710 CHAPTER 17 Cardiovascular emergencies Adult basic life support Basic life support (BLS) is the backbone of effective resuscitatio n following a cardiorespiratory arrest. The aim is to maintain adequate ventilation and cir culation until the underlying cause for the arrest can be reversed. 3 \200\2234 minutes wit hout adequate perfusion (less if the patient is hypoxic) will lead to irreversible cerebral damage. The usual scenario is an unrespon- sive patient found by staff, who alert the card iac arrest team. The initial assessment described below should have already been performed by the person \201 nding the patient. The same person should have also started car- diopu lmonary resuscitation (CPR). Occasionally you will be the \201 rst to discover the patien t, and it is important to rapidly assess the patient and begin CPR. The various stages in b asic life support are described here and summarized in Fig. 17.1 . 1. Assessment of the patient \200 Ensure safety of rescuer and victim \200 Check whethe r the patient is responsive . Gently shake victim and ask loudly \200\230 are you all right ? \200\231 (a) If victim responds, place him/her in the recovery position and get help. (b) If victim is unresponsive, shout for help and move on to assess airway (see below). 2. Airway assessment \200 Open the airway . With two \201 ngertips under the point of t he chin, tilt the head up. If this fails, place your \201 ngers behind the angles of the lower jaw and apply steady pressure upwards and forwards. Remove ill- \201 tting dentures and any obvious obstruction. If the patient starts breathing, roll the patient over into th e recovery position and try to keep the airway open until an orophyrangeal airway can be in serted. Keep airway open, look, listen, and feel for breathing . Look for chest movements, listen at the victim \200\231s mouth for breathing sounds and feel for air on yo ur cheek (for no more than 10 seconds). (a) If patient is breathing, turn them into the recovery position, check for continued breathing and get help. (b) If patient is not breathing, making occasional gasps, or weak attempts at breathing, se nd someone (or go for help if alone). (On return) start rescue breaths by giving two slow e ffective breaths, each resulting in a visible rise and fall in the chest wall. 3. Assessment of circulation \200 Assess signs of circulation by feeling the carotid puls e for no more than 10 s. (a) If there are signs of circulation but no breathing, continue rescue breaths and check for signs of breathing every 10 breaths (approximately one breath a minute). (b) If there are no signs of circulation start chest compression at a rate of 100 times per minute. Combine rescue breaths and compression at the rate of 15 compressions to two effec tive breaths. The ratio of compressions to lung in \202 ation remains the same for resuscitation with two persons. ADULT BASIC LIFE SUPPORT 711 Check responsiveness Shake and shout Open airway Head tilt/chin lift If breathing: recovery position Check breathing Look, listen, and feel Breathe 2 effective breaths Assess 10 s only Signs of a circulation No circulation Compress chest Circulation present Continue rescue breathing Check circulation every minute 100 per minute 15:2 ratio Send or go for help as soon as possible according to guidelines Fig. 17.1 Adult basic life support. For further information see The Resuscitation Council ( UK) website Y http://www.resus.org.uk/. 712 CHAPTER 17 Cardiovascular emergencies Adult advanced life support \200 It is unlikely that an effective spontaneous cardiac act ivity will be restored by basic life support without more advanced techniques (intubation f or effective ventilation, drugs, de \201 brillation, etc.). Do not waste time. As soon as help arrives, delegate CPR to someone less experienced in advanced cardiac life support (AC LS), so that you are able to continue. Attach the patient to a cardiac monitor as soon as possible to determine the cardiac rhythm and treat appropriately (see b Universal treatment algorithm, p. 716). Orophyrangeal (Guedel) or nasopharyngeal airways help maintain the patency of the airway by keeping the tongue out of the way. They can cause vomiting if the patient is not comatose. Endotracheal (ET) intubation is the best method of securing th e airway. Do not attempt this if you are inexperienced. See also Figs. 17.2 and 17.3. Establish venous access. Central vein cannulation (internal jugular or subclavian) is ideal but requires more training and practice, and is not for the inexper ienced. If venous access fails, drugs may be given via an ET tube into the lungs (except fo r bicarbonate and calcium salts). Double the dose of drug if using this route, as absorptio n is less ef \201 cient than IV. Post-resuscitation care \200 Try to establish the events that precipitated the arrest fro m the history, staff, witnesses, and the hospital notes of the patient. Is there an obvious cause (myocardial infarction (MI), hypoxia, hypoglycaemia, stroke, drug overdose or interaction, electrolyte abnormality, etc.)? Record the duration of the arrest in the notes, with the i nterventions, drugs (and doses) in chronological order. Examine the patient to check both lung \201 elds are being ventilated; check for ribs tha t may have broken during CPR. Listen for any cardiac murmurs. Check the neck veins. Examine the abdomen for an aneurysm or signs of peritonism. Insert a urinary catheter. Consider a nasogastric (NG) tube if the patient remains unconscious. Record the Glasgow Coma Score and perform a brief neurological assessment. \200 Investigations: electrocardiogram (ECG) (l ooking for MI, ischaemia, tall T waves ( i K + )); arterial blood gasses (ABG) (mixed metabolic and respiratory acido sis is common and usually responds to adequate oxygenation and ventilation once the circula tion is restored; if severe, consider bicarbonate); chest X-ray (CXR; check position of ET tube, look for pneumothorax); urea and electrolytes (U&Es), and glucose . \200 After earl y and successful resuscitation from a primary cardiac arrest, the patient may rapidly recov er completely. The patient must be transferred to high-dependency unit (HDU) or coronary ca re unit (CCU) to monitor for 12 \200\22324 h. Commonly the patient is unconscious post-arre st and should be transferred to the intensive therapy unit (ITU) for mechanical ventilation and haemodynamic monitoring and support for (cid:116)24 hours. ADULT ADVANCED LIFE SUPPORT 713 Change any venous lines that were inserted at the time of arrest for central lines inserted with sterile technique. Insert an arterial line and consider a pulmonary artery (PA) cathe ter (Swan \200\223Ganz) if requiring inotropes. Remember to talk to the relatives. Keep them informed of events and give a realistic (if bl eak) picture of the arrest and possible outcomes. \200 When appropriate, consider the pos sibility of organ donation and do not be frightened to discuss this with the relatives. Eve n if discussion with the relatives is delayed, remember corneas and heart valves may be use d up to 24 hours after death. Jaw lift to open the airway Jaw thrust (thrust the angle of the mandible upwards) Fig. 17.2 Opening airways. Reproduced with permission from Ramrakha P, Moore K, Sam M (2010 ). Oxford Handbook of Acute Medicine , 3rd ed. Oxford: Oxford University Press. 714 CHAPTER 17 Cardiovascular emergencies Insertion of oropharyngeal airway Insertion of nasopharyngeal airway Fig. 17.3 Insertion of nasopharyngeal airway. Reproduced with permission from Ramrakha P, M oore K, Sam M (2010). Oxford Handbook of Acute Medicine , 3rd ed. Oxford: Oxford University Press. This page intentionally left blank 716 CHAPTER 17 Cardiovascular emergencies Universal treatment algorithm \200 Cardiac rhythms of cardiac arrest can be divided into two groups: 1. ventricular \201 brillation/pulseless ventricular tachycardia (VF/VT) 2. o ther cardiac rhythms , which include asystole and pulseless electrical activity (PEA). The principal difference in treatment of the two groups of arrhythmias is the need for atte mpted de \201 brillation in the VF/VT group of patients. \200 Fig. 17.4 summarizes the a lgorithm for management of both groups of patients. VF/VT \200 VF/VT are the most common rhythms at the time of cardiac arrest. \200 Succes s in treatment of VF/VT is dependent on the delivery of prompt de \201 brillation. With ea ch minute, the chances of successful de \201 brillation decline by 7 \200\22310 % . Precordial thump : if arrest is witnessed or monitored, a sharp blow with a closed \201 s t on the patient \200\231s sternum may convert VF/VT back to a perfusing rhythm. It is part icularly effective if delivered within 30 s after cardiac arrest. Shock cycles are generally in groups of three. Initially 200 J, 200 J, and 360 J, with subsequent cycles at 360 J. After each shock (or sequence), the carotid pulse should be palpated only if the waveform c hanges to one usually capable of providing a cardiac output. The shock cycle is repeated every minute if VF/VT persists. \200 Myocardial and cerebral viability must be maintained after each shock cycle, with chest compressions and ventilation. In between cycles of de \201 brillation, reversible factors must be identi \201 ed and co rrected, the patient intubated (if possible) and venous access obtained. Adrenaline should be given every 3 minutes (1 mg IV and 2 \200\2233 mg via endotracheal route). Non-VF/VT rhythms \200 The outcome from these rhythms is generally worse than VF/VT unles s a reversible cause can be identi \201 ed and treated promptly. Chest compressions and ventilation should be undertaken for three minutes with each loop of the algorithm (1 min if directly after a shock). With each cycle, attempts must be made to intubate the patient, gain IV access and give adrenaline. Asystole \200 Atropine 3 mg IV should be given to block all vagal output. \200 In the p resence of P waves on the ECG strip/monitor, pacing (external or transvenous) must be considered. PEA \200 Identi \201 cation of the underlying cause and its correction are both vital fo r successful resuscitation. Resuscitation must be continued while reversible causes are bei ng sought. UNIVERSAL TREATMENT ALGORITHM 717 Cardiac arrest Precordial thump if appropriate BLS algorithm if appropriate Attach Defibrillator/Monitor Assess rhythm Check pulse VF/VT Non-VF/VT During CPR Correct reversible causes If not already: \200 Check electrodes, paddle position, and contact \200 Attempt/verify : airway & O2 IV access \200 Give adrenaline every 3 min. \200 Consider: amiodarone, at ropine/pacing buffers Defibrillate x3 as necessary CPR 3 min* *1 min if immediately after defibrillation CPR 1 min Potential reversible causes: \200 Hypoxia \200 Hypovolaemia \200 Hyper/hypokalaemia & metabolic disorders \200 Hypothermia \200 Tension pneumothorax \200 Tamponade \200 Toxic/therapeutic disorders \200 Thrombo-embolic & mechanical obstruction. Fig. 17.4 The advanced life support universal algorithm for the management of cardiac arres t in adults. For further information see The Resuscitation Council (UK) website Y http://ww w.resus.org.uk/. 718 CHAPTER 17 Cardiovascular emergencies Primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarc tion (see b p. 268) \200 Primary percutaneous coronary intervention (PCI) is the current gold standard reperfusion strategy for treatment of ST-segment elevation MI (STEMI). Primary PCI requires signi \201 cant coordination between the emergency services, communit y hospitals, and invasive centers. It must only be performed if: (1) a primary PCI program is available; (2) the patient presents to an invasive center and can undergo catheterizatio n without delay. Indication for primary PCI \200 All patients with chest pain and ST-segment elevation or new left bundle branch block (LBBB) ful \201 l primary PCI criteria (compare with indications for t hrombolysis). This will include a group of patients where ST-segment elevation may not ful \201 l thrombolysis criteria. In general, patients in whom thrombolysis is contraindicated should be managed by primary P CI. Cases where there is signi \201 cant risk of bleeding must be managed individually. ACUTE MI: THROMBOLYSIS PROTOCOL 719 Acute MI: thrombolysis protocol See Fig. 17.5 . Yes No Typical cardiac chest pain Within 12 hours of onset Typical ECG changes ST elevation \2201mm in \2202 contiguous leads Or New LBBB Contraindications to thrombolysis No Yes Internal bleed/surgery/injury/organ biopsy trauma/dental extraction \2072 weeks Any haemorrhagic CVA Other CVA, neurosurgery, head injury <2 weeks Know or suspected active peptic ulcer Pregnancy Any history of bleeding disorder or warfarin (INR >4.0) Management of high BP: If systolic BP >180 mmHg Bleep Med. Registrar for advice immediate or Thrombolyse immediately If diastolic BP >110 mmHg Reduce with IV nitrates start at 2 ml/hr. Thrombolyse immediately once BP <180/110 Yes No Anterior MI: Age \20775 yrs: <6 hrs pain onset Heparin bolus 5000 units followed by 1st dose reteplase New LBBB: Age \20775 yrs: <6 hrs pain onset Streptokinase 1.5 mega units Exactly 30 minutes later give 2nd dose reteplase Systolic BP<90 Previously had Streptokinase Followed by Heparin infusion Admit to CCU Fig. 17.5 Acute MI: thrombolysis protocol. BP = blood pressure; CVA = cerebrovascular accid ent; INR = international normalized ratio. 720 CHAPTER 17 Cardiovascular emergencies Acute myocardial infarction b ST elevation myocardial infarction (STEMI) p. 256 b STEMI: diagnosis p. 258 b STEMI: general measures p. 262 b STEMI: reperfusion therapy (thrombolysis) p. 264 b STEMI: reperfusion by primary PCI p. 268 b Rescue PCI p. 269 b STEMI: additional measures p. 270 b Right ventricular (RV) infarction p. 272 b STEMI: predischarge risk strati \201 cation p. 274 b STEMI: complications p. 276 b Ventricular septal defect post-MI p. 278 b Acute mitral regurgitation post-MI p. 280 b Pseudoaneurysm and free-wall rupture p. 281 b Cocaine-induced MI p. 282 b Ventricular tachyarrhythmias post-MI p. 284 b Atrial tachyarrhythmia post-MI p. 284 b Bradyarrhythmias and indications for pacing p. 285 b Bradyarrhythmias post-MI p. 285 b Hypotension and shock post-MI p. 286 b Non-ST elevation myocardial infarction (NSTEMI)/unstable angina (UA) p. 290 TREATMENT OPTIONS IN TACHYARRHYTHMIAS 721 Treatment options in tachyarrhythmias B-blockade if anxious Sinus tachycardia Look for cause Version to sinus rhythm (SR) Prevention Rate control Atrial \201 brillation (atrioventricular (AV) node) \200 Digoxin \200 B-blockade \200 calcium blocker (e.g. verapamil) Atrial \202 utter Supraventricular tachycardia (SVT) ( b p. 494) Amiodarone \200 Sotalol \200 Quinidine \200 Procainamide Flecainide \200 Amiodarone \200 Sotalol \200 Disopyramide \200 Synchronized DC shoc k Adenosine \200 B-blockade \200 Verapamil \200 (Vagal stimulation) Digoxin \200 Flecainide \200 Synchronized DC shock Junctional tachycardia (atrioventricular nodal re-entrant tachycardia (AVNRT)) ( b p. 498) Termination only \200 Synchronized DC shock At accessory pathway \200 Sotalol \200 Flecainide \200 Disopyramide \200 Quinidine \200 Amiodarone At AV node Accessory pathway tachycardias (i.e. atrioventricular re-entry tachycardia (AVRT)) ( b p. 4 98) Adenosine \200 B-blockade Termination and prevention \200 Lidocaine \200 Procainamide \200 Amiodarone \200 Ma gnesium Termination only \200 DC shock Ventricular tachycardia ( b p. 508) Flecainide \200 Disopyramide \200 Propafenone \200 B-blockade 722 CHAPTER 17 Cardiovascular emergencies Ventricular tachycardia: drugs See Table 17.1 . Table 17.1 Dosages of selected antiarrhythmics for the acute treatment of VT Drug Dosage Magnesium sulfate Loading dose 8 mmol (2g) IV over 2 \200\22315 min (repeat once if necessary) Maintenance dose 60 mmol/48 mL saline at 2 \200\2233 mL/h Lidocaine Loading dose 100 mg IV over 2 min (repeat once if necessary) Maintenance dose 4 mg/min for 30 min 2 mg/min for 2 h 1 \200\2232 mg/min for 12 \200\22324 h Procainamide Loading dose 100 mg IV over 2 min Repeat every 5 min to max 1 g Maintenance dose 2 \200\2234 mg/min IV infusion 250 mg q6h PO Amiodarone Loading dose 300 mg IV over 60 min via central line followed by 900 mg IV over 23 h or 200 mg PO tds x 1 week then 200 mg PO bd x 1 week Maintenance dose 200 \200\223400 mg od IV or PO Disopyramide Loading dose 50 mg IV over 5 min repeated every 5 min up to maximum 150 mg IV 200 mg PO Maintenance dose 2 \200\2235 mg/min IV infusion 100 \200\223200 mg q6h PO Flecainide Loading dose 2 mg/kg IV over 10 min (max 150 mg) Maintenance dose 1.5 mg/kg IV over 1 hour then 100 \200\223250 mcg/kg/h IV for 24 h or 100 \200\223200 mg PO bd SUPRAVENTRICULAR TACHYARRHYTHMIAS 723 Supraventricular tachyarrhythmias See Table 17.2 . Table 17.2 Dosages of selected antiarrhythmics for SVT Drug Dosage Digoxin Loading dose: IV 0.75 \200\2231 mg in 50 mL saline over 1 \200\2232 h PO 0.5 mg q12h for 2 doses then 0.25 mg q12h for 2 days Maintenance dose: 0.0625 \200\2230.25 mg daily (IV or PO) Propranolol IV 1 mg over 1 min, repeated every 2 min up to maximum 10 mg PO 10 \200\22340 mg 3 \200\223 4 times a day Atenolol IV 5 \200\22310 mg by slow injection PO 25 \200\223100 mg daily Sotalol IV 20 \200\22360 mg by slow injection PO 80 \200\223160 mg bd Verapamil IV 5 mg over 2 min; repeated every 5 min up to maximum 20 mg PO 40 \200\223120 mg tds Procainamide IV 100 mg over 2 min; repeated every 5 min up to maximum 1 g PO 250 mg q6h Amiodarone Loading dose: IV 300 mg over 60 min via central line followed by 900 mg IV over 23 h or PO 200 mg tds x 1 week then 200 mg PO bd x 1 week Maintenance dose: 200 \200\223400 mg od IV or PO Disopyramide IV 50 mg over 5 min; repeated every 5 min up to maximum 150 mg IV 100 \200\223200 mg q6h PO Flecainide 2 mg/kg IV over 10 min (max 150 mg) or 100 \200\223200 mg PO bd 724 CHAPTER 17 Cardiovascular emergencies Acute pulmonary oedema: assessment Presentation \200 Acute breathlessness, cough, frothy blood-stained (pink) sputum \200 Collapse, cardiac arrest, or shock \200 Associated fea tures may re \202 ect underlying cause: chest pain or palpitations \200\224 ? ischaemic heart disease (IHD)/MI, arrhythmia preceding history of dyspnoea on exertion \200\224 ? IHD, poor left ventricular (LV) function oliguria, haematuria \200\224 ? acute renal failure \200 seizures, signs of intracranial bleed. Causes A diagnosis of pulmonary ooedema or \200\230heart failure \200\231 is not adequate. An underlying cause must be sought in order to direct treatment appropriately. Causes may be divided into: \200 increased pulmonary capillary pressure (hydrostatic) \200 increas ed pulmonary capillary permeability \200 decreased intravascular oncotic pressure. Often there is a combination of factors involved (e.g. pneumonia, hypoxia, cardiac ischaemia); se e b Drugs for hypertensive emergencies, p. 760. The main differential diagnosis is acute (infective) exacerbation of chronic obstructive pu lmonary disease (COPD) (previous history, quiet breath sounds wheeze, fewer crackles). I t may be dif \201 cult to differentiate the two clinically. Principles of management 1. St abilize the patient \200\224 relieve distress and begin de \201 nitive treatment. 2. Look for an underlying cause. 3. Address haemodynamic and respiratory issues. 4. Optimize and i ntroduce long-term therapy. Initial rapid assessment \200 If the patient is very unwell (e.g. unable to speak, hypoxi c, systolic BP <100 mmHg), introduce stabilizing measures and begin treatment immediately before detail ed examination and investigations (see b Pulmonary oedema: management, p. 728). If the patient is stable and/or if there is doubt as to the diagnosis, give oxygen and diur etic, but await the outcome of clinical examination and CXR before deciding on de \201 nit ive treatment. Urgent investigations for all patients ECG Sinus tachycardia most common \200 ? any cardiac arrhythmia (atrial \201 brillarion (AF ), SVT, VT) ? evidence of acute ST change (STEMI, NSTEMI, unstable angina (UA)) ? evidence of underlying heart disease (left ventricular hypertrophy (LVH), p mitrale) ACUTE PULMONARY OEDEMA: ASSESSMENT 725 CXR To con \201 rm the diagnosis, looking for interstitial shadowing, enlarged hila, prominent upper lobe vessels, pleural effusion, and Kerley B lines. Cardiomegaly may or may not be p resent. Also exclude pneumothorax, pulmonary embolus (oligaemic lung \201 elds), and cons olidation \200 Typically d P a O 2 . P a CO 2 levels may be d (hyperventilation) or i dep ending on the severity of pulmonary oedema. Pulse oximetry may be inaccurate if peripherall y shut down \200 ? pre-existing renal impairment. Regular K + ABG U&Es measurements (once on IV diuretics) \200 ? anemia or leucocytosis, indicating the Full blood count (FBC) precipitant Echocardiography As soon as practical to assess LV function, valve abnormalities, ventricular septal defect (VSD), or pericardial effusion (ECHO) P a CO 2 = partial pressure of carbon dioxide in the arterial blood; P a O 2 = partial pres sure of oxygen in the arterial blood. Investigations for patients with pulmonary oedema All patients should have: \200 FBC, U&Es, C-reactive protein (CRP) \200 serial biochemi cal markers of myocardial injury (creatine kinase (CK), CK-MB, troponins) liver function tests (LFTs), albumin, total protein \200 ECG \200 CXR \200 ECHO ( transoesophageal echocardiography (TOE)) \200 arterial blood gasses. Where appropriate, c onsider: \200 septic screen (sputum, urine, blood cultures) \200 Holter monitor (?arrhy thmias) \200 coronary angiography (?IHD) \200 right and left heart catheter (if ECHO is unable to provide adequate information on pressures, shunts, valve disease) \200 endomyocardial biopsy (myocarditis, in \201 ltration) \200 multigated acquisition (MUGA) scan \200 cardiopulmonary exerci se test with an assessment of peak oxygen consumption. 726 CHAPTER 17 Cardiovascular emergencies Pulmonary oedema: causes Look for an underlying cause for pulmonary oedema. Increased pulmonary capillary pressure (hydrostatic) Mitral valve disease \200 Arrhythmia (e.g. AF) with pre-existing Left atrial pressure mitral valve disease \200 Left atrial myxoma \200 Ischaemia \200 Arrhythmia \200 Ao rtic valve disease \200 Cardiomyopathy \200 Uncontrolled hypertension \200 Pericardia l constriction \200 Fluid overload \200 High-output states (anemia, thyrotoxicosis, Left ventricular end-diastolic pressure (LVEDP) Paget \200\231s, AV \201 stula, beri-beri) Reno vascular disease. \200 L l R shunt (e.g. VSD) \200 Veno-occlusive disease. \200 Intracranial hemorrhage \200 Cerebral oedema \200 Post-ictal Pulmonary venous pressure Neurogenic High-altitude pulmonary oedema Increased pulmonary capillary permeability Acute respiratory distress syndrome (ARDS) Acute lung injury Decreased intravascular oncotic pressure i Losses (e.g. nephrotic syndrome, liver Hypoalbuminaemia failure) d Production (e.g. sepsis) \200 Dilution (e.g. crystalloid transfusion) Note: the critical LA pressure for hydrostatic ooedema = serum albumin (g/L) x 0.57. This page intentionally left blank 728 CHAPTER 17 Cardiovascular emergencies Pulmonary oedema: management Stabilize the patient \200 Patients with acute pulmonary oed ema should initially be continuously monitored and managed where full resuscitation facilit ies are available. Sit the patient up in bed. \200 Give 60 \200\223100 % oxygen by face mask (unless contrai ndicated, COPD). \200 If the patient is severely distressed, summon the \200\230on-call \200\231 anesthetist and inform ITU. If dyspnoea cannot be signi \201 cantly improved by a cute measures (below) the patient may require continuous positive airways pressure (CPAP) o r mechanical ventilation. Treat any haemodynamically unstable arrhythmia (urgent synchronized DC shock may be required (see b DC cardioversion, p. 818). Give: diamorphine 2.5 \200\2235 mg IV (caution abnormal ABGs) \200 metoclopramide 10 mg IV \200 furosemide 40 \200\223120 mg slow IV injection. Secure venous access and send blood for urgent U&Es, FBC, and cardiac enzymes (including troponin). Unless thrombolysis is indicated, take ABG. \200 If the systolic blood pressure is (cid:1 16) 90 mmHg and the patient does not have aortic stenosis: \200 give sublingual glyceryl trinitrate (GTN) spray (2 puffs) \200 start IV GTN infusion 1 \200\22310 mg/h, increase the infusion rate every 15 \200\223 20 minutes, titrating against blood pressure (aiming to keep systolic BP 7100 mmHg). If the systolic blood pressure is <90 mmHg, treat patient as cardiogenic shock (see b NSTEMI/UA: invasive versus non-invasive strategies, p. 301). Insert a urinary catheter to monitor urine output. \200 Repeat ABG and K + if the clinica l condition deteriorates/fails to improve, or after 2 h if there is improvement and the original sample was abnormal. Monitor pulse, BP, respiratory rate, O 2 saturation with a pulse oximeter (if an accurate reading can be obtained), and urine output. If the patient responds arrange appropriate investigations as listed on b Acute pulmonary o edema: assessment, p. 724 to help with further management. However, if there is further det erioration, speci \201 c measures should be taken to address problems. Further management The subsequent management of the patient is aimed at ensuring adequate v entilation/gas exchange and haemodynamic stability and correcting any reversible precipitin s of acute pulmonary oedema. \200 Assess the patient \200\231s respiratory function: does the patient require respiratory support? Assess the patient \200\231s haemodynamic status (see b Cardiogenic shock, p. 288): \200 is the patient in shock (?(see b Cardiogenic shock, p. 288). Look for an underlying cause (see b Pulmonary oedema: causes, p. 726). PULMONARY OEDEMA: MANAGEMENT 729 Conditions that require speci \201 c treatment: \200 acute aortic and mitral regurgitati on \200 diastolic LV dysfunction \200 \202 uid overload \200 renal failure \200 s evere anemia \200 hypoproteinaemia. If the patient remains unstable and/or deteriorates, assess their respira- tory function. Assessment of respiratory function \200 Wheeze may be caused by interstitial pulmonary oe dema. If there is a history of asthma, give nebulized salbutamol (2.5 \200\2235 mg), nebuli zed ipratropium bromide (500 mcg), and hydrocortisone (200 mg) IV. Consider commencing amin ophylline infusion. This will relieve bronchospasm, as well as \200\230off-load \200\231 b y systemic vasodilatation. However, it may worsen tachycardia, and can be arrhythmogenic an d lower K + (supplement to ensure K + 4 \200\2235 mmol/L). Indications for further respiratory support include: patient exhaustion or continuing severe breathlessness \200 persistent P a O 2 <8 kPa \200 rising P a CO 2 \200 persistent or worsening acidosis (pH < 7.2). CPAP : this may be tried for co-operative patients, who can protect their airway, and have adequate respiratory muscle strength and who are not hypotensive. The positive pressure red uces venous return to the heart and may compromise BP. Endotracheal intubation and mechanical ventilation may be required, and some positive end-expiratory pressure (PEEP) should be used. \200 Discuss the patient wit h the on-call anesthetist or ITU team early. Assess the patient \200\231s haemodynamic status It is important to distinguish between car diogenic and non-cardiogenic pulmonary oedema, as further treatment is different between th e two groups. This may be dif \201 cult clinically. A PA (Swan \200\223Ganz) catheter must be inserted if the patient \200\231s condition will allow. \200 Non-cardiogenic pulmonar y oedema occurs when the hydrostatic pressure within the capillary system exceeds the plasm a oncotic pressure. In patients with hypoalbuminaemia this will occur at a pulmonary capill ary wedge pressure (PCWP)<15 mmHg. The critical PCWP may be estimated by serum albumin (g/L ) x 0.57. Thus, a patient with a serum albumin of 15 g/L will develop hydrostatic pulmonary oedema at a LA pressure of 8 mmHg; a serum albumin of 30 g/L will require an LA pressure o f > 17 mmHg, and so on Cardiogenic pulmonary oedema is often associated with signi \201 cant systemic hypotension or low-output states. Contributing factors include conditions where there is \200\230mech anical \200\231 impairment to forward \202 ow (e.g. valvular heart disease (especially if acute), VSD), or severe myocardial disease (large MI, ongoing ischaemia, acute myocarditis , cardiomyopathy). 730 CHAPTER 17 Cardiovascular emergencies The gradient between PA diastolic pressure (PAD) and PCWP (PAD \200\223 PCWP) is generally <5 mmHg in cardiogenic and > 5 mmHg in non-cardiogenic pu lmonary oedema (e.g. ARDS). The pulse and BP are most commonly elevated due to circulating catecholamines and overactivity of the renin \200\223angiotensin system (RAS). Examination reveals sweating, cool \200\230shut-down \200\231 peripheries, high pulse volume (assess c arotid or femoral pulses). Management The general approach involves combination of diuretics, vasodilators inotrope s. Patients may be divided into two groups: \200 patients in shock (with systolic BP<100 mmHg) \200\224 see b Pulmonary oedema: management, p. 728 haemodynamically stable patients with systolic BP > 100 mmHg \200\224 (see b Pulmonary oedema, p. 726 \200\223733. Patients with systolic BP<100 mmHg \200 The patient is in incipient (or overt) shock. The most common etiology is cardiogenic shock but remember non-cardiogenic causes (e.g. ARDS, septic shock) . Optimal monitoring and access : central line PA catheter (Swan \200\223Ganz), urinary ca theter, arterial line (monitoring BP and ABG). Internal jugular lines are preferable, as th e risk of pneumothorax is lower. Ensure the patient is not under \201 lled, using PCWP as a guide (<10 mmHg) (mistaken diagnosis e.g. septic shock from bilateral pneumonia). Is there a mechanical cause that may require emergency surgery? Arrange an urgent ECHO to rule out: \200\224 VSD and acute mitral regurgitation (MR) in all patients with recent MI with/without new murmur (see b Ventricular septal defect post-MI, p.278; Acute mi tral regurgitation post-MI, p.280) \200\224 prosthetic heart valve dysfunction (e.g. dehiscence, infection) or pre-existing n ative aortic or mitral disease that may require surgery. Discuss the patient early on with cardiologist/cardiac surgeon. The choice of inotropic agent depends on the clinical condition of the patient and, to some extent, the underlying diagnosis: \200 Systolic BP 80 \200\223100 mmHg and cool peripher ies: start dobutamine infusion at 5 mcg/kg/min, increasing by 2.5 mcg/kg/min every 10 \200 \22315 minutes to a maximum of 20 g/kg/min until BP > 100 mmHg. This may be combined wit h dopamine (2.5 \200\2235 mcg/kg/min). However, tachycardia and/or hypotension secondary to peripheral vasodilation my limit its effectiveness. Phosphodiesterase inhibitors (enoximon e or milrinone) should be considered where dobutamine fails. Systolic BP <80 mmHg : give a slow IV bolus of adrenaline (2 \200\2235 mL of 1 in 10 000 solution Minijet ) and repeat if necessary. \200 Dopamine at doses of > 2.5 g/kg/min has a pressor action in addition to direct and indirect inotropic effects and may be used at higher doses (10 \200 \22320 mcg/kg/min) if the blood pressure remains low. However, it tends to raise the pulmon ary capillary \201 lling pressure further and should be combined with vasodilators (e.g. nitroprusside PULMONARY OEDEMA: MANAGEMENT 731 or hydralazine) once the blood pressure is restored (see below). Beware of arrhythmias at t hese doses. Adrenaline infusion may be preferred to high-dose dopamine as an alternative inotrope. Once the blood pressure is restored ( > 100 mmHg), vasodilators such as nitroprusside/hydralazi ne or GTN infusion should be added to counteract the pressor effects. Adrenaline can be com bined with dobutamine and/or a phosphodiesterase inhibitor, especially in the context of a poor ventricle. Intra-aortic balloon counter pulsation should also be used with/without inotropes in the co ntext of a potentially reversible cause for the pulmonary oedema and shock (e.g. ongoing my ocardial ischaemia, VSD, acute MR). Further doses of diuretic may be given. Patients with systolic BP \211 100 mmHg \200 Fu rther doses of diuretic may be given (furosemide 40 \200\22380 mg IV q3 \200\2234h or as a continuous infusion (20 \200\22380 mg/h)). Continue the GTN infusion, increasing the infusion rate every 15 \200\22320 min up to 10 mg /h, titrating against blood pressure (aiming to keep systolic BP 7100 mmHg). Angiotensin-converting enzyme inhibitors (ACE-Is) can be used if BP is adequate and there are no other known contraindications (e.g. RAS, renal failure). Arter iolar vasodilators (nitroprusside or hydralazine) may also be added in or used instead of G TN ( ACE-I) in patients with adequate BP. Arterial pressure should be monitored continuo usly via an arterial line to prevent inadvertent hypotension. Long-term management \200 Unless a contraindication exists, start an ACE-I, increasing th e dose to as near the recommended maximal dose as possible. In the context of LV impairment , ACE-Is have signi \201 cant prognostic bene \201 t. If ACE-Is are contraindicated or not tolerated, consider the use of hydralazine and long-acting oral nitrate in combination. If the patient is already on high doses of diuretics and ACE-Is, consider the addition spir onolactone (25 \200\22350 mg) (NB: monitor renal function and serum potassium). In the context of stable patients (no clinical features of failure) and poor LV function, B \200\223blockers have signi \201 cant mortality and some symptomatic bene \201 t (NB: st art with a very small dose and increase gradually every 2 weeks with regular monitoring). B isoprolol, carvedilol, and metoprolol can all be used. Ensure all arrhythmias are treated. \200 Digoxin can be used for symptomatic improvement. \200 Consider multisite pacing (biventricular) in the context of severe LV dysfunction, broad QRS complex MR on ECHO. Patients in AF, or with poor LV function should be considered for long- term anticoagulation. Patients <60 years with severe irreversible LV dysfunction and debilitating symptoms must be considered for cardiac transplantation. 732 CHAPTER 17 Cardiovascular emergencies Pulmonary oedema: speci \201 c conditions Diastolic LV dysfunction \200 This typically o ccurs in elderly hypertensive patients with LV hypertrophy, where there is impaired relaxation of the ventricle in diastole. There is mark ed hypertension, pulmonary oedema, and normal, or only mild, systolic LV impairment. With tachycardia, diastolic \201 lling time shortens. As the ventricle is \200\230stiff \200\231 in diastole, LA pressure is increased and pulmonary oedema occurs (exacerbated by AF, as \201 lling by atrial systole is lost). Treatment involves control of hypertension with IV nitrates (and/or nitroprusside), calcium-channel blockers (verapamil or nifedipine) and even certain B -bloc kers (e.g. carvedilol, bisoprolol). Fluid overload \200 Standard measures are usually effective. \200 In extreme circumstan ces, venesection may be necessary. \200 Check the patient is not anemic (hemoglobin (Hb) (cid:116) 10 g/dL). Remove 500 mL blood via a cannula in a large vein and repeat if necessa ry. If anemic (e.g. renal failure) and acutely unwell, consider dialysis. Known (or unknown) renal failure \200 Unless the patient is permanently anuric, large dos es of IV furosemide may be required (up to 1 g given at 4 mg/min) in addition to standard t reatment. If this fails, or the patient is known to be anuric, dialysis will be required. In patients not known to have renal failure, an underlying cause should be sought. Anemia \200 Cardiac failure may be worsened or precipitated by the presence of signi \201 cant anemia. Symptoms may be improved in the long term by correcting this anemia. Generally, transfusion is unnecessary with Hb > 9 g/dL unless there is a risk of an acute b leed. Treatment of pulmonary oedema will result in haemoconcentration and a \200\230rise \200\231 in the Hb. If the anemia is thought to be exacerbating pulmonary oedema, ensure that an adequate diuresis is obtained prior to transfusion. Give slow transfusion (3 \200\2234 h per unit) of packed cells, with IV furosemide 20 \200\22340 mg before each uni t. PULMONARY OEDEMA: SPECIFIC CONDITIONS 733 Hypoproteinaemia \200 The critical left atrial (LA) pressure at which hydrostatic pulmona ry oedema occurs is in \202 uenced by the serum albumin and approximates to serum albumin con centration (g/L) x 0.57. Treatment involves diuretics, cautious albumin replacement, spironolactone (if there is secondary hyperaldosteronism), and treatment of the underlying cause for hypoproteinaemia. 734 CHAPTER 17 Cardiovascular emergencies Acute aortic regurgitation Presentation \200 Sudden, severe aortic regurgitation (AR) pre sents as cardiogenic shock and acute pulmonary oedema. The haemodynamic changes are markedly different from those seen in chronic AR. The previous normal-sized LV results in a smaller effective forward \202 ow and higher LVEDP for the same degree of AR. Patients are often extremely unwell, tachycardic, peripherally shut down, and frequently ha ve pulmonary oedema. Unlike chronic AR, pulse pressure may be near normal. If available, ask for a history of previous valvular heart disease, hypertension, features of Marfan syndrome, and risk factors for infective endocarditis. Physical signs of severe AR include a quiet aortic closure sound (S 2 ); an ejection systol ic murmur over the aortic valve (turbulent \202 ow); high- pitched and short, early diast olic murmur (AR); quiet S 1 (premature closure of the mitral valve (MV)). Examine speci \201 cally for signs of an underlying cause (see b Aortic regurgitation, p. 170). Where there is no obvious underlying cause (e.g. acute MI), assume infective endocarditis until proven otherwise. Causes \200 Infective endocarditis \200 Ascending aortic dissection \200 Collagen vas cular disorders (e.g. Marfan) \200 Connective tissue diseases (large and medium vessel ar teritis) \200 Trauma \200 Dehiscence of a prosthetic valve. Diagnosis Diagnosis is based on a combination of clinical features and transthoracic and/or transoesophageal ECHO. Management Acute AR is a surgical emergency and all other management measures are only aime d at stabilizing the patient until urgent aortic valve replace- ment (AVR) can take place. The patient \200\231s clinical condition will determine the urgency of surgery (and mortali ty). Liaise immediately with local cardiologists. General measures (see b Pulmonary oedema: management, p. 728) \200 Admit the patient to intensive care or medical HDU. \200 Give oxygen, and begin treating any pulmonary ooedema with diuretics.