HEART FAILURE

A.Definition
Heart failure is a myocardium failure to maintain cardiac output and enough tissue perfusion Holloway, 2003: 189).
Heart failure is a heart disability condition to pump blood to whole body appropriate to metabolism need (Priyanto, 2001: 420).
Heart failure is a very complex clinical syndrome caused by disorder that causing ventricle disturbance ability to pump blood to whole body (Suryadipraja, 2001: 126).
Heart failure is a lack of heart contractility condition and ventricle disable to pump out blood as much as enter during diastole. It cause ventricle end diastole volume increase progressively (Corwin, 2001: 376).
Heart failure is signs and symptoms collection caused by disability of heart to pump enough blood to fulfill body metabolic need (Tambayong, 2000: 91).
Heart failure is heart disability to pump adequate blood to fulfill body metabolic need (Nanda, 2002).
From the definitions above if can be concluded that heart failure is complex heart disorders so that heart is disable to pump adequate blood to whole body to fill tissue metabolic need of oxygen and nutrition.

B.Etiology
1.Myocardium disorder (coroner arthroscleroses, arterial hypertension and muscle degenerative disease or inflammation).
2.Coronary atherosclerosis (cause myocardium dysfunction) so that cause hypoxia and acidosis (caused by lactate acid collection) and myocardium infarction.
3.Systemic and pulmonal hypertension.
4.Inflammation and degenerative myocardium infarct, this condition directly damage heart fiber, causing contractility decrease.
5.Others heart disease (disturbance of blood flow by heart, for example: semi lunar valve stenose, disability heart to fulfill blood, for example: pericardium temponade, constrictive pericarditis or AV valve stenose; abnormal heart empty, example: AV valve insufficiency; after load increasing suddenly caused by increase of systemic blood pressure, example: malign hypertension).
6.Systemic factor (fever, tyrotoxicose, hypoxia, anemia, acidosis and electrolyte abnormality). (Smeltzer & Bare, 2002: 806).

C.Pathofisiology
Mechanism as based of heart failure included disturbance ability of heart contractility, that cause cardiac output lower than normal. Heart frequency is an autonomous nerves system function. If cardiac output decrease, sympatic nerves system will fasten heart frequency to maintain cardiac output.
However in heart failure with main problems are damage and spasm heart fiber, decreasing of cardiac volume and normal cardiac output still can be maintained. Cardiac volume is amount of blood that is pumped in each contraction depend on 3 factors: preload, contractility and after load.
1.Preload
Is a synonym with Starling Law in heart that is said that amount of blood that filling heart directly equivalent with pressure that is caused by long heart fiber range.
2.Contractility
Based on changing contractility strength that happen in cell level and related to heart fiber long alter and calcium content.
3.After load
Based on the big of ventricle pressure, that must be produced to pump blood against differences pressure that is caused by arteriole pressure.
In heart failure, if one or three of the factors disturbed, the result is decreasing of heart volume. Easily, in definiting homodynamic measurement by invasive monitoring procedure that make congestive heart failure diagnose easier and make effective pharmacologic therapy applying easier. (Smeltzer & Bare, 2002: 805-806)

D.Heart failure classifications
1.Left heart failure
Left heart failure happen if left ventricle output less than totals blood volume that accepted from right heart by pulmonary circulation. Finally, obstruction happen in lung circulation and systemic blood pressure decrease.
Common etiology of left ventricle failure is myocardium infarction. The others etiology include systemic hypertension, stenosis or aorta insufficiency or cardiomyopaty. Mitral stenosis and mitral insufficiency also can cause Left Ventricle Failure symptom.
In the beginning level of Left Ventricle Failure, dipsnea appear if heart resaves over load. When the liquid begin to collect in pulmonary capillary, forming of interstitial edema cause defect when oxygenize. Decreasing of blood oxygen saturation, cause chemoreceptor stimulate respiratory center. In the beginning, respiratory rate increase for practice and even, in break. Short breath when physical activity (dipsnea when physical activity) is common symptom and relatively early. This individual can feel hard breathing if take a walk or much eat.
2.Right heart failure
Right heart failure happen if right ventricle output lack of increase from systemic vein circulation. As the effect, systemic vein circulation blocked and decrease output to lung.
Common etiology is left ventricle failure that cause increasing of pulmonary pressure, so that right ventricle more load.
Sign and symptom of Right Ventricle Failure is characterized by dependent edema and pitting, appear in sternum or sacrum in individual who is sitting. Expansism of lymph and liver can cause pressure in surroundings organs, respiratory included, and organ dysfunction. Ichteric and coagulation problem can happen in Right Ventricle Failure not decompensation, long and heavy. Asites also happens if there is severe Right Ventricle Failure and can cause respiratory restriction and pressure. (Tambayong, 2000)

E.Clinical Manifestation
Left Heart Failure: dipsnea, fatigue, ortopnea, paroxysmal nocturnal dipsnea, cough, heart grows up, rhythm gallop, S3/S4 additional heart sound, chines stoke respiratory, tachycardia, raunchy, pulmonary vein congestive.
Right Hear Failure: fatigue, edema, liver engorgement, anorexia, puffing, right heart grows up, rhythm gallop in right ventricle, murmur, increase of jugulars vein pressure, asites, hydrothorax, increasing vein pressure, heatomegali and pitting edema.
New York Heart Association (NYHA) classified client functional with heart failure into 4 classes:
Class 1: if client can do hard activity without complain
Class 2: if client can’t do harder activity from daily activity without complain
Class 3: if client can’t do daily activity without complain
Class 4: if client can’t do any activities and have to bed rest. (Ruhyanudin, 2007: 91)

F.Supporting Data
1.Laboratory:
a.Hematology: Hb and Ht relatively decrease, Leukocyte relatively increasing.
b.Electrolyte: K, Na, Cl, Mg increasing.
c.Kidney and lever function disturbances: ureum, creatinin, BUN increasing, complete urine, SGOT, SGPT increasing.
d.Blood glucose is increasing.
e.Cholesterol, triglycerides are increasing.
2.Electrocardiogram (ECG):
a.Coroner heart disease, ischemic, infarction.
b.Heart hypertrophy: LVH
c.Arhythmia.
d.Pericharditis.
3.Thorax Rontgen:
a.Alveolar edema.
b.Interstitial edema.
c.Pleura effusion.
d.Pulmonary vein dilatation.
e.Heart hypertrophy.
4.Echocardiogram: sketch rooms and heart’s valve.
5.Radio nuclear:
a.Evaluate left ventricle function.
b.Identify myocardium function disorder.
6.Catheteriztion:
a.To know pressure in heart circulation and lung.
b.To know oxygen saturation in heart’s rooms.
c.Endomyocarditis biopsy and heart muscle disorder.
d.Do research about electrophysiology and recurrent heavy ventricle arhythmia.
e.Severe of heart valve’s lesion.
f.Identify coroner artery obstruction.
g.Left ventricle angiography: identified hypo kinetic, ventricle aneurism, left ventricle function.
h.Coroner angiography: identified location of coroner artery stenosis. (Priyanto, 200: 121)

G.Management
1.Medical:
The main purpose of heart failure treatment:
a.Repair or get rid of hemodynamic disorders, neurohormonal abnormality and metabolism that appear, because these disorders determine prognosis.
b.Decrease morbidity risk and mortality because of heart failure.
c.Decrease symptom of heart failure and repair patient’ life quality.
Medicines to heart failure that now use basically are:
a.Diuretic
Beside digitalis, diuretic is a medicine that the longest and most used to heart failure and the advantages has known, because the diuresis will decrease patient complain quickly, heart pump power will decrease pre load and after load.
b.Positive inotropic
Digoxin is very advantages to heart failure that included atrium fibrillation. In the others research, digoxin also advantage to heart failure systolic dysfunction patient with sinus rhythm heart beat. In this research proved that digoxin can increase left ventricle ejecting fraction and guessed can decrease adrenosympatic activation effect that high in heart failure patient.
c.ACE Blocker
The effect of this medicine can directly decrease ventricle after load because can be dilatation systemic arteriole which in high resistant condition, decrease stimulation of adrenosympatic activity by change vasomotor tonus center, blocking angiotensin II receptor in sympatic nerve terminal which etiology of increase noradrenalin releasing, decrease (regression) left ventricle hypertrophy, block ventricle remodeling process, repair periphery blood flow, decrease of adrenosymatic tonus.
d.Vasodilator
Many vasodilators medicine which can decrease resistant and capacity small blood vessel, has other effect to vascular activity. For example: Flosequinan, has positive inotropic effect, while medicines calcium antagonist group have negative inotropic effect. Commonly vasodilator medicines have effect to decrease pre load and/or after load so that can decrease complain and signs heart failure.
e.Beta blockers
The most clinical experiment intention is centered in carvedilol, because carvedilol has more pharmacologic effects than others beta blockers, such as beta-1 blocker and beta-2 (can block tachycardia reflex), has vasodilator effect, has strong anti oxidant effect, anti inflammation and can prevent vascular smooth muscle proliferation, has cardio protection effect and block remodeling process. (Suryadipraja, 2001: 133-138)
2.Nursing
a.Additional rest
Patient need to take a rest physically or emotionally. Rest will decrease heart work, increase heart power stock and decrease heart pressure. Duration of lay also stimulate diuresis because lay down will repair kidney perfusion. Rest also decrease respiratory muscle works and use of oxygen.
b.Give comfortable position
The head of bed must be up 20 until 30 cm (8-10 inches) or patient sit on chair. In this position vein back flow to heart (pre load) and lung decrease, lung congestive decrease and lever pressure to diaphragm become minimal.
c.Vanish the anxiety
Because patient who suffer from heart failure experiences difficulty to maintain adequate oxygen, so they disposed worried and anxiety because hard to breath. This symptom disposed worst in night. Up the head of bed and turn on the lamp in the night often very useful. Patient who can not sleep on the bed may sit in the comfort chair.
d.Avoid stress
Emotional stress cause vasoconstriction, artery pressure increase, and heart beat fast. Give physical comfort and avoid situation that disposed can cause anxiety and agitation can help patient to relax.
e.Repair normal tissue perfusion
Easy daily practice can repair blood flow to periphery tissue. Adequate oxygenation and diuresis that appropriate also can repair tissue perfusion. Effective diuresis can decrease blood coagulation, so that increasing oxygen transportation capacity in vascular system. Enough rest very important to repair adequate tissue perfusion.
f.Patient education and think of caring at home
After heart failure controlled, patient is guided step by step to back to life style and to activity before sick early. Daily living activity must be planed to minimal apnea period and weakness. Every activity that can cause symptom must be avoided or adapted. Patient must be helped to know that heart failure can be controlled. (Smeltzer & Bare, 2002: 813-816)

H.Focus Intervention
1.Cardiac output decrease related to altered of myocardium contractility (Doenges, 2000: 55).
Purpose: Show vital sign in acceptable limit (disritmia controlled or gone) and free of heart failure symptom (for example: homodynamic parameter in normal, adequate liquid output).
Intervention:
a.Auscultation apical pulse, check the frequency, heart rhythm (record disritmia if there is telemetry).
b.Record heart sound.
c.Palpation periphery pulse.
d.Monitor blood pressure.
e.Asses skin of pale due to illness or fright and cyanosis.
f.Asses urine output, record decrease of output and urine concentrate.
g.Asses sensory alter, for example: lethargy, confuse, disorientation, anxiety and depression.
h.Give rest semi recumbent on bed or chair. Asses with physical assessment appropriate to indication.
i.Higher leg, avoid pressure under mouth. Motivate to passive or active sport. Increase of ambulation or activity as tolerance.
j.Give additional oxygen with nasal canal or masker as indication.
k.Give medicine as indication (diuretic, for example: furosemid (lasix); vasodilator, for example: nitrate (isodril); digoxin (lanoxin); captopril (capoten); morphine sulfate; tranquilizer or sedative; anti coagulation, for example: low doses heparin.
2.Excess liquid volume related to decreasing of glomerulus’s filtration flow (decrease of cardiac output) or increase of ADH production and natrium or water retention (Doenges, 2002: 59).
Purpose: Demonstrate stabile liquid volume with balance of intake and output, clear breath sound, vital sign in acceptable range, stabile body weight and there is no edema.
Intervention:
a.Asses urine output, record the amount and the color when diuresis happen.
b.Asses or count the balance of intake and output for 24 hours.
c.Weighting body weight every day.
d.Asses neck distance and periphery vessel. Look dependent body area to edema with or without pitting, record there’s edema for whole body.
e.Often change position. Higher leg if sit. Look skin surface, maintain to keep it dry and give rest as indication.
f.Auscultation breath sound, record decrease and/or additional sound, example: crackle. Record increase of dipsnea, tachipnea, ortopnea, nocturnal paroxysmal dipsnea and persistent cough.
g.Asses blood pressure and CVP (if there).
h.Asses intestine peristaltic. Record anorexia complain, nausea, abdomen distance, constipation.
i.Hepatomegali palpation. Record pain complain in abdomen right-up quadrant or push pain.
j.Give medicine as indication (diuretic, tiazid, kalium addition).
k.Maintain liquid or limiting natrium as indication.
3.High risk gas exchange damage related to alveolus capillary membrane changing (collecting or movement liquid into interstitial or alveoli area) (Doenges, 2000: 61).
Purpose: Demonstrate ventilation and adequate oxygen in tissue showed by Artery Blood Gas or oximetry in normal range and free respiratory distress symptom.
Intervention:
a.Auscultation breathes sound, record crackle.
b.Suggest patient to effective cough, deep breath.
c.Motivate often change position.
d.Maintain to sit on chair or bed rest with the head of bed up 20-30 degree, semi-fowler position. Support hands with pillow.
e.Monitor sketch of Artery Blood Gas, oximetry pulse.
f.Give additional oxygen as indication.
g.Give medicine as indication (diuretic, bronchodilator).
4.High risk for skin integrity damage related to edema (Doenges, 2000: 55-63).
Purpose: Maintain skin integrity and demonstrate action or prevent skin damage technical.
Intervention:
a.Look skin, record bone bump, edema, disturbance of area circulation or pigmentation or obesity.
b.Change position frequently on bed or chair, help active or passive range of motion practice.
c.Give often skin care, minimalize with moist or excretion.
d.Massage reddish area or whitish.
e.Avoid intramuscular medicine.
f.Give alternative pressure, sheep skin, elbow or heel protection.
5.Intolerance activity related to oxygen insufficiency to daily living activity (Carpentio, 2001).
Purpose: Demonstrate increase of tolerant activity that countable or forward with heart frequency or rhythm and blood pressure in normal limit and worm skin, pink and dry.
Intervention:
a.Record heart frequency, rhythm and altered of blood pressure before, being, after, activity as indication. Related to chest pain and short breath.
b.Increase rest (bed or chair). Limit activity on the basic pain or homodynamic responses. Give easy spare activity.
c.Limit visitor and/ or visit by patient.
d.Suggest patient to avoid increasing abdomen pressure, example strain abdominal muscles when defecating.
e.Explain increasing pattern step by step from activity level, example get up from chair if there’s no pain, ambulation and take a rest for an hour after eat.
f.Assess again signs/symptoms that show intolerant activity or need report to nurse or doctor.
g.Reconciliation to heart rehabilitation program.
6.Altered nutrition less than body requirement related to nausea, secondary anorexia caused by intestinal vein congestive and tired (Carpenito, 2001).
Purpose: Show increasing appetite and maintain or increase body weight.
Intervention:
a.Identify factor that can cause nausea or vomit.
b.Auscultation intestine peristaltic. Observe or palpation abdomen distance.
c.Weighing body weight as indication.
d.Give oral hygiene.
e.Consult nutritionist team support to give food that easy for digestive as balance nutrition.
f.Give parenteral as indication.
7.Ineffective air way clearance related to secret accumulation (Doenges, 2000).
Purpose: Identify or show act to reach effective air way clearance.
Intervention:
a.Assess frequency or respiratory depth and chest movement.
b.Auscultation lung area, record decrease area or there’s no air flow and adventitious breath sound.
c.Help patient for easy breath practice.
d.Give at least 2500 ml a day.