The Top 10 Categories of Cardiac Drugs
Introduction
This course is designed to introduce the
top ten cardiac drugs presently used in the treatment of cardiac failure and
myocardial infarction. Drugs are constantly being introduced to the
marketplace, with cardiac drugs being the most popular. Each drug category
addresses different issues related to cardiac function. Most of the drugs are
used together to achieve the best outcome for the patient. Finding the right
combination enables the medical community to provide the patient the maximum
benefit with the minimum amount of side effects.
We begin this study with an overview of the
heart and its function. It is essential to understand how the heart works so
that one may better understand the functionality of the drugs. Without a basic
knowledge of the heart as a pump, the actions of the drugs would not be useful.
Overview
of the Heart
The heart is made up of four chambers. They
are the right atrium, right ventricle, left atrium and left ventricle. Blood is
pumped through each chamber to supply oxygen to the organs of the body. The
heart acts as a pump, pushing the blood throughout the vasculature supplying
blood flow to the entire body.
The blood is pumped from the body through
the inferior and superior vena cava. From there it goes into the right atrium,
through the tricuspid valve into the right ventricle. From there the right
ventricle pumps the blood through the pulmonic valve to the pulmonary artery to
the lungs. The blood then takes on the oxygen from the lungs and goes to the
pulmonary vein. It is pumped into the left atrium, through the mitral valve to
the left ventricle. The left ventricle is the largest muscle in the heart and
is responsible for pumping the blood through the aortic valve into the aorta
and throughout the rest of the body.
The amount of blood pumped out of the
ventricles with each beat is called the cardiac output. The normal cardiac
output is between 4-6 liters per minute. Cardiac output is one way to judge if
the heart is functioning efficiently, and is determined by the heart rate and the
stroke volume. Stroke volume is the amount of blood ejected by the ventricle
with each beat.
Cardiac Output = Heart Rate x Stroke Volume
Another function of the heart that is
necessary to understand is that of preload. Preload is "a function of the volume of blood presented to the
left ventricle and also the compliance (the ability of the ventricle to stretch)
of the ventricles at the end of diastole." Preload involves the ability of
the heart muscle to stretch to accommodate the blood returned by the body. The
heart is made up of muscle that is elastic, and over time the elasticity of the
heart muscle decreases and the ventricles are not as pliable as they used to
be. Preload increases in patients with hypertrophy of the heart. Preload also
includes the amount of blood returned to the heart with each beat. If the heart
muscle is able to accommodate the amount of returned blood, then the cardiac
output is not affected. If, however, the heart has become less pliable and is
unable to eject the increased amount of blood, then the cardiac output will
decrease as well.
Afterload
is the stress the heart must overcome to eject the blood from the ventricles.
It is the amount of resistance the ventricles must push against to eject the
blood. This is especially important in the left ventricle. If the arteries in
the body are constricted or obstructed (such as in the case of
arteriosclerosis), the heart will have a greater resistance to overcome to get
the blood throughout the body. This resistance is often referred to as
"systemic vascular resistance" (SVR). This can have a direct effect
on the cardiac output. If the SVR is increased, the cardiac output will
decrease, since the heart must work harder to eject the blood.
Understanding these concepts will enable
the reader to better understand the drugs and their effects. Each drug affects
the heart in different ways, and some do not affect the heart at all, but
instead affect the vasculature it must pump against.
The main goal of inotropes is to provide
sufficient support for the heart to maintain adequate tissue perfusion. They
act to increase the stroke volume, allowing the heart to empty the ventricles
more completely. This increases the cardiac output and improves tissue perfusion.
All inotropes must be used with caution, however, since they can increase
myocardial oxygen consumption. Inotropes can have either alpha or beta effects.
Alpha effects include arterial and venous
constriction, increased systemic vascular resistance, and can also slightly
increase preload. Drugs with alpha effects act on the vasculature in the body
and not just the heart muscle.
Drugs with beta effects increase
contractility of the heart by increasing the stroke volume, which in turn
increases cardiac output. These medications act primarily on the heart muscle.
Dobutrex (dobutamine)
Dobutamine has been used for many years for
its wonderful alpha and beta effects. It is used mainly for cardiac
decompensation due to decreased contractility. Its actions fall into the beta
effects by providing increased
contractility and increased cardiac output. It is also a mild vasodilator.
Dobutamine is used primarily in
patients with congestive heart failure, left ventricular hypertrophy, and poor
cardiac output conditions such as cardiomyopathies and cardiogenic shock. It is
a beta-1 selective adrenergic drug.
Dobutamine is administered IV as a drip. It
is titrated to improve cardiac output and patient response. The adult
maintenance dosage is 2.5-10 mcg/kg/min, with a high of 40 mcg/kg/min.
Patients receiving this medication must be carefully
monitored for an increase in systolic blood pressure (SBP) and heart rate. If
the dosage is too high for the patient to tolerate, a marked increase in SBP
and heart rate, along with premature ventricular beats and anginal pain, may be
witnessed. It should not be used in patients with idiopathic hypertrophic
subaortic stenosis or hypovolemia. It should be used cautiously in patients
with atrial fibrillation and hypertension.
Pharmacokinetics:
Half-life: 2-5 min ~~ Onset: < 2 min ~~ Peak: < 10 min ~~ Duration: <
10 min
Intropin, Dopastat (dopamine)
Dopamine's effects are directly related to
its dose and it comes in IV drip only. In lower doses (2-5 mcg/kg/min),
dopamine stimulates the dopaminergic receptors causing renal vasodilation,
which causes an increased blood flow to the kidneys. This acts to increase
urinary output and decrease blood pressure in the process.
In low to medium doses (5-10 mcg/kg/min),
dopamine has positive inotropic effects, causing the release of norepinephrine.
This beta-1 adrenergic effect increases myocardial contractility, stroke
volume, and cardiac output.
In higher doses (>10 mcg/kg/min), it stimulates
the alpha receptors, causing vasoconstriction. This in turn increases the SVR
and blood pressure.
The side effects of dopamine are
tachycardia, ectopic beats, palpitations and hypertension. You may also see
headache, anginal pain, vasoconstriction, nausea, vomiting, and dyspnea.
Tachycardia, palpitations and vasoconstriction are especially common in higher
doses. It is contraindicated in patients with tumors that secrete
catecholamines, such as pheochromocytoma.
One of the major concerns with dopamine is the
risk of extravasation during IV administration. Use it cautiously in patients
with peripheral IV's, since infiltration can cause serious skin and muscle
damage. Such areas can be immediately remedied with Regitine (phentolamine) infiltration
of affected tissue. Some extravasation can become so severe that it may require
skin grafting.
Dopamine should not be used in patients
with compromised circulation to the extremities. Since higher doses can cause
vasoconstriction, these patients may experience even more severe occlusion,
increasing the risk of gangrene.
Pharmacokinetics:
Half-life: < 2 min ~~ Onset: 2-5 min ~~
Peak: rapid ~~ Duration: 10 min
Inocor (amrinone)
Inocor is used in the short-term management
of CHF. It increases contractility and is a vasodilator. Although it is not a
first line drug in the treatment of CHF, it is recommended for patients who are
not responding to digoxin, diuretics, or other vasodilators. It is one of only
2 agents in the inodilator (inotropes plus dilators) category.
Inocor is given IV. A bolus of 0.75 mg/kg
is given slowly over 2-3 minutes, followed by a maintenance drip of 2-15
mcg/kg/min. Patients should be closely monitored during administration. The IV
drip should not be continued for more than 48 hours.
A common side effect is a decrease in the
platelet count. In patients with thrombocytopenia, watch for bleeding.
Hypotension, cardiac dysrhythmias, nausea and vomiting can occur as well.
Inocor should be avoided in patients
sensitive to the drug, though it is often difficult to determine sensitivity
unless they have already received it in the past. Monitoring the patient with
the initial bolus and drip will help to determine if the infusion should be continued.
Patients who develop arrhythmias should have the drug discontinued.
Pharmacokinetics:
Onset: 2-5 min ~~ Peak: 10 min ~~ Duration: 0.5 to 2 hrs
Milrinone (Primacor)
Unlike amrinone, this inodilator agent is
used for both short and long-term management of CHF in patients who do not
respond to cardiotonics and diuretic/dilator therapy alone. It is given IV in a
loading dose of 50 mcg/kg, followed by a continuous infusion dose of 0.375
mcg/kg/min-0.75 mcg/kg/min.
Large numbers of end-stage heart failure
patients are treated with weekly 6-hour IV infusions. This has been shown to increase
the quality of life in these patients, and to decrease the number of
readmissions to the hospital for exacerbations of heart failure.
The primary side effect of milrinone
therapy is dysrhythmia, mainly ventricular in nature. As with amrinone,
thrombocytopenia and hypotension may also occur.
Pharmacokinetics:
Half-life: 2.3 hrs ~~ Onset: 5-15 min ~~ Peak: 6-12 hrs ~~ Duration: 8-12 hrs
Norepinephrine (Levophed)
Norepinephrine is a potent alpha-beta
vasoconstrictor. It is used mainly for hypotension that is refractory to other
medications, such as in the case of neurogenic shock. It is also commonly used
in patients immediately post-op CABG (coronary artery bypass graft) to increase
blood pressure short-term.
Norepinephrine can be deactivated by
alkaline solutions, so be cautious when administering and do not mix with other
medications or solutions. It is essential that the patient's blood pressure be
constantly monitored; therefore, an arterial line is imperative. Norepinephrine
should be given through a central line since extravasation to the tissues can
cause necrosis.
The usual range is from 0.5-30 mcg/min,
with the usual rate between 8 and 12 mcg/min, titrated to get the blood
pressure in the desired range. It is given IV only.
Side effects can include anxiety,
palpitations, and hypertension. Prolonged use of norepinephrine at high doses
can cause clamping down of the peripheral vessels and you may see mottling in
the lower extremities.
Although norepinephrine is used for
hypotension, it is contraindicated in hypotension caused by hypovolemia. In
those cases, fluid replacement is indicated as the best course of action.
Pharmacokinetics:
Half-life: < 5 min ~~ Onset: immediate ~~ Peak: 1-2 min ~~ Duration: 1-2 min
Lanoxin (digoxin)
Digoxin is one of the most popular drugs in
this category. It increases contractility and helps to control ventricular
response in atrial flutter, atrial fibrillation, and paroxysmal atrial
tachycardia by slowing AV conduction. It also helps to increase cardiac output,
and decrease edema associated with CHF.
Digoxin comes in IV and oral forms. Dosage
varies according to the patient; however, the usual dose is from 0.125-0.50
mg/day after an initial digitizing dose of 1-1.5 mg over 24 hours. Digoxin is
given IV push instead of by IV drip. The IV push dose should be given slowly to
decrease the risk of arrhythmias.
Digoxin has been known to cause many
different arrhythmias, so a patient who is receiving it for the first time
should be monitored. One of the main side effects of this drug is digoxin
toxicity. The most common early signs of toxicity are GI upsets such as nausea,
vomiting, and anorexia. Later signs are neurologic disturbances such as
headache, depression, weakness and confusion. The patient may describe a "yellow
light" or halo, which is a classic symptom of digoxin toxicity. To
determine this state, a digoxin level needs to be drawn.
A digoxin dose must be adjusted downward in
patients with renal insufficiency or hepatic dysfunction. Amiodarone can
increase the risk of toxicity. It is contraindicated in patients with
incomplete AV block. Also watch for increased risk of toxicity in patients
taking potassium-depleting diuretics.
Pharmacokinetics:
Half-life: 33-44 hrs ~~ Onset: 30-120 min ~~ Peak: 2-6 hrs ~~ Duration: 2-4
days
Adrenalin (epinephrine)
Epinephrine, an endogenous vasoactive
catecholamine, increases heart rate and automaticity throughout the cardiac
cells. It also increases myocardial electrical activity and force of
contraction. This, in turn, increases systemic vascular resistance and blood
pressure. Epinephrine is used mainly in cardiac arrest to increase the benefits
of defibrillation. Increasing the myocardial electrical activity increases the
chances of defibrillation causing a return to a normal rhythm.
Epinephrine also has another benefit. Since
it is a potent bronchodilator, it is used in anaphylactic shock. It inhibits
the bronchial tubes from closing down and causing respiratory arrest.
Epinephrine can be given either IV or
through the endotracheal tube. It should not be used in patients unless it is a
life-threatening situation. The normal dosage for adults is 0.5-1.0 mg,
repeated every 3-5 minutes for cardiac arrest. For severe anaphylaxis, a dose
of 0.3-0.5 mg is given followed by an IV drip.
Epinephrine needs to be protected from
light, since this can decrease its effectiveness. It can also be deactivated by
alkaline solutions--so do not mix it with any other drug.
Since epinephrine is a potent alpha-beta
adrenergic, side effects include palpitations, anxiety, tremors, nausea and
vomiting. These are rarely seen, however, since the main use for epinephrine is
in cardiac arrest situations. It can precipitate or exacerbate myocardial
ischemia, and may also induce ventricular ectopy in patients taking digoxin.
Pharmacokinetics (IV):
Half-life: < 5 min ~~ Onset: immediate ~~ Peak: 1-2 min ~~ Duration: 5 min
Vasodilators
Vasodilators can either act on the
arteries, the veins or both. They open the vessels up to decrease blood
pressure, systemic vascular resistance, and cardiac output. This causes a
decrease in preload and afterload.
Tridil (IV), Nitro-Bid (PO), Nitrostat (SL), Nitrol (Topical) (nitroglycerin)
The main action of nitroglycerin is coronary
artery dilatation. It opens the arteries of the heart and allows for increased
myocardial oxygen consumption. It is used mainly in myocardial infarct, angina,
and CHF.
Nitroglycerin comes in many forms. It can
be given IV drip, oral, sublingual, transdermal, or nasally. The sublingual or
nasal form is the method given to patients with a history of anginal attacks.
These methods work the fastest at bringing relief to chest pain. In the
hospital setting, the method of choice is IV drip. The usual beginning dose is
10 mcg/min. Titrate up by 5 mcg/min every 3-5 min to 20 mcg/min, and then by
10-20 mcg/min every 3-5 min until the patient states the chest pain is gone.
The main concern in nitroglycerin
administration is hypotension. Nitroglycerin is a potent vasodilator that can
decrease the blood pressure considerably. Prior to starting the IV drip or
giving the dose sublingually or nasally, take the blood pressure. If the
systolic BP is less than 90, the dose should be held unless the patient can be
supported with other medications, such as dopamine. Watch the blood pressure
closely during initial administration to be assured that the patient remains
hemodynamically stable.
The other side effect is headache. Although
the chest pain may be relieved, headache is the main complaint of patients on
nitroglycerin. Standard pain relievers do not relieve their headache, so
attempting to find an alternative to IV administration is encouraged. Other
side effects include flushing, bradycardia, syncope, and palpitations. Postural
hypotension (a significant decrease in blood pressure upon standing up) is also
seen, especially in patients who take this drug at home. Caution patients to
get up slowly. This will allow their cardiovascular system to compensate for
the vasodilation action of nitro.
Pharmacokinetics:
Onset Peak Duration
SL:
1-3
min...................unknown.....................30-60 min
Patch:
40-60
min.................unknown.....................8-24 hrs
IV:
immediate...............unknown.....................several
min
Nipride, Nitropress (sodium nitroprusside)
Most commonly called Nipride, this drug is
a potent arterial and venous dilator. Patients on this drug must have their
blood pressure monitored very closely, especially on initial administration.
The main use for Nipride is immediate reduction of blood pressure in a
hypertensive crisis. Nipride is rarely used for blood pressure control in other
situations; however, it may occasionally be used perioperatively, or for CHF
refractory to other treatments.
Nipride is administered IV only. Initial
dose is 0.3 mcg/kg/min with a range of 0.5-10 mcg/kg/min. You should not exceed
10 mcg/kg/min without expecting a severe decrease of blood pressure.
Once Nipride has been reconstituted, it
needs to be protected from light by wrapping aluminum around the IV bag.
Side effects include hypotension,
palpitations, reflex tachycardia, tinnitus, and photosensitivity. Watch for
cyanide toxicity in patients receiving higher doses and those on prolonged
therapy, as sodium nitroprusside is rapidly metabolized to cyanide in the red
blood cells and body tissues. Daily plasma thiocyanate levels need to be
monitored, especially in anuric patients.
Patients must have constant evaluation of
blood pressure during administration. Decreasing the blood pressure too rapidly
can cause nausea, diaphoresis, headache, muscle twitching, dizziness, and
retrosternal and abdominal pain. Increase the dose slowly to decrease the risk
of developing these side effects.
Pharmacokinetics:
Half-life: 2 min ~~ Onset: < 2 min ~~ Peak: 2-5 min ~~ Duration: 1-10 min
Apresoline (hydralazine hydrochloride)
Apresoline was a first line
antihypertensive for quite some time before the advent of new line drugs. It is
seeing a resurgence in popularity due to its potent arterial vasodilitation
properties. The benefit of Apresoline is that it acts directly on the vascular
smooth muscle, which has a greater effect on the arterioles. It also increases
heart rate and cardiac output, and decreases afterload.
Apresoline comes in both IV and oral forms.
The usual initial dose is a 5-10 mg IV push every 4-8 hours. Higher adult doses
of 20-40 mg IV may be necessary to achieve a normotensive state. Tablets come
in 10, 25, 50 and 100 mg doses.
Apresoline can cause reflex tachycardia,
which can be reduced with beta-blockers. It can also cause transient headache
and palpitations. Patients may complain of weight gain due to the sodium and
water retention properties of the drug.
Apresoline should be avoided in patients
with coronary heart disease, rheumatic heart disease, and lupus. Use cautiously
in patients with impaired renal function.
Pharmacokinetics:
Half-life: 4.2 hrs ~~ Onset: 30 min ~~ Peak: 2-8 hrs ~~ Duration: 2-5 days
Antiarrhythmics
The purpose of this class of drugs is to
decrease the speed of conductivity along the pathway, and to decrease
ventricular ectopy. It does this by altering the myocardial cell membrane and
interfering with the control of the pacemaker cells. It also reduces the rate
of automaticity in ectopic foci, causing less arrhythmic beats.
It must be remembered that whatever works
for the patient as an IV push must be followed by an IV drip to maintain the
benefits.
Cordarone (amiodarone)
This drug showed up on
the scene many years ago, but was not widely used until the present date. The
American Heart Association has named it the drug of choice in the treatment of wide complex tachycardias and
ventricular tachycardia (VT). It is also the primary drug in the treatment of
ventricular fibrillation (VF) and recurrent supraventricular tachycardia (SVT).
It is a class III antiarrhythmic.
The dose varies according to the situation.
In pulseless VT and VF, the dose is 300 mg IV push. In VT with a pulse, the
dose is 150 mg IV in 100 cc D5W over 10 minutes. It also comes in oral form of
200 mg tablets. For long-term ventricular arrhythmia management, a beginning
adult dose of 800-1600 mg per day is followed by a daily maintenance dose of
400 mg per day.
Side effects can be hypotension,
bradycardia, and AV block. Almost all patients exhibit corneal microdeposits,
which can lead to blurred vision. Severe, potentially fatal pulmonary toxicity
has been noted in some patients and begins with complaints of dyspnea, cough
with rales, and decreased breath sounds. In some cases, amiodarone can worsen
existing arrhythmias or produce new ones, a proarrhythmic effect.
Amiodarone should not be used in
conjunction with other antiarrhythmics. It may increase the effects of oral
anticoagulants. It can also increase the risk of digoxin toxicity.
Pharmacokinetics (PO ):
Half-life: 15-100 days ~~ Onset: 1-3 weeks ~~ Peak: 2-10 hrs ~~ Duration:
10-150 days
LidoPen, Xylocaine (lidocaine)
Although lidocaine's main claim to fame is
that of an antiarrhythmic, it can also be used as an anesthetic in lower doses.
Lidocaine has long been used as the main drug of choice in the treatment of
ventricular ectopic beats and runs of VT. It is a class Ib antiarrhythmic drug.
Lidocaine comes in IV form only. In the
treatment of arrhythmias, a loading dose of 50-100 mg (1.0-1.5 mg/kg), followed
by an IV drip of 1-4 mg/min.
Lidocaine can be extremely effective, but
patients must be watched closely for central nervous system toxicity. Initial
signs are tremors, disorientation and lightheadedness. This is easily resolved
upon discontinuation of the drug.
Lidocaine should not be used in patients
with supraventricular arrhythmias or Wolff-Parkinson-White syndrome. The dose
should be reduced for the elderly, since this can cause an increased risk of
CNS toxicity.
Pharmacokinetics (IV):
Half-life: 8 min ~~ Onset: 2-15 min ~~ Peak: 5-10 min ~~ Duration: 20-90 min
Pronestyl (procainamide)
Procainamide's main action is to slow
conduction through the myocardium. It increases the ventricular fibrillation
threshold, thereby slowing the reaction of the ventricles. It is used in the treatment
of ventricular arrhythmias (such as ventricular tachycardia) and slows the
conduction rate in atrial fibrillation. Although it is not considered to be the
main drug of action in these instances, it is used primarily when lidocaine or
amiodarone is not effective. It is a class Ia antiarrhythmic.
Procainamide comes in IV and oral forms. In
emergency situations, the dose is 20 mg/min IV until the arrhythmia is
converted. The maximum IV dose is 17 mg/kg. This maximum dose should never be
exceeded. The adult PO dose is 250-500 mg
every 3-6 hours, or for the long-acting form, 0.5 to 1 gram every 12 hours.
Procainamide is unique in that the
administration of the IV form should be stopped if the following occur:
maximum
dose has been reached
the
arrhythmia is converted
the patient
develops hypotension
the QRS is
widened by 50% of its original width
Side
effects can include anxiety, nausea, and convulsions. Watch for hypotension,
especially upon beginning the drug or increasing the drip rate. It should not
be used for patients with high degree heart blocks or PVC's in conjunction with
bradycardia.
Pharmacokinetics (IV):
Half-life: 3 hrs ~~ Onset: 10-30 min ~~ Peak: 10-60 min ~~ Duration: 3 hrs
Adenocard (adenosine)
Adenosine has the same action as those
drugs listed above. It slows conduction through the AV node, and also slows
impulses in the SA node. It is useful in restoring sinus rhythm in patients
with SVT. It is an unclassified antidysrrhythmic.
Adenosine comes in IV form only. The
initial dose is 6 mg over 1-2 seconds. A second dose of 12 mg may be given
within 1-2 minutes if the rhythm does not convert, and may be repeated every
1-2 minutes until the desired effect is obtained. It must be given rapidly,
since it has a very short half-life. Flush well after giving the dose.
Adenosine should not be given to patients
with second or third degree heart blocks, or sick sinus syndrome. It is also not
recommended in patients with atrial flutter or fibrillation, or VT.
The most frequent side effects are facial
flushing, pain in the chest/throat/jaw, and shortness of breath. Also watch for
new arrhythmias, especially PVC's and sinus bradycardia.
Pharmacokinetics:
Half-life: < 10 sec ~~ Onset: 1 min ~~ Peak: immediate ~~ Duration: 1-2 min
Norpace (disopyramide phosphate)
Norpace is another frequently used
antiarrhythmic. It is used mainly in the treatment of unifocal and multifocal
PVC's. It is also used for couplets and for episodes of VT. It is not used in
emergency situations. It is a class I antiarrhythmic.
Norpace comes in oral form in only two
strengths: 100 mg and 150 mg capsules.
Most often, patients on Norpace complain of
dry mouth. Other side effects include urinary hesitancy, constipation, blurred
vision, dizziness, fatigue, muscle weakness and headache. It should not be
given to patients with urinary retention, or second or third degree heart
blocks. It is of limited use in patients with poor left ventricular function,
due to its cardiovascular depressing effects.
Pharmacokinetics:
Half-life: 4-10 hrs ~~ Onset: 0.5-3.5 hrs ~~ Peak: 2.5 hrs ~~ Duration: 6-12
hrs
Beta-Blockers
Adrenergic neurohormones (circulating
catecholamines) stimulate the Beta 1 receptor cells and increase the heart
rate. Beta-blockers block the effect of
these neurohormones and decrease the heart rate. They slow the SA node
automaticity and the conductivity through the AV node. They also decrease myocardial oxygen demand and may also decrease
myocardial ischemia. The final
effect is a decrease in heart rate, decrease in blood pressure, decrease in
myocardial contractility, and a decrease in myocardial oxygen consumption.
As antiarrhythmic agents, beta-blockers are listed as class II.
The American Heart Association has listed beta-blockers as a treatment choice in
myocardial infarct. Studies have shown that they can decrease the risk of
reinfarct, and also decrease the risk of sudden death in patients suffering an
MI. Studies have also shown that if they are given within 4 hours of
thrombolytics, there is a decrease in the risk of reinfarction.
There are two different categories of
beta-blockers. Beta 1 blockers are
cardioselective. They act mainly on the cardiac cells, causing a decrease
in heart rate and decreased conduction through the AV node. They also depress
cardiac function. They come in both IV and oral forms. Some of the drugs in
this category are:
Sectral - acebutol
Tenormin - atenelol
Brevibloc - esmolol
Lopressor – metorpolol
The
second type of beta-blocker is Beta 2. Beta 2 blockers are non-selective. They
act on other cells beside the cardiac cells, yet still have the same effects as
the cardioselective Beta 1 blockers, in that they decrease heart rate and
decrease conduction through the AV node. The difference between the two
categories is that the non-selective Beta 2 blockers also affect pulmonary,
vascular, and uterine adrenergic receptors, and are used for other diagnoses
rather than just cardiac. For example, Inderal is also used in the treatment of
migraines.
The drugs in this category include:
Inderal - propanolol
Corgard - nadolol
Blocadren - tinolol
Normodyne, Trandate - labetolol
Visken – pindolol
All
beta-blockers can induce the same side effects. Some of those are hypotension,
exacerbation of CHF, and bronchospasm. Beta-blockers should be used cautiously
in patients with a history of COPD or asthma, since they can cause severe
bronchospasm in these patients.
One easy way to determine if a drug is a beta-blocker is to look for the name to end
in "lol."
Calcium Channel Blockers
Although many drugs are listed under the
heading of calcium channel blockers, this is the most chemically diverse group.
These drugs block the influx of calcium
across the slow channel during phase 2 of the action potential. In other words,
they cause a slowing of the rate between
the atria and ventricles. They can also produce relaxation of the coronary
vascular smooth muscle, and can dilate the coronary arteries.
The main use for these drugs is in the treatment of SVT and rapid ventricular
response rates. They are also successful
in the treatment of chronic stable angina, vasospasms, and hypertension.
They are listed as class IV antiarrhythmic agents.
Calcium channel blockers come in both IV
and oral form. Side effects are mainly related to their vasodilatation action,
such as decreased blood pressure and reflex tachycardia. Less extreme side
effects may include flushing, headache, and ankle edema.
When calcium channel blockers are used in
conjunction with beta-blockers, you may see increased effects, and they may
cause heart failure. Watch blood pressure closely and monitor heart rhythms for
any changes.
Here are some examples of calcium channel
blockers:
Calan, Isoptin - verapamil
Cardizem - diltiazem
Procardia - nifedepine
Cardene – nicardipine
ACE Inhibitors
(Angiotensin-Converting Enzyme)
ACE
inhibitors block the conversion of angiotensin I to angiotensin II, which happens
to be a potent vasoconstrictor. This group helps to decrease blood pressure.
They enhance the hypotensive effect of diuretics and other antihypertensives
such as beta-blockers.
Many studies have been done on the efficacy
of ACE inhibitors on CHF. The studies have shown conclusively that this line of
drug helps in the treatment of CHF by reducing
blood pressure and decreasing SVR. They are often used in combination with
diuretics and/or calcium channel blockers to manage heart CHF.
Most of these drugs are given orally. Only
Vasotec is available IV.
The main complaint of patients taking ACE
inhibitors is a persistent, dry,
irritating non-productive cough. Patients with renal dysfunction may show
an increase in their potassium levels. One of the benefits, however, is that
ACE inhibitors show less reflex tachycardias than other vasodilators.
ACE inhibitors are less effective when
administered with non-steroidal anti-inflammatory agents. They are also known
to increase lithium levels. All ACE inhibitors have detrimental effects on the
fetus and neonate.
Some of the more popular drugs in this
category are:
Capoten - captopril
Accupril - quinapril
Lotensin - benazepril
Monopril - fosinopril
Prinivil (Zestril) - lisinopril
Vasotec – enalapril
If you notice, ACE
Inhibitors all end in "pril."
Morphine
Your first question is "Why is
morphine listed in a class by itself?" That is a very good question.
Morphine is indeed a pain reliever, used mainly for the effects on the pain
centers. However, morphine has other properties as well.
It is the recommended pain reliever in patients experiencing chest pain from
angina or myocardial infarct. It has both analgesic and hemodynamic
properties, which is why it is a drug of choice.
Morphine increases venous capacitance. It causes peripheral vasodilation,
which causes a reduction in the SVR. It also helps to reduce pulmonary
congestion. By doing that, it reduces intramyocardial wall tension, which decreases myocardial oxygen requirements.
This helps to decrease the amount of damage caused by an MI, and reduces the
risk of extension in the infarcted area.
Morphine is given IV push. The dose is
between 2 and 5 mg given slowly,
preferably over 1-5 minutes. It may also be given by a variety of other
routes, including oral, IM, sustained release tablets, subcutaneous, rectal,
epidural, and intrathecal.
The main concern when giving morphine is
its effects on the respiratory center. Morphine can be a potent respiratory
depressant, so patients must be watched carefully to assure they maintain a
patent airway. Another side effect of morphine is hypotension.
The reversal agent for a morphine overdose
is naloxone (Narcan), given IV push in 1 mg.
Vasoconstrictors
Vasoconstrictors increase blood pressure by constricting the vessels. Their actions are systemic.
Pitressin (Vasopressin)
Vasopressin is a synthetic arginine
vasopressin that is identical to
endogenous vasopressin (ADH, or antidiuretic hormone). It is used to treat
diabetes insipidus. The adult dose is 5-10 units IM/SC, 2 to 4 times per day.
It is contraindicated in patients with chronic nephritis.
The American Heart Association's new
guidelines for 2001 list vasopressin as a first line treatment in VF/VT.
It is given IV with a dose of 40 units, to be given in one dose only. No repeated doses are to
be given, since the drug is long lasting (20 minutes).
The main side effects to watch for are
arrhythmias. Since this is still being studied, not much information is
available in this venue.
Glycoprotein IIb/IIIa Inhibitors
Classified as coagulation modifiers, this
group is used for the inhibition of
platelet aggregation. They reduce
coronary ischemia by blocking the enzyme glycoprotein IIb/IIIa that is
essential for platelet aggregation. Their main use is in the treatment of
MI, and it is one of the newer line of drugs in the treatment modality.
These drugs may be given PO
or IV. They have been proven to decrease MI complications after percutaneous
transluminal angioplasty (PTCA).
The main side effect with these drugs is bleeding. Patient histories must be
complete prior to giving these drugs. Contraindications would include:
Active bleeding or history of bleeding within the last 30
days.
Intracranial hemorrhage, aneurysm or stroke within the last
30 days.
Platelet count of less than 100,000 mm.
Systolic blood pressure of greater than 180 mm Hg.
Diastolic blood pressure of greater than 110 mm Hg.
Three
of the most popular IV drugs in this category are:
- Aggrestat - tirofiban
- Integrillin - eptifibatide
- Lovenox - enoxaprin
Three
of the most popular PO drugs in this category
are:
- Plavix - clopidogrel
- Trental - pentoxifylline
- Ticlid - ticlopidine
Oxygen
This must be one of the most forgotten
drugs that we use on a daily basis. Most often, oxygen is not even considered a
drug. However, it is considered one of the most important drugs in almost every
treatment. It is an essential component of cardiac resuscitation and emergency
cardiac care. Without oxygen, nothing else works!
Dosage varies greatly and can be
administered in many different forms. The simplest is by nasal cannula, but can
vary to a face mask, a non-rebreather mask, or to the maximum of an
endotracheal tube. The beginning dose is most often 2 liters by nasal cannula.
It can increase to a maximum dose of 15 liters or 100% oxygen. When using the
higher doses (greater than 6 liters) by nasal cannula, remember to add a "bubbler"
or water bottle for the comfort of the patient.
The way to determine the exact dose of
oxygen is through the use of a pulse oximeter, or SpO2 monitor. This monitor
can determine the concentration of oxygen in the blood by infrared readings through
the nailbeds. The oxygen content in the blood should be greater than 92%. If it
falls below that level, the oxygen concentration should be increased.
You can overdose a patient with oxygen, so
be careful when titrating the dose. Remember, COPD patients depend on their
hypoxic state as the stimulus for breathing! Oxygen toxicity may occur after a
prolonged support with high oxygen delivery.
Conclusion
You have now completed the study of the 10
most popular cardiac drug classifications. New drugs come on the market every
day. Some come into vogue while others fade away. If you remember the basics of
each category, you will never fail in your delivery of the right drug for the
right patient treatment.
Bibliography
- Hodgson, Barbara B., R.N.; Kizior, Robert J., B.S., R.Ph.; Saunders Nursing Drug Handbook 1999, W. B. Saunders, Philadelphia, 1999.
- Thelan, Lynne A.; Urden, Linda D.; Lough, Mary E.; Stacy, Kathleen M.; Critical Care Nursing, Diagnosis and Management. 3rd Edition, Mosby,
- Quick Drug Reference, accessed 8/02: http://www.ssgfx.com/CP2020/medtech/glossary/drugs.htm
- American Heart Association, Advanced Cardiac Life Support 2001 Guidelines.
- Deglin, Judith H; Vallerand, April H.;
- Lilley, Linda L., R.N., Ph.D.; Aucker, Robert S., PharmD; Pharmacology and the Nursing Process, 3rd edition, Mosby, St. Louis, 2001
