General Anesthesia Flashcards
what is the ultimate goal of anesthetic drugs
effect on brain: sedation and anesthesia
what is FA and what is FI
FA: alveolar fraction
FI: inspiratory fraction
why does FA differ from FI
because anesthetic is constantly being absorbed from the alveoli into the blood
if the anesthetic vaporizer is set to 2%, what is FI
2%
elimination involves both _________ and _________
biotransformation (metabolism) and clearance
what reflects the amount of anesthetic in the brain
alveolar concentration
how do we measure alveolar concentration (and therefore amt of anesthetic in the brain)
end-tidal concentration
what is the concept of dead space
the idea that not all anesthetic molecules are delivered to the alveoli (they can get caught up in the respiratory system)
alveolar concentration depends on what 5 things
1) inspired concentration (FI)
2) alveolar ventilation
3) solubility of inhalational anesthetic
4) cardiac output
5) tissue capacity and blood flow
what causes wasted ventilation
shallow breathing (dead space rebreathing)
what is the order of inhalational anesthetics from lowest to highest BGPC (and therefore fastest to slowest induction/recovery)
- desflurane
- H2O
- sevoflurane
- isoflurane
- halothane
- methoxyflurane
- ether
are inhaled anesthetics soluble in the lipid or aqueous component of blood
lipid
high solubility =
prolonged recovery and induction
solubility can be expressed as ___/____
FA/FI
describe how alveolar-venous tension difference influences amount of anesthetic in the brain
higher blood flow = faster uptake = decreased Fa = decreased amount in brain
lower CO = (higher/lower) solubility
higher CO = (higher/lower) solubility
lower = higher solubility
higher = lower solubility
normally, what percentage of CO goes to the brain in healthy animals
8%
what happens to the percentage of CO in the brain in animals in shock
it goes up to a very high percentage
when there is low CO, (higher/lower) percentage of the CO goes to the brain
higher
why do sick animals induce faster than healthy animals
they have less CO, so a higher fraction of the CO goes to the brain and the animal is induced faster
brain concentration will not rise significantly until
alveolar concentration starts to rise
anesthetic quantity in the blood is dependent on both
solubility and alveolar concentration
once you turn off iso, what happens to inspiratory concentration and what happens to end-tidal concentration
inspiratory will drop to 0 and end-tidal will slowly decline as the animal eliminates the anesthetic through breathing
do more or less soluble anesthetics have a higher degree of metabolism by the liver
more soluble
recovery depends on (3)
- movement from brain back to blood
- movement from blood back to alveoli
- removal from alveoli back to anesthetic circuit and eventually scavenging system
what are 4 properties of general anesthesia (what are 4 things we produce through inducing general anesthesia)
- muscle relaxation
- hypnosis
- amnesia
- analgesia
what is analgesia
reduced or absent perception of pain, in a conscious state
T/F all analgesics are general anesthetics
F
You need to do a procedure on an animal and you think it might be painful… based on the procedure, what 3 options do you have to control the animal/the animals pain
1) physical restraint
2) sedation and local anesthesia
3) general anesthesia
what are the 3 ways to perform general anesthesia and what is most commonly done
- inhalational
- total intravenous anesthesia (TIVA)
- partial intravenous anesthesia (PIVA)
PIVA most common
what are the 3 PHASES of anesthesia
1) pre-anesthetic
2) anesthetic
3) post-anesthetic
which of the following drugs are analgesics: (there are 3)
- opioids
- acepromazine
- alpha-2 agonists
- benzodiazepines
- ketamine
- alfaxalone
opioids, alpha-2 agonists, ketamine
which of the following drugs are NOT analgesics: (there are 3)
- opioids
- acepromazine
- alpha-2 agonists
- benzodiazepines
- ketamine
- alfaxalone
- acepromazine
- benzodiazepines
- alfaxalone
which of the following drugs are +/- at MAC reduction:
- opioids
- acepromazine
- alpha-2 agonists
- benzodiazepines
- ketamine
- alfaxalone
opioids and benzodiazepines
what are some benefits of pre-medicating your patients
- facilitates patient handling
- lowers dose of induction anesthetic needed
- lowers dose of inhalational anesthetic (MAC reduction)
- smoother induction
- smoother recovery (if still present in bloodstream during recovery)
- +/- analgesia
what is the best route to premedicate
IM
which of the induction drugs is the only analgesic
ketamine
which of the induction drugs is not a muscle relaxant
ketamine
which of the induction drugs always reduces MAC
ketamine and pentobarbital
what is neuroleptanesthesia
giving an opioid and a benzodiazepine to induce (only works for sick patients)
what induction anesthetic is good to induce on its own
propofol
what are examples of drug combinations that we can use to INDUCE a HEALTHY patient
- ketamine + diazepam/midazolam
- propofol/alfaxalone + diazepam/midazolam
- propofol alone
- inhalational anesthetic
what are advantages of using IV drugs to induce
1) rapid control of airways
2) rapid induction
3) smooth recovery
4) rapid adjustment in depth of anesthesia
what are 4 disadvantages of injectable induction
1) have to restrain patient
2) depends on patients hepatic and renal function
3) cardiopulmonary depression if you inject into artery
4) prolonged recovery if used for maintenance of anesthesia
what are advantages of inhalant anesthetic
1) does not require IV access
2) rapid recovery with newer agents
what are disadvantages of inhalant
1) requires fancy equipment
2) dose-dependent cardiopulmonary depression
3) excitement
4) pollution
5) cancer
what are 5 intubation routes
1) orotracheal
2) nasotracheal
3) pharyngostomy
4) tracheostomy
5) laryngeal mask
what are 5 things we can use to monitor the depth of anesthesia
1) ocular signs (palpebral, eye position)
2) muscle relaxation, muscle reflexes
3) RR depth and pattern
4) HR and BP
5) pharyngeal and upper airway reflexes
reflexes differ based on
species and drugs used
rules for monitoring are (strict/not strict)
not strict
what animals need a longer time before extubating
brachycephalics
where is the highest rate of death in horses (what phase)
post-anesthetic (recovery) phase
what do we monitor in recovery
cardiorespiratory and temperature (TPR)
what types of things do we give in recovery
fluids, analgesia, sedation
a lower MAC means (more/less) response to pain
less
inhalant/injectable anesthetics stimulate what 2 receptors
GABA and glycine
what triggers the respiratory center and where is this center located
chemoreceptors (peripheral and central) detect O2 and CO2 in the blood; located in the medulla and pons
what triggers the cardiovascular center and where is this center located
triggered by signals from baroreceptors in the carotid sinus and aortic arch; located in the medulla
what is respiration
the total process of delivering O2 and removing CO2
what are the 3 processes involved in respiration
1) gas exchange in the lungs
2) movement of gas in the bloodstream
3) transfer of gases at the cellular level
what is ventilation
the process of moving gases through the respiratory tract
does respiration or ventilation control O2 and CO2
ventilation
in an environment with no O2, what happens to ventilation and respiration
still ventilating because still moving air but not respirating because no O2
T/F ventilation is a part of respiration
T
what determines CO2 levels
minute ventilation (VE): RR x Vt
fill in the following:
low VE = ______ventilation = ____ CO2
high VE = ______ventilation = _____ CO2
hypo; high
hyper; low
why is it highly recommended to have a horse on a ventilator
depending on positioning, their organs can put pressure on the lungs and impact gas exchange
what is an issue with inhalant anesthetics and VE (think of Tainors graph)
when on inhalant anesthetic, the patient has a decreased ability to increase VE to compensate for higher CO2 (we may have to give breaths to counteract this)
physiologic dead space consists of:
anatomical and alveolar dead space
what does anatomical dead space consist of
air in the mouth, pharynx, larynx, trachea, bronchi and terminal bronchioles
what is alveolar dead space
air in the alveoli not participating in gas exchange (ex. due to atelectasis)
T/F PaCO2 = ETCO2
F
an animal that is panting/shallow breathing is ___________ but is not _______________-
ventilating; respirating
what is the consequence of panting/shallow breathing
less removal of CO2 from the lungs (may or may not impact O2 depending on FiO2)
what is the normal V/Q
0.8
V:
Q:
V: Ventilation
Q: CO or blood flow
what happens to V/Q when there is dead space
ventilating but not perfusing therefore V/Q = > 1
what happens to V/Q when there is a shunt
perfused but not ventilated therefore V/Q < 1
what are examples of a shunt
atelectasis, bronchoconstriction, complete small airway closure, vascular shunt
what pressure signifies relative hypoxemia and what pressure signifies absolute hypoxemia
relative: 80 mmHg
absolute: 60 mmHg
what is hypoxemia
low FaO2
what are 5 causes of hypoxemia
- low PiO2
- V/Q mismatch
- cardiac shunt
- hypoventilation
- diffusion barrier
what is PaO2 normally and under anesthesia
Normally: 93 mmHg
Under anesthesia: 663 mmHg
what determines the amount of O2 available to tissues
Hg content and saturation
you never want to see under what number on a pulse oximeter why
95; corresponds with PaO2 of 80 (patient is starting to get hypoxemic)
one molecule of Hg can carry how many molecules of O2
4
how easily does each of the 4 oxygen molecules bind
first one hardest, gets easier for each subsequent molecule
hypoventilation is _____ dependent whereas hypoxemia is ____ dependent
CO2; O2
at rest, how what % of delivered oxygen is being used by cells
25%
T/F if you have an anemic patient you can prevent hypoxemia by delivering 100% oxygen
F; only a small portion of oxygen is dissolved in blood so without adequate Hb the patient will still be hypoxemic
most oxygen is removed from Hb on the arterial or venous side
venous
________ effect occurs in the lungs and ________ effect occurs in the tissues
Haldane; Bohr
oxygen delivery to tissues is highly dependent on
Cardiac Output (CO)
stroke volume is dependent on (3)
preload, afterload, contractility
what is preload
amount of blood present in the ventricles at the end of diastole
what is the effect of preload on cardiac output
increases CO to a certain point (volume), at which point the cardiac mm can no longer recoil effectively and the CO will decrease
what is contractility
ability of the heart to contract in the absence of any changes in preload or afterload
how can we “cheat” increasing contractility of the heart
by giving ionotropic drugs that act as B1 agonists: dopamine, epinephrine, dobutamine
what is afterload and what is the effect on CO
resistance to ventricular ejection; decreases CO
what is the effect of vasoconstriction on afterload and what drugs will do this
increases: a agonists
what is the effect of vasodilation on afterload and what drugs will do this
decreases; a antagonists and B2 agonists
BP depends on
CO and SVR (systemic vascular resistance)
CO depends on
HR and SV
oxygen delivery (DO2) depends on
cardiac output and CaO2
T/F if you see a good BP while monitoring anesthesia you can conclude that CO is also good as there is a correlation between CO and BP
F; not necessarily
