ACUTE CORONARY SYNDROME

Acute Coronary Syndrome

Definition: a constellation of symptoms related to obstruction of coronary arteries with chest pain being the most common symptom in addition to nausea, vomiting, diaphoresis etc. Chest pain concerned for ACS is often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating.

Epidemiology
HIGH RISK POPULATION FOR CAD/ACS: INDIAN/WHITE/COLOURED INCREASING rate in Black population lifestyle/socioeconomic changes, urbanisation

Acute coronary syndrome

Based on ECG and cardiac enzymes, ACS is classified into:
STEMI: ST elevation, elevated cardiac enzymes NSTEMI: ST depression, T-wave inversion, elevated cardiac enzymes Unstable Angina: Non specific EKG changes, normal cardiac enzymes

MYOCARDIAL INFARCATION

Myocardial infarction
Definition

Other names: coronary occlusion- heart attack Myocardial infarction refers to the process by which myocardial tissue is destroyed in regions of the heart that are deprived of an adequate blood supply because of a reduced coronary blood flow (a prolonged lack of myocardial oxygenation leading to necrosis of a portion of the heart muscle).

Myocardial infarction
Etiology and pathopysiology

*Causes of reduced blood flow:

Narrowing of atherosclerosis a coronary artery owing to

A complete occlusion of an artery owing to embolus or a thrombus Myocardial necrosis caused by acute a coronary artery due to plaque erosion with imposed thrombosis) occlusion of rupture or

Myocardial infarction
Clinical manifestations

Symptoms Pain is the cardinal symptom of an MI

Anxiety and fear of impending death

Nausea and vomiting Breathlessness

Collapse/syncope

Myocardial infarction
Clinical manifestations (cont)

Physical signs Signs of sympathetic activation: pallor, sweating, tachycardia Signs of vagal activation: nausea,vomiting, bradycardia Signs of impaired myocardial function: hypotension, oligurea, cold peripheries Signs of complications: e.g. mitral regurgitation, pericarditis

Myocardial Infarction

Diagnostic evaluation
I. Electrocardiography
Is usually helpful in confirming the diagnosis.

Myocardial Infarction

II. Plasma biochemical markers

MI causes a detectable rise in the plasma concentration of enzymes and proteins that are normally within cardiac cells. The most widely used are creatine kinase (CK). A cardio-specific isoform of this enzyme (CK-MB) and the cardiospecific proteins troponin T & I.

Myocardial Infarction

Serial (usually daily) estimations are particularly helpful because it is the change in plasma concentrations of these markers that is of diagnostic value.

Myocardial Infarction

CK starts to rise at 4-6 hours, peaks at about 12 hours and falls to normal within 48-72 hours. Troponin T and I are released within 4-6 hours and remain elevated for up to 2 weeks.

Myocardial Infarction

III. Other blood tests 1. Leucocytosis 2. ESR 3. CRP (C-reactive protein)

IV. Chest X-ray : Cardiomegaly, pulmonary oedema

V. Echocadiography

Myocardial Infarction

Management:
Early management of acute myocardial infarction (AMI) require immediate access to medical and paramedical care and defibrillation facilities.

Myocardial Infarction
I. Immediate measures
High-flow oxygen I.V. access ECG monitoring 12-lead ECG I.V. analgesia (opiates) and antiemetic
Intravenous opiates e.g. morphine sulphate and antiemetics (metoclopramide) should be administered through an intravenous cannula and titrated by giving repeated small aliquots until the patient is comfortable.

Aspirin 300 mg

Myocardial Infarction

2. Acute reperfusion therapy Thrombolysis: successful thrombolysis leads to reperfusion with relief of pain, resolution of acute ST elevation. The sooner the patient is treated the better the results will be, any delay will only increase the extent of myocardial damage (minutes mean muscle).

Myocardial Infarction

Streptokinase 1.5 million U in 100 ml of saline given as an intravenous infusion over 1 hour is a widely used regimen. Streptokinase is antigenic and occasionally causes serious allergic manifestations, it may also cause hypotension.

Myocardial Infarction
Altephase (human tissue plasminogen activator or tPA) is a genetically engineered drug that is not antigenic and seldom causes hypotension. The major hazard of thrombolytic therapy is bleeding. (PCI) Primary percutaneous coronary intervention is the treatment of choice.

Myocardial Infarction
3. Maintaining vessel patency
Antiplatelet therapy Aspirin 75-300 mg/d Clopidogrel 75 mg/d Anticoagulant: subcutaneous heparin twice daily (low molecular weight heparin is now available).
N.B blockers and nitrates can be used as Adjunctive therapy

Myocardial Infarction

Complications of infarction Arrythmias Ventricular fibrillation Atrial fibrillation Sinus bradycardia Acute circulatory failure Embolism

Myocardial Infarction

Life-style modification - Stop smoking - Regular exercise - Diet (weight control, lipid lowering).

Myocardial Infarction
Secondary prevention drug therapy - Antiplatelet therapy - Statin b blocker - ACE inhibitor - Control diabetes and hypertension III. Rehabilitation

CARDIORESPIRATORY ARREST

SHOCK CARDIOGENIC

Cardiogenic Shock
Systemic hypoperfusion secondary to severe depression of cardiac output and sustained systolic arterial hypotension despite elevated filling pressures.

Etiologies

Acute myocardial infarction/ischemia LV failure VSR Papillary muscle/chordal rupture- severe MR Ventricular free wall rupture with subacute tamponade

Other conditions complicating large MIs Hemorrhage Infection Excess negative inotropic or vasodilator medications Prior valvular heart disease Hyperglycemia/ketoacidosis Post-cardiac arrest Post-cardiotomy Refractory sustained tachyarrhythmias Acute fulminant myocarditis End-stage cardiomyopathyHypertrophic cardiomyopathy with severe outflow obstruction Aortic dissection with aortic insufficiency or tamponade Pulmonary embolu Severe valvular heart disease -Critical aortic or mitral stenosis, Acute severe aortic or MR

Pathophysiology

Clinical Findings
Physical Exam: elevated JVP, +S3, rales, oliguria, acute pulmonary edema Hemodynamics: dec CO, inc SVR, dec SvO2 Initial evaluation: hemodynamics (PA catheter), echocardiography, angiography

4 Potential Therapies
Pressors Intra-aortic Balloon Pump (IABP) Fibrinolytics Revascularization: CABG/PCI

Refractory shock: ventricular assist device, cardiac transplantation

UNSTABLE ANGINA