General Anesthetics Flashcards

1
Q

General anesthesia

A

General anesthesia can be viewed as a controlled, reversible state of loss of sensation and consciousness.
The ideal general anesthetic state comprises analgesia, amnesia, loss of consciousness (absence of awareness), relaxation of skeletal, suppression of somatic, autonomic, and endocrine reflexes, and hemodynamic stability.
General anesthetics are subdivided on the basis of their route of administration… (1) INHALATIONAL (2) INTRAVENOUS

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2
Q

INHALATIONAL

A

Depth of anesthesia is determined by the concentration of an anesthetic in the brain—must be able to deliver an appropriate amount of the agent from the anesthetic machine to the brain.

Unlike most therapeutic agents inhalational anesthetics are administered as gases or vapors. Therefore a different set of physical principles applies

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3
Q

PARTIAL PRESSURE

A

in a mixture of gases the partial pressure of an anesthetic agent is directly proportional to its fractional concentration in the mixture

–when a gas is dissolved in blood or other body tissues—its PARTIAL PRESSURE is directly proportional to its concentration, but inversely proportional to its solubility in that tissue

–partial pressure is the driving force that moves that moves the gas from the anesthetic machine to the lung, from lung to blood, from blood to brain

-at theoretical equilibrium the partial pressures are EQUAL in all body tissues, alveoli, and the inspired gas mixture.
-because solubility varies from tissue to tissue as a consequence of differences in tissue lipophilicity—therefore the concentration will be different in different tissues.
—the partial pressure is the factor most easily controlled by the anesthesiologist—by adjusting the anesthetic machine to optimize partial pressure during induction.

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4
Q

ALVEOLAR VENTILATION

A
  • is the product of the rate of respiration and tidal volume less the pulmonary dead space, and the rate of induction of anesthesia is significantly influenced by factors that reduce alveolar ventilation.
  • —respiration depressants such as barbiturates or opioids
  • —pulmonary diseases, emphysema, COPD
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5
Q

LAW OF MASS ACTION

A

–initially at the alveoli space the partial pressure of the anesthetic is higher than the alveolar blood—gas moves into the blood——as the partial pressure of the anesthetic agent in the blood increases the gradient lessens and uptake slows

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6
Q

SOLUBILITY OF ANESTHETIC IN THE BLOOD

A

—-another important factor in the rise of arterial partial pressure
—this relationship is expressed as the blood : gas partition coefficient
the higher the solubility of an anesthetic gas in the blood, the more must be dissolved in the blood to produce a change in partial pressure (partial pressure is inversely proportional to solubility
–therefore the rate of rise of arterial partial pressure and speed of induction of anesthesia are the fastest for those gases least soluble in blood ( because the blood is acting as a reservoir for the drug)

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7
Q

CARDIAC OUTPUT

A

Cardiac output is the primary determinant of the rate of pulmonary blood low—–so it would seem that an increase in pulmonary blood flow would accelerate the induction of anesthesia—not –it has the opposite effect
–THE RATE OF ANESTHETIC INDUCTION DECREASES WITH INCREASEING CARDIAC OUTPUT

—Increased pulmonary blood flow means that the same volume of gas from the alveoli diffuses into a larger volume of blood per unit of time
—so initially you get a reduced concentration in the blood and the partial pressure is directly proportional to its concentration
–any increase in cardiac output usually results in the perfusion of tissues other than the brain
–also the opposite is true—example ???

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8
Q

Rate of Induction if Concentration of anesthetic in inspired-gas mixture

A

inc

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9
Q

Rate of Induction of Alveolar ventilation

A

inc

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10
Q

Rate of Induction Solubility of anesthetic in blood ( blood-gas partition coefficient)

A

dec

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11
Q

Rate of Induction of cardiac output

A

dec

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12
Q

Meyer and Overton originally observed

A

that the potency of anesthetic agents correlates highly to their lipid solubility, as measured by oil : gas partition coefficient
Also relates for inert gases xenon and argon

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13
Q

moa

A

According to the volume expansion theory, molecules of an anesthetic dissolve in the phospholipid bilayer lf the neuronal membrane, causing the membrane to expand. This impedes the opening of membrane ion channels necessary for the generation and propagation of action potentials

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14
Q

GABAA Complex

A

Inhalational Anesthetics have been postulated to have specific receptor binding sites on the GABAA Complex. It is not known how the inhalation anesthetics affect the Cl channel, since these agents do not affect the Cl channel in a similar manner as the BDZ’s or barb’s.

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15
Q

MINIMUM ALVEOLAR CONCENTRATION (MAC)

A

—expression of the potency of inhalational anesthetics
—MAC is a concentration that prevents 50 % of patients from responding to a painful stimulus, such as a skin incision
Mac ranges for surgery can range 1 to 2 but usually a MAC of 1.3 gives an ED99

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16
Q

NITROUS OXIDE

A

Nitrous oxide is a low molecular weight, odorless to sweet smelling, nonflammable gas of low potency and poor blood solubility that is commonly administered in combination with opioids or volatile anesthetics to produce general anesthesia. Although nitrous oxide is nonflammable, it will support combustion. Its poor blood solubility permits rapid achievement of an alveolar and brain partial pressure of the drug. Analgesic effects of nitrous oxide are prominent, but skeletal muscle relaxation is minimal.

  • -considered the most safest
  • –can nitrous oxide be used as a lone agent for surgical anesthesia???
  • —why???
  • –Inhalation anesthetics are additive (with Nitrous can use less of a more potent agent)
17
Q

HALOTHANE

A

—introduced in 1956-popular due to the (1) lack of flammability
(2) low incidence of toxic effects (3) rapid awakening
—–low margin of safety—circulatory depression—decreased cardiac contractility, hypotension, decreased cardiac output, and bradycardia
—cardiac arrhythmias
—-HALOTHANE HEPATITIS—hepatic failure—death
1 in 10,0000 maybe due to metabolism to immunogenic byproducts.
—releases bromide
—when combined with succinylcholine—Malignant hyperthermia

18
Q

ISOFLURANE

A

(A) decreases blood pressure predominately by decreased vascular tone
(B) most commonly used
(C) no renal or hepatic metabolism
(D) disadvantage —irritating to airways

19
Q

ENFLURANE

A

(A) significant release of fluoride with prolonged use and high doses
(B) may cause seizures with high doses
(C) less probability of arrhythmias than with isoflurane and halothane

20
Q

SEVOFLURANE

A

(A) less irritating to airways,
(B) does not produce tachycardia like isoflurane or desflurane, which maybe a preferable agent in patients prone to myocardial ischemia
(C) potential nephrotoxicity of Compound A, (the degradation produced by the interaction of sevoflurane with the carbon dioxide absorbant soda
lime)

21
Q

DESFLURANE

A

(A) not indicated for inhalation induction due to risk of laryngeal spasm
(B) special delivery system-desflurane is a liquid at room temperature

22
Q

INTRAVENOUS ANESTHETICS

A

-adds flexibility and permits the administration of lower concentrations of inhalation agents

23
Q

BENZODIAZEPINES

MIDAZOLAM

A

used only in anesthesia (I.V.)
–diazepam and lorazepam also used
no analgesia—used for procedures that do not induce a lot of pain, or as an adjunct for the inhalation anesthetics

24
Q

DROPERIDOL AND FENANYL (INNOVAR)

A

neuroleptic anesthesia

  • slow induction
  • may need ventilation
25
Q

KETAMINE

A

(A)MOA-not sure—agonist at opioid sigma receptors or antagonist at NMDA receptors (n-methyl-d-aspartate receptors)
(B) dissociative anesthesia— a dissociation from the environment,-eyes open, but unresponsive to pain
(C) analgesia and amnesia
(D) disadvantage-hallucinations, bad dreams, delirium, these effects may occur days or weeks later
(E) increases intracranial pressure- do not use in patients at risk for cerebral ischemia
(F) potent bronchodilator-well suited for patients at high risk for bronchospasms

26
Q

PROPOFOL

A

(A) M.O.A.—interaction with the GABAA receptors
(B) rapid redistribution and elimination very good for short procedures and outpatient surgery
(C) low incidence of nausea and vomiting
(D) pain upon injection

27
Q

ETOMIDATE

A

(A) M.O.A.—interaction with the GABAA receptors
(B) rapid onset and short duration of action-useful in short painless procedures- no analgesia
(B) relative lack of cardiovascular effects-useful in patients with impaired ventricular function, cardiac tamponade, or hypovolemia
(C) high incidence of spontaneous muscle movement and myoclonus
(D) pain upon injection

28
Q

(1) Name one long acting benzodiazepine used for anxiety?
(2) Name one long acting benzodiazepine used as a hypnotic?
(3) Name one short acting barbiturate?
(4) Name one drug used in the treatment of epilepsy?
(5) Name one drug that is a full Mu agonist

A

answer