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Medical > EP / EKG > Flashcards

EP / EKG Flashcards

1
Q

BP goal: - > 60 years

A

less than 150/90

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2
Q

BP Goal: -less than 60 years -CKD -DM

A

less than 140/90

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3
Q

Initial BP treatment: -Black

A

-Thiazide diuretic or -CCB *ACE/ARB not first line

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4
Q

Initial BP treatment -Other ethnicities

A

Any single agent or combination: -Thiazide -ACE/ARB -CCB

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5
Q

Initial BP treatment -all ethnicities with CKD or DM

A

ACE/ARB -alone or in combination with other agents

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6
Q

What did the ACCOMPLISH trial show?

A

dual therapy with ACE + CCB was superior to ACE + Thiazide in reducing CV events

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7
Q

What are indications for ambulatory BP monitoring?

A

-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

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8
Q

Define intrinsicoid deflection -Where is it seen?

A

-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

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9
Q

EKG findings of LVH:

A

-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

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10
Q

EKG Criteria for LVH (Sokolow and Lyone):

A

Precordial leads -Sv1 and R v5 or v6 > 35 mm -R v5 or v6 > 25 mm Limb leads -R aVL > 11 mm

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11
Q

EKG Criteria for LVH (Romhilt and Estes Point system)

A

**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

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12
Q

EKG Criteria for LVH (Cornell)

A

Men: Ravl + Sv3 > 28 mm Women: Ravl + Sv3 > 20 mm

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13
Q

EKG Criteria for left atrial abnormality

A

-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)

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14
Q

What four factors determine the transmembrane voltage (membrane potential) across the cell membrane in cardiac myocytes?

A

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

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15
Q

Cardiac Action potential: Phase 0

A

-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

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16
Q

Cardiac action potential: Phase 1

A

-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)

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17
Q

Cardiac action potential: Phase 2

A

-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

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18
Q

Mechanisms of tachyarrhythmias

A

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

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19
Q

Mechanism for Reentry tachycardias (must contain)

A

-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)

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20
Q

Initiation of a reentrant loop is thought to depend on this?

A

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

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21
Q

Mechanisms for terminating Reentry tachycardia

A

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

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22
Q

Key characteristics of RVH

A

-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)

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23
Q

EKG criteria for Right atrial enlargement

A

-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

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24
Q

Differential diagnosis of RAD

A

-RVH -Lateral wall MI -Left posterior hemiblock -COPD -Normal Young Adult

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25
Q

Differential diagnosis: Prominent R wave or R/S ratio in V1

A

-RVH -Ventricular Pre-excitation (WPW) -Posterior wall MI -Hypertrophic Cardiomyopathy -If qR pattern, incomplete RBBB with septal MI -Normal Variant

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26
Q

EKG findings: Acute PE

A

-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

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27
Q

RBBB diagnostic criteria

A

-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)

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28
Q

Causes of RBBB

A

-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)

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29
Q

Incomplete RBBB criteria

A

-RSR’ patterin in V1-V3 with QRS duration < 120 ms *Normal variant often seen in children (of no clinical significance)

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30
Q

RBBB pathophysiology

A

-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

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31
Q

Define “use dependence” -what class of drugs demonstrate this?

A

-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

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32
Q

Define “reverse use dependence” -what class of drugs demonstrate this?

A

-strength of blockade or action of the antiarrhythmic drug is enhanced at slower heart rates -Class III antiarrhythmics

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33
Q

Sodium channel blocking agents that are contraindicated in CAD or heart failure?

A

-Flecainide -Propafenone

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34
Q

Antiarrhythmic contraindicated in permanent AF or severe HF?

A

Droneaderone

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35
Q

Class I antiarrhythmics: -Ion effected -mechanism of action -examples

A

-Na -block inward sodium current during phase 0 of action potential -Procainamide, Quinidine, Disopyramide, Propafenone, Flecainide

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36
Q

Indications for PPM in SND - Class I

A

-Symptomatic sinus bradycardia and pauses -Symptomatic chronotropic incompetence -Symptomatic sinus bradycardia due to required drug therapy

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37
Q

Indications for PPM in SND - Class IIa

A

-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

38
Q

Indications for PPM in SND - Class IIb

A

-Minimally symptomatic patients with chronic HR < 40 bpm while awake

39
Q

Indications for PPM in SND - Class III

A

-SND in asymptomatic patients -SND in patients with symptoms documented in absence of bradycardia -Symptomatic bradycardia due to non-essential drug therapy

40
Q

Indications for PPM in AV nodal disease - Class I

A

-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

41
Q

Indications for PPM in AV nodal disease - Class IIa

A

-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

42
Q

Indications for PPM in AV nodal disease - Class IIb

A

-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

43
Q

Indications for PPM in AV nodal disease - Class III

A

-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)

44
Q

EKG criteria: Left Anterior Fascicular Block (LAFB)

A

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

45
Q

EKG findings: Ostium Primum ASD

A

-rSR’s’ in lead V1 + -Left axis deviation *Normal axis = Ostium secundum *Low atrial rhythm = sinus venosus ASD

46
Q

Describe EKG leads

A

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)

47
Q

What is poor R wave progression?

A

refers to the absence of the normal increase in size of the R wave in the precordial leads when advancing from V1-V6

48
Q

What does it mean/causes?

A

-Old anterior wall MI -LBBB or LAFB -LVH -RVH -Normal Variant -WPW -Dextrocardia or lead misplacement -Tension PTX with mediastinal shift -Congenital heart disease

49
Q

What to look for if an unexpected pause in sinus rhythm?

A

look at preceding T wave to ensure there is no “hidden” P wave that did not conduct because it came early

50
Q

STEMI area which may not demonstrate prominent EKG changes?

A

Lateral (especially high-lateral) wall -likely the result of the amount of myocardium involved and the site relative to the EKG electrodes

51
Q

What is Ashman phenomenon (Ashman beat)?

A

-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

52
Q

Define Atrial tachycardia

A

-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

53
Q

Atrial tachycardia: -Diagnosis

A

-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.

54
Q

Atrial tachycardia: -Treatment

A

-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)

55
Q

EKG finding of diffuse subendocardial injury, multivessel disease or LM disease?

A

-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)

56
Q

Class IA Antiarrhythmics

A

-Quinidine -Disopyramide -Procainamide

57
Q

Class IA Antiarrhythmics MOA

A

-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

58
Q

Class IA antiarrhythmic used in J wave syndromes (Brugada and early repolarization syndromes) to prevent recurrences of VF

A

Quinidine

59
Q

Procainamide uses and side effects

A

-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

60
Q

Class IB antiarrhythmics

A

Lidocaine Mexilitine

61
Q

Class IB antiarrhythmics uses

A

VT and VF -Lidocaine SE’s –> CNS toxicity (tinnitus, seizures, AMS, Coma) -Mexilitine SE’s –> tremor, blurred vision, dysphoria, dizziness)

62
Q

What increases the risk of Lidocaine toxicity?

A

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

63
Q

Class IC antiarrhythmics MOA

A

-Flecainide and Propafenone -block sodium channels with slow association/dissociation channel kinetics -prolong PR and QRS intervals (flecainide can also increase QT)

64
Q

Class IC antiarrhythmic contraindications

A

Structural heart disease

65
Q

Propafenone additional MOA

A

-sodium channel blockade -Voltage dependent calcium currents -Potassium currents -BB properties (pronounced in poor metabolizers via CYP2D6)

66
Q

Proarrhythmic events associated with Class IC antiarrhythmics (Flecainide, Propafenone)

A

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

67
Q

Contraindications to class IC antiarrhythmics

A

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

68
Q

EKG findings of Arrhythmogenic RV Cardiomyopahthy (ARVC)

A

-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

69
Q

Antiarrhythmic which has been shown to improve the efficacy of DC cardioversion in A-fib if used pretreatment?

A

Ibutilide

70
Q

Antiarrhythmics always administered in-hospital due to the risk of QT prolongation and Torsades des pointes VT?

A

-Ibutilide -Dofetilide

71
Q

Class IC antiarrhythmics adverse reaction in patients with A-fib? -Treatment?

A

-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

72
Q

Antiarrhythmics used for pharmacologic cardioversion of A-fib?

A

-Class IC (Flecainide, Propafenone) -Class III (Ibutilide, Dofetilide)

73
Q

Recommendations for anticoagulation in cardioversion of A-fib?

A

-3 weeks before and -4 weeks after

74
Q

Cardioversion of A-fib that does not require anticoagulation?

A

AF events of < 48 hours in duration

75
Q

What are the two strategies for anticoagulation in Cardioversion of A-fib?

A

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

76
Q

AV nodal blocking agent contraindicated in WPW with pre-excited AF?

A

nondihydropyridine CCBs (verapamil, Diltiazem)

77
Q

Considered in patients who have inadequate rate control after thorough trials of medical therapy and who fail or are not candidates for rhythm control?

A

AV node ablation + Permanent ventricular pacing

78
Q

Major adverse affect associated with AVN ablation and permanent pacing?

A

Right-ventricular pacing-induced cardiomyopathy

79
Q

What rhythm is present after AV nodal/junction ablation?

A

Junctional escape rhythm

80
Q

What is an alternative or treatment for RV pacing induced cardiomyopathy?

A

-upgrade to Biventricular pacemaker (Cardiac resynchronization therapy)

81
Q

Describe clinical outcomes of Sotalol use in patients with LVEF < 40% without defibrillators?

A

Increased Mortality -SWORD (Survival with Oral D-Sotalol trial) -OPTIC (Optimal Pharmacological Therapy in Cardioverter-Defibrillator Patients trial) -

82
Q

What did the SWORD trial (Survival with Oral D-Sotalol) show?

A

-Sotalol was associated with increased mortality in LVEF < 40% -Trial was stopped early owing to excess mortality in the group randomized to Sotalol

83
Q

What did the OPTIC (Optimal Pharmacological Therapy in Cardioverter-Defibrillator Patients) trial show?

A

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

84
Q

Typical (type I) atrial flutter is characterized by this:

A

“saw tooth” pattern in the inferior leads (II, III, aVF)

85
Q

What do ratios of > 2:1 in A-flutter indicate?

A

presence of underlying conduction system disease -A flutter typically presents with 2:1 block -must be present in absence of AV nodal blocking agents

86
Q

What are the indications for reduced dosing of Eliquis (Apixaban)?

A

-Age > 80 years -Body weight < 60 kg -Cr. > 1.5 *Reduce dose to 2.5 mg twice daily

87
Q

Benefit of Cardiac resynchronization therapy is highest when this is present

A

AV nodal ablation –> allows for maximal biventricular pacing

88
Q

What did the MADIT-RIT trial show?

A

-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

89
Q

In a typical EP study:

-How many catheters are used and where are they positioned?

A

3 catheters

  • Right atrium (RA)
  • Right Ventricle (RV)
  • “His position” (across the tricuspid valve)
90
Q
A
  • *

Medical (69 decks)

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