Clinical Electrophysiology Flashcards
3 Ways to Initiate Heart Beat
1- automaticity (gradual rate changes by changing slope of phase 4)
2- triggered (EADs and DADs)
3- re-entry (common -fast/slow - common)
Decreased and Increased Automaticity
- 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
EADs v DADs (+ causes of each)
- 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
What is the basic premise of re-entry?
- 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)
When should you be worried about LBBB?
If new LBBB in context of MI b/c means R coronary/L descending artery ischemia (bad prognosis)
Ashman’s Phenomenon
- transient block; R or L bundle temporarily loses ability to conduct quick enough (usually physiological and benign)
WPW
- 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)
2 Possible Re-entry Paths in WPW
- 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
What happens when a WPW patient gets a fib? How do you treat them?
- 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
AVNRT (+how to distinguish from WFW orthodromic tachy)
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)
Atrial Flutter
- 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
Ectopic Atrial Tachycardia
(least common) long RP interval and p waves not in sinus rhythm
Atrial Fibrillation
- 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
MAT
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
How can you tell the origin of a ventricular rhythm?
- If activation begins in L vent - RBBB shape
* If activation begins in R vent - LBBB shape (think - more severe version)
How long until a ventricular rhythm is considered “sustained”?
30 sec
7 Clues that a Wide QRS is Ventricular in Origin
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)
RVOT
- 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
Long QT (causes, main concern, tx)
- 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)
Brugada Syndrome
- 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
Treatment of Ventricular Rhythms in General
- 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
