A. Definition
Heart failure is a pathophysiological state of abnormality of cardiac function so that the heart is unable to pump blood to meet the metabolic needs of tissues and / or ability only if accompanied by abnormally elevated diastolic volume.
B. Etiology
Heart failure is the most frequent complication of all types of congenital and acquired heart disease. Physiological mechanisms that cause heart failure include the circumstances that increase the initial load, end load, or reduce myocardial contractility. Circumstances that increase the initial burden include aortic regurgitation and ventricular septal defect, and end load is increased in circumstances where there is aortic stenosis and systemic hipertansi. Myocardial contractility may decrease in myocardial infarction and cardiomyopathy.
C. Pathophysiology
Intrinsic abnormalities in myocardial contractility characteristic in heart failure due to ischemic heart disease, impairs the ability of effective ventricular emptying. Left ventricular contractility decreased sekuncup reduce bulk, and increase the residual ventricular volume. In response to heart failure, there are three primary mechanisms that can be seen: 1) increased sympathetic adrenergic activity, 2) Increased initial load due to activation of renin-angiotensin-aldosterone system, and 3) ventricular hypertrophy. Third kompensatorik response reflects an attempt to maintain cardiac output. Abnormalities in the working ventricle and decreased cardiac output state typically seen in the move.
With continued heart failure then the compensation will become increasingly less effective. The reduced bulk sekuncup in heart failure will evoke sympathetic responses kompensatorik. Increased adrenergic activity of catecholamines from sympathetic nerve merangang expenditure cardiac adrenergic nerves and adrenal medulla. Heart rate and force of contraction will increase to increase cardiac output. Peripheral artery vasoconstriction also occurs to stabilize the artery pressure and redistribution of blood volume by reducing blood flow to the lower organs such as skin and kidney metabolism, so that perfusion to the heart and brain can be maintained.
Decrease in cardiac output in heart failure will initiate a series of events: 1) decreased renal blood flow and glomerular filtration rate at last, 2) the release of renin from glomeruli juksta apparatus, 3) the interaction of renin with angiotensinogen in the blood to produce angiotensin I, 4) conversion of angiotensin I to angiotensin II, 5) stimulation of aldosterone secretion from the adrenal glands, and 6) retansi sodium and water in the distal tubules and collecting duct.
Last compensatorik response in heart failure is myocardial hypertrophy or increased wall thickness. Hypertrophy increases the number of sarkomer in myocardial cells, depending on the type of hemodynamic load resulting in heart failure, sarkomer can grow in parallel or serial. Myocardial response to volume load, as in aortic regurgitation, marked dilatation and increased wall thickness.
D. Classification.
Based on the pumping heart failure, heart failure is divided into left heart failure, right heart failure, and congestive heart failure. In left heart failure occurred dyspneu d'effort, fatigue, orthopnea, paroxysmal nocturnal dyspnea, cough, enlarged heart, clattering rhythms, ventricular heaving, clattering sound of S3 and S4, Cheyne Stokes breathing, tachycardia, pulsus alternans, ronkhi and pulmonary venous congestion.
In right heart failure resulting edema, liver engorgement, anorexia, and bloating. On physical examination found the right heart hypertrophy, heaving right ventricle, right atrium galloping rhythm, murmurs, signs of chronic lung disease, increased jugular venous pressure, P2 sound hardens, ascites, hidrothoraks, increased venous pressure, hepatomegaly, and pitting edema.
In congestive heart failure occurs manifestations combined left and right heart failure.
New York Heart Association (NYHA) functional classification made in 4 classes:
1. Class 1: If the patient can perform strenuous activity without complaint
2. Class 2: If the patient is unable to perform activities more weight than their daily activities without complaint
3. Class 3: When the patient is unable to perform daily activities without complaint.
4. Class 4: If the patient is unable to perform any activity and have bed rest.
E. Clinical manifestations
Clinical manifestations of heart failure should be considered relative to the degree of physical exercises that promote the onset of symptoms. At the onset, symptoms typically appear only on exercise or physical activity, decreased exercise tolerance and symptoms appear early with a lighter activity.
Diagnosis of congestive heart failure according to the Framingham criteria were divided into 2 major and minor criteria.
Major criteria:
1. Paroxysmal nocturnal dyspnea or orthopnea.
2. Increased jugular venous pressure
3. Wet Ronkhi not loud
4. Kardiomegali
5. Acute pulmonary edema
6. S3 galloping rhythm
7. Increased venous pressure> 16 cm H20
8. Hepatojugular reflux.
Minor criteria:
1.Edema ankle
2. Nighttime cough
3. Dispneu d'effort
4. Hepatomegaly
5. Pleural effusion
6. Vital capacity was reduced to 1 / 3 maximum
7. Tachycardia (.120x/menit)
F. Management
Heart failure treated with general measures to reduce the workload of the heart and selective manipulation of the three main determinants of myocardial function, either individually or through a combination of: 1) initial load, 2) contractility, and 3) the load end.
The principle of management of heart failure:
1. Improve oxygenation by reducing oxygen delivery and consumption of O2 through the rest / activity restrictions.
2. Improving cardiac muscle contractility.
Overcoming a reversible condition, including thyrotoxicosis, miksedema, and arrhythmias.
Digitalization
a. Doses of digitalis:
- Oral digoxin for rapid digitalization of 0.5 to 2 mg in 4-6 doses for 24 hours and continued 2 x 0.5 mg for 2-4 days
- 0.75 to 1 mg digoxin iv in 4 doses for 24 hours.
- Cedilanid iv 1.2 to 1.6 mg in 24 hours.
b. Dose support for failed jantun: digoxin 0.25 mg daily. For elderly patients and renal failure adjusted doses.
c. Dose of digoxin for atrial fibrillation supporting 0.25 mg
d. Rapid digitalization is given to cope with severe acute pulmonary edema:
- 1 to 1.5 mg digoxin iv slowly
- Cedilanid 04 to 0.8 mg iv slowly.
3. Lowering the burden of heart.
Lowering the initial burden with low-salt diet, diuretics and vasodilators.
a. Low-salt diet
In heart failure with NYHA class IV, use of diuretics, digoxin and angiotensin converting enzyme (ACE), is necessary given the short life expectancy.
For heart failure class II and III are given:
- Diuretics in low or medium doses (furosemide 40-80 mg)
- Digoxin in patients with atrial fibrillation and sinus disorders
- ACE inhibitors (captopril starting from a dose of 2 X 6.25 mg or equivalent to that of other ACE inhibitors, the dose increased gradually by taking into account the patient's blood pressure); isorbid dinitrat (ISDN) in patients with an impaired ability of the activity or the presence of persistent ischemia, starting dose of 3 X 10-15 mg. All medications should be titrated gradually.
b. Diuretics
That used frusemide 40-80 mg. Supporting an average dose of 20 mg. Side effects of hypokalemia can be treated with potassium salt supply or replaced with spironolactone. Another diuretic that can be used include hydrochlorothiazide, klortalidon, triamteren, amilorid, and etakrinat acid. The impact of diuretic which reduces the initial load does not reduce cardiac output or survival, but it is the first line treatment because it reduces symptoms and treatment and hospital care. Use of ACE inhibitors with potassium-sparing diuretics should be cautious because of possible occurrence of hyperkalemia.
c. Vasodilator
- Nitroglycerin 0.4 to 0.6 mg sublingual or 0.2 to 2 g / kg / min iv.
- Nitroprusid 0.5 to 1 ug / kg / min iv
- 2-5 mg oral prazosin
- ACE inhibitors: captopril 2 X 6.25 mg.
G. Reference
1. Beutler E, Lichtman MA, Coller BS, Kipps TJ, Seligsohn U, Williams WJ.Approach to the patient. In: Beutler E, Coller BS, Lichtman MA, Kipps TJ, editors.Williams hematology. 6th edition. New York: McGraw Hill.
2. Braunwald E. Heart Failure and Cor pulmonary. In: Kasper DL, Braunwald E, U.S. Fauchi et.al, eds. Harrison's principles of internal medicine 16th ed, 2003.
3. Francis, GS, Gassler JP, Sonnenblick, EH. Pathophysiology and diagnosis of heart failure. In The Heart. Fuster V, Alexander, RW., O'Rourke, AR. 10th edition.Volume 1. Mc. Graw Hill. P.655.
4. Gibbsons, RJ., Antman, EA., Alpert, J.S., et al. Guidelines for the evalution and management of chronic heart failure in the adult. ACC / AHA Practice guidelines - Full text. American college of cardiology and the American Heart Association, Inc..2001.
5. Joint National Committee. The 7th Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII).
6. Mohrman, DE & Heller, LJ. 2006. Cardiovascular Physiology, 6th edition. The McGraw-Hill Comp, Inc., Minnesota.
7. PAPDI, Textbook of Medicine, fourth edition, Department of Medicine Faculty of Medicine University of Indonesia, 2006.
8. Remme, W.J., Swedberg, K. Guidelines for the diagnosis and treatment of chronic heart failure: Task force for the diagnosis and treatment of chronic heart failure.European Heart Journal. 2001.
9. Schnall SF, Berliner N, Duffy Tp, Benz EJ. Approach to the adult and child with anemia. In: Hoffman R, Benz EJ, Shttil SJ, Furrie B, Cohen HJ, Silberstein LE, McGlove P, editors. Hematology: basic principles and practice. 3th edition. New York: Churchill Livingstone, 2000.
10. Swedberg, K., Chairperson. Guidelines for the diagnosis and treatment of chronic heart failure: full text (update 2005). The European society of cardiology 2005.
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