BEMS UNIVERSITY OF POONCH AJK

3. Myocardial Infarction
• Myocardial infarction or “heart attack” is an
irreversible injury to and eventual death of
myocardial tissue that results from ischemia
and hypoxia.
• Myocardial infarction is the leading killer of
both men and women in the United States.

4. • Critical myocardial ischemia can occur as a
result of increased myocardial metabolic
demand, decreased delivery of oxygen and
nutrients to the myocardium via the
coronary circulation, or both. An interruption
in the supply of myocardial oxygen and
nutrients occurs when a thrombus is
superimposed on an ulcerated or unstable
atherosclerotic plaque and results in
coronary occlusion.

5. • A high-grade (>75%) fixed coronary artery
stenosis caused by atherosclerosis or a dynamic
stenosis associated with coronary vasospasm can
also limit the supply of oxygen and nutrients and
precipitate an MI.
• Conditions associated with increased myocardial
metabolic demand include extremes of physical
exertion, severe hypertension (including forms of
hypertrophic obstructive cardiomyopathy), and
severe aortic valve stenosis.
• Other cardiac valvular pathologies and low cardiac
output states associated with a decreased mean
aortic pressure, which is the prime component of
coronary perfusion pressure, can also precipitate

6. Causes
• Most frequent cause is rupture of an
atherosclerotic lesion within coronary wall
with subsequent spasm and thrombus
formation
• Coronary artery vasospasm
• Ventricular hypertrophy
• Hypoxia
• Coronary artery emboli

7. Causes
• Cocaine
• Arteries
• Coronary anomalies
• Aortic dissection
• Pediatrics Kawasaki disease, Takayasu
arteritis
• Increased afterload which increases
myocardial demand

8. Risk factors for atherosclerosis
• Age
• Male gender
• Smoking
• Hypercholesterolemia and triglyceridemia
• Diabetes Mellitus
• Poorly controlled hypertension
• Type A personality

9. Risk factors for atherosclerosis
• Family History
• Sedentary lifestyle

10. Mechanisms of Myocardial damage
The severity of an MI is dependent of three
factors
• The level of the occlusion in the coronary
• The length of time of the occlusion
• The presence or absence of collateral
circulation

11. • The death of myocardial cells first occurs in the area
of myocardium most distal to the arterial blood
supply: the endocardium.
• As the duration of the occlusion increases, the area
of myocardial cell death enlarges, extending from
the endocardium to the myocardium and ultimately
to the epicardium.
• The area of myocardial cell death then spreads
laterally to areas of watershed or collateral
perfusion. Generally, after a 6- to 8-hour period of
coronary occlusion, most of the distal myocardium
has died. The extent of myocardial cell death defines
the magnitude of the MI. If blood flow can be
restored to at-risk myocardium, more heart muscle
can be saved from irreversible damage or death

12. Myocardial Infarction
Coronary blood flow and myocardial infarction
The location of a myocardial infarction will be largely
determined by which coronary blood vessel is occluded.
The two main coronary arteries supplying the myocardium
are:
a) the left coronary artery (which subdivides into the left
anterior descending and circumflex branches) and
b) the right coronary artery

13. Coronary Arteries for the heart
The two main coronary arteries supplying the myocardium are:
1. the left coronary artery (which subdivides into the left anterior descending
and circumflex branches) and
2. the right coronary artery

14. Myocardial Infarction
• The left anterior descending artery supplies blood to the
bulk of the anterior left ventricular wall, while the left
circumflex artery provides blood to the left atrium and the
posterior and lateral walls of the left ventricle.
• The right coronary artery provides blood mainly to the right
atria and right ventricles.
• Nearly 50% of all myocardial infarctions involve the left
anterior descending artery that supplies blood to the
main pumping mass of the left ventricle.
• The next most common site for myocardial infarction is
the right coronary artery, followed by the left

15. Myocardial Infarction
Morphology
A myocardial infarction may be:
a) transmural, meaning it involves the full thickness of the
ventricular wall, or
b) subendocardial, in which the inner one third to one half of
the ventricular wall is involved.
Transmural infarcts tend to have a greater effect on cardiac
function and pumping ability since a greater mass of
ventricular muscle is involved.

16. Signs and symptoms
• Acute MI can have unique
manifestations in individual patients.
The degree of symptoms ranges from
none at all to sudden cardiac death. An
asymptomatic MI is not necessarily less
severe than a symptomatic event, but
patients who experience asymptomatic
MIs are more likely to be diabetic.
Despite the diversity of manifesting
symptoms of MI, there are some
characteristic symptoms.

17. Signs and symptoms Contd.
• Chest pain described as a pressure
sensation, fullness, or squeezing in the midportion of
the thorax
• Radiation of chest pain into the jaw or
teeth, shoulder, arm, and/or back
• Associated dyspnea or shortness of breath
• Associated epigastric discomfort with or without
nausea and vomiting
• Associated diaphoresis or sweating
• Syncope or near syncope without other cause

18. Signs and symptoms Contd.
• An MI can occur at any time of the
day, but most appear to be clustered
around the early hours of the morning or
are associated with demanding physical
activity, or both. Approximately 50% of
patients have some warning symptoms
(angina pectoris or an anginal equivalent)
before the infarct.

19. Investigation / Cardiac
Biomarkers
• Cardiac biomarkers are protein molecules
released into the blood stream from
damaged heart muscle
• Since ECG can be inconclusive
, biomarkers are frequently used to
evaluate for myocardial injury
• These biomarkers have a characteristic
rise and fall pattern

20. Troponin T and I
• These isoforms are very specific for
cardiac injury
• Preferred markers for detecting myocardial
cell injury
• Rise 2-6 hours after injury
Peak in 12-16 hours
Stay elevated for 5-14 days

21. Creatinine Kinase ( CK-MB)
• Creatinine Kinase is found in heart muscle
(MB), skeletal muscle (MM), and brain
(BB)
• Increased in over 90% of myocardial
infraction
• However, it can be increased in muscle
trauma, physical exertion, post-
op, convulsions, and other conditions

22. Creatine Kinase (MB)
• Time sequence after myocardial infarction
Begins to rise 4-6 hours
Peaks 24 hours
returns to normal in 2 days
• MB2 released from heart muscle and
converted to MB1.
• A level of MB2 > or = 1 and a ratio of
MB2/MB1 > 1.5 indicates myocardial injury

23. Myoglobin
• Damage to skeletal or cardiac muscle
release myoglobin into circulation
• Time sequence after infarction
Rises fast 2hours
Peaks at 6-8 hours
Returns to normal in 20-36 hours
• Have false positives with skeletal muscle
injury and renal failure

24. Renal Failure and Renal
Transplantation
• Diagnostic accuracy of serum markers of
cardiac injury are altered in patients with
renal failure
• Cardiac troponins decreased diagnostic
sensitivity and specificity in patients
receiving renal replacement therapy
• Current data show levels of troponin I are
unaltered while levels of troponin T may
be elevated

25. CBC
• CBC is indicated if anemia is suspected as
precipitant
• Leukocytosis may be observed within
several hours after myocardial injury and
returns returns to levels within the
reference range within one week

26. Chemistry Profile
• Potassium and magnesium levels should
be monitored and corrected
• Creatinine levels must be considered
before using contrast dye for coronary
angiography and percutanous
revascularization

27. C-reactive Protein (CRP)
• C- reactive protein is a marker of acute
inflammation
• Patients without evidence of myocardial
necrosis but with elevated CRP are at
increased risk of an event

28. Chest X-Ray
• Chest radiography may provide clues to
an alternative diagnosis ( aortic dissection
or pneumothorax)
• Chest radiography also reveals
complications of myocardial infarction
such as heart failure

29. Echocardiography
• Use 2-dimentional and M mode
echocardiography when evaluating overall
ventricular function and wall motion
abnormalities
• Echocardiography can also identify
complications of MI ( eg. Valvular or
pericardial effusion, VSD)

30. Electrocardiogram
• A normal ECG does not exclude ACS
• High probability include ST segment
elevation in two contiguous leads or
presence of q waves
• Intermediate probability ST depression
• T wave inversions are less specific

32. Myocardial Infarction
Compensatory mechanisms of myocardial infarction
As a result of the hypotension and hemodynamic changes that accompany
a myocardial infarction, the cardiovascular system initiates a number of
reflex compensatory mechanisms designed to maintain cardiac
output and adequate tissue perfusion:
1.Catecholamine release : Increases heart rate, force of contraction and
peripheral resistance.
2. Sodium and water retention.
3. Activation of renin–angiotensin system leading to peripheral
vasoconstriction.
4. Ventricular hypertrophy.
Unfortunately, these compensatory changes may increase oxygen demand
and workload on the infarcted heart and worsen overall cardiac function.

33. Myocardial Infarction
Complications of myocardial infarction
Depending on the extent of the area involved in a myocardial infarction, a
number of complications might arise, including:
1. Rupture of weakened myocardial wall. Bleeding into pericardium may
cause cardiac tamponade and further impair cardiac pumping function.
This is most likely to occur with a transmural infarction. Rupture of the
septum between the ventricles might also occur if the septal wall is
involved in the infarction.
2. Formation of a thromboembolism from pooling of blood in the ventricles.
3. Pericarditis : Inflammation due to pericardial friction rub. Often occurs 1
to 2 days after the infarction.
4. Arrhythmia : Common as a result of hypoxia, acidosis and altered
electrical conduction through damaged and necrotic areas of the
myocardium. May be life-threatening and lead to fibrillation.

34. Myocardial Infarction
Complications of myocardial infarction
5. Reduced cardiac function : Typically presents with reduced
myocardial contractility, reduced wall compliance, decreased stroke
volume and increased left ventricular end diastolic volume.
6. Congestive heart failure may result if a large enough area of the
myocardium has been damaged such that the heart no longer pumps
effectively.
7. Cardiogenic shock : Marked hypotension that can result from
extensive damage to the left ventricle. The resulting hypotension will
trigger cardiovascular compensatory mechanisms that will further tax
the damaged myocardium and exacerbate impaired function.
Cardiogenic shock is associated with a mortality rate of 80% or
greater.

35. Myocardial Infarction
Rationale for therapy
 A main goal of intervention for myocardial infarction is to limit the
size of the infarcted area and thus preserve cardiac function.
 Early recognition and intervention in a myocardial infarction have
been shown to significantly improve the outcome and reduce
mortality in patients.
 If employed in the early stages of myocardial infarction, antiplatelet-
aggregating drugs such as aspirin and clot-dissolving agents such
as streptokinase and tissue plasminogen activator may be very
effective at improving myocardial blood flow and limiting damage to
the heart muscle.

36. Myocardial Infarction
Rationale for therapy
 Other drugs such as vasodilators, β -adrenergic blockers and ACE
inhibitors can also improve blood flow and reduce workload on the
injured myocardium and thus reduce the extent of myocardial
damage.
 The development of potentially life-threatening arrhythmias is also
common during myocardial infarction as a consequence of
hypoxia, acidosis and enhanced autonomic activity and must be
treated with appropriate antiarrhythmic drugs.
 Supportive therapies such as oxygen, sedatives and analgesics are
also utilized.

37. Myocardial Infarction
Treatment for myocardial infarction
1. Oxygen : Used to maintain blood oxygenation as well as tissue and
cardiac O2 levels.
2. Aspirin : If administered when myocardial infarction is detected, the
antiplatelet properties of aspirin may reduce the overall size of the
infarction.
3. Thrombolytic therapy :If employed in the first 1 to 4 hours following the
onset of a myocardial infarction, these drugs may dissolve clots in
coronary blood vessels and re-establish blood flow.
4. Vasodilator drugs : Intravenous nitroglycerin can increase blood flow to
the myocardium and reduce myocardial work.

38. Myocardial Infarction
Treatment for myocardial infarction
5.β -Blockers : Blunt the effect of catecholamine release on the
myocardium, reduce heart rate and myocardial work.
6. Pain management : Sublingual nitroglycerin, morphine if necessary
7. Antiarrhythmic drugs : To treat and prevent a number of potentially
life-threatening arrhythmias that might arise following a myocardial
infarction.
8. ACE inhibitors : the negative effects of vasoconstriction and salt and
water retention on the myocardium.

39. Myocardial Infarction
Thrombolytic Agents Used Clinically
a. Streptokinase : Derived from β -hemolytic streptococcus bacteria;
involved in the activation of plasmin
b. Anistreplase (APSAC) : Complex of human lys-plasminogen and
streptokinase; Administered as a prodrug
c. Alteplase (TPA): Recombinant tissue plasminogen activator
d. Urokinase : Endogenous human enzyme that converts
plasminogen to active plasmin
e. Routes of administration : Intravenous. for all of the above
f. Major unwanted effects : Internal bleeding, gastrointestinal
bleeding, stroke, allergic reactions

40. Myocardial Infarction
Pain Management in Myocardial Infarction
a. Sublingual nitroglycerin : Potent vasodilator of coronary
arteries, also dilates
b. peripheral arteries and veins to reduce preload and
afterload on the heart
c. Morphine sulfate : Powerful opioid analgesic that also
provides a degree of
d. sedation and vasodilatation; although the opioid
analgesics have little effect on
e. the myocardium, they are powerful respiratory
depressants

41. Myocardial Infarction
Aspirin
• Inhibits the cyclo-oxygenase pathway for the synthesis of
prostaglandins, prostacyclins and thromboxanes.
• Inhibits aggregation of platelets and is effective in
reducing myocardial infarction, stroke and mortality in
high-risk patients.

42. Myocardial Infarction
Key terms
• Cardiac tamponade : Excessive pressure that
develops from the accumulation of fluid in the
pericardium.
• Pericarditis : Inflammation of the pericardium.
• Stroke volume : Volume of blood ejected from
each ventricle per beat.
• End-diastolic volume : Volume of blood remaining
in the ventricle at the end of systole (contraction).