3.3 Post-Operative Cardiac Surgical Management & Low Cardiac Output Syndrome (LCOS)

Post-Operative Cardiac Surgical Management & Low Cardiac Output Syndrome (LCOS)

Quick Answer: Suspect low cardiac output when perfusion, urine output, venous saturation or lactate worsen after surgery. Check ventricular function, rhythm, filling, bleeding and residual lesions while supporting oxygen delivery. After a Norwood procedure, interpret oxygen saturation alongside systemic perfusion and the anatomy of the pulmonary blood supply.

Cardiopulmonary Bypass, Inflammation and Bleeding

Cardiopulmonary bypass (CPB) can activate inflammation and complement. Ischemia and reperfusion can contribute to transient myocardial stunning. Capillary leak and tissue edema can worsen lung compliance and ventricular filling. Edema and inadequate effective circulating volume may coexist. Consider the operation, bleeding, examination and echo before choosing a fluid or vasoactive intervention. Pediatric CPB inflammation study · AHA pediatric acute heart failure statement

Post-bypass coagulopathy

Dilution, platelet dysfunction, reduced fibrinogen, residual heparin and fibrinolysis can contribute to bleeding after bypass. With excessive drainage or instability, involve the surgeon while evaluating temperature, ionized calcium, platelet count, fibrinogen, coagulation testing and adequacy of heparin reversal. Surgical bleeding and impaired hemostasis can coexist.

Viscoelastic testing such as TEG or ROTEM can supplement conventional testing and clinical assessment. Comparing heparin-sensitive and heparin-neutralized channels can help distinguish residual heparin from other causes of delayed clot initiation. Compare the fibrin-based channel with overall clot strength before attributing a weak clot to platelets. Interpret lysis using the assay and the clinical context. Use the cardiac team's product and reversal protocol. A single assay result cannot distinguish all causes of bleeding or determine whether re-exploration is needed. Pediatric TAXI-CAB consensus · Pediatric ROTEM study

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Recognizing Low Cardiac Output Syndrome

Low cardiac output syndrome (LCOS) refers to inadequate forward flow and oxygen delivery for the child's metabolic needs. In a historical arterial-switch cohort with invasive measurements, the lowest cardiac index often occurred at 9–12 hours and 23.8% fell below $2.0\text{ L/min/m}^2$. That timing and study cutoff cannot serve as universal diagnostic criteria. A later pediatric CPB cohort did not identify a fixed nadir. Monitor from arrival through recovery. Arterial-switch study · Contemporary CPB cohort

• Examination and arterial waveform: Delayed refill, cooler extremities, weaker pulses, tachycardia and narrowing pulse pressure can accompany low flow. Compensatory vasoconstriction may maintain pressure while perfusion falls. Compare current findings with the postoperative baseline.
• Urine output and lactate: Falling output and rising lactate support concern when the examination deteriorates. Consider other contributors, including renal injury, the effect of epinephrine on lactate and postoperative changes in clearance.
• Venous oxygen saturation and near-infrared spectroscopy (NIRS): A fall in central venous oxygen saturation can reflect reduced delivery or increased demand. Interpret the change with hemoglobin, arterial saturation, catheter position and the operative anatomy. Cerebral and somatic NIRS provide regional trend information. A change should prompt evaluation in context.
• Rhythm, echo and the operative report: Check whether an arrhythmia or loss of AV synchrony explains the change. Assess both ventricular function and filling, valve regurgitation, effusion or clot, and the repair or palliation. If the trajectory is worse than expected or the echo cannot adequately assess a suspected lesion, discuss additional imaging, catheterization or surgical evaluation promptly. AHA residual lesions statement

Matching support to the physiology

1. Filling: Use examination, trends in filling pressure, drain output and echo. A high CVP can reflect impaired filling, ventricular dysfunction, increased intrathoracic pressure or other causes. When bleeding is likely, coordinate hemorrhage control and replacement. When an underfilled ventricle is likely, consider a small, reassessed volume challenge. With congestion, evaluate causes before giving more volume. Transfusion decisions depend on bleeding, hemoglobin, stage of repair and evidence of inadequate oxygen delivery. TAXI congenital heart disease recommendations
2. Contractility and arterial pressure: An inotrope such as epinephrine can support contractility in hypotensive low output. Milrinone adds inotropy, relaxation and vasodilation when pressure can tolerate it. Consider renal function and monitor for hypotension and arrhythmia. The PRIMACORP trial evaluated prophylaxis after corrective surgery. Its higher-dose arm used a loading infusion followed by continuous milrinone and had fewer LCOS events than placebo in the first 36 hours. Loading and maintenance decisions for an unstable child depend on pressure, renal function and the postoperative plan. Reassess flow and pressure before escalating. Correct measured electrolyte abnormalities, including low ionized calcium when appropriate. PRIMACORP trial · AHA pediatric cardiogenic shock statement
3. Rhythm and conduction: Temporary epicardial pacing can support symptomatic bradycardia or important AV block when pacing wires are available. Atrial pacing requires intact AV conduction. AV sequential or ventricular pacing may be needed with AV block, depending on lead availability and response. Postoperative junctional ectopic tachycardia (JET) can produce a narrow QRS or retain the baseline bundle branch pattern. Look for a junctional rate exceeding the atrial rate with AV dissociation, while recognizing that retrograde conduction can obscure it. An atrial-wire electrogram can clarify the mechanism. Correct fever and electrolyte abnormalities, provide analgesia and sedation, and reduce adrenergic stimulation if perfusion allows. Persistent instability can require specialist-guided cooling, an antiarrhythmic or pacing to restore synchrony after the rate slows. Pediatric postoperative JET treatment study · Pediatric postoperative arrhythmia cohort

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Single-Ventricle Palliation and Oxygen Delivery

Single Ventricle Reconstruction trial · AHA Fontan statement

Stage 1: Why saturation and perfusion can diverge

After Norwood palliation, systemic and pulmonary flow are in parallel. The distribution of ventricular output depends on the pressure gradients and resistance across both circuits, including the shunt or conduit, and on ventricular performance and any residual obstruction. An mBTT shunt can draw flow from the aorta during diastole, reducing systemic diastolic pressure and potentially compromising coronary perfusion. The RV-to-PA conduit avoids that direct aortic runoff pathway but has its own flow and ventricular consequences. With aortic atresia, coronary blood reaches the native ascending aorta by retrograde flow after reconstruction. To assess suspected arch obstruction, examine the reconstructed segment for narrowing and integrate Doppler and arm–leg pressure findings with perfusion. Post-Norwood coronary anatomy study · Post-Norwood recoarctation study

A higher arterial saturation can accompany greater pulmonary flow while systemic flow and delivery fall. The same saturation can also reflect better gas exchange. Interpret the direction of change with diastolic pressure, perfusion, venous saturation trends, lactate, ventilation and echo or other imaging. In a small immediate postoperative study, supplemental oxygen improved indices of systemic delivery. Another study found that increasing carbon dioxide could affect systemic vascular resistance and regional flow. Individualize oxygen and ventilation to the measured response and surgical physiology. If desaturation suggests obstruction of a shunt-dependent pulmonary circulation, urgently involve the cardiac team. AHA/AAP PALS supports oxygen, vasoactive agents and heparin when appropriate while preparing for urgent catheter or surgical intervention. Post-Norwood oxygen study · Post-Norwood carbon dioxide study · AHA/AAP PALS single-ventricle recommendations

Worked example: Arterial oxygen content is approximately $C_{aO_2} = 1.34 \times Hb \times S_{aO_2} + 0.003 \times P_{aO_2}$, with hemoglobin in g/dL, saturation as a fraction, and oxygen tension in mmHg. The result is in mL O₂/dL. Systemic oxygen delivery is $Q_s \times C_{aO_2} \times 10$ when $Q_s$ is in L/min, because 1 L equals 10 dL. With hemoglobin 12 g/dL, saturation 0.80 and oxygen tension 45 mmHg, the arterial content is about 13.0 mL O₂/dL. At $Q_s=1.0\text{ L/min}$, delivery is about 130 mL O₂/min. At $Q_s=0.7\text{ L/min}$ with the same arterial content, delivery falls to about 91 mL O₂/min. A stable oximeter reading can therefore coexist with falling delivery. Measured systemic oxygen transport after Norwood

Later Fontan complications

• Protein-losing enteropathy (PLE): Enteric protein loss can cause edema, ascites, hypoalbuminemia and diarrhea. Elevated venous pressure, altered mesenteric circulation and lymphatic dysfunction can contribute. The Fontan consensus uses fecal alpha-1 antitrypsin clearance above 27 mL/24 h without diarrhea or above 56 mL/24 h with diarrhea as evidence of enteric protein loss. Check urinary losses and other causes of hypoalbuminemia, and assess the Fontan pathway, filling pressures and lymphatic abnormalities with the specialist team. Fontan definitions consensus
• Plastic bronchitis: Branching airway casts can obstruct ventilation. Suspect it with cast expectoration or acute respiratory compromise in a child with Fontan circulation. Obstructing casts may require urgent bronchoscopic removal. A specialist team can consider lymphatic intervention in selected patients. Lymphatic intervention study
• Fontan-associated liver disease: Chronic venous congestion can lead to fibrosis and, in some patients, cirrhosis. Arrange longitudinal congenital cardiology and liver surveillance tailored to age, years since surgery and clinical findings. Normal transaminases alone cannot exclude liver disease. AHA Fontan statement · EASL–ERN position paper

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Open Sternum, Surgical Bleeding and Extracorporeal Support

• Delayed sternal closure: A covered open sternum may be used after selected operations when edema, bleeding or instability makes closure poorly tolerated. Approximation can restrict filling and impair hemodynamics or ventilation. Maintain the surgical dressing and monitoring plan, and let the team reassess readiness for closure based on clinical stability. Pediatric delayed closure cohort · Neonatal hemodynamic study
• Bleeding and suspected tamponade: Brisk or increasing bloody drainage with instability warrants immediate surgical assessment. Abrupt loss of drainage with hypotension, narrowing pulse pressure or rising filling pressure may signal retained blood or impaired filling. Check the drainage system for obstruction and notify the surgical team urgently. Use focused echo if it can be done without delaying treatment. Drain manipulation follows the surgical protocol. A localized clot may require surgical drainage. AHA residual lesions statement
• Postoperative arrest: Activate the cardiac surgical arrest response. Begin external compressions if emergency resternotomy is not immediately available. Early resternotomy is reasonable in an appropriately staffed and equipped ICU. AHA pediatric postoperative resuscitation guidance
• VA-ECMO: Seek timely assessment when a child cannot separate from bypass or has refractory low output despite correction of treatable causes and appropriate support. In an eligible postoperative child with refractory arrest, activate extracorporeal CPR through a capable program. Base the decision on the clinical trajectory, reversibility and surgical anatomy, including whether a residual lesion requires intervention. AHA/AAP PALS · AHA pediatric acute heart failure statement