Acute Coronary Syndrome - Ukdw - Okt13

ACUTE CORONARY
SYNDROME
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Page 1
What is Acute Coronary Syndrome

(ACS) ?
Acute Coronary Syndrome is when occlusion of
one or more of the coronary arteries occurs,
usually following plaque rupture, resulting in
decreased oxygen supply to the heart muscle.
ACS is the largest cause of death in U.S.
Majority of mortality associated with ST
Elevation Myocardial Infarction (STEMI).
Page 2
ACS Types
Page 3
Chest Pain
First symptom of those suffering myocardial
ischemia.
Called angina pectoris (angina pain)
Feeling of heaviness, pressure
Moderate to severe
In substernal area
Often mistaken for indigestion
May radiate to neck, jaw, left arm/ shoulder
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Due to :
oAccumulation of lactic acid in myocytes or
oStretching of myocytes
Three types of angina pectoris:

oStable, unstable and Prinzmetal
Page 5
Stable angina pectoris

Caused by chronic coronary obstruction
Recurrent predictable chest pain
Gradual narrowing and hardening of
vessels so that they cannot dilate in
response to increased demand of physical
exertion or emotional stress
Lasts approx. 3-5 minutes
Relieved by rest and nitrates
Page 6
Unstable Angina pectoris

Lasts more than 20 minutes at rest, or
rapid worsening of a pre-existing angina
May indicate a progression to M.I.
Page 7
Prinzmetal angia pectoris

(Variant angina)
Caused by abnormal vasospasm of normal
vessels (15%) or near atherosclerotic narrowing
(85%)
Occurs unpredictably and almost exclusively at
rest.
Often occurs at night during REM sleep
May result from hyperactivity of sympathetic
nervous system, increased calcium flux in
muscle or impaired production of prostaglandin
Page 8
Silent Ischemia
Totally asymptomatic
May be due abnormality in innervation
Or due to lower level of inflammatory
cytokines
Page 9
Acute Myocardial Infarction
Page 10
DEFINITION
qAcute myocardial infarction (MI) is defined as death or
necrosis of myocardial cells.
qMyocardial infarction occurs when myocardial ischemia
exceeds a critical threshold and overwhelms myocardial
cellular repair mechanisms that are designed to maintain
normal operating function and hemostasis.
qIschemia at this critical threshold level for an extended
time period results in irreversible myocardial cell damage
or death.
Page 11
PREVALENCE
qIn general, MI can occur at any age, but its
incidence rises with age.
qThe actual incidence is dependent upon
predisposing risk factors for atherosclerosis
qApproximately 50% of all MI's in the US occur in
people younger than 65 years of age.
qHowever, in the future, as demographics shift
and the mean age of the population increases, a
larger percentage of patients presenting with MI
will be older than 65 years
Page 12
Risk Factors:
Six primary risk factors have been identified with the
development of atherosclerotic coronary artery disease and
MI:
hyperlipidemia,
diabetes mellitus,
hypertension,
Smoking (Tobacco use),
male gender, and
family history of atherosclerotic arterial disease.
The presence of any risk factor is associated with doubling

the relative risk of developing atherosclerotic coronary
artery disease.
Page 13
Pathophysiology
Mechanisms of Occlusion:
Most MIs are caused by a disruption in the vascular
endothelium associated with an unstable
atherosclerotic plaque that stimulates the formation of
an intracoronary thrombus, which results in coronary
artery blood flow occlusion.
If such an occlusion persists long enough (20 to 40
min), irreversible myocardial cell damage and cell
death will occur.
Page 14
Pathophysiology (Cntd.)
The development of atherosclerotic plaque occurs over a
period of years to decades. The initial vascular lesion leading
to the development of atherosclerotic plaque is not known
with certainty.
The two primary characteristics of the clinically symptomatic
atherosclerotic plaque are a fibromuscular cap and an
underlying lipid-rich core.
Plaque erosion may occur due to the actions of
metalloproteases and the release of other collagenases and
proteases in the plaque, which result in thinning of the
overlying fibromuscular cap.
Hemodynamic forces applied to the arterial segment, can lead
to a disruption of the endothelium and fissuring or rupture of
the fibromuscular cap.
a site otherwise known as the plaque's "shoulder region."
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Vulnerable Plaque
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Mechanisms of Myocardial Damage:

qThe severity of an MI is dependent on three
factors:
The level of the occlusion in the coronary artery,
The length of time of the occlusion
The presence or absence of collateral circulation
qThe death of myocardial cells first occurs in the

area of myocardium that most distal to the
arterial blood supplythat is, the endocardium.
qAs the duration of the occlusion increases, the
area of myocardial cell death enlarges
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Structural, functional changes

q
q
q
q
q
q
Decreased contractility
Decreased LV compliance
Decreased stroke volume
Dysrhythmias
Inflammatory response is severe
Scarring results
Strong, but stiff; cant contract like healthy cells
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Page 23
SIGNS AND SYMPTOMS

AcuteMI may have unique presentations 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 MI's are more likely
to be diabetic.
Chest pain described as a pressure sensation, fullness, or squeezing in
the midportion of the thorax
Radiation of chest pain into the jaw/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
Impairment of cognitive function without other cause
A MI may occur at any time of the day, but most appear to be clustered
around the early hours of the morning and/or are associated with
demanding physical activity. Approximately 50% of patients have some
warning symptoms (angina pectoris or an anginal equivalent) prior to
the infarct.
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Nature of Pain
The pain of AMI is variable in intensity; in most patients it is
severe and in some instances intolerable.
The pain is prolonged, usually lasting for more than 30 minutes
and frequently for a number of hours.
Described as constricting, crushing, oppressing, or compressing;
often the patient complains of a sensation of a heavy weight or a
squeezing in the chest. Although the discomfort is typically
described as a choking, viselike, or heavy pain, it may also be
characterized as a stabbing, knifelike, boring, or burning
discomfort.
The pain is usually retrosternal in location, spreading frequently to
both sides of the anterior chest, with predilection for the left side.
Often the pain radiates down the ulnar aspect of the left arm,
producing a tingling sensation in the left wrist, hand, and fingers.
Some patients note only a dull ache or numbness of the wrists in
association with severe substernal or precordial discomfort. In
some instances, the pain of AMI may begin in the epigastrium and
simulate a variety of abdominal disorders, a fact that often causes
<MI> to be misdiagnosed as indigestion
Page 25
Nature of Pain
In other patients the discomfort of AMI radiates to the shoulders,
upper extremities, neck, jaw, and interscapular region, again
usually favoring the left side. In patients with preexisting angina
pectoris, the pain of infarction usually resembles that of angina
with respect to location. However, it is generally much more
severe, lasts longer, and is not relieved by rest and nitroglycerin.
In some patients, particularly the elderly, AMI is manifested
clinically not by chest pain but rather by symptoms of <acute> left
ventricular failure and chest tightness or by marked weakness or
frank syncope. These symptoms may be accompanied by
diaphoresis, nausea, and vomiting.
The recognition that pain implies ischemia and not infarction
heightens the importance of seeking ways to relieve the ischemia,
for which the pain is a marker. This finding suggests that the
clinician should not be complacent about ongoing cardiac pain
under any circumstances
Page 26
Other symptoms
Nausea and vomiting occur in more than 50 percent of patients
with transmural <MI> and severe chest pain, presumably owing
to activation of the vagal reflex or to stimulation of left
ventricular receptors as part of the Bezold-Jarisch reflex.
These symptoms occur more commonly in patients with
inferior <MI> than in those with anterior <MI>.
Occasionally, a patient complains of diarrhea or a violent urge
to evacuate the bowels during the <acute> phase of <MI>.
Other symptoms include feelings of profound weakness,
dizziness, palpitations, cold perspiration, and a sense of
impending doom.
On occasion, symptoms arising from an episode of cerebral
embolism or other systemic arterial embolism are the first signs
of AMI.
The aforementioned symptoms may or may not be accompanied
by chest pain.
Page 27
SILENT <MI>
Population studies suggest that between 20 and 60 percent
of nonfatal <MIs> are unrecognized by the patient and are
discovered only on subsequent routine ECG or postmortem
examinations.
Of these unrecognized infarctions, approximately half are
truly silent, with the patients unable to recall any
symptoms whatsoever. The other half of patients with socalled silent infarction can recall an event characterized by
symptoms compatible with <acute> infarction when
leading questions are posed after the ECG abnormalities
are discovered.
Unrecognized or silent infarction occurs more commonly
in patients without antecedent angina pectoris and in
patients with diabetes and hypertension
Page 28
ECG changes
q Pronounced, persisting Q waves
q ST elevation
q T wave inversion
Page 29
The Three Is
Ischemia = ST depression or T-wave inversion
Represents lack of oxygen to myocardial tissue
Page 30
The Three Is
Injury = ST elevation -- represents prolonged
ischemia; significant when > 1 mm above the baseline

of the segment in two or more leads
Page 31
The Three Is
Infarct = Q wave represented by first
negative deflection after P wave; must be
pathological to indicate MI
Page 32
What part of the heart is affected ?

II, III, aVF =
Inferior Wall
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Page 33
Inferior Wall MI
Page 34
Based on the EKG, which vessel in the

heart is blocked?
II, III & aVF = Inferior Wall MI =
Right Coronary Artery
blockage
Page 35
Which part of the heart is affected ?

Leads V1, V2, V3, and V4 =
Anterior Wall MI
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Page 36
Anterior Wall MI
Page 37

heart is blocked?
V1 - V4 = Anterior Wall
(Left Ventricle) =
Left Anterior
Descending Artery
Blockage
Page 38
What part of the heart is affected ?

l I,
aVL, V5 and V6
Lateral wall of left ventricle

I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Page 39
Lateral Wall MI
Page 40

heart is blocked?
I, aVL, V5 + V6 =
Lateral Wall =
Circumflex Artery
Blockage
Page 41
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Page 43
THERAPY
q The goals of therapy in AMI are the expedient
restoration of normal coronary blood flow and
the maximum salvage of functional
myocardium.
q These goals can be met by a number of
medical interventions and adjunctive therapies.
q The primary obstacles to achieving these goals
are the patient's failure to quickly recognize MI
symptoms and the delay in seeking medical
attention.
q When patients present to a hospital, there are a
variety of interventions to achieve treatment
goals.
Page 44
Time is Muscle
Page 45
Treatment
q
q
q
q
q
q
q
First 24 hours crucial

Hospitalization, bed rest
ECG monitoring for arrhythmias
Pain relief (morphine, nitroglycerin)
Thrombolytics to break down clots
Administer oxygen
Revascularization interventions: by-pass
grafts, stents or balloon angioplasty
Page 46
General Treatment Measures

q ASPIRIN
q CONTROL OF CARDIAC PAIN
Analgesics
q NITRATES
q BETA-ADRENOCEPTOR BLOCKERS
q OXYGEN
Limitation of Infarct Size
Page 47
THERAPY (Cntd.)
Antiplatelet Agents:
qAspirin in a dose of at least 160 mg and up to 325
mg should be administered immediately on
recognition of MI signs and symptoms and continued
daily indefinitely.
qOther antiplatelet agentsincluding clopidogrel,
ticlopidine, and dipyridamole-have not been shown
in any large-scale trial to be superior to aspirin in MI.
These other antiplatelet agents (specifically
clopidogrel) may be useful for patients who have a
true allergy to aspirin and for patients with known
resistance to aspirin's effects.11-13
Page 48
THERAPY (Cntd.)
qSupplemental Oxygen:
There are no published studies demonstrating that oxygen
therapy reduces mortality or morbidity of a MI.
qNitrates:
qBeta-blockers:
Beta-blocker therapy is recommended within 12 hours of MI
symptoms and is continued indefinitely.
Treatment with a beta-blocker reduces MI mortality
presumably by decreasing the incidence of arrhythmogenic
death.
Beta blockade decreases the rate and force of myocardial
contraction and decreases overall myocardial oxygen
demand. In the setting of reduced oxygen supply in MI, the
reduction in oxygen demand provided by beta blockade
minimizes myocardial injury and death.
Page 49
Heparin:
Unfractionated Heparin:
qIntravenous unfractionated heparin is recommended in
patients with a MI who undergo percutaneous
revascularization or fibrinolytic therapy with alteplase.
qIntravenous unfractionated heparin is also recommended
in patients with a MI who receive fibrinolytic therapy with
a non-selective fibrinolytic agent (urokinase,
streptokinase, anistreplase) and are at increased risk for
systemic emboli (prior embolic event, large or anterior
wall infarction, known left ventricular thrombus, or atrial
fibrillation).4
Page 50
Low-molecular-weight Heparin
(LMWH)
q
q
q
q
q
LMWH can be administered to MI patients not treated

with fibrinolytic therapy that have no contra-indication
to heparin.4
The LMWH class of drugs includes several agents that
have distinctly different anticoagulant effects.
These effects can be characterized by a given agent's
ratio of activity against factors Xa and IIa.
LMWHs have been proven to be effective in treating
acute coronary syndromes that are characterized by
unstable angina and non-Q-wave MI.
Their fixed doses are easy to administer, and
laboratory testing to measure their therapeutic effect is
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Page 51
Fibrinolytics:
qFibrinolytic therapy is indicated for patients with a
presentation compatible with MI and ST segment
elevation greater than 0.1 mV in 2 contiguous EKG
leads, or new onset of a bundle branch block, who
present less than 12 hours but not more than 24 hours
after symptom onset.4
qRestoration of coronary blood flow in MI can also be
accomplished pharmacologically with the use of a
fibrinolytic agent.As a class, the plasminogen activators
have been shown to restore coronary blood flow in 50%
to 80% of MI patients.
q The successful use of fibrinolytic agents provides a
definite survival benefit that is maintained for years
qA fibrinolytic is most effective when the "door-to-needle"
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time is 30 minutes or
less
Page 52
Percutaneous Coronary
Intervention:
Percutaneous coronary intervention is an
alternative therapy to fibrinolysis if performed
by a skilled operator supported by experienced
personnel performed in a well-equipped
catheterization laboratory.
Page 53
Percutaneous Coronary
Intervention:
The performance standard for primary percutaneous
intervention as a MI therapy is a "door-to-balloon" time of 90
minutes ( 30 minutes).4 Restoration of coronary blood flow
in a MI can be accomplished mechanically by percutaneous
coronary intervention (PCI). Mechanical revascularization by
PCI is used as a primary therapy in many well-equipped
medical centers and as an alternative to fibrinolysis when
fibrinolysis is not clearly indicated or contraindicated. PCI can
successfully restore coronary blood flow in 90% to 95% of a
MI patients
PCI provides a definite survival advantage over fibrinolysis for
MI patients who are in cardiogenic shock
Page 54
TIMI grading system:

Grade 0 = complete occlusion of the infarct-related
artery.
Grade 1 = some penetration of the contrast material
beyond the point of obstruction but without perfusion
of the distal coronary bed.
Grade 2 = perfusion of the entire infarct vessel into
the distal bed but with delayed flow compared with a
normal artery.
Grade 3 = full perfusion of the infarct vessel with
normal flow
Page 55
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ACUTE CORONARY

Free Powerpoint Templates

What is Acute Coronary Syndrome

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Three types of angina pectoris:

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Stable angina pectoris

Unstable Angina pectoris

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Prinzmetal angia pectoris

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Acute Myocardial Infarction

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The presence of any risk factor is associated with doubling

Free Powerpoint Templates

Free Powerpoint Templates

Free Powerpoint Templates

Free Powerpoint Templates

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Mechanisms of Myocardial Damage:

qThe death of myocardial cells first occurs in the

Structural, functional changes

Strong, but stiff; cant contract like healthy cells

Free Powerpoint Templates

Free Powerpoint Templates

SIGNS AND SYMPTOMS

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Free Powerpoint Templates

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ischemia; significant when > 1 mm above the baseline

Free Powerpoint Templates

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What part of the heart is affected ?

Free Powerpoint Templates

Free Powerpoint Templates

Based on the EKG, which vessel in the

Free Powerpoint Templates

Which part of the heart is affected ?

Free Powerpoint Templates

Based on the EKG, which vessel in the

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What part of the heart is affected ?

Lateral wall of left ventricle

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Free Powerpoint Templates

Based on the EKG, which vessel in the

Free Powerpoint Templates

Free Powerpoint Templates

Free Powerpoint Templates

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First 24 hours crucial

General Treatment Measures

Limitation of Infarct Size

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LMWH can be administered to MI patients not treated

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TIMI grading system:

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