Pediatric Hypotension: Think Hypovolemia

Pediatric hypotension, in the absence of cardiac pathology, should be considered hypovolemia until proven otherwise. Hypovolemia can precipitate respiratory failure, which then worsens hypotension in a vicious cycle. Hypovolemia can result in cardiac arrest.

Case: I was called to the emergency room to intubate an unresponsive, cyanotic, 5 year old girl. She looked pale and quite dehydrated, with sunken cheeks. According to the mother she had been suffering from vomiting, diarrhea and fever for several days. Blood pressure was 50/40 and pulse was 60, oxygen saturation was 65%. While an IV was inserted I hyperventilated her with 100% oxygen and then intubated the child. Pulse rose to 160 as her oxygen saturation rose to 90%. Lab work drawn with the IV start showed a blood glucose of 30. We immediately administered 2 mL/kg/dose of 25% solution of glucose and a 20 ml/kg bolus of crystalloid.

Blood pressure rose to 85/60. Pulse dropped to 120, and oxygen saturation rose to 95%. Glucose rose to 95 mg/dL. The child immediately woke up. She started to fight the endotracheal tube and the team decided to extubate her. She did well.

Although this child also had hypoglycemia, hypovolemia played a major role in her systemic shock. Hypovolemia, with inadequate volume replacement, is one of three major causes of cardiac arrest identified in the Pediatric Perioperative Cardiac Arrest Registry (P.O.C.A.) [1]. The other two were medication related, and respiratory due to airway obstruction secondary to laryngospasm. Here we concentrate on hypovolemia.

Why Do Children Have Less Cardiovascular Reserve?

Hypovolemia can easily cause pediatric hypotension because infants and toddlers have less cardiovascular reserve than adults. This lack of reserve impairs their ability to meet increased oxygen demand, further depressing the heart.

Illustration showing why infants have less cardiovascular reserve than adults

Poor perfusion can lead to hypoxemia, which can be an early sign of hypovolemia in children. Cardiac output is a product of stroke volume and heart rate. Either increasing stroke volume or increasing heart rate increases cardiac output. Humans rely on several mechanisms to increase stroke volume:

  • increasing intravascular volume by oral fluid intake if hypovolemic (not a rapid treatment)
  • vasoconstricting peripheral circulation: shifting more blood volume centrally from out of the limbs
  • increasing cardiac contractility — ejecting more blood with each beat

Limited Ability To Increase Stroke Volume

Infants and toddlers have limits on all 3 ways to increase stoke volume. They must be given liquids to drink and can’t go get more if they’re thirsty. They have low muscle mass and immature peripheral nervous systems, limiting their ability to mobilize circulation. And, their stiffer, less developed heart muscle has limited ability to increase contractility. The result is that pediatric cardiac output is essentially rate and volume dependent. Infants typically have normal heart rates greater than 100.

When faced with stresses such as hypovolemia, fever, or anemia, babies increase their heart rate over and above their baseline tachycardia to compensate. Babies can tolerate a heart rate up to 200 beats per min without evidence of heart failure.

However, there are limits. With little cardiovascular reserve, both hypovolemia and bradycardia quickly drop cardiac output and cause hypotension.

Bradycardia: A Cause and Effect of Pediatric Hypoxia!

Infants and young children have poorly developed sympathetic nervous systems. Hypoxia in an adult or older child usually triggers a sympathetic response, producing a tachycardia that improves oxygen delivery. Bradycardia is a late and very dangerous sign of imminent cardiovascular collapse.

In contrast, bradycardia in babies and young children may be the first sign of hypoxia—not the last. The small child’s immature nervous system has a better developed parasympathetic nervous system. Babies spend a lot of time eating and sleeping, and not so much time engaged in fight-or-flight activities. As a result, hypoxia triggers a vagal response and slows the heart. Consider bradycardia in a child to be caused by hypoxia until proven otherwise!

Infants and small children have a cardiac output that is rate dependent. Bradycardia significantly lowers cardiac output and oxygen delivery; hypoxia and hypercarbia worsen. Acidosis develops, further depressing the myocardium. Cardiac arrest can occur very quickly in the hypoxic child and must be treated urgently with oxygen, ventilation, and if needed, atropine.

Illustration showing cycle of how hypoxia induced bradycardia worsens hypoxia

What Is Hypotension in an Infant? 

To spot abnormal, you must know what normal is (2).

Table of systolic blood pressures indicating hypotension by age
Table indicating heart rates per age

Neonates, infants and small children normally have lower blood pressures than older children and adults. Treatment thresholds for neonatal systolic hypotension vary significantly, for example between North America (45.5 mmHg) and the internationally recommended threshold of 60 mmHg. Providers may tolerate hypotensive pressures in children because of a failure to recognize abnormal. (3)

Volume Treatment of Pediatric Hypotension Varies Greatly By Weight

Assuming normal heart function, treat hypotension with 10 ml/kg boluses of crystalloid, repeated as appropriate. Note that this would mean a mere 27 ml in a 2.7 kg premature neonate or a 50 ml bolus in a 5 kg baby, compared to a 700 ml bolus in a 70 kg adult.

You can see how the difference in scale can potentially lead to volume treatment errors for providers who infrequently manage children. Massive hemorrhage has been defined as a blood loss of 50% of circulating blood volume within a 3-hour period. For a 2.7 kg baby with a blood volume of 80 ml/kg (216 ml), massive blood loss would be 108 ml, an amount that could be safely ignored in an adult. A 10% blood loss for such an infant would be 21 ml, a volume that can be hard to measure intraoperatively. Hypovolemia from blood loss and hyperkalemia from transfusion of stored blood are the most common identifiable cardiovascular causes of death in the P.O.C.A. study (1)

As with most treatments, titration is prudent. Bolus. Observe the results. If need be bolus again. Observe the results. It is always easy to add more, not so easy to undo.

My instructors impressed upon me the two rules for providing safe pediatric anesthesia which have served me well over the years:

  • Pediatric hypotension is hypovolemia until proven otherwise!
  • Pediatric bradycardia is hypoxia until proven otherwise.

Follow this link to my review article in Airway Management on common problems in pediatric airway management and how to fix them: 10 Common Pediatric Airway Problems— And Their Solutions

May The Force Be With You

Christine E Whitten MD
Author: Anyone Can Intubate: a Step By Step Guide To Airway Management
Pediatric Airway Management: A Step By Step Guide


  1. Bhananker SM, Anesthesia-related cardiac arrest in children: update from the Pediatric Perioperative Cardiac Arrest Registry. Anesth Analg. 2007 Aug;105(2):344-50.
  2. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 1: Introduction to ACLS 2000: overview of recommended changes in ACLS from the guidelines 2000 conference. Circulation. 2000;102(8 Suppl):I86-9
  3. Nafiu O, et al. How do pediatric anesthesiologists define intraoperative hypotension? Paediatr Anaesth 2008 19 (11) 1048-1053

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