Temporary Mechanical Circulatory Support Devices

The primary goal of IABP counterpulsation is to increase myocardial oxygen supply while decreasing oxygen demand.

During diastole, the balloon inflates, resulting in a volume of blood being displaced toward the proximal aorta.

During systole, the balloon rapidly deflates, creating a vacuum effect resulting in a decrease in left ventricular (LV) afterload and a reduction in myocardial workload.

To optimize these two hemodynamic effects, the IABP must inflate and deflate in synchrony with the cardiac cycle.

The single most important determinant of effective counterpulsation is the timing of the IABP relative to the cardiac cycle.

Once proper timing has been established, IABP counterpulsation improves myocardial oxygen delivery via an increase in coronary perfusion pressure, reduces cardiac work by decreasing systolic blood pressure and afterload, and improves forward blood flow in patients with impaired cardiac contractile function.

The majority of patients exhibit a decrease in systolic pressure, an increase in diastolic pressure (which may subsequently enhance coronary blood flow to a territory perfused by an artery with a critical stenosis), a reduction in heart rate, a decrease in the mean pulmonary capillary wedge pressure (PCWP), and an increase in CO of 0.5 to 1.0 L/min.

Two indices measured during IABP counterpulsation are the tension-time index (TTI), which is the time integral of LV pressures during systole, and the diastolic pressure-time index (DPTI), which is the time integral of the proximal aortic pressures during diastole.

Proper balloon inflation augments diastolic pressure (i.e., increases DPTI), whereas rapid balloon deflation decreases LV afterload (i.e., decreases TTI).

The endocardial viability ratio (DPTI:TTI), which reflects the relationship between myocardial oxygen supply and demand, will increase with optimal IABP counterpulsation.

The appropriate timing of balloon counterpulsation to the mechanical events of the cardiac cycle must be monitored to ensure that the patient is deriving maximal hemodynamic benefit ( Fig. 24.2 ).

To maximize diastolic augmentation, the balloon should inflate at end systole, immediately after closure of the aortic valve.

Mean diastolic pressure correlates well with coronary perfusion and, hence, oxygen delivery.

Maximal coronary perfusion occurs when balloon inflation coincides with end systole.

The timing of balloon deflation, which decreases LV oxygen consumption, should occur at end diastole.

Loss of the optimal hemodynamic effect occurs when balloon IABP counterpulsation is not appropriately timed to the mechanical events of the cardiac cycle.

Four different scenarios involving faulty coupling of balloon IABP counterpulsation with the cardiac cycle have been described ( Fig. 24.3 ).

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  During early inflation, the balloon inflates before closure of the aortic valve. Pressure augmentation is thus superimposed upon the systolic aortic pressure tracing, leading to a decrease in LV emptying (a decrease in stroke volume), a decrease in cardiac output, an increase in LV afterload, and an overall increase in myocardial oxygen consumption.

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  In this scenario, there is loss of the distinct systolic peak of the central aortic pressure waveform and loss of the dicrotic notch (see Fig. 24.3A ).

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  To correct early inflation, the timing interval should be slowly increased until the onset of inflation occurs at the dicrotic notch.

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  During late inflation, the dicrotic notch on the aortic pressure waveform is clearly visualized.

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  The balloon inflates well beyond closure of the aortic valve. In this scenario, diastolic augmentation of the central aortic pressure is decreased, whereas LV afterload is minimally affected.

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  The classic morphologic finding on the central aortic pressure tracing is the presence of a distinct dicrotic notch, with the augmented diastolic pressure wave occurring well afterward (see Fig. 24.3B ).

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  To correct late inflation of the IABP, the timing interval should be gradually decreased until the onset of inflation coincides with the dicrotic notch on the arterial pressure waveform.

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  During early deflation, the balloon deflates prematurely; consequently, the benefits of diastolic augmentation are lost.

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  Analysis of the arterial pressure tracing reveals the presence of a peaked diastolic augmentation wave along with a U-shaped wave preceding the onset of systole (see Fig. 24.3C ).

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  To correct early deflation, the timing interval should be increased until the augmented diastolic wave becomes appropriate.

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  During late deflation, the balloon is deflated after the onset of systole and the opening of the aortic valve.

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  The resultant hemodynamic profile is like the one observed with early inflation: afterload is increased, leading to increased LV work and myocardial oxygen consumption along with reduced stroke volume and CO.

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  Analysis of the arterial pressure tracing usually reveals the loss of a distinct valley representing the end-diastolic pressure before the central aortic systolic wave (see Fig. 24.3D )

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  To correct late deflation, the timing interval should be decreased gradually until the balloon deflates before the onset of systole.

Absolute contraindications include significant aortic regurgitation, suspected aortic dissection, clinically significant abdominal or thoracic aortic aneurysm, distal aortic occlusion or severe stenosis, and chronic end-stage heart disease with no anticipation of recovery.

Relative contraindications include severe peripheral arterial disease (PAD), contraindications to anticoagulation, uncontrolled sepsis, and sustained tachyarrhythmias (heart rate > 160 beats/min).

The most commonly used approach for percutaneous placement is cannulation of the femoral artery ( Table 24.4 ).

Once it is concluded that the patient no longer requires circulatory support, the removal of the IABP is also a straightforward process ( Table 24.5 ).

No conclusive data support the requirement for intravenous anticoagulation in the setting of IABP use.

A trial of 153 patients found no difference in vascular complications in patients undergoing IABP therapy with and without continuous heparin anticoagulation.

Industry guidelines do not require continuous anticoagulation therapy, especially when the device is set at a 1 : 1 assist ratio.

Currently, it is reasonable to use intravenous heparin with the goal of maintaining an activated partial thromboplastin time of 60 to 75 seconds in a patient without contraindications to anticoagulation and when IABP counterpulsation therapy is planned for longer than 24 hours or at lower assist ratios.

Although no conclusive data exist in the literature, some authorities recommend gradual weaning of the balloon pump before it is finally removed.

In patients in whom the IABP was placed to treat hemodynamic instability, a gradual reduction in the assist ratio from 1 : 1 to 1 : 2 and then to 1 : 3 over several hours is frequently employed.

If hemodynamic stability is demonstrated at lesser assist ratios, the device can be removed safely.

Complications arising from IABP counterpulsation therapy can be categorized into vascular and nonvascular events.

In two studies of nearly 40,000 patients, death directly caused by an IABP or IABP placement was less than 0.05%.

Major complications—including major limb ischemia, severe bleeding, balloon leak, and death related directly to device insertion or to device failure—occurred in 2.6% of patients (see Table 24.3 ).

Vascular complications remain the most common serious complications to occur in patients with an IABP.

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  The most common types of vascular complications include limb ischemia, vascular laceration necessitating surgical repair, and major hemorrhage.

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  Arterial obstruction and limb ischemia can occur when the IABP is inadvertently placed into either the superficial or profunda femoral artery instead of the common femoral artery, because these arteries are usually too small to accommodate the IABP without compromising blood flow to the leg.

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  Prompt removal of the device and contralateral insertion (with avoidance of an excessively low needle puncture) is recommended.

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  Arterial dissection can occur with improper advancement of a guidewire with subsequent insertion of the IABP into a false lumen.

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  Less common vascular complications include spinal cord or visceral organ ischemia, cholesterol embolization, cerebrovascular accidents, sepsis, and balloon rupture.

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  The presence of PAD (including a history of limb claudication, femoral arterial bruit, or absent pulsations) has been the most consistent clinical predictor of complications.

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  These complications are more common in women (related to the size of the vessels) and patients with a history of diabetes mellitus and hypertension who are more likely to have PAD.

Because the helium gas used to inflate the balloon is insoluble in blood, helium embolization can cause prolonged ischemia or stroke.

These patients can be treated with hyperbaric oxygen to maintain tissue viability.

IABP counterpulsation therapy improves the hemodynamic and metabolic derangements that result from circulatory collapse.

Historically, this modality has been used mainly in the setting of acute ischemic syndromes associated with hemodynamic decompensation.