Saraf

Otonom

Simpatis
(reseptor Parasimpatis
adrenergik) (reseptor
kolinergik)
Simpato Simpatoli
mimetik tik
Muskari- Nikoti- Muskari-
nik nik nik
agonis agonis antagonis
 Reseptor yang
menerima signal dari
SSP menuju target
organ
 2 tipe reseptor
adrenergik:
› α-adrenergik
› Β-adrenergik
 Beta-Blocker (propanolol, metoprolol)
 Alpha-Blocker (prazosin, fentolamin)
 Bekerja sentral (metildopa, klonidin)
 Penghambat saraf adrenergik (reserpin,
guanetidin)
 Penghambat reseptor alfa dan beta(labetolol)
 Penghambat ganglion simpatis (trimetafan)
 Antagonis norepiphephrine and epinephrine
pada adrenoceptors β  afinitas
adrenoceptor β terblokade
 Angina pectoris / post myocard infark 
resepor Beta dihambat kontraktilitas
jantung akan menurun  frek menurun jadi:
› β-bloker : Menurunkan konsumsi O2 jantung 
kerja jantung ringan  mencegah stress
miokardial  mencegah serangan iskemik
 Takikardi
› β-bloker : menurunkan frek denyut jantung
 Hipertensi
› β-bloker : menurunkan resistensi perifer
 Glaukoma
› β-bloker : Menurunkan produksi aqueous humor
 Anxiolytic (Anti cemas)
› β-bloker : Menghambat epinefrin menurunkan
respon somatik (ex: palpitasi, gemetar, keringat
banyak)
 Hipertiroidism
› Mengontrol aritmia dan takikardia
 pharm properties
› variations in:
 Cardioselectivity (Non selective & selective)
 Membrane-stabilizing effects (local anestesi)
 Intrinsic sympathomimetic activity (some are partial
agonists)
 Lipid solubility
› these variations are generally of little clinical
significance
 2 important ones are lipid and agonist properties
 Propranolol was the first beta-blocker to enter
widespread use
 Propranolol is a non-selective beta-blocker,
demonstrating equal affinity for both beta1-
and beta2-receptors.
 Other : nadolol, timolol, and pindolol.
 Nonselective beta-blockers exert a wider
variety of extracardiac manifestations.
› metoprolol, esmolol, acebutolol, atenolol,
betaxolol
› relative selectivity for B1 receptor
› theoretically cause less bronchoconstriction and
peri vasodilation
 lose selective effects at higher doses
• lipophilic
• propanolol, metoprolol, oxprenolol, bisoprolol,
carevdilol
• readily absorbed from GI, metabolized in liver
• large volume of distrib, and penetrate BBB well
• hydrophilic
• acebutolol, atenolol, betaxolol, carteolol, nadolol.
sotalol
• less readily absorbed, not extensively metabolized
• long plasma half-lives
• = hepatic failure prolong t1/2 lipo, renal failure
prolongs hydrophilic
 “intrinsic sympathomimetic activity (ISA)
› acts as a partial agonist or partial antagonist.
› pindolol, alprenolol, acebutolol, carteolol,
dilevalol, oxprenolol
› cause little or no resting heart rate depression,
but block increased rate due to exercise
 useful if patient is naturally bradycardic at
rest
HIPERTENSI
 Hipertensi ditandai dengan peningkatan TD
sistolik >120mmHg dan TD diastolik
>90mmHg
 90% hipertensi essensial  tdk diketahui
secara pasti penyebabnya
 Insidensinya 4x lebih berisiko pada orang
kulit hitam
 Jenis kelamin laki-laki, usia, obesitas, gaya
hidup, rokok, alkohol  risiko meningkat
 Menurunkan curah jantung
› Beta blocker
› Penghambat syaraf adrenergik
 Menurunkan volume darah
› diuretik
 Menurunkan resistensi perifer
› Vasodilator
› ARB / AIIRA  menurunkan/ menghambat pembentukan
Angiotensin II.
› Calsium chanel blocker
› ACE inhibitor
› Penghambat reseptor alfa-adrenergik
› Obat yang bekerja sentral
 ACE inhibitor, ARB
(AIIRA), Alfa-blocker
 Beta-blocker
 CCB
 Diuretik

https://pathways.nice.org.uk/hypertension/management
 Congestive Heart Failure
› β-bloker : menghambat aktivitas saraf simpatis utk
mempertahankan stoke volume
 Asma Bronkhial
› β-bloker non selektif menyebabkan
bronkhokonstriksi
 Respon Vaskular berlebih
› β-bloker non selektif menghambat kerja β2 
vasokonstriksi yang berlebihan  akral dingin
 Bradikardi dan AV blok
› β-bloker menurunkan denyut jantung berlebih
dan menghambat konduksi atrial ke ventrikel
 Hypoglycemia pada diabetes mellitus
› β-bloker : menghambat pelepasan cadangan
glukosa hepar yang diinduksi oleh epinefrin
 Manifestations : bradycardia, hypotension,
arrhythmias, hypothermia, hypoglycemia, and
seizures.
 The presentation may range from
asymptomatic to shock.
 The goal of therapy in beta-blocker toxicity is
to restore perfusion to critical organ systems
by increasing cardiac output. This may be
accomplished by improving myocardial
contractility, increasing heart rate, or both
 Prognosis is largely dependent on the initial
response to therapy (6-12 h postingestion)
 Resusitasi cairan: If the patient is hypotensive, administer
20 mL/kg of isotonic intravenous fluids and place the
patient in the Trendelenburg position.
 inotropes and chronotropes : epinephrine and atropine,
for hypotension and bradycardia
 Glucagon can enhance myocardial contractility, heart
rate, and atrioventricular conduction
 Gastric lavage may be beneficial if the patient presents to
the ED within 1-2 hours of ingestion
 Multi-dose activated charcoal (MDAC) may be useful in
reducing bioavailability of nadolol and sotalol, probably
by removal of the drug through the enterohepatic
circulation.
 Hemodialysis may be useful in severe cases of atenolol
overdoses because atenolol is less than 5% protein bound
and 40-50% is excreted unchanged in urine. Nadolol,
sotalol, and atenolol (hidrophilic) are removed by
hemodialysis. Acebutolol is dialyzable. Propranolol,
metoprolol, and timolol (lipophilic) are not removed by
hemodialysis.
 Insulin : The currently recommended regimen
is a 1 U/kg of an insulin bolus followed by
continuous infusion of 1-10 U/kg/h, but
boluses of up to 10 U/kg and continuous
infusions as high as 22 U/kg/h have been used
with good outcomes and minimal adverse
events.
 Dextrose supplementation is typically
required to maintain euglycemia
 Monitoring : physical examinations, serial
electrocardiograms, and continuous
measurement of urinary output
 End points of therapy may include the
following:
› Heart rate >60 beats per minute (dr ranti
bilangnya 50-_-)
› Blood pressure >90 mm Hg systolic
› Evidence of good organ perfusion (improved
mentation or urine output)
Efek Positif
 Beta-blocker + diuretika  target terapi
Hipertensi lbh baik, mencegah postural
hipotensi dan tachycardi yang disebabkan
oleh diuretika (thiazide)
 B-bloker + hydralazine (vasodilator) 
mengurangi reflex tachycardi
 B-bloker + quinidine (anti-aritmia) 
mencegah atrial fibrilasi
Efek Positif
 Beta-blocker + neuromuskular-blockers,
(Succinycholine, Decamethonium)  sinergis
 B-bloker + Nitrat (anti angina)  sinergis,
menurunkan HR, meringankan kerja jantung
Efek Negatif
 B-bloker + prokainamide (antiaritmia) 
hipotensi
 B-bloker + alfa agonis (norepinefrin) 
vasokonstriksi berlebihan  ganggren
 B-bloker + Antiinflamasi (Natrium salisilat,
Fenilbutazon)  menurunkan potensi
antiinflamasi
 B-bloker + tembakau  antagonistik, perlu
peningkatan dosis b-bloker