Shock, cardiac arrest and resuscitation

Definition and Overview

Shock is a state of acute circulatory failure in which oxygen delivery to tissues is insufficient to meet metabolic demand, resulting in cellular dysfunction. In children, shock is defined clinically rather than by a fixed blood pressure threshold: hypotension is a late and pre-terminal sign in paediatric shock.

$$\dot{D}O_2 = CO \times CaO_2 = (HR \times SV) \times (Hb \times 1.34 \times SaO_2 + 0.003 \times PaO_2)$$

Shock occurs when $\dot{D}O_2$ falls below tissue $\dot{V}O_2$, or when tissue oxygen extraction is impaired despite adequate delivery (e.g. distributive shock).

Compensated shock: normal blood pressure maintained by tachycardia, increased SVR, and redistribution of flow. Children compensate vigorously due to high catecholamine reserve and ventricular compliance; decompensation is then abrupt.

Decompensated shock: hypotension present; imminent cardiovascular arrest if untreated.

Age-specific blood pressure thresholds (approximate lower limits of systolic BP)

Classification of Shock States

Recognising the predominant haemodynamic pattern guides therapy. Mixed shock is common in critically ill children.

Clinical Recognition

Primary Survey Findings

• Tachycardia is the earliest and most sensitive sign
• Peripheral perfusion: capillary refill time $> 2\,\text{s}$ (central $> 3\,\text{s}$ is more specific), skin temperature, mottling
• Pulse quality: compare central (brachial/femoral) versus peripheral; thready versus bounding
• Mental status: agitation, irritability, decreased responsiveness, reduced urine output ($< 1\,\text{mL/kg/hr}$ in children, $< 0.5\,\text{mL/kg/hr}$ in adolescents)
• Blood pressure: measure, but normal BP does not exclude shock; trend and pulse pressure matter

Warm versus Cold Shock

Clinically distinguishing warm from cold shock directs initial vasoactive choice, particularly in septic shock:

• Warm (vasodilated) shock: bounding pulses, flash CRT, wide pulse pressure, high cardiac output with low SVR
• Cold (vasoconstricted) shock: poor pulses, prolonged CRT, narrow pulse pressure, low cardiac output with elevated SVR

Investigations and Monitoring

Bedside

• Continuous ECG, pulse oximetry, ETCO₂ if intubated
• Point-of-care blood glucose (hypoglycaemia common in shocked child; treat if $< 3\,\text{mmol/L}$)
• Blood gas (arterial or venous): lactate, pH, base excess, $PaCO_2$, electrolytes
• Urinary catheter for output monitoring

Laboratory

• FBC, coagulation screen (DIC common in septic/meningococcal shock)
• Electrolytes, creatinine, urea, LFTs, calcium, magnesium, phosphate
• Blood culture before antibiotics; consider LP only when haemodynamically stable
• Troponin, BNP/NT-proBNP if cardiogenic shock suspected
• Group and hold; crossmatch if haemorrhagic

Imaging

• Chest X-ray: cardiomegaly, pulmonary oedema, pneumothorax
• Bedside point-of-care ultrasound (POCUS): cardiac function, pericardial effusion, IVC collapsibility, lung B-lines, pneumothorax
• ECG: arrhythmia, SVT mimicking shock in infants, myocarditis, Wolff-Parkinson-White

Haemodynamic Monitoring (escalating invasiveness)

• Non-invasive: NIBP, pulse oximetry waveform
• Invasive arterial line: continuous BP, arterial blood gas sampling
• Central venous access: CVP (limited standalone value but useful trend), ScvO₂ target $\geq 70\%$
• Advanced: PICCO (transpulmonary thermodilution), rarely PA catheter in paediatrics; echocardiography is preferred non-invasive CO assessment

Management

General Principles

1. Recognise early and act immediately. Call for senior support. Activate institutional rapid response if available.
2. Secure IV/IO access immediately. Intraosseous access is first-line if peripheral IV cannot be established within 60-90 seconds.
3. High-flow oxygen via non-rebreather mask; prepare for early intubation if deteriorating.
4. Identify and treat the underlying cause simultaneously with resuscitation.
5. Reassess after every intervention. Shock management is iterative.

Fluid Resuscitation

Initial bolus:

• Isotonic crystalloid (0.9% NaCl or Hartmann's/Plasmalyte)
• $10\text{-}20\,\text{mL/kg}$ IV/IO over 5-10 minutes (faster in haemorrhagic shock)
• Reassess after each bolus: heart rate, CRT, blood pressure, mental status, air entry

Limits and reassessment:

• After $40\text{-}60\,\text{mL/kg}$ without haemodynamic improvement, fluid-refractory shock is declared and vasoactive agents must be commenced
• Aggressive fluid administration in cardiogenic shock causes harm; use $5\text{-}10\,\text{mL/kg}$ boluses cautiously with frequent reassessment
• In septic shock, the FEAST trial established that aggressive bolus fluid in resource-limited settings increased mortality; contemporary practice emphasises titrated boluses with early vasopressor initiation when fluid-refractory
• In haemorrhagic shock, transition early to packed red cells (pRBC $10\text{-}20\,\text{mL/kg}$) and balanced blood product replacement (FFP, platelets in $1:1:1$ ratio for massive haemorrhage)
• Target: normalisation of HR, CRT, mental status, urine output, and lactate clearance; avoid pulmonary oedema

Specific fluid choices:

• Septic shock: balanced crystalloid preferred over 0.9% NaCl (hyperchloraemic acidosis risk)
• Hypovolaemic (haemorrhagic): blood products early; avoid excessive crystalloid
• DKA: see DKA protocol; 10 mL/kg bolus for shock, then controlled deficit replacement
• Anaphylaxis: crystalloid boluses; adrenaline is the primary intervention

Vasoactive Agent Selection

Commence via peripheral IV if central access is not immediately available; early central access preferred for ongoing infusions.

Septic Shock

• First-line: Adrenaline (epinephrine) for cold shock; noradrenaline (norepinephrine) for warm/vasodilated shock
• Australian/NZ PICU practice predominantly uses adrenaline as first-line in paediatric septic shock, particularly in children $< 12\,\text{years}$
• Adrenaline: start at $0.05\text{-}0.1\,\text{microgram/kg/min}$, titrate up to $0.5\text{-}1\,\text{microgram/kg/min}$
• Noradrenaline: start at $0.05\text{-}0.1\,\text{microgram/kg/min}$, titrate to effect

Catecholamine-Resistant Shock

When shock persists despite $\geq 0.3\,\text{microgram/kg/min}$ adrenaline or noradrenaline:

• Consider vasopressin $0.0003\text{-}0.002\,\text{U/kg/min}$ as vasopressor-sparing agent (V1 receptor mediated vasoconstriction, catecholamine-independent)
• Consider hydrocortisone for catecholamine-dependent/catecholamine-resistant shock with risk of adrenal insufficiency: $1\text{-}2\,\text{mg/kg}$ IV (max $100\,\text{mg}$) then $1\text{-}2\,\text{mg/kg/day}$ in divided doses
• Adrenal insufficiency more likely in: prolonged steroid use, purpura fulminans, pituitary/adrenal pathology

Cardiogenic Shock

• Avoid fluid boluses beyond $5\text{-}10\,\text{mL/kg}$ unless clearly preload-depleted
• Dobutamine $2\text{-}20\,\text{microgram/kg/min}$: positive inotropy, mild vasodilation; preferred if BP maintained ($\geq 70\,\text{mmHg}$ systolic)
• Milrinone $0.25\text{-}0.75\,\text{microgram/kg/min}$ (consider loading dose $25\text{-}50\,\text{microgram/kg}$ over 30-60 min if tolerated): phosphodiesterase-III inhibitor; inotropy plus lusitropy plus vasodilation; particularly useful post-cardiac surgery and in patients on beta-blockers
• Add noradrenaline or vasopressin if BP does not support dobutamine/milrinone monotherapy
• Levosimendan ($0.05\text{-}0.2\,\text{microgram/kg/min}$) as calcium sensitiser; evidence in paediatric low cardiac output syndrome is emerging

Anaphylaxis

• Adrenaline $10\,\text{microgram/kg}$ IM (max $500\,\text{micrograms}$) into lateral thigh immediately
• Repeat at 5-minute intervals if no response
• IV infusion $0.05\text{-}0.1\,\text{microgram/kg/min}$ if refractory or cardiovascular arrest
• Crystalloid boluses $20\,\text{mL/kg}$; adjuncts (antihistamine, corticosteroid) are not primary therapy

Vasopressor/Inotrope Summary Table

Airway and Ventilation

• Avoid delayed intubation in deteriorating shock
• Pre-oxygenate and haemodynamically optimise before induction (fluid bolus, vasopressor running)
• Ketamine $1\text{-}2\,\text{mg/kg}$ IV is preferred induction agent in shocked children: sympathomimetic; maintains SVR
• Avoid propofol in haemodynamically unstable children
• Suxamethonium $2\,\text{mg/kg}$ (infant) or $1\text{-}1.5\,\text{mg/kg}$ (child) for RSI; rocuronium $1.2\,\text{mg/kg}$ if suxamethonium contraindicated
• ETT size: cuffed $= \text{age}/4 + 3.5\,\text{mm}$; uncuffed $= \text{age}/4 + 4\,\text{mm}$
• Post-intubation: positive pressure ventilation reduces work of breathing and LV afterload (beneficial in cardiogenic shock); also reduces RV preload (harmful in obstructive/RV failure shock)

Complications and Special Considerations

Congenital Heart Disease and Shock

• Duct-dependent lesions (e.g. critical coarctation, HLHS, pulmonary atresia): shock presentation in neonate on day 2-7 as ductus closes; commence prostaglandin E1 (PGE1) $0.005\text{-}0.05\,\text{microgram/kg/min}$ without delay; intubate if apnoea (common PGE1 side effect)
• Single-ventricle physiology: balance of pulmonary-to-systemic blood flow (Qp:Qs); avoid hyperoxia (reduces PVR excessively, steals systemic flow); target $SpO_2\,75\text{-}85\%$ pre-Fontan
• Post-Fontan circuit: passive pulmonary flow dependent on CVP gradient; maintain euvolaemia and sinus rhythm; avoid high PEEP

Neurogenic Shock

• Triad: hypotension, bradycardia, warm vasodilation in setting of cervical/high thoracic cord injury
• Noradrenaline preferred to restore SVR; atropine or pacing for bradycardia
• Actively exclude haemorrhagic co-injury

Adrenal Crisis

• Suspect in: known adrenal insufficiency, prolonged corticosteroid use, Waterhouse-Friderichsen syndrome (meningococcaemia)
• Treatment: hydrocortisone $25\,\text{mg}$ (infant), $50\,\text{mg}$ (child 1-5 years), $100\,\text{mg}$ ($> 5\,\text{years}$) IV immediately, then maintenance dosing; fluid resuscitation; glucose correction

Refractory Shock and Mechanical Support

• When shock persists despite optimised pharmacotherapy, consider ECMO (VA-ECMO for cardiogenic; VV for isolated respiratory failure)
• ECMO as bridge to recovery (myocarditis), bridge to transplant (dilated cardiomyopathy), or bridge to decision
• Retrieve early to ECMO-capable centre before cardiac arrest where possible

PICU Framing for the Viva

• Always classify shock first (hypovolaemic/distributive/cardiogenic/obstructive) and identify reversible causes before titrating therapy
• Fluid responsiveness is not the same as fluid tolerance; repeated boluses without reassessment cause harm
• The sickest children (meningococcaemia, myocarditis) may look briefly compensated then crash: act before decompensation
• Lactate clearance ($> 10\%$ per hour) is a more useful resuscitation endpoint than any single haemodynamic parameter
• ScvO₂ $\geq 70\%$ alongside clinical markers guides adequacy of oxygen delivery
• Do not delay antibiotics beyond 1 hour in suspected septic shock; each hour of delay in paediatric sepsis is associated with increased mortality
• Early senior and subspecialty (cardiology, haematology, retrieval) involvement is a marker of good PICU practice, not failure