This issue has come up in the exam: Question 22 from the first paper of 2006, "Outline the indications for and the potential complications of Intra-Aortic Balloon Pump (IABP) insertion." The changing landscape of critical care literature offers some guidance for the use of IABP in the critically ill patient. I will separate the indications for IABP into three groups, on the basis of the existing evidence. This brief point-form summary offers a shortcut to answering that question without getting bogged down in an analysis of the literature supporting the use of this practice.
No choice but pump
- Failure to come off bypass
- Severe ischaemic mitral regurgitation or ventricular septal defect
with haemodynamic compromise, while waiting for repair
Probably harmless, but probably not useful
- High risk CABG patients (pre-op)
- High-risk PCI patients (pre-op)
- Cardiogenic shock while waiting for PCI
- Pulmonary oedema in spite of maximal medical management
- Takotsubo cardiomyopathy
- Neurogenic stress cardiomyopathy of subarachnoid haemorrhage
- Severe aortic stenosis
And of course, the main caveat is reversibility. The pump is a bridge. If there is nothing on the other shore, there is no need for a bridge. Additionally, to somewhat modify the cavalier statement above, there is never "no choice but pump", as that category could be easily renamed into "why not VA ECMO instead".
The time-poor exam candidate can safely stop reading here, as what follows is an extensive and rambling digression on the evidence behind the indications for IABP insertion. It is unclear that the college would ever expect anything further than the list of indications mentioned here. Judging by their brief model answer to Question 22, only a short point-form list of indications was expected.
Some patients fail to come off bypass. As circulation is restored, cardiac output remains low and coronary circulation is thus sub-optimal. These patients are effectively in cardiogenic shock. Historically, the poor coronary perfusion in these patients has been treated with IABP. Does it work? Hard to say. The mortality in this group has always been high; owing probably to the fact that their failure to wean from bypass is probably due to some sort of crippling cardiac disease. It is difficult to identify the IABP as an effective rescue measure, because frequently no rescue measure is effective and the patient dies anyway. One specific (small) study describes the experience of 26 patients all of whom failed to successfully separate from bypass post-CABG; of these 88% separated successfully after the IABP was inserted. Licker et al (2012) describes it as a "first line measure", quoting very old studies and pointing to the fact that historically it has been the third most common indication for IABP insertion in large cohort studies. Of course, there is still the open argument regarding this: why not just leave them on bypass and wait? Failure to wean from bypass is one of the applications of VA ECMO, and is discussed elsewhere.
For cardiogenic shock and such, we have great huge trials like the IABP-SHOCK II. But for the management of a uselessly flapping prolapsed mitral valve, or for infarct-related ventricular septal defect - for this we need to dip into the foggy past. In 1973, a group of investigators published on the use of IABP to stabilise the acutely broken patient with sudden onset of severe MR or VSD. The haemodynamic improvement was of secondary outcome measures, and there were only 11 patients enrolled. In spite of these defects, the physiological benefits remained enticing. IABP continued its use among this patient group in the ensuing decades. In 2013, another study (this one somewhat larger) had supported this practice. Among the IABP-treated patients, those who seemed to enjoy an improvement in survival were those who were in cardiogenic shock. And most of the improvement seemed to be in reducing pre-operative mortality. In short, in patients with acute ischaemia-associated mitral valve incompetence or ventricular septal defect, the IABP can be used to keep the patient alive while the surgeons wash their hands.
Ray Raper, in his chapter from Ohs Manual, discusses the use of IABP in the CABG patient. His Table 22.2 lists the indications for IABP use, for which the evidence was valid at the time of writing.
For the perioperative CABG patient, any two of the following features would qualify one for an IABP in the early 21st century:
If you score an IABP preoperatively, it is done immediately before knife goes to skin. Generally, the patient is already sedated for the procedure when the device is inserted. Apparently, only 1 hr of pre-op counterpulsation is enough. Question is, enough for what? The data regarding whether this intervention is useful or not is quite conflicting.
The initial studies of this intervention in "high risk" CABG patients had revealed a trend towards improvement. However, the Cochrane meta-analysis of their pooled data confirms that all trials were sponsored by Datascope (a balloon pump manufacturer) and the majority had the same author. This, from the viewpoint of bias, is upsetting.
These are the trials which have supported Raper's recommendations. Jan T Christenson tested the IABP in unstable angina, 70% left main stenosis, low (<35%) LVEF and re-do of the CABG. The results were positive. Sufficiently positive for the AHA/ACC to make their 2011 recommendations on the basis (it seems) of mainly Christenson data. Presumably, this also supported the listed indications in Oh's Manual.
However, Christenson et al appear to have been enrolling sicker patients into their studies, with some proportion of them being in the middle of an acute coronary syndrome. How, then, could you call this population "prophylactic"- surely the IABP was beneficial as a therapeutic measure in those who were actively infarcting? Trials which enrolled "truly" elective high-risk CABG patients have been less supportive of the practice. For instance, Ranucci et al (2013) of 110 elective high risk patient found no mortality benefit; in fact the steering committee killed the trial early because of futility. These were people with LVEF less than 35% but not in cardiogenic shock. None of the studied variables were different in the IABP group, suggesting it does nothing to improve perioperative morbidity for these people, and prompting for the authors to call for the practice to be abandoned "given the possible complications of intra-aortic balloon pump insertion, and the additional cost of the procedure". Similarly, Ferreira et al (2018) did not find any benefit. Results like these resulted in the downgrading of the recommendation, to the point where the ECS/ESC doesn't even mention preemptive IABP.
Massaging the data statistically can give rise to the impression that preemptive pre-CABG IABP is a good idea. For example Zangrillo (2015) and Rampersad (2017) performed meta-analysis (n = 625 and 1261) which favoured pre-emptive IABP. Depending on the reader's bias, this could be interpreted as ironclad evidence or as a demonstration of the limitations of meta-analysis as a tool of EBM.
A thoughtful reflection the meaning of these data (Townsley, 2018) suggests that at the time of writing the matter is far from settled. People like Gatti et al (2016) are publishing their experience (almost 20 years!) of putting in pre-op IABPs and confessing that their practice seems to have been driven by "a generic perception of improved immediate results" rather than any actual evidence for benefit. Landoni et al (2017) collected consensus opinions from a group of over 400 experts, and the best they could do is suggest that it "might" reduce mortality.
In summary, when posed with the question, "what are the indications for IABP", what should the Part II exam candidate write? Probably something about pre-operative CABG. The last time this was asked was in Question 22 from the first paper of 2006, when things seemed a lot more straightforward, i.e. the college examiners included pre-op CABG in their answer. There is clearly some support for this practice among them. It also does not hurt to know that the President of the College wrote "IABC has an established role in support of cardiac surgery" in his chapter for Oh's Manual (p. 302). Still if this comes up again, the savvy candidate will recognise that, like Landoni's group of 400 experts, the CICM examiners are a heterogeneous group who - if, say, trapped in an elevator and forced to come to a consensus on this issue - would not come to an agreement any stronger than "might reduce mortality". Thus, one would have mention this indication in the "probably harmless, but possibly not useful" category. To justify the "probably harmless" element one may fall back on IABP-SHOCK II data, which found no significant difference between groups in terms of harmful complications (re-infarction 3% vs. 1.3%, ischaemic complications 4.3% vs. 3.4%, bleeding: 3.3% vs. 4.4%, sepsis 15.7% vs. 20.5%).
Evidence for the use of IABP in MI and cardiogenic shock is sufficiently controversial that it has merited its own chapter. In brief, a 1994 trial published in Circulation had suggested that IABP use might improve coronary artery patency after a stent has been inserted. However, all the evidence in support of IABP use in AMI has been on the basis of studies which were performed on small groups of patients in the era before aggressive antiplatelet therapy. Subsequent investigations have failed to replicate this benefit. Overall, the use of IABP in high-risk PCI patients cannot be recommended, unless they are hemodynamically unstable, or they are having ongoing angina which is unresponsive to medical management. In short at this stage it seemed as if IABP in AMI may benefit some patients with ongoing angina, as bridging support while waiting for PCI, but AHA and ESC don't recommend it's routine use for all STEMI patients.
Cardiogenic shock is the territory of the IABP-SHOCK II trial. Their 30-day mortality was not reduced in their IABP group, suggesting that the IABP is not very useful in this setting. To be fair, their control group did enjoy a high rate of LVAD insertion, which some might view as cheating. However, this depressing result is consistent with the summed data from all previous studies. Again, the non-randomised (and smaller) studies were all positive, but as the quality of evidence improved, so did the observed benefit decrease. Furthermore, the studies which demonstrated a benefit all seemed to come from the thrombolysis and balloon angioplasty era. For the modern day (of drug-eluting stents), there is no convincing evidence that IABP improves mortality in post-AMI, post-PCI patients with cardiogenic shock. The 2013 revision of the AHA guidelines for STEMI still says that it "can be useful" in this setting, favouring it with a "Class IIa" recommendation.
Essentially, this indication is for decompensated heart failure in the setting of recent ischaemia. It is a frequently seen complication of a large infarct - the downtrodden myocardium struggles post-stent (or pre) and the patient suffers from pulmonary oedema which has all sorts of untoward effects, not the least of which is increased respiratory effort (with an associated increase in demand on the myocardium) and decreased oxygenation (requiring an increase in cardiac output to maintain DO2). The IABP can relieve this temporarily, by decreasing afterload. Early IABP experiments had demonstrated a decrease in PA wedge pressure.
In 2004, the AHA treated the IABP in these situations with a lukewarm "Class IIb" recommendation; according to that document, "it may be reasonable" to use the IABP in this setting. No mention of IABP for this indication exists in the 2013 guidelines - presumably this category is lumped together with cardiogenic shock.
Various authors have reported on the use of IABP in circumstances outside of the conventional.
A case report (and review of similar literature) suggests that in SAH patients with cardiogenic shock, the IABP is a useful adjunct. Without fulltext access, one can only guess how the patients were anticoagulated (or perhaps, not at all).
Because inotropes and catecholamine vasopressors are contraindicated in Takotsubo cardiomyopathy, the authors of one review conclude that the IABP "may be the preferred treatment strategy" in those patients who end up with significant haemodynamic collapse.
It is also counterintuitive to think of this as a strong indication for IABP, because surely the fixed obstruction to flow is the main limiting factor? In fact is afterload reduction not a bad thing in AS? Critical valve stenosis patients were actually excluded from the first SHOCK trial because of this concern. However, the subsequent UNLOAD study by Khot et al (2003) demonstrated that afterload reduction actually helps, and is safe in AS (they were using nitroprusside). There is unfortunately also only weak and fragile evidence for the IABP in this setting, and one could not call this a "hard indication" with a straight face.
For example, Aksay et al (2011) produces a case series from the Cleveland clinic where they put pumps into patients with severe AS who presented in cardiogenic shock (they put pumps into everybody, but the 35 severe AS patients were of specific interest in this study). Cardiogenic shock by itself may be an indication for IABP (the controversy surrounding this is discussed in more detail above), but in this instance the complicating factor of severe AS makes the whole thing more somewhat different from a perioperative point of view (the mortality being in the realms of 70%). Only 9 of these 35 patients had a concomitant acute coronary syndrome, i.e. these people had cardiogenic shock as defined mainly by cardiac output measurements (mean CI was 1.77), all due to their critically narrowed valves (mean area, 0.6 cm2).
It seems the real benefit of IABP in these scenarios is the fact that it allows the haemodynamically unstable patient to stabilise for long enough to undergo valve surgery safely. This seems to have a positive effect on their mortality - instead of around 70% dead, 91% of the Cleveland patients survived. This is certainly because of the AVR - among the IABP patients who were treated medically, all but 1 died. It is unclear what would have happened if all the unstable patients underwent AVR anyway, without the pump. The authors attributed the main advantage from IABP in AS to the slightly increased cardiac output it offers (CI increased by 0.6 on average, which does not seem like much even though it was a 33% improvement). There is probably some haemodynamic benefit from pushing extra blood into the coronaries in diastole, as the LVH associated with AS tends to produce subendocardial ischaemia in absence of good diastolic coronary flow. By increasing subendocardial blood flow, the IABP effectively permits the monstrously huge LV to contract even harder, improving cardiac output in spite of persistent AS.