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Drugs to raise blood pressure (Table 12.14)
Hypotension is initially treated with intravenous fluids, lightening of anesthesia, and asking the surgeon not to compress major vessels such as the vena cava (if that was responsible for reducing preload). Sometimes elevating the legs and thereby increasing venous return can help to improve cardiac output and arterial blood pressure. In addition, several drugs are available to improve myocardial con-tractility, increase arterial resistance, and decrease venous capacitance through adrenergic effects (Table 12.14).
The old standby still finds common use. We rely on its three-armed effects, alpha and beta stimulation as well as a release of norepinephrine from postganglionic sympathetic nerve terminals. Ten to 20 mg intravenously will increase heart rate and arterial pressure and stimulate the CNS, which we usually do not observe when we give the drug during anesthesia. It has a duration of action of about 20 minutes.
Epinephrine (adrenalin in Britain) and norepinephrine (and noradrenalin) are the two catecholamines we find circulating in blood. Norepinephrine is liberated from sympathetic nerve terminals and the adrenal medulla, while epinephrine comes only from the adrenal gland. Chemically, these two transmitter substances are identical but for a methyl group on the amine gracing epinephrine but not norepinephrine (NOR=N Ohne (German for “without”) Radical). The drugs dowhat sympathetic stimulation does. Being physiologic transmitter substances, these catecholamines have a fleeting effect. Single bolus injections last only for a matter of a few minutes.
The body makes extensive use of these catecholamines when fight, fright, or flight call for cardiovascular, pulmonary, muscular, ocular, and intestinal adjust-ments. It is amazing how well these substances with overlapping adrenergic effects orchestrate their actions to an optimal end-result of sympathetic stimulation. Clinically, we are limited to giving one drug or the other, counting on just one or the other effect. For example, low doses of epinephrine may reduce blood pressure a little through a beta2 effect, while larger doses raise pressure and accelerate heart rate. With norepinephrine, we see primarily increased pressure without tachycar-dia – as long as the baroreceptors are active. Typical doses used in the operating room might start with 10 to 20 mcg of epinephrine as a single i.v. bolus to help the average adult patient through a spell of hypotension, for example during ana-phylaxis. Usually reserved for more dire situations, we titrate a norepinephrine infusion to effect, starting perhaps with 0.1 mcg/kg/min. Epinephrine can also be given by continuous infusion. During cardiac resuscitation when we assume the body to have become very much less responsive to circulating catecholamines, doses as high as 1 mg epinephrine as a bolus have been used.
A biochemical forerunner to norepinephrine, dopamine also finds clinical use. It has the – undeserved – aura that in low rates of infusion, e.g., 1–3 mcg/kg/min, it can support blood pressure while maintaining renal perfusion and promoting diuresis. In larger concentrations, it turns into a vasopressor with renal vaso-constriction, just as norepinephrine, which it can liberate from post-ganglionic sympathetic terminals.
A synthetic catecholamine, dobutamine is a selective β1 agonist with greater effect on contractility than heart rate. It improves cardiac output in patients in cardiac failure. Because of its rapid metabolism, we administer dobutamine as an infusion at 2 to 10 mcg/kg/min, titrated to effect.
Another synthetic catecholamine, isoproterenol activates both β1 and β2 recep-tors with great vigor (2–10 times the potency of epinephrine). We use this agent to (i) increase heart rate, (ii) decrease pulmonary vascular resistance, andrarely, bronchodilate (i.v. or as an aerosol). Typical of β1 agonism, heart rate, contractility and cardiac output increase while β2 vasodilation reduces SVR. The net effect is a fall in diastolic and mean blood pressures. Isoproterenol also induces arrhythmias.
An old standby, phenylephrine sees vasoconstrictive service in nose drops and as an intravenous, pure α1 agonist. We expect to see both venous and arterial vasoconstriction with the typical intravenous bolus of 40 to 100 mcg, which should raise blood pressure for about 5 minutes. Because of its relatively short duration of effect, we can also infuse it at a rate of about 10 to 100 mcg/min (titrated to effect). Lacking effects at the β receptors, the drug will not increase heart rate or contractile force. Instead, a baroreceptor response can lead to lower heart rates.
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