1. Ventricular perfusion 
-L ventricle is perfused only in diastole, because the pressures generated with L ventricle contraction prevent anterograde flow through the coronary arteries in the L myocardium
-R ventricle, however, is perfused during systole and diastole and in fact more so in systole, because the pressures generated on the R side are not high enough to prevent flow through coronaries while systolic BP is higher than diastolic BP. The R heart is very sensitive to loss of perfusion-- so in someone with acute-onset pulmonary HTN, hypotension develops because of decreased CO (decreased LV preload), and CVP increases due to back-pressure of blood. Both of these things decrease RV perfusion, lead to  ischemia, and sometimes will decompensate into precipitous R heart (and thus L heart) failure. People who die from acute pHTN often will have microinfarcts of RV. (link: coronary blood flow) {paper in Circulation on right ventricular function and failure}
2. Acute PE
-In acute PE, the mechanism of hypoxia is counterintuitive. A clot that obstructs flow to one part of the lung will shift blood to remaining tissues, however if you think about it, 100% of the blood will still be oxygenated. CO2 and O2 (except in extreme cases) are perfusion-limited, not diffusion limited. So by these measures, there should be no hypoxemia in PE. What actually happens is that the embolus releases inflammatory factors that result in alveolar dysfunction and atelectasis, leading to decreased ventilation in the remaining segments of perfused lung (decreased V/Q ratio). {Am J Resp Crit Care Med paper on BALs done in patients with PEs} Additionally, if you clot off one part of the lung, you will increase perfusion to the rest of the lungs (i.e. if you clot off one lung, you double perfusion of the other lung). This will cause increased blood flow to all parts of the lung, including areas that are naturally less-ventilated (bases, lung that already was atelectic because your patient has been immobilized in bed for a month in the ICU, etc), and also cause decreased ventilation.
3. PE & hypotension: 
-increased pulmonary resistance => decreased ventricular pre-load => decreased hypotension
-When pulmonary vascular occlusion > 75%, its estimated that the R ventricle must generate systolic pressures > 50mmHg and pulmonary artery pressures > 40mmHg to maintain pulmonary perfusion.
4. Lab findings in acute PE
-Decreased pO2 from above explanation
-Decreased pCO2-- tachypnea triggered by hypoxia will lead to the patient blowing off pCO2
-Metabolic alkalosis 2/2 tachypnea
-Elevated troponins from R heart failure
-D-dimer: 80-95% sensitivity depending on the type of test, 40-60% specificity. Most useful in patients who are of moderate risk; people who are high-risk based on history and exam should go straight to CT-PE, while those who are low risk will remain low-risk even after a positive d-dimer.
5. Vein of Labbe drains posterior temporal lobe into transverse sinus. If you cut it during surgery, you will cause temporal lobe ischemia. If there is a sinus thrombus in the sigmoid or transverse sinus, it can cause backup of blood through the vein of labbe and cause swelling and ischemia of the temporal lobe.
6. According to the cardiac literature, if you transfuse platelets in someone with a new stent, their chance of clotting off that stent is 10-15%. So in someone with PVD and cerebral VD who comes in anticoagulated on aspirin and plavix, thrombocytopenic, who gets a new stent put in their cerebral vasculature (i.e. aneurysm), who then develops a brain bleed, is a very difficult person to manage. If you stop their anticoagulation or transfuse platelets, they may stroke out or have an MI and/or clot off their fresh stent. However, if you try to operate on them while they are on aspirin and plavix and thrombocytopenic (even small craniotomy, burr hole, drain), you could cause even more bleeding than what they originally had. Plavix is very unforgiving for neurosurgery. Whether it is better to stop the anticoagulation or keep the anticoagulation and transfuse platelets is controversial.
7. Someone who gets a bare-metal stent has to be anticoagulated for 30 days, and someone who gets a drug-eluting stent has to to be a/c for 12 months: elective surgery is contraindicated during this time. The drugs are tacrolimus and rapamycin and other drugs which inhibit the process of re-epithelialization; once a stent is epithelialized, it is much less thrombogenic.
8. Hepatic failure causes the buildup of agents that cause generalized vasodilation (i.e. of the splanchnic arteries) which can lead to increased CO and eventually, to high-output cardiac failure. Because of this vasodilation, you can have patients who have significantly increased intravascular volume and still be exhibiting signs of decreased end-organ perfusion (i.e. decreased FeNa in the urine, pre-renal labs). So, if you have an ICU patient in end-stage liver disease who has massive pulmonary effusions that are leading to bad hypoxemia, and you see that he is up 3L and his labs show a pre-renal picture (decreased FeNa, increased BUN/Cr ratio, hyperosmotic urine, signs of AKI) you can't necessarily assume that the volume is all extravascular/interstitial, and that his intravascular volume is low, and that aggressive diuresis will not affect his pulmonary function. If his increased volume is intravascular, aggressive diuresis will certainly lead to worsening of end-organ perfusion, but it will also likely ameliorate the pulmonary effusions-- and ultimately, the latter is more important as organ perfusion is moot if you can't oxygenate someone's blood. Of course the balance between the two must be weighted-- how bad are the effusions vs end organ dysfunction? If someone has a pH of 7.1 and a pO2<30 on max ventilator settings (incl 100% FiO2), nitrous, and 3 pressors, it's worth sacrificing the kidneys to save the lungs; you can fix ESRD, you can't fix dead.
8. Layers of scalp: SCALP mnemonic. Skin, cutaneous fat/vessels, aponeurosis (galea), loose connective tissue (contains nerves of scalp and blood vessels), periosteum. If you do a craniotomy you have to close the galea really well, especially if their dura/skull is compromised, as it will prevent CSF leak. When doing a craniotomy, you also want to remove the entire scalp including the periosteum, you don't want to separate it in the loose connective tissue layer as you risk damaging nerves and vessels therin. The only circumstance in where you would want to remove it is if you want to use the periosteum to regenerate dura. It is better than duraguard and other synthetic dural replacements.
9. For an average healthy patient, MAP < 60 = hypotension. 
10. Hemodynamic resuscitation: rhythm/rate, preload, contractility, afterload. In that order. If you don't have a perfusion rhythm, none of the others matter; if you're volume depleted, increasing contractility will not help much.

1. Shortcut neuro exam for a patient with a LEFT frontal lobe lesion that you're worried about getting larger: key to understanding is that this area is important for language (close to Broca's). So test language production by talking to them, asking them to ID objects (hold up a pen, ask if they can name what it is and what it does), ask them to repeat a phrase.
2. Shortcut neuro exam for RIGHT frontal lobe lesion: there isn't one. Generally, R frontal lesions will not produce symptoms unless they are large enough to create mass-effect problems (i.e. L sided weakness from compression of M1 on the R side), i.e. extremely large. Smaller frontal lesions can produce seizures, but this is not specific to R frontal.
3. During brain surgery where you're utilizing somatosensory evoked potentials, (e.g.  if you're operating on the spinal cord you want to check peripheral innervation, near the brainstem you want to check cranial nerves) do not use potent inhaled gases because they dampen the potentials. Use propofol and fentanyl.
4. Pulmonary AVMs can allow the passage of clots (+/- infected) through the lungs into the systemic circulation, esp brain. They are associated with significant (>10%) rates of stroke, TIA, and brain abscess. One way to diagnose them is to see late-onset of bubbles in echo.
5. Elevated CK/rhabdo: Hydrate aggressively & alkalinize the urine by adding bicarb to the IV fluids. Theoretically, alkalinization prevents the breakdown of myoglobin into nephrotoxic metabolites, and also to reduce crystallization of uric acid in the tubules.
6. DDx for pulsatile tinnitus:
-Vascular malformation in the ear: AVM, aberrant vessel
-Increased flow through ear: anemia, hyperthyroid
-Increased pressure transduction into the middle ear: superior canal dehiscence
7. Mass that has low signal (i.e. darker than CSF, which is bright white) on T2- meningioma or lymphoma.
8. Three categories of otitis media;
-Acute otitis media: can be recurrent or persistent
-Otitis media with effusion
-Chronic otitis media: implies tympanic perforation with chronic drainage
9. Indications for ear tubes:
-Recurrent otitis media, defined strictly as 6+ episodes of AOM in one year, 4+ episodes of AOM for two years, 3+ episodes of AOM for 3 years
-Complicated AOM (i.e. mastoiditis)
-AOM refractory to antibiotic treatment
10. Ear tubes 
-May or may not reduce the incidence of AOM, but AOM with ear tubes is much less painful than AOM without ear tubes
-If you have tubes, you get ear-drop administered antibiotics which can result in MICs in the 1000s, very effective treatment.

1. Trauma IV resuscitation:
-Need at least 16-18 gauge IV, order of preference for IV access sites: Large bore antecubital/peripheral > subclavian/fem/IJ > IO > venous cut down
-Fluids: if need to replenish <30% of total body water resuscitation use crystalloid, 30-40% add colloid to crystalloid to prevent fluid overloading, >40% add blood to prevent diluting out RBCs, platelets, coags
-Goals: SBP>80-100, hct 25-30
2. Trauma surgery anesthesia:
-Use general with ET tube because it's fast on, can be held for as long as necessary, and you can ventilate them; disadvantages are that it can worsen hypovolemia by decreasing vascular tone, you need to be able to get a tube in, and you can't do a neuro exam.
3. TBI: 
-GCS <8, severe TBI, 33-55% mortality
-GCS 9-12 moderate TBI, GCS 13-15 mild TBI, 2-3% mortality
-LOC is the hallmark of TBI
-Get to CT ASAP to r/o bleed.
4. ICP management, general principles: 
-Avoid hypoxemia, since that will lead to cerebral vessel dilation and worsening of ICP. Intubate early, use PEEP early.
-Keep the head elevated relative to body
-Control pain, even in obtunded patients; the ICP will rise to pain even in these people.
-Control temperature, as hyperthermia will increase CMRO2
5. Hyperventilation will reduce ICP and brain edema by leading to cerebral vasoconstriction. However, over time this will lead to ischemia, with elevating lactate and glutamate levels. So do this, but only for short periods of time, and only if you think there is a risk of herniation. Goal is pCO2 of 25-30
6. Osmotic diuretics like mannitol and hypertonic saline (3%) will decrease ICP from diuresis. Do not use glucose as your osmotic agent, as it readily crosses BBB. Know that the brain will eventually adjust to these osmotic diuretics, and they will become less effective over time. Also, osmotic diuretics are only effective if the BBB is intact, otherwise they will just cross over and possibly cause worse complications.
7. Steroids have not been shown to reduce mortality in patients with ICP. 
8. Barbituates like hyperventilation will reduce cerebral perfusion and reduce ICP, however they will also cause systemic hypotension that require pressors, which then will negate the ICP-reduction effect of the barbituates.
9. For chest trauma, rule out pneumothorax before you initiate positive pressure ventilation lest you cause a pneumothorax. Ventilate with low tidal volumes (<6ml/kg ideal body weight) and low PEEP. Ues double lumen ET tube for lung resections.
10. For chest trauma, get in A-lines, central lines and large bore IVs above the diaphragm-- if there is trauma to the great vessels in the chest, femoral or lower extremity lines will do you no good.

1. Malignant Hyperthermia:
-50% AD inherited mutations in ryanodine/dihydropurine, 50% spontaneous
-Risk factors: myopathies, muscular dystrophies, people susceptible to rhabdo.
-Early Clinical signs: muscle (esp masseter) contraction, hypercarbia (ET CO2>60), respiratory acidosis (aerobic metabolism) and metabolic acidosis (anaerobic metabolism)
-Late clinical signs: hyperthermia (up to 45 deg C, can increase at 1 degree every 5 mins), hyperkalemia leading to v-tac, v-fib, bigeminy, myoglobinuria
-Can happen anytime intra or postop
2. Treatment/Prevention of MH:
-Prevention: Avoid succinylcholine, all potent inhaled agents esp halothane. Use propofol, alone or with NO.
-Treatment: Turn off agent, run 100% O2 at max settings to flush out inhaled agent, give dantrolene (can give multiple times if it doesn't work), run fast VBG to detect hyperkalemia, treat if its present, watch CK/myoglobin levels.
3. Treatment of hyperthyroid
-Propanolol decreases symptoms and prevents peripheral T4 to T3 conversion
-PTU is faster-onset than methimazole, but more toxic (hepatitis, vasculitis, agranulocytosis)
-Methimazole is slower onset an relatively safer, although can also cause agranulocytosis
-Wolff-chaikoff effect: large doses of iodine prevents release/synthesis/organificaiton of thyroid hormone. Lasts around 10 days, after which there is an escape phenomenon (downreg of Na-I symporters, decreasing internal iodine concentration). Thought to be mechanism of hypothyroidism caused by iodine containing drugs (amiodarone).
4. Hyperthyoid & anesthesia 
-Don't use anticholinergics, as they may contribute to increased HR
-Paralytics OK
-Don't use aspirin, as it prevents thyroid hormone from binding to thyroglobulin and can increase free concentrations of thyroid hormone.
-Don't use desflurane, as if you infuse a lot of it fast it can stimulate the symp nervous system.
-Regional anesthesia may be preferable, as it causes sympathetcomy. Don't use epinephrine in your lidocaine... obviously.
-Epidural > spinal as it is slower onset, less acute perturbations of vital signs
5. Intraop Hyperthyroid 
-Operate on someone only if it is emergent, delay all other surgery until euthyroid
-IV esomolol during surgery-- short acting, fast off, B1 selective. Goal HR <85
-If you need phenylephrine, use less because there is increased sensitivity
-Thryoid storm usually happens 6-18 hours postop, rather than intraop. Treat with chilled fluids, esmolol drip.
6. GERD can present a lot like an MI: both can cause severe midsternal squeezing chest pain, both can be relieved by nitroglycerin (can relieve esophageal spasm)
7. Open cholecystectomies require subcostal incisions that hurt, and as a result people don't breathe well afterwards and frequently end up with pneumonia or atelectasis and prolonged, complicated hospital stays. Lap choles are safer, even in obese patients with restrictive lung disease where you're worried about being able to ventilate them.
8. Open prostatectomies can be complex too as they can be associated with a lot of bleeding. In lap/robotic prostatectomies, it's really tough to ventilate because people need to be in very steep trendelenburg, and all of their abdominal contents press hard on their lungs; their ET CO2 may go up to 60s. You also have to be careful of fluids because they can get head edema pretty quickly-- run these cases pretty dry.
9. Hyperglycemia is much better in surgery than hypoglycemia; its ok to be high 100s, 200s. If someone is a touch low, run them on D5 or D10 drip; if they're really low (like 40s) then give them half an amp of D50 bolus.
10. If you need to run a lot of fluids (i.e. trauma, hemorrhage), you want at least a 16 gauge IV, with the following locations in descending order of preference: antecubital/peripheral > subclavian/IJ/femoral >> IO line >>> venous cut-down.

1. Tranexamic acid (lysine derivative, binds plasminogen and prevents conversion to plasmin and activation of fibrinolysis) reduces all-cause mortality in bleeding trauma patients, with no increase in incidence of DVT/PE/stroke. {Lancet, CRASH-2 trial: international multicenter randomized placebo-controlled trial, total N>20,000}. The most amazing part of this is that they managed to get an N of 20,000 in a placebo controlled RCT. Additional analysis shows that transexamic acid should be given as soon as possible after trauma; it decreases mortality when given within 3 hours, but actually slightly increases it when given after 3 hours. In total knee replacement surgery, it decreases bleeding, transfusion need, and does not increase risk of DVT; benefit is increased when it is given early-on in surgery.
2. Oral airways: correct length is corner of mouth to angle of mandible. Any shorter, and it'll be pushing against the tongue and actually can cause irritation that worsens airway collapse.
3. FiO2 achievable with NC, around 30-40%; with non-rebreather mask (valves to prevent breathing in room air or exhaled air), closer to 70-80%.
4. Systolic BP at which you lose ability to palpate pulses: radial around 80, femoral around 60, and carotid around 40.
5. Mask induction vs IV induction: IV induction is faster (you blaze through stage 2), you have more control, and you already have an IV through which you can push drugs if something goes wrong. Mask induction is slower, especially in adults; in kids its pretty fast because they're smaller and the gas distributes faster. Benefits of mask induction is you don't have to stick an awake person, which is especially helpful in peds. Sevo is the gas of choice for mask induction, as it is the least irritating-- des and iso are pretty unpleasant to breathe in. If you have a particularly squirmy, uncooperative kid, the best thing to do is hold him down, mask him with 8% sevo and hope he goes under before he breaks loose.
6. If you overdose phenylephrine, if someone is young and healthy with good organs and they can take the hypertension/bradycardia, you can just wait it out. If someone is old and you're worried about cerebral hemorrhage or acute decompensated heart failure, then reverse with a short-acting vasodilator like nitroglycerin. Nitroprusside is more powerful, and must be dosed more carefully. You can also use a-antagonists like phenoxybenzamine and phentolamine.
7. When you would reach for albumin over crystalloids when volume resuscitating: 
-Hypoalbuminemic patients: End stage liver failure, burns
-People who can't tolerate large volumes: CHF, renal failure
8. Induction agents: 
-Fentanyl/Midazolam: old school. You need massive doses of these two to induce general anesthesia, and because of that (and their relatively longer-acting nature), the patients will be out for a long time and will likely take a long time to be extubated. Benefits are that this combo is extremely cardioprotective (more so than etomidate). It does not cause cardiac depression or hypotension. In big cardiac surgery cases with patients with bad hearts, you want to use these.
-Propofol: 1-2mg/kg for adults, 3-4 mg/kg kids since kids redistribute and metabolize so much faster and more efficiently. Pros: On fast (30 seconds) off fast (end of effect is redistribution, not metabolism/excretion; redistribution half life is 2-4 mins), abolishes pharyngeal reflexes so good to use to put in ET/LMA. Associated with less post op n/v. Cons: Causes most hypotension and apnea, burns going in to the IV (give lidocaine first), higher risk of infection given weird suspension of drug in oils.
-Etomidate: Pros: less myocardial depression than propofol, and doesn't cause tachycardia like ketamine: good for old people with subpar hearts but not undergoing major cardiac surgery. Cons: burns even worse than propofol, possible adrenal insuffieincy.
9. Transfusions:
-As aforementioned, @ 7 for most people, @10 for people with serious cardiorespiratory illness. Never transfuse past 12-- you get no more O2 carrying benefit and you do start to get sludging. This is extremely relevant post microsurgery (i.e. flaps), where sludging in small vessels can cause serious damage.
-FFP is roughly equivalent to pRBC for volume; cryo is a smaller volume so good for people you don't want to volume overload.
-Exchange transfusions take time to set up
-Irradiated blood kills off the white cells; this is important for people that are immunosuppressed (post chemo, transplant) and those with immune deficiency
10. Demerol 12.5 mg stops postoperative shivering very effectively.

1. More facts about coagulation: 
-Factor XIII important for polymerizing fibrinogen and solidifying clots.
-Hemophilia A is much more common than B (85%/15%)
-Bleeding into the joints/muscles should be treated after 3-5 hours, bleeding into head and neck, GI, or brain should be treated within 30 min-1 hour.
-Cryo has F VIII but not F IX.
-Contraindications for FFP: immunodeficiency, availability of a specific factor treatment.
-Desmopressin will increase F VIII levels in someone with <1% activity of F VIII by 2-4%; in someone with much higher levels of activity, it may increase up to 8%.
2. Arterial lines measure BP more accurately and in real-time (vs intermittently) compared to an external blood pressure cuff. They are also good for frequent blood sampling for ABG. They are useful in surgeries where you expect significant changes in blood pressure or blood volume (large fluid shifts/blood loss). They are also useful in surgeries where it is important to track the ABG closely (i.e. intracranial surgery where blood [CO2] affects cerebral perfusion, or lung resection where you're worried about ventilation or oxygenation)
3. Central lines have 2 primary functions: 
-Central access to give drugs that would be unsafe to give in peripheral lines: i.e. pressors, where you may cause ischemia of distal organs, or CaCl, which can cause wicked burns.
-Monitoring: particularly CVP, which assuming no lung pathology, is a proxy for ventricular end-diastolic pressure i.e. preload. This way, if the person becomes hypotensive, you can determine if it is cardiogenic, vasogenic, or hypovolemic.
4. Inhaled anesthesia effects: 
-decreases the amplitude of evoked potentials-- relevant for neuro/spine surgery.
-increases RR, decreases TV
-causes peripheral vasodilation; this redistributive volume alone can cause a 1.5 degree C drop in core body temperature. When patients are hypothermic, coagulation factors and platelets worsen, bleeding risk increases.
-bronchodilation: can be used to treat status asthmaticus.
5. LMA: less invasive, less risk of dental injury, less spasm of bronchi or larynx (esp in asthmatics), however its placement is less secure esp the smaller LMAs in kids and it does not protect against aspiration. It is only able to be used in patients who are spontaneously breathing (no paralytics), where the risk of aspiration is low and the surgery is <2-3 hours (because any more than that and you will start accumulating gastric juices that can then be aspirated.
6. ET: more invasive, more complications; more secure, protects against aspiration. Use in patients at increased risk of aspiration (bad GERD, DM gastroparesis, emergency surgery where the pt has not had time to be NPO for long enough, surgery >2-3 hours), laproscopic surgery-- because the air in the belly increases intraabdominal pressure, means higher vent pressures are required for adequate ventilation, and >20 cmH20 pressure ventilating via LMA will lead to filing stomach with air, making the surgeon's job harder.
7. Dealing with bronchospasm while intubated: albuterol into endotracheal tube (much of the drug will get stuck to the walls of the tube, so give 10-20 puffs and chase with air), or can increase dose of inhaled anesthetics, i.e. "go deeper", since they cause bronchodilation.
8. Adult airways are cylindrical, kids are conical with the smallest diameter at the cricoid cartilage (only tracheal cartilage that is a complete ring). When intubating adults, a cuff is needed to obstruct a portion of the trachea to deliver effective positive pressure beyond it; but if the right diameter tube is chosen, a cuff is theoretically not necessary in children since the cricoid cartilage should act as a seal against air regurgitation. However IRL, estimating the correct size may be difficult, requiring several attempts and the associated mucosal trauma that always accompanies multiple attempts of any sort of invasive procedure. The problem with a cuff is that it reduces the diameter of the tube that you can use-- this is mostly relevant in neonates/NICU babies where the tubes are already so small that even a small reductions will significantly reduce airflow.
9. Pressure of the ET tube or its cuff on the walls of the tracheal mucosa can cause ischemia or even future stenosis; in order to minimize this risk, fill the cuff/fit the tube to leak at a pressure of 20cmH20: less than that and you won't be able to ventilate adequately, tighter than that and you'll cause unnecessary damage.
10. EKG in surgery for non-cardiac patients: 
-5 leads in most adults (can see arrhythmia, some ischemia changes although no precordial leads)
-3 kids in most kids: rhythm only, cannot see ischemia, since you're rarely worried about ischemia in kids.

1. Ventilators:
-Pressure support: machine gives pre-set pressure either in CPAP (only inspiratory pressure) or BiPAP (inspiratory pressure and expiratory pressure aka PEEP) and records the volume. Normal setting 10/5. Before extubation, will try 5/0 (i.e. no PEEP). You still need the 5 inspiratory pressure because it compensates for the incresaed difficulty breathing in through the tube (more resistance to airflow). Patients control their own tidal volume, breathe on their own.
-Volume support: machine gives pre-set amount of volume, records the pressures needed to achieve that volume. You want low pressures, as they indicate good lung compliance; increased pressures may be seen in laproscopic surgery (blowing up the belly with air), obese patients, and those in trendelenburg for the same reason-- increased pressure against the abdominal surface of the diaphragm, makes it harder to fill the lungs. Patients are not breathing on their own.
-In surgery with general anaesthesia, wean from volume support to pressure support to spontaneous breathing. When weaning from volume to pressure, make sure they can breathe on their own-- have them take 2 deep breaths; check end-tidal CO2 to make sure they're breathing on their own.
2. Explanation for decreased O2 sats after intubation:
-Mainstem intubation
-Atelectasis
-FiO2 is too low.
3. ARDS: decreased surfactant, decreased lung compliance, require increased filling pressures to open alveoli and maintain oxygenation. Patients take shallower, more frequent breaths (vs opiates: they take fewer, deeper breaths). Protip: If your CO2 is rising, you are not ventilating enough, and increasing FiO2 (oxygenation) will not necessarily help.
4. In people with any disease which may lead to thrombocytopenia, avoid spinal or epidural anesthesia as you may cause an epidural hematoma. Think both acquired (ITP, sequestration, leukemia, drug-induced: ie heparin/thymoglobulin, chemotherapy, antibiotics, peroxidase inhibitors) and inherited causes of marrow failure (i.e. Fanconi's anemia)
5. Feeding tubes:
-Dobhoff feedings are associated with less issues of bloating/gastroparesis compared to NG feedings
-NG tubes can stay in longer, are more comfortable to wear
-OG tubes are less traumatic to insert (nasal mucosa is very vascular)
-In kids who are g-tube dependent, a nissen fundoplication will decrease risk of reflux and aspiration.
6. Respiratory depression:
-Opiates: fewer, deeper breaths
-Inhaled anesthetics: more frequent, shallower breaths.
7. Etomidate can be associated with adrenal suppression that occurs days later; treat the hypotension with stress-dose steroids (100mg). However, it causes less cardiac depression than propofol.
8. Preoperative assessment key questions:
-Reason for surgery
-History of problems with anesthesia (n/v, awareness), or in kids who have never had surgery-- family hx of problems with anesthesia
-Time of last consumption of water and food.
-PMHx (particularly organ dysfunction, airway issues)
9. Preoperative assessment relevant ROS:
-Neuro: seizures, TIA
-Cards: Exercise tolerance!! HTN, MI/CAD, CHF, valvular dx, arrhythmia.
-Pulm: COPD (bronch/emphysema), asthma, smoking status, OSA, recent URI (increases risk of bronchospasm)
-GI: GERD,
-Renal/Liver: any dysfunction
-Endo: thyroid, DM, adrenals
-Heme: anemia, bleeding dx
-MSK: arthritis (for positioning), neuromuscular dx
10. Preoperative assessment: exam 
-Airway: Mallampati, thyromental distance, neck flexion/extension, jaw thrust
-Other: lungs CTAB, heart RRR, disconjugate gaze

1. No statistically significant association between cranberry juice consumption and UTI prevention {Cochrane review, 2013, total N>4,473.} From the abstract: "Data included in the meta-analyses showed that, compared with placebo, water or not treatment, cranberry products did not significantly reduce the occurrence of symptomatic UTI overall (RR 0.86, 95% CI 0.71 to 1.04) or for any the subgroups: women with recurrent UTIs (RR 0.74, 95% CI 0.42 to 1.31); older people (RR 0.75, 95% CI 0.39 to 1.44); pregnant women (RR 1.04, 95% CI 0.97 to 1.17); children with recurrentUTI (RR 0.48, 95% CI 0.19 to 1.22); cancer patients (RR 1.15 95% CI 0.75 to 1.77); or people with neuropathic bladder or spinal injury (RR 0.95, 95% CI: 0.75 to 1.20). Overall heterogeneity was moderate (I² = 55%). The effectiveness of cranberry was not significantly different to antibiotics for women (RR 1.31, 95% CI 0.85, 2.02) and children (RR 0.69 95% CI 0.32 to 1.51). There was no significant difference between gastrointestinal adverse effects from cranberry product compared to those of placebo/no treatment (RR 0.83, 95% CI 0.31 to 2.27). Many studies reported low compliance and high withdrawal/dropout problems which they attributed to palatability/acceptability of the products, primarily the cranberry juice." (c/o Hopkins PodMed podcast)
2. Hemodialysis vs peritoneal dialysis (quality of life considerations): hemodialysis requires vascular access in the form of a graft or shunt, which has to be put in surgically, and it requires needlesticks multiple times a week. It requires regular trips to a dialysis center for hours at a time (unless you have home hemodialysis units), it makes you feel tired, and it has risks of infection/clots. Peritoneal dialysis requires the placement of a PD catheter (surgical) and risks peritonitis. However it can be done at home, by the user, even while sleeping. It requires good patient compliance/upkeep and a certain amount of patient responsibility
3. Hemodialysis vs peritoneal dialysis (outcomes):
-From uptodate:
"In a study of 27,015 patients from Australia and New Zealand, compared with hemodialysis, peritoneal dialysis was associated with a higher survival from day 90 to day 365 (HR 0.89, 95% CI 0.81-0.99) [40]. These benefits were most significant among younger patients without comorbid conditions. After one year, however, peritoneal dialysis was associated with markedly higher mortality (HR 1.33, 95% CI 1.24-1.42).

 However, a propensity-score analysis, (in which peritoneal dialysis patients were matched with hemodialysis patients with known covariates) showed no difference in mortality between groups prior to one year (HR 0.99, 95% CI 0.89-1.10) and an increase in mortality associated with peritoneal dialysis after one year (HR 1.35, 95% CI 1.27-1.42)."
4. Bile leak is a complication after liver resection: with an incidence of up to 5-10% by some estimates. Opiate-induced sphincter of oddi spasm leads to backing up of bile into the liver, which causes leakage/oozing of bile out of the cut surface of liver. Diagnose by running T-bili on the drain output. Bile is irritating to the peritoneal cavity, and can cause nausea and ileus. Treat with ERCP and stenting of the bile duct.
5. If a patient's hemoglobin is falling after major abdominal surgery, think dilutional vs occult bleed. Dilutional bleeding will be signaled by proportional decreases in all cell counts, will be associated with net positive fluids, and will be limited in scope. If your hemoglobin is dropping quickly and significantly, think occult bleeding. Look at the drain outputs (if they are not increasing, think hematoma vs poorly positioned drains), consider u/s or CT scan to look for the source of bleeding. Other less likely sources: sequestration, hemolysis, marrow failure.
6. Thymoglobulin can cause thrombocytopenia and leukopenia. They run the drug against an RBC adsorbent to eliminate anti-RBC antibodies, so it should not cause hemolysis/anemia.
7. Kidney and pancreas transplants are highly immunogenic and require strong immunosuppression. Livers are less so, and it's estimated that up to 20% of people do not actually need immunosuppression after a liver transplant, however it is unclear which people these are.
8. Pancreas transplants used to have the duct connected to the bladder, to measure amylase levels in the bladder as a means to track rejection. However this resulted in severe bicarb losses that were hard to replete, as well as bladder wall irritation from pancreatic enzymes. Now the duct is connected to small bowel. Islet cell transplants are indicated only in people who have difficult to control type 1 diabetes who have hypoglycemic unawareness.
9. Lead in neurons can interfere with Ca-mediated vesicle release of neurotransmitters, causing a botulism-like effect.
10. In pancreas/islet transplants, HLA matching is more complicated: if the match is poor, there will be an allo-rejection of the organ as too foreign. However, if the match is too good, the organ may be susceptible to destruction by the same autoantibodies that caused the destruction of the recipient's original pancreas, causing the type 1 diabetes.

1. Contraindications to receiving liver transplant vary by center, but the following are generally accepted:
-uncorrectable cardiopulmonary disease severe enough to be prohibitive for surgery
-extra-hepatic metastatic disease
-active alcohol and drug use
-(at some centers) advanced age, advanced AIDS
2. Contraindications to liver donation:
-Active malignancy (exception: primary brain tumor with no VP shunt)
-a-HIV seropositivity
-Sepsis, although this retrospective study found that organs from bacteremic donors had the same outcomes as those from non-bacteremic donors {Transplantation, 1999, n=1775}
3. Zinc is a treatment option for wilson's disease, as it prevents uptake of Cu. Good for asymptomatic and pregnant patients; symptomatic patients require chelating agents, like d-penicillamine.
4. Rapid progression of hypoxia and CXR findings- think PCP pneumonia. Treatment of choice is bactrim, PO or IV in more severe cases.
5. Healing after major abdominal surgery: Fascia is the last layer to heal; at 1 month postop, an average healthy person will be ~70% healed, and at 3 months postop they will be 100% healed. Advise no heavy lifting or anything else that significantly increases intra-abdominal pressure during that time.
6. Liver resection facts:
-Before surgery, consider IR embolization of venous supply of ipsilateral side to cause hypertrophy of the contralateral (i.e. remaining) lobe, to boost remnant liver function
-After major resection, watch phos, watch synthetic function closely esp INR (patients tend to crash 2-3 days post-op), watch for infection (fever, WBC), watch for bile leak, bleeding. Expect rising LFTs, lower protein.
7. Someone with BUN>100 is not a surgical candidate because of platelet dysfunction. I.e. the ESRD patient who needs dialysis will need a quinton or permacath placed first to dialyze down their uremia before they can get a fistula or graft for dialysis.
8. If someone's LVAD power usage is increasing, think clot-- the machine has to use more energy than before to maintain cardiac output, it's likely that there's something obstructing. Normal power is <10. LDH is a good marker for thrombosis. To prevent clotting, most people on an LVAD will have a goal INR of 1.5-2, although some people who may be hypercoagulable (as evidenced by clotting off their LVAD multiple times) may require much higher INRs. Remember that you can't put someone on plavix and walk away, assuming they're anticoagulated-- a significant portion (estimated 15-50%) of the population is resistant to plavix.
9. Lung cancer:
-Average doubling time 108 days (varies 20 to 800)
-Normal cigarettes => squamous cell CA, low-tar cigarettes => adenocarcinoma (peripheral cancer-- people think its safer so they inhale more deeply).
-Frequently produce paraneoplastic syndromes, and is assoc with hypertrophic pulmonary osteoarthritis/clubbing that is rapidly cured by tumor resection. People with lung cancer can present initially as "arthritis"
-Small cell is not operable; it responds well to chemo, but invariably comes back in 1 year, resistant and incurable.
10. Lung cancer resection: 
-Stage IIIA: possibly resectable; Stage IIIB: minimally resectable; Stage IV: not resectable
-Risk evaluation: FEV1<30%, DLCO<30, MVO2<10-15: poor risk:
-Palliation for effusion: sclerosing agents injected into the pleural space, i.e. talc, or a pleurx drain at home, will cause autosclerosis in 4-8 weeks.
-Palliation of obstruction: stent, radiation beam or ET brachytherapy

1. Contraindications to renal transplant: 
-Active infection
-Active metastatic malignancy with shortened expected lifespan.
-Active substance abuse
-Reversible renal failure
-Life expectancy: variable; almost all centers will not do it if life expectancy is <1 year, most will not do it <5 years since that is the expected half life of a kidney.
2. Relative/soft contraindications to renal transplant
-Severe, uncorrectable cardiac or pulmonary disease such that the risks of surgery are high-- CAD, CHF, etc.
-Severe, uncorrectable peripheral or cerebral vascular disease
-Active hepatitis or severe chronic liver disease.
-Malnutrition
-Significant medical, psych, or social barriers to post-transplant compliance with immunosuppressants.
-Severe hyperparathyroidism
3. After a partial liver resection, the regenerative process consumes phosphate, at times very rapidly, and someone's phosphate can go from normal to very low in a matter hours. The pathogenesis is thought to be related to the increased production of ATP and nucleotides for the synthesis of proteins and DNA replication. In patients who have undergone liver resections, their phosphate needs to be aggressively replenished, IV if PO is not fast enough. In adults (>18 years), phosphate is normally 2.5-4.5 mg/dL (in kids, its higher, age 1-7 is around 4.5-5.5). You want to keep these people around the upper limit of normal.
4. If you're going to do a TIPS procedure on someone, make sure that their hepatic artery is patent. If you shunt the portal vein to the cava, and their hepatic artery is clotted off (common after transplant), you will cause ischemia of the entire liver.
5. ATN affects proximal tubules, not distal, so kidneys still respond to ADH. In patients with ATN, they lose the ability to pull back solutes so their urine will have the same electrolyte concentrations as blood, i.e. whatever you put in them IV or PO. If they are hypernatremic, however, realize that that may trigger ADH secretion, which will pull back water and make the urine appear more concentrated and may give a false illusion of normal function. In reality, people who are experiencing ATN (say after transplant) generally will produce a more dilute urine; this may be because of more widespread damage (involving tubules) that makes the kidneys unable to pull back water. Or this may be due to fewer functional glomeruli, increased filtration pressure combined with more tubular dysfunction through the remaining ones. In any case, the results is that if you're giving someone NS and they're peeing out 1/2NS, they will become hypernatremic so watch for that. 24 hour urine electrolytes are much more accurate than spot checks, as they adjust for short-term variations in ADH
6. Hepatorenal syndrome-- there is nothing wrong with the kidneys per se, at least not at first. The physiology is essentially prerenal, involving a combo of shunt away from the kidneys (splanchnic vasodilation) and global vasoconstriction in the kidneys unresponsive to NO treatment. If the patient receives a liver transplant, the hepatorenal will be cured. Otherwise, over time, ischemia will develop and irreversible damage. The time frame is thought to be around 3 mos-- before then, do not transplant a kidney! Just dialyze them.
7. A gunshot wound to the head can trigger DIC, as brain lipids released into the blood can activate the coagulation pathway. These people may or may not be good organ donors, depending on the extent of organ thrombosis. Kidneys for example-- if you have a big clot that lead to whole-kidney ischemia, that organ isn't going to be transplantable, but microvascular occlusions will heal over time.
8. In someone with diabetic retinopathy, the significant fluid shifts and vital sign changes that inevitably accompany surgery can cause rupture and bleeding of the eye vessels. Before you go for surgery, they may need laser retina surgery to stabilize their retinopathy-- get clearance from optho.
9. Dialysis can cause b-2 microglobulin amyloidosis, since dialysis machines are not always good at clearing it. Clinical symptoms are mostly related to joint/bone pain: carpel tunnel syndrome, scapulohumeral periarthritis, spondyloarthropathy, cystic bone lesions. You can get also get deposits in the GI tract that may interfere with absorption. Longer, slower dialysis leads to lower incidence of this since it clears the amyloid better (overnight is best), as do some high-flux dialysis membranes.
10. If someone is going to be on a ventilator for a long time (>1-2 weeks), they have to get a trach. Endotracheal tubes are associated with increased morbidity with long-term use.

1. Carotid artery anatomy facts: 
-In 10% of people, both L and R common carotids come off of the innominate artery, making the placement of a carotid shunt harder
-The internal carotid has zero branches in the neck, the first branch of the external carotid is the superior thyroid artery. You can use this fact to identify which vessel is which after the bifurcation.
2. Nerve-related complications of carotid artery surgery
-Don't cut the vagus nerve
-Hypoglossal nerve runs around there-- if you cut it, there will be ipsilateral tongue deviation, resulting in speech alterations. They'll eventually learn to work with it and it'll get better, but their speech will never be the same.
-Glossopharygneal nerve is higher up, and you might need to dissect up if their bifurcation is high. Be careful-- if you take down CN IX, their pharynx will collapse; people describe it as impossible to swallow.
-Superior laryngeal: if you cut this, there will be vocal cord paralysis; if you cut both sides, they won't be able to breathe and they will be trach dependent for the rest of their lives. So if someone's got bilateral carotid disease, don't do them both at once; do one, then get ENT to scope them make sure vocal cords are ok, then do the other.
3. Presenting symptoms of carotid artery disease: 
-Syncope and dizziness are a frequent cause of referrals to vascular surgery, but they almost never have carotid disease as the underlying cause. Unless its an unusual case of 4-vessel disease, syncope and/or dizziness almost always due to cardiac, pulm, heme, tox, and/or volume considerations instead of carotid stenosis.
-Bruit-- listen to the heart to rule out valvular disease with neck radiation
-Neurological symptoms: TIA-style focal neuro deficits like weakness, paresthesias, speech (L carotid supplies speech centers in brain). TIAs formally are defined as <24 hours, but often will last only minutes. Amarosis fugax from embolization to opthalmic artery.
4. Diagnosis of carotid disease: 
-U/S doppler; look at the velocity, greater stenosis = higher velocity. Greater than 300 cm/s systolic 100 cm/s diastolic indicates severe disease. One thing to consider: in u/l carotid stenosis or occlusion, flow through the other artery will increase to compensate, and may give a false positive doppler.
-Confirm with CT angiogram.
5. When to operate: 
-Asymptomatic: >80% occlusion.
-Symptomatic: >50% occlusion
-Risk of triggering stroke in someone with no history of stroke: <1%. Risk in someone with a history of stroke: 4-5%. Use downstream filters during the procedure.
6. Stent vs Endarterectomy 
-SAPPHIRE trial: {NEJM, RCT, n=334} high-risk population, essentially similar outcomes. Less revision with shunt, slightly less risk of stroke (p=0.053) with stent slightly on top.
-CREST trial: {NEJM, RCT, n=2502}. At the time of procedure, stenting is associated with increased incidence of stroke or death, surgery associated with MI. 4 years after the procedure, stent is associated with slightly increased risk of stroke compared to endarterectomy.
7. Choosing your procedure: 
-Stent in people who would be harder to operate on: previous neck surgery, neck radiation, any scarring (i.e. 2/2 bad infection or abscess), VNS in place, etc.
-Bypass graft if you can't get a stent and can't do an endarterectomy: outcomes not as good long term
-Don't do a TPA catheter, you will shower downstream clots and cause TIA/stroke. (sidenote: don't use tpa cathether for upper extremity DVTs too, you will shower PEs and cause/worsen pulmonary hypertension and R heart failure)
8. During endarterectomy surgery: 
-Use a filter at the distal end of the artery to catch any small clots that may embolize during procedure
-Cut open the artery proximal to occlusion, extend to past occlusion. When you repair, don't just sew together the ends, you'll cause stenosis, make a U and use a graft to make the roof.
9. Preventing brain ischemia during surgery, two options:
-Clamp and run, with brain monitoring-- either EEG, carotid stump pressures, or do it as an awake procedure and monitor neurological status throughout
-Temporary shunt while you work
-Cochrane review cites ~700 RCT patients, shows insufficient data to definitively prefer one method to the other.
10. If your carotid is 100% occluded, 1/3 will have a major stroke, 1/3 will have a TIA, and 1/3 will be completely asymptomatic.