Pharm Cardiac

Front 1

Class IA: Agents and their specifics

Quinidine
form
treatment of
may cause

Back 1

Oral 200-400 mg QID or IV 50-75 mg/hr
- Afib, supraventricular tachycardia (SVT), Wolff-Parkinson-
White (WPW)
- Can cause significant hypotension (alpha blocking
properties); anticholinergic effects

Front 2

IB: Prolong action potential duration in some tissues and dissociate from the channel with rapid kinetics

Lidocaine, mexiletine, (tocainide), (phenytoin)

Little effect on

Back 2

supraventricular dysrhythmias

Front 3

Class IB: Agents and their specifics
Lidocaine (prototypical agent)
- Used for

dose

affects phase

why?

may cause 4x

clearance

Back 3

emergent ventricular arrhythmias

(2mg/kg load then 1-4 mg/min)

Affects Na+ late in phase 2 = no QT prolongation
- Can affect premature ventricular contractions by delaying rate of
phase 4 depolarizations
- Can cause confusion, dizziness, tremors, seizures
Depends on hepatic clearance

Front 4

Mexiletine

prodrug of
dose
s/e

Back 4

- Oral prodrug of lidocaine
- 150 – 200 mg Q8H
- GI side effects in 40% of patients

Front 5

IC: Prolong action potential duration in some tissues and dissociate from the channel with slow kinetics

Not to be used in 2x

Back 5

HF or post-MI patients

Front 6

Class IC: Agents and their specifics
Flecainide

tx of

may cause

not used for

Back 6

WPW, paroxysmal Afib
- Can lead to QRS prolongation (by 25% or more); sudden cardiac
death if post MI
- 100-200 mg BID; pill in pocket technique
- Not to be used in patients with HF (predisposition to ventricular
tachyarrhythmias)

Front 7

Class IC: Agents and their specifics

Propafenone

may lead to

dose

Back 7

Not to be used in patients with HF (predisposition to ventricular
tachyarrhythmias)
- Hepatic metabolism
- Can lead to SA/AV/Bundle Branch block
- 150-300 mg Q8H

Front 8

Receptor Pharmacology

Endogenous catecholamines are
responsible for

Back 8

regulation of vascular
and bronchiolar smooth muscle tone and
myocardial contractility

Front 9

Receptor Pharmacology

Sympathetic adrenergic receptors of the autonomic nervous system located 3x

Back 9

vasculature, myocardium, and
bronchioles mediate these effects

Front 10

β-adrenergic receptors exist as two
discrete subtypes

Back 10

β 1 mainly in cardiac tissue

β 2 mainly in vasculature and pulmonary branches

Front 11

β 1 mainly in cardiac tissue 2 effects

Back 11

- Increases heart rate and force of contraction
- Increases velocity of conduction

Front 12

β 2 mainly in vasculature and pulmonary branches produces

Back 12

Vascular and bronchial dilatation

Front 13

α-receptors are also subdivided

type and location

Back 13

α1-receptors are postsynaptic and located in vasculature

α2-receptors are presynaptic auto regulatory receptors

Front 14

Sympathetic Nervous System
Signals sent from medulla
- Neurotransmitter:

Back 14

norepinephrine

Front 15

Norepinephrine binds to

Back 15

β1-adrenergic receptors in
the SA and AV nodes

Front 16

Norepinephrine binds to β1-adrenergic receptors in the SA and AV nodes

does 3x

Back 16

- Stimulates increase in the rate of depolarization
- Increases conduction velocity
- Decreases refractory period of the node

Front 17

Parasympathetic Nervous System
Vagus nerve innervates

3x

Back 17

SA/AV nodes and atria

Front 18

Parasympathetic Nervous System
Vagus nerve

Reduces pacemaker current by

Back 18

by decreasing probability of
Ca2+ channel opening

Increases the probability of K+ channel opening, achieving
maximum diastolic potential

Front 19

Parasympathetic Nervous System

Neurotransmitter: acetylcholine

Back 19

- Slows rate of discharge of SA node
- Slows conduction through AV node

Front 20

Class II: β-Adrenergic Blockers

Inhibit sympathetic input to

Back 20

the pacing regions
of the heart (not sotolol)

Front 21

Class II: β-Adrenergic Blockers
Block sympathetic stimulation of

and to

Back 21

Inhibit sympathetic input to the pacing regions
of the heart (not sotolol)
Block sympathetic stimulation of β receptors in the
SA and AV nodes

Front 22

Class II: β-Adrenergic Blockers

AV node is more sensitive - to

Back 22

o the effects of β1-receptors
blockers

Front 23

Β1-blockers affect action potentials of SA and AV
nodes by

ultimately

Back 23

Decrease rate of phase 4 depolarization
- Prolong repolarization
Decrease mortality post MI, decrease work load of
the heart

Front 24

Most common agents for supraventricular and
ventricular arrhythmias due to sympathetic
stimulation
Perioperative stress, thyrotoxicosis, pheochromocytoma

Back 24

Class II: β-Adrenergic Blockers

Front 25

7 Adverse effects of β-Adrenergic Blockers

Back 25

Adverse effects
Bradycardia
Hypotension
Myocardial depression
Bronchospasm (especially non-selective agents)
Blunting of hypoglycemia symptoms
Fatigue, mental depression
Up-regulation of receptors (with chronic administration)

Front 26

Abrupt discontinuation of β-Adrenergic Blockers

Back 26

- Abrupt discontinuation may lead to supraventricular tachycardia

Front 27

Class III: K+ Channel Blockers work by

may cause 2x

Back 27

Cause longer plateau phase and prolong
repolarization
Lengthening of plateau increases risk for early
afterdepolarizations and Torsades de pointes
Variety of agents available
- Each with different pharmacologic action
- Different “pockets” of use

Front 28

Amiodarone: used for

Back 28

Atrial and ventricular arrhythmias

Front 29

Amiodarone
Causes alteration of

Back 29

lipid membrane in which ion channels
and receptors are located

Front 30

Amiodarone:

Substantial toxicity;due to

Back 30

prolonged half-life (19 days)
Pulmonary fibrosis, Hyper/hypo thyroid, Hepatic toxicity
(elevated LFTs), Corneal microdeposits, Skin discoloration
(“smurf syndrome”)

Front 31

Amiodarone: Negative inotropic effects

Back 31

enhanced during anesthesia
(consider temporary pacer)

Front 32

Dronedarone (Maltaq)
Structural analog

Back 32

of amiodarone
Lacks iodine atoms

Front 33

First antiarrhythmic drug to demonstrate reduction in
mortality and hospitalization in atrial fibrillation patients

Back 33

Dronedarone (Maltaq)

Front 34

Class III: Agents and their specifics
Sotalol K+ Channel Blockers
used for

risk of

Back 34

Uses: ventricular tachycardia, ventricular fibrillation, atrial
tachydysrhythmias (atrial fibrillation)

Risk for Torsades de pointes increases with increasing
dose

Front 35

Class III: K+ Channel Blockers

Class III: Agents and their specifics
Ibutilide
- For new

Back 35

onset atrial fibrillation or flutter (within 7 days)

Front 36

Class IV: Ca2+ Channel Blockers
Affect SA and AV nodes

affects rise of

effective tx of 2x

Back 36

Slow the rise of action potential upstroke
Prolong repolarization of the AV node
Effective in treating re-entry arrhythmias
Specific to nondihydropyridine CCBs
Not for use in HF or post-MI with ventricular
dysfunction (negative inotrope)

Front 37

Class IV: Agents and their specifics
Verapamil
- Not effective for slowing ventricular rate in

Back 37

WPW

Front 38

Adenosine (Adenocard)
Inhibits 2x

Back 38

SA nodal, atrial, and AV nodal conduction More sensitive to effects on AV node

Inhibits cAMP-induced Ca2+ influx, suppressing Ca2+
dependent action potentials

Front 39

Adenosine (Adenocard)

Uses:

Back 39

Narrow complex paroxysmal supraventricular tachycardia
(PSVT)– 90% effective
WPW
NOT for Afib, Aflutter, ventricular tachycardia

Front 40

Digoxin works by

Back 40

Shortens refractory period in atrial and ventricular
myocardial cells
Prolongs effective refractory period and conduction
velocity of the SA node

Front 41

Digoxin
Used for control of

Back 41

ventricular response rate in atrial
flutter and fibrillation

Front 42

Digoxin

Mechanism: inhibits

Back 42

Mechanism: inhibits sodium-potassium ATPase,
increasing intracellular sodium concentration leading to
increased intracellular calcium concentration
Increases activity of the sodium-calcium exchanger, which
elevates intracellular calcium and improves cardiac
contractility
Also increases cardiac vagal tone which decreases cardiac
sympathetic activity

Front 43

Digoxin
Shortens

prolongs

Back 43

refractory period in atrial and ventricular
myocardial cells
Prolongs effective refractory period and conduction
velocity of the SA node

Front 44

Digoxin

Mechanism:

Back 44

inhibits sodium-potassium ATPase,
increasing intracellular sodium concentration leading to
increased intracellular calcium concentration
Increases activity of the sodium-calcium exchanger, which
elevates intracellular calcium and improves cardiac
contractility
Also increases cardiac vagal tone which decreases cardiac
sympathetic activity

Front 45

Digitalis
Side effects

Arrhythmia characterized by

Back 45

Arrhythmia characterized by slowing of atrioventricular conduction
Anorexia, nausea, and vomiting
Headache, fatigue, confusion, blurred vision, alteration of color
perception, and halos on dark objects

Front 46

Digitalis - Factors disposing to toxicity
Electrolyte disturbances

Back 46

- Hypokalemia can precipitate serious arrhythmias
- Hypercalcemia
- Hypomagnesemia

Front 47

Factors disposing to toxicity with dig

Back 47

Factors disposing to toxicity
Electrolyte disturbances
- Hypokalemia can precipitate serious arrhythmias
- Hypercalcemia
- Hypomagnesemia
Drug interactions
- Quinidine, verapamil, and amiodarone
Disease states
- Hypothyroidism, hypoxia, renal failure, myocarditis

Front 48

Importance of Electrolytes
Magnesium

Back 48

Influences Na-K ATPase, sodium channels,
potassium channels, calcium channels
Indicated for digoxin associated arrhythmias if
hypomagnesmia is present, Torsades de pointes

Front 49

Importance of Electrolytes
Potassium

Back 49

Increasing serum K results in resting potential
depolarizing action and membrane potential
stabilization
- Hypokalemia = early afterdepolarizations, delayed
afterdepolarizations, ectopic beats
- Hyperkalemia = slowing of conduction velocity