Routine BP measurement is commonly used as a surrogate for cardiovascular wellbeing, even in HIC countries.3–5 The BP is determined by CO and systemic vascular resistance (SVR). However, an “adequate” mean BP may not equate to an “adequate” CO (see Chapter 3); for example, neonates with high BP due to elevated SVR may actually have a reduced CO. Therefore ideally, CO and BP will need to be monitored simultaneously to determine tissue perfusion. Interpreting BP values, without an objective assessment of cardiac output (using echocardiography), as is followed in many LMICs, may be detrimental in neonates who are critically unwell. In the absence of echocardiography combining parameters like mean BP <30 mmHg and capillary refill time ≥3 seconds increases the sensitivity for detecting measures of low CO such as low superior vena cava (SVC).⁶ Hypotension, which occurs in one-third of preterm neonates,⁷ needs vigilant monitoring, due to its effect on the cerebral blood flow auto-regulation, particularly if the mean blood pressure falls to <30 mmHg.^8,9 Invasive BP monitoring, which may not always be possible in LMICs, needs adequate staff training, while non-invasive measurements need appropriate cuff sizes¹⁰ and tend to overestimate invasive BP values, particularly in immature hypotensive preterm infants.^11,12

The oxygenation index (OI) and the OSI are measures that reflect the severity of hypoxic respiratory failure (HRF) in a neonate and are used to trend the degree of oxygen impairment (Table 28.1). The OI is utilized in some centers to determine the need to initiate iNO and is part of the criteria for commencing ECMO.¹³ Limitations of the OI are that it is invasive, it requires an indwelling arterial catheter, and it is only intermittently performed. OSI is useful in settings where arterial catheter insertion and monitoring are difficult to perform, utilizes the saturation by pulse oximetry (SpO₂), and allows for continuous assessment of the severity of the HRF. In studies comparing OI and OSI in ventilated neonates the correlation coefficient compared strongly (0.89–0.95)^14,15 and was good in the SpO₂ range of 85–95% (r = 0.94). For ranges >95% or <65%, the correlation was poor (r = 0.75).¹⁶ OSI correlated more strongly with HRF in preterm infants <34 weeks (<28 weeks, r = 0.93; 28–33 weeks, r = 0.93) compared with late preterm (r = 0.86) and term (r = 0.70) infants.¹⁶ OSI can be used to predict various levels of OI,¹⁴ making it a potentially useful, noninvasive tool. The regression equation from the derived data showed strong linear association of OSI with OI. A simple relationship between the two measures is that OI values can be derived or predicted from OSI values based on the equation OI = 2 × OSI.¹⁴ The strong correlation between OI and OSI makes OSI a useful tool to predict OI in babies with HRF in an LMIC setting. There are, however, some caveats; specifically, SpO₂ and PaO₂ only correlate linearly when SpO₂ ranges between 80% and 97%, but not in the extremes, where OSI may be unreliable.

d. Assessment of capillary perfusion¹⁷

Plethysmography variability index (PVI)

(Figure 28.2) A useful, noninvasive parameter, also measured by pulse oximetry, is plethysmography variability index (PVI), which is a dynamic index (from 0 to 100) measuring the relative variability of the plethysmography waveform. Higher variability of the plethysmography waveform indicates preload dependence and the need for fluid administration. PVI is calculated as follows: ((PI_max – PI_min)/PI_max) × 100. It may be affected by clinical deterioration, hypotension, volume insufficiency, or other parameters such as ventilation.^22,23

In an Indian study²⁴ that evaluated the changes in PVI in preterm neonates with sepsis and associated hypovolemia, the mean PVI was 28% ± 5 and decreased by 11% ± 5 on resolution of shock. In neonates with associated hypovolemic shock, the average PVI at the onset of shock (31% ± 3) decreased in these infants on the management of hypovolemia by 14% ± 2. PVI correlated positively with the collapsibility of the inferior vena cava (IVC), which suggested need for fluids, though the correlation was weak. Multiple studies^25–27 indicate that PVI may be used as a marker of hypovolemia in hemodynamically unstable neonates, particularly in neonates with no access to cardiac ultrasound.

Preload assessment in neonates, using jugular venous pressure, is not possible due to the presence of a short neck. Cardiac ultrasound is a useful modality for fluid assessment and responsiveness but may have limited availability in LMIC. Some useful parameters in the echocardiographic assessment include (i) IVC diameter (Figure 28.3) and collapsibility index³¹; (ii) eyeballing of the left ventricle (LV) with “kissing ventricles” suggesting an underfilled LV³¹; (iii) reduced ejection fraction by the Simpson biplane method which uses LV end-diastolic areas³²; and (iv) variation in the velocity time integral (VTI) at the LV outflow tract (LVOT). A value of >15% predicts need for fluids with a sensitivity/specificity of >90%.^33,34 Low bedside BP measurement is a good, albeit late, indicator of volume status. As mentioned above, the plethysmography variability index is a new tool that could be used as an indicator of fluid status in resource-challenged settings.

Measurement of LV output equals the systemic blood flow, but only in the absence of a ductal shunt. Measurement of right ventricular (RV) output is reflective of the systemic venous return (in the absence of any atrial shunting). Flow measured in the SVC is normally between 30% and 50% of the total systemic blood flow.³⁵ Echocardiographic assessment of CO,³⁶ if available, is the only available modality in resource-restricted settings to measure CO. Although the intra-observer variability of the measurement is high, and inter-observer variability is even higher, it still remains a helpful noninvasive mode of measuring cardiac output.^37–40

Cardiac ultrasound may be used for comprehensive assessment of chamber dilatation, ventricular systolic function (fractional shortening, ejection fraction) (Figures 28.4 and 28.5) and diastolic function, the presence and direction of flow through transitional shunts (ductus arteriosus, foramen ovale), pulmonary artery pressures, cardiac outputs, and fluid status. It is helpful for enhanced characterization of the hemodynamics in neonates with a significant PDA, pulmonary hypertension, perinatal asphyxia and sepsis, and guiding escalation of inotropic/vasopressor or lusitropic support. There is, however, need for a close collaboration with a pediatric cardiology team to rule out undiagnosed structural heart disease.^41,42 More detailed description of echocardiographic parameters may be found in Chapters 9 and 10.