MYOCARDIAL INFARCTION

• Acute occlusion / obstruction of one of the coronary artery causing death/necrosis of

surrounding tissue due to complete deprivation of blood supply to the affected area
Inadequate blood supply and oxygen to the myocardium resulting in local necrosis
characterised by retrosternal chest pain radiating to neck, jaw, left shoulder anterior aspect of
forearm and 2 little fingers lasting for more than 30 min and not relieved by rest nitroglycerine.

CAUSES
Most frequent cause is rupture of an atherosclerotic lesion within coronary wall with
subsequent spasm and thrombus formation
Coronary artery vasospasm
Coronary artery emboli

RISK FACTORS
Non-modifiable
Modifiable
Precipitating factors or triggering factors

PATHOPHYSIOLOGY
● Cardiac cells will start necrosis after 15-20 min of ischemia
● The earliest tissue to become ischemic is subendocardium innermost layer of tissue in
the cardiac muscle
● If ischemia continues within 4-6 hours the entire thickness of the heart muscle become
necrosed
● If the thrombus is not completely blocked it will take about 12 hours for necrosis
HEALING PROCESS
● Inflammatory process is the body's response to cell death. Within 24 hours
● Dead cells release enzymes
● Leukocytes infiltrate the area
● Neutrophils and macrophages stimulate proteolytic enzymes and begin to remove
necrotic tissue - 4th day
● Necrotic muscle wall become thin
● Development of collateral circulation improves areas of poor perfusion and limit the
zones of injury and infarction
● Catecholamine mediated lipolysis and glycogenolysis occurs due to infarction
● This leads to increased plasma glucose and free fatty acids
● Oxygen depleted myocardium will use these for anaerobic metabolism
● At 10-14 days - New scar tissue will form
● By 6 weeks necrotic tissues replaced by scar tissue and the injured area is considered
healed
● Scarred areas is often less compliant than other healthy area
● These changes can affect the unaffected myocardium
● Compensation mechanism can lead to hypertrophy and dilation of normal myocardium -
Ventricular remodeling
● This can lead to late HEART FAILURE for the patients with atherosclerosis

DEGREE 'S OF MI
ZONE OF NECROSIS OR INFARCTION
• Death of heart muscle caused by extensive and complete oxygen deprivation, Irreversible
damage

ZONE OF INJURY
• Region of muscle surrounding the area of necrosis, inflamed and injured but still viable if
adequate oxygenation can be restored

ZONE OF ISCHEMIA - PENUMBRA

• Region of heart muscle surrounding the injury which is ischemic, but viable

CLASSIFICATION
There are two basic types of acute myocardial infarction:
1. TRANSMURAL
2. SUB - ENDOCARDIA

TRANSMURAL:
Transmural infarcts extend through the whole thickness of the heart muscle (from endocardium
to epicardium) and are usually a result of complete occlusion of the area's blood supply
It is associated with atherosclerosis involving major coronary arteries.
It can be sub classified into anterior, posterior, inferior, lateral or septal.
 Location of MI Leads affected Vessel Involved

Anterior wall V₂ to V4 Left anterior

descending artery
(LAD) - Diagonal
branch

Septal wall V1 and V₂ Left anterior

descending artery
(LAD) - Septal branch

Lateral wall I, aVL,V5,V6 Left coronary artery

(LCA) - Circumflex
branch

Inferior wall II, III, aVF Right coronary artery

(RCA) - Posterior
descending branch

Posterior wall V1 to V4 Left coronary artery

(LCA) - Circumflex
branch
Right coronary artery
(RCA) - Posterior
descending branch
SUBENDOCARDIAL:
It involves a small area in the subendocardial wall of the left ventricle, ventricular septum, or
papillary muscles.

ST ELEVATION MI
The current guidelines for the ECG diagnosis of the ST segment elevation myocardial infarction
require more than or equal to 1 mm of ST segment elevation in the limb leads, and more than or
equal to 2 mm elevation in the precordial leads.

NON ST ELEVATION MI
NSTEMI is characterized by an imbalance between myocardial oxygen supply and demand.
Most often, the syndrome develops because of decreased myocardial perfusion resulting from
coronary narrowing caused by nonocclusive thrombus formation subsequent to disruption of an
atherosclerotic plaque. In contrast, STEMI results from an occlusive thrombus.
Mo

NEW CLASSIFICATION
● Type 1 - Spontaneous myocardial infarction related to ischemia due to a primary
coronary event such as plaque erosion or rupture or dissection

● Type 2 - Myocardial infarction secondary to ischemia due to either increased oxygen

demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia,
arrhythmias, hypertension, or hypotension

● Type 3 - Sudden unexpected cardiac death with symptoms of STEMI or evidence of

fresh thrombus in a coronary artery by angiography and/or at autopsy

● Type 4 stents: - Associated with coronary angioplasty or stents

1.Type 4a - Myocardial infarction associated with PCI
2.Type 4b - Myocardial infarction associated with stent thrombosis as documented by
angiography or at autopsy

● Type 5 - Myocardial infarction associated with CABG

CLINICAL MANIFESTATIONS
Pain - This is severe, usually substernal retrosternal and epigastric and may radiate into the jaw,
shoulders and down the arms or to the back.
It is described as a heaviness, pressure, tightness, burning, crushing, constriction or tight band
around the chest and lasts for several hours.
It is unrelieved by NTG.
Commonly occurs in the early morning hours, occur when active or at rest or sleep or awake
Usually last for 20-30 minutes or more. Patient with diabetic neuropathy will have silent attacks
In an older patient it may be change in mental status, shortness of breath, dizziness etc

Extreme pallor and cool clammy skin - This is due to the decreased cardiac output and
redirection of blood away from the skin to the major organs.

Dyspnoea - This is due to either the pain or pulmonary congestion caused by pulmonary
hypertension and pulmonary oedema. There is also an increase in the myocardial oxygen
demand.

Nausea and vomiting- This is due to pain or due to vasovagal reflexes

General fatigue - This is due to reduced cardiac output and generalised muscle ischemia.

Cardiovascular manifestations - BP and HR elevated initially due to release of catecholamines

and later BP drop due to decrease cardiac output

Jugular venous distension, hepatic engorgement and peripheral edema right ventricular
dysfunction

Abnormal Heart sounds ventricular dysfunction s3 and s4 indicating

Decrease renal output due to decrease renal perfusion

Pyrexia - The patient's temperature rises upto 100.4 degree or 38 degree Celsius due to the
inflammatory process initiated by the necrotic tissue and widespread death of cells. This
normally occurs over 24 - 48 hours and returns to normal within 7 days.

Sense of Impending Doom - This is due to the release of adrenaline and other catecholamines
as a part of the compensation mechanism. And also due to the real fear of death exits.

DIAGNOSTIC EVALUATIONS
● History Collection
● Physical examination
● Elevated glucose Elevated plasma soon after MI
● ECG Changes
 ● CBC
● Chest X-Ray
● C REACTIVE PROTEIN
● Cardiac Biomarkers
● Echocardiography
● Coronary
● Angiography
● BNP

CARDIAC BIOMARKERS
-Cardiac biomarkers are protein molecules released into the bloodstream 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

1.TROPONIN T AND I
● Preferred markers for detecting myocardial cell injury
● Troponin T-levels increase 3 to 6 hours is similar to CK MB with regard to sensitivity, and
elevated for 14 to 21 days.
● Troponin I levels increase 7 to 14 hours after AMI. - Elevation persist for 5 to 7 days
2.CREATININE KINASE (CK-MB)
● Increased in over 90% of myocardial infarction or injury
 ● Serum levels increase within 4-6 hours after MI
● Peak in 12 to 18 hours
● Duration - 2-3 days
3.MYOGLOBIN
● Release when myocardial tissue injury occurs
● Rises within 2 hours after MI
● Peaks at 4-12 hours
● Returns to normal in 12 hours
● Have false positives with skeletal muscle injury and renal failure

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

LDH - elevate 14-24 hours after onset of myocardial damage

Peak within 48-72 hours
Return to normal within 7-14 days

AST (aspartate transaminase) -increase within several hours after onset of pain
• Peak-12-18 hours
• Return to normal within 3-4 days

C-REACTIVE PROTEIN (CRP)

C-reactive protein is a marker of acute inflammation
With elevated CRP are at increased risk of an event myocardial necrosis and inflammation

BNP:
• B-type natriuretic peptide (BNP) is released from ventricular myocardium when any
dysfunction occurs
• BNP is a marker for heart failure.

Leukocytosis- leukocytosis appears on the second day after AMI and disappears in one week
•Myeloperoxidase - leukocyte enzyme shown to be predictive in AMI

MANAGEMENT
Management of acute attack
Immediate management on the time of admission -
● Position the patient in an upright position
● Initiate oxygen by nasal cannula and keep oxygen saturation above 93% at a rate of 2-4
litre
● Establish an IV route to provide an access for emergency drug therapy
● Give SUBLINGUAL NTG and aspirin if not given before arrival at admission time
● On going investigations and cardiac monitoring with 12 lead ECG
 ● Morphine sulfate given for pain which is not relieved by NTG
● Monitor vital signs include pulse oximetry during first few hours after admission and each
15 to 30 min thereafter
● Maintain bed rest and limit activity for 12 to 24 hours
● Patient with ongoing angina with negative cardiac markers provide dual antiplatelet
therapy (aspirin and ticagrelor) and heparin

DRUG THERAPY
1.IV NTG- initial treatment of patient with ACS
• Goal of Therapy - to reduce angina and improve coronary blood flow
• Immediate action which will help to increase myocardial oxygen supply
• To decrease side effects of hypotension, titrate the dose down at night during sleep and titrate
the dose up during the day

2.MORPHINE SULFATE
• Drug of choice for chest pain which is unrelieved by NTG
• It's a vasodilator, decreases cardiac workload by lowering myocardial oxygen consumption and
decrease BP
• Morphine help to reduce anxiety and fear
• Monitor patient for signs of bradypnea or hypotension

3.BETA ADRENERGIC BLOCKERS

• It decreases myocardial oxygen demand by reducing heart rate, BP and contractility

4.Angiotensin converting enzyme inhibitors

It should start within 24 hours.
• It prevent ventricular remodeling and prevent or slow the progression of HF

5.ANTIDYSRHYTHMIC DRUGS
Dysrhythmias is most common complications after an MI. • Its self limiting but it is life
threatening, should treated

6.Lipid lowering drugs

7.Stool softeners - docusate sodium given to increase bowel movements and prevent straining
and the resultant vagal stimulation from the valsalva maneuver

● THROMBOLYTIC THERAPY
● PCI
● CABG
● LASER REVASCULARIZATION
● IABP
COMPLICATIONS OF MI/ACS
a. Congestive Cardiac Failure
b. Myocardial Rupture and aneurysm
c. Arrhythmia.
d. Pericarditis and dressler syndrome
e. Cardiogenic shock
f. Pulmonary edema
g. Pulmonary embolism
h. Recurrent MI
i. Complications due to necrosis of myocardium
j. Cardiac Arrest
k. Papillary muscle dysfunction

NURSING DIAGNOSIS
• Acute chest pain related to increased cardiac workload and decreased myocardial blood flow
• Ineffective cardiac tissue perfusion related to obstruction in the coronary artery
.activity intolerance related to imbalance between myocardial oxygen supply and demand
• Fear or anxiety related to threat of death
• Risk for decreased cardiac output related to infarcted myocardium / changes in electrical
conduction

PREVENTION
Stop Smoking
Regular Exercise
Diet control
limitation of alcohol intake
Avoid Mental Stress
Regular Health Check-Up

NURSING MANAGEMENT
• Acute intervention
• Pain assessment and relief
• Physiologic monitoring
• Promotion of rest and comfort
• Alleviation of stress and anxiety
. Understanding of the patients emotional and behavioral reactions

PAIN
Provide NTG, morphine, and supplemental oxygen as needed
Ongoing evaluation and documentation

MONITORING
• ECG monitoring - Monitor patient for ischemia by monitoring ST segment levels
Check glucose level to identify the silent ischemia
• Assess heart and breath sounds to find out early HF (dyspnea, tachycardia, pulmonary
congestion, distended neck veins)
• Routine vital signs and monitor intake output each shift
• Assess oxygenation status
• Nasal cannula is used to deliver oxygen and check the nares for irritation for dryness

REST AND COMFORT

• Bed rest for first few days after an MI
• Rest in a chair within 8-12 hours if it is uncomplicated MI
• Comfort measures can promote rest like quite environment, use of relaxation techniques, etc
• Gradually increase the activity

AMBULATORY AND HOME CARE

• Cardiac rehabilitation restoration of a person to an optimal state of function in six areas
• Physiologic, psychologic, mental, spiritual, economic and vocational