Mobitz type II block : failure to conduct P waves may occur regularly (eg 3:1) or irregular ly, but the PR interval remains constant (Fig. 3.13 ). Third degree (complete) heart block Atrial activity is not conducted to ventricles. With a proximal block (eg at the AV node), a proximal escape pacemaker in the AV node or bundle of His may take over, producing narrow QRS complexes at a rate of 8 50/min. With distal AV bl ock, a more distal escape pacemaker results in broad bizarre complexes at a rate of 8 30/mi n. Ventricular asystole may occur if the escape pacemaker stops discharging, unless a subsi diary pacemaker takes over (Fig. 3.14 ). Intraventricular conduction disturbances The intraventricular conducting system commences a s the bundle of His and divides into right and left bundle branches \200\224 the latter su bdivides further into antero-superior and postero-superior divisions. These two divisions a nd the right bundle branch are referred to as the \200\230fascicles \200\231. Blockage of 2 out of 3 fascicles = bifascicular block . \200 RBBB + left anterior hemiblock causes le ft axis deviation and RBBB pattern on ECG. RBBB + left posterior hemiblock causes right axis deviation and RBBB pattern on ECG. Trifascicular block is present when bifasciular block is accompanied by a prolonged PR inte rval. Note that true blockage of all 3 fascicles would cause complete heart block, so \200 \230trifascicular block \200\231 represents impending progression to complete heart block. 81 BRADYARRHYTHMIAS Fig. 3.11 ECG of \201 rst degree heart block. Fig. 3.12 ECG of Mobitz type I AV block. Fig. 3.13 ECG of Mobitz type II AV block. Fig. 3.14 ECG of complete AV block. 82 CHAPTER 3 Medicine Treatment of bradyarrhythmias The emergency treatment of bradycardia depends upon two impor tant factors: the clinical condition of the patient and the risk of asystole. Give O 2 , in sert an IV cannula and follow the 2010 European Resuscitation Council Guidelines shown oppo site ( www.resus.org.uk ). Atropine is the \201 rst-line drug. The standard dose is 500mcg IV, which may be repeated to a total of 3mg. Further doses are not effective and may result in toxic effects (eg psy chosis, urinary retention). Adrenaline (epinephrine) can be used as a temporizing measure prior to transvenous pacing i f an external pacemaker is not available. Give by controlled infusion at 2 \200\22310mcg/mi n, titrating up according to response (6mg adrenaline in 500mL 0.9 % saline infused at 10 \200\22350mL/hr). External transcutaneous pacing is available on most de \201 brillators. It allows a pacing current to be passed between 2 adhesive electrodes placed over the front of the chest and the back. Select external demand pacing mode at a rate of 70/min, then gradually i the paci ng current from zero until capture is shown on the monitor. Clinically, capture results in a palpable peripheral pulse at the paced rate and clinical improvement in the patient \200 \231s condition. Provide small doses of IV opioid sedation if the patient \201 nds ext ernal pacing very uncomfortable. Transvenous cardiac pacing is the treatment of choice for bradycardic patients who are at r isk of asystole. The technique should only be performed by an experienced doctor. The prefe rred route of access is the internal jugular or subclavian vein. However, if thrombolysis h as recently been given or is contemplated, or if the patient is taking anticoagulants, use the right femoral vein instead. Obtain a CXR to exclude complications. A correctly function ing ventricular pacemaker results in a pacing spike followed by a widened and bizarre QRS ( Fig. 3.15 ). Fig. 3.15 Paced rhythm. Permanent pacemakers and implantable de \201 brillators Increasingly sophisticated implant able devices are being used to manage arrhythmias. Occasionally, a patient will present to the ED with a malfunctioning pacemaker. Get urgent specialist advice. External trans- cutan eous pacing will provide temporary support whilst the problem is resolved. A special magnet may be needed to inactivate an implantable de \201 brillator which \201 res repeatedly. 83 TREATMENT OF BRADYARRHYTHMIAS Algorithm for the management of bradycardia (Fig. 3.16 ) See www.resus.org.uk Assess using the ABCDE approach \200 Give oxygen if appropriate and obtain IV access \200 Monitor ECG, BP, SpO2, record 12-lead ECG \200 Identify and treat reversible causes (e.g. electrolyte abnormalities) Adverse features? Shock \200 Syncope \200 Myocardial ischaemia \200 Heart failure NO YES Atropine 500 mcg IV YES Satisfactory response? NO Interim measures: Risk of asystole? Atropine 500 mcg IV repeat to maximum of 3 mg \200 Isoprenaline 5 mcg min \200\2231 IV \200 Adrenaline 2 \200\22310 mcg min \200\2231 IV \200 Alternative drugs* OR \200 Tran scutaneous pacing Recent asystole \200 Mobitz II AV block \200 Complete heart block with broad QRS \200 Ventricular pause >3s YES NO ! Seek expert help Arrange transvenous pacing Observe Alternatives include: \200 Aminophylline \200 Dopamine \200 Glucagon (if beta-blocker or calcium channel blocker overdose) \200 Glycopyrronium bromide can be used instead of atropine Fig. 3.16 Algorithm for the management of bradycardia. 8 4 T a c h y c a r d i a C H A P T E R 3 M e d i c i n e Assess using the ABCDE approach \200 Give oxygen if appropriate and obtain IV access \200 Monitor ECG, BP, SpO2, record 12-lead ECG \200 Identify and treat reversible causes (e.g. electrolyte abnormalities) a l g o r i t h m \200\223 w i t h Adverse features? Yes/Unstable Synchronized DC Shock Up to 3 attempts Shock \200 Syncope \200 Myocardial ischaemia \200 Heart failure Amiodarone 300 mg IV over 10 \200\22320 min and repeat shock; followed by: No/Stable Amiodarone 900 mg over 24 h p u l s e Broad Narrow Is QRS narrow (< 0.12s)? Narrow QRS Is rhythm regular? Broad QRS Is rhythm regular? Regular Irregular Regular Irregular Use vagal maneuvers \200 Adenosine 6 mg rapid IV bolus; if unsuccessful give 12 mg; if un successful give further 12 mg \200 Monitor ECG continuously Irregular narrow complex tachycardia Probable atrial fibrillation Control rate with: \200 -Blocker or diltiazem \200 Consi der digoxin or amiodarone if evidence of heart failure Seek expert help ! Sinus rhythm restored? If ventricular tachycardia (or uncertain rhythm): Possibilities include: \200 AF with bundle branch block treat as for narrow complex \200 Pre-excited AF consider amiodarone \200 Polymorphic VT (e.g. torsade de pointes - give magnesium 2 g over 10 min) No Seek expert help Amiodarone 300 mg IV over 20 \200\22360 min; then 900 mg over 24 h If previously confirmed Yes ! T A C H Y C A R D A SVT with bundle branch block: \200 Give adenosine as for regular narrow complex tachycard ia Probable re-entry paroxysmal SVT: \200 Record 12-lead ECG in sinus rhythm \200 If recur s, give adenosine again and consider choice of anti-arrhythmic prophylaxis Possible atrial flutter \200 Control rate (e.g. -Blocker) I A L G O R Fig. 3.17 Tachycardia algorithm with pulse (www.resus.org.uk). I T H M 8 5 86 CHAPTER 3 Medicine Tachyarrhythmias The single Resuscitation Council 2010 tachycardia algorithm (Fig. 3.17 ) ( see www.resus.org.uk ) is based on the fact that, irrespective of the exact underlying card iac rhythm, many of the initial management principles in the peri-arrest setting are the sa me: \200 Rapidly assess ABC. \200 Monitor cardiac rhythm and record a 12-lead ECG. \200 Provide O 2 . \200 Identify and treat reversible causes. \200 Assess for evidence of instability (signs of shock, syncope, signs of heart failure, or myocardial ischaemia) \200\224 these indicate the need for urgent intervention, initially in the form of synchro nized cardioversion. The unstable patient with tachyarrhythmia Synchronized cardioversion This requires two doct ors \200\224 one to perform cardioversion, the other (experienced in anesthesia) to provid e sedation/anesthesia and manage the airway. The patient will not be fasted and is therefor e at particular risk of aspiration. The arrhythmia may d cardiac output and i circulation t imes, so IV drugs take much longer to work than usual. If the \200\230sedation doctor \200 \231 does not appreciate this and gives additional doses of anesthetic drugs, hypotension a nd prolonged anesthesia may result. Electrical cardioversion is synchronized to occur with the R wave to minimize the risk of i nducing VF. Synchronized cardioversion is effective in treating patients who exhibit eviden ce of instability with underlying rhythms of SVT, atrial \202 utter, atrial \201 brilla tion, and VT \200\224 choose an initial level of energy according to the rhythm: \200 Fo r broad complex tachycardia or AF, start with 200J monophasic or 120 \200\223150J biphasic. If unsuccessful, i in increments to 360J monophasic or 150J biphasic. Start with a lower energy for atrial \202 utter and paroxysmal SVT \200\224 use 100J mon ophasic or 70 \200\223120J biphasic. If this is unsuccessful, increase in increments to 360 J monophasic or 150J biphasic. Amiodarone If cardioversion is unsuccessful after 3 synchronized shocks, give amio- darone 300mg IV over 10 \200\22320min and repeat shock. Give amiodarone by central vein when possi ble as it causes thrombophlebitis when given peripherally. However, in an emergency, it can be given into a large peripheral vein. 87 BROAD COMPLEX TACHYARRHYTHMIAS Broad complex tachyarrhythmias May be caused by VT, or rarely by SVT with aberrant conducti on. The default position should be that broad complex tachycardia is VT. Provide O 2 as app ropriate, insert an IV cannula and follow the Resuscitation Council guidelines (Fig. 3.17 ) and (www.resus.org.uk ). The priorities in broad complex arrhythmias associated with tricyclic overdose are airway m anagement, oxygenation, ventilation and correction of metabolic disorders: give IV bicarbon ate, but avoid anti-arrhythmic drugs (b Tricyclic antidepressant poisoning, p.194). Fig. 3.18 Evaluating ECGs: is it VT or SVT with aberrant conduction? VT is much more likely as a caus e of the broad complex tachycardia if: \200 The patient is > 60 years. \200 The patient has a history of IHD or cardiomyopathy. \200 There is clinical evidence of AV dissociati on (intermittent cannon \200\230a \200\231 waves seen on jugular venous pressure (JVP), \201 rst heart sound of vari- able intensity). Inverted P waves in lead II. \200 The frontal plane axis is bizarre ( \200\22390 to \200\223180 ). \200 The QRS is > 0.13sec. \200 There are \200\230capture \200\231 o r \200\230fusion \200\231 beats. \200 The QRS is bizarre, not resembling a bundle branch block pattern \200 All chest leads (V 1 \200\2236 ) are concordant (QRS complexes point the same way). R > R (or r ) in V 1 . \200 There is a deep S wave (either QS, rS or RS) in V 6 . Tors ades de pointes This is a rare form of polymorphic VT, associated with hypomagnesaemia, hyp okalaemia, long QT interval (congenital or drug related, eg sotalol, antipsychotics, antihi stamines, antidepressants). A constantly changing electrical axis results in QRS complexes of undulating amplitude. Usually paroxysmal, it may degenerate to VF. Get expert help and t reat with IV magnesium sulfate (2g over 10min = 8mmol or 4mL 50 % magnesium). Refractory ca ses may require overdrive pacing. Fig. 3.19 88 CHAPTER 3 Medicine Narrow complex tachyarrhythmias These are almost always of supraventricular origin. Underly ing rhythms include: \200 Sinus tachycardia. \200 Paroxysmal AV re-entrant tachycardia (often referred to as \200\230SVT \200\231). \200 AF with fast ventricular response. \200 Atrial \202 utter. \200 Atrial tachycardia. \200 Junctional tachycardia. Give O 2 , insert an IV cannula, and follow the algorithm in Fig. 3.17 ( www. resus.org.uk ). Det ermine if the rhythm is regular. Treat irregular rhythms (AF) as outlined in Fig. 3.17 . If the ventricular rate is exactly 150/min, atrial \202 utter with 2:1 block is likely (Fig . 3.20 ). The compromised patient with shock, syncope, acute cardiac failure, or cardiac ischaemia sh ould be treated with emergency electrical cardioversion. It is reasonable to give IV adenos ine while arranging the cardioversion, as long as this does not delay the procedure. For stable patients consider Vagal stimulation The most effective way is a Valsalva maneuve r while supine or tilted head down. Instruct the patient to attempt to blow the plunger out of a 50mL bladder tip syringe. If unsuccessful, in the young patient, massage the carotid sinus for 15sec (1 side only), by gently rubbing in a circular action lateral to the upper border of the thyroid cartilage. Carotid sinus massage may be dangerous (especially if ther e is a carotid bruit or previous stroke/TIA). Adenosine This temporarily blocks conduction through the AV node. It has a very short half- life (10 \200\22315sec). Adenosine can successfully terminate re-entrant tachycardias and m ay \200\230unmask \200\231 other conditions (eg atrial \202 utter) by temporarily produc ing a conduction block. It is contraindicated in 2 * or 3 * AV block, patients with WPW and asthmatics. The effects are blocked by theophylline and potentiated markedly (and dangerou sly) in the presence of dipyridamole, carbamazepine or in a denervated heart \200\224 seek advice. Warn the patient about transient \202 ushing and chest discomfort. Give adenosin e by fast bolus 6mg IV injection into an IV cannula in the antecubital fossa and \202 ush with 0.9 % saline (Fig. 3.17 ) while recording a rhythm strip. If unsuccessful, repeat wit h 12mg, then 12mg. If adenosine is contra-indicated, consider IV verapamil 2.5 \200\2235mg over 2min. Avoid ve rapamil in patients with cardiac failure, hypotension, concomitant B -blocker therapy, or W PW. Fig. 3.20 Narrow complex tachycardia. 89 ATRIAL FIBRILLATION Atrial \201 brillation Atrial \201 brillation is rapid, irregular, uncoordinated atrial activity, and is associated with an irregular ventricular response. Causes Acute AF may be associated with: IHD (33 % ), heart failure (24 % ), hyperten- sion (26 % ), and valvular heart disease (7 % ). Other cardiac causes are sick sinus syndrome, p ericarditis, in \201 ltrative heart disease, cardiomyopathy, myocardititis, congenital hea rt disease, and post-cardiac surgery. Non-cardiac causes include: sepsis, PE, thyrotoxicosis, electrocution, lung or pleural dise ase, chest trauma, hypokalaemia, hypovolaemia, hypothermia, drug abuse (eg cocaine). Paroxy smal AF sometimes occurs in \201 t athletes. Holiday heart: binge drinking or occasionally alcohol withdrawal may cause acute AF in pati ents with no other predisposing factors. AF usually resolves spontaneously within 48hr. The diagnosis of \200\230holiday heart \200\231 is one of exclusion after cardiac disease and other causes have been ruled out. Clinical features AF d cardiac output by 10 \200\22320 % , irrespective of underlying ventr icular rate. Clinical presentation varies according to the cause and effect of the AF. Some patients are asymptomatic; others suffer life-threatening complications (heart failure, an gina). Patients with underlying IHD may develop ischaemia during periods of rapid ventricul ar rate. Treatment Patients in AF can be treated with cardioversion or rate control. If signs of sho ck, syncope, acute cardiac failure, or ischaemia are present, consider electrical cardiover sion under sedation. Patients may also be chemically cardioverted with \202 ecainide 50 \200\223150mg IV (contraindicated in patients with cardiac disease) or amiodarone 300mg IV (safer in patients with cardiac disease). Both drugs may cause hypotension. If the patient has had symp- toms for longer than 48hr, they are at risk of cardiac thromboembolism and st roke when cardioverted, so instead, give rate control medications and commence IV or low mo lecular weight heparin. Rate control drugs include metoprolol 5mg IV and diltiazem (IV form not available in UK). Digoxin 500mcg IV is the drug of choice in patients with CCF. See 20 06 NICE guidelines ( www.nice.org.uk ). Atrial \201 brillation in Wolff Parkinson White syndrome This may result in an irregular, broad complex tachycardia. Impulses are conducted from the atria via the AV node and an ac cessory pathway. Do not give AV-blocking drugs (digoxin, verapamil, or adenosine) as this c an result in acceleration of conduction through the accessory pathway, leading to cardiovas cular collapse or VF. Seek expert help. Atrial \202 utter The typical atrial rate is 300/min, so a regular 2:1 block will give a QRS rate of 150/min. Variable block may result in an irregular rate. Consult with an expert to discuss treatment. 90 CHAPTER 3 Medicine Hypertensive problems Bear the following points in mind when managing a hypertensive patien t in the ED: \200 Most patients with hypertension are asymptomatic. \200 Hypertension i s an important risk factor for cardiovascular disease and stroke. Most patients found to be hypertensive in the ED do not require any immediate intervention or treatment, but do require careful follow- up \200\224 usually by their GP. Never intervene on the basis of a single raised BP measurement in the absence of any associated symptoms and signs. Approach Approach patients found to be hypertensive as follows: \200 Those with no previo us history of hypertension, and no other concerns or history of other conditions (eg diabet es, peripheral vascular disease, IHD, or stroke) \200\224 arrange follow-up and monitoring with GP. Those known to be hypertensive already on treatment \200\224 arrange follow-up and monitoring with GP. Those displaying evidence of end organ damage (eg LV hypertrophy, retinal changes, renal impairment) \200\224 refer to the medical team. Those with hypertension associated with pain, vasoconstriction (eg acute pulmonary oedema) or stroke \200\224 treat underlying cause where possible. Do not intervene in stroke assoc iated hypertension except under the direction of a neurologist or stroke specialist. Those with hypertension directly associated with symptoms or signs \200\224 contact the me dical team and consider whether intervention is appropriate (see below). Mild/moderate hypertension (diastolic 100 \200\223125mmHg) Ascertain if the patient has a p ast history of hypertension and is taking drug therapy for this. Examine for retinal change s and evidence of hypertensive encephalopathy. Investigate as appropriate (U&E, urinalysis, CXR, ECG). Further management will depend upon the BP and the exact circum- stances. If th e BP is moderately elevated (ie diastolic BP: 110 \200\223125mmHg) and the patient is sympt omatic, refer to the medical team. If the patient is asymptomatic with normal examination a nd renal function, he/she may be suitable for GP follow up. 91 HYPERTENSIVE PROBLEMS Severe hypertension (diastolic > 125mmHg) Patients with a diastolic BP > 125mmHg require ur gent assessment. Search for evidence of hypertensive encephalopathy : headache, nausea, vom iting, confusion, retinal changes (hemorrhages, exudates, papilloedema), \201 ts, focal n eurological signs, d conscious level. Ask about recent drug ingestion (eg ecstasy or cocain e \200\224 b pp. 214 & 215). Investigations Insert an IV cannula and send blood for U&E, c reatinine, and glucose. Obtain a CXR and ECG, and perform urinalysis. If there is d conscio us level, focal signs, or other clinical suspicion that the hypertension may be secondary t o stroke or intracranial hemorrhage, arrange an emergency CT scan. Management \200 Refer patients with a diastolic pressure > 125mmHg or evidence of hyperte nsive encephalopathy to the medical team. Resist commencing emergency treatment until consu ltation with an expert. There is a sig- ni \201 cant risk of complications (stroke or MI) if the BP is reduced rapidly. It may be appropriate to commence oral antihypertensive thera py using a B-blocker (eg atenolol or labetalol) or calcium channel blocker (eg nifedipine). If treatment is appropriate, commence an IVI of sodium nitroprusside, labetalol or GTN with continuous BP monitoring via an arterial line and admit to high dependency unit (HDU) or I CU. Sodium nitroprusside has a very short half-life ( 8 1 \200\2232min) and acts as a vasod ilator of both arterioles and veins. IV labetolol may be preferred if aortic dissection ( b p.92) or phaeochromocytoma are suspected. Beta-blockers are contraindicated in hypertension caused by cocaine, amphetamine or related sympathomimetic drugs ( b p.215), since B-blockade may cause unopposed A-adrenergic activi ty with paradox- ical hypertension and d coronary blood \202 ow. Hypertension in pregnancy Hypertension may be part of pre-eclampsia or eclampsia (see b p.5 92). Pre-eclampsia is diagnosed with 2 or more of: hypertension ( > 140/90), proteinuria an d oedema. This can be associated with haemolysis, elevated liver function tests (LFTs), low platelets (HELLP syndrome). Check urine for protein and check blood for FBC, LFT, platelet s, and coagulation screen. Call for senior obstetric help. Eclampsia is diagnosed with the onset of grand mal seizures after 20 weeks gestation, and carries a signi \201 cant mortal ity rate. 92 CHAPTER 3 Medicine Aortic dissection Remember: hypertensive patients with sudden, severe chest, and/or back pa in may have acute aortic dissection. Pathology Aortic dissection is longitudinal splitting of the muscular aortic media by a col umn of blood. The dissection may spread proximally (possibly resulting in aortic incompeten ce, coronary artery blockage, cardiac tamponade), distally (possibly involving the origin o f various arteries), or rupture internally back into the aortic lumen, or externally (eg in to the mediastinum, resulting in rapid exsanguination). More than 70 % of patients have a history of hypertension. It occurs more frequently in tho se with bicuspid aortic valve, Marfan \200\231s syndrome or Ehlers \200\223Danlos syndrome. Up to 20 % follow recent cardiac surgery or recent angiography/angioplasty. Dissection may be classi \201 ed Stanford type \200\230A \200\231 or \200\230B \200\231, according to whether the ascending aorta is involved or not, respectively. Overall mortali ty is 30 % (35 % type A and 15 % type B). Type A Type B Fig. 3.21 93 AORTIC DISSECTION History Aortic dissection may mimic the presentation of an MI, requiring a high index of su spicion. It typically presents with abrupt onset sharp, tearing or ripping pain (maximal at onset) in anterior or posterior chest. Migration of the pain may re \202 ect extension of the dissection. Syncope occurs in 8 10 % of patients, sometimes in the absence of any pain . Occasionally, patients can present with neurological de \201 cit associated with chest p ain. Examination The patient is usually apprehensive and distressed, with pain which is dif- \201 cult to alleviate, even using IV opioid. Clues to the diagnosis include: \200 An aor tic regurgitation murmur (30 % ). \200 Asymmetry or absence of peripheral pulses or a pul se de \201 cit (15 \200\22320 % ). \200 Hypertension. \200 Hypotension with features o f tamponade or neurological signs in asso- ciation with pain (eg secondary to spinal/caroti d artery involvement). Investigations \200 Send blood for U&E, glucose, FBC, coagulation, and cross-matching. \200 Obtain an ECG and CXR. Thoracic aortic dissection usually results in an abnormal CXR. One or more of the following changes may be seen: \200 A widened or abnormal mediastinum (present in 875 % ). \200 A \200\230double knuckle \200\231 aorta. \200 Left pleural effusion ( 8 20 % ). \200 Deviation of the trachea or nasogastric (NG) tube to the right. \200 Separation of two parts of the wall of a calci \201 ed aorta by > 5mm (the \200\230calcium sign \200\231). The ECG may demonstrate MI, LVH. or ischaemia. Note thatu 8 12 % of patients with aortic di ssection have a normal CXR and 8 30 % have a normal ECG. CT angiography or formal angiograp hy will provide the de \201 nitive diagnosis. In a haemodynamically unstable patient, tran s-oesophageal echo in theater may be the investigation of choice. Management On suspicion of aortic dissection: \200 Provide O 2 by face mask as appropriat e. \200 Insert 2 large-bore (14G) IV cannulae and cross-match for 6U (inform blood bank of suspected diagnosis). Give IV morphine and titrate according to response ( anti-emetic). \200 Call cardiotho racic team and cardiologist at an early stage. \200 Insert an arterial line (preferably r ight radial artery) and discuss with specialist teams how to control the BP (eg labetalol infusion). Arrange further investigation based upon specialist advice and available resources (eg aortography, echocardiography, CT scan, MRI). Type A dissections are usually treated surgically; type B lesions are usually treated medic ally. 94 CHAPTER 3 Medicine Haemoptysis Haemoptysis may be the chief or sole complaint of patients presenting to the ED . It always warrants investigation. Causes of haemoptysis Infection (URTI, pneumonia, TB, lung abscess) \200 Carcinoma (bronchial or laryngeal) \200 Bronchiectasis Respiratory Pulmonary oedema \200 PE \200 Ruptured aortic aneurysm (aorto-bronchial \201 stula) Cardiovascular Drugs (eg warfarin, heparin) \200 Inherited (eg Hemophilia, Christmas disease) Coagulation disorder Penetrating or blunt Trauma Goodpasture \200\231s, Wegener \200\231s granulomatosis Other Presentation Ascertain the exact nature and volume (eg \200\230bright red streaks \200\231 or \200\230dark brown granules \200\231). Patients sometimes have surprising dif \201 cu lty distinguishing vomited blood from that coughed up. Enquire about weight loss, and take a drug history and smoking history. Investigation \200 Send blood for FBC, coagulation screen, U&E, LFTs. \200 Request Grou p and Save if evidence of signi \201 cant hemorrhage. \200 If SpO 2 <94 % on air, or the patient has COPD, check ABG. \200 Obtain CXR and ECG. \200 Perform urinalysis \200 \224 if shocked, insert catheter and monitor output. \200 Collect sputum samples. Send fo r microscopy, culture, and sensitivity. \200 Initiate further investigations according to the likely diagnosis. Treatment \200 Airway : clear and secure (coughing/suction). Put on a face mask and shiel d if maintaining the airway or intubating. Ensure nearby high \202 ow suction. Massive he morrhage may require tracheal intubation. Whilst preparing for this, tilt trolley so that t he patient is head-down. Breathing : provide O 2 to maintain saturations at 94 \200\22398 % . If ventilation is inadequate, assist with bag and mask or tracheal tube. Circulation : insert a large bore (14G) IV cannula (use 2 if hypovolaemic). Give IV \202 uids/blood/clotting factors as clinically indicated ( b p.172). Further treatment Commence speci \201 c treatment measures aimed at life-threatening under lying cause (eg LVF, PE, infection, coagulopathy). In cases of large haemoptysis, it is app ropriate to admit for further investigation and treat- ment. If the patient is stable and h as only had a small amount of blood stained sputum, urgent outpatient investigation may be appropriate. 95 OXYGEN Oxygen Oxygen is the most commonly administered hospital therapy. In recent years, high \202 ow oxygen was widely used in the treatment of medical and surgical emergencies, and in itial resuscitation. There is now a move towards safer treatment with controlled oxygen the rapy. Common problems \200 Failure to prescribe oxygen. \200 Failure to check ABG in patients requiring oxygen therapy. \200 Failure to monitor or review patients on oxygen therapy. \200 Inadvertent administration of another gas other than oxygen. \200 Inadvertent disc onnection from the oxygen supply. \200 Depletion of an oxygen tank during transfer ( www. nrls.npsa.nhs.uk ). Oxygen cylinders When administering oxygen in the ED, always use piped oxygen from the wall outlet. Only use an oxygen cylinder when transporting the patient to t he radiology department or ward. Oxygen is highly \202 ammable. Do not take a cylinder ou t of its support cage and never let it fall. In the UK, oxygen cylinders are color-coded wh ite. The commonest small cylinder is B (or M-6), which holds 170L oxygen. The commonest lar ge cylinder is E (or M-24), holding 680L. Before a patient leaves the ED, always check that the cylinder is full. If the patient is being transferred to another hos- pital, check the re is enough oxygen for the journey. The formula is: Volume of cylinder in L/ \202 ow rate = minutes cylinder will last Oxygen requirements The aim of oxygen therapy is to optimize tissue oxygen delivery. Use pu lse oximetry to guide whether the patient requires supplemental oxygen. In previously healt hy patients, aim for SpO 2 94 \200\22398 % , but in patients with known COPD or type II res piratory failure, aim for SpO 2 88 \200\22392 % . Always take an ABG in patients with chron ic lung disease, to assess their optimal oxygen treatment (see b p.98 on ABG interpretation ). Repeat the ABG within 30 min after changing the inspired oxygen concentration. When asse ssing a critically ill patient, it is appropriate to give high \202 ow oxygen and to titr ate the inspired oxygen concentration (FiO 2 ) down according to the ABG results. Oxygen delivery \200 Use a high concentration oxygen reservoir mask (non-rebreathing mask) in hypoxic patients without chronic lung disease. Use a simple face mask for patients with a mild hypoxia, without chronic lung disease. Use a 28 % Venturi mask for patients with COPD or known type II respi- ratory failure. Use a tracheostomy mask for patients with tracheostomy. Prescribing oxygen The oxygen presc ription should include the target SpO 2 , the oxygen mask type and oxygen \202 ow rate. I n an emergency, it is appropriate to administer oxygen prior to prescribing, but do not for get to prescribe the oxygen after resuscitation. See www.brit-thoracic.org.uk. 96 CHAPTER 3 Medicine The dyspnoeic patient The normal adult respiratory rate is 11 \200\22318/min, with a tidal volume of 400 \200\223800mL. Acute dyspnoea is a common presenting symptom. Common causes of acute dyspnoea Cardiac \200 Cardiogenic pulmonary oedema ( b p.100). \200 MI ( b p.68). \200 PE ( b p.120). \200 Arrhythmias ( b p.80). Respiratory \200 Asthma ( b p.104) or exacerbation of COPD ( b p.108). \200 Pneumonia ( b p.110). \200 P leural effusion ( b p.103). \200 Pneumothorax ( b p.114). Trauma \200 Aspiration of FB or vomit ( b p.112). \200 Pneumothorax/haemothorax ( b p.334). \200 Flail chest ( b p.3 32). \200 Drowning incident ( b p.258). Other \200 Hypovolaemia or fever from any cause . \200 Hyperventilation syndrome ( b p.97). \200 Respiratory compensation for metabolic acidosis (DKA, salicylate over- dose). Approach Follow the ABC approach and resuscitate as necessary. The main aim of treatment is to correct life-threatening hypoxia. Enquire about speed of onset of dyspnoea, past medica l history and associated symptoms (cough, haemoptysis, fever, wheezing, chest pain). Examin e carefully, paying atten- tion to the respiratory rate, depth, and pattern. Apply a pulse oximeter. Pulse oximetry This is simple, rapid, safe, and non-invasive, but it does not provide infor - mation about ventilation or arterial partial pressure of carbon dioxide (pCO 2 ). A norma l oxygen saturation does not exclude signi \201 cant lung pathology (eg PE). Pulse oximetr y may be inaccurate or misleading in: \200 Poor peripheral perfusion/shock. \200 Methae moglobinaemia. \200 Hypothermia. \200 CO poisoning (see b p.208). SpO 2 values may be f alsely high as COHb reads as oxyhaemoglobin. COHb can be measured on venous blood gas testi ng or COHb pulse oximeter. Nail varnish/synthetic \201 ngernails (if a \201 nger probe is used). \200 Excessive movement. Correlate readings with clinical \201 ndings: a non-pulsatile trace (or heart r ate different from that on cardiac monitor) suggests the saturation reading is probably ina ccurate. 97 HYPERVENTILATION Hyperventilation Hyperventilation is breathing which occurs more deeply and/or more rapidly than normal. CO 2 is \200\230blown off \200\231, so that pCO 2 d . Hyperventilation may be primary ( \200\230psychogenic \200\231) or secondary. A classical secondary cause is DKA \200\224 Kussmaul \200\231s respiration represents respiratory compensation for a metabol ic acidosis. Secondary causes of hyperventilation \200 Metabolic acidosis (eg DKA, uraemia, sepsis, he patic failure). \200 Poisoning (eg aspirin, methanol, CO, cyanide, ethylene glycol). \200 Pain/hypoxia. \200 Hypovolaemia. \200 Respiratory disorders (eg PE, asthma, pneum othorax). Primary (psychogenic or inappropriate) hyperventilation Typically, the patient is agitated and distressed with a past history of panic attacks or episodes of hyperventilation. They m ay complain of dizziness, circumoral paraesthesia, carpopedal spasm, and occasionally sharp or stabbing chest pain. Initial examination reveals tachypnoea with equal air entry over b oth lung \201 elds, and no wheeze or evidence of airway obstruction. It is important to c onsider secondary causes (such as PE or DKA). Therefore, perform the following investigatio ns: \200 SpO 2. \200 ECG. \200 ABG if SpO 2 d , or if symptoms do not completely sett le in a few minutes. BMG. If symptoms do not completely settle in a few minutes, obtain: \200 CXR. \200 U&E, blood glucose, FBC. Treatment Do not sedate a patient who is hyperventilating. Once seriou s diagnoses have been excluded, use this information to help reassure the patient with prim ary hyperventilation. Often this is all that is required, but it may be helpful to try simp le breathing exercises (breathe in through nose \200\224 count of 8, out through mouth \200\224 count of 8, hold for count of 4 and repeat). Discharge the patient with arrangemen ts for GP follow-up. If these simple measures fail, reconsider the diagnosis and refer the patient to the medical team for subsequent observation and treatment. 98 CHAPTER 3 Medicine Arterial blood gasses Blood gas sampling is useful in assessing breathless patients, septic patients, diabetic patients in ketoacidosis, those who are critically ill and patients who have ingested poisons. This enables rapid measurement of blood pH, bicarbonate, O 2 and CO 2 . Most ED blood gas analysers will also measure blood glucose, K + , Hb, and lactate, so arterial or venous blood gas sampling will also test for anemia, hyperkalaemia, and hypogl ycaemia. Assessing respiratory function Arterial sampling helps in the assessment of a patient with low SpO 2 , or in patients with known lung disease (especially if they are receiving supple mental oxygen). If possible (caution required), take the \201 rst sample with the patient breathing room air. If this is not possible, document the inspired oxygen concentration. L ook speci \201 cally for: \200 Hypoxia, (pO 2 <10.6kPa on air). \200 Hypercarbia, (pCO 2 > 6.0kPa). \200 Bicarbonate retention (HCO 3 \200\223 > 28mmol/L). \200 Acidosis (p H <7.35). Differentiating between type I and type II respiratory failure In type I failure there is hypoxia with normal or d pCO 2 . In type II failure, there is hypoxia with i pCO 2 , and frequently an i HCO 3 \200\223 . In type II failure, the patient may develop life-t hreatening respiratory failure if administered high concentrations of oxygen. Aim to mainta in SpO 2 at 88 \200\22392 % , and recheck ABGs in 30min. Differentiating between acute and chronic type II respiratory failure Patients who normally have a slightly i pCO 2 will also show i HCO 3 \200\223 on ABG. The kidneys adapt over a period of days to retain bicarbonate, in attempt to buffer the respiratory acidosis (see no mogram inside front cover). Respiratory acidosis in a patient with chronic type II respira- tory failure ( i pCO 2 , i HCO 3 \200\223 and pH <7.35) indicates life-threatening impair ment of lung function. In acute respiratory failure, the lungs are unable to eliminate CO 2 (caused by d GCS or hypoventilation from any cause), which results in i pCO 2 and a respir atory acidosis. Patients may require ventilatory support. A venous blood sample will give a ccurate readings for K + , lactate, glucose, HCO 3 \200\223 , Hb and COHb. In addition, a normal venous pCO 2 will exclude hypercarbia. Other blood gas results Blood gas analysers calculate the base excess from the HCO 3 \200 \223 concentra- tion and pH. Levels < \200\2232mmol/L indicate that the patient has a metab olic acidosis. Levels > 2mmol/L indicate a metabolic alkalosis (for example, as a result of chronic bicarbonate retention in type II respiratory failure). 99 ARTERIAL BLOOD gasses Metabolic acidosis The usual pattern of results in metabolic acidosis is pH<7.35, HCO 3 \200\223 <24mmol/L and BE < \200\2232mmol/L. There may be compensatory hypocarbia (pCO 2 <4 .5kPa). Metabolic acidosis has many possible causes: \200 i Acid load (lactic acidosis, k etoacidosis, or ingestion of salicylates, methanol, ethylene glycol, or metformin). d Removal of acid (renal failure or renal tubular acidosis types 1 and 4). \200 Loss of b icarbonate from the body (diarrhea, pancreatic, or intestinal \201 stulas, acetazolamide, or renal tubular acidosis type 2). The anion gap The anion gap is the quantity of anions not balanced out by cations, (a measu rement of negatively charged plasma proteins). The normal value is 12 \200\22316mmol/L. It is measured by: (Na + + K + ) \200\223 (Cl \200\223 + HCO 3 \200\223 ) all measured in mmol/L Measuring the anion gap helps distinguish the cause of a metabolic acidosis. A high anion gap indicat es that there is excess H + in the body. The commonest cause of a high anion gap metabolic acidosis is lactic acidosis. Most blood gas analysers will measure lactate (normal <2.0mmol /L). Causes of a lactic acidosis \200 Tissue hypoperfusion (trauma with major hemorrhage, sept ic shock). \200 Tissue hypoxia (hypoxaemia, carbon monoxide or cyanide poisoning). \200 Hepatic failure. \200 Renal failure. \200 Ethylene glycol or methanol poisoning ( b p. 203; b p.202). \200 Cocaine or amphetamines ( b p.215). \200 Salicylate poisoning ( b p .189) or iron poisoning ( b p.201). \200 Biguanides (metformin). \200 Isoniazid. \200 Strenuous exercise. The other causes of a high anion gap metabolic acidosis are ketoacidos is (diabetic or alcohol induced) and renal failure. Causes of a normal anion gap metabolic acidosis are chronic diarrhea, pancreatic or intesti nal \201 stulas, acetazolamide, or renal tubular acidosis. The osmolal gap This is the difference between calculated serum osmolarity and laboratory m easured serum osmolality. Serum osmolarity can be calculated by: (2 \227 Na + ) + urea + glucose (all measured in mmol/L) Subtract the calculated result fr om the laboratory measured osmolality to give the osmolal gap. Normally this is <10mOsm/kg. An elevated osmolal gap can be caused by alcohol, methanol, ethylene glycol or acetone inge stion, mannitol, or sorbitol. 100 CHAPTER 3 Medicine