IUSM Indy General Anesthetics

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general anesthesia

Induction of a state of unconsciousness with the absence of pain sensation over the entire body, through the administration of anesthetic drugs.

balanced anesthesia

anesthesia produced by safe doses of 2 or more agents or methods of anesthesia, each of which contributes to the total desired effect.

Goal: desired actions summate; undesirable actions are minimized.

Name 4 of the preanesthetic medications considered preoperatively.

Benzodiazepines: help sedate; ↓ anxiety
Antihistamines: bronchodilation; ↓ bronchospasm
Antiemetics: anti-nausea
Opioids: if concerned of analgesia

Describe the proposed mechanisms of action of general anesthetics.

General anthetics ↑ activity of GABA receptors and K⁺ channels (enhancement of inhibitory synaptic activity) and ↓ activity of ACh receptors and NMDA glutamate receptors (reduction of excitatory synaptic activity)

Name 3 barbiturates

thiopental, thiamylal, methohexital

thiopental

Action: intravenous anesthetic- barbiturate
•rapid onset anesthesia (high lipid solubility → brain)

Pharmacokinetics
•terminated by redistribution
•TERMINAL t½ LONGER W/ CONSTANT INFUSION (BUT METHOHEXITAL- rapid CLEARANCE)

Clinical Use
•induction of anesthesia

Toxicity
•↓ cerebral metabolism + blood flow
•↓ BP
•↓ respiration
•paradoxical excitation (muscle tremors)- esp. methohexital
•hiccups- esp. methohexital

thiamylal

Action: intravenous anesthetic- barbiturate
•rapid onset anesthesia (high lipid solubility → brain)

Pharmacokinetics
•terminated by redistribution
•TERMINAL t½ LONGER W/ CONSTANT INFUSION (BUT METHOHEXITAL- rapid CLEARANCE)

Clinical Use
•induction of anesthesia

Toxicity
•↓ cerebral metabolism + blood flow
•↓ BP
•↓ respiration
•paradoxical excitation (muscle tremors)- esp. methohexital
•hiccups- esp. methohexital

methohexital

Action: intravenous anesthetic- barbiturate

Pharmacokinetics
•rapid onset anesthesia (high lipid solubility → brain)
•terminated by redistribution
•TERMINAL t½ LONGER W/ CONSTANT INFUSION (BUT METHOHEXITAL- rapid CLEARANCE)

Clinical Use
•induction of anesthesia

Toxicity
•↓ cerebral metabolism + blood flow
•↓ BP
•↓ respiration
•paradoxical excitation (muscle tremors)- esp. methohexital
•hiccups- esp. methohexital

Propofol

Action: intravenous anesthetic

Pharmacokinetics
•rapid onset + duration similar to barbituate
→ REDISTRIBUTION still important
•RAPID CLEARANCE compared to barbiturates

Clinical Use
•induction + maintenance anesthesia
→ LESS HANGOVER effect than thiopental
•↑ use as sedative outside OR (RIP MJ)
•poor analgesia

Toxicity
•same as barbiturates: ↓ cerebral blood flow + metabolism; ↓BP (hypotension); ↓ respiration
•PAIN ON INJECTION

Etomidate

Action: intravenous anesthetic

Clinical Use
•Induction anesthesia
•CARDIOSTABLE- used in pts with risk of HYPOTENSION
•poor analgesia

Toxicity
•same as barbiturates: ↓ cerebral blood flow + metabolism; ↓ respiration (except NO ↓BP)
•PAIN ON INJECTION (~propofol)
•significant NAUSEA + VOMITING (choking risk)
•SUPPRESSION of ADRENOCORTICAL STRESS RESPONSE (LONG TERM)

Drug interactions
•fentanyl prolongs elimination half-life

Ketamine

Action: intravenous anesthetic
•blocks GLUTAMATE receptors (not GABAergic)
•DISSOCIATIVE STATE: amnesia despite the pt being awake

Metabolism: liver

Clinical Use
•Byitself for short procedures; maintenance (multiple injections); induction followed by different agent
•ANALGESIA
•↑ BP/bronchodilator- useful in pts at risk for hypotension or bronchospasm
•children undergoing short painful procedure

Toxicity:
•same as barbituate: ↑ cerebral blood flow
•CATALEPTIC STATE
•EMERGENCE OF DELIRIUM: adults (not kids); disorientation, excitation, hallucinations
•analog of PCP- target NMDA receptor, drug of abuse

Drug interactions
•potentiates nondepolarizing muscle relaxants
•ketamine + theophylline predispose to seizures

Which intravenous anesthetics cause pain at the injection site?

propofol, etomidate

Which intravenous anesthetics shoud be used in pts at risk for hypotension?

etomidate, ketamine

Which intravenous anesthetic should be used in pts at risk for bronchospasm?

ketamine

Which intravenous anesthetics causes nausea and vomiting as well as suppresses the stress response?

etomidate

Which intravenous anesthetic cause cataleptic state?

Ketamine

Which intravenous anesthetic is associated with emergence delirium- disorientation, excitation, hallucinations?`

Ketamine

Which intravenous anesthetic shows slow clearance after continuous infusion?

thiopental

Which intravenous anesthetics cause a depressed respiratory drive?

all of them

Which intravenous anesthetics cause muscular rigidity?

opioids, ketamine

Why is Dalton's Law important for understanding how inhalation anesthetics are administered?

Ptotal = P₁+ P₂+ P₃
A high partial pressure of the gas in the lungs results in more rapid achievement of anesthetic levels in the blood.

Use Henry's Law to explain why although the partial pressure of a gas may be equal in all tissues, the concentration is not.

Concentrations of drug in liquid = partial pressure of gas x solubility (λ)

The amount of gas with affinity for liquid (soluble) does not contribute to partial pressure → not available to enter other tissues

Define partition coefficient and how it is used to explain the amount of time to induce anesthesia.

Ratio of concentrations of the anesthetic in two tissues when the partial pressure is the same in the tissues and is based on Henry's Law.

The higher the blood/gas partition coefficient, the longer it takes to induce anesthesia and the longer the duration of action

Why does a higher cardiac output result in slower induction of an inhaled anesthetic?

High cardiac output results in more rapid uptake such that the rate of rise in the alveolar partial pressure and the speed of induction are slowed → delay time to reach anesthetic equilibrium.

(If a lot of blood is moving through, it will be hard to saturate the system)

Name and describe the 4 major determinants of inhaled anesthetic concentration.

1. INSPIRED ANESTHETIC CONCENTRATION: Dalton's Law; high partial pressure of the gas in the lungs results in more rapid achievement of anesthetic levels in the blood

2. ALVEOLAR VENTILATION: the greater the ventilation,the more rapid is the rise in the alveolar and blood partial pressure of the agent and the onset of anesthesia.

3. BLOOD/GAS SOLUBILITY (λ b/g): the more rapidly a drug equilibrates with the blood, the more quickly the drug passes into the brain to produce anesthetic effects. Drugs with a low b:g partition coefficient equilibrates more rapidly than those with a higher blood solubility.

4. PULMONARY PERFUSION (CARDIAC OUTPUT): at high pulmonary blood flows, the gas partial pressure rises at a slower rate → speed of onset of anesthesia reduced. At low flow rates, onset is faster.

What is MAC and why is it used in inhalation anesthetics?

Minimum Alveolar Concentration (MAC)
•concentration of gas in the alveolar compartment that results in a lack of response to a noxious stimulus in 50% of subjects

USED TO COMPARE POTENCY OF INHALATION ANESTHETICS and esp. useful when combining inhalation anesthetics (just combine MACs)

How can MAC be monitored in real time?

At equilibrium, the concentration in the alveolar compartment closely approximates the concentration in expired air

Name the 2 limitations of MAC.

1. 50% of pts still respond
2. Absence of response to pain may not indicate loss of consciousness

halothane

Action: inhaled anesthetic
•hi b/g partition coefficient → slow induction, slow offset
•POTENT! (MAC = 0.75%)

Clinical use
•maintenance (discontinued in US)
•used in developing countries (popular in peds)

Toxicity
•metabolite toxicity- trifluoroacetylchloride
•↑ cerebral blood flow w/ potential to ↑ intracranial pressure (differs from propofol, thiopental)- like enflurane
•inhibits ventilatory response to ↑ CO₂or to hypoxemia
•LIVER TOXICITY- DRUG-INDUCED HEPATITIS AND HEPATIC NECROSIS
•MALIGANT HYPERTHERMIA-w/ all halogenated agents esp. halothane

Volatile anesthetics can cause malignant hyperthermia. How does malignant hyperthermia predispose patients to muscle rigidity?

Anesthetic agents trigger an increase in intracellular calcium in skeletal muscle.

enflurane

Action: inhaled anesthetic
•hi b/g partition coefficient → slow induction

Clinical use
•maintenance (diminished substantially in US)

Toxicity
•↑ cerebral blood flow w/ potential to ↑ intracranial pressure- like halothane
•inhibits ventilation response to ↑CO₂or to hypoxemia- like halothane
•↑ SEIZURE ACTIVITY

isoflurane

Action: inhaled anesthetic
•lower b/g partition coefficient than halothane (1.2 v 2.4) → induction can be achieved in 10 minutes

Clinical Use
•maintenance b/c PUNGENT ODOR
•most commonly used anesthetic in US for many years

Side effects
•tachycardia
•peripheral vasodilation and hypotension (common)
•DILATES CORONARY ARTERIES → CORONARY STEAL → AVOIDED IN PTS W/ CAD

desflurane

Action: inhaled anesthetic
•LOWEST b/g partition coefficient → rapid onset + rapid changes + rapid emergence (5-10 min)
•low fat solubility

Clinical Use
•maintenance (not induction due to airway irritant)
•outpatient surgeries

Side effects
•concentration dependent ↓ in BP BUT CO NOT affected
•COUGHING, SALIVATION, BRONCHOSPASM IN AWAKE PTS → strong AIRWAY IRRITANT → NOT used for induction
•may produce carbon monoxide with dry soda lime (CO₂absorbent)

sevoflurane

Action: inhaled anesthetic
•low b/g partition coefficient → rapid onset + rapid recovery

Clinical use
•induction
•outpt anesthesia + peds b/c not irritating to airway
•no significan tachycardia

Side effects
•some concern that interaction of sevoflurane with soda lime (CO₂absorbent) produces nephrotoxic substance "Compound A."
→FDA recommends sevoflurane be given as fresh gas flow

nitrous oxide

Action: inhaled anesthetic
•IMPOTENT (MAC = 105%)
•insoluble in blood and tissues → rapid induction + emergence

Clinical use
•weak anesthetic agent but significant analgesia
•used primarily as adjunct to other inhalational or IV anesthetics
•N2O CANNOT be used at concentration above 80% → HYPOXIA. Only used as adjunct to other anesthetics at [50-70%]

Side effects
•accumulates in gas-filled spaces → BOWEL DISTENTION + PNEUMOTHORAX + PAIN W/ OBSTRUCTED INNER EAR
•GIVE 100% O₂at END of anesthesia → avoid DILUTING O₂and causing "DIFFUSIONAL HYPOXIA"
•CONTRAINDICATED in pts with PULMONARY HTN due to ↑ vascular resistance

methoxyflurane

Action: inhaled anesthetic
•slow onset + offset

Clinical Use
•foreign ambulance services as an ER analgesic

Side Effects
•EXTENSIVE METABOLISM IN KIDNEY (only 35% excreted unchanged by exhalation) → production of FLUORIDE ions → KIDNEY damage

Which inhaled anesthetic causes gaseous space enlargement?

nitrous oxide

Which inhaled anesthetics cause metabolite toxicity?

trifluoroacetylchloride w/ halothane
kidney damage w/ methoxyflurane

Which inhaled anesthetics cause malignant hyperthermia?

Halogenated agents except nitrous oxide; halothane may be worse than others

A high blood-gas λ leads to a shorter or longer induction time?

LONGER

The lower the blood solubility of an anesthetic, the shorter its induction time

The lower the MAC, the stronger or weaker the potency of an inhaled anesthetic?

STRONGER

The lower the minimal concentration of an anesthetic required to prevent pain in 50% of subjects (MAC), the higher its potency

The lower the oil-gas λ, the stronger or weaker the potency of the inhaled anesthetic?

WEAKER

The higher the lipid solubility of an anesthetic, the higher its potency.

ENANTIOMERS CAN BE AN EXCEPTION TO THIS RULE.

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