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72 Cards in this Set

  • Front
  • Back

Class IC antiarrhythmics are contraindicated in

after MI (increases risk of polymorphic VT)

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

S/E of amiodarone
thyroid dysfunction, liver toxicity, pulmonary fibrosis, and skin hypersensitivity
advantages of the newest antiarrhythmic agent dronedarone
reduce hospitalization or death in Afib atrial or flutter, and less side effects cf amio
S/E of dronedarone
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
MOA of adenosine
blocks the A1 receptors in the AV node and can terminate reentrant SVTs
what is paroxysmal, persistent and permanent Afib
terminates on its own – paroxysmal; >7days – persistent; continuous and cardioversion has failed or no longer attempted – permanent
atrial fibrillation occurs in the absence of structural heart disease in a patient younger than 60 years
lone Afib
Afib >48 hours, two strategies before cardioversion
warfarin x 3 weeks then cardiovert or full anticoagulation then TEE, if NEG, then cardiovert
post cardioversion of Afib, next step?
4 weeks of warfarin with goal INR 2–3 because atrium is stunned
when should cardioversion be done emergently in Afib?
hypotension, angina or heart failure
goal INR in patients with rheumatic mitral stenosis and atrial fibrillation
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
Prasugrel in Afib?
There is currently no role for prasugrel for stroke prophylaxis in atrial fibrillation
RE–LY trial
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
Rivaroxaban for Afib?
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
when should oral anticoagulation be interrupted in patients with Afib needing invasive procedures
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
resting heart rate goal for Afib
<110 /min
“pill–in–the–pocket” approach for patients with symptomatic paroxysmal Afib
short–acting B–blocker or calcium blocker 30 minutes before flecainide or propafenone
anticoagulation after afib ablation
continue warfarin x 2–3 months, thereafter guided by CHADS2 score
Nonpharmacologic strategies for Afib
Afib ablation, AV node ablation, maze surgery
involves several incisions or ablations in the right and left atria to interrupt potential reentrant pathways required for atrial fibrillation maintenance

Maze surgery

causes of bradycardia
dysfunction of sinus node, AV node, or His–Purkinje system; + reversible causes KIDLAT! (hyperK, drugs, Lyme, Thyroid disease)
underlying cause of pathologic sinus bradycardia in most patients
fibrotic replacement of the sinus node associated with aging (other causes – infarction, surgery damage, infiltrative processes, inc vagal tone, meds, genetic diseases)
pathology in second degree AV blocks
Mobitz type 1 is disease within AV node, type 2 more worrisome suggesting His Purkinje disease; HR of progressing to CHB
two or more nonconducted P waves occur for each QRS complex
Advanced second–degree heart block, or high–grade heart block
pathology in CHB
conduction block in His bundle or below
treatment for symptomatic sinus bradycardia or heart block without reversible causes
permanent pacemaker
common causes of sinus tachycardia
pain, fever, anxiety, anemia; in younger, SVTs, in older, AFib, aflutter, Vtach; any age – PACs and PVCs
Class II and Class IV antiarrhythmics are contraindicated in
decompensated systolic HF or WPW syndrome
Class IC antiarrhythmics are contraindicated in
after MI (increases risk of polymorphic VT)
Class III agents (not amio)initiated, waht 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
usual rate of Aflutter
treatment of Aflutter
same as afib
usual site of flutter ablation
isthmus between IVC and TV
the most frequent paroxysmal SVTs
AVNRT, AV reciprocating tachycardia (AVRT), atrial tachycardia
short RP tachycardias
AVNRT, AVRT, junctional tachycardia
long RP tachycardias
atrial tachycardia, sinus tachycardia, atypical AVNRT, and permanent form of junctional reciprocating tachycardia
how does adenosine work in SVT?
Blocks AV node conduction transiently,interrupts reentrant circuit, terminates AVNRT, AVRT. slows rate to demonstrate P waves in other SVTs (Afib, ST, atrial tach)
most common paroxysmal SVT
treatment of AVNRT (7)
vagal maneuvers, adenosine, β–blockers, nondihydropyridine calcium channel blockers, antiarrhythmic agents, or cardioversion; cath ablation also has high success rate
a reentrant circuit that includes a bypass pathway and the AV node
Atrioventricular Reciprocating Tachycardia
WPW pattern vs syndrome
preexcitation pattern on ECG = "WPW pattern"; pattern + symptoms (tachycardia) = "WPW syndrome"
Risk factors for VF in patients with WPW syndrome (4)
a history of AVRT, a rapidly conducting bypass pathway, multiple bypass pathways, Ebstein anomaly.
first line therapy for patients with AVRT with symptoms and preexication, with history of rapid Afib
catheter ablation
preferred agents in AVRT
procainamide and amiodarone (slows conduction down bypass pathway acutely) and not AV nodal blocking medications
treatment of AVRT without preexcitation on EKG
catheter ablation, β–blockers or antiarrhythmic agents
treatment of PACs
if symptomatic, B blockers or calcium blockers; usually needs only reassurance
caused by an ectopic focus or area of micro–reentry that fires faster than the sinus rate
atrial tachycardia
treatment of atrial tach
β–blockers, calcium channel blockers, digoxin, or antiarrhythmic agents; cath ablation also an option
an irregular tachycardia that demonstrates three or more P waves of different morphologies and is usually associated with underlying pulmonary disease
multifocal atrial tach
treatment of MAT
treat pulmonary disease, electrolyte repletion, and, occasionally, β–blockers or calcium channel blockers
treatment of symptomatic PVCs
B blocker or calcium blocker; antiarrhythmic agents rarely required; cath ablation if medical therapy failed
define sustained VT
lasts >30 secs or produces hemodynamic collapse
*treatment of idiopathic VT
mild – no treatment; frequent or severe Sx – calcium blockers or beta blockers, class I or III antiarrhythmic, cath ablation; ICD is not indicated
the most common channelopathy
Long QT syndrome
mainstay of therapy in long QT syndrome
b blockers
drugs to avoid in long QT syndrome
haldol, sotalol, erythromycin
treatment for short QT syndrome
quinidine to prolong QT interval; offer ICD
what is Brugada syndrome
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
VT during times of high adrenergic tone, carrying a high risk of SCD
catecholaminergic polymorphic VT
treatment of catecholaminergic polymorphic VT
avoid exercise, beta blockers, ICD
fibrofatty infiltration of the right ventricle resulting from dysfunction of the desmosome
EKG findings in ARVC/D

Tinv V1–V3, epsilon wave

treatment of ARVC/D
avoid exercise, ICD; no medical therapy to delay progression; B blockers, sotalol, amio and cath ablation can reduce ICD shocks
treatment of symptomatic bradycardia (4)
atropine, if ineffective, dopamine and epinephrine, until transcutaneous or transvenous pacing is initiated (ADEPt)
NOTE: In infections of cardiac devices,
it is important to not attempt aspiration of the device site because this can damage the leads.
x most common cause of acute pericarditis
viral infection
How is diagnosis of pericarditis confirmed?
2 of 3 classic findings: CP, pleuritic; friction rub; diffuse ST segment elevation; if (+) unexplained pericard effusion on echo, only 1 of 3 necessary
unique feature of chest pain in acute pericarditis
worsens in recumbent position
pericardial friction rub is best auscultated at
left lower sternal border during suspended respiration while leaning forward
EKG in myopericarditis
concave downward ST segment elevation like MI