Cardiac Medications:

Whats With the Mixing & Matching?

Michele B. Collins MSN RN CCRN

September 2009

Sodium-Potassium Pump
Sodium OUTSIDE cell &
Potassium INSIDE cell
before depolarization
Cell has NEGATIVE charge
& must CONTRACT to
become POSITIVE
SA node has less negativity
so it serves as pacemaker

 With cell stimulation, cell permeability

allows sodium INTO cell & potassium
OUT of cell
With sodium, can only have STAT
(fast channel) contraction
Calcium (fast channel) also enters
cell,
leading to total controlled contraction

Cardiac Repolarization
Na+ - K+ pump
uses energy (ATP)
so SODIUM LEAVES
cell and
POTASSIUM
RETURNS to cell
Calcium also leaves
cell at this time

Cardiac Repolarization
If the S-A node
does not
generate an
impulse, another
cardiac site WILL
(reentry
phenomenon)

Statistically, if you take six

different drugs, you have an
80% percent chance of at least
one drug-drug interaction.

Wayne K. Anderson, Dean,

State University of New York
School of Pharmacy

Medications Discussed

Antiarrhythmics
Beta Blockers Ace Inhibitors
Calcium Channel Blockers
ACE Inhibitors
Angiotensin II Receptor Blockers (ARB)
Diuretics
Digitalis
Nitrates
Amiodarone

Why so Many?
In atrial fibrillation, used to
suppress arrhythmias
Often done to relieve the
symptoms associated with loss of
the atrial component to
ventricular filling (atrial kick) due
to atrial fibrillation or flutter.

 In individuals with ventricular

arrhythmias, used to suppress
arrhythmias. Antiarrhythmic
agents may be considered the
first-line therapy in the
prevention of sudden death in
certain forms of structural heart
disease

Automaticity
Refers to a cardiac muscle cell
firing off an impulse on its own
All cardiac cells can initiate an
action potential, however, only
some of these cells are designed
to routinely trigger heart beats
Found in the 'conduction system'
of the heart and include the SA
node, AV node, Bundle of HIS
and Purkinje fibers
Sinoatrial node is a single
specialized location in the atrium
which has a higher automaticity
(a faster pacemaker) than the
rest of the heart, and therefore is
usually responsible for setting
the heart rate, and initiating

Re-entry
Occurs when an electrical
impulse recurrently
travels in a tight circle
within the heart, rather
than moving from one
end of the heart to the
other and then stopping
If conduction is
abnormally slow in some
areas, part of the impulse
will arrive late and
potentially be treated as
a new impulse

 Can produce a sustained abnormal

circuit rhythm. Re-entry circuits are
responsible for atrial flutter, most
paroxysmal
supraventricular tachycardia, and
dangerous ventricular tachycardia.

 Conditions that
increase
automaticity
include
sympathetic nervo
us system
stimulation and
hypoxia

 Resulting heart rhythm depends on

where the first signal begins
if in sinoatrial node, the rhythm remains
normal but rapid
if an ectopic focus, many types of
dysrhythmia may ensue.

Positive Inotropes
THE EFFECTS OF STIMULATING ADRENERGIC
RECEPTORS

RECEPTOR
SITE
ACTION
alpha
peripheral blood vessels
vasoconstriction of
peripheral arterioles
beta 1
myocardium
increased
heart rate (chronotropic)
increased contraction force (inotropic)
inc. conduction
(dromotropic)
beta 2
peripheral blood vessels
vasodilation of
peripheral arterioles &
veins
bronchioles
bronchodilation

ANTIARRHYTMICS
(Vaughan Williams
classification)

Class I Membrane-stabilizing agen

Class II Beta-blocking agents
Class III Increase time for cell to
repolarize
Class IV Calcium Channel blockers

 Class I agents interfere with the sodium

(Na+) channel.
Class II agents are antisympathetic nervous system agents. Most
agents in this class are beta blockers.
Class III agents affect potassium (K+)
efflux.
Class IV agents affect calcium channels
and the AV node.
Class V agents work by other or unknown
mechanisms.

Class I Antidysrhythmics:
slow rate of spontaneous depolarization
of cardiac cells, thus decreasing
automaticity, increasing refractory
period, & decreasing susceptibility to
escape beats
Prolong QT interval.
Widen QRS interval: decreased Na+ influx
into the cell decreases conduction velocity
and lengthens the QRS interval)
CLASS I-A (quinidine, procainamide,
disopyramide)
Not often used today

Class 1c
Increases blockage of sodium
channel
Encainide, Tombocor, Rythmol
severe ventricular dysrhythmias

Class I: Sodium
channel blockers
Disopyramide (Norpace)
Flecainide
Procainamide
Propafenone (Rythmol)
Quinidine
Tocainide

Beta blockers
Decrease mortality in patients with
myocardial infarction
Decrease infarct size
Decrease ventricular dysrhytmias

Slow progression of heart failure (HF) and

prolong lifespan in patients with HF
Used in treatment of coronary artery
disease, heart failure (HF), &
dysrhythmia

Class II Agents: Beta

Blockers
Blockage of beta-1 receptors causes
Decreased force of contraction (- inotrope)
Decreased heart rate (-chronotrope)
Slowed conduction (-dromotrope)

These 3 mechanisms of action combine to

decrease myocardial oxygen demand
decrease cardiac workload & myocardial
oxygen needs
Treatment of supraventricular tachycardias.
They decrease conduction through the
AV node.

Side Effects

Angina
Fatigue, nightmares, & slow HR
Males may experience impotence
Patients with asthma or emphysema
may not be able to tolerate beta
blockers because of an increase in symptoms
of shortness of breath and wheezing
Depression
Weight gain
Assess for cough, fatigue, edema, and
other symptoms of HF
may mask hypoglycemia in diabetics;
check blood glucose frequently
Removed from blood during hemodialysis;
hold dose until treatment finished

Cardioselectivity

Acebutolol Sectrol
Atenolol
Tenormin
Esmolol
Brevibloc
Metoprolol Lopressor

Non Cardioselectivity
Propranolol Inderal
Labetalol normodyne, Trandate
(alpha
properties as well)
Carteolol Cartrol
Nadolol
Corgard
Pindolol
Visken
Timolol
Blocadren

Beta Blockers

Atenolol
Metoprolol
Propranolol
Sotalol
Bisoprolol
Nadolol

Carvedilol
Timolol
Nadolol
Betaxolol
Pindolol
Labetolol

Calcium Channel Blockers

Block movement of calcium into
smooth muscle cells in vessel walls
Calcium required for muscle
contraction; calcium channel
blockers cause relaxation and
dilatation of arteries
By this mechanism, lower BP
Dilate the coronary arteries so also
used in treatment of
angina

 Reduce cardiac contractility, PVR, &

myocardial O2 needs. Effective on
reentrant dysrhythmias that require AV
nodal conduction for their continuation
In contrast to beta blockers, they allow the
body to retain adrenergic control of heart
rate and contractility.
Some have a slowing effect on the heart
rate and are used in the treatment of
arrhythmia
Used in treatment of hypertension,
arrhythmia, and angina

Uses
Paroxysmal SVT, rate control for
a-fib and flutter
Dilate coronary
arteries/decreases BP
Potentiates effects of digoxin
Change position slowly.

Side Effects
Usually go away within a few hours to a day or so and are
not said to be permanent once the medication has "washed
out" of the system
Common side effects of these drugs include constipation,
dizziness, and weakness
Swelling of the feet and ankles
Excessive lowering of the blood pressure
Most common with first dose
Change position slowly

Rarely an excessively slow heart beat

Worsening of HF
Many calcium channel blockers come in an extended
release or sustained release preparation ( XL, SR) that is
convenient for once a day dosing. These tablets should not
be cut in half or crushed, as this would affect the rate of
drug release into the bloodstream.

Diltiazem (Cardizem)
Less negative inotropic activity than
verapamil
Dilates the coronary arteries
Treatment of supraventricular arrhythmias
Oral diltiazem is effective in treatment of
reentry tachycardia

 Adverse Effects: fewest adverse

effects of this category of drugs
Hypotension
- AV Block if patient is on Beta
Blocker therapy
Verapamil (Calan, Isoptin): severe
hypotension & bradycardia

Calcium Channel Blockers

Drugs in this
class include:
Nifedipine
Diltiazem
Verapamil
Amlodipine

Felodipine
Isradapine
Nicardipene
Nimodipine
Bepridil

ACE Inhibitors (pril)

Used to treat both hypertension and

Acute Coronary Syndrome
Inhibit conversion of angiotension I
to angiotension II >>> block
release of aldosterone >>>
reducing sodium & water retention

ACE Inhibitors
Act to lower the blood pressure
Dilate blood vessels
Help with cardiac emptying in HF

Good for patients with heart failure by lowering

the net resistance in the vascular bed, thereby
facilitating the hearts task of pumping blood.

Indications
Mild to severe hypertension
Treatment of heart failure
Given within 48 hours of MI to
prevent ventricular remodeling
& development of HF
Increase survival rate after MI

Side Effects
Hypotension
have person lie down for 3
hrs after first dose
temporarily D/C diuretics
when starting therapya
avoid potassium
supplements/salt
substitutes, diuretics (may
cause severe hypotension)

Hyperkalemia, renal
tubular damage
Cough
Angioedema

 Give one hour before meals

Hold enalapril or lisinopril until
after hemodialysis (both are
removed by dialysis)

Ace Inhibitors

Enalapril Vasotec
Lisinopril Zestril
Captopril
Capoten
Quinapril
Accupril
Benazopril
Fosinopril

ARBs
Related to ACE inhibitors
Used to treat hypertension
Block the action of angiotensin II to
constrict blood vessels
lower blood pressure
function in a similar way as the ACE
inhibitors, but do not cause the dry,
hacking cough that is sometimes
associated with ACE inhibitor use.

Angiotensin II Receptor
Blockers (ARBs)

Losartan
Valsartan
Candesartan
Irbesartan

Digitalis

First medication useful in

treating disorders of the
heartbeat (1800s)
Digitalis leaf from the foxglove
plant
Used to treat atrial fibrillation
and heart failure

Actions
Direct: increases myocardial contractility and
CO
Vagal effect on SA & AV nodes so decreases heart rate
Slows conduction through AV node (positive inotrope,
negative chronotrope and negative dromotrope)

Indirect

decreases diastolic cardiac size

reduces cardiac wall tension
increases renal Na+ & H2O excretion
decreases peripheral vasoconstriction

 Slows HR so used in treatment of

atrial fibrillation and atrial flutter
does not suppress or prevent
arrhythmias but only works to slow
them down and relieve symptoms
of palpitations

Frequently used in heart failure

(HF)
Reduces frequency of HF
exacerbations
Does not reduce mortality from HF

Digitalis Toxicity
anorexia, n & v, visual disturbances
lethargy, bradycardia, heart block,
tachydysrhythmias
Take apical heart rate for one full
minute before administering
Monitor digoxin levels: narrow
therapeutic window: 0.8-2.0 ng/ml
Monitor potassium levels: hypokalemia
more likely to become digtoxic

Drug Interactions
Decreased digoxin absorption with
antacids & laxatives
Decreased digoxin effect:
metoclopramide, aminoglycosides,
thyroid supplements
Increased digoxin effect
Amphotericin B, corticosteroids,
non-potassium-sparing diuretics,
amiodarone

Digoxin Fab (Digibind)

Used for life-threatening digoxin toxicity
Mechanism: antibody complex formation to digoxin
Adverse Events
exacerbation of heart failure or a-fib due to withdrawal of
digoxin
potential for complex dissociation with repeat toxicity in
end-stage renal disease
digoxin levels meaningless for 7 days post Digibind use.

Nitrates
Vasodilator: increases coronary blood flow
by dilating coronary arteries and improving
blood flow to ischemic regions of the heart
Decreases preload by dilating peripheral veins
Decreases afterload
Decreases myocardial oxygen demand to
decrease angina

 Used for angina, hypertension, MI

Used in heart failure to diminish
symptoms of shortness of breath
Do not reduce mortality in
coronary artery disease or heart
failure. Their use is principally for
symptom relief.

Short-acting: Nitroglycerin
For acute anginal attacks. SL dosage (0.4mg):
Instruct patient to lie down
Repeat at 5 minute intervals; if pain not
relieved, up to 3 tablets
If anginal pain persists after 3 doses, go to ED
Stay with patient and monitor VS (esp. BP)
Headache & hypotension are major side effects

Long-acting Nitrates:
Isordil, nitroglycerin ointment, nitroglycerin
transdermal patch
Ointment: use
appropriate
application paper;
dont rub in

Nitrate-free periods (6
10 hrs/ 24 hr period) to
prevent tolerance

Remove patch before

Rotate sites (remove
defibrillating as patch
old patch, ointments)
may explode
Avoid contact with
skin

Side Effects
Hypotension, diaphoresis, nausea
Tachy- and bradydysrhythmias
Headache; reflex tachycardia

Drug Interactions
Sympathomimetics, thyroid
hormones, nicotine
All increase cardiac workload so
counteract NTG effects

Nitrates
Drugs in this class include:
Isosorbide Dinitrate
Isosorbide Mononitrate

Amiodarone
Principal effect on cardiac tissue to
increase time for cell to repolarize
Mainly block potassium channels, thereby
prolonging repolarization.
Do not affect the sodium channel so conduction
velocity is not decreased
Used to treat atrial arrhythmias (atrial
fibrillation and atrial flutter) as well as
ventricular arrhythmias (ventricular fibrillation
Prevent re-entrant arrhythmias
results in "chemical antifibrillatory" action

Side Effects
Pulmonary fibrosis
Abnormal thyroid
function
Photophobia,
Nausea, vomiting
Blue-gray skin color
Seeing halos around
objects

 May take over 3 weeks to work;

half-life about 50 days
Monitor with patients in HF and
elderly for decreased BP and pulse
Assess for fluid retention

 Have patient swallow whole

Do not stop abruptly
Take one hour before meals or 2
hours after meals
High fat meals elevate levels
Use sunscreens and sunglasses when
outside

Drug Interactions
Anticoagulants increase
anticoagulation
Increased digoxin effects
Avoid grapefruit juice as it will
increase serum levels causing
hypotension

Class III Potassium

Channel Blockers
Amiodarone (Cordarone)
Dofetilide (Tikosyn)
Ibutilide (Corvert)

So How Does This

Relate to My Patients? HTN

Goal

Two primary regulatory factors

Blood flow (volume)

Peripheral Vascular Resistance (PVR)

Primary groups of drugs are used:

Diuretics
Adrenergic inhibitors (Beta-blockers)
Vasodilators
ACE inhibitors

Calcium antagonists

Pharmacologic
Treatment
For patients with systolic dysfunction
(ejection fraction <40%)
Angiotensin-converting enzyme (ACE)
inhibitors for all patients
Beta blockers for all patients except
Hemodynamic instability or
Dyspnea at rest with signs of
congestion

 Aldosterone antagonist (ACE

inhibitor or ARB) for those with
dyspnea at rest or
symptomatic patients who have
suffered a recent myocardial
infarction
ARB as a substitute for patients
intolerant of ACE inhibitors

 Digoxin only for patients who remain

symptomatic despite treatment with
Diuretics, ACE inhibitors, and beta
blockers
or for those in atrial fibrillation
Diuretics for symptomatic patients to
maintain appropriate fluid balance .

 HF patients on multiple medications

are at a risk of potential drug
interactions and side effects
risk of hyperkalemia is increased with
renal insufficiency treated with an
aldosterone antagonist and an ACE
inhibitor.

Goals for Mgt of Heart

Disease

Maximize blood flow to heart

muscle
Maximize preload & minimize
afterload
Maximize cardiac contractility
(inotropic effect)

 Reduce chances of clot formation

Reduce overall blood volume if
overload
Maintain heart rate between 60-80
beats/min to maximize cardiac
output and filling pressures

What Drugs Help to

Meet these Goals?
Maximize preload I.V. fluids, volume
expanders
Minimize afterload ACE inhibitors
Maximize cardiac
contractility Digoxin, Dopamine
Decrease preload,
inc coronary circulation
& reduce pulmonary
congestion Nitrates

What Drugs Help to

Meet these Goals (contd)?
Reduce chances of ASA or other anti-platelet
clot formation
agents
Reduce fluid
volume overload

Diuretics

Keep heart rate btw

Beta blockers &
60-80/min
Calcium-channel blockers
Dysrhythmias

Antidysrhytmics

Treatment Goals for HF

Relieve symptoms & improve quality of life

Prevent readmission to hospital, and/or
recurrent ischemic events
Reduce mortality
Medications used:

ACE Inhibitors
Beta Blockers
Diuretics
Vasodilators
Digitalis

ACE Inhibitors
Increase lifespan of
patients with heart failure
Effects on blood vessels
that seem to counteract
the process of
atherosclerosis and have
been shown to reduce
heart attack, stroke, and
mortality in CAD

Beta-Blockers
Lower blood pressure & slow heart
rate (including protection against
arrhythmias)
Helps lower risk of stroke and heart
attacks

Nitrates
Used to treat angina
Vasodilates and
stops chest pain by
increasing
myocardial oxygen
supply & decreasing
demand

Antidysrhythmic Drugs
Used to bring under control abnormal
rhythms of the heart (including atrial
fibrillation), so the heart can pump
more effectively

Antihypertensives
Used to control BP & risk of stroke &
MI
Categories
ACE Inhibitors
Beta-Blockers
Calcium-Channel Blockers

Managing the Cost

Patients may be taking two
to four drugs to
manage cardiac condition
in addition to meds for other
health issues such
as diabetes
Med treatment for a chronic
condition becomes expensive
with each drug added

 Even with worsening condition some

people try to limit costs
May or may not ask which can be
decreased or stopped

Best if medication regimen is kept

simple so patients without insurance
can purchase generic versions
without rationing their doses.

Refill Red Tape

Patients and HCPs often face red tape
when it comes to refills and
preapproved status.
If desired med is not on insurance
company's preferred list
Must complete preauthorization form
Also must talk with insurance company
about why that particular medication is
needed

 Patients receiving nonformulary drugs often pay

more
May only be able to get partially
filled prescriptions
Providers should seek generic or
less expensive alternatives
whenever possible

Simple Steps:
Lifestyle Changes
Decrease
sodium intake
Exercise &
weight loss

Preload or Afterload?
Arterial vasoconstriction
BP 190/124
Administration of hydralazine or nitroprusside
Administration of Nitroglycerin
Diuretic therapy
Arterial vasodilation

 List some positive and negative

aspects to the administration of beta
blockers

 The desired effect from the use of

diuretics in the patient with acute left
ventricular failure is to

 List some medications that decrease

myocardial contractility

 What are some of the signs &

symptoms of left sided heart failure?

 Your patient on digoxin has a

morning heart rate of 56 BPM and is
supposed to be discharged today.
Your first priority is to

 What are some positive and negative

aspects related to Nitroglycerin
administration?

A patient with a dysrhythmia is

placed on digoxin and metoprolol
(Lopressor). Because of the
combined effects of these drugs,
what area(s) need to be the most
closely monitored?