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Intra-aortic Balloon Counterpulsation

  • Author: Elias V Haddad, MD, FACC; Chief Editor: Karlheinz Peter, MD, PhD  more...
 
Updated: Dec 04, 2015
 

Overview

Intra-aortic balloon counterpulsation is a method of temporary mechanical circulatory support that attempts to create 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. 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, 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.[1] 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.[1] 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 refractory to pharmacologic therapy. 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.[2]

Frequency

According to an analysis by Goldberg regarding trends in the care for cardiogenic shock complicating acute myocardial infarction, overall use of IABP during the 10-year period from 1986-1997 was only 20%. However, a temporal trend toward increased use of IABP in this patient population was such that by 1997, 42% of patients received IABP support for cardiogenic shock that developed as a consequence of an acute myocardial infarction.[3]

Pathophysiology

The IABP improves many of the hemodynamic perturbations of circulatory failure and cardiogenic shock.[4] 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).

The downward spiral of cardiogenic shock. Myocardi 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. (Adapted from Hollenberg SM. Annals of Internal Medicine. 1999; 131(1): 47-59.)

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%.[5] 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.[5] 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.[5]

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.[6] 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.

Annotated arterial pressure tracing obtained from Annotated arterial pressure tracing obtained from intra-aortic balloon pump set to a 2:1 ratio. 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.[7] 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.[8] In addition, diastolic augmentation is most efficient the closer the balloon is to the aortic valve.[9] 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.[10] 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.[11] 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.[12] 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.[13] 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.[14]

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.

Chest radiograph demonstrating proper positioning Chest radiograph demonstrating proper positioning of an intra-aortic balloon pump catheter. Major landmarks are annotated on the radiograph.
Intra-arterial positioning of an intra-aortic ball Intra-arterial positioning of an intra-aortic balloon pump (IABP). Used with permission from Radiopaedia.org (http://radiopaedia.org/cases/intra-aortic-balloon-pump-and-icu-lines).

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.

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Indications

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).[15]

Interestingly, data from the recently published 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.[16]

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

  • 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). [17]
  • Unstable angina refractory to medical therapy (IIa) [18]
  • 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.[8]

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.[19, 20, 21, 22] 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.[23]

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.[24]

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.[25]

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 2012 Surviving Sepsis Campaign guidelines do not mention IABP in current management options.

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Contraindications

Absolute contraindications

See the list below:

Relative contraindications

See the list below:

  • Bilateral ileofemoral peripheral arterial disease
  • Presence of iliac arterial stents
  • Prosthetic ileofemoral grafts
  • Coagulopathy
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Equipment

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 currently available on the market.

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

Manufacturer Balloon Catheters (Brand Name) Nominal Balloon Volume, mL/Catheter Size, F Maximum Guidewire Caliber, in Maximum Insertable Length, mm
Maquet/Datascope MEGA 50/8, 40/7.5, 30/7.5 0.025 723
Fidelity 25, 34, 40/8 0.025 723 (25-40 mL)
Linear 25, 34, 40/8 0.025 723 (25-40 mL)
Sensation (fiberoptic compatible) 25, 34, 40/7 0.025 714 (25-40 mL)
Arrow Ultraflex 30, 40/7.5; 50/9 0.025 643 (30 mL)



693 (40, 50 mL)



Ultra 8 30, 40/8 0.025 643 (30 mL)



693 (40 mL)



Narrowflex 30, 40/8 0.03 643 (30 mL)



693 (40 mL)



RediGuard 30/7, 40/8, 50/9 0.025 693 (30-50 mL)
Fiberoptix (fiberoptic compatible) 30, 40, 50/7.5, 8, 9 0.025 643 mm (30 mL)



693 mm (40 mL)



660 mm (50 mL)



Abiomed iPulse 40/8 0.025 720 mm
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Technique

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 2 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.[26]

McBride et al described the insertion of an intra-aortic balloon pump (IABP) catheter via the axillary artery to allow for more patient mobility.[27] 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 4 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 pressure tracing with 1:2 cou Intra-aortic balloon pressure tracing with 1:2 counterpulsation ratio depicting the timing error of early balloon inflation.
  • 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 pressure tracing depicting th Intra-aortic balloon pressure tracing depicting the timing error of late balloon inflation.
  • 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 pressure tracing showing the Intra-aortic balloon pressure tracing showing the timing error of early balloon deflation.
  • 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 pressure tracing showing the Intra-aortic balloon pressure tracing showing the timing error of late balloon deflation.
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Complications

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%.[28] 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%.[28] 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%.[28]

The Benchmark Registry identified 4 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.[28]

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Potential Future and Controversies

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 the TandemHeart and Impella device.

TandemHeart (CardiacAssist, Pittsburgh, Pa) provides left atrial–to–femoral artery bypass and can be inserted under fluoroscopy in the cardiac catheterization laboratory without surgical implantation. The TandemHeart 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 extracorporeal membrane oxygenator configuration (ECMO).

In contrast, the Impella device (Abiomed, Danvers, Mass) provides direct unloading of the left ventricle (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. Current devices can provide flow rates up to 2.5 L/min; newer available devices provide up to 3.5 L/min and 5 L/min (5 L requires surgical implantation). It has been used for temporary support in the setting of high-risk percutaneous coronary intervention (PCI) and as a bridge to recovery in acute myocardial infarction. See image below.

Impella device positioned in the left ventricle. B Impella device positioned in the left ventricle. Blood from the left ventricle is pulled into the inlet area and expelled through the outlet distal to the aortic valve by a motor integrated into the catheter system.

The Protect II Study, a prospective, multicenter, randomized controlled trial (Abiomed, Inc) compared Impella 2.5-L system to IABP in preventing major adverse events during and after nonemergent high-risk PCIs. Four hundred fifty-two symptomatic patients 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 during nonemergent high-risk PCI. 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 =.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 =.066).[29]

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 the current 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.

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Contributor Information and Disclosures
Author

Elias V Haddad, MD, FACC Assistant Professor of Medicine, Associate Director, Interventional Cardiology Fellowship Program, Director, International Scholars Exchange Program, Vanderbilt Heart and Vascular Institute, Vanderbilt University Medical Center

Elias V Haddad, MD, FACC is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Coauthor(s)

Cheryl Hawa Robertson, MD Fellow, Division of Cardiovascular Medicine, Vanderbilt University Medical Center

Cheryl Hawa Robertson, MD is a member of the following medical societies: Alpha Omega Alpha, Student National Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Karlheinz Peter, MD, PhD Professor of Medicine, Monash University; Head of Centre of Thrombosis and Myocardial Infarction, Head of Division of Atherothrombosis and Vascular Biology, Associate Director, Baker Heart Research Institute; Interventional Cardiologist, The Alfred Hospital, Australia

Karlheinz Peter, MD, PhD is a member of the following medical societies: American Heart Association, German Cardiac Society, Cardiac Society of Australia and New Zealand

Disclosure: Nothing to disclose.

Additional Contributors

Craig T Basson, MD, PhD Translational Medicine Head – Cardiovascular, Translational Medicine Head - Diabetes and Metabolism, Novartis Institutes for BioMedical Research

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology, American Heart Association

Disclosure: Nothing to disclose.

Acknowledgements

John A McPherson, MD, FACC, FAHA, FSCAI Associate Professor of Medicine, Division of Cardiovascular Medicine, Director of Cardiovascular Intensive Care Unit, Vanderbilt Heart and Vascular Institute

John A McPherson, MD, FACC, FAHA, FSCAI is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, Society of Critical Care Medicine, and Tennessee Medical Association

Disclosure: Abbott Vascular Corp. Consulting fee Consulting

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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. (Adapted from Hollenberg SM. Annals of Internal Medicine. 1999; 131(1): 47-59.)
Annotated arterial pressure tracing obtained from intra-aortic balloon pump set to a 2:1 ratio. 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.
Intra-aortic balloon pressure tracing with 1:2 counterpulsation ratio depicting the timing error of early balloon inflation.
Intra-aortic balloon pressure tracing depicting the timing error of late balloon inflation.
Intra-aortic balloon pressure tracing showing the timing error of early balloon deflation.
Intra-aortic balloon pressure tracing showing the timing error of late balloon deflation.
Chest radiograph demonstrating proper positioning of an intra-aortic balloon pump catheter. Major landmarks are annotated on the radiograph.
Impella device positioned in the left ventricle. Blood from the left ventricle is pulled into the inlet area and expelled through the outlet distal to the aortic valve by a motor integrated into the catheter system.
Intra-arterial positioning of an intra-aortic balloon pump (IABP). Used with permission from Radiopaedia.org (http://radiopaedia.org/cases/intra-aortic-balloon-pump-and-icu-lines).
Table. Summary of Available Intra-aortic Counterpulsation Catheters
Manufacturer Balloon Catheters (Brand Name) Nominal Balloon Volume, mL/Catheter Size, F Maximum Guidewire Caliber, in Maximum Insertable Length, mm
Maquet/Datascope MEGA 50/8, 40/7.5, 30/7.5 0.025 723
Fidelity 25, 34, 40/8 0.025 723 (25-40 mL)
Linear 25, 34, 40/8 0.025 723 (25-40 mL)
Sensation (fiberoptic compatible) 25, 34, 40/7 0.025 714 (25-40 mL)
Arrow Ultraflex 30, 40/7.5; 50/9 0.025 643 (30 mL)



693 (40, 50 mL)



Ultra 8 30, 40/8 0.025 643 (30 mL)



693 (40 mL)



Narrowflex 30, 40/8 0.03 643 (30 mL)



693 (40 mL)



RediGuard 30/7, 40/8, 50/9 0.025 693 (30-50 mL)
Fiberoptix (fiberoptic compatible) 30, 40, 50/7.5, 8, 9 0.025 643 mm (30 mL)



693 mm (40 mL)



660 mm (50 mL)



Abiomed iPulse 40/8 0.025 720 mm
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