Neuraxial anesthesia physiology- ChatGPT

Question 1

Where does spinal anesthesia act, and how is it administered?

Answer 1

It acts in the subarachnoid space, directly bathing the spinal nerve roots in cerebrospinal fluid (CSF).

Question 2

What factors influence the spread of local anesthetic in spinal anesthesia?

Answer 2

• Baricity
• patient position
• volume and dose of LA
• injection site
• CSF volume

Question 3

What is baricity, and why is it important in spinal anesthesia?

Answer 3

Baricity is the density of the local anesthetic relative to CSF; it determines how the drug spreads under gravity:

• Hyperbaric: settles downward (heavier than CSF)
• Hypobaric: rises upward (lighter than CSF)
• Isobaric: remains near injection level

Question 4

How does patient position affect LA spread in hyperbaric solutions?

Answer 4

Hyperbaric solutions follow gravity—LA flows downward when patient is supine or in Trendelenburg.

Question 5

What is the effect of injection volume and dose on spinal spread?

Answer 5

Higher doses and volumes generally increase both cephalad spread and block density.

Question 6

What nerve fiber types are blocked in spinal anesthesia, in order?

Answer 6

B fibers (preganglionic autonomic) →
C & A-delta fibers (pain, temperature) → A-gamma→
A-beta→
A-alpha (motor, proprioception)

Question 7

What is differential blockade?

Answer 7

The phenomenon where autonomic, sensory, and motor fibers are blocked at different levels:

• Sympathetic block = highest
• Sensory block = 2 levels below
• Motor block = 2 levels below sensory

Question 8

What is the typical level difference between sympathetic, sensory, and motor block?

Answer 8

Sympathetic > Sensory (−2 levels) > Motor (−2 more levels)

Question 9

Why are smaller fibers (like C fibers) blocked before larger ones?

Answer 9

Smaller diameter and unmyelinated fibers have less resistance to local anesthetic diffusion and conduction block.

Question 10

Which fibers are responsible for motor function and proprioception?

Answer 10

A-alpha (motor), A-beta (touch/proprioception)

Question 11

What factors affect the onset and duration of spinal anesthesia?

Answer 11

Dose, baricity, lipid solubility, protein binding, patient characteristics (height, weight, age), and spinal CSF volume.

Question 12

How does protein binding affect spinal anesthetic duration?

Answer 12

Higher protein binding → longer duration of action.

Question 13

How does pregnancy affect spinal anesthesia?

Answer 13

Pregnancy reduces CSF volume (engorged epidural veins), increases sensitivity to LA, and accelerates onset and spread.

Question 14

Why is it important to match the baricity of the LA with patient positioning?

Answer 14

It allows predictable spread and block height; misalignment can cause inadequate or excessive blockade.

Question 15

What is the risk of using a hypobaric solution incorrectly?

Answer 15

LA may rise too far cephalad, leading to high spinal or total spinal anesthesia.

Question 16

What can result from excessive cephalad spread of spinal anesthesia?

Answer 16

High spinal block → hypotension, bradycardia, difficulty breathing, and possibly apnea.

Question 17

What role does the interspace level of injection (e.g., L3–L4) play in spinal anesthesia?

Answer 17

Determines the starting point for LA spread; higher punctures may risk cord injury if above L2.

Question 18

What type of anesthetic is most commonly used in spinal anesthesia?

Answer 18

Hyperbaric bupivacaine is commonly used due to predictable spread and duration.

Question 19

What is the typical duration of spinal anesthesia with bupivacaine?

Answer 19

90–120 minutes, depending on dose and additives.

Question 20

What additives can be used to prolong or enhance spinal anesthesia?

Answer 20

Opioids (e.g., fentanyl), vasoconstrictors (e.g., epinephrine), or clonidine.

Question 21

What are the functions of Aα nerve fibers?

Answer 21

Skeletal muscle motor

Question 22

What are the functions of Aβ nerve fibers?

Answer 22

Touch, pressure, proprioception

Question 23

What are the functions of Aγ nerve fibers?

Answer 23

Muscle spindle tone (intrafusal fibers)

Question 24

What are the functions of Aδ nerve fibers?

Answer 24

Sharp pain, cold temperature

Question 25

What are the functions of B fibers?

Answer 25

Preganglionic autonomic

Question 26

What are the functions of C fibers?

Answer 26

Dull pain, warm temperature, postganglionic autonomic

Question 27

What is a clinical example of a hyperbaric local anesthetic solution?

Answer 27

Bupivacaine with dextrose (0.75% in 8.25% dextrose)

Question 28

What is an example of an isobaric spinal anesthetic?

Answer 28

Plain bupivacaine (0.5% without dextrose)

Question 29

What is a clinical example of a hypobaric spinal anesthetic?

Answer 29

Bupivacaine mixed with sterile water

Question 30

How does obesity affect spinal anesthesia?

Answer 30

Decreased CSF volume (due to epidural fat and venous engorgement) may lead to more cephalad spread.

Question 31

How does aging affect spinal block characteristics?

Answer 31

Decreased CSF volume and vertebral space narrowing can cause faster and more extensive spread.

Question 32

How do spinal abnormalities (e.g., scoliosis, kyphosis) affect spinal anesthesia?

Answer 32

They cause asymmetric or unpredictable spread of local anesthetic.

Question 33

What is the spinal duration of lidocaine?

Answer 33

~45–75 minutes

Question 34

What is the spinal duration of tetracaine?

Answer 34

~90–120 minutes (longer with epinephrine)

Question 35

What is the spinal duration of ropivacaine?

Answer 35

~90 minutes; less motor block than bupivacaine

Question 36

What is a high spinal block and its symptoms?

Answer 36

Excessive cephalad spread to upper thoracic levels causing hypotension, bradycardia, dyspnea.

Question 37

What is a total spinal block and its symptoms?

Answer 37

LA spreads to cervical/brainstem levels → apnea, unconsciousness, possible cardiac arrest.

Question 38

In what order does block resolution occur after spinal anesthesia?

Answer 38

Motor function returns first, followed by sensory, then autonomic tone.

Question 39

How does neuraxial anesthesia affect preload and afterload?

Answer 39

Preload ↓ due to venodilation from sympathectomy. Afterload ↓ from partial arterial vasodilation.

Question 40

How is cardiac output affected by neuraxial anesthesia?

Answer 40

↓ Venous return → ↓ Stroke volume → ↓ CO. Initially may rise briefly due to compensatory vasodilation, then fall.

Question 41

What reflex can cause bradycardia and even asystole after neuraxial anesthesia?

Answer 41

The Bezold-Jarisch reflex — triggered by ventricular underfilling and mediated by vagal 5-HT₃ receptors.

Question 42

What is the reverse Bainbridge reflex, and when is it triggered?

Answer 42

A decrease in HR due to reduced atrial stretch when venous return falls.

Question 43

What causes sudden cardiac arrest during spinal anesthesia?

Answer 43

Unopposed parasympathetic tone due to blockade of cardiac accelerator fibers (T1–T4), often in young patients with high vagal tone.

Question 44

What are the stats on spinal/epidural-related cardiac arrest?

Answer 44

Spinal: ~7 per 10,000. Epidural: ~1 per 10,000. Onset: Usually 20–60 min post-block. Risks: High vagal tone, large blood loss, cement in ortho surgery.

Question 45

What vasopressors are used to prevent spinal-induced hypotension?

Answer 45

Phenylephrine and ephedrine.

Question 46

How do 5-HT₃ antagonists (like ondansetron) help in spinal anesthesia?

Answer 46

They block the Bezold-Jarisch reflex and mitigate reflex bradycardia and hypotension.

Question 47

What is the preferred fluid strategy to prevent spinal-induced hypotension?

Answer 47

Co-loading (15 mL/kg IV fluids immediately after the block). Preloading is less effective and no longer routinely recommended.

Question 48

How does positioning help prevent hypotension during spinal anesthesia?

Answer 48

Pelvic tilt (e.g., wedge under right hip) improves venous return and cardiac output.

Question 49

What are first-line treatments for spinal-induced bradycardia and hypotension?

Answer 49

Ephedrine if bradycardic and hypotensive. Atropine for bradycardia. Epinephrine if severe. IV fluids to support preload.

Question 50

Why should Trendelenburg positioning be used cautiously?

Answer 50

A tilt >20° may impair cerebral venous drainage, reducing brain perfusion.

Question 51

How does neuraxial anesthesia affect respiration in most patients?

Answer 51

Tidal volume, RR, and ABGs usually unchanged, but ERV and vital capacity decrease slightly due to loss of abdominal muscle function.

Question 52

Why do patients report dyspnea during high thoracic spinal blocks?

Answer 52

Loss of sensory feedback from the chest wall and inability to take deep breaths or cough effectively.

Question 53

What causes apnea after spinal anesthesia?

Answer 53

Usually due to brainstem hypoperfusion; rarely from direct LA neurotoxicity.

Question 54

What are the GI effects of sympathetic and parasympathetic blockade?

Answer 54

Sympathetic block (T5–L2): removes inhibition → ↑ peristalsis. Parasympathetic (vagus): continues promoting tone, motility, secretion.

Question 55

How does spinal anesthesia affect bladder function?

Answer 55

Sympathetic block above T10 relaxes sphincters. Opioids ↓ detrusor contraction and ↑ bladder capacity → Risk of urinary retention and need for Foley catheter.

Question 56

How does neuraxial anesthesia impact the endocrine/metabolic stress response to surgery?

Answer 56

It blunts the surgical stress response by blocking afferent nociceptive input, resulting in: ↓ Catecholamine release (epinephrine, norepinephrine), ↓ Cortisol secretion, ↓ Glucagon, ↓ Vasopressin, ↓ Renin and angiotensin levels.

Question 57

What are the clinical benefits of reducing the surgical stress response via neuraxial anesthesia?

Answer 57

Improved hemodynamic stability, Reduced hyperglycemia, ↓ Risk of immunosuppression, ↓ Myocardial oxygen demand, Potential ↓ thromboembolic events.