Obviously, having a helium-filled balloon in one's aorta is not a consequence-free experience.
The following is an incomplete list of all the various reasons one might not want to shove one of these things into the patient, and all the things that might go wrong if one fails to heed the warnings.
Here is a summary of the meat and potatoes in this chapter:
Mild limb ischaemia - 2.9%
Balloon leak - 1.0%
Major limb ischaemia - 0.9%
Haemorrhage - 0.8%
Leg amputation due to ischaemia - 0.1%
Atheromatous cholesterol emboli
Aortic or arterial dissection
Now, to the detail.
First, the hard contraindications.
Essentially, if your aortic valve is incompetent, the diastolic balloon inflation will (instead of nourishing the coronary circulation) send a jet of blood though the aortic valve back into the left ventricle, increasing the preload. The valve was already doing this in diastole (hence the diastolic murmur)- but now the counterpulsation actually augments the regurgitation.
However, some intensivists from Barcelona did it anyway. In their case, which is quite unique, the aortic valve was regurgitant because of decreased diastolic pressure (the patient was so shocked that their valve never closed fully). The consequence of IABP counterpulsation in their case report was actually a resolution of regurgitation.
The presence of an aortic dissection would make one think twice about inserting a balloon pump. Even if the balloon somehow fails to actually touch the flap, its pulsations will send more blood into the false lumen, expanding the dissection. Any clots forming inside it will be battered around and potentially expelled into the systemic circulation. In short, its not a good idea.
For the IABP, a large aneurysm is both a mechanical inconvenience and a source of embolic complications. remember that the diastolic augmentation relies considerably on the elastic recoil of the aorta. If the aorta has "springy" walls, they will recoil in response to balloon inflation, and increase the diastolic pressure, driving blood into the aortic root and into the coronary arteries.
What use, then, is a balloon pump in an aorta which has uselessly flaccid walls? The diastolic augmentation will be very poor.
Furthermore, an aneurysm is seldom empty. Typically, there is a mass of clot sitting inside it. One need expend very little effort to imagine the consequences of inserting a balloon into such a clot, and turning it on.
There are several reasons as to why one may wish to withhold the IABP from the septic patient. Firstly, the bacteria in the bloodstream hardly need another surface to deposit upon, and more hardware means more surfaces. But more importantly, septic shock results in an unworkably flaccid circulation, with loss of arterial elastic recoil. Again, diastolic augmentation will be frustrated.
I will not dwell too long on the obvious folly of accessing a major artery in somebody who has no way to form a clot. Even if you manage to get it in without massive haemorrhage, what are you going to do when its time to remove it?
In the patients who clot normally, however, the risk of haemorrhagic complications is about 0.8%
There are two aspects to this. Firstly, if one has a patient with femoral arteries that are made of wood and formed like corkscrews, one will have a devil of a time trying to advance one's guidewire, let alone the relatively rigid balloon catheter. Not only will you dislodge showers of cholesterol emboli; a dissection is much more likely, and there will be more hemorrhagic complications from the multiple attempts to access the vessel.
Peripheral vascular disease is not merely an access problem. Lets say you somehow managed to shove the IABP into such unworkable vessels. Now, you have you 7.5Fr catheter occupying a certain diameter of the femoral artery. In a patient with peripheral vascular disease, that diameter will be much more narrow than you would normally expect. Your IABP catheter may actually occlude more than 50% of the vessel lumen, and that would be bad if the leg was already hanging on by a thread. With greatly diminished flow, limb ischaemia would become more likely. Cold pale toes will alert you to the possibility that you have sacrificed the limb.
The patterns of bloodflow in a dynamically obstructing left ventricular outflow tract create a gradient between the LV chamber and the aorta. In systole, the LVOT will be obstructed more readily if there is a lower aortic end-diastolic pressure. Indeed, a higher afterload keeps the LVOT open for longer; thus anything that keeps the afterload low will result in a more rapid obstruction of the LVOT, and a worsening hemodynamic picture.
Indeed, the IABP may even induce LVOT obstruction where there formerly was none.
Whether or not you actually need anticoagulation is a whole other topic; but local policy may dictate your movements here. For instance, some centers may demand a therapeutic APTT (50-90) whereas others may prescribe a fixed heparin dose (15000 units over 24 hrs) and others may rely only on the effect of the elephant loading doses of platelet aggregation inhibitors you give people before they have their angiogram and stent.
In either case, most would agree that somebody with uncontrolled bleeding should not be anticoagulated. If the local trend is to anticoagulate the IABP patient, this move will be counterproductive to the progress of their subarachnoid haemorrhage or retroperitoneal hematoma.
Now, to look at the softer contraindications and the complications.
A large-scale review from 2001 has sifted through almost 17000 IABP experiences. They found that this very invasive procedure has a reasonably low complication rate, roughly 2.6%.
There are situations when IABP insertion is impossible because the arteries are hideously corkscrewed, and/or caked in thick calcified deposits. An attempt to insert a large-bore catheter through such unworkable plumbing can send showers of cholesterol-rich debris into the brain, the spine, and generally any damn where. And you might not notice this immediately.
This is not unique to the arterially challenged, although it obviously happens more frequently among these people. But, even though most of the people who require IABP counterpulsation will have some sort of atheromatous disease, this complication is reasonably uncommon.
So, now you got your balloon pump lodged in some atheromatous plaque, lifting up the intima in the descending aorta, and you are not aware that it has happened. And what do you do then? Naturally, you turn it on. Counterpulsation ensues, but the waveform looks weird, your augmentation is all wrong, and the balloon waveform looks abnormal in some non-specific way. You fiddle, you change its position, re-zero the transducers. All the while, the helium balloon is jackhammering at the atheroma, dissecting the aortic wall and expanding the intra-plaque haemorrhage. An embarrassing phone call to the cardiothoracic surgeon is typically the consequence.
In addition to embolic complications, there is a real chance that the jagged calcified barnacles on the aortic wall will shred the helium balloon membrane on its way up. This is far from ideal. Not only will the abovementioned barnacles likely dislodge and sail disgracefully into the systemic circulation, infarcting everything. Bits of balloon could also embolise. And then, you turn it on.
Helium is sent under considerable pressure directly into the descending aorta. If the machine senses a loss of helium pressure, it rapidly withdraws all helium, and shuts down; however some gas inevitably escapes into the systemic circulation, and this is not ideal.
Some degree of balloon leak seems to happen in about 1% of patients. Actual clinically significant helium embolism is much less common. A discussion of gas embolism is carried out in a chapter by the same name, in the Trauma section.
Thankfully, this is a very rare complication in this day and age. However, when it does happen, it is typically fatal, or at least extremely unpleasant. Given that bubbles rise, the natural direction for the gas is up - into the brain, or into the splanchnic circulation. In case you are wondering, experience with treating adventurous idiots suggests that hyperbaric oxygen is the most effective management strategy.
Naturally, the placement of an IABP catheter occupies some of the femoral arterial lumen, and this results in some decrease in blood flow to the leg. How significant this is depends on how poor the blood flow was to begin with.
Lets say that leg was already somewhat compromised, its perfusion borderline - then, any impediment to femoral blood flow will result in limb ischaemia.
This is present in the literature. About 2.9% of patients with IABP end up having some decrease in limb pulses; however, only 0.9% actually have to have the catheter removed because the limb is seriously threatened; and only 0.1% lose the limb because it is irreparably trashed.