AIO Anesthesia Toronto Notes 2023
• accidental extubation
• insufficient cuff inflation or cuff laceration: results in leaking and aspiration
• laryngospasm (see Extubation, A20, for definition)
• bronchospasm
• accidental extubation
Difficult Airway
• difficulties with bag-mask ventilation,supraglottic airway, laryngoscopy, passage ofETT through the
cords, infraglottic airway, or surgical airway
• algorithms exist for difficult airways (Can I Anesth 2013;60:1119- 1138),see .\ppcndkcs. A30
• preoperative assessment (history of previous difficult airway,airway examination) and preoxygenation are important preventative measures
• if difficult airway expected, consider:
• awake intubation
intubating with bronchoscope, fiberoptic laryngoscope, video laryngoscope, etc.
• if intubation unsuccessful after induction:
1 . CALL FOR HELP
2. ventilate with 100% O’ via bag and mask
3. consider returning to spontaneous ventilation and/or waking patient
• if bag and mask ventilation inadequate:
1 . CALL FOR HELP
2. attempt ventilation with oral airway
3. consider/attempt LMA
4. emergency invasive airway access(e.g.surgical or percutaneous airway, jet ventilation, and
retrograde intubation)
If you encounter difficulty with tracheal
intubation, oxygenation is more
important than intubation
Oxygen Therapy
• in general, the goal of O’therapy is to maintain arterial 02 saturation (SaO’
) >90%
• small decrease in saturation below SaO’of 90% corresponds to a large drop in PaO’
• in intubated patients, O’is delivered via the ETT
• in patients not intubated,there are many O:delivery systems available; the choice depends on O’
requirements (F
'
iO’
) and the degree to which precise control ofdelivery is needed
• cyanosis can be detected at Sa02 <85%,frank cyanosis at Sa02 - 67%
100 -1
90 Tp H -
12,3-BPG
iTemp 80 -
70 -
--
60 - 12,3-BPG
fTemp 50 -
3«- Low Flow Systems oo
• provide O’
at flows between 0-10 L/min
• acceptable iftidal volume 300-700 mL, respiratory'rate (RR) <25 breaths/min, consistent ventilation
pattern
• dilution of 02 with room air results in a decrease in Fi02
• an increase in minute ventilation (tidal volume x RR) results in a decrease in ROi
• e.g. nasal cannula (prongs)
well tolerated if flow rates <5-6 L/min;drying of nasal mucosa at higher flows
nasopharynx acts as an anatomic reservoir that collects O2
delivered O 2 concentration (FiOa) can be estimated by adding 4% for every additional litre of O’
delivered
provides FiO’
of 24-44% at 02 flow rates of 1-6 L/min
33 - 3
20 .
10 -
-
j
0
) 1(f 20504,
05lS 60
,
70 d096 lOb ' '
PaO?
Figure8. Hb02saturation curve
Reservoir Systems Composition of Air
• use a volume reservoir to accumulate 02 during exhalation, thus increasing the amount of ()2 available 78.1% nitrogen
for the next breath 20.9% oxygen
0.9% argon
0.04% carbon dioxide • simple face mask
• covers patient’
s nose and mouth and provides an additional reservoir beyond nasopharynx
• fed by small bore O2 tubing at a rate of at least 6 L/min to ensure that exhaled CO:is flushed
through the exhalation ports and not rebreathed
• provides F
'
iO’of 55% at O2 flow rates of 10 L/min
• non-rebreather mask
a reservoir bag and a series of one-way valves prevent expired gases from re-entering the bag
during the exhalation phase, the bag accumulates with 02
provides FiO’of 80% at O2 flow rates of 10-15 L/min
n
High Flow Systems
• generate flows of up to 50-60 L/min
• meet/exceed patient’
s inspiratory flow requirement
• deliver consistent and predictable concentration ofO2
• Venturi mask
delivers specific F
'
iOi by varying the size of air entrapment
» O’ concentration determined by mask'
s port and NOT the wall flow rate
enables control of gas humidity
• Fi02 rangesfrom 24-50%
+
AL GRAWANY
All Anesthesia TorontoNotes 2023
Ventilation
• ventilation is maintained with PPV in patients given muscle relaxants
• assisted or controlled ventilation can also be used to assist spontaneous respirations in patients not
given muscle relaxants as an artificial means of supporting ventilation and oxygenation
Mechanical Ventilation
• indications for mechanical ventilation
Tracheostomy
Tracheostomy should be considered in
patients who require ventilator support
(or extended periods ol time. Shown
to improve patient comfort and give
patients a better ability to participate in
rehabilitation activities
apnea
• hypoventilation/acute respiratory acidosis
intraoperative positioninglimitingrespiratory excursion (e.g. prone,Trendelenburg)
required hyperventilation (to lower 1CP)
• deliver PEEP
• increased intrathoracic pressure (e.g. laparoscopic procedure)
• complications of mechanical ventilation
airway complications
a tracheal stenosis,laryngeal edema
• alveolar complications
a ventilator-induced lung injury (barotrauma, volutrauma, atelcctatrauma), ventilatorassociated pneumonia (nosocomial pneumonia), inflammation, auto-PEEP, patient-ventilator
asynchrony
cardiovascular complications
» reduced venous return (secondary to increased intrathoracic pressure),reduced cardiac
output,hypotension
• neuromuscular complications
a muscle atrophy
a increased ICP
• metabolic complications
a decreased CO’due to hyperventilation
a alkalemia with overcorrection ofchronic hypercarbia
Changes in peak pressures in ACV
and tidal volumes in PCV may reflect
changes in lung compliance and/or
airway resistance- patient may be
getting better or worse
Positive End Expiratory Pressure
(PEEP)
• Positive pressure applied at the
end of ventilation that helps to
keep alveoli open,decreasing V/O
mismatch
. Used with all invasive modes of
Ventilator Strategies ventilation
• mode and settings are determined based on patient factors (e.g.idealbody weight, compliance,
resistance) and underlyingreason for mechanical ventilation
• hypoxemic respiratory'failure:ventilator provides supplemental 02,recruits atelectatic lung segments,
helps improve V/Q mismatch,and decreases intrapulmonary shunt
• hypercapnic respiratory failure:ventilator augments alveolar ventilation;may decrease the work of
breathing, allowingrespiratory muscles to rest
Monitoring Ventilatory Therapy
Pulse oximetry.ETCO2 concentration
Regular arterial blood gases
Assess tolerance regularly
Modes of Ventilation
• assist-control ventilation (ACV) or volume control (VC)
everybreath is delivered with a pre-set tidal volume and rate or minute ventilation
extra controlled breaths may be triggeredby patient effort;ifno effort is detected within a
specified amount oftime the ventilator will initiate the breath
• pressure control ventilation (PCV)
a minimum frequency is set and patient may trigger additionalbreaths above the ventilator
allbreaths delivered at a pre-set constant inspiratory pressure
in traditional PCV, tidal volume is not guaranteed, thus changes in compliance and resistance
affect tidal volume
• synchronous intermittent mandatory ventilation (SIMV)
ventilator provides controlled breaths (either at a set volume or pressure depending on whether in
VC or PCV,respectively)
patient can breathe spontaneously (these breaths may be pressure supported) between controlled
breaths
• pressure support ventilation (PSV)
• patient initiates all breaths and the ventilator supports each breath with a pre-set inspiratory
pressure
• useful for weaning off ventilator
• high-frequency oscillatory ventilation (HEOV)
» high breathing rate (up to 900 breaths/min in an adult), very low tidal volumes
used commonly in neonatal and paediatric respiratory failure
• occasionally used in adults when conventional mechanical ventilation Is falling
• non-invasive positive pressure ventilation (NPPV)
• achieved without intubation by using a nasal or face mask
• Bi-level positive airway pressure (BiPAP): increased pressure (like PSV ) on inspiration and lower
constant pressure on expiration (i.e. PEEP)
• CPAP:delivers constant pressure on both inspiration and expiration
Patients who develop a pneumothorax
while on mechanical ventilation require
a chest tube
Causes of Intraoperative Hypoxemia
Inadequate Oxygen Supply
eg. breathing system disconnection,
obstructed or matpositioned ETT, leaks in
the anesthetic machine,loss of oxygen
supply
Hypoventilation
Ventilation-Perfusion Inequalities
e.g. atelectasis,pneumonia, pulmonary
edema,pneumothorax
Reduction in Oxygen Carrying Capacity
e.g. anemia, carbon monoxide
poisoning, methemoglobinemia.
hemoglobinopathy
leftward Shift of the HemoglobinOxygen Saturation Curve
e.g. hypothermia, decreased 2,3-BPG,
alkalosis,hypocarbia. carbon monoxide
poisoning
Right-to-left Cardiac Shunt
LJ
+
A12 Anesthesia Toronto Notes 2023
Table 3. Causes of Abnormal End Tidal CO2 Levels
Hypocapnea (Decreased CO2) Hypercapnea (Increased CO2)
Reservoir
Hyperventilation
Hypothermia (decreased metabolic rate)
Decreased pulmonary blood flow (decreased cardiac output)
Technical issues
Incorrect placemenl ol sampling catheter
Inadequate sampling volume
Hypoventilation
Malignant hyperthermia, other hypermetabolic states
Improved pulmonary blood flow after resuscitation or hypotension
Technical issues
Water in capnogtaphy device
Anesthetic breathing circuit error
Inadequate fresh gasflow
Rebreathing
Exhausted soda lime
Faulty circuit absorber valves
Low bicarbonate
Fresh
gas inlet
VCarbon J dioxide
! absorber
Uni
- direcbonal '
valves
limb Inspiratory>'
Q*j X^
Expiratory
lb V/0 mismatch
Pulmonary thromboembolism
Incipient pulmonary edema
Air embolism Y piece
n
Intraoperative Management <55 -
2
/
lj
Temperature Figure 9. The anesthesia circuit
Causes of Hypothermia (<36.0°C)
• intraoperative temperature losses are common (e.g.90% of intraoperative heat loss istranscutaneous),
due to:
OK environment (e.g. cold room, IV fluids, instruments)
• open wound
• prevent with forced air warming blankets/warm-water blankets, heated humidification of inspired
gases, warmed IV fluid, and increased OK temperature
Causes of Hyperthermia (>37.5-38.3°C)
• drugs(e.g. atropine)
• blood transfusion reaction
• infection/sepsis
• medical disorder (e.g. thyrotoxicosis)
• hypermetabolic states(e.g.malignant hyperthermia, neuroleptic malignantsyndrome,
pheochromocytoma)
• over
-zealous warming efforts
Impact of Hypothermia (<36°C)
• Increased risk of wound infections
due to impaired immune function
- Increases the period of
hospitalization by delaying healing
• Reduces platelet function and Impairs
activation of coagulation cascade,
increasing blood loss and transfusion
requirements
• Triples the incidence of VT and
morbid cardiac events
. Decreases the metabolism of
anesthetic agents,prolonging
postoperative recovery
Sec landmark Anesthesiology Trillstable for nort
nlornuboa on results from study of Wound Infection
a nd Temperature,which detailsthe impactof
mxmotbennia on wound healing and length of stay
asseen in 200 patieimaged 18-80 yr who underwent
electhee colorectalsurgery.
Heart Rate
Cardiac Arrest
• pulseless arrest occurs due to 4 cardiac rhythms divided into shockable and non-shockable rhythms
shockable:ventricular fibrillation (VF) and ventricular tachycardia (pVT)
non-shockable:asystole and pulseless electrical activity (PEA)
• for VF/pVT, key to survival is good early CPK and defibrillation
• for asystole/ PEA, key to survival is good early CPK and exclusion of all reversible causes
• reversible causes of PEA arrest (5 Hs and 5 Ts)
5 Hs: hypothermia, hypovolemia, hypoxia, hydrogen ions (acidosis), hypo/hyperkalemia
• 5 Ts: tamponade (cardiac), thrombosis(pulmonary), thrombosis (coronary), tension
pneumothorax, toxins (overdose/poisoning)
when a patientsustains a cardiac arrest during anesthesia, it is important to remember that there
are other causes on top of the Hs and Ts to consider (e.g.local anesthetic systemic toxicity (LAST),
excessive anesthetic dosing, etc.)
• for management of cardiac arrest,see Appendices, A30
Intraoperative Tachycardia
• tachycardia - HK >100 bpni;divided into sinus tachycardia ( HK = 100-150 bpm) or supraventricular
tachycardia (SVT)
• SVT: can be further divided into narrow complex or wide complex tachycardia
narrow complex:atrial fibrillation/flutter, accessory pathway mediated tachycardia, paroxysmal
atrial tachycardia
• wide complex:VT,SVT with aberrant conduction
• causes ofsinus tachycardia
shock/hypovolemia/blood loss
anxiety/pain/light anesthesia
full bladder
anemia
+
A13 Anesthesia Toronto Notes 2023
febrile illness/sepsis
drugs (e.g.atropine, cocaine, dopamine, epinephrine, ephedrine, isoflurane, isoproterenol,
pancuronium) and withdrawal
hyper- metabolic states:malignant hyperthermia, neuroleptic malignant syndrome,
pheochromocytoma, thyrotoxicosis,serotonin syndrome
•for management of tachycardia,see Appendices, A30
Intraoperative Bradycardia
•bradycardia - HR <50 bpm; most concerning are 2nd degree (Mobitz type 11) and 3rd degree heart
block, which can both degenerate into asystole
•causes of sinus bradycardia
• increased parasympathetic tone vs. decreased sympathetic tone
• must rule out hypoxemia
• arrhythmias (see Cardiology and Cardiac Surtterv. C19)
• baroreceptor reflex due to increased ICE or increased BP
• vagal reflex (oculocardiac reflex, carotid sinus reflex, airway manipulation)
• drugs (e.g. opioids,edrophonium, neostigmine, halothane, digoxin, p-blockers)
high spinal/epidural anesthesia
• hypothermia and hypothyroidism
•for management of bradycardia,see Appendices, A30
Intraoperative
m
Shock Box
SHOCKED
Sepsis or Spinal shock
Hypovolemic/Hemorrhagic
Obstructive
Cardiogenic
anaphylactiK
Endocrine'other (e.g. Addison'
s disease,
hyperthyroidism, transfusion reaction)
Drugs
BP
a- CO x SVR. where CO - SV x HR
SV is a function of preload, afterload,
and contractility
Blood Pressure
Causes of Intraoperative Hypotension/Shock
• shock:inability of cardiovascular system to maintain adequate end-organ perfusion and delivery of
02 to tissues
a)septic shock
see Infectious Diseases,1D20
b)spinal/neurogenic shock
decreased sympathetic tone
hypotension without tachycardia or peripheral vasoconstriction (warm skin)
c) hypovolemic/hemorrhagic shock
most common form of shock, due to decrease in intravascular volume
d) obstructive shock
obstruction of blood into or out of the heart
increased J VP, distended neck veins, increased SVR,insufficient CO
e.g. tension pneumothorax, cardiac tamponade, pulmonary embolism (and other emboli-i.e.
fat, air)
e) cardiogenic shock
inability of the heart to pump an adequate volume of blood
increased|VP, distended neck veins, increased SVR, decreased CO
e.g. myocardial dysfunction, dysrhythmias, ischemia/infarct, cardiomyopathy, acute valvular
dysfunction
f) anaphylactic( K)shock
see Emergency Medicine. PR29
g) endocrine/other
transfusion reaction, Addisonian crisis, thyrotoxicosis, hypothyroid, aortocaval syndrome
see Hematology and Endocrinology
h) drugs
vasodilators, high spinal anesthetic interfering with sympathetic outflow
Causes of Intraoperative Hypertension
• inadequate anesthesia causing pain and anxiety
• pre-existing H I N, coarctation,or preeclampsia
• hypoxemia/hypercarbia
• hypervolemia
• increased intracranial pressure
• full bladder
• drugs (e.g.ephedrine, epinephrine,cocaine, phenylephrine, ketamine) and withdrawal
• allergic/anaphylactic reaction
• hypermetabolic states:malignant hyperthermia,neuroleptic malignantsyndrome,serotonin
syndrome,thyroid storm,pheochromocytoma (see Endocrinology,E29, E40)
n
LJ
Fluid Balance and Resuscitation
• total requirement = maintenance + deficit + ongoing loss
• in surgical settings, thisformula must take into account multiple factors including preoperative
fasting/decreased fluid intake, increased losses during or before surgery, and fluids given with blood
products and medications
• increasingly, Enhanced Recover)'After Surgery protocols recommend consumption of clear fluids up
to 2 h prior to surgery
+
A14 Anesthesia TorontoNotes 2023
•both inadequate fluid resuscitation AND excessive fluid administration increase morbidity
postoperativelv
Maintenance Fluid
•average healthy adult requires approximately 2500 mL water/d
200 mL/dGl losses
800 mL/d insensible losses (respiration, perspiration)
1500 mL/d urine (beware of renal failure)
• maintenance should not exceed 3 mL/kg/h
•increased requirements with fever,sweating, Cil losses (vomiting, diarrhea, NG suction),adrenal
insufficiency, hyperventilation, and polyuric renal disease
•decreased requirements with anuria/oliguria, SIADH, highly humidified atmospheres, and CHT
•maintenance electrolytes
Na ’
: 3 mEq/ kg/d
K'
: I mEq/kg/d
•4-2-1 rule: 4 mL/h first 10 kg, 2 mL/h next 10 kg, I mL/h for every kg after to calculate maintenance
fluid requirement
alternatively, may add 40 to adults who weigh £20kg to calculate maintenance fluid requirement
in mL/h
•e.g. a 50 kg patient'
s maintenance requirements
fluid = (4 mL/h x 10 kg) t (2 mL/h x 10 kg) + (1 mL/h x 30 kg) *40 mL/h + 20 mL/h + 30 mL/h =
90 mL/h * 2160 mL/d
Na '= 150 mhq/d (therefore 150 mEq/2.16 L/d « 69 mEq/L)
K* = 50 rnEq/d (therefore 50 mEq/2.16 L/d *23 mEq/L)
•above patient'
s requirements roughly met with 2/3 dextrose 5% in water (D5W), 1/3 normalsaline
(NS) 0.9%
• 2/3 + 1/3at 100 mL/h with 20 mEq KC1 per litre
Fluid Deficit
• patientsshould be adequately hydrated prior to anesthesia
• total body water (TBW)
= 60% or 50% of total body weight for an adult male or female, respectively
(e.g.for a 70 kg adult male TBW = 70 x 0.6 = 42 L)
• total Na '
content determines ECE volume; [ Na ' ] determines ICE volume
• hypovolemia due to volume contraction
extra-renal Na floss
« Gl: vomiting, NG suction, drainage, fistulae, diarrhea
skin/respiratory:insensible losses (fever),sweating, burns
vascular: hemorrhage
renal Na ’
and H:0loss
diuretics
osmotic diuresis
hypoaldosteronism
salt-wasting nephropathies
renal H’
O loss
diabetes insipidus (central or nephrogenic)
hypovolemia with normal or expanded ECE volume
decreased CO
redistribution
• hypoalbuminemia:cirrhosis, nephrotic syndrome
• capillary leakage: acute pancreatitis,rhabdomyolysis, ischemic bowel,sepsis, anaphylaxis
• replace water and electrolytes as determined by patient’s needs
• with chronic hyponatremia, correction must be done gradually over >48 h to avoid central pontine
myelinolysis
TBW (42 U
I
1
23 1 3
ICFI28 L) ECFI14 L1
1
i i
3/4 1/4
Interstitial (10.5 L) Intravascular (3.5 L)
(Starting's forces maintain balance)
Figure 10. Total body water division
in a 70 kg adult
Table 4. Signs and Symptoms of Dehydration
Percentage of
Body Water Loss
Severity Signs and Symptoms
3% Decreased skin turgor,sunken eyes, dry mucous membranes, dry tongue,reduced sweating
Oliguria, orthostatic hypotension,tachycardia,low volume pulse, cool extremities,reduced
filling of peripheral veins and CVP, hemoconcentration,apathy
Profound oliguria or anuria and compromised CNS function with or without altered sensorium
Mild
6% Moderate
9% Severe
What are the Ongoing Losses?
• traditionally thought that fluid loss during surgery resulted from blood loss, losses from Eoley
catheter, NG,surgical drains, and minor losses due to sequestration of fluid into other body
compartments
• fluid therapy accounting for these losses often resulted in excess crystalloid administration
• goal-directed fluid regimens associated with lower rate of postoperative complications compared to
predetermined calculations, these can be done using point of care ultrasound ( HOCUS), esophageal
doppler, or pulse or pressure variation available either using arterial line monitoring or certain pulse
oximetry
n
J
+
A15 Anesthesia Toronto Notes 2023
IV Fluids
Colloids»s.Crystalloids lor Floid Resuscitationin
Critically IIIPeople
tncteare 06 Syst ter 20t8:C0000567
Purpose:lo assesseftect of colloids vs.crystal cIs
incnticaly illpatients on mortality,need for
transfusions or renal replacement therapy,and
adverse events.
Methods Systematic ev enof tCTs and qsasi-RCTs
irvolvmg trauma,boms,or medical conditons (i.e.
sepsis).Searched CENTRAL.MEDLINE.andEmdase.
Outcomes:65 studes.30020 pancipants.Serenes,
dertrans.aibsmm or FfP (moderate-certainty
erdence).or gelatins (ton-certainty evidence) vs.
crystalloids has no difference onmortality.Starches
slightly increase the need for bindtransfusion
(moderate-certairty evidence),and a bumin or FFP
may make littleor no difference to the need for
renalreplacement therapy (lorn-certainty erdencel.
Evdence for blood transfusions for deifans.and
aSummorfFP.isaittrtain.
• replacement fluids include crystalloid and colloid solutions
• IV fluids improve perfusion but NOT O’
carrying capacity of blood
Initial Distribution of IV Fluids
• H’
O follows ions/molecules to their respective compartments
Crystalloid Infusion
• salt-containing solutions that distribute only within ECF
• consensus guidelines recommend use of balanced crystalloid (i.e. Ringer’
s lactate) over NS for routine
replacement and resuscitation
• maintain euvolemia in patient with blood loss: 3 mL crystalloid infusion per 1 mL of blood loss for
volume replacement (i.e. 3:1 replacement)
• best practice is to use goal-directed therapy
• if large volumes are to be given, use balanced fluids such as Ringer’s lactate or Plasmalyte’, as too
much NS may lead to hyperchloremic metabolic acidosis
Colloid Infusion
« includes protein colloids (albumin and gelatin solutions) and non-protein colloids (dextrans and
starches, (e.g. hydroxyethyl starch) (HES))
• distributes within intravascular volume
• 1:1 ratio (infusiomblood loss) only in terms of replacing intravascular volume
• the use of HES solutions is controversial because of recent RCl'
s and meta-analyses highlighting
their renal (especially in septic patients) and coagulopathic side effects, as well as a lack of specific
indications for their use
colloids are being used based on mechanistic and experimental evidence but there is a paucity of
definitive studies investigating theirsafety and efficacy;routine use of colloids should be avoided
Calculating Acceptable Blood Losses
(ABL)
• Blood volume
term infant
adult male
adult female
80 mL/kg
70 mL
'
kg
60mL/kg
• Calculate estimated blood volume
(EBV) (e g.in a 70 kg male,approx.
70 mL'kg)
EBV - 70 kg x 70 mL'
kg- 4900 mL
• Decide on a transfusion trigger.i.e.
the Hb level at which you would
begin transfusion (e.g.70 g/Lfor
a person with Hb(initial) ~150 g/L)
Hb(final) =70 g/L
• Calculate
ABL -Hb(i) -HbfflxEBV
Table 5. IV Fluid Solutions
ECF Ringer’s
Lactate
0.9% NS 0.45% NS D5W
in D5W
2/3 D5W Plasmalyte
1/3 NS
mEq/L Na‘ 142 130 1S4 77 51 140
K 4 4 5
Ca:" 4 3
Mg Hb(i)
'
'
3 3
-150 - 70 x 4900
ct- 103 109 154 77 51 98 150
-2613 mL
• Therefore,in order to keep the Hb
level above 70 g/L.FtBCs would have
to be given after approximately 2.6 L
of blood has been lost
HC03- 27 28’ 27
mOsm/L 280-310 273 308 154 252 269 294
pH 7.4 6.5 5.0 4.5 4.0 4.3 7.4
’ConvertedIrom lactate
Table 6. Colloid HES Solutions
Concentration Plasma Volume
Expansion
Duration (h) Maximum Daily Dose
(mL/kg)
Transfusion Infection Risks
Virus Risk per1unit
pRBCs
Voluven 6% 4-6 33-50 3
Pentaspan1
1:1
10% 1:1.24.5 18-24 28
HIV 1in 21million
Hepatitis C virus
Hepatitis Bvirus
1in13 million
Blood Products 1in25 million
HTLV 1m1-1.3 million
• see Hematology, H54
Symptomatic
Bacterial Sepsis
1in 40.000 from
platelets and1in
250.000 from SBC
West Nile virus No cases since 2003
Source:C4kimJL Pidkertce PR Bloody Easy Fourth
E&ticoed.Tor onto:Snnrytrcok and Women's Coftege
HeatttiScience Centre:2016
+
A16 Anesthesia Toronto Notes 2023
Induction
toenroniinis.Secdsykhorne for Sapid
Sepaer.ee InducticnIntubation
C ochraae 06 SrstIn20«:C0002788
Pirpoie:Ine“
et raciroums treetesursbatug
conditions comparable to“ose of soctnylcbofse
during RSJ iJrtsi«tio- s.
Methods:Systematic rer ew of ICTs or CCIs wi'a
dose of at least 0.6opt)for rotaroseaasd1erg ng
for SiCtnr'
tfOlire.
lesolts:S0tr.-ai.it51berttrperis.SotccySci-a me
was super®.'to rocaroaeafor actiering eiceBest
rt*
atso ro-dtoa(M0.86.95% Cl 0.810 52) ard
dinically acceptable nrtubaboucosdtiocs {IS057.
95% Cl 055-055).
Conclusion:SutanjictKPtcse treated Superior
irtabatoa coed-toss tomaroonra aacberng
excellent andctacatj acteptePe istsPatng
conditions.
Routine Induction vs. Rapid Sequence Induction
• routine induction is the standard in general anesthesia; however, an RSI is indicated in patients at risk
of regurgitation/aspiration (see Aspiration, A5 )
• RSI uses
1. pre-determined doses of induction drugs given in rapid succession to minimize the time patient is
at risk for aspiration (e.g. from the time svhen they are unconscious without an HIT until the time
when the HIT is inserted and the cuff inflated)
2. no bag mask ventilation
3. cricoid pressure may be applied (although there are some exceptions, e.g. trauma to upper airway)
4. use of rapid onset muscle relaxant (i.e. SCh)
Table 7. Comparison of Routine Induction vs. RSI
Steps Routine Induction RSI
Equipment Preparation Check equipment,drugs,suction,and monitors;prepare an alternative laryngoscope blade and a second ETT tube
one size smaller,suction on
100% 02for 3minor 4-8 vital capacity breaths:reduce risk of hypoxemia during apneic period following induction
Most
Soluble
Haiothare
Pre-Oxygenationl
Denitrogenation
Pre-Treatment Agents
Iscriurane
Use agent of choice to blunt physiologic Use agent of choice to blunt physiologic responses to airway
responses to airway manipulation 3 min prior manipulation:if possible,give 3 min prior to laryngoscopy,but
can skip this step inan emergentsituation
Use IV or inhalation induction agent of choice Use pre-determined dose of fast acting induebon agentof choice
Muscle relaxant of choice given after the onset Predetermined dose of fast acting muscle relaxant (SCh or high
dose rocuronium) given IMMEDIATELY after induction agent
DO NOT bag ventilate - can increase risk of aspirabon
Cricoid pressure (Sellick Maneuver) toprevent regurgitation
Sevo;jrsne
to laryngoscopy
Induction Agents Desflurane
Muscle Relaxants Least
of the induction agent Soluble Nitrous Oxide
Ventilation
Additional Helpful
Maneuvers
Bag-mask ventilation
External Laryngeal Manipulation using
Backwards.Upwards.Rightward Pressure
(BURP)
Intubate,inflate cuff,confirm ETT position Intubate once paralyzed (
“
45 s after SCh given),inflate cuff.
confirm ETT position:cricoid pressure maintained untilETT cuff
inflated and placement confirmed
Secure ETT.and begin manual/machine ventilation
Figure 11. Solubility of volatile
anesthetics in blood
Intubation
Effects of CricoidPresssre Compared with a Sfaaa
Procedurein the Sapid SeqaenceInduction of
A nesthesia:TheIrisBaadoaizedClinicalTrial
JAMA Sarg 2015:154|T|5-17
Purpose:To determne :f cricoidress.'
c nqaets
Dulmocary £sp-
'ction pec
-? e.ndergoi-grapid
seq.e:ce sdaction (SSI)of aKSlftesa.
Methods:Jrtozedc
*d c Jtelio
assess3472 patiatsnotary!tugrapidsetjsoce
induction of aresttesia at W academe centers.
Results:ResritsdesMStratedthatOctets
_nde:go;-g anesfesic asirgRSI eper.erce
ncreasedpmeriaaof palaonary aspiration
using ocodpressure»aes compared to thessaa
condition.
Conclusion:This stsdy prordeseiiJe:eto show
tre:ie:g5tof cmdp*ess^
*e -iRSI ard^3indthat
iissuper.or to tSe sham procedine inprevoSag
asptratkuL
Secure
Induction Agents
•induction of general anesthesia may be achieved with intravenous agents and/or volatile inhalational
agents
Intravenous Agents
•IV induction agents are non-opioid drugs used to provide hypnosis, amnesia, and blunt reflexes to
laryngoscopy
•these are initially used to establish the plane of anesthesia rapidly and smoothly
most commonly used is propofol or ketamine
a continuous propofol infusion may be used as an alternative to inhalational volatile agents
during the maintenance phase of general anesthesia. An indication would be malignant
hyperthermia
Table 8. Intravenous Induction Agents
Propofol
(Diprivan:
)
Thiopental (sodium
thiopental, sodium
thiopentone)'
Ketamine (Ketalar 1,
Ketaject )
Benzodiazepines (midazolam Etomidate
(Versed (.diazepam (Valium ),
lorazepam (Ativan ))
Methohexital
(Brevital )
Alkylphenol- hypnotic Short acting thiobarbiturate Phencyclidine (PCP) derivative -
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