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32 Cards in this Set
- Front
- Back
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Cardiac muscle disease
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always aerobic
not 100% dependent on glucose like the brain |
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Myocardial O2 needs
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HR, contractile force, muscle mass, wall tension determine need for O2
reduction in O2 supply or increased O2 demand will disturb balance work (O2 demand) increased by: -increased heart rate -increased force of contraction -ventricular dilation or hypertrophy *left ventricle has increased demand because its thicker and works against systemic system while right works against pulmonary |
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Oxygen is delivered via coronary arteries
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arteries dilate in hypoxia
ischemia (decreased delivery of blood and O2) may be transient, reversible deficit of blood flow ischemia > 30-45 minutes leads to necrosis --> muscle cells don't reproduce themselves **coronary blood flow only occurs during diastole** |
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Progression of heart disease
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myocardium goes from aerobic to anaerobic metabolism--> local acidosis (pH down)
hypoxia, acidosis, decreased energy availability impairs ventricular function --> decreased energy = less contraction = cant push blood to body ECG --> T wave inversion and ST segment depression angina pectoris (chest pain) relieved by vasodilators indicates ischemia |
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Progression chart
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1. decreased perfusion to heart
2. partially/totally ischemic cells 3. totally --> NO ATP: cells gone -CK, LDH, troponin release --> monitor for heart damage level 4. partially --> anaerobic, reduced ATP -dysrhythmia ** down ATP = down contractibility = down CO = life threatening ** ** SNS up = HR up to try to conpensate ** |
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Infarction leads to functional changes
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decreased wall compliance (scar tissue does not contract/ relax), abnormal wall motion (dead zones)
reduced contractility, reduced SV, decreased ejection fraction --> percent of blood in ventricle not emptying at right volume increased ESV and EDV, increased ED pressure in ventricle --> dilated heart |
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Myocardial infarction chart
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1. myocardial infarction
2. decreased contractility 3. decreased ejection fraction and increased left ventricle end diastolic volume OR decreased renal perfusion and increased renin angiotensin release 4. increased preload OR increased afterload 5. renal failure OR hypertension (increased HR to get blood pushed out) |
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Body perceives a decreased blood pressure and volume and tries to correct deficit
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compensation mechanisms create a SNS stimulation (increases O2 demand)
generalized vasoconstriction, salt and fluid retention ventricular dilation and hypertrophy |
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Complications of MI
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primary complication is development of arrhythmia (90%) --> disrupt conduction pathway
CHF in 50% of patients cardiogenic shock in 10-15% of patients -at least 40% of ventricle damaged -severe drop in BP, total body hypoxemia and metabolic acidosis (leads to hypoxia) -reduced coronary perfusion, increased pulmonary congestion --> buildup of blood behind ventricle -80-90% mortality papillary muscle (puts tension on chordae tendonae so valves dont flop open) dysfuction leading to valve incompetence cardiac rupture with cardiac tamponade --> bleeds into pericardial sac (CT) which increases pressure and compresses the heart, fatal ventricular aneurysms, thromboembolism (blood clot from heart to brain), pericarditis |
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signs of myocardial ischemia and infarcts --> Infarction triad
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1. severe prolonged chest pain with sweating, nausea, anxiety
2. increase in specific cardiac enzymes -CK MB increases within hours --> acute diagnosis - LDH 1 up over 2-3 days -AST levels indicate muscle damage 3. changes in ECG -pronounced Q wave, elevated ST segment, inverted T wave |
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Lab tests
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myoglobin --> muscle tissue being destroyed, rapid increase in 2 hours from onset
CK --> creatin kinase, storage for muscle tissue, shoots up then decreases over time of onset CK-MB--> myocardial marker, steep increase after onset troponin I --> specific for cardiac muscle, steep increase after onset LDH --> rises slowly after onset, LDH 1 is cardiac which will be greater then LDH 2 (striated muscle) AST --> muscle/ liver damage |
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Predictors of trouble
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C receptive protein, homocysteine, MPO, metabolic syndrome
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C-reactive protein
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serum marker of inflammation that rises with atherosclerosis **inflammatory**
better predictor of MI then cholesterol historically not measured, no specific way to decrease -aspirin can help |
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homocysteine
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amino acid --> increased levels increase risk of MI
folate, B12, B6 needed for breakdown increases associated with high LDL, poor vasodilation, increased risk of thrombosis |
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Myeloperoxidase (MPO)
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measured with apolipoprotein A1
increased levels of MPO plus decreased levels of normal apoA1 raises risk of MI *try to predict person in trouble --> change diet/ lifestyle* |
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Metabolic syndrome (syndrome X)
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increased BP
high visceral fat (apple body shape), insulin resistence, high LDL, obesity increased risk of MI, stroke, Type 2 diabetes runs in families **many things wrong** |
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Diagnosing metabolic syndrome
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waist measurement (apple shape)
blood pressure 130/85 or higher triglycerides >150 mg/DL - not spilling glucose into urine fasting glucose >110 mg/dL *normal <100* may also see increased C reactive protein and increased fibrinogen/plasminogen activator --> create clots in blood stream more then normal |
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Dysrhythmia/arrhythmia
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most common complication of MI
results from disruption of normal conduction pathways in myocardium (already had MI) predisposing factors: -ischemia, hypoxemia, lactic acidosis -ANS activity from stressful situation -electrolyte imbalances (K) -various drugs may have tachycardia, bradycardia, ectopic beats (something other then SA node driving beat but still in atria, affects P wave), escape beats (AV node becomes pacemaker, atria not driving beat, ventricles contract quicker) |
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Ventricular premature beats are most common dysrhythmia
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ventricular tachycardia --> HR > 120bpm, severe reduction in CO
ventricular fibrillation --> total disruption of pathways, no effective systole, need defibrillator heart block --> delay/ blockage coming from SA node -primary --> all beats conducted, prolonged PQ wave -secondary --> some beats conducted -tertiary --> total block, no impulses get through, escape rhythm --> SA and AV nodes arent communicating |
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Atrial arrhythmia does occur
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tachycardia --> HR > 150bpm
atrial flutter (rates up to 300/min) may lead to atrial fibrillation -decreases preload of heart -AV node doesn't usually conduct > 180bpm |
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Risk factors for arrhythmia
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same as MI
smoking --> number/day more important then length of time smoking obesity, high caloric intake metabolic syndrome |
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Heart failure
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most common complication of all forms of heart disease --> acquired or congenital
no cure caused by heart infections or valve problems |
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Mechanisms of heart failure
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occurs when heart cant pump enough blood to meet O2 demand of body
-myocardial failure --> specific abnormalities of muscle -circulatory failure --> blood delivery problem (atherosclerosis) -congestive heart failure --> blood pools in capillary beds in organs no single biochemical mechanism explains all cases |
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Factors leading to CHF
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increased preload (aortic regurgitation, ventricular septal defects)
-volume overload = dilation increased afterload (aortic stenosis, systemic hypertension) -pressure overload = hypertrophy = increased O2 demand reduced contractility (infarcts, myopathy, scar tissue) impaired filling/ejection (AV valve stenosis, pericarditis, cardiac tamponade |
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Forward failure
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symptoms result from inadequate CO or downstream flow --> out into body from L ventricle, lack of blood going downstream
-compensation requires increased myocardial work = increased O2 demand = increased risk of ischemia weakness, fatigue most common early signs late stages result in multiple organ dysfunction -immediate result is increased HR |
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Backward failure
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symptoms from backup of blood behind failing ventricle: upstream failure --> trouble getting through system and heart
-pulmonary congestion--> L sided failure -edema of systemic organs--> R sided failure impaired function in one ventricle will eventually cause backward failure of other--> usually L side first then R side |
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Left ventricular failure
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depressed Frank Starling curve (decreased contractility= negative inotropic)
limited cardiac reserve, heart less compliant weak rapid pulse cardiac cachexia hear S3 in early diastole --> blood bouncing off walls, filling ventricle will hear it |
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Left failure forward/backward effects
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backward:
-dyspnea on exertion, orthopnea (trouble breathing while laying down), cough, paroxysmal noctural dyspnea (trouble breathing at night), cyanosis, basilar crackles forward: -fatigue, oliguria (decreased urine production), increased HR, faint pulses, restlessness, confusion, anxiety |
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S/S of upstream (backward) left failure
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dyspnea on exertion most common (pulmonary)
weakness/fatigue nonproductive cough hemoptysis (coughting up blood) dysphagia --> enlarged left atrium/pulmonary vein compresses esophagus |
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S/S of downstream (forward) left failure
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ischemia of organs as shift circulation to heart, lungs, brain
-decreased renal perfusion pallor, cyanosis as decreased skin perfusion XS sweating as decreased ability to loose heat changes in mental status--> insomnia, restlessness, confused |
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Right failure forward/ backward effects
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most common effect of L failure
backward: -hepatomegaly, ascites, splenomegaly, anorexia, subcutaneous edema, jugular vein distention forward: same as left forward failure |
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Upstream (backward) S/S of R failure (cor pulmonale)
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cor pulmonale --> heart problems secondary to pulmonary problems (L sided failure first)
elevation of jugular pressure and distention of veins hepatomegaly, tenderness anorexia, sense of fullness/nausea peripheral edema leading to generalized body edema (anasarca --> edema through whole body) increased urination at night (nocturia) |
