kuliah gagal jantung

8/7/2019 kuliah gagal jantung

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Preload

contractility

Afterload

Left ventricular size

Myocardial fibershortening

Heart rate

Arterial

Pressure

stroke volume

Peripheral

Resistance

CardiacOutput

Skema Komponen Komponen Penentu Aktivitas Jantung

Dikutip dari : Harrisons Internal Medicine ed.12 Vol.I


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Causes of Heart FailureCauses of Heart Failure


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Exacerbating orExacerbating orPrecipitating Factors of HFPrecipitating Factors of HF


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Kerusakan katup

Gagal jantung kronikRemodeling ventrikel kiri &

disfungsi kronik ventrikel kiri

Edema paru akut

Kerusakan myokard

Disfungsi ventrikel kiri

akut

ToksinVirusIskemiaHipertensi

Dispnea

Lelah

Edema

Hospitalisasi

Kematian

Penyebab Dasar & Manifestasi Gagal Jantung

Dikutip dari : Clinical Pharmacology, 4 th ed., Melmon and Morellis, 2000


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curah jantung

suplai darah ginjal

curah jantung(via kompensasi)

remodelling

Angiotensin II

sekresi renin

afterload preload frekuensi denyut

aktivitas simpatis

Firingsinus karotis

kontraktilitas

Respons Kompensasi Selama Kegagalan Jantung Kongestif

Dikutip dari : Basic & Clinical Pharmacology, 8 th ed., Katzung, 2001


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Spironolacton

AT antagonis

ACE-I

Vasodilator

preload afterloadLipid modulatorObat anti diabetes

InsulinIHD

Anti iskemia

PG

NO

BK

Vasodilatasi Inaktif

AI

AII

Kerusakan

myokard

Disfungsi

jantung

Otak

NE

Digoxin

AVPAldosterone vasokonstriksi Stress oksidatif Stimulasi myokard

Retensi air Retensi

garam

Worsening HFDisfungsi endothel

Sitokin Neurohormon

tanda & gejala kualitas hidup, lama perawatan RS Kematian akibatkegagalan pompajantung

Kematian akibat

aritmia ventrikel

Faktor resiko :

Diabetes,

dislipidemia

performa jantung

blockerAntioksidan-blocker

ACE-I, -blocker, diuretic,

digoxin, nitrat

ACE-I, -blockerTransplantasi

Hipertensi

amiodarone

Antihipertensi


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Terapi Gagal Jantung Sistolik

Berikan diuretika untuk mencapaiuevolemia

Tambahkan ACE inhibitor

Tidak toleran terhadap ACEinhibitor

Toleransi baik terhadap ACE inhibitor

TambahkanARB

Tambahkan - blocker, lakukan titrasidosis

Tambahkan - blocker

Tidak toleran terhadap - blocker

Toleransi baikterhadap - blocker

Tidak toleran

terhadap - blocker

Toleransi baik

terhadap - blocker

Lanjutkan terapi dengan

diuretika, ARB, dan - blocker


diuretika & - blocker,pertimbangkanpenambahanspironolakton

Tambahkan ARBatauspironolakton

Lanjutkan terapi dengandiuretika, ACE inhibitordan - blocker(memiliki bukti efikasipaling besar)


diuretika, ACE inhbitor dan ARBatau spironolakton

Dikutip dari : Finding The Optimal Combinationtherapy, Cleveland Clinic Journal of Medicine, Vol.69,2002


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Angiotensin Converting Enzyme Inhibitors Commonly Used for Chronic Heart Failure Treatment

DRUGUSUAL

STARTINGDOSE (mg)

DOSERANGE

TIMETO

ONSET(H)

PEAKEFFECT

(H)

T1/2 (H) PRODRUG

ROUTE OFELIMINATION

Captopril 6.25 6.25 50 mgtid

0.3 1 2 N Renal

Enalaprilmaleate

2.5 2.5 bid 1 4 6 11 Y Renal

Lisinopril 2.5 5 35mg/day 1 4 6 13 N Renal

Ramipril 2.5 5 10 mgbid

1 2 3 6 12 Y R+H 70/30

Quinapril 5 10 20 mgbid

1 4 3 Y Renal

Trandolapril 1 1 4 mg/day 2 6 8 16 24 Y R+H 30/70

ABBREVIATION : R+H, renal + hepatic

Dikutip dari : Clinical Pharmacology, 4th ed., Melmon & Morellis, 2000


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Therapeutics classification of subsets in acute myocardial infarction

SubsetSystolic ArterialPressure (mmHg)

Left VentricularFilling Pressure

(mmHg)

Cardiac Index(L/min/m2)

Therapy

1. Hypovolemia < 100 20 > 2.5 Diuretics

3. Peripheral congestion < 100 10 20 > 2.5 None, or vasoactivedrugs

4. Power Failure < 100 > 20 < 2.5 Vasodilators, inotropicdrugs

5. Severe shock < 90 > 20 < 2.0 Vasoactivedrugs,inotropic drugs,vasodilators, circulatoryassist

6. Right ventricularinfarction

< 100 RVFP > 10LVFP < 15

< 2.5 Provide volumereplacement for LVFP,inotropic drugs, avoid

diuretics

7. Mitral regurgitation,ventricular septal defect

< 100 > 20 < 25 Vasodilators, inotropicdrugs, circulatory assist,surgery

The numerical values are intended to serve as general guidelines and not as absolute cutoff points. Arterial

pressures apply to patients who were previously normotensive and should be adjusted for patients who were

previously hypertensive.

(RVFP and LVFP = right and left ventricular filling pressure.)

Dikutip dari : Basic & Clinical Pharmacology, Katzung, 2001


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S

T

R

O

K

E

V

O

L

U

M

E

VENTRICULAR FILLING PRESSURE

Normal Congestive symptoms

Low output symptoms

I

D

I + V + DV

I + V

Respons Hemodinamik terhadap Intervensi Farmakologik pada Gagal Jantung

I : inotropic agent; V : vasodilator; D : diuretic

Dikutip dari : Pharmacological Basis of Therapeutics, Goodman & Gilmans, 10thed., 2001


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Penyebab Resistensi terhadap Diuretika pada Gagal Jantung

Dikutip dari : Pharmacological Basis of Therapeutics, 10th ed., Goodman & Gilmans, 2001

Ketidakpatuhan pada regimen terapi dan / atau asupan Na+ yang berlebihan pada diet

Penurunan perfusi ginjal dan laju filtrasi glomerulus akibat :

Deplesi volume intravaskuler yang berlebihan dan hipotensi akibat pemberian diuretika yang agresif dan / atau terapi

vasodilatorPenurunan curah jantung oleh karena makin memburuknya gagal jantung, aritmia atau oleh penyebab primer pada

jantung lainnya

Reduksi selektif pada tekanan perfusi glomeruler yang menyertai pemberian awal dan atau peningkatan dosis terapi

dengan ACE inhibitor

Obat obat antiinflamasi non steroid (NSAIDs)

Kelainan primer pada ginjal (misalnya, emboli kolesterol, stenosis arteri renalis, drug induced interstitial nephritis,

uropati obstruktif)

Penurunan atau gangguan absorpsi diuretika oleh karena edema dinding usus dan penurunan aliran darah

splannikus


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Bradykinin

Inactive

peptide

Nitric Oxide

Prostacyclin

Angiotensinogen

Angiotensin I

Renin

ACE inhibitors

ACE

(Kininase)

Non ACE dependent

patways, e.g., chymase

AT1 receptors AT2 receptors

AldosteroneVasoconstriction

Sympathetic stimulation

Cellular hypertrophy

Renovascular effects

AT1 receptor antagonist

Angiotensin II

Bradykinin

receptors

The renin angiotensin aldosterone systemDikutip dari : Pharmacological Basis of Therapeutics, Goodman & Gilmans, 10th ed., 2001


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OUTFLOW RESISTANCE

S

T

R

O

K

E

V

O

L

U

M

E

normal Hypertension

Myocardial dysfunction, moderate

Myocardial dysfunction,severe

Relationship between ventricular outflow resistance and stroke volume in patients with systolic ventricular

dysfunction

Dikutip dari : Pharmacological Basis of Therapeutics, Goodman & Gilmans, 10th ed., 2001


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Peran Potensial Aldosterone pada Patofisiologi Gagal Jantung

MEKANISMEEFEK PATOFISIOLOGI

Peningkatan retensi natrium Edema, peningkatan tekanan pengisian jantung

Peningkatan ekskresi kalium dan magnesium Aritmogenesis dan resiko henti jantung mendadak

Penurunan uptake norepinefrin dari myokard Potensiasi efek NE terhadap remodeling danaritmogenesis

Penurunan sensitivitas baroreseptor Penurunan aktivitas parasimpatis dan resiko hentijantung mendadak

Fibrosis myokard, proliferasi fibroblast Remodeling dan disfungsi ventrikel

Perubahan ekspresi kanal natrium Peningkatan eksitabilitas dan kontraktilitas otot jantung

Dikutip dari : Pharmacological Basis of Therapeutics, 10

th

ed., Goodman & Gilmans, 2001


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Obat obat Vasodilator yang Digunakan pada Terapi Gagal Jantung

ikutip dari : Pharmacological Basis of Therapeutics, 10th ed., Goodman & Gilmans, 2001

KELAS OBATCONTOH MEKANISME KERJA

VASODILATASIPENURUNAN

PRELOADPENURUNANAFTERLOAD

Nitrat Organik Nitroglycerin,

isosorbide dinitrate

Vasodilatasi yang diperantarai

oleh NO

+++ +

Donor Nitric Oxide (NO)

Nitroprusside Vasodilatasi yang diperantaraioleh NO

+++ +++

Angiotensin convertingenzyme inhibitors(ACEI)

Captopril,enalapril, lisinopril

Hambatan pembentukanangiotensin, penurunandegradasi bradykinin

++ ++

Angiotensin receptorblockers

Losartan,candesartan

Blockade reseptor angiotensin ++ ++

Phosphodiesteraseinhibitors

Milrinone,inamrinone

Hambatan degradasi cAMP ++ ++

Direct acting Hydralazine,minoxidil Tidak diketahui + +++

Subtype selective 1

adrenergic receptorantagonists

Doxazosin,prazosin Hambatan selektif reseptor1

+++ ++

Non subtype selective adrenergicreceptor antagonists

Phentolamine Hambatan non selektif reseptor

+++ +++


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Guidelines for Pharmacological Management of Ambulatory Patients with Heart Failure

NYHA Functional Class IMild HF

II III IV

Severe HF

Diuretics

ACE inhibitors

-receptor blockers

Consider use Consider use

Digoxin - atrial fibrillation

Digoxin - sinus rhythm Consider use

Spironolactone Consider use

-

: Routinely used: Drugs should be consideredDikutip dari : Pharmacological Basis of Therapeutics, Goodman & Gilmans, 10th ed.,


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Classification & DrugTherapy of Heart Failure


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Treatment Algorithm for Chronic Heart Failure


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Outcome Evaluation of Chronic HF

Volume status

Exercise tolerance

Overall symptoms

Quality of Life (QoL)

Adverse drug reaction (ADR)

Disease progression & Cardiac function


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Acute Heart Failure

Hemodynamic category :

Volume status : Wet / dry

Wet volume/fluid overload

Dry EuvolemicEuvolemicPerfusion adequacy : Warm / cool

Warm adequate cardiac output (CO) to perfuse

peripheral tissues


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Clinical Presentation

Subset I (Warm&Dry)

Cardiac index (CI) > 2.2L/min/m2, pulmonary capillarywedge pressure (PCWP) < 18

mmHg

Patient considered wellcompensated & perfused,without evidence of congestion

No immediate interventionnecessary except optimizingoral medication & monitoring

Subset II (Warm&wet)

CI > 2.2 L/min/m2, PCWP 18 mmHg

Patients adequately perfused &shows signs & symptoms ofcongestion

Main goal is to reduce preload(PCWP) with loop diuretics

and vasodilators


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Subset III (Cool & Dry)

CI < 2.2L/min/m2, PCWP < 18mmHg

Patients are inadequately perfused& not congested

Hypoperfusion leads to increasedmortality, elevating death ratesfour-fold compared to those whoare adequately perfused

Treatment focuses on increasingCO with positive inotropic agentsand/or replacing intravascularfluids

Fluid replacement must beperformed cautiously, as patientscan rapidly become congested

Subset IV (Cool & wet)

CI < 2.2 L/minute per square meter,PCWP >18 mm Hg

Patients are inadequately perfusedand congested

Classified as the most complicatedclinical presentation of AHF with theworst prognosis

Most challenging to treat; therapytargets alleviating signs andsymptoms of congestion byincreasing CI as well as reducingPCWP, while maintaining adequate

mean arterial pressure

Treatment involves a delicate balancebetween diuretics, vasodilators, andinotropic agents

Use of vasopressors is sometimesnecessary to maintain blood pressure


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Usual Hemodynamic Effects of Commonly Used

Intravenous Agents for Treatment of Acute or Severe

Heart Failure

*Recombinant BNP

*

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