Resuscitation

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Resuscitation

INTRODUCTION

Without intervention, cardiac arrest may lead to permanent neurological injury after just three minutes. The interventions that contribute to a successful outcome after a cardiac arrest can be conceptualized as a chain – the Chain of Survival (Fig. 47.1).

The four links in this chain are:

This chapter includes some background to the epidemiology and the prevention of cardiac arrest. It details the principles of initiating CPR in-hospital, defibrillation, advanced life support (ALS), post-resuscitation care and potential modifications to ALS when cardiac arrest occurs intraoperatively.

EPIDEMIOLOGY

Ischaemic heart disease is the leading cause of death in the world. In Europe, sudden cardiac arrest is responsible for more than 60% of adult deaths from coronary heart disease. In Europe, the annual incidence of emergency medical services (EMS)-treated out-of-hospital cardiopulmonary arrest (OHCA) for all rhythms is 35 per 100 000 population. The annual incidence of EMS-treated ventricular fibrillation (VF) arrest is 17 per 100 000 and survival to hospital discharge is 10.7% for all-rhythm and 21.2% for VF cardiac arrest. There is some evidence that long-term survival rates after cardiac arrest are increasing. On initial heart rhythm analysis, about 25–35% of OHCA victims have VF, a percentage that has declined over the last 20 years. Immediate CPR can double or triple survival from VF OHCA. After VF OHCA, each minute of delay before defibrillation reduces the probability of survival to discharge by about 10%.

The incidence of in-hospital cardiac arrest is difficult to assess because it is influenced heavily by factors such as the criteria for hospital admission and implementation of a do-not-attempt-resuscitation (DNAR) policy. The reported incidence of in-hospital cardiac arrest is in the range of 1–5 per 1000 admissions. Data from the American Heart Association’s National Registry of CPR indicate that survival to hospital discharge after in-hospital cardiac arrest is 17.6% (all rhythms). The initial rhythm is VF or pulseless VT in 25% of cases and, of these, 37% survive to leave hospital; after pulseless electrical activity (PEA) or asystole, 11.5% survive to hospital discharge. Preliminary data from the United Kingdom National Cardiac Arrest Audit (NCAA), which includes all individuals receiving chest compressions and/or defibrillation and attended by the hospital-based resuscitation team (or equivalent) in response to a 2222 call, indicates that the survival to hospital discharge after all-rhythm cardiac arrest is 19.5%.

PREVENTION

Out of hospital, recognition of the importance of chest pain enables victims or bystanders to call the EMS and receive treatment that can prevent cardiac arrest.

Cardiac arrest in hospital patients in unmonitored ward areas is not usually a sudden unpredictable event; it is also not usually caused by primary cardiac disease. These patients often have slow and progressive physiological deterioration, involving hypoxaemia and hypotension that has been unnoticed by staff, or recognised but treated poorly. Many such patients have unmonitored arrests, and the underlying cardiac arrest rhythm is usually non-shockable; the preliminary NCAA data show that survival to hospital discharge for this group is just 7%.

Guidelines for Prevention of In-Hospital Cardiac Arrest (Resuscitation Council (UK))

1. Place critically ill patients, or those at risk of clinical deterioration, in areas where the level of care is matched to the level of patient sickness.

2. Monitor such patients regularly using simple vital sign observations (e.g. pulse, blood pressure, respiratory rate, conscious level, temperature and SpO2). Match the frequency and type of observations to the severity of illness of the patient.

3. Use an early warning score (EWS) system or ‘calling criteria’ to identify patients who are critically ill, at risk of clinical deterioration or cardiopulmonary arrest, or both.

4. Use a patient vital signs chart that encourages and permits the regular measurement and recording of vital signs and, where used, early warning scores.

5. Ensure that the hospital has a clear policy that requires a timely, appropriate, clinical response to deterioration in the patient’s clinical condition.

6. Introduce into each hospital a clearly identified response to critical illness. This will vary between sites, but may include an outreach service or resuscitation team (e.g. medical emergency team (MET)) capable of responding to acute clinical crises. This team should be alerted, using an early warning system, and the service must be available 24 hours a day.

7. Ensure that all clinical staff are trained in the recognition, monitoring, and management of the critically ill patient, and that they know their role in the rapid response system.

8. Empower staff to call for help when they identify a patient at risk of deterioration or cardiac arrest. Use a structured communication tool to ensure effective handover of information between staff (e.g. SBAR – Situation-Background-Assessment-Recommendation).

9. Agree a hospital do-not-attempt-resuscitation (DNAR) policy, based on current national guidance. Identify patients who do not wish to receive CPR and those for whom cardiopulmonary arrest is an anticipated terminal event for whom CPR would be inappropriate.

10. Audit all cardiac arrests, ‘false arrests’, unexpected deaths, and unanticipated intensive care unit admissions, using a common dataset. Audit the antecedents and clinical responses to these events. All hospitals should consider joining NCAA (http://www.resus.org.uk/pages/NCAA.htm).

CARDIOPULMONARY RESUSCITATION

The division between basic life support and advanced life support is arbitrary – the resuscitation process is a continuum. The keys steps are that cardiorespiratory arrest is recognized immediately, help is summoned, and CPR (chest compressions and ventilations) is started immediately and, if indicated, defibrillation attempted as soon as possible (ideally, within 3 min of collapse).

The sequence of actions and outcome depends on:

image Location – out-of-hospital versus in-hospital; witnessed versus unwitnessed; monitored versus unmonitored.

image Skills of the responders – in some public places staff may be trained in CPR and defibrillation. All healthcare professionals should be able to recognize cardiac arrest, call for help, and start resuscitation.

image Number of responders – single responders must ensure that help is coming. If other staff are nearby, several actions can be undertaken simultaneously.

image Equipment available – AEDs are available in some public places. In hospital, ideally, the equipment used for CPR (including defibrillators) and the layout of equipment and drugs should be standardized throughout the hospital. AEDs should be considered for clinical and non-clinical areas where staff do not have rhythm recognition skills or rarely need to use a defibrillator.

image Response system to cardiac arrest and medical emergencies – outside hospital the EMS should be summoned. In hospital, the resuscitation team can be a traditional cardiac arrest team (called when cardiac arrest is recognized) or a MET.

High-Quality CPR

The quality of chest compressions is often poor and, in particular, frequent and unnecessary interruptions often occur. Even short interruptions to chest compressions may compromise outcome. The correct hand position for chest compression is the middle of the lower half of the sternum. The recommended depth of compression is at 5–6 cm and the rate is 100–120 compressions min− 1. Allow the chest to recoil completely in between each compression. If available, use a prompt and/or feedback device to help ensure high-quality chest compressions. The person providing chest compressions should change about every 2 min, or earlier if unable to continue high-quality chest compressions. This change should be done with minimal interruption to compressions.

During CPR, perfusion of the brain and myocardium is, at best, 25% of normal; successful ROSC is more likely the higher the coronary perfusion pressure (CPP). Chest compressions increase the amplitude and the frequency of the VF waveform and increase the likelihood that attempted defibrillation will be successful. Pauses in chest compressions of just 10 seconds before shock delivery (pre-shock pause) reduce the chances of successful defibrillation. Frequent interruptions in chest compressions reduce survival from cardiac arrest: each time chest compressions are stopped the CPP decreases rapidly and takes time to be restored to the same level once the compressions are restarted.

ADVANCED LIFE SUPPORT

Arrhythmias associated with cardiac arrest are divided into two groups: shockable rhythms (VF/VT) and non-shockable rhythms (asystole and PEA). The principle difference in management is the need for attempted defibrillation in patients with VF/VT. Subsequent actions, including chest compression, airway management and ventilation, vascular access, injection of adrenaline, and the identification and correction of reversible factors, are common to both groups. The ALS algorithm (Fig. 47.3) provides a standardized approach to the management of adult patients in cardiac arrest.

Shockable Rhythms (VF/VT)

The first monitored rhythm is VF/VT in approximately 25% of cardiac arrests, both in or out of hospital. VF/VT will also occur at some stage during resuscitation in about 25% of cardiac arrests with an initial documented rhythm of asystole or PEA. Having confirmed cardiac arrest, help (including a defibrillator) is summoned and CPR initiated, beginning with chest compressions, with a compression:ventilation (CV) ratio of 30:2. When the defibrillator arrives, chest compressions are continued while applying self-adhesive pads. The rhythm is identified and treated according to the ALS algorithm.

Sequence of Actions

image If VF/VT is confirmed, charge the defibrillator while another rescuer continues chest compressions.

image Once the defibrillator is charged, pause the chest compressions, quickly ensure that all rescuers are clear of the patient and then give one shock. The person doing compressions, or another rescuer may deliver the shock. This sequence should be planned before stopping compressions.

image Resume chest compressions immediately (30:2) without reassessing the rhythm or feeling for a pulse.

image Continue CPR for 2 min, then pause briefly to check the monitor:

image On completion of CPR for 2 min, pause briefly to check the monitor:

image If intravascular (i.v./intraosseous) access has been obtained, give adrenaline 1 mg and amiodarone 300 mg once compressions have resumed. On completion of CPR for 2 min, pause briefly to check the monitor:

If an organized rhythm is seen during a 2-minute period of CPR, do not interrupt chest compressions to palpate a pulse unless the patient shows signs of life (this may include a sudden increase in end-tidal carbon dioxide [PECO2] if this is being monitored) suggesting ROSC. If there is any doubt about the existence of a pulse in the presence of an organized rhythm, resume CPR. If the patient has ROSC, begin post-resuscitation care.

Defibrillation Strategy

Single Versus Three-Shock Strategy: If defibrillation is attempted immediately after the onset of VF, it is unlikely that chest compressions will improve the already very high chance of ROSC associated with second or third shocks (i.e. myocardial levels of oxygen and adenosine triphosphate are likely to be adequate for the first minute or so). Thus, if VF/VT occurs during cardiac catheterization or in the early post-operative period after cardiac surgery (when chest compressions could disrupt vascular sutures), consider delivering up to three-stacked shocks before starting chest compressions. This three-shock strategy may also be considered for an initial, witnessed VF/VT cardiac arrest if the patient is already connected to a manual defibrillator – this situation will exist perioperatively if defibrillation pads were applied before induction of anaesthesia.

Non-Shockable Rhythms (PEA and Asystole)

Pulseless electrical activity (PEA) is defined as the absence of any palpable pulse in the presence of cardiac electrical activity that would be expected to produce a cardiac output. There may be some mechanical myocardial contractions that are too weak to produce a detectable pulse or blood pressure – this is sometimes described as ‘pseudo-PEA’. PEA may be caused by reversible conditions that can be treated if they are identified and corrected. A relative overdose of an induction drug is a well-recognized cause of intraoperative cardiac arrest.

Sequence of Actions for Asystole

Whenever a diagnosis of asystole is made, check the ECG carefully for the presence of P waves because the patient may respond to cardiac pacing when there is ventricular standstill with continuing P waves. There is no value in attempting to pace true asystole.

During CPR

During the treatment of persistent VF/VT or PEA/asystole, there should be an emphasis on giving good-quality chest compressions between defibrillation attempts, whilst recognizing and treating reversible causes (4 Hs and 4 Ts), and whilst obtaining a secure airway and intravascular access. Healthcare providers must practise efficient coordination between CPR and shock delivery. A shock is more likely to be successful if the pre-shock pause is short (less than 10 seconds).

Potentially Reversible Causes

Potential causes or aggravating factors for which specific treatment exists must be sought during any cardiac arrest (Table 47.1).

Minimize the risk of hypoxia by ensuring that the patient’s lungs are ventilated adequately with 100% oxygen.

Pulseless electrical activity caused by hypovolaemia is usually due to severe haemorrhage. Restore intravascular volume rapidly with fluid, coupled with urgent surgery to stop the haemorrhage.

Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia, and other metabolic disorders are detected by biochemical tests or suggested by the patient’s medical history, e.g. renal failure. A 12-lead ECG may be diagnostic. Intravenous calcium chloride is indicated in the presence of hyperkalaemia, hypocalcaemia, and calcium-channel-blocking drug overdose.

Suspect hypothermia in any drowning incident; use a low-reading thermometer.

A tension pneumothorax may be the primary cause of PEA and may follow attempts at central venous catheter insertion. Decompress rapidly by needle thoracocentesis or urgent thoracostomy, and then insert a chest drain.

Cardiac tamponade is difficult to diagnose because the typical signs of distended neck veins and hypotension are obscured by the arrest itself. Rapid transthoracic echocardiography with minimal interruption to chest compression can be used to identify a pericardial effusion. Cardiac arrest after penetrating chest trauma is highly suggestive of tamponade and is an indication for resuscitative thoracotomy.

In the absence of a specific history, the accidental or deliberate ingestion of therapeutic or toxic substances may be revealed only by laboratory investigations. Where available, the appropriate antidotes should be used, but most often treatment is supportive.

The commonest cause of thromboembolic or mechanical circulatory obstruction is massive pulmonary embolus. If cardiac arrest is likely to be caused by pulmonary embolism, consider giving a fibrinolytic drug immediately. Ongoing CPR is not a contraindication to fibrinolysis. Fibrinolytic drugs may take up to 90 min to be effective; give a fibrinolytic drug only if it is appropriate to continue CPR for this duration.

Use of Ultrasound Imaging During Advanced Life Support: Several studies have examined the use of ultrasound during cardiac arrest to detect potentially reversible causes. This imaging provides information that may help to identify reversible causes of cardiac arrest (e.g. cardiac tamponade, pulmonary embolism, ischaemia (regional wall motion abnormality), aortic dissection, hypovolaemia, pneumothorax). When ultrasound imaging and appropriately trained clinicians are available, use them to assist with assessment and treatment of potentially reversible causes of cardiac arrest. The integration of ultrasound into advanced life support requires considerable training to ensure that interruptions to chest compressions are minimized. A sub-xiphoid probe position has been recommended. Placement of the probe just before chest compressions are paused for a planned rhythm assessment enables a well-trained operator to obtain views within 10 seconds.

Resuscitation in the Operating Room

Patients in the operating room are normally monitored fully and there should be little delay in diagnosing cardiac arrest. High-risk patients will often have invasive arterial pressure monitoring, which is invaluable in the event of cardiac arrest. If cardiac arrest is considered a strong possibility, apply self-adhesive defibrillation patches before induction of anaesthesia.

Asystole and VF will be detected immediately but the onset of PEA might not be so obvious – loss of the pulse oximeter signal and end-tidal CO2 are good clues and should provoke a pulse check. If asystole occurs intraoperatively, stop any surgical activity likely to be causing excessive vagal activity – if this is the likely cause, give 0.5 mg atropine. Start CPR and immediately look for other reversible causes. The atropine dose can be repeated up to a total of 3 mg. A completely straight line suggests that a monitoring lead has become detached.

In the case of PEA, start CPR while looking quickly for reversible causes. Give fluid unless you are certain the intravascular volume is adequate. Stop giving the anaesthetic. While a vasopressor will be required, in these circumstances 1 mg of adrenaline may be excessive. Give a much smaller dose of adrenaline (e.g. 50–100 µg) or another vasopressor (e.g. metaraminol) initially; if this fails to restore the cardiac output, increase the dose.

Cardiac Arrest Caused by Local Anaesthetic

Systemic toxicity of local anaesthetics involves the central nervous system and the cardiovascular system and occurs when a bolus of local anaesthetic inadvertently enters the circulation, usually during regional anaesthesia. Severe agitation, loss of consciousness, with or without convulsions, sinus bradycardia, conduction blocks, asystole and ventricular tachyarrhythmias can all occur. Patients with cardiovascular collapse or cardiac arrest attributable to local anaesthetic toxicity should be treated with i.v. 20% lipid emulsion in addition to standard ALS. Guidelines for treatment with lipid emulsion have been produced by the Association of Anaesthetists of Great Britain and Ireland (http://www.aagbi.org): give an initial i.v. bolus of 20% lipid emulsion followed by an infusion at 15 mL kg− 1 h− 1; give up to three bolus doses of lipid at 5-minute intervals and continue the infusion until the patient is stable or has received up to a maximum of 12 mL kg− 1 of lipid emulsion.

Airway Management and Ventilation

There are no data supporting the routine use of any specific approach to airway management during cardiac arrest. The best technique depends on the precise circumstances of the cardiac arrest and the competence of the rescuer. During CPR with an unprotected airway, two ventilations are given after each sequence of 30 chest compressions. Once a tracheal tube or supraglottic airway device (SAD) has been inserted, the lungs are ventilated at a rate of about 10 breaths min− 1 and chest compressions continued without pausing during ventilation.

Several alternative airway devices have been considered for airway management during CPR for those not skilled in tracheal intubation or when attempted intubation fails. There are published studies on the use during CPR of the Combitube, the classic laryngeal mask airway (cLMA), the Laryngeal Tube (LT) and the i-gel, but none of these studies have been powered adequately to enable survival to be studied as a primary endpoint. Currently, the choice of these devices depends entirely on local preference.

Tracheal intubation should be attempted during cardiac arrest only by trained personnel, such as anaesthetists, who are able to carry out the procedure with a high level of skill and confidence. Prolonged attempts at tracheal intubation are harmful; the pause in chest compressions during this time will compromise coronary and cerebral perfusion. No intubation attempt should interrupt chest compressions for more than 10 seconds; if intubation is not achievable within these constraints, bag-mask ventilation is restarted.

Waveform capnography is the most sensitive and specific way to confirm and continuously monitor the position of a tracheal tube in victims of cardiac arrest and should supplement clinical assessment (auscultation and visualization of the tracheal tube passing between the vocal cords). There is concern that low pulmonary blood flow during CPR may not result in detectable exhaled carbon dioxide and that a correctly placed tracheal tube may then be removed in error. However, several studies have indicated that exhaled carbon dioxide is detected reliably during CPR, except after prolonged cardiac arrest (> 30 min) when pulmonary flow may be negligible. Existing portable monitors make capnographic initial confirmation and continuous monitoring of tracheal tube position feasible in almost all settings where intubation is performed, including out of hospital, emergency departments, and in-hospital locations.

Assisting the Circulation

Intravascular Access

Peripheral venous cannulation is quicker, easier to perform, and safer than attempting central venous access. Drugs injected peripherally must be followed by a flush of at least 20 mL of fluid. Any attempt at central venous line insertion must be achieved with minimal interruption to chest compressions. If i.v. access cannot be established within the first 2 min of resuscitation, consider gaining intraosseous (IO) access. Intraosseous delivery of resuscitation drugs will achieve adequate plasma concentrations.

Resuscitation drugs can also be given via a tracheal tube, but the plasma concentrations achieved using this route are very variable and generally considerably lower than those achieved by the i.v. or IO routes, particularly with adrenaline. Given the ease of gaining IO access and the lack of efficacy of tracheal drug administration, do not give drugs via the tracheal tube.

Drugs

Adrenaline: Despite the widespread use of adrenaline during resuscitation, and several studies involving vasopressin, there is no placebo-controlled study that shows that the routine use of any vasopressor at any stage during human cardiac arrest increases neurologically-intact survival to hospital discharge. A recent prospective, randomized trial of adrenaline versus placebo for out-of-hospital cardiac arrest has documented higher rates of ROSC with adrenaline for both shockable and non-shockable rhythms. The optimal dose of adrenaline is not known, and there are no data supporting the use of repeated doses. There are few data on the pharmacokinetics of adrenaline during CPR. The optimal duration of CPR and number of shocks that should be given before giving drugs is unknown. On the basis of expert consensus, for VF/VT, adrenaline is given after the third shock once chest compressions have resumed, and then repeated every 3–5 min during cardiac arrest (alternate cycles).

Anti-Arrhythmic Drugs: No anti-arrhythmic drug given during human cardiac arrest has been shown to increase survival to hospital discharge, although amiodarone has been shown to increase survival to hospital admission after shock-refractory VF/VT. Based on expert consensus, give amiodarone 300 mg by bolus injection (flushed with 20 mL of 0.9% sodium chloride or 5% dextrose) after the third shock. A further dose of 150 mg may be given for recurrent or refractory VF/VT, followed by an infusion of 900 mg over 24 h. Lidocaine 1 mg kg− 1 may be used as an alternative if amiodarone is not available, but do not give lidocaine if amiodarone has been given already.

Although the benefits of giving magnesium in known hypomagnesaemic states are recognized, the benefit of giving magnesium routinely during cardiac arrest is unproven. Give an initial i.v. dose of 2 g (= 8 mmol or 4 mL of 50% magnesium sulphate) for refractory VF if there is any suspicion of hypomagnesaemia (e.g. patients on potassium-losing diuretics); it may be repeated after 10–15 min. Other indications are: ventricular tachyarrhythmias in the presence of possible hypomagnesaemia; torsade de pointes VT; digoxin toxicity.

Bicarbonate: Cardiac arrest causes a combined respiratory and metabolic acidosis because pulmonary gas exchange ceases and cellular metabolism becomes anaerobic. The best treatment of acidaemia in cardiac arrest is chest compression; some additional benefit is gained by ventilation. During cardiac arrest, arterial blood gas values may be misleading and bear little relationship to the tissue acid–base state – analysis of central venous blood may provide a better estimation of tissue pH. Giving sodium bicarbonate routinely during cardiac arrest and CPR, or after ROSC, is not recommended. Give sodium bicarbonate 50 mmol if cardiac arrest is associated with hyperkalaemia or tricyclic antidepressant overdose. Repeat the dose according to the clinical condition of the patient and the results of repeated blood gas analysis.

Mechanical CPR

At best, standard manual CPR produces coronary and cerebral perfusion that is just 30% of normal. Several CPR techniques and devices may improve haemodynamics or short-term survival when used by well-trained providers in selected cases. However, the success of any technique or device depends on the education and training of the rescuers and on resources (including personnel).

PERI-ARREST ARRHYTHMIAS

Cardiac arrhythmias are common in the peri-arrest period and treatment algorithms for both tachycardia (Fig. 47.4) and bradycardia (Fig. 47.5) have been developed to enable the non-specialist to initiate treatment safely. In all cases, oxygen is given, an i.v. cannula is inserted and the patient is assessed for adverse signs. Whenever possible, record a 12-lead ECG; this will help determine the precise rhythm, either before treatment or retrospectively, if necessary with the help of an expert. Correct any electrolyte abnormalities.

The presence or absence of adverse signs or symptoms will dictate the appropriate treatment for most arrhythmias. The after adverse factors indicate that a patient is unstable because of the arrhythmia:

Depending on the nature of the underlying arrhythmia and clinical status of the patient, immediate treatments can be either electrical [cardioversion (tachyarrhythmias) or pacing (bradyarrhythmias)] or pharmacological. If the patient has adverse factors electrical therapy is likely to be appropriate. Drugs usually act more slowly and less reliably than electrical treatments and are usually the preferred treatment for the stable patient without adverse signs.

Tachycardias

If the patient is unstable and deteriorating, synchronized cardioversion is the treatment of choice. In patients with otherwise normal hearts, serious signs and symptoms are uncommon if the ventricular rate is < 150 min− 1. For a broad-complex tachycardia or atrial fibrillation, start with 120–150 J biphasic shock and increase in increments if this fails. Atrial flutter and regular narrow-complex tachycardia will often convert with lower energies: start with 70–120 J biphasic. If cardioversion fails to restore sinus rhythm, and the patient remains unstable, give amiodarone 300 mg i.v. over 10–20 min and re-attempt electrical cardioversion. The loading dose of amiodarone can be followed by an infusion of 900 mg over 24 hours.

The treatment for stable tachycardias is outlined in Figure 47.4. A regular broad-complex tachycardia is likely to be VT or a supraventricular rhythm with bundle branch block. In a stable patient, if there is uncertainty about the source of the arrhythmia, give adenosine.

Regular narrow-complex tachycardias include:

Vagal manoeuvres or adenosine will terminate almost all AVNRT or AVRT within seconds. Failure to terminate a regular narrow-complex tachycardia with adenosine suggests an atrial tachycardia such as atrial flutter. If adenosine is contraindicated, or fails to terminate a regular narrow complex tachycardia without demonstrating that it is atrial flutter, give a calcium-channel blocker, for example verapamil 2.5–5 mg i.v. over 2 min or diltiazem.

An irregular narrow-complex tachycardia is most likely to be AF or sometimes atrial flutter with variable AV conduction. If there are no adverse features, treatment options include:

In general, patients who have been in AF for more than 48 h should not be treated by cardioversion (electrical or chemical) until they have been fully anticoagulated for at least three weeks, or unless trans-oesophageal echocardiography has shown the absence of atrial thrombus. If cardioversion is required more urgently, give an i.v. bolus injection of heparin followed by a continuous infusion to maintain the activated partial thromboplastin time (APTT) at 1.5 to 2 times the reference control value.

If the aim is to control heart rate, the drugs of choice are beta-blockers, diltiazem (oral only in the UK), or verapamil. Digoxin and amiodarone may be used in patients with heart failure. Magnesium can also been used although the data supporting this are more limited.

If the duration of AF is less than 48 h and rhythm control is considered appropriate, electrical or chemical cardioversion may be attempted. Seek expert help and consider flecainide. Amiodarone may also be used but is less effective.

Bradycardia

If adverse signs are present, give i.v. atropine 500 µg, and, if necessary, repeat every 3–5 min to a total of 3 mg. In the intraoperative setting, stop any surgical activity likely to be causing vagal stimulation.

If treatment with atropine is ineffective, consider second line drugs. These include isoprenaline (5 µg min− 1 starting dose), adrenaline (2–10 µg min− 1) and dopamine (2–10 µg kg− 1 min− 1).

Transcutaneous pacing will be required if there is an inadequate response to drugs. Temporary transvenous pacing should be considered if there is a history of recent asystole; Mobitz type II AV block; complete (third-degree) heart block (especially with broad QRS or initial heart rate < 40 min− 1) or evidence of ventricular standstill of more than 3 seconds.

POST-RESUSCITATION CARE

The Post-Cardiac-Arrest Syndrome

The post-cardiac-arrest syndrome, which comprises post-cardiac-arrest brain injury, post-cardiac-arrest myocardial dysfunction, the systemic ischaemia/reperfusion response, and persistence of the precipitating pathology, often complicates the post-resuscitation phase. Post-cardiac-arrest brain injury manifests as coma, seizures, varying degrees of neurocognitive dysfunction and brain death. Post-cardiac-arrest brain injury may be exacerbated by microcirculatory failure, impaired autoregulation, hypercarbia, hyperoxia, pyrexia, hyperglycaemia and seizures. Significant myocardial dysfunction is common after cardiac arrest but typically recovers by 2–3 days. The whole body ischaemia/reperfusion that occurs with resuscitation from cardiac arrest activates immunological and coagulation pathways contributing to multiple organ failure and increasing the risk of infection. Thus, the post-cardiac-arrest syndrome has many features in common with sepsis, including intravascular volume depletion and vasodilation.

Airway and Breathing

Hypoxaemia and hypercarbia both increase the likelihood of a further cardiac arrest and may contribute to secondary brain injury. Several animal studies indicate that hyperoxaemia causes oxidative stress and harms post-ischaemic neurones. A clinical registry study documented that post-resuscitation hyperoxaemia was associated with worse outcome, compared with both normoxaemia and hypoxaemia. As soon as arterial blood oxygen saturation can be monitored reliably (by blood gas analysis and/or pulse oximetry), titrate the inspired oxygen concentration to maintain the arterial blood oxygen saturation in the range of 94–98%. Consider tracheal intubation, sedation and controlled ventilation in any patient with obtunded cerebral function. There are no data to support the targeting of a specific arterial PCO2 after resuscitation from cardiac arrest, but it is reasonable to adjust ventilation to achieve normocarbia and to monitor this using the end-tidal PCO2 and arterial blood gas values.

Disability (Optimizing Neurological Recovery)

Temperature Control

Therapeutic Hypothermia: Animal and human data indicate that mild hypothermia is neuroprotective and improves outcome after a period of global cerebral hypoxia-ischaemia. Cooling suppresses many of the pathways leading to delayed cell death, including apoptosis (programmed cell death). Hypothermia decreases the cerebral metabolic rate for oxygen by about 6% for each 1 °C reduction in temperature and this may reduce the release of excitatory amino acids and free radicals.

All studies of post-cardiac-arrest therapeutic hypothermia have included only patients in coma. There is good evidence supporting the use of induced hypothermia in comatose survivors of out-of-hospital cardiac arrest caused by VF and there is lower level evidence supporting cooling after cardiac arrest from non-shockable rhythms and after in-hospital cardiac arrest. Cooling should be started as soon as possible after ROSC (pre-ROSC cooling is being investigated) with the aim of maintaining temperature in the range of 32–34 °C for 24 h.

The practical application of therapeutic hypothermia is divided into three phases: induction, maintenance, and rewarming. External and/or internal cooling techniques can be used to initiate cooling. An infusion of 30 mL kg− 1 of 4 °C 0.9% sodium chloride or Hartmann’s solution decreases core temperature by approximately 1.5 °C and can easily be started prehospital. Other methods of inducing and/or maintaining hypothermia include: simple ice packs and/or wet towels; cooling blankets or pads; intranasal cooling; water or air circulating blankets; water circulating gel-coated pads; intravascular heat exchanger; and cardiopulmonary bypass.

In the maintenance phase, a cooling method with effective temperature monitoring that avoids temperature fluctuations is preferred. This is best achieved with external or internal cooling devices that include continuous temperature feedback to achieve a set target temperature. Plasma electrolyte concentrations, effective intravascular volume and metabolic rate can change rapidly during both cooling and rewarming. Control rewarming at 0.25–0.5 °C per hour.

Prognostication

Two thirds of those dying after admission to ICU after out-of-hospital cardiac arrest die from neurological injury. A quarter of those dying after admission to ICU after in-hospital cardiac arrest die from neurological injury. A means of predicting neurological outcome that can be applied to individual comatose patients is required. Many studies have focused on prediction of poor long term outcome (vegetative state or death), based on clinical or test findings that indicate irreversible brain injury, to enable clinicians to limit care or withdraw organ support. The implications of these prognostic tests are such that they should have 100% specificity or zero false positive rate, i.e. no individuals eventually have a ‘good’ long-term outcome despite the prediction of a poor outcome.

Impact of Therapeutic Hypothermia on Prognostication

There is inadequate evidence to recommend a specific approach to prognosticating poor outcome in post-cardiac-arrest patients treated with therapeutic hypothermia. There are no clinical neurological signs, neurophysiological studies, biomarkers, or imaging modalities that can predict neurological outcome reliably in the first 24 h after cardiac arrest. Potentially reliable prognosticators of poor outcome in patients treated with therapeutic hypothermia after cardiac arrest include bilateral absence of N20 peak on SSEP ≥ 24 h after cardiac arrest and the absence of both corneal and pupillary reflexes three or more days after cardiac arrest. Given the limited data, decisions to limit care should be based on the results of more than one prognostication tool (e.g. clinical examination and EEG). In most cases, treatment withdrawal decisions should be delayed until at least 3 days after return to normothermia.

DECISIONS RELATING TO CARDIOPULMONARY RESUSCITATION

It is essential to identify patients for whom cardiopulmonary arrest represents an anticipated terminal event and in whom CPR is inappropriate. All institutions should ensure that a clear and explicit resuscitation plan exists for all patients. For some patients this will involve a do-not-attempt-resuscitation (DNAR, also described as DNACPR) decision. National guidelines from the British Medical Association (BMA), Resuscitation Council (UK) and the Royal College of Nursing (RCN), and more recently from the General Medical Council, provide a framework for formulating local policy. The main messages from the BMA/RC(UK)/RCN guidance are:

image Decisions about CPR must be made on the basis of an individual assessment of each patient’s case.

image Advance care planning, including making decisions about CPR, is an important part of good clinical care for those at risk of cardiorespiratory arrest.

image Communication and the provision of information are essential parts of good quality care.

image It is not necessary to initiate discussion about CPR with a patient if there is no reason to believe that the patient is likely to suffer a cardiorespiratory arrest.

image Where no explicit decision has been made in advance there should be an initial presumption in favour of CPR.

image If CPR would not restart the heart and breathing, it should not be attempted.

image Where the expected benefit of attempted CPR may be outweighed by the burdens, the patient’s informed views are of paramount importance. If the patient lacks capacity, those close to the patient should be involved in discussions to explore the patient’s wishes, feelings, beliefs and values.

image If a patient with capacity refuses CPR, or a patient lacking capacity has a valid and applicable advance decision refusing CPR, this should be respected.

image A DNAR decision does not override clinical judgement in the unlikely event of a reversible cause of the patient’s respiratory or cardiac arrest that does not match the circumstances envisaged.

image DNAR decisions apply only to CPR and not to any other aspects of treatment.

DNAR Decisions in the Perioperative Period

General or regional anaesthesia may cause cardiovascular or respiratory instability that requires supportive treatment. Many routine interventions used during anaesthesia (for example tracheal intubation, mechanical ventilation or injection of vasoactive drugs) could be considered to be resuscitative measures. The AAGBI has produced guidance for managing DNAR decisions in the perioperative period. The anaesthetist and the surgeon should review DNAR decisions with the patient, or their representative if they lack capacity, as part of the consent process. The DNAR decision can be suspended, modified, or remain valid during the procedure. The DNAR management option would normally apply while the patient remains in the operating room and post anaesthetic care unit.

FURTHER READING

Association of Anaesthetists of Great Britain & Ireland, Do not attempt resuscitation (DNAR) decisions in the perioperative period. Available at http://www.aagbi.org/sites/default/files/dnar_09_0.pdf

British Medical Association, Resuscitation Council (UK) and Royal College of Nursing. Decisions relating to cardiopulmonary resuscitation, 2007. www.resus.org.uk

Deakin, C.D., Morrison, L.J., Morley, P.T., et al. Advanced life support chapter collaborators. Part 8. Advanced life support. International consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation. 2010;81(Suppl. 1):e93–e174.

Deakin, C.D., Nolan, J.P., Soar, J., et al. European resuscitation council guidelines for resuscitation 2010 Section 4. Adult advanced life support. Resuscitation. 2010;81:1305–1352.

General Medical Council Treatment and care towards the end of life: good practice in decision making. General Medical Council: London, 2010. isbn:978-0-901458-46-9, www.gmc-uk.org.

Nolan, J., Soar, J., Lockey, A., et al, Advanced life support, sixth ed. Resuscitation Council UK: London, 2011. isbn:978-1-903812-22-8.

Nolan, J.P. Resuscitation guidelines, 2010. Resuscitation Council (UK): London, 2010. isbn:978-1-903812-21-1, www.resus.org.uk.

Nolan, J.P., Hazinski, M.F., Billi, J.E., et al. Part 1. Executive summary. International consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation. 2010;81(Suppl. 1):e1–e25.

Nolan, J.P., Neumar, R.W., Adrie, C., et al. Post–cardiac arrest syndrome. Epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Resuscitation. 2008;79:350–379.

Nolan, J.P., Soar, J., Zideman, D.A., et al. Guidelines writing group. European Resuscitation Council Guidelines for Resuscitation 2010 Section 1. Executive summary. Resuscitation. 2010;81:1219–1276.

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