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P A R T 8
Drugs acting on the cardiovascular system
leaving the cell, prolonging the action potential and
slowing conduction and heart rate. Digoxin is effective
in the treatment of atrial arrhythmias. The drug exerts
a positive inotropic effect, leading to increased cardiac
output, which increases perfusion of the coronary
arteries and may eliminate the cause of some arrhyth-
mias as hypoxia is resolved and waste products are
removed more effectively.
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TABLE 45.2 Types of arrhythmias and drugs of choice for treatment
Arrhythmia
Antiarrhythmic drugs
Atrial
Flutter or fibrillation
Class Ic: flecainide
Class III: amiodarone, sotalol
Class IV: diltiazem
Other: adenosine
Other: digoxin
Paroxysmal atrial tachycardia (PAT)
Other: digoxin
Supraventricular tachycardia (SVT)
Class Ic: flecainide, propafenone*
Class II: esmolol* (short-term), propranolol
Class IV: diltiazem, verapamil (IV)
Other: adenosine* (SVT, including those caused by using alternative
conduction pathways)
Ventricular
Premature ventricular contractions (PVCs)
Class Ib: lignocaine*
Tachycardia or fibrillation
Class Ib: lignocaine
Life-threatening ventricular arrhythmias
Class Ia: disopyramide, procainamide
Class Ic: flecainide (X), propafenone
Class III: amiodarone*, sotalol (X)
*Drug of choice; (X) not drug of choice; proarrhythmic.
Care considerations for
people receiving antiarrhythmic agents
Assessment: History and examination
■
■
Assess for contraindications or cautions:
any known allergies to these drugs
to avoid
hypersensitivity reactions
; impaired liver or kidney
function,
which could alter the metabolism and
excretion of the drug
; any condition that could
be exacerbated by the depressive effects of the
drugs (e.g. heart block, HF, hypotension, shock,
respiratory dysfunction, electrolyte disturbances)
to avoid exacerbation of these conditions
; and
current status of pregnancy and breastfeeding
to prevent potential adverse effects on the fetus
or baby
.
■
■
Perform a physical assessment
to establish a
baseline before beginning therapy and during
therapy to determine the effectiveness of therapy
and evaluate for any potential adverse effects.
■
■
Assess the person’s neurological status, including
level of alertness, speech and vision and reflexes,
to identify possible CNS effects
.
■
■
Assess cardiac status closely, including pulse,
blood pressure, heart rate and rhythm,
to identify
changes requiring a change in the dosage of the
drug or the presence of adverse effects
; auscultate
heart sounds, noting any evidence of abnormal
sounds,
for early detection of heart failure
; and
anticipate cardiac monitoring
to evaluate heart rate
and rhythm and aid in identifying arrhythmia
.
■
■
Monitor respiratory rate and depth, and auscultate
lungs, for evidence of adventitious sounds
to
identify respiratory depression and detect changes
associated with heart failure.
■
■
Inspect abdomen
for evidence of distension
;
auscultate bowel sounds
to evaluate GI motility.
■
■
Evaluate skin for colour, lesions and temperature
to detect adverse reactions and to assess cardiac
output
.
■
■
Obtain a baseline ECG
to evaluate heart rate and
rhythm
; monitor the results of laboratory tests,
including full blood count,
to identify possible
bone marrow suppression
, and renal and liver
function tests,
to determine the need for possible
changes in dose and identify toxic effects.
Implementation with rationale
■
■
Titrate the dose to the smallest amount needed to
achieve control of the arrhythmia
to decrease the
risk of severe adverse effects.
■
■
Continually monitor cardiac rhythm when
initiating or changing dose
to detect potentially
serious adverse effects and to evaluate drug
effectiveness.
