The use of drugs to treat shock is based on one or more of the following types of actions: vasoconstriction, cardiac stimulation, and reversal of some of the vicious cycles in the production of shock. There are 4 groups of drugs which are useful in the treatment of shock. Predominantly vasoconstriction, such as angiotensin, methoxamine and phenylephrine. The last 2 are sympathomimetic drugs with pure vasoconstrictor action. The major hemodynamic pattern accompanying the rise in systemic blood pressure is an elevation in total systemic vascular resistance but a fall in cardiac output. Levarterenol, although a predominant vasoconstrictor, can potentially stimulate the heart if the vagal mechanism for cardiac slowing is blocked. Predominantely cardiac stimulants such as mephentermine, ephedrine and methamphetamine. All these examples are sympathomimetic drugs which stimulate the heart and have either a weak vasoconstrictor or even a weak vasodilator action. A new quinazaline compound has been reported to stimulate the heart even in the presence of acidosis. Blockade of sympathetic vasoconstriction of shock by drugs which block the sympathetic pathways. This can be accomplished by the classical sympathetic blocking drugs which interfere with the nervous and humoral mechanism for vasoconstriction. There is reasonable evidence from animal experiments that survival from hemorrhagic shock can be prolonged by inducing vasodilatation. Blockade of humoral agents which dilate the systemic blood vessels. In recent years, histamine, plasma kinins, serotonin, and isoproterenol have been shown to be important in the causation of special forms of experimental shock. There are corresponding blocking agents which are highly selective in nature and are under investigation for their clinical use. The new drugs which block the adrenergic beta receptors to the heart may also influence the coronary vasodilator mechanism and can deter the use of such drugs in the presence of heart disease.