EP Flashcards
Triple therapy
Decrease INR to 2-2.5
Ebsteins
a/w bypass tract WPW -> AVRT
Pre-excitation
short PR, slurred upstroke before QRS
Orthodromic AVRT
R-P interval >70ms (long RP tachycardia)
Narrow complex
Antegrade through AVNode
Retrograde thru accessory pathway
Antidromic AVRT
Antegrade conduction down accessory pathway (pre-excited tach)
Retrograde up AV Node
Wide QRS, RBBB since venticle activated from lateral side first instead of septal (normal AVN)
Pre-excited AF
complex irregular rhythm
high risk of RR int <250ms
Tx: ibutilide/procainamide/DCCV
NO AVN agents - 1:1 conduction and death (no verapamil, BB, adenosine)
PPM indications
Sx brady acquired AVB with Sx brady Escape rate <40bpm Pauses >3s in SR Pauses >5s in AF s/p AVN ablation alternating BBB SND in EPS Chronotropic incompet Mobitz II or CHB (3rd deg)
LQTS
Syncopal event with long QT on ECG Genetic testing needed refrain from competitive sports put on BB tx Screen family members
ICD LQTS
1) cardiac arrest
2) VT/Syncope while on BB
LQTS 1
BB tx if symptomatic 30-35% KCNQ1 - loss of fxn (K) broad based regular t wave Swimming/excercise
LQTS 2
BB tx if symptomatic 25-30% KCNQ2 - loss of fxn (K) low voltage notched t wave Alarm clock
LQTS3
5-10%
SCN5A - gain of fxn (Na+ (opp of brugada)
long ST segment with normal twave (narrow)
Sleep
Risk
Highest - QTc>500, LQT1,2, male LQT3
CRT-D
RBBB QRS>150ms
Afib unknown duration
don’t use amio as has cardioversion capability
CCB (vereapamil, diltiazem - neg ionotropes) ok if no CHF/LV dysfxn/AV blcok
AV Block during MI
AWMI - CHB - incidence lower than in IWMI, myocardial injury greater and block is below node
IWMI - incidence higher of CHB, higher or in AVN, less myocardial injury
Pre-excited AF
IV ibutilide
Procainamide
DCCV
NO AVNodal agents or BB or adenosine -> 1:1 AF ->VT/VF
Sx WPW
Class I - catheter ablation
BIVI Pacing
beneficial if 100% paced
If only paced 25% of time - needs AV node ablation to prevent rapid afib rate control (not candidate for rhtym control 2/2 BP or HF).
SVT
adenosine
metoprolol
if broncospasm can use VERAPAMIL
DCCV
Procainamide only for pre-excited afib
DO NOT USE BB/AVN agents - can cause 1:1 conduction down pathway and ->VT/VF
VT
wide QRS atypical RBBB R>r' QRS>140 S>R V6 Precordial concordance of QRS
Torasades de point
Magnesium tx…
Hypersensitive carotid sinus syndrome
10 seconds carotid massage
asystole>3 sec or BP drop >50mm Hg
cardioinhibition -vagal nerve stim
vasodpression -sympathetic nerve withdrawwal
Tx: Dual chamber PPM (cardioinhib component)
Vasodepressor component - augment salt/water, removal of diuretics or vasodepressor meds, use of fludrocortisone or midodrine
Vasovagal syncope
Upright posture >30s
deaphoriss, warmth, nausea, palor
hypotension/brady
hot environments/dehydration
Dx - tilt table h&p
Tx: water/sodium, postural maneuvers
BB, midodrine, flucortisone
PPM if syncopal episodes with asystole
Prevent inappopriate ICD shocks
MADIT RIT
Program higher VT/VF rate cutoffs
more detection only zones
AF isn’t fixed with anti-tach pacing
Primary prevention montior zone 160 to first tx zone one or more tx zone detection 6-10 seconds lowest tx zone 185-200 ATP attempt >1 unless pacing needed set VVI 40
Secondary prevention
set lowest VT zone 10-20bpm below lowest clinically relevant VT rate
Idiopathic left ventricular VT
left posterior fasicle - RBBB morph with superior axis + LAD (neg forces in inferior leads)
sensitive to VERAPAMIL
Typical Aflutter
Typical - isthmus dependent TV annulus (counter clock)
- narrow isthums between IVC & TV essential
- ECG pattern - flutter waves upright in V1, negative in II, III, aVF (sawtooth) - counterclock wavefront
Less common - clockwise isthmus dependent AFL - sawtooth pattern is superior in inferior leads
Non-isthmus dependent aflutter
- seen after cardiac surgery or AF ablation (IE PVI ablation line gaps, linear roof line, mitral isthmus line) or congenital heart disease
- gaps in lines create substrate for left atypical AFL
- absense of sawtooth pattern
- ablation of cavotricuspid isthmus will not termminate non-isthmus dependent AFL
Indications for EP study
Post infarct patient with syncope
EF<40 AND NSVT - EPS to determine inducible VT (MUSTT, MADIT)
Atrial Tach (AT)
Long RP tachycardia - pwave morph/PR interval distinct from SR - gradual rate increase and decrease
DOES NOT terminate with AVB (not dep on AVN)
can have
Crista terminalis, CS, bahcman’s bundle, MV annulus, PV
Dx: IV adenosine can show P-waves but will not terminate
Tx: BB/CCB, Class I agents or ablation
Sinus node dysfunction
Sinus node recovery tiem (SNRT) >525ms abnormal
Pacing indications
Sinus node dz
I - Sx sinus brady or pauses
-Sx chronotropic incompet
-sx sinus brady due to required drug therapy
IIa HR<40 Sx c/w brady but clear assoc between brady and sx unclear
-unexplaned syncope and abn SN fxn on EPS
asystole >3 sec in Sr, >5 sec pause in afib
alternative R/LBBB
syncope due to spontaneous carotid sinus hypersen with asystole >3 sec
Patient activated event monitor
record ecg immediate prior to and during event
Tilt table
orthostasis or postural orthostatic tachy
Syncope causes
1) Arrythmias
- syncope at onset before barorectors can restore BP
2) Structure obstructions - ie PE, HOCM, AS, Ao Diss
3) Hypotensive failure - dehydration, hypotensive Rx, autonomic neuropathy, initial orthostatic hypotension
4) Reflex mediated - vasovagal, carotid sinus syncope, IWMI hypotnesion/brady (Bezold=Jarisch response)
BiviICD
LVEF<35%
LBBB
QRS > 150ms
NYHA II-IV(ambulatory)
Mobtiz I vs II
Carotid sinus massage worsens AV conduction so Mobitz I (AV dz) will worsen conduction V-rate
improves His Purk conduction in mobitz II
Excercise improves AVN conduction - will worsen His purkinje conduction so Mobitz II will worsen V-rate
CHB vs AV dissociation
CHB - AV node doesn’t conduct anything to ventricles - atrial rate faster than ventricular or jnc escape rhtym
AV dissociation - ventricular rate similar to or slightly faster than a-rate - occasional atrial signals will come through AV node and see as “capture beats” or fuse with ventricular beats “fusion beats” -> suggestive of VT (must be >100bpm?)
Afib stroke risk
CHADS2
CHF, HTN, Age>75, DM, Stroke/TIA(2)
CHA2DS2-VASc
CHF, HTN, Age>65(1)>75(2), DM, Stroke/TIA(2), vascular dz (PAD, MI, CAD)
Cryo vs RF ablation
RF
More durable ablation
More risk of PPM/CHB
AVNRT
short RP tachycardia
negative p-wave at terminanl of QRS
Atach and aflutter not likely terminated with adenosine (will cease AV conduction temporarily and see p-waves only but will start again)
PVC localization
1) Morphology - RBBB - comes from left, LBBB - comes from right
2) Axis -
RVOT VT
LBBB
inferior axis (large postive deflections in inferior leads)
late precordial R wave transition
LCC VT
RBBB
inferior axis
early R wave transition
Brugada pattern SCN5A LOSS OF FXN Na+
Sodium channel blockers 1c (flecanide, proprafenone) can unmask brugada in pt with otherwise normal ecg
Can cause polymorphic VT/VF
push up V1/V2 leads to 2nd / 3rd ICS
ICD if h/o SCD
2nd prev ICD if spontaneous type I brugada (off drugs) and h/o syncope
Pt without spontaneous ECG type 1 brugada (drug needed to see) and no symptoms do not need ICD
Avoid fever triggers
If shocks with ICD - QUINIDINE
Torsades
can be caused by QT prolongation on CLass III agents (sotolol, dofetilide)
Neurogenic syncope
Droxidopa, midodrine, fludrocortisone
Intracardiac electrocardiogram
Surface ECG High RA His CS RV
AVNRT - see first atrial reading in His with short V->A time - rules out any tachycardia using an accessory pathway since V-A time would have to be longer
typical AVNRT - see pseduo r’ (short RP interval) - very short VA interval
Left atrial tachycardia - earliest atrial activation would have to be coronary sinus electrode
Reduce ICD shocks
patients with structural heart dz & reduced EF
Sotolol and amiodararone reduce ICD shocks & mortality
DO NOT USE Ic (flecanide, proprafeone) - inc’d risk of VT
Pre-excited AF
risk of SCD
procainamide or ibutilide (IV) or DCCV if unstable
DO NOT IMPLANT ICD
needs catheter ablation
DO NOT USE AVN (BB, CCB, adenosine) agents -> deg to VF…
Catheter ablation risks
Typical AVNRT - 1% risk CHB
AVRT (bypass tract) - left heart - 1% risk of CVA/TIA
Atach - high crista terminalis - 1% phrenic nerve injury
Afib/Atach mapped to PV - 1% PV stenosis
CPVT
Bidirectional VT
DAD diastolic Ca overload (like dig toxicity)
- SCD-> ICD
- Syncope or Asx - BB (nadolol, propranolol) +- flecandie (ryanadine receptor stabilizer)
Breakthrough left denervation
EAD
from Class III antiarrythmics
prolong QT - work better in slower HR (rev use dep)
inc likelihood that ectopy will bring AP back to depolarization and set up torsades
Treatment - pacing/isoproteronol
DAD
diastolic calcium O/L
Dig toxicity
CPVT
Tx with BB, CCB or flecanide for CPVT
Need to slow HR
(use dependence)
DO NOT OVERDRIVE PACE
