Cardiac+conditions 2

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Congenital Heart Disease Anatomic Defects ○ Children develop while forming in fetal development (wk 4-7), can see during week 8. ○ Several reasons: • Febrile illness (high fever) • Lupus • Diabetes • Maternal Alcoholism • Meds - Anti-convulsant meds, lithium. Hemodynamic Alterations ○ Abnormal shunting of blood from one side of heart to another. ○ Problem with heart going from fetal to outside of the womb circulation ○ Shunting from right to left side of heart or left to right side. (mixing of blood) Status of Tissue Oxygenation ○ Cyanotic • Right to left - Mixing of blood occurs, deoxygenated blood goes out to rest of circ, therefore ppl b/c cyanotic. ○ Acyanotic • Left to right - no cyanotic effect. Congenital Heart Disease Patent Ductus Arteriosus ○ Blood goes from RA to RV to Pulm artory directly to aorta ○ Premi babies take longer for duct to close • Underdeveloped, also in SNS, might have to do with messages not related, not pressures not being as they should be to close the gaps. ○ Can be seen on Xray ○ If does not close, can be repaired surgically, patch over ductus opening. Ventricular Septal Defect ○ Opening between both ventricles through septum. ○ Size determines severity. ○ Left side is higher pressure system than right, therefore oxygenated blood in left ventricle shunts into right ventricle. Leads to increased size in pulmonary artery and vein. • Pulmonary hypertension and progressive cyanosis. ○ Quicker rate of blood returning to left atrium, less time for oxygenation, more deoxygenated blood returning to left atrium - become cyanotic. ○ Echocardiogram - test used to determine where and size of opening. ○ Only surgically work on symptomatic individuals. ○ Can also use catheter, through femoral artery, attach/close the septum (new) Can have more than one congenital heart defect.

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Valvular Heart Disease ○ Can occur on any valve in heart. Stenosis ○ Occurs on any valve ○ Aortic Stenosis • Narrowing/thickening of valve leaflets, takes more blood pressure to push through opening • Most common in men, older people, high cholesterol, atherosclerotic condition. • Progressive condition, not symptomatic until advanced state (when 1/4 of usual size symptoms present:)  Angina, syncope, symptoms of heart failure. Characteristic heart murmur, follow with echocardiograms also. • • Surgical - valve replacement (don't want to replace too early) Prolapse • Ballooning back of valve leaflets, don't close nicely, can open a little allowing some blood to regurgitate back through. (Big floppy valves) • Can occur without regurgitation, but most people end up with regurgitation. ○ Mitral Valve Prolapse • Valve becomes fibrotic, usually asymptomatic, may have some chest pain atrest, disnea (difficulty breathing), fatigue, anxiety, palpitations and light headedness.

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• Hear click in the heart Regurgitation • Incomplete closure of valve (ie. Mitral) • Can be due to Rheumatic Heart Disease, stretching of papillary muscles, won't close effectively. • Can be an acute cause, body not as able to tolerate. • If occurs slower then body compensates, therefore can have condition for years before symptoms present. • Puts more pressure on side of the heart (left for mitral), affects stroke volume and further pulmonary congestion. Longer process. • Best to get to problem before symptoms present. • Can surgically repair, decrease pressure in heart.

Rheumatic Heart Disease Due to complication with Rheumatic Fever ○ Caused by group A. Beta-hemolytic streptocaucus (iestrep throat, pharyngeal) [not due to skin] ○ May cause interation between immune system and antigens from strep, deposits in heart tissue - effects heart valves, veins, and SQ tissue. ○ Acute • Strep throat • Involvement of CT, necrosis in joints, heart valves. • Further damage to these tissues - can cause permanent damage, common cause of mitral stenosis. • Treat with antibiotics ○ Chronic phase • Rheumatic fever --> heart disease • Use surgery to replace damaged heart valves. Beta Streptococcus Rheumatic Heart Disease Treatment Endocarditis ○ Inflammatory process, infectious, inner layer of heart valve invaded by bad acting bacteria on heart valves which destroy underlying tissue. ○ Already have heart disease. ○ See in Heart valve replacement patients, and other people with implants in heart (opportunistic bacteria possible cause) ○ Staphylococcus, Strepcoccus, Enterococcus ○ Easily released and can travel through circ system --> cerebral circ or peripheral circ. ○ Heart murmurs as vegetation grows. Subacute infective endocarditis ○ Don't appear as sick, develops over months, to an already damaged heart valve. ○ Fever, signs of systemic infex Acute infective endocarditis (IE)

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○ Occurs in heart valve that is previously normal. ○ See in IV drug users, introducing microorganisms into blood stream. ○ Become very sick, fever, signs of systemic infex. Antibiotic prevention Valve Replacements ○ Determined by: • Life expectancy • Follow up care needed Metal Valves ○ Need a lot of follow up treatment, constant anti-coagulant therapy for life. Last a long time. ○ Younger individual ○ Antibiotic therapy Tissue Valves ○ Pork! ○ Good for ten years. ○ Older person ○ Antibiotic therapy

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Coronary Heart Disease Atheroma ○ Plaque that forms. Atherosclerosis ○ Hardening of arteries ○ Develops from laying down of a fibro fatty lesion in the lining of a vessel. ○ See in large/medium sized arteries. ○ Begins as insidious (slow, hidden) process throughout life span, no knowledge of occuring for years after. ○ Risk factors: • High cholesterol, increased age, family history of Coronary heart Disease (men below the age of 55, women b4 menopause), cigarette smoking, obesity, HTN, diabetes, and more. Stable plaques ○ Stay there until mechanical trauma occurs (HTN, hemorrhage) Unstable Plaques ○ Caused by Endothelial injury, cause damage to inner lining of artery • mechanical (high pressure), sends more platelets/monocytesto area, lipids accumulate and form in smooth muscle cells or endothelial cells until a plaque structure develops (smooth muscle cells, macrophages, other leukocytes) • Plaques sit for several years. ○ Body tries to heal area where damage occurs, more platelets and macrophages forming a thrombus and an occlusion. ○ Give lipitor/statin drugs to stabilize plaques. Cardiac Arrest ○ Cessation of pumping of the heart can be caused by many reasons. ○ Versus MI - decreased O2 to certain area of heart, MI can lead to cardiac arrest. Coronary Heart Disease Risk Factors High blood lipid level High cholesterol. High blood pressure a. 140/90, but there are other stages Cigarette Smoking (tobacco) a. If person quits after several years, lessons risk but still has risk. Family history Diabetes Obesity Secondary lifestyle (couch potatoes) Alcohol Myocardial Infarction (MI) ○ Imbalance b/t O2 supply and demand for its needs, severity determines disease process, not severe --> agima, severe --> MI or sudden death.

Atherosclerosis most common cause (vessel over 50% occluded/blocked), difficulty of cells to function. Ischemic Heart Disease http://www.healthcentral.com/animation/408/13/Heart_Attack.html Something sitting on chest, not everyone experiences in same way, mainly men.  Chest pain radiates up neck, down arm, up to jaw, to shoulders.  Unrelenting nausea  Diaphoretic (sweaty), pale  Abnormal heart sounds, pericardial friction rub (inflammatory reaction in potential space, hear rubbing sensation, painful) Women, can be chin, under bra line, under ear. Causes: ○ Sudden blockage of Coronary Artery • No blood supply getting to myocardial tissue, will die if not relieved. • 10 seconds before myocardial cells feel effects (cellular metabolism), after afew minutes lose ability to contract, pumping function is hampered, anaerobic process occurs, lactic acid builds up. • Cardiac cells stay alive for 20 minutes without O2. ○ Hemorrhage into an atheromatous plaque ○ Arterial spasm ○ Sudden greatly increased myocardial oxygen requirements ○

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Myocardial Infarction Complications Arrhythmias ○ Irregular heart rhythm due to damaged heart muscle, irregular signal. ○ Bradycardia (slower heart rate, heart block) in non lethal instances. Heart Failure Intracardial thrombi ○ In lining of the heart muscle --> decreased space for heart to fill, decreased output. Pericarditis ○ Inflammation in potential space. Cardiac Rupture ○ Usually in septum (very lethal) Papillary Muscle Dysfunction ○ Ischemia over papillary muscles - impair closure, valves can be wide open. Ventricular Aneurysm ○ Aneurysm (thinning of the wall/vessel where blood accumulates underneath, stretching wall/muscle until thins, can lead to rupture) in lining of the muscle, usually in the ventricle. Myocardial Infarction Diagnoses ○ ECG • Can show MI ○ Blood Tests

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• CKMB (bradykin kinase), Troponin <-- peak after MI Treatments ○ Thrombolytics • Giving streptikinase, some clot busters. ○ Coronary Angioplasty, PCI (percutaneous coronary angioplasty) • See ballon angioplasty Balloon Angioplasty

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Angioplasty and a stent - run stent through catheter, blow stent to side of wall to hold up against wall.

Other Treatments 1. ASA (Aspirin) 1. Lipid lowing drugs a. Even is normal BP 1. Dietary Changes a. Lower cholesterol, less sodium, leaner meat, more good fats, less processed foods.

1. C-Reactive Protein a. Blood test, predictor of future coronary events. a. Marker of inflammation in body (chronic) 1. Homocysteine a. Independent risk factor for development of Coronary disease. a. May promote atherosclerotic plaques. a. Often from dietary insufficiency of B6, B12, folate.

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Angina ○ Inabil of coronary arteries to meet O2 demand. ○ Associated with fixed coronary obstruction. ○ Transient discomfort (3-5mins at a time) may be from lactic acid buildup. ○ Relieved with rest or nitrates. ○ Usually Substernal chest pain. Stable Angina ○ Narrowing of coronary arteries, not meeting metabolic needs of pericardium, particularly after stressful activity (stairs). ○ Sit and rest, angina goes away. Prinzmetal Angina ○ Chest pain due to transient Ischemia, usually occurs in sleep REM cycle. ○ Caused by vasospasm of arteries, may or may not have athersclerotic condition. • No long term damage, but there is pain. Silent Ischemia ○ No pain, may be due to difference in SNS. ○ See in patients that had coronary artery bypass, and transplants. Mental stress-induced Ischemia ○ Increased heart rate, BP, increased Myocardial O2 demand that is not met. ○ Unknown whether mental stress leads to MI.

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Hypertension Primary HTN Secondary HTN Isolated Systolic HTN Complicated HTN Malignant HTN

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Hypotension Orthostatic (postural) Hypotension ○ Acute ○ Chronic Treatment

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Cardiomyopathy Types: Ischemic Restrictive Hypertrophic Dilated

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Heart Failure Acute or Chronic Right Sided Left Sided

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Aneurysms Abdominal Aortic Aneurysm

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Veins Venous Insufficiency Varicose Veins

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Embolism Fat Air Foreign Material

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Arterial Thrombus Thrombus vs Embolism Arterial Thrombus Gangrene

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Edema Increased Capillary Permeability Low Plasma Proteins Increased Hydrostatic Pressure Lymph Obstruction Edema

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