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SUMPHARM > Antiarrythmias > Flashcards

Antiarrythmias Flashcards

1
Q

How does heart contract?

A 
Depolarization. Changes resting membrane potential via Na, Ca, Cl, K. 
K intracellular (-), 
Na Extracelluar (+). 
3 Na out 2 K in= change in potential
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2
Q

What does M gate means?

A

m=Activation gate at channels (intramembrane protein or phosophlipid). h= inactivation.
RESTING m= closed, h = open or closed

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3
Q

What is speed of Na and Ca channels state?

A

Na- fast, Ca-slow L channel more +

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4
Q

During ventricular contraction what is gate status?

A

Phase 0-Na/Ca m and h gate= OPEN QRS on EKG

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5
Q

What ion do SA and AV node depend for depolarization?

A

Calcium channels

Atria and ventricular rely on NA channels

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6
Q

What are phases seen in purkinje fibers?

A

Phase 1- Cl exit.
Phase 2- plateau, Ca in K out= contraction
Phase 3- rapid repolarizations K out T wave
Phase 4- resting Na out K in, flat in ventricle

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7
Q

How do pacemaker cells contract?

A

Depolarize via special hyperpolization ion channels. HYPERKALEMIA= SLOW PACEMAKER. HYPOKALEMIA=FAST PACEMAKER

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8
Q

How do formation disturbance affect arrhythmia mechanisms?

A

Affects slope of Phase 4 by 1. DEC slope d/t vagal stimulation, B-blockade bradycardia 2. INC slove d/t HYPOkalemia, B-stimulation fiber stretch, acidosis, INC HR

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9
Q

How do conductance disturbance affect arrhythmia mechanisms?

A

HYPERKALEMIA- extracellular potassium DEC APD (AP duration), slow impulse, DEC pacemaker rate, flattens Phase 4. HYPOKalemia- INC APD, INC pacemaker rate, INC Slope of phase 4

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10
Q

What is seen in fibers related to disturbing impulse conduction?

A

Normally conduction meet and extinguish each other.

IF a block d/t damage, pulses re-enter into tissue where impulse bifurcates

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11
Q

What exaggerate arrhythmia?

A

Ischemia, Hypoxia, Acidosis-formation issue, Excessive catehcholimines- Ca issue, Electoryles, Drug toxics, scarred stretced cardiac tissue- dec impulse geneation (SIMIlar to MSK injury)

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12
Q

How do anti-arrhythmic drugs DEC ectopic (outside) pacemaker activity?

A
  1. DEC conduction, excitably, INC APD
  2. Block Na or CA channels
  3. Prefer Phase 0 upstroke and Phase 2 plateau. NO binding during resting phase
  4. Reduce Phase 4 slope
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13
Q

Why does the EBM state antiarrhymics are poison with therapeutic effects?

A

At higher does, ischemia, hyperkalemia, and INC HR- the drugs can affect normal tissue-

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14
Q

What Drug class are Na channel blocker lengthen APD?

A

CLASS 1A- Discopyramidine, Quinidine, Procainamide (Double Quarter Pounder)

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15
Q

What Drug class are Na channel blocker that Shorten APD?

A

CLASS 1B- Lidocaine and Mexiletene (w/ lettuce and mayo)

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16
Q

What Drug class are Na channel blockers that slow bind to NA channel no effect APD?

A

CLASS 1C- Flecaine and Propafenone (Fries please)

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17
Q

What Drug class is Sympatholytic- reduce SNS/adrenerig/Epi/NE activity?

A

CLASS II- Propanol, Beta Block

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18
Q

Which Class prolongs refractory period, Prolongs APD, most blocking of outward K+ channels, thus HYPOkalemia, (less K outward, INC slope of Phase 4, less repolarization) INC APD, INC pacemaker Rate. BUT arrythmia may occur.)

A

CLASS III-Ibutilide, Solatol, Amiodarone, Dronedarone

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19
Q

Mr. Heme was DX w/ Afib has NO CVD, but has COPD and HTN. What class drugs are ideal for him?

A

BB and CCB (Class 4)

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20
Q

Mrs. Hart has A. Fib with LV dyfs and HF. Which drug is ideal for her?

A

BB and Digoxin, Amiodarone

** AVOID CB

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21
Q

If a pt has A.fib what 2nd line drug is ideal, but with Caution d/t SE?

A

Amiodarone.

**AVOID w/ COPD

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22
Q

What are MC used anitarrythmics?

A

BB, CCB and amiodarone. LEAST- LIDOcaine

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23
Q

This drug is Class 1A, with a-blockade vagolytic and blocks K channels, used for Malaria IV. Rare for Afib. flutter, WPW, VT?

A

Quinidine: USE; RATE ADE- 1. Ears, 2. vision,3. HYPOtension. 4. INC HR in a.fib d/t AV node. treat-digoxin CCB, BB

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24
Q

This drug is Class 1A, with a-blockade vagolytic and **ganglionic blockade, with a **metabolite the prolongs APD?

A

PROCAINAMIDE- USE- RATE VT, post MI (2nd line). INJ ONLY. ADE: Lupus, Agranulocytosis, MDD, Psychosis
(PRO crazy)

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25
Q

This drug is Class 1A, with a-blockade vagolytic, with renal adjustment?

A

DISOPYRAMIDE- USE: afib, wpw, psvt, VT life ADE- anticholinergic, AVOID BPH, NEG iontropic (contraction) **worsen HF

26
Q

This class 1B drug is used in VENTRICULAR ARRY ONLY?

A

LIDOCAINE- USE: ischemia post MI, not for prevention only during arrhythmias.
ADE- poor oral abs. IV ONLY, LIVER toxic, CNS depression, seizure, paresthesia, proarrhtymic HIGH dose

27
Q

What topical anesthesia is for post herpetic neuralgia, endotracheal, urethral?

A

LIDOCAINE patch, Oral prep, or catheter patches

28
Q

This class 1B drug is used in VENTRICULAR ARRY ONLY and Neuropathic pain?

A

MEXILETINE: PO,
ADE: drowsy, agitation, twitch, seizures. LONG HALF life

29
Q

This Class 1C drug that has min B AV blk affect is NOT USED in structural CVD d/t negative inotrophic cardia affect?

A

FLECAINIDE; AF, *chemical converter.
ADE; 7hr t1/2, *AVOID in CAD and VT and MI. Dizzy, vision tremor. Metallic taste.
DI- Ritonovir: CYP inbib, INC Flec

30
Q

This Class 1C drug that has min B AV blockade, proarrhytmic, bronchospasm, neg. inotropic effect?

A

PROPAFENONE: ADE AVOID MI.
1. Dizzy, vision
DI- FQs proarrthymia

31
Q

This solo class II drug is BB only NO INC in APD, DEC slope of phase 4-thus bradycardia btwn next AP?

A

PROPANOLOL- USE; Post MI DEC mortally, thyrotoxicosis, pheochromcytoma,
RATE AFib, sinus tachy, VT-acute,

32
Q

This is the MC class 3 drug w/ less proarrhythmic risk, RATE and RHYthm of atrial and ventricle?

A 
AMIODARONE. ADE: 
1. Pulmonary fibrosis 
2. Photosensitivity skin** 
3. Halos of light d/t corneal ASX 
4. Thyroid dfx 
5- Neurologic 
6. Liver toxic 
7. Severe bradycardia 
8 IV- phlebitis
33
Q

What should be monitored with Amiodarone?

A

**LFT and TSH and PT/INR

34
Q

Amiodarone INC this drug level, high risk bc most CVD are on this drug?

A

Digoxin INC

Wafarin- hypoprothrominenia (less clots, inc bleeding) DEC warfarin dose 30-50%

35
Q

What drugs with Amiodarone will INC Torsades and Prolong QT?

A

**Phenothiazines and FQs

36
Q

What other DIs with Amiodarone?

A
  1. Fentanyl anesthesia,
  2. Ritonavir- inhbit CYP of amiodarone INC
  3. Phenytoin- DEC amiodarone
37
Q

How should amidarone be dosed?

A

Loading dose needed to reach SS.

IV- Nexterone- no PVC pipe issue

38
Q

What Class 3 agent is rhythm control with INC in death?

A

Dronedarone

ADE- Long QT DI- Cyp inhib-TCA long QT, Digoxin, Statins

39
Q

This class 3 drug INC APD used in AF for NSR rhythm control, BB?

A

Sotalol ADE: Renal, DI-FQ INC arrhythmia, *NSAIDs DEC HTN effect

40
Q

This Class 3 drug enhances slow NA depolarization during plateau phase, prolongs depolarization. NO K block. Prolong QT?

A 
Ibutilide. MOU- electrical cardioversion post op 
ADE- pro-arrhythmic. AVOID other class and NO long QT drugs
41
Q

This Class 3 drug BLOCK k channels?

A

Dofetilide. MOU- conversion to NSR ADE- RENAL , arrhythmic Discontinue

42
Q

What drug slows SA node, and prolongs AV node during refractory period?

A

CCB- Verapamil, Dilitaxem

ADE- ONLY for SVT. may covert VTACh to VFib. MAY cause AV Blocks

43
Q

What anti-arrhythmic non class is vagal stimulation, INC APD inhibits NA K Atpase pump?

A

DIGOXIN- INC K+ conductance, Ca enters.
PNS activity in ATRIA and AV
USE- Ventricular RATE in AFIB

44
Q

What inhibits Ca and activate K currents?

A

Adenosine binds to receptors cause RATE control for PSVT re-entry.
Depresses AV node,
Inhibits SA.
Goal convert to NSR.

45
Q

What are ADE of Adensoine?

A

Facial flushing, dyspnea, chest pressure.
DI. Theophyline.
Dose- INJ- 5-9sec half life***Max 2-3 doses,

46
Q

What can cause slowed SA node?

A

INC Potassium- lengthens REpolarization, thus SA node not triggered.

47
Q

What INC early action depolar and delayed depolar?

A

HYPOKalemia- NO depolarization, thus SA starts quick

48
Q

What electrolyte if low will induce Digoxin arrhythmia?

49
Q

What other Drugs are used of ACLS?

A
  1. Epi- vasoconstrictor, tachycardia- USE VF, VT
  2. Vasopressin- vasoconstrictor
  3. Atropine: bradycardia PNS effect dry mouth etc.
  4. Dopamine- INC renal blood flow, POS inotrope, INC HTN 5. Isoproeneral- Beta 1-2 agonist, INC HR
50
Q

What can improve survival post MI from VF or VT?

A

**BB and Amiodarone

51
Q

This condition has risk of stroke in this chamber, d/t stasis and DEC CO?

A

A. Fib-palpitation, DOE, CP, dizzy.
Paroxysmal- self terminates
Persistent- end >7days, Permanent- NO RHYTHM control

52
Q

What is important with care of AFib?

A
  1. Ventricle rate control
  2. Conversion to NSR
  3. Anticoagulation- Age and Stroke INC risk
53
Q

What is difference with rhythm control vs Rate control?

A

Rhythm- atria and nodes,
Rate- Ventricles.
EBM- AVOID Rhythm focus on RATE for A. Fib

54
Q

What are rate control goals?

A
  1. HR <80 for SX AF
  2. Rest 60-80, <110
  3. AVOID CCB, Digoxin, Amiodarone in HF. NO Dronderone for ventricular rate control
  4. Use loading and maintenance dose
55
Q

What are goals for rhythm control?

A
  1. NSR
  2. prevent AF
    3 limit drug toxicity
  3. Class 3- hospital via direct cardioversion and BB out patient
56
Q

What Rhythm control drugs are used in Pt WITHOUT structural CVD?

A
  1. Dofetilide, Dronerdarone, *Flecainide, *Propafenone, Sotalol.
  2. Amiodarone
  3. Cather ablation.
57
Q

What Rhythm control drugs are used in Pt WITH structural CVD?

A

CAD- Dofetilide, Dronerdarone, Sotalol.

HF- Amiodarone Dofetilide

58
Q

What will help a pt stay converted to NSR?

A

Most remain NSR 1yr add anti arrythmic INC chance

59
Q

If Afib is present 48hr, what must be done 1st?

A

Warfarin maintain INR x3 wks and 4 wk after conversion.

60
Q

When are AF drugs ideal?

A

recent onset of AF when electrical not available

61
Q

Who are less likely to via electrical conversion?

A

Overweight and CMP, long duration

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