Case October 2026 - Severe LV Dysfunction with Stasis

Case description

A term infant developed profound cardiovascular collapse after a difficult delivery, requiring advanced resuscitation, ventilation and vasoactive support. Severe myocardial dysfunction followed, predominantly affecting the left ventricle (LV). During an overnight period of persistent shock, targeted neonatal echocardiography (TNE) was used to identify how systemic flow was being maintained and to guide an attempt at stabilisation. The cause of the myocardial injury remained uncertain. NT-proBNP was 6,738 ng/L, and high-sensitivity troponin I was markedly elevated at 12,754 ng/L. Total creatine kinase (CK) was 279 U/L. At the time, trace blood was noted in the endotracheal tube, and chest radiography showed pulmonary vascular congestion, raising concern for pulmonary venous hypertension with evolving pulmonary oedema in the setting of severe LV dysfunction. PEEP was increased to 7 cm H₂O due to these concerns (see chest radiography). A 12-lead ECG was performed and outlined ST segment anomalies highly suggestive of ischemia.

The key physiology was severe LV systolic dysfunction with relatively preserved right ventricular (RV) performance. A large patent ductus arteriosus (PDA) carried right-to-left flow into the descending aorta, with retrograde flow in the aortic arch. A small, restrictive patent foramen ovale (PFO) shunted from the left atrium to the right atrium. This was not simply a desaturation problem: the RV and ductus were supporting systemic perfusion while native LV ejection was markedly compromised. Cardiovascular support included prostaglandin E1 to preserve ductal patency and vasoactive agents including epinephrine and dobutamine. The bedside priorities were to sustain systemic perfusion through the available pathways, support ventricular performance, and reassess the response to treatment. Mechanical ventilation, analgesia and seizure treatment were concurrent components of intensive care. Therapeutic hypothermia, initiated for neonatal encephalopathy, was interrupted during the early rescue period because of haemodynamic instability. This was an individualised decision, not a general recommendation to withhold cooling. Serial TNE was interpreted alongside oxygen saturations, near-infrared spectroscopy (NIRS) and lactate. The question was not whether one blood pressure or saturation value had improved, but whether forward flow and tissue oxygen balance were improving together.

Laboratory trends (post-ductal arterial blood gases) during the course of the management

Discussion

The combination of right-to-left ductal flow and left-to-right atrial flow should prompt assessment for severe left heart dysfunction, rather than attribution of the saturation split to pulmonary vascular disease alone. [1] Here, the ductus provided a systemic pathway from the RV. The resemblance to a duct-dependent circulation was functional, not a diagnosis of hypoplastic left heart syndrome. Preserving the ductus addressed access to systemic flow; it did not correct LV failure. [2] The restrictive PFO was also important. It permitted some oxygenated pulmonary venous blood to reach the right heart, but could limit left atrial decompression and contribute to pulmonary venous hypertension. A normal-range RV output could not be equated with adequate systemic output, because RV ejection divided between pulmonary flow and flow through the ductus.

In this setting, lowering pulmonary vascular resistance could increase flow toward the lungs and return to a severely impaired LV, while reducing the share of RV output available through the ductus. Inhaled nitric oxide therefore required reassessment in the context of LV function and pulmonary venous congestion. This is a case-specific physiological concern, not a reason to avoid pulmonary vasodilation in every infant with LV dysfunction. Guidance stresses echocardiographic assessment of LV function before iNO treatment. [3] Neither severe postductal hypoxaemia nor excessive RV afterload was desirable. Oxygenation and ventilation needed to be considered together with ventricular performance, shunt direction and tissue perfusion—not adjusted solely to erase a preductal–postductal saturation difference.

The Doppler change was in the LV aortic velocity time integral (VTI), not the RV outflow. With comparable sampling, beam alignment and outflow area, a higher VTI supports an increase in native LV forward stroke volume. It does not establish a doubling of total systemic cardiac output: heart rate, outflow dimensions and shunt contributions also matter. [1] Estimated RV output remained approximately 180–200 mL/kg/min on serial assessment. The rise in NIRS, fall in lactate and improvement in postductal saturation were consistent with improved tissue oxygen balance. For a given haemoglobin, arterial oxygenation and metabolic demand, increased systemic flow can reduce fractional oxygen extraction and raise systemic venous saturation. This can improve the oxygen content of RV blood reaching the descending aorta through the PDA. However, saturation changes do not distinguish increased oxygen delivery from reduced oxygen consumption. [4] Postductal saturation was not a direct measurement of mixed venous saturation: atrial admixture, pulmonary venous oxygenation and the relative ductal and native aortic contributions also influenced it. NIRS similarly reflected regional oxygen balance, not a direct cardiac output measurement. Evidence from other RV-supported neonatal circulations reinforces the need to interpret NIRS alongside other haemodynamic data. [5] The rescue period achieved temporary improvement in perfusion markers and native LV forward flow, while severe LV dysfunction persisted. Several treatments changed together, so the response cannot be attributed to one intervention. The teaching point is the use of repeated TNE to follow a fragile circulation and assess the immediate response—not evidence of myocardial recovery or definitive rescue.

Coronary perfusion pressure: a potential cycle of worsening myocardial dysfunction 

Coronary perfusion depends on the pressure gradient driving blood from the aortic root through the myocardial circulation. For the LV, particularly its vulnerable subendocardium, the diastolic driving pressure is commonly approximated as aortic root diastolic pressure minus LV end-diastolic pressure (LVEDP). An elevated LVEDP therefore reduces this gradient even when aortic diastolic pressure is unchanged. In this case, both components could become unfavourable: poor systemic output could lower aortic diastolic pressure, while impaired LV relaxation and emptying could increase LVEDP and intramyocardial compressive forces. Left atrial hypertension would support concern for elevated LV filling pressure, although it would not directly measure LVEDP. With markedly reduced native LV ejection, coronary inflow could also depend substantially on ductal blood travelling retrogradely through the arch to the aortic root, analogous to the pathway supporting coronary perfusion in HLHS with aortic atresia. Any deterioration in RV output or ductal supply could further compromise aortic root perfusion. Limited oxygen enrichment of this blood could additionally reduce coronary oxygen delivery, while tachycardia shortens diastolic perfusion time and increases myocardial oxygen demand. Together, these mechanisms could create a vicious cycle: inadequate myocardial oxygen delivery worsens contraction and relaxation, further reducing forward flow and increasing filling pressures, which then further compromises coronary perfusion. This is a physiological explanation for potential deterioration, rather than evidence that coronary pressure or myocardial ischaemia was directly measured in this infant. 

Why postductal saturation is influenced by systemic venous oxygenation 

In this case, right-to-left ductal flow contributed substantially to descending aortic perfusion, making lower-body oxygenation dependent on the oxygen content of blood ejected by the right ventricle. This blood contains systemic venous return together with oxygenated pulmonary venous blood crossing the left-to-right atrial communication. Although the PFO was anatomically small and restrictive, its size alone does not establish the volume of shunting or its contribution to oxygen enrichment. Postductal arterial saturation was therefore influenced by systemic venous oxygenation, atrial admixture and the relative contributions of ductal flow and native LV ejection. It should not be interpreted as a direct measurement or a reliable numerical estimate of mixed venous saturation. Preferential streaming and changes in pulmonary venous oxygenation further complicate this relationship. When systemic oxygen delivery falls relative to metabolic demand, increased tissue oxygen extraction can lower systemic venous saturation and, in turn, the saturation of RV blood reaching the descending aorta through the PDA. However, low postductal saturation alone cannot quantify systemic blood flow or distinguish reduced oxygen delivery from increased oxygen consumption. The observed rise in postductal saturation was compatible with improved oxygen balance, but could also reflect changing atrial admixture, pulmonary venous oxygenation and native LV contribution. Its interpretation was strengthened by concurrent assessment of LVOT VTI, cerebral and renal NIRS, lactate, haemoglobin and clinical perfusion.

Key teaching points

Management focused on four major principles:

1. Optimize RV-supported systemic circulation

• Prostaglandin E1 to maintain ductal patency

• Acceptance of differential saturations

• Utilization of the RV as a systemic pump

2. Minimize pulmonary overcirculation

• Discontinuation of inhaled nitric oxide

• Avoidance of excessive oxygen exposure

• Oxygen titration using preductal saturations

3. Support systemic perfusion

• Optimization of epinephrine and dobutamine to support inotropy

• PGE to maintain RV-dependent systemic circulation

• Introduction of hydrocortisone for relative adrenal insufficiency possibility, as well as possible adrenal hit (ischemia)

4. Reduce metabolic demand

• Fentanyl infusion for sedation and metabolic suppression

• Additional sedative/antiepileptic medications when seizure activity was suspected

Evolution during the TNE-driven hours of management:  One of the most remarkable aspects of this case was the progressive improvement in markers of systemic blood flow despite persistently severe ventricular dysfunction. Serial TnECHO assessments demonstrated approximately a two-fold increase in ventricular outflow VTI, suggesting a substantial increase in effective forward blood flow. Concurrently, cerebral and somatic NIRS values increased from the low 20% range to approximately 50-60%, indicating improved regional oxygen balance (oxygen delivery and extraction). Lactate levels decreased from approximately 11 mmol/L to 5 mmol/L, supporting improved systemic perfusion and a reduction in anaerobic metabolism. Preductal oxygen saturation remained consistently near 100% on minimal oxygen supplementation, while postductal saturations improved dramatically from approximately 30% to 70%. This improvement likely reflected increasing mixed venous oxygen saturation secondary to enhanced systemic blood flow. As tissue oxygen extraction decreased and systemic oxygen delivery improved, venous return to the right atrium became progressively more oxygenated. This resulted in higher right atrial and right ventricular saturations and consequently higher oxygen content in blood traversing the ductus arteriosus into the descending aorta, explaining the marked improvement in postductal saturations. While initially anuric, the urine output appeared and remained approximately 0.5 mL/kg/hr, suggesting improving end-organ dysfunction.

This case highlights several important concepts in neonatal hemodynamics:

1. Differential saturations must be interpreted in their haemodynamic context. A postductal saturation near 30% remains profoundly concerning. In this patient, improvement in postductal saturation served as a bedside marker of improving mixed venous oxygen saturation and systemic oxygen delivery.

2. The ductus arteriosus can become a life-saving conduit. In severe isolated LV failure, maintaining ductal patency may permit the right ventricle to temporarily assume a systemic circulatory role.

3. TnECHO should be integrated with physiologic monitoring. The increase in VTI paralleled improvements in NIRS, lactate clearance, blood pressure, and oxygenation patterns, providing a coherent picture of improving systemic blood flow.

4. Metabolic demand matters. Beyond vasoactive support, deliberate reduction of oxygen consumption through sedation and minimization of physiologic stress likely contributed to restoration of the balance between oxygen delivery and oxygen demand.

Targeted Neonatal Echocardiography Views Obtained During the Management

Mitral insufficiency Doppler derived gradient and LA pressure estimation: The calculations of 19 and 21 mmHg assume that the postductal umbilical arterial systolic pressure approximates LV systolic pressure. That assumption is particularly uncertain here, because the descending aorta is substantially supplied by the RV through the PDA. Peak MR gradient and peak arterial pressure also need not occur simultaneously. Subtracting this from the contemporaneous arterial systolic pressure would suggest elevated LA pressure if arterial pressure approximates LV systolic pressure; however, this assumption is uncertain in the present ductally supported circulation. The subtraction method has supporting validation in selected patients, but not specifically this neonatal physiology. 

Clot in the left atrial appendage due to stasis at follow-up echocardiography

The development of a left atrial appendage (LAA) thrombus in this neonate illustrates how severe left ventricular (LV) dysfunction can drive intracardiac thrombogenesis through Virchow's triad, even in the absence of atrial fibrillation. The LAA is a heavily trabeculated, blind-ending pouch whose normal contraction and washout ordinarily protect against clot formation; when contractility falls and blood stagnates, it behaves as a static reservoir predisposed to thrombosis (Beigel et al., JACC: Cardiovascular Imaging, 2014; Naksuk et al., JACC: Clinical Electrophysiology, 2016). In patients in sinus rhythm, the mechanism linking cardiomyopathy to LAA thrombus is thought to involve deterioration of LAA flow together with elevated filling pressures—because the appendage sits within a fixed pericardial space above the LV free wall, diastolic LV distension can further impair its emptying (Naksuk et al., JACC: Clinical Electrophysiology, 2016). Consistent with this, severe LV dysfunction, left atrial dilatation, and reduced ejection fraction are independent, clinically identifiable predictors of LAA thrombus, and the LAA accounts for a substantial share of intracardiac thrombi in non-atrial-fibrillation cardiomyopathy patients who sustain embolic events (Brickner et al., American Journal of Cardiology, 1994; Lin et al., JACC: Heart Failure, 2021). This pathophysiology is directly relevant to the neonate: children with dilated or inflammatory cardiomyopathy carry an estimated period prevalence of intracardiac thrombus of roughly 14–16%, with risk highest at presentation and within the first months, and lower ejection/shortening fractions distinguishing those who clot from those who do not (Giglia et al., Circulation [AHA Scientific Statement], 2013). Importantly, thrombus can arise even in children receiving prophylactic antithrombotic therapy, underscoring that anticoagulation mitigates but does not eliminate the stasis-driven risk conferred by profound ventricular dysfunction (Giglia et al., Circulation, 2013; Payne et al., Journal of the American College of Cardiology, 2023). The present case therefore reinforces the importance of vigilant echocardiographic surveillance—including dedicated interrogation of the LAA—and early consideration of systemic anticoagulation in neonates with severely depressed systolic function and attendant intracardiac stasis.

• Incubator Podcast - #461 - [🫀 From The Heart] - Blue Baby, Gray Baby: Severe LV Dysfunction Masquerading as PPHN

• LV Dysfunction in the Newborn - Dr Kasper Kyng - September 2026 - YouTube of the Neonatal Hemodynamics Research Center - TNE Foundation Curriculum

• The Left Heart Phenotype - Neonatal Hemodynamics Research Centre Speaker: Dr. Jack Wren - TNE/NPE Foundations Lecture Series: Lecture 54.

• The Determinants of Ventricular Function - Neonatal Hemodynamics Research Centre - Speaker: Dr. Luc Mertens TNE/NPE Foundations Lecture Series: Lecture 26.