Receptor
Receptor site action
α-1
Glycogenolysis, gluconeogenesis, constricts vascular smooth muscle, relaxes GI tract
α-2
Constricts vascular smooth muscle, decreases insulin secretion and norepinephrine release
β-1
Increases heart rate and contractility, secretion of renin
β-2
Glycogenolysis, gluconeogenesis, relaxes vascular smooth muscle and bronchioles
∆-1
Increases renin release, dilates vascular smooth muscle
∆-2
Constricts smooth muscle, inhibits norepinephrine release
Ephedrine is an indirect acting vasopressor that has both alpha (vasoconstriction) and beta (increased heart rate) receptor effects. Ephedrine’s principal mechanism of action is to cause the release of norepinephrine from neuronal storage vesicles at the nerve terminus. This additional norepinephrine in the synaptic space then binds to and activates adrenergic receptors. Ephedrine is usually administered to patients who have both low blood pressure and low heart rate. In addition to having vasopressor effects, ephedrine is also a bronchodilator, and it can be administered to patients who are in bronchospasm.
Phenylephrine acts on alpha receptors causing increased vascular resistance and blood pressure. It has no beta agonist effects and frequently causes a reflex bradycardia (i.e. high blood pressure stimulates baroreceptors thereby decreasing heart rate). Phenylephrine is usually administered to patients who have low blood pressure and high heart rates. It must be used with caution in patients with ischemic heart disease, as it can actually decrease cardiac output.
Norepinephrine acts on both alpha and beta receptors, with alpha activity predominating. Norepinephrine leads to increases in blood pressure primarily by causing increased systemic vascular resistance. Because of baroreceptor mediated reflex bradycardia, cardiac output may actually decrease with the administration of norepinephrine – in spite of an increase in blood pressure.
Dopamine acts on alpha, beta, and dopamine receptors, depending on the dose administered. At low doses (<3 mcg/kg/min), dopamine will redistribute blood flow to the kidneys and may increase urine output. At higher doses, alpha and beta receptor actions predominate, leading to increased cardiac contractility and systemic vascular resistance.
Table 7.2 depicts commonly used vasopressors and their sites of action, and Table 7.3 depicts dosing regimens for these drugs.
Table 7.2
Receptor actions of commonly used vasopressors
Drug | Direct | Indirect | Site of action |
|---|---|---|---|
Ephedrine | + | ++ | α, β |
Phenylephrine | + | α | |
Norepinephrine | + | α, β | |
Dopamine | ++ | + | α, β, D (dopamine receptor) |
Table 7.3
Vasopressor dosing
Ephedrine | 2.5–10 mg IV bolus |
Phenylephrine | 40–100 mcg IV bolus or 20–150 mcg/min infusion |
Norepinephrine | 0.01–0.1 mcg/kg/min infusion |
Dopamine | 2–20 mcg/kg/min infusion |
Antiemetics
Postoperative nausea and vomiting (PONV) is one of the leading reasons for patient complaints, delayed postoperative discharge, and patient dissatisfaction with their anesthesia experience. There are various mechanisms by which surgery and anesthesia can cause nausea and vomiting, and consequently there are many different drugs available for prevention and treatment.
Serotonin antagonists are the mainstay of antiemetic prophylaxis and PONV treatment. These drugs work by blocking 5HT3 receptor binding. Ondansetron is by far the most commonly used serotonin antagonist, but dolasetron and granisetron are also available. Patients at moderate to high risk for PONV can be given a prophylactic serotonin antagonist prior to surgery, but current guidelines for low risk patients are to treat only those who exhibit nausea and vomiting postoperatively. Side effects sometimes include headache, lightheadedness or drowsiness.
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