1) Coronary artery disease, including conditions like atherosclerosis, angina, acute coronary syndrome, and myocardial infarction, involve a reduction in blood flow to the heart muscles. 2) Atherosclerosis is a buildup of plaque in the coronary arteries that can restrict blood flow. Myocardial infarction occurs when an artery is completely blocked, killing a section of heart muscle. 3) Risk factors include age, family history, smoking, lack of exercise, obesity, high cholesterol, and conditions like hypertension and diabetes. Chest pain and other symptoms depend on the specific condition. Diagnosis involves electrocardiograms, cardiac enzyme tests, and other exams. Treatment focuses on restoring blood flow, reducing risk factors,

1. TAMANNA INSTITUTE OF ALLIED
HEALTH SCIENCES
PRESENTED BY
MS. JYOTI SHRIVASTAVA
ASSISTANT LECTURER, TIAHS
SUBJECT: MEDICAL-SURGICAL NURSING-II
TOPIC: CORONARY ARTERY DISEASE

2. CORONARY ARTERY DISEASE

3. INTRODUCTION
• Coronary artery disease is the most prevalent type of
cardiovascular disease in adults. It include group of
disorder that are related to coronary artery, an artery that
supply oxygenated blood to the heart muscles it self.
• CORONARYARTERY DISEASE include:
Coronary atherosclerosis
Angina pectoris
Acute coronary syndrome
Myocardial infarction

4. DEFINITION
• Atherosclerosis, an abnormal accumulation of lipid or fat and
fibrous tissue in the lining of arterial blood vessel walls. These
substance block and narrow the coronary vessels in a way that
reduces blood flow to the myocardium.
• Atherosclerosis involves a repetitious inflammatory response
to injury of the artery well and subsequent in the structural and
biochemical properties of the arterial walls.

5. CORONARY ATHEROSCLEROSIS

6. RISK FACTORS
NON MODIFIABLE
RISK FACTORS
• Age
• Gender
• Family history
MODIFIABLE RISK FACTORS
• Smoking
• Lack of exercise (sedentary lifestyle)
• Stress
• obesity
• High dietary fat
• Elevated serum cholesterol level (low
density lipoprotein) known as bad
cholesterol also called hyperlipidemia
• Alcohol consumption
• HTN and DM
• Metabolic syndrome

7. PATHOPHYSIOLOGY
• Atherosclerosis is thought to begin as fatty streaks of lipids that are deposited in
intima of arterial wall.
• These lesions commonly begin early in life. Genetics and environmental factors
are involved in the progression of lesions.
• The development of atherosclerosis over many years involves an inflammatory
response, which begins with injury to the vascular endothelium.
• The injury may be initiated by smoking, hypertension, and other factors.
• The presence of inflammatory cells, such as Monocytes (macrophages). The
macrophages ingest lipids, becoming “foam cells” that transport the lipids into
the arterial wall.
• Activated macrophages also release biochemical substances that can further
damage the endothelium, attracting platelets and initiating clotting.

8. • Smooth muscle cells within the vessel wall subsequently proliferate and for a fibrous cap over
a core filled with lipid and inflammatory infiltrate. These deposits, called ATHEROMAS or
PLAQUES, protrude into lumen of the vessel, narrowing it and obstructing blood flow.
• Plaque may be stable or unstable, depending on the degree of inflammation and thickness of
the fibrous cap.
• If the fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can
resist the stress of blood flow and vessel movement. If the cap is thin and inflammation is
ongoing, the lesion becomes what is called the vulnerable plaque.
• At this point, the lipid core may grow, causing it to rupture and hemorrhage into the plaque. A
ruptured plaque is a focus for thrombus formation. The thrombus may then obstruct blood
flow, leading to ACUTE CORONARY SYNDROME (ACS), which may result in
MYOCARDIAL INFARCTION (MI) if quick action is not taken.

10. CLINICAL MANIFESTAIONS
• Chest pain (angina
pectoris)
• Acute coronary
syndrome
• Myocardial infarction
• Diaphoresis
• ECG changes
• Dysrhythmias
• Chest heaviness
• Dyspnea
• fatigue

11. ANGINA PECTORIS

12. INTRODUCTION
• Angina pectoris is a clinical syndrome which is
characterized by episodes of pain or pressure in the
anterior chest. The cause is insufficient coronary
blood flow, resulting in a decreased oxygen supply
when there is increased myocardial demand for
oxygen in response to the need for oxygen exceeds
the supply.

13. DEFINITION
• Angina is not a disease, but is a symptom of impending
coronary artery disease condition marked by severe pain in the
chest, often also spreading to the shoulders, arms, and neck,
owing to an inadequate blood supply to the heart.
• NOTE: Chest pain may be accompanied by other symptoms
(such as nausea, shortness of breath, or pain in the neck,
shoulder, jaw, arm, or back). Angina pectoris typically occurs
concurrently with coronary heart disease and is often
precipitated by physical exertion or emotional stress.

14. TYPES OF ANGINA
ANGINA
STABLE ANGINA
UNSTABLE ANGINA
INTRACTABLE OR REFRECTORY
ANGINA
VARIANT ANGINA
SILENT ISCHEMIA

15. Continue…..
STABLE ANGINA
• Predictable and consistent pain that occurs on exertion and is relieved by rest and
nitroglycerin (vasodilator).
UNSTABLE ANGINA
• Also called pre-infarction angina or (crescendo angina): symptoms increase in frequency and
severity; may not be relieved with rest or nitroglycerin. In this there is reduced blood flow in a
coronary artery, often due to rupture of an atherosclerotic plaque, but the artery is not
completely occluded. This is an acute situation that sometimes referred to as preinfarction
angina because patient will likely have an MI if prompt intervention do not occur.
INTRACTABLE OR REFRACTORYANGINA
• Severe incapacitating chest pain.
SILENT ISCHEMIA
• Objective evidence of ischemia (such as ECG changes, with a stress test) but patient reports
no pain.

16. CLINICAL MANIFESTATION
• Produce pain or other symptoms, varying in severity from mild
indigestion to a choking or heavy sensation in the upper chest that
ranges from discomfort to agonizing pain accompanied by severe
apprehension (anxiety/feeling of uneasiness) and feeling of
impending death.
• The pain is often felt deep in the chest behind the sternum
(retrosternal chest pain)
• The pain or discomfort is poorly located and may radiate to the
neck, jaw, shoulders, and inner aspects of the upper arm, usually left
arm. The patient often feels tightness or heavy choking or strangling
sensation that has a viselike (tight and firm like screw), insistent
quality.

17. A feeling of weakness or
numbness in the arms,
wrists, and hands as well as
shortness of breath, pallor,
diaphoresis, dizziness or
lightheadedness and nausea
and vomiting may
accompany with the pain.
ANGINA PECTORIS

19. DIAGNOSTIC TESTS
DIAGNOSTIC
HISTORY RELATED TO CLINICAL MANIFESTATION
A 12 LEAD ECG
MAY SHOW
CHANGES
INDICATIVE OF
ISCHEMIA SUCH AS
T-WAVE INVERSION
LAB TEST INCLUDE CRPAND
CARDIAC BIOMARKERS
PHARMACOLOGIC STESS TEST
IVASIVE PROCEDURES

20. MEDICAL MANAGEMENT
MEDICATION ACTION
1. NITRATES: Nitroglycerin, iso-sorbite
dinitrate,
1. VASODILATOR: relaxes veins when given
in small doses and relaxes arteries when
given in large doses.
2. BETA BLOCKER: metaprolol, atenolol 2. Blocks beta receptors and reduces myocardial
oxygen consumption.
3. CALCIUM CHANNEL BLOCKER:
Amplodipine, diltiazem
3. NEGATIVE INOTROP: used for
vasospasm, given in patients who do not
response to the beta- blocker.
4. ANTI-PLATELET: aspirin, clopidogrel, 4. Prevention of platelet aggregation.
5. ANTICOAGULANT: fractionated heparin
and unfractionated heparin (LMWH:
Enoxaparin, daltaparine)
5. Prevention of thrombus formation

21. ASSESSING ANGINA
• ASK FOR THE FOLLOWING:
1. “where is the pain (or prodomal symptoms)? Can you point to it?”
2. “can you feel the pain anywhere else?”
3. “how would you describe the pain?”
4. “is it like the pain you had before?”
5. “can you rate the pain on a 0-10 scale, with 10 being the most pain?”
6. “when did the pain begin?”
7. “How long does it lasts?”
8. “What brings on the pain?”
9. “What helps the pain to go away?”
10. “Do you have any other symptoms with the pain?”

22. ACUTE CORONARY SYNDROME AND
MYOCARDIAL INFARCTION

23. ACUTE CORONARY SYNDROME AND
MYOCARDIAL INFARCTION
• ACS is an emergent situation characterized by an acute
onset of myocardial ischemia that results in myocardial
death (i.e. MI) if definitive interventions do not occur
promptly. (Although the terms coronary occlusion, heart
attack, and MI are used synonymously, the preferred term
is MI). The spectrum of ACS includes unstable angina,
Non ST-segment elevation MI (NSETMI) and ST-
segment elevation MI (STEMI).

24. MYOCARDIAL INFARCTION
INTRODUCTION
• MI results from occlusion of one
of the coronary arteries which
stem from:
1. Atherosclerosis
2. Coronary thrombosis/ embolism
3. Platelet aggregation
4. Coronary artery stenosis/ spasm
5. Decreased blood flow with
shock and hemorrhage
6. Direct trauma

25. DEFINITION
• MI can be defined as the area of the myocardium is
permanently destroyed, typically because plaque rupture and
subsequent thrombus formation result in complete occlusion of
the artery.
• Vasospasm (sudden constriction or narrowing) of a coronary
artery , decrease oxygen supply (e.g. from acute blood loss,
anemia, or low blood pressure) and increased demand for
oxygen (e.g. from rapid heart rate, thyrotoxicosis or ingestion
of cocaine are other causes of MI).
• In each case a profound imbalance exist between myocardium
oxygen supply and demand.

26. Continue…..
• The area of infarction
develops over minutes to
hours. As the cells are
deprived of oxygen,
ischemia develops,
cellular injury occurs and
the lack of oxygen results
in infarction or death of
cells.

27. 3 AREAS WHICH DEVELOP IN
MYOCARDIAL IFARCTION
MYOCARDIAL
INFARCTION
ZONE OF INFARCTION
ZONE OF INJURYZONE OF ISCHEMIA

28. AREAS OF INVOLVEMENT

29. CLASSIFICATION OF MYOCARDIAL
INFARCTION
MYOCARDIAL INFARCTION
ANATOMIC CLASSIFICATION DIAGNOSTIC CALSSIFICATION
•TRANSMURAL INFARCTION
•SUB ADENOCARDIAL INFARCTION
•INTRAMURAL INFARCTION
•ST-SEGMENT ELEVATION
MYOCARDIAL INFARCTIONC(STEMI)
• NON ST-SEGMENT ELEVATION
MYOCARDIAL INFARCTION(NSTEMI)

30. ANATOMIC MYOCARDIAL
INFARCTION
TRANSMURAL INFARCTION
• The zone of infarction extend from endocardium to
epicardium.
SUBADENOCARDIAL INFARCTION
• The zone of infarction in limited to endocardial muscles.
INTRAMURAL INFARCTION
• Seen in patchy areas of the myocardium, equally
associated with angina pectoris.

31. DIAGNOSTIC MYOCARDIAL
INFARCTION
MYOCARDIAL INFARCTION
ST-SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
NON ST-SEGMENT ELEVATION
MYOCARDIAL INFARCTION

32. ST- SEGMENT ELEVATION MYOCARDIAL
INFARCTION
• ST- Segment Elevation
• T- wave inversion
• Q- wave development
• Severe enzyme
elevation
• Reciprocals

33. NON ST-SEGMENT ELEVATION MYOCARDIAL
INFARCTION
• ST-Segment depression
• T- wave changes
• No Q-wave
development
• Mild enzyme elevation
• No reciprocals

34. PATHOPHYSIOLOGY OF MYOCARDIAL
INFARCTION
DUE TO PREDISPOSING RISK FACTORS
PREMATURE, ACCELARATED ATHEROSCLEROSIS
PROGRESSIVE
NARROWING OF BLOOD
VESSELS
RISK FOR EXCESSIVE
BLOOD CLOT
FORMATION

35. ISCHEMIA OF
HEART MUSCLE
THROMBOEMBOLISM
HYPOXIA
NECROSIS

36. AEROBIC TO
UNAROBIC
METABOLISM
RELEASE OF
LYSOZOMAL
ENZYMES
DECREASED
MYOCARDIAL
CONTRACTILITY
LACTIC ACID
FORMATION
ALTERED
DEPOLARIZATION
DECREASED
CARDIAC
OUTPUT

37. CHEST PAIN AND
MUSCLE SPASM
RENAL ISCHEMIA
AND OLIGURIA
ALTERED
REPOLARIZATION
MYOCARDIAL
INFARCTION

38. CLINICAL MANIFESTATIONS
CARDIOVASCULAR
• Chest pain or discomfort not relieved by rest or nitroglycerine, palpitations.
Heart sounds may include S3, S, and new onset of murmur.
• Increased jugular venous distension may be seen if the MI has caused heart
failure.
• Blood pressure may be elevated because of sympathetic stimulation or
decreased because of decreased contractility, impending Cardiogenic shock
or medications.
• Irregular pulse may indicate atrial fibrillation.
• In addition to ST- segment and T-wave changes, ECG may show
Tachycardia, Bradycardia or other Dysrhythmias.

39. Continue….
RESPIRATORY
• Shortness of breath, Dyspnea, Tachypnea, and crackles if mi has caused pulmonary congestion. Pulmonary
edema may be present.
GASTROINTESTINAL
• Nausea and Vomiting
GENITOURINARY
• Decreased urinary output (oliguria) may indicate Cardiogenic shock.
SKIN
• Cool, clammy, diaphoretic and pale appearance due to sympathetic stimulation may indicate Cardiogenic
shock.
NEUROLOGIC
• Anxiety, restlessness and lightheadedness may indicate increased sympathetic stimulation or a decrease in
contractility and cerebral oxygenation. The same symptoms may also herald Cardiogenic shock.
PSYCHOLOGICAL
• Fear with feeling of impeding doom, or denial that anything is wrong.

40. DIAGNOSTIC TEST
1.PATIENT HISTORY
• Ask the patient regarding characteristics of pain and other sign and symptoms.
• History of previous cardiac and other illness.
• Family history of heart disease
• Ask patient’s life style and history regarding risk factors of MI.
2.ELECTROCARDIOGRAM
• Classic T-wave inversion, Q-wave development, ST-segment elevation.
3.ECHOCARDIOGRAM
• The echocardiogram is used to evaluate ventricular function. It may be used to
assist in diagnosing an MI, especially when ECG is non-diagnostic. The
echocardiogram can detect hypo kinetic and a kinetic wall motion and determine
the ejection fraction.

41. Continue….
4. LABORATORY TESTS
• This test include
measurement of cardiac
biomarkers and cardiac
enzymes. Such as creatine
kinase and isoenzymes
(CK-MB, CK-BB, CK-
MM).

42. Continue….

43. MEDICAL MANAGEMENT
EMERGENCY MEDICAL
MANAGEMENT OF MI
MONA
• M: MORPHINE
SULPHATE
• O: OXYGENATION
• N: NITROGLYCERINE
• A: ASPIRIN

44. LONG TERM TREATMENT OF MI
1. FIBRINOLYTIC DRUGS
• Fibrinolytic drugs act as thrombolytic
by activating plasminogen to form
plasmin, which degrades fibrin and so
breaks up the thrombi. Such as
Streptokinase
2. ANTIPLATELET AGENT
• Long-term low-dose aspirin reduces
overall mortality, non-fatal re-
infarction, non-fatal stroke and
vascular death.
• Clopidogrel, in combination with low-
dose aspirin

45. Continue….
3.BETA-BLOCKERS
• When started within hours of
infarction, beta-blockers reduce
mortality, non-fatal cardiac arrest
and non-fatal re-infarction. Such
as atenolol, metaprolol,
4.CALCIUM-CHANNEL
BLOCKERS
• diltiazem or verapamil can be
used if a beta-blocker cannot be
used but diltiazem and verapamil
are contra-indicated in patients
with left ventricular dysfunction.
5.ANGIOTENSIN-CONVERTING
ENZYME (ACE) INHIBITORS
• These reduce mortality whether or not
patients have clinical heart failure or
left ventricular dysfunction. They also
reduce the risk of non-fatal heart
failure. Such as enalpril
6.CHOLESTEROL-LOWERING
AGENTS
• Ideally, initiate therapy with a statin
as soon as possible for all patients
with evidence of cardiovascular
disease (CVD) unless contra-
indicated. E.g. Atorvastatin

46. SURGICAL MANAGEMENT OF MI
SURGICAL
MANAGEMENT
ANGIOPLASTY
CABGSTENTS

47. ANGIOLPLASTY
• Angioplasty, also known as balloon
angioplasty and percutaneous transluminal
angioplasty (PTA), is a minimally invasive,
endovascular procedure to widen narrowed or
obstructed arteries or veins, typically to treat
arterial atherosclerosis. A deflated balloon
attached to a catheter (a balloon catheter) is
passed over a guide-wire into the narrowed
vessel and then inflated to a fixed size. The
balloon forces expansion of the blood vessel
and the surrounding muscular wall, allowing
an improved blood flow. A stent may be
inserted at the time of ballooning to ensure
the vessel remains open, and the balloon is
then deflated and withdrawn. Angioplasty has
come to include all manner of vascular
interventions that are typically performed
percutaneously

48. CORONARYARTERY BYPASS GRAFTING
(CABG)
• Coronary artery bypass
surgery, also known as coronary
artery bypass graft (CABG,
pronounced "cabbage") surgery,
and colloquially heart bypass or
bypass surgery, is a surgical
procedure to restore normal blood
flow to an obstructed coronary
artery. A normal coronary artery
transports blood to and from the
heart muscle itself, not through
the main circulatory system.

49. STENT
• A stent is a metal or plastic tube
inserted into the lumen of an
anatomic vessel or duct to keep the
passageway open, and stunting is the
placement of a stent.
• Coronary stents are placed during a
coronary angioplasty. The most
common use for coronary stents is in
the coronary arteries, into which a
bare-metal stent, a drug-eluting stent,
a bioabsorbable stent, a dual-therapy
stent (combination of both drug and
bioengineered stent), or occasionally
a covered stent is inserted.

50. NURSING MANAGEMENT
ASSESSMENT
 Assess for the general condition of the client.
 Assess for the pain: location, intensity, frequency.
 Assess for the level of pain on analogue pain scale.
 Assess for other signs and symptoms with pain.
 Assess for lab investigation for CRP and cardiac
biomarkers (CK-MB, CK-BB, CK-MM)

51. NURSING DIAGNOSIS
1.Acute Pain related to Decreased myocardial blood flow
and Increased cardiac workload/oxygen consumption
possibly evidenced by client’s verbalization, distraction
of behaviors such as crying, restlessness
• GOAL: 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.

52. NURSING INTERVENTIONS RATIONALE
•Identify precipitating event, if any: frequency, duration, intensity, and
location of pain.
•Helps differentiate this chest pain, and aids in evaluating possible
progression to unstable angina.
•Observe for associated symptoms: Dyspnea, nausea and vomiting,
dizziness, palpitations, desire to maturate.
•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.
•Evaluate reports of pain in jaw, neck, shoulder, arm, or hand (typically on
left side).
•Cardiac pain may radiate. Pain is often referred to more superficial sites
served by the same spinal cord nerve level.
•Place patient at complete rest during anginal episodes. •Reduces myocardial oxygen demand to minimize risk of tissue injury.
•Elevate head of bed if patient is short of breath. •Facilitates gas exchange to decrease hypoxia and resultant shortness of
breath.
•Monitor heart rate and rhythm. •Patients with unstable angina have an increased risk of acute life-
threatening dysrhythmias, which occur in response to ischemic changes
and/or stress.
•Monitor vital signs every 5 min during initial anginal attack. •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 response if
cardiac output falls.

53. Continue….
•Stay with patient who is experiencing pain or appears
anxious.
•Anxiety releases catecholamine, which 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. Restrict
visitors as necessary.
•Mental/emotional stress increases 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.
•Provide supplemental oxygen as indicated. •Increases oxygen available for myocardial uptake and
reversal of ischemia.
•Administer nitroglycerine sublingually as prescribed
by doctor.
•Act as vasodilator to reduce preload.
•Administer analgesic morphine sulphate,
acetaminophen.
•Alleviate pain

54. Continue….
2. Acute Anxiety related to anticipated death Possibly evidenced
by Apprehension, uncertainty, restlessness
• GOAL: To reduce anxiety and help client to Verbalize
awareness of feelings of anxiety and healthy ways to deal with
them.
INTERVENTION RATIONALE
•Assess the general condition of the client,
well being, appearance and feelings.
•To get the base the line data and plan for
intervention.
•Explain purpose of tests and procedures:
stress testing.
•Reduces anxiety attributable to fear of
unknown diagnosis and prognosis.

55. •INTERVENTION •RATIONALE
•Promote expression of feelings and fears.
Let patient/SO know these are normal
reactions.
•Verbalization of concerns reduces
tension, verifies level of coping, and
facilitates dealing with feelings.
•Encourage family and friends to treat
patient as before.
•Reassures patient that role in the family
and business has not been altered.
•Tell patient the medical regimen has been
designed to limit future attacks and
increase cardiac stability.
•Encourages patient to test symptom
control, to increase confidence in medical
program, and to integrate abilities into
perceptions of self.
•Administer sedatives, tranquilizers, as
prescribed by the physician
•May be desired to help patient relax until
physically able to reestablish adequate
coping strategies.

56. 3. Risk for Decreased Cardiac Output may be related to
blockage of the major coronary artery possibly evidenced
by Inotropic changes (transient/prolonged myocardial
ischemia) and Alterations in rate/rhythm and electrical
conduction.
• GOAL: Report/display decreased episodes of Dyspnea,
angina, and dysrhythmias.
• Demonstrate increased activity tolerance.
• Participate in behaviors/activities that reduce the
workload of the heart.
Continue….

57. •INTERVENTION •RATIONALE
•Assess the general condition of the client. •To get the baseline data and for planning.
•Maintain bed or chair rest in position of comfort during
acute episodes.
•Decreases oxygen demand therefore reducing myocardial
workload and risk of decompensation.
•Monitor vital signs and cardiac rhythm. •Tachycardia may be present because of pain, anxiety,
hypoxemia, and reduced cardiac output.
•Auscultate breath sounds and heart sounds. Listen for
murmurs.
•S3, S4, or crackles can occur with cardiac decompensation.
•Provide for adequate rest periods. Perform self-care
activities, as indicated.
•Conserves energy, reduces cardiac workload.
•Stress importance of avoiding straining down, especially
during defecation.
•Valsalva maneuver causes vagal stimulation, reducing
heart rate (Bradycardia), which may be followed by
rebound tachycardia, both of which may impair cardiac
output.

58. •Encourage immediate reporting of pain for
prompt administration of medications as
indicated.
•Timely interventions can reduce oxygen
consumption and myocardial workload and
may minimize cardiac complications.
•Assess for signs and symptoms of heart
failure.
•Angina is only a symptom of underlying
pathology causing myocardial ischemia.
Disease may compromise cardiac function to
point of decompensation.
•Administer supplemental oxygen as needed. •Increases oxygen available for myocardial
uptake to improve contractility, reduce
ischemia, and reduce lactic acid levels.
•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
indicated.
•Determines adequacy of respiratory
function and/or O2 therapy.

59. Continue….
• Administer medications as indicated: Calcium channel blockers: diltiazem,
nifedipine, verapamil, Amplodipine
• 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.
• Beta-blockers: atenolol , nadolol, Propranolol (Inderal), esmolol
• These medications decrease cardiac workload by reducing heart rate and systolic
BP. Note: Overdosage produces cardiac decompensation.
• Acetylsalicylic acid (ASA), other Antiplatelet agents: ticlopidine , eptifibatide
(Integrilin)
• 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.

60. Continue….
4. Risk for Ineffective Tissue Perfusion may be related to
Reduction/interruption of blood flow, e.g.,
vasoconstriction, hypovolemia/shunting, and
thromboembolic formation
• GOAL: Demonstrate adequate perfusion as individually
appropriate, e.g., skin warm and dry, peripheral pulses
present/strong, vital signs within patient’s normal range,
patient alert/oriented, balanced I&O, absence of edema,
free of pain/discomfort.

61. •NURSING INTERVENTIONS
•RATIONALE
•Investigate sudden changes or continued alterations in mentation
(changes in LOC, mentation, stupor).
•Cerebral perfusion is directly related to cardiac output and is also
influenced by electrolyte and/or acid-base variations, hypoxia, and
systemic emboli.
•Inspect for pallor, cyanosis, mottling, cool and clammy skin. Note
strength of peripheral pulses.
•Systemic vasoconstriction resulting from diminished cardiac output
may be evidenced by decreased skin perfusion and diminished
pulses.
•Monitor respirations, note work of breathing. •Cardiac pump failure and/or ischemic pain may precipitate
respiratory distress; however, sudden or continued Dyspnea may
indicate thromboembolic pulmonary complications.
•Monitor intake, note changes in urine output. Record urine specific
gravity as indicated.
•Decreased intake or persistent nausea may result in reduced
circulating volume, which negatively affects perfusion and organ
function. Specific gravity measurements reflect hydration status and
renal function.
•Monitor laboratory data: ABGs, BUN, creatinine, electrolytes,
coagulation studies (PT, aPTT, clotting times).
•Indicators of organ perfusion and function. Abnormalities in
coagulation may occur as a result of therapeutic measures.
•Administer medications as indicated:
•Antiplatelet agents: aspirin, abciximab, clopidogrel.
•Anticoagulants: heparin or Enoxaparin
•To relieve sign and symptoms.

62. Continue….
5.Risk for imbalanced Fluid Volume: more than body
requirement may related to Decreased organ perfusion
(renal), Increased sodium/water retention, Increased
hydrostatic pressure or decreased plasma proteins.
• GOAL: Maintain fluid balance as evidenced by BP
within patient’s normal limits.
• Be free of peripheral/venous distension and dependent
edema, with lungs clear and weight stable.

63. •NURSING INTERVENTIONS •RATIONALE
•Auscultate breath sounds for presence of
crackles.
•May indicate pulmonary edema secondary to
cardiac decompensation.
•Note JVD, development of dependent edema. •Suggests developing congestive heart failure
or fluid volume excess.
•Measure I&O, noting decrease in output,
concentrated appearance. Calculate fluid balance.
•Decreased cardiac output results in impaired
kidney perfusion, sodium and water retention, and
reduced urine output.
•Weigh daily. •Sudden changes in weight reflect alterations
in fluid balance.
•Maintain total fluid intake at 2000 mL/24 hr
within cardiovascular tolerance.
•Meets normal adult body fluid requirements, but
may require alteration or restriction in presence of
cardiac decompensation.
•Provide low-sodium diet/beverages. •Sodium enhances fluid retention and should
therefore be restricted during active MI phase
and/or if heart failure is present.

64. Continue….
•Administer diuretics: Frusemide
(Lasix), spironolactone with
hydrochlorothiazide (Aldactazide),
Hydralazine (Apresoline).
•May be necessary to correct fluid
overload. Drug choice is usually
dependent on acute or chronic nature of
symptoms.
•Monitor potassium as indicated. •Hypokalemia can limit effectiveness of
therapy and can occur with use of
potassium-depleting diuretics.

65. Continue….
6.Activity Intolerance may be related to Imbalance between
myocardial oxygen supply and demand, Presence of
ischemic/necrotic myocardial tissues, Cardiac depressant
effects of certain drugs (beta-blockers, antiarrhythmics)
Possibly evidenced by Alterations in heart rate and BP with
activity, Development of dysrhythmias, Changes in skin
color/moisture, Exertional angina, Generalized weakness
• GOAL: Demonstrate measurable/progressive increase in
tolerance for activity with heart rate/rhythm and BP within
patient’s normal limits and skin warm, pink, dry.
• Report absence of angina with activity.

66. •NURSING
INTERVENTIONS
•RATIONALE
•Document heart rate and rhythm and changes
in BP before, during, and after activity.
Correlate with reports of chest pain or
shortness of breath.
•Trends determine patient’s response to
activity and may indicate myocardial oxygen
deprivation that may require decrease in
activity level and/or return to bed rest,
changes in medication regimen, or use of
supplemental oxygen.
•Encourage rest initially. Thereafter, limit
activity on basis of pain and/or adverse
cardiac response. Provide non-stress
diversional activities.
•Reduces myocardial workload and oxygen
consumption, reducing risk of complications.
•Instruct patient to avoid increasing
abdominal pressure (straining during
defecation).
•Activities that require holding the breath and
bearing down (Valsalva maneuver) can result in
Bradycardia (temporarily reduced cardiac output)
and rebound tachycardia with elevated BP.

67. •Activities that require holding the breath
and bearing down (Valsalva maneuver) can
result in Bradycardia (temporarily reduced
cardiac output) and rebound tachycardia
with elevated BP.
•Progressive activity provides a controlled
demand on the heart, increasing strength
and preventing overexertion.
•Review signs and symptoms reflecting
intolerance of present activity level or
requiring notification of nurse or physician.
•Palpitations, pulse irregularities,
development of chest pain, or Dyspnea
may indicate need for changes in exercise
regimen or medication.
•Refer to cardiac rehabilitation program. •Provides continued support and/or
additional supervision and participation in
recovery and wellness process.

68. Continue….
7.Deficient Knowledge May be related to Lack of
information/misunderstanding of medical condition/therapy needs,
Unfamiliarity with information resources, Lack of recall Possibly
evidenced by Questions; statement of misconception, Failure to
improve on previous regimen, Development of preventable
complications
• GOAL: Verbalize understanding of therapeutic regimen.
• List desired action and possible adverse side effects of medications.
• Correctly perform necessary procedures and explain reasons for
actions.

69. •NURSING
INTERVENTIONS
•RATIONALE
•Assess patient or SO level of knowledge
and ability and desire to learn.
•Necessary for creation of individual
instruction plan.
•Be alert to signs of avoidance (changing
subject away from information being
presented or extremes of behavior).
•Reinforces expectation that this will be a
“learning experience.” Verbalization
identifies misunderstandings and allows
for clarification.
•Present information in varied learning
formats: programmed books, audiovisual
tapes, question and answer sessions,
group activities.
•Natural defense mechanisms, such as
anger or denial of significance of
situation, can block learning, affecting
patient’s response and ability to
assimilate information.

70. •Reinforce explanations of risk factors, dietary
and/or activity restrictions, medications, and
symptoms requiring immediate medical attention.
•Using multiple learning methods enhances
retention of material.
•Encourage identification and reduction of
individual risk factors (smoking/alcohol
consumption, obesity).
•Provides opportunity for patient to retain
information and to assume control and participate
in rehabilitation program.
•Warn against isometric activity, Valsalva maneuver,
and activities requiring arms positioned above
head.
•These behaviors and chemicals have direct adverse
effects on cardiovascular function and may impede
recovery, increase risk for complications.
•Stress importance of follow-up care, and identify
community resources and support groups.
•Reinforces that this is an ongoing and continuing
health problem for which support and assistance is
available after discharge.
•Emphasize importance of contacting physician if
chest pain, change in anginal pattern, or other
symptoms recur.
•Timely evaluation and intervention may prevent
complications.
•Encourage patient and SO to share concern and
feelings.
•Depressed patients have a greater risk of dying 6–
18 mo following a heart attack.