Lesson 1 Cardiac Glycosides, Antianginals, and

Antidysrhythmics/Antiarrhythmmics

Site: New Era University Printed by: Charmaine Elyza M. Nolasco

Course: NCM104-18-Pharmacology copy 1 Date: Monday, 26 June 2023, 11:33 AM
Lesson 1 Cardiac Glycosides, Antianginals, and
Book:
Antidysrhythmics/Antiarrhythmmics
 Table of contents

1. Introduction

2. Learning Objectives

3. Content

4. VIdeo Cardiac Glycoside

5. Video Nitrates

6. Antiarrhythmic Drugs

7. Video
 1. Introduction

The cardiac drugs affect the function of the heart in three main ways. They can affect the force of contraction of the heart muscle (inotropic
effects), they can affect the frequency of the heart beat or heart rate (chronotropic effects) or they can affect the regularity of the heart beat
(rhythmic effects). Drugs can also affect blood vessels by altering the state of compression of the smooth muscle in the vessel wall, altering its
diameter and accordingly directing the volume of blood stream. Such medications are classified as vasoconstrictors or vasodilators depending
on the smooth muscle lining contraction and relaxation respectively. Treatment of cardiovascular (CV) disease often requires the administration
of numerous medications for long periods of time to patients likely to be old and suffering from a range of comorbid conditions.
 2. Learning Objectives

1. Differentiate the actions of cardiac glycosides, antianginal drugs, and antidysrhythmic drugs.

2. Describe the signs and symptoms of digitalis toxicity.

3. Compare the side effects and adverse reactions of nitrates, beta blockers, calcium channel blockers, quinidine, and procainamide.

4. Apply the nursing process, including patient teaching, related to cardiac glycosides, antianginal drugs, and antidysrhythmic drugs.
 3. Content

1. Cardiac Glycosides

Cardiac glycosides are a group of drugs derived from digitalis, a substance that occurs naturally in foxglove plants. The most commonly used
cardiac glycoside is digoxin.

Cardiac glycosides: Digoxin

Actions Indications

Inhibits sodium-potassium–activated adenosine Heart failure

triphosphase, an enzyme that regulates the Atrial fibrillation and flutter
amount of sodium and potassium inside the cell, Supraventricular tachycardia
resulting in increased intracellular levels of
sodium and calcium. Nursing considerations

Promotes movement of calcium from
extracellular to intracellular cytoplasm
and strengthens myocardial contraction.
Acts on the central nervous system to
enhance vagal tone, slowing contractions
through the sinoatrial and atrioventricular
nodes and providing an antiarrhythmic
Monitor the patient for adverse effects,
such as fatigue, agitation, hallucinations,
arrhythmias, anorexia, nausea, and
diarrhea.
Withhold the drug if the apical pulse is
less than 60 beats/minute, and notify the
prescriber.
Periodically monitor serum potassium
and digoxin levels.
Assess renal function because digoxin is
excreted by the kidneys.

effect.

NOTE:

Because digoxin has a long half-life, a loading

dose must be given to a patient who requires
immediate drug effects, as in supraventricular
arrhythmia. By giving a larger initial dose, a
minimum effective concentration of the drug in
the blood may be reached faster.

Loading doses should be avoided in patients with

heart failure to prevent toxicity.

a. Drug interactions

Rifampin, barbiturates, cholestyramine, antacids, kaolin and pectin, sulfasalazine, neomycin, and metoclopramide reduce the therapeutic
effects of digoxin.

Calcium preparations, quinidine, verapamil, cyclosporine, tetracycline, nefazodone, clarithromycin, propafenone, amiodarone, spironolactone,
hydroxychloroquine, erythromycin, itraconazole, and omeprazole increase the risk of digoxin toxicity.

Amphotericin B, potassium-wasting diuretics, and steroids taken with digoxin may cause hypokalemia (low potassium levels) and increase
the risk of digoxin toxicity.

The herbal preparations St. John’s wort and ginseng can increase levels of digoxin and increase the risk of toxicity

a. Adverse reactions

Because cardiac glycosides have a narrow therapeutic index (margin of safety), they may produce digoxin toxicity. To prevent digoxin toxicity, the
dosage should be individualized based on the patient’s serum digoxin concentration.
Signs and symptoms of digoxin toxicity include:

nausea and vomiting • insomnia

abdominal pain
diarrhea • confusion
headache
• vision changes (blurred or yellow vision)
irritability
depression • arrhythmias (bradycardia)

• complete heart block.

Nursing process Digoxin toxicity

These nursing process steps are appropriate for patients Digoxin has a
undergoing treatment with cardiac glycosides. narrow therapeutic index, so a
dose adequate to produce
Assessment therapeutic effects may
produce signs of toxicity.
Obtain a history of the underlying condition before therapy.
Individuals with hypokalemia
Monitor drug effectiveness by taking the patient’s apical pulse can develop digoxin
for 1 minute before each dose. Evaluate the electrocardiogram toxicity even when their digoxin
(ECG) when ordered, and regularly assess the patient’s levels aren’t elevated.
cardiopulmonary status for signs of improvement.
Signs of digoxin
Monitor digoxin levels (therapeutic blood levels range from 0.5 toxicity includes:
to 2 ng/mL). Obtain blood for digoxin levels 8 hours after the
• slow to rapid
last dose by mouth (PO).
ventricular rhythms
Closely monitor potassium levels.
• nausea and vomiting
Be alert for adverse reactions and drug interactions.
• blurred vision
Key nursing diagnoses
• anorexia
Decreased cardiac output related to underlying condition.
• abdominal discomfort
Risk for injury related to possible adverse reactions and
• mental changes.
digoxin toxicity.
Antidote
Deficient knowledge related to drug therapy.
Digoxin immune Fab is an
Planning outcome goals
antigen-binding fragment
Cardiac output will improve as evidenced by vital signs, urine (Fab) derived from specific
output, and level of consciousness. anti-digoxin antibodies.
Dosage is determined by the
Risk for digoxin toxicity will be minimized. serum digoxin level or the
estimated amount of
The patient will demonstrate correct drug administration and
digoxin ingested.
will verbalize correct symptoms of digoxin toxicity.

Implementation

Keep in mind that patients with hypothyroidism are extremely

sensitive to cardiac glycosides and may need lower doses.
Reduce the dosage in patients with impaired renal function.

Before giving a loading dose, obtain baseline data (heart rate

and rhythm, blood pressure, and electrolyte levels) and
question the patient about recent use of cardiac glycosides
(within the previous 3 weeks). The loading dose is always
divided over the first 24 hours unless the clinical situation
indicates otherwise.

Evaluation

Patient has adequate cardiac output.

Patient has no evidence of digoxin toxicity.
Patient and his family demonstrate an understanding of drug
therapy.

Teaching about digoxin
If digoxin is prescribed, review these points
with the patient and his caregivers:
Digoxin helps strengthen the heartbeat and
relieve ankle swelling, shortness of breath,
and fatigue, which can accompany a heart
problem.
Take digoxin and other heart medications as
prescribed, usually once daily, at the same
time each day.
Don’t miss any doses of the medication.
Don’t take a double dose of the medication if
a dose is missed.
Don’t take any over-the-counter medications
or herbal remedies without first consulting
with your prescriber.
You will need to have periodic physical
examinations, electrocardiograms, and blood
tests (for digoxin as well as electrolyte levels)
to see whether changes in dosages are
needed.
1. Antianginals
1. Coronary Artery Disease
Complementary and
Alternative Therapies
• Ginseng may falsely elevate
digoxin levels.
• Psyllium may decrease
digoxin absorption.
• Hawthorn may increase the
effect of digoxin.
• Licorice can potentiate the
effect of digoxin; it promotes
potassium loss (hypokalemia),
which increases the effect of
digoxin, and it may cause
digitalis toxicity.
• Aloe may increase the risk
of digitalis toxicity. It increases
potassium loss, which
increases the effect of digoxin.
• Ma-huang, or ephedra,
increases the risk of digitalis
toxicity.
• Goldenseal may decrease
the effects of cardiac
glycosides and may increase
the effects of
antidysrhythmics.
Limit salt intake and be sure to get enough
potassium. Follow the diet set by your
prescriber, and don’t take salt substitutes,
such as potassium chloride, without first
consulting with your prescriber.
Use the same brand and type of digoxin all
the time because forms and concentrations
are different and aren’t interchangeable.
Take your pulse as instructed by your
prescriber; count your pulse before each
dose. If it’s less than 60 beats /minute, call
your prescriber.
Don’t crush digoxin capsules. Tablets may be
crushed and can be taken with or after meals.
If taking the liquid form of digoxin, measure
accurately to prevent overdosage.
Report adverse effects, such as changes in
heart rate or rhythm, nausea, vomiting, or
vision problems, to your prescriber. These
signs and symptoms may mean that your
dosage needs to be changed.
 One of the leading causes of death in United States
Narrowing or occlusion of a coronary artery
Narrowing causes myocardial ischemia

a. Atherosclerosis

Most common etiology of CAD

Caused by presence of plaque

Figure 2.1 Atherosclerosis in the coronary arteries

Source: Mullvihill, Mary Lou; Zelman, Mark; Holdaway, Paul; Tompary, Elaine; Raymond, Jill, HUMAN DISEASES: A SYSTEMIC APPROACH, 6th
edition., © 2006. Reprinted and electronically reproduced by permission of Pearson Education, Inc., Upper Saddle River, New Jersey.

Blood Flow to Heart

– Myocardium receives blood via coronary arteries

– Diverge into smaller branches around heart

– Provide continuous supply of oxygen and nutrients

a. Angina Pectoris

Acute chest pain due to insufficient O2 to myocardium

Accompanies physical exertion or emotional excitement
Causes increased myocardial oxygen demand
Signs and Symptoms

– Steady, intense pain in anterior chest

– Pain radiating to left shoulder, left arm, spine, jaw

– Fear of impending death

– Pallor, dyspnea, diaphoresis

– Tachycardia, elevated blood pressure

– Pain diminishes with physical rest and/or stress reduction

Classification

– Classic/Stable angina is fairly predictable as to frequency, intensity, duration.

o Usually relieved by rest

– Vasospastic angina (Variant or Prinzmetal) caused by spasms of coronary arteries

– Silent angina occurs in absence of angina pain

– Unstable angina (preinfarction) when episodes occur more frequently, more intense, during periods of rest

Pharmacologic Management of Angina

Table 1 Selected Drugs for Angina and Myocardial Infarction


Drug
ORGANIC NITRATES
Isosorbide dinitrate (Dilatrate SR,
Isordil)
Isosorbide mononitrate (Imdur, Ismo,
Monoket)
Nitroglycerin (Nitrostat, Nitro-Dur, Nitro- SL; 1 tablet (0.3-0.6 mg) or 1 spray
Bid, others)
BETA-ADRENERGIC BLOCKERS
Atenolol (Tenormin)
Metoprolol (Lopressor, Toprol XL) (see
page 354 for the Prototype Drug box)
Nadolol (corgard)
Propranolol (Inderal, Inderal LA) (see
page 399 for the Prototype Drug box)
Timolol (Betimok) (see page 773 for the
Prototype Drug box)
CALCIUM CHANNEL BLOCKERS
Route and Adult Dose
(max dose where indicated)
PO; 2.5-30 mg qid (max:480
mg/day)
PO; 20 mg qid (max: 240 mg/day
sustained release)
(0.4-0.8 mg) every 3-5 min. (max:
three doses in 15 min.)
PO; 25-50 mg/day (max: 100
mg/day)
PO; 100 mg bid (max: 400 mg/day)
PO; 40 mg once daily (max: 240
mg/day)
PO; 10-20 mg bid-tid (mx: 320
mg/day)
PO (for MI); 10 mg once daily
Adverse Effects
Headache, postural hypotension,
flushing of face, dizziness, rash
(transdermal patch), tolerance
Anaphylaxis, circulatory collapse
due to hypotension, syncope due
to orthostatic hypotension
Fatigue, insomnia, drowsiness,
impotence or decreased libido,
bradycardia, confusion
Agranulocytosis, laryngospasm,
Steves-Johnson syndrome,
anaphylaxis; if the drug is abruptly
withdrawn, palpitations, rebound
hypertension, life-threatening
dysrhythmias or MI may occur
Amlodipine (Norvasc) PO; 5-10 mg/day (max: 10 mg/day) Flushed skin, headache, dizziness,
peripheral edema, light-
headedness, nausea, diarrhea

Bepridil (Vascor) PO; 200 mg/day (max: 360 mg/day)

Hepatotoxicity, MI, HF, confusion,

Ditiazem (Cardizem, Cartia XT, Dilacor
XR, others)
mood changes
PO; regular release: 30 mg tid-qid
(max: 480 mg/day); extended
release: 20-240 mg bid (max: 180
mg/day)

PO; 20-40 mg tid or 30-60 mg SR

bid (max: 120 mg/day)
Nicardipine (Cardene)

PO; 10-20 mg tid (max0: 180

mg/day)
Nifedipine (Adalat, Procardia, others)
(see page 339 for the Prototype Drug
box) PO; 80 mg tid-qid (max: 48 mg/day)

PO; (Covera-HS) 180-540 mg once

daily at bedtime
Verapamil (Calan. Covera-HS) (see page
401 for the Prototype Drug box)

MISCELLANEOUS DRUGS

Ranolazine (Ranexa) PO; 500-1000 mg bid (max: 2000 Dizziness, headache, constipation,
mg/day) nausea

Prolongation of QT interval,
bradycardia, palpitations,
hypotension

Note: Italics indicate common adverse effects; underlining indicates serious adverse effects.

Nitrates

• Relax both arterial and venous smooth muscle; dilate coronary arteries

• Short-acting—Terminate acute angina episode, half-life 1 – 3 minutes

• Long-acting—Decrease severity and frequency of episodes

• Reduce heart workload, lower myocardial oxygen demand

• Adverse effects: hypotension, dizziness, headache, flushing of face, rash

• Prototype drug: nitroglycerin (Nitrostat)

Prototype Drug Nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others)

Therapeutic Class: Antianginal Drug Pharmacologic Class: Organic nitrate, vasodilator

ACTIONS AND USES ADVERSE EFFECTS

Nitroglycerin, the oldest and most widely used The adverse effects of nitroglycerin are usually
organic nitrate, can be delivered by a number of cardiovascular in nature and rarely life threatening.
different routes: sublingual, PO, lingual, IV, Because nitroglycerin can dilate cerebral vessels,
transmucosal, transdermal, topical and extended- headache is a common side effects and may be severe.
release forms. It is taken while an acute angina Occasionally, the venous dilation caused by nitroglycerin
episode is in progress or just prior to physical produces reflex tachycardia. Some health care providers
activity. When given sublingually, it reaches peak prescribe a beta-adrenergic blocker to diminish this
plasma levels in 2 or 4 minutes, thus terminating undesirable increase in heart rate. Many of the side
angina pain rapidly. Chest pain that does not respond effects of nitroglycerin diminish after a few doses.
within 10 to 15 minutes after two or three doses of
sublingual nitroglycerin may indicate MI and
emergency medical services should be contacted.
The transdermal and oral extended-release forms are
for prophylaxis only because they have a relatively
slow onset of action.

ADMINISTRATION ALERTS Contraindications: Nitroglycerin should not be given to

patients with preexisting hypotension or with high
intracranial pressure or head trauma. Drugs in this class
are contraindicated in pericardial tamponade and
For IV administration, use a glass intravenous (IV)
constrictive pericarditis because the heart cannot
bottle and special IV tubing because plastic
increase cardiac output to maintain blood pressure when
absorbs nitrates significantly, thus reducing the
vasodilation occurs. Sustained-release forms should not
patient dose.
be given to patients with glaucoma because they may
Cover the IB bottle to reduce the degradation of
increase intraocular pressure. Dehydration or
nitrates due to light exposure.
hypovolemia should be corrected before nitroglycerin is
Use gloves when applying nitroglycerin or
administered; otherwise, serious hypotension may result.
ointment to prevent self-administration.
Pregnancy category C.

INTERACTIONS

ADMINISTRATION ALERTS Drug-Drug: Concurrent use with phosphodiesterase-5

inhibitors such as sildenafil (Viagra), vardenafil (Levitra)
Onset Peak Duration
or tadalafil (Cialis) may cause life-threatening
1-3 min 4-8 min 30-60 min hypotension and cardiovascular collapse. Use with
sublingual sublingual; sublingual alcohol and antihypertensive drugs may cause additive
hypotension.
2-5 min buccal; 4-10 min buccal; 2 h buccal; 18-
40-60 min 1-2 h 24 h
transdermal transdermal transdermal
Lab Tests: Nitroglycerin may increase values of urinary
patch; patch; patch;
catecholamines and vanillymandelic acid (VMA)
concentrations.
12 h topical Topical ointment Topical ointment
ointment 12 h 12 h

Herbal / Food: Use with hawthorn may result in additive

hypotension.

Treatment of Overdose: Hypotension may be reversed

with administration of IV normal saline. If
methemoglobinemia is suspected, methylene blue may
be administered.

Safety and Quality Improvement: Preventing medication error

Understanding Rate Versus Dose

The Institute for Safe Medication Practices (ISMP) reported an incident in which a nitroglycerin intravenous drip was set to infuse at 60 mL/hr
rather than 60 mcg/min. With the medication concentration used (50 mg/250 mL) the patient actually received 200 mcg/min instead of the
ordered 60 mcg/min. Investigation of this incident revealed that the nurses were using a handwritten, nonstandard dosing table rather than one
that corresponded to the available concentrations of premixed solutions in the hospital. According to the report, the patient became hypotensive
but recovered.

It is crucial to understand the difference between “mL/hr” and “mcg/min” when programming infusion pumps; rates are not interchangeable with
ordered doses! In addition, using standardized dosing charts that correspond to available concentrations of solutions is important. Some
facilities also require double-checking of infusion pump settings before medication therapy is begun.

www.ismp.org/Newsletters/nursing/Issues/NurseAdviseERR200506.pdf.

Beta-adrenergic Blockers

• Reduce the cardiac workload by slowing heart rate and reducing contractility

• First-line drug for angina pain

• Adverse effects: fatigue, insomnia, drowsiness, impotence, bradycardia, confusion

• Prototype drug: atenolol (Tenormin)

Prototype Drug Atenolol (Tenormin)

Therapeutic Class: Antianginal Drug Pharmacologic Class: Beta-adrenergic blocker

ACTIONS AND USES ADVERSE EFFECTS

Atenolol is one of the most frequently prescribed Being a cardioselective beta1-adrenergic blocker, atenolol
drugs in the United States due to its relative safety has few adverse effects on the lung. The most frequently
and effectiveness in treating a number of chronic reported adverse effects of atenolol include fatigue,
disorders, including HF, hypertension, angina and MI. weakness, bradycardia and hypotension.
The drug selectively blocks beta1-adrenergic
receptors in the heart. Its effectiveness in treating
angina is attributed to its ability to slow heart rate
Black Box Warning: Abrupt discontinuation should be
and reduce contractility, both of which lower
avoided in patients with ischemic heart disease; doses
myocardial oxygen demand. As with other beta
should be gradually reduced over a 1-to 2-week period. If
blockers, therapy generally begins with low doses,
angina worsens during the withdrawal period, the drug
which are gradually increased until the therapeutic
should be reinstituted.
effect is achieved. Because of its 7-to 9-hour half-life,
it may be taken once daily.

Contraindications: Because atenolol slows heart rate, it

ADMINSTRATION ALERTS
During IV administration, monitor ECG
continuously; BP and pulse should be assessed
before, during and after the dose is administered.
Assess pulse and BP before oral administration.
Hold if the pulse is below 60 beats per minute or if INTERACTIONS
the patients is hypotensive.
Atenolol may precipitate bronchospasm in
susceptible patients with initial doses.
Pregnancy category D.
PHARMACOKINETICS
should not be used in patients with severe bradycardia,
atrioventricular (AV) heart block, cardiogenic shock or
decompensated HF. Due to its vasodilation effects, it is
contraindicated in patients with severe hypotension.
Drug-Drug: Concurrent use with CCBs may result in
excessive cardiac suppression. Use with digoxin may
slow AV conduction, leading to heart block. Concurrent
use of atenolol with other antihypertensive may result in
additive hypotension. Anticholinergics may cause
decreased absorption from the gastrointestinal (GI) tract.

Onset Peak Duration

Lab Test: Atenolol may increase values of the following
1h 2-4 h 24 h blood tests: uric acid, lipids, potassium, creatinine and
antinuclear antibody.

Herbal / Food: Unknown.

Treatment of Overdose: The most serious symptoms of

atenolol overdose are hypotension and bradycardia.
Atropine or isoproterenol may be used to reverse
bradycardia. Atenolol can be removed from the systemic
circulation by hemodialysis.

Calcium Channel Blockers

• Inhibit the transport of calcium into myocardial cells, relax arteriolar smooth muscle

• Reduce cardiac workload; bring more oxygen into myocardium

• Adverse effects: hypotension, bradycardia, heart failure, constipation, headaches, dizziness, edema

• Prototype drug: diltiazem (Cardizem, Cartia XT, Dilacor XR, others)

• Role of the Nurse

– Assess vital signs

– Hold medication if patient hypotensive (heart rate of 60 or below)

– Obtain blood pressure in lying, sitting, and standing positions

– Assess for signs of heart failure

– Obtain daily weights

– Assess bowel functions

Prototype Drug Diltiazem (Cardizem, Cartia XT, Dilacor XR, others)

Therapeutic Class: Antianginal Drug Pharmacologic Class: Calcium channel blocker

ACTIONS AND USES ADVERSE EFFECTS

Like other CCBs, diltiazem inhibits the transport of Adverse effects of diltiazem are generally not serious and
calcium into myocardial cells. It has the ability to are related to vasodilation: headache, dizziness and
relax both coronary and peripheral blood vessels, edema of the ankles and feet. Abrupt withdrawal may
bringing more oxygen to the myocardium and precipitate an acute angina episode.
reducing cardiac workload. It is useful in the
treatment of atrial dysrhythmias and hypertension as
well as stable and vasospastic angina. When given
Contraindications: Diltiazem is contraindicated in
as sustained-release capsules, it is administered
patients with AV heart block, sick sinus syndrome, severe
once daily.
hypotension or bleeding aneurysm or those undergoing
intracranial surgery. This drug should be used with
caution in patients with renal or hepatic impairment.
ADMINSTRATION ALERTS

During IV administration, the patient must be

continuously monitored and cardioversion INTERACTIONS

equipment must be available.

Drug-Drug: Concurrent use of diltiazem with other
Extended-release tablets and capsules should not
cardiovascular drugs, particularly digoxin or beta-
be crushed or split.
adrenergic blockers, may cause partial or complete heart
Pregnancy category C.
block, HF or dysrhythmias. Diltiazem may increase
digoxin or quinidine levels when taken concurrently.
Additive hypotension may occur if used with ethanol,
PHARMACOKINETICS beta, blockers or antihypertensive.

Onset Peak Duration

30-60 min 2-3 h 6-8 h Lab Test: Unknown.

(immediate (immediate (immediate
release); 2-3 h release); 6-11 h release); 12 h
(extended (extended (extended Herbal / Food: St. John’s wort and ginseng may decrease
release) release) release) the effectiveness of diltiazem. Garlic, hawthorn and
goldenseal may increase the antihypertensive effect of
diltiazem.

Treatment of Overdose: Atropine or isoproterenol may be

used to reverse bradycardia caused by diltiazem
overdose. Hypertension may be reversed by a
vasopressor such as dopamine or dobutamine. Calcium
chloride can be administered by slow IV push to reverse
hypotension or heart block induced by CCBs.

Figure 2.2 Mechanisms of Action of Drugs Used to Treat Angina

a. Myocardial Infarction

Occurs when a coronary artery becomes completely occluded

Deprived of oxygen supply, affected area of myocardia become ischemic, and myocytes begin to die in about 20 minutes

Figure 2.3 Blockage and reperfusion following myocardial infarction: (2) blockage of left coronary artery with resultant myocardial ischemia; (3)
infusion of thrombolytics; (4) thrombus dissolving and ischemia clearing. Source: Pearson Education.

Thrombolytics

• Dissolve clots obstructing coronary arteries

• In cases of acute MI, for restoring circulation to myocardium

• Narrow margin of safety between dissolving clots and producing serious adverse effects, particularly excessive bleeding

• Prototype drug: reteplase (Retavase)

• Role of the Nurse

– Assess for conditions that may place patient at increased risk for bleeding

– Start IV and arterial lines, and insert Foley catheter

– Monitor vital signs and intake and output

– Monitor changes in laboratory values

– Assess for changes in neurological status

– Assess for dysrhythmia

Prototype Drug Reteplase (Retavase)

Therapeutic Class: Drug for dissolving blood clots Pharmacologic Class: Thrombolytic
ACTIONS AND USES ADVERSE EFFECTS

Prepared through recombinant DNA technology, The most serious adverse effect of reteplase is abnormal
reteplase acts by cleaving plasminogen to form bleeding. Bleeding may be prolonged at injection sites
plasmin. Plasmin then degrades the fibrin matrix of and catheter insertion sites. Dysrhythmias may occur
thrombi. Like other drugs in this class, reteplase during myocardial reperfusion.
should be given as soon as possible after the onset
of MI symptoms. Administered by IV bolus, it usually
acts within 20 minutes. A second bolus may be
Contraindications: Reteplase is contraindicated in
injected 30 minutes after the first, if needed to clear
patients with active bleeding or history of CVA or who
the thrombus. After the clot has been dissolved,
have had recent surgical procedures.
therapy with from forming. Reteplase may be used
off-label to treat acute and chronic deep venous
thrombosis and occluded catheters.
INTERACTIONS

Drug-Drug: Concurrent therapy with aspirin,

ADMINSTRATION ALERTS anticoagulants and platelet aggregation inhibitors will
produce an addictive anticoagulant effect and increase
Reconstitute the drug immediately prior to use
the risk of bleeding.
with diluent provided by the manufacturer; swirl to
mix – do not shake.
Do not give any other drug simultaneously
through the same IV line. Lab Test: Reteplase degrades plasminogen in blood
Reteplase and heparin are incompatible and must samples, thus decreasing serum plasminogen and
never be combined in the same solution. fibrinogen levels.
Pregnancy category C.

Herbal / Food: Ginkgo biloba should be avoided because

PHARMACOKINETICS it may increase the risk of bleeding.

Onset Peak Duration

Immediate Unknown Unknown Treatment of Overdose: There is no specific treatment

for overdose.

Nitrates

Assist diagnosis of MI: paint that persists 5–10 mins after administration, may indicate MI.
Arterial and venous dilation; relieve coronary artery vasospasm.
Role of the Nurse:

– Obtain blood pressure and monitor

– IV nitrates have greatest risk for severe hypotension

– Educate patient that alcohol is contraindicated with nitrates If hypotension occurs, withhold nitrates.

Beta-adrenergic blockers

Reduce myocardial oxygen demand; slow impulse conduction through the heart
Can reduce MI mortality if administered within 8 hours of onset.
Role of the Nurse:

– Assess apical heart rate

– Obtain blood pressure and continue to monitor

– Monitor respiratory status

– Monitor serum glucose levels

– Educate patient not to stop medications abruptly

ACE inhibitors
 Increased survival for those MI patients administered captopril (Capoten) or lisinopril (Prinivil, Zestoretic).
Most effective when administered within 24 hours of onset of symptoms
Role of Nurse

– Monitor patient's condition

– Provide education on prescribed drug treatment

– Obtain vital signs and medical and drug history

– Obtain information on lifestyle and dietary habits

3. Dysrhythmias

• Abnormalities of electrical conduction or rhythm in heart

• Also known as arrhythmias

• Can range from harmless to life- threatening

Frequency in Population Difficult to Predict

• Symptoms range from none to sudden death

• Still, dysrhythmias estimated to be quite common

• Persistent/severe dysrhythmias increase risk of stroke and heart failure

Flow of Electrical Impulses through Normal Heart

• Dysrhythmias defect in conduction of electrical impulses across myocardium

• Action potentials

– Signal cardiac muscle cells to contract; beat in a synchronized manner

• Sinoatrial (SA) node—pacemaker

– Automaticity

– Sinus rhythm

• Atrioventricular (AV) node

• Atrioventricular bundle (bundle of His)

• Right and left bundle branches

• Purkinje fibers

• Ectopic foci; ectopic pacemakers

Conduction System

Purpose is to regulate heat and maintain cardiac output

Figure 3.1 Normal conduction pathway in the heart

Occurrence of Dysrhythmias

• Can occur in both healthy and diseased hearts

• Disrupt regulation of heart

• May decrease cardiac output

• Closely associated with certain conditions

– Heart disease

– Myocardial infarction

Classification of Dysrhythmias

• Location

– Atrial or ventricular

• Type

– Flutter, fibrillation, block

• Atrial fibrillation most common

Types of Dysrhythmia

• Atrial or ventricular tachycardia

• Atrial or ventricular flutter

• Atrial or ventricular fibrillation

• Heart block

• Premature atrial or premature ventricular contractions (PVCs)

• Sinus bradycardia

Table 2 Types of Dysrhythmias

Name of Dysrhythmia Description

Atrial or ventricular tachycardia Rapid heartbeat greater than 100 beats/min. in adults; ventricular
tachycardia is more serious than atrial tachycardia

Atrial or ventricular flutter Rapid, regular heartbeats; may range between 200 and 300 beats/min.
atrial may require treatment but is not usually fatal; ventricular flutter
requires immediate treatment

Atrial or ventricular fibrillation Very rapid; uncoordinated contractions with complete disorganization
of rhythm; ventricular fibrillation requires immediate treatment

Heart block Blockage in the electrical conduction system of the heart; may be
partial or complete; classified as first, second or third degree

Premature atrial or premature An extra beat often originating from a source other than the SA node;
ventricular contractions (PVCs) only considered serious if it occurs in high frequency; may be a
precursor of more serious dysrhythmias.

Sinus bradycardia Slow heartbeat, less than 60 beats per minute, originating in the
sinoatrial (SA) node; may require a pacemaker

Electrocardiogram (ECG)

• Measures wave of electrical activity across the myocardium

• Used to diagnose many types of heart conditions

• Changes to wave patterns or timing can reveal certain pathologies

Figure 3.2 Relationship of the electrocardiogram to electrical conduction in the heart

Action Potentials

• Electrical impulses across myocardium

• Found in neural and cardiac cells

• Created by changes in extra- and intracellular ion polarization

• Cell membrane with negative membrane potential = polarized

– Negative membrane potential

– Na+ and Ca++ outside cell

– K+ inside cell

Generation of Action Potential

• Sodium ion channels open

– Sodium ions rush in, cause depolarization

• Calcium ion channels open

– Calcium ions enter cell, stimulate cardiac muscle contraction

§ SA and AV cells depolarize in response to calcium–ion influx

Repolarization

• Return to polarized state

• Sodium pump removes Na+

• Potassium ion channels allow K+ to move back into cell

Pharmacological Strategies to Terminate Dysrhythmias

• Block potassium–, sodium–, or calcium–ion channels

• Prolong refractory period

– Brief period in conduction cycle when myocardial cells cannot produce another action potential
Figure 3.3 Ion channels in myocardial cells

Nonpharmacological Therapies for Dysrhythmias

• Cardioversion and defibrillation

– Serious types of dysrhythmias

– Electrical shock stops all electrical impulses in heart and allows SA node to regain control

• Catheter ablation—Identify and destroy aberrant cardiac cells that cause dysrhythmias

• Cardiac pacemaker—Paces heart at set rate

• Implantable cardioverter defibrillator (ICD)—combination of pacemaker and defibrillator

Antidysrhythmic Drugs

• Primary mechanisms of action

– Blocking conduction (flow of ions)

– Altering automaticity (autonomic activity)

• Use is declining significantly

– Can worsen or create new dysrhythmias

– Nonpharmacological therapy is improving

Antidysrhythmic Drug Groups

• Five groups

– Class I: sodium channel blockers

§ Block sodium ion channels and suppress ectopic activity

– Class II: beta-adrenergic antagonists

§ Slow heart rate, decrease conduction velocity through AV node

– Class III: potassium channel blockers

§ Delay repolarization and lengthen refractory period—stabilize dysrhythmias

– Class IV: calcium channel blockers
§ Reduce automaticity in SA node and slow impulse conduction through AV node; slow heart rate
– Miscellaneous antidysrhythmic drugs: Slow conduction through AV node and/or decrease automaticity of SA node
Table 3 Antidysrhythmic Drugs
Drug
CLASS IA: SODIUM CHANNEL BLOCKERS
Disopyramide (Norpace)
Procainamide
Quinidine gluconate
Quinidine sulfate
CLASS IB: SODIUM CHANNEL BLOCKERS
Lidocaine (Xylocaine) (see page 247 for IV; 1-4 mg/min. infusion rate (max: Nausea, vomiting, drowsiness,
the Prototype Drug box)
Mexiletine (Mexitil)
Phenytoin (Dilantin) (see page 181 for
the Prototype Drug box)
CLASS IC: SODIUM CHANNEL BLOCKERS
Flecainide (Tambocor)
Propafenome (Rythmol)
CLASS II: BETA-ADRENERGIC BLOCKERS
Route and Adult Dose
Adverse Effects
(max dose where indicated)
PO; (immediate release): 400-800 Nausea, vomiting, diarrhea, dry
mg in divided doses mouth, urinary retention
PO; (extended release): 300 mg bid May produce new dysrhythmias or
worsen existing ones;
hypotension, blood dyscrasias
(quinidine) and lupus
IV; 100 mg every 5 minutes at a rate
(procainamide)
of 25-50 mg/min. (max: 1g)
PO; 324-648 mg tid-qid (max: 3-4
g/day)
PO; 200-400 mg tid-qid (max: 3-4
g/day); therapeutic serum drug
level is 2-5 mcg/Ml
3 mg/kg. per 5-10 min.) dizziness, lethargy
PO; 200-300 mg tid (max: 1,200 May produce new dysrhythmias or
mg/day) worsen existing ones,
hypotension, bradycardia, central
nervous system (CNS) toxicity
(lidocaine), malignant
PO; 100-200 mg tid (max: 625
hyperthermia (lidocaine), status
mg/day)
epilepticus if abruptly withdrawn
(phenytoin)
IV; 50-100 mg every 10-15 min. until
dysrhythmia is terminated (max:
1g/day)
PO; 100 mg bid (max: 400 mg/day) Nausea, vomiting, dizziness,
headache, palpitations
PO; (immediate release): 150-300
mg tid May produce new dysrhythmias or
worsen existing ones; hypotension
bradycardia
PO; (sustained release): 225 mg bid
Acebutolol (Sectral)
Esmolol (Brevibloc)
Propranolol (Inderal, InnoPran XL)
CLASS III: POTASSIUM CHANNEL BLOCKERS
Amiodarone (Cardarone, Pacerone)
Dofetilide (Tikosyn)
Dronedarone (Multaq)
Ibutilide (Corvert)
Sotalol* (Betapace, Betapace AF,
Sorine)
CLASS IV: CALCIUM CHANNEL BLOCKERS
Diltiazem (Cardizem, Dilacor, Taztia XT, IVl 5-10 mg/h continuous for a
Tiazac) (see page 371 for the Prototype maximum of 24 h (max: 15 mg/h)
Drug box)
Verapamil (Calan, COvera-HS Verelan)
MISCELLANEOUS DRUGS
PO; 200-600 mg bid (max: 1,200
mg/day)
IV;50 mcg/kg/min. maintenance
dose (max: 200 mcg/kg/min.)
PO 10-30 mg tid-qid (max: 480
mg/day)
IV: 0.5-3.1 mg every 4 hours
PO; 400-600 mg/day (max: 1,600
mg/day as loading dose)
PO; 125-500 mcg bid based on
creatinine clearance
PO; 400 mg bid
IV; 1 mg infused over 10 min
PO; 80 mg bid (max: 320 mg/day)
PO; 240-480 mg/day
IV; 5-10 mg direct: may repeat in
15-30 min if needed
Fatigue, insomnia, drowsiness,
impotence or decreased libido,
bradycardia, confusion
Agranulocystosis, laryngospasm,
Steves-Johnson syndrome,
anaphylaxis; if the drug is abruptly
withdrawn, palpitations, rebound
hypertension, life-threatening
dysrhythmias or myocardial
ischemia may occur
Blurred vision (amiodarone),
photosensitivity, nausea, vomiting,
anorexia
May produce new dysrhythmias or
worsen existing ones;
hypotension, bradycardia,
pneumonia-like syndrome
(amiodarone), angioedema
(dofetilide), CNS toxicity
(ibultilide)
Flushed skin, headache, dizziness,
peripheral edema, light-
headedness, nausea, diarrhea
Hepatotoxicity, MI, heart failure
(HF), confusion, mood changes
Adenosine (Adenocard, Adenoscan) IV; 6-12 mg given as a bolus Facial flushing, dyspnea, chest
injection every 1-2 min. as needed warmth
(max: 12 mg/dose)

May produce dysrhythmias or

PO; 0.125-0.5 mg qid; therapeutic worsen existing one
serum drug level is 0.8-2 mg/mL
Digoxin (Lanoxicaps) (see page 353 for
the Prototype Drug box)
Nausea, vomiting; headache and
visual disturbances

May produce new dysrhythmias or

worsen existing ones

Note: Italics indicate common adverse effects; underlining indicates serious adverse effects.

*Sotalol is a beta blocker, but because its cardiac effects are similar to those of amiodarone, it is considered a
class ill drug.

Sodium Channel Blockers (Class I)

• Prototype drug: procainamide (Pronestyl)

• Mechanism of action: to block sodium ion channels, which slows rate of impulse conduction across heart

• Primary use: to correct atrial and ventricular dysrhythmias

• Adverse effects: Creates new dysrhythmias or worsens existing ones

– Lupus effect, nausea, vomiting, abdominal pain, headache

– High doses can produce CNS effects

Role of the Nurse: Sodium Channel Blockers

– Monitor ECG for changes

– Monitor for hypotension, changes in level of consciousness, diarrhea

– Teach patient to take medication as directed and to avoid alcohol

– Contraindicated when patients have heart failure or renal impairment

Prototype Drug Procainamide

Therapeutic Class: Class IA antidysrhythmic Pharmacologic Class: Sodium channel blocker

ACTIONS AND USES Black Box Warning: Chronic administration may result in
an increased titer of antinuclear antibodies ANAs). A
Procainamide is an older drug, approved in 1950, lupus-like syndrome may occur in 30% to 50% of patients
that is chemically related to the local anesthetic who are taking drug for more than a year. Procainamide
procaine. Procainamide blocks sodium ion channels should be reversed for life-threatening dysrhythmias
in myocardial cells, thus reducing automatically and because it has the ability to produce new dysrhythmias or
slowing conduction velocity prolongs the refractory worsen existing ones. Agranulcytosis, bone marrow
period and can suppress dysrhythmias. The most depression, neutropenia, hypoplastic anemia and
common dosage form is the extended-release tablet; thrombocytopenia have been reported, usually within the
however, procainamide is also available in first 3 months of therapy. Complete blood counts should
intravenous (IV) and intramuscular (IM) be monitored carefully and the drug discontinued at the
formulations. The therapeutic serum drug level is 4 first sign of potential blood dyscrasia.
to 8 mcg/mL. The use of procainamide has declined
significantly due to the development of more specific
and safer drugs.
Contraindications: Procainamide is contraindicated in
patients with complete AV block, severe, HF, blood
dyscrasias and myasthenia gravis.
ADMINSTRATION ALERTS

Reconstitute the drug immediately prior to use

with diluent provided by the manufacturer; swirl to
mix – do not shake.
Do not give any other drug simultaneously
through the same IV line.
Reteplase and heparin are incompatible and must
never be combined in the same solution.
Pregnancy category C.

PHARMACOKINETICS

Onset Peak Duration

Immediate Unknown Unknown

Prototype Drug Procainamide

Therapeutic Class: Class IA antidysrhythmic Pharmacologic Class: Sodium channel blocker

ADMINSTRATION ALERTS PHARMACOKINETICS (PO)

Use the supine position during IV administration Nausea, vomiting, abdominal pain, hypotension and
because severe hypotension may occur. headache are common during procainamide therapy.
Pregnancy category C. High doses may produce CNS effects such as confusion
or psychosis.

PHARMACOKINETICS (PO)
INTERACTIONS
Onset Peak Duration
Drug-Drug: Additive cardiac depressant effects may
Immediate IV; occur if procainamide is administered with other
1-1.5 h 3-4 h
10-30 min IM antidysrhythmics. Additive anticholinergic drugs.

Lab Test: Procainamide may increase values for the

following: AST, ALT, serum alkaline phosphatase, LDH and
serum bilirubin. False-positive Coombs test and ANA
titers may occur.

Herbal / Food: Unknown.

Treatment of Overdose: Supportive treatment is targeted

to reversing hypotension with vasopressors and
preventing or treating procainamide-induced
dysrhythmias.

Beta-adrenergic Blockers (Class II)

• Prototype drug: propranolol (Inderal)

• Mechanism of action: to block beta receptors, which reduces automaticity and slows conduction velocity across myocardium

• Primary use: to treat atrial dysrhythmias associated with heart failure

• Adverse effects: bradycardia, hypotension with dizziness and fainting

– Bronchospasms, hypoglycemia, diminished libido

• Role of the Nurse: Beta-adrenergic Blockers

– Contraindicated in patients with heart block, severe bradycardia, AV block, asthma

– Monitor for hypotension and hypoglycemia

– Elderly patients may show signs of cognitive impairment

– Teach patients to measure heart rate, to rise slowly, to report signs of heart failure
Potassium Channel Blockers (Class III)

• Prototype drug: amiodarone (Cordarone)

• Mechanism of action: to block potassium-ion channels in myocardial cells, which prolongs refractory period of heart

• Primary use: to treat resistant ventricular tachycardia, atrial dysrhythmias with heart failure

• Adverse effects: blurred vision, pneumonia-like syndrome, bradycardia, hypotension

– Can create new dysrhythmias or worsen existing ones

• Role of the Nurse: Potassium Channel Blockers

– Use cautiously in patients with heart block

– Do not use during pregnancy (category C) or lactation

– Monitor for vision changes, palpitations, jaundice, abdominal pain

– Avoid sun exposure; take with food

Prototype Drug Amidarone (Cordarone, Pacerone)

Therapeutic Class: Class III antidysrhythmic Pharmacologic Class: Potassium channel blocker
ACTIONS AND USES
Amiodarone is structurally similar to thyroid
hormone. It is approved for the treatment of resistant Amiodarone may also cause blurred vision, rashes,
ventricular tachycardia that may prove life
threatening and it has become a drug of choice for dizziness and hypotension. Because this medication is
the treatment of atrial dysrhythmias in patients with concentrated by certain tissues and has a prolonged half-
HF. In addition to blocking potassium ion channels, life, adverse effects may be slow to resolve.
some of this drug’s actions on the heart relate to its
blockade of sodium ion channels. Amiodarone is
available as oral tablets and as an IV infusion. IV
infusions are limited to short-term therapy, normally
only 2 to 4 days. When given orally, its onset of
action may take several weeks. Its effects, however
can last 4 to 8 weeks after the drug is discontinued,
because it has an extended half-life that may exceed
100 days. The therapeutic serum level of amiodarone
is 0.5 to 2.5 mcg/mL.
ADMINSTRATION ALERTS
Hypokalemia and hypomagnesemia should be
corrected prior to initiating therapy.
Pregnancy category D.
PHARMACOKINETICS (PO)
Onset Peak Duration
2-3 d PO; 2 hr IV 3-7 h 10-150 days
Prototype Drug
Therapeutic Class: Class III antidysrhythmic
Pharmacologic Class: Potassium channel blocker
ADVERSE EFFECTS
The most serious adverse effect is pulmonary toxicity.
photosensitivity, nausea, vomiting, anorexia, fatigue,
Black Box Warning: Amiodarone causes a pneumonia-
like syndrome in the lungs. Because the pulmonary
toxicity may be fatal, baseline and periodic assessment
of lung function is essential. Amiodarone has
prodysrhythmic action and may cause bradycardia,
cardiogenic shock or AV block. Mild liver injury is
frequent with amiodarone.
Contraindications: Amiodarone is contraindicated in
patients with severe bradycardia, cardiogenic shock, sick
sinus syndrome, severe sinus node dysfunction or third-
degree AV block.
INTERACTIONS
Drug-Drug: Amiodarone can increase serum digoxin
levels by as much 70%. Amiodarone greatly enhances the
actions of anticoagulants: Thus, the dose of warfarin
must be cut by as much as half. Use with beta-adrenergic
blockers or calcium channel blockers may cause or
worsen sinus bradycardia, sinus arrest or ABV block.
Amiodarone may increase phenytoin levels two-to
threefold.
Lab Test: Amiodarone may increase values for the
following tests: nuclear antibody, ALT, AST and serum
alkaline phosphatase T4.
Herbal / Food: Use with Echinacea may cause an
increased risk of hepatotoxicity. Aloe may cause an
increased effect of amiodarone.
Treatment of Overdose: Treatment of amiodarone
overdose is targeted to reversing hypotension with
vasopressors and bradycardia with atropine or
isoproterenol.
Amidarone (Cordarone, Pacerone)
ACTIONS AND USES ADVERSE EFFECTS

Amiodarone is structurally similar to thyroid The most serious adverse effect is pulmonary toxicity.
hormone. It is approved for the treatment of resistant Amiodarone may also cause blurred vision, rashes,
ventricular tachycardia that may prove life photosensitivity, nausea, vomiting, anorexia, fatigue,
threatening and it has become a drug of choice for dizziness and hypotension. Because this medication is
the treatment of atrial dysrhythmias in patients with concentrated by certain tissues and has a prolonged half-
HF. In addition to blocking potassium ion channels, life, adverse effects may be slow to resolve.
some of this drug’s actions on the heart relate to its
blockade of sodium ion channels. Amiodarone is
available as oral tablets and as an IV infusion. IV
Black Box Warning: Amiodarone causes a pneumonia-
infusions are limited to short-term therapy, normally
like syndrome in the lungs. Because the pulmonary
only 2 to 4 days. When given orally, its onset of
toxicity may be fatal, baseline and periodic assessment
action may take several weeks. Its effects, however
of lung function is essential. Amiodarone has
can last 4 to 8 weeks after the drug is discontinued,
prodysrhythmic action and may cause bradycardia,
because it has an extended half-life that may exceed
cardiogenic shock or AV block. Mild liver injury is
100 days. The therapeutic serum level of amiodarone
frequent with amiodarone.
is 0.5 to 2.5 mcg/mL.

Contraindications: Amiodarone is contraindicated in

ADMINSTRATION ALERTS
Hypokalemia and hypomagnesemia should be
corrected prior to initiating therapy.
Pregnancy category D.
patients with severe bradycardia, cardiogenic shock, sick
sinus syndrome, severe sinus node dysfunction or third-
degree AV block.

INTERACTIONS

PHARMACOKINETICS (PO)
Drug-Drug: Amiodarone can increase serum digoxin
levels by as much 70%. Amiodarone greatly enhances the
Onset Peak Duration
actions of anticoagulants: Thus, the dose of warfarin
2-3 d PO; 2 hr IV 3-7 h 10-150 days must be cut by as much as half. Use with beta-adrenergic
blockers or calcium channel blockers may cause or
worsen sinus bradycardia, sinus arrest or ABV block.
Amiodarone may increase phenytoin levels two-to
threefold.

Lab Test: Amiodarone may increase values for the

following tests: nuclear antibody, ALT, AST and serum
alkaline phosphatase T4.

Herbal / Food: Use with Echinacea may cause an

increased risk of hepatotoxicity. Aloe may cause an
increased effect of amiodarone.

Treatment of Overdose: Treatment of amiodarone

overdose is targeted to reversing hypotension with
vasopressors and bradycardia with atropine or
isoproterenol.

Prototype Drug Procainamide

Therapeutic Class: Class IA antidysrhythmic Pharmacologic Class: Sodium channel blocker

ADMINSTRATION ALERTS PHARMACOKINETICS (PO)

Use the supine position during IV administration Nausea, vomiting, abdominal pain, hypotension and
because severe hypotension may occur. headache are common during procainamide therapy.
Pregnancy category C. High doses may produce CNS effects such as confusion
or psychosis.

PHARMACOKINETICS (PO)
INTERACTIONS
Onset Peak Duration
Drug-Drug: Additive cardiac depressant effects may
Immediate IV; occur if procainamide is administered with other
1-1.5 h 3-4 h
10-30 min IM antidysrhythmics. Additive anticholinergic drugs.

Lab Test: Procainamide may increase values for the

following: AST, ALT, serum alkaline phosphatase, LDH and
serum bilirubin. False-positive Coombs test and ANA
titers may occur.

Herbal / Food: Unknown.

Treatment of Overdose: Supportive treatment is targeted

to reversing hypotension with vasopressors and
preventing or treating procainamide-induced
dysrhythmias.

Calcium Channel Blockers (Class IV)

• Prototype drug: verapamil

• Mechanism of action: to block calcium ion channels, which reduces automaticity and slows myocardial (AV) conduction velocity

• Primary use: to treat supraventricular dysrhythmias

• Adverse effects: bradycardia, hypotension, headache

• Role of the Nurse: Calcium Channel Blockers

– Do not use for patients with sick sinus syndrome, heart block, severe hypotension, cardiogenic shock, or congestive heart failure

– Monitor for hypotension, especially in elderly

– Do not use during pregnancy (category C) or lactation

– Report palpitations, blood pressure changes, edema, shortness of breath

Prototype Drug Verapamil (Calan, Covera-HS, Isoptin Sr, Verelan)

Therapeutic Class: Class IV antidysrhythmic, antihypertensive, antianginal

Pharmacologic Class: Calcium channel blocker

ACTIONS AND USES ADVERSE EFFECTS

Verapamil was the first CCB approved by the food
and Drug Administration (FDA). The drug acts by
inhibiting the flow of calcium ions both into
myocardial cells and in vascular smooth muscle. In
the heart, this action slows conduction velocity and
stabilizes dysrhythmias. In the vessels, calcium
channel blockade lowers BP, reducing cardiac
workload. Verapamil also dilates the coronary
arteries, an action that is important when the drug is
used to treat angina.
Adverse effects are generally minor and include
headache, flushed skin, constipation and hypotension.
Because verapamil can cause bradycardia, patients with
HF should be carefully monitored.
Contraindications: Verapamil is contraindicated in
patients with AV heart block, sick sinus syndrome, severe
hypotension or bleeding aneurysm or those undergoing
intracranial surgery. Use with caution in patients with
renal or hepatic impairment.

ADMINSTRATION ALERTS

Swallow the capsule whole: Do not open or allow INTERACTIONS

patients to chew the contents.
Drug-Drug: Verapamil is metabolized by hepatic CYP
Pregnancy category C.
enzymes and exhibits many drug-drug interactions.
Verapamil has the ability to elevate blood levels of
digoxin (Lanoxin, Lanoxicaps). Because digoxin and
PHARMACOKINETICS (PO) verapamil both slow conduction through the AV node,
their concurrent use must be carefully monitored to avoid
Onset Peak Duration bradycardia. Use with other antihypertensive drugs,
including beta blockers, may cause additive hypotension.
30-90 min (4-8 h 3-7 h (2 h
1-2 hr PO; 1-5 Verapamil should not be administered with statins
(extended extended
min IV because the risk of myopathy increases significantly.
release) release)

Lab Test: Unknown.

Herbal / Food: Grapefruit juice may increase verapamil

levels. Hawthorn may have additive hypotensive effects.

Treatment of Overdose: Treatment of verapamil

overdose is targeted to reversing hypotension with
vasopressors. Calcium salts such as calcium chloride
may be administered to increase the amount of calcium
available to the myocardium and arterioles.

Miscellaneous Antidysrhythmics

• Examples: digoxin (Lanoxin) and adenosine (Adenocard)

• Mechanism of action: to decrease automaticity of SA node and slow conduction through AV node but not act by blocking ion channels

• Primary use: for digoxin—certain types of atrial dysrhythmias; for adenosine—serious atrial tachycardia

• Adverse effects: Creates new dysrhythmias or worsens existing ones

– Digoxin: nausea, vomiting, headache, visual disturbances

– Adenosine: facial flushing, dyspnea

• Role of the Nurse: Miscellaneous Drugs for Dysrhythmias

– Monitor heart rate and blood pressure

– Report symptoms of digoxin toxicity

Drug Therapy for Dysrhythmias: Nursing Process

• Assessment
– Complete health history

– Assessment of cardiac output

– Baseline ECG to compare throughout therapy

• Nursing diagnoses

– Ineffective Tissue Perfusion

– Knowledge Deficit

– Risk for Injury

– Decreased Cardiac Output

• Planning

– Improved cardiac output

– Understanding of drug therapy

– Prevention of adverse effects

• Implementation

– Monitor cardiac rate and rhythm

– Monitor IV site

– Investigate possible causes of dysrhythmia

– Observe for correct administration of drugs and adverse effects

• Evaluation

– Ideal outcome criteria

• Improved cardiac output

• Patient verbalization of understanding of drug therapy

• Prevention of adverse effects

Key Concepts

1. Coronary artery disease (CAD) is one of the leading causes of mortality in the United States. The primary defining characteristic of CAD is
narrowing or occlusion of a coronary artery. The narrowing deprives cells of needed oxygen and nutrients, a condition known as
myocardial ischemia.

1. The most common etiology of CAD in adults is atherosclerosis, the presence of plaque, a fatty, fibrous material within the walls of the
coronary arteries.

1. Angina pectoris is acute chest pain caused by insufficient oxygen reaching a portion of the myocardium; it usually accompanies physical
exertion or emotional excitement. These events cause increased myocardial oxygen demand.

1. The classic presentation of angina pectoris is steady, intense pain in the anterior chest, sometimes accompanied by a crushing or
constricting sensation. The discomfort radiates to the left shoulder and proceeds down the left arm. It may also extend posteriorly to the
thoracic spine or move upward to the jaw. In some patients, the pain is experienced in the mid-epigastrium or abdominal area. Emotional
distress may accompany the discomfort—a feeling of panic with fear of impending death. There is usually pallor, dyspnea with cyanosis,
diaphoresis, tachycardia, and elevated blood pressure.

1. Women do not always present with the classic symptoms of angina. In women, gastric distress, nausea and vomiting, a burning sensation
in the chest or chest wall, overwhelming fatigue, and sweating may be more common symptoms.
 1. Angina pectoris episodes are usually of short duration. With physical rest and/or stress reduction, the increased demands upon the heart
diminish, and the discomfort subsides within 5–10 minutes.

7. Angina is classified as stable or unstable. The pain associated with stable angina is usually relieved by rest. When episodes of angina arise
more frequently, have added intensity, and occur during periods of rest, this condition is called unstable angina. Two other types of angina are
vasospastic and silent angina. Vasospastic (or Prinzmetal’s) angina is caused by spasms of the coronary arteries; silent angina is a form of the
disease that occurs in the absence of angina pain. One or more coronary arteries are occluded, but the patient remains asymptomatic.

8. Angina pain often parallels the signs and symptoms of a heart attack. The nurse must accurately identify and differentiate the two
conditions, because the pharmacological interventions related to angina differ considerably from those of myocardial infarction (MI). MI,
however, carries a high mortality rate if appropriate treatment is delayed.

9. Healthy lifestyle habits can prevent CAD in many individuals and slow the progression of the disease in those who have plaque buildup.

10. Factors that reduce incidence of CAD include limited alcohol consumption, elimination of foods high in cholesterol and saturated fats,
elimination of tobacco use, maintenance blood pressure in the normal range, regular exercise, maintenance of optimum weight, maintenance of
blood glucose levels within normal range, and limited sodium intake.

11. When coronary arteries are significantly obstructed, percutaneous coronary intervention (PCI) is necessary. Plaque is either removed
(atherectomy) or compressed against the vessel wall (angioplasty), often with a stent inserted to prevent plaque from returning to its previous
state. Coronary artery bypass graft (CABG) surgery is for cases of severe coronary obstruction that cannot be effectively removed by PCI. A
portion of a vein from the leg or chest is used to create a bypass artery to create a new path for blood to flow and avoid the obstruction.

12. Although various drug classes are used to treat disease, antianginal medications may be placed into three categories: organic nitrates, beta-
adrenergic antagonists, and calcium channel blockers (CCBs). The primary means by which antianginal drugs accomplish these goals is by
reducing the myocardial demand for oxygen. This may be accomplished by slowing the heart rate; dilating veins so the heart receives less blood
(reduced preload); causing the heart to contract with less force (reduced contractility); and lowering blood pressure, thus offering the heart less
resistance when it is ejecting blood from its chambers (reduced afterload).

13. Ranolazine (Ranexa) is a newer drug for angina that acts by shifting the metabolism of cardiac muscle cells so that they use glucose as the
primary energy source rather than fatty acids. This decreases the metabolic rate and oxygen demands of myocardial cells and is considered the
only antianginal that acts through its metabolic effects, rather than hemodynamic effects.

14. Organic nitrates: Dilation of veins reduces the amount of blood returning to the heart, so the chambers contain a smaller volume, reducing
the heart’s workload and lowering the myocardial oxygen demand. Organic nitrates relieve chest pain and make angina episodes less frequent.
Short-acting nitrates are the drugs of choice for terminating an acute angina episode. Long-acting nitrates are used to decrease the frequency
and severity of angina episodes. These drugs relax both arterial and venous smooth muscle.

Prototype drug: nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others). The mechanism of action is to relax both arterial and venous smooth
muscle, thus decreasing the workload on the heart and lowering myocardial oxygen demand. The drug is used while an acute angina episode is
in progress or just prior to physical activity. Adverse effects include severe headache and reflex tachycardia. Most side effects diminish after a
few doses.

15. Nursing Process:

Assessment: The nurse’s assessment role includes careful monitoring of the patient’s condition and providing education as it relates to the
prescribed drug treatment; obtaining baseline vital signs, medical and drug history, lifestyle and dietary habits, and with which activities the
patient was involved at the onset of the symptoms; and obtaining a detailed description of the symptoms, including frequency and severity, and
any pharmacological treatment initiated by the patient.
Nursing diagnoses: Possible nursing diagnoses include: Knowledge Deficit regarding condition; Therapeutic Regimen, and Potential Side Effects
of Medications; Ineffective Therapeutic Regimen Management related to complexity of therapy and cost of medications; and Risk for Hypotension
related to side effects of medications.

Planning: Goals for patients receiving drugs for angina pectoris and myocardial infarction include the patient’s ability to explain angina pectoris
and needed medications and to verbalize the ability to follow prescribed therapy.

Implementation: Encourage compliance with the medication regimen. Provide additional education regarding the medication regimen, such as
consultation with the clinical pharmacist, written and/or visual educational material, and home health visits to ensure the patient’s ability to
follow prescribed therapy.

Evaluation: The ideal outcome criteria for evaluation of the plan of care are that patients are free of or are having reduced episodes of angina
with limited side effects and that patients are able to verbalize the importance of taking prescribed medications to assist them in their continued
management of the disease.

16. Beta-adrenergic antagonists: These are the first-line drugs for preventing angina pain. They reduce the cardiac workload by slowing the
heart rate and reducing contractility. These drugs are as effective as the organic nitrates in decreasing the frequency and severity of angina
episodes caused by exertion. Unlike with the organic nitrates, tolerance does not develop to the antianginal effects of the beta blockers.

Prototype drug: atenolol (Tenormin). The mechanism of action is to selectively block beta1-adrenergic receptors in the heart. Its effectiveness in
treating angina is attributed to its ability to slow the heart rate and reduce contractility, both of which lower myocardial oxygen demand. The
primary use is for the prophylaxis of chronic angina. Adverse effects include hypotension, bradycardia, and fatigue.

17. Calcium channel blockers (CCBs): used when beta blockers are not tolerated well by a patient. CCBs relax arteriolar smooth muscle, thus
lowering blood pressure. This reduction in afterload decreases myocardial oxygen demand. They also dilate coronary arteries and bring more
oxygen to the myocardium. Some CCBs also slow conduction velocity through the heart, decreasing heart rate and contributing to the reduced
cardiac workload.

Prototype drug: diltiazem (Cardizem, Cartia XT, Dilacor XR, others). The mechanism of action is to inhibit the transport of calcium into
myocardial cells, reducing cardiac workload and bringing more oxygen to the myocardium. Adverse effects include headache, dizziness, and
edema of the ankles and feet. Abrupt withdrawal may precipitate an acute anginal episode.

18. An acute coronary syndrome is a collection of symptoms that occur when a coronary artery is suddenly blocked, usually by a piece of plaque
that has broken off and occluded a portion of the coronary artery. The two primary types of acute coronary syndromes are unstable angina and
myocardial infarction (MI). Both are caused by the same pathophysiology and have the same patient presentation.

19. Necrosis of myocardial tissue, which may be irreversible, releases certain marker enzymes, which can be measured in the blood to confirm
the patient has experienced an MI versus unstable angina.

20. An electrocardiogram can give important clues as to the extent and location of the MI. The infarcted region of the myocardium is
nonconducting and usually produces abnormalities of Q waves, T waves, and S-T segments. When the ST segment is elevated (STEMI), the MI
must be treated aggressively because mortality is very high in this group of patients.

21. Thrombolytics are given in cases of acute MI. They dissolve the clots obstructing the coronary arteries. They need to be administered within
24 hours of the onset of MI symptoms. Thrombolytics have a narrow margin of safety between dissolving clots and producing serious adverse
effects, most notably excessive bleeding.
Prototype drug: reteplase (Retavase). Reteplase acts by cleaving plasminogen to form plasmin. Plasmin then degrades the fibrin matrix of
thrombi, dissolving the clots obstructing the coronary arteries. The primary use is to restore circulation to the myocardium. The primary risk of
thrombolytics is excessive bleeding due to interference with the normal clotting process. Dysrhythmias may also occur.

22. Antiplatelet and anticoagulant drugs are given as soon as an MI is suspected. Aspirin and clopidogrel (Plavix) are used for their antiplatelet
and anticoagulant properties. Glycoprotein IIb/IIIA inhibitors are antiplatelet agents with a different mechanism of action than aspirin.

23. Nitrates dilate arteries and veins, reducing myocardial oxygen demand. They are used for MIs, especially to relieve coronary artery
vasospasm, which may be present during the acute stage of MI. Nitrates are discontinued after discharge from the hospital, unless needed to
treat stable angina pain.

24. Beta-adrenergic blockers reduce myocardial oxygen demand. They slow impulse conduction through the heart, thereby suppressing
dysrhythmias. They reduce mortality of MIs if administered within 8 hours of MI symptom onset. Beta blocker therapy continues for the
remainder of the patient’s life.

25. Angiotensin-converting enzyme (ACE) inhibitors have been shown to increase survival for patients following an acute MI. They are most
effective when therapy is started within 24 hours of the onset of symptoms.

References

Adams, M.P., et al (2018). Pharmacology for Nurses: A Pathological Approach, 3rd

Edition: Pearson Canada

McCuistion L.E. (2018). Pharmacology: A Patient-Centered Nursing Process Approach

9th Edition: St.Louis, Missouri: Elsevier

4. VIdeo Cardiac Glycoside
5. Video Nitrates
6. Antiarrhythmic Drugs
7. Video