RSMH Palembang

HEART FAILURE

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

HEART FAILURE • •

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

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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 Compensated 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  Bukan OK HF • LV compliance / distensibility 

• 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 

Mekanisme Kompensasi pada Heart Failure •

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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 sarcomerg 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  • Metabolisme Anaerob

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 g. Ventric. Disinergi

II.

III.

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 Gangguan Ritme / Konduksi a. Standstill b. Fibrilasi c. Takhikardi – Bradikardi  berat d. Gangguan konduksi

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

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 Ronkhi basah kedua basal paru

CIRCULATORY CIRCUIT

PARU

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

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 • Mengurangi retensi Na & air

Myocardial Failure

Inotropic

Pump Failure COP ⇊

COP on demand

Tekanan Vena 

Vasodilator Vasokonstriksi simpatis ⇈ Renin release

Resistensi Perifer ⇈

Edema Perifer

Edema Pulm.

Diuretik Retensi Na / H2O

Angiotensin I

CEI Angiotensin II

Aldosterone

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.

2.

3.

4.

Acute mechanical overload • Acute Cor Pulmonale • Hipertensi • Acute Volume Overload Chronic severe overload • High COP (beri-beri, Paget’s disease) • Value & Congenital Heart Disease Gangguan pengisian (Impaired Cardiac Filling) • Pericardial Restruction • Restrictive Myocardial Disease • Obstruksi mekanik (MS – TS – Tumor) • Tachycardi Low Cardiac output  Heart block / bradicardy

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 diperngaruhi  - 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 :  performance • Saraf simpatis • Catecholamin • Inotropik agent • Depressant • Mass lost • Intrinsic myocardial depression

Left Ventricular Function Curve

End diastolic Pressure

Stroke volume

End diastolic volume

End diastolic volume

Stroke Volume

Left Ventricular Function Curve

End diastolic volume

LV Size PVR Preload

Contractility

Stroke Volume Myocard fiber short

COP HR

Afterload

B.P

CONTRACTILE STATE OF MYOCARD

EDV

Posisi Tekanan Intrathoracal Atrial Contrib Venous Return

Ventrikel Performance

Blood Volume

Otot Seklet STRETCHING

EDV

The Heart Failure Milieu : From Molecular Biodynamics to a Clinical Syndrome DNA

Contractile proteins

Molecular Genetic

Heritable disorders

Cellular, Organelle

Volume overload/ pressure overload Hormone signal transduction

Contraction

CELL

Pump

HEART

Physiologic milieu

Compensation

Integrated Organism: Man Prevention Treatment

Necrosis Toxins Remodeling Compensatory responses Decompensation

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

Disease Process

Mechanical Dysfunction Myocardial infarction Cardiomyopathy Myocarditis Drug/toxin-induced Systemic disease effects

The Heart Failure Milieu : Compensatory Mechanisms

Disease process

Ventricular dysfunction

Renal Renin-angiotensin-aldosterone Salt/water retention

Ventricular Dilation Hypertrophy

Hemodynamic abnormalities

Compensatory mechanisms

Sympathetic Increased contractility Tachycardia Increased venous tone Increased arterial tone

Renal Considerations in Heart Failure

The

Angiotensinogen (liver)

Renin release Angiotension I

Angiotension II

Thirst

Sodium retention (direct tubular effect)

Vasoconstriction

Angiotensinconverting enzyme

Aldosterone secretion

Kidney

Diuretic therapy Distal tubular sodium load

In

Renal perfusion pressure

Heart

Other K+, Ca2+, prostaglandins

Failure

Atrial natriuretic factor

Vasopressin

The Heart Failure Milieu : Clinical Presentation

Physical findings Disease process

Ventricular dysfunction

Physical findings Azotemia Hyponatremia Hypocalemia Hypomagnesemia Hyperuricemia Acidosis/alkalosis Hypoxia/O2 desaturatuion Decreased MVO2

Hemodynamic abnormalities

Peripheral edema Ascites Vascular congestion Jugular venous distension Rales Tachycardia Hypotension Cachexia Disease-specific findings

Metabolic changes Compensatory mechanisms Symtoms and physical findings

Symptoms Fatique and weakness Dyspnea and fluid retention syndromes Nocturia Gastrointestinal symptoms Diminished mentation

The Heart Failure Milieu : Disease process

End-Organ Failure and Death Systemic organ failure Renal failure Hepatic failure Respiratory failure Multi-organ failure Pulmonary embolism Peripheral (cerebral embolism)

Ventricular dysfunction

Hemodynamic abnormalities Metabolic changes Compensatory mechanisms End-Organ Failure

Lethal arrhythmia Electrolyte abnormalities Elevated catecholamine levels Ischemia Drug-proarrhythmia

Symtoms and physical findings

Death Sudden Death

Responses to Hemodynamic Overload Pressure overload

Volume overload

Systolic wall stress

Diastolic wall stress Mechanical transducers Intracellular signals Ventricular remodeling

Paralel sarcomeres

Concentric hypertrophy

Series sarcomeres Normal

Eccentric hypertrophy