Sympathomimetic amines
Mimic stimulation of sympathetic nervous system either directly or indirectly. They can be endogenous or synthetic.
Direct synthetic
Dobutamine (B1)
Dopexamine (B2)
Isoprenaline
Direct endogenous
Adrenaline (low dose beta, high dose alpha)
Noradrenaline (potent alpha, mild beta)
Dopamine (DA1 at low dose, beta at intermediate, alpha at high dose)
Non-catecholamines
Ephedrine (direct and indirect)
Metaraminol
Phenylephrine
Phosphodiesterase inhibitors
Competitive inhibition of phosphodiesterase III. This reduces breakdown of cyclic AMP increasing calcium release within the myocyte. Examples are milrinone and enoximone. They cause an increased cardiac output with a reduction in preload, making them useful in heart failure. However they can have a profound hypotensive effect if a loading dose is used and so they are often combined with a catecholamine.
Digoxin
An oral positive inotrope used in the treatment of heart failure. Also used as rate control in supraventricular tachycardias as it increases vagal tone. Digoxin reversibly binds to and inhibits the Na/K ATPase pump. This increases intracellular sodium, meaning there is less passive exchange for sodium and calcium resulting in an increased intracellular calcium concentration. It has a very narrow therapeutic index, and it’s toxic effects are worse in hypokalaemia and hypercalcaemia.
It’s antiarrhythmic effects are also solely due to an increased vagal tone, therefore they are often ineffective in sympathetically driven arrhythmias such as in sepsis.
Direct calcium sensitisers
Levosimendan is a relatively new drug that can modifiy the response of myofilaments to calcium without altering the availability of the ion. It enhances binding of Troponin-C to calcium. This causes inodilation and an increase in cardiac output of about 30%, supposedly without increasing myocardial oxygen demand. It is used in cardiogenic shock and has a very long half-life of about 80 hours.
Glucagon
This is a naturally occurring polypetide secreted by the alpha cells in the pancreas. It is able to directly stimulate adenyl cyclase in the myocyte, bypassing the Beta-1 adrenoceptor. However to do this you require a very large dose, which has been historically used to treat beta blocker overdose.
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