Cardiac Pulmonary Edema

Oleh: Abdurahman Wahid, S.Kep, Ns

Introduction
Kasus ini sering ditemukan di IRD.
Biasanya ditemukan pada pasien gagal jantung.
Mortality Rate ranging 15-20%.
Definition
Pulmonary edema yang terjadi akibat
peningkatan tekanan hidrosatik kapiler
sekunder dari peningkatan tekanan vena
pulmonalis
Pathophysiology mechanisms:
Ketidakseimbangan mekanisme Starling

Kerusakan epitel alveoli
Sumbatan Lymphatic
Idiopathic (unknown) mechanism
Q = K(P
cap
- P
is
) - l(P
cap
- P
is
)
The Starling relationship
Q = K(P
cap
- P
is
) - l(P
cap
- P
is
),
Q is net fluid filtration;
K is a constant called the filtration coefficient;
P
cap
is capillary hydrostatic pressure, which tends to force fluid out of the
capillary;
P
is
is hydrostatic pressure in the interstitial fluid, which tends to force
fluid into the capillary;
l is the reflection coefficient, which indicates the effectiveness of the
capillary wall in preventing protein filtration;
the second P
cap
is the colloid osmotic pressure of plasma, which tends
to pull fluid into the capillary;
the second P
is
is the colloid osmotic pressure in the interstitial fluid,
which pulls fluid out of the capillary.
Pengaruh Kerusakan Jantung Terhadap
Edema Paru
Obstruksi aliran atrium
Disfungsi Sistolik Ventrikel kiri
Disfungsi Diastolik Ventrikel kiri
Disritmia
Hypertropi ventrikel kiri
Overload volume ventrikel kiri
Infark Miokard
Sumbatan aliran ventrikel kiri
Meliputi dinding kapiler dan
alveoli
Bagian terpenting, adalah
interstitial space yang
terdapat antara dinding
kapiler dan alveoli
Drainase via pembuluh
lymphe.
Proses Pertukaran gas dan aliran
limfatik
Regulasi Cairan
Ingat kembali konsep starling:
Pulmonary capillary pressure is normally 8-12 mm Hg.
Colloid osmotic pressure is 28 mm Hg.
Peran Limfatik
removing solutes, colloid, and liquid from the interstitial
space at a rate of approximately 10-20 mL/h
in the presence of chronically elevated LA pressure, the
rate of lymphatic removal can be as high as 200 mL/h
Tahapan Pulmonary Edema
Tahap I Tahap II Tahap III
Terjadi peningkatan
tekanan tekanan
Atrium kiri.Tidak
terjadi gangguan
dalam pertukaran gas
Cairan dan coloid
mulai memasuki
interstitium namun
sistem limfatik masih
bisa membuang
kelebihan cairan.
Pada tahap ini
mungkin sudah
muncul gejala ringan
pada jalan nafas
Pada tahap ini terjadi
akumulasi cairan
lebih dari 500 cc di
ruangan intersitial.
Pada fase ini cairan
sudah masuk ke
alveoli.
ALVEOLAR
FLOODING !!
Sudah terlihat
gangguan pertukaran
gas
History
Patients develop a sudden onset of extreme
breathlessness, anxiety, and feelings of
drowning.
Munculnya gejala batuk merupakan
penanda CPE pada pasien dengan
disfungsi ventrikel kiri
Sputum berbusa dan kemerahan
Pemeriksaan Fisik
Sitting upright, lapar udara, agitasi, cemas,
diaphoresis
Hypertension sering muncul terutama akibat kondisi
hyperadrenergik. Hypotension menandakan
masalah pada LV
Auskultasi
Paru: rhonki basah terutama pada sisi terbawah paru
Jantung: S3 ==> menandakan CPE berasal dari jantung
Pasien dengan kelainan ventriel kanan biasanya
menunjukkan tanda tanda gagal jantung kanan;
oedema, hepatomegali
Lab
Complete blood count
Serum electrolyte measurements
Blood urea nitrogen (BUN) and creatinine
determinations
Pulse oximetry
Arterial blood gas analysis
Electrocardiography
Plasma BNP and NT-proBNP Testing
(BNP) and N -terminal proBNP (NT-proBNP)
synthesized by cardiac myocytes.
BNP cutoff value of 100 pg/mL .
Values of 100-400 pg/mL may be related to various
pulmonary conditions
NT-proBNP
NT-proBNP has a longer half-life (120 min)
than that of BNP (20 min).
The cutoff value > 450 pg/mL (<50 years)
BNP 100 pg/mL
NT-proBNP is less accurate than BNP in
patients older than 65 years.
Echo
For identifying a mechanical etiology :
Acute papillary muscle rupture
Acute ventricular septal defect
Cardiac tamponade
Contained LV rupture
Valvular vegetation with resulting acute severe
mitral, aortic regurgitation
Management
ABCs of resuscitation.
Medical treatment focuses on 3 main goals:
reduction of pulmonary venous return
(preload reduction).
reduction of systemic vascular resistance
(afterload reduction).
inotropic support.
Preload Reduction
Nitroglycerin;
iV NTG, mulai dengan 10mcg/min kemudian dapat ditingkatkan hingga
100mcg/min. alternative NTG diberikan 3 mg IV boluses setiap 5 menit
Diuretics ;
Premedication with drugs that decrease preload (eg, NTG) and afterload (eg,
angiotensin-converting enzyme [ACE] inhibitors) before the administration of
loop diuretics can prevent potential adverse hemodynamic changes.
Morphine sulfate
Afterload Reduction
ACE inhibitors;
Enalapril 1.25 mg IV or captopril 25 mg, given sublingually.
Angiotensin II receptor blockers
Nitroprusside
Catecholamines
Dobutamine , Dopamine
Norepinephrine;
Norepinephrine is generally reserved for patients with profound hypotension (eg,
systolic blood pressure < 60 mm Hg).
Phosphodiesterase inhibitors
Calcium sensitizers;
Thank You