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Aspiration of arterial blood during systole with reinfusion during diastole decreased
cardiac work without compromising coronary perfusion Harkin-1960s
Intravascular volume displacement with latex balloons - early 1960s
The Intra-aortic balloon pump (IABP) is a mechanical device that is used to decrease
myocardial oxygen demand, left ventricular systolic work, left ventricular end-diastolic
pressure, and wall tension while at the same time increasing cardiac output. By increasing
cardiac output it also increases coronary blood flow and therefore myocardial oxygen delivery.
The primary goals of IABP treatment are to increase myocardial oxygen supply and
decrease myocardial oxygen demand. Secondary, improvement of cardiac output (CO),
ejection fraction (EF), an increase of coronary perfusion pressure, systemic perfusion and a
decrease of heart rate, systemic vascular resistance occur.
Principles of the IABP
Counterpulsation: A technique that synchronizes the external pumping of blood with the
heart's cycle to assist the circulation and decreasing the work of the heart.
Counterpulsation pumps when the heart is resting to increase blood flow and oxygen to
the heart. Counterpulsation stops pumping when the heart is working to decrease the
heart's workload and lessen oxygen demand.

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Since 1979, a percutaneous placement of the IAB via the femoral artery using a modified
Seldinger technique allows an easy and rapid insertion in the majority of situations. After
puncture of the femoral artery a J-shaped guide wire is inserted to the level of the aortic
arch and then the needle is removed. The arterial puncture side is enlarged with the
successive placement of an 8 to 10,5Fr dilator/sheath combination. Only the dilator needs
to be removed.
Continuing, the balloon is threaded over the guide wire into the descending aorta just
below the left subclavian artery. The sheath is gently pulled back to connect with the
leak-proof cuff on the balloon hub, ideally so that the entire sheath is out of the arterial
lumen to minimize risk of ischemic complications to the distal extremity. Recently
sheathless insertion kits are available. Removal of a percutaneously placed IAB may
either be via surgical removal or closed technique. There are alternative routes for
balloon insertion. In patients with extremely severe peripheral vascular disease or in
pediatric patients the ascending aorta or the aortic arch may be entered for balloon
insertion. Other routes of access include subclavian, axillary or iliac arteries

Correct placement of Intra-Aortic Balloon

It is inserted into the descending aorta via the femoral artery either percutaneously
or by surgical cut-down.

It should be positioned so that the tip is approximately 1 to 2 cm below the origin of the
left subclavian artery and above the renal arteries.

After correct placement of the IAB in the descending aorta with it`s tip at the distal aortic
arch (below the origin of the left subclavian artery) the balloon is connected to a drive console.
The console itself consists of a pressurized gas reservoir, a monitor for ECG and pressure wave
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recording, adjustments for inflation/deflation timing, triggering selection switches and battery
back-up power sources. The gases used for inflation are either helium or carbon dioxide. The
advantage of helium is its lower density and therefore a better rapid diffusion coefficient.
Whereas carbon dioxide has an increased solubility in blood and thereby reduces the potential
consequences of gas embolization following a balloon rupture.
Correct positioning is critical in order to avoid blocking off the subclavian or renal
arteries. So placement if confirmed by flouroscopy or Chest X-ray. The tip should be visible
between 2nd and 3rd intercostal space.
Table 1: Hemodynamic effects of IABP Therapy

Factors Affecting Diastolic Augmentation

1. Patient Hemodynamics
Heart Rate, Stroke Volume, Mean Arterial Pressure, System Vascular Resistance

2. Intra-Aortic Balloon
IAB in Sheath, IAB Position, Kink in IAB Catheter, IAB Leak, Low Helium


Timing, IAB Augmentation Control (Inflation & Deflation)

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It then rapidly inflates immediately following aortic valve closure to augment (To make
(something already developed or well under way) greater, as in size, extent) diastolic
coronary perfusion pressure. When inflated, the balloon blocks 85-90% of the aorta.
Complete occlusion would damage the walls of the aorta, red blood cells, and platelets.
The balloon rapidly deflates just before ventricular systole to reduce the impedance (A
measure of the total opposition to current flow in an alternating current circuit) to left
ventricular ejection
Inflation and deflation are synchronized to the patients cardiac cycle. Inflation at the
onset of diastole results in proximal and distal displacement of blood volume in the aorta.
Deflation occurs just prior to the onset of systole.

Inflation of IABP:
The balloon is inflated during diastole in sync with the closure of the aortic valve.

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The blood in the aortic arch above the level of the balloon is pushed backward providing
increased coronary artery blood flow and increased myocardial oxygen supply.
Inflation of IABP Causes
o Increased coronary perfusion pressure
o Increased systemic perfusion pressure
o Increased O2 supply to both the coronary and peripheral tissue
o Increased baroreceptor response
o Decreased sympathetic stimulation causing decreased Heart Rate, decreased
Systemic Vascular Resistance, and increased Left Ventricular function
Deflation OF IABP
The balloon rapidly deflates just before ventricular systole to reduce Left Ventricular
work helps to decrease afterload.
The space where the balloon was inflated creates an empty space where the blood doesn't
have to flow against any resistance.
Deflation causes
o Deflation creates a "potential space" in the aorta, reducing aortic volume and
o Afterload reduction and therefore a reduction in myocardial oxygen consumption
o Reduction in peak systolic pressure, therefore a reduction in LV work
o Increased Cardiac Output
o Improved ejection fraction (The amount of blood pumped out of a ventricle
during each heart beat. The ejection fraction evaluates how well the heart is
pumping; Normally 50 - 70 percent) and forward flow
Preload is defined as the amount of blood volume or pressure in the left ventricle at the end
of diastole (i.e. the resting phase of the heart). Factors affecting preload include:
Aortic insufficiency
Circulating blood volume
Mitral valve disease

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Some medications (i.e. vasoconstrictors, vasodilators)

Afterload is the resistance that the heart must overcome in order to eject the blood volume
from the left ventricle. Afterload can be affected by:
Aortic valvular stenosis
Arterial vasoconstrictors and vasodilators
Peripheral arterial constriction
Balloon Inflation : Hemodynamics

Inflation of the balloon occurs at the onset of diastole. At the beginning of diastole,
maximum aortic blood volume is available for displacement because the left ventricle has
just finished contracting and is beginning to relax, the aortic valve is closed, and the
blood has not had an opportunity to flow systemically.

The pressure wave that is created by inflation forces blood superiorly into the coronary
arteries.This helps perfuse the heart.

Blood is also forced inferiorly increasing perfusion to distal organs (brain, kidneys,
tissues, etc.)

Benefits of Accurately timed Inflation :

- Coronary artery blood flow and pressure are increased.. Increased perfusion may increase the
oxygen delivered to the myocardium.
- Coronary collateral circulation is potentially increased from the increased CPP (coronary
perfusion pressure)
-Increased diastolic pressure also increases the perfusion to distal organs and tissues.
-Systemic perfusion pressure is increased.
Balloon Deflation : Hemodynamics

The balloon remains inflated throughout diastole.

At the onset of systole, the left ventricle has to generate a pressure greater than the
AEDP (Aortic End Diastolic Pressure) to achieve ejection. But the sudden loss of aortic
pressure caused by the deflation of the balloon reduces this afterload.

The left ventricle does not have to generate as much pressure to achieve ejection since the
blood has been forced from the aorta.
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This lower ejection pressure reduces the amount of work the heart has to do resulting in
lower myocardial oxygen demand.

Benefits of accurately timed Deflation:

The pressure that the LV must generate is less throughout the systolic phase. Therefore,
afterload is reduced which decreases myocardial oxygen demands.
Reduced afterload allows the LV to empty more effectively so SV (stroke volume) is

Enhanced forward CO.

Also decreases the amount of blood shunted from left to right in cases of intraventricular
septal defects.

Physiological Effects of IABP


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Schematic representation of coronary blood flow, aortic and left ventricular pressure wave
form with / without IABP. (Effects on DPTI and TTI . Balloon inflation during diastole
augments diastolic pressure and increases coronary perfusion pressure as well as
improving the relationship between myocardial oxygen supply and demand (DPTI:TTI
To achieve optimal effect of counterpulsation, inflation and deflation need to be correctly
timed to the patients cardiac cycle. This is accomplished by either using the patients ECG
signal, the patients arterial waveform or an intrinsic pump rate. The most common method of
triggering the IAB is from the R wave of the patients ECG signal. Mainly balloon inflation is set
automatically to start in the middle of the T wave and to deflate prior to the ending QRS
complex. Tachyarrhythmias, cardiac pacemaker function and poor ECG signals may cause
difficulties in obtaining synchronization when the ECG mode is used. In such cases the arterial
waveform for triggering may be used.
It is important that the inflation of the IAB occurs at the beginning of diastole, noted on the
dicrotic notch on the arterial waveform. Deflation of the balloon should occur immediately prior
to the arterial upstroke. Balloon synchronization starts usually at a beat ratio of 1:2.

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1. Early Inflation - Inflation of the IAB prior to aortic valve closure

Waveform Characteristics :
Inflation of IAB prior to dicrotic notch.
Diastolic augmentation encroaches onto systole, (may be unable to distinguish).
Physiologic effects:
Potential premature closure of the aortic valve.

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Potential increase in LVEDV and LVEDP.

Increased left ventricular wall stress or afterload.
Aortic regurgitation.
Increased MV02 demand.
2. Late Inflation - Inflation of the IAB markedly after closure of the aortic valve

Waveform Characteristics:

Inflation of IAB after the dicrotic notch.

Absence of sharp V.

Physiologic Effects:
- Sub-optimal coronary artery perfusion
- Sub-optimal diastolic augmentation
3. Early Deflation - Premature deflation of the IAB during the diastolic phase
Waveform Characteristics

Deflation of IAB is seen as a sharp drop following diastolic augmentation.

Sub-optimal diastolic augmentation.

Assisted aortic end diastolic pressure may be <= the unassisted aortic end diastolic

Assisted systolic pressure may rise.

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Physiologic Effects:
- Sub-optimal coronary perfusion
- Potential for retrograde coronary blood flow
- Angina may occur as a result of retrograde

coronary blood flow

- Sub-optimal afterload reduction & Increased MV02 demand.

4. Late Deflation- Late deflation of the IAB during the diastolic phase.

Waveform Characteristics:

Assisted aortic end diastolic pressure may be equal to the unassisted aortic end diastolic
Rate of rise of assisted systole is prolonged.

Diastolic augmentation may appear widened.

Physiologic Effects:
Afterload reduction is essentially absent.
Increased MV02 consumption due to the left ventricle ejecting against a greater resistance
IAB may impede left ventricular ejection and increase the afterload
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1. Refractory Unstable Angina

2. Impending Infarction
3. Acute MI
4. Refractory Ventricular Failure
5. Complications of Acute MI [i.e. acute MR or VSD, or papillary muscle rupture]
6. Cardiogenic Shock
7. Support for diagnostic, percutaneous revascularization, and interventional procedures
8. Ischemia related intractable ventricular arrhythmias
9. Septic Shock
10. Intraoperative pulsatile flow generation
11. Weaning from bypass
12. Cardiac support for non-cardiac surgery
13. Prophylactic support in preparation for cardiac surgery
14. Post surgical myocardial dysfunction/low cardiac output syndrome
15. Myocardial contusion
16. Mechanical bridge to other assist devices
17. Cardiac support following correction of anatomical defects
Medical Indications:
- Cardiogenic shock, Pre-shock syndrome, MI,Unstable Angina,Bridging device to other
mechanical assist, Cardiac support for hemodynamically
challenged patients with
mechanical defects like valvular stenosis or ventricular septal defect.
Surgical Indications:
-Post surgical Myocardial Dysfunction, Cardiac support following correction of
anatomical defects.
Severe aortic insufficiency
Aortic aneurysm
Aortic dissection
Limb ischemia
Aortic dissection
Severe peripheral vascular disease

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Severe calcific aorta-iliac disease or peripheral vascular disease

Sheathless insertion with severe obesity, scarring of the groin, or other contraindications
to percutaneous insertion

Renal failure and bowel ischemia

Neurologic complications including paraplegia
Heparin induced thrombocytopenia
Side Effects and Complications of IABP Therapy
1. Limb Ischemia:
2. Excessive bleeding from insertion site:
3. Balloon leak / IAB rupture:
4. Infection
5. Aortic perforation and/or dissection
6 .Compartment syndromes may develop after IAB removed..

Contractility refers to the velocity and vigor of contraction during systole.

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