M O N I TO R I N G A N E S T H E T I Z E D PAT I E N T

"MONERE~ - to monitor or to watch and warn

MONITORING - represents the process by which the anesthesiologist recognized and evaluate
potential physiologic problems by identifying prognostic trends in a timely manner.
PHYSOLOGIC MONTORING
Involves continuous assessment of the patient's condition with special
emphasis on detection of change.
This can be accomplished in 2 ways:
1.) Anesthesiologist qualitatively assess the patient's condition continuously by
monitoring with their senses (touch, hearing and sight)
2.) Anesthesiologist quantitatively assess the patient's condition by periodically
making specific measurements.
Careful observations of the anesthetized patient serves several purposes:
1.) Patient responds to anesthesia and operation with changes in breathing, heart rate,
blood pressure and other variables.
- these allows the anesthesiologist to regulate the depth of anesthesia
appropriately.
2.) treatment of such physiologic derangement as blood loss, hypothermia,
hypertension, arrhythmias, organ ischemia, metabolic changes or pulmonary dysfunction
requires systematic assessment.
3.) Vigilant observation supplemented by automatic alarms detects unexpected
catastrophies such as myocardial infarction and airway obstruction.

STANDARDS FOR BASIC ANESTHETIC MONITORING

The first standard states that anethesia personnel shall be present in the operating
room throughout the conduct of all general anesthetics, regional anesthetics and
monitored anesthesia care.
The second standard states that the patient's oxygenation, ventilation, circulation and
temperature shall be continually evaluated.
MONITORS can be :
a. Basic monitor (sense of touch, hearing, sight, and smell)
b. Essential monitors
1. Pulse oximeter
2. Non-invasive blood pressure devices
3. Capnograph
4. Temperature probes
S. ECG
6. Precordial or esophageal stethoscope

Monitoring Devices- these supplement the anesthesiologist's perception with sensors that
provide more sensitive and continuous assessment.
These systems must be accurate during stable and changing
conditions, precise, reliable, safe, inexpensive and practical.
Invasive Monitors - penetrate the body through the skin or via an orifice.
Monitors do not interpret data and do not substitute for a sound clinical judgment
Most important monitor of the patient's condition is a "Vigilant and a
Thoughtful Observer"

OXYGENATION
During all anesthetics an assessment of blood oxygenation is required
to ensure adequate oxygenation at all times.
 The patient's blood oxygen saturation is determined by pulse
oximetry.
Pulse oximeters should be equipped with an audible pulse~tone and
the pitch should change when the oxygenation drops, warning the
anesthesiologist of a change in the patient's status.
~. Hypoxemia results in irreversible organ injury if not detected and
treated within a minute.

CIRCULATION
The anesthesiologist continuously assess circulation through observation
of the patient, blood pressure and continuous ECG.
Heart rate and blood pressure must be checked at least every S minutes,

Blood pressure is the lateral pressure exerted by the blood in the arteries as it
flows.
Indicator of the adequacy of circulation during anesthesia.
Changes in systolic blood pressure correlates with changes in
myocardial oxygen requirement.
Changes in diastolic blood pressure reflect coronary perfusion
pressure.
Pulse pressure -the difference between the systolic and diastolic pressure.

VENTILATION
This must be monitored during all anellthetics.
Accomplished using qualitative clinical signs such as:
1. Chest excursion
2. Auscultation of breath sounds
Quantitatively through continuous carbon dioxide monitoring of
expired gas (CAPNOGRAPHY)
Measures end tidal carbon dioxide which is a clinical estimate of
the PaCO2, assuming ventilation and perfusion in the lungs are
appropriately matched.
End tidal CO2 - 36- 44 mmHg
Determination of end tidal carbon dioxide concentration confirms the
adequacy of ventilation.

CAPNOGRAM - a graphic display of airway PC02 as a function of time.

 TIME (SECONDS)

Initial stage of expiration ( devoid of CO2)

CO2 containing 8as
Plateau represents alveolar gas CO2 content (end tidal carbon dioxide)
Downslope begins with inspiration

- Correct placement of an endotracheal tube or larynseal mask must be confirmed by sustained

presence of CO2 for greater than 3 breaths.

CAUSES OF A DECREASED END TIDAL CO2 (ETC02)

Breathing circuit disconnection during mechanical ventilation

Low cardiac output (hypo-perfuslon) ; failing cardiac output
Accidental extubation
Pulmonary embollsm
Airway obstruction
Venous air embolism
Hypothermia ( decrease CO2 production)
HypometabolLsm
HyperventUation
~. Cardiac arrest

CAUSES OF iNCREASED END TIDAL CO2 (ETCO2)

Hypoventilation
Malisnant hyperthermia (increase in CO2 production)
Sepsis
Skeletal muscle activity
RePreathing of C02
Tracheal intubation can be distinguished from esophaseal intubation by the consistent
concentration of carbon dioxide in the exhaled 8as from trachea.
In healthy individual undersoing 8eneral anesthesia the difference between PaC02 and ETC02 is
5-7 rnmHB.

TEMPERATURE

- Temperature regulation by the hypothalamus is impaired during general

anesthesia
- Heat loss is common in surgery due to the exposed state of the skin, operating
room environment, and both general anesthesia and regional anesthesia
inhibiting thermoregulatory control
Site of temperature monitoring:

I. Skin - may not reflect core temperature(3-4 degree centigrade below)

IL Axilla - approximately 1 degree centigrade below core temperature
IlL Rectum - does not reflect rapid change of temperature
IV. Esophagus -probe is placed on the lower third of the esophagus,
- Accurately reflect core and blood temperature,
V. Nasopharynx - reflects brain temperature because of its proximib/to the internal carotid artery
contraindicated in head trauma or with evidence of CSF rhinorrhea.
VL External auditory meatus - retie
c tcore temperature because thetymp " membrane ~s" m
" close
anlc
proximity to the internal carotid artery.
Vii. Bladder Catheter - approximates core temperature when urine flow is hish.
Viii. Pulmonary artery catheter- an accurate measure of core temperature but expensive and invaslve.
"Temperature monitoring is required to allow the anesthesiologist to detect changes in body
temperature while the patient is anesthetized."

HYPOTHERMIA- a clinical state of subnormal body temperature in which the body is unable to generate
enough heat for bodily functions.

Perioperative hypothermia commonly results from:

1 . Anesthetic induced inhibition of thermoregulation
2 . Cold ambient environment in the operating room
3 . Heat loss during surgical exposure

Core temperature of 35 degree centigrade (95 degrees Fahrenheit) upper limit of hypothermia
Those at greatest risk for developing hypothermia include:
1. Elderly
2. Burned patients
3. Neonates
4. Patients with spinal cord Injuries
Adverse effects of hypothermia:
1. Cardiac dysrhythmias due to changes in cardiac repolarization
2. Potentiation of anesthetic drugs and neuromuscular blockade
3. Coagulopathy
4. Increase vascular resistance
5. Decrease availability of oxygen
6. Post- operative shivering

How anesthetics predisposes one to hypothermla:

1 . Heat loss is common during general anesthesia because the anesthetic alter the
thermoregulation.
2 . Prevent shivering.
3 . Produces peripheral vasodilatation.

Opioids - reduces the vasoconstrtctive mechanism of heat conservation by their sympatholytic

properties.
Barbiturates - causes peripheral vasodilation.
Muscle Relaxants - reduces muscle tone and prevent shivering thermogenesis.
Regional Anesthesia - may produce sympathetic blockade, muscle relaxation and sensory blockade of
thermal receptors.

Small children and infants are especiaUy prone to hypothermia because of the
increased ratio of body surface to weight.
Elderly are susceptible to hypothermia because of the limited compensatory mechanism.

HYPERTHERMIA - intraoperatlve rise in body temperature of two degrees centigrade per hour.
-less common than hypothermia and may result from:

1.
Malignant hyperthermia 2.
Fever secondary to stress of surgery 3.
Inappropriate to warm the patient 4.
Sespsis

increase in body temperature do not provide the earliest warnings of malignant

hyperthermia, whose first sign is increased in carbon dioxide production.

ELECTROCARDIOGRAM
 The intraoperatlve monitoring of the ECG was described in 1918 and remains the most and
practical monitor for the detection of disorders of cardiac rhythm and conduction.
>
Surface recording of the electrical activity of the myocardlum (electrical potential generated by
myocardial cells).
>
Displays cardiac electrical activity only; it says nothlng about the adequacy of the myocardial
pump function.
/ It's routine intraoperative use allows:
1. Detection of dysrhythmias
2. Detection of myocardial ischemia.
3. Conduction abnormalities.
4. Peacemaker malfunction.
5. Electrolyte disturbances.

- The ECG is most valuable if mordtoring begins before Induction of anesthesia.

-Any abnormal or marginal ECG findings ls less worrisome If It Is present in the preoperative
ECG and remains unchanged throughout the perloperatlve period.
-It becomes more troublktg if it first appears or worsens intraoperatlvely.

Einthoven - in 1906, invented the first ECG using a string ga|vanometer to measure the current
generated during a cardiac impulse.

Rhythm disturbances under

anesthesia: 1. Supraventricular
2. Ventricular

The differentiation is important because rhythm disturbances differ in their: 1. Etiology

2. Effect on the cardiovascular system
3. Treatment
4. Prognosis
>
Atrial Tachycardia is common during anesthesia and usually not associated with
significant hemodynamic instability.
>
Ventricular tachycardia is a medical emergency associated with hypotension and poor
cardiac output requldng immediate intervention.

ECG gives an accurate assessment of:

1. Rate
2. Rhythm
3. Degree of oxygenation of the heart muscle

CENTRALVENOUS PRESSURE
;~ 80% of the blood volume ~ in the venous circulation.
) , Reflects the right heart competence.
An index of the circulatlng blood volume and preload to the right ventdcki.
)~ It measures the pressure exerted by the blood returning to the right side of the heart
and the ability of the right side of the heart to manage this return effectively.

Normal CVP = 2-15 cm water (1.5 -11 torr)

) , The above values should always be interpreted together with other parameters
monitored like arterial blood pressure, pulse, peripheral circulation.
A decrease in CVP suggest:
1. Hypovolemla
2. Increase In venous capacitance as vasodllatation following sympathetic blockade.

- Fall in venous pressure takes place before the fall in arterial pressure.
 In a failing heart venous pressure is increased because if the heart action fails there is
backing up of blood on the venous side of circulation.
) ' An increase in CVP with a normal cardiac function suggests:
1. Hypervolemia
2. Vasoconstriction
3. increase in intrathoracic pressure
)~ An increase tn CVP in the presence of arterial hypotenslon suggests cardiac dysfunction.

Blood Pressure Diagnosis Fluids Drugs

1. Low Low or normal Hypovolemia increase

2. High Normal Hypervolemia Stop or decrease Diuretics
3. High Low Cardiac failure Restrict Diuretics and Digitalis.

Indications for CVP monitoring:

1. In elderly patients undergoing extensive surgical operation.
2 . Patients in whom a large blood or fluid exchange is expected to prevent overhydration or
overtransfusion.
3 . In patients known to have cardiac disease.
4 . Major traumatic surgery.
S . Anticipation of major blood loss during surgery.
6. in patients with uncertain preoperative volume status.
7. Facilitation of postoperative care in critically ill patients.
8 . Craniotomy or Cervical laminectomy when either is clone in the upright position to treat
potential air embolism.
9 . Multiple transfusion.
10. Open heart surgery.
11. During and following removal of pheochromocytoma.

ECHOCARDIOGRAPHY
)~ Transesophageal echocardiography (TEE) is expensive but can be useful continuous
perioperative monitor for heart anatomy and function.

TEE - useful in differentiating hypovolemia from poor myocardial contractility as a cause for
depressed cardiac output syndrome.
- in addition to the assessment of myocardial function and ischemia anatomic and
functional disorders of heart valves are frequently best assessed with the use of TEE.

INHALATIONAL ANESTHETICS
GENERAL ANESTHESIA - an altered physiologic state characterized by reversible loss of
consciousness, analgesia of the entire body, amnesia and some degree of muscle relaxation.
Anesthetic drugs have been shown to depress excitatory transmission in the spinal cord particularly
at the level of the dorsal horn interneurons that are involved in pain transmission.
),
Unconsciousness and amnesia probably mediated by cortical anesthetic action.
~,
Suppression of purposeful withdrawal from pain is related to subcortical structures such as the
spinal cord or brain stem.

Inhaled anesthetics are sufficient alone to provide complete anesthesia.

PROPERTIES OF AN IDEAL INHALATIONAL ANESTHETIC:

1 . Predictable in onset and emergence.
2 . Provide muscle relaxation.
3 . Cardio stability and bronchodilatation.
4 . Should not trigger malignant hyperthermia and other significant side effects like nausea
and vomiting.
 II. Inflammable
6. Undergo no blo transformation within'the body.
7. Allow easy estimation of concentration at the sight of action.
I. OLDER INHALAT1ONAL ANESTHETIC AGENTS:
1. Ether - flammability
2. Cyclopropane - flammability
3. Ruoroxene- flammability, hepatoxicity
4. Methoxyflurane - nephrotoxicity
5. Chloroform - hepatoxicity
6. Trichloroethylene - re acted with soda lime to form toxic gas known as phosgene
7. Nitrous oxide - lack potency
The above lnhalational anesthetic have unfortunate properties and side effects.

II. NEWER INHALTIONAL ANESTHETIC AGENTS :

1 . Halothane-substituted halogenated alkane
2. Influrane
3 . I s o fi u r a n e " l
4 . Sevofiurane ~.. substituted halogenated ether
5 . D e s fi u r a n e _ J
Despite the effectiveness of the inhaled anesthetics, they are the most difficult
drug to use for the following reasons :
1. Narrow margin of safety
2. Variation amongpatlents
~" So that constant attention of the dose and continuous physiologic monitoring of
the patient are required.
Concentration effective for producing surgical anesthesia frequently cause
significant effect on the central nervous system, respiratory, circulatory and
neuromuscular functlon.
- Thus this requires continuous life support.

POTENCIES OF ANESTHETIC GASES COMPARED

)> Using minimal alveolar concentration (MAC)

MAC - concentration of I atmosphere that abolishes motor response in 50% of patients in response
noxious stimuli (surgical incision)
Measurement of MAC assumes that alveolar concentration directly
reflects partial pressure of the anesthetic at its sight of action.

FACTORS THAT INFLUENCES MAC

1. Age
> The highest MAC are found in infants at 6-12 months of age
MAC decreases with Increasing age as well as in prematurity
2. Temperature
Hypothermia decreases MAC ( for every Celsius degree drop in temperature
MAC decreases approximately 2-5%
]> Hyperthermla.increases MAC
3. Electrolytes
> Hypernatremla decreases MAC
4.. Drugs
Oplolds , barbtturates, alpha 2 blockers , calclum channelblockers decreases
MAC
CNS stimulants (cocaine) increases MAC
S. Alcohol intoxication
) , Acute alcohol Intoxication decreases MAC
Chronic alcoholism increases MAC
FACTORS THAT DO NOT AFFECT MAC :
Hypocarbla / hypercarbla
2. Gender
3. Thyroid function
Hyperkalemia
BLOOD GAS PARTITION COEFFICIENT (SOLUBILITY OF INHALED ANESTHETICS IN THE |}LOOD)
~> Describes the distribution of anesthetic between blood and gas at the same parttal
pressure.
A higher blood gas partition coefficient correlates with a greater concentration of
anesthetic in the blood ~ higher solubility
A greater amount of anesthetic is taken by the blood whtch acts as a reservoir thus
reducing the alveolar concentration and thus slowing the rate of induction.

Alveolar concentration - the principal factor in determining the onset of action.

MAC Blood-Gas Partition Coefficient

'Enflurane 1.68 1.8
"Isoflurane 1.1S 1.4
Desflurane 6.0 0,42
Halothane 0.77 2.3
Nitrous Oxide 104 0.47
Sevoflurane 1.7 0.65

]~ The higher the blood gas partition coefficient the greater the anesthetic solubility and
the greater its uptake by the pulmonary circulation, as a consequence of this high
solubility alveolar partial pressure rises more slowly and thus induction is prolong.
The second factor that affects uptake is alveolar blood flow which is essentially equal to
cardiac output in the absence of pulmonary shunting.
If the cardiac output drops to zero, so will anesthetic uptake.
As cardiac output increases, anesthetic uptake increases. The rise in
alveolar partial pressure slows and thus induction is delayed.
~" The final factor affecting uptake is the partial Pressure difference between alveolar gas
and venous blood.
The greater the uptake of the anesthetic agent, the greater the
difference between inspired and alveolar concentration, the slower the
rate of induction.
;~ Low output states predisposes patient to overdosage with soluble agents since the rate
of rise in aIveoiar concentration will be markedly increased.

- The most important route for inhalational anesthetic is the alveolus.

Factors that would influence speed of induction (that which increases alveolar anesthetic
concentration - speed onset):
1. Increasing the delivered concentration of anesthetic,
2 . High flow within the breathing circuit.
3 , Increasin8 mlnuteventllatlon.

That which decrease alveolar concentration slow onset of volatile induction:

1. An increase in cardiac output.
2. Decreased minute ventilation.
3. High lipid anesthetic solubility.
4 . Low flow within the breathing circuit.

Many factors that speed induction also speed recovery.

NITROUS OXIDE
> The only inorganic anesthetic gas in clinical use. 04n~~
N o n - fl ~ m m a b l e b u t I I k ~ o x y g e n I t s u p p o r t ~ n ,
Its chculatory effects are explained by its tendency to stimulate the sympathetic
nervous system.
~ , Unlike other inhalatlonal agents, it does not provide significant muscle relaxation
It may increase the incidence of postoperative nausea and vomiting.

-- CAN EXPAND CLOSED AIR SPACES,

NzO is 30x is more soluble than nitrogen; N~O will diffuse Into an air filled space
much more rapidly than N~ that diffuse out, so that as a result N20 oxide carl incrtase
the volume in a closed body cavity with distensible walls such as an obstructed bowel
cavity, pneumothorax, pneumopericardlum or air emboli.

= SECOND GAS EFFECT

Nitrou$oxide has the highest MAC (104) - it is not potent enough to be
used alone and must be used in combination with other anesthetic.
High concentration of nitrous oxide will augment not only its owr
uptake but that of a concurrently administered anesthetic. NitroLs
oxide is insoluble in blood so that its rapid absorption in the alvecli
results in an abrupt rise in alveolar concentration of the accompanying
volatile anesthetic.
The concentration effect of one gas upon another results in secor,d gas
effect. This phenomenon should speed the onset of anesthetic
induction.

= DIFFUSION HYPOXIA
When nitrous oxide is abruptly discontinued, its rapid diffusion from the
blood to the alveolus decreases the oxygen concentration (tensio 1) in
the lung leading to a brief period of decreased oxygen concentration.
Administer 1.O0% oxygen at the end of the case can eliminate the
above" problem.

= BONE MARROW TOXICITY

Prolonged exposure to anesthetic concentration of nitrous oxide results
in bone marrow depression leading to megaloblastic anemia.

VENTILATORY EFFECTS OF VOLATILE ANESTHETICS

Dose dependent depression of ventilation mediated directly through
medullary centers and indirectly through effects on intercostal muscle
function.
~" Volatile anesthetics lead to a decrease in tidal volume and an incr,.=ase
in respiratory rate ~ rapid shallow breathing pattern.
The ventilator~response to hyper carbla Is also attenuated by incr( asing
the delivered concentration of anesthetic.

AIRWAY IRRITATION :
Lack of airway irritation for sevoflurane and nitrous oxide so that t hese
two agents could be used along with oxygen for a pleasant mask
induction in children.
ts~f!urane and desfiur~ne h~ve z punl]ent odor ;r; ~ui~t ir~:~:~ng
and may cause r_oulzhin~ and ~vp_n larvn~Q~l ~p=~m
Desflurane is used only for maintenance of anesthesia.
AIRWAY RESISTANCE :
Volatile anesthetics appear to decrease airway resistance by a dire ct
relaxing effect on bronchial smooth muscles and by decreasing the
broncho constricting effect of hypocapnia.
 Desflurane has no effect on airway resistance, non- smokers but
produce broncho constriction In smokers.
Nitrous oxide has no effect on airway resistance.
The brocncho constricting effect of histamine release also appear to be
decreased when an inhalational anesthetic is administered.

M UCOCILIARY CLEARANCE :
Appear to be diminished by volatile anesthetics principally throul~:h
interference with ciliary beat frequency.
The effects of dry inhaled gases, positive pressure ventilation and high
inspired oxygen content also contribute to ciliary impairment.
The physiologic response to hypoxia and hypercarbla is bluntJ.=d by
volatile anesthetic in a dose dependent fashion.

These effects maybe summarized according to "3Rs"

- rapid respiration
- reduced tidal volume
- regular duration with loss of the awake respiratory variability

CARDIOVASCULAR EFFECTS OF VOLATILE ANESTHETICS

I. Maintenance of mean arterial pressure:
All of the volatile inhaled anesthetics reduce arterial pressure in a dose dependent
fashion.
N20 is the only inhaled anesthetic that does not drop the blood pressure:
II. Suppression of sympathetic nervous system activity:
~* Three inhaled anesthetics - NzO,/liOflurane andDesflurane actually increase
sympathetic activity usually in a dose dependent fashion.
IlL Maintenance of heart rate:
~* All of the inhaled anesthetics tend to increase the heart rate at least at the same
concentration.
- These effects may represent sympathetic stimulation, a reflex tachycardia from
the reduction in arterial pressure or actions on the baroreceptors.
Halothane
Shown to increase the sensitivity of the myocardium to the action of
catecholamlnes resulting ~n premature ventricular contraction and
tachydysrrhythmias.
Compared with adults, children undergoing hatothane anesthesia appear lo be
relatively resistant to this sensitizing effect although halothane had been., hown
to have a cholinergic vagally induced bradycardic effect in children.
 The Indu~lon ajent Ihould hive I flit onnt Ind de©reiN Intrlocullr prlIiur!
Take In to consideration:
Ketamine can increase intraocular pressure
Etomidate can cause myoclonus and therefore can increase intraocular pressure
Propofol and Thiopental - best option
A patients should be assessed before laryngoscopy with the goal .... --) total paralysis as
coughing on the tube remarkably increase intraocular pressure
;~ REMEMBER : basic blinking, stress, and intubation can all increase intraocular pressure

CLINICAL PEARL:
~> Benzodiazepine and opiods have synergistic effect with intravenous induction requiring
adjustment in dosing.
Ketamine is the best induction for hypovolemic trauma patients as long as there is no risk for
increase in intracranial pressure.
increase cerebral blood flow, intracraniai pressure and cerebral metabolism is due to its
stimulation of the sympathetic nervous system.
It is also a good inducting agents inactive bronchospastic disease.

~> All other inducting agents cause a decrease intracranial pressure by decreasing cerebral blood
flow and cerebral metabolic rate.
EFFECT ON OTHER ORGAN SYSYTEM

I. LOW SOLUBILITY IN SKELETAL MUSCLE AND FAT

>" When inhaled anesthetics get into the blood stream, they are distributed or absorbed
into skeletal muscle and fat. This volume of distribution can be large providing a
significant depot which must be cleared so that the patient can emerge from the
anesthetic.
N20 and desflurane are insoluble in blood, smaller quantities are stored in the body
during a given anesthetic thus shortening the time for emergence.
II. DIRECT SKELETAL MUSCLE RELAXATION
Desflurane and sevoflurane cause the most relaxation of the skeletal muscles folk,wed
closely by isoflurane.
N20 has little effect on skeletal muscle.
III. NOT BEING A TRIGGER FOR MALIGNANT HYPERTHERMIA
Malignant hyperthermia is a rare genetically based disorder of calcium metabolisr~
which usually presents as a complication of anesthesia.
All of the volatile inhaled anesthetic~ (isoflurane, sevoflurane and desflurane can I rigger
a malignant hyperthermia crisis an d must be scrupulously avoided If a patient ha: a
history of malignant hyperthermia In the family.
IV. LOW HEPATIC METABOLISM
A simple mnemonic to remember the hepatic metabolism of inhaled anesthetics : o
called the rule of 2's
Hal~thane roughly 20% metabolized
Enflurane 2%
Isoflurane 0.2%
Desflurane 0.02 %
Sevoflurane 4% (2x2)
Ntrous Oxide negligible
Of the inhaled anesthetics that are now avallabie clinically, sevoflurane undergoe; the
most hepatic metabolism.\
IV. LACK OF ORGAN TOXICITY
Unfortunately all of the inhaled anesthetics have the potential to cause different :ypes
of organ toxicity.
Hepatic toxicity is a concern of IsoflOrane and desflurane
Renal toxicity is a concern with sevoflurane.
Bone marrow toxicity is a concern with nitrous oxide.
Under hypoxic conditions, halothane may undergo reductive metabolism produd NI
metabolites that may cause hepatic necrosis.
Halothane hepatitis is secondary to an auto immune hypersensitivity reactior.
~' Fluoride is another potentially toxic product of anesthetic metabolism.
Fluoride associated renal dysfunction has been linked to the use of rnethoxyflurane
and greatly contributed to the withdrawal of methoxyflurane from the market.
The fluoride produced by sevoflurane has been implicated in renal dysfunction but
because sevoflurane is not so lipid soluble as methoxyflurane and the time of
exposure (fluoride burden) is much less.
Soda lime can also degrade sevoflurane.
;~ Desflurane - is much more than any volatile anesthetic has been associated with the
production of carbon monoxide.

CENTRAL NERVOUS SYSTEM EFFECTS

I.ANALGESIA
]~ Of at! ths inhaled anesthetics only nitrous oxide has analgesic effect, this DroDer~Y i~
klmckmd with n=lo~mnm
II POTENCY
Of the volatile inhaled anesthetics isoflurane is the most potent having a MAC of 1.15 %
Sevoflurane has a MAC of 2.05%
Desflurane has a MAC of 6%
Nitrous oxide has a MAC of 104%
 NzO not potent enough to be used alone and must be used in combination with other
anesthetl¢~.
CLINCAL PEARL
ISOFLURANE
Dilates coronary arteries particularly if its concentration is abruptly increased tho*Jgh
not as a potent dilator as nitroglycerin.
Dilation of normal coronary arteries could theoretically divert blood away from the
stenotic lesions (CORONARY STEEL SYNDROME) causing myocardial ischemia during
episodes of tachycardia or drop in perfuslon pressure thus avoided in patients with
coronary artery disease.
DESFLURANE
Its low solubility in blood and body tissues cause a very rapid wash-in and wash-o Jt of
the anesthetic (fastest induction and emergence).
SEVOFLURANE
An excellent choice for smooth and rapid inhalational induction in pediatrics and adult
patients due to its non- pungency and rapid increases in alveolar anesthetic
concentration.
Metabolized to fluoride ion, strong bases that accumulate In the carbon dioxide
absorbent at low gas flows can degrade sevoflurane to a nephrotoxic bi product.
Produces compound A which is potentially nephrotoxic metabollte.
ENFLURANE
Can produce fast frequency and high voltage activity on the EEG that often progresses
to spike-wave activity which is in distinguishable from changes that accompany a
seizure.
This likelihood of enflurane evokes seizure activity is increased when the concentlation
of enflurane exceeds 2MAC or when hyperventilation of the lungs lowers the PACD2
below 30 mmHg.

Like most general classes of anesthetics, inhalation anesthetics vary in their properties. Some are
desirable, some are not. Thus, their use is tailored to a specific patient or a specific situation.

LOCAL ANESTHETICS

drugs that block the generation and propagation of impulses in excitable tissues most
notably the spinal cord, spinal nerve roots, and peripheral nerves but also skeletal
muscles, cardiac muscle and brain.

WHAT ROLE DO LOCAL ANESTHETICS PLAY IN THE PRACTICE OF ANESTHESIOLOGY :

use to provide regional anesthesia for surgery.
To provide post operative analgesia for painful surgical procedures.
Attenuate the pressor response to tracheal Intubation, decrease coughing during
tntubation and extubatlon
J~ For anti arrhythmlc effect.
Local anesthetic molecule consists of three bulldin8 blocks
ESTER OR AMIDE LINKAGE

AROMATIC RING QUARTERNARY AMINE

(Lipophiltc) (Hydrophi|ic)
the Intermedtlte cloth connecting the lipophlltc head and the hydrophUic tail contains an amide ]r an
ester linkage thus subdhddir~ the clinically useful local anesthetic into:
I. AMINO ESTERS
1.) Cocaine
2.) Chleroproc~ne
3.) procaine
4.) tetraCalne
\\, AMINO AMIOll
1.) Lldocalne
2.) Bupivacaine
3.) Mepivacalne
4.) Prilocalne
S.) Oebucalne
6.) Ropivacaine
METABOLISM OF LOCAL ANESTHETICS:
ESTERS - undergo hydrolysis by pseudocholinesterases found principally in plasma. \.

AMIDES- undergo enzymatic biotransformatlon primarily in deliver. L

ELECTROPHYSILOGIC EFFECTS OF LOCAL ANESTHETICS :

» The accepted mechanism of action for clinically utilized local anesthetics is direct inhibition of
the voltage gated sodium channels
)- Initiated by binding of the local anesthetic molecule with receptors located in the channel this
receptor local anesthetic interaction prevents the sodium flux needed for initiation and
propagation of the action potential.
ALLERGIC POTENTIAL
);;> Esters produces metabolites related to PABA (responsible for the allergic reaction) so that they
are more likely to produce allerglc reaction thari the amides.
» Allergic reaction following the use of focal anesthetics may also be due to methylparaben or
other preservatives in commercial preparation of local anesthetics
)- There is no cross sensitivity between classes of local anesthetics
)- Patients may experience palpitations induced by epinephrine containing local anesthetics.
WHAT DETERMINES LOCAL ANESTHJETIC POTENCY
)- The higher lipid solubility the greater the potency.
)- Lipid solubility correlates potency

Agent Lipid solubility Relative potency Protein Binding Duration

Procaine <1 1 5 short
2 Chloroprocaine >1 3 short
Mepivacaine 1 1.5 75 medium
Lidocaine . 3 2 65 medium
Bupivacaine 28 8 95 long
Tetracaine 80 8 85 long
Etidocaine 140 8 95 long
Ropivacaine 14 8 94 long

)-There are multiple measurements of local anesthetic potency that are analogous to the MAC of
inhalational anesthetics.
Cm - minimum concentration of local anesthetics that will block nerve impulse conduction.
This measure of relative potency is affected by several factors :
1. Nerve fiber size , type and myelination ·
2. pH (acidic antagonize block)
3. frequency of nerve stimulation (access oflocal anesthetic to the sodium receptor is enhanced
by repeatedly opening the sodium channel )
4. electrolyte concentration ( hypokalemia and hypercalcemia antagonize blockade
WHAT FACTORS INFLUENCE THE DURATION OF ACTION OF LOCAL ANESTHETICS
> the greater the protein binding , the longer the duration of action
> the duration of action is also influenced by peripheral vascular effects ofthe local anesthetics.
> Lidocalne, prilocaine and mepivacaine provide anesthesia of similar duration.
Udocalne is a more potent vasodilator, increasing absorption and metabolism of the drug thus
hai: thg thortor cll nic•I blockade than that produced by prilocaine or mepivacaine.
WWAT OCTCnUllJCC LOCAL lll ~HMHI C ONSH TIME
»- The clegree of ionization; the closer the pKa of the local anesthetic to tissue pH the more rapid
the c nset time.
0 .
pKa ··defined as the pH at which the ionized and unionized form exist in equal concentration .
 ~ The latency of 1 local anesthetic can also be shortened by uslns a hiaher concentration and by
using carbonated local anesthetic solution to adjust the local pH •

Agent pKa Onset Time

Procaine 8.9 Slow
2 Chloroprocalne 9.1 Very quick
Mepivacaine 7.7 Quick
Lidocaine 7.8 Quick
Bupivacalne 8.1 Moderate
Tetratcaine 8.4 Slow
Etldocaine 7.9 Quick
Ropivaca ine 8.1 Moderate

How does the onset of anesthesia proceed in a peripheral nerve block?

» Conduction blockade proceeds from the outermost (mantle) to the innermost (core) nerve
bundles. 1

Mantle fibers inervate proximal sturctures and core fibers inervate distal structures
DIFFERENTIAL BLOCKADE
» Describes blockade of the components of a peripheral nerve that proceet;ls at different rates:
a) Loss of sympathetic functions
b) Loss of pinprick sensation
c} Touch and temperature descrimlnation
d} Loss of motor functions
MAXIMUM SAFE DOSES OF LOCAL ANESTHETICS
DRUG MAXIMUM DOSE (mg/kg}
Procaine 7
Cloroprocaine 8-9
Tetracalne 1.5
Lidocaine 5 or 7 (w/ epinephrine) ·
Meplvacalne s
Bupivacaine 2.5
Etidocaine s
WHY ARE -EPINEPHRINE AND PHENYLEPHRINE OFTEN ADDED TO LOCAL ANESTHETICS?
» These drugs cause local tissue vasoconstriction thus limiting the uptake of the local anesthetic
into the vasculature therefore prolonging its effect and reducing its toxic potential.
CONTRAINDICATIONS TO LOCAL ANESTHETIC WITH EPINEPHRINE
1. Unstable angina pectorls
2. Cardiac dysrrhythmlas
3. Hypertension
4. Peripheral nerve blocks to fingers

lipid solubility of the local anesthetic determines potency.

pKa of the local anesthetic determines onset.
Protein binding of the local anesthetic determines duration of action.

TOXICITY OF LOCAL ANESTHETICS

Systemic toxicity is due to :
1. Elevated plasma local anesthetic level
a. Inadvertent lntravascular injection
b. Less frequently as a result of systemic absorption of local anesthetic .from the injection
site
SYSTEMIC VASCUlAR ABSORPTION OF LOCAL AN~~TMCTtc vAi\1€C AT 01~~1:'.0t:MT ~IT~
lntercostal nerve block > caudal > eoidural > brachia! olexus > sciatic > subcutaneous
 /

Because the intercostals nerve is surrounded by a rich vascular supply local anesthetic
injected to this area will be more rapidly absorbed • increasing the likelihood
of achieving toxic levels.
Toxicity from local anesthetics involves the cardiovascular system and the central nervous system.
The central nervous system is more sensitive to the toxic effects of the local anesthetics and is the one
that is affected first.

CENTRAL NERVOUS SYSTEM TOXICITY IS MANIFESTED BY THE FOLLOWING:

1. Light headedness, tinnitus, peri-oral numbness, confusion
2. Muscle twitching, auditory and visual hallucination
3. Tonic - clonic seizures, unconsciousness, respiratory arrest
CARDIO TOXICITY IS MANIFESTED BY THE FOLLOWING :
1. Hypertension, Tachycardia
2. Decreased contractility and cardiac output, hypotension
3. Sinus bradycardia, ventricular dysrrythmias, circulatory arrest
LOCAL ANESTHETIC INDUCED CNS TOXICITY MANIFEST WITH EXCITATION - - - • SEIZURE
LOSS OF CONSCIOUSNESS
LOCAL ANSETHETIC INDUCED CVS TOXICITY MANIFEST AS HYPOTENSION - - - .... CONDUCTION
BLOCKADE ----.•CARDIAC ARREST

CARDIOTOXICITY WITH VARIOUS LOCAL ANESTHETICS

~ The ratio of the dosage requi;ed for irreversible cardiovascular collapse and the dosage that
produces CNS toxicity is much lower for bupivacaine and etidocaine than for lidocaine.
~ Pregnancy, acidosis, and hypoxia increases the risk of cardio toxicity with bupivacaine.
~ Cardiac resuscitation is more difficult following bupivacaine induced cardiovascular collapse.
This may be related to the lipid solubility of bupivacaine which results in a slow dissociation of
the drug from cardiac - Na channel ·(fast in - slow out)
~ By contrast recovery from less lipid soluble lidocaine is rapid (fast in -fast out)
~ In an effort to minimize the risk of cardiac toxicity in the event of an accidental intravenous
injection avoid the use of bupivacaine concentration greater than .5 percent especially in
obstetric epidural anesthesia.

NEUROTOXIC!TY FROM LOCAL ANESTHETICS Demyelinzation

2 complications have been described after spinal and epidural anesthesia :
1. Transient neurologic symptom - manifest in the form of moderate to severe pain in the lower
back, buttocks and posterior thigh. . ·
The symptoms appear within 24 hours of spinal and epidural anesthesia and generally
resolve within seven days.
2. Cauda equina syndrome - diffuse injury to the lumbo- sacral plexus
The mechanism of neural injury is thought to be that non- homogeneous distribution of
spinally injected local anesthetic may expose sacral n_erve roots to a high concentration
of local anesthetic with consequent toxicity
Avoid injecting large amounts of local anesthetic in the sub- arachnoid space, specially if
less than an anticipated response is obtained with the initial dose.
Important adverse effects of local anesthetics although rare may occur from:
I. Systemic '1bsorption
II. Local tissue toxicity
Ill. Allergic reactions Demyelinzation
Disruption fo blood brain
IV. Drug specific effects Increase vasa vasorum

I. Systemic Toxicity
» The magnitude of local anesthetic systemic absorption depends on :
1. The dose injected
2. The specific site of injection
3. The inclusion of a vasoconstrictor in the local anesthetic solution.

SiglJS a~mptoms of CNS toxicity:

~'f.gtit"'fieadedness, tinnitus, perioral numbness, and confusion. .·; .
2. Muscle twitching, auditory and visual hallucinations.
3. Tonic-clonic seizures, unconsciousness, respiratory arrest.

Signs and symptoms of CVS toxicity:

1. Hypertension, tachycardia
2. Decreased contractility and cardiac output, hypotension
3. Sinus bradycardia, ventricular dysrrhythmias, circulatory arrest

» Establishment of maximal acceptable local anesthetic doses for performance of regional

anesthesia is an attempt to limit plasma concentration that can result from systemic
absorption of these drugs.
» Local anesthetic induced CNS toxicity manifest with excitation 7 seizures 7 loss of
consciousness.
» Local anesthetic induced CVS toxicity manifest with hypotension 7 condu.c tion blockade
7cardiac arrest.

Local anesthetics are neuronal depressants and the onset of seizures is thought to
reflect selective depression of cortical inhibitory neurons leaving excitatory pathways
unopposed.
• Higher doses may affect inhibitory and excitatory pathways resulting in CNS
depression and even coma (these effects parallel anesthetic potency).
• High plasma concentration of local anesthetics can produce profound
hypotension due to relaxation of arteriolar vascular smooth muscle and direct
myocardial depression.

CARDIOTOXICITY WITH VARIOUS LOCAL ANESTHETICS

» Part of the cardiac toxicity reflects the ability of local anesthetic to block cardiac sodium
iron channels ~ cardiac automaticity and conduction of cardiac impulses are impaired.
» The ratio of the dosage required for irreversible cardiovascular collapse are the dosage
that produce CNS toxicity is much lower for bupivacaine and etidocaine than for
lidocaine.
- Such findings support the concept that bupivacaine has greater cardiac toxicity
which have been the driving force for the development of ropivacaine and
levobupivacaine.

- Bupivacaine has the highest risk_Qf producing severe cardiac dysrrhythmias and
irreversible cardiovascular collapse, so that use of more than 0.5 %
concentration should be avoided especially in obstetric analgesia.
 - Pregnancy, acidosis and hypoxia Jncreases the risk of cardiotoxicity with
bupivacaine.

- Cardiac resuscitation is more difficult following bupivacqine induced

cardiovascular collapse. This is related to lipid solubility of bupivacaine which
result in slow dissociation of the drug from cardiac sodium channels (fast in -
slow out)

- By contrast recovery from less lipid soluble lidocaine is rapid (fast in - fast out)

PRILOCAINE
» Local anesthetic associated with the risk of Methemoglobinemia.
» Metabolized in the liver to 0-toluidine which is capable of oxidizing hemoglobin to
Methemoglobin.
» In a dose greater than 600 mg can produce clinical methemoglo~inemia making the
patient appear cyanotic.
~ The above condition is spontaneously reversible or maybe treated by IV methylene blue
(1-2 mg/kg)

ROPIVACAINE
» A new amide local anesthetic that is structurally and behaviorally similar to bupivacaine.
~ Like bupivacaine it is highly protein bound and has lengthy duration of action, however
it is less cardio toxic.
» Capable of providing differential blockade (it is capable of separating sensory and motor
blockade) • this characteristic may make ropivacalne an ideal anesthetic for use
in obstetric procedure.

" EMLA" cream (eutectic mixture of local anesth.etic)

~ Consists of a 1:1 mixture of 5% lidocaine and 5% prilocaine
» Dermal analgesia this requires a contact time of ~t least 1 hour under an occlusive
dressing.
This should not be used on :
1. Mucous membrane
2. Broken skin
3. lnJants less than 1 month old
4. Patients with predisposition to methemoglobinemia.

The rate of systemic absorption is proportionate to the vascularity of the site of injection.
The presence of vasoconstrictor causes vasoconstriction at the site of drug
administration leading to decrease in drug absorption.
Decrease absorption of local anesthetic through t he use vasoconstrictors will result in:
1. Increases neuronal uptake
2. Enhances the quality of the block
3. Prolongs the duration of action
4. limit toxic side effect

Muscle twitching heralds the onset of tonic-cloni.c seiiures--.. respiratory arrest often
follows.

Benzodiazepines and hyperventilation decreases cerebral blood flow and drug exposure (raises
the threshold of local anesthetic induced seizures)
Management of local anesthetic
,! .
toxicity :
'
~ Adequate ventilation an oxygenation should be maintained
~ Thiopental (1-2 mg/kg) given quickly and reliably terminates seizures
~ Intravenous lidocaine ( 1.5 mg/kg) decreases cerebral blood flow and attenuates the rise
of in intracranial pressure that accompanies intubation in-patients with decrease
intracranial compliance.

CLINICAL PEARL

);> Local anesthetics will not occur in acidotic tissues

)'> Factors determining the onset duration and potential complications of a regional block
with local anesthetics include:
1. Site of injection
2. The dose of the local anesthetic
3. Physiochemical properties
~ The addition of epinephrine to local anesthetic is useful to :
1. Detect intravascular injection
2. To increase duration of the blockade
3. To prevent systemic absorption and toxicity
INTRAVENEOUS ANESTHETICS

INTRAVENOUS INDUCTING AGENTS

An intravenous injected drugs use to induce unconsciousness at the onset of general
anesthesia but allows rapid recovery after termination of its effects.
QUAUT1ES OF AN IDEAL INTRAVENOUS ANESTHETICS
I. Rapid nearly instantaneous onset without causing pain on injection.
2. Smooth induction without any signs of muscular twltchlngs and excitement.
3. Safe and cause minimal perturbation of cardiovascular and respiratory function.
4. Short acting allowing the patient to awaken rapidly to full normal CNS function.
5 . Metabolism to Inert substances and excretion would be rapid and complete so
that ac~cumulatlon would not occur thereby allowing the drug to be used as a
constant Infusion over long periods of time.
6 . Amnesia for Intraoperatlve event should be complete.
No ideal intravenous inducting drugs exist but many agents possess most of the desired
physical and pharmacologic properties.
With increasing age the total volume of distribution increases and elimination clearance
decreases so that longer lasting drugs effects.
Older patients are more sensitive to Intravenous anesthetics thus dose reduction are
required.

Appropriate dosing of intravenous anesthetics requires consideration :

1. Intravascularvolume status
2. Comorbldities
3. Age
4. Chronic medications
I. BARBITURATES
Derived (Tom barblturic acid only the shorter acting barbiturates have clinical use
in anesthesia
Thiobarbiturates (3-5mg/kg)
1. Thlopental "L_ similar potency and pharmacologic profile
2. Thlam.ylal _J-
Oxybarblturates (1.5mg/k8)
1. Methohexital
Has a greater potency than the thlobarbiturates and is associatecl with a high
Incidence of myoclonic like muscle tremors and other signs of excitatory activity.

THIOPENTAL
Highly alkaline a 2.S% solution has a pH of 11
Will precipitate when added to an acidic solution (LR)
Accidental Intraarterlal Injection of,barbiturates mat result in the formation of crystals in
arterioles and capillaries causing intense vasoconstriction, thrombosis and even tissue
necrosis causing chemical endarterltls.

Management :
Treat with tntraarterlal administration of ltdocalne, heparaine.
)~ Geriatric patients require a 30% to 40% reduction in the usual adult dose
because of a decrease of the volume of the central compartment and a slowed
redistribution of the drug from the vessel rich tissue to lean muscle.
Contralndtcatlon: Absolute
1, Porphyrla
Increase in amino levullnic acid synthetase activity Increases porphyrin synthesis
(abdominal pain, neurotoxlclty, autonomic dysfunction, peripheral nerve
denlage, as well as intercostal and phrenlc nerve damage.)
 2. ~Jlerly
} * There is an Increased risk of histamine release with thiopental when compared
with other barbiturates secondary to the sulfur molecule in its chemical
structure.
Relative contraindication:
1. Hypovolemla
) * Due to cardiovascular depression, thlopental may result in slRnlflcant
hypotension.
~" If slowly titrated to loss of consciousness, thiopental maybe used successfully.
2. Hepatic failure
)" Metabolism maybe delayed resultln8 in a prolonlled ffect,

CENTRAL NERVOUS SYSTEM EFFECT

Reduces the brain's oxyRen consumption and may reduce ischemla-inducad
brain damage.
)* Used for the treatmeot of increased Intracranlal pressure.
CARDIOVASCULAR EFFECTS
Direct myocardial depression.
Decreases MAP secondary to peripheral vasodllatation.
Maintained cardiac output secondary to reflex tachycardla and vaRolytic effects.
RESPIRATORY EFFECTS
All intravenous anesthetics produces respiratory depression, decreases tidal
volume and minute ventilation as well as right shift in carbon dioxide responsive
curve.

TERMINATION OF EFFECTS
) * AS plasma concentration falls, some drug leaves the highly perfused organs
(brain) to ma!ntain equilibrium.
}~ This redistribution is responsible for termination of effects of many anesthetic
druEs.
This explains the awakenin8 from the effects of thiopental not due to
metabolism or excretion but rather to redistribution of the drug from the brain
to the muscle.

I1. ETOMIDATE
), A carboxyleted Imtdazole.
Unlike the barbiturates it may have dlsinhtbitory effect on the part of the
nervous system that controls extra pyramidal motor activity.
- this Inhibition is responsible for a 30-60% incidence of myodonus.
Dissolve In propylene Rlycol thus this solution often causes pain on injection that
can be lessened by a prior injection of lidocaine.
CARDIOVASCULAR EFFECTS
> This drui~ Is dlsttnl[uished from the other intravenous agents by its minimal
effects on the cardiovascular system,
a. Myocardial contractility and cardiac output are maintained
b. Mild decrease in MAP
} , Thb lru8 is the agent of choice whenever cardiovascular stability is potentially
an Imue.
) , Kncmm to cause edrenocortical suppression resulting to increased morbidity in
cdecany iii patients.
) . Thedo,~ for induction is 0.2-0.4 mE/k8 IV

po~-l~e dde effects

1. klrenocort~l suppression
 2. Myocionus
3. Actlvetion of seizure

III. KETAMIN E
> A phencydldlne derivative
Produces dose dependent CNS depression to a so called DISSOCIATIVE ANESTHETIC
STATE characterized by profound analgesia and amnesia and nystasmus
Induction dose :
1-2 mR/k8 IV -'I,_ producing an effect lasting for 10-20 minutes
4-8 mR/l~ IM-J '
AJthough recovery to full orientation may require an additional 60-90 minutes.

CARDIOVASCULAR EFFECTS
1. Stimulation of the sympathetic nervous system ---) Increase In MAP
2. Increasi~s heart rate aff~rdlac output
~> This Is an excellent Inductinll alent for hypovolemlc patient
) " However If catecholamlne stores are exhausted (end-stage shock ) Induction may result
In decrease MAP and a decrease In cardiac output.
METABOUSM
)~ Extensively metabolized In the liver to NORKETAMINE which is 1/3 to 1/5 as potent as the
parent compound.

THE GOOD ABOUT KETAMINE

1. Significant analgesic effect
2 . No suppression of the cardiovascular system and respiratory system
3 . Dose related unconsdousness and dlssocllltlve state of analResla
4 , Fast onset
5 . Bronchial smooth muscle relaxation (asthmatic induction)

THE BAD ABOUT KETAMINE

1. Related to phencyclldlne (LSD) - may cause hallucinations and disturbing dreams especially in
adults (PHSYCOMIMETIC REACTION)
Less likely in patients treated with benzodlazeplne, barbiturates, or propofol
2 . Not as amnestlc as benzodiasepioe
3. Dilates the pupil and trlsers nystaEmus,
4 . Increase cerebral metabolic rate for oxygen, cerebral blood flow and Intracranial pressure
(minimized by hyperventllatlon of the lungs and pretreatment with benzodlazeplne)
S. Increa~ salivation M-) laryngos spasm
6 . Can activate epilel~J:~enlc fosl In patients with known seizure disorder
7 . It~crelsed mu~ke toni with purposeless movements of the extremities

Co~trelndlcation :
> ContrMndlcated In pltients with Intracranlal pathology, as it Increases Intracrankd pressure and
tumbrel bbod flow.
IV.PROPOFOL

) Most ~ ~ Intravenous drub for Induction of anesthesia.

M ECHANI.Td¥1 OF ACTION
> The ~ by ,dnlch It Induces a state of general anesthesia may involve f~cllltatlon of
Inhibita(y neum~wwmKter mediated by GABA.
It MS ~ ~ because it is associated with :
1. I~1 k~ of ~U~lousness

|, Snml~ly fewer residual effects on patient's brain

CARDIOVASCULAR EFFECTS
1. MyocardLal depressant effect greater than thiopental
2 . Markedly decreases MAP up to 40~ secondary to peripheral vasodllatation
3 . Blockade of erterLal baroreceptor response to hypertension
4 . Minimal effecton heart rate
5. Decreased cardiac output
6. No reflex tachvcardla
AvaiLable as :
1~ aqueous solution (10mg/ml) available for Intravenous administration containing soy bean oil,
gtvcero! and ~ lecithin.

ADVERSE EFFECTS
1 . Allergies- patients with a history of previous allergic reaction to pmpofot or allerl~ to soy
beans and eggs.
A history of egg allergy does not necessarily contraindicate the use of propofol because most
egg allergy involve the reaction to egg white (albumin)
The above formulation can cause pain during injection
2 , Pregnancy-shouldbeusedcautiouslyforlnductionsecondarytoltsabllitytodecreaseMAP
it crosses the placenta rapidly and can lead to neonatal depression
3 . HypercholesterolemLa - it can result in a further increase in serum trlglycaddes.
4 . Muscle relaxants- use a non-histamine muscle relaxants to prevent bronchospasm
5. Cardiovascular challenged patients - patients who are hypovolemic or who have cardiovascular
disease may not tolerate the decrease In MAP and myocardial depression associated with
pmpofol.

Metabellsm
It is rapidly cleared from the central compartment by hepatic metabolism,

Dose;
It is used as a holus for the induction of anesthesia io adults (1-S-2 mg/kg W)
IV infusion rate for hypnosis 100200 mcgJkg/min
For sedation 25-7S mcg~min
The administration of propofoi can cause slliniflcant pain upon injection which can be
attenuated by using intravenous needle placadln a Large vain and or administerinR lidocaine at
.5-1 mgJiF~ IV Just prior to injecting propofor
Propofol has never been associated with a case of malignant hyperthermia, so it is the agent of
choice for general anesthesia In this setting.

APPROPRIATE INDUCTING AGENTS FOR ACTIVE WHEEZING /TRAUMA PATIENTS

When a patient Is actively wheezing and scheduled for elective surgew the case should be
postponed un~ the patient has been adequately optimized for surgery (broncho dilators,
Improvement of cold symptoms)
In any patient with a history of asthma or prone to histamine release Propofol or ketemtne is the
best optJon.
Propofol has shown to decrease airway resistance after incubation
Ketamlne Is a Oroncho lllaT~r and may be the Inducting agent of choice in apatient with active
wheezlrql requiring emergency surgery,
TRAUMA PATIENTS
Generally Intnlvascu~rly volume depleted
Kemmb~ ts ~e drug of choice secondary to its maintenance of MAP by stimulating the
sym e~ nervous system
> In all hylPevolemic patient administer the smallest dose possible titreting to loss of

PATIENT WITH A SCREW DRIVER IN HIS EYE, NEEDS EMERGENCY SURGERY, JUST EATEN A FULL MEAL
> The gilman/concern is the risk of aspiration
> In are/trauma patient it is considered to have a full stomach secondary to delayed
 > The Induction agent should have a fast onset and decrease intraocular pressure
Take In to consideration:
Ketamlne can increase Intraocular pressure
Etomldate can cause myoclonus and therefore can Increase lntraocular pressure
Propofol and Thiopental - best option
A patients should be assessed before laryngoscopy with the goal ---) total paralysis as
coughing on the tube remarkably increase intraocular pressure
)* REMEM8ER : basic bllnkin¢ stress, and Intubatlon can all increase Intraocular pressure

CLINICAL PEARL:
Benzodiazeplne and oplods have synerEIstic effect with Intravenous induction requiring
idju~tmcnt in doslnll,
Ketimlne Is the best induction for hypovotemlc trauma patients as long as there is no risk for
increase in Intracranlal pressure.
increase cerebral blood flow, Intracranial pressure and cerebral metabolism Is due to its
stimulation of the sympathetic nervous system.
it is also a Rood inducting agents Inactive bronchospastlc disease.

A~~ ~ther ~nduct~n~ a~ents cause a decrease ~ntracrania~ pressure by decreasin~ cerebra~ b~~~d
flow and cerebral metabolic rate.