CASE PRESENTATION

ON
MYOCARDIAL
INFARCTION
\

• IDENTIFICATION DATA
• PRESENTING COMPLAINTS
• PRESENT HISTORY OF ILLNESS
• PAST HISTORY OF ILLNESS
• FAMILY HISTORY
• DIETARY HISTORY
• PERSONAL HISTORY
• SOCIO-ECONOMIC STATUS
• PHYSICAL EXAMINATION
• NEUROLOGICAL EXAMINATION
MYOCARDIAL
INFARCTION

Presented By

Lt Harsha Varghese
ICU Update Trainee

CH (EC) Kolkata
• Introduction
• Definition
• Incidence
• Related Anatomy & Physiology
• Risk Factors
• Etiology
• Pathophysiology
• Clinical Manifestations
• Investigations
• Management
 DEFINITION

“Myocardial Infarction (MI) occurs because of

sustained ischemia, causing irreversible myocardial cell
death.”
- Lewis Medical Surgical Nursing

“Myocardial Infarction is a disease condition caused by

reduced blood flow in a coronary artery due to
atherosclerosis and occlusion of an artery by an
embolus or thrombus.”
 INCIDENCE
• In industrial countries MI accounts for 10-25% of
deaths

• Incidence is higher in elderly people, about 5% occur

in people under age 40.

• Males have higher risk.

• 80-90% due to thrombus formation

RELATED ANATOMY & PHYSIOLOGY
 TYPES OF MI
• BASED ON LOCATION
1) Anterior Wall MI/ Septal Wall MI
Obstruction in
Left Anterior Descending
Artery (LAD)
ECG
:ST segment elevation
In the anterior leads(V3, V4)
: T segment depression
In the inferior leads(II,III,aVF)
AWMI (Contd..)
TYPES (Contd)
2) Posterior Wall/ Lateral Wall MI
Obstruction of the Left Circumflex Artery
(LCx)

ECG
: ST segment Depression
: Upright T waves
: Tall, broad R waves

Isolated PWMIs are rare

TYPES(Contd)
3) Inferior Wall MI

Obstruction of Right
Coronary Artery (RCA)

ECG
: ST segment elevation in
Inferior leads(II,III,aVF)
: Reciprocal ST segment
Depression in lateral leads
(I, aVL, V5, v6)
 RISK FACTORS
Risk Factors of MI can be broadly classified as

- Non- Modifiable Risk Factors

- Modifiable Risk Factors
 NON MODIFIABLE RISK FACTORS

1) AGE: more than 40 years

2) FAMILY HISTORY: can be genetically inherited

3) GENDER: 3 times more in men than in women

 MODIFIABLE RISK FACTORS

1) HYPERTENSION: Excess strain and resulting

damage eventually leads to atherosclerosis

2) SMOKING: Inferior wall MI> anterior wall MI,

chemicals in the cigarette smoke causes the blood to
thicken and form clots, nicotin & CO mainly affect
the CV system

3) OBESITY: Leads to increased cholesterol levels in

body which in turn causes atherosclerosis
4) SEDENTARY LIFE STYLE: physical inactivity
and lack of exercise with unhealthy eating practices
leads to obesity

5) DIABETES MELLITUS: Usually cause silent MI

due to diabetic neuropathy( nerve disease), which can
damage the nerves that controls the heart, contributes to
the formation of atherosclerotic plaque.

6) STRESS: excess stress hormones predisposes to MI,

adrenalin, noradrenalin and cortisol( HR, BP)

7) HIGH LIPID LEVELS: high lipids builds up in the

walls of arteries causing atherosclerosis, arteries
become narrower and blood flow slows down
COMPARISON
BOOK PICTURE PATIENT PICTURE
AGE > 40 YRS 37 YRS
MALE> FEMALE GENDER MALE
GENETIC FACTORS FAMILY HISTORY OF
CARDIAC DISEASE
PRESENT
HYPERTENSION -
SMOKING CHRONIC SMOKER
OBESITY -
SEDENTARY LIFE STYLE -
DIABETIS MELLITUS FRESHLY DETECTED
STRESS EDUCATION OF CHILDREN
HIGH LIPID LEVELS DETECTED DURING MI
 PATHOPHYSIOLOGY
Any of the risk factors

Atherosclerosis of Coronary artery

Narrowing of Lumen

Insufficient blood flow to Myocardium

Increased oxygen demand of myocardial cells

Oxygen deficit
Anaerobic Myocardial cell death occurs inflammation
glycolysis

Accumulation of CK-MB & Troponin are Fever

Lactic acid released

Irritation of myocardial
nerve fibres
Transmission of
pain to Myocardium

Chest pain stimulation of

radiating towards shoulder vomiting centre
& arms
Nausea & Vomiting
SNS stimulation

Catecholamine Diaphoresis cold & clammy skin

 CLINICAL MANIFESTATIONS
BOOK PICTURE PATIENT PICTURE
CHEST PAIN Upper abdominal pain,
CHARACTERISTIC: severe, continous in nature,
immobilizing pain radiating to chest and arms
Usually described as
Heaviness, Pressure, Tightness Chest Burn
or Burning
LOCATION: Substernal,
Retrosternal, Epigastric
RADIATION: radiating to
neck, jaw, shoulder, arm or
back
DURATION: lasts for >20 min
 BOOK PICTURE PATIENT PICTURE
NAUSEA & VOMITING 4-5 episodes of vomiting
Due to the stimulation of since morning on
vomiting centre by severe 26.01.2021
pain
FEVER due to the No fever during the time of
inflammatory process admission, developed high
caused by myocardial cell grade fever later on
death
DIAPHORESIS due to
increased catecholamine
release due to sympathetic
nervous system stimulation
 BOOK PICTURE PATIENT PICTURE
Cold and clammy skin
(cold sweat)
CARDIO-VASCULAR
MANIFESTATIONS
1) Hypotension Hypotension (vasopressor
2) Oliguria due to support)
decreased cardiac
contractility
3) Dyspnoea Dyspnoea was present
DIAGNOSTIC TESTS
1) ELECTRO CARDIO GRAM (ECG)
- The classic ECG change are;
: T wave inversion
: ST Segment elevation
: Abnormal Q wave

2) CARDIAC MARKERS
These are proteins released in to the blood from necrotic
heart muscle after an MI. These are,
: Troponin T
: Troponin I
: CK-MB
: Myoglobin
 CARDIAC CHARACTERISTIC
MARKERS
Troponin I • Most sensitive & specific
• Rises in 4-12 hrs
• May remain elevated upto 2 weeks
• Normal value <0.3 ng/ml
Troponin T • Most sensitive & specific
• Normal value <0.2 ng/ml

Myoglobin • Lacks specificity

• Rises in 1-4 hrs, first serum cardiac marker to
appear after MI
• Returns to normal within 24 hrs
CK-MB • Rises in 4-12 hrs
• Returns to normal value within 36-48 hrs
• Normal value 2-6 ng/ml
3) LACTATE DE HYDROGENASE (LDH)
- isoenzyme LDH-1 is found in the heart muscles
and LDH-2 in the blood, LDH-1>LDH-2 suggest MI.
- Also increased during hemolysis

4) ASPARTINATE TRANSAMINASE (AST)

-not specific to heart damage
- one of the liver transaminase

5)PRO-B TYPE NATRIURETIC PEPTIDE (Pro-BNP)

-Marker for Acute Congestive Heart Failure
-Identifies cardiac and non cardiac causes
-released due to changes in pressure in the heart
6) CORONARY ANGIO GRAPHY (CAG)
-To detect percentage of blockage
- Determine type of MI

7) CHEST X-RAY
- To rule out cardiomegaly
COMPARISON
BOOK PICTURE PATIENT PICTURE
ECG ECG done on 26/01/2021 s/o
-ST Elevation in V1-V6,aVL
CARDIAC MARKERS Troponin I +ve
LDH : increased
CK-MB : increased
AST : increased
2 D ECHO LVEF 30-35%
MANAGEMENT
-Medical Mgt
- Surgical Mgt
-Nursing Mgt
Goals Of Medical Management Are:
• Restoration of the balance between oxygen supply and
demand to prevent further ischemia

• pain relief

• Prevention and treatment of complications

1) OXYGEN
-Reduces myocardial injury
- start @ 4 L/Min by Nasal Prongs
- patients with severe chronic heart failure,
pulmonary edema, or complication of MI may require
BiPAP, Endotracheal Intubation & Mechanical
Ventilation

2) ASPIRIN
- 160-325 mg stat
- Reduces mortality by 30%
- Cause rapid anti-thrombotic effect & near total
inhibition of Thromboxane A2 production
3) NITRATES- SUBLINGUAL NITROGLYCERIN
- Not given if systolic BP<90mmHg, bradycardia
-10 mg sublingual stat
-anti anginal, vaso dilator: relaxes vascular smooth muscle,
decreased pre-load and after-load, decrease systemic vascular
resistance, reduces cardiac oxygen demand

4)ANALGESIA
-IV Morphine 2-4 mg every 5 min
 DEFINITIVE MEDICAL MANAGEMENT

1) REPERFUSION THERAPY
A) PERCUTANEOUS CORONARY INTERVENTION
- First line of treatment in confirmed MI
- Goals are: open blocked artery within 90 minutes of hospital
arrival (Door to Balloon)
: to locate the blockage
: to assess the severity of blockage
: to determine the presence of collateral circulation
: to evaluate left ventricular function
: to opt the optimal treatment modality (IABP, STENT)
B) THROMBOLYTIC THERAPY (Door to Needle)
- Stop infarction process by dissolving the thrombus in the
coronary artery and reperfusing the myocardium.
- TENECTIPLASE: TPA
- ALTEPLASE
- RETEPLASE

C) CABG
- Failed medical management
- Sternotomy & CardioPulmonary Bypass
-Internal Mammary Artery, Saphenous veins, Radial artery
COMPARISON
BOOK PICTURE PATIENT PICTURE
OXYGEN Patient was placed on oxygen support
by face mask in 5 AF, in CH EC after
the cardiac arrest, he required
mechanical ventilation
ASPIRIN Tab Aspirin 300 mg stat given
NITRATE -
MORPHINE Inj Morphine 1.5 mg given
THRMBOLYTIC Inj tenectiplase 40 mg given Failed
THERAPY thrombolysis
PCI PAMI to LAD done on 27.01.2021
POBA(Plain Old Ballon Angioplasty)
stenting done, TPI inserted
 NURSING MANAGEMENT
Goals are:
- Relief of pain
- Preservation of myocardium
- Immediate and appropriate treatment
- Effective coping with illness-associated anxiety
- Reduction of risk factors
NURSING DIAGNOSIS
1) Ineffective gas exchange related to increased oxygen demand
as evidenced by hypoxia
2) Ineffective tissue perfusion related to disease condition as
evidenced by hypovolumia
3) Decreased cardiac output related to changes in myocardial
contractility
4) Acute pain related to tissue ischemia as evidenced by reports
of chest pain, facial grimacing, restlessness
5) Imbalanced nutrition less than body requirement related
decreased intake as evidenced by nasogastric feed, ventilatory
support
6) Activity intolerance related to imbalance between myocardial
oxygen supply and needs
7) Anxiety related to disease condition, hospital stay, fear of
death
8) Altered sleep pattern related to disease conditions,
environmental disturbances
9) Ineffective coping mechanisms related to knowledge deficit as
evidenced by anxiety
10)Knowledge deficit related to disease as evidenced by patient
asking queries about his present condition and prognosis
HEALTH EDUCATION
- INFORMATION
- EDUCATION
- COMMUNICATION

DISCHARGE PLANNING
 COMPLICATIONS OF MI
The Complications Of MI Include:
- Dysrhythmias
- Heart Failure
- Cardiogenic Shock: when nutrients & oxygen are
inadequate due to left ventricular dysfunction
- Papillary Muscle Dysfunction: muscles near to
mitral valve, may cause mitral valve regurgitation,
requires MVR
- Ventricular Aneurysm: when the damaged wall is
thin, it bulges out during contraction
- Pericarditis
- Dressler Syndrome: pericarditis with effusion and
fever 4-6 days after MI, due to immune reaction in the
necrotised heart tissue
THANK YOU