Cv System Exam 2_17: Antiarrhythmics

Front 1

phase 0: myocardial cells

Back 1

Front 2

phase 1: myocardial cells

Back 2

Front 3

phase 2: myocardial cells

Back 3

Front 4

phase 3: myocardial cells

Back 4

Front 5

phase 4: myocardial cells

Back 5

Front 6

phase 0 nodal cells

Back 6

Front 7

phase 3 and 4: nodal cells

Back 7

Front 8

Class IA, IB, IC

Back 8

Na channel blockers

Front 9

Class II

Back 9

Beta blockers

Front 10

Class III

Back 10

K+ channel blockers and others that prolong repolarization

Front 11

Class IV

Back 11

CCBs

Front 12

What will slow down conduction velocity in fast response tissue (eg ventricular myocytes)

Activating Ca channels
Blocking Ca channels
Activating K channels
Blocking K channels
Activating fast Na channels
Blocking fast Na channels

Back 12

Blocking fast Na channels; the target is phase 0 Na+ chanels

Front 13

What will slow down conduction velocity in nodal tissue?

Activating Ca channels
Blocking Ca channels
Activating K channels
Blocking K channels
Activating fast Na channels
Blocking fast Na channels

Back 13

block Ca2+ channels; target phase 0 Ca2+ channels

Front 14

What will prolong the ERP in fast response tissue (eg ventricular myocytes)

Blocking Ca channels
Activating K channels
Blocking K channels
Activating fast Na channels
Blocking fast Na channels

Back 14

block K+ channels; ERP- effective refractory period... prolong ERP to stay depolarized longer.
Phase 2: Ca2+influx
Phase0: Na+ chanels only

Front 15

Which of the following will break the reentrant circuit in the ventricles? (select all that apply)

Blocking Ca channels
Activating K channels
Blocking K channels
Activating fast Na channels
Blocking fast Na channels

Back 15

blocking K+ channels and fast Na+ channels: need to block conduction and extend refractory period... blocking Ca2+ channels will shorten AP duration as will activatin K+ channels

Front 16

what causes A flutter?

Back 16

reentry over a large anatomically fixed circuit

Front 17

what causes A fib?

Back 17

multiple wandering reentrant circuits within the atria... a rapid focal discharge may trigger

Front 18

A flutter

Back 18

"sawtooth EKG- Reg Ireg R-R

Front 19

A fib

Back 19

"squiggles" EKG- Irreg Irreg R-R

Front 20

Pharmacological Treatment of Atrial Fibrillation and Flutter

Back 20

rate and rhythm control (slow AV node)

Front 21

phase 0: nodal Ca2+ influx

Back 21

Front 22

what kind of drugs will slow AV conduction?

Back 22

verapimil, diltiazem, digoxin, beta blockers

Front 23

A fib: phase 0- Na+ influx
phase 3- K+ eflux

Back 23

Front 24

**A fib/flutter rhythm control drugs

Back 24

Front 25

**A fib/flutter rate control drugs

Back 25

Front 26

Atrial Flutter/Fibrillation: Pharmacological Treatment - Summary

Back 26

Slow the ventricular rate
-Rate control
-Decrease the activity of the AV node
Pharmacological cardioversion and prevention
-Convert to/maintain in NSR
-Rhythm control
-Stop reentry

Front 27

How else can you convert atrial fibrillation to NSR?

Back 27

DC cardioversion

Front 28

Monomorphic VT

Back 28

Usually a structural abnormality supporting a reentry circuit, most commonly a region of an old infarction

Front 29

Ventricular fibrillation

Back 29

Multiple small wavelets of reentry

Front 30

How do you stop pulseless VT or VF?

Back 30

hemodynamicaly unstable: shock 'em
-some drugs assist with reentry elim but can't cardiovert

Front 31

How do you prevent VT or VF?

Back 31

Implanted Cardiac Defibriliator
Reentry elimination drugs

Front 32

V fib

Back 32

phase0: Na
phase3: K

Front 33

AV Nodal Reentry - Sinus rhythm

Back 33

Front 34

AV nodal reentry

Back 34

Front 35

AV nodal reentry-arrhythmia

Back 35

Front 36

AV Nodal Reentry - Sinus rhythm

Back 36

Front 37

AV Nodal Reentry - Arrhythmia

Back 37

Front 38

AV Nodal Reentry

Back 38

Front 39

AV Nodal Reentry

Back 39

Front 40

Atrioventricular reentrant tachycardia(Bypass tract or WPW)

Back 40

see where the arrows meet? self-extinguishing Delta waves

Front 41

Atrioventricular Reentrant Tachycardia(Bypass tract or WPW)

Back 41

Front 42

Atrioventricular Reentrant Tachycardia

Back 42

Front 43

Atrioventricular reentrant tachycardia(Bypass tract or WPW)

Back 43

Front 44

Atrioventricular reentrant tachycardia(Bypass tract or WPW)

Back 44

Front 45

Atrioventricular reentrant tachycardia(Bypass tract or WPW): With Atrial Fibrillation/Flutter

Back 45

Front 46

Atrioventricular reentrant tachycardia(Bypass tract or WPW): With Atrial Fibrillation/Flutter

Back 46

Front 47

Myocardium/His-Purkinje System

Back 47

Front 48

What will help with AF/Flutter plus WPW?

Back 48

Accessory tract
Convert AF to NSR
-block Na channels
-block K channels
DO NOT block AVN... can make it worse

Front 49

What is the biggest problem with ALL antiarrhythmic drugs?

Back 49

proarrhythmic effect

Front 50

Class I antiarrhythmic drugs

Back 50

Na channel blockers

Front 51

Na Channel Blockers- general principles

Back 51

Block fast Na channels in the open and/or inactivated state

Agents differ on rate of recovery from block
Class 1A - - intermediate
Class 1B - - very fast
Class 1C - - very slow

Front 52

Cardiac Action Potential- Myocardium/His-Purkinje System

Back 52

Front 53

Class 1B – normal tissue

Back 53

Front 54

Class 1C – normal tissue

Back 54

Front 55

What about ischemic or damaged tissue?

Back 55

Front 56

In ischemic tissue, there is an increase in steady state block of fast Na channels (ie number of channels blocked during phase 4 or at the start of phase 0)

Back 56

In ischemic tissue, there is an increase in steady state block of fast Na channels (ie number of channels blocked during phase 4 or at the start of phase 0)

Front 57

what happens to phase 0 w/ lidocaine in damaged tissue?

Back 57

less steep slope

Front 58

Na channle blockers work better in ______ tissue and ____ heart rates.

Back 58

Work better in depolarized/damaged tissue and faster heart rates

Front 59

:)

Back 59

Front 60

What happens if you have a high steady state block of fast Na channels in normal tissue (e.g., not involved in the reentry arrhythmia)

Back 60

precipitate cardiac arrythmia

Front 61

Would Class 1B or 1C drugs have a higher chance of precipitating a cardiac arrhythmia from Na channel blockade?

Back 61

class 1C... comes off more slowly

Front 62

Quinidine MOA

Back 62

Blocks Na channels with an intermediate recovery time
-Open state blocker
-Moderate phase 0 depression
-Decreases conduction velocity in fast response tissue

Blocks K channels
-Lengthens the AP duration and increases the ERP

Front 63

Class IA effects in fast response tissue

Back 63

Front 64

Class IA effects in ectopic foci

Back 64

Front 65

Quinidine: Effect of Na channel blockade - Summary

Back 65

Decreases conduction velocity
-Fast response tissue
Decreases excitability
Decreases pacemaker rate
-Especially in ectopic pacemakers
-Little effect on SA node automaticity and HR
Works better in depolarized or damaged tissue than normal tissue

Front 66

Quinidine: Effect of K channel blockade - Summary

Back 66

Prolongs effective refractory period (ERP)

Front 67

What type of arrhythmias will quinidine be useful in treating?
A fib
V tach/fib
AVNRT
AVRT

Back 67

all the above

Front 68

Narrow QRS atrioventricular reentrant tachycardia (WPW)

Back 68

Front 69

Quinidine: clinical use

Back 69

Atrioventricular reentrant tachycardia or Wolff-Parkinson-White (WPW) syndrome
-Suppresses inciting premature impulses
-Slows conduction and prolongs ERP in accessory pathway

AV nodal reentrant tachycardia
-Suppresses inciting premature impulses
-Slows conduction and prolongs ERP in the retrograde fast pathway

Front 70

Quinidine: AEs

Back 70

Abdominal pain, nausea, vomiting, and diarrhea
30%-50% - mechanism not understood
Initial increase in ventricular rate when treating atrial flutter or fibrillation (i.e. prior to cardioversion).. inhibits vagal effect on heart

Front 71

p

Back 71

Front 72

What can you do to prevent this when quinidine is used for cardioversion of AF?
Epi
CCB
Mg2+
K+ blocker

Back 72

CCB... give an AVN blocker prior to administration quinidine

Front 73

Quinidine: AEs

Back 73

Torsades de pointes
-From K+ channel blockade
-2-3%
-In contrast with other drugs, plasma concentrations are often normal or even subtherapeutic

Front 74

p

Back 74

Front 75

What would happen to the QT interval if you prolong the AP duration?

Back 75

prolong QT interval

Front 76

Quinidine: AEs

Back 76

Toxic concentrations can depress cardiac electrical activity in any part of the heart-precipitate arrhythmias or asystole
Hypotension
Blocking a receptors
IV use (dont useIV)

Front 77

Quinidine: AEs

Back 77

CNS toxicity: Cinchonism
-Tinnitus
-Hearing loss
-Dizziness
-Headache
-Disturbed vision
-Confusion

Front 78

Quinidine: AEs

Back 78

Rare – hepatitis – reversible
Rare – allergic reactions
Rash, fever, immune-mediated thrombocytopenia (Ab’s to quinidine-plateletcomplex causes platelets toaggregate and lyse)

Front 79

Quinidine: interactions

Back 79

Increase serum digoxin concentrations

Front 80

Procainamide : summary

Back 80

Similar blockade of Na and K channels

Procainamide (**use IV)
-Less antimuscarinic effect
-Short half life
-Lupus-like syndrome
-Ganglionic blocker

Front 81

Procainamide: MOA

Back 81

Class IA Sodium Channel Blocker
Similar to quinidine except:
-Less effective at suppressing abnormal ectopic pacemaker -activity
-Less antimuscarinic activity
-Does not block a receptor

Front 82

Procainamide: PK

Back 82

IV, IM, or Oral
1/2 life= 3-5 hrs

Front 83

Procainamide: CU

Back 83

Most supraventricular and ventricular arrhythmias
-Comparable to quinidine
-Except also used (IV) cardioversion ventricular tachycardia
Not drug of choice for chronic use
-Frequent dosing and side effects

Front 84

Procainamide: AEs

Back 84

Cardiac
-Similar to quinidine
GI
-Nausea and diarrhea
Lupus-like syndrome (20-30%)
-80% of patients have an increase in antinuclear antibodies
-Arthralgia, fever, chills, myalgia, hepatomegaly pleuropericarditis, and hemorrhagic pericardial effusions with tamponade

Front 85

Procainamide (ProcanbidAdverse Effects

Back 85

Hypotension
-With rapid IV use and at high plasma concentrations

Ganglionic blockade:
decreases PVR and BP

Front 86

What does urinary retention and dry mouth remind you of?

Back 86

atropine

Front 87

Class IB Na channel blockers

Back 87

Lidocaine
Mexiletine
Phenytoin

Front 88

Lidocaine MAO

Back 88

Blocks fast Na channels in open or inactivated state
Very fast recovery from block
Minimal effect on normal tissue
Greatest effect on depolarized and/or rapidly driven tissue

Front 89

Class IB effects in fast response tissue

Back 89

Front 90

p

Back 90

Front 91

p

Back 91

Front 92

p

Back 92

Front 93

p

Back 93

Front 94

What type of arrhythmias will lidocaine treat?

Back 94

V fib/tach

Front 95

p

Back 95

Front 96

Lidocaine: metabolism?

Back 96

IV: extensive 1st pass (liver metabolism)

Front 97

what is lidocaine used for?

Back 97

V tach cardioversion

Front 98

Lidocaine AEs; large doses

Back 98

AV block
Sinus brady
asystole
decreased contractility (decreaes CO causing hypotension)
Ventricular arrythmias (low proarrythmic effct)
CNS: parethesia, tremor nausea, local anesthetic effect

Front 99

Mexiletine

Back 99

Class IB Na channel blocker
-oral lidocaine analogue

Front 100

mexiletine CU

Back 100

V tach and fib prevention

Front 101

Class IC Na channel blockers

Back 101

Flecainide
Propafenone

both oral

Front 102

Flecainimide MOA

Back 102

Na channel blocker with long recovery from blockade

Front 103

q

Back 103

Front 104

What type of arrhythmias will flecainide treat

Back 104

A fib
V tach/fib
AVNRT
AVRT
A fib/WPW

Front 105

Flecainide CU

Back 105

effective for most arryhmias
"pill in pocket" for A fib

**only for pts withOUT structural heart Dz... less prone to proarrythmic activity

Front 106

Cardiac Arrhythmia Suppression Trial(CAST)

Back 106

Flecainide significantly increased the rate of nonfatal cardiac arrest and total mortality in patients with recent MI, asymptomatic or symptomatic ventricular arrhythmias, and mild to moderate left ventricular dysfunction.

Front 107

Flec AEs

Back 107

Cardiac
-Proarrhythmic effects because of the marked Na channel blockade
-Mostly ventricular tachycardia and fibrillation
-AV block
Blurred vision, dizziness, nausea, headache, dyspnea

Front 108

Flecainide contraindications

Back 108

Hx MI
HF
-Negative inotropic effect and increased risk of proarrhythmias

AV block or bundle branch block

Front 109

Propafenone

Back 109

-Sodium Channel Blocker (Class IC)
-Similar to Flecainide
-Also blocks b receptors

Front 110

Beta Receptor Antagonists (pint pickle)

Back 110

Propranolol (Inderal, InnoPran XL)
Nadolol (Corgard)
Timolol (Timoptic, Betimol, Istalol)
Pindolol (Visken)
Carteolol (Cartrol, Ocupress)
Levobunolol (Betagan)

Front 111

Beta Receptor Antagonists (maybe)

Back 111

Metoprolol (Lopressor, Toprol XL)
Atenolol (Tenormin)
Acebutolol (Sectral)
Betaxolol (Betoptic, Kerlone)
Bisoprolol (Zebeta)
Esmolol (Brevibloc)

Front 112

Beta Blockers (Class II): what do they do?

Back 112

block Beta1s on heart

Front 113

Beta Blockers (Class II): end result

Back 113

SA node
-Negative chronotropic effect
AV node
-Decreased conduction velocity
-Increased ERP
Prevent arrhythmias triggered by excess catacholamines

Front 114

b Blockers (Class II): clinical use

Back 114

Reduce sudden cardiac death in post MI patients
-Increase in circulating catecholamine is correlated with the development of arrhythmias

Front 115

What type of arrhythmias will b blockers be useful in treating?
A fib
V tach/fib
AVNRT
AVRT
A fib w/ WPW

Back 115

A fib, AVNRT, AVRT

Front 116

q

Back 116

Front 117

Beta Blockers (Class II)

Back 117

Control ventricular rate in patients with atrial flutter or fibrillation

Front 118

Beta Blockers (Class II): some more clinical use

Back 118

AV nodal reentrant tachycardia
Narrow QRS atrioventricular reentrant tachycardia (WPW)

Front 119

b Blockers (Class II): prevent arrythmias triggered by ___ or ____ stress

Back 119

physical or emotional
-congenital long QT syndrome
-atrial flutter or fibrilation

Front 120

Long QT Syndrome

Back 120

Mutations in six genes produce abnormal cardiac K or Na channels
Human ether-a-go-go-related gene (HERG)
Encodes major subunit of IKr

Front 121

K Channel Blockers (Class III)

Back 121

Amiodarone
Dronedarone
Sotalol
Ibutilide
Dofetilide

Front 122

Amiodarone MOA

Back 122

Blocks K channels
-Prolong AP duration
-Increase the ERP
Blocks inactivated Na channels
-Relatively rapid rate of recovery
-Decrease conduction velocity
-Decreases excitability

Front 123

Amiodarone MOA

Back 123

Blocks K channels
-Prolong AP duration
-Increase the ERP
Blocks inactivated Na channels
-Relatively rapid rate of recovery
-Decrease conduction velocity
-Decreases excitability

Front 124

MOA 2

Back 124

Weak Ca channel blocker
-Decrease phase 4 slope in SA node
-Coronary and peripheral vasodilation
Non competitive a and b blocker

Front 125

AmiodaroneEnd Result

Back 125

Inhibits abnormal automaticity
Increases atrial, AV node, and ventricular ERP
Decreases AV conduction and conduction in atria and ventricles
Sinus bradycardia

Front 126

Amiodarone Pharmacokinetics

Back 126

Oral or IV
Very lipid soluble
-Large volume of distribution
-T1/2 = 13-103 day
-Loading dose for several weeks
-Plasma levels for nine months after stopping drug

Front 127

What type of arrhythmias will amiodarone be useful in treating?

Back 127

A fib, V tach, V fib, AVNRT, AVRT

Front 128

Amiodarone clinical use

Back 128

Atrial fibrillation and flutter
-Slow ventricular response
-Convert to sinus rhythm – usually converts within 24 -hours
-Maintain sinus rhythm after cardioversion
-Used at lower doses – less toxicity
Ventricular fibrillation and tachycardia
ACLS for VF/pulseless VT

Front 129

ARREST trial demonstrated a 29% increase in survival to hospital rate when amiodarone was given in the first minutes after cardiac arrest due to ventricular fibrillation/pulseless ventricular tachycardia

Back 129

ARREST trial demonstrated a 29% increase in survival to hospital rate when amiodarone was given in the first minutes after cardiac arrest due to ventricular fibrillation/pulseless ventricular tachycardia

Front 130

How will amiodarone prevent reentry?

Back 130

slow conduction and prolong ERT in the reentrant pathway

Front 131

Amiodarone clincal use

Back 131

AV nodal reentrant tachycardia
Atrioventricular reentrant tachycardia (WPW)

Front 132

Amiodarone clincal use

Back 132

AV nodal reentrant tachycardia
Atrioventricular reentrant tachycardia (WPW)

Front 133

Amiodarone advantages and disadvantages

Back 133

Advantage
-Very low proarrhythmic effect
No negative inotropic effect
Disadvantage
-Non cardiac side effects which are dose related and cumulative

**A drug of choice for treating arrhythmias in patients with heart failure

Front 134

Amiodarone AEs

Back 134

Nausea, vomiting, abdominal pain, constipation
Deposit in tissues
-Cornea
-Skin
--Photosensitivity
--Bluish-gray coloration of the skin

Front 135

Amiodarone AEs

Back 135

Elevation of liver enzymes
-Rare – hepatitis
Either hypothyroidism or hyperthyroidism
-Structural analog of thyroid hormone
-Contains large amount of iodine
-Cytotoxic effect on thyroid follicle cells

Front 136

Amiodarone AEs

Back 136

Pneumonitis leading to pulmonary fibrosis
-Can be rapidly progressive and fatal
-Cough – usually the first symptom
Peripheral neuropathy
-Ataxia, tremor, numbness in the fingers or toes, dizziness, muscle weakness
Bradycardia/AV block
Prolongs the QT interval
-Very low incidence of torsades de pointes

Front 137

Because of the potential for serious adverse effects, the FDA requires that a Medication Guide be given to patients that are prescribed amiodarone

Back 137

Because of the potential for serious adverse effects, the FDA requires that a Medication Guide be given to patients that are prescribed amiodarone

Front 138

Amiodarone

Back 138

Serious drug interactions
Digoxin
Warfarin
Drugs that prolong QT interval

Front 139

What is the difference between amiodarone and dronedarone???

Back 139

Front 140

Dronedarone has a similar chemical structure as amiodarone

Back 140

Similar spectrum of electrophysiological activity
Low proarrhythmic effect
Clinical trials
-Effective in suppressing recurrences of atrial fibrillation

Front 141

There is no iodide in dronedarone.What does that do?

Back 141

The iodine in amiodarone makes it more lipophilic
-Elimination half life of dronedarone is 1-2 days
-Dronedarone is potentially less toxic!!
Antithyroid properties have not been seen with dronedarone

Front 142

Does that mean Dronedarone is a wonder drug??

Back 142

Front 143

Does that mean Dronedarone is a wonder drug??

Back 143

ANDROMEDA Trial
-NYHA class II–IV (predominantly class III–IV) heart failure
-Trend toward increased mortality
-Terminated early
ATHENA Trial
-Mostly NYHA Class II HF, some Class III HF
-No hemodynamic instability
-Reduced cardiovascular hospitalization or death from any cause

Front 144

Dronedarone has a black box warning

Back 144

Contraindicated in patients with NYHA Class IV heart failure or NYHA Class II – III heart failure with a recent decompensation requiring hospitalization or referral to a specialized heart failure clinic.

Front 145

Dronedarone

Back 145

Reports of severe liver injury, including liver failure leading to transplant
Rare

Front 146

Sotalol MOA

Back 146

Non selective Beta blocker
-Decreased activity of the SA node
-Decreased AV nodal conduction
Blocks K channels
-Prolong the AP duration and increase ERP in atria, ventricles, AV node

Front 147

What effect would sotalol have on conduction velocity in fast response tissue?
increase
decrease
same

Back 147

same. K+ blocker, not Na+ blocker

Front 148

How does sotalol stop reentry in atria or ventricles?

Back 148

K+ blocker... prolong ERP in reentrant circle

Front 149

Sotalol clinical use

Back 149

Supraventricular and ventricular arrhythmias
-Ventricular arrhythmias
-Atrial fibrillation/flutter
-AV nodal reentrant tachycardia
-Atrioventricular reentrant tachycardia (WPW)

Front 150

Sotalol AEs

Back 150

Torsades de pointes (3-5%)
-Dose related
-From prolonging repolarization
-Prolongs QT interval
Fatigue, sinus bradycardia, dyspnea
-beta blockade

Front 151

Ibutilide and and Dofetilide summary

Back 151

Both prolong the ERP (block K channels)
Ibutilide – IV for conversion of atrial fibrillation and flutter to NSR
Dofetilide – oral for conversion of atrial fibrillation and flutter to NSR and used chronically to maintain NSR

Front 152

some more Ibutilide

Back 152

Both have relatively high incidence of torsades de pointes
Ibutilide – shown to increase incidence sustained polymorphic VT in those with HF or low LVEF
Dofetilide – does not reduce CO (no negative inotropic effect) and not shown to have a negative effect on morality in patients with heart failure

Front 153

Ibutilide Mechanism

Back 153

Blocks K channels
Promotes the influx of Na through slow inward Na channels
This prolongs the AP duration and increased ERP

Front 154

Ibutilide clinical use

Back 154

IV for the conversion of recent onset atrial fibrillation or flutter
-Effective in approximately 30 minutes
Increases the efficacy of DC cardioversion in refractory patients with atrial fibrillation/flutter
-Decreases cardioversion energy requirement

Front 155

Ibutilide Adverse Effects

Back 155

Torsades de Pointes
Prolongs the QT interval
Ventricular arrhythmias
Bundle-branch block, AV block, sinus bradycardia
Nausea, vomiting, headache

Front 156

Dofetilide summary

Back 156

K channel blocker
Oral drug used for atrial fibrillation and flutter
Mandated risk management program

Front 157

Dofetilide mechanism

Back 157

Selectively blocks K channels
-Prolong the AP duration and increase the ERP
Works in the atria, ventricles, and purkinje fibers

Front 158

Dofetilide clincal use

Back 158

Atrial fibrillation or atrial flutter
-Conversion to NSR
-Maintenance of NSR

Front 159

Dofetilide AEs

Back 159

Torsades de pointes
Prolong the QT interval
Ventricular tachycardia
Headache, dizziness

Front 160

How can you minimize the chance of getting dofetilide-induced torsades de pointes?

Back 160

Therapy is initiated in the hospital
Dose is calculated based on creatinine clearance and its effect on the QT interval

Front 161

Calcium Channel Blockers (Class IV)

Back 161

Verapamil (Calan)
Diltiazem (Cardizem
**Nifedipine and the other DHP’s are not useful as antiarrhythmic drugs

Front 162

q

Back 162

Front 163

What effect will verapamil have on AV nodal conduction velocity and ERP?

Back 163

Block AVN
Decrease velocity
increase ERP

Front 164

Calcium Channel Blockers (Class IV) clinical use

Back 164

AV nodal reentrant tachycardia
-Terminate – IV
-Prevent – oral
Slow ventricular rate in patients with atrial fibrillation or flutter
Narrow QRS atrioventricular reentrant tachycardia (WPW)

Front 165

q

Back 165

Front 166

Would you use verapamil alone in a patient with atrial fibrillation and WPW?

Back 166

No, it may shorten the ERP in the accessory pathway, enhance antegrade conduction and worsen the arrhythmia

Front 167

Miscellaneous Antiarrhythmic Agents

Back 167

Adenosine (Adenocard, Adenoscan)
Magnesium Sulfate
Atropine
Digoxin

Front 168

Adenosine mech

Back 168

Activate adenosine receptors
-Only in atria, SA node, and *AV node
Activate ACh sensitive K current
-Hyperpolarization (marked)
Inhibit cAMP-induced Ca influx
-Decrease conduction velocity (AV node)
-Increase refractoriness (AV node)

Front 169

q

Back 169

Front 170

What cardiac drugs are notable for causing AV block?

Back 170

adenosine
Beta blockers
CCBs (non-DHPs)
Digoxin

Front 171

Adenosine Pharmacokinetics

Back 171

Half life ~ 10 sec.
Administered by rapid IV bolus

Front 172

Adenosine clinical use

Back 172

AV nodal reentry or WPW
-Termination
-Restores sinus rhythm in 10-20 seconds in 85-100% of the cases
Not effective for atrial flutter, atrial fibrillation, or ventricular tachycardia
Wide-complex tachycardia diagnosis

Front 173

Adenosine Advantage

Back 173

Adverse reactions last for less than 1 minute

Front 174

Adenosine Adverse Effects

Back 174

Transient asystole
Dyspnea
-Bronchoconstriction
-May last longer in asthmatics
Chest pain or fullness – may -mimic angina
-Related to bronchospasm
Facial flushing
-From vasodilation (20%)

Front 175

A 58-year-old male presents to the emergency department with substernal chest pain. An ECG reveals ST-segment elevation. While treating him he develops ventricular fibrillation. He is successfully defibrillated. Before discharge his blood pressure is 137/80, pulse 105 bpm. He claims that his heart rate always runs high. He has a history of hypertension, coronary artery disease, Stage C, NYHA Class II heart failure. His current medications are ramipril, furosemide and aspirin. Which of the following agents would be most useful in preventing a reoccurrence of the arrhythmia (chronic therapy)?

Back 175

adenosine

Front 176

Magnesium Sulfate mechanism

Back 176

unknown, probably blocks Ca2+ channels

Front 177

Magnesium Sulfate clinical use

Back 177

Ventricular tachycardia or torsades de pointes
-Mg suppresses EADs
Digitalis induced arrhythmias
-Especially if hypomagnesemia is present

Front 178

Magnesium Toxicity

Back 178

Flushing
Diaphoresis
Hypotension
Depressed deep tendon reflexes
Muscle paralysis
Hypothermia
Circulatory collapse
Cardiac, CNS, or respiratory depression

Front 179

more toxicity

Back 179

Magnesium levels > 12 mEq/ml may be fatal due to
-Respiratory arrest
-Cardiac arrest secondary to complete heart block