Seminars in Fetal and Neonatal Medicine xxx (xxxx) xxxx

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Seminars in Fetal and Neonatal Medicine

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Superior vena cava flow: Role, assessment and controversies in the

management of perinatal perfusion
Koert de Waala,∗, Martin Kluckowb
a
John Hunter Children's Hospital Department of Neonatology and University of Newcastle, Newcastle, NSW, Australia
b
Royal North Shore Hospital Department of Neonatology and University of Sydney, Sydney, NSW, Australia

ARTICLE INFO ABSTRACT

Keywords: The superior vena cava (SVC) is a large vein responsible for the venous return of blood from structures located
Superior vena cava superior to the diaphragm. The flow in the SVC can be assessed with Doppler ultrasound and can be used as a
Echocardiography proxy for cerebral perfusion. Early clinical research studies showed that low SVC flow, particularly if for a
Perfusion prolonged period, was associated with short term morbidity such as intraventricular hemorrhage, mortality, and
Newborn
poorer neurodevelopmental outcomes. However, these findings have not been consistently reported in more
Hemodynamics
recent studies, and the role of SVC flow in early management and as a predictor of poor long-term neurode-
velopment has been questioned. This paper provides an overview of SVC assessment, the expected range of
findings, and reviews the role of SVC flow as a diagnostic and monitoring tool for the assessment of perinatal
perfusion.

1. Introduction
Perfusion of an organ or tissue is generally defined as the amount of
blood flow per unit tissue volume. The volume of blood flowing through
the circulatory system is dependent upon the pressure difference within
the measured blood vessel, vessel length, blood viscosity, and internal
vessel diameter. This physiologic principle of blood flow can be used to
estimate blood flow, and thus perfusion. Although many different
techniques are used to measure blood flow in newborns, cardiac ul-
trasound is the one most commonly utilized in clinical practice [1].
During the transition from fetus to newborn, the use of left or right
ventricular output as an indicator of systemic blood flow may not be
accurate because of left-to-right shunts across the patent ductus arter-
iosus (PDA) and foramen ovale. Therefore, measurement of cardiac
input via the superior vena cava (SVC) has been proposed as a proxy for
global cerebral blood flow in the transitional period [2]. As venous
return is the primary contributor of cardiac output, SVC flow can also
be used as a proxy for systemic blood flow
The SVC is a large vein responsible for the venous return of blood
from structures located superior to the diaphragm [3]. The right and
left brachiocephalic veins, also known as the innominate veins, join to
form the superior vena cava behind the first rib space on the right. The
SVC descends downwards to where the azygos vein drains just prior to
the point at which the SVC penetrates the fibrous pericardium, and
terminates in the superior and posterior portion of the sinus venarum of
the right atrium.
Under normal circumstances, blood flow in the SVC is biphasic, with
systolic velocity (S wave) greater than early diastolic velocity (D wave)
and minimal velocity reversal during atrial contraction (A wave). [see
Fig. 1] Respiration induces cyclic changes to this flow pattern, de-
pending on variations in intrathoracic and intraabdominal pressure,
intrapericardial pressure, pericardial constraint, and the inter-
dependence between the four cardiac chambers [4]. In adults, SVC flow
accounts for approximately 30% of total venous flow into the heart,
which can increase to over 50% with hypoxia, hypotension, and/or
cardiac dysfunction. SVC flow is 37% of the left ventricular output in
uncomplicated preterm infants without a patent ductus arteriosus and
50% in term babies [2,5]. It is estimated that 80% of the total SVC flow
is venous return from the head, but exact ranges have not been estab-
lished. SVC flow measurements as a proxy for cerebral perfusion are not
recommended if anatomical SVC or inferior vena cava (IVC) variants
are present.
2. SVC flow assessment
SVC flow measurement was first described in children and newborns
by Salim et al. to help better understand pulmonary blood flow after a
cavopulmonary anastomosis [5]. A few years later Tamura et al.

∗
Corresponding author. John Hunter Children's Hospital, Lookout road, New Lambton, NSW, 3205, Australia.
E-mail address: koert.dewaal@health.nsw.gov.au (K. de Waal).

https://doi.org/10.1016/j.siny.2020.101122

1744-165X/ © 2020 Elsevier Ltd. All rights reserved.

Please cite this article as: Koert de Waal and Martin Kluckow, Seminars in Fetal and Neonatal Medicine,
https://doi.org/10.1016/j.siny.2020.101122
K. de Waal and M. Kluckow
Fig. 1. SVC flow pattern.
described serial changes in SVC flow in 17 healthy term infants, but it
was the publication of 2 pivotal papers by Kluckow and Evans that
brought awareness of SVC flow as blood flow measure [2,6,7]. SVC flow
was minimally affected by fetal shunts such as the foramen ovale (in-
creasing right ventricular output) and the patent ductus arteriosus
(increasing left ventricular output), and could thus be used as a general
measure of cerebral perfusion and cardiovascular adequacy during the
transition from fetus to newborn.
All researchers have used the velocity time integral (Vti) method to
calculate SVC flow in mL/kg/min using the formula Vti x π x (mean
SVC diameter2/4) x heart rate/body weight, but the methodology of
measuring vessel diameter and the probe position to capture the
Doppler signal varies from study to study (Table 1). Most current stu-
dies have adopted the method proposed by Kluckow and Evans, where
the mean of minimum and maximum SVC diameter is captured from the
parasternal view and then averaged over 3 cardiac cycles. The Vti was
captured using a subcostal view and averaged over 10 cardiac cycles to
minimize the impact of respiration, although in clinical practice 4–6
cycles are often used.
The feasibility of image acquisition is close to 100% with good
image quality in about 80% of the acquisitions. However, up to 64%
variability of the calculated SVC flow has been reported between ob-
servers [2,8–10]. Alternative methods of SVC flow measurement have
been proposed in an effort to improve reproducibility. Harabor et al.
explored the variability between Vti measurements taken from the
subcostal view and the suprasternal view [11]. They found good cor-
relation and comparable variability, but angle correction was needed in
most suprasternal views. Ficial et al. proposed measuring SVC cross-
Table 1
Ultrasound methods of assessment of SVC flow.
SVC diameter
Salim 1995 [5] Parasternal view
Maximum diameter from 2D images
Tamura 1998 [6] Not detailed
Kluckow 2000 [2] Parasternal view
Average of minimum and maximum diameter from 2D images
Meyer 2012 [54] Parasternal view
Average of minimum and maximum diameter from M mode images
Ficial 2017 [12] Short axis view
Average of minimum and maximum SVC cross sectional area from 2D images
2
Seminars in Fetal and Neonatal Medicine xxx (xxxx) xxxx
sectional area from a modified short axis view, as previous MRI studies
showed that the SVC is often crescent shaped rather than round or oval
[12]. Although the group reported reduced interobserver variability
from 31% to 18%, data on variability need to be interpreted in the
context of what variation was measured, the equipment used, and
training and experience of the operators. Repeatability can be assessed
by examining the same scan obtained by one investigator using offline
analysis or having the actual image acquisition repeated by a second
observer. Scan-rescan repeatability could induce changes in heart rate
and respirations that contribute to the variation measured. In a recent
multicenter study with highly experienced operators, the median in-
terobserver variability was as low as 6% [13]. Small but statistically
significant differences in SVC flow were found between observers and
between sites, with diameter being the principal source of measurement
variation. From the above findings, it remains important for clinicians
to test the variability of newly used ultrasound parameters using their
own equipment and in their own hands. Interobserver variability can be
reduced with local training of standardized calliper placement, and
using a training tool that permits early recognition of outliers to trigger
review by a more experienced operator [14].
SVC flow measurements have been compared to phase contrast
cardiac MRI [15]. Acknowledging the differences from scan-rescan
variability (the echocardiography was performed at a median of 3.67 h
after the MRI), a significant mean bias of −13.7 ml/kg/min was found
because of higher cross-sectional areas and lower Vti with MRI. How-
ever, these data cannot specify which measurement technique should
be considered the gold standard in newborns, especially in preterm
infants. MRI is likely to be superior in accurately obtaining cross
Vti Comments
Subcostal view
Suprasternal view 5-7 cardiac cycles
No angle correction
Subcostal view 10 cardiac cycles
Subcostal view 10-15 cardiac cycles
Suprasternal view 8-10 cardiac cycles
No angle correction
K. de Waal and M. Kluckow
sectional area, but in preterm infants with higher heart rates, MRI
significantly underestimates true maximum velocity secondary to the
relative low frame rate (20 images per cardiac cycle) compared to the
current generation ultrasound machines (commonly > 50 images per
cardiac cycle). MRI is also impractical in the small, very premature
infant in the first days of life when perfusion information is most cri-
tical.
3. SVC flow and correlation with other measures of cerebral
perfusion
Several studies have compared SVC flow and other ultrasound blood
flow measures against regional cerebral saturation measured with near
infrared spectroscopy (NIRS) [16–20]. Although most studies showed
association between the 2 measures, the correlation was not optimal
and results could be contradictory, and dependent on the clinical con-
dition of the population studied. Regional cerebral saturation is de-
pendent on oxygen delivery and local metabolic rate, which might be
less dependent under optimal clinical conditions. Correlation between
SVC flow and NIRS improved in infants with low blood flow, supporting
this hypothesis. Similar strength relationships between SVC flow and
amplitude integrated EEG were found [21,22].
4. SVC flow reference ranges and values
The mean SVC flow rate in healthy term infants is around 80 mL/
kg/min but can range from 29 to 195 mL/kg/min if measured in the
first few days of life [2,8,9,23,24]. Ranges of SVC flow rates for preterm
infants are generally comparable but should be interpreted according to
concomitant interventions that can affect blood flow, such as illness,
mechanical ventilation and the use of inotropes at the time of the as-
sessment [2,25] (Table 2). The lowest SVC flow is usually recorded
around 3–12 h after birth, with a gradual increase thereafter until
24–48 h after birth. After the transitional phase, the SVC flow remains
relatively stable at 85–90 mL/kg/min in preterm infants [26].
5. SVC flow and clinical outcomes
Few studies have explored whether blood flow is associated with
clinical outcome. Physiology and animal data describe that prolonged
periods of low blood flow lead to inadequate oxygen delivery, lactic
acidosis, and cell damage. However, the threshold for irreversible da-
mage will vary per individual and disease process. Thus, it is not easy to
determine the true definition of low blood flow. Low and pathologically
low ventricular outputs (< 150 and < 120 mL/kg/min respectively)
are associated with morbidity and mortality and generally used to de-
fine low blood flow in preterm infants [27]. Early clinical research
studies showed that low SVC flow, particularly if prolonged, was as-
sociated with short term morbidity, mortality, and poorer neurodeve-
lopmental outcomes [28,29]. Low SVC flow is most commonly defined
as < 41 mL/kg/min, based on the lowest value found in 25 stable
preterm infants at 24 h of age [2].
5.1. SVC flow and intraventricular hemorrhage in preterm infants
The original paper by Kluckow and Evans describes how low SVC
flow is associated with the development of late intraventricular he-
morrhage (IVH) [7]. It was hypothesised that a cycle of ischemia and
loss of autoregulation, followed by reperfusion was the driver of this
increased risk of IVH. Other studies using different ultrasound para-
meters, aEEG and/or NIRS have confirmed the association between low
blood flow and ischemia-perfusion, and the increased risk of IVH
[19,21,30–32]. Not all reports show a consistent or strong association
between low SVC flow and IVH, especially when SVC flow measure-
ments were implemented as part of routine clinical practice. Holberton
et al. analysed scans of 161 preterm infants less than 30 week gestation
3
Seminars in Fetal and Neonatal Medicine xxx (xxxx) xxxx
obtained in the first 24 h of life [33]. The authors found a weak asso-
ciation between low SVC flow and morbidity on univariate analysis, but
this association disappeared when this was corrected for gestational age
and fluid loading on multivariate analysis. The finding could possibly
be explained because these were selected babies who were only scanned
during office hours and not at a predefined postnatal age. The authors
also reported a relatively high mean SVC flow for the whole population
(114 mL/kg/min) and defined low SVC as < 41 mL/kg/min, thus
possibly misclassifying patients because of an alternative method of
measuring SVC flow. Bates et al. scanned 108 preterm infants < 28
weeks at a median of 7 h of age [34]. They reported a relatively high
IVH rate of 43% but could not find a relationship between low SVC flow
and IVH when gestational age was added to a multivariate analysis. A
nested substudy by Popat et al., using < 55 mL/kg/min as a threshold,
also failed to find an association between low SVC flow and late IVH
[35].
Risk factors for low SVC flow have changed over time. Osborn et al.
compared 2 cohorts between 1995 and 1998 and found that the odds
ratio for late IVH from low SVC flow in the first 24 h of life reduced
from 20.4 to 5.2 [30]. Gestational age remained the most important risk
factor for low SVC flow, and importantly, the average mean airway
pressure in the first 12 h of life. It is likely that IVH is a multifactorial
complication of prematurity, and that a single measurement of low
blood flow early after birth is not consistently associated with the de-
velopment of late IVH in the current era of neonatal intensive care, with
different approaches to respiratory support and other treatments that
can affect blood flow [36].
5.2. SVC flow and heart-lung interactions
SVC flow can be used to study heart-lung interactions and help
guide optimal lung distention. Flow in the IVC cannot consistently be
measured using the Doppler Vti method, as the IVC can fully collapse
with changes in intrathoracic pressure. Simultaneous measurement of
SVC flow and RVO can provide additional insight into total venous
return, and how this is affected by changing intrathoracic and intra-
abdominal pressures. Increasing PEEP or mean airway pressure in in-
fants with lung disease generally reduces RVO but without changing
SVC flow, suggesting reduced venous return from the IVC [37,38]. No
changes in SVC flow or RVO were found in preterm infants with sig-
nificant lung disease randomized between conventional ventilation and
HFOV, or when changing positive end-expiratory pressure (PEEP) be-
tween 4, 6 or 8 cmH2O in preterm infants receiving CPAP for evolving
chronic lung disease [39,40]. Fajardo used the LVO: SVC ratio to show
that an increase in PEEP from 2 to 8 cmH2O produces a modest but
consistent decrease in left-to-right shunting through the PDA in venti-
lated preterm infants [41]. Abdel-Hady et al. studied the effect of re-
moving CPAP in stable preterm infants without significant lung disease
and found that SVC flow and RVO could increase by 30% [42]. From
the available data, it seems that alterations in PEEP or mean airway
pressure affect venous return dependent upon lung compliance, and
that before and after measurements of SVC flow can help determine the
optimal balance between lung distention and blood flows.
5.3. SVC flow in infants with hypoxic-ischaemic encephalopathy
SVC flow can help diagnose autonomic dysfunction in infants with
hypoxic ischaemic encephalopathy (HIE). Kumagai et al. studied a
small cohort of term infants with HIE, and found a 2 to 3 times higher
SVC flow beyond 12 h of age in infants with moderate to severe HIE
with abnormalities on MRI compared to infants with a normal MRI or
control infants with mild HIE [43]. This pattern was similar to what was
seen using heart rate variability or NIRS [44–46]. With intact auto-
nomic function and cerebral autoregulation, one would expect a de-
crease in heart rate and cerebral blood flow due to reduced demand.
The infants who were severely affected by hypoxia were not able to
K. de Waal and M. Kluckow Seminars in Fetal and Neonatal Medicine xxx (xxxx) xxxx

Table 2
Clinical studies that report on SVC flow presented for stable preterm infants, preterm cohorts, healthy term infants and term cohorts. CRT; capillary refill time, CPT;
central peripheral temperature, aEEG; amplitude integrated EEG, PEEP; positive end expiratory pressure, PDA, patent ductus arteriosus, PNA: Postnatal age, HIE,
hypoxic ischemic encephalopathy. A full reference list for included studies is available from the authors.
Study Year Comments Population N First echo Low SVC Definition Mechanical Inotropes Severe IVH
(PNA) flow (%) ventilation (%) (%) (%)

PRETERM, WELL
Kluckow 2000 Stable < 30 week 25 5h 0 0 0
Groves 2008 Stable < 31 week 14 5h 0 0 0
Sloot 2010 Stable < 32 week 62 7 days 0 0 0
PRETERM INFANTS
Kluckow 2000 Intraventricular hemorrhage < 30 week 126 5h 38 < 41 ml/kg/min 76 23 10
Osborn 2002 Inotropes < 30 week 42 3h 100 < 41 ml/kg/min 100 100 22
Evans 2002 Middle cerebral artery, blood pressure < 30 week 126 5h 38 < 41 ml/kg/min 76 23 10
Osborn 2003 Ventilation modes < 29 week 43 3h 16 < 41 ml/kg/min 100 51 7
Osborn 2003 Indomethacin < 30 week 70 4h 34 < 41 ml/kg/min 100 0 9
Osborn 2004 CRT, CPT, blood pressure < 30 week 122 3h 34 < 41 ml/kg/min 94 34 14
West 2006 aEEG < 31 week 40 5h 67
Hart 2006 Mixed venous saturation < 34 week 17 8h 35 < 41 ml/kg/min 100
Paradisis 2006 Milrinone < 29 week 29 3h 37 < 45 ml/kg/min 100 100 10
Osborn 2007 Cardiac contractility < 30 week 106 3h 42 < 41 ml/kg/min 98 40
Groves 2008 blood pressure < 30 week 80 5h 6 < 41 ml/kg/min 91
Miletin 2008 Intraventricular hemorrhage < 1500 g 38 18 h 21 < 40 ml/kg/min 44 17
de Waal 2007 PEEP changes all 50 18 h 100
Groves 2008 Descending Aorta flow < 31 week 80 5h 54
Stark 2008 Microvascular blood flow < 37 week 96 24 h 5
Abdel-Hady 2008 CPAP on/off < 33 week 25 7 days 0 0
de Waal 2009 lung recruitment < 30 week 34 5h 12 < 41 ml/kg/min 100 26
Moran 2009 Near infrared spectroscopy < 1500 g 27 18 h 19 < 40 ml/kg/min 78 11 11
Paradisis 2009 Milrinone < 30 week 90 3h 18 < 45 ml/kg/min 100 40
Sehgal 2010 Pre/post surfactant < 32 week 16 21 min
de Waal 2010 Septic shock < 33 week 20 15 days 100 75
Miletin 2010 Cortisol, illness severity < 1500 g 54 18 h 9 < 41 ml/kg/min
Takahashi 2010 Perfusion index < 32 week 24 3h 40 < 40 ml/kg/min 8
Takami 2010 Near infrared spectroscopy < 29 week 16 3h 13 < 40 ml/kg/min 50 56
Paradisis 2012 Magnesium sulphate < 30 week 87 4h 38 < 41 ml/kg/min 91 33 8
Holberton 2012 Intraventricular hemorrhage < 30 week 165 13 h 4 < 41 ml/kg/min 98 66 13
de Buyst 2012 PDA and fluid restriction < 32 week 18 14 days 44
Sommers 2012 Placental transfusion < 32 week 51 6h 2 < 45 ml/kg/min 45
Meyer 2012 Placental transfusion < 30 week 30 16 h 33 < 55 ml/kg/min 17 10 7
Shah 2013 aEEG, blood pressure < 29 week 92 12 h 20 < 45 ml/kg/min 73 35 10
Sirc 2013 Near infrared spectroscopy < 1250 g 22 6h 41 < 41 ml/kg/min 80 18
Katheria 2013 Pre/post surfactant all 20 8h 100
Ficial 2013 Cardiac MRI all 49 11 days 0 0
Beker 2014 PEEP changes < 35 week 34 5 days 0 0
Katheria 2014 Placental transfusion < 32 week 60 5h 90 33 10
Fajardo 2014 PDA and PEEP changes < 31 week 16 6 days 100
Lakkundi 2014 INSURE surfactant < 29 week 68 6h 13 < 45 ml/kg/min 6 10 3
Katheria 2015 Placental transfusion < 32 week 154 7h 17 4
Beker 2015 PEEP changes < 30 week 30 43 days
Cerbo 2015 Near infrared spectroscopy < 32 week 60 6h 21 < 40 ml/kg/min 62 38 12
Bravo 2015 Near infrared spectroscopy, dobutamine < 31 week 126 8h 22 < 41 ml/kg/min 55 28 13
Katheria 2016 Placental transfusion < 32 week 125 17 2
Popat 2016 Placental transfusion < 30 week 266 3 h 11 < 41 ml/kg/min 60 10 5
Bates 2016 Intraventricular hemorrhage < 28 week 108 7 h 9 < 41 ml/kg/min 47
Popat 2018 Variability < 30 week 40 6 h 66
Janaillac 2018 Near infrared spectroscopy, perfusion < 28 week 20 6 h 25 < 41 ml/kg/min 70 10
index
Hwang 2018 PDA and caffeine < 37 week 54 6 days 60
El-Naggar 2019 Placental transfusion < 32 week 73 5h 14 < 55 ml/kg/min 52 16 14
Ruangkit 2019 Placental transfusion < 36 week 101 1 day
TERM, WELL
Kluckow 2000 Well term 14 17 h
Groves 2008 Well term 13 12 h
Lee 2010 Well term 20 12 h
Hochwald 2014 Well term 12 62 h
Ha 2018 Well term 56 12 h
Katheria 2012 Well, gestational diabetes term 50 8h
Banait 2013 Well, small for gestational age term 52 7 days
TERM, UNWELL
Kumagai 2012 HIE term 22 5h
Hochwald 2014 HIE, pre/post rewarming term 16 62 h
Montaldo 2018 HIE, pre/post rewarming term 64 48 h
Mahoney 2018 Variability > 34 week 41 36 h

4
K. de Waal and M. Kluckow
produce this expected physiological response to hypothermia. High SVC
flow could still be documented at the time of rewarming, suggesting
that this finding is reflective of ongoing autonomic dysfunction [23,44].
5.4. SVC flow, PDA shunt and volume load
SVC flow can be used to estimate pulmonary blood flow and guide
fluid restriction in preterm infants with a PDA [47,48]. Evaluation of
left-to-right shunt volume through the PDA remains challenging, but
some researcher would advocate the ratio between LVO and SVC flow
to assess volume load or systemic hypoperfusion [49].
6. Treating and preventing low SVC flow
There are limited data on how best to treat low SVC flow or low
cardiac output in newborn infants. In a crossover design, Osborn et al.
randomized 42 preterm infants with low SVC flow to receive either
dopamine or dobutamine [50]. At the highest dose, dobutamine pro-
duced a greater increase in blood flow than dopamine. However, 40%
of infants failed to increase or maintain SVC flow in response to either
inotrope, and no significant differences in mortality or morbidity were
found. Bravo et al. randomized 28 preterm infants with low SVC flow to
dobutamine or placebo [51]. The time to achieve a normal SVC flow
(> 41 mL/kg/min) was 30–60 min shorter with dobutamine, but this
difference was not statistically significant. Response rate was high in
both groups, over 90%. The study did show some promising clinical
benefits, as the rate of severe IVH was 12% in the dobutamine group
compared to 33% in the placebo group, and similar to the 10% severe
IVH rate found in infants in the control group who did not develop low
SVC flow.
Milrinone, a selective inhibitor of type III cAMP phosphodiesterase
isoenzyme in cardiac and vascular muscles, has been attempted to
prevent low SVC flow [52]. After optimising the dosing regimen for
Milrinone in preterm infants, Paradisis et al. randomized 90 preterm
infants at risk for developing low SVC flow (determined by a predictive
model from previous observational cohorts), with a goal to maintain
SVC flow above 45 mL/kg/min [53]. Success rates were comparable
between the Milrinone and placebo group, but a significant portion of
infants required additional inotropes for low blood pressure.
Placental transfusion has been extensively studied as an interven-
tion to prevent low blood flow in preterm infants. Increased he-
moglobin can be achieved by delaying clamping of the cord by 30–60 s
or by milking of the cord. Early studies showed that placental trans-
fusion produced a significantly higher SVC flow in the first few days of
life, and with fewer infants developing low SVC flow [54–56]. The
largest randomized trial to date including 266 preterm infants < 30
weeks’ gestation could not find a significant difference in SVC flow with
placental transfusion, nor the number of infants who developed low
SVC flow [57]. Placental transfusion was associated with a lower RVO,
possibly suggesting increased right ventricular afterload from the in-
creased hemoglobin content. Placental transfusion has many clinical
benefits, including reduced mortality and morbidity in term and pre-
term infants and is recommended for all vigorous newborns. However,
it might not be the answer to preventing low SVC flow.
7. Should we use SVC flow in clinical practice?
SVC flow is a valuable parameter to inform clinicians about perfu-
sion and cerebral blood flow during the transition from fetus to new-
born. Considerable and/or persistently low blood flow is associated
with increased risk of morbidity and mortality, and serial SVC flow
measurements starting early after birth can help detect those infants at
risk. The diagnostic accuracy of SVC flow to predict poor perfusion will
improve when adding clinical parameters, such as blood pressure and
other measurement techniques for multimodal hemodynamic mon-
itoring [58]. SVC flow and cardiac output are considered key
5
Seminars in Fetal and Neonatal Medicine xxx (xxxx) xxxx
hemodynamic goals in neonatal shock and can be used to target
treatments [59]. SVC flow is an excellent monitoring technique for
assessing heart-lung interactions, PDA shunt volume, and for diag-
nosing autonomic dysfunction in HIE.
The main limitation of SVC flow and cardiac output measurements
is that they are not a true measure of myocardial function. Blood flow
represents the interaction between the heart and the vessels.
Ventricular-arterial coupling is an excellent parameter of cardiovas-
cular efficiency and pathways to heart failure, but it provides limited
insight into intrinsic myocardial function. Adding additional proxy
parameters of preload, myocardial fibre shortening, and changes in
ventricular shape and size are necessary to gain a better understanding
of myocardial function and dysfunction [60].
SVC flow is one of the best studied cardiac ultrasound parameters in
neonatology, and it is thus surprising that SVC flow and cardiac output
are not frequently mentioned in echocardiography guidelines for
newborns [61,62]. M-mode derived fractional shortening is still the
backbone of functional echocardiography in neonates, even though M-
mode parameters are being phased out of adult cardiology. For neonatal
cardiac ultrasound to progress, we should embrace well studied para-
meters such as SVC flow, acknowledging its limitations, and extend our
research to newer cardiac ultrasound assessment techniques to help
identify and treat infants at risk of impaired perfusion in the perinatal
period.
Practice points
• SVC flow is a proxy of cerebral blood flow and cerebral per-
fusion, and one of the best studied hemodynamic parameters
in neonatal intensive care
• SVC flow is minimally influenced by fetal shunts, and is thus
well suited as a hemodynamic monitoring parameter early
after birth
• SVC flow can provide the clinician with information about the
risk of cerebral compromise and provide insight into heart-
lung interactions
Research directions
• SVC
risk.
flow alone might not be sufficient to identify infants at
• Adding novel hemodynamic parameters to blood flow mea-
surements could increase our insight into hemodynamic
compromise in newborns
• More research is needed to reveal how best to treat or prevent
transitional low blood flow
Funding
None.
Declaration of competing interest
None declared.
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