Dysrhythmics Flashcards

1
Q

Autorhythmic cells

A

Cardiac cells that create their own resting membrane potential
(SA and AV node cells)

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2
Q

Contractile cells

A

Cardiac cells responsible for the heart’s pumping activity

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3
Q

Automaticity

A

Heart’s ability to spontaneously generate an electrical impulse

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4
Q

Depolarization

A

Electrical stimulation/impulse that generates an action potential
(cell becomes less negative)

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5
Q

Repolarization

A

Membrane potential returns to resting/polarized state (more negative)

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6
Q

Conduction velocity

A

Speed in which electrical impulses are transmitted

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7
Q

Refractory period

A

Time frame after depol. where cells can’t be excited again

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8
Q

Absolute refractory period

A

In-excitable period regardless of impulse strength

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9
Q

Relative refractory period

A

The cell is partially repolarized

A strong stimulus could cause depolarization

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10
Q

Vaughan-William Class I Agents

A

Sodium Channel blockers

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11
Q

Vaughan-William Class II Agents

A

Beta blockers

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12
Q

Vaughan-William Class III Agents

A

Potassium channel blockers

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13
Q

Vaughan-William Class IV Agents

A

Non-dihydropyridine calcium channel blockers

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14
Q

Class IA agents and MOA

Double, Quarter, Pounder

A

Disopyramide, Quinidine, Procainamide

Moderate inhibition of phase 0
Prolongs absolute refractory period/repolarization (QT interval)

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15
Q

Class IB agents and MOA

Lettuce, Mayo, Pickles

A

Lidocaine, Mexiletine, Phenytoin

Mild inhibtion of Phaso 0,
Shortens absolute refractory period/repolarization (good for VT/VF

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16
Q

Class IC agents and MOA

Fries, Please

A

Flecainide, Propafenone

Major inhibition of Phase 0
Minimal effect on absolute refractory period/minimal prolongation of repolarization

17
Q

Class I agents MOA

A

Na+ channel blockade (C>A>B)
delay automaticity
slows conduction velocity
varying effects on repolarization

18
Q

Procainamide

A

IV
Ventricular arrhythmias
LD: 500-600mg IV over 25-30 mins
MD: 2-6 mg/min by cont. IV infusion
AEs: hypotension, HF, 1st degree AV block, lupus erythematosus-like syndrome, blood dyscrasias (agranulocytosis, bone marrow suppression, neutropenia, thrombocytopenia)
Active metabolite acts as Class III agent
Substrate of CYP 2D6
Ethanol reduces serum conc.
dose adjust in renal (CrCl<50)/hepatic impairment
TDM: procainamide: 4-10mcg/ml, NAPA: 12-25mcg/ml, combo: 10-30 mcg/ml

19
Q

Disopyramide

A

Norpace
Oral
Ventricular arrhythmias
IR: 100-150mg q6h ATC
CR: 200-300mg q12
Dose adjust in renal dysfunction (CrCl <40) and hepatic dysfunction
CYP3A4 substrate
TDM: 3-7mcg/mL
Beers list: HF inducer, anticholinergic AEs
Take on empty stomach
AEs: hypotension, exacerbate HF, xerostomia, constipation, urinary hesitancy

20
Q

Quinidine

A

Atrial fibrillation/atrial flutter, Ventricular arrhythmias
Gluconate: ER: 648mg PO q8
Sulfate: IR: 200-400mg PO q6h, ER: 300mg q8-12h
(267mg quinidine gluconate = 200mg quinidine sulfate)
Metabolized by CYP3A4 (maj) and eliminated by P-gp
Strong inhibitor of CYP 2D6/P-gp
Dose adjust in CrCl <10, use caution in hepatic impairment
Contraindications: thrombocytopenia, 2nd/3rd degree heart block, concurrent use of quinolone antibiotics (prolong QT interval)
TDM: 3-8mcg/ml
AEs: GI distress, diarrhea, dizziness, fatigue, HA, palpitations, cinchoism

21
Q

Class IA pearls

A

use dependence, TDM, all can be pro-dysrhythmic
avoid in structural heart disease and/or CAD
Notorious for QT-prolongation

22
Q

Class IB Pearls

A

treatment of ventricular arrhythmias
use caution in hepatic disease and HF
higher CNS-related AEs
avoid in pts w/ structural heart disease and/or CAD

23
Q

Lidocaine

A

Xylocaine
VF/pulseless VT, hemodynamic monomorphic VT
1-1.5 mg/kg bolus
Refractory VF/pulseless VT: 0.5-0.75 mg/kg bolus every 5-10 mins (max cumulative dose: 3 mg/kg)
Cont infusion: 1-4mg/min
AEs: heart block, CNS toxicity (seizures, altered mental status, somnolence), N/V
Pearls: lower dose w/ hepatic dysfunction, maj substrate of CYP1A2 and CYP3A4
Contraindications:allergy to corn/corn-related products, severe degrees of SA/AV block(except in artificial pacemakers)
TDM: avoid levels >5 mcg/ml (CNS toxicity)

24
Q

Mexiletine

A

Ventricular arrhythmias
200-300mg PO q8 initially, after dysrhythmia is controlled q12h
Max/day: 1.2g
AEs: GI distress, N/V, dizziness, ataxia, hepatotoxicity, blood dyscrasias, DRESS
Pt counseling: take w/ food, avoid diets/meds that increase urinary pH
Pearls: maj substrate of CYP 1A2 and 2D6, caution in hepatic impairment and/or HF
Contraindications: 2nd/3rd degree AV block (except w/ artificial pacemaker), cardiogenic shock

25
Q

Class IC clinical pearls

A

primarily for supraventricular tachycardia in outpatient setting, avoid in pts w/ structural heart disease and/or CAD

26
Q

Flecainide

A

Tambocor
Paroxysmal a-fib, paroxysmal supraventricular tachycardia
50-100mg PO q12h (max/day 300-400mg)
Pearls: maj substrate of CYP 2D6, caution in hepatic dysfunction, dose adjust in CrCl<35ml/min
Contraindications: ritonavir, pre-existing 2nd/3rd degree AV block
Pt counseling: strict vegetarian diet decreases clearance due to increased urinary pH, milk may decrease absorption
AEs: dizziness, HA, fatigue, nausea, visual disturbances, dyspnea

27
Q

Propafenone

A

Rythmol
Paroxysmal a-fib, paroxysmal supraventricular tachycardia
ER cap: initial 225mg q12 may increase to max of 425mg q12
IR tab: initial: 150mg q8, may increase to max of 300mg q8
Monitor: CBC w/ differential for agranulocytosis, LFTs, ECG for heart block/bradycardia
Pearls: use w/ caution in pts on BBs, CYP2D6 substrate, inhibits P-gp, dose adjust in hepatic dysfunction, avoid grapefruit juice
AEs: unusual taste, n/v, dizziness, fatigue, blurred vision

28
Q

Vaughan-William Class II MOA

A

Autorhythmic cells: inhibits sympathetic activity decreasing SA/AV node automaticity and conduction velocity

Contractile cells: membrane stabilizing activity, increases AP duration and effective refractory period

Beta blockers w/ MSA: propranolol and metoprolol
Beta blockers w/o MSA: esmolol

29
Q

Propranolol

A

Inderal
30-320 mg/day divided q6-8h (Max/day 640mg)
Pearls: non-selective beta blocker, can be used to treat arrhythmias caused by hyperthyroidism
Drug-drug interactions: metabolized by CYP1A2 and 2D6 (fluoxetine), ethanol increases/decreases plasma levels
high protein diet can increase bioavailability (~50%)

30
Q

Esmolol

A

Brevibloc
Continuous infusion: 500mcg/kg/min over 1 min, then 50mcg/kg/min (max 200mcg/kg/min)
Pearls: good for low BP/HR, short half-life (9mins) metabolized by blood cell esterases
Transition to oral BB: reduce infusion by 50% 30mins after first dose of oral alternative

31
Q

Vaughan-William Class III MOA

A

K+ channel blockade (inhibits Phase 3)

Prolongs refractory period/repolarization

32
Q

Vaughan-William Class III agents

A

Amiodarone (Pacerone/Cordarone)
Dofetilide (Tikosyn)
Sotalol (Betapace/Betapace AF)

33
Q

Amiodarone

A

blocks all 4 Vaughan-William Classifications
treats atrial and ventricular arrhythmias
oral: 200-1600 mg/day
IV: 150-300mg rapid bolus, then 1mg/min for 6hrs, tehn 0.5mg/min for 18hrs
AEs: hypotension, bradycardia, hypothyroidism, hyperthyroidism, n/v, acute/chronic liver impairment, photosensitivity, pulmonary toxicity (pneumonitis, fibrosis), peripheral neuropathy, optic neuritis