This is a three part series- “IABP 101” designed to simply refresh or introduce the basic concepts of applying diastolic augmentation for the high risk cardiac patient. Again, some of the concepts here will seem to be fairly rudimentary for a seasoned perfusionist, but if it’s your first day in a perfusion program- then elementary reverts to elemental- as in a prerequisite foundation for any training program delivered to perfusionists.
This pdf file can be found by clicking here: www.icufaqs.org/IABPFAQ.doc
Have an excellent day!
What is an intra-aortic balloon pump?
An intra-aortic balloon pump is a device that basically does two good things for a heart in trouble. These two effects correspond to the two movements that the balloon makes, namely: inflation and deflation. The balloon itself looks like a wire coat-hanger with a transparent plastic hotdog on the end, which inflates and deflates in careful timing with certain parts of the cardiac cycle of systole and diastole. The balloon is inserted into the femoral artery, threaded up, and the tip is placed so that it sits just below the aortic arch – this is usually done in the cath lab under fluoro, but can be done at the bedside in an emergency.
The balloon is “driven” to inflate and deflate by this device, the console. The helium does the inflation lives in a small (very small) tank, and the timing of the movements is controlled in careful synch with the rate and rhythm of the heart. It has to be VERY precise, for reasons we’ll get into.
Why is an IABP inserted?
Two reasons: first, to help perfuse the coronary arteries, when they are nearly closed by tight lesions. If you try to visualize the cardiac cycle, think of the heart during diastole: the chamber walls open up, and on the left side of the heart, the valve leading from the LV to the aorta – the aortic valve – flips shut. The aorta has just been filled by the previous systolic contraction, and now with the aortic valve closed, it rebounds a little, like a garden hose with a pulse of water going through it – the walls stretch a bit with each systole, and then spring back a bit, creating a small backwards pressure towards the heart. The openings leading to the coronary arteries are actually in the wall of the aorta, just above the aortic valve, and the arteries fill passively during diastole. The balloon is timed to inflate at the end of diastole, creating a forcible pressure backwards along the aortic arch, pushing blood actively through the coronary arteries.
The second reason is for the management of acute cardiogenic shock. This is what the deflation movement does.
What is diastolic augmentation?
Inflation of the balloon during diastole increases coronary perfusion pressure which is normally derived from the end-diastolic aortic root pressure.
How much volume does the balloon hold?
The balloon itself can hold different volumes, 34cc, 40cc, and 50cc.
Why do they use helium?
“The advantage of helium is its lower density and therefore a better rapid diffusion coefficient.” What I think this means is that helium, being very light, and not very dense, is easier to push and pull in and out of the balloon through the line tubing. I’m not sure what happens if the helium gets into the patient – I remember being told that it’s physiologically inert – maybe the patient talks funny?
NB: Balloon Tech Gary says that the “rapid diffusion coefficient” means that the helium will dissolve very quickly in the blood if the balloon were to leak some into the circulation. Hopefully not a whole lot of helium: if the balloon were to rupture, a bolus of helium would act just like any other gas/air embolus in the circulation – for any sign of balloon rupture (like blood in the balloon line), the console must be shut down immediately, and the balloon removed.
What are tight lesions?
Tight lesions are the narrow spots along the lumens of the coronary arteries that make for all the trouble – if they’re nearly closed, say >95%, then the patient may develop spontaneous angina (“unstable angina”).
What is stable angina? Unstable angina?
Stable angina is the ischemic chest pain that a patient gets early in the development of their coronary lesions – they get the pain under stable, predictable conditions, like climbing a flight of stairs. Unstable angina is the pain the patients get as the coronary lesions get tighter. This angina can strike spontaneously, without any exertion, and represents worsening CAD.
What is LMNOP?
LMNOP are the initials that some people use to remember the maneuvers to make for cardiac ischemia: Lasix (assuming they’re “wet”), Morphine, Nitrates, Oxygen, and Position (sit them up if they’re short of breath – unless they’re hypotensive!). If LMNOP doesn’t work, then you have to think about putting in a balloon pump to forcibly perfuse the coronaries.
How do I know if the balloon is working?
You know that the balloon is working if the patient’s chest pain goes away! You also want to look at their EKG to see if their ischemic changes, if any, have resolved – remember, some diabetic patients, and we see lots of them – don’t have chest pain with ischemia, so you have to be careful. There are “anginal equivalents” – meaning, the patient becomes ischemic, but instead of having pain, does something else – breaks into a sweat maybe, becomes short of breath…
What if the balloon goes in, and they’re still having symptoms?
If the ischemia isn’t controlled with IABP insertion, they probably need to go for an emergent CABG or stent procedure, since something is probably about to infarct.
What are V-waves? Why do they come and go?
V-waves are a sign of ischemia – they can show up as part of a PCW waveform, and in this context it means that the patient has developed “ischemic MR” – mitral regurgitation. The idea is that the ischemia has affected the papillary muscles that control the mitral valve.
They’ve stopped working properly, and the valve starts leaking. You can use the presence of V-waves as an indicator that the patient is still in ischemic trouble – sometimes this is useful if a patient is intubated and can’t tell you they’re having pain, or in people who don’t have pain, like diabetics with neuropathy sometimes. The goal would be the same as treating someone with ischemic changes on their 12-lead – you want to see the v-waves go away. Look for the oxygenation to worsen with v-waves, since the valve is letting blood flow backwards towards the lungs – look for it to improve once the valve is working again.
What is cardiogenic shock?
“Cardiogenic” means that the shock state is being caused by heart failure: the pump isn’t pumping. Why not?
Remember that there are three parts of a blood pressure, and the common kinds of shock are caused by bad things happening to one of those: pump, volume, and arterial squeeze. Which one is this?
What is afterload?
Afterload is the resistance that the heart is looking at, as it tries to pump blood out into the entire arterial system.
(Preload is the volume arriving in the LV, measured as the wedge pressure. What number would tell you the preload of the RV?)
Remember that the arterial bed as a whole can squeeze, and loosen. If the arterial squeeze is high, then the heart has a harder time pushing blood into the tight vessels – so looser is better! Not too loose! Afterload corresponds to the SVR number – normal is around 1000, septic would be low, and cardiogenic would be high. Remember – high is tight, low is loose.
SVR rises in cardiogenic shock, the arteries tighten, trying to keep blood pressure up… is this a good thing?
What is afterload reduction?
Since a high afterload makes it harder for the LV to empty itself, it adds to the work that the failing heart has to do – bad! So the goal is to lower the afterload – to dilate the arterial “bed” – to lower the SVR. You can do this with drugs, like NTG or nipride, but if the patient has a systolic pressure of 90 – probably not a good idea!
So now comes the IABP. The balloon, deflating just at the beginning of systole, creates an area of lower pressure in the aorta – which helps the LV empty itself, and takes a lot of the workload off it – mechanical afterload reduction. Almost everyone with cardiogenic shock died of it before the IABP came along for this purpose.
Why can’t we just use pressors?
Well – you could, and sometimes you have to, even with the balloon pump working. But do you really want to add a pressor to failing heart muscle? Probably not – you want to avoid things that make the heart work harder, things that increase “MV02” – myocardial oxygen consumption. Dobutamine – the beta pressor – would be the drug of choice. You sure you want to use it?
What about the other pressors? Remember, the alpha receptors are in the arteries, and pressor-izing the arteries in this situation would be bad – it increases afterload resistance, and those arteries are probably already quite tightened up – that’s the reflex response the body uses to try to maintain blood pressure if cardiac output falls. These people already have bad peripheral perfusion – they’re so tight that they may not have detectable pulses – add an alpha pressor and they might lose their fingers!
Now – see? This is the mirror, the opposite of the reflex response that the body uses to compensate in sepsis, in which the patient has a loose arterial bed, and the compensation is really elevated cardiac output. SVR in sepsis would be… high or low? Low – correct. See that? Two reflex responses available for two different situations.
So – what might happen if the balloon insertion went “dirty”?
How can I tell if the balloon is working?
Simple: if the balloon goes in for chest pain/ischemia, you look for the patient’s pain and EKG changes to go away. Those nasty v-waves should go away too, if they were there before, and MR going away should improve oxygenation quickly. “Un-flash”…
If the balloon goes in for cardiogenic shock, then blood pressure should improve as the cardiac output comes up. The SVR should come down, and you should be able to wean some on the dobutamine.
What should happen to the urine output, and the wedge pressure?
The PCW should go down for two reasons – the balloon should improve the blood supply to a hurting LV and help it pump better – empty itself better. Afterload reduction from deflation should help PCW go down because of the mechanical advantage the balloon gives to the LV. With better cardiac output, urine output should improve – remember that somebody needs to check the X-ray to make sure the the tip of the balloon is in the right position – too low and it can obstruct the renal arteries, which tends to be bad for the kidneys.
How do I know if the patient is balloon dependent?
“Balloon dependent” describes a patient who is cardiogenic, and whose heart depends on the mechanical assistance from the IABP to keep blood pressure up. Pause the IABP – their BP falls. This patient is obviously not ready to wean from the balloon yet. A patient with a big MI producing cardiogenic shock may recover enough function in about a week’s time to wean.
How is a balloon inserted? Who does the procedure?
An IABP is inserted by an interventional cardiologist, usually in the cath lab under fluoroscopy, using much the same technique as any central line placement. Very rarely the balloon is put in at the bedside, but this is usually in a near-code situation – it’s been many years since I’ve seen this done. Careful placement is needed to avoid placing the balloon too high or low, and the patient must have an x-ray to confirm proper placement of the balloon tip. This can be read by the balloon techs, but has to be confirmed by a knowledgeable doc.
What is balloon timing?
Timing is everything in life, and the IABP is no exception. If you think about it even for a moment, you’ll realize that if the balloon is still inflated in the aorta, when the heart is trying to pump blood into that aorta – well, that would be a bad thing. So the timing of both inflation and deflation must be carefully looked after.
Why does the balloon inflate at the dicrotic notch?
The balloon is supposed to inflate towards the end of diastole. So – the walls of the heart open up, the chambers fill, and the aortic valve flips shut. It turns out that the anatomical openings – the ostea – leading to the coronary arteries are in the wall of the aorta, just above the valve, and at the end of diastole the aorta rebounds a little bit, and the coronaries perfuse – passively. Now, if your ischemic patient needed more than just passive perfusion – what could you do? Inflate the balloon. How do you know when to inflate? It turns out that the dicrotic notch, coming at the end of diastole, indicates exactly the event we want – the closure of the aortic valve. Once the valve is closed, the balloon inflates, and blood is forcibly pushed backwards along the aortic arch, and into the coronary arteries under pressure, improving perfusion.
Why do we use the arterial wave for timing?
Simple: we use the arterial wave to look for the dicrotic notch, to use as the marker for inflating the balloon. Use the inflation knob to move the inflation wave leftwards, until it meets the dicrotic notch.
But there’s also the “balloon pressure waveform”. What’s that for?
The arterial wave comes from the patient, so it doesn’t tell you anything about the balloon itself. The balloon pressure wave tells you if the balloon is inflating or deflating properly. Usually in my experience if the balloon is timing well and producing a good-looking waveform, then the balloon waveform is taking care of itself.
What is diastolic augmentation?
Remember that the balloon inflates at the end of diastole, just after the aortic valve closes – the rapid inflation is what augments the perfusion of the coronary arteries through the ostea. This rapid inflation can produce a pressure wave that’s actually higher than the patient’s systolic pressure, and that high pressure wave is referred to as diastolic augmentation. That’s the high waveform in the middle of the three peaks.
How does inflation help?
Inflation helps by forcibly perfusing the coronary arteries, instead of letting them be perfused passively. Look at the “PDP” point in the diagram below – that’s the pressure perfusing the coronaries generated by the inflation of the balloon. A lot of pressure! This is often enough to control angina/ischemia along with ischemic symptoms, and can stabilize an ischemic patient until they can go to either the cath lab or the OR.
Deflation Timing: What is the “point of isovolumic contraction”?
This refers to the point in the cardiac cycle when the chambers have filled with blood at the end of diastole – the chamber walls are building up pressure to start systolic contraction, and this is the point at which the heart is working the hardest.
What is “myocardial stroke work”?
Myocardial stroke work is the effort that the heart puts out with each systolic contraction. In cardiogenic shock, the pump is having a hard time pumping – so stroke work is something you want to try to reduce – which is exactly what balloon deflation does.
How does deflation help?
Rapid deflation of the balloon creates an area of lowered pressure in the aorta just ahead of the emptying left ventricle. Sort of like suction. The suction helps empty the ventricle with each beat, and takes some of the workload off of the cardiogenic heart. Almost everyone with cardiogenic shock died before the invention of the IABP because there was no way to assist the failing LV – now the survival numbers are pretty good.
The two big bad timing errors are early inflation and late deflation.
What is early inflation?
Early inflation is just that – the inflation knob is turned too far to the left, and the inflation wave actually comes before the dicrotic notch. To the left of it. This means that the balloon is inflating before the aortic valve closes, pumping backwards into the LV, which is already having a hard time emptying itself…
What is late deflation?
Late deflation is when the balloon remains inflated too long – the heart is trying now to pump against an inflated balloon. The deflation knob has been turned too far to the right – move it back towards the center.
What if the patient codes?
There is a mode called “internal 80” built into most of the consoles that allows the balloon to inflate and deflate “blindly” at a rate of 80 bpm, and possibly generate some blood pressure. In the current Datascope 300cs- this rate can be adjusted down to a rate of 50 BPM?
This mode has occasionally (and incorrectly) been called “a pacing mode” so if you hear a cardiologist asking for it- just clarify with them as to what it is they truly want. Clearly if you are doing CPR- they are asking for anything that will generate some sort of Q or CO.
When should we start weaning the balloon? What is “stunned myocardium”?
It depends on why the balloon went in. Remember that there are two main reasons for an IABP – to help keep tight lesions open in the coronary arteries (inflation), or to help a failing LV in cardiogenic shock (deflation). The first reason includes ballooning a patient for just a day or two after stent placement, after which hopefully they’d tolerate a rapid wean and removal. In that situation, anticoagulation is really of critical importance – do you want to be the one that let the patient clot off her brand new stents?
The second situation is more difficult, but hopefully somewhat predictable. The idea is that a heart that’s been hit by cardiogenic shock will need a certain amount of time to recover. What is there to recover? It turns out that around the area of infarct (you don’t have acute cardiogenic shock without a big infarct) is an area that is still alive, still ready to pump, but dazed, or as they say “stunned”. This area of “stunned myocardium” will eventually come back to work, but not for a given period of time, usually about a week. So the person who may have an EF of 12% right after an enormous MI may have a much better EF a week later, after the stunned areas come back and start to work. The goal of ballooning this patient is to get them through that period of time, with the balloon functioning as an LVAD – a left-ventricular assist-device.
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www.rxlist.com (a very useful site for finding pharmaceutical info)
https://critcare.lhsc.on.ca – the website of the London (Ontario) Health Sciences Centre, Critical Care Division
www.ispub.com/journals/IJTCVS/Vol2N2/iabp.html – The Internet Journal of Thoracic and Cardiovascular Surgery
www.cardio-info.com/_disc6/0000007e.htm the Johns Hopkins protocol cited in the CV Talk Educators and Professionals Discussion Group
www.datascope.com/ca/abstract_1.html “Vascular Complications from Intraaortic Balloons: Risk Analysis
www.datascope.com/ca/pdf/preinservice_self_study_guide.pdf “Pre-Inservice Self-Study Guide To Intra-Aortic Balloon Counterpulsation.