Anesthesia Flashcards

1
Q

What determines the resting potential of a nerve cell?

A

The resting potential arises from two activities:
1. The sodium/potassium ATPase, which moves three sodium ions outside the cell for every two potassium ions inside the cell and produces a net loss of positive charges and results in a negative intracellular charge.
2. Facilitated diffusion of potassium outside the cell.

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2
Q

What is the resting potential value of a nerve cell membrane?

A

All cells have a resting potential: an electrical charge across the plasma membrane with the interior of the cell negative with respect to the exterior. The size of the resting potential can vary, but in excitable cells it is about −70 millivolts (mV).

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3
Q

Describe the ionic relations in the cell for sodium, potassium, chloride, and calcium ions

A
  1. The sodium/potassium ATPase produces:
    a. A concentration of Na+ outside the cell that is some 10 times greater than that inside the cell. b. A concentration of K+ inside the cell some 20 times greater than that outside the cell
  2. The concentrations of chloride ions (Cl−) and calcium ions (Ca2+) are maintained at greater levels outside the cell.
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4
Q

Describe the depolarization of a nerve cell membrane.

A

Before an action potential can be formed, the nerve cell membrane is depolarized by either a mechanical stimulus (sound, stretch, etc.) or a neurotransmitter (eg, acetylcholine). This allows the facilitated diffusion of sodium into the cell, which reduces the resting potential at that area on the cell and creates an excitatory postsynaptic potential or EPSP.

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5
Q

Describe the formation of an action potential.

A

If the initial depolarization stimulus reaches a threshold voltage of –50 mV, then an action potential will be generated from that area of the cell membrane. This opens hundreds of voltage-gated sodium channels and creates a massive influx of sodium. The sudden complete depolarization of the membrane opens up more of the voltage-gated sodium channels in adjacent portions of the membrane. In this way, a wave of depolarization sweeps along the cell. This is the action potential, or nerve impulse.

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6
Q

Why is the action potential an all-or-nothing event?

A

If the critical threshold of a −50 mV membrane depolarization is reached, then an action potential will be produced,
if not, then no action potential will result. Strong stimuli produce no stronger action potentials than weak ones.

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7
Q

How is membrane repolarization reestablished?

A
  1. Diffusion of potassium ions out of the cell.
  2. Closure of sodium channels.
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8
Q

What is the refractory period?

A

A second stimulus applied to a neuron less than 0.001 second after the first will not trigger another impulse. The membrane is depolarized, and the neuron is in its refractory period. Not until the −70 mV polarity is reestablished will the neuron be ready to fire again.

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9
Q

How long does the refractory period last?

A

Varies, in some human neurons the refractory period lasts only 0.001 to 0.002 seconds. This means that the neuron
can transmit 500 to 1,000 impulses per second.

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10
Q

What is the node of Ranvier?

A

Myelinated neurons are encased in a fatty sheath called the myelin sheath, which is the expanded plasma membrane of an accessory cell called the Schwann cell. Where the sheath of one Schwann cell meets the next the axon is unprotected. This area is called the node of Ranvier.

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11
Q

Why is conduction in myelinated neurons faster than in unmyelinated ones?

A

Voltage-gated sodium channels of myelinated neurons are confined to the nodes of Ranvier. The inflow of sodium ions at one node creates just enough depolarization to reach the threshold of the next. In this way, the action potential jumps from one node to the next. This results in much faster propagation of the nerve impulse than is possible in unmyelinated neurons.

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12
Q

What is a conduction block?

A

It is the reversible interruption of conduction within a neural structure by a local anesthetic.

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13
Q

When does conduction block occur?

A

It occurs when local anesthetic molecules occupy enough sodium channels within an axon to interrupt its activity.

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14
Q

How does conduction block by a local anesthetic occur?

A

Local anesthetics act by binding to open-gated sodium channels causing them to remain inactive, thus preventing subsequent depolarization

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15
Q

Why do local anesthetics have a higher potency for nerves with a higher frequency of stimulation?

A

Nerve that have a higher frequency of stimulation have more activated open sodium channels that are more
susceptible to the action of local anesthetics.

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16
Q

Why are myelinated nerves easier to block then unmyelinated ones?

A

In myelinated nerves, only the nodes of Ranvier need to be exposed to local anesthetic for conduction block to
occur. In unmyelinated fibers, the full length and circumference of the nerve must be exposed to local anesthetic.

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17
Q

Why are myelinated nerves easier to block then unmyelinated ones?

A

In myelinated nerves, only the nodes of Ranvier need to be exposed to local anesthetic for conduction block to
occur. In unmyelinated fibers, the full length and circumference of the nerve must be exposed to local anesthetic.

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18
Q

During local anesthesia, what is the sequence of blockade and which nerve fibers are affected?

A
  1. Vasodilation (nerve type B, preganglionic autonomic, sympathetic, light myelin)
  2. Loss of pain and temperature sensation (nerve types A-􏰀 and C, moderate and no myelin, respectively) 3. Loss of pressure sensation (nerve type A-􏰁, heavy myelin)
  3. Loss of motor function (nerve type A-􏰂, heavy myelin)
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19
Q

What three structures make up the anesthetic molecule?

A
  1. aromatic ring (hydrophobic)
  2. tertiary amine (hydrophilic)
  3. intermediate chain (contains either an amide or ester bond)
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20
Q

Local anesthetics are classified into which two groups?

A
  1. Amino esters
  2. Amino amides
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21
Q

What is the pH of local anesthetic solutions?

A

Local anesthetics are weak base with a pKa ranging from 7.7 to 9.1. Commercially prepared solutions are prepared as hydrochloride salts of the cation with a pH of 5.0 to 6.0 without epinephrine and a pH of 2.0 to 3.0 with epinephrine. This is why they burn so much.

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22
Q

How can pain from local anesthetic blocks be minimized?

A

The pain associated with use of local anesthetics can be decreased by adding sodium bicarbonate to the anesthetic. Alkalinization of the local anesthetic solution allows the anesthetic to enter the nerve more quickly thereby increasing the rapidity of onset and effectiveness. Normal dose for sodium bicarbonate is 1 mEq/10 mL lidocaine and 0.1 mEq/20 mL bupivacaine. It can decrease the pain of local anesthetic injection by adding 1 mL sodium bicarbonate for every 9 mL local anesthetic.

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23
Q

The pharmacological activity of local anesthetics is determined by which three physiochemical properties?

A
  1. lipid solubility
  2. protein binding 3. pKa
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24
Q

How does lipid solubility affect the action of local anesthetics?

A

Increased lipid solubility of a local anesthetic will increase its potency because nerve cell membranes are highly
hydrophobic. Increased nerve block will occur because of facilitated entry across the nerve cell membrane.

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25
Q

How does protein binding affect the action of local anesthetics?

A

Local anesthetics with a higher protein binding will have greater contact with the nerve membrane and thus a
longer duration of action.

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26
Q

How does the pKa affect the action of local anesthetics?

A

The pKa of a local anesthetic determines the speed of onset of the nerve conduction block. Fifty percent of the anesthetic will exist in its basic and cationic form at a given pKa. The nonionized basic form has the highest lipid solubility and hence highest speed of onset. Because local anesthetics are prepared as hydrochloride salts with a pH of 5.0 to 6.0, some delay in onset will occur because of physiological buffering which is required to establish a significant base form concentration.

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27
Q

In what two ways can the onset of local anesthetics be accelerated?

A
  1. Preparation of the local anesthetic solution as a hydrocarbonate salt instead of a hydrochloride salt. 2. Addition of sodium bicarbonate to the local anesthetic prior to injection.
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28
Q

List four ester local anesthetics.

A
  1. procaine
  2. tetracaine 3. benzocaine 4. cocaine
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29
Q

List three amide local anesthetics.

A
  1. lidocaine
  2. bupivacaine
  3. prilocaine
    Note that these all have an “i” before the “-aine.”
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30
Q

How are esters metabolized?

A

Esters are rapidly hydrolyzed by plasma pseudocholinesterase that creates a short plasma half-life. Products of metabolism include para-aminobenzoic acid (PABA), which can be associated with hypersensitivity reactions in certain patients.

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31
Q

How are amides metabolized?

A

Liver cells metabolize amides intracellularly. Because of this longer process, an accumulation of repeated doses can cause systemic toxicity. Patients with poor liver function and congestive heart failure will have a significantly prolonged amide half-life. Normal half-life is 2 to 3 hours and unlike esters, true allergies are rare.

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32
Q

What types of toxicities are related to local anesthetics?

A
  1. direct tissue toxicity (buffers, preservatives, potential for intraneural injection) 2. systemic toxicity (CNS, cardiac, methemoglobinemia)
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33
Q

What factors determine the toxicity of a local anesthetic?

A
  1. potency or lipid solubility (increased CNS toxicity)
  2. total dose delivered
  3. rate of plasma uptake
  4. protein binding
  5. site of injection (highly vascularized tissues increase the rate of uptake)
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34
Q

How does the addition of epinephrine reduce a local anesthetic’s toxicity?

A

Produces vasoconstriction which:
1. decreases vascular uptake
2. lowers peak plasma levels
3. slows time course to peak level (reduced CNS toxicity)

35
Q

What toxic effects are associated with the addition of epinephrine?

A
  1. hypertension
  2. tachycardia
  3. cardiac arrhythmia 4. myocardial ischemia
36
Q

Name three factors that decrease seizure threshold and increase the risk of CNS toxicity

A
  1. hypercarbia
  2. hypoxia 3. acidosis
37
Q

Name two agents that can be used to treat seizures following CNS toxicity.

A
  1. benzodiazepine (increases seizure threshold and can prevent seizure activity) 2. sodium thiopental
38
Q

Describe the evolution of local anesthesia-induced CNS toxicity.

A
  1. CNS excitation (occurs first):
    a. dizziness
    b. light-headedness
    c. tinnitus
    d. circumoral numbness
    e. metallic taste in the mouth
    f. loss of consciousness
    g. muscular twitching
    h. convulsions
  2. CNS depression (occurs later): a. respiratory depression
    b. cardiorespiratory arrest
39
Q

What are the effects of local anesthetic toxicity on the cardiovascular system?

A
  1. Increased sodium channel blockade within the cardiac conduction system causes:
    a. decreased Purkinje fiber firing and prolonged conduction time
    b. long PR interval
    c. widened QRS complex
    d. sinus bradycardia and asystole
    e. direct myocardial depressant
    f. ventricular arrhythmia (increased reentrant pathway activity)
40
Q

What measures can be used to prevent or minimize systemic reactions to local anesthetics?

A
  1. Avoid intravascular injections (frequent aspirations while injecting).
  2. Always use smallest possible dose and concentration.
  3. Add epinephrine (avoid in digits and in patients with ischemic heart disease).
  4. Premedication with benzodiazepine (elevates convulsive threshold). 5. Use a small test dose.
41
Q

What measures can be used to treat toxic systemic reactions to local anesthetics?

A
  1. Always follow principles of ACLS.
  2. Convulsions:
    a. hyperventilation with O2 to reduce PaCO2
    b. Diazepam, Midazolam, Pentothal 50 to 100 mg IV
42
Q

What is the estimated adult toxic dose of lidocaine without epinephrine?

A

Maximal dose/kg: 5 mg/kg
Maximal single dose: 300 mg

43
Q

What is the estimated adult toxic dose of lidocaine with epinephrine?

A

Maximal dose/kg: 7 mg/kg Maximal single dose: 500 mg

44
Q

What is the maximum total dose of epinephrine in a healthy adult?

A

0.25 mg.

45
Q

How is a concentration of 1:200,000 of epinephrine prepared?

A

Add 0.05 mg (or 0.05 mL of 1:1000 concentration) of epinephrine to each 10 mL of local anesthetic solution used
(maximum of 50 mL of local anesthesia).

46
Q

What is the onset and duration of 1% lidocaine with and without epinephrine?

A

Lidocaine 1%
Onset: 5–10 min Duration: 45–60 min
Lidocaine 1% with Epinephrine
Onset: 3–5 min Duration: 60–120 min

47
Q

Describe the various indications and concentrations for lidocaine.

A
  1. Local infiltration: 0.5% to 1% (45–60 min)
  2. Intravenous regional anesthesia (IVRA): 0.5% 40 mL total for upper extremity (45–60 min) 3. Peripheral nerve block: 1% to 2% (1–3 hr)
  3. Motor nerve block: 2% (60–80 min)
48
Q

What common local anesthetics are used for peripheral nerve blocks?

A

Agent
2-Chloroprocaine Lidocaine Mepivacaine Bupivacaine Etidocaine
Concentration (%)
2–3 1–2 1–2
0.25–0.5 0.5–0.75
Duration (min)
30–75 45–120 120–300 300–720 300–720

49
Q

What causes methemoglobinemia?

A

The oxidation of hemoglobin from its ferric to ferrous form by prilocaine and benzocaine. Visible cyanosis can
occur when concentrations exceed 4 g/dL and tissue hypoxia and cyanosis can be treated with methylene blue.

50
Q

Allergic reactions to local anesthetics are most often associated with which agents?

A

A true allergic response to local anesthetics is very rare. Most allergies are associated with ester agents, which are metabolized to PABA, which can also be found throughout the pharmaceutical and cosmetic industries. Allergies to amides are even rarer and have been linked to methylparaben which is a preservative added to multidose vials of lidocaine to retard bacterial growth.

51
Q

What different types of anesthesia are available for the upper extremity?

A
  1. general
  2. regional:
    a. brachial plexus blocks (interscalene, supraclavicular, infraclavicular, axillary) b. bier block IVRA
    c. peripheral nerve blocks (radial, ulnar, and median nerves at elbow and wrist) d. metacarpal blocks
    e. digital nerve blocks
52
Q

What are the advantages of using regional anesthesia in the upper extremity?

A
  1. decreased morbidity in high-risk patients
  2. prevention of all afferent stimuli from reaching CNS (prevention of vasoconstriction, vasodilation effect) 3. postoperative pain relief
  3. decreased postoperative nausea and vomiting
  4. emergency procedures (full stomach)
  5. earlier ambulation
  6. outpatient surgery
53
Q

What are the disadvantages of using regional anesthesia in the upper extremity?

A
  1. extra time required for block to be effective
  2. incomplete or failed block
  3. residual numbness or paresthesia
  4. potential infection, hematoma, nerve injury 5. potential toxicity from intravascular injection
54
Q

What are some contraindications to using regional anesthesia?

A
  1. local sepsis, infection
  2. allergy to local anesthetics
  3. coagulopathy, anticoagulant therapy 4. uncooperative patient
  4. peripheral nerve damage
55
Q

Which nerves form the brachial plexus?

A

The union of the anterior primary divisions of C5–8 and T1 forms the brachial plexus with variable contributions from C4 and T2.

56
Q

Briefly describe the organization of the brachial plexus.

A
  1. Robert-roots (five of them, C5–T1)
  2. Taylor-trunks (three of them, superior, middle, and inferior)
  3. Drinks-divisions (six of them, an anterior and posterior division for each trunk) 4. Coffee-cords (three of them, posterior, lateral, and medial)
  4. Black-branches or named peripheral nerves
57
Q

Which peripheral nerve originates from the lateral, medial, and posterior cords?

A
  1. lateral cord: musculocutaneous nerve and contribution to medial nerve
  2. medial cord: ulnar nerve, medial antebrachial and medial brachial cutaneous nerves, contribution to median nerve
  3. posterior cord: radial and axillary nerves
58
Q

Name the four types of brachial plexus blocks to the upper extremity.

A
  1. interscalene block
  2. supraclavicular block 3. infraclavicular block 4. axillary blockade
59
Q

What are the advantages and disadvantages of the interscalene brachial plexus block (ISB)?

A

Indications:
Shoulder surgery, upper arm surgery
Advantages:
Effective analgesia for surgery or arthroscopy of the shoulder
Disadvantages:
Frequently misses:
1. medial cutaneous nerve of the arm
2. intercostobrachial nerve
3. ulnar nerve
Not suitable for hand anesthesia (sparing of C8 and T1) ulnar nerve
Failure rate 8.7%
Complications:
1. 100% ipsilateral phrenic nerve block (C3–5)
2. Horner syndrome
3. hoarseness, dysphagia, blurred vision
4. involvement of recurrent laryngeal and cervical sympathetic nerves can occur

60
Q

What are the advantages and disadvantages of the supraclavicular brachial plexus block?

A

Indications:
Surgery of the arm, elbow, and hand
Advantages:
Well suited for long surgery or prolonged postoperative pain relief
Complete, prompt, long-acting block
Arm can be in a comfortable position (modified Brown’s plumb-bob approach Disadvantages:
Pneumothorax 0.4% to 6%
Ipsilateral phrenic nerve paralysis 60%
Occasional Horner syndrome

61
Q

What are the advantages and disadvantages of the infraclavicular brachial plexus block?

A

Indications:
Surgery of the arm, elbow, and hand
Advantages:
Long-acting hand and arm anesthesia
Reliable block of musculocutaneous and axillary nerves
Lower risk of pneumothorax compared to supraclavicular block Uses more obvious landmarks then Supraclavicular Block (SCB) Disadvantages:
Increased risk of intravascular puncture as the plexus surrounds the subclavian artery at this level

62
Q

What are the advantages and disadvantages of the axillary brachial plexus block?

A

Indications:
Most widely used brachial plexus block in hand surgery Advantages:
Simple, safe, and reliable technique
Well suited for outpatient surgery
Remote from neck and thorax
Disadvantages:
Can miss the musculocutaneous nerve and thus the lateral antebrachial cutaneous nerve Complications:
Intravascular injection
Soreness or bruising of the axilla, persistent numbness

63
Q

Describe the relationship of the radial, ulnar, and median nerves to the axillary artery.

A
  1. The radial nerve is posterior to the axillary artery.
  2. The ulnar nerve is inferior to the axillary artery.
  3. The median nerve is superior to the axillary artery.
64
Q

What is a Bier block and how is it performed?

A
  1. An intravenous catheter is placed as distally as possible in the operated limb and the upper extremity is elevated
    and exsanguinated with an Esmarch bandage starting from distal to proximal.2. A dual tourniquet is placed on the operated arm and the proximal cuff is inflated prior to removal of the Esmarch bandage.
  2. Lidocaine 0.5% (40–50 mL) without preservatives is injected slowly (smaller doses of 30 mL can be used if a forearm tourniquet is used).
  3. The proximal tourniquet cuff can be deflated after 20 minutes after confirming that the distal tourniquet cuff has been inflated to avoid escape of intravascular local anesthetic into the central circulatory system.
  4. This distal cuff is inflated over an anesthetized area and can be tolerated for an additional 40 minutes.
  5. A minimum occlusion time of 20 minutes is recommended based on peak plasma values of local anesthetics.
65
Q

What are the advantages and disadvantages of a Bier block?

A

Advantages:
Ease of administration
Rapid onset
Rapid recovery of motor function
Suitable for outpatient surgery
Disadvantages:
Tourniquet pain when procedure longer than 1 hour
Accidental or early release of tourniquet can lead to toxic intravascular injection Loss of anesthesia following cuff deflation
Exsanguinations of painful extremity
Postoperative pain

66
Q

What are contraindications to using a Bier block (IVRA)?

A
  1. Any condition which precludes to use of a tourniquet: a. sickle cell anemia
    b. severe peripheral vascular disease
    c. established soft tissue infection
    d. tumors
67
Q

What are some causes of postoperative neuritis?

A
  1. tourniquet pressure above 250 mm Hg
  2. limb position during surgery (eg, pressure over ulnar nerve at the elbow)
  3. duration of tourniquet time >2 hours
  4. regional blocks:
    a. sharp needles instead of bevel block needles
    b. intraneural injection
    c. perineural hematoma
    d. seeking paresthesia
    e. higher concentrations than necessary of local anesthetics
68
Q

Name four types of peripheral nerve blocks.

A
  1. elbow block
  2. wrist block
  3. metacarpal block 4. digital block
69
Q

Elbow block

A
  1. Rarely performed because of variations and overlapping of the distribution of the nerves.
  2. Only allows for 20 to 30 minutes of tourniquet time.
  3. Individual elbow blocks most useful for supplementing anesthesia following incomplete brachial plexus blocks.
70
Q

Describe the landmarks for performing ulnar, median, radial, and medial and lateral antebrachial cutaneous nerve blocks at the elbow.

A

Ulnar: posterior to the medial epicondyle, 3 to 5 cm proximal
Median: medial to brachial artery, medial to biceps tendon, slightly above line between epicondyles Radial: anterior aspect of the lateral epicondyle, lateral to the biceps tendon
Medial and lateral antebrachial cutaneous nerves: subcutaneous ring block around the elbow

71
Q

What are the advantages and disadvantages of using wrist blocks?

A

Advantages:
Simple to perform
Retained motor function (except intrinsics)
Disadvantages:
Surgery time limited because of tourniquet pain after 20 to 30 minutes

72
Q

Describe the landmarks for performing ulnar, median, and superficial radial nerve blocks at the wrist

A

Ulnar: radial to the flexor carpi ulnaris tendon, at the level of proximal wrist crease and in the direction of the pisiform bone. (Can also be injected dorsally at the same point to block the dorsal ulnar cutaneous nerve.)
Median: between the palmaris longus and flexor carpi radialis tendons at the level of the proximal wrist crease. Superficial branch of radial nerve: base of the extensor pollicis longus tendon and across the anatomical snuffbox
lateral to the radial artery.

73
Q

How many nerve branches supply the digits?

A

Four nerve branches supply digital sensation: two volar and two dorsal branches along the respective sides of each
digit.

74
Q

How does the ulnar nerve distribution differ from the median nerve distribution distal to the DIP joint?

A

In the small finger, the dorsal digital nerve extends up to the end of the finger, whereas in the median nerve distribution the volar digital nerve supplies a dorsal branch that comes off distal to the PIP joint. Dorsal branches need also to be blocked for complete finger anesthesia.

75
Q

What kind of approaches can be used for a digital nerve block?

A
  1. Volar approach:
    a. common digital nerve
    b. proximal to the common digital arterial communications
    c. skin wheal made over the flexor tendon proximal to the distal palmar crease, and 2- to 3-mL lidocaine
    without epinephrine is injected on each side of the flexor tendons
    d. more painful than the dorsal approach
  2. Dorsal approach:
    a. less painful
    b. allows simultaneous blockade of dorsal branches without a second stick
    c. injection to the side of the extensor tendons proximal to the web and then palmar to block the volar digital
    nerves
  3. Intrathecal or flexor tendon sheath approach:
    a. Single injection of 2 mL into the flexor tendon sheath at the level of the distal palmar crease or
    metacarpophalangeal flexion crease
    b. Rapid onset
76
Q

What should be avoided during digital blockade?

A
  1. use of epinephrine
  2. circumferential ring blocks
  3. excessive or prolonged digital tourniquet 4. excessive local anesthetic volume injection
77
Q

What does a stellate ganglion block interrupt?

A

Sympathetic innervation of the upper extremity.

78
Q

What are the two types of central nerve blockade available?

A
  1. Epidural anesthesia: this occurs when a local anesthetic is injected into the epidural space and generally requires a large volume of anesthetic. Mostly used to block sensory function, not motor function, and often performed as a continuous block; eg, obstetrics.
  2. Spinal anesthesia: this occurs when a local anesthetic is injected into the subarachnoid space cerebrospinal fluid (CSF) and requires smaller volumes of anesthetic compared to epidural anesthesia. Used to block sensory and motor functions.
79
Q

List five potential complications from central nerve blockade.

A
  1. Hypotension: results from vasodilation; risk: patients who are hypovolemic
  2. High spinal: spinal anesthetic migrates cephalad; T1–4: blocks sympathetic innervation to heart (bradycardia, decreased cardiac output), above C4 (phrenic nerve, apnea)
  3. Spinal headache: because of continued CSF leak through the dura; treatment: caffeine, fluids, blood patch.
  4. Urinary retention: common
  5. Spinal cord injury
80
Q

What is balanced anesthesia?

A

Uses several different categories of drugs to achieve desired anesthesia, results in less of each drug and less toxicity.

81
Q

What are the different stages of anesthesia?

A

Stage 1: amnesia (from induction to loss of consciousness)
Stage 2: delirium (most dangerous stage, can have injurious pain response, eg, N&V, laryngospasm, hypertension,
tachycardia, uncontrolled movements)
Stage 3: surgical anesthesia (target point, no pain response)
Stage 4: overdose (shallow or absent respirations, hypotension, dilated and nonreactive pupils)

82
Q

Which muscle relaxant is not recommended for induction in burn patients and why?

A

Succinylcholine. An increase in the number of muscle receptor sites for acetylcholines has been documented in burn patients. Succinylcholine is an agonist of acetylcholine and can be responsible for a large and sometimes fatal release of potassium up to 2 years after the initial burn injury. Nondepolarizing muscle relaxants as well as careful monitoring with a nerve stimulator are recommended.

83
Q

Describe the patient American Society of Anesthesiologists (ASA) classification for anesthesia.

A

The ASA scale is the following:
ASA1: patient is a healthy individual with no major systemic disease
ASA 2: patient has a one-system, well-controlled disease
ASA 3: patient with multisystem disease or well-controlled major system disease ASA 4: patient with severe, incapacitating, poorly controlled, or end-stage disease ASA 5: patient with imminent danger of death with or without surgery
“E”: patient who qualifies for emergency surgery

84
Q

Which general anesthetic is most commonly associated with cardiac arrhythmias?

A

Halothane.