at 5-min intervals according to the response (see Ch. 8, p. 143). If the circulation is compromised to a degree that is immediately life-threatening, adrenaline 500 micrograms may be given by slow i.v. injection at a rate of 100 micrograms/min (i.e. 1 ml/min of the dilute 1 in 10 000 solution) with continuous monitoring of the ECG. This course requires extreme caution and use of a further x 10 dilution (i.e. a 1 in 100 000 solution) may be preferred as providing finer control and greater safety The s.c. route is generally not recommended as there is intense vasoconstriction, which slows absorption.
Adrenaline is used in anaphylactic shock because its mix of actions, cardiovascular and bronchial, provide the best compromise for speed and simplicity of use in an emergency; it may also stabilise mast cell membranes and reduce release of vasoactive autacoids (see p. 280). Patients who are taking nonselective p-blockers may not respond to adrenaline (use salbutamol i.v.) and indeed may develop severe hypertension (see below).
Adrenaline (topical) decreases intraocular pressure in chronic open-angle glaucoma, as does dipivefrine, an adrenaline ester prodrug. They are contra-indicated in closed-angle glaucoma because they are mydriatics. Hyperthyroid patients are intolerant of adrenaline.
Accidental overdose with adrenaline occurs occasionally. It is rationally treated by propranolol to block the cardiac p effects (cardiac arrhythmia) and phentolamine or chlorpromazine to control the a effects on the peripheral circulation that will be prominent when the P effects are abolished. Labetalol (a + p block) would be an alternative. P-adrenoceptor block alone is hazardous as the then unopposed oc-receptor vasoconstriction causes (severe) hypertension (see Phaeochromocytoma, p. 494). Use of antihypertensives of most other kinds is irrational and some may also potentiate the adrenaline.
Noradrenaline (norepinephrine) (chiefly a and p, effects)
The main effect of administered noradrenaline is to raise the blood pressure by constricting the arterioles and so raising the total peripheral resistance, with reduced blood flow (except in coronary arteries which have few otj-receptors). Though it does have some cardiac stimulant (pj) effect, the tachycardia of this is masked by the profound reflex bradycardia caused by the hypertension. Noradrenaline is given by i.v. infusion to obtain a gradual sustained response; the effect of a single i.v. injection would last only a minute or so. It is used where peripheral vasoconstriction is specifically desired, e.g. vasodilation of septic shock. Adverse effects include peripheral gangrene and local necrosis; tachyphylaxis occurs and withdrawal must be gradual.
Isoprenaline (isopropylnoradrenaline) is a nonselective P-receptor agonist, i.e. it activates both Pj-and P2-receptors. It relaxes smooth muscle, including that of the blood vessels, has negligible metabolic or vasoconstrictor effects, but a vigorous stimulant effect on the heart. This latter is its main disadvantage in the treatment of bronchial asthma. Its principal uses are in complete heart block and occasionally in cardiogenic shock (hypotension).
Dopamine activates different receptors depending on the dose used. At the lowest effective dose it stimulates specific dopamine (Dj) receptors in the CNS and the renal and other vascular beds (dilator); it also activates presynaptic autoreceptors (D2) which suppress release of noradrenaline. As dose is raised, dopamine acts as an agonist on P1-adrenoceptors in the heart (increasing contractility and rate); at high doses it activates oc-adrenoceptors (vasoconstrictor). It is given by continuous i.v. infusion because, like all catecholamines, its t\ is short (2 min). An i.v. infusion (2-5 micrograms/kg/min) increases renal blood flow (partly through an effect on cardiac output). As the dose rises the heart is stimulated, resulting in tachycardia and increased cardiac output. At these higher doses, dopamine is referred to as an 'inoconstrictor'.
Dopamine is stable for about 24 h in sodium chloride or dextrose. Subcutaneous leakage causes vasoconstriction and necrosis and should be treated by local injection of an a-adrenoceptor blocking agent (phentolamine 5 mg, diluted).
It may be mixed with dobutamine. For CNS aspects of dopamine, agonists and antagonists: see Neuroleptics, Parkinsonism.
Dobutamine is a racemic mixture of d- and 1-dobutamine. The racemate behaves primarily a pj-adrenoceptor agonist with greater inotropic than chronotropic effects on the heart; it has some a-agonist effect, but less than dopamine. It is useful in shock (with dopamine) and in low output heart failure (in the absence of severe hypertension).
Dopexamine is a synthetic catecholamine whose principal action is as an agonist for the cardiac P2-adrenoceptors (positive inotropic effect). It is also a weak dopamine agonist (thus causing renal vasodilatation) and inhibitor of noradrenaline uptake thereby enhancing stimulation of cardiac f31 receptors by noradrenaline. It is used occasionally to optimise the cardiac output, particularly perioperatively.
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