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 pressureThe 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 distalaspiration/flushingor 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 bothIndications::

Indications Acute cardiac failure refractory to pharmacologic intervention

Low-output states after CPB

Hypotension and low CI (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 present. 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.CONTRAINDICATIONSThe 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 ruptureUncontrolled 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 unusedin situto 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 offin situexcept when the patient is anticoagulated because of the risk of thrombus formation on the balloon.

DURATION OF USEHemodynamic 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 considereRoutine careThe 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.VascularVascular 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).

Other-Cholesterol 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