DR ROWAN MOLNAR ANAESTHETICS STUDY GUIDE PART V

Properties of NMBDs

PROPERTIES OF NMBDS

Highly polar molecules Low VD ( ~ ECF volume) Do not cross BBB/placenta Renally excreted (with exceptions) Range of actions at other ACh receptors Histamine releasers (most) Decrease VO2 /ATP & heat production

“SUX” VERSUS THE NDNMBDSSuxamethonium

Rapid onset (30s) Fasciculations Transient rise in ICP,

IOP, IAP/IGP, K+. Rapid offset

(usually) by hydrolysis in

plasma Unpredictable

effects in repeat dosing

Nondepolarisers

Slower onset (3-7m) No fasciculations Little to no effect on

ICP, etc. Varying durations

with different drugs OK for prolonged

use by boluses or infusion

NONDEPOLARISING RELAXANTSFirst generation

Curare/tubocurarine

Alcuronium Metocurine Gallamine Pancuronium

“Modern” agents Vecuronium Atracurium cisAtracurium Rocuronium Mivacurium

Brown = curare derivativesBlue = aminosteroids (the “oniums”)

Green = benzisoquinolines (the “uriums”)

SIDE EFFECTS OF SUXAMETHONIUM

Myalgia MH trigger Masseter spasm Phase II block Raises ICP Raises IOP Bradycardia

(Usually in infants or with 2nd dose)

Raises serum K+ Exaggerated action

& K+ rise in denervation, burns, muscle injury

Prolonged action with pseudochlinesterase variants/deficiency.

Histamine release Anaphylaxis (1:5000)

PROBLEMS WITH NONDEPOLARISERS

Slow onset – not usually a major problem Slow offset (situation/agent dependant) Awareness Hypothermia –reduced heat production Autonomic side effects Interactions Failure to reverse/recurarisation

PARALYSIS OBVIOUSLY MANDATES CONTROLLED VENTILATION

Modern anaesthetic machines are all equipped with ventilators.

Usual mode is volume controlled (delivers a set size of breath, a set number of times a minute) with or without PEEP.

Most can also give, or be adapted to give, pressure controlled ventilation, which is the mode of choice for paediatric patients (who usually have uncuffed tubes, and hence a small leak).

THE PHYSIOLOGY OF CONTROLLED VENTILATION“Spontaneous ventilation sucks; Controlled

ventilation blows”

Maintains constant minute volume & enables titration to desired pCO2 – vital in neurosurgery & acidotic patients.

Uptake of volatile agents therefore usually higher than in spontaneously breathing patient -> more CVS depression.

Recruits alveoli & prevents collapse: minimises shunt. Raises mean intrathoracic pressure – & hence RAP, so

reduces venous return & cardiac output – especially in head up position & with pneumoperitoneum – e.g. laparoscopic cholecystectomy.

Risk of barotrauma – esp. w/high tidal volume or pressures.

PHARMACOLOGY 5:LOCAL ANAESTHETIC AGENTS

Local anaesthetics are membrane stabilisers that block depolarisation in nerves

Non specific blockers of: All sensory fibres (not just pain) Motor fibres Autonomic fibres (mainly sympathetics in most

blocks) Hence can produce analgesia & arreflexia in the

distribution of the nerves blocked. Lower concentrations of LA agents effect predominantly

smaller axons: pain (Aδ & C fibres), temperature, & autonomic (unmyelinated sympthetic post-ganglionic fibres)

“YOUR FRIENDLY LOCAL ANAESTHETIC MOLECULE”THINK OF A PERSON STANDING IN THE WATER

– KEEPING THEIR HEAD HIGH & DRY

Head: benzene ring (lipophilic)

Body: (intermediate chain) with either ester or amide link.

Tail: (feet) – hydrophilic due to tertiary nitrogen capable of accepting proton & rendering molecule water soluble. (This is the form it is in in the ampoule)

NH+

A-

N N

ECF

NH+

ICF“THE VOYAGE OF THE MOLECULE LIGNOCAINE”

Cl-N

H+

Lignocaine hydrochloride injected

HCO3-

H2O + CO2

Tissue buffering

Freebase lignocaine diffuses across cell membrane

H+

Lower intra-cellular pH leads to re-ionization

Sodium channel

UNDERSTAND THIS, AND YOU WILL KNOW: Why local anaesthetics sting on injection

(because of the low pH needed to maintain ionised state)

Why their onset of action is not immediate(because of the buffering/diffusion/reionisation steps)

Why local anesthesia is poorly effective in inflamed/ infected tissue (because of the lack of buffering capability in acidotic

tissue) Why LAs exhibit tachyphylaxis

(exhaustion of buffering capability)(& why cocaine users end up needing nose reconstructions – from repeated insult to the

nasal septum from an acid substance that is also a vasoconstrictor - which inhibits circulatory

dilution of the acid load)

LOCAL ANAESTHETIC AGENTS

AGENT

Lignocaine (“Xylocaine”)Bupivicaine (“Marcain”)Ropivicaine (“Naropin”)Levobupivicaine

(“Chirocaine”)Prilocaine (Citanest”)

Max dose:Plain (+Adr)

4 (7) mg/kg2 mg/kg

3-4mg/kg4 mg/kg

7(9) mg/kg

LOCAL ANAESTHETIC PROBLEMS

Failed block - multiple causes High block (spinals/epidurals) CNS toxicity

at high dose or with inadvertent IV injection

Selective cardiotoxicity (bupivicaine) Needle/injection trauma

Nerve damageOther – e.g pneumothorax

ADJUVANT AGENTS USED WITH LAS

Adrenaline – prolongs blockade, allows increased dose (lignocaine/prilocaine)

Bicarbonate – Decreases acidity - speeds onset of block

Hyaluronidase –Aids diffusion (Eye & brachial plexus blocks)

Glucose (spinals) – to produce hyperbaric solutions Narcotics (neuraxial) – synergistic analgesia Other analgesics – e.g clonidine in neuraxial

blocks.

MODES OF LOCAL ANAESTHESIA

(a) Peripheral Surface

Topical (incl EMLA) Nebulised Intrapleural/

peritoneal Infitration Intravenous regional Nerve/plexus blocks

Multiple types

(b) Neuraxial Epi(extra)dural

Single shot vs catheter Bolus vs infusion LA only vs combinations Includes caudal blocks

Spinal/subarachnoid Usually single shot LA only or LA/narcotic

Combination (CSE)

SOME COMMON NERVE/PLEXUS BLOCKS

Eye blocks:Peribulbar, retrobulbar,

Sub-Tenons Superficial cervical

plexus block Brachial plexus

blocks:Axillary, supraclavicular,

interscalene Paravertebral blocks

Intercostal blocks Ilio-inguinal block Dorsal penile nerve

block Pudendal nerve

block Femoral (+/- LCNT)

block Ankle blocks

SPINAL ANAESTHESIA Relatively quick, defined end-point for

placement Small volume of LA Usually single shot – “fire & forget” Block level depends on spread – varies with:

VolumeSpeed of injectionBaricity

Minimal respiratory effects – unless high block Autonomic effects: - Vasodilatation @ T12 &

up - Bradycardia @ T4 & up

EPIDURAL ANAESTHESIA Alone, or with GA, or as CSE. Cervical (rare), thoracic, lumbar, caudal Usually catheter placement (except caudal) High volumes LA +/- adjuvants. “Band” phenomenon. Autonomic effects similar to spinal, but slower

onset

CONSIDERATIONS IN REGIONAL BLOCKADE

Consent/communication IV access Adjuvant sedation/analgesia Time involved Failed block/backup plan Management of side effects/reactions