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84 Cards in this Set

  • Front
  • Back

Patient response to inhalational ether anesthesia

1. pupil size


2. respiratory patterns


3. patient movement


4. muscle tone

Stages of Anesthesia

1. Stage 1


2. Stage 2 -Excitement stage


3. Stage 3 -Surgical Stage (4 planes)


4. Stage 4 - Medullary paralysis

Stage 1

Stage of anesthesia that involves mental depression, tolerance to painful stimulation, intact airway reflexes and amnesia increases with depth

Stage 2

* non-purposeful movement


* irregular breathing, HR


* dilated, divergent pupils


* heightened airway reflexes


*common in mask inductions


*theory of disinhibition

Stage 3

* Begins with return of rhythmic breathing


* Increasing depression of:


- Sensory


- Motor


- Reflex (autonomic)


- Mental

Stage 3, Plane 1

* Pharyngeal reflexes depressed


* Laryngeal reflexes intact


*Corneal/eyelash reflex depressed

Stage 3, Plane 2

-Laryngeal reflexes now depressed


- Increased chance for aspiration



*Good for intubation

Stage 3, Plane 3

- Remaining airway reflexes depressed


- Plane of "surgical anesthesia"


*Target before first surgical incision is made

Stage 3, Plane 4

*Rocking boat respirations


*Patient would need assistance with respirations

Stage 4

Apnea, no reflexes, fixed dilated pupils

Pharmacokinetics

1. what the body does to the drug


2. the study of drug disposition

pharmacokinetics describes...

1. absorption


2. distribution


3. metabolism


4. excretion

Absorption

Movement of drugs across biological membranes, may be passive (no energy required) or active (against gradient)


*depends on route of administration


*IV, oral, IM


* Oral, nasal, rectal, transdermal

Uncharged drugs are ____ soluble.

lipid

ionized drugs are ___soluble.

water

it is easier to move these drugs across membranes

uncharged

degree of ionization

*describes amount of drug present in each form (ionized vs. nonionized)


*depends on whether drug is acid or base


* depends on the solution the drug is immersed in

water is

polar and ionized


pKa

An acid dissociation constant that is specific for each drug.


pH at which the drug exists 50% in ionized form and 50% in non-ionized form

acid drug in acid solution has more drug in the ____ form

non-ionized form

base drug in acid solution has more drug in the __ form

ionized form

distribution

movement of drug to site of action


Distribution affected by these 3 things

-local/organ blood flow


-first-pass hepatic extraction


- degree of protein binding

Metabolism

Drug half-life


Conversion of drug for excretion


The rate of metabolism determines the intensity and duration of a drug's pharmacological effect.

Excretion

-Renal


-ionized fraction =excreted


-nonionized fraction= reabsorbed

Pharmacodynamics

what the drug does to the body

drug binds to this on a cell to produce an effect

receptor

Labels of axes on curve that describes relationship between drug and pharmacologic effect

X-axis = drug dose


Y-axis = intensity of drug effect

How does the slope change on dose/response curve if using a drug of higher potency?

slope becomes steeper

Type of drug half-life that measures effect of drug

functional (effective)

Type of drug half-life that measures concentration of drug itself

metabolic (biological)

first order kinetics

certain fraction of drug reduces over time, dependent on drug concentration in the body

zero order kinetics

Concentration of drug in the body does not impact the rate of metabolism. Certain amount of drug is metabolized per specific unit of time.


Ex. ethyl alcohol, dilantin

Theory of disinhibition
The CNS inhibitory system is anesthetized first so excitatory system dominates for some time during stage 2 of anesthesia until it too is inhibited.
Rocking boat
Intercostal muscles and diaphragm and thorax muscles start to work independently
PRMM
Ether anesthesia monitored these: pupils, respiratory, muscle tone and movement
4 pharmokinetics
ADME
Absorption distribution metabolism excretion
Fresh gas flow
Amount or fraction delivered, what we set (Fd)
Alveolar fraction FA
Concentration building up in the lungs
Inspired fraction Fi
How much is actually going to the pt, sampling port tells us this number
Arterial fraction Fa
Arterial blood supply
Dalton's law of partial pressures
The concentration of a gas is directly proportional to its partial pressure
Brain partial pressure/concentration is directly proportional to
Alveolar concentration/partial pressure at equilibrium. Brain to brain at any time though.
Factors affecting the rise of alveolar tension curves
1. Uptake of anesthetic agent
2. ventilation changes
3. Concentration/second gas effects
Uptake of anesthetic agents
A. Solubility of the agent
B. Alveolar blood flow (=perfusion=CO)
C. Arterial-to-venous partial pressure differences
Ostwald solubility coeff
B:g partition coefficient at 37 Celsius
Ostwald solubility coeff
B:g partition coefficient at 37 Celsius
Blood gas partition coefficient
Solubility coefficient
Solubility coefficient
The ratio of concentrations of the agent between the blood and alveolar gas space at equilibrium
Reflects the capacity of each phase to accept an anesthetic agent
Equilibrium between 2 phases means
Partial pressures of the agent are the same in both phases so theres no net movement.
When you will get the maximum clinical effect from an agent.
B:G solubilities
Metho 12
Halothane 2.5
Isoflurane 1.4
Sevo 0.69
Nitrous 0.47
Des 0.42
Xenon 0.12
Calculate concentration of agent
B= CX/(X+1)
A+B=C or C-B=A
Concentration formula
B:G solubility coeff X alveolar/gas concentration = blood concentration
Blood gas solubility tells you
Speed of induction
High solubility speed of induction
Slow
What does oil gas solubility tell you?
Greater affinity = greater potency
O/G solubilities of agents
Measures agents affinity for lipid membrane.
Metho. 970
Halothane 224
ISO. 98
Sevo. 55
Desflurane. 19
Nitrous. 1.4
O:G solubility is inversely proportional to dosage for the agent
^ O:G = decreased dose needed for effect

More lipid soluble means more potent and higher solubility number
Mac50
Minimum alveolar concentration at 1 atm pressure that prevents skeletal muscle movement in 50% of patients in response to a painful stimulus
* listed with at least 100% O2 or 70% nitrous
Mac awake
No agent used
0.3 - 0.5 x MAC50
Mac 99
1.3xMAC
MacBAR
1.7-2.0 x MAC50
Blocks autonomic reflexes
SE= decreased HR, BP, RR
MAC is inversely proportional to
Oil gas solubility
So higher solubility means less MAC needed to get effect
Factors that increase MAC (HHCCP)
Hyperthermia
Excess pheomelanin production/red hair
Induced catecholamine levels
Cylcosporine -depressant
Hypernatremia
Decrease MAC
Hypothermia
Increased age
Pre-op meds
Depressed catecholamine levels
Alpha -2 agonists
Acute ETOH ingestion
Pregnancy and <72 hrs postpartum
Lithium
Lidocaine
Opioids (neuraxial)
Ketanserin- can depress CNS by blocking alpha 1 receptors, serotonin and histamine
PaO2 < 38 mmHG
BP < 40 mmHG
CPB
Hyponatremia
No effect on MAC
Agent metabolism
Chronic ETOH abuse
Length of anesthesia
PaCO2 15-95 mmHG
PaO2 > 38 mmHG
BP > 40 mmHG
Hyper/hypokalemia
Thyroid dysfunction
3. Concentration/second gas effects
Over pressuring. The higher the Pi the more rapidly the PA approaches Pi
Alveolar blood flow is equal to
CO in absence of shunting
Increased CO will do what to induction time
Slow it down
Changes in CO have more effect on
High solubility agents because they tend to go into the blood whilst the low solubility will stay in alveoli more
Increased CO + low solubility
Fast induction
Right to left shunt
Arterial and venous blood mixes. Low solubility gases take longer for induction to happen because too much diluting of blood and harder to build up Pa
Arterial-to-venous partial pressure
Difference between amount of agent in arterial and venous blood
Affected by:
-tissue/blood partition coefficient
- blood flow to the tissue
- blood/tissue agent concentration gradient
Tissue groups
1. vessel rich group - brain heart liver kidneys exocrine glands. 10% body wt but gets 75% of CO
2. Muscle group- 50% body wt, 20% CO
3. Adipose group- 20% body wt, 6% CO, high affinity for gases and harder to induce x20
4. vessel poor group -bone, ligaments, hair, teeth, cartilage. Minimal effect on uptake of anesthetic
* adipose and muscle groups take longer to wear off
Uptake= solubility x CO x Pa-v
If solubility is 0 then no uptake. Zero means nothing going to target tissue
Ventilation changes
Increasing ventilation speeds up induction. Less of an effect when using the low solubility agents since they like to stay in alveoli
Second gas effect
Seen with nitrous. rapid diffusion of nitrous oxide. Affects mainly high solubility agents. Combination of concentrating and augmenting tracheal inflow effects. Rapid diffusion of nitrous out of lungs causes gas to be actively drawn into the lungs (augmented inflow). Second gas is the anesthetizing gas
* faster induction
Also affecting uptake:
ventilation perfusion mismatches
-affects the arterial fraction (concentration) - constriction
- impedence between alveolar space and blood -pneumothorax, bronchial intubation -collapsed alveoli
-longer time to clinical anesthesia/barrier -COPD, emphysema
Elimination of inhaled anesthetics
-biotransformation
- transcutaneous
- exhalation - main why
diffusion hypoxia
fink phenomenon
- elimination of nitrous wen pt is breathing room air
Causes hypoxia and hypocarbia
Dilution of alveolar oxygen/CO2 levels. Need to give 100% but make sure u balance it so u dont eliminate all CO2 reserves.
Hypoxia
Prepulmonary- anoxic/hypoxic
Pulmonary-
Post-
Stagnant- no blood flow ...CO
Anemic- Hgb issues, decreased O2
Histotoxic- tissues damage /CO poisoning
Stages of hypoxia
Pre-crisis stage PO2 60-55 saO2 80%
Crisis stage - po2 40-45 saO2 70% air hunger
Terminal stage- po2 <25%
Oxygen atelectasis
Due to inspiration of high concentrations of oxygen
Displaces nitrogen from the alveoli
Alveoli collapse when oxygen is absorbed out (no nitrogen left to keep alveoli patent)!
Give RA to replace N
Long cases add RA to mixture
retrolental fibroplasia or retinopathy of prematurity
With premies who dont have fully vascularized retinas. Increased O2 causes abnormal vascularization and fibrous tissue formation