Keywords/TrueLearn Flashcards
Acute vs Chronic Phenytoin on NDMB
Acute: prolonged
Chronic: resistance and shortened duration
Gentamicin + NDMB (why)
Interacts w/ Ca -> Disrupts ACh vesicle release
Depresses receptor sensitivity to ACh
NSAIDs on RBF (why)
Decreased - inhibit afferent R.A. dilation by PGs
Acoustic impedence equation
Which variable is more important?
Point of ultrasound gel?
Impedence (Z) = (medium density) x (propagation speed of sound)
Density is more important (propagation speed is similar in all body mediums)
Gel = reduce DENSITY between probe and skin
Ketamine emergence delirium: tx?
Barbs, benzos, propofol
Systemic local absorption: locations from most to least (8)
Tracheal Intercostal Caudal Epidural Brachial Plexus Spinal Femoral/Sciatic SubQ
Leads for atrial dysrhythmias
Leads for myocardial ischemia
Atria: II > V1 (biggest P waves)
Ischemia: V5 alone (but II + V4 if can do 2 leads is best for both)
Bainbridge reflex
Atrial stretch -> inhibited vagus -> tachycardia
Hering-Breuer reflex
Lung stretch (PPV/CPAP) -> inhibited inspiration
4 causes of A-A instability
Downs
RA
Achondroplasia
Trauma
MC cause of mortality from blood transfusion
Pathophysiology?
TRALI (ALI w/in 6h of transfusion) - 5-10% mortality
Anti-leukocyte donor ABs attack pulm leukocytes
Does succ have increased aspiration risk? Why or why not?
NO - increased LES tone > increased intragastric tone
Spironolactone: electrolyte abnormalities?
Hyper-K, hypo-Na
Sensitivity and Specificity equations
Sensitivity = TP/TP+FN Specificity = TN/TN + FP
How to monitor lovenox effect via lab?
Factor Xa activity
Signs of propofol infusion syndrome
Lactic acidosis Cardiac failure Rhabdo Renal failure Hyperkalemia Hyper-TG Hepatomegaly Pancreatitis
Propofol + Lidocaine mixture –> ??
How to best avoid?
Small lipid droplets w/ possibility for embolic risk
20mg per 200mg propofol, and do it right before using
Chronic opioid use on endocrine?
- Decreased HPA axis (low cortisol) and HPG axis (low testosterone/estrogen)
Ester vs amide local anesthetics: metabolism location
Ester: plasma cholinesterase
Amide: liver
Variable bypass vs Desflurane vaporizers: use at high altitude
Variable bypass: mostly compensates for decreased Atm
Des: constant CONCENTRATION but no change in partial pressure, therefore must increase percentage according to how low the Atm is
Hypoparathyroidism tx
Vit D and Ca++ supplementation 1st
How do NSAIDs cause renal dysfunction
Impaired vasodilation of AFFerent arterioles -> decreased RBF
Glucose/insulin management peri-op (Glc goal, IV vs SQ insulin, etc)
IV Insulin (short-acting, titratable) in acute situation or sx Goal glc < 180 (stricter w/ CV or neuro sx) SQ: variable peripheral vasodilation in sx = no consistent uptake -- OK in normal pre-op or pacu patient
Electrolyte/channel flow in phase 0-4 of cardiac myocyte AP
0: V-gated Na+, K outflow decreases
1: Na close, K open (transient outward)
2: Slow L-type Ca channels vs slow delayed K channels
3: Ca close, rapid K rectifier channels open
4: Na/K ATPase pumps Na out and K in, K gradient balance causes resting potential
Side effects of closed circuit ventilation
- Increased PONV via re-breathing of acetone or CO
- Risk of hypoxia if enough O2 not supplied
- Effect of temperature on CBF
- Effect of pO2 on CBF
- Each 1 degree C drop in temp = 6% drop in CBF
- CBF maintained despite pO2 until <50, then CBF rises precipitously
Effect of myasthenia gravis on NDMBs and Succ
MG: sensitive to NDMBs, resistant to succ but not dangerous
Effect of prolonged NDMBs on Succ use
Prolonged NDMBs -> increased NAChRs -> Succ dangerous
Effect of pyridostigmine and chronic steroids on muscle relaxation
Both cause resistance, therefore must monitor twitches
Pyridostigmine –> more ACh around to combat the NDMB
Steroids –> remember that NDMBs are steroidal, so maybe some increased resistance to steroids over time if chronic
Lab abnormalities of excess mannitol (before diuresis)
- Hypervolemic dilutional hyponatremia
- Dilutional hypo-HCO3 = metabolic acidosis
- Hyperkalemia (via solvent drag and leak from increased intracellular K+ stores due to loss of H20)
Lab abnormalities of excess mannitol (after diuresis)
Hypovolemic hypernatremia, hypokalemia, alkalosis (loss of Na and hence K and H+ in the urine)
6 indications for FFP transfusion
- MTP dilutional coagulopathy
- Factor deficiency(s)
- AT3 deficiency
- TTP
- Hepatic insufficiency coagulopathy
- Warfarin reversal
Why is FFP frozen for storage?
Factors V and VIII will degrade above 4 degrees C
Meperidine in renal dysfunction
Normeperidine -> seizures
MAC aware and MAC-BAR levels
MAC aware = 0.3-0.5 MAC (loss of recall, voluntary reflexes)
MAC BAR = 1.7-2 MAC
Side effects of magnesium toxicity
- Weakness -> loss of DTRs -> flaccid paralysis and respiratory arrest (reduced acetylcholine/catecholamine release)
- EKG changes (long PR and QRS) -> nodal block -> cardiac arrest
- Sedation (loss of neurotransmitter release)
- Warm/flushed (hypotension, vasodilation)
- N/V (hypotension, etc)
Cause of magnesium side effects
Inhibition of Na/K - ATPase
- Loss of release of neurotransmitters -> weakness, hypotension, sedation
- Direct inhibition of vasoconstriction and vasoconstrictors
Effects of neuraxial on PFTs, cough, forced exhale, etc
- Greatly reduced cough and forced exhalation pressure due to abdominal muscle weakness
- Small reduction in VC and FEV1
Reason for dyspnea in neuraxial anesthesia (assuming no high spinal)
Loss of proprioception to chest wall and abdominal muscles, thus loss of feeling of breathing (psychiatric)
Reasons to avoid cephalosporins with prior penicillin reaction
- Penicillin reaction < 10 years ago AND/OR…
- IgE reaction (bronchospasm, angioedema, anaphylaxis)
- Severe non-IgE (SJS, TEN, organ failure/damage, DRESS)
Gas law that explains why high altitude results in under-dosing of volatile
Dalton’s law:
P(x) = [ P(b) - P(h2o) ] * F
Gas law that explains why hypercarbia results in hypoxia
Alveolar gas equation:
PaO2 = PIO2 - (PaCO2 / R) + correction factor
Gas law that explains why increasing the volume percentage of a volatile increases the speed of induction
Henry’s law:
C = P x solubility
Increased partial pressure (P) -> increased concentration in the blood (and hence the brain)
Gas law that explains why V1/T1 = V2/T2
Charles Law (King Charles is under constant PRESSURE)
Gas law that explains why P1V1 = P2V2
Boyles Law (Water boyles at constant TEMPERATURE)
Gas law that explains why P1/T1 = P2/T2
Gay-Lussac Law
Describe standard error of the mean
Equation?
With larger populations, different groups of samplings would have different means. SEM is the standard deviation of all those sample means over all possible samples drawn from that population
SEM = SD / square root of n
Example: n = 100, SD = 10 –> SEM = 10/10 = 1
Result of giving succ after neostigmine
Why?
Same as with pyridostigmine or edrophonium?
Prolonged phase 1 duration
Unsure exactly why, but possibly due to decreased plasma cholinesterase activity and/or direct interaction with succ
Not nearly as much, not sure why
Possible side effects of bicarb administration
- Conversion to CO2 -> worsened acidosis if not exhaled
- CO2 into brain -> cerebral vasodilation, increased ICP/CBF
- Binding of Ca –> transient hypocalcemia -> impaired CV function
- Alkalosis -> K driven intracellularly -> hypo-K
- Loss of acidosis -> loss of peripheral/pulmonary vasoconstriction -> hypotension
When should FFP not be used? (4)
- Vitamin K deficiency that can be corrected w/ vit K
- Primary volume expander
- To replace a factor if the specific recomb. factor is avail.
- INR < 1.8 w/o bleeding
Factors that increase closing capacity
ACLS-S
- Age
- COPD/Chronic bronchitis
- Left ventricular failure (increased pulm blood volume)
- Smoking
- Surgery
Factors that decrease FRC
PANGOS
- Pregnancy
- Ascites
- Neonate
- General anesthesia
- Obesity
- Supine
MetHb treatment
G6PD?
Methylene blue (Met = Met)
Ascorbic acid (met blue causes hemolysis)
COHb treatments
B12, sodium thiosulfate
Cause of bradycardia after succ
Activation of mAChR’s at SA node (more in kids b/c higher vagal tone)
When would you expect phase 2 block w/ succ
When would you NOT?
- Prolonged continuous administration
- Very large dose
- NOT: after 2 regular doses spread apart
How to adjust neo/glyco drugs in CRF?
No adjustment - drug excretions are prolonged but in equal doses there are no significant toxicities after 1 dose - maximal doses still apply as normal
Normal P50 of oxyHb
27
Effect of hypophosphatemia on SaO2
When is this likely to be seen
Decreased (low 2,3-DPG maybe?)
Critical care patients (maybe refeeding?)
Is doxorubicin toxicity limited to cardiotoxicity?
NO - affects just about every organ system and is cumulative
Effects of benzos and opioids on inhalational induction
Benzos - improved induction
Opioids - worsened induction (apnea risk)
Low dose vs high dose ketamine - receptor interaction
Low dose (<50 mg) - NMDA non-competitive inhibitor in midbrain High dose (1-2 mg/kg) - opioid receptors (can be altered by naloxone)
Explain alfentanil CSHT curve
- Long to start (<1-2 hours) b/c low plasma clearance
- Low plateau after 2 hours
Alfentanil metabolism
Patient-specific hepatic CYP clearance
Metabolism of different benzos (w/ significance)
Lorazepam, oxaz, temaz (LOT): glucuronidation (no active metabolites, less susceptible to CYP-altering agents)
Midaz, Diaz: oxidation -> active metabolites
Definitions of data types:
- Nominal
- Ordinal
- Interval
Test types for each
Nominal: distinct result categories
Ordinal: A range of data where difference between each is variable (pain score, mild/mod/sev, etc)
Interval: numerical structured range of data (1,2,3)
Nominal = chi-squared / McNemar / logistic regression Interval = t-test / ANOVA Ordinal = chi-squared / Wilcoxon-Mann-Whitney / Friedman / Kruskal-Wallis
Why does hypercalcemia cause polyuria?
Initial treatment?
1) calcium salts damage renal parenchyma
2) extra calcium inhibits ADH activity
Initial tx = SALINE INFUSION
Can opioids be used as the primary sedative/hypnotic for general anesthesia? Why or why not?
NO - ceiling effect of MAC, cannot reach 1 MAC and obviously have significant side effects at high doses
How does sepsis affect SvO2?
Sepsis can cause EITHER increased OR decreased SvO2
- Increased: high C.O., peripheral blood shunting
- Decreased: increased O2 consumption from sick tissue
Effect of C.O., cyanide, and MetHb on SvO2
INCREASED – decreased O2 utilization by tissues
Anterior vs Posterior ischemic optic neuropathy - MC cause
AION: cardiac sx
PION: spine sx (prone)
Airway closure vs emptying in lung locations during forced exhalation
Closure: base (thus can’t empty)
Emptying: apex (b/c airways still open)
Esophageal detector device: ETT placement confirmation in code (no perfusion) state
Squeeze bulb, will not get air return if in esophagus b/c walls will collapse
Ideal wait time after DES
When can 180 days after DES be ignored?
365 days
Emergency surgery (risk of no sx > risk of thrombosis)
See varying side effects of barbiturates
Flagged in TL (test 21)
Highest to lowest LA absorption by block
ICEBaLLSS Intercostal Caudal Epidural Brachial plexus Lower limb SubQ
Type 2 DM:
- Insulin resistance vs deficiency
- Is insulin deficiency reversible?
- Degree of hyper-glc vs degree of deficiency
- Resistant –> loss of beta cell mass (deficient)(burnout)
- Reversible PARTIALLY w/ improved glc
- More severe high-glc -> more severe deficiency
Vasopressin levels in septic shock
After surgery, how long to vasopressin levels stay elevated for?
Initial burst –> depletion
A few days
Bezold-Jarisch reflex
What else might you see in this situation?
Depleted preload in ventricle –> reflexive bradycardia and decreased inotropy –> hypotension
Carotid baroreceptor -> tachycardia and increased inotropy (is generally slower to kick in when drop in preload is very quick)
How do PPIs and H2 blockers decrease gastric volume AND increase gastric pH?
Decrease SECRETION of acid, thus stomach empties over time and becomes more alkalotic
Does not directly stimulate gastric emptying
Garlic as supplement: use?
Concern?
Prevent atherosclerosis (lower BP/TGs/thrombus/plt agg)
Irreversible platelet inhibition (d/c 7d b4 surgery)
Ginkgo as supplement: uses?
Concern?
Several (vasoregulation, antioxidant, modulate neurotransmitters, alter PAF)
Inhibit platelet activating factor (d/c 36h b4 surgery)
Ginsing as supplement: uses?
Concerns?
Several
- Inhibit platelet aggregation and prolong PT/PTT in vitro
- Hypoglycemia (lower post-prandial blood glucose)
- D/c at least 1d (prefer 7d for platelet inhibition)
Saw palmetto: use?
Concern?
BPH
Excessive bleeding (unknown cause, no rec’s)
Learn about digoxin interactions
Flagged test 21
QT interval in hypo vs hypercalcemia?
Hypo: prolonged QT
- Less Ca-mediated K-channel opening causes
prolonged repolarization
Hyper: shortened QT
Learn all the EKG changes w/ electolyte anomalies
…
Recommended IO locations
- Proximal humerus (3rd best)
- Proximal (best) and distal (2nd best) (not mid - variable bone thickness) tibia
- Manubrium (uncommon now)
Why is IO better than central line in emergency? (4)
- Higher 1st success rate
- Lower infection rate
- Faster than central line placement
- Equivalent for fluid administration
Is fat/marrow embolism common in IO placement?
Yes (40-90%) - but no evidence of PaO2 changes or morbidity
Look up Bayes theorum
…
What is in cryo?
- VIII:C
- VIII:vWF
- Fibrinogen
- XIII
- Fibronectin
MetHb -> change in SvO2?
Decreased: changed Hb Fe causes impaired O2 binding –> functional anemia and decreased SaO2 –> decreased SvO2
Sepsis -> change in SvO2?
Increased: microvascular shunting in acidotic tissue leads to decreased O2 utilization + increased cardiac output from decreased SVR, etc
CO poisoning -> change in SvO2?
Increased: decreased O2 utilization
Asthma + nasal polyps…think what?
ASA/NSAID-induced asthma
Succ in asthma?
Succ IS associated w/ histamine release BUT has not been shown to cause bronchoconstriction
Beta-1 selective beta blockers
BEAM
- Bisoprolol
- Esmolol
- Atenolol
- Metoprolol
How to calculate total AMOUNT of dissolved O2…
How to calculate total PERCENTAGE of O2 that is dissolved…
Amount = 0.003 * PaO2
% = Amount / CaO2 CaO2 = (Hb * 1.36 * SaO2) + (0.003 * PaO2)
Cyanide poisoning -> change in O2 delivery?
Dilutional anemia -> change in O2 delivery?
Increased delivery to compensate for decreased usage ability
Decreased delivery due to decreased Hb molecules per second (body compensates by increasing C.O.)
TEG values/meanings…
- R
- K
- Alpha angle
- Max amplitude (MA)
- Teardrop shape of curve?
R = time to start clotting (nml 5-10 min) = coag factors or heparin admin (tx = FFP)
K = time from initial clot formation to 20mm amplitude of curve (1-3 min) = fibrinogen (tx = cryo)
Alpha angle = slope/speed of clot formation (nml = 50-70 degrees) = fibrinogen (tx = cryo)
MA = maximal width of clot strength (nml = 50-70 nm) = platelets
Teardrop shape = too fast fibrinolysis = anti-fibrinolytics (TXA, etc)
- Normal fibrinolysis by 30 min = 0-8%
Morphine epidural vs addition of clonidine
- Length
- Strength
- Side effects
What about adding it to fentanyl?
Longer, stronger (clonidine longer than morphine) Less PONV (less morphine needed, less catecholamine release) Less morphine-related pruritis, etc 2/2 less needed More hypotension (resolved w/ fluid)
NOT added benefit w/ fentanyl
Why is alfentanil so short-onset?
Lowest pKa (6.5) = very high non-ionized fraction at physiologic pH (89%) – so very fast onset despite only moderate lipid solubility (sufenta > fent > alfent > morphine)
Ankylosing spondylitis…mask, intubation, neuraxial
Difficult mask (TMJ) Difficult intub (c-spine) Difficult neuraxial + increased hematoma risk from multiple attempts
Neuraxial and Lovenox rules:
- How long after last dose
- How long to restart after doing
- How to restart while catheter is in
- How long to restart after catheter removal
Therapeutic - 24h (before doing AND to restart)
Prophylactic - 12h (before doing AND to restart)
While catheter is in - 1x/day prophylactic 12h later
4h to restart after removal of catheter
Blood transfusion + abdominal/chest/flank/back pain, hypotension, bronchospasm, hematuria, shock, pulmonary edema, renal failure, shock
Tx?
Acute hemolytic transfusion reaction (ABO)
- Stop transfusion
- Maintain UOP (fluids, diuretics) w/ possible alkalinization to prevent hemoglobin deposits
- Support BP
- Bronchodilators as needed
- Check for hematuria
Blood transfusion 24h ago –> fever, hemolytic anemia, jaundice
Cause?
Tx?
Delayed (2nd exposure) hemolytic transfusion reaction
Non-major RBC antigens (Kell, Kidd, Duffy, etc)
Usually nothing, may need some support if very anemic or renal failure
2 causes of febrile non-hemolytic transfusion reactions
Tx?
Prevention?
- Cytokines from WBCs
- Recipient antibodies against donor WBCs or platelets
Tx = tylenol/benadryl
Prevention = leukoreduction
GVHD - cause
Donor WBCs against immunocompromised host who cannot fight back
