Heart Failure

After completing this section of the chapter, you should be able to meet the following
objectives:

• Explain how the Frank-Starling mechanism, sympathetic nervous system,

renin–angiotensin–aldosterone mechanism, natriuretic peptides, endothelins, and myocardial
hypertrophy and remodeling function as adaptive and maladaptive mechanisms in heart failure.

• Differentiate high-output versus low-output heart failure, systolic versus diastolic heart failure,
and right-sided versus left-sided heart failure in terms of causes, impact on cardiac function, and
major manifestations.

• Differentiate chronic heart failure from acute heart failure syndromes and methods of
diagnosis, assessment, and management.

1. Definition
Heart failure has been defined as a complex syndrome resulting from any functional or structural
disorder of the heart that results in or increases the risk of developing manifestations of low
cardiac output and/or pulmonary or systemic congestion.

Summary the syndrome of heart failure can be produced by any heart condition that reduces the
pumping ability of the heart

Penyebab
Tersering : coronary artery disease, hypertension, dilated cardiomyopathy, and valvular heart
disease.

Memo
• Pada gangguan sistolik maka darah tidak mampu di pompa ventrikel
• Pada gangguan diastolik ada keanehan dalam fase relaksasi dan pengisian ventrikel
__________________________________________
Disfungsi sitolik
• people with heart failure often use their cardiac reserve at rest. [Meningkatkan Cardiac Output
ketika aktifitas]. For them, just climbing a flight of stairs may cause shortness of breath
because they have exceeded their cardiac reserve.
• Ejeksi berbanding lurus dengan fungsi mikoradium.
• Penurunan ejeksi menyebabkan peningkatan preload, dilatasi vent, ketegangan vent, > tek
diastol. The rise in preload is thought to be a compensatory mechanism to help maintain
stroke volume through the Frank-Starling mechanism despite a drop in ejection fraction.
• Preload meningkat -> cairan berkumpul di atrium -> edema pulmonar dan vaskular
• Gangguan sistolik dapat di diagnosis lewat cardiac output mauapun fraksi ejeksi, kemudian
secara manifestasinya lewat deteksia danya gagal jantung kiri dan kongesti pulmonal
(mungkin maksudnya edem pulmonal)
_________________________________________
Disfungsi Diastolik
• Pada disfungsi diastolik: Although such hearts contract normally, relaxation is abnormal. The
abnormal filling of the ventricle compromises cardiac output, especially during exercise
• Penyebab : ekspansi ventrikel yg terhalang (oleh perikardium), penebalan dinding ventrikel
dan pengecilan ukuran ruang (myocardial hypertrophy, hypertrophic cardiomyopathy) ,
kemudian ada delay relaksasi ketika diastol (Aging).

Suara 001
0:19

• An increase in heart rate shortens the diastolic filling time

• Thus, diastolic dysfunction can be aggravated by tachycardia or an arrhythmia and improved
by a reduction in heart rate, which allows the heart to fill over a longer period.
1. Disfungsi diastol ini bisa menyebabkan peningkatan tekana intravena karena darah yg tidak
leluasa dalam memasuki ventrikel kiri
2. Kemudian darah dari ventrikel kiri masuk kembali ke atrium kiri sekaligus ke vena pulmonar
menyebabkan paru menjadi penuh sehingga muncul gejala dyspnea (sesak nafas)
3. Terjadi penurunan cardiac output bukan karena ketidak mampuan dalam ejeksi namun karena
bertambahnya volume berlebih (preload)

___________________________________________
Disfungsi jantung kanan
• Daily measurement of weight can be used as a means of assessing fluid accumulation in a
person with chronic heart failure.
• there is accumulation or congestion of blood into the systemic venous system. This causes
an increase in right ventricular end-diastolic, right atrial, and systemic venous pressures.
• Right-sided heart failure also produces congestion of the viscera. As venous distention
progresses, blood backs up in the hepatic veins that drain into the inferior vena cava, and the
liver becomes engorged. This may cause hepatomegaly and right upper quadrant pain
• Pada gagal jantung kanan yang kronik terjadi , kematian sel hepatik, Asites, terlihat secara
visual peningkatan tekanan vena jugular dalam keadaan berdiri maupun duduk.
• Kegagalan ventrikel kiri merupakan penyebab tersering dari gagal ventrikel kanan
• Disfungsi vent kanan bisa disebabkan oleh tehalangnya aliran darah ke paru atau buruknya
kemampuan pompa ventrikel kanan
• Pulmonary hypertension occurs in people with chronic pulmonary disease, severe pneumonia,
pulmonary embolus, or aortic or mitral stenosis.
• When the right heart failure occurs in response to chronic pulmonary disease, it is referred to
as cor pulmonale.
• Other common causes include stenosis or regurgitation of the tricuspid or pulmonic valves,
right ventricular infarction, and cardiomyopathy.
• Gangguan ventrikel kanan dapat disebabkan juga oleh tetraology of fallot dan ventrikel septal
defek
________________________________________
Disfungsi jantung kiri
• Terjadi gangguan dalam mengalirkan darah dari pulmonal dengan tekanan rendah menuju
ateri sistemik dengan tekanan yang tinggi
•
• Peningkatan tekanan pulmonalbdisebabkan darah dari pulmonal yang tertahan disana karena
darah terakumulasi di ventrikel kiri dan atrium kiri
Terjadinya edema pulmonal terjadi dengan cara :
1. Meningkatnya tekanan filtrasi kapiler yang memasukkan darah kedalam paru-paru, tekanan
ini lebih tinggi dari tekanan osmotik koloid kapiler
2. Kemudian karena tekanan koloid lebih rendah dari tekanan filtrasi maka darah kan pindah ke
interstitium dan terjadi edema
• Kenapa bisa terjadi paroxymal nocturnal dyspnea? Hal ini terjadi karena, ketika seseorang
tidur tekanan gravitasi hilang dari paru-paru yang menyebabkan cairan yang terakumulasi di
bagian tubuh bawah akan kembali ke vaskular dan cairan akan di redistribusikan ke sirkulasi
pulmonal
• Penyebab dari disfungsi jantung kiri dan edema pulmonal adalah infrak miokardial akut.
Dimana hal ini juga yang membuat disfungsi jantung kiri terjadi dengan sangat cepat
• Infrak miokardial akut dapat berujung pada hypokinesis, akinesis, kongesti pulmonal dan
edema pulmonal
Ada 2 cara masing masing organ mempengaruhi satu sama lain:
1. Jantung -> paru
2. Paru -> jantung
_______________________________________
Low-Output Failure
• Low-output failure is characterized by clinical evidence of systemic vasoconstriction with
cold, pale, and sometimes cyanotic extremities
• In advanced forms of low-output failure, marked reductions in stroke volume are evidenced
by a narrowing of the pulse pressure
Penyebabnya :
1. Ischemic Heart disease
2. Cardiomyopathy
________________________________________
Heart compensatory Mechanism
• catecholamines released with sympathetic nervous system stimulation also may contribute
to the high rate of sudden death seen with heart failure.
• Peningkatan tahanan vaskular -> meningkatkan preload dan stress ventrikel
• Gagal jantung bisa menyebabkan reseptor beta-adrenergik tidak berfungsi dengan baik dan
berakibat vasokonstriksi.
• Low cardiac output -> decrease renal blood flow -> angiotensin II (stimulate ADH and
aldosteron) -> water retension -> fluid acumulation -> ventricular hypertrophy -> peningkatan
kebutuhan oksigen (pelebaran ventrikel) dan tegangan didnding jantung meningkat ->
mekanisme frank starling gagal, inotrpy berkurang dan berujung pada gagal jantung.

Kompensasi secara neurohormonal

• Jadi ANP dan BNP banyak diasosiasikan dengan gagal jantung
• ANP dan BNP akan berimteraksi dengan menghambat angiotensin II sehingga retensi cairan
menurun
_______________________________________
Acute Heart Failure Syndrome
Merupakan keadaan dimana terdapat perubahan bertahap maupun secara cepat dari tanda
maupun gejala dari gagal jantung. Hal ini utamanya diebabkan oleh edema paru parah karena
peningkatan filling pressure dari ventrikel kiri baik dengan maupun tanpa cardiac output yang
rendah. Sindrom ini bisa muncul juga dari gagal jantung kronik yang muncul dalam beberapa
episode dan berujung pada sindrom gagal jantung akut
• AHFS are thought to encompass three different types of conditions:
1. Worsening of chronic systolic or diastolic dysfunction that appears to respond to
treatment, approximately 80%
2. New-onset acute heart failure that occurs secondary to a precipitating event such as
a large myocardial infarction or a sudden increase in blood pressure superimposed on a
noncompliant left ventricle
3. Worsening of end-stage/advanced heart failure that is refractory to treatment, with
predominantly left ventricular systolic dysfunction associated with a low-output state.
• The difference between new-onset AHFS and AHFS caused by chronic heart failure is in
the degree of physiologic response, which is more pronounced in the new-onset AHFS and
subtler in chronic heart failure because of the compensatory pathophysiology
• new-onset AHFS, the person will have a stronger sympathetic response with enhanced
pulmonary vascular permeability causing rapid and dramatic symptoms of pulmonary edema.
• Because many compensatory mechanisms operate in people with chronic heart failure, they
tolerate higher pulmonary vascular pressures
• Perubahan regulasi neurohormonal juga dapat menstimulasi angiotensin-aldosteron

Manifestasi Klinis
Pada dasarnya manifestasi klinis dari gagal jantung berdasarkan tingkat disfungsi jantung :
1. Shortness of breath due to congestion of the pulmonary circulation is one of the major
manifestations of left-sided heart failure
2. Dyspnea
3. Orthopnea
4. Paroxysmal nocturnal dyspnea
5. cardiac asthma, Bronchospasm
6. Cheyne-Stokes Respiration (sebagai risiko yang memperburuk gagal jantung)
7. Cyanosis
8. AF
9. Cachexia

Respiratory
A subtle and often overlooked symptom of heart failure is a chronic dry, nonproductive cough
that becomes worse when the person is lying down. Bronchospasm due to congestion of the
bronchial mucosa may cause wheezing and difficulty in breathing. This condition is sometimes
referred to as cardiac asthma.

Cheyne-Stokes respiration is a pattern of periodic breathing characterized by gradual increase

in depth (and sometimes rate) of breathing to a maximum, followed by a decrease resulting in
apnea. The recurrent cycling of hypoventilation/apnea and hyperventilation may also increase
sympathetic activity and predispose to arrhythmias
Acute pulmonary edema is a life threatening condition in which capillary fluid moves into the
alveoli. With the decreased ability of the lungs to oxygenate the blood, the hemoglobin leaves
the pulmonary circulation without being fully oxygenated, resulting in shortness of breath and
cyanosis. The accumulated fluid in the alveoli and airways causes lung stiffness, makes lung
expansion more difficult, and impairs the gas exchange function of the lung. The person with
severe pulmonary edema is usually seen sitting and gasping for air, the pulse is rapid, the skin is
moist and cool, and the lips and nail beds are cyanotic. As the pulmonary edema worsens and
oxygen supply to the brain drops, confusion and stupor appear. The movement of air through
the alveolar fluid produces fine crepitant sounds called crackles, which can be heard with chest
auscultation. As fluid moves into the larger airways, the crackles become louder and coarser.
Terakhir diubah: 8 Jun 2019