Jerry P. Nolan
Heerajnarain Bulluck and Derek Hausenloy
Imran Ahmad and Martin John
Ehsan Ahmadnia, Phil Ostrowski, and Sussana Price
Defibrillation is the passage of an electrical current of sufficient magnitude across the myocardium to depolarize a critical mass of cardiac muscle simultaneously, enabling the natural pacemaker tissue to resume control. To achieve this, all defibrillators have three features in common:
• A power source capable of providing direct current.
• A capacitor that can be charged to a predetermined energy level.
• Two electrodes that are placed on the patient’s chest, either side of the heart, across which the capacitor is discharged.
Successful defibrillation is defined as the absence of ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT) at 5 s after shock delivery, although the ultimate goal is return of spontaneous circulation (ROSC).
Factors affecting defibrillation success
Defibrillation success depends on sufficient current being delivered to the myocardium. However, the delivered current is difficult to determine because it is influenced by transthoracic impedance (electrical resistance) and electrode position. Furthermore, much of the current is diverted along non-cardiac pathways in the thorax and, as a result, as little as 4% reaches the heart.
Current flow is inversely proportional to transthoracic impedance; however, biphasic defibrillators can measure the transthoracic impedance and adjust the energy delivered to compensate. Their efficacy is therefore independent of transthoracic impedance (impedance compensation). It is necessary to ensure good contact between self-adhesive pads and the patient’s skin.
Transmyocardial current during defibrillation is likely to be maximal when the electrodes are placed so that the area of the heart that is fibrillating lies directly between them (i.e. ventricles in VF/pVT, atria in atrial fibrillation [AF]). Therefore, the optimal electrode position may not be the same for ventricular and atrial arrhythmias.
When attempting to defibrillate a patient in VF/pVT, the standard procedure is to place one electrode to the right of the upper sternum below the clavicle. The apical pad is placed in the mid-axillary line, approximately level with the V6 electrocardiograph (ECG) electrode. Although the electrodes are marked positive and negative, each can be placed in either position. Other acceptable pad positions include:
One electrode anteriorly, over the left precordium, and the other electrode on the back behind the heart, just inferior to the left scapula (anteroposterior).
One electrode placed in the mid-axillary line, approximately level with the V6 ECG electrode or female breast and the other electrode on the back, just inferior to the right scapula (posterolateral).
Each electrode on the lateral chest walls, one on the right and the other on the left side (bi-axillary).
Strategies before defibrillation
Safe use of oxygen during defibrillation
In an oxygen-enriched atmosphere, sparking from poorly applied defibrillator paddles can cause a fire and significant burns to the patient. The use of self-adhesive electrodes is far less likely to cause sparks than manual paddles—no fires have been reported in association with the use of self-adhesive electrodes. The following are recommended:
Take off any oxygen mask or nasal cannulae and place them at least 1 m away from the patient’s chest.
Leave the ventilation bag connected to the tracheal tube or supraglottic airway device; no increase in oxygen concentration occurs in the zone of defibrillation, even with an oxygen flow of 15 l/min.
Alternatively, disconnect the ventilation bag from the tracheal tube or supraglottic airway device and move it at least 1 m from the patient’s chest during defibrillation.
If the patient is connected to a ventilator leave the ventilator tubing (breathing circuit) connected to the tracheal tube unless chest compressions prevent the ventilator from delivering adequate tidal volumes. In this case, the ventilator is usually substituted by a ventilation bag, which can be left connected or detached and removed to a distance of at least 1 m. Ensure that the disconnected ventilator tubing is kept at least 1 m from the patient or, better still, switch the ventilator to standby during the period of the resuscitation attempt; modern ventilators generate high oxygen flows when left disconnected. Patients in the critical care unit may be dependent on positive end-expiratory pressure (PEEP) to maintain adequate oxygenation; during cardioversion, when the spontaneous circulation potentially enables blood to remain well oxygenated, leave the critically ill patient connected to the ventilator during shock delivery.
Cardiopulmonary resuscitation versus defibrillation as the initial treatment
In any unwitnessed cardiac arrest, those responding should provide high-quality, uninterrupted cardiopulmonary resuscitation (CPR) while a defibrillator is retrieved, attached, and charged. Attempt defibrillation as soon as possible; a period of CPR (e.g. 2–3 min) before rhythm analysis and shock delivery is not recommended.
There is no conclusive evidence that a single shock strategy increases rate of ROSC or reduces recurrence of VF compared with three stacked shocks but, because outcome is improved by minimizing interruptions to chest compressions, single shocks are recommended for most situations. The duration of pre-shock and post-shock pauses should be minimized.
Continue CPR while a defibrillator is retrieved and applied; as soon as the defibrillator is available, assess the rhythm and attempt defibrillation when indicated.
Continue chest compressions while charging the defibrillator. During compressions, ensure all rescuers stand clear other than the individual performing chest compressions.
When defibrillating, ensure that the total interruption to chest compressions is less than 5 s and resume chest compressions immediately after defibrillation.
Immediately after a shock do not delay CPR for rhythm reanalysis or a pulse check.
Continue CPR (30 compressions: 2 ventilations) for 2 min until rhythm reanalysis is undertaken and another shock is given (if indicated). Even if the defibrillation attempt is successful, it takes time until the post-shock circulation is established and a pulse is not usually palpable with a perfusing rhythm immediately after defibrillation.
Patients can remain pulseless for over 2 minutes and the duration of asystole before ROSC can be longer than 2 min in as many as 25% of successful shocks.
Witnessed and monitored VF/pVT cardiac arrest
If a patient has a monitored and witnessed cardiac arrest in a high care area and a manual defibrillator is rapidly available:
Confirm cardiac arrest and shout for help.
If the initial rhythm is VF/pVT, give up to three quick successive (stacked) shocks.
Rapidly check for a rhythm change and, if appropriate, check for a pulse and other signs of ROSC after each defibrillation attempt.
Start chest compressions and continue CPR for 2 min if the third shock is unsuccessful.
Deliver the first shock with energy of at least 150 J. The shock energy for a particular defibrillator is based on the manufacturer’s guidance. Those using manual defibrillators should be aware of the appropriate energy settings for the type of device used, but, in the absence of this and if appropriate energy levels are unknown, for adults use the highest available shock energy for all shocks.
For subsequent shocks, there is no evidence to support either a fixed or escalating energy protocol, although an escalating protocol may be associated with a lower incidence of refibrillation. If the first shock is not successful and the defibrillator is capable of delivering shocks of higher energy it is reasonable to increase the energy for subsequent shocks. With manual defibrillators it is also appropriate to consider escalating the shock energy in patients when refibrillation occurs.
1. The sequence for using a defibrillator in manual mode is described. Because of the interruption in chest compressions caused by automatic rhythm analysis, shock advisory or automated external defibrillator (AED) mode should be used only by those unfamiliar with rhythm interpretation.
2. Confirm cardiac arrest—check for normal breathing and pulse simultaneously.
3. Call resuscitation team.
4. Perform uninterrupted chest compressions while applying self-adhesive defibrillation/monitoring pads—one below the right clavicle and the other in the V6 position in the mid-axillary line.
5. Plan actions before pausing CPR for rhythm analysis and communicate these to the team.
6. Stop chest compressions; confirm VF/pVT from the ECG. Ensure this pause in chest compressions is no longer than 5 s.
7. Resume chest compressions immediately; warn all rescuers other than the individual performing the chest compressions to ‘stand clear’ and remove any oxygen delivery device as appropriate.
8. The designated person selects the appropriate energy on the defibrillator and presses the charge button. Choose an energy setting of at least 150 J for the first shock and the same or a higher energy for subsequent shocks.
9. Ensure that the rescuer giving the compressions is the only person touching the patient.
10. Once the defibrillator is charged and the safety check is complete, tell the rescuer doing the chest compressions to ‘stand clear’; when clear, give the shock.
11. After shock delivery immediately restart CPR using a ratio of 30:2, starting with chest compressions. Do not pause to reassess the rhythm or feel for a pulse. This pause in chest compressions should be brief and no longer than 5 s.
12. Continue CPR for 2 min; the team leader prepares the team for the next pause in CPR.
13. Pause briefly to check the monitor.
14. If VF/pVT, repeat steps 6–12 and deliver a second shock.
15. If VF/pVT persists repeat steps 6–8 and deliver a third shock. Resume chest compressions immediately. Give intravenous (IV) adrenaline 1 mg and amiodarone 300 mg IV while performing a further 2 min of CPR. Withhold adrenaline if there are signs of ROSC during CPR.
16. Repeat this 2 min of CPR—rhythm/pulse check—defibrillation sequence if VF/pVT persists.
17. Give further adrenaline 1 mg IV after alternate shocks (i.e. approximately every 3–5 min).
18. If organized electrical activity compatible with a cardiac output is seen during a rhythm check, seek evidence of ROSC (check for signs of life, a central pulse or arterial waveform, and end-tidal CO2).
19. If there is ROSC, start postresuscitation care.
20. If there are no signs of ROSC, continue CPR and switch to the non-shockable algorithm.
21. If asystole is seen, continue CPR and switch to the non-shockable algorithm.
If electrical cardioversion is used to convert atrial or ventricular tachyarrhythmias, the shock must be synchronized with the R wave of the ECG (VF and pVT do not require synchronized shocks). By avoiding the relative refractory period in this way, the risk of inducing VF is minimized.
Conscious patients must be anaesthetized or sedated before synchronized cardioversion is attempted.
Most manual defibrillators incorporate a switch that enables the shock to be triggered by the R wave on the electrocardiogram. Electrodes are applied to the chest wall and cardioversion is achieved in the same way as attempted defibrillation, but there may be a slight delay between pressing the buttons and the discharge of the shock when the next R wave occurs.
If synchronization fails, choose another lead and/or adjust the amplitude. In patients with VT who are unstable, give unsynchronized shocks to avoid prolonged delay in restoring sinus rhythm.
Shock energies for cardioversion
For a broad-complex tachycardia or AF, start with 120–150 J and increase in increments if this fails.
Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower-energy shocks: start with 70–120 J. For AF and atrial flutter use anteroposterior defibrillator pad positions when it is practicable to do so.
Temporary cardiac pacing is an invaluable procedure in life-threatening or potentially life-threatening situations. However, the associated complication rates are high and therefore the decision for its use needs to be taken judiciously.
Temporary cardiac pacing provides a potentially life-saving measure for supporting the heart in patients with haemodynamic compromise owing to a disturbed conduction system. Depending on the particular indication for temporary cardiac pacing and the availability of suitable equipment and skilled personnel, there exist several types of temporary cardiac pacing.
Because of the high complication rates associated with temporary pacing (both immediate and in the short term), this procedure should be avoided as far as possible and used as quickly as possible when required.
Indications for temporary cardiac pacing
The setting of an acute myocardial infarction
• Second- or third-degree atrioventricular (AV) block.
• Symptomatic junctional bradycardia.
• New bundle branch block (particularly left bundle branch block) or bifascicular block in patients with an anterior/lateral myocardial infarction (MI).
Not related to an acute MI
• P-wave asystole.
• Second- or third-degree AV block without escape rhythm.
• Tachyarrhythmias secondary to bradycardia.
• Overdrive suppression of tachyarrhythmias.
• To prevent or treat torsades de pointes.
Prophylactic temporary cardiac pacing
• Postcardiac surgery (especially tricuspid and aortic valve surgery, ventricular septal defect (VSD) or ostium primum repair).
• During permanent pacemaker generator change in pacing dependent patients.
• During right coronary artery angioplasty (especially during rotablation).
Types of temporary cardiac pacing
Temporary transcutaneous cardiac pacing
This non-invasive approach is used if temporary transvenous cardiac pacing is not immediately available. Self-adhesive electrode pads are placed on the left anterior chest between the xiphoid process and the left nipple, and posteriorly below the left scapula and spine. These are attached to the external pulse generator. Conscious patients should be given sedation to minimize discomfort.
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 under fluoroscopic guidance. Where fluoroscopy is unavailable, pacing wires can be placed using balloon-tipped catheters.
Check the fluoroscopy equipment, pacemaker box, and defibrillator are functioning properly.
Put on a lead apron and a sterile gown and gloves.
Obtain central venous access (see Chapter 7, ‘Insertion of central venous catheters’). The right internal jugular vein offers easiest access to the right ventricle and is the recommended approach. The right subclavian vein is the most comfortable for the patient. The right femoral vein should be considered if the above fail (but is not recommended because of the risks of deep vein thrombosis, infection, and the need for the patient to remain continuously supine).
Insert a venous sheath that is one size larger than the pacing wire, which is usually 5F or 6F in size.
Right ventricular lead placement: from the right atrium, advance the pacing wire across the tricuspid valve and into the right ventricle. If it does not cross the tricuspid valve, rotate it so that it faces the lateral wall of the right atrium and forms a loop, and then prolapse the loop into the right ventricle. Entering the right ventricular outflow tract and then withdrawing the pacing wire will allow the tip to position in the apex. Maintain some slack in the pacing wire.
Right atrial lead: on entering the right atrium, the preformed ‘J’ shape of the atrial pacing wire should reform. Rotate the pacing wire and position the tip in the right atrial appendage.
Connect the pacing wire(s) to the pacing box and check for stability of the pacing wire(s) by asking the patient to cough, sniff, and take some deep breaths. Exclude diaphragmatic pacing.
Obtain a chest radiograph (CXR) to exclude a pneumothorax and check the position and integrity of the pacing wire(s). The atrial pacing wire should face anteriorly and loop upwards on a lateral CXR. The ventricular pacing wire should resemble the outline of a ‘sock’ on a posteroanterior (PA) CXR.
Temporary transoesophageal cardiac pacing
This approach obviates the requirement for central venous access or sterile precautions and may be considered when fluoroscopy is unavailable. It comprises a transoesophageal pulse generator and gelatine bipolar pill electrodes (for the oral route) or transoesophageal pacing catheters (for the nasal route).
Temporary epicardial cardiac pacing
This involves directly stimulating the epicardium of the atria and/or ventricle using electrodes sutured to the epicardium at the time of cardiac surgery. The pacing wires are pulled through an incision in the skin and secured to the external 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 perforation, tamponade, and disruption of coronary anastomoses are the recognized complications.
Setting the pacemaker up
Check the pacemaker box has a fresh battery and ensure the connections are secure and correct.
Determine the capture threshold
Capture describes the ability of the electrical impulse to initiate a myocardial depolarization.
Turn the pacemaker rate to 10 bpm above the intrinsic rate and increase the pacemaker output to 3 volts.
Slowly decrease the output until loss of capture occurs, then increase it until capture reoccurs after every pacer spike. This is the capture threshold (aim for <1.0 and <1.5 volts for ventricular and atrial wires, respectively). Set output at 2–3 times the threshold or at 3 volts, whichever is higher.
Reset the pacemaker to the prescribed rate.
Determine the sensitivity threshold
Sensitivity refers to the ability of the pacemaker to detect intrinsic myocardial activity. The sensitivity dial indicates the minimum voltage that the pacemaker can sense. Therefore, decreasing the sensitivity dial actually increases pacemaker sensitivity and vice versa.
Set the pacing rate at 10 bpm below the intrinsic rate.
Lower the pacemaker output to 0.1 volts to prevent competitive pacing.
Increase the sensitivity dial until the sense indicator stops flashing and the pace indicator starts flashing.
Slowly decrease the sensitivity dial until the sense indicator flashes continuously. This value is the sensing threshold. 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 2 mV.
Reset pacemaker to prescribed rate.
Pacemaker mode and variables
The three-letter code corresponds to the chamber paced (‘V’ for ventricle and ‘D’ for dual chamber), the chamber sensed, and the response to sensing (‘I’ means pacing is inhibited on sensing intrinsic myocardial activity).
VVI is for ventricular pacing only.
DDD is for dual chamber pacing, allowing AV sequential pacing, which may benefit patients with a low cardiac output state or those patients with a ‘stiff’ left ventricle.
AV interval (~150 ms): this is the time interval between a paced or sensed event in the atrium to a paced event in the ventricle.
Upper rate limit (~135 bpm): this is the maximum rate at which the ventricles will pace, as determined by tracking the atrial rate.
PVARP (postventricular atrial refractory period, ~300 ms): this time interval limits how early after a paced or sensed ventricular beat an atrial event can trigger a ventricular paced event.
Caring for patients with pacemakers
Proper care of the temporary cardiac pacing system includes daily assessment of the patient’s haemodynamic status and examination of the insertion site for signs of infection. The underlying heart rhythm, sensitivity, and capture thresholds should be determined daily, provided that pacing is occurring <90% of the time.
The absence of pacing spikes on the ECG
This may be due to failure to pace when the intrinsic rate is less than the pacing rate, or it may be because the intrinsic rate is greater than the set pacemaker rate.
Failure to pace
This describes the failure of the pacemaker box to deliver an electrical impulse and is indicated by the absence of pacing spikes when the intrinsic heart rate is less than the pacemaker rate.
Failure to capture
This describes the failure of an electrical impulse to initiate a myocardial depolarization and is revealed by the failure of an appropriately timed pacing spike to be followed by either a ‘P’ wave or a widened ‘QRS’ complex. The capture threshold often doubles in the first few days due to endocardial oedema. Therefore, try increasing the output to restore capture.
Failure to sense or undersensing
This describes the failure of the pacemaker to detect intrinsic myocardial activity. It is indicated by regular pacing spikes unrelated to the intrinsic rhythm, which may or may not capture. Try decreasing the sensitivity dial (thereby increasing pacemaker sensitivity).
Inappropriate or oversensing
This describes the situation where the pacemaker is misinterpreting skeletal activity or ‘P’ and ‘T’ waves as ‘QRS’ complexes and is inhibiting pacemaker activity, causing bradycardic episodes. Try increasing the sensitivity dial (thereby decreasing pacemaker sensitivity).
Causes of failure to pace, capture, or sense
• Pacemaker box malfunction or flat battery.
• Insecure or incorrect lead connections.
• Malpositioned, damaged, or displaced pacing wire.
• MI/fibrosis adjacent to wire tip.
• Myocardial perforation.
• Certain drugs such as class I antiarrhythmics.
• Electrolyte disturbances that widen the QRS and delay its upstroke, causing undersensing.
The intra-aortic balloon pump (IABP) was developed in the 1960s to provide circulatory support for patients in cardiogenic shock. It is now the most commonly used mechanical assist device in clinical practice and helps manage unstable patients from a broad spectrum of cardiac disease. An appreciation of the underlying principles and how the balloon pump operates is essential when dealing with patients supported by this device.
The primary aim of the balloon pump is to improve cardiac function by increasing myocardial oxygen supply and reducing demand. It works on the principle of counterpulsation: diastolic inflation and rapid systolic deflation within the aorta. Diastolic balloon inflation causes proximal and distal displacement of blood, which translates into improved coronary bloodflow and systemic perfusion. Rapid balloon deflation at the onset of systole reduces left ventricular afterload and myocardial oxygen demand.
Haemodynamic effects of intra-aortic counterpulsation
• Improved cardiac output.
• Improved ejection fraction.
• Increased coronary perfusion pressure.
• Reduced heart rate.
• Reduced systemic vascular resistance.
The IABP consists of a double-lumen balloon catheter that is attached to a pump console used to control balloon inflation and deflation. The outer lumen of the catheter is used to deliver gas (20–50 ml) to the balloon and the inner lumen is used for guidewire railroading during insertion, and arterial waveform monitoring after deployment. Helium is used as the inflating driving gas since its low viscosity facilitates rapid transfer from console to balloon. Helium also absorbs very rapidly in blood in case of balloon rupture.
• Cardiogenic shock.
• Mechanical complications of acute MI (mitral regurgitation (MR) or VSD).
• Cardiac support for high-risk patients undergoing percutaneous coronary intervention or coronary artery bypass grafting.
• Weaning from cardiopulmonary bypass.
• Refractory unstable angina.
• Postcardiac arrest myocardial dysfunction.
• Bridge to mechanical assist device placement or heart transplantation.
• Severe aortic valve dysfunction.
• Abdominal or thoracic aortic aneurysm.
• Aortic dissection.
• Severe peripheral vascular disease.
• Irreversible brain damage.
The IABP is normally inserted percutaneously into the femoral artery using a modified Seldinger technique, although the brachial and axillary arteries or an open surgical aortic approach can be used. The balloon catheter is advanced over a guidewire usually under fluoroscopic guidance to lie 2–3 cm distal to the left subclavian artery (Figure 2.1). If fluoroscopy is not available, the IABP position can be checked with a CXR or transoesophageal echocardiogram.
Proximal IABP malposition can result in left subclavian artery occlusion during balloon inflation, whilst a distally placed IABP can obstruct the renal arteries.
Once the IABP is secured in place, the patient can be nursed in the 30° head-up position but should not sit upright. Sitting may cause inward balloon migration, which increases the risk of aortic arch perforation and subclavian artery occlusion. Flexion of the leg in the sitting position may also kink the balloon, which can oppose adequate inflation.
To achieve optimal circulatory support, IABP counterpulsation is crucially dependent on synchronizing balloon inflation and deflation with the cardiac cycle. Balloon inflation should occur after aortic valve closure and deflation immediately before aortic valve opening. This can be accomplished by controlling the movement of gas between console and balloon in response to triggers from the patient’s ECG, arterial waveform, pacing spike, or at an internally preprogrammed rate.
The most commonly used trigger is the ECG. With this mode, balloon inflation occurs on the midpoint of the T-wave (diastolic onset), whilst deflation begins at the peak of the R-wave (systolic onset). Difficulties in synchronization may arise with this triggering source during tachyarrhythmias, CPR, or any setting where the ECG trace is poor. In such cases, arterial waveform triggering may be used instead.
When the arterial waveform is used as a trigger, balloon inflation occurs on the dicrotic notch, which corresponds to aortic valve closure. Deflation takes place immediately before the next arterial upstroke (aortic valve opening). More recently, balloon pumps have incorporated fibreoptic pressure sensors and flow algorithms to set inflation timing accurately for when aortic valve closure occurs.
An optimal arterial waveform should contain a sharp and pronounced ‘V-wave’ at the dicrotic notch, followed by a second augmented diastolic peak, which is ideally higher than the systolic pressure (Figure 2.2).
The initial augmentation ratio is usually set to 1:1 (every cardiac cycle receives augmentation). Lower ratios (1:2 or 1:3) are used to assess underlying cardiac function and aid balloon pump weaning.
The most common cause of inadequate balloon counterpulsation is failure to synchronize balloon inflation and deflation with the cardiac cycle. The IABP arterial waveform can be used to diagnose timing errors and assess response to manual adjustment.
When balloon inflation occurs early (before aortic valve closure), the left ventricular wall stress and myocardial oxygen demand increases. The arterial waveform shows augmentation prior to the dicrotic notch.
When balloon inflation is late (markedly after aortic valve closure), the augmentation of coronary perfusion is suboptimal. The arterial waveform shows a reduced diastolic augmentation commencing after the dicrotic notch in the absence of a sharp V-wave.
With early deflation (markedly before aortic valve opening), afterload reduction is suboptimal and retrograde coronary flow can potentially occur. The arterial waveform shows a pronounced reduction in pressure before late diastole.
Late deflation increases afterload and myocardial oxygen consumption. Essentially, the balloon remains inflated for too long, resulting in a widened appearance of the diastolic augmentation waveform, an impaired assisted aortic end-diastolic pressure, and a prolonged rate of rise of assisted systole.
Advances in technology have reduced the incidence of IABP-related morbidity and mortality in recent years.
The complications of IABP use are listed as follows.
• Limb ischaemia.
• Femoral artery thrombus.
• Peripheral embolization.
• Femoral vein cannulation.
• Arterial injury.
• AV fistula.
• False aneurysm.
• Visceral ischaemia.
• Compartment syndrome.
Limb ischaemia is the most common serious complication associated with IABP use and many patients receiving counterpulsation therapy already have pre-existing vascular risk factors. Regular monitoring of peripheral pulses, capillary refill, and limb temperature is advised. If there are any signs of ischaemia, the balloon pump must be removed.
Rapid balloon inflation and deflation causes trauma to red blood cells and platelets, which can lead to a haemolytic anaemia and thrombocytopenia.
There is also a risk of balloon surface thrombus formation and embolization (particularly at low augmentation rates), so most patients are anticoagulated with systemic heparin. This increases the risk of bleeding and development of heparin-induced thrombocytopenia.
Compartment syndrome presents as pain, swelling, and hardness of the calf. Treatment is urgent removal of the balloon with or without fasciotomy.
Balloon rupture with the potential for gas embolization is a rare complication but should be suspected if there is blood in the tubing and a loss of inflation pressure. Treatment is to turn the console off and remove the balloon pump.
Weaning and removal of the balloon pump
Weaning the balloon pump should be considered when relative haemodynamic stability has been attained and inotropic support is lowered. This is achieved gradually by reducing the augmentation frequency (up to 1:8) and/or lowering the balloon inflation volume (usually in 10–20% increments).
The balloon pump is usually removed once haemodynamic stability is established and systemic anticoagulation is normalized. The balloon is disconnected from the pump and then gently withdrawn and removed percutaneously. Direct pressure needs to be applied over the puncture site for at least 30 mins following removal. Pedal pulses should be confirmed by palpation or Doppler assessment and the patient should be monitored for bleeding and limb ischaemia.
Mechanical circulatory support of the heart has been possible for over half a century; however, owing to disappointing results in the critically ill, its use was largely limited to paediatric cardiorespiratory failure and longer-term cardiac support with ventricular assist devices. The emergence of respiratory extracorporeal membrane oxygenation (ECMO) as successful extracorporeal support for patients with severe acute respiratory failure due to the H1N1 pandemic has led to cardiac ECMO (also referred to as extracoporeal life support or ECLS) being revisited for adults. This chapter outlines the types of support available, and the indications/contraindications, in particular for acute circulatory support.
Indications for mechanical circulatory support
Use of mechanical circulatory support is indicated in patients with ventricular failure when cardiac output has fallen to a level such that other organ failure secondary to poor perfusion is likely to occur, despite maximal medical therapy. The most common causes of acute cardiac failure requiring circulatory support are acute myocardial ischaemia and cardiac surgery. In these circumstances, extracorporeal or percutaneous devices are used for short-term support to allow time for cardiac function to recover (‘bridge to recovery’) or for consideration of implantation of a longer-term device (‘bridge to bridge’). Medium-term (extracorporeal pulsatile) devices are usually used as a bridge to recovery or cardiac transplantation.
Long-term mechanical circulatory support
Cardiac assist devices are blood pumps that partially support or entirely replace the function of the left and/or right ventricle. A left ventricular assist device (LVAD) takes in blood from the left atrium or left ventricle and ejects it into the ascending or descending aorta. As a result, left ventricular preload is decreased and cardiac output increased, restoring organ perfusion. A right ventricular assist device (RVAD) takes blood from the right atrium and ejects it into the pulmonary artery. Some patients may require biventricular support using two VADs (BiVAD). Pumps can be implantable or paracorporeal and cannulation may be direct (via thoracotomy) or percutaneous. Pumps may produce pulsatile flow or continuous flow. Total artificial hearts that replace the heart completely are also available. Nearly all devices require patients to receive systemic anticoagulation.
Patients with slowly deteriorating chronic heart failure may be managed with long-term surgically implanted systems either as a bridge to recovery or transplantation, or, rarely, as permanent (‘destination’) therapy. In a randomized clinical trial of LVAD implantation versus medical therapy in 129 patients ineligible for cardiac transplantation, patients receiving an LVAD (HeartMate) survived longer and had better functional status (REMATCH study). In transplant candidates, those with an LVAD are more likely to survive until transplantation, and have non-inferior post-transplantation outcomes to patients who were not bridged with an LVAD.
Contraindications to implanted VAD support
• Contraindication to anticoagulation.
• Aortic regurgitation—greater than mild (for LVAD).
• Multiple organ failure.
• Interagency registry for mechanically assisted circulatory support (INTERMACS) I or II.
• Right ventricular dysfunction (for LVAD—consider BiVAD).
Types of pump
Blood is pumped by pneumatic or electric motor-driven compression of a blood reservoir. Prosthetic valves in the circuit prevent reverse flow. Pumps require adequate preload and afterload—stroke volume (SV) decreases with very high afterload unless drive line pressure is increased.
• Thoratec paracorporeal VAD (PVAD): extracorporeal single chamber (plastic sac) pump used for short- and medium-term support. A vacuum is used to enhance filling of the blood sac that is then compressed to produce an SV of 65 ml with total flows up to 6.5 l/min. Access cannulae contain mechanical one-way valves. Can be used as a long-term VAD.
• Abiomed BVS 5000 and AB5000: extracorporeal pumps with two blood chambers—a gravity-filled atrium and a pneumatically compressed ventricle. Two polyurethane valves are positioned within the pump. These pumps have been used extensively for temporary support for left, right, or both ventricles. The AB5000 can be used in the longer term as a bridge to transplantation or recovery.
• HeartMate LVAD: implantable long-term support for bridge to transplant, recovery, or destination therapy. Contains porcine valves and a pump surface that allows a cellular lining to develop and there is therefore less requirement for anticoagulation. Maximum SV is 85 ml.
• HeartMate XVE LVAD: similar to HeartMate but uses an electric motor rather than air to eject blood.
• Novacor LVAD: intracorporeal device that includes pusher plates to produce flow. Porcine valves are used in the cannulae. This device is only suitable for left ventricular support, but can be used in the long term.
No valves are included in circuits with these pumps and filling occurs by suction from the pump. Centrifugal pumps are used for short-term extracorporeal support and axial pumps are placed intracorporeally for longer-term ventricular assistance.
Centrifugal pumps accelerate bloodflow from the inlet at the centre of a rotating plate to the outflow at the periphery. These pumps (and axial impellers) are sensitive to changes in preload and afterload and therefore flow may vary considerably at the same pump revolutions per minute (rpm). They are used to provide temporary cardiac support. Pumps with bearings produce local heat that has been associated with an increased incidence of thrombotic complications.
• Medtronic Bio-pump (BioMedicus): extracorporeal centrifugal pump with bearings.
• CentriMag (Thoratec/Levitronix): a small extracorporeal pump, in which the impeller is rotated by a magnetic field, without bearings. Delivers up to 10 l/min, and can be used as an LVAD and/or an RVAD for up to 28 days.
Axial impeller pumps are smaller than other pumps and have a lower blood-contacting surface area than pulsatile pumps. All models require intracorporeal placement. Blood is pumped by a rotating screw or propeller. There has been considerable interest recently in using this type of pump for long-term ventricular support because of their smaller size and reduced risk of infection.
• Jarvik 2000: small axial pump, rotating at 8000–12000 rpm that is implanted into the apex of the left ventricle and ejects into the descending thoracic aorta, providing left ventricular support. It can be implanted using a left thoracotomy. Used for bridge to transplant but has also been used for destination therapy.
• MicroMed DeBakey and HeartMate II/III, Incor (Berlin Heart), HeartWare HVAD, Heart Assist 5 (Reliant): axial pumps implanted with inflow from the ventricle and outflow in the ascending aorta (LVAD) or pulmonary artery (RVAD).
Complications associated with VADs
Echocardiography (transthoracic and transoesophageal) is valuable in diagnosing and managing VAD-associated problems.
• Air embolus.
• Right ventricular failure—right ventricular dysfunction is common after LVAD implantation and up to 30% of patients may subsequently require RVAD support. Many patients will require inotropic support and pulmonary vasodilators.
• Cannula obstruction.
• Right-to-left shunting through patent foramen ovale (LVAD).
• Multiple organ failure.
Total artificial hearts
Although total artificial hearts (complete replacement of both ventricles) are not yet widely used, their potential advantages over LVADs include the absence of arrhythmias and the potential to manage patients with biventricular failure. Challenges exist, however, including removal of the atria, resulting in loss of atrial natriuretic peptide, with subsequent fluid retention and requirement for haemofiltration. Anticoagulation also remains a challenge in hearts with mechanical valves.
Catheter-based temporary assist devices
A number of assist devices that can be used without the need for a thoracotomy are available. These devices are for short-term support (<10 days) until recovery occurs or longer-term support is arranged. Indications for use include high-risk percutaneous coronary intervention and cardiogenic shock (INTERMACS I or II) of potentially reversible aetiology, either until cardiac function improves or as a bridge to surgical (long-term) LVAD implantation or to transplantation. Contraindications to insertion include right ventricular failure (biventricular support will be required), severe aortic stenosis (for axial flow pumps), and inadequate peripheral arterial vessels for device placement.
Axial flow pumps
The Impella (Abiomed) and HeartMate PHP (Thoratec) are catheter-mounted axial flow pumps that are passed from the femoral artery retrogradely across the aortic valve into the left ventricle. Blood enters the pump in the left ventricle and is ejected into the aorta. A number of different size Impellas are available, with the most commonly used being the 2.5 and 5.0. The LP2.5 (size 12F) is inserted percutaneously via the femoral artery and can pump up to 2.5 l/min. The larger LP5.0 requires insertion via femoral artery cut-down and can pump up to 5 l/min. The HeartMate PHP is inserted percutaneously via a 14F sheath and can pump over 4 l/min. Versions that can be placed during cardiac surgery are available. The Impella LD5.0 is placed through the ascending aorta into the left ventricle.
Right ventricular assist is also possible using the Impella RP device. With an inflow suction port placed surgically in the right atrium and outflow cannula in the pulmonary artery, the system can pump up to 5.5 l/min.
The Tandem Heart (Cardiac Assist) is an extracorporeal centrifugal pump. The inflow cannula is passed from the femoral vein into the left atrium via a transseptal puncture. The outflow cannula is placed via the femoral artery into the iliac artery. The system can pump up to 5 l/min and be used for up to 14 days. This makes it suitable for temporary support post-MI or postcardiac surgery. A right-sided option is available (Protek Duo), which also provides the opportunity to have an oxygenator in the circuit, thereby giving the potential for percutaneous cardiorespiratory support whilst avoiding full ECMO.
Percutaneous short-term VAD (pVAD) support is appealing because of the potential wider applicability of pumped circulatory support. A number of small randomized controlled trials comparing IABP with pVAD have been undertaken, all of which show improved haemodynamics but also an increase in bleeding complications, with no overall improvement in mortality when compared with IABP. With respect to right-sided support, a number of small, non-randomized studies have shown improved immediate and short-term haemodynamics; however, for all these devices, the longer-term benefits remain unclear.
ECMO for respiratory failure can usually be provided without the need for circulatory support (venovenous [VV]-ECMO) and is described in Chapter 1, ‘Extracorporeal membrane oxygenation (ECMO)’. Some patients may require combined circulatory and respiratory support, e.g. patients with pulmonary oedema because of severe left ventricular dysfunction. In these circumstances, temporary combined cardiac and pulmonary support can be achieved using venoarterial (VA)-ECMO. Blood is withdrawn from a right atrial or central venous cannula, pumped by an extracorporeal pump through an oxygenator, and returned into the aorta. Cannulae can usually be placed percutaneously. A centrifugal pump is often used in this situation.
Uses of VA-ECMO
• Neonatal respiratory distress syndrome (VV-ECMO is also used).
• Failure to wean from cardiopulmonary bypass.
• Cardiogenic shock (potentially reversible/transplant recipient).
• Heart failure (bridge to VAD/transplant).
• Acute respiratory distress syndrome with acute right ventricular failure (alternatively, right-sided support with oxygenator).
• Pulmonary embolism, pulmonary hypertension.
Mechanical circulatory support is likely to see technological advances in the coming years, particularly in the domains of miniaturization, efficiency, and automation. The anticoagulant properties of the prosthetic (blood interface) surfaces are likely to improve, reducing the thrombosis risk, and perhaps reducing the systemic anticoagulation required.
The cohort of patients in whom mechanical circulatory support is deemed appropriate is likely to increase, particularly as the potential harms and limitations of pharmacological therapies are better appreciated. This process is likely to be accelerated if VADs become more justifiable economically.
The role of VA-ECMO in the setting of cardiac arrest (both in-hospital and out-of-hospital), known as ‘ECPR’, is being investigated.
Targeted temperature management (TTM) is defined as an active therapy to achieve and maintain a specific target temperature for a defined duration. The chosen target temperature is usually in the range of 32–36°C and, for this reason, this treatment is also referred to as mild therapeutic hypothermia.
TTM is used to prevent or mitigate various types of neurological injury but is currently used most commonly in patients who remain comatose after initial resuscitation from cardiac arrest and in neonates at risk of hypoxic-ischaemic injury. Two randomized controlled trials published in 2002 showed improved neurological outcome among patients remaining comatose after resuscitation from VF/pVT cardiac arrest (mainly out-of-hospital) who were treated with mild (32–34°C) hypothermia compared with no temperature control. Some observational studies have shown an association between the use of mild hypothermia and improved outcome among patients with non-shockable initial rhythms (i.e. asystole or pulseless electrical activity) and after in-hospital cardiac arrest (IHCA), although a more recent observational study from the USA has shown an association between the use of mild therapeutic hypothermia and worse outcome after IHCA. The International Liaison Committee on Resuscitation recommends the use of TTM for selected patients who remain comatose following a witnessed cardiac arrest.
Two randomized clinical trials of therapeutic hypothermia (target 33°C) versus therapeutic normothermia (target 36.8°C) after out-of-hospital cardiac arrest (OHCA) and IHCA in children both failed to show significant improvement in functional outcome at 1 year with hypothermia. In the OHCA study, there were numerically more survivors with good functional outcome in the hypothermia group, leading some experts to criticize the study for being underpowered.
TTM has also been used for the treatment of severe traumatic brain injury, stroke, hepatic failure, ischaemic spinal cord injury, and MI. However, in none of these conditions has the use of TTM proven in high-quality randomized clinical trials to be beneficial.
Practical application of TTM
Following publication of the TTM randomized clinical trial, which showed no difference in survival when treating OHCA patients at a target temperature of 33°C or 36°C, clinicians have generally adopted either 33°C or 36°C as their preferred target temperature. The practical application of TTM is divided into three phases: induction, maintenance, and rewarming.
External and/or internal cooling techniques can be used to initiate and maintain TTM. If a target temperature of 36°C is chosen, for the many postcardiac arrest patients who arrive in hospital with a temperature less than 36°C it is best to let them rewarm spontaneously and to activate a temperature management device when they have reached 36°C. If a target temperature of 33°C is chosen, initial cooling is facilitated by neuromuscular blockade and sedation, which will prevent shivering. Magnesium sulfate, a naturally occurring N-methyl-D-aspartate (NMDA) receptor antagonist, that reduces the shivering threshold slightly, can also be given to reduce the shivering threshold. An infusion of 30 ml/kg of 4°C 0.9% saline or Hartmann’s solution will decrease core temperature by approximately 1.0–1.5°C but this technique should not be undertaken prehospital, where careful monitoring is difficult. In one prehospital randomized clinical trial this intervention was associated with increased pulmonary oedema (diagnosed on the initial CXR) and an increased rate of rearrest during transport to hospital.
The maintenance phase at 36°C is the same as for other target temperatures; shivering, for example, does not differ between patients treated at 33°C and 36°C. When using a target of 36°C, the rewarming phase will be shorter.
Methods of inducing and/or maintaining TTM include:
• Simple ice packs and/or wet towels—these methods are inexpensive but may be more time-consuming for nursing staff, may be associated with greater temperature fluctuations, and do not enable controlled rewarming. Ice-cold fluids alone cannot be used to maintain hypothermia but even the addition of simple ice packs may control the temperature adequately.
• Cooling blankets or pads.
• Water or air circulating blankets.
• Water circulating gel-coated pads.
• Oesophageal cooling.
• Transnasal evaporative cooling—this technique enables cooling before ROSC and is undergoing further investigation in a large randomized controlled trial.
• Intravascular heat exchanger, placed in the femoral or internal jugular veins.
• Extracorporeal circulation.
In the maintenance phase, a cooling method with effective temperature monitoring that avoids temperature fluctuations is preferred. This is best achieved with cooling systems that include continuous temperature feedback. The temperature is monitored from a thermistor placed in the bladder and/or oesophagus. There are no data indicating that any specific cooling technique increases survival when compared with any other cooling technique; however, intravascular devices enable more precise temperature control compared with external techniques.
Physiological effects and complications of hypothermia
Induction of hypothermia will lead to the activation of counter-regulatory mechanisms to decrease heat loss, including an increase in sympathetic tone, vasoconstriction of skin vessels, and shivering. Shivering increases oxygen consumption by 40–100% and is associated with increased risk of cardiac events; however, these observations have been made in the postoperative setting, where hypothermic patients are awake and have a high metabolic rate, increased oxygen consumption, a high heart rate, and a general stress-like response. These adverse events are linked to the haemodynamic and respiratory responses rather than to shivering per se, and the side-effects are largely absent in controlled hypothermia where patients are sedated, ventilated, and have low heart rates. However, shivering can generate significant amounts of heat and can significantly decrease cooling rates; for this and other reasons it should be aggressively treated (especially in the induction phase of cooling). Shivering responses are thought to decrease markedly when the temperature decreases below 33.5–34.0°C, although in the TTM trial the incidence of shivering was similar at a target temperature of 33°C and 36°C. The occurrence of shivering in cardiac arrest survivors who undergo mild induced hypothermia is associated with a good neurological outcome; it is a sign of a normal physiological response.
Mild induced hypothermia increases systemic vascular resistance and causes arrhythmias (usually bradycardia). The bradycardia caused by mild induced hypothermia may be beneficial (like the effect achieved by beta-blockers); it reduces diastolic dysfunction and is associated with good neurological outcome.
Mild induced hypothermia causes a diuresis and electrolyte abnormalities such as hypophosphataemia, hypokalaemia, hypomagnesaemia, and hypocalcaemia.
Hypothermia decreases insulin sensitivity and insulin secretion, and causes hyperglycaemia, which will need treatment with insulin.
Mild induced hypothermia impairs coagulation and may increase bleeding, although this effect seems to be negligible and has not been confirmed in clinical studies.
Hypothermia impairs the immune system and increases infection rates. Mild induced hypothermia is associated with an increased incidence of pneumonia; however, this seems to have no impact on outcome. An observational study documented a reduced incidence of pneumonia with the use of prophylactic antibiotics and, in another observational study, early use of antibiotics was associated with improved survival.
The serum amylase concentration is commonly increased during hypothermia but the significance of this is unclear.
The clearance of sedative drugs and neuromuscular blockers is reduced by up to 30% at a core temperature of 34°C.
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 owing to the immunosuppressive effects of hypothermia.
Treatment of hyperpyrexia
A period of hyperthermia (hyperpyrexia) is common in the first 48–72 h after cardiac arrest. Several studies have documented an association between postcardiac arrest pyrexia and poor outcomes. The development of hyperthermia after a period of mild induced hypothermia (rebound hyperthermia) is associated with increased mortality and worse neurological outcome. There are no randomized controlled trials evaluating the effect of the treatment of pyrexia (defined as ≥37.6°C) compared to no temperature control in patients after cardiac arrest, and the elevated temperature may only be an effect of a more severely injured brain.
Although when treating the postcardiac arrest patient the target temperature is typically maintained for 24 h, many intensive care clinicians will keep using temperature control systems to ensure normothermia for up to 72 h post-ROSC or until the patient awakens if less than 72 h.
The TTM2 study will compare a target temperature of 33°C with treatment of pyrexia only (triggered at a threshold of 37.8°C and then targeted at 37.5°C). Maintaining controlled normothermia may be just as difficult as maintaining controlled hypothermia because the shivering response is normally maximal in the range of 36–37°C but the set point is elevated in patients with fever.
Antipyretic drugs such as paracetamol can be used as adjunctive treatment to lower temperature. A major advantage is that these drugs do not activate the shivering response. However, their effectiveness (especially in non-infectious fever) is relatively low; the average temperature decrease in patients treated with high doses of paracetamol is 0.1–0.7°C.
Many animal studies show benefit for mild hypothermia when it is used as part of a TTM treatment strategy after resuscitation from cardiac arrest. Although two randomized trials also showed improved neurological outcome with the use of mild hypothermia in comatose adults with ROSC after VF/pVT OHCA, by today’s standards these studies are of low quality. The TTM trial has shown no difference between TTM with temperatures of either 33°C or 36°C, and two paediatric studies have shown no benefit with TTM versus controlled normothermia in OHCA and IHCA. Although TTM remains a standard of care for the treatment of adult comatose survivors of OHCA, the optimal target temperature is unknown.
Multiple choice questions and further reading
Interactive multiple choice questions to test your knowledge on this chapter and additional further reading can be found in Appendix Chapter 2 Multiple choice questions and further reading