Wednesday, October 13, 2010

DRUGS FOR SHOCK

Therapeutic aids


Pulmonary Artery Catheter
The differential diagnosis of the shock state is usually relatively straightforward. The clinical setting in conjunction with physical examination is often sufficient to guide diagnosis and therapy.

However, occasionally the cause of the shock state is unclear, in which case homodynamic parameters derived form a pulmonary artery catheter may provide valuable insight into the principal mechanism underlying the shock state.

Inotropes
Volume resuscitation, should precede pharmacological aids.
Drugs should be considered, when tissue perfusion is inadequate, after fluid administration.

Dopamine
Dopamine is an endogenous sympathetic amine, and is a biosynthetic precursor of epinephrine, which also acts as central and peripheral neurotransmitter effect. At low dose (1-3 µg/kg/min) dopamine may increase renal blood flow and diuresis.
At moderate doses (5 µg/kg/min) stimulation of cardiac beta-receptors produces increases in contractility and cardiac output with little effect on heart rate or blood pressure.
With increasing doses (5-10 µg/kg/min), Beta-adrenergic effects predominate, further increases in cardiac output are accompanied by increases in heart rate and blood pressure.
At higher doses (more than 10 µg/kg/min), peripheral vasoconstriction, from increasing alpha-activity becomes more prominent, resulting in
elevation of systemic vascular resistance,
blood pressure,
and myocadial oxygen consumption.

Dobutamine
Dobutamine is a synthetic adrenegic agonist.
The predominant effect is an increase in cardiac contractility with little increase in heart rate.
Dobutamine also has a peripheral vasodilating effect resulting from Beta2-receptor activation that is independent of any increase in cardiac output.
The combination of increased contractility, and reduction in afterload, contribute to improved left ventricular emptying and a reduction in pulmonary capillary wedge pressure.
As a result of these properties, dobutamine is an ideal agent when the therapeutic goal is to improve cardiac output rather than to improve blood pressure.
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