Ep Flashcards
Post mi arrhythmia a are
Re entrant variety
SSS
Complete heart block is not part of it
Ead and dad
EAD triggered activity bradycardia torsades.
dAD. Digitixicity
Critical part of reentry circuit is
Slow conduction
Pro can challenge
Help ful in brugada and quinidine may be the treatment
Signal average EKG
Slow conduction from scar s/p mi
Cardiac action potential
Phase O I Na Phase 1 I to Phase 2 I kr, I ca, I k Phase 3 I ks Phase 4 I Na, I ca
Procan challenge
H P disease,and brugada
CRT indication
Class 1 EF150
Class2 same with qrs >120
Syncope
1-3% ER admits and 6% hospitalizations
3-5 sec hypoperfusion can cause syncope
Carotid hypersensitivity > 3 sec pause
Dabigatran
Less ich more GI bleed
Antiarrhythmic statagies
Decrease automaticity phase 4
Decrease conduction velocity phase 0
Change refractory period phase 2&3
BB and ca blockers
Effect k and ca phase 4 so they are week
Lidocaine be cautious
CHF and hepatic dysfunction
Dronedarone
Do not use in CHF and permanent afib
Pallas study.
Athena was good out come with afib
Adenosine can cause
Afib
Adenosine
Avnrt/avet terminated
Focal AT av block increases do not usually terminate
Afib/ flutter unmask AF av block increases
High chad score
Need anticoagulation even if the pt is in NSR
AFFIRM
Rate control and rhythm control both are equal
New anti coagulants
Dabi direct thrombin RE-LY study
Rivaroxaban Xa rocket study
Apixaban Xa. Aristotle study
AF ablation
Success 60-80%
Repeat 80%
Symptoms
Paroxysmal AF
LA < 5 cm
No CHF copd sleep apnea
Ischemic heart disease
Amio
Difetilide
Svt
At is automatic
Avnrt/ avrt are reentrant
AVNRT
Fast And slow pathways
Simultaneous AV activation
pseudo R waves
AVRT
WPW
Orthodromic - down AV
Antideomic - retrograde through AV
AT
Originate in at risk tissue without AV node, purkinje system or Accessary pathway starting or maintaining it.
Could be multi focal MAT
Idiopathic out flow VT
cAMP mediated triggered
Caffein stress exercise
LBBB with inferior axis
Beta blockers
Transplant
Higher baseline sinus rate Sinus node dysfunction in half the patients PVC PAC 60% normal RBBB could be from biopsies 70% AV block uncommon could be rejection VT/VF mean rejection SVT allograft rejection
VT
Reentrant arrhythmia
Brugada
May be triggered by fever
Icd trials
AIVD secondary prevention trial
MADIT-2 and SCD-HeFT are primary prevention death benifit by 1 year 31%
Icd
In appropriate shock in 25%
Afib
Chad score 0 ASA
1 either Asa or Coumadin
2 Coumadin and xarelto or pradaxa
Idiopathic VT
First degree AV block with RBBB and left axis
A flutter
More common in copd CHF and smoking
Non isthmus dependent after surgery
Isthmus dependent has saw tooth in 2,3,F
Idiopathic vt
RBBB with inferior axis
Arvd
Desmosomal protein
20-30years
LBBB
T inverted V1-V3
Gating of cell membrane
Inward rectifier Ikach/ado operated by acetyl choline or adenosine
Delayed rectifier
Ikr and Iks
Trigger activity
Depends on preceding AP and do not arise from quiet cells
EAD
Slow rates
Reduction in outward currents
Increase inward current 1A,3 anti arrhythmias
K channel
Pacing abolishes EAD
Torsades effects phase 3 action potential
DAD
Arises from fully depolarized membrane
Phase 4 AP
Ca overload digitoxicity calstabin2
Initiated by Premature stimulation and show over drive acceleration
Class 1anti arrhythmic
Prolong the ratio of the effective refractory period to APD
Flecanide has slow kinetics use dependent block at slow rates
Class3
Prolongs AP increAses refractory period. Block Ikr, principle mechanism for these drugs
Reverse use dependence APD prolongation greater in slower rates
Ca channels
T type in the nodes L type in the myocardium
Ikr Iks channels
Responsible for rapid repolarization of cell membrane during phase 3 of AP
Adenosine
A1 AV block
A2b vaso dilatation
A3,4 bronchi spasm
Regadenoson selective A2A agonist
