This topic has come up multiple times in the CICM second part exam, and will appear again and again.
The most important reference for this is the new ERC/ESICM guidelines from 2021, and (to a slightly lesser extent) the AHA post-cardiac arrest care guidelines from 2015.
The action of cooling a human body to 32 or so degrees has a series of untoward consequences, and is not to be taken lightly. However, the benefits may be considerable. Much of the strategies of supporting the post-arrest patient revolve around managing the consequences of hypothermia. Question 24 from the second paper of 2011 addresses these strategies in a "outline the important management principles" sort of way. The AHA, via the Circulation, have published a comprehensive set of guidelines for post-resuscitation care, which Australia has more or less adopted. These guidelines were the basis of this summary chapter. It has subsequently been updated to incorporate the 2021 ESC/ESICM material.
Supportive management, in brief summary:
Disability (.. or prevention thereof)
Fluids and renal function
Gastrointestinal and nutritional support
And now, the same material but with relentless detail:
There is a discrete series of events which takes place after circulation is restored.
First, there is the frantic hour or so organising some basic life support equipment, transferring the patient to the ICU, and ringing all the various specialties. During this time, one should really get started on cooling the patient. Some definitive management typically takes place to reverse and repair the pathological process which led to the arrest.
Then, there is the 24 hours of therapeutic temperature management, during which the patient is kept at some 32-36 degrees or so. Then comes the passive rewarming, and gradual wean of sedating infusions.
Once sedation and paralysis are wearing off, 72 hours post arrest, one can begin to think about prognostication.
One would like the measured PaO2 around 100mmHg. Not too low, not too high. Hyperoxia certainly seems to increase mortality (OR around 1.8). I wont even mention hypoxia. Normoxia is the clear winner. Even though that is a dog study I linked to, the outcome is clear- neurological recovery is better with 21% FiO2. The ESC recommend the oxygen saturation target be set to 94% if you have no
One does not wish to have an abnormal PaCO2, as studies have shown it to be harmful - specifically, in one prospective cohort the odds ratio of poor outcome was found to be in excess of 2. Both high CO2 and low CO2 were associated with a poor outcome (the poor outcome in this case would be a CPC grade of 3 or less).
The AHA recommends one targets a MAP of >65mmHg, and a SBP of >90mmHg. ESC want an SBP of 100mmg, because they had to be different. One may do this with vasopressors and inotropes if one feels that they are warranted, but here the European and American guidelines leave the intensivist unsteered towards any specific choice of drug or technique.
Not only is a high BSL on admission a negative prognostic indicator, it also continues to be harmful in the ensuing 24 hours. The AHA guidelines recommend you aim to keep the BSL between 8 and 10 mmol/L (ESC give 7.8-10 mmol/L as the range). NG feeding can commence during TTM, especially if one has decided to cool to only 36 degrees.
There will be lung injury. Not only is there likely to be pulmonary oedema and aspiration of stomach content; you will also have pulmonary contusions, broken ribs, chest wall bruising, and who knows what else. Mechanical ventilation is going to be required, and positive pressure will help with many of these problems.
Furthermore, the act of taking over the respiratory function with a machine improves the demands on the heart. A significant proportion of cardiac output is dedicated to the effort of respiration, and this proportion increases as the effort increases; it stands to reason that a mandatory mode of ventilator support will reduce the demands on the failing ventricle.
In spite of the presence of an ARDS-like respiratory failure, the AHA recommends that permissive hypercapnea be avoided, and that normal minute ventilation be maintained. They confirm that their is no unique ventilation strategy for post-arrest patients, and suggest routine respiratory support.
There is good evidence (discussed at length elsewhere) that mild therapeutic hypothermia or at least "temperature management) improves neurological recovery and mortality among comatose survivors of cardiac arrest. It is contraindicated for patients who are not comatose, and for patients in whom there is uncontrolled bleeding.
The AHA, in determining who gets hypothermia, suggests that it be offered to anybody who is not following verbal commands after cardiac arrest. Furthermore, though the good quality studies are predominantly in hemodynamically stable survivors of out-of-hospital VF arrest, the AHA recommends therapeutic hypothermia be offered to survivors of arrest from any cause, in or out of hospital.
Though the evidence for this is derived from studies of neurological outcomes among stroke patients, the AHA still recommends that hyperthermia be avoided in cardiac arrest survivors.
With the recent evidence come to light, even more emphasis has been placed on the careful control of temperature in the post-arrest setting.
Though these people are already unconscious, sedation has a role to play. Opiates may decrease shivering, for instance; general anaesthetics may reduce the risk of seizures. However, there is no data to recommend any one specific drug combination over another. In the setting of therapeutic hypothermia, one can fall back on raw pharmacokinetic data, and avoid benzodiazepines (as their clearance is decreased 100-fold at 32°).
The combination of propofol and remifentanil may be the most pharmacologically suitable combination, on these grounds. Neither AHA nor ESC guidelines try to teach intensivists to suck eggs here, but they do mention that we should preferentially use short-acting agents.
There is good evidence that the prevention of shivering decreases left ventricular workload. The 2013 AHA statement mentions neuromuscular blockade as a valid measure to control shivering, and cautions that it must be used for the shortest possible time, and weaned as soon as is practical. However, no studies are quoted.
In contrast, the older 2003 ILCOR statement makes a firm recommendation that sedation and neuromuscular blockade be used to control shivering. The argument is that in all of the trials of therapeutic hypothermia, sedation and neuromuscular blockade were used, and given the promising outcomes of those trials it would be reasonable to reproduce this technique.
This topic has come up in the CICM SAQs (Question 18 from the first paper of 2018) and therefore merits its own revision chapter. In summary, the old 2015 AHA recommendations were strongly in favour of coronary angiography in post-arrest patients if there was ECG evidence of STEMI. They were more ambiguous with regards to patients who were not haein ST elevation. The PROCAT registry from Paris confirms that among the STEMI patients, 96% had significant coronary artery lesions on angiography- which is not surprising. What was surprising was the incidence of these lesions among the non-STEMI crowd - 58% of those patients also had significant coronary artery lesions. Those patients did not have any ST segment elevation on their post-ROSC ECG. This suggests that cardiac arrest itself strongly suggests cardiac pathology when there is no other immediately obvious cause. However, this was not enough to push the AHA over the line and merit a recommendation. The ESC are more permissive here, recommending an angiogram be considered for anybody with "ECG evidence of myocardial ischaemia", i.e. no ST elevation but ECG changes and a high probability of coronary occlusion (eg. an unstable rhythm)
The AHA has nothing firm to recommend on these topics. Invariably, evidence is either of poor quality or altogether absent. All that can be said is that there is no data for or against the use of these therapies. But of course you are going to treat their arrhythmias, and you are going to maintain their organ perfusion with some mixture of fluids, vasopressors and inotropes. Just like everybody else does.
What is the point, one might ask. The inevitable result will be "globally reduced systolic function". Indeed, TTE has a significant role to play in the peri-arrest setting, where you might discover a massive PE or pericardial tamponade, and avert some sort of impending disaster. Thus, in the diagnosis of pericardial effusion and massive PE a TTE is critically important. Outside of these conditions I have not been able to find any studies which call specifically for TTE to answer some sort of critically important post-resuscitation question. However, all the guidelines recommend echocardiography as a part of the hemodynamic monitoring options, and suggest that early echo will "enable the extent of myocardial dysfunction to be quantiﬁed", implying that this is useful.
Of course, one can tailor one's inotropes more easily when one has confirmation of this "global dysfunction" rather than the vague impression that it is probably present.
The AHA strongly recommends an EEG as soon as practical after return of spontaneous circulation. This has nothing to do with prognostication. Seizures occur in 5-20% of comatose post-cardiac arrest patients, and if left untreated they will result in excitotoxicity and worsening neurological outcomes. Given that you just paralyzed your shivering hypothermic patient, you will not be able to detect these clinically.
However, once you have found seizures, you might be tempted to treat them, and here you will run into trouble. Anticonvulsant prophylaxis does not seem to improve neurological outcome. Additionally, reactive treatment of seizures in the post-cardiac arrest patient seems to be ineffective, as these seizures are refractory to traditional anticonvulsant agents. So, after strongly recommending an EEG, the AHA has nothing to offer to treat the seizures aside from standard management protocols for status epilepticus. The ESC, writing from the vantage point of 2021, recommended valproate or levitiractam to treat post-arrest seizures.
Having recently traumatised the heart with direct current and compressions, one might expect the typical biomarkers of myocardial injury to diminish in sensitivity. In other words, how do you discriminate between the troponin rise of a myocardial infarction, and the troponin rise of a defibrillator-fried myocardial contusion?
One study attempted to discern the usefulness of biomarkers in the post-arrest setting. CK was found to be "worthless" - they even use that word in the abstract. However, troponins at 12 hours post arrest (with a cut-off of 0.6 ng/ml, or 600 ng/L) had 96% sensitivity and 80% specificity for myocardial infarction.
This is pretty poor. Having to wait for 12 hours to develop the suspicion that you patient's arrest was precipitated by a heart attack is far from ideal. The role of serial troponins in the post-arrest patient is more likely to be useful in monitoring for reinfarction, rather than as a primary diagnostic measure.