Transcript for:
CNS Ischemic Response Mechanisms tutorial

[Music] K team my name is Ben and let's go through the central nervous system es schic response the early phase so step one what's happened is we've got some cranial insult so we've had a bang or Blow To The Head and this is going to lead to Hemorrhage and vasogenic edema Hemorrhage so we're going to get bleeding and we're going to get vasogenic Adema so swelling inside our skull as that bleeding and swelling builds up we get an increase an intracranial pressure so this is a pressure inside the skull because our skull doesn't move any increase in pressure is going to cause a problem it's going to cause compression of our cerebral arteries Our arteries are things that provide our nutrition to the brain and so we get a decreased cerebral profusion pressure that is cerebral profusion pressure is the pressure that means our brain gets blood so cerebral means brain and cerebral profusion pressure is our mean arterial pressure so our blood pressure that's forcing the blood into the brain take away the intracranial pressure so the pressure inside the skull if our intracranial pressure increases then our cerebral profusion pressure is going to decrease so that's a problem what the body does to accommodate is we can shift our cerebral spinal fluid into the spinal cavity that's going to make a bit more room in the brain so what that's called is the Monro C hypothesis here's our brain our Cal spinal fluid and our blood as the pressure builds up in one compartment so here's our brain taking up more space because of the bleed then other compartments have to lose volume so here's our cerebral spinal fluid being shunted out into the spinal cavity that's the brain trying to relieve some of that intracranial pressure so cerebral profusion pressure can increase unfortunately if the bleed and the swelling continues then the compression of our cerebral arteries will still continue and we're going to end up with hypoxia and hypocapnea decrease oxygen and increase carbon dioxide to our brain to try to get more blood in there in our response we get cerebral vasod dilation the blood vessels going into the brain to dilate and open up to achieve more blood flow and that is the early response for our central nervous system ischemic response boom all right team that brings us to the late phase of the central nervous system ischemic response so remember cerebral profusion pressure is our mean arterial pressure take away our intracranial pressure intracranial pressure is building up building up inside the skull our cerebral profusion pressure the amount of blood flow getting to the brain is decreasing that leads to hypoxia decreased oxygen and hypocapnia increased carbon dioxide if we can't change the intracranial pressure the next thing we can look to fix is our mean arterial pressure so you want to increase our blood pressure the formula for blood pressure is blood pressure equals cardiac output times our total peripheral resistance to fix this problem water try to fix this problem our our sympathetic nervous system is going to stimulate systemic basoc constriction if we Vaso constrict systemically so the rest of our body that's going to increase our total peripheral resistance which is going to increase our blood pressure our mean arterial pressure increases hopefully that's going to improve our cerebral profusion pressure and so this brings us to the first part of Cushing's Triad which are the symptoms we look for the clinical signs on a patient who has increased intracranial pressure either via a stroke or a traumatic brain injury so first one if our central nervous system stimulates systemic phas of constriction it's going to increase blood pressure so Cushing's tray the first sign is an increase in our systolic blood pressure blood pressure too high is not good because it can lead to lots of problems like a stroke or a attack so we've got these Barrow receptors which are in the arch of the aort and they sense this increased blood pressure and they say well this is no good we got to do something about it so they're going to stimulate our parasympathetic nervous system our rest and digest and the Vagas nerve is going to cause decrease in heart rate the second step in Cushing's Tri is Brady cardia or decreased heart rate so now your client is going to present present with like two opposing symptoms increased systolic blood pressure with decreased heart rate so if that bleed continues and the swelling continues inside the brain we are going to get increasing intracranial pressure and we've got this increased blood pressure forcing more blood in which is going to cause more pressure again and this increased intracranial pressure eventually is going to press down on our brain stem so our brain stem is a deep part of our brain and it's involved in the critical for Life responses so things like breathing so the last phase of our chrisan Triad Shan Stokes respirations which are irregular respirations your patient breathing patterns will become irregular fast slow shallow deep all over the place so if you see this pattern and you're taking someone's respirate we don't want to just hold for 15 seconds count and then you times by four because you may catch them in a a fast pace or a slow place so we want to count for 30 seconds to a minute to get a more accurate representation okay this person is getting quite sick then the buildup of intracranial pressure all the hypoxia or the hypocapnea is going to cause exto toxicity and that's going to proceed on to neuronal death and unfortunately probably death of our client all right team that was the central nervous system ischemic response [Music] boom [Music] the n