6.3 Obstructive Shock

AHA PALS Provider Pediatric Advanced Life Support

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1 Chapter 1: Course Overview & Exam Logistics

1.1 Current Exam Facts 1.2 Audience, Prerequisites & Study Plan

2 Chapter 2: Systematic Pediatric Assessment

2.1 Pediatric Assessment Triangle (PAT) 2.2 Evaluate–Identify–Intervene Sequence 2.3 Primary Assessment: ABCDE 2.4 Secondary Assessment, SAMPLE & Vitals by Age

3 Chapter 3: Respiratory Distress & Failure

3.1 Respiratory Distress vs Failure 3.2 Recognition & Immediate Intervention Priorities 3.3 Oxygen Delivery & Basic Airway Support

4 Chapter 4: Airway Problems & Ventilation Strategies

4.1 Upper Airway Obstruction 4.2 Lower Airway, Lung Tissue Disease & Disordered Control 4.3 Bag-Mask Ventilation & Advanced Airways During CPR

5 Chapter 5: Shock Fundamentals & Hypovolemia

5.1 Compensated vs Hypotensive (Decompensated) Shock 5.2 Hypovolemic Shock 5.3 Isotonic Fluid Bolus 10–20 mL/kg & Reassessment

6 Chapter 6: Distributive, Cardiogenic & Obstructive Shock

6.1 Distributive & Septic Shock Pathway 6.2 Cardiogenic Shock 6.3 Obstructive Shock

7 Chapter 7: Pediatric BLS & High-Quality CPR

7.1 High-Quality CPR Metrics 7.2 Compression-Ventilation Ratios 7.3 CPR Quality Monitoring: ETCO2 & Diastolic BP

8 Chapter 8: Pediatric Cardiac Arrest Algorithm

8.1 Arrest Recognition & Systematic Approach 8.2 VF/pVT & Defibrillation Energy 8.3 Asystole & PEA 8.4 Epinephrine in Arrest: Dose & Timing

9 Chapter 9: Bradycardia & Narrow-Complex Tachycardia

9.1 Bradycardia with Poor Perfusion 9.2 Sinus Tachycardia vs SVT 9.3 Stable SVT: Vagal Maneuvers & Adenosine

10 Chapter 10: Unstable Tachycardia & Wide-Complex Rhythms

10.1 Unstable Tachycardia & Synchronized Cardioversion 10.2 Wide-Complex Tachycardia & VT with Pulse 10.3 Antiarrhythmics for Tachycardia with Pulse

11 Chapter 11: Reversible Causes & Special Circumstances

11.1 Reversible Causes: The H's and T's 11.2 Special Circumstances at Exam Level 11.3 Extracorporeal CPR (ECPR) Overview

12 Chapter 12: Post–Cardiac Arrest Care

12.1 Post-ROSC Oxygenation & Ventilation 12.2 Post-Arrest Hemodynamic Support 12.3 Temperature Control & Glucose 12.4 Neuroprognostication & Transport

13 Chapter 13: Vascular Access & Core Pharmacology

13.1 IV and Intraosseous Access 13.2 Epinephrine Dosing in Depth 13.3 Amiodarone, Lidocaine & Adenosine 13.4 Weight-Based Dosing Aids & Drugs to Avoid Routinely

14 Chapter 14: Team Dynamics & Megacode Readiness

14.1 High-Performance Team Roles 14.2 Closed-Loop Communication 14.3 Constructive Intervention, Debriefing & Exam Integration

6.3 Obstructive Shock

Key Takeaways Explain This Topic AI

Obstructive shock is inadequate cardiac output caused by a mechanical barrier to venous return or outflow—not primary pump failure or pure volume loss.

Core pediatric causes: tension pneumothorax, cardiac tamponade, massive pulmonary embolism, and ductal-dependent systemic blood flow lesions in neonates.

Tension pneumothorax: unequal breath sounds, tracheal deviation, hypoperfusion—immediate needle decompression, not endless fluids.

Tamponade: muffled sounds, distended neck veins, poor perfusion—fluids may temporize; definitive therapy is drainage (pericardiocentesis) when indicated.

Ductal-dependent systemic flow lesions may present with shock as the ductus closes—oxygen support and prostaglandin E1 (PGE1) are exam-level interventions while arranging urgent specialty care.

Last updated: August 2026

Mechanical Obstruction of Blood Flow

Obstructive shock occurs when a mechanical barrier prevents adequate venous return to the heart or adequate outflow from the heart/lungs, so cardiac output falls despite a myocardium that may be intrinsically capable of contracting. Preload may be low because blood cannot enter the thorax or heart chambers; afterload may be extremely high because outflow is blocked; or filling may be impaired because the heart is externally compressed. The unifying PALS message: identify and relieve the obstruction —fluids and vasoactives alone will not permanently fix a tension pneumothorax, tamponade, massive embolus, or closing ductus in a ductal-dependent neonate.

Compare the four shock families you now own:

Shock type Core problem First-line theme
Hypovolemic Lost circulating volume Isotonic 10–20 mL/kg boluses + reassess

Distributive Maldistribution / vasodilation / leak Fluids + cause therapy (antibiotics, IM epi) + vasoactives if needed

Cardiogenic Pump failure Cautious 5–10 mL/kg fluids + inotropes + treat rhythm
Obstructive Mechanical barrier Relieve obstruction (decompress, drain, open ductus, etc.)

Mixed pictures occur (trauma with blood loss and tension pneumothorax). Always reassess after each intervention.

Tension Pneumothorax

Air under pressure in the pleural space collapses the lung and shifts the mediastinum, kinking great veins and impairing venous return. Cardiac output plummets—this is obstructive shock and a pre-arrest emergency.

Recognition clues
Severe respiratory distress or failure, hypoxia
Decreased or absent breath sounds on the affected side
Hyperresonance on the affected side (when assessed)
Tracheal deviation away from the affected side (late)
Distended neck veins (variable in young children)
Tachycardia progressing to hypotension and bradycardia
History of trauma, positive-pressure ventilation, or underlying lung disease
Immediate intervention

Perform immediate needle decompression of the affected side per training and protocol, followed by definitive chest tube thoracostomy when available. Support airway and oxygen. Do not delay decompression to obtain a chest radiograph if the clinical diagnosis of tension physiology is clear. Fluids may support blood pressure briefly but do not replace decompression .

Exam trap: choosing only another fluid bolus for a trauma patient with unilateral absent breath sounds and shock. The correct action is decompress the chest.

Cardiac Tamponade

Fluid (blood or effusion) in the pericardial sac raises intrapericardial pressure, impairs diastolic filling, and reduces stroke volume—classic obstructive physiology.

Recognition clues
Poor perfusion, tachycardia, hypotension
Muffled heart sounds
Distended neck veins / signs of elevated venous pressure
Pulsus paradoxus when measurable
History of chest trauma, post-cardiac surgery, or pericardial disease
Electrical alternans or low voltage on ECG when available; enlarged cardiac silhouette may appear on imaging

Beck’s triad (hypotension, muffled sounds, elevated venous pressure) is taught widely but may be incomplete in children—do not require the full triad to act when suspicion is high.

Immediate intervention

Give oxygen; support ABCs. Isotonic fluid boluses may temporarily improve filling pressures and cardiac output as a bridge. Definitive therapy is pericardial drainage ( pericardiocentesis or surgical drainage) when indicated by clinical instability and available expertise. Arrange expert help early. Endless fluids without drainage will fail as intrapericardial pressure continues to limit filling.

Massive Pulmonary Embolism

Large PE obstructs pulmonary arterial flow, strains the right ventricle, and collapses left-ventricular preload—obstructive shock with severe hypoxemia. Pediatric PE is less common than adult PE but occurs with hypercoagulable states, central lines, congenital heart disease, and immobilization.

Recognition clues
Sudden dyspnea, hypoxemia, chest pain (if verbal)
Clear lungs or minimal findings despite profound hypoxemia
Signs of right-heart strain and shock
Risk factors as above
Immediate intervention

Support oxygen and ventilation; circulatory support per shock care; urgent expert consultation for imaging and reperfusion strategies (anticoagulation, thrombolysis, or other therapies in appropriate settings). PALS-level emphasis: recognize that this is not simple hypovolemia and that repeated fluids alone will not clear the vascular obstruction.

Loading diagram... Obstructive Shock: Cause → Immediate Action

Ductal-Dependent Systemic Blood Flow Lesions (Neonates)

Some neonates depend on a patent ductus arteriosus to supply systemic blood flow. Examples discussed at exam level include severe coarctation of the aorta , interrupted aortic arch, critical aortic stenosis, and hypoplastic left heart syndrome (HLHS) variants. When the ductus constricts in the first days of life, systemic perfusion collapses—the neonate presents in shock , often with gray color, weak pulses (sometimes differential upper vs lower extremity pulses in coarctation), metabolic acidosis, oliguria, and respiratory failure.

Recognition clues
Age typically first 1–2 weeks of life as ductal constriction occurs
Shock without clear hypovolemic losses
Differential pulses or blood pressures (upper > lower) in coarctation patterns
Single loud S2, murmur variable; gray/ashen appearance
Poor response to fluid boluses alone; progressive lactic acidosis
Immediate intervention (exam-level)

Support airway, breathing, and oxygen carefully—follow neonatal/cardiac guidance; many ductal-dependent systemic-flow lesions are managed with attention to balancing systemic and pulmonary circulations under specialist direction.

Obtain vascular access; correct hypoglycemia and support blood pressure.

Start prostaglandin E1 (PGE1, alprostadil) infusion to reopen or maintain ductal patency when a ductal-dependent lesion is suspected—this is the disease-specific therapy that can restore systemic flow.

Urgent pediatric cardiology / neonatal intensive care transfer; echocardiography confirms anatomy.

PGE1 can cause apnea —be ready to support ventilation. Exam items test whether you recognize the neonate in shock from ductal closure and choose PGE1 + supportive care + specialty transfer , not endless crystalloid alone.

Related concept: ductal-dependent pulmonary flow

Some cyanotic lesions depend on the ductus for pulmonary blood flow (e.g., severe pulmonary stenosis/atresia patterns). Those neonates present with profound cyanosis as the duct closes. PGE1 is again the bridge therapy. For obstructive shock framing, focus on ductal-dependent systemic flow lesions that present with hypoperfusion and shock; know that PGE1 is the shared exam-level pharmacologic bridge for ductal-dependent physiology.

Do Not Treat Obstruction With Endless Fluids Alone

Fluids have a limited bridging role (especially tamponade, some PE states) by raising filling pressures, but they do not remove the mechanical problem . If a vignette screams tension physiology, tamponade, PE, or closing-ductus neonatal shock, the correct answer names the cause-specific intervention (decompress, drain, specialist reperfusion pathway, PGE1)—not "another 20 mL/kg and recheck in an hour."

Putting Chapters 5–6 together
Is the child in shock? (perfusion, mentation, urine, lactate/acidosis context, BP for age)

Compensated or hypotensive?

Which type—hypovolemic, distributive, cardiogenic, obstructive—or mixed?

Intervene: oxygen/airway, access, type-specific fluids/drugs, cause control, reassess, escalate.

Clinical scenario (synthesis)

A 4-day-old neonate becomes poorly feeding, gray, and tachypneic with weak femoral pulses, delayed capillary refill, and severe metabolic acidosis. Multiple fluid boluses produce little improvement. Think ductal-dependent systemic blood flow lesion with ductal constriction —start PGE1, support ABCs, correct glucose, and arrange emergent cardiology/NICU care. A different child after blunt chest trauma develops sudden hypoxia, absent left breath sounds, tracheal deviation, and hypotension— tension pneumothorax —needle decompress immediately. A postoperative cardiac patient with muffled sounds, high venous pressure signs, and shock— tamponade —bridge with oxygen/fluids and pursue drainage.

Master obstructive shock and you complete the four-type shock framework tested throughout the Shock domain.