Intra-aortic Balloon Pump (IABP)

• IABP is the most commonly used device for mechanical circulatory support

• First placed 1968 in New York at Maimonides Medical Center by Adrian Kantrowitz and colleagues

• Consists of two parts:

  • the intra-aortic balloon itself (IAB), a double lumen catheter 7–8 French size;
  • console containing the controller, pump and helium cylinder

• 3 lumens (previously 2 lumens)

  • Helium gas lumen
    • connected to the balloon and allows balloon inflation
  • Arterial central arterial lumen
    • connects to the tip and allows monitoring of the aortic waveform of the proper augmentation of the arterial pressure.
    • connect to heparin saline line
    • through which we advance the balloon pump into the aorta
    • it takes 0.025 inch wire (or 0.018 inch wire)
      • Does not take take a 0.035 inch wire, i.e. traditional wire we use to advance catheter.
  • Fiberoptic line
    • allows monitoring of the aortic waveform using fiber optic plethysmography technology.
    • Use this line for monitoring the arterial waveform as it is more reliable and more durable
    • If this becomes dysfunctional, then you can connect the arterial line cable if you haven’t, and you can use it to monitor the arterial waveform.

• The outer lumen of the balloon is a gas containing chamber and the inner lumen is open to the aorta and is used for direct arterial pressure monitoring. Helium is less soluble than some other gases (e.g., CO2) and it is also less dense, which reduces travel time along the circuit and allows quick inflation and deflation of the balloon. IABP is usually positioned in the descending thoracic aorta through one of the femoral arteries using the Seldinger technique. (Source)

• An IABP can be implanted via the femoral artery or by means of percutaneous or axillary artery cut-down in a retrograde configuration, allowing for monitored patient ambulation.

• Positioned in the descending aorta below the left subclavian and above the renal arteries.

• Inflates at the beginning of diastole and deflates just at the beginning of systole during the isovolemic contraction.

  • This deflation is the most important aspect of balloon pump as it creates a vacuum that ↓ the afterload on the left ventricle.

• The failing left ventricle is extremely sensitive to afterload (more so than the normal left ventricle) so that the ↓ in afterload will allow an increase in the ejection stroke volume of the LV, and will ↓ oxygen demands.

• Inflation in diastole will improve coronary flow, which mostly occurs in diastole for the left heart, 85% of coronary flow to the left heart occurs in diastole.

• Benefit over the entire cardiac cycle → net benefit is a reduction in LV cardiac work and myocardial oxygen consumption

  • early diastole: inflates to improve coronary arterial perfusion
    • balloon will start to inflate when systole ends, AV closes
  • systole: deflates to provide assistance with afterload reduction

• The IABP inflation occurs at the dicrotic notch. You can see it on the left on the downslope during unassisted systole. When the IABP is on, you will no longer see this dicrotic notch (it fuses it with it).

  • The dicrotic notch corresponds with the end of the T wave (called "end of T inflation")

• The balloon inflates throughout diastole and just as we get isovolemic contraction (corresponds to peak of R wave), the balloon deflates (called "R-wave autodeflation")

• The balloon pump is actually triggered by the EKG → inflates at the end of T and deflates at the peak of R.

  • 📝 Can also be triggered by pressure (I think there are other options, but I’ve only ever used ECG or pressure. Pressure less helpful in end-stage/transplant-listed patients.)

• IABP ↑ cardiac output by ~20%, up to 0.5-1 liter/minute and ↓ LVEDP and PCWP by ~20%. These effects are driven by the ↓ in afterload and facilitation in ↑ stroke volume.

  • More so in severe MR
  • Less so in severely depressed LV with LV Cardiac Power Index (LVCPI) <0.33 W/m2
    • Because the LV must have some intrinsic function to be able to generate some extra stroke volume to fill and replace volume in that vacuum in the aorta. So an extremely depressed ventricle may not be able to generate that extra cardiac output because it does not have a stroke volume reserve.

• The reduction in afterload provided by the IABP ↓ myocardial O2 demands → ↓ myocardial ischemia

• Improved RV hemodynamics

  • IABP support can also improve RV hemodynamics, possibly related to ventricular interdependence. The reduction in LV filling pressures promotes more physiologic interventricular positioning, thereby improving the septal contribution to RV function.
  • believed to augment RV function in those with high right-sided filling pressures by increasing flow (diastolic > systolic) through the right coronary artery.

• IABP inflation in diastole ↑ aortic diastolic pressure. This, in conjunction with & LVEDP…

  • improves the gradient that drives coronary flow (recall, aortic diastolic pressure minus LVEDP is the gradient that drives coronary flow)
  • improves coronary flow in shock/low flow states with non-obstructed coronary arteries or post-PCI.
    • By contrast, Impella generally improves coronary flow more than balloon pump in unobstructed coronary arteries.
  • Does not improve coronary flow across severely stenotic arteries, even in shock
    • If you have a significant flow limiting coronary obstruction, balloon pump does not ↑ coronary flow across that obstruction. It has to be unobstructed or after you do PCI, this is the only time balloon pump will increase your coronary flow.
    • There is one paper that suggests that Impella increase a flow past the coronary stenosis (whereas balloon pump does not)

Counterpulsation: The balloon inflates during diastole and displaces the blood in the aorta, increasing diastolic and mean pressure and thus augmenting coronary perfusion. During systole, the balloon deflates, producing some vacuum effect and therefore reducing the afterload for the left ventricle (LV) and systolic pressure. This results in improved emptying of the heart, and therefore reduction of the wall stress of the heart. Other important hemodynamic effects of IABP include: reduction of the heart rate (by 20%), decrease in the pulmonary capillary wedge pressure (by 20%) and rise in cardiac output (by 0.5 L/min or by 20%). The magnitude of the effects can vary and depends on many factors: the volume of the IABP (bigger balloons, 50cm3, displace more volume, hence are more effective), its optimal position (the tip of the IAB should be located 2 cm caudally to the origin of the left subclavian artery which is easily confirmed by chest X-ray as 2 cm above the tracheal bifurcation, i.e. carina), optimal timing of the inflation/deflation cycle, heart rate and aortic compliance. (Source)

The maximum hemodynamic effect from IABP counterpulsation is achieved when it is set to inflate just after the aortic valve closure (dicrotic notch on the arterial trace) and deflate just before aortic valve opening (upstroke part on the arterial waveform of the next cardiac cycle). (Source)

• Assisted end-diastolic pressure is lower than the unassisted end-diastolic pressure
• Assisted systole will have a lower peak than with unassisted systole
  • started at a lower end-diastolic with assistance
• Peak diastolic pressure is our augmentation pressure
• Modes
  • 1:1 - every beat
    • inflation with every cardiac cycle
  • 1:2 - every other beat
  • 1:3 - every third beat
  • NOTE: the 1:2 and 1:3 modes are not very supportive and should not be used routinely. They are only valuable for weaning and for adjustment of inflation timing.
• Advantages
  • Easy to place and remove
  • Cost effective ($800-$1000)
  • Low complication rate (bleeding, peripheral ischemia, sepsis, CVA)
• Disadvantages
  • When placed femoral, patient is on bedrest
  • Balloon can rupture
  • Infection
  • Device can move - should have daily CXR

Waveforms

• The console will display 3 major waveforms
  • ECG (green)
    • connected to the console via the green port
    • the console will pick up the best EKG leads that shows you the best QRS and the best T
  • Arterial aortic waveform (red, I’ve also seen yellow)
  • Balloon inflation gas waveform (blue)

Improper IABP Timing

Early/late inflation as well as early/late deflation could lead to suboptimal diastolic augmentation and reduced hemodynamic benefits of the IABP. Timing of IABP is important as too early or too late inflation or deflation can in fact worsen cardiac output and increase preload. (Source) (Source)

• Early inflation
  • balloon inflates during late systole, before the aortic valve has closed
  • arterial waveform shows augmentation occurring prior to the dicrotic notch
  • ↑ LVEDP/V, ↑ LV wall stress, ↑ myocardial O2 consumption, ↓ CO
  • ==aortic regurgitation is made worse==
• Late Inflation (“half-ass job”)
  • balloon inflates after closure of the aortic valve
  • arterial waveform shows:
    • diastolic augmentation commencing after the dicrotic notch, i.e. absence of a sharp V at the dicrotic notch
    • reduced diastolic augmentation (compared to optimal timing)
• Early Deflation (“half-ass job”)
  • balloon deflates during late diastole, rather than with onset of systole
  • arterial waveform shows:
    • a pronounced drop in pressure before late diastole
    • assisted aortic end-diastolic pressure may be ≤ unassisted aortic end-diastolic pressure
    • the assisted systolic pressure may increase
  • Augmentation of coronary perfusion and afterload reduction are suboptimal.
  • Also, there is the potential for retrograde coronary (and carotid) blood flow, which may exacerbate angina. Myocardial oxygen demand may increase.
• Late Deflation
  • balloon deflates after systole has begun → still inflated, so obstructs forward flow
  • arterial waveform shows:
    • assisted aortic end-diastolic pressure ≥ unassisted aortic end-diastolic pressure
    • rate of rise of assisted systole is prolonged
    • diastolic augmentation may appear widened
  • Afterload is increased and myocardial oxygen consumption is increased.

Role of IABP in Cardiogenic Shock

• IABP dramatically improves SvO2, CPO and PCWP in decompensated HF-shock (en Uil CA et al, Eurointervention 2019), whereas the hemodynamic effect is limited in MI-shock (ISAR-SHOCK trial), hence the lack of mortality benefit? (IABP-SHOCK II trial)
• Why may this be?
  • HF-shock is much more afterload-sensitive than MI-shock, as the LV is more dilated in HF shock (hence more wall stress, which equals more afterload)
  • HF-shock is more severely vasoconstricted than Ml-shock, where inappropriate vasoplegia may be present
    • The more vasoconstricted you are, the more you get augmentation with that balloon pump
  • More profound hemodynamic compromise in MI shock and less tissue adaptation (↓ ability of tissue O2 extraction)
    • By contrast, in chronic heart failure shock the tissues may have already adapted to ↓ O2 delivery. ∴ you need higher output to achieve the same tissue oxygenation in MI-shock
  • More sinus tachycardia in MI shock→ Less IABP response
    • Sinus tachycardia impedes the ability of the balloon pump to augment
  • Functional moderate or severe MR is frequently seen in HF-shock and is readily ameliorated by IABP.
    • Recall, MR is very responsive to balloon pump.
• No improvement in survival based on studies, IABP-SHOCK II trial being the largest of them
  • ESC recommends against routine use of IABP support for CS
  • ACC/AHA downgraded the use of IABP in patients failing pharmacologic therapy from a class I to IIa indication

Indications

• Acute congestive heart failure exacerbation with hypotension
• MI with ↓ LV function leading to hypotension
• MI with complications causing cardiogenic shock
• Low cardiac output after CABG
• Bridge to definitive treatment in patients with:
  • Intractable angina or myocardial ischemia
    • In these cases, the IABP works similarly to giving the patient nitroglycerin or calcium channel blockers. In the case of cardiac O2 demand, we are improving afterload and indirectly preload. And the advantage of balloon pump in this scenario is that you’re not risking dropping the pressure like with nitroglycerin or CCBs. You are actually improving the blood pressure while reducing myocardial ischemia.
    • It’s also like giving the patient beta blocker → making the heart function better with less oxygen.
    • 👆 This is actually how balloon pump is useful in supporting complex PCI. It helps the LV tolerate more ischemia during our balloon inflations and stent manipulation. And it allows a quick recovery of ischemia soon after you open the occlusion with your balloon. So faster recovery of ischemia and faster recovery of any potential hemodynamic compromise.
  • Refractory heart failure
  • Intractable ventricular arrhythmias
• Prophylaxis or adjunct treatment in high risk PCI

Contraindications

• Moderate to severe Al
• Aortic dissection
• Severe PVD
• Uncontrolled bleeding diathesis
• Uncontrolled sepsis

Anticoagulation with IABP

Per Getinge (IABP manufacturer), heparin drip is optional regardless of inflation setting (1:1 from 1:3) from perspective of Getinge, the IABP manufacturers. They say as long as IABP is not on standby for longer than 30 minutes, you do not need anticoagulation. Limited data but Suchith did find some evidence to support this (here and here)

Trials

IABP-SHOCK II trial

• tl;dr: “In patients with acute MI complicated by cardiogenic shock, there was no difference in 30-day mortality with IABP placement.” (Source)

ISAR-SHOCK trial

• Impella LP 2.5 versus IABP

BCIS-1 Trial

• IABP vs no IABP in patients with low EF undergoing high-risk PCI

Resources