Acute Pulmonary Edema

Oleh : dr. Faisol Siddiq

Stase IGD Internship RSUD Sleman
 Identitas Pasien
• Nama : Ny. H
• Jenis kelamin : Perempuan
• Umur : 68 th
• Alamat : Jetis, Donokerto Turi Sleman
• Pekerjaan : PNS
• Agama : Islam
• Tgl Masuk RS : 20 September 2015 pukul
04.00 via IGD
• No. RM : 2834**
• Pembayaran : BPJS
• Indikasi rawat inap : Terapi
 KELUHAN UTAMA

Sesak nafas yang memberat sejak

1 jam yang lalu.
Sesak nafas memberat sejak 1 jam yll. Sesak tidak
membaik dengan istirahat. Sesak nafas jika tidur
berbaring (+), Sesak malam hari (+). Riwayat
Hipertensi (+) tidak terkontrol, DM (+) tidak
terkontrol. Riwayat Alergi (-), Riwayat Asma (-),
Pembengkakan jantung (+)

OS pernah dirawat di RS dengan keluhan serupa.

KU: sedang, kesadaran compos mentis,
tampak sesak
Vital Sign
TD 180/110 mmHg, posisi berbaring, lengan kanan,
tensi jarum, manset dewasa
RR 29 kali/menit
N 110 kali/menit, simetris, ireguler, isi cukup, tegangan
kuat
T : afebris
Pemeriksaan Kepala Leher
Kepala
Inspeksi
Mata : conjunctiva anemis (-), sklera ikterik (-)
Hidung : epistaxis (-), suara sengau (-)
Mulut : mukosa kering (-), pucat (-), gusi berdarah (-), faring hiperemis (-
), tonsila dbn
Palpasi
Nyeri tekan (-)
Leher
Inspeksi
o Tekanan vena jugularis : 5 + 2
o Jejas (-)
Palpasi
o Limfonodi : tak teraba
o Massa (-)
 PEMERIKSAAN THORAX

Temuan Penting :
 RBB pada kedua paru, Kardiomegali
 Pemeriksaan extremitas

• Nadi kuat
• Akral hangat
• CRT < 2 detik
• Sianosis (-)
• Palmar eritema (-)
• Anemis (-)
• Edema tungkai (-/-)
• Clubbing finger (-)
 Resume pemeriksaan fisik

• TD 180/110
• RR 29 kali/menit
• Nadi 110 kali/menit reguler
• Thorax-paru : RBB paru bilateral
• Thorax-jantung : kardiomegali (+)
 DIAGNOSIS KERJA

Edema Pulmo Akut

CHF NYHA CF IV ec HHD
 Plan

Monitor KU dan vital sign

O2 NRM 10 lpm
EKG
GDS
Infus RL lini
DC
Inj. Furosemide 2A
EKG
 EKG

Irama : Sinus
Frekuensi : 110 kpm
Axis : dbn
Morfologi : T inverted
V3-V6, P mitral lead II
 Deviasi : LVH, LAH

GDS = 230 mg/dL

Ro Thorax
 Temuan Penting

Tampak corakan vaskular bertambah,

perselubungan inhomogen perihiler &
pericardial
CTR > 0.5
 DIAGNOSIS KLINIS

Edema Paru Akut

CHF e.c HHD dd IHD (Cek CKMB &
LDH)
DM2O tidak terkontrol
 TERAPI

Infus RL 0,9% mikro lini

Inj. Furosemide 2A dilanjutkan Drip
Furosemid 5A dalam 50 cc NaCl 0,9 % syringe
pump kecepatan 2.5cc/jam
KSR 1x1
Spironolacton 1x25 mg
Valsartan 1x4 mg
Inj. Pantoprazole 1A/24 jam
Simvastatin 1x10 mg
Aspilet 4x75 mg
CPG 4x80 mg
ISDN Sublingual 5 mg
 Pulmonary edema

Cardiogenic pulmonary edema (also termed

hydrostatic or hemodynamic edema)
Noncardiogenic pulmonary edema (also
known as increased-permeability pulmonary
edema)
Difficult to distinguish because of their
similar clinical manifestations
Microvascular Fluid Exchange
in the Lung
Fluid and solutes that are filtered from the
circulation into the alveolar interstitial space do not
enter the alveoli because the alveolar epithelium is
composed of very tight junctions
It moves proximally into the peribronchovascular
space
The lymphatics remove most of this filtered fluid
from the interstitium and return it to the systemic
circulation
Microvascular Fluid Exchange
in the Lung
Cardiogenic Pulmonary Edema
Increased hydrostatic pressure in the
pulmonary capillaries
elevated pulmonary venous pressure
increased left ventricular end-diastolic pressure
and left atrial pressure
As left atrial pressure rises further (>25 mm
Hg)
edema fluid breaks through the lung epithelium
flooding the alveoli with protein-poor fluid
Microvascular Fluid Exchange
in the Lung
Noncardiogenic pulmonary edema
increase in the vascular permeability of the lung
resulting in an increased flux of fluid and
protein into the lung interstitium and air spaces
 Classic Symptom

Interstitial edema causes dyspnea and

tachypnea
Alveolar flooding leads to arterial
hypoxemia
Cough and expectoration of frothy edema
fluid
 Stepwise Approach

The noninvasive approaches for diagnosis

will inevitably lead to the misclassification
of some patients
repeated and ongoing assessment is necessary
requiring simultaneous diagnosis and treatment
10 percent of patients with acute pulmonary
edema have multiple causes of edema
 Laboratory Testing

BNP is secreted predominantly by the cardiac

ventricles in response to wall stretch or increased
intracardiac pressures
BNP level below 100 pg per milliliter indicates
that heart failure is unlikely (negative predictive
value, >90 percent)
BNP level greater than 500 pg per milliliter
indicates that heart failure is likely (positive
predictive value, >90 percent)
 Laboratory Testing

BNP levels between 100 and 500 pg per milliliter

provide inadequate diagnostic discrimination
BNP can also be secreted by the right ventricle,
and moderate elevations have been reported in
patients with acute pulmonary embolism, cor
pulmonale, and pulmonary hypertension
Chest Radiography
 Example X-Ray of Kerley B Lines

Kerley B lines are caused by peri-vascular edema, with a base

on the pleural surface of the lung and extending horizontally a
variable, but usually short, distance toward the center of the
chest.

Source Unknown
 Echocardiography

The first approach to assessing left

ventricular and valvular function in patients
in whom the history, physical and laboratory
examinations, and the chest radiograph do
not establish the cause of pulmonary edema
Less sensitive in identifying diastolic
dysfunction
Does not rule out cardiogenic pulmonary
edema
 Pulmonary-Artery
Catheterization
Assess the pulmonary-artery occlusion pressure
Is considered the gold standard for determining the
cause of acute pulmonary edema
Monitoring of cardiac filling pressures, cardiac
output, and systemic vascular resistance
Common complications included hematoma at the
insertion site, arterial puncture, bleeding,
arrhythmias, and bloodstream infection
Measurement of central venous pressure
should not be considered a valid substitute
for pulmonary-artery catheterization
available data suggest that there is often a poor
correlation between the two
 Guidelines

There are currently no published guidelines

from professional societies between
cardiogenic and noncardiogenic pulmonary
edema
 Conclusions and
Recommendations
Treatment can be provided while the
diagnostic steps are taken
begin with a careful history and physical
examination
chest radiograph
electrocardiogram
measurement of plasma BNP
transthoracic echocardiogram
pulmonary-artery catheter
 Edema Paru Akut

Edema paru akut adalah timbunan cairan di

pembuluh darah dan parenkim paru yang
pada sebagian besar kasus disebabkan oleh
gagal jantung akut.
Gagal jantung akut adalah penurunan fungsi
jantung yang mendadak dengan atau tanpa
didahului kelainan jantung.
 Penyebab edema pulmo akut terbanyak
adalah karena SINDROMA KORONER
AKUT dan HIPERTENSI.
 Tanda & Gejala

Tergantung berat ringannya gagal jantung.

Sesak saat aktifitas
Sesak bila berbaring
Iktus bergeser ke lateral
Ronki basah basal bilateral paru
Batwing appearance pada foto polos
Terapi
Tatalaksana Edema Paru
Akut
 Refferensi

Pulmonary edema: pathophysiology and

diagnosis. NCBI. 2011
Advance Cardiac Life Support. 2015
Thanks for your attention