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Cardiology > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

resting charge cardiac cell

A

K potential- -96 mV

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2
Q

AP of sinus node

A

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

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3
Q

afterdepolarizations

early vs late

A

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

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4
Q

reentry examples

A

AVNRT, AVRT, atrial flutter, scar related VT

needs to have slow conduction on one path

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5
Q

TWA

A

t wave alternans

beat to beat alternation of t wave amplitude: felt due to spatial dispersion of refractoriness

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6
Q 
Conduction intervals
AA
PA
AH
HV
A

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

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7
Q

Syncope types

A

reflex mediated
orthostatic
cardiovascular

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8
Q

CRT

A 
Class 3 chf 
ivcd> 120 ms
EF<35%
Sinus rhythm 
class 2 indications if afib
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9
Q

2nd degree av block

A

type 1 / mobitz 1/ wenkebach
prolonging pr interval - within av node

type 2 sudden failure of conduction- infrahissian

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10
Q

Pacer indication EPS

A

HV > 60msec with symptoms

HV>100
alternating BBB

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11
Q

strategies of AA meds

A

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)

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12
Q

1a and 1c vs 1b AA

A

1a and 1b sodium channel blockers prolong repolarization
quinidine, procain. & flecainide/propafenone

1c shorten repolarization- lidocaine/mexilitene

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13
Q

1c AA caution:

A

paresthesias, chest pain, diplopia
pro arrhythmic- increased mort with structural HD
can slow a flutter causing 1:1 AV conduction- need av blockade

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14
Q

class 3 AA

A

prolongs phase 3
blocks cardiac potassium channels
amio, sotolol, dofetilide, ibutilide, dronedarone-
amio also decrease conduction velocity (phase 0) and automaticity (phase 4)

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15
Q

svt types

A

automatic: atrial tachycardia
reentry: avnrt, avrt

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16
Q

svt irregular differential

A

multifocal atrial tachycardia
atrial fibrillation
atrial flutter with variable block
atrial tachycardia with variable block

17
Q

regular svt differential:

A

sinus tachycardia
no p waves: avnrt, junctional tachycardia
p waves present: sinus tach, atrial tach, atrial flutter, avnrt, avrt

18
Q

AVNRT

A

narrow complex, regular fast, rapid onset
2 pathways- 1 fast, 1 slow
simultaneous A V activiation- may not see p waves (r’ perhaps)

19
Q

Accessory Pathways

direction

A 
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
20
Q

assymptomatic preexcitation

A 
class 1 observe
class 2a ablate
21
Q

atrial tachycardias

rates, types, etiologies, mechanism

A

up to 250/min
focal or multifocal
fibrosis, inflammation, lung dz, catecholamine, albuterol, caffeine, digoxin (atrial tachy with 2:1 block)
automatic, triggered, reentrant

22
Q

atrial flutter

A

macrorentrant- usually ra origin, but post afib ablation may be on left side

23
Q 
Pregancy:
amiodarone
b blockers
sotalol
quindine, flecanide
A

Class 3:
atenolol shouldnt be used- brady in newborns, fetal growth restriction and respiratory depression
amio abnl fetal thyroid

24
Q

b blocker possible fetal complications:

A

intrauterine growth retardation, newborn bradycardia, reduced placental weight, hypoglycemia

should not cause structural heart dz- not asd ect

25
Q

idiopathic VT with “normal hearts”

A 
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
26
Q

Heart transplant arrhythmias

sinus rate

A

vagal denervation- hr 80’s or more
partial sympathetic denervaton

sinus node dysfunction: usually better by 3 mths
VT/VF think MI, rejection

27
Q

SVT in transplant

A

common with rejection- fibrosis, edema- consider empiric steroid rx

adenosine supersensitivity: 5x

28
Q

PVCs and reduced EF

A

> 24% cardiomyopathy

> 10% may cause cardiomyopathy

29
Q

WCT
hx
exam
ecg

A

prior heart dz 90%
cannon a waves, variable s1
ecg criteria

30
Q

ECG diagnosis

A

av dissociation (slow vt 1/3 have va conduction)
concordance : all neg or positive
bizzare axis
capture/fusion beats

31
Q

morphologic criteria for vt

A

V1: mono or biphasic favors VT
V1: triphasic favors svt
broad or notched qrs favors VT
V6 r/s 60ms to onset favors vt

32
Q

avR in VT

A

large R wave favors VT

33
Q

SCD : primary electrical disorders

A

QT long- K or Na channelopathies, causing abnl repolarization
Brugada- SCN5A gene Na channel
Catacholaminergic VT- card ca handling RYR2 and CASQ2

34
Q

QT syndrome subtypes

A

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

35
Q

Brugada ECGs

A

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

36
Q

risk stratify scd

A

eps neg predictive value not good
SAECG, HRV not good
EF better, but not adequate

37
Q

Long qt

Types with precipitator of events

A

Lqt1 >60% exercise induced

Lqt2 and 3: 40% emotion, 30% sleep

38
Q

Torsades channel

A

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.

39
Q

MRI hyperenhancement

A

Scar- not viable

Cardiology (15 decks)

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