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Patho Test 3: 1

Cardiac

QuestionAnswer
What Causes myocarditis? Bacteria, fungal, protozoan, and viral infections
What can also cause myocarditis? Rheumatic fever, diptheria, heat stroke, and radiation
WHat is myocarditis? Inflammation of the myocardium, which is the heart muscle
Pericarditis? inflammation of the pericardium
What can cause pericarditis? TB, Mycosis, collagen disease, urmeia, fungi, neoplosms, radiation, traum, MI it has a variety of causes
What are the two main clinical manifestations? Pain, and a friction rub
What do you do to diagnose pericarditis? EKG, Echo CT, MRI
In Pericarditis what falls and what rises pressure wise? Falling arterial pressure and rising venous pressure you also have distant heart sounds
How do you treat Pericarditis Bedrest, Meds-analgesics, NSAID's helps w/ inflammaiton, corticosteroids, ABT, antipyretics
Chronic Pericardites inflammation that has thickened the pericardium, s/s are edema, crackles
How do you preven Mycocarditis? Immunizations, increase physiscal activity, avoid competitive sports,gradually increase activity
what is endocarditis? attack of organism, gets in body and is a bacterial invasion,can get in through mouth or surgery, in blood stream,
who is endocarditis common in? older people and high instance of IV drug use
how do you diagnose Endocarditis? H&P blood culture, echo and CT
what is the first s/s of endocarditis? Flu like symptoms, splinter hemmorages of under fingernails, roth spots in retina, petechiae in conjunctiva
Complications of Endocarditis? Mycardial erosoin, which is bacteria is hanging from heart valves treat with antibiotics before invasive procedures
What is Pericardial effusion? fluid in the pericardial cavity, may accompany CHF, Heart surgery, trauma, also renal failure
S/S of pericardial effusion sudden or gradual, can result in cardiac tamponade
What is cardiac Tamponade? Muffled heart sounds, falling aterial pressure, narrowed pulse pressure, rising venous pressure ect.. these are related to not getting blood out: Dyspnea, pain, anxiety, syncope, distened neck veins, edema
Pericardial Effusion assessmetn and dx and management GET TRAY READY, EKG, examine fluid that is withdrawn
Cardiomyopathies: primary and secondary Primary: Heart muscle diseases of unknown origin, silent onset, so s/s until disease is well advanced Secondary:OUtside of heart, MI and have complications because of another cardiovascular disease
There are 3 types of cardiomyopathies list them dilated, hypertrophic, restrictive
Hypertrophic thickend hyper kinetic ventricular muscle mass, uncoordinated contractions and impaired relaxation
s/s of hypertrophic A fib is precursor to sudden death, dyspnea is most common, chest pain, fatigue, syncope
How do you treat hypertrophic? Beta blockers, ca channel blockers, surgical removal of part of mycardium, have to put in automatic internal defiblilator
Dilated cardiomyopathy Most common, dilation of all 4 chambers, cardiac failure, initation is alcohol, cocaine, genetic, pg, and aging, DM or thyroid
Dilated what happens to heart? Heart becomes enlarged and the wall becomes thinner
S/S of dilated Weakness, fatigue, periphial edema, tachycardia, leads to death
TX of dilated releave heart failure adn work laod with digoxin, diuretics, and afterload, reducing drugs, or heart transplant
Restrictive rarest form, stiff ventricular impaired diastolic feeling, it gets fibroused and rigid adn non compliant, major diff, is restrictive diastolic feeling, low stroke volume and CHF
Phase o rapid depolariztion ions switch side
Phase1 early repolarization peak of the action potential stops sodium channels with decrease in socdium permability
phase 2 the plateau, caused by the slower calcium sodium channels opening, calcium plays a role in the contractility in the cardiac muscle
phase 3 final rapid repolariaztion down slope of action potential, calcium sodium channels close and increase K permebility
phase 4 resting, sodium out potassium in
what are the two catagories of dysrythmia Superventricular and Ventricular
EKG a picture of the electrical conduction of the heart. easy quick 2,3, or 12 leads
Ejection fraction amount of blood % beening pumped in the first quarter of systole normal is 60-80 %.
Cadiac reserve how much an individual can increase CO as needed
preload amount of blood the heart must pump with each beat
afterload the pressure needed for the heart to pump blood into the aorta
Cardiac contractility heart can change the force of contraction without changing resting
inotropic something that can modify the contractility
heart rate the frequency the ventricles contract, the blood is ejected , filling time
dopomine increases blood pressure and contractility
arterial circulationq impairment can lead to echemia and infarction
what are the three causes of hypercholestrolemia genetics, nutrition and metobolic disease
Risk factors of coronary heart disease nonmodifiable risks-less than 45 for men and 55 for womenlipid risk factors- total chlosterol less than 200, LDL cholestorol is less than 130, Tri- less than 150, HDL greater than 40Nonlipid risk factors- hypertention less than 140/90, cig smoking,DM,
Probable risk factors Lipoproteins, small LDL particles, HDL subtypes, apolipoprotein B, Homocysteine, Fibrinogen, High-sensitivity C-reactive protein, Impaired fasting glucose
CAD largest killer in the US, great advances in treatment but no decline in death rate
two types of lesions in CAD stable and unstable
stable angina eschemia r/t athoersclerosis and phasospasms and thrombus
what brings on stable angina activity stress and cold
what relieves angina rest
where is the pain located with stable angina anywhere from the neck to the stomach
how do you treat stable angina prevent MI stop activity beta blocker CABG PTCA
CABG coronary artery bypass-graft
Variant angina caused by vaasospasma with or without the disease looks like Reynolds in heart
treatment for variant angina calcium channel or nitrate
Silent mydocaridial eschmeia ischemia without angina, common in patients with Dm, old MIS, and elderly
unstable angina new angina or recent accelerted angina, caused by plaque distrubtiion or repair
Diagnosis for unstable angina EKG, BP, and Cardiac markers
Segment elevation MI eschmic death of myo tissue, may or may not have a T wave
S/S of segment elevation abrubt onset, extreme pain, SOB, weakness, naseua and vomiting, tachecardia, feelings of impending dome, shock, sudden death due to dysrythmias
How long do you have to prevent permanent damage to prevent the segment elevation MI 1 hour (15-20) min is ideal
Myoglobulins (MB) cardiac marker; O2 carrier, released 1 hour after MI, not the best indicator
Creatine Kinese (CK) released 4-8 hours after MI,
What are the most specific cardiac markers for MI? CK and MB
Troponine Cardiac specific and peaks later, its the best one to tell how long ago the MI happened, once it gets to this level its pass the level of treatment
Mitral stenosis opening being narrowed, obstruction of blood flow from the LA to the LV
If Mitral stenosis backs up where does it go? lungs
Diagnosis of Mitral Stenosis H/P- Echo, heart cath
Mitral Regergetation Rheumatic fever
Endocarditis congenital heart defects, diet pills
Mitral regergetation backs up it goes where? left atrium
Aortic Stenosis calcification of the valves also narrowing of the aortic valve
What does aortic stenosis cause the left ventrivcle to do? thicken
Aortic stenosis is most common with what ages? 70-90
Aortic regergetation etiology-endocarditis, congenital hear defects, syphllis, aneurysms, aging, Marfins,
In aortic regergetation it will back up where LV
S/S of aortic regergettation most patients do not have smyptoms, water hammer pulse, visible pulses, murmur, angina, fainting
Diagnosis of aortic regergetation Echo, EkG, TEE, Stress test, and heart cath
Valve replacement: 2 types Disk Mechanical valves and Ball and socket
How do you treat Aortic Regurgitation? Treat CHF and dysthrithmias, also can do aortic valve replacement
Created by: JoeNLind
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