Cardiotronic Medications

Cardiotronic Medications- drugs used to increase the contractility of the heart muscle
for patients experiencing heart failure( a condition in which the heart fails to pump blood around
the body effectively causing Congestive Heart Failure (CHF)
Treatment: involves helping the heart muscle to contract more efficiently to restore
system balance.
Causes: Coronary Artery Disease is the leading cause of heart failure due to the
insufficient flow of blood to meet oxygen demands of the myocardium.
Hypertension
Cardiomyopathy
Valvular disease
Congenital heart abnormalities
Signs and Symptoms:
Left-Sided Heart Failure

Right-Sided Heart Failures

Reflects engorgement of the pulmonary veins,

Occurs as a result of COPD or other lung

which eventually leads to difficulty breathing

diseases that elevate pulmonary pressure

Patients complain of rapid, shallow

causing a congestion and back up of blood in

the systemic system.

respirations (tachypnea)
breathing discomfort (dyspnea)
difficulty breathing when lying down

(orthopnea)
coughing and coughing up blood
(hemoptysis), fluid in the lungs called

(pulmonary edema in severe cases)

increased heart rate
GI upset
abnormal pain
decreased peripheral pulses
oxygen deficiency (Hypoxia)
anxiety

Treatments:

Jugular venous pressure (JVP)

(enlargement of the liver)
Swelling in the legs(edema)
Increased urine output(nocturia)
excessive voiding during the night
Splenomegaly
Hepatomegaly
Decreased renal perfusion when
upright
Increased perfusion when supine
nocturia
Feels weak and fatigue

Vasodilators (ACE Inhibitors and Nitrates) lightens the hearts workload Decrease
workload of overworked cardiac
muscle
Diuretics (reduce blood volume and workload) -Decrease blood volume, which
decreases venous return and blood pressure
Beta-Adrenergic Agonists (Beta Blockers that decreases the hearts workload by
activating sympathetic reaction resulting in increased contraction and calcium flow

KEY POINTS
In HF, the heart pumps blood so ineffectively that blood builds up,
causing congestion in the cardiovascular system.

HF can result from damage to the heart muscle combined with

an increased workload related to CAD, hypertension, cardiomyopathy,

valvular disease, or congenital heart abnormalities. As the heart pump
fails, the muscle cells can no longer work to move calcium into the cell,
and cardiac contractions become weak and ineffective.

Signs and symptoms of HF result from the backup of blood in

the vascular system and the loss of fluid in the tissues. Right-sided HF
is characterized by edema, liver congestion, elevated JVP, and nocturia,
whereas left-sided failure is marked by tachypnea, dyspnea, orthopnea,
hemoptysis, anxiety, and poor oxygenation of the blood.

Treatment agents include vasodilators (to lighten the hearts

workload), diuretics (to reduce blood volume and workload), betablockers (to decrease the hearts workload by activating sympathetic
reaction), human B-type natriuretic peptides (to decrease the hearts
workload by vasodilatation and suppression of the response to the
sympathetic reaction), and cardiotonic (inotropic) agents (to stimulate
more effective muscle contractions).

Cardiac Glycosides: Cardiotronic Drugs

The result is a decrease in the hearts workload and relief of HF, atrial flutter, atrial
fibrillation and paroxysmal atrial tachycardia
Digoxin increases intracellular calcium and allows more calcium to enter myocardial cells during
depolarization causing the following effects:
Increased force of myocardial contraction (a positive inotropic effect)
Increased cardiac output and renal perfusion (which has a diuretic effect,
increasing urine output and decreasing blood volume while decreasing renin release
and activation of the reninangiotensinaldosterone system)
Slowed heart rate, owing to slowing of the rate of cellular repolarization
(a negative chronotropic effect)
Decreased conduction velocity through the atrioventricular (AV) node

Pharmacokinetics
Digoxin is available for oral and parenteral administration. The drug has a rapid onset of action and
rapid absorption (30120 minutes when taken orally, 530 minutes when given intravenously). It is
widely distributed throughout the body. Digoxin is primarily excreted unchanged in the urine.
Because of this, caution should be exercised in the presence of renal impairment because the drug
may not be excreted and could accumulate, causing toxicity.
TABLE 44.1 DRUGS IN FOCUS Cardiotonic Agents

Drug Name

Usual Dosage

Usual Indications

Cardiac Glycosides
digo

Adult: loading dose 0.751.25 mg PO or 0.1250.25

Treatment of acute heart
mg IV, then maintenance dose of 0.1250.25 mg/d
failure (HF), atrial
PO; decrease dose with renal impairment
arrhythmias
xin (Lanoxin)
Pediatric (dose based on age): 1060 mcg/kg PO or 8
50 mcg/kg IV loading dose; maintenance is 25%
30% of loading dose
Phosphodiesterase Inhibitors
milri 50 mcg/kg IV bolus over 10 min, then 0.375 0.75
Short-term management of
mcg/kg/min IV infusion; do not exceed 1.13 mg/kg/d; HF in adults receiving
reduce dose in renal impairment
digoxin and diuretics

none
(Primacor)

Contraindications and Cautions

Cardiac glycosides are contraindicated in the presence of allergy to any component of
the digitalis preparation to prevent hypersensitivity reactions.
Digoxin is contraindicated in the following conditions: ventricular tachycardia or
fibrillation,which are potentially fatal arrhythmias and should be treated with
other drugs;
Heart block or sick sinus syndrome, which could be made worse by slowing of
conduction through the AV node;
Idiopathic hypertrophic subaortic stenosis (IHSS)because the increase in
force of contraction could obstruct the outflow tract to the aorta and cause severe
problems;
Acute MI because the increase in force of contraction could cause more muscle
damage and infarct;
Renal insufficiency because the drug is excreted through the kidneys and toxic
levels could develop; and
Electrolyte abnormalities (e.g., increased calcium, decreased potassium,
decreased magnesium), which could alter the action potential and change the effects
of the drug.

Adverse Effects
headache
weakness
drowsiness
vision changes (a yellow halo around objects is often reported)
GI upset and anorexia
Arrhythmias may develop because the glycosides affect the action potential and conduction
system of the heart.
Digoxin *********
Very narrow therapeutic window
Drug levels must be monitored
0.5 to 2 ng/mL

 Low potassium levels increase its toxicity

Adverse Reactions with taking Digooxin

Cardiovascular- Dysrhythmias, including bradycardia or tachycardia
CNS-Headaches, fatigue, malaise, confusion, convulsions
Eye-Colored vision (seeing green, yellow, purple), halo vision, flickering lights
GI- Anorexia, nausea, vomiting, diarrhea

Digoxin Toxicity
digoxin immune Fab (Digibind) therapy
Hyperkalemia (serum potassium greater than 5 mEq/L) in a digitalis-toxic patient
Life-threatening cardiac dysrhythmias
Life-threatening digoxin overdose

The patients cardiac status should be monitored continually while the drug is given and for
several hours after the infusion is finished. Because there is a risk of hypersensitivity reaction
to the infused protein, life-support equipment should be on standby.
Serum digoxin levels will be very high and unreliable for about 3 days after the digoxin
immune Fab infusion because of the high levels of digoxin in the blood. The patient should not
be redigitalized for several days to 1 week after digoxin immune Fab has been use because of
the potential of remaining fragments in the blood.

PHOSPHODIESTERASE INHIBITORS
The phosphodiesterase inhibitors (Table 44.1) belong to a second class of drugs that act as
cardiotonic (inotropic) agents. These include milrinone (Primacor).

Types
Inamrinone (Inocor): Approved only for use in patients with HF that has not
responded to digoxin, diuretics, or vasodilators
Milrinone (Primacor): Short-term management of HF in patients who are
receiving digoxin and diuretics

Therapeutic Actions and Indications

The phosphodiesterase inhibitors block the enzyme phosphodiesterase. This blocking effect leads to
an increase in myocardial cell cyclic adenosine monophosphate (cAMP), which increases calcium
levels in the cell (Figure 44.4). Increased cellular calcium causes a stronger contraction and prolongs
the effects of sympathetic stimulation, which can lead to vasodilation, increased oxygen
consumption, and arrhythmias. These drugs are indicated for the short-term treatment of HF that
has not responded to digoxin or diuretics alone or that has had a poor response to digoxin, diuretics,
and vasodilators. See Table 44.1 for usual indications for each drug. Because these drugs have been
associated with the development of potentially fatal ventricular arrhythmias, their use is limited to
severe situations.

Pharmacokinetics
Inamrinone and milrinone are available only for intravenous use. These drugs are widely distributed
after injection. They are metabolized in the liver and excreted primarily in the urine.

Contraindications and Cautions

Phosphodiesterase inhibitors are contraindicated in the presence of allergy to either of
these drugs or to bisulfites to avoid hypersensitivity reactions.
Severe aortic or pulmonic valvular disease, which could be exacerbated by increased
contraction;
Acute MI, which could be exacerbated by increased oxygen consumption and increased
force of contraction
Fluid volume deficit, which could be made worse by increased renal perfusion; and
ventricular arrhythmias, which could be exacerbated by these drugs.
Caution should be exercised in the elderly, who are more likely to develop adverse
effects.
Adverse Effects
ventricular arrhythmias (which can progress to fatal ventricular fibrillation)

hypotension, and chest pain.

GI effects include nausea, vomiting, anorexia, and abdominal pain.
Thrombocytopenia occurs frequently with inamrinone, and it also can occur with milrinone.
Hypersensitivity reactions associated with these drugs include vasculitis, pericarditis, pleuritis,
and ascites.
Burning at the intravenous injection site is also a frequent adverse effect

Clinically Important DrugDrug Interactions

Precipitates form when these drugs are given in solution with furosemide. Avoid this combination in
solution. Use alternate lines if both of these drugs are being given intravenously.
p. 740

Prototype Summary: Milrinone

Indications: Short-term treatment of HF in patients who have not responded to digitalis,

diuretics, or vasodilators.
Actions: Blocks the enzyme phosphodiesterase, which leads to an increase in myocardial cell
cAMP, which increases calcium levels in the cell, causing a stronger contraction and prolonged
response to sympathetic stimulation; directly relaxes vascular smooth muscle.
Pharmacokinetics:
Route

IV

Onset

Immediate

Peak

10 min

Duration

8 hr

T1/2: 2.33.5 hours, metabolized in the liver and excreted in urine and feces.
Adverse Effects: Arrhythmias, hypotension, nausea, vomiting, thrombocytopenia, pericarditis,
pleuritis, fever, chest pain, burning at injection site.

Nursing Implications
Assess history, drug allergies, contraindications
Assess clinical parameters, including:
BP
Apical pulse for 1 full minute
Heart sounds, breath sounds
Weight, I&O measures
ECG
Serum labs: potassium, sodium, magnesium, calcium, renal, and liver function
studies
Before giving any dose, count apical pulse for 1 full minute
For apical pulse less than 60 or greater than 100 beats/min
Hold dose
Notify prescriber
Hold dose and notify prescriber if patient experiences signs/symptoms of toxicity
Anorexia, nausea, vomiting, diarrhea
Visual disturbances (blurred vision, seeing green or yellow halos around objects)
Nesiritide or milrinone
Use an infusion pump, assess IV site
Monitor Blood pressure (assess for hypotension), intake and output, heart rate and
rhythm, daily weights, respirations
Monitor for therapeutic effects

 Increased urinary output

Decreased edema, shortness of breath, dyspnea, crackles, fatigue
Resolution of paroxysmal nocturnal dyspnea
Improved peripheral pulses, skin color, temperature
Monitor for adverse effects

KEY POINTS
The cardiac glycoside digoxin increases the movement of calcium into the heart

muscle. This results in increased force of contraction, which increases blood flow to
the kidneys (causing a diuretic effect), slows the heart rate, and slows conduction
through the AV node. All of these effects decrease the hearts workload.
Phosphodiesterase inhibitors block the breakdown of cAMP in the cardiac

muscle. This allows more calcium to enter the cell (leading to more intense
contraction) and increases the effects of sympathetic stimulation (which can lead to
vasodilation but also can increase pulse, blood pressure, and workload on the heart).
Phosphodiesterase inhibitors are associated with severe effects. They are

reserved for use in extreme situations. They are only available for IV use.

SUMMARY
HF, a condition in which the heart muscle fails to effectively pump blood through the

cardiovascular system, can be the result of a damaged heart muscle and increased demand to work
harder.

The sarcomerethe functioning unit of the heart muscleis made up of protein fibers: thin

actin fibers and thick myosin fibers, which react with each other when calcium is present to
inactivate troponin. The fibers slide together, resulting in contraction. Failing cardiac muscle cells
lose the ability to effectively use energy to move calcium into the cell, and contractions become
weak and ineffective.
Cardiotonic (inotropic) agents are one class of drugs used in the treatment of heart failure.

These agents directly stimulate the muscle to contract more effectively.

Cardiac glycosides increase the movement of calcium into the heart muscle. This results in

increased force of contraction, which increases blood flow to the kidneys (causing a diuretic effect),
slows the heart rate, and slows conduction through the AV node. All of these effects decrease the
hearts workload. Digoxin is the cardiac glycoside most commonly used to treat HF.
Phosphodiesterase inhibitors block the breakdown of cAMP in the cardiac muscle. This

allows more calcium to enter the cell (leading to more intense contraction) and increases the
effects of sympathetic stimulation (which can lead to vasodilation but also can increase pulse,
blood pressure, and workload on the heart). Because these drugs are associated with severe effects,
they are reserved for use in extreme situations.

MULTIPLE CHOICE
Select the best answer to the following.
1. A nurse assessing a patient with heart failure (HF) would expect to find which of the following:
a.

Cardiac arrest

b.

Congestion of blood vessels

c.

A myocardial infarction

d.

A pulmonary embolism

2. Calcium is needed in the cardiac muscle

a.

to break apart actinmyosin bridges.

b.

to activate troponin.

c.

to promote contraction via sliding.

d.

to maintain the electrical rhythm.

3. When assessing a patient with right-sided HF, the nurse would expect to find edema
a.

in gravity-dependent areas.

b.

in the hands and fingers.

c.

around the eyes.

d.

when the patient is lying down.

4. Angiotensin-converting enzyme (ACE) inhibitors and other vasodilators are used in the early treatment of HF. They act to
a.

cause loss of volume.

b.

increase arterial pressure and perfusion.

c.

cause pooling of the blood and decreased venous return to the heart.

d.

increase the release of aldosterone and improve fluid balance.

5. A nurse is preparing to administer a prescribed cardiotonic drug to a patient based on the understanding that this group of drugs
act in which way?
a.

They block the sympathetic nervous system.

b.

They block the reninangiotensin system.

c.

They block the parasympathetic influence on the heart muscle.

d.

They affect intracellular calcium levels in the heart muscle.

6. A nurse would instruct a patient taking Lanoxin (digoxin) for the treatment of HF to do which of the following?
a.

Make up any missed doses the next day.

b.

Report changes in heart rate.

c.

Avoid exposure to the sun.

d.

Switch to generic tablets if less expensive.

7. A nurse is about to administer Lanoxin to a patient whose apical pulse is 48 beats/min. She should
a.

give the drug and notify the prescriber that the heart rate is low.

b.

retake the pulse in 15 minutes and give the drug if the pulse has not changed.

c.

retake the pulse in 1 hour and withhold the drug if the pulse is still less than 60 beats/min.

d.

withhold the drug and notify the prescriber that the heart rate is below 60 beats/min.

8. Before giving digoxin to an infant, the nurse should

a.

notify the prescriber that the dose is about to be given and recheck the ordered dose.

b.

check the apical pulse and have another nurse double-check the dose.

c.

make sure that the infant has eaten, has a full stomach, and has been given an antacid.

d.

check the apical pulse and give the drug very slowly.

Select all that apply.

1. Heart failure (HF) occurs when the heart fails to pump effectively. Which of the following could cause HF?
a.

Coronary artery disease

b.

Chronic hypertension

c.

Cardiomyopathy

d.

Fluid overload

e.

Pneumonia

f.

Cirrhosis

2. A client develops left-sided HF after a myocardial infarction (MI). Which of the following would the nurse expect to find during
the client assessment?
a.

Orthopnea

b.

Polyuria

c.

Tachypnea

d.

Dyspnea

e.

Blood-tinged sputum

f.

Swollen ankles