Angina pectoris,DEFINITIONS,Aetiology,CLINICAL FEATURES,RISK FACTORS for angina pectoris
Angina pectoris
A. DEFINITIONS
1. Angina pectoris is chest pain due to ischemic infarction generated and temporary or reversible. (The basics of nursing kardiotorasik, 1993)
2. Angina pectoris is a chronic syndrome, in which the client had an attack of typical chest pain that is like a button, or feel heavy in the chest that sometimes spreads to the left arm which arise at the time and soon lost activity when the activity stops. (Prof. Dr. Sjaifoellah H. M. Noer, 1996)
3. Angina pectoris is a term used to describe the type of discomfort that are usually located in the region retrosternum. (Practical Guide Cardiovascular)
B. Aetiology
1. Ateriosklerosis
2. Coronary artery spasm
3. Anemia
4. Arthritis
5. Aortic insufficiency
C. RISK FACTORS
1. Can be Modified (Modified)
a. Diet (hyperlipidemia)
b. Cigarettes
c. Hypertension
d. Stress
e. Obesity
f. Less activity
g. Diabetes Mellitus
h. Use of oral contraceptives
2. Can not be changed
a. Age
b. Gender
c. Ras
d. Hereditary
e. Personality Type A
D. ATTACK trigger
Trigger that can cause attacks include:
1. Emotions
2. Stress
3. Heavy physical work
4. Eve is too hot and humid
5. Too full
6. Many smoking
E. CLINICAL FEATURES
1. Substernal chest pain radiating retrosternal ataru to the neck, throat, internal regions of the scapula or the left arm.
2. Quality of pain like a heavy pressure, such as pressing, hot, sometimes just a bad feeling in the chest (chest discomfort).
3. Duration of pain lasted 1 to 5 minutes, no more daari 30 minutes.
4. Pain lost (reduced) when a break or giving nitroglycerine.
5. Accompanying symptoms: shortness of breath, feeling tired, sometimes comes a cold sweat, palpitations, dizzines.
6. EKG: ST segment depression, inverted T wave seen.
7. EKG is often normal at the time the attack did not arise.
F. TYPE ATTACKS
1. Stable angina pectoris
? classically associated with exercise or activity that increases oxygen demand niokard.
? pain go away with rest or cessation of activities.
? pain duration from 3 to 15 minutes.
2. Unstable angina pectoris
? nature, places and spread of chest pain can be similar to stable angina pectoris.
? Adurasi attacks can occur for longer than stable angina pectoris.
? triggers can occur in a state of rest or on mild tigkat activities.
? Less responsive to nitrate.
? More often found depresisegmen ST.
? It can be caused by atherosclerotic plaque rupture, spasmus, thrombus or platelet aggregate.
3. Prinzmental angina (variant angina).
? chest pain or pain occur at rest, often the morning.
? Pain caused koroneraterosklerotik vessels spasmus.
Elevaasi ? ECG showed ST segment.
? Tend to develop into acute myocardial infaark.
? arrhythmias may occur.
G. Pathophysiology and Pathways
Mechanism of occurrence of angina pectoris based on ketidakadekuatan supplied oxygen to the cells resulting from myocardium kekauan luminal narrowing of the arteries and coronary arteries (coronary ateriosklerosis). It is not known exactly what causes ateriosklerosis, it is clear that no single factor was responsible for the development of ateriosklerosis. Ateriosklerosis is penyakir coronary arteries are most commonly found. As the workload of a network increases, the oxygen demand also increases. If demand increases in the healthy heart is dilated and artei coronary megalirkan more blood and oxygen keotot heart. However, if the coronary arteries have narrowed due to kekauan or ateriosklerosis and can not be dilated in response to the increased need for oxygen, then there ischemic (lack of blood supply) myocardium.
The presence of endothelial injury resulting in a loss of production No (Oksid0 nitrate which is used to inhibit a variety of reactive substances. In the absence of this function can menyababkan smooth muscle to contract and arising spasmus aggravate coronary luminal narrowing due to a myocardial oxygen supply decreases. Refinements or block is not cause such symptoms appear until they’ve been achieving 75%. If the narrowing is more than 75% and triggered by the excessive activity of the coronary blood supply will be reduced. myocardium cells use anaerobic glycogen for their energy needs. metabolism produces lactic acid which lowers pH myocardium and cause pain. If kenutuhan energy heart cells decreases, the oxygen supply becomes inadequate and muscle cells to re-establish oxidative phosphorylation energy. This process does not produce lactic acid. With the disappearance of lactic acid pain will subside.
Thanks for the information. Angina pectoris is squeezing or tightening within the chest. It is also called chest pain. There are many causes of insufficient supply of blood to heart, angina pectoris such as stress, tension, excessive exertion. Angina pectoris is separated into two categories stable and unstable. Unstable angina pectoris is very much serious than stable angina. It is a minor issue but regular check is needed to prevent it. For more details refer
http://www.insideheart.com/etiology-of-angina-pectoris.html