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Phar 505 > Arrhythmias: Action potential, ECG, and antiarrhythmics > Flashcards

Arrhythmias: Action potential, ECG, and antiarrhythmics Flashcards

1
Q

What is automaticity, what is excitability, conductivity

A

Ability of a cell to initiate an electrical impulse, ability of cell to respond to electrical stimuli, ability of cells to receive and transmit an electrical impulse between adjacent cells

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2
Q

What is ectopy, what is the normal conduction system

A

Situation in which an electrical impulse is generated outside of the normal conduction system, SA node

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3
Q

What is the normal heart rate produced by SA node, how does the electrical current travel

A

60-100 bpm, current disseminates down left and right atria and move to the AV node, entering the ventricle system and then transmitted through the Bundle of HIS, spreads among the bundle branches until reaching the Purjinke Fibers causing contracting

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4
Q

What are other sources of automaticity, what BPM do they produce

A

AV node: 40-60 bpm, Bundle branches: 40-60 bpm, Purkinje Fibers: 20-40 bpm

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5
Q

What is affected by parasympathetic nodal conduction, what drives the conduction

A

The vagal tone (SA node, AV node, and Atrial response)/ catecholamines, acetylcholine, Calcium channel activity

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6
Q

What is affected by sympathetic nodal conduction, what drives the conduction

A

Mycotes/ catecholamines, Sodium channels, Potassium channels, calcium channel activity

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7
Q

What controls the rate of the SA node, what is it

A

The funny current: slow inward depolarizing Sodium inward currents

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8
Q

What are the three phases of SA node conduction, what, brief summary of each phase

A

Phase 4: Spontaneous depolarization to threshold, Phase 0: Depolarization throughout the cell due to the action potential
Phase 3: Repolarization of the cell

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9
Q

What occurs during phase 4 for the SA node

A

The funny current causes the cell to depolarize, once the cell hits -50mV T-type calcium channels aid in depolarizng the cell, once the cell hits -40mV L-type calcium channels open driving depolarization of the cell until action potential occurs

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10
Q

What causes depolarization throughout the cell

A

L-type calcium channels as the T-type calcium channels and funny currents start to close

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11
Q

What causes repolarization during Phase 3, what dominates ion movement and provides automatcity

A

Potassium channels open and potassium efflux until the cell is back to -60mV to which the potassium channels close, the funny current

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12
Q

What are the phases in cardiac myocyte action potentials

A

Phase 4: Slow depolarization from potassium leaks and small rush of sodium and calcium ions due to gap junctions
Phase 0: Rapid depolarization due to sodium ion influx
Phase 1: Brief repolarization due to sodium channels closing and potassium channels AND calcium channels open
Phase 2: Plataeu contraction due to balanced potassium efflux and calcium influx
Phase 3: Repolarizastion due to calcium channels closing and potassium channels staying open long enough for the cell to reach resting potential. Once the cell hits resting potential potassium channels close

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13
Q

What is the P-wave, QRS-Wave (upper limit ms), T-wave, RR-interval

A

P-wave: atrium depolarization, ventricular muscle depolarization (120 ms), ventricular repolarization, Time between R-R peaks for the QRS complexes

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14
Q

What is the PR interval, what should the ms be if it is normal, what does it mean if it is higher than the normal range

A

Delay through the AV node, 200 mv or less , 1st degree AV block

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15
Q

What is the QT interval, what effects it, what is the equation for QTc

A

Start of ventricular contraction to ventricular end of relaxation, potassium efflux, QTc (sec)= QT (sec)/√RR (sec)

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16
Q

What is considered prolonged QTc in men, women

A

Greater than 470, greater than 480

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17
Q

T/F: If the wave ends on the right side of midway point of an RR interval it is normal while on the left side means a possible arrhythymia

A

False: if the T wave ends before the halfway point then it is normal but if the T wave is to the right side of the midpoint between the RR-interval then it is prolonged

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18
Q

What are the three ways the arrhythmias can occur

A

Increased automaticity, Triggered activity, re-entry

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19
Q

What is the physiological change seen in increased automaticity, where can it occur, how can this lead to arrhythymias

A

Increased phase 4 slope increasing the heart rate, SA node and other tissues,the rate of spontaneous impulse generation exceeds that of the SA node

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20
Q

What are characteristics of increased automaticity, medications that possibly cause, conditions that possibly cause

A

Initiating beat is identical to subsequent beats/ digoxin and catecholamines/ Hypoxia, cardiac dilation, hypokalemia

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21
Q

What are the mechanisms to decrease automaticity what medication classes are given to achieve these effects

A

Decrease the slope of phase 4 (beta-blockers)/ elevate threshold potential (sodium and calcium channel blockers)/ increase maximum diastolic potential (adenosine and acetylcholine)/ increase action potential duration (potassium channel blockers)

22
Q

What is the physiological change seen in triggered events, what are the two types of triggered depolarizations

A

Repetitive mini membrane depolarizations occurring after depolarization but before phase 4/ delayed after depolarization (DAD) and early depolarization (EAD)

23
Q

How does DAD occur, EAD

A

Calcium overload either in the cytoplasm or SR resulting in a DAD after an action potential possibly causing a second beat if threshold is reached/ cardiac repolarization is delayed causing prolonged action potentials

24
Q

T/F:Delayed after-depolarizations are associated with fast heart beats while Early after-depolarizations are associated with slow heart beats

A

True

25
Q

What are medications that can cause afterdepolarizations, what are causes strictly associated with DAD, casues associated with EAD

A

Procainamdie, quinidine, digoxin toxicity/ myocardial ischemia, adrenergic stress, digitalis intoxication, CPVT, catecholamines/ Hypokalemia and class 1a anti-arrhythmic drugs or anything that blacks potassium channels

26
Q

What are ways to prevent DADs and the medication class that do so

A

Reduce calcium influx into the cell while decreasing SR load and spontaneous calcium release from SR (calcium channel blockers )/ elevate the threshold required to create the abnormal stroke (sodium channel blockers)

27
Q

What are way to prevent EADs

A

shorten the action potential duration with isoproterneol, magnesium WITHOUT normalinzing repolarization or QT

28
Q

What is the common causes of arrhythymias, what needs to be present for it to occur

A

reentry/ Two impulse pathways, prolonged refractory in one of the paths, slowed conduction in the other pathway

29
Q

What are the two types of rerentry, what is the difference between the two

A

Functionally defined reentry and anatomically-defined reentry/ Heterogeneity in refractoriness among regions of the heart cause anatomically defined while scarring results in tissues having varied conduction velocities thereby promoting multiple pathways of conduction

30
Q

T/F: Anatomically defined reentry is fixed and is futher caused by CAD, left-ventricular dysfunction or MI while functionally defined reentry is associated with atrial ventricular nodal reentry (AVNRT)

A

False: Anatomically defined reentry is fixed and is associated with (AVNRT) while functionally defined reentry is caused by conditions such as CAD, left-ventricular dysfunction and MI

31
Q

What are drug classes that manage anatomical reentry by increasing refractory period AND decrease conduction velocity, what manages but ONLY INCREASES refractory period, what manages but ONLY DECREASES conduction velocity

A

Potassium channel blcokers, adenosine, calcium channel blockers/ Potassium channel blockers/ sodium channel blockers

32
Q

What types of arrhythymias can be caused by reentry, triggered events, and increased automaticity

A

Atrial fibrillation and ventricular tachycardia

33
Q

T/F: Atrial flutter is only caused by reentry

A

True

34
Q

T/F: The VW classification system for the class 1 AADs is sub-stratified based on how tightly the drugs hold onto the sodium channels in phase 0

A

True

35
Q

What is the MOA of class 1a AADs,

A

Sodium is help onto, thereby decreasing the conduction velocity (slope of phase 0), Potassium efflux in phase 3 is slowed thereby prolonging repolariztion (refractory period and lengthening the action potentials)

36
Q

What is the MOA of class 1b AADs, when are they only used

A

Sodium is held very briefly possibly shortening the refractory period, Vtach only and otherwise rapidly driven tissues

37
Q

What is the MOA of class 1c AADs, what is required for them to be used

A

Sodium is held onto very tightly significantly decreasing the conduction velocity, normal sinus rthym

38
Q

What are the class 1a AADs, how do they effect an ECG

A

Quinidine, Disopyramide , Procainamide (IV)/ Increase QRS and QT interval

39
Q

What are the class 1b AADs, class 1c AADs

A

Mexiletine (PO) and Lidocaine (IV), decrease QT/ Propafenone and Flecanide, increase PR interval and QRS

40
Q

What antiarrythmic binds to sodium channels when it is in an inactivated state, ischemic tissue and faster rates

A

Lidocaine

41
Q

What AADs are metabolized by CYP3A4

A

quinidine, disopyramide, lidocaine, and propafenone

42
Q

What AADs are metabolized by CYP2D6, which of these is also metabolized by CYP1A2 as well

A

mexiletine, flecainide, propafenone/ mexiletine

43
Q

What AADs are eliminated renally

A

NAPA (procainamide active metabolite), 50% of flecainide

44
Q

If someone has moderate to severe liver disease what AAD should be reduced by 20%-30%

A

Propafenone

45
Q

What drug interactions should be cautioned when using flecainide, why

A

Cimetidine increase levels, flecanide increase digoxin

46
Q

What drug interactions should be cautioned when using propafenone, why

A

warfarin and grapefruit juice increase propafenone levels

47
Q

What are side effects associated with using 1a and 1c AADs

A

bradycardia, heart block, hypotension

48
Q

Which 1a cannot be used in heart failure patients

A

Disopyramide

49
Q

T/F: If a patient has an atrial flutter an AV blocking agent (beta-blocker/non-DHP CCBs) is used in conjunction with 1a or 1c agents

A

True

50
Q

T/F: 1c against are not used in post-MI or HF patients

A

True

51
Q

What type of arrhythmia causes Torsade de pointes

A

Reentry and Triggered activity

Phar 505 (33 decks)

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