Print this pageNursing heart failure is a condition that the inability of the heart to pump blood throughout the body in accordance with metabolic needs.
Etiology
Causes of heart failure:
1. Mechanical disturbances.
1. Increased pressure load
- Central (aortic stenosis).
- Peripheral (systemic hypertension).
b. Increased volume load.
- Valve regurgitation
- Shunt
- Increasing preload
c. Obstacles ventricular filling
- Mitral or tricuspid stenosis.
d. Perikard constriction, tamponade.
e. Retriksi endokardial or myocardial.
f Aneurysma ventricular.
2. Myocardial abnormalities.
1. Primary
- Cardiomyopathy
- Neuromuscular disorders.
- Myocarditis
- Metabolic (DM).
- Poisoning.
b. Secondary
- Ischaemia (coronary heart disease)
- Inflammation
- Systemic disease
- Obstrutif chronic lung disease
- Drugs that depressed myocardial
Three. Arrhythmia
- Ventricular stanstill
- Ventricular fibrillation
- Takhikardi or extreme bradycardia
- Impaired conduction
Originator of heart failure
Hypertension, myocardial infarction, arrhythmias, anemia, febrile, pulmonary embolism, stress and infection.
Pathophysiology
The function of the heart as a pump is indicated by its ability to meet an adequate blood supply to all parts of the body, either in the resting state maupan when experiencing physiological stress.
Basic physiological mechanisms of heart as stroke volume (contents sekuncup), cardiac output (cardiac output), heart rate (heart rate), preload (initial load) and the after-load (end load) and contractility is very influential in the mechanism of heart failure.
Stroke volume (SV) is the amount of blood in pompakan by ventricular contractions each time.
Cardiac output (CO) is the amount of blood in the ventricle pompakan every minute.
CO ═ heart rate / min x SV
Three factors affecting the stroke volume is:
Preload, Describes the myocardium of pressure on the end diastolic phase or just prior to ventricular contraction. Clinically described as "ventricular filling." According to Frank Starling law; the greater the content of the heart during diastolic, the greater the amount of blood pumped into the aorta.
Aortic pressure afterload Describes the total (impedance) that holds ventricular ejection. When systemic arterial pressure increased by the work of the heart will also rise.
Contractility is the intrinsic ability of myocardial fibers to contract. Increased stroke volume describes the increase in contractility and reverse, the decline in stroke volume describes the decline in contractility.
Response Kompensatorik
As a result of heart failure, it happens that the body compensatory mechanisms include:
1. Increased sympathetic adrenergic activity. Increased sympathetic activity may stimulate spending adrenergic catecholamines from adrenergic nerves of the heart and adrenal medulla. This will increase the contractility and heart rate, which will ensure the cardia output. Increased contractility and pulse rate is very dependent on the sympathetic response of the body. Another consequence of this mechanism of muscle contraction, so the heart must pump more strongly again because of increased peripheral resistance.
2. Increased preload. RAA system activation (renin Angiotensin Aldosterone) causes the sodium salt and water retention by the kidneys. The increase this initial load will increase myocardial contraction according to Starling law.
3. Ventricular hypertrophy. Ventricular wall thickening without penambahab heart size will cause the heart to work harder to meet the needs of the body
Third kompensatorik response illustrates the effort to maintain cardiac output, heart failure, but if this continues then the compensation becomes ineffective semalin. Nursing
1. Increased pressure load
- Central (aortic stenosis).
- Peripheral (systemic hypertension).
b. Increased volume load.
- Valve regurgitation
- Shunt
- Increasing preload
c. Obstacles ventricular filling
- Mitral or tricuspid stenosis.
d. Perikard constriction, tamponade.
e. Retriksi endokardial or myocardial.
f Aneurysma ventricular.
2. Myocardial abnormalities.
1. Primary
- Cardiomyopathy
- Neuromuscular disorders.
- Myocarditis
- Metabolic (DM).
- Poisoning.
b. Secondary
- Ischaemia (coronary heart disease)
- Inflammation
- Systemic disease
- Obstrutif chronic lung disease
- Drugs that depressed myocardial
Three. Arrhythmia
- Ventricular stanstill
- Ventricular fibrillation
- Takhikardi or extreme bradycardia
- Impaired conduction
Originator of heart failure
Hypertension, myocardial infarction, arrhythmias, anemia, febrile, pulmonary embolism, stress and infection.
Pathophysiology
The function of the heart as a pump is indicated by its ability to meet an adequate blood supply to all parts of the body, either in the resting state maupan when experiencing physiological stress.
Basic physiological mechanisms of heart as stroke volume (contents sekuncup), cardiac output (cardiac output), heart rate (heart rate), preload (initial load) and the after-load (end load) and contractility is very influential in the mechanism of heart failure.
Stroke volume (SV) is the amount of blood in pompakan by ventricular contractions each time.
Cardiac output (CO) is the amount of blood in the ventricle pompakan every minute.
CO ═ heart rate / min x SV
Three factors affecting the stroke volume is:
Preload, Describes the myocardium of pressure on the end diastolic phase or just prior to ventricular contraction. Clinically described as "ventricular filling." According to Frank Starling law; the greater the content of the heart during diastolic, the greater the amount of blood pumped into the aorta.
Aortic pressure afterload Describes the total (impedance) that holds ventricular ejection. When systemic arterial pressure increased by the work of the heart will also rise.
Contractility is the intrinsic ability of myocardial fibers to contract. Increased stroke volume describes the increase in contractility and reverse, the decline in stroke volume describes the decline in contractility.
Response Kompensatorik
As a result of heart failure, it happens that the body compensatory mechanisms include:
1. Increased sympathetic adrenergic activity. Increased sympathetic activity may stimulate spending adrenergic catecholamines from adrenergic nerves of the heart and adrenal medulla. This will increase the contractility and heart rate, which will ensure the cardia output. Increased contractility and pulse rate is very dependent on the sympathetic response of the body. Another consequence of this mechanism of muscle contraction, so the heart must pump more strongly again because of increased peripheral resistance.
2. Increased preload. RAA system activation (renin Angiotensin Aldosterone) causes the sodium salt and water retention by the kidneys. The increase this initial load will increase myocardial contraction according to Starling law.
3. Ventricular hypertrophy. Ventricular wall thickening without penambahab heart size will cause the heart to work harder to meet the needs of the body
Third kompensatorik response illustrates the effort to maintain cardiac output, heart failure, but if this continues then the compensation becomes ineffective semalin. Nursing