Glenn Circulation #3: Determinants of Post-Glenn SpO₂

After a bidirectional Glenn procedure, systemic arterial oxygen saturation is not determined by pulmonary gas exchange alone. The Glenn circulation creates a partial-mixing circulation, in which oxygenated pulmonary venous blood and desaturated systemic venous blood returning from the lower body mix before systemic ejection.

Therefore, post-Glenn SpO₂ should be understood as the result of two major physiologic inputs:

1. Pulmonary venous saturation (SpvO₂)
2. Systemic/mixed venous saturation (SvO₂)

The practical implication is important: a low SpO₂ after Glenn is often not simply an oxygenation problem; it may be an oxygen-delivery problem.

1. Core Physiology: Post-Glenn SpO₂ Is a Mixing Saturation

In the bidirectional Glenn circulation, SVC blood flows passively into the pulmonary arteries, while IVC blood returns directly to the heart. Pulmonary venous blood then mixes with systemic venous blood within the functional single ventricle before being ejected to the systemic circulation.

Theoretical analyses of bidirectional cavopulmonary physiology have shown that arterial saturation and systemic oxygen delivery are influenced by several interacting variables: pulmonary venous saturation, systemic venous saturation, cardiac output, oxygen consumption, hemoglobin concentration, and the balance between pulmonary and systemic flow [1, 2].

In simple terms:

Post-Glenn SpO₂ = the final saturation after mixing highly oxygenated pulmonary venous blood with partially desaturated systemic venous blood.

This explains why increasing FiO₂ alone may have only a limited effect if the main problem is low SvO₂.

2. Pulmonary Venous Saturation: Important, but Often Already Near Maximal

Pulmonary venous saturation reflects the effectiveness of pulmonary oxygen uptake. In many stable post-Glenn patients, SpvO₂ is already close to 100%. Once pulmonary venous blood is nearly fully saturated, additional gains from increasing FiO₂ are modest.

However, SpvO₂ may fall in the presence of pulmonary pathology or impaired pulmonary mechanics, including:

• Atelectasis
• Pulmonary edema
• Pneumonia or airway obstruction
• Ventilation-perfusion mismatch
• Pleural effusion or pneumothorax
• Pulmonary venous obstruction
• Elevated pulmonary vascular resistance
• Excessive intrathoracic pressure impairing passive Glenn flow

In these settings, lung optimization remains essential. Management should include adequate ventilation, lung recruitment, avoidance of hypoventilation, correction of acidosis and hypercarbia, and reduction of pulmonary vascular tone when clinically indicated.

Inhaled nitric oxide may be useful when pulmonary vasoconstriction or elevated cavopulmonary pressure is suspected, but it should be understood as a therapy targeting pulmonary vascular resistance, not as a universal treatment for all causes of post-Glenn desaturation.

3. Mixed Venous Saturation: The More Modifiable Lever

In many post-Glenn patients, SvO₂ is the more clinically modifiable determinant of systemic SpO₂. SvO₂ reflects the balance between systemic oxygen delivery and systemic oxygen consumption.

When systemic oxygen delivery is inadequate, tissues extract more oxygen from the blood. As a result, systemic venous blood becomes more desaturated. When this low-saturation venous blood mixes with pulmonary venous blood, the final systemic SpO₂ decreases.

This concept is supported by physiologic studies in single-ventricle circulation, which emphasize that tissue oxygenation may be optimized not simply by maximizing oxygen delivery, but by maintaining favorable systemic venous saturation and minimizing excessive oxygen extraction [2].

4. Three Major Ways to Improve SvO₂

A. Increase Cardiac Output

Improving cardiac output increases systemic oxygen delivery. When more oxygen is delivered to the tissues, less oxygen needs to be extracted from each unit of blood, and SvO₂ rises.

Key targets include:

• Adequate preload
• Preserved ventricular function
• Appropriate heart rate and rhythm
• Low atrioventricular valve regurgitation
• Avoidance of excessive afterload
• Relief of anatomic obstruction in the Glenn pathway or pulmonary arteries

Clinical studies after bidirectional cavopulmonary shunt have shown that postoperative oxygenation is influenced by hemodynamic factors, including ventricular volume loading and SVC pressure [3]. The Glenn procedure also unloads the single ventricle by removing the volume burden of a systemic-to-pulmonary shunt, which can improve ventricular efficiency and systemic hemodynamics [4].

B. Decrease Oxygen Consumption

SvO₂ decreases when oxygen consumption rises. This is particularly important in infants and children after cardiac surgery, where fever, agitation, respiratory distress, pain, seizures, or sepsis can markedly increase metabolic demand.

Common causes of increased oxygen consumption include:

• Fever
• Pain or agitation
• Increased work of breathing
• Sepsis or systemic inflammation
• Seizure activity
• Excessive catecholamine stimulation
• Inadequate sedation or analgesia

Reducing oxygen consumption can improve SvO₂ even without changing lung function. In practical terms, adequate analgesia, temperature control, reduction of respiratory effort, and avoidance of excessive stress are part of oxygenation management after Glenn.

C. Optimize Hemoglobin

Hemoglobin is a major determinant of arterial oxygen content. Saturation tells us the percentage of hemoglobin bound to oxygen, but it does not tell us how much hemoglobin is available to carry oxygen.

Thus, a patient may have an acceptable SpO₂ but still have poor oxygen delivery if hemoglobin is low.

In single-ventricle physiology, hemoglobin optimization can improve systemic oxygen delivery and reduce peripheral oxygen extraction. This may raise SvO₂ and secondarily improve systemic SpO₂ after mixing. Studies of oxygen transport in single-ventricle palliation have shown that hemoglobin concentration and systemic oxygen transport are closely linked [5, 6].

5. Pulmonary Vascular Resistance: Important, but Not the Whole Story

Pulmonary vascular resistance remains highly relevant in Glenn physiology because pulmonary blood flow is passive and depends on a low-resistance pulmonary vascular bed. Elevated PVR increases SVC pressure, reduces pulmonary blood flow, and may worsen systemic oxygenation.

However, PVR should not be viewed as the only determinant of post-Glenn SpO₂. Even with acceptable pulmonary vascular resistance, systemic saturation may remain low if cardiac output is poor, oxygen consumption is high, or hemoglobin is inadequate.

This distinction is important. The bedside question should not be only:

“Is the pulmonary vascular resistance high?”

It should also be:

“Is systemic oxygen delivery adequate relative to metabolic demand?”

6. Bedside Framework for Low SpO₂ After Glenn

When post-Glenn SpO₂ is lower than expected, the evaluation should be systematic.

1. Pulmonary venous saturation problem

Consider:

• Atelectasis
• Pulmonary edema
• V/Q mismatch
• Pneumonia
• Pneumothorax or pleural effusion
• Pulmonary venous obstruction
• Inadequate ventilation

Management focus:

• Optimize ventilation
• Recruit lung volume
• Treat pulmonary pathology
• Avoid acidosis and hypercarbia
• Consider pulmonary vasodilator therapy when appropriate

2. Low pulmonary blood flow problem

Consider:

• Elevated pulmonary vascular resistance
• Glenn pathway obstruction
• Branch pulmonary artery stenosis
• High intrathoracic pressure
• Low SVC driving pressure
• Dehydration or inadequate preload

Management focus:

• Assess Glenn pressure
• Evaluate pulmonary arteries and anastomosis
• Avoid excessive positive pressure ventilation
• Optimize volume status
• Treat elevated PVR

3. Low SvO₂ problem

Consider:

• Low cardiac output
• Ventricular dysfunction
• AV valve regurgitation
• Anemia
• Fever
• Pain or agitation
• Increased work of breathing
• Sepsis or systemic inflammation

Management focus:

• Improve cardiac output
• Optimize hemoglobin
• Reduce oxygen consumption
• Control fever and agitation
• Follow lactate, NIRS, urine output, acid-base status, and venous saturation

7. Clinical Teaching Point

Post-Glenn SpO₂ is best understood as a balance between SpvO₂ and SvO₂.

Because SpvO₂ is often already near maximal, the most effective way to improve systemic saturation is frequently to improve SvO₂ by:

• Increasing cardiac output
• Decreasing oxygen consumption
• Optimizing hemoglobin
• Maintaining low pulmonary vascular resistance
• Ensuring unobstructed cavopulmonary flow

The central concept is:

Post-Glenn desaturation is often not a pure lung problem. It is frequently a systemic oxygen delivery problem.

This physiologic perspective helps avoid overemphasis on FiO₂ alone and directs attention toward the broader determinants of oxygen transport: ventricular performance, hemoglobin concentration, metabolic demand, venous saturation, and passive pulmonary blood flow.

References

[1] Santamore WP, Barnea O, Riordan CJ, Ross MP, Austin EH. Theoretical optimization of pulmonary-to-systemic flow ratio after a bidirectional cavopulmonary anastomosis. Am J Physiol. 1998;274(2):H694-H700.

[2] Diller GP, Uebing A, Willson K, Davies LC, Dimopoulos K, Thorne SA, Gatzoulis MA, Francis DP. Analytical identification of ideal pulmonary-systemic flow balance in patients with bidirectional cavopulmonary shunt and univentricular circulation: oxygen delivery or tissue oxygenation? Circulation. 2006;114(12):1243-1250.

[3] 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.

[4] 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.

[5] 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.

[6] Li J, Zhang G, McCrindle BW, Holtby H, Humpl T, Cai S, Caldarone CA, Redington AN, Van Arsdell GS. Profiles of hemodynamics and oxygen transport derived by using continuous measured oxygen consumption after the Norwood procedure. J Thorac Cardiovasc Surg. 2007;133(2):441-448.

[7] Li J, Zhang G, Holtby H, Guerguerian AM, Cai S, Humpl T, Caldarone CA, Redington AN, Van Arsdell GS. The influence of systemic hemodynamics and oxygen transport on cerebral oxygen saturation in neonates after the Norwood procedure. J Thorac Cardiovasc Surg. 2008;135(1):83-90.e2.

[8] Naito Y, Aoki M, Watanabe M, Ishibashi N, Agematsu K, Sughimoto K, Fujiwara T. Factors affecting systemic oxygen delivery after Norwood procedure with Sano modification. Ann Thorac Surg. 2010;89(5):1498-1504.

[9] Hoffman GM, Mussatto KA, Brosig CL, Ghanayem NS, Musa N, Fedderly RT, Jaquiss RD, Tweddell JS. Systemic venous oxygen saturation after the Norwood procedure and childhood neurodevelopmental outcome. J Thorac Cardiovasc Surg. 2005;130(4):1094-1100.