and Rh-incompatible blood as well as antigens that screening does not reveal causes antigen-antibody rxn causing hemolysis, agglutination; histamine and serotonin released from mast cells and platelets; disseminated IV coagulation triggered, resulting in coagulation problems; chills, fever, hives, or dyspnea during transfusion alerts of potential rxn; blood/urine specimens examined w/ used blood to confirm incompatibility; transfusion protocol mandates set of baseline patient vitals taken beforehand and in designated intervals; at first indication of symptoms, blood transfusion stopped immediately, blood/urine samples abstained at that time w/ untransfused blood; antihistamines, anaphylaxis according to protocol treats; prognosis varies w/ amount of blood, rxn cause, speed of intervention; careful typing and crossmatching of blood mandatory; two assistants to gather patient info on blood bag and orders beforehand prevents

Classic Hemophilia

Hereditary bleeding disorder from lacking of clotting factors; can be mild, moderate, or severe; any unusually prolonged bleeding episode, easy bruising, hematomas, excessive epistaxis in male child suggests; first sign can be ecchymosis at birth, bleeding from circumcision; joint swelling and pain suggests bleeding in joints; if male infant/toddler/child has unexplained prolonged bleeding and symptoms, prompt assessment req; X-linked genetic disorder in males, hemophilia transmitted by asymptomatic carrier mother to son; Factor VIII, a clotting factor in intrinsic clotting cascade, is inactive; any minor trauma can cause bleeding; diagnosis based on clinical picture and history; normal platelet count, bleeding time, prothrombin time, prolonged partial thromboplastin time, and factor VIII assay of 0-30% grounds diagnosis; cannot be cured, but treatment stops deformities; concentrated factor VIII (AHF) stops bleeding, transfusions of blood sometimes necessary; avoiding bleeding causes, avoiding getting HIV; life-long blood transfusions possible; no prevention known

Disseminated IV Coagulation

Simultaneous hemorrhage and thrombosis; secondary to other diseases; oozing of blood from needle puncture sites, mucus membranes, or incisions noted; bleeding in form of purpura, wound hematomas, petechiae; hematemesis, hematuria, bloody stools, weakness, headaches, air hunger, tachycardia; med emergency if suffering condition at home; thrombin activates prod of fibrin, causing clots to form when not needed (in microcirculation e.g.); thrombin causes platelet aggregation, forming more clots; fibrinolytic system is activated by thrombin in plasma; thrombin  causes excess fibrinolysis and bleeding; predisposed by hypotension, hypoxemia, acidosis, stasis of capillary blood; diagnosis based on clinical picture, history of probable precipitating events; platelet count and fibrinogen reduced, PT prolonged; IV heparin inhibits additional microthrombi and aggregation of platelets from happening; platelet replacement, plasma clotting factors administered if serious hemorrhage; condition is life-threatening; prognosis guarded, prevention unlikely