14.2 Shock States

14.2 Shock States

Quick Answer: Neonatal shock is inadequate oxygen delivery. Classify it as hypovolemic, distributive/septic, cardiogenic, or obstructive (tamponade, tension pneumothorax, left-heart obstruction). Warm shock is vasodilated with flash refill and bounding pulses; cold shock is vasoconstricted or low-output with delayed refill. Give isotonic crystalloid in about 10 mL/kg aliquots and reassess—not a blind 20 mL/kg dump. Epinephrine is the usual first catecholamine for neonatal septic or undifferentiated shock. Hydrocortisone is for catecholamine-refractory shock. This section is taxonomy and sequence; catheter choice, waveforms, and the access menu live in chapter 3.

The Neonatal CCRN Test Plan lists shock states as a multisystem problem (multisystem domain 20%). Cardiovascular hemodynamic instability in chapter 3 is the monitoring-and-access leaf: UAC versus UVC, damping, and which lumen may carry a vasoactive. Do not retake that chapter here. Tamponade as an acquired cardiac diagnosis is introduced there; here tamponade is one of three obstructive physiologies you must separate from empty-tank and pump-failure shock.

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Shock is delivery, not a cuff number

Cardiac output times oxygen content must meet consumption. Neonates raise heart rate first; hypotension is late. Tachycardia, delayed central refill (often taught as longer than about 3 seconds), oliguria near or below about 1 mL/kg/hour after day 1, mottling, weak pulses, a widening core-to-peripheral temperature gap, and a rising lactate diagnose shock while the mean blood pressure still looks typical for weight. Chapter 3 already drilled that recognition. Your new job is to name which circuit failed and to choose the first therapy that matches that circuit.

Typical heart-rate conversation ranges still help you hear tachycardia: a term infant often sits near 120–160 beats/min when quiet; many preterm infants run 140–180. Persistent rates above those bands without pain, fever, anemia, or agitation are a perfusion clue. A so-called normal rate in a gray, oliguric infant is not reassuring—it may mean compensation is ending.

Mixed pictures are the rule in septic neonates: leak plus vasodilation plus cytokine myocardial depression. Name the dominant physiology on this hour's exam, then treat what is in front of you. Recheck after each intervention; the warm infant can become cold in one hour.

Warm versus cold

Warm (vasodilated) shock: flash capillary refill, bounding pulses, wide pulse pressure, pink or flushed skin, often still making some urine. Systemic vascular resistance is low. This is the classic early septic/distributive picture in a term infant who still has vascular tone to lose.

Cold (vasoconstricted or low-output) shock: delayed refill, thready pulses, mottling, cool extremities, narrow pulse pressure, quiet precordium or a large liver depending on cause. This can be hypovolemic, cardiogenic, obstructive, or late septic shock after compensation fails.

Exam trap: assuming every septic neonate is warm. Preterm infants often present cold and gray. Another trap: treating cold cardiogenic shock with repeated 10 mL/kg boluses because shock means fluid. A third trap: calling bounding pulses tamponade. Tamponade narrows the pulse pressure and muffles sounds; runoff and early septic vasodilation widen them.

Hypovolemic shock

History usually tells you: feto-maternal hemorrhage, subgaleal hemorrhage after vacuum or forceps, surgical blood loss, a huge gastric or chest-tube output, or an uncovered ELBW infant with massive transepidermal water loss. The heart is small, the liver is not huge, and the lungs are not wet from pump failure. Fontanelle and skin turgor help in a dehydrated term infant; they help less in a 500-gram infant under a radiant warmer.

Treatment: stop the loss, replace with isotonic crystalloid about 10 mL/kg, reassess perfusion, lactate, and liver size, then repeat if the tank is still empty. If the loss is blood, think red cells, not endless saline that dilutes oxygen content. Glucose and ionized calcium still matter in a crashing neonate—empty and hypoglycemic is two problems. Do not use hypotonic fluid as a shock bolus. Do not infuse the bolus into an infiltrated PIV and call the volume given. NRP logic for hypovolemia during delivery-room resuscitation is the same 10 mL/kg idea, not a 20 mL/kg pediatric dump.

Third-space hypovolemia in NEC or abdominal catastrophe can look like sepsis because it is often both. You still give 10 mL/kg aliquots, but you also get a surgeon and you watch that the abdomen is not so tight that ventilation and venous return collapse (an obstruction-adjacent picture).

Septic / distributive shock

Sepsis produces vasodilation, capillary leak, and myocardial depression. Early disease may look warm; late disease looks cold. Antibiotics and source control—including line removal—are part of shock treatment, not a separate paperwork track. Section 14.1 covers EOS versus LOS coverage; here the circulation is the topic. Every hour of untreated bacteremia is an hour of leak and cytokine myocardial injury.

Sequence used in this independent guide (not an AACN-published algorithm poster):

1. Airway, ventilation, temperature, and glucose. Hypoxemia and hypothermia worsen pulmonary vascular resistance and shock. Hypoglycemia mimics and worsens poor perfusion.
2. Rapid 10 mL/kg isotonic aliquots with reassessment. More leak may need more volume, but watch the liver edge and the lungs. If crackles and hepatomegaly appear, you have left empty-tank physiology.
3. Epinephrine infusion as the usual first catecholamine for neonatal septic or undifferentiated shock (inotropy plus vasoconstriction). Chapter 3 covers central venous delivery versus UAC: do not run epinephrine in an artery. A peripheral IV is an emergency bridge only; watch the limb.
4. If the infant remains hypotensive and vasodilated, additional vasopressor effect—further epinephrine titration or vasopressin in many NICUs—may be needed. Dopamine remains in many unit drawers as a mixed inotrope-vasopressor; do not treat old receptor-dose folklore as three different drugs.
5. Hydrocortisone for refractory shock after volume and catecholamines, especially when relative adrenal insufficiency is plausible (extreme prematurity, catecholamine-resistant vasoplegia). This is not a first-syringe drug for every hypotensive infant, and this guide will not invent an AACN-official milligram table. Congenital adrenal hyperplasia crisis is an endocrine leaf; septic hydrocortisone is a shock-refractory tool.

Milrinone is an inodilator/lusitrope. It is the wrong first drug for empty, vasodilated warm shock. It can help a failing, high-afterload ventricle once blood pressure can tolerate afterload reduction—that decision overlaps chapter 3 and the cardiac-surgery chapter, not the first 10 minutes of septic collapse.

Cardiogenic shock

The pump is the problem: perinatal asphyxia, enteroviral myocarditis, cardiomyopathy, tachyarrhythmia, or a volume-overloaded failing ventricle. The liver enlarges, the infant is gray, pulses are weak, and the lungs may be wet. More volume can finish the ventricle. A large liver plus pulmonary edema is not an invitation to 20 mL/kg.

Support: treat the rhythm if that is the cause (dysrhythmia section in chapter 3), open the duct with PGE1 if a ductal-dependent lesion is possible, consider inotrope (often epinephrine) and, when blood pressure allows, afterload reduction with milrinone as taught in the instability chapter. Avoid stacked 10 mL/kg boluses. Targeted neonatal echocardiography, when available, is a shock-class tool: empty versus full, squeezing versus stunned, tamponade versus poor function.

Therapeutic hypothermia for HIE (chapter 11) can further drop heart rate and output. Shock during cooling is not just cold skin. Rewarming can vasodilate. Those are cardiogenic and distributive overlays on an asphyxiated myocardium, and they preview the multi-organ section that follows.

Obstructive shock: three must-not-miss entities

Cardiac tamponade. Classic after a deep UVC or PICC that perforates into the pericardium, or after postoperative bleeding. Sudden collapse, muffled sounds, conceptually equalizing filling pressures, narrowed pulse pressure, and a quiet-looking heart on radiograph or ultrasound. Stop the infusion. Do not give a victory lap of 10 mL/kg. Prepare for emergency pericardiocentesis. Chapter 3.2 details the cardiac diagnosis; this paragraph is the shock-type classification: it is obstructive, not hypovolemic. Fluid that helps an empty tank can finish a compressed heart.

Tension pneumothorax. Sudden decompensation on positive pressure, asymmetric breath sounds, transillumination in a small infant, mediastinal shift, rising ventilation pressures or a high-frequency oscillator that suddenly looks wrong, and bradycardia. The obstruction is extra-cardiac: high intrathoracic pressure wrecks venous return. Needle thoracentesis and chest-tube evacuation reverse it. Another 10 mL/kg will not open the chest. Respiratory pleural disease is taught in the respiratory chapters; here it is a shock cause. High PEEP, massive gas trapping, and abdominal compartment physiology are cousins: they obstruct venous return without a pericardial effusion.

Left-heart obstruction. Critical coarctation, interrupted aortic arch, and hypoplastic left heart with a closing PDA produce obstructive shock as ductal tissue tightens: poor lower-body perfusion, a pre- and post-ductal saturation or blood-pressure gradient, and a gray lower half. The bolus-and-dopamine reflex misses PGE1 and the anatomy question. This is why a septic-looking day-2 term infant still needs the congenital-heart differential from the transition chapter. Four-limb blood pressures and simultaneous pre/post-ductal saturations are shock tests, not optional extras.

A pulmonary hypertensive crisis can obstruct right-ventricular output. The infant is livid, pre- and post-ductal saturations split or collapse, and blood pressure falls because left-heart filling falls. Treat PPHN physiology (oxygen, ventilation, iNO as indicated in the respiratory chapters); more saline may raise RV wall stress without fixing the blockage.

How this differs from chapter 3

If a stem is about a rounded arterial waveform after a blood draw, you are in chapter 3. If a stem is about which shock class and whether to give 10 mL/kg, epinephrine, hydrocortisone, PGE1, or a chest tube, you are here.

Worked scenarios

1. Three-day-old with NEC, tense abdomen, heart rate 190, refill 4 seconds, history of third-spacing: hypovolemic plus septic. Give 10 mL/kg, obtain cultures, start antibiotics, call surgery. Do not treat this as tamponade because the abdomen is tight—unless a deep line was just manipulated and the sounds went muffled.
2. PICC infant, flash refill, bounding pulses, wide pulse pressure, temperature instability: warm septic shock. Volume carefully, epinephrine, antibiotics, hydrocortisone if still hypotensive after catecholamines. Review whether the line should come out.
3. Deep UVC advanced yesterday, sudden collapse, muffled sounds: obstructive tamponade. Stop the line. Pericardiocentesis pathway. No 20 mL/kg.
4. Day-2 infant, differential cyanosis, absent femoral pulses, shock: left-heart obstruction. Start PGE1, not stacked saline.
5. Ventilated 26-week infant with a sudden high-pressure alarm, a transilluminating chest, and bradycardia: tension pneumothorax. Evacuate air. Fluid does not replace a chest tube.

Exam traps: 20 mL/kg as the neonatal default; hydrocortisone as the first drug before volume and epinephrine; milrinone as the first drug in empty warm shock; treating tamponade or tension pneumothorax with fluid marathons; forgetting PGE1 in left-heart obstruction; and answering a waveform question with a shock-class lecture.