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169 Cards in this Set
- Front
- Back
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characteristics of pain
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duration, quality, location, radiation, frequency, alleviating or precipitating factors, associated symptoms
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chest pain in acute coronary syndrome
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substernal opressive quality described as tightness, heaviness or pressure; in MI pain lasts >20-30min; constant in frequency, precipitated by exercise, radiates to left shoulder
inferoposterior MI can present with upper abdominal pain, nausea, hypotension and dizziness or fainting (due vagal reflexes) transient ischemia is releived with nitroglycerin associated symptoms are diaphoresis, tachypnea and anxiety |
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musculoskeletal or pulmonary chest pain
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described as sharp or knife-like and reproduced by changes in position or palpation
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tachycardia/tachypnea
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nonspecific but seen in MI or pulmonary embolism
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blood pressure in evaluation of chest pain
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difference of >20mmHg between two arms suggests aortic dissection (70%); hypotension is seen in massive pulmonary embolism or cardiac shock and it could also be seen in inferoposterior MI
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fever in evaluation of chest pain
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suggests pneumonia or mediastinitis
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signs of atherosclerosis
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corneal lipid rings
narrowed retinal arteries pigment and hair changes in legs may be seen in acute coronary syndrome |
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chest wall exam in chest pain evaluation
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check for tender areas, respiratory motion, respiratory retractions or accessory muscle use; if palpation reproduces the pain consider musculoskeletal etiology
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heart sounds in chest pain evaluation
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wide physiologic splitting of S2 (inspiration) --> right bundle branch block or right ventricular infarction
paradoxical splitting (expiration) --> LBBB or anterior/lateral infarction S3 --> heart failure S4 --> angina or infarction; aortic regurgitation --> aortic dissection mitral regurgitation --> angina or infarction due to papillary muscle dysfunction |
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lung auscultation in chest pain evaluation
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assymetry of breath sounds in spontaneous pneumothorax; absent lung sounds in spontaneous pneumothorax or pleural effussion
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work-up of chest pain
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all patients should have 12-lead ECG (MI diagnostic findings are ST elevation or Q waves in 50%, ischemia findings are ST depression or T wave inversion in 35%)
CK-MB, troponins T I C chest x-ray |
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differential diagnosis of chest pain
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noncardiovascular: costochondritis, hiatal hernia, GERD, peptic ulcer, gallbladder disease
cardiovascular: MI, aortic stenosis, myocarditis, pericarditis, dissecting aortic aneurysm, mitral valve prolapse pulmonary: embolism, pulmonary hypertension, pneumothorax |
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costochondritis differentiating features
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pain exacerbated with inspiration; reproduced with chest wall palpation
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hiatal hernia differentiating features
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reflux of food, relief with antacids
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GERD differentiating features
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acid reflux, relief with antacids
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peptic ulcer differentiating features
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epigastric pain worse 3h after eating
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gallbladder disease differentiating features
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right upper quadrant pain and tenderness
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myocardial infarction differentiating features
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severe pain > 20 minutes
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aortic stenosis differentiating features
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systolic ejection murmur
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myocarditis differentiating features
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vague mild pain
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pericarditis differentiating features
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sharp pain, worse with lying down, relieved by sitting up
diffuse ST elevation responds to analgesics |
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dissecting aortic aneurysm differentiating features
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sharp, tearing pain also felt in the back
loss of pulses, wide mediastinum on x-ray diagnosis confirmed by CT, MRI, transesophageal ultrasound or aortography |
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mitral valve prolapse differentiating features
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transient pain, midsystolic click, young females
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pulmonary embolism differentiating features
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tachypnea, dyspnea, cough, pleuritic pain, hemoptysis
diagnosis confirmed by CT, lung scan or pulmonary angiogram |
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pulmonary hypertension differentiating features
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signs of right ventricle failure
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pneumothorax differentiating features
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sudden onset of pain and dyspnea
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major modifiable IHD risk factors
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high cholesterol, tobacco, hypertension, physical inactivity, obesity, diabetes
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uncontrollable IHD risk factors
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age, sex, heredity
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minor IHD risk factos
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sex hormones and stress
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cholesterol levels in ischemic heart disease
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the higher the level, the more risk for IHD; LDL is most important to consider (>100mg/dL)
low HDL (<40mg/dL) hypertriglyceridemia (>150mg/dL) high HDL/cholesterol ratio high lipoprotein A |
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stable angina presentation
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cardiac chest pain episodes on exertion relieved by rest that last 5-15min; ST depression in seen during attack
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stable angina diagnosis
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perform baseline ECG then exercise stress test which is positive when there is >2mm ST depression and/or drop of >10mmHg in systolic pressure
this test is diagnostic (67% sens, 70% spec), determines severity, effectiveness of treatment and functional capacity; contraindicated in most other cardiac diseases can also use thallium nuclear stress test (82% sens, 95% spec), dobutamine or adenosine stress test, stress echocardiogram patients with stable angina need evaluation of severity |
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stable angina management
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acute episodes --> sublingual nitroglycerin
long-term --> long-acting nitrates (isosorbide), beta-blockers, aspirin, statins, modification of risk factors after evaluating severity decide on revascularization (stent or bypass) |
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differentiate NSTEMI and unstable angina diagnosis
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if there are ECG signs + elevated cardiac markers --> NSTEMI
if normal cardiac markers 6-24 hours after presentation --> unstable angina |
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unstable angina presentation
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cardiac chest pain episodes occuring at rest or of increasing severity, frequency and duration resistant to nitrates
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thrombolytic therapy
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beneficial in STEMI but not NSTEMI; in NSTEMI ischemia is mostly due to thrombus-related embolization and platelet-rich instead of fibrin-rich thus thrombolytics are not effective
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ECG diagnosis in NSTEMI
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ST segment deviation (>0.5mm) or new T-wave inversion (>2mm)
but normal ECG or minor changes in up to 50% |
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high-risk features of UA/NSTEMI
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repetitive or prolonged chest pain (>10min)
elevated biomarkers persistent ECG changes hemodynamic instability (SBP<90) sustained ventricular tachycardia syncope LV EF <40% diabetes chronic kidney disease prior PTCA or CABG |
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UA/NSTEMI management
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beta-blocker
antiplatelet: aspirin and clopidogrel (300mg loading, 75mg/day) anticoagulant; unfractionated heparin or enoxaparin for 48-72 hours or until angiography glycoprotein IIb/IIIa inhibitors: abciximab, tirofiban (diabetics), eptifibatide invasive: early coronary angiography (48 hours) and revascularization recommended in NSTEMI or high-risk patients |
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STEMI diagnosis
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clinical symptoms plus ECG:
persistent ST elevation of >1mm in two contiguous limb leads ST elevation of >2mm in two contiguous chest leads new LBBB pattern cardiac biomarkers are not needed for initial diagnosis |
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STEMI atypical presentation
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elderly or diabetics can present with nausea or dyspnea as sole symptom
as many as 20% are silent (symptoms not severe enough for patient) |
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STEMI general management
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cardiac monitor
oxygen therapy IV line aspirin nitroglycerin morphine |
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localizations of STEMI
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inferior, anteroseptal, anterior, lateral, posterior
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inferior STEMI ECG localization
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leads II, III and aVF; artery is right coronary
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anteroseptal STEMI ECG localization
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leads V1-V3; LAD artery
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anterior STEMI ECG localization
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leads V2-V4; LAD artery
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lateral STEMI ECG localization
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leads I, aVL, V4-V6; artery is LAD or circumflex
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posterior STEMI ECG localization
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leads V1-V2 --> tall broad initial R wave, ST depression, tall upright T wave
usually in association of inferior or lateral STEMI artery is posterior descending |
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abnormal Q wave
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>25% the height of partner R wave
greater than 0.04sec and 2mm deep Q waves are normal in lead III |
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ECG evolution of STEMI
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hyperacute T waves (immediately to 6-24 hours)
ST elevation (immediately to 1-6 weeks) Q waves (1/several days to years/never) T wave inversion (6-24 hours to months-years) |
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reperfusion therapy
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PCI (angioplasty/stents) are preferred if <12 hours and <90 minutes from first medical encounter; if PCI is unavailable or too late then thrombolytic therapy
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thrombolytic therapy
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appropiate in place of PCI if >12 hours of onset of STEMI
streptokinase and alteplase by IV infusion reteplase and tenecteplase by rapid bolus tPA is most common in US due to antibody formation streptokinase is contraindicated if had been given within 1 year to same patient |
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absolute contraindications to thrombolytic therapy
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active bleeding
significant closed head or facial trauma within 3 months suspected aortic dissection prior intracranial hemorrhage ischemic stroke within 3 months |
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relative contraindications to thrombolytic therapy
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recent major surgery (<3 weeks)
traumatic/prolonged cardiopulmonary rescucitation recent internal bleeding active peptic ulcer severe poorly controlled hypertension ischemic stroke <3 months |
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antiplatelet therapy in STEMI
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aspirin (to all patients) and clopidogrel (300mg) to patients undergoing PCI or fibrinolysis; with long-term maintanance of 75mg (up to 1 month after fibrinolysis or 1 year after stent)
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anticoagulant therapy in STEMI
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unfractionated heparin (or perhaps enoxaparin) an GP IIb/IIIa inhibitors should be used in conjunction with PCI; only heparin in case of fibrinolytic therapy
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heparin dosages in STEMI
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in PCI it depends on concomitant use of GP Iib/IIIa inhibitors
in fibrinolysis --> unfractionated heparin in initial bolus of 60 units/kg, followed by initial infusion of 12 units/kg (max 1,000/h) adjusted to attain activated PTT to 1.5-2 times control enoxaparin may be used in patients <75 but dose adjustment in renal patients |
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CABG indications
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should be considered in patients who failed PCI or persistent ischemia resistant to drugs; patient should have suitable anatomy
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discharge medications after acute coronary syndrome
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aspirin (75mg indefinitely)
clopidogrel (75mg upto 1 year after PCI or 1 month or if aspirin contraindicated) beta-blocker (if heart failure carvedilol or metoprolol) ACE inhibitors (if heart failure) statins to all patients should be initiated in hospital short-acting nitrates or isosorbide if continuous frequent pain warfarin in those at risk for systemic thromboembolism ABCDE |
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drug treatments shown to reduce mortality in IHD
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statins
aspirin beta-blockers CABG in triple vessel or left main disease |
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dysrhythmias as ACS complication
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bradycardia (treat with atropine)
premature beats supraventricular tachycardias (atrial tachycardia, fibrillation, flutter) ventricular tachyarrhythmias (ventricular tachycardia, accelerated idioventricular rhythm, fibrillation) |
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conduction abnormalities as ACS complication
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1st, 2nd and 3rd degree heart blocks, hemiblocks, branch blocks
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mechanical dysfunction as ACS complication
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heart failure (left/right or biventricular)
true or pseudoventricular aneurysm acute mitral regurgitation ventricular septal rupture free wall rupture mechanical problems are treated with emergency surgery |
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ischemia as ACS complication
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recurrent infarction or extension
post-infarction angina after thrombolytics or PCI requires bypass surgery |
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sudden cardiac death
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is a complication of ACS; most commonly ventricular fibrillation or tachycardia
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thromboembolic complications of ACS
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mural thrombus
deep vein thrombosis due to prolonged immobilization ischemic stroke |
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right ventricular infarction
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often a complication of inferior MI (30%); diagnosed with ECG and treated with fluids (if its complication)
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hypercoagulable states as nonatherosclerotic cause of MI
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polycythemia vera
thrombocytosis factor V Leyden protein C deficiency antiphospholipid antibodies |
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vasculitis as nonatherosclerotic cause of MI
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SLE, PAN, takayasu, Kawasaki
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coronary spasm
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due to prinzmetal or cocaine abuse which are nonatherosclerotic causes of MI
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Prinzmetal angina
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episodes of severe angina due to coronary vasospasm
occurs at rest (night or morning hours) ST elevation and can be associated with MI, ventricular arrhythmias or sudden death, migraines exercise stress tests and angiography are normal diagnose with ergonovine |
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coronary embolus as nonatherosclerotic cause of MI
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atrial myxoma, atrial or ventricular thrombus
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compensatory mechanisms in heart failure
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cardiac: Frank-Starling, tachycardia, ventricular dilation;
neuronal: increased sympathetic adrenergic, reduced vagal activity; hormonal: vasopressin, catecholamines and BNP, renin-angiotensin-aldosterone system |
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systolic heart failure
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decreased ventricle contraction, dilation and EF<45% due to ischemic cardiomyopathy, dilated cardiomyopathy
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dyastolic heart failure
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filling of one or both ventrciles is impaired with normal EF; can be due to amyloidosis
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congestive heart failure
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syndrome of dyspnea, fatigue, peripheral edema, high JVP and pulmonary edema with crackles
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causes of heart failure
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70% are due to ischemic heart disease
hypertensive, alcoholic and other cardiomyopathies valvular disease congenital heart disease |
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precipitating factors in heart failure
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important to exclude in diagnosis
excessive dietary Salt uncontrolled Hypertension cardiac Ischemia myocardial Infarction Infections Thyrotoxicosis Arrhythmias Anemia "SHIIIT precipitates A failure" |
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heart failure presentation
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dyspnea
orthopnea paroxysmal nocturnal dyspnea fatigue pulmonary rales peripheral edema ascites hepatomegaly jugular venous distention displaced apical impulse |
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cardiac Vs. pulmonary dyspnea
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cardiac is more sudden, not associated with sputum production, without history of pulmonary disease, no lung disease evidence on x-ray, cardiomegaly seen on x-ray
pulmonary dyspnea is the contrary |
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classification of heart failure severity
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Class I: no limitation of daily activities
Class II: mild limitation, can perform mild exertion Class III: marked limitation, only comfortable at rest Class IV: confined to bed or chair; physical activity or rest brings discomfort |
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heart failure work-up
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check cardiac enzymes to exclude ischemia or MI
x-ray to exclude infection test of choice is echocardiography for diagnosis and classification (ejection fraction) chest x-ray to exclude infection shows cardiomegaly, vascular redistribution, Kerley B-lines, interstitial edema ECG indentifies hypertrophy, ischemia or precipitating arrhythmias BNP is 97% sensitive for decompensated HF |
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heart failure management
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first line: ACEi + carvedilol/metoprolol + spironolactone + furosemide +- digitalis
ACE inhibitors improve survival and reduce hypertrophy and symptoms; loop diuretics decrease congestive symptoms; betablocker decrease mortality, reduce hospitalizations and improve ejection fraction; other vasodilators: nitrates/hydralazine used if ACEi or ARB are contraindicated; digitalis does not improve survival but reduces severe symptoms; if dyastolic HF use less diuretics and vasodilators and give CCBs (verapamil) to slow heart rate and allow filling; spironolactone decrease mortality |
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pulmonary edema
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medical emergency
tachypnea, expectoration, cyanosis, nocturnal dyspnea, rales, ronchi, wheezing; x-rays: prominent pulmonary vessels, enlarged cardiac silhouette, Kerley B lines, pleural effusions ECG: to determine if arrhythmia treatment: morphine, furosemide, sitting patient upright, oxygen, nitroglycerin (reduce preload), digoxin (if atrial fibrillation), IV ACEi |
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mitral stenosis etiology
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abnormal mitral leaflets are affected due to rheumatic fever autoimmune deposits
reduced left ventricular filling, increased left atrial and pulmonary pressure, forward and right heart failure ensues |
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mitral stenosis presentation
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systemic embolism
atrial fibrillation dyspnea orthopnea hemoptysis hoarseness paroxysmal nocturnal dyspnea fatigue right heart failure pulmonary rales decreased pulse pressure loud S1 with opening snap following S2 diastolic rumble sternal lift |
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mitral stenosis auscultation
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pulmonary rales, loud S1 with opening snap following S2, diastolic rumble, sternal lift
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mitral stenosis diagnosis
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chest x-ray: large left atrium (double-density right heart border, posterior displacement of esophagus and elevated left mainstem bronchus), Kerley B lines, large pulmonary arteries
ECG: signs of left atrial hypertrophy, left/right atrial abnormalities, atrial fibrillation echocardiography: thickening of mitral valve leaflets, left atrial enlargement |
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mitral stenosis management
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diuretics, salt restriction, digitalis and anticoagulants if atrial fibrillation
if drugs fail --> surgical valve replacement or commissurotomy |
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acute etiology of mitral regurgitation
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rupture of chordae tendinae
papillary muscle rupture endocarditis (valvular destruction) trauma |
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chronic etiology of mitral regurgitation
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Calcifications
Hypertrohpic cardiomyopathy Endocardial cushion defect Endocarditis Fibroelastosis Papillary muscle dysfunction Rheumatic fever mitral Prolapse severe left ventricular dilation "regurgitation by CHEF PReP" |
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mitral regurgitation pathogenesis
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retrograde left ventricle flow into left atrium increases atrial pressure and decreases forward output which results in volume overload, decreased afterload (flow is eased into left atrium) which allow compensated increased ejection fraction which eventually leads to left ventricular dysfunction
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mitral regurgitation presentation
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dyspnea, orthopnea, paroxysmal nocturnal dyspnea; if severe, right sided failure;
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mitral regurgitation auscultation
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hyperdynamic and displaced (downward left) left ventricular impulse
carotid upstroke diminished holosystolic apical murmur S3 with widely split S2 distended neck veins |
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mitral regurgitation diagnosis
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x-ray: cardiac enlargement and possble pulmonary congestion
ECG: left ventricular hypertrophy and left atrial enlargement echocardiography: mitral valve can prolapse; distended neck veins |
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mitral regurgitation management
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therapy: digitalis, diuretics, ACEIs, warfarin; if symptoms persist or are severe: surgery
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mitral prolapse presentation
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most are asymptomatic; can have lightheadedness, palpitations, syncope, chest pain
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mitral prolapse auscultation
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mid-systolic click and late systolic murmur at apex, worsens with Valsalva, improves with squatting
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mitral prolapse complications
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arrhythmias
sudden death CHF bacterial endocarditis valve calcifications transient cerebral ischemic attacks |
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mitral prolapse diagnosis
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clinical + doppler echocardiography which shows systolic displacement of mitral leaflets into left atrium
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mitral prolapse management
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endocarditis prophylaxis (in severe cases)
betablocker for chest pain or arrhythmias antiarrhythmics surgery rarely necessary |
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aortic stenosis etiology
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due to age-related calcification of the valve or calcification and fibrosis of congenitally bicuspid valve; also rheumatic fever
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aortic stenosis pathogenesis
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stiff aortic valve increases afterload and left ventricular pressure which results in concentric hypertrophy
noncompliant ventricle and S4 gallop with increased LVEP the heart has increased oxygen demands with decreased coronary flow due to thickness |
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aortic stenosis presentation and auscultation
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angina
syncope dyspnea pulsus pardus et tardus carotid thrill systolic ejection murmur in aortic area S4 gallop |
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mitral stenosis diagnosis
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ECG: right ventricular hypertrophy, atrial fib
chest x-ray: large left atrium and pulmonary artery with increased lung vascularity echocardiography: thickening of mitral valve leaflets, left atrial enlargement |
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mitral stenosis management
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endocarditis prophylaxis no longer recommended
if symptomatic: surgical valve replacement or balloon valvuloplasty |
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aortic stenosis Vs. aortic valve sclerosis
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both have systolic murmur but in aortic valve sclerosis carotids don’t have delayed upstroke
no hypertrohpy in ECG no excursion of valve leaflets in ecochardiography no hemodynamically significant aortic valve gradient |
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aortic stenosis Vs. hypertrophic obstructive cardiomyopathy
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both have systolic murmur but in HOC there's characteristic change in murmur with maneuvers; large septal Q waves; characteristic echocardiographic features (asymmetrical hypertrohpy)
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aortic stenosis Vs mitral regurgitation
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both have systolic murmurs but in MR is holosystolic and radiates to axilla, not carotids
carotid upstroke normal dilated ventricle aortic valve normal in eco |
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aortic stenosis Vs. pulmonic stenosis
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both have systolic murmurs but in pulmonic stenosis it does not radiate to neck; it's loudest on left sternal border and increases with inspiration; chest x-ray and EKG reveal enlarged right heart and valve stenosis
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aortic regurgitation etiology
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hypertension (most common)
infectious endocarditis syphillis ankylosing spondylitis Marfan rheumatic fever aortic dissection aortic trauma |
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aortic regurgitation pathogenesis
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valve insufficiency leads to volume overload of left ventricle with compensating Frank-Starling; dilation, overstretching and decreased contraction force; if acute, can have large LEVEDP because ventricle is not adapted; acute pulmonary edema can occur; lower systolic blood pressure is due to regurgitation of blood out of aorta and decreased SVR; there's increased systolic pressure and widened pulse
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aortic regurgitation presentation
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dyspnea
diastolic decrescendo, systolic flow and Austin-Flint (presystolic low-pitched apical) murmurs Duroziez sign (murmur over femoral) S3 when decompensated |
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aortic regurgitation diagnosis
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chest x-ray: LV and aortic dilation
EKG: LV hypertrophy with volume overload (narrow deep Q waves in left precordial leads) echocardiogram: dilated LV and aorta, LV volume overload, fluttering of anterior mitral valve leaflet |
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aortic regurgitation management
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endocarditis prophylaxis not recommended; salt restriction, ACEIs, aortic valve replacement
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dilated cardiomyopathy etiology
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most common is idiopathic
drugs --> Doxorubicin, Cyclophosphamide, Vincristine, Alcohol infections --> Tuberculosis, Coxsackie metabolic --> Uremia, chronic Hypophosphatemia, Hypokalemia, Hypocalcemia peripartum toxins --> arsenic, cobalt, lead |
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dilated cardiomyopathy presentation
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signs of left and right systolic heart failure
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dilated cardiomyopathy diagnosis
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x-ray: cardiomegaly/pulmonary congestion
EKG: sinus tachycardia, arrhythmias, conduction abnormalities echo: gold standard, dilated left ventricle, decreased wall motion, mitral regurgitation |
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dilated cardiomyopathy differential
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valvular heart disease
coronary artery disease hypertensive heart disease |
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dilated cardiomyopathy management
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treated as those with systolic heart failure
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hypertrophic cardiomyopathy etiology
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autsomal dominant in 60% or sporadically
aortic stenosis hypertension |
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hypertrophic cardiomyopathy pathogenesis
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unexplained myocardial asymmetrical hypertrophy results in reduced compliance of left ventricle and hypercontractility; increased ejection fraction to 80-90%; obstruction of blood flow
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contractility in obstruction of hypertrophic cardiomyopathy
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increased contractility increases obstruction: digitalis, beta stimulats (isoproterenol, epinephrine), tachycardia, premature beats
decreased contractility decreases obstruction: betablockers, heavy sedation/anesthesia, CCBs |
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preload in obstruction of hypertrophic cardiomyopathy
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reduced preload increases obstruction: valsalva, low volemia, standing, nitroglycerin, vasodilators, tachycardia
increased preload decreases obstruction: increased volemia, squatting, bradycardia, betablockers |
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afterload in obstruction of hypertrophic cardiomyopathy
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reduced afterload increases obstruction: hypovolemia, nitroglycerin, vasodilators
increased afterload decreases obstruction: hypervolemia, squatting, alfa stimulation, handgrip exercise |
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hypertrophic cardiomyopathy presentation
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dyspnea
angina presyncope syncope palpitations large jugular A wave S4 systolic murmur mitral regurgitation murmur |
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hypertrophic cardiomyopathy diagnosis
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EKG: LV hypertrophy, pseudo Q waves, ventricular arrhythmias
echo: gold standard, asymmetrical hypertrophy, systolic anterior motion of mitral valve, midsystolic closure of aortic valve |
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hypertrophic cardiomyopathy treatment
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betablockers, CCBs, surgery in severe cases
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restrictive cardiomyopathy etiology
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Neoplasia
Hemochromatosis Amyloidosis Radiation Sarcoidosis Scleroderma "restrictive Neo-HeARtSS" |
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restrictive cardiomyopathy pathogenesis
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myocardium is rigid and noncompliant, impeding ventricular filling and altering diastolic function similar to constrictive pericarditis
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restrictive cardiomyopathy manifestations
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dyspnea
exercise intolerance weakness elevated jugular venous pressure edema hepatomegaly ascites S3, S4 Kussmaul sign |
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restrictive cardiomyopathy diagnosis
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x-ray: mild cardiomegaly, pulmonary congestion
EKG: low voltage, conduction disturbances, Q waves echo: characteristic texture with thickening of all cardiac structures |
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restrictive cardiomyopahty treatment
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no good therapy; eventually die from CHF; consider heart transplant
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acute pericarditis etiology
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idiopathic
viral infections vasculitis metabolism disorders neoplasms trauma drug reactions |
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acute pericarditis presentation
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substernal or left-sided chest pain worsened by lying down, coughing and deep inspiration, relieved by sitting up and leaning forward
pericardial friction rub best heard with stethoscope diaphragm as patient sits forward and forced expiration |
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acute pericarditis diagnosis and treatment
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EKG may be diagnostic with diffuse ST elevation and upright T waves at onset of pain
treat etiology and anti-inflammatories "acute pericarditiST" |
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pericardial effusion etiology
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can be transudate (CHF, overhydration, hypoproteinemia) or exudate (TB, neoplasia) or hemopericardium (aortic aneurysm, aortic dissection, penetrating trauma, free wall rupture, bleeding due to coagulation defects)
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pericardial effusion diagnosis and treatment
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echo is gold standard showing echo-free space between posterior pericardium and posterior left ventricular epicardium; or heart swinging freely in pericardial sac; x-ray shows water-bottle configuration of cardiac silhouette; treat with pericardiocentesis and etiology cure
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cardiac tamponade etiology
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neoplasia
viral TB or suppurative pericarditis intrapericardial hemorrhage wounds postpericardiotomy uremia mediastinal radiotherapy vasculitis |
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cardiac tamponade manifestations
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dyspnea
fatigue orthopnea neck vein distention hypotension decreased heart sounds pulsus paradoxus (dissapearance during inspiration) |
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cardiac tamponade diagnosis and treatment
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clinical + echo + catheterization to confirm left and right atrial pressures
pericardiocentesis, subxiphoid surgical drainage |
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Kussmaul sign
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jugular venous distention that increases with inspiration
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constrictive pericarditis etiology
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thickening of pericardium due to idiopathic
open-heart surgery thoracic radiation postviral infection |
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constrictive pericarditis manifestations
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dyspnea on exertion
orthopnea (50%) right congestion signs Kussmaul sign distant heart sounds early diastolic apical pericardial knock confused with S3 |
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constrictive pericarditis diagnosis
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CT is gold standard and shows pericardial thickening and calcifications
x-ray: normal heart EKG: low-voltage T waves |
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2nd degree Mobitz I AV block
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progressive prolongation of PR interval until P wave is blocked and ventricular beat is dropped
normal QRS PR interval shortens after dropped beat; RR interval narrows progressively; RR interval is narrower after dropped beat |
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2nd degree Mobitz II AV block
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blocked ventricular beat not preceded by PR changes
site of block is usually infranodal wide or narrow QRS if PR is prolonged, the duration is constant |
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3rd degree AV block
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all atrial beats are blocked; complete dissaciation between PR and QRS
due to fibrous degenerative changes in elderly, inferior or posterior infarction, infiltrative or granulomatous diseases, digitalis, ankylosing spondylitis Adam-Stoke (sudden asystole or ventricular tachyarrhythmias) are common associated with bradycardia and congestion treat with pacemaker |
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paroxysmal supraventricular tachycardia presentation
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ectopic tachyarrhythmias with sudden onset and termination
regular rhythm between 130-220 beats initiated by supraventricular premature beat 80% are by re-entry; |
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paroxysmal supraventricular tachycardia treatment
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right carotid massage is first line
IV verapamil or adenosine is preferred second line or IV propanolol, esmolol or digitalis cardioversion if unstable |
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multifocal atrial tachycardia
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irregular supraventricular rhythm between 100-200 beats
QRS preceded by P but P waves vary in morphology |
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atrial flutter
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regular rhythm with ventricular rate of 125-150 and atrial rate of 250-300; treat with cardioversion if unstable OR digitalis, verapamil, betablockers
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atrial fibrillation etiology
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associated with heart disease (rheumatic fever, coronary artery disease, CHF, hypertension)
noncardiac (hyperthyroidism, hypoxemia, alcohol intoxication) lone AF (~30%, no structural disease) idiopathic |
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atrial fibrillation presentation
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supraventricular tachyarrhythmia with disorganized fribrillatory waves that replace P waves that vary in morphology and are irregular along with rapid ventricular response (iregularly irregular); shortness of breath, dizziness, palpitations
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EKG in flutter Vs. atrial fibrillation
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flutter waves that replace P waves (atrial contractions) are more regular than fibrillatory waves which are irregularly irregular
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atrial fibrillation diagnosis
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exam: severity, clinical type (paroxysmal, persistent, first episode), frequency, duration, precipitating factors and associated disease
x-ray: lung disease EKG: verifies rhythm, LVH, pre-excitation, prior MI echo: LVH, valve disease, atrial size thyroid function: exclude hyperthyroidism |
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atrial fibrillation management
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if hemodynamically unstable --> sedation and cardioversion
else --> control rate with diltiazem, verapamil, B-blocker or digoxin if no spontaneous conversion to sinus rhythm and AF > 48 hours --> immediate cardioversion else --> anticoagulation and elective cardioversion in 3 weeks if AF persists --> long-term anticoagulation (warfarin) and rate control; catheter ablation is also common |
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cardioversion drugs
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amiodarone, defetilide, felicanide, ibutilide, propafenone, quinidine
"PROPer cardioversion DEFEcates amiodarone" drugs to maintain sinus rhythm: amiodarone, disopyramide, defetilide, flecainide, propafenone, sotalol "PROPer rhythm DEFEcates Amiodarone and DISses Sotalol" |
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complications of cardioversion
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thromboembolism --> both electrical and pharmacologic
use anticoagulants if elective cardioversion torsade de pointes --> drug cardioversion |
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Wolf-Parkinson-White syndrome diagnosis
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ventricle is pre-excited by accesory pathway (Kent bundle); associated with paroxysmal supraventricular arrhythmia, atrial fibrillation and flutter
EKG shows short PR interval, wide QRS wave and delta waves "delta PRwIDE" |
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Wolf-Parkinson-White syndrome management
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if hemodynamically unstable --> immediate electrical cardioversion
else --> procainamide (digoxin, CCBs and BBs can inhibit normal pathway and are not indicated) definitive treatment is ablation |
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ventricular tachycardia etiology
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3 or more consecutive ventricular beats at rate >120b/min with wide and bizarre QRS
due to IHD MI cardiomyopathies mitral prolapse metabolic imbalances digoxin toxicity thioridazines |
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ventricular tachycardia presentation
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hypotension, CHF, syncope, cardiac arrest
variation in systolic pressure and intesity of heart sounds, intermittent canon waves in jugular venous pulse, extra heart sounds wide split between S1 and S2 due to asynchronous ventricular beats |
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ventricular tachycardia management
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if pulse is not present --> treat as ventricular fibrillation
else if stable pulse --> O2, IV access, lidocaine/amiodarone or procainamide or if hemodynamically unstable, cardioversion if unstable pulse --> O2, IV access, sedation, electrical cardioversion (100, 200, 300, 360J) |
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differential diagnosis of arrhythmias by QRS complex
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wide and regular: VT, SVT aberration, WPW
wide and irregular: AF rarely narrow and regular: ST, PSVT, AFL narrow and irregular: AF, MAT |
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torsades de pointes etiology
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undulating QRS on EKG baseline initiated by long-QT arrhythmias; drugs:
quinidine procainamide disopyramide phenothiazines thioridazine tricyclics lithium hypokalemia hypomagnesemia subarachnoid or intracerebral hemorrhage |
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torsades de pointes diagnosis and treatment
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undulating QRS
recurrent dizziness syncope treat underlying disorder replace antiarrhythmic with lidocaine or phenytoin cardiac pacing isoproterenol (shortens QT) if hemodynamically unstable then electrical cardioversion |
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ventricular fibrillation presentation
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significant activity on EKG with completely disorganized pattern
dead person (no pulse, no breathing, etc…) with VF EKG |
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ventricular fibrillation treatment
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CPR, electrical cardioversion, epinephrine, amiodarone (follow ACLS pulseless arrest algorhythm)
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