IDENTITAS PASIEN

Nama : Tn. A
Jenis kelamin : Laki-laki
Usia : 46 tahun
Alamat : Kp. Godog Jaya
Pekerjaan : Montir
Tanggal masuk : 14-09-2016

ANAMNESIS

Keluhan Utama
Sesak sejak 10 hari SMRS

Riwayat Penyakit Sekarang

Seorang laki-laki datang ke RSUD Cianjur mengeluh sesak sejak 10 hari sebelum masuk rumah
sakit. Sesak dirasakan tiba-tiba, sesak dirasakan bertambah ketika sedang beraktivitas dan
berkurang ketika istirahat. Pada saat tidur pasien sering terbangun pada malam hari karena
sesak, pasien lebih nyaman bila tidur menggunakan 3-4 bantal atau dengan posisi duduk. Pada
saat sesak napas tidak disertai bunyi ngik-ngik, pasien juga tidak merasa sesak nafas apabila
terkena debu, bulu ataupun cuaca dingin. Bengkak pada kaki disangkal. BAB dan BAK lancar
tidak ada keluhan.
Delapan hari sebelum masuk rumah sakit, keluhan disertai dengan perut yang terasa, kembung,
nyeri pada ulu hati (+), nyeri dirasakan hilang timbul. Lemas pada seluruh tubuh (+) cepat lelah
meskipun melakukan aktivitas ringan (+) misalnya jalan ke kamar mandi.
Pusing (+) demam (-) batuk kering (+) hilang timbul, batuk lebih sering malam hari. Napsu
makan berkurang seiring dengan adanya mual (+), muntah (+) sebanyak 2x setiap habis makan,
tidak disetai adanya darah.
Lima hari sebelum masuk rumah sakit, terdapat keluhan lain, yaitu bengkak pada kedua
kakinya, bengkak tidak berkurang walau beristirahat.
Sehari sebelum masuk rumah sakit, keluhan sesak bertambah berat, dan keesokan pagi nya
pasien dibawa ke rumah sakit dengan keluhan sesak (+), batuk kering (+) terutama pada malam
hari, bengkak pada kedua kaki, perut terasa kembung, mual (+), muntah (+) sebanyak 3x sejak
semalam, tidak disertai darah, lemas seluruh badan, penurunan napsu makan, BAB dan BAK
lancar.

Riwayat penyakit dahulu

 Riwayat hipertensi ( + ) sejak setahun yang lalu, namun tidak terkontrol.
 Riwayat DM disangkal
 Riwayat batuk lama > 2 minggu disangkal, asma disangkal
 Riwayat menjalani pengobatan paru yang 6 bulan disangkal
 Riwayat sakit kuning disangkal
 1 tahun yang lalu pasien mangaku pernah dirawat karena pembengkakan jantung

Riwayat penyakit dalam keluarga

 Ayah --> meninggal karena penyakit jantung.

Riwayat Pengobatan
 Sebelumnya pasien berobat ke puskesmas, lalu sempat dirujuk ke RS Cimacan, lalu
dirujuk ke RSUD Cianjur.

Riwayat Alergi
 Riwayat alergi makanan, debu, obat dan cuaca disangkal.

Riwayat Psikososial
 Semenjak sakit nafsu makan pasien menurun. Dahulu pasien mengaku suka makan
makanan yang asin gurih, bersantan atau berlemak, sering mengonsumsi kopi dan
,minuman bersoda, merokok kurang lebih 30th, tetapi pasien mengaku sekarang sudah
berhenti merokok.
PEMERIKSAAN FISIK
Keadaan umum : tampak sakit sedang
Kesadaran : komposmentis

Tekanan darah : 140/90 mmHg

Nadi : 80x/m, regular, kuat angkat isi cukup
RR : 28x/menit, regular
Suhu : 36,6oC (aksilla)

Status Generalis
Sistem Deskripsi
Kepala Bentuk normocephal, warna rambut hitam, distribusi rambut
merata, rambut tidak mudah rontok
Mata Konjungtiva anemis (-/-), sklera ikterik (-/-), refleks cahaya
(+/+), kornea jernih (+/+)
Hidung Sekret (-/-), epistaksis (-/-), septum deviasi (-/-), nafas cuping
hidung (-)
Mulut Mukosa mulut dan bibir lembab, tidak terdapat sianosis,
faring hiperemis (-), tonsil (T1-T1), stomatitis (-), lidah kotor
(-).
Telinga Normotia, simetris, serumen (-/-).
Leher Tidak didapatkan pembesaran KGB, pembesaran kelenjar
tiroid (-), JVP tidak terlihat adanya peningkatan
Jantung Inspeksi: iktus kordis tidak tampak
Palpasi: iktus kordis teraba di ICS VI linea anterior axilaris
sinistra
Perkusi:
Batas kanan jantung : ICS IV linea parasternalis dextra
Batas kiri atas jantung : ICS III linea parasternal sinistra
Batas kiri bawah jantung: ICS VI linea anterior axilaris
sinistra
Auskultasi: BJ I dan BJ II normal, murmur (-), gallop (-)
Paru Inspeksi : dada simetris (+/+), retraksi dinding dada (-/-
)
 Palpasi : Vokal fremitus sama di kedua lapang paru
Perkusi : Sonor pada ke 2 lapang paru, batas paru dan
hepar setinggi ICS 5
Auskultasi : suara dasar vesikuler (+/+), rales (+/+),
wheezing (-/-)
Abdomen Inspeksi : cembung (+), scar (-), caput medusa (-)
Auskultasi : bising usus (+) normal
Palpasi : nyeri tekan epigastrium (+)
Perkusi : timpani
Ekstremitas teraba hangat, CRT kurang dari 2 detik, edema (-/-),sianosis
atas (-/-)
Ekstremitas teraba hangat, CRT kurang dari 2 detik, edema (+/+), tampak
bawah eritema pada tungkai bawah +/+, sianosis (-/-)

PEMERIKSAAN PENUNJANG

Pemeriksaan Laboratorium tanggal 14-09-2016

Pemeriksaan Hasil Rujukan Satuan
Hematologi
Hemoglobin 15,2 13.5 – 17.5 g/dl
Hematokrit 45,4 42 – 52 %
Eritrosit 5,68 4.7-6.1 10^6/ul
Leukosit 9.1 4.8 – 10.8 10^3/ul
Trombosit 155 150 – 450 10^3/ul
MCV 80.0 80 – 84 fL
MCH 26.8 27–31 pg
MCHC 35 33 – 37 %
RDW-SD 45 37 – 54 fL
PDW 16.9 9–14 fL
MPV 13.1 8 – 12 fL
Differential
LYM% 31.4 26 – 36 %
MXD % 9.4 0 – 11 %
NEU% 57.7 40–70 %
EOS% 1.3 1-3 %
BAS% 0.2 <1 %
 Absolut
LYM# 1.43 1.00 – 1.43 10^3/μL
MXD # 0.43 0 – 12 10^3/μL
NEU# 2.63 1.8 – 7.6 10^3/μL
EOS # 0.06 0.02 – 0.50 10^3/μL
BAS # 0.01 0.00 – 0.10 10^3/μL
Kimia Klinik
Glukosa Rapid Sewaktu 124 < 180 mg/dL
Faal Ginjal
Ureum 42 10-50 mg%
Kreatinin 1.2 0-1 mg%
Elektrolit
Na 137.2 135-148 mEq/L
K 4.12 3.50-5.30 mEq/L
Ca 1.07 1.15-1.29 mmol/L

Pemeriksaan Laboratorium tanggal 17-09-2016

Pemeriksaan Hasil Rujukan Satuan

Elektrolit
Na 136.1 135-148 mEq/L
K 3.89 3.50-5.30 mEq/L
Ca 1.19 1.15-1.29 mmol/L
Gambaran EKG tanggal 14-09-2016

Interpretasi EKG :
1. Irama : sinus
2. Axis : normal
3. HR : 72 x/m
4. Gel. P : 0.04 – 0.1 mV
5. PR interval : 0.20 sec
6. Q patologis :
7. QRS duration : 0.06 sec
8. R/S V1 : > ½ --> RVH
9. R/S S V3 + R aVL: 30 mm --> kriteria cornell > 28 mm LVH
10. S persisten –
11. Segmen ST : depresi ST pada V5, V6
12. Gel. T : T inverted pada 1, Avl, v5, v6
13. Gel. U -
Pemeriksaan Rontgen Thoraks tanggal 16-09-2014

Kesan: Kardiomegali
Daftar Masalah :
1. Dekompensasi Cordis kanan kiri FC III
2. Gastritis
3. Hipokalemi

Analisa Masalah

1. Dekompensasi Cordis FC III – IV

A. Definisi

B. Etiologi
C. Tanda dan Gejala
 D. Diagnosa berdasarkan kriteria Framingham
Diagnosa gagal jantung dapat menggunakan kriteria Framingham, yaitu 2 kriteria mayor
atau 1 kriteria mayor dan 2 kriteria minor.

Kriteria Mayor : Kriteria minor :

o Paroksismal nocturnal dispneu o Edema ekstremitas
o Distensi vena leher o Batuk malam hari
o Rales o Dispnea d’effort
o Kardiomegali o Hepatomegali
o Edema paru akut o Efusi pleura
o Gallop S3 o Penurunan kapasitas vital 1/3 dari
normal
o Peninggian tekanan vena jugularis o Takikardia
o Refluks hepatojugular

Pada pasien didapatkan 4 kriteria mayor dan 4 kriteria minor, dinyatakan (+) dekom
cordis menurut kriteria Frammingham.
E. Tanda decompensatio cordis kanan dan kiri

Tanda kongesti vena pulmonalis (gagal jantung kiri)

• Dipsneu
• Ortopneu
• Wheezing atau ronki pada auskultasi paru
• Batuk
Tanda kongesti vena sistemik (gagal jantung kanan)
• Peningkatan tekanan vena jugularis
• Edema perifer : palpebra udem, udem tungkai
• Hepatomegali

F. Pemeriksaan Penunjang gagal jantung

o Pada EKG ditemukan hipertrofi ventrikel kiri, kelainan gelombang ST dan T
o Foto thoraks terdapat pembesaran jantung dan bendungan
 o Pada echocardiography terlihat pembesaran dan disfungsi ventrikel kiri, kelainan
bergerak katup mitral saat diastolik

G. Klasifikasi fungsional

Tanda kongesti vena pulmonalis (gagal jantung kiri)

o Dipsneu
o Ortopneu
o Wheezing atau ronki pada auskultasi paru
o Batuk
Pada pasien, decompensatio cordis termasuk klasifikasi fungsional C menurut AHA
dan klasifikasi fungsional III menurut NYHA.

H. Penatalaksanaan
2. Gastritis
A. Definisi
Gastritis is a condition in which the stomach lining—known as the mucosa—is
inflamed.

B. Penyebab
Helicobacter pylori (H. pylori) infection causes most cases of chronic nonerosive
gastritis. H. pylori are bacteria that infect the stomach lining. H. pylori are
primarily transmitted from person to person. In areas with poor sanitation, H.
pylori may be transmitted through contaminated food or water. In industrialized
countries like the United States, 20 to 50 percent of the population may be
infected with H. pylori. Rates of H. pylori infection are higher in areas with poor
sanitation and higher population density. Infection rates may be higher than
80 percent in some developing countries.
C. Gejala klinis
Many people with gastritis do not have any symptoms, but some people
experience symptoms such as
• upper abdominal discomfort or pain
• nausea
• vomiting
These symptoms are also called dyspepsia.
Erosive gastritis may cause ulcers or erosions in the stomach lining that can
bleed. Signs of bleeding in the stomach include
• blood in vomit
• black, tarry stools
• red blood in the stool.

D. Komplikasi
Most forms of chronic nonspecific gastritis do not cause symptoms. However,
chronic gastritis is a risk factor for peptic ulcer disease, gastric polyps, and
benign and malignant gastric tumors. Some people with chronic H. pylori
gastritis or autoimmune gastritis develop atrophic gastritis. Atrophic gastritis
destroys the cells in the stomach lining that produce digestive acids and enzymes.
Atrophic gastritis can lead to two types of cancer: gastric cancer and gastric
mucosa-associated lymphoid tissue (MALT) lymphoma.
E. Diagnosa
The most common diagnostic test for gastritis is endoscopy with a biopsy of the
stomach. The doctor will usually give the patient medicine to reduce discomfort
and anxiety before beginning the endoscopy procedure. The doctor then inserts
an endoscope, a thin tube with a tiny camera on the end, through the patient’s
mouth or nose and into the stomach. The doctor uses the endoscope to examine
the lining of the esophagus, stomach, and first portion of the small intestine. If
necessary, the doctor will use the endoscope to perform a biopsy, which involves
collecting tiny samples of tissue for examination with a microscope. Other tests
used to identify the cause of gastritis or any complications include the following:
• Upper gastrointestinal (GI) series. The patient swallows barium, a liquid
contrast material that makes the digestive tract visible in an x ray. X-ray images
may show changes in the stomach lining, such as erosions or ulcers.
• Blood test. The doctor may check for anemia, a condition in which the blood’s
iron-rich substance, hemoglobin, is diminished. Anemia may be a sign of chronic
bleeding in the stomach.
• Stool test. This test checks for the presence of blood in the stool, another sign
of bleeding in the stomach.
• Tests for H. pylori infection. The doctor may test a patient’s breath, blood, or
stool for signs of infection. H. pylori infection can also be confirmed with
biopsies taken from the stomach during endoscopy.

F. Tatalaksana
Medications that reduce the amount of acid in the stomach can relieve symptoms
that may accompany gastritis and promote healing of the stomach lining. These
medications include
• antacids, such as aspirin, sodium bicarbonate, and citric acid (Alka-Seltzer);
alumina and magnesia (Maalox); and calcium carbonate and magnesia (Rolaids).
Antacids relieve mild heartburn or dyspepsia by neutralizing acid in the stomach.
These drugs may produce side effects such as diarrhea or constipation.
• histamine 2 (H2) blockers, such as famotidine (Pepcid AC) and ranitidine
(Zantac 75). H2 blockers decrease acid production. They are available both over
the counter and by prescription.
 • proton pump inhibitors (PPIs), such as omeprazole (Prilosec, Zegerid),
lansoprazole (Prevacid), pantoprazole (Protonix), rabeprazole (Aciphex),
esomeprazole (Nexium), and dexlansoprazole (Kapidex). All of these drugs are
available by prescription, and some are also available over the counter. PPIs
decrease acid production more effectively than H2 blockers.
Depending on the cause of the gastritis, additional measures or treatments may
be needed. For example, if gastritis is caused by prolonged use of NSAIDs, a
doctor may advise a person to stop taking NSAIDs, reduce the dose of NSAIDs,
or switch to another class of medications for pain. PPIs may be used to prevent
stress gastritis in critically ill patients.
Treating H. pylori infections is important, even if a person is not experiencing
symptoms from the infection. Untreated H. pylori gastritis may lead to cancer or
the development of ulcers in the stomach or small intestine. The most common
treatment is a triple therapy that combines a PPI and two antibiotics—usually
amoxicillin and clarithromycin—to kill the bacteria. Treatment may also include
bismuth subsalicylate (Pepto-Bismol) to help kill bacteria. After treatment, the
doctor may use a breath or stool test to make sure the H. pylori infection is gone.
Curing the infection can be expected to cure the gastritis and decrease the risk of
other gastrointestinal diseases associated with gastritis, such as peptic ulcer
disease, gastric cancer, and MALT lymphoma.

3. Hipokalemi
A. Definisi
Hypokalemia can result from insufficient dietary potassium intake, intracellular
shifting of potassium from the extracellular space, extrarenal potassium loss, or
renal potassium loss (Table 21–3). Cellular uptake of potassium is increased by
 insulin and beta-adrenergic stimulation and blocked by alpha-adrenergic
stimulation. Aldosterone is an important regulator of total body potassium,
increasing potassium secretion in the distal renal tubule.
B. Etiologi
The most common cause of hypokalemia, especially in developing countries, is
gastrointestinal loss from infectious diarrhea. The potassium concentration in
intestinal secretion is ten times higher (80 mEq/L) than in gastric secretions.

Hypokalemia in the presence of acidosis suggests profound potassium depletion

and requires urgent treatment. Selflimited hypokalemia occurs in 50–60% of
trauma patients, perhaps related to enhanced release of epinephrine.
Hypokalemia increases the likelihood of digitalis toxicity. In patients with
heart disease, hypokalemia induced by beta-2-adrenergic agonists and
 diuretics may substantially increase the risk of arrhythmias. Numerous
genetic mutations affect fluid and electrolyte metabolism, including disorders of
potassium metabolism (Table 21–4). Magnesium is an important cofactor for
potassium uptake and maintenance of intracellular potassium levels. Loop
diuretics (eg, furosemide) cause substantial renal potassium and magnesium
losses. Magnesium depletion should be considered in refractory
hypokalemia.
C. Gejala Klinis
Muscular weakness, fatigue, and muscle cramps are frequent complaints in mild
to moderate hypokalemia.
D. Pemeriksaan Laboratorium
Urinary potassium concentration is low (< 20 mEq/L) as a result of extrarenal
loss (eg, diarrhea, vomiting) and inappropriately high (> 40 mEq/L) with renal
loss (eg, mineralocorticoid excess, Bartter syndrome, Liddle syndrome).
The transtubular [K+] gradient (TTKG) is a simple and rapid evaluation of net
potassium secretion. TTKG is calculated as follows:

Hypokalemia with a TTKG > 4 suggests renal potassium loss with increased
distal K+ secretion. In such cases, plasma renin and aldosterone levels are helpful
in differential diagnosis. The presence of nonabsorbed anions, such as
bicarbonate, increases the TTKG.
E. Temuan pada EKG
The electrocardiogram (ECG) shows decreased amplitude and broadening of T
waves, prominent U waves, premature ventricular contractions, and depressed
ST segments.
F. Penatalaksanaan
Oral potassium supplementation is the safest and easiest treatment for mild
to moderate deficiency. Dietary potassium is almost entirely coupled to
phosphate—rather than chloride—and is therefore not effective in
correcting potassium loss associated with chloride depletion from diuretics
or vomiting. In the setting of abnormal kidney function and mild to moderate
diuretic dosage, 20 mEq/d of oral potassium is generally sufficient to prevent
 hypokalemia, but 40–100 mEq/d over a period of days to weeks is needed to treat
hypokalemia and fully replete potassium stores.
Intravenous potassium is indicated for patients with severe hypokalemia and for
those who cannot take oral supplementation. For severe deficiency, potassium
may be given through a peripheral intravenous line in a concentration up to 40
mEq/L and at rates up to 10 mEq/h. Concentrations of up to 20 mEq/h may be
given through a central venous catheter. Continuous ECG monitoring is
indicated, and the serum potassium level should be checked every 3–6 hours.
Avoid glucose-containing fluid to prevent further shifts of potassium into the
cells. Magnesium deficiency should be corrected, particularly in refractory
hypokalemia.
Patients with unexplained hypokalemia, refractory hyperkalemia, or clinical
features suggesting alternative diagnoses (eg, aldosteronism or hypokalemic
periodic paralysis) should be referred for endocrinology or nephrology
consultation.
Patients with symptomatic or severe hypokalemia, especially with cardiac
manifestations, require cardiac monitoring, frequent laboratory testing,
and potassium supplementation.

From CMDT 2015 Page 868-870

Follow Up

Tanggal S O A P
15-09-16 Sesak nafas Kes : CM 1. Dekompensa 1. Dekompensasi
si Cordis FC Cordis FC III
+, sesak saat TD : 140/90
III - IVFD D5%
aktivitas N : 80 x/m 2. Gastritis 100 cc/24 jam
3. Hipokalemi - O2 2-4 lt/m
ringan dan S : 36,5 oC
jika sesak
saat istirahat, RR : 26 x/m - Ramipril 1 x
2,5 mg
nyeri dada -, Mata : ca -/-, si -/-
Asites dan udem
mudah lelah Leher : JVP tidak  belum
perbaikan
+, batuk +, meningkat
- Furosemide 3
mual +, Cor : BJ I dan II x 40 mg iv
2. Gastritis 
muntah -, normal, murmur -,
Belum perbaikan
nyeri ulu hati gallop – - Omz 1 x 40
mg iv
+, rasa penuh Pulmo : VBS kanan
- Sukralfat 3 x
pada perut +, = kiri, wh -/-, rales 10 ml
4. Hipokalemi
bengkak pada +/+
- KSR 1 x
kedua kaki +, Abd : cembung, BU 600 mg
BAB dan +, NT epigastrium
BAK tidak +,
ada keluhan Eks : edema
tungkai +/+

16-09-16 Sesak nafas + Kes : CM 1. Dekompensas 1. Dekompensasi

i Cordis FC Cordis FC III
berkurang, TD : 120/80
III - IVFD D5%
sesak saat N : 80 x/m 2. Gastritis 100 cc/24 jam
3. Hipokalemi - O2 2-4 lt/m
aktivitas S : 36,5 oC
jika sesak
ringan, nyeri RR : 24 x/m - Ramipril 1 x
2,5 mg
dada -, Mata : ca -/-, si -/-
Asites dan udem
mudah lelah Leher : JVP tidak  belum
perbaikan
+, batuk +, meningkat
- Furosemide 3
mual +, Cor : BJ I dan II x 40 mg iv
2. Gastritis 
muntah -, normal, murmur -,
Belum perbaikan
nyeri ulu hati gallop – - Omz 1 x 40
mg iv
+, rasa penuh
- Sukralfat 3 x
pada perut +, 10 ml
3.Hipokalemi
 bengkak pada Pulmo : VBS kanan - KSR 1 x
600 mg
kedua kaki +, = kiri, wh -/-, rales
BAB dan +/+
BAK tidak Abd : cembung, BU
ada keluhan +, NT epigastrium
+ berkurang
Eks : edema
tungkai +/+

17-09-16 Sesak nafas + Kes : CM 1. Dekompe 1. Dekompensasi

Cordis FC III
berkurang, TD : 110/80 nsasi
- IVFD D5%
sesak saat N : 84 x/m Cordis FC 100 cc/24 jam
- O2 2-4 lt/m
aktivitas S : 36,5 oC III
jika sesak
ringan, nyeri RR : 24x/m 2. Gastritis - Ramipril 1 x
2,5 mg
dada -, Mata : ca -/-, si -/- 3. Hipokale
Asites dan udem
mudah lelah Leher : JVP tidak mi  belum
perbaikan
+, batuk +, meningkat
- Furosemide 3
mual +, Cor : BJ I dan II x 40 mg iv
2. Gastritis 
muntah -, normal, murmur -,
Belum perbaikan
nyeri ulu hati gallop – - Omz 1 x 40
mg iv
-, rasa penuh Pulmo : VBS kanan
- Sukralfat 3 x
pada perut +, = kiri, wh -/-, rales 10 ml
3. Hipokalemi
bengkak pada +/+

kedua kaki +, Abd : cembung, BU perbaikan
- KSR 1 x
BAB dan +, NT epigastrium -
600 mg
BAK tidak Eks : edema
ada keluhan tungkai +/+

18-09-16 Sesak nafas + Kes : CM 1. Dekompensas 1. Dekompensasi

i Cordis FC Cordis FC III
berkurang, TD : 100/70
III - IVFD D5%
nyeri dada -, N : 88 x/m 2. Gastritis 100 cc/24 jam
3. Hipokalemia - O2 2-4 lt/m
batuk +, mual S : 36,5 oC
jika sesak
-, muntah -, RR : 22 x/m - Ramipril 1 x
2,5 mg
 nyeri ulu hati Mata : ca -/-, si -/- Asites dan udem
 belum
-, rasa penuh Leher : JVP tidak
perbaikan
pada perut + meningkat - Furosemide 3
x 40 mg iv
berkurang, Cor : BJ I dan II
2. Gastritis 
bengkak pada normal, murmur -, Belum perbaikan
- Omz 1 x 40
kedua kaki gallop –
mg iv
+/+ Pulmo : VBS kanan - Sukralfat 3 x
10 ml
berkurang, = kiri, wh -/-, rh +/+
3. Hipokalemi 
BAB dan Abd : cembung, BU Perbaikan
- KSR 1 x
BAK tidak +, NT epigastrium -
600 mg
ada keluhan Eks : edema
tungkai +/+

19-09-16 Sesak nafas + Kes : CM 1. Dekompe 1. Dekompensasi

nsasi Cordis FC III
berkurang, TD : 100/70
Cordis FC - IVFD D5%
nyeri dada -, N : 88 x/m III – IV 100 cc/24 jam
2. Gastritis - O2 2-4 lt/m
batuk +, mual S : 36,9 oC
3. Hipokale jika sesak
-, muntah -, RR : 20 x/m mi - Ramipril 1 x
2,5 mg
nyeri ulu hati Mulut : mukosa
Asites dan udem
-, rasa penuh lembab, lidah kotor  belum
perbaikan
pada perut + -
- Furosemide 3
berkurang, Cor : BJ I dan II x 40 mg iv
2. Gastritis 
bengkak pada normal, murmur -,
Belum perbaikan
kedua kaki gallop – - Omz 1 x 40
mg iv
+/+ Pulmo : VBS kanan
- Sukralfat 3 x
berkurang, = kiri, wh -/-, rh -/- 10 ml
-
BAB dan Abd : supel, BU +
BAK tidak normal, NT
ada keluhan epigastrium -

20-09-16 Sesak nafas + Kes : CM 1. Dekompe 1. Dekompensasi

nsasi Cordis FC III
berkurang, TD : 100/70
Cordis FC - IVFD D5%
nyeri dada -, N : 88 x/m III – IV 100 cc/24 jam
2. Gastritis
batuk +, mual S : 36,5 oC 3. Hipokale - O2 2-4 lt/m
mi jika sesak
-, muntah -, RR : 20 x/m
- Ramipril 1 x
nyeri ulu hati Mulut : mukosa 2,5 mg
Asites dan udem
-, rasa penuh lembab, lidah kotor
 belum
pada perut -, - perbaikan
- Furosemide 3
bengkak pada Cor : BJ I dan II
x 40 mg iv
kedua kaki normal, murmur -, 2. Gastritis 
Belum perbaikan
+/+ gallop –
- Omz 1 x 40
berkurang, Pulmo : VBS kanan mg iv
- Sukralfat 3 x
BAB dan = kiri, wh -/-, rh -/-
10 ml
BAK tidak Abd : supel, BU +
ada keluhan normal, NT -