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Heart rate changes during positive pressure ventilation after asphyxia-induced bradycardia in a porcine model of neonatal resuscitation
  1. Maria Liza Espinoza1,2,
  2. Po-Yin Cheung2,3,
  3. Tze-Fun Lee2,3,
  4. Megan O’Reilly2,3,
  5. Georg M Schmölzer2,3
  1. 1 Department of Pediatrics, University of Calgary, Calgary, Alberta, Canada
  2. 2 Centre for the Studies of Asphyxia and Resuscitation, Royal Alexandra Hospital, Edmonton, Alberta, Canada
  3. 3 Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada
  1. Correspondence to Dr Georg M Schmölzer, Neonatal Research Unit, Centre for the Studies of Asphyxia and Resuscitation, Royal Alexandra Hospital, Edmonton, AB T5H 3V9, Canada; georg.schmoelzer{at}me.com

Abstract

Background The Neonatal Resuscitation Program (NRP) states that if adequate positive pressure ventilation (PPV) was given for a low heart rate (HR), the infant’s HR should increase within the first 15 s of PPV.

Objective To assess changes in HR in piglets with asphyxia-induced bradycardia.

Methods Term newborn piglets (n=30) were anaesthetised, intubated, instrumented and exposed to 50 min normocapnic hypoxia followed by asphyxia. Asphyxia was achieved by clamping the tube until severe bradycardia (defined as HR at <25% of baseline). This was followed by 30 s adequate PPV and chest compression thereafter. Changes in HR during the 30 s of PPV were assessed and divided into four epochs (0–10 s, 5–15 s, 10–20 s and 20–30 s, respectively).

Results Increase in HR >100/min was observed in 6/30 (20%) after 30 s of PPV. Within the epochs 0–10 s, 5–15 s or 10–20 s no piglet had an increase in HR >100/min. Additional 10/30 (33%) had a >10% increase in HR.

Conclusion In contrast to NRP recommendation, adequate PPV does not increase HR within 15 s after ventilation in piglets with asphyxia-induced bradycardia.

  • newborn
  • infants
  • neonatal resuscitation
  • asphyxia
  • heart rate

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What is already known on this topic?

  • Positive pressure ventilation (PPV) should be initiated in the delivery room when an infant’s heart rate (HR) is <100/min.

  • Adequacy of PPV should be assessed by observing an increase in HR.

  • HR >100 beats/min can be achieved by either gradual increase over at least 60 s with PPV or rapid increase with sufficient lung aeration.

What this study adds?

  • Adequate PPV for 30 s increases HR in only 20% of piglets with asphyxia-induced bradycardia.

  • Clinicians should not expect an increase in heart rate  after  15  s  of positive pressure ventilation  if there is severe bradycardia  

Introduction

The seventh edition of the Neonatal Resuscitation Program (NRP) textbook recommends to initiate positive pressure ventilation (PPV) in the delivery room when an infant’s heart rate (HR) is <100/min.1 Adequacy of PPV should be assessed by observing an increase in HR, however if HR does not increase chest rise should be assessed to gauge PPV.1 The seventh edition of the NRP textbook further states that ‘if positive pressure ventilation (PPV) was started because the baby had a low heart rate (HR), the baby’s HR should begin to increase within the first 15 s of PPV.’1 Indeed, observational studies reported that a rising HR is a very reliable surrogate for adequate ventilation.2 3 The same studies further reported that HR in a bradycardic infant does not increase within the first 15 s of PPV. The rise in HR follows two distinctive patterns: a gradual rise to HR >100 beats/min over at a period of at least 60 s or a rapid increase within 5 s after lung aeration (median (IQR) of 126 (96–160) s from birth in newborn infants).2–4

The study aimed to examine the changes in HR during adequate PPV in piglets with severe bradycardia induced by asphyxia.

Methods

This was a secondary analysis of our previously published randomised controlled animal trials.5 6 The original trials were conducted in accordance with the Animal Research Reporting of In Vivo Experiments guidelines and approved by the Animal Care and Use Committee (Health Sciences), University of Alberta (AUP00000237). For this secondary analysis, we included 30 newborn mixed breed piglets (1–4 days of age, weighing 1.8–2.3 kg) from the original study with respiratory function data. The piglets were instrumented as previously described in our experimental protocol of neonatal resuscitation.5 6 Briefly, piglets were tracheotomised with an endotracheal tube inserted and tightly secured without air leak. After stabilisation, piglets were exposed to 50 min of normocapnic hypoxia, followed by an asphyxiation period until HR decreased to <25% of baseline, which was achieved by disconnecting the ventilator and clamping the endotracheal tube. Fifteen seconds later, PPV with 100% FiO2 at 40–60 breaths/min was given through a Neopuff T-Piece (Fisher & Paykel, Auckland, New Zealand) for 30 s and followed by chest compression as per protocol. The default settings for the Neopuff were peak inflation pressure (30 cmH2O), positive end expiratory pressure (5 cmH2O) and gas flow 8 L/min. Return of spontaneous circulation (ROSC) was defined as an unassisted HR >100 bpm, which was accessed by ECG, for at least 15 s.

Monitoring devices

HR was continuously measured and recorded using an ECG with a Hewlett Packard 78833B monitor (Hewlett Packard, Palo Alto, CA). A respiratory function monitor (NM3, Respironics, Philips, Andover, Massachusetts, USA) was used to continuously measure expiratory tidal volume, airway pressures and gas flow. The gas flow sensor was placed between the endotracheal tube and the ventilation device.

Data collection and analysis

Demographics of study piglets were recorded. During the 30 s of PPV prior to the start of chest compression, changes in HR were assessed and divided into four epochs: 0–10 s, 5–15 s, 10–20 s and 20–30 s. Expiratory tidal volumes were measured and analysed using Flow Tool Physiologic Waveform Viewer (Philips Healthcare, Wallingford, Connecticut, USA). Response to PPV was categorised into four groups: (1) ROSC defined as an unassisted HR >100/min; (2) an increase in HR defined as a >10% increase in HR from bradycardic baseline; (3) no change in HR defined as <10% change (either increase or decrease) from bradycardic baseline; and (4) a decrease in HR defined as a >10% decrease in HR from bradycardic baseline. The data are presented as mean (±SD) and median (IQR) for parametric and non-parametric variables, respectively. The data were tested for normality and compared using analysis of variance with Bonferroni post-test. P values <0.05 were considered statistically significant. Statistical analyses were performed with Stata (Intercooled 10, StataCorp, Texas, USA).

Results

A total of 30 piglets were analysed and their characteristics at baseline and their blood gas values at the start of PPV are presented in table 1. The asphyxiation period was 131 (50–300) s. The HR at end of asphyxia was 53 (49–57)/min and PPV was given to all piglets for a duration of 30 s. The HR of the 0–10 s epoch was 49 (36–55)/min, the 5–15 s epoch 52 (38–60)/min, the 10–20 s epoch 52 (37–62)/min and the 20–30 s epoch 58 (35–99)/min. Temporal changes in HR are presented in figure 1 and adequate PPV was provided throughout the 30 s of resuscitation as shown by expiratory tidal volumes.

Figure 1

Changes in heart rate and tidal volume delivery during each epoch for four different groups: animals with (A) return of spontaneous circulation (ROSC) (n=6); (B) gradual increase in heart rate (n=10); (C) no change in heart rate (n=7); and (D) decrease in heart rate (n=7) (◯=mean (SD) heart rate in beats/min, ■=mean (SD) delivered tidal volume in mL/kg).

Table 1

Demographics of included piglets

Within the 0–10 s epoch we observed 0/30 ROSC, 6/30 (20%) piglets had an increase in HR, 7/30 had a no change in HR and 17/30 had a decrease in HR.

Within the 5–15 s epoch we observed 0/30 ROSC, 10/30 (33%) piglets had an increase in HR, 16/30 had a no change in HR and 4/30 had a decrease in HR with one piglet having a decrease in HR to 0/min.

Within the 10–20 s epoch we observed 0/30 ROSC, 10/30 (33%) piglets had an increase in HR, 15/30 (50%) had a no change in HR, and 4/30 had a decrease in HR with one piglet having a decrease in HR to 0/min, and 1/30 already being in cardiac arrest with 0/min HR.

Within the 20–30 s epoch we observed ROSC in 6/30 (20%) piglets, 10/30 (33%) had an increase in HR, 7/30 had a no change in HR, and 5/30 (17%) had a decrease in HR, and 2/30 already had 0/min HR with no further change in HR.

Discussion

The NRP textbook states that ‘if PPV was started because the baby had a low HR, the baby’s HR should begin to increase within the first 15 s of PPV.’1 However, two observational studies in the delivery room reported that HR in a bradycardic infant did not increase within the first 15 s of PPV.3 4 The rise in HR was either gradual with an increase over at least 60 s to reach an HR >100 beats/min or rapidly once lung aeration has occurred.2 3 This is further supported by a recent study by Hooper et al, who reported that it took a median (IQR) of 126 (96–160) s from birth for HR to exceed 100 beats/min in premature infants <32 weeks’ gestation.4 Furthermore, the HR increase only followed 28 (21–36) s after gas exchange occurred. These observations contrast the statement by NRP that an infant’s HR should begin to increase within the first 15 s of PPV.1

In the current study, we examined the effect of adequate PPV on changes in HR in asphyxiated newborn piglets (figure 1). Overall, after 30 s of PPV we observed that only half of the piglets had an increase in HR with a rapid rise in only 6/30 piglets and a gradual increase in 10/30 piglets. The remaining piglets had changes in HR ranging from increases to decreases within the 30 s and within each piglet. Indeed, only one-third of piglets had an increase in HR with 15–20 s of adequate PPV. Our data challenge the current NRP statement and clinicians should not expect an increase in HR after 15 s of PPV if there is severe bradycardia. Interruption of PPV for HR assessment after 15 s of PPV may indeed be detrimental. In addition to adequate PPV, time to observe an increase in HR will further depend on the infants’ lung compliance, lung resistance, disease state (eg, premature rupture of membranes or antenatal steroid administration), state of labour or pressures used during PPV.

Limitations

Other than undergone fetal to neonatal transition, all piglets were anaesthetised and sedated which differ from delivery room resuscitations. Piglets were intubated using a tightly secured endotracheal tube to prevent any endotracheal tube leak, which allowed accurate assessment of respiratory function for this study. During delivery room resuscitation, the loss of tidal volume might be even higher as mask leak exacerbates. Despite distribution of cardiac output in the fetus and post-transitional neonate during asphyxial episodes are qualitatively similar, the impact of this study to infants remains to be investigated because of the above limitations.

Conclusion

Contrary to the current NRP guidelines which state that HR should increase after 15 s of PPV, no ROSC was observed within the first 15 s of PPV in piglets with asphyxia-induced bradycardia.

Acknowledgments

We thank the public for donation of money to our funding agencies: GMS is a recipient of the Heart and Stroke Foundation/University of Alberta Professorship of Neonatal Resuscitation, a National New Investigator of the Heart and Stroke Foundation Canada and an Alberta New Investigator of the Heart and Stroke Foundation Alberta. We thank the Neonatal Resuscitation Program, Canadian Pediatric Society (http://www.cps.ca/en/grants-bourses/details/nrp-research-grant) for supporting the study. This research has been facilitated by the Women and Children’s Health Research Institute through the generous support of the Stollery Children’s Hospital Foundation.

References

Footnotes

  • Contributors Conception and design: GMS, PYC. Drafting of the article: MLE, GMS, PYC, TFL, MOR. Critical revision of the article for important intellectual content: MLE, GMS, PYC, TFL, MOR. Final approval of the article: MLE, GMS, PYC, TFL, MOR.

  • Funding This study was funded by the Women and Children’s Health Research Institute, Edmonton, Alberta; Heart and Stroke Foundation of Alberta; Heart and Stroke Foundation of Canada; Neonatal Resuscitation Program; and Canadian Paediatric Society.

  • Disclaimer The sponsors of the study had no role in study design, data collection, data analysis, data interpretation or writing of the report.

  • Competing interests None declared.

  • Ethics approval Animal Care and Use Committee (Health Sciences), University of Alberta (AUP00000237)

  • Provenance and peer review Not commissioned; externally peer reviewed.

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