Drugs found in the drug tray:
Albuterol 17 gm (Proventil)
Drugs: albuterol & levabuterol (R-isomer of albuterol)
Drug Category: quick-relief medication for asthma
Mode of Action: bronchodilation by adenylate cyclase activation &  cAMP
Uses: relief of acute symptoms/bronchospasm, preventive treatment prior to exercise
induced asthma (2 hrs duration; 80% patients)
Adverse Effects: acute: have not been able to separate tremor from bronchodilation;
chronic: no impact on chronic airway inflammation traditionally because of
desensitization (but may be due to inducing phosphodiesterase, PDE3B & PDE4D, gene
products)
Therapeutic comment:
 drugs achieve 75% of max effect w/in 5 minutes
 90 g/puff exercise
 emergency 6-12 puffs or nebulizer—3 treatments every 20 minutes
Calcium Chloride 10 % in 10 ml syringe
Indications: Hypocalcemia; Cardiac arrest; Hyperkalemia; Toxicity, magnesium; Tetany,
neonatal; Tetany, secondary to parathyroid deficiency; Tetany, secondary to vitamin D
deficiency; Hypocalcemia, secondary to exchange transfusion; Colic, secondary to lead
toxicity; Toxicity, lead, adjunct
Off-label Indications: Not clinically relevant: Carcinoma, Medullary Thyroid
(diagnosis); Neuromuscular Blockade (antagonize); Zollinger-Ellison (diagnosis)
• In the treatment of hypocalcemia in conditions requiring a prompt increase in plasma
calcium levels (e.g., neonatal tetany and tetany due to parathyroid deficiency, vitamin D
deficiency and alkalosis) and for the prevention of hypocalcemia during exchange
transfusions.
• As adjunctive therapy in the management of acute symptoms in lead colic.
• In the treatment of magnesium intoxication due to overdosage of magnesium sulfate.
• In severe hyperkalemia, to combat deleterious effects on electrocardiographic (ECG)
funtion, pending correction of the potassium level in the extracellular fluid.
• In cardiac resuscitation, particularly after open heart surgery, when epinephrine fails to
improve weak or ineffective myocardial contractions.
Calcium chloride injection, 10% is irritating to veins and must not be injected into tissues,
since severe necrosis and sloughing may occur. Great care should be taken to avoid
extravasation or accidental injection into perivascular tissues.
Solutions should be warmed to body temperature. Injections should be made slowly
through a small needle into a large vein to minimize venous irritation and avoid
undesirable reactions. It is particularly important to prevent a high concentration of
calcium from reaching the heart because of the danger of cardiac syncope. If injected
into the ventricular cavity in cardiac resuscitation care must be taken to avoid injection
into the myocardial tissue.
Cefazolin 1 gm vial (Ancef)
1st Generation Cephalosporin
-Superior 1st gen for parenteral use; longest t½ (90min.; most others are 60 min).
-1st generation are most active cephalosporins for infections caused by Gram (+)
bacteria, especially sensitive staphylococci and streptococci; Gram (-) usually effective
against Proteus sp., E. coli, and Klebsiella, but - lactamase producing strains may be
resistant.
-least irritating after I.M. injection but all the cephalosporins are irritating after injection
-has the smallest volume of distribution (therefore giving highest blood levels).
-Used for urinary tract and skin infections; not much ABX difference with other 1st
generations.
Dexamethasone 20 mg/ 5 ml vial (Decadron)
Anti-inflammatory potency: high
Na+ retention potency: none
Duration of action: long
Given: PO, IM, IV
– Hydrocortisone; prednisone; prednisolone; methylprednisolone; triamcinolone;
betamethasone; dexamethasone
– ADME: given IV, PO, applied to skin, nose, and airways; highly PP bound to albumin
and corticosteroid binding proteins; highly metabolized in liver (reduction of double bond
at 4,5 position leads to inactive compound; 3-ketone is reduced to alcohol which can be
sulfated or glucuronidated and excreted in urine)
– Special concerns: w/drawal releases (-) feedback on CRH & ACTH acute adrenal
insufficiency; W/drawal syndrome – due to lack of feedback on adrenal (fever, myalgia,
arthralgia, malaise; usually occurs w/ continuous high dose tx)
– Carbohydrate metabolism:  gluconeogenesis;  glycogen formation; OVERALL: 
formation and storage of glucose
– Lipid metabolism:  lipolysis; redistribution of fat (Cushing’s – buffalo hump, moon
face, loss of fat in arms and legs)
– CNS effects: affect behavior, mood balance, brain excitability; high dose can cause
irritability, insomnia, restlessness, psychosis; maintaining glucose balance has indirect
effects
– Blood effects:  RBC’s and neutrophils;  lymphocytes, eosinophils, monocytes,
basophils (amt  of T cells > amt  of B cells); high levels lead to  lymphoid tissue
mass and vice-versa
– Anti-inflammatory effects:  synthesis/release of pro-inflammatory factors
(eicosanoids, PG’s, HETE’s, LT’s)
– Other effects: chronic use suppresses pituitary release of ACTH, GH, TSH, LH; large
doses antagonize effect of vitD on Ca2+ absorption; important for fetal lung development
Doxapram 400 mg/ 20 ml vial (Dopram)
DRUG CLASS: Analeptics; Stimulants, central nervous system
Indications: Pulmonary disease, chronic; Chronic obstructive pulmonary disease; Apnea,
post-anesthetic; Hypercapnia, acute; Respiratory depression, postoperative; Toxicity,
central nervous system depressants
Doxapram HCl produces respiratory stimulation mediated through the peripheral carotid
chemoreceptors. As the dosage level is increased, the central respiratory centers in the
medulla are stimulated with progressive stimulation of other parts of the brain and spinal
cord.
The onset of respiratory stimulation following the recommended single IV injection of
doxapram HCl usually occurs in 20-40 seconds with peak effect at 1-2 minutes. The
duration of effect may vary from 5-12 minutes.
The respiratory stimulant action is manifested by an increase in tidal volume associated
with a slight increase in respiratory rate.
A pressor response may result following doxapram administration. Provided there is no
impairment of cardiac function, the pressor effect is more marked in hypovolemic than in
normovolemic states. The pressor response is due to the improved cardiac output rather
than peripheral vasoconstriction. Following doxapram administration, an increased
release of catecholamines has been noted.
When the possibility of airway obstruction and/or hypoxia have been eliminated,
doxapram may be used to stimulate respiration in patients with drug-induced
postanesthesia respiratory depression or apnea other than that due to muscle relaxant
drugs.
To pharmacologically stimulate deep breathing in the postoperative patient. (A
quantitative method of assessing oxygenation, such as pulse oximetry, is
recommended.)
Diphenhydramine 50 mg/ 1 ml vial
DRUG CLASS: Antihistamines, H1
Indications: Parkinson's disease; Conjunctivitis, allergic; Transfusion
reaction; Anaphylaxis, adjunct; Motion
sickness; Angioedema; Urticaria; Dermatographism
Diphenhydramine HCl is an antihistamine with anticholinergic (drying) and sedative
effects. Antihistamines appear to compete with histamine for cell receptor sites on
effector cells.
Diphenhydramine is widely distributed throughout the body, including the CNS.
Diphenhydramine HCl has an atropine-like action and therefore should be used with
caution in patients with a history of lower respiratory disease including asthma,
increased intraocular pressure, hyperthyroidism, cardiovascular disease or hypertension.
Droperidol 5 mg/ 2 ml vial (Inapsine)
DRUG CLASS: Anesthetics,
general; Antiemetics/antivertigo; Anxiolytics; Sedatives/hypnotics
Indications: Nausea; Vomiting
Off-label Indications: Clinically relevant: Anesthesia, General; Anesthesia, Regional
(adjunct); Psychotic Disorder; Sedation, Conscious; Not clinically relevant: Delirium
Cases of QT prolongation and/or torsades de pointes have been reported in patients
receiving droperidol at doses at or below recommended doses. Some cases have
occurred in patients with no known risk factors for QT prolongation and some cases
have been fatal.
Cases of QT prolongation and serious arrhythmias (e.g., torsades de pointes) have been
reported in patients treated with droperidol. Based on these reports, all patients should
undergo a 12-lead ECG prior to administration of droperidol to determine if a prolonged
QT interval (i.e., QTc greater than 440 milliseconds for males or 450 milliseconds for
females) is present. If there is a prolonged QT interval, droperidol should NOT be
administered. For patients in whom the potential benefit of droperidol treatment is felt to
outweigh the risks of potentially serious arrhythmias, ECG monitoring should be
performed prior to treatment and continued for 2-3 hours after completing treatment to
monitor for arrhythmias.
Droperidol produces marked tranquilization and sedation. It allays apprehension and
provides a state or mental detachment and indifference while maintaining a state of
reflex alertness.
Droperidol produces an antiemetic effect as evidenced by the antagonism of
apomorphine in dogs. It lowers the incidence of nausea and vomiting during surgical
procedures and provides antiemetic protection in the postoperative period.
Droperidol potentiates other CNS depressants. It produces mild alpha-adrenergic
blockade, peripheral vascular dilatation and reduction of the pressor effect of
epinephrine. It can produce hypotension and decreased peripheral vascular resistance
and may decrease pulmonary arterial pressure (particularly if it is abnormally high). It
may reduce the incidence of epinephrine-induced arrhythmias, but it does not prevent
other cardiac arrhythmias.
The onset of action of single intramuscular and intravenous doses is from 3-10 minutes
following administration, although the peak effect may not be apparent for up to 30
minutes. The duration of the tranquilizing and sedative effects generally is 2-4 hours,
although alteration of alertness may persist for as long as 12 hours.
Epinephrine 1: 10,000 in 10 ml pre-filled syringe
DRUG CLASS: Adrenergic agonists; Bronchodilators; Inotropes; Ophthalmics
Indications: Rhinitis, allergic; Glaucoma, open-angle; Asthma; Serum sickness; Cardiac
arrest; Angioedema; Urticaria; Anaphylaxis; Anesthesia, local, adjunct; Anesthesia,
spinal, adjunct; Uterine contraction, inhibition
Off-label Indications: Not clinically relevant: Hemorrhage, Gastrointestinal; Hemorrhage,
Renal Arterial
Epinephrine is a sympathomimetic drug, acting on both alpha and beta receptors. It is
the drug of choice for the emergency treatment of severe allergic reactions (Type I) to
insect stings or bites, foods, drugs, and other allergens. It can also be used in the
treatment of idiopathic or exercise-induced anaphylaxis. Epinephrine when given
subcutaneously or intramuscularly has a rapid onset and short duration of action. The
strong vasoconstrictor action of epinephrine through its effect on alpha adrenergic
receptors acts quickly to counter vasodilation and increased vascular permeability which
can lead to loss of intravascular fluid volume and hypotension during anaphylactic
reactions. Epinephrine through its action on beta receptors on bronchial smooth muscle
causes bronchial smooth muscle relaxation which alleviates wheezing and dyspnea.
Epinephrine also alleviates pruritis, urticaria, and angioedema and may be effective in
relieving gastrointestinal and genitourinary symptoms associated with anaphylaxis.
In general, the most common uses of epinephrine are to relieve respiratory distress due
to bronchospasm, to provide rapid relief of hypersensitivity reactions to drugs and other
allergens, and to prolong the action of infiltration anesthetics. Its cardiac effects may be
of use in restoring cardiac rhythm in cardiac arrest due to various causes, but it is not
used in cardiac failure or in hemorrhagic, traumatic, or cardiogenic shock.
Esmolol 100 mg/ 10 ml vial (Brevibloc)
DRUG CLASS: Antiadrenergics, beta blocking; Antiarrhythmics, class II
Indications: Tachycardia, supraventricular; Tachycardia, intraoperative; Tachycardia,
postoperative; Hypertension, perioperative
Off-label Indications: Not clinically relevant: Ischemia, Myocardial; Tachyarrhythmia
Esmolol HCl is a beta1-selective (cardioselective) adrenergic receptor blocking agent
with rapid onset, a very short duration of action, and no significant intrinsic
sympathomimetic or membrane stabilizing activity at therapeutic dosages. Its elimination
half-life after intravenous infusion is approximately 9 minutes. Esmolol HCl inhibits the
beta1 receptors located chiefly in cardiac muscle, but this preferential effect is not
absolute and at higher doses it begins to inhibit beta2 receptors located chiefly in the
bronchial and vascular musculature.
Esmolol HCl is rapidly metabolized by hydrolysis of the ester linkage, chiefly by the
esterases in the cytosol of red blood cells and not by plasma cholinesterases or red cell
membrane acetylcholinesterase. Total body clearance in man was found to be about 20
L/kg/h, which is greater than cardiac output; thus the metabolism of esmolol HCl is not
limited by the rate of blood flow to metabolizing tissues such as the liver or affected by
hepatic or renal blood flow. Esmolol HCl has a rapid distribution half-life of about 2
minutes and an elimination half-life of about 9 minutes.
Using an appropriate loading dose, steady-state blood levels of esmolol HCl for dosages
from 50-300 μg/kg/min (0.05-0.3 mg/kg/min) are obtained within 5 minutes. (Steadystate is reached in about 30 minutes without the loading dose.) Steady-state blood levels
of esmolol HCl increase linearly over this dosage range and elimination kinetics are
dose-independent over this range. Steady-state blood levels are maintained during
infusion but decrease rapidly after termination of the infusion. Because of its short halflife, blood levels of esmolol HCl can be rapidly altered by increasing or decreasing the
infusion rate and rapidly eliminated by discontinuing the infusion.
Esmolol HCl has been shown to be 55% bound to human plasma protein, while the acid
metabolite is only 10% bound.
Esmolol HCl is indicated for the treatment of tachycardia and hypertension that occur
during induction and tracheal intubation, during surgery, on emergence from anesthesia,
and in the postoperative period, when in the physician's judgment such specific
intervention is considered indicated.
Etomidate 40 mg/ 20 ml syringe (Amidate)
DRUG CLASS: Anesthetics, general
Indications: Anesthesia, adjunct; Anesthesia, general
Etomidate is a hypnotic drug without analgesic activity. Intravenous injection of
etomidate produces hypnosis characterized by a rapid onset of action, usually within 1
minute. Duration of hypnosis is dose dependent but relatively brief, usually 3-5 minutes
when an average dose of 0.3 mg/kg is employed. Immediate recovery from anesthesia
(as assessed by awakening time, time needed to follow simple commands and time to
perform simple tests after anesthesia as well as they were performed before
anesthesia), based upon data derived from short operative procedures where
intravenous etomidate was used for both induction and maintenance of anesthesia, is
about as rapid as, or slightly faster than, immediate recovery after similar use of
thiopental. These same data revealed that the immediate recovery period will usually be
shortened in adult patients by the intravenous administration of approximately 0.1 mg of
intravenous fentanyl, 1 or 2 minutes before induction of anesthesia, probably because
less etomidate is generally required under these circumstances.
The most characteristic effect of intravenous etomidate on the respiratory system is a
slight elevation in arterial carbon dioxide tension (PaCO2).
Reduced cortisol plasma levels have been reported with induction doses of 0.3 mg/kg
etomidate. These persist for approximately 6-8 hours and appear to be unresponsive to
ACTH administration.
The intravenous administration of up to 0.6 mg/kg of etomidate to patients with severe
cardiovascular disease has little or no effect on myocardial metabolism, cardiac output,
peripheral circulation or pulmonary circulation. The hemodynamic effects of etomidate
have in most cases been qualitatively similar to those of thiopental sodium, except that
the heart rate tended to increase by a moderate amount following administration of
thiopental under conditions where there was little or no change in heart rate following
administration of etomidate. There are insufficient data concerning use of etomidate in
patients with recent severe trauma or hypovolemia to predict cardiovascular response
under such circumstances.
Etomidate induction is associated with a transient 20-30% decrease in cerebral blood
flow. This reduction in blood flow appears to be uniform in the absence of intracranial
space occupying lesions. As with other intravenous induction agents, reduction in
cerebral oxygen utilization is roughly proportional to the reduction in cerebral blood flow.
In patients with and without intracranial space occupying lesions, etomidate induction is
usually followed by a moderate lowering of intracranial pressure, lasting several minutes.
All of these studies provided for avoidance of hypercapnia. Information concerning
regional cerebral perfusion in patients with intracranial space occupying lesions is too
limited to permit definitive conclusions.
Reduced plasma cortisol and aldosterone levels have been reported following induction
doses of etomidate. These results persist for approximately 6-8 hours and appear to be
unresponsive to ACTH stimulation. This probably represents blockage of 11 betahydroxylation within the adrenal cortex.
Furosemide 20 mg/ 2 ml vial (Lasix)
Mode of Action: Actively secreted into PCT; acts on ascending loop of Henle (specifically
the Na+,K+,Cl- transporter) to inhibit the reabsorption of chloride
Uses: treatment of CHF (#1 diuretic for CHF), edema—various pathophysiologies (useful
in pulmonary edema because they produce short-term  in venous capacitance),
treatment of hypertension
Adverse Effects: allergy (related to sulfonamides), hypokalemia, hyponatremia &
dehydration, hyperglycemia (less common than w/ thiazides), hyperuricemia (excretion
of this drug in PCT will interfere w/ uric acid excretiongout), GI upset, ototoxicity
(ethacrynic acid especially, loop diuretics + aminoglycosides)
Urine composition: volume , sodium and chloride , potassium , bicarbonate ,
calcium  (supports renal calculus formation; negative calcium balance)
*Rapid onset of action (w/in minutes of IV administration), efficacy independent of acidbase balance, effective even w/ poor renal function; furosemide is twice daily &
torsemide is longer duration of action—once a day
Heparin 1000 units/ ml in 10 ml vial
Drug Category: heparin subclass of anticoagulants
Mode of Action: attaches to & activates antithrombin III  which complexes w/ serum
proteases to inactivate their protease activity
ADME: first cleared by initial saturable process (endothelial cell & macrophage
clearance) & secondly by slower, non-saturable renal clearance (w/ prolonged
admininstration  renal predominates); administrated subcutaneous or IV
Adverse Effects: unwanted bleeding  function of improper dosing (overdose can be
treated w/ protamine a positively charged drug that binds & inactivates heparin), allergic
reactions, chronic usage in dialysis patients or those undergoing chronic anticoagulation
therapy may develop osteoporosis, immediate re-occlusion of an arterial thrombosis w/
withdrawal of heparin, transient thrombocytopenia, peripheral necrosis in fingers & toes
from white clots
Precautions/Contraindications: patients w/ bleeding disturbances, pathologies prone to
bleeding (esophageal varices, active TB, or GI ulcerations), or w/ known hypersensitivity
*enoxapirin (Lovenox) similar to heparin w/ small molecular weight
--has longer ½ life: subcutaneous injection once daily
--does not produce thrombocytopenia & less chances of developing osteoporosis
--safe during pregnancy
Hetastarch 6 % in NS 500 ml (Hespan)
DRUG CLASS: Plasma expanders
Indications: Hypovolemia; Leukapheresis, adjunct
Off-label Indications: Not clinically relevant: Cryoprotective Agent (long-term storage of
whole blood); Plasma Volume Expander (during cardiopulmonary bypass); Priming Fluid
(for perfusion during extracorporeal circulation)
The plasma volume expansion produced by hetastarch approximate those of 5% human
albumin. Intravenous infusion of hetastarch results in expansion of plasma volume that
decreases over the succeeding 24 to 36 hours. The degree of plasma volume expansion
and improvement in hemodynamic state depend upon the patient's intravascular status.
Hetastarch molecules below 50,000 molecular weight are rapidly eliminated by renal
excretion. A single dose of approximately 500 ml of hetastarch (approximately 30 g)
results in elimination in the urine of approximately 33% of the dose within 24 hours. This
is a variable process but generally results in an intravascular hetastarch concentration of
less than 10% of the total dose injected by two weeks. A study of the biliary excretion of
hetastarch in 10 healthy males accounted for less than 1% of the dose over a 14-day
period. The hydroxyethyl group is not cleaved by the body, but remains intact and
attached to glucose units when excreted. Significant quantities of glucose are not
produced as hydroxyethylation prevents complete metabolism of the smaller polymers.
The addition of hetastarch to whole blood increases the eryathrocyte sedimentation rate.
Therefore, hetastarch is used to improve the efficiency of granulocyte collection by
centrifugal means.
Hetastarch is contraindicated in patients with known hypersensitivity to hydroxyethyl
starch, or with bleeding disorders, or with congestive heart failure where volume
overload is a potential problem. Hetastarch should not be used in renal disease with
oliguria or anuria not related to hypovolemia.
Hydralazine 20 mg/ 1 ml amp
Drug Category: arterial vasodilator
Mode of Action:  BP by arterial vasodilatation  release of NO from endothelial cells 
acts on vascular smooth muscle  activate guanylate cyclase 
 intracellular cGMP  relaxation of vascular smooth muscle
ADME: Important step in metabolic pathway is N-acetylation  slow acetylators don’t
metabolize drug as quickly exaggerated response
Adverse Effects: reflex tachycardia give  blocker, edema  give diuretics
3rd progressive step in controlling HTN: start w/ diuretic, add  blocker, and then arterial
vasodilator
also: nausea, headache, palpitations, sweating, and reversible Lupus-like syndrome
Precaution/Contraindications: slow acetylators; patients w/ underlying heart disease 
may induce anginal attacks & ischemic arrhythmias
Ketorolac 30 mg/ 1 ml vial (Toradol)
DRUG CLASS: Analgesics, non-narcotic; Nonsteroidal anti-inflammatory
drugs; Ophthalmics
Indications: Pain, moderate to severe; Conjunctivitis, allergic; Inflammation,
ophthalmic; Pain, ophthalmic; Photophobia, postoperative; Pruritus, ocular
Off-label Indications: Clinically relevant: Inflammation, Ocular; Not clinically
relevant: Miosis, Intraoperative; Pain, Postoperative
Toradol, a nonsteroidal anti-inflammatory drug (NSAID), is indicated for the short-term
(up to 5 days in adults) management of moderately severe acute pain that requires
analgesia at the opioid level. It is NOT indicated for minor or chronic painful conditions.
Toradol is a potent NSAID analgesic, and its administration carries many risks. The
resulting NSAID-related adverse events can be serious in certain patients for whom
Toradol is indicated, especially when the drug is used inappropriately. Increasing the
dose of Toradol beyond the label recommendations will not provide better efficacy but
will result in increasing the risk of developing serious adverse events.
Toradol can cause peptic ulcers, gastrointestinal bleeding and/or perforation. Therefore,
Toradol is CONTRAINDICATED in patients with active peptic ulcer disease, in patients
with recent gastrointestinal bleeding or perforation, and in patients with a history of
peptic ulcer disease or gastrointestinal bleeding.
Ketorolac tromethamine is a nonsteroidal anti-inflammatory drug (NSAID) that exhibits
analgesic activity in animal models. Ketorolac tromethamine inhibits synthesis of
prostaglandins and may be considered a peripherally acting analgesic. The biological
activity of ketorolac tromethamine is associated with the S-form. Ketorolac tromethamine
possesses no sedative or anxiolytic properties.
The peak analgesic effect of Toradol occures within 2-3 hours and is not statistically
significantly different over the recommended dosage range of Toradol. The greatest
difference between large and small doses of Toradol by either route was in the duration
of analgesia.
Labetalol 100 mg 20 ml vial
Drug Category: sympatholytic mixed antagonist
Mode of Action: selective for 1 block & non-selective for  block  does not produce
reflex tachycardia because  are block too (potency for  is 5X stronger but 
predominates because of innervated ’s on blood vessels);  plasma renin
Uses: due to dual action, especially useful in patients w/ both HTN and angina, HTN
emergencies, treat rebound HTN from clonidine w/drawal
Adverse Effects: orthostatic hypertension, sexual impotence
*Initially causes vasodilatation  chronic basis  both peripheral resistance and heart
rate; oral or IV administration; metabolized by the liver
Lidocaine (local) 2% 5 ml vial
Local anesthetics inhibit impulse conduction along the axon. This action is mediated by
inhibition of inward current through Na+ ion channel.
All local anesthetics bind to open or closed (not resting) Na+ channel to:
1) reduce Na+ conductance by  # of Na+ channels remaining in inactivated state (rest
block);
2) slow recovery of inactivated Na+ channels to resting state (rate-depend, time-dep, or
use-dep block)
-Local anesthetics consist of a lipophilic segment and a charged amine segment
connected in an amide or ester linkage. Mode of metabolism and incidence of allergy
are determined by chemical composition, either ester or amide.
-Each local anesthetic drugs can also be characterized by its molecular wt and lipid
solubility. As the MW and lipid solubility , drugs become more potent as local
anesthetics; dissociate more slowly f/ inactivated Na+ channel (longer ½ life for rate-dep
block); and are more toxic when released into the systemic circulation. As MW and lipid
solubility , the drugs have improved access to the site of action through the cell
membrane in their uncharged form. Larger, more lipophilic drugs also release more
slowly f/ their binding site on the Na+ channel. Access of local anesthetics to the Na+
channel is proposed to occur only f/ the cytoplasm, not ECF.
Duration of action of a local anesthetic is determined by its retention at the site of admin.
Termination of local anesthesia is largely dependent upon tissue blood flow. Toxicity is
determined by its plasma [ ].
-The factors determining the rate of absorption of a local anesthetic agent into the
systemic circulation include:
1) dosage;
2) intrinsic blood flow at site of injection;
3) inclusion of a vasoconstrictor at injection site;
4) physicochemical properties of the local anesth;
5) pH at injection site
-Overdosage, failure to follow well-established guidelines for dosages, is a principle
cause of local anesthetic toxicity. Systemic absorption following application of a local
anesthetic to a highly vascular tissue (mucosal surfaces) is faster than following
administration to a relatively avascular tissue (tendon).
-The principal determinant of the rate of absorption into the systemic circulation is blood
flow at the site of drug admin. All local anesthetics (w/ exception of cocaine) produce
local vasodilatation. Vasoconstrictors such as epi (1:100,000), phenylephrine
(1:20,000), or NE (1:100,000) prolong the duration of action of local anesthesia by  rate
of systemic absorption of the anesthetic f/ site of action. The slower systemic absorption
also  plasma drug [ ], reducing CV and CNS toxicity. Vasoconstrictors are more
effective in prolonging duration of action and reducing systemic toxicity for short-acting
agents such as procaine and lidocaine, than w/ longer-acting agents such as tetracaine
and bupivacaine.
Toxicity:
-Determined by: 1) properties of the local anesthetic;
2) rate of absorption of local anesthetic into systemic circulation.
-Allergy (acute anaphylaxis) to local anesthetics is not uncommon and is most common
w/ ester types containing p-aminobenzoate (procaine, tetracaine). Allergy with the
amide types is rare.
-Systemic toxicity primarily effects 2 organ systems: CNS & CV system.
-Systemic toxicity w/ lidocaine and most other locals occurs w/ overdosage (failure to
follow established guidelines for admin). If no more than 500 mg of lidocaine is
administered to full-sized adult, any systemic toxicity which may occur will be mild.
Toxicity is more common in children as dose and [ ] of the local injected to produce local
anesthesia is larger in relation to body mass and ability to metabolize drug than w/
adults.
-Deaths following local anesthetic administration generally occur b/c:
1) local anesthetics are used in a pt also receiving CNS depressants such as barb’s or
opiates;
2) a clinician is not prepared for respiratory depression most commonly observed as a
serious toxicity of local andministration. Hypercapnia and acidosis facilitate seizure
activity. Although grand mal seizures are often reported to precede respiratory arrest,
the progression to later stages of toxicity may be observed in absence of prodromal
signs. Respiratory and and oxygenation support must be available even w/ infiltration
anesthesia commonly performed in Dr’s or dentist’s office. If an anticonvulsive drug is
needed for tonic-clonic seizures assoc w/ local anesthetics, IV diazepam is DOC for
anticonvulsant activity.
Most commonly used local anesthetic and antiarrhythmics drug. It is metabolized in the
liver to 2 metabolites which lack antiarrhythmics drug activity while retaining CNS
stimulatory activity. Has a short duration of activity as a local anesthetics and
antiarrhythmic drugs. Although it can be used safely as a local w/o concomitant admin
of a vasoconstrictor, the use of a vasoconstrictor prolongs its duration of action and 
peak systemic lidocaine [ ] observed in plasma
Lidocaine (cardiac) 100 mg/ 5 ml syringe
Drug Category: Class IB antiarrhythmic
Hemodynamic Effects: mild negative inotropic agents, little ability to vasodilate, C.O. &
BP are NOT affected EXCEPT in severe heart failure
Electrophysiologic Effects: in normal rapid response tissue  shortens action potential
duration,  phase 0 upstroke (prolongs recovery of inactivated channels) &  conduction
( conduction only @ high HR); in ischemically damaged cardiac tissue  prolong
refractory period & slow or block conduction (even @ low HR); may cause QT
shortening; little effect on slow response tissues
Uses: ventricular arrhythmias: 1)accompanying acute MI, 2)following cardiac surgery, &
3)due to digitalis intoxication
ADME: IM or IV injection, initial bolus followed by constant infusion  bolus has little
antiarrhythmic effects due to rapid distribution to other tissues; absorbed orally but not
effective due to rapid liver metabolism; metabolites build up in chronic treatment 
grand mal seizures
Adverse Effects: neurologic sequelae, muscle tremors, restlessness, blurred vision,
nystagmus, insomnia; large over dose  focal or grand mal seizures, respiratory
depression, hypotension; MAY BE PROARRHYTHMIC
*lidocaine exhibits Vmax depression only @ high HR whereas quinidine exhibits Vmax
depression @ moderate and high HR (neither exhibit Vmax depression @ slow HR)
*this is because class IB bind & unbind in msec & class IA bind & unbind in sec
Metoclopramide 10 mg/ 2 ml vial (Reglan)
DRUG CLASS: Antiemetics/antivertigo; Gastrointestinals; Stimulants, gastrointestinal
Indications: Nausea, secondary to cancer chemotherapy; Vomiting, secondary to cancer
chemotherapy; Gastroesophageal reflux disease; Nausea, postoperative; Vomiting,
postoperative; Intubation, intestinal; Gastroparesis, diabetic; Testing, gastrointestinal,
adjunct
Off-label Indications: Clinically relevant: Headache, Vascular; Hiccups, Persistent; Not
clinically relevant: Anorexia Nervosa; Aspiration Pneumonitis (prophylaxis); Gastric
Emptying, Slow; Gastric Stasis (in preterm infants); Gastric Stasis,
Postsurgical; Lactation, Postpartum; Ulcer, Peptic; Vertigo
Metoclopramide stimulates motility of the upper gastrointestinal tract without stimulating
gastric, biliary, or pancreatic secretions. Its mode of action is unclear. It seems to
sensitize tissues to the action of acetylcholine. The effect of metoclopramide on motility
is not dependent on intact vagal innervation, but it can be abolished by anticholinergic
drugs.
Metoclopramide increases the tone and amplitude of gastric (especially antral)
contractions, relaxes the pyloric sphincter and the duodenal bulb, and increases
peristalsis of the duodenum and jejunum resulting in accelerated gastric emptying and
intestinal transit. It increases the resting tone of the lower esophageal sphincter. It has
little, if any, effect on the motility of the colon or gallbladder.
In patients with gastroesophageal reflux and low LESP (lower esophageal sphincter
pressure), single oral doses of metoclopramide produce dose-related increases in LESP.
Effects begin at about 5 mg and increase through 20 mg (the largest dose tested). The
increase in LESP from a 5-mg dose lasts about 45 minutes and that of 20 mg lasts
between 2 and 3 hours. Increased rate of stomach emptying has been observed with
single oral doses of 10 mg.
The antiemetic properties of metoclopramide appear to be a result of its antagonism of
central and peripheral dopamine receptors. Dopamine produces nausea and vomiting by
stimulation of the medullary chemoreceptor trigger zone (CTZ), and metoclopramide
blocks stimulation of the CTZ by agents like l-dopa or apomorphine which are known to
increase dopamine levels or to possess dopamine-like effects. Metoclopramide also
abolishes the slowing of gastric emptying caused by apomorphine.
The onset of pharmacological action of metoclopramide is 1-3 minutes following an IV
dose, 10-15 minutes following IM administration, and 30-60 minutes following an oral
dose; pharmacological effects persist for 1-2 hours.
Mivacurium 20 mg/ 10 ml vial (Mivacron)
–Compete w/ Ach for nicotinic sites and thus prevent Ach depolarization of endplate. All
are highly charged molecules and do not penetrate BBB.
–Produce NO reduction in pain sensation. Flaccid paralysis is produced w/ smaller
muscles being affected 1st and larger muscles, including diaphragm, being more
refractory to blockade. Recovery occurs in reverse order.
–Primary medical use is to produce needed muscle relaxation during surgical
procedures (ab muscle relaxation) as well as to permit lower levels of general
anesthetics to be used (don’t need to relax muscle tone w/ general anesthetic alone).
General anesthetics also produce varying degrees of muscle depression (halothane,
isofurane, enflurane). NMJ blocking dose must be adjusted accordingly.
–There are many “spare” nicotinic receptors at endplate (high safety factor). 75% of
receptors at endplate must be blocked before decrement in fxn is observed. Recovery is
complete after 75% become occupied.
–Choice of which agent to use in a particular instance depends on 2 effects of
compounds (autonomic or other additional actions) and route of elimination. Pt’s w/
renal disease would exhibit prolonged action w/ a drug eliminated primarily by kidney.
Hepatic elimination might present a problem w/ cirrhosis pt. Hypotension might be
problematic in some pts w/ CV disease whereas histamine induced bronchiolar
constriction would be untoward in asthmatics. Artificial respiration equipment should
always be on hand when any of these drugs are used.
–Shortest duration of drug action of any of the competitive NMJ blocking drugs.
–Clearance is by inactivation w/ plasma cholinesterase.
Naloxone 0.4 mg/ 1 ml vial (Narcan)
DRUG CLASS: Antagonists, narcotic; Antidotes
Indications: Overdose, opiate; Diagnosis, opiate intoxication; Poisoning, opiate
Off-label Indications: Clinically relevant: Opioid Dependence (diagnosis); Not clinically
relevant: Coma, Alcohol-induced; Coma, Clonidine-induced; Dementia, Senile; Edema,
Pulmonary (high altitude); Neurological Deficits, Ischemic; Respiratory Failure,
Acute; Shock, Cardiogenic; Shock, Septic
Naloxone HCl prevents or reverses the effects of opioids including respiratory
depression, sedation and hypotension. Also, it can reverse the psychotomimetic and
dysphoric effects of agonist-antagonists such as pentazocine.
Naloxone HCl is an essentially pure narcotic antagonist, i.e., it does not possess the
"agonistic" or morphine-like properties characteristic of other narcotic antagonists;
naloxone HCl does not produce respiratory depression, psychotomimetic effects or
pupillary constriction. In the absence of narcotics or agonistic effects of other narcotic
antagonists, it exhibits essentially no pharmacologic activity.
When naloxone HCl injection is administered intravenously, the onset of action is
generally apparent within 2 minutes; the onset of action is only slightly less rapid when it
is administered subcutaneously or intramuscularly. The duration of action is dependent
upon the dose and route of administration of naloxone HCl. Intramuscular administration
produces a more prolonged effect than intravenous administration. The requirement for
repeat doses of naloxone HCl, however, will also be dependent upon the amount, type
and route of administration of the narcotic being antagonized.
Odansetron 4 mg/ ml (Zofran)
DRUG CLASS: Antiemetics/antivertigo; Serotonin receptor antagonists
Indications: Nausea, secondary to cancer chemotherapy; Vomiting, secondary to cancer
chemotherapy; Nausea, postoperative; Vomiting, postoperative; Nausea, secondary to
radiation therapy; Vomiting, secondary to radiation therapy.
Ondansetron is a selective 5-HT3 receptor antagonist. While ondansetron's mechanism
of action has not been fully characterized, it is not a dopamine-receptor antagonist.
Serotonin receptors of the 5-HT3 type are present both peripherally on vagal nerve
terminals and centrally in the chemoreceptor trigger zone of the area postrema. It is not
certain whether ondansetron's antiemetic action in chemotherapy-induced nausea and
vomiting is mediated centrally, peripherally, or in both sites. However, cytotoxic
chemotherapy appears to be associated with release of serotonin from the
enterochromaffin cells of the small intestine. In humans, urinary 5-HIAA (5hydroxyindoleacetic acid) excretion increases after cisplatin administration in parallel
with the onset of vomiting. The released serotonin may stimulate the vagal afferents
through the 5-HT3 receptors and initiate the vomiting reflex.
Ondansetron is extensively metabolized in humans, with approximately 5% of a
radiolabeled dose recovered as the parent compound from the urine. The primary
metabolic pathway is hydroxylation on the indole ring followed by glucuronide or sulfate
conjugation.
Promethazine 25 mg/ 1 ml amp (Phenergan)
DRUG CLASS: Antiemetics/antivertigo; Antihistamines, H1; Phenothiazines
Indications: Rhinitis, allergic; Rhinitis, vasomotor; Conjunctivitis, allergic; Transfusion
reaction; Anaphylaxis, adjunct; Motion sickness; Pain,
adjunct; Sedation; Dermographism; Urticaria; Nausea; Vomiting; Allergic reactions
Off-label Indications: Not clinically relevant: Hemolytic Disease of the Newborn
Promethazine HCl is a phenothiazine derivative which possesses antihistaminic,
sedative, antimotion-sickness, antiemetic, and anticholinergic effects. Promethazine is a
competitive H1 receptor antagonist, but does not block the release of histamine.
Structural differences from the neuroleptic phenothiazines results in its relative lack
(1/10) of dopamine antagonist properties. In therapeutic doses, promethazine HCl
produces no significant effects on the cardiovascular system. Clinical effects are
generally apparent within 5 minutes of an IV injection and within 20 minutes of an IM
injection. Duration of action is 4-6 hours, although effects may persist up to 12 hours.
Promethazine HCl is metabolized in the liver, with the sulfoxides of promethazine and Ndesmethylpromethazine being the predominant metabolites appearing in the urine.
Following IV administration in healthy volunteers, the plasma half-life for promethazine
has been reported to range from 9-16 hours. The mean plasma half-life for promethazine
after IM administration in healthy volunteers has been reported to be 9.8 ± 3.4 hours.
Promethazine HCl injection is indicated for the following conditions:
Amelioration of allergic reactions to blood or plasma.
In anaphylaxis as an adjunct to epinephrine and other standard measures after
the acute symptoms have been controlled.
For other uncomplicated allergic conditions of the immediate type when oral
therapy is impossible or contraindicated.
For sedation and relief of apprehension and to produce light sleep from which the
patient can be easily aroused.
Active treatment of motion sickness.
Prevention and control of nausea and vomiting associated with certain types of
anesthesia and surgery.
As an adjunct to analgesics for the control of postoperative pain.
Preoperative, postoperative, and obstetric (during labor) sedation.
Intravenously in special surgical situations, such as repeated bronchoscopy,
ophthalmic surgery, and poor-risk patients, with reduced amounts of meperidine
or other narcotic analgesic as an adjunct to anesthesia and analgesia.
Propofol 20 ml vial
–Rapid onset.
–Used to induce general anesthesia and to produce conscious sedation.
–Undergoes rapid redistribution w/ α-phase ½ life of 2-8 min and β-phase ½ life of 30-60
min similar to barb’s.
–Termination of general anesthetic activity is consistent w/ rapid distribution, lasting 1020 min.
–Milky white emulsion. Anaphylactoid rexns can occur, but are probably a result of the
emulsifying agent rather than the active agent (2,6-diisopropylphenol).
–Can inhibit platelet fxn and  bleeding times although this is a short-lived phenomenon.
Scopolamine 0.4 mg/ 1 ml vial
Class:Anticholinergics; Antiemetics/antivertigo; Cycloplegics; Gastrointestinals; Mydriatic
s; Ophthalmics; Preanesthetics; Sedatives/hypnotics
Indications: Irritable bowel syndrome; Spasticity; Iridocyclitis; Motion
sickness; Preanesthesia; Sedation; Nausea; Vomiting; Delirium
tremens; Diverticulitis; Dysentery; Cycloplegia induction; Gastrointestinal
spasm; Mydriasis induction; Paralysis Agitans; Parkinsonism, postencephalitic
Off-label Indications: Clinically relevant: Bowel Syndrome,
Irritable; Parkinsonism; Sialorrhea; Not clinically relevant: Synechiae
Scopolamine hydrobromide is one of the major antimuscarinic agents that inhibit the
action of acetylcholine (ACh) on autonomic effectors innervated by postganglionic
cholinergic nerves as well as on smooth muscles that lack cholinergic innervation. It
exerts little effects on the actions of ACh at nicotinic receptor sites such as autonomic
ganglia. The major action of this antimuscarinic agent is a surmountable antagonism to
ACh and other muscarinic agents.
As compared with atropine, scopolamine differs only quantitatively in antimuscarinic
actions. Scopolamine has a stronger action on the iris, ciliary body and certain secretory
glands such as salivary, bronchial and sweat. Scopolamine, in therapeutic doses,
normally causes drowsiness, euphoria, amnesia, fatigue and dreamless sleep with a
reduction in rapid-eye-movement sleep. However, the same doses occasionally cause
excitement, restlessness, hallucinations or delirium, especially in the presence of severe
pain. Scopolamine depresses the EEG arousal response to photo-stimulation. It is more
potent than atropine on the antitremor activity (parkinsonism) in animals induced by
surgical lesions. Scopolamine is effective in preventing motion sickness by acting on the
maculae of the utricle and saccule.
Scopolamine, although less potent than atropine, has been used frequently in
preanesthetic medication for the purpose of inhibiting the secretions of the nose, mouth,
pharynx and bronchi and reduces the occurrence of laryngospasm during general
anesthesia. Scopolamine is less potent in the decrease of cardiac rate, but not in the
changes of blood pressure or cardiac output. Like other antimuscarinic agents,
scopolamine has been used widely in the treatment of peptic ulcers and as an
antispasmodic agent for GI disorders. This is due to the fact that scopolamine reduces
salivary secretion, the gastric secretion (both the volume and acid content), and also it
inhibits the motor activity of the stomach, duodenum, jejunum, ileum and colon,
characterized by a decrease in tone, amplitude and frequency of peristaltic contractions.
Sodium Bicarbonate 50 mEq/ 50 ml syringe
DRUG CLASS: Alkalinizing agents; Electrolyte replacements
Indications: Acidosis, metabolic
Off-label Indications: Not clinically relevant: Anemia, Sickle Cell; Contrast Media Toxicity
(prophylaxis)
Intravenous sodium bicarbonate therapy increases plasma bicarbonate, buffers excess
hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of
acidosis.
Sodium bicarbonate in water dissociates to provide sodium (Na+) and bicarbonate
(HCO3-) ions. Sodium (Na+) is the principal cation of the extracellular fluid and plays a
large part in the therapy of fluid and electrolyte disturbances. Bicarbonate (HCO3-)is a
normal constituent of body fluids and the normal plasma level ranges from 24 to 31
mEq/liter. Plasma concentration is regulated by the kidney through acidification of the
urine when there is an excess. Bicarbonate anion is considered "labile" since at a proper
concentration of hydrogen ion (H+) it maybe converted to carbonic acid (H2CO3) and
thence to its volatile form, carbon dioxide (CO2) excreted by the lung. Normally a ratio of
1:20 (carbonic acid; bicarbonate) is present in the extracellular fluid. In a healthy adult
with normalkidney function, practically all the glomerular filtered bicarbonate ion is
reabsorbed; less than 1% is excreted in the urine.
Sodium bicarbonate injection, USP is indicated in the treatment of metabolic acidosis
which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency
due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest
and severe primary lactic acidosis. Sodium bicarbonate is further indicated in the
treatment of certain drug intoxications, including barbiturates (where dissociation of the
barbiturate-protein complex is desired), in poisoning by salicylates or methyl alcohol and
in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of
hemoglobin and its breakdown products. Sodium bicarbonate also is indicated in severe
diarrhea which is often accompanied by a significant loss of bicarbonate.
Treatment of metabolic acidosis should, if possible, be superimposed on measures
designed to control the basic cause of the acidosis - e.g., insulin in uncomplicated
diabetes, blood volume restoration in shock. But since an appreciable time interval may
elapse before all of the ancillary effects arebrought about, bicarbonate therapy is
indicated to minimize risks inherent to the acidosis itself.
Vigorous bicarbonate therapy is required in any form of metabolic acidosis where a rapid
increase in plasma total CO2 content is crucial - e.g., cardiac arrest, circulatory
insufficiency due to shock or severe dehydration, and in severe primary lactic acidosis or
severe diabeticacidosis.
Solu-Cortef 100 mg vial (Cortisone)
See also dexamethasone for corticosteroid overview
Prepared Syringes:
Atropine 0.4 mg/ ml in 5 ml syringe
DRUG CLASS:
Antiarrhythmics; Anticholinergics; Antidotes; Cycloplegics; Mydriatics; Ophthalmics; Prea
nesthetic
Indications: Anesthesia, adjunct; Bradycardia; Cycloplegia; Heart
block; Mydriasis; Toxicity, cholinergic drugs; Toxicity, mushroom; Toxicity,
organophosphate; Inflamation, uvea, adjunct; Pylorospasm; Suppression, vagal
activity; Spasm, gastrointestinal; Colic, biliary; Colic, ureteral
This antocholinergic preparation blocks the responses of the sphincter muscle of the iris
and the accomodative muscle of the ciliary body to cholinergic stimulation, producing
pupillary dilation (mydriasis) and paralysis of accomodation (cycloplegia).
Cisatracurium 2 mg/ ml in 10 ml syringe (Nimbex)
DRUG CLASS: Musculoskeletal agents; Neuromuscular blockers,
nondepolarizing; Relaxants, skeletal muscle
Indications: Anesthesia, adjunct
The neuromuscular blocking potency of cisatracurium besylate is approximately 3-fold
that of atracurium besylate. The time to maximum block is up to 2 minutes longer for
equipotent doses of cisatracurium besylate compared to atracurium besylate. The
clinically effective duration of action and rate of spontaneous recovery from equipotent
doses of cisatracurium besylate and atracurium besylate are similar.
Isoflurane or enflurane administered with nitrous oxide/oxygen to achieve 1.25 MAC
(Minimum Alveolar Concentration) may prolong the clinically effective duration of action
of initial and maintenance doses, and decrease the average infusion rate requirement of
cisatracurium besylate. The magnitude of these effects may depend on the duration of
administration of the volatile agents. Fifteen (15) to 30 minutes of exposure to 1.25 MAC
isoflurane or enflurane had minimal effects on the duration of action of initial doses of
cisatracurium besylate and therefore, no adjustment to the initial dose should be
necessary when cisatracurium besylate is administered shortly after initiation of volatile
agents. In long surgical procedures during enflurane or isoflurane anesthesia, less
frequent maintenance dosing, lower maintenance doses, or reduced infusion rates of
cisatracurium besylate may be necessary. The average infusion rate requirement may
be decreased by as much as 30-40%.
Glycopyrrolate 0.2 mg/ ml in 5 ml syringes (Robinul)
DRUG CLASS: Anticholinergics; Gastrointestinals
Indications: Anesthesia, adjunct; Ulcer, peptic
Glycopyrrolate, like other anticholinergic (antimuscarinic) agents, inhibits the action of
acetylcholine on structures innervated by postganglionic cholinergic nerves and on
smooth muscles that respond to acetylcholine but lack cholinergic innervation. These
peripheral cholinergic receptors are present in the autonomic effector cells of smooth
muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, exocrine glands
and, to a limited degree, in the autonomic ganglia. Thus, it diminishes the volume and
free acidity of gastric secretions and controls excessive pharyngeal, tracheal, and
bronchial secretions.
Glycopyrrolate antagonizes muscarinic symptoms (e.g., bronchorrhea, bronchospasm,
bradycardia, and intestinal hypermotility) induced by cholinergic drugs such as the
anticholinesterases.
The highly polar quaternary ammonium group of glycopyrrolate limits its passage across
lipid membranes, such as the blood-brain barrier, in contrast to atropine sulfate and
scopolamine hydrobromide, which are highly non-polar tertiary amines which penetrate
lipid barriers easily.
With IV injection, the onset of action is generally evident within one minute. Following
intramuscular administration, the onset of action is noted in 15-30 minutes, with peak
effects occurring within approximately 30 to 45 minutes. The vagal blocking effects
persist for 2-3 hours and the antisialagogue effects persist up to 7 hours, periods longer
than for atropine.
Neostigmine 5 ml syringe
DRUG CLASS: Cholinesterase inhibitors; Musculoskeletal agents; Stimulants, muscle
Neostigmine inhibits the hydrolysis of acetylcholine by competing with acetylcholine for
attachment to acetylcholinesterase at sites of cholinergic transmission. It enhances
cholinergic action by facilitating the transmission of impulses across neuromuscular
junctions. It also has a direct cholinomimetic effect on skeletal muscle and possibly on
autonomic ganglion cells and neurons of the central nervous system. Neostigmine
undergoes hydrolysis by cholinesterase and is also metabolized by microsomal enzymes
in the liver. Protein binding to human serum albumin ranges from 15 to 25 percent.
Neostigmine bromide is poorly absorbed from the gastrointestinal tract following oral
administration. As a rule, 15 mg of neostigmine bromide orally is equivalent to 0.5 mg of
neostigmine methylsulfate parenterally, due to poor absorption of the tablet from the
intestinal tract. In a study in fasting myasthenic patients, the extent of absorption was
estimated to be 1 to 2 percent of the ingested 30-mg single oral dose. Peak
concentrations in plasma occurred 1 to 2 hours following drug ingestion, with
considerable individual variations. The half-life ranged from 42 to 60 minutes with a
mean half-life of 52 minutes.
Rocuronium 10 mg/ 1 ml syringe or 1 ml in 10 ml syringe
(Zemuron)
DRUG CLASS: Musculoskeletal agents; Neuromuscular blockers,
nondepolarizing; Relaxants, skeletal muscle
Indications: Anesthesia, adjunct
Rocuronium bromide injection is a nondepolarizing neuromuscular blocking agent with a
rapid to intermediate onset depending on dose and intermediate duration. It acts by
competing for cholinergic receptors at the motor end-plate. This action is antagonized by
acetylcholinesterase inhibitors, such as neostigmine and edrophonium.
Following IV administration of rocuronium bromide injection, plasma levels of rocuronium
follow a 3 compartment open model. The rapid distribution half-life is 1-2 minutes and
the slower distribution half-life is 14-18 minutes. Rocuronium is approximately 30%
bound to human plasma proteins. In geriatric and other adult surgical patients
undergoing either opioid/nitrous oxide/oxygen or inhalational anesthesia, the observed
pharmacokinetic profile was essentially unchanged.
Succinylcholine 20 mg/ ml in 10 ml syringe
–Administered IV to produce short-acting depolarizing block of skeletal muscle lasting
about 5 min. Short action is related to metabolism by plasma and liver
pseudocholinesterases to succinic acid and choline.
–About 1/3000 pts have a genetic defect producing a virtual absence of
pseudocholinesterase and thus have a much prolonged blockade.
–Some pts w/ severe liver dz may exhibit a similar prolonged response de to lack of NZ
(pseudocholinesterase) synthesis. In these cases, metabolism of succinylcholine can be
hastened by administering plasma w/ normal pseudocholinesterase levels.
–Does release histamine. Also stimulates autonomic ganglia and may cause a mild of
BP and bradycardia due to ganglionic effects. Rarely produces a syndrome known as
malignant hyperthermia which may be related to the initial intense muscular
contractions.
–Tends to  eye, CSF, and GI pressure and thus may be contraindicated in glaucoma
pts, those w/ suspected brain tumors, and immediately after meals.
–The short duration of action has made it one of the DOC to relax laryngeal muscles
prior to intubation and as an adjuvant prior to electroconvulsive shock therapy. When
infused for longer times, the nature of the blockade reverts to an apparent
desensitization (phase II blockade) of the nicotinic receptors and takes on the
characteristics of long term competitive antagonism. It is generally not recommended for
long term administration.
Controlled Substances not in the drug tray:
Fentanyl (Sublimaze)
DRUG CLASS: Analgesics, narcotic; Anesthetics, general
Indications: Anesthesia, adjunct; Anesthesia, general; Pain, cancer; Anesthesia,
induction; Pain, chronic
Off-label Indications: Not clinically relevant: Pain, Post-operative
Fentanyl citrate is a narcotic analgesic. A dose of 100 μg (0.1 mg) (2.0 ml) is
approximately equivalent in analgesic activity to 10 mg of morphine or 75 mg of
meperidine. The principal actions of therapeutic value are analgesia and sedation.
Alterations in respiratory rate and alveolar ventilation, associated with narcotic
analgesics, may last longer than the analgesic effect. As the dose of narcotic is
increased, the decrease in pulmonary exchange becomes greater. Large doses may
produce apnea. Fentanyl appears to have less emetic activity than either morphine or
meperidine. Histamine assays and skin wheal testing in man indicate that clinically
significant histamine release rarely occurs with fentanyl. Recent assays in man show no
clinically significant histamine release in dosages up to 50 μg/kg (0.05 mg/kg) (1 ml/kg).
Fentanyl preserves cardiac stability and blunts stress-related hormonal changes at
higher doses.
Sublimaze (fentanyl citrate) injection is indicated for:
• Analgesic action of short duration during the anesthetic periods, premedication,
induction and maintenance, and in the immediate postoperative period (recovery
room) as the need arises.
• Use as a narcotic analgesic supplement in general or regional anesthesia.
• Administration with a neuroleptic such as droperidol injection as an anesthetic
premedication, for the induction of anesthesia and as an adjunct in the
maintenance of general and regional anesthesia.
• Use as an anesthetic agent with oxygen in selected high risk patients, such as
those undergoing open heart surgery or certain complicated neurological or
orthopedic procedures.
Midazolam (Versed)
–Most selected for high anxiolytic potency in relation to their CNS depressive effects.
–All BDZ’s possess sedative-hypnotic properties to varying degrees, which are
extensively used clinically to facilitate sleep.
–Have largely replaced barbiturates as sedative agents b/c of relative safety.
–Receptors for BDZ’s found in CNS (thalamus, limbic system, cerebral cortex). They
form part of a GABAA receptor-chloride ion channel macromolecular complex.
–The GABAA recep is a membrane chloride channel that mediates most of the rapid,
inhibitory neurotransmission in CNS. (BDZ’s do NOT work on GABAB recep)
–BDZ’s  frequency of GABA-mediated Cl- ion channel opening
t½: 3hrs
Duration of action: Ultra short (<6 hrs)
Main clinical use: Sedation (peak=15-30 min)
Ephedrine
DRUG CLASS: Adrenergic agonists; Bronchodilators; Decongestants, nasal
Indications: Bronchospasm, acute; Hypotension, secondary
Therapeutic doses of ephedrine produce mainly relaxation of smooth muscle and, if
norepinephrine stores are intact, cardiac stimulation and increased systolic and usually
increased diastolic blood pressure. Its vasopressor effect results largely from increased
cardiac output and to a lesser extent from peripheral vasoconstriction. Pressor
responses to parenteral ephedrine are slower but more prolonged than those produced
by epinephrine. Ephedrine stimulates both alpha and beta receptors and its peripheral
actions are due partly to norepinephrine release and partly to direct effect on receptors.
Ephedrine may deplete norepinephrine stores in sympathetic nerve endings, so that
tachyphylaxis to cardiac and pressor effects of the drug may develop. Central nervous
system effects are similar to those of amphetamine drugs but less pronounced. The
central effects of ephedrine are overshadowed to a large extent by its peripheral actions.
Ephedrine is rapidly and completely absorbed following parenteral injection. Pressor and
cardiac responses to ephedrine persist for 1 hour following intramuscular or
subcutaneous administration of 25-50 mg.
Ephedrine sulfate injection is indicated primarily to counteract the hypotensive effects of
spinal or other types of nontopical conduction anesthesia. It is also useful as a pressor
agent in hypotensive states following sympathectomy, or following overdosage with
ganglionic-blocking agents, antiadrenergic agents, veratrum alkaloids or other drugs
used for lowering blood pressure in the treatment of arterial hypertension. The drug is
sometimes injected to relieve acute bronchospasm, but it is less effective than
epinephrine for this purpose.