Hyperlucent lung \201 eld compared to the contralateral side. Loss of clarity of the diap hragm outline. \200\230Deep sulcus \200\231 sign, giving the appearance of an inverted dia phragm. A particularly clear part of the cardiac contour. with a needle, followed by formal chest drain insertion. 3. Repeated needle aspiration may be suf \201 cient in spontaneously breath- ing patients without respiratory failure. 4. Chest drain insertion. This may need to be done under ultrasound or CT guidance if localized due to surrounding lung \201 brosis. A small pneumothorax (<10% hemithorax) may be left undrained, but prompt action should be i nstituted if cardiorespiratory deterioration occurs. Patients should not be transferred bet ween hospitals, particularly by airplane, with an undrained pneumothorax. Drains may be rem oved if not swinging/bubbling for several days. Bronchopleural \201 stula Denoted by cont inual drainage of air. Usually responds to conservative treatment with continual applicatio n of 5kPa negative pressure; this may take weeks to resolve. For severe leak and/or comprom ised ventilation, high frequency jet ventilation and/or a double-lumen endobronchial tube m ay be considered. Surgical intervention is rarely necessary. PNEUMOTHORAX 369 Lung rim Clear cardiac contour Deep sulcus Fig 22.3. Chest X-ray appearance. See also: Chest drain insertion, p84; Respiratory imaging, p158; Dyspnoea, p346; Respirator y failure, p350. 370 CHAPTER 22 Respiratory disorders Haemothorax Usually secondary to chest trauma or following a procedure, e.g. cardiac surger y, chest drain insertion, central venous catheter insertion. Spontaneous haemothorax is rar e, even in patients with clotting disorders. Clinical features \200 Stony dullness. \200 Decreased breath sounds. \200 Hypovolaemi a and deterioration in gas exchange (if large). Diagnosis \200 Erect chest X-ray \200\224blunting of hemidiaphragm and progressive loss of basal lung \201 eld. Supine chest X-ray \200\224increased opacity of affected hemithorax plus decrease d clarity of cardiac contour on that side. Large-bore needle aspiration to con \201 rm pre sence of blood. A small- bore needle may be unable to aspirate a haemothorax if it has clot ted. Management 1. If small, observe with serial X-rays and monitor for signs of cardiores- piratory deterioration. 2. Ensure any coagulopathy is corrected by administration of fresh frozen plasma and/or platelets or other blood products as indicated. 3. Ensure crossmatched blood is available for urgent transfusion if necessary. 4. If signi \201 cant in size or patient becomes symptomatic, insert large-bore chest drai n, e.g. size 28Fr. The drain should be directed postero-inferi- orly toward the dependent a rea of lung and placed on 5kPa suction. 5. If drainage exceeds 1000mL or >200mL/h for 3 \200\2234h despite correcting any coagulopathy, contact a thoracic surgeon. 6. Factor VIIa may be considered for intractable bleeding though only an- ecdotal reports of bene \201 t exist. 7. Drains inserted for a haemothorax may be removed after 1 \200\2232 days if no further bleeding occurs. Perforation of an intercostal vessel during chest drain insertion may cause considerable bl eeding into the pleura. If deep tension sutures around the chest drain fail to stem blood l oss, remove the chest drain and insert a Foley urethral catheter through the hole. In \202 ate the balloon and apply traction on the catheter to tamponade the bleeding vessel. If th ese meas- ures fail, contact a thoracic surgeon. HAEMOTHORAX 371 See also: Chest drain insertion, p84; Coagulants and anti \201 brinolytics, p322; Bleeding disorders, p468; Multiple trauma (1), p582; Multiple trauma (2), p584. 372 CHAPTER 22 Respiratory disorders Haemoptysis \200 May range from a few specks of blood in expectorated sputum to massive pulmonary hemorrhage . Likely to disrupt gas exchange before hypovolaemia is life-threatening. May be a presenti ng feature of a patient admitted to intensive care or may result from critical illness and its treatment. \200 Causes Massive haemoptysis \200 Disruption of a bronchial artery by acute in \202 ammation or invasion (e.g. pulmonary neo plasm, trauma, cavitating TB, bronchiectasis, lung abscess, and aspergilloma). Rupture of a rterio-venous malformations and bronchovascular \201 stulae. Pulmonary infarction seconda ry to prolonged pulmonary artery catheter wedging or pulmonary artery rupture. \200 Minor haemoptysis \200 \200 Intrapulmonary in \202 ammation or infarction (e.g. pulmonary embolus). Endotracheal tube trauma (e.g. mucosal erosion, balloon necrosis, trauma from the tube tip, trauma to a trach eostomy stoma, trauma from suction catheters). Tissue breakdown in critically ill patients (e.g. tissue hypoperfusion, coagulopathy, poor nutritional state, sepsis, and hypoxaemia). Investigation and assessment Assess cardiorespiratory function and monitor closely. Massive haemopt- ysis may require resuscitation and urgent intubation. The diagnosis may be sugges ted by the history and a chest X-ray may identify a cavitating lesion. Lower lobe shadowing on a chest X-ray may be the result of overspill of blood from elsewhere in the bronchial t ree. Early surgical intervention should be prompted by a changing air- \202 uid level, per sistent opaci \201 cation of a previous cavity, or a mobile mass. Early bronchoscopy may i dentify the source of haemoptysis although only while bleeding is active. Blood in multiple bronchial ori \201 ces may be confusing but saline lavage may leave the source visible. R igid bronchoscopy is useful in massive haemoptysis allowing oxygenation and wide bore sucti on. Management \200 Basic resuscitation (high FIO2, endotracheal intubation, and blood transfusion) is needed f or cardiorespiratory compromise. Correction of coagulopathy is a priority. Bronchoscopy all ows direct instillation of 1 in 200,000 epinephrine if the source of hemorrhage can be foun d or, alternatively, endobronchial tamponade with a balloon catheter. In cases of severe he morrhage from one lung, a double-lumen endotracheal tube may prevent some overspill to the other lung while de \201 nitive treatment is organized. De \201 nitive treatment may incl ude radiological bronchial artery embolisation or surgical resection. Induced hypotension m ay be useful in bronchial artery hemorrhage. In cases of pulmonary artery hemorrhage, PEEP may be used with mechanical ventilation to reduce pulmonary bleeding. \200 \200 HAEMOPTYSIS 373 See also: Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68; Continuous positive airway pressure, p70; Fibreoptic bronchoscopy, p88; Coagulation mo nitoring, p222. 374 CHAPTER 22 Respiratory disorders Inhalation injury Causes include smoke, steam, noxious gasses, and aspiration of gastric co n- tents. Clinical features \200 \200 \200 \200 \200 \200 \200 \200 Dyspnoea, coughing. Stridor (if upper airway obstruction). Bronchospasm. Signs of lung/loba r collapse (especially with aspiration). Signs of respiratory failure. Cherry-red skin colo r (carbon monoxide). Agitation, coma. ARDS (late). General principles of management 1. High \202 ow, high concentration O2 targeting an SaO2 of 92 \200\22398%. 2. Early intubation if upper airway is compromised or threatened. 3. Ea rly bronchoscopy if inhalation of soot, debris, vomit suspected. Speci \201 c conditions Smoke inhalation \200 Smoke rarely causes thermal injury beyond the major bronchi as it has a low speci \201 c h eat content. However, soot is a major irritant to the upper airways and can produce very ra pid and marked in \202 ammation. Urgent laryngoscopy should be performed if soot is presen t in the nares, mouth, or pharynx. If soot is seen or the larynx appears in \202 amed, per form early endotracheal intubation. As the upper airway can obstruct within minutes, it is advisable to intubate as a prophylactic measure rather than as an emergency where it may pr ove impossible. After intubation, perform urgent bronchoscopy with bronchial toilet using w armed 0.9% saline to remove as much soot as possible. Commence benzylpenicillin 1.2gqds IV. Speci \201 c treatment for poisons contained within smoke (e.g. carbon monoxide, cyanide) . \200 Steam inhalation \200 \200 Consider early/prophylactic intubation. Steam has a much higher heat content than smoke and can cause injury to the whole respiratory tract. Consider early bronchoscopy and lavage wi th cool 0.9% saline. Aspiration of gastric contents \200 Early bronchoscopy and physiotherapy to remove as much particulate and liquid matter as pos sible. Either cefuroxime plus metronidazole, or clindamycin for 3 \200\2235 days. Some auth orities argue that antibiotics are unnecessary. Corticosteroid therapy has no proven bene \201 t. INHALATION INJURY 375 See also: Fibreoptic bronchoscopy, p88; Antimicrobials, p326; Basic resuscitation, p338; In haled poisons, p534; Burns \200\224 \202 uid management, p592; Burns \200\224general manag ement, p594. 376 CHAPTER 22 Respiratory disorders Pulmonary embolus \200 Usually arises from a DVT in femoral or pelvic veins. Risk increases with prolonged immobil ity, polycythaemia, or hyperviscosity disorders. Amniotic \202 uid embolus. Fat embolus a fter pelvic or long bone trauma. Right heart source, e.g. mural thrombus. \200 \200 Clinical features \200 \200 Pleuritic-type chest pain, dyspnoea 9 haemoptysis. The patient with a major embolus often p refers to lie \202 at. Dyspnoea improves due to increased venous return and right heart l oading. Deterioration in gas exchange: may \201 nd a low PaO2, low or high PaCO2, and a m etabolic acidosis. Cardiovascular features, e.g. tachycardia, low/high BP, and collapse. Ch est X-ray: may be normal but a massive embolus may produce fewer vascular markings (pulmona ry oligaemia) in a hemithorax 9 a bulging pulmonary hilum. A wedge-shaped peripheral pulmon ary infarct may be seen after a few days following a smaller embolus. ECG: acute right vent ricular strain, i.e. S1Q3T3, tachycardia, right axis deviation, right bundle branch block, P pulmonale. Echocardiogram: may reveal evidence of pulmonary hypertension and acute right ventricular strain. A large embolus may be visualized. D-dimers: a normal value probably ex cludes a pulmonary embolus. \200 De \201 nitive diagnosis \200 \200 \200 \200 CT scan with contrast: the investigation of choice for major embolus. Echocardiography: may identify embolus. Pulmonary angiography. Ventilation-perfusion scan: degree of certainty i s reduced if area of non- perfused lung corresponds to any chest X-ray abnormality. Fat glo bules or fetal cells in pulmonary artery blood may be found in fat and amniotic \202 uid embolus, respectively. General management 1. FIO2 0.6 \200\2231.0 to maintain SaO2 93 \200\22398%. 2. Lie patient \202 at to increase venous return. 3. Fluid challenge to optimize right heart \201 llin g. 4. Epinephrine infusion if circulation still compromised. 5. Mechanical ventilation may be needed. Gas exchange may worsen due to loss of preferential shunting and decreases in cardiac output. Management of blood clot embolus Start anticoagulation with low molecular weight heparin ad justed for weight. Consider thrombolysis if there is a major embolus and cardio- vascular c ompromise, and embolectomy if the patient remains moribund. Otherwise, at 24 \200\22348h, c ommence warfarinisation regimen but continue heparin for further 2 \200\2233 days after ade quate oral dosing. Management of fat embolus Other than general measures including oxygenation, \202 uid res uscitation, and right heart loading, treatment remains controversial. Various authori- ties advocate corticosteroids, heparinisation, or no speci \201 c therapy. PULMONARY EMBOLUS 377 Drug dosages Low molecular weight heparin regimens Subcutaneous low molecular weight heparin is given until oral anticoagulant therapy is full y established. Dalteparin: 200 units/kg (max. 18,000 units) every 24h (or 100 units/kg twice daily if incr eased risk of hemorrhage) Enoxaparin: 1mg/kg 12-hourly or 1.5mg/kg (150 units/kg) every 24h Tinzaparin: 175 anti-Xa units/kg once daily Unfractionated heparin regimen IV heparin is given until oral anticoagulant therapy is fully established. 80 units/kg bolus (do not exceed 8,000 units initial bolus) followed by 18 unit/kg/h (not t o exceed 1,800 units/h) titrated to achieve APTT 2 \200\2233x normal. Thrombolytic regimens rtPA: (100mg over 90min) should be given followed by a heparin infusion (24,000 \200\22336, 000 units/d) to maintain the partial thromboplastin time at 2 \200\2233x normal. This is th e treatment of choice if surgery or angiography is contemplated. Streptokinase (500,000 units as a loading dose over 30min followed by 100,000 units/h for 2 4h). NB. Central venous catheters should ideally be inserted pre-thrombolysis by an experienced operator to minimize the risk of bleeding/haematoma. Key papers Task Force Report of the European Society of Cardiology. (2000) Guidelines on di agnosis and management of acute pulmonary embolism. Eur Heart J 21: 1301 \200\22366. Konstantinides S, for the Management Strategies and Prognosis of Pulmonary Embolism-3 Trial Investigators. (2002) Heparin plus alteplase compared with heparin alone in patients with submas- sive pulmonary embolism. N Engl J Med 347: 1143 \200\22350. British Thoracic Society guidelines for the management of suspected acute pulmonary embolis m. (2003) Thorax 58: 470 \200\22384. See also: Ventilatory support \200\224indications, p44; Blood gas analysis, p154; Coagulati on monitoring, p222; Anticoagulants, p318; Thrombolytics, p320; Basic resuscitation, p338; Cardiac arrest, p340. This page intentionally left blank 379 Chapter 23 Cardiovascular disorders Hypotension 380 Hypertension 382 Tachyarrhythmias 384 Bradyarrhythmias 386 Acute coronary s yndrome (1) 388 Acute coronary syndrome (2) 390 Heart failure \200\224assessment 392 Heart failure \200\224management 394 380 CHAPTER 23 Cardiovascular disorders Hypotension The overall management aim is to maintain a minimum mean arterial pres- sure th at will ensure adequate tissue perfusion. This will vary between patients so individual tit ration is necessary. A normal BP does not guarantee an adequate cardiac output; circulatory support should aim to achieve ade- quate blood \202 ow as well as an adequate pressure. For patients in extremis, \201 rst-line treatment options should include external cardiac massage and epinephrine 0.05 \200\2230.2mg IV boluses (1mg in cardiac arrest). BP elevatio n should not be excessive as this may compromise tissue perfusion. Assessment of hypotension Hypotension requires treatment if there are signs of poor tissue perfusion (e.g. oliguria, confusion, altered consciousness, cool peripheries, metabolic aci dosis). This will usually be at mean BP <60mmHg (higher if patient has a hypertension histo ry) with xxx Speci \201 c treatment should be given for the underlying cause, e.g. hemorrh age, acute myocardial infarction, arrhyth- mias, pulmonary embolus, sepsis, and poisoning. Initial treatment of hypotension Most cases require \202 uid as \201 rst-line managemen t to restore an adequate circulating volume. Exceptions may include acute heart failure, ar rhyth- mias, cardiac tamponade, and pneumothorax. In cases of severe haemor- rhage, blood s hould be used as soon as available; if life-threatening, group speci \201 c or O negative blood should be used considered. Pharmacological treatment If hypotension persists after restoring an adequate circulating v olume, the appropriate choice of drug treatment depends on whether there is myo- cardial fa ilure (signs of low cardiac output or known measured low stroke volume) or peripheral vascu lar failure (warm, vasodilated periphery, or measured normal/high stroke volume). A low str oke volume should be treated with an inotropic agent (e.g. epinephrine, dobutamine) and per i- pheral vascular failure with a vasopressor (e.g. norepinephrine). Inotropic support Most hypotensive patients requiring inotropes (epinephrine, dopamine, or dobutamine) should have \202 ow monitoring. Titrating against BP alone carries the danger of inappropriate vasoconstriction and reduced cardiac output. The agent should be titrated against stroke volume as tachycardia may maintain output. Dobutamine and PDE inhibitors (e .g. milrinone) can cause excessive vasodilatation and hypotension. Vasopressors Once stroke volume has been corrected, norepinephrine (or high-dose dopamine) should be titrated against mean BP. In most patients, 60mmHg is an adequate target, but may need to be higher to ensure organ perfusion in the elderly and previous hypertensives. Pre ssors may reduce cardiac output. This effect should be monitored and corrected by adjustmen t of dose. Vasopressin (or its synthetic analog, terlipressin) is increasingly used for hig h output, catecholamine-resistant, vasodilatory shock. Care should be taken to avoid excess ive peripheral constriction or impairment of organ perfusion. HYPOTENSION 381 Drug dosages Epinephrine Infusion starting from 0.05mcg/kg/min Dobutamine Infusion from 2.5 \200\22325mcg/kg/min Dopamine Infusion from 2.5 \200\22330mcg/kg/min Norepinephrine Infusion starting from 0.05mcg/kg/min Vasopressin 0.01 \200\2230.04U/min for sepsis Terlipressin 0.25 \200\2230.5mg bolus, repeated at 30min intervals as necessary to maximum 2mg Key papers Russell JA, for the VASST Investigators. (2008) Vasopressin versus norepinephrin e infusion in patients with septic shock. N Engl J Med 358: 877 \200\22387. Annane D, for the CATS Study Group. (2007) Norepinephrine plus dobutamine versus epine- phr ine alone for management of septic shock: a randomized trial. Lancet 370: 676 \200\22384. See also: Intra-aortic balloon counterpulsation, p102; Blood pressure monitoring, p164; Art erial cannulation, p166; Colloids, p246; Inotropes, p264; Vasopressors, p268; Basic resusci tation, p338; Cardiac arrest, p340; Fluid challenge, p348; Pneumothorax, p368; Haemothorax, p370; Pulmonary embolus, p376; Acute coronary syndrome (1), p388; Acute coronary syndrome (2), p390; Heart failure \200\224 assessment, p392; Upper gastrointestinal hemorrhage, p412 ; Bleeding varices, p414; Intra- abdominal bowel perforation and obstruction, p418; Lower i ntestinal bleeding and colitis, p420; Abdominal sepsis, p422; Pancreatitis, p424; Sepsis an d septic shock \200\224treatment, p560; Multiple trauma (1), p582; Spinal cord injury, p590 ; Burns \200\224 \202 uid management, p592; Post-partum hemorrhage, p638; Amniotic \202 uid embolus, p640. 382 CHAPTER 23 Cardiovascular disorders Hypertension Often de \201 ned in adult patients as a diastolic pressure >95mmHg and a sys tolic pressure >180mmHg. Common causes in intensive care \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Idiopathic/essential. Agitation/pain, especially where muscle relaxants are used. Excessive vasoconstriction, e.g. cold, vasopressor drugs. Head injury, cerebrovascular accidents. Dr ug-related. Dissecting aneurysm, aortic coarctation. Vasculitis, thrombotic thrombocytopaen ic purpura. (Pre-)eclampsia. Aortic coarctation (may present acutely in adulthood). Endocri ne, e.g. phaeochromocytoma (rare). Renal failure, renal artery stenosis (rare). Spurious \200\224underdamped transducer system. Indications for acute treatment Hypertensive encephalopathy, heart failure, eclampsia, and acute dis- secting aneurysm are the prime indications for rapid and aggressive, albeit cont rolled, reduction of blood pressure. In other conditions, especially chronic hypertension and following acute neurological event s, e.g. head injury, cerebrovascular accidents, a rapid reduction in BP may adversely affec t perfusion. Hypertension after a cerebral event is not usually treated unless very high, e .g. mean BP >140 \200\223150mmHg, systolic BP >220 \200\223230mmHg. In this instance, contr olled and partial reduction is mandatory, e.g. with sodium nitroprusside infu- sion with co ntinuous invasive monitoring. In the presence of a raised ICP, a cerebral perfusion pressur e \211 60 \200\22370mmHg is usually targeted. Hypertensive crisis Occurs when symptomatic (increasing drowsiness, seizures, papilloedema, retinopathy) in the presence of elevated sy stemic pressures. The diastolic BP usually exceeds 120 \200\223130mmHg and the mean BP >140 \200\223150mmHg, although encephalopathy can occur at lower pressures. Principles of manag ement 1. Adequate monitoring (invasive BP, ECG, CVP, cardiac output, urine output). 2. Consider pain, hypovolaemia, hypothermia, and agitation. 3. Consider speci \201 c treat ment, e.g. phaeochromocytoma, thyroid crisis, aortic dissection, in \202 ammatory vasculitis. 4. Slow intravenous infusion of nitrate or nitroprusside. Other options include labetalol o r esmolol infusions, hydralazine (IV or IM). Sublingual nifedipine or IV hydralazine may so metimes produce precipitate falls in BP. Use cautiously and start with low doses. 5. Aim to reduce to mildly hypertensive levels unless dissecting aneu- rysm where systolic BP should be lowered <100 \200\223110mmHg. After certain types of surgery (e.g. cardiac, ao rtic), control of systolic BP <100 \200\223120mmHg may be requested to reduce risk of bleed ing. 6. Longer-term oral treatment, e.g. calcium channel blocker, ACE inhibi- tor, should be instituted. HYPERTENSION 383 Drug dosages GTN 0.5 \200\22320mg/h Sodium nitroprusside 0.5 \200\2231.5mcg/kg/min, increased slowly to 0.5 \200\2238mcg/ kg/min Labetalol 50mg IV over 1min repeated every 5min to maximum 200mg Metoprolol 5mg slow IV or 0 \200\2230.1mg/kg/h Esmolol 50 \200\223200mcg/kg/min Hydralazine 5 \200\22310mg slow IV, followed by 50 \200\223150mcg/min See also: Blood pressure monitoring, p164; Intracranial pressure monitoring, p200; Vasodila tors, p266; Hypotensive agents, p270; Intracranial hemorrhage, p448; Subarachnoid hemorrhag e, p450; Stroke, p452; Pre-eclampsia and eclampsia, p634. 384 CHAPTER 23 Cardiovascular disorders Tachyarrhythmias If pulses are not palpable or there is severe hypotension, a tachyarrhythm ia requires cardiac massage and urgent DC cardioversion. Otherwise, the initial treatment p rior to diagnosis includes correction of hypoxaemia, potassium (to ensure a plasma K+ 4.5 \200\2235.8mmol/L) and magnesium (targeting plasma levels of 1.5 \200\2232mmol/L). Causes of tachyarrhythmias Where possible, the cause should be treated. Speci \201 c treat ment should be given as appropriate, e.g. for hypovolaemia, hypotension (may also be due to the arrhythmia), acute myocardial infarction, pain, anemia, hypercapnia, fever, anxiety, t hyrotoxicosis, and digoxin toxicity. Diagnosis Broad complex tachycardia Assumed to be ventricular tachycardia (VT) until proven otherwise (e.g. slows with adenosine). Regular complexes with AV dissociation (fusion beat s, capture beats, QRS >140ms, axis < \200\22330*, concordance) suggest VT. If there is no A V dissociation, the arrhythmia is probably supraventricular with aberrant conduction; adeno sine may be used as a diagnostic test since SVT may respond and VT will not. Irregular broa d complexes are probably atrial \201 brillation with aberration. Torsades de pointes are a form of ventricular tachycardia with a variable axis. Narrow complex tachycardia The absence of P waves suggests atrial \201 brillation. A P wa ve rate >150 suggests SVT, whereas slower rates may represent sinus tachycardia or atrial \202 utter with block. P waves are abnormal ( \202 utter waves) in atrial \202 utter an d QRS complexes may be irregular in variable block. Extremely fast SVT may be due to a re-e ntry pathway with retrograde conduc- tion and premature ectopic atrial excitation. In Wolff Parkinson White syndrome, the re-entry pathway inserts below the His bundle allowing rapid AV conduction and re-entry tachyarrhythmias. Prior to onset of the arrhythmia, there may b e a short PR interval and a delta wave. Treatment Ventricular tachycardia Lidocaine, amiodarone, or magnesium is the mainstay of dr ug treatment. Overdrive pacing may be used if a pacing wire is in situ, capturing the ven- tricle at a pacing rate higher than the arrhythmia and gradually reducing the pacing rate. Torsades de pointes may be exacerbated by anti-arrhythmics so magnesium or overdrive pacing are safest. Supraventricular tachycardia and atrial \202 utter Carotid sinus massage may be used in p atients with no risk of calci \201 ed athero- matous carotid deposits. Amiodarone, adenosi ne, or magnesium is usually the most useful drugs in the critically ill. Verapamil may be u sed if complexes are narrow (no risk of misdiagnosed ventricular tachycardia) although this drug and other AV node blockers should be avoided in re-entry tachycardias. Atrial \201 brillation If onset <48 hours, cardiovert, especially if haemodynamic comprom ise. If rate control desired, B-blockers are \201 rst-line; digoxin has a secondary role. TACHYARRHYTHMIAS 385 Drug dosages and cautions Adenosine 6mg IV as a rapid bolus. If no response in 1min give 12mg followed by a repeat 12mg. Verapamil 2.5mg IV slowly. If no response, repeat to a maximum of 20mg. An IV infusion of 1 \200\2231 0mg may be used. 10mL CaCl2 10% should be available to treat hypotension associated with ve rapamil. Verapamil should be avoided in re-entry tachyarrhythmias since ventricular respons e may increase. Life-threatening hypotension may occur in misdiagnosed ventricular tachycar dia and life- threatening bradycardia may occur if the patient has been B-blocked. 1mg/kg I V as a bolus, followed by an infusion of 2 \200\2234mg/min. Lidocaine Amiodarone 5mg/kg over 20min, then infused at up to 15mg/kg/24h in 5% glucose via a central vein. Avoi d with other class III agents (e.g. sotalol) since QT interval may be severely prolonged. Magnesium 20mmol MgSO4 over 2 \200\2233h. In an emergency it may be given over 5min. See also: Electrical cardioverversion, p94; ECG monitoring, p162; Electrolytes (Na+, K+, CT , HCO3 Antiarrhythmics, p272; Basic resuscitation, p338. \210\222), p212; 386 CHAPTER 23 Cardiovascular disorders Bradyarrhythmias If peripheral pulses are not palpable, a bradyarrhythmia requires external cardiac massage and treatment as for asystole. For asymptomatic brady- cardia, treatment m ay not be required other than close monitoring and correction of the cause. The exception t o this is higher degrees of heart block occurring after an acute anterior myocardial infarc tion where pacing may be required prophylactically. Causes Where possible, treat the cause. Common causes for which speci \201 c treat- ment m ay be required include hypovolaemia, hyperkalaemia, hypotension (may also be due to the arr hythmia), acute myocardial infarction, digoxin toxicity, B-blocker toxicity, hyperkalaemia, hypothyroidism, hypopitui- tarism, and raised intracranial pressure. Digoxin toxicity may require treat- ment with anti-digoxin antibodies. Diagnosis Sinus bradycardia Slow ventricular rate with normal P waves, normal PR interval, and 1:1 AV conduction. Heart block \200 Normal P waves, a prolonged PR interval, and 1:1 AV conduction suggest 1* heart block. In 2 * heart block, the ventricles fail to respond to atrial contraction intermittently. This ma y be associated with regular P waves and an increasing PR interval until ventricular depola risation fails (Mobitz I or Wenkebach) or a normal PR interval with regular failed ventricu lar depolarisation (Mobitz II). In the latter case, the AV conduction ratio may be 2:1 or m ore. In 3* heart block, there is complete AV dissociation with a slow, idioventricular rate . Absent P wave bradycardia Absent P waves may represent slow atrial \201 brillation or sin o-atrial dys- function. In the latter case, there will be a slow, idioventricular rate. Treatment Hypoxaemia must be corrected in all symptomatic bradycardias. First- line drug tr eatment is usually atropine 0.3mg or glycopyrronium bromide 200mcg IV. If the arrhythmia fa ils to respond, 0.6mg followed by 1.0mg atropine may be given. Failure to respond to drugs requires temporary pacing. This may be accomplished rapidly with an external system if ther e is haemodynamic compromise or by transvenous placement. Other indica- tions for temporary pacing are shown opposite. Higher degrees of heart block after an anterior myocardial infa rction will usually require perma- nent pacing. BRADYARRHYTHMIAS 387 Indications for temporary pacing \200 Persistent symptomatic bradycardia. \200 Blackout s associated with: \200 \200 \200 Cardiovascular collapse. Inferior myocardial infarc tion with symptomatic 3* heart block. Anterior myocardial infarction with: \200 \200 \200 3* heart block. 2* heart block. RBBB and left posterior hemiblock. \200 \200 3 heart block. RBBB and left posterior hemiblock. Alternating RBBB and LBBB. See also: Temporary pacing (1), p96; Temporary pacing (2), p98; ECG monitoring, p162; Chron otropes, p274; Basic resuscitation, p338. 388 CHAPTER 23 Cardiovascular disorders Acute coronary syndrome (1) Anginal pain Ischaemic or, rarely, spasmodic constriction of co ronary arteries resulting in pain, usually precordial, pressing or crushing, and 9 radiatio n to jaw, neck, or arms. The sedated, ventilated patient will not usually complain of pain, but signs of discomfort may be apparent, e.g. sweating, hypertension, tachycardia. Regular ly scrutinize the ECG for ST segment and/or T wave changes. A spectrum of severity is present, ranging from stable angina to myo- cardial infarction. A nginal attacks may have recently increased in frequency and/or severity, persist longer, re spond less to nitrates, and occur at rest or after minimal exertion. Pathophysiology \200 Myocardial oxygen supply-demand imbalance usually due to coronary artery atheroma 9 disrupt ion of plaque or new non-occlusive thrombus formation. Spasm (Prinzmetal angina) is uncommo n. Vasopressor drugs may compromise myocardial perfusion by further constricting an already stenosed vessel. Vasodilator drugs may also compromise myocardial perfusion by a \200\230 coronary steal \200\231 phenomenon where blood \202 ow is re-distributed away from stenos ed vessels. Diagnosis \200 \200 \200 Symptoms, especially chest pain but also non-speci \201 c, e.g. sweating. ECG changes: ST segment elevation/depression, T wave inversion. No rise in cardiac enzymes or troponin abov e the myocardial infarction threshold. Dyskinetic areas of myocardium may be seen on echoca rdiography or angiography. Treatment \200 \200 \200 \200 Ensure adequate oxygenation. Correct hypotension and tissue hypoperfusion. Consider drug ca uses, e.g. vasopressors. Glyceryl trinitrate (0.5mg SL) or nitrolingual spray (0.4 \200\223 0.8mg), repeated as necessary. If symptoms are severe and/or persisting, maintain bed rest. Aspirin 75mg od PO (unless contraindicated). \200 For continuing angina \200 \200 \200 IV nitrate infusion, e.g. glyceryl trinitrate, isosorbide trinitrate. Consider B-blocker (u nless contraindicated), e.g. metoprolol. Consider calcium antagonist if B-blocker contraind icated though not on its own, e.g. diltiazem. LMW heparin and clopidogrel (unless contraind icated). Consider GP2b3a inhibitor (IV epti \201 batide or tiro \201 ban) in addition to aspirin + clopidogrel, if considered at high-risk of MI or death. If symptoms or ST segment changes persist despite optimal pharmacological intervention, inform cardiologist with a v iew to angiography and possible angioplasty or surgery. \200 ACUTE CORONARY SYNDROME (1) 389 Key papers Yusuf S for the Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators. (2001) Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 345: 494 \200\223502. Task Force for Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of European Society of Cardiology. (2007) Guidelines for the diagnosis and treatment of no n- ST-segment elevation acute coronary syndromes. Eur Heart J 28: 1598 \200\223660. See also: Coronary revascularisation techniques, p104; ECG monitoring, p162; Echocardiograp hy, p192; Cardiac function tests, p216; Vasodilators, p266; Anti-anginal agents, p276; Acut e coronary syndrome (2), p390; Heart failure \200\224assessment, p392. 390 CHAPTER 23 Cardiovascular disorders Acute coronary syndrome (2) Diagnosis of myocardial infarction Rise and/or fall of cardiac biomarkers (preferably troponin) above upper reference limit plus evidence of myocardial is chaemia with \211 1 of: \200 \200 \200 \200 Symptoms of ischaemia. ECG changes of new ischaemia (new ST \200\223T changes or new LBBB). Pathological Q waves on ECG. New loss of myocardium or new regional wall motion abnormalit y. Management of uncomplicated infarction \200 \200 \200 Oxygen \200\224to maintain SaO2 \211 98%. Good venous access and continuous ECG monitoring . Appropriate and prompt monitoring plus investigations as indicated, e.g. echocardiography , angiography, cardiac output monitoring. Adequate pain relief. Aspirin. Urgent referral fo r percutaneous coronary intervention (PCI) or, if not available, early thrombolysis. Early B-blockade. Gradual mobilization. Do not delay arterial or central venous cannulation if cl inically indicated. An experienced operator should perform these procedures to minimize the risk of bleeding. Avoid the subclavian route. \200 \200 \200 \200 Complications of myocardial infarction \200 \200 \200 \200 Cardiopulmonary arrest. Continuing chest pain \200\224may be ischaemic or pericarditic in o rigin. Pump failure. Hypotension \200\224apart from cardiogenic shock, consider hypovolaemi a (e.g. post-diuretics) or a reaction to a thrombolytic agent. Tachyarrhythmias/bradyarrhyt hmias. Valve dysfunction \200\224predominantly mitral. Pericardial tamponade (rare). Ventri cular septal defect (unusual, often presents 2 \200\2235 days later). Complications of thro mbolytic therapy: arrhythmias, bleeding, hypotension, anaphylactoid reaction. \200 \200 \200 \200 Management of complicated infarction In addition to general measures for the uncomplicated infarction: \200 Cardiopulmonary arrest \200\224cardiopulmonary resuscitation. \200 Con tinuing ischaemic chest pain \200\224IV nitrate and heparin infusions, aspirin, clopidogrel , calcium antagonist, and B-blocker (unless contraindicated); consider urgent angiography 9 stenting or surgery. Pericarditic chest pain \200\224consider non-steroidal anti-in \202 ammatory agent. Management of heart failure. Tachyarrhythmia \200\224anti-arrhythmics, sync hronized DC cardioversion. Bradycardias \200\224chronotrope, consider temporary pacing. Val ve dysfunction \200\224heart failure management; consider surgery. Pericardial tamponade \200\224pericardial aspiration. Ventricular septal defect \200\224heart failure management, consider surgery. Management of thrombolysis complications. \200 \200 \200 \200 \200 \200 \200 ACUTE CORONARY SYNDROME (2) 391 Drug dosages Diamorphine 2.5mg IV. Repeat PRN + anti-emetic Streptokinase 1.5 million units in 100mL 0.9% saline IV over 1h rtPA (alteplase) 15mg IV bolus, then 0.75mg/kg over 30min, then 0.5mg/kg over 1h to a maximal dose of 100mg. This is then followed by heparin for 24 \200\22348 h. Tenecteplase For acute MI: IV bolus of 0.5mg/kg over 10s, followed by heparin for 24 \200\22348h. Reteplase Two IV boluses of 10U given 30min apart, followed by heparin for 24 \200\22348h. Aspirin 150mg PO od Clopidogrel 300mg PO loading dose, then 75mg PO od Atenolol 50mg PO od (increase to 100mg od if not hypotensive and HR exceeds 70bpm) or 5mg slow IV bo lus Propranolol 10 \200\22340mg PO qds (titrate to HR of 60bpm) Isosorbide dinitrate 2 \200\22340mg/h IV GTN 10 \200\223200mcg/min IV or 0.5 \200\2231mg SL Diltiazem 60mg PO tds Nifedipine 5 \200\22310mg SL or PO tds Atropine 0.3mg IV. Repeat to maximum of 2mg Lidocaine 1mg/kg slow IV bolus, then 2 \200\2234mg/min Amiodarone 5mg/kg over 20min, then infused up to 15mg/kg/d in 5% glucose via central vein. (In emergen cy, give 150 \200\223300mg in 10 \200\22320mL 5% glucose over 3min.) Key papers Task Force on management of acute myocardial infarction of the European Society of Cardiology. (2003) Management of acute myocardial infarction in patients presenting with ST segment eleva- tion. Eur Heart J 24: 28 \200\22366. Thygesen K for the Joint ESC/ACCF/AHA/WHF Task Force for the Rede \201 nition of Myocardia l Infarction. (2007) Universal de \201 nition of myocardial infarction. Circulation 116: 2 634 \200\22353. See also: Intra-aortic balloon counterpulsation, p102; Coronary revascularisation technique s, p104; ECG monitoring, p162; Echocardiography, p192; Cardiac function tests, p216; Vasodi lators, p266; Anticoagulants, p316; Thrombolytics, p320; Basic resuscitation, p338; Cardiac arrest, p340; Hypotension, p380; Tachyarrhythmias, p384; Bradyarrhythmias, p386; Acute cor onary syndrome (1), p388; Heart failure \200\224assessment, p392. 392 CHAPTER 23 Cardiovascular disorders Heart failure \200\224assessment Impaired ability of the heart to supply adequate oxygen an d nutrients to meet the demands of the body \200\231s metabolizing tissues. Major causes \200 \200 \200 \200 \200 \200 \200 \200 Myocardial infarction/ischaemia. Drugs, e.g. B-blockers, cytotoxics. Tachyarrhythmias or br adyarrhythmias. Valve dysfunction. Sepsis. Septal defect. Cardiomyopathy/myocarditis. Peric ardial tamponade. Clinical features Decreased forward \202 ow leading to poor tissue perfusion \200 \200 \200 \200 Muscle fatigue leading ultimately to hypercapnia and collapse. Confusion, agitation, drowsi ness, coma. Oliguria. Increasing metabolic acidosis, arterial hypoxaemia, and dyspnoea. Increased venous congestion secondary to right heart failure \200 \200 \200 \200 Peripheral oedema. Hepatic congestion. Splanchnic ischaemia. Raised intracranial pressure. Increased pulmonary hydrostatic pressure from left heart failure \200 \200 Pulmonary oedema, dyspnoea. Hypoxaemia. Investigations Test Diagnosis ECG Myocardial ischaemia/infarction, arrhythmias Chest X-ray With left heart failure: pulmonary oedema (interstitial perihilar ( \200\230bat \200\231s w ing \200\231) shadowing, upper lobe blood diversion, Kerley B lines, pleural effusion) 9 ca rdiomegaly Low cardiac output and stroke volume, low mixed venous oxygen saturation (<60%), raised PAWP (with left heart failure), raised RAP (with right heart failure). V waves with mitral or tricuspid regurgitation Flow monitoring Blood tests Low SaO2, variable PaCO2, base de \201 cit >2 mmol/L, hyperlactataemia, low venous O2, (mi xed or central venous), raised cardiac enzymes, troponin, BNP, thyroid function (if indicat ed) Echocardiogram Poor myocardial contractility, ventricular akinesia, hypokinesia or dyskinesia, pericardial effusion, valve stenosis or incompetence Notes Peripheral oedema implies total body salt and water retention, but not necessarily in travascular \202 uid overload. HEART FAILURE \200\224ASSESSMENT 393