11.6 Gas Balancing, Hemodynamics & NIRS
Key Takeaways
- Stage 1 single-ventricle targets are patient- and center-specific. Saturations around 75%–85% and avoidance of unintended hypocapnia are common teaching points, while subambient oxygen or inspired CO2 is restricted to specialist protocols with continuous gas analysis.
- NIRS provides regional trends that vary by patient, sensor site, and device. A falling somatic value relative to cerebral baseline may support concern for systemic hypoperfusion, but must be correlated with examination, lactate, pressure, urine output, venous saturation, and echocardiography.
- Subambient oxygen at an FiO2 of 0.16 to 0.20 raises pulmonary vascular resistance through hypoxic pulmonary vasoconstriction and requires a congenital-cardiac protocol with calibrated blending, continuous oxygen analysis, and alarms.
- In Glenn and Fontan circulations there is no subpulmonary pump, so pulmonary blood flow depends entirely on the transpulmonary gradient between central venous pressure and left atrial pressure.
11.6 Gas Balancing, Hemodynamics & NIRS
Therapeutic Gas Manipulation of PVR & SVR
When pulmonary flow appears excessive relative to systemic flow, first confirm anatomy, shunt or conduit patency, ventricular function, hemoglobin, preload, vascular tone, ventilation, and perfusion. Oxygen, carbon dioxide, airway pressure, and specialized gas mixtures affect PVR, but manipulate them only to a congenital-cardiac team's explicit targets.
+-----------------------+---------------------+---------------------+-----------------------+
| Clinical Intervention | Effect on PVR | Effect on SVR | Impact on Qp/Qs Ratio |
+-----------------------+---------------------+---------------------+-----------------------+
| Supplemental Oxygen | Usually decreases | Context dependent | May increase Qp/Qs |
| above prescribed need | PVR | | in parallel flow |
+-----------------------+---------------------+---------------------+-----------------------+
| Subambient Oxygen | Controlled Increase | Unchanged | Decreases Qp/Qs |
| (FiO2 0.16 to 0.20) | (Hypoxic Vasoconstr)| | (Preserves Systemic) |
+-----------------------+---------------------+---------------------+-----------------------+
| Hyperventilation | Usually decreases | Context dependent | May increase Qp/Qs |
| and alkalosis | PVR | | |
+-----------------------+---------------------+---------------------+-----------------------+
| Controlled higher CO2 | Usually increases | Context dependent | May decrease Qp/Qs |
| if prescribed | PVR | | |
+-----------------------+---------------------+---------------------+-----------------------+
| PEEP | U-shaped effect; | Can reduce preload | Must be titrated to |
| | recruitment matters | and cardiac output | mechanics/perfusion |
+-----------------------+---------------------+---------------------+-----------------------+
1. Subambient Oxygen Therapy ($\text{FiO}_2\text{ }0.16\text{ to }0.20$)
- Rationale: When an infant with parallel circulation exhibits pulmonary flooding and systemic steal on room air ($\text{FiO}_2 = 0.21$), the clinician can intentionally lower inspired oxygen below atmospheric levels.
- Physiology: Delivering an inspired fraction of oxygen between $0.16\text{ and }0.20$ ($16%\text{ to }20%\text{ }\text{O}_2$) induces mild, controlled alveolar hypoxia. This stimulates physiological hypoxic pulmonary vasoconstriction (HPV), increasing PVR. Higher PVR restricts pulmonary runoff and forces single-ventricle output across the neo-aorta into the systemic bed.
- Delivery Engineering: Medical nitrogen ($100%\text{ }\text{N}_2$) is blended with medical compressed air using a precision subambient gas mixer or dedicated blender circuit.
- Safety controls: Subambient oxygen is not routine respiratory care. Use it only under a congenital-cardiac protocol with calibrated blending, an independent continuous oxygen analyzer and alarms, redundant monitoring, and a prescribed lower limit. Stop and escalate for worsening perfusion, acidosis, arrhythmia, or hypoxemia.
2. Controlled Permissive Hypercapnia & Inhaled Carbon Dioxide ($i\text{CO}_2$)
- Avoid unintended hypocapnia and alkalosis. Some congenital-cardiac protocols accept controlled higher PaCO2 to influence PVR, but the prescribed PaCO2 and pH depend on anatomy, stage, cerebral perfusion, lung mechanics, and systemic perfusion.
- A few specialist centers use precisely blended inhaled CO2. This is not routine therapy: it requires a written protocol, calibrated analyzers and alarms, appropriate scavenging and monitoring, and direct cardiac-intensive-care oversight.
3. PEEP Titration
- Titrate PEEP to lung recruitment, resistance, compliance, oxygenation, venous return, and cardiac output. Both atelectasis and overdistension can raise PVR; a fixed PEEP range cannot reliably “balance” every single-ventricle circulation.
Advanced Hemodynamic Monitoring in the Pediatric Cardiac ICU
1. Arterial Line & Pulse Pressure Analysis
- Catheter Sites: Right radial artery (pre-ductal site, reflecting coronary and cerebral perfusion) or femoral artery.
- Waveform Analysis:
- In patients with a modified BT shunt, a low diastolic pressure (e.g., $60/25\text{ mmHg}$) indicates significant diastolic runoff into the low-pressure pulmonary bed. Diastolic pressure is the driving pressure for coronary blood flow; severe diastolic runoff precipitates subendocardial ischemia.
- Pulse-pressure variation: Dynamic indices are often unreliable in small children and after cardiac surgery because tidal volume, spontaneous effort, rhythm, shunts, chest compliance, and right-heart physiology violate their assumptions. Use them only when validated conditions are met and never as a stand-alone fluid trigger.
2. Central Venous Pressure (CVP)
- Interpretation: Use the patient’s baseline, catheter position, waveform, ventilation, filling conditions, and surgical stage; there is no single normal CVP that fits every critically ill infant.
- Post-Glenn & Post-Fontan importance: In Glenn and Fontan circulations, there is no subpulmonary pump; pulmonary blood flow is driven exclusively by the pressure difference between CVP and left atrial pressure (the transpulmonary gradient). A high or rising venous pressure can reflect high PVR, pulmonary-artery obstruction, elevated atrial pressure, ventricular or valve dysfunction, volume status, or positive-pressure effects. Interpret the trend with transpulmonary gradient, output, imaging, and catheter data; sustained elevation can accompany low output, effusions, ascites, and later Fontan complications.
3. Near-Infrared Spectroscopy (NIRS)
NIRS uses near-infrared light to estimate regional tissue hemoglobin oxygen saturation. The signal is weighted toward the venous microcirculation but the exact arterial/venous contribution is not fixed; it reflects the local balance between oxygen delivery ($\text{DO}_2$) and oxygen consumption ($\text{VO}_2$):
- Sensor placement: A forehead sensor trends cerebral regional saturation; a flank sensor can trend somatic or renal-region saturation.
- Interpretation: Expected values and the relationship between sites vary with device, anatomy, hematocrit, oxygenation, temperature, sensor position, and individual baseline. A substantial fall from baseline or divergence between cerebral and somatic trends can support concern for altered regional oxygen delivery.
- Clinical action: Check signal and sensor placement, then correlate with perfusion, lactate, pressure, urine output, venous saturation, gases, and echocardiography. NIRS alone neither proves systemic steal nor diagnoses bowel or renal ischemia.
NPS Exam Traps
Exam Trap 1: Panicking Over SpO2 78% in a Stage 1 Norwood Patient
A post-Norwood infant with SpO2 78%, PaO2 40 mmHg, stable pressure, reassuring perfusion, and urine output 1.8 mL/kg/hr may already be within the team's prescribed range. Do not raise FiO2 from the saturation alone. Verify the target and trends, examine work of breathing and perfusion, review lactate and NIRS or venous saturation when available, and communicate with the cardiac team. Those numbers do not mathematically prove Qp/Qs of 1.0 or “perfect” balance.
Exam Trap 2: The "SpO2 95% Reassurance" Trap
A rising saturation can accompany pulmonary overcirculation, but saturation alone is not diagnostic. If it rises with falling pressure, oliguria, lactate elevation, or poor perfusion, urgently involve the congenital-cardiac team, correct unintended hyperventilation toward the prescribed target, and consider specialized gas balancing only under the center protocol.
Exam Trap 3: Dismissing Low Somatic NIRS when Blood Pressure is Normal
A low or falling somatic NIRS trend despite preserved pressure warrants assessment rather than reassurance. Verify the signal and correlate it with lactate, examination, urine output, venous saturation, and echocardiography; do not diagnose bowel infarction or systemic steal from one NIRS number.
An intubated 6-day-old infant with Hypoplastic Left Heart Syndrome awaiting Stage 1 surgical palliation is monitored in the neonatal cardiac intensive care unit. The patient is receiving mechanical ventilation on room air (FiO2 0.21). The bedside monitor shows a heart rate of 148 bpm, blood pressure of 64/38 mmHg (mean 46 mmHg), and an SpO2 of 91%. Continuous multi-site Near-Infrared Spectroscopy (NIRS) displays a cerebral regional saturation (rScO2) of 66% and a somatic/renal regional saturation (rSsO2) of 41%. Arterial blood gas reveals a pH of 7.32, PaCO2 38 mmHg, PaO2 54 mmHg, and lactate 3.8 mmol/L. How should the clinical team interpret these monitoring findings, and what physiological event is impending?