Lecture 7 - Local and General Anaesthetics Flashcards
Local anaesthetics - General function
Locally applied chemicals that can disrupt nerve transmittion and inhibit the perception of pain
- Differ in duration, site of metabolism, and potency
Local anaesthetics - Uses
- Topical application –> burns and small cuts
- Injections –> Dental applications
- Epidural and intrathecal –> obstetic procedures and major surgery
Local anaesthetics - Sites of action
- Brain
- Spinal cord
- Neurons
- Nerve endings
Local anaesthetics - Mechanism of action
- Reduces resposes to pain by inhibiting sensory nerves
- Blocks conduction by blocking voltage-gated sodium channels
- Blocks sensory nerves at doses that do not inhibit motor nerve function
Define
Saltatory Conduction
a rapid mode of signal transmission along myelinated neurons, where the electrical impulse “jumps” from one node of Ranvier to the next
How do local anaesthetics travel in the body?
They are weak bases so they travel as uncharged or positively charged molecules in the body
Local anaesthetics - Esters
- Short duration
- metabolized by enzymes in blood and skin
- Ex. Procaine, Cocaine, Tetracaine
Local anaesthetics - Amides
- Long duration
- metabolized by liver
- Ex. Lidocaine, Prilocaine, Bupivacaine, Articaine
Why is epinephrine added to lidocaine?
- EPI is a vasoconstrictor so it makes the effect of the lidocaine last longer
- reduces toxicity of local anaesthetics and controls bleeding
Define
Use-dependent inhibition in local anaesthetics
some local anesthetics bind preferentially to open state of voltage-sensitive Na+ channels
What does the cationic form of local anaesthetics do in neurons?
Enters the cell and bind to the cytoplasmic side of the sodium ion channel protein and prolongs the inactivation state –> increasing the refractory period
LA Routes of Administration
Topical application
- Surface anaesthetic
Combination topical anaesthesia - TAC (tetracaine, adrenaline, cocaine)
- LET (lidocaine, epinephrine, tatrecaine)
- EMLA (eutectic mixure of local anaesthetics)
LA Routes of Administration
Parenteral administration
- Intradermal
- Epidural or caudal blockade
- Perineural or paravertabral blockade
- Spinal blockade
- Beir block (intravenous regional anaesthesia)
- Infiltration (injection, subcutaneous tissue)
- Regional nerve block (inject a nerve root)
Monitored anaesthesia care (MAC)
- Intravenous sedation with midazolam, followed by propofol and/or fentanyl
- Induces conscious sedation, minimal response to pain, can speak but has an
altered state of awareness
Stages of Anaesthesia and CNS Depression
Stage 1 - Analgesia
Euphoria, giddiness, loss of pain, loss of consciousness
Slow wave EEG
Stages of Anaesthesia and CNS Depression
Stage 2 - Excitement (Delirium)
Increased sympathetic tone, elevated blood pressure and heart rate, hypereaction to stimulation
Burst suppression and slow wave EEG
Stages of Anaesthesia and CNS Depression
Stage 3 - Surgical anaesthetics plane 1-4
- Sleep, normal blood pressure and respiration
- Dilated pupils, loss of corneal reflex
- Skeletal muscle relaxation
- Paralysis of diaphragm, hypotension
Burst suppression EEG
Stages of Anaesthesia and CNS Depression
Stage 4 - Medullary paralysis
Respiratory paralysis which leads to circulatory collapse and death
Isoelectric EEG
General anaesthesia - Induction
- Time required to take a patient from a conscious stae to stage 3
- GA inductions are generally smooth and rapid and usually injected
General anaesthesia - Maintenence
The depth of anaesthesia is continually monitored by vital signs: body temperature, breath, blood pressure, heart beat (ECG), and general observation of the patient
General anaesthesia - Mechanisms of action
Inhibit CNS activity by interacting with membrane ion channels
1) Enhancing GABAa receptors
2) Block NMDA recpetor
What GAs interact with the GABAa receptor to enhance its function?
Benzodiazepines, barbiturates, etomidate, and propofol
How do GAs enhancing GABAa receptors affect neurons?
GAs activate GABAa receptors and allow chloride ions to move into the cell which inhibits or hyperpolarizes the neuron
What is NMDA receptor?
Ionotropic glutamate receptor (excitatory)
What is NMDA antagonized by?
Nitrous oxide and ketamine (blocks cation movement and depolarization)
Define
Dissociative anaesthetics
Form of anaesthesia characterized by catalepsy, catatonia, analgesia, and amnesia
Does not always involve loss of consciousness and state of GA
GA Routes of Administration
Inhalation
Nitrous oxide, desflurane, sevoflurane, diethyl ether, halothane, isoflurane, enflurane
GA Routes of Administration
Intravenous
Rapid delivery of drug to the blood
- pentobarbitol, thiopental, propofol, ketamine, etomidate
