Studi Kasus di SMF Kardiologi

PJK OMI ANTEROSEPTAL + DCFC IV

+ HT Stage II + DMND V +
Hiperkalemia

PRESENTED by

apt. Nurul Masyithah, M.Farm

 PATIENT DATABASE
▪ Nama : Tn. S
▪ No. RM : 1244. xx. xx
▪ Umur : 62 tahun
▪ Tgl MRS : 12 September 2015
▪ Ruang : Camelia
▪ Diagnosa : PJK OMI Ant. Septal + HT St. II + DCFC IV + DMND V + Hiperkalemia
▪ Anamnesa awal : KU : Px sesak nafas sejak 2 minggu, memberat 1 hari SMRS
dirasakan sepanjang hari, minum banyak, tidur dengan 3 bantal, kaki bengkak sudah 3
minggu terahir, pitting oedema (+), Paru : rh (-/+) basah, cor : bising, mual (-), muntah (-),
nyeri ulu hati (+).
▪ RPD : DM (+) 13 tahun, HT kronik tidak terkontrol, Px dinyatakan PJK
namun tidak kontrol.
▪ RPO : Glibenklamid.
2
 HASIL KONSUL
Tanggal Kesimpulan
14/09 PX dengan PJK OMI ant. Septal + HT st. II + DCFC IV + DMND V + Hiperkalemia
Konsul Mohon pemeriksaan funduskopi guna penegakan Dx nefropati diabetik
Mata Kesimpulan :-
Kesimpulan : Px DM tp.II + S.ND V + Hiperkalemi
Saran :
1. Diet B3 2100 kkal
12/09
2. Balance cairan i:O 4500ml
Konsul IPD
3. Inf. Pz 7 tpm
4. Inj. Ca. Gluconas 1 amp. Iv bolus
5. Inj. D40% + insulin Actrapid 4 unit iv bolus 2x (interval 30 menit)

HASIL ELECTROCARDIOGRAM
TANGGAL EKG
11/09/15 Irama sinus 75x/menit. Axis normal. OMI anteroseptal
14/09/15 Irama sinus 76x/menit. Axis normal. OMI anteroseptal
15/09/15 Irama sinus 80x/menit. Axis normal. OMI anteroseptal
16/09/15 Irama sinus 73x/menit. Axis normal. OMI anteroseptal
17/09/15 Irama sinus 78x/menit. Axis normal. OMI anteroseptal
3
 PERKEMBANGAN DIAGNOSA

DATE DIAGNOSTICS

PJK OMI ant. Septal + HT st. II + DCFC IV + DM tp.2 + S. ND V +

12/09/15
Hiperkalemia

13/09/15 PJK OMI ant. Septal + HT st. II + DCFC II + DM tp.2 + S. ND V + Hiperkalemia

14/09/15 PJK OMI ant. Septal + HT st. II + DCFC II + DM tp.2 + S. ND V + Hiperkalemia

15/09/15 PJK OMI ant. Septal + HT st. II + DCFC II + DMND V + Hiperkalemia

16/09/15 PJK OMI ant. Septal + HT st. II + DCFC II + DMND V + Hiperkalemia

17/09/15 PJK OMI ant. Septal + HT st. II + DCFC I + DMND V + Hiperkalemia

4
 DATA LABORATORIUM
Tanggal
Nilai 12/09 12/09
Data Lab
Normal Pukul Pukul 14/09
Tanggal
02.08 09.20
DATA Nilai 12/09 12/09
HCT 41.3-52.1 32.9 30.61
LAB Normal Puk Puk 14/0 15/0 16/0
ul ul 9 9 9
MCV 86.7-102.3 91.3
02.08 09.20
MCH 27.1-32.4 29.3
10.5
HB 13,3-16,6 10.5 MCHC 29.7-33.1 32.1
6
RDW 12.2-14.8 14.2
Leukosit 3,37-10 4.97 5.01 GDA 40-121 133 196
151. GD2PP 166
Trombosit 150-450 172
3 HbA1C 4.3-6.0 8.6
RBC 3,69-5,46 3.60 Kolesterol
<200 140
K 4,0-5,5 6,3 5.2 5.4 5.2 5.3 total
Na 136-145 138 131 139 132 138
Trigliserida 30-150 71
Cl 98-107 117 107 109 102 106
HDL 40-60 37
BUN 7-18 39 45 25
LDL 00-99 88
SCr 0,6-1,3 5.36 5.0 5.6
CRP 0.0-0.9 0.1
SGOT < 41 41 5
Albumin 3,4-5,0 3.02 3.3 3.3
BLOOD GASSES URINALYSIS
Tanggal Tanggal
Data Lab Nilai Normal Nilai
Data Lab 12/09
12/09 Normal
pH 7,35-7,45 7.40
Eritrosit - 1+
PCO2 35-45 28
Leukosit - Neg
PO2 80-100 126
Nitrit - Neg
HCO3 22-26 17.3
Glukosa - Neg
BE -3,5-2,00 -7.5
BJ 1,003-1,030 1.020
TCO2 23-30 18.2
pH 4,5-8,0 7.0
SO2 94-98% 99
Protein - 2+
Temp 00,00 37.0
Keton - Neg
Data Lab Nilai Normal 12/09 Urobilinogen < 1,0 1
CKMB 0,18-300 34.2 Bilirubin - Neg
Troponin 0,02-0,06 0.032 Warna Other
Kejernihan Clear
*Hasil pemeriksaan kalium meningkat. Sampel baik mohon konfirmasi klinis bila tidak sesuai
klinik mohon sampel baru 6 6
 Data Klinik
DATA 12/9 13/9 14/9 15/9 16/9 17/9
Suhu 36.5 36.5 36.5 36.7 36.8 36.5
Nadi 72-84 72 70 82-88 78 72
RR 24-32 20 20 18-20 20 18
150-169/
TD 150/76 150-160/90 160/100 160/90 150/90
80-90
aicd - - - - - -
JVP ↑ ↑/
KU lemah cukup cukup cukup cukup cukup
GCS 456 456 456 456 456 456
Sesak ↓↓ - - - - -
Mual/ muntah -/- -/-
Supel met – Supel met – Supel met – Supel met – Supel met – Supel met –
Abdomen
BU + N BU + N BU + N BU + N BU + N BU + N
Extremitas AHKM AHKM AHKM AHKM AHKM AHKM
Rh --+/--+ ---/--- ---/--- ---/--- ---/--- ---/---
Wh -/- ---/--- ---/--- ---/--- ---/--- ---/---
P(Ves/Ves) +/+ +/+ +/+ +/+ +/+ +/+
Edem -+/-+ --/-- -+/-+ minimal --/-- --/-- --/--
C es (-) m(-) g(-) es (-) m(-) g(-) es (-) m(-) g(-) m(-) g(-) m(-) g(-) m(-) g(-)
7
 PROFIL TERAPI
TANGGAL
REGIMEN
OBAT
DOSIS 12/9 13/9 14/9 15/9 16/9 17/9

2100 TKRPRG
Diet B3 √ √ √ √ √
kkal/hari 1900 kkal
O2 nasal 3 lpm √ √ √ √
Pump 2.5
Furosemid Inj 1-0-0 2x1 √ √ √ √
mg/jam
Spironolakton 1x25 mg √ √
Captopril 3x12.5 mg √ √
Amlodipin 0-0-10 mg 1x5 mg √ √ √ √ √
Atorvastatin 0-0-20 mg 0-0-80 mg √ √ √ √ √
ASA 1x100 mg √ √ √ √ √ √
1 amp iv
Inj. Ca Glukonas √ √ √ √ √
bolus
Drip D40 √ √ √ √ √
4x selang 3x selang
Actrapid 4 IU √ √ √
½ jam 1 jam
D10 + 10 IU insulin
√ √ √
7 tpm
Kalitake 3x1 sach √ √ √ √ √ √
8
 OBAT KRS

OBAT REGIMEN DOSIS

Furosemid 40mg 1x sehari (pagi)
Amlodipin 10 mg 1x sehari
Atorvastatin 20 mg 1x sehari (malam)
ASA 100 mg 1 x sehari
3x sehari dalam 30 cc air 30 menit
Kalitake
sebelum makan

9 9
 HYPERTENSION IN DIABETIC
NEPHROPATHY

Van Buren, P.N., Toto, R. 2011. Hypertension in Diabetic Nephropathy: Epidemiology, Mechanisms, and Management. Adv
Chronic Kidney Dis. 18(1): 28–41. 10
TREATMENT IN DIABETIC
NEPHROPATHY

11 11
 DIURETICS THERAPY
TANGGAL
REGIMEN
OBAT
DOSIS 12/9 13/9 14/9 15/9 16/9 17/9

Pump 2,5
Furosemide Inj 1-0-0 2x1 √ √ √ √
mg/jam

Spironolakton 1 X 25mg √ √
DATA 12/9 13/9 14/9 15/9 16/9 17/9
150-169/80-
TD 150/78 150-160/90 160/100 160/90 150/90
90
Sesak ↓↓ - - - - -

P(Ves/Ves) +/+ +/+ +/+ +/+ +/+ +/+

-+/-+
Edem -+/-+ --/-- --/-- --/-- --/--
minimal
Tanggal
DAT
Nilai 12/09 12/09 14/09 15/09 16/09
A
Normal Pukul Pukul
LAB
02.08 09.20
K 4,0-5,5 6,3 5.2 5.4 5.2 5.3
BUN 7-18 39 45 25
SCr 0,6-1,3 5.36 5.0 5.6
12
 DIURETICS IN PATIENT WITH
HEART FAILURE
INITIAL DAILY DURATION
DRUG SPECIAL POINTS SIDE EFFECTS CONTRAINDICATIONS
DOSE OF ACTION
LOOP DIURETICS
20-160 mg orally Loop diuretics can cause
once daily or worsening
divided dose. A renal function (especially
dosage of 5 to 20 when used in patients with Loop and thiazide diuretics are
mg/h IV by hypovolemia), contraindicated in
4-6 h orally,
FUROSEMIDE continous Least expensive ototoxicity,hyperuricemia, hypotension/shock
2 h IV
infusion ( or less hypocalcemia, (systolic BP < 90 mm Hg),
preferably, 20- hypokalemia, dehydration, hypernatremia, anuria
100 mg of IV hyponatremia, and
boluses every 6- depletion of thiamine
12 hours levels
POTASSIUM-SPARING DIURETICS
require frequent
monitoring for
hyperkalemia.
Aldosterone antagonists are
They are not as
Spironolactone can cause contraindicated in
useful for their
serious hyperkalemia and hypotension/shock
25–50 mg orally diuretic effects,
SPIRONOLAKTON 2-3 d metabolic acidosis. It can (systolic BP < 90 mm Hg),
once daily but have been
cause gynecomastia or dehydration, hypernatremia,
shown to reduce
breast pain anuria, hyperkalemia, severe renal
mortality
insufficiency (SC > 2.5 mg/dL).
in patients with
advanced heart
failure

Pater et al, 2007. Optimal Use of Diuretics in Patients with Heart Failure. 13
 PHARMACOKINETICS/
PHARMACODYNAMICS
PK/PD FUROSEMIDE SPIRONOLAKTON

Structure

Oral (30-60 minutes)

Onset of Action Gradual : maximum diuretic effect reached on third day
IV : 5 minutes

Oral : 6-8 hours

Duration Diuresis persists for 2-3 days after discontinuance
IV : 2 hours

Well absorbed following oral administration, peak

65% (normal renal function)
Absorption serum concentrations of spironolactone usually attained
45% (renal failure)
within 1-2 hours

Protein binding 98% 91-98%

30 minutes (normal renal function)

t½ 78-84 minutes
9 hours (renal failure)

50% (oral), 80% (iv) excreted unchanged in

Elimination Urinary & biliary
urine within 24 hours

Serum electrolytes, renal function, & blood

Monitor Serum potassium, sodium, & renal function
pressure.

Lexicomp. 2015 14
 MANAGEMENT HYPERTENSION

James, Paul. A et al. 2014. Evidence-Based Guideline for theManagement of High Blood Pressure in Adults Report
15 Fromthe
15
PanelMembers Appointed to the Eighth Joint National Committee (JNC 8). American Medical Association
 ANALYSIS THERAPY
ANTIHYPERTENSION
TANGGAL
OBAT REGIMEN DOSIS
12/9 13/9 14/9 15/9 16/9 17/9
Spironolakton 1x25 mg √ √
Captopril 3x12.5 mg √ √
Amlodipin 0-0-10 mg 1x5 mg √ √ √ √ √

DA Tanggal
12/9 13/9 14/9 15/9 16/9 17/9 DAT NILAI
TA
A NORMA 12/09 12/09 14/0 15/0 16/0
Na LAB L Pukul Pukul 9 9 9
72-84 72 70 82-88 78 72
di 02.08 09.20
150- K 4,0-5,5 6,3 5.2 5.4 5.2 5.3
150/ 150- 160/1 160/ 150/
TD 169/
76 160/90 00 90 90 SCr 0,6-1,3 5.36 5.0 5.6
80-90

▪ ACE-i atau ARB dalam monoterapi maupun kombinasi merupakan strategi yang paling efektif
dalam ESRD akan tetapi memiliki resiko terjadi hiperkalemia.
▪ CCB hampir tidak memiliki efek dalam meningkatkan kalium tetapi dapat meningkatkan serum
kreatinin dan mempunyai efek samping edema yang besar.
▪ Pemilihan obat antihipertensi dalam kasus ini mempertimbangkan risk dan benefit pasien dan
obat yang dipilih adalah amlodipin. Pemilihan amlodipidin kurang sesuai karena kurang memiliki
benefit dibandingkan dengan ACE-i dalam penatalaksanaan CKD dan HF terutama dg
penurunan EF (rekomendasi IA), sehingga kami lebih menyarankan penggunaan ACE-i tanpa
spironolakton serta perlu monitoring ketat serum kalium pasien. 16
 META ANALYSIS OF BLOOD
PRESSURE-LOWERING
AGENTS

Palmer, Suetonia C et al. 2015. Comparative e fficacy and safety of blood pressure-lowering agents in adults with
17 diabetes
and kidney disease: a network meta-analysis. Lancet 2015 Vol.385 Page.2047–56 17
 ATORVASTATIN
TANGGAL
OBAT REGIMEN DOSIS
12/9 13/9 14/9 15/9 16/9 17/9

Atorvastatin tab 0-0-20 mg 0-0-80 mg √ √ √ √ √

Tanggal
Intensive lipid-lowering after an ACS event regardless
of baseline LDL (off-label use) Data Lab Nilai Normal 12/09 12/09
Oral: Initial: 80 mg once daily; adjust based on patient (02.08) (09.20)
tolerability (Cannon 2004; Pederson 2005; Schwartz 2001). Kolesterol total <200 140
Note: Currently, the ACC/AHA guidelines for UA/NSTEMI
do not specify which statin to use (ACCF/AHA [Anderson Trigliserida 30-150 71
2013]). Also consider the ACC/AHA Blood Cholesterol HDL 40-60 37
Guideline recommendations (Stone 2013).
LDL 00-99 88

▪Analisis Terapi Atorvastatin :

Pemilihan atorvastatin telah sesuai dengan guideline dari AHA karena pada pasien dengan
resiko tinggi terjadinya gangguan cardiovascular (ACS) lebih dipilih high intensity statin
(atorvastatin). Penggunaan atorvastatin dosis tinggi (80mg) sesuai dengan guideline dimana
dengan dosis tinggi efek dari atorvastatin juga meningkat, namun pada pasien ESRD efektifitas
dan keamanan statin dosis tinggi masiih belum jelas sehingga sebaiknya digunakan dosis yang
lebih kecil (pada pasien dosis diturunkan menjadi 20 mg).
18
18Meta-Analysis.
Yan et al., 2015, High-Intensity Statin Therapy in Patients with Chronic Kidney Disease : A Systematic Review and
 19
19Meta-Analysis.
Yan et al., 2015, High-Intensity Statin Therapy in Patients with Chronic Kidney Disease : A Systematic Review and
 PLEOTROPIC EFFECT OF STATIN
Pleotropic effect of statin (Mishra, 2008)

Lipid Independent :
 Decrease LV mass
- Inhibit angiotensin I-mediated cardiomyocyte hypertrophy
Lipid Dependent : - Decrease extracellular signal-related kinase (ERK ½) activity,
 Decrease vascular ERK phosphorylation, RAS membrane targeting and activation
atherosclerosis - Antihypertensive
 Decrease myocardial  Decrease LV fibrosis
infarction - Decrease inflammation (decreased C-reactive protein,
 Decrease cerebral interleukin-6), immune activation, oxidative stress, oxygen free
vascular accident radicals
 Decrease peripheral - Alter matrix metalloproteinase activity
vascular disease  Increase arterial compliance
- Decrease vascular atherosclerosis, endothelin synthesis
- Improve endothelial function
- Increase nitric oxide

20
20 108-114
Mishra, T.K. 2008. Role of Statin in Heart Failure. Journal of Indian Academy of Clinical Medicine, Vol.9, No.2:
 ANTIPLATELET THERAPY
TANGGAL
OBAT REGIMEN DOSIS
12/09 13/09 14/09 15/09 16/09 17/09
ASA 1x100 mg √ √ √ √ √ √

ASPIRIN
Irreversibly inhibits cyclooxygenase-1 and 2
(COX-1 and 2) enzymes, via acetylation,
which results in decreased formation of
prostaglandin precursors; irreversibly inhibits
formation of prostaglandin derivative,
thromboxane A2, via acetylation of platelet
cyclooxygenase, thus inhibiting platelet
aggregation; has antipyretic, analgesic, and
anti-inflammatory properties
21
21
Opie, Lionel H. and Gersh, Bernard J. 2013. Drugs for the Heart eighth edition. Elsevier Saunders
 DRUG INTERACTIONS
DRUG MECHANISM RISK
Salicylates may diminish the antihypertensive effect of
ACE Inhibitors. They may also diminish other beneficial
pharmacodynamic effects desired for the treatment of Risk C :
ACE inhibitors CHF. The effects are likely dose-related. 100 mg doses Monitor
aspirin appear to cause no problems, whereas 300 mg therapy
doses appear to significantly affect ACE Inhibitor
efficacy

Salicylates may diminish the diuretic effect of loop Risk C :

Loop diuretics diuretics. Loop diuretics may increase the serum Monitor
concentration of salicylates. therapy

▪Analisis Terapi ASA :

Penggunaan ASA sudah sesuai dengan guideline dimana ASA digunakan untuk
mencegah timbulnya agregasi platelet, mencegah pelepasan isi granul platelet, dan
mencegah vasokontriksi platelet mediated vascular.

Lexicomp. 2015 22 22
 INSULIN
THERAPY
TANGGAL
OBAT
12/9 13/9 14/9 15/9 16/9 17/9
D10 + 10 IU
insulin 7 √ √ √
tpm

Tanggal
Nilai 12/09 12/09
Data Lab
Normal Pukul Pukul 14/09
02.08 09.20
GDA 40-121 133 196
GD2PP 166
HbA1C 4.3-6.0 8.6

1. Pemberian terapi insulin dimulai tanggal 14/9 karena dari data lab menunjukkan peningkatan GDA
dan GD2PP, sehingga sudah sesuai diberikan basal insulin 10 IU + D10 secara infus kontinyu
untuk mencegah terjadinya hipoglikemia pada pasien.
2. Perlu dilakukan pemeriksaan data lab lebih lanjut mengenai gula darah pasien serta HbA1C
setelah 3 hari pemberian Insulin, sehingga tidak dapat merekomendasikan terapi insulin pasien
tersebut
McCulloch, D.K. 2015. General Principles of Insulin Therapy in Diabetes Mellitus. Uptodate. 23
 TREATMENT OF HYPERKALEMIA

Yelena Mushiyakh, MD1, Harsh Dangaria, MD2, Shahbaz Qavi, MD2, Noorjahan Ali, MD2, John Pannone, MD1 and David Tompkins,
24 MD1.
24
2011. Treatment and pathogenesis of acute hyperkalemia. Citation: Journal of Community Hospital Internal Medicine Perspectives.
 HYPERKALEMIA THERAPY
TANGGAL
REGIMEN
OBAT
DOSIS 12/9 13/9 14/9 15/9 16/9 17/9

Spironolakton 1x25 mg √ √
Captopril 3x12.5 mg √ √
Inj. Ca Glukonas 1 amp iv bolus √ √ √ √ √
Drip D40 √ √ √ √ √
4x selang 3x selang 1
Actrapid 4 IU √ √ √
½ jam jam
Kalitake 3x1 sach √ √ √ √ √ √

Tanggal

DATA Nilai 12/09 12/09

LAB Normal Puk Puk 14/0 15/0 16/0
ul ul 9 9 9
02.08 09.20

K 4,0-5,5 6,3 5.2 5.4 5.2 5.3

Na 136-145 138 131 139 132 138
Cl 98-107 117 107 109 102 106
BUN 7-18 39 45 25
SCr 0,6-1,3 5.36 5.0 5.6 25 25
 EFFICACY (EBM) OF KALITAKE
REFERENCES RESULT
1. Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion exchange
resins for the treatment of hyperkalemia: are they safe and
effective? J Am Soc Nephrol 2010; 21:733 Weak evidence suggests that sodium
2. SCHERR L, OGDEN DA, MEAD AW, et al. Management of polystyrene sulfonate can lower the serum
hyperkalemia with a cationexchange resin. N Engl J Med 1961; potassium, usually after multiple doses are
264:115 given over one to five days; single doses
3. FLINN RB, MERRILL JP, WELZANT WR. Treatment of the oliguric are not very effective . However, laxative
patient with a new sodiumexchange resin and sorbitol; a therapy (eg, sorbitol) may produce an
preliminary report. N Engl J Med 1961; 264:111 equivalent reduction in the serum potassium
4. FLEISHER DS. Cation exchange resin therapy for hyperkalemia in
infants and children. J Pediatr 1961; 58:486.
Calcium polystirene sulfonate do not
appear to have superior efficacy as
compared with laxatives alone .
FLINN RB, MERRILL JP, WELZANT WR. Treatment of the oliguric
The reduction in the serum potassium was
patient with a new sodiumexchange
larger in those given sorbitol alone (from 6.3
resin and sorbitol; a preliminary report. N Engl J Med 1961; 264:111
to 4.6 meq/L) than in those given sodium
polystyrene sulfonate combined with
sorbitol (from 6.6 to 5.2 meq/L)
In other hyperkalemic patients who meet all of the following criteria, we suggest therapy with a cation
exchange resin rather than with repeated doses of insulin and glucose (Grade 2C) :
1.Potentially life threatening hyperkalemia.
2.Dialysis is not readily available.
3.Other therapies to remove potassium (eg, diuretics, rapid restoration of kidney function) have failed or
are not possible.

Treatment and Prevention of Hyperkalemia in Adults. Uptodate. 2015 26 26

MECHANISM ACTION OF KALITAKE
 MECHANISM ACTION:
In the gut, sodium polystyrene sulfonate takes up potassium (and calcium and
magnesium to lesser degrees) and releases sodium. Each gram of resin may
bind as much as 1 meq of potassium and release 1 to 2 meq of sodium. Thus, a
potential side effect is exacerbation of edema due to sodium retention.

ANALYSIS THERAPY OF HYPERKALEMIA

1. Pemberian terapi Ca glukonat dan D40+insulin dipakai pada kondisi hiperkalemia (dengan kadar
berapapun di atas normal) dengan perubahan EKG atau kadar kalium lebih dari 6.5 tanpa
perubahan EKG. Tetapi pada tanggal 12&13/09 saat pemberian Ca glukonat dan D40 + insulin tidak
didapatkan hasil EKG.
2. Setelah hyperkalemia teratasi, pada tanggal 13-16 September tetap mendapatkan terapi Ca
Glukonas dan D40 + Insulin serta kalitake oral. Dari data EKG, tidak terdapat perubahan EKG.
Sebaiknya setelah hiperkalemia terkoreksi dan mencapai nilai normal serta tidak didapatkan
perubahan EKG, cukup dengan pemberian kalitake oral khususnya pada pasien ini mengalami
CKD yang rentan untuk terjadinya resiko hiperkalemia. Penggunaan kalitake tidak melebihi dosis
yang di tentukan dan tidak sebagai single dose tapi multiple dose dengan dosis 3 x sehari.
3. Pemberian captopril dan spironolakton tetap diberikan pada tanggal 12-13 September, meskipun
telah dalam kondisi hiperkalemia. Kombinasi captopril dengan spironolakton berpotensi untuk
menyebabkan terjadinya hiperkalemia
4. Menghindari makanan yang tinggi kalium (pisang, apel, brokoli, dll) untuk mencegah resiko
terjadinya hiperkalemia.
27
 RANITIDINE

TANGGAL
REGIMEN
OBAT 12/9 13/9 14/9 15/9 16/9 17/9
DOSIS

Inj. Ranitidine 2x1 amp √ √ √ √ √ √

DATA 12/9 13/9 14/9 15/9 16/9 17/9

Mual/ muntah -/- -/-

Nyeri uluhati +

• Analisis Terapi Ranitidin :

 Pemberian terapi ranitidin diindikasikan karena pada saat MRS tgl 12/09
pasien mengeluhkan nyeri ulu hati.
 Dosis ranitidin sudah sesuai untuk gastritis 2x1 amp (25mg).
 Pada tanggal 13/09 tidak ada keluhan mual muntah dan nyeri ulu hati tetapi
pemberian Ranitidin tetap dilanjutkan.
 Dilihat dari kondisi pasien, pasien sudah bisa makan sehingga pemberian
ranitidin iv perlu dievaluasi kembali.
28
 PKPD & MECHANISM OF
RANITIDINE

PK/PD RANITIDINE

Onset of Action 1 hr(PO/IV)

Duration 4-5 hr (IV/IM); 4-6 hr(PO)

Vd 1.4L/kg

Protein binding 10-19%

t½ 2.5-3 hr (PO); 2-2.5(IV)

Elimination Urine (30%; PO;70% IV)

29
 SUMMARY
1. Pemberian obat antihipertensi pada pasien dengan DM, CKD, HF, dan hiperkalemia
memerlukan pertimbangan risk dan benefit dari efikasi serta efek samping obat.
2. Penggunaan spironolakton sebaiknya dihentikan dari hari pertama sejak ditegakkan
diagnosa hiperkalemia. Penggunaan amlodipin sebaiknya diganti captopril yang mempunyai
benefit untuk pasien HF dan CKD daripada resiko hiperkalemia dengan monitoring ketat
serum kalium.
3. Pemakaian diuretik Furosemid memberikan manfaat pada pasien gagal jantung dengan
edema dengan tetap monitoring profil gula darah dan elektrolit terkait pasien dengan DM
dan hiperkalemia.
4. Pemberian kombinasi Ca glukonas, D40 + Insulin serta Kalitake untuk penatalaksanaan
hiperkalemia sebaiknya ditinjau kembali, mengingat kadar kalium pasien telah normal dan
tidak ada perubahan EKG.
5. Pemakaian Atorvastatin sudah sesuai dan memberikan benefit lebih terkait stabiliasi plak
khususnya pada pasien dengan riwayat PJK.
30
 DAFTAR PUSTAKA
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