Clinical Electrophysiology

Question 1

3 Ways to Initiate Heart Beat

Answer 1

1- automaticity (gradual rate changes by changing slope of phase 4)

2- triggered (EADs and DADs)

3- re-entry (common -fast/slow - common)

Question 2

Decreased and Increased Automaticity

Answer 2

• Decreased automaticity - sick sinus syndrome (alternating tachy-brady) w/ poss sinus pauses > 3 sec OR chronotropic incompetence (cannot reach 60% max heart rate w/ exercise)
  
  • Give pacemaker for sick sinus syndrome
• Increased automaticity - inappropriate tachycardia OR some junctional tachycardia

Question 3

EADs v DADs (+ causes of each)

Answer 3

• EADs (early after depolarization) - in phase 2 or 3
  
  • Acidosis, hypoxia, hypokalemia, ischemia right after MI
• DADs (delayed after depolarization) - in phase 4 but b/f threshold
  
  • Digoxin/digitalis toxicity

Question 4

What is the basic premise of re-entry?

Answer 4

• Common upper pathway —> slow AND fast conducting limbs —> common lower pathway
• If normal… fast limb beats slow limb and that is what is passed to common lower
• If very premature beat… neither fast or slow is conducted b/c neither has recovered (no beat)
• If only slightly premature beat… fast path has not recovered (longer recovery time) so only slow is conducted —> gets to common lower soon (tachycardia) and goes up fast limb (cyclic)

Question 5

When should you be worried about LBBB?

Answer 5

If new LBBB in context of MI b/c means R coronary/L descending artery ischemia (bad prognosis)

Question 6

Ashman’s Phenomenon

Answer 6

• transient block; R or L bundle temporarily loses ability to conduct quick enough (usually physiological and benign)

Question 7

WPW

Answer 7

• Accessory path - bypasses AV node so ventricle can be depolarized early
• R-sided Accessory Path - close to SA node so FASTER –> prominent delta waves
• L-sided Accessory Path - further from SA node so SLOWER –> Less prominent delta wave/less pre-excitation
• On EKG… short PR (accessory shorter interval than AV node) and wide QRS (b/c some ventricle depolarized early via accessory and some at normal time) and delta waves (leading into QRS)

Question 8

2 Possible Re-entry Paths in WPW

Answer 8

• 1- Orthodromic Tachy -conduction passes through AV node originally then back up accessory pathway (counter-clockwise)
  
  • Normal, narrow QRS b/c QRS from normal conduction pathway then retrograde P wave
• 2- Antidromic Tachy - conduction passes through accessory originally then back up AV (clockwise)
  
  • Wide QRS b/c QRS from accessory pathway

Question 9

What happens when a WPW patient gets a fib? How do you treat them?

Answer 9

• Normally when a fib happens the AV node is decrementing so when it gets a lot of signals it slows down firing (protective) so not all a fib firing is relayed to ventricle
• In WPW… the accessory pathway does transmit sporadic atrial firing to ventricles —> ventricular fibrillation (can cause immediate death)
• Treat w/ procainamide or amiodarone b/c these work on ventricles too; DO NOT use beta blockers, digoxin, Ca channel blockers b/c these will stop AV which further favors the accessory path

Question 10

AVNRT (+how to distinguish from WFW orthodromic tachy)

Answer 10

AV Node Re-entrant Tachy (much smaller circuit)

• Perfectly timed premature beat —> slow path to AV node has recovered but fast has not —> retrograde flow through fast path back tp atrium
• SO wide QRS b/c slow conducting path wins and retrograde p wave
• Shorter R-retro p interval (~60 ms - simultaneous) b/c smaller circuit than WPW sequential ventricle then atrial contraction (~220 ms)

Question 11

Atrial Flutter

Answer 11

• Macro circuit that moves counter-clockwise (up atrial septum - across AV valve - down medially along AV valve)
• Negative flutter waves in inferior leads; saw tooth p waves
• Treat w/ anti-coagulants like a fib

Question 12

Ectopic Atrial Tachycardia

Answer 12

(least common) long RP interval and p waves not in sinus rhythm

Question 13

Atrial Fibrillation

Answer 13

• Multiple waves depolarize parts of atrium at diff times so not a synced contraction; irreg irreg
• Risk of stroke so use anticoagulation (Warfarin - must monitor INR)
• Causes - hypertension, sleep apnea, CAD, COPD, alcohol, thyroid disease, etc

Question 14

MAT

Answer 14

Multifocal Atrial Tachycardia

• Mult, discrete locations w/in atrium all activating ventricle through normal system
• Irreg irreg but w/ p waves (p waves all have diff shape)
• Do NOT use anticoagulation

Question 15

How can you tell the origin of a ventricular rhythm?

Answer 15

• If activation begins in L vent - RBBB shape

* If activation begins in R vent - LBBB shape (think - more severe version)

Question 16

How long until a ventricular rhythm is considered “sustained”?

Answer 16

30 sec

Question 17

7 Clues that a Wide QRS is Ventricular in Origin

Answer 17

1- Hx CAD

2- past MI

3- Hx L vent dysfunction (dec EF)

• EKG

4 - AV dissociation (atrial and vent rates appear to be unconnected)

5- capture beat (appears normal)

6- fusion beats (when normal and ventricular beat at same time so QRS is summation of two)

7- concordance in pericordial leads (V1-V6 deflection all in same direction)

Question 18

RVOT

Answer 18

• Right Ventricular Outflow Tract Tachy
• Totally normal ventricular tachycardia
• Looks like LBBB (b/c R ventricle is origin), inferior axes exacerbated and triggered during exercise/stress

Question 19

Long QT (causes, main concern, tx)

Answer 19

• Genetic defect in K+ and Ca++ channels
  
  • Treat w/ beta blockers and pacers, stellate ganglia sympathectomy, implantable defibrillator
  • Romano-Ward (dominant)
  • Jervell-Lange-Nielsen (recessive w/ deafness)
• Acquired - drugs (ex- Dofetilide), hypokalemia, hypo magnesium
• Main concern = peak of T wave is vulnerable period for spontaneous PVC to cause ventricular tachy or ventricular fibrillation (longer QT = longer vulnerable period)
  
  • If ventricular arrhythmia is sustained —> cyclic (Tornado de pointes)

Question 20

Brugada Syndrome

Answer 20

• Auto dominant cardiac channel disorder
• Pseudo-RBBB w/ ST elevation in V1 and V2
  
  • Can sometimes be unmasked/discovered if pt on Na channel blocker (anti-arrhythmic) —> these abnormal EKG findings
• Recommend implantable defibrillator and avoiding Na channel blockers

Question 21

Treatment of Ventricular Rhythms in General

Answer 21

• If asymptomatic - none
• If symptomatic but normal heart- still not necessary unless interfering w/ daily activities then use beta blocker
• If abnormal heart structure due to past MI (coronary artery disease)
  * If patient has significant LV dysfunction (low EF) then use implantable defibrillator (primary prevention)
  * If patient survives sudden cardiac death then put in implantable defibrillator (secondary prevention)
  * Anti-arrhythmic drugs not as effective
• If abnormal heart structure for other reasons (dilated cardiomyopathy, hypertrophic cardiomyopathy, sarcoidosis, tetralogy of Fallot) - still use implantable defibrillator if LV dysfunction
• If abnormal heart for cellular reasons (long QT, Brugada) - still likely use implantable defibrilator