Expert commentary by Douglas Chamberlain
A 50-year-old Asian male with a history of hypertension and hypercholesterolemia has become acutely unwell with central chest pain and shortness of breath whilst eating dinner at a nearby local restaurant. Bystander first aid had initially taken place but the patient has deteriorated to full cardiac arrest. The ambulance service is at the scene within 6 minutes and initiates advanced life support measures and obtains a return of spontaneous circulation.
They telephone the priority call for your department to receive this patient within the next few minutes. The 2 junior doctors on duty with you ask how the patient should best be managed both during and after the cardiac arrest.
See Box 2.1 for a clinical summary of cardiac arrest.
A key reason for the improvement in outcomes after cardiac arrest is based on improvements in each of the links of the resuscitation chain: community response, ambulance service, emergency department, intensive care specialist, and cardiologists.
The days of just thinking about advanced life support (ALS) protocols and the 4Hs and 4Ts are also numbered. For optimal management one must now need to think about another paradigm—the 8Cs; Choosing wisely on whom it is appropriate to perform CPR; Communication and Control (leadership) of the arrest; the importance of Compressions; Cutting the time between last compression and shocking; Cardiac echo during pulse check, Cooling post ROSC; considering Cardiac Catheterization and Critical care management by protocol. The importance of the 9th C—cardiac arrest centres—is up for debate.
It is essential to remember that no resuscitation drugs or advanced airway interventions have been shown to increase survival to hospital discharge. However, ‘basic skills’ of compressions and defibrillation have. The temptation to use ‘advanced skills’, whilst not worrying about the life-preserving ‘basic’ skills, must always be resisted.
The treatment options during ALS are limited. The recent updates however have further rationalized how, when and why we use the resources at hand:
• Delivery of drugs via a tracheal tube is no longer recommended—if intravenous access cannot be obtained, drugs should be delivered by the intra-osseous (IO) route. Drugs can be given just as quickly and serum levels established just as rapidly by IO compared to a central line.9
• Despite the lack of human data, the use of adrenaline is still recommended. This is based largely on animal data and increased short-term survival ROSC rates.10,11 No certainty exists as to the optimal dose of adrenaline or exactly when to give it; however, expert consensus recommends its use directly after the third shock and after every other shock thereafter, or if in pulseless electrical activity (PEA) then straight away and after every other 2-minute cycle. The theoretical risks of giving adrenaline even if there is a ROSC after the third shock are minimal compared to the theoretical benefits.
• Amiodarone should be given after the third shock and a further 150 mg if in refractory VF. It has been shown to improve short-term outcome of survival compared with placebo and Lignocaine in shock-resistant VF.12,13
• Routine administration of magnesium in cardiac arrest does not increase survival14 and it is not recommended unless Torsades de Pointes is suspected.
• Routine administration of sodium bicarbonate during cardiac arrest and CPR or after ROSC is also not recommended. However, if cardiac arrest is associated with hyperkalaemia or tricyclic antidepressant overdose then administration is warranted.
• Routine fibrinolysis is also not recommended,18 although consider fibrinolytic therapy when cardiac arrest is thought to be due to an acute pulmonary embolus; just make sure that you are prepared to do prolonged CPR after you have given fibrinolysis—for up to an hour.19,20
Intubation is often a moot point during arrests. It is accepted that this is the optimal oxygen delivery system but also that intubation should not interrupt compressions, something that it does frustratingly often.21 Common practice now exists that in the first couple of cycles intubation is deferred for risk of interfering with compressions. If there has been no ROSC within a couple of cycles, to then intubate, but by the most senior personnel available and only during the time needed for a pulse check. If unsuccessful or debatable whether the intubation was successful, then it is easier to go back to an ‘I-GEL’ supraglottic device and the patient oxygenated through that.
Clinical question: Does the quality of chest compressions affect the outcome of cardiac arrest?
The 2010 guidelines emphasize the key factors that improve chances of ROSC following a CA—good compressions and early defibrillation with minimal gap between CPR and defibrillation.2 Although this statement may sound simple, this inevitably requires the cocoordinating skills of an organized and focused team leader.
Good chest compressions generate a small but significant amount of blood flow to the brain and myocardium and increase the likelihood of successful defibrillation. When compressing the chest think about rate (aim for 100/min, with a 30:2 ratio for breaths), depth (at least 5 cm) and allow the chest to completely recoil;22,23 compressions should take the same amount of time as time for recoil.
The interposed abdominal compression technique uses compressions of the abdomen during relaxation phase of chest compressions to enhance venous return. However, there is conflicting evidence as to its benefit.24–26
Active compression–decompression CPR can also enhance venous return. It is a hand-held suction device that literally lifts the chest up during decompression. This creates a negative intrathoracic pressure during decompression and thus enhances venous return.27–30
Although the concept is promising, the reality is not as positive as the theory would suggest and results have been mixed. Some studies have shown improved haemodynamics,28–31 but these surrogate markers haven’t affected the clinical reality. A meta-analysis of 12 studies showed no improvement in outcomes using active compression–decompression vs standard CPR.33
The impedence threshold device should also theoretically improve outcome, and may therefore increase cardiac output. It is a valve that limits air entry into the lungs during active lung recoil between chest compressions. This decreased intrathoracic pressure increases venous return and thus may increase cardiac output. It is theoretically best used with an endotracheal tube, but it has been used with a face mask.34
Unfortunately a recent meta-analysis showed increased rates of ROSC but no improvement in rates of survival;35 the Resuscitation Council thus does not currently recommend it. However, a high-quality RCT showing the use of both impedance threshold device and active compression–decompression, showed potential benefits.36
There are manual devices to help with compressions. Mechanical chest compressors theoretically should increase survival, by increasing cardiac output. There are two main systems on the market: the LUCAS, a gas-driven sternal compressing device that incorporates a suction cap for active decompression and the Autopulse, a constricting band and backboard which pneumatically constricts the chest.
Animal models have shown improved haemodynamics and short-term survival using the LUCAS vs standard CPR,37,38 and also improved haemodynamics with the Autopulse.39–41 However, RCTs have not shown an overall survival benefit with the use of devices.42–45
But, for prolonged CPR (e.g. whilst going to the catheter lab) following hypothermic arrest, overdoses, and thrombolysis following CPR, as well as prolonged ambulance journeys—especially where compressions in a moving vehicle are difficult and less effective—the use of such devices may facilitate CPR and they are starting to be used more frequently.47
The key to survival is ‘simple’ compressions. If done properly, manual compressions can be effective and life-saving; do not use the excuse of not having a mechanical compressor in the case of poor quality compressions. Unfortunately, the quality of chest compressions during in-hospital CPR is frequently sub-optimal.48,49 To improve CPR quality during an arrest, it is imperative that metronomes are used to maintain the rate at 100/minute.50 Feedback devices should be also used to make sure depth and recoil are adequate.
Many studies have shown that by 2 mins, chest compressions lose some of their effectiveness because of rescuer fatigue.51 The role of the team leader is to ensure optimal compressions and that includes organizing the rotation of compressors.
Interruptions in external chest compression reduces the chances of successful defibrillation.52 Procedures such as intubation and quick-look echo,53 if required, should be done with the minimal interference in compressions and only done during the time needed for a pulse check. Even a 5–10 second delay will reduce the chances of the shock being successful.52,54,55
Although checking for safety is something that has been drummed into all of us, the risk of being hurt by a DC shock is negligible, especially if gloves are worn.56 The best way to reduce the pre-shock pause thus remains to compress whilst charging, preferably using manual mode defibrillation. The person doing compressions should do a safety check whilst charging, and then he/she should press the defibrillate button. It is an effective way to keep the pause to a minimum and if a shock is delivered, he/she has no-one else to blame!
After a shock, you must restart CPR straight away without waiting for a pulse check. Even if the defibrillation was successful, it takes time until the post-shock circulation is established and it is also very unusual to feel a pulse immediately after successful defibrillation. Compressing even if you do have a ROSC it is unlikely to do any harm.57–59 Not compressing whilst discussions continue and then realizing you do not have a ROSC will, however, cause harm so advice remains to go straight back to compressions after a shock.
The days of doing stacked shocks are long gone. Interruptions in external CPR reduce the chance of successful defibrillation60 and stacked shocks helped create that delay. There is evidence that the single-shock protocol increases survival61–63 so never be seduced by the temptation to administer more than one external shock.
Despite the panacea of advanced treatments, the multitudes of studies, and all the collected findings of resuscitation researchers, it is still the basics that improve survival; effective, interruption-free CPR and effective coordinated single-shock defibrillation.
Few realize how poorly basic life support is generally performed. The universal errors are shown in any analysis of electronic downloads. It is salutary for those who have performed resuscitation attempts to see subsequently how they have performed. All must realize, however, that the procedure, conceptually simple as it is, is very hard to perform well in real emergencies. The key points have already been highlighted, but a few points are worth stressing. Intubation can be useful if performed by someone skilled in the procedure, but unfortunately all too often this leads to excessive number of ventilations at the expense of compressions. Ideally, no pause in compressions should ever exceed 10 seconds, again hard to achieve. As mentioned, the pause between the last compression and shock delivery is of particular importance, and with the use of manual defibrillation (as opposed to automated) this can be less than 3 seconds. The value of adrenaline in cardiac arrest is currently a hot topic. A recent large meta-analysis showed no survival (to discharge) benefit, even though there were increased rates of ROSC and increased survival-to-hospital rates.64 Another observation study showed that adrenaline increased ROSC rates but caused a decrease in survival and survival with good neurological outcome.65 But counter to this, an observational study in the BMJ in 2014 showed that the earlier adrenaline was delivered the better the outcome.66 The conclusion is that we are not sure what to do! Use the latest Resuscitation Council guidelines but never let the use of drugs substitute the effectiveness of CPR and electricity.
No studies have shown that the use of echo improves the final outcome in cardiac arrest however it does help in ruling out reversible causes.67 A subxiphoid position for the probe used during a pulse check is the ideal way to perform an echo during cardiac arrest.68 The key is for the team leader to ensure that the use of echo does not interfere with compressions.
Lack of any cardiac motion is highly predictive of death,69–71 and so it may help in making the decision to stop in futile but emotionally charged, difficult circumstances. Paediatric cardiac arrest is inevitably one such occasion, and the use of an objective and visual marker such as echo can facilitate a timely and appropriate conclusion to resuscitation efforts.
In the pre-hospital environment, the patient has an uncomplicated supraglottic airway placed and an intra-osseous line inserted into his right humeral head. The pre-hospital tem perform 2 cycles of CPR on the shockable algorithm with 2 asynchronous shocks. A three-point pulse check reveals a palpable pulse but no significant respiratory effort. The patient is stabilized and brought into hospital, but shows no signs of waking up or ‘biting on the tube’ so ongoing ventilation continues with a bag-valve mask.
Clinical question: should we be performing therapeutic hypothermia on all patients post ROSC regardless of initial rhythm?
There are strong theoretical arguments for the beneficial effects of therapeutic hypothermia, especially if applied early or even during cardiac arrest. During cardiac arrest there is interruption of cerebral blood flow and a cascade of ischaemic insults. Once cardiac output is restored, reperfusion injury compounds the deleterious effects of the original ischaemia. Mild hypothermia reduces cerebral metabolic rate, and reduces production of cytotoxic chemicals and free radicals.74 Hypothermia also reduces cerebral blood flow during the reperfusion period thus decreasing the impact of the reperfusion injury.74 A period of hyperthermia (hyperpyrexia) is common in the first 48 hrs after cardiac arrest and several studies have shown an association between post-cardiac-arrest pyrexia and poor outcomes.72,73
Over the last few years there has been an increasing amount of research into therapeutic hypothermia. Evidence has shown the benefits of therapeutic hypothermia (at least compared to no temperature control which is different to normothermia). It has become the treatment modality of choice, with good evidence for arrests of VF/VT origin and poorer quality evidence for non-shockable initial rhythms. It should be noted that there is only evidence for therapeutic hypothermia in patients who remain obtunded following return of spontaneous circulation. Those who are starting to wake should not be put back to sleep so as to cool down the brain, but allowed to wake up ‘naturally’ on a high-dependency unit.
Prior to 2013, there have been four RCTs75–78 looking into therapeutic hypothermia post arrest of which one, the HACA trial75 was of a high quality. However, the pooled data in the three meta-analyses79–81 also showed an improved outcome with therapeutic hypothermia, with 6–7 patients treated per 1 survivor with a good quality of life.
Additionally, numerous observational studies82–97 have shown the effectiveness of the therapy in real life, and not just the efficacy in studies. A meta-analysis98 of these non-randomized data, including from PEA arrests, confirmed an odds ratio of 2.5 in favour of good neurological outcome after cooling. The registry data99–101 also confirmed similar survival rates to those presented in the published RCTs.
There is a paucity of high-quality evidence for hypothermia in the management of post-ROSC PEA / asystolic arrests, and no RCTs looking into this. However, there is some low-quality evidence based on non-randomized trials, observational studies, and registry data to argue that it should be used. Added to the biological plausibility of the treatment in this group of patients, it is reasonable to strongly consider treatment in selected individuals, especially those with short ROSC times.102
In 2013, a landmark study confused what we all thought we knew.103 There was no difference in outcome between patients cooled to 33 ̊C or 36 ̊C. Does this mean we should continue to cool to 33 ̊C or just cool between 33–36 ̊C? The jury is still out, but if the temperature is above 36 ̊C there is no question; make sure it is between 33–36 ̊C.
Evidence showing the correlation between time to start cooling and outcome is available, but this too is not of the best quality.104 However, until new evidence comes to light, current recommendations are to be initiating cooling in the ED if not started pre-hospital and that clinicians should be following the protocols of the two main studies that have been shown to improve outcome. In those studies75,–76 the cooling was pre-hospital or in the ED, where there was a median time of 105 mins from ROSC to commencement of cooling. Very few patients would get from ROSC to ITU in less than 105 mins and so it is imperative to start the cooling in the ED or earlier. However, a recent RCT showed no survival benefit in starting pre-hospital cooling with 2 litres of cold saline.105 The inference we should take from this isn’t that early cooling is ineffective, but that early cooling with 2 litres of normal saline is ineffective.
Although there have been excellent adoption rates of therapeutic hypothermia in ITU,106,107 in 2009/2010 a telephone survey showed only 35 % of EDs started therapeutic hypothermia in the ED (120) and of those 55 %would cool only for VF/VT. This is clearly an area that ED physicians should be looking at improving. It is easy to start cooling in the ED with the easiest ways being the use Ice bags placed around the major vessels, cold towels, and 30 ml/kg−1 of 4 ̊C saline or Hartmann’s. A lack of financial resources for equipment can thus not be a credible excuse for ignoring this treatment modality, and EDs need to give the optimal care in the resuscitation room and not wait till they get to ITU.
Most agree that hypothermia is an important treatment modality after out-of-hospital cardiac arrest, but many years are likely to pass before we learn how to use the treatment to maximum effect. Whilst its use after non-shockable rhythms has not been proven beyond doubt, most accept it and act accordingly. However, we do not know how important it is to cool pre-hospital nor indeed whether cooling should ideally be started intra-arrest. Teamwork is important so that if pre-hospital hypothermia has been initiated, it should be continued in hospital. We lack evidence on whether we should aim to reach target temperature quickly, which in any case is not possible with most methods in common use. We can, however, be reassured that using the various conventional methods do provide overall benefit even though they may not be optimal.
The ITU outreach team join you in the resuscitation room and agree to help to initiate the cooling measures required. Cooling packs are obtained and applied to the patient but the ITU team inform you that it will take at least an hour to free a bed in the critical care unit and request that you ‘optimize’ the patient as best as possible in the resus room setting.
Clinical question: What measures can be initiated in the post-ROSC phase to maximize the chance of return to baseline status?
Successful ROSC is not the end of the resuscitation process but just the start. Post-resuscitation care must start immediately post resuscitation (pre-hospital or in the ED) and not delayed till we get the patient into the intensive care. It is not fair on our patients to think that post-resuscitation care is the concern for the intensive care staff solely.
Some consider the post-cardiac arrest phase a syndrome comprising brain and myocardial dysfunction alongside a body-wide ischaemia/reperfusion injury. Generally the longer the down-time and the longer the duration of CPR, the worse the symptoms will be. Other factors exacerbate the symptoms; microcirculatory failure, impaired autoregulation, hypercarbia, hyperoxia, pyrexia, hyperglycaemia, and seizures. Minimizing these factors helps reduce the symptoms. Specific measures also improve outcome, such as therapeutic hypothermia. It must be remembered that in the first 48 hrs you cannot predict from initial neurology the final neurological outcome and so ongoing decisions with regard to whether the patient should go to ITU should not be based on initial neurological findings.
The post-arrest management proceeds along a step-by-step fashion. However alongside this, the appropriateness of post-arrest management to intensive care needs to be carefully assessed. If a 95-year-old with severe dementia from a nursing home has been brought in following a ‘successful’ post arrest, this does not mean that we need to continue inappropriate and undignified treatment. Extubation and tender loving care may well be in the patient’s best interest and what we should do. What is appropriate is a consideration of the rationale as to why he/she was resuscitated in the first place and make sure that appropriate community systems are in place to prevent inappropriate attempts at CPR. Not only is it inhumane for the patient, it can inadvertently deter staff from being enthused to perform appropriate resuscitation attempts.
However, if it is appropriate to manage a patient in the intensive care unit, then they should have the most up-to-date, evidence-based treatment available.
If the patient is actively pulling at the endotracheal tube in a coherent way and is waking up appropriately, then it is sensible to extubate and send to a high-dependency ward. Otherwise, a critical care management bundle started in the ED and continued in the intensive care department should be used.
Make sure the airway is secure, use CO2 monitoring and keep the patient sedated and initially muscle-blocked as required. Hypoxaemia and hypercarbia both can cause problems by increasing the likelihood of a further cardiac arrest and contributing to secondary brain injury. Clinical registry data has also shown an association between hyperoxaemia and poor outcome.108
As soon as a reliable saturation monitor is functioning, titrate the oxygen sats to 94–98 %. As soon as an arterial line has been placed aim for a normocapnia. This includes for transfer; the days of having an old-fashioned portable ventilator which only gives ‘air mix’ and ‘no air mix’ (100 % oxygen) must be resigned to the history books.
Once A and B are sorted, perform an ECG and aim to get the patient’s blood pressure to a reasonable MAP which can perfuse brain and kidney. Post cardiac arrest, it is common to get myocardial dysfunction leading to low blood pressure and, more importantly, reduced cardiac output. If management of arrhythmias and simple fluids has not improved things, then insertion of a CVP line in the resuscitation room along with appropriate use of vasoactive agents is what is required. If this fails, consider cardiology review for an aortic pump and angiography.109,110
If the ECG shows ST elevation, then it is commonly accepted that the patient should undergo early coronary angiography and percutaneous coronary intervention (PCI). However, it is known that a lack of chest pain and/or lack of ST elevation does not indicate that the patient has not had acute coronary occlusion.111 We must, therefore, ask the cardiologists to consider this intervention at the earliest possible opportunity in all post-cardiac-arrest patients who are suspected of having a cardiac arrest of cardiac origin, regardless of ECG findings.109–118
Recent guidelines say that all post-arrest patients of presumed cardiac origin should go immediately from the resuscitation room to the angiography suite. These guidelines have a good evidence base.119
There is no point to all this management if we produce patients with a poor quality of life. Therefore management interventions to preserve neurological function are of the highest priority. Seizures or myoclonus or both occur in 5–15 % of patients who achieve ROSC. Seizures show a threefold increase in cerebral metabolism and may cause cerebral injury; they therefore must be treated promptly with anti-epileptic medications. In practice this means adding in phenytoin and increasing the propafol infusion rate for comatosed intubated patients who are fitting.
Glucose control is very important. High blood glucose after resuscitation is associated with a poor neurological outcome. If BMs are high, start a sliding scale and aim for a blood glucose of ≤ 10 mmoll−1 (180 mgdl−1). However, too strict glucose control should not be implemented because of the increased risk of hypoglycaemia.121,122
Although none doubt the importance of good chest compressions, the details of post-resuscitation care are less well accepted and certainly poorly practised. The author has stressed measures that deserve careful attention from all in the field. The need for this is all too evident by comparing outcome ratios between hospitals for patients admitted with ROSC after an out-of-hospital cardiac arrest, but exactly the same considerations apply to those who arrest in hospital, especially if resuscitation was prolonged.
Post-resuscitation care is as essential as care during a cardiac arrest. It should start as soon as a pulse has been obtained and not wait until the patient is in the intensive care unit. The large variations of outcome need to be narrowed by routinely following post-arrest care bundles.
As a team leader awaiting a patient who has had a successful ROSC pre hospital, it is imperative that you plan for post-resuscitation care prior to the patient arriving. Arranging your team and planning for possible deteriorations is essential. The team leader should run through a checklist prior to the patient arriving so that all equipment is checked (including capnography) and all personnel know their role. Drugs should be readied to keep the patient sedated and ET tube secure (i.e. infusion of sedatives set up and neuromuscular junction blockers drawn up). Cooling equipment should be assembled and clear instructions given about whose role it is to start or continue this. Liaison with ITU and cardiologists should occur prior to the patient arriving.
How may the management of cardiac arrest and post-resuscitation care change?
When this type of question is asked people inevitably always look to new scientific advances. Greater improvements in outcome however may be achieved by focusing more on the areas that we know work, including improving community CPR and AED uptake as well as cardiac arrest prevention and appropriate post-arrest management and better education. In terms of education the future of improvement lies in learning from feedback of performance during the cardiac arrest and immediate aftermath, both of the technical quality of CPR and also the team dynamics.123 An ideal world would allow us to have a team debrief after every arrest where we watch real-time video and analyse areas of potential improvement.
There are of course future scientific developments that we may yet see.
The actual way we do CPR may change. At best, standard manual CPR produces coronary and cerebral perfusion that is just 30 % of normal. Although manual chest compressions are often performed very poorly,50, adjuncts to CPR have never consistently been shown to be superior to conventional manual CPR in RCTs.
However in 2011, Aufderheide et al.36 combined the use of a manual compressor and an impedance threshold device, a valve that limits air entry into the lungs during chest recoil thus decreasing intrathoracic pressure and increasing venous return to the heart. This showed an improvement—an odds ratio of 1.58 for the chances of survival with a good neurological outcome for all arrests of presumed cardiac origin.
A trial is currently underway into the role of cooling prior to obtaining ROSC124 using an intranasal cooling system. The results are due January 2016.
It may soon be possible to predict how likely there will be successful defibrillation from the fibrillation waveforms. This may mean that in the future shock/CPR protocols will be more fluid and adapt to the clinical picture.
The days are long gone when it is sufficient only to know the ALS protocols in order to be a team leader. The role must now include coordinating the team, adapting the management to the specific situation, using feedback devices to optimize care, and most importantly, making sure that the basics are performed proficiently: good compressions, early defibrillation with the briefest possible interval between CPR and shock, along with optimal post-arrest care. These measures are the core strategies to achieve the best possible survival rate from cardiac arrest.
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