Reports of pain varying in frequency, duration, and intensity (especially as

condition worsens)

Narrowed focus

Distraction behaviors (moaning, crying, pacing, restlessness)

Autonomic responses, e.g., diaphoresis, blood pressure and pulse rate

changes, pupillary dilation, increased/decreased respiratory rate

Desired Outcomes

Report anginal episodes decreased in frequency, duration, and severity.

Demonstrate relief of pain as evidenced by stable vital signs, absence of

muscle tension and restlessness

Nursing Interventions

Rationale
Pain and decreased cardiac output may
stimulate the sympathetic nervous system
to release excessive amounts of
norepinephrine, which increases platelet

Instruct patient to notify nurse

immediately when chest pain occurs.

aggregation and release of thromboxane

A2. This potent vasoconstrictor causes
coronary artery spasm, which can
precipitate, complicate, and/or prolong an
anginal attack. Unbearable pain may cause
vasovagal response, decreasing BP and
heart rate.
Provides information about disease

Assess and document patient response to

medication.

progression. Aids in evaluating

effectiveness of interventions, and may
indicate need for change in therapeutic
regimen.

Identify precipitating event, if any:

Helps differentiate this chest pain, and

frequency, duration, intensity, and location

aids in evaluating possible progression to

of pain.

unstable angina.

Observe for associated symptoms:

Decreased cardiac output (which may

dyspnea, nausea and vomiting, dizziness,

occur during ischemic myocardial episode)

palpitations, desire to micturate.

stimulates sympathetic and

Nursing Interventions

Rationale
parasympathetic nervous system, causing
a variety of vague sensations that patient
may not identify as related to anginal
episode.

Evaluate reports of pain in jaw, neck,

Cardiac pain may radiate. Pain is often

shoulder, arm, or hand (typically on left

referred to more superficial sites served by

side).

the same spinal cord nerve level.

Place patient at complete rest during

Reduces myocardial oxygen demand to

anginal episodes.

minimize risk of tissue injury.

Elevate head of bed if patient is short of

Facilitates gas exchange to decrease

breath.

hypoxia and resultant shortness of breath.

Patients with unstable angina have an

Monitor heart rate and rhythm.

increased risk of acute life-threatening

dysrhythmias, which occur in response to
ischemic changes and/or stress.
Blood pressure may initially rise because
of sympathetic stimulation, then fall if

Monitor vital signs every 5 min during

initial anginal attack.

cardiac output is compromised.

Tachycardia also develops in response to
sympathetic stimulation and may be
sustained as a compensatory response if
cardiac output falls.
Anxiety releases catecholamines, which

Stay with patient who is experiencing pain

or appears anxious.

increase myocardial workload and can

escalate and/or prolong ischemic pain.
Presence of nurse can reduce feelings of
fear and helplessness.

Maintain quiet, comfortable environment.

Mental/emotional stress increases

Restrict visitors as necessary.

myocardial workload.

Provide light meals. Have patient rest for 1

hr after meals.

Decreases myocardial workload associated

with work of digestion, reducing risk of
anginal attack.

Nursing Interventions
Provide supplemental oxygen as indicated.

Rationale
Increases oxygen available for myocardial
uptake and reversal of ischemia.

Administer antianginal medication(s) promptly as indicated:

Nitroglycerin has been the standard for
Nitroglycerin: sublingual (Nitrostat),

treating and preventing anginal pain for

buccal, or oral tablets, metered-dose

more than 100 yr. Today it is available in

spray.

many forms and is still the cornerstone of

antianginal therapy.
Rapid vasodilator effect lasts 1030 min

sublingual isosorbide dinitrate (Isordil)

and can be used prophylactically to

prevent, as well as abort, anginal attacks.
Long-acting preparations are used to
prevent recurrences by reducing coronary
vasospasms and reducing cardiac

Sustained-release tablets, caplets:

(Nitrong, Nitrocap T.D.), chewable tablets
(Isordil, Sorbitrate), patches,
transmucosal ointment (Nitro-Dur,
Transderm-Nitro)

workload. May cause headache, dizziness,

light-headedness, symptoms that usually
pass quickly. If headache is intolerable,
alteration of dose or discontinuation of
drug may be necessary. Note: Isordil may
be more effective for patients with variant
form of angina. Reduces frequency and
severity of attack by producing continuous
vasodilation.

Beta-blockers: acebutolol (Sectral),

Reduces angina by reducing the hearts

atenolol (Tenormin), nadolol (Corgard),

workload. Note: Often these drugs alone

metoprolol (Lopressor), propranolol

are sufficient to relieve angina in less

(Inderal)

severe conditions.

Calcium channel blockers: bepridil

(Vascor), amlodipine (Norvasc), nifedipine
(Procardia), felodipine (Plendil), isradipine
(DynaCirc), diltiazem (Cardizem)
Analgesics: acetaminophen (Tylenol)

Produces relaxation of coronary vascular

smooth muscle; dilates coronary arteries;
decreases peripheral vascular resistance.
Usually sufficient analgesia for relief of
headache caused by dilation of cerebral

Nursing Interventions

Rationale
vessels in response to nitrates.
Potent narcotic analgesic may be used in
acute onset because of its several
beneficial effects, e.g., causes peripheral
vasodilation and reduces myocardial
workload; has a sedative effect to produce

Morphine sulphate (MS)

relaxation; interrupts the flow of

vasoconstricting catecholamines and
thereby effectively relieves severe chest
pain. MS is given IV for rapid action and
because decreased cardiac output
compromises peripheral tissue absorption.
Ischemia during anginal attack may cause
transient ST segment depression or
elevation and T wave inversion. Serial

Monitor serial ECG changes.

tracings verify ischemic changes, which

may disappear when patient is pain-free.
They also provide a baseline against which
to compare later pattern changes.

Risk for Decreased Cardiac Output

Risk factors may include

Inotropic changes (transient/prolonged myocardial ischemia, effects of

edications)

Alterations in rate/rhythm and electrical conduction

Desired Outcomes

Report/display decreased episodes of dyspnea, angina, and dysrhythmias.

Demonstrate increased activity tolerance.

Participate in behaviors/activities that reduce the workload of the heart.

Nursing Interventions
Maintain bed or chair rest in position of
comfort during acute episodes.

Rationale
Decreases oxygen demand therefore
reducing myocardial workload and risk of
decompensation.
Tachycardia may be present because of
pain, anxiety, hypoxemia, and reduced
cardiac output. Changes may also occur in

Monitor vital signs and cardiac rhythm.

BP (hypertension or hypotension) because

of cardiac response. ECG changes
reflecting dysrhythmias indicate need for
additional evaluation and therapeutic
intervention.
S3, S4, or crackles can occur with cardiac
decompensation or some medications

Auscultate breath sounds and heart

(especially beta-blockers). Development of

sounds. Listen for murmurs.

murmurs may reveal a valvular cause for

chest pain (aortic stenosis, mitral stenosis)
or papillary muscle rupture.

Provide for adequate rest periods. Perform

Conserves energy, reduces cardiac

self-care activities, as indicated.

workload.

Stress importance of avoiding straining

Valsalva maneuver causes vagal

Nursing Interventions

Rationale
stimulation, reducing heart rate

down, especially during defecation.

(bradycardia), which may be followed by

rebound tachycardia, both of which may
impair cardiac output.

Encourage immediate reporting of pain for

Timely interventions can reduce oxygen

prompt administration of medications as

consumption and myocardial workload and

indicated.

may minimize cardiac complications.

Desired effect is to decrease myocardial
oxygen demand by decreasing ventricular

Monitor and documents effects or adverse

response to medications, noting BP, heart
rate, and rhythm.

stress. Drugs with negative inotropic

properties can decrease perfusion to an
already ischemic myocardium.
Combination of nitrates and beta-blockers
may have cumulative effect on cardiac
output.
Angina is only a symptom of underlying

Assess for signs and symptoms of heart

pathology causing myocardial ischemia.

failure.

Disease may compromise cardiac function

to point of decompensation.

Evaluate mental status, noting

Reduced perfusion of the brain can

development of confusion, disorientation.

produce observable changes in sensorium.

Peripheral circulation is reduced when

Note skin color and presence and

quality of pulses.

cardiac output falls, giving the skin a pale

or gray color (depending on level of
hypoxia) and diminishing the strength of
peripheral pulses.

Administer supplemental oxygen as

needed.

Increases oxygen available for myocardial

uptake to improve contractility, reduce
ischemia, and reduce lactic acid levels.

Monitor pulse oximetry or ABGs as

Determines adequacy of respiratory

indicated.

function and/or O2 therapy.

Measure cardiac output and other

Cardiac index, preload/afterload,

Nursing Interventions

Rationale
contractility, and cardiac work can be
measured noninvasively through various
means, including thoracic electrical
bioimpedance (TEB) technique. Useful in

functional parameters as indicated.

evaluating response to therapeutic

interventions and identifying need for
emergency care. Note: Evaluation of
changes in heart rate, BP, and cardiac
output requires consideration of patients
circadian hemodynamic variability.

Administer medications as indicated:

Calcium channel blockers: diltiazem
(Cardizem), nifedipine (Procardia),
verapamil (Calan), bepridil (Vascor),
amlodipine (Norvasc), felodipine (Plendil),
isradipine (DynaCirc)

Beta-blockers: atenolol (Tenormin),

nadolol (Corgard), propranolol (Inderal),
esmolol (Brevibloc);

Although differing in mode of action,

calcium channel blockers play a major role
in preventing and terminating ischemia
induced by coronary artery spasm and in
reducing vascular resistance, thereby
decreasing BP and cardiac workload.
These medications decrease cardiac
workload by reducing heart rate and
systolic BP. Note: Overdosage produces
cardiac decompensation.
Useful in unstable angina, ASA diminishes

Acetylsalicylic acid (ASA), other

antiplatelet agents: ticlopidine (Ticlid);
glycoprotein IIb/IIa, abciximab (ReoPro),
eptifibatide (Integrilin)

platelet aggregation and clot formation.

For patients with major GI intolerance,
alternative drugs may be indicated. New
antiplatelet medications are being used IV
in conjunction with angioplasty. Oral forms
are under investigation.

IV heparin

Bolus, followed by continuous infusion, is

recommended to help reduce risk of
subsequent MI by reducing the thrombotic
complications of plaque rupture for
patients diagnosed with intermediate or

Nursing Interventions

Rationale
high-risk unstable angina. Note: Use of
low-molecular-weight heparin is increasing
because of its more efficacious and
predictable effect with fewer adverse
effects (less risk of bleeding) and longer
half-life. It also does not require
anticoagulation monitoring.

Monitor laboratory studies: PTT, aPTT.

Discuss purpose and prepare for stress
testing and cardiac catheterization, when
indicated.

Evaluates therapy needs and

effectiveness.
Stress testing provides information about
the health and strength of the ventricles.
Angioplasty (also called percutaneous
transluminal coronary angioplasty [PTCA])
increases coronary blood flow by
compression of atheromatous lesions and
dilation of the vessel lumen in an occluded
coronary artery. Intracoronary stents may
be placed at the time of PTCA to provide
structural support within the coronary

Prepare for surgical intervention,

artery and improve the odds of long-term

angioplasty with/without intracoronary

patency. This procedure is preferred over

stent placement, valve replacement,

the more invasive CABG surgery. CABG is

CABG, if indicated.

the recommended treatment when testing

confirms myocardial ischemia as a result
of left main coronary artery disease or
symptomatic three-vessel disease,
especially in those with left ventricular
dysfunction. Note: Stent placement may
also be effective for the variant form of
angina where periodic vasospasms impair
arterial flow.

Prepare for transfer to critical care unit if

Prolonged chest pain with decreased

Nursing Interventions

Rationale
cardiac output reflects development of

condition warrants.

complications requiring more emergency

interventions.

Decreased Cardiac Output

Nursing Diagnosis

Decreased Cardiac Output

May be related to

Altered myocardial contractility/inotropic changes

Alterations in rate, rhythm, electrical conduction

Structural changes (e.g., valvular defects, ventricular aneurysm)

Possibly evidenced by

Increased heart rate (tachycardia), dysrhythmias, ECG changes

Changes in BP (hypotension/hypertension)

Extra heart sounds (S3, S4)

Decreased urine output

Diminished peripheral pulses

Cool, ashen skin; diaphoresis

Orthopnea, crackles, JVD, liver engorgement, edema

Chest pain

Desired Outcomes

Display vital signs within acceptable limits, dysrhythmias absent/controlled,

and no symptoms of failure (e.g., hemodynamic parameters within acceptable
limits, urinary output adequate).

Report decreased episodes of dyspnea, angina.

Participate in activities that reduce cardiac workload.

Nursing Interventions

Rationale

Auscultate apical pulse, assess heart rate,

Tachycardia is usually present (even at

rhythm. Document dysrhythmia if

rest) to compensate for decreased

telemetry is available.

ventricular contractility. Premature atrial

contractions (PACs), paroxysmal atrial
tachycardia (PAT), PVCs, multifocal atrial
tachycardia (MAT), and atrial fibrillation

Nursing Interventions

Rationale
(AF) are common dysrhythmias associated
with HF, although others may also
occur. Note: Intractable ventricular
dysrhythmias unresponsive to medication
suggest ventricular aneurysm.
S1 and S2 may be weak because of
diminished pumping action. Gallop

Note heart sounds.

rhythms are common (S3and S4), produced

as blood flows into noncompliant
chambers. Murmurs may reflect valvular
incompetence.
Decreased cardiac output may be reflected
in diminished radial, popliteal, dorsalis

Palpate peripheral pulses.

pedis, and post tibial pulses. Pulses may

be fleeting or irregular to palpation, and
pulsus alternans (strong beat alternating
with weak beat) may be present.
In early, moderate, or chronic HF, BP may
be elevated because of increased SVR. In

Monitor BP.

advanced HF, the body may no longer be

able to compensate, and profound
hypotension may occur.
Pallor is indicative of diminished peripheral
perfusion secondary to inadequate cardiac

Inspect skin for pallor, cyanosis.

output, vasoconstriction, and anemia.

Cyanosis may develop in refractory HF.
Dependent areas are often blue or mottled
as venous congestion increases.

Monitor urine output, noting decreasing

Kidneys respond to reduced cardiac output

output and concentrated urine.

by retaining water and sodium. Urine

output is usually decreased during the day
because of fluid shifts into tissues but may
be increased at night because fluid returns

Nursing Interventions

Rationale
to circulation when patient is recumbent.

Note changes in sensorium: lethargy,

confusion, disorientation, anxiety, and
depression.

May indicate inadequate cerebral perfusion

secondary to decreased cardiac output.
Physical rest should be maintained during

Encourage rest, semirecumbent in bed or

acute or refractory HF to improve

chair. Assist with physical care as

efficiency of cardiac contraction and to

indicated.

decrease myocardial oxygen demand/

consumption and workload.

Provide quiet environment: explain

Psychological rest helps reduce emotional

therapeutic management, help patient

stress, which can produce

avoid stressful situations, listen and

vasoconstriction, elevating BP and

respond to expressions of feelings.

increasing heart rate.

Commode use decreases work of getting

Provide bedside commode. Have patient

to bathroom or struggling to use bedpan.

avoid activities eliciting a vasovagal

Vasovagal maneuver causes vagal

response (straining during defecation,

stimulation followed by rebound

holding breath during position changes).

tachycardia, which further compromises

cardiac function.

Elevate legs, avoiding pressure under

Decreases venous stasis, and may reduce

knee. Encourage active and passive

incidence of thrombus or embolus

exercises. Increase activity as tolerated.

formation.

Check for calf tenderness, diminished

Reduced cardiac output, venous pooling,

pedal pulses, swelling, local redness, or

and enforced bed rest increases risk of

pallor of extremity.

thrombophlebitis.
Incidence of toxicity is high (20%)

Withhold digitalis preparation as indicated,

because of narrow margin between

and notify physician if marked changes

therapeutic and toxic ranges. Digoxin may

occur in cardiac rate or rhythm or signs of

have to be discontinued in the presence of

digitalis toxicity occur.

toxic drug levels, a slow heart rate, or low

potassium level.

Administer supplemental oxygen as

Increases available oxygen for myocardial

Nursing Interventions

Rationale

indicated.

uptake to combat effects of hypoxia.

A variety of medications may be used to

Administer medications as indicated:

increase stroke volume, improve

contractility, and reduce congestion.
Diuretics, in conjunction with restriction of
dietary sodium and fluids, often lead to
clinical improvement in patients with
stages I and II HF. In general, type and

Diuretics: furosemide (Lasix), ethacrynic

acid (Edecrin), bumetanide (Bumex),
spironolactone (Aldactone).

dosage of diuretic depend on cause and

degree of HF and state of renal function.
Preload reduction is most useful in treating
patients with a relatively normal cardiac
output accompanied by congestive
symptoms. Loop diuretics block chloride
reabsorption, thus interfering with the
reabsorption of sodium and water.
Vasodilators are the mainstay of treatment
in HF and are used to increase cardiac

Vasodilators: nitrates (Nitro-Dur,

Isordil); arterial dilators: hydralazine
(Apresoline); combination
drugs: prazosin (Minipress);

output, reducing circulating volume

(venodilators) and decreasing SVR,
thereby reducing ventricular
workload. Note: Parenteral vasodilators
(Nitropress) are reserved for patients with
severe HF or those unable to take oral
medications.

ACE inhibitors: benazepril (Lotensin),

captopril (Capoten), lisinopril (Prinivil),
enalapril (Vasotec), quinapril (Accupril),
ramipril (Altace), moexipril (Univasc).

ACE inhibitors represent first-line therapy

to control heart failure by decreasing
ventricular filling pressures and SVR while
increasing cardiac output with little or no
change in BP and heart rate.

Angiotensin II receptor

Antihypertensive and cardioprotective

antagonists: eprosartan (Teveten),

effects are attributable to selective

irbesartan (Avapro), valsartan (Diovan);

blockade of AT1(angiotensin II) receptors

Nursing Interventions

Rationale
and angiotensin II synthesis.
Increases force of myocardial contraction
when diminished contractility is the cause
of HF, and slows heart rate by decreasing

Digoxin (Lanoxin)

conduction velocity and prolonging

refractory period of the atrioventricular
(AV) junction to increase cardiac efficiency
/output.
These medications are useful for shortterm treatment of HF unresponsive to

Inotropic agents: amrinone (Inocor),

milrinone (Primacor), vesnarinone (ArkinZ);

cardiac glycosides, vasodilators, and

diuretics in order to increase myocardial
contractility and produce vasodilation.
Positive inotropic properties have reduced
mortality rates 50% and improved quality
of life.
Useful in the treatment of HF by blocking

Beta-adrenergic receptor

the cardiac effects of chronic adrenergic

antagonists:carvedilol (Coreg), bisoprolol

stimulation. Many patients

(Zebeta), metoprolol (Lopressor);

experience improved activity tolerance and

ejection fraction.
Decreases vascular resistance and venous
return, reducing myocardial workload,

Morphine sulfate.

especially when pulmonary congestion is

present. Allays anxiety and breaks the
feedback cycle of anxiety to catecholamine
release to anxiety.

Antianxiety agents and sedatives.

Promote rest, reducing oxygen demand

and myocardial workload.

Anticoagulants: low-dose heparin, warfarin

May be used prophylactically to prevent

(Coumadin).

thrombus and embolus formation in

presence of risk factors such as venous
stasis, enforced bed rest, cardiac

Nursing Interventions

Rationale
dysrhythmias, and history of previous
thrombotic episodes.
Because of existing elevated left

Administer IV solutions, restricting total

amount as indicated. Avoid saline
solutions.

ventricular pressure, patient may not

tolerate increased fluid volume (preload).
Patients with HF also excrete less sodium,
which causes fluid retention and increases
myocardial workload.
Fluid shifts and use of diuretics can alter

Monitor and replace electrolytes.

electrolytes (especially potassium and

chloride), which affect cardiac rhythm and
contractility.
ST segment depression and T wave
flattening can develop because of

Monitor serial ECG and chest x-ray

changes.

increased myocardial oxygen demand,

even if no coronary artery disease is
present. Chest x-ray may show enlarged
heart and changes of pulmonary
congestion.
Cardiac index, preload, afterload,
contractility, and cardiac work can be

Measure cardiac output and other

functional parameters as indicated.

measured noninvasively by using thoracic

electrical bioimpedance (TEB) technique.
Useful in determining effectiveness of
therapeutic interventions and response to
activity.

Monitor laboratory studies:

BUN, creatinine.

Elevation of BUN or creatinine reflects

kidney hypoperfusion.
May be elevated because of liver

Liver function studies (AST, LDH).

congestion and indicate need for smaller

dosages of medications that are detoxified
by the liver.

Nursing Interventions

Rationale

Prothrombin time (PT), activated partial

Measures changes in coagulation

thromboplastin time (aPTT) coagulation

processes or effectiveness of anticoagulant

studies.

therapy.
May be necessary to correct

Prepare for insertion and maintenance of

pacemaker, if indicated.

bradydysrhythmias unresponsive to drug

intervention, which can aggravate
congestive failure and/or produce
pulmonary edema.

Prepare for surgery as indicated:

Heart failure due to ventricular aneurysm
or valvular dysfunction may require
valve replacement, angioplasty, coronary
artery bypass grafting (CABG).

aneurysmectomy or valve replacement to

improve myocardial contractility/ function.
Revascularization of cardiac muscle by
CABG may be done to improve cardiac
function.
Cardiomyoplasty, an experimental
procedure in which the latissimus dorsi
muscle is wrapped around the heart and

Cardiomyoplasty.

electrically stimulated to contract with

each heartbeat, may be done to augment
ventricular function while the patient is
awaiting cardiac transplantation or when
transplantation is not an option.
Other new surgical techniques include
transmyocardial revascularization
(percutaneous [PTMR]) using CO2 laser

Transmyocardial revascularization.

technology, in which a laser is used to

create multiple 1-mm diameter channels
in viable but underperfused cardiac
muscle.

Assist with mechanical circulatory support

An intra-aortic balloon pump (IABP) may

system, such as IABP or VAD, when

be inserted as a temporary support to the

Nursing Interventions

Rationale
failing heart in the critically ill patient with
potentially reversible HF. A batterypowered ventricular assist device (VAD)
may also be used, positioned between the
cardiac apex and the descending thoracic

indicated.

or abdominal aorta. This device receives

blood from the left ventricle (LV) and
ejects it into the systemic circulation,
often allowing patient to resume a nearly
normal lifestyle while awaiting heart
transplantation. With end-stage HF,
cardiac transplantation may be indicated.

. Impaired Gas Exchange

Nursing Diagnosis

Risk for Impaired Gas Exchange

Risk factors may include

Alveolar-capillary membrane changes, e.g., fluid collection/shifts into

interstitial space/alveoli

Possibly evidenced by

Not applicable. A risk diagnosis is not evidenced by signs and symptoms, as

the problem has not occurred and nursing interventions are directed at
prevention.

Desired Outcomes

Demonstrate adequate ventilation and oxygenation of tissues by

ABGs/oximetry within patients normal ranges and free of symptoms of
respiratory distress.

Participate in treatment regimen within level of ability/situation.

Nursing Interventions
Auscultate breath sounds, noting crackles,
wheezes.

Rationale
Reveals presence of pulmonary congestion
and collection of secretions, indicating
need for further intervention.

Instruct patient in effective coughing,

Clears airways and facilitates oxygen

deep breathing.

delivery.

Encourage frequent position changes.

Helps prevent atelectasis and pneumonia.

Maintain chair or bed rest, with head of

bed elevated 2030 degrees, semi-

Reduces oxygen demands and promotes

Fowlers position. Support arms with

maximal lung inflation.

pillows.
Place patient in Fowlers position and give

To help patient breath more easily and

supplemental oxygen.

promote maximum chest expansion.

Nursing Interventions

Rationale
Hypoxemia can be severe during
pulmonary edema. Compensatory changes
are usually present in chronic HF. Note: In

Graph graph serial ABGs, pulse oximetry.

patients with abnormal cardiac index,

research suggests pulse oximeter
measurements may exceed actual oxygen
saturation by up to 7%.

Administer supplemental oxygen as

Increases alveolar oxygen concentration,

indicated.

which may reduce tissue hypoxemia.

Administer medications as indicated:

Diuretics: furosemide (Lasix)

Reduces alveolar congestion, enhancing

gas exchange.
Increases oxygen delivery by dilating

Bronchodilators: aminophylline

small airways, and exerts mild diuretic

effect to aid in reducing pulmonary
congestion.