ANESTHESIA NOTES

LEVEL VI MBCHB
2019
COMPILED BY NAILA KAMADI
 OUTLINE
Introduction to anesthesiology & pharmacology of anesthesia – 4

Local anesthetics – 20

Inhalational anesthetics – 77

Intravenous anesthetics – 127

Muscle relaxants – 169

Analgesics – 180
 Outline
Preoperative assessment & preparation – 214
Anesthetic & critical care monitoring records – 241
Basic principles of mechanical ventilation – 275
Cardiopulmonary & cerebral resuscitation – 305
Clinical scenarios in shock management – 331
Post – operative care – 377
Specialized techniques in anesthesia & critical care – 409
Tutorial notes – 461
1. INTRODUCTION
18/1/2019
BY: DR. NABULINDO M. SUSANE
PEDIATRIC ANESTHESIOLOGIST
DEPARTMENT OF ANESTHESIA UON
 Definition
• Anesthesia is the reversible drug – induced
loss of sensation to perform medical and
surgical procedures
• Types:
• General anesthesia: loss of consciousness
• Regional anesthesia: limited to a specific
part of the body with no loss of
consciousness.
 History
• Genesis 2:18 – 25
• So the Lord God caused the man to fall into a
deep sleep…
• 400 – 300BC: Egyptian surgeons half –
asphyxiated children undergoing circumcision by
first almost strangling them
• Physical restraint
• 1846: start of the era of modern anesthesia. 1st
delivery of ether.
 Aims/ components of
anesthesia
1. Loss of consciousness
2. Amnesia
3. Muscle relaxation
4. Analgesia
 Anesthesia practice
• Patient safety
• Safety aspects: anesthesia personnel (personal
environment), equipment & drugs, monitoring
• In anesthesia, there is immediacy of drug
results e.g. over – administration of Propofol
will result in cardiac arrest. This informs the
emphasis on patient safety.
• Adequate and appropriate planning & vigilance
is very important in anesthesia.
 Scope of cover
• Medical management of anesthetized
patients
• Protection of life & vital organ function
• Acute & chronic pain relief
• Cardiopulmonary & cerebral resuscitation
• Pulmonary & special medical care unit
• Critical patient transfer
 Equipment
• Basic airway management
• Anesthesia delivery systems
• Physiological monitors
• Anesthesiologist’s presence &
mindset
 Drugs & medication
• Array of pharmacological agents
• Interactions and adverse outcomes
with patients medical condition or
concurrent therapy
• Understanding the potential for
harm
 Anesthesia entry points
• Physician anesthesiologist
• Registered Clinical Officer (RCO)
• Certified registered Nurse
 Involves team work
• Anesthetic assistants
• All medical specialties
• Residents & MOs
• Nurses
• Physiotherapists
• Nutritionists
• Laboratory/ radiology
 Interest
• Sophisticated technology (physics)
• Scientific challenges
• ? Lifestyle
• ? Income
 Career
• Challenging under pressure
• Life threatening interventions
• Limit of care
• Detail
 Risks
• Ethics
• Medico – legal issues
• Addiction & drug abuse
 Level VI Emphasis
• Vascular access
• Airway management
• Medical diseases & anesthesia
• Pre – op assessment & post – op care
• Principles of resuscitation
• Pain management
 Level VI anesthesia
academic profile
• Clinical attachment evaluation
• Log entry
• Core tutorials
• Lectures
 Examination
• CAT
• Exit examination input
• Mentorship
2. PHARMACOLOGY OF
LOCAL ANESTHETIC
AGENTS
15th/2/2019
BY: DR. OLUROTIMI AARON
PEDIATRIC ANESTHESIA FELLOW, UON
 Objectives
• Recall how an action potential is generated
& propagated.
• Classify local anesthetics (LAs).
• Describe mechanisms of action,
pharmacokinetics & toxic effects of LAs.
• Describe the clinical applications of LAs &
use of adjuvants.
 Outline
• Introduction
• Chemistry
• Pharmacokinetics (PKs)
• Pharmacodynamics (PDs)
• Clinical applications:
• Neuraxial blocks: spinal & epidural
• Bier’s block/ Intravenous Regional Neural Anesthesia
• Peripheral blocks
• Conclusion
 Introduction
• LA drugs are used widely for the provision of anesthesia &
analgesia both intra – & post – operatively.
• Understanding the pharmacology of these agents as a group
as well as the differences between specific drugs, enables
the anesthetist to use them safely to maximum effect.
• When applied near the axons, LA drugs cause reversible &
complete blockade of neuronal transmission.
• There are a variety of formulations as well as, routes &
methods of administration. They can cause severe systemic
toxicity if used inappropriately.
 The benefits of LA
techniques include:
•Quick recovery.
•↓ complications.
•Early feeding.
•Short hospital stay.
 What are LA anesthetics?
• These are agents that produce a transient &
reversible loss of sensation to pain (analgesia)
in a specific/ circumscribed region of the
body without the loss of consciousness.
• This is accomplished by disruption of
afferent neural traffic via inhibition of
impulse generation or propagation.
• Normally, the process is predictable &
completely reversible.
• Recovery is normally spontaneous, predictable,
& without residual effects.
 History
Agent Discoverer Year
Cocaine, the
Cocaine Niemann 1860
first of such
Benzocaine Salkowski 1895 agents, isolated
Procaine Einhorn 1904 by Niemann in
Dibucaine Meischer 1925 1860 &
introduced into
Tetracaine Eisler 1928
clinical use by
Lidocaine Lofgren 1943 Koller in 1884
Chloroprocaine Marks, Rubin 1949 as an
Mepivacaine Ekenstam 1956 ophthalmic
anaesthetic.
Bupivacaine Ekenstam 1957
Ropivacaine Sandberg 1989
 Structure of an LA agent
• Most local anesthetic agents
consist of a lipophilic group
(e.g., an aromatic ring) connected
by an intermediate chain via
an ester or amide to an
ionizable/ hydrophilic group
(e.g., a tertiary amine)
Cont.
 Chemistry of LAs
• They are weak bases (pKa = 8 –
9) with 3 structural parts:
1. Hydrophilic end: amine
2. Lipophilic end: aromatic
group
3. An amino ester or amino
amide bond
Cont.
 Cont.
•The intermediate bond is
the basis of classifying LAs
into:
1. Amino esters
2. Amino amides
 Amino Esters
• They include: cocaine, procaine (Novocain),
chloroprocaine, tetracaine (pontocaine), benzocaine
• Amino esters have only one [i] in their names.
• They are metabolized by plasma esterases/
pseudocholinesterases & hence have a shorter half life.
• MC used as topical agents in ophthalmic surgery.
• They carry a higher risk of anaphylactic reactions
due to PABA, a metabolite of procaine & benzocaine.
 Amino Amides
• They include: lidocaine/ lignocaine/ xylocaine,
bupivacaine/ Marcaine, levobupivacaine/
chirocaine, ropivacaine/ naropin,
mepivacaine/ carbocaine/ isocaine,
dibucaine, prilocaine, articaine, etidocaine.
• These are more stable as they are metabolized in
the liver.
• They carry a lesser risk of allergic reaction.
 LAs in common use
LA MW pKa Protein Binding
ESTERS
Tetracaine 264 8.4 80%
Chloroprocaine 271 9.1 0%
AMIDES
Lignocaine 234 7.8 65%
Bupivacaine 288 8.1 95%
Ropivacaine 274 8.1 94%
Levobupivacaine 288 8.1 95%
 Chemistry
• LAs are weak bases. The pKa of most is in the range
8 – 9.
• The cationic form is the most active. The
uncharged form is important for rapid penetration
of biologic membranes.
• Most LA agents consist of a lipophilic group
(aromatic ring), an intermediate chain (an amide or
an ester) & an ionizable amine group.
• Optimal activity requires a delicate balance between
the lipophilic and hydrophilic ends.
• LAs are usually less effective in infected tissue.
 Pharmacology/
characteristics of LA
1
Speed of onset: PKa α
Speed of onset of action

Potency: Lipid solubility 𝛼 Potency

Duration of action: Protein binding 𝛼 Duration of Action

 Cont.
1. PKa correlates with onset of action: LAs with PKa closer to
tissue pH e.g. lidocaine (pH 7.74) have a faster onset of action
since the LA exists in its non – ionized form & ∴ it crosses
biological membranes faster.
2. Lipid solubility correlates with potency: The higher the lipid
solubility, the more potent the LA e.g. bupivacaine, etidocaine,
tetracaine are potent LAs.
3. Protein binding correlates with DoA: the higher the protein
binding the longer the duration of action of the agent.
• Bupivacaine has 95% protein binding & it is a long – acting
amino amide LA; Lidocaine has 65% protein binding & it is a
medium acting amino amide LA.
 Systemic absorption of LA depends on
blood flow which is determined by:
• Site of injection
• Presence of vasoconstrictors:
epinephrine, phenylephrine
• LA agent: more lipid soluble agents that
are highly tissue bound are also more
slowly absorbed.
 Distribution depends on organ
uptake which is determined by:
• Tissue perfusion
• Tissue/ blood partition coefficient
• Tissue mass: muscle provides the greatest
reservoir for distribution of LA agents.
 Metabolism and excretion:
Ester – type LAs
• Ester type LA are hydrolyzed rapidly in the blood
by pseudocholinesterase. Individuals with
atypical pseudocholinesterase may exhibit
features of toxicities to ester type LAs.
• Termination of action of intrathecally injected
esters e.g. tetracaine depends on their
redistribution into blood stream as CSF doesn’t
have esterases.
• In contrast to other esters, cocaine is partially
metabolized (N – methylation & ester hydrolysis)
in the liver & partially excreted unchanged in
the urine.
 Amide – type LAs
• The amide linkage of the amide LAs is
metabolized (N – dealkylation & hydroxylation) by
microsomal enzymes in the liver. Rate of amide
metabolism depends on the specific agent
(prilocaine>lidocaine>mepivacaine>ropivacaine>b
upivacaine).
• Toxicity of the amide type LA is more likely in
patients with liver disease & in those with ↓
hepatic blood flow (CCF, 𝛽 – blockers or H2RA)
 Cont.
• Prilocaine is the only LA metabolized to
O – toluidine which produces
methaemoglobinemia in a dose –
dependent fashion. Benzocaine can also
cause dangerous levels of
methaemoglobinemia.
• Rx: IV Methylene blue 1 – 2mg/kg of a
1% solution over 5 minutes.
 Mechanism of action
• The excitable membrane of axons maintains
a transmembrane potential of 90 to -60mV.
• During excitation, there is depolarization
leading to the opening of Na+ channels.
• Repolarization is mediated by the exit of K+
from the cell.
• LA bind to receptors near the intracellular
end of Na+ channel.
 Cont.
• The smaller & the more lipophilic the molecule the
faster the rate of interaction with the Na+ channel
receptor. Potency is thus, positively correlated
with lipid solubility , i.e., Potency ∝ lipid
solubility
• Nerve fibers differ in their sensitivity to LA
blockade on the basis of size & myelination:
• Small nerve fibers are more sensitive than large
nerve fibers, whereas, myelinated fibers are
blocked before the non – myelinated ones.
Myelination
• Sensitivity to LA blockade ∝
Size of nerve fiber
Cont.
 Cont.
• LAs act by reversibly blocking
the fast voltage gated Na +
ion channels in axons hence
hindering the initiation &
propagation of action potentials.
• This manifests as a blockage of
sensory & motor function.
Cont.
 Sequence of clinical
anesthesia
• Sympathetic block (vasodilation).
• Loss of pain & temperature
sensation.
• Loss of proprioception.
• Loss of touch & pressure sensation.
• Loss of motor function.
 Cont.
LA pKa Onset Duration (+ Epi.) Max Dose (+ Epi.)
Procaine 9.1 Slow 45 – 90 mins. 8mg/kg – 10mg/kg
Lidocaine 7.9 Rapid 120 – 240 mins. 4.5mg/kg – 7mg/kg
Bupivacaine 8.1 Slow 4 hours – 8 hours 2.5mg/kg – 3mg/kg
6 – 10
min
Prilocaine 7.9 Medium 90 – 360 mins. 5mg/kg – 7.5mg/kg
 LA techniques
• Infiltration anesthesia: injection into the vicinity of
peripheral nerve endings.
• Regional anesthesia
• Intravenous Regional Anesthesia (IVRA/ Bier
block)  commonly 40mL of 0.5% prilocaine is used
for manipulation of Colles’ fracture. Also 0.25 – 0.5%
plain lidocaine (max. 3mg/kg) can be used.
• Intrathecal block/ spinal anesthesia
• Epidural
 Cont.
• Truncal blocks: Transversus
Abdominis Plane (TAP) block
• Peripheral nerve block
(usually done under U/S
guidance)
• Plexus: brachial, lumbar
• Individual or group of nerves
 Cont.
• Surface anesthesia/ topical: on intact skin e.g.
EMLA (eutectic mixture of local anesthetic)
cream which contains a 1:1 mixture of 5%
lidocaine & 5% prilocaine bases in an oil – in –
water emulsion.
• Dermal analgesia sufficient for beginning an IV
line requires contact time of at least 1h under
an occlusive dressing. Usual depth of
penetration is 3 – 5mm & DoA is 1 – 2h.
• Applications: STSG harvesting, laser removal
of portwine stains, lithotripsy & circumcision
• S/Es: skin blanching, erythema, edema
 Lidocaine
• Also a Class IB antiarrhythmic.
• Relatively rapid onset of action
• Intermediate duration
• Combination with a longer – acting agent such as
bupivacaine may produce a balance of onset & duration
between the 2 component agents alone.
• Cardiotoxic potential at equivalent levels of central
1
nervous toxicity is about that of bupivacaine.
9
 Bupivacaine
• Long – acting
• Slow onset of action
• Prone to causing myocardial depression with
slow & difficult reversal
• Due to high affinity for cardiac proteins
• Contraindicated for IV regional anaesthesia
(Bier’s block).
• Strictly observe the dosing limits.
 Adjuvants used in LA techniques:
Adrenaline/ epinephrine
• This is a vasoconstrictor that ↓ vascularity
of the area.
• Effects:
• ↓ systemic absorption of the drug.
• ↑ duration of nerve blockade.
• Greater margin of safety for systemic
toxicity.
• ↓ surgical bleeding.
 Cont.
• Epinephrine – containing solutions should not
be injected in the proximity of end – arteries
such as the penile, ophthalmic (central artery of
the retina) or digital arteries since there is no
collateral circulation to supplement the supply if
vasoconstriction is severe.
• Hence it is CI in fingers, nose, phallus
• Epinephrine containing solutions are relevant for
local infiltration & peripheral nerve blocks.
 Cont.
• Bicarbonate: ↑ tissue pH → higher
proportion of non – ionized drug, which
diffuses into the neurone more rapidly 
speed of onset of anesthesia is ↑.
• Glucose: ↑ the baricity of the solution to >
than that of CSF. When administered along
with a spinal anesthetic this results in more
controlled spread of solution within the
intrathecal space.
 Cont.
• Hyaluronidase: facilitates the spread
through the connective tissues following
subcutaneous injection.
• Opioids (like fentanyl)  relevant in spinal
& epidural
• Clonidine, ketamine, dexmedetomidine,
neostigmine
• Adjuvants generally ↓ the standard dose of
LA required.
 Maximum doses of LA
Max. dose – Max. dose +
LA Epi. (mg/kg) Epi. (mg/kg)
Lidocaine 3 7
Bupivacaine 2 2

Ropivacaine 3 3
Prilocaine 6 —
 LA toxicity
• LAs may be toxic if sufficient
amounts are absorbed into the
systemic circulation.
• Clinical toxicity appears to relate to
the effects of the drug on other
excitable membranes in the CNS &
CVS.
 Cont.
• CNS effects:
• Tingling of lips & circumoral numbness (MC first sign)
• Slurred speech
• ↓ LOC
• Seizures
• Cardiac effects on a variety of ion channels may cause:
• Arrhythmias
• ↓ myocardial contractility
• Cardiac arrest
 Cont.
• Other clinical problems are more specific to
particular drugs.
• The incidence of allergy to PABA, a metabolite of
many esters has been mentioned.
• Prilocaine is metabolized to O – toluidine which
can cause methaemoglobinemia in susceptible
individuals
• Cocaine is inherently, a potent vasoconstrictor
& may cause problems in patients already on
vasoconstricting drugs such as monoamine
oxidase inhibitors, tricyclic antidepressants.
 Cont.
• Allergic reactions: True allergic reactions are
associated with amino – ester linked LAs.
• Tissue toxicity
• Primarily myotoxicity & neurotoxicity can
be produced by all LAs if high
concentrations are used
• E.g. transient neurologic symptoms, cauda
equina syndrome (CES)
 Cont.
• Systemic toxicity
• Methaemoglobinemia: prilocaine used in Bier’s
block treated by Evans blue
• Severe systemic LA toxicity: CVS & CNS toxicity
• Result from systemic absorption of LA
• Dependent on:
• Fraction of unbound drug within the plasma
• Peak plasma concentration
• Rate of ↑ of plasma concentration
• Plasma clearance
• Plasma pH
 Management of severe LA
toxicity

Recognition Definitive
Immediate
of signs of treatment (±
supportive Follow up
severe circulatory
management
toxicity arrest)
 1. Recognition of signs of
severe toxicity
• CNS manifestations: sudden alteration in mental
status (converse with the patient during
anesthetic administration to detect this as
soon as possible), severe agitation or LOC, ±
GTCs.
• Cardiovascular collapse: sinus bradycardia,
conduction blocks, asystole & ventricular
tachyarrhythmias may all occur
• LA toxicity may occur some time after an
initial injection.
 2. Immediate Supportive
Management
• Stop injecting the LA.
• Call for help
• Maintain the airway: positioning, oropharyngeal
airway, mask ventilation, intubation in that order
• Give 100% supplemental O2 & ensure adequate lung
ventilation
• Confirm or establish IV access
• Control seizures: give a BDZ, thiopental or propofol
in small incremental doses.
• Assess cardiovascular status throughout.
 3a. Definitive treatment
with circulatory arrest
• Start CPR using standard protocols.
• Manage arrhythmias
• Consider the use of cardiopulmonary bypass if
available
• Give IV lipid emulsion
• Continue CPR throughout treatment with lipid
emulsion.
• Note that recovery from LA – induced
cardiac arrest may take >1h so DO NOT
STOP CPR PREMATURELY.
 3b. Definitive treatment
without circulatory arrest
• Use conventional therapies to treat:
• Hypotension: vasoactive drugs e.g.
adrenaline
• Bradycardia: vagolytic drugs e.g. atropine
• Tachyarrhythmias: antiarrhythmics
• Lidocaine should not be used in this case.
• Consider IV lipid emulsion
 4. Follow up
• Arrange for safe transfer to a clinical
area with appropriate equipment and
suitable staff until sustained recovery is
achieved.
• Exclude pancreatitis by:
• Regular clinical review
• Daily amylase or lipase assays for 2
days
 Essential precautions
before administering LA
• Ensure there is a secure IV line & adequate
resuscitation equipment & medications.
• Use the lowest, effective dose of LA.
• Administer large volumes of the LA injection in divided
doses.
• Continuous monitoring of vital signs.
• Before each injection, aspirate through the needle or
catheter to ensure that it is not in the intravascular
compartment.
• Use an IV marker e.g. adrenaline when a high dose of LA
is to be given.
 Summary
• Safe use of LAs
• Choice of agent
• Dosing limits
• Essential precautions
• Toxicity
• Early recognition & management is
paramount.
 References
• Sullivan, P. Anaesthesia for Medical
Students
• Smith T, et el. Eds. Fundamentals of
Anaesthesia
• Morgan & Mikhail’s Clinical
Anesthesiology
3. PHARMACOLOGY OF
INHALATIONAL
ANESTHETICS
1st/2/2019
BY: DR. ANTHONY
GATHERU
 Classification
General
anesthetics

Inhaled Intravenous

Volatile
Barbiturates Dissociative Opioids BDZ
Gas: N2O liquids:
(Thiopental) (Ketamine) (Fentanyl) (Midazolam)
Halothane
 Volatile agents/ vapors
• Fluorinated hydrocarbons/
halogenated compounds:
Halothane, Isoflurane, Sevoflurane,
Desflurane, Enflurane
• Ethers: Diethyl ether, ethylene
• Others: chloroform, cyclopropane
 Mechanism of action
• Remains unknown.
• It appears that volatile agents preferentially
potentiate inhibitory GABAA receptors &
2 pore domain K+ channels.
• Anesthetic gases N2O & Xenon inhibit
excitatory channels. The most important
one is N – methyl – D – aspartate
channel.
 Inhalational anesthetic
agents are used in GA for:
• Induction: halothane; sevoflurane.
• Maintenance of anesthesia: isoflurane,
sevoflurane, halothane & desflurane  they
can be administered continuously.
• Carrier gas: N2O
• Analgesia: N2O esp. in dental procedures.
N2O is never used alone; it is usually
administered with O2 (Entonox).
 Pharmacokinetics:
Uptake of the inhalational anesthetic is
dependent on the following:
• Inspired concentration/ partial pressure:
• If the alveolar concentration (FA) is approaching
the inspired concentration of the anesthetic
agent (FI) induction of anesthesia will occur
faster.
• FA correlates directly with the partial pressure of
the inhaled anesthetic agent in the inspired gas
mixture. The ↑ the inspired partial pressure, the
↑ the rate of rise of FA & thus induction is
accelerated.
 Cont.
• Alveolar ventilation:
• An ↑ in alveolar ventilation causes an ↑ rate
FA
at which FA approaches FI, i.e. = 1. The
FI
magnitude of the effect depends on the
solubility of the agent in blood, i.e., blood:
gas partition coefficient.
• Hyperventilation ∴ ↑ the speed of induction
of anesthesia with agents that would
normally have a slow onset e.g. halothane.
 Cont.
• Blood solubility of the agent:
• When an anesthetic with low blood solubility diffuses from the
lung into the arterial blood, relatively few molecules are required
to raise its partial pressure in blood & ∴, the arterial tension rises
rapidly e.g. N2O, desflurane, sevoflurane. Such drugs have a
comparatively rapid onset of action.
• NB: desflurane is pungent & is a poor induction agent.
• Conversely, for anesthetics with moderate to high solubility e.g.
halothane, isoflurane, more molecules dissolve (i.e. it is taken
up faster into the blood stream) before partial pressure changes
significantly & arterial tension of the gas ↑ less rapidly. Such
agents have a medium rate of onset of action
 Cont.
• CO & hence alveolar blood flow:
• ↑ CO  ↑ alveolar blood flow  ↑ uptake of
FA
anesthetic into blood  ↓ rate at which =1↓
rate of induction of anesthesia. FI

• This is because an ↑ CO will also ↑ anesthetic

agent distribution into all tissues (not just the
CNS). Since cerebral blood flow is well auto –
regulated, ↑ CO will ultimately ↑ delivery of
anesthetic to other non – neural tissues.
• ↑ CO is seen in: hyperthyroidism, pregnancy etc.
 Cont.
• The difference in partial pressure
between alveolar gas & venous
blood.
• This depends on uptake of anesthetic
by tissues (including non – neural
ones). The greater the difference, the
more time it will take to achieve
equilibrium with brain tissue.
 Distribution depends on:
• Vessel rich group: organs receiving a
higher blood supply receive more drug
concentrations e.g. the kidney.
• Blood tissue solubility: agents that are
more lipid soluble distribute into the brain
faster & are more potent (Meyer – Overton
Theory).
Pharmacological properties of
inhaled anesthetic agents
 Biotransformation/ metabolism
• Modern inhaled anesthetics are eliminated mainly by
ventilation & are only metabolized to a very small
extent. A large fraction is excreted unchanged.
• Metabolism may have important implications for their
toxicity. E.g. halothane is eliminated more rapidly during
recovery than enflurane since more of halothane (>40%)
as compared to enflurane (<10%) is metabolized during an
average anesthetic procedure.
• Rank of order of hepatic metabolism is as follows:
• Halothane > enflurane > sevoflurane > isoflurane >
desflurane > N2O
• N2O is not metabolized by human tissues. Can be
broken down by GIT bacteria.
 Elimination
•Inhaled anesthetic
agents are mainly
eliminated in the lungs.
 Factors affecting rate of recovery
from inhalational anesthesia
• Blood: gas partition coefficient of agent: agents
that are relatively insoluble in blood & brain e.g.
N2O, desflurane, sevoflurane are eliminated/
washed out faster than the more soluble agents e.g.
halothane, isoflurane leading to a more rapid
recovery. Recovery from halothane – & isoflurane –
based anesthesia is predictably less rapid.
• Tissue solubility of agent
• Pulmonary blood flow
• Magnitude of ventilation: hyperventilation
speeds recovery
 Pharmacodynamics
• Mechanism of action: they produce
anesthesia by enhancing inhibitory
channels & attenuating excitatory
channels in the brain & spinal cord
• Effects:
• Relaxation of skeletal muscle
• Unconsciousness, amnesia, analgesia (only
N2O has this ability) & immobility
 CNS effects
• ↓ Cerebral Metabolic Rate (CMR) which ↓
cerebral blood flow.
• Volatile agents also cause cerebral VD; the net
effect on cerebral blood flow depends on
concentration of anesthetic delivered.
• Administration of high concentrations of volatile
anesthetics is undesirable in patients with
increased ICP.
• Hyperventilation  ↓ PaCO2  Cerebral VC
 CVS effects
• Halothane, Enflurane, Isoflurane, Desflurane & Sevoflurane all ↓
normal cardiac contractility (halothane & enflurane >
isoflurane, desflurane & sevoflurane. Hence they ↓ MAP in a
dose – dependent fashion.
• ↓ Systemic Vascular Resistance (SVR): seen with isoflurane,
sevoflurane & desflurane more. These preserve CO but ↓ preload
& afterload.
• N2O also depresses cardiac function but it is offset by
concomitant activation of the SNS.
• ↓ myocardial O2 consumption
• Coronary VD & improved myocardial oxygenation
• Sensitization to epinephrine.
 Guedel’s Signs of depth of anesthesia derived
from observations of the effects of inhaled
diethyl ether
• Stage I  analgesia: Initially, analgesia without
amnesia then amnesia develops later in stage I.
• Stage II  excitement: Patient appears delirious, may
vocalize but is completely amnesic. ↑ RR, HR, BP;
duration is shortened by rapidly ↑ concentration of agent.
• Stage III  Surgical anesthesia: Begins with ↓ RR, HR
& extends to complete apnea; there are 4 planes of stage
III based on changes in ocular movements, eye reflexes &
pupil size, indicating increasing depth of anesthesia
• Stage IV  Medullary depression: Represents severe
CNS depression including the vasomotor center in the
medulla & respiratory center in the brain stem. Without
circulatory and respiratory support, death rapidly ensues.
 Minimum Alveolar
Concentration (MAC)
• Anesthetic potency is currently defined
as the minimum alveolar concentration
of the anesthetic that prevents
movement in response to a standard
surgical stimulus (surgical skin incision)
in 50% of the subjects. It reflects the end
tidal concentration of the gases in the
alveoli.
 Cont.
• MAC mirrors brain partial pressure & it ∴
allows comparisons of potency between agents &
provides a standard for experimental evaluations.
• Remember gases move from a region of high
concentration to one of lower concentration.
Equilibrium occurs between the brain & the
alveolar concentrations of the agent.
• Anesthetic potency is described by the MAC
required to prevent a response to a surgical incision.
• LOC typically precedes the absence of stimulus –
induced movement.
 Factors which support the use
of MAC
• MAC is invariant with a variety of noxious
stimuli.
• Individual variability is small.
• Sex, height, weight & anesthetic duration do
not alter MAC. Doses of anesthetics in
MAC’s are additive.
• Note that MAC is non – linear
 Cont.
Characteristics Isoflurane Sevoflurane Desflurane N2O Xenon
Boiling Point 48 59 23 - 89 - 108
(0C)
B:G coefficient 1.4 0.68 0.4 0.47 0.12
at 370C
Oil: Gas 91 47 26 1.4 1.9
coefficient at
370C
MAC 1.15 2.0 6.0 104 71
Metabolism 0.2 5 0.02 0 0
 Cont.
• The less soluble an inhalational
anesthetic is e.g. N2O, desflurane
& sevoflurane, the faster the onset
& offset of action.
• In our set up, Sevoflurane is the
most available agent with the
fastest onset & offset of action.
 Factors that affect MAC values
• Factors that ↑ anesthetic requirements:
• Hypernatremia
• Hyperthermia
• Chronic ethanol consumption
• Sympathomimetics: Acute amphetamines,
ephedrine, cocaine
• Infants (highest MAC at 6 months)
• Genetics (red hair)
 Cont.
• Factors which ↓ anesthetic requirements:
• Hypoxia
• Hypercabia
• Hypothermia
• Metabolic acidosis
• Hyponatremia
• Sedative drugs
• ↑ age: there is a 6% ↓ in MAC per decade of age.
• Acute ethanol consumption
• Severe anemia (Hb < 5g/dL)
• Pregnancy
• Hypotension
 Nitrous Oxide
• This is a gas at ambient pressure & room
temperature.
• Colorless & odorless. Mostly an induction
agent as it does not have a pungent smell.
• Cheap
• Non – flammable but supports combustion
• MAC: 104%; metabolism: 0%.
 Cont.
• Relatively insoluble in blood.
• The only inhalational agent with analgesic
action.
• It has an ability to expand air filled spaces
e.g. it may worsen pneumothorax, intestinal
obstruction. It is contraindicated in middle –
ear surgeries.
• Elimination mainly by exhalation.
 Cont.
• The 2nd gas effect:
• Even though N2O is poorly soluble in blood,
large amounts are taken up from the
alveoli during induction because it is
administered in such large quantities (2 – 6
ml/min). As a result, the remaining gases
e.g. isoflurane, enflurane become more
concentrated in the alveoli & therefore
their uptake is enhanced..
 Effects
• N2O can ↑ cerebral blood flow & ↑ ICP by
activation of the sympathetic nervous
system.
 Halothane
• An alkane: halogenated ethane derivative.
• Doesn’t have an ether base unlike the
rest of the fluorinated hydrocarbons
• Non – flammable.
• Relatively non – pungent.
• Intermediate solubility in blood. Most
potent since it has the lowest MAC of 0.75.
 Cont.
• ↓ SVR, ↓ myocardial contractility & is
arrhythmogenic (esp. when using
catecholamines)
• It is oxidized by cytochrome P450
• Elimination is majorly via lungs to toxic
metabolite.
• Can cause immune mediated hepatitis
that may be lethal. It is avoided in developed
countries.
 Isoflurane
• Halogenated methyl ethyl ether. 2nd most potent of
the volatile anesthetics. Non – flammable liquid at
room temperature
• Has a pungent smell & irritates the airway. It is
avoided during induction when the reflexes are still
active but is used for maintenance.
• Has great physical stability
• More cardiostable than halothane
• Biotransformation happens to a smaller extent
• Main route of elimination is lungs
 Sevoflurane
• Fluorinated methyl isopropyl ether. Sweet smelling.
• Low blood: gas solubility hence LOC comes faster
• Rapid smooth induction & rapid recovery: agent of
choice for induction esp. in children
• Minimal effect on the CVS.
• Bio transformed by cytochrome enzymes to a small
extent; majorly eliminated unchanged through the
respiratory system.
• Compound A formation when exposed to soda lime.
It is nephrotoxic.
 Properties of the ideal
anesthetic agent
• Preparation
• Easily administered
• Chemically stable
• Long shelf life, compatible with other
components of the breathing circuit e.g.
soda lime, metals & plastics
• Non – flammable
• Cheap
 Cont.
• Pharmacokinetics
• Low blood/gas solubility: rapid
onset, rapid offset, adjustable depth
• Minimal metabolism: as substrates
are usually toxic; allows use in
patients with chronic kidney
disease
• Predictable in all age groups
 Cont.
• Pharmacodynamics
• High potency (allows high FiO2)
• High therapeutic index
• Analgesic e.g. N2O.
• Minimal side effects
 Physical properties
• Non – flammable, non – explosive at room
temperature (RTP)
• Stable in light
• Liquid & vaporizable at RTP i.e. low latent heat of
vaporization.
• Stable at RTP, with long shelf life
• Stable with soda lime as well as plastics and metals
• Environmentally friendly, no ozone depletion e.g.
Xenon
• Cheap (like N2O) and easy to manufacture
 Biological
• Pleasant to inhale (e.g. sevoflurane) non irritant
(unlike isoflurane), induces bronchodilation (e.g.
halothane)
• Low blood: gas solubility i.e. fast onset
• High oil: water solubility, high potency
• Minimal effects on other systems
• No biotransformation: should be excreted via the
lungs unchanged
• Non toxic to operating theater personnel
• Analgesic
 Monitoring depth of GA
• Individual variations in patient drug
requirements can lead to occasional over dosage
or under dosage with anesthetic agents
• Inadequate GA: signs develop in response to
stress or painful stimulus. Such signs include:
• Movement, ↑ RR or HR & ↑ BP, sweating
• Awareness & recall, though rare, can lead to
PTSD
 Cont.
• The EEG:
• The transition from a state of wakefulness to
a state of GA is accompanied changes in the
brain’s spontaneous electrical activity
recorded from electrodes placed on the scalp.
• The EEG reflects compound synaptic activity
of both excitatory and inhibitory synapses.
• Epileptic – like patterns may be seen with
sevoflurane & enflurane but frank clinical
seizure activity has been observed with
enflurane.
 Others
• Bispectral Index (BIS)
• Evoked potentials
• MAC (gold standard)
• Limb isolation
• Hemodynamic parameters
 Vaporizers
• Purpose: deliver reliable accurate & adjustable
concentration of anesthetic vapor.
• Oxygen & N2O act as carrier gases.
• The anesthetic vapor is diluted with fresh gas in one of 2
ways:
• Variable bypass vaporizers/ plenum vaporizers:
fresh gas flow (FGF) enters the vaporizer containing the
halogenated anesthetic.
• Measured flow vaporizers: halogenated anesthetic is
injected into the chamber containing the FGF.
 Vaporizers safety features
• Agent – specific, keyed & color coded filling
devices help prevent filling a vaporizer with the
wrong agent.
• Overfilling of these vaporizers is minimized because
the filler port is located at the maximum safe
liquid level.
• Vaporizers are firmly secured to a vaporizer
manifold on the anesthesia workstation &
therefore problems associated with vaporizer tipping
are less frequent.
• Contemporary interlock systems prevent the
administration of more than one inhaled anesthetic
 Cont.
• Color coding:
• Red: Halothane
• Purple: Isoflurane
• Yellow: Sevoflurane
• Blue: Desflurane
 Factors that influence
vaporizer output
• Flow rate: the output of the vaporizer is generally less
than the dial setting at very low (<200ml/min) or very
high (>15l/min).
• Temperature: automatic temperature compensating
mechanisms in bypass chambers maintain a constant
vaporizer output with varying temperatures
• Back pressure: intermittent back pressure e.g. positive
pressure ventilation causes higher vaporizer output in the
dial setting
• Carrier gas composition
• Ambient pressure
 Cylinders
• Oxygen: Black body & white shoulder
• Nitrous oxide: Blue
• Entonox: Blue body; blue & white shoulder
• Cyclopropane: Orange
• Medical air: Gray body; black & white
shoulder
4. PHARMACOLOGY OF
INTRAVENOUS
ANESTHETICS
 Introduction
• General anesthesia is composed
of:
• Analgesia
• Anterograde amnesia
• Loss of consciousness
• Muscles relaxation
 The following are the qualities of
an ideal IV anesthetic agent:
• Rapid & smooth onset of action
• Short duration (can be prolonged by infusion or
intermittent boluses)
• Antiemetic (free from PONV)
• Free from ‘hangover’ (headache, dizziness)
• Ability to decrease cerebral blood flow, cerebral
metabolism, ICP & IOP.
• Minimal cardiorespiratory depression
• Minimal risk of histamine release, allergic reaction
or anaphylaxis
 Cont.
• Drug compatibility & stability in solution.
• Rapid metabolism into inactive metabolites since
hangovers result from active metabolites e.g.
• Pethidine  Norpethidine; ketamine 
norketamine; alcohol  aldehydes; diazepam 
temazepam & desmethyldiazepam.
• Pain – free on injection & no tissue necrosis on
extravasation (diazepam commonly causes this)
• High potency (steep dose response relationship)
with minimal accumulation.
 Mechanisms of action of IV
anesthetics
• Interaction with GABA: some
sedative/ hypnotic agents stimulate
GABA resulting in sedation,
hypnosis & unconsciousness.
Examples include: BDZs,
Etomidate, Propofol,
Barbiturates, Eltanolone (a
steroid)
 Cont.
• Interaction with NMDA (N – Methyl – D
– Aspartate) an excitatory
neurotransmitter system: NMDA
receptor antagonists include
dextromethorphan, ketamine,
phencyclidine, N2O, ethanol etc.
These are associated with
hallucinations, dissociation & analgesia.
 Classification of IV anesthetic
agents.
• Barbiturates: thiopentone, methohexitone, thiamylal
etc.
• BDZs: Diazepam, Midazolam, Lorazepam
• Phenol derivatives: propofol
• Imidazole derivatives: etomidate
• Phencyclidine derivatives: ketamine
• Narcotics/ Opioids: Fentanyl, Alfentanil, Sulfentanil,
Remifentanil, Pethidine, Morphine
• Steroids: Althesin, Eltanolone
• Eugenols: Propanidid (sometimes classified as a steroid)
 Clinical uses of IV anesthetic
agents
• Induction of GA: can be used either singly or in
combination (co – induction) for smooth & rapid effect
(dosages dependent on age, weight, co – existing diseases,
premedication & Coadministration with other drugs)
• Total Intravenous Anesthesia: has rapid onset, short
duration, high potency & availability; easy to use infusion
pumps have made this possible even in very ill & unstable
patients.
• Neuroleptanalgesia/ neuroleptanesthesia: a state of
quiescence, altered awareness & analgesia produced by
the administration of a combination of narcotics & a
neuroleptic agent (commonly fentanyl and droperidol).
Has been overtaken by TIVA in modern practice.
 Cont.
• Monitored Anesthesia Care (M.A.C): IV
anesthetic agents used in combination with
regional anesthesia for sedation/ hypnosis to
minimize fear, anxiety and discomfort.
• Sedation: during endoscopic procedures and
radiological studies.
• Management of status epilepticus: IV agents
such as thiopentone and BDZs have been
administered through infusion for acute stages.
 1. BARBITURATES
• Include: Thiamylal, Thiopental,
Methohexital, Pentobarbital,
Secobarbital, Phenobarbital
• MoA:
• Depression of Reticular Activating System
which controls consciousness by an
agonist action at the GABAA resulting
in an increased duration of opening of
the Cl- specific channel.
 Cont.
• Structure – Activity Relationships:
• Substitution at carbon C5 determines hypnotic
potency & anticonvulsant activity.
• Phenyl group in phenobarbital is
anticonvulsive. Methyl group in Methohexital
is not.
• Replacing O2 at C2 (oxybarbiturates) with a
sulfur atom (thiobarbiturates) increases lipid
solubility e.g. thiopental & thiamylal have
greater potency, more rapid onset of action &
shorter duration of action.
 PK
• Prior to introduction of propofol, thiopental,
thiamylal & Methohexital were frequently
administered IV for induction of GA in adults &
children.
• The duration of sleep doses of highly lipid –
soluble barbiturates (thiopental, thiamylal &
Methohexital) is determined by redistribution.
• Prolonged use of thiopental and thiamylal can
cause long duration coma due to slow elimination
and large volume of distribution. PPB is high.
 Cont.
• Barbiturates are principally biotransformed via
hepatic oxidation to inactive water soluble
metabolites.
• Methohexital is cleared by the liver more
rapidly than thiopental hence full recovery of
psychomotor function is more rapid following
Methohexital due to its enhanced metabolism.
• Renal excretion is limited to water soluble end
products of hepatic biotransformation.
Methohexital is excreted in feces.
 PD
• CVS: ↓ BP; reflex tachycardia; CO is thus
maintained; effects vary markedly depending
on rate of administration, dose, volume
status, baseline autonomic tone & pre-
existing cardiovascular disease.
• Resp. system: ↓ the medullary ventilatory
center  hypercapnia & hypoxia
 Cont.
• CNS: cerebral vasoconstriction & ↓ in cerebral
blood flow & ICP (∴ CPP increases).
• Renal: ↓ renal blood flow & GFR
• Hepatic: ↓ hepatic blood flow and induction of
hepatic enzymes; promote aminolevulinic acid
synthetase which stimulates the formation of
porphyrin. This may precipitate acute
intermittent porphyria or variegate porphyria in
susceptible individuals.
 Side effects
• Methohexital produces pain on
injection. Reduce pain by using large
veins or IV LA.
• Dysgeusia with thiopental
• Excitement e.g. tremors, hyper –
tonus, hiccups with Methohexital
 2. BDZ
• Include: Diazepam, Lorazepam, Midazolam
• MoA: Bind GABAA receptors  ↑ the
frequency of opening of the associated Cl- ion
channel
• Flumazenil (an imidazobenzodiazepine) is a
specific BDZ – receptor antagonist.
 P/K
• Commonly administered PO, IM & IV to provide
sedation, or less commonly, to induce GA.
• Midazolam can be administered intranasal,
buccal, sublingual for preoperative sedation.
• IM injections of diazepam are painful &
unreliably absorbed.
• Induction of GA with midazolam is convenient
only with IV administration.
 Cont.
• Lipid solubility:
• Diazepam: readily penetrates BBB
• Midazolam is water soluble at reduced pH
but is lipid soluble at physiologic pH
• Lorazepam is moderately lipid soluble
• Redistribution is responsible for awakening.
• All 3 are highly protein bound (90 – 98%)
 Cont.
• Metabolism: hepatic
• Phase I metabolites of diazepam are
pharmacologically active
• Excretion is chiefly via urine.
• Enterohepatic circulation produces a 20
peak in diazepam plasma concentration 6 –
12 h following administration.
 P/D
• CVS: minimal depressant effects at GA
doses; given alone they ↓ MAP, CO & PVR
slightly; sometimes ↑ HR
• Resp.: ↓ ventilatory response to CO2
• Ventilation MUST be monitored in all
patients receiving IV BDZ & resuscitation
equipment must be immediately available.
 Cont.
• CNS: ↓ CMR, cerebral blood flow & ICP;
effective in preventing & controlling GTCs.
Oral sedative doses often produce
anterograde amnesia. Have a mild muscle –
relaxing property mediated at the spinal cord
level &not at the NMJ. Have anxiolytic,
amnestic & sedative effects that progress, in
a dose – dependent manner to stupor &
unconsciousness.
• Have no direct analgesic properties.
 D/Is
• The following inhibit metabolism of BDZs:
cimetidine, erythromycin
• Heparin: displaces diazepam from protein –
binding sites hence ↑ the free drug concentration.
• Opioids + BDZs  marked ↓ in MAP & PVR
• BDZs ↓ MAC of volatile anesthetics by as much
as 30%.
• CNS depressants like ethanol, barbiturates
potentiate the sedative effects of BDZs.
 3. PROPOFOL
• Phenol derivative
• Oil – water emulsion hence not physically soluble
in water
• Needs to be refrigerated as it is a good culture
medium; administered within 6h of opening the
ampule
• Very painful on injection & ∴, to ↓ pain
administer the following before giving Propofol:
• IV formulation of lidocaine
• Short acting opioid e.g. fentanyl
 Cont.
• Brain – arm circulation time: 30s
(highly lipid soluble); DOA: 5 – 7 mins
(10mins max); Plasma Protein Binding
(PPB) is about 80%
• Metabolized in the liver into inactive
water soluble metabolites that are
excreted via the kidneys.
 Effects of Propofol
• CNS: ↓ O2 utilization by the brain while
maintaining its perfusion, i.e., the brain is
nice & quiet. Doesn’t cause hallucinations,
nausea or vomiting.
• CVS: can cause significant hypotension by ↓
the SVR.
• Resp.: causes apnea by ↓ RR & tidal volume
(Propofol is thus not safe for use in an out of
ideal theater set up)
 Uses of Propofol
• Indications: neurosurgery
• Contraindications:
• Hypotensive patient e.g. ruptured ectopic,
intestinal obstruction, dehydration
• In ICU due to Propofol Infusion Syndrome
(find out)
 4. Etomidate
• Imidazole derivative; dissolved in propylene glycol
for injection; causes pain on injection that can be
lessened by a prior IV injection of lidocaine.
• MoA:
• Depresses the RAS
• Mimics the inhibitory effects of GABA (↑ GABAA
receptor’s affinity for GABA)
• Has disinhibitory effects on the parts of the
nervous system that control extrapyramidal motor
activity hence 30 – 60% incidence of myoclonus
with etomidate induction of GA.
 P/K
• Available as IV formulation only
• Primarily used for induction of GA
• Very rapid onset of action due to great lipid
solubility; highly PPB
• Redistribution is responsible for awakening
• Metabolism: hepatic & by plasma esterases
• Excretion: urinary
 P/D
• CVS: minimal effects; mild ↓ in PVR hence slight
↓ in MAP.
• Respiratory: minimal effects. Even induction
doses usually do not result in apnea unless
opioids have also been administered.
• CNS: ↓ CMR, cerebral blood flow & ICP; CPP is
well maintained; PONV is more common; lacks
analgesic properties.
• Endocrine: Induction doses transiently cause
adrenocortical suppression
 D/Is
• Fentanyl: ↑ plasma levels & prolongs
half life
• Opioids: ↓ myoclonus
 5. Ketamine
• Structural analogue of phencyclidine
• Used for: IV induction of anesthesia esp. in
settings where its tendency to produce
sympathetic stimulation are useful e.g.
hypovolemia, trauma.
• When IV access is lacking, it is useful for
IM induction of GA in children &
uncooperative adults
 Cont.
• Stable in the environment.
• Comes in a vial with a dark rubber
top.
• Water soluble
• Cheaper compared to Propofol
• Doesn’t cause any pain on injection
 MoA
• Antagonist at the N – methyl – D – Aspartate
(NMDA) receptor, a sub – type of the excitatory
glutamate receptor.
• It dissociates the thalamus (which relays sensory
impulses from the RAS to the cortex) from the
limbic cortex (which is involved with the
awareness of sensation, resulting in
dissociative anesthesia. The patient appears
conscious (e.g. eye – opening, swallowing, muscle
contracture) but is unable to process or respond
to sensory input.
 P/K
• Can be administered PO, intranasal, rectal, IV, IM, SC,
epidural.
• Dose:
• Induction: IV  1 – 2 mg/kg; IM  3 – 5 mg/kg
• Sedation (almost always in combination with propofol): IV
2.5 - 15𝜇g/kg/min
• Has rapid brain uptake & subsequent redistribution
(distribution t1/2 is 10 – 15 min.) because:
• More lipid soluble & less protein bound than thiopental;
Induces ↑ cerebral blood flow & CO
• Brain – arm circulation time: 60 – 90s; longer DOA of 15 – 20
mins. Awakening is due to redistribution from brain to
peripheral compartments.
 Cont.
• Hangover effect: ketamine is metabolized in the
liver & one of its metabolites called norketamine is
active hence prolonging the action of ketamine.
Norketamine is responsible for the characteristic
excitatory phenomenon in patients
(hallucinations, involuntary movements, night
mares esp. in females). It may result in convulsions.
To reduce the phenomena, co – administer ketamine
with BDZs.
• It induces hepatic enzymes hence patients
develop tolerance on multiple doses of ketamine.
• End products of metabolism are excreted renally.
 Effects of ketamine
CVS:
• Causes ↑ in MAP, HR & CO indirectly
via central stimulation of the SNS.
• Use with caution in: coronary artery
disease, uncontrolled HTN, CHF,
arterial aneurysms
• Beneficial in hypotensive patients.
 Cont.
Resp.:
• Causes bronchodilation & ↑ secretions
(overwhelming bronchorrhea & rhinorrhea;
attenuate with anticholinergic e.g.
glycopyrrolate, atropine); ventilatory drive is
minimally affected by induction doses &
upper airway reflexes remain largely intact.
• Beneficial in asthmatics.
 Cont.
CNS:
• Causes ↑ CMR, cerebral blood flow & ICP.
• Precludes use in neuro – anesthesia but if combined with BDZ & controlled
ventilation, but not N2O it is not associated with ↑ ICP.
• Has undesirable psychotomimetic side effects e.g. disturbing dreams & delirium
during emergence & recovery which are less common in:
• Children
• Patients pre – medicated with BDZs
• Combination with propofol in a TIVA technique

• Induces analgesia (opioid sparing), amnesia as well as unconsciousness.

 D/Is
• Synergistic interaction with volatile agents.
• Additive interaction with propofol, BDZ & other
GABA – receptor mediated agents
• Diazepam & midazolam attenuate ketamine’s
cardio stimulatory effects
• Diazepam prolongs ketamine’s elimination half
life.
• 𝛼 – & 𝛽 – blockers unmask the direct myocardial
depressant effects of ketamine which are normally
overwhelmed by sympathetic stimulation.
5. PHARMACOLOGY OF
MUSCLE RELAXANTS
15/1/2019
BY: DR. MWITI
 Classification of skeletal
muscle relaxants:

Neuromuscular
blocking drugs Spasmolytics
(NMBDs)
 1. NMBDS
Depolarizing (agonists): Succinylcholine

Non – depolarizing (antagonists)

• Isoquinoline derivatives: atracurium,
cisatracurium, mivacurium, doxacurium,
tubocurarine, metocurine
• Steroid derivatives: Pancuronium,
pipecuronium, rocuronium, vecuronium
• Gallamine
 2. Spasmolytics
Centrally acting
•Diazepam
•Baclofen
•Tizanidine
•Pregabalin, Progabide, Glycine, Idrocilamide, Mephenesin
& related drugs, Cannabis

Peripherally acting
•Dantrolene sodium
•Botulinum toxin
 Drugs for treating acute
local muscle spasm
• Cyclobenzaprine
• Carisoprodol
• Chlorphenesin
• Chlorzaxozane
• Metaxalone
• Methocarbamol
• Orphenadrine
 Succinylcholine/
Suxamethonium
• MoA: Succinylcholine (Sux.) Attaches to nicotinic
receptors & acts as an agonist resulting in
depolarization of the NM end plate. Unlike
acetylcholine (Ach) that is instantly destroyed by
acetylcholine esterase (AChE), Sux.:
• Persists at a high concentration in the synaptic
cleft.
• Remains attached to the receptor for a longer
time.
• Provides constant stimulation of the receptor.
 Cont.
•Blockade by Sux. therefore is
divided into 2 sequential
phases:
• Phase I (depolarizing)
• Phase II (desensitizing)
 PK
• Very rapid OOA (within 1 minute); very brief DOA (5 – 10
mins)
• It is rapidly hydrolyzed by butyrylcholinesterase/
pseudocholinesterase
• The initial metabolite succinylmonocholine has a weak
NM blocking action. This is further metabolized to
succinic acid & choline
• NM blockade by either SC or mivacurium may be
prolonged in patients with an abnormal genetic variant of
plasma cholinesterase
• The dibucaine number is a test for ability to
metabolize SC, which can be used to identify such
patients
 PD
• Skeletal muscles: paralysis follows IV admin of Sux.
• Transient muscle fasciculation occurs over the chest &
abdomen within 30s. The arms, neck & leg muscles are
initially relaxed followed by facial and pharyngeal
muscles. The resp. muscles including the
diaphragm are paralyzed last.
• CVS:
• Can cause arrhythmias when administered during
halothane GA.
• Has –ve inotropic & chronotropic effect which can be
attenuated by an anticholinergic like atropine.
 Adverse effects
• Hyperkalemia
• Cases of trauma esp. burns, nerve
damage, closed head injury, spinal cord
injury
• N – M disease e.g. muscle dystrophy
• Peritoneal infection
• Renal failure
 Cont.
• ↑ intragastric pressure (but also ↑ LES
pressures so ↓ risk of aspiration)
• Post – operative myalgia and muscle damage
• Increased IOP
• Malignant hyperthermia (Rx: 1 mg/kg IV
dantrolene then repeat PRN up to a max of
10mg/kg)
5. PHARMACOLOGICAL
TREATMENT OF ACUTE
PAIN
15/2/2019
DR. T. M. MWITI
 Introduction
• Pain
• Common complaint
• Common component of diagnostic &
therapeutic procedures
• Pain is usually generally poorly managed
• Analgesia is part of the triad of
anesthesia, i.e., unconsciousness &
muscle relaxation
 Definitions
• Pain is an unpleasant sensory & emotional
experience associated with actual or potential
tissue damage, or described in terms of such
damage [IASP].
• Acute pain: pain temporarily related to injury
and that resolves during the appropriate healing
period
• Persisting/ subacute pain: pain that persists
after tissue healing for < 3 months.
• Chronic pain: is that which lasts ≥ 3 months
 Cont.
• Nociceptive pain
• Pain arising from actual or threatened damage to
non – neural tissue.
• Is due to the activation of nociceptors.
• Induces immobilization for appropriate tissue/
organ healing
• May be somatic or visceral
• Neuropathic pain
• Pain caused by a lesion or disease of the
somatosensory nervous system e.g. painful
diabetic neuropathy (treated with duloxetine).
 Causes of acute pain
• Trauma
• Burns
• Surgery & other therapeutic & diagnostic
procedures
• Inflammatory conditions
• Infective processes
• Colic, kidney stones
• Sickle cell crises
Physiology of pain
 Clinical presentation of acute pain
• Background pain: slow dull pain is transmitted
by C fibers
• Acute pain is transmitted by Aδ fibers
• Breakthrough pain: e.g. in end of dose failure
• Procedural pain
• Post – procedural pain: higher intensity than
the usual background pain
• Psychologic/ anticipatory pain: occurs when
initial pain was not well controlled
 Acute pain treatment
• Acute pain intensity is worst in the
1st few days.
• Pharmacologic and non –
pharmacologic approaches e.g.
acupuncture, massaging, cold
compresses are used.
 Goals of acute pain treatment
• Adequate analgesia
• Physical rehabilitation
• Prevention of acute complications of pain & its
management:
• Complications include: HTN, tachycardia,
hypercoagulability and VTE (immobility),
pneumonia and atelectasis, insulin
insensitivity, anxiety, central sensitization
• Prevention of chronification of pain
 Strategy
• Treatment of underlying disease process
• Round the clock interventions for
background pain e.g. tramadol QID
• On – demand medication for breakthrough
(incidental & procedural) pain
• Preemptive management of some adverse
effects of therapies e.g. change of dressing
• Re – evaluation
 1. Opioids
• Cornerstone of management for acute, severe
pain
• Effective: “cost of opioid use?”
• A variety with different ranges of potency & DoA
• Different routes of administration
• Morphine 1mg/kg then reassess after 10
minutes to assess the effective dose
• Titrated to effect
 Cont.
• Clinically relevant side effects: respiratory depression,
nausea & vomiting, itch, constipation
• Antidote: naloxone
• Analgesia comes before the side effects
• Tolerance, physical dependence, addiction (psychological
dependence)
• Examples: morphine, fentanyl, codeine, DF 118
(dihydrocodeine), remifentanil, oxycodone, methadone,
hydromorphone, buprenorphine, tramadol
• Fentanyl cannot be used orally as it undergoes first
pass metabolism
 2. Paracetamol
• Opioid dose sparing
• Antipyretic
• Excellent risk profile & few contraindications
• Should be used regularly at its maximal dose, TDS or QID
in all patients
• Contraindications: liver disease
• Cautious use: severe malnutrition, alcoholics
• Toxicity in adults is commonly due to combinational
tablets.
• Antidote for paracetamol toxicity: N – acetylcysteine
 Cont.
• Maximum PO or PR dose for children (acute
administration for 2 to 3 days)
• 60mg/kg/ day in term neonates and infants
• 90mg/kg/day in children aged between 6
months and 12 years
• Maximum doses of IV paracetamol
• 30mg/kg/day in neonates and infants
• 40 to 60 mg/kg/day in children
• 1g QID in adults
• Maximum adult dose: 4g/ day (1g q6h)
 3. NSAIDs
• Non – selective COX inhibitors & selective
COX – 2 inhibitors
• Effective analgesia, anti – inflammatory &
anti – pyretic
• Synergistic with opioids (1 + 1 = 4)
• Not recommended for routine use in patients
with ↑ risk of renal failure, peptic ulceration
• Caution in the elderly
 Cont.
• Often first line
• Chemically diverse compounds
• Traditional (non – specific) NSAIDs
• Selective COX – 2 inhibitors
• Most widely prescribed drugs for acute
& chronic pain
 Classification
Salicylates Aspirin, diflunisal, salsalate

Propionic acid derivatives Ibuprofen, dexibuprofen, ketoprofen,

(Profens) dexketoprofen, naproxen, fenoprofen,
flurbiprofen, oxaprozin, loxoprofen
Acetic acid derivatives Indomethacin, diclofenac, nabumetone,
tolmetin, sulindac, etodolac, ketorolac
Enolic acid derivatives Piroxicam, isoxicam, meloxicam, tenoxicam,
(Oxicams) droxicam, lornoxicam
Fenamic acid derivatives Mefenamic acid, flufenamic acid, tolfenamic
(Fenamates) acid, meclofenamic acid
Phenylpyrazolones Phenylbutazone, oxyphenbutazone
COX – 2 selective inhibitors Celecoxib, rofecoxib, valdecoxib
 Cont.
• Action:
• Inhibition of COX 1 & 2  inhibition of
PG synthesis
• Anti – inflammatory & analgesic
effects
• Analgesic equipotency, analgesic ceiling
• Switching to a different NSAID may be
considered if the first is ineffective
 A/E
• GI
• More with non – selective NSAIDs
• Cause for concern
• Increased risk of GI ulcers on
endoscopy
• Serious upper GI complications;
hemorrhage, perforation & obstruction
 Cont.
• Risk factors of GI A/Es.
• Patients > 65
• Patients with a history of PUD
• Patient taking: steroids,
anticoagulants, aspirins
 Adverse effects
•Therapeutic approaches to
reduce GI toxicity
•Coadministration of PPI
with traditional NSAIDs
•Use COX – 2 inhibitors
 Cardiovascular risk of NSAIDs
• A class effect of all NSAIDs
• Includes
• Thrombotic events
• New onset HTN
• Worsening pre – existing HTN by
water retention
 Others
• Respiratory: bronchospasm in
susceptible asthmatics
(traditional NSAIDs); use COX -
2
• Naproxen is not better than the
rest
 Renal toxicity
• Transient decrease in renal function
• Occur more often in patients with
underlying renal disease e.g. in DM,
burns, trauma
• May alter responses to thiazides or loops
• Fluid retention and edema in come
patients
 Adjuvants
• Ketamine
• Powerful analgesic at sub – anesthetic doses (0.25 – 0.5
mg/kg IV)
• Post – op infusion for up to 48 hrs.
• Opioid sparing esp. in opioid exposed patients e.g. sickle
cell disease
• A/Es: hallucinations (give BDZ, like diazepam)
• Anticonvulsants & antidepressants
• Gabapentin, pregabalin, amitriptyline, nortriptyline
• Neuropathic pain: duloxetine
• Burn itch: gabapentin
 Pharmacological: adjuvants
• 𝜶 – 2 adrenergic blockers:
clonidine, dexmedetomidine
• IV lignocaine infusion; do it under
continuous ECG monitoring
• A/Es: arrhythmias, convulsion
• Bupivacaine gives a quick cardiac
arrest.
 Regional analgesic techniques
• Wound infiltration
• Epidural analgesia
• Conventional
• Patient controlled epidural analgesia
• LAs, opioids
• Neural blocks
• Peripheral nerves
• Plexus blocks
• Other truncal blocks: transversus abdominis plane
block, paravertebral block
 Patient Controlled Analgesia
(PCA)
• Allows patient to administer preset doses of
an analgesic on demand.
• Gives a patient sense of control over pain
• Types
• IV patient controlled analgesia (IV PCA)
• Patient controlled epidural analgesia
(PCEA)
• Trans – dermal – on trials
 Multimodal analgesia
• Use of several different analgesics and
routes of administration, which then act
synergy
• Improves the effectiveness of pain relief
• Reduces the maximal dosage and adverse
effects
• Procedure specific
 Treatment options in relation to magnitude of post –
op pain expected following different types of surgery
Mild intensity pain Moderate intensity pain Severe intensity pain
e.g. inguinal hernia, varices, e.g. hip replacement, e.g. thoracotomy, upper abdominal surgery,
laparoscopy hysterectomy, jaw surgery aortic surgery, knee replacement
1. Paracetamol and wound infiltration with
local anaesthetic
2. NSAIDs (unless contraindicated)
3. Epidural local analgesia or major
peripheral nerve or plexus lock or opioid
injection (IV PCA)

1. Paracetamol and wound infiltration with local anaesthetic

2. NSAIDs (unless contraindicated)
3. Regional block anaesthesia (single shot or continuous infusion) or opioid
injection (IV PCA)

1. Paracetamol and wound infiltration with local anaesthetic agents

2. NSAIDs (unless contraindicated)
3. Regional block anaesthesia
Add weak opioid or rescue analgesia with small increments of strong opioid if necessary
WHO analgesic ladder initially
developed for cancer pain
 Non – pharmacological methods
• Psychological techniques: relaxation
techniques, CBT
• Distraction: music therapy, virtual
reality, bubble blowing, play therapy
 Conclusion
• Pain is a subjective experience
• Acute pain is a common presenting symptom
• Opioids are useful but should be used
appropriately (titrate to effect)
• Paracetamol has few contraindications
• NSAIDs are useful but can cause serious adverse
effects
• Consider regional analgesia
• Best approach: multimodal analgesia.
The first to apologize is
the bravest.
The first to forgive is
the strongest.
The first to forget is the
happiest.
1. PRE – OPERATIVE
ASSESSMENT &
PREPRATION
25/1/2019
BY: PROF. MURIITHI
 Introduction
• The assessment & preparation of a patient before
operation is paramount for epidemiological
studies have indicated that inadequacies in the
above may be a major contributory factor to the
primary anesthetic causes of perioperative
mortality.
• ∴ means of establishing fitness for anesthesia
(i.e. anesthetic assessment clinics), although
uncommon, are paramount.
 Cont.
• Due to improved anesthetic practices, death
due to anesthesia is now rare.
• The morbidity & mortality of surgery are
due to factors present before, during &
after operation e.g. blood loss, tissue
damage, enforced fasting, immobility, pain
& hypoxia
 3 factors are to be considered for surgery
in a patient with an intercurrent illness
1. The nature, extent & urgency of the
operation.
2. The effect of the operation & associated
morbidity on the patient’s homeostatic
mechanisms.
3. The effect of anesthesia.
• NB: the nature of the anesthetic must be
decided upon in light of factors (a) & (b).
 The purpose of the preoperative
visit:
• Establish rapport with the patient.
• Obtain a history & perform a P/E.
 History & P/E
• Direct questions: on items of particular
anesthetic relevance e.g. hereditary
conditions like porphyria, malignant
hyperpyrexia, hemophilia etc.
• Cardiovascular & respiratory conditions e.g.
dyspnea, angina etc.
• History of pregnancy, drug allergies, smoking,
alcohol intake, drug interaction history
• Physical examination: all systems of the body.
Document in the case records.
 Special assessment of fitness for surgery
American Society of Anesthesiologists, ASA
Physical Status Scale (1 – 6 Grades)
2. A patient with mild 3. A patient with a
systemic disease but no systemic disease &
1. A normal healthy functional impairment significant functional
individual e.g. hypertensive impairment; not
controlled on DASH diet, incapacitating e.g.
pregnancy, obesity poorly controlled DM

4. A systemic disease & 5. A moribund patient

6. A declared brain
severe impairment of not expected to survive
dead person whose organs
function that is a > 24hrs without
are to be removed for
constant threat to life operation e.g.
donor purposes
e.g. recent history of MI intracranial bleed
 Pre – operative investigations
• Remember the purpose of the patient visit.
• Clinical history & PE represent the best
method of screening for the presence of
disease.
• Routine lab tests on patients apparently
healthy on clinical examination & history
may be of little use & may be a waste of
resources.
 Cont.
• Before ordering for any investigations
(lab & others), ask yourself the
following questions:
• Will this investigation yield
information not revealed by P/E?
• Will the results of investigation alter
the management of the patient?
 These investigations may be
necessary
• Full Hemogram:
• Hemoglobin: major surgeries that may involve large
blood loss, age > 50yrs, menstruating females,
suspected SCD, history of anemia, blood dyscrasias or
malignancy, congenital heart disease, chronic disease
states
• WBC count: suspected infection or ISS
• Platelet count: history of abnormal bleeding or
bruising, liver disease, blood dyscrasias, chemotherapy,
hypersplenism
• Group & Cross Match
• RBS: patients on steroids, DM or vascular disease
 Cont.
• Urinalysis: ?DM, ?UTI; also for genito – urologic
procedures.
• U/E/Cr: > 65 yrs.; if there is h/o diarrhea, vomiting,
renal or hepatic diseases; abnormal nutritional
state; patients on diuretics, digoxin, anti – HTN,
steroids or hypoglycemic; cardiovascular disease or
on cardiac medication; IVF for > 24hrs..
• LFTs: patients with hepatic disease; abnormal
nutritional states or metabolic disease; alcoholics;
drug therapy with agents that may affect liver
function
• Pregnancy test: if uncertain of status.
 Cont.
• BGA: all patients with dyspnea at rest
and patient scheduled for thoracotomy
• Coagulation tests (PTT & INR) in
patients with history of bleeding
disorders or patients receiving
anticoagulant therapy or with liver
disease, drug abuse; significant chronic
alcohol abuse; malabsorption or poor
nutrition.
 Cont.
• CXR:
• If age > 60 yrs.
• H/O cardiac/ respiratory disease
• Metastases
• Before thoracic surgery
• Others: anticipated difficult intubation
• Cervical spine flexion/ extension X – rays: in
patients with RA or Down’s syndrome. Not done
routinely.
 Cont.
• ECG: history or sign of cardiac disease; age >50
yrs.; male smoker > 45 yrs.; history actual or
suspected of heart disease or HTN; cardiac drugs;
chronic or acute on chronic pulmonary disease
• Pulmonary function tests e.g. PEV, PEFR, FVC
& FEV1: candidates for preoperative PFTs include
patients:
• Considered for pneumonectomy; with moderate to
severe pulmonary disease scheduled for major
abdominal or thoracic surgery; with severe
dyspnea on mild or moderate exertion or at rest;
with chest wall & spinal deformities; who are
morbidly obese; with obstructive airway lesions.
 Airway evaluation
• This is assed as follows:
• History e.g. difficult intubation in the past,
sleep apnea
• P/E
• Radiographs (some times)
• PFTs
• Direct fiber – optic examination
 Anatomical factors associated
with difficult laryngoscopy
• Short muscular neck e.g. in Cushing
syndrome, obesity
• ↓ atlanto – occipital distance (↓ neck
extension , requires x – ray , 2 fingers or
less)
• Prominent/ protruding upper incisors
• Edentulous state: associated with poor fit
of anesthesia mask.
• Long, high arched palate
 Cont.
• Receding lower jaw e.g. in elderly people that
have lost teeth; in Pierre Robin Syndrome
• Limited range of motion of TMJ & cervical
spine.
• ↑ anterior depth mandible
• ↑ posterior depth of mandible (jaw opening)
• Macroglossia
• Hair style: heap of hair on the back of the
head
 Pre operative assessment of the
airway
1. General appearance of the neck, face, maxilla &
mandible
2. Jaw movement R/O trismus
3. Head extension & neck movement
4. The teeth & oropharynx.
5. The soft tissue of the neck
6. Recent chest & cervical spine X – rays
7. Previous anesthetic records
 Etiological factors of difficult
intubation
Anesthetist factors:
• Inadequate preoperative assessment
• Inadequate equipment preparation
• Inexperience, poor technique
Equipment
• Malfunction
• Unavailability
• No trained assistant
 Cont.
Patient
• Congenital conditions:
• Syndromes: Down’s, Pierre Robin,
Treacher Collins, Marfan’s
• Achondroplasia, cystic hygroma,
encephalocele
 Cont.
• Acquired conditions:
• ↓ jaw movements: trismus (infection  abscess,
tetanus, fracture); fibrosis (post – infection,
radiotherapy, trauma); rheumatoid arthritis (RA);
ankylosing spondylitis (AS), tumors, jaw wiring
• ↓ neck movement: RA, OA, AS (bamboo spine),
cervical fracture/ instability/ fusion
• Airway: edema (infection, abscess, trauma,
angioedema, burns); compression (goiter, surgical
hemorrhage); scarring (radiotherapy, infection,
burns); tumors/ polyps; foreign body; nerve palsy
• Morbid obesity, pregnancy, acromegaly
 Mallampati test
• This is one of many clinical tests done to predict
difficult laryngoscopy & intubation.
• None of these tests are totally reliable but their
use may complement routine examination of the
airway.
• Mallampati test predictive value may be
strengthened if the thyromental distance is <
6.5cm.
• Mallampati classification correlates with the
view obtained at laryngoscopy.
 The Mallampati Score
(The patient must fully extend the tongue, i.e.,
maximal mouth opening)

Class I: soft palate, fauces, uvula & pharyngeal pillars.

Class II: only soft palate, fauces & uvula visible.

Class III: only soft palate & base of uvula visible

Class IV: soft palate not visible; hard palate is visible.

 Preparation of the patients
a) The history, physical examination &
laboratory investigations – are all geared
towards good or sound pre – operative
preparation
b) Any abnormality or disease detected should
be managed before any surgery unless it is
a serious emergency
c) The preparation will also include
premedication.
 Premedication objectives
• Allay anxiety and fear: anxiolytics e.g. BDZ,
Barbiturates (1h pre – op)
• ↓ secretion: use anti – sialagogue e.g. atropine
(0.4 – 0.6 IM), scopolamine (0.2 – 0.4 IM),
glycopyrrolate (0.2 – 0.4, IM)
• Anticholinergics also prevent bradycardia &
hypotension during laryngoscopy & surgical
manipulation
• ↓ the hypnotic effect of GA agents
• ↓ post – operative nausea & vomiting (PONV):
antiemetics
 Cont.
• Produce amnesia to reduce awareness: BDZ e.g. midazolam
• ↓ volume & ↑ pH of gastric contents: incase the patient vomits &
regurgitates the risk of developing Mendelson syndrome is lower
with ↑ pH
• H2RA: ranitidine 50 – 100mg IV 1h before surgery
• Omeprazole PO 3 – 4 h before surgery; IV 30 minutes before
surgery
• Antacids
• Prokinetics: metoclopramide 15 – 30 minutes before surgery
• Attenuate vagal reflexes/ sympathoadrenal responses.
• Analgesia: Morphine
2. ANESTHETIC & CRITICAL
CARE MONITORING
RECORDS
1ST/3/2019
BY: DR. T. CHOKWE
 Outline
• Definition of monitoring.
• Importance of monitoring.
• What monitoring involves.
• Importance of keeping records.
• Few tips on keeping good
records.
 Monitoring
• Monitor derived from Latin word
“monere” meaning “to warn”
• It is to interpret available clinical
data to help recognize present or
future mishaps or unfavorable
system conditions.
 Characteristics of critical care/
anesthesia monitoring
• Continuous
• By trained personnel
• Dynamic
 Relevance
•Assessment/ evaluation of
a patient’s condition
•Patient safety
•Trending of parameters
 What does monitoring involve
•Parameters that are
observed/ felt
•Parameters that are
measured
 Historically
•Visual monitoring of
respiration and overall
clinical appearance.
•Finger on arterial (radial)
pulse.
 Harvey Cushing
• Famous neurosurgeon & father of anesthesia
monitoring & records.
• 1896: started continuous pulse, RR
monitoring.
• Popularized Codman’s anesthetic chart
• 1901: Riva – Rocci Sphygmomanometer (BP)
• Emphasized the relationship between vital
signs & neurosurgical events.
Cushing’s BP machine
 Transitions in clinical
records
• What’s important is clarity of
records & trending of the
records.
• Figures should be interrogated
in relation to the circumstances
surrounding the patient.
 Standards for basic intra –
operative monitoring (ASA)
• Qualified anesthesia personnel shall be
present (physically & mentally) in the room
throughout to conduct all GA, RA & MAC.
• During all anesthetic procedures, the
patient’s respiratory (ventilation,
oxygenation), circulation & temperature
shall be continually evaluated.
 Basic essentials
• Presence of anesthesia provider
• Pulse oximetry
• Non invasive BP
• ECG
• Temperature
• Capnography
• Pain monitoring: very important esp. to an anesthetist.
It can influence other parameters as pain may cause
tachycardia & HTN.
 Advanced essentials
• Dictated by clinical
circumstances; are done to obtain
information that would otherwise
not be available by basic
monitors. Requires complex
equipment
 CVS Monitors
• Invasive BP
• CVC
• Pulmonary artery catheterization
• CO2 measurement
• Tracheo – esophageal echocardiography
(TEE)
• Blood loss measurement
 Respiratory System Monitors
• Airway pressure measurement
• Disconnection alarm
• Stethoscope (pericardial & esophageal)
• Spirometry
• FiO2 monitoring
• CO2 monitoring
• Anesthetic gas analysis
• Blood gas monitoring
 CNS monitoring
• EEG
• Evoked potentials
• Cranial nerve monitoring
• Cerebral blood flow measurement
• Monitoring of cerebral oxygenation
• Monitoring of anesthetic depth
• Bispectral Index Monitoring
 Monitoring of metabolism
• Tissue oxygenation
• Indirect calorimetry
• Fluid & electrolyte status
monitoring
• Blood gas & acid base status
monitoring
 Neuromuscular function
monitoring
• Clinical tests
• Conscious patient
• Unconscious patient
• Gold standard: peripheral nerve
stimulation
 Role of information
• Interpret & make decisions
• Intervene
• Optimize
• Record
• NOTE: “if it is not written/
documented, it was not done”
 Record keeping
• The quality of medical records is
a direct reflection of the quality of
medical practice.
• To achieve and maintain a high
standard of medical practice,
proper medical documentation is
essential.
 Cont.
• All doctors have a responsibility to
maintain clear, accurate, adequate
and contemporaneous medical
records of their patients.
• Systematic record keeping helps in
ensuring patients’ problems are
followed and properly looked after.
 Purposes for written records
• Written communication
• Permanent record for accountability
• Legal record of care
• Teaching
• Research and data collection
 Types of records
• Paper based records
• Electronic records
• Data filled/ keyed into computers
• Data stored in monitors
• Videos/ photographs
• Audio recordings
 What should be recorded
• For you: documentation is a
substitution of your memory
(which tends to fail).
• For a 3 party: Paint a picture so
rd
clear they can visualize the
situation.
• Be legible for self & others to read
• Avoid altering records.
 S.O.A.P
• Subjective: what happened
• Objective: what did you find?
(observations, monitors)
• Assessment: what do you think?
• Plan: What did you do?
The Anesthetic Chart
 Write legibly: you can read your own
handwriting but can any one else read?
 Tips on good record keeping
• Write down patient’s name & identification
on each leaflet.
• Include date and time: Record as soon as
possible
• Avoid abbreviations e.g. 30 year old female
with PID or neonate with TOF
• Avoid unnecessary (personal) comments e.g.
OMG!
 Cont.
• Clearly write your name at the end(own your
notes)
• Avoid altering records
 Basics of medical records
• Professional • Legible, spelling correct
• Accurate • Honest
• Consistent • No duplication
• Thorough • Plain language
• Clear • Relevant information
• Brief/ concise • Clearly write/ sign your
name
• Paint the picture
 Summary
• Monitoring is an integral part of anesthesia
and critical care
• Monitoring is continuous & dynamic &
requires the presence of trained personnel.
• Good record keeping is key in patient
management
• Records are tools of communication
between medical personnel & they are a
secure evidence.
3. BASIC PRINCIPLES OF
MECHANICAL VENTILATION
25/1/2019
BY: DR. OLANG’
 Outline
 Introduction
 Classification of mechanical ventilators
 Indications for mechanical ventilation
 Goals of mechanical ventilation
 Modes of ventilation
 Complications of mechanical ventilation
 Weaning from mechanical ventilation
 Introduction
• 1928, the first mechanical ventilator.
• It was a negative – pressure ventilator,
known as the Drinker – Shaw tank
ventilator or the “iron lung”.
• Made up of a metal cylinder engulfing
patient up to the neck.
• A vacuum pump created negative pressure
in the chamber, resulting in chest
expansion.
 Cont.
• Change in chest geometry ↓ the
intrapulmonary pressure allowing room air to
flow into the patient's lungs as well as venous
return. Therefore, in negative pressure
ventilation venous return happens during
inspiration.
• When the vacuum was terminated, the
negative pressure dropped to zero (atmospheric
pressure) & the elastic recoil of the chest &
lungs permitted passive exhalation.
• There was no need for endotracheal or
tracheostomy tube.
Drinker – Shaw tank ventilator
 Cont.
• Drinker – Shaw tank ventilator was cumbersome &
uncomfortable with no access to patient (1928).
• 1931, Emerson introduced the Emerson tank
ventilator used extensively during the polio
epidemics 1940s & 1950s.
• Today, Negative – pressure ventilators have been
replaced by Positive – pressure ventilators
(inspiration results in positive intrapulmonary
pressure; venous return is thus during
expiration when intrapulmonary pressures are
reducing due to elastic recoil).
 Cont.
• Positive – pressure ventilation means that
pressure is applied at the patient's airway
through an endotracheal or tracheostomy
tube (insp. is +ve as opposed to –ve in
spontaneous respiration)
• The positive pressure causes the gas to
flow into the lungs until the ventilator
breath is terminated, i.e. the respiratory
cycle.
• Elastic recoil of the chest results in passive
exhalation by pushing the tidal volume out.
Mechanical ventilation is indicated:

• When spontaneous ventilation is

inadequate to sustain life.
• As a measure to control ventilation in
critically ill patients esp. in extremes of
ages.
• As a prophylaxis for impending collapse
of other physiologic functions.
 Cont.
• During the polio epidemic in Scandinavia
& the United States in the early 1950s it
was noted that manual mechanical
ventilation ↓ mortality from 80  25%.
• This was, however, found to be labour
intensive leading to the gradual
adaptation of positive – pressure machines
used in the operating rooms for use in the
ICUs.
Classification of positive pressure ventilators
• Ventilators are classified by their method of
cycling from the inspiratory phase to the
expiratory phase.
• The signal to terminate the inspiratory activity
of the machine is either:
1. A preset volume (for a volume – cycled
ventilator)
2. A preset pressure limit (for a pressure –
cycled ventilator) OR
3. A preset time factor (for a time – cycled
ventilator).
 Cont.
• Volume – cycled ventilation is the
most common form of
ventilator cycling used due to its
production of a consistent
tidal volume.
• Sometimes pressure – ventilation
may be indicated for adequate
oxygenation of the patient.
Indications for mechanical ventilation
• Respiratory failure (hypoxia, acidosis, hypercarbia etc.)
• Cardiopulmonary arrest
• Trauma esp. of head, neck and chest
• Cardiovascular impairment: strokes, tumors, infection,
emboli, trauma
• Neurological impairment: drugs, poisons, myasthenia
gravis, GBS, bulbar poliomyelitis, quadriplegia etc.
• Pulmonary impairment: infections, tumors,
pneumothorax, COPD, trauma, pneumonia, poisons,
ARDS, Acute Lung Injury (ALI)
 Goals of mechanical ventilation
• Treat hypoxemia
• Treat acute respiratory acidosis
• Relief of respiratory distress
• Prevention or reversal of atelectasis by
putting positive pressure to expand the
alveoli
• Resting of ventilatory muscles e.g. in
morbid tachypnea
 Modes of ventilation
•Basically 2 modes:
1. Spontaneous: no
machine involvement
except in negative –
pressure ventilation.
2. Mechanical: machine
involved
 Cont.
• Mechanical ventilation is essentially
a process that replaces all or part of the
action of the inspiratory muscles as well
as the neural control of breathing. It can
be classified as:
1. Invasive
2. Non – invasive ventilation i.e.
without endotracheal or
tracheostomy tube.
Non – Invasive Ventilation (NIV/ NPPV) for OSA, Central
Hypoventilation Syndrome/ Ondine’s curse
 Respiratory cycles
• 2 basic types of respiratory cycles can be
defined.
1. Controlled cycle (initiated by the
ventilator): the ventilator “controls” the
inspiratory phase by replacing the
respiratory muscle effort & the neural control
by the patient. The patient is paralyzed.
2. Assisted cycle (initiated by the patient):
the ventilator only “assists” the inspiratory
muscles that are active. The patient is not
paralyzed.
 Cont.
• The cycle of the mechanical ventilator can also be classified
according to variables that are controlled during inspiration, i.e.,
• Time
• Flow
• Volume OR
• Pressure
• In clinical practice, hybrid modes (assist – control) are
utilized e.g. in preterm neonates who are predisposed to getting
apneic attacks so set Synchronized Intermittent Mechanical
Ventilation on the machine.
 Controlled ventilation
• Every breath is fully supported by the
ventilator. In classic control modes, patients
were unable to breathe except at the
controlled set rate. They were deeply sedated
&/or paralyzed.
• In newer control modes, machines may act in
assist control, with a minimum set rate & all
triggered breaths above the rate are also
fully supported.
 Cont.
1. VCV – Volume Cycled/Controlled
Ventilation:
• The cycle depends on a predetermined
tidal volume (normally 6 – 8mls/Kg
but varies with the
pathophysiology).
2. PCV – Pressure Cycled/ Controlled
Ventilation:
• The cycle depends on a predetermined
(based on clinical condition) peak
inspiratory pressure (PIP).
 Assisted ventilation
• Assist Control (A/C): the patient is able to trigger a
positive pressure inflation with each breath.
• Synchronized Intermittent Mandatory Ventilation
(SIMV): the patient is able to trigger only a pre – set
number of positive pressure inflations.
• Pressure Support (PS): this is a flow – limited mode of
ventilation (not volume – limited or pressure – limited).
Delivers inspiratory pressure until the predetermined is
achieved (~25% of peak). Clinician sets inspiratory
pressure, applied PEEP (Positive End Expiratory
Pressure), and FiO2 (Fraction of Inspired Oxygen).
Patient triggers each breath.
• PEEP therefore compromises venous return resulting
in ↓ CO & hypotension.
 Cont.
• CPAP (Continuous Positive Airway
Pressure): Continuous level of positive
airway pressure. Patient initiates all
breaths. Functionally similar to PEEP.
Good for OSA (Obstructive Sleep Apnea),
cardiogenic pulmonary edema
• BPAP (Bi – level Positive Airway
Pressure): Mode used during NPPV or
NIV. It delivers a set IPAP and EPAP.
Tidal Volume is determined by difference
between IPAP – EPAP.
 Cont.
• Pressure – regulated volume control (PRVC) : A
form of PACV (Pressure Assist-Control Ventilation) that
uses tidal volume as a feedback control for continuously
adjusting the pressure target. Clinician sets tidal volume
target and the ventilator then automatically sets the
inspiratory pressure.
• Airway Pressure Release Ventilation (APRV): Time
–triggered, pressure-limited, and time-cycled mode. High
continuous positive airway pressure (P high) is delivered
for a long duration (T high) and then falls to a lower
pressure (P low) for a shorter duration (T low). Allows
spontaneous breathing (with or without PS) during both
the inflation and deflation phases.
 Cont.
• Biphasic Ventilation: similar to APRV, except
that T low is longer during biphasic ventilation,
allowing more spontaneous breaths to occur at P
low.
• Adaptive Support Ventilation (ASV):
Ventilator delivers a desired minute ventilation
set by clinician. Breaths are pressure-control +
pressure support for triggered breaths to achieve
desired respiratory rate. Automatically adjusts
respiratory rate and inspiratory pressure to
achieve
 Cont.
• High-frequency ventilation (HFV):
Keeps the lung inflated for extended
period of time to maximize alveolar
recruitment. HFV uses very high
breathing frequencies (120 – 900
breaths/min) coupled with very small
tidal volumes (<1 mL/kg) to provide gas
exchange in the lungs. Supplied by
either jets or oscillators.
Complications of mechanical ventilation
• Barotrauma/ Volutrauma/ pneumothorax
• Nosocomial/Ventilator Associated Pneumonia: the
protective mucociliary complex is bypassed.
• Cardiovascular complications e.g. hypotension/low
cardiac output
• Airway complications
• GI hemorrhage (stress ulcers)
• Failure of tracheostomy stoma to close
• Equipment failure
• Trauma during intubation
• Ventilator dependence
Weaning from mechanical ventilation
• Weaning is the process of
liberating the patient from
mechanical support and
from endotracheal tube.
 Stages of weaning

Treatment of acute respiratory failure

Suspicion that weaning may be possible

Assessment of readiness to wean

Spontaneous Breathing Trial (SBT)

Extubation (while ready to possibly re – intubate)

 Weaning failure

• Failed SBT
• Re – intubation &/or resumption
of ventilatory support following
successful extubation OR
• Death within 48h following
extubation
How to determine the patient is ready for
weaning?
• A reducing oxygen requirement to achieve
adequate SPO2.
• The primary indication for mechanical
ventilation has been sorted out.
• Patient tolerates SBT.
8. CARDIOPULMONARY &
CEREBRAL RESUSCITATION
18/1/2019
BY: DR. NABULINDO M. SUSANE
PEDIATRIC ANESTHESIOLOGIST
DEPARTMENT OF ANESTHESIA UON
 Introduction
• Historically, it was considered impossible, even blasphemous to
attempt to reverse ‘death’
• Man has always wanted to prevent loss of a loved one:
• Old testament Elisha (800 BC)
• Hippocrates (460 – 375 BC)
• One should introduce a cannula into the trachea along the jaw
bone so that air can be drawn into the lungs
• May 1958: Journal of the American Medical Association (JAMA)
• Skillful performance of expired air breathing is an easily learned,
lifesaving procedure. It has revived many victims unresponsive to
other methods and has been proved…’
 Cont.
• 1960 JAMA:
• Chest compression buys time until the external
defibrillator arrives on the scene
• Anyone, anywhere can now initiate cardiac
resuscitative procedures. All that is needed is 2
hands
• 1960 report closed chest cardiac massage + mouth to
mouth ventilation  modern era of CPR
• 16 September 1960 Maryland Medical Society
• 2 techniques of mouth to mouth ventilation + CPR
should be used together
 What is CPR?
• A first aid technique to help people who suffer a
cardiac arrest
• Involves doing chest compressions and
breaths to keep the casualty alive until a
defibrillator arrives
• The MC pre – arrest event is usually an
arrhythmia hence the use of a defibrillator (&
adrenaline)
• CPR on its own is unlikely to restart someone's
heart
 Why CPR?
• Life saving skill
• The only known effective method of
keeping someone alive after
arresting
 Recognition of arrest
• Unresponsive
• Are there signs of life?
• Is breathing normal in terms of rhythm &
rate?
 Scenarios
• Outside hospital
• Lay person
• Trained person
• In – hospital: trained personnel, team effort
 Cardio – respiratory arrest
• Outside hospital: BLS
• In – hospital:
• Basic  Advanced life support
 Simplified adult BLS
• Unresponsive
• No breathing or no normal breathing (only
gasping) 
• Activate emergency response (get
defibrillator) 
• Start CPR (push hard & push fast)  (cycle)
check rhythm/ shock if indicated; repeat
every 2 mins.
 Adult CPR
[DRs. CAB]
Danger
• Ensure there are no dangers to yourself, the
casualty or other bystanders
• Dangers:
• Moving vehicles, electricity, eater, other
people and smoke/ fire
• Needles, blood
• Only help if it is safe for you to do so
 [DRs. CAB]
Response
• If there is no response, the casualty is
unconscious

Shout for help

• Shout for help & get defibrillator
 [DRs. CAB]
• Compressions
• Airway
• Breathing
 Call an ambulance/ chest
compressions
• Call an ambulance
• Commence the chest compressions
• Push down (2 – 2.5 in) 30 times at a
rate of 100 – 120 compressions/
minute
 Airway & Breathing
• No breathing or no normal breathing (gasping)
• Airway maneuvers:
• Chin lift
• Jaw thrust
• Assist ventilation: Bag & mask
• Rate 8 – 10/ min
• Avoid excessive ventilation as it overfills the
lungs & compromises venous return
• Mouth to mouth/ mask/ tube
 Compression: ventilation ratio
• Depends on the age of the patient and how many
rescuers are at the scene
• If alone: 30 compressions to 2 breaths (30:2)
• If more than one rescuer: 15 compressions to 2
breaths (15:2)
• Established advance airway:
• Continuous compression at a rate of ≥100 &
breaths at 8 – 10/ min without interruption
 Defibrillators
• Automated External
Defibrillator (AED) used in an out
of hospital setting.
• Conventional defibrillator is found in
the setting.
• Ensure you know how it works
 To shock or not?
• Shockable rhythms
• Ventricular fibrillation (commonest pre –
arrest arrhythmia in adults)
• Ventricular tachycardia
• Non – shockable rhythms
• Asystole
• Pulseless Electrical Activity (PEA)
 Reversible causes of cardiopulmonary
arrest
[H’s & T’s)
• Hypovolemia
• Hypoxia
• H+ ion (acidosis)
• Hypo/ hyperkalemia
• Hypothermia
• Hypo/ hyperglycemia
 Cont.
• Tension pneumothorax
• Tamponade (cardiac)
• Toxins
• Thrombosis (pulmonary)
• Thrombosis (coronary)
• Trauma
 Post – arrest care after return of
spontaneous circulation (ROSC)
• Multidisciplinary
• Neuroprotection
• Ventilation
• Sedation & analgesia
• Temperature control: targeted, normothermia
• Glucose control: <10mmol/L; avoid hypo/
hyperglycemia
• Seizure control: most patients start seizing
after ROSC due to the preceding period of brain
hypoxia during the arrest.
 Cont.
• Deal with injuries e.g. rib fractures due to
CPR, trauma
protect other organs – kidneys: maintain
normovolemia
• Comprehensive history & full assessment
• Transfer
• Investigations
 PEDIATRIC CPR
[DRs. ABCR]
• Usually due to hypoxia
• 5 Rescue breaths
• Compression ratio: always 15
compressions to 2 breaths regardless of
the number of rescuers (15:2).
• Techniques of chest compression:
• 2 fingers (neonates)
• Heel of the palm
 Cont.
• Danger
• Response
• shout for help
• Airway
• Breathing
• Circulation
• ROSC (post – care)
9. CLINICAL SCENARIOS
IN SHOCK MANAGEMENT
8 /3/2019
TH

BY: DR. C. MWANGI

 Objectives
• Definition
• Pathophysiology
• Classification
• Management principles
 Introduction
- Shock is important since it is a cause of
reversible & preventable deaths.
- You will definitely encounter it in your
clinical practice & it affects all age groups.
- early recognition is key as it is a major
cause of morbidity & mortality – 20%.
- Mortality is high in cases of:
- Diarrhea & vomiting
- Trauma
 Recap
• Components of the CVS
• Fluid: blood
• Pipes: Arteries, veins, capillaries
• Pump: Heart
• CO = Stroke volume X Heart Rate
• BP = CO X Peripheral Vascular Resistance
(PVR)
Cont.
 Definition
• Circulatory shock happens when
tissue perfusion is reduced. The
blood flow is inadequate to meet the
body’s metabolic needs.
• The result is cellular & organ system
dysfunction.
Cont.
 Pathophysiology
• Initial stage
• Hypo – perfusion causing
hypoxia
• Anaerobic metabolism 
decreased ATP
• Metabolic acidosis due to lactic
and pyruvic acid
 Cont.
• Compensatory stage
• Neural, hormonal & biochemical mechanisms
activated to reverse the condition
• Baroreceptors sense hypotension  increased
adrenaline and noradrenaline  increased in
HR  increased BP (BP = CO X SVR)
• Vasoconstriction: divert blood to the CNS
• RAAS  increase in ADH – water retention
• Hyperventilation due to acidosis
Initial

Compensatory
 Cont.
• Progressive stage
• Compensatory mechanisms begin to fail
• Sodium ions build up within
• Potassium ions leak out
• Increase in metabolic acidosis  increased
vasodilation
• Leaky capillary membrane
• Increase in viscosity
Cont.
 Cont.
• Refractory stage
• Decreased blood supply
• Cellular necrosis
• Irreversible organ damage
 Cont.
• The clinical manifestations are
due to:
• The stimulation of the
sympathetic system and
neuroendocrine stress responses
• Symptoms of inadequate oxygen
 Signs
• Hypothermia
• Dry mouth
• Cold & mottled skin, sunken eyes, sunken fontanelle, decreased
skin turgor
• Rapid, weak and thready pulse
• Poor capillary refill
• Hypotension
• Tachypnea
• Anxiety, restlessness, altered mental state
• Decreased UOP
 Classification (Hinshaw & Cox)
• Hypovolemic shock
• Cardiogenic shock
• Distributive shock
• Septic shock
• Anaphylactic shock
• Neurogenic shock
• Obstructive shock
 Hypovolemic shock
• Reduced circulatory volume
• Causes:
• Hemorrhage
• Diarrhea
• Vomiting
• Burns
Cont.
 American College of Surgeons, Advanced
Trauma Life Support (ATLS) classification
Class I Class II Class III Class IV
Blood loss ≤750 750 – 1500 1500 – 2000 ≥ 2000
Blood loss (% of ≤15 15 – 30 30 – 40 ≥ 40
blood volume)
PR/ min < 100 > 100 > 120 ≥ 140
BP Normal Normal Decreased Decreased
Pulse pressure Normal or Decreased Decreased Decreased
increased
Capillary refill test Normal Positive Positive Positive
RR 14 - 20 20 – 30 30 – 40 < 35
UOP ≥30 30 – 30 5 – 15 Negligible
CNS mental status Slightly anxious Mildly anxious Anxious and Confused, lethargic
confused
Fluid replacement Crystalloid Crystalloid Crystalloid Crystalloid + blood
(3:1 rule
 Cardiogenic shock
• Failure of the heart to pump effectively
• Causes:
• MI
• Arrhythmias
• CCF
• Valvular disorders
• Congenital cardiac disease
 Cont.
• Distended jugular veins due to
increased jugular venous pressure
• Murmurs
• Arrhythmias
 Distributive shock
• Dilatation of blood vessels
insufficient intravascular volume of blood
relative hypovolemia  decreases SVR
• Types
• Septic
• Neurogenic
• Anaphylactic
 Unique signs & symptoms
• Normal or markedly reduced CRT (1 – 2 s)
• Systemic VD resulting in hypotension
• Warm skin due to VD
 Septic shock
• Systemic infection causing VD
• Endotoxins released by gram negative
organisms E. coli, proteus, pseudomonas
• Toxins by gram +ve organisms (Streptococci,
pneumococci) & fungi
• Signs:
• Fever
• DIC
 Anaphylactic shock
• This is caused by a severe
anaphylactic reaction to an
allergen or foreign protein.
 Signs and symptoms
• Skin eruptions and large bumps
• Localized edema esp. around the
face.
• Breathlessness & cough due to
narrowing of the airways & swelling
of the throat.
 Neurogenic shock
• Usually caused by trauma to the
spinal cord
• Results in the sudden loss of
autonomic and motor reflexes below
the injury level
• Causes:
• Spinal cord injury
• Drug induced: spinal anesthesia
 Cont.
•Profound bradycardia in
high spinal injuries due to
loss of cardiac accelerating
nerve fibers from the
sympathetic nervous system
at T1 – T4.
 Obstructive shock
• Flow of blood is obstructed which impedes
circulation and can result in circulatory arrest.
• Common causes:
• Cardiac Tamponade: due to pericardial
effusion; prevents venous return.
• Constrictive pericarditis in which the
pericardium shrinks and hardens.
• Tension pneumothorax
• PTE
Cont.
 MANAGEMENT
• Aim
• Restore & maintain the blood circulating
volume
• Ensure oxygenation and BP are adequate
• Re – establishing maintaining perfusion to
organs
 CLINICAL IMPRESSION:
YES NO
Consciousness
CPR
Breathing
Colour

Primary Assessment A, B, C, D, E Intervention at every point.

Secondary Assessment - Focused history: SAMPLE Intervention

- Focused examination

Diagnostic tests & Medication Intervention

 Focused History
• S: Signs & Symptoms
• A: Allergies
• M: Medication currently taking
• P: PMH
• L: Last meal
• E: Events surrounding current presentation
 Cont.

FLUIDS

CIRCULATION

INOTROPIC
SUPPORT
 Clinical shock:
Circulation can be managed with
• Fluids • Inotropic support
• Cardiogenic: 5 – • Adrenaline
10mls/kg • Noradrenaline
• Hypovolemic: • Dobutamine
20mls/kg
• Dopamine
• Distributive: 40 –
• Milrinone
60mls/kg
• Obstructive: sort out
the primary problem
 Fluids
• Differences
• Colloids (have HMW molecules that stay
intravascular) vs. crystalloids (tend to
extravasate)
• Hartman’s vs. NS vs. Dextrose (Read,
electrolyte, constitution, pH)
• Dose:
• Colloids: blood loss 1:1
• Crystalloids: blood loss 3:1 (administer 3
times the crystalloid to replace blood loss)
 Cont.
• 5% Dextrose is not favorable:
• Dextrose is broken down and the fluid
extravasates very fast resulting in edema if
given in large quantity.
 Fluid end points
• 3 – 4 boluses
• Watch out for signs of fluid overload
• Crepitations
• Hepatomegaly
• Edema
• If non – responsive to fluids consider
inotropic support
 Cont.
• Hypovolemic shock: restore circulating
volume
• Cardiogenic shock:
• Main goals are improving the heart’s
effectiveness as a pump, hence:
• Re – establish circulation to myocardium
• Minimize heart muscle damage
 Cont.
• Distributive shock:
• Septic shock: antibiotics, inotropic
support, fluids
• Anaphylactic shock: adrenaline,
corticosteroids, fluids
• Neurogenic shock: fluids, vasopressors
 Cont.
• Obstructive shock:
• Remove obstruction, i.e.,
• Tension pneumothorax
• PTE
• Cardiac tamponade
 Conclusion
• Early recognition & diagnosis is key.
• Fluids are the main stay of
management.
 Additional reading
• Endocrine shock
• 2016 management of sepsis
guidelines
• Principle of peripheral and
central IV access in pediatrics &
adults
10. POST – OEPRATIVE
CARE
1 /3/2019
st

BY: DR. T. CHOKWE

 Introduction
• Post – operative care begins pre
– operatively.
• The clinician must have
anticipated all possible
adventures intra - & post
operatively.
• Patient care should be
optimized.
 Emergence phase
• Recovery from anesthesia can range
from being simple &
uncomplicated to life
threatening.
• It must be managed by skilled
medical and nursing personnel since
it causes great physiological stress
acutely.
Level of care depends on:
• Underlying illness
• Duration & complexity of surgery
• Anesthetic interventions
• Risk of complications
• Transfer of patients:
• Ambulatory, general wards,
• HDU or ICU.
 Management principles
• Assessment, monitoring & intervention

• Control of sepsis

• Nutrition

• Co-morbidity management
 Principles of monitoring
• Trends rather than absolute numbers are preferred.
• Continuous monitoring is done at individualized
frequencies.
• Parameters
• Temperature
• Pulse rate
• Blood pressure
• Respiratory rate
• Pain assessment (resting vs. moving)
• Urine output
 Post – Anesthesia Care
Unit
An open ward design/ recovery room.
Has basic intra – operative level
monitors including:
Oxygen delivery points
Suction apparatus
Resuscitation trolley
 Cont.
• Staffing:
• Anesthesiologist(s).
• Nurses trained in:
• Anesthesia emergence care
• Airway management and ACLS
• Acute post – surgical complications
 1st Post – operative assessment
• Intra – operative history
• Premorbid state
• Interventions in theater
• PMH
• Medications
• Allergies
• Intra – operative complications
• Post – operative instructions
• Recommend Rx & Prophylaxis
 Respiratory status assessment
• Oxygen saturation

• Breathing effort/ accessory muscle use

• Respiratory rate

• Symmetry of respiration/expansion

• Breath sounds, percussion notes

 CVS status assessment
• Hands: warm or cool, pink or pale

• Capillary refill

• Pulse rate, volume & rhythm

• Blood pressure

• Conjunctival pallor
 Volume and fluid balance
• Urine color & rate of production
• Drains & wound soiling
• Jugular Venous Pressure
 Fluid management
• Replacement of deficits
• Deficit is calculated to assess the degree of
dehydration
• Replacement is done: volume for volume
• Crystalloids: N/S & R/L
• Ongoing losses: drains, vomiting,
• Replacement: volume for volume
• Crystalloids: RL, N/S
 Mentation
•The pre – morbid state must
be recorded.
•Assess the:
•Level of consciousness
•Responsiveness
 Common post – operative
complications
• General or specific to the type of surgery undertaken.
• Highest incidence: 1 – 3 days postop
• Distinct temporal patterns of occurrence:
• Immediate (may be associated with the surgery or
anesthetic interventions)
• Early
• Several days after the operation
• Throughout the post – operative period
• Late
 General Post – Op complications
 Immediate:
 Airway obstruction, hypoventilation,
hypoxemia
 Primary hemorrhage
 Hypothermia
 Delayed emergence from anesthesia
 Post – operative nausea & vomiting
(PONV).
 Cont.
• Shock: blood loss, AMI, PTE or sepsis.
• Low urine output: inadequate fluid
replacement intra- & post –
operatively.
• Electrolyte imbalances
• Hypoglycemia
• Hyperglycemia
 Respiratory complications
• Airway obstruction
• Causes
• Laryngospasm
• Soft tissue swelling around the pharynx
• Foreign bodies (loose teeth)
• Hypotonia of pharyngeal muscles
• Viscous fluids (blood)
 Airway security
•Head tilt / chin lift
•Clear the airway
•Airways adjuncts
•Endotracheal
instrumentation
 Hypoventilation
• Opioid drugs
• Hypothermia
• Parenchymal lung disease
• Muscle weakness
• Residual effects of relaxants
• Pain
• Obesity
 Hypoxemia
• A reduced inspired oxygen fraction, N2O
• Hypoventilation
• Ventilation or perfusion mismatch
• Lung collapse or atelectasis
• Bronchospasm
• Pulmonary edema
• Pneumothorax
• PTE
 Delayed emergence
•Poor reversal
•Failure to regain
consciousness 30 – 60
minutes after GA.
 Causes of delayed emergence
• Residual anesthetic

• Sedative & analgesic drug effect

• Perioperative stroke / seizure.

• Hypothermia

• Marked metabolic disturbances

• Comorbidity – esp. hepatorenal system

 Post – operative pain
• Consequences of undertreated pain
• Respiratory: depression/ Hypo –
ventilation
• CVS: tachycardia, HTN, O2 demand, DVT
• Endocrine / Immunologic defects
• Autonomic dysfunction
• Anxiety/psychiatric consequences
• Delayed wound healing, Urine retention
 Modalities of management
• Parenteral: opioids, NSAIDs

• Regional techniques: epidural/ spinal/ nerve

blocks, local infiltration

• Patient – controlled analgesia

• Oral: NSAIDs, opioids, paracetamol

 Fever
• Infections

• Drug / blood reactions

• Tissue damage

• Neoplastic disorders

• Metabolic disorders: thyroid storm, phaechromocytoma,

adrenal crisis, porphyria, neuroleptic malignant syndrome

 Changes in perfusion
• Hypotension: More significant as it impairs end organ perfusion

• HTN: May result in end organ damage e.g. aneurysms

• Pre – operative BPs should be known. What is optimal is what has been

perfusing the patient and not what is described as normal in the texts.
 Criteria for ward transfer
• Independently maintains a secure airway with
intact reflexes
• Spontaneously breathing with adequate oxygen
saturations
• Hemodynamically stable

• (Awake): can raise alarm when something is going

wrong.

• Normothermic & Pain free

 Aldrete Score
Activity Respiration Circulation Consciousness Oxygen
Saturation
2. Moves all 2. Breaths deeply 2. BP + 20 2. Fully awake 2. SpO2 > 92% on
extremities and coughs freely. mmHg of pre – room air.
voluntarily/ on anesthetic level
command

1. Moves 2 1. Dyspneic, 1. BP + 20 – 50 1. Arousable on 1: Supplemental

extremities shallow or limited mmHg of pre – calling O2 required to
breathing anesthetic level maintain SpO2 >
90%

0. Unable to 0. Apneic 0: BP + 50 0. Not responding 0: SpO2 < 92%

move extremities mmHg of pre – with O2
anesthetic level supplementation
 Cont.
•To release a patient from
the PACU, an ideal score
of above 7 is required.
 Summary
• Respiratory and cardiovascular status most
important consideration ‘post –
anesthetically’
• Airway complications demand immediate
attention.
• Pain must be adequately controlled.
• Fluid management entails maintenance
requirements, replacement deficits and
ongoing losses.
11. SPECIALIZED
TECHNIQUES IN
ANESTHESIA AND CRITICAL
CARE
22/2/2019
BY: DR. GACII
 Outline
• Aortic clamping
• Cardiopulmonary bypass
• One – lung anesthesia
• Hypotensive anesthesia
• Non – invasive PPV
• Hyperbaric O2 chamber
 1. Aortic clamping
• Indications
• Aneurysm
• Tumors impinging on aorta
• Stenosis/ coarctation of the aorta
• Dissection
 Anatomy
• Key arteries supplying the spine
• Radicular artery
• Artery of Adamkiewicz (Great radicular
artery)
• These should be kept in mind as the aorta is
clamped to prevent development of post – op
paraplegia.
 Problems of clamping
• Spinal cord injury and paraplegia
• Hypotension
• Interruption of supply to Artery of
Adamkiewicz
• Mesenteric/ bowel ischemia
• Renal ischemia/ AKI
• Hepatic ischemia
• The CNS organs are the most vulnerable.
 Cont.
• Hemodynamic swings
• When the clamp is on: HTN
proximal to the clamp with
accompanying LV strain, ↓ CO, ↑
catecholamine and renin –
angiotensin release lead to
vasoconstriction
 Protective measures
• Maintain a minimum MAP of about 40 – 60mmHg
• Steroids: to mitigate the systematic inflammatory
response to clamping; to protect the spinal cord from
ischemic inflammation
• Hypothermia 33 – 340C: if the clamping period lasts
longer than the usual 2h. Hypothermia slows down
metabolism & reduces energy requirements.
• Mannitol 0.5mg/kg: prevents swelling in CNS
• Frusemide: prevents swelling in the CNS
• Dopamine: for support of MAP
 Problems on clamp removal
• Declamping shock: due to reperfusion injury
& sudden vasodilation
• Sudden decrease in afterload
• Severe hypotension (up to 70% drop)
• Release of vasodilating metabolites from
the ischemic lower body
• Hypokalemia and hypocalcemia
• Decrease in contractility & CO
 Protective measures
• Volume expansion
• Vasoconstrictors: phenylephrine
• Reduce anesthetic dose
• Reduce/ stop vasodilator administration
• Staged unclamping
• Main strategy: keeping the BP normal
 Other strategies for SC protection
• Intravenous thiopentone
• Intrathecal papaverine
• Methylprednisolone
• Magnesium sulphate
• Mannitol
• Beta blockers
• Aortic shunt
 2. Cardiopulmonary Bypass
• Technique used in open heart surgery
(OHS) allowing the surgeons to operate
on a blood – less motionless heart.
• This also protects the myocardium
during OHS.
 Principle of action of heart lung
machine (Pump oxygenator)
• Venous blood is drained by cavity into a venous
reservoir.
• Blood pumped from reservoir to an artificial
lung (oxygenator).
• Oxygenated blood is pumped back into patient's
circulation (aorta)
• Heart is by passed
• Note that the heart lung machine is at a lower
level than the patient. Drainage of blood from
the patient is by gravity
 Time temperature
Module

Blood level detector

Air bubble detector

Pump Head

Pump Head
controls
 Other functions of the pump
oxygenator
• Scavenging shed blood from
operating field.
• Cooling and warming patients
• Cool when on bypass
• Warm when coming off bypass
• Delivers cardioplegia
Normal circulation
 Before bypass
• Heparin 3mg/kg given to prevent any clots
forming in the circuits.
• Activated Clotting Time: ≥ 480s
• All air removed from the bypass circuit
tubing since air can embolize.
 Onset of By Pass
• By-pass started gradually
• Anesthetist administers
sedation/analgesic/muscle relaxant
• Ventilation stopped
• Venous blood runs by gravity into the venous
reservoir
• Flow is gradually increased to cardiac index
of 2.4 – 3.2L/min/m2
 On By – Pass Checklists
• Anesthetist's: MAP, blood gases,
cardiac activity, level of anesthesia,
UOP, Bleeding.
• Perfusionist’s: Blood flow rate, arterial
line pressure, oxygen flow, oxygen
saturation, MAP, coagulation status
(ACT), temperature.
 Cross – clamp & cardioplegia
• After bypass, the patient is cooled depending
on the procedure
• Traditionally: 28 – 300
• Congenital anomalies: may go down to 180
• Cross clamp is applied
• Cardioplegia is infused into the coronaries at
a dose of 10 – 20ml/kg to arrest the heart in
diastole when the heart is relaxed and easy
to work on.
 What is the cross clamp and what
is it’s purpose
• The cross-clamp is a clamp placed across
the aorta & it has 2 main functions:
• To prevent blood flowing back into the
heart
• To allow all the cardioplegia given to be
directed through the coronary openings
 Aortic Cannula
Cross-clamp

Cardioplegia
in

Carioplegia cannula
 Myocardial protection
• Heart normally uses 70% of 02 in blood entering
the coronaries
• Myocardial protection is vital during
cardiopulmonary bypass to reduce the 02
consumption of the heart to a minimum.
• This is achieved via:
• Cardioplegia of the heart in diastole reduces
oxygen utilization
• Cooling of the heart reduces O2 utilization
• Venting the heart: something is put to drain all
the remaining blood in the heart
 Cont.
1. Arrests heart – reduces oxygen consumption (up
to 80%)
2. Arrests heart in diastole – heart is pliable and
easy to operate on
3. Blood cardioplegia – maintains aerobic
metabolism
4. Re – administered approximately every 20mts
(10 – 20mls/kg)
 Components of cardioplegia
• Potassium: Causes electromechanical arrest
• Sodium: Prevents cellular edema. Creates a slightly
hyperosmolar solution
• Calcium: Restores Ca2+ that has been chelated by citrate in
blood
• Bicarbonate: Increases pH to 7.6 – 7.8
• Tromethamine: Increases pH indirectly by combining with
H+ to form bicarbonate
• Glucose & Mannitol: Increases osmolarity. Prevents
intracellular edema
 Other methods of myocardial
protection
• Cooling: Reduces O2 consumption by 10 – 15%
• Venting the heart: Prevents inadvertent re-warming by
blood returning from the lung circulation
• Taping down venous cannulae (caval occlusion): Prevents
systemic blood return around the venous cannulae
• Addition of substrates such as glutamate and aspartate:
Reduces myocardial ischemic injury. Replenish
myocardial ATP stores
 Effects of CPB
• Cardiopulmonary bypass is an abnormal circulatory state
• Effects caused by
• Non – pulsatile flow through circulation
• Hemolysis
• Hemodilution: keep track of the Hb
• Exposure of blood to foreign forces sparks off an
immune response
• Stress response
• Inflammatory response
 Process of termination of CPB
• Patient is rewarmed: If the heart is too cold
<340C there may be ventricular arrhythmias
• Cross clamp is removed. The heart then
starts to beat as coronaries are perfused with
blood.
• Sedation analgesia is repeated
• Vents are stopped
 Cont.
• Arterial flow from the machine is reduced while
venous line to machine is gradually clamped to
fill the heart; inotropic agents may be used to
facilitate this process.
• As heart fills, it starts ejecting (starling’s law)
• Pump stopped and venous line totally clamped
• Heparin reversed with protamine
• Blood remaining in the reservoir can be returned
to patient
 One Lung Ventilation (OLV)
• Purpose:
• Protection of healthy lung from infected/
bleeding one
• Diversion of ventilation from damaged airway
or lung
• Improved exposure of surgical field
• Problems
• Excess airway manipulation
• Risk of movement intraoperative and hypoxia
• More stimulation of airways
 Physiology of OLV
• One lung is collapsed and non –
dependent
• One lung is not collapsed and dependent
• Non – aerated lung goes hypoxic 
pulmonary vasoconstriction  reduces
the VQ mismatch
• Blood is diverted into the aerated lung
 Lateral position
• Hypovolemia
• Compression of heart or greater
vessels
• Thoracic epidural sympathetic
blockade
• Air trapping & high PEEP
 Methods to achieve one lung
ventilation
• Double lumen Endobronchial Tube
• Carlens Tube, Left Robertshaw
tube, Right Robertshaw tube
• Ordinary ETT in one bronchus
• ETT with bronchial blocker
• Separate bronchial blocker inserted
in ordinary ETT
Double lumen endobronchial tube
 Sizing: by patient’s height
• By patients height
• < 165cm 35 – 37F
• 165 – 179cm 37 – 39F
• >179cm 39 – 41F
 Principles of OLV
• Maintain two-lungs as long as possible

• Start 100% O2 then titrate FiO2

• Monitor inspiratory pressures and tidal volumes and adjust the

ventilator to minimize barotrauma
• Monitor closely SpO2and ET CO2

• Surgical field. Is non-dependent lung collapsed?

• VT 8-10 ml/kg

• Keep PaCO2 35 – 40 mmHg

• Low PEEP < 5 cm H2O

 Hypotensive anesthesia
• Purpose
• Reduce blood loss
• Decreases surgical time
• Improved penetration of cement in joint
replacement surgery
• PDA ligation
• Functional endoscopic sinus surgery
• Principle: MAP > 50mmHg
 Techniques
• GA
• Inhalational
• IV: dexmedetomidine, propofol
• Combined
• Regional (lower limb surgery)
• Spinal
• Epidural
 High frequency jet ventilation
• When conventional methods of ventilation
fail to oxygenate e.g. in ARDS, lung
contusion
• Delivers small tidal volumes (1 – 3ml/kg) at
high frequencies 60 – 600 cycles/ minute
• Expiration is passive
• Needs and ETT with a special connector.
 Indications
• Ventilation of stiff lungs e.g. ARDS
• Reduces over distension and
volutrauma
• Prevents cyclical collapse and
expansion of stiff lungs
 Disadvantages
• Pneumothorax,
• Pneumopericardium
• Pneumomediastinum
• SC emphysema
• Hypotension
• Mucosal trauma
• Tracheal necrosis
• Atelectasis
• Hypercapnia
 Non Invasive PPV (NIPPV)
• Ventilation of patients with positive pressure
without intubation/ tracheostomy e.g. in
patients with COAD.
 Features
• Improves oxygenation
• Increases resting lung volume
• Used in type II respiratory failure and does not cause CO2
retention
• Reduces work of breathing: combination of pressure support and
PEEOP reduces diaphragmatic effort & prevents fatigue.
• Reduces RR & dyspnea
• NIPPV is used as intermittent therapy – usually 6 – 12 hr./day
• Patient is awake and un – sedated
• Only effective if no leaks in the system
 Patients likely to benefit from
NIPPV
• Acute hypercapnic respiratory failure –
COPD
• Chronic restrictive lung disease
• Post – extubation resp. failure
• Cardiogenic pulmonary edema when you
don’t want to intubate
• PCP
 Patients excluded from NIPPV
• Hemodynamic instability
• Unable to keep airway: airway obstruction
• In respiratory arrest
 Hyperbaric O2 therapy
• For cyanide poisoning, CO poisoning, gas
gangrene, decompression sickness and air
embolism
• 100% O2 under pressure
• Increased dissolved O2
• Trials
• Connective tissue disorders, compartment
syndromes, chronic ulcers, radiation ulcers
You cannot breathe the air
of anxiety & expect to live
in an atmosphere of peace.
Trust is a choice.
Make it today.
#Jesus_Is_The_Prince_Of_Peace
ANESTHESIA TUTORIAL NOTES
LEVEL VI MBCHB
2019

COMPILED BY EFFIE NAILA

 OUTLINE

INTRAVENOUS ANESTHETICS – 463

MUSCLE RELAXANTS – 479

ANESTHESIA EQUIPMENT – 489

AIRWAY MANAGEMENT – 547

1. INTRAVENOUS ANESTHETICS
14/1/2019
BY: DR. CAROLINE
 Definition

• Anesthesia: loss of sensation

• Types of anesthesia:
– General: patient is not awake
•IV anesthetics
•Inhalational anesthetics
– Regional: patient is awake
 Aims of anesthesia

•Loss of consciousness
•Amnesia
•Analgesia
•Muscle relaxation
•Sedation/ hypnosis
 Stages of anesthesia

1.Induction
2.Maintenance
3.Reversal
 DEPTH OF ANESTHESIA

•Assignment: what are the clinical signs

to assess depth of anesthesia?
 Ideal characteristics of IV anesthetics

• Pharmacokinetics: A drug that is metabolized in the body into inactive

metabolites that are readily excreted
• Pharmacodynamics:
– Rapid onset of action (OOA)
– Short duration of action (DOA) for almost immediate reversal
– Highly potent
– A drug without CNS symptoms e.g. convulsions, hallucinations, night
mares, ↑ metabolic use of oxygen by brain, dissociative anesthesia, nausea
& vomiting (ideally the drug should be an antiemetic)
– A drug that is a bronchodilator, that does not ↓ tidal volume, that does not
↑ secretions, that doesn’t cause laryngospasm or cough
– A cardio – stable drug (does not cause hypotension, hypertension or
dysrhythmia)
– A drug that does not cause any form of renal or hepatic insufficiency
– A drug that does not cause histamine release
 Cont.

• Physical
– The drug should be stable in the environment e.g. Propofol requires
refrigeration
– The drug should be cheap
– The drug that is not decomposed by light
– The drug should be soluble in water hence it can be mixed in water
and diluted to different concentrations
– Drug shouldn’t be painful when injected e.g. sodium thiopental can
cause a lot of tissue necrosis upon extravasation
 MoA in the CNS

• Neurotransmitters:
– Inhibitory: GABA, glycine
– Excitatory: glutamate
• Anesthetics potentiate the effect of
inhibitory neurotransmitters & inhibit the
effect of excitatory neurotransmitters
 Classification

• Imidazole: etomidate (best IV anesthetic; but very expensive)

• Phenol derivative: Propofol
• Ketamine
• Benzodiazepine: midazolam, diazepam, lorazepam
– Diazepam and midazolam are the MC used because of their potency.
Midazolam has a better pharmacokinetic profile than diazepam but
it is expensive.
• Barbiturates: sodium thiopental
– Others: phenobarbitone, methohexital, thiamylal
• Opioids: fentanyl
– Never used alone as the sole agent of anesthesia since they can only
cause adequate surgical anesthesia at toxic doses
 Different uses of IV anesthetics

• Induction
• Maintenance (total intravenous anesthesia, TIVA)
– Preferred in patients with: severe cardiac disease, COPD
(inadequate absorption of the inhalational anesthetic due
to dysfunctional alveolar - capillary membrane)
– In TIVA the drug needs to keep being bloused so there is a
waxing and waning effect; pumps are required to give
target control infusions.
 Cont.

• Sedation: monitored care anesthesia, CT

scan rooms, endoscopy, COD in burns unit
• Barbiturate induced coma in status
epilepticus
• ECT
• Neuroleptanalgesia
 Propofol

• Phenol derivative
• Oil – water emulsion hence not physically soluble in water
• Needs to be refrigerated as it is a good culture medium; administered
within 6h of opening the ampule
• Very painful on injection & ∴, to ↓ pain administer the following before
giving Propofol:
– IV formulation of lidocaine
– Short acting opioid e.g. fentanyl
• Brain – arm circulation time: 30s (highly lipid soluble); DOA: 5 – 7 mins
(10mins max); Plasma Protein Binding (PPB) is about 80%
• Metabolized in the liver into inactive water soluble metabolites that
are excreted via the kidneys.
 Effects of Propofol

• CNS: ↓ O2 utilization by the brain while

maintaining its perfusion, i.e., the brain is nice
& quiet. Doesn’t cause hallucinations, nausea
or vomiting.
• CVS: can cause significant hypotension by ↓ the
SVR.
• Resp.: causes apnea by ↓ RR & tidal volume
(Propofol is thus not safe for use in an out of
ideal theater set up)
 Uses of Propofol

•Indications: neurosurgery
•Contraindications:
– Hypotensive patient e.g. ruptured ectopic,
intestinal obstruction, dehydration
– In ICU due to Propofol Infusion Syndrome
(find out)
 Ketamine

• Stable in the environment. Comes in a vial with a dark rubber top.

Water soluble
• Can be given IV, SC, IM, rectal or via inhalation
• Cheaper compared to Propofol
• Doesn’t cause any pain on injection
• Brain – arm circulation time: 60 – 90s; longer DOA of 15 – 20 mins
• Hangover effect: ketamine is metabolized in the liver & one of its
metabolites called norketamine is active hence prolonging the action
of ketamine. Norketamine is responsible for the characteristic
excitatory phenomenon in patients (hallucinations, involuntary
movements, night mares esp. in females). It may result in convulsions.
To reduce the phenomena, co – administer ketamine with BDZs.
 Effects of ketamine

• CNS: Ketamine ↑ cerebral metabolism, ICP & cerebral blood

flow & hence it is NOT good for neuro – anesthesia.
• Resp.: causes bronchodilation; doesn’t depress the
respiratory system as much when used correctly; causes ↑
secretions (overwhelming bronchorrhea & rhinorrhea). To ↓
secretions, an anti – sialagogue like atropine may be used.
• CVS: causes ↑ in HR & BP; it is not good for coronary disease
patients but is safe for hypotensive patients.
• It has analgesic properties & will thus ↓ the dosage
requirements for other analgesics like opioids.
2. MUSCLE RELAXANTS
15/1/2019
BY: DR. MWITI
 Classification of skeletal muscle relaxants:

Neuromuscular
blocking drugs Spasmolytics
(NMBDs)
 1. NMBDS

Depolarizing (agonists): Succinylcholine

Non – depolarizing (antagonists)

• Isoquinoline derivatives: atracurium,
cisatracurium, mivacurium, doxacurium,
tubocurarine, metocurine
• Steroid derivatives: Pancuronium, pipecuronium,
rocuronium, vecuronium
• Gallamine
 2. Spasmolytics

A. Centrally acting
a. Diazepam
b. Baclofen
c. Tizanidine
d. Pregabalin, Progabide, Glycine, Idrocilamide,
Mephenesin & related drugs, Cannabis
B. Peripherally acting
a. Dantrolene sodium
b. Botulinum toxin
 Drugs for treating acute local muscle spasm

• Cyclobenzaprine
• Carisoprodol
• Chlorphenesin
• Chlorzaxozane
• Metaxalone
• Methocarbamol
• Orphenadrine
 Succinylcholine/ Suxamethonium

• MoA: Succinylcholine (Sux.) Attaches to nicotinic

receptors & acts as an agonist resulting in
depolarization of the NM end plate. Unlike
acetylcholine (Ach) that is instantly destroyed by
acetylcholine esterase (AChE), Sux.:
– Persists at a high concentration in the synaptic
cleft
– Remains attached to the receptor for a longer time
– Provides constant stimulation of the receptor
 Cont.

•Blockade by Sux. therefore is

divided into 2 sequential
phases:
– Phase I (depolarizing)
– Phase II (desensitizing)
 PK

• Very rapid OOA (within 1 minute); very brief DOA (5 – 10 mins)

– It is rapidly hydrolyzed by butyrylcholinesterase/
pseudocholinesterase
• The initial metabolite succinylmonocholine has a weak NM blocking
action
• This is further metabolized to succinic acid and choline
• NM blockade by either SC or mivacurium may be prolonged in patients
with an abnormal genetic variant of plasma cholinesterase
• The dibucaine number is a test for ability to metabolize SC, which
can be used to identify such patients
 PD

• Skeletal muscles: paralysis follows IV admin of Sux.

– Transient muscle fasciculation occurs over the chest &
abdomen within 30s. The arms, neck & leg muscles are
initially relaxed followed by facial and pharyngeal
muscles. The resp. muscles including the diaphragm are
paralyzed last.
• CVS:
– Can cause arrhythmias when administered during
halothane GA
– Has –ve inotropic & chronotropic effect which can be
attenuated by an anticholinergic like atropine.
 Cont.

• Hyperkalemia
– Cases of trauma esp. burns, nerve damage, closed head injury, spinal
cord injury
– N – M disease e.g. muscle dystrophy
– Peritoneal infection
– Renal failure
• ↑ intragastric pressure (but also ↑ LES pressures so ↓ risk of aspiration)
• Post – operative myalgia and muscle damage
• Increased IOP
• Malignant hyperthermia (Rx: Img/kg IV dantrolene then repeat PRN up to
a max of 10mg/kg)
3. ANESTHESIA EQUIPMENT
16/1/2019
BY: DR. MURIITHI
 I. Monitoring devices

•Capnography: this is the measurement

of carbon dioxide in a patient’s
exhaled breath over time.
•Pulse oximeter
•Blood Pressure Machine
The Normal Capnograph
Capnography
 II. SUPRAGLOTTIC AIRWAY DEVICES

• These are devices that keep the upper

airway clear for unobstructed ventilation.
They include:
– Laryngeal Mask Airway
– I – gel
– Guedel Airway/ Oropharyngeal Airway
LARYNGEAL MASK AIRWAY
 CONT.
• This is an alternative to mask
ventilation during GA.
• It however does not protect against
aspiration of gastric contents and is
therefore contraindicated in full
stomach patients.
• Complications:
– Aspiration
– Sore throat
– Tongue numbness/ cyanosis
– Laryngospasm
I – GEL SINGLE USE SUPRAGLOTTIC AIRWAY
• This is an innovative 2nd generation
supraglottic airway device.
• It is designed to create a non – inflatable,
anatomical seal of the hypo - pharyngeal,
laryngeal & perilaryngeal structures whilst
avoiding compression trauma.
• It has a bite guard & a hole through which
gastric contents can regurgitate to avoid
aspiration.
• Sizes are weight specific & they range from
0 – 5.
GUEDEL/ OROPHARYNGEAL AIRWAY
• May be made of elastomeric material,
metal or plastic.
• Is shaped according to the natural
curvature of the mouth.
• Is hollow to allow for passage of air,
vomitus, secretions & suction tube.
• It has a flange at the buccal end to
prevent the oropharyngeal axis from
moving deeper into the mouth and a
means to fix the airway in place.
• Sizing: measure from the incisor to the
angle of the jaw
NASOPHARYNGEAL AIRWAY

•This is used to
maintain the
airway in patients
with an intact gag
reflex e.g. trismus,
mouth trauma
 III. INFRAGLOTTIC DEVICES

•These provide access to the

airway by means of opening the
trachea below the glottis for
ventilation or maintenance of
the airway. They are invasive.
 Endotracheal Tube (ETT)

•Flexible tube placed in the trachea

•Delivers anesthetic gases directly from
the anesthetic machine to the lungs
•Placement of an ETT bypasses the oral
& nasal cavities, pharynx & larynx.
 Advantages

• Open airway
• Less anatomical dead space
• Allows precision in the administration of
anesthetic agents
• Prevents pulmonary aspiration
• Responds to respiratory emergencies
• Monitors respirations
 Properties of an ETT

• Materials
– Polyvinyl chloride: clear and stiffer
– Red rubber: flexible and less traumatic, absorbent, and
may kink or collapse
– Silicone: pliable, strong, less irritating, resist collapse
• Length
– Standard lengths
– Scale marks distance from patient end (centimeters)
• Size
– Measured by internal diameter (ID)
– Range from 1 mm to 30 mm
 Parts of the ETT

• Patient end: beveled

• Machine end
• Connector
• Cuff
• Pilot balloon & valve
 Endotracheal Tube
• A  Valve with syringe attached.
• B  Pilot balloon
• C  Machine end
• D  Connector
• E  Tie
• F  Measurement of length from the
patient end (cm)
• G  Measurement of internal diameter
(mm)
• H  Inflated cuff
• I  Patient end (left – facing bevel)
• J  Murphy eye (prevents blockage)
ARMORED/ REINFORCED ETT

• Just like standard ET tubes,

armored/ reinforced tubes
have the typical left – facing
bevel tip & Murphy eye.
• Their distinctive feature is a
metal wire coil embedded in
the wall of the tube shaft.
• They are less likely to occlude
through kinking.
PRE – FORMED ETT (SOUTH/ NORTH – FACING)

• Indications for a North –

Facing ETT
– Maxillofacial surgery
• Indications for a South –
Facing ETT
– Adenoidectomy
– Eye surgery
Double Lumen ETTs

•They are used for 1

lung anesthesia for
lung procedures
involving 1 lung.
ETT insertion procedure checklist
 Laryngoscope

• Used to increase the visibility of the larynx while

placing an ET tube.
• Parts
– Handle containing batteries (a laryngoscope is held with
the left hand)
– Blade to depress tongue and epiglottis
– Light source to illuminate the throat
• They come in various sizes.
• Types
– Miller blades
– McIntosh blades
Cont.
Laryngoscope handles and blades

A. Size 4 Miller blade

B. Size 4 McIntosh blade.
C. Size 2 Miller blade.
D. Size 1 McIntosh blade.
E. Laryngoscope handle with size 00
Miller blade in unlocked position.
F. Laryngoscope handle with size 3
McIntosh blade in locked position
(note that the light turns on when
the blade is locked).
 CONT.

•The Miller Laryngoscope is used in

infants & neonates as well as for
difficult intubations. It allows one to
lift both the epiglottis & the tongue.
•The Macintosh Laryngoscope allows
one to lift just the base of the tongue
MAGILL’S FORCEPS

• Indications:
– For difficult intubations
– For insertion of throat packs in
children
• Cuffing in children may result in
compression injury since the
narrowest part of their airway is
just below the vocal cords 
laryngeal mucosal ischemia 
post – extubation laryngeal
stenosis.
 IV. Breathing Systems

• Carries anesthetic and oxygen from the fresh

gas inlet to the patient
• Conveys expired gases (containing CO2) away
from the patient
• May be:
– Rebreathing (part of anesthetic machine)
– Non – rebreathing (separate unit from
anesthetic machine)
 Classification

• Open: Fresh gas flow (FGF) from atmosphere alone (no circuit).
• Semi – open: FGF from atmosphere, some apparatus e.g.
Schimmelbusch mask, hand cupping gas from T – piece ± added
O2 etc.
• Closed: Closed to atmosphere; FGF = uptake, CO2 removed.
• Semi – Closed: Closed to atmosphere; FGF > uptake; excess
scavenged; can be
– Semi – Closed Non – Rebreathing (typical ICU ventilator) or
– Semi – Closed Rebreathing (e.g. typical circle circuit);
CO2 removal by absorber or FGF
 Alternative classification by Conway:

•Without CO2 absorbers: Mapleson

type, Resuscitation Bags
•With CO2 absorbers: Circles, Waters
(to-and-fro)
Mapleson Circuits
 Mapleson A (Magill’s circuit)

• FGF enters at the end remote from the

patient.
• There is an expiratory valve at the face
mask end.
• Designed to get the reservoir bag away
from the patient during maxillofacial
surgery.
 Mapleson B & C systems

• FGF at the face mask end where the patient is.

• The Mapleson type C system has no corrugations
unlike the type B.
• These are inefficient since once the bag is full during
expiration, FGF is vented.
• Not suitable for spontaneous breathing since
rebreathing is inevitable (with C02 entering the
tubing unless FGF exceeds the peak inspiratory flow
rates.
 Mapleson D, E & F systems

• FGF enters at the patient's end.

• The D system has an expiratory valve proximal to the
reservoir bag with FGF at the patient’s end.
• The E system (Ayer’s T – piece) has the valve & FGF
at the patient’s end & includes no reservoir bag. It’s
commonly used in pediatric patients.
• The F system (Jackson – Rees modification of the
Ayre’s T – Piece) includes a reservoir bag with the
valve & FGF at the patient's end.
 Closed circuits

• These are also called circle/ CO2 absorption circuits.

• In this case gases are recycled.
• The gases are humidified using the following means:
– Heat Moisture Exchange/ Bacterial Filter
– Bubbling gas through a water bath
• The tube is connected so a canister containing soda
lime which absorbs CO2. Soda lime contains: 94%
Ca(OH)2, 5% NaOH, 1% KOH, 0 – 2% Silica & 14 – 19%
H20.
 Cont.

• Ca(OH)2 free soda lime reduces compound A

production markedly.
• Desiccated soda lime can produce CO.
• Silicates prevent powdering.
• Fresh soda lime has a pH of 12 which decreases as
CO2 is absorbed.
• White S/L contains ethyl violet; critical pH is 10.3.
• Pink S/L contains phenolphthalein; critical pH is 7
where it becomes colorless.
 Cont.

•Reactions of CO2 with soda lime

– NaOH + CO2 + H2O  Na2CO3 + H2O +
Heat
– Na2CO3 + Ca(OH)2  Ca2CO3 + NaOH
 HUMIDIFIERS

•There are 2 types of humidifiers:

– Heat Moisture Exchange/
Bacterial Filter
– Bubbling gas through a water bath
 HME

• This contains a hygroscopic

structure that traps moisture
& heat in the patients
breath.
• Has disposable &
undisposable parts.
• Has a port for sampling gases
going into the patient.
 SPINAL NEEDLE

• These come in different sizes.

• They have a tightly fitting removable
stylet to avoid tracking epithelial
cells into the subarachnoid space.
• They can be classified as either:
– Sharp (cutting) – tipped e.g.
Quincke needle
– Blunt – tipped/ pencil point e.g.
Whitacre needle (↓ incidence of
post – dural puncture headache)
 Cont.

• A smaller gauge, pencil point needle

provides a much more difficult
subarachnoid access but the risk of a post
– spinal headache is lower.
• A bigger gauge needle provides better
subarachnoid access but with a greater
risk for a post – spinal headache.
 Indications of a spinal needle

• Administration of spinal anesthesia for

operations below the level of the
umbilicus.
• Diagnostic Lumbar Puncture.
• Therapeutic Lumbar Puncture.
• Administration of intrathecal
chemotherapy.
 Specific technique for spinal anesthesia

• Approaches:
– Midline
– Paramedian: preferred in patients with
severe scoliosis & kyphoscoliosis
• Patient position:
– Lateral decubitus
– Sitting
– Prone
 Specific technique for spinal anesthesia

• Assemble requirements
• Infiltrate with LA
• Identify landmarks: below L1
• Advance spinal needle slowly from the skin through
deeper structures, angling slightly towards the head
until 2 ‘pops’ are felt. The 1st is the penetration of
the ligamentum flavum & the 2nd that of the dura –
arachnoid membrane. Successful dural puncture is
confirmed by withdrawing the stylet to verify free
flow of CSF.
 Cont.

• With small-gauge needles, (<25 g), aspiration

may be necessary to detect CSF.
• If free flow occurs initially, but CSF cannot be
aspirated after attaching the syringe, the
needle likely will have moved.
• Persistent paresthesias or pain with injection
of drugs should alert the clinician to withdraw
and redirect the needle.
 Layers penetrated on spinal anesthesia

• Skin
• Subcutaneous tissue
• Supraspinous ligament
• Interspinous ligament
• Ligamentum flavum
• Epidural space
• Dura matter
• Subdural space
• Arachnoid matter
• Subarachnoid space.
Factors affecting the dermatomal spread of anesthesia
 Baricity of LA solution

• This is the density of LA solution relative to CSF density.

• CSF has a specific gravity/ baricity of 1.003 – 1.008 at 370C. A
hyperbaric solution of LA is denser/ heavier than CSF whereas a
hypobaric solution of LA is less dense/ lighter than CSF.
• LA can be made hyperbaric by addition of glucose or hypobaric by the
addition of sterile water or fentanyl.
• With the patient in a head – down position, a hyperbaric solution
spreads cephalad & a hypobaric solution spreads caudad. Vice versa is
true in a head – up position. In lateral position, a hyperbaric solution
will spread towards the dependent position.
• An isobaric solution tends to remain at the level of injection. An
anesthetic solution is mixed with CSF (1:1) to make them isobaric.
 Cont.

• Hyperbaric solutions tend to move to the most

dependent area of the spine (normally T4 – T8
in the supine position). With normal spinal
anatomy, the apex of the thoracolumbar
curvature is T4. In the supine position, this
should limit a hyperbaric solution to produce a
level of anesthesia at or below T4.
 Cont.

1
• Lumbar CSF volume ∝
dermatomal spread
– ↑ intraabdominal pressure or conditions that cause
engorgement of epidural veins (pregnancy, ascites,
large abdominal tumors) thus ↓ CSF volume are
associated with greater dermatomal spread for a
given volume of injectate.
• Site of injection: the more cephalad the site, the
more cephalad the level.
Spinal anesthetic agents
 Spinal anesthetic agents

• Hyperbaric bupivacaine and tetracaine are 2 of the

MC used agents for spinal anesthesia.
– Both are relatively slow in onset (5 – 10 min) and
have a prolonged duration (90 – 120 min).
– Spinal tetracaine produces motor blockade more
consistently than dose an equivalent dose of
bupivacaine.
• Only preservative free solutions are used.
 Adjuvants

• Addition of vasoconstrictors (𝛼 adrenergic

agonists, epinephrine 0.1 – 0.2mg) & opioids
enhance quality &/or prolong duration of spinal
anesthesia.
• Vasoconstrictors seem to delay uptake of LA
from CSF and may have weak spinal analgesic
properties.
• Opioids & clonidine can also be added to
improve both quality and duration.
 Cont.

• Epinephrine prolongs duration of bupivacaine modestly; of

tetracaine by >50%.
• Phenylephrine prolongs tetracaine anesthesia; has no effect
on bupivacaine spinal blocks.
• Experience with ropivacaine is limited but it has been used.
• Lidocaine & procaine: relatively rapid onset (3 – 5min) &
short duration (60 – 90 min); duration only modestly
prolonged by vasoconstrictors.
– Lidocaine is no longer used by some due to the
phenomenon of transient neurological symptoms & Cauda
Equina Syndrome (CES)
 EPIDURAL NEEDLE

• Standard epidural needle is typically a 17 – 18

gauge & has a blunt level with a gentle curve of
15 – 300.
– The blunt curved tip theoretically helps to
push away the dura after passing the
ligamentum flavum instead of penetrating it.
• The layers penetrated include:
– Skin, subcutaneous tissue, supraspinous
ligament, Interspinous ligament, ligamentum
flavum, epidural space
• The Tuohy needle is MC used. The straight
needles (Crawford needles) may have a greater
incidence of dural puncture but they facilitate
passage of an epidural catheter.
 Cont.

• An epidural can be used as a single shot

technique or with a catheter that allows
intermittent boluses &/or continuous infusion.
• Can be used for surgical anesthesia, obstetric
analgesia, post – operative pain control &
chronic pain management.
Agents for epidural anesthesia
 Major C/I to Neuraxial anesthesia

• Patient refusal
• Bleeding diathesis
• Severe hypovolemia
• Elevated ICP (particularly with an intracranial
mass)
• Infection at the site of injection
• Severe aortic stenosis
• Severe mitral stenosis
 Relative C/I

• Sepsis
• Uncooperative patient
• Demyelinating lesions
• Pre – existing neurological deficits
• Severe spinal deformity
• Severe LV outflow obstruction: HCM
 Complications of Neuraxial anesthesia

• Adverse or exaggerated physiological responses:

urinary retention, high block, total spinal anesthesia,
cardiac arrest, anterior spinal artery syndrome,
Horner’s syndrome
• Complications related to needle/ catheter
placement: backache, dural puncture leak (post –
dural headache, diplopia, tinnitus), Neural injury,
Bleeding, arachnoiditis, meningitis, epidural abscess
• Drug toxicity: systemic LA toxicity, transient
neurological symptoms, Cauda Equina Syndrome
4. AIRWAY MANAGEMENT
17/1/2019
BY: DR. GACII
 INTRODUCTION

• Airway management comprises measures to

keep the upper airway patent in the patient
with an at risk airway e.g. reduced level of
consciousness, inhalational burns, head & neck
tumors, trauma, GA, foreign bodies
(emergency do abdominal thrusting) etc.
 OBJECTIVES

•Airway anatomy and function.

•Differences between pediatric/adult
airway.
•Evaluation of the airway.
•Clinical management of the airway.
 Airway anatomy

• Upper airway:
– Nasal & oral cavities
– Pharynx
– Larynx
– Trachea
– Principle Bronchi
• Lower airway
 5 differences between pediatric and adult airway

More rostral/ cranial Relatively larger Omega, Ω – shaped

larynx: C2 – 3 tongue epiglottis

Funnel shaped
larynx: narrowest
part of the Angled vocal cords
pediatric airway is
the cricoid cartilage
 1. More cranial/ rostral larynx

• The laryngeal apparatus develops from the brachial clefts & descends
caudally. The infant’s larynx is higher in the neck (C2 - 3) compared
to the adults (C4 – 5).
 2. Relatively larger tongue

•Obstructs the airway.

•Obligate nasal breathers.
•Straight laryngoscope blade
completely elevates the epiglottis & is
preferred for pediatric laryngoscopy.
 3. Omega, Ω – shaped epiglottis

• Adult epiglottis is broader with its axis

parallel to the trachea.
• Infant epiglottis is omega – shaped (Ω) & is
angled away from the axis of the trachea.
• It is more difficult to lift an infant’s
epiglottis with a laryngoscope blade.
 4. Funnel shaped larynx

• The narrowest part of the infant’s larynx is the

underdeveloped cricoid cartilage, whereas in the
adult it is the glottis opening (vocal cord).
• Tight fitting ETT may cause edema & trouble upon
extubation.
• Uncuffed ETT is preferred for patients < 8yrs. Old
• Fully developed cricoid cartilage occurs at 10 – 12
yrs. Of age.
ADULT INFANT
 5. Angled vocal cords

• Infant’s vocal cords have more angled

attachment to trachea whereas adult
vocal cords are more perpendicular.
• Difficulty in nasal intubations where
blindly placed ETT may easily lodge in
anterior commissure rather than in the
trachea.
 Evaluation of the airway

•History
•Physical examination
•Special investigations
 History

•History of difficult airway.

•Complications during intubation
– Desaturation.
– Bradycardia.
•Airway symptoms/diseases
 P/E: Signs of airway obstruction

• Hoarse voice
• Decreased air entry & exit
• Stridor
• Retraction of suprasternal/ supraclavicular/
intercostal space
• Tracheal tug
• Restlessness
• Cyanosis
 Cont.

•Assess:
– Ease of opening and maintenance of
the airway
– Teeth
– Neck movement
 Anatomic features associated with difficult airway management

• Short muscular neck

• Receding mandible
• Protruding maxillary incisors
• Long high arched palate
• Inability to visualize the uvula
• Limited TMJ mobility
• Limited cervical spine mobility
 Mallampati’s classification

•Used to assess the difficult of

intubation & risk of sleep apnea
•Use in combination with other ways of
assessing the airway
 Special investigations

•CT scan
•MRI
 PRINCIPLES OF AIRWAY MANAGEMENT

• First step is positioning the airway. How to open

the airway:
– Non – equipment methods:
•Head – tilt (sniff position): small pillow,
flexion at shoulder & extension at upper neck
•Chin lift
•Jaw thrust
Place the patient in a lateral decubitus position
to prevent aspiration as they are being taken to
hospital.
 Cont.

• Equipment methods of keeping the airway patent::

– Tongue depressor
– Suction
– Oropharyngeal airway/ Guedel airway
– Nasopharyngeal airway
– Laryngeal Mask Airway
– Combitube
• To secure the airway: Endotracheal Intubation.
OROPHARYNGEAL/ GUEDEL AIRWAY
NASOPHARYNGEAL AIRWAY
 Bag & Mask Ventilation

• This is a must know life saving skill

• Involves the use of a face mask & ambu bag to
ventilate the patient
• Masks/ bags come in different sizes hence one
has to use the correct size for each patient
• Techniques:
– One hand
– Two hands
 Endotracheal Intubation

• Indications:
– Airway protection: unconsciousness, trauma,
inhalational burns, airway lesions
– Maintenance of airway patency: trauma,
inhalational burns, airway lesions
– Pulmonary toilet
– Application of Positive Pressure Ventilation (PPV)
– Maintenance of adequate oxygenation
 Requirements of endotracheal intubation

• Laryngoscope: curved/ straight, working,

appropriate size
• Endotracheal tube (ETT): cuffed/ non
cuffed; appropriate size & a size smaller
• KY jelly
• Suction
• Stylet
 Cont.

• Airway: oro/ nasopharyngeal

• Bag & mask
• Drugs: Sedative, Muscle relaxant
• Oxygen
• Monitoring devices: Stethoscope, pulse
oximeter, ECG, capnography
• Strapping/ tape to secure the tube
• An assistant
LARYNGOSCOPE
 CONT.

•The Miller Laryngoscope is used in

infants & neonates as well as for
difficult intubations. It allows one to
lift both the epiglottis & the tongue.
•The Macintosh Laryngoscope allows
one to lift just the base of the tongue
ENDOTRACHEAL TUBE
 ETT sizing (internal diameter in mm)

Age Size Length

Premature 2-3 6–7
Term 3-5 7–9
Infants 4 9 – 11
Children (2 – 10y) Age Age
X4 + 12
4 2
Pre - adolescents 6.0 18 – 20
Adolescents 6.5 – 8 21 - 24
 Procedure of endotracheal intubation

• Position:
– Sniffing position for adults
– Neutral position for children & infants
• Administer drugs: sedation, muscular
relaxation, muscarinic blockade
• Bag & Mask Ventilation (BMV) until patient
is relaxed
 Direct laryngoscopy

• Hold the handle with the left hand.

• Insert the blade through the right side of
the mouth sweeping the tongue away.
• Lift the laryngoscope vertically to lift the
base of the tongue off the vocal cords.
 Cont.

•Insert the tip of the ET tube through

the groove on the right side of the
laryngoscope blade.
•Ensure you visualize the tube going
through the vocal cords (1 monitor of
st

intubation).
 Summary of technique of routine intubation

• (Preoxygenation)
• Administration of sedative
• Adequate mask ventilation
• Administration of rapidly acting NMBD
• Intubation
• Confirm tube in trachea
 RAPID SEQUENCE INTUBATION

• This is a special process of ET intubation that is used in

emergencies e.g. obstetrics when the patient:
– Is at a high risk of pulmonary aspiration
– Has impending airway compromise
• It differs from the normal in that artificial ventilation is
generally not provided from the time the patient goes apneic
(on sedatives) until after successful intubation is achieved.
This minimizes insufflation of air into the patient’s stomach
which might otherwise provoke regurgitation & consequent
aspiration.
• Good candidates for RSI are patients with a full abdomen e.g.
intestinal obstruction, pregnancy etc.
 Procedure for RSI

1. Assemble requirements as for ETT plus a trained assistant

2. Pre – oxygenate with 100% O2 for 3 – 5 minutes
3. Apply cricoid pressure/ Sellick maneuver (this is the only
cartilage that’s a complete ring) to obstruct the esophagus
& prevent regurgitation
4. Administer rapid onset sedative & muscle relaxant (there is
no mask ventilation).
5. Proceed with inserting the ETT with minimal delay.
6. Release the cricoid pressure.
 How to know the tube is in the right place:

• Visualization of the ETT tip going through the vocal cords.

• 5 – point auscultation (2 points on the upper chest, 2 points
on the lower chest & at the epigastrium)
– Check for air entry
– Listen for gurgling sounds
• End Tidal CO2 (ETCO2) on capnography, (at least 3 – 5 waves)
is the gold standard for confirming intubation
• Observe the chest rise & fall
• Large spontaneous exhaled TV
 Cont.

• Fibreoptic visualization of cartilaginous

rings of the trachea and tracheal carina
• Respiratory gas moisture disappearing on
inhalation & reappearing on exhalation
• No gastric distention
• Reservoir bag having the appropriate
compliance
 Difficult airway

• May be:
– Difficult intubation
– Difficult ventilation
 Techniques for difficult ventilation

• Oral/ nasal airway

• 2 – person mask ventilation
• LMA
• Surgical airway access
• Esophageal – tracheal combitube
 Techniques for difficult intubation

• Stylet
• Alternative laryngoscope blades
• Awake intubation
• Blind intubation (oral or nasal)
• Fibreoptic intubation
• Surgical airway access
 Failed intubation

• Call for help

• Reposition the patient
• Do BMV to oxygenate the patient as you buy
time
– If you can’t ventilate, do a
cricothyroidotomy
• Use the adjuncts e.g. supraglottic airways
• Consider a formal tracheostomy
 Procedure for cricothyroidotomy

• Take a knife & incise the cricothyroid

membrane.
• Put a 4.5 – 5 tube.
• This will oxygenate the patient for about 20
minutes
• Complications: bleeding, surgical emphysema
• Plan for a formal tracheostomy
 Complications of ETT

• Malposition: Esophageal intubation, bronchial

intubation (too deep).
• Trauma: tooth damage; lip, tongue mucosal
laceration;, dislocated mandible;
retropharyngeal dissection; cervical spine
injury; cords;
• Physiologic reflexes: HTN, arrhythmia, raised
ICP & IOP; laryngospasm (esp. when
intubating a patient that isn’t adequately
sedated & relaxed), bronchospasm
 CONT.

• Tube malfunction:
– Obstruction of the tube (usually by mucus plug) in patients
that are intubated for the long term
• Murphy’s eye is to prevent obstruction
– Cuff perforation
– Kinking of the tube
– Dislodging of the tube
• Aspiration
• Infection
 Extubation

• Prepare as for intubation

• Be ready to reintubate
• Have a way to supplement oxygen
 END

Always render more & better service

than is expected of you no matter what
your task may be; for the measure of a
man’s greatness is not the number of
servants he has, but the number of
people he serves.
#Jesus_Over_All