Clinical overview
Roughly 85% of term babies establish regular respiration within 10–30 seconds of birth, and the great majority of the rest respond to drying, stimulation and a clear airway. Only a small minority — classically around 1 in 10 babies need some help and far fewer than 1 in 100 need full resuscitation (standard NRP teaching) — require active inflation breaths, and chest compressions or drugs are needed in only a fraction of those. The corollary is that neonatal resuscitation is overwhelmingly about establishing effective ventilation: a dry, warm, well-ventilated newborn almost always recovers. Cardiac arrest in the newborn is, with rare exception, the end-stage of respiratory failure, not a primary cardiac event — which is why the priority order differs fundamentally from adult ACLS.
The registrar must be able to demonstrate the resuscitation drill under pressure, assess using the Apgar score correctly (and know its limits), interpret a cord blood gas to time and characterise an intrapartum insult, and recognise the spectrum of birth injuries. In South Africa, where birth asphyxia and intrapartum-related events remain a leading cause of early neonatal death and a recurring theme in perinatal mortality audit, competent resuscitation at every level of care — from a district labour ward to a tertiary unit — is a core registrar skill. Every birth attendant should anticipate the need, prepare the equipment, and be able to deliver effective positive-pressure ventilation. See also Initiation of respiration and Neonatal transition for the underlying physiology.
Core knowledge
The physiology of transition and asphyxia
At birth the fetus must clear lung fluid, establish a functional residual capacity, drop pulmonary vascular resistance and switch from placental to pulmonary gas exchange. The first effective breaths are generated against high surface tension; this is why aerating the lung — not chest compression — is the engine of newborn resuscitation. When gas exchange fails (cord compression, abruption, prolonged labour, shoulder dystocia), the fetus passes through a stereotyped sequence first described in experimental work: primary apnoea (a period of no breathing with maintained heart rate, responsive to stimulation), then gasping, then terminal (secondary) apnoea (heart rate and gasping fail; only positive-pressure ventilation will recover the baby). Clinically you cannot reliably tell primary from secondary apnoea at the bedside, so treat every apnoeic, non-vigorous newborn as if in terminal apnoea and ventilate.
Apgar score
The Apgar score (Virginia Apgar, 1953 — standard teaching) is a structured description of the newborn's condition at fixed time points, assigned at 1 and 5 minutes, and continued every 5 minutes (10, 15, 20) while resuscitation continues if the 5-minute score is < 7. It scores five signs 0–2:
| Sign | 0 | 1 | 2 |
|---|---|---|---|
| Appearance (colour) | Blue/pale all over | Body pink, extremities blue (acrocyanosis) | Pink all over |
| Pulse (heart rate) | Absent | < 100/min | ≥ 100/min |
| Grimace (reflex irritability) | No response | Grimace | Cry / cough / sneeze |
| Activity (tone) | Limp | Some flexion | Active motion |
| Respiration | Absent | Slow / irregular / weak | Strong cry |
The Apgar is a descriptor of condition and response, not a trigger for resuscitation — you do not wait for the 1-minute score to begin (heart rate and breathing drive intervention from the first seconds). It has poor sensitivity and specificity for long-term neurological outcome; a low score reflects many things (prematurity, sedation, sepsis, malformation, hypotonia) besides hypoxia. A persistently low Apgar (e.g. ≤ 3 at 5 and 10 minutes) carries more prognostic weight than a single 1-minute value but must always be interpreted alongside the cord gas, the clinical course and evidence of evolving encephalopathy. Record the score honestly, including the components and the interventions in progress at the time.
Cord blood gas
Paired arterial and venous umbilical cord sampling, taken from a doubly-clamped segment of cord immediately after delivery, gives an objective, retrospective measure of the fetal acid–base state at birth — far more reliable than the Apgar for documenting intrapartum hypoxia. The artery reflects the fetal/placental condition; the vein reflects maternal–placental supply. Correctly drawn, the arterial pH and base deficit should be the more acidotic of the pair (this also confirms you truly sampled an artery and a vein).
Commonly taught thresholds (standard physiology / textbook canon — confirm exact local cut-offs):
- Normal term arterial pH ≈ 7.18–7.38 (mean ~7.26).
- Significant acidaemia: arterial pH < 7.10.
- Severe metabolic acidaemia (a component of the consensus definition of an acute intrapartum hypoxic event): arterial pH < 7.00 and base deficit ≥ 12 mmol/L.
Interpret the pattern, not just the pH:
- Respiratory acidosis (low pH, high pCO₂, near-normal base deficit) suggests a recent, acute event — e.g. cord compression in the final minutes — with little time for lactate to accumulate. Generally a better prognosis.
- Metabolic acidosis (low pH, high base deficit/lactate, pCO₂ not the main driver) implies a more prolonged hypoxic-ischaemic insult with anaerobic metabolism.
- Mixed acidosis combines both.