pharm exam 3 arrhythmias Flashcards

(49 cards)

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

22
Q

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

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

25
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
1A 1B 1C
26
Disopyramide what drug class? restrict use to ___ ventricular arrhythmias
Na+ channel blocker, 1A | life-threatening
27
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!
``` Na+ channel blocker, 1A SLE (Lupus) half life NAPA renal failure ```
28
Quinidine what drug class? VERY irritating to the __ can also cause __ Quinidine may increase mortality in treatment of __ or __
Na+ channel blocker, 1A GI tract Cinchonism atrial fibrillation or atrial flutter
29
Cinchonism includes:
``` Blurred vision Tinnitus Hearing loss Diaphoresis Confusion Psychosis ```
30
Lidocaine contraindication: __ syndrome: Sudden collapse into unconsciousness
Adam-Stokes
31
Flecainide what class? Has ___ effects
Na+ channel blocker, 1C | pro-arrhythmic
32
All Class __ Antiarrhythmics are PROARRHYTHMIC!
1
33
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 __
sympathetic sinus ; velocity pacemaker effective refractory period (ERP)
34
Esmolol beta blocker is only used for __ control of arrhythmia
rapid
35
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 __
3 repolarization ERP tachyarrhythmias QT-interval
36
Currently the most effective antiarrhythmic for ventricular arrhythmias; however, it is also the most toxic =
Amiodarone
37
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
AST or ALT fibrosis Blue-gray Corneal Hypo Hypo gait/ataxia memory Sleep brady
38
Amiodarone half life ranges from __-__ days!! Initial response is __-__ , peak response takes __-__ PO duration: Up to __ days after D/C of therapy
35-110 2 days to 3 weeks ; 1 week to 5 months 50
39
AKA: “less toxic Amiodarone”; but not as effective as Amiodarone at maintaining sinus rhythm =
Dronedarone
40
__ in Class 3 is pregnancy X
Dronedarone
41
``` Each of these can cause a substantial __ in Dofetilide plasma concnetrations. (↑ F and ↓ Cl) Verapamil Cimetidine Trimethoprim Ketoconazole Prochlorperazine Megestrol HCTZ ```
increase
42
Dofetilide | BBW: Hospitalize minimum of __ days during initiation
3
43
Ibutilide | BBW: May cause potentially fatal ___
arrhythmias
44
``` Sotalol Contraindication: __ Formulations indicated for ventricular and atrial arrhythmias are different: Betapace = __ Betapace AF = ___ ```
asthma ventricular atrial
45
only the ___ CCB's are approved as antiarrhythmics
nondihydropyridine
46
Ca2+ Channel Blockers: 
Class IV MOA Decreases conduction velocity and prolongs __, especially at the __. Prolongs phase __ of the AP
repolarization | AV node ; 2
47
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
vagal ; parasympathomimetic AV node
48
Digoxin toxicity When K+ levels are __, Digoxin can more easily bind to the pump exerting its __ effects
low | inhibitory
49
Adenosine MOA POWERFUL __, especially in the coronary circulation; but VERY __ acting used for the rapid treatment of supraventricular tachycardias
vasodilator | short