Indications for temporary cardiac pacing The setting of an acute myocardial infarction (AMI ) \200 \200 Asystole, 2nd or 3rd degree atrioventricular (AV) block with symptoms , New trifascicular b lock,. 2nd or 3rd degree AV block without symptoms but fol- lowing an anterior AMI. \200 Not related to an AMI \200 \200 \200 \200 Asystole. 2nd or 3rd degree AV block with symptoms. Sinus or junctional bradycardia with sy mptoms. Tachyarrhythmias secondary to bradycardia. Overdrive suppression of tachyarrhythmias \200 To prevent or treat Torsade de Pointes. Prophylactic temporary cardiac pacing Pre-operative patient with symptoms and: \200 \200 Sinus node disease or 2nd degree AV block (type I). Bifascicular/trifascicular block. Pre-operative patient without symptoms and: \200 2nd degree (type II) or 3rd degree AV block. Complications of transvenous pacing These include pneumothorax, haemothorax, infection, ina dvertent arterial puncture, non-sustained VT as the pac- ing wire is maneuvered across the tricuspid valve, throm- boembolism with pulmonary embolism, and myocardial perforation with cardiac tamponade. The setting of cardiac surgery \200 \200 Valvular surgery (especially tricuspid and aortic). Ventricular septal defect (VSD) closure or ostium pri- mum repair. Biatrial pacing to reduce post-operative AF. Temporary transoesophageal cardiac pacing This approach obviates the requirement for centra l venous access or sterile precautions, and may be considered when \202 uoroscopy is unav ailable. It comprises a transoesophageal pulse generator and gelatine bipolar pill electrod es (for the oral route) or transoesophageal pacing catheters (for the nasal route). During the replacement of a permanent pacemaker and rarely for right coronary artery angiop lasty. Types of temporary cardiac pacing Temporary transcutaneous cardiac pacing This non-invasive approach is used if temporary trans- venous cardiac pacing is not immediately available. S elf- adhesive electrode pads are placed on the left anterior chest between the xiphoid proc ess and the left nipple, and posteriorly below the left scapula and spine. These are attach ed to the external pulse generator. Conscious patients should be given sedation to minimize discomfort. Temporary epicardial cardiac pacing This involves directly stimulating the epicardium of th e atria and/or ventricle using electrodes sutured to the epi- cardium at the time of cardia c surgery. The pacing wires are pulled through an incision in the skin and secured to the e xternal chest wall. By convention, the atrial wires and the ventricular wire exit from the right and left side of the sternum, respectively. Infection, myocardial damage and/or perfo ration, tamponade and disruption of coronary anas- tomoses are the recognized complications . Temporary transvenous cardiac pacing This procedure requires suitable equipment and skilled personnel as stipulated by American Heart Association guidelines. Cannulation of a central vein allows a pacing wire to be placed in the right ventricle and/or the right atrium unde r \202 uoroscopic guidance. Where \202 uoroscopy is unavailable, pacing wires can be pl aced using balloon- tipped catheters. Setting the pacemaker up \200 Check the pacemaker box has a fresh battery and ensure the connections are secure and corre ct. Turn the pacemaker box on and set the pacing rate at 90 \200\223110bpm for cardiac surg ery, 50bpm for sinus rhythm and 70 \200\22390bpm for heart block or bradycardias. The procedure \200 Check that the \202 uoroscopy equipment, pacemaker box and de \201 brillator are functio ning properly. 55 CHAPTER 2.2 Temporary cardiac pacing Troubleshooting The absence of pacing spikes on the ECG This may be due failure to pace whe n the intrinsic rate is less than the pacing rate. Or it may be because the intrinsic rate is greater than the set pacemaker rate. Determine the capture threshold Capture describes the ability of the electrical impulse to initiate a myocardial depolarization. \200 Turn the pacemaker rate to 10bpm above the intrinsic rate and increase the pacemaker output to 3V. Slowly decrease the output until loss of capture occurs, then increase it until cap ture reoccurs after every pacer spike. This is the capture threshold (aim for <1.0 and <1.5 V for ventricular and atrial wires, respectively). Set output at 2 \200\2233 times the thre shold or at 3V, whichever is higher. Reset the pacemaker to the prescribed rate. Failure to pace This describes the failure of the pacemaker box to deliver an electrical im pulse, and is indicated by the absence of pacing spikes when the intrinsic heart rate is le ss than the pacemaker rate. See checklist below. Failure to capture This describes the failure of an electrical impulse to initiate a myocar dial depolarization, and is revealed by the failure of an appropriately timed pacing spike to be followed by either a \200\230P \200\231 wave or a widened \200\230QRS \200\231 comp lex. The capture threshold often doubles in the \201 rst few days due to endo- cardial oe dema. Therefore, try increasing the output to restore capture. Determine the sensitivity threshold Sensitivity refers to the ability of the pacemaker to d etect intrinsic myocardial activity. The sensitivity dial indicates the minimum voltage tha t the pacemaker is able to sense. Therefore, decreasing the sensitivity dial actually incre ases pacemaker sensitivity, and vise versa. \200 \200 Set the pacing rate at 10bpm below the intrinsic rate. Lower the pacemaker output to 0.1V t o prevent com- petitive pacing. Increase the sensitivity dial until the sense indicator sto ps \202 ashing and the pace indicator starts \202 ashing. Slowly decrease the sensitivi ty dial until the sense indica- tor \202 ashes continuously. This value is the sensing th resh- old. Set the sensitivity dial at half the sensitivity threshold value. If there is no underlying rhythm and sensitivity cannot be determined, set the sensitivity dial at 2mV. R eset pacemaker to prescribed rate. Failure to sense or undersensing This describes the failure of the pacemaker to detect intr insic myocardial activity. It is indicated by regular pacing spikes unrelated to the intrin sic rhythm, which may or may not capture. Try decreasing the sensitivity dial (thereby incr easing pacemaker sensitivity). Inappropriate or oversensing This describes the situation where the pacemaker is misin- ter preting skeletal activity or \200\230P \200\231 and \200\230T \200\231 waves as \200\230 QRS \200\231 complexes, and is inhibiting pacemaker activity, causing bradycardic episodes. Try increasing the sensitivity dial (thereby decreasing pacemaker sensitivity). Pacemaker mode and variables \200 VVI for ventricular pacing only. \200 DDD for dual-ch amber pacing, allowing AV sequential pacing, which may bene \201 t patients with a low car diac output state or those patients with a \200\230stiff \200\231 left ventricle. The thre e letter code corresponds to the chamber paced ( \200\230V \200\231 for ventricle and \200 \230D \200\231 for dual chamber), the chamber sensed and the response to sensing ( \200\230 I \200\231 means pacing is inhibited on sensing intrinsic myocar- dial activity). AV interv al ( 150ms): this is the time interval between a paced or sensed event in the atrium and a paced event in the ventricle. Upper rate limit ( 135bpm): this is the maximum rate the vent ricles will pace at, as determined by tracking the atrial rate. PVARP (post-ventricular atr ial refractory period, 300ms): this time interval limits how early after a paced or sensed ventricular beat an atrial event can trigger a ventricular paced event. Causes of failure to pace, capture or sense \200 Pacemaker box malfunction or \202 at b attery. \200 Insecure or incorrect lead connections. \200 Malpositioned, damaged or dis placed pacing wire. \200 Myocardial infarction/ \201 brosis adjacent to wire tip. \200 Myocardial perforation. \200 Certain drugs such as class I antiarrhythmics. \200 Elect rolyte disturbances which widen the QRS and delay its upstroke, causing undersensing. Futher reading Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the manageme nt of patients with acute myocardial infarction. J Am Coll Cardiol 2004; 44: 671 \200\22371 9. Francis GS, Williams SV, Achord JL, et al. Clinical competence in insertion of temporary tr ansvenous ventricular pacemaker: ACP/ACC/AHA Task Force Statement. Circulation 1994; 89: 19 13 \200\2236. Gammage MD. Temporary cardiac pacing. Heart 2000; 83: 715 \200\22320. Overbay D, Criddle L. Mastering temporary invasive cardiac pacing. Crit Care Nurse 2004; 24: 25 \200\22332. Caring for patients with pacemakers Parker J, Cleland JGF. Choice of route for insertion of temporary pacing wires: recommendat ions of the medical practice commit- tee and council of the British Cardiac Society. Br Hea rt J 1993; 70: 294 \200\2236. Proper care of the temporary cardiac pacing system includes daily assessment of the patient \200\231s haemodynamic status and examination of the insertion site for signs of infection . The underlying heart rhythm, sensitivity and cap- ture thresholds should be determined da ily, providing pac- ing is occurring <90% of the time. Timothy PR, Rodeman BJ. Temporary pacemakers in critically ill patients: assessment and man agement strategies. AACN Clin Issues 2004; 15: 305 \200\22325. 56 I AHMAD Intra-aortic balloon counterpulsation pump Intra-aortic balloon pumps were introduced in the 1960s for patients in cardiogenic shock; since then their use has been expanded into other clinical situations to provide earlier ha emodynamic support in the management of patients with ischaemia or dysfunctioning myocardiu m. The primary aims of intra-aortic counterpulsation are: 1 to increase myocardial oxygen s upply 2 to decrease myocardial oxygen demand The secondary effects are: 1 to improve cardia c output 2 to improve ejection fraction 3 increased coronary perfusion pressure 4 a reducti on in heart rate 5 a reduction in systemic vascular resistance. represents the closure of the aortic valve and the onset of diastole, it is here where the balloon is in \202 ated, displacing blood towards the openings of the coronary arteries, t hus increasing coronary artery perfusion. The start of systole is represented by the arteri al upstroke and de \202 ation of the balloon occurs just prior to this point, immediately before the aortic valves open, thus allowing the forward \202 ow of blood. Errors in timing Errors can occur with the timing of the intra-aortic balloon pump, and thi s may result in different waveform character- istics and various physiological effects. Ear ly in \202 ation occurs before the dichrotic notch, and the balloon in \202 ates against a closed aortic valve; this results in a poorly de \201 ned dichrotic notch, which lies be tween the unassisted systole waveform and the augmented diastolic waveform. Late in \202 a tion results in diastolic augmentation occurring after the dichrotic notch, and this result s in suboptimal coronary artery perfusion. Early de \202 ation occurs during diastole, thu s an early and sudden drop in diastolic augmentation is seen on the arte- rial waveform; th is results in suboptimal afterload reduc- tion and coronary artery perfusion. Late de \202 ation is when the balloon remains in \202 ated for too long, thus remaining in \202 ated during systole, resulting in a wid- ened appearance of the diastolic augmentation waveform , reduced assisted aortic end-diastolic pressure and a pro- longed rate of rise of assisted systole. Late de \202 ation impedes left ventricular ejection and increases the afterload . Physiology The balloon assists cardiac function by in \202 ating and de \202 at- ing duri ng the cardiac cycle, using helium gas. Helium is the preferred gas as it has a low density and a rapid diffusion coef \201 cient, therefore allowing rapid in \202 ation and de \202 ation of the balloon. The balloon in \202 ates at the onset of diastole, augmenting c oronary blood \202 ow by the proximal displacement of blood, thereby increasing myocardia l oxygen supply. De \202 ation occurs just prior to systole, lowering systolic blood press ure and afterload, thus reducing myocardial oxygen demand. For optimal effect, counterpulsa tion must be timed cor- rectly to the patient \200\231s cardiac cycle. This is achieved by either the patient \200\231s ECG signal or the arterial waveform. Indications \200 \200 \200 \200 \200 \200 ECG signal The most common method used for triggering is the ECG signal, and the R wave is used as the trigger for balloon in \202 ation. In \202 ation starts at the middle of the T wave and the balloon de \202 ates before the end of the QRS complex. Dif \201 culties i n synchronization may arise in cases of tachyar- rhythmias, pacemakers and poor ECG signal; in such cases the arterial waveform may be used for triggering instead. Left ventricular failure Cardiogenic shock Unstable refractory angina Mechanical complicati ons of AMI Post-myocardial infarction ventricular irritability Cardiac support for high ris k general surgery patients and percutaneous transluminal coronary angioplasty (PTCA) patien ts Septic shock Weaning from cardiopulmonary bypass Arterial waveform The two phases of the cardiac cycle can be identi \201 ed on the arteria l waveform (Fig. 2.3.1). The dichrotic notch \200 Contraindications \200 \200 \200 \200 \200 \200 Augmented diastolic pressure Severe aortic valve dysfunction Abdominal aortic aneurysm Thoracic aortic aneurysm Aortic d issection Severe peripheral vascular disease Irreversible brain damage Non- augmented systolic pressure Reduced systolic pressure Insertion of the balloon pump The balloon is inserted percutaneously via either femoral art ery. A modi \201 ed Seldinger technique allows easy and rapid insertion. The balloon cathe ter is passed into the aorta, over a guide wire, and should lie just distal to the subclavi an artery. If not using \202 uoroscopy, a CXR must be done to con \201 rm the position o f the balloon tip. The guide wire can then be removed from the central lumen, which can now be used for arterial pressure monitoring. Reduced aortic end- diastolic pressure Dicrotic notch Unassisted aortic end- diastolic pressure Fig. 2.3.1 Arterial waveform showing augmented pressure 57 CHAPTER 2.3 Intra-aortic balloon counterpulsation pump Balloon perforation or rupture is indicated by blood in the tubing, low augmentation or gas loss. Treatment is to turn the console off and change the balloon. Compartment syndrome pr esents as pain, swelling and hardness of the calf. Treatment is urgent removal of the ballo on with or without fasciotomy. The balloon physically damages platelets during in \202 ati on and de \202 ation, and this may result in thrombocytopaenia. All patients on balloon pu mps should be anticoagulated using heparin, so beware of heparin-induced thrombocyto- paeni a as the cause of the low platelets. If the balloon is placed too proximally, then the left subcla- vian artery may become occlu ded, and if the balloon is too distal, then the renal arteries may become occluded. Once th e balloon is secured in place, the patient should not be allowed to sit up, but can be nurs ed in a 30 head up posi- tion. Sitting may result in the balloon migrating inwards, with the risk of perforating the arch of the aorta and occlusion of the subclavian artery. Flexi on of the leg in the sitting position may kink the balloon, which will prevent adequate in \202 ation. Complications The incidence of complications occurring as a result of bal- loon pumps has d ecreased over the years, and balloon pump-induced death has decreased signi \201 cantly. A ll reported complications are listed below, the most common being vascular. Removal of the balloon pump Patients need to be weaned off the balloon pump by reduc- ing t he balloon frequency. 1:1 indicates that in \202 ation and de \202 ation occurs with ever y cycle, which is the setting most patients are started on. 1:2 indicates in \202 ation an d de \202 ation with every other cycle, and 1:3 indicates in \202 ation and de \202 a- t ion for every 3rd cycle. The frequency is gradually weaned from 1:1 to 1:3, or more dependi ng on the console, as the patient requires less support. Once the patient tolerates less su pport on the balloon pump, indicated by cardiovascular stability and the absence of myocard ial ischaemia, it can then be removed. To remove the balloon, make sure anticoagulation has been weaned, disconnect the balloon from the pump, then gently pull back and remove. Direc t pressure then needs to be applied over the puncture site for at least 30min. Pedal pulses should be con \201 rmed by palpation or Doppler, and the patient should be monitored for bleeding and limb ischaemia. Vascular \200 \200 \200 \200 \200 \200 \200 Limb ischaemia Femoral artery thrombosis Peripheral embolization Femoral vein cannulation A rterial injury AV \201 stula False aneurysm Balloon related \200 Perforation \200 Rupture \200 Incorrect position \200 Gas embo lization \200 Entrapment Further reading Akyurekli Y, Taichmann JC, Keon WJ. Effectiveness of intraaortic bal- loon counter pulsation and systolic unloading. Can J Surg 1980; 23: 122 \200\2236. Other \200 \200 \200 \200 \200 Hemorrhage Visceral ischaemia Infection Compartment syndrome Thrombocytopaenia Barnett MG, Swartz MT, Peterson GJ et al. Vascular complica- tions from intraaortic balloon s: risk analysis. J Vasc Surg 1994; 71: 328 \200\22332. Eltchaninoff H, Dimas AP, Whitlow PL. Complications associated with percutaneous placement and use of intraaortic balloon counter pulsation. Am J Cardiol 1993; 71: 328 \200\22332. The most common vascular complication is limb ischaemia; this may be because many of these patients suffer from co- existing diseases such as diabetes, hypertension and peripheral va scular disease. The patients must therefore have their peripheral pulses, capillary re \201 ll and limb tem- perature checked regularly, and the balloon must be removed immediate ly if there are any signs of ischaemia. Other vascular injuries generally require surgical inter- vention. Freedman RJ. The intra-aortic balloon pump system: current roles and future directions. J Appl Cardiol 1991; 6: 313 \200\2238. Mercer D, Doris P, Salerno TA. Intra-aortic balloon counter pulsa- tion in septic shock. Can J Surg 1981; 24: 643 \200\22345. Moulopoulos SD, Topaz S, Koloff WJ, et al. Diastolic balloon pump- ing (with carbon dioxide ) in the aorta \200\224a mechanical assistance to the failing circulation. Am Heart J 1962; 63: 669 \200\22375. 58 J CORDINGLEY Cardiac assist devices Pneumatic \200 Over the last few years there have been major develop- ments in cardiac assist device techn ology for both tempo- rary and longer term haemodynamic support for patients with severe ca rdiac failure. Thoratec VAD: extracorporeal single chamber (plastic sac) pump used for short and medium-te rm support. A vacuum is used to enhance \201 lling of the blood sac that is then compress ed to produce an SV of 65ml with total \202 ows up to 6.5l/min. Access cannulae contain m echanical one-way valves. Can be used as a long-term VAD. Abiomed BVS5000 and AB5000: extra corporeal pumps with two blood chambers \200\224a gravity- \201 lled atrium and a pneumati cally compressed ventricle. Two polyurethane valves are positioned within the pump. These p umps have been used extensively for temporary support for left, right or both ventricles. T he AB5000 can be used for longer term as a bridge to transplantation or recovery. HeartMate LVAS: implantable long-term support for bridge to transplant, recovery or destination ther apy. Contains porcine valves and a pump surface that allows a cellular lining to develop, a nd therefore there is less requirement for anticoagulation. Maximum SV is 85ml. General description Cardiac assist devices are blood pumps that partially sup- port or enti rely replace the function of the left or right ventricle. A left ventricular assist device (LVAD) takes in blood from the left atrium or left ventricle and ejects usually into the as cending or descending aorta, but sometimes more peripherally. As a result, LV preload is de creased and car- diac output increased, restoring organ perfusion. A right ventricular assi st device (RVAD) takes blood from the right atrium and ejects into the pulmonary artery. So me patients may require biventricular support using two VADs. Pumps can be extracorporeal o r intracorporeal, and cannulation may be direct via thoracotomy or percutaneous. Some pumps produce pulsatile \202 ow and others continuous. Total arti \201 cial hearts that repla ce the heart completely are also available. Recently percutaneously placed devices providin g LV support have come into clinical use. Nearly all devices require patients to receive sy stemic anticoagulation. Electric motor driven \200 HeartMate XVE LVAS: similar to HeartMate LVAS but uses an electric motor, rather than air t o eject blood. Novacor LVAS: intracorporeal device that includes pusher plates to produce \202 ow. Porcine valves are used in the cannulae. This device is only suitable for LV supp ort, but can be used long term. Indications for cardiac assist device Use of a cardiac assist device is indicated in patien ts with cardiac failure when cardiac output has fallen to a level such that other organ fai lure secondary to poor perfusion is likely to occur, despite maximal medical therapy. The m ost common causes of acute cardiac failure requiring cir- culatory support are acute myocar dial ischaemia and fol- lowing cardiac surger y. In these circumstances, extracorporeal or percutaneous devices for short-term support are used to allow time for cardiac function to recover or for consideration of implantation of a longer term device. Medium-term (extracor poreal pulsatile) devices are usually used as a bridge to recovery or cardiac transplantati on. Patients with slowly deteriorating chronic heart failure are more likely to be managed with long-term intracorporeal (surgically implanted) systems that allow patients to leave h ospital, and are implanted either as a bridge to recovery or transplantation or rarely as p ermanent (destination) therapy. In a randomized clinical trial of LVAD implantation vs medi cal therapy in 129 patients ineligible for cardiac transplantation, patients receiving an L VAD (Heartmate) survived longer and had better functional status (REMATCH study). Non-pulsatile No valves are included in circuits with these pumps, and \201 lling occurs by suction from the pump. Centrifugal pumps are used for short-term extracorporeal support and axial pumps are placed intracorporeally for longer term ven- tricular assistance. Centrifugal Centrifugal pumps accelerate blood \202 ow from the inlet at the center of a rotating plate to the out \202 ow at the periph- ery. These pumps (and axial impellers) ar e sensitive to changes in preload and afterload, and therefore \202 ow may vary considera bly at the same pump revolutions per minute (rpm). They are used to provide temporary cardi ac sup- port. Pumps with bearings produce local heat that has been associated with an incre ased incidence of thrombotic complications. \200 Medtronic Bio-pump (BioMedicus): extracorporeal cen- trifugal pump with bearings. Levitroni x (Centrimag): a small extracorporeal pump, in which the impeller is rotated by a magnetic \201 eld, without bearings. Can be used as an LVAD and/or an RVAD for up to 28 days. Contraindications to VAD support \200 Contraindication to anticoagulation \200 Aortic r egurgitation \200\224greater than mild (for LVAD) \200 Multiple organ failure Axial Axial impeller pumps are smaller than other pumps and have a lower blood-contacting s urface area than pulsatile pumps. All models require intracorporeal placement. Blood is pum ped by a rotating screw or propeller. There has been considerable interest recently in usin g this type of pump for long-term ventricular support because of their smaller size and red uced risk of infection. \200 Types of pump Pulsatile Blood is pumped by pneumatic or electric motor-driven compression of a blood reservoir. Pro sthetic valves in the circuit prevent reverse flow. Pumps require adequate preload and afte rload \200\224stroke volume (SV) decreases with very high afterload, unless drive line pres sure is increased. Jarvik 2000: small axial pump, rotating at 8000 \200\22312000rpm that is implanted into the apex of the left ventricle and ejects into the descending thoracic aorta, providing LV sup port. Can be implanted using a left thoracotomy. 59 CHAPTER 2.4 Cardiac assist devices Two sizes are available. The LP2.5, size 12F, is inserted per- cutaneously via the femoral artery and can pump up to 2.5l/min. The larger LP5.0 requires insertion via femoral artery cut down, and can pump up to 5l/min. Versions of the pump that can be placed during cardiac surgery are available. The LD5.0 is placed through the ascending aorta into the left ventr icle. Right ventricular assist is also possible using the RD device. With an in \202 ow su ction port placed surgically in the right atrium and out- \202 ow cannula in the pulmonar y artery the system can pump up to 5.5l/min. The Impella devices can be used for up to 10 d ays. Used for bridge to transplant, but has also been used for destination therapy. Micromed DeB akey and HeartMate II: axial pumps implanted with in \202 ow from the ventricle and out \202 ow in the ascending aorta (LVAD) or pulmonary artery (RVAD). Complications associated with VADs Echocardiography (TTE and TOE) is very valuable in diag- nosing and managing VAD-associated problems. Acute \200 \200 \200 Hemorrhage Air embolus Right ventricular failure Tandem Heart The Tandem Heart (CardiacAssist Inc., Pittsburgh, PA, USA) is an extracorporea l centrifugal pump. The in \202 ow cannula is passed from the femoral vein into the left a trium via a transeptal puncture. The out \202 ow cannula is placed via the femoral artery into the iliac artery. The system can pump up to 5l/min and be used for up to 14 days. This makes it suitable for temporary support post-myocardial infarction or post-cardiac surgery . Percutaneous short-term LVAD support is appealing because of the potential wider applicab ility of pumped cir- culatory support. Clinical outcome studies of percutane- ous LVAD supp ort are awaited. RV dysfunction is common after LVAD implantation, and up to 30% of patients may subsequentl y require RVAD sup- port. Many patients will require inotropic support and pul- monary vaso dilators. \200 \200 \200 \200 Cannula obstruction Haemolysis Arrhythmias Right to left shunting through patent foramen ov ale (LVAD) Multiple organ failure Chronic \200 \200 \200 \200 \200 Venoarterial extracorporeal membrane oxygenation ECMO for respiratory failure can usually b e provided with- out the need for circulatory support (VV ECMO) and is described in Chapter 1.14. Some patients may require combined circulatory and pul- monary support, e.g. patient s with ARDS combined with acute right ventricular failure, for example post-pneumon- ectomy . In these circumstances, temporary combined car- diac and pulmonary support can be achieve d using venoarterial extracorporeal membrane oxygenation (VA ECMO). Blood is withdrawn from a right atrial cannula, pumped by an extracorporeal pump through an oxygena- tor and retur ned into the aorta. Cannulae can usually be placed percutaneously. A centrifugal pump, e.g. Levitronics/ Centrimag, is often used in this situation. Thrombus formation/hemorrhage Stroke Infection Valve failure Device failure Total arti \201 cial hearts Although total arti \201 cial hearts that completely replace both ventricles have been produced, they have not been used widely. Potential advantages ov er intracorporeal LVADs include absence of arrhythmias and potential RV failure. Catheter-based temporary assist devices Recently a number of assist devices that can be use d with- out the need for a thoracotomy have become available. These devices are for short-t erm support (<10 days) until recovery occurs or longer term support is arranged. Indication s for use include cardiogenic shock of any cause, either until cardiac function improves or as a bridge to sur- gical (long-term) LVAD implantation or to transplantation. A further u se being investigated is during high risk revascu- larization (surgical or medical) in orde r to decrease myco- cardial oxygen demand in a large area of ischaemic myocardium. Contrain dications to insertion include RV failure (biventricular support will be required) and inad e- quate peripheral arterial vessels for device placement. Uses of VA ECMO \200 Neonatal respiratory distress syndrome (VV ECMO is also used) Failure to wean from cardiopu lmonary bypass Short-term support of left or both ventricles when com- bined with acute pul monary failure ARDS with acute right ventricular failure. \200 Further reading Boehmer JP, Popjes E Cardiac failure: mechanical support strategies. Crit Care Med 2006; 34: 268 \200\22377. Impella The Impella (Abiomed Europe, Aachen, Germany) has a catheter-mounted axial \202 o w pump that is passed from the femoral artery retrogradely through the aortic valve into th e left ventricle. Blood enters the pump in the left ventri- cle and is ejected into the aor ta. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term mechanical left ventricular assistance for end-stage heart failure (REMATCH Study). N Engl J Med 2001; 345: 1435 \200\22343. 60 K POLDERMAN Therapeutic cooling rapid re-warming after therapeutic hypothermia can re-trigger harmful processes and adverse ly affect outcome. The rate of re-warming should be even slower (0.05 \200\223 0.1 C/hr) w hen hypothermia has been used in patients with TBI. Therapeutic hypothermia is being used with increasing fre- quency to prevent or mitigate va rious types of neurological injury. Currently, its most frequent usage is in patients who r emain comatose following witnessed cardiac arrest with restoration of spontaneous circulati on (ROSC). Two rand- omized controlled trials and 15 non-randomized studies have shown that neurological outcome in this category of patients can be improved by mild (32 \200\22334 C) hypothermia. Preliminary \201 ndings suggest that patients with other initial rhythms, such as asystole and pulseless electrical activity, may also bene \201 t from therapeutic cooling. Guidelines from the European Resuscitation Council and the American Heart Associa tion formally recommend the use of hypo- thermia for selected patients who remain comatose fol- lowing a witnessed cardiac arrest. Hypothermia can also be used for numerous other ind ica- tions including severe traumatic brain injury, stroke, hepatic failure, ischaemic spin al cord injury, myocardial infarction and numerous others. Some of these indications requir e longer treatment periods, with a concomitant increase in the risk of side effects. Practical aspects Induction of hypothermia will lead to the activation of counter-regulator y mechanisms to decrease heat loss, including an increase in sympathetic tone, vasoconstric tion of skin vessels and shivering. Shivering increases oxygen consumption by 40 \200\22310 0% and has been linked to increased risk of morbid cardiac events; however, these observati ons have been made in the post-operative setting, where hypo- thermic patients are awake an d have a high rate of metabo- lism, increased oxygen consumption, excess work of breathing, a high heart rate and a general stress-like response. These adverse events are linked to t he haemo- dynamic and respiratory responses rather than to shiver- ing per se, and the side effects are largely absent in controlled hypothermia where patients are sedated, venti- la ted and have low heart rates. However, shivering can gen- erate signi \201 cant amounts of heat and can signi \201 cantly decrease cooling rates; for this and other reasons it shou ld be aggressively treated (especially in the induction phase of cooling). Shivering respon ses decrease markedly when the temperature decreases below 33.5 \200\22334.0 C. Cardiovasc ular effects of cooling include bradycardia and a rise in blood pressure. Hypothermia \200 \231s effect on myocardial contractility is variable (depending on heart rate and \201 ll ing pressure); in most patients, myocardial contractility will increase, although mild dias tolic dysfunction may develop in some patients. Clinically signi \201 cant arrhythmias may occur, but only if core temperature decreases below 30 C. The most important long-term si de effect of hypothermia is an increased risk of infections (especially of the respira- tor y tract and/or wounds) and bedsores. The most important potential side effects of cooling a re: \200 Hypovolemia through hypothermia-induced cold diure- sis. If uncorrected this can cause hypotension. Hypothermia per se does not decrease blood pressure. Electrolyte disord ers (cooling causes urinary loss of K, Mg, P as well as intracellular shift; rapid re-warmi ng can cause hyperkalaemia). Hyperglycaemia (cooling can cause insulin resistance and decre ased insulin secretion). Shivering (can be controlled with magnesium, meperid- ine, quick-a cting opiates, propofol or benzodiazepines; additional therapeutic options include ketanser in, cloni- dine, tramadol, urapidil and doxapram). Skin injuries/bedsores (prolonged direct exposure of the skin to ice or ice-packs can cause burns; cooling causes vasoconstriction in the skin; and wound infections can develop more easily due to the immunosuppressive effe cts of hypothermia). Infections, especially airway and wound infections. De \201 nitions Induced hypothermia: an intentional reduction of a patient \200\231s core temperature below 36.0 C. Therapeutic hypothermia: controlled induced hypothermia, i.e. in duced hypothermia with potentially harmful effects such as shivering being controlled or su ppressed. Temperature range usually 32 \200\22335.9 C. A separate but closely related issu e is the use of controlled normothermia (therapeutic fever management). Several studies hav e demonstrated a link between fever (irrespec- tive of its cause) and a worsening of neurol ogical outcome in many types of neurological injury, including post-ischaemic injury follow ing cardiac arrest. This correlation persists after multivariate analysis, and observations from animal studies strongly suggest that the link is causal. Therefore, sympto- matic con trol of fever is becoming an increasingly accepted goal of therapy in patients with neurocr itical illness. Therapeutic normothermia: bringing down and maintaining core temperature wi thin a range of 36.0 \200\22337.5 C in a patient with fever, with the potentially deleteri ous effects such as shivering being controlled or suppressed. Temperature management in cri tically ill patients poses special challenges for attending physicians and nurses, as the i nduction strategy and proper management of side effects can have a substantial impact on ou tcome. The hypothermia treatment period can be divided into three distinct phases: Induction phase Aim: to achieve temperatures \211 34 C and then target tem- perature as q uickly as possible. In this phase, a small over- shoot ( \211 1 C) should be regarded as a cceptable provided core temperature remains >30 C. Maintenance phase Aim: to control core temperatures tightly within a narrow range, with no or minor \202 uctuations (maximum 0.2 \200\2230.5 C). Precautions \200 Treat infections early and aggressively; consider antibi- otic prophylaxis; perform frequen t cultures of blood and other sites. Re-warming phase Aim: slow and controlled rise in temperature, target rate 0.2 \200\2230.3 C/h, maximum acceptable rate 0.5 C/h. Reason: 61 CHAPTER 2.5 Therapeutic cooling Use appropriate sedation and analgesia (animal data sug- gest loss of protective effects if sedation is insuf \201 cient; sedation also facilitates cooling by preventing shivering a nd causing vasodilation). Adjust ventilator settings (cooling causes dO2 consump- tion and dCO2 production); adjust feeding rate (cooling decreases metabolism by 7 \200\22310% per C decrease below 37 C). Blood gas analysis and clotting parameters are affected by tempera ture. Most laboratories warm samples to 37 C before analysis. If blood gas results have no t been analyzed at the patient \200\231s true core temperature, values can be estimated wit h the following rule of thumb: for pO2, subtract 5mm Hg for every 1 C below 37 C; for pCO 2, subtract 2mm Hg for every 1 C below 37 C; for pH, add 0.012 points for every 1 C belo w 37 C. Adjust drug dosage (drug clearance, especially by the liver, may change; this incl udes clearance of sedatives, opiates and paralyzing agents. Precaution: use bolus doses dur ing induction phase, avoid high maintenance doses). Avoid core temperature \211 30 C (ris k of arrhythmias arises at temperatures \211 28 \200\22330 C). Hypothermia does not cause arrhythmias at temperatures \211 30 C. Avoid \200\230overtreating \200\231. Bradycardia , mild metabolic acido- sis and a slight rise in lactate levels, liver enzymes and amylase are normal consequences of hypothermia, and usually do not require treatment. Avoid long-te rm paralysis. Paralysis can mask inadequate sedation and seizures, and can have adverse con se- quences such as increased risk of critical illness polyneu- romyopathy. Treat shivering with one of the other agents listed above. Consider platelet administration before surgery or inva- sive procedures during cooling. General measures: provide good basic intensive ca re (many of the side effects of cooling can be prevented or controlled with proper intensiv e care treatment). by external cooling, the patient \200\231s normal counter-regulatory mechanisms will be act ivated. Indeed shivering may be more pronounced than in hypothermic patients, because where as at 33 C the shivering response is absent or signi \201 cantly blunted, at 36 \200\2233 7 C the counter-regulatory mechanisms are working at maximum capacity. Therefore, maintain ing controlled normothermia is often more dif \201 - cult than maintaining controlled hypo thermia, and extra efforts may be required to combat shivering. This is a prob- lem especia lly in non-ventilated patients, because the doses of sedatives required to control shiverin g may be so large that they can induce respiratory failure. Antipyretic drugs such as parac etamol (acetaminophen) or aspirin can be used as adjunctive treatment to lower tem- peratur e. A major advantage is that these drugs do not activate the shivering response. However, t heir ef \201 cacy (especially in non-infectious ( \200\230central \200\231) fever is relat ively low; the average temperature decrease in patients treated with high doses of paraceta mol or aspirin is 0.1 \200\2230.7.