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oxygen consumption (VO2) is less than O2 demand and the neonate relies increasingly on anaerobic metabolism to maintain energy substrate Accordingly, shock results from either impaired oxygenation, O2-carrying capacity, or delivery, all of which is often compounded by an elevated O2 demand Oxygenation and O2 content (CaO2) are compromised due to the mixing of systemic and pulmonary venous return; thus systemic blood flow (Qs) must compensate to maintain adequate tissue oxygenation The health of the neonate with a fUVH and shock will be compounded by an elevated O2 demand The primary factors responsible for an increase in metabolism include increased ventilatory demand and impaired respiratory mechanics, resulting in a marked increase in respiratory muscle VO2 and corresponding DO2; elevated myocardial O2 demand; and elevated total body VO2 due to catecholamine exposure (endo- and exogenous sources) Assessment of Systemic Oxygen Delivery (See Also Chapter 70) Standard “hemodynamic” parameters such as blood pressure, heart rate, and arterial oxygen saturations (SaO2), and the perfusion exam may not provide an accurate indication of the adequacy of DO2 The SaO2 may be elevated, indicating a generous Qp, but that does not necessarily have to occur at the expense of Qs and DO2 if the total cardiac output (CO) is adequate Conversely, an “acceptable” SaO2 (e.g., 80%) does not indicate adequate DO2 if the total CO is limited A normal or elevated blood pressure does not indicate adequate DO2 as SVR may be compensating for a low Qs This is a particularly important consideration in patients with a fUVH and multidistribution physiology, as an elevated and rising SVR/pulmonary vascular resistance (PVR) ratio creates a positive feedback cycle that culminates in tissue hypoxia and shock As Qs falls and becomes limited, neurohormonal activation ensues, which—if systolic function is impaired—causes stroke volume and CO to decrease while increasing the SVR/PVR ratio, thus increasing the Qp/Qs And in this instance the increase in Qp is occurring at the expense of the systemic circulation One strategy that may be used to assess Qs and DO2 is the use of venous and or cerebral NIRS oximetry, which relies on the use of a manipulated and simplified Fick equation: where ScvO2 is the central venous O2 saturation obtained from the jugular vein, superior vena cava, or inferior vena cava–right atrial juncture and SaO2 − ScvO2/SaO2 is the oxygen extraction ratio (O2ER).37a A cerebral NIRS O2 saturation may be used a surrogate for regional (cerebral) and global (ScvO2) VO2/DO2 analysis; however, there are important factors to consider, which are discussed elsewhere DO2 is coupled to metabolism, which is accomplished by viscera modulating vasomotor tone, blood flow, and regional DO2 The O2ER increases from normal (25% to 30% or so) when DO2 becomes limited A O2ER of 50% to 60% is consistent with impending shock and the critical O2ER (defined by the onset of anaerobic metabolism and fall in VO2 without a decrement in O2 demand) is 60% or so.38 Clinical findings consistent with impending or existing shock include an elevated O2ER that is approaching if not exceeding the “critical” O2ER and lactic acidosis An important limitation of lactate levels is that the O2ER must exceed critical levels for lactate production to exceed its clearance The principles of initial simultaneous assessment and management are outlined in Table 71.2 The top priority should be to establish access for the initiation of prostaglandin, correction of acidosis, and initiation of inotropic support The dose of prostaglandin needed to open the constricted ductus arteriosus is 0.1 to 0.2 µg/kg per minute, which is 10 to 20 times higher than that needed to maintain patency typically 0.01 µg/kg per minute Apnea can occur with the initiation of high-dose prostaglandin; therefore the patient should be prepared for intubation The caveat to intubating the neonate in shock is that tachypnea may be a response to a profound metabolic acidosis; therefore minute ventilation should be high until the metabolic component has been corrected Partial correction of the acidosis with sodium bicarbonate should be considered prior to intubation Supplemental oxygen should be administered with caution, as once the patency of the ductus arteriosus has been reestablished, oxygen can decrease PVR and increase maldistribution of flow into the pulmonary vascular bed It is generally recommended not to “intubate for transport,” as preoperative intubation carries risk during the procedure; it also increases the mortality risk for subsequent surgery, the likelihood of earlier extubation, and the hospital length of stay.39–42 Table 71.2 ABC Approach to Simultaneous Assessment and Management of a Neonate in Shock With a Functionally Univentricular Heart Assessment Management Airway/Access/Antibiotics Placement of an airway should occur, occasionally following partial correction of acidosis with sodium bicarbonate Peripheral, umbilical, or central access Antibiotics are typically started, particularly if the birth has been premature Breathing Tachypnea is common secondary to pulmonary edema from left atrial hypertension (restrictive atrial septal defect), increased lung water (from increased pulmonary blood flow), and to compensate for metabolic acidosis Titrate oxygen for a saturation of 80%–85% and mixed venous oxygen saturation >50% In most cases supplemental oxygen is not necessary when the patency of the arterial duct is established (see Chapter 70) Circulation Prostaglandin initiation at high dose 0.1–0.2 µ/kg per minute, with reduction to lowest effective dose once ductal patency is confirmed, typically 0.01 µg/kg per minute Volume administration 10 mL/kg isotonic fluid boluses as necessary Inotropic support for failing ventricle with dopamine or epinephrine, consideration for milrinone to reduce systemic vascular resistance (although pulmonary vascular resistance may fall as well) Inspired gases to potentially elevate pulmonary vascular resistance and improve systemic oxygen delivery are controversial and used variably at different centers Urgent bilateral pulmonary artery banding for stabilization achieves the same goal with more predictability and little effect on the preoperative vascular tone of the pulmonary endothelium.2,46,47 Once the neonate has been stabilized, a comprehensive evaluation for endorgan function should occur This includes assessment for intracranial hemorrhage and ischemic brain injury, necrotizing enterocolitis, and testing of hepatic and renal function However, if the neonate remains unstable without end-organ recovery, worsening end-organ injury, and ongoing acidosis, bilateral pulmonary artery banding can be performed to increase systemic blood flow and decrease flow to the pulmonary vascular bed, thus allowing for end-organ recovery This strategy has been shown to improve systolic blood pressure, renal function, and acidosis with recovery of end organ function, allowing for more definitive surgical palliations including the Norwood operation and transplantation.43–45