Pulse Oximetry and the Neonate.

Evaluation of the newborn who has cyanosis requires prompt and logical assessment. Although entities such as polycythemia and methemoglobinemia must be considered, the diagnoses that must be addressed most urgently are primary respiratory disease, congenital heart disease (CHD), and persistent pulmonary hypertension of the newborn (PPHN). These categories of disease are not mutually exclusive, as in the case of meconium aspiration with PPHN, but their distinct pathophysiologic mechanisms account for different results in diagnostic testing. The essence of PPHN lies in the pathologic failure of pulmonary artery pressure to decline postnatally. Although pulmonary artery pressure varies directly with pulmonary vascular resistance (PVR), pulmonary blood flow, and pulmonary capillary wedge pressure, the first of these plays the most prominent role in PPHN. Persistently elevated PVR may result from the perinatal failure to elaborate nitric oxide and/or prostaglandin I2 in addition to increased production of phosphodiesterase-3 or -5, endothelin-1, reactive oxygen species, and rhokinase. The net effect is right ventricular dysfunction as well as right-to-left shunting across fetal channels (ie, the patent foramen ovale and ductus arteriosus), which results in decreased pulmonary blood flow. The affected infant develops ventilation/perfusion mismatch, hypoxemia, and acidosis that can lead to left ventricular dysfunction, decreased output, and shock.When differentiating PPHN from cyanotic CHD, the clinician must pay careful attention to patient history; familial occurrence of CHD; and risk factors for PPHN, including sepsis, perinatal asphyxia, intrauterine growth restriction, andmaternal medications (eg, selective serotonin reuptake inhibitors, indomethacin) (Table 1). On physical examination, the clinician should auscultate for heart murmurs, compare upper and lower extremity pulses, assess for hypotension associated with the patient’s cyanosis, and examine the cardiac silhouette on chest radiography. For many years, the “hyperoxia test” was used to distinguish the 3 major causes of cyanosis. Arterial blood gases were obtained before and after infants were placed in 100%oxygen. If an initially low PaO2 rose to equal to or greater than 150 mm Hg following hyperoxia, the likely diagnosis was respiratory disease. Nonresponders with either cyanotic CHD or PPHN were subsequently hyperventilated. Decreased PaCO2 and alkalosis would dilate the pulmonary vasculature in PPHN, resulting in increased PaO2, which would not be the case in cyanotic CHD. Recently, echocardiography with color Doppler directional flow has supplanted the hyperventilation phase of the hyperoxia test. However, use of blood gases is limited by the technical difficulty in obtaining them by arterial puncture; a falsely low PaO2 may result when an infant’s crying leads to increased right-to-left shunting. Also, changes in clinical status may not be evident during the interval between the 2 samplings. Consequently, the routine introduction of pulse oximetry into the care of neonates has had a significant impact. AUTHOR DISCLOSURE Dr Roth has disclosed no financial relationships relevant to this article. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.