Glenn Circulation #1: Principle of Stage 2 Palliation

The bidirectional Glenn circulation is a stage 2 palliation for patients with single-ventricle physiology. Its central principle is simple but physiologically profound: superior vena cava (SVC) blood is redirected directly into the pulmonary arteries, thereby removing a major portion of pulmonary blood flow from the workload of the systemic ventricle.

Before Glenn, the systemic ventricle often supports both systemic and pulmonary circulations. In this setting:

Systemic ventricular output = Qs + Qp

After Glenn, SVC-derived pulmonary blood flow bypasses the ventricle and enters the pulmonary arteries passively. As a result:

Systemic ventricular output ≈ Qs

This transition reduces ventricular volume loading while maintaining pulmonary blood flow through a cavopulmonary pathway [1, 2].

1. The Pre-Glenn Problem: Pulmonary Blood Flow Is “Stolen” from Systemic Output

In first-stage single-ventricle palliation, pulmonary blood flow is commonly supplied by a systemic-to-pulmonary source, such as a shunt, ductal stent, or right ventricle–to–pulmonary artery conduit.

This arrangement provides oxygenation, but it also creates a fundamental hemodynamic burden:

• The systemic ventricle must pump blood to the body.
• The same ventricle must also supply pulmonary blood flow.
• Pulmonary runoff competes with systemic perfusion.
• Excessive Qp increases pulmonary venous return and ventricular preload.

Thus, pulmonary blood flow is functionally “borrowed” from the systemic circulation. If Qp is excessive, systemic perfusion may be compromised; if Qp is inadequate, systemic oxygen saturation falls.

The Glenn operation is designed to reduce this parallel-circulation burden.

2. The Glenn Concept: Removing Pulmonary Circulation from the Systemic Ventricle

The Glenn operation connects the SVC to the pulmonary artery, usually as a bidirectional cavopulmonary anastomosis.

This produces three major physiological changes:

1. SVC flow becomes pulmonary blood flow

Venous return from the upper body flows directly into both pulmonary arteries.

2. The systemic ventricle is volume-unloaded

The ventricle no longer needs to generate the SVC-derived component of pulmonary blood flow.

3. Pulmonary blood flow becomes passive and non-pulsatile

There is no subpulmonary ventricle. Flow depends on venous pressure, pulmonary vascular resistance, pulmonary artery anatomy, and downstream atrial/ventricular filling pressure.

This is why Glenn circulation is not simply an anatomic shunt. It is a conversion from ventricular-driven pulmonary blood flow to venous-driven pulmonary blood flow.

3. The Lungs Are Placed Between the SVC and the Systemic Ventricle

A useful surgical and physiological concept is:

The lungs are placed between the SVC and the systemic ventricle.

The sequence becomes:

SVC → pulmonary artery → pulmonary vascular bed → pulmonary veins → atrium → systemic ventricle

This means that the lung circulation is now interposed within the upper-body venous return pathway. Pulmonary blood flow is no longer generated by ventricular contraction, but by the pressure gradient from the SVC through the pulmonary vascular bed into the atrium.

Therefore, Glenn flow is especially dependent on:

• SVC flow volume
• Low pulmonary vascular resistance
• Unobstructed branch pulmonary arteries
• Unobstructed pulmonary venous return
• Low atrial pressure
• Favorable ventricular diastolic function
• Avoidance of high intrathoracic pressure

This passive system explains why Glenn patients are sensitive to changes in ventilation, acid-base status, pulmonary vascular tone, and venous return.

4. Passive Pulmonary Blood Flow: A Low-Resistance System Is Essential

In normal biventricular physiology, the right ventricle actively ejects blood into the pulmonary arteries. In Glenn physiology, this pump is absent.

Flow is driven by:

SVC pressure − atrial pressure

and opposed by:

pulmonary vascular resistance + anatomic pathway resistance

Therefore, even a modest increase in resistance can reduce pulmonary blood flow. Important causes include:

• Elevated PVR
• Pulmonary artery stenosis or distortion
• Pulmonary venous obstruction
• High left atrial or common atrial pressure
• Ventricular diastolic dysfunction
• High positive-pressure ventilation
• Atelectasis, hypoxia, hypercarbia, or acidosis

Clinical outcomes after bidirectional Glenn are strongly influenced by the pulmonary vascular bed and preoperative hemodynamic status. In a large contemporary series, elevated PVR was an important risk factor for adverse outcome and failure to progress successfully through staged palliation [2].

5. Oxygen Saturation After Glenn: Flow, Resistance, and Venous Mixing

After Glenn, systemic saturation is determined by the balance between:

• Oxygenated pulmonary venous return generated by SVC-to-pulmonary flow
• Deoxygenated IVC return that still enters the heart without passing through the lungs

Because only SVC blood is routed to the pulmonary arteries, Glenn physiology is inherently partially cyanotic.

Two mechanisms are particularly important.

A. Flow-related desaturation

If SVC flow decreases, pulmonary blood flow decreases.

Examples include:

• Low cardiac output
• Hypovolemia
• SVC obstruction
• Reduced cerebral/upper-body venous return
• Increasing IVC proportion with growth
• Venovenous collateral formation

As the child grows, the IVC contribution to total venous return increases. Therefore, the Glenn circulation is usually a transitional stage rather than the final circulation.

B. Resistance-related desaturation

If PVR increases, Glenn flow decreases.

Examples include:

• Hypoxia
• Hypercarbia or hypocarbia-related changes in cerebral/SVC flow
• Acidosis
• Atelectasis
• Elevated airway pressure
• Pulmonary artery stenosis
• Pulmonary venous obstruction

Cerebral oxygenation and perfusion may change significantly during conversion from systemic-to-pulmonary shunt physiology to Glenn physiology, emphasizing that Glenn circulation alters not only pulmonary blood flow but also upper-body venous and cerebral hemodynamics [3]. Early postoperative arterial oxygenation is also influenced by age, ventricular volume loading, and postoperative SVC pressure; higher SVC pressure correlates with lower oxygen saturation [4].

6. Why PVR Matters So Much

In Glenn physiology, PVR is not merely one variable among many. It is one of the central determinants of whether the circulation works.

When PVR is low:

• SVC pressure can remain acceptable.
• Pulmonary blood flow improves.
• Oxygen saturation is more stable.
• Ventricular preload is reduced without severe cyanosis.

When PVR is high:

• SVC pressure rises.
• Pulmonary blood flow falls.
• Systemic saturation decreases.
• Pleural effusions, venous congestion, or Glenn failure may occur.
• Progression to Fontan becomes less favorable.

Computational and experimental models also support this principle: Glenn performance changes substantially across different PVR conditions, with higher PVR increasing SVC pressure and reducing the efficiency of cavopulmonary flow [5].

7. Additional Antegrade Pulmonary Blood Flow: Helpful or Harmful?

One important surgical question is whether to leave an additional source of pulmonary blood flow at the time of Glenn.

Potential advantages:

• Higher systemic oxygen saturation
• Better pulmonary artery growth
• More pulsatile pulmonary flow
• Longer period of acceptable palliation in selected patients

Potential disadvantages:

• Persistent ventricular volume loading
• Higher SVC or pulmonary artery pressure
• Pleural effusions or venous congestion
• Potential negative impact on later Fontan physiology if flow is excessive

The literature is mixed. Some studies show that persistent antegrade pulmonary blood flow improves oxygen saturation and pulmonary artery growth without worsening early Fontan outcomes [6]. Other reports highlight that additional pulmonary blood flow may be useful in selected patients but remains controversial because of the tradeoff between oxygenation and ventricular unloading [7, 8]. Larger series suggest that Glenn with antegrade pulmonary blood flow can serve as effective temporary palliation before Fontan, or even longer-term palliation in selected patients who are suboptimal Fontan candidates [9].

The key concept is not simply whether antegrade flow exists, but whether it is controlled. Too little flow causes cyanosis; too much flow recreates the pre-Glenn problem of ventricular volume overload.

8. Surgical Principles

The surgical objective is to create a wide, low-resistance, non-obstructive cavopulmonary pathway.

Important technical principles include:

• A tension-free SVC-to-PA anastomosis
• Avoidance of SVC narrowing
• Preservation of branch pulmonary artery geometry
• Avoidance of pulmonary artery distortion
• Assessment of bilateral SVC anatomy when present
• Consideration of azygos vein management
• Evaluation of Glenn pressure and oxygen saturation after separation from bypass
• Careful decision-making regarding additional antegrade pulmonary blood flow

Because Glenn flow is passive, even mild anatomic narrowing may have meaningful physiological consequences.

9. Clinical Interpretation: What Makes a Good Glenn Circulation?

A favorable Glenn circulation requires alignment of anatomy, resistance, and ventricular function.

Key features include:

• Low PVR
• Adequate pulmonary artery size
• No significant branch PA stenosis
• No pulmonary venous obstruction
• Low atrial pressure
• Good systemic ventricular systolic and diastolic function
• Controlled atrioventricular valve regurgitation
• Acceptable SVC pressure
• Adequate systemic oxygenation
• Absence of excessive collateral burden

The Glenn operation therefore functions as both a palliation and a physiological test. It determines whether passive venous pulmonary blood flow can support the patient before Fontan completion.

10. Summary

The bidirectional Glenn circulation redirects SVC return directly to the pulmonary arteries. This removes SVC-derived pulmonary blood flow from the systemic ventricular workload and reduces ventricular volume overload.

The central transformation is:

• Before Glenn: the systemic ventricle supplies both Qs and Qp.
• After Glenn: the systemic ventricle supplies mainly Qs, while SVC flow passively supplies the lungs.

This makes Glenn circulation effective, but also fragile. Oxygenation depends on the interaction between SVC flow, PVR, pulmonary artery anatomy, atrial pressure, ventricular diastolic function, airway pressure, and the presence or absence of additional pulmonary blood flow.

In short:

The Glenn circulation converts pulmonary blood flow from ventricular-driven flow to passive venous flow. Its benefit is ventricular volume unloading; its vulnerability is dependence on low pulmonary resistance and adequate SVC return.

References

[1] Allgood NL, Alejos J, Drinkwater DC, Laks H, Williams RG. Effectiveness of the bidirectional Glenn shunt procedure for volume unloading in the single ventricle patient. Am J Cardiol. 1994;74(8):834-836.

[2] Alsoufi B, Manlhiot C, Awan A, Al-Fadley F, Al-Ahmadi M, Al-Wadei A, McCrindle BW, Al-Halees Z. Current outcomes of the Glenn bidirectional cavopulmonary connection for single ventricle palliation. Eur J Cardiothorac Surg. 2012;42(1):42-49.

[3] Bertolizio G, DiNardo J, Laussen P, Polito A, Pigula F, Zurakowski D, Kussman B. Evaluation of cerebral oxygenation and perfusion with conversion from an arterial-to-systemic shunt circulation to the bidirectional Glenn circulation in patients with univentricular cardiac abnormalities. J Cardiothorac Vasc Anesth. 2015;29(1):95-100.

[4] Aeba R, Katogi T, Kashima I, Omoto T, Kawada S, Omae K. Factors influencing arterial oxygenation early after bidirectional cavopulmonary shunt without additional sources of pulmonary blood flow. J Thorac Cardiovasc Surg. 2000;120(3):589-595.

[5] Esmaily-Moghadam M, Hsia TY, Marsden AL; Modeling of Congenital Hearts Alliance (MOCHA) Investigators. The assisted bidirectional Glenn: a novel surgical approach for first-stage single-ventricle heart palliation. J Thorac Cardiovasc Surg. 2015;149(3):699-705.

[6] Gray RG, Altmann K, Mosca RS, Prakash A, Williams IA, Quaegebeur JM, Chen JM. Persistent antegrade pulmonary blood flow post-Glenn does not alter early post-Fontan outcomes in single-ventricle patients. Ann Thorac Surg. 2007;84(3):888-893.

[7] McElhinney DB, Marianeschi SM, Reddy VM. Additional pulmonary blood flow with the bidirectional Glenn anastomosis: does it make a difference? Ann Thorac Surg. 1998;66(2):668-672.

[8] Mainwaring RD, Lamberti JJ, Uzark K, Spicer RL. Bidirectional Glenn. Is accessory pulmonary blood flow good or bad? Circulation. 1995;92(9 Suppl):II294-II297.

[9] Calvaruso DF, Rubino A, Ocello S, Salviato N, Guardì D, Petruccelli DF, Cipriani A, Fattouch K, Agati S, Mignosa C, Zannini L, Marcelletti C. Bidirectional Glenn and antegrade pulmonary blood flow: temporary or definitive palliation? Ann Thorac Surg. 2008;85(4):1389-1395.