OBAT OBAT PADA

JANTUNG

CHRONOTROPIK ---- S.A. NODE

INOTROPIK -- OTOT JANTUNG
DROMOTROPIK ---- SISTEM KONDUKSI
REMODELING--- HIPERTOPI
VASCULER JANTUNG -- ENDOTHEL
RITME JANTUNG -- > ElEKTRO FISIOLOGIS
MENGGANTI SEL MIOSIT - STEM SEL

OBAT OBAT UNTUK

PAYAH JANTUNG

CARDIAC GLIKOSIDA
DIURETIKA
ACE INHIBITOR
VASODILATOR

CONGESTIVE HEART FAILURE

NOREPINEPRIN

ANGIOTENSIN II

PRELOAD DAN AFTER LOAD

ARGININ VASOPRESIN

RETENSI GARAM DAN AIR

BEBAN JANTUNG MENINGKAT

MYOCARDIAL HYPERTROPHY

DISFUNGSI MIOKARDIUM

AKTIFITAS NEUROENDOKRIN PADA CHF

SNSA
-ADRENERGIC
STIMULATION

MYOCARDIAL DYSFUNCTION

VASOCONSTRICTION

CARDIAC ENLARGEMENT

Na RETENTION

ATRIAL STRECTCH

ALDOSTERONE

ANF RELEASE
Na LOSS
VASODILATATION
RENIN INHIBITION

RAS, AVP
H2O RETENTION

FUNGSI POMPA JANTUNG GAGAL

KOMPENSASI NEURAL
AKTIVITAS SIMPATIS

KONTRAKSI JANTUNG
KONSTRIKSI PEMB.

KOMPENSASI HORMONA
RENIN ANGIOTENSIN
ALDOSTERON
ARGININ VASO PRESIN

RETENSI GARAM DAN AIR

KONSTRIKSI PEMB. DARA

MENINGKATKAN OUT PUT JANTUNG

KEGAGALAN JANTUNG TERATASI
MEMPERBERAT BEBAN

MEMPERBERAT BEBAN

GAGAL JANTUNG TAMBAH BERAT

KOMPENSASI PENINGKATAN AKTIVITAS SIMPATIS

ALPHA 1
PEMB. DARAH
VASO KONSTRIKSI

BETA 1
OTOT JANTUNG

BETA 1
JUXTA GLOMER

INOTROPIK +
CHRONOTROPIK

RENIN ANGIO
TENSIN ALDS.

VASO KONSTRIKSI
ALDOSTERON
ANTI DIURETIK HORMON

RETENSI GARAM DA AIR

Drugs for CCF

Drugs for CCF

The most common symptoms of

CCF includes shortness of breath,
edema and fatigue.
Causes of heart failure includes
Coronary artery disease (CAD),
Hypertension, Diabetes,Mitral
valve disease and Chronic alcohol.

Drugs for CCF

Heart failure is the progressive

inability of the heart to supply
adequate blood flow to vital
organs.
It is classically accompanied by
significant fluid retention.
It is a leading cause of mortality
and morbidity.

Drugs for CCF

Vasodilators ACE Inhibitors

Diuretics
Beta blockers
Digoxin
Other Cardiac Inotropes
Dobutamine, Milrinone

ACE Inhibitors for

CCF

ACE Inhibitors for CCF

Drugs for CCF

Angiotensin Converting Enzyme
(ACE) Inhibitors :
ACE inhibitors improve mortality,
morbidity, exercise tolerance, left
ventricular ejection fraction.
Captopril, Lisinopril, Enalapril,
Ramipril, Quinapril.

Drugs for CCF

Angiotensin Converting Enzyme
(ACE) Inhibitors :
Reduction in arterial resistance
(afterload)
Reduction in venous tension
(preload)
Reduction in aldosterone secretion
Inhibition of cardiac and vascular
remodeling

Drugs for CCF

Angiotensin Converting Enzyme
(ACE) Inhibitors :
Adverse effects :
Dry irritating persistent cough
Hyperkalemia
Angioedema
Fetal toxicity

Drugs for CCF

Angiotensin Receptor AT-1
blockers (ARB) :
Losartan, Irbesartan, Candesartan
Competitive antagonists of
Angiotensin II (AT-1).
No inhibition of ACE or Cough.

Drugs for CCF

Vasodilators :
Isosorbide dinitrate and
hydralazine also used specially in
patients who cannot tolerate ACE
inhibitors.
Amlodipine and prazosin are other
vasodilators can be used in CCF.

Nitrates in CCF

Drugs for CCF

Diuretics :
These are useful in reducing the
symptoms of volume overload by
decreasing the extra cellular
volume
decreasing the venous return

Drugs for CCF

Diuretics :
Loop diuretics like furosemide and
bumetanide are the most
effective and commonly used.
Thiazides are effective in mild
cases only.

Drugs for CCF

Diuretics : Adverse effects :
Loop diuretics and thiazides
cause hypokalemia.
Potassium sparing diuretics help
in reducing the hypokalemia due
to these diuretics.

Drugs for CCF

Potassium Sparing Diuretics :
Spironolactone :
Aldosterone inhibition minimize
potassium loss, prevent sodium
and water retention, endothelial
dysfunction and myocardial
fibrosis.

Drugs for CCF

Spironolactone : Aldosterone
antagonist
Spironolactone can be added to
loop diuretics to modestly
enhance the diuresis; more
importantly, improve survival.

Drugs for CCF

Beta blockers for congestive
cardiac failure :
Acts primarily by inhibiting the
sympathetic nervous system.
Increases beta receptor
sensitivity
(up regulation).
Anti-arrhythmic properties.
Anti-oxidant properties.

Beta blockers in CCF

Drugs for CCF

Beta blockers for CCF :
Start at low dose and monitor for
bradycardia
Carvedilol and Metoprolol are the
most commonly used for CCF
amongst beta blockers

Drugs for CCF

Cardiac glycosides : Digoxin :
Inhibition of Na/K ATPase pump
increase intracellular sodium
concentration eventually
increase cytosolic calcium.
It restores the vagal tone and
abolishes the sympathetic over
activity.

Cardiac glycosides

Digitalis
Sourced from foxglove plant
1785, Dr. William Witherings
monograph on digitalis
Has a profound effect on the
cardiac contractility

EFEK FARMAKOLOGI DIGITALIS

EFEK LANGSUNG
OTOT JANTUNG
SA NODE
AV NODE
PURKINYE
EFEK TIDAK LANGSUNG
PENURUNAN AKYTIVITAS SIMPATIS
PENINGKATAN AKTIVITAS PARA SIMPATIS

DIGITALIS

INOTROPIK POSITIF
OUTPUT JANTUNG

KONSTRIKSI ARTERI
KONSTRIKSI VENA

AKTIVITAS SYMPATIS
CHF MEMBAIK

BRADIKRDI
KONDUKSI

DILATASI ARTERI
DILATASI VENA

FEVER, MAYOR SURGERY, HYPOKSMIA

THYROTOKSIKOSIS, TAKIKARDI

Digoxin in CCF

Drugs for CCF

Cardiac glycosides : Digoxin :
Increase the refractoriness of AV
node thus decrease ventricular
response to atrial rate.
Digoxin is used as a first-line drug
in patients with congestive heart
failure who are in atrial fibrillation.

KERACUNAN DIGITALIS:

GEJALA EKSTRA CARDIAC:

GASTROINTESTINAL : MUAL MUNTAH NAUSEA ANOREK
NEUROMUSKULAR: KELEMAHAN OTOT KELEMAHAM UMU
PSIKIS: CEMAS, HALUSINASI, DELIRIUM
KELUHAN MATA: KABUR, FOTO POBI PANDANGAN KIUN

GEJALA INTRA CARDIAC :

BRADIKARDI
PERLAMBATAN KODNDUKSI A-V
A-V BLOK
BIGEMINUS
TRIGEMINUS
VENTRIKULAR TAKHI KARDI
VENTRIKULAR FIBRILASI

Drugs for CCF

Digoxin : Adverse effects / Precautions
:
Nausea, vomiting, gynecomastia,
visual disturbances and psychosis.
Ventricular bigeminy, AV block and
bradycardia.
Amiodarone and verapamil can
increase the plasma concentration
of digoxin by inhibiting its excretion.

Drugs for CCF

Digoxin toxicity treatment:

Toxicity can be treated with
higher than normal doses of
potassium.
Digoxin antibody (digibind) is
used specifically to treat lifethreatening digoxin overdose.

Drugs for CCF

Cardiac Inotropes :
Phosphodiesterase III Inhibitors
Positive inotropic and vasodilator
INO-DILATOR ; Eg., Milrinone
Dobutamine is a beta-1 agonist
which increase contractility and
cardiac output.

Drugs for CCF

Conclusion :
ACE inhibitors are cornerstone in the
treatment of CCF.
Beta blockers are used in selected
patients (mild/moderate failure, low
dose)
Diuretics and digoxin are other drugs
useful in CCF in select patients.

STAGE

DISABILITY

CLASS 1
MILD

No symptoms Can perform ordinary

activities without any limitations

CLASS 2
MILD

Mild symptoms - occasional

swelling Somewhat limited in ability to
exercise or do other strenuous activities

CLASS 3

Noticeable limitations in ability to

exercise or participate in mildly
strenuous activities
Comfortable only at rest

MODERATE
CLASS 4
SEVERE

Unable to do any physical activity

without discomfort Some HF symptoms
at rest
45

Antidysrhythmic Agent

Arrhythmia

Heart condition where disturbances in

Pacemaker impulse formation

Contraction impulse conduction
Combination of the two

Results in rate and/or timing of contraction

of heart muscle that is insufficient to
maintain normal cardiac output (CO)
To understand how antiarrhythmic drugs
work, need to understand
electrophysiology of normal contraction of
heart

Mechanisms of Cardiac
Arrhythmias
Result from disorders of impulse
formation, conduction, or both
Causes of arrhythmias
Cardiac ischemia
Excessive discharge or sensitivity to
autonomic transmitters
Exposure to toxic substances
Unknown etiology

Dysrhythmia
Any deviation from the normal
rhythm of the heart
Antidysrhythmics
Drugs used for the treatment and
prevention of disturbances in cardiac
rhythm

Resting Membrane
Potential: RMP

This difference in the electronegative

charge.
Results from an uneven distribution of
ions (sodium, potassium, calcium)
across the cell membrane.
An energy-requiring pump is needed to
maintain this uneven distribution of
ions.
Sodium-potassium ATPase pump

ANTIARRHYTHMIC DRUGS
CLASS Mechanism of Action Drug name
IA
Na+Channel blocker Disopyramide, procainamide,
quinidine
IB
Na+Channel blocker Lidocaine, mexiletine,
tocainide
IC
Na+Channel blocker Flecainide, propafenone
II
Adrenoreceptor blocker
Esmolol, metoprolol,
pindolol,
propranolol
III
K+Channel blocker
Amiodarone,
bretylium, sotalol
IV
Ca++ Channel blocker Diltiazem, verapamil
Other antiarrhythmic drugs
Adenosine, digoxin

Action Potential

A change in the distribution of ions causes

cardiac cells to become excited.

The movement of ions across the cardiac

cells membrane results in the propagation
of an electrical impulse.

This electrical impulse leads to contraction

of the myocardial muscle.

Vaughan Williams
Classification

Class 1
Class Ia
Class Ib
Class Ic

Class II
Class III
Class IV
Other

Vaughan Williams
Classification
Class I

Membrane-stabilizing agents
Fast sodium channel blockers
Divided into Ia, Ib, and Ic agents, according
to effects

Vaughan Williams
Classification
Class I
moricizine

General Class I agent

Has characteristics of all three subclasses
Used for symptomatic ventricular and lifethreatening dysrhythmias

Vaughan Williams
Classification
Class Ia
quinidine, procainamide, disopyramide

Block sodium channels

Delay repolarization
Increase the APD
Used for atrial fibrillation, premature atrial
contractions, premature ventricular contractions,
ventricular tachycardia, Wolff-Parkinson-White
syndrome

Vaughan Williams
Classification
Class Ib
tocainide, mexiletine, phenytoin,
lidocaine

Block sodium channels

Accelerate repolarization
Decrease the APD
Used for ventricular dysrhythmias only
(premature ventricular contractions, ventricular
tachycardia, ventricular fibrillation)

Vaughan Williams
Classification
Class Ic
encainide, flecainide, propafenone

Block sodium channels (more pronounced

effect)
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter

Vaughan Williams
Classification
Class II
Beta blockers: atenolol, esmolol,
petaprolol, propranolol

Reduce or block sympathetic nervous system

stimulation, thus reducing transmission of
impulses in the hearts conduction system
Depress phase 4 depolarization
General myocardial depressants for both
supraventricular and ventricular dysrhythmias

Vaughan Williams
Classification
Class III
amiodarone, bretylium, sotalol, ibutilide

Increase APD
Prolong repolarization in phase 3
Used for dysrhythmias that are difficult to treat
Life-threatening ventricular tachycardia or
fibrillation, atrial fibrillation or flutterresistant to
other drugs
Sustained ventricular tachycardia

Vaughan Williams
Classification
Class IV
verapamil, diltiazem

Calcium channel blockers

Depress phase 4 depolarization
Used for paroxysmal supraventricular
tachycardia; rate control for atrial fibrillation
and flutter

Vaughan Williams
Classification
Other Antidysrhythmics
digoxin, adenosine

Have properties of several classes and are

not placed into one particular class

Antidysrhythmics
Digoxin

Cardiac glycoside

Inhibits the sodium-potassium ATPase pump

Positive inotropeimproves the strength of cardiac

contraction

Allows more calcium to be available for contraction

Used for CHF and atrial dysrhythmias

Monitor potassium levels, drug levels, and

for toxicity

Antidysrhythmics
adenosine (Adenocard)

Slows conduction through the AV node

Used to convert paroxysmal supraventricular
tachycardia to sinus rhythm
Very short half-life
Only administered as fast IV push
May cause asystole for a few seconds
Other side effects minimal

Antidysrhythmics:
Side Effects
ALL antidysrhythmics can cause
dysrhythmias!!

Hypersensitivity reactions

Nausea
Vomiting
Diarrhea
Dizziness
Blurred vision
Headache

CLINICAL
PHARMACOLOGY OF
ANTIANGINAL DRUGS.
CLINICAL
PHARMACOLOGY OF
ANTIARRHYTHMIC

ISCHEMIC HEART DISEASE

There are 35 risk factors for development of IHD
3 most important ones are

big triple

hypercholesterolaemia
arterial hypertension
smoking
95 % of patients with IHD are observed to have
aterosclerotic changes in coronary arteries

Antianginal (coronary
active) drugs
a group of drugs which using different
mechanisms
even
out
irregularities
between myocardium need in oxygen and
its blood supply by coronary arteries
clinically it is manifested by removal or
prevention
of
stenocardia
attacks
(improvement of disease current) and
increasing
of
patients
tolerance
to
physical load

ANTIANGINAL (CORONARY
ACTIVE) DRUGS
. Nitrates and sidnonims which are
close to the first ones
. Bets-adrenoblockers
. Antagonists of calcium ions
. Activators of potassium channels

Inhibitors of ATE
Antiaggregants and anticoagulants
Drugs with metabolic influence
miocardium

on

NITRATES
nitroglycerin
isosorbid dinitrate
isosorbid-5mononitrate

MECHANISM OF ACTION
OF NITRATES

Interaction with sulfhydryl (SH-)

groups
(nitrate receptors) inside
cells of vascular smooth muscles
Stimulation
of
formation
of
endothelial factor of relaxation of
vessels (RF) nitrogen oxide (NO)
Decreasing of ionized 2+ contents
Relaxation, dilation of vessels,
including coronary vessels

MECHANISM OF ACTION
OF NITRATES
Decreasing
of tone of venules decreasing of preloading (income

of blood into heart during diastole) decreasing of work of left

ventricle and heart output
Decreasing of tone of arterioles decreasing of afterloading
(decreasing of arterial pressure, end diastolic pressure in left
ventricle and its volume, decreasing of tension of myocardium wall
decreasing of heart need in oxygen
improvement of blood float in ischemic zone of myocardium
redistribution of coronary blood circulation with increasing of
perfusion of subendocardial areas
dilation of large coronary vessels if they are in spasm or narrowed
with aterosclerotic mass
development of anastomoses between arteries in myocardium (in
case of prolonged administration)

NITROGLYCERINE

Tablets (under the tongue)

1 % alcohol or oil solution (under the
tongue)
aerosol
Latent period - 2-3 min
Duration of action - 20-30 min
ampoules 1 % solution intravenously
dropply 0,01% solution
prolonged forms of nitroglycerine:
trinitrolong, sustak, nitrong, ointment,
plaster

SIDE EFFECTS OF
NITROGLYCERINE
bursting, pulsating headache
decreasing of arterial pressure
(heartbeat, dizziness, collapse)
skin redness, feeling of fever

Contraindications for
nitroglycerine use

Close-angled form of glaucoma

increasing of intracranial
pressure, insult

acute myocardium infarction (in

case of presence of hypotonia
and collapse)

PROLONGED FORMS OF
NITROGLYCERINE

Trinitrolong polymer films (0,001 g or 0,002

g of nitroglycerine) action develops immediately,

lasts for 3-5 hours
Sustac Susta-mite (contains 0,0026 g of
nitroglycerine) and Sustac-forte (0,0064 g of
nitroglycerine)
beginning of action after 10 min,
maximal action after 1 hour,
duration of action 4-5 hours
Nitrong microcapsule form of nitroglycerine of
prolonged action
latent period 30-60 min,
maximal effect - after 3-4 hours,
action duration - 6-8 hours

SIDE EFFECTS OF NITRATES

bursting, pulsating headache
decreasing of arterial pressure
(heartbeat, dizziness, collapse)
skin redness, feeling of fever
development of tolerance
nitrate dependence
syndrome of cancellation

Other nitrates

Nitrosorbid isosorbid dinitrate

latent period 30-50 min,

duration of action 4-6 hours and more
With sublingual administration of the drug latent period
grows short to 3-5 min

buccal form (Dinitrolslrbilong)

tablets of prolonged action (Isoket-retard)

ointment

aerosol

drugs for intravenous introduction

Isosorbid-5-mononitrate
- pharmacologically active metabolite of isosorbid
dinitrate
duration of action - from 6 till 24 hours

SYDNONIMS
Molsydomin corvaton sydnopharm

is metabolized in liver forming a substance SIN-1a

which contains free N group (doesnt need previous
interaction with SH-groups)
nitrogen oxide stimulates guanilatecyclase that activates
synthesis of cGMP

cGMP causes dilation of vessels

2 mg of molsydomin = 0,5 mg of nitroglycerine

Molsydomin

latent period - 20 min (5-10 min if

administered sublingually), action duration - 6
hours.
can be used for prophylaxis and releasing
stenocardia attacks in patients with glaucoma
(doesnt increase intraoccular pressure)
indicated for patients who make breaks in
using nitrates to decrease tolerance towards
them
doesnt lead to development of tolerance
(doesnt
need
previous
combining
with
sulfhydryl groups)
absence of cancellation syndrome

BETA-ADRENOBLOCKERS

Mechanism of action during stenocardia

blockade of 1-adrenoreceptors of heart: decreasing

of power and frequency of heart contractions and
as follows cardiac need in oxygen
decreasing of thrombocyte aggregation and
prevention of thrombus formation
increasing of diastole duration improvement of
coronary vessels saturation with blood
improvement of perfusion of ischemic areas of
myocardium
Decreasing of calcium ions accumulation releasing
of cardiac muscle tension, improvement of
metabolic processes, increasing of ATP synthesis
in case of acute myocardium infarction increasing
of blood supply of ischemic areas of heart,
decreasing of size of infarction seat, prevention of
development of cardiac arrhythmias

CALCIUM IONS ANTAGONISTS

1. Derivatives of difenilalkilamin (verapamil)
2. Derivatives of benzothiazepine (dylthiazem)
3. Derivatives of dyhydropyridine (nifedipin,
amlodipin, nimodipin)
Drugs of 1 and 2 groups dominantly influence on
heart (depress automatism of sinus node,
conductivity through conductive heart system) ,
show antiarrhythmic, antiangina and
hypotensive action.
Derivatives of dyhydropyridine (group of nifedipin)
decrease blood pressure and cause dilation of
coronary vessels, cause reflective tachycardia

Nifedipin - corinfar - fenigidin adalate

Doesnt depress conductivity in
myocardium,
has a weak antiarrhythmic action
Maximal concentration of the drug in
blood occurs after 45-60 min after
administration orally and after 2-3
min if administered sublingually
Effect lasts for 4-6 hours

Antagonists of calcium ions

derivatives of dyhydropyridine
of generation (amlodipin,
isradipin, nicardipin)

almost dont cause tachycardia

are indicated for prolonged treatment
of patients with stabile stenocardia
arent indicated in case of non stabile
stenocardia (long lasting latent period)

Usage of calcium ions antagonists

Drugs

Illness
Hypertension

Verapamil

Dylthiazem

Nifedipin

Stenocardia

Verapamil

Dylthiazem

Nifedipin

Supraventric
ular tachyarrhythmia

Verapamil

Dylthiazem

Possible
combination with
-blockers
-recommended drug

Dylthiazem

Nifedipin

Felodipin

Amlodipin

Amlodipin

Felodipin

--should be used carefully

Amlodipin

ACTIVATORS OF POTASSIUM
CANALS
NICORANDIL

activates 2+-depending potassium canals

causes relaxation of smooth muscles of
vessels
coronary, arteriolar and venous
vasodilation
improvement of blood supply of myocardium,
decreasing of pre- and afterloads of heart,
decreasing of myocardial need in oxygen,
separation of ischemic damage zone

Acetylsalicylic acid

80-100 mg per day as

antiaggregative drug, decreases risk
of development of acute myocardium
infarction and decreases mortality of
patients with IHD
In many world countries it is also
used a basis treatment drug of IHD
which can be used for years

ACUTE MYOCARDIUM
INFARCTION

one of the main reasons of disablement and

mortality of people of employed age in many world
countries, including Ukraine
men suffer from MI almost 5 times more often than
women
Mortality of patients with MI during first two hours
starting from the beginning of the process makes
around 50 % of all mortal cases connected with MI
the most often death causes acute cardiacvascular insufficiency (angina pectoris, lung
edema, cardiogenic shock), heart rupture, heavy
cardiac arrhythmia
other complications of MI thrombosis and emboli,
acute and chronic heart aneurisms, Dreslers
syndrome, chronic cardiac insufficiency

TREATMENT OF MYOCARDIUM
INFARCTION
three stages

Immediate treatment decreasing pain and

treatment of stop of heart beats
Early treatment separation of zone of
infarction seat and prevention of early life
threatening
complications
(cardiac
arrhythmias, acute cardiac insufficiency)
Further treatment prevention and therapy
of late complications of MI, prophylaxis of
recurrent MI and death of the patients

TREATMENT OF ACUTE
MYOCARDIUM INFARCTION
Releasing of pain and
prophylaxis of cardiogenic shock

nitroglycerin (1 tablet under the tongue every 7-10

min.)
Neuroleptanalgesia (fentanil with droperidol),
morphine, omnopon, promedol (in combination with
atropine, dimedrol, aminasine)
nitrous oxide in combination with neuroleptics
in case of remaining pain non narcotic analgesics in
combination with antihistamine and neuroleptic drugs
to increase arterial pressure during cardiogenic shock
intravenously dropply dopamine (drugs of choice),
noradrenalin, mesaton
sometimes glucocorticosteroids are used

TREATMENT OF ACUTE
MIOCARDIUM INFARCTION
Size limitation
of infarction seat

Intravenous dropply introduction of

0,01 % nitroglycerin solution

Administration of -adrenoblockers

TREATMENT OF ACUTE
MYOCARDIUM INFARCTION
Treatment and prophylaxis of heart
arrhythmias
Treatment of ventricular arrhythmias i.v. slowly 0,2
% solution of xycain, novocainamid intramuscularly
Prophylaxis of ventricular extrasystolia and
tachycardia magnesium sulfate (intravenous
dropping introduction of 4-5 % solution),
-adrenoblockers
Arrhythmias of atrial origin heart glycosides,
antagonists of calcium ions
Bradycardia - isadrin, atropine sulfate, alupent (i.v.)

TREATMENT OF ACUTE
MYOCARDIUM INFARCTION
CORRECTION OF BLOOD CLOTTING
thrombolytic drugs
streptokinase (1,5 mln OD), urokinase (2 mln
OD), aktilise recombinant tissue activator of
plasminogen (100 mg) intravenous
after performing of thrombolytic therapy intravenous
introduction of heparin, at first 10 000 OD, after 1000
OD per hour during 24-48 hours

anticoagulants of indirect action

acetylsalicylic acid
(80-100-300 mg per day)

TREATMENT OF ACUTE
MYOCARDIUM INFARCTION
Treatment of heart insufficiency

i.v. furosemid (40-120 mg); i.v. dropply nitroglycerine

(12-20 hours), morphine
i.v. dropply dopamin and dobutamin
heart glycosides in tachysystolic form of scintillating
arrhythmia or fluttering of atria with moderate leftventricular insufficiency

General measures

oxygen inhalation
correction of acid-base balance