anaestheticsgeneral
Table of Contents
general anaesthesia
see also:
traditional stages of anaesthesia
- stage of analgesia
- no amnesia until late in stage.
- stage of excitement
- delirium, excited, amnesic, irregular respiration, vomiting, incontinence.
- stage of surgical anaesthesia
- recurrence of regular respiration;
- 4 planes described according to pupil size, eye reflexes & ocular movements
- 4 EEG phases of maintenance anaesthesia:
- phase 1: light anaesthesia - decrease in EEG beta activity (13-30Hz), increase in alpha activity (8-12Hz) and delta activity (0-4Hz)
- phase 2: intermediate state - an increase in alpha and delta activity in the anterior leads compared to posterior leads “anteriorization”, and EEG resembles stage 3 non-REM (slow-wave) sleep
- phase 3: deep anaesthesia - EEG characterised by flat periods interspersed with periods of alpha and delta activity
- phase 4: profound anaesthesia - EEG is flat, isoelectric and this phase induced by barbiturates or propofol is often used as a neuroprotective function in neurosurgery, or in Mx of status epilepticus.
- approximates brain-stem death as patients are:
- unconscious, have depressed brain stem reflexes, do not respond to nociceptive stimuli, have no apnoeic drive
- require cardiorespiratory and thermoregulatory support
- stage of medullary depression
- severe depression of vasomotor & respiratory centres
- ⇒ death without full circulatory & resp. support
signs of induction of anaesthesia
- failure of patient to track movement of your finger with their eyes +/- onset of nystagmus
- blinking increases
- oculocephalic, eyelash and corneal reflexes are lost but pupillary light reflex remains
- heart rate typically increases unless opiates or benzodiapines have been administered prior to or during induction
- while BP may rise or fall
signs of inadequate general anaesthesia
- heart rate and/or BP may rise dramatically
- perspiration
- tearing
- changes in pupil size
- return of muscle tone and movement if not paralysed by muscle relaxants
- changes in EEG measures of brain activity
mechanism of action of general anaesthetics
- NB. we still do not understand the mechanism of consciousness
- actual mechanisms are complex
- primary mechanism appears to be suppression of excitatory neurons
- it appears many agents act by suppressing neuronal activity in the brain stem arousal centres - the lateral dorsal tegmental areas of the pons and the midbrain paramedian region.
- apnoea is partly due to actions on GABA[sub]A[/sub] interneurons in the respiratory control network in the ventral medulla and pons.
- the rapid atonia following a propofol bolus is thought to be due to actions on the spinal cord as well as the pontine and medullary reticular nuclei that control antigravity muscles
- microtubule quantum effect hypothesis of consciousness
- 1st proposed by Penrose
- these microtubules are affected by inert gases such as xenon which do have anaesthetic effects
pharmacokinetics of inhaled general anaesthetics
- depth of anaesthesia determined by concentration in CNS.
uptake from lungs & distribution
- Concentration of a gas is proportional to its partial pressure (tension).
- Rate at which a given concentration of anaesthetic is achieved in CNS depends upon:
solubility of gas:
- blood:gas partition coefficient = relative affinity for blood cw air
- poorly soluble gases (ie. low blood:gas partition coefficient) (eg. N2O):
- relatively few molecules are needed to diffuse to raise arterial tension
- ⇒ perfusion limited
- ⇒ high arterial tensions develop rapidly
- ⇒ faster induction of anaesthesia
- ⇒ at equilibrium, arterial tension closer to alveolar tension
- eg. N2O reaches ~90% of its alveolar tension but methoxyflurane only 20%
anaesthetic | blood:gas coefficient | brain:blood coefficient | MAC |
---|---|---|---|
nitrous oxide | 0.47 | 1.1 | >100% ie. cannot be used alone for GA |
sevoflurane | 0.69 | 1.7 | 2.0 |
isoflurane | 1.4 | 2.6 | 1.4 |
enflurane | 1.8 | 1.4 | 1.68 |
halothane | 2.3 | 2.9 | 0.75 |
methoxyflurane | 12.0 | 2.0 | 0.16 |
inspired concentration
- proportional to alveolar tension achieved
- ⇒ higher concentrations increase rate of rise of arterial tension
- ⇒ increase rate of induction of GA
- THUS, use 3-4% halothane initially then maintenance of 1-2%
pulmonary minute ventilation
- proportional to rate of rise of arterial tension achieved effect greatest on high soluble gases (eg. methoxyflurane, halothane) eg. 4x minute ventilation ⇒ doubles arterial tension of halothane in 1st 10'
pulmonary blood flow
- increased cardiac output SLOWS rate of rise of arterial tension less time of blood in contact with alveolus larger volume of blood exposed to gas
- ⇒ shock increases rate of induction esp. for high-soluble drugs
arterio-venous concentration gradient
- the greater the difference, the longer the time required for equilibration gradient depends on degree of uptake in tissues which depends upon:
- tissue perfusion (brain,heart,liver,kidneys > muscle > adipose)
- solubility in that tissue
elimination
- rate of recovery from GA depends on redistribution away from brain & elimination.
elimination by lungs
- depend on factors as for uptake BUT:
- while uptake can be increased by increasing inspired concentration, the reverse process cannot be enhanced as cannot reduce conc. below zero.
- tension in various tissues is variable (ie. not zero as at start of GA) & depends on:
- solubility in tissues, perfusion of tissues
- duration of GA - longer duration ⇒ higher tissue tensions ⇒ slower recovery
- poorly soluble gases are “washed out” faster ⇒ rapid recovery
hepatic metabolism
- esp. methoxyflurane (→ release of fluoride ions) & halothane (15-20% metabolised).
dose-response characteristics
Minimum Alveolar Concentration (MAC):
- partial pressure of alveolar gas as a % of 760mmHg that results in immobility in 50% pts when exposed to noxious stimuli such as surgical incision ie. represents the ED50 on a conventional quantal dose-response curve
- THUS is a measure of relative anaesthetic potency
- it gives NO information about the slope of this curve, but in general, it is steep ie. >95% pts may fail to respond to surgical incision @ 1.1MAC !!
- individual pts require between 0.5 - 1.5 MAC for GA
- MAC values decrease with age but NOT affected by sex, height or weight.
- MAC values may decrease substantially when adjuvant drugs used (eg. opiates).
effects of inhaled general anaesthetics on organ systems
CVS:
- halothane, enflurane
- ⇒ decreased cardiac output but no effect on total peripheral resistance (TPR) ⇒ decreased BP
- myocardial depressant effect ⇒ reduced myocardial oxygen needs
- isoflurane ⇒ marked decrease in TPR but little effect on cardiac output ⇒ decreased BP
- all GA's tend to increase right atrial pressure (RAP)si
- GA's alter heart rate via direct effect on no-atrial (SA) node &/or via autonomic effects
- halothane sensitises myocardium to catecholamines ⇒ risk of ventricular fibrillation (VF)
Resp:
- all GA's except N2O decrease tidal volume & increase resp. rate → decreased minute ventilation
- all GA's
- ⇒ increase resting PaCO2
- ⇒ increase apnoeic threshold
- ⇒ decreased ventilatory response to hypoxia - important in recovery phase where this response needed
- ⇒ depress mucociliary function → pooling of mucus
- ⇒ tend to cause bronchodilation
CNS:
- all GA's ⇒ decrease metabolic rate of brain
- most GA's
- ⇒ increase cerebral blood flow via decreased cerebral vascular resistance
- ⇒ raised intracranial pressure (least with N2O)
- NB. although N2O has low GA potency, it has marked analgesic & amnesic effects
Renal:
- all GA's
- ⇒ decreased effective renal blood flow (RBF) & glomerular filtration rate (GFR)
- ⇒ increased filtration fraction
- ⇒ increased renal vascular resistance ⇒ impaired autoregulation
- methoxyflurane ⇒ flouride ions and other metabolites ⇒ irreversible polyuric renal failure
Liver:
- all GA's ⇒ decreased hepatic blood flow (15-45% of pre-GA flow)
- halothane ⇒ possible hepatotoxicity
Uterus:
- most (not N2O) ⇒ potent uterine muscle relaxation
- ⇒ helpful in manipulations of fetus during delivery
- ⇒ risk of haemorrhage in D&C's, etc.
Blood:
- N2O ⇒ prolonged exposure causes megaloblastic anaemia
Muscle:
- GA's esp. with volatile gases or suxamethonium in susceptible pts ⇒ malignant hyperthermia
- ⇒ tachycardia, hypertension
- ⇒ acidosis, hyperkalaemia, muscle rigidity, hyperthermia
- Rx: IV dantrolene, lower temperature & restore electrolyte & acid-base balance
anaestheticsgeneral.txt · Last modified: 2024/06/27 11:41 by gary1