This document defines myocardial infarction and provides epidemiological data. It begins by defining myocardial infarction as the irreversible necrosis of heart muscle due to prolonged ischemia resulting from a blockage in a coronary artery. It then notes that over 735,000 Americans have heart attacks each year. Risk factors include increasing age, male sex, hypertension, dyslipidemia, diabetes, smoking, obesity, physical inactivity, and excessive alcohol consumption. The pathophysiology involves rupture of an atheromatous plaque leading to thrombus formation and coronary artery occlusion, causing ischemia and eventual cell death.

1. • Subtitle
MYOCARDIAL
INFARCTION

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DEFINITION
• Acute myocardial infarction (AMI), commonly known as a
heart attack, is the irreversible necrosis of heart muscle
secondary to prolonged ischemia.
• Results from an imbalance in oxygen supply and demand,
caused by plaque rupture with thrombus formation in a
coronary vessel, resulting in an acute reduction of blood
supply to a portion of the myocardium.

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EPIDEMIOLOGY
• Every year about 735,000 Americans have a heart
attack. Of these, 525,000 are a first heart attack and
210,000 happen in people who have already had a
heart attack.
• In 2010, approximately 1 in 6 people in the United
States died of Acute Myocardial Infarction.
• Approximately every 34 seconds, 1 American has a
coronary event, and approximately every 1 minute 23
seconds, an American will die of one.
The incidence of MI in India is 64.37/1000 people in
men aged 29-69 years

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EPIDEMIOLOGY
Prevalence of myocardial infarction by age and sex

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EPIDEMIOLOGY
Annual number of adults per 1000 having diagnosed heart attack or fatal
coronary heart disease (CHD) by age and sex

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EPIDEMIOLOGY
Incidence of heart attack or fatal coronary heart disease by age, sex, and race

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RISK FACTORS

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RISK FACTORS
• Increasing age and male sex. Individuals aged older than
45 years have an eight times greater risk for AMI.
Even after menopause, when women's death
rate from heart disease increases, it's not as
great as men's
• Hypertension, dyslipidemia,and
diabetes
“A case-control study of AMI in 52 countries,
comprising 15,152 cases and 14,820 controls,
was conducted. Among the important risk factors
for AMI in both men and women were raised,
history of hypertension, and diabetes”

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RISK FACTORS
• Smoking increases a person's risk for heart disease to
about 4 times greater than non-smokers.
• Obesity and physical inactivity People who have excess
body fat — especially at the waist — are more likely to
develop heart disease even if they have no other risk
factors.
• Lack of exercise has been linked to 7–12% of cases
• Acute and prolonged intake of high quantities of
alcoholic drinks (3-4 or more) increase the risk of a heart
attack

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PATHOPHYSIOLOGY
Coronary Arterial Occlusion.
• Rupture of high-risk atheromatous plaque in the coronary arteries is a primary
causative factor in the development of AMI.
• When exposed to subendothelial collagen and necrotic plaque contents,
platelets adhere, become activated, release their granule contents, and
aggregate to form microthrombi.

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• Vasospasm is stimulated by mediators released from platelets.
• Tissue factor activates the coagulation pathway, adding to the bulk of the
thrombus.
• Within minutes, the thrombus expands to completely occlude the vessel
lumen.
PATHOPHYSIOLOGY

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• In approximately 10% of cases, AMI occurs in the absence of the typical coronary
atherothrombosis.
PATHOPHYSIOLOGY
Vasospasm Emboli Others
• Intravascular
Platelet
aggregation
• drug ingestion
(e.g., cocaine or
ephedrine)
• Vegetations of
infective
endocarditis,
• Intracardiac
prosthetic
material
• Vasculitis,
• Hematologic
abnormalities
(e.g., sickle cell
disease),
• Amyloid
deposition,
• Vascular
dissection,
• Aortic stenosis,
• Lowered systemic
blood pressure
(e.g., shock)

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Myocardial Response.
• Coronary arterial obstruction diminishes blood flow to a region of
myocardium causing ischemia, rapid myocardial dysfunction, and
eventually—with prolonged vascular compromise — myocyte death.
• The anatomic region supplied by that artery is referred to as the area
at risk.
PATHOPHYSIOLOGY

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PATHOPHYSIOLOGY

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• Experimental and clinical evidence shows that only severe ischemia lasting 20
to 30 minutes or longer leads to irreversible damage (necrosis) of cardiac
myocytes.
• This delay in the onset of permanent myocardial injury provides the rationale
for rapid diagnosis in acute MI—to permit early coronary intervention to
establish reperfusion and salvage as much “at risk” myocardium as possible.
PATHOPHYSIOLOGY

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PATHOPHYSIOLOGY

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• The earliest detectable feature of myocyte necrosis is the disruption of the
integrity of the sarcolemmal membrane, allowing intracellular macromolecules
to leak out of necrotic cells into the cardiac interstitium and ultimately into the
microvasculature and lymphatics.
• Intracellular myocardial proteins into the circulation forms the basis for blood
tests that can sensitively detect irreversible myocyte damage, and are important
for managing AMI.
PATHOPHYSIOLOGY

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PATHOPHYSIOLOGY
• Time to elevation of CKMB, cTnT and cTnI is 3 to 12 hrs
• CK-MB and cTnI peak at 24 hours
• CK-MB returns to normal in 48-72 hrs, cTnI in 5-10 days, and cTnT in 5 to
14 days

19. • MIs can be located in the
anterior, septal, lateral,
posterior, or inferior walls
of the left ventricle.

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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 subendocardial wall of the left ventricle, ventricular septum,
or papillary muscles.
A transmural infarct is sometimes referred to as an “ST elevation
myocardial infarct” (STEMI) and a subendocardial infarct as a “non–ST
elevation infarct” (NSTEMI).

23. CLASSIFICATION

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A transmural acute myocardial infarct, predominantly of the
posterolateral left ventricle (arrow). Note the myocardial hemorrhage
at one edge of the infarct that was associated with cardiac rupture,
and the anterior scar (arrowhead), indicative of old infarct.

25. ASSESSMENT
HISTORY
• patients with MI describe a heaviness, squeezing, choking, or smothering
sensation.
• Patients often describe the sensation as “someone sitting on my chest.”
• The substernal pain can radiate to the neck, left arm, back, or jaw.
• Unlike the pain of angina, the pain of an MI is often more prolonged and
unrelieved by rest or sublingual nitroglycerin.
• Associated findings on history include nausea and vomiting, especially for the
patient with an inferior wall MI.
• These gastrointestinal complaints are believed to be related to the severity of
the pain and the resulting vagal stimulation.

26. PHYSICAL EXAMINATION
• patients usually appear restless and in distress.
• The skin is warm and moist.
• Breathing may be labored and rapid. Fine crackles, coarse crackles, or rhonchi may
be heard when auscultating the lungs.
• an increased blood pressure related to anxiety or a decreased blood pressure
caused by heart failure.
• The heart rate may vary from bradycardia to tachycardia.
• When the patient is placed in the left lateral decubitus position, abnormalities of
the precordial pulsations can be felt. These abnormalities include a lack of a point
of maximal impulse or the presence of diffuse
• A fourth heart sound is heard in almost all patients with MI, whereas a third heart
sound is detected in only about 10% to 20% of patients.
• Transient systolic murmurs may be heard
• After about 48 to 72 hours, many patients acquire a pericardial friction rub
• Patients with right ventricular infarcts may present with jugular vein
distension, peripheral edema, and an elevated central venous pressure.

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• Chest pain
• most common symptom
• described as a sensation of tightness, pressure, or
squeezing.
• not relieved by rest, position change or nitrate
administration.
• Pain radiates most often to the left arm, but may also
radiate to the lower jaw, neck, right arm, back,
and upper abdomen, where it may mimic heartburn.
• Levine's sign, in which a person localizes the chest
pain by clenching their fists over their sternum.
SILENT AMI - 20-30% subjects don’t have chest pain, common in patients with
diabetes mellitus, hypertension, & in elderly patients.

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• Nausea and Vomiting
• Vomiting results as a reflex from severe pain.
• Vasovagal reflexes initiated from area of ischemia.
• Shortness of breath (dyspnea)
• the damage to the heart limits the output of the left ventricle,
causing left ventricular failure and consequent pulmonary edema.
• Diaphoresis (an excessive form of sweating),
• Light-headedness, and
• Palpitations
• Loss of consciousness
• inadequate blood flow to the brain and cardiogenic shock.
• Sudden death
• due to the development of ventricular fibrillation

29. DIAGNOSTICS
• After collecting patient health history, a series of EKG’s should be
taken to rule out or confirm MI.
• 12 lead EKG’s can help to distinguish between ST-elevation MI’s and
Non-ST-elevation MI’s.

30. Normal Sinus Rhythm

31. ANGINA
Stable
• Chest pain caused by the build up of lactic acid and irritation to the myocardial
nerve fibers.
• Chest pain caused by the 4 E’s.
• Pain is usually relieved with rest, pain meds and nitrates.

32. VARIABLE/PRINZMETAL/SPASM
• Transient ischemia that occurs unpredictably and almost always at rest.
• Pain is caused by vasospasm of the arteries.
• ST segment elevations will be noted.

33. UNSTABLE
• Chest pain at rest or with exercise and tends to last greater than 15
minutes.
• This results in reversible myocardial ischemia but is a sign that an
infarct is soon to come.
• EKG will reveal ST segment depression and T wave inversion.

34. STEMI
• ST segment elevations
• T wave changes
• Q wave development
• Enzyme elevations
• Reciprocals

35. NSTEMI
• ST segment depressions
• T wave changes
• No Q wave development
• Mild enzyme elevations
• No reciprocals

36. STEMI VS. NSTEMI

37. SERUM CARDIAC MARKERS
• Myocardial cells produce certain proteins and enzymes associated with
cellular functions.
• When cell death occurs, these cellular enzymes are released into the blood
stream.
• CPK and troponin

38. CPK
• Creatine Phosphokinase
• Begin to rise 3 to 12 hours after acute MI.
• Peak in 24 hours
• Return to normal in 2 to 3 days

39. TROPONIN
• Myocardial muscle protein released into circulation after injury.
• These are highly specific indicators of MI.
• Troponin rises quickly like CK but will continue to stay elevated for 2 weeks.
• Myoglobin-lacks cardiac specificity.

40. SERUM CARDIAC MARKERS

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• MONA- B
• Morphine
• Oxygen
• Nitroglycerin
• Aspirin / Clopidogrel
• Beta-Blockers
• Other Early Hospital Therapies
• ACE Inhibitors
• Non- Dihydropyridine Calcium Channel Blockers.
• Fibrinolytics
• ~Targeted temperature management

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• Revascularization procedures
• Percutneous Coronary Intervention / Angioplasty.
• Coronary Artery By –Pass (CABG).
• Transmyocardial Laser Revascularization

43. MANAGEMENT
EARLY MANAGEMENT
• The patient’s history and 12-lead ECG are the primary methods
used to determine initially the diagnosis of MI.
• The ECG is examined for the presence of ST segment elevations
of 1 mV or greater in contiguous leads.
• 1. Administer aspirin, 160 to 325 mg chewed.
• 2. After recording the initial 12-lead ECG, place the patient on a
cardiac monitor and obtain serial ECGs.
• 3. Give oxygen by nasal cannula.

44. • 4. Administer sublingual nitroglycerin (unless the systolic blood
pressure is less than 90 mm Hg or the heart rate is less than 50 or
greater than 100 beats/minute).
• 5. Provide adequate analgesia with morphine sulfate. Provide
adequate analgesia with morphine sulfate.

45. THROMBOLYTIC THERAPY
• Thrombolytic drugs lyse coronary thrombi by converting plasminogen to
plasmin.
• Thrombolytic therapy provides maximal benefit if given within the first 3
hours after the onset of symptoms.
• Significant benefit still occurs if therapy is given up to 12 hours after onset
of symptoms.
Contraindications
■ Previous hemorrhagic stroke at any time; other stokes
or cerebrovascular events within 1 year
■ Known intracranial neoplasm
■ Active internal bleeding (does not include menses)
■ Suspected aortic dissection

46. THROMBOLYTIC THERAPY
Cautions/Relative Contraindications
■ Severe uncontrolled hypertension on presentation (blood pressure
>180/110 mm Hg)
■ History of prior cerebrovascular accident or known intracerebral disease
not covered in contraindications
■ Current use of anticoagulants in therapeutic doses (international
normalized ratio [INR] ≥2:3); known bleeding diathesis
■ Recent trauma (within 2–4 weeks), including head trauma
or traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation (CPR)
or major surgery (<3 weeks)

47. • ■ Noncompressible vascular punctures
• ■ Recent (within 2–4 weeks) internal bleeding
• ■ For streptokinase/anistreplase: prior exposure (especially within 5
days to 2 years) or prior allergic reaction
• ■ Pregnancy
• ■ Active peptic ulcer
• ■ History of chronic severe

48. PRIMARY PERCUTANEOUS
TRANSLUMINAL
CORONARY ANGIOPLASTY (PTCA)
• (PTCA) is an effective alternative to reestablish blood flow to ischemic
myocardium.
• Primary PTCA is an invasive procedure in which the infarct-related coronary
artery is dilated during the acute phase of an MI without prior
administration of thrombolytic agents.
• Primary PTCA may be an excellent reperfusion alternative for patients
ineligible for thrombolytic therapy.
• The nurse must carefully monitor the patient after a primary PTCA for
evidence of complications.
• These complications can include retroperitoneal or vascular hemorrhage,
other evidence of bleeding, early acute reocclusion, and late restenosis.

49. INTENSIVE AND INTERMEDIATE
CARE MANAGEMENT
• Prophylactic antidysrhythmics during the first 24 hours of hospitalization are not recommended.
• IV nitroglycerin is continued for 24 to 48 hours.
• Daily aspirin is continued on an indefinite basis.
• Clopidogrel may be used for patients who are intolerant of aspirin.
• IV beta blocker therapy should be administered within the initial hours of the evolving infarction,
followed by oral therapy provided there are no contraindications.
• Beta blockers are one of the few pharmacological agents
• that have been shown to reduce morbidity and mortality
• in the patient with an MI.
• They reduce oxygen demand by decreasing the heart rate and contractility.
• They also increase coronary artery filling by prolonging
• diastole.

50. • Calcium channel blockers may be given to patients in whom beta blocker
therapy is ineffective or contraindicated.
• Angiotensin-converting enzyme (ACE) inhibitors are administered to patients
with anterior wall MI and to patients who have an MI with heart failure in the
absence
• of significant hypotension.
• ACE inhibitors help prevent ventricular remodeling (dilation) and preserve
ejection fraction.
• Heparin is given to patients undergoing percutaneous or surgical
revascularization and for those receiving thrombolytic therapy with alteplase.
• Low–molecular-weight heparin should be used for patients with non–Q-wave
MI

51. Hemodynamic Monitoring
• Use of a pulmonary artery catheter for hemodynamic monitoring is
indicated in the patient with MI who has severe or progressive congestive
heart failure or pulmonary edema, cardiogenic shock, progressive
hypotension, or suspected mechanical complications.
Additional Diagnostic Tests:
• Radionuclide Imaging
• Echocardiogram
• Stress Test
• Coronary Angiography

52. FIBRINOLYTIC THERAPY
• Indicated for patients with STEMI MI’s.
• Should be given within 12 hours of symptom onset.
• Fibrinolytics will break down clots found within the
vessles
• Contraindications: post op surgical patients, history of
hemorrhagic stroke, ulcer disease, pregnancy, ect.

53. CARDIAC CATHETERIZATION
• A diagnostic angiography which includes angioplasty and possible
stenting.
• Performed by an interventional cardiologist with a cardiac surgeon
on stand by.
• Percutaneous procedure through the femoral or brachial artery.

54. CARDIAC CATHETERIZATION
• Upon arrival to the cath lab all actue MI patients will
receive:
• A bolus dose of plavix
• IV Integrelin
• Heparin dose either subcu or IV drip
• Angiomax : a DTI may be substituted for heparin and integrelin.

56. CORONARY ARTERY BYPASS GRAFT
• Surgical treatment where saphenous vein is harvested
from the lower leg and used to bypass the occluded
vessels.

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Lifestyle modifications:
• Smoking cessation: Two years after cessation, the risk of AMI
drops by 50%
• Alcohol moderation and prevention of illicit drug use.
• Physical activity and exercise:
• Exercise 30 minutes per day 7 days a week.
• Physical activity can help control blood cholesterol, diabetes and
obesity, as well as help lower blood pressure.
• losing even 10% from current weight, can lower your heart
disease risk.

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Diet modification
• Diets rich in soluble fiber, vegetables, fruits, and whole
grains, and low in saturated fat/trans fat and cholesterol
should be encouraged.
• Lipid management:
• Saturated fat (<7% of total calories),
• cholesterol and trans fatty acids (<200 mg/day),
• plant stanols/sterols (2 g/day),
• viscous fiber (10 g/day),
• Olive oil, rapeseed oil and related products are to be used
instead of saturated fat
• use of omega-3 fatty acids (fish)

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Management and control of comorbid diseases
• Hypertension should be managed.
• Patients with CAD should have their blood pressure maintained at less than 130/80
mm Hg.
• This may be achieved using a multimodal approach, which includes diet modification,
lifestyle changes, exercise, and medications.
• Diabetes control should be appropriate
• According to the 2007 AHA guideline for management of patients with STEMI, the
goal for HbA1c in diabetic patients should be less than 7%
Patient education:
• Patients, their family members, and the community should be educated properly,
especially on how to detect and respond to an episode of AMI

61. • Exercise
• Eat Healthy
• Don’t Smoke
• Don’t Drink

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