Transcript Pharmacology and the Nursing Process, 4th ed. Lilley/Harrington

Pharmacology in Nursing
Antidysrhythmic Drugs
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Conditions Causing
Dysrhythmias
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CAD
MI
Cardiac Surgery
Valvular disease
Hypoxia
Electrolyte imbalance
Acid/Base imbalance
Hypovolemia
External forces
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Antidysrhythmics
Dysrhythmia
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Any deviation from the normal rhythm of the heart
Antidysrhythmics
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Drugs used for the treatment and prevention of
disturbances in cardiac rhythm
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Cardiac Cell
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Inside the resting cardiac cell there exists a
net negative charge relative to the outside of
the cell
This difference in the electronegative charge
results from an uneven distribution of ions
(sodium, potassium, calcium) across the cell
membrane
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Resting membrane potential (RMP)
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Resting Membrane Potential
(RMP)
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An energy-requiring pump is needed to
maintain this uneven distribution of ions
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Sodium-potassium ATPase pump
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Action Potential
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A change in the distribution of ions causes cardiac
cells to become excited
The movement of ions across the cardiac cell’s
membrane results in an electrical impulse spreading
across the cardiac cells
This electrical impulse leads to contraction
of the myocardial muscle
Results in excitation of cardiac muscle fibers, weak
electrical current
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Action Potential (cont’d)
Four phases
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The SA node and the Purkinje cells each have
separate action potentials
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3 Types of Electrical Current
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Resting Membrane Potential: Sodium
Potassium Pump activated, membrane is
relatively permeable to K+, but much less to
Na+ and Ca+
Depolarization: cell membrane suddenly
becomes permeable to sodium, sodium
enters cell, sharp increase in positivity,
potassium migrates outside of cell
Repolarization: re-establishment of resting
membrane potential
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Four Phases to Action Potential
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Phase 1: Fast sodium channel closes ; period
of repolarization begins
Phase 2: Calcium ion influx occurs through
slow channels
Phase 3: Potassium ions flow outward, cell is
repolarized to baseline
Phase 4: Resting membrane potential
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Action Potential Duration
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Absolute or effective refractory period
Relative refractory period
Threshold potential
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Automaticity or pacemaker activity
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Electrocardiography
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ECG or EKG
P wave
PR interval
QRS complex
ST segment
T wave
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Common Dysrhythmias
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Atrial dysrhythmias
Supraventricular dysrhythmias
Ventricular dysrhythmias
Ectopic foci
Conduction blocks
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Supraventricular Dysrhythmias
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Ventricular Dysrhymias
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Ventricular Fibrillation
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Premature Ventricular
Contractions
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Atrial Fibrillation
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Atrial Fibrillation with Rapid
Ventricular Response
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Bradycardia & Heart Blocks
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Vaughan Williams Classification
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System commonly used to classify
antidysrhythmic drugs
Based on the electrophysiologic effect of
particular drugs on the action potential
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Vaughan Williams
Classification (cont’d)
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Class I
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Class Ia
Class Ib
Class Ic
Class II
Class III
Class IV
Other
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Vaughan-Williams Classification
Class
Basic Mechanism
Comments
I
Sodium-channel blockade
Reduce phase 0 slope and peak
of action potential
IA
-moderate
Moderate reduction in phase 0
slope; increase APD, increade
ERP
IB
-weak
Small reduction in phase o slope
IC
-strong
Pronounced reduction in phase 0
slope
II
Beta-blockade
Block sympathetic activity,
reduce rate and conduction
III
Potassium-channel
blockade
Delay repolarization, increase
action potential
IV
Calcium-channel blockade
Block L-type calcium channels,
reduce rate and conduction, most
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at SA
& AV
Vaughan Williams Classification:
Mechanism of Action
Class I
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Membrane-stabilizing drugs
Sodium channel blockers
Divided into Ia, Ib, and Ic drugs, according
to effects (weak to strong)
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
Class Ia: quinidine, procainamide,
disopyramide
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Block sodium (fast) channels
Delay repolarization
Increase the APD
Used for atrial fibrillation, premature atrial
contractions, premature ventricular contractions,
ventricular tachycardia, Wolff-Parkinson-White
syndrome
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
Class Ib: mexiletine, phenytoin, lidocaine,
tocainide
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Block sodium channels
Accelerate repolarization
Increase or decrease the APD
Used for ventricular tachyarrhythmias only
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Premature ventricular contractions, ventricular tachycardia,
ventricular fibrillation
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
Class Ic: flecainide, propafenone , moricine
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Block sodium channels (more pronounced effect)
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter, WolffParkinson-White syndrome, supraventricular
tachycardia dysrhythmias
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
Class II: b-blockers: atenolol, esmolol,
metoprolol, propranolol, nadolol, sotalol
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Reduce or block sympathetic nervous system
stimulation, thus reducing transmission of impulses in
the heart’s conduction system
Depress phase 4 depolarization
General myocardial depressants for both
supraventricular and ventricular dysrhythmias
Also used as antianginal & antihypertensive drugs
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
Class III: amiodarone, sotalol,* ibutilide,
bretylium
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Increases action potential
Prolong repolarization in phase 3
Used for dysrhythmias that are difficult to treat
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Life-threatening ventricular tachycardia or fibrillation, atrial
fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia
*Sotalol also exhibits Class II properties
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Drug to Know:
Amiodarone (Cordarone)
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Classification: Antiarrhythmics (class III)
Indication: Life-threatening ventricular
arrhythmias , part of ACLS protocol
Action: Prolongs action potential, slows sinus
rate, prolongs QT interval, suppresses
arrhythmias
Side Effects: Dizziness, fatigue, pulmonary
fibrosis, CHF, bradycardia, hypotension, hypo
or hyperthyroidism, nausea, vomiting,
constipation, anorexia, corneal microdeposits,
photosensitivity
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Amiodarone
Nursing Assessment
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Monitor ECG continuously during IV therapy
Monitor for QT prolongation
Assess for signs of pulmonary toxicity
Assess for signs of thyroid dysfunction
Monitor BP for hypotension
Regular ophthalmic exams for oral route
Monitor for neurotoxicity
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Vaughan Williams Classification:
Mechanism of Action and Indications
(cont’d)
Class IV: verapamil, diltiazem
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Calcium channel blockers
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Inhibit slow-channel (calcium-dependent) pathways
Depress phase 4 depolarization
Reduce AV node conduction
Used for paroxysmal supraventricular tachycardia;
rate control for atrial fibrillation and flutter
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3 Classes of Calcium Channel
Blockers
Dihydropyridines
amlodipine (Norvasc)
nicardipine (Cardene)
nimodipine (Nimotop)
Non-dihydropyridines
Verapamil (Calan)
Diltiazem (Cardizem)
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Vaughan Williams Classification:
Other Antidysrhythmics
digoxin, adenosine
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Have properties of several classes and are not
placed into one particular class
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Unclassified Antidysrhythmic
adenosine (Adenocard)
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Slows conduction through the AV node
Used to convert paroxysmal supraventricular
tachycardia to sinus rhythm
Very short half-life—less than 10 seconds
Only administered as fast IV push
May cause asystole for a few seconds
Other adverse effects minimal
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Adenosine Injection
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Antidysrhythmics: Adverse
Effects
ALL antidysrhythmics can cause dysrhythmias!
 Hypersensitivity reactions
 Nausea
 Vomiting
 Diarrhea
 Dizziness
 Blurred vision
 Headache
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Nursing Implications
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Obtain a thorough drug and medical history
Measure baseline BP, P, I&O, and
cardiac rhythm
Measure serum potassium levels before
initiating therapy
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Nursing Implications (cont’d)
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Assess for conditions that may be
contraindications for use of specific drugs
Assess for potential drug interactions
Instruct patients regarding dosing schedules
and adverse effects to report to physician
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Nursing Implications (cont’d)
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During therapy, monitor cardiac rhythm, heart
rate, BP, general well-being, skin color,
temperature, heart and lung sounds
Assess plasma drug levels as indicated
Monitor for toxic effects
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Nursing Implications (cont’d)
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Instruct patients to take medications as
scheduled and not to skip doses or double up
for missed doses
Patients who miss a dose should contact their
physician for instructions if a dose is missed
Instruct patients not to crush or chew any oral
sustained-release preparations
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Nursing Implications (cont’d)
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For class I drugs, monitor ECG for QT
intervals prolonged more than 50%
IV infusions should be administered with
an IV pump
Solutions of lidocaine that contain
epinephrine should not be given IV—they are
to be used ONLY as local anesthetics
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Nursing Implications (cont’d)
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Ensure that the patient knows to notify health
care provider of any worsening of
dysrhythmia or toxic effects
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Shortness of breath
 Edema
 Dizziness
 Syncope
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Chest pain
 GI distress
 Blurred vision
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Nursing Implications (cont’d)
Patients taking b-blockers, digoxin, and other
drugs should be taught how to take their own
radial pulse for 1 full minute, and to notify
their physician if the pulse is less than
60 beats/minute before taking the next dose
of medication
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Nursing Implications (cont’d)
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Monitor for therapeutic response
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Decreased BP in hypertensive patients
Decreased edema
Decreased fatigue
Regular pulse rate
Pulse rate without major irregularities
Improved regularity of rhythm
Improved cardiac output
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Nonpharmacologic Treatment of
Cardiac Dysrhythmias
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Pacemaker
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Catheter Ablation
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Direct current cardioversion
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Implantation of AICD
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