Percutaneous ventricular assist devices (pVADs) increasingly are being used in patients with cardiogenic shock (CS) as a bridge to recovery, decision, durable device, or cardiac transplantation [1]. By far the most common cause of CS is myocardial infarction. However, acute regurgitant valve failure, myocarditis, postcardiotomy shock, and acute or chronic heart failure also may present with end-organ dysfunction from hypoperfusion due to cardiac pump failure, the hallmark of this syndrome.

Though fibrinolytics and primary percutaneous coronary intervention (PCI) have improved mortality in patients who experience shock from acute myocardial infarction, little progress in the medical treatment of cardiogenic shock has been made over the last few decades; overall mortality remains greater than 40% [2]. The mainstay of medical treatment continues to be inotropes and vasopressors, but when used to temporize the patient hemodynamically in the short term, it actually contributes to end-organ dysfunction, arrhythmia, increased myocardial oxygen consumption, and increased mortality in the long term [3]. Frequently, they do not provide enough support to maintain adequate perfusion and hemodynamic stability. Unfortunately, once end-organ dysfunction occurs, it not only leads to increased mortality but can prevent the patient from being a candidate for advanced heart failure therapies such as durable ventricular assist devices or cardiac transplantation. In conditions where myocardial recovery is possible, medical therapy may not provide enough support to keep the patient alive and preserve end-organ function until recovery can occur.

While some pVADs have been studied for temporary support during “high-risk” PCI, there has been far less research on the role of these devices in the end-stage heart failure patient. This chapter strives to explain how these devices can be utilized in this patient population.

Currently, there are multiple percutaneous devices available for use in end-stage heart failure patients, and the choice of device or devices is dependent on multiple variables. Is RV failure, LV failure, or biventricular failure present? How much hemodynamic support is needed? Does the patient have respiratory failure, circulatory failure, or both? Does the patient have any absolute or relative contraindications for a particular device? What is the ease and rapidity of device deployment and what is the available operator’s comfort deploying the device? What is the ancillary staff’s level of comfort and experience caring for a patient with the device? What is the next step in management of the patient? The answer to each of these questions is important to determine the most appropriate device for the patient. There is no one-size-fits-all device, and there often is not a single solution to a patient conundrum.

Ultimately, all pVADs serve as a bridge to something, whether it is recovery, decision, durable device, or cardiac transplantation. If the patient has a condition at baseline that precludes them from bridging to advanced therapies or recovery, a pVAD should not be placed. A candid conversation about the possibility of failure to recover or about conditions that disqualify the patient from advanced therapies should take place with the patient and family beforehand whenever possible.

The intra-aortic balloon pump (IABP) is the oldest and most widely used pVAD currently in use for left ventricular support. Invented in 1968, it works on the principle of counterpulsation to pressure unload the heart and, to a lesser extent, increase coronary perfusion [4–6]. The dual lumen catheter with a balloon at its distal end typically is inserted through the femoral artery and passed retrograde to the proximal descending aorta just distal to the ostium of the subclavian artery (◘ Fig. 29.1). It is then connected to the controller which causes the balloon to inflate and deflate with the timing of the cardiac cycle. One lumen is the channel by which the balloon is inflated, and a second lumen facilitates a guide wire for placement and transduces an aortic pressure tracing when the catheter is in place. Helium is used to inflate and deflate the balloon due to its low viscosity, allowing rapid movement of the gas into and out of the balloon. Helium is able to be more rapidly absorbed by the body in the case of balloon rupture, decreasing the chance of occurrence of a fatal air embolism. Inflation of the balloon during diastole causes both retrograde and antegrade displacement of blood, augmenting diastolic blood flow and pressure. The retrograde flow into the coronary arteries increases coronary blood flow (CBF), and the antegrade displacement increases forward flow to the body, increasing the mean arterial pressure (MAP). Rapid deflation of the balloon at the onset of ventricular systole creates suction, dropping the pressure in the aorta and thus raising forward flow. This decrease in pressure and increase in flow results in a reduction in afterload, decreased LVEDP, rise in stroke volume, and therefore cardiac output. Myocardial ischemia is reduced through multiple mechanisms including decreasing oxygen consumption by lessening ventricular wall tension and coronary microvascular resistance and improving CBF both through a rise in diastolic pressure and a drop in LVEDP. IABP has been shown to increase cardiac output by 0.5 L/min in patients with cardiogenic shock [4].

Technically, the IABP is easy to place. It requires only one arterial access, most commonly 8F, though other sizes are available. A radiopaque tip allows placement under fluoroscopy, but bedside placement with “guestimate distance” is feasible with position later confirmed by the use of a chest X-ray. An experienced operator can insert a balloon in approximately10 min. Insertion via the femoral artery prohibits ambulation, though safety and efficacy have been demonstrated with insertion through the subclavian, axillary, or brachial arteries [7]. These approaches should be performed under fluoroscopic guidance.

The IABP has some limitations. Its performance is dependent on a relatively stable electrical rhythm, intrinsic heart function, vascular tone, correct placement of the balloon in the aorta, and timing of balloon inflation and deflation. It has limited, if any, support in right ventricular failure. It should not be used in patients with more than mild aortic insufficiency as increasing diastolic retrograde flow would raise LVEDP and thus worsen their hemodynamics. Severe atherosclerosis or tortuous vessels can also be a contraindication to IABP placement. Potential complications include bleeding, infection, thrombocytopenia, limb ischemia, embolization to distal vessels including stroke, and compromise of subclavian or renal artery perfusion by forward or backward migration of the balloon. Vascular injury can occur at the entry site or at any point along the aorta including the ostia of the visceral arteries.

Earlier studies on IABP use in patients with myocardial infarction showed improved mortality or a trend toward it. The SHOCK trial demonstrated lower in-hospital mortality of patients with myocardial infarction who received IABP in addition to thrombolytic therapy or early revascularization with PCI or coronary artery bypass graft surgery [8]. GUSTO-I showed a trend toward improved 30 day and 1 year mortality in early IABP and thrombolytic therapy, although this improved mortality comes with an increased risk in bleeding [9]. Subsequent analysis of registry data showed this mortality benefit only held in patients undergoing thrombolytic therapy and not in cases of primary PCI [10]. Meta-analyses of IABP use in infarct-related cardiogenic shock cases not only showed no improvement in mortality but also demonstrated an increased risk of complications including stroke [11]. In spite of the current data, IABP is still widely used and has some class II indications in the current guidelines [12].

The challenge arises with patient selection. With its limited CO augmentation of 0.5 lpm, IABP provides little support when end-organ perfusion is impaired. It is more effective in ischemic situations or acute instability, but it rarely provides adequate support for a prolonged period of time. Thus, while helpful in the post-MI patient, it is not a good durable bridge strategy for more than a day or two. Consequently, if the recovery of end-organ function is not significant, which would reflect adequate hemodynamic support, escalation to next stage therapy is often needed. Most evaluations for transplant or LVAD cannot occur in a day, and, more often than not, the next level of support is another pVAD.

The TandemHeart^® (CardiacAssist, Inc., Pittsburgh, PA) is a continuous-flow pVAD that works in parallel with the heart to augment cardiac output and volume unload the heart. It is FDA approved for up to 6 h of support for procedures not requiring full bypass support, though there are reports of it being in excess of 3 weeks. The TandemHeart is a magnetically driven extracorporeal centrifugal pump that indirectly unloads the LV by transferring oxygenated blood from the left atrium to the iliac arteries and perfusing the aorta retrograde. Access to the left atrium is obtained by passing a catheter to the right atrium by femoral vein access and performing a transseptal puncture and dilation to place the 21F inflow cannula (◘ Fig. 29.2). The outflow cannula is placed in the iliac artery via access of the femoral artery with either a 15F or 17F cannula. In patients with smaller femoral vessels or with peripheral vascular disease, two 12F cannulae can be placed bilaterally to decrease the potential for vascular compromise. The amount of flow can range from 2.5 to 4 L/min depending on the size of the cannulae and the speed of the pump.

The TandemHeart decreases LV preload, filling pressures, and wall stress and improves peripheral tissue perfusion. Due to its parallel circuit to the heart and its unloading distally, stroke volume is reduced, and the ventricular afterload is increased. Though myocardial oxygen demand is lowered due to lessened preload and wall stress, this increase in afterload leaves the absolute effect on myocardial oxygen consumption dependent on the hemodynamic severity of the cardiogenic shock [5, 6]. This device must be placed under fluoroscopy or with intracardiac or transesophageal echocardiographic guidance by an operator skilled in transseptal puncture, often limiting this technology to larger, tertiary centers. Aortography with runoff should be performed before placement to evaluate the iliac arteries. Placement of the device takes 30–45 min when done by an experienced operator. Systemic heparinization is required, and the device is FDA approved for the addition of an oxygenator to the circuit for gas exchange.

Contraindications to placement of the TandemHeart include right or left atrial thrombus, moderate or severe aortic insufficiency, ventricular septal defect, bleeding diathesis and coagulopathies, or significant peripheral vascular disease. Possible complications include bleeding at insertion sites, cardiac perforation and tamponade, infection, and embolic events – including stroke, limb ischemia, vascular injury, hemolysis, desaturation from migration of the left atrial cannula, or right to left shunting, paradoxical embolus, arrhythmia, or creation of an ASD from transseptal puncture.

Though studies of its use in cardiogenic shock after AMI show the TandemHeart provides more support and improves hemodynamics to a greater degree than IABP, no mortality benefit has been demonstrated [13]. In studies powered to detect mortality benefit, an increased risk of bleeding and vascular complications has been seen. Small case series demonstrated utility using the TandemHeart as a bridging device to advanced therapies such as durable device [14] and transplant and as bridge to recovery [15].

Moreover, TandemHeart has been used with limited success to provide RV support in certain clinical conditions such as isolated RV failure from RV infarct and pulmonary hypertension, in conjunction with other PVADs for biventricular failure and for temporary RV support after placement of a durable LVAD [16]. For RV support, both the inflow and outflow cannulae are placed by venous access, usually in the bilateral femoral veins. The inflow cannula is placed in the right atrium and the outflow located in the main pulmonary artery to support and offload the RV. When the distance from the femoral vein to the pulmonary artery is too long, the outflow cannula can be put in the pulmonary artery via the internal jugular. With its highly technical insertion needs, only high volume, tertiary centers are capable of maintaining the skill set necessary for proficiency. Its flexibility to potentially provide biventricular support is a plus. It does have a tendency to migrate over time, and, like all pVADs, risks of complications rise with prolonged support.

The Impella Recover LP (Abiomed Inc., Danvers, MA) devices have become an increasingly popular pVAD option due to their ability to deliver a significant amount of support and their relative ease of deployment requiring only a single arterial access.

The Impella 2.5 and Impella CP are the most commonly used iterations of the Impella family of devices, and they are installed using the same platform [17, 18]. A miniature axial flow pump is mounted on a pigtail catheter, and using standard catheterization techniques, it is passed retrograde across the aortic valve and placed in the left ventricular cavity with TEE or fluoroscopic visualization (◘ Fig. 29.3). Blood is pumped from the left ventricle through the inlet into the proximal ascending aorta by continuous flow. Up to 2.5 and 3.5 L/min of flow can be delivered by the Impella 2.5 and Impella CP, respectively. The amount of flow is dependent on the size of the pump, the speed of the impeller, and the pressure gradient between the ventricle (inflow) and aorta (outflow).

The Impella 2.5 is indicated for up to 6 h of use during high-risk PCI to prevent hemodynamic instability. The Impella CP is indicated for up to 6 h for partial circulatory support in procedures not requiring cardiopulmonary bypass. Studies comparing the Impella 2.5 and Impella CP with IABP in patients in cardiogenic shock associated with AMI showed superior hemodynamics in the Impella group, but to date there is no mortality benefit [17, 18].

The Impella 5.0 operates with the same type of pump as the Impella 2.5 and CP, but due to its large size it requires a surgical cut down for catheter placement. This procedure can be performed by the CV surgeon or a vascular surgeon in conjunction with a cardiologist. The Impella 5.0 generates a larger amount of flow, up to 5 L/min, than the Impella 2.5. Though the Impella 5.0 was developed initially for femoral artery access, placement in the axillary or subclavian artery (◘ Fig. 29.4) is safe and effective in providing support with the added benefit of allowing the patient to sit in a chair, ambulate, and rehabilitate while it is in place [17, 18].

Indications for the use of the Impella 5.0 are circulatory support with no cardiopulmonary bypass or circulatory support using an extracorporeal bypass control unit for up to 6 h, but it can provide adequate support for over 45 days [17, 18]. Case studies demonstrated successful utilization of the Impella 5.0 as bridge from ECMO to durable device [19], as support in acute rejection after orthotopic heart transplantation [20], for LV support in RV failure as a bridge to RV recovery and durable LVAD [21], as bridge to recovery in myocarditis [22], and as bridge to cardiac transplantation [23]. Results from some small case series suggest survival improved in patients with severe and profound shock after ST elevation myocardial infarction with immediate Impella 5.0 treatment compared to Impella 2.5 support alone [24].

Contraindication to placement of any of the Impella LP devices includes moderate or greater aortic insufficiency, the presence of a mechanical aortic valve, aortic stenosis with valve area less than 1.5 cm², a heart constrictive device, severe PVD that would impair the ability to place the device, or LV thrombus. The potential complications include bleeding, infection, vascular injury, hemolysis, stroke, cardiac perforation or tamponade, damage to the aortic valve, device malfunction, or arrhythmia. Hemolysis from mechanical shearing can also occur in 5–10% of patients but usually responds to device repositioning. If renal failure from persistent hemolysis occurs, the device should be removed.

Development of the Impella device greatly expanded the temporary support world for end-stage heart failure patients. With growing resistance to implanting durable VADs in the INTERMACS 1 patient, the Impella 5.0 allows adequate hemodynamic support for these patients, appropriate end-organ recovery of function, and a higher rate of success for the eventual cardiac replacement option. With the axillary implant option, these patients can also avoid the deconditioning that results from groin access mandatory bed rest restrictions. While the Impella 5.0 does require a mini-surgical approach, the single vessel access, no need to cross cardiac chambers and axillary implantation makes it poised to be the most currently balanced device for intermediate support in this patient population.

Extracorporeal membrane oxygenation (ECMO) offers pulmonary or cardiopulmonary support depending on its configuration. With its improved technology, it is having a “comeback” of sorts.