Modified Blalock–Taussig Shunt vs RV–PA Conduit in the Norwood Circulation

Concept and anatomic context

Following the Norwood procedure for hypoplastic left heart syndrome (HLHS), systemic output is routed from the right ventricle (RV) to the neo-aorta. Because native pulmonary blood flow (PBF) is interrupted, a source of PBF (“Qp”) must be created surgically. Two standard options are used:

• Modified Blalock–Taussig shunt (mBTS): a 3.5–4.0 mm PTFE graft from the neo-aorta (or innominate/subclavian) to a branch pulmonary artery.
• Right ventricle–to–pulmonary artery conduit (RV–PA; Sano): a short, ring-reinforced 5–6 mm PTFE graft from the RV free wall to the main pulmonary artery.

Both establish Qp in single-ventricle physiology but impart distinct pressure–flow signatures that drive different trade-offs.

Hemodynamic profiles

mBTS

• Flow pattern: relatively continuous (systolic and diastolic) Ao→PA flow.
• Aortic/Coronary effects: diastolic runoff lowers neo-aortic diastolic pressure (DBP), risking subendocardial ischemia (“coronary steal”).
• Pulmonary circuit: a steadier driving pressure may stimulate PA growth but predisposes to higher Qp and systemic hypoperfusion if systemic vascular resistance (SVR) is not defended.
• Clinical corollaries: deliberately maintain higher SVR to preserve DBP; avoid excessive reductions in PVR (no hyperoxia/hypocarbia); careful ventilator titration.

RV–PA conduit

• Flow pattern: predominantly pulsatile systolic RV→PA flow with minimal diastolic runoff.
• Aortic/Coronary effects: typically higher neo-aortic DBP and improved coronary perfusion reserve at a given SVR. Multiple early clinical series showed higher DBP with RV–PA relative to mBTS [2–4].
• RV consequences: requires a ventriculotomy with potential for regional RV dysfunction, arrhythmogenic substrate, and proximal conduit/anastomotic stenosis over time.
• Clinical corollaries: more stable DBP and often less need for pharmacologic vasoconstriction to meet saturation targets, but vigilant surveillance for conduit obstruction is essential.

Bedside management principles (shared, with different weights)

Balance Qp:Qs

Target Qp ≈ Qs (systemic SaO₂ typically mid-70s to mid-80s). Manipulate:

• PVR: FiO₂ (avoid hyperoxia), PaCO₂ (allow mild hypercarbia), PEEP and lung volume.
• SVR: vasoactive strategy (norepinephrine/vasopressin commonly required with mBTS).
• O₂ carrying capacity: modestly higher Hb can support DO₂ at lower Qp.

Protect coronary perfusion (DBP-dependent)

• mBTS: actively defend DBP (e.g., ≥40–45 mmHg in many programs) and watch for ischemic ECG change, rising lactate, or low SvO₂ despite “good” saturations.
• RV–PA: DBP is usually more forgiving; RV performance and conduit patency become the rate-limiting steps.

Monitoring essentials

Arterial line for beat-to-beat DBP; cerebral and somatic NIRS to detect maldistribution (high-Qp/low-systemic flow or conduit restriction); lactate/SvO₂/urine output for global perfusion; echocardiography for shunt/conduit patency, branch PA flow symmetry, RV function, and neo-aortic valve/root.

Practical “when to favor which”

mBTS may be preferred when

• Avoiding an RV incision is a priority (marginal RV function, arrhythmia concerns).
• Branch PAs are hypoplastic and may benefit from steadier driving pressure.
• Re-entry planning disfavors conduit takedown.

RV–PA may be favored when

• Coronary reserve is tenuous and diastolic runoff must be minimized.
• There is prior instability from low DBP or labile SVR.
• The program has reliable surveillance and low threshold for catheter relief of stenosis.

Evidence summary: The Pediatric Heart Network Single Ventricle Reconstruction (SVR) randomized trial showed superior 12-month transplant-free survival with RV–PA vs mBTS (74% vs 64%), but the advantage diminished beyond one year and reinterventions/complications were more frequent with RV–PA [1]. Multiple physiologic studies demonstrated higher DBP with RV–PA [2–4]. A pooled meta-analysis reported lower interstage mortality and ICU stay with RV–PA but more interventions overall [7]. Long-term observational follow-up found no sustained survival difference by shunt type [8].

Common complications and targeted mitigations

mBTS

• Low DBP/ischemia → increase SVR (vasopressors), avoid excessive PVR reduction; consider smaller shunt at index operation in borderline cases.
• Excess Qp/systemic hypoperfusion → permissive hypercarbia, moderate PEEP, judicious inodilators.
• Shunt thrombosis → institution-standard anticoagulation; urgent cath/surgical revision.
• Branch PA distortion (esp. LPA) → anticipate in planning; early cross-sectional imaging if asymmetry emerges.

RV–PA

• Conduit stenosis (often proximal) → falling sats, rising gradient, RV dilation; early balloon/stent or surgical revision. Increased shunt/PA reintervention burden with RV–PA was noted in single-center and network reports [1,5,6].
• RV dysfunction/arrhythmia → optimize afterload and coronary supply; rhythm monitoring; minimize ventriculotomy and use low-profile patches.
• Endocarditis risk → prophylaxis and vigilance.

Technical notes that shape physiology

• Size selection matters: 3.5 vs 4.0 mm (mBTS) and 5 vs 6 mm (RV–PA) materially alter Qp; bigger is not always better.
• Geometry: gentle curves without kinks; short, ringed RV–PA graft; mBTS distal anastomosis oriented to avoid LPA distortion.
• Antithrombotic strategy: heparin early then aspirin ± additional agents per institutional risk stratification.
• Pre-Stage II catheterization insights: In the SVR cohort, RV–PA was associated with smaller mid-branch PA diameters and more severe PA or shunt obstruction, whereas mBTS showed more hemodynamic abnormalities related to diastolic runoff—illustrating that mechanisms and trade-offs truly differ [6].

Take-home comparison (one-glance)

• mBTS: continuous Ao→PA flow; ↓ aortic DBP → potential coronary steal; no ventriculotomy; often greater dependence on SVR management; good PA growth when geometry is favorable.
• RV–PA: systolic RV→PA flow; preserves DBP → better coronary reserve; ventriculotomy-related risks and conduit stenosis burden; often steadier systemic perfusion early; more catheter/surgical reinterventions during interstage [1,5–7].

References

[1] Ohye RG, Sleeper LA, Mahony L, Newburger JW, Pearson GD, Lu M, et al. Comparison of shunt types in the Norwood procedure for single-ventricle lesions. N Engl J Med. 2010;362(21):1980-1992.

[2] Bradley SM, Simsic JM, McQuinn TC, Habib DM, Shirali GS, Atz AM. Hemodynamic status after the Norwood procedure: a comparison of right ventricle-to-pulmonary artery connection versus modified Blalock-Taussig shunt. Ann Thorac Surg. 2004;78(3):933-941.

[3] Ghanayem NS, Jaquiss RDB, Cava JR, Frommelt PC, Mussatto KA, Hoffman GM, Tweddell JS. Right ventricle-to-pulmonary artery conduit versus Blalock-Taussig shunt: a hemodynamic comparison. Ann Thorac Surg. 2006;82(5):1603-1609.

[4] Edwards L, Morris KP, Siddiqui A, Harrington D, Barron D, Brawn W. Norwood procedure for hypoplastic left heart syndrome: BT shunt or RV-PA conduit? Arch Dis Child Fetal Neonatal Ed. 2007;92(3):F210-F214.

[5] Tabbutt S, Dominguez TE, Ravishankar C, Marino BS, Gruber PJ, Wernovsky G, et al. Outcomes after the stage I reconstruction comparing the right ventricular to pulmonary artery conduit with the modified Blalock-Taussig shunt. Ann Thorac Surg. 2005;80(5):1582-1591.

[6] Aiyagari R, Rhodes JF, Shrader P, Radtke WA, Bandisode VM, Bergersen L, et al. Impact of pre-stage II hemodynamics and pulmonary artery anatomy on 12-month outcomes in the Pediatric Heart Network Single Ventricle Reconstruction trial. J Thorac Cardiovasc Surg. 2014;148(4):1467-1474.

[7] Loomba RS, Shah PH, Chandrasekar S. Short-term outcome comparison of Norwood procedures with right ventricle to pulmonary artery conduit versus modified Blalock-Taussig shunt: a meta-analysis. Ann Pediatr Cardiol. 2011;4(2):145-149.

[8] Ballweg JA, Dominguez TE, Ravishankar C, Gaynor JW, Nicolson SC, Spray TL, Tabbutt S. A contemporary comparison of the effect of shunt type in hypoplastic left heart syndrome on the hemodynamics and outcome at Fontan completion. J Thorac Cardiovasc Surg. 2010;140(3):537-544.