Electronic Resource for Doctors in Training




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VT should be 5 - 7ml.kg (350 - 450 ml)

  • PaCO2 should be 6 - 8 kPa

  • PIP should be less than 30 cm H2O


    The main exclusion to hypercapnoeic ventilation is in patients suspected of having sustained brain injury, when PaCO2 should be maintained at between 4.5 kPa and 5.5 kPa).


    WHEN USING BIPAP, IT IS VERY EASY FOR TIDAL VOLUME & MINUTE VOLUME TO CHANGE.


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    RONE POSITION VENTILATION



    In general patients will be turned prone for the night and returned to the supine position for the day.


    1. All drips must be carefully managed.

    2. Intra-arterial lines may be easier to manage in the foot, or the hand (wrist) needs to be placed above head

    3. Expect oxygenation to continue to improve for up to 8 hours after first adopting prone position. It may then start to fall again, as pulmonary oedema starts to reaccumulate at the most dependent part of the lungs, and atelectesis starts to return.

    4. Turn soon after the plateau reached and see what the time course of change is

    5. Remember good eye protection (drops, gelpads)

    6. Often the patient can be managed 12 hours prone, 4 hours supine etc, which gives access for examination etc etc

    7. Ventilate the patent using IPPV NOT BIPAP

    8. You will be expected to be present during turning, often managing the head/airway


    If the patient needs defibrillation/countershock, get on with it using back paddle pushed under the patient. Ask yourself whether the arrest is because the patient was underventilated (tube kinked or fell out)





    PROTOCOL FOR DECANNULATION: TRACHEOSTOMY







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    If the tracheostomy has been performed using the non-surgical percutaneous technique always assume that reinsertion of the tube will be difficult. The tube is placed between tracheal rings which may immediately take up their original anatomical shape (the rings close down like fingers in a tightly closed fist). In these circumstances, if there is doubt:


    • Have a bougie ready

    • Have a small tracheostomy tube available

    • Be prepared to re-intubate via the ORAL route (ie you need sedation, relaxant and a full intubation tray available).


    Make sure that the physio knows you are likely to decannulate.


    You are not advised to decannulate in the small hours of the morning!


    1. Stop feeding (NG or oral) 2 hours before decannulation.

    2. Check that the ABG or saturation is satisfactory.

    3. Put the patient on high flow oxygen before decannulation.

    4. Get the post-extubation oxygen system running (eg hot water humidifier, nebuliser, etc) before decannulation.

    5. Suck out the contents of the stomach through the naso- or oro-gastric tube

    6. If the patient is semi-conscious, consider whether decannulation (or even changing to a non-cuffed tube) is appropriate. They should not usually be decannulated if they are unable to clear secretions or do not have a cough reflex.

    7. Cut the ties/tapes.

    8. The nurse will usually push the suction catheter down the tracheostomy tube until the patient coughs. If the patient does NOT cough, reconsider whether the airway will be secure when the tube is removed.

    9. Deflate the cuff.

    10. Pull out the tracheostomy tube, while suctioning all the time with the suction catheter. This will suck out secretions lodged above the cuff and any in the stoma.

    11. If you are replacing the tracheostomy tube with (say) a speaking (fenestrated) tube, slide this in through the stoma, and immediately pull out the bougie. Hold the tube in: usually the patient will cough vigorously. If you are placing a speaking tube slide in the inner tube and ask the patient to talk! Then put on the humidification system!

    12. If decannulation is to be complete, cover the wound with a non-adherent dressing, and then tape over this with some very sticky dressing (usually "sleek"), which sticks well as stops air leaks. The patient should then receive humidified oxygen (at least for a few hours).


    Do not start nasogastric feeding for at least 2 and preferably 4 hours; the larynx remains incompetent for quite long periods. You can probably guess this because the patient originally tolerated a trache-tube without coughing, and the hoarse voice indicates incomplete closure of the vocal cords, or leakage of air from the stoma.

    PROTOCOL FOR TREATMENT OF PERSISTENT HYPOXAEMIA IN ACUTELY ILL PATIENTS







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    This protocol is aimed to assist management of patients suffering from ALI or ARDS. It assumes that mechanical causes of hypoxaemia have been excluded ie inadvertent endobronchial intubation, lobar collapse due to bronchial obstruction (sputum, foreign body), pneumothorax. It is sensible to exclude obvious problems with a chest X-ray and, if necessary, bronchoscopy. Every effort should be made to maintain PaO2 >9kPa and SpO2 >93%

    For the purposes of this protocol, persistent hypoxaemia will be defined as a PaO2 of <8.5kPa, or a SpO2 of <91% for >12 hours when receiving an FIO2 of >0.6 (i.e. a PaO2/FIO2 ratio <14kPa).

    Other indications are:

    (a) PaO2 of <7.5kPa, or a SpO2 of <88% for >2 hours if breathing 85% oxygen

    (b) inability to raise PaO2 above 8kPa


    Patients should already be receiving hypercapnoeic ventilation (PaCO2 >7.5 kPa) and low level EEP (5 cm H2O)


    TREATMENT REGIMENS ARE:

    1. IRV

    2. Prone position ventilation

    3. Nitric oxide therapy

    4. Usually modalities will be added in that order.




    1. Hypercapnoeic ventilation is indicated in all patients. Accept an FIO2 of 0.7-0.8 for 24 hours

    2. IRV should begin immediately. Minimise peak airway pressures using BIPAP or other means of pressure limited ventilation

    3. Perform a recruitment manoeuvre (prolonged (10-15 seconds) & repeated (3-4) breaths

    4. Prone position ventilation is indicated if FIO2 >0.8 for >12 hours or "1" or "2" are ineffective

    5. Nitric oxide therapy indicated if prone position is ineffective, or not practical.

    6. Therapies should be continued until FIO2 <0.7. Prone positioning should be discontinued before nitric oxide therapy.

    PROTOCOL FOR BRONCHO-ALVEOLAR LAVAGE IN MECHANICALLY VENTILATED PATIENTS IN CRITICAL CARE







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    CHOICE OF AREA FOR BRONCHO-ALVEOLAR LAVAGE

    Outside the Intensive Therapy Unit, broncho-alveolar lavage is performed on a single lung segment, usually the segment showing consolidation. Unfortunately, in the critically ill patient in the ITU, radiological evidence or clinical signs pointing to a particular area of interest are often lacking, and the segmental area to undergo lavage should be chosen at the time of fibreoptic bronchoscopy. Not uncommonly, however, there is no obvious area, and lavage should be performed in three different segments.


    METHOD

    1) Prior to lavage (as for any bronchoscopy) the patient must be ventilated (pre-oxygenated) with 100% oxygen for at least 5 (and preferably 20) minutes.

    2) The sealed suction unit etc must be replaced with a bronchoscope swivel adaptor.

    3) Immediately prior to bronchoscopy, minute and tidal volume set up on the ventilator should be increased by 25% to accommodate the gas loss due to bronchoscopic suction and leakage around the swivel. In these circumstances, this is sensible practice even when the ventilator is pressure cycled.

    4) The patient requires adequate sedation. If an oral tube is present, the patient will require a muscle relaxant, to prevent biting on the endotracheal tube/fibrescope: it is not usually possible to insert a bite guard. Sedation is best achieved with a benzodiazepine (midazolam or diazepam). Propofol may cause significant hypotension. An additional bolus of an opioid may be helpful.

    5) The sputum trap may require changing prior to lavage, particularly if lignocaine has been used as a local anaesthetic.

    6) Following formal bronchoscopy, three sub-segmental areas are chosen for lavage. The bronchoscope is pushed into the segment until it is stuck and can be pushed no further. This effectively "plugs" and isolates the segment, although large changes in lung volume with ventilator inflation may unplug the fibrescope. Sixty (60) ml of warmed (37oC) saline is injected into the segment. After a 2 second delay, this is aspirated into the suction trap. Aspiration is repeated.

    7) The other two areas are now lavaged. It is important that volumes are limited to 180 ml (total), if both lungs are lavaged. Bilateral lavage with high volumes (500 ml) can (and does) cause significant hypoxaemia.

    8) If the trap is more than half full, it must be replaced, otherwise the whole sample may be inadvertently suctioned away.

    9) At the end of the procedure, minute and tidal volume should be readjusted.

    10) Pre-oxygenation should be continued for at least 10 minutes after completion of the procedure.

    4.0 HAEMODYNAMICS – CONTENTS







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    Introduction

    Determinants of Cardiac Output

    Monitoring

    Mean Arterial Pressure

    Urine output

    Arterial Wave Form Analysis

    Central Venous Pressure

    Non Invasive Haemodynamic Parameters

    Vasoactive Drug Therapy

    Fluid Replacement - Colloids, Blood Products & Albumin

    Haemodialysis

    What is CVVH?

    How does CVVH work?

    Practical management

    Protocol

    Resources

    Important Conditions/Guidelines

    Acute Renal Injury

    Arrhythmia

    Surviving Sepsis

    Guidelines for Doctrecogin Alpha

    Myocardial Infarction

    Organ Failure

    Pyrexia

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    dult Protocol for Meningococcal Septicaemia


    Main Contents

    4.0 HAEMODYNAMICS







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    Insufficient cardiac output (heart rate x stroke volume) will over time yield inefficient anaerobic metabolism that cannot be sustained indefinitely. It is for this reason that matching output to demand is a critical factor within critical care and it requires a careful and rationalised titration of specific drugs or fluids.


    - HAEMODYNAMIC MANAGEMENT IN CRITICAL CARE


    Some patients in critical care can respond very well to straight forward basic management. However, it is not uncommon for some patients to present a significant challenge. There may be a whole host of issues, (often more than one) that present a consequent challenge for ensuring that the patient is optimised. Some examples include:


    • Cardiac impairment (e.g. poor LV function, conduction abnormalities)

    • Pain and/or agitation

    • Renal and/or hepatic dysfunction

    • Poor ventilation (e.g. high lung volumes/pressures)

    • Sepsis

    • Poor hydrational status pre critical care

    • Third space loss (e.g. low albumin)

    • Difficult IV access (e.g. practically difficult or inability due to coagulopathy)

    • Presence of other significant co-morbidities



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    DETERMINANTS OF CARDIAC OUTPUT


    PRELOAD

    Pre contractile fibre stretch in diastole is known as preload. Starling’s Law dictates that muscle fibre length at end diastole influences the vigour of contraction. Therefore, ejected volume will increase as filling occurs. However, in cardiac failure or excessive delivery of fluid, the ventricle can become preload insensitive and there will be less ejected volume associated with filling. Other issues can result in reduced diastolic compliance (e.g. hypertension, valve dysfunction, high PEEP)

    Preload is measured in critical care though the use of CVP monitoring.

    • Low preload usually suggests circulating volume is too low

    • High preload usually suggests circulating volume is too high


    CVP reliability should be used with caution in patients where there is evidence of cardiac impairment or suspected problems with afterload and/or contractility


    AFTERLOAD

    This is the muscular tension that is developed during systole per unit of blood flow. The systolic wall stress is affected by blood pressure, wall thickness and ventricular volume. Moderate changes can usually be met by increases in heart rate, contractility or preload so output remains the same. Once these reserves are met, then afterload can significantly rise. On the other hand, if afterload is too low, then efforts to compensate can result in significant changes to heart rate, contractility and preload until the patient becomes severely compromised


    Non invasive cardiac output monitoring allows for observation of systemic vascular resistance which provides a means of measuring the degree of afterload. Systemic Vascular Resistance is measured


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    ONTRACTILITY


    Contractility refers to the ability of the myocardium to contract. This can be affected by many stimuli and these can be independent of the preload and afterload status of the patient, (some examples include electrolye abnormalities, acid base balance, ischemia, anoxia, drugs and toxins). Changes in contractility are rare. For example:

    • Increased sympathetic stimulation to the heart increases contractility and HR.

    • Increased contractility increases stroke volume and an increase in preload.

    • Increase in preload results in an increased force of contraction and does not require a change in contractility.

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