E1: AntiARRhythMICS Flashcards

1
Q

What are the three sources of a cardiac arrhythmia?

A

disease, injury, or DRUGS

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2
Q

normal contractions at a faster rate

A

Tachycardia

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3
Q

all areas may not follow normally (can affect atria or ventricles);

A

flutters

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4
Q

uncoordinated contractions

A

fibrillations

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5
Q

normal contractions at a slower rate

A

bradycardia

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6
Q

complete _______ = His Purkinje system cut in half; therefore atria and ventricles work independently

A

HEART BLOCK

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7
Q

5 transmembrane phases! Plateau where net influx of Ca+ through Ca+ channels is slightly more than the efflux of K+ channels

A

Phase 2

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8
Q

5 transmembrane phases! early, partial repolarization through the efflux of K+ ions

A

Phase 1

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9
Q

5 transmembrane phases! restoration of ionic concentrations via the Na+K+ and the Na+Ca+ exchange pump = resting membrane potential is reestablished (-90 mV)

A

Phase 4

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10
Q

5 transmembrane phases! predominant efflux of K+ ions

A

Phase 3

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11
Q

5 transmembrane phases! influx of Na+ ions through fast channels to generate the upstroke (depolarization)

A

Phase 0

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12
Q

5 transmembrane phases! absolute (effective) refractory period = Phases ___,___,___, & most of ____.

A

0,1,2,most of 3

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13
Q

5 transmembrane phases! Middle of phase 3 to beginning of phase 4 =

A

relative refractory period

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14
Q

synonymous with DEPOLARIZAITON…a mechanism that PROTECTS the heart from all other ectopic impulses

A

ABSOLUTE refractory period

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15
Q

The time when only a strong stimulus can cause depolarization…Occurs when repolarization is almost complete

A

Relative Refractory period

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16
Q

All cells are repolarized and ready to respond in a normal fashion

A

Nonrefractory phase

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17
Q

In the __________ period all fast Na+-channels are voltage-inactivated and closed, which prevents sustained tetanus.

A

absolute refractory

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18
Q

What are the 3 areas of the heart with pacemaker activity?

A

SA node, AV node, Purkinje Fibers

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19
Q

What drives automaticity?

A

Spontaneous opening and closing of K+ channels.

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20
Q

The further away from _______ that the cell is maintained, the harder it will be to get the cell to depolarize

A

resting and threshold membrane potentials

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21
Q

Effective Refractory Period (absolute refractory period) in cells in _______ areas is longer than in _______ cells

A

pacemaker…myocardial

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22
Q

Myocardial cells repolarize quickly and have to wait for the pacemakers to repolarize before firing again

A

Myocardial….pacemakers

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23
Q

*different arrhythmias require that the _________ be lengthened or shortened

A

Effective/Absolute Resting Potential

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24
Q

Yes, I am going to do this to you. GET SOME! What are the 5 indications for Antiarrhythmias? WHATS THE MOST COMMON????

A

1.Paroxysmal ATRIAL tachycardia, 2.Paroxysmal VENTRICULAR tachycardia, 3.Atrial fibrillation (A FIB IS MOST COMMON), 4.Ventricular ectopic arrhythmias, 5.Digoxin-induced arrhythmias…GOOD JOB DAWG!

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25
Q

What are the 4 Contraindications for Antiarrhythmics?

A
  1. Complete A-V heart block 2.Congestive heart failure 3. Hypotension 4.Known hypersensitivity to the drug
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26
Q

IA: Na+ channel blocker (_______): Blocks conduction; ______ duration of AP

A

medium…. prolongs

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27
Q

IB: Na+ channel blocker (____): Blocks conduction; _______ ERP; _______ the AP

A

fast… decreases…shortens

28
Q

IC: Na+ channel blocker (_____): Blocks conduction; _____ effect on ERP; _____ conduction without affecting the ____

A

slow….little…slows…AP

29
Q

II: Beta blocker: ________ SA node automaticity; reduces _______ activity

A

Decreases…SYMpathetic

30
Q

III: K+ channel blocker: ______ the AP; prolongs phase ___ repolarization

A

Prolongs…3

31
Q

IV: Ca+ channel blocker: Slows conduction velocity at the ______; ______ firing rate of SA and AV nodes

A

AV node… decreases

32
Q

What are the 3 methods of Class I Na+ blocking antiarrythmic drugs?

A

1.Decrease Excitability 2.Decrease conduction velocity 3.Prolong effective refractory period

33
Q

Class IA: slow ______, prolong ____, increase _____

A

conduction, AP, ERP

34
Q

Class IA: _______ = toxic; can produce fatal arrhythmias

– Made from bark of CINCHONA tree = overdose leads to cinchonism

A

QIUN-iD-ine

35
Q

Class IA: _________ after cardioversion to maintain normal rhythm

A

Prophylaxis

36
Q

Class IA: Site of action: _______

A

Atrial tissues

37
Q

Class IA: ________-Derivative of the local anesthetic _______…Many adverse effects = reversible _____-like
syndrome in 25% of patients

A

Procain-amide…..procaine…LUPUS-like

38
Q

Class IA: Used for treatment of VENTRICULAR arrhythmias, as an ALTERNATIVE to quinine and procainamide

A

DIS-o-pyramide (NorPACE)

39
Q

Class IB: decrease duration of AP by ________/________ repolarization (ERP) = ________ rate so overcome ventricular ectopic foci…WHAT IS THE DRUG OF CHOICE? (Treats _______ arrythmias)

A

shortening/decreasing….speeds up…LIDOCAINE…(treats ventricular arrythmias)

40
Q

Which Class IB drug would I give during an MI?

A

LIDOCAINE

41
Q

Where do Class IB’s act?

A

the ventricles!

42
Q

Class IB drug: anticonvulsant/antiarrhythmic….Prolongs ERP and suppresses ventricular pacemaker automaticity; shortens action potential in the heart… **remember this drug causes gingival hyperplasia

A

Phenytion (Dilantin)

43
Q

Which Class IB drug? Structurally related to lidocaine….Serious ventricular arrhythmias; suppression of PVCs

A

mex-il-et-ine (mexico! woo!)

44
Q

Which class IB drug? Suppression of life-threatening ventricular arrhythmias

A

TO-cain-ide

45
Q

Class Ic-MARKED conduction _______…site of action=_____

A

slowing!…ventricles

46
Q

What are the names of these Class IC badasses? Approved only for use of refractory ventricular arrhythmias (life-threatening)…Serious safety concerns: Cause arrhythmias because of profound effect on Na+ channels in healthy heart tissue as well…think Tamborine Rhythm!

A

FLE-CAIN-ide (TAMBocor)…PRO-paf-en-one(RYTHMol)

47
Q

Approved only for use of refractory ventricular arrhythmias (life-threatening)

A

Class IC Antiarrythmias

48
Q

Beta Blockers are ALSO considered Class ____ antiarrythmics!

A

II

49
Q

What channel type do Class III antiarrythmics block? What effect does this have on the AP? On the heart in general?

A

Potassium Channel Blockers! Prolongs the AP (longer Ref Period)..Slows Heart

50
Q

What are our two examples of Class III antiarrythmics? (one Dr. S made us say out loud and together)

A
  1. AMI-O-DaR-ONE 2.Sot-A-LOL(nonselective beta blocker)
51
Q

Which drug has IODINE and therefore long term use causes BLUE SKIN & thyroid disease?

A

AMI-O-DaR-ONE….do, dare,dedi,datum-to give iodine=”io-dar” :) LATIN!!!

52
Q

Class IV Antiarrythmics are Ca2+ channel blockers have a ________ CHRONOtropic effect and a ________ INOtropic effect on the heart.

A

negative…negative

53
Q

WHAT IS THE DRUG OF CHOICE FOR CARDIAC ARRYTMIAS???? What is a side effect? Think real hard about what type of drug it is…

A

VERA-PAM-IL..ca2+ blocker-GINGIVAL HYPERPLASIA!

54
Q

What is a good Diagnostic drug for arrhythmias? (Class IV)

A

Adenosine

55
Q

This CROSSOVER drug is indicated for A-fib, flutter, & congestive heart failure….(a class IV antiarrythmic)

A

DIG-OX-IN

56
Q

DigOXin-Increases ERP
– ______ conduction velocity
– _______ inotropic effect…Which one helps with congestive heart failure?

A

Decreases… Positive (more force)(helps with congestive heart failure)

57
Q

Treating the Tom BradyArrythmias: what brady drug can also be used to SLOW DOWN salivation for a dental procedure?!

A

AtroPine!

58
Q

Treating the Tom BradyArrythmias: What tis the name of the BETA (1&2) AGONIST that is synthetic Epinephrine?

A

Iso-Pro-Ter-On-oL

59
Q

What two minerals can we use to treat Ectopic Pacemakers?

A

Potassium & Magnesium (Mg) haha

60
Q

What is a good sign of CinChonism? (a side affect of the Class 1A antiarrythmic Quinidine)

A

TINNITUS!

61
Q

Drug Interactions with Antiarrhythmics: The vagal blocking effects of antiarrhythmic drugs and anticholinergics (e.g. atropine) can act synergistically and lead to _______

A

tachycardia

62
Q

Drug Interactions with Antiarrhythmics: Therapeutic effects of antiarrhythmics are increased by _______ (and reduced in hypokalemia)

A

potassium

63
Q

Saliva-inhibiting drugs should not be administered to a patient who is prone to arrhythmias, as they may cause _______…e.g. _______

A

tachycardia….atropine

64
Q

Lidocaine solutions used to treat arrhythmias are not the same as dental anesthetics that contain lidocaine = no epinephrine and different _______ = not interchangeable

A

buffering

65
Q

Gingival hyperplasia may be seen with _______ drugs… Dr. Taylor St. Vincent clinic..

A

Ca+channel blocker