Diastole and Coronary Blood Flow

Because the majority of coronary flow occurs in diastole, an increase in diastolic pressure has the potential to augment coronary flow as well as flow to other end organs. Diastolic pressure may in fact be augmented substantially, in part because balloon inflation is rapid, yielding an abrupt increase in volume and effecting a rapid rise on the pressure-volume curve. A variety of physical and biologic parameters, including compliance characteristics of the aorta and vascular bed, affect the degree of augmentation.¹⁶ The extent of peak pressure rise has been reported in a range from minimal to near doubling of diastolic pressure.^17,18 However, increase in diastolic pressure and hence coronary perfusion pressure may not result in an increase in coronary flow because autoregulation modulates this potential and because in normal patients, end organs capable of autoregulation maintain flow without significant change.

Despite both several decades of experimentation in animal models and attempts to assess coronary flow in a variety of clinical settings in humans, the effect of IABP on coronary flow remains incompletely defined. Experimental and clinical data fail to show change in flow in native coronary arteries19,20 or in bypass grafts²¹ regardless of the severity of coronary stenosis.²² Although total coronary blood flow may not increase, coronary blood flow velocity has consistently been demonstrated to rise.^17,23,24 In turn, data from a thrombolysis in myocardial infarction (MI) model suggest that the pulsatile waveform generated by IABP during diastole may contribute to improved time to coronary reperfusion without concomitant increase in coronary blood flow;²⁵ in all likelihood this improvement reflects the enhancement in peak flow velocity that may also help prevent reocclusion.²³ However, pulsatile flow may have additional benefit: in a randomized study comparing cardiopulmonary bypass with or without concomitant IABP, multiple parameters of whole-body perfusion were superior in the pulsatile flow setting.²⁶ In general, augmentation of blood flow appears most likely to occur in patients in profound shock.^17,24,27 Thus, most of the benefits of IABP are related to improvement in hemodynamics with secondary relief of ischemia. Amelioration of ischemia may in turn result in improved LV function and additional improvement in hemodynamics.

Systole and Myocardial Mechanics

Although the IABP is generally described as both improving myocardial oxygen supply and lowering myocardial oxygen demand, the predominant effect is the latter. This is based on decreased afterload and wall stress with increased stroke volume and cardiac output, in particular in patients with low-output states. In general, the magnitude of hemodynamic response is proportional to the extent of depression of cardiac function.¹⁶ Because stroke volume improves, heart rate stays the same or tends to decrease even as cardiac output rises. Reduction in LV end-diastolic pressure and improved cardiac output is associated with lower left ventricular heart filling and pulmonary arterial pressures, whereas systolic pressure typically decreases and mean blood pressure stays the same in hemodynamically stable patients. In patients in shock, mean blood pressure rises and systolic pressure may increase as well. When IABP placement results in improved end-organ perfusion, as evidenced by signs such as better urine output, the overall prognosis is generally improved.¹² Reduction in left-sided heart filling and pulmonary artery pressures also leads to reduced right ventricular (RV) afterload; thus, IABP insertion may be helpful in some patients with right-sided heart failure.²⁸ Although ejection phase indices tend to improve with unloading, the extent of augmentation of cardiac output is limited by the overall reserve in LV systolic function. Thus, at the extremes of ventricular dysfunction, even with excellent positioning of the balloon and timing as well as large IABP volumes, the IABP may not provide sufficient augmentation of cardiac output in some patients. A variety of other parameters have been used to assess the effect of IABP in shock, most prominently the cardiac power index (mean systemic pressure times cardiac index), which is the strongest hemodynamic correlate of outcomes.²⁹

Effects on Organs Other Than the Heart

The effect of IABP on flow to end organs other than the heart is also incompletely characterized. In the cranial circulation, as in the heart, net flow does not appear to increase in patients with a stable hemodynamic state. Further, with balloon deflation, there is some evidence for transient reversal of blood flow as well,³⁰ although this may be a consequence of early deflation (see discussion under “Timing”). Similarly, overall carotid flow is not changed in this setting.³¹ During hypothermia while patients are under cardiopulmonary bypass, pulsatile augmentation as obtained by the IABP does appear to improve cerebral oxygenation.³² Indirect evidence again suggests additional benefit in the setting of shock, with better cerebral blood flow, a setting in which there is modest clinical experience with using IABP in patients with refractory cerebral vasospasm.³³ Despite improvement in cardiac output with IABP, gastric tonometry has not shown improvement in the splanchnic circulation in CS patients,³⁴ and renal vein thermodilution has failed to show improvement in overall renal blood flow.³⁵ In cardiac surgery patients who subsequently developed low-output syndrome, however, IABP did have a positive effect on gastric tonometery.³⁶

Balloon Dimensions

The available IABP catheters range in gas volume from 25 to 50 mL and in shaft lengths from approximately 60 to 72 cm. The actual length of the balloon segment varies by manufacturer and balloon volume: Commercial balloon lengths are in the range of 16.5 to 26 cm. Although balloon volume does affect the degree of diastolic augmentation³⁸ and cardiac output³⁹and may be particularly important in patients with severe, refractory CS, little difference was found in IABP effectiveness between 32-mL and 40-mL balloons in one study,⁴⁰ and risk to the patient is significantly higher if inflated balloon diameter approximates or exceeds aortic diameter (see “Complications”). Thus the decision for IABP size is typically based on patient size and severity of hemodynamic compromise, with the 40-mL balloon used in approximately three fourths of patients.⁴¹ A special consideration for balloon volumes is patient air transport; rapid changes in altitude will lead to increased (during ascent) or decreased (with descent) volume, requiring monitoring to ensure that appropriate balloon volume is maintained.⁴²

Because it is essential to locate the balloon below the origin of the left subclavian artery at the upper margin and above the renal arteries at the lower (a “safe zone”; Fig. 7.4), the tolerances are relatively low. Studies looking at the length of this segment in Japanese patients found a range of 21 to 25 cm, with good correlation between patient height and length of this segment (although in the relatively short Japanese population, the balloon lengths frequently exceeded the “safe zone” length for individual patients).⁴³ Recommendations vary by manufacturer: A 50-mL size I is generally recommended for patients taller than 6 feet (183 cm), and the 25-mL is used for patients shorter than 5 feet (152 cm). Recent changes in technology have allowed for larger diameter balloons to be available for shorter patients (e.g., a 50-mL IABP on an 8 F shaft is now available for patients 5′4″ [162 cm] and taller). In general, larger balloon sizes lead to improved unloading and augmentation with greater blood volume displacement. Early balloon models were designed to be occlusive during inflation, and experimental data have demonstrated optimal augmentation with 100% occlusion of the aorta.^38,39 Such full occlusion is generally avoided because of potential trauma to the aorta, ischemia to the spinal circulation, or abrasion of the balloon, which might contribute to a risk of rupture. The generally accepted value for ratio of balloon to aorta size is 80% to 90%; in the study by Igari⁴³ in Japanese patients, the range of commercially available balloon diameters was noted to be 14 to 15 mm, whereas aortic diameter mean at the level of the renal arteries was 17.5 ± 3.2 mm, within the accepted 80% to 90% range, although at least one 50-mL balloon has an expanded diameter of 18 mm (Arrow International, Inc., Reading, PA). In an earlier study in Americans, 90% of midthoracic aortas were larger than 19 mm.⁴⁴ Balloons are typically made of polyurethane or polyethylene, with materials chosen to allow rapid inflation-deflation cycles and tolerate an average of 100,000 to 150,000 cycles per day. Experimental materials with heparin and hydrophilic coatings have been developed to address thrombosis risk and trauma to the vasculature during device passage^45,46 but are not generally available.

Balloon Console

IABPs are driven by complexly engineered consoles with extensive artificial intelligence designed to recognize electrocardiographic rhythms and hemodynamics, with the ability to trigger balloon inflation either from the ECG (including paced rhythms) or from pressure waveforms, although in some settings, such as during cardiopulmonary bypass, an automatic trigger at a preset rate can be used. Tachyarrhythmias and irregular rhythms have substantial influence on the effectiveness of the IABP, the former in part because of the disproportionately shorter diastolic filling periods, and the latter because of difficulties predicting the timing of occurrence of the dicrotic notch, although improved algorithms have been incorporated.⁴⁷ The central lumen of the balloon is typically connected to a transducer and separate ECG leads are connected to the console. A series of alarms identify leaks in the IABP circuit, high or low pressure, loss of trigger signals, blood in the gas line, low battery, and other anomalies that foreshadow or indicate impending or existing system failures. (Figure 7.5 demonstrates the control panel of a modern IABP console.) Modern IABPs using fiber-optic technology permit automatic calibration in patients after insertion and automatic recalibration on a periodic basis or whenever the algorithms detect a change in patient condition.

Femoral Access

Every effort should be made to ensure that femoral puncture is above the femoral bifurcation and below the inguinal ligament (Fig. 7.7). An excellent practice is to place a short 5 F or 6 F pilot sheath in the femoral artery and to perform angiography of the common femoral artery to confirm sheath entry below the inferior excursion of the inferior epigastric artery; punctures above this landmark correlate strongly with retroperitoneal hemorrhage.⁵¹ Puncture below the femoral head drastically increases the likelihood of puncture into the femoral bifurcation vessels (77% of femoral bifurcations are at or below the inferior margin of the femoral head⁴⁹), which in turn is associated with acute leg ischemia due to vascular obstruction, and pseudoaneurysm formation upon balloon removal is more likely because of lack of the anvil of the femoral head against which to perform manual compression. If the pilot sheath is found to have entered outside the common femoral artery on femoral angiography, consideration should be given to switching to the contralateral side. Using fluoroscopy to aid in puncturing the common femoral artery at a point over the lower half of the femoral head is a recommended technique to ensure proper sheath placement.

Sheathless Insertion

The use of a sheathless insertion technique has been recommended to reduce complications.⁵² Sheaths typically add between 0.6 and 0.8 mm to the overall diameter required to place a device, so the sheath for an 8 F balloon approximates 10 F in outer diameter. “Going sheathless” therefore has the advantage of having the device occupy less space in the common femoral artery and has been described as reducing vascular complications with an odds ratio greater than 2 : 1.^53,54 Although retrospective analysis of large patient subsets presents compelling data that the sheathless approach is superior for reducing complications,⁵⁵ this finding has not been universally confirmed.^50,56 The latest data suggest that about 80% of IABPs are inserted with a sheath.⁴¹ The sheathless approach is most compelling in diabetic patients, women, and patients with known peripheral vascular disease or small body surface area. Sheathless insertion of an IABP requires careful preparation of the tissue track to allow atraumatic entry of the balloon tip into the artery directly through the skin over a wire. Spreading of tissue and predilatation with a dilator are essential. Fibrosed tissue tracks or thickened/calcified arterial walls frequently resist sheathless entry. In some cases, a stiff guidewire provides an adequate rail along which to slide the naked balloon catheter into the vessel.

Balloon Advancement and Positioning

Once suitable access is gained, guidewire passage to the aortic arch is ideally performed under fluoroscopic guidance. Without fluoroscopy at the bedside, approximating the distance from the femoral puncture to a point near the top of the descending aorta is imprecise and adds to the risk of trauma/ischemia to head and neck vessels, the aorta, or the renal arteries. In the critical care setting, transesophageal echocardiography is a suitable alternative to fluoroscopy for enabling precise balloon placement.⁵⁷ If fluoroscopy is not used, prompt postprocedure radiography to confirm location is imperative.

If guidewire passage meets resistance, alternative approaches include use of guidewires that are hydrophilic, steerable, or both.⁵⁸ If significant iliac stenosis is noted, balloon dilatation or stenting of the iliac artery is an accepted practice with high success rate both for achieving passage of the IABP and as an adjunct to preventing distal ischemia.^59,60 As more cardiologists become skilled in endovascular intervention, the ability to perform combined iliac stenting and IABP placement is expanding.⁶¹

Once the balloon has been advanced to a point 1 to 2 cm inferior to the left subclavian artery origin (see Fig. 7.4)—typically near the top of the descending aorta—the guidewire is withdrawn and the central lumen flushed. The vacuum port (minus its one-way valve) is connected to gas line tubing that in turn is connected to the console, and the dead space is purged and then filled with helium. The central catheter lumen is connected to a transducer on the console. After triggering is initiated, typically on every other beat, fluoroscopy should be used to confirm balloon location and filling, and pressure contours should be evaluated for appropriateness of timing (see later discussion under “Timing”). Once the timing is considered satisfactory, continuous pumping can be initiated. If necessary, the balloon should be repositioned with the console turned to standby to avoid trauma to the aorta.

The distal circulation should be assessed carefully after IABP placement. Distal ischemia is relatively common. The most likely cause of acute ischemia is obstruction of the artery by the catheter shaft itself. If ischemia occurs hours or days after insertion, the possibility of thrombus, typically secondary to stagnant blood in the confined space of a small or diseased vessel, should be considered as well. A technique for addressing distal limb ischemia—placement of a small sheath retrograde in the contralateral femoral artery and antegrade in the ipsilateral common femoral or superficial femoral artery—if performed by expert hands, can occasionally salvage an ischemic limb without forcing removal of the IABP⁶² (Fig. 7.8). There is some evidence that IABP inflation properties and hemodynamic effects may be superior in the patient positioned horizontally than with the patient tilted at a 30-degree angle.⁶³ Postprocedure and subsequent monitoring of left arm pressures can lead to early diagnosis of inadvertent balloon advancement obstructing left subclavian artery inflow, a phenomenon to which the restless patient who flexes the thigh is predisposed.

Alternate Access Routes

Multiple alternatives to percutaneous femoral access have been described, all associated with higher complication rates. In part, this difference in rates is selection related: Patients with severe peripheral vascular disease have multiple comorbid conditions that affect IABP complications. In addition, introduction of a balloon into a peripheral vessel smaller than the common femoral artery or into a large central vessel through a surgical approach of necessity creates hazards associated with the introduction, maintenance, and withdrawal of the IABP.

Approaches described to date include the brachial, subclavian, axillary, iliac, transthoracic, and translumbar arteries. Although the brachial approach has been successful in isolated cases,64,65 and sheathless entry reduces the overall diameter of lumen encroachment to less than 3 mm, the potential for complications is substantial. They include not only vascular injury and ischemia of the hand but also potential neurologic consequences from formation of thrombus on an indwelling catheter underneath the origin of the right common carotid artery (as the shaft traverses from the right subclavian artery to the innominate artery) as well as under the left common carotid artery and subclavian artery origin.⁶⁶

Iliac insertion through a conduit has been used for patients in whom femoral access is not adequate or who are not candidates for ventricular assist devices: With retroperitoneal placement, patients can be at least partially ambulatory during prolonged counterpulsation.⁶⁷ Other routes of access that have been described are via the subclavian⁶⁸ and axillary arteries,^69,70 with or without conduits, and generally with an eye toward allowing modest ambulation during prolonged IABP use. A transthoracic approach has been described, with placement via the ascending aorta into the standard descending aortic location.^71,72 The morbidity rate associated with these surgical placements is significantly higher,⁷³ in part because they typically involve longer IABP indwelling times as well as the comorbidity issues already mentioned.

Late Inflation and Early Deflation

Gross errors in inflation and deflation lead to failure to obtain benefit from IABP and occasionally to significant hemodynamic compromise. Early in the history of IABP deployment, it was appreciated that inflation throughout the period from closure of the aortic valve to its subsequent opening was necessary for optimal hemodynamic effect.¹⁶ Both late inflation and early deflation reduce augmented LV stroke volume and result in decreased peak diastolic coronary velocity;²³ the latter is demonstrated with transthoracic Doppler ultrasound, a tool that can potentially be used to optimize timing. An additional concern exists with early deflation: The abrupt decrease in IABP volume during diastole can lead to reversal of both coronary and other end organ (e.g., cerebral) flow back into the aorta, shunting blood from vital end organs.³⁰

Early Inflation

Early inflation results in increased afterload late in LV ejection with consequent impairment of LV systolic function. The ejection phase is shortened, LV end-systolic pressure rises, and stroke volume decreases; inflation, in the range of 130 to 190 ms before the dicrotic notch, results in a 20% decrease in stroke volume.⁷⁴ This effect may not be seen if early balloon inflation is less pronounced; no hemodynamic effect was noted when IABP inflation occurred 50 ms before the dicrotic notch. Regardless, although early inflation theoretically lengthens diastole and allows for a longer period of diastolic augmentation, the net effect does not appear to be salutary. In addition, early inflation carries theoretical risks associated with the increased afterload and wall stress, including aneurysm formation and rupture in the peri-MI period.

Late Deflation

Similarly, late balloon deflation could be expected to interfere with ventricular ejection and decrease stroke volume. In fact, somewhat counterintuitively, a similar 110- to 180-ms delay in IABP deflation appears to have salutary effects and is associated with a stroke volume increase of 18%,⁷⁴ which apparently results from both an increase in diastolic filling period and an augmented decrease in afterload later in the cycle. This finding confirms a prior observation by Kern and associates⁷⁵ and suggests that, in general, most operators have timed deflation too early. The beneficial effect occurs with timing deflation to be simultaneous with LV ejection; delaying deflation beyond the range described, however, raises concerns similar to those described for early inflation.

Electrocardiogram Triggering

When the ECG is used as the trigger, the descending slope of the T wave correlates best with the onset of diastole³⁸ and is the usual timing for balloon inflation. Deflation is typically timed to the R wave, which denotes a short time delay after the onset of electrical systole. Algorithms were developed early to effect prompt deflation and prevent inflation in the setting of ectopy, and IABP software recognizes pacemaker spikes in contrast to QRS complexes as well. As in the findings described previously,^74,75 deflation timed to the J point, with adjustment for the delay between onset of isovolumic systole and aortic valve opening, and perhaps slightly later, was shown early in the IABP literature to improve stroke volume.³⁸

Other Considerations

A common problem has been proper timing in patients with underlying arrhythmias. Atrial fibrillation has been particularly vexing, with unpredictable beat-to-beat intervals. An algorithm to predict the occurrence of the distance between the QRS and the dicrotic notch was developed in the mid-1990s.⁷⁶ Newer dicrotic notch prediction algorithms using high-fidelity micromanometer pressure sensors have been described.⁴⁷ However, atrial fibrillation poses difficulties beyond timing alone; rapid ventricular rates result in a disproportionate decrease in the diastolic interval and limit the effectiveness of IABP because of the inherently short period of counterpulsation,⁷⁷ including subtraction of the fixed time interval required for shuttling helium into and out of the balloon. Operating at 1 : 2 rates may be required in this setting.

Lack of augmentation despite proper timing should result in troubleshooting the IABP console, checking with fluoroscopy to visualize inflation of the balloon and confirm the level of balloon placement, and excluding kinking of the gas line or other mechanical failures. Apparently normal IABP function with absence of hemodynamic improvement should raise a suspicion that the patient has a baseline hemodynamic state that will not benefit from LV unloading, in particular hypovolemia, sepsis, or profound hemodynamic collapse, as well as a number of conditions described subsequently (see “Contraindications”).

Overall, timing of IABP should result in diastolic pressure augmentation and lowering of assisted peak systolic pressure when possible, with the former a generally used end point for patients with shock and the latter the primary goal in patients with more stable hemodynamics at the time of IABP insertion.

Cardiogenic Shock

The classic understanding of CS has been stunning or irreversible loss of a large amount of myocardium (≥40%) with resultant low output and compensatory elevated systemic vascular resistance to maintain central organ perfusion pressure. The definition of CS has varied, but the essential elements are persistent tissue hypoperfusion secondary to cardiac dysfunction in the presence of adequate filling pressure (and elevated left-sided heart filling pressure). The most common current definition is hypotension (blood pressure < 90 mm Hg systolic) for more than 30 minutes, with low cardiac index (less than 1.8 L/minute/m² without support or less than 2.2 L/minute/m² with support), and finally, elevated filling pressure (pulmonary artery wedge pressure > 15 mm Hg or LV end-diastolic pressure > 18 mm Hg or RV end-diastolic pressure > 10-15 mm Hg).⁹⁴ Data from the SHOCK (SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK) trial have called several classic assumptions into question,⁹⁵ in part because some of the patients in this trial with CS had relatively preserved ejection fractions, whereas other patients with apparently much larger amounts of dysfunctional or nonfunctional heart muscle were hemodynamically compensated.

Although the incidence of CS has declined,⁹⁶ it remains significant; the most recent estimates are that it is seen in approximately 6% of acute MIs. Mortality rate, once described as high as 80% (though variable in the literature, primarily because of the multiple definitions used), has declined in part because of better interventional tools,⁹⁷ because patients with coronary artery disease are receiving better long-term medical therapy, which in turn helps limit infarct size, and because the pharmacotherapy for CS itself has improved. Mortality rate remains high, however, with a nearly 40% in-hospital death rate reported in the Benchmark Registry.⁴⁸

IABP use in CS dates to the beginning of the IABP experience, and it results in predictable hemodynamic improvement in the majority of patients. IABPs have been shown to be beneficial in the setting of acute MI and CS when patients are not treated with PCI. The National Registry of Myocardial Infarction (NRMI) 2 compared results in patients with CS who received adjunct IABPs and those who did not.⁹⁸ Although mortality rate was not affected in patients undergoing primary angioplasty, those receiving only thrombolytic therapy had a significantly higher mortality rate (67% without IABP vs. 49% with IABP). Similar findings were shown in the SHOCK trial⁹⁹ as well as a meta-analysis of more than 10,000 STEMI patients with CS.¹⁰⁰ A small and underpowered randomized trial also suggested that patients with Killip class III or IV heart failure after MI have lower mortality rates when treated with fibrinolysis combined with IABP than when treated with fibrinolysis alone.¹⁰¹ There is some basis for these findings from animal data, which suggest improved reperfusion when thrombolysis without other intervention is combined with IABP use.²⁵

Mechanical Complications of Acute Myocardial Infarction

Afterload reduction has significant hemodynamic benefits in patients with abnormal unloading of the left ventricle into the right ventricle (ventricular septal rupture) or left atrium (severe mitral regurgitation).¹²⁰ The theoretical effect of counterpulsation in lowering afterload is in improving the ratio of forward flow through the aortic valve. The physiologic benefit in acute mitral insufficiency (mitral regurgitation) is widely accepted, resulting in a higher percentage of patients with severe mitral regurgitation and CS receiving IABP support than patients with CS alone.¹²¹ The mechanism of benefit appears to be lowered aortic impedance with consequent improvement in cardiac output, and modest decrease in regurgitant fraction.¹²² The IABP is in use in nearly all (98%) patients in this setting undergoing mitral valve repair, compared with less than half (43%) of those treated without surgery, a difference also influenced by selection issues. As with acute mitral regurgitation, 75% of ventricular septal rupture patients in the SHOCK registry underwent IABP placement.¹²³ Although systolic pressure did rise (from a median 81 mm Hg to 102 mm Hg) with institution of IABP in patients with ventricular septal rupture, mortality rate was dismal in both groups. In-hospital survival rate was only 13% with ventricular septal rupture, compared with 45% with severe mitral regurgitation. Nevertheless, IABP use is an essential element of intervention in acute ventricular septal rupture, and one goal of therapy has been stabilization before closure of the defect is undertaken.¹²⁴

Acute Myocardial Infarction without Shock

IABP use for uncomplicated acute MI is controversial. As with many modalities that lower myocardial oxygen demand, IABP theoretically helps decrease infarct size, even when reperfusion does not take place.¹⁰⁶ However, a number of older trials and two randomized trials from the past decade did not demonstrate compelling risk-to-benefit ratios with routine IABP use in acute MI patients undergoing PCI,^125,126 nor did a more recent study assessing myocardial infarct size using cardiac MRI.¹²⁷ The findings conform to a meta-analysis that showed no benefit along with a small increase in stroke and bleeding.¹⁰⁰ Economic analysis did not demonstrate significant increase in hospital costs in patients randomly assigned to undergo routine IABP insertion in this setting.¹²⁸ The potential benefit of the IABP in maintaining higher infarct artery patency has been demonstrated in two randomized studies showing that an open artery is more likely at 5 days¹²⁹ and at 3 weeks¹³⁰ in patients randomly assigned to IABP placement.

IABP has been used to manage recurrent ischemia and malignant ventricular arrhythmias in the peri-infarction setting, although the evidence base for these indications is less compelling, and both are class II indications (see Box 7.1) in patients with STEMI.⁹¹

Unstable Angina

IABP use in unstable angina dates from an era in which the available alternatives were medical therapy and coronary bypass surgery, and IABP was utilized to stabilize patients before they were taken to the operating room. In certain settings, such as severe left main coronary artery disease discovered in the cardiac catheterization laboratory or in unstable angina with attendant hemodynamic instability, this approach is still appropriate.¹³¹ Reducing myocardial oxygen demand frequently stabilizes these patients, and the IABP may have additional benefits during subsequent revascularization in the cardiac catheterization laboratory or operating room, as discussed later.

Prophylactic Use for Coronary Intervention

Prophylactic use of an IABP prior to PCI has generally been considered to be a sound strategy for high-risk patients, typically defined as having acute coronary syndrome with hemodynamic instability, severe LV dysfunction and extensive coronary disease, or left main/last remaining vessel intervention. Prophylactic IABP insertion in this setting had substantially better outcomes than rescue IABP placement according to retrospective multivariate analysis,¹³² including evaluation of high-risk patients with severely depressed LV ejection fraction¹³³ undergoing angioplasty and patients undergoing unprotected left main PCI,¹³⁴ though the level of evidence base was generally weak. BCIS-1 (Balloon Pump-Assisted Coronary Intervention Study) randomly assigned patients to elective use of IABP prior to PCI in high-risk patients. Whereas it failed to demonstrate a significant benefit, a nonsignificant trend to decreased morality rate was seen (4.6% vs. 7.4%) and may reflect the underpowered nature of the trial. There was significant crossover in this study as well; crossover tends to dilute the power of studies that examine the use of already available technology, particularly when there is a perception on the part of clinicians that the device is efficacious, even if the efficacy is unproven.¹³⁵ IABP use in this setting is currently class IIb,⁹² and is discussed further in this chapter under “Newer Technologies.”

A partial explanation for the less-than-compelling evidence for the use of prophylactic IABP in this setting is the misconception that IABP provides adequate protection to allow prolonged ischemia in a critical vascular bed during coronary intervention. With total occlusion of flow to a large amount of myocardium, such as with unprotected left main angioplasty or angioplasty of a sole remaining vessel, hemodynamics may be preserved during the procedure, and ischemia and necrosis may be limited by lowering of myocardial oxygen demand effectuated by IABP. However, because cardiac output remains dependent on LV ejection, myocardial oxygen demand is substantially higher than when temporary cardiac or cardiopulmonary bypass is used, and significant stunning or necrosis or both of heart muscle can occur despite IABP use during high-risk angioplasty.

Cardiac Surgery

IABP is utilized in approximately 10% to 15% of patients undergoing cardiac surgery, with substantial rise in the rate in the past decade.¹³⁶ About half of this use is for coronary bypass patients; two-thirds of the CS patients in the Society of Thoracic Surgeons database had insertion of IABPs.¹³⁷ A number of studies have demonstrated a favorable influence on outcomes, including mortality rate.^138–140 Nevertheless, there is considerable variability in use among centers, reflecting a lack of consensus regarding indications for perioperative IABP use.^136,141 The vast majority of IABP insertions occur preoperatively.^136,137 The effectiveness of this approach has been controversial. One small randomized trial of high-risk patients demonstrated lower mortality rate, higher postoperative cardiac index, and shorter intubation time, intensive care unit (ICU) stay, and hospitalization in patients with preoperative IABP placement.¹³¹ Mortality rate benefit was also observed in a retrospective single center experience¹⁴² as well as a meta-analysis.¹⁴³ In contrast, a propensity analysis suggested excess mortality rate in nearly 2,000 patients receiving preoperative IABP insertion compared with 28,000 who did not.¹⁴⁴ Because of the limitations of propensity analysis, it is possible that selection bias determined the unfavorable outcomes associated with preoperative IABP use. Patients most likely to benefit from preoperative IABP insertion are those with depressed LV function, unstable angina or recent MI, or left main coronary artery disease or those who are undergoing repeat thoracotomy.

Several mechanisms can be postulated for superior outcomes with preoperative IABP insertion. Counterpulsation can provide hemodynamic support during anesthesia induction and during the stress of surgery before cardiopulmonary bypass is begun.140,145 As already described, IABP with pulsatile flow during cardiopulmonary bypass also appears to have favorable effects on end-organ perfusion^26,146,147 with protection of both coronary and cerebral blood flow.¹⁴⁸ IABP insertion can also be used to assess prognosis; requirement for catecholamine support and overall hemodynamics 1 hour after institution of perioperative balloon pump insertion is highly predictive of overall outcome.¹⁴⁹

Although studies have reported the mortality rate in high-risk patients treated with IABP as high as 53%, preoperative placement of an IABP was associated with substantially lower morbidity and mortality rates (24%), while postoperative insertion, in this case creating bias toward late insertion in situations with bad outcomes, was associated with a 63% mortality rate.¹⁵⁰ In the STS database, operative mortality rate in CS patients, the majority of whom received IABP, was high, ranging from 20% with isolated CABG to 33% for CABG and valve surgery and 58% for CABG and ventricular septal repair.¹³⁷ Similarly, a nonrandomized study of patients with an ejection fraction of 25% or less compared patients who were treated with preoperative IABP with those who were not. Mortality rate was 2.7% in the former group compared with 11.9% in the latter group, despite the presence of New York Heart Association (NYHA) class III or IV heart failure in 92% of the former and only 55% of the latter.¹³⁸ Several other post hoc analyses have found results consistent with advantages of preoperative IABP.^151,152

Outcomes in addition to mortality rate that were superior in patients undergoing preoperative IABP insertion were duration of IABP support, length of hospital stay, and postoperative LV ejection fraction in a randomized study of high-risk patients with ejection fraction of 30% or less.¹⁵³ Similarly, preoperative use of an IABP in high-risk off-pump CABG patients appears to be favorable.^154,155 Thus, although the evidence base is incomplete, the overall preoperative use of IABP is growing.¹³⁶ Cost analysis appears to be favorable; combining high-risk cohorts randomly assigned to receive preoperative IABP placement or not,^131,145 costs were 36% less in patients with preoperative IABP insertion because of shorter IABP treatment time, shorter hospitalizations, and lower use of critical care facilities.¹⁵⁶

Congestive Heart Failure

IABP has been used successfully in a variety of settings that results in congestive heart failure, including fulminant myocarditis¹⁵⁷ and severe decompensated aortic stenosis.¹⁵⁸ On the basis of case reports, the device has also been helpful as adjunctive therapy for myocardial depression secondary to drug toxicity,^159,160 myocardial contusion,¹⁶¹ anaphylaxis,¹⁶² thyrotoxicosis,¹⁶³ multiple sclerosis,¹⁶⁴ and even lightning strike.¹⁶⁵ Animal data suggest some benefit in the setting of RV failure;¹⁶⁶ the mechanism appears to be lowered pulmonary vascular resistance with consequent improvement in RV ejection.²⁸ IABP insertion has also improved outcomes in patients with acute RV failure after heart transplantation.¹⁶⁷

Finally, IABP has been used as a bridge to transplantation, typically with placement in the axillary or external iliac arteries to allow ambulation during prolonged counterpulsation.¹⁶⁸ With development of a range of LV assist devices designed for long-term implantation, the use of IABP for this indication has waned.¹⁶⁹

Miscellaneous Indications

Limited data suggest that IABP placement during cardiopulmonary resuscitation has favorable effects.170,171 The device has been used in pregnancy in patients undergoing heart surgery with an eye toward preserving uterine and fetal flow during cardiopulmonary bypass.¹⁷² In patients at high risk for cardiac events during noncardiac surgery (e.g., recent MI, LV failure, unrevascularized ischemic myocardium),^173,174 IABP has been shown to have significant benefits for outcome,¹⁷⁵ although the evidence base consists largely of case reports;^176,177 a randomized trial has not been performed. Prophylactic IABP insertion seems particularly appropriate in high-risk patients undergoing emergency noncardiac surgery.¹⁷⁷

Use of the Intra-aortic Balloon Pump

Overall, the existing data suggest that IABP is underutilized. In more than 23,000 patients in CS reported by NRMI 2, only 31% were treated with IABP. As is the case for a number of other interventions, women were less likely to undergo IABP placement; there was an age and race difference as well, with lower rates in nonwhites and older patients.¹⁷⁸ A number of studies from the 1990s demonstrated less than 25% use of IABP in CS;^104,179 this figure contrasts with 86% utilization in the SHOCK trial.¹⁰² Although some exclusion criteria in the latter may have improved suitability for IABP in the cohort enrolled in the study, the threefold higher use of the device in the SHOCK trial is consistent with wide underuse in clinical practice, similar to findings for a variety of pharmacologic and invasive interventions in acute MI.⁹⁰

Vascular Complications

Vascular complications including limb ischemia are the most common serious adverse events related to IABP insertion. Amputation is rare (0.1%),⁴¹ but major limb ischemia, defined in the Benchmark Registry as “loss of pulse or sensation, or abnormal limb temperature or pallor requiring surgical intervention,” occurred in 1.3% of cases.¹⁹⁰ Minor limb ischemia, defined as not requiring surgery and improving with balloon removal, occurred in another 1.2% in the same series. These numbers are consistent with steady improvement over the past decade: A smaller but still substantial earlier series from India involving 911 patients (with a much higher proportion of diabetic patients and likely significantly smaller body surface area) reported a 5.9% incidence of major vascular complications, and 5.8% rate of minor vascular complications.⁵³ This series used a 9.5 F shaft IABP, which has been shown to have higher vascular complication rates than the 8 F shaft balloons that have been available for the past decade.¹⁹¹ Vascular complications, likely in part because of comorbid conditions, are associated with a much higher overall mortality rate—as much as a twofold increase.⁸⁸

Trauma to the aorta has been reported, with paraplegia caused by spinal necrosis due to subadventitial hematoma,¹⁹² cholesterol embolization to spinal and mesenteric arteries,¹⁹³ and aortic dissection¹⁹⁴ as well as no obvious cause in some patients. The presence of friable atheroma in the descending aorta has been associated with embolization.¹⁹⁵ IABP use has been identified as an independent predictor for neurologic complications of percutaneous intervention, although whether this is due to embolic phenomena or confounding variables has not been established.¹⁹⁶

A complication particular to IABP is thrombocytopenia, occurring presumably because of destruction of platelets that adhere to the IABP surface, although the mechanism remains unclear. Critical care patients who have IABPs in place and are heparinized have a 7 : 1 odds ratio of a 50% drop in platelet count compared with patients without IABPs who are placed on heparin therapy at similar doses,¹⁹⁷ lowering the likelihood that heparin-induced thrombocytopenia is the etiologic factor.

Mechanical Failure

Several complications of mechanical failure of the balloon or console have serious consequences. Rupture of the balloon was more common early in the IABP era, with an incidence reported to range from 1.7%¹⁹⁸ to 5.2%.¹⁹⁹ Typically the diagnosis was made by the appearance of blood in the gas lumen, with triggering of alarms. The usual site of rupture has been at a point when the aorta is at its nadir in diameter along the course of the IABP. Small vessel size is associated with abrasion of the IABP (thus the observation that is it more common in women²⁰⁰ likely correlates with their smaller body surface area); similar concerns arise for larger balloon sizes. Rupture of the balloon with a major gas leak, a rare event, has been reported to cause stroke secondary to gas embolization.²⁰¹ Hydrophilically coated balloons hold some promise for further reducing the risk of rupture through potentially decreasing abrasion of the balloon surface.⁴⁶ Fracturing of the IABP can occur with entrapment, including separation and migration of part of the device.²⁰² Clot may also form in the gas lumen after loss of balloon integrity and has been reported to interfere with balloon deflation, requiring use of a thrombolytic agent in the gas line to allow balloon deflation and removal of the balloon.²⁰³

Treating Complications Related to the Intra-aortic Balloon Pump

Several approaches to managing IABP-related complications have been proposed. Limb ischemia has traditionally been most successfully treated by removal of the IABP,53,204 even in patients wholly dependent on the balloon, in order to avoid loss of limb. This situation has occasionally forced physicians and families to choose between loss of limb and patient survival. Surgical femoral-femoral shunting performed at the bedside with exteriorization of the graft has been described as one potential approach.²⁰⁵ As previously mentioned, we have performed percutaneous nonsurgical external femoral-femoral shunting to effectively address limb ischemia by placing one sheath retrograde into the femoral artery contralateral to the IABP and another antegrade in the ipsilateral vessel, connecting the two sheaths with tubing and a flow regulator (see Fig. 7.5).⁶² Infusion of prostaglandin E₁ through the balloon central lumen has been shown to relieve lower limb ischemia in a small series, presumably through increase in caliber of collateral vessels or relief of spasm in the common femoral or iliac system.²⁰⁶

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