The practicalities of starting ICU call and the fundamentals of care for ICU level patients

Dr Peter Mc Cauley SpR in Anaesthesiology Version 1.0, March 2020 The practicalities of starting ICU call and the fundamentals of care for ICU level patients

Disclaimer The author has made every effort to ensure the accuracy of this booklet. However, given the time sensitive nature of the COVID-19 pandemic, this booklet version 1.0 has been released ahead of schedule, to make it available as soon as possible. All efforts to proofread and edit the contents have been made and users of this booklet should do so in conjunction with all official guidelines, policies and resources as appropriate.

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Table of Contents Introduction ...... 4 The ICU Referral ...... 5 The practicalities of intubating in ICU ...... 9 Setting up for the night ahead! ...... 12 Ventilation ...... 14 Mechanics of ventilation and gas exchange ...... 14 Peak, mean and plateau pressure ...... 21 Modes of Ventilation ...... 24 Non-invasive Ventilation (NIV) ...... 27 High Flow Nasal Oxygen (HFNO) ...... 30 ARDS...... 31 Recruitment Manoeuvres ...... 33 Ventilation in the Prone position...... 34 Inhaled Nitric Oxide (iNO) ...... 37 The ABG ...... 38 Vasopressors, inotropes and inodilators ...... 41 Dialysis ...... 45 Sepsis ...... 51 Shock ...... 54 Sedation and analgesia in the ICU ...... 56 Nutrition in the ICU ...... 59 Care Bundles ...... 61 Common ICU conditions on call ...... 62 Delirium ...... 62 Lactate ...... 63 Tachycardia/PVCs ...... 64 Temperature spikes ...... 65 Blood transfusions ...... 66 Ventilator dysynchrony ...... 67 End of life Care ...... 69 The Cardiac patient ...... 70 The Neurosurgery patient ...... 75 Conclusion: ...... 81

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Introduction Initially this booklet was designed for those about to be put onto the ICU rota (usually anaesthetic trainees). Now this booklet is also written considering the potential heath crises we face with the arrival of COVID-19 to Ireland. For most, even with anaesthetic training, starting ICU call is an incredibly stressful time. Essentially, you’ve been in theatre every day with assigned Consultants on-site, who are commonly present for most inductions, especially any sick or unstable patients. Now, you are being thrust into the realm of ICU. You are expected to manage the sickest patients in the hospital, often having to intubate haemodynamically unstable patients with a Consultant who is off-site, or busy elsewhere. These are the very patients you wouldn’t be inducing alone in theatre. However, now you have to, sometimes in unfamiliar environments like the wards, the Cath lab, or ED! This is particularly true of COVID-19 patients. Furthermore, we may end up in a situation where non anaesthetic trained NCHDs (whilst not expected to intubate) may have to look after critically ill patients (who would otherwise be in ICU), titrating vasopressor support and oxygen therapy. Anaesthetic trainees may find themselves directing this care. Of course, it may be stressful, but remember the vast majority of trainees will not only get through it, they will thrive on it!

The following booklet is designed to familiarise you with key concepts of ICU care, the practicalities of being on call, and to provide clinical pearls and tips for dealing with everyday ICU on-call issues. In reality, it’s not all about assessing sick patients on wards or ED; a lot of ICU call involves housekeeping issues – charting fluids, electrolytes, blood etc.

Already, the response of medical and nursing staff to the outbreak of COVID-19 has been inspirational, between those in isolation willing to come back to work as soon as feasible, and those who have been incredibly flexible with work patterns to ensure continuation of high-quality care. I must also, personally, commend the Anaesthetic Department in CUH, who to date, have shown excellent leadership, and a genuine care and empathy for both patients and staff alike. I would like to thank them all for their support in this endeavour. I have no doubt we will face this challenge together as a medical community, provide the best care we can for ourselves, and our patients, and ultimately come away stronger for it.

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The ICU Referral What patients need to come to ICU In a nutshell, patients who require organ support over and above that which can be given on the wards. (Please understand that what we consider normal ward level care now, may change in the context of COVID -19.) Another important category here are patients who are at significant risk of deterioration, where a period of intensive treatment now may prevent a prolonged ICU admission later. These patients may not need immediate ICU transfer but likely will in the near future. This presents a potential window of opportunity to admit them to ICU now, in an effort to prevent a deterioration in the very near future (typically in the next hours or days) that will result in a more prolonged ICU stay. This is particularly true of COVID-19 patients. You do not want to intubate unless you have to, but remember that intubation itself is considered source control, and it may be wise to intubate early, if you feel the patient is ultimately heading that way.

Firstly, let’s look at categories of patient care. You will likely hear the phrases like ‘level 2’ or ‘level 3’ care. But what does that mean?

Levels of Care: · Level 0 – patient can be cared for on a general ward · Level 1 – the patient is either at risk of deterioration or has just stepped down from higher care. These patients should be treated on an acute ward (e.g. an observation ward) · Level 2 – the patient needs more frequent obs, or support for a single failing organ or is postoperative. This category also includes patients who have stepped down from a higher-level care. HDU care could be considered level 2 care. · Level 3 – patients requiring advanced respiratory support (i.e. intubation) or patients with 2 or more organ failures. This is ICU care.

You are likely to be involved in level 2 care and definitely involved in level 3 care in ICU. These are HDU and ICU patients respectively. If COVID-19 becomes widespread, it is likely non-anaesthetic staff and trainees may have to care for at least level 2 patients on the wards, and possibly level 3.

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So, how to assess how sick patients are and what level of care they need? When called about an ICU review, make sure to get as much information as possible over the phone. Although you might feel like you’re interrogating the person on the end of the phone, it is crucial for the following reason: · Whilst it helps you form an idea of how sick the patient is, you may have a whole host of other tasks awaiting you, or indeed other patients to review. It is important to get as much information as possible so that you can prioritise your tasks. Therefore, don’t be shy about asking for clinical information.

If patients are being referred to ICU it is because they require management not achievable at ward level. They will largely, although not entirely, fall into the following broad (and often overlapping) categories:

· Low GCS/not protecting their airway –? needs intubation · Respiratory failure -? needs intubation · Low blood pressure –? needs vasopressors · Severe acidosis/renal failure -? needs dialysis.

We will deal with each of these topics, and others in more detail later.

So, if patients are referred to you, you should at least get (or be given): · Detailed history and details of clinical findings. Ask for current observations – HR, BP, O2 saturations · You should also have relevant investigations – which should include bloods at a minimum and should also include a CXR, particularly if respiratory failure is the reason for the consult (unless so urgent and acute that there was no time e.g. a patients GCS is suddenly 3, they are peri-arrest etc.) · You should also have ABG (or VBG) results in practically all cases. Whilst it will obviously give information on respiratory status, measurement of lactate is a vital component in the assessment of sepsis. It will also provide information about the patient’s metabolic status (very relevant in all critically ill patients). · You should also be given an indication of fluid balance and trends of urine output. Patients sick enough to warrant ICU review should have a catheter and an accurate fluid balance chart commenced, if there is not already one being documented.

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Your job when reviewing the patient is a global review of the patient and a determination of whether the patient can be managed on the ward, or whether they need ICU care. If they need intubation, vasopressors, dialysis etc, this decision is usually easy and obvious. Cases are often more nuanced, and quite often you will decide that a trip to ICU now for 24 hours may prevent an ICU admission in 2 days that may last weeks. You may see an opportunity to pull a patient out of a potential spiral. Recognising this comes with experience.

The investigations and observations are objective facts and they may clearly point to the need for ICU care. However, you may find yourself in situations where the observations aren’t too bad, but you just don’t like ‘the look’ of the patient. Trust your instincts. Seek advice early and do not refuse an ICU admission without discussing it first with your Consultant. No Consultant (no matter how much you think they don’t want to be contacted) wants to come into work in the morning and hear form a Medical or Surgical Consultant that their patient arrested on the wards, having been reviewed by ICU on the wards but not admitted to the unit. Always take heed of the nurses, they usually know the patient the best out of anyone. Sometimes the patient will visibly deteriorate before the observations show it, and the nurse, having been with the patient, is your clue to this. A concerned nurse, therefore, should always be taken seriously.

So, in summary, use the objective evidence and trust your instincts. As a rule of thumb – if you walk away from a situation thinking “I wonder if I should” then the answer is you should!! If you think “I wonder should I bring that patient to ICU” then you should.

Remember that younger patients, and particularly children, will compensate for a long time with normal observations, but will ultimately decompensate very rapidly when they do decompensate. Older frail patients may also decompensate quickly, but often have little compensation, so the warning signs will be there earlier as a continuing decline.

Do not fall into the trap of grading your patients in severity of sickness. We all (at least subconsciously) wonder if the ward patient is worse than any of our current ICU patients. As you become more senior, it is an important skill to have, as it is vital for bed management issues. However, when starting ICU call, this is not your concern and it should not factor into your decision-making. You must first decide whether the patient warrants ICU care. If the answer is yes, then and only then, can you worry about the logistics of how that happens. This will usually involve bed management and your Consultant. This will become especially relevant if there is a sustained outbreak of COVID -19. We may have to use the PACU and operating theatres for ventilated patients. There will be people whose job it is to decide who goes where. Your job will be to decide if someone warrants intubation etc.

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Lastly, if you think a patient might need to come to ICU, but equally might not after a specific treatment (e.g. bolus of fluids) then follow up post intervention to make sure the patient has actually improved. You might think the ward will be proactive in keeping you in the loop. Quite often they’re not – the nurse has other patients and the Medical Reg is now busy in ED etc. Just because you’ve heard nothing, do not assume things have improved.

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The practicalities of intubating in ICU (See COVID -19 suggestions at the end) It’s now you truly realise you’ve gone from theatre, where you’ll often have a Consultant present, anaesthetically trained nurses, plenty of space, and a well patient that came in for some minor procedure, to the sickest patients who need ICU care. You might be on the wards and have a frail elderly patient, with saturations of 92% on a non-rebreather mask and a blood pressure of 72/46. Now you have no Consultant on site, your space is severely limited, there are nurses running everywhere (trust me this happens!) and there are machines beeping in your bay, the bay next to you and so on, just adding to a cacophony of noise and distraction.

Your job is to control as much of the environment as you possibly can. Make sure you have all your airway equipment, and all the monitoring you would like. Move the bed away from the wall and make sure you have enough space to intubate. Make sure you know who’s giving the drugs, who’s doing cricoid pressure etc. Plan it in so far as you can with people having clearly identified and assigned roles.

Clinical Pearls: Firstly, ask yourself why am I intubating this patient? Is it for respiratory failure, airway protection etc? Answering this first question will inform the answer to the second – how quickly do they need to be intubated? Does it need to be done on the ward? Maybe you have time to get to ICU which, although not theatre, is at least more controlled! Do you have time to get help? Even if you think you don’t have time, someone can arrange for help to be on the way as you proceed.

Tips and tricks: · Intubate in a familiar environment – if you have time (and unless the patient is peri-arrest you do!) bring the patient to ICU/theatre first!! In over 5 years of ICU call, I can count on less than 2 hands how often I have intubated on the ward. · Unless you are intubating in a hurry, put in an arterial line first!! (if you have time to bring them to ICU, then you very likely do!) Patients will become haemodynamically unstable at intubation, so having an arterial line is invaluable. · If you need help, don’t be afraid to ask. It is NOT a sign of weakness, but rather of strength. · Don’t underestimate the value of pre-oxygenation. Hold the facemask tightly – if you get good bag movement awake and a good CO2 trace on capnography, you are more likely (but not guaranteed) to be able to bag post induction, should the need arise. · Have the bougie open and out. They only cost a few cents, and they take longer than you think to get out of the package and ready, and that can be vital in a rapidly desaturating patient.

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· Pre-form the bougie by creating a small anterior curve in it. Yes, they have a curve at the end already, like a hockey stick. However, I would advise to curve the entire bottom third of the bougie anteriorly. Why? Because the likely reason you are going to need a bougie, is for an anterior larynx. · Use what you are familiar with. Don’t use a McGrath for the first time intubating an ICU patient. The technique is slightly different, and you will find yourself with a wonderful view of the larynx and an inability to place the tube. Remember, the McGrath becomes essentially useless in situations of vomiting and high secretion loads, blood etc.

And now the big question – what drugs do I use? What’s the dose? This one comes down to experience. There is no dose/kg or a combination of drugs to be given. However, the following is some helpful advice.

LESS is always more in ICU. You can give more of a drug, but you can’t take it away once it’s given. Patients in extremis with a low GCS will likely NOT remember an intubation, even if you gave them no drugs. Whilst in theatre your priority is to safely intubate and prevent awareness, in ICU your role is to KEEP THE PATIENT ALIVE. In most scenarios their brain will be scrambled, and they will be haemodynamically unstable. I have intubated with no drugs, except muscle relaxant (colloquially referred to as the ‘strong arm and an apology’ technique. Alternatively, using lidocaine in a ‘spray as you go’ technique is also an option.)

It might seem obvious to say, but give drugs close to the cannula site, not further up through a 3-way tap with lots of dead space to pass through before it reaches the patient.

Unless I am worried about raised ICP and intracranial bleeding, I usually give boluses of phenylephrine or ephedrine, or both, before giving any induction drugs. Alternatively, in a very unstable patient you can run a phenylephrine infusion peripherally (or indeed noradrenaline peripherally, through a large cannula for a short period of time) or noradrenaline centrally.

What if the peripheral noradrenaline extravasates? Whilst not a desired outcome, it’s still better than doing CPR. Again, your job is to safely intubate whilst keeping the patient alive.

It is important to be wary of a distressed patient with a blood pressure of 90/50. This blood pressure is with distress – a sympathetic surge. Administering sedating drugs removes this sympathetic drive and can cause a precipitous fall in BP. Yes, patients have arrested following only 1mg of midazolam and nothing else.

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In theatre you give fentanyl to offset the stimulation of intubation. In ICU that stimulation is your friend. It increases the blood pressure. You’re not trying to cause the patient any pain but causing some discomfort they won’t remember is a lot better than asking colleagues to start CPR.

Your first attempt should be your best and you give yourself the best chance with a fully relaxed patient. Use suxamethonium or rocuronium unless contraindicated. The DAS guidelines support this view. Despite almost all ICU intubations being rapid sequence, it is reasonable to attempt 1 or 2 bag mask ventilations at low pressures and low volumes while waiting for the relaxant to work. The advantages are several fold. It provides a little more oxygen, but more importantly it tells you that you CAN bag-mask-ventilate the patient. Now when you go to tube you can relax a little bit knowing that in the worst-case scenario, you can definitely bag the patient. But what if you couldn’t when you tried? That was without an OPA, or an LMA or a 2-hand technique – so you still have many options should you need to bag. Furthermore, the muscle relaxant will be working by then which is likely to help. (obviously this is not the case during this upcoming COVID-19 outbreak)

Always use capnography. Believe me, the CO2 colourimeter is useful, but in a large patient who will temporarily desaturate no matter how quick or good your technique, and who will also take a while to recover saturations, you do not want to be second guessing the placement of your tube, particularly if it was a tricky tube with a bougie and limited views.

So, in summary: As giving drugs goes, less is more · Limit dead-space when giving drugs · Stimulation can be your friend in ICU · Beware the distressed hypotensive patient · Always use capnography

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COVID – 19 intubations: · Full PPE for all cases – includes full face visors, as well as goggles. Intubation is high risk for infection. · Pre-oxygenate with a tight mask. Avoid NIV/airvo for this if possible. Give at least 5 mins. True COVID-19 patients are likely to have significant lung disease, be very PEEP dependent and will desaturate rapidly. Pre-oxygenate sitting up to improve FRC as much as practical. · Avoid bag-mask ventilation if possible. This is where prolonged pre-oxygenation is important. If absolutely required – use low tidal volumes. · Be careful with doses of induction agents as above, but give adequate doses of muscle-relaxants. (experienced anaesthetists could consider giving muscle relaxant first followed by induction agent in particularly high-risk cases – to reduce the time from apnoea to intubation.) · Do not start ventilation, or bag the patient until the cuff is fully inflated (and make sure fully inflated, not air slowly in, as done in theatre)

Setting up for the night ahead! The evening handover is the most important interaction you will have on your ICU call shift. It will entirely determine the flow of your night and its direction. Facing into a night without any available ICU beds is very different to knowing you have 4 potential beds if needed (hopefully not!). During your evening clinical handover of patients, ensure you ascertain the following:

· If someone is very sick, what is their escalation protocol – are they for full resus etc? · If someone is dying, what is the palliation plan? – e.g. extubation, wean vasopressors, start subcutaneous infusions etc. · Who are your dischargeable patients? and in what order? Can they go to a ward? Do they need to go to PACU/Recovery, or need a telemetry bed etc?

Some general points! In general, call your Consultant or the 3rd on if you are not sure about anything. When you are more experienced, you may discuss at the handover round with the Consultant what things to call about. For example, a Consultant may be happy for you to admit and treat a simple respiratory sepsis needing intubation etc without the need to ring them.

If you see a patient who needs ICU treatment and is likely to pass away before the ICU Consultant would get to review them on a morning ward round, then inform the Consultant overnight.

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Keep it Simple! The key to surviving those first few months of ICU is to keep it simple. Yes, ICU involves complex patient cases with advanced and complex care needs. However, the treatments overnight can be simplified as: 1. Patient has respiratory failure or decreased consciousness level. They need intubation and ventilation 2. Patient has circulatory shock and requires vasopressors/inotropes. They need a central line and art line 3. Patient has acute renal failure or severe metabolic acidosis and needs dialysis. They require a vascath.

Believe it or not these are things you can already do before starting in ICU. You may not have put in a vascath, but it is effectively a large CVC. (see dialysis section for more on this).

Whilst an oft frowned upon sentiment, your basic job overnight is to “keep them alive ‘til 8.05.”

If you can intubate and ventilate, put in a CVC and maintain a blood pressure with vasopressors/inotropes, and insert a vascath overnight for urgent dialysis, you will very likely keep the patient alive overnight!

The other components of care (e.g. antibiotics, fluids, blood etc) are all things you’ve been doing since internship anyway. The more nuanced ICU-specific issues are covered later.

ICU call is as much a state of mind as it is clinical acumen and skills. You really can simplify ICU in your head to the above interventions. You can perform most, if not all of them already. Therefore, if you can keep it simple, you’ve half the battle won already. Hopefully doing this will demystify ICU call.

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Ventilation Mechanics of ventilation and gas exchange This is a massive topic and it’s easiest to begin with basic MCAI level physiology.

At its simplest level, ventilation involves the movement of gases down a pressure gradient into the lungs where gas exchange occurs, followed by the release of gases out. Normal inspiration creates a negative pressure (i.e. sub atmospheric) so the gas moves into the lung. This is an active process all of the time. Expiration involves the recoil of diaphragm and lungs and is usually passive. It can however be active (for example in asthma when someone is working hard to overcome the bronchoconstriction in expiration). In situations where the patient can’t breathe for themselves, and we need to ventilate them, we can’t create the negative pressure that they do. Instead we use positive pressure to create a gradient and inflate the lungs – hence the term Intermittent Positive Pressure Ventilation (IPPV)

So, what are the factors involved in oxygenating the patient? 1. How much gas gets in? The amount of effective gas exchange depends on several factors: Fio2 - How much Oxygen are we breathing in – if we stood in a room with no oxygen, our bronchi and alveoli could be working perfectly, be beautifully compliant – but we’d still die rapidly. Clearly then, the Fio2 is important. On the wards, you’ll meet patients with pneumonia, pulmonary oedema etc. These conditions interfere with gas exchange by creating increased ventilation/perfusion mismatch. Put simply, these are areas of the lung that are receiving blood flow (perfusion) but no gas exchange – this is known as a shunt. The patient’s effort, or work of breathing, might be normal, but their saturations might be low because of ineffective gas exchange. Here increasing the Fio2 may restore oxygenation effectively. But what if we give someone 100% oxygen (Fio2 1.0) and they’re only taking shallow breaths, or are really struggling to breathe? They won’t maintain their saturations for long. Increasing the Fio2 alone will not work. This brings us to point 2 – the mechanics of ventilation.

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2. The pressure gradient created. Recall from basic physics that: Pressure = flow x resistance This is a critical concept and not that hard to understand. It stands to reason, that at a constant pressure, the higher the resistance, the lower the flow rates. So, if one whole lung is plugged off, there will be higher resistance and consequently less flow of vital gases at a given pressure. If we rearrange the formula, we find that: Flow = Pressure/Resistance So, in order to maintain flow in higher resistances, we need to increase the pressure. This is the key concept behind positive pressure ventilation. We are providing a pressure gradient to allow ventilation (i.e., the FLOW of gases into the lung to achieve a volume of gas in the alveoli). How much pressure we need depends on several factors, especially the resistance. The highest-pressure value in the gradient we create is known as the peak inspiratory pressure. (PIP)

Therefore, it is fair to say that the flow of gases down into the alveoli is based on: Flow = pressure (that we dial into the ventilator i.e. the PIP)/ Resistance (both from the patient and ventilator tubing, size of the ETT etc)

Smaller ETTs have higher resistance. Imagine trying to blow a paper ball off a table using a straw. The smaller the straw, the harder it is – you need to create more pressure (by blowing harder) to move the ball.

Longer ETTs also have increased resistance. Imagine trying to blow the ball with a 10cm straw versus how much pressure you’d need if the straw was 10 foot long. The longer the tube, the bigger the dead-space This is why many intensivists cut ETTs – it reduces the dead space AND plays a small role in decreasing resistance.

So, the rule of thumb in ICU is a large tube (bigger than theatre) and cut short (unless contra-indicated e.g. where the face is going to swell as in severe burns)

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3. Alveolar pressure So now we have created a sufficient pressure gradient to overcome resistance and create enough flow for gases to arrive in the alveoli. Alveoli behave as spheres, so the pressure now needed to inflate the alveolus to a given volume now depends on the compliance in the following relationship: Alveolar pressure = Volume/compliance.

Again, this is easy to understand – if I only want a small volume, I don’t need as much pressure to achieve it, all things being equal. So, the higher the volume needed, the higher the pressure needed to achieve it. Compliance – how compliant the alveolus is (i.e. how easy does it expand for us). Very compliant alveoli at constant pressure achieve better volumes, and poorly compliant lungs need higher pressures just to achieve the same volumes. So in order for gases to get in, we require a pressure gradient to allow flow and overcome the resistance of the tubing (and the bronchi and bronchioles), and we also needs a pressure gradient to fill the alveoli with volume (which depends on how compliant the alveoli are)

Volume itself is important too. A patient is going to have better oxygenation if they breathe in 500mls of oxygen compared to 50mls. If their tidal volume is too small, they will desaturate quickly, even on 100% oxygen. So…the amount of pressure you need to achieve effective gas flow and alveolar expansion (effective ventilation) is:

Airway pressure = flow x resistance + volume/compliance

4. PEEP PEEP is positive end-expiratory pressure. Normally, at the end of expiration, alveoli return to baseline pressure. With PEEP, we maintain a constant pressure at the end of expiration, not allowing it to fall to 0. So, with a PEEP of 5cm water, there is a minimum pressure of 5cm in the alveoli at the end of expiration. Similarly, a PEEP of 10cm will maintain a pressure of 10cm at the end of expiration.

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Now you might say that for flow you need a pressure gradient and you’d be right. You might also say that if you have a PEEP of 10cm (meaning the lowest pressure at the end of expiration is 10cm water, not zero) you will surely need even more pressure to keep the same gradient – i.e. you will have need a higher PIP. Your logic would be the following:

If effective ventilation was achieved with a peak pressure (PIP) of 20cm and PEEP of 0 (a gradient of 20cm water) then surely a PEEP of 10, needs a PIP of 30 to maintain the gradient?

This is not quite the case for the following reason: The hardest part of blowing up a balloon is at the very start with no air in it, and at the very end, when its already full. It’s much easier to inflate a balloon when there’s some air already in it.

Therefore, by splinting the alveoli open with PEEP we make them easier to expand with the next breath. This improves the compliance of the alveoli and this makes them expand easier. Recall from earlier that with better compliance, higher volumes are achieved for the same pressure.

So, putting it together – yes, we have increased the pressure at the end of expiration, in theory meaning we need higher pressures in inspiration to maintain a gradient. However, because the alveolar compliance is improved, less pressure is needed in the alveolus to expand it and we need less of an overall gradient! We therefore use PEEP to improve alveolar compliance and to prevent alveolar collapse. So, the total airway pressure is actually:

Airway pressure = flow x resistance + Volume/compliance + PEEP

Airway pressure = pressure needed to overcome resistance in tubes + pressure needed to inflate alveoli + PEEP

Patients in respiratory distress are often working hard at breathing – here they are working to create as much negative pressure in inspiration as possible (remember atmospheric pressure stays the same) – this will create a larger pressure gradient allowing more gas flow. More flow equals higher volumes. Therefore, they are working hard to increase their tidal volumes.

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You’ll also see them in a tripod position, or pursed lip breathing. This represents the patient attempting to create their own PEEP, turning expiration into an active process. This can expend a lot of energy and cause them to tire quickly. As you know, oxygen is required for aerobic respiration, so the more energy used in active expiration, the more oxygen required, and consumed by the patient. This creates an increasing spiral where low oxygen levels are causing the patient to increase their work of breathing, but increasing work of breathing uses up and requires more and more oxygen. This is how patients can rapidly decompensate.

So now we see that PEEP increases compliance and can reduce the work of breathing. Remember, blood flowing to a collapsed alveolus does not partake in gas exchange (shunting). But if you manage to keep the alveolus open with PEEP, it will partake in gas exchange and therefore improves ventilation-perfusion (V/Q) matching and hence oxygenation.

5. Time Another important concept is time. This is also logical. A breath in lasting 3 seconds is going to allow more oxygen flow and higher volumes than a breath lasting 1 second. This is referred to as inspiratory time and forms the I part of the I:E ratio.

The I:E ratio refers to the relative lengths of inspiration and expiration. An I: E of 1:2 means that 1/3rd of the breath is inspiration and 2/3rds are expiration.

An I:E ratio of 1:4 is 1/5th inspiration and 4/5ths expiration and so on…!

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Now that we know how ventilation works, we can work out different ways to increase the amount of oxygen going in by manipulating things like pressure, volume, time etc. We can therefore increase oxygenation by: · Increasing Fio2 · Increasing airway pressures to allow more flow, overcome resistance or further inflate alveoli resulting in higher volumes. (in practice this refers to mean airway pressure – we will discuss this below) · Increasing tidal volumes (instead of increasing the pressure to achieve this as in point 2). This works for patients with small tidal volumes of <4mls/kg and is ineffective at tidal volumes >4mls/kg. · Using PEEP. This improves alveolar compliance. Decreasing the work of breathing may also decrease the patient’s oxygen consumption and thus their O2 requirement. It helps improve V/Q by reducing shunt and increasing mean airway pressure. · Prolonging the inspiratory time. This allows longer inspirations, allowing more time for oxygen to get in. · In clinical practice, increasing Fio2 and PEEP are the most common and important interventions we use to increase oxygenation.

What about eliminating CO2? Firstly, remember that there is anatomical and physiological dead space. This is important to remember. Let’s say the dead space is 150mls and your tidal volume is 200mls. You only have 50mls of effective gas exchange. If you have a respiratory rate of 12, this gives effective minute gas exchange of 50mls x 12 = 600mls. If you increase the rate to 20, its now 50mls x 20 = 1200mls But what if you increased the tidal volume to 550mls? Now you have effective gas exchange of 400mls per breath. Keeping the rate at 12, our effective gas exchange is now 4,800mls (4 times higher than if we had just simply increased the rate. Thus, effective ways to improve CO2 elimination include: · Increasing the tidal volume (it may not change the dead space in real terms i.e., it’s still 150mls, but it massively increases effective gas exchange). However, in practice we ventilate almost all non-head injury patients with tidal volumes <6mls/kg. · Increasing respiratory rate – allows more CO2 to be exhaled. · Prolonging the expiration time (the E part of the I:E ratio) – allowing more time for CO2 to be exhaled · Reducing dead space – strategies included improving V/Q matching by using PEEP like we mentioned above. · Cutting the ETT to reduce the anatomical dead space (although the effect is likely to be small)

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· In practice, increasing the respiratory rate is the most commonly used intervention.

So now you know how to increase oxygenation and improve CO2 elimination. But remember that it can be difficult to do both at the same time. Prolonging the expiration time, must by definition reduce the inspiration time. Let’s work through an example of this.: If the RR is 12, then each breath cycle lasts 5 seconds. (60sec/12 = 5secs) If the I:E ratio is 1:2, then 1.66secs are inspiration and 3.33seconds are expiration If you keep the RR as 12 but increase the I: E to 1:3, then only 1.25secs are inspiration and 3.75 seconds are expiration. This could be problematic if oxygenation is an issue.

Now assume we keep the I:E ratio at 1:2 but we increase the RR to 20. Now each breath lasts 3 seconds (60sec/20 = 3secs). Now we only have 1 second of inspiration and 2 seconds of expiration.

Thus, you must remember that altering settings may have consequences you may not consider or desire. This is why you will often hear a PO2 of 8kPa and a PCO2 of 8kPa is acceptable. Chasing a lower PCO2 in a hypoxic patient may make the hypoxia worse. This is the nuance of ICU. You can learn the theory and know the ways to increase oxygenation or eliminate CO2. The true skill is in balancing your approach to achieve a safe and effective level of both, not necessarily a textbook idealistic result.

From a practical viewpoint being on call – clearly poor oxygenation will kill a patient quicker than hypercarbia, therefore your initial priority is always oxygenation. When this is restored, you can then tweak things to address high PCO2s.

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Peak, mean and plateau pressure Peak Pressure This is the highest pressure in inspiration and known as the peak inspiratory pressure, as outlined above. The peak pressure is only transient in nature, and is not the pressure throughout the breath cycle. This is instead known as the mean airway pressure.

Mean Airway Pressure Using a simple analogy of blood pressure, the peak inspiratory pressure is analogous to systolic pressures, whereas your mean airway pressure is analogous to your mean arterial pressure. We know it is the mean arterial pressures that are important for perfusion. A BP of 120/10 will have poor perfusion despite the systolic pressure, whereas a BP of 120/80 will be much better – owing to the higher mean arterial pressure. In the same way, it is the mean airway pressure that is important for oxygenation. To finish out the analogy, PEEP is like the diastolic pressure.

So, what’s the plateau pressure, and why bother with it? Remember, mean airway pressure is the mean pressure throughout the entire breath cycle. Remember also that airway pressure is: Airway pressure = flow x resistance + volume/compliance + PEEP.

So, it’s a combination of pressure needed to deliver gas flow to the alveoli and then pressure to inflate the alveoli. A peak pressure of 30cm water in a totally obstructed airway is being used entirely to overcome resistance, and none of it is getting to the alveolus. So how do we know how much pressure is in the alveolus?

The factual answer is we don’t. But if we don’t have any flow, then by and large, the pressure left, is the pressure within the alveolus. Therefore, if we do an inspiratory hold (allow a breath in and then hold that breath) we find a plateau pressure. Essentially, we have inflated the lungs and then stopped all flow. No pressure is required to overcome resistance and provide flow, so the pressure measured at end inspiration with no gas flow is used as a surrogate marker for alveolar pressure.

From a clinical viewpoint this is important. If your peak and plateau pressures are roughly the same, then there isn’t much resistance to flow. If the peak and plateau pressures are both high, then that must mean high pressures are needed to inflate the alveoli.

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If, however, the peak pressure is very high, but plateau is not, then a lot of the pressure is being used to overcome the resistance to flow (in the airways) – this is the scenario you see in asthma.

What is intrinsic PEEP? Imagine you blow air into a balloon. There’s a narrowing of the balloon stem so only a small bit gets out, leaving some behind. Now you blow more air in, and again only a small bit gets out leaving even more behind. Clearly the volume of the balloon will continue to increase as you are being continuously left with more and more air in it. This air creates a pressure inside the balloon. This is the exact same with the lungs. If air is trapped in the alveoli (e.g. in the case of bronchospasm where narrowing bronchi prevent the outflow of air) then that trapped air increases and creates its own pressure. Remember that by setting a PEEP, we intentionally leave air in the lungs to help compliance.

But also remember, that the other difficult time to inflate a balloon is when its already full. So too much PEEP can worsen compliance. PEEP generated from air trapping over and above any PEEP we set on the ventilator is known as intrinsic PEEP.

Therefore, the total PEEP = PEEP + intrinsic PEEP.

How do we know if there is intrinsic PEEP? Again, remember simply, that PEEP is the pressure at the end of expiration. So, if we allow an expiration and then hold the breath, allowing no flow, then the pressure we record is the pressure at the end of expiration (I.e. the PEEP). If we had set a PEEP of 5cm water and the pressure on an expiratory hold is 5cm water, then there is no intrinsic PEEP. If, however we set a PEEP of 5cm water and the PEEP measured on expiratory hold is 12cm, then there must be intrinsic PEEP.

Total PEEP = PEEP + intrinsic PEEP. Therefore, if Total PEEP is 12 and set PEEP is 5, then intrinsic PEEP must be 7cm water.

Just as an aside, and for completeness, if you have massive gas trapping, you increase the volume in the thoracic cavity, thus increasing the pressure. This in turn decreases the venous return and can cause significant haemodynamic instability up to and including cardiac arrest.

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Clinical Pearl: If you intubate an asthmatic (and you really don’t want to unless you have to!) and they suffer a cardiac arrest immediately post intubation, you should disconnect the ventilator or C-circuit and push on the chest to expel any trapped air and rule that out as a cause.

Why does all this even matter? Surely you just dial up a pressure and a volume you want to ventilate the patient at and once you don’t go too high on volumes and pressures, everything will be ok? Not quite! Increasing evidence points to a condition known as Ventilator induced lung injury (VILI) from inappropriate ventilator settings. That’s beyond the scope of this but it is important to know that ventilators, whilst vital for keeping patients alive, can cause lung injuries too.

Furthermore, most will be familiar with the concept of lung protective strategies, especially in ARDS. The rationale for this is quite simple actually. In ARDS, you have some alveoli that are very stiff and non-compliant, and some alveoli that are quite compliant. Therefore, if you use really high pressures to try to inflate the non-compliant, stiff alveoli, the compliant alveoli will massively inflate at those same pressures and cause lung injury. Hence, for ARDS, we use a combination of restricted airway pressures, and low tidal volumes to prevent lung injury due to variable compliance of different parts of the lung.

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Modes of Ventilation From theatre you will almost certainly be familiar with:

· Pressure control ventilation (PCV) · Volume control ventilation (VCV) · PSV Pro (also known as Pressure Support in ICU – PS for short) · PCV-VG (Pressure control ventilation – volume guaranteed. In ICU this is known as PRVC – pressure regulation volume control, but is essentially the same thing)

Modes you will be less familiar with:

· SIMV – (synchronised intermittent mandatory ventilation) · CPAP/PS (continuous positive airway pressure/pressure support) – a commercial example you may have heard of is Bi-PAP.

Pressure Control. Put simply, you set up the inspiratory pressure, the respiratory rate and PEEP. Because the pressure is fixed, the actual tidal volumes themselves may vary (not ideal where you want to control the TV closely e.g. ARDS) Usually, slightly better tidal volumes are achieved for a given pressure in this mode. So, a peak inspiratory pressure (PIP) of 20cm water may achieve a tidal volume of 420mls, whereas if you used volume control, setting a TV of 420mls may require the machine to produce a PIP of 24. This becomes important at the higher ends of peak pressure.

There are modes (depending on the ventilator) that allow assist modes. Here you dial in your desired PIP, RR and PEEP as normal. If the patient attempts to breathe, the ventilator will assist the patient’s breath, rather than initiating its own. If the patient’s respiratory rate is higher than what you set, there will be no initiated breaths and only patient assisted ones. If the patient’s respiratory rate is lower, there will be some assisted and some ventilator-initiated breaths.

Volume Control Here, you set up the tidal volume, respiratory rate and PEEP. The ventilator will use whatever pressure necessary to achieve this tidal volume (subject to an alarm limit that acts like a circuit breaker. If the PIP alarm is 35cm water and the tidal volume you dialled in requires more pressure than that to achieve it, the breath will cut off once 35cm is reached). So, while the tidal volume is relatively fixed, the pressure is the variable here. Again, like the pressure assist modes, there are volume assist modes that work in the same way, Due to the different variables, the risk of PCV is volutrauma, and the risk of VCV is barotrauma.

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PRVC This simply combines a set tidal volume, at the lowest pressure to achieve it, and tries to combine the best features of both PCV and VCV without the risks of volutrauma and barotrauma. In this mode you set the tidal volume, respiratory rate and PEEP, just like VCV, and the machine will do its best to keep the pressure as low as possible.

Pressure support The patient breathes themselves. Here you set up the respiratory pressures. Instead of setting a PIP, you set a pressure that will be used to support the breaths that the patient initiates. You do not set up a respiratory rate – it is dependent on the patient initiating breaths. You also set the PEEP. (It’s essentially like Bi-pap but with a tube in, rather than using a mask). So, the key difference between this and PCV is the lack of a back-up RR being set. Most ventilators will default to a backup mode if the patient doesn’t breathe but don’t assume this!! The endotracheal tube and breathing circuits have inherent resistance so patients generally need a minimum pressure support of 5-7cm even when breathing well, just to overcome this resistance. It is unusual to leave a tubed patient on just PEEP. At this point it is useful to clarify the subtle difference between PEEP and CPAP. PEEP is positive end expiratory pressure and applies the set pressure at the END of expiration. CPAP is continuous positive airway pressure and ensures this pressure is maintained throughout the breath cycle – inspiration and expiration.

SIMV (Synchronised Intermittent Mandatory Ventilation) In many ventilators, this is used as the ‘assist mode’ in PCV and VCV. Recall above that you can have assist modes in both PCV and VCV. Remember, this mode either initiates breaths itself, or assists patient breaths depending on the circumstances. Some models of ventilators use SIMV instead. Like the MV bit suggests, it delivers mandatory breaths (in the event the patient doesn’t initiate a breath themselves.) Like the synchronised suggests, it synchronises with the patient if they do initiate a breath and therefore this mode can both initiate and assist breaths. The mandatory breaths can be in volume control or pressure control mode, and the assist mode is usually in the form of pressure support. So…

In SIMV-VC – (that is SIMV – volume control) the mandatory breaths are volume controlled and you therefore set the tidal volume, respiratory rate and PEEP just like volume control ventilation. If the patient’s breaths exceed the rate you set, they will be assisted breaths and how assisted they are depends on what pressure support you set to assist them (just like the pressure support mode above). So, in essence, you have volume control ventilation and pressure support modes running at the same time. Only pressure support mode will be used if patient is breathing themselves, and volume control mode will kick in if the patient is not breathing at all. A combination of both is used if the patient is breathing but at less than the rate you dialled in.

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In SIMV-PC – (that is SIMV – Pressure Control) the mandatory breaths are in pressure control and the assisted breaths are in pressure support mode. Which mode is active is exactly as above depending on the patient’s own respiratory rate.

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Non-invasive Ventilation (NIV) (you may hear the term ‘Nippy’ in ICU to mean this also)

CPAP or CPAP/PS? Remember from above, CPAP is continuous positive airway pressure (slightly different to PEEP). It is very useful in type 1 respiratory failures, especially pulmonary oedema.

CPAP/PS is bilevel positive airway pressure (a commercial trademark you may be familiar with is Bi-PAP, however, it is more correctly termed CPAP/PS.) It is comprised of inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). This is analogous to the CPAP/Pressure Support mode of a ventilator. An IPAP of 20 and EPAP of 6 is the same as CPAP of 6 and PS of 14 (since 6+14 will give and total inspired pressure of 20). Similarly, an IPAP of 10 and an EPAP of 4 is analogous to CPAP 4, PS 6. Continuous positive pressure is applied throughout the breath, as in CPAP, with additional pressure provided to assist inspiration, hence bi-level. CPAP keeps the alveoli open to prevent collapse and increase compliance.

The additional pressure provided during inspiration assists the breath and helps in several ways: · It increases the tidal volume and provides more pressure to the lungs, improving flows and alveolar volumes. The higher volumes will improve both oxygenation and CO2 removal (it improves CO2 removal by reducing dead-space and reducing V/Q mismatching). · It reduces the work of breathing. This helps decrease likelihood of patient fatigue and also reduces O2 consumption and requirements. · It is therefore useful in type 1 and type 2 respiratory failure as it facilitates improved oxygenation, decreased work of breathing and increased CO2 elimination by decreasing dead-space and improving V/Q matching by reducing shunt.

Advantages include: · Non-invasive - therefore no sedation required · Avoids risks associated with intubation. May avoid intubation altogether. · Can be managed on the ward

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Indications: · Hypoxia despite a high Fio2 (type 1 respiratory failure) · Hypercarbia (usually above 8kPa) but chronic type 2 patients may have a baseline PCO2 above 8kPa · Mild respiratory acidosis · Weaning from mechanical ventilation

Contraindications: · Needs to be urgently intubated – due to severe organ dysfunction of severe haemodynamic instability. · Unconscious (or the old adage – GCS below 8, intubate!!) · Severe agitation (will not tolerate a tight mask needed to create a seal) · Severe acidosis – intubate instead · Inability to get/maintain a seal – orofacial abnormalities, agitation as above. · Recent Upper GI surgery, especially involving anastomosis. · Pneumothorax, pneumomediastinum etc · If COVID-19 suspected, and likely to ultimately need intubation, consider early intubation.

Practical aspects: NIV takes time for a patient to adapt to. Typically, it is described as the feeling of breathing with your head sticking out of a fast-moving car (not recommended). It requires a tight seal for the generation of pressure, and this can be uncomfortable for patients. In some cases, it can cause skin breakdown and ulceration. NIV can cause stomach inflation (hence the contraindication in recent GI surgery) and increase risk of aspiration. You should consider the placement of a wide bore NG on drainage to prevent this.

Although patients can be managed on the wards on NIV, frail patients may benefit from ICU transfer for a number of reasons. The 1:1 or 1:2 nursing care can often ensure better patient compliance from coaching, positive reinforcement etc. It also allows the placement of an arterial line, facilitating repeated sampling and changing settings. It can also allow you to judiciously use titratable sedation (e.g. a dexmedetomidine infusion) to tolerate the mask. NIV will cause increased aerosolization in the case of COVID-19 so be cautious. You will recall from earlier chapters that increasing airway pressure will increase oxygenation whilst increasing inspiratory pressures will generally increase tidal volumes, also improving oxygenation.

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Therefore, to address oxygenation you can: · Increase Fio2 · Increase PEEP (EPAP) (improves alveolar compliance, prevents collapse, improves V/Q matching) · Increase IPAP – increases tidal volume, reduces work of breathing

To increase CO2 elimination, you can: · Increase PEEP (EPAP – improves atelectasis, improves V/Q matching) · Increase IPAP – increases tidal volume which can reduce dead-space, improving gas exchange.

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High Flow Nasal Oxygen (HFNO) HFNO is designed to provide high Fio2, and high oxygen flow rates. The delivered oxygen is warmed and can have almost 100% humidification. It is usually well tolerated by patients, particularly in comparison to NIV. Whilst standard nasal cannulae provide 1-4L/min and facemasks up to 15L/min (think your non-rebreather) – HFNO can provide up to 60L/min

What are the perceived advantages of HFNO2? 1. Tolerance - although not universally so, HFNO is usually well tolerated by the patient, especially in comparison to NIV. 2. Humidification and warming. This helps with tolerance. It also helps with O2 consumption. Normally we are nasal breathers – during nasal breathing we warm and humidify the air. This requires energy. Respiratory distress results in higher breathing flow rates (meaning more gas to warm and humidify) and often results in a switch to oral breathing (bypassing the usual nasal method). This results in increased consumption of O2 and energy expenditure in an attempt to warm and humidify the air. HFNO is thought to help in this regard. 3. High Fio2. Remember from basic physiology that a driving flow of oxygen will entrain air (and by doing so reduce the Fio2). High flow rates limit entrainment and therefore achieve a higher Fio2 4. Reduced dead space. The high flow rates facilitate CO2 washout and create a reservoir of oxygen in the respiratory tree. This reduces dead space. 5. The high flows cause expansion of the upper airways. Some of this is transmitted to the lower airways. It is thought that each increase in flow rate by 10L results in an equivalent PEEP of 1cm H20

Who to consider for HFNO? · Patients with type 1 respiratory failure · As an aid to intubation – especially in the obese or pregnant patient, or a potentially difficult airway (see the THRIVE study) · During the extubation process. · It is particularly useful in paediatrics. The ‘dose‘ is 2L/kg

It might sound obvious, but do not persist with either HFNO or NIV in a patient that should be intubated. It may buy you a little time to perform a controlled intubation, but it should not alter your decision to intubate in those who warrant it.

HFNO will also increase aerosolization in the context of COVID-19.

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ARDS Acute respiratory distress syndrome is characterised by: · Acute onset – within 1 week · Bilateral chest opacification on imaging, not explained by effusions, collapse. · Not attributable to cardiogenic pulmonary oedema, fluid overload · A Pa02/Fio2 (P/F ratio) of <300mmHg.

What’s a PF ratio? It’s the ratio of PaO2 to the fractional inspired Fio2. For example, a patient with a PaO2 of 10kPa on room air is very different to a patient with a Pa02 of 10Kpa on 100% Oxygen. The P/F ratio therefore considers the amount of oxygen we are giving the patient to achieve the measured Pa02. Remember, that to change from kPa to mmHg, we multiple to a factor of 7.5

So, a Pa02 of 10kPa = PaO2 of 75mmHg Now we divide that by the Fio2. Let’s say it’s 0.4 75mmHg/0.4 = 187.5. Therefore, our P/F is 187.5 If, however our patient is actually receiving an Fio2 of 0.8, then their P/F is: P/F = 75mmHg/0.8 = 93.75

· P/F of 200- 300 is mild · p/F of 100-200 is moderate · P/F <100 is severe.

This makes sense. Our first patient had a PaO2 of 75mmHg (10Kpa) on an Fi02 0f 0.4 which is moderate. Our second patient has the same Pa02 but requires much more oxygen to achieve this and is clearly sicker. Their P/F is 93.75 and they are in the severe category. Getting into the pathophysiology of ARDS is beyond the scope of this but in essence, diffuse inflammatory changes in the lung result in reduced compliance, increased dead space that can improve over time, or progress to chronic fibrotic lung changes.

Ventilatory management: (lung protective measures) · Tidal volume of 4-6mls/kg (max 8mls/kg) of IDEAL body weight · Plateau pressures < 30 (not peak – remember plateau pressures are a surrogate for alveolar pressure) · PEEP – minimum 5cm, usually much higher (in reality >10cm water)

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· In COVID-19 one could expect to use PEEP in the range of 10-20cm H20 and often >15cmH20.

Clinical Pearl: Your goal here is for ADEQUATE oxygenation and ventilation, not perfect. Therefore, you don’t use high pressures and volumes to get better numbers. It is safer for the patient to have plateau pressures below 30 and oxygen saturations of 90%, than pressures of 50 to achieve saturations of 94%. Therefore, when you are on call and there is a patient with ARDS in the unit – make sure the acceptable parameters are agreed.

THIS IS OFTEN:

PO2 >8, PCO2 <8,

PH >7.25

SATURATIONS >88%

HOWEVER, THIS WILL DEPEND ON CASE BY CASE BASIS.

Other strategies: · Early aggressive antibiotics – treat the cause. · Conservative fluid management (decreases ventilator days but no effect on mortality) · Nitric oxide – this improves oxygenation by improving V/Q mismatch. It’s essentially a temporising measure. · Proning – this again improves V/Q mismatch, improving oxygenation. Proning comes with its own risks and has not been proven to improve mortality (although there is a trend towards improved mortality). Patients are usually proned for 16 hours, returned supine and then reassessed for further proning. Do not prone someone without senior advice. · Muscle relaxation may be needed for ventilator asynchrony. · Extra-corporeal membrane oxygenation, or ECMO. ECMO is done in the Mater and Crumlin, while CO2 removal can be done elsewhere. It is similar in concept to cardiopulmonary bypass, and the filters are there to provide gas exchange – 02 and CO2, before being returned to the body. This is highly specialist. It was used most prominently during the H1N1 epidemic and may feature again with COVID-19.

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Recruitment Manoeuvres Most anaesthetists will be familiar with recruitment manoeuvres. Essentially this involves increasing the inspiratory pressures to open up collapsed alveoli, and then keeping them open. This is where we get the term recruitment – you are recruiting alveoli that have been become collapsed or atelectatic (known as de-recruited alveoli).

Anaesthetist in theatre do this normally by switching to bag ventilation. This should not be done in cases of COVID-19, as doing so would involve breaking the circuit. Instead, the ventilator should be used, and the circuit kept intact!

There are many different recruitment manoeuvres, and all have limited evidence. By way of example: · One method, known as the staircase method, involves increasing the Peak Inspiratory Pressure (PIP) to 15cm water above PEEP. You then increase the PEEP (keeping the PIP 15cm water above it) every 2 minutes to from 15cm, to 20cm, to 30cm, to 40 cm (at 40cm, your PIP will be 55cm H20). You then reduce the PEEP again slowly back down to between 15cm and 20cm water, and leave the PEEP at this level to keep the newly recruited alveoli open.

· Another method is to increase the PEEP sequentially and then maintain and inspiratory hold (this is effectively what most anaesthetists do with bag ventilation. It is important to remember this is effectively a Valsalva manoeuvre and may be very poorly tolerated by patients who are already haemodynamically unstable).

· There are other methods such as RAMP (which is a long slow increase in respiratory pressure up to 40cm water).

Clinical Pearl: Use whichever you are comfortable with, but be careful with regard to the patients haemodynamics. Ensure they are adequately sedated. I personally muscle relax the patient, as recruitment can be extremely stimulating, and often poorly tolerated without deep sedation, or muscle relaxation.

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Ventilation in the Prone position. Who do we prone, and why? Prone positioning is performed to improve oxygenation in ARDS patients, when lung protective strategies have failed to achieve the desired outcome. As mentioned above, some studies have demonstrated a trend towards improved mortality, but to date, owing to limitations of these studies, they cannot be said to definitely show an improvement in mortality. They do however, show an improvement in oxygenation and gas exchange. The logic for this is easy enough to follow:

In the supine position, most of the blood is pooled in the posterior lungs. However, the posterior lungs are most prone to atelectasis and collapse. This means simply, that the posterior lungs are getting most of the blood flow, but not most of the ventilation, causing ventilation/perfusion mismatch – called V/Q mismatch. Areas of the lung that have little ventilation, but increased blood flow cause “shunting” of blood – where blood is shunted through the lungs without being involved in gas exchange.

The reasons the posterior lungs are more prone to atelectasis and collapse include (but are not limited to): · Transpulmonary pressure gradients – the gradients are bigger in the ventral lungs, allowing more effective ventilation in the ventral lungs. Remember that pressure gradients drive flow, and hence ventilation. · The weight of the lungs themselves in the supine position promotes atelectasis and collapse. · The weight of the heart and diaphragm – both squeeze different parts of the posterior lung parenchyma. · The reduction in Functional Residual Capacity (FRC) from the abdomen in supine positioning. · Disease processes themselves (such as COVID-19) can often attack the posterior lungs

Proning helps in the following way: · Pronging makes the posterior lungs non-dependent, and therefore improves the transpulmonary gradient, promoting ventilation to these parts. · Only a small amount of ventral lung is compressed in proning, whereas you have now taken compression off the posterior lungs, again promoting ventilation. There are much less compressive effects of the heart, diaphragm, and lungs themselves. · Some studies suggest that an unsupported abdomen in proning can increase FRC, thereby creating a reservoir of oxygen and improving oxygenation.

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· Although the ventral lungs are now dependent, the majority of blood still flows to the posterior lungs. Now that you are better ventilating these parts (as mentioned in the above points), you are improving ventilation of those lung parts AND oxygenation and gas exchange of the blood vessels. This reduces shunting of blood and overall improves gas exchange.

As mentioned above, proning should generally only be considered when lung protective strategies have failed! Based on our knowledge above about the physiology of proning patients, we can predict that those most likely to benefit are those with diffuse oedema, or those with dependent (posterior) alveolar atelectasis/collapse.

The practicalities of proning in ICU: There is a natural fear among staff in the ICU (nurses and NCHDs alike) about proning patients. There is a risk that lines (arterial lines, CVCs, catheters etc) may be dislodged, or the patient may be accidentally extubated. Then there comes the anxiety about having limited access to the patient when proned (e.g. access to ETT etc) and difficulties with CPR in the event of cardiac arrest.

However, despite these concerns, studies have shown a benefit to oxygenation and a tendency towards mortality benefit (although not proven), so it should be considered in all patients who are failing on standard lung protective ventilation strategies.

Proning the patient can be done in a number of ways, the most important thing is that it is done safely: · It can be done as a log roll on the sheets · A second bed/trolley can be used to transfer the patient supine initially, before rolling prone onto their bed again.

Whatever way it is done, the following is important: · There should be an anaesthetist present for proning, and returning supine. This is so they can reintubate immediately if required. · I personally would advocate fully muscle-relaxing the patient before proning (you do not want the patient to cough out the tube). In reality, the patient is likely to be muscle-relaxed already as part of your protective ventilation strategy, and before you consider proning. · One person should be assigned to mind lines and access to ensure there is enough slack, so that they don’t become dislodged on turning. Although the person on the airway (usually the anaesthetist) will call all the actions, all members should be ready to stop if the person minding vascular access requests so.

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· Proning lasts 16 hours. Unlike theatre, the face is turned side to side and the patient is not face down. Patients are then turned supine after 16 hours, and usually remain so for 8 hours before consideration for proning again. · I would certainly advise common sense here. If the patient is prone for 16 hours at 7am, it is absolutely reasonable to wait until after 8am to return supine, when there are more staff around.

Contraindications to proning: · Major haemodynamic instability, where the patient will not tolerate large fluid shifts involved in turning, and the potential anterior chest wall compression of being proned · Spinal instability – you must be able to move the neck laterally in both directions when prone · Pregnancy · Recent sternotomy/tracheostomy · Raised intracranial pressure · Significant unstable fractures

Clinical Pearl: Much like theatre, care must be taken when assessing the patient’s final position. They are at significant risk of retinal damage and blindness (reduced by having the head turned) and nerve compression injuries (reduced by ensuring all areas e.g. radial head are well protected from compression). Ensure your ETT is well secured, as well as all vascular access. Have a low threshold for continuing a neuromuscular blockade infusion throughout the proning period. Further to this, ensure adequate analgesia and sedation when using muscle relaxant.

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Inhaled Nitric Oxide (iNO) Inhaled nitric oxide is used to improve oxygenation. What follows is a brief review of pulmonary physiology to explain its role.

The purpose of the lungs is to receive oxygen and expel carbon dioxide. In order to effectively achieve gas exchange, it must match ventilation and perfusion (V/Q matching). When an alveolus does not receive oxygen, and becomes hypoxic, the accompanying blood vessels are constricted in an attempt to divert blood towards alveoli that are receiving oxygen. This is termed hypoxic pulmonary vasoconstriction. It is why patients with chronic hypoxia develop raised pulmonary pressures, and ultimate develop pulmonary hypertension and right heart failure.

Nitric oxide is a vasodilator. When it reaches an alveolus, it causes a local effect of vasodilation on the blood vessels. This increases flow to the alveoli that receive nitric oxide. (Remember, if they are receiving nitric oxide, then they are likely receiving oxygen too).

This has the net effect of matching ventilation to perfusion better, whilst also reducing hypoxic pulmonary vasoconstriction. It overall reduces pulmonary pressures and can relieve some strain on the right heart.

All of this combined increases pulmonary blood flow, reduces pulmonary pressures and right heart strain, and improves ventilation/perfusion matching. By improving ventilation/perfusion matching, we improve oxygenation and gas exchange.

It does not alter the underlying pathology, so it is used as a temporising measure whilst antibiotics, diuresis etc is used to treat the underlying condition.

Nitric oxide is started at 20ppm (its maximum therapeutic dose) and is sequentially reduced over time. Whilst some units have actual nitric oxide ventilators (that deliver both nitric oxide, and ventilate the patient), many units add nitric oxide into the existing ventilator circuit.

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The ABG Whole textbooks can be written about the ABG. It is important to keep it simple and be systematic in your approach. Remember, that for every acid-base balance disturbance, your body will attempt to correct it. Therefore, there are often multiple acid-base disturbances at the same time. Let’s take it step by step: pH – (Normal 7.35-7.45) pH<7.35, you already know to be on the lookout for metabolic (low bicarbonate, negative base excess, high lactates) or respiratory causes (high PCO2) or both as you progress through the ABG. Similarly, a pH of 7.45 will have you wondering if the alkalosis is metabolic (high bicarbonate) or respiratory (low PCO2)

PCO2 – (Normal 4.5 -6kPa) A high PCO2 is a respiratory acidosis (which may be the primary issue, or it may be a response to a metabolic disturbance), and a low PCO2 is a respiratory alkalosis (which is nearly always in response to a metabolic acidosis or an anxious patient hyperventilating)

PO2 – (normal >13.3) PO2 <8 is respiratory failure

Bicarbonate – (normal 22-28) Low bicarbonates are seen in metabolic acidosis. High bicarbonates are seen in metabolic alkalosis (very commonly as a compensation for respiratory acidosis – a high PCO2) although this often takes several days to achieve

Base excess – (Normal levels are -2 to +2) Bicarbonate is a base and an important buffering agent. The base excess refers to the apparent surplus or deficit of bicarbonate for a given acid-base disturbance. A positive base excess means you have an excess of bicarbonate (a metabolic alkalosis), whereas a negative base excess beyond -2 would indicate a deficit of bicarbonate and thus a metabolic acidosis. This is really useful to know in compensatory states as we will see below.

Na+/K+/Cl-. These are important values themselves, but they are also used to calculate the anion gap. Put simply the blood is full of cations (positively charged chemicals such as sodium and potassium) and anions (negatively charged chemicals such as chloride and bicarbonate.)

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Normally the body has tight control of the gap between cations and anions, and when added up the gap should be <15. An anion gap of >15 suggests there is some anion floating in the blood not accounted for by the substances in the equation. If the patient is acidaemic with an elevated anion gap this points to potential diagnosis (all of which involve anions floating in the blood). The acronym is MUDPILES: Methanol, Uraemia, DKA, Paraldehyde, Infection, Lactic acidosis, Ethanol, Salicylates.

Now let’s look at some gases: pH 7.21 PCO2 4.0 PO2 13 HCO3- 12 BE -11 Na 135 K4.8 C-115

· So, we have a PH of 7.21 – an acidosis · Our PCO2 is low so that’s a respiratory alkalosis (but the overall pH is low, so overall, we still have an acidosis) · Our P02 is acceptable · Our bicarbonate is 12 – this Is low and is indicative of a metabolic acidosis (well it had to be as the patient has an acidosis and we’ve already established its not respiratory) · The BE is -11. This indicates a deficit of bicarbonate, further pointing to a metabolic acidosis (this might seem obvious, and it is, but you’ll see the value of BE in the next example) · The calculated AG is normal.

pH7.18 PCO2 7.4 PO2 10.6 HCO3- 22 BE -9 AG normal

· So here again we have an acidosis with a pH of 7.18 · The PCO2 is elevated so we have a respiratory acidosis. · The bicarbonate is normal so surely this is a respiratory acidosis? · This is where the Base excess comes in. The ABG is telling us that we have a respiratory acidosis, but it is ALSO TELLING US THERE IS A DEFICIT OF

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BICARBONATE. Therefore, although the bicarbonate is technically normal, it is low for this acid-base balance.

It may be that the patient is a chronic CO2 retainer, (we don’t have that information), but we do know that relative to the pH, the bicarbonate is low. Therefore, we have a metabolic acidosis. Here, we now have a mixed acidosis – with a high PCO2 and a relatively low bicarbonate. This patient should not be dismissed as respiratory acidosis, and causes for metabolic acidosis should investigated. Maybe the lactate is high? Maybe they have renal failure? Maybe they have sepsis? They could have respiratory sepsis causing a respiratory acidosis and a metabolic acidosis at the same time.

These cases are designed to show that the ABG can be easily deciphered when using a systematic approach, and looking for clues with the bicarbonate level and the base excess. The Base excess is key in determining whether the bicarbonate is at an appropriate level. Remember it may be in the normal range and still be relatively low, indicating a metabolic acidosis.

It is possible to have a metabolic alkalosis, particularly in cases of protracted vomiting, but this is more commonly seen in pyloric stenosis in Paediatrics.

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Vasopressors, inotropes and inodilators Vasopressors exert their effects by causing vasoconstriction and therefore increasing systemic vascular resistance. They therefore increase MAP by increasing total peripheral resistance (TPR). Inotropes increase the contractility of the heart and increase MAP by increasing cardiac output. Inodilators (explained below) have a dual effect of inotropy in cardiac muscle, but vasodilatory effects on vascular smooth muscle.

To understand this better, lets briefly review adrenoreceptor physiology: Recall that there are 2 main types of adrenoreceptor: alpha and beta, which themselves are subdivided into alpha 1 and alpha 2, and beta 1, beta 2 and beta 3.

Alpha 1 receptors are post synaptic receptors found especially in vascular smooth muscle, but also cardiac and bronchial muscle amongst other places. Activation of alpha 1 receptors causes vasoconstriction. Examples include phenylephrine and noradrenaline Alpha 2 receptors are presynaptic receptors and work to inhibit presynaptic release of neurotransmitters, most notably noradrenaline. Activation of alpha 2 receptors therefore reduce vasoconstriction and effects include a drop in blood pressure. They also have a role in mediating pain. Examples are clonidine and dexmedetomidine, the former of which is particularly useful for pain. The potential for hypotension using clonidine is the reason it should not be given as a bolus.

Beta 1 receptors are particularly prominent in cardiac tissue. Stimulation of beta 1 receptors results in positive chronotropy (heart rate) and inotropy (force of contractility) – both of which increase cardiac output. Beta 2 receptors are more commonly found in smooth muscle and activation results in vasodilation (which is why adrenaline in very low doses is actually a vasodilator through stimulation of beta 2 receptors). You will be well familiar with beta 2 receptors activation causing bronchial smooth muscle relaxation, hence the role of beta 2 agonists (salbutamol in asthma, and conversely, the risk of bronchospasm that can be seen with beta blocker use). Furthermore, in the maternity setting, beta 2 agonists cause uterine relaxation and can therefore be used as a tocolytic (inhibition of uterine contractions). (Beta 2 receptors also play an important role in glucose control via glycogenolysis and gluconeogenesis. This is why glycogen is indicated in the treatment of moderate to severe beta blocker overdose). Beta 3 receptors do exist and have a role in lipolysis, and a role in the thermogenesis of new-born babies.

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Dopamine receptors – there are 5 subtypes with multiple effects on various body organs ranging from cardiovascular effects, to movement disorders (Parkinson’s disease) to nausea and vomiting (chemoreceptor trigger zone etc.) Dopamine has varying effects on the cardiovascular system, ranging from vasodilation at low doses, to vasoconstriction at higher doses. It is seldom used. It’s historical popularity derived from the fact it can be given peripherally.

Lastly regarding adrenoreceptors, recall that they are G-protein coupled. Without diving too much into the physiology, it is important to realise that stimulatory aspect of G proteins exert their effect by increasing levels of cAMP. Examples are Beta receptors and alpha 1 receptors.

Conversely G inhibitory proteins (as seen in alpha 2 receptors which inhibit the release of noradrenaline) reduce the amount of cAMP.

Overall, cAMP in cardiac muscle causes increased contractility (inotropy) and chronotropy (heart rate) but cAMP in vascular smooth muscle decreases contractility and promotes vasodilation.

So now we know cAMP plays a vital role in the mediating the effects of adrenoreceptors, causing increased cardiac contractility, but also vasodilation. cAMP is inactivated by phosphodiesterase. So, the logic follows that if you inhibit phosphodiesterase, the net effect is increased cAMP.

Therefore, phosphodiesterase inhibitors are known as inodilators – they cause simultaneous inotropy and vasodilation through the effects of increased cAMP. Commonly used examples in clinical practice include milrinone and enoximone. These drugs cause both systemic vasodilation and pulmonary arterial vasodilation – hence their use in pulmonary hypertension and right ventricular failure. (reducing pulmonary artery pressures reduces the afterload of the right ventricle, hence how it is considered helpful in right ventricular failure)

Remember that the point of using these drugs is to maintain effective tissue perfusion.

Mean Arterial Pressure = Cardiac Output (heart rate x stroke volume) x total peripheral resistance MAP = CO (HR x SV) X TPR

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Therefore, to maintain MAP we can either increase the TPR (e.g. noradrenaline) or increase the cardiac output (fluids to increase stroke volume, adrenaline to increase contractility and heart rate). Which ones we use will therefore depend on the clinical scenario.

Based on our above knowledge, the treatment of various conditions becomes quite logical: · Patients with septic shock (distributive shock) are vasodilated and hence benefit from increasing TPR (i.e. noradrenaline) · Patients with cardiac failure (e.g. post op cardiac patients) benefit from positive inotropy and/or chronotropy so these patients may require adrenaline or milrinone. Because milrinone causes vasodilation, it is not unusual to need to combine it with a vasopressor such as noradrenaline to maintain a reasonable TPR. Increasing the cardiac output whilst also decreasing TRP may actually result in a lower overall MAP. · Remember that stroke volume is important. Patients therefore need adequate filling time in diastole to achieve this. Hence, tachycardia may be very undesirable in these patients and poorly tolerated. Drugs acting to increase inotropy all increase chronotropy to various degrees (adrenaline, dobutamine, milrinone) so be cognisant of this.

Examples of drugs we use routinely and their actions: Noradrenaline – predominantly alpha 1 agonist. Therefore, causes vasoconstriction and increases MAP by increasing TPR. Particularly good in vasodilatory states e.g. septic shock.

Adrenaline – alpha 1 and beta effects. At low doses beta effects dominate and it leads to increased contractility, chronotropy and cardiac output. At higher doses (e.g. the 1mg dose in cardiac arrest) alpha 1 effects dominate and increased TPR occurs.

Phenylephrine – alpha 1 agonist – therefore increases MAP by vasoconstriction, increasing TPR.

Ephedrine and Metaraminol are both alpha 1 and beta agonists. With metaraminol alpha 1 effects predominate. However, the beta activation reduces the prevalence of reflex bradycardia seen with the likes of phenylephrine. Ephedrine has predominant beta effects but some alpha 1 effects. It mostly works by stimulating the release of endogenous neurotransmitters, hence the phenomenon of tachyphylaxis after repeated dosing.

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Dobutamine acts on beta receptors, particularly cardiac beta 1 receptors. It therefore increases contractility (inotropy) and heart rate (chronotropy). Remember increased chronotropy may be undesirable.

Isoprenaline is a beta receptor agonist. It is sometimes used as an infusion in bradycardic states that compromise cardiac output.

Milrinone/enoximone are phosphodiesterase inhibitors and are known as inodilators. They increase cAMP and are useful for right or left ventricular failure and for pulmonary hypertension. Remember both can cause unwanted tachycardia and they may need combination with a vasopressor (e.g. noradrenaline) to offset the vasodilatory effects.

Dopamine was previously used to increase cardiac output, but it has largely fallen out of favour outside of paediatrics.

Lastly, vasopressin can be used as (you guessed it) a vasopressor. It works on vasopressin receptors, which are particularly prominent in the splanchnic circulation. It causes vasoconstriction here and a diversion of blood to the more ‘vital organs. It should therefore be used in caution in patients with potentially compromised gut blood flow, and is contraindicated in those with bowel ischaemia.

Its main use is in addition to noradrenaline when high doses of noradrenaline are reached. This is for 2 reasons. Firstly, its acts by a different mechanism so may be beneficial to noradrenaline even when noradrenaline is working well. Secondly, at high doses, increasing noradrenaline has little additional benefit, and most units would advocate the addition of vasopressin if noradrenaline doses are rising above 30mcgs.

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Dialysis What is it? Who needs it? Do they need to go on it overnight? All these questions ran through my head before I started ICU call for the first few times. I worked in theatre – I had no experience of dialysis. So, let’s break it down and keep it very simple and practical. Remember, it’s a whole specialty in itself – you don’t need to know everything. The basics will do just fine!

Very simply put, dialysis is a process that takes over the job of a failing or failed kidney(s). We use it to get rid of toxins, excess fluid and for the regulation of electrolytes etc. Patients with established renal failure are on intermittent haemodialysis 2-3 times/week. This involves taking large volumes of blood through the dialysis circuit, removing toxins, replacing electrolytes etc. Sessions usually last 3hours. Because lots of blood is taken and dialysed, the patient needs to be haemodynamically stable to achieve this.

A dialysis patient with a BP of 80/40 will not tolerate taking large quantities of blood out of an already struggling circulation for the purposes of dialysis. But they still need to be dialysed. The solution is to dialyse them at a slow, steady rate continuously, rather than trying to fit it all in in 3 hours. It causes much less haemodynamic instability. So, this is where CVVH (continuous veno-veno haemodialysis) comes in. We use it in sick, haemodynamically unstable patients where intermittent dialysis would not only be poorly tolerated, it could kill the patient.

So now we know what CVVH is and why it’s used in preference for intermittent haemodialysis. But who needs it? When do we start it?

This can be divided into those that need urgent dialysis (overnight, on-call) and those that need urgent dialysis but can wait until the morning. Urgent cases: · Hyperkalaemia (either very high to start (>7mmol/L) or remains elevated despite maximal medical treatment (>6.5mmom/l) or those with ECG changes at any elevated level. · Severe metabolic acidosis. There is no absolute parameter here, but convention would consider a pH <7.2 and/or very high lactates. · Severe fluid overload (more specifically pulmonary oedema) that does not respond to diuretics · Severe uraemia · Severe drug poisoning in a dialysable drug

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Clinical pearl. · The kidneys are responsible for filtering and reabsorbing bicarbonate. Remember that low levels of bicarbonate are seen in metabolic acidosis. Failing kidneys cannot retain bicarbonate, hence why acute renal failure is associated with metabolic acidosis. · One of the reasons a pH of 7.2 is picked, is because inotropes and vasopressors are less effective at low pH. Therefore, improving a patient’s pH can improve response to vasopressor therapy.

Note that none of the above include creatinine levels, urine output etc. These are all important factors when determining who ultimately needs dialysis, although not necessarily as important factors in deciding who needs it in the next hour or two. It’s obvious that rising creatinine and falling urine outputs will sound alarm bells about renal failure. There are several different criteria for this. In practice, you will get a feeling for it over time, even if you don’t apply a particular set of criteria. (AKIN or RIFLE are common criteria used).

Other indications: · Uraemic encephalopathy, coagulopathy · Severe sodium disturbance - <115 or >165 · Hyperthermia (by taking blood out of the body, it naturally becomes a bit colder than body temperature. For this same reason, any low-grade pyrexia and especially temperature spikes on dialysis should be taken seriously, as the true temperatures are likely higher, and are artificially lower due to the circuit.

So now we know who we need to put on dialysis overnight, and who will ultimately need it, but can wait until the morning. How do we go about it?

Vascaths These are inserted exactly like a central line and come in different lengths. The Internal jugular vein is preferred where possible. Whilst femoral vascaths are acceptable and do work, they have higher infection rates. Furthermore, dialysis relies on good flows, so if a patient is flexing their hips, it can interfere with flow. Agitated patients kicking their legs around will interfere with dialysis flows. Rule of thumb (not an absolute) is a 15cm for RIJ, 15-20cm for LIJ and 20cm for femoral. Subclavian veins can and are used. Remember the subclavian vein is non-compressible and vascaths are large, so be cautious in picking what patients to put them in.

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They often come with 2 dilators, but the technique of insertion is the exact same as a standard central line. It’s important to ensure proper dilation over the wire, especially in the groin. I have had several instances where I’ve wired a difficult vessel only to not properly dilate. This causes a kink in the wire under the skin and makes it impossible to thread the vascath over it – essentially you must start again! When you have dilated, you can (very gently) move the wire slightly forwards and backwards with the dilator still in situ. If the wire moves freely with the dilator sitting over it, then you haven’t kinked it. If there will be a delay in using the vascath it is good to consider heparin locking it. You don’t want it clotting off and becoming useless after you’ve gone to the trouble of putting it in.

Continuous Veno-Veno Haemodialysis (CVVH) How do I prescribe it? Nurses will ask you to prescribe an exchange rate – what’s that? Firstly, there will be protocols in the ICU for starting patients on dialysis. They are easy to follow. For understanding purposes, the exchange rate is the amount of blood being filtered per minute. Think of it as the machine’s GFR. We would like a GFR of approximately 30mls/kg/min. So, for a 70 kg person, we would like a 2.1L exchange rate. (30mls x 70kg = 2100mls/min). For an 80kg person it would be 2.4L and so on.

Can we use heparin? Undoubtedly you will be asked this. Dialysis can be cumbersome to set up and programme for the nurses and neither you nor they would like the blood passing through the filter to clot. If the filter clots off, no more blood can pass through it so the whole dialysis circuit must be taken down. We often use heparin in the dialysis circuit to try to prevent it clotting off. There will be a protocol for the nurses to follow.

But I don’t want the patient to get heparin? Using heparin in this instance is for priming the dialysis circuit to prevent it clotting off. Very little actually goes into the patient, so you are not heparinising a patient in the same way that an intravenous infusion does.

Ok but I still don’t wat to use heparin? You have 4 options. 1. Use nothing and hope the filter doesn’t clot 2. Use flolan – it causes localised platelet inhibition, again only working on the filter and trying to prevent clotting by inhibiting platelets 3. Use citrate dialysis. 4. Pre-filter dilution

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What is citrate dialysis? Citrate is a compound that chelates calcium (i.e. it mops it up). You might recall from haematology that calcium is a critical co-factor in the clotting cascade. Therefore, by chelating calcium, it works as an anticoagulant. It negates the need for heparin and does not anticoagulate the patient. The key difference from your point of view is the nurses will ask you about calcium levels. Now that you have removed all the calcium in the circuit, you need to replace it into the blood before the blood gets back to the patient. You don’t wat the filter to clot, that’s the whole point of using citrate, so you must add it back after the filter. Ionised calcium is used as measurement and there will be clear protocols on how much to give depending on values.

So, let’s just use citrate in everyone? Not quite. Yes, it can be used in most cases, and is becoming more preferentially used in most cases as it clots far less than other dialysis circuits, even those with heparin. However, citrate can be toxic, and it is metabolised by the liver. Therefore, it can’t be used in severe liver failure. Citrate is also part of the pyruvate-lactic acid cycle. Therefore, it can’t be used in high lactates. Citrate is a base and therefore can’t be used in severe alkalosis.

In short, use citrate with caution if:

· Liver failure · High lactates, · Alkalosis.

What’s pre-filter dilution? Do not get bogged down here. If a filter has been clotting a lot, another technique is to dilute the blood as it comes out of the vascath and before it reaches the filter. It makes the blood less concentrated, making it less likely to clot the filter. But, by making the blood less concentrated, it decreases the concentration gradients that dialysis relies on, so it reduces the effective dialysis. Still, that may be more than acceptable over a constantly clotting filter.

What are access pressures and return pressures? The access pressure is the negative pressure required to “draw out” a sufficient amount of blood from the vascath to bring to the filter. Very negative pressures could mean that the lumen is up against a wall, or the patient is profoundly dry, or there is a kink obstructing flow etc.

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The return pressure is the pressure required to push the fluid from the filter back into the vascath and into the vein. Of course, very high pressures could mean you re in an artery but hopefully you’d have spotted that at insertion time! High return pressures could involve a kink in the circuit or in the vascath, or the lumen could be sitting up against a wall.

So, what can I do about it? · Ensure there are no kinks · You could reposition the vascath slightly so it’s not abutting the wall of the vessel. · You can switch the access and return arms. Yes, vascaths are colour coded red and blue. However, sometimes the problem can be fixed by switching the tubing over.

What’s a high filter pressure? (or transmembrane pressure – known as TMP) This is telling you the pressure in the filter is increasing. It is usually a sign that the filter is beginning to clot. It is important to recognise this, especially in unstable patients. If the filter clots off, all the blood in the filter and on its way to the filter will be stuck there. The patient has now lost a lot of their circulation as its sitting in the circuit and going into the bin. Therefore, especially in unstable patients, if the filter pressure is rising, you should consider washing back all the blood into the patient before it clots and deciding to take the filter down before it clots off.

What do I do with balances? Nurses will ask you what balance you want. They mean the net fluid balance on dialysis. So, if I want an even balance, they will replace any fluid lost. Similarly, if the drug infusions amount to 1.5L over 24hours, they will take off 1.5L fluid via the dialysis circuit so the patient is in even balance. If you are dialysing the patient for the purposes of removing fluid (amongst other things) you will want a negative balance. This is usually achieved by deciding on an hourly balance. For example, if you ask the nurses to take off 50mls/hr via dialysis, in theory your patient should be net 1.2L negative after 24 hours. If you ask for 100mls/hr, the patient should be 2.4L negative. In practice, it is usually less than this due to infusions, feed etc. All of these need to be accounted for when calculating total balance and what you want to achieve.

It is generally prudent to start on an even balance. Quite often, you are using CVVH because the patient is haemodynamically unstable, and they may be on vasopressors or inotropes. Removing fluid from their circulation may make them more unstable so it is usually wise to establish them on dialysis first before trying to remove any fluid.

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By the same token, if someone is on very high doses of vasopressors/inotropes e.g. the very sick patient on noradrenaline, vasopressin and adrenaline, starting dialysis involves withdrawing blood to pass to the filter. This may be extremely poorly tolerated, and, in this scenario, you may actually need a bolus of fluid to maintain circulatory volume while you are trying to start the dialysis. (even if you are dialysing them with the ultimate goal of removing fluid – remember it is possible to be very oedematous and intravascularly extremely dry!)

Clinical pearl: Using dialysis allows the removal of toxins/fluids etc and the regulation of electrolytes. If a patient has renal failure and hyponatraemia, dialysing them will correct the sodium. So, if starting dialysis on a patient with a sodium <125mmol/L, be careful – the same rules of correction apply, and you don’t want to correct it too fast. The general idea here is to dialyse them with lower exchange rates (so there’s less filtration – yes, your toxins will take longer to be removed, but your sodium won’t correct as fast!)

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Sepsis This topic is massive and whole books are dedicated to it. The most important thing in relation to sepsis is early recognition and immediate commencement of treatment.

What is Sepsis? The latest consensus documents define sepsis as “life-threatening organ dysfunction caused by a dysregulated host response to infection.” The reason this definition was changed from the old SIRS criteria is because anyone with, say for example tonsillitis, can have a temp of >38 and an accompanying heart rate of >100bpm. This may in fact be an appropriate response to the infection. Thus, the new definition points out the dysregulated host response to infection.

Septic shock is a particularly severe form of sepsis associated with circulatory, metabolic and/or cellular compromise. Such patients have a significantly increased mortality and are identified by the need for vasopressors to maintain MAP (caused by circulatory compromise) and an elevated lactate (a sign of cellular/metabolic derangement).

The old SIRS criteria have since been replaced by the Sequential Organ Failure Assessment Score (SOFA). A Score of >2 indicates a mortality of >10%. SOFA score considers the following factors:

· PaO2 · Fio2 · Whether the patient is receiving mechanical ventilation · Platelet count · GCS · Bilirubin · MAP (and within that the need for vasopressors) · Creatinine

In place of SIRS at the bedside is now a test known as the Quick SOFA or qSOFA score. This looks at 3 factors:

· Altered mental state · Respiratory rate >22bpm · Systolic blood pressure <100mmHg

2 or more of these clinical findings in a patient with a suspected infection correlate with poorer outcomes. (The pneumonic used is HAT – hypotension, altered mental state, tachycardia).

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When called to see a sick patient for ICU review – always think SEPSIS. Even if the cause is very clearly cardiac etc, this does not rule out concomitant infection. As mentioned above, early recognition and treatment is the key to effective management and improved outcomes. Indeed, one study suggested that every hour delay in antibiotic administration correlated strongly with an increased mortality in the region of 7% per hour delay. The Sepsis 6 bundles are used in all hospitals in Ireland, and you should be very familiar with them. The principal is to give 3 and take 3. (hence the term sepsis 6)

In the first hour you give: 1. Oxygen 2. Antibiotics 3. Fluids

You take: 1. Blood cultures 2. Lactates (hence the need for a blood gas) 3. Urine output (hence why catheters and fluid balance charts are important)

If not already clear, it should now be clear that every patient referred to ICU should have a lactate level and urine output measured.

With regards to antibiotics – consult your local hospital guidelines (and these are prone to change). This is important as in two hospitals less than 5 miles apart, the aminoglycoside of choice varies from gentamicin to amikacin, owing to a localised resistance to gentamicin in one of the hospitals but not in the other. Ideally cultures should be taken prior to antibiotics but DO NOT DELAY ANTIBIOTICS waiting for cultures.

Make sure you examine the patient properly – although the nurses are excellent at head to toe assessments, don’t rely on that. You don’t want to be the NCHD that hands over a case of sepsis of unknown origin, only to find out they had a rip-roaring sacral wound infection, had you looked.

Take cultures from all sites – blood cultures (peripheral and line cultures if there is an indwelling line), MSU/CSU cultures, sputum if relevant, stool samples, wound swabs etc.

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Start broad and narrow your cover as culture results become available. Have a low threshold for involving Microbiology.

With regards to Specific drugs such as vancomycin – people get very confused about this. Firstly, check if your hospital has guidelines on this. Vancomycin works by having a minimum level at all times - for ICU patients this is 15-20. There are 2 measurements therefore used in vancomycin dosing – the peak level and the trough level. Of most relevance to ICU is the trough. · The peak level (usually up to 40) will tell you that the dose is correct in terms of the peaks not being too high. · The trough will tell you that the timing interval is right., whilst also giving dosing clues. Adequate peak levels and low troughs means there is too big a time gap between doses. Adequate peaks and high troughs indicate that you are dosing too frequently. In places that don’t routinely measure peaks, the altering of vancomycin dosing is a bit more nuanced.

Dosing is generally 15mg/kg (unless severe renal failure) – you can therefore assume adequate peaks with this and adjust your timing to achieve the appropriate troughs.

Clinical Pearls: Patients who are receiving renal doses of any medication in ICU that then begin dialysis will need a reconsideration of that dose to reflect the fact that dialysis is improving their clearance and they may warrant higher dosing. The opposite is true as a patient is being trialled off dialysis during the period of renal recovery.

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Shock Broadly, shock is a state of circulatory failure resulting in tissue hypoperfusion, organ failure and death.

There are 4 types of shock: 1. Distributive shock -e.g. sepsis. The preload and afterload are both decreased but contractility is increased. This is often termed “hyperdynamic circulation”. Patients are often vasodilated and warm to touch, which provides a clue. Causes are sepsis and neurogenic shock (spinal cord injury)

2. Cardiogenic shock. Acute ventricular failure e.g. post MI, malignant dysrhythmias (which can affect filling time and therefore effective stroke volume – don’t forget that dysrhythmias can cause cardiogenic shock)

3. Obstructive shock: Impedance to blood flow. Examples here are cardiac tamponade and tension pneumothorax

4. Hypovolaemic shock: e.g. dehydrations, burns, pancreatitis. Patients are often cold and shut down peripherally.

By far the commonest shock you will see is hypovolaemic and distributive (particularly septic shock). In general, ICU treatment of shock involves fluid and vasopressors/inotropes, which treats hypovolaemic and distributive shock respectively. It is however important to remember other causes. A deteriorating post cardiac surgery patient or a rheumatoid arthritis patient may have a large pericardial effusion causing tamponade and no amount of fluids, antibiotics or noradrenaline is going to treat that without a pericardiocentesis. The same is true of tension pneumothorax.

Beware of neurogenic shock, especially in a trauma patient:

· Lesions above T4 are associated with hypotension · Lesions above T2 can exhibit bradycardia · Lesions in the region C3,4,5 affect the diaphragm but remember that accessory muscles of breathing are affected by low cervical and high thoracic nerves, so C3- 5 may be intact, but respiratory function may be significantly affected.

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You will hear some people refer to anaphylactic shock, or toxic shock etc – these are indeed shocked states but fall into the above categories (both are distributive shock).

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Sedation and analgesia in the ICU Why bother with sedation? Having vascaths, central lines etc and especially endotracheal tubes are uncomfortable for the patient. Patients with a strong gag reflex will need sedation to tolerate an endotracheal tube. So, it’s important from a patient-comfort point of view. It’s also important from your point of view – an uncomfortable patient may pull out arterial lines, central lines and tubes, with the obvious clinical risk of associated deterioration, not to mention the dreaded phone call to the ICU Reg saying we need new central and art lines etc.

Increasing evidence points to PTSD post ICU care. This is reduced with appropriate levels of patient comfort. It is, however, important not to over sedate a patient. It can lead to muscle weakness (especially respiratory), increased length on the ventilator, reduced mobility, which can lead to pressure sores, infection etc So, sedation is important for patient comfort, but it’s important not to over-do it.

Why bother with pain relief if they’re sedated? · Although sedated, they are not anaesthetised. Pain is a significant contributing factor to discomfort (requiring higher doses of sedation that may not be needed with adequate analgesia). · Pain is a risk factor for delirium, increased length of ventilator days, prolonged ICU stay etc. · Having an ETT is uncomfortable and can be painful, especially suctioning etc. Many Intensivists would advocate that all intubated patients should have some form of analgesia. · Remember also that many of your patients may be post-op. Furthermore, their underlying conditions may be painful; - e.g. ischaemic limb and things like chest drains are particularly uncomfortable for patients.

In short therefore, it is important to treat a patient with appropriate analgesia to prevent discomfort, whilst also considering sedation itself to ensure comfort. Balance is important though, as overdoing both can have their own consequences as above. The principles of good sedation and analgesia involve having a comfortable patient whose pain is well controlled and who is calm.

Remember that benzodiazepines can contribute to delirium, so where possible, use analgo-sedation. (sedation with analgesic properties). Fentanyl is a strong analgesic and is somewhat sedating. Clonidine is quite sedating and has analgesic properties.

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Your choice of sedation is influenced by several factors, including the patient’s pain. One thing to consider is the half-life of the drug and its elimination. If you are likely to attempt an extubation soon, or if they need to be neurologically assessed off sedation, morphine and midazolam (both longer acting) may be best avoided and something like propofol and fentanyl used instead. Cardiovascular stability is important. Propofol is a good drug by infusion but be careful with it in haemodynamically unstable patients – use morphine/midazolam instead.

You can use any combination you like – the rule of thumb is to use short acting infusions if likely to extubate soon, and longer acting if not or if quite unstable (you’re not likely to extubate an unstable patient soon anyway!). The use of remifentanil is controversial, especially with concerns regarding hyperalgesia. It can be used for short periods, but when weaning off it, longer acting opioids should be considered.

Do not forget the possibility of opioid/benzodiazepine withdrawal post extubation. A patient who has been on these for several weeks and is now extubated, should have them weaned to prevent withdrawal, rather than abruptly stopped. Finally, do not use propofol as in infusion in children, due to the risk PRIS (Propofol infusion syndrome).

Clinical pearls: · Analgesia is not vastly different in ICU to the wards. · Paracetamol should still be given (unless contraindicated) and can be given NG, IV or PR. It is an effective drug and should not be avoided just because the patient is in ICU · NSAIDS are best avoided in ICU except with the direction of a senior. ICU patients are at risk of stress ulcers and if hypotensive, renal impairment is common. · Opiates can be given by IV infusion in the case of intubated patients, by intermittent bolus by the nurses (with or without a low dose background infusion) or by PCAs on the wards (again with or without a low background infusion) · Clonidine is a good drug as it provides both analgesia and sedation. Dexmedetomidine is in the same family so do not use both together. From experience, dexmedetomidine is more sedating and less analgesing, with clonidine being the opposite. · Ketamine in doses of <0.25mg/kg are less likely to cause dissociative anaesthesia and is excellent for analgesia. · Do not forget the importance of neuropathic pain, especially in patients with pre- existing pain or those post thoracotomy etc. Caution in renal failure. · Regional analgesia is common in post op patients but can also be used for rib fractures etc so familiarise yourself with policies regarding the removal of epidural

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and wound catheters and timing of LMWH. Epidural catheters should be removed by day 4.

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Nutrition in the ICU This is a very important aspect of ICU care. Malnutrition has been shown to increase morbidity and mortality. It contributes to weakness leading to prolonged ventilation and increased risks of infection, wound and skin breakdown. Many patients in the ICU are in a catabolic state and require nutritional support throughout this period.

Where possible, the enteral route should be used. Oral is obviously the best, but where this is not possible, the NG route is the preferred alternative. There are 2 types of NG: Narrow bore tubes are used exclusively for feeding Wide bore NG tubes are used for both feeding and can be used for aspirating stomach contents, or on free drainage/suction in the context of vomiting, particularly in small bowel obstruction.

Therefore, in all intubated patients, it is a good idea to insert a wide bore NG at the time of intubation. You won’t get a better chance. You have sedated and muscle-relaxed the patient for intubation anyway, so now is a good time to site an NG also.

If you anticipate the patient to be intubated for >24hours, thus precluding the oral route, you should consider early feeding. On the contrary, if you consider a patient to be suitable for extubation, then consider holding the feed for 6 hours prior to extubation.

If gastric emptying is an issue, then a naso-jejunal tube can be inserted (also known as post-pyloric feeding). Initial studies suggested this was helpful in pancreatitis, but latest studies do not show any benefit of NJ over NG in this situation.

There are lots of different feed types – dieticians will prescribe the appropriate one for each patient, but the general principles are: · Jevity is the standard feed. Jevity Plus is higher in fibre and useful for GI patients · Nepro is generally used for renal patients. It generally has higher kCal/ml. It is therefore useful in fluid restricted patients. Further consideration for renal patients includes the amount of sodium and potassium in the feed. · Pulmocare can be used in COPD patients as lower levels of carbohydrates in this feed reduces the production of carbon dioxide · Elemental feeds are available for patients with short gut syndrome or pancreatitis

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Prokinetics? The NG is usually aspirated every 4hours and the volume measured (This is known as the Gastric Aspirate Volume – The GAVs). The generally accepted convention is for volumes of >250mls to be considered significant. At this point it is reasonable to temporarily stop feeding and consider the introduction of prokinetics.

· Metoclopramide is used to improve gastric emptying · Erythromycin reduces gastric residual volumes and should be limited to 5 days duration in total. Prokinetics have not been shown to reduces incidence of VAP (ventilator associated pneumonia) or overall mortality.

TPN: The European and American Societies differ in how soon to start TPN. Generally, TPN should be strongly considered in patients who will not commence enteral feed within 5 days and definitely within 7 days. TPN is a lipid emulsion and it is ripe for causing infection in the line. This is why TPN is interrupted as little as possible and has its own dedicated line. A line used for TPN should not be routinely used for anything else, even when TPN is not actively running (obviously it can be used in a dire emergency). In some patients, they may transition from TPN to enteral feeds and will have both running simultaneously.

What is refeeding syndrome? This is a whole spectrum of metabolic derangement that occurs when feeding is reintroduced to a patient that has recently had prolonged fasting e.g. post op, or an acute admission who was unwell and not eating for days prior to admission. While you should consider feeding a patient early in ICU, it is important on-call to be aware of the features of refeeding syndrome. When a patient is starved, their metabolism moves to fatty acid metabolism. When you reintroduce carbohydrates, you have a change to carbohydrate metabolism and a large increase in insulin. This causes significant shifts in fluid, electrolytes and glucose levels. So now you can predict that patients will have: · Hypokalaemia, hypoglycaemia, fluid shifts that can result in hypotension, pulmonary oedema and cardiac failure. · Furthermore, these electrolyte shifts affect kidney function causing sodium and water retention. · Low phosphate and magnesium are also a feature. All of these can result in arrhythmias, MI, respiratory muscle weakness. Therefore, on call, it is important to recognise this and replace electrolytes appropriately. It is usually prudent to hold the feeds until the morning, when senior staff can decide on further feeding regimes.

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Care Bundles Care bundles are protocols designed to reduce complications associated with various aspects of ICU care. Examples include: General ICU admission bundles, Ventilator bundles, CVC bundles.

· General admission bundles include: o Stress ulcer prophylaxis (PPIs), DVT prophylaxis, early enteral feeding in ventilated patients. · Ventilator bundles are designed to reduce the incidence of VAP. Aspects include: o Nursing at 45 degrees head up, regular closed suctioning, meticulous hygiene, sedation breaks and avoidance of over sedation, Stress ulcer prophylaxis (PPI) and DVT prophylaxis. · CVC bundles involves protocols reading the access and use of CVCs: Aspects include o Siting: subclavian >internal jugular> femoral (with regards to sepsis). o Meticulous hand hygiene, daily review of CVC indication (remove if not needed).

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Common ICU conditions on call Delirium It is an altered conscious and cognitive state that develops rapidly and fluctuates considerably. It is characterised by inattention. It can by hypoactive, hyperactive (harder to manage) or both.

What’s a CAM-ICU? And while we’re at it, what’s an RAAS? CAM-ICU is a confusion assessment method in ICU for detecting delirium. There are 4 components.

· Acute change · Inattention · Altered level of consciousness · Disorganised thinking. The Richmond Agitation sedation Scale is a scoring system that allows communication of how agitated (+4), calm (0) or profoundly sedate (-5), further allowing for documentation of fluctuations.

Treatment. Firstly, treat the cause: Pain, sepsis, dehydration, constipation, acute withdrawal (often missed – patients on fentanyl/morphine/midazolam when intubated, and then nothing when extubated), hypoxia, altered sleep-wake cycle, electrolyte abnormalities etc. Re-orientation and reassurance may be helpful Family members, a familiar face may help Pharmacological Treatment: · 1st line is haloperidol – can be given IV. Caution in prolonged QTc · 2nd line is olanzapine. Can be given sublingually, safer in prolonged QTc · Can consider alpha-2 agents such as dexmedetomidine as a titratable infusion · Benzodiazepines (BDZ) only work in the case of alcohol and BDZ withdrawal. Otherwise, BDZ can actually contribute to delirium · Melatonin is used widely, 2mg nocte in an effort to restore the sleep/wake cycle.

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Lactate Lactate is produced by most tissues in the body, in particular the muscles, and is generally cleared by the liver. Anaerobic metabolism causes a shift away from the Krebs cycle and into the Cori cycle where lactate is produced. Thus already, we can fairly obviously deduce that high lactates can be seen in:

· Areas of anaerobic metabolism – can be seen in hypoxia or a shift towards it (e.g. DKA) · Areas of tissue hypoperfusion – again causing anaerobic metabolism here – this could be generalised hypoperfusion from low MAP or organ specific e.g. ischemic bowel or ischaemic limb. The commonest cause here is SEPSIS causing low MAP. · Since it is cleared by the liver, liver failure causes a high lactate. · Seizures or excessive work of breathing cause anaerobic muscle activity and increased lactate. Therefore, this is why you might see a high lactate in someone with a normal MAP but severe respiratory distress. · Certain drugs can cause high lactates – most notably adrenaline in ICU, but metformin, theophylline and B-agonists can too (this is commonly seen in acute asthmatics who have been given repeated doses of salbutamol).

Therefore, in short high lactates are commonly caused by (amongst a large list of things) · Sepsis · Hypovolaemia · Ischaemia · Liver failure · Drugs

This is why people often give fluids in response to a high lactate. The goal is to restore circulating volume to enhance perfusion. This is especially true of patients on vasopressors. Remember vasopressors cause vasoconstriction and can divert blood flow to the vital organs, leaving other areas, most notably the peripheries, hypo-perfused. This can cause elevated lactates.

Be careful not to overload patients in cardiac failure by them giving them too much fluid. Also, it may take time for the liver to clear lactate, so don’t keep giving fluids to a falling lactate or you run the risk of overloading the patient in a quest to treat a number that was already improving. Look at the bigger clinical picture and don’t always treat a number.

It is a good habit to listen for bowel sounds in cases of elevated lactate and to ensure the LFTs have not recently become acutely deranged. You should also ensure adequate oxygenation to ensure aerobic metabolism and avoid hyperglycaemia where possible.

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Tachycardia/PVCs Remember from basic physiology that cardiac pacemaker cells exhibit automaticity and a decaying membrane potential. Remember also that action potentials are all-or-nothing events, and depend on a certain threshold being reached. This itself is dependent of electrochemical gradients, most notably involving sodium influx and potassium efflux.

Therefore, low extracellular levels of potassium can alter these important gradients and lead to easier depolarisations and thus PVCs and tachycardia. Therefore, in instances of PVCs or fast a-fib, you should in the first instance treat easy and reversible causes. This includes maintaining a potassium level of >4mmol/L and administering magnesium. In this case, magnesium works a cell membrane stabiliser.

Other things to look out for are:

· Is the patient under sedated? · Do they have adequate analgesia? · Have they missed regular doses of B-blockers etc because they are now on noradrenaline? · Electrolyte levels – potassium (aim > 4mmol/L) and magnesium (aim >1mmol/L)

If these measures fail, you now want to look at strategies for controlling the rate. · Beta-blockers may be contraindicated due to blood pressure concerns and digoxin is often contraindicated as many ICU patients have renal dysfunction. · In this instance amiodarone is your drug of choice. It involves a bolus dose of 150mg or 300mg (use the higher dose if the patient is on vasopressors) and then an infusion of 900mg over 23 hours. · Remember, an unstable tachyarrhythmia should be treated with a synchronised shock as per ACLS guidelines.

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Temperature spikes Cultures should be taken during a temperature spike as this can coincide with a bacteraemia (transient or otherwise) and produce the best chance of detecting a positive yield. There are arguments over what temperature 38C v 38.3C etc – use your clinical judgement. Cultures should be taken from all appropriate sites (peripherally and from central lines, catheters, drains, sputum, swabs etc) A very important point to note is that being on dialysis involves blood outside the body and patients naturally trend towards a cooler temperature. Therefore, any temperature spike on dialysis should be taken seriously as the temperature would likely be even higher were it not for the dialysis.

Refer to your antimicrobial guidelines but a general rule of thumb: (Remember you may need to further broaden already broad cover depending on your clinical suspicions)

· If suspecting UTI/pyelonephritis, add in a gram-negative cover e.g. gentamicin/amikacin · If there are indwelling lines (e.g. CVC) add in gram positive cover e.g. vancomycin/linezolid · If you are not sure and the patient is within 1 week of presentation, consider atypical cover e.g. clarithromycin/ciprofloxacin · If the patient has had bowel surgery, or has diarrhoea and C diff is possible – consider anaerobic cover e.g. metronidazole · If the patient is extremely septic and on multiple antibiotics or has upper GI pathology or is immunocompromised (e.g. oncology, haematology patients) consider antifungal e.g. fluconazole/anidulafungin/ambisome. Fluconazole is particularly heavy on the liver so be careful with this in septic patients with liver dysfunction. Anidulafungin or ambisome can be used, but ambisome can’t be used in renal failure.

Again, as mentioned in the sepsis bundles, do not delay antibiotics waiting on cultures.

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Blood transfusions Remember 2 things about blood: · It is a lifesaving treatment · It is a potentially fatal treatment.

So, who gets blood overnight? This is where common sense is vital. Studies have not shown a consistently proven benefit of Hb >9g/dL compared to Hb >7g/dL. There may be some evidence that above >8 is better in cardiac. (the old thinking that cardiac patients need Hb >10g/dL is not supported by robust evidence). It is reasonable to aim for a Hb of >8g/dL in elderly or frail patients. Consider it also in hypoxic patients – remember Hb is needed for O2 transport.

Obviously actively bleeding or unstable patients with low Hb <8g/dL need blood. Furthermore, a hypovolaemic patient with a Hb of 8.5g/dL is likely to need blood (remember, if they are hypovolaemic, they are haemo-concentrated and this Hb result is like to be artificially elevated. (It is always wise to look at the haematocrit when looking at a Hb results).

Patients who have drifting haemoglobins over the course of days and is 7.8g/dL do not routinely need blood overnight. Blood transfusions can cause significant reactions; therefore, your instinct should be not to routinely transfuse overnight unless the patient needs it urgently or is likely to deteriorate without it before morning. Indeed, it is fair to assume a patient with a Hb of 7.4g/dL at 3 am will ultimately need blood, but if they are stable otherwise and not a cardiac patient, it can generally wait until the morning when more staff are around. This is just a rule of thumb and nothing can replace your won clinical judgement, or just plain common sense.

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Ventilator dysynchrony Simply put, this is a situation where the ventilator and the patient are not in tandem. It may be that the ventilator is trying to deliver a back-up breath on top of the patients own triggered breathing, or that the patient is breathing over and on top of a ventilated breath (so-called breath stacking). This can lead to significant derangements in gas exchange, hypoxia and hypercarbia.

The first thing to look at is the patient under sedated or in pain. Either may cause tachypnoea in the patient and ventilator dysynchrony.

Next you should look at the ventilator settings. Is the patient on a synchronised mode? This means that the ventilator should support a patient’s own breath if the patient initiates one, and not try to trigger its own mandatory back-up breaths. You may be in pressure control or volume control mode without either assist mode (available in some ventilators) or SIMV mode. It may even be that the patient is suitable for plain CPAP and PS and doesn’t actually need the ventilator to try deliver its own breaths at any stage.

How a patient triggers the ventilator is important. They can trigger it one of 2 ways. · Flow triggered · Pressure triggered. This simply means that the patient must exceed a set flow or pressure threshold for the ventilator to recognise the patient effort and assist the breath.

In some instances, it may be that the patient is not being sufficiently detected by the ventilator and making the ventilator more sensitive to patient effort will allow better synchrony and less back up breaths.

More commonly however, the ventilator is too sensitive to what it thinks are patient breaths, when they might not be. It will therefore erroneously try to support a breath that was never properly triggered. Changing the sensitivity and increasing the threshold the patient must meet to trigger the ventilator will often reduce levels of desynchrony, as the ventilator will not now try to support what it thinks are 40 small breaths.

Another option is to decrease the back-up ventilator rate if the patient has a reasonable respiratory rate and tidal volumes from supported breaths. An alternative is to increase the backup rate in an effort to inhibit or override small patient efforts. You don’t want the ventilator to support breaths of 60 breaths per minute

Page 67 of 81 The practicalities of starting ICU call and the fundamentals of care for ICU level patients is you can avoid it. However, altering the trigger sensitivities will likely have better results.

Whether to increase or decrease back-up breaths, and flow/pressure triggers comes with experience. Lastly, if you are really stuck – do what you do in theatre – give muscle relaxant. Remember ICU care is not general anaesthesia, so if you are giving muscle relaxant, ensure adequate sedation.

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End of life Care An important aspect of ICU care is end of life treatment. It is important to have Consultant input into these decisions. From a purely legal perspective, the withdrawal of care, or the decision not to institute care (e.g. to start dialysis) is a purely medical decision. From a practical perspective, it is always important to have the family on board with treatment decisions.

One thing to always remember is that an elderly patient that is ventilated, on large doses of noradrenaline, adrenaline, haemodialysis etc – could (in some intensivists eyes) be considered to be receiving ongoing continuous aggressive resuscitation. Suffering a cardiac arrest in this context is to suffer a cardiac arrest in the context of already maximal life-sustaining support. Attempts at ACLS are likely to be futile here and indeed the dignity of the patient may be better suited by allowing natural death.

Of course, each situation is different. A 24year old, otherwise healthy individual on massive supports may have a reversible pathology and attempts at ACLS may be warranted despite massive supports. Indeed, the same may also be true of the elderly patient in certain circumstances. The purpose of the above paragraph is to get you to appreciate the bigger picture here. When you come on shift for the night, it is always useful to clarify a patient’s resus status, especially if they are on large levels of support.

Decisions may involve full resus, continuing to escalate therapy but not to intervene in the event of arrest, capping therapies at current levels, or beginning the process of palliation.

The process of palliation is somewhat different in ICU to the general wards. It is important to agree a plan with the Consultant in charge. Some will advocate keeping the patient intubated but decreasing the Fio2 to room air, whereas others may extubate the patient. Some may wean the vasopressors, whereas others may be quicker to stop them altogether.

In any case, be careful with the use of intravenous morphine and midazolam. Yes, it is important to keep patients comfortable, and IV is the preferred route for almost everything in ICU. An ICU Doctor in the NHS was accused of euthanising a patient because they administered the morphine and midazolam intravenously to a palliative patient. That is not to say you can’t do it in any circumstances, it more so highlights the need for Consultant level input into treatment.

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The Cardiac patient Cardiac patients do have some important differences to general ICU patients. However, the principles of management are the same. Most of your cardiac patients will be post-op. The following is a brief description of the operative procedures in cardiac surgery:

Most patients undergoing cardiac surgery will have a median sternotomy. (there are some less invasive procedures such as mini-mitral valve surgery). This allows access to the mediastinum and the heart.

Whilst beating heart CABGs are done in some specialist centres, performing a CABG or valve surgery requires access to a bloodless, motionless heart. In order to achieve this, a large cannula is inserted into the left atrium and another large cannula is inserted into the aorta. To do this, and to proceed with bypass, the patient must be fully anticoagulated with heparin to an ACT of >480. This prevents the circuit from clotting off, which could be devastating. Blood is withdrawn from the atrium, passes through an oxygenator (which is essentially an external lung). The oxygenator will oxygenate the blood and remove C02 before returning it to the aorta. In this way the heart and the lungs are bypassed, giving a relatively bloodless heart.

Next, cardioplegia solution is given (which contains potassium) and this is injected into the coronary arteries, the coronary veins, or both. This causes a diastolic cardiac arrest, hence providing the motionless heart. Of course, the fact that the heart isn’t beating doesn’t matter as the blood is being bypassed anyway (withdrawn from left atrium, oxygenated and returned to the aorta)

At the end of surgery, the heparin is reversed with protamine to return the patients clotting to normal. Any spare blood from the bypass circuit is returned to the patient at the end of surgery (it is important to realise this contains heparin) The sternotomy is closed, and the patient is brought to ICU. Fast-track cardiac surgery aims to extubate the patient within 6 hours of return to ICU.

During this time, the ICU care is similar to all other patients in ICU:

· Adequate gas exchange · Maintaining normotension · Re-warmed to normothermia · Adequate analgesia

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There are some nuances to be aware of with cardiac ICU patients: When the patient comes off bypass in theatre and is given protamine, they may have a normal ACT. However, they are then given blood left over from the bypass circuit, containing heparin. Therefore, their ACT may rise again. In this instance they may need more protamine when they get to ICU. Whilst protamine reverses heparinisation, too much protamine actually has anticoagulant effects and can promote bleeding. Therefore, if in any doubts, discuss dosing with ICU Consultant/Senior, or Cardiothoracics. Protamine itself can cause significant hypotension for several reasons: anaphylaxis, anaphylactoid reaction, and due to a transient rise in pulmonary artery pressures. The rise in pulmonary artery pressure puts significant strain on the right heart and can lead to acute right ventricular failure so be cautious.

It is important to maintain an adequate MAP for the patient. However, in cases where the aorta has been opened (known as aortotomy - especially in an aortic valve replacement) you do not want very high systolic pressures as this can promote aortic dissection/rupture of aortotomy. Therefore, your target is generally a MAP of 70 and a systolic of <120mmHg.

The indications for a return to theatre are generally due to bleeding. This decision will ultimately be up to Cardiothoracics.

The main reasons cardiac patients deteriorate post op are: · Hypovolaemia. This can be due to bleeding. Bleeding itself can be due to coagulopathy (in which case the treatment involves replacing products) or surgical (for example an errant suture etc) · Being on a bypass circuit causes a polyuria, haemodilution and leaky capillaries. All of these can contribute to hypovolaemia. · Vasoplegia – vessels become dilated after bypass and can be poorly responsive to vasopressors. This occurs particularly in cases where patients are on bypass for longer than 2 hours. · Graft or valve failure. The valve may come loose and obstruct outflow. The graft may kink and restrict blood supply – essentially causing an MI · Low cardiac output state. This is where the ventricles have poor function and is commonly seen postop. As opposed to vasoplegia (where the treatment is vasopressors), the treatment here is inotropy. · Patients post cardiac surgery are very dependent on cardiac filling. They do not tolerate arrythmias well (many will come to ICU post-surgery with pacing wires in and being actively paced). The commonest arrythmia postop is A-fib and should be treated as it is poorly tolerated. · Rewarming – remember that as a patient warms, they vasodilate. Patients are often cold (temps ~35) coming to ICU so BP drops with rewarming · Cardiac tamponade – try not to miss this post surgery Page 71 of 81 The practicalities of starting ICU call and the fundamentals of care for ICU level patients

· Sepsis – do not forget sepsis can be a cause of deterioration in any patient, cardiac included · Tension pneumothorax – patients often come back with chest drains in situ, but these can kink. Also, we generally put CVCs into the RIJ whereas chest drains are inserted into the left lung so watch out for a right sided pneumothorax. · Inotropes/vasopressors inadvertently stopped or changed from the theatre pumps to the ICU pumps. Patients who are dependent on inotropes do not tolerate any interruptions. Therefore, patients should have inotropes and vasopressors running through 2 lines at the same time and be satisfied that the new line has filled the dead space of the CVC and is now infusing. Only then should you discontinue the initial infusion · Hypertension is important to treat also. Common causes are overuse of vasopressors/inotropes. Other causes include inadequate sedation (remember the patient may still be muscle-relaxed upon return from theatre)

Cardiac Arrest in a cardiac patient. There are differences!!

Principles: The goal is to restore circulation as quickly as possible, whilst also avoiding adrenaline (if possible), particularly in the context of a shockable rhythm. Failed ROSC within 5 minutes of resuscitation should lead to a re-sternotomy and internal cardiac massage/defibrillation. From a practical viewpoint, given how long it takes to open and prepare the re-sternotomy kit, ask the nursing staff to open the kit as soon as an arrest is called.

Differences: If a shockable rhythm (pulseless VT or VF) – the initial treatment is 3 stacked shocks (150J x3) in the first minute of arrest. Chest compressions may be delayed for up to 1 minute to allow for this. If this fails, conventional CPR should commence with a view to re-sternotomy as soon as possible. (The dose of direct defibrillation using cardiac paddles is 10-20J). Amiodarone should be given if progressing to a re-sternotomy Similarly, in cases of bradycardia or asystole, compressions may be delayed in order to attempt pacing. If this fails, external compression should be started with a view to re- sternotomy as soon as possible and ideally within 5 minutes of arrest onset.

PEA is treated according to standard ACLS protocol. It might seem obvious, but don’t forget to turn off sedation or vasodilators which will make your job of achieving ROSC even harder.

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A short word on post cardiac arrest care: · Keep patients sedated for 24 hours to reduce cerebral metabolic oxygen demands. · Employ neuroprotective strategies, as you would for a neuro patient (nurse at >30 degrees, control the PCO2, maintain a good MAP for cerebral perfusion, and indeed other organ perfusion). · Maintain adequate oxygenation. · Control temperature and avoid pyrexia. Latest evidence has moved away from deliberate hypothermia but supports normothermia and an avoidance of pyrexia. Aim for a temperature of 35-36 degrees and use a cooling blanket if necessary.

A word on fast-track cardiac surgery: · The aim of this is to have a patient extubated within 6 hours of completing surgery. The usual targets of extubation apply (i.e. neurologically appropriate, good gas exchange, haemodynamically stable etc).

Balloon Pumps: Put simply, this is a device that is inserted into the femoral artery and advanced under echo or fluoroscopic guidance to sit just distal to the subclavian artery (approx. 3cm). It is used for low cardiac output states, usually in the context of left ventricular failure. Positioning is important – too high can obstruct the left subclavian artery. Too low can obstruct the renal arteries, or the mesenteric arteries and cause either renal failure or bowel ischaemia/infarction.

It has a helium filled balloon at the distal tip. This intermittently inflates and deflates. It inflates in DIASTOLE and deflates during systole. (Therefore, it is known as a counter pulsation device). Because it deflates in systole, it reduces cardiac afterload. It reduces left ventricular systolic pressure and left ventricular end-diastolic pressure. This ultimately decreases myocardial work and myocardial oxygen demand, whilst increasing cardiac output. Its inflation in diastole is designed to augment blood flow, especially to the coronary arteries, although the real effects are variable. It may increase renal blood blow in the context of increased cardiac output. However, remember that poor placement will actually decrease renal blood flow.

The IABP inflates in diastole based on one of 2 triggers 1. ECG – it triggers on the mid T wave 2. Pressure sensing – based on the dicrotic notch

This is important because if the patient arrests with an IABP, it is important to switch the device from ECG (which is what it normally uses) to pressure sensing so that it will assist with counter pulsation during CPR.

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How much the machine works can be programmed. · 1:1 means it assists every heartbeat · 1:2 is every second beat and 1:3 is every 3rd beat. · Moving from 1:1 to 1:3 is usually done in the context of weaning and assessing the ongoing need for the device. 1:3 is not left for long as the device runs the risk of clotting.

Clinical Pearl: If a patient with an IABP develops worsening renal failure or rising lactates, this may be in the context of the low cardiac output state that the IABP is trying to treat. However, do not overlook the fact the poor positioning may be causing interrupted renal and/or mesenteric blood flow.

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The Neurosurgery patient To understand the goals of treatment for a neuro patient, it is first important to revise neurophysiology – in particular the CPP, ICP, CVP and the Munroe Kelly doctrine. Cerebral perfusion pressure = MAP (at the level of the circle of Willis) – CVP or ICP (whichever is higher). Cerebral perfusion pressure is the pressure gradient driving cerebral blood blow. Simply put, it is the pressure difference between the cerebral arterial input pressure and the output pressure (usually the CVP, but sometimes the ICP if this is higher).

Recall the Munro-Kelly doctrine. The brain is like a fixed box, made up of blood, CSF and tissue. If the pressure rises in one, it must decrease in the others to compensate. This keeps the pressure in the brain constant allowing controlled cerebral perfusion pressure and blood flow. So if pressure in the brain rises, that is to say the ICP rises (e.g. due to trauma), the first thing that happens is CSF is shunted from the brain to the spine and venous blood is shunted from intracranial vessels to the extracranial vessels. This reduces the CVP and ICP and an effort to maintain the cerebral perfusion pressure, and hence cerebral blood flow.

At the extreme end of this, and by way of remembering, consider this: If the ICP was higher than the MAP reaching the brain (i.e. the pressure inside the brain is already higher than the blood pressure reaching it!) there would be no blood flow at all. Similarly, if the venous sinuses thrombosed completely and blocked venous output, very soon the blood would be stuck in the brain, the pressure would rise, and blood flow would cease.

Hopefully now we understand the importance of maintaining cerebral perfusion pressure. Remember that pressure is related to flow, and flow is related to diameter. So, for the same pressure, large vessels will allow large flows of blood, whereas constricted vessels will allow smaller flows. Therefore, we must consider another important concept:

Cerebral vasodilation and constriction. It has been shown that cerebral vessels constrict and dilate in a near linear fashion with PCO2 levels. Low PCO2 levels cause vasoconstriction to a level of 4kPa and rising PCO2 cause predictable vasodilation up to 12KPA. Therefore, it’s important to control the PCO2 to have some element of control over total cerebral blood flow. There is another important factor with PCO2 control. Damaged brain vessels lose their vasoactivity. They may be somewhat dilated by comparison to the other vessels. This can be advantageous in terms of ensuring there is adequate blood flow to the most affected area. However, high PCO2 and generalised cerebral vasodilation may mean that the damaged area (although vasodilated itself) is vasoconstricted relative to the rest of the

Page 75 of 81 The practicalities of starting ICU call and the fundamentals of care for ICU level patients cerebral blood vessels. This would deprive them of vital blood flow. This is another reason therefore, to control the PCO2.

As well as losing is vasoactivity, damaged areas of the brain may have increased permeability and become prone to oedema. This is the theory behind the use of hypertonic saline. Hypertonic saline renders the blood hypertonic relative to the brain tissue and causes a gradient that promotes water to move from the brain into the blood stream. Hence you are aiming to reduce cerebral oedema. The now expanded volume is sensed by the kidneys and results in a diuresis. It is normal to target serum sodium levels of 150-155 as a guide to “dosing” this therapy.

· When we understand the above concepts, it is not hard to understand the key concepts of neurological patient care. The critical concept to remember is that this care is aimed to prevent secondary or further brain injury, the primary brain injury is what has gotten you to this situation. · Nurse the patient at >30 degrees head up. This allows for adequate venous drainage and keeping the CVP low. Furthermore, ensure that ETT ties are not so tight as to obstruct venous drainage. · Maintain CPP of >60 (if the patient has an ICP monitor in, liaise directly with neurosurgeons. Normally, pressures <20 are desirable and definitely <25. Your CPP is calculated by: CPP = MAP – ICP . · So, for example, a patient with an ICP of 18 needs a MAP of at least 78 to achieve a CPP of 60. Patients will often require noradrenaline to maintain higher MAPs. · CAVEAT: Beware of the patient with an acute SAH who has an unsecured aneurysm (i.e. not coiled or operated on yet) – liaise with neuro regarding target systolic BPs and MAPs as too high may risk rupture. · Ensure adequate oxygenation. · Ensure normocapnia. Usually we target PCO2s of 4-4.5 (and definitely <5kPa) – remember it is related to generalised cerebral blood flow and has impacts on flow to damaged brain. · Ensure adequate sedation/analgesia – this is essentially allowing the brain to rest/recover. As propofol is quite vasodilatory and you are aiming for higher MAPs, many centres go with morphine/midazolam for deep sedation. · Ensure normothermia and avoid shivering (cooling blankets and/or muscle relaxant may be needed) · Treat any seizures early and aggressively. · With raised ICP consider hypertonic saline. Whilst we mostly use Hartmann’s in ICU patient, standard fluids in neuro is generally Normal Saline when not using hypertonic regimes. · Patients at risk of, or suffering from, cerebral vasospasm are given nimodipine NG to treat this. Some centres still use Triple H therapy - which is o Hypertension (ensures and adequate MAP) o Hypervolaemia (aims to increase cerebral blood flow for a given MAP))

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o Haemodilution (in theory makes the blood less viscous facilitating cerebral blood flow) · Aggressive treatment of sepsis or other organ failure. · Watch out for Diabetes insipidus – very large urine outputs.

Clinical Pearls Liaise with neurosurgery before attempting to wean a patient’s sedation. Some postoperative patients are deliberately deeply sedated for several days to allow brain rest and recovery. SAH itself can lead to transient left ventricular failure and to neurogenic pulmonary oedema. Therefore, some SAH patients can become hypoxaemic in the absence of cardiac pulmonary oedema or respiratory sepsis, so watch out for this. Be careful with hypertonic saline or mannitol in patients with poor ventricular function – both treatments are designed to draw water into the intravascular space and can cause cardiac overload.

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Status epilepticus Status epilepticus is either:

· A seizure lasting greater than 5minutes duration · More than one seizure without recovery in between

The patient requires rapid assessment and treatment. Like always, follow the ABC approach. Whilst your goal is to treat and terminate the seizure, you do not want to miss a compromised airway.

The decision to intubate is a clinical one and will be determined by asking yourself the following: Is the airway compromised? Can the patient maintain airway patency? As you know, most patients who present with seizures do not get intubated. However, have a low threshold to intubate patients who have status epilepticus as they are unlikely to maintain their airway indefinitely. What is the likely clinical course? Here, with an isolated seizure, recovery is expected, including a rapid improvement in GCS and the ability to then maintain their own airway. This is often the reason this cohort are not intubated, despite a transient low GCS. If, however, you are facing status, you are facing the possibility of protracted seizures and a prolonged low GCS. Here, it is wise to intubate. Is gas exchange compromised? Like all patients, if hypoxia is an issue, or hypercarbia (in the context of low GCS) then intubation is warranted, regardless of whether you think the seizure will terminate soon. Rapid assessment of breathing and circulation follows along the usual principles. Establish IV access as early as possible – ideally concomitant with assessment and ALWAYS CHECK GLUCOSE!!

Treatment: · Benzodiazepines are first line therapy: · Lorazepam 0.1mg/kg to a maximum of 4mg as a bolus, repeated if necessary · Diazepam can be used as an alternative at 0.15mg/kg up to a max bolus dose of 10mg · In intubated patients, boluses of midazolam and infusions of midazolam can be given.

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Second line agents: · Phenytoin – bolus dose is 20mg/kg, given at a rate of 25-50mg/min. Therefore, phenytoin loading for an 80kg patient is 1600mg and should be given no faster than over 32 minutes. If seizures persist, a further dose of 5-10mh/kg can be given but no more than a max of 30mg/kg total. Note: Phenytoin can precipitate if given in same line as dextrose or benzodiazepines. Therefore, always give phenytoin through a separate IV line with full cardiac monitoring.

· Levetiracetam (Keppra) given at a dose of up to 60mg/kg to a max of 4.5g over 15minutes · Sodium Valproate – loading dose of 30mg/kg and infusion of 10mg/kg

If no IV access: · Midazolam 5 -10mg IM, buccal or intranasal. (5mg if <40kg, 10mg if >40kg). · Rectal diazepam (0.2mg/kg) to a max dose of 20mg. Studies suggest midazolam is superior

Refractory Status Epilepticus: (You may hear the term NORSE which stands for New Onset Refractory Status Epilepticus)

· This patient will definitely need intubation · Treatment options here are based on the above treatments (i.e. phenytoin, levetiracetam etc) but also infusions. · Midazolam, propofol and thiopentone infusions are all used. Just remember that thiopentone has an extremely long half-life.

Some general points. The worldwide adult mortality for generalised convulsant status epilepticus is as high as 20% from a first episode. Therefore, you should acknowledge that this is a serious life- threatening condition. There are many associated serious systemic effects including life-threatening cardiac arrythmias, hypoxia and respiratory failure, hyperthermia (from muscle activity). Seizures lasting longer than 30 minutes are strongly associated with increased risk of long-term neurological disability – hence the need for early and aggressive treatment of seizures. Once under control, look for underlying causes – electrolytes, metabolic, traumatic, malignancy etc.

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Nonconvulsive status epilepticus: This is a state of status epilepticus without motor features. It therefore requires a high index of suspicion. The definition differs from generalised convulsive status epilepticus, in that the duration is 10mins without recovery (as opposed to 5). Although not formally in the definition, most also accept seizures (without motor effects) without full recovery in-between.

Non convulsive status has many classifications. In short,

· they can be associated with or without coma. · They can be generalised (such as a typical absence type seizure) or focal (with or without impairment of consciousness)

Causes are multifactorial, including an underlying epileptiform disorder, but NCSE is also seen in critically ill patients, particularly those with encephalopathy. It has been well associated with B-lactam and fluoroquinolone antibiotics, chemotherapy and immunosuppressive agents.

Clinical features are often non-specific and usually revolve around impairment of consciousness. There may be aphasia or mutism, lip smacking, rhythmic myoclonic type jerking, or no discernible features at all. Therefore, a high index of suspicion is required (these are the patients who are unresponsive but appear to have open eyes with a blank expression).

It can be hard to distinguish from hypoactive delirium, stroke, encephalopathy. This is amongst the many reasons why encephalopathic (or presumed encephalopathic patients) should have an EEG. EEG is the key to accurate diagnosis

Treatment should revolve around non-sedating anticonvulsants such as: · Phenytoin, levetiracetam, valproate etc · If benzodiazepines are to be used, midazolam is used preferentially due to its shorter duration of action.

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Conclusion: I would like to thank you for taking the time to read this ICU booklet. When writing this, my mind was cast back to when I first started ICU call, with all the anxiety and trepidation that accompanied that. The content is based around my own clinical experience of ICU call and the day to day care of ICU patients. I consciously decided to begin most sections with an overview of physiology, or of the topic, in the hope that this will aid understanding. I have made every effort to ensure that all clinical information is both relevant and up to date.

It is my hope that you will learn something from this booklet and from my previous experiences. This is not intended as an encyclopaedia of ICU care, but rather a whistle- stop tour of the common things you will encounter on ICU call and with ICU patients. This is the first version, and this will no doubt be amended and revised, especially as treatments constantly evolve. I am always delighted to hear any feedback and suggestions that anyone may have. Please feel free to contact me with any such feedback or suggestions at [email protected].

Is Mise le Meas, Dr Peter Mc Cauley MB BCh BAO MRCPI FCAI PDip in Health Sciences (Clinical Education) SpR in Anaesthesiology

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