Pharm Unit 1 Flashcards
Definition of anesthesia?
Lack of feeling or sensation, artificially induced loss of ability to feel pain
Definition of regional anesthesia?
Insensibility caused by interrupting the sensory nerve conduction of a particular region of the body - peripheral, spinal, epidural
- Level of consciousness is unchanged (unless sedatives are used)
- Ventilatory/airway protection is maintained
Definition of sedation?
A spectrum of consciousness between “awake” and “unconscious”
What are examples of anesthesia from 4000 to 400 BC?
Plants (poppy, coca leaves), acupuncture, ethylene fumes beneath Apollo’s temple, cannabis vapor, carotid compression
What was Hippocrates view of anesthesia?
None is needed, it is the job of the patient to stay still so that the Dr may do their work (accommodating the operator)
Who wrote the materia medica? What is it?
Dioscordies a surgeon in Nero’s army. It is a pharmacology volume.
Give an example of anesthesia from Roman/Greek times
Mandragora and wine, together had a hallucinogenic effect
What was the change in anesthesia in the middle ages?
Preference for inhaled agents began, such as a mix of opium, mandrake, hemlock, hyposcyamus (L-isomer of atropine) and water. Reversed with vinegar
What was the first volatile anesthetic? What was its problem? Who discovered it?
Diethyl ether, Valerius Cordus
Who invented IV access?
Sir Christopher Wren and Robert Boyle
Who discovered NO and oxygen?
Joseph Priestly
Who discovered the basic elements and suggested NO for surgical pain control?
Humphry Davy - also discovered K+, Na+, Ca2+, Mg2+
Which dentist found that NO patients had no recall of pain/injury?
Horace Wells
Who started mixing volatiles with air to improve cyanosis?
Andrews a Chicago surgeon
Who re-visited ether as an anesthetic combined with whiskey?
Crawford Long
Who found a way to purify Ether?
Dr. Robinson Squibb
Other than flammable, what are disadvantages of ether?
Prolonged induction/emergence, high incidence of nausea/vomiting
Who defined pain as actual or potential tissue damage?
Sir James Simpson
Who discovered epidemiology?
Dr. John Snow
Who used cocaine for eye surgery?
Dr. Koller
Who did the first regional block with cocaine? Type of block?
Dr. Halsted, Mandibular block
Who completed the 1st spinal anesthetic with cocaine?
Dr. August Bier - developed Bier block
Describe the Bier block
You elevate the arm, let blood drain. Wrap the arm tightly to squeeze out more blood. Inflate a BP cuff to prevent flow of blood into the arm, then inject lidocaine. The arm should stay numb until either the lidocaine is metabolized, or blood flow is restored
1st CRNA?
Sister Mary Bernard
Mother of anesthesia?
Alice Magaw
Who opened one of the earliest anesthesia schools?
Agatha Hodgins
Issue with cyclopropane? Halothane?
C = highly explosive
H = Slow onset and can cause hepatitis. Good because it causes bronchodilation
Compare speeds of Desflurane, Sevoflurane and Isoflurane
Des = fastest onset and emergence
Sevo = in between
Isoflurane = slowest onset/emergence of the three
Who did much of the research on modern volatiles?
Dr. Edmund Egar
What causes amnesia?
Stimulation of inhibitory transmission (GABA) or inhibition of stimulatory transmission (ACh)
What is the anesthesia triad?
Amnesia, Analgesia and Muscle relaxation
What was the first muscle relaxant?
Curare - Decreased amount of anesthesia due to relaxation, decreased mortality
Which surgeon was responsible for 3 deaths from 1 operation?
Dr. Liston
Who opened the Cleveland clinic?
George Crile
- Light nitrous/oxygen anesthesia
- Local infiltration of procaine
Who began anesthetic records, BP, and HR measurements?
Harvey Cushing - Regional blocks prior to emergence from ether
What is Neurolept anesthesia?
You “screw up the brain” to induce amnesia. Involves lots of anti-psychotics and minimal muscle relaxants/opioids.
What is stage 1 of anesthesia? Each plane?
Stage 1 = beginning of induction to LOC
1st plane = no amnesia/analgesia
2nd plane = amnesia, but only partially analgesic (versed, fentanyl)
3rd plane = complete analgesia/amnesia
What is stage 2 of anesthesia?
LOC to onset of automatic breathing. Eyelash reflex disappears, coughing/vomiting/struggling can still occur. This is when we want people to not bother the patient. Laryngospasm a risk as well. You want to get through this stage as fast as possible
What is stage 3 of anesthesia? Each plane?
Stage 3 = onset of automatic respiration to respiratory paralysis
1st plane = automatic respiration to cessation of eyeball movements
2nd plane = cessation of eyeball movements to beginning of intercostal muscle paralysis. Tear secretion increases
3rd plane = beginning/completion of intercostal muscle paralysis. Pupils dilate, desired plane prior to muscle relaxants
4th plane = complete intercostal paralysis to diaphragmatic paralysis (apnea)
What is stage 4 of anesthesia?
Stoppage of respiration to death
What stages do you extubate at? Why?
1 or 3, 2 has a high incidence rate of laryngospasm, N/V
What stage do you intubate at?
Stage 3
Per lecture, what common pressor agent has a high incidence of tachyphylaxis?
Ephedrine
Which receptors/proteins are intracellular?
Insulin, steroids, milrinone
What is the 1 compartment model?
Drug gets injected, goes to heart, circulates through the central circuit and goes to vessel rich groups, then they can leave and go to other places and then be excreted
What is the 2 compartment model?
Drugs go into the central compartment and then into the periphery and from there can go other places such as fat or proteins prior to excretion.
What drugs are listed as sensitive to first pass metabolism?
Lidocaine, propranolol, demerol, fentanyl, sufentanil, alfentanil
What protein do acidic drugs bind to? Basic?
Acid = albumin
Base = A1-Acid Glycoprotein
What factors can caused decreased plasma proteins?
- Age
- Hepatic disease
- Renal failure
- Pregnancy
- malnutrition
What happens to the fraction of free drug if the normal free fraction of drug is 2% and 50% of plasma proteins are lost?
ThenThe free fraction of drug is 4%…. It doubles!
Poor protein binding and lipophilic results in a ______ volume of distribution
Big volume of distribution - Thiopental, diazepam
Highly protein bound to plasma proteins results in a ______ volume of distribution
small - warfarin
Which drugs are generally more inactive, water or lipid soluble?
Water
What metabolizes most of our anesthesia drugs?
Liver microsomal enzymes
What are the primary functions of phase I reactions? Phase II?
Phase I = Redox and hydrolysis to increase drugs in polarity to prepare them for phase II
Phase II = Make drugs more water soluble via some form of a conjugation reaction
What is the primary microsomal enzyme? And the most common of that family?
CYP450, and the most common of that subclass is CYP3A4
Induction vs inhibition?
Induction: enzyme activity is increased leading to a shorter duration of a drug metabolized by the enzyme
Inhibition: enzyme activity is reduced leading to a greater duration
For most anesthetic drugs clearance is _______
constant
In flow-limited clearance, _____ limits the metabolic rate
In capacity-limited clearance, ______ is the limiting factor
Q or blood flow
the liver’s ability to metabolize
Rate of drug metabolism equation
R = Q (C inflow – C outflow)
Elimination half-time vs elimination half-life?
HT = time to get rid of 50% from the plasma
HL = time to get rid of 50% from the body (tissues for example, hard to measure)
Context sensitive half time?
This is half-time related to an infusion. Basically, the longer an infusion goes, the longer it takes for its effects to wear off.
Does ionized or non-ionized more easily cross barriers?
Non-ionized
What is the mental trick to remember how to solve ionization problems?
Weak Acid PK after pH (a for after), weak base pK before pH (b for before)
Why would a LA not work for a necrotic limb in regards to pH?
Many LA’s are weak bases, if the pH is too low, the LA is likely to ionize and therefore not work
How can individual variability influence pharmacodynamics?
Elderly
- Decreased cardiac output… To brain and liver…
- Decreased protein binding
- Increased body fat
Enzyme activity - Acute vs chronic alcohol ingestion
Genetic disorders
- Atypical cholinesterase activity
- Malignant hyperthermia
Definition of chiral?
A molecule with asymmetric centers
What is the term for a right rotation of light? Left?
R = Dextrorotatory
L = Levorotatory
Why do we give anti-anxiety meds in pre-op?
To reduce catecholamine cascade
Sedative vs hypnotic?
S = drug that induces sleep or calm
H = Drug that induces hypnosis or sleep
In regards to an EEG, is even/odd on the left or right?
Odd = left, Even = right
BIS terms: SQI, EMG, EEG and SR?
SQI: signal quality index, want this maxed
EMG: you want none, meaning no muscle movement
EEG: all brain electrical activity into one waveform
SR: suppression ratio, tells us how often the EEG has been flat
Goal BIS range?
40 - 60
What are the 5 main effects of BZDs?
Anxiolysis, sedation, anterograde amnesia, anticonvulsant action and spinal-cord mediated skeletal muscle relaxation
Alpha 1 vs Alpha 2 in a GABA receptor?
Alpha 1 = sedative, amnestic and anti-convulsant
Alpha 2 = anxiolytic and skeletal muscle relaxer
What BZD clears the fastest?
Versed
What BZD is an aspiration risk?
Versed
What BZD can produce an isoelectric baseline?
Valium
What BZD is best for a COPD patient?
Diazepam(Valium)
What BZD is not dependent on hepatic enzymes?
Ativan
What BZD is the most potent sedative/amnestic?
Ativan
What BZD is the most potent muscle relaxer?
Valium
What BZD has the slowest onset of action?
Ativan
What BZD does not have active metabolites?
Ativan
Relationship of CBF and CRMO to EEG?
Direct correlation, as CBF and CRMO increase, the EEG waveform number should increase
At what BIS are patients going to be unconscious? At what level do they have less than a 5% chance to return to consciousness within 50 seconds?
Bis less than 58 = unconscious
Bis less than 65 for the 5% chance
What is important to note about the spinal-cord mediated skeletal muscle relaxation with BZDs?
It is not adequate for surgery, you will still need muscle relaxants or paralyzers. It does NOT potentiate NMBD
Why did BZDs replace barbiturates?
Less tolerance, less potential for abuse, fewer and less serious side effects, and do not induce hepatic microsomal enzymes
How does a BZD work?
Binds to a GABA receptor, which increases affinity for GABA to bind to receptor causing the chloride channel to open, hyperpolarizing the target and making it harder to excite
What other drugs/chemicals can bind to GABA sites (hint think GABA potentiation)?
Barbiturates, etomidate, propofol and alcohol, clonidine, precedex
In general are BZDS highly/poorly protein bound and water/lipid soluble?
Highly protein bound and highly lipid soluble
What are the general effects of BZDs on the EEG?
Decreased a-alpha activity, antegrade amnesia, some unable to produce isoelectric state
What drugs/chemicals are synergistic with BZDs?
Alcohol, injected anesthetics, opioids, alpha-2 agonists (clonidine, precedex, guanfacine), inhaled anesthetics
What is a potential anecdotal concern with BZDs intraop?
Reduced platelet aggregation
What is the relationship of the imidazole ring to BZD drug availability in pH changes?
If the pH is less than 3.5, the ring is open, water soluble and protonated
If the ph is greater than 4.0, the ring is closed, lipid soluble and non-protonated
Which drugs are known to cause inhibition of P-450 enzymes and decrease BZD metabolism?
Cimetidine, erythromycin, CCBs, anti-fungals and fentanyl
Which BZD is good for induction with neuropathology? Why?
Versed - No change in ICP if decreased intracranial compliance
What is the Vd for versed?
1-1.5 L/kg (large)
Dosing range for versed in children and adults for sedation?
C = 0.25-0.5 mg/kg Oral (peak 20 - 30 minutes)
A = 1 - 5 mg IV, peak 5 minutes
Induction dose of versed?
0.1 - 0.2 mg/kg IV over 30 - 60 seconds given AFTER 50 - 100 mcg of fentanyl
Post-op dose for sedation for versed?
1 - 7 mg/hr IV
Why is post-op sedation with versed now discouraged?
Markedly delays awakening (active metabolites) and can negatively impact the immune T cells
What BZD is not a vesicant?
Versed
List the BZDs from shortest to longest E1/2 times
Versed (2 hours) < Ativan (14 hours) < Valium (20 - 40 hours)
What is the onset of valium?
Onset 1-5 minutes
What is the valium dosage for anti-convulsant actions?
0.1 mg/kg IV
At what dose does valium begin to cause hypercapnia (it is still the BZD of choice for COPD patients)
0.2 mg/kg IV, and in general, the ventilatory depression is countered by the stimulation of the surgery
Which BZD has the most minimal impact on the CV system?
Valium
Induction dose for valium?
0.5 - 1.0 mg/kg IV (decrease by 25 - 50% for elderly)
What is the structural difference of Ativan to Serax?
It has an extra Cl atom
What is the elimination half time of ativan?
14 hours
When is the peak effect of Ativan?
20-30 minutes with IV dose
Dosing range for Ativan?
1 - 4 mg IV
Which of the BZD doesn’t require propylene glycol for solubilizing?
Versed
What is the metabolism route for flumenazil?
Via hepatic microsomal enzymes in inactive metabolites
Dosing guidelines for flumenazil?
0.2 mg IV and titrate to consciousness, repeat by 0.1 mg q1m to 1 mg total
Dosing range for flumenazil to reverse sedation and abolish therapeutic dose?
Reverse sedation = 0.3 - 0.6 mg
Abolish therapeutic dose = 0.5 - 1 mg
What would you suspect with unconscious/overdose AND 0.5-1mg of flumazenil without change?
Other intoxicants
What is the duration of flumazenil?
30-60 min
What is the rate for continuous infusion of flumazenil?
0.1-0.4 mg/hr
Flumazenil acts as a _________ to prevent/reverse BZD activity
competitive antagonist
What releases endogenous histamine?
Basophils and mast cells
Effects of histamine in the body?
Contraction of smooth muscle in the airways, secretion of stomach acid, release of neurotransmitters in the CNS (ACh, norepi, serotonin)
What drugs can induce histamine release?
Morphine, mivacurium, protamine and atracurium. If any of these are given you must treat with an H1 and an H2 antagonist
What does histamine do to H1 receptors? H2?
H1 = “bee sting”, hyperalgesia and inflammatory pain, allergic rhino-conjunctivitis s/sx
H2 = elevates cAMP (beta-1 like stimulation) and increase acid/volume production
H1 can activate
muscarinic, cholinergic, 5-HT3 and a-adrenergic
H2 can activate
5-HT3, and B-1
What are the general effects of H1/H2 receptor activation?
Hypotension, capillary permeability, flushing, prostacyclin release, tachycardia
Where are the H1 receptor?
In the vestibular system, airway smooth muscle and cardiac endothelial cells
What is an advantage of H1 antagonists?
They have little to no tachyphylaxis
H1 antagonist s/e and drug examples?
S/E = blurred vision, urinary retention, dry mouth, drowsiness (1st gen only)
Drugs = benadryl, phenergan (these are the 1st gen), zyrtec and claritin
What is benadryl given for?
Anti-pruritic, pre-treat for allergy for IVP dye and anaphylactic reactions
- May inhibit afferent arc of oculo-emetic reflex
E1/2 time for benadryl?
7 - 12 hours
What are some positive effects of Benadryl?
Stimulates ventilation by augmenting the relationship of hypoxic/hyper-carbic drives
What is the dosing range for benadryl?
25 - 50 mg IV
Primary use for phenergan?
Anti-emetic
E1/2 for phenergan?
9 - 16 hours
What are the secondary uses for Phenergan?
As a rescue drug for PONV and reduce peripheral pain level (has anti-inflammatory action)
What are the black box warning for Phenergan?
Vesicant (limb loss) and respiratory arrest bronchospasm in children under the age of 2
Dose and onset for phenergan?
12.5 - 25 mg IV and 5 minutes
How do H2 receptor antagonists work?
Decrease hypersecretion of gastric fluid from the gastric parietal cells, decrease cAMP, decrease gastric volume, increase pH
General S/E of H2 receptor antagonists?
Diarrhea, HA, skeletal muscle pain, weakened gastric mucosa (infection concerns for the lung), bradycardia, increase in serum creatinine
H2 receptor drug examples?
Cimetidine (tagamet), ranitidine (zantac) Famotidine (pepcid)
How is tagamet metabolized?
In the liver via CYP450, cleared in the urine
Downside of Tagamet?
Strongly inhibits CYP450 (drugs like warfarin, phenytoin, lidcaine, TCAs, propranolol, nifedipine, Demerol and Valium can last longer)
S/E of Tagamet?
Bradycardia, hypotension, increased prolactin, impotence (inhibits dihydrotestosterone from binding)
Dosing range for Tagamet?
150 - 300 mg IV (1/2 the dose in renal impairment)
How is Zantac metabolized?
In the liver and cleared by the kidneys
Relationship of Zantac to CYP450?
Does bind, but more weakly than Tagamet and does not inhibit the enzyme
Dosing range for Zantac?
50 mg diluted to 20 cc given over 2 minutes (1/2 the dose in renal impairment)
How is Pepcid metabolized?
Hepatic metabolism, renally cleared
Relationship of Pepcid to CYP450?
No interference
Only H2 antagonist that inhibits CYP450?
Tagamet
What drug is indicated to inhibit the oculo-emetic reflex?
Benadryl
Most potent H2 antagonist? What is its E1/2 time?
Famotidine(Pepcid), 2.5 - 4 hours (the longest of the H2 blockers)
What does Pepcid interfere with?
Phosphate absorption
MOA of PPIs
Irreversible binding to acid secretion “pumps”
- Inhibit the movement of protons (H+) across the gastric parietal cells
- Up to 5 days onset (3)
Dosing range for Pepcid?
20 mg IV (1/2 the dose in renal impairment)
General trends for PPIs?
Takes 3 - 5 days to fully “work”, most effective at controlling gastric acidity and decreasing volume
What are side effects are PPI’s generally associated with with?
Bone fractures, Lupus, nephritis, C-Diff, vitamin b-12 deficiency, magnesium deficiency
What drugs can PPI’s negatively affect?
Inhibits warfarin metabolism, and blocks enzyme that activates Plavix
PPI drugs
Omeprazole (Prilosec), Pantoprazole (Protonix), Lansoprazole (Prevacid) Dexlansoprazole (Dexilent)
How is Omeprazole unique from other PPI’s?
It is a prodrug and enteric-coated - protonates in parietal cells to active form
Omeprazole metabolism?
By CYP enzymes, theoretically inhibits other drugs but not in a clinically significant manner
Omeprazole dose?
40 mg in 100 CC NS over 30 minutes or PO 3 hours prior to surgery
Omeprazole S/E?
HA, Agitation, AMS (it can cross the BBB), ABD pain, N/V, flatulence, small bowel bacterial overgrowth
Protonix metabolism?
CYP, no significant drug interactions
What H2 antagonist is Protonix just as “fast” as?
Ranitidine. Takes about 1 hour to decrease gastric volume and increase pH
Protonix has ________ bioavailability and _______ E ½ time compared to prilosec
greater, longer
Protonix dosing?
40 mg in 100 ml over 2 - 15 minutes
Drug of choice for GERD?
PPI
Drug of choice for Gastric ulcers?
PPI
Drug of choice for GI hemorrhage?
PPI after EGD
Drug of choice for NSAID ulcerations (specific drug, not class)?
Omeprazole and d/c NSAIDs
Drug of choice for Aspiration pneumonitis prevention (take timeframe into account)?
Less than 24 hours = H2 Antagonist
Greater than 24 hours = PPI
Drug of choice for intermittent s/sx of reflux?
H2 antagonists
Difference between particulate and non-particulate antacids?
P = aluminum and magnesium based, and its aspiration is just as bad as an acidic aspiration (don’t reduce volume and increase pH enough especially relative to the NP antacids)
NP = sodium, carbonate, citrate, bicarbonate base - neutralizes acid
Long term downsides to antacids?
Can delay gastric emptying and acid rebound is a concern
Concerns with magnesium, calcium and sodium based antacids?
M = diarrhea and neurologic/neuromuscular impairment
C = hypercalcemia
S = increased Na load = extra strain on the CV system d/t fluid overload
Downside of giving an antacid prior to surgery?
It does increase gastric volume
Dosing for sodium citrate?
15 - 30 ml, give right before surgery as it wears off in 30 - 60 minutes
Antacids neutralize acid → base + acid = ?
SALT, CO2 AND WATER
What drug would you give if the patient had a full stomach?
A dopamine blocker because it increases gastric motility (prokinetic)
Basic effects of dopamine blockers on gastric motility?
- Increases lower esophageal sphincter tone
- Stimulates peristalsis
- Relaxes pylorus and duodenum (Gastric emptying and intestinal transit)
Side effects of dopamine blockers on antagonizing dopamine receptors?
- Not administered to patients with dopamine depletion/inhibition
- Extrapyramidal reactions (easily crosses BBB)
- Orthostatic hypotension
- Some effects on chemoreceptor trigger zone (Esp cinv and s/p csection but < 5-Ht3 drugs)
- No change in gastric ph
Can you give a patient with Parkinson’s dopamine receptor blockers?
No - already low on dopamine
Dopamine receptor blocker drugs?
Reglan, Domperidone and Droperidol (Inapsine)
What is the best drug for diabetic gastroparesis?
Metoclopramide (reglan)
S/E of Metoclopramide (reglan)?
ABD pain, muscle spasms, hypotension, sedation, increased prolactin release, neuroleptic malignant syndrome, decrease plasma cholinesterase levels
What medication can cause neuroleptic malignant syndrome?
Metoclopramide (reglan)
What are the results of Metoclopramide (reglan) decreasing plasma cholinesterase levels?
Slows metabolism of succinylcholine, mivacurium, ester LA
S/Sx of neuroleptic malignant syndrome?
High temp, muscle rigidity, tachycardia, confusion
Dosing for Reglan?
10 - 20 mg IV over 3 - 5 minutes 15 - 30 minutes prior to induction
Which dopamine receptor blocker does not cross the BBB?
Domperidone
What was Droperidol originally prescribed for?
Schizophrenia and psychosis
Which dopamine blocker has the highest risk for extrapyramidal s/sx and NMS (neuroleptic malignant syndrome)?
Droperidol
What is advantageous about Droperidol?
More effective than Reglan and just as effective as Zofran (plus its cheaper)
Black box warning for Droperidol?
QT elongation -> Torsaddes, and has A LOT of drug interactions with medications that can affect the heart
Dosing for Droperidol?
0.625 - 1.25 mg IV
What meds need to be avoided when giving Droperidol (inapsine)?
Avoid other CNS depressants - barbiturates, opioids, general anesthetics
Describe the process of serotonin release
Released from chromaffin cells of the gut→ stimulates vagal afferents via 5HT3 receptors → vomiting
Highest concentration of 5HT3 receptors?
Brain and GI tract
5HT3 antagonists?
Ondansetron (Zofran), Granisetron (Kytril) and Dolasetron (Anzemet)
5HT3 antagonists don’t work for what kind of N/V?
Not effective for motion sickness/vestibular stimulation
Advantages of Zofran? S/E?
Advantages = no CNS activity, no Dopamine/histamine/adrenergic/cholinergic activity.
S/E = HA, diarrhea, QT elongation
Dosing for Zofran? Half life?
4 - 8 mg IV, and about 4 hours
When do you give Zofran to prevent PONV?
end of procedure
What is the theory of why Decadron works for N/V?
- Inhibition of prostaglandin synthesis and control endorphin release
- Because it is an anti-inflammatory it can reduce opioid use = lesser chance of NV
Decadron onset?
Takes 2 hours to kick in and lasts for 24 hours
When should you give decadron for PONV prevention?
2 hours before procedure ends or beginning of procedure if shorter
Why would you give decadron more than 2 hours before the procedure ends?
Reduce airway edema from difficult intubation - increase dose to 12-20 mg
S/E of decadron?
Hyperglycemia (minimal if not many doses are given) and perineal burning/itching if given too fast IVP
Dosing of Decadron?
Varies, start with 4 - 8 mg, uptitrate if needed
Primary effects of Scopolamine patch?
Sedation, Anti sialagogue (fancy speak for dry mouth), reduce motion sickness, mydriasis cycloplegia (pupil dilation)
Scopolamine dosing and timing?
Apply 4 hours preop, lasts 24 - 72 hours, gives a 140 mcg priming dose then 1.5 mg over 72 hours.
Best site for Scopolamine patch?
Post-auricular, secondary = wrist or back
Why would you give scopolamine over other anticholinergics (atropine and glycopyrrolate?
Scopolamine is better for sedation, drying secretions, mydriasis, and motion-induced N/V
How do broncho dilators work?
- G stimulatory and activate cAMP = broncho relaxation, decrease Ca entry and contractile sensitivity to Ca
- Reduce inflammation and directly relax smooth muscle
Bronchodilators have a similar structure to _______
epinephrine
How much airway relaxation does a SABA achieve?
15% increase in FEV
How much of an inhaled SABA reaches the lungs?
12%
How much does an ETT reduce drug delivery if aerosolized into the tube?
by about 50 - 70%
Beta agonist S/E?
Tremor, tachycardia, transient decrease in arterial oxygenation, hyperglycemia
Inhaled beta agonist drugs?
Albuterol (proventil) and Levo-albuterol (xopenex)
Difference between Albuterol (proventil) and Levo-albuterol (xopenex)
albuterol works better than xopenex but has more side effects
Which PPI can cross the BBB?
Omeprazole
What would you give to an OB patient with a full stomach going into surgery?
Sodium Citrate (Bicitra)
How do dopamine blockers help with full stomach?
Stimulate peristalsis, constrict the esophageal sphincter tone and relax the pylorus/duodenum (lower tract)
With these drugs, which one requires the RN to wash their hands after administration?
Scopolamine patch - if you don’t, and say rub you eye you could severely dilate it
Who made the first anesthesia machine with nitrous and oxygen?
Hewitt
Which dentist was an early proponent of ether?
William Morton
What 2 people were early experimenters with chloroform? Their professions?
Sir James Simpson and Dr. John Snow, obstetricians
Who discovered that chloroform had hepatotoxicity in children?
Guthrie
Who discovered that light chloroform created fatal VF in animals?
Levy
Who understood early on shorter surgeries were preferable?
Dr. Liston (killed 3 men in one surgery)
Who worked at the cleveland clinic and was first to use local infiltration of LA using procaine?
Dr. George Crile
Who started using regional blocks and kept strict records of vital signs?
Harvey Cushing
What metabolizes Valium?
CYP3A4
What receptors are in the lipid bilayer?
Opioids, BZDs, B-blockers, catecholamines and NMBD’s
What receptors are intracellular?
Insulin, steroids, Milrinone
What receptors are circulating proteins?
Anti-coagulants
What was organized to explore young deaths with chloroform? It’s findings?
The Hyderabad commissions - deaths related to apnea -> hypoxia -> cardiovascular collapse
When discovered, what was Isoflurane’s advantages over Halothane?
Less N/V, safer and quicker onset than Halothane
Who discovered that end-tidal concentration correlated to movement, or MAC?
Dr. Egar
What classes of drugs are most common to pre-op?
BZD’s, H1/H2 blockers and bronchodilators
What drugs are most common to induction?
Etomidate, ketamine, propofol and narcotics
What classes of drugs are most common to maintenance of anesthesia?
Inhalation drugs, NMBD’s, pressors, blockers
What classes of drugs are used in emergence of anesthesia?
NMB reversal, local anesthetics
Ventilation vs Oxygenation
V = getting oxygen to the alveoli
O = getting the oxygen from the alveoli to the tissues
Define pre-emptive analgesia
The idea that the longer you can prevent the brain from recognizing pain, the lesser the sensation of pain will be when it is eventually recognized
What is an alternative reason that early NO anesthesia was able to induce unconsciousness not related to NO?
Hypoxia, they were breathing pure nitrous oxide, so the LOC could be due to hypoxia
Which volatile has a high vapor pressure (evaporates easily) and the highest MAC?
Desflurane
What is a potential concern with sevoflurane?
Toxic interactions with the soda lime (mostly disproven)
Why is Domperidone not available in the US?
Due to dysrhythmia and sudden death concerns
What is advantageous of Domperidone?
Does not cross the BBB (unlike reglan) and no anti-cholinergic activity
What sub-unit of GABA is most abundant?
Alpha-1
How is versed metabolized?
In the liver by CYP3A4
Why is versed useful in patients with CHF?
While it can increase HR and decrease BP, it reduces SVR and maintains the CO.
What is unique to versed in being used with intubation?
It does not inhibit the BP/HR response, so lesser chance of hypotension
What was the country of origin of Dr. Koller, and who was his colleague?
Viennese and Sigmund Freud
What is a disadvantage of desflurane?
Requires a large quantity to achieve anesthesia
What technique was used in the 1980s to combat surgical stimulation causing change in vitals despite lack of patient movement?
High dose opioid technique
What trend was adopted in the 2000s to reduce opioid use?
The multi-modal approach
What changes occur in the case of pheochromocytoma?
Decreased B-receptors due to constant catecholamine release = harder for our pressor drugs to work
Which BZD and 1 other drug has a large VD, poor protein binding and lipophilic?
Valium and Thiopental
What anti-coagulant is highly protein bound to plasma proteins and a small VD?
Warfarin
What molecules prefer to be renally excreted? Hepatically?
Renal = ionized or water soluble
Hepatic = non-ionized or lipid soluble
When solving PK equations, what type of number do you want?
Negative, the more negative it is, the more likely it will be non-ionized and therefore lipid soluble
What kinds of drugs (general class, not specific drugs) does BIS have a high correlation with? Low?
High = hypnotic drugs
Low = narcotics
Where would you find Alpha-1 receptors? Alpha-2?
1 = cerebral cortex, and thalamus
2 = Hippocampus and amygdala
How does valium compare to Ativan in behavior at the GABA site?
Valium dissociates faster from GABA, so it has a shorter duration of action and longer E 1/2 time
What is one huge advantage of valium?
Minimal effects on the cardiovascular system, even with induction doses (used to be used frequently in CV cases)
What classification of drug action do H1/H2 antagonists fall under?
Inverse agonists
What must you avoid with Droperidol?
CNS depressants: barbiturates, opioids, GA
What are the 4 major effects of scopolamine?
Sedation, Anti-sialagogue (dry mouth) Mydriasis cycloplegia (dilated pupils) and motion sickness prevention
Contraindications to a dopamine receptor blocker?
Pt’s with dopamine depletion, extrapyramidal reactions, orthostatic hypotension
