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pharm exam 3 > pharm exam 3 arrhythmias > Flashcards

pharm exam 3 arrhythmias Flashcards

1
Q

Conduction velocity is determined by regulation of the action potential, specifically the slope of phase ___ depolarization

A

0

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2
Q

The ____/____ refractory period is the time during which cardiac cells cannot conduct nor propagate an action potential

A

effective/absolute

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3
Q

The ___ refractory period is the time during which cardiac cells may conduct and propagate action potentials secondary to strong electrical stimuli

A

relative

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4
Q

resting membrane potential

in the ventricle =

AV node =

SA node =

A
  • 75 mv
  • 70 mv
  • 60 mv
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5
Q

Upon depolarization, an influx of ___ raises the gradient from a negative value towards a positive value, allowing for conduction of the electrical current

During repolarization, the gradient returns back to baseline as ___ effluxes

A

cations (Na+ and/or Ca2+)

K+

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6
Q

Mechanisms responsible for cardiac arrhythmias are generally divided into 2 major categories:

1)
2)

A

1) abnormal impulse formation
- abnormal automaticity
- triggered activity

2) abnormal conduction
- conduction delay
- re-entry

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7
Q

During triggered activity, heart cells contract ___

example = torsades

A

twice

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8
Q

____ produces no cardiac output and causes most cases of sudden cardiac arrest

A

v fib

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9
Q

Arrhythmias are defined by location and rate

____ arrhythmias arise from abnormalities in the SA node, atrial tissue, AV node, or bundle of His.

____ arrhythmias originate from below the bundle of His.

A

Supraventricular

Ventricular

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10
Q

T wave =

A

ventricular repolarization

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11
Q

_____ reflects the duration of the ventricular action potential

A

QT interval

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12
Q

Mechanism of sinus bradycardia:

what are some causes?

A

decreased SA node automaticity

MI, hypothyroidism, drug induced, hyperkalemia

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13
Q

consistent prolonged PR interval =

A

First degree AV block

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14
Q

prolongation of PR interval until a QRS complex is dropped =

Almost always a disease of the AV node

A

second degree AV block type 1 (wenckebach)

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15
Q

PR interval remains constant and does not increase with each cardiac cycle prior to the ”dropped” QRS complex =

Almost always a disease of His-Purkinje System

A

second degree AV block type 2 (Mobitz II)

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16
Q

third degree heart block aka

A

complete heart block

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17
Q

condition in which the nerve impulse generated in the sinoatrial node (SA node) in the atrium of the heart can not propagate to the ventricles =

A

complete heart block

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18
Q

mechanism of AV block:

what are some causes?

A

prolonged conduction

MI, drug induced, hyperkalemia, increased vagal tone, myocarditis, AV nodal disease

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19
Q

Atrial Fibrillation and Atrial Flutter are ____ arrhythmias

A

supraventricular

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20
Q

mechanism of supraventricular arrhythmia =

A

Enhanced automaticity and reentrant circuits

21
Q

v tach = 3 or more consecutive ___ at a rate exceeding 100 bpm and a wide QRS interval

A

PVCs

22
Q

Specific variety of ventricular tachycardia w/ QRS complexes that appear to twist around the ECG baseline =

A

torsades

23
Q

Sodium channel blockers MOA:
blocking the channels leads to a decrease in the slope of phase __. This causes a decrease in ___ velocity in non-nodal tissue (atrial and ventricular muscle, Purkinje system). Ultimately, blocking Na+ channels reduces the __ of action potential transmission w/i the heart. This can serve as an important mechanism of suppressing ___ that are caused by abnormal conduction

A

0 ; conduction

velocity
tachycardia’s

24
Q

Na+ Channel Blockers

__ drugs have the greatest decreasing effect on phase 0

__ drugs have the smallest effect on phase 0

__ drugs are intermediate in their effect on phase 0

A

1C

1B

1A

25
Q

Na+ Channel Blockers and Effective Refractory period (EFP)

Class __: Increase ERP
Class __: Decrease ERP
Class __: No effect on ERP

Increasing the ERP can interrupt tachycardia caused by reentry mechanisms by prolonging the duration that normal tissue is unexcitable

A

1A
1B
1C

26
Q

Disopyramide

what drug class?
restrict use to ___ ventricular arrhythmias

A

Na+ channel blocker, 1A

life-threatening

27
Q

Procainamide

what drug class?
Positive ANA may develop drug induced __
extremely short __
50% metabolized to an active metabolite known as __
NAPA may accumulate in patients with __
If you don’t metabolize it quickly enough, it will have anti-arrhythmic effects!

A 
Na+ channel blocker, 1A
SLE (Lupus)
half life
NAPA
renal failure
28
Q

Quinidine

what drug class?
VERY irritating to the __
can also cause __
Quinidine may increase mortality in treatment of __ or __

A

Na+ channel blocker, 1A
GI tract
Cinchonism
atrial fibrillation or atrial flutter

29
Q

Cinchonism includes:

A 
Blurred vision
Tinnitus
Hearing loss
Diaphoresis
Confusion
Psychosis
30
Q

Lidocaine

contraindication: __ syndrome: Sudden collapse into unconsciousness

A

Adam-Stokes

31
Q

Flecainide

what class?
Has ___ effects

A

Na+ channel blocker, 1C

pro-arrhythmic

32
Q

All Class __ Antiarrhythmics are PROARRHYTHMIC!

A

1

33
Q

β-Blockers: Class II MOA

inhibit ___ influences on cardiac electrical activity, thereby decreasing __ rate, decrease conduction __ (which can block reentry mechanisms), and inhibit aberrant __ activity

Also, BB’s increase action potential duration and the __

A

sympathetic
sinus ; velocity

pacemaker

effective refractory period (ERP)

34
Q

Esmolol beta blocker is only used for __ control of arrhythmia

A

rapid

35
Q

K+ Channel Blockers: 
Class III MOA

These drugs bind to and block the K+ channels that are responsible for phase __ repolarization. Blocking these channels slows/delays __, which leads to an increase in action potential duration and an increase in __. these drugs are very useful in suppressing ___ caused by reentry mechanisms

On the ECG, this increases the __

A

3
repolarization
ERP
tachyarrhythmias

QT-interval

36
Q

Currently the most effective antiarrhythmic for ventricular arrhythmias; however, it is also the most toxic =

A

Amiodarone

37
Q

Amiodarone side effects:

1) Increased liver __ or __ levels (as high as 40-50% in some studies, check at baseline and Q6 months)
2) Pulmonary __ (check PFT at baseline and Q12 months)
3) __ color skin
4) __ deposits
5) Proarrhythmic
6) __tension
7) __thyroidism
8) Abnormal __
9) Impaired ___
10) Involuntary movement
11) __ disturbances
12) __cardia
13) AV block

A

AST or ALT

fibrosis
Blue-gray
Corneal

Hypo
Hypo
gait/ataxia
memory

Sleep
brady

38
Q

Amiodarone
half life ranges from __-__ days!!
Initial response is __-__ , peak response takes __-__
PO duration: Up to __ days after D/C of therapy

A

35-110
2 days to 3 weeks ; 1 week to 5 months
50

39
Q

AKA: “less toxic Amiodarone”; but not as effective as Amiodarone at maintaining sinus rhythm =

A

Dronedarone

40
Q

__ in Class 3 is pregnancy X

A

Dronedarone

41
Q 
Each of these can cause a substantial \_\_ in Dofetilide plasma concnetrations. (↑ F and ↓ Cl)
Verapamil
Cimetidine
Trimethoprim
Ketoconazole
Prochlorperazine
Megestrol
HCTZ
A

increase

42
Q

Dofetilide

BBW: Hospitalize minimum of __ days during initiation

A

3

43
Q

Ibutilide

BBW: May cause potentially fatal ___

A

arrhythmias

44
Q 
Sotalol
Contraindication: \_\_
Formulations indicated for ventricular and atrial arrhythmias are different:
Betapace = \_\_
Betapace AF  = \_\_\_
A

asthma

ventricular
atrial

45
Q

only the ___ CCB’s are approved as antiarrhythmics

A

nondihydropyridine

46
Q

Ca2+ Channel Blockers: 
Class IV MOA

Decreases conduction velocity and prolongs __, especially at the __. Prolongs phase __ of the AP

A

repolarization

AV node ; 2

47
Q

Digoxin MOA in Atrial Fibrillation/Flutter:

Activates __ efferent nerves to the heart (__ effect). Vagal activation can reduce the conduction of electrical impulses w/i the __ to the point where some of the impulses will be blocked. When this occurs, fewer impulses reach the ventricles and ventricular rate falls.
Digoxin also increases ERP within the AV node

A

vagal ; parasympathomimetic

AV node

48
Q

Digoxin toxicity

When K+ levels are __, Digoxin can more easily bind to the pump exerting its __ effects

A

low

inhibitory

49
Q

Adenosine MOA

POWERFUL __, especially in the coronary circulation; but VERY __ acting

used for the rapid treatment of supraventricular tachycardias

A

vasodilator

short

pharm exam 3 (1 decks)

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