End tidal CO2 in cardiac arrest

Measuring end-tidal CO2 in cardiac arrest patients is helpful for

  1. confirming tracheal tube placement
  2. assessing the effectiveness of chest compressions
  3. predicting likelihood of return of spontaneous circulation (ROSC), in that a persistently low ETCO2 tends to predict death, whereas a high or rising ETCO2 is associated with a higher chance of ROSC.

It may be however that its predictive ability depends on the type of cardiac arrest, and how far into the resuscitation you’ve got when you measure the ETCO2. Consider this new study from Slovenian pre-hospital emergency physicians:

Methods: The study included two cohorts of patients: cardiac arrest due to asphyxia with initial rhythm asystole or pulseless electrical activity (PEA), and cardiac arrest due to arrhythmia with initial rhythm VF or pulseless VT. The causes of asphyxia were: asthma, severe acute respiratory failure, tumor of the airway, suicide by hanging, acute intoxication, pneumonia and a foreign body in the airway.PetCO2 was measured for both groups immediately after intubation and repeatedly every minute, both for patients with or without return of spontaneous circulation (ROSC). We compared the dynamic pattern of PetCO2 between groups. Resuscitation procedures were performed by an emergency medical team (emergency medical physician and two emergency medical technicians or registered nurses) in accordance with 2005 ERC Guideline

Results: Between June 2006 and June 2009 resuscitation was attempted in 325 patients and in this study we included 51 patients with asphyxial cardiac arrest and 63 patients with VF/VT cardiac arrest. The initial values of PetCO2 were significantly higher in the group with asphyxial cardiac arrest (6.74 ± 4.22 kilopascals (kPa) versus 4.51 ± 2.47 kPa; P = 0.004). In the group with asphyxial cardiac arrest, the initial values of PetCO2 did not show a significant difference when we compared patients with and without ROSC (6.96 ± 3.63 kPa versus 5.77 ± 4.64 kPa; P = 0.313). We confirmed significantly higher initial PetCO2 values for those with ROSC in the group with primary cardiac arrest (4.62 ± 2.46 kPa versus 3.29 ± 1.76 kPa; P = 0.041).

A significant difference in PetCO2 values for those with and without ROSC was achieved after five minutes of CPR in both groups (asphyxial arrest: 6.09 ± 2.63 kPa versus 4.47 ± 3.35 kPa; P = 0.006; primary arrest: 5.63 ± 2.01 kPa versus 4.26 ± 1.86; P = 0.015)

In mmHg, the PetCO2 values for those with and without ROSC after five minutes of CPR was: asphyxial arrest: 42.3 ± 20 mmHg versus 34 ± 25.5 mmHg; P = 0.006; primary arrest: 42.8 ± 15.3 mmHg versus 32.3 ± 14.1 mmHg; P = 0.015

Graphically, this difference in ROSC vs non-ROSC PetCO2 for both groups appeared to be even greater at ten minutes, with higher statistically significance (p<0.001), although the values of PetCO2 are not given in the paper.

In all patients with ROSC the initial PetCO2 was again higher than 1.33 kPa (10.1 mmHg).

Conclusions: The dynamic pattern of PetCO2 values during out-of-hospital CPR showed higher values of PetCO2 in the first two minutes of CPR in asphyxia, and a prognostic value of initial PetCO2 only in primary VF/VT cardiac arrest. A prognostic value of PetCO2 for ROSC was achieved after the fifth minute of CPR in both groups and remained present until final values. This difference seems to be a useful criterion in pre-hospital diagnostic procedures and attendance of cardiac arrest.

The authors summarise with the following key messages:

  • Initial values of PetCO2 are higher in asphyxial cardiac arrest than in primary cardiac arrest.
  • Initial values of PetCO2 in asphyxial cardiac arrest do not have a prognostic value for resuscitation outcome.
  • The prognostic value of PetCO2 for ROSC was achieved after the fifth minute of CPR in both groups and remained present until the final values.
  • The values of PetCO2 seem to be useful in differentiating the causes of cardiac arrest in a pre-hospital setting.

I think that last one’s a bit of a stretch. For me, this paper confirms that the longer you are into a cardiac arrest resuscitation, the worse news a low PetCO2 is. The lack of predictive value of initial PetCO2, particularly in the asphyxia group, is interesting but not surprising.

The dynamic pattern of end-tidal carbon dioxide during cardiopulmonary resuscitation: difference between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest
Critical Care 2011, 15:R13

UK children sedation guideline

Despite the huge number of articles in the literature on paediatric sedation, one still encounters acrimonious debates about the appropriateness of non-anaesthetists doing it. How refreshing then, to see that the UK’s National Institute for Health & Clinical Excellence (“NICE”) has tackled this subject and come up with some reasonable recommendations. I’ve as yet only read the summary, but some of the good things are:

  • No unachievable ‘two doctors present’ rule: ‘Two trained healthcare professionals should be available during sedation
  • Differentiating painless imaging from painful procedures
  • Monitoring standards that are appropriate for the age of child and depth of sedation (no mandatory blood pressure or ECG monitoring unless deep sedation; end-tidal capnography in deep sedation).
  • Acknowledgement of the special features of ketamine: ‘Ketamine is a dissociative agent: the state of dissociative sedation cannot be readily categorised as either moderate or deep sedation; the drug is considered to have a wide margin of safety.’
  • Recognition that specialists other than anaesthetists may have specialist sedation and airway skills

There are some rather conservative recommendations on fasting, although the wording of the guideline in my interpretation allows some flexibility if ketamine is used for an emergency procedure.

Sedation in children and young people
National Institute for Health & Clinical Excellence

Propofol and the heart

I don’t normally blog about animal studies, but on reading a review of recent(-ish) shock research I was interested in the following piece that describes the effect of diffrent induction agents on rat heart muscle:

Sedation is frequently necessary in patients with septic shock, and therefore Zausig and colleagues investigated the effects of dose-dependent effects of various induction agents (propofol, midazolam, s(+)-ketamine, methohexitone, etomidate) in a Langendorff heart preparation from rats rendered septic by CLP. Propofol exerted the most pronounced depressant effects on both the maximal systolic contraction and the minimal diastolic relaxation, and cardiac work. Furthermore, propofol only adversely deleteriously affected the myocardial oxygen supply- demand ratio. In contrast, s(+)-ketamine was associated with the best maintenance of cardiac function. Within the limits of the study – that is, the use of an ex vivo isolated organ model – the authors concluded that s(+)-ketamine may be an alternative to the comparably inert etomidate, the use of which is, however, limited due to its endocrine side effects.

Of course we should be cautious about extrapolating animal lab work to clinical practice, but this supports my position of vehement opposition to the injudicious use of propofol for RSI in critically ill patients!

Year in review 2009: Critical Care – shock
Critical Care 2010, 14:239 Full text

Pre-hospital therapeutic hypothermia

A Czech study demonstrated effective pre-hospital therapeutic cooling of post-cardiac arrest patients using fairly modest amounts of intravenous saline at 4°C: the administration of 12.6 ± 6.4 mL/kg (1,032 ± 546 mL) of 4°C normal saline led to a tympanic temperature decrease of 1.4 ± 0.8°C (from 36.2 ± 1.5 to 34.7 ± 1.4°C; P < 0.001) in 42.8 ± 19.6 minutes. No ice packs were applied.

Before other emergency medical services adopt this, it should be noted that all these patients were managed in the field by emergency physicians who administered sedatives and neuromuscular blockers. It’s a European thing.

Pre-hospital cooling of patients following cardiac arrest is effective using even low volumes of cold saline
Critical Care 2010, 14:R231 Full text

Prone ventilation in ARDS

Prone ventilation can improve refractory hypoxaemia in ARDS but its effects on mortality have not been impressive in some studies which may be underpowered or include patients with less severe hypoxaemia. An updated meta-analysis showed significantly reduced ICU mortality in the four recent studies that enrolled only patients with ARDS, as opposed to ARDS/ALI (odds ratio = 0.71; 95% confidence interval = 0.5 to 0.99; P = 0.048; number needed to treat = 11). There may also be benefit from a greater duration of prone positioning.

An updated study-level meta-analysis of randomised controlled trials on proning in ARDS and acute lung injury
Critical Care 2011, 15:R6 Full text

Extracorporeal CPR

Extracorporeal cardiopulmonary resuscitation (E-CPR) using extracorporeal membrane oxygenation (ECMO) support during inhospital cardiac arrest has been attempted to improve the outcome of cardiopulmonary resuscitation (CPR). A retrospective, single-center, observational study from Korea analysed a total of 406 adult patients with witnessed inhospital cardiac arrest receiving cardiopulmonary resuscitation for >10 mins.

How their system works: An ECMO cart was transported to the CPR site within 5–10 mins during the day and within 10–20 mins during the night shift. The decision to use E-CPR was dependent on the CPR team leader. Application of ECMO was usually considered under conditions of prolonged arrest (when there was no ROSC after 10–20 mins of CPR), recurrent arrest (when ROSC could not be maintained), or when the patient could not be expected to recover as a result of underlying severe left ventricular dysfunction or coronary artery disease despite a short CPR duration (end-stage heart failure requiring transplantation, left main coronary artery occlusion, etc)

The primary end point was a survival discharge with minimal neurologic impairment.

No. ECMO. I said ECMO.

85 patients underwent E-CPR and 321 underwent C- CPR. ECMO implantation was successful in 94.1% (80 of 85) in the E-CPR group, except for three cannulation failures and two ECMO flow failures. There was a signficantly greater proportion of patients with primary cardiac disease in the E-CPR group. Propensity score matching was used to balance the baseline characteristics and cardiopulmonary resuscitation variables that could potentially affect prognosis. In the matched population (n = 120), the survival discharge rate with minimal neurologic impairment in the extracorporeal cardiopulmonary resuscitation group was significantly higher than that in the conventional cardiopulmonary resuscitation group (odds ratio of mortality or significant neurologic deficit, 0.17; 95% confidence interval, 0.04-0.68; p = .012). In addition, there was a significant difference in the 6-month survival rates with minimal neurologic impairment (hazard ratio, 0.48; 95% confidence interval, 0.29-0.77; p = .003; p <.001 by stratified log-rank test). In the subgroup based on cardiac origin, extracorporeal cardiopulmonary resuscitation also showed benefits for survival discharge (odds ratio, 0.19; 95% confidence interval, 0.04-0.82; p = .026) and 6-month survival with minimal neurologic impairment (hazard ratio, 0.56; 95% confidence interval, 0.33-0.97; p = .038; p = .013 by stratified log-rank test).

The authors conclude that extracorporeal cardiopulmonary resuscitation showed a survival benefit over conventional cardiopulmonary resuscitation in patients who received cardiopulmonary resuscitation for >10 mins after witnessed inhospital arrest, especially in cases of cardiac origin. These results contrast with these recently published French findings in patients receiving ECMO after out-of-hospital cardiac arrest.

Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: A comparison with conventional cardiopulmonary resuscitation
Crit Care Med. 2011 Jan;39(1):1-7

Better outcomes with conventional CPR

A very large nationwide Japanese observational study examined outcomes in out-of-hospital cardiac arrest patients who received CPR from lay rescuers. They compared conventional CPR (with mouth-to-mouth and chest compressions) with compression-only CPR. Over 40 000 patients were included.

Conventional CPR was associated with better outcomes than chest compression only CPR, for both one month survival (adjusted odds ratio 1.17, 95% confidence interval 1.06 to 1.29) and neurologically favourable one month survival (1.17, 1.01 to 1.35). Neurologically favourable one month survival decreased with increasing age and with delays of up to 10 minutes in starting CPR for both conventional and chest compression only CPR. The benefit of conventional CPR over chest compression only CPR was significantly greater in younger people in non-cardiac cases (P=0.025) and with a delay in start of CPR after the event was witnessed in non-cardiac cases (P=0.015) and all cases combined (P=0.037).

The authors conclude that conventional CPR is associated with better outcomes than chest compression only CPR for selected patients with out of hospital cardiopulmonary arrest, such as those with arrests of non-cardiac origin and younger people, and people in whom there was delay in the start of CPR.

Outcomes of chest compression only CPR versus conventional CPR conducted by lay people in patients with out of hospital cardiopulmonary arrest witnessed by bystanders: nationwide population based observational study
BMJ 2011; 2011; 342:c7106 Full Text

Cervical spine guideline

The UK College of Emergency Medicine has produced guidelines on the management of cervical spine injury in the ED

Since I have a bit of a ‘thing’ about the obsession with cervical immobilisation, I’m reproducing here an excerpt from the guideline regarding this topic:

In 1998, Hauswald published retrospective data that compared the neurological outcomes of 334 patients with blunt traumatic cervical spinal injury who all had spinal immobilisation performed (New Mexico) with 120 patients with blunt traumatic cervical spinal injury that had no spinal immobilisation performed (Malaya). There was a non-significant increase in neurological disability in the immobilised group. Though this comparison is flawed, the author’s argument that any cord injury from blunt trauma occurs at the time of the impact, that subsequent movement is very unlikely to cause further damage, and that alert patient will develop a position of comfort with muscle spasm protecting the spine appears credible. It is widely accepted that it may be harmful for patients with pre-existing vertebral anatomical abnormalities eg ankylosing spondylitis to have their neck forced into an unnatural position and such patients usually have their neck supported in a position of comfort with or without a collar.

A Cochrane review updated in 2009 by Kwan et al concluded that in the absence of any randomised controlled trials the low incidence of unstable injuries of the cervical spine amongst those immobilised raised the possibility that immobilisation may be associated with a higher morbidity and mortality than non-immobilisation. In a recent literature review, Benger and Blackman concluded that alert, co-operative trauma patients do not require cervical spine immobilisation unless their conscious level deteriorates or they find short-term support of a collar helpful.

The evidence both for and against cervical spine immobilisation is weak. Although Hauswald’s study is intriguing, if we accept a 1-2% prevalence of unstable cervical spine injury following blunt trauma and hypothesise that 1 in 10 patients with unstable cervical spinal injuries would suffer a spinal cord injury as a consequence of non-immobilisation of their neck then only 1 in 500 -1,000 patients would be harmed as a result, which exceeds Hauswald’s study population. There is a need for large randomised multi-centre trials to determine the risk:benefit ratio of neck immobilisation. However, the current practice of cervical spine immobilisation has been so widely adopted and the consequence of causing or exacerbating a spinal injury so catastrophic that such trials may not be supported by ethical committees….Though evidence that the use of cervical collars prevents secondary injury is lacking, no evidence could be found to contradict this statement and it is, therefore, supported.

The guideline does not specify what exactly they mean by cervical spine immobilisation. Clinical practice ranges from one-piece hard or semi-rigid collars (eg. Stifneck) to more comfortable two-piece collars (eg. Philadelphia), tape and sandbags alone, or ‘triple immobilisation’ (collar, sandbags and tape). It is perhaps the obsessive adherence to the latter in the absence of a single piece of supportive evidence that I find bewildering.

Fortunately most Australian practice I’ve witnessed settles on a collar or manual immobilisation, with early application of a two-piece collar in those patients who require prolonged immobilisation.

The College guideline provides a helpful and pragmatic summary of the evidence to date and a digestible list of recommendations that could guide both departmental practice and postgraduat exam revision.

Guideline on the management of alert, adult patients with potential cervical spine injury in the Emergency Department
College of Emergency Medicine 2010 (PDF)