The September 2017 SAQ featured a question on the balloon pump, with marks mostly for knowing the indications/contraindications, complications and physiological rationale for the device.
It reappeared in the September 2020 CRQ with a 71% pass rate. The examiners commended candidates' knowledge in view of "relatively limited exposure" to the device, though lamented poor understanding of the applied physiology.
The IABP reared its head again in March 2023, with a paltry 44% pass rate. The exam report decries poor candidate understanding of the physiology despite the device's "relatively common" use. Quite why trainee exposure to the IABP should have gone from limited to common in 3yrs I don't know...
The definitive resource is Deranged Physiology's remarkable ten-section tour de force on the device, taken from their CICU page, though LITFL's one-pager is perhaps more manageable.
The intra-aortic balloon pump (IABP) is mechanical circulatory support device which utilises a counter-pulsation mechanism
Device
The device is typically a 7.5Fr cathether with a sausage-shaped balloon (25 - 50ml volume) at the distal end
The cathether is plumbed into an arterial line transducer
The balloon is connected to a source of Helium gas via a console, which contains a pump for balloon inflation/deflation
The balloon inflates/deflates in sequence with the cardiac cycle
When fully inflated, the balloon fills 80 - 90% of the thoracic aortic volume
Not uncomfortable; can't feel the balloon inflating/deflating
Positioning
Inserted via the femoral artery using a Seldinger technique by an interventional cardiologist
Appropriate position in the descending thoracic aorta can be confirmed by:
Pressure transducer confirming arterial position
Fluoroscopy-guided insertion (or CXR): tip just above level of left main bronchus or 2nd - 3rd intercostal space
TOE: tip 1 - 2cm distal to origin of the left subclavian artery
Measure length of insertion: from insertion point to umbilicus + distance from umbilicus to sternal angle [crude]
The distal end of the balloon should lie superior to the renal arteries
Timing of balloon inflation/deflation
The balloon inflates in LV diastole
This occurs ∽40ms before the dicrotic notch (i.e. mid-T-wave) - the beginning of diastole
The balloon deflates in LV systole
This occurs in time with the peak of the R-wave - the end of diastole
As one might be able to tell, setting this inflation/deflation cycle in time with the ECG is possible
This works in AF, though naturally the R-R interval varies
This works in the presence of misshapen QRS complexes by changing the R-wave sensory to "peak" type i.e. the peak QRS voltage
Other timing methods are possible:
ECG (see above)
Arterial pressure (useful if there is no reliable ECG trace but there is arterial pressure e.g. during CPR/cardiac arrest)
Pacemaker timing (e.g. if ECG monitoring isn't possible or patient has an open chest)
Asynchronous timing (a flat rate of ~80bpm, which may also be useful in asystole)
Anticoagulation
There is conflicting evidence and non-uniform practice with regards to anticoagulation once the device is in situ
Some suggestion that no anticoagulation does not increase the risk of thrombotic complications
Nevertheless, some people will some degree of anticoagulation even if just heparinised saline flushing of the catheter
Weaning
The device is normally set up in a 1:1 ratio i.e. for every cardiac contraction there is a balloon counterpulsation and augmentation
Weaning occurs by reducing this ratio; 1:2 and then 1:3
The balloon, when deflated, is extremely pro-thrombogenic so should not be left in situ deflated; the device should instead be removed
Principles
The overall aim is to improve myocardial oxygen supply/demand and thus LV performance
Oxygen supply
The inflation of the balloon in diastole leads to increased mean aortic diastolic pressure
As CBF = AoDBP - LVEDP, there is increased coronary blood flow and myocardial oxygen supply
The balloon also 'pushes' blood distally, with increased systemic blood flow and therefore better MAP/organ perfusion inc. renal blood flow (approx. 25%)
(I.e. the IABP increased the diastolic pressure-time index [DPTI])
Oxygen demand
The deflation of the balloon in early systole leads to decreased aortic systolic pressure
There is therefore a reduced afterload i.e. the LV has to generate less pressure to ensure forward flow
Isovolumetric contraction is shorter and therefore myocardial oxygen demand is reduced (approx. 30%)
(I.e. the IABP reduces the tension-time index [TTI])
The LV becomes a much happier place, with:
Better stroke volume and therefore increased cardiac index (approx. 25%)
Better coronary blood flow and myocardial oxygen supply/demand balance
Reduced afterload and preload
In all cases the cause of cardiogenic mischief must be reversible
No choice but to use IABP unless VA-ECMO is to hand
Failure to come off cardiopulmonary bypass
Severe ischaemic MR or VSD, awaiting surgery
Evidence base is dubious but probably not harmful
Prior to high-risk CABG or PCI
Those in cardiogenic shock awaiting PCI (no 30-day mortality benefit according to the 2012 IABP-SHOCK II trial)
Post-MI (/PCI)
Pulmonary oedema despite maximal medical management
Experimental
Takotsubo cardiomyopathy
Severe aortic stenosis
Neurogenic stress cardiomyopathy following SAH
As a pseudo-REBOA in massive UGIB
Absolute
Moderate or severe AR
Thoracic aortic aneurysm (either untreated or stented)