Anita Yadav MPharm(Clinical Pharmacy), Pokhara Unuversity

1. Anita YadavAnita Yadav
Roll. No: 1Roll. No: 1
Mpharm(Clinical Pharmacy)Mpharm(Clinical Pharmacy)
School of Health Science, Pokhara UniversitySchool of Health Science, Pokhara University
Lekhnath-12, Kaski, PokharaLekhnath-12, Kaski, Pokhara

2.  Myocardial infarction (MI) or acute myocardial
infarction (AMI), commonly known as a heart attack, is
the interruption of blood supply to part of the heart, causing
some heart cells to die.
 Either one of the following criteria satisfies the diagnosis
for an acute, evolving, or recent myocardial infarction:
1. Typical rise and gradual fall (troponin) or more
rapid rise and fall (CK-MB) of biochemical markers of
myocardial necrosis with at least one of the following:
a. Ischemic symptoms
b. Development of pathologic Q waves on the
electrocardiogram
c. Electrocardiographic changes indicative of
ischemia (ST segment elevation or depression)
d. Coronary artery intervention (e.g., coronary
angioplasty).
2. Pathological findings of an acute myocardial
infarction

3.  Myocardial infarction is the leading cause of death in
the United States and is the most common cause of
death in the industrial world as well.
 The good news is that the survival rate for patients
who seek medical treatment for an acute MI is up to
90% to 95%.

4.  With approximately 50% of all acute MI’s in the
United States occurring to people under the age of
65; this disease is no longer thought to be a
“disease for the elderly”
 The actual incident of suffering an acute MI
depends on the number of pre-disposing factors
for atherosclerosis.

5.  High Blood Cholesterol (Hyperlipidemia) – An elevated
”total” cholesterol level is major component of
atherosclerotic plaque build up which causes the
development of an acute MI.
 Diabetes Mellitus – Patients with DM have a substantially
greater risk of developing atherosclerotic vascular disease
at an accelerated rate. This acceleration occurs regardless
of whether the patient has insulin dependant or non insulin
dependant diabetes.
 Hypertension – High blood pressure (squeezing of arteries
and veins) has consistently been associated with an
increased risk of developing an acute MI (both systolic and
diastolic elevations).

6.  Smoking – Tobacco contains certain components that
are known to damage vessel walls. The body’s
response to this damage elicits the formation of
atherosclerosis thereby increasing the risk of an acute
MI.
 Male Gendered – The incidence of developing an
acute MI is greater for men than women however;
with age this risk narrows.
 Family History – A family history of premature
coronary disease increases and individuals risk of
developing atherosclerosis and acute MI. Family
history includes both genetic components and learned
behaviors (i.e. smoking and high fat diets).

7.  Most patients who sustain an MI have coronary
atherosclerosis.
 The thrombus formation occurs most often at the
site of an atherosclerotic lesion, thus obstructing
blood flow to the myocardial tissues.
 Plaque rupture is believed to be the triggering
mechanism for the development of the thrombus
in most patients with an MI.
 When the plaques rupture, a thrombus is formed
at the site that can occlude blood flow, thus
resulting in an MI.

8.  Irreversible damage to the myocardium can begin
as early as 20 to 40 minutes after interruption of
blood flow.
 The dynamic process of infarction may not be
completed, however, for several hours.
 Necrosis of tissue appears to occur in a
sequential fashion.
 It is demonstrated that cellular death occurs first in
the subendocardial layer and spreads like a
“wavefront” throughout the thickness of the wall of
the heart.

9.  a substantial amount of myocardial tissue can be
salvaged if flow is restored within 6 hours after the
onset of coronary occlusion.
 The cellular changes associated with an MI can
be followed by:
1. the development of infarct extension (new
myocardial necrosis),
2. infarct expansion (a disproportionate thinning
and dilation of the infarct zone), or
3. Ventricular remodeling (a disproportionate
thinning and dilation of the ventricle).

11.  Several factors determine the size of the resulting MI.
 These factors include the extent, severity, and
duration of the ischemic episode; the size of the
vessel; the amount of collateral circulation; the status
of the intrinsic fibrinolytic system; vascular tone; and
the metabolic demands of the myocardium at the time
of the event.
 MIs most often result in damage to the left ventricle,
leading to an alteration in left ventricular function.
 Infarctions can also occur in the right ventricle or in
both ventricles.

12.  The term transmural infarction is used to imply an
infarction process that has resulted in necrosis of the
tissue in all the layers of the myocardium.
 Because the heart functions as a squeezing pump,
systolic and diastolic efforts can be significantly altered
when a segment of the heart muscle is necrotic and
nonfunctional.
 If the area of the transmural infarction is small, the
necrotic wall may be dyskinetic, a term meaning
“difficulty in moving.”
 If the damage to the myocardial tissue is more
extensive, the myocardial muscle may become akinetic,
meaning “without motion.”

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

16. 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.

17. 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
contraction.

18.  On auscultation, the first heart sound may be
diminished as a result of decreased contractility.
 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.

19. The Electrocardiogram
 An ECG can be used to detect patterns of
ischemia, injury, and infarction
Ischemia.
 On the ECG, myocardial ischemia results in T-
wave inversion or ST segment depression in the
leads facing the ischemic area.
 The inverted T wave representative of ischemia is
symmetrical, relatively narrow, and somewhat
pointed.

20.  ST segment depressions of 1 to 2
mm or more for a duration of 0.08
second may indicate myocardial
ischemia.
 Ischemia also should be suspected
when a flat or depressed ST segment
makes a sharp angle when joining an
upright T wave rather than merging
smoothly and imperceptibly with the T
wave

21. Injury.
 the injury process begins in the subendocardial layer and
moves throughout the thickness of the wall of the heart like
a wave.
 If the injury process is not interrupted, it eventually results
in a transmural MI.
 On ECG, the hallmark of acute myocardial injury is the
presence of ST segment elevations.
 In the normal ECG, the ST segment should not be elevated
more than 1 mm in the standard leads or more than 2 mm
in the precordial leads.
 With an acute injury, the ST segments in the leads facing
the injured area are elevated.
 The elevated ST segments also have a downward concave
or coved shape and merge unnoticed with the T wave

22. (A)ST segment elevation without T-
wave inversion.
(B) ST segment elevation with T-wave
inversion.
The elevated ST segments have
a downward concave or coved shape and
merge unnoticed with the T wave.

23. Infarction. When myocardial injury persists, MI is the result.
 During the earliest stage of MI, known as the hyperacute phase,
the T waves become tall and narrow. This configuration is
referred to as hyperacute or peaked T waves.
 Within a few hours, these hyperacute T waves invert.
 Next, the ST segments elevate, a pattern that usually lasts from
several hours to several days.
 In addition to the ST segment elevations in the leads of the ECG
facing the injured heart, the leads facing away from the injured
area may show ST segment depression.
 This finding is known as reciprocal ST segment changes.
 Reciprocal changes are most likely to be seen at the onset of
infarction, but their presence on the ECG does not last long.
 Reciprocal ST segment depressions may simply be a mirror
image of the ST segment elevations.

24.  Within a few days after the MI, the elevated ST
segments return to baseline.
 Persistent elevation of the ST segment
 may indicate the presence of a ventricular
aneurysm.
 The T waves may remain inverted for several
weeks, indicating areas of ischemia near the
infarct region.
 Eventually, the T waves should return to their
upright configuration.
 The Q waves do not disappear and therefore
always provide ECG evidence of a previous MI.

26.  To attain an accurate view of the right ventricle,
right-sided chest leads are recorded by placing
the six chest electrodes on the right side of the
chest using landmarks analogous to those used
on the left side
 To detect posterior wall abnormalities, three of the
precordial electrodes are placed posteriorly over
the heart.

27. Laboratory Tests
 Creatine Kinase
 CK-MB appears in the serum in 6 to 12 hours,
peaks between 12 and 28 hours, and returns to
normal levels in about 72 to 96 hours.
 Serial samplings are performed every 4 to 6 hours
for the first 24 to 48 hours after the onset of
symptoms
 Creatine Kinase Isoforms: CK-MB1 is the isoform
found in the plasma, and CK-MB2 is found in the
tissues. In the patient with an MI, the CK-MB2 level
rises, resulting in a CK-MB2 to CK-MB1 ratio
greater than one

28.  Myoglobin: Myoglobin is an oxygen-binding
protein found in skeletal and cardiac muscle.
Myoglobin’s release from ischemic muscle occurs
earlier than the release of CK.
 The myoglobin level can elevate within 1 to 2
hours of acute MI and peaks within 3 to 15 hours.
 Because myoglobin is also present in skeletal
muscle, an elevated myoglobin level is not specific
for the diagnosis of MI. onsequently, its
diagnostic value in detecting an MI is limited

29.  Troponin. (troponin T and troponin I):
 Troponin I levels rise in about 3 hours, peak at 14
to 18 hours, and remain elevated for 5 to 7 days.
 Troponin T levels rise in 3 to 5 hours and remain
elevated for 10 to 14 days

31. 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.

32.  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.

33.  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
■ Suspected aortic dissection

34. 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)

35.  ■ Noncompressible vascular punctures
 ■ Recent (within 2–4 weeks) internal bleeding
 ■ Pregnancy
 ■ Active peptic ulcer
 ■ History of chronic severe

36.  (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.

37.  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.

38.  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

39. 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

40. Vascular Complications
 Recurrent ischemia
 Recurrent infarction
Mechanical Complications
 Left ventricular free wall rupture
 Ventricular septal rupture
 Papillary muscle rupture with
acute mitral regurgitation
Myocardial
Complications
 Diastolic dysfunction
 Systolic dysfunction
 Congestive heart failure
 Hypotension/cardiogenic
shock
 Right ventricular infarction
 Ventricular cavity dilation
 Aneurysm formation

41. Pericardial Complications
 Pericarditis
 Pericardial effusion
Thromboembolic
Complications
 Mural thrombosis
 Systemic thromboembolism
 Deep venous thrombosis
 Pulmonary embolism
Electrical
Complications
 Ventricular tachycardia
 Ventricular fibrillation
 Supraventricular
tachydysrhythmias
 Bradydysrhythmias
 Atrioventricular block
(first, second, or third
degree)

42.  Using the research-based guidelines developed by the
American College of Cardiology and the American Heart
Association decreases in-hospital mortality rate post MI
from 15.3% to 8.3%. Emergency treatment of acute
STEMI includes:
◦ Fibrinolytic therapy (Streptokinase, or alteplase, or
reteplase) are used to stimulate lysis of the clot or through
mechanical opening the occluded artery.
◦ Anticoagulants: Heparin co-administration with fibrinolytic
therapy.
◦ Beta-blockers (metoprolol or atenolol) to prevent
dysrhythmias.
42

43. ◦ Anti-diabetic agents for tight glucose control to improve
survival rate.
◦ Angiotensin-Converting Enzyme (ACE) Inhibitors: These
include lisinopril and captopril and are helpful in prevention
of heart failure.
43

44. • Acute Pain related to oxygen supply and demand
imbalance
• Anxiety related to chest pain, fear of death,
threatening environment
• Decreased Cardiac Output related to impaired
contractility
• Activity Intolerance related to insufficient
oxygenation to perform activities of daily living,
deconditioning effects of bed rest
• Risk for Injury (bleeding) related to dissolution of
protective clots

45.  Handle patient carefully while providing initial care,
starting I.V. infusion, obtaining baseline vital signs,
and attaching electrodes for continuous ECG
monitoring.
 Maintain oxygen saturation greater than 92%.
 Administer oxygen by nasal cannula if prescribed
 Encourage patient to take deep breaths may
decrease incidence of dysrhythmias by allowing the
heart to be less ischemic and less irritable; may
reduce infarct size, decrease anxiety, and resolve
chest pain.

46.  Morphine –Morphine is also beneficial in reducing the
hemodynamic workload by increasing venous
capacitance and reducing systemic vascular
resistance (therefore decreasing myocardial oxygen
demand).

47.  Nitroglycerin – Nitrates such as Nitroglycerin
cause vasodilation of the vessels and help to
decrease cardiac oxygen demand, cardiac
preload and afterload while increasing cardiac
output.
 Aspirin – Antiplatelet therapy (specifically aspirin)
is now a standard therapy for the treatment of
angina and acute MI. The primary mechanism is
believed to be related to irreversible inhibition of
the cyclooxygenase pathway of platelets (blocking
the formation of thromboxane A2 and
thromboxane A2-induced platelet aggregation). I

48.  Heparin –Heparin is thought to keep the blood thinner and
prevents clotting. This allows for easier blood travel
through the vessels that are affected by narrowing and
atherosclerosis.
 Beta Blockers –Being able to decrease the work load of the
heart assists with improving cardiac output and lessens the
severity of the damage caused by the acute MI. Beta
blockers can actually interrupt an evolving MI, limit the
infarct size and decrease the risk of ventricular arrhythmias
by decreasing oxygen demand.

49.  Calcium Channel Blockers – Calcium channel blockers
prohibit the entry of calcium into smooth muscle. This
assists with dilating coronary arteries and veins which in
turn provides an increase in overall cardiac blood flow.
Calcium channel blockers also decrease systemic blood
pressure, total peripheral resistance and cardiac
afterload.

 ACE inhibitors – An Angiotensin converting enzyme;
ACE inhibitors block to the conversion of Angiotensin I to
Angiotensin II (which is a potent vasoconstrictor). The
goal of and ACE inhibitor is to decrease blood pressure
and afterload without increasing heart rate or the
workload of the heart.

50.  Dopamine – Dopamine has both a and b-adrenergic effects (as well
as dopaminergic effects). At low doses (2-5 mcg/kg/min) it
increases renal and mesenteric blood flow. At moderate doses (5-
10 mcg/kg/min) it has a positive inotrope affect which increases
blood pressure and cardiac output. At larger doses (10-20
mcg/kg/min) it exhibits a pure alpha stimulation which causes
peripheral vasoconstriction with both increased systemic vascular
resistance (SVR) and afterload.
 Dobutamine – Dobutamine stimulates B-receptors of the heart and
provide a direct acting positive inotrope effect. Dobutamine
increases stroke volume and cardiac output by increasing cardiac
contractility. By increasing contractility and cardiac output; there is
more oxygen rich blood available for damaged tissue.

51.  Larry Stanton is a 46-year-old man transported by
paramedics to the ED of a large community
hospital. He presents with severe, substernal chest
pain for the last 6 hours. He states he was fine until
about an hour after he ate breakfast. The pain
radiates to his jaw and neck and is accompanied by
N/V and diaphoresis. Father with heart failure and
Type 2 DM and questionable history of “mild heart
attack” at age 42; mother alive with HTN. He has
one sister who is 48, alive and well, and one brother
who died suddenly at age 46.

52.  Q. Which findings in this patient’s case history are
consistent with acute STEMI?
 Q. What risk factors for the development of
coronary artery disease are present in this
patient?
 Q. What non-pharmacologic therapeutic
alternative can also achieve the immediate goal in
this patient?
 Q. Based on this presentation, what is the initial
therapy in this patient?