Single Ventricle and Anesthesia Management

Hem Joshi; Daniel Germeroth

Single Ventricle and Anesthesia Management

Author: Hem R. Joshi Editor: Daniel R. Germeroth Updated: 6/22/2025 10:55:42 PM

Introduction

Congenital heart disease (CHD) is one of the most common congenital disorders, with an incidence of up to 9.1 per 1000 live births.[1] Lesions with single ventricle physiology account for approximately one-fifth of those cases.[2] Single ventricle physiology refers to a group of congenital heart defects in which only 1 functional ventricle is responsible for pumping blood to both the systemic and pulmonary circulations. Anatomically, this may involve 1 well-developed ventricle with a hypoplastic counterpart or 2 well-formed ventricles with significant inflow or outflow obstruction. Functionally, however, a single ventricle supports both circulatory systems.

For this physiology to be sustained, complete mixing of systemic and pulmonary venous blood must occur, after which the single ventricle pumps the mixed blood into the systemic and pulmonary circulations. As a result of this mixing, hypoxemia is common, especially during the transition from parallel to fetal circulation to the series circulation of postnatal life. In some cases, immediate medical or surgical intervention is necessary after birth to properly direct blood flow and ensure survival. Anesthesiologists frequently care for infants with single ventricle physiology in both the cardiac catheterization laboratory and the operating room. Understanding this complex physiology is essential for safe and effective perioperative management.

Function

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Function

Congenital cardiac lesions with single ventricle physiology can be broadly categorized based on ventricular anatomy into 2 main groups:

Single ventricle physiology with a single anatomical ventricle: Examples include hypoplastic left heart syndrome, tricuspid atresia, and hypoplastic right heart syndrome.
Single ventricle physiology despite 2 well-developed ventricles: Examples include tetralogy of Fallot with pulmonary atresia, truncus arteriosus, severe neonatal arch stenosis or interrupted aortic arch, heterotaxy syndrome (where venous return drains into both atria), double inlet left ventricle, double outlet right ventricle, unbalanced atrioventricular canal defect, mitral atresia with a normal aortic root, and Ebstein anomaly.[3][4]

Single Ventricle Physiology with a Single Anatomical Ventricle

In these conditions, 1 ventricle is severely underdeveloped or hypoplastic, and the entire circulatory workload is managed by a single functional ventricle. Survival depends on ensuring that all venous return is directed to this ventricle and that blood is effectively distributed to the systemic and pulmonary circulations.

Hypoplastic left heart syndrome

In hypoplastic left heart syndrome, oxygenated blood from the pulmonary veins enters the right atrium via an atrial septal defect (ASD) or patent foramen ovale (PFO), where it mixes with systemic venous return. The right ventricle pumps this mixed blood into the pulmonary artery. Systemic circulation is maintained via retrograde flow through a patent ductus arteriosus (PDA) into the hypoplastic ascending aorta. Thus, systemic blood flow is ductal-dependent, and survival relies on maintaining atrial-level communication and ductal patency.

Tricuspid atresia

In tricuspid atresia, systemic venous blood enters the left atrium through an ASD or PFO, mixing with pulmonary venous return. The well-developed left ventricle then pumps this mixed blood into the aorta for systemic circulation, and to the pulmonary circulation either through a PDA or a ventricular septal defect (VSD). As the right ventricle is hypoplastic or absent, survival is dependent on both atrial-level communication and a patent ductus.

The surgical approach to these lesions involves a staged palliation, gradually transitioning from parallel to series circulation. This includes:

Stage 1: Norwood procedure
Stage 2: Bidirectional Glenn shunt or hemi-Fontan
Stage 3: Fontan procedure

Single Ventricle Physiology Despite Two Well-Developed Ventricles

In some congenital lesions, both ventricles are anatomically well-developed, but significant inflow or outflow obstruction from 1 ventricle leads to functional single-ventricle physiology. Relieving the obstruction may allow for the restoration of biventricular circulation in such cases.

Issues of Concern

All congenital lesions resulting in single ventricle physiology share several key characteristics. Despite their anatomical differences, these conditions are united by a typical hemodynamic pattern that significantly impacts oxygenation, perfusion, and long-term management. These characteristics include the following:

Venous return convergence: Both systemic and pulmonary venous return must be directed to a single functional ventricle.
Complete blood mixing: Oxygenated and deoxygenated blood fully mix within the heart, typically resulting in systemic oxygen saturations between 75% and 80%.
Parallel circulation: The single ventricle perfuses both the systemic and pulmonary circulations in a parallel rather than series configuration.
Flow distribution governed by vascular resistance: The relative resistances of the pulmonary and systemic vascular beds primarily determine the distribution of cardiac output between the 2 circuits.
Associated pulmonary abnormalities: Pulmonary vascular or structural abnormalities of varying severity are often present due to an underlying congenital cardiac lesion.

While fetal echocardiography can detect these lesions in utero, affected fetuses typically remain asymptomatic. This is due to a PFO and a PDA, which allow adequate blood mixing and diversion between circulations. However, these neonates may rapidly decompensate after birth as pulmonary vascular resistance (PVR) falls and the fetal parallel circulation transitions to the postnatal series circulation. The survival of these neonates depends on 2 critical factors:

Unrestricted mixing of systemic venous blood with oxygenated pulmonary venous blood.
A patent conduit from the single functional ventricle to the systemic and pulmonary circulations.

The site of blood mixing varies by lesion, most commonly occurring at the atrial level via a PFO or ASD. However, the atrial septum is intact or restrictive in approximately 6% of patients with single ventricle physiology.[5] These individuals require emergent atrial septostomy, septectomy, or septoplasty—sometimes with stent placement—to establish adequate interatrial communication for effective mixing and systemic oxygenation.[6]

After adequate mixing, blood is directed into the single functional ventricle, which pumps it to both circulations. Depending on the lesion, this ventricle may have 1 of 2 configurations:

Two outlets (eg, double-outlet left ventricle, double-outlet right ventricle, or unbalanced atrioventricular canal defects): In these cases, an adequately sized VSD is necessary to allow the ventricle to eject blood into both outflow tracts. If the VSD is restrictive, emergent ventricular septostomy or septectomy may be required to ensure unimpeded flow.
A single outlet (eg, hypoplastic aortic arch or pulmonary atresia): Here, cardiac output is directed through a single vessel, with blood shunted to the alternate circulation via a PDA. In these cases, maintaining ductal patency is critical; this may require prostaglandin E1 infusion, PDA stenting, or the creation of a surgical shunt, such as a central shunt or Blalock–Thomas-Taussig shunt.[7][8]

Physiologically, the single ventricle receives and pumps the entire cardiac output, resulting in pressure and volume overload. This increased workload leads to elevated myocardial oxygen demand. Diastolic runoff into the pulmonary circulation can also reduce coronary perfusion pressure, predisposing the myocardium to ischemia.[9][10] Individuals affected are highly sensitive to preload, afterload, and myocardial oxygen supply-demand balance changes. When there is unrestricted outflow from the single ventricle, the distribution of blood between the systemic and pulmonary circulations is primarily determined by the relative resistances of each vascular bed.[11]

Following birth, decreased PVR due to lung expansion leads to increased pulmonary blood flow and relative systemic hypotension. Management may require interventions such as intubation with controlled hypoventilation, and in some cases, inhaled nitrogen or carbon dioxide administration to increase PVR and balance systemic perfusion.[12] Inotropic support may also be necessary to maintain adequate cardiac output and tissue perfusion.

Several factors influence the resistance of the pulmonary and systemic circuits, thereby altering blood flow distribution (see Table. Factors Influencing Pulmonary and Systemic Circuit Resistances).

Table. Factors Influencing Pulmonary and Systemic Circuit Resistances

		Physiological parameters	Pharmacological parameters
Facilitate pulmonary blood flow (Qp) (Decrease PVR/SVR ratio)	Decreased pulmonary resistance	Higher FiO2 Hypocarbia, Alkalosis, Spontaneous ventilation Judicious PEEP	Nitric oxide, sildenafil, milrinone, propofol
	Increased systemic resistance	Pain, anxiety, Valsalva	Ketamine Systemic vasoactive therapy (epinephrine, norepinephrine)
Facilitate systemic blood flow (Qs) (Increase PVR/SVR ratio)	Increased pulmonary resistance	Lower FiO2, Hypercarbia Acidosis Hypothermia Pain, anxiety, Valsalva Positive pressure ventilation Atelectasis	Epinephrine, norepinephrine nitrous oxide
	Decreased systemic resistance	Adequate analgesia	Milrinone, propofol Systemic vasodilators Volatile anesthetics

FiO2, fraction of inspired oxygen; PEEP, positive end-expiratory pressure; PVR, pulmonary vascular resistance; Qp, pulmonary blood flow; Qs, systemic blood flow; SVR, systemic vascular resistance

In patients with single ventricle physiology, the ideal pulmonary-to-systemic blood flow ratio (Qp:Qs) is approximately 1:1, assuming minimal aortopulmonary collateral flow and no intrinsic pulmonary abnormalities. This balance, known as balanced circulation, optimizes both oxygenation and systemic perfusion.[13] An oxygen saturation between 75% and 85% is considered a reliable surrogate marker of balanced circulation.[14]

Oxygen saturations above this range indicate excessive pulmonary blood flow, which may result in poor lung compliance, hepatomegaly, and systemic hypoperfusion due to the diversion of blood away from systemic circulation.[15] Chronic pulmonary overcirculation can also lead to pulmonary vascular remodeling and pulmonary hypertension. Conversely, saturations below this range indicate pulmonary undercirculation, with insufficient oxygenation of systemic blood. Various anatomical and physiological pulmonary abnormalities are often present in patients with single ventricular physiology, further complicating the already complex univentricular circulation. These abnormalities may include endothelial dysfunction, altered pulmonary blood flow, venovenous and aortopulmonary collaterals, valvular dysfunction, and obstruction of pulmonary venous return.[16]

Clinical Significance

The clinical presentation of patients with single ventricle physiology is highly variable, even among individuals with similar anatomic lesions. Some may remain relatively asymptomatic due to adequate blood flow through a PDA or atrial/ventricular septal defects. Others may present in critical condition requiring intubation, mechanical ventilation, multiple vasopressors, and, in severe cases, extracorporeal membrane oxygenation.

The primary goal of preoperative assessment is to evaluate and optimize systemic perfusion while minimizing end-organ dysfunction from chronic hypoxemia or hypoperfusion. An oxygen saturation of 75% to 85% typically suggests balanced circulation. Clinical signs such as crackles, pulmonary edema, or increased work of breathing may indicate pulmonary overcirculation. Preoperative echocardiography and cardiac catheterization data are essential for evaluating ventricular function, shunt patency and gradients, pulmonary-to-systemic blood flow ratios, and the presence of aortopulmonary collateral vessels. Optimizing hemoglobin levels and maintaining a hematocrit of around 40% helps enhance peripheral oxygen delivery.

Because these patients are preload-dependent and poorly tolerate abrupt changes in afterload, prolonged fasting should be avoided, and maintenance fluids should be continued when feasible. Additionally, anxiety and pain can cause unpredictable shifts in pulmonary and systemic vascular resistances, further burdening the single ventricle. Therefore, appropriate premedication and minimizing stressful stimuli are critical components of preoperative care.

Intraoperative Management

Patients with single ventricle physiology are susceptible to changes in preload, afterload, myocardial contractility, and PVR/SVR. Factors that contribute to maintaining balanced circulation, such as lower tidal volumes, prevention of atelectasis, controlled interstitial lung water, and hypoxic pulmonary vasoconstriction, can be easily disrupted during induction and intubation. Therefore, a deliberate, well-planned anesthetic technique is essential.

In addition to standard American Society of Anesthesiologists monitoring, patients with single ventricle physiology often require invasive monitoring, such as arterial blood pressure, central venous pressure, and regional tissue oxygenation monitoring (eg, near-infrared spectroscopy), depending on the surgical procedure. Upper extremity arterial lines may be unreliable in patients with a Blalock-Taussig-Thomas shunt due to runoff from the subclavian artery on the shunted side. Similarly, a PDA may create discrepancies between pre- and postductal oxygenation monitors.

Preoxygenation with high inspired oxygen concentrations (FiO2) can exacerbate pulmonary overcirculation. At the same time, too low an FiO2 may compromise apnea time and oxygen reserves, resulting in hypoxemia and hypercarbia, which can impair pulmonary blood flow and oxygenation. Typically, an FiO2 of 40% to 60% is employed to balance these effects.

All volatile anesthetics reduce cardiac output in a dose-dependent manner, primarily through systemic vasodilation (decreasing SVR). Sevoflurane has the most favorable profile regarding hemodynamic stability.[17] Consequently, intravenous induction is usually preferred. However, inhalation induction may be appropriate when the stress of intravenous access could provoke significant hemodynamic compromise. In such cases, lower concentrations should be used and reduced immediately after induction.

Nitrous oxide is typically avoided, as it significantly increases PVR. Among intravenous agents, propofol is known to cause a marked reduction in SVR and cause myocardial depression, which can significantly reduce cardiac output and divert blood away from pulmonary circulation.[18] Etomidate is considered a safer option due to its minimal cardiovascular impact.[19] Ketamine can also be used in patients with preserved ventricular function, as it increases SVR through catecholamine release without significantly affecting PVR. Fentanyl and dexmedetomidine have minimal effects on myocardial contractility, SVR, and PVR, making them well-suited for use in this population.[9]

The intraoperative goal in patients with single ventricle physiology is to maintain balanced circulation with a Qp:Qs ratio of 1:1. The target oxygenation saturation is typically 75% to 85%, corresponding to a PaO2 of 40 to 50 mm Hg. The Qp:Qs ratio can be controlled by adjusting FiO2 and ventilation parameters. To reduce pulmonary overcirculation, both decreasing FiO2 and increasing PaCO₂ can be employed, and vice versa when pulmonary blood flow is insufficient.[20] A slightly elevated PaCO2 (45–55 mm Hg), as mild hypercapnia increases cerebral oxygenation—a helpful strategy in lower systemic oxygen saturations—can be achieved via mild hypoventilation.

Positive pressure ventilation increases intrathoracic pressure, resulting in decreased venous return, increased PVR, and reduced cardiac output.[21] Therefore, spontaneous ventilation is often preferred, as it helps maintain favorable hemodynamics by lowering PVR, improving preload, and preserving cardiac output. When mechanical ventilation is required, a tidal volume of 8 to 12 mL/kg with positive end-expiratory pressure of 3 to 5 cm H2O is generally recommended to optimize oxygenation and prevent atelectasis.[22]

Maintaining adequate diastolic blood pressure is essential to ensure coronary perfusion, and avoiding tachycardia is critical to reduce myocardial demand and enhance oxygen delivery.[23] Special attention should be paid to maintaining shunt patency in patients with central or Blalock-Taussig-Thomas shunt-dependent pulmonary blood flow. Reduced pulmonary blood flow can lead to shunt thrombosis due to blood stasis, resulting in acute cessation of pulmonary perfusion and rapid hemodynamic collapse. In such scenarios, venoarterial extracorporeal membrane oxygenation may be necessary to support the patient until shunt flow is restored.

Following each procedure, the risks and benefits of early extubation should be carefully considered. The hemodynamic consequences of stress from inadequate analgesia or of hypoventilation and hypercapnia due to residual anesthesia or narcosis must be weighed against the potential advantages of extubation and the return of spontaneous ventilation. Given their minimal impact on balanced circulation, fentanyl and dexmedetomidine are commonly used to facilitate smooth emergence from anesthesia.

Enhancing Healthcare Team Outcomes

Single ventricle lesions encompass a variety of congenital cardiac defects characterized by significant heterogeneity in anatomy and physiology. Patients with these conditions may present for various emergent or elective cardiac and noncardiac procedures. With advancements in cardiology, imaging technologies, anesthesia, surgical techniques, and critical care, approximately 70% of infants born with single ventricle physiology survive into adulthood.[24]

Optimal care requires a thorough understanding of the complex anatomical variations and the unique physiology associated with these lesions. Management priorities include maintaining balanced circulation, preserving myocardial function, and ensuring adequate systemic oxygen delivery. Successful outcomes depend on close collaboration and communication among cardiologists, surgeons, anesthesiologists, intensivists, respiratory therapists, and nursing staff, all functioning cohesively as an interprofessional team.

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