Pharmacology

·         Emergency drugs via an endotracheal tube:

E-LAINE: Endotracheally- lidocaine, atropine, isoproterenol, naloxone, and epinephrine

·         VOLATILE ANESTHETICS

1. Speed of onset of volatile anesthetics is increased by increasing the delivered concentration of anesthetic, increasing the fresh gas flow, increasing alveolar ventilation, and using non-lipid-soluble anesthetics.
2. Volatile anesthetics lead to a decrease in tidal volume and an increase in respiratory rate, resulting in a rapid, shallow breathing pattern.
3. MAC is decreased by old age or prematurity, hyponatremia, hypothermia, opioids, barbiturates, alpha2 blockers, calcium channel blockers, acute alcohol intoxication, and pregnancy.
4. MAC is increased by hyperthermia, chronic alcoholism, and CNS stimulants (e.g., cocaine).
5. The physiologic response to hypoxia and hypercarbia is blunted by volatile anesthetics in a dose-dependent fashion.
6. Because of its insolubility in blood and rapid egress into air-filled spaces, nitrous oxide should not be used in the setting of pneumothorax, bowel obstruction, pneumocephalus, or during middle ear surgery.
7. Degradation of desflurane by desiccated absorbents may lead to carbon monoxide production, theoretically exposing and poisoning the patient.

·         Potassium hydroxide (KOH)-containing absorbents are the stronger bases and result in greater CO production. From greatest to least, KOH-containing absorbents are Baralyme (4.6%) > classic soda lime (2.6%) > new soda lime (0%) > calcium hydroxide lime (Amsorb) (0%). Choice of volatile anesthetic also determines the amount of CO produced and at equiMAC concentrations, desflurane > enflurane > isoflurane. Sevoflurane and halothane lead to little or no CO.

·         Nitrous oxide, administered to pregnant rats in concentrations greater than 50% for over 24 hours, has been shown to increase skeletal abnormalities. The mechanism is probably related to the inhibition of methionine synthesis, which is necessary for DNA synthesis; the mechanism may also be secondary to the physiologic effects of impaired uterine blood flow by nitrous oxide. Although direct effects have not been seen in humans, it may be prudent to limit the use of nitrous oxide in pregnant women.

·         MUSCLE RELAXANTS

1. Metabolism of relaxants is more important that pharmacological reversal for termination of relaxant effect.
2. Train-of four assessment is highly subjective and has been repeatedly demonstrated to underestimate residual neuromuscular blockade.
3. It may be a best practice to administer reversal agents to all patients receiving nondepolarizing relaxants.
4. Leave clinically weak patients intubated and support respirations until the patient can demonstrate return of strength.

·         patterns of stimulation produced by nondepolarizing agents:

1.       Repetitive stimulation (TOF or tetanus) is associated with fade in the muscle response.

2.       Following a tetanic stimulus, response to subsequent stimulations is increased (posttetanic facilitation). This may be due to increased ACh release or increased sensitivity at the end plate

·         patterns of stimulation produced by depolarizing relaxants:

1.       The single-twitch, TOF, and tetanus amplitudes are uniformly decreased at any level of blockade. There is lack of fade in response to TOF and tetanus and lack of posttetanic facilitation.

2.       A desensitization or phase II blockade may develop with prolonged exposure to SCH. Phase II blockade has the same twitch characteristics as nondepolarizing blockade

·         Conduction blockade proceeds from the outermost (mantle) to the innermost (core) nerve bundles. Generally speaking, mantle fibers innervate proximal structures and core fibers innervate distal structures.

·         Ropivacaine is a new amide local anesthetic that is structurally and behaviorally similar to bupivacaine. Like bupivacaine, it is highly protein bound and has a lengthy duration of action. It is, however, less cardiotoxic.

Ropivacaine is capable of providing differential blockade. In other words, it is possible to separate its sensory and motor anesthetic properties. With ropivacaine, sensory anesthesia may be provided without a significant degree of motor blockade. These characteristics may make ropivacaine an ideal anesthetic for use in obstetric procedures.

·         INOTROPES AND VASODILATOR DRUGS

1. Clinically manifest congestive heart failure with preserved left ventricular systolic function (EF > 35%) in the absence of ischemia and valvular pathology suggests diastolic heart failure.
2. Nesiritide may be beneficial for the management of precardiac transplant patients with increased pulmonary vascular resistance as well as renal failure.
3. Vasopressin has a role in blood pressure maintenance in septic shock and other shock states.
4. Beneficial effects of nitroglycerin and other nitrates in anginal therapy result from platelet effects, a reduction in MVO2, and improved coronary perfusion.
5. Because of its narrow therapeutic ratio and adverse interactions with fluid and electrolyte shifts, digitalis is rarely used intraoperatively as an inotrope.
6. There is now scientific evidence that low-dose dopamine is ineffective for prevention and treatment of acute renal failure and for protection of the gut.

·          

·         SMR:

1. Shortest acting SMR : Succinylcholine ( SCh)

2. Shortest acting Non-depolarising / Competitive SMR : Mivacurium

3. Fastest acting SMR : SCh (1-1.5 min).

4. Fastest acting ND-SMR : Rocuronium(1-2 min).

Rocuronium is an agent of intermediate duration but of rapid onset and lower potency. Its rapid onsets allows it to be used as an alternative to succinylcholine in rapid-induction anesthesia and in relaxing the laryngeal and jaw muscles to facilitate tracheal intubation

(* Note : Rapacuronium is the fastest acting ND/SMR, but due to it's broncho-constrictive side effects is withdrawn from the market, so in the question if 'Rocuronium' is not there go for Rapacuronium).

5. Longest acting SMR : Doxacurium

6. Most potent SMR: Doxacurium.

7. Least potent SMR : Gallamine.

8. Maximum histamine release : dTC (d-tubocurarine)

9. Minimum histamine release : Vecuronium.

NOTE : Succinylcholine, mivacurium, doxacurium, and atracurium also cause histamine release, but to a lesser extent unless administered rapidly. The ammonio steroids, pancuronium, vecuronium, pipecuronium, and rocuronium, have even less tendency to release histamine after intradermal or systemic injection. Histamine release typically is a direct action of the muscle relaxant on the mast cell rather than IgE-mediated anaphylaxis.

10. SMR undergoing Hoffmann elimination : Atracurium , Cisatracurium.

( The metabolite of Atracurium called Laudanosine can accumulate (theoretically/on prolonged use) to induce Seizures.

The benzylisoquinolines group that includes d-TC, Atracurium, Cis-atracurium, Doxacurium and Mivacurium- 'tend to release Histamine' : The least histamine releasing among this group is Cis-atracurium.

11.   SMR used in Asthmatics : Atracurium, Vecuronium.

12.   SMR used to reduce BP : d-TC.

13.   SMR used to maintain BP : Pancuronium.

14.   SMR which is cardiostable (commonly used) : Vecuronium.

15.   SMR safe in Hepatic Failure & Renal Failure : Atracurium, Cisatracurium.

16.   SMR contraindicated in Pregnancy and Renal failure : Gallamine.

17.   Pancuronium is Vagolytic and thus it can produce tachycardia.

·         Muscle relaxants - onset and duration of action list:

Succinyl choline

Mivacurium

Rocuronium

Vecuronium

Atracurium

Cisatracurium

Piperacuronium

d-tubocurarine

Pancuronium

Doxacurium

So Marry Rosy Victoria's Attractive Sister, Prepared To Please Doctors. ( in PREPARE = Two P s indicate piperacuronium and please indicates pancuronium )

·         Daycare anaesthetic agents

1. Alfentanyl

2. Propofol

3. Isoflurane (congener)

4. Midazolam

5. Mivacurium

6. Sevoflurane

·         TIMETABLE FOR DISCONTINUATION OF ANTIPLATELET AGENTS BEFORE SURGERY

Aspirin--Irreversible defect-5-10 days

Cilostazol-Reversible inhibition of platelet aggregation-3 days

Clopidogrel-Irreversible defect-7-10 days

Dipyridamole-Inhibits platelet aggregation-2 days

NSAIDs-Reversible defect-4-5 half-lives before surgery

Ticlopidine-Irreversible defect-7-10 days