Resuscitation

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 conceptualised as the ‘chain of survival’ ( Fig. 28.1 ). The four links in this chain are:

early recognition – to potentially enable prevention of cardiac arrest – and call for help;
early cardiopulmonary resuscitation (CPR);
early defibrillation; and
post-resuscitation care.

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.

Science and guidelines

The 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations summarises the current science underpinning CPR. The European Resuscitation Council and Resuscitation Council (UK) Guidelines for Resuscitation 2015 are derived from the 2015 consensus document and have been used as source material.

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–treated out-of-hospital cardiopulmonary arrest (OHCA) for all rhythms is 40 per 100,000 population; ventricular fibrillation (VF) arrest accounts for about one third of these. The incidence of VF is declining and has been reported most recently as 23% among treated arrests of cardiac cause. Survival to hospital discharge is 8%–10% for all rhythms and approximately 21%–27% for VF cardiac arrest. 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 (IHCA) is difficult to assess because it is influenced by factors such as the criteria for hospital admission and implementation of a ‘do not attempt cardiopulmonary resuscitation’ (DNACPR) policy. The reported incidence of IHCA 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 IHCA is 17.6% (all rhythms). There is some evidence that these survival rates are increasing. Data from the UK National Cardiac Arrest Audit (NCAA) show that survival to hospital discharge after IHCA is 18.4% (all rhythms). The initial rhythm is VF or pulseless ventricular tachycardia (VT) in 16.9% of cases, and 49% of these survive to leave hospital; after pulseless electrical activity (PEA) or asystole, 10.5% survive to hospital discharge. All these individuals received chest compressions, defibrillation, or both, and attendance by a resuscitation team. Many patients sustaining an IHCA have significant comorbidity, and strategies to prevent cardiac arrest are important.

Prevention

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

Cardiac arrest in hospital patients in unmonitored ward areas is not usually a sudden, unpredictable event 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.

Guidelines for the 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. HR, BP, respiratory rate, conscious level, temperature and S p o ₂ ). 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 among sites but may include an outreach service or resuscitation team (e.g. medical emergency team) capable of responding to acute clinical crises. This team should be alerted, using an early warning system, and the service must be available 24 h.
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. Situation-Background-Assessment-Recommendation or SBAR).
9.
Agree on a hospital DNACPR 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. Increasingly, DNACPR decisions are being incorporated into wider treatment plans such as the Recommended Summary Plan for Emergency Care and Treatment (ReSPECT) – also known in the United States as Physician Orders for Life-Sustaining Treatment. These focus more on what will be done for the patient rather than what will be withheld.
10.
Audit all cardiac arrests, false arrests, unexpected deaths and unanticipated ICU admissions using a common dataset. Audit the antecedents and clinical responses to these events. All hospitals should consider joining NCAA ( https://www.icnarc.org/Our-Audit/Audits/Ncaa/About ).

Cardiopulmonary resuscitation

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

Diagnosis of cardiac arrest

Many trained healthcare staff may not be able to assess a patient's breathing and pulse sufficiently reliably to confirm cardiac arrest. Agonal breathing is common in the early stages of cardiac arrest; it is a sign of cardiac arrest and should not be confused as being a sign of life or circulation. Agonal breathing can also occur during chest compressions as cerebral perfusion improves but is not indicative of a return of spontaneous circulation (ROSC). Delivering chest compressions to a patient with a beating heart is unlikely to cause harm.

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 5–6 cm and rate 100–120 compressions min ⁻¹ . The chest should be allowed to recoil completely in between each compression. If available, a prompt or a feedback device should be used 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.

Starting CPR in hospital

The sequence of actions for initiating CPR in hospital is shown in Fig. 28.2 .

Fig. 28.2, In-hospital resuscitation algorithm.

Advanced life support

Arrhythmias associated with cardiac arrest are divided into two groups: shockable rhythms (VF/pulseless VT); and non-shockable rhythms (asystole and PEA). The principle difference in management is the need for attempted defibrillation in patients with VF/pulseless VT. Subsequent actions, including chest compression, airway management, ventilation, vascular access, injection of adrenaline and the identification and correction of reversible factors, are common to both groups. The ALS algorithm ( Fig. 28.3 ) provides a standardised approach to the management of adult patients in cardiac arrest.

Shockable rhythms (VF/pulseless VT)

The first monitored rhythm is VF/pulseless VT in approximately 25% of cardiac arrests, both in or out of hospital. Ventricular fibrillation/pulseless 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 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

If VF/pulseless VT is confirmed, charge the defibrillator while another rescuer continues chest compressions. Choose an energy setting of at least 150 J for the first shock and the same or a higher energy for subsequent shocks, or follow the manufacturer's guidance for the particular defibrillator.
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. This pause in chest compressions should be brief and no longer than 5 s.
Resume chest compressions immediately (CV ratio 30 : 2) without reassessing the rhythm or feeling for a pulse.
Continue CPR for 2 min, then pause briefly to check the monitor.
If VF/pulseless VT persists:
- Give a further (second) shock and, without reassessing the rhythm or feeling for a pulse, resume CPR (CV ratio 30 : 2) immediately after the shock, starting with chest compressions.
On completion of CPR for 2 min, pause briefly to check the monitor.
If VF/pulseless VT persists:
- Give a further (third) shock and, without reassessing the rhythm or feeling for a pulse, resume CPR (CV ratio 30 : 2) immediately after the shock, starting with chest compressions.
If 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 VF/pulseless VT persists:
- Give a further (fourth) shock; resume CPR immediately and continue for 2 min.
- Give adrenaline 1 mg with alternate cycles of CPR (i.e. approximately every 3–5 min).
If organised electrical activity is seen during this brief pause in compressions, seek evidence of ROSC (check for signs of life, a central pulse and end-tidal CO ₂ if available).
- If there is ROSC, start post-resuscitation care.
- If there are no signs of ROSC, continue CPR and switch to the non-shockable algorithm.
If asystole is seen, continue CPR and switch to the non-shockable algorithm.
If a rhythm compatible with a pulse is seen during a 2-min period of CPR, do not interrupt chest compressions to palpate a pulse unless the patient shows signs of life suggesting ROSC.
If there is any doubt about the existence of a pulse in the presence of an organised rhythm, resume CPR.
If the patient has ROSC, begin post-resuscitation care.

Precordial thump

A single precordial thump has a very low success rate for cardioversion and is only likely to succeed if given within the first few seconds of the onset of a shockable rhythm. There is more success with pulseless VT than with VF. Delivery of a precordial thump must not delay calling for help or accessing a defibrillator. It is reasonable to attempt a precordial thump if VF occurs intraoperatively, but do not delay the call for a defibrillator.

Witnessed and monitored VF/pulseless VT in the cardiac arrest

If a patient has a witnessed and monitored cardiac arrest in the catheter laboratory, coronary care unit (CCU) or critical care area or whilst monitored after cardiac surgery, and a manual defibrillator is rapidly available:

confirm cardiac arrest and shout for help;
if the initial rhythm is VF/pulseless VT, 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; and
start chest compressions and continue CPR for 2 min if the third shock is unsuccessful.

This three-shock strategy may also be considered for an initial, witnessed VF/pulseless VT cardiac arrest if the patient is already connected to a manual defibrillator (e.g. intraoperative cardiac arrest where defibrillation pads had been applied before the operation).

Non-shockable rhythms (PEA and asystole)

Pulseless electrical activity 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. Pulseless electrical activity 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-recognised cause of intraoperative cardiac arrest.

Sequence of actions for PEA and asystole

Start CPR (CV ratio 30 : 2) and inject adrenaline 1 mg as soon as i.v./intraosseous access is achieved.
Continue CPR (CV ratio 30 : 2) until the airway is secured, then continue chest compressions without pausing during ventilation.
Recheck the patient after 2 min.
If electrical activity compatible with a pulse is seen, check for a pulse and signs of life:
- If a pulse or signs of life are present, start post-resuscitation care.
- If no pulse or no signs of life are present (PEA or asystole):
  - Continue CPR.
  - Recheck the rhythm after 2 min and proceed accordingly.
  - Give further adrenaline 1 mg every 3–5 min (during alternate 2-min loops of CPR).
If VF/pulseless VT at rhythm check, change to the shockable rhythm algorithm.

During CPR

During the treatment of persistent VF/pulseless VT or PEA/asystole, there should be an emphasis on giving good-quality chest compressions between defibrillation attempts, whilst recognising and treating reversible causes ( Table 28.1 ) and whilst obtaining a secure airway and i.v./intraosseous 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 5 s).

Table 28.1

Reversible causes of cardiac arrest

4 Hs	4 Ts
Hypoxia	Tension pneumothorax
Hypovolaemia	Tamponade (cardiac)
Hypothermia	Toxic substances
Hyper-/hypokalaemia Hypocalcaemia Acidaemia Other metabolic disorders	Thromboembolism Pulmonary embolism Coronary thrombosis

Optimising the quality of cardiopulmonary resuscitation

Several defibrillator models incorporate CPR feedback systems. These comprise either a puck that is placed on the sternum or modified defibrillator patches, both of which incorporate an accelerometer that enables measurement of chest compression rate and depth. Measurement of the changes in chest impedance enable ventilation rate to be recorded. These modified defibrillators can provide audio feedback in real time, and downloaded data can be used for team debriefing after the event. Use of a CPR feedback device results in CPR performance that is closer to that specified in the guidelines, but this has yet to be shown to improve survival.

Potentially reversible causes

Potential causes or aggravating factors for which specific treatment exists must be sought during any cardiac arrest (see Table 28.1 ):

Minimise the risk of hypoxaemia 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 overdose of calcium channel blocking drugs.
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 CVC insertion. Decompress rapidly by needle thoracentesis or urgent thoracostomy, and then insert an intercostal 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 most common 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 ALS

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, 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 minimised.

A subxiphoid 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 s. Pseudo-PEA describes the echocardiographic detection of cardiac motion in the presence of a clinical diagnosis of PEA. The diagnosis of pseudo-PEA is important because it carries a better prognosis than true PEA and will influence treatment.

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 CO ₂ 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 and give atropine 0.5 mg. 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 i.v. fluids unless you are certain intravascular volume is adequate. Stop giving the anaesthetic. Although a vasopressor will be required, in these circumstances adrenaline 1 mg 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 in the prone position

Cardiac arrest in the prone position is rare but challenging. Risk factors include:

cardiac abnormalities in patients undergoing major spinal surgery;
hypovolaemia;
venous air embolism;
wound irrigation with hydrogen peroxide (no longer recommended); and
poor patient positioning with occluded venous return.

Consider applying self-adhesive defibrillation patches preoperatively to patients deemed at high risk from cardiac arrest. Chest compression in the prone position can be achieved with or without sternal counter-pressure.

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