Nursing Care of Coronary Heart Disease - 5 Diagnosis Interventions

at 10:32 PM
Posted by imam kom

Coronary heart disease is mainly caused by the process of atherosclerosis which is a degenerative
disorder. Coronary heart disease is the imbalance between myocardial oxygen supply needs.

Coronary heart disease occurs due to:

 Narrowing of the coronary arteries

 Decreased blood flow / cardiac output
 The increase in myocardial oxygen demand
 Coronary artery spasm

Main causes of atherosclerosis. Although influenced by many factors, due to degenerative

disorder, it often causes sudden death and attacked very productive age.

Input to the oxygen demand imbalance, namely:

1. Hypoxemia (ischemia), caused by vascular disorders (coronary arteries). On ischemic

vascular abnormalities that are reduced tissue perfusion to metabolic elimination caused
by (eg lactic acid) decreased as well, so it will be faster symptoms appear.
2. Hypoxia (anoxia), caused by lack of oxygen in the blood. Actual input of oxygen to the
myocardium depends on the oxygen in the blood and the coronary arteries. Oxygen in the
blood depends on the oxygen can be taken up by the blood. So influenced by Hb, lungs
and oxygen in the breathing air.

Palpitations are manifestations of coronary heart disease although not specific. Manifestations of
coronary heart disease varies depending on the degree of coronary artery blood flow. When
coronary flow is still sufficient for the tissue will not cause any complaints / clinical
manifestations. Factors that affect large and coronary flow properties such as the state of
anatomical and mechanical factors, autoregulation system and peripheral resistance.

The trigger factor that adds to ischemia such as, physical activity, stress, etc.. Angina pectoris is
the main symptom specific and typical for coronary heart disease. Shortness of breath began to
feel short of breath while doing activities that are sufficiently severe, increasing shortness of
breath. At a more advanced state of heart failure can occur.

5 Nursing Diagnosis and Interventions of Coronary Heart Disease

1. Nursing Diagnosis : Acute Pain related to heart tissue ischemia, or blockages in the coronary
arteries.

Objective: The client is expected to be able to demonstrate a decrease in chest pain, showed a
decrease in pressure and how relaxation.

Interventions:

 Monitor and review the characteristics and location of pain.

 Monitor vital signs (blood pressure, pulse, respiration, consciousness).
 Instruct the patient to immediately report instances of chest pain.
 Create an atmosphere of calm and comfortable environment.
 Teach and encourage the patient to do relaxation techniques.
 Collaboration in: Giving oxygen and drugs
 Measure vital signs before and after treatment.

2. Nursing Diagnosis: Activity Intolerance related to imbalance between oxygen supply and
demand, and the presence of necrotic tissue in myocardial ischemia.

Objective: The client shows an increase in the ability to perform activities (blood pressure, pulse,
rhythm within normal limits) the absence of angina.

Interventions:

 Record the heart rhythm, blood pressure and pulse before, during and after the activity.
 Instruct the patient to have more rest first.
 Instruct the patient not to "push" at the time of defecation.
 Explain to the patient about the stages of activity that may be performed by the patient.
 Show to patients about physical signs that activity exceeds the limit.

3. Nursing Diagnosis : Risk for Decreased Cardiac Output related to changes in the rate,
rhythm, cardiac conduction, decrease preload or increased SVR, miocardial infarction.
Objective: There is no decrease in cardiac output during the action of nursing.

Interventions:

 Perform blood pressure measurements (compare the two arms in a standing position,
sitting and lying down, if possible).
 Assess the quality of the pulse.
 Note the development of the S3 and S4.
 Auscultation of breath sounds.
 Stay with the patient at the time of the activity.
 Serve food that is easy to digest and reduce the consumption of kafeine.
 Collaboration in: serial ECG examination, chest radiographs, administering medications
anti dysrhythmias.

4. Nursing Diagnosis : Risk for Impaired Tissue Perfusion related to decreased blood
pressure, hypovolemia.

Objective: During done nursing action is not a decline in tissue perfusion.

Interventions:

 Assess the changes in consciousness.

 Inspection of the pale, cyanosis, cold skin and peripheral pulse degradation.
 Assess the Homans sign (pain in calf on dorsoflextion), erythema, edema.
 Assess respiration (rhythm, and effort into breathing).
 Assess gastrointestinal function (bowel sounds, abdominal distention, constipasi).
 Monitor intake and output.
 Collaboration in: Examination ABG, BUN, serum ceratinin and electrolyte.

5. Nursing Diagnosis : Risk for Excess Fluid Volume related to decreased organ perfusion
(renal), increased sodium retention, decreased plasma protein.

Objective: There is an excess of fluid in the body of the client during the treatment.

Interventions:

 Auscultation of breath flare (examine the crackless).

 Assess the jugular vein distension, increased occurrence of edema.
 Measure intake and output (fluid balance).
 Assess the weight every day.
 Instruct the patient to consume a maximum of 2000 total liquids cc/24 hours.
 Serve a meal with a low-salt diet.
 Collaboration in the provision of diuretics.
http://screware.blogspot.com/2013/06/nursing-care-of-coronary-heart-disease.html
Nursing Interventions:

1. Monitor blood pressure, apical heart rate, and respirations every 5 minutes during an
anginal attack.
2. Maintain continuous ECG monitoring or obtain a 12-lead ECG, as directed, monitor for
arrhythmias and ST elevation.
3. Place patient in comfortable position and administer oxygen, if prescribed, to enhance
myocardial oxygen supply.
4. Identify specific activities patient may engage in that are below the level at which anginal
pain occurs.
5. Reinforce the importance of notifying nursing staff whenever angina pain is experienced.
6. Encourage supine position for dizziness caused by antianginals.
7. Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker
and calcium channel blocker therapy. These drug must be tapered to prevent a “rebound
phenomenon”; tachycardia, increase in chest pain, and hypertension.
8. Explain to the patient the importance of anxiety reduction to assist to control angina.
9. Teach the patient relaxation techniques.
10. Review specific factors that affect CAD development and progression; highlight those
risk factors that can be modified and controlled to reduce the risk.

Acute Pain

Acute Pain: Unpleasant sensory and emotional experience arising from actual or potential tissue
damage or described in terms of such damage; sudden or slow onset of any intensity from mild
to severe with anticipated or predictable end and a duration of <6 months.

May be related to

 Decreased myocardial blood flow

 Increased cardiac workload/oxygen consumption

Possibly evidenced by

 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
Instruct patient to notify nurse immediately
when chest pain occurs.
Assess and document patient response to
medication.
Identify precipitating event, if any: frequency,
duration, intensity, and location of pain.
Observe for associated symptoms: dyspnea,
nausea and vomiting, dizziness, palpitations,
desire to micturate.
Evaluate reports of pain in jaw, neck, shoulder,
arm, or hand (typically on left side).
Place patient at complete rest during anginal
episodes.
Elevate head of bed if patient is short of breath.
Monitor heart rate and rhythm.
Monitor vital signs every 5 min during initial
anginal attack.
Rationale
Pain and decreased cardiac output may
stimulate the sympathetic nervous system to
release excessive amounts of norepinephrine,
which increases platelet 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 progression.
Aids in evaluating effectiveness of
interventions, and may indicate need for change
in therapeutic regimen.
Helps differentiate this chest pain, and aids in
evaluating possible progression to unstable
angina.
Decreased cardiac output (which may occur
during ischemic myocardial episode) stimulates
sympathetic and parasympathetic nervous
system, causing a variety of vague sensations
that patient may not identify as related to
anginal episode.
Cardiac pain may radiate. Pain is often referred
to more superficial sites served by the same
spinal cord nerve level.
Reduces myocardial oxygen demand to
minimize risk of tissue injury.
Facilitates gas exchange to decrease hypoxia
and resultant shortness of breath.
Patients with unstable angina have an 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 cardiac
output is compromised. Tachycardia also
develops in response to sympathetic stimulation
and may be sustained as a compensatory
 Nursing Interventions
Stay with patient who is experiencing pain or
appears anxious.
Maintain quiet, comfortable environment.
Restrict visitors as necessary.
Provide light meals. Have patient rest for 1 hr
after meals.
Provide supplemental oxygen as indicated.
Administer antianginal medication(s) promptly as indicated:
 Nitroglycerin: sublingual (Nitrostat),
buccal, or oral tablets, metered-dose
spray.
 sublingual isosorbide dinitrate (Isordil)
 Sustained-release tablets,
caplets: (Nitrong, Nitro Cap T.D.),
chewable tablets (Isordil, Sorbitrate),
patches, transmucosal ointment (Nitro-
Dur, Transderm-Nitro)
 Beta-blockers: acebutolol (Sectral),
atenolol (Tenormin), nadolol (Corgard),
metoprolol (Lopressor), propranolol
(Inderal)
 Calcium channel blockers: bepridil
(Vascor), amlodipine (Norvasc),
nifedipine (Procardia), felodipine
(Plendil), isradipine (DynaCirc),
diltiazem (Cardizem)
Rationale
response if cardiac output falls.
Anxiety releases catecholamines, which
increase myocardial workload and can escalate
and/or prolong ischemic pain. Presence of nurse
can reduce feelings of fear and helplessness.
Mental/emotional stress increases myocardial
workload.
Decreases myocardial workload associated with
work of digestion, reducing risk of anginal
attack.
Increases oxygen available for myocardial
uptake and reversal of ischemia.
Nitroglycerin has been the standard for treating
and preventing anginal pain for more than 100
yr. Today it is available in many forms and is
still the cornerstone of antianginal therapy.
Rapid vasodilator effect lasts 10–30 min 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 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.
Reduces angina by reducing the heart’s
workload. Note: Often these drugs alone are
sufficient to relieve angina in less severe
conditions.
Produces relaxation of coronary vascular
smooth muscle; dilates coronary arteries;
decreases peripheral vascular resistance.
 Nursing Interventions
 Analgesics: acetaminophen (Tylenol)
 Morphine sulphate (MS)
Monitor serial ECG changes.
Rationale
Usually sufficient analgesia for relief of
headache caused by dilation of cerebral 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 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 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

Decreased Cardiac Output: Inadequate blood pumped by the heart to meet metabolic demands
of the body.

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.
Monitor vital signs and cardiac rhythm.
Auscultate breath sounds and heart sounds.
Listen for murmurs.
Provide for adequate rest periods. Perform self-
care activities, as indicated.
Stress importance of avoiding straining down, reducing heart rate (bradycardia), which may be
especially during defecation.
Encourage immediate reporting of pain for
prompt administration of medications as
indicated.
Monitor and documents effects or adverse
response to medications, noting BP, heart rate,
and rhythm.
Assess for signs and symptoms of heart failure.
Evaluate mental status, noting development of Reduced perfusion of the brain can produce
confusion, disorientation.
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 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
(especially beta-blockers). Development of
murmurs may reveal a valvular cause for chest
pain (aortic stenosis, mitral stenosis) or
papillary muscle rupture.
Conserves energy, reduces cardiac workload.
Valsalva maneuver causes vagal stimulation,
followed by rebound tachycardia, both of which
may impair cardiac output.
Timely interventions can reduce oxygen
consumption and myocardial workload and may
minimize cardiac complications.
Desired effect is to decrease myocardial oxygen
demand by decreasing ventricular 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
pathology causing myocardial ischemia.
Disease may compromise cardiac function to
point of decompensation.
observable changes in sensorium.
 Nursing Interventions
Note skin color and presence and quality of
pulses.
Administer supplemental oxygen as needed.
Monitor pulse oximetry or ABGs as indicated.
Measure cardiac output and other functional
parameters as indicated.
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),
These medications decrease cardiac workload
nadolol (Corgard), propranolol (Inderal),
by reducing heart rate and systolic BP. Note:
esmolol (Brevibloc);
Overdosage produces cardiac decompensation.
 Acetylsalicylic acid (ASA), other
antiplatelet agents: ticlopidine (Ticlid);
glycoprotein IIb/IIa, abciximab
(ReoPro), eptifibatide (Integrilin)
 IV heparin
Rationale
Peripheral circulation is reduced when cardiac
output falls, giving the skin a pale or gray color
(depending on level of hypoxia) and
diminishing the strength of peripheral pulses.
Increases oxygen available for myocardial
uptake to improve contractility, reduce
ischemia, and reduce lactic acid levels.
Determines adequacy of respiratory function
and/or O2 therapy.
Cardiac index, preload/afterload, contractility,
and cardiac work can be measured
noninvasively through various means, including
thoracic electrical bioimpedance (TEB)
technique. Useful in 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 patient’s circadian
hemodynamic variability.
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.
Useful in unstable angina, ASA diminishes
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.
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 high-risk unstable angina. Note:
Use of low-molecular-weight heparin is
 Nursing Interventions
Monitor laboratory studies: PTT, aPTT.
Discuss purpose and prepare for stress testing
and cardiac catheterization, when indicated.
Prepare for surgical intervention, angioplasty
with/without intracoronary stent placement,
valve replacement, CABG, if indicated.
Prepare for transfer to critical care unit if
condition warrants.
https://nurseslabs.com/4-angina-coronary-artery-disease-nursing-care-plans/4/
Rationale
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.
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 artery and improve the odds of
long-term patency. This procedure is preferred
over the more invasive CABG surgery. CABG
is 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.
Prolonged chest pain with decreased cardiac
output reflects development of complications
requiring more emergency interventions.