DEPARTMENT OF PHYSIOLOGY

TOPIC-: MYOCARDIAL INFARCTION AND

ITS ECG FINDINGS
MODERATOR -: Dr. Dipti Bania (Professor and HOD, Physiology)
Dr. Nandita Dutta( Associate professor , Physiology)

Presented by:
Pragyan Pritam Saikia(Roll no. 69)
Reetupritom Borah (Roll no. 76)
Jaya Bharti (Roll no. 43)
Daibik Roy Chowdhury (Roll no. 25)
MYOCARDIAL INFARCTION

DEFINITION-:
 Myocardial infarction (MI) is defined as a diseased condition
which is caused by reduced blood flow in a coronary artery
due to atherosclerosis and occlusion of an artery by an
embolus or thrombus

 MI or also known as heart attack is the irreversible

damage of myocardial tissue caused by prolonged
ischemia and hypoxia. It is a leading cause of morbidity
and mortality worldwide.
#BASIC ANATOMY OF CORONARY
CIRCULATION

 Coronary blood supply-:

 Left coronary artery(LCA): supplies left side of the
heart
 Right coronary artery (RCA): supplies right side of
heart

 Collateral circulation –it is a network of small, pre-

existing blood vessels that can develop and
enlarge to provide an alternative blood supply to
the heart when a major coronary artery is blocked.
 #Pathophysiology- Ischemia and
Necrosis
 Ischemia – It is a condition characterized by a
restriction in blood supply to a tissue, muscle or
organ leading to shortage of oxygen and this
decreased oxygen supply leads to anaerobic
metabolism that cause tissue damage.
 This leads in depletion of ATP which causes failure of Na+/k+ pump, cellular swelling and
rupture.
 Necrosis – It is the death of body tissue caused by
 injury, disease or lack of blood flow , leading to
 cell membrane rupture and release of cellular contents ,
 triggering inflammation.
 Wavefront phenomenon-:There is transmural progression
Of necrosis from subendocardium to epicardium
#HEMODYNAMIC CHANGES IN MI-:
 Decreased cardiac output -:
Mechanism –
MI damage the heart muscle , reducing the heart’s ability to pump
effectively This leads to a decrease in stroke volume and
consequently , a reduction in cardiac output ( cardiac output =
heart rate x stroke volume)
Consequence-
A lower cardiac output leads to inadequate blood flow to vital
organs, resulting in symptoms like fatigue , shortness of breath ,
and in severe cases organ dysfunction.
 Increased peripheral resistance -:
Mechanism:
In response to the reduced cardiac output , body attempts to maintain blood pressure by
constricting blood vessels, which increases peripheral resistance (the resistance of blood flow in
the peripheral blood vessels)
Consequence:
The increased resistance can further exacerbate the problem, making it harder for the heart to
pump blood and leading to a vicious cycle.
 Hemodynamic instability and cardiogenic shock -:
If the heart pumping function is severely compromised , it can lead to hemodynamic instability ,
where blood pressure drops dangerously low , and the body’s organs are not adequately perfused.
In severe cases , this can progress to cardiogenic shock, a life- threatening condition where the
heart can not pump enough blood to meet body’s need.
#Types of myocardial
infarction-:
It is classified into five types based on the underlying causes and
circumstances-
 TYPE 1- it is the most common type , occurring due to spontaneous
event like plaque rupture ,fissuring or dissection in a coronary artery ,
leading to blood clot (thrombus)and reduced blood flow to heart
muscle.
 TYPE 2 – this type occurs when the heart’s oxygen supply and
demand are out of balance , but not due to primary coronary event .
This can be caused by factors like increased oxygen demand (eg.
Hypertension) or decreased supply (eg. Coronary artery spasm,
hypotension)
 Type 3 (MI resulting in death )- this type refers to sudden , unexpected cardiac death where
biomarker values are unavailable , meaning the patient dies before blood samples can be drawn or
biomarkers appear in the circulation,
 Type 4 (MI resulting in percutaneous coronary intervention)- this type is associated with procedures
like PCI (angioplasty) and can be further divided into type 4a and type 4b
 Type 5- this MI is related to coronary artery bypass grafting surgery

#Mechanism of coronary occlusion

Coronary occlusion or blockage of a coronary artery, is primarily caused by the buildup of plaque
(atherosclerosis)leading to narrowing and potentially complete blockage of the artery, or by a blood
clot forming on a plaque that has ruptured.
 Atherosclerosis-
 It is a condition where plaque, composed of fatty deposits, cholesterol,and other substances
accumulates on the inner walls of the arteries
 this causes the arteries to narrow and become less flexible , a process called stenosis.over
time the plaque can grow, further restricting blood flow and potentially leading to complete
blockage
 Plaque rupture and thrombus formation:
 Plaques can become unstable and rupture,
exposing the underlying tissue to blood.
 This triggers cascade of events, including
platelet aggregation and clot formation
(thrombus).the thrombus can then completely
block the coronary artery , leading to a heart
attack(myocardial infarction).
 Coronary artery spasm:
 In some cases , coronary occlusion can also
result from a coronary artery spasm, a
temporary constriction of the artery’s muscles
which can reduce or block blood flow
 Other causes:
 in rare instances, coronary occlusion can occur due to other factors , such as embolization
(a blood clot travelling from another part of the body)or inflammation of coronary arteries.

# Clinical presentation and symptoms-

Key symptoms-:
o Chest pain /discomfort-
It typically occurs in the center or left side of the chest and can last for more than a few
minutes or come and go. The pain may radiate to the arms , jaw, neck ,back or shoulders
Other common symptoms –:
• Shortness of breath
• Sweating
• Nausea or vomiting
• fatigue
• Light-headedness or dizziness
• Anxiety or a feeling of impending doom
• Heartburn or indigestion

Atypical presentation-:
• Common in elderly, diabetics and women
• Epigastric pain, fatigue and syncope.
 # Diagnosis of MI -:
 Diagnosing a myocardial infarction (MI) or heart attack involves a combination of assessing
symptoms, performing an electrocardiogram (ECG), and analyzing cardiac biomarkers like
troponin.

1. Clinical Evaluation:

Symptoms:
• Patients may experience chest pain, discomfort, squeezing, or heaviness that can radiate to
the left arm, shoulder, neck, jaw, or back. Other symptoms include shortness of breath,
nausea, sweating, dizziness, or lightheadedness .
Physical Examination:
• A physical exam may reveal signs of low-grade fever, pale and cool, clammy skin, and other
cardiovascular findings.
2. Electrocardiogram (ECG):
 Purpose:
An ECG charts the heart's electrical activity and can reveal signs of a past or recent heart attack.
 Findings:
ECG changes associated with MI include ST-segment elevation or depression, T-wave inversion,
and the development of pathological Q waves.
 Importance:
ECG is a cornerstone in the diagnosis of MI and should be obtained and interpreted quickly.
3. Cardiac Biomarker Testing:
Purpose:
 Blood tests can detect elevated levels of proteins
released by damaged heart muscle cells.
Key Biomarkers:
 Troponin: Cardiac isoforms of troponins
I and T are the established biomarkers of
cardiomyocyte injury.
 Other Markers: Creatine kinase (CK)
and CK-MB can also be measured.
Importance:
 The rise and/or fall in serial troponin measurements are essential for the diagnosis of MI.
4. Imaging Tests:
Echocardiogram:
 Uses sound waves to create images of the heart, helping to identify damaged areas and assess
heart function.
Coronary Angiography:
 A catheter is inserted into an artery and guided to the heart to visualize the coronary arteries
and identify blockages or narrowings.
Cardiac CT or MRI:
 These tests can provide detailed images of the heart and chest, helping to assess the extent of
heart damage.
5. Diagnosis Confirmation:
 A diagnosis of MI is usually made when there is a rise and/or fall of cardiac biomarkers (like
troponin) along with supportive evidence such as typical symptoms, ECG changes, or imaging
evidence of new loss of viable myocardium or new regional wall motion abnormality.
 #Compensatory mechanisms and cardiac output
1. Sympathetic Nervous System Activation:
 Increased Heart Rate and Contractility:
The sympathetic nervous system is activated, leading to an increase in heart rate (tachycardia) and
myocardial contractility, which helps to maintain cardiac output despite the damage caused by the
infarction.
 Peripheral Vasoconstriction:
The sympathetic nervous system also causes peripheral vasoconstriction, increasing systemic vascular
resistance and blood pressure to maintain blood flow to vital organs.
2. Renin-Angiotensin-Aldosterone System (RAAS) Activation:
 Sodium and Water Retention:
The RAAS is activated, leading to increased sodium and water retention by the kidneys, which can
increase blood volume and further contribute to increased blood pressure.
 Vasoconstriction:
Angiotensin II, a product of the RAAS, also causes vasoconstriction, further increasing blood pressure.
 # Complications of MI –:
 Electrical Complications:
 Arrhythmias:
Irregular heartbeats, including premature ventricular beats, tachycardia, and bradycardia, can
occur due to damage to the heart's electrical conduction system.
 Heart Block:
Damage to the heart's electrical pathways can lead to a heart block, where the heart's electrical
signals are disrupted, potentially causing a slow heart rate.
 Ventricular Tachycardia/Fibrillation:
Rapid, potentially life-threatening heart rhythms that can occur in the ventricles, the heart's
lower chambers.
 Mechanical Complications:
 Heart Failure:
Damage to the heart muscle can lead to reduced pumping ability, causing fluid buildup in the lungs
and other parts of the body.
 Cardiogenic Shock:
A severe form of heart failure where the heart is unable to pump enough blood to meet the body's
needs, leading to dangerously low blood pressure and organ damage.
 Myocardial Rupture/Aneurysm:
Weakened heart tissue can rupture, leading to a sudden, potentially fatal cardiac event, or form an
aneurysm, a bulge in the heart wall.
 Ventricular Septal Rupture:
A tear in the wall between the heart's ventricles, leading to a dangerous blood flow between the
chambers.
 Papillary Muscle Rupture:
Damage to the papillary muscles, which control the heart valves, can lead to mitral valve regurgitation,
where blood flows backward through the valve.
 # Treatments of Myocardial Infarction
The treatment of myocardial infarction (MI) includes the
following approaches:
1. Rest and Recovery
•Absolute body rest is crucial to minimize the
workload on the heart.
•Overactivity can lead to the "coronary steal"
syndrome, where blood preferentially flows to normal
heart tissues, depriving the ischemic area​.

2. Drug Therapy
•Vasodilators: Nitroglycerin and other nitrate drugs
help relieve anginal pain by improving blood supply.
•Beta Blockers (e.g., Propranolol): Reduce heart rate
and oxygen demand, decreasing stress on the heart​.
3. Surgical Interventions
 Aortic-Coronary Bypass Surgery: Uses grafted veins to bypass
blocked coronary arteries, restoring normal blood flow.
 Coronary Angioplasty: A balloon catheter is used to expand
the narrowed artery.
 Stenting: Metal stents are placed to keep arteries open.
 Laser Therapy: Experimentally used to dissolve arterial
plaques

4. Long-Term Recovery and Rehabilitation

 The infarcted heart muscle is replaced by scar tissue, and
surrounding muscle may hypertrophy to compensate for lost
function.
 Collateral circulation development aids recovery.
 Physical activity must be gradually reintroduced
5. Pain Management
•Morphine or other opioid analgesics: Used to relieve severe chest pain
and anxiety, reducing sympathetic stimulation that could worsen heart
workload.

6. Thrombolytic Therapy (Fibrinolysis)

•Tissue Plasminogen Activator (tPA),
Streptokinase, or Urokinase: Used to dissolve
clots in the coronary arteries if PCI (angioplasty)
is not immediately available.
 7. Antiplatelet and Anticoagulant
Therapy
•Aspirin: Inhibits platelet
aggregation and prevents further clot
formation.
•Clopidogrel or Ticagrelor: Used
alongside aspirin for stronger platelet
inhibition.
•Heparin or Low-Molecular-
Weight Heparin (LMWH): Prevents
8.
clotOxygen Therapy
extension and further
•thrombosis.
Supplemental oxygen is given to
patients to increase oxygen
delivery to ischemic heart tissues
and reduce hypoxia.
9. Management of Arrhythmias
•MI patients are at high risk of developing
ventricular fibrillation or tachycardia.
Treatments include:
• Defibrillation for life-threatening
arrhythmias.
• Antiarrhythmic drugs (e.g.,
Amiodarone, Lidocaine) to stabilize
heart rhythm.

10. Blood Pressure Control

•ACE Inhibitors (e.g., Enalapril, Ramipril):
Prevent heart remodeling and lower afterload.
•ARBs (e.g., Losartan, Valsartan):
Alternative for patients intolerant to ACE
11. Cholesterol Management
•Statins (e.g., Atorvastatin,
Rosuvastatin): Lower LDL cholesterol
and stabilize atherosclerotic plaques to
prevent future heart attacks.

12. Lifestyle Modifications Post-MI

•Smoking cessation to improve
cardiovascular health.
•Dietary changes: Low-fat, high-fiber,
and heart-healthy diet.
•Weight management to reduce risk
factors like hypertension and diabetes.
•Regular but controlled exercise after
cardiac rehabilitation to strengthen the
ECG CHANGES IN

MYOCARDIAL
INFARCTION
BASIC TERMINOLOGIES :

 ST Segment : The ST segment on an electrocardiogram (ECG) is the

flat, isoelectric line between the end of the QRS complex (J point) and
the beginning of the T wave, representing the period when the
ventricles are between depolarization and repolarization.

 J Point :The J point is the junction between the QRS complex and the
ST segment, and it's a crucial reference point for measuring ST
segment changes.
Ischemia and Infarction

Ischemia refers to a reduction in blood flow,

leading to oxygen deprivation, while
infarction is the tissue death that results from
prolonged or complete cessation of blood flow,
often a consequence of ischemia.
Role of ECG in Myocardial
Infarction :
ECG is done to diagnose and localise the area
of infarction , and to find the duration of infarct
.
ST Elevation Myocardial
Infarction (STEMI)
Characteristics :
 ST segment elevation over area of damage :
- ST elevation > 1 mm
- present in 2 or more contiguous leads
 ST depression in leads opposite infarction
 Inverted T waves
 Pathological Q waves
 It occurs in Transmural Ischemia .
Stages of ECG in STEMI :

1. Hyperacute Phase :
Tall peaked T waves – Symmetric
2. Acute Phase :
- ST segment elevation
> 1mm above borderline in 2 or more contiguous leads
3. Evolving Phase :
Here , T waves gets inverted .
4. Fully Evolved Phase :

Pathological Q Waves : >0.04 sec and >1/3 of the R wave

Pathological Q Waves : >0.04 sec and >1/3 of the R wave

5.Healed Phase :

Pathological Q Wave
 Physiological Basis of ST
Elevation
The : change in AMI is ST segment elevation. This
hallmark of ECG
occurs due to three mechanisms that operate in sequence:
1. Rapid repolarization of the infarcted tissue: Within few
seconds of infarction, the infarcted tissue rapidly repolarizes due
to fast opening of K+ channels. Therefore, the membrane
potential of the infarcted area is higher than the membrane
potential of the normal surrounding area during the later part of
repolarization. This makes the normal region negative to the
infarcted region. As normally current flows from positive to
negative region, in AMI, the current flows from infarcted area to
the surrounding areas and also towards the electrode placed on
the infarcted area. This causes increased positivity between the
S and T waves in ECG and results in ST elevation.
2.Decreased RMP of infarcted muscle fibers: Loss of
intracellular K+ decreases resting membrane potential in
the infarcted muscle cell. This causes current flow into the
infarcted tissue during diastole, which causes TQ segment
depression in ECG that manifests as ST elevation.

3. Delayed depolarization of infarcted cells: Infarcted

muscle fibers depolarize very slowly in comparison to the
surrounding normal fibers. This makes the infarcted tissue to
be relatively positive to the normal tissue, especially in early
part of repolarization, and causes ST segment elevation.
In chronic case, the dead infarcted tissue forms scar tissue
and becomes electrically silent. Therefore, the infarcted tissue
becomes negative relative to the normal tissue. The ECG
manifestations of this negativity are many, though the
common feature is the appearance of Q wave, which was not
Location of MI :
The hallmarks of ‘Acute MI’ is :

1. Elevation of ST segment in the leads overlying the area of infarct .

2. Depression of ST segment in the reciprocal leads .

Example 1 :
Example 1 Answer : Anterolateral Wall MI
with Septal involvement .
Example 2 :
Example 2 Answer :Inferior Wall MI
Non-ST-Elevation Myocardial
Infarction (NSTEMI)
ECG features can be any of the following :
1. ST depression (70-80 % Sensitivity)
2. T wave inversion (10-20% Sensitivity)
3. Both ST depression and T wave inversion
4. Normal ECG
5. It occurs in Subendocardial ischemia .
T Wave Inversion in NSTEMI

 Atleast 1mm deep

 Present in >2 contiguous leads
 Dynamic ( not present in old ECG )

NOTE : T wave inversion is a normal variant in Lead III , aVR and V1 .

Example of T Wave Inversion :
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