MYOCARDIAL INFARCTION

Introduction

The heart requires a balance between oxygen supply and oxygen demand in order to function properly.
The integrity of the arteries is an important determinant of oxygen supply to the heart muscles. Any
disorder that reduces the lumen of one of the coronary arteries may cause a decrease in the blood flow
and oxygen delivery to the area of the myocardium supplied by that vessel and lead to acute coronary
syndromes of angina, acute myocardial infarction (AMI), and sudden cardiac death.

"Myo" means muscle, "cardial" pertains to the heart, and "infarction" means death of tissue due to lack
of blood supply

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack,
results from the partial interruption of blood supply to a part of the heart muscle, causing the heart
cells to be damaged or die.

Definition: An acute myocardial infarction is also known as heart attack, coronary occlusion or simply a
“coronary”, which is a life threatening condition characterized by the formation of localized necrotic areas
within the myocardium.- Joyce M Black

CAUSES

 Occlusion (blockage) of a coronary artery

 An unstable collection of cholesterol and fatty acids and white blood cells in the wall of an artery
 psychological stress or physical exertion
 The period of intense exercise
 Poor physical condition
 Stress on atheromas
 Acute severe infection, such as pneumonia

RISK FACTORS

Important risk factors are

 previous cardiovascular disease,

 older age, tobacco smoking,
 high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and
 low levels of high density lipoprotein (HDL) cholesterol,
 diabetes, high blood pressure, lack of physical activity and obesity,
 chronic kidney disease,
 excessive alcohol consumption, the abuse of illicit drugs (such as cocaine and amphetamines),
chronic high stress levels
 Gender: At any given age men are more at risk than women, particularly before menopause, but
because in general women live longer than men ischemic heart disease causes slightly more total
deaths in women.
 Diabetes mellitus (type 1 or 2)
 High blood pressure
 Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly
high low-density lipoprotein, low high-density lipoprotein and high triglycerides
 Tobacco smoking, including secondhand smoke
 Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and sulfur
dioxide but not ozone.
 Family history of ischemic heart disease or myocardial infarction particularly if one has a first-
degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction
(defined as occurring at or younger than age 55 years (men) or 65 (women).
 Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist
circumference or waist-hip ratio).
 Lack of physical activity.
 Psychosocial factors including, low socio-economic status, social isolation, negative emotions
and stress increase the risk of myocardial infarction and are associated with worse outcomes after
myocardial infarction. Socioeconomic factors such as a shorter education and
lower income (particularly in women), and unmarried cohabitation are also correlated with a
higher risk of MI.
 Alcohol — Studies show that prolonged exposure to high quantities of alcohol can increase the risk
of heart attack.
 Oral contraceptive pill – women who use combined oral contraceptive pills have a modestly
increased risk of myocardial infarction, especially in the presence of other risk factors, such as
smoking.

Classification:
The two main types of acute myocardial infarction, based on pathology, are:
Transmural infarction- Transmural infarcts extend through the whole thickness of the heart
muscle and are usually a result of complete occlusion of the area's blood supply.
Subendocardial (nontransmural) infarction - involves a small area in the sub endocardial wall of
the left ventricle, ventricular septum, or papillary muscles.

Pathophysiology
 Change in the condition of the plaque in the coronary artery

Activation of platelets

Formation of a thrombus

Ischemia of tissue in the region supplied by the artery

Coronary blood supply less than demand

Myocardial cell death

 Altered repolarization of myocardium

Release of lysosomal enzymes

Anaerobic glycolysis

Myocardial irritability

Decreased contractility

Stimulation of the Decreased left

Sympathetic nervous ventricular function

system

increased increased increased preload decreased

oxygen needs after load. Cardiac output

Clinical manifestations:

Cardiovascular
Chest pain or discomfort, palpitations.
Heart sounds may include S3, S4, and new onset of a murmur.
Increased jugular venous distention
Blood pressure may be elevated because of sympathetic stimulation or decreased
because of decreased contractility,
Pulse deficit may indicate atrial fibrillation.
ST-segment and T-wave changes, ECG may show tachycardia,
bradycardia, and dysrhythmias.
Respiratory
Shortness of breath, dyspnea, tachypnea, and crackles
Pulmonary edema may be present.
Gastrointestinal
Nausea and vomiting.
Genitourinary
Decreased urinary output may indicate cardiogenic shock.
Skin
Cool, clammy, diaphoretic, and pale appearance
Dependent edema may also be present due to poor contractility.
Neurologic
Anxiety, restlessness, light-headedness
Headache, visual disturbances, altered speech, altered motor function,
Changes in level of consciousness
Psychological
Fear with feeling of impending doom,
Diagnostic evaluation

It is recommended that all clients with a suspected AMI ingest aspirin and obtain baseline
cardiac serum makers and a 12 lead ECG within 10 minutes of arrival in the emergency
department

Recommended methods of identifying acute cardiac ischemia in emergency department are

tropin T serum levels and echocardiography based on appropriate triage, 30 day survival rates,
and cost effectiveness.

Electrocardiography:-

 When blood flow to the heart is decreased, ischemia and necrosis of the heart muscle
occur.
 These conditions are reflected in altered Q wave, ST segment and T wave on the 12 lead
ECG.
 12 lead ECG examines the heart from 12 views, with the view provided from the V5 lead
being the most sensitive in detecting abnormalities.
 The Q wave change is significant; normally the Q wave is small or absent.
 Ischemic tissue produces an elevation in the ST segment and a peaked T wave or
inversion of the T wave.
 ST segment elevation is considered significant if greater than 1 mm.
 Through the course of an MI, changes occur first in the ST segment, then the T wave,
and finally the Q wave.
 The 12 lead ECG can be used to determine the location of the infarct.
  Leads V1 and V2 face the septum of the heart, leads V3 and V4 face the anterior wall of
the left ventricle, and V5 and V6 face the lateral wall of the left ventricle.

Laboratory tests

Laboratory findings include elevated levels of serum creatinine kinase (CK) MB isoenzyme,
cardiac troponin T, and cardiac troponin T and cardiac troponin I.

Historically elevation in lactate dehydrogenase (LDH) MI iso enzyme, serum aspartate

transaminase (AST), leukocytes and erythrocyte sedimentation rate ( ESR) have aided in the
diagnosis of AMI.

CK – MB (serum creatinine kinase):-

Increase 3 to 6 hours after the onset of chest pain, peak in 12 to 18 hours and return to normal
levels in 3 to 4 days.

Myoglobin:-

Is a heme protein found in striated muscle fibres. Myoglobin is rapidly released when
myocardial muscle tissue is damaged. Because of the rapid release it can be detected within 2
hours after AMI.

Troponin

The cardiac troponin complex is a basic component of the myocardium that is involved in the
contraction of the myocardial muscle.

Cardiac troponin T is similar to CK- MIS with regard to sensitivity and levels increase within 3 to
6 hours after pain has started. Levels remain elevated for 14 to 21 days.

cardiac troponin I levels increase 7 to 14 hours after AMI . Elevation persists for 5 to 7 days.

LDH ( lactate dehydrogenase)

It is released into the serum when myocardial damage occurs. Serum levels of LDH elevate 14
to 24 hours after onset of myocardial damage, peak within 48 to 72 hours.

AST ( aspartate transaminase )

Serum level of AST increase within several hours after the onset of chest pain, peak within 12 to
18 hours.

Leukocytosis:- ( 10,000 to 20,000 mm)

Appears on the second day after AMI and disappears in 1 week

Imaging studies

Positron emission tomography:-

Is used to elevate cardiac metabolism and to assess tissue perfusion. It can be used to detect
CHD, assess coronary artery flow reserve, measure absolute myocardial blood flow, detect AMI.

Magnetic resonance imaging:

Helps identify the site and extend of an MI, assess the effects of reperfusion therapy and
differentiate reversible and irreversible tissue injury.

Echocardiography:-

It is useful in assessing the ability of the heart walls to contract and relax. The transducer is
placed on the chest and images are relayed to a monitor screen.

Trans esophageal echocardiography :-

It is an imaging technique in which the transducer is placed against the wall of the esophagus.
This technique is particularly useful for viewing the posterior wall of the heart.

Medical management

Major goals of care for clients with AMI include the following:-

 Initiating prompt care

 Reducing pain
 Delivering successful treatment for the acute pain and reperfusion of the myocardium
 Preventing complications
 Preventing remodeling and heart failure

MONA- B

Morphine

Oxygen

Nitroglycerin

Aspirin / Clopidogrel

Beta-Blockers
Rehabilitating and educating the client and significant others.

Treat the acute attack immediately:-

Clients with manifestations of AMI must receive immediate treatment
 Delay may increase damage to the heart and reduce the chance of survival
 The client is given oxygen, an intravenous IV line is inserted and the client is connected
to a heart monitor
 The client experiencing AMI needs immediate admission to a hospital with a coronary
care unit if possible
 The first 24 hours after AMI is the time of highest risk for sudden death.
 There is a significant benefit if treatment is administered within first hour of onset.

Reduce pain:-

 Upon admission, the client who complains of chest pain is admitted to the emergency
department, given oxygen therapy and placed on ECG monitoring.
 An IV line is placed, serum cardiac makers are drawn and a 12 lead ECG is undertaken
within 10 minutes.
 Pain control is a priority and pain is usually treated with iv morphine.
 Oxygen is used to treat tissue hypoxia.

Monitor heart rhythm:-

Because dysrhythmias are common, ECG monitoring is essential and anti-dysrhythmias

medications should be at hand.

Improve perfusion:-

 The general principles of pharmacology that is treatment of AMI consist of anti-

ischemic and anti-thrombotic therapies.
 Anti- ischemic therapy usually consists of beta blockade and iv nitroglycerine.
 Anti-thrombotic therapy continues with medications that lyse the clot that forms
part of the blockage of the coronary artery.
 Thrombotic therapy includes streptokinase, urokinase, urokinase plasminogen
activator and reteplase.
 Thrombolytic agents should be given within an hour after the onset of chest pain.
 Heparin is continued after thrombolytic agent is administered.
 Not all clients with MI are suitable candidates for thrombolytic therapy.
 History of recent cerebral vascular accident, surgery, pregnancy or use of anti-
coagulants is contraindications.
  Complications of thrombolytics include bleeding, allergic reactions and stroke.
 Guidelines suggest that thrombolytic therapy should be initiated within 30 minutes
or PTCA should be initiated within 60 minutes.
 Anti-dysrhythmic agents are initiated.
 Clinicians begin beta-blockade and angiotensin converting enzyme (ACE) inhibitors
within 72 hours of onset to reduce ventricular remodeling and mortality.

Nursing Considerations

 Minimize the number of times the patient’s skin is punctured.

 Avoid intramuscular injections.
 Draw blood for laboratory tests when starting the IV line.
 Start IV lines before thrombolytic therapy; designate one line to use for blood draws.
 Avoid continual use of noninvasive blood pressure cuff.
 Monitor for acute dysrhythmias, hypotension, and allergic reaction.
 Monitor for reperfusion: resolution of angina or acute ST-segment changes.
• Check for signs and symptoms of bleeding: decrease in hematocrit and hemoglobin values,
decrease in blood pressure, increase in heart rate, oozing or bulging at invasive procedure sites,
back pain, muscle weakness, changes in level of consciousness, complaints of headache
• Treat major bleeding by discontinuing thrombolytic therapy and any anticoagulants; apply
direct pressure and notify the physician immediately.
• Treat minor bleeding by applying direct pressure if accessible and appropriate; continue to
monitor.
Determine the location of MI:-

Determining the exact coronary vessel that has infracted is done through analysis of the 12 lead
ECG and is validated with coronary angiography to determine the degree of occlusion.

Complications:

 Arrythmias and conduction defects with possible sudden death

 Extension of infarction or re-infarction
 Congestive heart failure
 Cardiogenic shock
 Pericarditis
 Mural thrombosis
 Myocardial wall rupture
 Cardiac tamponade
 Ventricular aneurysm formation
 ACUTE CORONARY SYNDROME

Introduction: Acute coronary syndrome is a term used to describe a range of conditions

associated with sudden, reduced blood flow to the heart.

Definition:

Acute coronary syndrome (ACS) is a syndrome (set of signs and symptoms) due to
decreased blood flow in the coronary arteries such that part of the heart muscle is unable to
function properly or dies.

Acute coronary syndrome is commonly associated with three clinical manifestations:

 ST elevation myocardial infarction (STEMI, 30%),

 Non ST elevation myocardial infarction (NSTEMI, 25%)
 Unstable angina (38%).

Causes:
Acute coronary syndrome happens because blood flow has slowed or stopped in the arteries that
supply blood to the heart.
Acute coronary syndrome is typically caused by coronary artery disease. Coronary artery disease,
also called heart disease, is caused by atherosclerosis, or hardening of the arteries.
Atherosclerosis causes a substance called plaque to build up in the coronary arteries. Plaque causes
angina by narrowing the arteries. The narrowing limits blood flow to the heart muscle. A heart
attack happens when blood flow is completely blocked.
Risk factors
The risk factors for acute coronary syndrome are the same as those for other types of heart
disease. Acute coronary syndrome risk factors include:

 Older age (older than 45 for men and older than 55 for women)
 High blood pressure
 High blood cholesterol
 Cigarette smoking
 Lack of physical activity
 Unhealthy diet
 Obesity or overweight
 Diabetes
 Family history of chest pain, heart disease or stroke
 For women, a history of high blood pressure, preeclampsia or diabetes during pregnancy
Signs and symptoms

 Chest pain or discomfort, which may involve pressure, tightness or fullness

 Pain or discomfort in one or both arms, the jaw, neck, back or stomach
 Shortness of breath
 Feeling dizzy or lightheaded
 Nausea
 Sweating

Diagnostic Evaluation:

 History and physical examination

 Electrocardiogram (ECG): Abnormal or irregular impulses can indicate poor heart

function due to a lack of oxygen to the heart.
 Chest Xray
 Exercise stress test
 Echocardiogram
 Nuclear Imaging studies
 Electron beam Ct scan
 Positron emission tomography
 Coronary Angiography
 Laboratory studies:
 Cardiac Troponin
 CBC
 CK-MB
  C-reactive protein
 Myoglobin
 Homocysteine
 Lipid profile

MANAGEMENT:

Collaborative therapy

1) Acute Coronary syndrome

 12 lead and continuous ECG monitoring

 IV access
 Oxygen therapy
 Drug therapy
 Nitroglycerin: Nitrates produce their principal effects by following mechanisms :
 Dilating peripheral blood vessels: Decreases venous blood return to heart so myocardial
oxygen demand is decreased because of reduced cardiac work load.
 Dilating Coronary arteries and collateral vessels: Increase the blood flow to ischemic
areas of heart.
 Sublingual NTG usually relieves the pain in about 3 min.

 Morphine sulphate: Functions as an analgesic and sedative. Acts as a vasodilator to

reduce preload and myocardial oxygen consumption.

 Aspirin : Inhibits cyclogenase, which in turn produces thromboxane A 2 a potent platelet

activator

 Beta adrenergic blockers : Inhibit the sympathetic nervous stimulation of the heart.
Reduce heart rate, contractility and BP. Decrease the after load
Ex: Atenolol, Carvedilol, Metoprolol

 ACE inhibitors: Prevent the conversion of angiotensin I to angiotensin II. Decrease the
endothelial dysfunction.
Ex: Captopril, Enalapril

2. Unstable Angina/ Non ST segment Elevation (NSTEMI)

Acute intensive drug therapy

 Nitroglycerin
 Antiplatelet therapy ( Aspirin, clopidogrel)
  Anticoagulation therapy ( Heparin) : Prevents the conversion of fibrinogen to fibrin

Coronary Angiography

PCI: 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.

3. ST SEGMENT ELEVATION MI (STEMI)

Emergent perfusion therapy:
 PCI
 Thrombolytic therapy : Breaks up fibrin meshwork in clots. Used only in ST –Segment
elevation MI
EX: Reteplase
Alteplase

 CABG Surgery : Coronary artery bypass grafting (CABG) is a type of surgery that
improves blood flow to the heart.

The goals of CABG may include:

 Improving your quality of life and reducing angina and other CHD symptoms
 Allowing you to resume a more active lifestyle
 Improving the pumping action of your heart if it has been damaged by a heart attack
 Lowering the risk of a heart attack (in some patients, such as those who have diabetes)
 Improving your chance of survival

Concurrent drug therapy

 Antiplatelet therapy
 Anticoagulant therapy

Nursing Management for Percutaneous Coronary Intervention

Pre procedure care: (AT WARD LEVEL)

1. The nurse should check for obtained orders from the doctor and consent should be
taken by the doctor
2. Patient should be on NBM for 2 to 6hrs
3. The nurse should call nursing aid boy/lady for cath site preparation ( radial or femoral
site)
4. Check for lab investigation ( HB%, serum creatinine, screening status) if any abnormal
inform report to the doctor
5. The nurse should fill out the pre cath checklist.
 6. The nurse should make sure that the dentures removal if any
7. Remove all the jewellary and hand over to relatives.
8. Check for vital signs and peripheral pulse and document

Procedure: (IN CATH LAB)

1. Identify the patient with Name, UHID OR IP number and check the patient ID band.
2. Before taking the patient in to the cath lab nurse should ensure that the all emergency
equipment is in working condition(defibrillator ,oxygen facility and suction facility ) and
all she should ensure that the emergency drugs are in place
3. The nurse performs the TIME OUT just before start of the procedure.
4. During the procedure the cath lab nurse should assist the doctor
5. The procedure involves injecting a contrast agent into arterial system and performing
radiographic studies. Angiography is performed in an interventional laboratory or a
special procedures room in the radiology department.
6. The procedure is performed under sterile conditions. Local anesthesia is given at the
puncture site, and a catheter is placed percutaneously .after injection of a contrast
agent through the catheter, fluoroscopy may be performed. Series of pictures of the dye
movement are taken.

Post procedure care:

1. Frequent assessment of vital signs and neurologic function and distal pulse checks, with
particular attention to the extremity that has been punctured.
2. Check puncture site for any bleeding or hematoma
3. Bed rest for 6 to 8hrs, with punctured extremity keeping straight alignment for a trans
femoral approach.
4. Continuous intravenous (IV) hydration for 6 to 8hrs to assist with contrast excretion.
Encourage oral fluid intake AND monitor for urine output.
5. NOTE : special precaution to be taken for CKD cases on maintenance hemodialysis
(preferably patient can be taken for HD)
6. Assessment of BLOOD UREA NITROGEN, CREATININE levels then next day.
7. Resumption of pre procedure diet and medication.

Complications:
 Allergic reaction to contrast medium
 Vessel wall perforation
 Emboli
 Renal failure
 Pseudo aneurysm
 Arrhythmias
 Heart attack and stroke.
 Bleeding and hematoma at puncture site.

Prevention
  Eat a heart-healthy diet that has lots of fruit, vegetables, whole grains, and lean protein.
 Stay at a healthy weight. Lose weight if you need to.
 Be active.
 A safe level of exercise.
 Don't smoke.
 Manage other health problems, including diabetes, high blood pressure, and high
cholesterol.
 Lower your stress level. Stress can damage your heart.
 Take a daily aspirin if doctor advises it.

Complications of Acute Coronary Syndrome

• Acute pulmonary edema
• Heart failure
• Cardiogenic shock
• Dysrhythmias and cardiac arrest
• Pericardial effusion and cardiac tamponade

NURSING MANAGEMENT:

Assessment

Obtain baseline data on current status of patient for comparison with ongoing status. Include
history of chest pain or discomfort, difficulty breathing (dyspnea), palpitations, unusual fatigue,
faintness (syncope), or sweating (diaphoresis).
Perform a complete physical assessment, which is crucial for detecting complications and any
change in status. The examination should include the following:
• Assess level of consciousness.
• Evaluate chest pain (most important clinical finding).
• Assess heart rate and rhythm; dysrhythmias may indicate not enough oxygen to the
myocardium.
• Assess heart sounds; S3 can be an early sign of impending left ventricular failure.
• Measure blood pressure to determine response to pain and treatment; note pulse pressure,
which may be narrowed after an MI, suggesting ineffective ventricular contraction.
• Assess peripheral pulses: rate, rhythm, and volume.
• Evaluate skin color and temperature.
• Auscultate lung fields at frequent intervals for signs of ventricular failure (crackles in lung
bases).
• Assess bowel motility; mesenteric artery thrombosis is a potentially fatal complication.
• Observe urinary output and check for edema; an early sign of cardiogenic shock is
hypotension with oliguria.
• Examine IV lines and sites frequently.

• Ineffective cardiac tissue perfusion related to reduced coronary blood flow

• Risk for imbalanced fluid volume
• Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left
ventricular dysfunction
• Death anxiety
• Deficient knowledge about post-ACS self-care
Planning and Goals

The major goals of the patient include relief of pain or ischemic signs (eg, ST-segment changes)
and symptoms, prevention of myocardial damage, absence of respiratory dysfunction,
maintenance or attainment of adequate tissue perfusion, reduced anxiety, adherence to the
self-care program, and absence or early recognition of complications.

Relieving Pain and Other Signs and Symptoms of Ischemia

• Administer oxygen in tandem with medication therapy to assist with relief of symptoms
(inhalation of oxygen reduces pain associated with low levels of circulating oxygen).
Acute Coronary Syndrome and Myocardial Infarction Acute Coronary Syndrome and Myocardial
Infarction
• Assess vital signs frequently as long as patient is experiencing pain.
• Assist patient to rest with back elevated or in cardiac chair to decrease chest discomfort and
dyspnea.
Improving Respiratory Function
• Assess respiratory function to detect early signs of complications.
• Monitor fluid volume status to prevent overloading the heart and lungs.
• Encourage patient to breathe deeply and change position often to prevent pooling of fluid in
lung bases.
Promoting Adequate Tissue Perfusion
• Keep patient on bed or chair rest to reduce myocardial oxygen consumption.
• Check skin temperature and peripheral pulses frequently to determine adequate tissue
perfusion.
Reducing Anxiety
• Develop a trusting and caring relationship with patient; provide information to the patient
and family in an honest and supportive manner.
• Ensure a quiet environment, prevent interruptions that disturb sleep, use a caring and
appropriate touch, teach relaxation techniques, use humor, and provide spiritual support
consistent with the patient’s beliefs. Music therapy also helpful.
Provide frequent and private opportunities to share concerns and fears.
• Provide an atmosphere of acceptance to help patient know that his or her feelings are
realistic and normal.
Monitoring and Managing Complications
Monitor closely for cardinal signs and symptoms that signal onset of complications.

TEACHING PATIENTS SELF-CARE

• Identify the patient’s priorities, provide adequate education about heart-healthy living, and
facilitate the patient’s involvement in a cardiac rehabilitation program.
• Work with the patient to develop a plan to meet specific needs to enhance compliance.

CONTINUING CARE
• Provide home care referral if warranted.
• Assist the patient with scheduling and keeping follow-up appointments and with adhering to
the prescribed cardiac rehabilitation regimen.
• Provide reminders about follow-up monitoring, including periodic laboratory testing and
ECGs, as well as general health screening.
• Monitor the patient’s adherence to dietary restrictions and to prescribed medications.
• If the patient is receiving home oxygen, ensure that the patient is using the oxygen as
prescribed and that appropriate home safety measures are maintained.
• If the patient has evidence of heart failure secondary to an MI, appropriate home care
guidelines for the patient with heart failure are followed.