Mechanical Circulatory Assist Devices

Mechanical Circulatory Assist Devices

Michael A. Chen*

*Debra Laurent and Julie A. Shinn are authors of Nursing Care Plan 26-1

Mechanical circulatory assist devices have been used since the 1960s. Intra-aortic balloon pump (IABP) catheters are the most commonly used devices. Other circulatory support devices, once restricted to a few large centers, are now becoming more widely available for temporary use in the cardiac catheterization laboratory, as an adjunct to cardiac surgery, as well as being implanted for short-, intermediate-, and even long-term ventricular assistance (i.e., “destination therapy”). Such devices are used to support circulation temporarily when the injured (left or right) ventricular myocardium cannot generate adequate cardiac output. One such device has been used successfully to support a patient for nearly seven and a half years.1 With the aging of the population and the improved treatment of coronary artery disease and myocardial infarction (MI), the incidence of heart failure is increasing; in the coming years the numbers of patients who have acute severe and end-stage heart failure will increase. Typically, less than 2,500 patients per year receive cardiac transplants in the United States due to a limited donor pool, making mechanical assist devices an important long-term therapy as well.2 In November 2002, the Food and Drug Administration approved the use of the HeartMate (Thoratec Laboratories, Inc., Pleasanton, CA) left ventricular assist device (LVAD) for permanent or destination therapy in patients who are not appropriate candidates for heart transplantation.3

With early recognition, the often rapid hemodynamic deterioration of patients with acute left ventricular (LV) failure can be arrested with circulatory assist devices. The type of device used depends on the degree of myocardial injury, the degree of LV functional impairment, the anticipated length of therapy as well as other factors (including what is available locally). The purpose of therapy is to stabilize the patient until: (1) the left ventricle recovers from acute injury; (2) mechanical problems causing acute failure (e.g., ruptured ventricular septum) can be surgically corrected; (3) heart transplantation can be performed; or (4) a decision is made to place a device as “destination therapy,” for patients who are not candidates for transplant. The goal of a circulatory assist device is to stabilize or improve hemodynamics and secondary organ function. The major principles governing all devices are that they: (1) decrease or take over LV workload; (2) enhance oxygen supply to the myocardium; and (3) partially or totally support the systemic circulation and thus, other organ perfusion. The extent to which each principle can be achieved depends on the type of device used. An IABP offers only partial support, whereas implantable right ventricular assist devices (RVADs), LVADs, and BiVADs can assume the total workload of the right, left, or both ventricles, respectively. In addition, there are devices that provide intermediate levels of support. Most cardiovascular critical care nurses encounter patients requiring IABP support. In addition, this chapter will describe other types of circulatory assist devices.


The IABP was introduced in the late 1960s as a therapy for cardiogenic shock after MI.4 Since then, its application has expanded to include patients with other etiologies of acute LV failure, including before or after cardiac surgery, from acute myocarditis, and in patients with chronic heart failure who experience acute hemodynamic deterioration. Other indications include support during high-risk percutaneous coronary intervention (PCI), reducing major adverse coronary events and procedural complications.5,6 They can be used for patients with unstable angina, refractory ventricular arrhythmias (particularly when ischemia driven), and for patients with mechanical complications of acute MI, such as papillary muscle rupture or ventricular septal rupture, as a bridge to surgical repair. It is estimated that over 70,000 IABP are placed each year in the United States alone.4 Display 26-1 lists the most common indications for IABP placement from a review of nearly 17,000 patients who received the therapy from 1996 to 2000.7


The intra-aortic balloon is constructed of a biocompatible, nonthrombogenic material and mounted on a catheter constructed of the same material. An opening at the catheter-balloon connection allows pressurized gas (usually helium) to move in and out of the balloon, causing inflation and deflation to occur. Most catheters have two lumens: an inner lumen for central pressure monitoring at the catheter tip and a second lumen for the gas. Properly positioned, the distal tip of the balloon catheter rests just distal to the origin of the left subclavian artery and the proximal end of the balloon is positioned proximal to the renal arteries. Figure 26-1 illustrates proper anatomic position of the IABP catheter. (See Figure 12-3 in Chapter 12.) The tip of the catheter is radio-opaque so that its position can be verified with a chest x-ray. The catheter is inserted via a direct femoral or iliac arteriotomy or by percutaneous insertion using the Seldinger technique with or without a sheath. Although a direct arteriotomy approach is rarely used today, prior designs made it mandatory, and it may still be the optimal choice for a patient with severe peripheral vascular disease (when direct visualization is desired) or for pediatric patients. The approach requires an incision in the groin for access to the femoral or iliac artery. This technique is more invasive and time consuming, and requires surgical removal. The percutaneous technique is faster, less
invasive and allows for easy bedside removal. In all catheters, the balloon is wrapped tightly around its own guide wire so that it slides easily through a sheath or directly into the artery. Once in proper position, the balloon is inflated, resulting in unwrapping of the balloon, allowing inflation and deflation to commence. This catheter is secured to the skin by sutures. Figure 26-2 illustrates the percutaneous insertion technique utilizing an introducer sheath.

A newer design (SupraCor) has recently been introduced. This device can be placed in the ascending aorta for use after cardiac surgery. In an animal model, the device was shown to increase blood flow in saphenous vein and internal mammary bypass grafts, when a standardly placed IABP did not.8

Physiologic Principles

The two goals of IABP therapy are to increase coronary artery perfusion pressure and thus coronary artery blood flow, and to decrease LV workload by lowering LV afterload. These goals are achieved by displacement of volume in the aorta during systole and diastole with alternating inflation and deflation of the balloon. A typical adult-sized balloon contains 40 mL of gas or volume. For smaller adult patients, a 35-mL balloon is available; for larger patients, a 50-mL balloon is available. Placing a smallersized balloon (shorter) in smaller patients is important because a larger (longer) balloon could extend into the abdominal aorta, potentially compromising blood flow to the renal vasculature or even the lower extremities and exposes the balloon to abrasion (and even rupture) from calcified abdominal aortic atherosclerotic plaques.

Figure 26-1 Proper placement of the intra-aortic balloon catheter is just distal to the left subclavian artery and proximal to the renal arteries. (From Shinn, J. A. [1986]. Intra-aortic balloon pump counterpulsation. In C. M. Hudak, B. M. Gallo, & T. S. Lohr [Eds.], Critical care nursing: A holistic approach [4th ed., p. 190]. Philadelphia: J.B. Lippincott).

Figure 26-2 Percutaneous insertion of the balloon catheter through an introducer or sheath. Note the right wrap of the balloon. (From Bull, S. O. [1983]. Principles and techniques of intra-aortic balloon counterpulsation. In S. L. Woods [Ed.], Cardiovascular critical care nursing [p. 171]. New York: Churchill Livingstone.)

The size of the catheters range from 7 to 9.5 French. When the balloon is rapidly inflated at the onset of diastole, an additional 35 to 50 mL (depending on the balloon size) of volume is suddenly added to the aorta. This acute increase in volume creates an early diastolic pressure rise in the aortic root (where the coronary ostia lie), increasing coronary artery perfusion pressure. Figure 26-3 illustrates this effect. Because ischemic coronary beds are maximally vasodilated, no further autoregulatory increases in flow are possible, and flow is pressure dependent.9, 10, 11 IABP inflation provides this enhanced pressure. The early diastolic pressure increase is referred to as the diastolic augmentation. Diastolic augmentation increases coronary perfusion pressure and in addition, by increasing overall mean arterial pressure, also contributes to enhanced flow to other organs.

This augmented diastolic pressure gradually falls, as diastolic pressure normally does when diastolic run-off occurs. Rapid evacuation of gas out of the balloon during deflation removes 35 to 50 mL of volume (the same amount used in inflation) out of the aorta. This sudden drop in aortic volume rapidly decreases pressure. Deflation is timed to occur at the end of diastole, just before the patient’s next systole. Effective deflation, which decreases end-diastolic pressure, decreases the impedance or afterload that the ventricle must contract against to open the aortic valve and sustain ejection during systole. The lower the impedance, the lower the wall stress, and, therefore, the lower the LV workload. In cardiogenic shock, high systemic vascular resistance contributes to greater impedance, resulting in a greater workload for the failing
left ventricle. With properly timed deflation, which lowers end-diastolic pressure and impedance to ejection, the LV workload is reduced. Figure 26-4 illustrates this effect. Systolic pressure is decreased when deflation of the balloon is timed properly. As a result of decreased afterload, there is more effective forward flow during systole. Improved forward flow contributes to decreased endsystolic volume in the ventricle. Improved emptying leads to decreased subsequent preload, which also contributes to decreasing LV workload. Cardiac output is increased and so is the mean arterial pressure. The need for compensatory tachycardia is reduced and heart rate is expected to fall, further decreasing myocardial oxygen demand. Better systemic perfusion helps to reverse the acidosis often seen in shock and improves secondary organ dysfunction related to the previous hypoperfused state. Although there is significant patient-to-patient variability, the expected beneficial outcomes of IABP therapy are listed in Displays 26-2 and 26-3.10,12

Figure 26-3 Balloon inflation during diastole displaces volume retrograde toward the aortic root. The result is increased coronary artery perfusion pressure. Enhanced distal flow may also occur. (From Quaal, S. J. [1984]. Comprehensive intra-aortic balloon pumping [p. 82]. St. Louis: C.V. Mosby.)

Figure 26-4 Impedance or resistance to left ventricular (LV) ejection is decreased by abrupt balloon deflation before systole. Properly timed deflation decreases aortic end-diastolic pressure (A0EDP), which decreases the workload of the left ventricle. (From Quaal, S. J. [1984]. Comprehensive intra-aortic balloon pumping [p. 83]. St. Louis: C.V. Mosby.)


Because inflation of the balloon during diastole increases pressure in the aortic root, significant aortic regurgitation is a contraindication to IABP therapy. Inflation would otherwise increase regurgitation and thus LV workload. The presence of an aortic aneurysm is also a contraindication to IABP therapy. Trauma or rupture of the aneurysm can occur during IABP insertion. Dislodgement of adjacent thrombus can occur during insertion or from balloon inflation resulting in embolization. These risks are all unacceptable. Severe peripheral vascular occlusive disease in the femorial or iliac artery contraindicates IABP therapy. Catheter insertion may be difficult or impossible, and occlusion of the affected vessel, dissection, and dislodgement of plaque from the vessel wall are all possibilities as well. These potential problems can be avoided by selecting an alternate method of insertion. In the cardiac surgery patient, the catheter may be inserted directly into the thoracic aorta, although this method requires reopening the sternotomy incision to remove the catheter. The catheter can also be placed antegrade in the aorta via the right subclavian/axillary artery.13 This approach requires a subperiosteal clavicular resection to access the artery, but is less invasive than a sternotomy incision. Newer catheters of smaller diameter minimize the risk of occluding distal blood flow. In addition, the ascending aorta device described above (SupraCor) could be considered. Uncontrolled sepsis and coagulopathy are other contraindications. Lastly, if invasive therapies are contrary to the goals of care (e.g., comfort care in a patient who is very unlikely to survive despite even heroic measures), IABP therapy should not be utilized.

Proper Timing and Expected Clinical Outcomes

Proper timing of IABP therapy is crucial to achieving the beneficial hemodynamic changes described above. Proper timing requires coordination of inflation and deflation of the balloon with the patient’s cardiac cycle. To evaluate balloon timing properly, the assist ratio is set at 1:2, meaning the balloon is assisting every other cardiac cycle. In this way, the observer can compare the effect of balloon inflation and deflation with unassisted beats. Most patients tolerate this ratio well, at least for a brief period. The R wave from the ECG, pacemaker spikes on the ECG, or the arterial systolic pressure can be used to identify individual cardiac cycles. Each can act as signals for the IABP console to discriminate systole from diastole. The R wave signals the onset of electrical depolarization, which immediately precedes mechanical systole. A ventricular pacemaker spike essentially represents the same event. Arterial systolic pressure signals the onset of mechanical systole. Any of these reference points can be used to determine when deflation of the balloon should optimally occur. An arterial waveform is necessary to determine the onset of mechanical diastole and systole and to verify timing. Diastole has begun when the dicrotic notch (which results from aortic valve closure) appears on the arterial waveform. Balloon inflation is timed to occur at this point in the cardiac cycle. The deflation point can be optimally adjusted by observing the end-diastolic drop in pressure created by balloon deflation. The goal is to create the greatest pressure drop possible. Ideally, there would be at least a 10 mm Hg difference between end-diastolic pressure without the balloon effect and the end-diastolic pressure created by balloon deflation. Evidence that afterload reduction has occurred is seen in the following systolic pressure. With afterload reduction, the next systolic pressure after balloon deflation is lower than the systolic pressure with no balloon effect, which is evidence that LV workload has been decreased. Five criteria can be used to determine the effectiveness of IABP timing, as illustrated on the arterial pressure tracing (Fig. 26-5) and detailed below.

Figure 26-5 Criteria for effective intra-aortic balloon pump (IABP) timing: (1) inflation occurs at the dicrotic notch; (2) the slope of rise of balloon inflation is straight and runs parallel with the preceding systolic upstroke; (3) augmented diastolic pressure is at least equal to the preceding systolic pressure; (4) end-diastolic pressure at balloon deflation is lower than the preceding unassisted end-diastolic pressure; (5) the next systolic pressure is assisted systole and is lower than the preceding systole, which was not affected by balloon deflation. (From Shinn, J. A. Intra-aortic balloon pump counterpulsation. In C. M. Hudak, B. M. Gallo, & T. S. Lohr [Eds.], Critical care nursing: A holistic approach [5th ed., p. 213]. Philadelphia: J.B. Lippincott, 1990.)

  • Criterion 1. Inflation must occur at the dicrotic notch, which is the beginning of diastole. Inflation actually should be timed to obliterate the notch. The interval between the onset of systolic upstroke and the point of balloon inflation should not be shorter than the interval between the systolic upstroke and dicrotic notch on the unassisted beat. Inflation that occurs too early can abbreviate systole by causing premature aortic valve closure, reducing stroke volume, and therefore cardiac output. Late inflation (past the dicrotic notch) shortens the duration of assistance, thus reducing the period of maximal augmented diastolic pressure.

  • Criterion 2. The upstroke of balloon inflation should be sharp and parallel with the preceding systolic upstroke. This inflation creates a V-shaped appearance, with the nadir of the V being the point of inflation. The sharp upslope ensures that maximal early augmentation is occurring. A slope that is not straight may indicate that the balloon is inflating late, perhaps mistiming off of an artifact during early diastole. In this case, the loss of the V configuration also is evident.

  • Criterion 3. The augmented diastolic pressure peak should be at least equal to the preceding systolic pressure peak. A decrease in this pressure peak may indicate gas loss from the balloon. This loss can occur by natural diffusion. A balloon normally requires refilling every 1 to 2 hours because of natural diffusion of gas through the membrane. Most consoles automatically purge and
    refill the balloon and catheter at least every 2 hours. An abrupt loss of the pressure peak may indicate the development of a balloon or catheter leak. Occasionally, augmentation greater than the systolic pressure is not achievable because the balloon is too small relative to the aorta. Ideally, the balloon should occlude 85% to 90% of the aorta when fully inflated. If there is a size mismatch, diastolic augmentation pressure may be reduced, and may even be less than the patient’s systole.

  • Criterion 4. The balloon deflation should occur at the end of diastole. Proper deflation results in a drop in pressure at the end of diastole. This drop in pressure creates an end-diastolic pressure much lower than diastolic pressure without the balloon effect. Timing is adjusted so that the lowest pressure possible is achieved. It is important to make sure that the systolic upstroke that follows is straight and that a sharp, V-shaped configuration is present. The V shape indicates that systole began immediately after deflation. Any plateau indicates that deflation occurred too early, diminishing (or obliterating) the intended reduction in afterload. Late deflation, on the other hand, results in higher impedance because the balloon remains inflated at the onset of systolic ejection, creating more work for the LV. An end-diastolic pressure that is the same or greater than the end-diastolic pressure without balloon assistance is evidence of late deflation. The systolic pressure in the following beat may be the same or lower than the unassisted systole because of the inability of the failing ventricle to work against the higher impedance to ejection.

  • Criterion 5. Finally, the observer should note what effect balloon deflation has on the next systolic pressure, for the reasons just described. The goal is to ensure that the lower systolic pressure that follows balloon deflation is caused by afterload reduction and not by improper timing, which resulted in late deflation. Proper balloon fit has an impact on the ability to achieve afterload reduction. If the balloon size is small, then volume displacement may have less of an effect on lowering end-diastolic pressure. Figure 26-6 illustrates the four possible errors that can occur with timing.

Figure 26-6 Possible errors in balloon timing. (From Shinn, J. A. [1986]. Intra-aortic balloon pump counterpulsation. In C. M. Hudak, B. M. Gallo, & T. S. Lohr [Eds.], Critical care nursing: A holistic approach [4th ed., p. 198]. Philadelphia: J.B. Lippincott.)


IABP therapy carries a relatively low risk of additional morbidity in a generally sick population. In the series of nearly 17,000 patients with IABPs placed (from 1996 to 2000) mentioned above, the incidence of any complication was 7% and major complications (i.e., severe bleeding, major acute limb ischemia, death from IABP insertion, or failure) was 2.6%.7 Vascular complications have been reported to range from 6% to 25% of cases depending on the report.14, 15, 16 Vascular injuries include plaque dislodgement, dissection, laceration, and compromise of the circulation to the distal extremity. Peripheral nerve injury is another possible complication of insertion (particularly if a cut down approach is used). Compromised circulation can occur any time during IABP therapy as a result of the presence of the indwelling catheter, compartment syndrome, or embolus from thrombus formation along the catheter or on the balloon.17 The incidence of limb ischemia ranges from 5% to 35%.17,18 Although intravenous heparin is generally used with IABP, there is little evidence that heparin reduces limb ischemia, and one randomized trial of 153 patients did not find a difference in such events.19

Complications are more common in patients with peripheral vascular occlusive disease, in women, those who are smaller (body surface area [BSA] <1.8 m2), and in patients with a history of stroke, transient ischemic attacks, and diabetes.7,17,20, 21, 22, 23 Risk is decreased with sheathless insertion and with smaller balloon sizes.22,24,25 In addition, operator’s and hospital-staff’s experience likely play a part.26 Nurses monitor for and prevent compromised circulation by carefully assessing peripheral perfusion; preventing the patient from flexing the hip of the affected extremity, which may compromise blood flow; and maintaining coagulation times within prescribed parameters by careful titration of any prescribed anticoagulants. The nurse should be aware that multiple or prolonged attempts at insertion increase the risk of vascular injury and thrombus formation. Infection at the insertion site is reported to occur in less than 5% of patients, with an increase risk after 7 days of therapy. Insertion site infections may dictate the removal of the IABP catheter. Careful efforts must be made to maintain the sterility of insertion site dressings. Other problems that may be encountered include thrombocytopenia; compromised circulation to the left subclavian, renal, or mesenteric arteries because of balloon malposition; and bleeding from the insertion site or other line insertion sites. Mechanical problems related to the balloon include improper timing or a leak or perforation in the balloon, necessitating its removal. A leak in the balloon becomes evident as augmentation becomes less effective. Eventually, blood backs up in the catheter and can be detected. When a leak has occurred, the balloon must be removed immediately to avoid the possibility of gas embolus or balloon entrapment. Entrapment occurs when blood enters the balloon and becomes a large, hardened mass. The size makes it difficult to remove without a surgical intervention.

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Jan 10, 2021 | Posted by in NURSING | Comments Off on Mechanical Circulatory Assist Devices
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