UAS PELAYANAN KEFARMASIAN

Dosen Pengampu : apt. Sumaryana, S.Si., M. Sc

Disusun oleh :

Nyai Melati Pratama (A) 19405021118

PROGRAM STUDI PROFESI APOTEKER

FAKULTAS FARMASI

UNIVERSITAS WAHID HASYIM SEMARANG

2020
 ANALISIS KASUS
Tn. Mukidi umur 70 tahun, BB/TB: 65 kg/170 cm, Riwayat Masuk RS : masuk RS pada
tanggal 20 Januari 2020 jam 04.00, pasien mengeluh sesak nafas sejak 1 minggu yang lalu,
memberat dengan aktivitas, sedikit berkurang dengan istirahat.

Diagnosis : CHF NYHA III, DM tipe 2, HT stage-2, IHD (Ischemic Heart disease)
Riwayat penyakit keluarga : -

Riwayat penyakit dahulu : Ca colon sejak Des 2018 sudah kemo 5 x, HT dan DM Riwayat
penyakit lain : Operasi laparotomi

Riwayat pengobatan : Amlodipin 1 x 10 mg, candesartan 1 x 16 mg, novorapid 8-8-8 unit

Riwayat alergi : alergi Penicilin, alergi gin gin

1. SOAP
a. Subjective : Tn. Mukidi umur 70 tahun, Riwayat Masuk RS : masuk RS pada
tanggal 20 Januari 2020 jam 04.00, pasien mengeluh sesak nafas sejak 1 minggu
yang lalu, memberat dengan aktivitas, sedikit berkurang dengan istirahat
 Riwayat penyakit keluarga :-
 Riwayat penyakit dahulu : Ca colon sejak Des 2018 sudah kemo 5 x, HT
dan DM
 Riwayat penyakit lain : Operasi laparotomi
 Riwayat pengobatan : Amlodipin 1 x 10 mg, candesartan 1 x 16 mg,
novorapid 8-8-8 unit
 Riwayat alergi : alergi Penicilin, alergi gin gin
b. Obyektif
BB : 65 kg
TB: 170 cm,
 Diagnosis : CHF NYHA III, DM tipe 2, HT stage-2, IHD (Ischemic Heart
disease)
Tanda Vital Tn. Mukidi selama di rumah sakit:
Monitoring Januari
20-01 21-01 22-01 23-01 24-01 25-01 26-01 27-01 28-01 29-01 30-01
TD (120/80 130/90 160/90 150/100 140/90 180/100 170/80 160/100 180/90 160/90 180/90 170/80
mmHg)
Suhu(°C) 36 37 36 36 37 37 37 37 37 36 36
Nadi 80-90 72 90 80 88 90 86 90 80 90 80 90
(x/menit)
RR 20 24 22 20 22 20 20 20 22 22 20 20
(x/menit)
Nyeri - 3-3-2 2-2-2 2-3-3 3-0-0 0 0 0 0 0 0
Urin (ml) - 1300 900 1600 1300 800 1200 1200 1200 1100 400

Riwayat pengobatan saat ini :

Tanggal
Nama obat
20 21 22 23 24 25 26 27 28 29
Adalat oros 30 mg/24 jam po √
Amlodipin 10 mg/24 jam P.o √ √ √ √ √ √ Stop
Ampicillin sulbactam 1,5 gr/8 jam iv √ √
Asam Folat 1 mg/24 jam P.o √ √ √ √ √ √
Atorvastatin 40 mg/24 jam P.o √ √ √ √ √ √
Azytromycin 500 mg/24 jam po √
Bicnat 500 mg/8 jam P.o √ √ √ √ √ √ √ √
Candesartan 16 mg/24 P.o √ √ √ √ √ √ √ √ √ √
Clopidogrel 75 mg/24 jam P.o √ √ √ √ √ √ √
Concor 2,5 mg/24 jam po √ √
Digoxin 0,25 mg/24 jam P.o √ √ √ √ √ √ Stop
Furosemid (Pg-Sore) 40 mg- 20 mg I.v √ Stop
Furosemid 1 amp/ekstra iv √
Furosemid 20 mg/12 jam IV √ √ Stop
Furosemid 40 mg/24 jam po √ √
Infus D 10% 20 tpm √
Infus D 40% 2 Flash √
Infuse RL 10 tpm √ √ √ √ √ √ √ √ √
ISDN 5 mg/8 jam P.o √ √ √ √ √ √ √ √ √ √
Lantus 14 unit Sc √ √ √ √ Stop
Metformin (malam) 500 mg/24 jam P.o √ √ √ √ √ √ √ √
N-asetilsistein 200 mg/8 jam P.o √ √ √ √ √ √ √ √ √ √
New diatab 600 mg/8 jam po √ √ √ √ √ Stop
Novorapid 8-8-8 unit Sc √ √ √ √ √ √ √ √ √
Paracetamol k/p 500 mg/8 jam po √ √ √ √
Spironolacton 100 mg/24 jam P.o √ √ √ Stop
Spironolacton 25 mg/24 jam P.o √
Hasil Laboratorium
Tanggal
Parameter Normal Pemeriksaan
20-Jan
13-16 g/dl 11
Hb
40-54 % 35
Hematokrit
4.4-5.9 10^6µL 3.5
Eritrosit
27-32 PG 31.4
MCH
76-96 Fl 89.9
MCV
29-36 g/dL 34.9
MCHC
3.8-10.6 10^3 6.3
Leukosit µL
150-400 10^3 272
Trombosit µL
4.6-14.8 % 5.2
RDW
4-11 Fl 9.2
MPV

Kimia Klinik
Tanggal Pemeriksaan
Parameter Normal
20 21 22 23 24 25 26 27 28 29
GDS 80-160 mg/dl 139 146 199 179 151 147 153 153 150 130
SGOT 15-34 U/L 34
SGPT 15-60 U/L 17
Albumin 3.4-5 g/dl 3.2 3.2 3.3 2.9 2.9 2.9 3.2 3.2 3.2 3.3
Ureum 15-39 mg/dl 43 31
Kreatinin 0.6-1.3 mg/dl 1.4 2.1
Mg 0.74-0.99 mmol/l 0.86
Ca 2.12 – 2.52 mmol/l 2
Elektrolit
Na 136-145 mmol/l 144
K 3.5-5.1 mmol/l 3.3
Cl 98-107 mmol/l 110
 Normal Tanggal Pemeriksaan
Parameter
20-01-20
GDP 80-109 mg/dL (baik), 110-125 99
mg/dL (sedang), >126 mg/dL
(buruk)

G2PP 80-140 mg/dL (baik), 145-179 178

mg/dL (sedang), >180 mg/dL
(buruk)

HbA1c 6.0-8.0 % 7.4

Kolesterol <200 mg/dL 300
TG <150 mg/dL 121
HDL 40-60 mg/dL 60
LDL 0-100 mg/dL 20
Asam urat 3.5-7.2 mg/dL 6.8

Hasil lab Urine

Parameter Normal Tanggal Pemeriksaan

20-Jan

Warna Kekuningan

Kejernihan Jernih

Bj 1.003-1.025 1.008

Protein NEG 00 ↑
(mg/dl)

Ph 4.8-7.4 5.5

Reduksi NEG NEG

(mg/dl)

Urobilinogen NEG Normal

(mg/dl)

Aseton NEG NEG

(mg/dl)

Nitrit NEG NEG

Lekosit esterase 25 /uL

Blood 50 /uL
 Sedimen

Epitel 0.0 – 40.0 3.6

/uL

Epitel tubulus 0.0-6.0 /uL 2.6

Eritrosit 0.0-25 /uL 54.3

Lekosit 0.0-20 /uL 5.6

Sekresi-ekskresi 0.0-0.5 /uL 1.6

Silinder-patologi NEG /LPK NEG

Granula halus NEG /LPK 0.1

Silinder hialin 0.00-1.20 0.84

/uL

Silinder epitel NEG /LPK NEG

Silinder eritrosit NEG /LPK NEG

Silinder leukosit NEG /LPK NEG

Mukus 0.0-0.5 /uL 0.14

Yeast cell 0-25 /uL 0.5

Bakteri 0-100 /uL 70.7

 Problem Medis Assesmen Plan
Ischemic Heart Adalat Oros (Nifedipine) METO
disease, Hipertensi  Indikasi :angina, 1. Monitoring tekanan
stage II hipertensi darah kurang dari
c. Assesment 130/80 mmHg (A)
 Dosis/ Pasien: 2. Monitoring heart
30mg/24 jam rate
 DRP:
Adanya interaksi MESO :
metformin dengan 1. Monitoring TD
nifedipine pada fase tidak kurang dari
farmakodinamik 90/60 mmHg
antagonis (monitor 2. Edema perifer
hipoglikemia)
PLAN:
Menyarankan untuk
menghentikan adalat
oros dan melanjutkan
terapi amlodipine
dengan penurunan
dosis menjadi 5 mg

Literatur :
DiPiro et al., 2017
Perki, 2015
Madsacepe,2020
2.PCNE ESC Guidlines,2012
(Chaplin, 2019)
A. Problem
Ischemic Heart Amlodipine METO
Medik
disease, Hipertensi  Indikasi :angina, 1. Monitoring tekanan
Masalah Terapi Obat : NO PROBLEM
stage II hipertensi darah kurang dari
Alasan Target (SMART)
130/80 mmHg
Terapi untuk CHF NYH IIIDosis
sudahPasien:
Tekanan Darah Turun
10 mg/24Detak
jam PO 2. Monitoring heart
sesuai jantung Normal
 DRP: rate
Kemungkinan Solusi 1. Interaksi amlodipin
Implementasi
dengan metformin MESO :
- -
pada fase
CHF NYH III Solusi yang dipilih farmakodinamik
Monitoring 1. Monitoring TD
Terapi Tetap Dilanjutkan -TD (monitor tidak < 90/60 mmHg
antagonis
hipoglikemia)
-HR
2. Efek samping
- Monitoring Efek2. samping
Edema perifer
obat
edema- kepatuhan Minum obat
3. Edema
- Periode sesak napas paru dan
dari dada (urine
batuk output)

PLAN:
Problem Medik Terapi amlodipin
Hipertensi Masalah Terapi Obat : M2.1 dilanjutkan dan
Alasan Target (SMART)menyarankan untuk
1. Adalat oros tidak tepat, menurunkan dosis
TD: 130/70-139/79
digunakan karena tidak amlodipine menjadi 5
masuk ke algoritma mg untuk menurunkan
hipertensi dan gagal jantung. risiko edema
P1.1 Pemilihan obat tidak
sesuai dengan guideline Literatur :
2. Adanya interaksi metformin DiPiro et al., 2017
MIMS, 2020
 dengan nifedipine pada fase
farmakodinamik antagonis
(monitor hipoglikemia)
Kemungkinan Solusi Implementasi
Terapi obat dihentikan I.3.5 Obat A3.1 Intervensi dilanjutkan,
dihentikan penerimaan tidak diketahui

Solusi yang dipilih Monitoring

I1.3 Diusulkan pada penulis resep Tekanan darah

Problem Medik
Masalah Terapi Obat : P6.3
Alasan Target (SMART)
Penggunaan insulin tidak GDP 80-109 mg/dL
diperlukan karena kadar HbA1C G2PP 80-140 mg/dL
7,4 HbA1C 6-8%
DM
Kemungkinan Solusi Implementasi
Hanya digunakan metformin A3.1 Intervensi dilanjutkan,
penerimaan tidak diketahui

Solusi yang dipilih Monitoring

I1.3 Diusulkan pada penulis resep Kadar gula darah
Problem Medik
Masalah Terapi Obat P1.3
Alasan Target (SMART)
Penggunaan ISDN tidak tepat
indikasi karena pasien tidak
mengalami nyeri dada

Kemungkinan Solusi Implementasi

IHD Disarankan untuk Penghentian I1.5 intervensi diajukan,
pemberian obat I3.5 penerimaan tidak diketahui

Solusi yang dipilih Monitoring

Hanya digunakan jika terjadi Elektrolit dalam serum
serangan nyeri dada

Problem Medik
Masalah Terapi Obat : No Problem
Alasan Target (SMART)
Terapi untuk anemia sudah sesuai HB 13-16 g/dL, Hematokrit 40-
54%, eritrosit 4,4-5,9 106µL

Anemia Kemungkinan Solusi Implementasi

Solusi yang dipilih Monitoring

HB, hematocrit, eritrosit

B. Problem
Medik
Terapi tanpa Masalah Terapi Obat : P1.3, P6.1
 Alasan Target (SMART)
1. Antibiotik – tidak tepat Nyeri berkurang (paracetamol)
indikasi (dilihat dari data lab)
2. Infus D10, D40 – pasien
tidak mengalami
hipoglikemia
3. New diatabs – pasien tidak
terindikasi diare
indikasi dan
4. Bicnat – tidak tepat indikasi
tidak tepat
5. Paracetamol – waktu
penggunaan
pemberian tidak tepat
Kemungkinan Solusi Implementasi
Paracetamol digunakan hanya Intervensi diterima (A1), terapi
ketika terjadi nyeri (tgl 21-24) dihentikan (I3.1)

Solusi yang dipilih Monitoring

I1.3 Diusulkan pada penulis resep I1.5 intervensi diajukan,
penerimaan tidak diketahui
 3. SBAR
Kasus pasien
Situation Tn. Mukidi umur 70 tahun, Riwayat Masuk RS : masuk RS pada tanggal
20 Januari 2020 jam 04.00, pasien mengeluh sesak nafas sejak 1 minggu
yang lalu, memberat dengan aktivitas, sedikit berkurang dengan istirahat.
Diagnosis : CHF NYHA III, DM tipe 2, HT stage-2, IHD (Ischemic Heart
disease)
Background Pasien mendapatkan resep
Adalat oros 30 mg/24 jam po
Amlodipin 10 mg/24 jam P.o
Ampicillin sulbactam 1,5 gr/8 jam iv
Asam Folat 1 mg/24 jam P.o
Atorvastatin 40 mg/24 jam P.o
Azytromycin 500 mg/24 jam po
Bicnat 500 mg/8 jam P.o
Candesartan 16 mg/24 P.o
Clopidogrel 75 mg/24 jam P.o
Concor 2,5 mg/24 jam po
Digoxin 0,25 mg/24 jam P.o
Furosemid (Pg-Sore) 40 mg- 20 mg I.v
Furosemid 1 amp/ekstra iv
Furosemid 20 mg/12 jam IV
Furosemid 40 mg/24 jam po
Infus D 10% 20 tpm
Infus D 40% 2 Flash
Infuse RL 10 tpm
ISDN 5 mg/8 jam P.o
Lantus 14 unit Sc
Metformin (malam) 500 mg/24 jam P.o
N-asetilsistein 200 mg/8 jam P.o
New diatab 600 mg/8 jam po
Novorapid 8-8-8 unit Sc
Paracetamol k/p 500 mg/8 jam po
Spironolacton 100 mg/24 jam P.o
Spironolacton 25 mg/24 jam P.o
Assesement  Pemberian Infus dextrose 40% dan dextrose 10% tidak digunakan
karena itu untuk pasien hipoglikemi, sedangkan pasien tidak
mengalami hipoglikemi
 Pengobatan hipertensi dan gagal jantung
1. ACEI atau ARB + diuretic + betabloker (kombinasi sudah
tepat)
2. ARB = Candesartan = dosis tidak sesuai
3. Diuretic = furosemide
4. Betabloker= concor (bisoprolol)
 Pengobatan dengan Digoxin
Tidak perlu diberikan karena digunakan untuk penguat jantung,
sedangkan pasien tidak mengalami lemah jantung
 Pengobatan Hipertensi dan DM
 Kombinasi spironolakton dan furosemide (sudah sesuai)
Tetapi dosis awal spironolakton diturunkan menjadi 25 mg/hari
p.o , bukan 100 mg. Jika untuk dosis pemeliharaan bisa dinaikkan
 menjadi 50 mg/hari
 Antiplatelet (clopidogrel) dapat digunakan untuk mencegah
pembekuan darah.
 Pada pasien hipertensi + DM, kadar darah akan meningkat
sehingga menyebabkan darah lebih kental dan mudah membeku.
Sehingga pembekuan darah akan berlangsung lama. Maka nya
diberikan antiplatelet
 Pada data kolesterolnya tinggi
 Terapi DM Tipe 2
Metformin, lantus, dan novorapid = dipilih salah satu (lihat dari
kerjanya)
 Terapi tanpa indikasi /dan tidak tepat cara penggunaan
a. Bicnat tidak diberikan karena tidak mengalami gagal ginjal
b. New diatab Tidak diberikan karena tidak diare
c. Paracetamol Waktu pemberian tidak sesuai (pemberian tidak
tepat)
d. Adalat oros Tidak tepat, tidak digunakan karena tidak masuk ke
algoritma hipertensi+komplikasi gagal jantung jantung
e. Antibiotic azitromisin dan ampisilin tidak ada indikasi infeksi
Recommendatio Di sarankan agar ISDN hanya digunakan jika terjadi serangan saja dan
n Direkomendasikan untuk memonitoring terapi dan efek samping obat
 DAFTAR PUSTAKA

BNF, 2020. Royal Pharmaceutical Society. Ed 79.

Chaplin, S. (2019). Chronic heart failure in adults: diagnosis and management. Prescriber,
30(1), 16–18. https://doi.org/10.1002/psb.1730
Makani, M., & Setyaningrum, N. (2017). Pola penggunaan furosemid dan perubahan
elektrolit pasien gagal jantung di Rumah Sakit X Yogyakarta. Jurnal Ilmiah Farmasi,
13(2), 57–68. https://doi.org/10.20885/jif.vol13.iss2.art3
MIMS,2020 Online, https://www.mims.com/indonesia/drug/info.
Medscape,2020 Online, https://reference.medscape.com/

DiPiro, J.T., Talbert, R.L., Yee, G.C., Matzke, G.R., Wells, B.G., and Posey, L.M.,
2017,Pharmacotherapy A Pathophysiologic Approach 10th Edition, Mc Graw Hill
Education, New York.

National Heart, Lung, and Blood Institute (NIH), 2019, Ischemic Heart Disease, Departemen
of Health and Human Service, Bethesda.

Perkeni, 2015, Konsensus Pengelolaan dan Pencegahan Diabetes Mellitys tipe 2 di

Indonesia, PB Perkeni, Jakarta.

Perki, 2015, Pedoman Tatalaksana Gagal Jantung, Perhimpunan Dokter Spesialis

Kardiovaskular Indonesia, Jakarta.

Perki, 2015, Pedoman Tatalaksana Hipertensi pada Penyakit Kardiovaskular, Perhimpunan

Dokter Spesialis Kardiovaskular Indonesia, Jakarta

Yancy, Clyde, W., Jessup, M., Bozkurt, B., and Butler, J., 2017, 2017 ACC/AHA/HFSA
Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart
Failure, Journal of the American College of Cardiology, 62, 1495-1539.
 Lampiran
Terapi HT stage 2 dengan IHD & CHF NYHA II-IV

Perki, 2015 halaman 36

Dipiro et al,2017 halaman 57

 Terapi CHF NYHA II-IV dengan DM

Perki,2015 halaman 36

Perki, 2015 halaman 37

Konsensus Penatalaksanaan Hipertensi 2019 halaman 50

Perki, 2015 halaman 25
ACC/AHA/HFSA FOCUSED UPDATE
CLINICAL STA
AND GUID
 LINES
MENTS
2017 ACC/AHA/HFSA Focused Update of the
2013 ACCF/AHA Guideline for the
Management of Heart Failure
A Report of the American College of Cardiology/American Heart
Association Task Force on Clinical Practice Guidelines and the Heart Failure
Society of America

WRITING GROUP MEMBERS* Developed in Collaboration with

the American Academy of Family
Clyde W. Yancy, MD, MSc, MACC, FAHA, FHFSA, Chair Physicians, American College of
Mariell Jessup, MD, FACC, FAHA, Vice Chair Chest Physicians, and International
Society for Heart and Lung Trans-
Biykem Bozkurt, MD, PhD, FACC, FAHA*† plantation
Javed Butler, MD, MBA, MPH, FACC, FAHA*‡
ACC/AHA Task Force Members,
Donald E. Casey Jr, MD, MPH, MBA, FACC§ see page e150
Monica M. Colvin, MD, FAHA║

Mark H. Drazner, MD, MSc, FACC, FAHA, FHFSA‡

Gerasimos S. Filippatos, MD*

Gregg C. Fonarow, MD, FACC, FAHA, FHFSA*‡
Michael M. Givertz, MD, FACC, FHFSA*¶
Steven M. Hollenberg, MD, FACC#

JoAnn Lindenfeld, MD, FACC, FAHA, FHFSA*¶

Frederick A. Masoudi, MD, MSPH, FACC**
Patrick E. McBride, MD, MPH, FACC††

Pamela N. Peterson, MD, FACC, FAHA‡

Lynne Warner Stevenson, MD, FACC*‡

Cheryl Westlake, PhD, RN, ACNS-BC, FAHA, FHFSA¶

2017;136:e137– e161. DOI:

10.1161/CIR.0000000000000509.

*Writing group members are required to recuse themselves from voting on sections to which their
specific relationships with industry may apply; see Appendix 1 for detailed information. †ACC/AHA
Task Force on Clinical Practice Guidelines Liaison. ‡ACC/AHA Representative. §ACP Representative.

‖ ISHLT Representative. ¶HFSA Representative. #CHEST Representative. **ACC/AHA Task Force on

Performance Measures Representative. ††AAFP Representative.

The American Heart Association requests that this document be cited as follows: Yancy CW, Jessup
M, Bozkurt B, Butler J, Casey DE Jr, Colvin MM, Drazner MH, Filippatos GS, Fonarow GC, Givertz
MM, Hollenberg SM, Lindenfeld J, Masoudi FA, McBride PE, Peterson PN, Stevenson LW, Westlake

C. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management
of heart failure: a report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation.
 ◼ natriuretic peptide biomarker
Key Words: AHA Scientific Statements ◼ angioedema ◼ sleep apnea
© 2017 by the American College
◼ angiotensin-converting enzyme inhibitors ◼ angiotensin receptor blockers ◼
of Cardiology Foundation, the
angiotensin receptor- neprilysin inhibitor ◼ beta blockers
American Heart Association, Inc.,
◼ ferric carboxymaltose ◼ focused update ◼ heart failure
◼ hypertension ◼ iron deficiency and the Heart Failure Society of
America
◼ ivabradine ◼ natriuretic peptides

Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e137

Downloaded from http://ahajournals.org by on July 18, 2020
Yancy et al

TABLE OF CONTENTS
Preamble..........................................................................e138
1. Introduction................................................................e139
1.1. Methodology and Evidence Review....................e140
1.2. Organization of the Writing Group.....................e141
1.3. Document Review and Approval........................e141
6. Initial and Serial Evaluation of the HF Patient.............e141
6.3. Biomarkers..........................................................e141
6.3.1. Biomarkers for Prevention:
Recommendation....................................e142
6.3.2. Biomarkers for Diagnosis:
Recommendation....................................e142
Since 1980, the American College of Cardiology (ACC) and
American Heart Association (AHA) have translat- ed scientific
evidence into clinical practice guidelines (guidelines) with
recommendations to improve cardio- vascular health. These
guidelines, which are based on systematic methods to evaluate
and classify evidence, provide a cornerstone for quality
cardiovascular care. The ACC and AHA sponsor the development
and pub- lication of guidelines without commercial support, and
members of each organization volunteer their time to the writing
and review efforts. Guidelines are official policy of the ACC and
AHA.

6.3.3. Biomarkers for Prognosis or Added

Risk Stratification: Recommendations........e142

7. Treatment of Stages A to D........................................e144

7.3. Stage C.............................................................e144

7.3.2. Pharmacological Treatment for Stage

C HF With Reduced Ejection Fraction:
Recommendations...................................e144

7.3.2.10. Renin-Angiotensin System

Inhibition With Angiotensin-
Converting Enzyme Inhibitor
or Angiotensin Receptor
Blocker
or ARNI: Recommendations . e144

7.3.2.11. Ivabradine: Recommendation.....e145

7.3.3. Pharmacological Treatment for Stage C
HFpEF: Recommendations.......................e146
9. Important Comorbidities in HF...................................e147

9.2. Anemia: Recommendations................................e147

9.5. Hypertension (New Section)...............................e149

9.5.1. Treating Hypertension to Reduce the
Incidence of HF: Recommendation..........e149
9.5.2. Treating Hypertension in Stage C
HFrEF: Recommendation.........................e149

9.5.3. Treating Hypertension in Stage C

HFpEF: Recommendation........................e149

9.6. Sleep-Disordered Breathing:

Recommendations..............................................e149

References.......................................................................e151

Appendix 1. Author Relationships With Industry

and Other Entities (Relevant).....................e156

Appendix 2. Reviewer Relationships With Industry

and Other Entities (Comprehensive)..........e158

Appendix 3. Abbreviations..............................................e161

PREAMBLE
 Intended Use
Practice guidelines provide
recommendations applica- ble to patients
with or at risk of developing cardiovas-
cular disease. The focus is on medical
practice in the United States, but guidelines
developed in collabora- tion with other
organizations may have a global impact.
Although guidelines may be used to inform
regulatory or payer decisions, their intent is
to improve patients’ quality of care and
align with patients’ interests. Guide- lines
are intended to define practices meeting
the needs of patients in most, but not all,
circumstances and should not replace
clinical judgment.
Clinical Implementation
Guideline recommended management is
effective only when followed by healthcare
providers and patients. Adherence to
recommendations can be enhanced by
shared decision making between
healthcare providers and patients, with
patient engagement in selecting
interventions based on individual values,
preferences, and associated conditions and
Downloaded from http://ahajournals.org by on July 18, 2020
comorbidities.
Methodology and Modernization
e138 August 8, 2017
The ACC/AHA Task Force on Clinical Practice Guidelines
(Task Force) continuously reviews, updates, and modi-
fies guideline methodology on the basis of published
standards from organizations including the Institute of
Medicine1,2 and on the basis of internal reevaluation.
Similarly, the presentation and delivery of guidelines are
reevaluated and modified on the basis of evolving tech-
nologies and other factors to facilitate optimal dissemi-
nation of information at the point of care to healthcare
professionals. Given time constraints of busy healthcare
providers and the need to limit text, the current
guideline format delineates that each recommendation
be support- ed by limited text (ideally, <250 words) and
hyperlinks to supportive evidence summary tables.
Ongoing efforts to further limit text are underway.
Recognizing the impor- tance of cost-value
considerations in certain guidelines, when appropriate
and feasible, an analysis of the value of a drug, device,
or intervention may be performed in accordance with
the ACC/AHA methodology.3
To ensure that guideline recommendations remain
current, new data are reviewed on an ongoing basis,
with full guideline revisions commissioned in approxi-
mately 6-year cycles. Publication of new, potentially
practice-changing study results that are relevant to an
existing or new drug, device, or management strategy
will prompt evaluation by the Task Force, in
consultation with the relevant guideline writing
committee, to de- termine whether a focused update
should be commis- sioned. For additional information
and policies regard- ing guideline development, we
encourage readers to
Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509
 2017 ACC/AHA/HFSA Heart Failure Focused Update

consult the ACC/AHA guideline methodology

CLINICAL STATEMENTS
Guideline-Directed Management
manual4 and other methodology articles. 5–8

Selection of Writing Committee
Members
The Task Force strives to avoid bias by selecting experts
from a broad array of backgrounds. Writing commit-
tee members represent different geographic regions,
sexes, ethnicities, races, intellectual perspectives/biases,
and scopes of clinical practice. The Task Force may also
invite organizations and professional societies with re-
lated interests and expertise to participate as partners,
collaborators, or endorsers.
AND GUIDELINES
and Therapy
The term guideline-directed management and therapy
(GDMT) encompasses clinical evaluation, diagnostic
testing, and pharmacological and procedural treat-
ments. For these and all recommended drug treat-
ment regimens, the reader should confirm the dosage
by reviewing product insert material and evaluate the
treatment regimen for contraindications and interac-
tions. The recommendations are limited to drugs, de-
vices, and treatments approved for clinical use in the
United States.

Class of Recommendation and Level

Relationships With Industry and Other
Entities
The ACC and AHA have rigorous policies and meth-
ods to ensure that guidelines are developed without
bias or improper influence. The complete relationships
with industry and other entities (RWI) policy can be
found online. Appendix 1 of the current document
lists writing committee members’ relevant RWI. For
the purposes of full transparency, writing committee
mem- bers’ comprehensive disclosure information is
available online. Comprehensive disclosure
information for the Task Force is also available online.
of Evidence
The Class of Recommendation (COR) indicates the
strength of the recommendation, encompassing the
estimated magnitude and certainty of benefit in pro-
portion to risk. The Level of Evidence (LOE) rates the
quality of scientific evidence that supports the inter-
vention on the basis of the type, quantity, and con-
sistency of data from clinical trials and other sources
(Table 1).4–6
Glenn N. Levine, MD, FACC, FAHA
Chair, ACC/AHA Task Force on Clinical
Practice Guidelines

Evidence Review and Evidence Review

Committees providers, and biostatisticians. When a formal systematic review
has been commissioned, the recom- mendations developed by
When developing recommendations, the writing com- the writing committee on the basis of the systematic review are
mittee uses evidence-based methodologies that are marked with“SR”.
based on all available data.4–7 Literature searches focus
on randomized controlled trials (RCTs) but also include
registries, nonrandomized comparative and
descriptive studies, case series, cohort studies,
systematic reviews, and expert opinion. Only key
references are cited.

An independent evidence review committee (ERC)

is commissioned when there are 1 or more questions
deemed of utmost clinical importance that merit
formal systematic review. This systematic review will
strive to de- termine which patients are most likely to
benefit from a drug, device, or treatment strategy and
to what degree. Criteria for commissioning an ERC and
formal systematic review include: a) the absence of a
current authoritative systematic review, b) the
feasibility of defining the ben- efit and risk in a time
frame consistent with the writing of a guideline, c) the
relevance to a substantial number of patients, and d)
the likelihood that the findings can be translated into
actionable recommendations. ERC members may
include methodologists, epidemiologists, healthcare
 1. INTRODUCTION
The purpose of this focused update is to
update the “2013 ACCF/AHA Guideline for
the Management of Heart Failure”9 (2013
HF guideline) in areas in which new
evidence has emerged since its publication.
For this update and future heart failure
(HF) guidelines, the Heart Failure Society of
America (HFSA) has partnered with the ACC
and AHA to provide coordinated guid- ance
on the management of HF.
The scope of the focused update
includes revision to the sections on
biomarkers; new therapies indicated for
Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509
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stage C HF with reduced ejection fraction (HFrEF);
updates on HF with preserved ejection fraction
(HFpEF); new data on important comorbidities,
including sleep apnea, anemia, and hypertension; and
new insights into the prevention of HF.
This focused update represents the second part of a 2-
stage publication; with the first part having been pub-
lished as the “2016 ACC/AHA/HFSA Focused Update
on New Pharmacological Therapy for Heart Failure,”10
which introduced guidance on new therapies, specifi-
cally for the use of an angiotensin receptor–neprilysin
inhibitor (ARNI) (valsartan/sacubitril) and a sinoatrial
node modulator (ivabradine). That focused update was
published concurrently with the European Society of
Cardiology’s complete guideline, “2016 ESC Guidelines
August 8, 2017 e139
Yancy et al

Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions,
Treatments, or Diagnostic Testing in Patient Care* (Updated August 2015)

for the Diagnosis and Treatment of Acute and Chronic
Heart Failure.”11
1.1. Methodology and Evidence Review
To identify key data that influence guideline
recommen- dations, the Task Force and members of
the 2013 HF guideline writing committee reviewed
clinical trials that were presented at the annual
scientific meetings of the
ACC, AHA, and European Society of Cardiology and
other scientific meetings and that were published in
peer-reviewed format from April 2013 through
Novem- ber 2016. The evidence is summarized in
tables in the Online Data Supplement. All
recommendations (new, modified, and unchanged) for
each clinical section are included to provide a
comprehensive assessment. The text explains new and
modified recommendations, whereas
recommendations from the previous guideline
 e140 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509
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that have been deleted or superseded no longer ap-
pear. Please consult the full-text version of the 2013
HF guideline9 for text and evidence tables supporting
the unchanged recommendations and for clinical areas
not addressed in this focused update. Individual
recom- mendations in this focused update will be
incorporated into the full-text guideline in the future.
Recommenda- tions from the prior guideline that
remain current have been included for completeness,
but the LOE reflects the COR/LOE system used when
the recommendations were initially developed. New
and modified recommen- dations in this focused
update reflect the latest COR/ LOE system, in which
LOE B and C are subcategorized for greater
specificity.4–6 The section numbers corre- spond to the
full-text guideline sections.
1.2. Organization of the Writing Group
For this focused update, representative members of
the 2013 HF guideline writing committee were invit-
ed to participate. They were joined by additional in-
vited members to form a new writing group, which
is referred to as the 2017 HF focused update writing
group. Members were required to disclose all RWI rel-
evant to the data under consideration. The group was
composed of experts representing general cardiolo-
gists, HF and transplantation specialists, electrophysi-
ologists, pharmacists, and general internists. The 2017
HF focused update writing group included representa-
tives from the ACC, AHA, and HFSA, as well as the
American Academy of Family Physicians, American
College of Chest Physicians, American College of Phy-
sicians, and International Society for Heart and Lung
Transplantation.
1.3. Document Review and Approval
The focused update was reviewed by 2 official
reviewers each nominated by the ACC, AHA, and HFSA;
1 reviewer each from the American Academy of Family
Physicians, American College of Chest Physicians, and
International Society for Heart and Lung
Transplantation; and 19 in- dividual content reviewers.
Reviewers’ RWI information is published in this
document (Appendix 2).
This document was approved for publication by the
governing bodies of the ACC, AHA, and HFSA.
6. INITIAL AND SERIAL
EVALUATION OF THE HF PATIENT
6.3. Biomarkers
Assays for BNP (B-type natriuretic peptide) and NT-
proBNP (N-terminal pro-B-type natriuretic peptide),
which are both natriuretic peptide biomarkers, have
been used increasingly to establish the presence and
2017 ACC/AHA/HFSA Heart Failure Focused Update
CLINICAL STATEMENTS
severity of HF. In general, both natriuretic peptide bio-
AND GUIDELINES
marker values track similarly, and either can be used
in patient care settings as long as their respective ab-
solute values and cutpoints are not used interchange-
ably. Notably, BNP, but not NT-proBNP, is a substrate
for neprilysin. Therefore, ARNI increases BNP levels 12
but not NT-proBNP levels.13 Note that the type of natri-
uretic peptide assay that has been performed must be
considered during interpretation of natriuretic peptide
biomarker levels in patients on ARNI. In 2 studies with
ARNI, NT-proBNP levels were reduced,12,14 with the
reduction in 1 study being associated with improved
clinical outcomes.12
A substantial evidence base exists that supports the
use of natriuretic peptide biomarkers to assist in the
di- agnosis or exclusion of HF as a cause of symptoms
(eg, dyspnea, weight gain) in the setting of chronic
ambula- tory HF15–21 or in the setting of acute care with
decom- pensated HF,22–30 especially when the cause of
dyspnea is unclear. The role of natriuretic peptide
biomarkers in population screening to detect incident
HF is emerg- ing.31–37 Elevated plasma levels of
natriuretic peptide biomarkers are associated with a
wide variety of cardiac and noncardiac causes (Table
2).38–42 Obesity may be as- sociated with lower
natriuretic peptide concentrations, and this may
modestly reduce diagnostic sensitivity in morbidly
obese patients.42
Table 2. Selected Potential Causes of Elevated
Natriuretic Peptide Levels38–41
Cardiac
HF, including RV syndromes
Acute coronary syndromes
Heart muscle disease, including LVH
Valvular heart disease
Pericardial disease
Atrial fibrillation
Myocarditis
Cardiac surgery
Cardioversion
Toxic-metabolic myocardial insults, including cancer chemotherapy
Noncardiac
Advancing age
Anemia
Renal failure
Pulmonary: obstructive sleep apnea, severe pneumonia
Pulmonary hypertension
Critical illness
Bacterial sepsis
Severe burns
Modified from Table 8 of the 2013 HF guideline. 9
HF, indicates heart failure; LVH, left
ventricular hypertrophy; and RV, right
ventricular.
 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e141
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 Yancy et al

Because of the absence of clear and consistent evi-
dence for improvement in mortality and
cardiovascular outcomes, 43–62 there are insufficient
data to inform spe- cific guideline recommendations
related to natriuretic peptide–guided therapy or serial
measurements of BNP or NT-proBNP levels for the
purpose of reducing hospi- talization or deaths in the
present document.
Like natriuretic peptides, cardiac troponin levels
may be elevated in the setting of chronic or acute
decom- pensated HF, suggesting myocyte injury or
necrosis.63 Troponins I and T respond similarly for acute
coronary syndromes and acute decompensated HF.
Elevations in either troponin I or T levels in the setting
of acute HF are of prognostic significance and must be
interpreted in the clinical context.64
In addition to natriuretic peptides and troponins,65–67
multiple other biomarkers, including those of inflam-
mation, oxidative stress, vascular dysfunction, and
myo- cardial and matrix remodeling, have been
implicated in HF.68–71 Biomarkers of myocardial fibrosis,
soluble ST2 receptor, and galectin-3 are predictive of
hospitaliza- tion and death and may provide
incremental prognos- tic value over natriuretic peptide
levels in patients with HF.72–74 Strategies that combine
multiple biomarkers may ultimately prove beneficial in
guiding HF therapy in the future, but multicenter
studies with larger deri- vation and validation cohorts
are needed.75,76 Several emerging biomarkers await
validation with well-defined outcome measures and
prognostic accuracy before they can reach the clinical
arena.77–84
This section categorizes the role of biomarkers into
prevention, diagnosis, prognosis, and added risk strati-
fication to clarify evidence-based objectives of their
use in clinical practice.

6.3.1 Biomarkers for Prevention: Recommendation

Biomarkers: Recommendation for Prevention of HF
COR LOE Recommendation Comment/Rationale
IIa B-R For patients at risk of developing HF, natriuretic peptide NEW: New data suggest that
biomarker– based screening followed by team-based care, natriuretic peptide biomarker
See Online Data including a cardiovascular specialist optimizing GDMT, can be screening and early intervention
Supplements A and useful to prevent the development of left ventricular may prevent HF.
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B. dysfunction (systolic or diastolic) or new-onset HF. 85,86

In a large-scale unblinded single-center study (STOP-HF [The St Vincent’s Screening to Prevent Heart Failure]), 85 patients at risk of HF
(identified by the presence of hypertension, diabetes mellitus, or known vascular disease [eg, stage A HF]), but without established left
ventricular systolic dysfunction or symptomatic HF at baseline, were randomly assigned to receive screening with BNP testing or usual
primary care. Intervention-group participants with BNP levels of ≥50 pg/mL underwent echocardiography and were referred to a
cardiovascular specialist who decided on further investigation and
management. All patients received further coaching by a specialist nurse who emphasized individual risk and the importance of adherence to
medication and healthy lifestyle behaviors. BNP-based screening reduced the composite endpoint of asymptomatic left ventricular dysfunction
(systolic or diastolic) with or without newly diagnosed HF.85 Similarly, in another small, single-center RCT, accelerated up-titration of renin-
angiotensin-aldosterone system antagonists and beta blockers reduced cardiac events in patients with diabetes mellitus and elevated NT-
proBNP levels but without cardiac disease at baseline. 86 Developing a standardized strategy to screen and intervene in patients at risk of HF
can be difficult because of different definitions of HF risk, heterogeneity of prevalence in different populations, variable duration until clinical HF
or left ventricular dysfunction develops, and variable interventions for risk factor modification or treatment. Further studies are needed to
determine cost-effectiveness and risk of such screening, as well as its impact on quality of life (QoL) and mortality rate.

6.3.2 Biomarkers for Diagnosis: Recommendation

Biomarkers: Recommendation for Diagnosis
CO LO Recommendation Comment/Rationale
R E
I A In patients presenting with dyspnea, measurement of MODIFIED: 2013 acute and chronic
natriuretic peptide biomarkers is useful to support a recommendations have been combined into
See Online Data a diagnosis section.
diagnosis or exclusion of HF.15–24,28–30
Supplements A and
B.
Natriuretic peptide biomarker testing in the setting of chronic ambulatory HF provides incremental diagnostic value to clinical judgment, especially
when the etiology of dyspnea is unclear. 15–21 In emergency settings, natriuretic peptide biomarker levels usually have higher sensitivity than
specificity and may be more useful for ruling out than ruling in HF. 20 Although lower values of natriuretic peptide biomarkers exclude the presence
of HF, and higher values have reasonably high positive predictive value to diagnose HF, clinicians should be aware that elevated plasma levels for
both natriuretic peptides have been associated with a wide variety of cardiac and noncardiac causes (Table 2). 38–41

6.3.3 Biomarkers for Prognosis or Added Risk Stratification: Recommendations

Biomarkers: Recommendations for Prognosis
COR LOE Recommendations Comment/Rationale
Measurement of BNP or NT-proBNP is useful for establishing 2013 recommendation remains current.
I A
prognosis or disease severity in chronic HF.16,87–92
e142 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509
 2017 ACC/AHA/HFSA Heart Failure Focused Update

CLINICAL STATEMENTS
AND GUIDELINES
Biomarkers: Recommendations for Prognosis (Continued)
COR LOE Recommendations Comment/Rationale
I A Measurement of baseline levels of natriuretic peptide MODIFIED: Current recommendation
biomarkers and/ or cardiac troponin on admission to the emphasizes that it is admission levels of
See Online Data hospital is useful to establish a prognosis in acutely natriuretic peptide biomarkers that are
Supplements A and decompensated HF.27,93–100 useful.
B.
Higher levels of natriuretic peptide biomarkers on admission are usually associated with greater risk for clinical outcomes, including all-cause and
cardiovascular mortality, morbidity, and composite outcomes, across different time intervals in patients with decompensated HF. 20,27,29,93–101 Similarly,
abnormal levels of circulating cardiac troponin are commonly found in patients with acute decompensated HF, often without obvious myocardial
ischemia or underlying coronary artery disease (CAD), and this is associated with worse clinical outcomes and higher risk of death.95,99,102,103
Studies have demonstrated incremental prognostic value of these biomarkers to standard approaches of cardiovascular disease risk
assessment.29,95 However, there were differences in the risk prediction models, assay cutpoints, and lengths of follow-up.29 Furthermore, not all
patients may need biomarker measurement for prognostication, especially if they already have advanced HF with established poor prognosis or
persistently elevated levels of biomarkers in former settings. Therefore, assays of natriuretic peptide biomarkers for incremental prognostication
should not preclude good clinical judgment; an individualized approach to each patient is paramount.

IIa B- During a HF hospitalization, a predischarge natriuretic peptide NEW: Current recommendation reflects
NR level can be useful to establish a postdischarge new observational studies.
See Online Data prognosis.93,96,104–113
Supplements A and
B.
Predischarge natriuretic peptide biomarker levels and the relative change in levels during hospital treatment are strong predictors of the risk of
death or hospital readmission for HF.93,96,104–113 Several studies have suggested that predischarge natriuretic peptide biomarker levels had higher
reclassification and discrimination value than clinical variables in predicting outcomes. 96,106,108–111 Patients with higher predischarge levels and
patients who do not have a decrease in natriuretic peptide biomarker levels during hospitalization have worse outcomes. 96,106,108–111 Although
observational or retrospective studies have suggested that patients with natriuretic peptide biomarker reduction had better outcomes than those
without any changes or with a biomarker rise, 93,107,112,113 targeting a certain threshold, value, or relative change in these biomarker levels during
hospitalization may not be practical or safe for every patient and has not been tested in a prospective large-scale trial. Clinical assessment and
adherence to GDMT should be the emphasis, and the prognostic value of a predischarge value or relative changes does not imply the necessity
for serial and repeated biomarker measurements during hospitalization.
IIb B- In patients with chronic HF, measurement of other clinically MODIFIED: 2013 recommendations have
NR available tests, such as biomarkers of myocardial injury or been combined into prognosis section,
See Online Data fibrosis, may be considered for additive risk resulting in LOE change from A to B-NR.
Supplements A and stratification.27,95,98,99,103,114–119
B.
Biomarkers of myocardial fibrosis (eg, soluble ST2 receptor, galectin-3, high-sensitivity cardiac troponin, and others) are predictive of
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hospitalization and death in patients with HF and also are additive to natriuretic peptide biomarker levels in their prognostic value. 117,119–126 A
combination of biomarkers may ultimately prove to be more informative than single biomarkers.127

Figure 1. Biomarkers Indications for Use.

Colors correspond to COR in Table 1. *Other biomarkers of injury or fibrosis include soluble ST2 receptor, galectin-3, and high-
sensitivity troponin. ACC indicates American College of Cardiology; AHA, American Heart Association; ADHF, acute decom-
pensated heart failure; BNP, B-type natriuretic peptide; COR, Class of Recommendation; ED, emergency department; HF, heart
failure; NT-proBNP, N-terminal pro-B-type natriuretic peptide; NYHA, New York Heart Association; and pts, patients.
Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e143
 Yancy et al

7. Treatment of Stages A to D
7.3. Stage C
7.3.2. Pharmacological Treatment for Stage C HF With Reduced Ejection Fraction: Recommendations
(See Figure 2 and Table 3).

7.3.2.10. Renin-Angiotensin System Inhibition With Angiotensin-Converting Enzyme Inhibitor or Angiotensin

Receptor Blocker or ARNI: Recommendations
Recommendations for Renin-Angiotensin System Inhibition With ACE Inhibitor or ARB or
ARNI
COR LOE Recommendations Comment/Rationale
ACE-I: A The clinical strategy of inhibition of the renin-angiotensin NEW: New clinical trial data
system with ACE inhibitors (Level of Evidence: A),128–133 OR prompted clarification and
ARB: A important updates.
ARBs (Level of Evidence: A), 134–137 OR ARNI (Level of Evidence:
I
B-R)138 in conjunction with evidence- based beta blockers, 9,139,140
ARNI: B- and aldosterone antagonists in selected patients, 141,142 is
R recommended for patients with chronic HFrEF to reduce
morbidity and mortality.
Angiotensin-converting enzyme (ACE) inhibitors reduce morbidity and mortality in heart failure with reduced ejection
fraction (HFrEF). Randomized controlled trials (RCTs) clearly establish the benefits of ACE inhibition in patients with
mild, moderate, or severe symptoms of HF and in patients with or without coronary artery disease. 128–133 ACE inhibitors
can produce angioedema and should be given with caution to patients with low systemic blood pressures, renal
insufficiency, or elevated serum potassium. ACE inhibitors also inhibit kininase and increase levels of bradykinin, which
can induce cough but also may contribute to their beneficial effect through vasodilation.
Angiotensin receptor blockers (ARBs) were developed with the rationale that angiotensin II production continues in the
presence of ACE inhibition, driven through alternative enzyme pathways. ARBs do not inhibit kininase and are
See Online Data
associated with a much
Supplements 1,
lower incidence of cough and angioedema than ACE inhibitors; but like ACE inhibitors, ARBs should be given with
2,
caution to patients with low systemic blood pressure, renal insufficiency, or elevated serum potassium. Long-term
18-20.
therapy with ARBs produces hemodynamic, neurohormonal, and clinical effects consistent with those expected after
interference with the renin-angiotensin system and have been shown in RCTs 134–137 to reduce morbidity and mortality,
especially in ACE inhibitor–intolerant patients.
In ARNI, an ARB is combined with an inhibitor of neprilysin, an enzyme that degrades natriuretic peptides, bradykinin,
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adrenomedullin, and other vasoactive peptides. In an RCT that compared the first approved ARNI, valsartan/sacubitril,
with enalapril in symptomatic patients with HFrEF tolerating an adequate dose of either ACE inhibitor or ARB, the
ARNI reduced the composite endpoint of cardiovascular death or HF hospitalization significantly, by 20%. 138 The benefit
was seen to a similar extent for both death and HF hospitalization and was consistent across subgroups. The use of
ARNI is associated with the risk of hypotension and renal insufficiency and may lead to angioedema, as well.
The use of ACE inhibitors is beneficial for patients with prior 2013 recommendation repeated for clarity
I ACE-I: A
or current symptoms of chronic HFrEF to reduce morbidity in this section.
and mortality.128–133,143
ACE inhibitors have been shown in large RCTs to reduce morbidity and mortality in patients with HFrEF with mild,
moderate, or severe symptoms of HF, with or without coronary artery disease. 128–133 Data suggest that there are no
differences among available ACE inhibitors in their effects on symptoms or survival. 143 ACE inhibitors should be started
at low doses and titrated upward to doses shown to reduce the risk of cardiovascular events in clinical trials. ACE
inhibitors can produce angioedema and should be given with caution to patients with low systemic blood pressures,
See Online renal insufficiency, or elevated serum potassium (>5.0 mEq/L). Angioedema occurs in <1% of patients who take an
Data ACE inhibitor, but it occurs more frequently in blacks and women. 144 Patients should not be given ACE inhibitors if they
Supplement are pregnant or plan to become pregnant. ACE inhibitors also inhibit kininase and increase levels of bradykinin, which
18. can induce cough in up to 20% of patients but also may contribute to beneficial vasodilation. If maximal doses are not
tolerated, intermediate doses should be tried; abrupt withdrawal of ACE inhibition can lead to clinical deterioration and
should be avoided.
Although the use of an ARNI in lieu of an ACE inhibitor for HFrEF has been found to be superior, for those patients
for whom ARNI is not appropriate, continued use of an ACE inhibitor for all classes of HFrEF remains strongly advised.
The use of ARBs to reduce morbidity and mortality is 2013 recommendation repeated for clarity
I ARB: A recommended in patients with prior or current symptoms of in this section.
chronic HFrEF who are
intolerant to ACE inhibitors because of cough or
angioedema.134–137,145,146
ARBs have been shown to reduce mortality and HF hospitalizations in patients with HFrEF in large RCTs.134–137
Long-term therapy with ARBs in patients with HFrEF produces hemodynamic, neurohormonal, and clinical effects
consistent with those expected after interference with the renin-angiotensin system. 145,146 Unlike ACE inhibitors, ARBs do
not inhibit kininase and are associated with a much lower incidence of cough and angioedema, although kininase
inhibition by ACE inhibitors may produce beneficial vasodilatory effects.
Patients intolerant to ACE inhibitors because of cough or angioedema should be started on ARBs; patients already
See Online Data
tolerating ARBs for other indications may be continued on ARBs if they subsequently develop HF. ARBs should be
Supplements 2 and
started at low doses and titrated upward, with an attempt to use doses shown to reduce the risk of
19.
cardiovascular events in clinical trials. ARBs should be given with caution to patients with low systemic blood
pressure, renal insufficiency, or elevated serum potassium (>5.0 mEq/L). Although ARBs are alternatives for
patients with ACE inhibitor–induced angioedema, caution is advised because some patients have also developed
angioedema with ARBs.
Head-to-head comparisons of an ARB versus ARNI for HF do not exist. For those patients for whom an ACE
inhibitor or ARNI is inappropriate, use of an ARB remains advised.
e144 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509
 2017 ACC/AHA/HFSA Heart Failure Focused Update

CLINICAL STATEMENTS
AND GUIDELINES
Recommendations for Renin-Angiotensin System Inhibition With ACE Inhibitor or ARB or
ARNI (Continued)
COR LOE Recommendations Comment/Rationale
In patients with chronic symptomatic HFrEF NYHA class II NEW: New clinical trial data necessitated
I ARNI: B- or III who tolerate an ACE inhibitor or ARB, replacement this recommendation.
R by an ARNI is recommended to further reduce morbidity
and mortality.138
Benefits of ACE inhibitors with regard to decreasing HF progression, hospitalizations, and mortality rate have been shown
consistently for patients across the clinical spectrum, from asymptomatic to severely symptomatic HF. Similar benefits have
been shown for ARBs in populations with mild-to-moderate HF who are unable to tolerate ACE inhibitors. In patients with
mild-to- moderate HF (characterized by either 1) mildly elevated natriuretic peptide levels, BNP [B-type natriuretic
peptide] >150 pg/mL or NT-proBNP [N-terminal pro-B-type natriuretic peptide] ≥600 pg/mL; or 2) BNP ≥100 pg/mL or NT-
proBNP ≥400 pg/mL with a prior hospitalization in the preceding 12 months) who were able to tolerate both a target
dose of enalapril (10 mg twice daily) and then subsequently an ARNI (valsartan/sacubitril; 200 mg twice daily, with the
ARB component equivalent to valsartan 160 mg), hospitalizations and mortality were significantly decreased with the
See Online Data
valsartan/sacubitril compound compared with enalapril. The target dose of the ACE inhibitor was consistent with that known
Supplements 1 and
to improve outcomes in previous landmark clinical trials.129 This ARNI has been approved for patients with
18.
symptomatic HFrEF and is intended to be substituted for ACE inhibitors or ARBs.
HF effects and potential off-target effects may be complex with inhibition of the neprilysin enzyme, which has multiple
biological targets. Use of an ARNI is associated with hypotension and a low-frequency incidence of angioedema. To
facilitate initiation
and titration, the approved ARNI is available in 3 doses that include a dose that was not tested in the HF trial; the
target dose used in the trial was 97/103 mg twice daily. 147 Clinical experience will provide further information about
the optimal titration and tolerability of ARNI, particularly with regard to blood pressure, adjustment of concomitant HF
medications, and the rare complication of angioedema. 14
ARNI should not be administered concomitantly with ACE NEW: Available evidence demonstrates a
III: B-R inhibitors or within 36 hours of the last dose of an ACE potential signal of harm for a concomitant
Harm inhibitor.148,149 use of ACE inhibitors and ARNI.

Oral neprilysin inhibitors, used in combination with ACE inhibitors can lead to angioedema and concomitant use is
contraindicated and should be avoided. A medication that represented both a neprilysin inhibitor and an ACE inhibitor,
See Online omapatrilat, was studied
Data in both hypertension and HF, but its development was terminated because of an unacceptable incidence of
Supplement 3. angioedema148,149 and associated significant morbidity. This adverse effect was thought to occur because both ACE and
neprilysin break down bradykinin, which directly or indirectly can cause angioedema. 149,150 An ARNI should not be
administered within 36 hours of switching from or to an ACE inhibitor.
ARNI should not be administered to patients with a NEW: New clinical trial data.
III: C-EO
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history of angioedema.
Harm
Omapatrilat, a neprilysin inhibitor (as well as an ACE inhibitor and aminopeptidase P inhibitor), was associated with
a higher frequency of angioedema than that seen with enalapril in an RCT of patients with HFrEF.148 In a very large
RCT of hypertensive patients, omapatrilat was associated with a 3-fold increased risk of angioedema as compared
with enalapril.149 Blacks and smokers were particularly at risk. The high incidence of angioedema ultimately led to
N/A cessation of the clinical development of
omapatrilat.151,152 In light of these observations, angioedema was an exclusion criterion in the first large trial assessing
ARNI therapy in patients with hypertension153 and then in the large trial that demonstrated clinical benefit of ARNI
therapy in HFrEF.138 ARNI therapy should not be administered in patients with a history of angioedema because of the
concern that it will increase the risk of a recurrence of angioedema.

7.3.2.11. Ivabradine: Recommendation

Recommendation for Ivabradine
COR LOE Recommendation Comment/Rationale
Ivabradine can be beneficial to reduce HF hospitalization for NEW: New clinical trial data.
patients with symptomatic (NYHA class II-III) stable chronic
IIa B-R HFrEF (LVEF ≤35%) who are receiving GDEM*, including a beta
blocker at maximum tolerated dose, and who are in sinus
rhythm with a heart rate of 70 bpm or greater at rest. 154–157

Ivabradine is a new therapeutic agent that selectively inhibits the If current in the sinoatrial node, providing heart rate
reduction. One RCT demonstrated the efficacy of ivabradine in reducing the composite endpoint of cardiovascular
death or HF
hospitalization.155 The benefit of ivabradine was driven by a reduction in HF hospitalization. The study included patients
with HFrEF (NYHA class II-IV, albeit with only a modest representation of NYHA class IV HF) and left ventricular
See Online ejection fraction (LVEF) ≤35%, in sinus rhythm with a resting heart rate of ≥70 beats per minute. Patients enrolled
Data included a small number with paroxysmal atrial fibrillation (<40% of the time) but otherwise in sinus rhythm and a small
Supplement 4. number experiencing ventricular pacing but with
a predominant sinus rhythm. Those with a myocardial infarction within the preceding 2 months were excluded.
Patients enrolled had been hospitalized for HF in the preceding 12 months and were on stable GDEM* for 4
weeks before initiation of ivabradine therapy. The target of ivabradine is heart rate slowing (the presumed benefit
of action), but only 25% of patients studied were on optimal doses of beta-blocker therapy.9,139,140,155 Given the well-
proven mortality benefits of beta-blocker therapy, it is important to initiate and up titrate these agents to target
doses, as tolerated, before assessing the resting heart rate for consideration of ivabradine initiation.155

*In other parts of the document, the term “GDMT” has been used to denote guideline-directed
management and therapy. In this recommendation, however, the term “GDEM” has been
used to denote this same concept in order to reflect the original wording of the
recommendation that initially appeared in the “2016 ACC/AHA/HFSA Focused Update on
New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline
for the Management of Heart Failure.” 10

Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e145

 Yancy et al
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Figure 2. Treatment of HFrEF Stage C and D.

Colors correspond to COR in Table 1. For all medical therapies, dosing should be optimized and serial assessment exercised.

*See text for important treatment directions. †Hydral-Nitrates green box: The combination of ISDN/HYD with ARNI has not
been robustly tested. BP response should be carefully monitored. ‡See 2013 HF guideline. 9 §Participation in investigational studies
is also appropriate for stage C, NYHA class II and III HF. ACEI indicates angiotensin-converting enzyme inhibitor; ARB, angiotensin
receptor-blocker; ARNI, angiotensin receptor-neprilysin inhibitor; BP, blood pressure; bpm, beats per minute; C/I, contraindication;
COR, Class of Recommendation; CrCl, creatinine clearance; CRT-D, cardiac resynchronization therapy–device; Dx, diagnosis;
GDMT, guideline-directed management and therapy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; ICD,
implantable cardioverter-defibrillator; ISDN/HYD, isosorbide dinitrate hydral-nitrates; K+, potassium; LBBB, left bundle-branch block;
LVAD, left ventricular assist device; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSR, normal sinus rhythm; and
NYHA, New York Heart Association.

7.3.3. Pharmacological Treatment for Stage C HFpEF: Recommendations

Recommendations for Stage C HFpEF
CO LOE Recommendations Comment/Rationale
R
Systolic and diastolic blood pressure should be controlled in 2013 recommendation remains current.
I B patients with HFpEF in accordance with published clinical
practice guidelines to prevent morbidity. 164,165

Diuretics should be used for relief of symptoms due to volume 2013 recommendation remains current.
I C
overload in patients with HFpEF.

Coronary revascularization is reasonable in patients with CAD 2013 recommendation remains current.
IIa C in whom symptoms (angina) or demonstrable myocardial
ischemia is judged to be having an adverse effect on
symptomatic HFpEF despite GDMT.
Management of AF according to published clinical practice 2013 recommendation remains current
IIa C
guidelines in patients with HFpEF is reasonable to improve (Section
symptomatic HF. 9.1 in the 2013 HF guideline).
The use of beta-blocking agents, ACE inhibitors, and ARBs 2013 recommendation remains current.
IIa C in patients with hypertension is reasonable to control
blood pressure in patients with HFpEF.
e146 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509
 2017 ACC/AHA/HFSA Heart Failure Focused Update

CLINICAL STATEMENTS
AND GUIDELINES
Recommendations for Stage C HFpEF (Continued)
CO LOE Recommendations Comment/Rationale
R
IIb B-R In appropriately selected patients with HFpEF (with EF ≥45%, NEW: Current recommendation reflects
elevated BNP levels or HF admission within 1 year, estimated new RCT data.
See Online glomerular filtration rate >30 mL/min, creatinine <2.5 mg/dL,
Data potassium <5.0 mEq/L), aldosterone receptor antagonists might
Supplement C. be considered to decrease hospitalizations.83,166,167

Mechanistic studies have suggested that mineralocorticoid receptor antagonists can improve measures of diastolic function in patients with HFpEF,
possibly by a similar effect on remodeling. 83,168
The TOPCAT (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist) trial 166 investigated the effects of
spironolactone on a combined endpoint of death, aborted cardiac death, and HF hospitalization in patients with HFpEF. A small reduction
(HR=0.89) in this composite endpoint did not reach statistical significance, although HF hospitalization was reduced (HR=0.83); known side
effects of hyperkalemia and rising creatinine were seen more commonly in the treatment group. 166 An unusual amount of regional variation was
seen in this trial, prompting a post-hoc analysis 167 that showed that rates of the primary endpoint were 4-fold lower in Russia/Georgia than in
North America and South America (the Americas). Rates in the Americas were comparable to those in other HFpEF trials.169,170 The post-hoc
analysis showed efficacy in the Americas (HR=0.83) but not in Russia/Georgia (HR=1.10). Moreover, a sample of the Russia/Georgia population,
despite having been in the active treatment arm, had nondetectable levels of the metabolite of spironolactone. These post- hoc analyses have
significant limitations, but they suggest that in appropriately selected patients with symptomatic HFpEF (with ejection fraction [EF] ≥45%, elevated
BNP level or HF admission within 1 year, estimated glomerular filtration rate >30 mL/min creatinine <2.5 mg/dL, and potassium <5.0 mEq/L),
particularly in those with elevated BNP levels, use of spironolactone might be considered with close monitoring of potassium and renal function.
Confirmatory studies are required.
With regard to the use of mineralocorticoid receptor antagonists, creatinine should be <2.5 mg/dL in men or <2.0 mg/dL in women (or estimated
glomerular filtration rate >30 mL/min) and potassium should be <5.0 mEq/L. Careful monitoring of potassium, renal function, and diuretic dosing
represents best practices at initiation and during follow-up thereafter to minimize risk of hyperkalemia and worsening renal function.
The use of ARBs might be considered to decrease 2013 recommendation remains current.
IIb B
hospitalizations for patients with HFpEF.169

III: No Routine use of nitrates or phosphodiesterase-5 inhibitors to NEW: Current recommendation reflects
B-R
Benefit increase activity or QoL in patients with HFpEF is new data from RCTs.
ineffective.171,172
See Online
Data
Supplement C.
Nitrate therapy can reduce pulmonary congestion and improve exercise tolerance in patients with HFrEF. However, the NEAT-HFpEF (Nitrate’s
Effect on Activity Tolerance in Heart Failure With Preserved Ejection Fraction) trial171 randomized 110 patients with EF ≥50% on stable HF therapy,
not including nitrates, and with activity limited by dyspnea, fatigue, or chest pain, to either isosorbide mononitrate or placebo and found no
Downloaded from http://ahajournals.org by on July 18, 2020

beneficial effects on activity levels, QoL, exercise tolerance, or NT-proBNP levels. On the basis of this trial, routine use of nitrates in patients with
HFpEF is not recommended. This recommendation does not apply to patients with HFpEF and symptomatic CAD for whom nitrates may provide
symptomatic relief. Phosphodiesterase-5 inhibition augments the nitric oxide system by upregulating cGMP activity. The RELAX
(Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Heart Failure with Preserved Ejection Fraction) trial172
randomized 216 patients with EF ≥50% on stable HF therapy and with reduced exercise tolerance (peak observed V o2 <60% of predicted) to
phosphodiesterase-5 inhibition with sildenafil or placebo. This study did not show improvement in oxygen consumption or exercise tolerance.
III: No Routine use of nutritional supplements is not recommended 2013 recommendation remains current.
C
Benefit for patients with HFpEF.

9. IMPORTANT COMORBIDITIES IN HF
9.2. Anemia: Recommendations

Recommendations for Anemia

CO LOE Recommendations Comment/Rationale
R
IIb B-R In patients with NYHA class II and III HF and iron deficiency NEW: New evidence consistent
(ferritin <100 ng/mL or 100 to 300 ng/mL if transferrin with therapeutic benefit.
See Online saturation is <20%), intravenous iron replacement might be
Data reasonable to improve functional status and QoL.173,174
Supplement D.
Routine baseline assessment of all patients with HF includes an evaluation for anemia in addition to other baseline laboratory measurements.
Anemia is independently associated with HF disease severity, and iron deficiency appears to be uniquely associated with reduced exercise
capacity. When iron deficiency is diagnosed and after full evaluation for cause, intravenous repletion of iron, especially in the setting of
concomitant hepcidin deficiency in HF, may improve exercise capacity and QoL. Studies examining correction of iron deficiency in HF have
demonstrated improvement in surrogate endpoints, such as QoL, NT- proBNP, and LVEF; however, controlled trials have been underpowered to
detect reductions in hard clinical endpoints. The FAIR-HF (Ferric Carboxymaltose Assessment in Patients With Iron Deficiency and Chronic
Heart Failure) trial173 demonstrated improvements in NYHA class and functional capacity over a short-
term exposure. The CONFIRM-HF (Ferric Carboxymaltose Evaluation on Performance in Patients With Iron Deficiency in Combination with Chronic
Heart Failure) trial174 included a larger cohort of patients (n=304) and demonstrated improvements in 6-minute walk test. A meta-analysis of 5
prospective controlled studies (631 patients) evaluated the effect of intravenous iron on deaths, hospitalizations, and other events in patients with
HF and iron deficiency.175 Patients receiving intravenous iron experienced limited but statistically significant improvements in functional capacity and
LVEF but no reduction in mortality rate. The FAIR-HF
2 trial is underway to further address the potential benefit of intravenous iron in HF associated with iron deficiency. Therefore, a strong
recommendation for intravenous iron repletion must await the results of an appropriately powered trial on morbidity and mortality. There is an
uncertain evidence base for oral iron repletion in the setting of anemia associated with HF.
Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e147
 Yancy et al

Recommendations for Anemia (Continued)

COR LOE Recommendations Comment/Rationale
III: No In patients with HF and anemia, erythropoietin-stimulating NEW: Current recommendation reflects new
B-R
Benefit agents should not be used to improve morbidity and evidence demonstrating absence of
mortality.176 therapeutic benefit.
See Online
Data
Supplement D.
Small studies evaluating the treatment of anemia in patients with HF have suggested a trend toward improvement in functional capacity and
reduction in hospitalization with the use of erythropoietin-stimulating agents, 177–182 but results have varied183 and have been limited because of
sample size. Although a meta-analysis of 11 RCTs (n=794) comparing erythropoietin-stimulating agents to control in patients with HF
demonstrated significant improvements in
6-minute walk, exercise duration, peak V o2, NYHA functional status, EF, BNP, HF-related hospitalizations, and QoL, 184 in the STAMINA-HeFT
(Study of Anemia in Heart Failure) trial, 183 darbepoetin alfa was not associated with significant clinical benefits. In the largest RCT to date
(n=2278), correction of anemia with darbopoetin alfa did not result in benefit and resulted in a significant increase in the risk of thromboembolic
events and a nonsignificant increase in fatal and
nonfatal strokes, supporting findings from other trials. 176,185–188 In summary, the strongest evidence on erythropoietin-stimulating agent therapy in HF
suggests lack of benefit and increased adverse events. Therefore, erythropoietin-stimulating agent therapy cannot be recommended in patients
with HF and anemia.

Table 3. Drugs Commonly Used for HFrEF (Stage C HF)

Mean Doses
Drug Initial Daily Maximum Achieved in Reference
Dose(s) Doses(s) Clinical Trials s
ACE inhibitors
Captopril 6.25 mg TID 50 mg TID 122.7 mg QD 158
Enalapril 2.5 mg BID 10–20 mg BID 16.6 mg QD 129
Fosinopril 5–10 mg QD 40 mg QD N/A —
Lisinopril 2.5–5 mg QD 20–40 mg QD 32.5–35.0 mg 130
QD
Perindopril 2 mg QD 8–16 mg QD N/A —
Downloaded from http://ahajournals.org by on July 18, 2020

Quinapril 5 mg BID 20 mg BID N/A —

Ramipril 1.25–2.5 mg QD 10 mg QD N/A —
Trandolapril 1 mg QD 4 mg QD N/A —
ARBs
Candesartan 4–8 mg QD 32 mg QD 24 mg QD 137
Losartan 25–50 mg QD 50–150 mg QD 129 mg QD 136
Valsartan 20–40 mg BID 160 mg BID 254 mg QD 134
ARNI
Sacubitril/valsartan 49/51 mg BID (sacubitril/valsartan) 97/103 mg BID 375 mg QD; target dose: 24/26 138
(therapy may be initiated at 24/26 mg (sacubitril/valsartan) mg, 49/51 mg OR 97/103 mg
BID) BID
If channel inhibitor
Ivabradine 5 mg BID 7.5 mg BID 6.4 mg BID (at 28 d) 6.5 155–157
mg BID (at 1 y)
Aldosterone antagonists
Spironolactone 12.5–25 mg QD 25 mg QD or BID 26 mg QD 142
Eplerenone 25 mg QD 50 mg QD 42.6 mg QD 159
Beta blockers
Bisoprolol 1.25 mg QD 10 mg QD 8.6 mg QD 160
Carvedilol 3.125 mg BID 50 mg BID 37 mg QD 161
Carvedilol CR 10 mg QD 80 mg QD N/A —
Metoprolol succinate 12.5–25 mg QD 200 mg QD 159 mg QD 139
extended release (metoprolol
CR/XL)
Isosorbide dinitrate and hydralazine
Fixed-dose combination 20 mg isosorbide dinitrate/37.5 40 mg isosorbide 90 mg isosorbide dinitrate/ 162
mg hydralazine TID dinitrate/75 mg ~175 mg hydralazine QD
hydralazine TID
Isosorbide dinitrate 20–30 mg isosorbide dinitrate/25–50 40 mg isosorbide dinitrate N/A 163
and hydralazine mg hydralazine TID or QD TID with 100 mg
hydralazine TID
 Modified (Table 15) from the 2013 HF guideline. 9

ACE indicates angiotensin-converting enzyme; ARB, angiotensin receptor blocker; ARNI,

angiotensin receptor-neprilysin inhibitor; BID, twice daily; CR, controlled release; CR/XL,
controlled release/extended release; HF, heart failure; HFrEF, heart failure with reduced ejection
fraction; N/A, not applicable; QD, once daily; and TID, 3 times daily.

e148 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509

 2017 ACC/AHA/HFSA Heart Failure Focused Update

CLINICAL STATEMENTS
9.5. Hypertension (New Section)

AND GUIDELINES
9.5.1. Treating Hypertension to Reduce the Incidence of HF: Recommendation
Recommendation for Prevention
CO LOE Recommendations Comment/Rationale
R
I B-R In patients at increased risk, stage A HF, the optimal blood NEW: Recommendation reflects new RCT
pressure in those with hypertension should be less than data.
See Online Data 130/80 mm Hg.189–193
Supplements E and
F.
A large RCT demonstrated that in those with increased cardiovascular risk (defined as age >75 years, established vascular disease, chronic
renal disease, or a Framingham Risk Score >15%), control of blood pressure to a goal systolic pressure of <120 mm Hg, as determined by
blood pressure assessment as per research protocol, was associated with a significant reduction in the incidence of HF191 and an overall
decrease in cardiovascular death. Blood pressure
measurements as generally taken in the office setting are typically 5 to 10 mm Hg higher than research measurements; thus, the goal of <130/80
mm Hg is an approximation of the target blood pressure in conventional practice. Targeting a significant reduction in systolic blood pressure in
those at increased risk for cardiovascular disease is a novel strategy to prevent HF.

9.5.2. Treating Hypertension in Stage C HFrEF: Recommendation

Recommendation for Hypertension in Stage C HFrEF
COR LOE Recommendation Comment/Rationale
I C-EO Patients with HFrEF and hypertension should be prescribed NEW: Recommendation has been
GDMT titrated to attain systolic blood pressure less than 130 adapted from recent clinical trial data but
See Online Data mm Hg.191 not specifically tested per se in a
Supplements E and F. randomized trial of patients with HF.

Clinical trials evaluating goal blood pressure reduction and optimal blood pressure–lowering agents in the setting of HFrEF and concomitant
hypertension have not been done. However, it is apparent that in those patients at higher risk, blood pressure lowering is associated with fewer
adverse cardiovascular events.
GDMT for HFrEF with agents known to lower blood pressure should consider a goal blood pressure reduction consistent with a threshold now
associated with improved clinical outcomes but not yet proven by RCTs in a population with HF.

9.5.3. Treating Hypertension in Stage C HFpEF: Recommendation

Recommendation for Hypertension in Stage C HFpEF
Downloaded from http://ahajournals.org by on July 18, 2020

COR LOE Recommendation Comment/Rationale

I C-LD Patients with HFpEF and persistent hypertension after NEW: New target goal blood pressure
management of volume overload should be prescribed GDMT based on updated interpretation of recent
See Online Data titrated to attain systolic blood pressure less than 130 mm clinical trial data.
Supplements E and F. Hg.9,167,169,170,195–199
The use of nitrates in the setting of HFpEF is associated with a signal of harm and, in most situations, should be avoided. For many common
antihypertensive agents, including alpha blockers, beta blockers, and calcium channel blockers, there are limited data to guide the choice of
antihypertensive therapy in
the setting of HFpEF.172 Nevertheless, RAAS inhibition with ACE inhibitor, ARB (especially mineralocorticoid receptor antagonists), and
possibly ARNI would represent the preferred choice. A shared decision-making discussion with the patient influenced by physician judgment
should drive the ultimate choice of antihypertensive agents.

9.6. Sleep-Disordered Breathing: Recommendations

(Moved from Section 7.3.1.4, Treatment of Sleep Disorders in the 2013 HF guideline.)

Recommendations for Treatment of Sleep Disorders

COR LOE Recommendations Comment/Rationale
IIa C-LD In patients with NYHA class II–IV HF and suspicion of sleep- NEW: Recommendation reflects
disordered breathing or excessive daytime sleepiness, a formal clinical necessity to distinguish
See Online sleep assessment is reasonable.200,201 obstructive versus central sleep
Data apnea.
Supplement
G.
Sleep disorders are common in patients with HF. A study of adults with chronic HF treated with evidence-based therapies found that 61% had
either central or obstructive sleep apnea. 202 It is clinically important to distinguish obstructive sleep apnea from central sleep apnea, given the
different responses to treatment. Adaptive servo-ventilation for central sleep apnea is associated with harm. 203 Continuous positive airway pressure
(CPAP) for obstructive sleep apnea improves sleep quality, reduces the apnea-hypopnea index, and improves nocturnal oxygenation. 200,201

IIb B-R In patients with cardiovascular disease and obstructive sleep NEW: New data demonstrate the limited
apnea, CPAP may be reasonable to improve sleep quality and scope of benefit expected from CPAP for
See Online obstructive sleep apnea.
daytime sleepiness.204
Data
Supplement
G.
In patients with sleep apnea, a trial evaluated the impact of CPAP with usual therapy versus usual therapy alone on subsequent cardiovascular
events, including HF.204 In this RCT of >2700 patients, there was no evidence of benefit on cardiovascular events at a mean follow-up of 3.7 years for
CPAP plus usual care compared with usual care alone. Improvements in sleep quality were noteworthy and represented the primary indication for
initiating CPAP treatment.204 However, in patients with atrial fibrillation (AF) (a frequent comorbidity noted with HF), the use of CPAP for obstructive
sleep apnea was helpful. In a trial of 10 132 patients with AF and obstructive sleep apnea, patients on CPAP treatment were less likely to
 progress to more permanent forms of AF than were patients without CPAP.205

Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e149

Yancy et al

Recommendations for Treatment of Sleep Disorders (Continued)

COR LOE Recommendations Comment/Rationale
III: B-R In patients with NYHA class II–IV HFrEF and central sleep apnea, NEW: New data demonstrate a signal of
Harm adaptive servo-ventilation causes harm. 203 harm when adaptive servo-ventilation is
See Online used for central sleep apnea.
Data
Supplement
G.
Mortality rate (all cause and cardiovascular) was higher with adaptive servo-ventilation plus GDMT than with GDMT alone in a single RCT to test
the addition of adaptive servo-ventilation (≥5 hours/night, 7 days/week) to GDMT in patients with HFrEF and central sleep apnea.203 A
similar risk has been seen in another trial, and a third trial of adaptive servo-ventilation in central sleep apnea and HF was aborted because of
ethical concerns. The weight of evidence does not support the use of adaptive servo-ventilation for central sleep apnea in HFrEF.

Gayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice Presi-

ACC/AHA TASK FORCE MEMBERS dent, Office of Science Operations
Glenn N. Levine, MD, FACC, FAHA, Chair; Patrick T. O’Gara, Jody Hundley, Production Manager, Scientific Publications,
MD, FACC, FAHA, Chair-Elect; Jonathan L. Halperin, MD, Office of Science Operations
FACC, FAHA, Immediate Past Chair*; Sana M. Al-Khatib, MD,
MHS, FACC, FAHA; Kim K. Birtcher, PharmD, MS, AACC; Bi-

ykem Bozkurt, MD, PhD, FACC, FAHA; Ralph G. Brindis, MD, Steven R. Houser, PhD, FAHA, President Nancy Brown,
MPH, MACC*; Joaquin E. Cigarroa, MD, FACC; Lesley H. Cur- Chief Executive Officer
tis, PhD, FAHA; Lee A. Fleisher, MD, FACC, FAHA; Federico
Gentile, MD, FACC; Samuel Gidding, MD, FAHA; Mark A. Rose Marie Robertson, MD, FAHA, Chief Science and Medicine Officer
Hlatky, MD, FACC; John Ikonomidis, MD, PhD, FAHA; José
*Former Task Force member; current member during the writing effort.
Joglar, MD, FACC, FAHA; Susan J. Pressler, PhD, RN, FAHA;
Duminda N. Wijeysundera, MD, PhD

PRESIDENTS AND STAFF

American College of Cardiology
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American Heart Association

 FOOTNOTES
This document was approved by the American
College of Cardiology Clinical Policy Approval
Committee, the American Heart Association
Science Advisory and Coordinating Com- mittee,
the American Heart Association Executive
Committee, and the Heart Failure Society of
America Executive Committee in April 2017.
The Comprehensive RWI Data Supplement
table is avail- able with this article at
http://circ.ahajournals.org/lookup/
suppl/doi:10.1161/CIR.0000000000000509/-/DC
1.
The Data Supplement is available with this
article at
http://circ.ahajournals.org/lookup/suppl/doi:10.11
61/ CIR.0000000000000509/-/DC2.
This article has been copublished in the
Journal of the American College of Cardiology
and the Journal of Cardiac Failure.
e150 August 8, 2017
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 Yancy et al

Appendix 1. Author Relationships With Industry and Other Entities (Relevant)—2017 ACC/AHA/HFSA
Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure (December 2015)

Institutional, Voting
Ownership Organizational, Recusa
Committe Speake / Person or Other Exper ls By
e Member Employment Consulta rs Partnershi al Financial t Section
nt Bureau p/ Researc Benefit Witnes *
Principal h s
Clyde W. Northwestern None None None None None None None
Yancy, Chair University Feinberg
School of Medicine,
Division of Cardiology
—Professor of
Medicine and Chief;
Diversity and Inclusion
— Vice Dean
Mariell Fondation Leducq— None None None None None None None
Jessup, Vice Chief Scientific Officer
Chair
Biyke Baylor College of None None None • Novartis None None 7.3.2.10,
m Medicine, Department of 7.3.2.11,
Bozkur Medicine— Professor of 7.3.3, and
t Medicine; Cardiology 9.5.
Section, DeBakey VA
Medical Center—Chief;
The Mary and Gordon
Cain Chair &
W.A. “Tex” and
Deborah Moncrief, Jr.—
Chair; Winters Center
for Heart Failure
Research—Director;
Cardiovascular
Research Institute—
Associate Director
Downloaded from http://ahajournals.org by on July 18, 2020

Javed Butler Stony Brook University • Bayer† • Novartis† None • Amgen None None 7.3.2.10,
— Division Chief of • Boehringe (DSMB)† 7.3.2.11,
Cardiology r 7.3.3, and
Ingelheim 9.5.

• CardioCell†
• Luitpold
• Medtronic
• Merck†
• Novartis†
• Relypsa†
• Takeda
• Trevena†
• Z Pharma
• Zensun
Donald Thomas Jefferson None None None None None None None
E. College of Population
Casey, Health— Faculty;
Jr Alvarez & Marsal
IPO4Health—Principal
and Founder
Monica University of Michigan— None None None None None None None
M. Colvin Associate Professor of
Medicine, Cardiology

Mark University of Texas None None None None None None None
H. Southwestern Medical
Drazne Center—Professor,
r Internal Medicine

Gerasimos National and None None None • Bayer† None None 7.3.2.10,
S. Kapodistrian University • Bayer (DSMB) 7.3.2.11,
Filippatos of Athens; Attikon 7.3.3, 9.2,
University Hospital, • Novartis† and 9.5.
Department • Servier
of Cardiology, Heart Pharmaceuticals
Failure Unit—Professor †
of Cardiology • Vifor
Gregg Ahmanson-UCLA • Amgen None None • Novartis† None None 7.3.2.10,
C. Cardiomyopathy Center • Janssen 7.3.2.11,
Fonaro — Director; UCLA Pharmaceutica 7.3.3, and
w Division of Cardiology
 —Co-Chief ls 9.5.
• Novartis†
(Continued )

e156 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509

 2017 ACC/AHA/HFSA Heart Failure Focused Update

Appendix 1. Continued

CLINICAL STATEMENTS
Institutional, Voting
Ownership Organizational, Recusa

AND GUIDELINES
Committe Speake / Person or Other Exper ls By
e Member Employment Consulta rs Partnershi al Financial t Section
nt Bureau p/ Researc Benefit Witnes *
Principal h s
Michael M. Brigham and • Merck None None None None None 7.3.2.10,
Givertz Women's Hospital— • Novartis 7.3.2.11,
Professor of 7.3.3, and
Medicine 9.5.

Steven M. Cooper University None None None None None None None
Hollenberg Hospital—Director,
Coronary Care Unit,
Professor of Medicine

JoAnn Vanderbilt Heart and • Abbott None None • AstraZeneca None None 6.3,
Lindenfeld Vascular Institute— • Janssen • Novartis† 7.3.2.10,
Director, Advanced Heart Pharmaceutica 7.3.2.11,
Failure and Transplant ls 7.3.3, 9.5,
Section—Professor of and 9.6.
Medicine • Novartis
• Relypsa†
• ResMed†
Frederick A. University of Colorado, None None None None None None None
Masoudi Anschutz Medical
Campus—Professor of
Medicine, Division of
Cardiology

Patrick E. University of Wisconsin None None None None None None None
McBride School of Medicine and
Public Health—
Professor of Medicine
and Family Medicine;
Associate Director,
Preventive Cardiology
Downloaded from http://ahajournals.org by on July 18, 2020

Pamela N. University of Colorado, None None None None None None None
Peterson Denver Health Medical
Center—Associate
Professor of Medicine,
Division of Cardiology

Lynne Brigham and Women’s None None None • Novartis— None None 7.3.2.10,
Warner Hospital PARENT trial 7.3.2.11,
Stevenson Cardiovascular (PI) 7.3.3, and
Division—Director, • NHLBI— 9.5.
Cardiomyopathy and INTERMA
Heart Failure Program CS (Co–
PI)
Cheryl Azusa Pacific None None None None None None None
Westlak University, School of
e Nursing, Doctoral
Programs— Professor

This table represents the relationships of committee members with industry and other entities
that were determined to be relevant to this document. These relationships were reviewed and
updated in conjunction with all meetings and/or conference calls of the writing committee
during the document development process. The table does not necessarily reflect relationships
with industry at the time of publication. A person is deemed to have a significant interest in a
business if the interest represents ownership of ≥5% of the voting stock or share of the
business entity, or ownership of ≥$5000 of the fair market value of the business entity, or if
funds received by the person from the business entity exceed 5% of the person’s gross income
for the previous year. Relationships that exist with no financial benefit are also included for the
purpose of transparency. Relationships in this table are modest unless otherwise noted.
According to the ACC/AHA, a person has a relevant relationship IF: a) The relationship or interest relates to the same or similar subject matter, intellectual
property or asset, topic, or issue addressed in the document; or b) the company/entity (with whom the relationship exists) makes a drug, drug class, or device
addressed in the document, or makes a competing drug or device addressed in the document; or c) the person or a member of the person’s household has a
reasonable potential for financial, professional, or other personal gain or loss as a result of the issues/content addressed in the document.

*Writing committee members are required to recuse themselves from voting on sections to
which their specific relationships with industry and other entities may apply.
†Significant relationship.
 ACC indicates American College of Cardiology; ACCF, American College of Cardiology
Foundation; AHA, American Heart Association; DCRI, Duke Clinical Research Institute;
DSMB, data safety monitoring board; HFSA, Heart Failure Society of America; NHLBI,
National Heart, Lung, and Blood Institute; INTERMACS, Interagency Registry for Mechanically
Assisted Circulatory Support; PARENT, Pulmonary artery pressure reduction with entresto;
UCLA, University of California, Los Angeles; and VA, Veterans Affairs.

Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e157

 Yancy et al

Appendix 2. Reviewer Relationships With Industry and Other Entities (Comprehensive)—2017 ACC/AHA/
HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure (October 2016)

Institutional,
Ownership Organizational
Speake / Person , or Other Exper
Reviewer Representatio Employment Consultant rs Partnershi al Financial t
n Bureau p/ Researc Benefit Witnes
Principal h s
Kim K. Official University of • Jones & None None None None None
Birtche Reviewer— Houston College of Bartlett
r ACC/AHA Pharmacy— Clinical Learning
Task Force on Professor
Clinical
Practice
Guidelines
Akshay Official Brigham and • Medscape None None None • Novartis* None
S. Desai Reviewer— Women’s Hospital— Cardiology • Thoratec
HFSA Director, Heart *
Failure Disease • Merck
Management,
Advanced Heart • Novartis*
Disease Section, • Relypsa*
Cardiovascular • St. Jude
Division; Medical*
Associate
Professor of
Medicine, Harvard
Medical School
Anita Official Michael E. DeBakey None None None • NIH* • AHA None
Deswal Reviewer— VA Medical Center— • AHA
AHA Chief of Cardiology; (GWTG
Director, Heart Failure Steering
Program; Baylor Committee)
College of Medicine— †
Professor of Medicine
• HFSA†
Downloaded from http://ahajournals.org by on July 18, 2020

Dipti Official Newport Coast None None None None • St. Jude Medical None
Itchhaporia Reviewer— Cardiology—Robert
ACC Board and Georgia Roth
of Trustees Endowed Chair for
Excellence in
Cardiac Care;
Director of Disease
Management
Ileana L. Official Montefiore Medical • Relypsa None None None None None
Piña Reviewer— Center—Associate
AHA Chief for Academic
Affairs, Cardiology;
Professor of
Medicine &
Epidemiology and
Population Health—
Albert Einstein
College of Medicine
Geetha Official University of Missouri- None None None None None None
Raghuveer Reviewer— Kansas City School of
ACC Board Medicine—Professor
of Governors of Pediatrics;
Children's Mercy
Hospital— Pediatric
Cardiology
James Official Tufts Medical Center • Lantheus None None • Gilead (DSMB) • Abbott None
E. Reviewer— —Chief, Division of Medical • GlaxoSmithKli Laboratorie
Udelso HFSA Cardiology Imaging ne (DSMB) s
n • AHA*
• NHLBI
• Otsuka • Circulation/
Circulation:
Heart Failure†
• HFSA
(Executive
Council)†
• Pfizer/
GlaxoSmithKlin
e
• Sunshine Heart
Mary Norine Official St Vincent Heart None None None None • Corvia Medical None
Walsh Reviewer— Center of Indiana— • Otsuka
 ACC Board Medical Director, • PCORI
of Trustees Heart Failure and • Thoratec
Cardiac
Transplantation
(Continued )

e158 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509

 2017 ACC/AHA/HFSA Heart Failure Focused Update

Appendix 2. Continued
Institutional,
Ownership Organizational
Speake / Person , or Other Exper
Reviewer Representatio Employment Consulta rs Partnershi al Financial t
n nt Bureau p/ Researc Benefit Witnes
Principal h s
David Organization Newark Beth Israel • Maquet • Novartis None • XDx* None None
A. al Reviewer Medical Center— • Otsuka* • NIH*
Baran — ISHLT Director of Heart
Failure and
Transplant Research
Kennet Organization Wm. S. None None None None • CHEST None
h al Reviewer Middleton
Casey — CHEST Memorial
Veterans Hospital
—Director, Sleep
Medicine
M. Fuad Jan Organization Aurora None None None None None None
al Reviewer Advanced
— CHEST Healthcare—
Cardiologist
Kenneth Organization Georgetown University None None None None None None
W. Lin al Reviewer School of Medicine—
— AAFP Clinician Educator
Track, Associate
Professor
Joaquin Content Oregon Health & None None None None • ACC/AHA† None
E. Reviewer— Science University— • AHA†
Cigarroa ACC/AHA Clinical Professor of
Task Force on Medicine • ASA†
Clinical • Catheterization
Practice and
Guidelines Cardiovascular
Intervention†
• NIH
• Portland Metro
Downloaded from http://ahajournals.org by on July 18, 2020

Area AHA
(President)†
• SCAI
Quality
Interventiona
l Council†
Lee A. Content University of • Blue None None • Johns • Associatio None
Fleishe Reviewer— Pennsylvania Health Cross/Blue Hopkins n of
r ACC/AHA System—Robert Shield* (DSMB) University
Task Force on Dunning Dripps • NQF† Anesthesiologist
Clinical Professor of s†
Practice Anesthesiology • Yale University
• NIH
Guidelines and Critical Care;
Chair, Department
of Anesthesiology
& Critical Care
Samuel Content Nemours/Alfred I. • FH Foundation† None None • FH None None
S. Reviewer— duPont Hospital for • International Foundation†
Gidding ACC/AHA Children—Chief, FH • NIH*
Task Force on Division of Pediatric Foundation†
Clinical Cardiology
Practice
Guidelines
James Content Massachusetts • Critical None None • Amgen None None
L. Reviewe General Hospital— Diagnostic (DSMB)
Januzzi r Hutter Family s* • Boeringe
Professor of • Novartis* r
Medicine in the Field Ingelhei
of Cardiology • Phillips
m
• Roche (DSMB)*
Diagnostic
• Janssen
s*
Pharmaceutica
• Sphingotec* ls (DSMB)
• Prevencio*
José Content UT Southwestern None None None None None None
A. Reviewer— Medical Center—
Joglar ACC/AHA Professor of
Task Force on Internal Medicine;
Clinical Clinical Cardiac
Practice Electrophysiology
Guidelines — Program
Director
 Edward Content Johns Hopkins None None None None None None
K. Reviewe Cardiology—E.
Kasper r Cowles Andrus
Professor in
Cardiology
(Continued )

Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509 August 8, 2017 e159

 Yancy et al

Appendix 2. Continued

Institutional,
Ownership Organizational
Speake / Person , or Other Exper
Reviewer Representatio Employment Consulta rs Partnershi al Financial t
n nt Bureau p/ Researc Benefit Witnes
Principal h s
Wayne C. Content University of • Abbott None None • NIH • Amgen* None
Levy Reviewe Washington— Laboratorie • Novartis* • AHA
r Professor of s
Medicine • St. Jude • HeartWare*
• Biotronik Medical* • Novartis*
• GE Healthcare
• Resmed*
• HeartWare
• Thoratec
• PharminIN
Judith Content SUNY Downstate None None None None • Associatio None
E. Reviewe Medical Center— n of Black
Mitchell r Director/Heart Cardiologists†
Failure Center;
SUNY
Downstate College
of Medicine—
Associate Professor
of Medicine
Sean Content Mount Sinai School of • Acorda None None • Thoratec† None None
P. Reviewer— Medicine—Associate Therapeutic • NIH†
Pinney ACC Heart Professor of s
Failure and Medicine, Cardiology • Thoratec
Transplant
Council • XDx
Randall Content Cleveland Clinic • BioControl None None • Medtronic • St. Jude Medical None
C. Reviewer— Department of • Medtronic • NIH*
Starling ACC Heart Cardiovascular
Failure and Medicine—Vice • Novartis • Novartis†
Transplant Chairman, Department • St. Jude
Council of Cardiovascular Medical
Downloaded from http://ahajournals.org by on July 18, 2020

Medicine; Section †
Head,Heart Failure &
Cardiac Transplant
W.H. Content Cleveland Clinic None None None • NIH* • Alnylam None
Wilson Reviewe Foundation—Assistant Pharmaceutica
Tang r Professor of Medicine ls
• NIH
• NHLBI
• Roche
• Novartis
• Thoratec
Emily J. Content Columbia University None None None • Bayer† None None
Tsai Reviewe College of • Bristol-
r Physicians & Myers
Surgeons— Squib†
Assistant Professor
of Medicine, Division • NHLBI*
of Cardiology
Duminda N. Content Li Ka Shing None None None • CIHR (DSMB)† None None
Wijeysunder Reviewer— Knowledge Institute of • CIHR*
a ACC/AHA St.
Task Force on Michael’s Hospital • Heart and
Clinical — Scientist; Stroke
Practice University of Foundation of
Guidelines Toronto—Assistant Canada*
Professor, • Ministry of
Department of Health &
Anesthesia and Long- term
Institute of Health Care of
Policy Management Ontario*
and Evaluation • PCORI
DSMB)†

This table represents the relationships of reviewers with industry and other entities that were
disclosed at the time of peer review, including those not deemed to be relevant to this document.
The table does not necessarily reflect relationships with industry at the time of publication. A person
is deemed to have a significant interest in a business if the interest represents ownership of
≥5% of the voting stock or share of the business entity, or ownership of ≥$5000 of the fair market
value of the business
entity, or if funds received by the person from the business entity exceed 5% of the person’s
gross income for the previous year. A relationship is considered to be modest if it is less than
significant under the preceding definition. Relationships that exist with no financial benefit are
also included for the purpose of transparency. Relationships in this table are modest unless
otherwise noted. Names are listed in alphabetical order within each category of review.
American College of Physicians did not provide a peer reviewer for this document.
*Significant relationship.
†No financial benefit.
AAFP indicates American Academy of Family Physicians; ACC, American College of
Cardiology; ACCF, American College of Cardiology Foundation; AHA, American Heart
Association; ASA, American Stroke Association; CHEST, American College of Chest Physicians;
CIHR, Canadian Institutes of Health Research; DSMB, data safety monitoring board; FH, familial
hypercholesterolemia; GWTG, Get With The Guidelines; HFSA, Heart Failure Society of
America; ISHLT, International Society for Heart and Lung Transplantation; NIH, National
Institutes of Health; NHLBI, National Heart, Lung, and Blood Institute; NQF, National Quality
Forum; PCORI, Patient-Centered Outcomes Research Institute; SCAI, Society for Cardiac
Angiography and Interventions; SUNY, State University of New York; UT, University of Texas;
and VA, Veterans Affairs.

e160 August 8, 2017 Circulation. 2017;136:e137–e161. DOI: 10.1161/CIR.0000000000000509

 2017 ACC/AHA/HFSA Heart
Failure Focused Update

Appendix 3. Abbreviations
ACE = angiotensin-converting enzyme
ARB = angiotensin-receptor blocker
ARNI = angiotensin receptor–neprilysin inhibitor
BNP = B-type natriuretic peptide
BP = blood pressure
COR = Class of Recommendation
CPAP = continuous positive airway pressure
EF = ejection fraction
GDMT = guideline-directed management and therapy
HFpEF = heart failure with preserved ejection fraction
HFrEF = heart failure with reduced ejection fraction
LOE = Level of Evidence
LVEF = left ventricular ejection fraction
NT-proBNP = N-terminal pro-B-type natriuretic peptide
QoL = quality of life
RCT = randomized controlled trial
Downloaded from http://ahajournals.org by on July 18, 2020
See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/331567800

Pola penggunaan furosemid dan perubahan elektrolit pasien gagal jantung di

Rumah Sakit X Yogyakarta

Article · December 2017

DOI: 10.20885/jif.vol13.iss2.art3

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 Jurnal Ilmiah Farmasi 13(2) Agustus-Desember Tahun 2017, Hal.57-68

ISSN: 1693-8666

available at http://journal.uii.ac.id/index.php/JIF

Patterns of furosemide use and electrolyte imbalance in heart failure

patients at
Hospital X Yogyakarta

Pola penggunaan furosemid dan perubahan elektrolit pasien gagal jantung di

Rumah Sakit X Yogyakarta

Mawaqit Makani, Ndaru Setyaningrum*

Program Studi Farmasi FMIPA Universitas Islam Indonesia

*Corresponding author. Email: ndaru.setyaningrum@uii.ac.id

Abstract
Background: Heart failure is the final stage of all heart diseases or heart defects affecting the pericardium,
heart valves, and myocardium. Furosemide is a drug commonly used in heart failure patients. The diuretic
effect of furosemide can cause depletion of fluids and electrolytes in the body.

Objective: This study aimed to determine the use of furosemide and evaluate the electrolyte levels in
patients with heart failure.

Method: This research used the descriptive observational cross-sectional design. Data were collected
retrospectively based on the medical records of patients with heart failure in X Hospital Yogyakarta for the
period 2011-2014, and patients should be eligible for the inclusion criteria.

Results: The results showed that intravenous furosemide 3x1 was used the most with 32 patients (45%).
The effects of furosemide on the levels of electrolytes showed 7 patients (17%) experienced mild
hyponatremia events and 10 patients (25%) had hypokalemia (4 patients with mild hypokalemia, 6 patients
with moderate hypokalemia). Intravenous furosemide of 20 mg/2ml was given to patients with edema, and
40 mg furosemide was orally administered to patients who have recovered from edema.

Conclusion: The response to furosemide therapy based on electrolyte levels was found 7 patients (17%)
mild hyponatremia; 4(10%) mild hypokalemia and 6(15%) moderate hypokalemia

Keywords: heart failure, furosemide, therapeutic response

Intisari
Latar belakang: Gagal jantung merupakan tahap akhir dari seluruh penyakit jantung atau kelainan jantung
yang berpengaruh terhadap perikardium, katup jantung, dan miokardium. Furosemid merupakan obat
umum yang digunakan pada pasien gagal jantung. Efek diuretik furosemide dapat menyebabkan deplesi
cairan dan elektrolit dalam tubuh.

Tujuan: Tujuan dari penelitian adalah untuk mengetahui pola penggunaan furosemid dengan melihat kadar
elektrolit pasien.

Metode: Penelitian ini merupakan penelitian deskriptif dengan rancangan cross sectional. Pengumpulan
data yang digunakan dalam penelitian ini adalah data sekunder yang diambil dari data rekam medik pasien
di RS PKU Muhammadiyah Yogyakarta Periode 2011-2014 yang memenuhi kriteria inklusi.
Hasil: Hasil penelitian ini menunjukkan bahwa furosemid intravena 3x1 (20mg/2ml) paling banyak
digunakan pada 32 pasien (45%). Respon terapi furosemid dilihat dari kadar elektrolit yaitu; 7 pasien (17%)
mengalami kejadian hiponatremia ringan, 10 pasien (25%) mengalami hipokalemia (4 pasien hipokalemia
ringan, 6 pasien hipokalemia sedang). Pemberian furosemid intravena 20 mg / 2ml diberikan pada pasien
yang mengalami edema. Sedangkan pemberian furosemid 40 mg oral diberikan pada pasien yang
mengalami perbaikan kondisi setelah edema.

Kesimpulan: Respon terapi furosemid berdasarkan tinjauan kadar elektrolit ditemukan 7 (17%) hiponatremia
ringan, 4 (10%) hipokalemia ringan dan 6(15%) hipokalemia sedang

Kata kunci: gagal jantung, furosemid, respon terapi

57
 58 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

1. Pendahuluan
Dekade terakhir ini pengobatan gagal jantung mengalami banyak perubahan. Pengobatan
tidak hanya meringankan gejala tetapi sudah mengarah pada mencegah timbulnya gejala gagal
jantung serta mencegah progresivitas gagal jantung. Dengan demikian akan menurunkan
angka kematian. Masalah gagal jantung tidak hanya menyangkut jantung itu sendiri tetapi
reaksi atau respon dari tubuh penderita akibat menurunnya fungsi jantung. Respon dari tubuh
antara lain menurunnya aliran darah tepi, tidak normalnya struktur dan fungsi otot rangka,
perubahan fungsi paru, retensi air dan natrium (Parker et al., 2008 & Price, S.A., Wilson, L.M.,
2005)
Data di seluruh rumah sakit di Yogyakarta menunjukkan penyakit-penyakit kardiovaskuler
seperti jantung, stroke, hipertensi atau dikenal sebagai penyakit CVD (Cardiovasculer Disease)
menempati urutan paling tinggi penyebab kematian. Berdasarkan data morbiditas rawat jalan
dan rawat inap serta kematian di rumah sakit se-DIY tahun 2007, diketahui bahwa persentase
kematian akibat penyakit gagal jantung di RS DIY sebesar 2,9 %, sedangkan data pada tahun
2008 menunjukkan jumlah kematian akibat penyakit jantung sebesar 3,07% (Dinas Kesehatan
Provinsi DIY, 2010). Furosemide digunakan pada pasien dengan CHF untuk meningkatkan
ekskresi Na urin dengan target membangun kembali dan memelihara keseimbangan Na dan
euvolemia (Weber, K., 2004).

2. Metode penelitian
Penelitian ini merupakan penelitian deskriptif observasional dan mengikuti rancangan
potong lintang. Pengumpulan data dilakukan pada pasien ICU dan ruang inap RS X Yogyakarta
menggunakan data rekam medik pasien gagal jantung yang menggunakan furosemid. Data
penelitian diambil untuk kasus pasien selama 2011-2014 yang memenuhi kriteria inklusi yaitu
pasien berusia diatas 30 tahun ,memiliki pemeriksaan elektrolit lengkap, dan menjalani rawat
inap minimal 5 hari. Sampel penelitian dieksklusikan apabila pasien hanya memjalani satu kali
pemeriksaan elektrolit dan memiliki riwayat penyakit ginjal. Analisis data dilakukan secara
deskriptif untuk menggambarkan karakteristik pasien yang menggunakan furosemide, pola
penggunaan furosemide, dan respon terapi setelah pemberian furosemide.

3. Hasil dan pembahasan

 59 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

3.1. Karakteristik pasien

Penelitian ini dilakukan pada pasien ICU dengan diagnosa gagal jantung yang
menggunakan furosemid di RS X Yogyakarta. Sejumlah 23(57%) merupakan pasien laki – laki
dan sisanya 17 (43%) pasien perempuan (Gambar 1).

Gambar 1. Distribusi pasien gagal jantung yang menjalani rawat inap di RS X

Yogyakarta periode 2011-2014 berdasarkan Jenis Kelamin

Secara teoritis ada perbedaan risiko antara laki-laki dan perempuan pada usia muda.
Laki-laki memiliki risiko lebih tinggi dibanding perempuan karena secara alami perempuan
memproduksi hormon estrogen sehingga berisiko rendah terkena penyakit jantung
dibandingkan laki-laki. Perbedaan ini akan hilang ketika perempuan tersebut mengalami
menopouse (Hunt et al., 2009).
3.1.2. Karakteristik pasien berdasarkan usia
Klasifikasi umur dalam penelitian ini dibagi menjadi dua golongan yaitu dewasa dan lanjut
usia. Golongan umur dewasa dibagi menjadi dua kelas, hal ini berkaitan dengan umur diatas 40
tahun sebagai faktor risiko munculnya penyakit gagal jantung pada usia dewasa. Data distribusi
pasien gagal jantung berdasarkan umur ditunjukkan dalam Tabel 1.

Tabel 1. Distribusi pasien gagal jantung yang menjalani Rawat Inap di RS X Yogyakarta
periode 2011-2014 berdasarkan Umur

Pasien Umur (tahun) Jumlah Persentase (%)

(pasien)
Dewas 31-40 2 5,00
a
41-50 4 10,00
51-60 6 15,00
Lanjut usia ≥ 61 28 70,00
Total 40 100,00

Pada Tabel 1., pasien gagal jantung dewasa lebih sedikit dibandingkan dengan pasien
gagal jantung lanjut usia. Prevalensi gagal jantung meningkat seiring peningkatan usia.
Kejadian gagal jantung 12 kali lebih tinggi pada usia lebih dari 75 tahun dibanding rentang usia
45 – 54 tahun.
 60 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

Penelitian di Rotterdam menunjukkan hal yang mirip bahwa prevalensi gagal jantung rentang usia 55 –
64 tahun adalah 1% sedangkan prevalensi gagal jantung pada usia lebih dari 85 tahun sebesar 10% (Bui
et al., 2011). Jumlah pasien gagal jantung pada tabel I menunjukkan peningkatan dua kali lipat
dibandingkan umur 31-40 tahun. Data yang terdapat di ACC/AHA Practice Guidelines 2005
menyebutkan bahwa umur diatas 40 tahun merupakan faktor risiko yang dapat memicu
munculnya penyakit gagal jantung. Pada usia diatas 40 tahun mulai terjadi penurunan fungsi
fisiologi tubuh, kemungkinan ini akan lebih sering muncul pada individu yang menjalani pola
hidup yang tidak sehat seperti jarang berolahraga, makan makanan yang mengandung banyak
kolesterol, dan alcohol (Hunt et al., 2009).

3.1.3. Distribusi pasien berdasarkan penyakit penyerta

Data hasil penelitian menunjukkan bahwa sebagian besar pasien gagal jantung yang
menjalani rawat inap di RS X Yogyakarta periode 2011-2014 selain terdiagnosis gagal jantung,
juga terdiagnosis penyakit penyerta. Dalam penelitian ini, dilakukan penelusuran data pasien
dengan penyakit penyerta berdasarkan ACC/AHA Practice Guidelines 2005, jenis penyakit
penyerta pada pasien gagal jantung dibagi menjadi 2 yaitu kardiovaskular dan non-
kardiovaskular. Penyakit penyerta kardiovaskular meliputi hipertensi, dyslipidemia, diabetes
mellitus, fibrilasis atrial (AF), penyakit jantung koroner (IHD), infark miokard, angina pektoris.
Adapun penyakit penyerta non- kardiovaskular meliputi gagal ginjal, penyakit pernafasan
(PPOK, asma), kanker, anemia, gangguan tiroid, hepatitis dan HIV.

Tabel 2. Distribusi pasien gagal jantung yang menjalani rawat inap di RS X Yogyakarta
periode 2011-2014 dengan dan tanpa penyakit penyerta

Diagnosis Jumlah Persentase (%)

(pasien)
Gagal jantung tanpa penyakit penyerta 1 2,00
Gagal jantung dengan penyakit penyerta 5 13,00
non
kardiovaskular
Gagal jantung dengan penyakit penyerta 14 36,00
kardiovaskular dan non- kardiovaskular
Gagal jantung dengan penyakit penyerta 19 49,00
kardiovaskular
Total 40 100,00

Berdasarkan Tabel 2, pasien gagal jantung yang memiliki penyakit penyerta

kardiovaskular yaitu 19 pasien (49%). Penyakit penyerta kardiovaskuler menjadi penyakit
penyerta yang dominan dialami pasien di RS X Yogyakarta. Hasil analisis data menunjukkan
bahwa hipertensi merupakan penyakit kardiovaskular penyerta gagal jantung yang paling
banyak diderita pasien gagal jantung
 61 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

yaitu sebanyak 26 pasien (38%), sedangkan infark miokard adalah penyakit penyerta yang jarang
diderita oleh pasien gagal jantung yang menjalani rawat inap di RS X Yogyakarta periode 2011-2014.
Peningkatan tekanan darah yang terjadi dalam jangka waktu panjang akan menyebabkan terjadinya
hipertrofi ventrikel (penebalan dinding ventrikel) yang dapat menurunkan kelenturan otot jantung.
Selain itu, aldosteron juga dapat menyebabkan retensi natrium dan air yang
menyebabkan terjadinya penumpukan cairan atau edema (Lacy et al., 2009-2010).
Penyakit penyerta diabetes cukup tinggi pada pasien gagal jantung di RS X Yogyakarta.
Pada pasien diabetes akan terjadi penurunan nitrit oksida yang merupakan senyawa vasodilator
akibat defisiensi insulin atau kerusakan reseptor insulin pada sel endotel. Kejadian
hiperglikemia juga dapat menghambat produksi nitrit oksida, yang dapat menyebabkan
vasokonstriksi yang selanjutnya akan meningkatkan tekanan darah dan beban kerja jantung.
Pasien diabetes dapat mengalami komplikasi mikrovaskular maupun makrovaskular yang
berhubungan dengan kejadian kardiomiopati atau tidak berfungsinya otot jantung (Hunt et al.,
2009 & Lacy et al., 2009-2010),
Hipertensi dan diabetes mellitus dapat berperan dalam perkembangan disfungsi sistolik
atau diastolik baik secara langsung atau berperan (bersama dislipidemia) pada perkembangan
ischemic heart disease (IHD) sehingga hipertensi, diabetes mellitus dan dislipidemia terutama
hiperlipidemia menjadi penyakit penyerta utama pada gagal jantung (Lacy et al., 2009-2010).
Pada pasien gagal jantung yang mengalami IHD dapat terjadi angina pektoris atau infark
miokard, sehingga kedua penyakit tersebut merupakan penyakit penyerta pada gagal jantung
yang jarang terjadi.
3.2. Gambaran dosis dan kombinasi penggunaan furosemid
3.2.1.Gambaran dosis furosemid pada masing – masing cara pemberian
a. Penggunaan furosemid oral
Furosemid merupakan obat yang memiliki kemampuan untuk meningkatkan ekskresi
natrium dalam urin dan mengurangi tanda-tanda fisik dari retensi cairan padapasien dengan
gagal jantung. Pada tabel 4. dan 5. akan terlihat pola penggunaan dosis furosemid secara
intravena maupun oral
Dilihat dari tabel 4 penggunaan furosemid oral pada pasien gagal jantung yang paling
sering diberikan adalah 40 mg per hari dengan pemberian selama 5 hari. Berdasarkan data
yang diperoleh penggunaan furosemid oral maksimal yang digunakan pada pasien gagal
jantung adalah 3 x 40 mg. Hal ini berarti bahwa penggunaan maksimal furosemid pada pasien
dalam penelitian ini adalah120 mg per hari. American Heart Association dan Drug Information
Handbook menjelaskan bahwa pemberian awal furosemid oral yaitu 20 sampai 80 mg per dosis.
Sedangkan untuk pemeliharaan dapat dilakukan peningkatan dosis secara bertahap dari 20
sampai 40 mg setiap 6 sampai 8 jam
 62 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

untuk efek yang diinginkan dengan interval sekali atau dua kali sehari, dengan dosis harian
maksimum 600 mg pada kondisi edema (Hunt et al., 2009 & Pramudianto, A., & Evaria, 2009)

Tabel 3. Pola penggunaan sediaan furosemid oral di RS X Yogyakarta periode 2011-2014

∑ Hari/ ∑ Jumlah Persentase

Frekuensi Pasien (%)
(pasien)
1 2 3 4 5 6 7 8 9 10
Satu kali - - - - - - - - - 1 1 5
20 mg
Dua - - - - - - 1 - - - 1 5
kali
40mg
Tiga kali 2 - 3 - - - - - - - 5 25
40 mg
Satu kali 3 2 3 - 3 1 - - - - 12 65
40 mg

b. Penggunaan furosemid intravena

Penggunaan furosemid intravena ini diberikan pada pasien yang mengalami kelebihan
cairan atau memiliki risiko lainnya yang dapat memperparah kondisi jantung. Pola penggunan
sediaan furosemid intravena di RS PKU Muhammadiyah Yogyakarta dapat dilihat pada tabel V.
Pada tabel V, penggunaan furosemid intravena yang dominan digunakan adalah 3 x 20 mg/ 2
ml yaitu sebanyak 32 pasien (45%). Sedangkan pasien yang memiliki frekuensi 2 x 20 mg/ 2 ml
ada 19 pasien (27%), 1
x 40 mg/ 4 ml dan 1 x 20 mg/ 2 ml masing-masing ada 2 pasien (3%), dan 3 x 40 mg/ 4 ml ada 16
pasien (22%).

Tabel 4. Pola penggunaan sediaan furosemid intravena di RS X Yogyakarta periode 2011-2014

∑ Hari/ ∑ Jumlah Persentase

Frekuensi Pasien (%)
(pasien)
1 2 3 4 5 6 7 8 9 10
Satu kali 20 mg - - 1 - - 1 - - - - 2 3
Satu kali 40 mg 2 - - - - - - - - - 2 3
Tiga kali 40 mg 3 5 6 1 - - 1 - - - 16 22
Dua kali 20 mg 5 6 2 1 1 1 1 1 1 - 19 27
Tiga kali 20 mg 1 2 4 4 8 6 2 1 3 1 32 45

3.3. Kombinasi obat pada penggunaan furosemid

Penyakit gagal jantung merupakan penyakit yang tidak hanya terkait jantung itu sendiri
tetapi reaksi atau respon dari tubuh penderita akibat menurunnya fungsi jantung. Sehingga
pada penderita gagal jantung akan diberikan beberapa obat penyerta yang akan meningkatkan
kualitas hidup pasien.
 63 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

Obat-obat lain yang digunakan oleh pasien gagal jantung di RS X Yogyakarta ditunjukkan oleh
tabel 6.
Penyakit gagal jantung merupakan penyakit yang tidak hanya terkait jantung itu sendiri
tetapi reaksi atau respon dari tubuh penderita akibat menurunnya fungsi jantung. Sehingga
pada penderita gagal jantung akan diberikan beberapa obat penyerta yang akan meningkatkan
kualitas hidup pasien. Obat-obat lain yang digunakan oleh pasien gagal jantung di RS X
Yogyakarta ditunjukkan oleh Tabel 5.

Tabel 5. Obat lain yang berpengaruh terhadap perkembangan klinis pasien

Klasifikasi Nama obat Jumlah Persentas

obat (pasien) e
%
Hidroklorotiazid 3 2
Diuretik Spironolakton 15 11
Preparat Renapar 1 1
kalium Aspar K 15 11
Karvedilol 8 6
Kaptopril 11 8
Obat lain
Klopidogrel 15 12
Digoxin 19 15
Asering 4 3
Cairan NaCl 17 14
RL 22 17

Berdasarkan Tabel 5, spironolakton dan aspar-k memiliki persentase tertinggi sebagai

obat yang sering digunakan yaitu sebesar 11 % untuk masing-masing obat-obat tersebut. Hal
ini karena diuretik menyebabkan ekskresi kalium bertambah, sehingga pada dosis besar atau
pemberian jangka lama diperlukan tambahan kalium (berupa KCl). Penggunaan furosemid
dosis rendah mungkin tidak diperlukan kombinasi dengan suplemen kalium hanya
menganjurkan tambahan makanan yang mengandung banyak kalium daripada memberikan
preparat kalium. Namun hal ini akan berbeda jika penggunaan furosemid dosis tinggi atau
penggunaan jangka panjang.
Pada penelitian ini infus yang dominan digunakan adalah infus NaCl, ringer laktat, dan
asering. Setiap infus memiliki komponen elektrolit yang berbeda, sehingga setiap pemberian
memiliki indikasi yang berbeda pula. Selain dapat mengimbangi dari penggunaan furosemid
sebagai asupan cairan yang dapat membantu keseimbangan elektroit, cairan infus ini dapat
memberikan efek yang tidak menguntungkan pada pasien. Ketidakseimbangan elektrolit akibat
cairan infus dapat dilihat pada Tabel 6.
 64 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

3.4 Gambaran ketidakseimbangan elektrolit pasien gagal jantung

Tabel 6. Ketidakseimbangan elektrolit pada pasien gagal jantung di RS X Yogyakarta 2011-

2014
Ketidakseimbangan elektrolit Frekuensi Jumlah
(pasien)
Hiperkalemia 3 x 40 mg/ 4 ml 1
3 x 20 mg/ 2 ml 1
3 x 20 mg/ 2 ml 1
Hiperkloremia
2 x 20 mg/ 2 ml 1
1 x 40 mg* 1
Jumlah (pasien) 5
Keterangan :*=Pemberian oral

Hiperkloremia terjadi lebih banyak dari pada hiperkalemia. Hal ini dapat terjadi akibat
pemberian infus yang diberikan pada masing-masing pasien. Pada dasarnya penyesuaian
cairan ini diperlukan karena hiperkloremia dapat menyebabkan penurunan bikarbonat sehingga
menyebabkan ketidakseimbangan asam-basa atau asidosis metabolik. Apabila keadaan ini
terjadi terus-menerus dapat memengaruhi sistem syaraf pusat dan dapat menyebabkan koma
(Price, S.A., Wilson, L.M., 2005)
Pada pasien yang mengalami dehidrasi (syok hipovolemik dan asidosis) pada kondisi:
gastroenteritis akut, demam berdarah dengue (DHF), luka bakar, syok hemoragik, dehidrasi
berat, trauma dapat diberikan cairan asering. Ringer laktat juga dapat digunakan untuk
mengembalikan keseimbangan elektrolit pada keadaan dehidrasi dan syok hipovolemik. Namun
ringer laktat menjadi kurang disukai karena menyebabkan hiperkloremia dan asidosis
metabolik, karena akan menyebabkan penumpukan asam laktat yang tinggi akibat metabolisme
anaerob. Sedangkan NaCl juga dapat diberikan pada pasien dengan kondisi yang sama pada
penggunaan asering maupun ringer laktat namun pemberian cairan ini sesuai dengan
kebutuhan cairan setiap pasien (Garg &Garg, 2000).

3.3. Respon terapi furosemid

Respon terhadap diuretik tergantung pada konsentrasi obat dan tentu saja saat masuk ke
dalam urin. Pasien dengan gagal jantung ringan merespon positif terhadap dosis rendah karena
dapat menyerap diuretik secara cepat dari usus dan mengantarkan obat ini dengan cepat ke
tubulus ginjal. Namun, karena peningkatan gagal jantung, penyerapan obat mungkin tertunda
oleh edema sehingga
 65 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

pengiriman obat dan respon terhadap konsentrasi intratubular yang diberikan terganggu.
Penilaian respon terapi dalam penelitian ini dapat dilihat dari kadar elektrolit pasien, derajat
udem, tekanan vena jugular, balance cairan dan keluhan pasien.
Pada Tabel 7 pemeriksaan yang paling banyak dilakukan adalah penilaian kadar elektrolit.
Hal ini karena dalam penelitiankadar elektrolit menjadi parameter utama yang mudah diamati.
Penilaian elektrolit dilakukan pada semua pasien gagal jantung dalam penelitian ini. Sedangkan
parameter lainnya yaitu balance cairan terdapat 35 pasien (23%), edema 23 pasien (16%), dan
JVP 7 pasien (5%). Setiap pasien mendapatkan pemeriksaan yang berbeda-beda sesuai
dengan kondisi penyakit ataupun kemampuan ekonomi pasien. Distribusi penilaian respon
terapi dan keluhan pasien dapat dilihat pada Tabel 7.

Tabel 7. Distribusi perkembangan klinis pasien gagal jantung di RS X Yogyakarta 2011-2014

Parameter Jumlah Persentase (%)

perkembangan klinis (pasien)
JVP 7 5,00
edema 23 16,00
Balance cairan 35 23,00
Elektrolit 40 28,00
Sesak 40 28,00
JVP = Jugularis Venous Pressure

Pada pemeriksaan tekanan vena jugular misalnya, tidak dilakukan pada semua pasien
yang mengalami gagal jantung. Walaupun sebenarnya pemeriksaan ini perlu dilakukan untuk
melihat adanya perubahanvolume dan tekanan di dalam atrium kanan yang apabila meningkat
maka hal tersebut menandakan adanya indikasi gagal jantung kanan ataupun edema (Stason,
et al., 1966).Namun karena keterbatasan biaya maka pemeriksaan tekanan vena jugular tidak
dilakukan pada setiap pasien. Pemeriksaan balance cairan juga tidak dapat dilakukan setiap
waktu, karena pemeriksaan ini hanya dilakukan di ruang khusus seperti ICU (Intensive Care
Unit). Sedangkan pengukuran edema dapat dilakukan dengan pitting edema (edema
ekstermitas) dan dengan foto thoraks untuk edema paru. Data pada tabel 8 menunjukkan
bahwa seluruh pasien dalam penelitian ini mengalami sesak nafas. Parker (2008) menyatakan
salah satu manifestasi utama gagal jantung adalah sesak nafas.
Pada Tabel 8, dapat dilihat ketidakseimbangan elektrolit yang dialami pasien setelah
penggunaan furosemid. Dari Tabel 8, 6 pasien mengalami kejadian hiponatremia ringan, 10
pasien mengalami hipokalemia (4 pasien hipokalemia ringan, 6 pasien hipokalemia sedang).
Pada 40 pasien
 66 | Makani, M, & Setyaningrum N. /Jurnal Ilmiah Farmasi 13(2) Agustus-Desember 2017, 57-68

yang menggunakan furosemid tidak tedapat pasien yang mengalami penurunan kadar klorida,
namun beberapa pasien mengalami hiperklorida. Respon furosemid terkait tinjauan terhadap
kadar elektrolit pasien dapat dilihat pada Tabel 8.

Tabel 8. Tinjauan kadar elektrolit setelah pemberian akibat furosemid pada pasien
gagal jantung RS X Yogyakarta 2011-2014
Elektrolit Normal Ringan Sedan
g
Sodium 33 7 -
Pottasium 30 4 6
Chloride 40 - -

Keterangan:

Hiponatremia ringan = 125-135 mEq/L, Hipokalemia ringan = 3.0-3.4 mEq/L, Hipokalemia sedang = 2.5-3.0
mEq/L

Hiponatremia biasanya hanya gejala ringan atau tanpa gejala sehingga pengobatan harus
disesuaikan dengan kondisi klinis. Hiponatremia pada pasien euvolemic dapat dikelola dengan
pembatasan cairan dan pembatasan obat yang mempengaruhi ekskresi.
Respon penggunaan furosemid tidak hanya dipengaruhi oleh dosis yang diberikan kepada
setiap pasien, namun juga dipengaruhi oleh sediaan yang diberikan. Respon penggunaan
furosemid dapat dilihat pada Tabel 9 dan 10.

Tabel 9. Respon penggunaan furosemid oral pada pasien gagal jantung RS X Yogyakarta
2011-2014
Respon
Frekuensi Dosis Jumlah (Pasien) Elektrolit
Sesak
Hiponatremia Hipokalemia
3x1 40 mg 5 - - <
2x1 40 mg 1 - 1 pasien <
1x1 40 mg 12 - - <
1x½ 20 mg 1 - - <

Tabel 10. Respon penggunaan furosemid intravena pada pasien gagal jantung RS X Yogyakarta
2011-2014
Respon
Jumlah Elektrolit
Frekuensi Dosis Sesak
(pasien) Hiponatremia Hipokalemia
(kasus)
(kasus) (kasus)
 3x2 40 mg / 4 ml 16 2 3 <
1x2 40 mg / 4 ml 2 - - +
3x1 20 mg / 2 ml 32 2 6 2 (+)
2x1 20 mg / 2 ml 19 1 1 4 (+)
1x1 20mg / 2 ml 2 - - +

Dari Tabel 9 dan 10, dapat dilihat bahwa ketidakseimbangan elektrolit lebih sering
dialami oleh pasien yang menerima furosemid intravena. Tidak hanya dosis yang dapat
mempengaruhi respon dari suatu obat, namun juga jalur pemberian yang diberikan kepada
setiap pasien.
Dari tabel diatas dapat dilihat bahwa yang memiliki potensi besar menurunkan kadar
elektrolit adalah pasien dengan dosis dan frekuensi 3 x 40 mg/ 4 ml. Hal ini sesuai dengan
fungsi dari diuretik itu sendiri yaitu meningkatkan ekskresi urin dan mengurangi tanda-tanda
fisik dari retensi cairan pada pasien dengan gagal jantung (Hunt et al., 2009).
3.5. Keterbatasan penelitian

Penelitian ini memiliki beberapa keterbatasan yang cukup berpengaruh dalam hasil akhirnya
terutama dalam proses penghambilan data rekam medis pasien. Banyak rekam medis yang sulit
dipahami tulisannya. Monitoring pemasukan dan pengeluaran tubuh serta kadar elektrolit tubuh,
JVP, dan balance cairan yang terkait dengan penggunaan furosemid hanya dilakukan apabila
pasien berada dalam ICU atau jika dokter meminta petugas untuk memonitoringnya sehingga
tidak dapat mengoptimalkan makna dari penggunaan furosemid. Selain itu perubahan kadar
elektrolit tidak hanya dipengaruhi oleh furosemid tetapi juga obat-obat lain.

4. Kesimpulan
Pemberian furosemid intravena 20 mg / 2ml diberikan pada pasien yang mengalami edema.
Sedangkan pemberian furosemid 40 mg oral diberikan pada pasien yang mengalami perbaikan
kondisi setelah edema. Respon terapi furosemide berdasarkan tinjauan kadar elektrolit
ditemukan 7(17%) hiponatremia ringan; 4(10%) hipokalemia ringan dan 6(15%) hipokalemia
sedang.
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