Category Archives: PHARM

Prehospital and Retrieval Medicine

Pre-hospital NIV

"The driver's dyspneic - pass the Boussignac valve!"

Pre-hospital non-invasive ventilation for patients with acute dyspnoea features in two journals this month. Researchers at the Ambulance Service New South Wales published an evidence-based review of pre-hospital NIV for acute cardiogenic pulmonary oedema, concluding that there are probable benefits.

Background Non-invasive ventilation (NIV) is increasingly being implemented by many ambulance jurisdictions as a standard of care in the out-of-hospital management of acute cardiogenic pulmonary oedema (ACPO). This implementation appears to be based on the body of evidence from the emergency department (ED) setting, with the assumption that earlier administration by paramedics would give benefits with regard to inhospital mortality and the rate of endotracheal intubation beyond those seen when initiated in the ED. This paper sought to identify and review the current level of evidence supporting NIV in the prehospital setting.

Methods Electronic searches of Medline, EMBASE, CINAHL, Cochrane Database of Systematic Reviews and Cochrane Database of Controlled Trials were conducted and reference lists of relevant articles were hand searched.

Results The search identified 12 primary studies documenting the use of NIV, either continuous positive airway pressure or bi-level non-invasive ventilation, for ACPO in the out-of-hospital setting. Only three studies were randomised controlled trials, with none addressing inhospital mortality as a primary outcome measure. The majority of articles were non-comparative descriptive studies.

Conclusion Early prehospital NIV appears to be a safe and feasible therapy that results in faster improvement in physiological status and may decrease the need for intubation when compared with delayed administration in the ED. There is weak evidence that is may decrease mortality. The cost versus benefit equation of system-wide prehospital implementation of NIV is unclear and, based on the current evidence, should be considered with caution.

Prehospital non-invasive ventilation for acute cardiogenic pulmonary oedema: an evidence-based review.
Emerg Med J. 2011 Jul;28(7):609-12
At the same time, the National Association of EMS Physicians has published a position statement on noninvasive positive pressure ventilation, for the general indication of acute dyspnoea. It states:

The general indication for NIPPV is dyspnea accompanied by early respiratory failure in patients with intact protective airway reflexes and mental status. The majority of NIPPV studies have focused on patients with acute pulmonary edema.

However, NIPPV may prove useful with other reversible disease processes such as chronic obstructive pulmonary disease or asthma exacerbations. While utilized in in-hospital practice, the role of NIPPV for pneumonia-associated respiratory failure is less clear. While some clinicians advocate the use of NIPPV to augment oxygenation prior to ETI in the in- hospital setting, there are no studies evaluating this strategy in the prehospital setting.

 
Noninvasive positive pressure ventilation: resource document for the National Association of EMS Physicians position statement.
Prehosp Emerg Care. 2011 Jul-Sep;15(3):432-8
Full Text of Position Statement

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

How about pre-hospital tranexamic acid?

The CRASH 2 trial showed improved outcomes in trauma from the administration of the antifibrinolytic drug tranexamic acid. A further analysis of the data has shown that benefit was only seen in CRASH-2 when tranexamic acid was administered within 3 hours of injury1.
An accompanying editorial2 makes the following interesting points:

  • Acute traumatic coagulopathy is a hyperacute process in which systemic fibrinolysis releases D-dimers that are detectable within 30 min of injury.
  • Those severely injured patients who develop acute coagulopathy are much more likely to die and to die early.
  • Once fully activated, fibrinolysis has been shown to continue unabated until endogenous antifibrinolytic elements are restored.
  • The earlier that tranexamic acid is administered, the more likely it might be to prevent full activation of fibrinolysis.
  • Hospital massive transfusion protocols incorporate fresh frozen plasma that contains all the endogenous antifibrinolytic elements in plasma and so the place for tranexamic acid in high income countries with such protocols is unclear.
  • The best place for tranexamic acid in developed trauma systems might actually be in the prehospital environment, where trauma bypass policies have extended prehospital times and the administration of plasma is uncommon and often impractical.

BACKGROUND: The aim of the CRASH-2 trial was to assess the effects of early administration of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage. Tranexamic acid significantly reduced all-cause mortality. Because tranexamic acid is thought to exert its effect through inhibition of fibrinolysis, we undertook exploratory analyses of its effect on death due to bleeding.

METHODS: The CRASH-2 trial was undertaken in 274 hospitals in 40 countries. 20,211 adult trauma patients with, or at risk of, significant bleeding were randomly assigned within 8 h of injury to either tranexamic acid (loading dose 1 g over 10 min followed by infusion of 1 g over 8 h) or placebo. Patients were randomly assigned by selection of the lowest numbered treatment pack from a box containing eight numbered packs that were identical apart from the pack number. Both participants and study staff (site investigators and trial coordinating centre staff ) were masked to treatment allocation. We examined the effect of tranexamic acid on death due to bleeding according to time to treatment, severity of haemorrhage as assessed by systolic blood pressure, Glasgow coma score (GCS), and type of injury. All analyses were by intention to treat. The trial is registered as ISRCTN86750102, ClinicalTrials.gov NCT00375258, and South African Clinical Trial Register/Department of Health DOH-27-0607-1919.

FINDINGS: 10,096 patients were allocated to tranexamic acid and 10,115 to placebo, of whom 10,060 and 10,067, respectively, were analysed. 1063 deaths (35%) were due to bleeding. We recorded strong evidence that the effect of tranexamic acid on death due to bleeding varied according to the time from injury to treatment (test for interaction p<0.0001). Early treatment (≤1 h from injury) significantly reduced the risk of death due to bleeding (198/3747 [5.3%] events in tranexamic acid group vs 286/3704 [7.7%] in placebo group; relative risk [RR] 0.68, 95% CI 0.57-0.82; p<0.0001). Treatment given between 1 and 3 h also reduced the risk of death due to bleeding (147/3037 [4.8%] vs 184/2996 [6.1%]; RR 0.79, 0.64-0.97; p=0.03). Treatment given after 3 h seemed to increase the risk of death due to bleeding (144/3272 [4.4%] vs 103/3362 [3.1%]; RR 1.44, 1.12-1.84; p=0.004). We recorded no evidence that the effect of tranexamic acid on death due to bleeding varied by systolic blood pressure, Glasgow coma score, or type of injury.

INTERPRETATION: Tranexamic acid should be given as early as possible to bleeding trauma patients. For trauma patients admitted late after injury, tranexamic acid is less effective and could be harmful.

1. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial
Lancet. 2011 Mar 26;377(9771):1096-101
2. Tranexamic acid for trauma
Lancet. 2011 Mar 26;377(9771):1052-4

Tympanic monitoring for targeted temperature management

As the authors of this study point out, the reliability of tympanic temperature monitoring is still under debate. Since invasive measures of core temperature employed in the ICU may not be practicable in the pre-hospital setting, it would be helpful to employ a simpler method in the field, particular if we are implementing targeted temperature management post-cardiac arrest. In this small study of ten patients (with 558 temperature measurements) there was a high degree of correlation between tympanic and oesophageal temperature (r=0.95, p<0.0001, 95% CI 0.93 to 0.96) and also between tympanic and bladder temperature (r=0.96, p<0.0001, 95% CI 0.95 to 0.97). This finding is apparently in keeping with results obtained from patients undergoing cardiac surgery.

Objective Prehospital induction of therapeutic hypothermia after cardiac arrest may require temperature monitoring in the field. Tympanic temperature is non-invasive and frequently used in clinical practice. Nevertheless, it has not yet been evaluated in patients undergoing mild therapeutic hypothermia (MTH). Therefore, a prospective observational study was conducted comparing three different sites of temperature monitoring during therapeutic hypothermia.
Methods Ten consecutive patients admitted to our medical intensive care unit after out-of-hospital cardiac arrest were included in this study. During MTH, tympanic temperature was measured using a digital thermometer. Simultaneously, oesophageal and bladder temperatures were recorded in a total of 558 single measurements.
Results Compared with oesophageal temperature, bladder temperature had a bias of 0.019°C (limits of agreement ±0.61°C (2SD)), and tympanic measurement had a bias of 0.021°C (±0.80°C). Correlation analysis revealed a high relationship for tympanic versus oesophageal temperature (r=0.95, p<0.0001) and also for tympanic versus bladder temperature (r=0.96, p<0.0001).
Conclusions That tympanic temperature accurately indicates both oesophageal and bladder temperatures with a very small discrepancy in patients undergoing MTH after cardiac arrest is demonstrated in this study. Although our results were obtained in the hospital setting, these findings may be relevant for the prehospital application of therapeutic hypothermia as well. In this case, tympanic temperature may provide an easy and non-invasive method for temperature monitoring.

Tympanic temperature during therapeutic hypothermia
Emerg Med J. 2011 Jun;28(6):483-5

RSI complications increase with intubation difficulty


A substudy of a large randomised controlled trial comparing etomidate with ketamine for RSI in the pre-hospital environment, emergency department, and intensive care unit examined immediate complication rates in relation to the intubation difficulty scale score (IDS).
They used the 7-criteria IDS previously developed and evaluated. The variables included in the IDS are as follows:

  1. the number of attempts excluding the first;
  2. the number of extra operators;
  3. the number of additional techniques utilised;
  4. the Cormack grade (0–3 points, grade 1 giving no IDS points);
  5. the intensity of lifting force required (0 points if normal, 1 point if increased);
  6. the need to apply external laryngeal pressure (0 or 1 point, application of cricoid pressure (Sellick manoeuvre) does not alter the score)
  7. vocal cord position (abduction, 0 points; adduction, 1 point). Each criterion was scored and recorded by the physician who performed the procedure.

The sum gives the IDS score, and a score of 0 indicates an easy tracheal intubation at the first attempt by a single operator using a single technique, with a good view of the glottis and abducted vocal cords. Intubation was considered difficult if the score was greater than 5.
There was a positive linear relationship between IDS score and complication rate, and difficult intubation appeared to be a significant independent predictor of death.

OBJECTIVES: To evaluate the association between emergency tracheal intubation difficulty and the occurrence of immediate complications and mortality, when standardised airway management is performed by emergency physicians.

METHODS: The present study was a substudy of the KETAmine SEDation (KETASED) trial, which compared morbidity and mortality after randomisation to one of two techniques for rapid sequence intubation in an emergency setting. Intubation difficulty was measured using the intubation difficulty scale (IDS) score. Complications recognised within 5min of endotracheal intubation were recorded. We used multivariate logistic regression analysis to determine the factors associated with the occurrence of complications. Finally, a Cox proportional hazards regression model was used to examine the association of difficult intubation with survival until 28 days.

RESULTS: A total of 650 patients were included, with mean age of 55±19 years. Difficult intubation (IDS >5) was recorded in 73 (11%) patients and a total of 248 complications occurred in 192 patients (30%). Patients with at least one complication had a significantly higher median IDS score than those without any complications. The occurrence of a complication was independently associated with intubation difficulty (odds ratio 5.9; 95% confidence interval (CI) [3.5;10.1], p<0.0001) after adjustment on other significant factors. There was a positive linear relationship between IDS score and complication rate (R(2)=0.83; p<0.001). The Cox model for 28-day mortality indicated that difficult intubation (hazard ratio 1.59; 95%CI [1.04;2.42], p=0.03) was a significant independent predictor of death.

CONCLUSION: Difficult intubation, measured by the IDS score, is associated with increased morbidity and mortality in patients managed under emergent conditions.

Morbidity related to emergency endotracheal intubation—A substudy of the KETAmine SEDation trial
Resuscitation. 2011 May;82(5):517-22

Infant CPR causing rib fractures

An increase in rib fractures was observed at autopsy in infants who had undergone CPR, which is temporally related to the introduction of guidelines stressing the hand-encircling two-thumb method of CPR and compression depths of 1/3 – 1/2 the anteroposterior diameter of the chest, which has been shown in previous studies to produce higher coronary perfusion pressures and more consistently correct depth and force of compression than the “two-finger” technique.
Previous posts here have reported a CT scan-based mathematical modelling study that suggested compressing to 1/3 anteroposterior chest wall diameter should provide a superior ejection fraction to 1/4 depth and should generate less risk for over-compression than 1/2 AP compression depth, and another post described a small case series of 6 PICU patients requiring CPR for cardiac arrest due to primary cardiac disease in which blood pressure as measured by an arterial line increased when the depth of chest compression was increased from one third to one half of the chest wall diameter (using the hand-encircling method).
What should we do about this? I think the take-home message is to be mindful of the risk of rib fractures and to avoid over-compression, but to follow the guidelines. Another valuable point was made by the authors:

“Regardless of the reason for the increased incidence, the possibility of CPR-related rib fractures needs to be seriously considered in the evaluation of any infant presenting with rib fractures, when there is a history of CPR, so as not to misinterpret the finding as evidence of non-accidental/inflicted injury.”

An infant NOT requiring CPR. And a happy doctor.

OBJECTIVE: A recent increase in the number of infants presenting at autopsy with rib fractures associated with cardio-pulmonary resuscitation (CPR) precipitated a study to determine whether such a phenomenon was related to recent revision of paediatric resuscitation guidelines.

METHODS: We conducted a review of autopsy reports from 1997 to 2008 on 571 infants who had CPR performed prior to death.

RESULTS: Analysis of the study population revealed CPR-related rib fractures in 19 infants (3.3%), 14 of whom died in the 2006-2008 period. The difference in annual frequency of CPR-related fractures between the periods before and after revision of paediatric CPR guidelines was statistically highly significant.

CONCLUSIONS: The findings indicate that CPR-associated rib fractures have become more frequent in infants since changes in CPR techniques were introduced in 2005. This has important implications for both clinicians and pathologists in their assessment of rib fractures in this patient population.

Increased incidence of CPR-related rib fractures in infants-Is it related to changes in CPR technique?
Resuscitation. 2011 May;82(5):545-8

Drugs in cardiac arrest – guess what works?

Just like epinephrine (adrenaline), amiodarone does not increase survival to hospital discharge in cardiac arrest patients. I doubt his will deter the people in the resuscitation room with their stopwatches from handing me these drugs and telling me I ought to be giving them though.

Amiodarone - a load of balls

 

AIMS: In adult cardiac arrest, antiarrhythmic drugs are frequently utilized in acute management and legions of medical providers have memorized the dosage and timing of administration. However, data supporting their use is limited and is the focus of this comprehensive review.

METHODS: Databases including PubMed, Cochrane Library (including Cochrane database for systematic reviews and Cochrane Central Register of Controlled Trials), Embase, and AHA EndNote Master Library were systematically searched. Further references were gathered from cross-references from articles and reviews as well as forward search using SCOPUS and Google scholar. The inclusion criteria for this review included human studies of adult cardiac arrest and anti-arrhythmic agents, peer-review. Excluded were review articles, case series and case reports.

RESULTS: Of 185 articles found, only 25 studies met the inclusion criteria for further review. Of these, 9 were randomised controlled trials. Nearly all trials solely evaluated Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF), and excluded Pulseless Electrical Activity (PEA) and asystole. In VT/VF patients, amiodarone improved survival to hospital admission, but not to hospital discharge when compared to lidocaine in two randomized controlled trials.

CONCLUSION: Amiodarone may be considered for those who have refractory VT/VF, defined as VT/VF not terminated by defibrillation, or VT/VF recurrence in out of hospital cardiac arrest or in-hospital cardiac arrest. There is inadequate evidence to support or refute the use of lidocaine and other antiarrythmic agents in the same settings.

The use of antiarrhythmic drugs for adult cardiac arrest: A systematic review
Resuscitation. 2011 Jun;82(6):665-70

Single bag for adults and kids

A nice idea – using a single adult self-inflating bag for the resuscitation of adult and paediatric patients, marked to identify compression points that deliver specific tidal volume ranges. Might be useful in situations where equipment needs to be minimised, such as military or pre-hospital settings.

AIM: To overcome limitations of inaccurate tidal volume (TV) delivery by conventional selfinflating paediatric and adult bags during paediatric and adolescent resuscitation, we designed a novel target volume marked bag (TVMB) with four compression points marked on an adult bag surface. The aim of this study was to evaluate the TVMB in delivering preset TV.

METHODS: Fifty-three subjects (28 doctors, 17 nurses, 8 paramedics) participated in this simulation trial. TVMB, paediatric bag and adult bag were connected to a gas flow analyser for measuring TV and peak inspiratory pressure (PIP). In a random cross-over setting, participants delivered 10 ventilations using the adult bag, paediatric bag or TVMB in each of four target volume ranges (100-200ml, 200-300ml, 300-400ml, 400-500ml). We compared TV and PIP for the adult bag, paediatric bag and TVMB in each subject.

RESULTS: Compared with the paediatric bag, TVMB showed higher rates of accurate TV delivery in the 200-300ml target volume range (87-90% versus 32-35%; p<0.05). Compared with the adult bag, TVMB showed higher rates of accurate TV delivery in all target volume ranges (75-90% versus 45-50%; p<0.05). The frequency of too high or low TV delivery was higher with the adult bag than TVMB (20-30% versus 0-5%; p<0.05). There was no significant difference in PIP between the paediatric bag and TVMB (within 5cm H(2)O; p<0.05).

CONCLUSIONS: TVMB could deliver accurate TV in various target volume ranges for paediatric and adolescent resuscitation.

Resuscitation. 2011 Jun;82(6):749-54