Circulatory insufficiency is inadequate tissue oxygen delivery for the infant's metabolic demand. It may occur with low BP, normal BP, or even transiently high BP if systemic blood flow is inadequate or oxygen extraction is failing.
Cardiogenic shock is a subtype in which the dominant problem is impaired myocardial performance, severe loading abnormality, arrhythmia, or a structural/ductal lesion that prevents adequate forward flow.
| Term | Practical Definition | How It Changes Management |
|---|---|---|
| Hypotension | BP below expected range for GA/postnatal age, or lower than the infant's usual trend. It is a sign, not a diagnosis. | Confirm accuracy, correlate with perfusion, identify systolic vs. diastolic pattern. Do not automatically give fluid or dopamine. |
| Circulatory insufficiency | Inadequate systemic blood flow or O₂ delivery causing organ hypoperfusion. | Use full perfusion assessment and investigate cause. Target preload, contractility, afterload, SVR, O₂ content, or ductal physiology. |
| Compensated shock | Perfusion is threatened but BP may be preserved by vasoconstriction and catecholamine response. | Tachycardia, cool extremities, delayed refill, rising lactate, or oliguria may appear before hypotension. Escalate early. |
| Decompensated shock | BP falls because compensatory mechanisms fail. | Immediate intervention — correct airway, O₂ delivery, glucose, calcium, acidosis, infection, blood loss, structural/ductal lesions. |
| Cardiogenic shock | Poor tissue perfusion caused mainly by inadequate myocardial contractility or a lesion/arrhythmia limiting forward flow. | Avoid excessive afterload, excessive fluid, therapies that worsen PVR/SVR mismatch. Obtain echo and cardiology input. |
| Refractory shock | Persistent circulatory insufficiency despite initial volume correction (when indicated) and appropriate vasoactive therapy. | Reassess: ductal-dependent CHD, tamponade, pneumothorax, adrenal insufficiency, sepsis/NEC, arrhythmia, PPHN/RV failure, incorrect line/drug delivery, or ongoing bleeding. |
These are reference distributions, not treatment triggers. A number below the listed percentile in a well-perfused infant with a normal lactate and good urine output is a reason to look harder, not a reason to start a pressor.
| Postconceptual age (weeks) | Systolic — 3rd percentile | Mean — 3rd percentile | Diastolic — 3rd percentile |
|---|---|---|---|
| 24 | 32 | 26 | 15 |
| 25 | 34 | 26 | 16 |
| 26 | 36 | 27 | 17 |
| 27 | 38 | 27 | 17 |
| 28 | 40 | 28 | 18 |
| 29 | 42 | 28 | 19 |
| 30 | 43 | 29 | 20 |
| 31 | 45 | 30 | 20 |
| 32 | 46 | 30 | 21 |
| 33 | 47 | 30 | 22 |
| 34 | 48 | 31 | 23 |
| 35 | 49 | 32 | 24 |
| 36 | 50 | 32 | 25 |
Baylor Table 3-4 — preterm values in mmHg, from the Northern Neonatal Nursing Initiative data on systolic blood pressure in babies below 32 weeks in the first year of life (Archives of Disease in Childhood: Fetal & Neonatal Edition 1999;80:F38–F42).
| Healthy term neonate | Day 1 | Day 2 | Day 3 | Day 4 |
|---|---|---|---|---|
| 95th percentile — systolic | 78 | 83 | 86 | 88 |
| 95th percentile — mean | 57 | 62 | 64 | 65 |
| 50th percentile — systolic | 65 | 69 | 70 | 71 |
| 50th percentile — mean | 48 | 51 | 53 | 55 |
| 5th percentile — systolic | 54 | 57 | 59 | 63 |
| 5th percentile — mean | 39 | 41 | 41 | 43 |
Baylor Table 3-5 — term values in mmHg, adapted from Kent AL, Kecskes Z, Shadbolt B, Falk MC. Normative blood pressure data in the early neonatal period. Pediatric Nephrology 2007;22(9):1335–41.
Systolic hypotension means a low stroke volume — from reduced preload, impaired contractility, or increased afterload. Diastolic hypotension means impaired filling, a low systemic vascular resistance, or an inadequate intravascular volume. Treating the mean alone hides which of these you are looking at.
| Mechanism (systolic hypotension) | Pathophysiology | Clinical examples |
|---|---|---|
| Decreased preload | Reduced pulmonary blood flow lowers left atrial volume, or pulmonary venous return is obstructed | PPHN; high mean airway pressure impairing systemic venous return; partial or total anomalous pulmonary venous connection |
| Impaired diastolic filling | Hypertrophic obstructive cardiomyopathy; cardiac tamponade; left ventricular non-compaction | |
| Increased afterload | Failure to adapt to a change in loading conditions, so contractility falls | Loss of the low-resistance placenta at birth; post-PDA-ligation syndrome; coarctation, interrupted arch, critical aortic stenosis; congenital heart disease with high resistance |
| Elevated systemic vascular resistance | Cold shock with vasoconstriction redistributing blood to vital organs; exogenous vasopressors | |
| Pump failure | Structural anomalies | Hypoplastic left heart syndrome, Shone's complex |
| Arrhythmia | SVT, VT, junctional rhythm, atrial flutter, AVNRT | |
| Impaired contractility from myocardial injury or ischaemia | Hypoxic-ischaemic encephalopathy; cardiomyopathy; congenital coronary artery anomalies |
| Mechanism (diastolic hypotension) | Clinical examples |
|---|---|
| Enlarged vascular bed | Patent ductus arteriosus; bronchopulmonary sequestration, giant haemangioma, arteriovenous malformation |
| Vasodilation | Systemic inflammatory response (NEC or septic shock); medications such as phenobarbital, midazolam or morphine; autonomic dysregulation |
| Hypovolaemia | Capillary leak in NEC or septic shock; haemorrhage (intracranial, feto-maternal); transepidermal water loss; excessive urine losses — physiologic diuresis, post-obstructive diuresis, diabetes insipidus |
BP is easy to measure but an incomplete surrogate for systemic blood flow. A neonate can have acceptable MAP with high SVR and low cardiac output, or low MAP with preserved systemic blood flow and good organ perfusion.
Treatment decisions should be based on a pattern: BP trend plus perfusion signs, lactate/base deficit, urine output, acid-base status, O₂ requirement, and echo/POCUS findings.
| BP Pattern | What It May Suggest | Immediate Bedside Response |
|---|---|---|
| Low systolic, relatively preserved diastolic | Low stroke volume from low preload, impaired contractility, excessive afterload, or obstructed filling | Assess volume history, cardiac function, lung volume/MAP, obstruction, ductal-dependent systemic flow |
| Low diastolic + wide pulse pressure | Low SVR, PDA run-off, AVM/VGAM, sepsis/NEC vasodilation, medication effect, or adrenal insufficiency | Evaluate for PDA/hyperdynamic precordium, bounding pulses, low UO, sepsis signs, medication exposure, echo for run-off |
| Both systolic and diastolic low | Severe low flow, combined myocardial dysfunction + vasodilation, decompensated sepsis, hemorrhage, or terminal transition | Resuscitate immediately, correct reversible factors, start physiology-matched vasoactive support |
| Normal BP with poor perfusion | Compensated shock, high SVR/low CO, cold sepsis, severe PPHN, ductal-dependent lesion, or obstructive emergency | Do not be reassured by BP alone; obtain lactate, gas, CXR, pre/postductal SpO₂, echo/POCUS |
| High BP with poor perfusion | Excess vasoconstriction, pain/agitation, high afterload, renal/vascular cause, or inappropriate vasoactive dose | Reassess vasoactive choice, pain/sedation, line accuracy, renal status, LV function |
Oxygen delivery = cardiac output × arterial O₂ content. Cardiac output = heart rate × stroke volume. Stroke volume depends on preload, contractility, afterload, ventricular compliance, rhythm, and cardiopulmonary interactions.
In preterm infants, immature myocardium and immature autonomic regulation limit the ability to increase stroke volume. In term infants with PPHN or ductal lesions, the same BP may represent very different pulmonary and systemic flows.
| Variable | Bedside Meaning | Common Neonatal Disruptors | Corrective Strategy |
|---|---|---|---|
| Preload | Amount of blood returning to and filling the ventricles | Blood loss, capillary leak, dehydration, excessive mean airway pressure, tamponade, impaired pulmonary venous return, PPHN with poor pulmonary blood flow | Treat the cause. Use cautious volume only when hypovolemia is likely. Reduce excessive airway pressure if it impairs venous return. |
| Contractility | Myocardial ability to generate forward flow | Asphyxia/HIE, acidosis, hypoglycemia, hypocalcemia, myocarditis, cardiomyopathy, sepsis, ischemia, post-PDA closure syndrome, arrhythmia | Correct metabolic factors; use inotrope/inodilator guided by echo and perfusion. |
| Afterload | Resistance the ventricle must eject against | High SVR from cold shock or pressors; high PVR in PPHN; outflow obstruction; postnatal loss of low-resistance placenta in ELGAN | Avoid therapies that worsen ventricular output. Consider afterload reduction/inodilation when BP allows. |
| SVR | Systemic vascular tone | Low in warm sepsis, vasodilating drugs, adrenal insufficiency; high in cold shock or excessive vasopressors | Use vasopressor for low SVR; avoid excess alpha effect if poor LV performance is the primary problem. |
| PVR | Pulmonary vascular tone affecting RV afterload and pulmonary blood flow | Hypoxia, acidosis, hypercarbia, atelectasis, overdistension, MAS, pneumonia, CDH, sepsis, HIE | Optimize lung volume, oxygenation, pH, sedation; iNO when appropriate; RV support. |
| Oxygen content | Amount of O₂ carried in arterial blood | Anemia, hypoxemia, methemoglobinemia, poor ventilation/oxygenation | Correct oxygenation/ventilation; consider pRBC for anemia/hemorrhage based on clinical context. |
Circulatory insufficiency should be suspected when clinical signs and laboratory trends show impaired O₂ delivery, even before hypotension develops.
| Domain | Concerning Signs | Important Caveats |
|---|---|---|
| General appearance | Lethargy, irritability, poor tone, temperature instability, worsening apnea, poor feeding | Sedation, hypothermia, prematurity, and neurologic injury can mask clinical signs |
| Perfusion | Weak pulses, cool extremities, mottling, pallor, central cyanosis, delayed capillary refill, differential pulses | Capillary refill is affected by ambient temperature and examiner technique; use trends and multiple signs |
| Heart rate/rhythm | Tachycardia, bradycardia, narrow variability, SVT, heart block, frequent ectopy | Preterm infants may not mount robust tachycardia; therapeutic hypothermia lowers HR |
| Respiratory | Rising O₂ need, labile saturations, tachypnea, pulmonary edema, apnea, ventilatory failure | PPHN, pulmonary disease, left-sided obstruction, and sepsis may overlap |
| Renal perfusion | Oliguria, rising creatinine, worsening fluid overload, or post-obstructive diuresis | UO may be delayed on day 1; affected by AKI, diuretics, and obstruction |
| Metabolic | Rising lactate, worsening base deficit, hypoglycemia/hyperglycemia, hypocalcemia, acidosis | Epinephrine can increase lactate; interpret lactate in context and follow trend |
| Blood pressure | Low MAP, falling trend, wide pulse pressure, narrow pulse pressure, upper/lower extremity difference | Validate cuff size, arterial waveform, zeroing, limb location, and agitation before acting |
| Test / Monitor | Why It Matters | When to Prioritize |
|---|---|---|
| Continuous cardiorespiratory + pre/postductal SpO₂ | Detects hypoxemia, differential cyanosis, arrhythmia, and response to resuscitation | All unstable neonates; suspected PPHN, CHD, shock, severe respiratory disease |
| Arterial blood pressure (arterial line when available) | Beat-to-beat BP; blood gas access | Refractory shock, vasoactive infusion, severe PPHN, ELGAN instability, postoperative/cardiac |
| Blood gas with lactate and base deficit | O₂ delivery, ventilation, acid-base status, and trend response | Any infant with poor perfusion, rising respiratory support, suspected sepsis/NEC, PPHN, or CHD |
| Glucose, iCa, Na, K, Cr, LFTs | Correctable metabolic problems worsen contractility and vascular response | Initial shock workup; during vasoactive or steroid therapy |
| CBC, reticulocyte, type/screen, coagulation | Identifies anemia, hemorrhage, infection, thrombocytopenia, DIC | Shock with pallor, bleeding, abruption, fetomaternal hemorrhage, sepsis/NEC, liver congestion |
| Cultures and inflammatory evaluation | Sepsis/NEC shock may present with poor perfusion before hypotension | Clinical sepsis, maternal infection risk, NEC signs, unexplained deterioration |
| Chest/abdominal radiograph | Lung disease, pulmonary edema, cardiomegaly, pneumothorax, line malposition, NEC | Respiratory decompensation, suspected PDA/heart failure, obstructive emergency, line placement |
| ECG | Arrhythmia, conduction abnormality, ischemic clues, chamber strain | Tachyarrhythmia, bradyarrhythmia, cardiogenic shock, abnormal pulses, cardiomegaly |
| Functional echo / targeted neonatal echo | Structural disease, PDA, PPHN, ventricular function, preload, shunts, output, tamponade | Early in refractory shock, PPHN, suspected CHD, poor response to first therapy, ELGAN instability |
| NIRS (if available) | Regional oxygenation trend; cerebral and somatic O₂ delivery | Complex hemodynamics, postoperative/cardiac, severe shock trend monitoring |
| Shock Phenotype | Typical Clues | Common Causes | Initial Treatment Direction |
|---|---|---|---|
| Hypovolemic / Hemorrhagic | Pallor, weak pulses, metabolic acidosis, falling hematocrit, abruption/cord history | Placental abruption, cord laceration, twin-to-twin, internal hemorrhage, severe dehydration | NS 10 mL/kg while preparing pRBC/FFP. Do not delay blood products when hemorrhage is likely. |
| Distributive / Vasodilatory | Warm extremities early, bounding pulses, low diastolic BP, wide pulse pressure, rising lactate | Sepsis, NEC, systemic inflammation, vasodilating drugs, adrenal insufficiency | Antibiotics/source control; cautious fluid if preload depleted; vasopressor for low SVR; hydrocortisone for catecholamine-resistant shock |
| Cardiogenic / Myocardial Dysfunction | Poor pulses, hepatomegaly, gallop, pulmonary edema, cardiomegaly, oliguria, acidosis, poor ventricular function on echo | HIE/asphyxia, myocarditis, cardiomyopathy, arrhythmia, ischemia, severe acidosis, hypoglycemia, hypocalcemia, post-PDA closure | Correct metabolic factors; avoid excessive fluid; inotrope/inodilator by function and BP; cardiology involvement |
| Obstructive | Sudden collapse, ventilation difficulty, muffled heart sounds, unilateral breath sounds, extreme PPHN/RV failure, tamponade | Tension pneumothorax, cardiac tamponade from line perforation, critical outflow obstruction, severe PPHN, obstructed TAPVR | Fix the obstruction: needle decompression/chest tube, pericardiocentesis, urgent cardiology/surgery; support O₂ delivery while acting |
| Ductal-Dependent Systemic Flow | Shock in first days/weeks, weak femoral pulses, differential BP, acidosis, poor feeding, gray appearance, may worsen after ductal closure | Coarctation, interrupted arch, critical aortic stenosis, HLHS variants, severe LV outflow obstruction | Start PGE₁; avoid excessive O₂ if it steals systemic flow; correct acidosis; urgent echo/cardiology/transport |
| PPHN / RV Failure | Severe labile hypoxemia, pre/postductal gradient, loud P2, RV dilation/dysfunction, high PVR, poor LV preload | MAS, pneumonia, RDS, CDH, HIE, sepsis, pulmonary hypoplasia, maladaptation | Optimize lung volume, oxygenation, pH, sedation; iNO if eligible; SVR support; consider milrinone or PGE₁ by echo physiology |
| High-Output Failure / Steal | Wide pulse pressure, bounding pulses, cardiomegaly, pulmonary overcirculation, low diastolic BP, end-organ hypoperfusion | Large PDA, AVM, vein of Galen malformation, large hemangioma, bronchopulmonary sequestration | Echo/imaging; support perfusion; manage run-off lesion; avoid therapies that worsen pulmonary overcirculation |
| Clinical Pattern | Preferred First Thinking | Common Therapy Choices | Avoid / Caution |
|---|---|---|---|
| Low BP + poor perfusion + likely blood loss | Hypovolemia/hemorrhage until proven otherwise | NS 10 mL/kg while obtaining pRBC; pRBC 10–15 mL/kg when hemorrhage/anemia is likely; FFP/platelets if coagulopathy/active bleeding | Do not rely on crystalloid alone with ongoing hemorrhage. Do not delay blood products. |
| Low diastolic BP + wide pulse pressure + bounding pulses | Low SVR or run-off lesion | Echo for PDA/AVM; vasopressor if vasodilatory shock; manage PDA/run-off lesion if hemodynamically significant | Repeated fluids may worsen pulmonary edema and systemic steal. |
| Low systolic BP + weak pulses + pulmonary edema/hepatomegaly | Low stroke volume / myocardial dysfunction | Echo; dobutamine/epinephrine or milrinone depending on BP and ventricular function; correct acidosis, glucose, calcium; consider diuresis only after perfusion is supported | Avoid dopamine-only escalation if afterload worsens output; avoid large fluid loads. |
| Hypoxemia + pre/postductal gradient + RV dysfunction | PPHN with inadequate pulmonary blood flow and RV strain | Optimize lung recruitment and pH; iNO for eligible term/late preterm; norepinephrine/vasopressin if LV function adequate; milrinone if function and BP allow; consider PGE₁ for RV unloading by echo | Avoid atelectasis, overdistension, acidosis, agitation, systemic hypotension. Exclude CHD before iNO when possible. |
| Shock in early neonatal period + weak femorals/differential BP | Ductal-dependent systemic blood flow | PGE₁ · echo/cardiology/transport · cautious O₂ strategy · correct acidosis · support ventilation | Do not wait for a murmur. Avoid excessive O₂ and hyperventilation if they reduce PVR and steal systemic flow. |
| Sepsis/NEC + warm shock | Low SVR with inflammatory vasodilation and capillary leak | Cultures, antibiotics, source control; cautious fluid if depleted; norepinephrine/epinephrine/vasopressin by function; hydrocortisone for catecholamine-resistant shock | Avoid volume overload; reassess lungs after each bolus. |
| Sepsis/NEC + cold shock | High SVR/low flow, possible myocardial dysfunction | Echo; inotrope if dysfunction; epinephrine may be useful; consider vasodilatory strategy only with expert echo-guided care | A pure vasoconstrictor may worsen CO if SVR is already high. |
| Refractory shock despite high catecholamines | Wrong phenotype, adrenal insufficiency, ongoing source, obstruction, or poor drug delivery | Check line/pump/concentration; repeat echo; consider hydrocortisone; seek cardiology/endocrinology/ECMO/transport input | Do not keep escalating one drug without revisiting the diagnosis. |
Dose ranges below are educational starting ranges. Verify against local formulary, drug concentration, central/peripheral policy, renal/hepatic function, and pharmacy guidance before bedside use.
| Drug | Typical Neonatal Starting Range | Best Physiologic Use | Main Cautions / Monitoring |
|---|---|---|---|
| Dopamine | Start 5 mcg/kg/min; usual 5–15 mcg/kg/min; consider switching if no response by 10–15 mcg/kg/min | Raises BP more reliably than dobutamine short-term in preterm hypotension; useful when BP/SVR support desired and ventricular function is acceptable | May increase HR, O₂ consumption, arrhythmia risk, PVR more than SVR; may reduce systemic flow despite MAP increase. Do not use reflexively. |
| Dobutamine | Start 5 mcg/kg/min; usual 2–15 mcg/kg/min | Inotropy and improved stroke volume/CO — especially LV dysfunction or low systemic blood flow with acceptable BP | May lower BP via vasodilation; less effective for raising MAP; titrate to perfusion/echo rather than MAP alone. |
| Epinephrine | Start 0.01–0.03 mcg/kg/min; usual 0.01–0.3 mcg/kg/min | Systolic dysfunction, cold shock, low CO, or when both inotropy and vasopressor effect are needed | Tachycardia, hyperglycemia, ↑ lactate, arrhythmia, ↑ PVR at higher doses; interpret lactate trend carefully. |
| Norepinephrine | Commonly 0.02–0.2 mcg/kg/min; local ranges vary | Low SVR/warm shock; PPHN with systemic hypotension and adequate LV function — raising SVR may support right-to-left shunt reduction | Excess vasoconstriction can impair flow; monitor perfusion, lactate, extremities, UO, and echo. |
| Milrinone | Often 0.2–0.75 mcg/kg/min; most neonatal pathways avoid loading dose in hypotension | Inodilator: myocardial dysfunction + high afterload, RV dysfunction, post-cardiac surgery/low output, PPHN + ventricular dysfunction when BP is adequate | Can cause hypotension; accumulates with renal dysfunction/oliguria; monitor BP, rhythm, platelets, renal function. |
| Vasopressin | Baylor/TCH: 0.005–0.04 units/kg/hr — check local units and concentrations carefully | Catecholamine-resistant vasodilatory shock; low SVR with tachycardia where more beta stimulation is undesirable; selected PPHN/systemic hypotension | Hyponatremia, excessive vasoconstriction, ischemia risk, dose-unit errors; monitor Na, perfusion, UO, abdominal/skin signs. |
| Hydrocortisone | Baylor: 1 mg/kg IV once; if persistent/recurrent: 1 mg/kg/dose q8h × 24–48h; taper off by day 5 if tolerated | Catecholamine-resistant hypotension; suspected relative adrenal insufficiency; sepsis-related vasoplegia in at-risk preterm or critically ill neonate | Hyperglycemia, hypertension, infection risk, impaired bone mineralization, intestinal perforation — especially with concurrent indomethacin/NSAID. Avoid routine cortisol testing unless local practice supports it. |
| PGE₁ (alprostadil) | Common starting range 0.01–0.05 mcg/kg/min; titrate to ductal response and side effects | Suspected ductal-dependent systemic or pulmonary blood flow; critical CHD while awaiting echo/transport | Apnea, hypotension, fever, flushing; secure airway for transport when clinically indicated; ensure reliable IV access and cardiology involvement. |
| Inhaled Nitric Oxide (iNO) | 1–20 ppm initial dose in eligible ventilated term/late-preterm infants after lung recruitment and CHD exclusion when possible | PPHN/hypoxic respiratory failure with elevated PVR and recruitable lung disease; improves oxygenation and reduces ECMO need in term/near-term population | Limited evidence in preterm rescue; monitor methemoglobin and NO₂; avoid abrupt wean below 5 ppm; nonresponse should trigger reassessment. |
Extremely preterm infants frequently have low measured BP during transition because of immature autonomic tone, immature myocardium, PDA physiology, changing SVR after placental separation, insensible water losses, and relative adrenal immaturity. Many do not have true hypovolemia.
A large PDA reduces diastolic pressure and systemic perfusion by run-off into the pulmonary circulation. Signs: wide pulse pressure, bounding pulses, worsening respiratory status, pulmonary edema, low UO, and feeding intolerance.
A pressor that only raises MAP may not correct systemic steal. Therapy should consider ductal significance, pulmonary overcirculation, systemic flow, renal/mesenteric perfusion, and timing of medical or procedural closure.
PPHN shock may be driven by high PVR, poor pulmonary blood flow, reduced LV preload, RV dilation/dysfunction, systemic hypotension, or a combination. Echo is essential to distinguish physiology and exclude structural heart disease.
Core treatment: lung recruitment without overdistension, avoidance of acidosis, adequate preductal oxygenation, sedation/minimization of agitation, surfactant when lung disease is present, iNO when indicated, targeted systemic support. If LV function is adequate, norepinephrine or vasopressin may improve systemic pressure and shunt direction; if ventricular function is impaired, inotropy or inodilation may be needed.
Perinatal asphyxia can cause myocardial injury, PPHN, renal injury, acidosis, hypoglycemia, hypocalcemia, and impaired vascular tone. Therapeutic hypothermia lowers HR and alters drug clearance — trends are more important than isolated values.
Management: correct metabolic factors, evaluate ventricular function and PPHN, support O₂ delivery, avoid unnecessary volume loading when myocardial dysfunction or renal injury is present.
Shock developing as the ductus closes should be considered ductal-dependent systemic blood flow until proven otherwise. Coarctation, interrupted arch, critical aortic stenosis, and HLHS variants may present with acidosis, weak femoral pulses, differential BP, poor feeding, respiratory distress, or gray appearance — sometimes without a murmur.
Excess O₂ and hyperventilation can lower PVR and increase pulmonary run-off in selected lesions. O₂ targets should be individualized with cardiology input.
Neonatal septic shock may present with low, normal, or high BP. Early cold shock may have intense vasoconstriction with poor perfusion and preserved BP; warm shock may show vasodilation, wide pulse pressure, and low diastolic BP. NEC shock adds capillary leak, acidosis, myocardial depression, coagulopathy, and possible surgical source.
Treatment: antibiotics and source control, careful fluid resuscitation by perfusion and lung status, vasoactive support matched to SVR and ventricular function, correction of metabolic factors, and hydrocortisone for catecholamine-resistant shock.
After PDA ligation or device closure, sudden removal of the low-resistance ductal pathway can increase LV afterload and reduce LV output. Typical syndrome: systolic hypotension and worsening ventilation/oxygenation several hours after closure.
Anticipate the physiology: monitor closely after closure, obtain echo when unstable, support LV systolic performance, consider dobutamine or milrinone when LV output and afterload mismatch dominate.
IDM infants may have impaired diastolic filling and hypertrophic cardiomyopathy with preserved or hyperdynamic systolic function. Hypotension may reflect poor filling rather than poor contractility.
Before starting vasoactive medications: assess preload, obstruction, ventricular filling, and outflow gradients. Excess inotropy may worsen dynamic obstruction; cardiology/echo guidance is important.
High-output lesions can create severe diastolic run-off, pulmonary overcirculation, cardiomegaly, heart failure, and systemic hypoperfusion. The clue is wide pulse pressure and signs of heart failure rather than simple low contractility.
Management: echo and neurovascular/cardiology consultation, support of systemic perfusion, avoidance of excessive fluid, and definitive lesion-specific therapy when feasible.
Shock drugs buy minutes; these are the agents that carry an infant through weeks of volume or pressure overload while the underlying lesion is addressed.
| Class | What it does | Practical detail and cautions |
|---|---|---|
| Loop diuretics (furosemide) |
Reduce extracellular fluid volume, so preload falls and hepatic congestion and pulmonary oedema ease | First line for heart failure (low certainty evidence, weak recommendation) — used for symptom relief, since paediatric trials have not shown long-term efficacy or mortality benefit. Oral bioavailability is poor: use a 1:2 conversion when moving from IV to oral — that is, the oral dose is double. If diuresis is inadequate, adding a thiazide may be considered. |
| ACE inhibitors (captopril, enalapril) |
Block angiotensin II and aldosterone → vasodilation, lower SVR, reduced afterload, higher cardiac output; they also attenuate the cardiac remodelling that drives heart failure forward | Captopril's short half-life means 2–4 doses a day; enalapril acts longer through enalaprilat and can be given once or twice daily. There is no head-to-head evidence, so choose on dosing convenience, response and tolerability. Adverse effects: hypotension, hyperkalaemia, rising BUN and creatinine, anuria, acute kidney injury, rarely angioedema. In preterm infants ACE inhibitors carry a high incidence of acute kidney injury. |
| β-blockers (propranolol, carvedilol) |
Reverse adrenergic myocardial dysfunction, damp neurohormonal activation, act as antiarrhythmics and slow the rate. Carvedilol adds α-1 blockade with vasodilatory, antioxidant and antiproliferative properties | Adult mortality benefit is established; whether the same holds in paediatric heart failure is unclear. Propranolol is the commonest agent for infant hypertension and arrhythmia; carvedilol is the usual choice in paediatric heart failure. Both come as liquids. Avoid in acute decompensated heart failure — hypotension and transient worsening are expected at initiation. Contraindicated in symptomatic bradycardia or heart block and in significant hypotension; use caution in reactive airway disease. |
The pathophysiology is the same in all three columns — elevated pulmonary vascular resistance. What changes the drug choice is how well the right and left ventricles are still coping.
| Echo finding | Intact ventricular function | Impaired ventricular function | Severely impaired function |
|---|---|---|---|
| RV afterload | ↑ | ↑↑ | ↑↑↑↑ |
| RV contractility | ↑↑ | ± | Markedly reduced |
| LV preload | Normal or low | Normal or low | Low |
| LV afterload / systolic function | Normal or low | Reduced | Markedly reduced |
| Ventricular septum | Normal | Flattened | Bowing into the left ventricle |
| Tricuspid regurgitation jet velocity | Normal | Normal to raised | Raised |
| TAPSE | Normal | Reduced | Markedly reduced |
| Suggested vasoactive approach | Pulmonary vasodilators and epinephrine; add milrinone if the diastolic pressure is within the normal range | All of the above, plus consider norepinephrine or vasopressin | |
Pulmonary maldevelopment, maladaptation and hypoplasia raise pulmonary resistance, which raises RV afterload — the right ventricle dilates and hypertrophies, relaxation in early diastole is impaired, and the sustained RV pressure narrows the coronary perfusion gradient, producing RV ischaemia. The left ventricle is affected from fetal life: it is smaller and less compliant, reduced pulmonary blood flow lowers LV preload, and septal bowing from the dilated right ventricle impairs LV filling and stroke volume. Management is individualized to which ventricle the echo shows is failing — not to a single CDH recipe.
| Problem | Most Useful Clues | Best Next Action |
|---|---|---|
| Low MAP in a well-perfused ELGAN | Warm, good pulses, normal/improving lactate, adequate UO, stable O₂ need | Observe closely; verify measurement; repeat perfusion assessment; consider echo if persistent/worsening |
| Low MAP + rising lactate | Poor capillary refill, weak pulses, metabolic acidosis, oliguria | Treat as circulatory insufficiency; investigate phenotype and start targeted support |
| Wide pulse pressure | Low diastolic BP, bounding pulses, murmur may be present, pulmonary edema | Evaluate for PDA/AVM/low SVR; echo early |
| Narrow pulse pressure | Poor stroke volume, cool extremities, weak pulses | Evaluate contractility, preload, afterload, obstruction, and arrhythmia |
| Shock + severe hypoxemia | Pre/postductal gradient, labile saturations, high O₂ need | Consider PPHN, CHD, lung disease, or combined physiology; optimize lung and obtain echo |
| Shock + no femoral pulses | Upper/lower BP gradient, acidosis, poor feeding, gray appearance | Start PGE₁ and urgent echo/cardiology |
| Shock + sudden ventilatory collapse | Asymmetric breath sounds, high pressures, positive transillumination | Treat tension pneumothorax immediately if suspected |
| Shock + UVC/UAC recently placed | Pericardial effusion, arrhythmia, hepatic injury, abdominal distension, bleeding | Check line position; use POCUS/CXR; treat tamponade or malposition immediately |
| Issue | How Sources Differ | Neonatology Academy Synthesis |
|---|---|---|
| BP threshold | Older/protocol-based sources use numeric BP cutoffs; Baylor emphasizes correlation with perfusion and physiology | Use thresholds as screening tools, not automatic treatment triggers. Treat circulatory insufficiency, not MAP alone. |
| Volume boluses | Some stabilization algorithms include early volume; Baylor warns nonspecific boluses in preterm infants are often transient and may be harmful | Give volume when hypovolemia/hemorrhage is likely. Avoid repeated empiric boluses in ELGAN, PDA, myocardial dysfunction, or pulmonary edema. |
| Dopamine vs. dobutamine | Traditional protocols favor dopamine; evidence shows dobutamine may improve systemic flow more in selected low-output infants | Choose dopamine when BP/SVR support is the goal and function is acceptable; choose dobutamine when contractility/systemic flow is the main problem and BP can tolerate it. |
| Hydrocortisone | Baylor provides structured refractory-hypotension approach; discourages routine cortisol testing; other sources mention steroids less specifically | Use hydrocortisone for catecholamine-resistant shock or suspected adrenal insufficiency after reassessing phenotype; avoid NSAID overlap when possible. |
| Functional echocardiography | Modern neonatal hemodynamic literature strongly supports physiology-driven echo; older guidelines depend more on clinical signs and drug algorithms | Echo/POCUS should guide fluid, inotrope, vasopressor, pulmonary vasodilator, and PGE₁ decisions when available. |
| PPHN and shock | Baylor integrates PPHN physiology into circulatory insufficiency; CHD-focused sources emphasize ruling out ductal lesions | Always exclude CHD when hypoxemia/shock is unclear. Treat PPHN by optimizing lungs, RV/LV function, SVR/PVR balance, and shunt direction. |
| Mistake | Why It Is Dangerous | Better Practice |
|---|---|---|
| Treating every low MAP with dopamine | MAP may rise while systemic flow worsens, especially with LV dysfunction or high afterload | Identify phenotype; use echo/perfusion/lactate trends |
| Repeated saline boluses without evidence of hypovolemia | Can worsen pulmonary edema, PDA steal, BPD risk, IVH risk, and myocardial stretch | Use 10 mL/kg increments only when indicated; reassess after each bolus |
| Missing ductal-dependent systemic blood flow | Shock may not improve until ductal patency is restored | Start PGE₁ when early neonatal shock suggests left-sided obstruction or ductal systemic dependence |
| Calling PPHN without excluding CHD | iNO and O₂ strategies may be unsafe or ineffective in selected structural lesions | Obtain echo early; use pre/postductal saturations and clinical context |
| Ignoring line malposition or tamponade | UVC/UAC complications can cause rapid collapse | Verify line position; use POCUS/CXR when deterioration follows line placement |
| Using hydrocortisone too casually | Hyperglycemia and intestinal perforation risk with concurrent indomethacin | Reserve for refractory hypotension or suspected adrenal insufficiency; document rationale |
| Interpreting lactate without context | Epinephrine, seizures, hypoxia, sampling delay, and liver dysfunction affect lactate | Follow trend and combine with perfusion, pH, UO, and vasoactive dose |
| Failing to reassess after an intervention | Shock physiology changes quickly; the initial diagnosis may be wrong | Set a reassessment interval and target after every bolus or drug titration |