Neonatal cardiac physiology differs from that of the adult in several ways. At birth, the neonatal myocyte is not fully developed; making the heart less able to respond to volume loading with an increased cardiac output. This is due to the higher proportion of fibrous tissue to contractile tissue, as compared to that of an adult. Due to the heart’s immature T-tubule and sarcoplasmic reticulum, the neonate relies heavily on calcium flux through the sarcolemma for myocyte function. This myocyte contraction is highly dependent on ionized plasma calcium.
Cardiac output is the product of heart rate and stroke volume. Unlike adults, neonates possess a limited ability to increase cardiac output by increasing stroke volume. Instead, neonatal cardiac output is significantly dependent on heart rate, indicating they have less preload reserve. Neonatal oxygen requirements are also much greater than the adult, which requires the neonatal heart to function at near maximal capacity.
Relative dominance of the sympathetic and parasympathetic system changes as the neonate develops. The parasympathetic system is fully formed shortly after birth, while the sympathetic innervation is incomplete. This predisposes the neonate to pronounced vagal responses.
Prior to anatomic closure of the foramen ovale or ductus ateriosus, neonates may, in times of stress, revert to a fetal pattern of circulation. This may lead to shunting in either direction, as the balance of SVR and PVR dictate. Sepsis, hypoxia, hypercarbia, hypothermia, or pain may precipitate this by increasing PVR. PVR approaches adult values by about two months of age.
Lactate is the primary fuel source for the immature myocardium in contrast the adult myocardium which utilizes fatty acids for energy.