Overview (intro - clinical manifestations, causes, risk factors, complications, prevention) Assessment, diagnosis (Med and Nursing),

Overview

A heart attack, also called a myocardial infarction, can be fatal, but treatment has improved dramatically over the years. It is defined by
the demonstration of myocardial cell necrosis due to significant and sustained ischemia. It is usually, but not always, an acute manifestation of
atherosclerosis-related coronary heart disease. MI results from either coronary heart disease, which implies obstruction to blood flow due to plaques
in the coronary arteries or, much less frequently, to other obstructing mechanisms (e.g. spasm of plaque-free arteries).

Introduction

Myocardial infarction is the end result of either acute or chronic myocardial ischemia. Myocardial ischemia differs
slightly from myocardial hypoxia in that ischemia results in a stasis of waste products of cellular metabolism in addition
to a lack of oxygen delivery, leading to cellular damage above and beyond that from hypoxemia. Myocardial infarction is
a pathologic diagnosis and, depending on whether it is acute or chronic, is characterized by loss of normal
cardiac myocyte structure (i.e., myocytolysis, coagulative necrosis, inflammatory cell infiltration, and fibrosis).
Myocardial infarction has a host of causes and is a leading cause of cardiovascular disease and death in humans. The
vast majority of myocardial infarction in people stems from coronary artery disease and atherosclerosis, both of which
are relatively uncommon in the veterinary patient population. In dogs, collateral circulation of the coronary arterial
supply is relatively extensive, so the probability of irreversible myocardial ischemia from any one coronary arterial
occlusion may be lower in this species.

The clinical manifestations of myocardial ischemia and infarction in veterinary patients can range from nonspecific
symptoms to severe life-threatening arrhythmias and congestive heart failure. Thus, clinical suspicion of myocardial
infarction should lead to aggressive management and supportive care. Prognosis depends on the severity of clinical
signs, presence of concurrent disease, and response to initial therapy.
clinical manifestations

While the classic symptoms of a heart attack are chest pain and shortness of breath, the symptoms can be quite varied. The most common
symptoms of a heart attack include;

 pressure or tightness in the chest

 pain in the chest, back, jaw, and other areas of the upper body that lasts more than a few minutes or that goes away and comes back
 shortness of breath
 sweating
 nausea
 vomiting
 anxiety
 feeling like you’re going to faint
 a fast heart rate
 sense of impending doom

It’s important to note that not all people who have heart attacks experience the same symptoms or the same severity of symptoms.

Chest pain is the most commonly reported symptom among both women and men. However, women are a bit more likelyTrusted Source than
men to have more of the “atypical” symptoms, such as:
  shortness of breath
 jaw pain
 upper back pain
 lightheadedness
 nausea
 vomiting

In fact, some women who have had a heart attack report that their symptoms felt like the symptoms of the flu.

Heart attack symptoms vary

Not all people who have heart attacks have the same symptoms or have the same severity of symptoms. Some people have mild pain; others have
more severe pain. Some people have no symptoms. For others, the first sign may be sudden cardiac arrest. However, the more signs and symptoms
you have, the greater the chance you're having a heart attack.

Some heart attacks strike suddenly, but many people have warning signs and symptoms hours, days or weeks in advance. The earliest warning
might be recurrent chest pain or pressure (angina) that's triggered by activity and relieved by rest. Angina is caused by a temporary decrease in
blood flow to the heart.

The vast majority of heart attacks occur because of a blockage in one of the blood vessels that supply your heart. This most
often happens because of plaque, a sticky substance that can build up on the insides of your arteries (similar to how pouring
grease down your kitchen sink can clog your home plumbing). That buildup is called atherosclerosis.
 Causes a heart attack

Sometimes, plaque deposits inside the coronary (heart) arteries can break open or rupture, and a blood clot can get stuck
where the rupture happened. If the clot blocks the artery, this can deprive the heart muscle of blood and cause a heart attack.

Heart attacks are possible without a blockage, but this is rare and only accounts for about 5% of all heart attacks. This kind of
heart attack can occur for the following reasons:

 Spasm of the artery: Your blood vessels have a muscle lining that allows them to become wider or narrower as needed.
Those muscles can sometimes twitch or spasm, cutting off blood flow to heart muscle.
 Rare medical conditions: An example of this would be any disease that causes unusual narrowing of blood vessels.
 Trauma: This includes tears or ruptures in the coronary arteries.
 Obstruction that came from elsewhere in the body: A blood clot or air bubble (embolism) that gets trapped in a
coronary artery.
 Electrolyte imbalances: Having too much or too little of key minerals like potassium in your blood can cause a heart
attack.
 Eating disorders: Over time, an eating disorder can cause damage to your heart and ultimately result in a heart attack.

Who is most at risk for a heart attack?

Several key factors affect your risk of having a heart attack. Unfortunately, some of these risk factors aren't things you can
control.

 Age and sex.

  Family history of heart disease.
 History of preeclampsia, a condition that can develop during pregnancy.
 Lifestyle.
 If you have certain health conditions or diseases.
Age and sex

Your risk of heart attack increases as you get older, and your sex also influences when your risk of a heart attack starts to
increase:

 Men: The risk of heart attack increases greatly at age 45.

 Women: The risk of heart attack increases greatly at age 50 or after menopause.
Family history

If you have a parent or sibling with a history of heart disease or heart attack — especially at a younger age — your risk is even
greater. That risk increases with the following:

 Your father or a brother who was diagnosed with heart disease at age 55 or younger.
 Your mother or a sister who was diagnosed with heart disease at age 65 or younger.
Lifestyle

The lifestyle choices you make can also affect your risk of having a heart attack. The following lifestyle factors increase your
risk of heart attack:

 Lack of physical activity.

  A diet high in sodium, sugar and fat.
 Smoking or tobacco use (including smokeless or chewing tobacco and vaping).
 Drinking too much alcohol.
 Drug abuse (especially in younger individuals).
Other diseases and health conditions

The following health conditions can increase your risk of heart attack:

 Diabetes.
 Obesity.
 High blood pressure (hypertension).
 High cholesterol (hyperlipidemia).
 Eating disorders (especially in younger individuals).

Complications

Myocardial infarction (MI) is usually the result of thrombosis in a coronary artery, triggered by fissuring or rupture of an atheromatous
plaque. Platelets and fibrin are deposited on the damaged plaque resulting in the formation of a clot and the occlusion of the artery.
This article is an overview of the most common complications associated with MI. complications includes;
Sudden death

Disturbance of rate, rhythm and conduction

Cardiogenic shock

Cardiac rupture

Heart failure
Angina pectoris

Thromboembolism

Pericarditis

Ventricular septal defect

Ventricular aneurysm

Ruptured papillary muscles

Dressler’s syndrome

Shoulder hand syndrome

Can I prevent having a heart attack?

In general, there are many things that you can do that may prevent a heart attack. However, some factors beyond your control
— especially your family history — can still lead to a heart attack despite your best efforts. Still, reducing your risk can
postpone when you have a heart attack and reduce the severity if you have one.

How can I reduce my risk of having a heart attack?

Although there are several risk factors that you can’t control, there are many ways you can help yourself and reduce your risk
of a heart attack. These include:

 Schedule a checkup: Find a primary care provider and see them at least once a year for a checkup or wellness visit. An
annual checkup can catch many of the early warning signs of heart disease, including signs that you can't feel. These
include your blood pressure, blood sugar levels, cholesterol levels and more.
  Quit tobacco products: This includes smokeless tobacco and all vaping products.
 Exercise regularly: Aim for 20 to 30 minutes of moderately intense physical activity a week.
 Eat a healthy diet: Examples include the Mediterranean or Dash diets. A plant-based diet approach is an excellent
alternative.
 Maintain a healthy weight: Your primary care provider can advise you on a healthy goal weight and provide you
resources and guidance to help you reach that goal.
 Manage your existing health conditions: This includes high cholesterol levels, high blood pressure and diabetes.
 Reduce your stress: Consider techniques such as yoga, deep breathing and meditation.
 Take your medications: Don’t just take medications when you remember to or when you have a doctor’s appointment
coming up.
 Keep all your medical appointments: Seeing your healthcare providers regularly can help uncover heart-related issues
or other medical problems you didn't know you had. This can also help treat problems sooner rather than later.

Being an active contributor to your health doesn't mean you have to make lifestyle changes all on your own. Ask your primary
care provider and other providers on your healthcare team for help. They can provide the information and resources you need,
and point you to services from which you might benefit.

If you've already had a heart attack, your healthcare provider will recommend a cardiac rehabilitation program. This program's
goals are to reduce your chance of a second heart attack. These medically supervised programs provide counseling and focus
on the same healthy living goals listed above.
Nursing assessment:
One of the most important aspects of care of the patient with MI is the assessment.

 Assess for chest pain not relieved by rest or medications.

 Monitor vital signs, especially the blood pressure and pulse rate.
 Assess for presence of shortness of breath, dyspnea, tachypnea, and crackles.
 Assess for nausea and vomiting.
 Assess for decreased urinary output.
 Assess for the history of illnesses.
 Perform a precise and complete physical assessment to detect complications and changes in the patient’s status.
 Assess IV sites frequently.
 Assess for chest pain (with or without radiation to jaw, neck, arm)
 Assess for shortness of breath
 Assess for dizziness
 Assess for diaphoresis
 Assess for atypical symptoms such as nausea, weakness, change in mentation, heartburn, or frequent belching
 Assess for ST changes of 1 mm or more
 Assess for Tachyarrhythmias
 Assess for Levine’s sign (clutching chest).
ASSESSMENT FOR PATIENTS WITH MYOCARDIAL INFARCTION

SKIN: cool, clammy, diaphoretic, and pale, appearance due to sympathetic stimulation from loss of contractility may indicate cardiogenic shock. Dependent edema may also be
present due to poor contractility.

RESPI: shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary congestion. Pulmonary edema may be present.

CARDIO: chest pain or discomfort, palpitations. Heart sounds may include S3, S4, and new onset of murmur. Increased jugular venous distention 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. pulse deficit may indicate atrial fibrillation. In addition to ST-segment and T-wave changes, ECG may show tachycardia, bradycardia, and dysrhythmias

GI: nausea and vomiting.

GENITOURINARY: decreased urinary output may indicate cardiogenic shock

NEURO: anxiety, restlessness, light-headedness may indicate increased sympathetic stimulation or a decrease in contractility and cerebral oxygenation. The same symptoms may
also be heard in cardiogenic shock. Headache, visual disturbances, altered speech, altered motor function, and further changes in level of consciousness may indicate cerebral
bleeding if patient is receiving thrombolytics.
 MANAGEMENT OF MYOCARDIAL INFARCTION
Diagnostic Studies

 Blood Tests
o Cardiac enzymes and isoenzymes: CPK-MB(isoenzyme in cardiac muscle): Elevates within 4–8 hr, peaks in 12–20
hr, returns to normal in 48–72 hr.
 LDH:Elevates within 8–24 hr, peaks within 72–144 hr, and may take as long as 14 days to return to normal.
An LDH1 greater than LDH2 (flipped ratio) helps confirm/diagnose MI if not detected in acute phase.
 Troponins:Troponin I (cTnI) and troponin T (cTnT): Levels are elevated at 4–6 hr, peak at 14–18 hr, and
return to baseline over 6–7 days. These enzymes have increased specificity for necrosis and are therefore
useful in diagnosing postoperative MI when MB-CPK may be elevated related to skeletal trauma.
 Creatinine Kinase (CK-MB): Increased in over 90% of MI patients. Time sequence after MI: Begins to rises
4-6 hours, Peaks 24 hours, returns to normal after 2 days.
o Myoglobin: A heme protein of small molecular weight that is more rapidly released from damaged muscle tissue with
elevation within 2hr after an acute MI, and peak levels occurring in 3–15 hr.
o Electrolytes: Imbalances of sodium and potassium can alter conduction and compromise contractility.
o WBC: Leukocytosis (10,000–20,000) usually appears on the second day after MI because of the inflammatory
process.
o ESR: Rises on second or third day after MI, indicating inflammatory response.
o C-Reactive protein (CRP) – Is the marker of acute of acute inflammation. Patients without evidence of myocardial
necrosis but with elevated CRP are at increased risk of MI.
o Chemistry profiles: May be abnormal, depending on acute/chronic abnormal organ function/perfusion.
o ABGs/pulse oximetry: May indicate hypoxia or acute/chronic lung disease processes.
 o Lipids (total lipids, HDL, LDL, VLDL, total cholesterol, triglycerides, phospholipids):Elevations may reflect
arteriosclerosis as a cause for coronary narrowing or spasm.
 Diagnostics Tests
o ECG: ST elevation signifying ischemia; peaked upright or inverted T wave indicating injury; development of Q waves
signifying prolonged ischemia or necrosis.
. ECG (Electrocardiogram)
ECG is the most important test and should be done within 10 minutes of presentation.
For STEMI, initial ECG is usually diagnostic, showing ST-segment elevation ≥ 1 mm in 2 or more contiguous leads subtending the damaged area.

9 Steps to ECG Interpretation

Reading an electrocardiogram (ECG) correctly can more precisely pinpoint any cardiovascular anomalies a patient may experience. Medicomp,
leaders in ECG patch technology, offers the following guidelines to interpret an ECG since every patient relates symptoms differently, and cardiac
rhythms will vary from one individual to the next.

 Is the rhythm regular? Check the QRS segment of the ECG to determine if the depolarization within the ventricles is regular. Measuring the
distance between one R to the next can determine if that baseline measurement matches all other R-to-R distances within a given amount of
time, typically six to ten seconds. If any irregularities are noted, ask the patient if these abnormalities are persistent. If so, look for symptoms
associated with C.H.A.P.S. – chest pain, hypotension, altered mental state, poor perfusion, or shortness of breath.
 Calculate heart rate. Take a six- or ten-second radial pulse and multiply for a one-minute reading. Determine from the reading whether the
patient is experiencing bradycardia, tachycardia, superventricular tachycardia, or ventricular tachycardia with a pulse.
 Diagnose the P waves. Determine if the P waves are present, upright on the cardiac monitor, and followed by the QRS segment. If all three
are within normal limits, chances are the electrical impulse began in the SA node, as it should.
 Measure the P-R interval. Calculate the time between the P wave and the beginning of the QRS segment. A typical P-R interval is 0.12 to 0.20
seconds, with a prolonged P-R interval suggesting a blockage or delay through the AV node.
 Measure the QRS segment. The normal duration of the QRS segment is 0.04 to 0.10 seconds. A prolonged QRS segment could signify a
bundle branch block. Bundle branch blocks may be benign, but combined with other factors may indicate heart disease.
 Check the T wave. The T wave should be upright and follow the QRS segment. Inverted T waves may indicate a lack of oxygen to the heart,
peaked T waves suggest hyperkalemia, flat T waves may indicate low potassium, and a raised ST segment may suggest a heart attack.
 Note any ectopic beats. Fibers outside the SA node that stimulate the heart to beat cause premature atrial contractions, premature junctional
contractions, or premature ventricular contractions. Any ectopic beats should be counted to determine the interval, shape, and whether they
appear singularly or in groups.
 Determine the origin. With all the above information in place, look for these elements.
o Sinus: regular rhythm with 60-100 beats per minute; P waves upright, round, and occurring before the QRS segment; normal P-R
interval; normal QRS duration.
o Atria: Rhythm may or may not be regular; QRS segment is normal with abnormal P waves (premature, flat, notched, peaked, inverted,
or hidden).
o Junctional: Is the P wave junctional, inverted before, during or after the typical QRS segment?
o Ventricular: If the rhythm originates below the SA node, the QRS segment will be wide and unusual with no P waves.
o Paced rhythm: Low voltage pacer spikes before the QRS should be reviewed.
 Correctly identify the rhythm. Measure the information from the ECG against the patient’s symptoms and vital signs. This will give a much
better understanding of how to begin treatment.

o Chest x-ray: May be normal or show an enlarged cardiac shadow suggestive of HF or ventricular aneurysm.
 o Two-dimensional echocardiogram: May be done to determine dimensions of chambers, septal/ventricular wall
motion, ejection fraction (blood flow), and valve configuration/function.
o Nuclear imaging studies: Persantine or Thallium:Evaluates myocardial blood flow and status of myocardial cells,
e.g., location/extent of acute/previous MI. Cardiac blood imaging/MUGA: Evaluates specific and general ventricular
performance, regional wall motion, and ejection fraction. Technetium: Accumulates in ischemic cells, outlining
necrotic area(s).
o Coronary angiography: Visualizes narrowing/occlusion of coronary arteries and is usually done in conjunction with
measurements of chamber pressures and assessment of left ventricular function (ejection fraction). Procedure is not
usually done in acute phase of MI unless angioplasty or emergency heart surgery is imminent.
o Digital subtraction angiography (DSA): Technique used to visualize status of arterial bypass grafts and to detect
peripheral artery disease.
o Magnetic resonance imaging (MRI): Allows visualization of blood flow, cardiac chambers/intraventricular septum,
valves, vascular lesions, plaque formations, areas of necrosis/infarction, and blood clots.
o Exercise stress test: Determines cardiovascular response to activity (often done in conjunction with thallium
imaging in the recovery phase).

Cardiac markers
Cardiac markers (serum markers of myocardial cell injury) are cardiac enzymes (eg, creatine kinase-MB isoenzyme [CK-MB]) and cell contents
(eg, troponin I, troponin T, myoglobin) that are released into the bloodstream after myocardial cell necrosis. The markers appear at different times
after injury, and levels decrease at different rates. Sensitivity and specificity for myocardial cell injury vary significantly among these markers, but
the troponins (cTn) are the most sensitive and specific and are now the markers of choice. Recently, several new, highly sensitive assays of
cardiac troponin (hs-cTn) that are also very precise have become available. These assays can reliably measure cTn levels (T or I) as low as 0.003
to 0.006 ng/mL (3 to 6 pg/mL); some research assays go as low as 0.001 ng/mL (1 pg/mL).

Coronary angiography
Coronary angiography most often combines diagnosis with percutaneous coronary intervention (PCI—ie, angioplasty, stent placement). When
possible, emergency coronary angiography and PCI are done as soon as possible after the onset of acute myocardial infarction (primary PCI). In
many tertiary centers, this approach has significantly lowered morbidity and mortality and improved long-term outcomes. Frequently, the infarction
is actually aborted when the time from pain to PCI is short (< 3 to 4 hours).
Angiography is obtained urgently for patients with STEMI, patients with persistent chest pain despite maximal medical therapy, and patients with
complications (eg, markedly elevated cardiac markers, presence of cardiogenic shock, acute mitral regurgitation, ventricular septal defect,
unstable arrhythmias). Patients with uncomplicated NSTEMI whose symptoms have resolved typically undergo angiography within the first 24 to
48 hours of hospitalization to detect lesions that may require treatment.

MRI Findings of Myocardial Infarct

After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing ischemia (ECG findings or symptoms),
hemodynamic instability, recurrent ventricular tachyarrhythmias, and other abnormalities that suggest recurrence of ischemic events. Some
experts also recommend that angiography be done before hospital discharge in patients with STEMI who have inducible ischemia on stress
imaging or an ejection fraction < 40%.

Treatment of Acute MI

 Prehospital care: oxygen, aspirin, nitrates, and triage to an appropriate medical center

A reliable IV route must be established, oxygen given (typically 2 L by nasal cannula), and continuous single-lead ECG monitoring
started. Prehospital interventions by emergency medical personnel (including ECG, chewed aspirin [325 mg], and pain management
with nitrates) can reduce risk of mortality and complications. Early diagnostic data and response to treatment can help determine the
need for and timing of revascularization.

 Drug treatment: Antiplatelet drugs, antianginal drugs, anticoagulants, and in some cases other drugs
  Reperfusion therapy: Fibrinolytics or angiography with percutaneous coronary intervention or coronary artery bypass surgery
 Postdischarge rehabilitation and chronic medical management of coronary artery disease

Hospital admission
 Risk-stratify patient and choose reperfusion strategy
 Drug therapy with antiplatelet drugs, anticoagulants and other drugs based on reperfusion strategy

On arrival to the emergency room, the patient's diagnosis is confirmed. Drug therapy and timing of revascularization depend on the clinical picture
and diagnosis.

For STEMI, reperfusion strategy can include fibrinolytic therapy or immediate PCI. For patients with NSTEMI, angiography may be done within 24
to 48 hours of admission if the patient is clinically stable. If the patient is unstable (eg, ongoing symptoms, hypotension or sustained arrhythmias),
then angiography must be done immediately (see figure Approach to myocardial infarction ).

Mechanical Ventilation
A mechanical ventilator is a machine that helps a patient breathe (ventilate) when he or she cannot breathe on his or her own for any reason. There
are many benefits, but a major risk is infection.

What is a mechanical ventilator?

A mechanical ventilator is a machine that helps a patient breathe (ventilate) when they are having surgery or cannot breathe on their own due to a
critical illness. The patient is connected to the ventilator with a hollow tube (artificial airway) that goes in their mouth and down into their main airway
or trachea. They remain on the ventilator until they improve enough to breathe on their own.
Why do we use mechanical ventilators?

A mechanical ventilator is used to decrease the work of breathing until patients improve enough to no longer need it. The machine makes sure that
the body receives adequate oxygen and that carbon dioxide is removed. This is necessary when certain illnesses prevent normal breathing.

What are the benefits of mechanical ventilation?

The main benefits of mechanical ventilation are the following:

 The patient does not have to work as hard to breathe – their respiratory muscles rest.
 The patient's as allowed time to recover in hopes that breathing becomes normal again.
 Helps the patient get adequate oxygen and clears carbon dioxide.
 Preserves a stable airway and preventing injury from aspiration.

It is important to note that mechanical ventilation does not heal the patient. Rather, it allows the patient a chance to be stable while the medications
and treatments help them to recover.

What are the risks of mechanical ventilation?

The main risk of mechanical ventilation is an infection, as the artificial airway (breathing tube) may allow germs to enter the lung. This risk of infection
increases the longer mechanical ventilation is needed and is highest around two weeks. Another risk is lung damage caused by either over inflation
or repetitive opening and collapsing of the small air sacs Ialveoli) of the lungs. Sometimes, patients are unable to be weaned off of a ventilator and
may require prolonged support. When this occurs, the tube is removed from the mouth and changed to a smaller airway in the neck. This is called a
tracheostomy. Using a ventilator may prolong the dying process if the patient is considered unlikely to recover.
 Ventilator and Patient Monitoring

Patient monitoring and ventilator checks are generally performed every 4 hours in the hospital. This is important to guarantee proper ventilator
function and to know if there is a patient issue. Such as:

 the patient needs suctioning

 the patient needs a breathing treatment
 the equipment is functioning properly
 it also helps protect against accidental changes that may occur with the controls

VENTILATOR ALARMS

The ventilator is equipped with safety alarms. An alarm will sound if the ventilator exceeds or drops below certain limits. Always look at and attend to
the patient first. Address the alarm situation second.

. Low pressure alarm: Indicates that the pressure in the ventilator circuit has dropped. Low pressure alarms are usually caused by a leak or
disconnect. Start at the patient and work your way towards the vent checking for loose connections. This can also include a leak at the site where the
tracheostomy tube enters the neck. If they are struggling for air, disconnect the circuit from the patient and manually ventilate with a resuscitation bag
(AMbu bag). Then call for help.

. Low Minute Ventilation (Ve): This alarm will sound when the amount of air taken in perminute drops below a set value. It will act similar to a low
pressure alarm and usually indicates some kind of a leak or disconnect in the system.
. High pressure alarm: This will sound when the pressure in the circuit has increased. It helps protect the lungs from high pressures delivered from
the ventilator. Secretions, water in the tubing, or kinks in the tubing can cause high pressure. Suction the patient and look for other sources. If this
does not fix the problem, disconnect the patient from the circuit and manually ventilate with an AMbu bag. Then call for help.

Low Volume alarm

Low exhaled volume alarms are triggered by air leaks. These are most frequently secondary to ventilatory tubing disconnect from the patient's
tracheal tube but will also occur in the event of balloon deflation or tracheal tube dislodgement

High Frequency alarm

High pressure alarm: This will sound when the pressure in the circuit has increased. It helps protect the lungs from high pressures delivered
from the ventilator. Secretions, water in the tubing, or kinks in the tubing can cause high pressure. Suction the patient and look for other sources.

Apnea Alarm

In the case of a Low Rate Alarm (often labeled "Apnea" alarm), back up ventilation may be provided, depending on settings. An agitated or
fatigued patient may have an increase in respiratory rate. Sedated patients or patients with impaired neuromuscular function may also have a
decreased respiratory rate
Drug treatment of acute myocardial infarction
All patients should be given antiplatelet drugs, anticoagulants , and if chest pain is present, antianginal drugs. The specific drugs used depend on
the reperfusion strategy and other factors; their selection and use is discussed in Drugs for Acute Coronary Syndrome . Other drugs, such as beta-
blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins, should be initiated during admission (see table  Drugs for Coronary Artery
Disease).
Patients with acute myocardial infarction should be given the following (unless contraindicated):

 Antiplatelet drugs: Aspirin, clopidogrel, or both (prasugrel or ticagrelor are alternatives to clopidogrel)

 Anticoagulants: A heparin (unfractionated or low molecular weight heparin) or bivalirudin
 Glycoprotein IIb/IIIa inhibitor when PCI is done
 Antianginal therapy usually nitroglycerin
 Beta-blocker
 ACE inhibitor
 Statin

All patients are given aspirin 160 to 325 mg (not enteric-coated), if not contraindicated, at presentation and 81 mg once a day indefinitely
thereafter. Chewing the first dose before swallowing quickens absorption.  Aspirin reduces short-term and long-term mortality risk. In patients
undergoing PCI, a loading dose of clopidogrel (300 to 600 mg orally once), prasugrel (60 mg orally once), or ticagrelor (180 mg orally once)
improves outcomes, particularly when administered 24 hours in advance. For urgent PCI, prasugrel and ticagrelor are more rapid in onset and
may be preferred.

Either a low molecular weight heparin (LMWH), unfractionated heparin, or bivalirudin is given routinely to patients unless contraindicated (eg, by
active bleeding). Unfractionated heparin is more complicated to use because it requires frequent (every 6 hours) dosing adjustments to achieve
target activated partial thromboplastin time (aPTT). The LMWHs have better bioavailability, are given by simple weight-based dose without
monitoring aPTT and dose titration, and have lower risk of heparin-induced thrombocytopenia . Bivalirudin is recommended for patients with a
known or suspected history of heparin-induced thrombocytopenia. Anticoagulants are continued for:

 Duration of PCI in patients undergoing this procedure

 Duration of hospital stay (in patients on LMWH) or 48 hours (in patients on unfractionated heparin) in all other cases

Consider a glycoprotein IIb/IIIa inhibitor during PCI for high-risk lesions (high thrombus burden, no reflow).  Abciximab, tirofiban,
and eptifibatide appear to have equivalent efficacy, and the choice of drug should depend on other factors (eg, cost, availability, familiarity). This
agent is continued for 6 to 24 hours.
Chest pain can be treated with nitroglycerin or sometimes morphine. Nitroglycerin is preferable to morphine, which should be used judiciously (eg,
if a patient has a contraindication to nitroglycerin or is in pain despite nitroglycerin therapy). Nitroglycerin is initially given sublingually, followed by
continuous IV drip if needed. Morphine 2 to 4 mg IV, repeated every 15 minutes as needed, is highly effective but can depress respiration, can
reduce myocardial contractility, and is a potent venous vasodilator. Evidence also suggests that  morphine use interferes with some P2Y12
receptor inhibitors. A large retrospective trial showed that morphine may increase mortality in patients with acute myocardial infarction (1, 2).
Hypotension and bradycardia secondary to morphine can usually be overcome by prompt elevation of the lower extremities.

Standard therapy for all patients with unstable angina includes beta-blockers, ACE inhibitors, and statins.  Beta-blockers are recommended unless
contraindicated (eg, by bradycardia, heart block, hypotension, or asthma), especially for high-risk patients. Beta-blockers reduce heart rate,
arterial pressure, and contractility, thereby reducing cardiac workload and oxygen demand.  ACE inhibitors may provide long-term cardioprotection
by improving endothelial function. If an ACE inhibitor is not tolerated because of cough or rash (but not angioedema or renal dysfunction),
an angiotensin II receptor blocker  may be substituted. Statins are also standard therapy regardless of lipid levels and should be continued
indefinitely.

Reperfusion therapy in acute myocardial infarction

 For patients with STEMI: Immediate percutaneous coronary intervention or fibrinolytics
 For patients with NSTEMI: Immediate percutaneous coronary intervention for unstable patients or within 24 to 48 hours for stable patients

For STEMI patients, emergency PCI is the preferred treatment of ST-segment elevation myocardial infarction when available in a timely fashion
(door to balloon-inflation time < 90 minutes) by an experienced operator. If there is likely to be a significant delay in availability of PCI,
thrombolysis should be done for STEMI patients meeting criteria (see Infarct extent). Reperfusion using fibrinolytics is most effective if given in the
first few minutes to hours after onset of myocardial infarction. The earlier a fibrinolytic is begun, the better. The goal is a door-to-needle time of 30
to 60 minutes. Greatest benefit occurs within 3 hours, but the drugs may be effective up to 12 hours. Characteristics and selection of  fibrinolytic
drugs are discussed elsewhere.

Unstable NSTEMI patients (ie, those with ongoing symptoms, hypotension, or sustained arrhythmias) should proceed directly to the cardiac
catheterization laboratory to identify coronary lesions requiring PCI or coronary artery bypass grafting (CABG).
For uncomplicated NSTEMI patients, immediate reperfusion is not as urgent because a completely occluded infarct-related artery at
presentation is uncommon. Such patients typically undergo angiography within the first 24 to 48 hours of hospitalization to identify coronary
lesions requiring PCI or CABG.
Fibrinolytics are not indicated for any NSTEMI patients. Risk outweighs potential benefit.

Choice of reperfusion strategy is further discussed in Revascularization for Acute Coronary Syndromes .
Rehabilitation and post-discharge treatment
 Functional evaluation
 Changes in lifestyle: Regular exercise, diet modification, weight loss, smoking cessation
 Drugs: Continuation of antiplatelet drugs, beta-blockers, ACE inhibitors, and statins

Patients who did not have coronary angiography during admission, have no high-risk features (eg, heart failure, recurrent angina, ventricular
tachycardia or ventricular fibrillation after 24 hours, mechanical complications such as new murmurs, shock), and have an ejection fraction  > 40%
whether or not they received fibrinolytics usually should have stress testing of some sort before or shortly after discharge (see table  Functional
Evaluation After Myocardial Infarction ).
Nursing Planning, Goals. Priorities, Interentions and Evaluation for myocardial infraction
Planning & Goals
To establish a plan of care, the focus should be on the
following:
 Relief of pain or ischemic signs and symptoms.
 Prevention of myocardial damage.
 Absence of respiratory dysfunction.
 Maintenance or attainment of adequate tissue perfusion.
 Reduced anxiety.
 Absence or early detection of complications.
 Chest pain absent/controlled.
 Heart rate/rhythm sufficient to sustain adequate cardiac
output/tissue perfusion.
 Achievement of activity level sufficient for basic self-care.
 Anxiety reduced/managed.
 Disease process, treatment plan, and prognosis understood.
 Plan in place to meet needs after discharge.
Nursing Priorities
 Relieve pain, anxiety.
 Reduce myocardial workload.
 Prevent/detect and assist in treatment of life-threatening
dysrhythmias or complications.
 Promote cardiac health, self-care.
Nursing Interventions
 Administer oxygen along with medication therapy
to assist with relief of symptoms.
 Encourage bed rest with the back rest elevated to
help decrease chest discomfort and dyspnea.
 Encourage changing of positions frequently to help keep fluid from
pooling in the bases of the lungs.
 Check skin temperature and peripheral pulses frequently to monitor
tissue perfusion.
 Provide information in an honest and supportive manner.
 Monitor the patient closely for changes in cardiac rate and rhythm,
heart sounds, blood pressure, chest pain, respiratory status, urinary
output, changes in skin color, and laboratory values.
Evaluation
After the implementation of the interventions within the
time specified, the nurse should check if:
 There is an absence of pain or ischemic signs and symptoms.
 Myocardial damage is prevented.
 Absence of respiratory dysfunction.
 Adequate tissue perfusion maintained.
 Anxiety is reduced.

Discharge and Home Care Guidelines

The most effective way to increase the probability that the
patient will implement a self-care regimen after discharge is to
identify the patient’s priorities.

 Education. This is one of the priorities that the nurse must teach the
patient about heart-healthy living.
 Home care. The home care nurse assists the patient with scheduling
and keeping up with the follow-up appointments and with adhering
to the prescribed cardiac rehabilitation management.
 Follow-up monitoring. The patient may need reminders about follow-
up monitoring including periodic laboratory testing and ECGs, as well
as general health screening.
 Adherence. The nurse should also monitor the patient’s adherence to
dietary restrictions and prescribed medications.
 INDEPENDENT:

 Obtain full description of pain from client including location,

intensity (0 to 10), duration, characteristics (dull or crushing), and
NURSING DIAGNOSIS FOR MYOCARDIAL INFARCTION radiation. Assist client to quantify pain by comparing it to other
experiences.
INEFFECTIVE BREATHING PATTERN R/T ALTERED
HEART CONTRACTILITY  Review history of previous angina, anginal equivalent, or MI pain.
Discuss family history if pertinent.
Independent:
 Instruct client to report pain immediately.
 Auscultate chest, noting presence/character of breath sounds,
presence of secretions. INDEPENDENT:

 Review chest x-rays as indicated.
 Encourage slower/deeper respirations, use of pursed-lip technique,
and so on.
 Elevate height of bed as appropriate.
 Maintain calm attitude while dealing with client and SO.
Dependent:
 Provide quiet environment, calm activities, and comfort measures,
for instance, dry or wrinkle-free linens and backrub. Approach
client calmly and confidently.
 Assist or instruct in relaxation techniques, such as deep, slow
breathing and distraction.
DECREASED CARDIAC TISSUE PERFUSION R/T REDUCED
CORONARY BLOOD FLOW

 Administer oxygen at lowest concentration as indicated. Independent:

 Maintain optimal cardiac output.

ACUTE PAIN R/T CARDIAC TISSUE ISCHEMIA  Consider the need for potential embolectomy, heparinization,
 vasodilator therapy, thrombolytic therapy, and fluid rescue.

 If patient is overweight, encourage weight loss to decrease venous

disease.

 Keep patient warm, and have patient wear socks and shoes or
sheepskin-lined slippers when mobile. Do not apply heat.

 Educate patient about nutritional status and the importance of

paying special attention to obesity, hyperlipidemia, and
malnutrition.

Dependent:

 Administer nitroglycerin (NTG) sublingually for complaints

of angina.

 Maintain oxygen therapy as ordered.