cardiac arrhythmias: an energizer · 2018-05-04 · cardiac arrhythmias: an energizer jackoline...

Cardiac Arrhythmias: An Energizer

JACKOLINE COSTANTINO, PHARMD

PGY-2 CARDIOLOGY PHARMACY RESIDENT

DAVIDE VENTURA, PHARMD, BCCCP

CLINICAL PHARMACY SPECIALIST-CARDIOLOGY

FLORIDA HOSPITAL ORLANDO; ORLANDO, FL

Disclosures

Presenters have no actual or potential conflicts of

interest related to the content of this presentation

Objectives

Review the cardiac myocytes electrophysiology

Review the cardiac anatomy and physiology of the cardiac conduction system

Review the pharmacology of antiarrhythmic medications and classification scheme

Outline pharmacokinetics & pharmacodynamics properties of antiarrhythmic medications

Review guidelines recommendations for common arrhythmias and therapeutic options

Given a patient case, utilize guidelines to treat presenting arrhythmia

Agenda

Electrophysiology Pharmacotherapy Patient Cases

Causes of Arrhythmias

Coronary artery disease Hypertension

Cardiomyopathy Valve disorders

Electrolyte abnormality

(Na+, Ca2+, K+)

Myocardial infarction

Cardiac surgery Drug induced

Congenital & Genetics Age

Cardiac Anatomical Circuitry

Cardiac Electrophysiology-Non-Nodal Tissue

Cardiac Electrophysiology-Nodal Tissue

4

Cardiac Electrophysiology-Nodal Tissue

03

4

2

Electrocardiogram (ECG or EKG)

P wave: Atrial

depolarization

PR interval: AV nodal

conduction time

QRS: Depolarization of

ventricles,

repolarization of the

atria

T-wave: Ventricle

repolarization

QT interval: Ventricle

APD

Origins of Dysrhythmias

•Depressed automaticity

•Enhanced automaticity

Abnormal impulse generation

•Delayed after depolarization

•Early after depolarization

Triggered activity

•Conduction block

•Re-entry phenomenon

•Accessory tract pathways

Abnormal impulse conduction

Iwasaki Y, el al. Circulation. 2011;124:2264-74

Origins of Dysrhythmias

Iwasaki Y, el al. Circulation. 2011;124:2264-74

Abnormal Impulse Conduction

Re-entry

Anatomically defined circuit

Unidirectional block

Impulse with slow

conduction

Re-Entry Mechanism

A

• Normal conduction around scar tissue; both limbs capable of receiving conduction

B• Both arms are refractory

C1

• One limb is refractory/blocked and the other limb is receptive

C2

• Blocked limb completes repolarization, signal enters retrograde and re-entry occurs

Accessory Electrophysiology

Audience Response Question #1

All of the following statements are true EXCEPT:

1. Fast channel action potentials are driven by calcium influx in phase 0

2. Slow channel action potentials are driven by calcium influx in phase 0

3. Unidirectional blocks can result in re-entry circus rhythms

4. Early after depolarization is often a result of loss of potassium channel function as well as congenital anomalies (LQTS) and can lead to TdP

5. Only option A is FALSE

6. Only option B is FALSE

Agenda


Goals of Antiarrhythmic Agents

Decrease conduction velocity

Change duration of effective refractory period (ERP)

Suppress abnormal automaticity

Prevent secondary events (ie. embolic strokes)

Antiarrhythmic Pharmacotherapy

Vaughan-Williams Classification

Class I

•Sodium Channel Blocker

Class II

•Beta Blocker

Class III

•Potassium Channel Blocker

Class IV

•Calcium Channel Blocker


Class Ia

Quinidine Procainamide Disopyramide

Slows the rate of Na channel opening Phase 0

Prolong action potential and ERP by blocking potassium channels

Decreases the slop of Phase 4 spontaneous depolarization

Increases QRS and QT interval

Therapy Overview

Drug CommonUses

Target Effect Pharmacokinetics (PKT) Common Side Effect

Disopyramide AF, VF, hypertrophic obstructivecardiomyo-

pathy

INa, IKr QRS prolonged QTc prolonged; increased DFT

Onset: 0.5-3.5h,T1/2: 4-10 h -> increased with HF;

Metab: H-dealkylation;Excr: U/F

Anticholinergiceffects, prostatism,

QT interval, negative inotrope

Procainamide VT INa, IKr QRS prolonged QTc prolonged; increased DFT

Onset: 10-30 min, T1/2: 2–5 h(FA vs SA); NAPA 6–8 h T1/2

prolonged in renal/hep dysfxn. Anephric: proc 11 h/NAPA 42 h; Metab: H (NAT/Cyp

2D6); Excr: U

TdP, AVB, hypoTN; exacerbate HFrEF;Lupus symptoms,

N/D, blood dyscrasias

Quinidine T, VF (Short QT

syndrome, Brugada), AF

INa, Ito, Ikr,

M, α-receptor

QRS prolonged QTc prolonged; increased DFT

Onset: 1-2hT1/2: 6-8 h; longer in HF, liver cirrhosis, older

age; Metab: H (Cyp 2D6/3A4)/ I: CYP 2D6 (St),P-gp (increases digoxin, BB, TCAs);

Excr: U

Cinchonism,abdominal cramps,

n/v/d, TdP, worsening HF,

ventricular arrhythmias, fever

AVB: AV-block; CYP: Cytochrome P-450; H: Hepatic; R: Renal; M: Major; St: Strong; SA: Slow acetylators; FA: Fast acetylators; PM: Poor metabolizer; EM: Extensive metabolizer; NAT: N-acetyltrasferase

Pearls

Pearls

Quinidine • Prevents SCD • AE present in 38% of patients

• Alternative to ICD in select patients • Reduces ICD shocks

Procainamide • Provokes suspected Brugada Syndrome• Poor outcomes for use by EMS outside responders

• Superior to lidocaine and amiodarone for VT termination• Poor outcome for routine prophylaxis use for post MI ventricular arrhythmias

Disopyramide • Pyridostigmine for anticholinergic effects • Ameliorates symptoms of exertional SOB, pre-syncope and syncope due to obstructive HCM

• Synergistic effects when given with metoprolol, verapamil or diltiazem for atrial fibrillation

Parker M, et al. J Pharm Practice, 2016;29(1):77-86

http://www.acc.org/latest-in-cardiology/articles/2014/07/18/15/12/ten-pearls-for-the-use-of-antiarrhythmic-drugs-for-atrial-fibrillation


Class Ib

Lidocaine Mexiletine Phenytoin

Shortens phase 3, repolarization by blocking small sodium plateau current

Decreases the duration of the cardiac action potential

High affinity for open and inactivated Na channels with rapid unbinding

during diastole, hence little cumulative effect on QRS in NSR

Drug CommonUses

Target Effect PKT Common Side Effect

Lidocaine VT, VF INaNo marked effect on most intervals; QTccan slightly shorten

Onset: 0.5hT1/2: 1-3h; prolonged in HF, liver dz,

renal disease.Metab: H (Cyp 3A4/2D6/IA2/2C9) I:

CYP 1A2 (St)/2D6 Excr: U

Bradycardia, hemodynamic collapse, AVB, sinus arrest,

delirium, psychosis, seizure, nausea, tinnitus, dyspnea,

bronchospasm

Mexilitine T, VF, PVC, has a role in

patients with LQT syndrome

INa No marked effect on most intervals; QTccan slightly shorten

Onset: 30-120 minT1/2: 12-20h (PM)

7-11h (EM); Metab: H (CYP 2D6 (M)/1A2 (M); I: CYP 1A2 (St);

Excr: U

Arrhythmias, dizziness,N/V,D, ,tremor, CP, angina,insomnia, blurred vision,

tinnitus

Therapy Overview

Pearls

Pearls

Lidocaine • Refractory VT/Cardiac arrest• Amiodarone and procainamide more effective for termination of stable VT

• Works preferentially on ischemic tissues

Mexilitine • Oral equivalent of lidocaine• Congenital long QT syndrome

• Useful for recurrent ICD shocks

Phenytoin • Not used for antiarrhythmic properties• If bradycardic, check free phenytoin level, and consider using another agent if patients are symptomatic




Class Ic

Flecainide Propafenone

Slows the rate of Na channel opening Phase 0

Slow conduction in all the myocardial tissues, with minor effect on duration

of action ad refractoriness

Automaticity is reduced by increase in the threshold potential rather than

decrease in the slope of the phase 4 depolarization

Drug Common Use

Target Effect PKT Common Side Effects

Flecainide VT, PVC (inthe absence

of SHD);CPVT,

AVNRT, AVRT, AF

INa, IKr, IKurPR prolonged

QRS prolonged;increased DFT

Onset: 1hT1/2: 12-27h (PM); 10-14

(EM)Metab: H (CYP 2D6

(M)/1A2)/ I: CYP 2D6;Excre: U

SND, AVB, drug-inducedBrugada syndrome,monomorphic VT in

patients with a myocardial scar, exacerbation of

HFrEF, dizziness, tremor, vision disturbance,dyspnea, nausea

Propafenone VT, PVC (inThe absence

of SHD), AVNRT,

AVRT, AF

INa, IKr, Ikur,

Betareceptor

PR prolongedQRS prolonged;increased DFT

Onset: 3.5hT1/2: 10-32h (PM); 2-10

(EM)Metab: H (CYP 2D6

(M)/1A2)/2D6 / I: CYP1A2/2D6; Excre: U

HF, AVB, drug-inducedBrugada syndrome,

dizziness, fatigue, N/D, xerostomia, tremor,

blurred vision

Therapy Overview

Pearls

Pearls

Flecainide • Avoid in structural heart disease • ICD, drug and ablation refractory VT• Provokes suspected Brugada Syndrome

• Reduces exercise-induced ventricular arrhythmias with catecholaminergicpolymorphic VT

Propafenone • Significant beta-blocking properties that cause bradycardia and heart block• Increases digoxin levels

• ICD drug and ablation refractory VT• Modest efficacy to suppress RV outflowtract (RVOT) VA/PVC although with a far higher rate of recurrence than catheter ablation



Vaughan-Williams Classification (Class II-Beta blockers)

Drug Common Use


Acebutolol AF, VT, PVC Beta 1, Mild ISA

Sinus rate slowed

AV nodalrefractoriness

increased

ActiveMetabolite T1/2:

8–13 h; (prolonged with

Renal impairment) Metab: H; Excr: F 60%, U

40%

Bradycardia, hypotension, HF, AVB,

Dizziness,fatigue, anxiety,

impotence, hyper/hypoesthesia

Atenolol AF, VT, PVC,

ARVC,LQTS

Beta 1receptor

Sinus rate slowed


increased

T1/2: 6–7 h (prolonged with renal impairment)

Metab: H Excr: F 50%, U40%

Bradycardia, hypotension, HF,AVB, Dizziness,

fatigue, depression,impotence

Therapy Overview

Bennet MT, et al. Europace. 2014;16:1847-1851

Drug Common Use


Bisoprolol AF, VT, PVC

Beta 1receptor

Sinus rate slowedAV nodal

refractorinessincreased

T1/2: 9-12h Metab: H Excr: U

Chest pain,bradycardia, AVB, Fatigue,

insomnia, diarrhea

Carvedilol AF, VT, PVC

Beta 1 and 2Receptors,

alpha receptor



T1/2: 7–10 hMetab: H

Excr: F

Bradycardia, hypotension, AVB, edema, syncope,

Hyperglycemia, dizziness, fatigue, diarrhea

Therapy Overview

Drug Common Use


Esmolol AF, VT, AVNRT, AVRT

Beta 1 receptor



T1/2: 9 minMetab: RBCEsterases,

Excr: U

Bradycardia, hypotension, HF, AVB, Dizziness, nausea

Metoprolol AF, VT, PVC,

AVNRT, AVRT

Beta 1 receptor



T1/2: 3–4 hMetab: H

Excr: U

Bradycardia,hypotension, AVB, Dizziness, fatigue,

diarrhea, depression, dyspnea

Nadalol AF, VT, PVC, LQTS,

CPVT

Beta 1 and 2 receptors



T1/2: 20–24 hMetab: none

Excr: U

Bradycardia, hypotension, HF, AVB, edema,dizziness, cold

extremities, bronchospasm

Therapy Overview


Drug Common Use


Propranolol AF, VT, PVC,LQTS,

AVNRT, AVRT

Beta 1 and 2 receptors, INa



Onset: 1hT1/2: IR 3-6h, ER 8-10h,Metab: H (CYP 2D6);

Excre: U

Bradycardia, hypotension, HF, AVB, sleep disorder, dizziness, nightmares, hyperglycemia,

diarrhea, bronchospasm

Therapy Overview


Pearls

Pearls

• Better safety profile than other antiarrhythmics• Effective treatment of VA and reducing the risk of SCD• Often first-line antiarrhythmic therapy• First line therapy for some cardiac channelopathies (e.g., long QT syndrome,

catecholaminergic polymorphic ventricular tachycardia) • Post AMI beta blocker use reduced mortality vs other antiarrhythmic’s increased

mortality• Long-term side effects include: hypercholesteremia, hyperglycemia, erectile dysfunction





Class III

Amiodarone Ibutalide Sotalol Dofetilide Dronedarone

Blocks the potassium inward channel

Increases AP and ERP without affecting phase 0

Prolong QT and PR interval

Drug Common Use


Amiodarone AF, VT, VF, PVC, AVNRT

INa, ICa, IKr, IK1 IKs,

Ito, Beta receptor,

Alpha receptor

nuclear T3receptor

Sinus rate slowedQRS prolongedQTc prolonged


increased;increased DFT

Onset: IV: 6-8 hrs;PO: 2 days

T1/2: 26-107 dMetab: H (Major DDI‘s: CYP 3A4,

2C8)Excr: F

Hypotension, bradycardia, AVB,TdP, corneal micro deposits, thyroid,

N/V, constipation, skin discoloration, dizziness,

peripheral neuropathy, tremor, hepatitis, cirrhosis, pulmonary

fibrosis or pneumonitis

Dofetilide SVT (AVNRT, AVRT, AF)

IKrSinus rate slowed

QTc prolongedAV nodal


T1/2: 6-10 hMetab: H (Major DDI‘s: CYP 3A4)

Excr: U/F

QT prolongation, Tdp, Contraindicated for BL QTc interval

or QTc >440 ms† or 500 ms inw/ ventricular conduction

abnormalities

Therapy Overview

Drug Common Use


Dronedarone AF INa, ICa, IL-

ACh, IKr, IK1

IKs,Ito, Beta receptor

Sinus rate slowedQTc prolonged

AV nodal refractoriness

increased

T1/2: 13-19Metab: CYP 3A4,I: CYP 3A4, 2D6;

Excr: F

QT prolonged, HF, Bradycardia, liver disease; AKI, allergic dermatitis,

N/V/D; structurally similar to Amiodarone (Interstitial pulm dz,

pneumonitits, pulm fibrosis)

Ibutalide Chemicalcardioversion for AF, WPW,

postop AF

IKr T1/2: 6hMetab: CYP 3A4, 2D6, oxidation;

Excr: U

QT prolongation, Tdp, AVB, hypotension, nausea

Sotalol AF, VT, VF, PVC

IKr, Beta 1 and 2

receptor

Onset: IV: 5 min, PO: 1-2 hr;T1/2: 12 h

Metab: noneExcr: U

Bradycardia, hypotension,syncope, TdP, Fatigue,

dizziness, weakness, dyspnea, bronchitis, depression, N/D

Therapy Overview

PearlsPearls

Amiodarone • Do not use: COPD or Interstitial lung disease, Cataracts, Thyroid issues, true Iodine allergy• Yearly: Visual fundascope/slant lamp, PFTs, CXR, Thyroid test• Skin: Blue/gray from iodine deposition: Consider reducing the dose• If patients state Iodine allergy ask about multivitamins (~100mcg iodine), table salt, contrast

Dofetilide • Switching to sertraline for SSRI best option • Other MAJOR CI: Bactrim, azithromycin, verapamil, megestrol, ketoconazole, cimetidine, prochlorperazine, dolutegravir, grapefruit. • Always get EKG 2 hour post dose and CMP

• First 6 doses require inpatient monitoring• No longer on REMS program• Use Cockcroft-Gault with actual body weight

Dronedarone • Does not contain Iodine, less lipophilic than amiodarone, less Vd and shorter half-life. • CI with permanent AF, NYHA Class IV HF, or symptomatic HF with recent decompensation, heart blocks or SSS, hx of amiodarone toxicity

•Empirically reduce digoxin by 50% • Increases dabigatran levels

Sotalol • Current formulation is a racemic mixture (old data only D-isomer) with beta blocker properties, it’s not a substrate of CYP 450 system nor P-gp. Avoid other QTc prolonging meds concomitantly; renally adjust




Class IV

Verapamil Diltiazem

Block L-type calcium cannels

Decrease rate of phase 4 in SA/AV node

Slows conduction and prolongs the ERP

Slows phase 0 upstroke in nodal tissue

Drug Common Use Target Effect PKT Common Side Effects

Diltiazem VTspecifically

RVOT,idiopathic

LVT

ICa-L

Sinus rate slowed

PR prolongedAV nodal

conduction slowed

T1/2: IV 2–5h, IR: 4.5–12h, ER 12 h,

and severe hepatic impairment 14–

16 h; Metab: H- CYP3A4/

2C9/2D6: I: CYP 2D6/ 3A4/2C9/P-gp

Excr: U

Hypotension, edema, HF, AVB, bradycardia, exacerbation of

HFrEF, headache, rash

Verapamil VT (specificallyRVOT,

Verapamil sensitive

idiopathicLVT)

ICa-LT1/2: 3–7 h

Metab: H-CYP 3A4 (M)/1A2/2C9;

I: CYP 2D6/3A4/1A2/2C9/ P-gp;

Excr: U

Hypotension, edema, HF, AVB, bradycardia, exacerbation of

HFrEF, headache,rash, gingival hyperplasia,constipation, dyspepsia

Therapy Overview

Pearls

Pearls

Diltiazem • CI in HFrEF EF (< 40%)• IR and ER total daily dose are equivalent• Diltiazem can increase dofetilide levels despite not being contraindicated like verapamil

Verapamil • Do not use in heart failure with reduced EF (<40%)• Helpful for cerebral vasospasm due to the inhibitory effects on the sympathetic ganglia (not seen with diltiazem) due to T-type calcium channel blockade• Major inhibitor of opioid, anticoagulant, and transplant medications• Contraindicated to use with dofetilide



Other Antiarrhythmic'sDrug Mechanism of Action PKT Common Side Effects

Digoxin • Inhibits the Na/K/ATP pump in cardiac tissue • Stimulates Ca influx and increased contractility• Positive inotropic effect • Decreased ventricular rate to fast atrial arrhythmias

Onset: IV 5-60 min, PO 1-2h

T1/2: 36-48 hMetab: H (complicated

metabolism); Excr: U

Bradycardia, AVB, anorexia, N/V, visual

changes and arrhythmias w/ digoxin toxicity (levels

>2 ng/mL)

Ivabradine • Selective inhibition of the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (f-channels) within the SA node resulting in slowing firing in the SA node, and ultimately reducing heart rate

T1/2: 2h; effective ~6h;Metab: Extensive CYP 3A4;

Excr: U

Bradycardia, Phosphenes, AF, AVB, angioedema

Ranolazine • Antianginal agent, blocks late Na channel current and less potent on funny channel (rapid delayed potassium rectifier Ikr)

T1/2: 7h, metabites: 6-22h;Metab: CYP3A4 and 2D6,

Excr: U/F

Bradycardia, hypotension, minor QT prolongation (< 10 msec), dizziness, HA, confusion, constipation,

dyspnea

Pearls

Pearls

Digoxin • Common AE for toxicity are diarrhea, and halo around lights • Do not administer with antacids/divalent cations (Ca, Mg, Fe)

• Really adjust, and pay attention to indication of use (HF vs AF)

Ivabradine • FDA approved for use in HF in the US• Should only be used when goal directed therapies for HF are maintained and HR > 70

• Off-label use for refractory inappropriate sinus tachycardia (IST)• Off-label use for stable angina for patients refractory or intolerant of beta blockade

Ranolazine • Not typically used as an antiarrhythmic • Was found to reduce and inhibit TdP in multiple models• “pill-in-the-pocket therapy for pharmacologic cardioversion

• Post CT surgery AF• Use for refractory AF with anti-angina dosing (500-1000mg BID)




A 45 year old female presents to her PCP complaining of upper respiratory tract

symptoms that have persisted for the last 13 days without resolution. She’s

currently febrile, with facial pressure and colorful nasal discharge. She has a

history of IVDU with a bioprosthetic valve replaced 2 months ago and postop

atrial fibrillation. Her current medications are amiodarone, methadone and

warfarin. Azithromycin 500mg x 3 doses is prescribed and patient is sent home.

What life threatening side effect(s) could potentially be propagated with this

new medication?

1. Gingival hyperplasia

2. Torsade de Pointes (TdP)

3. Diarrhea

4. Angioedema


Which of the following antiarrhythmic agent(s) would be an

appropriate option for a patient presenting with AF with a history of

ICM HFrEF (EF < 40%) and COPD?

1. Flecainide

2. Dronedarone

3. Dofetilide

4. Sotalol

5. Options 3 & 4

6. None of the above

Agenda


Ventricular Arrhythmias

Supraventricular Arrhythmias

Atrial Fibrillation

Guidelines Algorithms

Ventricular Fibrillation/Flutter

Associated with structural heart disease:

Exceptions: Long QT syndrome, drugs, or inherited disorders (Brugada Syndrome)

Ventricular fibrillation (VF):

The ventricles quiver

Minimal to no blood is pumped from the heart

Ventricular flutter (V-flutter):

Sequence of consecutive ventricular premature beats and rate ~250-350 beats/min

Sustained vs non-sustained:

Sustained: 3 or more consecutive beats lasting > 30 seconds

Non-sustained: < 30 seconds of coupled ventricular beats with rate > 100 beats/min

Ventricular Fibrillation

Ventricular Tachycardia

Al-Khatib SM, et al. 2017 VA/SCD Guidelines. Circulation. 2017;000:e000–e000



Atrial Fibrillation


Supraventricular Tachycardia (SVT)

Types of SVT

Atrial fibrillation/ Flutter

Paroxysmal SVT

AVRT (AV re-entry tachycardia)

AVNRT (AV nodal re-entry

tachycardia)

Wolff-Parkinson-White Syndrome

(WPW)

IST (Inappropriate sinus tachycardia)

Two causes

Re-entry

Increased automaticity

Page RL, et al. 2015 SVT Guidelines. J Am Coll Cardiol. 2016;67(13):e27-115



Atrial Fibrillation


Atrial Fibrillation (AF)/Flutter

Paroxysmal AF

Terminates within 7 days of onset

Persistent AF: Continuous AF for > 7

days

Long-standing AF: Continuous AF > 12

months

Permanent AF

Decision to abandon effort to gain

NSR

Nonvalvular AF: Absence of

rheumatic mitral valve stenosis, valve

replacement, or mitral valve repair

Atrial Fibrillation

Atrial Flutter

January CT, et al. 2014 Atrial Fibrillation Guidelines. J Am Coll Cardiol. 2014;64(21):e1-76

Patient Case #1

K.R. is a 62-year-old man with a history of hypertension, an MI 3 years ago, and

paroxysmal AF. Serum creatinine today is 0.9. His LVEF is 55%. He takes

hydrochlorothiazide 25 mg once daily, metoprolol tartrate 100 mg twice daily,

lisinopril 20 mg once daily, aspirin 81 mg once daily, atorvastatin 20 mg once

daily, and warfarin 5 mg once daily (INR 2.2). He continues to have palpitation

and dizziness episodes once or twice weekly, which last about 4–6 hours. Which

is the most appropriate therapy at this time?

1. Amiodarone 400mg twice daily x 4 weeks, then 200mg once daily

2. Sotalol 80 mg every 12 hours

3. Flecainide 100mg every 12 hours

4. Propafenone ER 225mg every 12 hours

Patient Case #2

J.M. is a 64-year-old man with no history of cardiovascular disease who presents

to the ED with palpitations, dizziness, and lightheadedness. His ECG reveals SVT

with no evidence of pre-excitation. His blood pressure in the ED is 102/80 mm

Hg and heart rate is 131 beats/minute. Neither cough nor carotid sinus massage

is effective for terminating his arrhythmia. In addition, J.M.’s SVT is not responsive

to adenosine 6 mg IV, followed by two doses of adenosine 12 mg IV. Which is

the most appropriate treatment?

1. Digoxin 0.5 mg IV

2. Diltiazem 0.25mg/kg IV, then 5 mg/hr infusion

3. Ibutalide 1mg IV over 10 minutes

4. Procainamide 50 mg/min infusion to total dose 17mg/kg, then 3mg/min

infusion

Patient Case #3

A.B. is a 65-year-old woman who was admitted to the cardiac intensive care unit today with an acute MI. Her echocardiogram reveals an LVEF of 30%. A.B. has a history of hypertension and dyslipidemia. Her serum creatinine is 1.0 mg/dL and she weighs 57 kg. While in the cardiac intensive care unit, she has dizziness and palpitations, and her blood pressure is 95/68 mm Hg. Her ECG reveals VT at a rate of 125 beats/minute, and has lasted longer than 30 seconds. Which is the most appropriate treatment?

1. IV Amiodarone 150mg over 10 minutes, then 1mg/min x 6 minutes, then 0.5mg/min x 18 hours

2. IV Sotalol 75mg every 12 hours

3. IV Verapamil 2.5-5mg every 15-30 minutes

4. IV Procainamide 50mg/min infusion to total dose of 17mg/kg then 1 mg/min infusion

Patient Case #4

A.S. is a 75-year-old woman who presents to the ED with palpitations, dizziness, and light-headedness that began about 4 hours ago. She has a history of hypertension and diabetes mellitus. Medications prior to admission include lisinopril 20 mg daily, hydrochlorothiazide 25 mg daily, and metformin 1000 mg once daily in the evening. Her blood pressure in the ED is 78/52 mm Hg, heart rate is 170 beats/minute, and respiratory rate is 24 breaths/minute. On arrival at the ED, she begins to lose consciousness. Her ECG reveals AF. Which is the most appropriate treatment?

1. Immediate direct current cardioversion

2. Amiodarone 300 mg IV over 1 hour

3. Diltiazem 0.25 mg/kg IV over 2 minutes

4. Digoxin 0.25 mg IV every 4 hours to total dose of 1.5 mg

Patient Case #5

A.B. has her VT terminated by drug therapy. Her medical team ascertains that she is at increased risk of recurrent VT and sudden cardiac death. Which treatment option is preferred to reduce her risk of sudden cardiac death?

1. Amiodarone 400 mg orally once daily

2. Sotalol 160 mg orally twice daily

3. Implantation of an ICD

4. Catheter ablation

Summary

Antiarrhythmic medications can typically have multiple targets and work to reduce

multiple types of arrhythmias

Due to the non-selectivity of most of the antiarrhythmic medications the side effect

profiles can be extensive and require frequent and continuous monitoring

Drug-Drug interaction and kinetic properties of these medications are important

factors to consider when initiating or deescalating therapies

The guidelines algorithms provide a quick glance at levels of recommendation but

lack more granular recommendations

Cardiac Arrhythmias: An Energizer

JACKOLINE COSTANTINO, PHARMDPGY-2 CARDIOLOGY PHARMACY RESIDENT

[email protected]

DAVIDE VENTURA, PHARMD, BCCCPCLINICAL PHARMACY SPECIALIST-CARDIOLOGY

FLORIDA HOSPITAL ORLANDO; ORLANDO, FL

cardiac arrhythmias: an energizer · 2018-05-04 · cardiac arrhythmias: an energizer jackoline...

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