Myocardial oxygen demand can be met if there is a balance between supply and oxygen demand. Decrease in myocardial oxygen supply may be harmful to myocardial function. Coronary heart disease caused by an imbalance between myocardial oxygen supply and demand. When myocardial oxygen demand increases, the oxygen supply must also increase. Increased oxygen demand occurs on: tachycardia, increase myocardial contractility, hypertension, hypertrophy, and dilatation of the ventricles. To increase the supply of oxygen in a sufficient amount of coronary artery flow should be improved.
Four factors that affect cardiac oxygen demand:
* The frequency of heart rate
* Power contraction
* Muscle Mass
* Voltage ventricular wall
The imbalance between supply and oxygen demand can be caused:
* Narrowing of coronary arteries (atherosclerosis), which is the most common cause.
* Decrease in blood flow (cardiac output).
* Increased myocardial oxygen demand
* Coronary artery spasm.
Suply demand
Suply demand
Suply demand
Pathogenesis
Coronary artery atherosclerosis is a cause of coronary artery disease are most commonly found. In coronary atherosclerosis, there is accumulation of lipids and fibrous tissue in the coronary artery so that narrow the coronary artery lumen.
Mechanisms of atherosclerosis:
* In the tunica intima containing lipid deposits occur much cholesterol.
* Occur complex atherosclerotic plaque consists of fat, fibrous tissue, collagen, calcium, cellular debris and capillaries.
* Changes degenerative artery wall.
* Coronary artery luminal narrowing.
CHD RISK FACTORS
Risk factors irreversible:
* Age
* Gender
* Family history / genetic
* Race
Reversible risk factors:
* Hyperlipidemia, hypercholesterolemia
* Hypertension
* Smoking
* Diabetes mellitus
* Obesity
* Stress psychologic
* Type of personality
* Lack of sports activities
Clinical manifestations
* Without symptoms
* Angina pectoris
* Acute Myocardial Infarction
* Arrhythmias
* Suck heart
* Sudden deaths
PATOFISOLOGI
Ischemia
Ischaemia is a condition of oxygen shortage is temporary and reversible. Decrease in oxygen supply will improve the mechanism of anaerobic metabolism. Long ischemia can cause muscle death or necrosis. State that continued necrosis can cause death of heart muscle (myocardial infarction). Ventriekel left is the living heart of the most susceptible to ischemia and infarction, due to left ventricular oxygen demand greater for contraction. Anaerobic metabolism is not very effective addition to the energy produced is not large enough also enhances the formation of lactic acid that may reduce the PH cell (lactic). Ischaemia is typically marked changes in ECG: T inversion, and ST segment depression.
Combined effects of hypoxia, decrease in energy supply, as well as acidosis can quickly disrupt the function of the left ventricle. Strength of contraction in the affected areas susceptible to interference, muscle fibers shorten, as well as its velocity decreases. Changes in these contractions can be caused decrease in cardiac output. Ischemia can cause pain as the result of excessive accumulation of lactic acid. Angina pectoris is chest pain that accompanies myocardial ischemia.
Angina pectoris can be divided: of angina pectoris stable (stable of angina), angina pectoris unstable (unstable wind), a variant of angina (angina prinzmetal).
Stable angina pectoris: chest pain belonging to stable angina is the pain that arises when performing activities. The pain of not more than 15 minutes and lost the rest.
Unstable angina pectoris (UAP): The chest pain arising UAP at rest, the pain lasts for more than 15 minutes and an increase in pain.
Variant angina: Unstable angina is caused by coronary artery spasm.
Infarction
Ischemia lasting more than 30 minutes can cause irreversible cell damage and muscle death (necrosis). Part of experiencing myocardial necrosis or infarction will cease to contract permanently.
Nursing care
* Review: a complaint of pain, disease history, risk factors.
* Physical examination: TTV, peripheral perfusion, capillary reffil, arterial pulsation, heart sounds: S3, S4, murmurs, lung sounds: Ronchi, whezing.
* Response psychological: depression, anxiety, worry.
* ECG: T inversion, ST depression
* Laboratory: Routine blood, cardiac enzymes, lipid profile.
* Echocardiogram
* Kateterisasi heart
* Photo thoracic
Nursing Diagnosis
* Decrease in cardiac tissue perfusion
* Changes in breathing pattern
* Changes in comfort; pain
* Intolerance activity
* Anxiety
Management of
* The most effective management is to detect and mitigate risk factors.
* Reducing cardiac oxygen demand by decreasing heart work
* Increase the oxygen supply of heart
* Coronary revascularization
Coronary revascularization
Coronary revascularization is a way to improve vascularities blood vessels to the heart. Three mechanisms revaskkularisasi
Coronary were: PTCA (Percutaneous Transluminal Coronary Angioplasty), revascularization with CABG surgery, therapy Thrombolytics.
PFS REHABILITATION PROGRAM
Rehabilitation of heart disease is a series of efforts to help cure the patient in order to return quickly to normal life. Rehabilitation aims to restore the PFS physical condition, mental and social one as optimal as possible so that achieved self ability to run activities at home or occupation.
Phase I Program
Courses are given in all patients who are still in care at the hospital. Program implemented as soon as possible in patients with stable hemodynamics since the ICCU, inpatient unit, until the patient home. Length of training: 7-14 days. Types of exercise: 5 minute warm-up that includes exercises arm muscles, legs, hips in a rhythmic and repetitive. Components of core exercises is the road / bike with a load that can be gradually increased according to response to exercise. The exercise ended with cooling for 5 minutes.
Phase II Program
Is an advanced program whose implementation as soon as possible after the patient's home. Length of training: 6-8 weeks 3x/minggu held for one hour. Types of exercise: warm-up for 5-10 minutes of stretching, followed by riding a stationary bike and walking for 30-45 minutes. The exercise ended with cooling for 10 minutes.
Phase III Program
Is a long term program with a community base. Conducted after the patients completed the Phase II program through the heart exercise test and achieve aerobic capacity. Length of training: 1-3 months
Pathophysiology
Risk Factors
Atherosclerosis
PSS Myocardial Blood Supply
Myocardial ischemia
Necrosis / infarction
PSS myocardial contractility
PSS Bulk Heart
Heart Failure
Death
