AHESTHESIA

Anesthesia – Greek aísthēs (is) - capacity for sensation or feeling; sensitivity + [an] – negation
Analgesia – lack of pain sensation

Anesthesia as a medical phenomenon

The main goal of anesthesia as a medical workmanship is to protect the patient from the
operative stress. This is done through monitoring and control of the vital functions of the human body
during surgery or other invasive procedures.

The operative stress was extensively studied and one of the most lucrative concepts was proposed by
H. Laborit and P. Huguernard, with their theory of the “oscillating postagressive syndrome”, meaning an
exaggerated physiological reaction which creates the state of shock in its form and mechanisms. According to
this concept the reaction of the human body in this case involves all the organ systems and have numerous
expressions, like increase in sympathetic tone as well as endogenous catecholamine level with an increase in
heart rate and blood pressure, known nowadays as common hemodynamic response to a nociceptive stimulus,
etc. From this point of view anesthesia is designed to modulate and even counteract these phenomena.

In the past in order to prevent the appearance of shock various anaesthetic combinations use to be
used: potentialised anaesthesia (diethazine, promethezine and pethidine) and the “Lytik cocktail”
(chlorpromazine, prometazine, pethidine), which later on became the famous neurolept-anesthesia (i.e
combination of dropridol – a neuroleptic/ antipsychotic with antiemetic properties and extrapyramidal side-
effects + an opioid).

As a complex event/process anesthesia consists of several steps:

I. Evaluation of the Patient and Preoperative Preparation

Preoperative Assessment
Preoperative Medication
II. Equipment Preparation
III. Patient Positioning
IV. Anesthesia Induction
V. Anesthesia Course/Maintenance and Monitoring
VI. Emergence from Anesthesia and Recovery

The last three steps refer to anesthesia itself and are usually presented as stages of general anesthesia.

Dr. Crawford Long administered the first anesthesia using an ether-saturated towel applied to his
patient‟s face on March 30, 1842, in the American state of Georgia. The surgical patient went on to have two
small tumors successfully removed from his neck. Dr. Long received the world‟s first anesthetic fee: $0.25.
Nowadays ether is not used any more as an anesthetic being replaced by modern drugs and techniques and
the anesthesiologists fee in developed countries is one of the highest in the medical field.

According to Miller's Anesthesia Seventh edition and following P.Woodbridge concept, the purpose of
anesthesia can be distilled down to several basic components/end points: (Stress-Free Anesthesia, p.29-30)
hypnosis
analgesia (lack of pain and other types of sensation which also blunts autonomic reflexes = autonomic
nervous system stability)
muscle relaxation
 Out of these four components, analgesia and autonomic nervous system stability are of paramount
importance and should be present in any type of anesthesia (local/regional or general). Hypnosis and muscle
relaxation can be optional depending on a number of circumstances, including type of surgery (e.g. during a
peripheral nerve blockade hypnosis can be replaced by a light sedation; profound muscle relaxation will
appropriate during hip replacement surgery)

Anesthesia starts with patient assessment and preoperative preparation. These serve to optimize the safety
of anesthetic experience.

Preoperative evaluation and medication. ASA anesthesia risk score

Assessment include: general state of health, previous anesthetics, current drug usage, allergy, drug abuse and
addiction, menstrual and obstetric history and organ systems review as well as physical examination and
laboratory tests and investigations.

The purpose of the pre-operative assessment is three-fold:

• To review the medical and psychological status of the patient

• To identify factors which may impact on the perioperative course, to take measures to optimize those factors
where possible, and to delay surgery if necessary
• To inform patient, alleviate anxiety and establish rapport

This evaluation takes the form of a directed history, physical examination and laboratory exam. On history,
the anesthesiologist attempts to elicit symptoms of cardiac or respiratory disease as well as a history of any
other major medical illnesses, past or present.
ASA Score Hepatic or renal disease may impact on metabolism
ASA class Description and excretion of anesthetic agents, fluid balance
A normal healthy patient in need of surgery for
and coagulation status. The patient‟s medications
1
a localized condition. are reviewed including any history of adverse drug
2 A patient with mild to moderate systemic reactions. The patient‟s and their relative‟s previous
disease; examples include controlled anesthetic experience is reviewed. The physical
hypertension, mild asthma. examination focuses on the cardiac and respiratory
3 A patient with severe systemic disease;
examples include complicated diabetes, (including airway) systems. Recording baseline
uncontrolled hypertension, stable angina. vital signs is important, as is detecting any
4 A patient with life-threatening systemic unstable, potentially reversible conditions such as
disease; examples include renal failure or congestive heart failure or bronchospasm. The
unstable angina.
A moribund patient who is not expected to
airway is assessed for ease of intubation. Routine
5
survive 24 hours with or without the operation; pre-op laboratory investigations have not been
examples include a patient with a ruptured shown to improve patient outcome. Therefore,
abdominal aortic aneurysm in profound laboratory studies are ordered only as indicated,
hypovolemic shock. according to the medical status of the patient and
6 A brain stem dead patient whose organs are
being removed for donor purpose the nature of the planned surgery. Studies are rarely
For emergency cases the suffix/letter code “E” is used ordered to establish a “baseline” but rather to detect
abnormalities that require correction prior to
surgery. The traditional “CBC and urinalysis” is no
longer required in healthy patients having minor surgery. An electrocardiogram (ECG) is ordered on patients
who are known to have cardiac disease or in whom risk factors (including age) are present. Routine pre-
operative chest x-rays are not required prior to most procedures. The anesthesiologist will commonly assign
an “ASA class” (see table) to the patient. The ASA (American Society of Anesthesiologists) classification
was defined in the 1940„s as an attempt to identify operative risk. As the patient‟s underlying health is the
most important determinant of peri-operative risk, the ASA class does correlate to overall peri-operative risk.
 Compared with younger patients, elderly patients may be at a greater risk for perioperative
complications because of age-related concomitant diseases and declines in basic organ function that are
independent of disease. In the table below there is a summary of some age-related changes important for
anesthesia delivery:

Age related changes

Decreased Cardiac Output, Resting an Maximum Heart Rate
Increased Systemic vascular resistance and Systolic blood pressure
Loss of skeletal muscle mass, Decrease in Total body water (e.g. 20
-30% reduction in blood volume by 75 years of age)
Increase in body fat (= increased volume of distribution)
Decrease in dose requirements (i.e. decreased tolerance) for volatile
anesthetics, opioids, barbiturates, benzodiazepines

A special attention is paid to Airway Assessment. The anesthesiologist must always perform a
thorough preoperative airway assessment, regardless of the planned anesthetic technique. The purpose of the
assessment is to identify potential difficulties with airway management and to determine the most appropriate
approach. The airway is assessed by history, physical examination and occasionally, laboratory exams. On
history, one attempts to determine the presence of pathology that may affect the airway. Examples include
arthritis, infection, tumors, trauma, morbid obesity, burns, congenital anomalies and previous head and neck
surgery. As well, the anesthesiologist asks about symptoms suggestive of an airway disorder: dyspnea,
hoarseness, stridor, sleep apnea. Finally, it is important to elicit a history of previous difficult intubation by
reviewing previous anesthetic history and records.

The physical exam is focused towards the identification of anatomical features which may predict
airway management difficulties. It is crucial to assess the ease of intubation. Traditional teaching maintains
that exposure of the vocal cords and glottis opening by direct laryngoscopy requires the alignment of the oral,
pharyngeal and laryngeal axes. The “sniffing position” optimizes the alignment of these axes and optimizes
the anesthesiologist‟s chance of achieving a laryngeal view. An easy intubation can be anticipated if the
patient is able to open his mouth widely, flex the lower cervical spine, extend the head at the atlanto-occipital
joint and if the patient has enough anatomical space to allow a clear view. Each of these components should
be assessed in every patient undergoing anesthesia:

• Mouth opening: Three fingerbreadths is considered adequate mouth opening. At this point in the exam,
the anesthesiologist also observes the teeth for overbite, poor condition and the presence of dental prosthetics.
• Neck motion: The patient touches his chin to his chest and then looks up as far as possible. Normal range of
motion is between 90 and 165 degrees.
• Adequate space: Ability to visualize the glottis is related to the size of the tongue relative to the size of the
oral cavity as a large tongue can overshadow the
Class 1 Soft palate, larynx. The Mallampati classification (see table)
uvula, tonsillar assigns a score based on the structures visualized
pillars can be
seen
when the patient is sitting upright, with the head
As above except
in a neutral position and the tongue protruding
Class 2
tonsillar maximally. Class 1 corresponds well with an
pillars not seen easy intubation. Class 4 corresponds well with a
Class 3 Only base of difficult intubation. Classes 2 and 3 less reliably
uvula is seen predict ease of intubation. The thyromental
Class 4 Only tongue and distance is also an important indicator. The
hard palate distance from the lower border of the mandible
can be seen to the thyroid notch with the neck fully extended
Table x. Mallampati Score should be at least three to four fingerbreadths. A shorter distance may
indicate that the oral-pharyngeal-laryngeal axis will be too acute to achieve good visualization of the larynx.
As well, a short thyromental distance may indicate inadequate “space” into which to displace the tongue
during laryngoscopy. Combining Mallampati classification with thyromental distance and other risk factors

Predictive signs of a difficult airway:
Morbid obesity
short, thick neck (short thyromental
distance < 3 fing.)
neck stiffness with limited mobility
limited mouth opening and III – IV
Mallampati score
magnetic resonance imaging may be required.
(morbid obesity, short, thick neck, protuberant teeth,
retrognathic chin), will increase the likelihood of
identifying a difficult airway. No assessment can
completely rule out the possibility and so the clinician
must always be prepared to manage a difficult airway.
Laboratory investigations of the airway are rarely
indicated. In some specific settings, cervical spine x-rays,
chest ray, flow-volume loops, computed tomography or

The induction of anesthesia abolishes the normal laryngeal reflexes that prevent inhalation
(“aspiration”) of stomach contents. Due to gastric, biliary and pancreatic secretions (which are present even
during fasting), a stomach is never “empty”. NPO (nil per os) indicates the restriction of oral intake for a
period of time prior to surgery, minimizing the volume, acidity and solidity of stomach contents. Such
measures reduce both the risk of aspiration occurring as well as the severity of pneumonitis, should an
aspiration event occur.

Premedication
Premedication can include medication that the patient takes routinely as well as medication that may
be prescribed specifically for the pre-operative period. Generally speaking, patients should be given their
usual medication on the morning of surgery with a sip of water. It is particularly important that patients
receive their usual cardiac and antihypertensive medications pre-operatively. Discontinuation of beta-
blockers, calcium channel blockers, nitrates or alpha-2 agonists (clonidine) can lead to rebound hypertension
or angina.Similarly, most medications taken for chronic disease should be continued on the morning of
surgery as well as throughout the peri-operative period. This is particularly important for most
antidepressants, thyroid replacement and anticonvulsants.

There are certain medications that may need to be discontinued in the pre-operative period. Examples
include monoamine oxidase inhibitors and anticoagulants. Patients on platelet inhibitors such as aspirin
represent a special group of patients who must be considered on an individual basis such that the risk of
stopping the aspirin is weighed against the risk of surgical site bleeding. For example, a patient who is on
aspirin because of the recent insertion of a coronary stent must receive their aspirin throughout the peri-
operative period. On the other hand, if the patient is on aspirin for primary prevention then it is usually
discontinued a full week before surgery to allow return of normal platelet function.

Some medications are ordered specifically for the preoperative period. Examples include anxiolytics,
antibiotics, bronchodilators, anti-anginal medication and anti-emetics. Currently, pre-operative sedation is
used less frequently than it has been in the past as it can delay awakening at the end of anesthesia. A delayed
recovery is particularly undesirable in the outpatient surgical population where a return of cognitive function
is required prior to discharge home. Furthermore, a preoperative visit has been shown to be at least as
effective as pharmacologic means in allaying anxiety in surgical patients. Nonetheless, there is a role for pre-
operative sedation in very anxious patients or in those for whom anxiety would be deleterious, such as the
cardiac patient.

For most types of surgery, antibiotics are ordered preoperatively to reduce the incidence of wound
infection. Antibiotics may also be ordered to reduce the risk of bacterial endocarditis in at-risk patients
though the current recommendations from the American Heart Association are much more restrictive than
they have been in the past. As discussed, aspiration prophylaxis may be ordered in high risk patients. This
includes agents which decrease the volume and/or acidity of gastric secretions (ranitidine, sodium citrate) as
well as agents which increase gastric emptying (metoclopramide). A history of systemic steroid use may
require the delivery of a peri-operative course of steroids.
Some of the eventual goals for preoperative medication can be summarized as follows:
Anxiety relief
Sedation
Amnesia
Analgesia
Infection prevention
Drying of airway secretions
Prevention of autonomic nervous system responses
Reduction of gastric fluid volume and increased pH
Antiemetic effects
Reduction of anesthetic requirements
Facilitate induction of anesthesia

General Anesthesia. GA Stages

As mentioned above, general anesthesia is a tetrad of amnesia (unconsciousness), analgesia, control

of autonomic reflexes and muscle relaxation. Amnesia (unconsciousness) is usually induced by intravenous
anesthetic agents and then maintained by using inhalational anesthetic agents. Analgesia is provided by
various analgesic drugs or by regional/peripheral nerve blocks. Muscle relaxation component of general
anesthesia is not required in all patients or surgical procedures. Muscle relaxants are used to facilitate tracheal
intubation, mechanical ventilation or surgical procedure.

Amnesia or unconsciousness may be produced by various drugs, which depress the central nervous
Most of general anesthetics act through
nervous system (CNS). Commonly used anesthetic agents (e.g.
such recptors as: propofol, thiopentone,) produce unconsciousness in one arm-
GABA brain circulation time with transient depression of cardio-
NMDA respiratory function. However, for some drugs the doses
2PK, etc. required to produce anesthesia are so large that the
rapidly producing unconsciousness cardiovascular and respiratory depression commonly occur,
(e.g onset of hypnosis after thiopental
intravenous injection is 30-60 seconds) and recovery cab be delayed for hours (e.g. benzodiazepines).
Ideally intravenous anesthetic agent should be able to produce
rapid loss of consciousness and recovery from its effect should be quick without any hangover effects.

In patients with appropriate fasting, general anaesthesia is induced, usually, by administering short
acting opioid analgesic agent (fentanyl or fentanyl derivates) followed by slow injection of intravenous
anesthetic agent (propofol) with simultaneous assessment of verbal response or eyelash reflex of patient.
When unconsciousness is induced, if needed muscle relaxant is administered. Patient‟s airway is maintained
using laryngeal mask airway (LMA) or endotracheal tube. General anesthesia is commonly maintained by
inhalational anesthetic agent and ventilating the lungs with oxygen and nitrous oxide or air. If anesthesia is
induced and maintained only by intravenous anesthetics it is termed Total Intravenous Anesthesia (TIVA).

Induction
The goal of the induction phase of anesthesia is to induce unconsciousness in a fashion which is
pleasant, rapid and maintains hemodynamic stability. If the anesthetic plan includes control of the airway and
ventilation then the induction phase also aims to achieve muscle relaxation to facilitate endotracheal
intubation. Anesthesia can be induced by having the patient breathe increasing concentrations of inhaled
gases by mask (avoiding agents like isoflurane or desflurane, which can irritate airway because of their
pungent smell). While there are settings where this is the desired technique, it tends to be slow and can be
unpleasant. More commonly, anesthesia is induced with short acting intravenous agents such as propofol,
ketamine, thiopental or etomidate, followed by a muscle relaxant if indicated. In most cases, a non-
depolarizing muscle relaxant (NDMR) is used.
 During this stage a special attention is paid to airway management. The key aim of airway
management is to clear or bypass the obstructed airway, assist or replace spontaneous ventilation and protect
the lungs from aspiration. Rapid assessment and institution of a patent airway, ventilation and oxygenation
of lungs is essential in preventing secondary damage to the brain and other organs due to hypoxia. A wide
range of airway management devices are available. Choice of device depends on the individual patient and
the experience of the attending medical personnel. Airway devices can be generally classified in to two
groups, those which are less invasive and placed above the level of glottis are known as supra-glottic devices.
Those that place within the trachea (below the level of glottis) are known as infra-glottic devices. Below is a
short list of such devices.

Airway management devices

Supra-glottic Infra-glottic

-Various types of masks - Endotracheal tube

-Laringeal Mask Airway - Cricothyroidotomy
-Esophageal- tracheal - Tracheostomic tube
Combitube

Endotracheal intubation is considered to be the optimal form of airway management. It is considered

to be superior to other advanced airway management techniques for the following reasons:

1. Airway is reliably isolated from foreign material in the oropharynx.

2. Suction of inhaled particles from the lower respiratory tract is possible.
3. More effective ventilation of lungs.

There are three simple maneuvers that can be used to relieve the obstruction of the airway caused by
the tongue. These maneuvers generate a position similar to “sniffing position”. Same maneuvers can be used
to facilitate tracheal intubation:
• Head tilt – can be attained by placing one hand on the patient‟s forehead and tilting the head back gently, keeping the thumb and
index finger free to close patient‟s nose if rescue breathing is required
• Chin lift - Patient‟s chin is lifted to open the airway using the finger tips of the other hand
• Jaw thrust - After identifying the angle of the mandible, the ring and little fingers are placed behind the angle, the index and
middle finger placed over the body of mandible to apply steady upwards and forward pressure to lift the mandible. The thumbs are
used to open the mouth slightly by downward displacement of the chin This is the only technique that can be done if there is a
suspicion of cervical spine injury.

Endotracheal intubation is usually performed during direct laryngoscopy with the visualization of
respective structures and advancement of the tracheal tube between the vocal folds with confirmation of
correct tube position:

Vallecula
Vocal fold
Epiglottis

Aryepiglotic
Cuneiform fold
cartilage

Corniculate Trachea
cartilage
Practically this stage usually starts with a rapid sequence induction to be performed as follows:
1. Suction apparatus is checked and kept readily available.
2. Pre-oxygenation of patient with 100% oxygen for 3-5 minutes.
3. Application of cricoid pressure (Sellick‟s maneuver) by assistant.
4. Induction with pre-calculated dose of induction agent followed immediately by intubating dose of
depolarizing muscle relaxant (succinylcholine). A rapidly acting non-depolarizing agent (e.g. rocuronium) is
commonly used in a so-called “modified” rapid sequence induction.
5. Intubation of trachea, cuff inflation and verification of proper tube position.

Cuff pressure is essential in endotracheal tube management. Guidelines recommend a cuff pressure of
20 to 30 cm H2O. Inflation of the cuff in excess of 30 cm H2O damages the tracheal mucosa by
compromising capillary perfusion

Criteria for successful tracheal intubation

- Carbon dioxide in exhaled gases (CO2 by capnometry)

- Bilateral rising of the chest during ventilation and bilateral equal breath sounds
- Absence of air movement during epigastric auscultation
- Condensation (fogging) of water vapor in tube during exhalation
- Refilling of reservoir bag during exhalation
- Maintenance of arterial oxygenation (SpO2 by puls-oximetry)

Maintenance
If no further agents were administered following the induction of anesthesia the patient would
awaken within minutes. Therefore, maintenance of anesthesia requires the delivery of pharmacologic agents
with the aim of achieving the “four components of anesthesia” and hemodynamic stability throughout the
surgical procedure. A further consideration is the length of the procedure and the need to awaken the patient
at the end of the case.
The maintenance phase of anesthesia involves the use of inhaled agents, opioids and non-
depolarizing muscle relaxants (NDMR). The anesthesiologist must be ever vigilant. Problems related to the
airway, breathing and circulation (ABC‟s) are most critical and can occur during any phase of anesthesia.

Emergence from anesthesia

During the emergence phase of anesthesia, the patient begins to return to his pre-operative state of
consciousness. In most cases, the anesthesiologist aims to awaken the patient at the end of the operative
procedure prior to transfer to the post-anesthetic care unit (PACU). How “awake” must the patient be? Ideally
the patient is conscious enough to obey commands and support his own airway. At the very least, the patient
must have adequate spontaneous ventilation but may need minimal assistance to maintain patency of the
airway. In between these two states lies a wide spectrum of level of consciousness. Patient factors as well as
the anesthetic technique determine the rate at which emergence from general anesthesia occurs.
Emergence requires the offset of effect of the anesthetic agents. This is achieved by administering the
anesthetic drugs in appropriate doses at the appropriate time according to the anticipated length of the
procedure. The anesthesiologist relies on the normal metabolism and excretion of drugs to achieve offset of
effect. Active reversal of drug effect through the administration of another drug also plays a role in
emergence. The most common example of this is the reversal of muscle relaxation. The action of all non-
depolarizing muscle relaxants can be reversed prior to emergence from anesthesia. The anticholinesterase
drugs, sometimes termed “reversal agents” are edrophonium, neostigmine and pyridostigmine .
Aside from muscle relaxants, anesthetic agents are rarely actively reversed in order to achieve
emergence. There is no “antidote” to the inhaled agents; offset of effect relies on the timely discontinuation of
administration followed by excretion through the lungs. While an opioid antagonist (naloxone) exists, there
are several disadvantages to using it to reverse opioid effect at the end of surgery. Firstly, unless very
carefully titrated, its use will lead to a startled, hyper-alert patient who complains of pain at the operative site.
Hypertension, tachycardia, myocardial ischemia and pulmonary edema may result. Secondly, the duration of
effect of the antagonist is shorter than that of many of the opioid agonists therefore “re-narcotization” in the
PACU is a risk. Finally, Naloxone is an expensive drug whose use adds unnecessarily to the cost of the
anesthetic. Flumazenil is a specific benzodiazepine antagonist which may play a role in the occasional
surgical patient whose decreased level of consciousness is attributed to benzodiazepines. Like naloxone,
flumazenil has a shorter duration of action than most of the benzodiazepine agonists therefore rebound
sedation may occur.
If an endotracheal tube is used to maintain the airway intra-operatively, it must be removed at some
point during the emergence phase of anesthesia. It is important to time the extubation properly, so as to avoid
the potential post-extubation complications:
• airway obstruction
• aspiration
• inadequate ventilation
• laryngospasm

Goals of Recovery
At the end of the operative procedure, care and monitoring of the patient is handed over from the
anesthesiologist to the nurse in the postoperative care setting as the patient enters the period of recovery. For
most patients, this occurs in the Post-Anesthetic Care Unit (PACU). However, some patients, such as those
requiring prolonged post-operative ventilation or close hemodynamic monitoring, may instead be admitted
directly to the Intensive Care Unit. Prior to transporting the patient from the operating room, the
anesthesiologist must ensure the presence of the following:
• patent airway (provided either by an awake patient, oral airway or endotracheal tube)
• adequate ventilation
• stable hemodynamics
• adequate pain control

Any identified problems must be corrected before leaving the operating room to avoid transporting
an unstable patient.

Problems during general anesthesia can appear at any stage of anesthesia but during induction and
emergence from anesthesia they are more common. Such problems, teremed as complications can be
summarized as follows:
Allergic reactions (anesthetics – 5%, muscle relaxants – 50%, antibiotics – 8%, infusion fluids – 3%,
latex – 17%)
Aspiration of gastric content
Failed intubation
Failed ventilation
Acute airway obstruction (bronchispasm, laryngospasm)
Pneumothorax
Hypotension
Malignant hyperthermia (triggered by Succinylcholine or Volatile Anesthetic)
Cardiac arrest
Below is a table with the risk level for such complications:
Risk level Verbal Anesthesia/medical
(ratio) scale examples

1: 1-9 Very common Pain 1:2, Sore throat 1:2 (ETT), Delirium, PONV 1:4, Cognitive difunction, Diziness,
Headache

1: 10 – 99 Common Thrombophlebitis 1:10, Severe pain 1:10, Dural puncture headache (1:10), Pneumotorax
(spraclavicular block), Miocardial re-infarction (< 3mo after MI), Difficult intubation

1:100 – 999 Moderately CVA (general surgery) 1:100, Loss of vision (cardiac surg) 1:100, Dental damage, Prioperative
common death 1:100 (1 mo) or 1:500 (at 2 days), Awareness, Failure to intubate, Sezures

1:1000 - 9999 Less Systemic LA toxicity (regional block) 1:1500, Cardiac arrest 1:1500 (spinal), Death 1:5000
commmon (ASA 3-4),

1:10000 - Rare Anaphylaxis 1:10000, Systemic LA toxicity (epidural) 1:10000, Death (related to anesthesia)
99999 1:50000, Malignant hyperthermia

1: 100000 - Very rare Death (related to anesthesia ASA 1-2) 1:100000, Paraplegia (spinal/epidural) 1:100000, etc.
999999
ETT – endotracheal tube, PONV – postoperative nausea and vomiting, MI – myocardial infarction, LA – local anesthetic, ASA –
American Society of Anesthesiologists (score)

Inhalational anesthetics

Inhalational anesthetic agents Mecanism of action

• Inhalational anesthetics have been shown
A) Volatile anesthetics to affect many different ion channels, second
- Halothane messengers, and metabolic processes
• GABA, NMDA, glycine receptor subunits,
- Isoflurane 2PK receptors have all been shown to be
- Sevoflurane affected
- Desflurane • Potency of anesthetic has been roughly
linked to lipid solubility and is revealed by
- Enflurane MAC
B) Gases • Part of mechanism may involve anesthetic
agents dissolving in lipophilic sites on cells
- Nitrous Oxide
- Xenon

Halothane Isoflurane
• The most potent of the clinically used • Highly pungent (risk for airway irritation
inhalational agents (MAC 0.75%) not to be used for induction!)
• Can be used to induce and maintain • Second most potent of the clinically used
anesthesia inhalational agents (MAC 1.2%)
• Does not have analgesic effect •Highly popular for neuroanesthesia
• Moderate muscle relaxation effect • Has been implicated for causing “coronary
• Causes vasodilation – decreases BP steal” – dilation of “normal” coronary arteries
causing blood to be diverted away from maximally
• Increases ICP dilated, stenotic vessels to vessels with more
• Causes bronchodilation adequate perfusion
• Sensitises the heart to catecholamines, so it • Causes vasodilation – decreases BP -
is liable to cause cardiac arrhythmias, minimal compared to halothane
occasionally fatal • Increases ICP (usually at above 1 MAC;
short lived) - minimal compared to halothane
• Can cause severe liver injury (1:10000)
• At 2 MAC produces electrically silent EEG
• Its use in developed countries has been
mostly replaced by newer agents
 Sevoflurane
• Half as potent as isoflurane (MAC 2.15%)
• Rapid uptake and elimination
• Sweet smelling, non-pungent
•Quick uptake and sweet smell make this
agent very popular for inhalational
induction
• Potent bronchodilator
Desflurane
• Very fast uptake and elimination
• Low potency (MAC 6.6%)
• Very pungent (risk for airway irritation not
to be used for induction!)
•Can cause breath-holding, bronchospasm,
laryngospasm, coughing, salivation when
administered to an awake patient via face
mask
• Can cause an increased sympathetic
response (tachycardia, hypertension)
when inspired concentration is increased
rapidly

Nitrous Oxide MAC of Inhaled Anesthetics

MAC is the minimum alveolar concentration of

• Can induce hypnosis but has a low potency
(MAC 104% - can never reach 1 MAC- can inhaled anesthetic that prevents movement in 50% of
induce dillutional hypoxia!) subjects in response to a painful (surgical incision)
• Insoluble in blood - facilitates rapid uptake stimulus.
and elimination
• Commonly administered as an anesthetic
adjuvant Anesthetic MAC
• Does not produce skeletal muscle relaxation Halothane 0.75%
• Can diffuse into air filled cavities and cause Enflurane 1.7%
expansion of air filled structures (pneumo- Isoflurane 1.2%
thorax, bowel, middle ear, ET tube balloons,
Sevoflurane 2.0%
etc.) – avoided for on-pump heart surgery and
Nitrous oxide (N2O) 104%
neurosurgery, especially in sitting position
(because of the risk of gaseous emboli) Desflurane 6.0%
• Myocardial depression may be unmasked in
CAD or severe hypotension MAC is an indicator of anesthetic potency and is
• NMDA antagonist -> has analgesic effects inversely related to anesthetic potency (i.e. lower
• NOT a trigger for MH (unlike volatile agents) MAC=higher potency) and can be used for comparing IA
potency

Intravenous anesthetics

Intravenous Anesthetics (IA) IA Pharmacodynamics

Mechanism of Action
• It is widely believed that most IV anesthetics exert
their sedative and hypnotic effects via interaction
with GABA receptors
– GABA is the primary inhibitory neurotransmitter
in the CNS
– Activation of receptor causes increased chloride
conductance, and therefore hyperpolarization
(promotion of inhibition)
– Other IV anesthetics exert effect via NMDA
receptors (Ketamine) or alpha-2 receptors
(Dexmedetomidine)
• Propofol and Barbiturates decrease the rate of
dissociation of GABA and its receptor
• Benzodiazepines increase the efficiency of GABA-
receptor and chloride ion channel coupling
• The principle pharmacologic effect of IV
anesthetics is to produce increasing sedation and
eventually hypnosis. They can be used to induce
loss of consciousness at the beginning of an
anesthetic or used as infusions to maintain
general anesthesia
• All hypnotics also affect other major organ
systems
– They produce a dose-dependent respiratory
depression (exception: Ketamine)
– They produce hypotension and cardiac
depression
– A large hemodynamic depressant effect can be
seen in the elderly and those with pre-existing
cardiovascular disease
• These patients often exhibit decreased dose
requirement
 Barbiturates (Thiopental)
• Highly alkaline (pH 9)
• Can precipitate in acidic solutions (DO NOT MIX
with Rocuronium or LR)
• Intra-arterial injection can cause intense
vasoconstriction, thrombosis and tissue necrosis;
treat with papaverine and lidocaine or regional
anesthesia-induced sympathectomy and
heparinization
• Induction dose 3-5 mg/kg in adults, 5-6 mg/kg in
children, 6-8 mg/kg in infants
• Rapidly redistributed into peripheral compartments
(accounts for short duration of action)
• Larger doses can saturate the peripheral
compartments resulting in a prolonged duration of
action
• Decreases CBF, ICP
– Causes sedation and EEG burst suppression in larger
doses (previously commonly used for neurosurgical
procedures)
• Anticonvulsant activity – Exception: Methohexital
• Decreases muscular tonus
• Cardiovascular depression by central and peripheral
(decreases SVR, direct myocardial depressant –
hypotension) effects
• Dose-dependent respiratory depression
• Can produce laryngospasm and bronchospasm
• Contraindications to anesthesia with barbiturates
include: allergy to barbiturates, liver failure,
hypotensive states, bronchial asthma
Ketamine
• Produces a dissociative anesthetic state
– profound analgesia and amnesia despite
maintenance of consciousness
– High incidence of psychomimetic
reactions/ hallucinations (attenuated by co-
administration of midazolam)
• Induction dose 1-2 mg/kg
• NMDA antagonist – analgesic effect
(implications in prevention/ treatment of
chronic pain)
• Increases BP, CBF, ICP - – Contraindicated
in neurosurgical procedures
• Most likely to preserve airway reflexes
among the IV anesthetics
• Minimal respiratory depression
• Cardio-stimulating effects secondary to
direct sympathetic stimulation
• Intrinsic myocardial depressant, may be
significant in severely ill patients with
depleted catecholamine reserves
• Increases PVR
• Causes bronchodilation
• Causes increased oral secretions

Propofol Benzodiazepines
(Diazepam, Midazolam)
• Produced in an egg lecithin emulsion - is
relevant to patient allergies
• All benzodiazepines have anxiolytic,
• Pain on injection occurs in 32-67% of subjects;
amnestic, sedative, hypnotic, anticonvulsant
attenuated with IV lidocaine or administering the
properties (but not analgesia!)
drug in a larger vein, can cause thrombophlebitis
• Has central muscular relaxation properties
• Used for continuous sedation, induction and
• Premedication dose 0.04-0.08 mg/kg IV
maintenance
(typically 1-2 mg)
• Induction dose 1.5-2.5 mg/kg
• Induction dose 0.1-0.2 mg/kg IV
– Children require higher doses (larger Vd and
• Decreases CBF, ICP - does not produce EEG
higher clearance)
burst suppression
– Elderly require lower doses (smaller Vd and
• Causes cardiovascular depression -
decreased clearance)
decrease SVR and BP when used as induction
• Infusion doses ~100-200 mcg/kg/min for
dose
hypnosis and ~25-75 mcg/kg/min for sedation
• Causes dose-dependent respiratory
• Depresses cerebral cortex
depression – exaggerated when combined
• Has a rapid onset and recovery
with opioids and in patients with chronic
• Minimal mental confusion on awakening
respiratory disease
• Decreases CBF and ICP;
• Anticonvulsant properties (used in
• Anticonvulsant properties
seizures after a local anesthetic overdose)
• Decreases SVR (arterial and venous), direct
• Flumazenil is a specific antagonist – Very
myocardial depressant
short acting – 45-90 minutes of action
• Dose-dependent respiratory depression
following 1-3 mg dose
• Has anti-emetic properties – often used for
• May see re-sedation as benzodiazepine is
TIVA cases and as a background infusion for
eliminated more slowly compared to effects
patients with PONV
of flumazenil
Muscle relaxants (Neuromuscular Blocking Agents – NMBA) : types, mechanism of action

Muscle relaxation is one of the four components of general anaesthesia. Muscle relaxation is not always
required during general anaesthesia. NMBA are used during general anaesthesia if patient needs tracheal
intubation, mechanical ventilation, or the nature of surgical procedure demands muscle relaxation. These
drugs act at neuromuscular junction.

Muscle relaxants are classified as:

• Depolarizing muscle relaxant (Depolarizing NMBA) : Suxamethonium
• Non-depolarising NMBA: Atracurium, Rocuronium, Vecuronium

NMBA Mechanism of Action Depolarizing NMBA:

• Action potential depolarizes motor
neuronCa++ influxvesicles fuse and
release AChAch across synaptic cleft and
binds nicotinic receptors
• When ACh binds both α subunits, receptor
ion channel opens with ion movement of Na+
and Ca++ in, K+ out
Succinylcholine
(Suxamethonium)
• Structure: two ACh molecules joined by
methyl groups
• Mechanism of action: ACh receptor agonist
and prolonged muscle depolarization
• Intubating Dose: 1 – 1.5 mg/kg
• If you use a defasciculating dose of roc
(0.03mg/kg), intubating dose of sux is higher
(1.5 – 2mg/kg)
• Onset: within 30-60 sec; duration ~10 min
depending on dose (often used for rapid
sequence induction and intubation)
• Diffuses away to extracellular fluid, then is
rapidly metabolized by pseudocholinesterase =
plasma cholinesterase = butyrylcholinesterase)
• ~1:3000 individuals are homozygous for an
abnormal plasma cholinesterase, and paralysis
can last 3-8 hours. .

Nondepolarizing NMBA
Suxamethonium Side Effects • Mechanism of action: competitive inhibition
of nicotinic Ach receptor (nAChR) at the NMJ.
• Hyperkalemia • There are presynaptic nAChR which mobilize
ACh containing vesicles. These presynaptic
• Fasciculations (can be decreased with
nAChR have a slightly different structure than
defasciculating dose of rocuronium = postsynaptic nAChR. Some nondepolarizing
0.03 mg/kg 3 minutes prior to sux) agents block both pre- and postsynaptic nAChR.
• Cardiac Rhythm Disorders; • Two structural classes:
•Bradycardia (especially in children -- often 1. Benzylisoquinolinium = “-urium”
given with atropine). • Cisatracurium, Doxacurium, Atracurium,
• Tachycardia Mivacurium, d-Tubocurarine
• Anaphylaxis (approx. 1:5000 – 1:10,000) • Some can cause histamine release (d-
Tubocurarine >> Atracurium and Mivacurium)
• Myalgia
2. Aminosteroid = “-onium”
• Malignant Hyperthermia • Pancuronium, Vecuronium, Rocuronium,
•Trismus Pipecuronium
• Increased ICP, IOP • Vagolytic effects (Pancuronium > Rocuronium
• Increased intragastric pressure and lower > Vecuronium)
esophageal sphincter pressure. • The most used nondepolarizing agents are the
intermediate duration (aprox. 30 min) agents
rocuronium, cisatracurium, pipecuronium,
vecuronium.
• Neostigmine with glycopyrrolate are most
commonly used “ND NMBA reversal agents” in
the OR.
Opioid analgesics

Basic Opioid Pharmacology Opioid Receptor Subtypes and Their

Effects
• Analgesia produced by mu (µ) opioid receptor
Receptor Clinical effect Agonists
agonism in the brain (periaquaductal gray matter)
Supraspinal (μ1) Morphine
and spinal cord (substantia gelatinosa) μ Respiratory depression (μ2) Met-enkephalin
• Well-known side effect profile: Physical dependence B-Endorphin
– Sedation, respiratory depression Muscle rigidity Fentanyl
– Itching, nausea/vomiting, constipation/ileus, Morphine
urinary retention κ Sedation Nalbuphine
– Bradycardia, hypotension Spinal analgesia Butorphanol
Dynorphin
– Miosis, chest wall rigidity
Oxycodone
• Opioids are hemodynamically stable when given Analgesia Leu-enkephalin
alone, but cause ↓CO, SV, and BP in combination δ Behavioral B-Endorphin
with other anesthetics Epileptogenic
• Reduces MAC of volatile anesthetics Pentazocine
σ Dysphoria Nalorphine
• Effect of pure agonists can be reversed by an
Hallucinations Ketamine
antagonist (Naloxone)

Opioids
Morphine
– Slow peak time (~80% effect at 15 minutes, but peak
analgesic effect is at ~90 minutes)
– Active metabolite, morphine-6-glucuronide, has
analgesic properties and is renally excreted (not clinically
relevant unless patient has renal failure)
– Can cause histamine release
Hydromorphone (Dilaudid)
– “A rapid onset morphine” --> Peak effect in 5-10
minutes.
– About 8-fold more potent than morphine (i.e. 1 mg
Dilaudid = 8 mg morphine)
– No active metabolites, no histamine release
– Common choice for post-op analgesia and PCA
Opioids
Fentanyl
– Is a synthetic opioid
– Fast onset & short duration of action (peak effect
at 3-5 minutes; effect site half-life ~30 minutes
– ~100-fold more potent than morphine
– Causes less histamine release than Morphine
– Can be used as an adjunct to Spinal/Epidural
anesthesia and for short postoperative analgesia
– Very cheap
Sufentanil
– Fast onset, but slightly slower than fentanyl
– 10-fold more potent than fentanyl (i.e. 5 mcg
sufentanil ~ 50 mcg fentanyl).
– More rapid recovery than fentanyl
– Commonly used as infusion

Opioids Strategies for Opioid Use

• For a standard GETA induction, use fentanyl to
blunt the stimulation caused by DL and intubation
Alfentanil
• For brief, intense stimulation (e.g. retrobulbar
– Fastest onset time of all opioids (~90 seconds); pKa =
block, rigid bronchoscopy), consider a bolus of
6.5, so it crosses the blood-brain barrier rapidly
short-acting opioid like remifentanil or alfentanil
– Also causes more N/V, chest wall rigidity, and
• For intra-op analgesia:
respiratory depression
– Fentanyl is rapidly titratable, but requires
– Brief duration
Stages of action
of general due to rapid redistribution
anesthesia frequent redosing; it may be more “forgiving” if
Remifentanil overdosed
– Peak effect time ~90 seconds – Morphine has a long onset time to peak effect,
– Unique pharmacokinetics - metabolized by plasma but gives prolonged analgesia during the case and
esterases into the post-op period
– Short context-sensitive half-time after termination of – Hydromorphone is rapidly titratable (like
infusion with predictable offset in ~5-10 minutes fentanyl) with prolonged analgesia (like morphine)
Anesthesia and monitoring equipment. Monitoring during anesthesia
The Anesthetic Machine
The purpose of the anesthetic machine is to deliver gases to the patient in precise, known
concentrations. Although the anesthetic machine has evolved substantially over the years, the essential
features have remained remarkably constant. Some of the important components of a modern anesthetic
machine are depicted in the figure below.
Gases (oxygen, air and nitrous oxide) come from pipelines entering the operating room through the
wall. Tanks on the back of the anesthetic machine provide an alternate source of those gases should the wall
supply fail. Although 100% oxygen can be delivered to the patient, usually a mixture of oxygen (with air or
nitrous oxide) is selected. The relative concentrations of the gases to be delivered are controlled by
flowmeters (one flowmeter for each gas) found on the left hand side
Main components of of the anesthetic machine. The anesthetic machine also allows the
anesthesia machine are: delivery of a precise concentration of volatile agent. The volatile
Anesthesia circuit
Gase sourse
anesthetic gases, such as sevoflurane and desflurane, are contained in
Flowmeters liquid form in the vaporizers mounted on the machine. The gas
Vaporizer, mixture from the flowmeters flows through the vaporizer and the
Ventilator volatile anesthetic agent is added to the mixture in gaseous form. The
concentration of the volatile gas in the final mixture is determined by
a dial on or near the vaporizer. For safety reasons, only one volatile agent can be delivered at a time. The
ventilator allows positive pressure ventilation of the anesthetized patient. The ventilator can be set to deliver a
specific tidal volume (in which case pressure varies according to lung compliance) or to achieve a certain
peak inspiratory pressure (in which case volume varies according to lung compliance). The ventilator moves
the gas mixture through the common gas outlet and into the anesthetic circuit, the tubing that connects to the
patient‟s airway.
There are different types of anesthesia circuits (AC). A simple categorization of AC is conditionally
based on the way the inhalation (open type circuits) or exhalation
Advantages of a Circle System:
(closed type circuits) is performed and includes following AC
Conservation of gases
versions: (1) Open; (2) Semi-open; (3) Semi-closed and (4) Closed
Conservation of heat
(or Circle System). The gases exhaled by the patient can be partially
Conservation of moisture
(Semi-closed Circuit) or totally (Closed Circuit or Circle System) re-
Minimal operating room
pollution
inhaled by the patient. For these circuits an increase in CO2 can be a
problem.

The vast majority of general anesthetics today are delivered through a circle system. The circle
circuit has a CO2 absorber, a canister containing a hydroxide mixture (soda lime) that absorbs CO2. The
absorption of CO2 allows the expired gas to be recycled, thus minimizing the excessive cost and pollution
that would otherwise result. There are several other types of circuits which are useful in specific clinical
situations or are of historical interest. For more details on AC:
http://www.anesthesia2000.com/physics/Chemistry_Physics/physics14.htm

The origin and pathways of gas flow that applies to most anesthetic machines is depicted in schematic
form below. It is imperative that all anesthesia equipment undergo regular checks and maintenance. It is the
responsibility of the anesthesiologist to ensure that the equipment is in functioning condition prior to the
administration of every anesthetic. The pre-operative checklist can be found on every anesthetic machine.
Figure. Anesthesia machine (general view and conceptual scheme)

Monitoring the anesthetized patient

Provides information that improves the safety of anesthesia and provides a means to asses physiological
functions during anesthesia. Monitoring during anesthesia will include:
Presence of an Anesthetist
Heart Rate (q 5 min)
Blood Pressure (non-invasive vs invasive)
ECG (continuous – the 2nd lead is recommended because better reveal P wave)
Ventilation (observing the respiratory bag; auscultation; Capnometry/End Tidal CO2)
Disconnect Monitors (pressure alarms)
Oxygen analyzer (inspired oxygen concentration)
Pulse-Oxymeter
Electroencephalogram, intracranial pressure, evoked potentials
Temperature
Urine output
Other (Cardiac output, Central venous pressure (CVP), PCWP, etc.)

Capnography – measures exhaled CO2 Capnometry:

Is a method for measuring CO2

concentration in the exhaled air
It’s use is mandatory during low-
flow anesthesia
Graphical recording is defined as
capnography
Can be used for early detection of
CO2 reinhalation
Is a method of confirmation of
proper endotracheal tube
placement
Local anesthetics: mechanism of action. Differential blockade

Local anesthetics(LA): classification and clinical characteristics

Local anaesthetic drugs can reversibly block the nerve conduction and produce loss of sensation. The first LA
used in medical practice was cocaine. LA can be classified in to amides or esters depending upon the
chemical link between the amino and aromatic chain.

Esters Amides
Contain ester linkage. They are hydrolysed Contain amide linkage. They are
in the body by plasma esterases. They are metabolised by amidases in liver.
more likely to produce hypersensitivity Hypersensitivity reaction to amides are
reaction very rare.
Examples: Examples:
Cocaine, Lidocaine
Procaine Lignocaine,
Amethocaine Prilocaine,
Tetracaine Bupivacaine
Benzocaine Ropivacaine.

Local Anesthetics (LA) Clinical Usage

- Provide anesthesia and analgesia by Provide anesthesia and analgesia
disrupting the conduction of impulses throughseveral routes of delivery
along nerve fibers Topical
- LAs block voltage-gated sodium channels Infiltration
– Reversibly bind intracellular alpha IV
subunit Epidural
– Inhibit the influx of sodium, thus Intrathecal (Spinal)
preventing an action potential from being Perineural (Regional)
reached
-LAs are less effective in inflammation Differential Block : Small diameter (A delta)
because of impaired dissociation and and myelinated nerves are most susceptible,
delayed penetration trough cellular thus sensory loss precedes motor weakness
membrane

Effects of Epinephrine Added to the Factors influencing LA tissue uptake

LA Solution: (absorbtion):
Prolongs duration of anesthesia Anesthetic concentration
Reduces systemic absorbtion Tissue blood flow (vascularisation)
Increases intencity of blockade LA Tissue solubility
Reduces surgical bleeding
Signals intravascular injection
Decreases the latency to onset of
anesthesia
 LA Toxicity
- CNS toxicity
• Local anesthetics readily cross the blood brain
barrier
• Clinical manifestations: Lightheadedness,
tinnitus, tongue numbness > CNS depression,
seizure > coma
- Cardiovascular toxicity
• Dose dependent blockade of Na channels >
disruptions of cardiac conduction system >
bradycardia, ventricular dysrhythmias, decreased
contractility, cardiovascular collapse/ circulatory
arrest
• Bupivacaine especially has severe CV side
effects
• Approximately 3x the amount of local
anesthetics are required to produce
cardiovascular toxicity than CNS toxicity
• Addition of Epinephrine allows for early
detection of intravascular injection and also
increases the max allowable dose
Treatment of LA toxicity
- Initial management:
– Stop local anesthetic
– Give benzodiazepines for seizure, avoid
propofol when there are signs of CV instability.
– Begin ACLS: CPR, securing airway.
– Reducing individual epinephrine doses to <1
mcg/kg.
AVOID: vasopressin, Ca channel blockers, Beta
blockers, and local anesthetics
• Initiate early intralipid (IL) therapy
– Bolus IL 20% 1.5 ml/kg, followed by infusion
of 0.25 ml/kg/min
– May repeat loading doses (max 3 total doses)
– May increase infusion rate to 0.5 ml/kg/min if
BP is still low. Not to exceed 10 ml/kg in the
first 30 mins.
– Consider early initiation of cardiopulmonary
bypass

LA Drug Formulary

Drug Concen- Clinical Maximum Potency Toxicity Onset Duration

tration Uses Dose (mg) (units)** (units)** Latency of action
(%) (minutes) (hours)
Infiltration 180 –
Procaine 0,25 – 0,5 PNB 600- 1 1 8-15 0,5 – 1,5*
(Novocaine) Epidural 1400*
Spinal
Topical
Lidocaine 0,25 - 5 Infiltration 100 – 3-5 1,5 5 - 10 0.5 - 4
PNB 600*
Epidural
Spinal
Infiltration
Ropivacaine 0,75 - 1 PNB 200 - 300 6-7 1 10 - 20 2 - 10
Epidural
Infiltration
Bupivacaine 0.25 – PNB 25 – 200* 7-8 2 5 - 20 2-9
0,75 Epidural
Spinal
Levobupivacaine 0,25 – 0,5 Epidural 25 - 150 7 2 15 - 20 3-9
Spinal
Infiltration
Mepivacaine 0,25 - 4 Epidural 100–600* 3 -5 1 – 1,5 5 - 10 1 – 1,5
Spinal
*- with Epinephrine 1:200000; **- compared with Procaine = 1 unit; PNB – peripheral nerve block

Local/Regional Anesthesia
Regional anesthesia involves the introduction of drugs (LA) with the intention of blocking the nerve
supply to a specific part of the body such as a limb. In most cases it provides safer alternative to
general anesthesia as well as prolonged postoperative analgesia. Regional anesthesia is achieved by
using local anesthetic drugs that block nerve conduction.
Types of Local/Regional Anaesthesia

A. Central Neural Blocks

Spinal anesthesia
Epidural anesthesia
B. Peripheral Nerve Blocks (sciatic nerve, brachial plexus, etc)
C. Intravenous Regional Anesthesia (IVRA)
D. Topical and Infiltration anesthesia
E. Others: Intrapleural analgesia, ophthalmic anesthesia

Advantages/Benefits of Local/Regional Anesthesia

Conscious patient - able to warn of adverse effects (during carotid surgery, and trans-urethral
resection of prostate), less interruption of oral intake.
Avoidance of adverse effects of general anesthesia like nausea, vomiting, sore throat and
hang over.
Minimal interference with respiratory function when appropriate regional technique is
chosen and reduced interference with hemodynamic function
Avoids hazards of unconsciousness like aspiration of gastric contents, anatomical damage to
skin, joints, nerves etc.
Better postoperative pain relief (extended block), decreased narcotic use, faster recovery and
discharge (e.g. in one day surgery)
Reduced blood loss particularly with pelvic and hip surgery.
Decreased incidence of pneumonia and deep vein thrombosis

Disadvantages of Local/Regional Anesthesia

Requires a skilled operator to insert
Not always effective
Risk of intravascular injection (LA systemic toxicity)
Difficult to cover multiple sites of pain
Risk of infection from infusion catheter

Correct needle placement/site of injection during Local/Regional Anesthesia can be

confirmed by various techniques:
Ultrasound
Paresthesia technique
Use of peripheral nerve stimulator

Technics for Local/Regional anesthesia

Local Anesthesia
Local anesthesia refers to the infiltration of a local anesthetic agent at the surgical site and is usually
performed by the surgeon. This technique is appropriate for superficial procedures such as dental surgery,
breast biopsy or carpal tunnel release. Local anesthesia may be used in an unmonitored setting. However,
often it is used in combination with sedation in which case monitoring is required. While local anesthesia is
inadequate for more invasive procedures such as those involving the body cavities, local infiltration is often
used as an adjunct in post-operative pain management. Care must be taken to avoid intravascular injection
and to avoid exceeding the toxic dose of the local anesthetic in use.

Regional Anesthesia
Regional anesthesia involves the blockade (with local anesthetics) of the nerve supply to the surgical
site. This may be achieved by blocking peripheral nerves (e.g. ankle block) or by blocking the spinal cord
and/or nerve roots (spinal, epidural block). A single nerve block may be sufficient (e.g. ulnar nerve block for
repair of 5th digit) or a group of nerves may need to be blocked (e.g. brachial plexus block for forearm
fasciotomy).
While regional techniques are perceived to be “safer” than general anesthesia, they do carry risks of
their own. The most serious “early” complication of a peripheral nerve block is local anesthetic toxicity. The
most worrisome “late” complication is neuropraxis or nerve injury. The central neuraxial blocks have many
potential complications, both early and late, which will be discussed in the next section.
There are some patients in whom a regional technique offers at least short term benefits over general
anesthesia. For example, in those undergoing total hip arthroplasty, the use of spinal or epidural anesthesia is
associated with less intra-operative blood loss, less postoperative hypoxemia and a lower risk of post-
operative deep venous thrombosis formation. While it seems intuitive that physiologic homeostasis is more
readily achieved when regional anesthesia is employed, the anesthesiologist must always remain vigilant.
Principles of pre-operative assessment and preparation must be applied just as vigilantly to the patient
undergoing regional anesthesia.
Many different types of surgical procedures can be performed while the nerves that supply the
surgical site are rendered insensate. This method is called “neural blockade” or “nerve block”. Various
techniques of neural blockade comprise what is known as regional anesthesia. During regional anesthesia, the
anesthesiologist must not only monitor and manage the patient‟s physiologic status but must also ensure that
the patient remains calm and cooperative. The anesthesiologist must be alert to the development of
complications and must also be prepared to convert to a general anesthetic at any point in the procedure.
The main tissues layers a needle passes while performing Epidural/Spinal anesthesia as well as
locations of Epidural and Spinal Spaces are presented in the following scheme:

EPIDURAL ANESTHESIA

CSF
Skin Subcutan. Spraspinous Interspinous Ligamentum Epidural Dura Arachniod Subarch. Pia
Ligament Ligament Flavum space Mater Mater Space Mater

SPINAL ANESTHESIA

Contraindications to Local/Regional Anesthesia

A) Absolute: Patient refusal, anesthetist‟s inexperience and localised infection at the site
B) Relative: Abnormal anatomy or deformity, coagulation disorders, neurological disease

Complications of Local/Regional Anesthesia

1. Technical: failure of the technique, direct trauma to nerves and blood vessels (bleeding and
hematoma), pneumothorax with intercostal and intrapleural block.
2. Excessive local anesthetic volume can result in total spinal during epidural and phrenic nerve
block during brachial plexus block.
3. Those related to specific technique: Hypotension, bradycardia and headache following spinal or
epidural analgesia. Rare possibility of nerve injury with peripheral nerve blocks.
4. Drug related: Local anesthetic toxicity due to intravascular injection or systemic absorption,
overdose of local anesthetic, anaphylactoid reaction and methaemoglobinaemia (prilocaine)

Epidural anesthesia (EA)

Epidural and spinal anesthesia can be used for procedures involving the abdomen, perineum or lower
extremities. The two blocks differ by virtue of the anatomic space into which local anesthetic (LA) is
delivered. Understanding the anatomy of the region (see figure ) is crucial to understanding the blocks.
The most important landmark for performance of lumbar EA (and Spinal) are the vertebral spinal
processes (define the midline) and the iliac crests (a line drawn between the crests – Tuffier line – crosses
L4), which identify the spaces selected for insertion of the epidural or spinal needle. In epidural anesthesia, a
tiny plastic catheter is placed through the needle into the epidural space, which is the anatomic space located
just superficial to the dura. An epidural catheter can be placed at any point along the spinal column. Epidural
catheters placed for surgical anesthesia or analgesia are most commonly used at the thoracic or lumbar
regions depending on the site of the surgery.
A LA solution is delivered through the catheter. LA blocks the spinal nerves roots. From the epidural
space, it is slowly absorbed into the subarachnoid space. The volume of anesthetic delivered and the site of
the catheter determine the level or “height” of the block. The presence of an indwelling catheter allows the
block to be extended in height or duration as required. Insertion of an epidural catheter is done in a strictly
sterile fashion. After local infiltration, a specially designed 17 or 18 gauge epidural needle (common trade
names Tuohy®) is inserted into the spinous interspace. A special
syringe, filled with air or saline is attached to the hub of the needle.
While advancing the needle, the anesthesiologist maintains pressure
on the syringe in order to sense
In Epidural Anesthesia the
the resistance of the tissue
local anesthetic, an opioid
being traversed. The epidural
and sometime a
space is a “potential space”
vasodilator is injected in
such that when it is entered
the epidural space which is
with the needle, a sudden loss about 4-8 mm large at L2-4
of resistance is detected. The level and acts here on the
syringe is then removed so that roots of spinal nerves.
a catheter can be threaded
through the needle into the epidural space (see figure), after which
the needle is removed. Once the catheter is in place, the
anesthesiologist “tests” the catheter to ensure that neither blood nor

Figure . 5 Anatomical landmarks

cerebral spinal fluid (CSF) can be aspirated. While delivering LA
in small (3 ml) aliquots, the anesthesiologist observes for
for Spinal/Epidural anesthesia
symptoms or signs of incorrect catheter placement.
If the catheter is situated in one of the veins of the epidural plexus then the patient may experience
symptoms of local anesthetic toxicity: tinnitus, perioral numbness, metallic taste in the mouth and
dizziness, psychomotor agitation, seizures, cardiac and respiratory arrest. Allergic reaction is also a
possibility. If the catheter is situated in the intrathecal space, then the patient will develop a sensory/motor
block rapidly after the administration of only a small amount of LA.
In the absence of any signs or symptoms of incorrect catheter placement, the full dose of LA is
delivered over 10-20 minutes. Some LA‟s, such as lidocaine, have a relatively rapid onset of effect but also
have a relatively shorter duration of action. Bupivacaine, while possessing a slower onset of effect, has a
longer duration of action.
Complications of Epidural Anesthesia

Complication Incidence (%) Management

Dural puncture 0.16 – 1.3 Bed rest, analgesia, hydration, blood
patch
Headache 16 -86 Bed rest, analgesia, hydration,
suspect dural pucture
Nereve or Spinal Cord Injury 0.016 – 0.56 Immediate neurological assessment
Catheter migration 0.15 – 0.18 Remove catheter and re-site if
appropriate
Epidural Hematoma 0.0004 – 0.03 MRI or CT, immediate neurological
Epidural Abscess 0.01 – 0.05 assessment, antibiotics
Respiratory Depression 0.13 – 0.4 Decrease in opioid concentration
may be required
Hypotension 3 - 30 I/V fluids + vasopressors,
temporarely reduce or stop infusion
Pruritus 10 Naloxone I/V + antihistamine
Urinary Retension 10-30 (in male) Catheterisation
Motor Block 3 Check for catheter migration,
temporarely cease infusion

Spinal anesthesia (SA)

Spinal anesthesia involves the blockade of the nerves of the spinal cord and cauda equina by injection
of LA into the intrathecal space. The important anatomy is depicted in figure above. Because the LA is
injected in close proximity to its site of action, much smaller volumes are required (1-3 ml) and the onset of
effect (within 5 minutes) is rapid relative to epidural anesthesia. The choice of LA used is based primarily on
the anticipated length of procedure. Spinal lidocaine provides surgical anesthesia for procedures lasting up to
75 minutes however its use has been limited by the associated increased incidence of postoperative
radiculopathies. A similar duration of action shows mepivacaine. Spinal bupivacaine will provide up to 3.5
hours of anesthesia and is considered to be safe. The addition of opioids (e.g. fentanyl) to the local anesthetic
solution can extend the duration of block.
However, if the block dissipates prior to the end of the procedure there is no way to extend the block
at that point. Spinal anesthesia is performed under strict asepsis. The patient may be sitting or curled in the
lateral position. A special small-bore “spinal needle” is used (22-27 gauge). The needle is inserted at a lower
lumber interspace and is advanced through the dura. Because the dura is a tough membrane, a definite “pop”
is often felt as the needle passes through into the intrathecal space. The stylet of the needle is removed and
cerebrospinal fluid (CSF) is observed in the lumen of the needle. The local anesthetic is then injected and the
needle removed.
The height of the required block depends on the surgical procedure. The height of the block achieved
is determined by many factors including the mass and volume of LA administered, the position of the patient
and the baricity or “heaviness” of the LA relative to CSF. The complications of spinal anesthesia are similar
to those of epidural anesthesia with a few exceptions. Because of the small dose of LA required, LA toxicity
is not an issue even if intravascular injection occurs. Dural puncture is required for spinal anesthesia therefore
“spinal headache” is always a risk, especially in young adult patients. The use of needles which are smaller-
bore and have a “pencil-point” tip helps to decrease the incidence of post-dural puncture headache.
For some procedures, the anaesthetist may choose to combine the rapid onset and reliable, dense
block of a spinal anesthetic with the post-operative analgesic effects of an epidural. This is called combined
spinal and epidural anaesthesia (CSE).
 The contraindications to SA are similar to the ones listed under Local/Genereal Anesthesia and
include:
Patient refusal
Infections of the skin at the puncture site
Hypovolemia
Coagulation abnormalities

https://epratama.files.wordpress.com/2008/12/lecture-note-clinical-anaesthesia.pdf

https://www.mededcoventry.com/Specialties/Anaesthetics/Handbook/

https://www.ucl.ac.uk/anaesthesia/StudentsandTrainees/Year4PerioperativeWorkbookv13