Arrhythmia Mayo Flashcards
(107 cards)
1
Q
what lead sites over R atrial appendage?
A
v1
2
Q
Wandering pacemaker
A
MAT with HR <100
3
Q
Treatment for MAT
A
CCB
4
Q
When is warfarin preferred over DOAC (for AF)? (2)
A
“valvular afib”
Mitral stenosis
Mechanical heart valve
5
Q
When do you anticoagulate regardless of CHADS VASC?
A
Mitral stenosis
Mechanical heart valve
HOCM
6
Q
What AC to use in ESRD/dialysis patients?
A
Apixaban
Warfarin
7
Q
Cardioversion anticoagulation management
A
Afib < 48hrs then OAC 4 weeks after DCCV
Afib >48hrs or unknown then OAC 4 weeks before DCCV and 4 weeks after DCCV
TEE/DCCV if not on OAC for 3 weeks
8
Q
ACS and Afib
A
Urgent DCCV if hemodynamically unstable, ischemia, high rate
IV beta blockers for patients in afib RVR with ACS
If recent PCI: triple therapy 1-4 weeks, then discontinue aspirin
If PCI >1year, OAC monotherapy is ok
9
Q
DOAC
A
Preferred over warfarin (less intracranial bleeding)
DO NOT give in MS and mechanical valves
Monitor renal function
10
Q
RP interval
A
Short RP = AVRNT or AVRT
Long RP = ST or AT
11
Q
Regular narrow complex SVTs
A
12
Q
Short RP hints
A
Pseudo R prime in V1
Pseudo S wave in II
13
Q
WPW pattern vs syndrome
(pre-excitation)
A
Syndrome = accessory pathway
Orthodromic (down through His)
If symptomatic, then risk stratify: exercise stress test, holter, EPS
- Low risk: abrupt loss of pre-excitation (vs slow loss)
- Increase sympathetic tone–>AV node conducts better than accessory pathway) = slow loss of pre-excitation
14
Q
Typical flutter
A
Cavotricuspid isthmus dependent
Terminal + in V1 and Terminal - in II/III/AVF
Discordant
15
Q
Atypical flutter
A
Non-cavotricuspid isthmus dependent
Terminal + in V1 and Terminal + in II/III/AVF
Discordant
16
Q
Substages of afib
A
Paroxysmal < 7 days
Persistent > continuous 7 days
Longstanding persistent >1 year
17
Q
Stroke risk factors not in CHADS2VASC
A
18
Q
Anticoagulation in afib algorithm
A
19
Q
Afib risk factors/lifestyle
A
HEADTOES
Heart failure, exercise, arterial HTN, DM, tobacco, obesity, ethanol, sleep
*Weight loss has most impact
Sleep apnea? caffeine cessation
20
Q
Afib trials
A
AFFIRM-no difference rate or rhythm control
EAST-AFNET-early rhythm control had mortality benefit
CASTLE-AF-ablation in AF with HFrEF had mortality benefit
21
Q
Rate vs rhythm control
A
Rhythm control
- Reduced EF and high afib burden
- HF
- Recent afib
- Symptomatic afib
22
Q
How to treat pre-excited afib?
A
IV procainamide
IV ibultilide
DC cardioversion
Rhythm: beat to beat variability
HARMFUL meds to give: digoxin, amiodarone, beta blockers, diltiazem, verapail —» potentially cause conduction through accessory pathway +/-VT
23
Q
How to treat afib in patients with HF?
A
Amiodarone
Avoid CCB
24
Q
Pharmacologic cardioversion
A
Class 1C: flecainide, propafenone-avoid with structural heart disease SE: decrease BP/HR, flutter, VT
Class III: IV ibulitide if LVEF >40%. SE: torsades (give IV mag before). IV amiodarone-long time to convert. SE: bradycarida, hypotension
25
AAD in patients with afib WITHOUT structural heart disease?
Dofetilide, dronedarone, flecainide, propafenone. Then amiodarone. Then sotalol.
**What is structural heart disease in context of AAD? CAD, Hx MI, HOCM, Low EF
26
AAD in patients with afib WITH structural heart disease?
Dofetilide, amiodarone, dronedarone. Then solalol.
DO NOT GIVE FLECAINIDE, PROPAFENONE
**What is structural heart disease in context of AAD? CAD, Hx MI, HOCM, Low EF
27
Indications for catheter ablation
Symptomatic AF
Asymptomatic AF-young patient
HF
28
HF and afib
Higher chance benefit from ablation (compared to AAD)
AAD
AVN ablation + device (CRT or PPM)
29
Ablation complications
Acute
Volume overload
Recurrent atrial arrhythmia
Cardiac tamponade
Hemidiaphragm nerve palsy (elevated diaphragm on one side)
Subacute
PV stenosis
Recurrent atrial arrhythmia
Stiff LA syndrome
30
SVT: Management-Chronic Suppression
Catheter ablation best
AAD if failed catheter ablation or unable to ablate
31
SVT: Management-Acute Termination
Unstable: cardiovert
Stable: Vagal, adenosine, IV AV nodal blockers
32
EKG concepts
L and R mirror images
V1 = anterior to posterior
33
Approach to identifying VT
1. VA dissociation= capture beats, fusion beats
2. Axis - northwest (AVR positive)
3. Precordial transition - concordance
4. Septal activation
5. Slow initial, fast terminal slopes in VT
Structural heart disease (MI, CHF, Device, valvular disease)
Lead II or AVR: time to first peak >40ms
34
Concordance
No precordial transition (V1 to V6) = concordance
Focus area at base = positive concordance
Focus area at apex = negative concordance
35
Septal activation
RBBB - septal activation from L to R
- aberrancy: no V1 Q or V6 R, monophasic complexes, no notching
LBBB - septal activation from R to L
- aberrancy: no V6Q
36
VT: management
WPW or pre-excited afib = give procainamide
If stable VT, amiodarone or lidocaine
37
Idiotpathic VT
No structural heart disease (normal ECG and normal echo)
Origin: outflow tracts, papillary muscles, perivenous areas
LBBB morphology
Positive at inferior leads
Rarely associated with cardiac death
Tachy induced CM if burden >10%
Mechanism:
-Delayed after-depolarizations for RVOT
-Abnoraml automaticity for papillary muscle
38
RVOT VT
Type of idiopathic VT
Mechanism: Delayed after depolarizations
39
Fascicular VT
RBBB morphology (V1 positive)
Relatively narrow
Negative in inferior leads
Young person, exercise related
Verapamil sensitive
40
Scar based VT
Areas of surviving myocardial fibers-areas of slow conduction
Re-entry VT - monomorphic VT
41
ARVC
Problem: cell to cell adhesions. Desmosome protein mutation
LBBB TWI V1-V3, epsilon wave (terminal QRS is fractionated)
42
Sarcoid VT
VT and heart block (septal involvement)
Dx: FDG uptake (for cardiac inflammation)
Tx: long term immunosuppression
43
Bundle branch re-entry
NICM with tachycardia that resembles sinus rhythm
44
Polymorphic VT
Prolonged QT
Long QT, current leak, threshold reach and another depolarization
Early depolarizations = R on T phenomenon
Polymorphic VT --> look for ischemia
Torsades (long QT) = check electrolytes, genetic causes
45
VT management
Idiopathic VT
-Drugs-beta blocker, CCB, anti-arrhythmics, adenosine (RVOT)
-Ablation
-No ICD
Scar based VT
- Drugs (K channel blockers)-amiodarone, sotalol, dofetilide
-ICD
-If recurrent, ablation
*mexilitine as adjunct, not primary
Polymorphic VT
-Magnesium (2g), pacing to shorten QT, avoid QT prolonging meds, isoproterenol/dopamine to increase HR, correct underlying causes
46
BBB pattern in V1
V1 = anterior lead
RV is anterior
RBBB pattern in V1 (pos V1)
- Ventricular activation posterior to anterior (originate from LV)
LBBB pattern in V1 (neg V1)
- Ventricular activation anterior to posterior (originate from RV)
-Ie RVOT VT
47
PVC burden
>10% is significant and risk of CM
If symptomatic, can treat. Symptoms from next beat (increased filling)
Treatment: beta-blockers, CCB
48
Meds to avoid with structural heart disease
Flecainide and propafenone
Structual heart disease-->treat with K channel blockers (sotalol, amiodarone, dofetilide). Amiodarone not great for long term treatment due to side effect profile
Mexilitine is weak and used as adjunct
49
Brugada pattern
Syndrome if pattern AND:
- Associated with syncope
- At least one relative
- Positive genetic test (loss of function SCN51 Na channel)
Affects men 9x more
Avg age 40yo
Trigger: fever
Type 2 and 3 dont matter unless they degenerate to type 1 with stress (fever, drug challenge-flecainide, procainaide, hyperthermia)
ECG taken with leads up (depending on where RVOT is), can elicit Brugada pattern
Incompletely penetrance provocable by exogenous stressor
Tx
- ICD for secondary prevention
- Quinidine
- RVOT epicardial ablation
50
Catecholaminergic polymorphic VT
Calcium induced calcium release. Leaky Ca channels (Ryr2)-->diastolic calcium overload-->delayed after depolarizations
Exertion induced VT
No structural heart disease
Phenotypically mimics PLQT
Dx: exercise induced bidirectional VT
Tx:
-NO ICD
-Nadolol and fleicainide
51
Approximating QT from ECG
1. Use lead II and V5 (avoid V2 and V3)
2. If QT less than 1/2 R to R interval, then QTc will be <460ms
3. If sinus arrhythmia or afib, need to avg
4. Low HR = QTc underestimated, high HR = QTc overestimated
5. Wide QRS
---QTC (adjusted) = QTc- (wide QRS-120ms)
52
LQTS: mech, TW, trigger, Tx
LQT1=loss of IKS, 35-45% = wide, slow T wave. Adrenaline, swimming. Tx: BB (nadolol, propranolol) +/- denervation therapy
LQT2 =loss IKR, 30-35% = wide, double hump T wave. Auditory, post-partum. Tx: BB (nadolol, propranolol)
LQT3=leaky Na channels, 5-30% = normal T wave after long isoelectric segment. Non-activity. Tx: BB (nadolol, propranolol) +/- late Na blocker (mexilitine, ranolazine)
BB=DO NOT USE atenolol or metoprolol
Tx:
-Drugs-non-selective beta blocker-nadolol or propranolol +/-mexilitine/ranolazine
-L cardiac sympathetic denervation
-ICD- - Primary prevention: QTC>550ms and NOT LQT1. Secondary prevention for cardiac arrest
53
QT threshold?
>500ms = pro-arrhythmogenic
Dont care if:
-Amiodarone causes prolonged QT but never arrhythmogenic
-BBB
Care if:
- Meds
- Electrolytes
- Genetics (80-90% can be found-loss of function of voltage gated K channel)
54
Channelopathy genetic yield
Brugrada
- loss of function Na channel SCN51
- 10% (PR normal) to 40% (PR prolonged)
Catecholaminergic polymorphic VT
- Leaky RyR2 Ca channels
- 60-70%
PQTS
- loss of function voltage gated K channel
- 80-90%
55
Anti-arrhythmic drugs
Class 1 (block Na channels)
- 1a - procainamide, quinidine = increase AP
- 1b - lidocaine = decrease AP
- 1c - flecainide, propafenone (most pure, prolongs QRS)
Class 3 (block K channels)
- amiodarone, sotalol, dofetilide
56
Class 1 drugs
Slows Na into cell --> depolarization takes longer --> wide QRS
Typical patient profile:
Recent onset PAF
Highly symptomatic
No structural heart disease
57
Class III drugs
Class 3 (block K channels)
- amiodarone, sotalol, dofetilide
Slows K out of cell --> repolarization takes longer --> prolong QT
Typical patient profie
Persistent AF
Structural heart disease (CAD, LV dysfunction, ACHD)
No renal dysfunction
Adherence is key (with sotalol, dofetilide)
Amiodarone = last resort
Okay for old age, renal dysfunction, structural heart disease, failed AAD or ablation
58
Proarrhythmia*
1. Slowed conduction promotes re-entry (Class 1c-flecainide, propafenone)
2. Prolonged repolarization promotes EAD (Class 3-amiodarone, sotalol, dofetilide)
3. Ca overload = triggered delayed after depolarizations (digoxin)
59
Re-entry (class 1c drugs)
Class III antiarrhythmics (K blocker)
-Prolong repolarization --> reduce excitable gap
Class I antiarrhythmics (Na blocker)
-Slow conduction --> excitable gap longer --> can be pro-arrhytmic
60
CAST trial
MI patients received 1c AAD vs placebo and had increased mortality. No class 1c AAD in structural heart disease
61
Early after-depolarization (EAD)
Prolonged repolarization
62
Delayed after-depolarization (DAD)
-High intracellular calcium
-CPVT and digoxin mechanisms
-Not pause dependent (triggered by isoproterenol, pacing, exericise/stress
-Bidirectional VT
Dig toxicity worse with hypokalemia
CPVT better with flecainide
63
Bidirectional VT
64
Use-dependence channel block
-Drug binds to inactivated state
-Greater effect at faster HR
-Drugs: class 1c-flecainide, propafenone
-Effective for terminating tachycarrhthmias (pill in pocket)
-Monitor pharmacologic effect with stress. QRS widening. Expect 10% above baseline. If 15-20% above then stop or dose reduce.
65
Reverse use-dependence channel block
-Drug effect greatest at rest state
-Greater effect at slower HR
-Drugs: class III-amiodarone, sotalol, dofetilide
-Effective for maintianing SR (as opposed to converting)
-Monitor pharmacologic effect with resting QT
-Potential for pause-dependent polymorphic VT. Avoid class III meds in patients with bradycardia and pauses
66
Which AAD are renally cleared?
Sotalol
Dofetilide
Digoxin
67
What drugs interact with amiodarone?
Causes increased levels of:
Warfarin
Digoxin
Colchicine
Cyclosporine/tacrolimus
68
Afib AAD: no structural heart disease
1st line
flecainide
propafenone
sotalol
2nd line
amiodarone
dofetilide
69
Afib AAD: with structural heart disease
1st line
amiodarone
dofetilide
70
Afib AAD: with CAD
1st line
Dofetilide
Sotalol
2nd line
Amiodarone
71
VT AAD
72
Drug monitoring
73
Syncope
Definition: abrupt LOC and inability to maintain postural tone
74
Cardiac vs Non cardiac syncope
Cardiac
-Structural-valvular (AS), ACS, obstructive CM, myxoma, dissection, pericardial disease, PE, vascular steal
-Arrhythmogenic-AV block, SN dysfunction, SVT, inherited syndromes (LQTS, brugada, CPVT, ARVD)
Non-cardiac
-Vasovagal
-Carotid sinus synddrome
-Orthostasis
-Postural orthostatic hypotension syndrome (POTS)
-Inappropriate sinus tachycardia
75
Reflex syncope
Def: due to reflex that causes vasodilation or bradycardia (vasovagal, carotid sinus, situational)
76
Vasovagal
Counter pressure maneuvers-cross legs
77
Orthostasis
78
POTS
Triggers: heat, large meals, ETOH
79
Tilt test-normal/abnormal
80
Tilt test-cardio vs vaso
Cardioinhibitory - 3 second pause - dc-PPM or anticholinergics
Vasodepressor - >50mmHg fall-midodrine, fludrocortisone, SSRI
81
Tilt test-POTS
BP same but HR increase by at least 30bmp
82
Syncope and driving
83
Out of hospital arrest
ICDs prevent SCD but not treat. If have ICD, avoid shocks (AAD, ablation, device programming)
Patients who dont need ICD=reversible substrates:
-Pre-excitation, VF/VT within 48hrs MI, drugs/electrolyte, RVOT VT (ablatable)
84
Conduction disease
Atrial (sinus node dysfunction)-sinus bradycardia or sinus arrest/sinus with competing junctional
AV node-narrow QRS.
Infranodal-wide WRS, slower focus
AV block at AV node=low risk death
AV block infranodal=high risk of syncope/death
85
PPM indications - sinus node dysfunction
86
PPM indication - AV node or infranodal block
EPS if unsure level of block (AV nodal vs infranodal)
Reversible AVB-lyme, drugs, OSA, physiologic (vagal, sleep)
PACE:
-Irreversible, symptomatic slow afib, symptomatic AV block on drugs, neuromuscular (myotonic dystrophy)
87
Pacemaker indications
PACE:
-Irreversible, symptomatic slow afib, symptomatic AV block on drugs, neuromuscular (myotonic dystrophy)
88
Pacemaker and bifascicular block
89
Pacemaker and post TAVR / cardiac surgery patients
New LBBB 20-55%, 3rd AV block 5-25%. Higher risk with self-expanding valve. Baseline block higher risk.
After cardiac surgery, wait a week
90
Mode nomenclature
VV setting - atria not sensed
Try to maintain AV synchrony
91
Asynchronus pacing
pacemake does own thing, no sensing
92
P wave response
93
Pacemaker mediated tachycardia
V paced --> retrograde p wave to atria --> device sense atrial activity and triggers ventricular pacing
Can be triggered by PVC
PVARP: interval after sensed/paced ventricular event when atrial channel insensitive
Solution: extend PVARP (so retrograde p wave not sensed)
94
DDD and ventricular tracking in afib
Solution: DDD (tracking) mode switch to DDIR (non-tracking) when rate exceeds whatever set to
95
Ventricular failure to capture
Lead dislodged
Exit block (fibrosis around lead tip, needs higher energy to capture)
Lead failure
96
DDD-Ventricular output failure
Oversensing-thought saw ventricular activity so vpace inhibited
circuit interruption
97
VVI-oversensing and undersensing
1st paced beat early bc prior beat was not sensed (undersense)
2nd paced beat later bc sensed activity thats not really there (oversense)
*Oversensing leads to abnormal pacing inhibition or triggering from undesired sensing
*Undersensing-failure to recognize and act on native P or QRS
98
99
Lead fracture or insulation breath
High impedence = lead fracutre
Low impedence = insulation breach
100
Primary vs secondary SCD prevention
Primary
- Structural heart disease or electrical heart disease with increased risk of SCD. NO PRIOR cardiac arrest, unexplained syncope, sustained VT/VF (30 seconds)
Secondary
- SCD survivors, unexplained syncope, sustained VT/VF
101
ACS: Primary vs secondary SCD prevention
102
NICM: Primary vs secondary SCD prevention
103
ICD in HCM
104
ICD primary prevention
105
CRT
Lead at R and L ventricle (through coronary sinus and epicardial L ventricle)
Dyssynchrony = septum activated before free wall. Low EF. QRS 150ms
With resynchronization, EF and QRS should improve
ECG biventricular pacing
- R wave in V1 (LV pacing)
- Q in I (L sided lead), activating LV
CRT: better QOL, reduced mortality, reduced hospitalizations
106
Summary pearls
-sinus node dysfunction - pace only if symptomatic
-determine level of block-infra-hisian gets paced regardless of symptoms
-AVB after MI-RCA may need transient pacing
-neurocardiogenic sycope-pace if cardioinhibitory response
-PM-preserve AR synchrony, minimize RV pacing
-PM EG-failure of capture, failure of output, oversensing, undersensing
-primary and secdonary indications for PM. ICM wait 40days post-MI or 3 months after GDMT optimized
-CRT indications
107
