Unstable angina and AMI

Applied anatomy

HEART 

The heart is a conical hollow muscular organ situated in the middle mediastinum. It is enclosed within the pericardium. It is responsible for blood circulation.ti is an organ with four chambers- right and left atria right and left ventricles.The two atria receive venous blood. The right ventricle propels blood to the lungs and the left ventricle propels blood around the system circulation. 

Valves of the heart 

The valves of the heart maintain un directional flow of the blood and present is regurgitation in the opposite direction. There are two pairs of valve in the heart a pair of alriventricular valves and a pair of semilunar valves. The right alriventricular valves is known as the tricuspid valve because it has 3 cusps. It is also called the mitral valve.the semilunar valves include the aortic and pulmonary valves each having 3 semilunar cusps .

Conducting system of the heart 

The conducting system of the heart consist of the sinuatrial nide the atriventricular node the atriventricular bundle the right and left brancesh of the bundle and the subendocardial purkinje fibers. From the SA node which like the AV node and it's extension is composed of a specialized type of cardiac muscle fibers impulse are conducted to the AV node by atrial cardiac muscle fibers.The AV node bundle branches and subendocardial fibres form one continuous mass of conduction tissue.

Blood supply of the heart 

The heart is supplied by the the two Coronary arteries and their branches . The right and left coronary arteries arises dorm aortic sinuses at the beginning of the ascending aorta.  The veins that drain the myocardium do not have names that correspond to the arteries. 

A right Coronary after 

    It arises from the anterior aortic sinus of the ascensding aorta runsa between the root of the pulmonary to trunk and the right a circle.

B.left Coronary artery 

   It arises from the left aortic sinus of the ascensding aorta just above the aortic semilunar valves.

   it supplies the left atrium and left ventricle

Unstable Angina

Unstable angina is rapidly worsening angina or  severe angina at rest or prolonged and
severe ischaemic chest pain without ECG or enzymatic evidence of myocardial infarction.

PATHOGENESIS:
Fissuring of atheromatous plaque which is associated with thrombosis a
vasospasm.

TREATMENT

Initial Medical Management:

- Bed rest
- - Hospitalization in CCU
- I.V. access with 5% dextrose
- - 12-leads ECG - monitoring
- Continuous ECG-monitoring
- - High flow O2 inhalation.
- Correction of precipitating conditions such as:
- hypertension , arrhythmias, anaemia and hypoxaemia.

DRUG THERAPY

- Aspirin 150-325 x PO x daily or
- - Clopidegrol 75 mg × daily
- Heparin:
- - Unfractionated heparin
60-80 units/kg - bolus, followed by 14 units/kg/hr. infusion for 48 hrs.
Activated partial thromboplastin time ( APTT) should be measured every 6-
hour until a therapeutic level of 1.5-2 times the control value is achieved.

- Low-molecular-weight heparin:
- Enoxaparin 1 mg/kg S.C. 12-hourly or
- Dalteparin 120 mg/kg S.C. 12-hourly
b-blockers:

Atenolol 50-100 mg daily or
Metoprolol 50-100 mg 12-hour

calcium channel blockers:

- Verapamil 80-120 mg x 8-hourly xorally or
- Diltiazem 60-120 mg x 8-hourly × orally or
- Nifedipine or Amlodipine with B-blockers
if pain persists or recurs:
- Infusions of intravenous nitrates
- - Nitroglycerine 0.6-1.2 mg/hr. or
-Isosorbide dinitrate 1-2 mg/hr.
If Medical Management Fails:
- Coronary angiography
- - Percutaneous coronary angioplasty (PCA)
- Coronary artery bypass grafting (CABG)

MYOCARDIAL INFARCTION (MI)

Myocardial infarction is the acute ischaemic necrosis of the myocardium due to occlusion of coronary artery by atheromatous plaques. Atheromatous plaque rupture with superimposed thrombosis or coronary vessel spasm.

PATHOGENESIS OF MYOCARDIAL INFARCTION

Atherosclerotic coronary artery inflammation

Plaque rupture Lerosion

Platelet thrombus

Embolisation

Microvascular obstruction and dysfunction

Myocardial necrosis (infarction)

AETIOLOGY

It occurs usually due to formation of occlusive thrombus at a site of rupture of an
atheromatous plaque in a coronary artery.

RISK FACTORS

Major Risk Factors

- Cigarette smoking
- - Hypertension
- Diabetes mellitus
- - Hypercholesterolemia

MINOR RISK FACTORS
- Type A personality
- - Male sex
- Oral contraceptive pills for long period
- - Family history of premature coronary artery disease(< 55 yrs male, <65 yrs female)
- Lack of physical activity
Clinical Features
SYMPTOMS
Chest pain:
Site: Retrosternal
Severity:Very severe
Onset:Sudden, usually at rest
Duration:Prolonged
Character:Tight, heavy constricting
Radiation:Left shoulder, neck, jaw, left arm, ulnar border of forearm and hand,even to epigastrium and back.
Relief:Not by rest or nitrates, only by strong analgesic like morphine

ASSOCIATED SYMPTOMS
- Breathlessness
- - Restlessness
- Anxiety
- - Fear of impending death
- Nausea and vomiting-
- - Sweating
- Collapse or syncopal attack
Features of complications - Heart failure
- Shock.
Silent MI in elderly and diabetic patients

Physical Signs

: Signs of sympathetic activation: pallor, sweating, tachycardia

- Signs of vagal activation: vomiting, bradycardia
- Signs of impaired myocardial function:
- - Hypotension, Oliguria, Cold periphery
- Narrow pulse pressure
- - Raised JVP
- Prominent S3, quiet S1
- - Basal crepitations

- Signs of tissue damage: fever
- - Signs of complications: MR, pericarditis,

Differential Diagnosis

(i) Pericarditis
(ii) Myocarditis
(iii) Acute aortic dissection
(iv) Pneumothorax
(vi) Left ventricular failure

INVESTIGATIONS

(i) ECG: - ST-elevation (convexity upward)
Symmetrical T - wave inversion,.
- Pathological Q- wave
(ii) Plasma enzymes:
Creatine kinase myocardial Band (CK-MB) - specific for myocardial injury.

95% sensitive and specific for MI when measured within 24-36 hours of
chest pain.

Plasma CK-MB begins to elevate at 4-6 hours after the start of pain and
reaches a peak at 12-24 hours.

Condition with raised CK
   • Myopathy
   • DC shock
   • cardiopulmonary resuscitation
   • muscle trauma
   • intramuscular injection

- Troponin : T and I
   • Begins to elevate 4-6 hours after start of pain
   • remains elevated for 1-2 weeks
   • more specific CK - MB
   •
- Lactate dehydrogenase (LDH)
   • Routine use of LDH in the diagnosis of MI is no longer recommended.
   • in acute MI elevation in LDH are detectable at 12 hours after the onset of chest pain and peak in 24 - 72 hours
   • LDH levels remain elevated for 10-14 days after infarction
   • An LDH -1 to LDH-2 ratio greater then 1.0 considered evidence of MI.

III) random blood sugar blood urea serum creatinine and electrolytes.
iv) serum lipid profile
V) blood TC DC ESR polymorph nuclear leucocytosis high ESR.
Vi) chest x-ray
        - pulmonary oedema
        - cardiomegaly
        - pericardial effusion
Vii) echocardiography : To detect regional walk motion abnormalities and other complication of MI
Vii) Coronary ateriograohy and left ventriculography.

MANAGEMENT OF AN ACUTE MYOCARDIAL INFARCTION (MI)

A.EARLY MANAGEMENT

     • Complete bed rest 

     • aspirin 140-30mg chewed and clopidegrol 300mg loading then 75 mg daily. 

     • Admission in hospital under Coronary care unit 

     • O2 inhalation- vial nasal cannula if hypoxia 

     • I.V open with 5% dextrose 

     • continuous ECG monitoring and O2 saturation 

     • serial 12 leads ECG 

     • analgesic

     • tab nitroglycerin 0.5 mg S/L sos or 

     • tab Isosorbide 5mg S/L stat or sos 

     • tab. Isosorbide mononitrate 10-20 mg × po × BD 

     • laxative to avoid constipation 

THROMBOLYTIC DRUGS 

      • streptokinase 

      • Altepase

ANTICOAGULANTS 

      • low molecular weight heparin is performed in place of unfractionated heparin .

      • subcutaneous heparin 12,500 unit twice daily given in addition to oral aspirin may prevent reinfarction after successful thrombolysis and reduce the risk of thromboembolic complications.

Beta- blockers

    Atenolol 5mg -10mg IV .over 5 minutes 

    Metoprolol 5-15 mg IV.over 5 minutes followed by oral B- blockers.

Late management.

 a) risk stratification and further investigation 

    • Left ventricular function : ECG ECHOCARDIOGRAM AND CHEST X-RAY

    • ISCHEMIA : EXERCISE TOLERANCE TEST

     

b) routine drug therapy 

     • Aspirin 150mg ×po × daily 

     • b.blockers : atenolol 50 mg ×po× daily 

     • nitrite : Isosorbide mononitrate 10-20mg×po× daily 

     • ACE inhibitors: captopril 25 mg × TDs 

C) risk Factor modification 

      • Stop smoking

      • control weight

      • daily exercise

COMPLICATION OF ACUTE MYOCARDIAL INFARCTION 

A. Early 

     I) arrhythmias

                 • Ventricular fibrillation

                 • ventricular tachycardia

                 • atrial fibrillation

                 • sinus bradycardia

                 • heart block 

   iI) angina 

   III) cardiogenic shock 

   Iv) pericarditis

   V) thromboembolism 

   Vi) mechanical complications

                   - papillary muscles damage

                   - rupture of interventricular septum

                   - rupture of ventricle

                   

B) DELAYED COMPLICATIONS

        • Ventricular aneurysm

        • post mi syndrome 

        • 3Ps pericarditis 

                  pleural effusion

                  persistent pyrexia

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