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8/13/2019 EM I K7 CR Cardiac Failure
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Prof. Dr. T. Bahri Anwar, SpJP(K)Prof. Dr. Harris Hasan, SpPD,SpJP(K)
DEPARTEMEN KARDIOLOGI FK USU MEDAN
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TERMINOLOGI
DEFENISI
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SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION
LV-DYSFUNCTION VENTRICULAR DYSFUNCTION
PRECLINICAL STATE OF HEART FAILURE
ASYMPTOMATIC HEART FAILURE
SILENT HEART FAILURE
MILD HEART FAILURE
OVERT HEART FAILURE
PROGRESSIVE HEART FAILURE
REFRACTER HEART FAILURE
ACUTE HEART FAILURE CHRONIC HEART FAILURE
SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE
FORWARD FAILURE BACKWARD FAILURE
LEFT HEART FAILURE RIGHT HEART FAILURE
HIGH-OUTPUT FAILURE LOW-OUTPUT FAILURE
CONGESTIVE HEART FAILURE
END-STAGE HEART FAILURE
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1. Subjective Ada simptom HF (saat istirahat atau bekerja),Dan
2. Objective Ada bukti bahwa terjadi gangguan fungsi jantung
(cardiacdysfunction) saat istirahat,
Dan
3. Retrospective Ada respon (perbaikan) terhadap HF-nya dengan
pengobatan yang sesuai
Untuk dapat disebut HF, kriteria 1 dan 2 harus dipenuhi pada semua kasus.
Dan bila dengan kriteria 1 dan 2 masih meragukan maka digunakan kriteria 3.
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ETIOLOGI
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Myocardial infarction
Coronary thrombosis
Myocardial ischaemia
Coronary artery disease
Atherosclerosis, Left ventricular hypertrophy
Risk factors
(Hypertension, LDL, Diabetes, etc)
Arrhythmia & Loss of muscle
Sudden
death
Remodelling
Ventricular dilatation
Heart failure
Endstage
Heart Disease
Dzau & Braunwald, 1991
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Valvular
Infeksi : Myocarditis
Kongenital : ASD, VSD, PDA, Coarc-Ao
Cardiomiopati : bahan kimir, obat-obatan
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FAKTOR PENCETUS (EXACERBATE)
ANEMI
GANGGUAN GINJAL
GANGGUAN THYROID
PEMAKAIAN OBAT-OBAT CARDIODEPRESSANT
INFEKSI
KELEBIHAN CAIRAN KELEBIHAN ASUPAN GARAM
ALKOHOL
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PATOFISIOLOGI
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Gangguan fungsi pemompaan ventrikel
Aktivasi neurohormonal
Peningkatan konsentrasi neurohormones :
Noradrenaline
Angiotensin II
Vasopressin
Aldosterone
Retensi Na++ H2O di ginjalVasokonstriksi Hypertrophy dilatation
(remodeling)
Peningkatan signal transductionHeart Failure
Efek neuroendocrine pada heart failure
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PENAMPILAN
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SYMPTOMS
SENSITIVITY
(%)
SPECIFICITY
(%)
DYSPNOEA 66 52
ORTHOPNOEA 21 81
PAROXYSMAL
NOCTURNAL
DYSPNOEA
33 76
OEDEMA 23 80
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SIGNS
SENSITIVITY
(%)
SPECIFICITY
(%)
TACHYCARDIA 7 99
RALES 13 91
S3 31 95
JVP 10 97
OEDEMA 10 93
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NYHA Class I Tidak ada keterbatasan : aktivitas fisik biasa tidakmenimbulkan fatique, dyspnoea ataupun palpitasi
NYHA Class II Sedikit keterbatasan aktivitas fisik : merasa nyaman
ketika istirahat tetapi aktivitas fisik biasa sudah
menimbulkan fatique,Palpitasi atau dyspnoea
NYHA Class III Keterbatasan yang nyata pada aktivitas fisik : merasa
nyaman ketika istirahat tetapi symptom akan muncul
begitu ada aktivitas fisik yang lebih ringan dari biasa.
NYHA Class IV Rasa tidak nyaman setiapkali melakukan aktivitas fisik
apapun : symptom HF sudah tampak ketika istirahat dan
semakin tidak nyaman ketika melakukan aktivitas fisik.
SEVERITY
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DIAGNOSTIK
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NO IDEAL TEST
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1. Untuk memastikan bahwa si pasien memang menderita HF
2. Untuk memastikan etiologi dari HF
3. Untuk menentukan pola patofisiologinya sehingga dapat
ditentukan/dipilih strategi pengobatannya.4. Untuk menentukan penampilan HF-nya (apakah ada oedema
atau orthopnoe)
5. Untuk mengenal faktor-faktor yang dimiliki dalam kaitan
menentukan prognosa (prediksi morbidity dan mortality)
6. Untuk memprediksi apakah seseorang termasuk beresiko tinggi
mengalami HF
KOMPONEN DIAGNOSTIK
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TEST DIAGNOSTIK
EKG : 8% normal
THORAX FOTO : dikaitkan dengan klinis
dan EKG
LABORATORIUM : cardiac enzyme (khusus
pada acute exacerbation) dan ANP/BNP
untuk rule out test
ECHOCARDIORAPHY : EF
ANGIOGRAPHY
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EKG
PJK : Infark (baru atau lama), Iskemi ?
LVH ?
Aritmia ?
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THORAX FOTO
Kardiomegali ?
Tanda bendungan ?
Infiltrat, effusi pleura ?
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Alveolar edema
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Edema
Pitting edema
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LABORATORIUM
Darah Rutin
Urin Rutin
Fungsi Ginjal : Ureum, Kreatinin
Fungsi Hati : SGOT, SGPTElektrolit
Analisa Gas Darah
Fungsi Thyroid
Gula darah
Enzym Jantung
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ECHOCARDIOGRAPHY
Fungsi LV, pergerakan dinding jantung (wall motion)
Dimensi rongga-rongga jantung
Katub-katub jantungKelainan kongenital : ASD, VSD, dll
LV hypertrophy, aneurysma
Efusi perikardial
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ANGIOGRAPHY
Kateterisasi jantung kanan : kongenital ?
Kateterisasi jantung kiri : PJK ?
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EVOLUTION
AND
PROGRESSION
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Stage Deskripsi Contoh
A Pasien beresiko tinggi menderita HF oleh
karena adanya kondisi yang erat kaitannya
dengan terjadinya HF. Pada pasien ini
tidak ditemukan kelainan struktur maupunfungsi perikardium, miokardium atau katub
jantung dan belum pernah memperlihatkan
tanda dan gejala HF.
Hipertensi sistemik; penyakit jantung koroner; diabetes mellitus;
riwayat pemakaian obat cardiotoxic atau peminum alkohol; pernah
menderita demam rematik; ada riwayat keluarga yang menderita
cardiomyopathy.
B Pasien dengan penyakit yang telah
berdampak terhadap struktur jantung yang
erat kaitannya dengan terjadinya HF tetapi
belum pernah memperlihatkan tanda dan
gejala HF.
Fibrosis atau hypertrophy ventrikel kiri;
dilatasi ventrikel kiri atau kontraksinya melemah;
penyakit jantung katub asimptomatik; pernah mengalami infark
miokard sebelumnya.
C Pasien dengan gejala HF sebelumnya
atau sekarang, berkaitan dengan penyakit
jantung yang dideritanya.
Fatique atau dyspnoea akibat dysfungsi sistolik ventrikel kiri;
pasien asymptomatik yang tadinya telah mendapat pengobatan
terhadap gejala HF-nya.
D Pasien dengan penyakit jantung yanglanjut, menunjukkan gejala HF yang nyata
ketika istirahat meskipun pengobatannya
sudah maksimal dan membutuhkan
intervensi khusus.
Pasien yang sudah berulangkali di opname karena HF dantampaknya sulit keluar dari rumah sakit;
pasien opname yang sedang menunggu transplantasi jantung;
pasien yang dirawat di rumah dengan berbagai peralatan mekanis
untuk membantu sisrkulasi serta mengatasi keluhannya;
pasien yang sedang dalam ruang atau kondisi tertentu untuk
penetalaksanaan HF-nya.
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Perawatan ICCU (terutama bila akut)
Akses pembuluh darah (IV-line)
Posisi setengah duduk
O2nasal atau masker
Diuretik : Furosemide 50-100 mg bolus atau intermitten Digoxin : terutama bila ada aritmia (Atrial Fibrillasi)
- oral : 0.5 mg, bisa diulang setelah 6 jam
- i.v. : 0.5 mg selama 20 min, bisa diulang
setelah 6 jam Atasi faktor pencetus yang ada.
Obat-obat lain sesuai etiologi.
PENATALAKSANAAN
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Bila terjadi hipotensi :
Dobutamine 5-20 g/kgBB/menit
Dopamine 2.5-5 g/kgBB/menit
Adrenaline 1-12 g min-1
Noradrenaline 1-12 g min-1
Intra-aortic balloon pumping
KONDISI KHUSUS
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Blockers
AntiarrhythmicsAnticoagulants
Surgery
Revascularization
Valve replacementCardiac transplantation
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Stage A Stage B Stage C Stage D
Pts with :
Hypertension
CAD
DM
Cardiotoxins
FHx CM
THERAPY Treat Hypertension Stop smoking Treat lipid disorders Encourage regular
exercise Stop alcohol
& drug use ACE inhibition
Pts with :
Previous MI
LV systolic
dysfunction
Asymptomatic
Valvular disease
THERAPY All measures under
stage A ACE inhibitor Beta-blockers
THERAPY All measures under
stage A Drugs for routine use:
diureticACE inhibitorBeta-blockersdigitalis
THERAPY All measures under
stage A,B and C Mechanical assist
device Heart transplantation Continuous IV
inotrphic infusions forpalliation
Pts who havemarked symptomsat rest despitemaximal medicaltherapy.
Pts with :
Struct. HD
Shortness ofbreath and fatigue,reduce exercisetolerance
Struct.HeartDisease
DevelopSymp.of
HF
Refract.Symp.ofHF at
rest
Stages in The Evolution of HF and Recommended Therapy byStage
ACC/AHA Guidelines for theEvaluation and Management of Chronic Heart Failure in the Adult
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TERIMAKASIH
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MANAGEMENT
Drug therapy
Diuretics
Loop diuretics, e.g. frusemide (typically 40-120 mg d-1)orbumetanide(typically 1-4 mg d-1)
Nitrates
Nitrates, e.g.oral isosorbide mononitrate(30-120 mg d-1)
Vasodilators
Oral ACE inhibitors, e.g.captopril12.5-50 mg tid, enalapril10-20 mgbd or lisinopril10-20 mg d-1
Oral AT1 receptor antagonists, e.g.losartan50-100 mg d-1
In patients with renal dysfunction or intolerance of ACE inhibitorsand AT1 receptor antagonists, the combination of hydralazine, and anitrate is a suitable alternative. The regimen used in the VeHEFT-IItrial was hydralazine75 mg qid and isosorbide dinitrate40 mg qid,although different dosing intervals and nitrate preparations can beused to improve compliance.
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Causes and precipitating factors in AHF
1. Decompensation of pre-existing chronic heartfailure (e.g.cardiomyopathy)
2. Acute coronary syndromes
a) Myocardial infarction/unstable angina with
large extent of ischaemia and ischaemic
dysfunction
b) Mechanical complication of acute myocardialinfarction
c) Right ventricular infarction
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3. Hypertensive crisis
4. Acute arrhythmia (ventricular tachycardia,ventricular fibrillation, atrial fibrillation or flutter,other supraventricular tachycardia)
5. Valvular regurgitation (endocarditis, rupture of
chordae tendinae, worsening of pre-existingvalvular regurgitation)
6. Severe aortic valve stenosis
7. Acute severe myocarditis
8. Cardiac tamponade
9. Aortic dissection
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10. Post partum cardiomyopathy
11. Non-cardiovascular precipitating factorsa. lack of compliance with medical treatment
b. Volume overload
c. Infections, particularly pneumonia or septicaemia
d. Severe brain insulte. After major surgery
f. Reduction in renal function
g. Asthma
h. Drug abusei. Alcohol abuse
j. phaeochromocytoma
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12. High output syndromes
a) Septicaemia
b) Thyrotoxicosis crisisc) Anaemia
d) Shunt syndromes
P i di l i j
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Dyregulation of contractiliy
Frank Starling mechanism?
Force-frequency-relationship?
Catecholamine refractoriness
Neuroendocrine activation
Sympathetic nervous system
RAAS
ADH,endothelin,etcHypertrophy
Low cardiac output
Remodeling
Ischaemia
FibrosisMyocyte Death
Apoptosis
Necrosis
Acidosis, radical load
Coronary perfusionPeripheral perfusion? Myocardial oxygen consumption?
Reduced renal blood flowTachycardiaHypotension
Filling pressure?
Wall tension?Cardiac output? Blood volume ?
Vascular resistance?
Precipitating condition
Anaemia, thyroid disease,etc.Critical LV-Deterioration
Previous myocardial injury
Remodeling
Chronic heart failure
Afterload-Chronotropy/Inotropy/Lusitropy mismatch
Hypertensive crisis
Arrhythmias,etc.
Acute critical myocardial injury
Acute myocardial infarction
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Suspected Acute Heart Failure Assess Symptoms & Signs
Heart Disease?
ECG/BNP/X-ray?
Evaluate cardiac
function byEchocardiography/otherimaging
HEART FAILURE, assess by
Echocardiography
Characterize type and severity
Consider other diagnosis
Selected tests
(angio, haemodynamically
monitoring, PAC)
Normal
Abnormal
Abnormal
Normal
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Assessment of Ventricular Function Left
Ventricular Ejection Fraction
Reduced LVEF
Systolic LV dysfunction
Preserved LVEF
Error in evaluation, other causesof heart failure, Diagnostic error
(no heart failure
Diastolic
DysfunctionTransientSystolic
Dysfunction
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Goals of treatment of the patient with AHF
Clinical
symptoms (dyspnoea and/or fatigue
clinical signsbody weight
diuresis
oxygenation
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Laboratory
Serum electrolyte normalizationBUN and/or creatinine
S-bilirubin
Plasma BNP
Blood glucose normalization
Haemodynamic
pulmonary capillary wedge pressure to
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Outcome
Length of stay in the intensive care unit
Duration of hospitalization
Time to hospital re-admission
Mortality
Tolerability
Low rate of withdrawal from therapeutic measures
Low incidence of adverse effects
Acute Heart Failure
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If moribund BLS, ALS
Analgesia or sedation
Immediate Resuscitation
Patient distressed or in painYES
NO
Increase FiO2, consider
CPAP, NIPPV
NO
YES
Arterial oxygen saturation >95%
Pacing, antiarrhythmics etc
YES
YES
YES
NONormal Heart Rate and rhythm
Vasodilators, consider diuresis
if volume overload
NO
Mean BP >70 mmHg
Fluid challengeNOAdequate preload
Consider inotropes or further
afterload manipulation
Reassess frequentlyYES
NOAdequate Cardiac Output:
reversal of metabolic acidosis,
SvO2>65%, clinical signs of
adequate organ perfusion
Invasive monitoring eg
PAC may be require
Definitive Treatment
Diagnosis algorithm
Definitive Diagnosis
Acute Heart Failure
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Acute heart failure with systolic dysfunction
Oxygen/CPAPFurosemide vasodilator
Clinical evaluation (leading to mechanistic theraphy)
SBP < 85 mmHg
Volume Loading? Inotrope
and/or dopamine > 5
g/kg/min and/ornorepinephrine
No response: reconsider
mechanistic therapy
Inotropic agents
SBP 85-100 mmHg
Good response Oral
therapy furosemide,
ACEI
Vasodilator and/or
inotropic (dobutamine,
PDEI or levosimendan)
Vasodilator (NTG,
nitroprusside, BNP)
SBP > 100 mmHg
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Immediate surgical correction
Pericardiocentesis
Fluids
Inotropes
Consider IABP
DIAGNOSIS
Free wall rupture
Echocardiography
Pericardial effusion (especially if>10 mm)
Echodensities in the effusion
Echo signs of tamponade
Echocardiography
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Immediate surgical correction
Coronary Angiography
Urgent surgical
correction
Coronary Angiography
Stable patient
Medical Therapy
Unstable patientConsider :
IABP
Mechanical ventilation
PAC
Echocardiography
DIAGNOSIS VSR
VSR
Site
Size
Qp:Qs
Diagnosis uncertain
PACOximetry
O2step up>5% RA-RV
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Echocardiography
akinetic apex
Hyperdinamic basal IVS, SAM
Discontinue
positive inotropes
nitrates
IABP
Consider
-blockers
-agonists
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Medical therapy
Consider
IABP
Mechanical ventilation
PCI or CABG
VAD
Heart transplant
Cardiogenic shock fromm loss
of ventricular muscle mass
Low EF
No signs of mechanical complication
Echocardiography