Because anesthetics eliminate pain, and because pain can be a warning sign of complications, patients recovering from anesthesia must be protected from inadvertent harm until the anesthetic wears off. Caution the patient against activities that might result in unintentional harm.
Time Course of Local Anesthesia
Ideally, local anesthesia would begin promptly and would persist no longer (or shorter) than needed. Unfortunately, although onset of anesthesia is usually rapid (Tables 21.2 and 21.3), duration of anesthesia is often less than ideal. In some cases, anesthesia persists longer than needed. In others, repeated administration is required to maintain anesthesia of sufficient duration.
TABLE 21.2
Topical Local Anesthetics: Trade Names, Indications, and Time Course of Action
| Indications | Time Course of Action* | |||||
| Chemical Class | Generic Name | Trade Name | Skin | Mucous Membranes | Peak Effect (min) | Duration (min) |
| Amides | Dibucaine | Nupercainal | ✓ | <5 | 15-45 | |
| Lidocaine† | Xylocaine, Lidoderm, others | ✓ | ✓ | 2-5 | 15-45 | |
| Esters | Benzocaine | Many names | ✓ | ✓ | <5 | 15-45 |
| Cocaine | Generic only | ✓ | ✓ | 1-5 | 30-60 | |
| Tetracaine† | None‡ | ✓ | ✓ | 3-8 | 30-60 | |
| Others | Dyclonine | Sucrets (spray) | ✓ | <10 | <60 | |
| Pramoxine | Tronolane, others | ✓ | 3-5 | — | ||
TABLE 21.3
Injectable Local Anesthetics: Trade Names and Time Course of Action
| Time Course of Action* | ||||
| Chemical Class | Generic Name | Trade Name | Onset (min) | Duration (hr) |
| Amides | Lidocaine† | Xylocaine | <2 | 0.5-1 |
| Bupivacaine | Marcaine | 5 | 2-4 | |
| Mepivacaine | Carbocaine | 3-5 | 0.75-1.5 | |
| Prilocaine | Citanest | <2 | ≥1 | |
| Ropivacaine | Naropin | 10-30‡ | 0.5-6‡ | |
| Esters§ | Chloroprocaine | Nesacaine | 6-12 | 0.5 |
| Tetracaine† | Pontocaine | ≤15 | 2-3 | |
Onset of local anesthesia is determined largely by the molecular properties of the anesthetic. Before anesthesia can occur, the anesthetic must diffuse from its site of administration to its sites of action within the axon membrane. Anesthesia is delayed until this movement has occurred. The ability of an anesthetic to penetrate the axon membrane is determined by three properties: molecular size, lipid solubility, and degree of ionization at tissue pH. Anesthetics of small size, high lipid solubility, and low ionization cross the axon membrane rapidly. In contrast, anesthetics of large size, low lipid solubility, and high ionization cross slowly. Obviously, anesthetics that penetrate the axon most rapidly have the fastest onset.
Termination of local anesthesia occurs as molecules of anesthetic diffuse out of neurons and are carried away in the blood. The same factors that determine onset of anesthesia (molecular size, lipid solubility, degree of ionization) also help determine duration. In addition, regional blood flow is an important determinant of how long anesthesia will last. In areas where blood flow is high, anesthetic is carried away quickly, and effects terminate with relative haste. In regions where blood flow is low, anesthesia is more prolonged.
Use With Vasoconstrictors
Local anesthetics are frequently administered in combination with a vasoconstrictor, usually epinephrine. The vasoconstrictor decreases local blood flow and thereby delays systemic absorption of the anesthetic. Delaying absorption has two benefits: It prolongs anesthesia and reduces the risk for toxicity. Because absorption is slowed, less anesthetic is used and a more favorable balance is established between the rate of entry of anesthetic into circulation and the rate of its conversion into inactive metabolites.
It should be noted that absorption of the vasoconstrictor itself can result in systemic toxicity (e.g., palpitations, tachycardia, nervousness, hypertension). If adrenergic stimulation from absorption of epinephrine is excessive, symptoms can be controlled with alpha- and beta-adrenergic antagonists.
