Applied Physiology Lecture 2 9-13-11 Just to recap: for neurosurgery, we want to ↓ICV to ↓ICP. The cranium contains tissue, blood and CSF. Each can go up in volume and ↑ICP. If volume ↑, then pressure ↑= bad. So, we have to control the volume to be able to control the pressure. We can control blood flow with ventilation. ↑PCO2 ↑CBF ↑ICP ↑PaO2 ↓CBF ↓ICP Good range for ICP= 27-30mmHg. Brain can autoregulate within a 70-150mmHg range. For a posterior craniotomy, shunts can be involved, but we’ll talk about these later. The brain and glucose: brain requires a lot of glucose, which gets to the brain through the blood. ↑glucose ↑CBF ↑CBV ↑ICP On a side note, after you eat a big meal (post-perennial), lots of blood is diverted to your splanchnic vasculature, so that some also gets diverted from the brain, which is why you get sleepy. Brain function which is too much above normal is bad (= seizure). If you give more glucose = ↑blood flow= ↑ICP. You need to maintain a tight glucose control, so give insulin. You can ↓ the brain mass with tumor steroids (b/c it ↓ edema), but the steroid use causes hyperglycemia, which causes your CMRO2 to ↑ b/c the brain now has a lot of food. Therefore, you get ↑CBF ↑ICP. So, give insulin with it. PaCO2, or PCO2, is okay to a certain level, then it starts to ↑ almost linearly. If the brain activity ↑ too much, this is bad b/c it will cause a seizure. Low activity is good, especially when controlling ICP and ICV. Temperature also affects this greatly: ↑Temp (hyperthermia) ↑CBF ↑ICV ↑ICP. Hypothermia does exactly the opposite. At 37⁰C, the brain has 2 functions: 60% energy used to process information, etc. (do extra work) 40% energy used to keep brain tissue alive We can drop the temp of the brain to 17⁰C so that it is just warm enough to keep the brain cells alive, but not active. This is known as circulatory arrest, a procedure where the body is brought to 17⁰C to stop the blood flow and freeze the brain. Then the patient is essentially dead. When you bring them back/ warm them back up, they will be normal again. At this temperature, the brain will function at the bare minimum to keep itself intact and alive. We can do an EEG (electroencephalogram) to know the brain function of an individual. We should have a basic idea of how to read an EEG. At 17⁰C, you see an isoelectric EEG is where you see a flat line b/c there is no brain activity, but the brain is still alive. WAVE PURPORTED GENERATOR I Extracranial auditory nerve II Intracranial auditory nerve and/or cochlear nucleus III Superior olive IV Lateral lemniscus V Inferior colliculus VI Thalamus VII Thalamocortical radiation When you warm the patient back up, they will be normal. It takes about 2 hours to warm them back b/c you have to do this slowly. Why do we have to warm them slowly? We have protein in our body, just like an egg has protein in it. Our protein is all through the micro-vessels in our brain, our vasculature, cells, etc. If you heat an egg too quickly, you get scrambled eggs. If you heat a protein too quickly, it will denature and you will have scrambled eggs all throughout your body and you will die. These proteins in the vasculature have to carry all of the drugs and such throughout our body. Warm the patient slowly so you don’t denature the proteins and so that you protect the brain. We usually give a large dose of steroids (1g methylprednisolone). Why? To scavenge free radicals and protect the brain. We give this while we’re cooling the patient. We have to apply the principles of neuroanesthesia even when we are dealing with non-neuro cases. We put on a fem-fem bypass (machine hooked up to femoral vasculature on both sides of patient) to run their blood through this machine and cool them down to 17⁰C. We have to maintain PCO2, PaO2, temperature, glucose control, brain activity (no seizures/ hyperactivity), etc. What would be the desired viscosity of the blood during this procedure? If we thinned their blood and made them anemic, it would flow faster and ↑ their ICP. The blood has to go to the brain to give it O2 and glucose. Anemic blood gives less O2, so it would have to flow at a higher rate to deliver more blood to get the same amount of O2. This would also result in an ↑ heart rate. Viscous blood has the opposite effect. If the patient is given polycythemia (excessive RBCs), they would have viscous blood and slow down the flow. You could use erythropoietin to do this, but it would take a couple weeks, so that’s really not a good option here. You could also cut down on your fluid administration in _________________. However, giving them a lot of blood (↑ viscosity) winds up ↑CVP and ↓CPP (b/c CPP= MAP-CVP). Polycythemia ↑Blood viscosity ↓CBF Anemia ↓ Blood viscosity ↑CBF Initially, when this procedure was done, they would do just that: they would lower the fluid administration and “run them dry”. Now, however, they have found it is best to stay at normal blood viscosity, so they “run them even”. If the patient loses 100ml of urine, they give them 100ml NS. If they lose 300ml blood, they give them 900ml of NS or 300ml of blood. If you use a lot of crystalloid, it leaves the patient anemic and ↑CVP. You need to maintain fluid management. If you have a drain, you can drain the CSF out. If you have a brain tissue mass, give steroids. You can give diuretics: 0.5-1g/kg of mannitol 0.5mg/kg of lasix (a __________ diuretic). The half life of this drug is 6 hours b/c it lasts 6 hours (lasts six hours= lasix). The position of the patient is also important. You want to keep the head up to ensure venous drainage. During a sitting craniotomy, the neck is extremely flexed so it occludes the venous drainage in the EJ (external jugular vein). Also, when you tape the ETT around the head, sometimes the tape occludes the EJ, so you have to move/cut the tape. Ex: a patient is hit by a baseball bat and has a subdural hematoma. He can open his eyes to pain, he withdraws to pain and he doesn’t respond to commands. You are taking this patient from the ER to the OR, so what is the first thing you need to do? Calculate his GCS, which is 7, so you immediately know you need to intubate this patient (at a GCS of 8 or below, they can no longer maintain their airway). A patient’s GCS score = eye + verbal + motor. You have your mannitol and your lasix ready. PCO2 is 27mmHg b/c the patient has already been hyperventilated. The CT scan confirmed that the patient has all the signs of potential herniation. You have to put a central line in. Where should you put it? Do not put it in the IJ b/c we just discussed how the venous drainage there is occluded. So, preferably, the central line will be placed in the subclavian vein. You also need to know the complications of this procedure. Then what? Studies have shown that you should not give steroids in a trauma situation b/c it actually makes matters worse. You should really only give steroids if you are dealing with a tumor or a SCI (spinal cord injury). You also do not want to give Mannitol in this situation b/c it will function in the opposite fashion in which it normally would. In this situation, the Mannitol will actually go into the brain and bring the fluid into the brain with it, out of the vasculature so it would actually ↑ICP. The BBB should be intact. Next, you will want to put the patient’s head up and thereby somewhat ↓ flexion of the neck. Do not sit the patient up during the surgery or the surgery will not be able to be performed appropriately. Sitting craniotomies: say for instance that you have a patient with an infratentorial tumor (a tumor in the space which is on the bottom back of the cranium the below the tentorium and behind the brainstem). These tumors in this situation are always benign by histology but malignant by location if it grows it can crush the brainstem. Sitting craniotomies are becoming a thing of the past. Now they are mainly done in either prone or semi-lateral positions b/c of air embolism risks. All of the vessels in the cranium pull air in when the cranium is opened. The air from all of the vessels then goes into the SVC and the R atrium, so you wind up with air going into the pulmonary artery. We hope that the air goes into the lungs and gets absorbed. However, if the air pocket is too big, it will cause an air lock in the pulmonary artery, meaning you now have an air embolism in the blood vessel. This means that you are now getting ventilation to the lungs without perfusion because the blood can no longer get passed the air to the lungs, which means you have dead space. If the patient develops an air embolism, the PCO2 on the machine will read very low b/c CO2 is not getting out of the patient to actually be read by the machine because of the air embolism. EtN2 will ↑ because you are not ventilating properly and getting O2 in, which would usually get the N2 out. However, we don’t always have the EtN2 monitor on the machine. Therefore, you have to measure this with clinical signs to see if it is an air embolism or not (VAE= venous air embolism). With a VAE, you will also get a ↓ in bp b/c no O2 is getting delivered to the heart, so the heart starts to become ischemic. By the time we see all of this on the monitors, it’s almost too late. How do we see this sooner? We definitely want a central line to measure CVP (central venous pressure). We can use a precordial doppler, which is hooked to a really loud stethoscope to be able to hear the heart. If the heart sounds get squishy, then we know we have air in there. So, the heart sounds are squishy, we know we have a VAE, now what? We need to aspirate the air out via our central line. In order to do this, our central line has to be at the junction of the SVC and the R atrium, or we will not be able to successfully accomplish this. How do you know if your central line is in the right spot? If you go too far and you get the line into the R atrium, you will get PVCs. You could also try measuring the depth on the catheter, but this is not always consistent for each person, so it is not as accurate of a method. The best way to tell is with the use of an EKG lead on the end of our central line, along with a lead on the arm. With this set up, as you approach the SA node in the heart, you will start to see the P-wave on the EKG. As you line up next to the SA node, you will see a biphasic P-wave, which lets you know you are in the right spot. This is possible because the EKG is measuring the polarity sent out from the SA node. These are really the only types of central lines that are used in sitting craniotomies. Even more sensitive than the EKG central line is the TEE (transesophageal echocardiogram). This device will pick up an air bubble that is only 0.25cc in volume, but the TEE only senses the presence of the air; you still need the EKG central lines to be able to treat the issue and remove the air embolism. If you see that the patient is having an air embolism, lay them down flat. You can also give them epinephrine to make the R ventricle squeeze harder and be able to push the air block (VAE) out of the pulmonary artery into the lungs. At this point, we hope it gets absorbed in the lungs. If it is too massive, it will not be absorbed and the patient will code. At this point, the source of the air which caused the VAE still has not been cut off. To stop the air entry, place soaked gauze over the open surgical area to prevent air from entering the venous system. What is this VAE causing in the heart? At this point, you have an air block in your pulmonary artery, which means that the right side of your heart is essentially pushing against a wall, so the pressure in the R ventricle is ↑ due to the blocked exit. In turn, this is making the pressure in the R atrium ↑ as well. What do you do? You can give more fluid to push the air out However, if this does not work and the fluids cannot push the VAE into the lungs, the pressure in the R atrium will get so high that the patient will develop a PFO (patent foramen ovale); this means that the patient will have an intracardiac shunt that will shift all of the blood from the R atrium to the L atrium, which will then send it to the L ventricle and send deoxygenated blood out to the rest of the body. In a pediatric patient who is coming in for a craniotomy, the first thing you want to do is get an echo to see if the patient has a PFO (25% of the population does) before performing the procedure. In embryology, the septum between the 2 atria of the heart forms in such a way that it leaves a hole in the septum. The septum primum grows down from the top of the chamber which will be the 2 atria, connects with the bottom, then disconnects from the top of the chamber. Following that, the septum secundum grows down a portion of the way to the bottom and overlaps with the septum primum. The overlap/ flap in the middle leaves a gap called the foramen ovale. In most individuals, this is not an issue b/c the pressure in the L atrium is higher than that in the r atrium and this usually holds the flap closed. Additionally, while being held closed, most of the population’s foramen ovale proceeds to close/ grow shut. There is also a situation where the septa grow in such a way that there is no overlap at all, in which case the condition is considered to be a septal defect. Because of the situation described above, ASDs (atrial septal defects) and VSD (ventricular septal defects) are a contraindication to a sitting craniotomy. Back to our infratentorial tumor: this is in a bad location b/c if it ↑ in size, it can damage the brain stem. A sitting craniotomy is the best way to access this issue, but it presents problems with VAE and venous drainage. You must ensure that your patient is properly padded b/c we pay for all of the neuropathy that occurs legally and ______________________. Make sure PPP (all pressure points padded)!!! Everywhere that the patient in the position is touching the table/chair presents a potential for neuropathy. The patient in this position can also get hypotension due to blood pooling in the legs. You can ↑CVP (central venous pressure) with fluids or positive pressure ventilation can use big breaths or Valsalva maneuver. This will ↑CVP = ↑______. How does blood get back to the heart? The venous system uses muscular contractions and has valves. How about when a patient has varicose veins? The venous system also uses the intrathoracic pressure gradient to get the blood to return to the heart. The negative pressure created when inhaling air brings the lungs out and makes the SVC and IVC have cortico____________ suction. Ventilating the patient is done with positive pressure, so the opposite occurs and you wind up ↓ venous return. Therefore, you should not add PEEP to a patient who is intubated and has hypotension. The valsalva maneuver ↑ intrathoracic pressure ↓ venous return. This will force the air block into the left atrium and make the shunt b/w the atria even worse. With this situation, you want to turn your ventilator off , close the APL valve. You have a ↓bp which will lead to cardiac arrest b/c venous return has ↓ to a point ___________________________________________________________________. So, CVP looks high, but this is only because the patient is being artificially ventilated. PEEP makes VAE worse. Additionally, a bunch of nerves come from the area where the surgeon is operating. Dorsal respiratory group, ventral respiratory group3 Lower cranial nerves (and functions) V Trigeminal Facial sensation VI Abducens Eye abduction VII Facial Facial muscles (motor) VIII Acoustic Hearing IX Glossopharyngeal Gag reflex X Vagus Cough reflex, laryngeal muscles XI Spinal accessory Shoulder movement XII Hypoglossal Tongue movement During the craniotomy, they monitor the Facial nerve (VII) and BAEP (Brainstem auditory evoked potential) or BAER (response) (same thing) to make sure that the patient is not having nerve damage. They monitor the BAER by making a clicking noise by the ear and watching for a response. How do we maintain our patient? Hyperventilate them, keep them asleep, and paralyze them. To paralyze the patient, we want to use Rocuronium or another non-depolarizing MR. We would probably use Roc here b/c it is long acting and our case is going to take 6 hours. Now, the surgeon has finished and he thinks that there is a brainstem injury because the he is not getting a twitch in CN VII. What do you say? Check the MR and see if it reversed first (use train of 4, etc.). You cannot randomly reverse the MR in the middle of the case b/c you’ll get a _________________________ block, which lasts 12 hours, so you’ll be doing more harm than good. You want to make sure the MR is reversed by the time the surgeon is ready to monitor the nerves. For BAER, they need to use EEG to monitor that pathway (there are something like 18 pathways for it????) This is the only evoked potential which is NOT affected by anesthesia (Etomidate can affect it a little bit, but not enough so that it is clinically significant), so we NEVER take the blame if there is damage here. The Artery of Adamkiewicz/ the great radiculomedullary artery goes from the aorta to the spinal cord to supply the spinal cord with blood, etc. For the blood to flow through this artery to the spinal cord, the pressure needs to be higher on the side of the aorta. If the surgeon is fixing an aneurysm, and he has to clamp the aorta at points above and below where the artery exits the aorta, then the pressure on the aorta side is going to drop and you will lose that gradient and, consequently, blood flow to the spinal cord there. For this, you have to know the principles of physiology. A blood vessel comes up the thoracic aorta to the spinal cord, which normally does not have the pressure gradient to allow blood flow to the spinal cord (???not sure about that last sentence, but it was something like that and it makes sense???)So, you have to ↓ the pressure in the spinal cord with a lumbar drain to be able to ↑ passive perfusion to the spinal cord to keep it alive. Average CBF is 100mg/ml. BAEP has 7 peaks (we don’t have to know these for our boards). The time between 1 peak and the next is called latency. The height of the peak is the amplitude of the wave. If the amplitude ↓ by >50% (if it becomes <50% of what it originally was), or if the latency ↓ by >10%, this is bad. This means that the surgeon is pushing too much on the brainstem or causing damage. We do not take blame for this. VI VII VIII IX X Abducens Facial Acoustic Glossopharyngeal Vagus Disconjugate gaze Facial muscle paralysis Hearing loss Loss of gag reflex Vocal cord paralysis Cushing’s triad is HTN, bradycardia, and ↑ICP. HTN + tachycardia= the patient is too light. Hypotension + tachycardia= they’re hyppovolemic, or you just put their head up and the venous blood is temporarily pooling. HTN + bradycardia= vagal stimulation tell surgeon. Some of the post-operative concerns include damage to the nerves on this side this is easier to diagnose if you know these.