Paeds · acute-care-resuscitation-and-toxicology
Cardiogenic and obstructive shock
Also known as Paediatric cardiogenic shock · Obstructive shock in children · Cardiac tamponade · Tension pneumothorax · Low cardiac output syndrome · Pump failure shock
Fellowship guide to paediatric cardiogenic and obstructive shock: recognising the low cardiac output state from pump failure versus mechanical obstruction, the distinguishing bedside signs of cardiac tamponade (Beck triad, pulsus paradoxus) and tension pneumothorax, the cautious fluid and inotrope strategy for cardiogenic shock, the emergency needle decompression and pericardiocentesis that reverse obstructive shock, and the ANZ, AHA and European guideline differences.
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Overview & Definition
Shock is the failure of the cardiovascular system to deliver enough oxygen to the tissues to meet metabolic demand. It is not defined by a blood pressure reading — a child can be in shock with a normal blood pressure, because compensatory tachycardia and vasoconstriction keep the pressure up until late, and hypotension is a late and ominous sign.[1][17] Shock becomes decompensated when the blood pressure falls below the Pediatric Advanced Life Support hypotension thresholds for age — below 70 mmHg in infants, below 70 + (2 × age in years) mmHg from 1 to 10 years, and below 90 mmHg at 10 years and older.[17]
Paediatric shock is classified by its mechanism into four types: hypovolaemic (loss of volume), distributive (vasodilation, as in sepsis or anaphylaxis), cardiogenic (pump failure), and obstructive (mechanical obstruction to forward flow). This page owns the last two types. Cardiogenic shock is the failure of the heart to generate an adequate cardiac output because of impaired contractility, a structural lesion, or a pathological rhythm. Obstructive shock is the failure of forward flow because something mechanical is blocking the heart or the great vessels: cardiac tamponade, tension pneumothorax, or massive pulmonary embolism.[1][3]
The reason cardiogenic and obstructive shock are grouped together is that they share a cold, low-output phenotype and, crucially, they are the two shock types where aggressive fluid resuscitation can harm. Both demand early vasoactive support or physical decompression rather than the large-volume crystalloid boluses that rescue hypovolaemic and septic shock. Recognising the type within the first minutes of assessment is the skill that separates the safe from the dangerous resuscitation.[1]
You have read the opening of this topic. The complete unit — every section and its primary-source references — is part of the Paediatrics Fellowship fellowship atlas.
References17Show ledgerHide ledger
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- [11]Alsabri M, Abo-Elnour DE, Ayyad M, et al. Epidemiology and management of massive, sub-massive, and non-massive pediatric pulmonary embolism: a systematic reviews. BMC Pediatr, 2025.PMID 40287637
- [12]Ji D, Gill AE, Durrence WW, et al. Catheter-Directed Pharmacologic Thrombolysis for Acute Submassive and Massive Pulmonary Emboli in Children and Adolescents-An Exploratory Report. Pediatr Crit Care Med, 2020.PMID 31688811
- [13]Khalil M, Jux C, Rueblinger L, et al. Acute therapy of newborns with critical congenital heart disease. Transl Pediatr, 2019.PMID 31161078
- [14]Zaidi AU, Hutchins KK, Rajpurkar M Pulmonary Embolism in Children. Front Pediatr, 2017.PMID 28848725
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- [17]Singer CE, Pluta ID, Vintilescu SB, et al. Pediatric Shock Across Acute Emergencies: Age Patterns, Etiologic Subtypes, and Bedside Clinical Indicators in a Single-Centre Cohort. Children (Basel), 2026.PMID 41897079