Regionals LA Pharmacology Barry
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| Define regional anesthesia: | Insensibility of a part induced by interrupting the sensory nerve conductivity of that region of the body.
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| Regional anesthesia results from... | The result of a conduction blockade of specific peripheral nerves or nerve groups.
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| When was Cocaine first isolated from the coca plant? | 1855.
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| 1884- Carl Koller did what? | An ophthalmologist, he used topical cocaine for the first time during eye surgery.
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| 1884- Surgeon William Halsted (Hall) used cocaine for... | Mandibular and brachial plexus nerve blocks.
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| What happened in 1885? | Corning 1st use of spinal/epidural anesthesia in a dog (cocaine)
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| Who was the first to perform a lumbar puncture? | 1891- Heinrick Quinke performed a lumbar puncture for hydrocephalus.
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| When did Heinrick Quinke perform the first LP? | 1891.
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| 1898- August Bier... | Administered spinal anesthetic using 3 ml of 0.5% cocaine intrathecally for surgical anesthesia & published his results.
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| When was the first Bier block? | 1908- August Bier described intravenous regional anesthesia (Bier Block).
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| When was the first synthetic LA and who synthesized it? | 1904- Alfred Einhorn, synthesized Procaine (Novacaine).
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| 1905- Heinrich Braun... | Used Procaine as a local anesthetic. He also was the first to add epinephrine to prolong the effect of the local.
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| 1901- Ferdinand Cathelin and Jean Sicard introduced... | Caudal epidural anesthesia.
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| 1921- Fidel Pages reported using... | Epidural anesthesia for abdominal surgery.
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| What LA was introduced in 1855? | Cocaine.
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| What LA was introduced in 1904? | Procaine (Novocaine).
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| What LA's were introduced in the 1920's? | Dibucaine (Nupercaine) & Tetracaine (Pontocaine).
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| What's the brand name of Dibucaine? | Nupercaine.
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| What's the generic name of Nupercaine? | Dibucaine.
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| What's the generic name of Pontocaine? | Tetracaine.
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| What's the brand name of Tetracaine? | Pontocaine.
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| 1940’s- Lofgren and Lundquist introduced... | Lidocaine.
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| When was Lidocaine discovered and who was responsible? | 1940's, Lofgren and Lundquist.
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| 1955 what LA was discovered? | Chloroprocaine (Nesacaine).
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| When was Chloroprocaine (Nesacaine) discovered? | 1955.
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| What is the brand name of Chloroprocaine? | Nesacaine.
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| What is the generic name of Nesacaine? | Chloroprocaine.
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| 1957 what LA was discovered? | Mepivacaine (Carbocaine).
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| When was Mepivacaine (Carbocaine) discovered? | 1957.
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| What is the brand name of Mepivacaine? | Carbocaine.
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| What is the generic name of Carbocaine? | Mepivacaine.
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| 1969, what LA was discovered? | Prilocaine (Citanest).
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| When was Prilocaine (Citanest) discovered? | 1969.
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| What is the brand name of Prilocaine? | Citanest.
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| What is the generic name of Citanest? | Prilocaine.
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| 1963, what drug was synthesized? | Bupivacaine (Marcaine).
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| When was Bupivacaine (Marcaine) synthesized? | 1963.
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| What is the brand name of Bupivacaine? | Marcaine.
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| What is the generic name of Marcaine? | Bupivacaine.
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| 1972, what LA was discovered? | Etidocaine (Duranest).
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| What is the brand name of Etidocaine? | Duranest.
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| What is the generic name of Duranest? | Etidocaine.
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| 1996, what LA was discovered? | Ropivacaine (Naropin).
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| What is the brand name of Ropivacaine? | Naropin.
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| What is the generic name of Naropin? | Ropivacaine.
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| What are some common characteristics of LA's? | 1. Poorly H2O soluble
2. Weak base
3. Benzoic acid derivative joined by an ester linkage to a tertiary amine
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| Synthetic derivatives possess same 3 essential functional units: | 1. Hydrophilic chain (tertiary amine), joined to
2. Lipophilic portion (aromatic ring) by
3. An ester or amide linkage (hydrocarbon chain)
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| What are the ester LA's? | Cocaine, Procaine, Chloroprocaine, Tetracaine.
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| What are the amide LA's? | Lidocaine, Bupivacaine, Ropivacaine, Mepivacaine, Prilocaine, Etidocaine.
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| What are some general characteristics of LA esters? | 1. Are less stable (shorter shelf life)
2. Metabolized in the plasma by pseudocholinesterases
3. More prone to cause allergic reactions
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| What are some general characteristics of LA amides? | 1. More stable
2. Metabolized by liver
3. Rare allergies
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| LA's are poorly soluble in H2O. How are they prepared? | Commercially prepared as H2O soluble HCL salts.
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| LA'S are commercially prepared as H2O soluble HCL salts, making them acidic with a pH range of 4-7. This acidity is important for two reasons: | 1. At this pH they are highly ionized, it is this portion that is H2O soluble.
2. Epi (if added) needs an acidic pH as it is unstable in alkaline environments.
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| What is the method of action of LA's? | They inhibit the transmission of nerve impulses by preventing the passage of Na ions through their channels in the nerve membranes.
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| What are Na channels? | Na channels are integral membrane proteins that initiate and propogate action potentials.
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| What is the specific receptor for the LA's? | The alpha subunit of the Na channel in the nerve membrane.
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| What form of LA crosses the membrane? | Unionized (free base).
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| What happens after the free base crosses the membrane? | Once in the axoplasm; the base and the cationic (ionized) form “re”equilibrate.
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| When do LA's have the highest affinity for the Na channel? | When the Na channels are in the open and activated state (rather than in the resting state).
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| What form of the LA keeps the Na channel in a closed, inactivated state? | The unionized free base.
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| The ionized form sneaks in after an action potential has passed (and Na channels are open), and... | Attaches to a receptor site inside the Na channel and blocks it.
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| What is CM? | Minimum concentration. The minimum amount of drug needed to produce a block.
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| What factors influence minimum concentration? | 1. Potency of local anesthetic
2. Nerve diameter
3. Myelination
4. “frequency dependent blockade priniciple”
5. Position of nerve in nerve bundle
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| Blocking of impulse requires a defined length of fiber to be... | "Nonexcitable."
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| Myelinated fibers: conduction proceeds in jumps from one node of Ranvier to next. How many nodes need to be blocked for successful block? | To successfully block myelinated fibers; LA’s must generally inhibit 3 successive nodes of Ranvier.
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| Unmyelinated fibers: | 1. Usually conduct more slowly.
2. Often relatively resistant to LA’s despite smaller size.
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| Because of the “dual action” of the locals, the more action potentials that occur... | The more likely the local will encounter the Na channel in the open or inactive state.
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| The more action potentials that occur the more likely the local will encounter the Na channel in the open or inactive state. What is this called? | "Frequency dependent blockade” or “use dependence.”
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| What does "frequency dependent blockade" or "use dependence" explain? | This explains why some nerves that have a lot of action potentials are more sensitive to locals than others that have less action potentials.
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| Position of nerve in nerve bundle indicates what? | Those closer to the “mantle” blocked before those closer to “core.”
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| Fiber diameter indicates what? | 1. Smaller fibers “more sensitive”
2. Larger fibers “less sensitive”
“Locals will block smaller fibers at lower concentrations than are required by larger fibers of same type.”
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| As a group unmyelinated fibers... | Are more resistant to LA’s compared with some larger myelinated fibers.
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| Nerve fibers are classified as <blank> based on anatomical and functional properties. | A, B, and C.
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| A-fibers = | Motor efferent conduction.
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| How many A-fibers are there? | Four. Alpha, beta, gamma, and delta.
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| A-alpha: | Innervate skeletal muscle motor/proprioception.
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| A-beta: | Sensations of touch/pressure.
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| A-gamma: | Skeletal muscles for muscle tone.
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| A-delta: | Sensations of pain/temperature/touch.
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| Are A-fibers myelinated? | Yes, all of them.
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| T or F: A fibers: motor afferent conduction A-alpha: innervate skeletal muscle motor/proprioception A-beta: sensations of touch/pressure A-gamma: skeletal muscles for muscle tone A-delta: sensations of pain, temp., touch A fibers are all myelinat | False.
A fibers: motor EFFERENT conduction
A-alpha: innervate skeletal muscle motor/proprioception
A-beta: sensations of touch/pressure
A-gamma: skeletal muscles for muscle tone
A-delta: sensations of pain, temp., touch
A fibers are all myelinat
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| T or F: A fibers= motor efferent conduction A-alpha: innervate skeletal muscle motor/proprioception A-beta: skeletal muscles for muscle tone A-gamma: sensations of touch/pressure A-delta: sensations of pain, temp., touch A fibers are all myelin | False.
A fibers= motor efferent conduction
A-alpha: innervate skeletal muscle motor/proprioception
A-beta: SENSATIONS OF TOUCH/PRESSURE
A-gamma: SKELETAL MUSCLES FOR MUSCLE TONE
A-delta: sensations of pain, temp., touch
A fibers are all myeli
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| B-fibers: | 1. Preganglionic autonomic nerve fibers
2. Myelinated, frequently firing
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| Are B-fibers myelinated? | Yes.
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| True or false: B-fibers are 1. Postganglionic autonomic nerve fibers 2. Myelinated, frequently firing | False. B-fibers are
1. PREganglionic autonomic nerve fibers
2. Myelinated, frequently firing
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| True or false: B-fibers are 1. Preganglionic autonomic nerve fibers 2. Unmyelinated, frequently firing | False. B-fibers are
1. Preganglionic autonomic nerve fibers
2. MYELINATED, frequently firing
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| C-fibers: | 1. Pain (slow), reflex responses
2. Postganglionic autonomic
3. Unmyelinated, small fibers
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| Are C-fibers myelinated? | No.
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| True or false: C-fibers 1. Pain (slow), voluntary responses 2. Postganglionic autononic 3. Unmyelinated, small fibers | False. C-fibers
1. Pain (slow), REFLEX responses
2. Postganglionic autonomic
3. Unmyelinated, small fibers
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| True or false: C-fibers 1. Pain (slow), reflex responses 2. Preganglionic autonomic 3. Unmyelinated, small fibers | False. C-fibers
1. Pain (slow), reflex responses
2. POSTganglionic autonomic
3. Unmyelinated, small fibers
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| Talk about blocking B-fibers. | Blocked 1st. Exception to rule d/t rapid conduction velocity. So requires a minimum concentration of LA to block.
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| What fibers are these: Pain fibers, blocked by same conc. of local. | A delta and C fibers.
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| Order of nerve block recovery: | 1. A-alpha
2. A-beta
3. A-gamma
4. C and A-delta
5. Beta
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| STPTPMVP: | 1. Sympathetic
2. Temperature
3. Pain
4. Touch
5. Pressure
6. Motor
7. Vibration
8. Proprioception
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| Lipid solubility is related to... | Potency.
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| Potency is related to... | Lipid solubility.
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| Protein binding is related to... | Duration of action.
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| Duration of action is related to... | Protein binding.
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| PKa is related to... | Onset.
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| Onset is related to... | PKa.
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| All currently used locals have pKa's... | Higher than body pH.
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| A lower pKa will give you a... | More unionized drug at body pH.
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| The pH of the tissue becomes relevant in conditions of infection or inflammation, in which the pH may be more acidic. This acidity results in a... | Greater proportion of the ionized (charged) form of the anesthetic, thereby delaying or preventing the onset of action.
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| What vasoconstrictors are used with LA's? | Epinephrine and Phenylephrine.
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| What does Epinephrine do to the pH of your LA? | Makes it more acidic and increases its shelf life.
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| What are the two ways Epinephrine acts in conjunction with your LA? | 1. Decreases blood flow to area thus less taken up in blood and carried away; also increasing time fibers are exposed to increased concentrations (incr. block)
2. Also thought to exert presynaptic adrenergic receptor activity that contributes to analgesi
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| Talk about Sodium Bicarb and LA: | 1. Used clinically to speed onset of block
2. Increases amount of “nonionized” form available to cross membrane
3. Inconsistent
4. May see more effect with epinephrine containing locals
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| When and why do we use opioids with LA? | 1. Used with central blocks
2. Improves perioperative analgesia
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| Talk about alpha-2 adrenergic agonists. | 1. Used in central blockade
2. Enhances analgesia without opioid side effect profile
3. Binds to a-2 receptors on primary afferent fibers and several brainstem nuclei
4. Increases AcH and norepi in CSF and inhibits release of several neurotransmitters
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| Where do alpha-2 adrenergic agonists bind? | Alpha-2 receptors on primary afferent fibers and several brainstem nuclei.
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| Alpha-2 adrenergic agonists bind to alpha-2 receptors on primary afferent fibers and several brainstem nuclei. What do they do there? | Increase ACh and Norepi in CSF and inhibits release of several neurotransmitters.
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| What's the most common alpha-2 adrenergic agonist? | Clonodine.
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| True or false: Clonodine is an alpha-2 adrenergic antagonist that binds to alpha-2 receptors on primary afferent fibers and several brainstem nuclei. It increases ACh and Norepi in CSF and inhibits release of several neurotransmitters. | False. Clonodine is an alpha-2 adrenergic AGONIST that binds to alpha-2 receptors on primary afferent fibers and several brainstem nuclei. It increases ACh and Norepi in CSF and inhibits release of several neurotransmitters.
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| True or false: Clonodine is an alpha-2 adrenergic agonist that binds to alpha-2 receptors on primary efferent fibers and several brainstem nuclei. It increases ACh and Norepi in CSF and inhibits release of several neurotransmitters. | False. Clonodine is an alpha-2 adrenergic agonist that binds to alpha-2 receptors on primary AFFERENT fibers and several brainstem nuclei. It increases ACh and Norepi in CSF and inhibits release of several neurotransmitters.
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| True or false: Clonodine is an alpha-2 adrenergic agonist that binds to alpha-2 receptors on primary afferent fibers and several brainstem nuclei. It increases ACh and Norepi in CSF and inhibits release of several neurotransmitters. | True.
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| Tissue blood flow from most to least absorption of LA: | 1. IV
2. Intercostal
3. Tracheal
4. Caudal/paracervical
5. Epidural
6. Brachial plexus
7. Spinal
8. SubQ
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| What four factors influence absorption of locals? | 1. Tissue blood flow
2. Protein binding
3. Lipid solubility
4. Metabolism
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| Talk about metabolism of locals. | Very small amounts excreted unchanged in urine
Amides: primarily metabolized by the liver
Esters: hydrolysis by plasmacholinesterases
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| What is the active metabolite of Lidocaine? | Mono ethyl glycine xylidide.
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| What is a precaution of using Lidocaine in a patient with liver problems? | More chance of toxicity.
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| What is the metabolite of Prilocaine? | Ortho Toluidine.
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| What does Ortho Toludine do? | Converts hemoglobin to methemoglobin.
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| What is the treatment for Methemoblobinemia? | Methyline Blue.
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| Do locals easily cross the BBB? | Yes.
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| What are the two ways we can get CNS toxicity from locals? | Direct IV infusion or systemic absorption.
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| List the s/s of LA CNS toxicity from earliest and least dangerous to latest and most dangerous. | 1. Vertigo/Lightheadedness
2. “Tinnitius” Visual/auditory disturbances
3. Circumoral numbness
4. Ominous feelings
5. Muscle twitching
6. Convulsions
7. unconsciousness
8. Coma
9. Resp collapse
10. CV collapse
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| How can we prevent LA CNS toxicity? | 1. Choice of appropriate drug/dose
2. Frequent aspiration from catheter (epid)
3. Small “test doses”
4. Checking for systemic effects
5. Monitors
6. Slow injection
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| Treatment of LA CNS toxicity is dependent on severity. Know s/s and stop injection. How do you treat? | 1. Maintain patent airway
2. O2/barbs/benzo’s
3. Tx CV s/s
Initially excitation
Tachy, hypertension
Followed by depression
4. Decr CO, hypotension
Phenylephrine, ephedrine, norepi
Amniodarone, bretylium, vasopressin
5. Increased resuscitation tim
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| What is lipid resuscitation (20% intralipid)? | 1. Administer 1.5 mL/kg as an initial bolus; the bolus can be repeated 1- 2 times for persistent asystole.
2. Start an infusion at 0.25 mL/kg/min for 30-60 minutes; increase infusion rate up to 0.50 mL/kg/min for refractory hypotension.
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| What's the bolus dose for lipid resuscitation (20% intralipid)? | Administer 1.5 mL/kg as an initial bolus; the bolus can be repeated 1- 2 times for persistent asystole.
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| What's the infusion dose (after the bolus dose) for lipid resuscitation (20% intralipid)? | Start an infusion at 0.25 mL/kg/min for 30-60 minutes; increase infusion rate up to 0.50 mL/kg/min for refractory hypotension.
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| Where is Pseudocholinesterase produced, and where does it go? | Pseudocholinesterase is an enzyme produced by the liver and circulates in the plasma.
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| Ester LA's are derivatives of... | Benzoic acid.
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| What is a metabolic end product of ester LA? | Para-aminobenzoic acid (PABA).
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| Dibucaine (Nupercaine) Very potent, <blank> times as toxic as procaine. (Not used in clinical practice) | 15.
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| Dibucaine depresses the activity of... | Pseudocholinesterase.
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| Dibucaine number: If the individual is Heterozygote (one norm and one abnorm gene) how much depression? | 40%.
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| Dibucaine number: If the patient is Homozygote (2 abnormal genes) how much depression? | 20%.
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| If you have atypical plasma cholinesterase you are incapable of... | Metabolizing ester locals.
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| Talk about Dibucaine numbers and times. | Dibucaine number 80 = normal
Dibucaine number 40 = 20-30 minute block
Dibucaine number 20 = Very long wait, pt goes intubated to RR. Can last up to 8 hours.
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| What is a Dibucaine number? | Percentage of inhibition of Pseudocholinesterase.
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| Can Prilocaine induce methemoglobinemia? | Yes.
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| Normal Hb has iron in what state? | Ferrous (Fe++).
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| Met-Hb has iron in what state? | Ferric (Fe+++). O2 carrying capacity is poor.
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| What is the dose of Methylene Blue for methemoglobinemia? | Methylene blue 1-2mg/kg over 5 minutes.
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| Talk about Parabens. | 1. Paraben derivatives (have microbial actions) can cause allergic rxns.
2. Parabens are cytotoxic – do not use for spinal , epidural or intravenous regional anesthesia.
3. Needs to say Methylparaben Free or MPF
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| Novocaine/Procaine: max dose, duration, duration with epi: | Max dose: 12mg/kg
Duration: 30-60 minutes
Duration with epi: 30-90 minutes
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| Nesacaine/Chloroprocaine: max dose, duration, max dose with epi, duration with epi: | Max dose: 12 mg/kg
Duration: 30-60 minutes
Max dose with epi: 14 mg/kg
Duration with epi: 30-90 minutes
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| Pontocaine/Tetracaine: max dose, duration, duration with epi: | Max dose: 3 mg/kg
Duration: 1.5-2.5 hours
Duration with epi: 4-6 hours
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| Cocaine: max dose, duration: | Max dose: 3 mg/kg
Duration: 30-60 minutes
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| Lidocaine/Xylocaine: max dose, duration, max dose with epi, duration with epi: | Max dose: 4 mg/kg
Duration: 30-120 minutes
Max dose with epi: 7 mg/kg
Duration with epi: 120-360 minutes
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| Mepivacaine/Carbocaine: max dose, duration, max dose with epi, duration with epi: | Max dose: 4 mg/kg
Duration: 45-90 minutes
Max dose with epi: 7 mg/kg
Duration with epi: 120-360 minutes
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| Ropivacaine: max dose, duration: | Max dose: 3 mg/kg
Duration: 90-240 minutes
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| Bupivacaine/Marcaine: max dose, duration, max dose with epi, duration with epi: | Max dose: 2.5 mg/kg
Duration: 120-240 minutes
Max dose with epi: 3.2 mg/kg
Duration with epi: 180-420 minutes
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| Etidocaine/Duranest 1%: max dose, duration, max dose with epi, duration with epi: | Max dose: 6 mg/kg
Duration: 120-180
Max dose with epi: 8 mg/kg
Duration with epi: 180-420 minutes
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| How do LA affect CV system? | 1. Generally depressant (exception cocaine)
2. Cardiac Na channel blockade
3. Inhibition of ANS
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| How do LA affect Resp system? | 1. Lidocaine depresses hypoxic drive
2. Relax bronchial smooth muscle (IV)
3. Apnea from phrenic nerve paralysis (C-4)
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| What can IV Lidocaine do to CNS? | 1. Lidocaine (IV) decreases cerebral blood flow
2. Attenuates the rise in ICP from laryngoscopy
3. IV can reduce MAC up to 40%
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| What does Cocaine do to the CNS? | Stimulates it.
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| What LA's are the biggest culprits for CNS toxicity? | Chloroprocaine
Lidocaine 5%
Continuous subarachnoid, lithotomy, ischemia
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| What risk factors are associated with TNS (transient neurologic symptoms)? | Lido, litho, obesity, parasthesia.
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| How do LA's affect the immunologic system? | 1. Rare allergic rx
2. Uncommon to local
3. Usually preservative or rx to epi
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| MS and LA? | Myonecrosis with direct injection.
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| How do LA's affect the hematologic system? | 1. Decrease coagulation
2. Enhance fibrinolysis
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| How does the use of epi affect toxicity? | Use of epi reduces risk of toxicity (due to reducing blood flow).
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| Is Cauda Equina syndrome transient? | No. It is permanent.
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| What are some factors implicated in Cauda Equina syndrome? | Several things: usually 5% Lidocaine, Lithotomy position, ischemia to the nerve by hypothermia and hypotension and the use of continuous subarachnoid catheters (not common).
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To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
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