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Cardiology (inpatient) > antiarrythmics/random/hypertrophy/BBB > Flashcards

antiarrythmics/random/hypertrophy/BBB Flashcards

1
Q

Class 1a action

A

sodium channel blockers; depress phase 0 polarization; slow conduction; prolong polarization

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2
Q

Class 1b action

A

Shorten repolarization

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3
Q

Class 1c action

A

Depress phase 0 repolarization; slow conduction

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4
Q

Class II action

A

BB, slow AV conduction

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5
Q

Class III action

A

K channel blockers, prolong action potential

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6
Q

Class IV action

A

slow calcium channel blockers

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7
Q

Class V action

A

Adenosine: slows conduction time through AV node, interrupts reeentry pathways
digoxin: direct action on cardiac muscle and indirect action on cardiovascular system via ANS

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8
Q

Class Ia indications

A

SVT, Vtach, prevent Vfib, symptomatice ventricular premature beats

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9
Q

1b indications

A

Vtach, prevention of vfib, symptomatic ventricular premature beats

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10
Q

1c indications

A

life threatening vtach or vfib, refractory SVT

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11
Q

II indication

A

SVT, prevent Vfib

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12
Q

III indication

A

refractory Vtach, SVT

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13
Q

IV indication

A

SVT

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14
Q

V indication

A

SVT

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15
Q

1a examples

A

Quinidine, procainamide, disopyramide, moricizine

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16
Q

1b

A

lidocain, mexiletine

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17
Q

1c

A

flecainide, propafenone

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18
Q

II

A

esmolol, propanolol, metoprolol

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19
Q

III

A

amiodarone, sotalol, dofetilide, ibutilide

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20
Q

IV

A

verapamil, diltiazem

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21
Q

V

A

adenosine, digoxin

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22
Q

supraventricular arrhythmias

A

sinus bradycardia, sinus tachy, atrial premature beats, PSVT, afib, aflutter, junctional rhythms

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23
Q

sinus brady.

A

symptoms less than 50,
Weakness, pre-syncope/syncope, SOB

tx with atropine (vagolytic) or postivie chronotropic (epi or dopamine)

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24
Q

sinsus tachy (regular, narrow complex)

A

sx: palpitations, dizzy, SOB, angina

stable-valsalva , 1s push adenosine, then BB or CCB

Unstalbe- synchronized cardioversion

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25
Q

stable tachy with wide QRS

A

antiarrhytime infusion of procainamide, amiodarone or sotatlol

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26
Q

afib

A

most common, “holiday heart” excessive alcohol use or withdrawal

unstable- cardiovert at 200J
stable- 1) rate control w/BB , then CCB, then digoxin 2) anticoag (heparin or enoxaparin and warfarine or dibigatran, and rate control for 3-4 weeks prior to converstion

chemical converstion-flecanimide, propafenone, amiodarone, dronedrone or ibutilide

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27
Q

aflutter

A

unstable: cardioversion w/ 50 J
stable- anticoags, and rate control (metoprolol, esmolol, diltiazem or verapamil) prior to conversion

chemical conversion w/ IV ibultilide or synchronized cardioverstion w. 5 to 50 J can also be effective

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28
Q

chronic a flutter

A

dofetilide is primary choice, but dronedarone, amiodarone, sotalol, procainamide, and flecainide

29
Q

ventriculare premature beats (PVC)

A

tx w/ BB
may be benign or lead to sudden death; can occure w/ increasing frequency if myocardium is irritated by facots such as ischemia or electrolyte disturbance

30
Q

vtach

A

three or more consecutive ventricular premature beats; frequent complication of actue MI or dilated cardiomyopathy

unstable- shock! pulseless=unsynchronized,
pulse=synchronized

31
Q

torsades de pointes

A

polymoprhic vtac- continually changing axis; I V Mg

32
Q

Long QT

A

causes recurrent syncope; AT interval 0.5-0.7 sec long; ;tx- correct electorolyep abnormality, stop offending drug

33
Q

Brugada’s

A

think Asains and men; implantable defibrillator

34
Q

vfib

A

no effective pumping action
***Main cuase of sudden cardiac death
tx-non-synchronized defibrillation 120-200 J; amiodarone for 28-48 hours

35
Q

conduction disorders

A

sick sinus syndrome, AV blocks

36
Q

sick sinus syndrome

A

found in elderly, made worse by digitalis, CCB, BB, sympatholytic agents; collagen vasculare or metastaic dz, surgical injury, coronary artery dz; scarring of heart

tx permanent pacing

37
Q

AV block

A

delay or inerupption in the transmission of an ipulse from the atria to the ventericles

**key is the PR interval

38
Q

AV blokc symptoms

A

weakness, fatigue, light-headedness, syncope

39
Q

first degree

A

if the Ris far from the P, then you have a first degree. no tx really needed

40
Q

mobitz I (or a wekenbach)

A

longer, longer, longer, drop, then you have a wenckebach.

regular irregular, type 1 conduction delay usually in AV node

think athletes, elderly, ischemia, drugs (BB, CCB, anti-arrhythmics)
tx- is symptomatice and signs of hypoperfusion use atropine

41
Q

mobitz II

A

block usually in bundle of his,; almost always secondary to organic dz in infranodal system, almost always will progress to a complete heart block

(if some ps get through, then you have a mobitz II)

tx with pacemaker

42
Q

3rd degree

A

if p’s and q’s dont agree, then you have a 3rd degree

43
Q

what are sx of sick sinus syndrome?

A

mostly asx, but pt may have syncope, dizziness, confusion, heart failure, palpitations, decreased exercise intolerance

44
Q

what can cause a shortened PR interval?

A

junctional rhythm if inverted p wave

wolff-parkinson-white sydrome

45
Q

what can use a prolonged PR interval

A

AV blocks

46
Q

what affects the height and amplitude of a QRS complex?

A

size and direction of vectors in relations to the lead

47
Q

what would hypertrophy do to a QRS complex?

A

increase it bc more muscle to conduct through

48
Q

what would an infarct do to a QRS complex?

A

you would see higher voltage on the unopposed wave (other side)

49
Q

how do you calculate the axis?

A

look at I and AVF

if both negative=extreme R, if both positive then normal

50
Q

what is a RBBB

A

RV depolarization is delayed

51
Q

what is the criteria for reading a RBBB?

A

XRS prolongation >.12
slurred S wave in leads i and V6

RSR pattern in lead 1

52
Q

criteria for LBBB

A

QRS prolongations > .12

Broad monomorphic R waves in I and V6

Broad monomorphic S waves in V1

53
Q

what do you need to think of if there is a LBBB

A

AMI until proven otherwise

54
Q

criterai for a LPH

A

right axis deviation

s wave in lead 1 and q in III

55
Q

how to see left atrial enlargement

A

P wave in lead II: > .12
M shape=P mitrale
camel humpts

P wave in V1: v=biphasic second half of wave neg and deeper/wider

56
Q

what can cause LAE?

A

MS/MR, AS/AR, systemic HTN

57
Q

Right atrial enlargement

A

P in lead II: > 2.5 mm, Peak shape= P pulmonale

P in lead V1: IF biphasic, + half taller and wider than neg half

58
Q

causes of RAE

A

TS/R

pulmonary HTN,

Pulmonary embolism

59
Q

left ventricular hypertrophy

A

causd by pressure or volume overlad

**will see increased amplitude on EKG bc more cells=more action potentials

60
Q

what is LVH w/ strain

A

ST depression and or inverted T waves that are actually abnormal repolarization

61
Q

criteral for LVH

A

deepest S wave in V1 or V2 + tallest R wave in V5 or V6 = >/= 35 mm

62
Q

Right Ventricualr hypertrophy

A

Look at leads V1 and V2
R wave in these leads at least as tall as the depth of S wave (R:S ratio ≥ 1)
Early transition zone

63
Q

what can cuase RVH?

A 
Pressure overload: Pulmonary HTN, PE
Pulmonic stenosis/regurgitation
Ventricular septal defect
Tricuspid regurgitation
Severe mitral stenosis
64
Q

why would you see a flipped Twave in an MI

A

Zone of injury does not repolarize completely
Remains more positive than surrounding tissue, leading to ST elevation
T remains flipped

65
Q

what is the idea of a reciprocal change?

A

, the recording made by the lead on the wall exactly opposite an AMI is registering the reciprocal change of that AMI

66
Q

what is an example of a reciprocal change?

A

Inferior MI’s = Reciprocal changes in Anterior and Lateral Leads
Lateral MI’s = Reciprocal Changes in I, avL, V5, V6

67
Q

what EKG change is seen in hopthermia?

A

rounded osborn wave at the J point

68
Q

how to determie if pace maker is atrial or ventricular

A

look at pacer spikes

if where P wave should be- atrium

if where Q wave should be- ventricle

69
Q

what is sinus arrhythmia?

A

Representation of normal respiratory variation
Slower during exhalation and faster upon inhalation
Inhalation increases venous return by lowering intrathoracic pressure
Common in both young and elderly
Symptoms: usually none, occasionally palpitations
Evaluation: EKG
Treatment: None, normal clinical finding

Cardiology (inpatient) (14 decks)

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