Nursing Medical Emergency Patients E-Book

Philip Jevon

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 400

Veröffentlichungsjahr: 2010

Beschreibung

Nursing Medical Emergency Patients is a practical guide to the nursing care and management of patients with medical emergencies involving system failure. Following an initial chapter on assessment, the authors adopt a system-by-system approach, with an emphasis on the clinical features of medical emergencies, their assessment, diagnosis and treatment. Nursing Medical Emergency Patients is a vital resource for all nurses working with medical emergency patients, and provides an essential companion to both Monitoring the Critically Ill Patient and Treating the Critically Ill Patient. * Accessible and reader friendly * Integrates theory with practice * Adopts an evidence based approach * Includes chapter objectives, 'best practice' boxes and case studies * Refers to National guidelines and key initiatives e.g. outreach teams * Includes legal and ethical issues

Leseprobe

The Essential Clinical Skills for Nurses series focuses on key clinical skills for nurses and other health professionals. These concise, accessible books assume no prior knowledge and focus on core clinical skills, clearly presenting common clinical procedures and their rationale, together with the essential background theory. Their user-friendly format makes them an indispensable guide to clinical practice for all nurses, especially to student nurses and newly qualified staff.

Other titles in theEssential Clinical Skills for Nursesseries:

Clinical Assessment andMonitoring in ChildrenDiana FergussonISBN: 9781405133388

Intravenous TherapyTheresa FinlayISBN: 9780632064519

Respiratory CareCaia FrancisISBN: 9781405117173

Care of the Neurological PatientHelen IgguldenISBN: 9781405117166

ECGs for NursesPhil JevonISBN: 9780632058020

Monitoring the Critically Ill PatientSecond EditionPhil Jevon and Beverley EwensISBN: 9781405144407

Treating the Critically IllPatientPhil JevonISBN: 9781405141727

Pain ManagementEileen Mann and Eloise CarrISBN: 9781405130714

Leg Ulcer ManagementChristine Moffatt, Ruth Martin and Rachael SmithdaleISBN: 9781405134767

Practical ResuscitationEdited by Pam Moule and John AlbarranISBN: 9781405116688

Pressure Area CareEdited by Karen OuseyISBN: 9781405112253

Infection Prevention and ControlChristine PerryISBN: 9781405140386

Stoma CareTheresa Porrett and Anthony McGrathISBN: 9781405114073

Caring for the PerioperativePatientPaul Wicker and Joy O’NeillISBN: 9781405128025

Wound ManagementCarol Dealey and Janice CameronISBN: 9781405155410

Trauma CareElaine ColeISBN: 9781405162302

This edition first published 2008© 2008 Blackwell Publishing Ltd

Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing programme has been merged with Wiley’s global Scientific, Technical, and Medical business to form Wiley-Blackwell.

Registered officeJohn Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, United Kingdom

Editorial offices9600 Garsington Road, Oxford, OX4 2DQ, United Kingdom350 Main Street, Malden, MA 02148-5020, USA

For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell.

The right of the author to be identified as the author of this work has been asserted in accordance with the Copyright, Designs and Patents Act 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.

Library of Congress Cataloging-in-Publication Data

Jevon, Philip.Nursing medical emergency patients / Philip Jevon, Beverley Ewens, Melanie Humphreys.p.; cm. – (Essential clinical skills for nurses)Includes bibliographical references and index.ISBN-13: 978-1-4051-2055-5 (pbk. : alk. paper)ISBN-10: 1-4051-2055-X (pbk. : alk. paper) 1. Emergency nursing. I. Ewens, Beverley. II. Humphreys, Melanie. III. Title. IV. Series.[DNLM: 1. Emergencies–nursing. 2. Critical Care–methods. 3. Nursing Care–methods. WY 154 J58n 2008]

RT120.E4J49 2008610.73′6–dc222007047498

A catalogue record for this book is available from the British Library.

Set in 9 on 12 pt Palatino by SNP Best-set Typesetter Ltd., Hong KongPrinted in Singapore by Utopia Press Pte Ltd

1   2008

Contributors

Anthony Batson RMN, RGN, ENB 100, ENB 148, DN (LON), RCNT, RNT, BSc (Hons)

Senior Lecturer, Pre-registration Studies, University of Wolverhampton, Wolverhampton, UK

James Bethel RN, Emergency Nurse Practitioner, BSc (Hons) Clinical practice, PGD Emergency Care, PGC Learning and Teaching in HE

Senior Lecturer, Emergency Medicine, University of Wolverhampton, Wolverhampton, UK

Kate Deacon PgDip (Health Psychology), BA (Hons) Psychology, RGN, ENB 100

Senior Lecturer, Intensive Care, University of Wolverhampton, Wolverhampton, UK

Beverley Ewens, PG Dip Critical Care, BSc (Hons), PGCE, DPSN, ENB 100, RGN

Staff Development Nurse Practitioner Scholar, Joondalup Health Campus, Edith Cowan University, Western Australia

Fiona Foxall MA Medical Ethics & Law, BSc (Hons) Nursing Studies, DPSN, PGCE (FAHE), ENB 100, RGN

Head of Division, Continuing Professional Development, University of Wolverhampton, Wolverhampton, UK

Melanie Humphreys MA, BSc (Hons), DIPSIN, RGN, ONC, ENB 124

Senior Lecturer, Continuing Development Division, School of Health, University of Wolverhampton, Wolverhampton, UK

Philip Jevon RN, BSc (Hons), PGCE, ENB 124

Resuscitation Officer/Clinical Skills Lead, Honorary Clinical Lecturer, Manor Hospital, Walsall, UK

Gillian Maidens RMN, BSc (Hons), PGCE (Cert. ed) Senior Lecturer, Mental Health, University of Wolverhampton, Wolverhampton, UK

Sue Talbot MSc Advanced Nursing Practice, BSc (Hons) Educational Studies (Nursing), ENB 136, RNT, RGN

Senior Lecturer, Renal Care, University of Wolverhampton, Wolverhampton, UK

Christine Thompson PGDE, BSc, ENB 199, RGN

Senior Lecturer, Pre-registration Studies, University of Wolverhampton, Wolverhampton, UK

Foreword

Historically in the UK, medical emergencies would have occurred within limited areas within the acute hospital such as the emergency department, theatres and recovery and critical care units. However, a number of factors such as a shift of emphasis to care in the community, reduced hospital bed capacity and advanced medical technologies have resulted in hospital beds being occupied by only the acutely ill. This has necessitated all nurses working within the in-patient environment needing to recognise medical emergencies promptly and to instigate appropriate resuscitation. Delay in recognising signs and symptoms of deteriorating medical status can be fatal or severely compromise the patient’s full recovery to health. Furthermore, with the government directives to reduce junior doctors’ working hours nurses are in a pivotal position to be first responders to medical emergencies. Demographically, the UK has an ageing population and this has led to a dramatic increase in the number of people with several co-morbid long terms conditions such as heart failure, chronic respiratory and renal disease. Thus, even patients admitted to hospital for fairly routine procedures or investigations are likely to be predisposed to developing complications such as cardiac failure, pulmonary embolism and shock.

This text provides a user friendly and practical aid to student nurses and registered nurses who wish to further develop their knowledge and skills in responding to medical emergencies effectively. The text does not require the reader to have any previous experience of caring for emergency medical patients as it provides clear and precise guidance to all stages of the ABCDE approach for the most frequently occurring medical emergency situations. Chapter 12 assists us to understand the many complex ethical and legal issues related to the care and treatment of emergency patients in contemporary health care. The editors and contributors are to be commended on compiling this extremely useful text, which should be on the essential reading list for all pre-registration nursing curricula. In summary, this text emphasises the importance of thorough patient observation, which was recognised by Florence Nightingale who wrote

‘In dwelling upon the vital importance of observation, it must never be lost sight of what observation is for. It is not for the sake of piling up miscellaneous information or curious facts, but for the sake of saving life and increasing health and comfort’ (Nightingale, 1859)

REFERENCE

Nightingale, F (1859) Notes on Nursing. J B Lippincott, Philadelphia.

Acknowledgements

We extend our thanks to the contributing authors for their valuable contribution to this book. We have relied on their appraisal of the current literature, national recommendations e.g. Resuscitation Council (UK), National Institute for Clinical Excellence (NICE) and local guidelines, policies and procedures, together with utilising their clinical experience and expertise.

We are particularly grateful to our two Consulting Editors, Dr Adam Crawford McGuffie and Mr Saad Abdulla, for kindly reviewing the clinical accuracy of the text and making helpful and valuable suggestions to improve it.

Finally we are grateful to the staff at Blackwell Publishing for their advice, continued support and patience in all aspects of the publishing process.

Philip JevonMelanie HumphreysBeverley Ewens

Contents

Contributors

Foreword

Acknowledgements

Chapter 1   Overview of the treatment of medical emergencies

Philip Jevon

Chapter 2   Respiratory emergencies

Kate Deacon

Chapter 3   Cardiac emergencies

Melanie Humphreys

Chapter 4   Cardiovascular emergencies

Melanie Humphreys

Chapter 5   Shock

Beverley Ewens

Chapter 6   Neurological emergencies

Anthony Batson and Christine Thompson

Chapter 7   Acute renal failure

Sue Talbot

Chapter 8   Gastrointestinal emergencies

Beverley Ewens

Chapter 9   Endocrine emergencies

Philip Jevon

Chapter 10  Poisoning

James Bethel

Chapter 11  Critical care outreach service

Kate Deacon

Chapter 12  Ethical and legal issues

Fiona Foxall

Index

1 Overview of the Treatment of Medical Emergencies

Philip Jevon

INTRODUCTION

Medical emergencies can be life-threatening. Prompt recognition and effective early treatment of a patient with a medical emergency is paramount if deterioration of the patient is to be prevented and the chances of recovery are to be maximised. The aim of this book is to understand the treatment of medical emergencies.

The assessment and treatment of any patient with a medical emergency should follow the ABCDE approach advocated by the Resuscitation Council UK (Resuscitation Council UK, 2006). In this chapter a brief overview to this generic approach will be provided (a more detailed and comprehensive guide can be found in Treating the Critically Ill Patient, Jevon, 2007) and throughout the book its importance will be continually emphasised.

The aim of this chapter is to provide an overview to the treatment of medical emergencies.

LEARNING OUTCOMES

At the end of the chapter the reader will be able to:

list what emergency equipment should be available,

describe the assessment of a patient with a medical emergency,

state the aim of treating a patient with a medical emergency.

EMERGENCY EQUIPMENT

Wherever patients with medical emergencies are treated, procedures should be in place to ensure that all the essential monitoring and emergency equipment and emergency drugs/fluids are immediately available, accessible and in good working order (Jevon, 2001).

Oxygen

Facilities should be available for the delivery of high concentrations of oxygen: either piped oxygen to a wall-outlet behind the patient’s bed (preferable), or a portable oxygen cylinder, fitted with a variable oxygen-flow-rate meter capable of delivering up to 15 litres/min (Figure 1.1). There should also be adequate stocks of various oxygen-delivery devices, particularly non-rebreathe masks (see Figure 1.4, below).

Figure 1.1 A wall mounted oxygen cylinder, fitted with a variable oxygen-flow-rate meter capable of delivering up to 15 litres/min

Suction

Every clinical area should have access to a portable suction device. In addition, it is preferable if a wall-mounted suction device is available behind each patient’s bed (Figure 1.2). As suction is sometimes required immediately in a life-threatening situation, it is standard practice to store appropriate suction connection tubing, together with suction catheters (rigid and flexible), with the suction source; that is, suction can be quickly administered.

Monitoring devices

At the very least, an ECG monitor and a pulse oximeter should be available. Other monitoring facilities, for example capnography, may also be required in some clinical areas.

Figure 1.2 A wall-mounted suction device

Cardiopulmonary resuscitation trolley

A carefully set out and fully stocked cardiac arrest trolley is paramount, following Resuscitation Council guidelines (Box 1.1) (Resuscitation Council UK, 2004). The trolley should be spacious, sturdy, easily accessible and mobile; ideally each trolley in a healthcare establishment should be identically stocked to avoid confusion. A defibrillator should be immediately available and, where appropriate, for example on general wards, it should have an automatic or advisory facility (Jevon, 2001). Defibrillators with external pacing should be strategically located, for example in emergency departments, intensive care units (ICUs) and coronary care units (CCUs).

Box 1.1 Cardiopulmonary resuscitation equipment that should be available

Airway equipment

Pocket mask with oxygen port (should be widely available in all clinical areas)

Self-inflating resuscitation bag with oxygen reservoir and tubing (ideally, the resuscitation bag should be single-use; if not, it should be equipped with a suitable filter)

Clear face masks, sizes 3, 4 and 5

Oropharyngeal airways, sizes 2, 3 and 4

Nasopharyngeal airways, sizes 6 and 7

Portable suction equipment

Yankauer suckers

Tracheal suction catheters, sizes 12 and 14

Laryngeal mask airways (LMAs; sizes 4 and 5), or ProSeal LMAs (sizes 4 and 5), or Combitube (small)

Magill forceps

Tracheal tubes, oral, cuffed, sizes 6, 7 and 8

Gum elastic bougie or equivalent device

Lubricating jelly

Laryngoscope handles (×2) and blades (standard and long blade)

Spare batteries for laryngoscope and spare bulbs (if applicable)

Fixation for tracheal tube (e.g. ribbon gauze/tape)

Scissors

Selection of syringes

Oxygen mask with reservoir (non-rebreathing) bag

Oxygen cylinders

Cylinder key

Circulation equipment

Defibrillator (shock advisory module and or external pacing facility to be decided by local policy)

ECG electrodes

Defibrillation gel pads or self-adhesive defibrillator pads (preferred)

Selection of intravenous cannulae

Selection of syringes and needles

Cannula fixing dressings and tapes

Seldinger central venous catheter kit

Intravenous infusion sets

0.9% sodium chloride, 1000 ml × 2

Arterial blood gas syringes

Tourniquet

Drugs

(a) Immediately available prefilled syringes

Adrenaline (epinephrine) 1 mg (1 : 10,000) × 4

Atropine 3 mg × 1

Amiodarone 300 mg × 1

(b) Other readily available drugs

IV injections

Adenosine 6 mg × 10

Adrenaline 1 mg (1 : 10,000) × 4

Adrenaline 1 mg (1 : 1000) × 2

Amiodarone 300 mg × 1

Calcium chloride 10 ml of 100 mg/ml × 1

Chlorphaniramine 10 mg × 2

Furosemide 50 mg × 2

Glucose 10% 500 ml × 1

Hydrocortisone 100 mg × 2

Lignocaine 100 mg

Magnesium sulphate 50% solution 2 g (4 ml) × 1

Midazolam 10 mg × 1

Naloxone 400 mg × 5

Normal saline, 10 ml ampoules

Potassium chloride for injection (see National Patient Safety Agency Alert, www.npsa.nhs.uk)

Sodium bicarbonate 8.4%, 50 ml × 1

Other medications/equipment

Salbutamol (5 mg × 2) and ipratropium bromide (500 mg × 2) nebules

Nebulizer device and mask

Glyceryl trinitrate spray

Aspirin 300 mg

Additional items

Clock

Gloves/goggles/aprons

Audit forms

Sharps container and clinical waste bag

Large scissors

Alcohol wipes

Blood sample bottles

A sliding sheet or similar device should be available for safer handling

Source: Resuscitation Council UK (2004).

Routine checking of emergency equipment

All emergency equipment should be checked routinely following local protocols. It is recommended that cardiopulmonary resuscitation equipment should be checked on a daily basis by each ward or department responsible for it (Resuscitation Council UK, 2000). A system for daily documented checks of the equipment inventory should be in place (Jevon, 2001). The electronic equipment should be stored, maintained and checked following the manufacturer’s recommendations and those of the local electrobiomedical engineers’ department (EBME).

ASSESSMENT OF A PATIENT WITH A MEDICAL EMERGENCY

ABCDE assessment

A patient with a medical emergency will be critically ill. The Resuscitation Council UK (2006) has issued guidelines on the recognition and treatment of the critically ill patient. Adapted from the ALERT course (Smith, 2003), these guidelines follow the logical and systematic ABCDE approach to patient assessment and treatment:

Airway,

Breathing,

Circulation,

Disability,

Exposure.

When assessing the patient, a complete initial assessment should be undertaken, identifying and treating life-threatening problems first, before moving on to the next part of assessment. The effectiveness of treatment/intervention should be evaluated, and regular re-assessment undertaken. The need to alert more senior help should be recognised and other members of the multidisciplinary team should be utilised as appropriate so that patient assessment, instigation of appropriate monitoring and interventions can be undertaken simultaneously.

Irrespective of their training, experience and expertise in clinical assessment and treatment, all nurses can follow the ABCDE approach; clinical skills, knowledge, expertise and local circumstances will determine what aspects of the assessment and treatment are undertaken. Throughout this book, the ABCDE approach will be reinforced.

Prevention of cross-infection

When assessing and treating the critically ill patient, it is important to ensure that effective measures are taken to minimise the risk of cross-infection. Wash hands or use alcohol gel following local policy (Figure 1.3).

Figure 1.3 Hygienic hand-rub

Communication with the patient

Talk to the patient and evaluate the response: a normal response indicates that they have a clear airway, are breathing and have adequate cerebral perfusion; if they are unable to complete sentences in one breath, this may be an indication of extreme respiratory distress. An inappropriate response or no response could indicate an acute life-threatening physiological disturbance (Gwinnutt, 2006).

General appearance of the patient

Note the patient’s general appearance, their colour and whether they appear content and relaxed or distressed and anxious.

Senior help

During the assessment process, consider whether senior help should be requested. Evaluate MEWS score and alert medics/outreach if necessary (see p. 298).

Oxygen

Administer high concentrations of oxygen: use a non-rebreathe mask (Figure 1.4) connected to an oxygen flow rate of 15 litres/min (Smith, 2003). This will enable the delivery of an inspired oxygen concentration of approximately 95% (Jevon, 2007). Prior to application, carry out checks to ensure correct functioning as recommended by the manufacturer (Figure 1.5).

Patient-monitoring devices

Attach appropriate monitoring devices, for example pulse oximetry, ECG monitor and non-invasive blood-pressure monitoring, as soon as it is safe to do so (Resuscitation Council UK, 2006).

Figure 1.4 A non-rebreathe mask. Taken from Jevon, P (2007) Treating the Critically Ill Patient. Blackwell Publishing, Oxford, with permission

Figure 1.5 Ensure correct functioning as recommended by the manufacturer. (a) Attach the tubing to the oxygen source and set the oxygen flow rate. (b) Occlude the valve between the mask and the oxygen reservior bag to check that the bag fills up with oxygen. Taken from Jevon, P (2007) Treating the Critically Ill Patient. Blackwell Publishing, Oxford, with permission.

Assessment of airway

Look, listen and feel for the signs of airway obstruction. Partial airway obstruction will result in noisy breathing:

gurgling: indicates the presence of fluid, for example secretions or vomit, in the mouth or upper airway; usually seen in a patient with altered conscious level who is having difficulty or is unable to clear their own airway;

snoring: indicates that the pharynx is being partially obstructed by the tongue; usually seen in a patient with altered conscious level lying in a supine position;

stridor: high-pitched sound during inspiration, indicating partial upper-airway obstruction; usually due to either a foreign body or laryngeal oedema;

wheeze: noisy musical whistling type sound due to the turbulent flow of air through narrowed bronchi and bronchioles, more pronounced on expiration; causes include asthma and chronic obstructive pulmonary disease (COPD).

Complete airway obstruction can be detected by no air movement at the patient’s mouth and nose. Paradoxical chest and abdominal movements (‘see-saw’ movement of the chest) may be observed; central cyanosis (a late sign of airway obstruction) will develop if not treated rapidly.

If the patient’s airway is compromised, or is at risk of being compromised, take immediate action. Treat the underlying cause (Resuscitation Council UK, 2006); for example:

apply head tilt/chin lift to open the airway;

suction the airway if secretions, blood or gastric contents are present;

place the patient in the lateral position if breathing, but has altered conscious level;

if the patient is unconscious, insert an oropharyngeal airway to help maintain an oral airway (a nasopharyngeal airway may be helpful in a patient who is semi-conscious);

advanced airway intervention, for example tracheal intubation or tracheostomy, may be required in some situations;

administer high-concentration oxygen.

Assessment of breathing

Look, listen and feel to assess breathing.

Count the respiratory rate: normal respiratory rate is 12–20 breaths/min (Resuscitation Council UK, 2006). Tachypnoea is usually the first sign that the patient has a physiological upset, the cause of which may be respiratory (NCEPOD, 2005). Bradypnoea is an ominous sign and could indicate imminent respiratory arrest; causes include drugs such as opiates, fatigue, hypothermia, head injury and central nervous system depression.

Evaluate chest movement: chest movement should be symmetrical; unilateral chest movement suggests unilateral pathology, such as pneumothorax, pneumonia or pleural effusion (Smith, 2003).

Evaluate depth of breathing: only marked degrees of hyper-ventilation and hypoventilation can be detected; hyper-ventilation may be seen in metabolic acidosis or anxiety and hypoventilation may be seen in opiate toxicity (Ford et al., 2005).

Evaluate respiratory pattern: a Cheyne–Stokes breathing pattern (periods of apnoea alternating with periods of hyperpnoea) can be associated with brain-stem ischaemia, cerebral injury and severe left-ventricular failure (altered carbon dioxide sensitivity of the respiratory centre) (Ford et al., 2005).

Note the oxygen saturation (SpO2) reading: 97–100% is normal. A low SpO2 could indicate respiratory distress or compromise. Note that the pulse oximeter does not detect hypercapnia and that the SpO2 can be normal in the presence of a very high PaCO2 (Resuscitation Council UK, 2006).

Listen to the breathing: normal breathing is quiet. Rattling airway noises indicate the presence of airway secretions, usually due to the patient being unable to cough sufficiently or unable to take a deep breath in (Smith, 2003). The presence of stridor or wheeze indicates partial, but significant, airway obstruction (see above).

Check the position of the trachea: place the tip of the index finger into the suprasternal notch, let it slip either side of the trachea and determine whether it fits more easily into one or other side of the trachea (Ford et al., 2005). Deviation of the trachea to one side indicates mediastinal shift (e.g. lung collapse, pneumothorax, lung fibrosis or pleural fluid).

Palpate the chest wall: to detect surgical emphysema or crepitus (suggesting a pneumothorax until proven otherwise) (Smith, 2003).

Perform chest percussion: this is done as follows.

Place the left hand on the patient’s chest wall. Ensure that the fingers are separated slightly, with the middle finger pressed firmly into the intercostal space to be percussed (Ford et al., 2005).

Strike the centre of the middle phalanx of the middle finger sharply using the tip of the middle finger of the right hand (Ford et al., 2005). Deliver the stroke using a quick flick of the wrist and finger joints not from the arm or shoulder. The percussing finger should be bent so that its terminal phalanx is at right angles to the metacarpal bones when the blow is delivered, and it strikes the percussed finger in a perpendicular way. The percussing finger should then be removed immediately, like a clapper inside a bell, otherwise the resultant sound will be dampened (Epstein et al., 2003).

Percuss the anterior and lateral chest wall. Percuss from side to side, top to bottom, comparing both sides and looking for asymmetry.

Categorise the percussion sounds (see below).

If an area of altered resonance is located, map out its boundaries by percussing from areas of normal to altered resonance (Ford et al., 2005).

Sit the patient forward and then percuss the posterior chest wall, omitting the areas covered by the scapulae. Ask the patient to move their elbows forward across the front of the chest: this will rotate the scapulae anteriorly and out of the way (Talley & O’Connor, 2001). It may be helpful to offer the patient a pillow to lean on.

Again percuss from side to side, top to bottom, comparing both sides and looking for asymmetry. Don’t forget that the lung extends much further down posteriorly than anteriorly (Epstein et al., 2003).

Categorise the percussion sounds (see below).

The causes of different percussion notes are listed below (source, Ford et al., 2005):

resonant: air-filled lung;

dull: liver, spleen, heart, lung consolidation/collapse;

stony dull: pleural effusion/thickening;

hyper-resonant: pneumothorax, emphysema;

tympanitic: gas-filled viscus.

Auscultate the chest

Ask the patient to breathe in and out normally through their mouth.

Auscultate the anterior chest from side to side, and top to bottom. Auscultate over equivalent areas and compare the volume and character of the sounds and note any additional sounds. Compare the sounds during inspiration and expiration.

Note the location and quality of the sounds heard.

Auscultate the posterior chest, from side to side, and top to bottom. Auscultate over equivalent areas and compare the volume and character of the sounds and note any additional sounds. Compare the sounds during inspiration and expiration (Jevon & Cunnington, 2006).

Evaluate air entry, the depth of breathing and the equality of breath sounds on both sides of the chest. Bronchial breathing indicates lung consolidation; absent or reduced sounds suggest a pneumothorax or pleural fluid (Smith, 2003). In particular, note any additional breath sounds:

Wheezes (rhonchi): these are high-pitched musical sounds associated with air being forced through narrowed airways, for example asthma (Ford et al., 2005). This is usually more pronounced on expiration. Inspiratory wheeze (stridor) is usually indicative of severe upper-airway obstruction, for example by a foreign body or laryngeal oedema. If both inspiratory and expiratory wheezes are heard, this is usually due to excessive airway secretions (Adam & Osborne, 2005).

Crackles (crepitations): these are non-musical sounds, associated with reopening of a collapsed airway, for example pulmonary oedema (Ford et al., 2005). Crackles are usually localised in pneumonia and mild cases of bronchiectasis; in pulmonary oedema and fibrosing alveolitis, both lung bases are affected equally (Epstein et al., 2003).

Pleural friction rub: this can be heard as leathery/creaking sounds during inspiration and expiration, evident in areas of inflammation when the normally smooth pleural surfaces are roughened and rub on each other (Adam & Osborne, 2005).

Record peak expiratory flow rate: this provides a useful estimate of the calibre of the airways, particularly in asthma and COPD (Ford et al., 2005).

Evaluate the efficacy of breathing, work of breathing and adequacy of ventilation

Efficacy of breathing: air entry, chest movement, pulse oximetry, arterial blood gas analysis and capnography.

Work of breathing: respiratory rate and use of accessory muscles, for example neck and abdominal muscles.

Adequacy of ventilation: heart rate, skin colour and mental status.

If breathing is compromised, ensure a clear airway and administer a high concentration of oxygen. Positioning the patient in an upright position can be helpful in a patient who is breathing spontaneously. It is important to recognise and effectively treat immediately life-threatening conditions, such as acute severe asthma, pulmonary oedema, tension pneumothorax and massive haemothorax (Resuscitation Council UK, 2006). Patients with inadequate ventilation will need ventilatory support.

Assessment of circulation

Look, listen and feel to assess circulation.

Palpate peripheral and central pulses: check for presence, rate, quality, regularity and equality (Smith, 2003). A weak, thready pulse suggests a poor cardiac output and a bounding pulse may indicate sepsis (Resuscitation Council UK, 2006).

Check the colour and temperature of the hands and fingers: signs of cardiovascular compromise include cool and pale peripheries.

Measure the capillary refill time (CRT): apply sufficient pressure to cause blanching to the skin, for example on the sternum, for 5 s and then release (Figure 1.6). Normal CRT is less than 2 s; a prolonged CRT could indicate poor peripheral perfusion, although other causes can include cool ambient temperature, poor lighting and old age (Resuscitation Council UK, 2006).

Figure 1.6 Measuring the central capillary refill time (CRT). Taken from Jevon, P (2007) Treating the Critically Ill Patient. Blackwell Publishing, Oxford, with permission

Look for other signs of a poor cardiac output: these include altered conscious level and, if the patient has a urinary catheter, oliguria (urine volume less than 0.5 ml/kg per h) (Smith, 2003).

Look for signs of haemorrhage: for example from wounds or drains, or evidence of internal haemorrhage, such as abdominal swelling; concealed blood loss can be significant, even if drains are empty (Smith, 2003).

Measure blood pressure: systolic blood pressure (BP) of less than 90 mmHg suggests shock. A normal BP does not exclude shock because compensatory mechanisms increase peripheral resistance in response to reduced cardiac output (Smith, 2003). A low diastolic BP suggests arterial vasodilatation, for example anaphylaxis or sepsis. A narrowed pulse pressure – that is, the difference between systolic and diastolic readings (normal is 35–45 mmHg), suggests arterial vasoconstriction, for example cardiogenic shock or hypovolaemia (Resuscitation Council UK, 2006).

Assess the state of the veins: if hypovolaemia is present the veins could be under-filled or collapsed (Smith, 2003).

Interpret the ECG: determine whether a cardiac arrhythmia is present. A 12-lead ECG should be recorded as a priority in some situations, for example chest pain.

If the patient has compromised circulation (Resuscitation Council UK, 2006);

ensure the airway is clear and breathing is adequate;

administer high-concentration oxygen;

if shock present, insert one or more wide-bore cannulae (14–16-gauge), and start treatment directed at fluid replacement, haemorrhage control and restoration of tissue perfusion; administer a rapid fluid challenge, for example 500 ml normal saline (warmed) over 5–10–min;

if the patient has chest pain and acute coronary syndrome is suspected, treat initially with oxygen, aspirin, nitroglycerine and morphine.

Assessment of disability

Assess disability (central nervous system function) as follows.

Evaluate the patient’s level of consciousness: use the AVPU scale (see Box 6.1) or the Glasgow Coma Scale (GCS) (see Box 6.2) if a more objective assessment of conscious level is required, for example head injury (see Chapter 6 in this volume).

Examine the pupils: compare size, equality and reaction to light of each pupil.

Undertake bedside glucose measurement: exclude hypoglycaemia as a cause of altered conscious level.

If the patient has altered conscious level (Resuscitation Council UK, 2006):

review ABC: exclude or treat hypoxia and hypotension (both of which are possible causes of altered conscious level);

nurse in a lateral position, with particular attention to the airway;

review the patient’s medication chart: check for reversible medication-induced causes of altered conscious level, for example administer naloxone (opioid antagonist) for opioid toxicity.

Exposure

Expose the patient and undertake a thorough examination to ensure that important details are not over-looked (Smith, 2003). In particular, the examination should concentrate on the part of the body that is most probably contributing to the patient’s ill status, for example in suspected anaphylaxis, examine the skin for urticaria. Respect the patient’s dignity and minimise heat loss.

In addition (source, Resuscitation Council UK, 2006):

take a full clinical history and review the patient’s notes/charts;

study the recorded vital signs: trends are more significant than one-off recordings;

administer prescribed medications;

review laboratory results and ECG and radiological investigations;

ascertain what level of care the patient requires (e.g. ward, high-dependency unit, ICU);

document in the patient’s notes details of assessment, treatment and response to treatment.

THE AIM OF TREATING A PATIENT WITH A MEDICAL EMERGENCY

The aim of treating a patient with a medical emergency is the early anticipation and detection of abnormal physiology at a stage before organ failure is established and to initiate simple preventative therapies and interventions (Smith, 2003). The initial ABCDE assessment and treatment should be seen as a holding measure to keep the patient alive, and to produce some clinical improvement, so that definitive treatment may be initiated (Resuscitation Council UK, 2006). The aim of this book is to discuss the treatment of medical emergencies following the ABCDE approach.

CONCLUSION

Recognition and the effective treatment of a patient with a medical emergency is paramount. In this chapter the importance of ensuring that the necessary emergency equipment is available and the systematic approach to assessment following the ABCDE method have been described. In the remaining chapters of the book the specific treatment for individual medical emergencies will be discussed.

REFERENCES

Adam, S & Osborne, S (2005) Critical Care Nursing Science and Practice, 2nd edn. Oxford University Press, Oxford

Epstein, O, Perkin, G, Cookson, J & de Bono, D (2003) Clinical Examination, 3rd edn. Mosby, London

Ford, M, Hennessey, I & Japp, A (2005) Introduction to Clinical Examination. Elsevier, Oxford

Gwinnutt, C (2006) Clinical Anaesthesia, 2nd edn. Blackwell Publishing, Oxford

Jevon, P (2001) Advanced Cardiac Life Support. Butterworth Heinemann, Oxford

Jevon, P (2007) Treating the Critically Ill Patient. Blackwell Publishing, Oxford.

Jevon, P & Cunnington, A (2006) Chest examination Part 3. Chest auscultation. Nursing Times102(46), 26–7

National Confidential Enquiry into Patient Outcome and Death (NCEPOD) (2005) An Acute Problem? NCEPOD, London.

Resuscitation Council UK (2000) Cardiopulmonary Resuscitation: Guidelines for Clinical Practice and Training. Resuscitation Council UK, London

Resuscitation Council UK (2004) Recommended Minimum Equipment for In-Hospital Adult Resuscitation. Resuscitation Council UK, London

Resuscitation Council UK (2006) Advanced Life Support, 5th edn. Resuscitation Council UK, London

Smith, G (2003) ALERT Acute Life-Threatening Events Recognition and Treatment, 2nd edn. University of Portsmouth, Portsmouth

Talley, N & O’Connor, S (2001) Clinical Examination, 4th edn. Blackwell Publishing, Oxford

This chapter is based on the chapter ‘Overview of Treating the Critically Ill Patient’ which first appeared in Treating the Critically Ill Patient by Jevon (2007). It has been revised and updated.

2 Respiratory Emergencies

Kate Deacon

INTRODUCTION

Respiratory emergencies can result from an array of different causes, from acute exacerbation of a long-term chronic respiratory disease to acute traumatic injury. In the UK one in five deaths are caused by respiratory disease. In 2004 more people died from respiratory disease (117,000) than from ischaemic heart disease (106,000) (British Thoracic Society, 2006). Once changes in the coding for deaths caused by pneumonia are taken into account, mortality rates from respiratory disease seen in 2004 have changed little in 20 years (British Thoracic Society, 2006).

Large socio-economic effects are seen in mortality rates for respiratory diseases, more than for any other type of disease. Social class inequality is estimated to be associated with 40% of respiratory deaths (British Thoracic Society, 2006).

The burden for the NHS of respiratory disease is a significant one. In English NHS hospitals in 2004/2005 there were 845,000 inpatient admissions for respiratory disease (7% of admissions); 550,000 of these were emergency admissions (13% of emergency admissions) (British Thoracic Society, 2006). In 2004 the cost to the NHS of respiratory disease was calculated to be £3 billion with a total cost to the UK economy of £6.6 billion (British Thoracic Society, 2006).

LEARNING OUTCOMES

At the end of the chapter the reader will be able to:

define respiratory failure,

outline pulse oximetry and arterial blood gas (ABG) analysis,

discuss the treatment of chronic obstructive pulmonary disease (COPD),

discuss the treatment of asthma,

discuss the treatment of pneumonia,

discuss the treatment of acute respiratory distress syndrome (ARDS),

discuss the treatment of pneumothorax.

RESPIRATORY FAILURE

‘Respiratory failure is defined as a failure to maintain adequate gas exchange and is characterised by abnormalities in arterial blood gas tensions’ (British Thoracic Society Standards of Care Committee, 2002). Respiratory failure is split into two types, relating to the abnormalities seen in the arterial blood gases (ABGs). These are described in Table 2.1.

In type 1 (hypoxic) respiratory failure, ventilation is adequate but there is a problem with the exchange of oxygen. It is caused by a mismatch between ventilation and perfusion (V/Q mismatch). That is, the areas of the lung that are well ventilated are not well perfused with blood or vice versa.

Type 2 respiratory failure is caused by inadequate ventilation. As insufficient air reaches the areas of gas exchange, both PaO2 and PaCO2 are deranged.

Having an awareness of the effect of the type of respiratory failure a patient is experiencing is essential in ensuring that an appropriate method of monitoring oxygenation is employed.

Table 2.1 Types 1 and 2 respiratory failure

Type 1 respiratory failureType 2 respiratory failurePaO2 <8.0 kPaPaO2 <8.0 kPaPaCO2 normal or lowPaCO2 >6.0 kPa

Source: British Thoracic Society (2008).

PULSE OXIMETRY AND ARTERIAL BLOOD GAS ANALYSIS

Pulse oximetry (Figure 2.1) is a non-invasive method for assessing the oxygen saturation of haemoglobin in the peripheral circulation (SpO2 which has a direct correlation to arterial oxygen saturation (SaO2)). It involves a probe that usually sits on the end of a finger; a combination of red and infrared light is used to calculate how well haemoglobin is saturated with oxygen (Jevon & Ewens, 2007). It is one of the physiological observations that the National Institute for Health and Clinical Excellence (NICE) Short Clinical Guidelines Technical Team (2007) have recently recommended should be taken as standard (see Chapter 11 in this volume).

Pulse oximetry is non-invasive, cheap and fairly simple to use; however, one should be aware that it does not provide information about the level of CO2 in the patients blood, which would render it less suitable for use in patients with type 2 respiratory failure. For these measurements an ABG sample will need to be taken. Either samples can be obtained from a one-off arterial ‘stab’ using syringe and needle or an arterial line can be sighted which has a port to allow blood samples to be taken. Taking arterial stab samples requires a level of skill and can be very uncomfortable for the patient; consideration should therefore be given to sighting an arterial line if frequent samples are required. Box 2.1 shows normal ABG values. Note that these values are for a healthy adult; those with chronic respiratory disease may have varied baseline values. Analysis of ABG results is described in detail elsewhere (Jevon & Ewens, 2007).

Figure 2.1 A pulse oximetry monitor with finger probe

Box 2.1 Normal arterial blood gas values

pH      7.35–7.45PaCO2      35–45 mmHg (as well as kPa)PaO2      10.0–14 kPa (75–105 mmHg)Base excess      -2 mmol/+2 mmolHCO3      22–26 mmol/lSaO2      95–100%

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

COPD is an internationally recognised term that describes a spectrum of disease processes characterised by a chronic and progressive reduction in airflow. Although there may be an element of reversibility, most of the respiratory impairment is permanent and affects the upper airways, lung parenchyma and pulmonary circulation (Francis, 2006).

Specific diseases such as chronic bronchitis and emphysema are common causes of COPD; however, a small number have a diagnosis of emphysema without it progressing to a diagnosis of COPD (Selby, 2002). Also, whereas many smokers show symptoms of chronic bronchitis not all will develop the permanent airflow restriction of COPD as many will find that their symptoms disappear when they give up smoking (British Thoracic Society, 1997; Francis, 2006). Guidelines on the management of COPD have been published by NICE (NICE, 2004) and the Department of Health states that a National Service Framework for COPD will be published in 2008.

Incidence

At least 600,000 people in the UK have a diagnosis of COPD, a prevalence of 1%. However, one must be cognisant that diagnosis is usually made relatively late when definite symptoms have appeared (Calverly & Bellamy, 2000). In particular, smokers often ignore a persistent cough as simply being a side effect of the habit (Fehrenbach, 2002). In England alone in 2004 over 1 million hospital bed days were accounted for by COPD, and in the same year in the UK 27,478 people died from COPD, 23% of all respiratory deaths (British Thoracic Society, 2006). There is a strong socio-economic risk for COPD, with men of 20–64 years in manual unskilled occupations being 14 times more likely to die from COPD than those in professional ones (British Thoracic Society, 2006).

Pathogenesis

Chronic bronchitis is a state of mucus hypersecretion, defined as a productive cough on most days for 3 months for 2 con-secutive years (without alternative explanation) (Bourke, 2003). The airways of chronic bronchitic patients have mucus-gland hypertrophy and excess goblet cells. The accumulation of mucus and the presence of infection can aggravate airway obstruction.

Emphysema causes airflow obstruction from damage to the alveoli, the walls of which are broken down and become distended. This may follow a pattern known as centrilobular, where the distended air spaces are those immediately next to the terminal bronchiole with more distal ones intact, or panacinar, where distension is spread throughout the acinus from the terminal bronchiole to the distal spaces (see Figure 2.2) (Bourke, 2003; Halpin, 2003).

Panacinar emphysema is the characteristic pattern seen in patients with alpha-1 (a-1) anti-trypsin deficiency (Bourke, 2003). The terminal airways have no cartilage to keep them open and depend on the support of surrounding alveoli for this. Support is lost with the destruction of alveolar walls and the airways collapse during expiration, which leads to air trapping. With the destruction of alveolar walls capillary blood supply is also lost, leading to ventilation/perfusion mismatch.

Figure 2.2 Views of a lobule (left) and whole lung section (right) in (a) centrilobular and (b) panacinar emphysema

Causes

The single most important cause of COPD is cigarette smoking (British Thoracic Society, 1997; Bourke, 2003; Halpin, 2003). According to the British Thoracic Society COPD Consortium (2007) smoking is responsible for 95% of cases. COPD can develop in non-smokers but this is rare. Although nearly all COPD patients have smoked, only about 15% of smokers go on to develop clinically significant COPD (British Thoracic Society, 1997).

An inherited deficiency of the anti-protease a-1 anti-trypsin is associated with the development of severe emphysema with the risk being much increased in those with the deficiency who smoke (Global Initiative for Chronic Obstructive Lung Disease, 2006). A deficiency of a-1 anti-trypsin causes an imbalance between proteases and anti-proteases that leads to proteolytic destruction of lung tissue. However, this deficiency is stated to account for only 1–2% of severe COPD (Bourke, 2003; Halpin, 2003). There may be other heritable factors that have not yet been identified. A number of other factors have been shown to be implicated in the development of COPD. These are summarised in Box 2.2.

Box 2.2 Risk factors for COPD

Genes

Exposure to particles

Tobacco smoke

Occupational dusts, organic and inorganic

Indoor air pollution from heating and cooking with

biomass in poorly ventilated dwellings

Outdoor air pollution

Lung growth and development

Oxidative stress

Gender

Age

Respiratory infections

Socio-economic status

Nutrition

Comorbidities

Source: Global Initiative for Chronic Obstructive Lung Disease (2006).

Clinical features

There is great variability in the symptoms experienced by patients for different severities of airflow obstruction and in the rate of disease progression. Many patients with mild airflow obstruction will be asymptomatic (Halpin, 2003). Initially symptoms may be mild and intermittent but become more severe and continuous with severe airflow obstruction. The key symptoms of COPD are cough, wheeze and breathlessness (Halpin, 2003).

Chronic cough and sputum production are caused by mucus hypersecretion and infective exacerbations are commonly seen, which cause purulent secretions (Bourke, 2003). The patient often does not notice shortness of breath until a significant amount of respiratory function has been permanently lost, especially in those with a sedentary lifestyle; deterioration is usually gradual over a number of years (Bourke, 2003).

Investigations

NICE (2004), in their clinical guidance on the management of COPD, recommended the following investigations for all suspected COPD patients:

spirometry,

chest X-ray,

calculation of body mass index (BMI).

Further investigations may be necessary in some instances, as outlined in Table 2.2.

Diagnosis

There is not one specific test for COPD and diagnosis is made from the overall clinical picture. NICE (2004) state that a diagnosis of COPD should be considered in patients who:

are over 35;

are smokers or ex-smokers;

have any of these symptoms:

exertional breathlessness,

chronic cough,

regular sputum production,

frequent winter bronchitis;

have no clinical symptoms of asthma.

Clinical features that may differentiate between asthma and COPD can be seen in Table 2.3.

Table 2.2 Further investigations for COPD

Investigation

Role

Serial domiciliary peak-flow measurements

      

To exclude asthma if diagnostic doubt remains

α-1 Anti-trypsin

      

If early-onset, minimal smoking history or family history

Transfer factor for carbon monoxide (TLCO)

      

To investigate symptoms that seem disproportionate to the spirometric impairment

CT scan of the thorax

      

To investigate symptoms that seem disproportionate to the spirometric impairment

To investigate abnormalities seen on a chest radiograph

To assess suitability for surgery

ECG

      

To assess cardiac status if there are features of cor pulmonale

Echocardiogram

      

To assess cardiac status if there are features of cor pulmonale

Pulse oximetry

      

To assess need for oxygen therapy

If cyanosis or cor pulmonale is present, or if FEV1 <50% predicted

Sputum culture

      

To identify organisms if sputum is persistently present and purulent

Source: NICE (2004).

FEV1, forced expiratory volume in 1 s.

Table 2.3 Clinical features of COPD and asthma

COPDAsthma

Smoker or ex-smoker      

Nearly all      Possibly

Symptoms under age 35      

Rare      Common

Chronic productive cough      

Common      Uncommon

Breathlessness      

Persistent and progressive      Variable

Night-time waking with breathlessness and/or wheeze      

Uncommon      Common

Significant diurnal or day-to-day variability of symptoms      

Uncommon      Common

Source: NICE (2004).

If COPD seems likely from the above then spirometry should be performed to confirm airway obstruction. Airway obstruction is defined as (NICE, 2004; Global Initiative for Chronic Obstructive Lung Disease, 2006):

forced expiratory volume in 1 s (FEV1) <80% predicted,

and FEV1/forced vital capacity <0.7.

Treatment

In the UK guidance for COPD treatment is provided by the NICE clinical guidelines of 2004. Within this extensive guidance, recommendations are given for management of the chronic symptoms of mild, moderate and severe COPD as well as recommendations for acute exacerbations treated in hospital or at home.

Assess the patient following the ABCDE approach (Chapter 1). Evaluate MEWS score and alert medics/outreach if necessary (see p. 298).

Sit the patient in an upright position and administer oxygen. All critically ill patients should receive oxygen, including COPD patients. Caution should be exercised in COPD patients who have previously retained CO2 in whom high concentration of oxygen may precipitate respiratory failure; the aim is to maintain oxygen saturations at 90–92%. (Resuscitation Council UK, 2006). Commence pulse oximetry.

Administer nebulised bronchodilators; intravenous theophyl lines may also be required.

Assess the need for non-invasive ventilation, such as BiPAP (Bi level positive airways pressure).

Monitor the patient’s level of consciousness using AVPU and undertake regular pupillary assessment; if the patient’s conscious level starts to deteriorate, for example drowsiness, they may becoming hypoxic or hypercapnoeic.

If respiratory status is compromised, summon expert help immediately as tracheal intubation and mechanical ventilation may be required; whilst awaiting for help, provide ventilation as required.

Insert a wide-bore intravenous cannula (e.g. 14 gauge) and obtain blood sample for relevant investigations, including full blood count, urea and electrolytes, liver-function tests and glucose.

Ensure the following investigations are performed:

chest X-ray,

ABG (with record of inspired oxygen content),

ECG,

full blood count, urea and electrolytes,

Theophylline level if patient taking drug prior to admission,

sputum sample for microscopy and culture if purulent.

(NICE, 2004)

ASTHMA

‘Asthma is a condition which is characterised by episodes of reversible airway narrowing, associated with contraction of smooth muscle within the airway wall’ (Weinberger, 2004). Various definitions such as this exist which describe the key characteristics of the disease; however, there isn’t one agreed definition (BTS & SIGN, 2008).

There is considerable variation between patients in the severity of episodes experienced and the overall course of the disease. For some patients their illness is well controlled and they are asymptomatic between acute attacks whereas for others the illness can progress to a state of irreversible airway obstruction (Bourke, 2003).

Incidence

There are 5.2 million people in the UK with asthma; of these 1.1 million are children and 4.1 million are adults (Asthma UK, 2004). Although the number of children with asthma has fallen since a peak in the 1990s the number of adults with asthma has risen, with an increase of 400,000 between 2001 and 2004. Asthma caused 69,000 hospital admissions and 1400 deaths in the UK in 2002 (Asthma UK, 2004).

Figure 2.3 A healthy bronchus and an asthmatic bronchus

Pathogenesis