Tag Archives: resuscitation

Still no cardiac arrest survival benefit from epinephrine?

A double blind randomised controlled trial showed significantly better rates of return of spontaneous circulation and hospital admission with the use of adrenaline (epinephrine) compared with placebo. This effect was observed with both shockable and non-shockable initial cardiac arrest rhythms. There was no statistically significant difference in the primary outcome of survival to hospital discharge.
Interesting but unfortunate political factors appear to have prevented recruitment to the required numbers of patients for this study so it is underpowered for its primary outcome of survival to hospital discharge, which in the adrenaline group was double that in the placebo group, although this did not reach statistical significance. What was supposed to be a multi-centre study became a single centre one and it was not possible to continue as the study drugs reached their expiry date and no additional funding was available.
So do ROSC and survival to admission matter? The authors make the following point:


While not the primary outcome of our study, ROSC is an increasingly important clinical endpoint as the influence of post resuscitation care interventions (i.e.: therapeutic hypothermia, managing underlying cause, organ perfusion and oxygenation) on survival to hospital discharge are recognised.

Optimum dose and timing of adrenaline remain unknown, along with whether it impacts on long-term outcomes.


BACKGROUND: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades. The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

METHODS: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score – CPC).

RESULTS: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR=3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR=2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

CONCLUSION: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Resuscitation. 2011 Sep;82(9):1138-43

Pre-hospital ECMO

Two cases are reported of the pre-hospital institution of venoarterial extracorporeal membrane oxygenation (ECMO) for patients in cardiac arrest. One was from France and the other from Germany – both countries with mature physician-staffed pre-hospital systems. The two cases were a 9 yr old drowning victim1 and a 48 year old marathon runner2. They each received BLS then ACLS then ECMO, and both went from asystole to sinus rhythm after the institution of ECMO. Sadly both failed to neurologically recover and died in hospital.
If irreversible anoxic encephalopathy could be detected in the field, patients could be better selected for this intervention. An editorialist3 states:


Until we have a hand held device which can measure neuronal integrity on a cellular level in the field we must use our best judgement, and in many cases give the patient the benefit of the doubt by cannulating them, cooling for 24 h and then making a neurological assessment and withdrawing ECLS if necessary.

Other issues to consider are:

  • Can society afford this level of intervention?
  • Could this intervention, when associated with brain death, result in sufficiently recovered organs for transplantation?
  • How can the infrastructure be created to enable rapid institution of pre-hospital ECMO?

I suspect as the equipment becomes even more portable and self-maintaining, pre-hospital / retrieval physicians already expert in critical care interventions such as seldinger-guided vascular access will be the ones instituting this therapy. In the meantime, we await evidence of outcome benefit and some objective means of case selection.
1. Out-of-hospital extracorporeal life support for cardiac arrest—A case report
Resuscitation. 2011 Sep;82(9):1243-5
2. Out-of-hospital extra-corporeal life support implantation during refractory cardiac arrest in a half-marathon runner
Resuscitation. 2011 Sep;82(9):1239-42
3. Community extracorporeal life support for cardiac arrest – When should it be used?
Resuscitation. 2011 Sep;82(9):1117

Mouth-to-nose breathing

Interesting – mouth to nose breathing was more effective than mouth-to-mouth in simulated resuscitations using anaesthetised, apnoeic patients:


BACKGROUND: The authors hypothesized that mouth ventilation by a resuscitator via the nasal route ensures a more patent airway and more effective ventilation than does ventilation via the oral route and therefore would be the optimal manner to ventilate adult patients in emergencies, such as during cardiopulmonary resuscitation. They tested the hypothesis by comparing the effectiveness of mouth-to-nose breathing (MNB) and mouth-to-mouth breathing (MMB) in anesthetized, apneic, adult subjects without muscle paralysis.

METHODS: Twenty subjects under general anesthesia randomly received MMB and MNB with their heads placed first in a neutral position and then an extended position. A single operator performed MNB and MMB at the target breathing rate of 10 breaths/min, inspiratory:expiratory ratio 1:2 and peak inspiratory airway pressure 24 cm H₂O. A plethysmograph was used to measure the amplitude change during MMB and MNB. The inspiratory and expiratory tidal volumes during MMB and MNB were calculated retrospectively using the calibration curve.

RESULTS: All data are presented as medians (interquartile ranges). The rates of effective ventilation (expired volume > estimated anatomic dead space) during MNB and MMB were 91.1% (42.4-100%) and 43.1% (42.5-100%) (P < 0.001), and expired tidal volume with MMB 130.5 ml (44.0-372.8 ml) was significantly lower than with MNB 324.5 ml (140.8-509.0 ml), regardless of the head position (P < 0.001).
CONCLUSIONS: Direct mouth ventilation delivered exclusively via the nose is significantly more effective than that delivered via the mouth in anesthetized, apneic adult subjects without muscle paralysis. Additional studies are needed to establish whether using this breathing technique during emergency situations will improve patient outcomes.

Effectiveness of breathing through nasal and oral routes in unconscious apneic adult human subjects: a prospective randomized crossover trial
Anesthesiology. 2011 Jul;115(1):129-35

Better than FFP in trauma?

Replacement of clotting factors in bleeding trauma patients seems to be of benefit, but are coagulation factor concentrates safer than fresh frozen plasma? This retrospective study suggests they might be; prospective studies are recommended.

INTRODUCTION: Clinical observations together with recent research highlighted the role of coagulopathy in acute trauma care and early aggressive treatment has been shown to reduce mortality.
METHODS: Datasets from severely injured and bleeding patients with established coagulopathy upon emergency room (ER) arrival from two retrospective trauma databases, (i) TR-DGU (Germany) and (ii) Innsbruck Trauma Databank/ITB (Austria), that had received two different strategies of coagulopathy management during initial resuscitation, (i) fresh frozen plasma (FFP) without coagulation factor concentrates, and (ii) coagulation factor concentrates (fibrinogen and/or prothrombin complex concentrates) without FFP, were compared for morbidity, mortality and transfusion requirements using a matched-pair analysis approach.
RESULTS: There were no major differences in basic characteristics and physiological variables upon ER admission between the two cohorts that were matched. ITB patients had received substantially less packed red blood cell (pRBC) concentrates within the first 6h after admission (median 1.0 (IQR(25-75) 0-3) vs 7.5 (IQR(25-75) 4-12) units; p
CONCLUSION: Although there was no difference in overall mortality between both groups, significant differences with regard to morbidity and need for allogenic transfusion provide a signal supporting the management of acute post-traumatic coagulopathy with coagulation factor concentrates rather than with traditional FFP transfusions. Prospective and randomised clinical trials with sufficient patient numbers based upon this strategy are advocated.

The impact of fresh frozen plasma vs coagulation factor concentrates on morbidity and mortality in trauma-associated haemorrhage and massive transfusion.
Injury. 2011 Jul;42(7):697-701

It's up to you….

Sometimes you have nothing to lose by doing a procedure that you may never have done before, if the patient is going to die or deteriorate without it.
In today’s competency-based-training-and-accreditation climate (a good thing), how does one achieve competence in a procedure that may be too rare to have even been seen, let alone practiced under supervision and formally assessed?
I spend a lot of time and energy trying to convince colleagues and trainees that there are situations where the benefit-harm equation is in favour of acting, despite reservations they may have about inadequate experience or training. These situations often require ‘surgical’ procedures. What they have in common is that they are all relatively simple to perform, but may save a life, a limb, or sight which otherwise may almost certainly be lost.
How best to train for these procedures, some of which may be too rare even for ‘see one, do one, teach one’ in an entire residency program? Simulators? Animal labs? Cadavers?

Slide from 'Making Things Happen' Course

In my view, the answer is to use the most high fidelity simulator in the universe – the human brain. It is those professionals who mentally rehearse the scenario and visualise the procedure over and over who are most likely to act when the patient needs it most. Several colleagues of mine over the years can recount incidents in which the indications for a thoracotomy or hysterotomy were present but they failed to act, talking themselves out of doing the procedure with a range of excuses from ‘I hadn’t had enough training’ to ‘No-one in the room wanted to do it’. Don’t be one of those! Get simulating now – you have all the equipment you need!

Ten steps to making it happen – be prepared
1. Pick a procedure (eg. thoracotomy)
2. Be ABSOLUTELY CLEAR on the indications – this helps remove any doubt when the time comes
3. Learn how to do it (talk to colleagues, read a book)
4. Know where the required equipment is kept
5. Start practicing in your mind – visualise seeing the patient, what you will say to your staff, where you will locate your equipment, what you will do procedurally step-by-step
6. Visualise possible outcomes and what your next steps would be (tamponade plus cardiac wound in a beating heart, tamponade plus wound plus VF, return of spontaneous circulation with bleeding from internal mammary arteries)
7. Read more and talk to more colleagues based on questions arising from your ‘simulations’
8. Travel, go on a course, get access to animal or cadaver labs if that’s an option in your setting
9. Speak to people who have done it in YOUR context (eg. for a resus room thoracotomy, talk to emergency physicians who have done it there, rather than a cardiothoracic surgeon who has only ever done them in the operating room)
10. Find an excuse on shift to talk about it to colleagues and rehearse the steps, locate the equipment, and so on. Remember: REPETITION IS THE MOTHER OF SKILL!

What’s on your list of life/limb/sight-saving procedures that can’t wait for someone else to do? Did I miss any? Should skull trephination be there? Comments welcome!

Prehospital resuscitative hysterotomy


My colleagues and I describe a tragic case in this month’s European Journal of Emergency Medicine1. Our physican-paramedic team was called to the home of a collapsed 38-week pregnant female who was in asystolic cardiac arrest. A peri-mortem caesarean delivery was performed by the physician in the patient’s home and the delivered newborn required intubation and chest compressions for bradycardia before resuming good colour and heart rate. Sadly there was ultimately a fatal outcome for both patients, but this case reminds us of the indications for this intervention and for emergency and pre-hospital physicians to be prepared to do it. A literature search yielded only one other reported prehospital case in recent medical literature2.

1.Prehospital resuscitative hysterotomy
Eur J Emerg Med. 2011 Aug;18(4):241-2
2.Out-of-hospital perimortem cesarean section
Prehosp Emerg Care. 1998 Jul-Sep;2(3):206-8

How much oxygen after ROSC?


I reported a previous JAMA publication demonstrating an association between hyperoxia and mortality in patients resuscitated post-cardiac arrest. The same authors have published furthur data to better define the relationship between supranormal oxygen tension and outcome in postresuscitation patients. They hypothesised that a linear dose-dependent relationship would be present in the association between supranormal oxygen tension and in-hospital mortality.

Background– Laboratory and recent clinical data suggest that hyperoxemia after resuscitation from cardiac arrest is harmful; however, it remains unclear if the risk of adverse outcome is a threshold effect at a specific supranormal oxygen tension, or is a dose-dependent association. We aimed to define the relationship between supranormal oxygen tension and outcome in postresuscitation patients.

Methods and Results– This was a multicenter cohort study using the Project IMPACT database (intensive care units at 120 US hospitals). Inclusion criteria were age >17 years, nontrauma, cardiopulmonary resuscitation preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained. We excluded patients with hypoxia or severe oxygenation impairment. We defined the exposure by the highest partial pressure of arterial oxygen (PaO(2)) over the first 24 hours in the ICU. The primary outcome measure was in-hospital mortality. We tested the association between PaO(2) (continuous variable) and mortality using multivariable logistic regression adjusted for patient-oriented covariates and potential hospital effects. Of 4459 patients, 54% died. The median postresuscitation PaO(2) was 231 (interquartile range 149 to 349) mm Hg. Over ascending ranges of oxygen tension, we found significant linear trends of increasing in-hospital mortality and decreasing survival as functionally independent. On multivariable analysis, a 100 mm Hg increase in PaO(2) was associated with a 24% increase in mortality risk (odds ratio 1.24 [95% confidence interval 1.18 to 1.31]. We observed no evidence supporting a single threshold for harm from supranormal oxygen tension.

Conclusion– In this large sample of postresuscitation patients, we found a dose-dependent association between supranormal oxygen tension and risk of in-hospital death.

Relationship Between Supranormal Oxygen Tension and Outcome After Resuscitation From Cardiac Arrest
Circulation. 2011 Jun 14;123(23):2717-2722
Australasian investigators provided the following critique of the original JAMA study:

Unfortunately, these investigators used only the first set of arterial blood gases in the ICU to assess oxygenation, excluded close to 30% of patients because of lack of arterial blood gas data and did not adjust for standard illness severity scores. Their conclusion that hyperoxia is a robust predictor of mortality in patients after resuscitation form cardiac arrest was therefore potentially affected by selection bias and by insufficient adjustment for major confounders. Thus, their results are of uncertain significance and require confirmation.

They undertook their own study of 12,108 patients:

INTRODUCTION: Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients.
METHODS: We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined ‘hyperoxia’ as PaO2 of 300 mmHg or greater, ‘hypoxia/poor O2 transfer’ as either PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen (FiO2 ) < 300, ‘normoxia’ as any value between hypoxia and hyperoxia and ‘isolated hypoxemia’ as PaO2 < 60 mmHg regardless of FiO2. Mortality at hospital discharge was the main outcome measure.

RESULTS: Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO2 < 60 mmHg). The hyperoxia group had higher mortality (754 (59%) of 1,285 patients; 95% confidence interval (95% CI), 56% to 61%) than the normoxia group (911 (47%) of 1,919 patients; 95% CI, 45% to 50%) with a proportional difference of 11% (95% CI, 8% to 15%), but not higher than the hypoxia group (5,303 (60%) of 8,904 patients; 95% CI, 59% to 61%). In a multivariable model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95% CI, 1.1 to 1.6). However, once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxemia, time period matching and hyperoxia defined as PaO2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21).

CONCLUSIONS: Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.

Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest.
Crit Care. 2011 Mar 8;15(2):R90. [Epub ahead of print]
Open Access Full Text
What’s the best approach in the light of these differing results? My approach is to avoid hypoxia, since that’s probably bad, and to actively avoid overoxygenating as part of my general neuroprotection checklist in a post-cardiac arrest patient. It would seem prudent to follow the recommendations of ILCOR, summarised by the European Resuscitation Council guidelines as:

Recognition of the potential harm caused by hyperoxaemia after ROSC is achieved: once ROSC has been established and the oxygen saturation of arterial blood (SaO2) can be monitored reliably (by pulse oximetry and/or arterial blood gas analysis), inspired oxygen is titrated to achieve a SaO2 of 94–98%

Paeds BVM for adult resuscitation

Three hand-ventilation systems were used in a simulated adult resuscitation to determine the delivered volumes. The mean minute ventilation delivered by each of the three devices investigated was significantly different, with the paediatric (500-ml) self-inflating bag producing the result most consistent with the guideline.

There is a discrepancy between resuscitation teaching and witnessed clinical practice. Furthermore, deleterious outcomes are associated with hyperventilation. We therefore conducted a manikin-based study of a simulated cardiac arrest to evaluate the ability of three ventilating devices to provide guideline-consistent ventilation. Mean (SD) minute ventilation was reduced with the paediatric self-inflating bag (7.0 (3.2) l.min(-1) ) compared with the Mapleson C system (9.8 (3.5) l.min(-1) ) and adult self-inflating bag (9.7 (4.2) l.min(-1) ; p = 0.003). Tidal volume was also lower with the paediatric self-inflating bag (391 (52) ml) compared with the others (582 (87) ml and 625 (103) ml, respectively; p < 0.001), as was peak airway pressure (14.5 (5.2) cmH(2) O vs 20.7 (9.0) cmH(2) O and 30.3 (11.4) cmH(2) O, respectively; p < 0.001). Participants hyperventilated patients' lungs in simulated cardiac arrest with all three devices. The paediatric self-inflating bag delivered the most guideline-consistent ventilation. Its use in adult cardiopulmonary resuscitation may ensure delivery of more guideline-consistent ventilation in patients with tracheal intubation.

Comparison of the Mapleson C system and adult and paediatric self-inflating bags for delivering guideline-consistent ventilation during simulated adult cardiopulmonary resuscitation
Anaesthesia. 2011 Jul;66(7):563-7

Normal heart and respiratory rates in children


A large review has established normal ranges of heart rate and respiratory rate in children from birth to 18 years of age. Some of the results differed markedly from some existing ranges quoted, such as in the Advanced Paediatric Life Support Course.

BACKGROUND: Although heart rate and respiratory rate in children are measured routinely in acute settings, current reference ranges are not based on evidence. We aimed to derive new centile charts for these vital signs and to compare these centiles with existing international ranges.

METHODS: We searched Medline, Embase, CINAHL, and reference lists for studies that reported heart rate or respiratory rate of healthy children between birth and 18 years of age. We used non-parametric kernel regression to create centile charts for heart rate and respiratory rate in relation to age. We compared existing reference ranges with those derived from our centile charts.

FINDINGS: We identified 69 studies with heart rate data for 143,346 children and respiratory rate data for 3881 children. Our centile charts show decline in respiratory rate from birth to early adolescence, with the steepest fall apparent in infants under 2 years of age; decreasing from a median of 44 breaths per min at birth to 26 breaths per min at 2 years. Heart rate shows a small peak at age 1 month. Median heart rate increases from 127 beats per min at birth to a maximum of 145 beats per min at about 1 month, before decreasing to 113 beats per min by 2 years of age. Comparison of our centile charts with existing published reference ranges for heart rate and respiratory rate show striking disagreement, with limits from published ranges frequently exceeding the 99th and 1st centiles, or crossing the median.

INTERPRETATION: Our evidence-based centile charts for children from birth to 18 years should help clinicians to update clinical and resuscitation guidelines.

Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies
Lancet. 2011 Mar 19;377(9770):1011-8