myocardial infarction

MYOCARDIAL INFARCTION

BY ANIL MANDALIA

MSN

BHAVNAGAR (Gujarat) - IndiaBHAVNAGAR (Gujarat) - India

Mob:9898535498

Email : [email protected]

1

DEFINITION

• “Acute myocardial infarction (MI) is a clinical

syndrome that results from occlusion of a

coronary artery, with resultant death of

cardiac myocytes in the region supplied by cardiac myocytes in the region supplied by

that artery.

2

• A myocardial infarction (MI), commonly

known as a heart attack, results in the death

of heart muscle.

• The affected myocardial cells in the heart • The affected myocardial cells in the heart

are permanently destroyed.

3

• An MI occurs from a partial or complete

blockage of a coronary artery, which

decreases the blood supply to the cells of

the heart supplied by the blocked coronary the heart supplied by the blocked coronary

artery.

4

ETIOLOGY

• Acute coronary thrombosis (partial or total)

is associated with 90% of MIs.

– Severe CAD (greater than 70% narrowing of the

artery) precipitates thrombus formation.artery) precipitates thrombus formation.

7

ETIOLOGY

• Other etiologic factors include coronary

artery spasm, coronary artery embolism,

infectious diseases causing arterial

inflammation, hypoxia, anemia, and severe inflammation, hypoxia, anemia, and severe

exertion or stress on the heart in the

presence of significant CAD .

8

RISK FACTORS FOR CORONARY

ARTERY DISEASE 9

PATHOPHYSIOLOGY

Formation of Atherosclerosis

Formation of plaque

10

Formation of plaque

Release of collagen and proteases (within the plaque)

This results in thinning of the overlying fibromuscular cap

PATHOPHYSIOLOGY

Disruption of the endothelium and fissuring or rupture of the fibromuscular cap.

11

The loss of structural stability of a plaque

Disruption of the endothelial surface can cause the formation of thrombus via platelet-mediated

activation of the coagulation cascade.

PATHOPHYSIOLOGY

If a thrombus is large enough to occlude coronary blood flow, an MI can result

12

SIGNS AND SYMPTOMS

• Chest pain

• Diaphoresis, cool clammy skin, facial pallor

• Hypertension or hypotension• Hypertension or hypotension

• Bradycardia or tachycardia

• Premature ventricular and/or atrial beats

• Palpitations, severe anxiety, dyspnea

13

SIGNS AND SYMPTOMS

• Disorientation, confusion, restlessness

• Fainting, marked weakness

• Nausea, vomiting, hiccups• Nausea, vomiting, hiccups

• Atypical symptoms: epigastric or abdominal

distress, dull aching or tingling sensations,

shortness of breath, extreme fatigue

14

DIAGNOSTIC EVALUATION 1

5

ECG CHANGES

• Generally occur within 2 to 12 hours, but

may take 72 to 96 hours.

• Necrotic, injured, and ischemic tissue alter

ventricular depolarization and ventricular depolarization and

repolarization.

– ST segment depression and T wave inversion indicate a

pattern of ischemia.

– ST elevation indicates an injury pattern.

– Q waves indicate tissue necrosis and are permanent.

16

ECG CHANGES1

7

Evolution of the ECG during a

myocardial infarct

Time from onset of

symptomsECG Changes in the heart

Minutes

hyperacute T waves

(tall T waves), ST-

elevation

reversible ischemic

damage

18

elevationdamage

Hours

ST-elevation, with

terminal negative T

waves, negative T

waves (these can last

for days to months)

onset of myocardial

necrosis

Days Pathologic Q Waves scar formation

Necrosis of myocardium 1

9

Fibrosis of myocardium 2

0

ECG CHANGES

LM = Left main

21

RCA = Rt. Coronary Artery

LAD = Lt. anterior descending

RCX = Ramus circumflexus

ECG CHANGES2

2

ECG CHANGES2

3

ECG CHANGES

localisation ST elevationReciprocal ST

depressioncoronary artery

Anterior MI V1-V6 None LAD

Septal MI

V1-V4,

disappearance of

septum Q in leads none

LAD-septal

branches

24

septum Q in leads

V5,V6

branches

Lateral MI I, aVL, V5, V6 II,III, aVF LCX or MO

Inferior MI II, III, aVF I, aVLRCA (80%) or RCX

(20%)

Posterior MI V7, V8, V9

high R in V1-V3

with ST depression

V1-V3 > 2mm

(mirror view)

RCX

Right Ventricle MI V1, V4R I, aVL RCA

CARDIAC MARKERS

• All muscle cells, including cardiac muscle

cells contain protein enzymes or

biochemical markers that leak out into the

bloodstream when muscle cells are bloodstream when muscle cells are

damaged.

• A rise in a cardiac marker confirms cardiac

cell death.

25

CARDIAC MARKERS

SERUM TESTEARLIEST

INCREASE (HR)PEAK (HR)

RETURN TO

NORMAL

Total CK 3–6 24–36 3 days

26

Total CK 3–6 24–36 3 days

CK-MB:

isoenzyme

4–8 12–24 3–4 days

Myoglobin 1-3 4-12 3–4 days

Troponin T or I 3-4 4-24 1-3 Wk

Management

• Medical management

• Surgical Management

• Nursing managment

27

Medical management

• The goal of medical management is to…

– Minimize myocardial damage,

– Preserve myocardial function, and

– Prevent complications.– Prevent complications.

28

Goal

Goal Treatment

Minimize

myocardial damage

Thrombolytic medications or PTCA

29

Preserve myocardial

function

Reducing myocardial oxygen

demand and increasing oxygen

supply

Prevent

complications.

Effective use of “Golden Period”

Management in the Emergency

Department (MONA-THERAPY)

• M – Morphine - Acts as an analgesic and

sedative.

• Morphine is routinely administered by

repetitive (every 5 min) intravenous repetitive (every 5 min) intravenous

injection of small doses (2–4 mg) rather

than by the subcutaneous administration of

a larger quantity.

30



• O – Oxygen therapy - O2 should be

administered by nasal prongs or face mask

(2–4 L/min) for the first 6–12 h after

infarction.infarction.

31



• N – Nitroglycerin - Dilates peripheral

vessels, relaxes vascular smooth muscle,

and decreases preload. Up to three doses of

0.4 mg should be administered at about 0.4 mg should be administered at about

5-min intervals.

32



• A – Aspirin - Antiplatelet drug. Chewed or

dispersible 160–325-mg tablet .

• This measure should be followed by daily

oral administration of aspirin in a dose of oral administration of aspirin in a dose of

75–150 mg.

33

PHARMACOLOGIC THERAPY :

Thrombolytic:

• The purpose of thrombolytics is to dissolve

the thrombus in a coronary artery

(thrombolysis), allowing blood to flow (thrombolysis), allowing blood to flow

through the coronary artery again

(reperfusion), minimizing the size of the

infarction, and preserving ventricular

function.

34


Thrombolytic:

• streptokinase (Kabikinase, Streptase),

alteplase (Activase), and reteplase (r-PA,

TNKase). TNKase).

• Anistreplase (Eminase) is another

thrombolytic agent that may be used.

35


Analgesics:

• The analgesic of choice for acute MI is

morphine sulfate. Morphine is routinely

administered by repetitive (every 5 min) administered by repetitive (every 5 min)

intravenous injection of small doses

(2–4 mg) rather than by the subcutaneous

administration of a larger quantity.

36


Antithrombin agents :

• The standard antithrombin agent used in

clinical practice is unfractionated heparin

(UFH). The recommended dose of UFH is an (UFH). The recommended dose of UFH is an

initial bolus of 60 U/kg (maximum 4000 U)

followed by an initial infusion of 12 U/kg

per hour (maximum 1000 U/h). An

alternative to UFH for anticoagulation of

patients are the low-molecular-weight

heparin (LMWH) 37


Angiotensin-Converting Enzyme Inhibitors

(ACE-I) :

• It decreases the mortality rate and prevents

the onset of heart failure.the onset of heart failure.

38


Calcium Channel Blockers –

• Calcium channel blockers prohibit the entry

of calcium into smooth muscle. This assists

with dilating coronary arteries and veins.with dilating coronary arteries and veins.

• Calcium channel blockers also decrease

systemic blood pressure, total peripheral

resistance and cardiac afterload

39


Beta-adrenoceptor blockers :

• These drugs reduce myocardial oxygen

consumption by blocking the beta-

adrenergic sympathetic stimulation to the adrenergic sympathetic stimulation to the

heart. The result is a reduction in heart rate

and force of contraction. Eg. Propranolol

(Inderal), metoprolol (Lopressor, Toprol),

and atenolol (Tenormin)

40


Plaque stabilizing and lipid lowering :

• Atorvastatine, simvastatin rosuvastatine

groups of drugs are used for this purpose

41


Activity

• Complete bed rest for the first 12 h.

• In the absence of complications, patients should

be encouraged, under supervision, to resume an be encouraged, under supervision, to resume an

upright posture by dangling their feet over the

side of the bed and sitting in a chair within the

first 24 h.

• In the absence of hypotension and other

complications, by the second or third day patients

typically are ambulating in their room with

increasing duration and frequency.

42


Diet

• Either nothing or only clear liquids by

mouth for the first 4–12 h.

• The typical coronary care unit diet should • The typical coronary care unit diet should

provide ≤30% of total calories.

• Portions should not be unusually large, and

the menu should be enriched with foods

that are high in potassium, magnesium, and

fiber but low in sodium.

43


Bowels

• Morphine leads to constipation.A diet rich in

bulk, and the routine use of a stool softener

such as dioctyl sodium sulfosuccinate (200 such as dioctyl sodium sulfosuccinate (200

mg/d) are recommended.

• If the patient remains constipated despite

these measures, a laxative can be prescribed.

44

PHARMACOLOGIC THERAPY

Sedation

• Many patients require sedation during

hospitalization to withstand the period of

enforced inactivity with tranquillity.enforced inactivity with tranquillity.

• Diazepam (5 mg), oxazepam (15–30 mg), or

lorazepam (0.5–2 mg), given three or four

times daily, is usually effective.

45

SURGICAL MANAGEMENT :

Percutaneous Coronary Interventions

• Mechanical opening of the coronary vessel

can be performed during an evolving

infarction. infarction.

• Percutaneous coronary interventions (PCI),

including percutaneous transluminal

coronary angioplasty, coronary stenting,

and arthrectomy can be used instead of or

as an adjunct to thrombolytic therapy.

46

SURGICAL MANAGEMENT :

Surgical Revascularization

• Emergency CABG (Coronary Artery Bypass

Graft )surgery can be performed within 6

hours of evolving infarction. hours of evolving infarction.

48

Complications of MI4

9

27

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Thank you

50

An

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MS

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myocardial infarction

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