EP / EKG Flashcards
BP goal: - > 60 years
less than 150/90
BP Goal: -less than 60 years -CKD -DM
less than 140/90
Initial BP treatment: -Black
-Thiazide diuretic or -CCB *ACE/ARB not first line
Initial BP treatment -Other ethnicities
Any single agent or combination: -Thiazide -ACE/ARB -CCB
Initial BP treatment -all ethnicities with CKD or DM
ACE/ARB -alone or in combination with other agents
What did the ACCOMPLISH trial show?
dual therapy with ACE + CCB was superior to ACE + Thiazide in reducing CV events
What are indications for ambulatory BP monitoring?
-discrepancy between the BP readings at home and in-office (“white coat” hypertension) -Suspected paroxysmal hypertension (pheochromocytoma) -Suspected autonomic dysfunction -Hypertension refractor to treatment -Hypotensive symptoms while on antihypertensive therapy
Define intrinsicoid deflection -Where is it seen?
-time from onset of the earliest Q or R wave to the peak of the R wave in the lateral leads (aVL, V5-V6) -represents the time taken for excitation to spread from the endocardial to the epicardial surface of the left ventricle -R wave peak time is said to be prolonged if > 45 ms -Seen in: LAFB, LVH, LBBB
EKG findings of LVH:
-increased amplitude (voltage) of QRS -supported (and strengthened) by presence of secondary ST-T wave changes -Other: left atrial abnormality, LAD, and/or prolonged intrinsicoid deflection, prominent U waves may be present
EKG Criteria for LVH (Sokolow and Lyone):
Precordial leads -Sv1 and R v5 or v6 > 35 mm -R v5 or v6 > 25 mm Limb leads -R aVL > 11 mm
EKG Criteria for LVH (Romhilt and Estes Point system)
**5 or more = LVH, 4 or more = probably LVH** Amplitude (any of the following) = 3 points -Any limb lead R or S > 20 mm -Sv1 or Sv2 > 30 mm -Rv5 or Rv6 > 30 mm ST-T change = 3 points (1 with digitalis) Left atrial abnormality = 3 points Left axis deviation (-30 or more) = 2 points Intrinsicoid deflection = 1 point
EKG Criteria for LVH (Cornell)
Men: Ravl + Sv3 > 28 mm Women: Ravl + Sv3 > 20 mm
EKG Criteria for left atrial abnormality
-Prominent notching of P-wave (especially L2) with P-wave duration > 0.12s -Leftward shift of P-wave axis -Increased duration and depth of terminal negative portion of P in V1 ( > 0.04 mm-sec)
What four factors determine the transmembrane voltage (membrane potential) across the cell membrane in cardiac myocytes?
Concentration of ions on the inside/outside the cell -inside (high in Na and Ca) -Outside (high in K) -electrochemical gradients control the range of transmembrane voltages that can be achieved when ion channels open Permeability of the cell membrane to those ions (Ion conductances) -controlled by the opening/closing of specific ion channel proteins Activity of electrogenic transporters -Na-K ATPase, Na-Ca exchange, Ca transport pumps -maintain ion concentrations across the cell membrane Current flowing from neighboring interconnected myocytes via gap junctions -gap junction channel is composed of two connexons or hemichannels that connect across the intercellular space
Cardiac Action potential: Phase 0
-upstroke or rapid depolarization of the action potential -in most cells it is dominated by Na ions entering through voltage-gated Na channels -peak voltage may reach +30 - +40 mV -in SA and AV nodal tissue –> depolarization is carried mainly by T- and L-type Ca channels
Cardiac action potential: Phase 1
-initial or rapid early depolarization -caused by rapid inactivation of Na current (Ina) and by activation of transient outward current (Ito) carried mostly by K ions *Ito is composed of two components (Ito1, Ito2)
Cardiac action potential: Phase 2
-plateau of the action potential (several hundred msec long in some cardiac cells, such as Purkinje) -phase that distinguishes a cardiac action potential from a neuronal action potential -most complex part of the action potential because many small amplitude currents flow through several ion channels *Inward (depolarizing current) -late inactivating Na channels (INa) -L-type calcium channels (ICa-L) *Outward (repolarizing current) -K channels *(Ito) inactivation *activation of rapidly (Ikr), slowly (IKs), delayed rectifier K channels and electrogenic transporters
Mechanisms of tachyarrhythmias
Reentry -Atrial flutter -AV nodal reentrant tachycardia -AV reentrant tachycardia (WPW) -Atrial fibrillation (multiple reentrant loops) Abnormal automaticity -Atrial tachycardia -Accelerated junctional rhythm Triggered activity (EAD’s) -Torsades de pointes / LQTS Triggered activity (DAD’s) -Bidirectional VT due to Ca overload (digitalis toxicity, ischemia) -Outflow tract tachycardias / VT
Mechanism for Reentry tachycardias (must contain)
-areas with fast and slow conduction velocities -varying refractory periods in these areas (refractoriness is usually longer in the fast pathway -implied is that there must be a core about which the circuit moves (a fixed or functional core)
Initiation of a reentrant loop is thought to depend on this?
development of an area of unidirectional block so that an electrical wave front (action potential depolarization) may circulate in one direction around the re-entrant loop
Mechanisms for terminating Reentry tachycardia
interventions that modify action potential conduction -suppression of Na or Ca channels to slow or block conduction refractoriness -block or stimulation of K channels to change action potential duration and refractoriness functional properties -improving ischemia so that an area of functional or unidirectional block disappears interventions that electrically interrupt the conditions needed to maintain the re-entrant loop -delivering a small electrical shock to depolarize or block a small part of the re-entrant loop, delivering a large electrical shock to depolarize most of all of the re-entrant loop, or ablating tissue critical to the re-entrant loop
Key characteristics of RVH
-R/S ratio in V1 > 1 and R wave > 5mm -QR in V1 -RAD -Right atrial enlargement -S1Q3T3 pattern and S1S2S3 pattern *S1S2S3 pattern due to RVH = (SII > SIII)
EKG criteria for Right atrial enlargement
-peaked P (amplitude > 2.5 mm) in leads II, III, and aVF -Rightward shift in P-wave axis ( > +75) -Increased area ( >0.06 mm/sec or amplitude > 1.5 mm) of initial positive portion of P wave in V1
Differential diagnosis of RAD
-RVH -Lateral wall MI -Left posterior hemiblock -COPD -Normal Young Adult
Differential diagnosis: Prominent R wave or R/S ratio in V1
-RVH -Ventricular Pre-excitation (WPW) -Posterior wall MI -Hypertrophic Cardiomyopathy -If qR pattern, incomplete RBBB with septal MI -Normal Variant
EKG findings: Acute PE
-Rightward shift of the QRS axis ( > 90 or indeterminate) -S1Q3T3 pattern -Incomplete or complete RBBB (often transient) -ST-segment deviation (depression or elevation) in V1-V2 -Sinus tachycardia, atrial flutter, atrial fibrillation
RBBB diagnostic criteria
-Broad QRS > 120 ms -RSR’ pattern in V1-V3 (M-shaped QRS complex) -Wide, slurred S wave in the lateral leads (I, aVL, V5-V6)
Causes of RBBB
-RVT / cor pulmonale -PE -Ischemic heart disease -Rheumatic heart disease -Myocarditis or cardiomyopathy -Degnerative disease of the conduction system -Congenital heart disease (e.g. ASD)
Incomplete RBBB criteria
-RSR’ patterin in V1-V3 with QRS duration < 120 ms *Normal variant often seen in children (of no clinical significance)
RBBB pathophysiology
-activation of the RV is delayed as depolarization has to spread across the septum from the LV -LV is activated normally, meaning that the early part of the QRS is unchanged -Delayed RV activation produces a secondary R wave (R’) in the right precordial leads (V1-V3) and a wide, slurred S wave in the lateral leads -Delayed activation of the RV also gives rise to secondary repolarization
Define “use dependence” -what class of drugs demonstrate this?
-strength of blockade or action of the antiarrhythmic drug is enhanced at faster heart rates -at faster heart rates -> more sodium channels in an open or inactivated state -> these drugs have a greater binding affinity to their receptors in the open or inactivated state -Class I antiarrhythmics
Define “reverse use dependence” -what class of drugs demonstrate this?
-strength of blockade or action of the antiarrhythmic drug is enhanced at slower heart rates -Class III antiarrhythmics
Sodium channel blocking agents that are contraindicated in CAD or heart failure?
-Flecainide -Propafenone
Antiarrhythmic contraindicated in permanent AF or severe HF?
Droneaderone
Class I antiarrhythmics: -Ion effected -mechanism of action -examples
-Na -block inward sodium current during phase 0 of action potential -Procainamide, Quinidine, Disopyramide, Propafenone, Flecainide
Indications for PPM in SND - Class I
-Symptomatic sinus bradycardia and pauses -Symptomatic chronotropic incompetence -Symptomatic sinus bradycardia due to required drug therapy
Indications for PPM in SND - Class IIa
-HR < 40 bpm and symptoms consistent with bradycardia but clear association between bradycardia and symptoms is undocumented -Unexplained syncope and abnormal sinus node function on EP study
Indications for PPM in SND - Class IIb
-Minimally symptomatic patients with chronic HR < 40 bpm while awake
Indications for PPM in SND - Class III
-SND in asymptomatic patients -SND in patients with symptoms documented in absence of bradycardia -Symptomatic bradycardia due to non-essential drug therapy
Indications for PPM in AV nodal disease - Class I
-CHB or ASDB with bradycardia and symptoms or ventricular arrhythmias presumed due to block -CHB or ASDB with arrhythmias or other conditions requiring drug therapy resulting in bradycardia -CHB or ASDB with pause > 3 seconds, escape rate < 40 bpm or below the AV node -CHB or ASDB with A-fib and pause > 5 seconds -CHB or ASDB after cathter ablation of the AV junction -CHB or ASDB after cardiac surgery not expected to resolve -CHB or ASDB associated with neuromuscular disorders -Second-degree AV block of any type with symptomatic bradycardia -Second or third degree AV block with exercise without ischemia -CHB with HR > 40 bpm in the setting of cardiomegaly or LV dysfunction or site of block is below the AV node -Asymptomatic Mobitz II block with wide QRS
Indications for PPM in AV nodal disease - Class IIa
-CHB with HR > 40 bpm in asymptomatic individuals without cardiomegaly -Asymptomatic second-degree AV block with intra- or infra-Hisian block found on EPS -First or second-degree AV block with symptoms -Asymptomatic Mobitz II block with narrow QRS
Indications for PPM in AV nodal disease - Class IIb
-AV block of any degree in the setting of neuromuscular disease with or without symptoms - AV block in the setting of drug toxicity that my recur even when drug is withdrawn
Indications for PPM in AV nodal disease - Class III
-Asymptomatic first-degree AV block -Asymptomatic Mobitz I or Wenckebach block -AV block that is expected to resolve (reversible drug effect, Lyme disease, transient increase in vagal tone or during hypoxia and sleep apnea)
EKG criteria: Left Anterior Fascicular Block (LAFB)
LAD (usually between -45 and -90) Small Q waves with tall R waves (= ‘qR complexes’) in leads I and aVL Small R waves with deep S waves (=’rS complexes’) in leads II, III, aVF QRS duration normal or slightly prolonged (80-110 ms) Prolonged R wave peak time in aVL > 45 ms Increased QRS voltage in the limb leads **QRS voltage in aVL may meet voltage criteria for LVH (R wave > 11 mm), but there will be no LV strain pattern
EKG findings: Ostium Primum ASD
-rSR’s’ in lead V1 + -Left axis deviation *Normal axis = Ostium secundum *Low atrial rhythm = sinus venosus ASD
Describe EKG leads
Bipolar limb leads (frontal plane) -I, II, III Augmented unipolar limb leads (frontal plane) -aVR, aVL, aVF Unipolar chest / Precordial leads (horizontal plane) -V1, V2, V3 (Posterior Anterior) -V4, V5, V6 (Right, Left or Lateral)
What is poor R wave progression?
refers to the absence of the normal increase in size of the R wave in the precordial leads when advancing from V1-V6
What does it mean/causes?
-Old anterior wall MI -LBBB or LAFB -LVH -RVH -Normal Variant -WPW -Dextrocardia or lead misplacement -Tension PTX with mediastinal shift -Congenital heart disease
What to look for if an unexpected pause in sinus rhythm?
look at preceding T wave to ensure there is no “hidden” P wave that did not conduct because it came early
STEMI area which may not demonstrate prominent EKG changes?
Lateral (especially high-lateral) wall -likely the result of the amount of myocardium involved and the site relative to the EKG electrodes
What is Ashman phenomenon (Ashman beat)?
-occurs when a premature supra ventricular beat occurs before the right bundle branch has recovered from its refractory period –> results in the PVC being displayed as RBBB -frequently occurs with PAC’s, however can also be seen in A-fib, atrial tachycardia as R-R intervals can vary -No clinical significance, patient’s may feel palpitations
Define Atrial tachycardia
-least common form of PSVT (~10%) -long R-P tachycardia with P wave morphology and PR interval that are distinct from sinus rhythm -usually abnormal P-wave axis (inverted in the inferior leads II, III, aVF) -AV block may be present (generally a physiological response to rapid HR) -Not dependent on AV node –> will not terminate with AV block -May be periods of variable conduction with more P’s than QRS’s
Atrial tachycardia: -Diagnosis
-EKG findings -IV adenosine can be used acutely to promote AV block and expose P-waves -Automatic or micro-re-entrant focal rhythm would not be expected to terminate with adenosine -15-20% of AT’s can respond to IV adenosine.
Atrial tachycardia: -Treatment
-Often termination is spontaneous -Medical therapy (BB’s, CCB’s) often used for symptomatic relief if AT frequent -hemodynamic compromise –>cardioversion -Frequent, symptomatic episodes from a single focus with high AT burden –> catheter ablation (85-90% success rates)
EKG finding of diffuse subendocardial injury, multivessel disease or LM disease?
-Widespread horizontal ST depression (most prominent in I, II, V4-V6) -ST elevation in aVR > 1 mm -ST elevation in aVR > V1 *ST elevation in aVR is reciprocal to vector in anterior, inferior, lateral walls (ST depression)
Class IA Antiarrhythmics
-Quinidine -Disopyramide -Procainamide
Class IA Antiarrhythmics MOA
-slow conduction due to sodium channel blockade -block rapidly activating potassium channel (IKr) –> prolongation of the QT interval -Contraindicated in HF –> negative inotropic effects and potential for hypotension
Class IA antiarrhythmic used in J wave syndromes (Brugada and early repolarization syndromes) to prevent recurrences of VF
Quinidine
Procainamide uses and side effects
-Termination of A-fib in the setting of WPW (pre-excitation) -Used to unmask possible Brugada syndrome –> coved ST-segment elevation in right precordial leads -Can cause Drug-induced Lupus
Class IB antiarrhythmics
Lidocaine Mexilitine
Class IB antiarrhythmics uses
VT and VF -Lidocaine SE’s –> CNS toxicity (tinnitus, seizures, AMS, Coma) -Mexilitine SE’s –> tremor, blurred vision, dysphoria, dizziness)
What increases the risk of Lidocaine toxicity?
Heart failure -dose must be reduced by 50% Absence of P450 enzyme CYP2D6 -absent in 7% of the Caucasian population -Amiodarone and Citalopram will increase levels
Class IC antiarrhythmics MOA
-Flecainide and Propafenone -block sodium channels with slow association/dissociation channel kinetics -prolong PR and QRS intervals (flecainide can also increase QT)
Class IC antiarrhythmic contraindications
Structural heart disease
Propafenone additional MOA
-sodium channel blockade -Voltage dependent calcium currents -Potassium currents -BB properties (pronounced in poor metabolizers via CYP2D6)
Proarrhythmic events associated with Class IC antiarrhythmics (Flecainide, Propafenone)
Treatment of AF –> A flutter with RVR -should be used in conjunction AV nodal blocking agents Use dependent properties –> QRS widening at fast rates often mimicking VT
Contraindications to class IC antiarrhythmics
CAD and reduced LV function (particularly post-MI) -CAST (Cardiac Arrhythmia Suppression Trial): studied suppression ventricular arrhythmias post-MI -CASH (Cardiac Arrest Study Hamburg): prevention of sudden cardiac death and Brugada Syndrome -Sodium blockade may increase risk of VF
EKG findings of Arrhythmogenic RV Cardiomyopahthy (ARVC)
-Epsilon wave (most specific finding, seen in 30% of patients) -TWI in V1-V3 (85% of patients) -Prolonged S-wave upstroke of 55ms in V1-V3 (95% of patients) -Localized QRS widening of > 110msec in V1-V3 -Paroxysmal VT with LBBB morphology
Antiarrhythmic which has been shown to improve the efficacy of DC cardioversion in A-fib if used pretreatment?
Ibutilide
Antiarrhythmics always administered in-hospital due to the risk of QT prolongation and Torsades des pointes VT?
-Ibutilide -Dofetilide
Class IC antiarrhythmics adverse reaction in patients with A-fib? -Treatment?
-can convert A-fib –> A-flutter, resulting in 1:1 AV nodal conduction and dangerously rapid ventricular rates -AV nodal blocking agent should always be administered concomitantly
Antiarrhythmics used for pharmacologic cardioversion of A-fib?
-Class IC (Flecainide, Propafenone) -Class III (Ibutilide, Dofetilide)
Recommendations for anticoagulation in cardioversion of A-fib?
-3 weeks before and -4 weeks after
Cardioversion of A-fib that does not require anticoagulation?
AF events of < 48 hours in duration
What are the two strategies for anticoagulation in Cardioversion of A-fib?
Warfarin (INR > 2.0) or OAC for 3 weeks before / 4 weeks after cardioversion or TEE + Heparin/Lovenox/OAC immediately before Cardioversion –> Warfarin or OAC x 4 weeks after
AV nodal blocking agent contraindicated in WPW with pre-excited AF?
nondihydropyridine CCBs (verapamil, Diltiazem)
Considered in patients who have inadequate rate control after thorough trials of medical therapy and who fail or are not candidates for rhythm control?
AV node ablation + Permanent ventricular pacing
Major adverse affect associated with AVN ablation and permanent pacing?
Right-ventricular pacing-induced cardiomyopathy
What rhythm is present after AV nodal/junction ablation?
Junctional escape rhythm
What is an alternative or treatment for RV pacing induced cardiomyopathy?
-upgrade to Biventricular pacemaker (Cardiac resynchronization therapy)
Describe clinical outcomes of Sotalol use in patients with LVEF < 40% without defibrillators?
Increased Mortality -SWORD (Survival with Oral D-Sotalol trial) -OPTIC (Optimal Pharmacological Therapy in Cardioverter-Defibrillator Patients trial) -
What did the SWORD trial (Survival with Oral D-Sotalol) show?
-Sotalol was associated with increased mortality in LVEF < 40% -Trial was stopped early owing to excess mortality in the group randomized to Sotalol
What did the OPTIC (Optimal Pharmacological Therapy in Cardioverter-Defibrillator Patients) trial show?
Demonstrated superiority of amiodarone plus beta-blockers over sotalol for the suppression of ICD shock sin patients with ICD’s. *patients had to have LVEF < 40% to be enrolled
Typical (type I) atrial flutter is characterized by this:
“saw tooth” pattern in the inferior leads (II, III, aVF)
What do ratios of > 2:1 in A-flutter indicate?
presence of underlying conduction system disease -A flutter typically presents with 2:1 block -must be present in absence of AV nodal blocking agents
What are the indications for reduced dosing of Eliquis (Apixaban)?
-Age > 80 years -Body weight < 60 kg -Cr. > 1.5 *Reduce dose to 2.5 mg twice daily
Benefit of Cardiac resynchronization therapy is highest when this is present
AV nodal ablation –> allows for maximal biventricular pacing
What did the MADIT-RIT trial show?
-Multicenter Automatic Defibrillator Implantation Trial - Reduce Inappropriate Therapy -Investigated a strategy of a single zone at 200 bpm compared with conventional programming (VT zone - 170 bpm and VF zone - 200 bpm) -Trial also included a delayed-therapy arm that included a VT zone with a 60-second delayed detection -Showed that the single-zone program strategy resulted in a reduction in inappropriate therapies and improved survival
In a typical EP study:
-How many catheters are used and where are they positioned?
3 catheters
- Right atrium (RA)
- Right Ventricle (RV)
- “His position” (across the tricuspid valve)
- *
