The document discusses coronary artery anatomy and acute myocardial infarction. It describes: - The main coronary arteries that supply the heart and the regions each artery perfuses. - How atherosclerosis leads to plaque buildup in arteries, reducing blood flow to the heart. - How a plaque rupture can cause a clot that fully occludes a coronary artery, causing cell death in the myocardial region supplied by that artery - known as a myocardial infarction.

1. Chapter
Acute Myocardial Infarction
AMI

2. Coronary Arteries
• Blood supply to the
myocardium is by Rt & Lt
main coronary arteries.
• The left coronary artery
branches into; left anterior
descending (LAD) & the
left circumflex artery (LCA)
• The LAD perfuse the
anterior two thirds of the
ventricular septum,
anterior left ventricle &
most of bundle branches.
• Left circumflex perfuse left
lateral & left posterior
walls.
• The right coronary artery
(RCA) perfuse the right
ventricle, & the inferior
wall of the left ventricle.

3. Coronary Atherosclerosis
• Atherosclerosis is the abnormal accumulation of lipid
deposits & fibrous tissue within Arterial walls & lumen.
• In coronary atherosclerosis, blockages & narrowing of
the coronary vessels reduce blood flow & decreasing
oxygen supply to the myocardium.
• The inflammatory response involved with the
development of atherosclerosis begins with injury to
the vascular endothelium & progress over many years.
• Endothelium stop producing the normal Antithrombotic
& vasodilating agents.
• Symptoms occur with 75% or more occlusion (thanks
to the collateral circulation).

4. Atherosclerosis—Pathophysiology
• Triglycerides, hypertension, &
cigarette smoking cause damage
to the endothelium.
• Fatty substances, cholesterol,
cellular waste products, calcium,
& fibrin pass are deposited
forming lipid plaque (atheroma).
• WBC, smooth muscle cells, &
platelets to aggregate at the site,
forming a fibrous plaque.
• The plaque may rupture & a
thrombus might form, obstructing
blood flow leading to ACS which
may result in an AMI.

5. Atherosclerosis—Pathophysiology

6. Acute Coronary Syndrome
• Unstable angina
– Unexpected chest pain/discomfort occurring at
rest
• MI
– ST-segment elevation MI (STEMI)
– Non–ST-segment elevation MI (NSTEMI)

7. Atherosclerotic Plaque

8. Copyright © 2018 Wolters Kluwer • All Rights Reserved

9. Myocardial Infarction (MI)
▪ MI is precipitated by an imbalance between
oxygen supply & oxygen demand, most
commonly R/t a coronary artery thrombosis
• Other causes include embolism, anemia, coronary
artery spasm, arrhythmias
• Thrombus formation occurs most often at the site of
an atherosclerotic plaque.
• Dysfunctioning endothelium—activation of the
inflammatory response---- formation of atherosclerotic
plaque --- rupture of plaque --- thrombus formation --
occlusion of the coronary artery --- Irreversible
damage (necrosis) within 20 - 40 min.

10. MI
• Transmural MI infarction implies an infarction that resulted
in necrosis of the tissue in all the layers of the myocardium
(up to the epicardium)
• Transmural MI infarction compromises CO as area of
infarction may become dyskinetic with small infarction, or
akinetic with a large infarction.
• Determinants of ventricular function post MI include
infarction size, location, & type
❑ Size of Infarction is determined by:
o Extent, severity, & duration of ischemia
o Size of the vessel; & amount of collateral circulation
o Status of the intrinsic fibrinolytic system; & the metabolic
demands of the myocardium.

11. ❑ MIs Location:
▪ Anterior left ventricle
o Occlusion of left anterior descending (LAD)
▪ Lateral & posterior left ventricle
o Left circumflex artery
▪ Inferior left ventricle
o Occlusion of right coronary artery
▪ Inferior Right ventricle
o Occlusion of right coronary artery
MI

12. Types of MI Infarction
▪ STEMI= ST-segment elevation MI
• More common
• Usually the affected coronary artery is completely
occluded
• Mostly ends up with Q wave thus causing Q-wave
MI
• The primary goal of initial treatment is early
reperfusion therapy through administration of
fibrinolytics or mechanical reperfusion.

13. Types of MI Infarction
❑ NSTEMI = non ST-segment elevations MI
• Related to partially or intermittently occluding thrombus.
• Unstable angina (UA) & NSTEMI are difficult to distinguish
initially, both presented with similar symptoms & ECG
changes (significant ST-segment depression & T-wave
inversions)
• An elevated biomarker is detected with NSTEMI but not UA
• Management strategies for UA/NSTEMI include
Antiplatelet, Antithrombin, & Antianginal
• Fibrinolysis is contraindicated with NSTEMI & UA
• An invasive strategy is indicated in patients with positive
biomarkers or unstable clinical features.

14. Assessment/History
• Chest discomfort or pain, described as heaviness,
squeezing, or choking (the most common complaint)
• Patients describe as “someone sitting on my chest.”
• The substernal pain radiate to the neck, left arm, back, or
jaw
• Unlike the pain of angina, the pain of an MI is often more
prolonged & unrelieved by rest or sublingual nitroglycerin
• Nausea & vomiting, thus patients may initially seek relief
of the gastrointestinal symptoms through antacids & other
home remedies.
• Diaphoresis, dyspnea, weakness, fatigue, anxiety,
restlessness, confusion, shortness of breath, or a sense of
impending death.

15. Assessment/ Physical Examination
• May appear restless, agitated, in distress
▪ Cool pale moist skin & diaphoreses
• VS, low-grade fever, hypertension, & tachycardia or
hypotension & bradycardia
• Labored & rapid breathing, crackles
• Diminished heart sounds, murmurs, pericardial
friction rub
• JVD, heart failure, pulmonary edema

16. Diagnostic Tests/ECG
▪ An ECG can be used to detect patterns of ischemia,
injury, & infarction
• Ischemia—T-wave inversion, ST-segment depression
• Injury—ST-segment elevation
• Infarction—T-wave, ST-segment, & Q-wave changes
• Myocardial ischemia is caused by 70% occluded
coronary artery with & oxygen demand exceeding
oxygen supply
• uncorrected ischemic state leads to injury
• uncorrected injury leads to MI
• Ischemia & injury are reversible but infarction is
irreversible.

17. Effects of Ischemia, Injury, Infarction on
ECG
• Involve changes in the
T wave, the ST
segment, & the Q
wave in the leads
overlying the infarcted
area.

18. ECG Changes in AMI/Infarction
▪ Stage 1: Hyperacute or peaked T waves phase:
• T waves become tall & narrow, after a few hours,
these hyperacute T waves invert

19. ECG Changes during AMI
• Hyperacute T waves may precede ST segment
elevation (A) or seen at the same time with ST
elevation (B) during this acute phase.

20. ECG Changes in AMI/Infarction
▪ Stage 2: the ST segments elevate from several hours
to several days in the leads of the ECG facing the
infracted heart.
• 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.
• The leads facing away from the injured area may show
ST segment depression (reciprocal changes), most
likely to be seen at the onset of infarction & disappear
later

21. ECG Changes in AMI/Infarction
▪ Stage 3: development of Q waves
• Q waves compatible with an MI are usually 0.04
second or more in width or one-fourth to one-third the
height of the R wave
• Small, narrow Q waves may be seen in the normal
ECG in leads I, II, III, aVR, aVL, V5, & V6
• Q waves develop within the fist 24 to 48 hours after
the infarction

22. ECG Changes during AMI
▪ Last stage: few days after the MI
• The elevated ST segments return to baseline.
o 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 infarcted 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.
o Abnormal Q waves accompanied by ST segment
elevations indicate an acute MI.
o Abnormal Q waves accompanied by a normal ST segment
indicate a previous MI.

23. ECG Changes in AMI
Figure 21-8
Evolution of the electrocardiogram (ECG) in a patient with MI. A: Tall peak T waves
known as hyperacute T waves. B: Symmetrical T-wave inversions. C: ST-segment
elevation. D: Development of the Q wave.

24. The 12-lead ECG: Correlation of lead with the view
of the heart

25. The 12-lead ECG: Correlation of lead with the view
of the heart

27. Correlation of lead with the view of the heart

28. MI Location
Coronary
artery
ECG leads Clinical impact
Anteroseptal
MI
most
common
LAD
ventricular
septum,
anterior left
ventricle &
most of
bundle
branches.
V1 –V4
Q waves and
ST
segment
elevations
Significant
hemodynamic
Compromise:
CHF, pulmonary
edema, cardiogenic
shock;
intraventricular
conduction
disturbances (e.g.,
RBBB, LBBB)

29. Anterior MI
•

30. Septal MI
Acute septal MI is associated with ST elevation, Q wave formation and T wave
inversion in the leads overlying the septal region of the heart (V1 & V2)

31. MI Location Coronary artery ECG leads Clinical impact
Lateral wall MI Left circumflex
Perfuse the SA
node in 45% of
people and AV
node in 10% of
people
I, aVL, V5, V6,
Q waves, ST
segment
elevations
Some
hemodynamic
Changes
dysrrhythmias
such as sinus
arrest and
junctional
rhythm

32. Lateral wall MI
Figure 21-10
Twelve-lead ECG showing an acute lateral wall MI. ST-segment elevations can be seen in leads I, aVL, V5 &
V6. Note also the deep Q waves in II, III, and aVF & normal ST segments, indicating a previous inferior wall
MI.

33. Location
Coronary
artery
ECG leads Clinical impact
Posterior wall MI Left
circumflex
Perfuse
the SA
node in
45% of
people and
AV node in
10% of
people
V1 and V2
all upright R
waves
with ST segment
depression
(reciprocal
changes)
V7 - V9 (15
lead ECG) : Q
waves and ST
segment
elevation
Some hemodynamic
changes;
dysrrhythmias
such as sinus arrest
and junctional
rhythm

34. Posterior MI

35. MI Location Coronary artery ECG leads Clinical impact
Inferior wall
less common
than
anteroseptal
more common
than lateral or
posterior
RCA
Supplies SA
node in 50% of
people and the
AV node in 90%
of people
II, III, aVF
Q waves and ST
segment
elevation
Some
hemodynamic
changes
Potential for
significant
arrhythmias caused
by SA and AV node
dysfunction

36. Inferior wall MI
Figure 21-11
ECG showing an acute inferior wall MI. Note the ST-segment elevations in II, III, and aVF. The posterior
wall infarction is evidenced by a tall R wave, ST-segment depression, and inverted T wave in V1 and V2.

37. Types of MI
Location Coronary artery ECG leads Clinical impact
Right
ventricular
wall
50% of
patients will
have also
inferior MI
RCA
Supplies blood to
the SA node in
50% of people
and the AV node
in 90% of people
right precordial
chest leads
(RV1 through
RV6)
Q waves and
ST segment
elevations
Some
hemodynamic
changes
Potential for
significant
arrhythmias
caused by SA
and AV node
dysfunction

38. Inferior and RV MI
 Right ventricular
infarction. The six chest
leads have been
positioned on the right
side of the chest.
 Note the ST segment
elevation in RV4, RV5, &
RV6.
 ST segments in the
inferior leads (II, III,
aVF) indicating inferior
wall MI
Figure 21-13
Twelve-lead ECG showing right ventricular infarction. The six chest leads have been positioned on the right side of the
chest. Note the ST-segment elevation in RV4, RV5, and RV6. The ECG also shows elevated ST segments in the inferior
leads (II, III, aVF). Patients with an inferior wall MI often also have an infarction in the right ventricle.

39. Diagnostic tests/ Lab tests
• Cardiac Troponins
– Preferred biomarker
– Are proteins with two subforms (troponin T & troponin I,)
that are highly specific for cardiac muscle. (Troponin C
which is not sensitive to MI)
– Troponin levels are not detected in the healthy person &
not affected by skeletal muscle injury.
– Troponin I levels rise in about 3 to 12 hours, peak at 24
hours & remain elevated for 5 to 10 days.
– Troponin T levels rise in 3 to 12 hours, peaks in 12 hours-
2 days & remains elevated for 5 to 14 days.
– Excellent diagnostic markers for patients who present late
with symptoms of MI.

40. Diagnostic tests/ Lab tests
▪ Creatine Kinase (CK)
• CK is an enzyme found mainly in heart & skeletal
muscles. When heart muscle is damaged, CK is released
into the blood.
• Onset 6 to 8 hours after the MI, peaks within 12 to 28
hours, & returns to normal in 24 to 36 hours
• The isoenzyme (CK MB) offers a more definitive
indication of myocardial cell damage than total CK alone.
• CK-MB appears in the serum in 6 to 12 hours, peaks
between 12 & 28 hours, & returns to normal levels in
about 72 to 96 hours.
• In the patient with an MI, the CK-MB2 level rises
resulting in a CK-MB2 to CK-MB1 ratio greater than one

41. Diagnostic tests/ Lab tests
• Myoglobin
– Myoglobin is an oxygen-binding protein found in
skeletal & cardiac muscle (thus it is not specific to
the heart)
– Onset within 1 to 2 hours of acute MI & peaks
within 3 to 15 hours
– The early release of myoglobin makes it valuable
in helping to detect MI

42. Laboratory Tests

43. Management
▪ Early management
• An initial evaluation (Hx, PE, ECG, monitor) of the patient
should occur ideally within the first 10 minute
• Continuous cardiac monitoring & Serial ECGs required
• Administer Aspirin, 160 to 325 mg chewed, to diminishes
platelet aggregation
• Give oxygen by nasal cannula , use pulse oximeter, &
draw ABG.
o hypoxemia often occurs in patients with a myocardial
infarction because of pulmonary edema.
o If severe pulmonary edema is present & the patient is in
respiratory distress, intubation may be necessary
o Serum cardiac markers, CBC, chemistry, and lipid profile

44. Management
• Administer sublingual Nitroglycerin (unless the systolic BP
is less than 90 mm Hg or the heart rate is less than 50 or
greater than 100 beats/minute)
• Nitroglycerin promotes vasodilation but is relatively
ineffective in relieving pain in the early stages of a MI.
• Intravenous nitroglycerin is recommended for the first 24 to
48 hours for patients with acute MI & heart failure, large
anterior wall infarctions, persistent ischemia, or hypertension.
• Morphine is the drug of choice to relieve the pain of a MI.
o given intravenously in small doses (2–4 mg) & can be
repeated every 5 minutes until the pain is relieved.
o Close respiratory monitoring is indicated because morphine
can depress respirations

45. Management
▪ Percutaneous Transluminal Coronary
Angioplasty (PTCA)
• It is the RECOMMENDED method of reperfusion
• PTCA is an invasive procedure in which the infarct-
related coronary artery is dilated with a balloon catheter
and possibly stent placement after balloon dilatation
• PTCA is used for patients who present within 12 hours of
the onset of symptoms, with persistent ischemic
symptoms, OR for patients ineligible for thrombolytic
therapy
• A dose of 162 to 325 mg of Aspirin is given to the
patient before the primary PCI and the aspirin is
continued indefinitely
• Complications include retroperitoneal or vascular
hemorrhage, early acute reocclusion, & late restenosis

46. Management
• Fibrinolytic therapy
– Lyse coronary thrombi by converting plasminogen to
plasmin which degrade fibrin and fibrinogen
– The ideal door to drug time for these patients is 30
minutes. Once the patient is stabilized, the patient is
evaluated for transfer to a hospital for angiography and
revascularization within 3 to 24 hours.
– 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 the onset of symptoms, if PCI can not be
performed within 120 minutes
– Fibrinolytic therapy also is recommended for patients with
STEMI who are unable to receive PCI if there is clinical
and/or electrocardiographic evidence of ongoing ischemia
within 12 to 24 hours of symptom onset and a large area
of myocardium is at risk or hemodynamically unstable

47. Management
• The patient is closely monitored during and after the
infusion of a thrombolytic agent
• The nurse assesses the patient for resolution of chest
pain, normalization of elevated ST segments,
development of reperfusion dysrhythmias (accelerated
idioventricular rhythm, ventricular tachycardia, and AV
heart block) any allergic reactions, evidence of bleeding,
and the onset of hypotension
• The nurse monitor the development of complications
such as reocclusion of the coronary artery (chest pain,
ST segment elevation, and hemodynamic instability),
bleeding (urine and stool for blood or altered levels of
consciousness due to intracranial bleeding)

48. Absolute Contraindications to Fibrinolytic
Therapy
• Previous intracranial hemorrhage or cerebrovascular
events within 1 year
• Known malignant intracranial neoplasm (primary or
metastatic)
• Known structural cerebral vascular lesion (e.g.,
arteriovenous malformation)
• Active bleeding or bleeding diathesis (excluding menses)
• Suspected aortic dissection
• Significant closed-head or facial trauma within 3 months
• Intracranial or intraspinal surgery within 2 months
• For streptokinase/anistreplase: prior treatment within the
previous 6 months or prior allergic reaction

49. • Severe uncontrolled hypertension on presentation (blood
pressure >180/110 mm Hg)
• History of prior ischemic stroke greater than 3 months
• Known intracranial pathology not covered in contraindications
• Current use of anticoagulants in therapeutic doses
(international normalized ratio [INR] ≥2:3); known
bleeding diathesis
• Recent (within 2–4 weeks) internal bleeding
• Head trauma or traumatic or prolonged (>10 minutes)
• (CPR) or major surgery (<3 weeks)
• Pregnancy/ Dementia/ Active peptic ulcer
Relative Contraindications to Fibrinolytic
Therapy

50. Management/ Pharmacological therapy
▪ For management of dysrhythmias
o Easy access to atropine, lidocaine, amiodarone,
transcutaneous pacing patches, transvenous pacing
wires, a defibrillator, & epinephrine is essential
o Prophylactic Antidysrhythmics during the first 24
hours of hospitalization are NOT recommended
• IV Nitroglycerin is continued for 24 to 48 hours
• IV beta blocker therapy should be administered within
the initial hours of the evolving infarction, followed by
oral therapy (they reduce oxygen demand by
decreasing the heart rate and contractility)

51. Management/ Pharmacological therapy
• β Blockers & ACE inhibitors are initiated in the first 24
hours unless contraindicated.
• β Blockers are continued during & after hospitalization
• 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 (they prevent ventricular
remodeling (dilation) & preserve ejection fraction)
• Calcium channel blockers may be given to patients in
whom beta blocker therapy is ineffective or
contraindicated

52. Management/ Pharmacological therapy
• Heparin (IV or low molecular weight) is given to patients
MI because of the high risk of embolism
• Daily aspirin is continued on an indefinite basis.
• Clopidogrel is added to the aspirin regimen for patients
with an STEMI and is continued for 14 days.
• Thrombotic thrombocytopenic purpura is associated
with the prolonged use of Clopidogrel
• During the first several days after STEMI, it is important
to normalize the patient’s blood glucose levels.
– An insulin infusion may be required to achieve this
goal.
• Lipid management therapy is initiated if indicated.

53. Management
▪ Other interventions
• Hemodynamic monitoring
– Use of a pulmonary artery catheter (check
volume status, CO) .
– Invasive arterial monitoring is indicated

54. Complications
▪ Ventricular dysrhythmias that occur in the prehospital
phase cause the majority of sudden cardiac deaths.
▪ Recurrent myocardial ischemia
• Efforts are made to lower myocardial oxygen demand, to
relieve pain. Emergent PTCA or surgical revascularization
may be considered
▪ Cardiogenic shock
• Is the most serious myocardial complication of MI.
• Occurs because of the loss of contractile forces in the
heart (necrosis involves 40% or more of the left ventricle),
• Is the most common cause of in-hospital death for
patients with MI, with a mortality rate of nearly 80%.

55. Complications
▪ Manifestations: rapid, thready pulse, narrow pulse
pressure, dyspnea, tachypnea, inspiratory crackles,
distended neck veins, chest pain, cool, moist skin, oliguria,
and decreased mentation. Decreased PaO2 and respiratory
alkalosis, systolic BP <85 mm Hg, a mean arterial blood
pressure <65 mm Hg, PAWP >18 mm Hg (should be =18).
• Interventions to cardiogenic shock include oxygen supply,
IV dopamine, nitroprusside with a vasopressor (to reduce lt
ventricle workload), use of an intra-aortic balloon pump
(IABP)
• Other complications: ventricular septal wall rupture, left
ventricular wall rupture, pericarditis, DVT, pulmonary
embolism, ventricular dysrhythmias and conduction
disturbances

56. Nursing DX
• Chest Pain related to myocardial infarction, angina
• Decreased Cardiac Output: Electrical factors affecting
rate, rhythm, or conduction
• Decreased Cardiac Output: Mechanical factors related
to preload, afterload, or left ventricular failure
• Knowledge Deficit related to illness and impact on
patient’s future
• Anxiety, stress related to fear of illness, death, and
critical care environment
• Activity Intolerance related to decreased cardiac output
or alterations in myocardial tissue perfusion
• Risk for Ineffective Tissue Perfusion related to
thrombolytic therapy impact on myocardial tissue

57. ACLS

59. <3 hours