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72 Cards in this Set
- Front
- Back
Class IC antiarrhythmics are contraindicated in |
after MI (increases risk of polymorphic VT)
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Class III agents (not amio) initiated, what to watch out for? |
start in–patient over 3 days to monitor for torsades, if QTc >500 or increases by >15% or 60msec, decrease or discontinue dose |
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S/E of amiodarone
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thyroid dysfunction, liver toxicity, pulmonary fibrosis, and skin hypersensitivity
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advantages of the newest antiarrhythmic agent dronedarone
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reduce hospitalization or death in Afib atrial or flutter, and less side effects cf amio
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S/E of dronedarone
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increased crea but does not change GFR; do not use in NYHA II or III with recent decompensation or Class IV; should not be used as rate control agent in those with permanent AFib
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MOA of adenosine
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blocks the A1 receptors in the AV node and can terminate reentrant SVTs
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what is paroxysmal, persistent and permanent Afib
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terminates on its own – paroxysmal; >7days – persistent; continuous and cardioversion has failed or no longer attempted – permanent
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atrial fibrillation occurs in the absence of structural heart disease in a patient younger than 60 years
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lone Afib
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Afib >48 hours, two strategies before cardioversion
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warfarin x 3 weeks then cardiovert or full anticoagulation then TEE, if NEG, then cardiovert
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post cardioversion of Afib, next step?
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4 weeks of warfarin with goal INR 2–3 because atrium is stunned
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when should cardioversion be done emergently in Afib?
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hypotension, angina or heart failure
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goal INR in patients with rheumatic mitral stenosis and atrial fibrillation
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2–3
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If a mechanical heart valve is present in a patient with atrial fibrillation, the level of anticoagulation is based on the type of valve, with a minimum INR of
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2.5
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Prasugrel in Afib?
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There is currently no role for prasugrel for stroke prophylaxis in atrial fibrillation
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RE–LY trial
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dabigatran was shown to be superior to warfarin in preventing ischemic and hemorrhagic stroke, with a reduced risk of life–threatening bleeding but a higher risk of gastrointestinal bleeding
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Rivaroxaban for Afib?
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approved for prevention of stroke and systemic embolism in atrial fibrillation. It is noninferior to warfarin for stroke prevention with no difference in major bleeding, but demonstrates a reduction in intracranial hemorrhage
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when should oral anticoagulation be interrupted in patients with Afib needing invasive procedures
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If the patient has a low short–term risk (CHADS2 score of 0–2) and the duration of interruption is less than 1 week, then bridging is not needed. If the patient has a higher short–term risk (CHADS2 score of 5–6, recent stroke, mechanical or rheumatic mitral valve) or if the interruption is more than 1 week, then use of a bridging agent should be considered more strongly
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resting heart rate goal for Afib
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<110 /min
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“pill–in–the–pocket” approach for patients with symptomatic paroxysmal Afib
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short–acting B–blocker or calcium blocker 30 minutes before flecainide or propafenone
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anticoagulation after afib ablation
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continue warfarin x 2–3 months, thereafter guided by CHADS2 score
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Nonpharmacologic strategies for Afib
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Afib ablation, AV node ablation, maze surgery
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involves several incisions or ablations in the right and left atria to interrupt potential reentrant pathways required for atrial fibrillation maintenance
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Maze surgery |
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causes of bradycardia
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dysfunction of sinus node, AV node, or His–Purkinje system; + reversible causes KIDLAT! (hyperK, drugs, Lyme, Thyroid disease)
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underlying cause of pathologic sinus bradycardia in most patients
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fibrotic replacement of the sinus node associated with aging (other causes – infarction, surgery damage, infiltrative processes, inc vagal tone, meds, genetic diseases)
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pathology in second degree AV blocks
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Mobitz type 1 is disease within AV node, type 2 more worrisome suggesting His Purkinje disease; HR of progressing to CHB
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two or more nonconducted P waves occur for each QRS complex
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Advanced second–degree heart block, or high–grade heart block
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pathology in CHB
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conduction block in His bundle or below
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treatment for symptomatic sinus bradycardia or heart block without reversible causes
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permanent pacemaker
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common causes of sinus tachycardia
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pain, fever, anxiety, anemia; in younger, SVTs, in older, AFib, aflutter, Vtach; any age – PACs and PVCs
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Class II and Class IV antiarrhythmics are contraindicated in
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decompensated systolic HF or WPW syndrome
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Class IC antiarrhythmics are contraindicated in
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after MI (increases risk of polymorphic VT)
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Class III agents (not amio)initiated, waht to watch out for?
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start in–patient over 3 days to monitor for torsades, if QTc >500 or increases by >15% or 60msec, decrease or discontinue dose
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usual rate of Aflutter
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250–350
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treatment of Aflutter
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same as afib
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usual site of flutter ablation
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isthmus between IVC and TV
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the most frequent paroxysmal SVTs
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AVNRT, AV reciprocating tachycardia (AVRT), atrial tachycardia
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short RP tachycardias
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AVNRT, AVRT, junctional tachycardia
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long RP tachycardias
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atrial tachycardia, sinus tachycardia, atypical AVNRT, and permanent form of junctional reciprocating tachycardia
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how does adenosine work in SVT?
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Blocks AV node conduction transiently,interrupts reentrant circuit, terminates AVNRT, AVRT. slows rate to demonstrate P waves in other SVTs (Afib, ST, atrial tach)
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most common paroxysmal SVT
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AVNRT
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treatment of AVNRT (7)
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vagal maneuvers, adenosine, β–blockers, nondihydropyridine calcium channel blockers, antiarrhythmic agents, or cardioversion; cath ablation also has high success rate
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a reentrant circuit that includes a bypass pathway and the AV node
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Atrioventricular Reciprocating Tachycardia
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WPW pattern vs syndrome
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preexcitation pattern on ECG = "WPW pattern"; pattern + symptoms (tachycardia) = "WPW syndrome"
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Risk factors for VF in patients with WPW syndrome (4)
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a history of AVRT, a rapidly conducting bypass pathway, multiple bypass pathways, Ebstein anomaly.
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first line therapy for patients with AVRT with symptoms and preexication, with history of rapid Afib
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catheter ablation
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preferred agents in AVRT
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procainamide and amiodarone (slows conduction down bypass pathway acutely) and not AV nodal blocking medications
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treatment of AVRT without preexcitation on EKG
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catheter ablation, β–blockers or antiarrhythmic agents
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treatment of PACs
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if symptomatic, B blockers or calcium blockers; usually needs only reassurance
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caused by an ectopic focus or area of micro–reentry that fires faster than the sinus rate
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atrial tachycardia
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treatment of atrial tach
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β–blockers, calcium channel blockers, digoxin, or antiarrhythmic agents; cath ablation also an option
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an irregular tachycardia that demonstrates three or more P waves of different morphologies and is usually associated with underlying pulmonary disease
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multifocal atrial tach
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treatment of MAT
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treat pulmonary disease, electrolyte repletion, and, occasionally, β–blockers or calcium channel blockers
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treatment of symptomatic PVCs
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B blocker or calcium blocker; antiarrhythmic agents rarely required; cath ablation if medical therapy failed
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define sustained VT
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lasts >30 secs or produces hemodynamic collapse
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*treatment of idiopathic VT
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mild – no treatment; frequent or severe Sx – calcium blockers or beta blockers, class I or III antiarrhythmic, cath ablation; ICD is not indicated
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the most common channelopathy
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Long QT syndrome
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mainstay of therapy in long QT syndrome
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b blockers
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drugs to avoid in long QT syndrome
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haldol, sotalol, erythromycin
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treatment for short QT syndrome
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quinidine to prolong QT interval; offer ICD
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what is Brugada syndrome
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a pattern of 2 mm or greater J–point elevation, coved ST–segment elevation, and T–wave inversions in leads V1 to V3 with an increased risk of syncope, VF, and sudden cardiac arrest
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VT during times of high adrenergic tone, carrying a high risk of SCD
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catecholaminergic polymorphic VT
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treatment of catecholaminergic polymorphic VT
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avoid exercise, beta blockers, ICD
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fibrofatty infiltration of the right ventricle resulting from dysfunction of the desmosome
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ARVC/D
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EKG findings in ARVC/D
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Tinv V1–V3, epsilon wave |
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treatment of ARVC/D
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avoid exercise, ICD; no medical therapy to delay progression; B blockers, sotalol, amio and cath ablation can reduce ICD shocks
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treatment of symptomatic bradycardia (4)
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atropine, if ineffective, dopamine and epinephrine, until transcutaneous or transvenous pacing is initiated (ADEPt)
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NOTE: In infections of cardiac devices,
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it is important to not attempt aspiration of the device site because this can damage the leads.
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x most common cause of acute pericarditis
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viral infection
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How is diagnosis of pericarditis confirmed?
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2 of 3 classic findings: CP, pleuritic; friction rub; diffuse ST segment elevation; if (+) unexplained pericard effusion on echo, only 1 of 3 necessary
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unique feature of chest pain in acute pericarditis
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worsens in recumbent position
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pericardial friction rub is best auscultated at
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left lower sternal border during suspended respiration while leaning forward
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EKG in myopericarditis
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concave downward ST segment elevation like MI
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