HEART FAILURE. Ali Ghanie. Sub Divisi Kardiologi Bagian Penyakit Dalam FK UNSRI / RSMH Palembang

HEART FAILURE

Ali Ghanie

Sub Divisi Kardiologi Bagian Penyakit Dalam FK UNSRI / RSMH Palembang

• Heart Failure (Gagal Jantung) : gagalnya

jantung memompa darah pada kecepatan yang sesuai dengan kebutuhan jaringan

• Circulatory Failure & Overload : 1. Circulatory Failure :

a. Heart failure

b. Non cardiac (peripheral) circul. Failure • Venous return  (volume )

• Kapasitas vaskular bed  • Gangguan vaskular perifer • Oxyhemoglobin

2. Circulatory Congestion :

a. Cardiac  gagal jantung b. Non cardiac :

• Volume darah 

• Venous return  (vask. Resistance )

• Congestive heart failure (acute – chronic)  cardiac origin

• Myocardial dysfunction / failure  sistolik, diastolik • Forward failure – backward failure

• Left – VS Right Heart Failure • Latent Heart Failure

• Stress mekanik (after load / pre load)

Pressure over load

Volume overload

• Pressure overload

– Kontraksi > kuat : lebih lambat

– Hipertrofi konsentris (replikasi sarcomer paralel)

– Chamber tetap (<<)

– Kontraksi perunit  ( ttp total mass  ) • LV diastolic filling 

• LV compliance / distensibility 

Bukan OK HF

• Volume Over Load

– Hipertrofi eksentris (replikasi sarcomere seri) – Replikasi paralel (+) (o.k. wall stress)

– Pengosongan LV (PD MR) > cepat  wall tension <<

– Chamber >> ; tanpa kenaikan tekanan diastole – Bila compliance   tekanan diastole 

Responses to Hemodynamic Overload Pressure overload

Systolic wall stress

Mechanical transducers

Volume overload

Diastolic wall stress

Intracellular signals

Ventricular remodeling

Paralel sarcomeres Series sarcomeres

Mekanisme Kompensasi pada Heart Failure

• Autonomic nervous system

a. Jantung : HR, kontraktilitas , kecepatan relaxasi 

b. Circ. Perifer : Vasokonstriksi arterial (after load ) Vasokonstriksi venous (preload )

• Ginjal  R.A.A

a. Vasokonstriksi arterial (afterload ) b. Retensi Na – H₂0 (PRG & afterload ) c. Kontraktilitas 

• Frank – Starling Law of the Heart

Pemanjangan sarcomere pada akhir diastole Kenaikan volume, tekanan

• Hipertrofi  - Paralel (konsentris) - Seri (eksentris)

• Oksigen – Perifer

a. Redistribusi cardiac output

b. Kurva disosiasi oxygen – hemoglobin c. Ekstraksi O₂ jaringan 

PENYEBAB OVERALL HEART “PUMP”

FAILURE

I. Kelainan Mekanis :

a. Beban tekanan 

b. Beban volume   regurgitasi, preload

c. Obstruksi vent. Filling  MS. TS d. Konstriksi pericard

e. Endokard – miokard restriksi f. Ventric. Aneurysm

II. Kelainan otot ( miokard ) a. Primer :

 Miopati  Miokarditis

 Metabolik (DM)  Toxic (alcohol, etc)  Presbycardia

b. Sekunder :

 Disdinamik (sekunder o.k. mekanik)  Iskhemia

 Kelainan systemik  PPOM

 Obat

III. Gangguan Ritme / Konduksi

a. Standstill b. Fibrilasi

c. Takhikardi – Bradikardi  berat d. Gangguan konduksi

PUMP (OVERALL H.F.)

≁

Mycardial

Failure

• Overall HF  1. ∑ darah L. min // m2

2. Tekanan atrium

• Myocardial failure :

– me kecepatan & pemendekan unit otot jantung melawan afterload (systolic load)

Overall Heart Failure tanpa Myocardial

Failure

1. Acute mechanical overload

• Acute Cor Pulmonale

• Hipertensi

• Acute Volume Overload

2. Chronic severe overload

• High COP (beri-beri, Paget’s disease) • Value & Congenital Heart Disease

3. Gangguan pengisian (Impaired Cardiac Filling) • Pericardial Restruction

• Restrictive Myocardial Disease

• Obstruksi mekanik (MS – TS – Tumor) • Tachycardi

Myocardial – Failure tanpa overall H.F.

1. Systolic unloading of ventricle • Mitral Regurgitation

• Vasodilator drugs

2. Compensated myocardial failure 3. Segmental contraction disorder

• Iskhemik miokard transient • Infark miokard

Cardiac Performance (Kemampuan ?)

PREDIKTOR :

• Preload : - “a change in initial length”

- tegangan FFG ventrikel akhir diastole

dipengaruhi  - Venous Return

- Total volume - Distribusi volume Posisi tubuh tekanan intrathorak tekanan intrapericard tonus vena kontraksi atrium

• After load : “Force / Stress” pada ventrikel segera sesudah pemendekan otot ventrikel. dipengaruhi  - PVR

- Fisik arteri

- Volume pada ejeksi

• Kontraktilitas :



• Saraf simpatis • Catecholamin • Inotropik agent • Depressant • Mass lost

KLASIFIKASI

(Toleransi terhadap Latihan Jasmani)

• Menurut NYHA (New York Heart Association ) I. Aktifitas fisik tidak terbatas

II. Aktifitas fisik sedikit terbatas III. Aktifitas fisik sangat terbatas IV. Istirahat  sesak

• Subjektif  Anamnese

• Objektif  uji latih dengan beban, TMT, bicycle

Diagnosis

A. Gagal Jantung Kiri

– Dyspnea d’effort – Orthopnea

– Paroxysmal nocturnal dyspnea – Edema paru

– Pernapasan cheyne stokes – Hemoptisis – Berdebar – debar – Pembesaran jantung – Takikardi – S3 gallop – P2 mengeras

CIRCULATORY

CIRCUIT

Kanan Kiri

B. Gagal Jantung Kanan

– Lelah

– Mual, anorexia, rasa penuh pada perut – Sesak nafas  tidak menyolok

– JVP ˆ

– Hepar >>, nyeri tekan, ikterus (+) – Splenomegali

– Ascites

– Edema tungkai bawah – Hidrothorak

The Heart Failure Milieu : Compensatory Mechanisms Disease process Ventricular dysfunction Hemodynamic abnormalities Compensatory mechanisms Sympathetic Increased contractility Tachycardia

Increased venous tone Increased arterial tone

Renal Renin-angiotensin-aldosterone Salt/water retention Ventricular Dilation Hypertrophy

Heart Failure Milieu : Disease Process Mechanical Dysfunction Pressure Overload Hypertension Aortic/pulmonic valve stenosis Pulmonary hypertension Volume overload

Aortic, mitral, tricuspid valve insufficiency

Impaired Heart Filling

Pericardial disease Ventricular hypertrophy Myocardial restriction Mitral/tricuspid stenosis Myocardial Dysfunction Myocardial infarction Cardiomyopathy Myocarditis Drug/toxin-induced

Systemic disease effects

Disease Process

Renal Considerations in Heart Failure Angiotensinogen (liver) Angiotension I Angiotension II Thirst Sodium retention (direct tubular effect) Vasoconstriction Renin release Angiotensin- converting enzyme

The

Kidney

In

Heart

Failure

Aldosterone secretion Diuretic therapy Distal tubular sodium load Renal perfusion pressure Other K+, Ca2_+, prostaglandins Atrial natriuretic factor Vasopressin

The Heart Failure Milieu : Clinical Presentation Disease process Ventricular dysfunction Hemodynamic abnormalities Metabolic changes Symtoms and physical findings Compensatory mechanisms Physical findings Peripheral edema Ascites Vascular congestion

Jugular venous distension Rales Tachycardia Hypotension Cachexia Disease-specific findings Physical findings Azotemia Hyponatremia Hypocalemia Hypomagnesemia Hyperuricemia Acidosis/alkalosis Hypoxia/O₂ desaturatuion Decreased MVO₂ Symptoms

Fatique and weakness

Dyspnea and fluid retention syndromes

Nocturia

Gastrointestinal symptoms Diminished mentation

Symtoms and physical findings

Death

The Heart Failure Milieu :

End-Organ Failure and Death

Disease process Ventricular dysfunction Hemodynamic abnormalities Metabolic changes Compensatory mechanisms _End-Organ Failure Sudden Death

Systemic organ failure

Renal failure Hepatic failure Respiratory failure Multi-organ failure Pulmonary embolism

Peripheral (cerebral embolism)

Lethal arrhythmia

Electrolyte abnormalities

Elevated catecholamine levels Ischemia

The Heart Failure Milieu :

From Molecular Biodynamics to a Clinical Syndrome

Molecular Genetic Cellular, Organelle CELL HEART Integrated Organism: Man Prevention Treatment DNA Contractile proteins Contraction Pump Physiologic milieu Compensation Heritable disorders Volume overload/ pressure overload

Hormone signal transduction

Necrosis Toxins

Remodeling

Compensatory responses

Penatalaksanaan

1. Pengendalian faktor penyebab

• Prosedur operasi • Terapi medis

2. Pengendalian faktor pencetus

3. Memperbaiki faktor yang memperburuk 4. Terapi gagal jantungnya

Gagal Jantung

• Perbaikan daya pompa jantung • Pengurangan beban jantung

Myocardial Failure Pump Failure Inotropic COP ⇊ COP on demand Vasokonstriksi simpatis ⇈ Resistensi Perifer ⇈ Vasodilator Renin release Angiotensin I Angiotensin II CEI Tekanan Vena  Edema Perifer Edema Pulm. Retensi Na / H₂O Aldosterone Diuretik AT1 AT2 AII RB

ANGIOTENSINOGEN RENIN TISSUE RENIN ANGIOTENSIN I TISSUE ACE CHYMASE CATHEPSIN G ACE ANGIOTENSIN II CATHEPSIN G ELASTASE TPA BRADYKININ INACTIVE FRAGMENTS ARBs AT₁ AT₂ VASOCONSTRICTION RENAL NA+ REABSORPTION ALDOSTERONE SECRETION SYMPATHETIC ACTION VASOPRESSIN SECTION CELL GROWTH AND PROLIFERATION

VASODILATION

ANTIPROLIFERATION APOPTOSIS

Left Ventricular Function Curve

Stroke volume

End diastolic volume

End dias tolic Pres su re

Left Ventricular Function Curve

End diastolic volume

St

ro

ke

V

LV Size PVR B.P Stroke Volume COP Myocard fiber short HR Preload Contractility Afterload

EDV

CONTRACTILE STATE OF MYOCARD

Blood Volume Posisi Tekanan Intrathoracal Atrial Contrib Venous Return Otot Seklet STRETCHING EDV V entrik el Performance