Was there any bystander CPR ? Where a patient in cardiac arrest is brought to hospital by a mbulance, the cardiac arrest team (ED staff, the hospital team, or a combination of both) s hould already be present in the resuscitation room with all equipment ready to receive the patient. The team leader The team leader controls, co-ordinates, organizes the team and makes treatm ent decisions. 4 \200\2236 team members are optimal. Each should know their role. Perform r esuscitation in a calm, quiet, con \201 dent manner with minimal interruption to the perfo rmance of basic life support (BLS) or de \201 brillation. Start the following procedures simultaneously: \200 Continue BLS. \200 Remove/cut cloth ing from the upper body to allow de \201 brillation, ECG monitoring, chest compression, and IV access. Obtain the ECG trace (through de \201 brillator pads or monitor leads). If already attache d to an ECG monitor, note (print out if possible) the rhythm. Beware movement artifact, dis connected leads, electrical interference, etc. Follow the ALS algorithm ( b p.52). \200 Do not interrupt CPR except to perform de \201 brillation. 47 IN-HOSPITAL RESUSCITATION ALGORITHM In-hospital resuscitation algorithm 1 Collapsed/sick patient Shout for HELP and assess patient Signs of life? YES NO Assess ABCDE Recognize and treat Oxygen, monitoring, IV access Call resuscitation team CPR 30:2 with oxygen and airway adjuncts Call resuscitation team if appropriate Apply pads/monitor Attempt defibrillation if appropriate Advanced life support when resuscitation team arrives Handover to resuscitation team Fig. 2.3 1 Resuscitation Council (UK) guidelines , 2010 ( www.resus.org.uk ). 48 CHAPTER 2 Life-threatening emergencies Adult basic life support Airway and ventilation Usually in the ED, advanced airway techniqu es will be used from the outset. If basic techniques are used (Fig. 2.4 ): \200 With the patient on his/her back, open the airway by tilting the head and lifting the chin. (Use jaw thrust instead if neck trauma suspected.) \200 Remove any visible obstructions from the mouth, but leave well- \201 tting dentures in place. Aim for each breath to last 8 1sec and make the chest rise. After each breath, maintain the head tilt/chin lift, take your mouth away from the patient \200\231s and watch for the che st to fall as the air comes out. Fig. 2.4 Mouth to mouth ventilation. 1 1 Colquhoun MC et al . (1999). ABC of Resuscitation , 4th edition. BMJ Books, London. 49 ADULT BASIC LIFE SUPPORT Technique for chest compression (Fig. 2.5 ) \200 Place the heel of one hand over the midd le of the lower half of the patient \200\231s sternum, with the other hand on top. Extend o r interlock the \201 ngers of both hands and lift them to avoid applying pressure to the patient \200\231s ribs. Positioned above the patient \200\231s chest and with arms straight, press down to depress the sternum 5 \200\2236cm. Release all the pressure and repeat at a rate of 100 \200\223120/min. \200 Compression an d release phases should take the same time. \200 Use a ratio of 30 chest compressions to 2 ventilations (30:2). \200 Aim to change the person providing chest compressions every 2 min, but ensure that this is achieved without causing signi \201 cant pauses. Fig. 2.5 Chest compressions. 1 1 Colquhoun MC et al . (1999). ABC of Resuscitation , 4th edition. BMJ Books, London. 50 CHAPTER 2 Life-threatening emergencies Cardiac arrest management De \201 brillation \200 Most survivors have an initial rhythm of VF/VT. The treatment for this is de \201 brillation. With time, the chances of successf ul de \201 brillation and survival d dramatically. Adhesive de \201 brillator pads have r eplaced manual paddles in most hospitals. Place one pad to the right of the upper sternum b elow the clavicle, the other in mid-axillary line level with V 6 ECG electrode position. Av oid placement over the female breast. To avoid problems with pacemakers, keep pads > 15cm a way from them. \200 With biphasic de \201 brillators, use shock energy of 150J, for (mos tly older) monophasic de \201 brillators, select 360J energy. Plan for chest compressions to be as continuous as possible, with minimal delays. Having pa used brie \202 y to assess the rhythm, recommence compressions until the de \201 brillato r is charged. Pause brie \202 y to deliver a shock (removing O 2 sources and transdermal g lycerol trinitrate (GTN) patches), then immediately restart CPR with 30:2 compressions: ven tilation, and continue for 2min before reassessing the rhythm or feeling for a pulse. In monitored patients with pulseless ventricular tachycardia/ \201 brillation (VT/VF) wher e de \201 brillation is not immediately available, give a single precordial thump . With a tightly clenched \201 st, deliver one direct blow from a height of 820cm to the lower ha lf of the sternum. Airway management Techniques for securing the airway, providing oxygenation and ventilation are covered in b Airway obstruction: basic measures, p.324. Although tracheal intubation h as long been considered to be the gold standard de \201 nitive airway, only attempt this i f suitably experienced. Laryngeal mask airway is a readily available, rapid alternative, wh ich is easy to insert. Whatever method is used, aim to ventilate (preferably with 100 % O 2 ) using an inspiratory time of 1sec, a volume suf \201 cient to produce a normal rise of the chest, at a rate of 10/min. For patients with tracheal tubes or laryngeal mask airways, ventilate without interrupting chest compressions, which should be continuous (except for de \201 brillation or pulse checks as appropriate). End-tidal CO 2 monitoring is very usef ul to con \201 rm correct tracheal tube placement and indirectly measure cardiac output du ring CPR. Drugs There is little evidence that any drug improves outcome. Central venous cannulation i s dif \201 cult, has risks and interrupts CPR. Peripheral access is easy and quick. Having given a peripheral IV drug, give a 20mL saline bolus and elevate the limb for 10 \200\2232 0sec. If IV access is impossible, consider intraosseous route ( b p.640). It is no longer r ecommended for any drugs to be given by tracheal tube. Similarly, do not attempt intracardi ac injections. The \201 rst drug used in cardiac arrest (after oxygen) is adrenaline. In the case of VF/ VT, administer adrenaline after three shocks, whereas in asystole/PEA, give it as soon as p ossible (see b Adult life support algorithm, p.52). 51 CARDIAC ARREST MANAGEMENT Non-shockable rhythms: PEA and asystole Pulseless electrical activity ( PEA ) is the clinic al situation of cardiac arrest with an ECG trace compatible with cardiac output. PEA may be caused by: \200 Failure of the normal cardiac pumping mechanism (eg massive MI, drugs su ch as B -blockers, Ca 2 + antagonists or electrolyte disturbance, eg hypokalaemia, hyperkal aemia). Obstruction to cardiac \201 lling or output (eg tension pneumothorax, pericardial tampona de, myocardial rupture, pulmonary embolism (PE), prosthetic heart valve occlusion, and hypo volaemia). Prompt and appropriate correction of these can result in survival. Remember potentially rev ersible causes as the 4H \200\231s and 4T \200\231s (see Table 2.1 ). Table 2.1 4H \200\231s 4T \200\231s Hypoxia Tension pneumothorax Hypovolaemia Tamponade (cardiac) Hyper/hypokalaemia/metabolic disorders Toxic substances (eg overdose) Hypothermia Thromboembolic/mechanical obstruction Asystole is the absence of cardiac (particularly ventricular) electrical activity. If unsur e if the rhythm is asystole or \201 ne VF, continue chest compressions and ventilation in an attempt to increase the amplitude and frequency of VF, and make it more susceptible to de \201 brillation. Length of resuscitation The duration of the resuscitation attempt depends upon the nature o f the event, the time since the onset, and the estimated prospects for a successful outcome . In general, continue resuscitation while VF/pulseless VT persists, always provided that i t was initially appropriate to commence resuscitation. If VF persists despite repeated de \201 brillation, try changing pad position or de \201 brillator. Asystole unresponsive to treatment and arrests which last > 1hr are rarely associated with survival. However, except ions occur \200\224 particularly in younger patients, hypothermia, near drowning, and drug overdose. Mechanical CPR There are several devices available that can provide mechanical CPR. These i nclude the \200\230AutoPulse \200\231 circumferential load-distributing band chest compres sion device (comprising a pneumatically actuated constricting band and backboard) and the \200\230LUCAS \200\231 gas-driven sternal compression device (with accompanying suction cup to provide active decompression). Widespread use of these devices may develop if early enc ouraging results are con \201 rmed by larger studies. Mechanical CPR is potentially very u seful in situations where the resuscitation attempt is prolonged (eg cardiac arrest associa ted with hypothermia, poisoning or following \201 brinolytic treatment for PE), ensuring consistent CPR over a long period of time and freeing up an additional member of the team. 52 CHAPTER 2 Life-threatening emergencies Advanced life support algorithm 1 Unresponsive? Not breathing or only occasional gasps Call resuscitation team CPR 30:2 Attach defibrillator/monitor Minimize interruptions Assess rhythm Shockable (VF/Pulseless VT) Non-Shockable (PEA/Asystole) Return of spontaneous circulation 1 Shock Immediate post cardiac arrest treatment \200 Use ABCDE approach \200 Controlled oxygena tion and ventilation \200 12-lead ECG \200 Treat precipitating cause \200 Temperature control/ therapeutic hypothermia Immediately resume CPR for 2 min Minimize interruptions Immediately resume CPR for 2 min Minimize interruptions During CPR \200 Ensure high-quality CPR: rate, depth, recoil \200 Plan actions before i nterrupting CPR \200 Give oxygen \200 Consider advanced airway and capnography \200 C ontinuous chest compressions when advanced airway in place \200 Vascular access (intraven ous, intraosseous) \200 Give adrenaline every 3 \200\2235 min \200 Correct reversible c auses Reversible causes Hypoxia \200 Hypovolaemia \200 Hypo-/hyperkalaemia/metabolic \200 Hypothermia Thrombosis - coronary or pulmonary \200 Tamponade - cardiac \200 Toxins \200 Tension pneumothorax Fig. 2.6 1 Resuscitation Council (UK) guidelines , 2010 ( www.resus.org.uk ). 53 NOTES ON USING THE ADVANCED LIFE SUPPORT ALGORITHM Notes on using the advanced life support algorithm \200 Establish the underlying cardiac rhythm as quickly as possible in order to determine which \200\230loop \200\231 to follow to provide appropriate treatment \200\224 for VF/pulseless VT, the initial focus is de \201 brillation and good CPR; for asystole/PEA, the initial focus is good CPR, IV adrenalin e, and searching for potentially reversible causes. Do not interrupt CPR except to perform de \201 brillation. \200 Search for and correct p otentially reversible causes of the arrest. \200 Give IV adrenaline 1mg and amiodarone 30 0mg for VF/pulseless VT refractory to three shocks, followed by 1mg adrenaline every 3 \200 \2235min. A further dose of 150mg IV amiodarone may be given for recurrent or refractory VF /VT. Lidocaine (1mg/kg) IV is an alternative to amiodarone, but do not give it if amiodaron e has already been given. For torsade de pointes, and refractory VF in patients with suspected digoxin toxicity or hy pomagnesaemia (eg on K + losing diuretics), give IV magnesium sulfate 2g (= 8mmol = 4mL of 50 % solution). In asystole and PEA, give IV 1mg adrenaline as soon as possible and thereafter every 3 \200\2235min. Exercise caution before using adrenaline in arrests associated with cocaine or other sympathomimetic drugs. Atropine is no longer routinely recommended in asystole or slow PEA. \200 In PEA arrests associated with hyperkalaemia, hypocalcaemia, or Ca 2 + channel blocking drug or magnesium overdose, give 10mL 10 % IV calcium chloride (6.8mmol). With good quality CPR, acidosis develops slowly. Do not \200\230routinely \200\231 give an alkali. Give 50mL of sodium bicarbonate 8.4 % solution (50mmol) if arrest is associated wi th tricyclic overdose ( b p.194) or hyperkalaemia and consider it in patients with severe a cidosis (arterial pH<7.1, base excess less than \200\22310). Allow further administration to be guided by repeated arterial blood gas (ABG) results. Follow loops of the algorithm for as long as it is considered appropriate for the resuscita tion to continue. Provided that the attempt was commenced appropriately, it should not norm ally be stopped if the rhythm is still VF. Pacing and external cardiac percussion Pacing may be of value in patients with extreme brad yarrhythmias, but its value in asystole is unproven (except for rare cases of trifascicular block with P waves present). If there is a delay before pacing can be performed, external cardiac percussion can provide a cardiac output and \200\230buy time \200\231. Perform ext ernal cardiac percussion using a clenched \201 st: \200 Over the heart at a rate of 100 /min. \200 With a blow more gentle than a precordial thump. \200 Each blow should gener ate a QRS complex. If this, and a detectable output, is not achieved restart conventional CPR. 54 CHAPTER 2 Life-threatening emergencies Post-resuscitation care Features such as coma or pupil re \202 exes are unreliable prognos tic indicators in the early post-resuscitation phase. Accurate prognostication in an indivi dual patient is rarely possible before 24 \200\22372hr. Involve the intensive care unit/cri tical care unit (ICU/CCU) team early. Pending this and following ROSC \200 Ensure that the airway is protected ( b p.324). \200 Maintain oxygenation and ventilation. Correct hypoxia and prevent hypercapnoea under ABG guidance (may require IPPV). Use pulse oximetry to monitor SpO 2 non-invasively, titrat ing inspired oxygen concentration to achieve SpO 2 of 94 \200\22398 % . In intubated patients, insert an oro- or nasogastric tube to decompress the stomach. Obtain a 12-lead ECG and a CXR (check position of tracheal tube, central lines and presence of pneumothorax etc.). Optimize cardiac output: inotropes, vasodilators, \202 uids and/or diuretics may be neede d under haemodynamic monitoring guidance. If the arrest is associated with an acute coronar y syndrome, consider immediate thrombolysis and/or coronary revascularization. Cerebral blood \202 ow autoregulation is de \201 cient post-arrest. Maintaining arterial pressures \200\230normal \200\231 for the patient may prevent hypotensive hypoperfusion. i BP above the normal for the patient may worsen cerebral oedema. Seizures aggravate brain injury by i ICP and cerebral metabolic requirements. Treat with ap propriate anticonvulsants (as b p.149) and ensure adequate oxygenation and ventilation. Measure U&E, Ca 2 + , Mg 2 + , and correct abnormalities appropriately. \200 Obtain full blood count (FBC) to exclude anemia contributing to myocardial ischaemia and to provide an admission baseline. Both hypo- and hyperglycaemia compromise neurological outcome. Monitor plasma glucose conce ntration regularly and aim to avoid both hypo- and hyperglycaemia (keep the level (cid:100) 10mmol/L). No drug has been shown to improve cerebral outcome following cardiac arrest. The routine us e of steroids, mannitol, Ca 2 + channel blockers, etc., is unwarranted. When any drug is used, remember that pharmacokinetic pro \201 les are often impaired post- resuscitation. Dose adjustment and careful monitoring are needed. Avoid/treat hyperthermia with antipyretic or active cooling. \200 There is compelling dat a to support the early induction of mild therapeutic hypothermia (32 \200\22334 C) in pa tients who are comatose following out of hospital VF arrest. Mild hypothermia is believed t o be neuroprotective in this situation (and pending more data, may be of bene \201 t in ot her situations as well, eg other arrest rhythms, in-hospital arrests, pediatric patients). Cooling may be initiated by external techniques (cooling blankets, water or air circulating blankets) or internally by an infusion of 30mL/kg of 4 C 0.9 % saline \200\224 liaise with ICU. Mild hypothermia is typically maintained for 12 \200\22324hr. 55 POST-RESUSCITATION CARE Training Theoretical knowledge is important, but many of the skills required during the man agement of a cardiac arrest need expert teaching and supervised practice. Attend an approve d Resuscitation Council (UK) Advanced Life Support course (see www.resus.org.uk ) \200\224 preferably before starting in the ED. 56 CHAPTER 2 Life-threatening emergencies Central venous access Indications Central venous access may be required for: \200 Adminis tration of emergency drugs. \200 Central venous pressure measurement. \200 Administrati on of IV \202 uids, especially when peripheral veins are collapsed or thrombosed. Note : other routes (eg femoral vein) are generally preferable for giving large volumes rapidly. Transvenous cardiac pacing. Choice of vein The external jugular vein is often readily visible and can be cannulated eas ily with a standard IV cannula. The internal jugular and subclavian veins are generally used for central venous access in t he ED. Subclavian vein cannulation has a relatively high risk of pneumothorax, so the inter nal jugular vein is usually preferable, via a \200\230high \200\231 approach. When possibl e, use ultrasound (USS) guidance and the right side of the neck ( d risk of thoracic duct d amage). If, however, a chest drain is already in situ, use the same side for central venous cannulation. The femoral vein is useful for temporary access in severe trauma, burns, and in drug addict s with many thrombosed veins. Seldinger technique for central venous access The method of choice, because the relatively \201 ne needle d risk of complications such as pneumothorax. The technique involves inser ting a hollow metal needle into the vein. A \202 exible guidewire is threaded through the needle, which is then removed. A tapered dilator and plastic cannula are inserted over the guidewire and advanced into the vein. The guidewire and dilator are removed, and the cannu la secured. Once the cannula is in place, check that venous blood can be freely aspirated a nd secure the cannula. Precautions and problems Central venous access is a specialized technique with potentially life- threatening complications, including: pneumothorax, haemothorax, arterial puncture, t horacic duct damage, air embolism, and infection. \200 Expert supervision is essential. C annulation is particularly dif \201 cult and hazardous in hypovolaemic, shocked, or agitat ed patients. In such situations, consider whether it is possible to defer the procedure. USS has become widely available and is increasingly used by suitably trained ED specialists . It d complications and failure rates by clarifying the relative positions of needle, vein , and surrounding structures. Variant anatomy and vein patency can also be assessed by USS. Bleeding dyscrasias and anticoagulant treatment are contraindications to internal jugular and subclavian vein access. Severe pulmonary disease is a relative contraindication to central venous access, especiall y by the subclavian route, because a pneumothorax would be particularly dangerous. 57 CENTRAL VENOUS ACCESS Methods Use aseptic technique. If possible, tilt the trolley 10 head down to \201 ll t he internal jugular and subclavian veins and d risk of air embolus. After successful or att empted subclavian or internal jugular cannulation, take a chest X-ray (CXR) to check for pn eumothorax and the position of the cannula. External jugular vein The vein can be seen and felt as it crosses super \201 cially over t he sternomastoid muscle and runs obliquely towards the clavicle. Gentle pressure on the low er end of the vein will distend it. A standard IV cannula can easily be inserted into the e xternal jugular vein, but passing a catheter centrally may be dif \201 cult because of val ves and the angle at which the vein joins the subclavian vein. Internal jugular vein The internal jugular vein runs antero-laterally in the carotid sheath , parallel to the carotid artery, and deep to the sternocleidomastoid muscle. The high appr oach described has less risk of pneumothorax than lower approaches (Fig. 2.7 ). \200 Turn the patient \200\231s head away from the side to be cannulated. \200 Identify the caroti d pulse at the level of the thyroid cartilage. \200 Insert the needle 0.5cm lateral to th e artery, at the medial border of sternomastoid muscle. Advance the needle at an angle of 45 parallel to the sagittal plane, pointing towards th e ipsilateral nipple. The vein should be entered at a depth of 2 \200\2234cm and blood aspi rated freely. If it is not, try again slightly more laterally. Subclavian vein (infraclavicular approach) \200 Turn the patient \200\231s head away from the side of cannulation. \200 Identify the mid-clavicular point and the sternal notch. \200 Insert the needle 1cm below the mid-clavicular point and advance it horizontally belo w and behind the clavicle, aiming at a \201 nger in the suprasternal notch. The vein is u sually entered at a depth of 4 \200\2236cm (Fig. 2.8 ). Femoral vein Insert the needle 81cm medial to the femoral artery and just below the inguina l ligament, pointing slightly medially and with the needle at 20 \200\22330 to the skin. 58 CHAPTER 2 Life-threatening emergencies Sternomastoid muscle Carotid artery Fig. 2.7 Internal jugular cannulation. 1 Subclavian vein Clavicle Finger in suprasternal notch First rib Superior vena cava Fig. 2.8 Subclavian vein cannulation. 2 1 Rosen M et al . Handbook of Percutaneous Central Venous Catheterization. W.B. Saunders, London. 2 Cosgriff JH. An Atlas of Diagnostic and Therapeutic Procedures for Emergency Personnel . J.B. Lippincott, Philadelphia. 59 SEVERE SEPSIS AND SEPTIC SHOCK Severe sepsis and septic shock Septic patients have a systemic in \202 ammatory response s yndrome (SIRS) as a consequence of infection. Severe sepsis refers to septic patients with evidence of organ hypoperfusion. Septic shock is present when septic patients exhibit hypot ension unresponsive to intravenous \202 uid resuscitation. Systemic in \202 ammatory response syndrome This requires 2 or more of: \200 Body temper ature of > 38 C or <36 C \200 Heart rate > 90/min \200 Respiratory rate > 20 brea ths/min or PaCO 2 < 4.3kPa \200 WCC > 12 \227 10 9 /L or <4 \227 10 9 /L or > 10 % imma ture (band) forms Management Severely septic patients have SIRS with evidence of hypoperfusion (eg systolic B P <90mmHg and/or lactate > 3mmol/L). Obtain senior/ICU help early. Intensive therapy of sev erely septic patients focuses upon certain therapeutic goals : \200 CVP of 8 \200\22312mm Hg. \200 mean arterial pressure > 65mmHg. \200 urine output > 0.5mL/kg/hr. \200 centr al venous saturation > 65 % . Adopt the following approach: \200 Obtain senior/ICU assist ance now. \200 Assess and manage airway, breathing, circulation (ABC) \200\224 in partic ular, provide high \202 ow oxygen, secure good IV access and give an initial IV \202 ui d bolus of 20mL/kg of 0.9 % saline. Some patients may require early tracheal intubation and IPPV. Look for obvious sources of infection. \200 Check BMG (and treat if hypoglycaemic). \200 Take blood cultures before starting antibiotics (the choice of antibiotics will depend upon the likely cause and is considered on b p.60). Patients who remain hypotensive and/or have a lactate > 3mmol/L require central venous and arterial catheterization in an intensive care/ resuscitation setting, with IVI noradrenalin e to maintain mean arterial pressure > 65mmHg and IV 0.9 % saline 500mL boluses every 20min s to achieve CVP 8 \200\22312mmHg (12 \200\22315mmHg in mechanically ventilated patients). 60 CHAPTER 2 Life-threatening emergencies Shock Shock is a clinical condition characterized by failure to adequately perfuse and oxyg enate vital organs. Clinically, shock is recognized by: \200 Hypotension Generally consid ered to be systolic BP <90mmHg (in adults), but values may be higher in young, \201 t or previously hypertensive patients. Associated tachycardia ( > 100/min) is common, but may no t be present in patients with cardiac or neurological causes or in those taking B-blockers. A few patients with haemorrhagic shock have a paradoxical bradycardia. Altered consciousness and/or fainting (especially on standing or sitting up) may result from d cerebral perfusion. Poor peripheral perfusion Cool peripheries, clammy/sweaty skin, pallor, d capillary return, but note that in the early phase of endotoxic septic shock there may be vasodilatation wit h warm peripheries. Oliguria d renal perfusion with urine output <50mL/hr (in adults). \200 Tachypnoea. Classi \201 cation of shock Traditional classi \201 cation of types of shock is arti \201 cial \200\224 mixed aetiologies are common. Hypovolaemic shock \200 Blood loss: trauma, gastrointestinal (GI) bleed (haematemesis, me laena), ruptured abdominal aortic aneurysm, ruptured ectopic pregnancy. Fluid loss/redistribution ( \200\230third spacing \200\231) : burns, GI losses (vomiting, diarrhea), pancreatitis, sepsis. Cardiogenic shock \200 Primary : myocardial infarction (MI), arrhythmias, valve dysfuncti on, myocarditis. Secondary : cardiac tamponade, massive pulmonary embolus, tension pneumothorax. Septic shock (see b p.59) More common at the extremes of age, in patients with diabetes mel litus, renal/hepatic failure and the immunocompromised (eg HIV infection, underlying malign ancy, post-splenectomy, steroid therapy). Note that fever, rigors and i white cell count (W CC) may not be present. \200 Organisms responsible include Gram + ve and \200\223ve, esp ecially Staph. aureus, Strep . pneumoniae , N meningitidis , coliforms including enterococc i and Bacteroides (especially in patients with intra-abdominal emergencies, such as rupture d diverticular abscess). In the immunocompromised, Pseudomonas, viruses, and fungi may caus e septic shock. Anaphylactic shock: see b p.42. Neurogenic shock: see b p.382. Other causes These include poisoning ( b p.183) and Addison \200\231s disease ( b p.155). 61 SHOCK Management of shock Investigation and treatment should occur simultaneously. Get senior hel p immediately. \200 Address the priorities \200\224 ABC. \200 Give high \202 ow O 2 by mask. \200 Secure adequate venous access and take blood for FBC, U&E, glucose, liver f unction tests (LFTs), lactate, coagulation screen, and if appropriate, blood cultures. Monitor vital signs, including pulse, BP, SpO 2 , respiratory rate. \200 Check ABG. \200 Monitor ECG and obtain 12 lead ECG and CXR. \200 Insert a urinary catheter and monitor urine output hourly. \200 For shock associated with d effective circulating blood volume, give IV crystalloid (0.9 % saline) 20mL/kg as bolus. Give further IV \202 uids including colloid 9 blood (aim for haematocrit (Hct) > 30 % ) according to etiology and clinical res ponse (and in particular, pulse, BP, central venous pressure (CVP), and urine output). Use caution with IV \202 uid infusion in shock related to cardiogenic causes, and in ruptured or dissecting aortic aneurysm. Look for, and treat speci \201 cally, the cause(s) of the shock. Echocardiography, USS, CT , and/or surgical intervention may be required. Speci \201 c treatments include: \200 La parotomy : ruptured abdominal aortic aneurysm, splenic and/or liver trauma, ruptured ectopi c pregnancy, intra-abdominal sepsis. Thrombolysis/angioplasty : MI. \200 Thrombolysis : PE. \200 Pericardiocentesis/cardiac surgery : cardiac tamponade, aortic valve dysfunction. Antidotes : for certain poisons. \200 Antibiotics : sepsis. The choice of antibiotic will depend upon the perceived cause and local policies (eg ceftriaxone for meningococcal disea se). Where there is no obvious source, empirical combination therapy is advised (eg co-amox iclav + gentamicin + metronidazole). Obtain specialist microbiological advice early, especi ally in neutropaenic/immunocompromised patients. Inotropic and vasoactive therapy, assisted ventilation, and invasive monitoring (including arterial and CVP lines) are often needed as part of goal directed therapy. Get specialist I CU help early. 62 Chapter 3 Chapter 00 Medicine Electrocardiogram interpretation Chest pain Angina Acute coronary syndromes ST segment elev ation MI Myocardial infarction: electrocardiogram changes STEMI: treatment Pericarditis Bra dyarrhythmias Treatment of bradyarrhythmias Tachycardia algorithm \200\223with pulse Tachya rrhythmias Broad complex tachyarrhythmias Narrow complex tachyarrhythmias Atrial \201 bri llation Hypertensive problems Aortic dissection Haemoptysis Oxygen The dyspnoeic patient Hy perventilation Arterial blood gasses Cardiogenic pulmonary oedema Non-cardiogenic pulmonary oedema Pleural effusion Acute asthma: assessment Acute asthma: management COPD Pneumonia P ulmonary aspiration 64 66 67 68 70 72 76 78 80 82 84 86 87 88 89 90 92 94 95 96 97 98 100 102 103 104 106 108 1 10 112 63 Chapter 3 Medicine Spontaneous pneumothorax Deep venous thrombosis Pulmonary embolism Upper gastrointestinal b leeding Lower gastrointestinal bleeding Headache Subarachnoid hemorrhage Migraine Other cau ses of headache Acute confusional state (delirium) Dementia The unconscious patient Collaps e and syncope Acute generalized weakness Stroke Transient ischaemic attacks Seizures and st atus epilepticus Hypoglycaemia Hyperglycaemic crises Sodium derangements Addisonian crisis Thyrotoxic crisis Urinary tract infection Chronic renal failure Hyperkalaemia Hypokalaemia Porphyria Bleeding disorders Patients on anticoagulants Blood transfusion Sickle cell disea se 114 118 120 122 124 126 128 130 132 134 135 136 140 142 144 146 148 150 152 154 155 156 158 160 162 164 165 166 170 172 176 64 CHAPTER 3 Medicine Electrocardiogram interpretation The electrocardiogram (ECG) is normally recorded so that a de \202 ection of 10mm = 1mV. The recording rate is 25mm/sec, 1mm = 0.04sec, 1 large squa re = 0.2sec. There is an ECG ruler on the inside back cover. Follow a systematic approach. Rate Calculate the rate by dividing 300 by the number of large squares in one R \200\223R i nterval. Frontal plane axis Normally lies between \200\22330 * and + 90 * (see Fig. 3.1 ). With a normal axis, QRS complexes in I and II are both + ve. An axis more \200\223ve than \200\22330 * (I + ve, aVF and II \200\223ve) is left axis deviation (causes: left anteri or hemiblock, inferior myocardial infarction (MI), ventricular tachycardia (VT), Wolf Parki nson White (WPW) syndrome). An axis more + ve than + 90 * (I \200\223ve, aVF + ve) is righ t axis deviation (causes: pulmonary embolism (PE), cor pulmonale, lateral MI, left posterio r hemiblock). P wave Normally <0.12sec wide and <2.5mm tall. They are best seen in leads II and V 1 which are chosen for rhythm strips or monitoring. A tall peaked P wave in II may re \202 ect ri ght atrial hypertrophy; a widened bi \201 d P wave left atrial hypertrophy. P waves are ab sent in atrial \201 brillation (AF). PR interval Normally 0.12 \200\2230.2sec (<5 small squares). A short PR interval (abnormall y fast conduction between atria and ventricles) implies an accessory pathway (eg Wolf Parki nson White syndrome). A prolonged PR interval occurs in heart block ( \201 rst, second or third degree, see b Br adyarrhythmias, p.80). QRS width Normally 0.05 \200\2230.11sec (<3 small squares). Prolonge d QRS complexes may be due to: right bundle branch block (RBBB) (RsR or M shape in V 1 ), left bundle branch block (LBBB) (QS or W shape in V 1 with RsR or M shape in V 6 ), tricyc lic antidepressant poisoning ( b p.194), hypothermia, ventricular rhythms, and ectopics. Head \200\22390 aVR \200\223150 aVL \200\22330 Right Left 180 I 0 II +60 +120 III aVF +90 Feet Fig. 3.1 Diagram of the ECG frontal axis. 65 ELECTROCARDIOGRAM INTERPRETATION QRS amplitude The QRS amplitude can indicate left ventricular hypertrophy (LVH). Signs of L VH are: (S in V 2 + R in V 5 ) > 35mm; R in I > 15mm; R in aV L > 11mm. Q waves May be norm al in III, aV R , and V 1 , but are abnormal in other leads if > 0.04sec or > of the hei ght of the subsequent R wave. ST segment elevation is caused by: acute MI, pericarditis (concave up), ventricular aneurys m, Prinzmetal \200\231s angina, LVH, Brugada syndrome, hypertrophic cardiomyopathy, benign early repolarization. ST segment depression is caused by: ischaemia, digoxin, LVH with strain. QT interval = start of Q wave to end of T wave. QT c = QT \201\204 \210\232R \200\223R (Baz ett \200\231s formula). Normal QT c is <440msec. At rates of 60 \200\223100/min, QT should be <1/2 R \200\223R interval. A prolonged QT c predisposes to \200\230torsades de pointes \200\231 ( b Broad complex tachyarrhythmias, p.87) and is caused by acute MI, hypothermia, hypocalcaemia, drugs (quinidine, tricyclic antidepressants), certain congenital diseases (e g Romano \200\223Ward syndrome). T waves Abnormal if inverted in V 4 \200\2236 . Peaked T w aves are seen in early acute MI and hyperkalaemia ( b p.162). Flattened T waves (sometimes with prominent U waves) occur in hypokalaemia. R 1.0 PR segment ST segment m m 0 1 T 0.5 P P U 0 m m 1 P \200\223R interval Isoelectric line Q S QRS interval e g a t l o V ) V m Q \200\223T interval ( 0.0 0.2 0.4 Seconds 0.6 0.8 0.04 Fig. 3.2 66 CHAPTER 3 Medicine Chest pain Always take chest pain seriously. It may re \202 ect life-threatening illness. Triage patients with chest pain as \200\230urgent \200\231 and ensure that they are seen w ithin a few minutes. Ischaemic heart disease is understandably the \201 rst diagnosis to spring to mind in the middle-aged or elderly, but chest pain may have a variety of other di sease processes, many of which are also potentially life-threatening (Table 3.1 ). Table 3.1 The differential diagnosis of chest pain Common causes Less common causes Aortic dissection * Musculoskeletal (eg costochondritis) Acute coronary syndrome * Pneumothorax * Cholecystitis Herpes zoster Oesophageal rupture * Pancreatitis * Oesophagitis Pneumonia Pulmonary embolism * Vertebral collapse Obscure origin (eg precordial catch) Tabes dorsalis (very rare) Potentially rapidly fatal. Reaching the correct conclusion requires accurate interpretation of the history, examinatio n and investigations, bearing in mind recognized patterns of disease presentations. History Characterize the pain \200 Site (eg central, bilateral or unilateral). \200 Severity. \200 Time of onset and duration. \200 Character (eg \200\230stabbing \200\231, \200 \230tight/gripping \200\231, or \200\230dull/aching \200\231). \200 Radiation (eg to arm s and neck in myocardial ischaemia). \200 Precipitating and relieving factors (eg exercis e/rest/GTN spray). \200 Previous similar pains. Enquire about associated symptoms Breathl essness, nausea, and vomiting, sweating, cough, haemoptysis, palpitations, dizziness, loss of consciousness. Document past history, drug history, and allergies. Old notes and old ECG s are invaluable \200\224 request them at an early stage. Quickly consider contacting card iologists if acute coronary syndrome (ACS) is likely ( b ST segment elevation MI: treatment , p.76). Examination and resuscitation Evaluate Airway, Breathing, Circulation (ABC) and re suscitate (O 2 , venous access, IV analgesia) as appropriate. Listen to both lung \201 el ds and check for tension pneu- mothorax and severe left ventricular failure (LVF). Complete full examination. Investigations These depend upon the presentation and likely diagnosis, but an ECG and CXR are usually required. Remember that these may initially be normal in MI, PE and aortic dissection. Ensure that all patients receive ECG moni- toring in an area whe re a de \201 brillator is readily available. 67 ANGINA Angina Angina is de \201 ned as discomfort in the chest, arm, neck, or adjacent areas due to myocardial ischaemia. It can be brought on by exertion, cold weather and emotion. It occ urs when coronary artery blood \202 ow fails to meet the O 2 demand of the myocardium (eg during exercise, coronary artery spasm or anemia). Ischaemia may produce ST depression or inversion, which resolves on recovery. First presentation of angina Patients may come to the ED with angina as a \201 rst presen tation of ischaemic heart disease (IHD). Always consider the possibility of MI. In particul ar, suspect myocardial cell death with any pain lasting > 10min (even if relieved by glycer yl trinitrate (GTN)). A normal examination, normal ECG and normal baseline cardiac markers do not exclude MI. If in any doubt, admit the patient . If considering discharge, discuss w ith senior ED/medical staff. Atypical cardiac chest pain Patients with acute MI are occasionally sent home from the ED i nadvertently. Cardiac chest pain may be poorly localized, and may present with musculoskele tal features or gastrointestinal (GI) upset. In particular, patients with acute coronary sy ndromes commonly have chest wall tenderness. Some patients understandably play down symptom s in order to avoid admission to hospital. If the clinical history is suspicious of cardiac pain (especially in a patient with risk factors, such as family history of IHD, hypertensi on, smoking), then refer for admission. Do not be fooled by a normal ECG, normal examinatio n, or the fact that the patient is <30 years old. Remember that oesophageal pain may improv e with GTN and true cardiac pain may appear to improve with antacids. The decision whether or not to refer the patient for admission and investigation depends upon an assessment of t he risk of MI. In general, exclude an MI where chest pain lasting > 15min has some features of IHD. Also refer patients who look unwell, even if the chest pain lasts <15min. 68 CHAPTER 3 Medicine Acute coronary syndromes Coronary artery plaque rupture can result in a variety of ischaemi c conditions which fall under the overall term of \200\230acute coronary syndrome \200\231 and include unstable angina, non-ST segment elevation MI (NSTEMI) and ST segment elevation MI (STEMI). Patients labeled as having acute coronary syndrome, but without initial ST ele vation, comprise a relatively heterogenous group \200\224 some later proving (on the basis of elevated blood troponin levels) to have suffered an NSTEMI.