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)