Exam 2: Local Anesthetics Flashcards
1
Q
Local anesthetics
A
- Local anesthetics (LA) are drugs that reversibly block conduction of electrical impulses along nerve fibers They are a MAJOR component of clinical anesthesia and are increasingly being used to treat chronic and acute pain
2
Q
Nerve anatomy
A
- The axon, and extension of the neuron, is the functional of peripheral nerves
- Major components include axolemma and axoplasm
- Schwann cells surround each axon
- Nerves are considered either myelinated or unmyelinated based on type of axon covering
- Will be blocking axons of 1st order neurons
-
Not all nerves are created the same – how fast they’re affected, for how long they’re affected
- Un/myelinated
3
Q
SCHWANN CELLS
A
- Serve to support and insulate each axon
- Unmyelinated nerves - In smaller nerves, single Schwann cells cover several axons
- LA will get to these first! Bc not as much tissue to get through
- Myelinated nerves - In larger nerves, the Schwann cell covers only one axon and has several concentric layers of myelin
4
Q
Nerve anatomy - nodes of ranvier
A
- Nodes of Ranvier are periodic segments between Schwann cells along the axon that do not contain myelin
- Voltage-gated sodium (Na+) channels are located in these segments and are the primary site of LA action
- Action potentials jump from nerve to nerve, known as saltatory conduction
- To block impulses in myelinated fibers it is necessary for LA to inhibit channels in three successive nodes
- Must block at least 3 nodes to block the AP from going down
5
Q
Nerve anatomy - fasciculi
A
- Bundles of axons are called fasciculi
- Fasciculi are covered with three layers of connective tissue:
- Endoneurium is a thin, delicate collagen that embeds the axon in the fascicule
- Perineurium consists of layers of flattened cells that binds groups of fascicles together
- Epineurium surrounds the perineurium and is composed of connective tissue that holds fascicles together to form a peripheral nerve
- LA must diffuse through these layers to exert their effects
-
Will boil down to how much CT is surrounding that nerve! This is why nerves will look differently
- Nerves come out of spine and converge and diverge
-
Dermatomes are referring to nerve roots
- Vs. Myotomes
- Ex: C5 = endoneurium (ind nerve fibers) and probably perineurium (holding together several fascicles), C5 + C6 held together by epineuereum (bundles of nerves)
- Danger is when you actually inject under the perineurium – pressure/nerve injury/ischemia
6
Q
Nerve conduction physiology
A
- Resting membrane potential of axon
- -70 mV to -90 mV
- Caused by an imbalance axoplasm and extracellular fluid
- Physiologic mechanisms help create this
- Na+ – K+ pump in axolemma
- Intracellular ratio of potassium is 30:1
- Membrane impermeable to other ions (such as Na+)
- Excess of negatively charged ions in axoplasm
- Nernst equation
- Expresses the charge created by K+ concentration gradient
- When an electrical impulse is applied to a nerve, membrane potential is reversed due to influx of Na+
- Overrides K+ directed at maintaining potential
- Once membrane potential reaches 20mV, Na+ in inactive state
- Na+ - K+ pump restores resting membrane potential
- Three Na+ ions leave for each two K+ that enter
- LAs are going to block this! But they don’t alter the RMP!!
7
Q
Local Anesthetic MOA
A
(BASE, you know this bc it’s bound to an acid)
-
Bind to specific sites on the Na+ channel
- Preferential to open and inactive states
- To a lesser extent, also blocks:
- K+ channels
- Ca++ channels
- G protein-coupled receptors
- Block transmission of nerve impulses
- LA do not alter the resting transmembrane potential or threshold potential
- Modulated receptor hypothesis of LA action
- Preference to attach during active or inactive states
- Frequency-Dependent Blockade
- Resting nerve is less sensitive to LA than one repeatedly stimulated
- AKA “use-dependent” or “phasic block”
- Will see quicker block if they’re opening/closing their sodium channels compared to someone at rest ≅ ketamine (works best when someone is already ramped up – give it right at the time of surgical incision)
- ALL local anesthetics are weak bases, not ionized, so it diffuses across.
- Diffusion of an unionized base across the nerve sheath and membrane
- Re-equilibrium between the base and cationic forms in the axoplasm
- Binding of the cation to a receptor inside the sodium channel, resulting in its blockade and inhibition of Na+ conduction.
- Pref when open or inactive state.
8
Q
Differential blockade
A
- Nerves have different sensitivity when exposed to LA
- Small diameter and lack of myelin enhance sensitivity
- Larger nerves conduct impulses faster and are harder to block
- In general, preganglionic are blocked with low concentrations, followed by small C fiber and small A fibers resulting in a loss of pain and temperature.
- Touch and proprioception can still be present but not pain of surgical stimulation
- In an anxious patient any sensation can be seen as LA failure
- LA’s bind to smaller, unmyelinated nerves
-
If you want to know early if your block is working, you’ll see vasodilation, flushed
- Block small, preganglionic nerves 1st – that control SNS tone.
- Those nerves are running in the same channel as the sensory/motor nerves
- Why spinal epidural will see hypotension – 8 oz cup/8 oz container → 8 oz cup in 16 oz container
- Next will see loss of sensation
- Next will lose motor
9
Q
Fiber Type Aa:
fn, diameter, myelination, block onset
A
Aa = alpha
fn: proprioception, motor
“alpha motor neuron”
diameter 6-22 um
myelination - heavy
block onset - last (lots of myelin always takes a long time)
10
Q
Fiber type AB (A beta)
fn, diameter, myelination, block onset
A
- fn: touch, pressure “betta touch”
- diameter 6-22 um
- myelination: heavy
- block onset: intermediate
11
Q
Fiber Type A gamma:
fn
diameter
myelination
block onset
A
- fn: muscle tone “Grandma’s (gamma) got muscle tone!”
- diameter: 3-6 um
- myelination: heavy
- block onset: intermediate (only last one is Aa)
12
Q
Fiber type A Delta:
fn
diameter
myelination
block onset
A
- fn: pain, cold temp, touch
- “Manny was in TRI-delta - pain, cold, touch”
- diameter: 1-5 um
- myelination: heavy
- block onset: intermediate
13
Q
Fiber Type B
fn
diameter
myelination
block onset
A
- fn - preganglionic autonomic vasomotor
- diameter <3 um
- myelination - LIGHT
- block onset - early
14
Q
Fiber Type C Sypathetic
fn
diameter
myelination
block onset
A
- fn - postganglionic (autonomic) vasomotor
- diameter 0.3-1.3 um
- myelination - NONE
- block onset - EARLY
15
Q
Fiber Type C Doral Root
fn
diameter
myelination
block onset
A
- fn - pain, warm and cold temperature, touch
- diameter 0.4 - 1.2
- myelination - NONE
- block onset - EARLY
cold temp is Type A delta fiber, aaaaand Type C Dorsal Root fibers!! Double trouble, that’s why I’m always cold.
16
Q
2 people important to the hx of LA’s
A
- Karl Koller introduced Cocaine as the first LA in 1884
- Halsted recognized its potential for regional and spinal anesthesia
17
Q
LA’s have 3 characteristic segments
A
- An unsaturated, aromatic ring system (lipophilic portion of the molecule)
- A tertiary amine (hydrophilic portion of the molecule)
- Either an ester or an amide linkage binds the aromatic ring to the carbon group.
18
Q
Ester vs. Amide
A
- The ester or amide linkage relevant clinically because of its implications for metabolism, duration and allergic potential
- Esters metab in the plasma by plasma esterase – starts to be metab as soon as it gets into the circ → SHORTER ACTING
- Amide metab by the liver
- Changes in chemical structure affect drug potency, speed of onset, duration of action, and differential block potential
19
Q
Ester LA’s (5)
A
the one that doesn’t have “i’s”
Procaine
Chloroprocaine
Tetracaine
Cocaine
Benzocaine
20
Q
Amide LA’s (6)
A
the ones with “i’s” in them
Lidocaine
Mepivicaine
Prilocaine
Bupivicaine
Ropivicaine
Articaine
21
Q
Clinical Differences between Ester and Amide LA’s: ESTERS
A
- Ester metabolism is catalyzed by plasma and tissue cholinesterase via hydrolysis; occurs throughout the body and is rapid
- although LA allergy is uncommon, esters have a higher potential, and if pts exhibit an allergy to an ester, all esters should be avoided
- ester drugs tend to be shorter acting d/t ready metabolism; tetracaine is the longest acting ester
Aside:
- Breaks down into Paraminobenzoic acid (?)
- Tease out if it’s a true allergy bc HR 110 might have been lido that has Epi in it
- Amide had like 1-2 cases
- Of esters – tetracaine is longest acting, the rest of them at 90 minutes or less
- Amides might last 8+ hrs
22
Q
Clinical Differences between Ester and Amide LA’s: AMIDES
A
- Amides are metabolized in the liver by the CYP1A2 and CYP3A4 and thus a significant blood level may develop with rapid absorption
- Allergy to amides is extremely rare; there is no cross allergy among the amide class or between ester and amide agents
- Amides are longer acting bc they are more lipophilic and protein-bound. They require transport to the liver for metabolism
23
Q
Cm: Minimum Effective Concentration
A
- Cm is the minimum concentration of LA necessary to produce conduction blockade of a nerve impulse ≅ MAC
- Analogous with minimum alveolar concentration (MAC) for inhaled anesthetics
- Cm of motor fibers approximately twice that of sensory fibers
- Sensory anesthesia may not always be accompanied by paralysis
- Less LA is needed for intrathecal vs. epidural anesthesia
- Necessary to expose A fibers three nodes of Ranvier to LA
- A-delta and unmyelinated C fibers require similar concentrations
- Pre-ganglionic B fibers more readily blocked than any fiber
- EPIDURAL – never compromising the dura
- Injecting LARGE volume of drug, hoping it will spread to the area to hit the peripheral nerves coming out of
- Labor epidural – don’t want the parturient to be numb. Will tell them that we don’t want them to be numb.
- Low concentration and high volume
- If not working, give a small volume of high concentration
- Caudal = straight epidural
- SPINAL – we are going to compromise the dura
- Directly on the nerve, in a tube that’s filled with dura
- SC all the way to S5. Coccygeal ligament is what tethers the SC to the coccyx?
24
Q
Mantra with LA’s
A
“Always aspirate, never inject >5 mL”
25
PK/PD concepts (general) of LA's, and Potency
* An important distinction between LA and other medication is agents are meant to remain localized in the area of injection
* The higher the concentration injected, the faster the onset
* Systemic absorption results in termination of the drug
* *Some tissue has more vasculature than others – if highly vascularized, DOA won’t be as long.*
* Absorption also influences drug termination and toxicity
* The slower a LA is absorbed, the less likely toxicity
* Metabolism and elimination readily keep up
* Ester – if it gets into the circulation, it’s going to be metabolized quickly!
* Amide – bound to protein in the blood, will hang around longer. Gets to the heart, which has a lot of Na+ channels, so the amide will attach to those! Heart stops
* POTENCY
* Strong relationship between potency and lipid solubility
* Larger lipid-soluble LA are water insoluble and highly protein bound – longer DOA, **esp amide drugs** → severe cardiotoxicity (BUPIVICAINE)
* Lipid solubility correlates with:
* Protein binding
* Increased potency
* Longer duration of action
* Tendency for severe cardiac toxicity
26
PK/PD concepts of LA's: DOA, Onset
* DURATION OF ACTION
* Relationship between protein binding and lipid solubility
* Drug tends to remain in vicinity of Na+ channel
* LA are weak bases and bind to alpha1-acid glycoprotein
* Lesser extent to albumin
* Injection site also plays a major role in duration of action
* ONSET OF ACTION – “makes no sense”
* How readily a LA diffuse through axolemma depends on chemical structure
* LA are weak bases
* Basic drugs become more ionized when placed in a solution with a pH less than the pKa
* Drugs with a pKa closer to physiologic pH have faster onset
* Drugs that are more nonionized should be faster onset
* Chloroprocaine is the exception
* Made a very concentrated drug so it will work fast
* *Tetracaine – rarely used, just used when they ran out of \_\_\_ivacaine*
* *Starting to wear off, pts will get movement back but will still be numb*
* Know lido, bupivacaine, tetracaine.
* Lido – closer to physio pH – quicker onset
* More available drug
* DOA shorter
* Bupiv – 8.1 pH - slower onset
* Highly protein bound
* Less amt available, but will constantly be dropping off – longer DOA
* \> 8 hrs
* Tetracaine –
* Can base your pain mgmt plan on when the LA is going to wear off!
* Spinal is basically transected at the level at which youre injecting
27
PK: Absorption, and Vasomotor Action of LA's (which is PD, cmon now Falyar)
* LA cause relaxation of smooth muscle
* Lidocaine, ropivacaine and cocaine are exceptions
* Relaxation causes vasodilation that:
* Decreases duration of action
* Increases plasma concentration, potential toxicity
* Greater circulation to the area that vasodilated → more of the drug getting reabsorbed → shorter DOA
* ABSORPTION
* Speed of absorption has toxicity implications
* Also depends on where you inject!
* Total dose of LA determines plasma level, not volume or concentration
* Know the list below!!
28
Uptake of Local Anesthetics Based on Regional Anesthesia Technique
IV - **RESULT IN HIGHEST BLOOD CONCENTRATIONS**
Tracheal
Caudal
Paracervical
Epidural
Brachial
Sciatic
Subcutaneous - **RESULT IN LOWER BLOOD CONCENTRATIONS**
29
Possible Absorption Additives (8)
CD - SHEKD
* Clonidine
* Dexmedetomidine
* Epinephrine - to constrict at site of injection – prevent reabsorption – DOA is longer
* Opioids
* Sodium bicarbonate
* Ketorolac
* Dexamethasone
* Hyaluronidase
30
EPI (additive to LA)
* The shorter acting the drug, the greater affect from epi
* Bupivacaine – not gonna make that much of a difference on this one bc it’s already long-acting
* Epinephrine is a vasoconstrictor that reduces the rate of vascular absorption
* Increased duration and potency of block
* Decreases risk of systemic toxicity
* Does not prolong block for all LA to same extent
* Lidocaine, mepivacaine and procaine
* Local infiltration, peripheral nerve block and epidural
* Prilocaine and bupivacaine
* Prolonged with peripheral nerve block, but not epidural
31
Sodium Bicarb (additive to LA)
* Commonly used in epidural anesthesia
* In theory, adding bicarbonate raises the pH of the LA solution resulting in more drug in the nonionized state
* May result in less pain on injection
* Major limitation is the precipitation that can occur
* Dependent on commercially or “freshly mixed” with epinephrine
* Ex: labor epidural is 0.125% (numb but still want them to push, feel contractions) → to convert to a rapid surgical epidural – 2% lidocaine, still has to get thru the dura to get the effect
* Add sodium bicarb → make it alkalotic so it
* 1 mL sodium bicarb + 10 mL lidocaine
* Epidural catheter – can redoes, can adjust dosage and []. Spinals are one and done!
32
PK of LA's: Distribution, Metabolism, and Excretion
* DISTRIBUTION
* Absorption or injection of LA into systemic circulation results in rapid redistribution
* Distribution of esters and amides are similar
* Decrease in plasma concentration to highly perfused tissue
* Brain, heart and lungs receive most initially
* Can be concerning because of toxic levels to brain and heart
* Secondary distribution to rest of the body
* Muscle receives the most
* METABOLISM
* Metabolism differs according to ester or amide structure
* Plasma esterases catalyze the hydrolysis of ester LA
* Procaine and chloroprocaine have plasma half-life less than 1 minute
* Atypical plasma cholinesterase can increase possible toxicity
* Metabolism of amide LA occurs in the liver via CYP-450 enzyme
* Severe hepatic disease can prolong metabolism of these drugs
* Liver failure – lower proteins, so higher free fx of drug
* Can’t metabolize.
* EXCRETION
* Renal dysfunction affects clearance far less than hepatic failure
* Will affect protein binding to both AAG and albumin
33
PK/PD CONSIDERATIONS
* Pregnancy
* Mechanical changes
* Reduction in epidural space
* Hormonal changes
* Progesterone levels affect sensitivity to LA?
* Epidural space becomes engorged, compressed
* Ex 80 yo man could get 2 mL in a spinal
* Pregnant mother might have compression – 2 mL could cause excessive spread (goes to T4 – SNS preganglionic) cardioaccelerator – so now hypotensive, AND no BP compensation
* Will see exaggerated spread in pregnant women
34
LAST (progression of sx's)
* serious, but rare
* Local anesthetic systemic toxicity (LAST) is a serious but rare event during regional anesthesia
* Most commonly occurs from an inadvertent intravascular injection (goes past the liver, but if protein-bound won’t get metab, then goes up to the heart)
* Initial blocking of inhibitory neurons thought to cause seizures
* Blocking of cardiac ion channels results in bradycardia
* Ventricular fibrillation is most serious complication
* Shorter acting drugs thought to be less cardiotoxic
* Chemical properties play a role
* More potent agents higher lipid solubility and protein binding
* Classic clinical presentation: Rapid onset; usually **within a minute**
* 1. Progression of subjective symptoms: agitation, tinnitus, circumoral numbness, blurred vision and metallic taste
* “My ears are ringing”
* “I have a metal taste in my mouth”
* **Not a good sign, first few things you’ll see.**
* 2. Followed by: Muscle twitching, unconsciousness and seizures
* 3. Very high levels can result in: Cardiac and respiratory arrest
* Incident rate of last in regional anesthesia is 0.4 per 10,000
35
LAST most commonly seen in, and prevention/tx strategies
* Most commonly seen in:
* Epidural (epidural veins – if you give too much LA here or don’t appreciate that you punctured the dura and are now in the intrathecal space, will have problems)
* Axillary (but don’t really do these often)
* Interscalene (carotid and IJ vein) – brachial plexus
* Locations -
* *Always show up with neo and ephedrine, and that IV is patent*
* Prevention strategies include:
* Test dosing (could go into vein or thru the dura) – test dose is just to make sure you’re not in any of those spaces
* If you had lido-epi, you’ll see the effects of the EPI more than the 15 mg of lidocaine
* Incremental injection with aspiration
* Use of pharmacologic markers
* Ultrasound
* Treatment includes:
* Prompt recognition and diagnosis
* Airway management priority
* Seizure suppression
* Benzodiazepines
* Succinylcholine
* Prevent hypoxia and acidosis
* Lipid emulsion therapy - 1st bolus might not get it done
* Vasopressors
* Epinephrine \< 1 mg/kg
* Vasopressin – no
36
Lipid Emulsion Therapy MOA
* 1. Mechanism of action
* 2. Capture local anesthetic in blood (lipid sink)
* 3. Increased fatty acid uptake by mitochondria
* 4. Interference of Na+ channel binding
* 5. Promotion of calcium entry
* 6. Accelerated shunting
* “Lipid sink” – lipid adds to the blood and that ↓s the potency of the LA, binds to the Na+ channels
* Might use this therapy for drug ODs also!
* LAST – **think bupivacaine**
SOME SAY ropiv and bupiv are the same, but 0.5% of one ≠ 0.5% of the other
37
Lidocaine & Mepivicaine:
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
Max Dose (mg/kg) - 4
Max Dose with EPI (mg/kg) - 7
38
Ropivacaine & Bupivacaine:
## Footnote
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
Max Dose (mg/kg) - 3
Max Dose with EPI (mg/kg) - n/a
39
Procaine
## Footnote
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
Max Dose (mg/kg) - 12
Max Dose with EPI (mg/kg) - n/a
"It's a PRO, it's the highest max dose at 12"
40
Chloroprocaine
## Footnote
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
Max Dose (mg/kg) - 11
Max Dose with EPI (mg/kg) - 14
41
Prilocaine
## Footnote
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
Max Dose (mg/kg) -7
Max Dose with EPI (mg/kg) - 8.5
42
Tetracaine
## Footnote
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
Max Dose (mg/kg) - 3
Max Dose with EPI (mg/kg) - n/a
43
SIDE EFFECTS AND COMPLICATIONS: allergic rxns
* Allergic reactions
* More common in ester LA
* Esters are metabolized to and derivatives of **para aminobenzoic acid (PABA)** – known allergen
* Cross reactivity to other esters, but not amides
* *^ (If allergic to 1 ester, allergic to all esters)*
* Amide related allergies more commonly associated with preservative
* paraben, methylparaben or metabisulfite
* Spinal should be preservative free!!! Lidocaine, must check! The one that you use for starting lines will have preservatives in it.
44
SEs: Methemoglobinemia
* A condition of high concentrations of methemoglobin in blood
* Ferris form of hemoglobin (Fe2+) converted to ferric hemoglobin (Fe3+)
* Reduced oxygen carrying capability causing tissue hypoxia
* Hgb not accepting O2 !
* Presents as decreasing oxygen saturation not responsive to therapy
* Benzocaine-induced methemoglobinemia
* Rise in cases since 2006 – related to OTC sprays
* Many cases involving infants less than two
* Prilocaine can cause methemoglobinemia because of one of its metabolites o-toluidine
* Dosing should not exceed 2.5mg/kg
* Should be avoided in:
* Children under 6
* Pregnant women
* Patients taking other oxidizing drugs
* Treatment is methylene blue 1-2 mg/kg over 3 to 10 minutes – pulse ox changes
* High levels of methemoglobinemia may require transfusion or dialysis
45
SEs: Cauda Equina Syndrome (CES)
* Manifests as bowel and bladder dysfunction with lower extremity weakness and sensory impairment related to cord ischemia
* Risk factors include supernormal doses of LA (2-chloroprocaine, lidocaine) – used to use 4% lidocaine for spinals
* Sacral nerves are innervating bowels and bladder, perineum
* Maldistribution of LA within intrathecal space
46
SEs: Transient Neurologic Symptoms (TNS)
* Associated with intrathecal lidocaine
* Presents as burning, aching, cramp like pain in the low back and radiating down the thighs for up to five days post op
* Other risk factors include lithotomy position and outpatient surgery
47
Lidocaine: general info, and concentrations available
* Discovered in 1943 by Nils Löfgren in Sweden
* On the World Health Organization’s (WHO) List of Essential Medications – 1 out of 10
* Lidocaine is an amide local anesthetic
* Weak base
* pKa slightly above physiologic pH (= fair amount of nonionization = fairly rapid onset, short DOA)
* protein binding: 64% – 70% (nothing like bupivacaine)
* Duration of action
* Maximum dose
* Lidocaine 0.5%
* Lidocaine 1%
* Lidocaine 1.5% with epi 1:100,000
* Lidocaine 1.5% with epi 1:200,000 – labor epidural test dose
* Lidocaine 2%
* Lidocaine 4%
* Lidocaine 5%
48
Lidocaine: Jack of all trades
* Antiarrhythmic
* Topical
* Induction
* Nebulized
* Multimodal Pain Management
* Regional anesthetic
49
Lidocaine in ACLS algorithm, and Topical EMLA
* Depress myocardial automaticity
* Class IB
* Dosage VT/VF:
* 1 – 1.5 mg/kg IV/IO
* 0.5 – 0.75 mg/kg (refractory)
* 3 mg/kg (total)
* Maintenance Infusion: 1 – 4 mg/min (30 – 50 mcg/kg/min)
* TOPICAL EMLA (Eutetic Mixture of Local Anesthetics)
* 1:1 lidocaine:prilocaine mixture
50
Lidocaine Contraindications
* mucous membranes (super vascular, super well absorbed, maybe have methemoglobinemia)
* broken skin
* infants \< 1 month
* History methemoglobinemia
51
Lidocaine for pain of propofol
* Pain caused by phenol
* King et al. showed that 1 mL of 2% lidocaine reduced pain on injection from 70% to 30%
* Jalota et al. meta analysis showed to most significant interventions
* antecubital vein
* veno occlusion
* small dose of opioids
* Kaya et al. 20 mg lidocaine in 10 mL, with venous occlusion for 60 seconds (tourniquet, inject lidocaine and let it sit for a minute, and then release the tourniquet)
* Borazan et al. compared paracetamol to lidocaine pretreatment 1 minute before injection of propofol
* .5 mg/kg lidocaine and 1 mg/kg paracetamol equal
* 2 mg/kg paracetamol most effective \*but expensive\*
52
Lidocaine (multiple reasons to use for induction)
* Given intravenously on induction:
* Decrease pain of propofol
* Attenuate cardiovascular response to intubation
* Attenuate increase in intracranial pressure (ICP) in patients with decreased compliance
* Less protein bound – more free drug avail (not like bupivacaine)
* Injected into vein – not going to tissues
53
Lidocaine for Attenuation of SNS
* 1.5 mg/kg intravenous administration 1-3 min prior to laryngoscopy:
* Attenuate hypertension
* Attenuate rise of intracranial pressure
* Yokiaka et. al determined 2 mg/kg completely attenuates cough given 1-5 minutes prior to intubation
* Lidocaine 2% is 5 mL, 100 mg – most ppl’s IBW is 70 = 105 mg
54
Topical Lidocaine
* Decreasing “Emergence Phenomenon”
* Coughing
* Sore throat
* Dysphonia
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