Elsevier

Current Paediatrics

Volume 15, Issue 2, April 2005, Pages 143-150
Current Paediatrics

Applied physiology of newborn resuscitation

https://doi.org/10.1016/j.cupe.2004.12.002Get rights and content

Summary

Although the majority of newly born babies will establish normal respiration and circulation without help, up to 1–2% may require some resuscitation. Although the word ‘physiology’ induces narcolepsy in many doctors, the fetal and perinatal physiology governs many of the practical aspects of newborn resuscitation and is the basis for the differences from resuscitation later in life. Newly born babies lose heat faster than at any other time in life and until the first breath, the newborn lungs are completely filled with fluid, which is a state experienced during resuscitation at no other time. An understanding of the normal and abnormal perinatal physiology is important in appreciating the practical differences in the approach to caring for any baby in need of resuscitation and also in avoiding actions that may be detrimental in the longer term.

Section snippets

Background

The resuscitation of babies at birth is different from the resuscitation of all other age groups and knowledge of the relevant physiology and pathophysiology is essential. Resuscitation may be required in up to 1–2% of newborn babies; however, the majority of newly born babies will establish normal respiration and circulation without help. This article will describe the normal fetal and newborn physiology relevant to resuscitation and examine how that influences the practical approach to

Normal physiology

As pregnancy approaches term, a number of changes occur in preparation for the transition from intra to extra uterine life. The changes most relevant to resuscitation are those that affect the functioning of the lungs, cardiovascular system, respiration and metabolism including thermoregulation.

Pathophysiology

Our knowledge of the physiological changes due to peripartum hypoxia comes from animal experiments in the early 1960s.9, 12 The results of these experiments, which followed the physiology of newborn animals during acute, total, prolonged asphyxia and subsequent resuscitation are summarised in Figure 1, Figure 2, Figure 3.

When the placental blood supply is interrupted, the fetus attempts to breathe probably stimulated by increased carbon dioxide levels. Should these attempts fail to provide an

Response to resuscitation and assessment

A newborn baby who does not breathe may have experienced hypoxia but there may be other aetiologies. Premature infants may not start to breathe because of muscular weakness or poorly compliant lungs, but it must be realised that they are also more vulnerable to the effects of hypoxia. These babies are often in need of immediate intervention and the best way to assess the response to resuscitation is by assessing the heart rate. The best way to do this is with a stethoscope.13 It is clear from

Temperature control

Recent research in animals has suggested a possible advantage of moderate hypothermia for those few infants suffering hypoxic encephalopathy. Randomised controlled trials are in progress to assess this in human newborns. However, for the majority of babies requiring resuscitation at birth a thermoneutral environment would be the ideal for which we should aim. Cold stress will increase the oxygen requirements of all babies. Babies subjected to cold stress in the period immediately after birth

First inflations

In the apnoeic baby the first breaths are obviously important as they establish the resting lung volume and aerate the fluid-filled alveoli. They also initiate the fall in pulmonary vascular resistance. In term babies, peak pressures of 20–30 cm H2O may be required but ideally one should use the minimum pressure needed to achieve chest wall movement. Longer breaths at lower pressure may be more effective in displacing alveolar fluid.14 Most bag and mask systems have a blow-off set at 40 cm H2O

Heart rate and blood pressure

Hypoxia causes an initial rise in heart rate, cardiac output and blood pressure before they fall. The latter is maintained for some time by the increased stroke volume of each bradycardic beat and peripheral vasoconstriction. Early resuscitation provides oxygenated blood in the lungs, which, returned to the heart, causes the rate to increase. If, due to acidosis and hypoxia, the circulation has ceased to be effective, then chest compressions may be needed to affect this (Fig. 3). Success is

Pulmonary blood flow

Hypoxia increases pulmonary vascular resistance and pulmonary flow declines in parallel with cardiac output until the start of resuscitation. At that time rapid restoration of pulmonary arterial pressure is observed and this may exceed the baseline. This suggests that resistance remains raised for a time, although it returns to baseline within 5 min in piglets. In this animal model the pulmonary vascular resistance does not differ regardless of whether air or 100% oxygen is used.20

Metabolism

After a period of buffering, increasing base deficit is directly related to the duration of hypoxia. During reoxygenation base deficit continues to increase or plateau during the first 5 min. This is likely to be due to washout of lactic acid and other metabolites in peripheral tissues as perfusion improves. There is then a slow return to baseline values, which may take up to 4 h to normalise in ideal conditions.

In preterm or sick babies, hypoglycaemia may occur after resuscitation. There are no

Cerebral blood flow and oxygenation

Cerebral blood flow initially increases with hypoxia but then declines if it persists. Following significant hypoxia resuscitation may still restore cerebral blood flow but it can take a substantial time. The optimum time for restoration of cerebral blood flow in unknown. Cerebral blood volume increases with hypoxia and continues to increase after the initiation of resuscitation. It reaches a maximum at 5–10 min and returns to normal over the next 1–2 h. Brain oxygenation can only be measured

Conclusions

There are physiological and practical reasons for much of the present approach to resuscitation at birth. However, knowledge of the effects of perinatal hypoxia is almost entirely focused on acute hypoxia. In life, the fetus in trouble may be exposed to prolonged subacute hypoxia, which may go unnoticed for some time before ultimately presenting acutely. At present, therefore, we extrapolate from the acute models originating in the 1960s. Babies born prematurely have different problems and

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