INTENSIVE CARE

Cardiopulmonary resuscitation and post-resuscitation care

Jonathan Mackenney Jasmeet Soar

Learning objectives
After reading this article, you should be able to: C describe the recognition and treatment of cardiac arrest in adults according to current guidelines, understanding the importance of high-quality chest compressions and minimizing interruptions to chest compressions C describe a safe debrillation technique that includes a brief pause in chest compressions to conrm shockable rhythm, charging during chest compressions, and a brief pause in compressions for shock delivery C list post-cardiac arrest care interventions including the use of therapeutic hypothermia C understand the difculties of prognostication in comatose survivors of cardiac arrest

Abstract
Survival following cardiac arrest depends on early recognition and effective treatment with high-quality chest compressions with minimal interruption, ventilation, treatment of reversible causes, and debrillation if appropriate. Successfully resuscitated patients can develop a SIRS-like post-cardiac arrest syndrome. Post-cardiac arrest care includes coronary reperfusion, control of oxygenation and ventilation, circulatory support, glucose control, treatment of seizures, and therapeutic hypothermia. Prognostication in comatose survivors is challenging. Approximately one-third of cardiac arrest survivors admitted to intensive care are discharged home.

to hospital discharge. One-third of cardiac arrests survivors admitted to ICU are discharged from hospital and survival rates are improving. Most survivors have a good neurological outcome.

Keywords Asystole; cardiac arrest; cardiopulmonary resuscitation; debrillation; hypothermia; post-resuscitation care; pulseless electrical activity; ventricular brillation
Royal College of Anaesthetists CPD Matrix: 1B03, 1B04, 3C00.

The Chain of Survival

All four links in the Chain of Survival (Figure 1) must be strong to improve survival from cardiac arrest.

Early recognition and call for help

Recognition of the importance of chest pain and alerting the ambulance service can prevent out-of-hospital cardiac arrest. In the hospital, early identication of patients at risk of cardiac arrest using an early warning scoring system, alerting the resuscitation team or medical emergency team (MET), and appropriate treatment may prevent cardiac arrest. Here, we cover the issues following cardiac arrest.

Introduction
There are an estimated 50,000 cardiac arrests treated annually in the UK. Of these, about 60% occur out-of-hospital. Post-cardiac arrest patients who remain comatose after successful restoration of a spontaneous circulation (ROSC) account for one in 17 intensive care unit (ICU) admissions in the UK. Ventricular brillation (VF) or pulseless ventricular tachycardia (VT) is the presenting rhythm in most out-of-hospital cardiac arrests. Early debrillation is the effective treatment for VF/VT and each minute of delay decreases the chances of success by roughly 10%. Survival to hospital discharge after out-of-hospital cardiac arrest is 8e10%. The incidence of in-hospital cardiac arrest is about 1e5 per 1000 admissions. Survival is greatly increased if the rst rhythm recorded in cardiac arrest is shockable. In 80% of in-hospital cardiac arrests, however, the rst monitored rhythm is asystole or pulseless electrical activity (PEA). Approximately 15e20% of patients suffering in-hospital cardiac arrests survive

Cardiopulmonary resuscitation
Diagnosis of cardiac arrest Gasping (agonal breathing) after a sudden cardiac arrest (usually VF/VT) is common and can cause a delay in starting CPR. Rescuers should look for signs of life, including a pulse. If signs of life are absent or the rescuer is unsure, CPR should be started. In anaesthetized or intensive care unit (ICU) patients, the presence of monitoring will also help to make the diagnosis but should not cause delays in starting CPR. Chest compressions in a low cardiac output state are unlikely to be harmful. Chest compressions Chest compressions generate blood ow by increasing intrathoracic pressure and compressing the heart directly. At best, compressions achieve 25% of normal brain and myocardium perfusion. A higher coronary perfusion pressure (CPP aortic diastolic pressure e left ventricular end diastolic pressure) achieved during CPR is associated with improved ROSC. Each time chest compressions stop, the CPP decreases rapidly. On resuming

Jonathan Mackenney MRCP is a CT2 in ACCS Emergency Medicine in the Severn Deanery, UK. Conict of interest: none declared. Jasmeet Soar FRCA FFICM is a Consultant in Anaesthetics and Intensive Care Medicine at Southmead Hospital, North Bristol NHS Trust, UK. Conicts of interest: none declared.

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Figure 1 The chain of survival. CPR, cardiopulmonary resuscitation.

chest compressions, it takes time to achieve the same CPP that existed just before compressions were interrupted. Recent evidence points to the need for deeper chest compressions at a higher rate. The current recommended depth for chest compressions in an adult is 5e6 cm at a rate of 100e120 per minute. The compression to ventilation ratio is 30:2. Advanced life support (ALS) The ALS algorithm gives a standardized approach to cardiac arrest treatment (Figure 2). Airway and ventilation No specic airway and ventilation technique has been shown to improve cardiac arrest outcomes. Tracheal intubation by trained rescuers enables continuous chest compressions at 100e120 per minute without pauses for ventilations. Tracheal tube placement should be conrmed by auscultation of the chest during ventilation and waveform capnography. During effective CPR, there should be a carbon dioxide waveform. If no carbon dioxide is detected this should immediately raise the possibility of oesophageal intubation. Waveform capnography also provides a measure of CPR quality. High-quality CPR will increase end-tidal carbon dioxide, and ROSC is associated with a rapid increase in end-tidal carbon dioxide during CPR. The recommended ventilation rate is 10 per min as a higher rate decreases the CPP. Compared with bag-mask ventilation, early ventilation with a supraglottic device reduces the incidence of gastric distension and regurgitation. If a supraglottic airway (e.g. laryngeal mask airway, I-gel) has been inserted, attempt continuous chest compressions without stopping for ventilations. If excessive gas leakage results in inadequate ventilation of the patients lungs, interrupt chest compressions to enable ventilation.

event of a shockable rhythm, identify who will charge the debrillator and deliver the shock. Chest compressions should stop briey to analyse the ECG and conrm a shockable rhythm. Chest compressions should then immediately resume whilst the debrillator is charged. All other rescuers are instructed to stand clear and ensure no oxygen is owing across the chest (leave tracheal tubes or supraglottic devices attached to the breathing circuit or bag device). Once the debrillator is charged, the rescuer performing chest compressions also stands clear. The shock is delivered with no-one touching the patient. Chest compressions then immediately resume for a further 2 minutes. If there are delays due to difculties in rhythm analysis or rescuers still in contact with the patient, chest compressions should be resumed whilst another plan is made. Drugs Drug use during CPR is supported by very little evidence. Adrenaline (1 mg every 4e5 minutes) increases the CPP during CPR and is associated with improved ROSC. Recent observational studies suggest that adrenaline use may be associated with worse survival and neurological function at 1 month. Amiodarone (300 mg) given to patients in ventricular brillation (VF) refractory to debrillation attempts has only been shown to improve shortterm survival. Drug administration and attempts at intravenous access should not cause interruptions in chest compressions. The intra-osseous route should be used if intravenous access is not possible. The tracheal route is no longer recommended. Reversible causes Identify and treat reversible causes during CPR. These are divided into two groups of four based upon their initial letter e either H or T (Figure 2). Ultrasonography by trained rescuers whilst minimizing interruptions in CPR can help identify reversible causes (e.g. cardiac tamponade).

Debrillation
Debrillation creates a current across the myocardium to depolarize a critical mass of the cardiac muscle enabling natural cardiac pacemaker tissue to resume control. Every 5-second increase in the pre-shock pause (the interval between stopping CPR and shock delivery) halves the chance of successful debrillation. To minimize the pre-shock pause self-adhesive debrillation pads should be applied without stopping CPR. Before stopping chest compressions, the team should plan what to do if debrillation is appropriate including the importance of safety. Identify who will assess the electrocardiogram (ECG), and in the

Post-cardiac arrest care

Resuscitation from cardiac arrest triggers a systemic inammatory response syndrome (SIRS). This post-cardiac arrest syndrome consists of: (i) brain injury, (ii) myocardial dysfunction, (iii) systemic ischaemia/reperfusion response, and (iv) the precipitating disease that caused the cardiac arrest. A bundle of early post-cardiac arrest care using Airway, Breathing, Circulation, Disability, Exposure approach improves survival. The

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Resuscitation Council (UK)

ALS algorithm

Unresponsive? Not breathing or only occasional gasps Call resuscitation team

CPR 30:2 Attach defibrillator / monitor Minimize interruptions

Assess rhythm Shockable (VF / Pulseless VT) Non-shockable (PEA /Asystole)

1 Shock

Return of spontaneous circulation

Immediately resume CPR for 2 minutes Minimize interruptions

Immediate post-cardiac arrest treatment

Use ABCDE approach Controlled oxygenation and ventilation 12-lead ECG Treat precipitating cause Temperature control / therapeutic hypothermia

Immediately resume CPR for 2 minutes Minimize interruptions

During CPR
Ensure high-quality CPR: rate, depth, recoil Plan actions before interrupting CPR Give oxygen Consider advanced airway and capnography Continuous chest compressions when advanced airway in place Vascular access (intravenous, intraosseous) Give adrenaline every 35 minutes Correct reversible causes

Reversible causes
Hypoxia Hypovolaemia Hypo- /hyperkalaemia /metabolic Hypothermia Thrombosis - coronary or pulmonary Tamponade - cardiac Toxins Tension pneumothorax

Figure 2 Reproduced with permission from the Resuscitation Council (UK).

decision to admit a comatose post-cardiac arrest patient to ICU should be based predominantly on the patients status before the cardiac arrest. To optimize their chances of survival, patients resuscitated from cardiac arrest benet from admission to a designated cardiac arrest centre that offers both specialist ICU and cardiac catheter facilities. Airway and breathing Consider tracheal intubation, sedation and controlled ventilation in comatose patients after ROSC. Adjust oxygenation and ventilation to achieve normal arterial oxygen saturation (94e98%) and
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normocapnia. Hypocapnia, hypoxia and hyperoxia are all potentially harmful to the reperfused brain. Circulation Acute ST-segment elevation or new left bundle branch block on a 12-lead ECG and a typical history of acute myocardial infarction are indications for reperfusion therapy. Percutaneous coronary intervention (PCI) performed by an experienced team within 90 minutes of rst medical contact is the preferred technique for reperfusion. CPR is not a contraindication to thrombolysis if PCI is not available. About one-quarter of patients with primary

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cardiac arrest may have acute coronary artery occlusion despite no preceding chest pain and no acute ST elevation on a 12-lead ECG. Early PCI should therefore be considered for any cardiac arrest patient in whom an acute coronary syndrome is suspected. Haemodynamic instability caused by myocardial dysfunction is common after cardiac arrest and often resolves within 48 hours. Patients usually require large volumes of uid, inotropes and vasopressors to achieve haemodynamic stability. An intra-aortic balloon pump (IABP) can also provide mechanical assistance. Aim to maintain serum potassium at 4.0e4.5 mmol/litre and correct hypomagnesaemia. Patients resuscitated from VF cardiac arrest outside the context of treated coronary artery disease should be considered for an implantable cardioverter debrillator (ICD) before hospital discharge. Disability and exposure Cerebral hyperaemia immediately follows ROSC. This is followed 15e30 minutes later by global cerebral hypoperfusion. Normal cerebral autoregulation is lost, leaving cerebral perfusion dependent on mean arterial pressure (MAP). Hypotension can worsen any neurological injury. After ROSC, attempt to maintain the MAP at the patients usual level. Mild hypothermia suppresses many of the chemical reactions associated with reperfusion injury. Unconscious adult patients with spontaneous circulation after cardiac arrest should be cooled to 32e34 C. Cooling should be started as soon as possible and continued for at least 12e24 hours. Cooling can be rapidly induced by infusing 30 ml/kg of cold (4 C) crystalloid. There are numerous techniques to maintain hypothermia (e.g. surface, intravascular, intranasal cooling devices). Re-warm the patient slowly (0.25 C/hour) and avoid hyperthermia. The risk of a poor neurological outcome increases for each degree of body temperature over 37 C. Seizures and, or myoclonus occur in 5e15% of conscious patients after ROSC and 10e40% of comatose patients. Prolonged seizures are associated with a fourfold increase in mortality and should be rapidly controlled. Treat with benzodiazepines, phenytoin, propofol, or a barbiturate. Clonazepam is the treatment of choice for myoclonus. Alternative antimyoclonic drugs include sodium valproate, levetiracetam and propofol. Seizures or myoclonus are not always related to a poor prognosis: 17% of these patients survive with good neurological function. There have also been rare cases of good neurological recovery despite status myoclonus. Continuous electroencephalography monitoring should be used to detect seizures in patients receiving neuromuscular blocking drugs. Both a high and low blood glucose after ROSC is associated with a poor outcome. Aim to keep blood glucose between 4 and 10 mmol/litre. Prognostication Traditional markers of dismal prognosis at day 3 post-cardiac arrest are less reliable than previously thought, due to the use of therapeutic hypothermia. A signicant proportion of coma-

tose, cooled patients with a motor response to pain no better than extension at day 3 post-cardiac arrest later regain consciousness. Even absent brainstem reexes (pupillary response to light and corneal reexes) at day 3 can be unreliable. Hypothermia treatment and use of sedation can delay recovery of motor responses for 5e6 days after cardiac arrest. Reliable prognostication cannot be achieved until 3 days after return to normothermia and has to be multimodal. Prediction of a poor outcome should be based on at least two of the following: (i) incomplete recovery of brainstem reexes, (ii) myoclonus, (iii) an unreactive EEG, and (iv) absent cortical somatosensory evoked potentials (SSEPs). Unfortunately most ICUs do not have access to neurophysiology assessments.

Prognosis
In the UK, about one-third of ICU admissions after cardiac arrest survive to hospital discharge. Survival rates are improving but there is considerable variability between ICUs and regions. Most cardiac arrest survivors return home and have a good quality of life. Even those with good apparent survival can have neurocognitive and psychiatric problems. A

FURTHER READING Berdowski J, Berg RA, Tijssen JG, Koster RW. Global incidences of out-ofhospital cardiac arrest and survival rates: systematic review of 67 prospective studies. Resuscitation 2010; 81: 1479e87. Deakin CD, Nolan JP, Soar J, et al. European Resuscitation Council Guidelines for Resuscitation 2010. Section 4. Adult advanced life support. Resuscitation 2010; 81: 1305e52. Meaney PA, Nadkarni VM, Kern KB, et al. Rhythms and outcomes of adult in-hospital cardiac arrest. Crit Care Med 2010; 38: 101e8. Nolan JP, Laver SR, Welch CA, et al. Outcome following admission to UK intensive care units after cardiac arrest: a secondary analysis of the ICNARC Case Mix Programme Database. Anaesthesia 2007; 62: 1207e16. Nolan J, Soar J, Eikeland H. The chain of survival. Resuscitation 2006; 71: 270e1. Nolan JP, Soar J. Airway and ventilation techniques. Curr Opin Crit Care 2008; 14: 279e86. Nolan JP, Soar J, Zideman DA, et al. European Resuscitation Council Guidelines for Resuscitation 2010 section 1. Executive summary. Resuscitation 2010; 81: 1219e76. Oddo M, Rossetti AO. Predicting neurological outcome after cardiac arrest. Curr Opin Crit Care 2011; 17: 254e9. Zia A, Kern KB. Management of post cardiac arrest myocardial dysfunction. Curr Opin Crit Care 2011; 17: 241e6.

USEFUL WEBSITES European Resuscitation Council, www.erc.edu (accessed 5 May 2012). International Liaison Committee on Resuscitation, http://www.ilcor.org (accessed 5 May 2012). Resuscitation Council UK, www.resus.org.uk (accessed 5 May 2012).

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