Intra-Aortic Balloon Counterpulsation
Authors, Journal, Affiliations, Type, DOI
- Jeffrey C. Trost, L. David Hillis
- American Journal of Cardiology 2006;97:1391–1398
- Johns Hopkins University School of Medicine (Trost); University of Texas Southwestern Medical School (Hillis)
- Review article
- DOI: https://doi.org/10.1016/j.amjcard.2005.11.070
Overview
This pre-IABP-SHOCK II era review provides the definitive operational reference for IABP — covering device history, mechanics, timing, hemodynamic effects, indications, contraindications, and complications. It presents the Benchmark Registry as the largest complication dataset (n=16,909) and synthesises pre-2006 clinical evidence across cardiogenic shock, mechanical MI complications, intractable arrhythmias, and high-risk revascularization. The NRMI-2 analysis foreshadows the IABP-SHOCK II finding: IABP benefited thrombolysis-era patients but showed no survival benefit in the primary PCI era. Coronary blood flow augmentation is shown to be mechanistically inconsistent and absent distal to severe fixed stenoses.
Keywords
Intra-aortic balloon pump, counterpulsation, cardiogenic shock, hemodynamics, coronary blood flow, timing, complications, contraindications, ventricular septal rupture, high-risk PCI, CABG
Key Takeaways
History
- Concept of "counterpulsation" (blood displaced out of phase with cardiac cycle) first described experimentally by Adrian and Arthur Kantrowitz in 1952
- Harken proposed extracorporeal pump principle in 1958; first tested in animals 1962
- Moulopoulos et al developed intra-aortic device (catheter-mounted balloon) in 1962
- Kantrowitz et al (1968): first clinical IABP in 2 patients with cardiogenic shock — hemodynamic improvement in both; only 1 survived to hospital discharge
- Early balloons inserted via femoral arterial cutdown; Bregman et al (1980) described percutaneous insertion — now the standard technique
Device Construction and Insertion
- Double-lumen 8–9.5 Fr catheter; 25–50 mL polyethylene balloon at distal end
- Balloon sizing by patient height: <5 ft → 25 mL; 5–5'4" → 34 mL; 5'4"–6' → 40 mL; >6' → 50 mL
- Balloon diameter when expanded must not exceed 80–90% of descending thoracic aorta diameter
- Percutaneous femoral artery insertion via introducer sheath using over-the-wire technique; brachial artery also possible
- Surgical approaches (transthoracic, translumbar, iliac, subclavian, axillary) available but associated with higher periprocedural mortality than percutaneous
- Tip positioned 2–3 cm distal to origin of left subclavian artery (at level of carina), usually under fluoroscopic guidance
- Inner lumen: monitors systemic arterial pressure; outer lumen: delivers helium from console to balloon
- Helium used as inflation gas — low density facilitates rapid transmission; complete expansion confirmed fluoroscopically
Triggering and Timing
- ECG trigger: R wave peak = beginning of LV systole → balloon deflates; onset of diastole (middle of T wave) → balloon inflates; poor ECG quality/AF may produce inconsistent triggering
- Arterial pressure waveform trigger: inflate after aortic valve closure (dicrotic notch); deflate immediately before aortic valve opening (just before systolic upstroke)
- Cycling: 1:1 (maximum support), 1:2 (baseline for hemodynamic assessment), 1:4, 1:8 (weaning); IABP initially set at 1:2 to compare assisted vs unassisted beats
Timing Errors and Hemodynamic Consequences
| Error | Mechanism | Consequence |
|---|---|---|
| Early inflation (before aortic valve closure) | LV forced to eject against inflated balloon | ↑ LV afterload, ↑ myocardial O2 demand, worsening systolic function |
| Late inflation (well after diastole onset) | Delayed diastolic augmentation | Reduced coronary/diastolic perfusion benefit |
| Early deflation (before end of diastole) | Shortens augmentation period; transient pressure drop | Risk of retrograde flow from carotid/coronary arteries → cerebral/myocardial ischemia |
| Late deflation (after end of diastole) | Balloon still inflated at systole onset | Same as early inflation: ↑ LV afterload, ↑ O2 demand, worsening systolic function |
- Optimal waveform: peak diastolic augmentation > unassisted systolic pressure; both assisted end-diastolic and assisted systolic pressures < unassisted values
- Waveform should be examined at least daily by trained personnel
Concomitant Medications
- Unfractionated heparin standard therapy: target aPTT 50–70 seconds; however one RCT (n=153) showed no difference in limb ischemia rates with vs without heparin
- Non-functioning balloon must be removed within 30 minutes (thrombosis risk; deflated balloon in non-heparinized animals thromboses within 20 minutes)
- Balloon rupture → immediate heparin discontinuation + prompt IABP removal
- Elective removal: discontinue heparin ≥2 hours before; cycle at minimum 1:8 during interval to prevent stasis/thrombosis
- After IABP removal: patient immobile for ≥6 hours; extubation planning — remove IABP first while patient still sedated
Hematologic Effects
- Hemoglobin and hematocrit decrease modestly: mechanical hemolysis + access site bleeding (−2.3 g/dL vs −1.5 g/dL in non-IABP MI patients; P<0.05)
- Thrombocytopenia: mechanical platelet destruction and/or heparin-induced thrombocytopenia
- Monitor: daily hemoglobin/hematocrit, platelet count, and serum creatinine
Hemodynamic Effects — Systemic Pressure and LV Performance
- IABP hemodynamic effects depend on: (1) balloon volume, (2) heart rate, (3) aortic compliance
- Higher HR = shorter diastolic filling time = less augmentation per unit time
- Higher aortic compliance (lower SVR) = attenuated diastolic augmentation magnitude
- Hypotensive patients: IABP increases MAP (diastolic augmentation exceeds systolic decrease)
- Normotensive patients: little/no MAP change (maintained by circulatory autoregulation)
- CS/severe HF: IABP reduces systolic pressure ("unloads" failing heart); reduces LV wall tension and O2 demand; secondary preload reduction (LA/LVEDP); increases SV and CO
Hemodynamic Effects — Coronary Arterial Blood Flow
- Mechanism: diastolic aortic pressure augmentation should increase coronary flow (most coronary flow occurs in diastole)
- Evidence is conflicting: multiple studies show increase, several show no change or decrease — varies by patient hemodynamics, species, and measurement method
- Impaired autoregulation: IABP may augment coronary flow in patients with profound hypotension where autoregulation is overwhelmed
- Normal autoregulation range (perfusion pressure 45–125 mmHg): coronary flow is pressure-independent; IABP provides little benefit
- Fixed severe stenosis (>90% luminal narrowing): IABP-induced diastolic pressure increase is NOT transmitted to poststenotic segment → no poststenotic coronary flow benefit
Indications
Cardiogenic shock (~20% of all IABP insertions):
- SHOCK Trial Registry: IABP + thrombolysis 47% mortality vs IABP alone 52% vs thrombolysis alone 63% vs neither 77% (P<0.0001); confounded by higher revascularization rates in IABP group
- GUSTO-1 retrospective (n=310 CS): early IABP 1-year mortality 57% vs 67% without IABP (P=0.04); confounded — IABP group received more inotropes, pacing, ventilation, revascularization; major bleeding 47% vs 12%
- NRMI-2 (n=23,180 AMI-CS): IABP + thrombolysis 49% vs 67% without IABP (P<0.001 — benefit); but IABP + primary PCI 45% vs 47% (P=NS — no benefit) — key finding foreshadowing IABP-SHOCK II
- Hemodynamic improvement common but unclear survival benefit without concomitant revascularization
VSR or papillary muscle rupture with MR (~5% of IABP use):
- Small observational studies: hemodynamic and clinical improvement; one study showed improvement in intracardiac shunting, systemic pressure, and PAWP
Intractable ventricular arrhythmias:
- Fotopoulos et al (n=21 medically refractory VA): 18/21 showed reduction or abolition of arrhythmias with IABP — mechanistic basis likely improved coronary perfusion reducing ischemic trigger
Post-MI angina / unstable angina refractory to medical therapy (~12% of IABP use):
- Symptomatic and ECG improvement in small observational series
Refractory HF: IABP used as temporary bridge to cardiac transplantation only
High-risk PCI:
- No randomized data for pre-procedural prophylactic IABP in high-risk catheterization/PCI
- Routine post-PCI IABP after primary PCI in high-risk AMI (n=437 RCT): NOT indicated — no difference in death, reinfarction, or reocclusion
High-risk CABG (ongoing ischemia, decompensated HF, hemodynamic instability):
- Two nonrandomized series (n=251): lower in-hospital mortality with preoperative IABP
- Single RCT (n=52; ≥2 risk features): preoperative IABP → shorter CPB time, shorter postoperative IABP, higher cardiac index, shorter ICU stay, lower mortality (6% vs 25%; P<0.05)
- Routine IABP NOT recommended for left main CAD without ischemia, or poor LV function without overt HF
Septic shock: no human data; conflicting animal data
Contraindications
- Absolute: aortic regurgitation (worsens regurgitation); suspected/known aortic dissection (false lumen risk → extension/rupture); sizable abdominal aortic aneurysm (rupture risk)
- Relative: severe peripheral vascular disease uncorrectable by angioplasty/surgery; bilateral femoral-popliteal bypass grafts (contraindication to percutaneous femoral insertion); uncontrolled septicemia; bleeding diathesis
- Note: aortobifemoral bypass grafts are generally acceptable for percutaneous femoral IABP
Complications (Benchmark Registry; n=16,909)
- Any complication: 7%
- Major complications: 2.6%
- Major bleeding: 0.8%
- Limb-threatening ischemia: 0.9%
- Limb amputation: 0.1%
- IABP-related death: 0.05% (usually from aortic dissection/rupture)
- Additional: infection, balloon rupture, inadequate inflation/augmentation, hemolysis, thrombocytopenia
Predictors of major complications (multivariate):
- Age >75 years
- Peripheral vascular disease
- Diabetes mellitus
- Female gender
- Small body surface area (<1.65 m²)
Limitations of the Document
- Review article with no original RCT data
- Published 2006 — predates IABP-SHOCK II (2013), which definitively showed no 30-day or 6-year mortality benefit in AMI-CS
- Clinical evidence base is largely observational/retrospective with significant confounding by indication
- NRMI-2 and GUSTO-1 data subject to selection bias; non-randomized IABP assignment
- Benchmark Registry major complication rate (2.6%) substantially lower than later systematic reviews — likely reflects registry bias toward experienced centers and under-reporting
Key Concepts Mentioned
- concepts/IABP — device mechanics, hemodynamics, indications, contraindications, complications
- concepts/Temporary-Mechanical-Circulatory-Support — IABP as the foundational tMCS device
- concepts/Cardiogenic-Shock — IABP historical use and evidence in AMI-CS
Key Entities Mentioned
- None requiring new entity pages
Wiki Pages Updated
- Created: wiki/sources/iabp-ajc-2006.md
- Created: wiki/concepts/IABP.md
- Updated: wiki/concepts/Temporary-Mechanical-Circulatory-Support.md (source_count 5→6)
- Updated: wiki/sourceindex.md
- Updated: wiki/wikiindex.md