Intra-Aortic Balloon Pump (IABP)

Most recent study for cardiogenic shock showed no benefit (NEJM DOI 10.1056/NEJMoa1208410)


IABP Timing from Yen Chow

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inflation during early diastole increases coronary artery perfusion pressure, increases diastolic BP by 15-30% and increases SBP as well

40 cc is the typical balloon inflation to fill 80-90% of aortic diameter

advance the radioopaque marker to just distal to the takeoff of the left subclavian

never pull a balloon back through the sheath if it has been inflated, even after deflation

hold distal pressure for 2-3 heartbeats, then hold proximal pressure.

ideal timing is for the V to be located at the dichrotic notch

contraindicated in aortic regurgitation, aortic dissection, PDA,  and aortic aneurysm


how to use echo to place iabp

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Principles of Intra-Aortic Balloon Pump Counterpulsation

Murli Krishna, MBBS, FRCA, FFPMRCA; Kai Zacharowski, MD, PhD, FRCA


Cont Edu Anaesth Crit Care & Pain. 2009;9(1):24-28. ©2009 Oxford University Press

Posted 04/02/2009

Abstract and History



Intra-aortic balloon pump (IABP) remains the most widely used circulatory assist device in critically ill patients with

cardiac disease. The National Centre of Health Statistics estimated that IABP was used in 42 000 patients in the USA in

2002. Advances in technology, including percutaneous insertion, smaller diameter catheters, sheathless insertion

techniques, and enhanced automation, have permitted the use of counterpulsation in a variety of settings, with greater

efficacy and safety.



[1] described augmentation of coronary blood flow by retardation of the arterial pressure pulse in animal

models in 1952. In 1958, Harken

[2] suggested the removal of some of the blood volume via the femoral artery during

systole and replacing it rapidly in diastole as a treatment for left ventricular (LV) failure, so called diastolic

augmentation. Four years later, Moulopoulos and colleagues

[3] developed an experimental prototype of an IABP whose

inflation and deflation were timed to the cardiac cycle. In 1968, Kantrowitz

[1] reported improved systemic arterial

pressure and urine output with the use of an IABP in two subjects with cardiogenic shock, one of who survived to

hospital discharge. Percutaneous IABs in sizes 8.5-9.5 French (rather than 15 French used earlier) were introduced in

1979, and shortly after this, Bergman and colleagues

[4] described the first percutaneous insertion of IABP. The first

prefolded IAB was developed in 1986.

Basic Principles of Counterpulsation

Counterpulsation is a term that describes balloon inflation in diastole and deflation in early systole. Balloon inflation

causes ‘volume displacement’ of blood within the aorta, both proximally and distally. This leads to a potential increase in

coronary blood flow and potential improvements in systemic perfusion by augmentation of the intrinsic ‘Windkessel

effect’, whereby potential energy stored in the aortic root during systole is converted to kinetic energy with the elastic

recoil of the aortic root.

Physiological Effects of IABP Therapy

The primary goal of IABP treatment is to improve the ventricular performance of the failing heart by facilitating an

increase in myocardial oxygen supply and a decrease in myocardial oxygen demand. The overall haemodynamic effects

of IABP therapy are summarized in

Table 1 . Although these effects are predominately associated with enhancement of

LV performance, IABP may also have favourable effects on right ventricular (RV) function by complex mechanisms

including accentuation of RV myocardial blood flow, unloading the left ventricle causing reduction in left atrial and

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pulmonary vascular pressures and RV afterload.

[5] IABP inflates at the onset of diastole, thereby increasing diastolic

pressure and deflates just before systole, thus reducing LV afterload. The magnitude of these effects depends upon:

Balloon volume

: the amount of blood displaced is proportional i. to the volume of the balloon.

Heart rate

: LV and aortic diastolic filling times are inversely proportional to heart rate; shorter diastolic time

produces lesser balloon augmentation per unit time.


Aortic compliance

: as aortic compliance increases (or SVR decreases), the magnitude of diastolic augmentation



Myocardial Oxygen Supply and Demand

Inflation of IAB during diastole increases the pressure difference between aorta and left ventricle, the so-called diastolic

pressure time index (DPTI). The haemodynamic consequence of this is an increase in coronary blood flow and,

therefore, myocardial oxygen supply. Myocardial oxygen demand is directly related to the area under the LV systolic

pressure curve, termed as tension time index (TTI). Balloon deflation during systole causes a reduction in the LV

afterload, thereby decreasing TTI. Thus, the ratio of oxygen supply (DPTI) to oxygen demand (TTI), known as the

endocardial viability ratio (EVR), should increase if the IABP is working optimally. This can be evidenced by a decrease

in coronary sinus lactate.

Coronary Perfusion

According to the Hagen Poiseuille principle, flow through a tube is directly proportional to the pressure difference across

it and the fourth power of the radius while being inversely proportional to the length of the tube and the viscosity of fluid

flowing through it. Hence, in patients with severe coronary artery disease in whom autoregulation is perceived to be

absent, coronary blood flow is directly related to diastolic perfusion pressure. Therefore, IABP should theoretically

improve coronary flow in these patients.

Renal Function

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.

Haematological Effects

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.



Over the years, indications for the use of IABP have developed in clinical practice and are summarized along with

contraindications in

Table 2 .

Acute Myocardial Infarction

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 enhanced.

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.

Ventricular Arrhythmias

IABP is also effective in stabilizing patients with refractory ventricular ectopy after myocardial infarction by increasing

the coronary perfusion pressure, reducing ischaemia and trans-myocardial wall stress, and maintaining adequate

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systemic perfusion.

Cardiogenic Shock

This is life-threatening complication of acute myocardial infarction, is characterized by low cardiac output, hypotension

unresponsive to fluid administration, elevated filling pressures and tissue hypoperfusion leading to oliguria,

hyperlactaemia, and altered mental status. IABP therapy is considered to be a class I indication (ACC/AHA guidelines)

for the management of cardiogenic shock not rapidly reversed by pharmacological therapy.


Unstable Angina

Unstable angina refractory to drug 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.

Refractory Ventricular Failure

IABP has a role in managing patients with refractory ventricular failure outside the setting of acute myocardial infarction,

such as those with cardiomyopathy or severe myocardial damage associated with viral myocarditis. This can aid the

progression to more definitive treatments such as ventricular assist device or cardiac transplantation.

Cardiac Surgery

IABP is used for stabilization of patients with acute myocardial infarction referred for urgent cardiac surgery. IABP

support is often initiated in the cardiac catheterization laboratory and continued through the perioperative period.

Elective placement is considered in high-risk patients such as those with significant left main stem disease, severe LV

dysfunction (ejection fraction <30%), congestive heart failure, cardiomyopathy, chronic renal failure, or cerebrovascular

disease. 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.


The contraindications to IABP are summarized in

Table 2 . It is contraindicated in patients with aortic regurgitation

because it worsens the magnitude of regurgitation. 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. Similarly, aortic rupture can occur if IABP is inserted in patients with sizable abdominal

aortic aneurysms. Patients with end-stage cardiac disease should not be considered for IABP unless as a bridge to

ventricular assist device or cardiac transplantation.

IABP device placement should be avoided in patients with severe peripheral vascular disease. Percutaneous femoral

IABP device insertion is contraindicated in the presence of bilateral femoral-popliteal bypass grafts. Uncontrolled sepsis

and bleeding diathesis are relative contraindications to the placement of IABP device.

Technique of Insertion and Operation

The IABP device has two major components: (i) a double-lumen 8.0-9.5 French catheter with a 25-50 ml balloon

attached at its distal end; and (ii) a console with a pump to drive the balloon. The balloon is made of polyethylene and is

inflated with gas driven by the pump. Helium is often used because its low density facilitates rapid transfer of gas from

console to the balloon. It is also easily absorbed into the blood stream in case of rupture of the balloon.

Before insertion, the appropriate balloon size is selected on the basis of the patient’s height (as supplied by Datascope,

for a patient <152 cm in height, a balloon volume of 25 cc is appropriate; for height between 152 and 163 cm, balloon

volume 34 cc; for height 164-183 cm, balloon volume 40 cc, and for height >183 cm, balloon volume 50 cc). Smaller

balloons are available for paediatric use. The diameter of the balloon, when fully expanded, should not exceed 80-90%

of the diameter of the patient’s descending thoracic aorta.

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The IABP catheter is inserted percutaneously into the femoral artery through an introducer sheath using the modified

Seldinger technique. Alternative routes of access include subclavian, axillary, brachial, or iliac arteries. The catheter can

also be inserted surgically using a transthoracic or translumbar approach, but this is associated with an increased

periprocedural mortality.

[8] Once vascular access is obtained, the balloon catheter is inserted and advanced, usually

under fluoroscopic guidance, into the descending thoracic aorta, with its tip

∼2 to 3 cm distal to the origin of the left

subclavian artery (at the level of the carina). Intraoperatively, balloon placement can be ascertained using

transoesophageal echocardiography.

The outer lumen of the catheter is used for delivery of gas to the balloon and the inner lumen can be used for monitoring

systemic arterial pressure. Complications associated with IABP are summarized in

Table 3 .

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. Poor ECG quality, electrical interference, and cardiac arrhythmias can result in erratic balloon


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). IABP timing refers to inflation and deflation of the IAB in relation to the

cardiac cycle. The cardiac cycle is monitored by continuous display of 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


Figure 1.

One complete cardiac cycle and the corresponding waveform of the IABP during inflation and deflation.

Principles of Intra-Aortic Balloon Pump Counterpulsation

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Reproduced with permission from Datascope®

Suboptimal timing of inflation and deflation of the balloon will result in haemodynamic instability (Fig. 2A-D): Examples of

this include:

Early inflation

: inflation of the IAB before aortic i. valve closure (Fig. 2A).


Late inflation: inflation of the IAB markedly after closure of the aortic valve (Fig. 2B).


Early deflation: premature deflation of the IAB during the diastolic phase (Fig. 2C).


Late deflation: deflation of the IAB after the onset of systole (Fig. 2D).

Figure 2.


Waveform characteristics: inflation of IAB before dicrotic notch; diastolic augmentation encroaches

onto systole, may be unable to distinguish.

Physiological effects: potential premature closure of the aortic

valve; potential increase in LVEDV and LVEDP or PCWP; increased LV wall stress or afterload; aortic

regurgitation; increased MVO

2 demand. (B) Waveform characteristics: inflation of IAB after the dicrotic

notch; absence of sharp ‘V’.

Physiological effects: suboptimal coronary artery perfusion. (C) Waveform


: deflation of IAB is seen as a sharp decrease after diastolic augmentation; suboptimal

diastolic augmentation; assisted aortic end-diastolic pressure may be equal to or less than the unassisted

aortic end-diastolic pressure; assisted systolic pressure may increase.

Physiological effects: suboptimal

coronary perfusion; potential for retrograde coronary and carotid blood flow; suboptimal afterload

reduction; increased MVO

2 demand. (D) Waveform characteristics: assisted aortic end-diastolic pressure

may be equal to the unassisted aortic end-diastolic pressure; rate of increase of assisted systole is

prolonged; diastolic augmentation may appear widened.

Physiological effects: afterload reduction is

essentially absent; increased MVO

2 consumption because of the left ventricle ejecting against a greater

resistance and a prolonged isovolumetric contraction phase; IAB may impede LV ejection and increase

the afterload. Reproduced with permission from Datascope®

Principles of Intra-Aortic Balloon Pump Counterpulsation

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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


in situ except when the patient is anticoagulated because of the risk of thrombus formation on the balloon.

Patient care should be carried out with three primary goals in mind:

evaluation in terms of haemodynamic status, systemic perfusion, i. and relief of cardiac symptoms;

observation for early signs of complications including limb ischaemia, balloon malpositioning, thrombus formation,

bleeding, and infection;


iii. ensuring proper functioning of IABP, including correct timing, consistent triggering, and troubleshooting of alarms.

Table 1. Summary of Haemodynamic Effects of IABP Therapy


↓systolic pressure, ↑diastolic pressure

Left ventricle

↓systolic pressure, ↓end-diastolic pressure, ↓volume, ↓wall tension


↓afterload, ↓preload, ↑cardiac output

Blood flow

↑→ coronary blood flow

Table 2. Indications and Contraindications for the Use of IABP Therapy


Acute myocardial infarction Refractory LV failure

Cardiogenic shock Refractory ventricular arrhythmias

Acute MR and VSD Cardiomyopathies

Catheterization and angioplasty Sepsis


Refractory unstable angina Infants and children with complex cardiac



Cardiac surgery

Weaning from cardiopulmonary bypass


Absolute Relative

Aortic regurgitation Uncontrolled sepsis

Aortic dissection Abdominal aortic aneurysm

Chronic end-stage heart disease with no anticipation of



Aortic stents Severe peripheral vascular disease

Major arterial reconstruction surgery

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Table 3. Complications Associated with IABP

Transient loss of peripheral pulse

Limb ischaemia


Compartment syndrome


Aortic dissection

Local vascular injury—false aneurysm, haematoma, bleeding from the wound


Balloon rupture (can cause gas embolus)

Balloon entrapment

Haematological changes, for example thrombocytopenia, haemolysis

Malpositioning causing cerebral or renal compromise

Cardiac tamponade


Kantrowitz A. Experimental augmentation of coronary flow by retardation of the arterial pressure pulse. Surgery

(1953) 34:678-87.


Harken DE. The surgical treatment of acquired valvular disease. Circulation 2. (1958) 18:1-6.

Moulopoulos SD, Topaz SR, Kolff WJ. Extracorporeal assistance to the circulation and intraaortic balloon

pumping. Trans Am Soc Artif Intern Organs (1962) 8:85-9.


Bergman HE, Casarella WJ. Percutaneous intra-aortic balloon pumping: initial clinical experience. Ann Thorac

Surg (1980) 29:153-5.


Miller RD. Miller’s anaesthesia. In: Anesthesia for Cardiac Surgery—Nyhan D, Johns RA, eds. Elsevier.



Walls JT, Boley TM, Curtis JJ, Silver D. Heparin induced thrombocytopenia in patients undergoing intra-aortic

balloon pumping after open heart surgery. ASAIO J (1992) 38:M574-6.


Ryan TJ, Antman EM, Brooks NH, et al. 1999 update: ACC/AHA Guidelines for the Management of Patients

with Acute Myocardial Infarction: Executive Summary and Recommendations: A Report of the American College

of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of

Acute Myocardial Infarction). Circulation (1999) 100:1016-30.


Arafa OE, Geiran OR, Svennevig JL. Transthoracic intra-aortic balloon pump in open heart operations:

techniques and outcome. Scand Cardiovasc J (2001) 35:40-4.


Mercer D, Doris P, Salerno TA. Intra-aortic balloon counterpulsation in septic shock. Can J Surg (1981)



Pinkney KA, Minich LL, Tani LY, et al. Current results with intraaortic balloon pumping in infants and children.

Ann Thorac Surg (2002) 73:887-91.


11. Velez CA, Kahn J. Compartment syndrome from balloon pump. Catheter Cardiovasc Interv (2000) 51:217-9.

Sidebar: Key Points

Principles of Intra-Aortic Balloon Pump Counterpulsation

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The primary goal of intra-aortic balloon pump (IABP) treatment is to increase myocardial oxygen supply and

decrease myocardial oxygen demand.

Decreased urine output after the insertion of IABP can occur because of juxta-renal balloon positioning.

Haemolysis from mechanical damage to red blood cells can reduce the haematocrit by up to 5%.

Suboptimal timing of inflation and deflation of the balloon produces haemodynamic instability.

An IABP is thrombogenic; always anticoagulate the patient.

Never switch the balloon off while

in situ.

Reprint Address

Kai Zacharowski, MD, PhD, FRCA, Chair of Cardiovascular Anaesthesia and Critical Care, Consultant in Anaesthesia

and Critical Care, Department of Anaesthesia, Bristol Royal Infirmary, Bristol BS2 8HW, UK; Tel: +44 117 928

2301/2365; Fax: +44 117 926 8674; Email:

Murli Krishna, MBBS, FRCA, FFPMRCA

, Consultant in Anaesthetics & Pain Medicine, Frenchay Hospital, Bristol BS16


Kai Zacharowski, MD, PhD, FRCA

, Chair of Cardiovascular Anaesthesia and Critical Care, Consultant in Anaesthesia

and Critical Care, Department of Anaesthesia, Bristol Royal Infirmary, Bristol BS2 8HW, UK

Principles of Intra-Aortic Balloon Pump Counterpulsation

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From Lifeinthefastlane-Chris Nickson


One of your patients is a 58 year-old man who had a quadruple coronary artery bypass earlier in the day. He had poor cardiac output after the procedure and required the insertion of an intra-aortic balloon pump (IABP) to augment his cardiac function. The medical students on your team have a few questions for you concerning IABPs.

Can you answer them?


Q1. What is an intra-aortic balloon pump (IABP) and how does it work as a circulatory assist device?

Show answer

The IABP has two parts:

(1) a large bore catheter with a long sausage-shaped balloon at the distal tip, and

(2) a console containing a pump that inflates the balloon.

The balloon is designed to sit in the proximal descending aorta. It comes in various lengths according to body height, with balloon volumes of about 30-50 mL. The balloon is usually filled with helium gas, and when inflated should fill up 80-90% of the aortic diameter.

The IABP works by inflating and deflating at different phases of the cardiac cycle. Balloon inflation augments diastolic blood pressure and balloon deflation decreases afterload during systole .

IABP effects on the aortic pressure cycle. The dicrotic notch immediately precedes point C. Key: A. Unassisted End Diastolic Pressure, B.Unassisted Systolic Pressure, C.Unassisted Diastole, D. Reduced Systolic Pressure, E. Diastolic Augmentation, F. Assisted End Diastole Pressure (the unlabeled arrow!) (from

Balloon inflation in early diastole (usually triggered by the R wave on the ECG) increases diastolic blood pressure (E). This in turn increases systemic perfusion and coronary perfusion (at least in the hypotensive patient). Balloon inflation thus displaces blood both proximally and distally. The increase in coronary perfusion increases myocardial oxygen supply.

Balloon deflation occurs at the end of diastole resulting in a decreased end diastolic blood pressure (F). This reduces the aortic pressure at the start of systolic ejection, thus decreasing the afterload that the heart has to pump against. This decreases myocardial oxygen demand and improves systemic perfusion during systole.

This animation may help in visualising how the IABP works (bear with the funky accent! – you may need to increase the volume):

embedded by Embedded Video YouTube Direkt


Q2. What are the indications for IABP use?

Show answer

The IABP can be used whenever there is cardiac pump failure if:

  • it may resolve spontaneously, or
  • a corrective procedure is planned.

In other words, there has to be some hope of the patient being able to survive without an IABP in the future.

Some situations where an IABP is used include:

  • Cardiogenic shock after coronary artery bypass grafting (CABG) or acute myocardial infarction
  • unstable angina
  • Acute mitral incompetence
  • Planned cardiac transplant
  • ventricular arrhythmias refractory to conventional treatment
  • cardiotoxicity from poisoning, e.g. verapamil overdose


Q3. How is an IABP inserted and positioned?

Show answer

IABPs are usually inserted using the Seldinger technique via the femoral artery so that the tip of the catheter is advanced proximally into the aorta. Fluoroscopy is not essential for insertion, so an IABP can be placed emergently.

IABP’s must be appropriately positioned:

The balloon tip is positioned just distal to the origin of the left subclavian artery, and the entire balloon should lie above the renal arteries.

Here is a more detailed description of the steps involved in IABP insertion as described by Charles Gommersall:

  • heparinise patient prior to insertion of catheter providing there are no contraindications such as recent surgery.
  • prep skin
  • fully collapse balloon applying 30 ml vacuum with 60 ml syringe
  • insert needle into femoral artery at 45° and pass it through both walls of artery. Withdraw needle until strong pulsatile jet of blood is obtained
  • pass guidewire through needle and advance until tip is is in thoracic aorta. Wire should pass very easily
  • pass sheath over wire in similar manner to insertion of PA catheter sheath
  • pass balloon over guidewire through sheath. Must be inserted to at least the level of the manufacturer’s mark (usually double line) to ensure that entire balloon has emerged from sheath
  • balloon should be positioned so that the tip is about 1 cm distal to the origin of the left subclavian artery. If fluroscopy is not available during insertion the distance from the angle of Louis down to the umbilicus and then to the femoral artery insertion site should be measured to approximate the distance the balloon should be advanced and the position should be checked on CXR
  • remove wire. Return of blood via central lumen confirms that the tip is not subintimal and has not caused a dissection.
  • flush central lumen with heparin saline and connect to transducer to monitor intra-aortic pressure (the outer lumen transmits helium gas to the balloon)
  • monitor Doppler ankle pressures and compare with preinsertion value

Note: once the balloon has been inflated, even if it is then deflated, it must not be removed through the sheath for any reason – the sheath must be removed first.


Q4. When is an IABP contra-indicated?

Show answer

Contra-indications include:

  • Aortic insufficiency
  • Aortic dissection
  • Patent ductus arteriosus
  • Severe peripheral vascular disease
  • Thoracic aortic graft <12 months old
  • the patient’s cardiac index is too low for there to be a clinical benefit from IABP assistance


Q5. What are the determinants of IABP efficiency?

Show answer

IABP efficiency is determined by:

  • Timing of balloon inflation and deflation
  • Assist ratio (e.g. 1:1 – balloon inflation and deflation on every cardiac cycle – provides greater circulatory assistance than 1:2 or 1:4 – balloon inflation and deflation on every 2nd or 4th cardiac cycle )
  • Heart rate (efficiency is greatly decreased at heart rates >130/min)
  • Gas loss from balloon (balloon volume)
  • Minimum cardiac index of 1.2 – 1.4 L/min/m2 is required for IABP assistance to be clinically beneficial


Q6. How can IABP function be optimised?

Show answer

Optimisation can be achieved by ensuring that:

  • inflation of the balloon occurs at the dicrotic notch (forming the ‘V’)
  • the slope of rise of augmented diastolic waveform is straight and parallel to the systolic upstroke
  • the augmented DBP at balloon deflation exceeds or is equal to end-systolic BP
  • the end-diastolic BP at balloon deflation is lower than the preceding unassisted end-DBP by 15-20 mmHg
  • the assisted SBP (following a cycle of balloon inflation) is lower than the previous unassisted SBP by 5 mmHg


Q7. What are the complications of IABPs?

Show answer

Complications can occur during insertion, while the IABP is in use, during removal, or after removal.

During insertion

  • failure to advance catheter beyond iliofemoral system because of atherosclerotic disease (common)
  • aortic dissection and arterial perforation – may cause retroperitoneal hemorrhage.

During use

  • Ischemia
    • ischemia of the lower limbs (up to 25% of all IABP patients)
      • may occur while the IABP is in place, or hours after removal due to thromboembolic showers
      • ischemia usually results from thrombosis at the insertion site
      • Can affect contra-lateral leg due due to cholesterol emboli and thromboembolic showers from the balloon
      • Close neurovascular monitoring essential – sensorimotor loss generally mandates removal
      • Pulseless limb may need to be tolerated if IABP is life-saving
    • Visceral ischemia
    • Spinal ischemia
  • Balloon rupture causing helium embolus
      • this may be heralded by high balloon inflation pressures.
      • The key indicator of balloon rupture is the presence of blood in the connecting tubing.
      • Management involves immediate cessation of counterpulsation, placement of the patient head down and IAB removal. Consider giving broad spectrum antibiotics as the gas chamber of the balloon is not sterile.
  • Hemolysis and consumptive thrombocytopenia
  • Peripheral neuropathy
  • Catheter-related infection
  • Small perforation in balloon membrane
    • this may allow a small amount of blood to leak into balloon lumen. The blood is dessicated by the dry helium and forms a hard pellet which may stop the balloon from being removed without surgical aortotomy.

During or after removal:

  • Haematoma
  • Pseudoaneurysm
  • AV fistula


References and Links

  • Datascope’s IABP elearning modules
  • Gomersall C. Intra-aortic balloon pumping. 1999.
  • Krishna M, Zacharowski K. Principles of Intra-Aortic Balloon Pump Counterpulsation. Cont Edu Anaesth Crit Care & Pain. 2009;9(1):24-28.
  • Life in  the Fast Lane: Paul Young’s ICU Mind Maps – Intra-Aortic Balloon Pump [pdf]
  • Marino PL. The ICU Book (3rd edition). 2007; Wolters Kluwer.
  • Overwalder PJ. Intra Aortic Balloon Pump (IABP) Counterpulsation. The Internet Journal of Perfusionists. 2000;1:(1) (fulltext online)


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