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ETT should not have a cuff if the child is under
- 8 years of age
- less edema, barotrauma
- cricoid acts as a physiologic cuff
Sux induced bradycardia MOA? prevention?
- binds muscarinic SA Node receptors
- prevent: atropine 20mcg/kg 2 minutes prior (esp < 5yrs)
hyperkalemic cardiac arrest with sux from?
undiagnosed Duchenne muscular dystrophy
tall peaked T wave
- high pitched breath sound from turbulence
- inspiratory: extrathoracic obstruction (epiglottitis, Laryngotracheobronchitis, Retropharyngeal Abscess, Abscess,Subglottic FB
- expiratory: INTRATHORACIC =Bronchial Asthma, bronchiolitis, IntrathoracicFBRetropharyngeal
If radius is halved, resistance increases
Pediatric narrowest part of airway?
cricoid cartilage (< 8 years old)
Negative Pressure Pulmonary Edema (NPPE)
- cause: laryngospasm, ETT obstruction
- Presentation: frothy pink sputum, SOB, low SpO2, pulmonary edema on CXR.
- risk factor: young males
- tx: CPAP, IPPV, O2. pressors, volume, lasix, diuretic rarely.
wall vs cylinder
- wall: 50psi, Diameter (DISS)
- cylinder: 2200psi, Pin (PISS)
wall check valve:
- cylinder pressure closes
- prevents cylinder gas->wall & cylinder drainage
interchange before DISS
1st check valve for N2O
oxygen pressure sensor shutoff
Wall gas saftey devices
DISS, color, 2nd stage regulator
- O2 E 2200psi = 625L (volume/pressure proportional)
- N2O E 745psi = 1590L
- Air E 1800psi = 625L
- cylinder safety
- PISS, color, regulator
Which regulatory body controls production, standards and transportation of cylinder gases?
pathways for oxygen to flow:
- 1. Power Outlet for Ventilator
- 2. Oxygen Flush Valve
- 3. Pressure Sensor Shutoff Valve
- 4. Oxygen Supply Failure Alarm
- 5. Flow Meter Assembly
- 6. Vaporizers
- green, encased, 35-75 LPM, barotrauma,
- emergency: hirgh freq jet vent w crycothyrotomy
Oxygen Supply Failure Alarm triggered when?
- O2 < 28PSI
- adjactent to shutoff valve
Pressure sensor shutoff valve is held open by
- O2 psi>25
- allows N2O to flow meters
Second Stage Regulator
- before flowmeter, reduce 50->16psi
- O2 is last gas in failure
- variable orifice tubes
- Tapered with the smaller opening at the bottom where the gas enters and the larger opening at the top where the gas exits into the common manifold
Float indicators are read at the
Ball indicators are read at the
center of the ball.
oxygen flow meter is always located
to the right of the other flow meters (downstream) and closest to the common gas outlet
flow meters are aligned in a ______ fashion
vaporizer four paths:
- 1. Relief or Bypass Valve: open when the fresh gas flow exceeds the amount that will ‘pick up’ the set concentration of anesthetic vapor.
- 2. Temperature Bypass
- a. Hot: more vapor, more FGF bypass
- b. Cold: more liquid, more FGF to vaporizing chamber
- 3. Mixing Chamber: mix vaporized w FGF
- 4. Vaporizing Chamber: wicks increase surface are
oxygen content of N2O
16 ÷ 44 *100% = 36.36% by mass
In the vaporizer mixing chamber, gases are
- a) Concentration calibrated
- b) Flow over
- c) Agent specific
- d) Thermocompensated vaporizers
- BP 23.5C, partial pressue 669
- TEC-6 vaporizer is pressurized to 2 atmospheres and temperature is maintained
common gas outlet
- receives all the fresh gas and anesthetic vapors from the machine.
- composed of a 15-mm female slip joint with a coaxial 22-mm male connection with a retaining device to prevent inadvertent disconnection
- granule size 4 and 8 mesh.
- smaller granules->more absorptive surface area & more resistance to air flow
CO2 absorptive capacity
26L/100 g of absorbent
CO2 absorber byproduct
Compound A from SEVO (not with Amsorb)
- color(cant see middle, reversion, deactivation from storage)
- CO2 best indicator is capnogram
94% calcium hydroxide (Ca(OH)2)
Desiccated Absorbant + Inhaled Anesthetics
- Carbon Monoxide
- Desflurane ≥ enflurane > isoflurane >> halothane = sevoflurane
- Most associated with baralyme absorbant – now removed from market
- Soda lime also implicated
- Amsorb Plus is not associated with CO production (no degradation occurs)
- desiccated absorbant
- = HEAT (Fires). Don’t run at low flows
5% sodium hydroxide (2NaOH) catalyst
- 1% potassium hydroxide (KOH) activator.
- Silica : harden the compound and reduce dust \
- CO2 + H20 <-> H2CO3
- H2CO3 + 2NaOH (KOH) <-> Na2CO3 (K2CO3) + 2H20 + HEAT
- Na2CO3 (K2CO3) + Ca(OH)2 <-> CaCO3 + 2NaOH (KOH)
- 80% calcium hydroxide (Ca(OH)2)
- 20% barium hydroxide (Ba(OH)2) catalyst
- More stable than soda lime,
- does not need silica as a binder
- performs better in dry climates
- 15% less efficient based on weight
- as close to pt as possible
- preset alarm <30%
- calibrate daily
- rubber or neoprene
- used during spontaneous or manual ventilation.
- Adult size has 3 liter capacity;
- Pediatric size is 1 liter).
- Neck: 22-mm female fitting
- expands during exhalation as it accumulates exhaled gases and
- contracts during inhalation.
- Information about the patients respirations can be through visual and tactile observation.
reservoir bag max pressure
- 60cm H2O
- stretch bags to increase safety margin
- controls the amount of gas released to the scavenger and the amount of pressure and gas remaining in the breathing system and reservoir bag.
- spontaneous: APL fully opened
- manually or assisted: APL partial open, bag squeezed -> patient not scavenger
APL position: spontaneous
- Fully open
- decrease inspiration resistance
- close slightly if bag completely collapsed
Occupational Safety and Health (NIOSH) standards for anesthetic gases are as follows:
- Nitrous oxide: less than 25 PPM
- Halogenated agents with nitrous oxide: less than 0.5 PPM
- Halogenated agents alone: less than 2.0 PPM
- 660 nm - Reduced Hemoglobin (red)- deoxyhemoglobin
- 940 nm - Oxyhemoglobin (infrared)
- Depended on pulsatile flow
- (SaO2)= ratio of absorbance at these two wavelengths. A ratio of 0.4 is approximately a SaO2 of 100%.
Saturation (%)= PaO2 (mmHg)
- 100 >100 (FiO2 Dependent)
- 95= 90
- 90= 60 (danger!)
- 75= 40 (Mixed venous)
- 50= 27 (P50) (pt probably dead)
- Inc CO (C monoxide), and methemoglobin.
- O2 sat will show normal but O2 is lower
Similar light absorption at 660 nm and 940 nm (1:1 ratio); at high levels, SpO2 approaches 85%.
- Similar absorbance to O2Hb.
- 50% COHb, SaO2 = 50% on ABG, but SpO2 may be 95%, thus producing a falsely HIGH SpO2.
falsely LOW SpO2
dyes (methylene blue > indocyanine green > indigo carmine), blue nail polish, shivering, ambient light
NO EFFECT on SpO2
bilirubin, HbF, HbS, SuHb, acrylic nails, flourescein dye
- clinically apparent with 3 g/dl desaturated Hb
- Hb = 15 g/dl, cyanosis occurs at SaO2 = 80%
- Hb = 9 g/dl (i.e. anemia), cyanosis occurs at SaO2 = 66%.
- Four limb leads + V5 (left anterior axillary line, 5th ICS), allows monitoring of 7 leads simultaneously.
- – V5 is 75% sensitive for detecting ischemic events; II + V5 is 80% sensitive; II + V4 + V5 together is 98% sensitive.
BP Cuff too small
falsely HIGH BP
A-line Transducer Setup
- Zeroing = exposes the transducer to air-fluid interface at any stopcock, thus establishing Patm as the “zero” reference pressure.
- Leveling = assigns the zero reference point to a specific point on the patient; by convention, the transducer is “leveled” at the right atrium.
point at end of expiratory plateau
gradual expiratory upstroke, shortened plateau
- INCREASING BASELINE on Capnogram
- faulty expiratory valve
- inadequate inspiratory flow
- insufficient expiratory time
- CO2 absorber malfunction
max pressure per breath
volume controlled modes
- AC: Assist Control. You set the volume and the rate. The patient always gets this. If the patient tries to inhale the machine also will deliver a breath “assist”.
- SIMV: Synchronized Intermittent Mandatory Ventilation. You set the rate and the volume and also pressure support. Typically set the rate low to encourage patient to breathe. Extra breaths are supported by the pressure you preselect and the ventilator synchronizes breaths with the patient.
Pressure Control Mode.
Set rate & maximum peak airway pressure allowed. Tidal volumes vary in accordance with the pressures
- Set pressure support
- patient does all the work
- Ventilator gives this set pressure to augment what the paitent is doing.
- Useful for weaning.
- Set a backup breath every 30 seconds or patient will get nothing if they don’t breathe.
- Continuous Positive Airway Pressure
- Constant set pressure in cm H2O to the patient.
- The patient exhales against this.
- Positive End Expiratory Pressure.
- Leaves a little positive pressure behind at the end of expiration.
- Useful for preventing atelectasis and increasing oxygen levels as alveoli remain open.
- big breath every few minutes.
- Helps prevent atelectasis and mimics natural breathing.
- 1:2 normal
- shorten it to 1:1 if you are having problems with CO2 retention esp. in laparascopic surgery.
- Beware air trapping.
- COPDers like 1:3
- monitoring nondepolarizing NMBA
- number of twitches and the ratio between the 4th
- and 1st twitch are measured with the TOF.
TOF Surgical relaxation can be achieved when the patient has
2-3 twitches depending on location
Nerve stim setup
red proximal to heart
Four patterns of electrical stimulation:
- Single Twitch – a single pulse 0.2 msec induration given every 1 -10 secs
- Train of Four (TOF) – a series of fourtwitches given within 2 secs, each 0.2 msecin duration
- Tetany – a sustained 5 sec stimulus of 50to 100 Hz
- Double Burst – three stimulations followedby two stimulations, each set separated by750 msec
Sensitivity to NMBs
- Laryngeal muscles (VC)------most resistant
- Obicularis oculi
- Abdominal rectus
- Adductor pollicis
- Extraocular---------most sensitive
- monitor arm or orbicularis
Reversal of NMB is accomplished by using an
standard test of normal clinical function (NMB reversal)
- A sustained head lift for 5 secs remains the
- TOF ratio > 0.7
N.B. Neostigmine will potentiate
- phase I block from sux
- but will reverse a phase II block
If placing electrodes on the face, do not deliver more than
20 – 30 mA or you will stimulate facial muscles directly
Variability in muscle blockade
- (most resistant > most sensitive):
- vocal cords > diaphragm > currogator supercilii (muscle controlling the eyebrow) > abdominal muscles > adductor pollicis > pharyngeal muscles > extraocular
- ligand-gated CL ion channel
- HYPERPOLARIZES, less excitatory
- have GABA and BZD receptors
- ex. thiopental
- bind CNS GABA-A
- blocks CL channels
- stimulate FORMATION of GABA-> strong
- cant decrease pain
- LIVER, zero order
- quick redistribution, fat bound
- MOA: Na+ channel blocker, cannabinoid
- ++: antiemetic, anticonvulsive
- --: vasodilation, hTN, pain on injection
- metabolism: 1/2 life 1-2 hours, rapid redistribution, LIVER
- oil based, protein bound
- MOA: GABA-A, imidazole
- ++: rapid, less CV(no vasodilation), doesn't depress spinal cord activity
- --: adrenocortical suppressive (increased with BZD & narc), seizures
- quick redist, slightly slower than prop, STP
- MOA: NMDA, dissociative, uncompetetive channel blocker
- ++: analgesia, dissociative anesthesia(trauma), bronchodilation, counteract spinal sensitization (crush, amputation injuries)
- --: catecholamine release, elevated BP, hallucinations
- ionotropic receptor ->transfer of electrical signals brain &spinal column.
- To remain open, an NMDA receptor must bind to glutamate and to glycine.
- An NMDA receptor that is bound to glycine and glutamate and has an open ion channel is called "activated."
- Chemicals that deactivate the NMDA receptor are called antagonists.
- NMDAR antagonists fall into four categories:
- Competitive antagonists, which bind to and block the binding site of the neurotransmitter glutamate;
- glycine antagonists, which bind to and block the glycine site;
- noncompetitive antagonists, which inhibit NMDARs by binding to allosteric sites;
- uncompetitive antagonists, which block the ion channel by binding to a site within it.
- Ketamine is an uncompetetive channel blocker. Others include anti Parkinson drugs and some cough medicines such as dextramethorphin.
Why can ketamine sedate children?
Corpus Callosum in children is not fused. Therefore, no hallucinations
- not sole agent
- GABA on different "less powerful" receptor
- metabolism: LIVER,
- Reversed by: flumazenil
- Gprotein that release GABA & endorphins
- CNS & GI
ejection fraction avg
- normal breath
- 500 ccs in a healthy adult.
Inspiratory Reserve Volume:
- max extra volume above and beyond tidal volume.
- About 3 liters for most people.
- What’s left in the lungs after your most forceful expiration.
- About 1200 ccs for most people
Tidal volume plus inspiratory reserve volume. About 3500 ccs.
Functional Residual Capacity:
expiratory reserve volume plus residual volume. AKA what remains after a normal expiration. About 2300 ccs.
- IRV plus tidal volume plus expiratory reserve volume.
- AKA everything a person can do after inhaling as deeply as possible and exhaling as much as possible.
- About 4600 ccs.
Total lung capacity:
vital capacity plus residual volume. Have to calculate it.
point at which residual volume drops below the closure of alveoli. Normal people do not have to worry about this.
opiate receptors MOA
- hyperpolarizes cells, resulting in decreased transmission of impulses
- decreased release of acetylcholine (slow movements, respiratory depression).
difficult mask ventilation:
- large face
- facial deformity or injuries
- History of difficult intubation.
- Trach scar!
- Short thick neck, obesity
- History of snoring or OSA
- Mallampati score
- Ability to prognath!!!
- Thyromental distance
- Neck mobility
- Interincisor gap
- Poor (< 4 METS): eat, dress, bathe, walk slowly on 2 level blocks, light housework, light recreational activities, moderate house work
- Moderate (4-7 METS): climb a flight of stairs or walk up hill, walk briskly, heavy housework, sexual relations, moderate recreational activities
- Excellent (> 7 METS): climb stairs briskly or walk upstairs with 1-2 bags of groceries, heavy outdoor work, strenuous sports
3.5 mL O2 per kg of body weight x minutes
(between 7 days and < 1 month) is an active cardiac condition
Smoking cessation for at least
Zofran & SSRIs
- Have last meal by 8 pm night before surgery.
- “NPO after midnight”.
- Clear liquids (can see through it) 2 hours before procedure.
- Breast milk: 4 hours
- Formula/Nonhuman milk: 6 hours
- Everything else: 6-8 hours
preop Oral hypoglycemics :
hold day of surgery (24 hours for metformin)
- take half dose of long acting—
- hold short acting--
- do as first case.
- Check sugar before and after surgery.
- TAKE beta blockers, calcium channel blockers and alpha agonists.
- HOLD ACE inhibitors.
preop Psych/pain meds:
Take night before.
preop Aspirin and NSAIDS:
- hold for 5-7 days.
- Bridge patient with LMWH until 12 hours before surgery.
FA/Fi reaches 1 equilibrium is depended on
- a. Delivery into the lungs
- (Input into the Lungs)
- b. Uptake by the blood
- (Output from the Lungs)
more soluble the anesthetic
- (such as isoflurane)
- greater uptake
- slower the rate of induction
- lower the height of the FA/Fi ratio curve.
least soluble the anesthetic
- (nitrous oxide, desflurane),
- faster the rise of FA/Fi
- faster the rate of induction
- higher the height of the FA/Fi ratio curve.
pharmacokinetics of inhalational agents phases
- – Absorption
- – Distribution (to the CNS/brain = site of action)
- – Metabolism (minimal)
- – Excretion (minimal)
- ultimate goal is to establish a particular partial
- pressure of an agent in the alveoli (PA)
- partial pressure will equilibrate with the CNS tissue to produce an anesthetized state
- decrease CMO2 (cerebral metabolic rate)
- increase CBF (via direct vasodilatation) (may inc ICP)
- dose-related decrease in blood pressure
- muscle relaxant (except N2O)
- dose-dependent depression of the ventilatory response to hypercarbia and hypoxia
- Increase RR + decrease tidal volume = preserved minute ventilation
- MAC mirrors the brain partial pressure of an agent
- 1 MAC, 50% of anesthetized rats do not react to placement of a tail clamp.
- • MAC is an ED50 concentration.
- The ED95 is 95%, so at 1.3 MAC, 95% of patients will not respond to incision.
- MAC values are additive (e.g. 0.5 MAC isoflurane + 0.5 MAC N2O = 1 MAC
MAC-Awake (a.k.a. MAC-Aware)
- – The MAC necessary to prevent response to verbal/tactile stimulation.
- – Volatiles: ~0.4 MAC; N2O: ~0.6 MAC
- – The MAC necessary to blunt the autonomic response to a noxious stimulus
- – ~1.6 MAC
- – The MAC necessary to prevent laryngeal response to endotracheal intubation
- – ~1.3 MAC
- Use of (chronic) alcohol, cocaine, speed, ephedrine (enzyme induced)
- Pediatrics, esp. babies
- Redheads (yes!)
- Other anesthetic drugs
- Acute alcohol (drunk)
- (Chronic) amphetamines (catecholamine depleted)
- Severe Anemia
All inhaled anesthetics depress
- ventilation in a dose related manner.
- increase in PaCO2.
- decrease in tidal volume (TV).
- Since Minute Ventilation (MV) = TV X RR
- Minute ventilation decreases but to a lesser extent due to the offsetting increase in RR
- net decrease in MV with an associated increase in resting PaCO2 (gas breathing).
- This increase in resting PaCO2 can be used as an index for assessing respiratory depression by the inhalation agents.
All anesthetics decrease __(cv)
- arterial blood pressure by decreasing SVR
- Halothane by decreasing CO
- Most increase heart rate.
- Desflurane often very much so!
lower the cardiac output (? FA/FI)
the faster the rise in FA/FI (think redistribution)
lower the blood:gas solubility (?FA/FI)
the faster the rise in FA/FI (think nitrous)
High A Low A The higher the minute ventilation
the faster the rise in FA/FI (crosses the lungs faster!)
High (PA - Pv) Low (PA - Pv)
- At the beginning of induction, Pv is zero but rises rapidly (thus [PA-Pv] falls rapidly) and FA/FI increases rapidly.
- Later, during induction and maintenance, Pv rises more slowly so FA/FI rises more slowly.
- B, blood solubility;
- Q, cardiac output;
- A, minute ventilation;
- PA, Pv, pulmonary arterial and venous blood partial pressure.
- Low potency (MAC 104% - can never reach 1 MAC!)
- • Insoluble in blood
- – Facilitates rapid uptake and elimination (second gas)
- • Commonly administered as an anesthetic adjuvant (additive)
- • Does not produce skeletal muscle relaxation
- • Can potentially contribute to PONV, watch out.
- • Can diffuse into air filled cavities and cause expansion
- of air filled structures (pneumothorax, bowel, middle
- ear, ET tube balloons, pulmonary blebs, etc.)
- – Nitrous oxide can enter cavities faster than nitrous can leave
- – CONTRAINDICATED in these settings
- • Myocardial depression may be unmasked in CAD or hypotension
- Diffusion Hypoxia, theoretically
- • Highly pungent
- • Second most potent of the clinically used inhalational agents (MAC 1.2%)
- • Preserves flow-metabolism coupling in the brain
- – Highly popular for neuroanesthesia
- • Has been implicated for causing coronary steal
- – Dilation of normal coronary arteries causing blood to be diverted away from maximally dilated, stenotic vessels to vessels with more adequate perfusion
- • Causes vasodilation
- – Decreases BP!
- – Increases CBF (usually seen at 1.6 MAC)
- – Increases ICP (usually at above 1 MAC; short lived)
- • Minimal compared to halothane
- • At 2 MAC produces electrically silent EEG
- Slow onset, slow offset.
- Cheap ~$10/bottle
- Half as potent as isoflurane (MAC 1.8%)
- • Rapid uptake and elimination
- • Sweet smelling, non-pungent
- Quick uptake and sweet smell make this agent very popular for inhalational induction
- • Potent bronchodilator
- • Can form CO in desiccated CO2 absorbent
- – Can cause fires, don’t run at low flows.
- • Forms Compound A in CO2 absorbent (nephrotoxic)
- – Recommended to keep fresh gas flows >2 L/min
- Expensive ~$200/bottle
- Lowest blood:gas solubility coefficient (lower than N2O) Great for obese patients.
- • Very fast uptake and elimination
- • Low potency (MAC 6.6%). Run low flow or fill vaporizer a lot.
- • High vapor pressure. Must be stored in a heated, pressurized vaporizer.
- • Very pungent. Can cause breath-holding, bronchospasm, laryngospasm, coughing,salivation when administered to an awake patient via face mask (Just don’t do it. Use sevo.).
- • Can form CO in desiccated CO2 absorbent
- • Can cause an increased sympathetic response (tachycardia, hypertension) when inspired concentration is increased rapidly
- Intermediate cost ~$100/bottle
_____ is great for bronchospasm and asthma prevention.
- The problem comes when you shut it off.
If you are running a really long (~8hr) case, just use
Signs your patient is getting light
- Increase in HR or BP by 20% above baseline
- • Tearing
- • Dilated pupils
- • Coughing or bucking
- • Patient movement
- • Signs of consciouness on EEG monitor
- (Bispectral Index)
BIS (bispectral index:
- EEG monitoring and algorithms to produce
- numbers (0-100) relating to depth of anesthesia.
- – 65-85 = sedation
- – 30-65 = general anesthesia
- – <30 = too deep
- •Has been shown to be fairly good predictors of
- loss and regaining consciousness
- • Interpatient variability exists
- • Both have a noticeable time lag (~2min)
- • It is possible to display the raw EEG in real time, and interpret on your own.
Inhalation with decreasing respiratory depression:
Enf > Des = Iso > Sevo = Hal
Inhaled Anesthetics Cardiovascular Effects
- All anesthetics decrease arterial blood pressure.
- Most by decreasing SVR
- Halothane by decreasing CO
- Most increase heart rate.
- Halothane tend to maintain HR
- All decrease SVR.
- Exception is Halothane
- All produce no change in cardiac index.
- Exception is Halothane
N2O does not increase the PaCO2
- suggesting that
- substitution of this anesthetic for a portion of the volatile anesthetic would result in less
- depression of ventilation
- Commercial preparations in 2.5% solution
- with a pH of 10.5
- Effects due to interaction with inhibitory
- neurotransmitter gamma-aminobutyric acid
- (GABA) in the CNS
- After induction dose rapidly enters the
- brain and then rapidly redistributes to
- skeletal muscle (with termination of CNS
- effects) - wake up time is 15-20 min
- Hepatic metabolism - not renal
- Indications: Induction
- Treatment of increased ICP
- Cerebral protection
- Cardiovascular changes - vasodilation and
- increases in heart rate (baroreceptor reflex
- Histamine release can occur with rapid
- administration, but not clinically significant
- Formulated in soybean and purified egg
- emulsion - NO preservatives
- Irritation “burning” on infusion
- Susceptible to bacterial growth
- Vasodilation greater than with thiopental
- (related to rate of administration) with no
- baroreceptor reflex changes in heart rate
- Interacts with GABA receptors
- Short duration of action on the brain
- Reduces ICP and CMRO2
- Reduces respiratory efforts and
- depresses laryngeal reflexes
- Not depended on renal clearance
- Has short anti-emetic effects
- Pain on injection
- Rapidly enters the brain and
- awakening is the result of
- redistribution to inactive tissues
- Interacts with GABA receptors
- Side effects: Myoclonus on induction,
- adrenal suppression (up to 8 hours
- later), high incidence of PONV
- Cardiovascular: Hemodynamically
- stable profile (NO HISTAMINE
- Avoid in patients with acute porphyria
- (same with barbiturates like
- Ephedrine is an INDIRECT-acting
- synthetic noncatecholamine that
- stimulates both alpha- and betaadrenergic
- Action mediated by causing the release
- of endogenous catecholamines
- Therefore, cardiovascular effects similar
- to epinephrine
- Has weak direct alpha agonist effects
- Phenylephrine is a synthetic
- noncatecholamine that stimulates
- principally alpha receptors by a
- DIRECT effect (No BETA EFFECT)
- Peripheral vasoconstriction occurs
- with reflex baroreceptor bradycardia
- (differs from ephedrine) – drug of
- choice when hypotension with
- tachycardia is present
Single Twitch – a single pulse 0.2 msec in
duration given every 1 or 10 secs
Train of Four (TOF) – a series of four
- twitches given within 2 secs, each 0.2 msec
- in duration
Tetany – a sustained 5 sec stimulus of 50
to 100 Hz
Double Burst – three stimulations followed
- by two stimulations, each set separated by
- 750 msec
FADE is indicative of
- nondepolarizing agents and not of depolarizing agent such as succinylcholine (phase I block)
- Exception is during a phase II block
- FADE = T4/T1 Ratio < 1.0
- Sustain tetanic stimulus can be used
- minimize undetected fade after
Depolarizing Phase I
muscle fasiculations, NO FADE, TOF 1.0, NO post tetanic facilitation, augmented by anticholinesterase inhibitors
- Only widely available depolarizing muscle
- relaxant in the U.S.
- Consists of 2 ACh molecules linked together
- by a methyl group
- Ultra rapid onset (30-60 secs) with short
- duration (3-5 mins) – Facilitates rapid
- intubation during rapid sequence induction
- “Agonist” – mimics ACh effects but with
- prolonged duration because of slower rate
- of hydrolysis
- Causes prolonged depolarization of muscle
- Metabolized by butyrylcholinesterase
- After an IV dose - ~95% of initial dose is
- metabolized and only 5% reaches the NMJ
- However, termination of action by dissociation
- and diffusion away from NMJ
- (no pseudocholinesterase at NMJ)
- Characteristically see fasciculations; may see
- masseter spasm making intubation difficult
- (MS associated with MH)
Succinylcholine – Side Effects
- Cardiac – sinus bradycardia /
- Increases in IOP / ICP / IGP
- Trigger for Malignant Hyperthermia
- Masseter muscle spasm (Trismus)'
- Serum K+ increase ~0.5 mEq/L with
- Not prevented with priming
- Pt. with renal failure do not have greater
- increases in K+ levels
- Hyperkalemia may occur after
- administration of succinylcholine to patients
- Unrecognized muscular dystrophy
- Denervation injuries / Spinal cord injuries
- Upper motor neuron lesions
- Severe skeletal muscle trauma
- Intra-abdominal infections
- Severe hypovolemia and metabolic acidosis
Classification of NDMB Drugs
- According to Structural Classification –
- Nondepolarizing Drugs
- Steroids – Pancuronium, Pipecuronium,
- Vecuronium, Rocuronium, Rapacuronium
- Benzylisoquinolones –
- d-tubocurarine, Atracurium,
- cis-Atracurium, Mivacurium
- Intermediate acting (30-60 mins)
- Rapid onset – depends on dosing
- Dose: 0.6 – 1.2 mg/kg
- No histamine release
- Clearance: Biliary excretion / little
- renal excretion
- Alternative for RSI when
- succinylcholine is contraindicated /
- drawback – prolonged paralysis
- Intermediate acting (30-60 mins)
- Dose: 0.1 – 0.2 mg/kg
- No histamine release
- Clearance: Hepatic metabolism and
- renal excretion(small)
- Vecuronium is unstable in solution
- therefore supplied as a lyophilized
- powder that must be dissolved in
- sterile water before its use.
- Intermediate acting (30-60 mins)
- Dose: 0.4 – 0.6 mg/kg
- Histamine releaser
- MET: Hoffman elimination / ester
- Metabolism independent of liver or
- elimination independent of kidneys
- End product: Laudanosine –
- accumulation assoc. with Sz.
Cis - Atracurium
- Similar to Atracurium – more
- Dose: 0.15 – 0.2 mg/kg
- No histamine release
- MET: Exclusively by Hoffman
- elimination (no ester hydrolysis)
- Therefore no Laudonosine produced
- Long acting (> 1 hour)
- Dose: 0.08 – 0.12 mg/kg
- Clearance: Mostly renal excretion
- Avoid in renal dysfunction
- Use assoc. with HR, BP, CO
- Due to vagolytic effect and
- catecholamine release
- No histamine release
Reversal of NDMB
- Reversal of NMB is accomplished by
- using an anticholinesterase
- Reversal agent increase the conc. of
- ACh at the junctional clefts, so
- competition with the blocking drug is
- shifted in favor of the transmitter
- ACh, and transmission is restored
- Anticholinesterases act by inhibiting
Assessing Adequate NMB Recovery
- Tidal volume is a very insensitive
- clinical test for assessing residual
- muscle paralysis
- “Tongue depressor test” may be more
- sensitive to residual paralysis with
- TOF ratio < 0.9
- TOF ratio < 0.9 associated with
- abnormal pharyngeal function - risk
- of aspiration
- Amide - Lidocaine, Bupivacaine,
- Ropivacaine, Mepivacaine
- Most Likely to exist in stereoisomers with
- differing pharmacodynamics
- Esters - Procaine, 2-Chloroprocaine,
- Tetracaine, Cocaine
ester LA features
- metabolism: plasma cholinesterase
- short half life
- low allergenic
Amide LA features
- Hepatic metabolism
- longer serum halflife
- low allergenic
LA Duration of Action: Correlate with
- degree of protein binding.
- Higher protein binding Longer duration
- (Bupivacaine / Ropivacaine)
LA Lipid Solubility: correlates with
- potency of the LA
- Increase lipid solubility Increase potency
- Only free unbounded LA causes toxicity.
- Neurotoxicity - cauda equina syndrome, transient neurologic syndrome (TNS)
- Systemic Toxicity - seizures and cardiac toxicity
Transient Neurologic Syndrome
- Associated with spinal use of LIDOCAINE
- Presents after spinal anesthetic wears off
- and last for 48 to 72 hours
- Presentation: unilateral or bilateral back
- or buttock pain radiating down back or
- legs with no assoc. neurologic weakness
- TX: NSAIDS - spontaneously resolves
- Increase Incidence - lithotomy and
- ambulatory surgeries
LA Systemic Toxicity:
- Depends on serum level of unbounded
- Site of injection has significant bearing
- on serum level
- Higher vascular areas Higher serum levels
- Early signs of toxicity - CNS symptoms
- Cardiotoxicity: due to binding to sodium
- channels in the heart and disruption of
- conduction system
- Bupivacaine has high cardiotoxicity due
- to avidly binding to cardiac sodium
- channel receptors and slowly dissociating
- from them (“Fast in, Slow out”)
- The following are depended in
- biodegradation in the plasma (not
- hepatic nor renal)
- Succinylcholine / Mivacurium
- Atracurium / Cis-atracurium
- Local anesthetics - Esters
Regional Anesthesia - Spinal
- Clinical Uses: Lower extremity
- surgery (orthopedic), GU, C-sections,
- Decreased incidence of DVT
- Improved postop analgesia
- Less PONV
- Coagulopathy (LMWH, aspirin use)
- Ticlopidine (Ticlid): 10 -14 ds
- Clopidogrel (Plavix): 7 ds
- Systemic or localized infection
- Significant hypovolemia
- Patient refusal (equally important)
- Respiratory Effects:
- Minimal - Phrenic nerve unaffected
- However active exhalation affected
- (although normal exhalation is passive)
Regional Cardiovascular Effects:
- Secondary to sympathetic blockade
- Decrease in systemic vascular resistance
- Decrease in heart rate esp. if
- cardioaccelerators (T1-T4) affected
- Cardiac arrest can occur
- “High Spinal” - cerebral blood flow may
- be affected
- Phase I - Inspiration
- Phase II - Start of exhalation
- Phase III - Emptying of alveoli
- Phase IV - Start of inspiration
All anesthesia machines have
- 3 basic components:
- 1. A source of compressed gases.
- 2. Flowmeters to ensure delivery of
- known flows and concentrations
- these gases
- 3. Means of vaporizing and delivery
- known concentrations of inhalation
Carbon Monoxide Formation
- Desiccated Absorbant + Inhaled Anesthetics = Carbon Monoxide
- Desflurane ≥ enflurane > isoflurane >> halothane = sevoflurane
- Sevoflurane + desiccated absorbant = HEAT (Fires)
- Most associated with baralyme
- absorbant – now removed from
- Soda lime also implicated
- Amsorb Plus is not associated with CO
- production (no degradation occurs)
- Average incidence = 30%
- Prophylaxis not required in all
- ???? Who to treat ?????
- Risk factors assessment to determine
- Patient Related
- Gender: F>M
- Nonsmoking status
- Hx of PONV or motion sickness
- Surgical Related
- Length of surgery
- Type of surgery (Laparoscopic)
- Anesthetic Related
- Postoperative opioid use
- Volatile anesthetics
- Nitrous oxide
PONV Prophylaxis or Treatment
- Dopamine antagonist –
- metoclopramide, droperidol,
- Histamine antagonist –
- diphenhydramine, cyclizine, and
- Anticholinergics – scopolamine
- (transderm patch)
- Serotonin antagonist – ondansetron,
- dolasetron, granisetron
- Neurokinin antagonist – aprepitant
- (PO dosing only)
- Dexamethasone – unknown site of
HTN anesthesia mgt
- Perform your induction with higher doses of narcotic and lower doses of propofol. This serves two purposes.
- DL will cause an exaggerated sympathetic response with tachycardia and hypertension that may be severe. Blunt the patient very, very well with narcotic and lidocaine and limit DL time (15 seconds or less).
- Beware of blood pressure dropping during lull times in the case. Fluid load the patient, don’t be afraid to switch to colloid and keep phenylephrine/vasopressin and ephedrine close at hand.
- Blunt the patient very well before incision.
- Watch your EKG closely for ST changes.
- During the case, keep the patient’s MAP where it was at baseline. Remember your patient has “upregulated” to this MAP.
- Do not lower the MAP to where you think it should be. You may think you are doing the patient a favor. You are not. You risk loss of perfusion to organs, MI and stroke, or POCD if you do.
- Beware of hypertension which may be severe during emergence as the patient begins to awaken, feel pain, and buck.
- Narcotize the patient as well as you can to avoid pain.
- Deep extubate if you can to prevent bucking, or blunt with an LTA.
Coronary artery disease mgt
- 12 lead EKG if your patient is over 40 or has drug habits.
- med consult
- keep HR, BP within 20% of normal
- sedate before emergence
- Blunt the patient very well with midazolam and narcotic. Use as little propofol as possible. Avoid ketamine.
- Don’t hesitate to start a phenylephrine drip.
- Use a non depolarizer, no sux please.
- No desflurane.
- Blunt the patient well before DL, and limit to 15 seconds or less.
- Yes you can give them nitrous. Do if possible. More nitrous=less inhalational.
- Regional is always an option if the case is appropriate. Spinals are best avoided.
- Use non depolarizers as needed.
- Please use the ST segment analyzer function on the monitor and keep an eye on it.
- Keep your patient warm. Shivering increases myocardial oxygen demand
- Reversal of paralysis needs to be done carefully to prevent tachycardia.
- Deep extubate your patient if possible or blunt with an LTA to avoid bucking.
- Narcotize the patient well.
- Nitroglycerin boluses are your friend for the treatment of hypertension on emergence. It will drop BP nicely and quickly, wear off right away and will not affect the heart rate. Plus they dilate coronary vessels.
- Please order a 12 lead EKG in the PAR. Keep oxygen on longer.
Mitral Stenosis mgt
- Plan for an arterial line.
- Goals are “fast, forward, full”.
- Do not let the heart rate decrease.
- Maintain normovolemia as much as possible. In both cases, try not to overload but under-rescuscitation is very bad.
- Keep phenylephrine handy: try not to allow any decrease in SVR. This is very bad for aortic stenosis as the coronary arteries will not perfuse if this happens.
- Use more narcotic and less propofol.
- The mitral valve is incompetent, does not close fully and blood flows backwards into the left atrium.
- You will see signs of left atrial enlargement on the 12 lead EKG.
- You will see an enlarged heart on the CXR.
- General anesthesia is preferable.
- Regional in the form of peripheral nerve blocks is probably ok if MR is mild to moderate. Spinals and epidurals are not recommended d/t sympathectomy.
- Maintain the heart rate as much as possible. Some decreases in PVR benefit the patient, but there are limits.
- Deep GA can maintain the decreased PVR you want. Blunt the patient well with narcotics to avoid swings from surgical stimulation.
Aortic Regurgitation mgt
- The incompetent aortic valve allows blood to fall back into the left ventricle at end diastole.
- Will cause LV hypertrophy and increased oxygen demand by the heart.
- These patients often have angina—coronary arteries don’t perfuse well.
- You will need a medical or cardiac consult to determine level of optimization.
- Plan for an arterial line.
- Maintain the heart rate as best you can.
- Again, regional is best avoided if AR is severe. You can decrease PVR, this will help the patient, but don’t overdo it.
Mitral Valve Prolapse
- Left ventricle contracts and incompetent valve leaflet falls backwards into the left atrium.
- Present in 5% of the population.
- When listening you will hear a click type murmur.
- You need to maintain normovolemia. If you don’t you risk permanent prolapse of a leaflet during LV contraction.
- Keep the patient’s SVR at baseline in this case.
- Please no regional of MVP is severe: its effects on PVR.
- Place an arterial line, awake if necessary
- Keep the patient’s heart rate at baseline, avoid tachycardia.
- Blunt the patient very well with narcotic, lidocaine, etc. to avoid overtly sympathetic responses to DL or surgical stimulation.
- Keep phenylephrine or vasopressin handy.'
- Worn-out heart.
- It is best not to take these patients to surgery if possible.
- CHF must be under tight control and patient must be optimized. Medicine/cardiology must be involved.
- Anesthetic goal is to preserve cardiac output to the highest degree possible
- Place an awake arterial line with sedation and local.
- Induction generally speaking has to be done with midazolam/fentanyl only, and maintenance may have to be done with opioid drip and low dose gas.
- You will have to put them on the ventilator, they won’t be able to breathe for themselves. Warn them they might wake up still on the ventilator.
- Keep fluids to the bare minimum and keep lasix handy.
- Patient history is the best indicator. Chest X rays are rarely helpful.
- Ask patient for severity. Ask how often uses inhaler, how many ER visits, hospitalizations, or admissions.
- If asthma is severe ie has had admissions, intubations or placed on ventilator, a medicine consult is probably warranted for optimization
- Listen to the lungs day of surgery. If surgery is elective and patient is wheezing, cancel case.
- Remember that in most cases, the mere act of instrumenting the airway (intubation) can and often does trigger bronchospasm.
- Regional anesthesia is a good option whenever possible!
- Use regional anesthesia.
- Don’t intubate (LMA).
- Pre emptively treat asthmatic patients with albuterol.
- Sedate them well before bringing back.
- Turn on sevoflurane quickly while inducing.
- Blunt airway with LTA.
- Once tube is in, turn on sevoflurane quickly. Listen for wheezing right after taping tube. If you hear wheezing or if peak pressures are high, give more albuterol. Remember most of it is going to stick to the tube so plan accordingly.
- Keep patient as deep as you can on sevoflurane during case.
- Deep extubate the patient if you possibly can. You really should.
- Give albuterol again before you shut off the agent.
- Blunt the carina again with an LTA.
Post Induction Bronchospasm
- Try to prevent it by following the steps above. Some things are better to prevent than to treat.
- Severe post induction bronchospasm can be hard to diagnose!!! If they are that tight you will not see much end tidal and you might not hear any breath sounds!!
- If you are 100% sure you saw the tube go through the cords don’t take it out
- Give more albuterol. Remember most of it is going to stick to the plastic so plan accordingly.
- Turn up the agent: hand bag the patient.
- If all else fails, give a little epi.
- Loss of elastic recoil of the lungs. The patient can’t exhale.
- PFTs may or may not help you. A history is just as good.
- Assess exercise tolerance. If poor, then PFTs.
- Regional anesthesia, if possible, is a very good choice for these patients
- If general anesthesia cannot be avoided, remember these patients are chronic CO2 retainers. Your good intentions can be their worst nightmare.
- You cannot let them breathe spontaneously under general anesthesia.
- Warn the patient they might awaken still on the ventilator!
- Set the I:E ratio on the ventilator from 1:2 to 1:3 or more. Remember they take much longer to exhale than we do.
- You have to allow permissive hypercapnea. Remember they have upregulated and a 60/60 ABG is not unheard of in these patients. Don’t try to fix this.
- Don’t use nitrous.
- Use the least amount of narcotic. Ask surgeon to inject local.
Type 1 diabetes
- Assess level of conttol.
- Remember hypoglycemia under general anesthesia is extremely difficult to diagnose and the consequence is permanent brain damage.
- Tight control is key, 120-180.
- Assess for end organ damage
- Rule is one year of untreated diabetes ages the vasculature 10 years.
- Chronic hyperglycemia causes arterial lumen thickening, nutrients can’t pass well, healing is delayed.
- Vascular tone is impaired.
- Nephropathy is common, check kidney function tests and plan accordingly.
- If neuropathies are present, avoid regional.
- Beware of loss of joint mobility from glycolyisation of joints. This includes the neck and the mandible. Have patient show you prayer sign to assess.
- Beware of loss of autonomic control in these patients. Resting heart rate tachycardia or a heart rate that fails to respond to exercise is an ominous sign of the beginning of a denervated heart
- Delayed gastric emptying is a hallmark sign of diabetes. It is wise to pretreat them with reglan and/or treat them as a full stomach.
- Decreased sensation is ubiquitous in diabetes. Silent MIs are not unheard of. Always order a 12 lead EKG.
- Hold all PO oral hypoglycemics day of surgery, many say the night before too d/t risk of hypoglycemia in the perioperative period.
- Hold morning insulin.
- Schedule these patients first. Check their blood sugar morning of surgery.
- Don’t hang LR please. NS or Plasmalyte.
- Check serum glucose levels priodically.
- Obese persons are at great risk for hypertension (increased cardiac output) and cardiomegaly.
- Great risk of hyperlipedemia and coronary artery disease.
- Abnormal liver function: fatty liver.
- Rampant type II diabetes.
- Decreased lung volumes and capacities
- Chronic hypoxemia and obesity hypoventilation syndrome.
- Remember obesity imposes a restrictive ventilation defect in and of itself. Truncal obesity is the worst.
- Many obese patients are chronically hypoxic and hypercapnic.
- They have no inspiratory reserve.
- OSA is rampant.
- Make sure your blood pressure fits the patient. Too small and and it will read falsely high.
- You can place a regular sized cuff on the forearm.
- Obese people often have serious airway issues. Neck ROM and head extension are often limited. Thick heavy neck means redundant tissue which can be very difficult!
- Mouth opening may be limited: check.
- It is wise to treat them as a full stomach.
- Have a low threshold for awake fiberoptic intubation in these patients. Stand your ground if you have to. These patients have no oxygen reserve other than what you give them. If you don’t get the tube in on the first try, things can go very badly.
- Have the difficult airway cart ready if you are worried. Call for a glidescope as well.
- Avoid sedation. Plan to go very light on the opiates.
- Know which of your drugs should be based on ideal body weight and which actual. Plan accordingly.
- Regional is always an option but is likely to be difficult.
- Do not ever lie down an obese person.
- Preoxygenate the patient first. Put the oxygen on right after the pulse ox. Do not begin induction until the FeO2 is 95% or greater. This buys you time!
- Ramp the bed with sheets or shoulder rolls. Ear tragus equal to sternum.
Ramp obese patients until
tragus is aligned with sternum
- It is safest to induce with sux. Paralysis is going to cause serious lung compression so be prepared. Use less narcotic.
- Use desflurane if you possibly can.
- Obese patients cannot be allowed to breathe on their own. Keep them on the ventilator.
- If it is a laparascopic case, you have many challenges ahead
- Turn the agent off early. Be aware that it might take a long time to come off.
- Use narcotics very sparingly. Ketorolac is an option!
- Place your patient in reverse trendelenburg.
- Make sure all NMB is fully reversed.
- Beware of stage II breath holding. Use CPAP with your hands if needed.
- Extubate fully awake.
- Often goes hand in hand with obesity
- Very serious problem for all anesthesia providers and patient deaths have occurred.
- Patient breathing stops for >10 seconds during sleep due to pharyngeal muscle tone being lost.
- Also mandibular defects play a part
- Underdiagnosed and undertreated.
- Symptoms: frequent awakenings/microawakenings (most not noticed by the patient), heavy snoring and breathing stoppages (noted by spouse), daytime somnolence.
- Complications: memory problems, motor vehicle accidents, hypoxemia and hypecarbia, polycythemia, hypertension, pulmonary hypertension and right heart failure.
- ASK patients about these symptoms, especially if they are obese, have thick necks, malampatti 3-4 airways and redundant pharyngeal tissue and/or micrognathia!
OSA Anesthetic implications
- Warn the PAR. This is where most problems occur.
- If the patient is on CPAP, ask them to bring it with them. If they didn’t, ask the PAR to order one for you.
- Minimize narcotics. Ketorolac and local anesthesia is your friend.
- Think twice about sending the patient home after surgery. Someone should stay with them.
- If patient is willing, refer to a sleep specialist.
- Delineate: renally impaired versus renally dead.
- If on dialysis, should be followed by that service. Schedule elective surgery for the day after dialysis, due to fluid and electrolyte shifts that happen the day of dialysis.
- IV access may be difficult. If you absolutely cannot start an IV ask me to show you how to access a dialysis cath.
- If they have a shunt leave that arm/leg alone.
- #1 cause: hypertension
- #2 cause: diabetes
- Kidneys are very powerful and will continue to function during these disease progressions unnoticed by the patient.
- Anemia also accompanies this, and is worsened by dialysis.
- Hyperkalemia is rampant. Renal patients however generally tolerate a serum K of 5.5 with no symptoms.
- Check potassium levels morning of surgery. If higher than 5.5 cancel case if it is elective.
- Avoid using sux on renal patients if they are on dialysis and K is high.
- Regional anesthesia is always the best choice for this patients whenever possible. These patients are very well aware that they cannot metabolize or excrete our drugs.
- Limit IV fluids as much as you can.
Best drugs for renally impaired:
- Sux or cisatracurium.
- Remifentanyl or fentanyl.
- Volatiles are mostly OK.
Renally impared Avoid:
- Vec/Roc (ok if necessary but they will be paralyzed much longer)
- Meperidine/morphine/codeine (toxic metabolites)
- Best choice is to postpone any and all elective surgery until the baby is born.
- Unfortunately sometimes this is not possible.
- In cases of trauma, the pregnancy almost always is lost.
- surgery during the second or third trimester, if necessary, poses low risk to the fetus.
- Reason: organogenesis is generally done by then.
- Beware of inducing preterm labor! Explain this risk to the patient!
- OB/GYN will be involved
- Cardiac output increases by 50% during pregnancy.
- Oxygen reserve decreases dramatically due to a. hypermetabolic state and b. size.
- Airway difficulty increases!
- Warn the patient about risk of preterm labor.
- Have OB/GYN attach a fetal heart monitor. This will go to the OR with you along with a technician/RN who can monitor it.
- Nitrous and midazolam are teratogens. Don’t use them.
- Pregnant women are “full stomachs”. Treat them accordingly. Give them bicitra.
- Use regional if you possibly can.
- RSI is best.
- If later pregnancy, position her right side up to prevent IVC compression.
- Preoxygenate very, very well.
- Inhalationals, propofol are OK.
- Minimize narcotics. Ketorolac is now considered OK, but ask.
- Extubate fully awake.
- OB/GYN will monitor fetal heart tones in the PAR.