Intra-aortic Balloon Counterpulsation

Intra-aortic balloon counterpulsation is the most common form of mechanical circulatory support (MCS) used in the setting of myocardial ischemia and cardiogenic shock. ^{[1, 2]} This method of temporary mechanical circulatory support attempts to create a more favorable balance of myocardial oxygen supply and demand by 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 (PCWP). The following review discusses the hemodynamic, clinical, and technical aspects of this important modality for hemodynamic support.

History of the procedure

The principle of aortic counterpulsation was originally described by Dr Adrian Kantrowitz in 1959 using a dog model​ in which the hemidiaphragm was wrapped around the thoracic aorta, ^{[2, 3]} which, by electrical stimulation of the phrenic nerve, was made to contract during diastole. Altering the pressure characteristics of the cardiac cycle by augmenting diastolic pressure was postulated to improve coronary perfusion and take over as much as 25% of the pumping burden of the natural heart.

The modern intra-aortic counterpulsation device, which consists of a balloon mounted on a flexible catheter, was described by Moulopoulos et al at the Cleveland Clinic in 1962. ^{[2, 4]} The original description was of a latex tube tied around a polyethylene catheter with side holes. Carbon dioxide was used to inflate the balloon regulated via a 3-way solenoid valve. ^{[2, 4]} Balloon inflation occurred for a predetermined duration and was timed using the R wave on the electrocardiogram.

In 1971, Krakauer et al working with Adrian Kantrowitz described their experience in 30 patients who received intra-aortic balloon pump (IABP) support for cardiogenic shock secondary to myocardial infarction (MI) refractory to pharmacologic therapy. ^[5] In this series, most patients (25 of 30) achieved hemodynamic stabilization and reversal of shock after the introduction of counterpulsation. In the subgroup of patients developing medically refractory shock within the first 12 hours of infarction, 9 of the 20 survived to hospital discharge. ^[6]

Frequency

In the decades following their introduction, the IABP became an important adjunctive therapy in the management of cardiogenic shock, particularly in the setting of an acute MI. In the seminal SHOCK trial, published in 1999, IABP was used in 86% of patients, regardless of whether they were revascularized or not. ^[7]

In relatively recent years, the efficacy of IABP support in cardiogenic shock has come into question. ^[8] Data from 1998 compared to 2008 showed that IABP support of patients in cardiogenic shock fell from 36.5% in 1998 to 13.4% in 2008 (P< 0.0001). ^[9] In a large 2009-2013 study comprising data from 76,474 patients, Sandhu et al found 39% were supported with IABP while undergoing percutaneous coronary intervention (PCI) in the setting of cardiogenic shock. ^[10] The authors noted, however, that there was large variation across centers. In a study using the CathPCI Registry, IABP was used in 10.5% of all high-risk PCIs, whether due to unprotected left main artery as the target vessel, cardiogenic shock, severely depressed LV function, or ST-elevation myocardial infarction (STEMI). ^[11]

More recently, a study that analyzed ongoing prospective, observational data from the North American COVID-19 (coronavirus disease 2019) Myocardial Infarction (NACMI) registry to determine the frequency and clinical impact of MCS on STEMI that complicated COVID-19 found that IABP was the most frequently used MCS device in those with and those without COVID-19. ^[12]  Those with COVID-19 and STEMI who received an IABP had a significantly higher in-hospital mortality than individuals with STEMI but without COVID. 

Pathophysiology

The IABP improves many of the hemodynamic perturbations of circulatory failure and cardiogenic shock. ^[13] Therefore, understanding the pathophysiology of this dramatic manifestation of heart failure is important. Cardiogenic shock is characterized by end-organ tissue hypoperfusion, which initiates a series of counter-regulatory mechanisms. The classic understanding of the interplay between the underlying pathophysiology and counter-regulatory mechanisms is that of a downward spiral in which compensatory mechanisms such as peripheral vasoconstriction, tachycardia, and neurohormonal regulatory activation contribute to further worsening of left ventricular failure (see image below).

While a comprehensive discussion of the hemodynamics of cardiogenic shock is beyond the scope of this review, it is worthwhile to note the following:

Cardiogenic shock is the most common cause of death from acute myocardial infarction. According to data from the SHOCK registry, the mortality from cardiogenic shock complicating acute myocardial infarction is 50-80%. ^[14] In addition, data indicate that anterior myocardial infarction is the most common territory leading to cardiogenic shock. In the SHOCK registry, 55% of infarctions were anterior. ^[14] 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. The diagnosis is confirmed by demonstrating hemodynamic criteria consistent with myocardial dysfunction.

Mechanical complications of acute myocardial infarction can precipitate cardiogenic shock or contribute to preexisting cardiogenic shock. These include acute mitral regurgitation, postinfarction ventricular septal defect, and left ventricular free wall rupture. For more information, see Medscape Drugs & Diseases article Complications of Myocardial Infarction.

Catecholamine vasopressors to treat hypotension in the setting of cardiogenic shock should be used judiciously to maintain coronary perfusion pressure but also minimize additional myocardial oxygen demand through increasing afterload and genesis of dysrhythmias.

Reperfusion of ischemic myocardium has been shown to provide long-term survival benefit in the setting of cardiogenic shock related to acute myocardial infarction. ^[14]

The above highlights of cardiogenic shock pathophysiology set the stage for the following discussion of counterpulsation hemodynamics.

Effects of counterpulsation on systemic hemodynamics

The 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. ^[15] In a multicenter trial of counterpulsation in cardiogenic shock, a mean 30 mm Hg increase in diastolic pressure was observed with no significant change in heart rate.

The IABP pressure tracing in the image below shows the systemic hemodynamic effects of counterpulsation in a 2:1 configuration, whereby every other beat is assisted by balloon inflation. 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. ^[16] The magnitude of counterpulsation hemodynamic effect depends on several factors, including the relation of balloon volume to aorta size, heart rate and rhythm, and aortic compliance. ^[17] In addition, diastolic augmentation is most efficient the closer the balloon is to the aortic valve. ^[18] To minimize the risk of cerebral embolism, the ideal IABP position in modern practice is 1 or 2 centimeters distal to the origin of the left subclavian artery.

Effect of counterpulsation on coronary perfusion

In theory, the augmentation of diastolic pressure by counterpulsation should be transmitted to the epicardial coronary circulation, leading to an increase in myocardial perfusion. However, the data suggest that the degree of coronary artery stenosis and the state of coronary autoregulation cause significant variation in response to counterpulsation. Kimura et al, using an anesthetized dog model, showed that diastolic forward flow in the left anterior descending (LAD) increased by 12% during counterpulsation. However, with partial ligation of the left main to create a critical stenosis, the effect of counterpulsation to augment LAD flow was completely abolished. ^[19] In human subjects, data regarding augmentation of coronary flow by counterpulsation is inconsistent.

Transesophageal echocardiography (TEE) Doppler tracings from epicardial vessels obtained in patients with an IABP have shown increased Doppler velocities, suggesting augmented coronary flow. ^[20] The effect of diastolic augmentation on post-stenotic coronary flow has also been assessed using a Doppler angioplasty guidewire in patients undergoing angioplasty.

Kern studied coronary flow in 15 patients with a mean vessel narrowing of 95%. No significant increase in coronary flow augmentation was demonstrated in the post-stenotic segment, but angioplasty restored the effect of counterpulsation to augment coronary flow. ^[21] Because of the severity of luminal obstruction present in the population studied, the use of a guidewire beyond the stenosis may have adversely affected flow measurements. In addition, conclusions cannot be drawn regarding flow augmentation beyond less severe stenoses, since these were not studied.

Takeuchi addressed this issue by comparing 40 patients undergoing counterpulsation for typical indications using transthoracic Doppler echocardiography to measure coronary flow velocity. Analysis of the data stratified by lesion severity showed enhanced distal vessel flow regardless of the degree of stenosis present. ^[22] Nonetheless, a major contributor to the relief of ischemia by counterpulsation is via its effect to decrease afterload, left ventricular wall stress, and myocardial oxygen demand.

Relevant anatomy

The IABP is commonly introduced via the common femoral artery using a Seldinger technique. If placed in a cardiac catheterization laboratory, fluoroscopy is often used to confirm correct position of the device, but a chest radiograph can be used to confirm position after placement if fluoroscopy is not available. The tip of the balloon should be positioned 1-2 centimeters distal to the origin of the left subclavian artery. In the case of blind placement, the take-off of the left subclavian artery can be identified using the second rib as a landmark. The caudal end of the balloon should be positioned above the origin of the renal arteries. In most patients, the right and left renal arteries arise between the first and second lumbar vertebral bodies. ^[23]

The first image below shows a chest radiograph from a patient with an IABP in place with the major landmarks vital for proper positioning highlighted. The second image shows intra-arterial positioning of an IABP.

The aortic valve functions to prevent the regurgitation of blood from the aorta into the left ventricle during ventricular diastole and to allow the appropriate flow of blood—the cardiac output—from the left ventricle into the aorta during ventricular systole. For more information about the relevant anatomy, see Aortic Valve Anatomy.

Indications with evidence of benefit

American College of Cardiology/American Heart Association (ACC/AHA) 2013 guidelines for the management of ST elevation myocardial infarction (STEMI) and European Society of Cardiology (ESC) 2012 guidelines for the management of acute heart failure believe it is 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).

Data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-1) trial showed lower 1-year mortality in the cohort (68 of 310 subjects with cardiogenic shock) receiving early IABP support (57% vs 67%, P = 0.04). Of note, rates of major bleeding were also higher in the IABP cohort (47% vs 12%, P = 0.0001).

Use of data from the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial registry revealed that acute myocardial infarction patients receiving thrombolytic therapy with IABP support had a lower in-hospital mortality than those receiving thrombolytic therapy alone (47% vs 63%, P< .0001). ^[24]

Interestingly, data from the Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock (randomized, prospective, multicenter trial in Germany) showed that the use of IABP counterpulsation did not reduce 30-day mortality in patients with cardiogenic shock complicating acute myocardial infarction for whom early revascularization strategy was the planned-primary endpoint. There were 300 patients in the IABP group (40% mortality) versus 298 patients in the control group (41% mortality). No significant differences were noted in the secondary endpoints or in process-of-care measures, including the time to hemodynamic stabilization, the length of stay in the ICU, serum lactate levels, the dose and duration of catecholamine therapy, and renal function. ^[25]

Other class IC and IIa-b indications for IABP support include the following conditions:

• Acute mitral regurgitation (IC)

• Ventricular septal defect (VSD) as a complication of myocardial infarction (IC)

• Intractable ventricular arrhythmias: Fotopoulos reported on the use of counterpulsation in 21 patients with ventricular arrhythmias refractory to medical therapy. During IABP support, 18 of the 21 patients showed reduction or termination of the arrhythmias (IIa). ^[26]

• Unstable angina refractory to medical therapy (IIa) ^[27]

• Decompensated systolic heart failure as bridge to definitive mechanical support or transplantation: Counterpulsation therapy, owing to its effect to decrease cardiac work, left ventricular end-diastolic volume, and pulmonary capillary wedge pressure, is used as a temporizing measure in extreme LV failure. Current insertion techniques using the axillary artery have also allowed for more prolonged counterpulsation therapy in patients awaiting cardiac transplantation (IIb).

Indications with postulated benefit

Decompensated critical aortic stenosis

By decreasing the burden of coexisting ischemia, counterpulsation can lead to clinical stabilization in patients awaiting aortic valve replacement. The hemodynamic benefits of counterpulsation are altered in aortic stenosis because of fixed LV outflow obstruction. Case reports show that in patients with critical aortic stenosis, a blunted decrease in left ventricular systolic pressure is noted and IABP support results in an increase in the transvalvular gradient. ^[17]

Perioperative support for coronary artery bypass surgery, and for high-risk cardiac patients undergoing noncardiac surgery

The use of preoperative IABP in high-risk patients undergoing revascularization by coronary artery bypass graft surgery has been shown to reduce operative mortality in patients with high-risk characteristics including symptomatic heart failure and medically refractory angina. ^{[28, 29, 30, 31]} The use of IABP for noncardiac surgery in patients with high-risk cardiac disease has been based on case reports and anecdotal data; no clinical trials have examined the benefit of counterpulsation in this setting.

Percutaneous coronary intervention (PCI)

The routine use of IABP in high-risk patients undergoing PCI has been analyzed in a large, multicenter randomized trial. The Primary Angioplasty in Myocardial Infarction (PAMI-II) trial published data on 437 high-risk patients randomized to post-PCI IABP or traditional medical care. No significant difference was seen in the endpoints of death, reinfarction, or new-onset heart failure. ^[32]

In addition, the prophylactic use of an IABP as adjunctive therapy with primary PCI for an acute anterior myocardial infarction without evidence of shock has not been shown to reduce infarct size as measured by cardiac MRI. ^[33]

The Balloon Pump-Assisted Coronary Intervention Study (BCIS-1) study randomized high-risk patients undergoing PCI to routine prophylactic IABP support, and no benefit was observed in the patients supported with IABP. ^[34]

The IABP was evaluated against the Impella 2.5 device in the Protect II Study to compare the devices in preventing major adverse events during and after nonemergent high-risk PCIs in 452 symptomatic patients. ^[35] These individuals were randomized with complex 3-vessel disease or unprotected left main coronary artery disease and severely depressed LV function to IABP (n = 226) or Impella 2.5 (n = 226) support. The study found that the 30-day incidence of major adverse events was not different for patients with IABP or Impella 2.5 hemodynamic support (35.1% for Impella 2.5 vs 40.1% for IABP, P = 0.227). However, trends for improved outcomes were observed for Impella 2.5–supported patients at 90-days (40.6% for Impella 2.5 vs 49.3% for IABP, P = 0.066). ^[35]

Indications with no evidence to suggest benefit

Sepsis

The routine use of IABP is septic patients is not recommended, nor has it been shown to offer any consistent mortality advantages in various animal or human studies. The 2021 Surviving Sepsis Campaign guidelines do not mention IABP in current management options. ^[36]

Absolute contraindications

Absolute contraindications to intra-aortic balloon counterpulsation (IABP) include the following:

• Significant aortic regurgitation (no consensus on what degree of aortic regurgitation is an absolute contraindication)

• Aortic dissection

Relative contraindications

Relative contraindications to intra-aortic balloon counterpulsation (IABP) include the following:

• Bilateral iliofemoral peripheral arterial disease

• Abdominal aortic aneurysm

• Presence of iliac arterial stents

• Prosthetic iliofemoral grafts

• Coagulopathy

Advantages and disadvantages of mechanical circulatory support (MCS) devices

Intra-aortic balloon pump (IABP)

The IABP has the advantage of increasing coronary perfusion pressure (CCP) and reducing both left ventricular (LV) afterload and myocardial oxygen consumption. It can also be placed rapidly, it's possible to insert the device percutaneously, and no general anesthesia is needed. Anticoagulation is optional. ^[1]

Disadvantages and risks of the IABP include the fact there is no direct increase in cardiac output; access site complications include limb ischemia, bleeding, pseudoaneurysm, and vascular trauma; admission to the intensive care unit (ICU) is required for the duration of therapy; it is dependent on electrocardiography (ECG) tracings or arterial waveforms (poor function with cardiac arrhythmias, significant tachycardia); and severe thrombocytopenia may result. ^[1]

Impella device

Advantages of the Impella device include it allows percutaneous access; supports cardiac output up to 2.5, 4, 5, or 5.5 L/min flow (dependent on the model); reduces preload, afterload, and myocardial oxygen consumption, as well as pulmonary capillary wedge pressure; raises mean arterial pressure; is not dependent on ECG or arterial waveforms; has the potential for longer-term support if placed in an axillary artery; and is approved for up to 14 days of support (4 days for the 2.5 and CP models; 6 days for the 5 model; 14 days for the 5.5 and RP models). ^[1]

Disadvantages and risks of the Impella device include recommended anticoagulation, hemolysis, access site complications (eg, cutdown and/or vascular graft is required for the 5.0 and 5.5 devices); and potential valve damage (the device is contraindicated in the presence of coexisting mechanical aortic valve, aortic insufficiency, or aortic stenosis). ^[1]

TandemHeart system

Advantages of the TandemHeart system include it allows percutaneous access, supports cardiac up to 5 L/min flow (dependent on cannula size), reduces preload and afterload and oxygen demand, increases mean arterial pressure, reduces filling pressures, can support either venticle, is not dependent on ECG or arterial waveforms, and allows the addition of an oxygenator to the circuit. ^[1]

Disadvantages and risks of the TandemHeart system include required anticoagulation as well as transseptal puncture, in which the device is placed in the catheter lab guided by transesophageal echocardiography and the risk of tamponade or residual atrial septal defect is heightened; access site complications; increased LV afterload; and it is approved for only 6 hours of support in the United States or up to 30 days of support in Europe. ^[1]

Extracorporeal membrane oxygenator configuration (ECMO)

Advantages of ECMO include supporting cardiac output (up to 8 L/min flow), capability to provide full cardiopulmonary support, allows for rapid bedside cannulation (percutaneous insertion), continuous renal replacement therapy (CRRT) is possible via the ECMO circuit, and long-term support is also possible. ^[1]

Disadvantages and risks of ECMO include recommended anticoagulation, hemolysis, access site complications, required ongoing care by skilled staff (perfusionist, ECMO technician), no venous reservoir (volume sensitive), increased LV afterload if no LV vent is in place, stroke, venovenous ECMO does not provide LV support (respiratory function only), and venoarterial ECMO with a femoral cannula mixes antegrade (native cardiac output) and retrograde (ECMO) blood flow (resulting in blood mixing and hypoxia if respiratory failure develops). ^[1]

Selection of balloon size

Selection of balloon size is determined by the height of the patient. For patients shorter than 5 feet, a 25 cm³ balloon is recommended. A 34 cm³ balloon is available for patients 5 feet to 5 ft 4 inches tall. The most common balloon size is 40 cm³ for patients 5 ft 4 inches to 6 feet tall. A 50 cm³ balloon is available for patients taller than 6 feet.

The Table below summarizes the counterpulsation balloon catheters available on the market.

Table. Summary of Available Intra-aortic Counterpulsation Catheters (Open Table in a new window)

Device insertion

In modern usage, intra-aortic balloon counterpulsation is performed with a polyethylene balloon mounted on a flexible catheter positioned 1-2 cm below the origin of the left subclavian. The shaft of the balloon catheter contains two lumens: one allows for gas exchange from console to balloon; the second is used for catheter delivery over a guidewire and for monitoring of central aortic pressure after installation.

Balloon inflation is performed using helium, which, owing to its low density, can be rapidly exchanged through the tubing and catheter to allow for rapid balloon inflation and deflation during the cardiac cycle.

Insertion is generally performed via either one of the femoral arteries using a standard percutaneous Seldinger technique over a 0.030-inch guidewire provided with the balloon catheter.

The device catheter can be introduced via a sheath (usually 7.5, 8, or 9 French [F]). A sheathless approach can also be used in patients with peripheral vascular disease. The sheathless method has been shown to reduce limb ischemia, but the risk of infection and minor bleeding is increased with this method. ^[37]

McBride et al described the insertion of an intra-aortic balloon pump (IABP) catheter via the axillary artery to allow for more patient mobility. ^[38] This is performed via a cutdown, often using a 6-12 mm GoreTex or Dacron sleeve sewn onto the axillary artery to facilitate introduction of the device.

An IABP device can also be inserted via the brachial artery or subclavian artery or, during open-heart surgery, directly into the ascending or thoracic aorta.

Initial set-up and troubleshooting

Following installation, the balloon catheter is connected to the console and the system is purged with helium. The central lumen of the catheter is connected to pressure tubing and a pressure transducer to allow for monitoring of central aortic pressure.

Heparin should be given as a bolus and continuous infusion to maintain a partial thromboplastin time (PTT) of 60-80 seconds or an activated clotting time (ACT) of 1.5-2.0 times normal.

An appropriately timed IABP will effectively lower impedance to left ventricular (LV) ejection and augment diastolic pressure. However, improper timing can lead to inefficient LV support or counteract the intended purpose of therapy. The four timing errors to troubleshoot are as follows:

• Early balloon inflation (see image below) occurs prior to aortic valve closure. 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.

  Intra-aortic Balloon Counterpulsation. Intra-aortic balloon pressure tracing with 1:2 counterpulsation ratio depicting the timing error of early balloon inflation.

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• Late balloon inflation (see image below) occurs 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.

  Intra-aortic Balloon Counterpulsation. Intra-aortic balloon pressure tracing depicting the timing error of late balloon inflation.

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• Early balloon deflation (see image below) 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.

  Intra-aortic Balloon Counterpulsation. Intra-aortic balloon pressure tracing showing the timing error of early balloon deflation.

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• Late balloon deflation (see image 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.

  Intra-aortic Balloon Counterpulsation. Intra-aortic balloon pressure tracing showing the timing error of late balloon deflation.

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The Benchmark Counterpulsation Outcomes Registry published outcomes data on 16,909 patients undergoing IABP therapy between 1996 and 2000. The total incidence of major complications was 2.6%; incidence of minor complications was 4.2%. Specifically, the incidence of major limb ischemia, defined as loss of pulse, abnormal limb temperature, or pallor requiring surgical intervention, was 0.9%. ^[39] The incidence of bleeding associated with hemodynamic compromise, requiring transfusion or surgical intervention was 0.8%. In addition to vascular and bleeding complications, IABP may be associated with systemic cholesterol embolization, infection, and stroke.

The incidence of unsuccessful attempts at IABP placement recorded in the Benchmark Registry was low at 2.3%. ^[39] Complications attributed to device failure include balloon leak, balloon entrapment, and poor balloon inflation. Shear forces created by the balloon can lead to hemolytic destruction of red cells and platelets; therefore, daily blood counts should be monitored during IABP therapy. In-hospital mortality attributed to IABP placement in the Benchmark Registry was 0.05%. ^[39]

The Benchmark Registry identified four risk factors for major complications from IABP use: (1) age ≥75 years, (2) female gender, (3) peripheral arterial disease, (4) body surface area < 1.65 m². ^[39]

Intra-aortic counterpulsation remains the workhorse circulatory support device used by cardiovascular specialists. The device provides a minimally invasive method of support for failing left ventricular (LV) function by reducing afterload and improving myocardial oxygen supply-demand balance. However, the efficacy of counterpulsation depends on several factors, including intrinsic ventricular function. For this reason, the options of available circulatory support have also expanded to include peripherally inserted ventricular assist devices such as venoarterial extracorporeal membrane oxygenator configuration (ECMO) with percutaneous cannulation, the TandemHeart circuit, and the Impella family of devices.

The TandemHeart system provides left atrial–to–femoral artery bypass and can be inserted under fluoroscopy in the cardiac catheterization laboratory without surgical implantation. This system uses a transseptal cannula that allows direct unloading of the left heart, and, by providing a cardiac output independent of ventricular stroke volume, this device provides support only exceeded by traditional surgically implanted ventricular assist devices (VAD). An external centrifugal pump provides flow rates up to 4 L/min. In some centers, the venous-to-arterial bypass is interrupted by an oxygenator membrane and the venous cannula is placed in the right atrium. This provides complete pulmonary circulation bypass with an ECMO.

In contrast, the Impella device provides direct unloading of the LV using an integrated pump and catheter system. A 9F pigtail catheter carries a pump housing of 12F caliber, which pulls blood volume from the LV and ejects it into the ascending aorta. The devices can provide flow rates ranging from 2.5 L/min to 5.0 L/min (the 5.0 L device generally is performed by surgical implantation). It has been used for temporary support in the setting of high-risk percutaneous coronary intervention (PCI), for the management of shock, and as a bridge to recovery in acute myocardial infarction. See the image below.

Importantly, in comparison to modern intra-aortic balloon pump catheters, the percutaneous VAD systems are high-profile systems. The TandemHeart requires an arterial sheath caliber of 15-17F, and newer generation Impella devices use a 13-14F arterial sheath. However, advances in technology have allowed for development of a lower profile IABP. Initial devices required a surgical cutdown and were up to 15F in diameter, but, in recent years, lower profile devices able to fit through sheaths as small as 7.5F have entered the market. This has reduced vascular complications significantly and allowed for more widespread use of counterpulsation therapy. For this reason, counterpulsation will likely remain the most widely accessible form of mechanical hemodynamic support for the foreseeable future.

Use of IABP with veno-arterial extra-corporeal membrane oxygenation (VA-ECMO)

One limitation of the use of VA-ECMO in LV failure is that it can increase afterload and thus myocardial oxygen demand. This can result in unfavorable increases in LV end-diastolic pressure and consequent LV distention, and it can hamper efforts at LV myocardial recovery and weaning from ECMO. ^[40] Physiologically, IABP may have a synergistic effect with VA-ECMO by unloading the LV, providing enhanced pulsatility to flow and improving coronary blood flow. ^{[41, 42, 43, 44]} The addition of IABP to VA-ECMO may also effect cerebral blood flow.41 Groups have reported the use of combined VA-ECMO with IABP for the treatment of severe heart failure in critically ill individuals with promising results. ^{[45, 46]} Evidence-based guidelines are needed to help clinicians decide between a growing array of hemodynamic support devices and configurations.

Bridge to cardiac transplantation

Another emerging role for IABP is as a bridge to cardiac transplantation with placement via left axillary/subclavian arterial access. ^[47] The IABP can be inserted via a percutaneous or surgical cut-down technique, which can be effective and relatively low risk. In a study by Estep et al, 50 patients with end-stage heart failure underwent percutaneous insertion of a left axillary IABP, with a result of 92% total survival on IABP support and an 18-day median duration of use. ^[48] The outcome in 84% was successful transplantation, 6% escalated to a different form of mechanical support, and 8% died while on IABP. The rate of significant thrombotic or bleeding events was low: 8%. ^[48]

Compared to mechanical support with other devices such as ECMO, this technique has the potential advantage of allowing the patient to ambulate. ^[1] In a study by Umakanthan et al in which 18 patients underwent surgical placement of an axillary IABP, the duration of ambulatory support was 5 to 63 days. ^[49]  There was a statistically significant increase in the longest distance walked pre-IABP (411 ± 248 ft) compared to post-IABP (2655 ± 2426 ft) (P = 0.008).