Morgan And Makhail Chapter 7

Front 1

pharmacokinetics is

Back 1

The study of the relationship between a drug's dose, tissue concentration, and elapsed time

Front 2

pharmacodynamics is

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The study of drug action, including toxic
responses

Front 3

Three factors affect anesthetic uptake:

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solubility in the blood, alveolar blood flow, and the
difference in partial pressure between alveolar gas and venous blood.

Front 4

Low-output states predispose patients

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to overdosage with soluble agents, as the rate of rise in
alveolar concentrations will be markedly increased.

Front 5

seven factors that speed induction also speed recovery:

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elimination of rebreathing, high
fresh gas flows, low anesthetic-circuit volume, low absorption by the anesthetic circuit, decreased
solubility, high cerebral blood flow, and increased ventilation.

Front 6

General anesthesia is

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an altered physiological state characterized by reversible loss of
consciousness, analgesia of the entire body, amnesia, and some degree of muscle relaxation.

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unitary hypothesis proposes that

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that all inhalation agents share a common mechanism of action
at the molecular level. This is supported by the observation that the anesthetic potency of inhalation
agents correlates directly with their lipid solubility (Meyer–Overton rule).

Front 8

The minimum alveolar concentration (MAC) is

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is the alveolar concentration of an inhaled
anesthetic that prevents movement in 50% of patients in response to a standardized stimulus (eg,
surgical incision).

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Prolonged exposure to anesthetic concentrations of nitrous oxide can result in

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in bone marrow
depression (megaloblastic anemia) and even neurological deficiencies (peripheral neuropathies and
pernicious anemia).

Front 10

Isoflurane dilates

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coronary arteries, but is not nearly as potent a dilator as nitroglycerin or
adenosine.

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The low solubility of desflurane in blood and body tissues causes

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causes a very rapid washin and
washout of anesthetic.

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Rapid increases in desflurane concentration lead to transient but sometimes worrisome

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but sometimes worrisome
elevations in heart rate, blood pressure, and catecholamine levels that are more pronounced than
occur with isoflurane, particularly in patients with cardiovascular disease.

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The course of general anesthesia can be divided into three phases:

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(1) induction, (2) maintenance,
and (3) emergence.

Front 14

The actual composition of the inspired gas mixture depends mainly on 3x

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fresh gas flow rate,
the volume of the breathing system, and any absorption by the machine or breathing circuit.

Front 15

Because anesthetic agents are taken up by the
pulmonary circulation during induction, alveolar concentrations....

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lag behind inspired concentrations (FA/FI <
1.0). The greater the uptake, the slower the rate of rise of the alveolar concentration and the lower the FA:
FI ratio.

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the concentration of a gas is directly proportional

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to its partial pressure,

Front 17

The alveolar partial pressure is important because it determines

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partial pressure of anesthetic in the blood and, ultimately, in the brain.

Front 18

the partial pressure of the
anesthetic in the brain is directly proportional to its

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brain tissue concentration, which determines clinical
effect.

Front 19

the greater the uptake of anesthetic agent, the greater the difference between

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inspired and
alveolar concentrations, and the slower the rate of induction.

Front 20

The relative solubilities of an anesthetic in air, blood, and tissues are
expressed as

Back 20

as partition coefficients. Each coefficient is the ratio of the concentrations of the
anesthetic gas in each of two phases at equilibrium.

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Equilibrium is defined as

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equal partial pressures in the
two phases.

Front 22

The higher the blood/gas coefficient

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the greater
the anesthetic's solubility and the greater its uptake by the pulmonary circulation.

Front 23

As a consequence of this
high solubility ifalveolar partial pressure rises more slowly,

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induction is prolonged.

Front 24

Low-output states predispose patients to
overdosage

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overdosage with soluble agents, as the rate of rise in alveolar concentrations will be markedly increased

Front 25

The transfer of anesthetic from blood to tissues is determined by
three factors analogous to systemic uptake:

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tissue solubility of the agent (tissue/blood partition coefficient),
tissue blood flow, and the difference in partial pressure between arterial blood and the tissue.

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the concentration effect

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increasing the inspired concentration not only increases the alveolar concentration but also increases its
rate of rise (ie, increases FA/FI).

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Anesthetics can be eliminated by

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biotransformation, transcutaneous loss, or exhalation.

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The most important route for elimination of inhalation anesthetics is the

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alveolus.

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diffusion hypoxia is prevented by

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administering 100% oxygen for 5–10 min after
discontinuing nitrous oxide.

Front 30

(Meyer–Overton rule

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.the observation that the anesthetic potency of inhalation agents
correlates directly with their lipid solubility

Front 31

Neuronal membranes contain a multitude of hydrophobic sites in their

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phospholipid bilayer

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MAC is a useful measure because it mirrors

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it mirrors brain partial pressure, allows comparisons of potency between
agents, and provides a standard for experimental evaluations

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High altitude requires a

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a higher inspired concentration
of anesthetic to achieve the same partial pressure.

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MAC values for different anesthetics are roughly

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additive.

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MAC can be altered

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by several physiological and pharmacological variables (Table 7–4). One of the
most striking is the 6% decrease in MAC per decade of age, regardless of volatile anesthetic

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only inorganic anesthetic gas in clinical use

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Nitrous oxide

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nitrous oxide is as
capable as oxygen of

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supporting combustion.

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circulatory effects of nitrous oxide are explained by

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its tendency to stimulate the sympathetic
nervous system.

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.Hypoxic drive, the ventilatory response
to arterial hypoxia that is mediated by

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peripheral chemoreceptors in the carotid bodies, is markedly
depressed by even small amounts of nitrous oxide.

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increasing CBF and cerebral blood volume, nitrous oxide produces

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mild elevation of
intracranial pressure. Nitrous oxide also increases cerebral oxygen consumption

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Nitrous oxide appears to (renal)

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decrease renal blood flow by increasing renal vascular resistance. This leads
to a drop in glomerular filtration rate and urinary output.

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almost all nitrous oxide is eliminated by

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exhalation.

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Although nitrous oxide is insoluble in comparison with other inhalation agents, it is

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is 35 times more
soluble than nitrogen in blood.

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7 Examples of conditions in which
nitrous oxide might be hazardous include

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air embolism, pneumothorax, acute intestinal
obstruction, intracranial air (tension pneumocephalus following dural closure or
pneumoencephalography), pulmonary air cysts, intraocular air bubbles, and tympanic membrane
grafting.

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Because of the effect of nitrous oxide on the pulmonary vasculature, it should be avoided in patients
with

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pulmonary hypertension.

Front 46

Halothane is a (class)

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halogenated alkane

Front 47

a 2.0 MAC of halothane results in a

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50% decrease in blood pressure and cardiac
output

Front 48

inhibition of baroreceptors
in the aortic arch and carotid bifurcation

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causing a decrease in vagal stimulation and a compensatory rise
in heart rate

Front 49

Halothane and bronchials

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Halothane is considered a potent bronchodilator, as it often reverses asthma-induced bronchospasm.
In fact, halothane may be the best bronchodilator among the currently available volatile anesthetics.

Front 50

Halothane attenuates airway reflexes
and relaxes bronchial smooth muscle by

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inhibiting intracellular calcium mobilization.

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Halothane is oxidized in

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the liver by a particular isozyme of cytochrome P-450

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Contraindications to withhold halothane

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unexplained liver dysfunction following previous exposure, intracranial mass lesions because of the
possibility of intracranial hypertension, Hypovolemic patients and some patients with severe cardiac disease

Front 53

Isoflurane and cerebral

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Isoflurane reduces cerebral metabolic oxygen requirements, and
at 2 MAC it produces an electrically silent electroencephalogram (EEG). EEG suppression probably
provides some degree of brain protection during episodes of cerebral ischemia.

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Isoflurane is metabolized to

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trifluoroacetic acid.

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The structure of desflurane is very similar to that of isoflurane. In fact, the only difference is

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fluorine atom for isoflurane's chlorine atom.

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the low
solubility of desflurane in blood and body tissues causes

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a very rapid washin and washout of anesthetic.

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Desflurane metabolism

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Desflurane undergoes minimal metabolism in humans. Serum and urine inorganic fluoride levels
following desflurane anesthesia are essentially unchanged from preanesthetic levels.

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Desflurane, more than other volatile anesthetics, is degraded by desiccated carbon
dioxide absorbent into

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into
potentially clinically significant levels of carbon monoxide.

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metabolizes sevoflurane

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liver microsomal enzyme P-450 (specifically the 2E1 isoform)

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Anesthesia systems can be classified as 3 types

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Anesthesia systems can be classified as nonrebreathing, partial rebreathing, or total rebreathing
systems.

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nonrebreathing systems (open systems),

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the fresh gas flow into the breathing circuit exceeds
the patient's minute ventilation. All gases not absorbed by the patient are exhausted through the adjustable
pressure-relief valve, there is no flow through the CO2 absorber, and no gas is rebreathed by the patient.

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In partial rebreathing systems (semiopen or semiclosed),

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the fresh gas flow into the breathing circuit
is less than the minute ventilation provided to the patient but greater than the rate of uptake of all gases by
the patient. The difference between the fresh gas flow and patient uptake is equal to the exhaust volume
from the pressure-relief valve. Therefore, exhaled gas can take one of three courses: It can be evacuated
by the pressure-relief valve, absorbed by the CO2 absorber, or rebreathed by the patient.

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total rebreathing system (closed system)

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does not evacuate any gas through the adjustable
pressure-relief valve. This implies that all exhaled gases except CO2 are rebreathed, expired CO2 must be
eliminated by the CO2 absorber to prevent hypercapnia, and the total amount of fresh gas delivered to the
system must nearly equal the amount of gas taken up by the patient's lungs.

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Anesthesia establishes a basal metabolic rate that is dependent upon

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the patient's weight and body
temperature.

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Basal metabolic oxygen consumption ( O2) equals

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equals 10 times a patient's weight in kilograms to
the three-quarters power:
For a 70-kg patient, oxygen consumption is
Oxygen requirements decrease by 10% for each degree below 37.6°C:
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Carbon dioxide production is approximately XX% oxygen consumption

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80%

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Minute ventilation is the sum of

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alveolar ventilation and ventilation of anatomic dead space and
equipment dead space.

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Equipment dead space consists primarily of

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the ventilation lost to expansion of the breathing circuit
during positive-pressure ventilation.

Front 69

Anesthetic uptake by the pulmonary circulation depends upon 3 factors

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the agent's blood/gas partition
coefficient ( b/g), the alveolar/venous difference (CA–V), and the cardiac output ( ):

Front 70

The amount of anesthetic required to prime the
breathing circuit and the functional residual capacity is equal to

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their combined volume (approximately 100
dL) multiplied by the desired alveolar concentration (1.3 MAC).

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Modern agent-specific vaporizers deliver a constant

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constant concentration of agent regardless of flow.

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Each milliliter of liquid halothane, isoflurane, desflurane, or sevoflurane
represents

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approximately 200 mL (±10%) of vapor