Paeds SAQs · acute-care-resuscitation-and-toxicology
Shock in children: physiology and classification — formative SAQs
Two MedVellum formative short-answer questions on the physiology and classification of shock in children: recognising compensated shock from the whole child and the trend, grading severity, naming the haemodynamic phenotype, explaining why children maintain blood pressure until late, and applying the fluid-as-a-ceiling principle with early escalation. The marks and timing support transparent self-assessment. They are not an official board format or pass standard.
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Target exams
SAQ 1 — A febrile infant with a normal blood pressure
Question 1 — 10 formative marks; suggested time 15 minutes [1]
A nine-month-old infant has had two days of fever and poor feeding. At assessment the heart rate is 165, the respiratory rate is 50 with mild recession, the central pulses are felt but the peripheral pulses are weak, the skin is cool and mottled, the capillary refill is 4 seconds on the sternum, and the infant is irritable but rousable. The blood pressure is normal for age. The urine output is reduced. [2]
- Define shock and state whether this infant is in shock, justifying your answer from the findings given. (2 marks)
- Explain why a normal blood pressure does not exclude shock in this infant. (3 marks)
- Grade the severity of this infant's shock and explain the compensation-to-collapse trajectory that produces that grade. (3 marks)
- State the single most important bedside sign to follow, and what change would tell you the infant is now decompensating. (2 marks)
Full-credit answer — SAQ 1
Reveal full-credit answer for SAQ 1
1. Definition and whether this infant is in shock
Shock is the failure of oxygen and substrate delivery, or of cellular use, to meet tissue demand, producing a shift to anaerobic metabolism. This infant is in shock. The blood pressure is normal, but the whole circulation picture shows failing perfusion: tachycardia out of keeping with the illness, weak peripheral pulses, cool mottled skin, a capillary refill of 4 seconds, reduced urine output and irritability. Shock is a whole-child, trend-based diagnosis, never a single blood pressure number. [1] [9]
2. Why a normal blood pressure does not exclude shock
Cardiac output in infants is heart-rate dependent because stroke volume is relatively fixed. As stroke volume falls, the heart raises output by increasing heart rate, and the vasculature raises systemic vascular resistance to redirect the reduced output toward the brain and heart. This compensation holds mean arterial pressure in the normal range while perfusion to skin, gut and muscle quietly fails, which is exactly the picture here. Hypotension appears only when compensation finally breaks, at the haemodynamic cliff edge. Waiting for the blood pressure to drop would mean diagnosing shock only when the infant is nearly dead. [1] [2]
3. Severity grade and the compensation trajectory
This is compensated shock: the blood pressure is still normal for age, but perfusion is failing across multiple signs. The trajectory runs from compensated shock, through borderline decompensating shock, to decompensated shock with hypotension, and finally to irreversible shock with refractory organ failure. In the compensated phase tachycardia and vasoconstriction preserve blood pressure and cerebral perfusion while the tissues run anaerobic. The infant is in this phase now; the task is to recognise it and act before the cliff edge, because once hypotension arrives the fall to arrest is steep and fast. [1] [9]
4. The most important sign to follow, and the decompensation signal
The most important sign to follow is the heart rate together with the integrated perfusion trend, because a falling or abnormally low heart rate in a deteriorating infant is the hallmark of decompensation rather than recovery. The change that tells me the infant is decompensating is a falling heart rate with weak or absent central pulses, worsening mottling, falling consciousness and then hypotension for age. The moment any of these appears I treat as decompensated shock and move toward critical care and the arrest pathway. [1] [2]
SAQ 2 — A school-age child in septic shock
Question 2 — 10 formative marks; suggested time 15 minutes [5]
A five-year-old in a regional hospital has fever, warm flushed skin initially then cool mottled limbs, bounding pulses that become weak, a capillary refill that is flash then prolonged, altered consciousness, and a blood pressure that has now fallen below the threshold for age. The hospital has monitoring and intravenous access but no paediatric intensive care or vasoactive agents on site. [5]
- Classify this child's shock by haemodynamic phenotype and by severity, and explain why the picture changed over time. (3 marks)
- Outline your fluid strategy, stating the bolus philosophy and how you decide when fluid is no longer the answer. (3 marks)
- Explain the FEAST lesson and how it applies to this well-resourced child in septic shock. (2 marks)
- Describe your escalation to vasoactive support and retrieval, and why you do not wait for local options to fail. (2 marks)
Full-credit answer — SAQ 2
Reveal full-credit answer for SAQ 2
1. Phenotype, severity, and why the picture changed
This is septic shock: a distributive phenotype that has progressed from warm to cold as reserve was spent, with myocardial depression and relative hypovolaemia contributing a mixed picture. Early, the child was in warm distributive shock with vasodilation, a wide pulse pressure, bounding pulses and flash capillary refill. As the heart could no longer raise its output and the vessels could no longer maintain tone, the child crossed into cold, low-output shock with weak pulses, a narrow pulse pressure, prolonged refill and hypotension. By severity this is now decompensated shock because the blood pressure has fallen below the threshold for age with falling consciousness. Mixed physiology is expected in sepsis, which is why the phenotype must be read as the leading mechanism and revised after every reassessment. [1] [5]
2. Fluid strategy and when fluid is no longer the answer
I confirm shock from the integrated assessment, control obvious loss, and give an isotonic crystalloid aliquot of 10 to 20 mL per kilogram. Before each aliquot I state the response I expect, and after each I reassess the whole child for better pulse quality, warmer skin, a shorter refill, improved consciousness and more urine. The first-hour total is a ceiling, not a target: I repeat an aliquot only while the child remains in shock and is not showing overload. Fluid is no longer the answer when the child is no longer fluid-responsive (no improvement after an aliquot), when the phenotype is cardiogenic or clearly non-responsive, or when overload appears as a rising respiratory rate, basal crackles, hepatomegaly or gallop. At that point I stop fluid and start vasoactive support. [4] [5] [9]
3. The FEAST lesson applied here
FEAST found that saline or albumin bolus increased early mortality compared with no bolus in African children with severe febrile illness. Its correct lesson is that a fluid algorithm cannot be transplanted across populations, shock types and available rescue resources; it does not prove that every bolus is harmful everywhere. Here, in a well-resourced setting with a child in septic shock and critical care available, I still give up-front aliquots because the child is fluid-responsive and in decompensated shock, but I reassess rigorously after each, stop for overload or no benefit, and escalate to vasoactive support and retrieval rather than driving toward a fixed volume. [4]
4. Escalation to vasoactive support and retrieval
Because the child is now decompensated and this hospital has no vasoactive agents or paediatric intensive care, I call retrieval and critical care in parallel with resuscitation, before local options are exhausted. I agree the destination, the vasoactive agent to start on arrival or in transit, the escort and monitoring, the expected deterioration and the plan if transfer is delayed. The first vasoactive agent follows the phenotype: a cold, low-output state leans toward an inotrope such as adrenaline, while a warm, vasodilated state leans toward a vasoconstrictor such as noradrenaline. I do not wait for local options to fail, because the cost of delay in decompensated shock is arrest. [5] [9]
References
- [1]Bjorklund, Ashley Pediatric Shock Review Pediatrics in review, 2023.PMID 37777656
- [2]Fleming, Susannah Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies Lancet (London, England), 2011.PMID 21411136
- [3]Fleming, Susannah The Diagnostic Value of Capillary Refill Time for Detecting Serious Illness in Children: A Systematic Review and Meta-Analysis PloS one, 2015.PMID 26375953
- [4]Maitland, Kathryn Mortality after fluid bolus in African children with severe infection The New England journal of medicine, 2011.PMID 21615299
- [5]Weiss, Scott L Surviving Sepsis Campaign International Guidelines for the Management of Sepsis and Septic Shock in Children 2026 Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies, 2026.PMID 41869844
- [8]Schlapbach, Luregn J International Consensus Criteria for Pediatric Sepsis and Septic Shock JAMA, 2024.PMID 38245889
- [9]Davis, Allan de Caen The American College of Critical Care Medicine Clinical Practice Parameters for Hemodynamic Support of Pediatric and Neonatal Septic Shock: Executive Summary Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies, 2017.PMID 28723883