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Pharmacology 2 > Exam 3 - SVT > Flashcards

Exam 3 - SVT Flashcards

1
Q

What is the drug of choice for abolishing Acute SVT?

A

Adenosine

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2
Q

If AF PT is hemodynamically stable vs unstable what changes in the short-term goals?

A

Stable=Go with anticoagulation second

Unstable=Go with rhythm second

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3
Q

Newly discovered persistent AF is treated in what 4 steps?

A
  1. Rate control and anticoagulation as needed
  2. Antiarrythmic drug therapy
  3. Cardioversion
  4. Long-term antiarrythmic drug therapy
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4
Q

What med types are used for pharmacological rate control in AF?

A

Beta-blockers, CCB, Digitalis, Amiodarone, Dronedarone.

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5
Q

What two things used for non-pharmacological rate control?

A
  1. Pacing

2. Ablation

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6
Q

What two drugs are preferred for chemical cardioversion?

A
  1. Dofetilide

2. Ibutilide

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7
Q

Which three drug types prevent remodeling in AF?

A
  1. ACEI
  2. ARB
  3. CCB
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8
Q

Which Nonselective/Cardioselective/Mixed Beta-Blockers are used for rate control in AF?

A

Cardioselective: Atenolol, Metoprolol Succ and Tart
Nonselective: Propanolol, Nadolol
Mixed: Carvedilol, Labetolol

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9
Q

Which CCBs are used for rate control in AF?

A

Non-DI CCBs (Verapamil, Diltiazem)

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10
Q

Two cases where rate control is very important in AF?

A
  1. LV damage

2. Extensive CAD

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11
Q

What are some problems with Antiarrythmic drugs?

A

Limited efficacy long-term (recurrence likely), adverse drug reactions (may cause arrythmias)

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12
Q

Are Class I drugs used (QPDLFP)? Why or why not?

A

Very rarely. Old and dangerous; can cause arrythmias.

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13
Q

What percent with AF of people will fall out of NSR due to disease progress? What about those on Amiodarone?

A

50% will fall out due to disease progression. Amiodarone 2/3 will stay in NSR.

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14
Q

In a PT with persistent or paryoxysmal AF what is the first question to ask with regards to drug selection?

A

Is there structural heart disease or not

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15
Q

In PTs with AF and no structural heart disease what is the progression of drugs and other therapies?

A

D.D.F.P.S.->Amiodarone->Catheter Ablation

Dofetilidide, Dronedarone, Flecainide, Propafenone, Sotolol

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16
Q

When is Amiodarone used in AF? What can it cause?

A

Used for those who have failed previous therapy. Can crash CO.

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17
Q

If AF PT has structural heart disease what must you next determine?

A

If they have CAD or HF

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18
Q

If AF PT has CAD with structural heart disease what are treatment options

A

DDS->Amiodarine->Ablation

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19
Q

If AF PT has Heart Failure with structural heart disease what are treatment options?

A

Amiodarine or Dofetilides->Ablation

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19
Q

Which ion is blocked in the Class 1 drugs? What are the 6 Class 1 antiarrythmics?

A

Sodium

QPDLFP

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20
Q

What ions blocked in Class I, II, III, and VI

A

I=Na+
II=Ca++
III=K+
IV=Ca++

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21
Q

What ion is blocked in Class II drugs? What are they?

A

Calcium.

Beta-blockers.

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22
Q

What ion is blocked in Class III drugs? What are the 5?

A

Potassium

SAD.ID

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23
Q

Which ion is blocked in Class IV drugs? What are the two?

A

Calcium.

Verapamil and Diltiazem.

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24
Q

Three are three short-term treatment goals for AF patients if hemodynamically stable or unstable?

A
  1. Immediate rate control
  2. Drug or electrical cardioversion
  3. Anticoagulation

If hemodynamically stable then anticoagulation is number 2.

25
Q

What are the three long-term goals for AF patients?

A
  1. Rate Control
  2. Maintenance of Sinus Rhythm
  3. Stroke Prevention
26
Q

Which ions are blocked in sinus rhythm maintenance meds in AF?

A

Sodium=Class IA and Ic
Potassium=Class III
Calcium=Beta-Blockers

27
Q

Three category of meds which prevent remodeling in AF?

A
  1. ACE-I
  2. ARC
  3. CCBs
28
Q

What is the most common arrythmia world wide? What percent of them are over 65 y/o? How many times is their cardiac mortality and stroke risk increased?

A

AFib is most common. 80% over 65 y/o. 2x cardiac mortality, 5x stroke risk.

29
Q

Class I VW drugs all block what Ion?

A

Sodium

30
Q

What are the Class II VW drugs, mechanism, and which ion? Effect on action potention time, AV node, and conduction in ischemic tissue?

A

Beta-Blockers block calcium. Decreased beta-adrenergic sympathetic activity, prolonged action potential, slower conduction in ischemic tissue. Slots heart-rate, slows AV nodal conduction, and AV nodal refractoriness.

31
Q

Metroprolol MOA? Labeled and unlabeled uses?

A

CYP2D6 extensive 1st pass. Selective B1. Used when rate control immediately needed.
Unlabeled: Tachyrhythmias, Acute VT

32
Q

Carvedilol MOA? Labeled use? Unlabeled use?

A

Combo non-selective Beta-adrenergic and Alpha-adrenergic blocking activity. Based on dose.
Labeled use: HTN, angina, post-MI LVD and HF
Unlabeled: Rate mgm’t in select AF patients (post-MI, stable LVD, and HF)

33
Q

Sotolol MOA? Labeled use? Unlabeled use? Renal?

A

Dual purpose non-selective beta-blocker and potassium-blocker. Decreases rate and prolongs action potentials.
Labeled: Conversion of sustained VT, maintenance after AF converted to NSR.
Unlabeled: NSR maintenance in AF with hypertrophic cardiomyopathy with preserved LV mass and function.
Renal: Must be adjusted.

34
Q

Sotalol contraindications?

A
  1. Bradycardia
  2. 2-3rd degree heard block
  3. Long QT
  4. Heart Failure
  5. Cardiogenic shock
35
Q

Which of the “three main” Beta Blockers can be used in a patient with Heart Failure? Which cannot?

A

Safe in HF: Metoprolol and Carvedilol

CI in HF: Sotalol

36
Q

Which of the “three main” Beta Blockers cannot be used in a patient with Heart Block? Which can and in which type?

A

No use in Heart Block: Metoprolol and Carvedilol

Safe in 1st degree heart block only: Sotalol

37
Q

What is the class, MOA, indication, and CIs for Ibutilide?

A

Class III
MOA: K+ channel blocker, prolongs refractoriness
Converts acute Afib/Aflutter to NSR. Used with electric cardioversion to lower energy for shock.
CI: K less than 3.5, QT more than 440 msec, symptoms more than 48h

38
Q

What is the class, MOA, indication, and CIs for Dofetilide? Renal?

A

Class III
MOA: K+ blocker, prolongs refractoriness
Acute tx of AF to NSR and maintenance.
CI: QT more than 440 msec, uncorrected K+, CrCl less than 20

39
Q

What is the class, MOA, 3 indication, and CIs for Amiodarone?

A

Class III
MOA: K+, Na+, and Ca++ blocking. Prolongs AP and refractory period. Decrease AV and sinus node function.
Indications: Maintain NSR w/AF, breakthrough VT/VF, pulseless VT/VF
CI: Sever bradycardia, 2nd or 3rd degree AV block, cardiogenic shock

40
Q

Amiodarone half-life and use with anticoagulants? Amiodarine with antiarrythmics may cause what?

A

55 day half-life VERY LONG!

Warfarin + Amiodarone require half-doses.

Don’t double up on antiarrythmics! No Flacanid or Propadanone or else long Q-T phenomena!

41
Q

What is the class, MOA, indication, and CIs for Non-DI CCBs?

A

Class 4 Antiarrythmics.
MOA: Depress AV node conduction, increases AV refractoriness. Decreases pacemaker activity.
CI: 2nd-3rd degree AV block, SBP less than 90, others drug-specific

42
Q

What is the class, MOA, 3 indication, and CIs for Verapamil?

A

Class 4 Antiarrythmic
MOA: CCB slows AV nodal conduction. Smooth and vascular muscle relaxation, improved myocardial demand in CAD.
Indication: Paroxysmal SVT, rate control in AFib/flutt, HTN
Off-label: Migraine, mania, hypertrophic cardiomyopathy
CI: SBP less than 90, sick-sinus, 2nd-3rd degree block, AF w/reentry tachycardia, preexication syndrome

44
Q

What is the class, MOA, indication, and CIs for Diltiazem?

A

Class 4 antiarrythmic
MOA: CCB slows AV nodal conduction. Smooth and vascular muscle relax, improved myocardial oxygenation in CAD
Indication: Off-label for narrow and stable SVT after Adenosine and vagal maneuvers
CI: SBP less than 90, 2nd-3rd heart block, acute MI, decompensated HF, pulmonary congestion

45
Q

What are two non-VW agents?

A
  1. Adenosine

2. Digoxin

46
Q

Which category is better than Digoxin at reducing ventricular rate? Is Digoxin consistent at NSR correction? Toxicity?

A

Beta-blockers are more effective.

Inconsistent at NSR correction.

Digoxin can become toxic.

47
Q

What is the class, MOA, indication, and CIs for Adenosine?

A

No class.
MOA: Rapid and reversible AV block, slows AV node conduction interrupting re-entry pathways
Indication: Terminated SVT from AV nodal re-entry tachycardia
CI: WPW, 2nd or 3rd degree heart block, symptomatic bradycardia

48
Q

What can Adenosine help with the diagnosis of? Half-life and excretion?

A

Allows diagnosis of latent pre-excitation from accessory pathways in patients with atrial arrhythmias and normal ECG during sinus rhythm
Half-life: 10 seconds
Excretion: 30 seconds

49
Q

What is the class, MOA, indication, and CIs for Digoxin?

A

No class.
MOA: Inhibit Na+/K+ ATPase pump. AV nodal suppression, increase period, reduced conduction velocity by increased vagal tone
Indication: Rhythm control. Suppresses Afib induced VT
CI: Digoxin hypersensitivity, vfib

50
Q

What rhythm change can Digoxin cause from toxicity?

A

Prolonged PR-interval shows up at longer R-R on strip.

Sagging ST and ST segment depression.

51
Q

Which is the only antiarrythmic to DECREASE refractory period?

A

Lidocaine. Class Ib. Na+ blocker.

52
Q

What are the three types of SVT?

A
  1. Afib/Aflutter
  2. Paroxysmal Supraventricular tachycardia (PSVT)
  3. Atrial Tachycardia
53
Q

What is the last drug to use in paroxysmal or persistent atrial fibrillation only after medication risks have been considered and when other antiarrhythmic agents have failed or have been contraindicated?

A

Adenosine (make sure about this answer)

54
Q

Which two antiarrythmics are not used in PTs with structural heart disease?

A

Flecainide

Propafenone

55
Q

In PT with new AFib but no symptoms what is best rate-control med?

A

Metoprolol Succinate

56
Q

Does gingival hyperplasia happen with Amiodarone?

A

No

57
Q

Is Verapamil appropriate in a PT with wide-QRS tachycardia?

A

No

58
Q

What is Sotalol’s CrCl contraindication?

A

CrCl less than 40

59
Q

What is drug of choice for Torsades?

A

Magnesium

60
Q

What is done to Procainamide in a PT with history liver impairment?

A

Reduce Procainamide dose by 50%

Pharmacology 2 (17 decks)

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