Intra-aortic balloon counterpulsation is a method of temporary mechanical circulatory/hemodynamic

support that attempts to create more favorable balance of myocardial oxygen supply and demand
IABP is aimed at achieving haemodynamic stability until a definitive course of treatment or recovery
occurs. By decreasing myocardial work and SVR, intracardiac shunting, mitral regurgitation, or both (if
present) are reduced while coronary perfusion is enhancedThe intra-aortic balloon, by inflating during
diastole, displaces blood volume from the thoracic aorta.
In systole, as the balloon rapidly deflates, this creates a dead space, effectively reducing afterload for
myocardial ejection and improving forward flow from the left ventricle. The net effect is to decrease
systolic aortic pressure by as much as 20% and increase diastolic pressure
The catheter is inserted in most cases through a common femoral artery and advanced under
fluoroscopic guidance such that the distal end is positioned in the proximal descending aorta, usually
about one centimeter distal to the origin of the left subclavian arter (mnimize the risk of cerebral embolism
- - , diastolic augmentation is most efficient the closer the balloon is to the aortic valve) , The caudal end
of the balloon should be positioned above the origin of the renal arteries. Selection of balloon size is
determined by the height of the patient. .
A flexible catheter with one lumen that allows for either distal aspiration/flushing or pressure
monitoring and a second that permits the periodic delivery and removal of helium gas to a closed
balloon. The balloons are manufactured in sizes between 20 and 50 cc.
A mobile console that contains the system for helium transfer as well as computer control of the
inflation and deflation cycle.

Pumping is initiated and controlled by the console using input from both the aortic pressure and the
electrocardiogram. Inflation occurs immediately after aortic valve closure and deflation just before aortic
valve opening

Percutaneous insertion into common femoral artery high in descending thoracic aorta

Inflation is triggered from the R wave on the EKG and occurs during diastole,
immediately following closure of the aortic valve just after dicrotic notch
Balloon deflation occurs during isovolemic contraction (late diastole) just
prior to opening of the aortic valve.

The downward spiral of cardiogenic shock. Myocardial injury leads initially to diastolic dysfunction
resulting in increased left ventricular end-diastolic pressure (LVEDP), LV wall stress, and pulmonary
congestion. The onset of systolic dysfunction sets in motion a cascade of reflex mechanisms and
consequences of low cardiac output that exacerbate myocardial ischemia and myocardial dysfunction
mortality from cardiogenic shock complicating acute myocardial infarction is 50-80%
Cardiogenic shock is diagnosed at the bedside by observing the clinical signs of end-organ hypoperfusion
such as altered mental status, cool and mottled extremities, and oliguria

Expected changes in the hemodynamic profile in the majority of patients with cardiogenic shock include
Renal blood flow can increase up to 25%, secondary to increase in cardiac output. Decrease in urine
output after insertion of IABP should raise the suspicion of juxta-renal balloon positioning.
The haemoglobin levels and the haematocrit often decrease by up to 5% because of haemolysis from
mechanical damage to the red blood cells. Thrombocytopenia can result from mechanical damage to the
platelets, heparin administration, or both

Indications::
Indications
Acute cardiac failure refractory to pharmacologic intervention
Low-output states after CPB
Hypotension and low CI (<1.8) with high wedge pressure (>25 mmHg) despite
pressors
Cardiogenic shock 2/2 myocardial ischemia
Bridge to cardiac transplant
ACC/AHA 2013 class I indiciation- reasonable to use IABP therapy in the setting of acute myocardial
infarction where cardiogenic shock cannot be quickly reversed with pharmacologic therapy (class IIa/IIb
indications, respectively). It is to be used as a temporary stabilizing measure (prior to revascularization if
appropriate).
Severe mitral regurgitation secondary to papillary muscle dysfunction or rupture after myocardial
infarction can lead to significant haemodynamic instability. This can initially be managed by IABP, pending
definitive surgery.
In addition, intraaortic balloon pumping reduces mean systemic impedance and developed systolic
pressure, and causes a 14 percent decline in calculated peak left ventricular wall stress The reductions in
afterload and wall stress lead to a fall in myocardial oxygen consumption, which is one of the goals of
treatment of patients with myocardial ischemia
High-risk PCI we suggest not routinely placing an IABP electively before PCI in high-risk (as defined
in BCIS-1) patients. However, placement of an IABP prior to PCI is potentially of benefit in those patients
who are hemodynamically unstable before the procedure, or those who are judged highly likely to
become unstable during the procedure.
Refractory ventricular arrhythmias with severely impaired left ventricular function and those in
whom the arrhythmia compromises hemodynamic status and for whom the IABP may provide time to
implement appropriate therapy. During IABP support, 18 of the 21 patients showed reduction or
termination of the arrhythmias (IIa.
Unstable angina refractory to dru treatment is an indication for IABP. These patients are at increased risk
of developing acute myocardial infarction and death. By improving the haemodynamic condition of these
patients, IABP can facilitate further percutaneous interventions or bridge the patient to surgery.

Weaning from cardiopulmonary bypass may be difficult in cases where aortic cross-clamping is
prolonged, revascularization is only partially achieved, or pre-existing myocardial dysfunction is prese nt.
Separation from cardiopulmonary bypass may be marked by hypotension and a low cardiac index despite
the administration of inotropic drugs. The use of IABP in this setting decreases LV resistance, increases
cardiac output, and increases coronary and systemic perfusion, facilitating the patient's weaning from
cardiopulmonary bypass.

CONTRAINDICATIONS The following conditions are contraindications to IABP insertion:

Significant (more than mild) aortic regurgitation since the degree of aortic regurgitation will be
increased by counterpulsation -- because it worsens the magnitude of regurgitation.
Aortic dissection or clinically significant aortic aneurysm -- IABP insertion should not be attempted
in case of suspected or known aortic dissection because inadvertent balloon placement in the false
lumen may result in extension of the dissection or even aortic rupture
Uncontrolled sepsis
Uncontrolled bleeding disorder
Severe peripheral artery disease that cannot be pretreated with stenting. precludes insertion

using the concepts of systolic unloading and diastolic augmentation. As a consequence, cardiac output,
ejection fraction, and coronary perfusion are increased, with a concomitant decrease in left ventricular
(LV) wall stress, systemic resistance to LV ejection, and pulmonary capillary wedge pressure.
Inflation of IAB during diastole increases the pressure difference between aorta and left ventricle,
The console is programmed to identify a trigger for balloon inflation and deflation. The most commonly
used triggers are the ECG waveform and the systemic arterial pressure waveform. The balloon inflates
with the onset of diastole, which corresponds with the middle of the T-wave. The balloon deflates at the
onset of LV systole and this corresponds to the peak of the R-wave.
The balloon is set to inflate after the aortic valve closure (which corresponds to the dicrotic notch on the
arterial waveform) and deflate immediately before the opening of the aortic valve (which corresponds to
the point just before the upstroke on the arterial pressure waveform).
As the balloon inflates at the onset of diastole, a sharp and deep 'V' is observed at the dicrotic notch (Fig.
1). Balloon inflation causes augmentation of diastolic pressure and a second peak is observed. This peak
is referred to as diastolic augmentation. Diastolic augmentation is ideally higher than the patient's systolic
pressure except when reduced stroke volume causes a relative decrease in augmentation

. Depending upon the patient's haemodynamic status, the balloon is programmed to assist every beat
(1:1) or less often (1:2, 1:4, or 1:8). With haemodynamic improvement, the device can be 'weaned' to less
frequent cycling before complete removal. However, the device should never be left unused in situ to
prevent thrombosis.
The intra-aortic balloon pump inflates at the dicrotic notch leading to peak-augmented diastolic pressure.
As the balloon deflates, assisted end diastolic pressure is seen to be lower than unassisted end diastolic
pressure, and assisted systolic pressure is lower than unassisted systolic pressure.
To confirm maximal hemodynamic effect from the intra-aortic balloon pump, peak diastolic augmentation
should be greater than the unassisted systolic pressure and both assisted pressures should be less than
the unassisted pressures.
** Notice the increase in diastolic pressure, ** the decrease in peak systolic pressure on the
postassisted beat, and **the decrease in aortic end-diastolic pressure on the assisted beat.
The net effect on myocardial mechanics is to decrease myocardial oxygen consumption, increase cardiac
output, and lower peak left ventricular wall stress.

Weaning from IABP should be considered when the inotropic requirements are minimal, thus allowing
increased inotropic support if needed. Weaning is achieved gradually (over 6-12 h) reducing the ratio of
augmented to non-augmented beats from 1:1 to 1:2 or less and/or decreasing the balloon volume. The
balloon should never be turned off in situ except when the patient is anticoagulated because of the risk of
thrombus formation on the balloon.
DURATION OF USE Hemodynamic support with an intraaortic balloon pump (IABP) should be
continued as long as the benefits outweigh the risks. It should be removed as soon as the patient
stabilizes or sooner for complications. The risk of complications increases with the duration of
implantation.
i.

When the etiology of hemodynamic compromise necessitating mechanical support is thought to

be transient, periodic weaning trials can help determine optimal timing of IABP removal. In cases
where the indication is not expected to reverse without a definitive intervention (eg,
revascularization), the IABP can remain in place for as long as needed to bridge the patient to
that definitive procedure. Meticulous care of the catheter, as well as close monitoring of distal
circulation for vascular compromise, are necessary. When prolonged need for IABP support is
expected (eg, >10 to 14 days), insertion via axillary approach (preferably using graft conduit)
should be considere

Routine care The following routine care measures likely decrease complication rates:

A chest x-ray should be obtained after initial insertion and daily to document the position of the
catheter tip, which should be at the level of bifurcation of left and right main bronchi
Documentation of the distal pulses should occur before, after, and three times every day.
The pressure wave form should be evaluated by a practitioner knowledgeable with the use of the
system twice daily.
Daily measurement of the hematocrit, platelet count, and creatinine.
Anticoagulation.

COMPLICATIONS The in-hospital mortality was 21 percent, one-half of which occurred while the IABP
was in place. IABP-related mortality was only 0.5 percent.
Vascular Vascular complications (occurring in six to 25 percent of cases) remain the major risk
associated with intraaortic balloon pumping . The most common major complications include:
Limb (and visceral) ischemia
Vascular laceration necessitating surgical repair
Major hemorrhage
It is important that the IABP be inserted into the common femoral artery rather than one of its branches
(eg, the superficial or profunda femoral artery). Neither of the branches is generally large enough to
permit insertion without producing arterial obstruction and limb ischemia.
Arterial dissection is most often due to improper advancement of the guidewire with subsequent insertion
of the IABP into a false lumen. The balloon may function normally in this position. Dissection may be
diagnosed by ultrasonography and requires immediate balloon removal.
Less common vascular complications, due to IABP compromise of perfusion, include spinal cord ischemia
and visceral ischemia (including renal ischemia).
OtherCholesterol embolization is an infrequent occurrence that may result in limb loss -This complication
should be suspected in patients with thrombocytopenia, livedo reticularis, eosinophilia, and, with
renal atheroemboli, eosinophils in the urine sediment. Chronic anticoagulation may be detrimental in
this setting, promoting further embolization ..IABP should be removed in the presence of diagnosed
or suspected cholesterol embolization
Cerebrovascular accident is a rare complication of IABP, since the balloon is normally positioned
distal to the left subclavian artery. Cerebral ischemia only occurs when the IABP has been placed
too proximally or has accidentally migrated proximally, or the central balloon lumen has been flushed
vigorously and dislodged a thrombus.
Sepsis is uncommon unless counterpulsation continues for more than seven days. This
observation suggests that infections can be minimized by meticulous attention to sterile technique,
analogous to the care given to parenteral nutrition
Balloon rupture is an uncommon event, and is generally related to the balloon pumping against a
calcified plaque

Additional complications include a fall in platelet count, hemolysis, seromas, groin infection, and
peripheral neuropathy.
The higher complication rate in women is most likely related to the size of the iliac and femoral arteries.
Patients with diabetes and hypertension suffer more vascular complications due to an increased
incidence of peripheral arterial disease.
--------------A) Late inflation, -- long after closure of aortic valve, leading to inefficient diastolic pressure augmentation
and diminished coronary perfusion. This is rectified by setting balloon inflation to immediately after the
dicrotic notch

(B) early inflation, -- ) occurs prior to aortic valve closure. Impedes on systole -- The net
hemodynamic effect is an increase in left ventricular end-diastolic pressure (LVEDP), volume (LVEDV),
and wall stress, resulting in increased myocardial oxygen demand. This is rectified by setting balloon
inflation to occur immediately after the dicrotic notch.
(C) late deflation - below) leads to LV ejection against increased afterload, raising LV wall stress and
myocardial oxygen consumption. Adjustment of deflation to before the onset of systole prevents
counterpulsation from becoming counterproductive.
(D) early deflation. -- leads to submaximal diastolic augmentation and afterload reduction. Delay of
balloon deflation to just before the onset of systole will improve the quality of hemodynamic support from
counterpulsation