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
Q
PK/PD concepts (general) of LA’s, and Potency
A
- 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
- Strong relationship between potency and lipid solubility
26
Q
PK/PD concepts of LA’s: DOA, Onset
A
- 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
- Relationship between protein binding and lipid solubility
- 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
- Lido – closer to physio pH – quicker onset
27
Q
PK: Absorption, and Vasomotor Action of LA’s (which is PD, cmon now Falyar)
A
- 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
Q
Uptake of Local Anesthetics Based on Regional Anesthesia Technique
A
IV - RESULT IN HIGHEST BLOOD CONCENTRATIONS
Tracheal
Caudal
Paracervical
Epidural
Brachial
Sciatic
Subcutaneous - RESULT IN LOWER BLOOD CONCENTRATIONS
29
Q
Possible Absorption Additives (8)
CD - SHEKD
A
- Clonidine
- Dexmedetomidine
- Epinephrine - to constrict at site of injection – prevent reabsorption – DOA is longer
- Opioids
- Sodium bicarbonate
- Ketorolac
- Dexamethasone
- Hyaluronidase
30
Q
EPI (additive to LA)
A
- 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
Q
Sodium Bicarb (additive to LA)
A
- 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
Q
PK of LA’s: Distribution, Metabolism, and Excretion
A
- 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
- Brain, heart and lungs receive most initially
- 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
- Renal dysfunction affects clearance far less than hepatic failure
33
Q
PK/PD CONSIDERATIONS
A
- 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
- Mechanical changes
34
Q
LAST (progression of sx’s)
A
- 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
- 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.
- Progression of subjective symptoms: agitation, tinnitus, circumoral numbness, blurred vision and metallic taste
- Followed by: Muscle twitching, unconsciousness and seizures
- Very high levels can result in: Cardiac and respiratory arrest
- Incident rate of last in regional anesthesia is 0.4 per 10,000
35
Q
LAST most commonly seen in, and prevention/tx strategies
A
- 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
- 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
- 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
Q
Lipid Emulsion Therapy MOA
A
- Mechanism of action
- Capture local anesthetic in blood (lipid sink)
- Increased fatty acid uptake by mitochondria
- Interference of Na+ channel binding
- Promotion of calcium entry
- 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
Q
Lidocaine & Mepivicaine:
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
A
Max Dose (mg/kg) - 4
Max Dose with EPI (mg/kg) - 7
38
Q
Ropivacaine & Bupivacaine:
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
A
Max Dose (mg/kg) - 3
Max Dose with EPI (mg/kg) - n/a
39
Q
Procaine
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
A
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
Q
Chloroprocaine
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
A
Max Dose (mg/kg) - 11
Max Dose with EPI (mg/kg) - 14
41
Q
Prilocaine
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
A
Max Dose (mg/kg) -7
Max Dose with EPI (mg/kg) - 8.5
42
Q
Tetracaine
Max Dose (mg/kg)
Max Dose with EPI (mg/kg)
A
Max Dose (mg/kg) - 3
Max Dose with EPI (mg/kg) - n/a
43
Q
SIDE EFFECTS AND COMPLICATIONS: allergic rxns
A
- 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.
- More common in ester LA
44
Q
SEs: Methemoglobinemia
A
- 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
Q
SEs: Cauda Equina Syndrome (CES)
A
- 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
Q
SEs: Transient Neurologic Symptoms (TNS)
A
- 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
Q
Lidocaine: general info, and concentrations available
A
- 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
Q
Lidocaine: Jack of all trades
A
- Antiarrhythmic
- Topical
- Induction
- Nebulized
- Multimodal Pain Management
- Regional anesthetic
49
Q
Lidocaine in ACLS algorithm, and Topical EMLA
A
- 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
Q
Lidocaine Contraindications
A
- mucous membranes (super vascular, super well absorbed, maybe have methemoglobinemia)
- broken skin
- infants < 1 month
- History methemoglobinemia
51
Q
Lidocaine for pain of propofol
A
- 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
Q
Lidocaine (multiple reasons to use for induction)
A
- 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
Q
Lidocaine for Attenuation of SNS
A
- 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
Q
Topical Lidocaine
A
- Decreasing “Emergence Phenomenon”
- Coughing
- Sore throat
- Dysphonia
55
Q
A
