Cardiac

Failures and
Myocardial
Infarction
 What is Cardiac Failure?
 Cardiac failure/Heart failure is a clinical syndrome resulting from structural or functional
cardiac disorders that impair the ability of the ventricles to fill or eject blood. Although CF can
affect people of all ages, It is most common in people older than 75 years.
 In the past, CF was often referred to as congestive heart failure(CHF)or Chronic heart failure,
because many patients experience pulmonary or peripheral congestion with edema. Currently,
CF is recognized as a clinical syndrome characterized by signs and symptoms of fluid overload
or inadequate tissue perfusion.
 The term cardiac failure indicates myocardial disease in which impaired contraction of the
heart(systolic dysfunction) or filling of the heart(diastolic dysfunction) may cause pulmonary
or systemic congestion.
 Two major types of Cardiac failure:

1. Systolic Cardiac failure – The most common type and alteration in ventricular contraction,
which is characterized by a weakened heart muscle.

2. Diastolic Cardiac failure – Which is characterized by a stiff and noncompliant heart muscle,
making it difficult for the ventricle to fill.
Other types are:
1. Left-Sided Heart Failure – Pulmonary congestion occurs when the left ventricle cannot effectively pump
blood out of the ventricle into the aorta and the systemic circulation. The increased left ventricular end-
diastolic blood volume increases the left ventricular end-diastolic pressure, which decreases blood flow
from the left atrium into the left ventricle during diastole. The blood volume and pressure build up in the
left atrium, decreasing flow through the pulmonary veins into the left atrium. Pulmonary venous blood
volume and pressure increase in the lungs, forcing fluid from the pulmonary capillaries into the pulmonary
tissues and alveoli, causing pulmonary interstitial edema and impaired gas exchange.
The Clinical Manifestations:
 Cough
 Dyspnea
 Pulmonary crackles
 Low oxygen levels
 Orthopnea
 An extra heart sound, the S3, or ventricular gallop upon auscultation
2. Right-Sided Heart Failure – When the right ventricle fails, congestion in the peripheral tissues and the
viscera predominates. This occurs because the right side of the heart cannot eject blood effectively and
can not accommodate all of the blood that normally returns to it from the venous circulation. Increased
venous pressure leads to jugular venous distention(JVD) and increased capillary hydrostatic pressure
throughout the venous system.

The Clinical Manifestations:

 Edema of the lower extremities(dependent edema)
 Hepatomegaly
 Ascites
 Weight gain due to retention of fluid
Cardiac Failure Clinical Manifestations:
 Congestion:
1. Dyspnea
2. Orthopnea
3. Paroxysmal Nocturnal Dyspnea
4. Cough (recumbent or exertional)
5. Pulmonary crackles that do not clear with cough
6. Weight gain(rapid)
7. Dependent edema
8. Abdominal bloating or discomfort
9. Ascites
10. Jugular venous distention
11. Sleep Disturbance(anxiety or air hunger)
12. Fatigue
 Poor Perfusion/Low Cardiac Output:
1. Decreased exercise tolerance
2. Muscle wasting or weakness
3. Anorexia or nausea
4. Unexplained weight loss
5. Lightheadedness or dizziness
6. Unexplained confusion or altered mental status
7. Resting tachycardia
8. Daytime oliguria with recumbent nocturia
9. Cool or vasoconstricted extremities
10. Pallor or cyanosis
DIAGNOSTIC TESTS:

• Blood tests. Your doctor may take a blood sample to look for signs of diseases that can affect the heart. He or she
may also check for a chemical called N-terminal pro-B-type natriuretic peptide (NT-proBNP) if your diagnosis
isn't certain after other tests.
• Chest X-ray. X-ray images help your doctor see the condition of your lungs and heart. Your doctor can also use
an X-ray to diagnose conditions other than heart failure that may explain your signs and symptoms.
• Electrocardiogram (ECG). This test records the electrical activity of your heart through electrodes attached to
your skin. It helps your doctor diagnose heart rhythm problems and damage to your heart.
• Echocardiogram. An echocardiogram uses sound waves to produce a video image of your heart. This test can
help doctors see the size and shape of your heart along with any abnormalities. An echocardiogram measures your
ejection fraction, an important measurement of how well your heart is pumping, and which is used to help classify
heart failure and guide treatment.
• Stress test. Stress tests measure the health of your heart by how it responds to exertion. You may be asked to
walk on a treadmill while attached to an ECG machine, or you may receive a drug intravenously that stimulates
your heart similar to exercise.
• Sometimes the stress test can be done while wearing a mask that measures the ability of your heart and lungs to
take in oxygen and breathe out carbon dioxide. If your doctor also wants to see images of your heart while you're
exercising, he or she may use imaging techniques to visualize your heart during the test.
• Cardiac computerized tomography (CT) scan. In a cardiac CT scan, you lie on a table inside a doughnut-
shaped machine. An X-ray tube inside the machine rotates around your body and collects images of your heart
and chest.
• Magnetic resonance imaging (MRI). In a cardiac MRI, you lie on a table inside a long tubelike machine that
produces a magnetic field, which aligns atomic particles in some of your cells. Radio waves are broadcast toward
these aligned particles, producing signals that create images of your heart.
• Coronary angiogram. In this test, a thin, flexible tube (catheter) is inserted into a blood vessel at your groin or in
your arm and guided through the aorta into your coronary arteries. A dye injected through the catheter makes the
arteries supplying your heart visible on an X-ray, helping doctors spot blockages.
• Myocardial biopsy. In this test, your doctor inserts a small, flexible biopsy cord into a vein in your neck or groin,
and small pieces of the heart muscle are taken. This test may be performed to diagnose certain types of heart
muscle diseases that cause heart failure.
(New York Heart Association Classification of Cardiac/Heart Failure)

Classifications Signs and Symptoms

I No limitation of physical activity

Ordinary activity does not cause undue fatigue, palpitation, or
dyspnea

II Slight limitation of physical activity

Comfortable at rest, but ordinary physical activity causes
fatigue, palpitation, or dyspnea.

III Marked limitation of physical activity

Comfortable at rest, but less than ordinary activity causes
fatigue, palpitation and dyspnea.

IV Unable to carry out any physical activity without discomfort,

Symptoms of cardiac insufficiency at rest , If any physical is
undertaken, discomfort is increased
 Pathophysiology
 Regardless of the etiology, the pathophysiology of Cardiac failure results in similar
pathophysiologic changes and clinical manifestations. Significant myocardial dysfunction usually
occurs before the patient experiences signs and symptoms of CF such as shortness of breath,
edema, or fatigue.
As CF develops, the body activates neurohormonal compensatory mechanisms. These
mechanisms represent the body’s attempt to cope with the CF and are responsible for the signs and
symptoms that eventually develop. Understanding theses mechanism is important because the
treatment for CF is aimed at opposing them and relieving symptoms.
Systolic CF results in decreased blood ejected from the ventricle. The decreased blood flow is
sensed by baroreceptors in the aortic and carotid bodies. The sympathetic nervous system is then
stimulated to release epinephrine norepinephrine. The purpose of this initial response is to increase
heart rate and contractility and support the failing myocardium, but the continued response has
multiple negative effects. Sympathetic stimulation causes vasoconstriction in the skin, gastrointestinal
tract, and kidneys.
 A decrease in renal perfusion due to low CO and vasoconstriction then causes the release of renin by the
kidneys. Renin converts the plasma protein angiotensinogen to angiotensin I, which then circulates to the
lungs. Angiotensin-converting enzyme(ACE) in the lumen of pulmonary blood vessels converts angiotensin I
to angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and afterload. Angiotensin
II also stimulate the release of aldosterone from the adrenal cortex, resulting in sodium and fluid retention by
the renal tubules and an increase in blood volume. These mechanisms lead to the fluid volume overload
commonly seen in CF. Angiotensin, aldosterone and other neurohormones(e.g.,endothelin) lead to an increase
in preload and afterload, which increases stress on the ventricular wall, causing an increase in cardiac
workload. A counter-regulatory mechanism is attempted through the release of natriuretic peptides. Atrial
natriuretic peptide(ANP) and B-type natriuretic peptide(BNP; brain type) are released from the overdistended
cardiac chambers. These substances promote vasodilation and diuresis. However, their effect is usually not
strong enough to overcome the negative effects of the other mechanisms.
As the heart’s workload increases, contractility of the myocardial muscle fibers decreases. Decreased
contractility results in an increase in end-diastolic blood volume in the ventricle, stretching the myocardial
muscle fibers and increasing the size of the ventricle(ventricular dilation). One way the heart compensates for
the increased workload
Is to increase the thickness of the heart muscle(ventricular hypertrophy). However, hypertrophy results in
abnormal changes in structure and function of myocardial cells, a process known as ventricular remodeling.
Under the influence of neurohormones(e.g.,angiotensin II), enlarged myocardial cells become dysfunctional
and die early(a process called apoptosis), leaving the other normal myocardial cells struggling to maintain CO.
As cardiac cells die and the heart muscle becomes fibrotic, diastolic CF can develop, leading to further
dysfunction. A stiff ventricle resists filling, and less blood in the ventricles causes a further decrease in CO. All
of these compensatory mechanisms of CF have been referred to as the “vicious cycle of CF” because low CO
leads to multiple mechanisms that make the heart work harder, worsening the CF.
 What is the Etiology of Cardiac Failure?

Cardiac Failure can be caused by a number of conditions when patient has:

 Coronary Artery Disease
 Hypertension
 Cardiomyopathy
 Valvular Disorders
 Renal Dysfunction with volume overload
 Diabetes
 Atherosclerosis of the coronary arteries
  MEDICAL MANAGEMENT(Common meds used to treat Cardiac Failure)
MEDICATION THERAPEUTIC EFFECTS KEY NURSING CONSIDERATIONS

Angiotensin-Converting Enzyme Inhibitors BP and afterload Observe for symptomatic hypotension,

Lisinopril (Privinil) Relieves signs and symptoms of CF increased serum K, cough, and worsening
Enalapril (Vasotec) Prevents Progression of CF renal function.

Angiotensin Receptor Blockers BP and afterload Observe for symptomatic hypotension,

Valsartan(Diovan) Relieves signs and symptoms of CF increased serum K, cough, and worsening
Losartan(Cozaar) Prevents Progression of CF renal function.

Hydralazine and Isosorbide Dilates blood vessels Observe for symptomatic hypotension.
Dinitrate(Dilatrate) BP and afterload

Beta-Adrenergic Blocking Agents(B- Dilates blood vessels and afterload Observe for decreased heart rate , symptomatic
Blockers) Signs and Symptoms of CF hypotension, dizziness, and fatigue.
Metoprolol(Lopressor) Improves exercise capacity
Carvedilol(Coreg)
 MEDICATION THERAPEUTIC EFFECTS KEY NURSING CONSIDERATIONS

Diuretics Fluid volume overload Observe for electrolyte abnormalities, renal

Loop Diuretic: Signs and Symptoms of CF dysfunction, diuretic resistance, and decreased
Furosemide(Lasix) BP. Carefully monitor I&O and daily weight.

Thiazide Diuretics:
Metolazone(Zaroxolyn)
Hydrochlorothiazide(HCTZ)
Observe for hyperkalemia, hyponatremia
Aldosterone Antagonist: Improves CF symptoms in advanced CF
Spironolactone(Aldactone)

Digitalis I Improves cardiac contractility Observe for bradycardia and digitalis toxicity
Digoxin(Lanoxin) Signs and Symptoms of CF
 Nutritional Therapy
 Following a low sodium(no more than 2g/day) diet and avoiding excessive fluid intake are usually
recommended.

 Supplemental Oxygen (Additional Therapy)

 Oxygen therapy may become necessary as CF progresses. The need is based on the degree of pulmonary
congestion and resulting hypoxia.
 Some patients require supplemental oxygen only during periods of activity.
 Nursing Process (ADPIE)
 ASSESSMENT
 Nursing assessment for the patient with CF focuses on observation for effectiveness of therapy and for the
patient’s ability to understand and implement self-management strategies
 Health History : focuses on the signs and symptoms of CF, such as dyspnea, fatigue, and edema. Sleep
disturbances, particularly sleep suddenly interrupted by shortness of breath, may be reported.
 Physical Examination : The patient is observed for restlessness and anxiety that might suggest hypoxia from
pulmonary congestion. The patient’s LOC is also evaluated for any changes, as low CO can decrease the flow of
oxygen to the brain.
 Diagnosis
Nursing Diagnosis – Based on the assessment data, major nursing diagnoses may include the ff:
 Activity intolerance related to decreased CO
 Excess fluid volume related to the CF syndrome
 Anxiety-related symptoms related to complexity of the therapeutic regimen
 Powerlessness r/t chronic illness and hospitalization
 Ineffective family therapeutic regimen management
Collaborative Problems/Potential Complications:
 Hypotension, poor perfusion, and cardiogenic shock
 Dysrhythmias
 Thromboembolism
 Pericardial effusion and cardiac tamponade
 Planning and Goals
 Major goals for the patient may include promoting activity and reducing fatigue, relieving fluid overload
symptoms, decreasing anxiety or increasing the patient’s ability to manage anxiety, encouraging the patient to
verbalize his or her ability to make decisions and influence outcomes, and educating the patient and family about
management of the therapeutic regimen.
 Nursing Interventions:
 Promoting Activity Tolerance
 Minimizing Powerlessness
 Assisting Patients and Family to Effectively Manage the Therapeutic Regimen
- Monitoring and Managing Potential Complications
 Promoting Home and Community- Based Care
1. Educating Patients About Self-Care
2. Continuing Care
3. End-Of-Life Considerations

 Evaluation
1. Demonstrates tolerance for desired activity
2. Maintains Fluid Balance
3. Decreased Anxiety
4. Makes sound decisions regarding care and treatment
5. Patients and Family members adhere to therapeutic regimen
 What is Myocardial Infarction?
 Acute Coronary Syndrome is an emergent situation characterized by an acute onset of myocardial ischemia that
results in myocardial death. If definitive interventions do not occur promptly. Although the terms coronary
occlusion, heart attack, and myocardial infarction are used synonymously, the preferred term is “Myocardial
Infarction”.

 The spectrum of ACS includes unstable angina, NSTEMI, and ST-segment elevation myocardial
infarction(STEMI).
 CLINICAL MANIFESTATIONS:
 Chest pain
 Shortness of Breath
 Indigestion
 Nausea
 Anxiety
 Cool, pale and moist skin
 HR and RR may be faster than normal

 Assessment
- Obtain patient’s history includes the description of the presenting symptom(ex.pain), the history of previous cardiac
and other illnesses, and the family history of heart disease. The history should also include information about the
patient’s risk factors for heart disease.
PATHOPHYSIOLOGY
 Myocardial infarction ("heart attack") is the irreversible damage of myocardial tissue caused by prolonged
ischemia and hypoxia. This most commonly occurs when a coronary artery becomes occluded following the
rupture of an atherosclerotic plaque, which then leads to the formation of a blood clot (coronary thrombosis). This
event can also trigger coronary vasospasm. If a vessel becomes completely occluded, the myocardium normally
supplied by that vessel will become ischemic and hypoxic. Without sufficient oxygen, the tissue dies. The
damaged tissue is initially comprised of a necrotic core surrounded by a marginal (or border) zone that can either
recover normal function or become irreversibly damaged. The hypoxic tissue within the border zone may become
a site for generating arrhythmias. Collateral blood flow is an important determinant of infarct size and whether or
not the border zone becomes irreversibly damaged. Infarcted tissue does not contribute to tension generation
during systole, and therefore can alter ventricular systolic and diastolic function and disrupt electrical activity
within the heart. After several weeks, the infarcted tissue forms a fibrotic scar. Long-term consequences include
ventricular remodeling of the remaining myocardium (e.g., development of compensatory hypertrophy or
dilation), ventricular failure, arrhythmias and sudden death. Myocardial infarctions produce clinical symptoms
that include intense chest pain that may radiate into the neck, jaw or arms (i.e., referred pain), a sense of
substernal heaviness, squeezing or pressure, shortness of breath (dyspnea), fatigue, fainting (syncope), nausea,
sweating (diaphoresis), anxiety, sleeplessness, hypertension or hypotension (depending in part on the extent of
cardiac damage), tachycardia and arrhythmias.
Recent clinical research indicates that the symptoms may be very different between men and women. Chest pain is
less common in women. Instead, their most common symptoms are weakness, fatigue and dyspnea. The
pathophysiology of acute myocardial infarction is complex. Loss of viable myocardium impairs global cardiac
function, which can lead to reduced cardiac output, and if damage is severe, to cardiogenic shock. Systolic and
diastolic dysfunction are associated with ischemic myocardium. If left ventricular function is significantly impaired,
pulmonary congestion and edema can occur. Ischemia can also precipitate abnormal cardiac rhythms and conduction
blocks that can further impair function and become life-threatening in some cases. Reduced cardiac output and
arterial pressure can elicit baroreceptor reflexes that lead to activation of neurohumoral compensatory mechanisms
(e.g., activation of sympathetic nerves and the renin-angiotensin-aldosterone system) similar to what occurs during
heart failure. The pain and anxiety associated with myocardial infarction further activates the sympathetic nervous
system, which causes systemic vasoconstriction and cardiac stimulation (this explains why some patients become
hypertensive and have tachycardia). While sympathetic activation helps to maintain arterial pressure, it also leads to a
large increase in myocardial oxygen demand that can lead to greater myocardial hypoxia, enlarge the infarcted
region, precipitate arrhythmias, and further impair cardiac function. Sympathetic activation is responsible for the
diaphoresis (sweating) experienced by the patient. Renal hypoperfusion and sympathetic activation stimulate renin
release, which leads to increased plasma levels of angiotensin II and aldosterone that enhance renal retention of
sodium and water.
Diagnostic Findings:

• Electrocardiogram - This test records the electrical activity of your heart through electrodes attached to your
skin. It helps your doctor diagnose heart rhythm problems and damage to your heart.
• Blood tests. Your doctor may take a blood sample to look for signs of diseases that can affect the heart. He or she
may also check for a chemical called N-terminal pro-B-type natriuretic peptide (NT-proBNP) if your diagnosis
isn't certain after other tests.
• Echocardiogram. An echocardiogram uses sound waves to produce a video image of your heart. This test can
help doctors see the size and shape of your heart along with any abnormalities. An echocardiogram measures your
ejection fraction, an important measurement of how well your heart is pumping, and which is used to help classify
heart failure and guide treatment.
• Troponin - A troponin test measures the levels of troponin T or troponin I proteins in the blood. These proteins
are released when the heart muscle has been damaged, such as occurs with a heart attack. The more damage there
is to the heart, the greater the amount of troponin T and I there will be in the blood.
• Creatine Kinase and Its Isoenzymes - The creatine phosphokinase (CPK) isoenzymes test measures the
different forms of CPK in the blood. CPK is an enzyme found mainly in the heart, brain, and skeletal muscle.
Elevated CPK is an indicator of acute MI.
• Myoglobin - used detect muscle damage. When heart or skeletal muscle is injured, myoglobin is released into the
blood. Blood levels of myoglobin can rise very quickly with severe muscle damage and can be measured within a
few hours following an injury.
MEDICAL MANAGEMENT –
Medication Summary
The goals of pharmacotherapy for myocardial infarction are to reduce morbidity and to prevent complications. The main goals of
emergency department medical therapy are rapid intravenous thrombolysis and/or rapid referral for percutaneous coronary
intervention (PCI), optimization of oxygenation, reduction of cardiac workload, and pain control.

 Antiplatelet Agents
 Aspirin (Ascriptin, Bayer Aspirin, Aspirtab, Ecotrin, Durlaza)
Early administration of aspirin in patients with acute myocardial infarction has been shown to reduce cardiac
mortality rate by 23% in the first month.

 Clopidogrel (Plavix)
This agent has been shown to decrease cardiovascular death, myocardial infarction, and stroke in patients with acute
coronary syndrome (ie, unstable angina, non-ST elevation MI [NSTEMI], or ST-elevation MI [STEMI]).
 Prasugrel (Effient)
It is indicated for reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute
coronary syndrome (ACS) managed by means of percutaneous coronary intervention (PCI) who have either (a)
unstable angina or non-ST-elevation MI (NSTEMI) or (b) ST-elevation MI (STEMI) when managed with primary or
delayed PCI. The use of prasugrel is not recommended for patients with a history of stroke or transient ischemic
attack (TIA).

 Vorapaxar (Zontivity)
Vorapaxar reversibly inhibits protease-activated receptor 1 (PAR-1) which is expressed on platelets, but its long half-
life makes it effectively irreversible. It is indicated to reduce thrombotic cardiovascular events in patients with a
history of MI or with peripheral arterial disease. It is not used as monotherapy, but added to aspirin and/or
clopidogrel.
 Antithrombotic Agents
 Bivalirudin (Angiomax)
Bivalirudin, a synthetic analogue of recombinant hirudin, inhibits thrombin; it is used for anticoagulation in patients
with unstable angina who are undergoing PCI. With provisional use of glycoprotein IIb/IIIa inhibitor (GP IIb/IIIa
inhibitor), bivalirudin is indicated for use as an anticoagulant in patients undergoing PCI.

 Heparin
Heparin augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin. Heparin does
not actively lyse, but it is able to inhibit further thrombus formation and prevents reaccumulation of a clot after
spontaneous fibrinolysis.

 Enoxaparin (Lovenox)
Enoxaparin enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, it
preferentially increases the inhibition of factor Xa. Enoxaparin is indicated for the treatment of acute STEMI
managed medically or with subsequent PCI. It is also indicated for prophylaxis of ischemic complications caused by
unstable angina and non-Q-wave myocardial infarction.
 Glycoprotein IIb/IIIa Inhibitors
 Abciximab (ReoPro)
Abciximab is a chimeric human-murine monoclonal antibody. It binds to the platelet surface glycoprotein IIb/IIIa
(GPIIb/IIIa) receptor with high affinity, preventing the binding of fibrinogen and reducing platelet aggregation by
80%. Inhibition of platelet aggregation persists for as long as 48 hours after infusion stops.

 Tirofiban (Aggrastat)
Tirofiban is a nonpeptide antagonist of the glycoprotein IIb/IIIa receptor. It is a reversible antagonist of fibrinogen
binding, and when administered intravenously, it inhibits platelet aggregation by more than 90%.

 Eptifibatide (Integrilin)
Eptifibatide is a cyclic peptide that also reversibly inhibits platelet aggregation by binding to the glycoprotein IIb/IIIa
receptor. Blocks platelet aggregation and prevents thrombosis.
 Vasodilators
 Nitroglycerin IV (Nitro-Dur)
Nitroglycerin relaxes vascular smooth muscle via stimulation of intracellular cyclic guanosine monophosphate
production, causing a decrease in blood pressure. Nitrates are useful for preload reduction and symptomatic relief but
have no apparent impact on mortality rate in myocardial infarction.

 Beta-adrenergic blockers
 Metoprolol (Lopressor)
This category of drugs, which includes metoprolol (Lopressor) and esmolol (Brevibloc), has the potential to suppress
ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have
antiarrhythmic properties and reduce myocardial oxygen demand secondary to elevations in heart rate and inotropy.
 Esmolol (Brevibloc)
Esmolol is a useful drug for patients at risk of experiencing complications from beta-blockers, particularly reactive
airway disease, mild-to-moderate left ventricular dysfunction, and peripheral vascular disease. Its short half-life of 8
minutes allows for titration to desired effect, with the ability to stop quickly if necessary.
 Atenolol (Tenormin)
Used to improve and preserve hemodynamic status by acting on myocardial contractility, reducing congestion, and
decreasing myocardial energy expenditure.
 Angiotensin-Converting Enzyme Inhibitors
 Captopril
Captopril has a short half-life, which makes it an important drug for initiation of ACE inhibitor therapy. It can be
started at a low dose and titrated upward as needed and as the patient tolerates.

 Enalapril (Vasotec, Epaned)

Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels
of plasma renin and a reduction in aldosterone secretion. This agent helps to control blood pressure and proteinuria.

 Quinapril (Accupril)
Quinapril prevents conversion of angiotensin I to angiotensin II, resulting in increased levels of plasma renin and a
reduction in aldosterone secretion.

 Lisinopril (Zestril, Prinivil)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone
secretion.
 Angiotensin-Receptor Blockers
 Irbesartan (Avapro)
Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II at tissue receptor site. May induce more
complete inhibition of renin-angiotensin system than ACE inhibitors and does not affect response to bradykinin (less
likely to be associated with cough and angioedema).

 Candesartan (Atacand)
Candesartan blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete
inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely
to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.

 Valsartan (Diovan)
Produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower
blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine
vasopressin release, water intake, and hypertrophic responses. Use in patients unable to tolerate ACE inhibitors.
 Thrombolytics
 Alteplase, t-PA (Activase)
Alteplase (t-PA) is a fibrin-specific agent with a brief half-life of 5 minutes. Adjunctive therapy with IV heparin is
necessary to maintain the patency of arteries recanalized by t-PA, especially during the first 24-48 hours.

 Tenecteplase (TNKase)
Tenecteplase is a modified version of alteplase (t-PA) made by substituting 3 amino acids of alteplase. It can be given
as a single bolus over a 5-second infusion, instead of 90 minutes with alteplase. Tenecteplase appears to cause less
nonintracranial bleeding, but the risk of intracranial bleeding and stroke is similar to that of alteplase. Base the dose
using patient weight. Initiate treatment as soon as possible after the onset of acute STEMI symptoms. Because
tenecteplase contains no antibacterial preservatives, reconstitute immediately before use.
 Analgesics
 Morphine sulfate (Duramorph, MS Contin, Kadian, Avinza)
Morphine sulfate is the drug of choice for narcotic analgesia due to its reliable and predictable effects, safety profile,
and ease of reversibility with naloxone. Morphine sulfate is administered intravenously, may be dosed in a number of
ways, and commonly is titrated until the desired effect is achieved.

 PCSK9 Inhibitors

 Evolocumab (Repatha)
Human monoclonal IgG2 directed against PCSK9. Evolocumab binds to PCSK9 and inhibits circulating PCSK9
from binding to the LDLR, preventing PCSK9-mediated LDLR degradation and permitting LDLR to recycle back to
the liver cell surface. By inhibiting the binding of PCSK9 to LDLR, evolocumab increases the number of LDLRs
available to clear LDL from the blood, thereby lowering LDL-C levels.

 Alirocumab (Praluent)
Monoclonal antibody that binds to PCSK9. LDL-C is cleared from the circulation preferentially through the LDL
receptor (LDLR) pathway. PCSK9 is a serine protease that destroys LDLR in the liver, resulting in decreased LDL-C
clearance and increased plasma LDL-C.
 Supplemental Oxygen (Additional Therapy)
- Oxygen therapy may become necessary as MI progresses. Some patients require supplemental oxygen only during
periods of activity.
 Emergent Percutaneous Coronary Intervention - (PCI, formerly known as angioplasty with stent) is a non-surgical
procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood
vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis –
 Cardiac Rehabilitation - Cardiac rehab is a medically supervised program designed to improve your
cardiovascular health if you have experienced heart attack, heart failure, angioplasty or heart surgery. Cardiac
rehab has three equally important parts:
1. Exercise counseling and training: Exercise gets your heart pumping and your entire cardiovascular system
working. You’ll learn how to get your body moving in ways that promote heart health.
2. Education for heart-healthy living: A key element of cardiac rehab is educating yourself: How can you manage
your risk factors? Quit smoking? Make heart-healthy nutrition choices?
3. Counseling to reduce stress: Stress hurts your heart. This part of cardiac rehab helps you identify and tackle
everyday sources of stress.
NURSING PROCESS
 Assessment – Systematic assessment includes a careful history, particularly as it relates to symptoms: Chest pain
or discomfort, difficulty breathing(dyspnea), palpitations, unusual fatigue, faintness(syncope), or other possible
indicators of myocardial ischemia.
 Nursing Diagnosis
1. Acute Pain r/t increased myocardial oxygen demand and decreased myocardial oxygen supply.
2. Risk for decreased cardiac tissue perfusion r/t reduced coronary blood flow
3. Risk for imbalanced fluid volume
4. Risk for ineffective peripheral tissue perfusion r/t decreased cardiac output from left ventricular dysfunction
5. Anxiety r/t cardiac event and possible death
6. Deficient knowledge about post –ACS self-care
 Collaborative Problems/Potential Complications
1. Acute Pulmonary Edema
2. Heart Failure
3. Cardiogenic Shock
4. Dysrhythmias and cardiac arrest
5. Pericardial effusion and cardiac tamponade

 Planning and Goals:

 The major goals for the pt. include the relief of pain or ischemic signs and symptoms
 Prevention of myocardial damage and maintenance of effective respiratory function
 Maintenance or attainment of adequate tissue perfusion, reduced anxiety, adherence to the self-care program, and
early recognition of complications.
 Nursing Interventions:
1. Relieving pain and other signs and symptoms of ischemia
2. Improving Respiratory function
3. Promoting Adequate Tissue Perfusion
4. Reducing Anxiety
5. Monitoring and Managing Potential Complications
6. Promoting home and Community based care
- Educating Patients about self-care
- Continuing care
 Evaluation:
1. Experiences relief of angina
2. Has stable cardiac and respiratory status
3. Maintains adequate tissue perfusion
4. Exhibits decreased anxiety
5. Adheres to a self-care program
6. Has no complications