Arrhythmias Flashcards
resting charge cardiac cell
K potential- -96 mV
AP of sinus node
phase 4 gradually increase potential to threshold (Ca current and funny current Na
automaticity altered:autonom. NS, beta adren. stim increases If and lowers threshold voltage, increasing hr
parasym stim decreases If increasing threshold
afterdepolarizations
early vs late
oscillations in membrane voltage- not spontaneous, but require trigger
early afterdepolarization- long qt, brady aggrevates, torsade
delayed afterdepolarizations- during phase 4- dig toxic, catechol, bidirectional vt
reentry examples
AVNRT, AVRT, atrial flutter, scar related VT
needs to have slow conduction on one path
TWA
t wave alternans
beat to beat alternation of t wave amplitude: felt due to spatial dispersion of refractoriness
Conduction intervals AA PA AH HV
AA: sinus cycle length- 1200-600 msec (50-100 bpm)
PA: surface p wave to low RA - normal up to 30 ms
AH: atrial electro in his bundle to his bundle spike- represents AV
nodal conduction: 45-140 ms- autonomic influences
HV: His bundle spike to vent activation- little interference- 35-55ms
Syncope types
reflex mediated
orthostatic
cardiovascular
CRT
Class 3 chf ivcd> 120 ms EF<35% Sinus rhythm class 2 indications if afib
2nd degree av block
type 1 / mobitz 1/ wenkebach
prolonging pr interval - within av node
type 2 sudden failure of conduction- infrahissian
Pacer indication EPS
HV > 60msec with symptoms
HV>100
alternating BBB
strategies of AA meds
decrease automaticity phase 4 ( b and ca blocker)
change conduction velocity- change phase 0 and phase 4
change refractory period (increase phase 2 and 3)
1a and 1c vs 1b AA
1a and 1b sodium channel blockers prolong repolarization
quinidine, procain. & flecainide/propafenone
1c shorten repolarization- lidocaine/mexilitene
1c AA caution:
paresthesias, chest pain, diplopia
pro arrhythmic- increased mort with structural HD
can slow a flutter causing 1:1 AV conduction- need av blockade
class 3 AA
prolongs phase 3
blocks cardiac potassium channels
amio, sotolol, dofetilide, ibutilide, dronedarone-
amio also decrease conduction velocity (phase 0) and automaticity (phase 4)
svt types
automatic: atrial tachycardia
reentry: avnrt, avrt
svt irregular differential
multifocal atrial tachycardia
atrial fibrillation
atrial flutter with variable block
atrial tachycardia with variable block
regular svt differential:
sinus tachycardia
no p waves: avnrt, junctional tachycardia
p waves present: sinus tach, atrial tach, atrial flutter, avnrt, avrt
AVNRT
narrow complex, regular fast, rapid onset
2 pathways- 1 fast, 1 slow
simultaneous A V activiation- may not see p waves (r’ perhaps)
Accessory Pathways
direction
depolarize quickly- delta wave, short pr, widen qrs tachy: orthodromic- down avn, up bypass antidromic- down bypass, up avn- wide qrs class 3 rx: verapamil, diltiazem, digoxin class 1: ablation
assymptomatic preexcitation
class 1 observe class 2a ablate
atrial tachycardias
rates, types, etiologies, mechanism
up to 250/min
focal or multifocal
fibrosis, inflammation, lung dz, catecholamine, albuterol, caffeine, digoxin (atrial tachy with 2:1 block)
automatic, triggered, reentrant
atrial flutter
macrorentrant- usually ra origin, but post afib ablation may be on left side
Pregancy: amiodarone b blockers sotalol quindine, flecanide
Class 3:
atenolol shouldnt be used- brady in newborns, fetal growth restriction and respiratory depression
amio abnl fetal thyroid
b blocker possible fetal complications:
intrauterine growth retardation, newborn bradycardia, reduced placental weight, hypoglycemia
should not cause structural heart dz- not asd ect
idiopathic VT with “normal hearts”
normal EF LBBB appearance, upward inferior leads (inferior axis)- rv outflow tract origin RVOT- camp mediated, ppt caffeine, stress- rx with ablation, b blocker, ca blocker
Heart transplant arrhythmias
sinus rate
vagal denervation- hr 80’s or more
partial sympathetic denervaton
sinus node dysfunction: usually better by 3 mths
VT/VF think MI, rejection
SVT in transplant
common with rejection- fibrosis, edema- consider empiric steroid rx
adenosine supersensitivity: 5x
PVCs and reduced EF
> 24% cardiomyopathy
> 10% may cause cardiomyopathy
WCT
hx
exam
ecg
prior heart dz 90%
cannon a waves, variable s1
ecg criteria
ECG diagnosis
av dissociation (slow vt 1/3 have va conduction)
concordance : all neg or positive
bizzare axis
capture/fusion beats
morphologic criteria for vt
V1: mono or biphasic favors VT
V1: triphasic favors svt
broad or notched qrs favors VT
V6 r/s 60ms to onset favors vt
avR in VT
large R wave favors VT
SCD : primary electrical disorders
QT long- K or Na channelopathies, causing abnl repolarization
Brugada- SCN5A gene Na channel
Catacholaminergic VT- card ca handling RYR2 and CASQ2
QT syndrome subtypes
95% of lqt
lqt1: gene KCNQ1- IKs decrease- exercise related- b blocker
lqt2: HERgend: IKr decrease- vf with startling- b blocker
lqt3: SCN5A gene: INa increase- die in sleep
Brugada ECGs
type 1:rbbb coved st elevation with t inversion- pathognomic
type 2: rbbb saddle back st elevation 2 mm
type 3: rbbb saddle back with less than 2 mm st elevation
risk stratify scd
eps neg predictive value not good
SAECG, HRV not good
EF better, but not adequate
Long qt
Types with precipitator of events
Lqt1 >60% exercise induced
Lqt2 and 3: 40% emotion, 30% sleep
Torsades channel
Explanation: Suppression of Ikr (Rapid component of the delayed rectifier potassium current) is the principal mechanism of drug-induced QT prolongation and resultant torsade de pointes. Mutation of the slow component of the delayed rectifier current (IKs) results in congenital long QT syndrome (LQTS) type 1. A gain of function SCN5A mutation results in LQTS type III. A loss of function SCN5A mutation is present in ~ 20% of patients with Brugada syndrome. If is responsible for sinus node automaticity. IKACH-ADO acts as the adenosine receptor.
MRI hyperenhancement
Scar- not viable
