INTRAVENOUS ANESTHETICS
MOA The actions of benzodiazepines such as midazolam are
PROPOFOL (Diprivan)
Summar Propofol is a medication used in general anesthesia and for
y sedation.
Dosage Inj.:
10 mg/mL, 20 mL ampule (IV)
10 mg/mL, 50 mL pre‐filled syringe (IV)
10 mg/mL, 20 mL and 50 mL vial (IV)
Backgro Propofol is an intravenous anesthetic agent used for induction
und and maintenance of general anesthesia. IV administration of
propofol is used to induce unconsciousness after which
anesthesia may be maintained using a combination of
medications. Recovery from propofol-induced anesthesia is
generally rapid and associated with less frequent side effects
(e.g. drowsiness, nausea, vomiting) than with thiopental,
methohexital, and etomidate. Propofol may be used prior to
diagnostic procedures requiring anesthesia, in the
management of refractory status epilepticus, and for induction
and/or maintenance of anesthesia prior to and during
surgeries.
MOA The action of propofol involves a positive modulation of the
inhibitory function of the neurotransmitter gamma-
aminobutyric acid (GABA) through GABA-A receptors.
MIDAZOLAM (Benzodiazepines)
Summar a short-acting injectable benzodiazepine with rapid onset that
y is commonly used in seizures, anesthesia and anxiety
disorders
Dosage Inj.:
1 mg/mL, 5 mL ampule/vial (IM, IV)
5 mg/mL, 1 mL, 2 mL, 3 mL, 5 mL and 10 mL ampule (IM,
IV)
Backgro Midazolam is a short-acting hypnotic-sedative drug with
und anxiolytic, muscle relaxant, anticonvulsant, sedative,
hypnotic, and amnesic properties.6 It belongs to a class of
drugs called benzodiazepines. This drug is unique from others
in this class due to its rapid onset of effects and short duration
of action.6 Midazolam is available by oral, rectal, intranasal,
intramuscular (IM), and intravenous (IV) routes and has been
used in various biomedical applications, including dentistry,
cardiac surgery, and endoscopic procedures as pre-anesthetic
medication, and as an adjunct to local anesthesia.
mediated through the inhibitory neurotransmitter gamma-
aminobutyric acid (GABA), which is one of the major
inhibitory neurotransmitters in the central nervous system.
Benzodiazepines increase the activity of GABA, thereby
producing a sedating effect, relaxing skeletal muscles, and
inducing sleep, anesthesia, and amnesia. Benzodiazepines
bind to the benzodiazepine site on GABA-A receptors, which
potentiates the effects of GABA by increasing the frequency
of chloride channel opening. These receptors have been
identified in different body tissues including the heart and
skeletal muscle, although mainly appear to be present in the
central nervous system
FENTANYL (Opioid Agonist)
Summar an opioid analgesic used in anesthesia, for breakthrough
y cancer pain, or round the clock pain management
Dosage Inj.: 50 micrograms/mL, 2 mL and 10 mL ampule (IV)
Backgro Fentanyl, a potent opioid agonist, was developed in the 1950s
und to fill a need for strong and rapid analgesia. Because of these
characteristics, fentanyl is commonly used to treat chronic
cancer pain or in anesthesia. Fentanyl is related to other
opioids like morphine and oxycodone. Fentanyl's high potency
has also made it a common adulterant in illicit drugs,
especially heroin.
MOA Fentanyl binds to opioid receptors, especially the mu opioid
receptor, which are coupled to G-proteins. Activation of
opioid receptors causes GTP to be exchanged for GDP on the
G-proteins which in turn down regulates adenylate cyclase,
reducing concentrations of cAMP. Reduced cAMP decreases
cAMP dependant influx of calcium ions into the cell. The
exchange of GTP for GDP results in hyperpolarization of the
cell and inhibition of nerve activity.

SMOOTH MUSCLE RELAXANTS
SUCCINYLCHOLINE (Depolarizing Neuromuscular Blocking Agent)
Summar a depolarizing skeletal muscle relaxant used adjunctly to
y anesthesia and for skeletal muscle relaxation during
intubation, mechanical ventilation, and surgical procedures
Dosage Inj.: 20 mg/mL, 10 mL vial (IV)
Backgro Succinylcholine is a depolarizing skeletal muscle relaxant
und consisting of two molecules of the endogenous
neurotransmitter acetylcholine (ACh) linked by their acetyl
groups. It has been widely used for over 50 years, most
commonly in its chloride salt form, as a means of
neuromuscular blockade during intubation and surgical
procedures. Its rapid onset and offset, with effects beginning
within 60 seconds of intravenous administration and lasting
between four to six minutes, make succinylcholine
particularly useful in the setting of short medical procedures
requiring brief periods of muscle relaxation
MOA Succinylcholine is a depolarizing neuromuscular blocker,
meaning it causes a prolonged period of membrane
depolarization in order to exert its therapeutic effects. It binds
to the post-synaptic cholinergic receptors found on motor
endplates, thereby inducing first transient fasciculations
followed by skeletal muscle paralysis
ATRACURIUM (Nondepolarizing Neuromuscular Blocking Agent)
Summar a neuromuscular blocker indicated to relax muscles during
y mechanical ventilation under general anesthesia or intubation
Dosage Inj.: 10 mg/mL, 2.5 mL and 5 mL ampule (IV)
Backgro Atracurium is indicated as an addition to general anesthesia to
und facilitate endotracheal intubation and provide skeletal muscle
relaxation during surgery or mechanical ventilation.
Atracurium is a non-depolarizing neuromuscular blocking
drug of the benzylisoquinolinium class. It competes with
acetylcholine for binding sites.
MOA Atracurium is a non-depolarizing neuromuscular blocking
drug of the benzylisoquinolinium class. It is a competitive
antagonist of the alpha subunit of the postsynaptic nicotinic
receptor at the neuromuscular junction. It competes with
acetylcholine for binding sites. The binding of the
postsynaptic nicotinic receptor by atracurium prevents
depolarization of the motor endplate and subsequent skeletal
muscle contraction. Unlike binding of depolarizing agents,
binding of atracurium or other non-depolarizing agents does
not induce a receptor conformational change.
ROCURONIUM (Nondepolarizing Neuromuscular Blocking Agent)
Summar a vecuronium analog used to facilitate tracheal intubation and
y to relax skeletal muscles during surgery
Dosage Inj.: 10 mg/mL, 5 mL ampul/vial (IV)
Backgro Rocuronium is a non-depolarizing neuromuscular blocker
und widely used to produce muscle relaxation to help facilitate
surgery and ventilation of the lungs in elective and emergent
situations. It is one of the many non-depolarizing
neuromuscular blockers used but has the distinct advantage of
being fast-acting and reversible. The major indications for its
use are:
 - Provide airway muscle paralysis to facilitate LOCAL ANESTHETICS
endotracheal intubation in elective as well as
emergent conditions BUPIVACAINE
- Provide surgical paralysis to facilitate surgery Summar a local anesthetic used in a wide variety of superficial and
- Provide chest wall relaxation to facilitate mechanical y invasive procedures.
ventilation in critically ill patients who are under
Dosage Inj.:
adequate sedation
0.5%, 5 mL, 10 mL and 20 mL vial
- Provide a defasciculating dose to prevent
0.5%, 5 mL, 10 mL, 20 mL and 50 mL ampule/vial (local
fasciculations during depolarizing muscle paralysis to
infiltration)
prevent myalgias. (off-label)
0.5% 4 mL ampule (spinal) with 8% dextrose
- Prevent shivering in patients post cardiac resuscitation
0.5% (isobaric), 5 mL ampule (spinal)
after the return of spontaneous circulation during
Backgro Bupivacaine is a potent local anesthetic with unique
therapeutic hypothermia (off-label)
und characteristics from the amide group of local anesthetics.
It is vital to ensure that the patients who receive a muscle
Local anesthetics are used in regional anesthesia, epidural
relaxant like rocuronium are adequately sedated to prevent the
anesthesia, spinal anesthesia, and local infiltration. Local
risk of awareness. A patient can be paralyzed but awake and
anesthetics generally block the generation of the action
cannot show the motor signs of awareness.
potential in nerve cells by increasing the threshold for
electrical excitation. The progression of anesthesia is
SUGAMMADEX - is a γ-cyclodextrin derivative that has
dependent on factors such as the diameter, degree
been introduced as a novel agent to reverse the action of
of myelination, and conduction velocity of nerve fibers. In
rocuronium.
clinical practice, the order of a loss of nerve function is as
MOA Rocuronium acts by competing for cholinergic receptors at the
follows:
motor end-plate. This action is antagonized by
- Pain
acetylcholinesterase inhibitors, such as neostigmine and
- Temperature
edrophonium. Rocuronium acts by competitively binding to
- Touch
nicotinic cholinergic receptors. The binding of vecuronium
- Proprioception
decreases the opportunity for acetylcholine to bind to the
- Skeletal muscle tone
nicotinic receptor at the postjunctional membrane of the
MOA Bupivacaine is an amide local anesthetic that provides local
myoneural junction. As a result, depolarization is prevented,
anesthesia through blockade of nerve impulse generation and
calcium ions are not released and muscle contraction does not
conduction. These impulses, also known as action potentials,
occur. Evidence also suggests that nondepolarizing agents can
critically depend on membrane depolarization produced by the
affect ACh release. It has been hypothesized that
influx of sodium ions into the neuron through voltage-gated
nondepolarzing agents bind to postjunctional ("curare")
sodium channels. Bupivacaine crosses the neuronal membrane
receptors and may therefore interfere with the sodium and
and exerts its anesthetic action through blockade of these
potassium flux, which is responsible for depolarization and
channels at the intracellular portion of their pore-forming
repolarization of the membranes involved in muscle
transmembrane segments. The block is use-dependent, where
contraction.
repetitive or prolonged depolarization increases sodium
channel blockade. Without sodium ions passing through the
channel’s pore, bupivacaine stabilizes the membrane at rest
and therefore prevents neurotransmission.
While it is well-established that the main action of
bupivacaine is through sodium channel block, additional
analgesic effects of bupivacaine are thought to potentially be
due to its binding to the prostaglandin E2 receptors, subtype
 EP1 (PGE2EP1), which inhibits the production of
prostaglandins, thereby reducing fever, inflammation, and
hyperalgesia.
depolarize and will thus fail to transmit an action potential.
This facilitates an anesthetic effect by not merely preventing
pain signals from propagating to the brain but by aborting
their generation in the first place.
In addition to blocking conduction in nerve axons in the
peripheral nervous system, lidocaine has important effects on
the central nervous system and cardiovascular system. After
absorption, lidocaine may cause stimulation of the CNS
followed by depression and in the cardiovascular system, it
acts primarily on the myocardium where it may produce
decreases in electrical excitability, conduction rate, and force
of contraction

LIDOCAINE

Summar a local anesthetic used in a wide variety of superficial and

y invasive procedures.
Dosage Inj.:
1%, 20 mL ampul
2% (20 mg/mL), 2 mL, 5 mL, 20 mL and 50 mL ampul/vial
(IM/IV)
2%, 5 mL and 50 mL vial (epidural, local infiltration)
2%, 1.8 mL carpule (with epinephrine) (local infiltration)
Spray: 10%, 50 mL
Backgro Lidocaine is a local anesthetic agent commonly used for local
und and topic anesthesia, but it also has antiarrhythmic, and
analgesic uses and can be used as an adjunct to tracheal
intubation.
MOA Lidocaine is a local anesthetic of the amide type. It is used to
provide local anesthesia by nerve blockade at various sites in
the body. It does so by stabilizing the neuronal membrane by
inhibiting the ionic fluxes required for the initiation and
conduction of impulses, thereby effecting local anesthetic
action. In particular, the lidocaine agent acts on sodium ion
channels located on the internal surface of nerve cell
membranes. At these channels, neutral uncharged lidocaine
molecules diffuse through neural sheaths into the axoplasm
where they are subsequently ionized by joining with hydrogen
ions. The resultant lidocaine cations are then capable of
reversibly binding the sodium channels from the inside,
keeping them locked in an open state that prevents nerve
depolarization. As a result, with sufficient blockage, the
membrane of the postsynaptic neuron will ultimately not