Control gradients Physiolog processes Anatomic structures Diagnoses Expectation Goals Sensed info Effectors Recursion 1 Function 5. (R1F5) Function 4. (R1F4) Executive Internal / External interface Cortical neural activation and firing thresholds Specific neural activation thresholds Processes of cognition, judgement, planning. The initiation of voluntary motor movement Receiving, processing and redirecting incoming sensory signals (external and internal) Telencephalon inside scull, meninges (Cerebral circulation as part of F2) Diencephalon (thalmus / hypothalmus) and subcortical structures (eg pituitary, basal ganglia, circinate cortex + Cortical areas associated with sensation and perception States of processes: Neurologically not waking up. He isnt responding. He’s still deeply States of gradient: The temperature went up, it spiked last night. Mild unconscious, but pushing his way to the surface. He’s still deep deep deeply sedated, grade temperature. He’s non-responding. Mixed picture difficult to test beyond the point of comfort, almost comatose. Sedation has reduced his responsiveness. reflexes; a little brisker than normal. He's blind in his left eye as well. His lack of waking up was due to sedation still on board. His level of sedation was inappropriate. He's sufficiently sedated because he's quiet. He’s sedated so he’s a little calmer but still responding. He's able to obey in all four limbs and neurologically he's comfortable. Limb movement and strength was the same. He had very weak limb strength, muscle weakness. He’s also got brain failure when you think about it. His conscious state is lightening - his brain States of process: He was febrile over night. His temperature hasn’t actually works. He’s awake. He's quite alert and aware. He’s with it. He was appropriate. been variable and he was afebrile - he’s keeping his temperature under He’s a bit blurred out, lost the whole week or so. He had a go and he understood. No change control. He had a good gag reflex. His pupils are equal and reacting to in his mental state. I’m not sure of how much cognition he has. He’s got much more insight light. He localises pain. He’s got some level of ability to feel what I’m now. He looks depressed to me. doing to him. Expectations associated with processes: If he was responding I’d be saying what about Expectations associated with Gradients: His temp tells you about the increasing his morph and midaz. He’s neurologically responding even though he’s on patients metabolic rate. So we're just waiting his temp may peak at night. massive doses of sedation it means that he’s not lying there like a log, flat on sedation. Is You drop your body temperature because the blood is out of the body as it there something else going on - he’s on such a small sedative dose not to be flexing to goes through the filter. His temperature is going to be misrepresented with painful stimuli. Don’t know if it’s the urea or other toxins that should be removed by the the filter. Patients on a filter would normally drop to a temp of around 35, kidney, but when urea gets to 30 or 40 patients have impaired conscious state. his temps 37 in actual fact so take him off the filter and he’s probably Hyponatreamia if it gets severe enough can cause seizures. I’m querying whether he needs around 39. He's sedated so his pupil are pinpint as expected on morphine. sedation or pain relief. His temperature is high which might make him feel uncomfortable. Stress reflexes like heart rate and BP, facial expression - that would He might have an encephalopathy associated with multi organ failure, 'ARDs of the brain'. indicate that someones in pain. To turn off coughing requires a lot of You’re desperately sick makes your brain malfunction sedation. . Thinking that his lack of movement can be due to other neurologic problems - anyone who Expectations associated with Process: Its part of the stress response, is critically ill can develop a critical illness polyneuropathy - a diffuse disorder of the with just the stress response his temp will rise. His own body mechanisms peripheral nervous system as a consequence of just being sick. If we can get him through should get the temp down by themselves. When you and I get infection this probably his brain will be OK and he will wake up again. If he still cant move then we’ll we get fever; people who are neutropenic don’t often get fever or it might need to look at that problem more formally. Only time and improvement and stopping drugs be blunted. His reflexes are about lower brain function. He’s obviously will improve it. He may well be feeling apprehension, fear its hard to know. Emotional snuggled up to keep perfusion - he must have been cold at least in his recovery starts after the depression, which starts after they’re virtually better-I see this not feet. Because of his conscious state he would obstruct his airway. His uncommonly. Sleep is a problem in ICU’s, there are ways of dealing with this all of them temperature should go down with paracetamol. unsatisfactory. Drugged sleep is not as efficient as natural sleep and so sleep is a real issue. Sleep night patterns have a lot to do with recovery. He’ll need a more normal day/night pattern other wise he’ll become compromised from sleep deprivation. People who are about to 'go off' get a little irritable, start fiddling, dont interact as appropriately or respond to questions correctly, he might pull lines out adding another risk for infection. If he goes off he’s not going to cough when I ask him so his respiratory function may worsen. If your sitting out of bed its much better physiologically for your lungs. The biggest risk is that he wont cough when I ask him to, he wont participate in his own physio.Getting him out of bed will exhaust him. He probably wont last very long 20 minutes, but that’s OK. If he wasn’t sedated he'd probably be awake and anxious. Pain as well as agitation and restlessness might be associated with his foot. He's probably anxious and frightened of everything especially if he’s awake and he’s got the tube in his mouth and cant move much. If he showed signs of waking up then we’d wait on the tracheostomy- give him another few hours and maybe a day and see how he is neurologically and then maybe try to extubate. There might be a few short term memory problems. I imagine he would be able to tell me if he had pain. Pain wise he will probably deny it, as he took so long to tell someone he was sick to start with. Expectations associated with anatomy: He could have flicked off a clot or had some sort of stroke. If he did have a stroke you’d see lateral changes. If he’s had a cerebral event or he’s been hypoxic, or had a bleed on one side or a big intracerebral haemorrhage related to thrombocytopenia, then his prognosis is less than now which is already terrible, so there'd be no point continuing. Goals about Processes: We'll give him the benefit of the doubt and wait, particularly if he’s Goals about Gradients: the temp is something we monitor. We're trying responded a little bit. He needs less sedation. We’re not about to de-instrument so his dose to keeping him cool as much as we can. can be titrated to what he needs. Not too sedated, sedated to a point of safety. Now I want to make sure he’s sedated. If he has abdominal pain we want to know about it. Control pain and anxiety. Making him comfortable with fans/blankets. Keep him comfortable without sedating him. Keep him comfortable so I wont turn the sedation off completely. Find a balance between level of sedation and comfort. Reduce the sedation to see whether he’s actually going to wake up. Wake him up We wanted to know what his cerebral function was to keep him sedated. Sedation is designed for patient compliance with the treatment and Goals about Processes: Let him establish and regulate his own fluid patient comfort, humanitarian reasons, sedating him to the point where he tolerates his balance endotracheal tube. Nothing gained by him being uncomfortable and agitated. I don’t want him wide awake and miserable, I want to make sure he has no pain. My main goal is to assess his conscious state. Its time to start getting him up out of bed. He wont actually be mobilising independently, but sitting out of bed. His psychological recovery is very important, he needs to feel he’s getting better. And he needs to get up, move his pressure areas around, he needs to feel he’s moving. Get him to settle down. Re-orient him to the date and time and what's happened to him. Get him out of bed, shaved, washed, doing close to normal things as tolerated. I wont let him sleep all day. Try and give him a good sleep at night. Get him into a day/night pattern. Get him back to a more normal type of day. Get him to rest and relax and maintain a more normal sleep/wake pattern. Make sure he slow his expiration so that he slows the number of breaths he takes. So now I have a commitment to him his comfort, and dignity and death. Sensed information about Processes: I’ve greeted him; he’s appropriately looked at me. Sensed information about Gradients: His temperature is volatile, He responded appropriately to his name. Didn’t respond to direct verbal stimuli. I can see elevated. Normal temperature is 36.8. His temperature is 38. 38.4, 36.3, he’s immobile, not responding, doing nothing, eyes closed. No response to name, to 37.5. Spiked to 39.2. His temperature’s high even with his blood going interference - what we do to him. Nothing to verbal command eg poke your tongue out. He’s through the haemofilter circuit. Temperature with the filter off. His visual not communicating verbally or any other way. He doesn’t wake up to command, doesn't obey acuity- what was the normal state of his pupils how those had changed any commands. He’s obeys commands. He wasn’t purposefully responding to painful stimuli. with sedation. A good cough reflex elicited through the suctioning. I’m not getting any response to pain. He’s responsive in all hands and legs to painful stimul. Initiating coughs. He’s got a tiny bit of jaw movement to tube wiggling when He guards against painful stimuli tries to get rid of it. He's doing something.<doctor> yelled at I put that suction catheter all the way down, no cough reflex. Different limb him, he opened his eyes but closed them - not a huge response to narcan. Squeeze your actions, sometimes they flex sometimes they extend. His limbs are all fairly right hand, your left hand, wiggle your toes, look over here. Squeezed my hand from the stiff, he’s resisting all sorts of movement. Plantar reflexes (upgoing other side. Just going to feel your feet (plantars). Level of sedation. He hasn’t had any downgoing) just going to press your toes, response to pain- a bit of a sedatives for at least two, three, four days now. Sedated for most of admission. He’s sedated withdrawal. Non-responding to painful stimuli, pinch his ear or sternal rub. with Morphine and Midazolam. From his history he was on morphine before he came in. Tap you knee now. So I just give him a bit of a sternal rub. Im pressing on the finger tips to see if there’s any result just to see if he’s giving us any High dose of morphine. Relate his sedation to his level of consciousness. Turned off the response. Sensed information about processes: You can monitor lots of things off sedation and he became very agitated when they were suctioning. We used to use the the temperature. We cant monitor his temperature with the haemofilter. Ricker scale to titrate sedation. Every time you intervene, suction or movement, he goes He’s sweaty and hot, diaphorectic. Even though he hasnt got a bananas. When the family comes in he gets upset and starts to breath a lot. He didn’t jump temperature he feels clammy, sweaty. Sensation its hard to assess. when I touched him. He’s alert and awake. He was sitting there watching. He's alert, knows Reflexes- they open their eyes. They can blink their eyes. I look more at what the day and time is -orientation. Ask him the same questions during the shift to see if I his pupils now because he cant talk to me or move than if I had a fully get the same response or if the answers change. He tries to tell you what he wants. He said oriented patient, sitting up in bed doing things. Equal pupils, size and he was a bit hot.Questions to see what insight he’s got. Have a chat to see what his response to light. Pupils are small and fixed ahead. His pupils were pin interaction's like, whether they interact with you; whether they’re orientated. He's co- point, constricted and not reacting. His pupils are equal and reacting. He’s operative. In the last 24 hours he’s noticeably awake and obeying commands. No got no dolls eye reflex. All he does is cough and his pupils react. He wasn’t spontaneous movement. He was moving but he wasn’t doing what I asked him to do. coughing or biting. He's got a good gag reflex. Facial expressions Movement wasn’t purposeful or meaningful. He’s spontaneously moving. A very little grimacing. response, he opens his eyes, he turns his head and gave a half grimace. He opened his His limb didn’t do anything to weak. He's eyes but strength was equally command. had been lifting his hand to the tube. Movement in Sensed information about anatomy: CT Brain scan. arms and legs. He hasn’t slept for two days. Grabbing at himself. I can see he’s tired and doesn’t want to talk to me. Can he do two tasks at once. Confused, agitated prior to intubation. Agitated, moving about, very restless, thrashing around. Her speech was soft but correct and present but incomplete. Looks unsettled. Didn’t seem too uncomfortable. He’s told me he doesn’t remember anything but pain. He’s tired and he gets anxious. He woke up overnight and was distressed. He hasn’t been sleeping. Its been documented that he slept about 6 hours fully, but says he’s had no sleep. Fatigued. He's very jumpy.Looks like he’s very tense. Sensed information about anatomy: They did a Scan earlier in the week. Lateralising signs Effectors on processes: He has been on intravenous sedation, morphine 2mg /5mg/6mg Effectors on gradients: The Prisma haemofilter's got a warmer so she (analgesic) and midazolam 2 mg/5mg/6mg (anxiolytic) half and half, with boluses.The turned that off in the hope to cool him down. So the blood that’s coming morphine's a narcotic and midazolam's a sedative. Bolus doses of 1 mg sedation maybe. from his body will cool down. Because we’ve got the heater on the filter so He's requiring more sedation so we increased it. Just a little bit of sedation. Reduced his we can give heated fluid if we need to. Well the way she’d been treating sedation a bit. Sedations been off for 6 hours, reduced, turned off, cut back, halved. You him was wrapping him up with blankets. More cold washes and fans. could give him narcan and flomazinol to wake him up in a huge hurry. they're reversal agents to reverse the morphine and midazolam. Get him out of bed and giving him different stimulation, talk to him, encourage him, tell him how good he’s doing. They get sedated if agitated. Reassure him and work him through it. So there are many Effectors on process: Paracetamol. Four hourly- PRN Panadol. They different ways of trying to induce sleep most of them drug related. He’s been on chloral hadn’t had to give any further panadol, they’ve ordered it, orally. Keep hydrate to help him sleep overnight. Temazapam sublingually to help him sleep. He’d been regular analgesia to hold pain and PR panadol is the drug of choice at the given propofol to sleep. So I’ll sit him out of bed. Do like a bit of a yoga breathing-blow out moment as well as traminol. like with a balloon-they can understand that concept blow up a balloon. Been through his exercises and give him a bit of a break Function 3. (R1F3) Function 2. (R1F2) Internal automatic co-ordination Communication & distribution Neural activation thresholds in receptors Neural activation thresholds, pressure and concentration gradients Processing of information related to basic basic survival functions 1. Neural transmission. 2. Circulation. 3. Hormone secretion Midbrain (Medulla oblongata, Pons Varoli) 1. Neural transmission pathways. (Spinal cord & Autonomic NS). 2. Cardiovascular network including blood volume. 3. Endocrine / Exocrine States of gradient: His sedation is reducing his respiratory drive. States of gradient: Only on a small amount of inotropic support. He hasn’t had a big response (to filling), his circulation, so that’s disappointing. States of process: Hes got respiratory failure. He's got circulatory States of process: He's improved haemodynamically. His circulation is still his failure. He’s stable on a lot of support. Respiratory wise, circulatory biggest problem. We’ve lost ground from the circulatory point of view- a major wise he’s a bit more stable. He cant maintain his airway. circulatory dip from the procedure that’s persisted he’s had a bit of a rocky night. He’s got lousy circulation and good lungs. He’s got circulatory failure. He's not peripherally shut down. Expectations associated with Gradients: If he wakes up he Expectations associated with gradients: He might be in that category where should be able to regulate his own breathing. I plan to wake him up we've filled his vascular compartment but at the same time he’s continuing to and his blood pressure should come up. deteriorate. Now he’s deteriorated he’s getting very close to his limit. Circulation likes to be a bit fuller. The circulatory response to surgery is fastest. You end up with hyposecretion from your adrenal gland of cortisol maybe from the inotropes we give him or from too much endogenous adrenaline/catacholamines. Expectations associated with processes: He's breathing himself Expectations associated with processes: New infection will probably manifest suggesting his conscious state is lightening. They sometimes have itself as haemodynamic collapse- hypotension. But will his circulation benefit from a lot of difficulty breathing on the ventilator when they’re not more fluid. They can get an improvement in their circulation with filling. In terms of sedated. He's bombed that can depress his circulation. People’s magnitude, the circulation is his survival factor. Two factors now to help his blood pressure falls when they’re asleep. Circulation, lungs and circulation (filling and reduction in sedation). I thought that he was already on a lot kineys conflicting priorities of circulation, lungs and kidneys in terms of support inotrope wise. Its generally felt that between 50 and 100mg of of fluids. I think if he was more awake he would need less hydrocortisone every 6 hours would be a maintenance type of dose in a stress inotropes. situation - published trials have used approximately 200mg total per day. Goals about Gradients: Goals about gradients: Goals about processes: Have the patient lie there happily and let Goals about processes: We're going to fill him to see whether that can improve the ventilator do the breathing for him rather than having them his circulation. Continue haemodynamic support. I want to help this guys breath against the ventilator. circulation. Circulation's the major problem his worst thing that most needs to be addressed, our main priority at the moment is to try and keep his circulation stable and getting better. Sensed information about gradients: His blood pressure did go Sensed information about gradients: The difference in his circulation between up once we’d awoken him. when it (cytaramine - chemo) was started and when it wasn’t given. A thorough physical examination related to his peripheral nervous system, then formal tests of nerve function done by putting recording needles into muscle and electrically stimulating nerves and that will confirm neuropathy or not. Sensed informaiton about processes: He's chugging on the Sensed information about processes: Cardiovascular stability... I wanted to see ventilator, it keeps pressure limiting. See how he's breathing for the progress over the past few days; how much support. Its not that easy some himself. hormones- ACTH. Synthactin test. The PICO gives you a continuous cardiac index that you can compare.The indexes are around 3.5 to around 4. He's got pink good capillary return Effectors on gradients: Effectors on Gradients: We give a maintenance dose of steroid hormones. Unfortunately you cant titrate your cortisol dose to catecholamines. He’s on a lot of inotropic support. Effectors on processes: Light sedation Effectors on Processes: He was on adrenaline at the beginning. The reason we do the synthactin test is to see how we are going to interpret the synthacin test, its about learning about the synthactin test! Function 1i. (R1F1i) Function 1ii. (R1F1ii) Function 1iii. Metabolism Defence Reproduction Pressure and concentration gradients Biochemical concentration gradients Supply - Respiration, Ingestion / digestion, Waste processing Haemostasis, inflammation, opsonisation etc, antibody -Defaecation, Urination. Utilisation & Storage - Protein, / antigen reaction Fats, carbohydrates, vitamins & minerals Apparatus of: Respiration, GIT, Renal,. Integument, Structures associated with coagulation, & inflammation. Structures associated with immunity (cellular and humoral) Auxilliary organ function. Cellular immunity. Stress metabolism. Inflammatory response. Gastro-intestinal. Coagulation & clotting. Integumentary. Auxilliary organ function. Cellular immunity. Stress metabolism. Inflammatory Response. Gastro-intestinal. Coagulation and clotting. Auxilliary organ systems: Cellular immunity Stress metabolism: Inflammatory response Gastro-intestinal: Auxilliary organ systems: Cellular immunity: Stress metabolism: Inflammatory response: Gastro -intestinal: Coagulation and clotting: Auxilliary organ systems: Cellular immunity: Stress metabolism: Inflammatory response: . Gastro-intestinal: Coagulation and Clotting: Recursion 2 (Systems); Function 2 (Communication & Distribution) Function 5. Function 4. Internal / Executive R2CF External interface Control Cortical neural Specific neural gradients activation and firing activation thresholds thresholds Physiolog Processes of Receiving, processing processes cognition, and redirecting judgement, planning. incoming sensory The initiation of signals (external and voluntary motor internal) movement Anatomic Telencephalon Diencephalon (thalmus structures / hypothalmus) and subcortical structures (eg pituitary, basal ganglia, circinate cortex Diagnoses Expectation Goals Sensed info Effectors 2 (Systems); Function 2 (Communication & Distribution) Function 3. (R2CF3) Internal automatic co-ordination Neural activation thresholds in receptors Activation of Cardiac and Vasomotor centres in response to sensory inputs Cardiac and vasomotor centres in medulla and pons. Sensory pathways of Glossopharyngeal, Vagus and Herings nerve, chemo & baro-receptors States of gradients: He’s pretty fragile. Haemodynamically I think he’s a bit sensitive. His dependency on inotropes reflects increasing cardiovascular instability. His circulation is now much more robust. and able to cope with changes. His inotropic support has decreased. Propofol causes him to require an inotrope States of processes: The haemodynamic instability that he had over the weekend has to do with his sepsis. Hes still a bit dilated. His cardiovascular state is unstable, deteriorated. Although he’s haemodynamically stable, he’s stable on a lot of support.He’s stable he’s not fluctuating higher or lower, he's staying quite stable with support.The trend has been for improving status. He was quite stable, no particular problems . Expectations associated with gradients: He doesn’t cope in the sense that he could drop his BP. It would take a while before the effects of the bolus cause his BP to settle. His needs for filling and inotropes suggest that he's quite hyperdynamic. May not need quite so much of the inotropes if we look at everything else and realise that a lower blood pressure is still acceptable. His blood pressure mightcome up as a response to reducing sedation. Probably he was haemodynamically unstable, his blood pressures low and so on and he needs inotropes, but we may be treating a side effect with the inotropes. The regulatory curves shift to the right. Hypertensive people need higher pressures; all the regulatory curves will shift to the left. If he's able to maintain his MAP with the change in noradrenaline then there’s a degree of progress there. Expectations associated with processes: He's not accomodating - we'd have to go down by the amount of inotrope that we had to go up, when we turned him. You wouldn’t turn him every five minutes and expect him to cope without inotropes. Suggests that his haemodynamic state is not really stable at all. With someone who’s so sick they’re just hyperdynamic. Circulatory status is stressed from his illness. Haemodynamically just wean the inotropes slowly its not something I'm aggressively working towards, it would have an effect on his vasodilatory systems. He’s not mobilising his endogenous catecholamines. The major problem that’s going to kill him is his circulation reaching inotrope limits.. Goals about gradients: We need to keep him sedated but we need to keep his blood pressure up. As he’s able to manage his circulation, support is allowed to drift downwards. Goals about processes: Monitor him and know that he’s hyperdynamic. I have to think what can I do to make sure that we don’t have huge dips in his blood pressure. Well the major priorities are the cardiovascular system status quo. Don’t want to introduce beta-blockers etc and then have him become septic Sensed information about Gradients Significant amounts of inotropes to maintain cardiovascular stability. His inotropes coming down. The trend for the amount of support required is pretty much status quo. He’s had a a lot of hypotension. He was showing hyperdynamic figures all the time via the Swan. Looking at the haemodynamic parameters via the PICCO it’s a haemodynamic monitoring device - an alternative to a Swan-Ganz catheter. They removed/ inserted the Swan-ganz catheter. Sensed information about processes: Cardiovascular status overall. His circulations steady without support. Worsening haemodynamic instability. Increasiningly needed to give him boluses of noradrenaline. Turning and moving him makes the blood pressure go down. He’d had some synacthin tests done. Effectors on Gradients: You put him on his side he drops his blood pressure, you go up on the noradrenaline, you put him back onto his back, you cant turn off the noradrenaline, but you turn it down. Even a small boluses of morph and midaz cause large dips. Effectors on processes: Use inotropic (catecholamine) drug therapy to support his circulation. Give him extra doses of noradreanline. On some hydrocortisone. Function 2. (R2CF2) Communication & distribution Neural activation thresholds, pressure and concentration gradients 1. Neural transmission. 2. Circulation. 3. Hormone secretion 1. Motor & sensory pathways of spinal cord and peripheral autonomic nervous system., incl. Vagus, Glossopharyngeal and branches. 2. Circulating blood volume (plasma &cells). 3. Adrenal medulla / kidneys States of gradients: He's come off the noradrenaline. His circulation has improved because the noradrenaline's come down today from 7 come down to 1. States of processes: He’s not on the right inotrope combination now he’s got blue fingers. He’s also having an adverse effect from high dose noradrenaline. Noradrenalines well below the ceiling, so improving inotropes although still not much. Too much noradrenaline. . Reduced adrenal function. We do know that he had adrenal insufficiency. States of anatomy: Haemoglobins not bad. I noted that he was anaemic. He's got no obvious blood loss that I know of. Expectations associated with gradients: High dose inotropes, his prognosis is bad, on low dose inotropes his prognosis is better. We thought to go down on the inotrope but no. If he could maintain a MAP of 70, we could slowly start weaning the noradrenaline. As the propofol starts to wear off we can come down on the noradrenaline. Vasopressors have potential adverse effects - adrenal exhaustion. I have no idea why he turned the corner last night - his inotropes started coming down. We know that the endogenous hydrocortisone levels go low or are less than they should be in septic shock. Some hormones are easy to functionally assess, like insulin, but you cant assess catecholamines. Adrenal exhaustion or increased desensitisation of noradrenaline receptors - probably both. We have some evidence about what the right doses of hydrocortisone are- trials say approximately 200mgs per day. You’d expect him to have a cortisol level of 500 600, 700 or more, a normal cortisol level in a stressed patient. I suspect his is only 300 or 200. If we took any more fluid off we would effectively just have to increase his support with the noradrenaline most likely. Acute renal failure, you can accumulate potassium and that can become dangerous. Expectations associated with processes: I'm not expecting much because we didn’t reduce the intropes at all. Needs intropes in septic shock. Usually a mixture of adrenaline, dobutamine, but the effects maybe due more to the noradrenaline. Inotropes have deleterious effects on the periphery and implications for acidosis. If you're very haemodynamically unstable and on high doses of inotropes tissues are affected. Adrenaline tends to peripherally shut you down, there's a tendency to necrotic patches. He cant go with noradrenaline for the next four or five days, it'll be causing vasoconstriction. His adrenals are at risk, they're under performing. Low cortisol is reflected in vascular de-sensitisation but cortisol is important in most cellular functions. I think some of the inotropes are working against each other. The amount of proteins in his blood help to draw fluid out of his tissues into the vascular compartment. Kidneys produce erythropoietin which you need to produce red blood cells. He has a reduced O2 carrying capacity. Expectations associated with anatomy: We presume it’s a bleed into the retro-peritoneal space something like that. Goals for gradients: The inotrope limit should be revised to include the adrenaline to spare the blue fingers. We’re going to continue with the inotrope support to keep his MAP above 60, around 70. Turn down the sedation, so that weaning the noradrenaline and adrenaline will be a little bit easier. Try to wean the noradrenaline while maintaining his mean BP. We can start giving an AICE inhibitor to reduce high blood pressure. Goals for processes: Wean him very slowly. Wean the inotropes and stop drugs that aren't required. The Dobutamine’s staying, we’re just using noradrenaline to support blood pressure. Overall goal is to have this guy off inotropes, so reduce the inotropes. I think the ceiling, maximum dose, for the noradrenaline was 80mics.Try and wean down his hydrocortisone. Push his Hb up to 80's with packed red blood cells. Have a look and his HPA (Hypothalmic-Pituitary Axis), get his cortisol and ACTH. Sensed information about gradients: The inotrope dose is his primary indictor of progress whether he’s getting better or worse. Turn the norad up his blood pressure goes up if we turn it down his blood pressure goes down and if we turn it off his blood pressure goes right down. His norad has an upper limit of 75-80. The dose of inotropes have gone up, he's requiring more noradrenaline. He’s on high doses of noradrenaline, adrenaline, dobutamine. His inotropes are down significantly. Noradrenalines down to 30 from 60. Adrenalines unchanged. We've reduced the inotropes. His inotropes have been steadily increasing over the last few days- they peaked at midnight and since they’re coming down. He’s completely off the norad. Not on inotropes anymore. So in that I’m mentally graphing his noradrenaline it went up and peaked about 6 hours ago now its come down to 60. He was off noradrenaline, off inotropes. Blood pressure has fluctuated up and down, but hasn’t changed over the last couple of days, it fell quite precipitously over the weekend. Low red blood cells- 70, his Hb dropped down to 8, it was 11. His albumin was low yesterday. Sensed info about processes: His synacthin test had shown reduced adrenal function. We’ve looked at him for peripheral oedema. His hands are cold and swollen. Check out warmth, peripheral perfusion. No marks on his feet, toes looked good, everything was warm - well perfused. He looks a little bit oedematous. The Swan- ganz catheter is out now. The tests blood factors, synacthin. I’ve just done his K (Potassium) level. Effectors on gradients: When you’re blood pressure is low in states of sepsis, vasopressor therapy. Catecholamines – noradrenaline; beta-agonists – dobutamine and adrenaline. Noradrenaline is the drug of choice. The nurse adjusts the noradrenaline and adrenaline to maintain the mean arterial blood pressure. We can implement some adrenaline in conjunction with the noradrenaline. Giving hydrocortisone in an attempt to reduce the Noradrenaline. Give Normal Saline to try and give him some more volume in his arterial space. They used filling to restore BP,. Effectors on processes: The combination of adrenaline, noradrenaline and dobutamine, some are vasodilators some are vasoconstrictors they can work against each other. Now today we've got hydrocortisone. We havent had the hydrocortisone. Hypertension was resolved with analopril,- a vasodilatory and antihypertensive treatment - beta blockers. I also use endopril / atenolol. Blood transfusion. Function 1i. Distribution Blood Pressure gradients Blood flow as a function of pump pressure and vessel diameter (resistance and distensibility) and circulating volume Systemic Arterial Network (includes composition of arteries - endothelium, smooth muscle and exothelium), comprised of aorta and major supply branches (eg renal, pulmonary, carotid etc) States of gradients: He’s got a good blood pressure. BP’s been pretty stable. His blood pressure has stayed roughly the same. It hasn’t been as good the last 24 hours as it was the 14 hours before. He’s quite unstable with his blood pressure. He’s got enough fluid in his arterial tree.With that urine output his BP hasn’t been compromised. States of processes: He's got circulatory maldistribution. He’s becoming quite dilated and constricted. Hes dilated, with the sepsis and the temperature. His vasculature is dilated, peripheral vasodilation. He was a bit more constricted, not so much in a shocked state. His peripheral circulation is not too bad. He’s peripherally perfused. He's a bit dry. States of anatomy: He's got vascular disease, in his left leg we know he has poor circulation there. Expectations associated with gradients: If his blood pressures compromised he'll also drop his CVP. The systolic blood pressure determines the urine output not the MAP. The kidneys rely on blood pressure and the differential pressure across certain membranes in order to function. Perhaps his vascular resistance is still low due to vasodilation. Other things that could impinge on his mean arterial pressure, like if he’s not filled enough. Too much fluid came off the haemofilter so he’s dropped his blood pressure. If he’s undervolumed his blood pressure would drop. There's no advantage to having a blood pressure higher than it is now. Hypertensive patients run at high pressures and they’ll hypo- perfuse their vital organs if its less. I wouldn’t let someone get to 160 systolic in a normal situation. I would want to get his blood pressure down to 120 –140, - I would want a reasonable degree of hypertension before I intervened because I don’t want him to become hypotensive. Expectations associated with processes: People who're immuno-compromised, in septic shock get severe hypotension. They’re dilating because they’re fighting an inflammatory response. His circulations gone, it wasn't a big bleed. Hes dilated giving him a huge arterial vascular space. I’ll be happy to keep on filling him without too much account of the fluid balance - he’s vasodilated again. He has such a big vascular space that you need to fill it- they use a lot to fill them. His high dose noradrenaline doesnt seem to be excessively burdensome on his peripheral perfusion. Wouldn’t be surprised in a guy who has vascular disease like he does, with his age, would commonly have hypertension. If the blood pressure’s looking fantastic then I might think about weaning. I’ve found that if you drop the intropes they tend to fall in a hole. If he all of a sudden tightened up (vasoconstricted) then I'd drop the inotropes. He’s going to be here for a while there’s no use in stressing him out just so we can get the inotropes down - they’ll be fine. Expectations associated with anatomy: He might have vascular and arterial disease. I was expecting that his periphery would be a lot worse, you're especially concerned about the toes. There’s an increasing recognition of dissection of vessels as a cause of stroke syndrome so even if you’vegot normal carotids -the mechanism probably involves inflammation of arterial vessel walls; the destruction of platelets makes the vessel walls sticky, so damage to the vessel wall predisposes to major arterial thrombosis- you get clotting of major arteries and catastrophic things like half of the brain dies. Goals for gradients: The MAP is irrelevant, we choose a MAP that gives us a systolic of 105 that’s what we chose. Goals for his blood pressure can come down he doesn’t need a mean blood pressure of 80. To achieve the aims that were set eg MAP above 60 … 60-65; 75-80. I wanted to stabilize his BP for a couple of hours. We’ll allow the blood pressure to be up - don’t let it go down. At 150 systolic, I wouldn’t treat that. Goals for processes: Maintain cerebral perfusion, renal perfusion, cardiac perfusion but definitely cerebral perfusion- normal blood pressure for vital organ perfusion. General objective is to let him maintain his blood pressure as long as its above a particular level at whatever that is, rather than to bump that up artificially. Less requirements to maintain his circulation from a drug point of view. As soon as his blood pressure looks fairly stable I start to get rid of the inotropes. I want to be gentle with him, there’s no reason to wean him quickly. The main criteria for weaning was a mean arterial pressure above 65. In his situation it wouldn’t be such a bad thing to keep him in the short term fairly heavily flogged then reduce it later on. Sensed information about gradients: I’m scanning the blood pressure. His blood pressures constant - roughly the same over the past three days. The primary indicator is a blood pressure in the range systolic 105 to 115. His BP isnt going with his Pulmonary Artery pressure. I don’t go with MAPS (mean arterial pressures)- he’s got a very low diastolic -systolic of 105 and diastolic of 40. MAP on 60 to 65; 75 to 80. The inotropes had come down (were off)- his blood pressure was still higher than required, with systolic 140 to 150 and mean blood pressure 85, 90. He had some hypertension up to 160, 170 but it settled down. He’s maintaining systolic above 120. Dropped his MAP but it bounces back up. Sustained a low BP. Sensed information about processes: His blood pressure went down with the drop in adrenaline, but came up when I increased the Noradrenaline. He required filling as well as inotropes.You’re fixing his water when his blood pressure comes up and you can turn the Norad down. They’ve said that they weaned him and he suddenly crashed. I’m looking to see when he was last on vasopressor support. He's been unstable especially when you move or touch him. SVR was 200, that's very low. SVR '700. SVR was around 1400, its normally around 800 to 1000. I cant monitor his haemodynamics- no PICO or Swan. He’s on antihypertensives at home. His fingers - poor circulation to the tips of his fingers. I held his hand, I looked at the colour because they felt cold - they're blue, its bilateral, its not as bad on his feet. He’s not got severe cyanosis. Pulses present everywhere. Brisk capillary return and pedal pulses. Warm peripheries, hands, feet. His heels are a bit blue and red rimmed- you get this frost bite look. He was quite warm, but I couldn’t feel any pedal pulses. He was cold peripherally but good pulses - well perfused. Sensed information about anatomy: From his past history he had peripheral vascular disease - he was waiting a fem-pop bypass. Effectors on gradients: Noradrenaline vasoconstricts by stimulating adrenergic receptors in arterial/arteriolar smooth muscle. He’s mean arterial blood pressure is still above 65 without any support. Effectors on processes: Noradrenaline increases SVR, but it can restrict peripheral blood flow. Clonidine is used to reduce hypertension. Give Normal Saline to give him some more volume in his arterial space. Function 1ii. (R2CF1ii) Pump Intracardiac volume / pressure gradients Rhythmic myocardial contractility Heart comprised of right atrium, right ventricle, septa, left atrium, left ventrical, four cardiac valves, coronary arteries. States of gradients: Reduced atrial kick. States of processes: Well that’s an abnormal response it reflects intrinsic heart disease. He’s hyper-dynamic but he’s not as hyper-dynamic as he would be if he had a heart like you. Obstensibly he's got a cardiac problem. His Cardiac index is adequate. He has a soft fourth heart sound which comes and goes during respiration. He's a bit tachycardic Expectations associated with Gradients: Atrial Fibrillation can cause increased ischaemia via lack of the atrial kick, especially in a person who has a stiff left ventrical from hypertension. With AF - no atrial kick to push the blood from atrium to ventricle - less volume will go to the ventricle. Starlings law … rubber bands… stretch. In regards to the PICO measurements, I’m not totally convinced about the alternative preload measurements, the thoracic blood volume and extravascular lung water, so each patient is a trial of one - we’re matching what we think is going on clinicially with what we measure. There are some assumptions and potential inaccuracies but the trials suggest that PICOs are reasonable to use. Generally what’s happening to pressures in the right heart is happening in the left heart to a degree. Expectations associated with processes: High cardiac outputs. You look at this - great cardiac output normally 5 now its 10, nice hyperdynamic response but its incomplete, it should be 15. The normal hyperdynamic response to infection has been blunted by intrinsic heart disease. He may have some cardiac depression rather than left ventricular failure. The tachycardia decreases the diastolic time for perfusion of the heart. The atrial kick can be important to improving cardiac output. Perhaps his heart is not as strong as it could be, he only needs little bits of filling to accommodate a weak heart. He may have a degree of right heart failure. Expectations associated with anatomy: Heart size says a lot for physiological changes. My main concern is some sort of inflammatory response in the heart, eg pericarditis, that’s somehow restricting it a little bit. His leukocytes are up they were worried about endocarditis.The possibility of bacterial seeding from the swan ganz catheter is most feared - you get seeding on the cardiac valves and bacterial endocarditis. If he had any form of indwelling device eg a pace maker or a prosthetic heart valve you would assume that staph had colonized it and he would probably have 2 or 3 months of intravenous antibiotics. If its endocarditis or another unrealised site of infection, we could see in two days time a dramatic deterioration. I’ve seen that often, they do very well and suddenly they get a new sepsis and they're dead in 24 hours. I don’t know the state of his valves or his heart, he could have lots of problems and he’s nearly 80. Goals for processes: I wouldnt want his heart to be working hard. Goals for anatomy: Get the Swan out, its come up on my list now. Sensed information about Gradients: The PICO gives you a volume measure of pre-load as opposed to a pressure measure of a pre-load which is your CVP or your Wedge. Physiologically pre-load is a volume not a pressure measure. Sensed information about processes: continuous cardiac output from the PICO. The PICO and the Swan-Ganz both measure Cardiac output. PICO seems to measure up quite well, the cardiac output measurement seems to correlate with the Swan. The cardiac output was 16 litres, thats high, its come down to 6 Litres which is good. He’s got a cardiac output of 5. Had a small cardiac output. He's got a highish cardiac output. Slight tacycardia of 102 to 104. His heart rate around the 70, 80, 90. His heart rate is quickly trending up but its not a sustained, it’s a very quick up and down. Axis deviation. I’m looking for the progression of any changes on his ECG, any ischaemic changes on his ECG, scooping in his ST segment – non-specific ST changes. Just to see whether they’ve changed. Heart sounds were alright. I couldn’t hear anything other than S1 and S2. Heart sounds are difficult to assess. Muffled heart sounds. I’m going to listen to his heart for new signs on clinical examination eg a new murmur, gallop rhythm on auscultation. Hard to listen to heart sounds in someone who’s ventilated. Sensed information about anatomy: Look at his x-ray to check heart size. The Echo result from yesterday, showed trivial regurgitation in his tricuspid but no vegetations - we could have seen a bleed around his heart. Get a trans-oesophageal ECHO to look at heart function and his valves Function 1 iii. R2CF1iii) Return Intrathoracic pressure, cardiac & venous pressures Processes associated wityh hydrostatic fluid movement including volume (distensibility) skeletal muscular contraction, ventilation Venous and lymphatic networks, (comprised of endothelium, small smooth muscle, valves) States of gradients: We put two and a half liters in, it didn’t help the circulation or CVP. He was a little bit overloaded with fluid. I was mentally discounting it because he was underfilled. He’s not underfilled and he’s not over filled. He was well filled. States of processes: Happy with his level of filling, he’s been dry, he's been filled. Despite fillling his CVP didn’t go up - the fluids we gave didn’t fill or expand the intravascular compartment. We wanted colloids and blood to fill the vascular space - it didn’t and ended up in the tissues. I know already he’s got oedema everywhere. The fluid's maldistributed, its outside the circulation where its needed because he’s got a leaky circulation. The conc alb didn’t help his oedema at all. The actual volume of water in his vascular system is increasing even though you’ve got an even balance in and out. No swollen feet but hands swollen. Expectations associated with gradients: If his serum albumin was 14 I’d be thinking we’ll fill him with albumin, a colloid because it gives you the best blood pressure in the short term for less fluid. Take fluid from the intravascular space first, then you get a secondary redistribution out of the interstitium according to hydrostatic forces but that doesn’t happen immediately, so it may be that he’s a little volume depleted intravascularly. Water will come into vascular system with the increased plasma proteins. Normal physiology you would within a few hours redistribute body water. His Blood pressure's up - might be just a shift of fluids. A CVP less than 10 will benefit from fluid filling, upto 12 you could probably do it (without affecting the lungs), 12 to 16 might not. A drop in his CVP might reflect underfilling. You can fill people and they don’t actually get a rise in CVP. Low CVP suggests that intravascularly he’s a bit dry. Expectations associated with processes: By 24 hours the colloid particles aren’t being a colloid they’re only a colloid for 8 hours. With synthetic colloids like haemaccel the colloid pull power’s just temporary because once the gel's metabolised it's gone.We could re-start inotropes but before that we’ll probably give him a bit of filling - his CVP was lowish. We dont want to contribute to ARDS by giving him too much fluid. We could start wringing him out to get rid of the oedema. We'll need to reduce the inotropes to do anything with the oedema. You know you’ve got a patient who’s either volume overloaded or in heart failure. If he has a bit of right heart failure in which case filling may not have been a good idea. Perhaps the oedema could have something to do with right heart failure. If we continue to take off fluid then we might have to go back on the inotropes, but this is not desirable. If we dry him out he'll need more noradrenaline. I’ll have to be reasonably cautious with the filling but in turn you don’t want to underfill people. Expectations aassociated with anatomy: It’s the sort of thing you get with a blocked SVC - petechie only happen when there’s venous hypertension like when you leave a tournique up, so that suggests that there’s venous hypertension where the flairing on his abodmen is so I presume there’s some IVC occlusion and he’s got an anastomosis going through to his SVC through his abdominal wall, is it of any relevance to the condition probably not. Goals for gradients: CVP certainly upto 12 maybe even upto 16. Goal is CVP 10+/ - 2. Monitor his filling pressures. They're quite happy with a CVP of 5 so just reduce the maintenance fluids. Goals for processes: Keep him filled for circulation as opposed to drying out to help the lungs. Our fluid management is directed towards circulation.The doctors didn’t want to fill - we've had been trying to unload him. Priority is to dry him out. Keep him dry. Sensed information about gradients: Central Venous Pressure is 10; was higher; up a little; sitting about 8; is low. The PICO as a measure of filling. Looked at his Jugular Venous Pressure to ascertain his fluid status but he’s had so many lines in his neck its all swollen and you cant see his JVP. In some ways I think JVP's better than a CVP. The JVP is up around the ear lobe - he's wet. You cant see it; you lie the patient flat and you cant see it and you tip the patient head down and you still cant see it, then the patients dry. JVP's not prone to technical or reading error - you see a venous pressure wave there or not, but you don’t have as fine control over it.The CVP didn’t seem to be closely related to major changes in his state. Adequate serum albumin. His albumin's 27. Sensed information about processes: I notice we’ve taken off a bit of fluid via the haemofilter in the last couple of days. His fingers are double normal size. Looking at how his arms and legs are elevated. See if he is swollen (feet) or not, no oedema on the legs a bit on the hands but not much. Sensed information about anatomy: We noted a slight venular flairing over the left side of his abdomen its only on one side it’s long standing. I noticed a whole lot of petechei but only on the left. Effectors on Gradients: Colloid is broken down, it only has a half life of 12 hours or less. I’d use Haemaccel. And the idea of the albumin hopefully it’ll tend to stay in the circulation and draw fluid in from the tissues. You use colloids to get that fluid out of those spaces and into the circulation eg concentrated albumin. I’ve already gone down the list he doesn’t need blood he doesn’t need albumin. So the next thing is colloid - Haemaccel. So despite the filling and despite the albumax and concentrated albumin. Effectors on process: Give red blood cells - they’re the best way to fill someone cause red cells stay in the circulation without extravasation. Give intravenous fluid, give him more volume. Dried him out via the haemofilter. We’ve had the filling. He had some cautious filling. One mechanism for getting the noradrenaline dose down is to fill the patient with fluid. We didn’t have to use any GTN or nipride. Reduce his maintenance line down to 40 (ml/ hr ). Intravenous running at 80ml/ hour. Recursion 2 Function 1 (Metabolism ; Ventilation) Function 5. Function 4. Internal / External Executive interface Control gradients Cortical neural Specific neural activation activation and firing thresholds thresholds Physiol processes Processes of Receiving, processing and cognition, redirecting incoming sensory judgement, signals (external and internal) planning. The initiation of voluntary motor movement Anatomic structures Telencephalon Diencephalon (thalmus / hypothalmus) and subcortical structures (eg pituitary, basal ganglia, circinate cortex + Cortical areas associated with sensation and perception Diagnoses Expectations Goals Sensed info Effectors on 1 (Metabolism ; Ventilation) Function 3. (R2VF3) Internal automatic co-ordination 1. H + HCO3 D H2CO3 D H2O + CO2. Diffusion cross cell membranes, chemical activation Respiratory centres of midbrain. (dorsal and ventral respiraoty groups, pneumotaxic and apneustic centres) States of gradient: The patients been relatively stable, not requiring a lot of support. He's not accumulating CO2. He’s trying to clear CO2, he’s breathing up to clear it. His lactate its not contributing to any of his acidosis. He's got more lactate there than can be attributed to his acidosis. We lost his CO2 control - but it was technical. He was over ventilated for the first time. Its respiratory acidosis. Respiratory failure. His pH was within normal limits, he’s maintaining that himself. States of process: Sedated to the point that he could be depressing respiration. He’s not making any effort - he's overly sedated. He wasn’t completely sedated, as he was controlling his CO2 quite well. His respiratory center's working, so his respiratory center, tick. He’s got a strong respiratory drive and wants to breath for himself. He’s maintaining the rate side. His minute ventilation is adequate. He's setting the pace and rhythm of breathing. He stopped breathing for a time. His ventilator support is at low levels its not too bad. His minute ventilation is adequate to his needs. He's breathing some spontaneous breaths by himself on top of the ventilator breaths. With a modest amount of respiratory support, he's coping with quite a large stress. He wasn’t deep breathing enough. Wasn’t taking enough time to breath out – a little bit rushed He didnt cope exturbated. He's on minimal support. Its not normal for him. He’s much better now, he's breathing on his own. He’s not tired. H His blood gases were quite OK for his condition. He seems extremely comfortable. He was mouth breathing. His breathing is fine. States of anatomy: Decreased consciousness and decreased the safety of his airways. Expectations associated with gradients: I think that the sedation is the reason for his carbon dioxide going up. He could do with a bit of CO2 off-loading. The fact that his pH is affected tells you that its not normal for him, I mean if his pH was 7.4 with a CO of 59, 60 well that’s probably normal. We’re in full control of his ventilation, so we’re probably over-ventilating- his CO2's a bit down. He’s not breathing up at all which may indicate that he still needs support to control his carbon dioxide levels. Hopefully his respiratory status will improve so that he’s controlling it himself. Lactate is not a harmful substance - only if its associated with a severe acidosis. Expectations associated with processes: If we increased the sedation, we'd depress his respiratory centres, we'd have to put him on SIMV. We'll just wait awhile for his respiratory center to kick in. He's not breathing himself and I don’t know if its sedation or if we’re meeting his needs-I can only relate that to respiratory depression. He wouldn’t maintain an airway probably if he wasn’t on the ventilator. We’re looking at making progress we should be able to wean him. Couple of principles in weaning - if he can breath himself then why not; if he can do it himself adequately, even better. He may not be getting a chance to breathe, because we’ve set the rate of machine breaths too high. Sputum retention would be the major reason for him not going to the ward.There’s only a very small window in which he can trigger a breath. You turn the machine rate down and the overall rate doesnt change - his underlying rhythm to breath is close to that- You just make more time for him to breath. We don’t have much control over his tidal volumes. At 90Kgs he needs anything from 540 to 650 ml with each breath according to trials. In reality its not always easy to deliver that because we’re using a mode of ventilation (pressure controlled ventilation) where we cant regulate the volume. There’s never been a trial that showed that one regime (volume or pressure control) is better or worse than the other. If he deteriorated he’ll become more ventilator dependent. We extubated him then reintubated- he probably needed ventilating for a longer period. We’re starting to wean, we might be able to get him on CPAP, where he's breathing himself. Hiccoughing is going to be problematic, in that it may trigger a ventilator breath. We may find that he has a breath and a hiccough on top of that and peaks the pressures off and then the ventilator dumps the rest of the breath, so he’s not getting the same tidal volume, so hiccough and receive 200 mls. I hope to see him Expectations associated with anatomy: We think his underlying lung is unchanged but we’re not sure until we solve the technical problem they probably had a circuit leak, so we’re going to have a fresh start this morning. Goals for gradients: In regards to his acid base I wouldn’t mind keeping it within normal limits you know 7.35-7.45. Goals for processes: Start getting him to breath independently, off the ventilator with some humidification. I want to encourage him to breath himself just to maintain his own rhythmicity and also to try and slow down the deconditioning of his respiratory muscles. We can start having time off the ventilator. We want get some respiratory progress so we make sure that his ventilator is allowed to drift down. Sedate him but not to the point where he wont breath. Reduce his sedation and get him to breath a bit for himself, encourage him to initiate his own breaths. Keep him sedated so we can control his ventilation. To deliver the minute volume we're aiming for, he needs to be completely sedated. With that sedation make sure he gets good volumes. We’re trying to get him to breath by himself. We’re going to wait for him to wake-up so we can extubate. Keep him ventilated, we’re in no hurry to extubate. We’re just starting to wean Sensed information about gradients: Gases are stable. His blood pH was 7.5. He’s hyperventilating a bit -his CO2 is down a bit. His pH has been going down in the last 6 hours. His PaCO2s 59 with a pH 7.26, 7.3 - acidotic. He was acidotic last night and he’s still acidotic. Sensed information about processes: An increase/decrease in sedation. When he’s awake he’s fighting the ventilator so he’s not getting the tidal volumes he’s supposed to be getting, its affecting his CO2 and pH. During the night his gas exchange deteriorated, then he was breathing up. His respiratory rate is between 20 and 30 breaths per minute -went up to 30 to 35. He occaisionally breaths-up 2 to 5 breaths himself with good volumes. He wasn’t taking any of his own breaths. Increase apnoic periods, he’s not breathing for long periods of time. He’s breathing too fast, the respiratory rate is up. He became tacypnoeic. I look at him, his rate plus the monitor. He initiates breaths, breathing spontaneously. He's breathing 3 or 4 breaths more than the set rate. I notice that the ventilator set rate is 22 and his breathing rate is 22. The ventilator settings are another set of information and he himself is another set of information. He’s not on a ventilator. His ventilator support hasn’t changed. The ventilator rate, and his own respiratory rate are similar. He’s not on any mandatory breaths, he's breathing spontaneously, setting his breathing rate for himself. He’s making some spontaneous respiratory efforts now. He is spontaneously ventilating. He’s keeping his minute volume at what it was when he was fully ventilated. His minute ventilation is at least twice normal. Minute ventilation’s going up. He's in CPAP mode on the ventilator. He's on pressure control ventilation and he's achieving greater volumes. He's breathing too quickly. He’s able to get off the ventilator. Didn’t need to be re-tubed. It appeared to be spontaneous but the breaths were being triggered by the fluid in the tubing. He looked comfortable - he was coping extubated and he doesn’t appear to have any respiratory distress. Sensed information about anatomy: Mouth breathing. Effectors on Gradients: Requires a high minute volume to keep his pH there. They increased the rate to blow off CO2. Leave the tube in and move to CPAP and pressure support. He will be having time off the ventilator, on CPAP and 5-15 minutes in the hour he’ll be breathing spontaneously with a little bit of extra oxygen. Effectors on process: He’s taking a lot of sedation to control his respiration.The only way we would be able to reduce his respiratory drive is more sedation. CPAP and pressure support breaths, rather than having the machine mandatory breaths.The mode of ventilation is pressure controlled ventilation; the mode is SIMV. We can giving him a mandatory rate, controlled ventilation, or CPAP which supports his spontaneous rate, we haven’t dialed in a pre-set volume for each breath. Put them on some CPAP so that they are breathing by themselves but they’ve got that level of sedation that inhibits that. Sedate him and ventilate him with higher volumes and lower rate. SIMV pressure control mode allows him to take a breath. May have to make the pressure control trigger a little less sensitive. SIMV but only lightly sedated. I turned the sedation down so he'd breath more. Mechanical ventilation. CPAP; pressure support are spontaneous ventilator modes. We set his respiratory rate on the ventilator at 12-13. A rate of 16 means he’s only got about 4 seconds per respiratory cycle and say an inspiratory time of about 1 sec, so he’s only got a 3 second window to breath himself. We’re starting to wean, we’ve turned the rate down to 10. He was extubated. He’s just been on a trache shield. Function 2. (R2VF2) Communication & distribution 1. Neural activation thresholds. 2. Pulmonary artery pressure, left ventricular end diastolic pressure. 3. Gas pressure gradients to atmosphere 1. Neural transmission. 2. Circulation. 3. Inspiration from atmosphere (passive) 1. Spinal cord and autonomic pathways ( glossopharyngeal & vagus). 2. Pulmonary circulation 3. Pharynx States of gradient: Pulmonary hypertension. States of process: He’s fluid overloaded -we’ve pushed to a point of deteriorating another system we cant go any further in that direction ie circulatory filling now causing wet lungs. I think the x-ray is worse because he was pretty positive in terms of fluid balance. Perfusion problems in his lungs didn’t have a cardiac origin. He didn’t develop cardio-genic pulmonary oedema which was our concern. Expectations associated with gradients: Wedge of 18 is generally felt to be the cut- of mark between to distinguish cardiogenic from non-cardiogenic pulmonary oedema. He may well have longstanding pulmonary hypertension then it’d be higher than his normal PA pressure. Older people can have high pulmonary artery pressures.. Expectations associated with processes: We wanted to see if we took off two liters of fluid, his thoracic blood volume index would come down. Now again that x-ray appearance could be due to many things cardiac failure so the water leaks into the alveoli due to hydrostatic pressure, or that its non-cardiogenic pulmonary oedema or ARDs due to leaky capillaries. Once you wean off the nitric you can wean down the FiO2. Acid base, the kidney has a lot to do with acid base metabolism and regulation and if it’s not working then that can be a problem. Goals for gradients: Goals for processes: Dry him out despite his circulation. Dry him out. Make sure he's not too constricted cardiovascularly so he's not ventilating dead space. Pulmonary wise his pulmonary vasculature is actually vasoconstricted. They don’t want him to be too wet. Sensed information about gradients: Arterial / venous gases - venous saturation was 64%, which is quite OK; PvO2 / SvO2 fell down to about 40. His PaO2 is quite low, 50. His blood pH is about 7.26. PaCO2 its normal. The main measure of pulmonary circulatory pressures is the pulmonary capillary wedge pressure (Pcwp). His wedge pressures were generally below 18. The cutoff mark between cardiogenic and non-cardiogenic pulmonary hypertension is a wedge pressure of 18. He’s got a wedge less that 18 Pulmonary artery Pressure (PAP), rhythm and a high wedge. His pcwp was raised except that his PAP diastolic was not so high. PAP are very high- 70 over 35; 55-60 systolic mark. Sensed information about processes: Lung Function in relation to his positive fluid balance. Measure lung water via the PICO. Intrathoracic blood volume index. Instead of it being a right sided measurement like CVP, it’s a right to left, but it doesnt actually tell you whats going on in the pulmonary circulation, it neatly neglects the pulmonary circulation. We didn’t see his thoracic blood volume index come down and we didn’t see any change in him clinically. The normal value's said to be less than 10ml per kilo of body weight per meter squared- its indexed to the size of the patient. We're measuring anything from 18-19 on the PICO, is that very wet or moderately wet there's no data yet to tell us. Effectors on Gradients: Effectors on processes: Nitric oxide has been recognized as a highly specific pulmonary vasodilator. It acts on the Pulmonary vasculature. Nitric oxide causes vasodilation to the areas of the lungs best ventilated . It reduces V/Q mismatch by increasing perfusion at the bases. Because it’s a gas its carried to the bases which aren’t well perfused. Function 1i. (R2VF1i) Ventilation - pressure generation Sympathetic nervous system thresholds associated with neuromuscular activation Rhythmic muscular contraction relations generating cyclical negative intrathoracic pressures Diaphragm, abdominal muscles, intercostal muscles, pleura, ribs sternum, vertebrae States of processes: He has a big mechanical disadvantage to breathe with a distended abdomen so that his diaphragm is being pushed up from underneath. His thorax is being splinted by the mechanical situation. Everything's stacked against his breathing. He's pulling good volumes. His work of breathing's fine - not labouring. He’s doing his own work of breathing Expectations associated with gradients: Expectations associated with processes: We're worried about fluids and stuff collecting in his abdominal cavity and stopping his diaphragm. If he’s guarding his abdomen then his ventilation isn’t going to be as great. His lungs'd be as normal as you'd get if you did a lung biopsy - its a mechanical problem.He wont do any deep breathing, it would effect respiratory muscles, and if he didn’t have a trache he would certainly need one just to reduce the overall work. You find (with ventilation) when muscles have to work a week later they don’t work very well. CPAP probably does keep muscle tone going its probably good. Increased work of breathing would mean faster, but shallower breathing, and lower volumes will go to the lungs, new air wont reach where there’s gas exchange and the breathings too fast for expiration. Goals for gradients: Give him pain control so he can deep breath. Goals for processes: Keep his respiratory muscles functioning keep his muscles toned rather than wasting. Rest him over night. Sensed information about gradients: Sensed information about processes: As work of breathing increases the visible effort to maintain ventilation increases. I’m looking at his chest to see if he's using his accessory muscles. See his tummy moving there, it's a little less tense. Guarding his abdomen. Stomach rigidity. His stomach was quite lax, throughout the night it got a bit tense. It was a little less tense. He’s got a huge cough. He’s coughing. Tidal volumes, between 300 to 500. Tidal volumes are too shallow. His tidal volumes are low. His ability to maintain good volumes. Effectors on Gradients: Effectors on processes: Allow him to exercise those respiratory muscles. Being on a ventilator doesnt exercise respiratory muscles. The ventilator pushes the gas to a set volume so for 700; he doesn’t have to pull it. His respiratory muscles have to generate some degree of effort with CPAP. Well on CPAP his diaphragm still has to generate some negative pressure to trigger for the ventilator. Supported by the ventilator Function 1ii. (R2VF1ii) Ventilation - gas flow Gas partial pressure and temperature gradients Gas flow and distribution, humidification, filtration, expectoration Lungs, pleura, bronchioles, bronchi and upper airways, larynx, pharynx States of gradient: [Gas gradient: FIO2 its down to a reasonable level.] States of processes: [Ventilatory function: His lungs are working pretty well, are pretty good, have been stalwart, they've been great all the way through-the best part. Lung function did deteriorate yesterday. So now I’m saying lung functions good; not too bad. His lung function’s stable. He hasn’t lost anything in lung function although his x-ray’s worse. His lungs are worse than his circulation. His lung functions gone down with an increase in metabolic rate. We had no reserves from a ventilation point of view. He’s got to breath more with stiffer lungs. He’s got an increase in dead space. His compliance is reasonable, not flash. He hasn’t got a wheeze. The airway pressure is generated by coughing. He’s got sputum down there. He’s a mouth breather. He wasn’t breathing to his bases.] [Lung water: I cant continue filling because his x-ray has deteriorated. He’s also fluid overloaded. His lungs will tolerate filling. There's a bit of fluid on x-ray. Although his x-ray’s got worse I caused that (filling) he didn’t do it. Fluid has gone into the extravascular space in the lungs so with filling and deteriorating lung function. His total lung thoracic water was high. Intravascular Water is in his lungs.] [Pathology: He's got ARDS (Adult Respiratory Distress Syndrome).] [Ventilator: He’s still on moderate support. He’s extubated.] States of anatomy:. His x-ray this morning is unchanged. There wasn’t any marked collapse or consolidation. He's got basal consolidation and sputum retention. A bit of collapse in the lung. It looked like a right pleural effusion. Appearance of his lung fields has improved dramatically, which means that theres more inefficient ventilation. But although we’ve lost a bit in x-ray appearance we haven’t lost a significant amount in lung function. He told me he has terrible sinuses. Expectations associated with gradients: [Gas gradients: He’s got a lot of dead space ventilation which means that there’s air being breathed in and out without being exposed to blood for exchange of gas. His oxygen needs would go up. If you put the good lung down, oxygenation would decrease. People can usually deep breath on their side. ] Expectations associated with process: [Pathology: Straight pneumonia from bed rest; ventilator associated pneumonia, aspiration pneumonia during unconsciousness. Some people who are ventilated for a few days, develop ARDS. May have chronic lung disease. His lungs will be a bit stiff. The respiratory response to insult has a lag period of at least 24 hours. Hopefully the adverse response (to surgical insult) is too brief to have affected his lungs. If it was a prolonged insult we'd expect his lung function to go off - it went gone off in the first place in response to insult. The lungs can look disgusting (following ARDS) on x-ray for months even though other things have improved.] [Ventilators: If you’ve got a healthy lung you can just wind up the ventilation to 10 breaths by 700ml but with him 10 by 700 might give him extreme pressures. You use pressure rather than volume control when someone who’s got compliance problems. He’s requiring pressure to open up the lower airways, maybe water on the lungs as well. With low volumes the base of the lungs will collapse. A lot of his problems are due to positive pressure ventilation. Ventilators dont provide therapy, or fix problems with the lungs - mostly it makes them worse. In theory higher ventilator tidal volumes induce sheer that causes damage and can potentiate ARDS. Maybe he’ll get away without having a tracheostomy-he's been ventilated for a week he’s not far off having a tracheostomy. ] [ Lung water: Deteriorating lung function - I cant continue filling. His lungs are looking very wet - will they tolerate fluid filling, or do they need drying. I expected his lungs to be quite noisy, and that he’d be quite stiff in his ventilation.We expected that if we took 2 litres of water off, his lung water would come down demonstrating the validity of the PICO. If you’ve got a patient with florid pulmonary oedema what number will the PICO give to tell us how wet the lung is. I assume anything between 15-20 is wet - overseas units , using the PICO more often haven’t reported those things yet. Could go a CVP upto 12 without harm.] Expectations associated with anatomy: [Airways: Sputum in that instance was causing an obstruction at some point in his upper airway, so inspired gas probably wasn’t getting any further and saturations. Quite often it’s the turn that loosens sputum.] [Lung and pleura: Sometimes if they get a worsening collapse or plural effusion on one side so they're not going to ventilate as well] Goals for gradients: [Gas gradients: Decrease his FiO2 to 40. Start to wean his FIO2. Less oxygen the better. Reduce the FIO2. Improve his oxygenation and decrease his FI02. ] Goals for processes: [Lung water: Drying him out will help his lungs. Dry his lungs out a bit. Take the fluid from his lungs. Make sure we don’t overload him with fluids. I'll dry him out despite his circulation. His lungs are a higher priority at the moment. I’m assessing his lungs suitability for me to intervene further in his circulation. ] [Ventilators: Its time it started going down on his support. Control the pressure in his lung. Turn the pressure support down a little bit. Limit his tidal volumes. Lower his level of PEEP. Try to get his tube out within two or three days. We’re still waiting for nature to do the right thing with his lungs and his kidneys so he becomes independent of the ventilator. Keep him intubated for a longer period of time. Prepare for a tracheostomy. Extubate this morning. ] [ sputum clearance: Big project for the day will be getting his chest right. Clear the sputum in his chest sputum. Being extubated you want to get any secretions up, make sure he’s well oxygenated] Goals for anatomy: [Lungs: We’re supporting his ventilation hopefully in a manner that will not create further lung injury. Prevent lung injury. Get him to focus on the bottom of his lungs. Open all the basal areas. Get him sitting up, to aerate the bases of his lungs so try and get him off the hudson mask which is uncomfortable and get him onto nasal prongs} Sensed information about gradients: [Gas: Only FiO2 = 45%, = 60, =40, =30,oxygen. Increased oxygen. ] Sensed information about processes: [Ventilatory function: He's generating great tidal volumes. Reduced air entry. Decreased air entry at the bases.No wheezes. There wasnt any wheeze or any shortness of breath.] [lung function: If we were able to measure his lung compliance. His lungs aren’t so stiff that he’s pressure limiting before he gets an adequate volume. He’s not requiring a lot of pressure to expand his lungs to 700 or 800ml. ] [Lung water: The PICO measures lung water- whether the lungs are wet.] [Ventilators: On the same PEEP and FIO2. PEEP of 10, of 7. Pressure support of 10. High PIPS (Peak Inspiratory Pressures), around are 28 mark.Tidal volumes vary all the time. His PIPS dictate what volumes he’s getting. His minute ventilation is nearly double. ] [Lung water: Clinical examination - listening to his chest. Crackles ascultated anterior to midzones. Static course crackles. Lung sounds are clear. Lots of noises. Didn’t hear any true crackles. Widespread course and fine crackles. His lungs sounded not too bad. His chest sounded a Air entry is equal to both sides. Decreased air entry to the bases. Quiet in the bases. His chest sounds pretty clear on the right. On the left side there’s a few crackles where he’s had abnormalities on chest x-ray. Bronchial breath sounds in the left base and dull on the right. Just listening for extra sounds, clarity of air entry and symmetry of the breath sounds. He snores a lot. Microbiology from his sputum. The amount of sputum, suctioning up. Huge amounts, frequent, small amounts. Colour of sputum, still purulent looking. MRSA in his sputum. His sputum was clear. He can expectorate it only to a certain point. Time of extubation.You could do dead space measurement using Fowlers single breath washout, nitrogen washout test- done in a respiratory laboratory. He’s got a lot of oral secretions.] Sensed information about anatomy: [Apparatus of ventilation: We looked at his x-ray. Chest x-rays are one set of information. X-ray looked a bit better. X-ray still looks terrible. His lungs on chest x-ray look white. Darker in the lung fields now. On x-ray, we’ve seen an increased density of the pulmonary infiltrates compared to yesterday. Wet/dry looking x-ray. Residual pulmonary oedema on chest x-ray. Basal changes on x-ray. Subtle changes on the x-ray. His left lower lobe looked collapsed, consolidated on x-ray. No collapse or consolidation. Chest x-ray looked like ARDS. The position of the ET tube, ET tube moved forward. Lung biopsy.] [pharynx: Tongue was swollen, it was so oedematous, and dry and he was resisting having his teeth cleaned. He didn’t breath through his nose at all.] Effectors on gradients: [Gas: FIO2 had to go up. Machines giving pressure as well as oxygen. The ventilators giving a FIO2 50%, decrease to 25%. Slowly decreasing the oxygen. He’s on about 60% oxygen and 10 cm of PEEP.] Effectors on processes:[Ventilatory function: We intubated him - because his urea went up and sedation and increased confusion.] [Ventilation: Pressure support. Ventilation regulated by pressure control limit. Ventilatory breath up to the pressure limit; intrathoracic pressure. That the ideal ventilatory strategy is low tidal volume, and emphasis on PEEP to maintain oxygenation Ventilation regulated by a volume controlled cycle- the ventilator pushes the gas to a set volume, so for 700ml he will get around 680 to 700 every time he initiates a breath. Increase PEEP, 5, 8, 10 of PEEP. 15 of pressure support. On high flow when he CPAP’s on the ventilator. PEEP just keeps the airways open and avoids airway collapse. He’s on PEEP. Increase PEEP, 5, 8, 10 of PEEP. 15 of pressure support. On high flow when he CPAP’s on the ventilator. Chest physio, positoning the patient, suctioning, ventolin nebulisers to loosen the sputum. His minute ventilation has had to be increased. A nebuliser in the ventilator circuit and I prefer to use the MDI the medidose inhalers. Suction him and position him.} [pathology: On antibiotic coverage, Vancomycin. ] Effectors on anatomy: We electively intubated him. He had a tracheostomy yesterday- a single lumen tube Recursion 2, Function 1 (Metabolism ; Water & electrolytes) Function 5. Function 4. (R2EF4) Executive Internal / External interface Control gradients Cortical neural activation and Specific neural activation thresholds, firing thresholds concentration gradients (tonicity) Physiolog Processes of cognition, Receiving, processing and redirecting processes judgement, planning. The incoming sensory signals (osmoreceptors). initiation of voluntary motor Secretion of ADH movement Anatomic Telencephalon Thalmus, hypothalmus, Pituitary gland structures Diagnoses Expectations Expectations associated with Gradient: I wouldn’t want to take any more off, because I'm hoping not to send too much of a hypovolaemic signal to his sick kidneys Goals for process: Yesterday we were keen for him to re-establish his own fluid balance; that he should establish his own fluid balance within reason. So when I say we’re trying to get him even balance what I would like him to do is establish his own fluid balance. Goals Sensed info Effectors Function 3. (R2EF3) Internal automatic co-ordination Systemic blood pressure. Concentration gradients - tonicity. Circulating blood (plasma & cells) especially of hormones ADH, Angiotensin II, Aldosterone, Atrial naturetic peptide … Cerebral and systemic circulation (mainly aorta) States of gradient: His urea and creatinine seemed to have tapered in terms of how fast they’re going up. His urea and creatinine is coming down. States of process: Drying him out improved not only circulation but also oxygenation. He's in renal failure, acute renal failure. His figures for renal failure are pretty good, but not good enough to turn the haemodialysis Sensed information about gradients: Urea, creatinine, increase his tonicity. Sensed information about process: Extracellular fluid volume tells me about the Renin -angiotensin system. Function 2. (R2EF2) Communication & distribution - Renal Blood flow Arterial blood pressure, electrolyte especially sodium gradients Circulating volume and flow with renal autoregulatory mechanisms -Senses distal tubule sodium. Renin release. Minor Sympathetic innervation. Erythropoietin production Renal arteries and veins. Afferent / Efferent renal arteries, Juxtaglomerula apparatus, macula densa. Neural pathways (minor motor paths). States of gradient: Hyponatraemia is a problem, essentially we’re loosing salt. States of process: His fluid balance was positive Friday and negative yesterday then his vasculature closed up and he was very positive. He had a big positive. He’s a little bit on the positive side but that’s quite acceptable. He’s two litres negative. I confirmed that he was indeed fluid overloaded. He's not underloaded or overloaded. His fluid volume, he’s dry. Expectations associated with gradient: There is some argument with impending renal failure, that if you keep blood pressure high you maintain renal perfusion etc and prevent renal failure but that’s far from proven. Once you’re in established renal failure I don’t think blood pressure applies and we say that in an adult a mean arterial pressure around 70 should be adequate to most organ perfusion. You can keep the blood pressure up to increase or maintain glomerular filtration rate. Expectations associated with process: We don’t know whether ARF involves maldistribution of blood flow to the kidneys, at a deeper level maybe his kidneys’ look like his toes and kidney circulation is sort of similar to other organ circulations. You can either be depleted in salt, sodium, or Fluid balance reflects many things. He's probably euvolemic. Little and concentrated urine you know you’ve got a profoundly dry, undervolumed patient. I would match what’s going in with what’s coming out - with insensible loss he'll be drying out.You can take off too much fluid and that may compromise him especially his inotrope ceilings.Ureamia - urea accumulates and circulates.They accumulate oedema in the periphery. If the filter wasn’t there, he might go into pulmonary oedema. Reducing the amount of fluid coming off from 200 to a 100 that might help in 4, 5, 6 hours due to fluid redistribution between compartments. He wont be metabolising and getting rid of drugs, they'll accumulate. Patients with acute renal failure often become anaemic because the kidney produces erythropoietin, this is well known in patients with chronic renal failure where the kidneys are small and shrunken and don’t Haemofilters clot and you loose 300 ml of blood each time, there are multiple blood tests. Not sure whether urea is a neuro toxin. Goals for gradients: They want him positive to bring his CVP and BP up to keep his kidney’s flushed - to provide perfusion to his kidneys.. Goals for process: We’re supporting his circulation by trying to balance the fluids. We hadn’t made much progress in drying him out so we set a goal of approximately 150 ml per hour from the haemofilter but realistically you seldom get those goals. Compensate with the dialysis for the amount of fluids he’s getting in. Adjusted his filtrate when we get the TPN and Intralipid going. With his respiratory problems we don’t want him to be overloaded. Aim to achieve that with a status quo fluid balance. Trying to maintain what we call a zero net loss. So we want him filled. I want a positive fluid We’re not going to get his lungs any better unless we dry him out. Removing toxins and pull off fluid to help with the oedema. Sensed information about gradients: He had low sodium. He’s getting hyponatraemic. Sodium tells me about extracellular fluid volume. Sensed information about processes: Looks more swollen. oedematous, tells me a bit about his history of fluid resuscitation in the past few days, how sick he is .He was quite oedematous. The distribution of oedema is pretty much all over the whole body. Pitting oedema. Function 1ii. Filtration Glomerular filtration (Glomerular filtration rate) Urine production via filtration, absorption, secretion, active transport. Two kidneys States of gradient: States of process: Renal impairment. His kidneys aren’t working. About one quarter of renal function. Renal function was all but non-existent. Renal function still hasn’t changed a bit.There was some urine there but not enough . He’s been in renal failure what 5 or 6 days since he came in really. Acute renal failure he’s virtually anuric. He’s become anuric. His kidneys are totally non functioning. He’s still in renal failure. His kidneys will slowly start to work again. He’s making large amounts of urine He subsequently developed renal failure anyway. He's still got a degree of renal impairment. He’s in the polyuric phase of renal failure, so he's recovering. Urinary outputs Ok. His kidney's Expectations associated with process: There’s two components to renal function, fluid management and clearance of metabolic waste products - the two aren’t temporary linked. His kidneys are still being perfused with blood but he has renal tubular damage which will recover. Renal insult takes longer to turn around usually a week to ten days, so we hope his renal dysfunction resolves in the next 48 to 72 hours. He should start making urine anytime over the next few days. You get a return of urine production before you get a return of clearance of urea, creatinine and electrolytes. In two or three days he should start to clear toxins. He's making some urine so if we put more fluid in we can get him to pee it out. With a fluid challenge, I'd expect him to increase his urine. Even if he did have halfway normal renal function, he’d still need drug support.You can encourage the kidneys to work, push them along You might restart dialysis if you have excessive body salts particularly potassium or that there’s build up of wastes like urea and creatinine, or the blood is too acid. Out of control potassium. You can accumulate potassium with acute renal failure - thats dangerous- can cause serious arrhythmias.His kidneys might kick off without the filter. Getting better, he’ll be making large amounts of urine (in polyuric phase), we'll have to give him fluids to keep up. He’s had a huge diuresis so probably going in the polyuric phase. His high lactate would probably be coming from his haemofilter replacement fluid. Indwelling catheters carry risk of infection. You can use the haemofilter to filter off septic mediator substrates, then he’d still be producing urine. He is in renal failure so he wont clear any drugs. Drugs will stay around. If he had one dose today and two days later he still had plenty of drug, it confirms that his kidneys aren’t working well at toxin clearance. He has only some clearance of sedatives, morphine, and antibiotics like Goals for processes: We don’t want to give this guy too much fluid because he’s in renal failure and cant get rid of it. We don’t want to stop the Lasix which we’d started the previous day to get him to make urine. Aiming for about 150 ml/ hr urine output. Keep his urine up. Make sure that that he’s making urine. Aiming for at least 150 ml/ hr of urine. Take a break - leave his dialysis running until about an hour or two before surgery, then disconnect it. We don’t want to go back on the dialysis machine. So a total of about 1litre off via the haemofilter in the next 24 hours heading for a zero balance. Monitor fluid balance and urea and creatinine to see that the filter is helping. Prevent the haemofilter from packing up, keep it working to optimum, keep it from clotting up and clagging -get as much filter life as we can out of it.. To get him negative. Try to dry him out. Sensed informtion about process: His water/fluid balance- 6 hourly total balance. He’s about 3-4 liters positive of fluid in the last 18-24 hours. Fluid balance is inaccurate, the most accurate would be a daily weigh. Its too hard to weigh him so we have to rely on nurses counting what goes in compared to what goes out. His U&Es’ (Urea and Electrolyte) biochemistry had got down to almost normal. Creatinines about 240micmols; ureas about 30. Generally used a number of urea greater than 40mmol. Levels of urea and creatinine are coming down. Urea and creatinine was quite low. Degree of uraemia, how high your blood urea and creatinine are. The rise and fall of creatinine each day is no longer an indicator of renal function due to haemofiltration, they’re static. He’s got a return of urine production. Looking at his urine output. Initially he was anuric. He had no urine output. He still has non urine output. His urine output is dropping off. His urine output is low. His urine output was between zero to 10 ml/ hour. He every Ultrasound his bladder to see if there’s urine there. Ultrasound showed very small amount of urine, we’ll checkpassed 1.5 litres overnight. He’s got a return of urine production. I noted that he’s been making about 80 or 100ml/ hr of urine and just in the last 2 hours it was 30 or 45ml/ hour. Looking at the amount of urine from the kidneys - he’s making between 100 and 200mls/ hr of urine. He was actually making good volumes of urine. Urine output hasn’t changed for the last two or three days despite being off the haemofilter. The haemofilter.You get an hour output with the haemofiltration. Filter flow’s. I can see we're taking fluid off. The amount coming off the haemofilter. Electrolytes tell me tell me how well we’re filtering. Urea and creatinine are a flat line - its no longer an indication. He’s off the haemofilter. Change in his levels of drugs such as Vancomycin give you some degree of indication about his renal Effectors on process: Dry him out by taking off fluid via the haemofilter.You’re removing urea and creatinine plus its removing patient fluid. So we’ve got to manipulate his fluids he’s on 120ml/ hr of fluid input, 60 via the nasogastric and 60 via the IV. We could reduce his fluids by dropping his input. They're taking 50mls, 100 mls, 150 ml, 200mls per hour via the filter., but we’re only removing 50 mls per hour when you take into account his input. We could restart dialysis to get rid water. Take a bit more fluid out. They took too much fluid off. We couldn’t return the blood in the haemofilter back to the patient, so we ordered replacement blood. You lose about 300ml of blood when you change the filter. A urinary catheter was inserted. The filter was stopped yesterday. Use a diuretic, then can get him off his dialysis. Lasix at 25mg/hour IV. A smaller dose of a Lasix infusion. Instead of writing up a regular dose, we the dialysate and replacement fluid wont be dose and thereafter different to levels. You can vary concentrations of decided to give him just a on-off vancomycin heated. Filter using aaccordingmethod, you’d use pre-dilution for septic mediators to try and pull the larger molecules off rather than pull off your electrolytes. Haemofilter wasnt running with heparin. He’s not having any dialysis. They’d put in a vascath and haemofilter. Decided to leave the urinary catheter in to see if he's making urine. They turned off the anti-coagulation. PRISMA GAMBROS filtration units. They didn’t want a lactate free regime. Function 1iii. Elimination Pressure gradients (distention) Peristaltic contractions moving urine in forward direction Calyxes, ureters, bladder, urethra Recursion 3, Function 2 (Communication & Distribution) Function 5. Executive Function 4. Internal / External Function 3. Internal interface automatic co-ordination Control gradients Neural activation thresholds Neural activation thresholds, pressure Central pressure and in receptors and concentration gradients volume gradients Physiolog Activation of Cardiac and 1. Neural transmission. 2. Processes associated processes Vasomotor centres in Circulation. 3. with central pressure and response to sensory inputs Hormone secretion volume gradients - preload, Starlings Law Anatomic Cardiac and vasomotor 1. Motor & sensory pathways of spinal Arterial and Venous structures centres in medulla and pons. cord and peripheral autonomic networks, heart. Sensory pathways of nervous system.. 2. Glossopharyngeal, Vagus Circulating blood volume (plasma and and Herings nerve. cells). 3. Adrenal medulla Diangosis Expectations Goals Sensed info Effectors Function 2. Communication & Function 1i. (R3CF1i) distribution Distribution 1. Regional and local pressure Local plasma concentration gradients (eg oxygen, nitric oxide, hydrogen) and concentration gradients. 2. Neural activation thresholds 1. Circulation including Vasodilation and constriction via local autoregulatory mechanisms circulating vasoactives (eg catecholamines). 2. Regional/ local neural transmission 1. Systemic and regional Arteriolar, terminal arteriolar & capillary networks circulatory networks. 2. Some autonomic pathways especially of the Vagus nerve States of gradient: He’s got peripheral circulatory embarrassment or failure. States of process: His circulation is not getting to the periphery . He’s peripherally shut down. Using noradrenaline to the point of peripheral ischaemia. He’s not at that point but he’s telling us its an adverse effect. Blue fingers are not quite as bad as yesterday. His hands have deteriorated. His feet are blue. In spite of a cardiac output of 5 he’s still got blue toes. We've got increased permeability. He's got a leaky circulation associated with his acute illness. We Expectations about gradients: Expectations about processes: If he’s got peripheral shut down in his skin he's likely to be shutdown elsewhere in his other organs as well like his liver and kidneys. The skin - is perhaps representative of other organs. You can get digital ischaemia and necrosis. The blue fingers are relevant to the side effects of the noradrenaline. You can have ..noradrenaline with pink blue extremities. Cooling a patient can give you cold fingers as well. In maldistribution the body behaves as if parts of it are not being perfused, and this is a loss of control, regional blood Goals for processes: Yes that (Adrenaline) was to spare the blue fingers. Reconstitute those capillary membranes. Sensed information about gradients: Sensed information about processes: He’s got warm brisk capillary return. I can see he’s got blue finger tips. Look at his feet slightly blue nails. Looking at his other extremities. He’s not on Adrenaline - he hasn’t had blue fingers. Sensed information about anatomy: He’s got petechiae all over his belly. Effectors on Gradients: Put more blankets on he’s got a big cooling device there as well. Effectors on Processes: Adrenaline doesn’t cause as much peripheral constriction as noradrenaline but may be more chronotropic. Normal saline has shifted through the extracellular compartment. Function 1ii. (R3CF1ii) Rhythmic conduction Neural and neuro-muscular action potentials Polarisation, depolarisation of the conduction system triggered by SA node, Sino-atrial and Atrioventricular nodes, Bundles of His, Purkinje fibres, myocardium States of process: He is/was in Atrial fibrillation (AF). He's been having atrial ectopics and he had a bout of AF. He’s trying to go into AF, he’s just niggling away. He’s in asort of Atrial flutter. Recurrent AF. His AF is significant. He’s not in AF anymore. It wasn’t uncontrolled. His AF was quite controlled it wasnt a rapid rate. He’s in sinus rhythm. He's reverted back to sinus rhythm He had some AF during his highly septic phase. Expectations about gradients: I want to know what his potassium is knowing he has bouts of AF. A too low K can lead to arrythmias and leaving it too high can be fatal AF suggests cardiac irritability especially if magnesiums low. AF - I'd watch his blood pressure, because with AF he'd lose his atrial kick - less volume will go to the ventricle and the blood pressure drops. Loss of atrial kick reduces atrial filling time. If you’re BP's not compromised and the rate is acceptable you can live with that. In AF he'll require more noradrenaline; aboutthan sinus rhythm. Him being in sinus rhythm will his rhythm - the sodium/potassium Expectations more processes: Potassium's important for stabilising help me to reduce the pump. I'd know something was happening if he started having regular Ventricular Ectopics (VEs or PVCs). If his rate got up over a 125, 130, I'd be concerned that he was changing his pattern. I’m assuming that he has an inherent tendency to AF but he’s not in it for a cardiac reason, it was triggered by his sepsis. He’s a chronic AF. He’ll revert to sinus rhythm with amiodarone. If he got worse I'd revert the AF with DC shock, especially since he's on Amiodarone. If his AF got any faster, uncontrollled, you’d be considering other antiarrythmics. Goals for gradients: Make sure his K and Magnesium are normal. Goals for processes: Keep an eye on his heart rate knowing that he’s been in AF. Maintain him in sinus rhythm and monitor that. Keep him in sinus rhythm so we can get the norad down. We want to get the amiodarone off. Stop his amiodarone once AF has reverted. We’re keeping the amiodarone. Sensed information about gradients: Rapid rate AF which was compromising his BP. I’ll check his K and magnesium. Sensed information about processes: Amiodarone - he’s had some rhythm disturbance. He went into AF. He's still in AF. He went back into sinus rhythm for a couple of hours. Set my alarm rate at around 100, in AF it was around 120 130. He reverted back to sinus rhythm about midnight. Past history of AF. Rhythm stripe, you just look at the monitor. He was AF, Atrial Flutter, AF, Atrial Flutter. Looked at the 12 lead ECG to confirm that he is in AF. The arrythmias and the antiarrhythmic agents. From his ECG I noticed that his cardiac rhythm has improved. He had about the first 4 or 5 days of sinus rhythm. Effectors on gradients: Effectors on processes: Amiodarone, for his rhythm disturbance. Give a bolus of amiodarone. He’s still on theAmiodarone infusion to keep the levels up, but it has a long half life. We’ll turn off the amiodarone and see what his rhythm does. Start back on amiodarone or something else like digoxin. On a daily amiodarone. Gave him some amiodarone to reverted him back to sinus rhythm. Amiodarone’s a wonderful drug for acute use. I don’t tend to continue it on for a prolong period, so I would use it for the acute period and be quite happy to stop it and get them to earn further doses or further treatment. DC - shock. Zap him if amiodarone Function 1 iii. (R2CF1iii) Return to vascular compartment hydrostatic pressure, osmosis and diffusion gradients Hydrostatic fluid movement, solute diffusion, osmosis, active transport Interstitial venuole and lymphatic networks States of processes: He’s got quite a bit of peripheral oedema, he’s very oedematous. Possibly a bit more today. The flank oedema is dependent oedema. Expectations about gradients: In peripheral oedema there’s either an increased pressure favouring outward filtration of fluid. A bit of extra protein probably wouldn’t hurt to draw that fluid out. Expectations about processes: If the level of oedema increases then it could be the immune response - he'd have leaky capillaries. Colloids have no problems crossing leaking capillaries, red cells shouldn’t cross, they're too big to get through capillary pores, they'd have to break down. Most of the colloid's finished up outside the vascular compartment and hasn’t had a significant impact on intra vascular volume. Sensed information about gradients: Sensed information about processes: He's got petechiae all over his belly. He’s still got quite a lot of oedema. Yes, he’s very swollen. So I cant see his feet but I can see his oedema. His hands have got oedema so I’m seeing if its four limb oedema…his oedema was the same. I’m noting that he’s got oedema in his flanks now. He looks peripherally oedematous He’s still got quite a lot of oedema. Oedema is acceptable Effectors on processes: Albumin or a colloid to shift fluid into the intravascular space. I would have thought albumen. Recursion 3, Function 1 (Metabolism Ventilation) Function 5. Function 4. Internal Function 3. Executive / External interface Automatic co- ordination Control 1. H + HCO3 D 1. Neural activation Local neural gradients H2CO3 D H2O + thresholds. thresholds and CO2. 2. Pulmonary artery circulatory pressure , left pressure ventricular end gradients diastolic pressure Physiolog Diffusion cross cell 1. Neural Regional processes membranes, chemical transmission. brochodilation/ activation 2. Circulation. constriction Anatomic Respiratory 1. Spinal cord Larynx, structures centres of and autonomic trachea, midbrain. (dorsal pathways. bronchi and and ventral 2. Systemic upper respiraoty groups, venous and respiratory pneumotaxic and arterial tree apneustic networks incl. centres) heart Diagnoses Expectations Goals Sensed info Effectors lism Ventilation) Function 2. (R3VF2) Communication & distribution Gas partial pressure and temperature gradients. Transpulmonary circulatory pressure gradients Gas flow and distribution, Pulmonary circulatory blood flow. Physiological shunt. Lungs, pleura, bronchioles, bronchi and upper airways, larynx, pharynx . Pulmonary circulatory network States of process: His working diagnosis is ARDS. In other words fluid has extravasated from capillaries into his alveoli. Dead space ventilation at the alveolar level is one of the criteria for ARDS diagnosis. ARDS is tending to resolve. He went into APO yesterday. Expectations associated with gradients: I was expecting that he would not be oxygenating that well. Expectations about process: It could be a ventilation perfusion mismatch, there are other things that come into play besides, besides the ventilation. If you have leaky pulmonary capillaries you have water leaking out into the lungs- He's 4 liters positive- that’s one reason why his lungs might be a bit wet. If you're volume overloaded a proportion of that will leak out into the lung tissue, lung parenchyma. If he’s overloaded his gas exchange wouldn’t be as good. In ARDS you can get high pressures because the volume of lung water increases, it leaks out of the pulmonary capillaries into the alveoli. Its takes time for the fluid to go from the lungs back to the vascular system and for his Inspiratory pressures to come down. Expectations associated with anatomy: I think there are a lot of microthrombi in the micro pulmonary vasculature so a proportion of the alveoli have vessels that are thrombosed. We don’t want to cause any further any lung injury. Goals for gradients:Keep his SaO2 between 88 and 92 Sensed information about gradients: Saturations better 99 to 100 compared to 94 to 96. His oxygen requirements have come down. The parameters on his blood gas analysis were improved. His gas exchange wasn’t that different. Effectors on Gradients: PEEP open and avoids airway collapse which minimizes VQ mismatch at the lower end of the respiratory tree. Effectors on Processes: Nitric oxide crosses the pulmonary capilliary membrane there it acts on pulmonary vasculature causing vasodilation Function 1i. (R3VF1i) Alveolar gas exchange Gas partial pressure gradients Diffusion Terminal bronchioles, alveoli (incl surfactant) , alveolar membrane States of gradient: His overall oxygenation has been good. He’s required less oxygen to maintain arterial oxygenation within adequate physiological ranges saturations etc. Well his PO2 is good. His oxygenation went off. His oxygenation has remained satisfactory. His oxygen requirements are fine. Expectations associated with Gradients: Desaturation curves, affected by haemoglobin, temp. Expectations associated with process: Oxygenation will go off over at least a 24 hour period following the initial ARDS response. However we just needed to confirm in our minds that it was in fact ARDs. So we think oxygenation going off was to do with leaky capillaries ie ARDS. Goals for gradients: Improve his oxygenation, decrease his FI02. Goals for process: Reduce the FIO2 so you want a saturation around 90, 91 92. Goals for anatomy: Open the lower airways especially in the basal area. Keep more alveoli recruited for tomorrows extubation. Sensed information about gradients: His oxygenation ratio to his inspired oxygen concentration is improved. On 40% and a PaO2 of about 100 so that’s fine. Low Sats… But his oxygenation got better over the course of the night. A PaO2 of 140 or so, Sat’s are 100%. Sensed information about process: His blood gases during the day are perfect and saturation 99%.We want PO2 around 60s, 70's and now is around 70. His PaO2 is quite OK. Effectors on gradients: FiO2 can go up or down depending on PaO2 and SaO2 Function 1ii.(R3VF1ii) Capillary gas exchange 1. H + HCO3 D H2CO3 D H2O + CO2. 2. HbO D Hb + O Diffusion / dissociation. Pulmonary capillaries, capillary membranes, plasma, red blood cells States of gradient: His minute ventilation was inadequate for CO2 clearance. States of process: His CO2 is OK. He doesn’t really need a ventilator. He has an increased blood carbon dioxide Goals for process: To eliminate his carbon dioxide Sensed information for process: His PaCO2 went up even further. Carbon dioxide is starting to increase. PaCO2 has gone up from 56 to 67. Effectors on process: Minute volume and rate. His minute ventilation has had to be increased to reduce his CO2. Recursion 3, Function 1 (Metabolism: Water & electrolytes) Function 5. Executive Function 4. Internal / External Function 3. Internal interface automatic co-ordination Control gradients Cortical neural Specific neural activation Regional and local activation and firing thresholds, concentration arterial blood thresholds gradients (tonicity) pressure gradients Physiolog Processes of Receiving, processing and Blood flow under processes cognition, judgement, redirecting incoming pressure. planning. The initiation sensory signals of voluntary motor (osmoreceptors). Secretion movement of ADH Anatomic structures Telencephalon Thalmus, hypothalmus, Interlobar arteries & Pituitary gland veins Diagnosis Expectations Goals Sensed info Effectors Function 2. Communication & Function 1i. Filtration distribution Colloid osmotic Interstitial osmolarity, tubule solute concentration gradients (Na, K, HCO3, gradients between H, H2O, Glucose, amino acids) intracapillary space and interstitium Collect water and Diffusion, osmosis, secretion, absorption, active transport, acid/base solutes reabsorbed from buffering Loop of Henle Peritubular Capillaries Renal Cortex Nephrons : mainly proximal, distal and collecting tubules States of process: He doesn’t need that much Lasix. Renal figures his biochemistry are quite stable morning. The Haemofilter wasnt commenced for renal failure, but for acid-base. Renal failure can m high 9 or 10. Expectations associated with gradients: That will lead to what we call a naturesis or reduction, ex response in terms of the sodium of giving lasix by infusion. It has a variable effect. In some people th because you get rid of more water than sodium, in some like here it goes down cause you’re getting r we're seeing here-excreting sodium and the body not being able to pull that back because there’s stil Expectations associated with process: His requirement for Lasix to maintain his urine output is les him Lasix and see what happens.You’ve got the potential for overdoing it with the Lasix or more likely and loose potassium. His excretion’s is going to be slowed up a bit. Urinary output may have fallen be we might recommence the frusemide. You can push them along with drugs such as Lasix, which ind Goals for process: We don’t want to stop the Lasix. Start weaning the Lasix as tolerable - he needs Sensed information about gradients: His urea and creatinine were really high. The blood results, th normal limits as well. His urea, creatinine and potassium was elevated. His potassium was high. Sod Sensed information about process: Water clearance. His urea and creatinine are from the morning Effectors on gradients: He’s off his lasix infusion. Intermittent doses of frusemide, through his IV. I .He was on 25mg, 45mg of frusemide, Lasix. Titrating the Lasix to urine output. A smal dose of a La process: No fluid challenges. The filters’ been functioning to normalise U&Es. The haemofilter was bicarb. The filter’s not really there for water its to get rid of the nasties urea and creatinine. While the being maintained as good because of the haemodialysis machine. Function 1ii. Elimination Concentration gradients. Counter current multiplier mechanism. Diffusion (urea, H2O, Na), Active transport (Na, Cl, HCO3, Ca, Mg) Renal medulla Nephrons: descending and ascending Loop of Henle ures his biochemistry are quite stable but they’re not brilliant. Renal numbers haven’t improved this ut for acid-base. Renal failure can make him acidotic. He had a metabolic alkalosis. Lactate’s quite we call a naturesis or reduction, excretion of sodium in the kidneys. Now there’s a variable a variable effect. In some people their sodium stays normal, in some people it tends to go up e it goes down cause you’re getting rid of more sodium proportionately than water. That's what to pull that back because there’s still tubular dysfunction. six to maintain his urine output is less which means his kidneys are getting better. We could give rdoing it with the Lasix or more likely underdoing it. Now we're giving Lasix he's likely to diurese bit. Urinary output may have fallen because the lasix has stopped. If his urine output remains low with drugs such as Lasix, which induce them to get rid of water. ng the Lasix as tolerable - he needs to maintain a urinary output. were really high. The blood results, the urea was within normal limits and creatinine was within vated. His potassium was high. Sodium and Potassium are normal. and creatinine are from the morning blood tests. doses of frusemide, through his IV. I noticed that his Lasix infusion had been stopped 4 hours ago. to urine output. A smal dose of a Lasix infusion. He had a bolus dose of Lasix. Effectors on rmalise U&Es. The haemofilter was started for acid base balance. The filter’s taking off too much sties urea and creatinine. While the figures are good we cant turn the machine off. Figures are e.