Dopamine & dobutamine

DOPAMINE AND
DOBUTAMINE
 Presented by :
Dr.Vishal kr.
Kandhway

INTRODUCTION
 Dopamine is an endogenous natural
catecholamine that serve as both a
neurotransmitter and a precursor of nor
epinephrine synthesis.
 When given as an exogenous drug dopamine
activates a variety of receptors in dose
dependent manner.
 Regulates cardiac, vascular and endocrine
function.

RECEPTORS
o Dopamine acts through D1 , D2 as well as
adrenergic alpha and B1 receptors ( But not B2)
o D1 and D2 receptors are the most abundant
and widespread in areas receiving a
dopaminergic innervation ( namely the
striatum ,limbic system, thalamus and
hypothalamus) as are D2 receptors, which also
occur in the pituitry gland

MECHANISM OF ACTION
 At dose of 0.5 to 3 mcg /kg /min :-
Selectively activates dopamine specific
receptors in the renal and splanchnic
circulation.
Increase blood flow in these region.
Low dose dopamine also directly affects
renal tubular epithelial cells.
It causes an increase in urinary Na
excretion

 At dose of 3 to 10 mcg /kg /min :-
It stimulates B1 receptors in the heart and peripheral
circulation.
Increases myocardial contractility, increases heart rate and peripheral
vasodilatation
It increases myocardial oxygen demand, so when ever dopamine is
to be used oxygen must be supplemented
Over all increase in cardiac output
Contractile response to dopamine is modest when compared
to dobutamine

 At dose of > 10 mcg /kg / min :-
Dopamine produces a progressive activation of alpha
receptors in the systemic and pulmonary circulation
resulting in progressive pulmonary and systemic
vasoconstriction
This vassopressor effect by virtue of increasing ventricular
afterload

Dopamine not effective orally and does not
cross blood brain barrier in sufficient amounts
to cause CNS effects.

PHARMACOKINETICS
 Rapid metabolism of dopamine mandates its
use as a continuous infusion. A portion of the
positive inotropic effect of dopamine is due
to stimulation of release of endogenous
norepinephrine which may predispose to
development of cardiac disarrythmias never
theless, dopamine is less disarrythmogenic
than epinephrine
 It is used only intravenously .

CLINICAL USES
 Dopamine is often used in situation where
both cardiac stimulation and peripheral
vasoconstriction desired such as cardiogenic
shock
 Also used to correct the hypotension in the
septic shock .But norepinephrine become the
preferred vassopressor in this condition
 Low dose is often used in an attempt to
prevent or reverse acute renal failure

 Drug initially administered at a rate of 2 to 5
mcg / kg /min . During infusion ,pt require
clinical assessments of myocardial function
perfusion of vitals organs such as the brain ,
and the production of urine
 Most pts should receive intensive care with
monitoring of arterial and venous pressures
and ECG
 Reduction in urine flow ,tachycardia or the
development of arrhythmias may be
indications to slow or terminate the infusion

DOPAMINE IN PULMONARY OEDEMA
 The sympathomimetic amines dopamine is
potent ionotropic agents
 Used in pulmonary edema
 Forcefully contracts the heart and thus
decreases the pulmonary load

DOPAMINE INFUSION IN WHICH
FLUID ?
 D-5–Yes
 RL -- No
 NS -- No
 DNS-- No

Conti-
 Low dose simultaneously increases:
Glomerular filtration rate
Renal blood flow
Urine output

DOSE AND ADMINISTRATION
 Commercial preparation of dopamine are
concentrated drug solution [Containing 40 mg
/80 mg dopamine HCL /ml]
 Provided in small volume vial / ampoule in 5 ml
/10 ml
 THE Preparation must be diluted to prevent
intense vasoconstriction during drug infusion
 Always delivered into , large central veins

DOSING REGIMEN
 There are two recommended doses:-
 3 to 10 mcg /kg /min is for augmenting
cardiac output thereby increasing BP
 More than 10 mcg /kg /min is
recommended to increase the blood pressure
directly

INCOMPABILITIES
 dopamine is inactivated by higher PH So ,
alkaline fluids should not be infused along
with dopamine
 INFUSATE:-
 Use 5 ml 2 vials containing 40 mg /ml
dopamine HCL add to 500 ml isotonic saline

PRECAUTIONS
 Before dopamine is administered to pt in
shock ,hypovolemia should be corrected by
transfusion of whole blood , plasma or other
appropriate fluid

ADVERSE EFFECTS
o Tachyarrhythmia's are the most common
adverse effects of dopamine
o Malignant tachyarrhythmia [ Multifocal
ventricular ectopic , ventricular tachycardia ]
o The most feared complication of dopamine
infusion is limb necrosis
o Extravasations of drug through a peripheral
vein can be treated with local injection of
phentolamine [5 to 10 mg in 15 ml saline ]

Contd…
 Allergic reactions
 Delays gastric emptying
 If pt is on dopamine infusion and is to be
anaesthetized , he / she will be treated as a
full stomach pt
 Less dysarrytmogenic than epinephrine

Contd…
 Continuous infusion of dopamine increase
intraocular pressure
 Ventilation effects :-
Infusion of dopamine interferes with the
ventilatory response to arterial hypoxemia
They results in unexpected depression of
ventilation
ABG have been observed to deteriote
during infusion of dopamine

Contd…
 Hyperglycemia that is commonly present in
pts receiving a continuous infusion of
dopamine is likely to reflect drug induced
inhibition of insulin secretion

CONTRAINDICATION
 Pt receiving MAO inhibitors
 Pheochromocytoma
 Uncorrected tachyarrhythmia
 Ventricular fibrillation

DOBUTAMINE
Name of drug;
 Dobutamine (generic name)
 Synthetic catecholamine derived from Isoproterenol.
Class of drug;
 Sympathomimetic
 Potent alfa 1 adrenergic agonist & weak B1-B2 adrenergic agonist.
 Vasopressor

PHARMACODYNAMIC PROPERTIES
 MECHANISM OF ACTION;
 Directly stimulates beta adrenergic receptor.
 Stimulation of Adenyl cyclase activity.
 Doesn‘t cause release of nor epinephrine.
 Cardiac Stimulation.

 Positive inotropic effect on myocardium.
 Increase in cardiac output by increase in stroke volume.
 Decrease in peripheral resistance.
 Increased myocardialOxygen consumption by increasing
tachycardia & myocardial contractility.
 Weak effects on vascular tone causing Peripheral
vasodilation.
 Increase in urine flow.
 Doesn‘t affect Dopaminergic receptor.

PHARMACOKINETICS
 Following IV administration
 Onset of action is 2 min
 Peak plasma conc. of drug is 10 min after initiation
of an IV infusion.
 Metabolism; ( in liver)
 Plasma half-life is 2 min
 Excretion mainly through urine.

 Dosage of adult and the elderly;
 2.5-10 mcg/kg/min
 Rarely upto 40mcg/kg/min may be
required.

INDICATIONS
 Inotropic support
 Cardiac failure
 Open heart surgery
 Positve end expiratory pressure
 Alternative to exercise in Cardiac stress
testing.

CONTRAINDICATIONS
 Hypersensitivity to dobutamine.
 Pheochromocytoma
 Must not be used in myocardial ischemia, in
case of ;
 Recent myocardial infarction,
 Unstable angina pectoris,
 Stenosis of main left coronary artery,
 Heart failure

Precautions ;
 Use with extreme caution after myocardial
ischemia
 Dose is decreased if there is undue increase in
heart rate, systolic blood pressue or arrythmia is
precipitated.
 Mild hypokalemia may occur.
 Sulphite sensitivity;
 Use with caution in sulphite – sensitive patients
because it causes allergy.

OVERDOSE
Symptoms;
 Anorexia
 Nausea, vomiting, tremor
 Headache, chest pain
 Excessive Hypertention
 Tachycardia

MANAGEMENT OF TOXICITY
 The initial action to be taken;
 Discontinuing administration of drug.
 Ensuring oxygenation and ventilation.
 If product is ingested , then absorption of drug
from GIT may be decreased by giving
activated charcoal. It is better than emesis
and gastric lavage.

ADVERSE DRUG REACTION
 Immune system disorders;
 Hypersensitivity reactions including;
 rash
 fever
 Anaphylactic reactions and severe life-
threatening asthmatic episodes may be due to
sulphite sensitivity.

DOPAMINE AND DOBUTAMINE
COMBINED INFUSION
 The divergent pharmacologic effects of
dopamine and dobutamine make their use in
combination potentially useful.Infusion of the
combination of dopamine and dobutamine
have been noted to produce a greater
improvement in cardiac output, at lower
doses, than can be achieved by either drug
alone.

 REFERENCES :
 Stoelting’s Pharmacology & Physiology.
 K.D.Tripathi Of Pharmacology.

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