‫الحقيبة التعليمية‬

Prepared by
Khaled Mohamed Ahmed

Under supervision of
 Myocardial Infarction

Out Lines
• Definition

• Classification

• Signs & symptoms

• Causes

• Pathophysiology

• Complications

• Diagnosis

• Management

• Role of the nurse

• REFRRENCE
Objective

•
At the end of presentation the student able to define
myo cardialinfarction
•
At the end of the presentation the student able to
classified MI
•
At the endof the presentation the student able to
understandthe cause & pathophysiology of
myocardial infarction
•
At the end of the presentation able to management
thecase

ِ
Definition:

Myocardial infarction (MI) or acute myocardial

infarction (AMI), commonly known as a heart attack is
the interruption of blood supply to a part of the heart,
causing heart cells to die. This is most commonly due to
occlusion (blockage) of a coronary artery following the
rupture of a vulnerable atherosclerotic plaque, which is an
unstable collection of lipids (fatty acids) and white blood
cells (especially macrophages) in the wall of an artery. The
resulting ischemia (restriction in blood supply) and oxygen
shortage, if left untreated for a sufficient period of time, can
cause damage or death (infarction) of heart muscle tissue
(myocardium).

• Classification

Tran mural: associated with atherosclerosis involving

major coronary artery. It can be sub classified into anterior,
posterior, or inferior. 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: involving a small area in the

subendocardial wall of the left ventricle, ventricular septum,
or papillary muscles. Subendocardial infarcts are thought to
be a result of locally decreased blood supply, possibly from
a narrowing of the coronary arteries. The subendocardial
area is farthest from the heart's blood supply and is more
susceptible to this type of pathology.

S&S:

symptoms of acute myocardial infarction include sudden

chest pain (typically radiating to the left arm or left side of
the neck), shortness of breath, nausea, vomiting,
palpitations, sweating, and anxiety (often described as a
sense of impending doom)[1]. Women may experience fewer
typical symptoms than men, most commonly shortness of
breath, weakness, a feeling of indigestion, and fatigue.[2]
Approximately one quarter of all myocardial infarctions are
"silent", without chest pain or other symptoms.

Causes:

It isn’t known but there is risk factors

• Diabetes (with or without insulin resistance) -

the single most important risk factor for ischaemic
heart disease (IHD)
• Tobacco smoking
• Hypercholesterolemia (more accurately
hyperlipoproteinemia, especially high low density
lipoprotein and low high density lipoprotein)
• Low HDL
• High Triglycerides
• High blood pressure
• Family history of ischaemic heart disease (IHD)
• Obesity[27] (defined by a body mass index of
more than 30 kg/m², or alternatively by waist
circumference or waist-hip ratio).
• Age: Men acquire an independent risk factor at
age 45, Women acquire an independent risk factor at
age 55; in addition individuals acquire another
independent risk factor if they have a first-degree
male relative (brother, father) who suffered a coronary
vascular event at or before age 55. Another
independent risk factor is acquired if one has a first-
degree female relative (mother, sister) who suffered a
coronary vascular event at age 65 or younger.
 NOTES

Hyperhomocysteinemia (high homocysteine, a toxic

blood amino acid that is

elevated when intakes of vitamins B2, B6, B12 and folic

acid are insufficient)

• Stress (occupations with high stress index are

known to have susceptibility for atherosclerosis)
• Alcohol Studies show that prolonged exposure
to high quantities of alcohol can increase the risk of
heart attack
• Males are more at risk than females.[

Pathophysiology

A myocardial infarction occurs when an atherosclerotic

plaque slowly builds up in the inner lining of a coronary
artery and then suddenly ruptures, causing catastrophic
thrombus formation, totally occluding the artery and
preventing blood flow downstream.

Acute myocardial infarction refers to two subtypes of acute

coronary syndrome, namely non-ST-elevated myocardial
infarction and ST-elevated myocardial infarction, which
are most frequently (but not always) a manifestation of
coronary artery disease.[8] The most common triggering
event is the disruption of an atherosclerotic plaque in an
epicardial coronary artery, which leads to a clotting
cascade, sometimes resulting in total occlusion of the artery.
[48][49]
Atherosclerosis is the gradual buildup of cholesterol
and fibrous tissue in plaques in the wall of arteries (in this
case, the coronary arteries), typically over decades.[50] Blood
stream column irregularities visible on angiography reflect
artery lumen narrowing as a result of decades of advancing
atherosclerosis.[51] Plaques can become unstable, rupture,
and additionally promote a thrombus (blood clot) that
occludes the artery; this can occur in minutes. When a severe
enough plaque rupture occurs in the coronary vasculature, it
leads to myocardial infarction (necrosis of downstream
myocardium).[48][49]

If impaired blood flow to the heart lasts long enough, it triggers

a process called the ischemic cascade; the heart cells in the
territory of the occluded coronary artery die (chiefly through
necrosis) and do not grow back. A collagen scar forms in its
place. Recent studies indicate that another form of cell death
called apoptosis also plays a role in the process of tissue
damage subsequent to myocardial infarction.[52] As a result, the
patient's heart will be permanently damaged. This Myocardial
scarring also puts the patient at risk for potentially life
threatening arrhythmias, and may result in the formation of a
ventricular aneurysm that can rupture with catastrophic
consequences.

Injured heart tissue conducts electrical impulses more slowly

than normal heart tissue. The difference in conduction velocity
between injured and uninjured tissue can trigger re-entry or a
feedback loop that is believed to be the cause of many lethal
arrhythmias. The most serious of these arrhythmias is
ventricular fibrillation (V-Fib/VF), an extremely fast and
chaotic heart rhythm that is the leading cause of sudden cardiac
death. Another life threatening arrhythmia is ventricular
tachycardia (V-Tach/VT), which may or may not cause sudden
cardiac death. However, ventricular tachycardia usually results
in rapid heart rates that prevent the heart from pumping blood
effectively. Cardiac output and blood pressure may fall to
dangerous levels, which can lead to further coronary ischemia
and extension of the infarct.

The cardiac defibrillator is a device that was specifically

designed to terminate these potentially fatal arrhythmias. The
device works by delivering an electrical shock to the patient in
order to depolarize a critical mass of the heart muscle, in effect
"rebooting" the heart. This therapy is time dependent, and the
odds of successful defibrillation decline rapidly after the onset
of cardiopulmonary arrest
Complications

Complications may occur immediately following the heart

attack (in the acute phase), or may need time to develop (a
chronic problem). Acute complications may include heart
failure if the damaged heart is no longer able to adequately
pump blood around the body; aneurysm or rupture of the
myocardium; mitral regurgitation, particularly if the
infarction causes dysfunction of the papillary muscle; and
arrhythmias, such as ventricular fibrillation, ventricular
tachycardia, atrial fibrillation and heart block. Longer-term
complications include heart failure, atrial fibrillation, and
the increased risk of a second myocardial infarction

Diagnosis
The diagnosis of myocardial infarction is made by integrating
the history of the presenting illness and physical examination
with electrocardiogram findings and cardiac markers (blood
tests for heart muscle cell damage).[1][53] A coronary angiogram
allows visualization of narrowings or obstructions on the heart
vessels, and therapeutic measures can follow immediately. At
autopsy, a pathologist can diagnose a myocardial infarction
based on anatomopathological findings.

A chest radiograph and routine blood tests may indicate

complications or precipitating causes and are often performed
upon arrival to an emergency department. New regional wall
motion abnormalities on an echocardiogram are also suggestive
of a myocardial infarction. Echo may be performed in equivocal
cases by the on-call cardiologist.[54] In stable patients whose
symptoms have resolved by the time of evaluation, Technetium
(99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride
can be used in nuclear medicine to visualize areas of reduced
blood flow in conjunction with physiologic or pharmocologic
stress.[54][55] Thallium may also be used to determine viability of
tissue, distinguishing whether non-functional myocardium is
actually dead or merely in a state of hibernation or of being
stunned[56]
Management

Main article: Myocardial infarction management

An MI is a medical emergency which requires immediate

medical attention. Treatment attempts to salvage as much
myocardium as possible and to prevent further
complications thus the phrase "time is muscle".[75] Oxygen,
aspirin, and nitroglycerin are usually administered as soon
as possible. Morphine was classically used if nitroglycerin
was not effective however it may increase mortality in the
setting of NSTEMI.[76] A 2009 and 2010 review of high
flow oxygen in myocardial infarction found increased
mortality and infarct size,
Cardiac catheterization
• Patients with unstable angina and the following
clinical characteristics should be referred for
immediate cardiac catheterization:
o Cardiogenic shock
o Severe left ventricular dysfunction
o Angina refractory to medical therapy
o Acute mitral regurgitation
o New ventricular septal defect
o Unstable tachyarrhythmia
o To the management of unstable angina as
this trial focused on patients with stable disease.
o Based on the weight of the current
evidence, early invasive strategy benefits high-
risk patients with acute coronary syndrome. In
keeping with this, the current AHA/ACC
Guidelines recommend an invasive treatment
strategy for patients with high-risk clinical
predictors.

Surgical Care
Patients at moderate-to-high risk for adverse events, such as
those with ST depression greater than 1 mm on ECG,
troponin positivity or NQMI, or chest pain refractory to
medical therapy should be scheduled for cardiac
catheterization with likely revascularization within the next
48 hours. The TACTICS/TIMI-18 trial showed that this
early invasive strategy reduced 30-day rates of death,
myocardial infarction, or rehospitalization for unstable
angina from 19.4% to 15.9%, or a relative risk reduction of
18%.
FRISC II showed that even a delayed invasive strategy
(mean time to revascularization 4 d, 71% revascularization
rate vs 9% in the conservative arm) coupled with LMWH
(dalteparin) therapy provides durable benefit for individual
hard end points. At 1 year, the invasive group had
statistically significant reductions in death (2.2% vs 3.9%,
relative risk reduction, 43%) and myocardial infarction
(8.6% vs 11.6%, relative risk reduction, 26%).11

• FRISC II has been the only randomized clinical

trial able to show a mortality benefit. This was likely
because of the very strict criteria for revascularization,
which resulted in only 9% of the conservative arm
receiving percutaneous coronary intervention (PCI) or
coronary artery bypass graft (CABG). For example, in
the TACTICS/TIMI-18 study and other North
American trials, approximately 50% of the patients in
the conservative arm had some form of
revascularization, and not all in the invasive strategy
arm had indications for percutaneous coronary
intervention or coronary artery bypass graft.
Therefore, the benefits of revascularization were less
striking because of the narrower differences in rates of
revascularization.
• Of note, by 1 year, a catch-up phenomenon was
observed in patients who had initial conservative
management. By then, 52% had undergone
angiography, and 43% required revascularization. See
the image below.

• The cost-benefit ratio of an initial invasive

approach based on the FRISC II trial has been
estimated. At the cost of 15 extra coronary artery
bypass graft and 21 percutaneous coronary
intervention procedures, the benefit per 100 patients
per year is as follows:
o 1.7 lives saved
o 2 myocardial infarctions prevented
o 20 readmissions prevented
o Earlier and better symptom relief
 • Coronary artery bypass graft is usually the
preferred method for revascularization in patients with
the following conditions:
o Left main trunk artery stenosis
o Poor left ventricular function
o Significant 3-vessel coronary artery
disease or 2-vessel disease that involves the
proximal left anterior descending artery

Role of the Nurse

Prevention

The risk of a recurrent myocardial infarction decreases with

strict blood pressure management and lifestyle changes,
chiefly smoking cessation, regular exercise, a sensible diet
for patients with heart disease, and limitation of alcohol
intake.

Patients are usually commenced on several long-term

medications post-MI, with the aim of preventing secondary
cardiovascular events such as further myocardial
infarctions, congestive heart failure or cerebrovascular
accident (CVA). Unless contraindicated, such medications
may include:[59][60]

• Evidence supports the consumption of

polyunsaturated fats instead of saturated fats as a
measure of decreasing coronary heart disease.[61]
• Antiplatelet drug therapy such as aspirin and/or
clopidogrel should be continued to reduce the risk of
plaque rupture and recurrent myocardial infarction.
Aspirin is first-line, owing to its low cost and
comparable efficacy, with clopidogrel reserved for
patients intolerant of aspirin. The combination of
clopidogrel and aspirin may further reduce risk of
cardiovascular events, however the risk of hemorrhage
is increased.[62]
• Beta blocker therapy such as metoprolol or
carvedilol should be commenced.[63] These have been
particularly beneficial in high-risk patients such as
those with left ventricular dysfunction and/or
continuing cardiac ischaemia.[64] β-Blockers decrease
mortality and morbidity. They also improve
symptoms of cardiac ischemia in NSTEMI.

• ACE inhibitor therapy should be commenced

24–48 hours post-MI in hemodynamically-stable
patients, particularly in patients with a history of MI,
diabetes mellitus, hypertension, anterior location of
infarct (as assessed by ECG), and/or evidence of left
ventricular dysfunction. ACE inhibitors reduce
mortality, the development of heart failure, and
decrease ventricular remodelling post-MI.[65]

• Statin therapy has been shown to reduce

mortality and morbidity post-MI.[66][67] The effects of
statins may be more than their LDL lowering effects.
The general consensus is that statins have plaque
stabilization and multiple other ("pleiotropic") effects
that may prevent myocardial infarction in addition to
their effects on blood lipids.[68]

• The aldosterone antagonist agent eplerenone has

been shown to further reduce risk of cardiovascular
death post-MI in patients with heart failure and left
ventricular dysfunction, when used in conjunction
with standard therapies above.[69] Spironolactone is
another option that is sometimes preferable to
eplerenone due to cost.
 • Omega-3 fatty acids, commonly found in fish,
have been shown to reduce mortality post-MI.[70]
While the mechanism by which these fatty acids
decrease mortality is unknown, it has been postulated
that the survival benefit is due to electrical
stabilization and the prevention of ventricular
fibrillation.[71] However, further studies in a high-risk
subset have not shown a clear-cut decrease in
potentially fatal arrhythmias due to omega-3 fatty
acids.[72][73]

Blood donation may reduce the risk of heart disease for

men,[74] but the link has not been firmly established.
References

Circulation 113 (18): 2177–85.

doi:10.1161/CIRCULATIONAHA.105.610352.
PMID 16651468.
.http://circ.ahajournals.org/cgi/content/full/113/18/2177

1. ^ a b c Mallinson, T (2010). "Myocardial Infarction".

Focus on First Aid (15): 15.
http://www.focusonfirstaid.co.uk/Magazine/issue15/index
.aspx. Retrieved 2010-06-08.
2. ^ Kosuge, M; Kimura K, Ishikawa T et al. (March
2006). "Differences between men and women in terms of
clinical features of ST-segment elevation acute
myocardial infarction". Circulation Journal 70 (3): 222–
226. doi:10.1253/circj.70.222. PMID 16501283.
http://www.jstage.jst.go.jp/article/circj/70/3/222/_pdf.
Retrieved 2008-05-31.
3. ^ Erhardt L, Herlitz J, Bossaert L, et al. (2002).
"Task force on the management of chest pain" (PDF).
Eur. Heart J. 23 (15): 1153–76.
doi:10.1053/euhj.2002.3194. PMID 12206127.
http://eurheartj.oxfordjournals.org/cgi/reprint/23/15/1153.
4. ^ a b Robert Beaglehole, et al. (2004) (PDF). The
World Health Report 2004 - Changing History. World
Health Organization. pp. 120–4. ISBN 92-4-156265-X.
http://www.who.int/entity/whr/2004/en/report04_en.pdf.
5. ^ Bax L, Algra A, Mali WP, Edlinger M, Beutler
JJ, van der Graaf Y (2008). "Renal function as a risk
indicator for cardiovascular events in 3216 patients with
manifest arterial disease". Atherosclerosis 200 (1): 184.
doi:10.1016/j.atherosclerosis.2007.12.006.
PMID 18241872.
http://linkinghub.elsevier.com/retrieve/pii/S0021-
9150(07)00768-X.
6. ^ Pearte CA, Furberg CD, O'Meara ES, et al.
(2006). "Characteristics and baseline clinical predictors of
future fatal versus nonfatal coronary heart disease events
in older adults: the Cardiovascular Health Study".