MedicoNotebook: Anaesthesia

Showing posts with label Anaesthesia. Show all posts

0 EMLA - Eutectic Mixture of Local Anesthetics

EMLA - Eutectic Mixture of Local Anesthetics

Combination Lidocaine/prilocaine is a eutectic mixture of equal quantities (by weight) of lidocaine and prilocaine. A 5% emulsion preparation, containing 2.5% each of lidocaine/prilocaine.

Dermal Anaesthesia : Used to decrease needle phobia.

0 IVRA Intravenous Regional Anaesthesia

IVRA = Bier block anesthesia :

1. Both for Upper limb and Lower limb

2. Drugs : Lignocaine , Prilocaine

3. Bupivacaine is Contraindicated

4. Contraindications of IVRA :

Sickel cell disease
Raynaud's disease
Scleroderma

0 Celiac plexus block

Celiac plexus block :

MC complication : Hypotension (because of lumbar sympathetic block) (MCQ)

Used for pain relief in Pancreatic and Gastric Malignancies.

Stellate-ganglion block :
The stellate ganglion (or cervicothoracic ganglion or inferior cervical ganglion) is a sympathetic ganglion formed by the fusion of the inferior cervical ganglion and the first thoracic ganglion. Stellate ganglion is located at the level of C7.

Although located at C7 , the needle is inserted at the level of anterior tubercle of transverse process of C6 ( Chassaignac tubercle ) to avoid the piercing the pleura.

Used for upper extremity sympathetic dystrophies.

Signs of successful block :

Horner's syndrome (miosis , ptosis , enophthalmos)
Conjunctival Congestion
Nasal Stuffiness ( Guttmann's Sign )
Mueller's syndrome - injection of tympanic membrane and warmth of face.
Vasodilatation
Skin temperature increase.

MCQ point : NO Bradycardia

0 Epidural Anaesthesia

Epidural Anaesthesia :

Epidural space has Negative pressure.

Drugs:
Lignocaine : 1-2%
Bupivacaine : 0.25 - 0.5%

Drug required is high - 15 - 20ml (Penetrates intervertebral foramina into CSF)
So there are high chances of Total Spinal anaesthesia and LA toxicity.
Also epidural space has large number of veins - Venous plexus of Batson

Needle : Tuohy Needle , Crowford Needle

How to know if we are in the Epidural space ?
1. Loss of resistence (On piercing Ligamentum flavum)
2. Hanging drop technique. ( Gutierrez's sign )
3. Rapid injection in the space causes increase in rate and depth of respiration. ( Duran's Sign )
4. Absence of knee jerk after epidural block. (Westphal sign )

Advantages over Spinal Anaesthesia:

Less Hypotension
No headache
Level block can be done
Any duration can be performed.

Disadvantages :

Patchy block (therefore give fentanyl)
Chances of Unsuccessful block
High chance of total spinal
Expensive
Effect starts in 15-20mins [ therefore use combine Spinal and Epidural (CSE) ]

Caudal Block = Sacral epidural block : LSCS NOT Possible with this.

Drug injected - Xylocaine 2mg/kg , in Sacral hiatus.

Most commonly used in children

Good for Perineal surgeries and infra-umblical pain relief in children.

1 Spinal Anaesthesia

Spinal anaesthesia also called sub-arachnoid block (SAB)

Needles used :

Whitacre
Sprotte

These have pencil tip point end (therefore decrease post puncture headache)

Layers pierced :

Skin
Subcutaneus
Supraspinous ligament
Interspinous ligament
Ligamentum flavum (loss of ressistance felt as it is pierced)
Dura
Arachnoid - subarachnoid space

Drugs :

Lignocaine (5%- heavy due to dextrose )
Tetracaine (0.5% in 5% dextrose)
Bupivacaine (0.5% in 8% dextrose)

Factors affecting height of anaesthesia :

Dose (most important)
Baricity of solution
Volume of drug
Position of patient
Age
Height
Pregnancy
Abdominal Tumors

Effects of Spinal Anaesthesia :

Blocks Sympathetic system at the concerned level (therefore Increases Parasympathetic)

Thus Hypotension with Tachycardia (Marey's law) (tachycardia because T1-T4 sympathetic is intact and so there is compensatory tachycardia)

But with High Spinal Block -- there is Hypotension with Bradycardia (as T1-T4 sympathetic also blocked)

Other points to remember :

Autonomic block is 2 segments higher than sensory.

Maximum breathing capacity and active exhalation decrease because of intercostal paralysis.

Respiration is severely affected only if C3,4,5 involved (i.e very high spinal block)

Nausea, Vomiting

Vasodialator , therefore heat loss - shivering (T/t - Pethidine)

Successful sign -- Flacid and engorged Penis (due to paralysis of Nervi Ergentis )

Most Common Complication : Hypotension

Management for this

Prophylaxis

Curative

Colloids , Vasopressor

If Bradycardia

Post Spinal Headache : (Usually Occipital)

1. Low - pressure headache because of leak of CSF
Therefore structures in brain are dragged down.

2. Presents :

24 - 48hrs
Mostly > 90% in 7-10days
Almost all by 3weeks

3. Prevention : Use pencil tip needle

4. Curative T/t :

IV fluids
Analgesics
Inject 25 - 50 ml NS in epidural space
BEST -- Inject 15 - 20 ml autologus blood in epidural space (blood patch)

Other Complications (of Spinal Anaesthesia)

Cauda equina syndrome
Paraplegia
6th Nerve paralysis
1 , 9 , 10 nerve involvement
Anterior spinal artery syndrome
Meningitis
Backache

Contraindications :

Raised ICT
Refusal of patient
Infection at local site
Bleeding diasthesis
Hypotension , hypovolemia
Spinal deformities
Hypertension

Saddle block anesthesia :

A form of spinal anesthesia that produces loss of sensation in the buttocks, perineum, and inner thighs.
If a patient is kept sitting for several minutes after the injection of a small volume of a hyperbaric solution of local anaesthetic, a classical "saddle block" affecting only the sacral nerve roots will result.

0 Local Anaesthetic Drugs - Important points

Procaine :

1-2% for nerve block
Metabolized by Pseudocholinesterase
LA of choice in Malignant Hyperthermia

Chloroprocaine :

Shortest acting
High pKa but still Fast acting (this is an exception)
Most acidic of all LA
Contraindicated for spinal anaesthesia

Lignocaine

5% - heavy - spinal
4% - Surface
2% - Jelly for uretheral
1-2% - Extradural
1% - Nerve block
0.5% - IVRA
Maximum safe dose : 3mg/kg ,( if with adrenaline - 7mg/kg)

Bupivacaine :

Long acting
Dose : 2mg/kg (max. safe dose) , ( if with adrenalin - 3mg/kg.)
Never IV

Prilocaine :

S/E - Methemoglobenemia (T/t - Methylene blue)

0 LA - Salient points

The mechanism of local anesthetic(LA) action.

"B" represents an unionized local anesthetic and "BH+" represents an ionized.The blue is a voltage gated sodium channel(NaV) and the ionized anesthetic inhibits it in the intracellular fluid.

When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited.

Non Ionized - enters at Node of Ranvier

Ionized - blocks Na+ Channel

pKa -- is pH at which Ionized = Non Ionized

Anaesthetic Potency (related to) Hydrophobicity

Drug with lower pKa is Fast acting (exception - Chloroprocaine which has rapid onset and high pKa)

To increase Duration
1. Add Adrenaline

in Lignocaine - increases both sensory and motor block
in Bupivacaine - increases Only Sensory block

2. Add phenylephrine

Sodium bicarbonate : Decreases pKa -- increasing availability of unionized form , therefore increase onset of action.

CNS toxicity -- Bupivacaine > Etidocaine > Lidocaine = 4:2:1

All Local Anaesthetics are Negative Ionotropic

All are Vasodialator except Cocaine

Bupivacaine --} CNS:CVS = 1:3

Lignocaine ---} CNS:CVS = 1:7

Large dose of Prilocaine -- causes Methemoglobinemia (Treatment - Methylene Blue )

LA with Adrenaline is Contraindicated in :

Finger
Toes
Penis
Pinna

0 Peak plasma concentration after single shot LA

Peak plasma concentration after single shot LA
Maximum to Minimum (according to site of administration)

Intrapleural > Intercostal > Lumbar epidural > brachial plexus > Subcutaneus > Sciatic > Femoral

0 Local Anaesthetics

Local Anaesthetics :

ESTERS	AMIDES
Procaine Chloroprocaine (shortest acting) Tetracaine	Lidocaine Mepivacaine Prilocaine Bupivacaine Etidocaine Dibucaine (Longest acting)
Metabolized by Pseudocholinesterase( Plasma) (except Cocaine which is metabolized in liver)	Metabolized in Liver
Unstable	Stable
Metabolized to PABA – therefore Allergy	Low incidence of allergy
Mnemonic : EPPP	Bind to Alpha1 glycoprotein in plasma More intense and longer lasting anaesthesia

MedicoNotebook - Founder : DrShiviMudgal , Co-Founder : DrAyushGoel

0 Sequence of block by Local Anaesthetics

Sequence of block by Local Anaesthetics :

Temperature (Cold > Hot) - Pain - Touch - Deep pressure - Proprioception

Autonomic > Sensory > Motor

Recovery is opposite i.e Motor > Sensory > Autonomic

6 Nerve Fibers

Sensitivity to Pressure : A > B > C

Sensitivity to Hypoxia : B > A > C

Sensitivity to Local Anaesthetic : A gamma & A delta > A alpha & A beta > B > C
(Ref: Read text below)

Miller's Anaesthesia (7th ed , pg 921 , 922 )
"Different fiber types are differentially sensitive to local anesthetic blockade.
In vivo experiments in which continuous superperfusion of peripheral nerve allows equilibration with drug and experiments in which a drug bolus is delivered by percutaneous injection, analogous to clinical peripheral nerve block, show unequivocally that small myelinated axons (Aγ motor and Aδ sensory fibers) are the most susceptible to impulse annihilation. Next in order of block are the large myelinated (Aα and Aβ) fibers, and the least susceptible are the small, nonmyelinated C fibers.
In fact, in this last group, impulses in the slowest conducting population (conduction velocity of 0.5 to 0.8 msec) are the most resistant to local anesthetic.
The generalized notion that local anesthetics block the smallest fibers first or most is clearly wrong. "

0 Rapid sequence induction

Rapid sequence induction is used in cases of Full Stomach :

Normally induction sequence is

Pre O2 (3-4mins)
IV induction
Muscle relaxant
Bag + Mask IPPV
Intubation

In Rapid Sequence induction

Pre O2 (3-4mins)
IV induction
Fast Acting Muscle Relaxant
No Bag & mask
Intubate

0 Some Diseases and Anaesthesia

Porphyria :

Contraindicated drugs -

Thiopentone
Etomidate
Pentazocine

DOC - Propofol

Myesthenia Gravis :

Increased sensitivity to NDMR
Resistance to DMR
Sevoflurane is inhalational agent of choice
Atracurium (1/10th normal dose) is Muscle relaxant of choice.
Risk of post-op Respiratory failure.

Dystrophia Myotonica:

Tendency of Obstructive sleep apnea
Sch is Contraindicated (as it causes prolonged contraction)
Rapid sequence induction with Propofol and Rocuronium is used.

Duchenne Muscular Dystrophy :

Abnormal response to Sch and Volatile agents
IV induction preferred
Hyperkalemia common
NDMR duration is prolonged.

0 Muscle Relaxants - Important Points

Drugs NOT having Renal excretion : (SMAC)

Sch
Mivacurium
Atracurium
CisAtracurium

Histamine Release (MAST)

Mivacurium
Atracurium
Sch
Tubocurrarine

Ganglionic effects

Stimulation - Sch
Block - Tubocurrarine

Vagolytic Activiy

Gallamine
Pancuronium

Sympathetic Stimulation

Gallamine
Pancuronium

Metabolized Completely by Renal

Gallamine

MedicoNotebook - Founder : DrShiviMudgal , Co-Founder : DrAyushGoel

0 NDMR (some more points)

Non-depolarizing Muscle relaxants :

This is the second post on NDMR.
For Previous post - Click here

Drugs which antagonize the NDMR block :

Phenytoin
Carbamazepine
Calcium

Reversal of Block by :

1. Neostigmine

does not cross BBB
Muscarinic side effects - therefore give Atropine along with it.

2. Edrophonium

Short duration of action (therefore chances of recurarization)

3. Pyridostigmine

Longer duration

Signs of Adequate reversal :

Lift head for >5sec - Best Clinical Sign
Regular respiration
Spontaneous eye opening
Spontaneous Limb movements
Can protrude tongue
Able to cough
No Cyanosis

4 Non Depolarizing Muscle Relaxants (NDMR)

Non Depolarizing Muscle Relaxants (NDMR) :

No Muscle fassiculation.

Slow onset and slow dissociation.

Reversed by Neostigmine.

Muscle remains responsive to other stimulus (Therefore Neuromuscular monitor used).

Fade & Post tetanic stimulation.

Mild hypothermia antagonizes block.

Atracurium :

Metabolism - 75% by Hoffman degradation, 25 % by ester hydrolysis.
Metabolite - Laudanosine (pro convulsant)
Does not require any reversal agent

DOC in :

Renal and Hepatic failure cases.
Myesthenia Gravis - Use 1/10 th of normal dose

CisAtracurium :

3 times more potent
No histamine release
Non cumulative
Only Hoffman degradation
Laudanosine levels are lower.

Mivacurium :

Ultra Short
Metabolism - Plasma Cholinesterase (=Pseudo)
Ideal Muscle relaxant for Continuous infusion , day care surgery.

Doxacurium :

Most Potent
Long acting
Metabolism - Kidney

D Tubocurarine :

Long acting
Cause hypotension by ganglionic block

Vecuronium Bromide :

Most Haemodynamically stable
Minimum Vagolytic
Metabolism - Liver

Pancuronium :

Causes Hypertension and tachycardia (therefore good in Shock)
Long acting
Vagolytic
Causes Nor-epinephrine release

Rocuronium bromide :

Rapid onset (therefore can be used in full stomach)
Slightly vagolytic
Largely excreted unchanged in bile

Pipecuronium :

Longest acting
No vagolytic activuty

Rapacuronium :

Fastest Onset (among NDMR) ( Note: Overall Fastest Onset Muscle relaxant is Sch )
Increases incidence of bronchospasm.

Gallamine:

Maximum propensity for vagal blockade
Cross Placenta (therefore contraindicated in Pregnancy)
Also Contraindicated in Renal disease.

Alcuronium :

Anaphylaxis is common
Deterioration on exposure to sunlight.

Fastest onset agents are used in full stomach : (preference order as mentioned below)

Succinylcholine
Rapacuronium
Rocuronium

2 Succinylcholine

Succinylcholine = Suxamethonium chloride

Succinylcholine acts as a Depolarizing neuromuscular blocker (=DMR - Depolarising muscle relaxant)

Mnemonic : SSSS

FasSiculations
FaSt dissociation at receptors (Therefore Short acting )

Mnemonic : DND

Not reversed by Neostigmine
No fade or Post tetanic stimulation.

Potentiated by

Isoflurane
Respiratory Alkalosis
Hypothermia
Mg

Antagonised by : Acidosis and NDMR

Repeated use - causes Phase II block (similar to NDMR) -- (MCQ)

Other points about Sch :

Onset within 30 sec --- lasts 10-12 mins.
Bradycardia in children (especially after 2nd dose) (MCQ)
All presures are increased ( BP , ICP , IOP , Intra gastric )
Enzyme metabolism - by PseudoCholinestrase (= plasma = Butyrylcholinesterase) (read below in short about Cholinestrases )

Dibucaine Number :

The Dibucaine Number is a measure of the qualitative activity of Pseudocholinesterase and is the percentage of inhibition of the enzyme by the local anesthetic Dibucaine.

Normally 75 - 85 % inhibition , But if homozygous defficiency - then 30%

It is used to differentiate individuals who have substitution mutations of the Butrylcholinesterase enzyme.

Side effects :

Increase K+ (especially after Burns , spinal cord injury , stroke , cerebral palsy )

Therefore Sch is Avoided 48hrs - 9months after acute injury.

Post Op muscular pain which can be decreased by :

1. Self Taming (Pretreatment with small (10 mg) doses of succinylcholine)

2. Precurarization (NDMR + Sch)

3. Lignocaine

Malignant Hyperthermia

Note:

Sch is the MC drug which causes Malignant Hyperthermia.
All Fluranated inhalational anaesthetics & Lignocaine are other drugs which can cause Malignant Hyperthermia.

Allergy - releases histamine.

Contraindicated in Myotonic Dystrophy : as it causes severe muscle rigidity , preventing respiration and intubation.

Can cause Masseter spasm in children.

NeuroMuscular monitoring (Adductor Pollicis , Ulnar Nerve) (No use in Sch block)

TOF (Train of 4)
PTC ( Post tetanic count )
DBS ( Dual burst stimulation )
Tetanus

Cholinesterases :

True : RBC and Grey Matter.
Pseudo/False : Liver and Plasma.

2 Neuromuscular-blocking drugs

Neuromuscular-blocking drugs

These drugs fall into two groups:

Non-depolarizing blocking agents: These agents constitute the majority of the clinically relevant neuromuscular blockers. They act by competitively blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors.
Depolarizing blocking agents: These agents act by depolarizing the plasma membrane of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh.

0 Neuromuscular junction (NMJ)

Neuromuscular junction (NMJ):
The neuromuscular junction connects the nervous system to the muscular system via synapses between efferent nerve fibers and muscle fibers, also known as muscle cells.

Neuromuscular junction

presynaptic terminal
sarcolemma
synaptic vesicles
Acetylcholine receptors
mitchondrion

Points to remember : ( Mnemonic - MU CaR )

Acetylcholine Uploading into vesicles -- Magnesium (Mg)

Acetylcholine Release from vesicles -- Calcium (Ca)

Excitation-contraction coupling of vertebrate skeletal muscle :

Upon the arrival of an action potential at the presynaptic neuron terminal, voltage-dependent calcium channels open and Ca2+ ions flow from the extracellular fluid into the presynaptic neuron's cytosol.
This influx of Ca2+ causes neurotransmitter-containing vesicles to dock and fuse to the presynaptic neuron's cell membrane through SNARE proteins.
Fusion of the vesicular membrane with the presynaptic cell membrane results in the emptying of the vesicle's contents (acetylcholine) into the synaptic cleft, a process known as exocytosis.
Acetylcholine diffuses into the synaptic cleft and can bind to the nicotinic acetylcholine receptors on the motor end plate.
These receptors are ligand-gated ion channels, and when they bind acetylcholine, they open, allowing sodium ions to flow in and potassium ions to flow out of the muscle cell.
Because of the differences in electrochemical gradients across the plasma membrane, more sodium moves in than potassium out, producing a local depolarization of the motor end plate known as an end-plate potential (EPP).
This depolarization spreads across the surface of the muscle fiber and continues the excitation-contraction coupling to contract the muscle.
The action of acetylcholine is terminated when ACh diffuses away from the synapse or the enzyme acetylcholinesterase degrades part of ACh (producing choline and an acetate group).
The choline produced by the action of acetylcholinesterase is recycled — it is transported, through reuptake, back into the presynaptic terminal where it is used to synthesize new acetylcholine molecules.

ref:
http://en.wikipedia.org/wiki/Neuromuscular_junction

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