Arteriosclerosis - “hardening of the arteries”.

Atherosclerosis – build up of plaque (atheroma) on the lining of arteries.

End results for both are the same Stenosis of the lumen of artery Ulceration of plaque Rupture of plaque with thrombus formation Obstruction of blood flow Ischemia of tissue distal to thrombus

• Left Coronary Artery.• Anterior Descending (LAD)• Left Circumflex (LCx)

Right Coronary Artery

Inflammatory response secondary to injury is mostly widely accepted theory for development of atherosclerosis. Endothelial injury from shearing stresses,

radiation, chemicals, hyperlipidemia Inflammatory response Beginning of atheroma

Atherosclerosis Vasospasm Thrombus or embolusAtheroma Coronary Artery:

Slow obstruction: Fat plaque formation Thrombosis – formation of blood clot

Sudden obstruction: Embolism – separated blood clot

Non-modifiable Risk Factors Contributing To CAD

Heredity Increasing age Gender During reproductive years, women have a

much lower incidence of Coronary Heart Diseases (CHD) compared to men of similar age. The reason for this due to the protective effect of oestrogen.

Modifiable Major Risk Factors1- Elevated Serum lipids:

An elevated ”total” cholesterol level is major component of atherosclerotic plaque build up which causes the development of an acute MI.

2- Hypertension:This related to the shearing stress, causing

denuding injuries of the endothelial lining. Atherosclerosis, in turn, causes narrowed, thickened arterial walls and decreases the distensibility and elasticity of vessels.

3. Cigarette smoking: includes increases of plasma cholesterol

Triglycerides and fibrinogen, and platelet aggregation and decreases high –density lipoprotein (HDL).

4. Physical Inactivity:Physical active people have increased

HDL levels, and exercise enhances fibrinolytic activity, thus reducing the risk of clot formation.

5. Obesity:Obesity increases risk for CAD through increased

level of LDL, which are strongly implicated in arteriosclerosis” and hypertension.

6- Diabetes mellitus:Arterial wall exposure to abnormally high levels

of circulating insulin causes proliferation of smooth muscle cells inhibition of glycolysis and synthesis of cholesterol, triglyceride and phospholipids.

7- Stress and behavior patterns: Several behavior patterns have been

correlated with CAD. Type A behaviors include protectionism and a hard working, driving personality.

 8- Psychological traits:Depression, anxiety, and hostility have been

demonstrated to be associated with the risk of coronary artery disease and of adverse outcomes after acute coronary events.

DefinitionClinical syndrome characterized by episodes

of discomfort or pressure in the upper chest Result of ischemia Atherosclerosis is most common cause

Factors Known To Precipitate Typical Angina.

Physical exertion Exposure to cold Eating a heavy meal Stress or emotional situation

1. Stable angina:pain that occurs on exertion and is

relieves by rest or nitrate. The discomfort is usually relieves within 2-10 minutes by rest.

2. Unstable angina:the discomfort has become more frequent,

more easily triggered, more severe or prolonged or less responsive to nitrate therapy, and lasting more than 20 minutes.

3. Variant angina (Prinzmetal’s angina):This discomfort tends to be prolonged, severe

and not readily relieved by nitroglycerin. Variant angina is caused by spasm of the coronary arteries and can be accompanied by transient elevation of the segment.

4. Nocturnal angina:It occurs only at night but not necessary

when the person is in the recumbent position or during sleep.

 

5- Angina decubitus:It is chest pain that occurs only while the

person is lying down and is usually relieved by standing or sitting.

6- Silent ischemia:Approximately 70% of ischemic episodes in

patients with CHD are silent, making silent ischemia a more common occurrence than angina. In addition, up to 30% of symptomatic myocardial infarctions are silent.

 

Heaviness, squeezing, pressure, tightness in upper chest

Choking or smothering sensation

Indigestion or gas

Radiation to neck, jaw, shoulders and arms

Feeling of weakness or numbness in arms, wrists or hands

Associated symptoms Dyspnea Diaphoresis Dizziness N/V Anxiety

Diagnosis often made by evaluating clinical manifestations and history

12 lead ECGMay show T-wave inversions and ST segment depressions in the electrocardiograpgic leads

Stress test with or without nuclear scan or ECHO

Cardiac catheterization

Objectives of Medical Management of Angina *Decrease oxygen demands of myocardium or myocardial oxygen consumption* Increase oxygen supply

Treatment of Angina Pharmacologic therapy Control risk factors Revascularization

Invasive interventional procedures Coronary artery bypass grafting (CABG)

Nitrates – mainstay of treatment Dilate veins – decreases preload Dilate arteries – decreases afterload as

well as dilates coronary arteries Administer- spray, sublingually, PO, IV,

topically Side effects – hypotension, HA, flushing,

tachycardiaEx: Nitrostat SL or Tridil (nitroglycerin),

DO NOT administer with Viagra

Beta blockers Reduce myocardial oxygen consumption

by decreasing heart rate, contractility and blood pressure

Monitor heart failure clients for worsening failure

Side effects – hypotension, bradycardia, bronchial spasm, masks hypoglycemia

Ex: Lopressor or Toprol (metoprolol), Inderal (propranolol), Tenormin

Calcium channel blockers Dilate arteries which decreases workload

and O2 consumption

Decrease heart rate and myocardial contractility – decreases O2 consumption

Side effects - hypotension, bradycardia, constipation, edema, AV blocks

Ex: Adalat or Procardia (nifedipine), Cardene (nicardipine), Cardizem (diltiazem)

Antiplatelet medications Prevent platelet aggregation on atheroma

or thrombus EX: Aspirin and ticlopidine. side effects: GI irritation, bleeding,

increased bruising

Anticoagulants (Heparin)* Given IV in acute situations or

subcutaneous in non-acute situation* Monitor partial thromboplastin time (PTT) * Observe bleeding precautions

Anticoagulants (warfarin)* Used long term; given PO• Effects do not occur for 3-5 days

Oxygen therapy Administered usually at 2 L/min per nasal

cannula Increases amount of O2 delivered to

myocardium