Case Presentation Ta..Bsn II-c

Acute Myocardial
Infarction
21/12/7 Free Template from www.brainybetty.com 1

Acute Myocardial Infarction
Definition
The term myocardial infarction is derived

from myocardium (the heart muscle) and
infarction (tissue death due to oxygen
starvation)
Ischemic myocardial necrosis usually

resulting from abrupt reduction of coronary
blood flow to a segment of myocardium.

Epidemiology
It is a medical emergency, and the leading cause of death for
both men and women all over the world
Important Risk factors:

• Older age
• Male gender
• Family history
• Cigarette smoking
• Hypercholesterlemia (especially high LDL and low HDL)
• Diabetes
• High blood pressure
• Obesity (defined by a BMI of more than 30 kg/m2)
Most common cause of AMI is an

occlusive coronary thrombus at the
site of a pre-exixting atherosclerotic
plaque

Other causes:
• Coronary artery spasm
Variant angina
Cocaine abuse
• Coronary artery embolus

Atrial myxoma
Atrial or ventricular thrombus
• Vasculitis
• Hypercoagulable states
Polycythemia vera
Thrombocytosis

Mechanism of AMI
Over decades atherosclerosis causes gradual buildup

of cholesterol and fibrous tissue in plaques
in the wall of coronary arteries
Coronary artery lumen narrows as a result of

decades of advancing atherosclerosis
Plaques can become unstable due to inflammation,

rupture, and promote a thrombus that occludes the
artery; this can occur in minutes
Plaque rupture leads to myocardial infarction

A collagen scar forms in its place


Clinical Findings
Symptoms
• Chest pain:
• prolonged (>20 min)
sensation of tightness, pressure, squeezing
Radiation to left arm, lower jaw, neck, right arm, back, epigastrium
• Dyspnea: shortness of breath

• Diaphoresis: an excessive form of sweating
• Weakness or Fatigue
• Light-headedness
• Nausea and vomiting
• Palpitations
• Loss of consciousness
• Sudden death
• Silent, without chest pain or other symptoms
Diagram of pain zones in myocardial infarction

dark red = most typical area,
light red = other possible areas

Signs
General:
Appearance: Anxious and sweating

Tachycardia or Bradycardia
Blood pressure high or low
Fever: low grade
Jugular venous distention (JVD)±
Edema ±
Cyanosis ±
Chest:
Clear lungs, or basilar rales
Heart:
May be normal
Abnormally located ventricular Impulse
Soft heart sounds
Atrial gallop S4 or ventricular gallop S3
Systolic murmur due to papillary muscle or
ventricular septal rupture
Pericardial friction rub

ECG Change Onset Disappearance
Electrocardiogram (ECG)
Hyper acute T Immediately 6-24 hours
waves (Tall
Peaked T waves in
leads facing
infarction)
ST Segment Immediately 1-6 weeks

elevation
Q waves longer One to Years to never

than 0.04 sec several
days
T wave 6-24 hours Months to

inversion years
Main Coronary blood supply
Right Coronary Artery Left Coronary Artery

Arises from Aorta behind the Arises from the Aorta behind
right aortic sinus of valsalva the left aortic Sinus of valsalva
Supplies: Left anterior descending (LAD)
•Posterior Inferior wall of LV Supplies:
•Right Ventricle and atrium via Anterior wall of left ventricle
marginal branch Anterior two thirds of
•SA and AV node interventricular septum
Left Circumflex (LCX)
Supplies:
Lateral wall of left ventricle


Location of Myocardial Infarction
Area of Infarction ECG Changes in leads Artery involved
Inferior wall II, III, aVf Right Coronary

Anteroseptal V1-V3 Left anterior
descending
Anterior wall V2-V4 Left anterior
descending
Lateral wall I, aVL, V4, V5 and V6 Left anterior
descending or
circumflex
Posterior wall V1-V2: Tall broad Posterior
initial R wave, ST descending
depression, Tall
Upright T wave, in
association with
Inferior or lateral MI
Cardiac Enzymes
• Cardiac markers or cardiac enzymes are

proteins from cardiac tissue found in the blood
• These proteins are released into the

bloodstream when damage to the heart occurs,
as in the case of a myocardial infarction
• Serial measurement of cardiac enzymes is the

most valuable diagnostic test
• Creatinine Kinase (CK-MB) and Troponin I or T

(TNI) are the most specific and widely used
assays
CK-MB begins to elevate at 4-6 hours
after onsetof chest pain and peaks
at 12-24 hours
Troponin I begins to elevate 4-6

hours after onset of pain and
Remains elevated for 1-2 weeks

Chest X-Ray:
May be normal or may show signs of Congestive heart failure
Echocardiography:
Provides assessment of ventricular function and wall motion.
Doppler echo is used to diagnose post infarction mitral
regurgitation or ventricle septal defect
Other Laboratory tests:

Leukocytosis
Scintigraphic studies:
Angiography:
A chest X-ray
showed large
Cardiac silhouette
and
bilateral interstitial
markings
consistent with
pulmonary edema.

Diagnostic criteria
1. Clinical history of ischaemic type chest

pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers
such as CK-MB and Troponin I specific for
the heart

Types of AMI
STEMI : ST-elevation myocardial infarction

NSTEMI : Non-ST-elevation myocardial infarction
Q-wave infarction
Non-Q wave infarction

Treatment
A heart attack is a medical emergency

which demands immediate attention
The ultimate goal of the management in the

acute phase of the disease is to salvage
as much myocardium as possible and
prevent further complications.

General Measures
• CCU(coronnary care unit) Monitoring

• Oxygen(2-4 L/min)
• Aspirin
• Glyceryl trinitrate (nitroglycerin)
• Analgesia (usually morphine)

Reperfusion therapy
The concept of reperfusion has become

so central to the modern treatment of
acute myocardial infarction, that we are
said to be in the reperfusion era

Reperfusion therapy
• Thrombolytic therapy
• Percutaneous coronary intervention
(PCI)
• Bypass surgery

Fibrinolysis is the process

where a fibrin clot, the product
of coagulation, is broken down
by an enzyme plasmin
Fibrin-specific thrombolytic
agents have have the property
of fibrin-enhanced conversion
of plasminogen to plasmin.

Thrombolytic Agents
Recombinant tissue plasminogen
activator (rtPA)
Patients <70 years, Anterior MI, within 4 hours of onset and with
pump failure.
Streptokinase
Older patients with concomitant hypertension (>160mmHg), no
previous exposure to streptokinase or recent streptococcal
infection.
Urokinase
Alteplase
Reteplase
TenecteplaseFree Template from www.brainybetty.com
21/12/7 28
Thrombolytic therapy
Indications
1. Within 12 hours of the onset of typical chest pain of AMI
2. ST elevation of > 1mm in two contiguous leads or Q waves
3. New Left bundle branch block
Contraindications
1. Dissecting aortic aneurysm
2. Uncontrolled hypertension > 180/110
3. Active peptic ulcer
4. Bleeding Diathesis
5. History of cerebrovascular disease
6. Recent trauma or surgery especially of head or spine
7. Traumatic CPR
8. Pregnancy
Percutaneous coronary intervention (PCI)
• PCI done to abort a myocardial infarction is
known as primary PCI
• Goal of primary PCI: open the artery

preferably within 90 minutes of the patient
presenting to the emergency room
• Primary PCI involves performing a coronary

angiogram to determine the anatomical
location of the infarcting vessel, followed by
balloon angioplasty (and frequently
deployment of an intracoronary stent) of the
thrombosed arterial segment

Other pharmacologic agents given in AMI
• Beta blockers
• Angiotensen-converting enzyme
inhibitors
• Anticoagulation (typically with heparin)
• Antiplatelet agents such as Clopidogrel

Complications
1. Infarct extension and post infarction

Ischemia
• Inadequate blood flow though a recanalized vessel

or reocclusion
• Medical therapy with nitrates, beta blockers,
calcium channel blockers as well as heparin and
aspirin is given
• If medical therapy fails then early catheterization
and revascularization by Percutaneous
transluminal coronary angioplasty (PTCA) or
Coronary artery bypass graft (CABG) is performed
2. Life threatening arrhythmias
Electrical characteristics of the infarcted
tissue is changed so arrhythmias are a
frequent complication
The re-entry phenomenon may cause too fast
heart rates like ventricular tachycardia and
even ventricular fibrillation and ischemia in the
electrical conduction system of the heart may
cause a complete heart block

3. Myocardial Dysfunction
Cardiac dysfunction is proportionate to the extent of myocardial
necrosis
■Congestive heart failure:

signs/symptoms: Dyspnoea, Diffuse rales in the lung, Arterial
hypoxemia
Treatment: Oxygen, Diuretics, morphine sulphate, vasodilators nitrates,
ionotropic agents dopamine or dobutamine
■Hypotension and shock:

Systolic BP<100 mmHg, low urine output, cold extremities and
confusion
Treatment: Dopamine, Norepinephrin, Intra-aortic baloon
counterpulsation IABC

4. Mechanical defects
• Paplillary muscle rupture and Interventricular

septum rupture can occur in AMI
• Detected by appearance of new systolic murmer with

clinical deterioration and pulmonary edema
• Treatment is by surgical repair

5. Myocardial rupture
 Myocardial rupture is most common three to five days
after AMI
• Shear stress between the infarcted segment and the
surrounding normal myocardium makes it a nidus for
rupture
• Occur in the free walls of the ventricles
• The weakness may also lead to ventricular aneurysm
• Rupture is usually a catastrophic event that may result
a life-threatening process known as cardiac
tamponade

6. Pericarditis
• As a reaction to the damage of the heart muscle, inflammatory cells

are attracted and may reach out and affect the heart sac causing
pericarditis
• In Dressler's syndrome this occurs several weeks after the initial
event.
• Treated with aspirin, NSAIDs and later steroids
7. Mural Thrombus
• Common in large anterior infarctions

• Systemic embolization is a potential threat
• Detected by echocardiography
• Treatment is anticoagulation with heparin followed by warfarin
therapy

Post Infarction Management
Stress testing
Coronary angiography
Medical Therapy
Antiplatelet drug therapy: Aspirin or clopidogeral

Beta Blocker
ACE- Inhibitors
Lipid lowering Therapy
Smoking cessation
Regular exercise
Sensible diet for patients with heart disease,
Limitation of alcohol intake


Case Presentation Ta..Bsn II-c

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Case Presentation Ta..Bsn II-c

Uploaded by

Copyright:

Available Formats

Acute Myocardial

21/12/7 Free Template from www.brainybetty.com 1

The term myocardial infarction is derived

Ischemic myocardial necrosis usually

21/12/7 Free Template from www.brainybetty.com 2

Important Risk factors:

Most common cause of AMI is an

21/12/7 Free Template from www.brainybetty.com 4

• Coronary artery embolus

21/12/7 Free Template from www.brainybetty.com 5

Over decades atherosclerosis causes gradual buildup

Coronary artery lumen narrows as a result of

Plaques can become unstable due to inflammation,

Plaque rupture leads to myocardial infarction

21/12/7 Free Template from www.brainybetty.com 7

21/12/7 Free Template from www.brainybetty.com 8

• Dyspnea: shortness of breath

Diagram of pain zones in myocardial infarction

21/12/7 Free Template from www.brainybetty.com 10

Appearance: Anxious and sweating

21/12/7 Free Template from www.brainybetty.com 12

ST Segment Immediately 1-6 weeks

Q waves longer One to Years to never

T wave 6-24 hours Months to

Right Coronary Artery Left Coronary Artery

21/12/7 Free Template from www.brainybetty.com 14

21/12/7 Free Template from www.brainybetty.com 15

Inferior wall II, III, aVf Right Coronary

• Cardiac markers or cardiac enzymes are

• These proteins are released into the

• Serial measurement of cardiac enzymes is the

• Creatinine Kinase (CK-MB) and Troponin I or T

Troponin I begins to elevate 4-6

21/12/7 Free Template from www.brainybetty.com 18

Other Laboratory tests:

21/12/7 Free Template from www.brainybetty.com 20

1. Clinical history of ischaemic type chest

21/12/7 Free Template from www.brainybetty.com 21

STEMI : ST-elevation myocardial infarction

21/12/7 Free Template from www.brainybetty.com 22

A heart attack is a medical emergency

The ultimate goal of the management in the

21/12/7 Free Template from www.brainybetty.com 23

• CCU(coronnary care unit) Monitoring

21/12/7 Free Template from www.brainybetty.com 24

The concept of reperfusion has become

21/12/7 Free Template from www.brainybetty.com 25

21/12/7 Free Template from www.brainybetty.com 26

Fibrinolysis is the process

21/12/7 Free Template from www.brainybetty.com 27

• Goal of primary PCI: open the artery

• Primary PCI involves performing a coronary

21/12/7 Free Template from www.brainybetty.com 30

21/12/7 Free Template from www.brainybetty.com 31

1. Infarct extension and post infarction

• Inadequate blood flow though a recanalized vessel

21/12/7 Free Template from www.brainybetty.com 33

■Congestive heart failure:

■Hypotension and shock:

21/12/7 Free Template from www.brainybetty.com 34

• Paplillary muscle rupture and Interventricular

• Detected by appearance of new systolic murmer with

• Treatment is by surgical repair

21/12/7 Free Template from www.brainybetty.com 35