2. 3. 4. 5. 6. 7. 8. 9. Complications \200 Puncture of blood vessel at cricothyroid membrane may cause signi \201 cant intratracheal or external bleeding. Apply local pressure if this occurs after blade incision. If bleeding continues, insert mini-tracheotomy tube for a tamponading effect. If bleeding persists, in sert deep sutures either side of mini-tracheotomy; if this fails, contact surgeon for assis tance. Perforation of esophagus. Mediastinitis (rare). Pneumothorax. \200 \200 MINI-TRACHEOTOMY 83 See also: Tracheotomy, p80; Chest physiotherapy, p90; Atelectasis and pulmonary collapse, p 352. 84 CHAPTER 2 Respiratory therapy techniques Chest drain insertion Indications include drainage of air (pneumothorax), \202 uid (effus ion), blood (haemothorax), or pus (empyema) from the pleural space. Insertion technique 1. Use 28Fr drain (or larger) for haemothorax or empyema; 20Fr will suf \201 ce for a pure pn eumothorax. Seldinger-type drains with an integral guidewire are now available. The drain i s usually inserted through the 5th intercostal space in the mid-axillary line, \201 rst a nesthetizing skin and pleura with 1% lidocaine. Ensure that air/ \202 uid is aspirated. Ma ke a 1 \200\2231.5cm skin crease incision, create a track with gloved \201 nger (or force ps) to separate muscle \201 bres and open pleura. Insert drain through open pleura withou t trochar. Angle and insert drain to correct position (toward lung apex for pneumothorax an d lung base for haemothorax/effusion). CT scan or ultrasound is useful for directing placem ent for small collections. Connect to the underwater seal and keep bottle below level of he art. Secure drain to chest wall by properly placed sutures. Perform chest X-ray to ensure c orrect siting and lung rein \202 ation. Place on 5 \200\22310cmH2O (0.5 \200\2231.3kPa) ne gative pressure (low pressure wall suction) if lung has not fully expanded. 2. 3. 4. 5. 6. 7. 8. Subsequent management \200 \200 Do not clamp drains prior to removal or during transportation of patient. Drains may be rem oved when lung has re-expanded and no air leak is present (no respiratory swing in \202 u id level nor air leak on coughing). Unless long-term ventilation is necessary, a drain inse rted for a pneumothorax should usually be left in situ during IPPV. Remove drain at end-exp iration. Cover hole with thick gauze and Elastoplast ; a purse-string suture is not usuall y necessary. Repeat chest X-ray if indicated by deteriorating clinical signs or blood gas a nalysis. Complications \200 \200 Morbidity associated with chest drainage may be up to 10%. Puncture of an intercostal vesse l may cause signi \201 cant bleeding. Consider: (i) correcting any coagulopathy, (ii) plac ing deep tension sutures around drain, or (iii) removing drain, inserting a Foley catheter, in \202 ating the balloon, and applying traction to tamponade bleeding vessel. If these m easures fail, contact (thoracic) surgeon. Puncture of lung tissue may cause a bronchopleura l \201 stula. Consider suction (up to 15 \200\22320cmH2O), pleurodesis, high frequency ve ntilation, a double-lumen endobronchial tube or surgery. Extubate if feasible. Perforation of major vessel (often fatal); clamp but do not remove drain, resuscitate, contact surgeon, consider double-lumen ET tube. Infection: take cultures; antibiotics (staphylococcal 9 ana erobic cover); consider removing/resiting drain. Local discomfort/pain from pleural irritat ion may impair cough. Consider simple analgesia, subcutaneous lidocaine, instilling local a nesthetic, local or regional anesthesia, etc. Drain dislodgement; if needed, replace/resite new drain, depending on cleanliness of site. Don \200\231t advance old drain (infection ri sk). Lung entrapment/infarction: avoid milking drain in pneumothorax. CHEST DRAIN INSERTION 85 See also: Pleurla aspiration, p86; Basic resuscitation, p338; Pneumothorax, p368; Haemothor ax, p370. 86 CHAPTER 2 Respiratory therapy techniques Pleural aspiration Drainage of \202 uid from the pleural space using needle, cannula, or \202 exible small-bore drain. Increasingly being performed under ultrasound guidance. Blo od/pus often requires large-bore drain insertion. Indications \200 \200 \200 Improvement of blood gasses. Symptomatic improvement of dyspnoea. Diagnostic \200\230tap \200\231. Contraindications/cautions \200 Coagulopathy. Technique 1. 2. Con \201 rm presence of effusion by CXR or ultrasound. Select drainage site either by maxi mum area of stony dullness under percussion or under ultrasound guidance. Use aseptic techn ique. Clean area with antiseptic and in \201 ltrate local skin and subcutaneous tissues wi th 1% lidocaine. Advance into deeper tissues, aspirating to con \201 rm absence of blood, then in \201 ltrate with local anesthetic until pleura is pierced and \202 uid can be as pirated. Advance drainage needle/cannula/drain slowly through chest wall and intercostal sp ace (above upper border of rib to avoid neurovascular bundle). Apply gentle suction until \202 uid is aspirated. Withdraw 50mL for microbiological (M, C & S, TB stain, etc.), bioch emical (protein, glucose, etc.) and histological/cytological (pneumocystis, malignant cells , etc.) analysis, as indicated. Either leave drain in situ connected to a drainage bag or c onnect needle/cannula by a three-way tap to a drainage apparatus. Continue aspiration/drain age until no further \202 uid can be withdrawn or if patient becomes symptomatic (pain/dy spnoea). Dyspnoea or haemodynamic changes may occur due to removal of large volumes of \202 uid (>1 \200\2232L) and subsequent \202 uid shifts; if this is considered to be a po ssibility, remove no more than 1L at a time, either by clamping/ declamping drain or repeat ing needle aspiration after an equilibration interval (e.g. 4 \200\2236h). Remove needle/dr ain. Cover puncture site with \201 rmly applied gauze dressing. 3. 4. 5. 6. 7. 8. Complications \200 \200 Puncture of lung or subdiaphragmatic viscera. Bleeding. Fluid protein level \200 Protein >30g/L (NB. This should be viewed in the context of the plasma protein level) is an exudates; caused by: in \202 ammatory, e.g. pneumonia, pulmonary embolus, neoplasm, colla gen vascular diseases. Protein <30g/L is a transudate caused by: (i) raised venous pressure (e.g. heart failure, \202 uid overload), (ii) decreased colloid osmotic pressure (e.g. c ritical illness leading to reduced [plasma protein] from capillary leak and hepatic dysfunc tion, hepatic failure, nephrotic syndrome). PLEURAL ASPIRATION 87 See also: Chest drain insertion, p84; Basic resuscitation, p338; Pneumothorax, p368; Haemot horax, p370. 88 CHAPTER 2 Respiratory therapy techniques Fibreoptic bronchoscopy Indications Diagnostic \200 Collection of microbiological 9 cytological specimens (by bronchoalveolar lavage, protected brush specimen, biopsy). Cause of bronchial obstruction (e.g. clot, foreign body, neoplasm ). Extent of inhalation injury. Diagnosis of ruptured trachea/bronchus. \200 \200 Therapeutic \200 \200 Clearance of secretions, inhaled vomitus, etc. Removal of obstructing matter (e.g. mucus pl ug, blood clot, food, tooth). Proximal obstruction rather than consolidation is suggested b y the X-ray appearance of a collapsed lung/lobe and no air bronchogram. Cleansing/removing soot or other toxic materials, irrigation with saline. Directed physiotherapy 9 saline to l oosen secretions. Directed placement of balloon catheter to arrest pulmonary bleeding. To a id dif \201 cult endotracheal intubation. \200 \200 \200 Contraindications/cautions \200 \200 Coagulopathy. Severe hypoxaemia. Procedure It is dif \201 cult to perform bronchoscopy in a nasally intubated patient. A na rrow lumen scope can be used but suction is limited. 1. 2. 3. 4. 5. 6. Pre-oxygenate with FIO2 1.0. Monitor with pulse oximetry. Increase pressure alarm limit on ventilator. Lubricate scope with lubricant gel/saline. If unintubated, apply lidocaine gel to nares 9 spray to pharynx. Consider short-term IV sedation 9 paralysis. Insert scope nasa lly in a non-intubated patient or via the catheter mount port if intubated. An assistant sh ould support the ET tube during the procedure to minimize trauma to trachea and/or scope. I nject 2% lidocaine into trachea to prevent coughing and haemodynamic effects from tracheal/ carinal stimulation. Perform thorough inspection and any necessary procedures. If SpO2 \211 85% or haemodynamic disturbance occurs, remove scope and allow re-oxygenation before c ontinuing. Bronchoalveolar lavage is performed by instillation of at least 60mL of (prefera bly warm) isotonic saline into affected lung area without suction, followed by aspiration i nto a sterile catheter trap. All bronchoscopic samples should be sent promptly to the lab. After procedure, reset ventilator as appropriate. 7. 8. 9. 10. Complications \200 Hypoxaemia: from suction, loss of PEEP, partial obstruction of endotracheal tube, and non-d elivery of tidal volume. Haemodynamic disturbance, including hypertension and tachycardia ( related to hypoxaemia, agitation, tracheal stimulation, etc.). Bleeding. Perforation (unusu al though more common if biopsy taken). \200 FIBREOPTIC BRONCHOSCOPY 89 See also: Endotracheal intubtion, p42; Chest physiotherapy, p90; Atelectasis and pulmonary collapse, p352; Haemoptysis, p372; Inhalation injury, p374. 90 CHAPTER 2 Respiratory therapy techniques Chest physiotherapy The aim is to expand collapsed alveoli, mobilize chest secretions, or r e-in \202 ate collapsed lung segments. Though anecdotal experience suggests bene \201 t, no scienti \201 c validation of effectiveness has been reported. The current view is routi ne \200\230prophylactic \200\231 suctioning/bagging should be avoided in the critically il l. Indications \200 \200 \200 Mobilization of secretions. Re-expansion of collapsed lung/lobes. Prophylaxis against alveo lar collapse and secondary infection. Contraindications/cautions \200 Aggressive hyperin \202 ation in already hyperin \202 ated lungs, e.g. asthma, emphysema \200\224though can be very useful in removing mucus plugs. Undrained pneumothorax. Raised i ntracranial pressure. \200 Techniques Hyperin \202 ation Hyperin \202 ating to 50% above ventilator-delivered VT, ai ming to expand collapsed alveoli and mobilize secretions. VT is rarely measured, so either excessive or inadequate hyperin \202 ations may be given, depending on lung compliance and operator technique. Pressure-limiting devices ( \200\230blow-off valves \200\231) or manom eters can avoid excessive airway pressures. A recommended technique is slow inspiration, a 1 \200\2232s plateau phase, and then rapid release of the bag to simulate a \200\230huff \200\231 and mobilize secretions. Preoxygenation may be needed as PEEP may be lost and the delivered VT may be inadequate. Cardiac output often falls with variable blood pressure and heart rate responses. Sedation may blunt haemodynamic response. Full de \202 ation avoids air trapping. Suction Removing secretions from trachea and main bronchi (usually right). A cough re \202 ex may be stimulated to mobilize secretions further. Tenacious secretions may be loosened by instillation of 2 \200\2235mL 0.9% saline. Falls in SaO2 and cardiovascular disturbance may be avoided by pre-oxygenation. Percussion and vibration Drumming and shaking actions ov er chest wall to mobilize secretions. Inspiratory pressure support (Bird ventilator) The aim is to increase FRC and expand collap sed alveoli. Postural drainage Patient positioning to assist drainage \200\224depends on affected lung a rea(s). Complications of chest physiotherapy \200 Hypoxaemia: from suction, loss of PEEP, etc. \200 Haemodynamic disturbance affecting cardiac output, heart rate, and blood pressure (ma y be related to high VT, airway pressure, hypoxaemia, agitation, tracheal stimulation, etc. ). Direct trauma from suctioning. Barotrauma/volutrauma, including pneumothorax. \200 CHEST PHYSIOTHERAPY 91 General care to avoid need for urgent physiotherapy \200 \200 \200 \200 \200 Adequate humidi \201 cation avoids tenacious sputum and mucus plugs. Pain relief is import ant to encourage good chest expansion and cough. Position semi-recumbent to optimize use of respiratory muscles. Ensure nutrition is adequate to maintain muscle strength. Mobilizatio n and encouraging deep breathing may avoid infection. Requesting urgent physiotherapy Request Collapsed lung/lobe with no air bronchogram visible, i.e. suggesting proximal obstr uction rather than consolidation. Mucus plugging causing subsegmental collapse, e.g. asthma . Don \200\231t request Clinical signs of chest infection with no secretions being produced. Radiological consolidation with air bronchogram but no secretions present. See also: Minitracheotomy, p80; Fibreoptic bronchoscopy, p88; Atelectasisa and pulmonary co llapse, p352. This page intentionally left blank 93 Chapter 3 Cardiovascular therapy techniques Electrical cardioversion 94 Temporary pacing (1) 96 Temporary pacing (2) 98 Therapeutic hyp othermia 100 Intra-aortic balloon counterpulsation 102 Coronary revascularisation technique s 104 94 CHAPTER 3 Cardiovascular therapy techniques Electrical cardioversion Electrical conversion is used to convert a tachyarrhythmia to norm al sinus rhythm. This may be: \200 \200 \200 Emergency \200\224when the circulation is absent or severely compromised. Semi-elective \200\224when the circulation is compromised to a lesser degree. Elective \200\224when synch ronized cardioversion is performed to restore sinus rhythm for a non-compromising supravent ricular tachycardia. Synchronization requires initial connection of ECG leads from the patient to the de \201 b rillator so that the shock is delivered on the R wave to minimize the risk of ventricular \201 brillation. Newer, biphasic de \201 brillators require approximately half the energy setting of monophasic de \201 brillators. Indications \200 \200 \200 \200 Cardiac arrest, e.g. VF. Compromised circulation, e.g. VT. Restoration of sinus rhythm and more effective cardiac output. Lessens risk of cardiac thrombus formation. Contraindications/cautions \200 \200 \200 \200 Aware patient. Severe coagulopathy. Caution with recent thrombolysis. Digoxin levels in tox ic range. Complications \200 Surface burn. \200 Pericardial tamponade. \200 Electrocution of by standers. Technique (See algorithm opposite, \201 gure 3.1). \200 The chances of maintaining sinus rhythm are increased in elective cardioversion if K+ >4.5m mol/L and plasma Mg2+ levels are normal. Prior to de \201 brillation, ensure self and onlo okers are not in contact with patient, things attached to the patient, or the bed frame. To reduce the risk of super \201 cial burns, replace gel/gelled pads after every three shock s. Consider resiting paddle position (e.g. anteroposterior) if de \201 brillation fails. T he risk of intractable VF following de \201 brillation in a patient receiving digoxin is s mall unless the plasma digoxin levels are in the toxic range or the patient is hypovolaemic . ELECTRICAL CARDIOVERSION 95 Sedate (e.g. etomidate, propofol, fentanyl) \200 maintain airway \200 oxygenate (high F IO2) Patient aware? Yes No Place gelled pads oon chest Severe haemodynamic compromise? Defibrillate \200 output present: 200J Monophasic (150J biphasic) \200 pulseless VF/VT: 360J monophasic (150J biphasic) Yes No Improvement? No Place ECG leads \200 Ensure good venous access \200 Consent patient (if possible) Cardiac arrest protocol Set defibrillator to \200\234synchronized \200\235 Yes Initial shock - monophasic (biphasic) \200 AF or VT: 200 (120-150) J \200 Atrial flutte r/paroxysmal SVT: 100 (70-120) J repeat if needed, escalate to 360 (200) J Monitor closely Sinus rhythm restored? Yes No Consider antiarrhythmic agents repeated synchronized cardioversion Fig. 3.1 Algorithm for use of electrical cardioversion. Key paper Deakin CD, Nolan JP. European Resuscitation Council Guidelines for Resuscitation 2005. Section 3. (2005) Electrical therapies: Automated external de \201 brillators, de \201 brillation, cardioversion and pacing. Resuscitation 67(Suppl 1), S25 \200\22337. See also: Chronotropes, p274; Cardiac arrest, p340; Tachyarrhythmias, p384. 96 CHAPTER 3 Cardiovascular therapy techniques Temporary pacing (1) When the heart \200\231s intrinsic pacemaking ability fails, temporary internal or external pacing can be instituted. Internal electrodes can be endocardial (ins erted via a central vein) or epicardial (placed on the external surface of the heart at tho racotomy). The endocardial wire may be placed under \202 uoroscopic control or \200\230b lind \200\231 using a balloon \202 otation catheter. External pacing can be rapidly perfo rmed by placement of two electrodes on the front and rear chest wall when asystole or third degree heart block has produced acute haemodynamic compromise. It is often used as a bridg e to temporary internal pacing. It can also be used as a prophylactic measure, e.g. for Mob itz type II second degree heart block. Indications \200 \200 Third degree heart block. Mobitz type II second degree heart block when the circulation is compromised or an operation is planned. Overpacing (rarely; more successful with internal p acing). Asystole. \200 Complications Internal pacing \200 \200 \200 \200 As for central venous catheter insertion. Arrhythmias. Infection (including endocarditis). Myocardial perforation (rare). External pacing \200 Discomfort. Failure to pace 1. 2. No pacemaker spikes seen: check connections, check battery. No capture (pacing spikes but n o QRS complex following): poor positioning/dislodgement of wire. Temporarily increase outpu t as this may regain capture. Reposition/replace internal pacing wire. General 1. Check threshold daily as it will rise slowly over 48 \200\22396h, probably due to \201 br osis occurring around the electrodes. Overpacing may be used for a tachycardia unresponsive to anti-arrhythmic therapy or cardioversion. For SVT, pacing is usually attempted with the wire sited in the right atrium. Pace at rate 20 \200\22330bpm above patient \200\231s hear t rate for 10 \200\22315s, then either decrease rate immediately to 80bpm or slowly by 20bp m every 5 \200\22310s. If overpacing fails, underpacing may be attempted with the wire situ ated in either atrium (for SVT) or usually ventricle (for either SVT or VT). A paced rate o f 80 \200\223100bpm may produce a refractory period suf \201 cient to suppress the intrins ic tachycardia. Epicardial pacing done during cardiac surgery uses either two epicardial el ectrodes or one epicardial and one skin electrode (usually a hypodermic needle). The pacing threshold of epicardial wires rises quickly and may become ineffective after 1 \200\2232d. In asystole, paced rhythm does not guarantee cardiac output. 2. 3. 4. 5. TEMPORARY PACING (1) 97 See also: Temporary pacing (2), p98; Chronotropes, p274; Cardiac arrest, p340; Bradyarrhyth mias, p386. 98 CHAPTER 3 Cardiovascular therapy techniques Temporary pacing (2) Technique (for endocardial electrode placement) 1. If using \202 uoroscopy, move patient to X-ray suite or place lead shields around bed are a. Place patient on \200\230screening table \200\231. Staff should wear lead aprons. Use a septic technique throughout. Insert 6Fr sheath in internal jugular or subclavian vein. Sutu re in position. Connect pacing wire electrodes to pacing box (black = negative polarity = d istal, red = positive polarity = proximal). Set pacemaker to demand. Check box is working a nd battery charge adequate. Turn pacing rate to 30bpm above patient \200\231s intrinsic rhy thm. Set voltage to 4V. Insert pacing wire through sheath into central vein. If using ballo on catheter, insert to 15 \200\22320cm depth, then in \202 ate balloon. Advance catheter, viewing ECG monitor for change in ECG morphology and capture of pacing rate. If using scree ning, direct wire toward the apex of the right ventricle. Approximate insertion depth from a neck vein is 35 \200\22340cm. If pacing impulses not captured, (de \202 ate balloon), wi thdraw wire to 15cm insertion depth, then repeat step 4. Once pacing captured, decrease vol tage by decrements to determine threshold at which pacing is no longer captured. Ideal posi tion determined by a threshold \211 0.6V. If not achieved, re-position wire. If possible, ask patient to cough to check that wire does not dislodge. Set voltage at three times thres hold and desired heart rate on \200\230demand \200\231 mode. Tape wire securely to patient to prevent dislodgement. 2. 3. 4. 5. 6. 7. 8. Technique (for external pacing) 1. Connect pacing wire gelled electrodes to pacemaker. Place black (= negative polarity) elect rode on the anterior chest wall to the left of the lower sternum and red (= positive polari ty) electrode to the corresponding position on the posterior hemithorax. Connect ECG electr odes from ECG monitor to external pacemaker and another set of electrodes from pacemaker to patient Set pacemaker to demand. Turn pacing rate to 30bpm above patient \200\231s intrins ic rhythm. Set current to 70mA. Start pacing. Increase current (by 5mA increments) until pa cing rate captured on monitor. If pacing rate not captured at current of 120 \200\223130mA, resite electrodes and repeat steps 3 \200\2234. Once pacing captured, set current at 5 \200\22310mA above threshold. 2. 3. 4. 5. 6. TEMPORARY PACING (2) 99 See also: Temporary pacing (1), p96; Chronotropes, p274; Cardiac arrest, p340; Bradyarrhyth mias, p386. 100 CHAPTER 3 Cardiovascular therapy techniques Therapeutic hypothermia Induced (therapeutic) hypothermia is being increasingly used as a t ool to achieve neuroprotection and/or cardioprotection. Clear bene \201 t in terms of neur ological outcome exists for victims of cardiac arrest following VT or VF, and following asp hyxia in neonates. Ongoing work is examining its ef \201 cacy in ischaemic stroke, traumat ic head injury, subarachnoid haemor- rhage, hepatic encephalopathy, and haemorrhagic shock. Study results are either con \202 icting or too preliminary to make \201 rm recommendat ions. Timing and duration The optimal period following neurological injury for which outcomes may be positively in \202 uenced by hypothermia is uncertain. Human studies show bene \201 t from treatment durations ranging from 12 \200\22372h. From animal experiments, optimal eff ects are achieved when hypothermia is induced as rapidly as possible \200\224 \200\230time is brain \200\231. Studies show bene \201 ts can be realized even after delays of 8h befor e commencement. Ideally, target tempera- ture (currently 32 \200\22334*C) should be maintai ned as closely as possible, and rewarming should be slow and controlled to minimize reperfu sion injury. Various cooling systems are currently available, each with speci \201 c advan - tages and disadvantages. Cooling techniques These can be subdivided into non-invasive and invasive. Non-invasive \200 \200 \200 \200 \200 \200 Air- or water-circulating cooling blankets or pads. Ice packs in groins and axillae. Coveri ng body in wet sheets or spraying with alcohol. Exposing head. Fans to increase air circula tion. Immersion of body in cold water. Invasive \200 \200 Infusion of cold \202 uids. Irrigating (or instilling and draining at regular intervals) bladder and/or stomach and/or peritoneum with iced water. Specialized endovascular catheter s placed in a central vein, with iced sterile saline pumped through integral cooling balloo ns. Extracorporeal circulation. Infusion of cold \202 uid can be used in the induction phase of hypothermia maintained by non-invasive methods. Potential side effects \200 \200 \200 \200 \200 \200 \200 \200 \200 Infection. Pressure sores. Electrolyte disorders. Hyperglycaemia. Arrhythmias (low risk if core temperature kept >30*C). Increased bleeding tendency. Alterations in drug metabolism. Bradycardia. Thrombocytopaenia, leucopaenia. THERAPEUTIC HYPOTHERMIA 101 Key papers The Hypothermia after Cardiac Arrest Study Group. (2002) Mild therapeutic hypoth ermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 346: 549 \200 \22356. Polderman KH. (2004) Keeping a cool head: How to induce and maintain hypothermia. Crit Care Med 32: 2558 \200\22360. See also: Cardiac arrest, p340; Coma, p438; Head injury (1), p586 Head injury (2), p588; Hy pothermia, p600. 102 CHAPTER 3 Cardiovascular therapy techniques Intra-aortic balloon counterpulsation Principle A 30 \200\22340mL balloon is placed in the descending aorta. The balloon is in \202 ated with helium during diastole, increasing dias tolic blood pressure above the balloon which thus improves coronary and cerebral perfusion. The balloon is de \202 ated during systole, decreasing peripheral resistance and increasi ng stroke volume. No drug therapy exists which can increase coronary blood \202 ow while reducing peripheral resistance. Intra-aortic balloon counterpulsation may improve cardiac p erformance in situations where drugs are ineffective (see \201 gure 3.2). Indications It can be used to support the circulation where a structural cardiac defect is to be repaired surgically. It may also be used for acute circulatory failure where resoluti on of the cause of the cardiac dysfunction is expected. In acute MI, resolution of peri-inf arct oedema may allow spontaneous improvement in myocardial function; the use of balloon co unterpulsa- tion may provide temporary circulatory support and promote healing by improving myocardial blood \202 ow. Other indications include acute myocar- ditis and poisoning wi th myocardial depressants. It should not be used in aortic regurgitation as the rise in dia stolic blood pressure would increase regurgitant \202 ow. Insertion of the balloon The usual route is via a femoral artery. Percutaneous Seldinger ca theterisa- tion (9 an introducer sheath) provides a rapid, safe technique with minimal arte rial trauma and bleeding. Open surgical catheterisation may be needed in elderly patients w ith atheromatous disease. Check the balloon position on a chest X-ray to ensure that the ra dio-opaque tip is at the level of the 2nd intercostal space. Anticoagulation The presence of a large foreign body in the aorta requires systemic antico- agulation to prevent thrombosis. The balloon should not be left de \202 ated for longer t han a minute while in situ, otherwise thrombosis may develop despite anticoagulation. Control of balloon in \202 ation and de \202 ation Helium is used to in \202 ate the bal loon, its low density facilitating rapid transfer from pump to balloon. In \202 ation is c ommonly timed to the \200\230R \200\231 wave of the ECG, although timing may be taken from an arterial pressure waveform. Minor adjustment may be made to the timing to ensure that i n \202 ation occurs immediately after closure of the aortic valve (after the dicrotic notc h of the arterial pressure waveform) and de \202 ation occurs at the end of diastole. The \201 lling volume of the balloon can be varied up to the maximum balloon volume. The grea ter the \201 lling volume, the greater the circulatory augmentation. The rate at which ba lloon in \202 ation occurs may coincide with every cardiac beat or every 2nd or 3rd cardia c beat. Slower rates are necessary in tachyarrhythmias. Weaning of intra-aortic balloon cou nterpulsation may be achieved by reducing augmentation or the rate of in \202 ation. INTRA-AORTIC BALLOON COUNTERPULSATION 103 IABP off IABP on Assisted diastolic pressure Unassisted systolic pressure Assisted systolic pressure Unassisted end-diastolic pressure Assisted end-diastolic pressure Fig. 3.2 Arterial waveform with and without intra-aortic counterpulsation. See also: Inotropes, p264; Vasopressors, p268; Anticoagulants, p318; Heart failure \200\224 assessment, p392; Heart failure \200\224management, p394. 104 CHAPTER 3 Cardiovascular therapy techniques Coronary revascularisation techniques Principle Early restoration of blood \202 ow throug h an obstructed coronary vessel will prevent irreversible infarction and/or ongoing ischaem ia. Revascularisation leads to bene \201 t after acute coronary syndromes, including myoca rdial infarction. However, this is more often con \201 ned to symptom reduction rather tha n mortality bene \201 t over medical therapy with efforts to reduce risk factors. High-ris k patients, such as those with left main coronary artery disease, are more likely to show b etter survival rates. Techniques Pharmacological Thrombolytic agents remain in common usage, though contraindicat ed in 15 \200\22320%. Older drugs such as streptokinase are being replaced by recom- binant tissue plasminogen activators (rtPA) such as alteplase, reteplase, and tenecteplase \200 \224these are easier to administer and appear more effective. However, the rate of recanali sation at 90min is only 55 \200\22360% and there is a 5 \200\22315% risk of early or late r eocclusion. There is also a 1 \200\2232% risk of intrac- ranial hemorrhage (with 40% mortal ity) and an increased risk of bleeding elsewhere (e.g. gastrointestinal tract, cannula site s). Other anticoagulant agents are administered alongside rtPA or PCI (see below), includin g heparin, warfarin, and antiplatelet agents \200\224aspirin, clopidogrel, and the glycopro tein IIb/IIIa inhibitors (e.g. abciximab, epti \201 batide, and tiro \201 ban). Percutaneous Percutaneous coronary intervention (PCI) has evolved since the 1980s, when ste notic lesions were simply dilated by transluminal coronary angio- plasty (PTCA), to now inc lude stenting of these dilated areas using bare- metal and, more recently, drug-eluting ste nts. Though drug-eluting stents reduce the risk of restenosis and the need for repeat PCI, they carry an increased risk of \200\230very late stent thrombosis \200\231 plus undesired effects related to the stent polymer and the stent itself. Next-generation stents using ne w drugs, polymers, and drug delivery systems are in development to improve on current devic es. Surgical Coronary artery bypass grafting (CABG), though declining in recent years due to th e increasing use of preventive health measures and PCI tech- niques, still has an important role to play in bypassing stenotic lesions not amenable or suitable for PCI. While PCI is targeted at the \200\230culprit \200\231 lesion(s), CABG is directed at the epicardial ves sel, including the \200\230culprit \200\231 lesion(s) and possible future culprits. Patients with single-vessel disease are more likely to have PCI, while those with triple-ve ssel disease are more likely to undergo CABG. Despite the increased morbidity and recovery time of CABG, mortality is similar to PCI. The advantages of CABG over PCI are better relief of angina and a lower likelihood of subse quent reocclusion. The magnitude of the latter bene \201 t may decrease with drug-eluting stents. However, the increase in the rate of stroke with CABG offsets these advantages. CORONARY REVASCULARISATION TECHNIQUES 105 Critical care issues \200 Increased bleeding risk with the use of anticoagulant agents. The prolonged action of aspir in and clopidogrel on platelet function (lasting 3 \200\2237d after discontinuation) will h eighten the risk of bleeding, both peri-operatively and during critical illness. Fresh plat elet transfusions may be needed to restore platelet functionality. Similarly, warfarin has a prolonged duration of action that can be reversed with fresh frozen plasma, prothrombin c omplex concentrates (e.g. Octaplex ), or recombinant factor VIIa. A balance has to be soug ht between bleeding risk (or severity of an existing hemorrhage) and stent thrombosis from discontinuation of the drug(s). Arrhythmias \200\224commonly related to reperfusion and may occasionally be life-threatening. Mishaps related to PCI, including coronary artery ruptur e plus restenosis and acute occlusion of the stent. Complications related to CABG, includin g stroke, bleeding, and transient myocardial depression. See also: Anticoagulants, p318; Thrombolytics, p320; Acute coronary syndrome (1), p388; Acu te coronary syndrome (2), p390. This page intentionally left blank 107 Chapter 4 Renal therapy techniques Haemo(dia) \201 ltration (1) 108 Haemo(dia) \201 ltration (2) 110 Peritoneal dialysis 112 Plasma exchange 114 108 CHAPTER 4 Renal therapy techniques Haemo(dia) \201 ltration (1) Conventional haemodialysis requires a pressurized, puri \201 ed water supply, and a greater risk of haemodynamic instability due to rapid \202 uid an d osmotic shifts. Haemo(dia) \201 ltration can be arterio-venous, using the patient \200 \231s BP to drive blood through the haemo \201 lter, or pumped veno- venous. The latter is preferable as it does not depend on the patient \200\231s BP, and the pump system incorpor ates alarms and safety features. Continuous veno-venous haemo(dia) \201 ltration (CVVH or CVVHD) is increasingly the technique of choice. Blood is usually drawn and returned via a 1 0 \200\22312Fr double-lumen, central venous catheter (see \201 gure 4.1). Indications \200 \200 \200 \200 \200 \200 \200 Azotaemia (uraemia). Hyperkalaemia. Anuria/oliguria; to make space for nutrition. Severe me tabolic acidosis of non-tissue hypoperfusion origin. Fluid overload. Drug removal. Hypother mia/hyperthermia. Techniques CVVH relies on convection (bulk transfer of solute and water) to clear solute. I n CVVHD, dialysate \202 ows countercurrent to the blood, allowing small mol- ecules to di ffuse according to their concentration gradients. Membranes are usually hollow \201 bre polyacrylonitrile, polyamide, or polysulphone with a surface area of 0.6 \200\2231m2. Both CVVH and CVVHD are effective for small molecule clearance (e.g. urea). CVVH is better at larger molecule clearance and can remove substances up to the membrane pore size cut-off (usually 30 \200\22335kD). Filtrate is usually removed at 20 \200\22335mL/kg/h; \202 uid balance is adjusted by varying the rate of \202 uid replacement. High volume haemo \201 ltration involves much higher ultra \201 ltration rates (e.g. 50 \200\223100mL/kg/h, usua lly for short periods, e.g. 4h) in an effort to remove in \202 ammatory mediators. Variabl e outcomes are reported in studies. Creatinine and K+ clearances are higher with CVVHD, but \201 ltration alone is usually su f \201 cient if ultra \201 ltrate volume is adequate. (1000mL/h approximates to a creatin ine clearance of 16mL/min). CVVHD is preferred for pharmacologically-resistant hyperkalaemi a. Replacement \202 uid A balanced electrolyte solution buffers acidaemia and is titrated to desired \202 uid and electrolyte balance. Buffers include lactate (liver metabolized to bicarbonate) and bicarbonate. Acetate (metabolized by muscle) causes most haemodynamic inst ability and is now rarely used. Bicarbonate may be more ef \201 cient than lactate at reve rsing severe acidosis, but no outcome bene \201 t has been shown. Care is needed when givi ng Ca2+ since calcium bicarbonate may crystallize. In hypoperfused liver, lactate may be in ade- quately metabolized. Increasing metabolic alkalosis may be due to excessive buffer so use low buffer (30mmol/L l actate) replacement \202 uid. K+ can be added to maintain normokalaemia. 20mmol KCl in a 4.5L bag provides a concentra- tion of 4.44mmol/L. K+ clearance is increased by reducing th e concentra- tion within replacement \202 uid or dialysate. HAEMO(DIA)FILTRATION (1) 109 HAEMOFILTRATION Replacement fluid Anticoagulant Convection + solvent drag + ultrafiltration Blood to patient Blood from patient Ultrafiltrate HAEMODIAFILTRATION Replacement fluid Anticoagulant Diffusion + ultrafiltration Blood to patient Blood from patient Dialysis fluid Dialysate + ultrafiltrate Fig. 4.1 Circuit arrangement for haemo(dia) \201 ltration. Key papers Ronco C, Bellomo R, Homel P, et al. (2000) Effects of different doses in continu ous veno-venous haemo \201 ltration on outcomes of acute renal failure: a prospective rand omized trial. Lancet 356: 26 \200\22330. Bouman CS, Oudermans-Van Straaten HM, et al. (2002) Effects of early high-volume continuous venovenous haemo \201 ltration on survival and recovery of renal function in intensive ca re patients with acute renal failure: a prospective, randomized trial. Crit Care Med 30: 22 05 \200\22311. The VA/NIH Acute Renal Failure Trial Network. (2008) Intensity of renal support in critical ly ill patients with acute kidney injury. N Engl J Med 359: 7 \200\22320. See also: Haemo(dia) \201 ltration (2), p110; Oliguria, p398; Acute renal failure \200\224 diagnosis, p400; Acute renal failure \200\224management, p402. 110 CHAPTER 4 Renal therapy techniques Haemo(dia) \201 ltration (2) Anticoagulation The circuit can be anticoagulated with unfrac tionated heparin (200 \200\2232000IU/h), a prostanoid (prostacyclin or PGE1) at 2 \200\2231 0ng/kg/min, or a combination of the two. Other alternatives include regional citrate antico agulation, the low molecular weight heparinoid danaparoid, or direct thrombin inhibi- tors (e.g. lepirudin, argatroban). These agents are, as yet, under-evaluated for renal replaceme nt therapy and they risk important complications such as hypocalcaemia (with citrate) and p rolonged bleeding with the long half-lives of the thrombin inhibitors. Bivalirudin is a new agent related to hirudin and lepirudin but is reversible with a short half-life of only 25 min. No anticoagulant may be needed if the patient is auto-anticoagulated. Premature clotting may be due to mechanical kinking/obstruction of the circuit, insuf \201 cient anticoagulation, inadequate blood \202 ow rates, or lack of endogenous anticoagula nts such as antithrombin III. Usual \201 lter lifespan should be at least two days, but is often decreased in septic pa tients due to decreased endogenous anticoagulant levels. In this situation, consider use of fresh frozen plasma, a synthetic protease inhibitor such as aprotinin, or antithrombin III replacement (costly). Filter blood \202 ow Flow through the \201 lter is usually 100 \200\223200mL/min. Too s low a \202 ow rate promotes clotting. Too high a \202 ow rate will increase transmembra ne pres- sures and decrease \201 lter lifespan without signi \201 cant improvement in cl ear- ance of \200\230middle molecules \200\231 (e.g. urea). Complications \200 \200 \200 Disconnection leading to hemorrhage. Infection risk (sterile technique must be employed). E lectrolyte, acid-base or \202 uid imbalance (due to excess input or removal). Hemorrhage (vascular access sites, peptic ulcers) related to anticoagulation therapy or consumption co agulopathy. Heparin-induced thrombocytopaenia may rarely occur. Cautions \200 \200 \200 \200 \200 \200 \200 Haemodynamic instability related to hypovolaemia (especially at start). Vasoactive drug rem oval by the \201 lter (e.g. catecholamines). Membrane biocompatibility problems (especial ly with cuprophane). Drug dosages may need to be revised (consult pharmacist). Amino acid l osses through the \201 lter. Heat loss leading to hypothermia. Masking of pyrexia. HAEMO(DIA)FILTRATION (2) 111 See also: Haemo(dia) \201 ltration (1), p108; Coagulation monitoring, p222; Anticoagulants , p318.