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Owenpharm Block 3 > Anesthetics > Flashcards

Anesthetics Flashcards

1
Q

What is the natural state of Nitrous oxide when stored or delivered?

A

A gas, it is not a volatile liquid

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2
Q
  1. What is the rate of equilibration of Nitrous oxide? Why?
  2. How is this exploited therapeutically?
A
  1. Rapid. It is very insoluble in blood.
  2. It increases the concentration of other anesthetics and is useful to enhance induction with isoflurane, for example.
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3
Q
  1. What needs to be administered during emergence from Nitrous oxide?
  2. Why?
A
  1. 100% O2
  2. It’s rapid equilibration rate in alveoli decrease relative concentration of oxygen.
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4
Q

How is Nitrous oxide excreted?

A

99% via the lungs

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5
Q
  1. What are two clinical uses for Nitrous oxide?
  2. What is it not good for?
A
    1. Sedation and analgesia at 50% inhaled concentrations
    1. Adjunct to stronger anesthetics to reduce dose needed.
  3. General Anesthesia
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6
Q
  1. What is a primary contraindication for Nitrous oxide?
  2. What is a cardiac side effect of Nitrous oxide?
  3. Is respiratory suppression a major issue?
A
  1. Pneumothorax
  2. Negative inotrope, but sympathomimetic
  3. No
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7
Q
  1. What is the primary general mechanism for local anesthetics?
  2. What is the general resulting effect?
A
  1. They bind reversibly to a site within the pore of voltage gated Na+ channels. This blocks sodium entry when the channel is opened.
  2. Reversible nerve conduction blockade. This causes sensory loss and motor paralysis in innervated area.
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8
Q
  1. What is local infiltration anesthesia?
  2. What is nerve block anesthesia?
A
  1. Local injection of an agent irrespective of the course of cutaneous nerves
  2. Injection of local anesthetic around individual nerve or nerve plexus.
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9
Q
  1. What type of nerve fiber do local anesthetics act on?
  2. How does a local agent eliminate pain sensation?
  3. Is there any nerve damage that occurs with local agents?
A
  1. All nerve fibers
  2. Block AP initiation and propagation on nociceptive neurons.
  3. No, they are completely reversible.
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10
Q
  1. Where do local anesthetics bind?
  2. Do they bind in the uncharged or charged form?
  3. Are they weak acids, weak bases, strong acids or strong bases?
A
  1. On the intracellular side of the voltage-dependent sodium channel inside the channel.
  2. Binds in cation (charged) form
  3. They are all weak bases.
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11
Q
  1. How is potency measured in anesthetics?
  2. What is the relationship between dose of a gas and alveolar concentration?
A
  1. The “dose” of anesthetic that prevents movement in response to pain in 50% of patients
  2. Dose is directly related to and determined by its concentration at the alveolus.
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12
Q

What are three considerations of MAC (Minimum Alveolar Concentration) as a measure of anesthetic efficacy and potency?

A
  1. Measurable (concentration of anesthetic in end-tidal expired air)
  2. Correlates with concentration at site of action, the brain.
  3. End-point (lack of movement to pain) is easy to measure and define.
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13
Q

How is potency for IV anesthetics measured?

A

Free plasma concentration that produces loss of response to surgical incision in 50% of patients (EC50)

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14
Q

What are three likely targets of anesthetics?

A
  1. GABAA receptor Cl- channel. Results in hyperpolarization
  2. Inhibition of NMDA receptors. Results in reduced sodium and calcium influx. Some hyperpolarization
  3. Other membrane associated proteins like filling hydrophobic cavities and alteration of protein movement.
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15
Q
  1. Why do gaseous anesthetics have to be continuously administered?
  2. What route is typically used for induction because it is less frightening?
A
  1. They have very short half-lives.
  2. IV route typically used for induction.
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16
Q

How is rapid induction using IV anesthetic achieved?

A

All are hydrophobic and partition into the brain and spinal cord in one pass. Redistribution occurs when blood levels drop.

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17
Q
  1. What is Sodium thiopental?
  2. What is its onset of action?
  3. What is its duration of action?
  4. What is its half-life?
A
  1. A GABAA receptor agonist used to induce anesthesia
  2. 10-30 sec
  3. 10 min
  4. 12 hours
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18
Q

What is a unique about barbiturates in their side effects that can be exploited in a certain paitent population?

A

Since demand on the heart is reduced (which can result in precipitous drop in BP) they are not contra-indicated in patients with CAD.

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19
Q
  1. What is the mechanism for Propofol?
  2. What is its onset of action?
  3. What is its duration of action?
  4. What is are 2 unique side effects?
  5. What is the half-life?
A
  1. GABAA agonist
  2. 10-30 seconds (same as Sodium thiopental)
  3. 10 min. (same as Sodium thiopental)
  4. It is an antiemetic. Causes pain on injection.
  5. 3.5 hours (less hang-over than barbiturates)
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20
Q
  1. What needs careful monitoring during administration of Propofol?
A
  1. BP due to severe vasodilation and depression of myocardial contractility both secondary to blunted baroreflexes.
  2. More significant respiratory depression than thiopental.
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21
Q
  1. When would Etomidate be prefered for anesthesia?
  2. What are some noticeable side effects for Etomidate?
A
  1. In patients at risk for hypotension because it has little to no effect on BP.
  2. Pain on injection, Myoclonus, N/V, suppression of adrenocortical response
22
Q

What is the mechanism for Ketamine?

A

NMDA antagonist

23
Q

What are some major side effects for Ketamine?

A
  1. Nystagmus, salivation, lacrimation, increased tone
  2. Increased ICP
  3. Emergence Delirium
  4. Hypertension: indirect sympathomimetic effects
24
Q

What are special uses for Ketamine?

A
  1. Patients with bronchospasm
  2. Pediatric procedural sedation
25
Q
  1. What is the mechanism for Midazolam?
  2. What is its relative induction and duration compared to thiopental?
  3. How is it metabolized?
A
  1. GABAA agonist. It is a short acting benzo.
  2. Slower induction and longer duration
  3. By hydroxylation to an active metabolite.
26
Q
  1. What determines achievement of equilibrium of anesthetic gases?
  2. What is the important property of gases at each compartment barrier?
A
  1. balance of partial pressures (not concentrations)
  2. Partition coefficients
27
Q
  1. What is a partition coefficient?
  2. What does it mean for an anesthetic to have a low blood:gas PC?
  3. What does it mean for an anesthetic to have a high fat:blood PC?
A
  1. It determines the relative amounts of anesthetic in two compartments.
  2. High amounts are needed in inspired air. Equilibrium is reached quickly: induction and recovery are fast.
  3. Long half-life (hang over) due to slow release into blood.
28
Q

What factors affect induction with a gaseous anesthetic?

A
  1. Concentration in inspired air: affects partial pressure and rate of movement into blood
  2. Pulmonary ventilation: more important for moderate PC than low blood:gas PC.
  3. Pulmonary blood flow: increased flow slows rate of rise of arterial partial pressure. Also more important for moderate blood:gas PC.
  4. Arteriovenous concentration gradient: dependent on rate and extent of tissue uptake
29
Q

When does anesthesia occur chemically speaking?

A

When the brain partial pressure is equal to the MAC

30
Q

What does steady state of anesthetic gas mean?

A
  1. No net movement of gas at this stage
  2. Quick for gases with low blood:gas PC
  3. Slow for gases with high fat:blood PC
31
Q

Which partition coefficient determines the half-life of an anesthetic?

A

The blood:fat PC

32
Q
  1. What is the blood:gas PC of Isoflurane? What does this mean?
  2. What are the clinical uses for it?
A
  1. Moderate blood:gas PC which mean moderate rates of induction and recovery
  2. Mostly used for maintenance but can be used for induction. Especially used worldwide. Often used in combination with nitrous oxide to reduce amount needed.
33
Q

What are the side effects of Isoflurane?

A

Respiratory:

  • Airway irritant
  • Coughing
  • Decreases Tidal Volume and increases RR

Cardiovascular:

  • Myocardial depression → decreases BP
  • Arrythmias (sensitizes to catecholamines)
  • Cerebral vessel vasodilation → increased ICP
34
Q

What are the chemical properties of Desflurane?

A
  1. Very volatile at room temp → needs special equipment
  2. Very low blood:gas PC → rapid induction and recovery
35
Q
  1. What are the clinical uses for Desflurane?
  2. What are the side effects?
A
  1. Outpatient surgeries/maintenance, NO induction due to airway irritation.
  2. -Skeletal muscle relaxation (a good thing)
    - Similar cardiovascular effects to Isoflurane
    - Worse respiratory irritant w/ bronchospasm
36
Q
  1. What is the blood:gas PC of Sevoflurane?
  2. What makes it different from Iso- or Des-?
  3. What are the clinical uses for it?
A
  1. Very low blood:gas partition coefficient
  2. 5% metabolized to flouride ion in liver (may cause renal damage)
  3. Very popular inpatient and outpatient
    - Used to induce and maintain
    - Children and adults
    - NOT a respiratory irritant
37
Q

Why do local anesthetics have a higher affinity for inactive than unopened channels?

A

They bind to sodium channel on neurons easiest in open state.

Remember: unactivated → activated → inactive

38
Q

What consequences does a local anesthetic binding in an open state have?

A

Degree of block depends on the frequency of nerve stimulation and resting membrane potential.

39
Q

When is local anesthetic less effective? Why?

A

During infection or inflammation because of the decreased pH.

Remember:
pH = pKa + log ([unprotonated]/[protonated])
pKa lidocaine = 7.9

40
Q

What are the three most sensitive types of nerve fibers to local anesthetic?

A

Autonomic fibers
non-myelinated C fibers
Adelta fibers.

41
Q

What is the order in which sensation goes away with nerve blocks

A
  1. Pain
  2. Cold
  3. Warm
  4. Touch
  5. Deep pressure
  6. Motor

Recovers in reverse order

42
Q

What are the three steps of CNS toxicity with a local anesthetic?

A
  1. CNS stimulation is seen first:
    - Depression of cortical inhibitory neurons
    - Restlessness, tremors, convulsions
  • *2. CNS depression at higher doses:**
  • Drowsiness, general depression, respiratory depression, possible respiratory arrest

Death typically associated with respiratory depression

43
Q

What cardiovascular effects can occur from local anesthetic toxicity?

A
  1. General depression of CV system → usually after CNS symptoms develop
  2. Hypotension and arrhythmias can lead to cardiac arrest.
44
Q

What is the primary anesthetic use of Cocaine?

A

Topical anesthesia of the upper respiratory tract

45
Q

What is the relative potency, onset and duration of Procaine?

A
  • Low potency
  • Slow onset
  • Short duration
46
Q
  1. What is the relative potency, and duration of Tetracaine?
  2. What is it most frequently used for?
  3. What is it not used for?
A
  1. More potent and longer acting
  2. Widely used in spinal anesthesia and in topical ophthalmic preparations.
  3. Peripheral nerve block.
47
Q
  1. Why is benzocaine sold over the counter with low risk of toxicity?
A
  1. It have low water solubility and is too slowly absorbed to be toxic.
48
Q

What are the ester derivative local anesthetics?

A

Cocaine
Procaine
Tetracaine
Benzocaine

49
Q
  1. What is the relative onset, duration, efficacy of Lidocaine?
  2. How do we typically reduce the risk of toxicity?
A
  1. Fast onset, intermediate duration but longer than procaine and more effective than procaine.
  2. Administer with vasoconstrictor like Epinephrine
50
Q
  1. What are the benefits to using Bupivicaine over Lidocaine?
  2. What are the drawbacks?
A
  1. -Longer acting
    - Provides more sensory than motor block
  2. More cardiotoxic than equieffective doses of lidocaine.
51
Q

What is Ropivacaine?

A
  • Similar in action to bupivicaine but less toxic
  • Suitable for epidural and regional anesthesia
  • More motor sparing that bupivicaine

Owenpharm Block 3 (8 decks)

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