Unit 5 Flashcards
Alpha fibers
alpha-skeletal muscle motor, proprioception
Beta- touch, pressure
Gamma- Skeletal muscle tone
Delta- fast pain, temp, touch
Beta fibers
Preganglionc ANS fibers
C fibers
Sympathetic- postganglionic ANS fibers
Dorsal root- slow pain, temp, touch
Block onset
- B
- C
- A gamma and A delta
- A alpha and a beta
VGNaC
1 alpha unit
2 betas
Resting (-70 mV): closed
Active (-70 to +35 mV): opens, Na flows outside to inside
Inactive (+35 to -70 mV): closed, inactivation gate until membrane potential reestablished
LA can bind in active and inactive phases- more frequent depol means more time for blockade (use dependent or phasic blockade)
Resting membrane potential
-70
3 Na+ out and 2 K+ in
LAs do not impact resting membrane potential or threshold
Mechanism of action LA
Weak bases
After injection LA dissociates into uncharge base and ionized, conjugate acid
PKa’s higher than 7.4= > 50% will exist as ionized conjugate acid
Uncharged base enters cell and becomes ionized due to acidic ECF
Only ionized, conjugate acid binds to LA binding site on alpha subunit
LA molecule construction
Benzene ring- lipophilic
Intermediate chain- ester or amide (has NH in it)
Tertiary amine- hydrophilic
Ester LA’s
No i before Caine suffix
Benzocaine, cocaine, chloroprocaine, procaine, tetracaine
Pseudocholinesterase metabolism
Low allergic potential- cross sensitivity if allergy happens, due to PABA
Amide type
I before suffix Caine
Articaine, bupivicaine, etidocaine, lidocaine, mepivicaine, ropivicaine
Hepatic/P450 metabolism
Extremely rare allergies
Onset of action
PKA- closer to pH of blood= larger fraction uncharged and able to cross and get to receptor
Dose- give large dose of chlorprocaine cause isn’t very potent even with high pKa
Concentration- higher concentration onset’s quicker
Potency
Lipid solubility- can get inside drug and be available to bind to receptor
Intrinsic vasodilating effect- cocaine, chloroprocaine, and ropi dont vasodilate, lido does
Duration of action
Protein binding- tissue reservoir to extend DOA, preferably bind to alpha a acid glycoprotein but can bind to albumin
Lipid solubility
Intrinsic vasodilating effect
Addition of vasoconstrictors- prolongs
Amide pKa
Bupivacaine- 8.1
Ropivacaine- 8.1
Lido- 7.9
Prilocaine- 7.9
Ester pKa’s
Procaine- 8.9
Chloroprocaine- 8.7
Tetracaine- 8.5
PKa and LA
Degree of ionization increases as pKA gets further from physiologic pH
Faster onset at pKa close to blood (except chloroprocaine)
Benzocaine
PKa 3.5
Unionized at pH yet i has anesthetic activity
Site of LA and uptake
I Think Illogical Imposters Can’t Educate But Fabulous Schools Should IV Tracheal Interpleural Intercostal Caudal Epidural Brachial plexus Femoral Sciatic Subcutaneous
Amide max doses
Bupivicaine 2.5mg/kg, 175mg, with epi 3mg/kg, 175mg
Lidocaine 4.5 mg/kg, 300 mg, with epi mg/kg, 500mg
Ropivicaine 5 mg/kg, 200 mg
Mepivicaine 7 mg/kg, 400mg
Ester max doses
Procaine 7mg/kg, 350-600mg
Chloroprocaine 11mg/kg, 800mg
Lidocaine toxicity
1-5mcg/mL- analgesia 5-10mcg/mL- tinnitus, perioral numbness, skeletal muscle twitching, restlessness, vertigo, blurred vision, hotn, myocardial depression 10-15mcg/mL- seizures 15-25mcg/mL- coma, respiratory arrest >25mcg/mL- cardiovascular collapse
CNS factors that increase LAST risk
Hypercarbia
Hyperkalemia- raises membrane potential and makes depolarization more likely
Metabolic acidosis- ion trapping in brain
LA cardiac affinity
Bupivacaine>levobupivacaine>ropivacaine>lidocaine
Bupi risk increased with pregnancy, beta blockers, ca channel blockers, dig
Cocaine toxicity
Inhibits NE reuptake into nerve terminal- vasoconstrictive properties
SNS stim increases risk
Avoid with MAOIs, TCAs, sympathomimetic drugs
Beware of beta blockade due to unopposed alpha 1 stimulation
Nitro is best but use labetolol or beta blocker with alpha mixed in
Lipid emulsion for LAST
Bolus 20% 1.5mL/kg (lean body mass) over one minute
Infusion 0.25 mL/kg/min
Can repeat bolus up to 2 more times and increase infusion to 0.5
Infusion goes 10min after hemodynamic stability
Max dose 10mL/kg in 1st 30 min
Lipid MOA
Lipid sink- reservoir to sequester LA
Metabolic- increases fatty acid metabolism
Inotropic effect- increased Ca influx
Membrane effect- impairs binding to VgNaC
Avoid in LAST treatment
Beta blockers and Ca blockers
Tumescent anesthesia
PE most common causes of death
Solution of sodium chloride, lido, epi, and bicarb
Max lido dose 55mg/kg
Peaks at 12 hours and eliminated in 36 hours
Methemoglobinemia
Fe2+ on hemoglobin oxides to ferric form Fe3+-forms methemoglobin
Decreases O2 carrying capacity and shifts curve to L
Causes- benzocaine, cetacaine, prilocaine, EMLA, nitroprusside, nitroglycerin, sulfa, phenytoin
Methemoglobinemia S/S
Hypoxia Cyanosis- with normal PaO2 Chocolate colored blood Tachycardia Tachypnea Mental status changes Coma/death
Methemoglobinemia treatment
Methylene blue: 1-2 mg/kg over 5 min, max dose 7-8 mg/kg
Metabolized and reduces methemoglobin to hemoglobin
Neonates at high risk
EMLA
50/50 lido and prilocaine
Analgesia in 1 hour, max effect 2-3 hrs
Only to intact skin
Infants and kids have risk of methemoglobin
EMLA dosing
0-3 months or < 5 kg- 1 g, 10 cmsquared
3-12 months or >5kg- 2 g, 20cmsquared
1-6 years or >10kg- 10g, 100cmsquared
7-12 years or >20kg- 20g, 200cmsquared
Prolong duration of action
Epi- alpha 1 agonist, works better on intermediate action LAs
Decadron- acts on steroid receptor
Dextran- decreases uptake of LAs
provide supplemental analgesia
Clonidine- alpha 2 agonism in brain and SC
Epi- alpha 2 agonism
Opioids- spinal and epidural
Drugs that shorten onset time
Sodium bicarb
Increases number of lipid soluble molecules
Increasing fraction of nonionized base
Drugs that improve diffusion through tissues
Hyaluronidase Hinders spread of substances through tissues Used in ophthalmic blocks Reduces hematoma size Allergy potential
