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60 Cards in this Set
- Front
- Back
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Mcc of ischemic heart disease -
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coronary atherosclerosis
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4 main clinical syndromes of ischemic heart disease -
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1. Angina pectoris
2. Acute myocardial infarction 3. Sudden cardiac death 4. Chronic ischemic heart disease |
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STEMI:
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ST elevation - sign of transmural ischemia/infarction
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non-STEMI:
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ST depression - sign of subendocardial ischemia
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Angina pectoris -
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symptoms of pain/discomfort/pressure anywhere between eyebrows and waist
Pain from coronary insufficiency without infarction |
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Subtypes of Angina pectoris -
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Stable/classic angina
Unstable angina Prinzmetal or variant angina |
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Stable angina -
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Stenotic artery due to atherosclerosis of coronary arteries -> Decreased blood blow
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Pathogenesis of stable angina -
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Decreased oxygenation affects subendocardium (furthest from supply)
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Clinical presentation of stable angina -
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Exercise induced substernal chest discomfort, lasting less than 30 mins
Relieved by rest or nitro EKG -> ST depression |
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Unstable angina -
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severe dz with clot on pre-existing ruptured plaque
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Clinical presentation of unstable angina -
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Frequent pain, onset at minimum exertion or rest
Not relieved by rest/nitro May be STEMI/NON-STEMI Never do a stress test Not infarcted yet -> can progress to MI |
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Prinzmetal's angina -
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vasospasm of coronary arteries
often at the site of athero. plaque |
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Clinical presentation of Prinzmetal's angina -
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Comes on randomly -> not assoc with activity
EKG -> ST elevation |
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Acute myocardial infarction -
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Death of myocardium, secondary to loss of blood supply
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Causes of myocardial infarction -
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Thrombosis of coronary artery at site of athero. plaque
Hemorrhage into plaque with ballooning of plaque against opp wall Embolization of plaque into a distal branch |
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Clinical findings of MI -
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Severe retrosternal chest pain >30-45 mins, not relieved by nitro
Pain radiates to LEFT arm, shoulder, jaw or epigastrum Diaphoresis, anxiety, SOB Elderly & Diabetics might NOT have any pain |
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Criteria for diagnosis of MI -
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Serum enzyme levels
EKG changes Clinical symptoms |
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What is chronic ischemic heart disease?
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CHF from ischemic damage to heart muscle
Heart tissue replaced -> Non-contractile scar tissue Episodes of angina -> eventually Heart failure |
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Sudden cardiac death -
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Occurs from arrhythmia
Most pts have severe coronary stenosis Common causes - cocaine use, malformation of coronary arteries or conduction pathways |
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2 types of infarction -
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Transmural (Q-wave)
Subendocardial (non Q-wave) |
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Transmural aka Q wave infarction
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ST elevation on EKG aka STEMI
Poor collateral blood supply -> Full thickness infarction |
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Subendocardial infarction -
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ST depression on EKG (NON-STEMI)
Arterial obstruction in heart -> good collateral blood supply Thrombolytics can be given early, some muscle fibers salvaged, if given late -> increased reperfusion injury damage |
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Enzymes used in diagnosis of MI
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Troponin
Myoglobin CK-MB LDH |
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LDH -
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24-1 week
Sensitive, but not specific In MI, LDH1>LDH2 |
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Creatine Kinase (CK-MB)
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6h-72h
Sensitive, but not specific MB form more specific Best for diagnosing re-infarction (troponins will still be elevated, which would give a false positive) |
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Troponin
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8h - 1 week
Sensitive & Specific Gold standard for diagnosis |
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Myoglobin
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4h -24h
Sensitive but not specific Fast screen |
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What is secondary peak in these cardiac enzymes from?
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Reperfusion of partially infarcted tissue can "wash out" enzyme from the dead tissue and cause a secondary peak
Also skeletal muscle damage can cause increasked levels - not specific |
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Microscopic changes assoc with MI -
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0-30 mins: No visible change
30-2hr: "Wavy fibers" at edge, contraction bands 4-8hrs: Early nuclear changes, polys at edge 8-24hrs: Coagulative necrosis, PMNs 24-74hrs: Pallor (soft and yellow) grossly, dead fibers eaten up by macrophages Well developed coag necrosis 3-7 days: Red rim - grossly; granulation tissue, macros 1-7 weeks: Granulation tissue -> scar tissue (white, non-contr) |
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Early complications of MI:
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Cardiac arrhythmics -hours to days; MCD - V-fib
CHF (1st day) happens in large infarcts, with cardiogeic shock if 40% of LV infarcted Rupture of pericardium (3-7 days) weak granulation tissue replaced infarcted myocardium Fibrinous pericarditis (1-7) days: Chest pain relieved by leaning forward; friction rub heard on auscultation |
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Different types of ruptures in post MI and there complications:
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Rupture of ventricle -> Cardiac tamponade; hemopericardium (usually when infarct is soft - 4to 10 days)
Papillary muscle rupture -> mitral insufficiency Interventricular septum rupture -> L to R shunt |
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Late complications of MI:
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Mural thrombus -> ultimately embolization
Ventricle aneurysms - 4-8 weeks occurs in scarred area Auto-immune pericarditis (dressler's syndrome) 6-8 wks |
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What is Dressler's syndrome?
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happens post MI; 6-8 weeks
AutoAbs vs. pericardium Fever and friction rub |
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Post MI ventricular aneurysm -
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Happens between infarct and replacement by strong collagen
Precordial bulge during systole appearing 4-8 weeks after MI |
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Rhabdomyoma
Dz assoc: |
MC primary tumor of heart in children (skeletal muscle)
Dz assoc: Tuberous sclerosis |
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Cardiac myxoma -
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benign adult tumor of endocardium in left atrium -> sx due to blockade of MV
Presentation: dyspnea, syncope, SOB May hear diastolic murmur at apex |
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Gross/Microscopic presentation of cardiac myxoma -
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Grossly - large ball/valve
Microscopically - stellate cells |
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Ball-valve thrombus -
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Large ball like thrombus that usually appear in LA
Presentation: dyspnea, syncope, embolization of thrombus (stroke, etc) Diastolic murmur at apex |
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Fibrinous pericarditis etiology -
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Similar to myocarditis -coxsackie virus and trypansoma cruzi
SLE, collagen vascular disease, post mi, uremia Coxsackie - mcc |
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Fibrinous pericarditis pathology -
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Fibrinous type of pericardial exudate often accompanied by an effusion
Sometime constrictive pericarditis - by dense scar tissue with dystrophic calcification |
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Clinical findings in fibrinous pericarditis -
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Friction rub
Precordial chest pain - relieved when leaning forward, increases upon inspiration |
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Pericardial tamponade -
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hemorrhage into pericardial space -> compression of the heart
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Causes of pericardial tamponade -
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post mi rupture, aortic dissection, trauma
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Presentation of pericardial tamponade -
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Beck's tria ->
1. hypotension (assoc with pulsus paradoxicus) 2. neck vein distention jvd (kussmai's sign -> blood can't enter RA during inspiration) 3. muffled heart sounds |
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What is constrictive pericarditis?
Mcc Presentation - |
Incomplete feeling on cardiac chamber due to thickening of parietal pericardium
Tuberculosis - mcc, otherwise idiopathic Pericardial knock - due to ventricles hitting thickened parietal pericardium |
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What is cardiomyopathy?
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Group of diseases that primarily involve myocardium and produce myocardial dysfunction
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Types of cardiomyopathy -
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Dilated (congestive) (most common)
hypertrophic Restrictive |
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Dilated cardiomyopathy etiology -
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Idiopathic (mc)
Genetic causes Myocarditis Drugs (cocaine, adriamycin) Postpartum state, thiamine def(alcoholism) |
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Pathophys of DCM -
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Decreased contractility with a decreased EF (<40%) - not enough contractile muscle fibers overload
Systolic dysfunction type of LHF |
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Clinical findings in DCM -
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Global enlargement of heart
All chambers dilated ECG -> poor contractility |
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Hypertrophic CM Epidemiology -
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Mcc of sudden death in young adults
Familial form - mutation in heavy chains of beta myosin and in troponins Sporadically in elderly |
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Pathophys of HCM -
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Hypertrophy of myocardium
Disproportionately thickening of IV septum than free LV wall Obstruction of blood flow is below aortic valve -> because anterior wall of mitral valve is drawn against IV septum as blood exits LV Aberrant myofibers and conduction system in IV septum - these conduction disturbances responsible for sudden death Decreased diastolic filling - as muscle thickened so restricts the filling |
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Clinical findings in HCM -
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systolic ejection murmur
Murmur intensity increases with decreased preload (standing) murmur decreases upon increasing preload |
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Restrictive CM mcc -
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Tropical endomyocardial fibrosis-mcc
Infiltrative diseases such as Pompe's glycogenesis, amyloidosis, hemochromatosis, sarcaidosis Also endocardial fibroelastosis (thickening of endocardial fibroelastic tissues) in children |
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Pathophys in RCM -
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Decreased ventricular compliance
2ndary to infiltrative dz of myocardium Leads to LV diastolic dysfunction |
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Clinical findings in RCM -
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arrhythmias, CHF
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Detection of amyloidosis or hemochromatosis in RCM -
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Amyloidosis due to transthyretin protein - staining with congo red and apple green on birefringence
Hemochromatosis - prussian blue staining |
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Libman-sacks endocarditis -
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Assoc with SLE
Sterile vegetations located on mitral valve sruface - produces valve deformities and regurgitation problems |
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NBTE or marcantric endocarditis -
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Paraneoplastic syndrome
Sterile, non destructive vegetations on mitral valve because of procoagulant effect of circulating mucin from mucin producing tumors of colon and pancreas |
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Complications of marcantric endocarditis -
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Emoblization
May be secondarily infected |
