Seminars in Fetal and Neonatal Medicine 25 (2020) 101144

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Seminars in Fetal and Neonatal Medicine

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Assessment of neonatal perfusion

Samir Gupta a, b, *, Steven M. Donn c
a
School of Medical Physics & Engineering, Durham University, United Kingdom
b
Division of Neonatology, Sidra Medicine, Doha, Qatar
c
Department of Pediatrics, Division of Neonatal-Perinatal Medicine, C.S. Mott Children’s Hospital, Michigan Medicine, Ann Arbor, MI, USA

A R T I C L E I N F O A B S T R A C T

Keywords: Disorders of perfusion in newborn infants are frequently observed in neonatal intensive care units. The current
Perfusion assessment practices are primarily based on clinical signs. Significant technologic advances have opened new
Echocardiography avenues for continuous assessment at the bedside. Combining these devices with functional echocardiography
Hypotension
provides an in-depth understanding of perfusion and allows targeting therapy to the pathophysiology rather than
Shock
Monitoring
monitoring and targeting blood pressure. This change in approach is guided by the fact that perfusion disorders
Newborn can result from a number of causes and a single management approach might do more harm than good. This
approach has the potential to improve long term outcomes but needs to be tested in well-designed trials.

1. Introduction
Assessment and management of neonatal perfusion is an integral part
of neonatal intensive care. The routinely used clinical signs have a
limitation because of low sensitivity during early periods of impaired
perfusion and are deranged only when the newborn has progressed to a
state of uncompensated or irreversible shock [1]. Over the years there
have been key technologic advances that help complement the clinical
examination with bedside assessment tools. There is now a potential for
early diagnosis of neonatal perfusion impairment, which if timely
managed, could reduce morbidity and mortality. There are, however,
concerns that overzealous treatment could do more harm than good. The
selection of assessment tools is governed by striking a balance between
tests with high sensitivity but limited availability (such as functional
echocardiography, MRI) with tests enabling continuous assessment but
with only borderline sensitivity [such as near-infrared spectroscopy
(NIRS)].
With better understanding of transitional circulation and the het­
erogeneity of neonatal hemodynamic problems, it is now clear that one
size does not fit all. Clinicians have to understand the pathophysiology
of the hemodynamic problems to objectively match the therapy to the
cause rather than be guided by the traditional approaches to manage­
ment using volume, inotropes and vasopressors. This requires an un­
derstanding of the physiologic concepts of hemodynamics and the
pharmacodynamic properties of the pharmaceutical agents used for
management.
Over the years we have been treating hypotension rather than
impaired perfusion. Hypotension is a numerical or statistical value
connoting a blood pressure that is more than two standard deviations
from the mean. This may or may not represent a pathological state of
shock, which is derangement of perfusion. It is a condition connoting
circulatory failure, where tissues cannot be provided with adequate
oxygen or nutrients. This change in concept is pivotal for appropriate
management of hemodynamic disturbance and hence assessment of
neonatal perfusion is important in day to day practice.
2. What is perfusion and why is it important?
Perfusion is the delivery of blood to the tissue capillary bed. This
facilitates oxygen transport to the tissues (DO2), which in turn is utilized
for aerobic metabolism. In hypoxic or ischemic states, when the oxygen
delivery falls below the critical level,anaerobic metabolism commences
resulting in the production of lactic acid. To maintain oxygen delivery,
the cardio-pulmonary system has to function effectively and the sys­
temic vascular resistance should be maintained. The DO2 is dependent
upon the lungs, heart, vascular bed, and hemoglobin. Ventilation and
diffusion of gases are often affected in respiratory disorders and could
affect transitional circulation leading to pulmonary hypertension. The
heart is a pump and systolic or diastolic dysfunction can lead to pump
failure and states of shock. The vascular system is comprised of venous
and arterial sides. The venous bed accounts for preload, and the arte­
rioles maintain the systemic vascular resistance within the capillary bed

* Corresponding author. Lead for Neonatal Hemodynamics & Transitional Physiology Program, Sidra Medicine, Doha, Qatar.
E-mail address: Samir.gupta@durham.ac.uk (S. Gupta).

https://doi.org/10.1016/j.siny.2020.101144

Available online 1 August 2020

1744-165X/© 2020 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
S. Gupta and S.M. Donn
Fig. 1. Oxygen delivery and Determinants of myocardial function.
Fig. 2. Bedside non-invasive assessment.
Fig. 3. Stage of shock by cardiac output and blood pressure [Adapted from
deBoode et al. [19]].
affecting end organ perfusion of tissues. The oxygen carrying capacity is
dependent upon hemoglobin as the majority of oxygen is bound to he­
moglobin and only a small percentage is dissolved in the blood. Thus,
evaluation of perfusion should incorporate a global assessment of its
various components to diagnose perfusion problems.
2.1. Oxygen delivery (DO2) and cellular metabolism
The oxygen delivery is the product of cardiac output and oxygen
content (Fig. 1).
DO2 ¼ Cardiac output (CO) x Arterial oxygen content (CaO2)
2
Seminars in Fetal and Neonatal Medicine 25 (2020) 101144
The blood oxygen content is dependent on the hemoglobin concen­
tration of blood and the oxygen saturation, which in turn affects cellular
metabolism. The oxygen saturation is dependent on airway, breathing
and the fraction of inspired oxygen (FiO2). The common lung problems
in newborn babies can range from surfactant-deficient lung disease,
parenchymal disorders of the lung, congenital malformations (such as
diaphragmatic hernia) and intra-pleural collections of air or fluid. The
airway problems encompass obstruction by secretions or debris,
congenital abnormalities of the airway and chronic conditions, such as
bronchopulmonary dysplasia. These airway and lung problems should
be recognized and treated early to facilitate a smooth transition from
fetal to neonatal circulation; otherwise, if persistent, they can adversely
impact perfusion. Further discussion on monitoring and assessment of
lung disorders is beyond the scope of this article.
In ventilated infants, increasing airway pressure decreases the alve­
olar/capillary transmural pressure gradient, squeezing blood out of the
intra-alveolar capillaries, resulting in an increase in pulmonary vascular
resistance (PVR) and a decrease in pulmonary blood flow (PBF). It is
important to ventilate infants at functional residual capacity (FRC),
where the total PVR and alveolar PVR are minimum for the given lung
volume. Additionally, the extra-alveolar PVR is also coincidently low at
FRC. Thus, it allows successful perfusion of the lungs at the minimum
achievable PVR to optimize ventilation-perfusion matching [2].
The other determinant of cellular metabolism is the target blood
flow. The target blood flow is dependent upon cardiac output. The
cardiac output is the product of heart rate and stroke volume. Disorders
of heart rate can be caused by sepsis, arrhythmias, and pain, and could
affect cardiac output even if the stroke volume is maintained. To the
contrary, stroke volume is dependent upon myocardial performance.
The determinants of myocardial performance are preload, afterload, and
myocardial contractility. Different conditions, such as hypovolemia,
ischemia and elevated viscosity could thus affect myocardial perfor­
mance by affecting preload, contractility, and afterload, respectively.
Blood pressure is another important factor. Perfusion pressure is
reflected by mean blood pressure and is derived from systemic vascular
resistance and cardiac output. However, the systolic pressure can be
utilized to assess cardiac contractility and cardiac output, and the dia­
stolic pressure reflects the systemic vascular resistance, which can be
affected by inflammatory states, fetal shunts, and other conditions.
Once ventilation and hemoglobin are optimized, one should
concentrate on the hemodynamic assessment of perfusion using bedside
tools and clinical examination to prevent progression to uncompensated
and irreversible states of shock. It is important to understand and treat
the cause(s) of poor perfusion and direct therapy selectively rather than
blindly following a regimented approach with the potential for harm.
3. Clinical assessment of perfusion and its limitations
The clinical bedside assessment of perfusion in newborn infants has
been used routinely to direct decision making. The commonly advocated
signs include capillary refill time, urine output, heart rate, peripheral
color, base excess, lactate concentration, and blood pressure. The
acceptable limits for each measurement are embedded in practice, but
all of them reflect end organ perfusion. The derangement of end organ
perfusion reflects states of uncompensated or irreversible shock
requiring prompt intervention and treatment. However, early disorders
of perfusion are difficult to detect using clinical signs alone. Used in
conjunction with other monitoring could be more critical to decision
making.
A survey of neonatal intensive care units by Stranak et al. [3] re­
ported enormous variation in diagnosis, management, and clinical
practice. The diagnosis of hypotension in extremely low gestational age
infants continues to utilize mean blood pressure less than the gestational
age as the criterion by 73% of units across the 38 countries surveyed.
The use of mean blood pressure in clinical practice is related to the ease
of measurement rather than the objectivity. It is derived from systolic
S. Gupta and S.M. Donn
and diastolic pressures and reflects the perfusion pressure, but it does
not provide any information on the cause of an abnormal reading.
Widely practiced mean BP values less than the gestational age stem from
the recommendations of an expert working group of the British Asso­
ciation of Perinatal Medicine on audit measures and guidelines for
management of respiratory distress syndrome in preterm infants [4] but
is without sufficient evidence. Clearly, the practices over the last 30
years have changed, with more extremely preterm infants surviving, but
the extrapolation to practice from this old recommendation still con­
tinues to be used for lower gestational age groups. Another report of
mean blood pressure <30 mm of Hg for 1 h in infants <31 weeks’
gestation was reported to be associated with severe hemorrhage,
ischemic cerebral lesions, or death within 48 h [5]. Comprehensive
assessment of perfusion is more informative than relying solely on mean
blood pressure. The use of specific systolic and diastolic blood pressure
measurements is more important to guide therapy, as they reflect car­
diac function and systemic vascular resistance.
The other bedside signs used to assess perfusion have been reported
to have poor sensitivity, specificity, and predictive values. Superior vena
caval flow reflects the systemic venous return from the brain and upper
body and was reported to be poorly correlated with clinical signs, such
as capillary refill time (CRT), core-peripheral temperature difference,
and mean blood pressure. The sensitivity improved to 78% after
combining a mean BP < 30 mm Hg with a CRT >3 s. The authors sug­
gested that low upper body blood flow is common on the first postnatal
day and is associated with intraventricular hemorrhage, but clinical
signs such as BP and CRT have limitations in detecting low blood flow in
the first day of life [6]. Thus, clinicians should be cautious in using only
these clinical signs for decision making in infants with perfusion
disorders.
Base excess reflects acid-base hemostasis and chronic conditions
affected by renal compensatory mechanisms. However, in acute states a
negative base excess reflects metabolic acidosis and anaerobic meta­
bolism. It is a marker to be used with other parameters to assess hypoxic
states such as asphyxia, but on its own is a poor predictor for outcome.
Blood lactate concentrations reflect the perfusion state but are deranged
only if anaerobic metabolism is persistent. High lactate concentrations
can also be observed in poorly perfused peripheral tissues when a
capillary sample is taken for analysis. Rather than using a singular
lactate concentration, serial measurements are more helpful to predict
outcomes. It has been reported that in ventilated infants elevated lactate
concentrations, which do not decrease over 24 h, are associated with
high mortality [7].
4. Bedside monitoring
The determination of adequate circulation and perfusion should be
made based on the composite appraisal of hemodynamic variables [8].
For systematic assessment of the hemodynamic apparatus, bedside
monitoring can utilize various assessment tools, which can be grouped
based on level of assessment (Fig. 2). Broadly, this can be divided into
five assessments:
1. Preload
2. Contractility
3. Afterload
4. Capillary perfusion
5. End organ perfusion
4.1. Assessment of preload
Preload is dependent on cardiac compliance, circulating blood vol­
ume, and venous capacitance. The cardiac compliance is well described
by the relation between preload and stroke volume by Frank-Starling
curve. The ability of the heart to change its force of contraction- and
3
Seminars in Fetal and Neonatal Medicine 25 (2020) 101144
thus the stroke volume-is proportional to the blood present in the
ventricle at the end of diastole. The diastolic function of the heart is thus
important to allow filling of the ventricles and thus effective cardiac
output. In addition to cardiac compliance, a reduction in circulating
blood volume will lead to decreased preload and ventricular dysfunc­
tion. The reduction in circulating blood volume can be seen in acute or
chronic blood loss and third space losses seen in necrotizing enterocolitis
and systemic inflammatory response syndrome. In contrast, (abundant)
fluid administration might also impair ventricular function and cardiac
output. The venous capacitance and mean systemic filling pressure is
controlled by veins, as they hold 65% of the blood volume and are
sensitive to α1 and α2 adrenergic stimulation. This allow modulation of
the pressure from the arterial to the venous side.
Unlike pediatric and adult patients, the assessment of preload in
newborn infants is difficult, as the jugular venous pressure cannot be
reliably assessed. Echocardiography can be used to assess preload –
visualizing the heart, assessing inferior vena cava and superior vena
cava (SVC) flows. The “eye-balling” of the heart in the 4-chamber view
provides information about end-diastolic volume. The inferior vena cava
can be sampled using 2D echo. The SVC flow measurement was first
described by Kluckow et al. and has been widely used in clinical practice
albeit with some limitations [9]. Please refer to the article by deWaal
and Kluckow in this issue for a comprehensive review of SVC flow.
Indirect assessment of preload has been reported using Electric
velocimetry ICON®. An increase in stroke volume variation (SVV) and
thoracic fluid content (TFC) has been utilized in pediatric populations as
a marker for preload, but there is paucity of data in the newborn pop­
ulation [10]. Similarly, the Pleth-variability index (PVi) using the
Masimo® pulse oximeter has been described in adults as a marker to
assess preload status [11]. It is calculated from (Pimax – Pimin) x
100/Pimax. The bedside assessment of blood pressure gives reliable
qualitative information on preload in hypovolemic states, but this can be
a late sign when compensatory mechanisms fail.
4.2. Assessment of contractility (pump)
The cardiac output is dependent upon preload, afterload, and
contractility, the heart function. The assessment of cardiac function can
be done invasively using catheterization, but that is reserved for the
catheterization laboratory for cardiac intervention and pre-surgical
planning. For bedside assessment, the systolic and diastolic function
can be assessed to direct therapy. However, this requires expertise in
functional echocardiography. The indirect measures of cardiac function
utilize measurement of cardiac output. Echocardiography can assess
cardiac output for both the left and right ventricles, but the limitation is
that it only provides point-of-care assessment.
There are various non-invasive cardiac output (CO) assessment de­
vices available that have been reported to measure the CO continuously.
The ‘Thoracic electrical bio-impedance’ (TEB) device is a non-invasive,
easily applicable (four disposable surface electrodes), and continuous
CO measurement method for newborns. TEB is based on impedance
cardiographic technology and uses changes in thoracic electrical
impedance caused by the cardiac cycle: the difference in measured
voltage—produced by a small electrical current—caused by the change
in alignment of red blood cells in the aorta during systole respective to
diastole is used to calculate SV and CO. Examples of TEB are Electrical
Cardiometry (EC; ICON®, Ausculon®, Osypka Medical GmbH, Berlin,
Germany) and the bioreactance method (Starlin®, NICOM®; Cheetah
Medical Inc., Vancouver, WA, USA). The first method analyzes the
changes in signal amplitude and the latter method measures changes in
phase shift of thoracic impedance during the cardiac cycle. The mea­
surements obtained by these devices indirectly measure cardiac output
and are thus affected by loading conditions, such as fetal shunts and
congenital heart defects [12]. We longitudinally assessed ICON® and
observed that assessments done using ICON® correlated with assess­
ments using functional echocardiography for LVO but not for RVO. The
S. Gupta and S.M. Donn
ease of its use and bedside continuous display of data are helpful in the
early diagnosis of perfusion disorders and also to assess the response to
interventions [13–15]. Another non-invasive cardiac output assessment
utilizes transcutaneous Doppler technique. It is used in the ultrasonic CO
monitor (USCOM®, Sydney, NSW, Australia), continuous wave Doppler
device. USCOM® is designed for rapid, non-invasive measurement of CO
located at either the sternal notch (aortic valve; LVO) or parasternal
view (pulmonary valve; RVO). The cardiac output is calculated from the
measured blood flow velocity profile across the aortic or pulmonary
valves. The limitations of this method results from the use of a nomo­
gram based on the patient’s height, weight, and age for estimation of the
valve cross-sectional area. The measurements done by USCOM are not
inter-changeable with echocardiographic assessments [16].
4.2.1. Role of functional echocardiography
The echocardiographic assessment of cardiac function incorporates
2D, spectral Doppler, M-mode, tissue Doppler, and more recently
speckle tracking for strain analysis. Using these modalities, the systolic
and diastolic functions of the heart, cardiac output of left and right
ventricle, contractility of the left ventricle, ejection fraction, and
segmental dysmotility of the myocardium can be assessed [17–22]. This
also helps in assessing the right heart pressures and function and evi­
dence of pulmonary hypertension commonly associated in babies with
hypoxemia and poor cardiac function. The point-of-care assessments
using bedside functional echocardiography combined with continuous
assessment using non-invasive cardiac output monitoring seems a good
approach for continuous assessment of cardiac function to assess
perfusion.
The use of functional echocardiography in neonatal intensive care
units is increasing. There are concerns that if the measurements and
assessments are not performed by trained personnel, the risk of misdi­
agnosis could potentially delay intervention or result in inappropriate
treatment. In trained hands, therapy can be directed to the specific cause
to improve short and long-term outcomes [18,23–27].
4.3. Assessment of afterload
Afterload is defined as the force against which the heart must act in
order to pump the SV and largely depends on ventricular dimensions,
blood pressure, (systemic) vascular resistance, and vascular compliance.
With increasing afterload, the ventricular wall stress increases and the
echocardiography derived velocity of circumferential fiber shortening
decreases, resulting in a decrease in stroke volume. Echocardiographic
studies have reported an age-dependent relationship, suggesting that
newborn infants with an immature heart and a higher basal contractile
state, the myocardial performance is more sensitive to afterload [28,29].
High afterload can be observed in infants shortly after transition,
following ductal ligation, and in the presence of “cold” shock (low CO
and high SVR). Low afterload as a result of low vascular tone/SVR is a
cause of circulatory failure in neonates with “warm” shock (high CO and
low SVR). It is important to differentiate between these different pre­
sentations of shock, as they require other therapeutic approaches (ino­
tropes versus vasopressors) [30,31].
4.4. Assessment of capillary perfusion
The assessment of capillary perfusion at the bedside can be done
clinically using CRT. A CRT > 3 s is abnormally prolonged. The CRT
should be assessed centrally after applying pressure for 3–5 s and timing
the return of color. It is not possible to do it in babies undergoing
therapeutic hypothermia. The Masimo® pulse oximeter displays the
pulse wave contour, which has been used to assess capillary perfusion
using the perfusion index (Pi). Pi reflects the amplitude of the pulse
oximeter waveform and is calculated as the pulsatile infrared signal (AC
or variable component), indexed against the non-pulsatile infrared
signal (DC or constant component). Pi is expressed as a percentage
4
Seminars in Fetal and Neonatal Medicine 25 (2020) 101144
(0.02–20%). In the neonatal acute care setting, a low PI has been shown
to be an objective and accurate measure of acute illness. The determi­
nation of Pi is unambiguous and independent compared to subjective
means of assessing the health status of neonates. When combined with
the heart rate and pulse oximetry value, it can be an objective predictor
of illness severity in newborn infants [32]. In healthy term infants, a
cutoff value of 0.75 (10th centile) and 0.54 (3rd centile) was reported
from a study cohort of 1073 infants [33].
Mixed venous oxygen saturation (SvO2) represents the oxygen
reserve after tissue oxygen extraction. Under normal conditions, the
body extracts approximately 25–30% of oxygen from the arterial blood
resulting in an SvO2 of 70–75%. A decrease in SvO2 is either the result of
an increase in oxygen consumption or a decrease in CO. SvO2 can only
be measured from blood sampled from the main pulmonary artery,
which is not feasible in neonates. An alternative is to sample venous
blood from the right atrium or the caval veins (ScO2). While decreasing
values of SvO2 mostly reflect inadequate oxygen delivery or increased
consumption, normal or high values cannot be interpreted as normal
tissue oxygenation. A number of factors affect its measurement – sam­
pling site, intra-cardiac shunts, redistribution of blood during shock,
level of consciousness, and myocardial oxygen consumption [34].
4.5. Assessment of end-organ perfusion
The assessment of end-organ perfusion has historically utilized
clinical signs as described above. The various states of shock influence
end-organ perfusion, but the clinical signs are predictive only in
advanced or late stages of shock when it is either uncompensated or
irreversible. It is postulated that early intervention, if possible, could
improve outcome by preserving reasonable hemodynamics.
Near-infrared spectroscopy (NIRS) estimates regional blood flow,
regional tissue oxygenation, and—when simultaneously measured with
arterial oxygen saturation—also fractional tissue oxygenation extrac­
tion. End-organ perfusion can be assessed using NIRS in newborn in­
fants. So far, it is regarded as a research tool, but in the last decade there
is renewed interest with improving technology. Observational studies in
neonates evaluated the use of NIRS in the NICU to monitor cerebral/
splanchnic/renal circulation and in the delivery room with promising
results. Interventional trials evaluating the use of NIRS are in progress
[35]. Studies such as the SafeBoosC trial reported that episodes of ce­
rebral hypoxemia and hyperoxemia were significantly reduced in pre­
term infants monitored by NIRS. However, there was no difference in the
short-term outcome. A full overview of this topic is covered separately in
this issue [36].
5. Functional cardiac magnetic resonance imaging (fCMRI)
Cardiac MRI techniques can be used to assess ventricular function
and systemic perfusion in preterm and term newborns. The fast heart
rate, sedation, and transport to the MR scanner has limited the useful­
ness of this modality on the NICU. Because of the shape of the ventricles,
CMRI provides the highest sensitivity and specificity of cardiac function
measurement compared to other modalities, including echocardiogra­
phy. Groves et al. reported the feasibility of using CMRI in preterm in­
fants and demonstrated that CMRI provides additional value over
echocardiography [37].
6. Decision making in different types of shock
Neonatal hemodynamic perfusion disorders can be broadly grouped
into four types of shock:
a. Hypovolemic shock
b. Cardiogenic shock
c. Distributive shock
d. Obstructive shock
S. Gupta and S.M. Donn Seminars in Fetal and Neonatal Medicine 25 (2020) 101144

Practice points
1. Assessment of perfusion should take into account preload, afterload, and cardiac function.
2. Clinical signs of perfusion assess end organ perfusion and thus are not deranged until late into perfusion disorders.
3. Functional echocardiography is increasingly utilized for perfusion and hemodynamic assessment of infants presenting with impending shock.
4. Non-invasive bedside tools and techniques are increasingly utilized for longitudinal continuous assessment and trend analysis.

In hypovolemic shock, there is decreased intravascular blood volume.
This could result from a hemorrhagic disorder with acute or chronic
blood loss, or from non-haemorrhagic disorders, such as diabetes
insipidus, dehydration, or iatrogenic fluid imbalance. In these situations,
the preload is reduced and the cardiac function is initially preserved. If
persistent, the decreased end-diastolic volume leads to diastolic
dysfunction of the heart with resultant decreased systolic BP and
reduced end-organ perfusion. Appropriate history, detection, and
prompt treatment of hypovolemia can prevent acute kidney injury and
other systemic ischemic problems common with other causes of shock as
late events with a potential for long term complications.
Cardiogenic shock can be caused by prematurity, myocardial
hypoxemia-ischemia, myocarditis, cardiomyopathy, and arrhythmias. It
can also be associated with congenital heart defects pre- and post-
intervention. In these situations, the preload and afterload is normal
for gestational age. However, the myocardium can be poorly organized
(as in premature infants), subject to hypoxemia/ischemia, or with
myocardial dysfunction, as in myocarditis and cardiomyopathy. In these
situations, the blood pressure is initially compensated by compensatory
response mechanisms and/or iatrogenically by injudicious use of vaso­
pressors such as dopamine. The cardiac dysfunction and reduced cardiac
output can be detected by invasive and non-invasive assessment tools,
but echocardiography is important to assess the degree and extent of
cardiac dysfunction, and also to assess systolic/diastolic dysfunction.
Afterload reducing agents with positive ionotropic effects, such as
dobutamine, milrinone, or low dose epinephrine are drugs of choice in
the initial states. The arrhythmias are associated with reduced cardiac
output, and the treatment of the primary cause and conversion to a
normal sinus rhythm is required to maintain perfusion.
In distributive shock there can be loss of fluid into the third space with
reduced systemic vascular resistance (low diastolic BP as in warm shock)
with normal or high cardiac output as seen in sepsis and severe systemic
inflammatory response syndromes. In cold shock, to the contrary, the
blood pressure is maintained but the cardiac output is low with or
without low intravascular volume. In these situations, careful and
judicious use of fluid boluses and vasopressors to improve SVR (in warm
shock) and inotropes to improve cardiac contractility (in cold shock) is
advocated. Patients should be closely followed with functional echo­
cardiography and non-invasive continuous monitoring of perfusion to
manage further.
In obstructive shock, the baby can present with signs of decreased
preload, afterload, and cardiac function depending on the duration of
exposure and delay in treatment of the primary cause. Tension
pneumothorax, and cardiac tamponade (pneumo- or hemo-pericardium)
require prompt decompression. These are usually neonatal emergencies
that require prompt recognition and intervention. Clinical management
of different types of shock is covered in the article by Dempsey et al. in
this issue.
Shock can also be classified as:
1. Compensated shock
2. Uncompensated shock
3. Irreversible shock
By measurement of cardiac output and blood pressure, the state of
shock can be assessed at bedside. If the cardiac output is low and the
blood pressure is normal or high, the baby is in compensated shock. If
both cardiac output and blood pressure are low then the baby is already
in uncompensated shock. If the uncompensated state persists and affects
the end- organ perfusion with derangement of cellular metabolism, the
baby has entered into irreversible shock (Fig. 3).
Based on the assessment, the clinician should make an informed
decision on the state of perfusion and take decisive steps for
management:
� Adequate perfusion – No action
� Borderline perfusion – Monitor and review frequently
� Inadequate perfusion – Commence first line management and
request functional echocardiogram
� Grossly inadequate perfusion – Emergency management and urgent
functional echocardiogram
� No perfusion – “Crash” call
7. Conclusion
Management of perfusion has evolved over the last decade with
improvement in technology and the availability of bedside functional
echocardiography. Bedside continuous monitoring techniques are
rapidly evolving to complement clinical assessment and diagnose
inadequate perfusion states sooner rather than later. Basing decisions on
blood pressure alone is a questionable practice, and an extended
assessment beyond blood pressure seems the way forward. This under­
standing allows treating the cause of impaired perfusion rather than
following the heretofore regimented approach to management of hy­
potension. Although the long term data on the utility of new biomarkers
for perfusion assessment are lacking, a physiology-based approach

Research directions
1. Monitoring and trend analysis to diagnose infants during compensated shock.
2. Clinical short and long term outcomes of the physiologic approach to perfusion management requires investigation through well-designed
trials.
3. Methods to diagnose preload and assess fluid responsiveness in hypotensive newborn infants.

5
S. Gupta and S.M. Donn
seems logical and a step towards precision medicine. It is equally
important to recognize the limitations of the monitoring systems used,
and above all monitoring itself will not improve outcome unless a
rational physiologic approach is used.
Financial disclosure
The authors have indicated they have no financial relationships
relevant to this article to disclose.
Declaration of Competing Interest
The authors Competing Interest: None declared.
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