Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
54 Cards in this Set
- Front
- Back
|
4 specific general anaesthetic agents
|
1. Volatile liquids
2. Gases 3. Dissociative anesthetics 4. Neuroleptoanalgesis |
|
|
3 preanaesthetic induction agents
|
1. Barbituates
2. Etomidate 3. Propofol |
|
|
4 objectives of anaesthesia
|
1. Hypnosis
2. Analgesia 3. Hyporeflexia 4. Neuromuscular blockade (important for abdominal surgery) |
|
|
4 progressive stages of anaesthesia
|
1. Analgesia
2. Excitement 3. Surgical Anaesthesia 4. Medullary Anaesthesia |
|
|
What happens in stage I (analgesia)
|
The spinothalamic (pain) tract is interrupted b/c the dorsal horn is very susceptible. Amnesia, normal pupils, normal breathing
|
|
|
What happens in stage II (excitement)
|
Stage II shouldn't happen, but it will if inhibitory neurons are shut off too. Irregular breathing, dilated pupils, marked eye movement, no blink
|
|
|
What happens in stage III (surgical anaesthesia)
|
Ascending pathways of the reticular activating system are shut off
|
|
|
4 planes of stage III surgical anaesthesia
|
1. Eye movements stop, loss of facial and vagal reflexes
2. Respiratory depression, loss of corneal and laryngeal reflexes. Tonsillectomy 3. Decrease in inspiration, artifical respiration required, spinal reflexes suppressed. PREFERRED 4. Dilated, unresponsive pupils, no expiration (hypercapnia), carinal reflex gone (aspirate) |
|
|
What happens in stage IV
|
Cardio-respiratory collapse
|
|
|
Least and most powerful inhaled GA
|
N2O, Halothane
|
|
|
What is the induction phase?
|
How long it takes you to get to Stage III, Plane III. Less time is better
i. Short in hyperventilating with vent-limited (halothane), decreasing cardiac output. Children are naturally shorter. ii. Long in hyperventilating with perf-limited (N2O), hypoventilating in diff-limited (halothane), increased cardiac output, COPD. |
|
|
Solubility and induction general rule
|
The more soluble a GA, the longer the induction (why you hyperventilate with halothane to shorten it's induction) and the longer the recovery.
|
|
|
2 important factors in maintenance
|
1. Partial pressure of gas
2. Rate |
|
|
Why does N2O take effect quickly while halothane, which is more soluble, take longer?
|
i. More soluble GAs require higher concentrations to reach adequate anaesthetic concentrations in blood, because they dissolve
ii. Poorly soluble N2O does not dissolve, and raises the partial pressure of the capillary iii. N2O moves across the pressure gradient into the brain as fast as the blood can carry it there, and deactivates just as quickly. iv. Halothane, meanwhile, must continuously dissolve into the blood until the blood is saturated. Only then will its capillary pressure rise and it will move into the brain |
|
|
What is the VRG?
|
Vessel-rich group. It comprises highly perfused organs (brain, liver, kidneys, heart, lungs) It has the lowest capacity for anaesthetics, however, so the partial pressure of GA in lungs equilibrates most rapidly with the VRG
|
|
|
Simplified GA perfusion - circulatory phase
|
1. You inhale a GA
i. It is poorly soluble (perf-limited) a. It will diffuse rapidly from the blood into the VRG b. It will be rapidly inactivated ii. It is highly soluble (vent-limited) a. It must saturate the blood before entering the VRG. b. It will take a long time to deactivate |
|
|
Potency in GA
|
Has nothing to do with real pharma potency. A more lipid soluble anesthetic is more potent = less dose needed to induce anaesthesia
|
|
|
Highly lipid soluble anaesthetics
|
1. Are more potent
2. Accumulate in body fat |
|
|
MAC and potency
|
The most potent GAs have the lowest MAC (Mean alveolar concentration)
|
|
|
MAC
|
The percent alveolar concentration at 1 atm at which 50% of patients will not respond to a skin incision.
|
|
|
What does the rate of equilibration of a ventilation-limited anaesthetic depend on?
|
1. You set a partial pressure for halothane in the inspired air
2. How quickly the alveoli partial pressure equilibrates with the inspired partial pressure determines how quickly the VRG is dosed, so to speak. |
|
|
Are there antagonists to GAs?
|
No.
|
|
|
What is the analgesic index?
|
The MAC divided by the partial pressure that causes analgesia in 50% of patients. A high A.I means you stop feeling pain at a much lower dose than needed for surgery.
|
|
|
Major route of GA clearance?
|
Exhalation. Certain GAs undergo toxic metabolism in the liver.
|
|
|
Diffusion hypoxia
|
Rapid GAs like NO bounce out of blood and tissue so fast that they can displace oxygen.
|
|
|
Theories on why GAs work
|
1. Activate K channels
2. May directly activate GABA 3. May inhibit NMDA (ketamine, NO, xenon) |
|
|
Effects of GA on CNS
|
1. Depressed EEG
2. Depressed excitation 3. Depressed metabolism 4. Increase cerebral blood flow -- ventilate to avoid increased intercranial pressure |
|
|
What does GA do to respiratory fxn?
|
1. Decreased hypoxic reflex
2. Reflex to CO2 diminished 3. PaCO2 rises 4. Low VT 5. Pooling mucus |
|
|
GA on heart
|
1.Vagal stim
2. Sympathoadrenals to stress 3. Low BP due to low output |
|
|
What is catecholamine sensitization?
|
The heart is made more sensitive to endogenous catecholamines, predisposing to arrythmias in the presence of stress hormones. Halogenated GAs do this.
|
|
|
GAs on kidney
|
You pee less
|
|
|
GAs on liver
|
Decrease hepatic blood flow.
|
|
|
GAs on uterus
|
Relax.
|
|
|
Side effects of halothane
|
respiratory depression, cardiac arrythmia, poor analgesia, hepatotoxicity, malignant hyperthermia
|
|
|
Warning signs of malignant hyperthermia
|
bad response to succinylcholine, elevated CPK, muscle spasms and pain
|
|
|
What is the defect in malignant hyperthermia?
|
AD, Chromosome 19. Increased myoplasmic calcium disrupts mitochondria, causing anaerobic respiration and lactic acid buildup.
|
|
|
Antidote to malignant hyperthermia
|
Procaine. IV mannitol for the kidney, total body cooling, IV O2, DANTROLENE FOR MUSCLE.
|
|
|
Side effects of enflurane
|
RESPIRATORY DEPRESSION, cardiovasc depression, poor analgesic, epileptic induction
|
|
|
Isoflurane
|
The best and most expensive moderate GA. Can cause coronary steal
|
|
|
Desflurane
|
Indicated for outpatient surgery. Laryngospasms and sympathomimetic cardio effects
|
|
|
Nitrous Oxide
|
Mixed with halothanes to minimize bad inert effects. Must be given with O2. Does not relax or stage III a patient.
|
|
|
Sevoflurane
|
Pleasant odor, outpatient, is chemically unstable
|
|
|
Ketamine
|
Good analgesic/amnesic. Indicated for orthoped, musculoskeletal, and cutaneous cases. Emergence delirium. Not absorbed by the gut.
|
|
|
Mixture in neuroleptoanalgesia
|
1. Fentanyl -- analgesia
2. Droperidol --psychosedative antipsychotic 3. N2O for anaesthetic = You care about literally nothing |
|
|
Fatal side effect of droperidol
|
Torsades
|
|
|
What is the desired effect of neuroleptoanalgesia?
|
The patient can remain responsive to voice instructions.
|
|
|
Key induction agents
|
Short acting barbituates. INTUBATE.
|
|
|
Why do people wake up after induction agents are given?
|
Redistribution of the drug, not metabolism.
|
|
|
Why don't we use barbituates for anaesthesia?
|
No analgesia, hyporeflexia or relaxation
|
|
|
Major advantage and disadvantage of IV GAs?
|
Rapid induction, No control
|
|
|
Barbituate contraindication
|
Acute intermittent porphyria
|
|
|
Etomidate
|
Non-barbituate sedative induction agent
|
|
|
Propofol
|
Rapid anaesthetic induction, sedation during regional anaesthesia, and in patients requiring controlled ventilation
|
|
|
Why would you use anticholinergic medications in surgery?
|
Drying of bodily secretions and vasoconstriction
|
