Normal circulatory function depends on coordinated interaction
between the heart as the central pump and the microcirculation
at the tissue level to deliver oxygen and nutrients and remove
metabolic waste. Shock is an acute failure of
circulatory function to adequately deliver oxygen or
nutrients to tissues resulting cellular energy failure and
metabolic dysfunction.
In children, strong compensatory mechanisms are able to preserve blood pressure and shock may occur without hypotension. Therefore, Early recognition therefore relies on perfusion abnormalities, vital sign changes, and mental status rather than blood pressure alone.
Adequate tissue oxygenation depends on cardiac output (CO) and microvascular blood flow:
CO = Stroke Volume × Heart Rate
Stroke volume is influenced by:
These variables are regulated by sympathetic tone, endogenous catecholamines, nitric oxide, pH, oxygen tension, calcium homeostasis, and inflammatory mediators.
Infants have limited ability to increase stroke volume and rely heavily on heart rate to augment cardiac output, therefore, tachycardia is a key early sign of shock.
Decreases in preload, afterload, or contractility trigger compensatory mechanisms such as increased heart rate, increased SVR, and redistribution of blood flow. As shock progresses, these mechanisms fail, leading from compensated to uncompensated shock.
Blood pressure reflects the interaction of CO and SVR but is a late marker of shock in children. Normal blood pressure does not exclude significant hypoperfusion.
Low SVR may produce:
Hypotension indicates failure of compensatory mechanisms and impending cardiovascular collapse.
All shock states involve absolute or functional hypovolemia.
Maldistribution of capillary blood flow is common to all shock types and is driven by endothelial activation, inflammatory cytokines, PAMPs, DAMPs, microthrombi, and glycocalyx injury. This contributes to regional ischemia and progression to multiorgan dysfunction syndrome (MODS).
Restoration of blood flow may trigger oxidative and inflammatory injury, amplifying tissue damage even after global perfusion improves.
Mitochondrial dysfunction may impair oxygen utilization despite adequate delivery, leading to impaired ATP production and organ dysfunction. This phenomenon helps explain persistent organ injury in sepsis and trauma despite normalized hemodynamics.
| Shock Type | Examples | HR | BP | CO | Capillary Refill | Extremity Temp | SVR | Treatment |
|---|---|---|---|---|---|---|---|---|
| Hypovolemic | Hemorrhage Dehydration |
↑ | ↓ | ↓ | Delayed | Cool | High | Stop bleeding Fluid resuscitation (crystalloids) Blood products when indicated |
| Cardiogenic | Myocarditis Dysrhythmias Cardiomyopathy |
↑ | ↓ | ↓ | Delayed | Cool | High | Inotropes (epinephrine, milrinone) Caution with fluids Treat arrhythmias ECMO for refractory cases |
| Distributive | Sepsis Anaphylaxis |
↑ | ↓ or normal | ↓ or ↑ (early sepsis) | Flash or delayed | Warm or cool | Low or high | Sepsis: antibiotics, fluids, vasopressors Anaphylaxis: epinephrine, fluids, antihistamines, steroids |
| Neurogenic | Spinal cord injury Traumatic brain injury |
↓ | ↓ | ↓ | Flash or normal | Warm | Low | Fluid resuscitation Vasopressors (norepinephrine) Spinal stabilization |
| Obstructive | Cardiac tamponade Tension pneumothorax Pulmonary embolus Ductal-dependent congenital lesions |
↑ | ↓ | ↓ | Delayed | Cool | High | Pericardiocentesis Needle decompression / chest tube Anticoagulation or thrombectomy Prostaglandins for ductal-dependent lesions |
| Dissociative | Carbon monoxide poisoning Cyanide toxicity |
↑ | Normal or ↑ | ↑ | Normal | Normal | Low to normal | CO: high-flow oxygen, hyperbaric therapy Cyanide: hydroxocobalamin, sodium thiosulfate |
Hypovolemia, or decreased circulating blood volume, is the most common cause of shock in children. Worldwide, the leading etiology is gastrointestinal fluid loss from vomiting and diarrhea due to infection. Other causes include hemorrhage (trauma, postsurgical, gastrointestinal), plasma losses (burns, hypoproteinemia, pancreatitis), and extragastrointestinal water losses (glycosuric diuresis, heat stroke).
Acute hypovolemia reduces cardiac output due to decreased preload, triggering compensatory increases in heart rate and systemic vascular resistance (SVR). Baroreceptor-mediated sympathetic activation increases cardiac chronotropy and vasoconstriction, while adrenal epinephrine release augments these responses. Activation of the renin–angiotensin–aldosterone (RAA) system and antidiuretic hormone (ADH) promotes renal sodium and water retention. Angiotensin II further increases SVR through direct vasoconstriction.
Cardiogenic shock results from decreased cardiac output due to impaired myocardial contractility. Obstructive congenital heart lesions causing outflow obstruction are better classified as obstructive shock. Although myocardial depression may occur in all shock states, primary cardiogenic shock is caused by viral myocarditis, ALCAPA, incessant arrhythmias, drug ingestions (e.g., cocaine), metabolic derangements (e.g., hypoglycemia), and postoperative cardiac surgery complications.
Clinical signs include pulmonary rales, gallop rhythm, hepatomegaly, jugular venous distention, peripheral edema, and cardiomegaly on chest radiograph. Laboratory findings such as elevated CK, troponin, or BNP may indicate myocardial dysfunction but are not universally present.
As in hypovolemic shock, sympathetic activation, RAA system upregulation, ADH release, and natriuretic peptide secretion increase SVR to compensate for low cardiac output. However, the volume deficit in cardiogenic shock is functional rather than absolute.
Obstructive shock occurs when an acute mechanical obstruction to ventricular outflow impairs cardiac output. Causes include pulmonary embolus, cardiac tamponade, tension pneumothorax, and left-sided obstructive congenital lesions such as critical aortic stenosis, coarctation, interrupted aortic arch, and hypoplastic left heart syndrome.
A sudden decrease in cardiac output leads to increased SVR and functional hypovolemia. Rapid identification of the underlying cause is essential. Ductal-dependent congenital lesions typically present at 1–3 weeks of age after ductus arteriosus closure.
Distributive shock results from inappropriate vasodilation, peripheral blood pooling, and microvascular shunting. Common causes include sepsis, anaphylaxis, and drug ingestions. It often coexists with hypovolemic or cardiogenic components.
Pediatric sepsis has traditionally been defined using SIRS criteria. Severe sepsis includes organ dysfunction, and septic shock refers to cardiovascular dysfunction. Many children with sepsis have negative cultures, but microbial components trigger inflammatory and coagulation cascades leading to capillary leak, myocardial depression, and vasomotor instability.
Classic septic shock presents with high cardiac output and low SVR (“warm shock”), but more than half of children exhibit low cardiac output and high SVR (“cold shock”). Sepsis-3 redefined adult sepsis as life-threatening organ dysfunction from a dysregulated host response, with pediatric updates pending.
In anaphylaxis, mast cell degranulation releases histamine, proteases, and proteoglycans, followed by prostaglandins and leukotrienes. These mediators cause urticaria, airway edema, wheezing, profound vasodilation, and capillary leak. Reflex tachycardia increases cardiac output.
Neurogenic shock is caused by sudden loss of sympathetic stimulation to vascular smooth muscle, resulting in profound vasodilation and decreased SVR. Unopposed vagal tone leads to bradycardia or absence of the expected tachycardic response. It may occur after severe traumatic brain injury or cervical spinal cord injury.
Dissociative shock occurs when toxic metabolites or drugs impair cellular oxygen delivery or utilization despite normal or supranormal tissue perfusion. Examples include severe anemia, methemoglobinemia, and carbon monoxide poisoning. In these conditions, cells cannot effectively use oxygen, resulting in metabolic failure.
Key principle: Epinephrine is first-line for fluid-refractory pediatric septic shock. Norepinephrine is preferred in low-SVR (“warm”) shock. Agents may start peripherally or via IO in dilute form, but should transition to central access when available.
| Agent | Dose Range | Mechanism | Primary Use | Key Considerations |
|---|---|---|---|---|
| Epinephrine | 0.05–1 µg/kg/min | α₁, β₁, β₂ stimulation
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| Norepinephrine | 0.05–1 µg/kg/min | α₁, β₁ stimulation |
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| Dopamine | 5–10 µg/kg/min | α₁, β₁, β₂, D₁ stimulation
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| Vasopressin | 0.0002–0.004 units/kg/min Max: 0.04 units/min |
V1a receptor–mediated vasoconstriction
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| Dobutamine | 2.5–20 µg/kg/min | β₁ stimulation; mixed α agonist/antagonist |
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| Milrinone | 0.25–1 µg/kg/min | Type III phosphodiesterase inhibitor |
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Source control should begin as soon as IV access is obtained and fluid resuscitation is underway. Early identification and treatment of the underlying cause of shock is essential.
| Patient History | Antibiotic Choices | Additional Considerations |
|---|---|---|
| Previously healthy child with community‑acquired infection |
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| Suspected intra‑abdominal infection |
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| Immunocompromised patient (cancer, chronic disease, recent hospitalization, long‑term care, indwelling central line) |
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| Neonate |
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Infants under 2–3 months require coverage for: Group B Streptococcus, coagulase‑negative Staphylococcus, Listeria, E. coli, H. influenzae, and HSV. They are at increased risk for CNS infection → ensure adequate CNS‑penetrating doses.
Although rapid recognition and reversal of shock applies to all shock types, pediatric septic shock has been the focus of extensive protocol development and quality improvement efforts. The principles below emphasize sepsis-specific management but are broadly applicable to other shock states.
Frequent reassessment is essential to determine response to initial resuscitation. Improvement in clinical and laboratory parameters indicates successful reversal of shock.
| Parameter | Comment | Target |
|---|---|---|
| Heart rate | Tachycardia → hypovolemia or ongoing shock Bradycardia → severe shock in infants or neurogenic shock in older children |
Age‑specific |
| Respiratory rate | Tachypnea may reflect pulmonary disease or metabolic acidosis | Age‑specific |
| Systolic blood pressure | Hypotension is a late sign in children Wide pulse pressure (DBP <½ SBP) → low SVR (distributive/neurogenic shock) |
Age‑specific |
| Mean arterial pressure | Useful for titrating vasoactive therapy | Age‑specific |
| Diastolic blood pressure | Low DBP suggests vasodilation | Age‑specific |
| Capillary refill | Flash refill → warm shock Delayed refill → cold shock |
1–2 seconds |
| Extremity temperature | Warm = vasodilation; Cool = vasoconstriction | Normal warmth |
| Mental status | Lethargy, confusion, agitation → poor perfusion | Alert and age‑appropriate |
| Urine output | Marker of renal perfusion | <30 kg: >1 mL/kg/hr ≥30 kg: ≥30 mL/hr |
| Lactate | Elevated lactate (>2–4 mmol/L) → inadequate oxygen delivery | <2–4 mmol/L OR ≥10% decrease every 1–2 hrs |
| Age | HR (bpm) | RR (breaths/min) | SBP (mm Hg) | MAP (mm Hg) | DBP (mm Hg) |
|---|---|---|---|---|---|
| 0–7 days | 100–160 | <60 | >60 | >40 | >30 |
| 8–30 days | 100–160 | <60 | >65 | >45 | >30 |
| 31 days–<2 yrs | 90–160 | <50 | >70 | >50 | >35 |
| 2–<6 yrs | <140 | <30 | >75 | >50 | >40 |
| 6–<13 yrs | <130 | <24 | >85 | >60 | >45 |
| >13 yrs | <110 | <20 | >90 | >65 | >50 |
Vital Signs & Shock Monitoring References
Fluid‑refractory, catecholamine‑resistant shock is defined as persistent inadequate tissue perfusion despite ≥60 mL/kg of fluid resuscitation and high‑dose vasoactive support (epinephrine or norepinephrine ≥1 μg/kg/min). These patients have significantly higher mortality and require rapid escalation of care.