THE PHARMACOLOGY OF

ADRENERGIC RECEPTORS

M.T. Piascik

This study guide will facilitate the understanding of sympathomimetics and

sympatholytics and the adrenergic receptors at which these drugs interact.
The educational goal is to understand the uses in dental practice of drugs
that interact at the adrenergic receptors as well as toxicities that could
occur as a result of these interactions. In addition, dental patients are likely
to be taking drugs that act at these receptors. The presence of these drugs
could modify the actions of drugs prescribed in dental practice as well as
produce interactions that could have serious consequences.

Learning Objectives, Lecture I

1. Integrate pharmacodynamic principles to understand the actions of drugs

that interact with the adrenergic receptors and how these interactions are
relevant to dental practice.

2. Understand the effects of epinephrine and norepinephrine on the

cardiovascular system.

3. Understand the rationale and potential toxicities for the use of

epinephrine in dental practice.

4. Understand the mechanisms for drug interactions involving drugs used in

cardiovascular therapeutics as they relate to dental practice.

Key drugs
Epinephrine - Adrenalin
Norepinephrine- Levophed
PROPOSED
BINDING OF
NE TO THE
BETA
RECEPTOR

The adrenergic receptors which subserve the response of the sympathetic

nervous system have
been divided into two discrete subtypes: alpha adrenergic receptors (alpha
receptors) and beta adrenergic receptors (beta receptors). The
classification of these receptors, and indeed receptors in general, is based
on the interaction of agonists and antagonists with the receptors. The
actions of epinephrine, widely used in combination with local anesthetic
drugs, are produced as a result of interactions with these receptors.
Beta Receptor Systems

Most tissues express multiple receptors. However, the dominant beta

receptor in the normal heart is the beta1 receptor while the beta2 receptor is
the dominant regulatory receptor in vascular and non vascular smooth
muscle. Epinephrine activates both the beta1 and beta2-receptors.
Norepinephrine activates only the beta1-receptor.

Effect of Beta1 Receptor Activation on the Heart: Activation of the beta1

receptor leads to increases in contractile force and heart rate. Drugs that
activate the beta1 receptor can be used in heart failure to improve the
contractile state of the failing heart. Drugs that activate the beta1 receptor
also increase heart rate. Indeed, excess stimulation the beta1 receptor can
induce significant increases in heart rate and arrhythmias. Arrhythmias
are a major concern with drugs such as epinephrine that can be absorbed
systemically after intra-oral injection.
Effect of Beta2 Receptor Activation on Smooth Muscle: Activation of
the beta2 receptor leads to vascular and nonvascular smooth muscle
relaxation. Drugs that activate the beta2 receptor can be used to treat as
asthma (by relaxing airway smooth muscle) and premature labor (by
relaxing uterine smooth muscle).
ALPHA RECEPTORS SYSTEMS:

The receptor mediating the vasconstrictor actions of catecholamines is

referred to as an alpha receptor.
Alpha receptors have been further subdivided into alpha1 and alpha2
receptors. Both epinephrine and norepinephrine activates both the alpha1
and alpha2 receptors.

Presynaptic Alpha2 Receptors

Alpha2 receptors also exist presynaptically associated with nerve terminals.
Activation of these receptors inhibits the release of norepinephrine.
Norepinephrine acts at presynaptic alpha2 receptors to inhibit its own
release.

Norepinephrine acts at presynaptic alpha2 receptors to inhibit its own release.

Postsynaptic Alpha1 Receptors on Vascular Smooth Muscle:

Associated with vascular smooth muscle are a large number of alpha1

receptors relative to beta2 receptors. Activation of these receptors by
sympathetic nervous system transmission or drugs will result in
vasoconstriction and an increase in peripheral resistance and systemic
arterial blood pressure.
Applications to Therapeutics
Oral dosing of norepinephrine or epinephrine is not possible due to the
rapid metabolism of catechol nucleus in gastrointestinal mucosa and liver.
Therefore, these agents are given I.V., I.M., topically and in aerosol sprays.

Epinephrine is often used in combination local anesthetic agents to prolong

the duration of anesthetic action. This would include articaine, bupivacaine
or lidocaine. This combination is used because epinephrine can induce
vasoconstriction thus limiting the diffusion of the local anesthetic from the
site of injection. This not only prolongs the actions of the local anesthetic
but also to reduce the toxicity of the local anesthetic by limiting its systemic
absorption. Lidocaine in toxic doses can produce cardiac arrthythmias and
convulsions.
Epinephrine can also be topically applied in surgical procedures to induce
vasoconstriction and thus reduce blood loss. Epinephrine is used in the
treatment of shock and in emergency situations related to bronchial
asthma.

Clinical studies have shown that epinephrine blood levels increase

following its intraoral administration. The risk of this increase is dependent
on characteristics of the patient. For example, hypertensive patients or
those with other cardiovascular disease or patients taking other drugs that
affect sympathetic nervous system function are at higher risk than patients
without these conditions. Systemically absorbed epinephrine could also
increase heart rate and exacerbate cardiac rhythm disturbances or
myocardial ischemia.
Learning Objectives Lecture II

1. Understand the potential sites of action for sympathomimetics and the

difference between a direct and indirect acting agonist.

2. Understand the pharmacologic actions and therapeutic actions of drugs

that act at the beta1 and beta2 -adrenergic receptors as well as the alpha1 -
adrenergic receptor.

3. Know the mechanism of action and effects of amphetamine and cocaine.

4. Understand how the pressure of sympathomimetics alters the dental

management of patients.

Key Drugs*
Amphetamine-Adderall
Albuterol - Ventolin - 13th leading prescription drug in the US in 2003-
source- rxlist.com
Cocaine
Dopamine - Intropin
Methylphenidate - Ritalin - 102nd leading prescription drug in the US in
2003- source- rxlist.com
Phenylephrine - Neosynephrine

* A more complete list of sympathomimetics and their trade names can be

found on p. 110-111 of the Yagiela text.

Sympathomimetics: synthetic analogs of naturally occurring

catecholamines that mimic the actions of the endogenous
neurotransmitters. These agents can be divided into direct and indirect
acting sympathomimetics.

1. Direct acting agonists or antagonists can act at postsynaptic receptors.

2. Indirect acting agonists release neurotransmitters from presynaptic nerve

terminals to produce a sympathomimetic effect.

3. Inhibition of the membrane uptake of catecholamines by drugs such as

cocaine and tricyclic antidepressants produce a sympathomimetic effect.

4. Inhibition of monoamine oxidase by drugs such as Tranylcypromine.

SYMPATHOMIMETICS ACTING AT BETA RECEPTOR SYSTEMS

EXAMPLES:
Dopamine
Dobutamine
Beta2 agonists

Uses of Dopamine and Dobutamine

Congestive heart failure and cardiogenic shock.

In congestive heart failure, the failing heart is not able to eject blood as
efficiently as the normal heart. As a result there is a decrease in cardiac
output which triggers a host of compensatory actions. These include fluid
retention, vasoconstriction, an increase in peripheral vascular resistance,
an increase in the levels of circulating catecholamines and tissue hypoxia.
Dopamine and dobutamine activate the myocardial beta1 receptor and thus
increase the force of contraction of the failing heart. This will result in an
increase in cardiac output. These drugs are reserved for use in the acute
management of heart failure.

SELECTIVE BETA2 AGONISTS

These agents have a higher affinity (lower equilibrium dissociation
constant) for beta2 receptors when compared to beta1. Therefore, they
selectively activate beta2 receptors when compared to beta1.

Uses
1. Airways dysfunction; bronchial asthma, chronic bronchitis, emphysema
In airways dysfunction, beta2 selective agonists relax airways thus
decreasing airways resistance.

2. Premature labor
In premature labor, the beta2 selective agonists relax uterine smooth
muscle. Drugs that relax uterine smooth muscle are referred to as tocolytic
agents.

Side effects related to dental practice

1. Xerostomia, with inhaler usage.

ALPHA1 AGONISTS

Direct Acting Agents

These are synthetic agents that directly activate the alpha1 -adrenergic
receptor. These structural modifications of the parent catecholamine
nucleus result in drugs that are orally active and have longer plasma half-
lives. However, these same modifications result in lower affinity for the
receptor than do the endogenous agonists (epinephrine or norepinephrine).
There are two structural classes of alpha1 agonists phenethylamines which
are closely aligned in structure to epinephrine and the imidazolines,
compounds structurally unrelated to epinephrine. Levonordeferin is a
phenyethylamine that has been used in dental practice in combination with
local anesthetics.

Uses
1. Hypotension-to increase blood pressure during a surgical procedure
where a general anesthetic has induced hypotension

2. Ophthalmic preparations-to induce mydrasis also in topical preparations

for symptomatic release of eye irritation.

3. Cough and cold preparations-Induces constriction of nasal mucosa

decreases resistance to air flow.

Indirect Acting Sympathomimetics

These agents require the presence of endogenous catecholamines to
produce their effects. They have little activity if catecholamines are
depleted.

Cocaine: Blocks reuptake of monoamines into nerve endings. Cocaine

also has local anesthetic activity.

Amphetamine: Promotes the release of NE from nerve endings.

Amphetamine can also block the reuptake of norepinephrine.

Amphetamine-like compounds

1. Methylphenidate

A major site action of cocaine, amphetamine and amphetamine-like agents

is in the CNS. These drugs produce a feeling of well being and euphoria.
As a result the drugs carry a significant abuse liability. Both cocaine and
amphetamine are on the FDA schedule 2.

Uses of Cocaine (# 1 below), Amphetamine and Amphetamine-like

agents (2-4 below)

1. Cocaine has limited use as a local anesthesic and vasoconstrictor in

surgical procedures involving oral, laryngeal or nasal cavities.

2. Appetite suppression

3. Hyperactivity in children

4. Narcolepsy
Cautions Relevant to Dentistry

1) Cocaine and amphetamine-like agents (tricyclic antidepressants as well)

could potentiate the effects of direct acting agonists such as epinephrine.
Recall that epinephrine can be absorbed systemically after intraoral
administration. This epinephrine can be taken up by nerve terminals and
this uptake contributes to the the termination of the actions of epinephrine.
Thus, the risk of hypertension and other problems associated with systemic
absorption of epinephrine will be greater in patients taking cocaine or
amphetamine-like drugs.

2) An analog of amphetamine, methamphetamine, is produced illegally and

is a widely abused substance. Methamphetamine can be produced from
over the counter cough and cold medications such as pseudoephedrine.
Lithium, muriatic acid, sulfuric acid, red phosphorus and lye are used in this
preparation. When smoked these highly corrosive agents are vaporized
resulting in significant damage to teeth and gums.

Sympatholytics: synthetic analogs which bind to beta or alpha receptors

or act through other mechanisms to block the actions of endogenous
neurotransmitters or other sympathomimetics.

Learning Objectives Lecture III

1. Review the pharmacodynamic properties and characteristics of

antagonists.

2. Understand the pharmacologic properties and therapeutic uses of

clonidine, prazosin analogs, the beta blockers and MAO-inhibitors.

3. Understand the special precautions that exist for sympatholytic drugs in

dental practice.

Key Drugs*

Atenolol - Tenormin and various trade names - 4th leading prescription

drug in the US in 2003- source- rxlist.com
Clonidine - Minipres, various trade names
Propranolol - Inderal - various trade names
Terazosin - Hytrin

* A more complete list of sympatholytics and their trade names can be

found on p. 123 of the Yagiela text.
ALPHA2 AGONISTS AS SYMPATHOLYTICS
Clonidine

Actions and Therapeutic Uses

1. This drug stimulates alpha2 receptors in the nucleus tractus solitarius
(NTS) to decrease sympathetic outflow to the heart and blood vessels.

2. The decrease in sympathetic tone results in a decrease in peripheral

vascular resistance.

3. Clonidine is used in dental practice in the management of chronic pain. It

can be given orally or in patch form. Clonidine is a second-line
antihypertensive that has many other uses including opiate withdrawal,
nicotine withdrawal, vascular headaches, diabetic diarrhea, glaucoma,
ulcerative colitis and Tourette's syndrome.

Side Effects
The use of clonidine may result in clinical symptoms related to dry mouth,
such as difficulty in swallowing and speech. Chronic use of xerostomia-
producing drugs is associated with a higher incidence of oral candidiasis
and dental caries.

SELECTIVE ALPHA1-ANTAGONISTS
Prazosin and analogs, terazosin, doxazosin, trimazosin.

Effects on the Cardiovascular System:

1. Relaxes arterial and venous smooth muscle as well as nonvascular
smooth muscle.

2. Decreases peripheral vascular resistance and venous return with a

resultant decrease in systemic arterial blood pressure.

Uses
1. Hypertension

2. Benign prostatic hypertrophy

Tamsulosin specifically blocks the alpha1-receptor associated with the

prostate and is used to treat benign prostatic hypertropy.

The Relevance of Orthostatic Hypotension to Dental Practice

Orthostatic hypotension is a problem with prazosin analogs and to a lesser
extent tamsulosin. Significantly, orthostatsis is a problem that can be seen
with any vasodilator that affects the tone on venous smooth muscle. This
would include, organic nitrates, hydralazine, clonidine, minixodil and
the many drugs used to treat impotence. Orthostatic hypotension or
postural hypotension occurs when systemic arterial blood pressure falls by
more than 20 mmHg upon standing. In this situation, cerebral perfusion
falls and an individual may become light headed, dizzy or pass out. In
changing from the supine to the standing position, gravity tends to cause
blood to pool in the lower extremities. However, several reflexes, including
sympathetically mediated venoconstriction minimize this pooling and
maintain cerebral perfusion. If these reflex actions do not occur, then
orthostatic hypotension could result. By blocking the alpha1-receptors
associated with venous smooth muscle, prazosin-like drugs, inhibit the
sympathetically mediated vasoconstriction associated with postural
changes. Hence, orthostatic hypotension can occur. Drugs like clonidine
cause orthostasis due to its CNS actions that block the sympathetic
reflexes. Vasodilators such as nitrates, minoxidil, hydralazine or impotence
medications cause orthostasis because of their actions directly on the
vasculature. A consideration for patients being treated with some
sympatholytics is the patient's position during and after dental
procedures. Suddenly standing upright after being in a supine position in
the dental chair is very apt to cause syncope.

BETA ADRENERGIC RECEPTOR BLOCKERS

Cardiovascular Uses
Hypertension, ischemic heart disease, supraventricular
tachyarrhythmias.

1. These drugs are competitive antagonists of the beta adrenergic

receptors

2. Beta blockers are either selective for the beta1 receptor or nonselective
beta1 and beta2
antagonists.
3. Propranolol is the prototype Beta Blocker as well as the prototype of a
nonselective beta blocker.

4. By blocking the myocardial beta1 receptor beta blockers, a) decrease the

force and rate of myocardial contraction, b) Decreases renal renin secretion
with the net result of c) decreasing systemic arterial blood pressure

5. A major disadvantage of nonselective beta blockers is the fact that they

will block beta2
receptors associated with airway or vascular smooth muscle. This is a
problem in treating patients with airway dysfunction or peripheral vascular
disease such as alpha1 adrengeric
receptor-mediated vasoconstrictor tone will be unoppsed by the beta2
receptors. To overcome this disadvantage, antagonists that selectively
block the beta1 receptor have been developed.

6. Atenolol is the prototype selective beta1 receptor beta blocker.

Applications to Dentistry
Because nonselective β-blockers block β2-receptor mediated
vasodilation, there is a risk of a hypertensive episode following
administration of local anesthetic agents that contain epinephrine. In this
situation, the vasoconstrictor actions of epinephrine at α1 -receptors are
not opposed by the vasodilatory actions of β2-receptors resulting in an
exaggerated blood pressure response that could be deleterious in patients
with hypertension or ischemic heart disease.

Side Effects
1. Sedation, fatigue

2. Exacerbation of peripheral vascular disease, airway dysfunction

Monoamine Oxidase Inhibitors

1. These drugs inhibit monoamine oxidase and are used as
antidepressants in psychiatric practice.

2. A side effect that is not clearly understood is that these drugs can also
produce hypotension.

3. Can precipitate a hypertensive crisis. Patients taking MAO inhibitors

must not be given
drugs that have indirect sympathomimetic activity or are inactivated by
MAO. Occasionally,
the dentist may find reason to use the vasoconstrictor phenylephrine.
Because it causes even
a minor release of norepinephrine from adrenergic nerves and is subject to
metabolism by MAO,
phenylephrine must be avoided in patients taking MAO inhibitors.
Epinephrine and levonordefrin, which are most commonly found in local
anesthetic solutions, are not contraindicated, since they are direct agonists
and are largely inactivated by catechol-O-methyltransferase. Nonetheless,
the avoidance of hemostatic preparations containing high concentrations of
epinephrine is
recommended.

4. Opioids and other CNS depressants should be used cautiously and

usually at lower doses in
patients who are taking MAO inhibitors. Meperidine is absolutely
contraindicated. The dentist
should reinforce the physician's instructions to the patient about dietary
restrictions and
contraindications of several drugs for patients taking MAO inhibitors.

Uses
1. Hypertension

2. Depression
The following is a list of trade names for the drugs mentioned in this
handout. It is provided for your information.

Epinephrine Adrenalin Chloride

Phenylephrine Neo-synephrine
Isoproterenol Isuprel
Norepinephrine Levophed
Methoxamine Vasoxyl
Metaraminol Aramine
Clonidine Catapres
Methyldopa Aldomet
Guanabenz Wytensin
Oxymetazoline Afrin
Naphazoline Naphcon Forte Ophthalmic
Tetrahydrozoline Tyzine
Prazosin Minipress
Terazosin Hytrin
Doxazosin Cardura
Acebutolol Sectral
Atenolol Tenormin
Betaxolol Betopic, Kerlone
Bisoprolol Zebeta
Esmolol Brevibloc
Metoprolol Lopressor, Toprol XL
Carteolol Cartrol
Nadolol Corgard
Penbutolol Levatol
Pindolol Visken
Propanolol Inderal
Sotalol Betapace
Timolol Blocadren
Labetalol Trandate, Normodyne
Salmeterol Serevent
Albuterol Proventil, Ventolin
Bitolterol Tornalate
Isoetharine Bronkosol
Metaproterenol Alupent, Metaprel
Pirbuterol Maxair
Terbutaline Serevent
Guanethidine Ismelin
Reserpine -----

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Home » D » Digoxin (Digoksin) Bagian 1

Digoxin (Digoksin) Bagian 1

Digoxin (Digoksin) Bagian 1

Digoxin adalah glikosida jantung dengan efek inotropik positif

Kelas terapi Digoxin :

Agen Danshen

MEKANISME AKSI / FARMAKOLOGI DIGOXIN :

Gagal jantung kongestif: menghambat pompa Na/K ATP0-ase yang bekerja dengan
meningkatkan pertukaran natrium-kalsium intraselular sehingga meningkatkan kadar kalsium
intraseluler dan meningkatkan kontraktilitas
Aritmia supraentrikular : Secara langsung menekan konduksi AV node sehingga
meningkatkan periode refractory efektif danmenurunkan konduksi kecepatn - efek inotropik
positif, meningkatkan vagal tone, dan menurunkan dan menurunkan kecepatan ventrikular
dan aritmia atrial. Atrial fibrilasi dapat menurunkan sensitifitas dan meningkatkan toleransi
pada serum konsentrasi digoksin yang lebih tinggi

Digoxin adalah glycosida jantung

Mekanisme Tepat aksi belum sepenuhnya dijelaskan.

Properti farmakologis utama adalah kemampuannya untuk meningkatkan kekuatan dan

kecepatan miokard sistolik kontraksi (aksi inotropik positif) oleh tindakan langsung pada
miokardium baik pada pasien dengan nonfailing hati dan pada mereka dengan gagal jantung.

Menghambat aktivitas sodium-potasium-diaktifkan adenosine trifosfatase (Na + -K + -

ATPase), suatu enzim yang dibutuhkan untuk transpor aktif natrium di membran sel miokard

Hipotesis bahwa Aksi digoxin pada gagal jantung terutama oleh pelemahan aktivasi sistem
neurohormonal, bukan oleh aksi inotropik positif

Dosis Beracun menyebabkan penembusan kalium dari miokardium dan masuknya bersamaan
sodium (Natrium).
Hasil Toksisitas sebagian dari hilangnya kalium intrasel yang terkait dengan penghambatan
Na + -K + -ATPase.

Dengan dosis terapi, augmentasi kalsium masuknya ke protein kontraktil dengan peningkatan
resultan dari eksitasi-kontraksi kopling terlibat dalam aksi inotropik positif glikosida jantung;
peran Na + -K + -ATPase dalam efek ini adalah kontroversial.

CHF: Penyebab penurunan refleks resistensi perifer dengan meningkatkan kontraktilitas

miokard; ini mengkompensasi aksi vasokonstriktor langsung dan, karena itu, resistensi perifer
total biasanya berkurang.

CHF: Peningkatan kontraktilitas miokard dan cardiac output secara refleks mengurangi nada
simpatik, sehingga memperlambat peningkatan denyut jantung dan menyebabkan diuresis di
patients.a edematous

CHF: Peningkatan kontraktilitas miokard disertai dengan peningkatan konsumsi oksigen

miokard

CHF: Mengurangi akhir diastolik ventrikel tekanan dan meningkatkan kontraktilitas miokard
menghasilkan penurunan bersih atau tidak ada perubahan dalam consumption.a oksigen
miokard ada penurunan aliran darah koroner, dan pada pasien dengan gagal jantung
pemulihan kerja jantung yang efisien dapat meningkatkan sirkulasi koroner.

Mengurangi kecepatan konduksi melalui atrioventrikular (AV) node dan memperpanjang

periode refrakter efektif (ERP) AV node dengan meningkatkan aktivitas vagal, berdasarkan
efek langsung pada nodus AV, dan oleh efek simpatolitik

Dengan dosis terapi, dapat menyebabkan pemanjangan interval PR, memperpendek interval
QT, dan ST segmen depresi, tetapi efek EKG ini tidak ukuran kuantitatif dari tingkat
digitalization.

Dosis toksik meningkatkan automaticity (peningkatan depolarisasi diastolik spontan) dari

semua bidang jantung kecuali SA node.

Anoreksia, mual, dan muntah mungkin dimediasi oleh kemoreseptor yang terletak di
postrema daerah medulla.

SIFAT FISIKA KIMIA DIGOXIN :

Pemerian :
Digoksin merupakan kristal putih tidak berbau. Obat ini praktis tidak larut dalam air dan
dalam eter, sedikit larut dalam alkohol dan dalam kloroform dan sangat larut dalam piridin.

Digoksin adalah salah satu glikosida jantung (digitalis), suatu kelompok senyawa yang
mempunyai efek khusus pada miokardium. digoksin diekstraksi dari daun Digitalis lanata

NAMA KIMIA / IUPAC DIGOXIN ;

4-[(1S,2S,5S,7R,10R,11S,14R,15S,16R)-5-{[(2R,4S,5S,6R)-5-{[(2S,4S,5S,6R)-5-
{[(2S,4S,5S,6R)-4,5-dihydroxy-6-methyloxan-2-yl]oxy}-4-hydroxy-6-methyloxan-2-
yl]oxy}-4-hydroxy-6-methyloxan -2-yl]oxy}-11,16-dihydroxy-2,15-dimethyltetracyclo
[8.7.0.0^{2,7}.0^{11,15}] heptadecan -14-yl] -2,5-dihydrofuran-2-one

SMILES DIGOXIN :
[H][C@]12CC[C@]3([H])[C@]([H])(C[C@@H](O)[C@]4(C)[C@H](CC[C@]34O)C3=CC
(=O)OC3)[C@@]1(C)CC[C@@H](C2)O[C@H]1C[C@H](O)[C@H](O[C@H]2C[C@H](
O)[C@H](O[C@H]3C[C@H](O)[C@H](O)[C@@H](C)O3)[C@@H](C)O2)[C@@H](C)O
1

BOBOT MOLEKUL DIGOXIN :

Rata rata : 780.9385
Monoisotopic: 780.429606756

SEDIAAN DIGOXIN :
TABLET

FORMULA MOLEKUL DIGOXIN :

C41H64O14
MEREK / NAMA DAGANG DIGOXIN :
Digitek®,
Lanoxicaps®,
Lanoxin®
Fargoxin
Lanoxin

NAMA GENERIK :
Digoxin

SINONIM DIGOXIN :
12-Hydroxydigitoxin

PENGGUNAAN / INDIKASI DIGOXIN :

Digunakan untuk terapi digitalisasi dan pemeliharaan.

IV digunakan untuk digitalisasi cepat dalam situasi darurat

Digunakan terutama dalam pengelolaan profilaksis dan pengobatan CHF dan untuk
mengendalikan laju ventrikel pada takiaritmia supraventrikular (misalnya fibrilasi atrium atau
debar).
Digoxin adalah glikosida jantung yang tersisa di AS, terutama karena dapat diberikan melalui
berbagai rute, memiliki durasi aksi menengah dan farmakokinetik pada pasien dengan atau
tanpa insufisiensi ginjal telah secara ekstensif dipelajari.

CHF
Digunakan bersama dengan ACE inhibitor, diuretik, dan / atau agen memblokir β-adrenergik
dalam pengelolaan gejala CHF yang berhubungan dengan ventrikel kiri sistolik disfungsi.

Terapi dapat dimulai pada awal perkembangan gagal jantung pada pasien yang sudah mulai
tapi belum merespons gejalanya ke ACE inhibitor atau agen β-adrenergik blocker, alternatif,
digoxin dapat ditangguhkan sampai respons gejala pasien ke inhibitor ACE atau β-blocker
telah ditetapkan dan kemudian digunakan hanya pada pasien yang tetap bergejala saat
menerima ACE inhibitor atau agen β-adrenergik blocking.

Pada pasien CHF menerima digoxin tanpa inhibitor ACE atau β-blocker, digoxin tidak boleh
dihentikan, tetapi terapi yang tepat dengan ACE inhibitor dan / atau β-blocker harus dimulai.

Meredakan gejala dan meningkatkan status klinik. Efek Menguntungkan aditif dengan
mereka yang juga menggunakan inhibitor ACE dan / atau diuretik.

Meningkatkan curah jantung mengakibatkan diuresis dan mengurangi gejala-gejala gagal

jantung kanan yang disebabkan oleh kongesti vena sistemik (misalnya, edema perifer) dan
gagal jantung sisi kiri disebabkan oleh kongesti paru (misalnya, dyspnea, ortopnea, dan
paroxysmal nocturnal dyspnea).

Meningkatkan fraksi ejeksi ventrikel dan meningkatkan gejala gagal jantung (seperti yang
dibuktikan oleh kapasitas latihan, jantung rawat inap terkait kegagalan-dan perawatan
darurat), sementara tidak memiliki dampak nyata pada keseluruhan mortaliti.

Umumnya, yang paling efektif dalam pengelolaan kegagalan output-rendah sekunder untuk
hipertensi, arteri koroner atau penyakit jantung aterosklerotik, penyakit miokard primer,
kardiomiopati nonobstruktif, dan penyakit katup jantung.

Tidak dianjurkan untuk pasien dengan disfungsi ventrikel kiri sistolik asimtomatik (NYHA
gagal jantung kelas fungsional I) karena hanya pengobatan untuk mencegah perkembangan
gagal jantung diindikasikan pada pasien ini dan digoxin belum terbukti memiliki efek nyata
pada progression (perkembangan) tersebut.

Memperburuk obstruksi sebagai akibat dari efek inotropik pada pasien dengan idiopatik
stenosis subaorta hipertrofik

Pasien dengan gangguan tertentu yang melibatkan gagal jantung yang terkait dengan fraksi
diawetkan ventrikel kiri ejeksi (misalnya, kardiomiopati restriktif, perikarditis konstriktif,
penyakit jantung amiloid, cor pulmonale akut) mungkin sangat rentan terhadap toksisitas
digoxin.

Atrial Fibrillation dan Flutter

Manajemen tergantung pada situasi klinis dan kondisi pasien dan kecepatan ventrikel.
Antiaritmia lainnya (misalnya, agen memblokir β-adrenergik, diltiazem, magnesium) adalah
terapi lini pertama untuk fibrilasi atrium dan respon ventrikel yang cepat.

Karena konversi Atrial Fibrilasi ke irama sinus normal dapat berhubungan dengan emboli,
antikoagulan yang memadai dianjurkan sebelum pemberian digoxin ketika durasi fibrilasi
atrium > 48 jam,

Aritmia atrium yang berhubungan dengan tempat hipermetabolik sangat resisten terhadap
pengobatan digoxin, dan perawatan harus dilakukan untuk menghindari toxicity (toksisitas).

Pada pasien dengan aritmia atrium dan hipotiroidisme, persyaratan untuk digoxin adalah
pengurangan dosis.

Sinus Takikardia
Digunakan untuk memperlambat denyut jantung ketika sinus takikardia disebabkan oleh
CHF.

Ventrikel atau kompleks prematur atrium disebabkan oleh CHF dapat mengirimkan ketika
kegagalan diobati dengan digoxin, tapi obat tidak boleh digunakan untuk mengobati
kompleks prematur tanpa gagal jantung.

Umumnya tidak efektif dan tidak diindikasikan untuk sinus takikardia tanpa gagal jantung,
seperti yang disebabkan oleh demam, anemia, kehilangan darah, atau hipertiroid.

Paroxysmal Supraventricular Tachycardia

Digunakan untuk pencegahan dan pengobatan takikardia supraventricular paroksismal
(PSVTs) seperti takikardia paroksismal atrial, paroksismal AV junctional irama, atau
paroksismal atrial fibrilasi / flutter.

Pengobatan pilihan untuk takikardia atrium paroksismal mencakup langkah-langkah untuk

meningkatkan tonus vagus (seperti karotis pijat sinus, manuver Valsava, dan / atau tersedak)
atau administrasi adenosine.

Mungkin bermanfaat dalam pengelolaan profilaksis dan pengobatan regular supraventricular

(reciprocating) takikardia terkait dengan sindrom Wolff-Parkinson-White (WPW), tetapi
umumnya tidak sendirian karena dapat meningkatkan konduksi melalui jalur aksesori dan,
dengan adanya fibrilasi atrium atau flutter, menghasilkan kecepatan ventrikel yang sangat
cepat dan kejadian fibrillation ventrikel,

Umumnya tidak digunakan dalam pengobatan takiaritmia, terutama fibrilasi atrium atau
debar, ketika anomali konduksi AV tampak.

MI
Penggunaan di MI akut adalah kontroversial.
Disfungsi ventrikel kiri ringan setelah MI akut biasanya dirawat dengan diuresis sederhana
dan pengurangan afterload dan preload (misalnya, dengan nitrogliserin parenteral); terapi
inhibitor ACE juga mungkin tepat.

Hasil samar-samar dengan digoxin dalam hal kematian, dan kekhawatiran tentang
peningkatan mortalitas yang terkait dengan terapi milrinone jangka panjang telah mendorong
pengkajian ulang tentang penggunaan digoxin.

Dapat digunakan secara selektif selama pemulihan MI akut, tetapi umumnya disediakan
untuk aritmia supraventrikuler dan untuk sistolik gagal jantung ventrikel kiri yang refrakter
terhadap agents lini pertama.

Efektif untuk takiaritmia supraventrikuler terus-menerus pada MI akut

Digitalisasi cepat dapat memperlambat respon ventrikel yang cepat dan meningkatkan fungsi
ventrikel kiri pada takiaritmia supraventrikular, fibrillation terutama atrium

Mungkin sangat berguna untuk memperlambat respon ventrikel yang cepat pada disfungsi
ventrikel kiri.

Syok Kardiogenik
Nilai dalam pengobatan syok kardiogenik belum ditetapkan, tapi kadang-kadang digunakan,
terutama ketika edema paru.

Digunakan untuk meningkatkan fungsi ventrikel kiri pada syok kardiogenik dan atrial
fibrilasi atau debar dengan kecepatan ventrikel yang cepat.

Kejang Jantung
Mungkin bermanfaat, terutama dalam kaitannya dengan memblokir agen β-adrenergik, dalam
pengobatan angina pectoris saat kardiomegali dan CHF.

Tidak bermanfaat sendirian dalam pengobatan angina pectoris tanpa kardiomegali dan CHF.

Aritmia dan CHF Profilaksis selama Stres di Penyakit Jantung tanpa Kegagalan

Telah digunakan sebagai profilaksis untuk mencegah aritmia dan CHF penyakit jantung tanpa
kegagalan selama situasi stres tertentu (misalnya, pembedahan, penyakit berat, kehamilan).

Kegemukan
Jangan gunakan sendiri atau dalam kombinasi dengan obat lain sebagai anorexiant untuk
pengobatan obesitas, karena anoreksia disebabkan oleh digoxin adalah gejala toksisitas, dan
berpotensi aritmia yang fatal dapat terjadi.
Informasi Obat di OBat dRug Informasi
Baca bagian selanjutnya di Digoxin Bagian 2
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