Regional Introduction Flashcards
What are the three structures of that make up LA?
Aromatic Ring – fat soluble (hydrophobic)
Terminal Amine – water soluble (hydrophillic)
Intermediate link - Ester or Aminde
Generally what are three characteristics of Esters?
- -Are less stable (shorter shelf life)
- -Metabolized in the plasma by pseudocholinesterases
- -More prone to cause allergic reactions
Generally what are three characteristics of Amides?
- -More stable
- -Metabolized by liver
- -Rare allergies
Chemical structure of LA, what two important reasons why they are placed in an acidic environment (vial)?
This acidity is important for 2 reasons:
- –At this pH they are highly ionized, it is this portion that is H2O soluble
- –Epi (if added) needs an acidic pH as it is unstable in alkaline environments
- —NaHCO3 is often added to hasten onset
How is the potency of LA determined?
Lipid solubility or length of chain is related to potency
How is the duration of action of LA determined?
Protein binding is related to duration of action
How is the onset of an LA determined?
pKa is related to the onset
To successfully block myelinated fibers, LAs must block how many nodes?
To successfully block myelinated fibers; LA’s must generally inhibit 3 successive nodes of ranvier
What is the order of the Nerve fiber blockade? from first to last?
B fibers C and A delta Fibers A gamma Fibers A beta Fibers A alpha fibers
What are B fibers responsible for?
Autonomic and sympathetic efferent
What are C and A Delta fibers responsible for?
Temperature and touch
What are A Gamma fibers responsible for?
Muscle tone for skeletal muscles
What are A beta fibers responsible for?
Small motor with sensations of touch/pressure
What are A alpha fibers responsible for?
innervate skeletal muscle for large motor and proprioception
Are all A fibers myelinated or unmyelinated?
All A fibers are myelinated
What are B-fibers?
Preganglionic autonomic nerve fibers
B fibers myelinated or unmyelinated?
B fibers are myelinated
C fibers myelinated or unmyelinated?
C fibers are unmyelinated
What are C fibers?
pain (slow), reflex responses, postganglionic autonomic
What are A delta fibers?
sensations of pain (1st;fast), temp., touch
What a-1 agonists can you give as local anesthetic “adjuvants”?
Epinephrine
Phenylephrine
These are a-1 agonists
(vasoconstrictors)
How will Epinephrine effect the local anesthetic as an “adjuvants”?
- -Makes more acidic; increases shelf life
- -Prolongs & incr. intraneural conc. of LA’s
- -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)
- -Now also thought to exert presynaptic adrenergic receptor activity that contributes to analgesia
What will sodium bicarbonate do if you add it as an adjuvant to local anesthetics?
- -Used clinically to speed onset of block
- -Increases amount of “nonionized” form available to cross membrane
- -Inconsistent
- -May see more effect with epinephrine containing locals
What class are used as an adjuvant to local anesthetics, especially with central blocks? This improves perioperative analgesia as well.
Opioids
Also see a reduction of supraspinal side effects seen w. systemic opioids
Opioids and spinal analgesia modulated what fibers in the spinal cord?
A-delta & C fibers in the spinal cord
What type of affects does opioids and LA have?
A synergistic affect
What are major concerns/side effects with using opioids in conjunction with local anesthetics?
Pruritis
N/V
Urinary retention
If you use opioids in conjunction with local anesthetics, what other drugs will it require you to use less of?
Reduces the requirements of Volatile Anesthetics
What is the most commonly used alpha-2 adrenergic agonist in conjunction with local anesthetics?
Clonidine
Alpha-2 adrenergic agonists are used in why type of blockade?
Used in central blockade
What are alpha-2 adrenergic agonists suppose to do when it is used with local anesthetics?
It enhances analgesia without opioid side effect profile
Alpha-2 adrenergic agonists binds to a-2 receptors on which two sites in the body?
Binds to a-2 receptors on primary afferent fibers and several brainstem nuclei
Alpha-2 adrenergic agonists increases AcH and norepi in the (Blank) and inhibits the release of several other (Blank)?
Increases AcH and norepi in CSF and inhibits release of several neurotransmitters
Absorption of local anesthetics depends on many factors such as injection site. What is the order of injection site that will be more more vascular/ increase absorption?
Tissue blood flow: More vascular/ incr. absorption IV Intercostal Tracheal Caudal/paracervical Epidural Brachial plexus Spinal SubQ ****presence of epi will decrease absorption
Do Local anesthetics cross the BBB?
Yes
locals readily cross the BBB
CNS toxicity can occur with direct IV injection or by?
CNS toxicity can occur with direct IV injection or systemic absorption
What are signs and symptoms of local anesthetic toxicity?
S/S dose dependent
- Vertigo/Lightheadedness
- “Tinnitius” Visual/auditory disturbances
- Circumoral numbness
- Ominous feelings
- Muscle twitching
- Convulsions
- unconsciousness
- Coma
- Resp/ Cardio collapse
What are some ways that you can prevent local anesthetic toxicity? (not talking about adding epi)
- Choice of appropriate drug/dose
- Frequent aspiration from catheter (epid)
- Small “test doses”
- Checking for systemic effects
- Monitors
- Slow injection
What is the treatment for local anesthetic toxicity? (other than intralipid)
Dependent on severity -Stop injection -Know s/s -Maintain patent airway/O2 barbs/benzo’s -Tx CV s/s Initially excitation Tachy, hypertension Followed by depression --Decr CO, hypotension Fluids, phenylephrine, vasopressin, norepi --Cardiac arrest Amniodarone, vasopressin vs. epi and lidocaine Increased resuscitation time
If using 20% intralipid for local anesthetic toxicity, how do you give it?
- -Administer 1.5 mL/kg as an initial bolus; the bolus can be repeated 1- 2 times for persistent asystole.
- -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
How can you tell if a Local anesthetic is an Ester or Amide?
Esters have one i, Amides have 2 i’s.
How are esters and amides metabolized?
Esters are metabolized by pseudocholinesterase. Amides are cleared by the liver.
what is Pseudocholinesterase?
Pseudocholinesterase is an enzyme produced by the liver and circulates in the plasma.
What are ester local anesthetics derived from?
Ester local anesthetics are derivatives of benzoic acid.
What is the metabolic end product for an ester local anesthetic?
Para-aminobenzoic acid (PABA) is a metabolic end product of ester local anesthetics.
What is the toxic manifestations for lidocaine?
Toxic manifestations of Lido 4ug/ml. Tongue numbness, lightheadedness.
Whats the relationship between benzoic acid and PABA?
- -Benzoic acid = ester local anesthetics = PABA (Para-aminobenzoic acid)
- -PABA can cause allergic reactions
- -Esters cause allergic reactions more so than amides secondary to PABA
Which local anesthetic can can induce methemoglobinemia??
- —Prilocaine may induce methemoglobinemia.
- – O-toluidine is a metabolite of liver metabolism of prilocaine which may cause methemoglobinemia.
What is Methemoglobinemia?
—Methemoglobinemia: Normal hemoglobin has iron in the ferrous state (Fe++) Met-Hb has iron in the ferric state (Fe+++) O2 carrying capability is poor. Tx. Methylene blue 1-2mg/kg over 5 minutes.
Which preservative can cause an allergic reaction?
- —Paraben derivatives (have microbial actions) can cause allergic rxns.
- –Parabens are cytotoxic – do not use for spinal , epidural or intravenous regional anesthesia.
- –Needs to say Methylparaben Free or MPF
What are the Local Anesthetics clinical uses?
- –Topical
- –Infiltration (for Aline/Pline)
- -Field block
- -Nerve block
- -Intravenous regional anesthesia (Bier block)
- -Spinal anesthesia
- -Epidural anesthesia (caudal)
What are two types of Central nerve blocks?
Spinal and Epidural
What makes a Spinal block different from an epidural block?
- -Small volume
- -Direct-Sheath (in the spinal cord, right at the nerves)
- -Rapid onset
- -Total neural block (from this area and below) (BP will quickly drop)
What makes an epidural block different from a spinal block?
Large volume
Outside-Sheath
Slow onset (has to slowly diffuse into the sheath)
Block varies with dose
(the more volume you put the higher the block will be
What are some advantages from doing a peripheral block than doing a central one?
- -Segmental block (don’t see a huge sympathetocmy)
- -Slow onset = time to Rx side effects
- -Flexibility in density
- -Flexibility in duration
- -Less side effects
What are some disadvantages from doing a peripheral block than doing a central one?
- -More technical & more failure
- -More time consuming
- -Greater LA volume- [>toxicity risk]
- -Faulty block
What are some things you need to consider with peripheral nerve blocks in terms of equipment?
- -Usually to perform any peripheral nerve block, you will need specialized equipment
- -This equipment includes specially insulated needles and a nerve stimulator
- -They are hooked up to each other to generate a pulse current so that when you are near a nerve, you will see the area innervated by the nerve react
- -This helps you localize the nerve much more efficiently and makes the percentage of you getting a good block climb tremendously
- -It is no longer a completely “BLIND” technique
