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.