Physiology News Magazine

Full issue

Cardiac output diversity: Are children just small adults?


Cardiac output diversity: Are children just small adults?


Helen Ord, Southampton Children’s Hospital, UK

Michael J Griksaitis, Southampton Children’s Hospital & University of Southampton, UK

Understanding the phenotypical differences between children and adults is uncomplicated. The changes children undergo in terms of growth, stature and higher functions are easily apparent. What is not so clearly visible, is their physiological differences. Even the micro-architecture of cells differs and an understanding of this diversity helps us to manage conditions which alter their physiology in a detrimental way (Vrancken et al., 2018; Marijianowski et al., 1994). In this article we will focus on how the physiology of cardiac output varies with age.

What is cardiac output?

Cardiac output is the volume of blood pumped from the left or right ventricle, per unit time. It is most commonly used to describe the left ventricular (LV) output to the systemic circulation, and is a product of the stroke volume and heart rate. Adequate LV cardiac output is important to ensure sufficient oxygen delivery to tissues, irrespective of age.

In order to alter the cardiac output to match the end organ demand during disease states, or increased metabolic demand, there are many factors which can be altered with the end effect of changing heart rate or stroke volume.

It would appear logical that if there is a greater demand for an end product (oxygen, glucose), both an increased supply and increased rate of delivery is required. However, there is distinct diversity between the response of the neonatal, infant and young children’s cardiovascular system to demands on cardiac output, when compared to that of the adult.

How the neonatal heart differs

Newborn infants have a much higher metabolic rate and demand than adults, given their rate of growth, particularly in the first year of life. Their protein and glycogen stores are comparatively much less than adults.

When the neonatal heart is put under greater demand, the ability to increase cardiac output by increasing stroke volume is limited. This is because it has a relatively higher proportion of extracellular matrix (ECM), and a higher ratio of type I to type III collagen within the ECM. This lends it to being less compliant than the adult heart and thus, less accommodating of volume expansion with resultant increases in cardiac stroke volume (Marijianowski et al., 1994). There is evidence that following a myocardial infarction, the deleterious remodelling that occurs and leads to a less complaint heart is in part owed to a similar increase in the ratio of type I to type III collagen fibres (Wei et al., 1999). Therefore, given the relatively fixed stroke volume, the cardiac output of neonates and infants is very heart-rate dependant. This is a relatively unique difference in the age-dependent physiology.

The mechanics of cardiac output: Preload

The Frank–Starling curve represents changes in cardiac output for a given change in preload (or end diastolic volume). Such that, as end diastolic volume is increased (through increasing preload) this equates to a proportional increase in stroke volume, and therefore cardiac output. This is true to a point of optimal sarcomere stretch, after which further increases in preload do not equate to ongoing increases in cardiac output.

However, we know that the neonatal myocardium is less compliant. It therefore sits on a flatter part of the Starling curve, and the same increases in preload do not result in increasing cardiac output to that which may be observed in an adult. As mentioned, neonates are heart-rate dependent for their cardiac output. However, when beating too fast there is then reduced diastolic filling time. The normal heart rates therefore vary with age (Figure 1).

The mechanics of cardiac output: Contractility

Calcium is essential for the unique narrative of the cardiac action potential and for the excitation–contraction coupling by which the electrical action potential is converted to muscle contraction.

There are a number of factors related to calcium delivery and use in the neonatal myocardium which impair contractile ability. The sarcoplasmic reticulum (SR), which senses and triggers calcium-induced calcium release (CICR) in order to potentiate contraction is immature, as well as the T-tubules which invaginate into the myocyte to bring L-type calcium channels into closer contact with the SR ryanodine receptors (Ikonnikov and Yelle, 2013; Breatnach et al., 2017). There is evidence that these factors, alongside altered calcium handling, lead to generation of less force during contraction (Wiegerinck et al., 2009).

The pattern of LV contraction during systole differs between adults and neonates, with adult myocardial muscle fibres using optimal rotational physiology. Outflow from the adult ventricle is enhanced as the fibres of the apex move in a counter-clockwise direction with other fibres (basal) moving in the opposite direction (Vrancken et al., 2018).

There is some evidence that preterm infants (those delivered prior to 36 weeks gestation) display more negative (clockwise) basal rotation than their term counterparts. Furthermore, infants who have been exposed to hypoxia in the perinatal period, have further deleterious properties of LV physiology, displaying reduced LV torsion, twist and untwist rates compared to controls (Breatnach et al., 2017).

Diversity in maturity of autonomic innervation between the neonatal and adult heart also differs. Mature parasympathetic fibres predominate in the neonatal heart, leading to a more pronounced response of the vagal nerve (bradycardia). Given we have established the importance of heart rate in the control of cardiac output in neonates, one can understand the potential detrimental effects of this should the parasympathetic response be activated (a problem encountered in paediatric anaesthesia and critical care).

Beta-adrenergic receptor stimulation leads to increased inotropy, chronotropy and lusitropy in cardiac muscle. The neonatal heart has relatively less sympathetic innervation and beta-adrenergic receptors compared to the adult heart, leading to impaired contractility.

The mechanics of cardiac output: Afterload

Afterload is the pressure against which the left ventricle ejects blood during systole. Afterload is often primarily considered to be that of systemic vascular resistance, but it is also dependent upon aortic pressure and vascular compliance. There is some evidence that the neonatal heart is more sensitive to changes in afterload than the adult heart, in terms of ventricular performance (Rowland and Gutgesell, 1995).

The effects of ageing and hypertension on the systemic vascular resistance are also an example of differences in afterload and therefore cardiac function between adults and infants. There is a natural increase in blood pressure with age (Figure 1).

Clinical applications of the physiological differences

An understanding of the variances in alteration of cardiac output between young children and adults enables us to tailor our practical management and anticipate causation of physiological decline.

There is evidence to show the haemodynamic response of young children to sepsis (overwhelming blood-borne infection) is commonly that of increased systemic vascular resistance and myocardial dysfunction. In contrast, adults more commonly present in a hyperdynamic state of reduced systemic vascular resistance (SVR) and increased cardiac output.

Understanding this, alongside the specific mechanisms which impair cardiac output in children, means we can counter them with our treatment.

For example, if we understand that the very young patient has a poor preload reserve and a limited ability to intrinsically improve cardiac output by improving contractility, the addition of medication to reduce afterload (reduce pressure against which the left ventricle needs to pump) is likely to be of significant benefit. Figure 2 summarises the differences between neonatal and adult cardiac output that have been discussed here.


There are physiological differences as described in the cardiovascular system of the neonate when compared to the adult. This diversity is important when considering the clinical implications of management of critical illness.


Breatnach CR et al. (2017). Left ventricular rotational mechanics in infants with hypoxic ischaemic encephalopathy and preterm infants at 36 weeks postmenstrual age: a comparison with healthy term controls. Echocardiography 34(2), 232 – 239.

Ikonnikov G, Yelle D (2013). Physiology of cardiac conduction and contractility. [Online] McMaster Pathophysiology Review. Available at: [Accessed 30 May 2019]

Marijianowski MM et al. (1994). The neonatal heart has a relatively high content of total collagen and type I collagen, a condition that may explain it’s less compliant state. J Am Coll Cardiology 23(5), 1204 – 1208.

Rowland DG, Gutgesell HP (1995). Noninvasive assessment of myocardial contractility, preload and afterload in healthy newborn infants. Am J Cardiol 75(12), 818 – 281.

Vrancken SL et al. (2018). Neonatal hemodynamics: from developmental physiology to comprehensive monitoring. Front Pediatr 6:87. DOI: 10.3389/fped.2018.00087

Wei S et al. (1999). Left and right ventricular collagen type I/III ratios and remodelling post-myocardial infarction. J Card Fail 5(2), 117 – 126.

Wiegerinck RF et al. (2009). Force frequency relationship of the human ventricle increases during early postnatal development. Paediatric Res 65(4), 414 – 419.

Site search


Content Type

Sign up to our newsletter

Sign up to our newsletter