Just ran across this article on counterpulsion on Medscape. It sounds a lot like EECP, but is called SECP. I suppose any acceptance of one will lead to acceptance of the other? They sound very similar. Regards, Mark
Diastolic counterpulsation is an acceptable clinical method that is known to improve the perfusion of vital organs by increasing the mean aortic diastolic pressure. It also decreases left ventricular afterload and thus decreases left ventricular oxygen demand, which results in better left ventricular performance and a higher cardiac output. The technique is widely used in patients with acute ischemic syndromes and cardiogenic shock. Clinically, diastolic counterpulsation has been achieved in the past with an intraaortic balloon pump. This technology has been successfully used since it was clinically introduced in 1968 by Kantrowitz et al.[1] However, intraaortic balloon counterpulsation is associated with frequent complications, including arterial embolization, infection, trauma to the aorta and its main branches, lower extremity ischemia, and hemolysis.[2, 3]
A noninvasive alternative, external counterpulsation, was developed in the early 1960s.[4, 5] Inflatable cuffs are applied to the lower half of the body, including legs, thighs, and buttocks. Diastolic inflation of the cuffs mechanically shifts the intra-arterial blood pool toward the coronary arteries, aortic arch vessels, and renal arteries. The deflation of the cuffs with the onset of systole suddenly diminishes afterload and therefore results in improved left ventricular function. In addition, the diastolic compression of the lower extremities improves venous return to the heart. Several investigations have clearly demonstrated clinical benefits from this noninvasive technique, with improvement of compromised left ventricular function, decrease in symptoms, and improved survival in patients with extensive myocardial infarction, congestive heart failure, and cardiogenic shock.[6-9] However, to date there is no information about the effect of external counterpulsation on human renal and cerebral blood flow.
Current noninvasive technology allows for the quantitative measurement of renal and cerebral blood flow, and the purpose of this study was to evaluate the effect of external counterpulsation on cerebral and renal blood flow.
Methods
Patients
Carotid blood flow. Carotid blood flow evaluation during intermittent counterpulsation was performed in 35 patients. The age of the patients varied from 48 to 89 years. Mean age was 63 +/- 4 years. There were 26 men and nine women. All patients had atherosclerotic heart disease, and most of them (30 [83%] of 35) were symptomatic (New York Heart Association Class II or more).
Renal blood flow. The measurement of renal blood flow was performed in 18 patients during intermittent external counterpulsation. All these patients (aged 49 to 83 years, mean age 55 +/- 8 years; 14 men) had atherosclerotic heart disease.
Patients with contraindications for external counterpulsation were not included in this study. These contraindications included a history of recent lower extremity thrombophlebitis, severe lower extremity ischemia, lower extremity trauma (such as recent surgical incision or amputation), more than mild aortic insufficiency, severe congestive heart failure, uncontrolled hypertension, or uncontrolled arrhythmia. Patients receiving thrombolytic agents or anticoagulation therapy were also not included. The protocol for this study was approved by the investigational research review boards of the participating hospitals. All patients gave informed consent for the procedure.
External Counterpulsation
A sequential external counterpulsation (SECP) system (Cardiomedics, Inc., Irvine, Calif.) was used in all patients. This system sequentially compresses the legs from the ankles through the thighs by inflating two sets of flexible, fabric cuffs that inflate with air during each diastole.
The calves are compressed first; the thighs are compressed approximately 20 msec later. Thus blood is shifted from the lower extremities toward the aorta. Inflation results in a cuff pressure up to 225 mm Hg. The timing and duration of each inflation is synchronized with the surface electrocardiogram. The pressure cuffs are inflated at the onset of diastole (near or at the peak of the T wave) and are deflated with the onset of systole (just after the QRS complex). Finger plethysmography allowed us to identify the arterial systolic pressure wave and the diastolic augmentation wave. This tracing, which is simultaneously monitored with the electrocardiogram, is useful for adjusting the onset of inflation and deflation as well as the level of pressure during inflation. In each patient, the diastolic inflation pressure was gradually increased over a period of 1 to 2 minutes. The pressure was increased to a point at which the peak diastolic pressure wave reached the height of the systolic pressure wave, as seen on the finger plethysmograph (Fig. 1). In most patients, this point could be achieved with diastolic inflation pressures between 150 and 180 mm Hg. After 30 minutes of effective counterpulsation, it was abruptly stopped (with the cuffs deflated). All patients tolerated the procedure well without side effects. There were no complications.
Figure 1. (click here to zoom image) Electrocardiogram and pulse waveform during sequential external counterpulsation. Note augmented diastolic pressure wave (D).
Monitoring of Carotid Blood Flow Velocity
Studies of the left common carotid artery were performed in each patient with a 7.5 mHz linear array imaging transducer with color Doppler imaging of carotid blood flow. The pulsed Doppler sample volume was placed in the middle of the lumen of the artery with an angle correction of <=60 degrees. Doppler spectra were displayed and recorded before external counterpulsation (baseline), every 5 minutes during counterpulsation, and immediately after counterpulsation. The diameter of the carotid artery at the site of the sample volume was measured before and during external counterpulsation.
Monitoring Renal Artery Blood Flow Velocity
Visualization of renal artery blood flow was performed with Duplex ultrasonography with a 2.5 mHz transducer. After imaging the aorta, the right renal artery was identified and its blood flow was identified by color flow mapping. With the pulsed volume at the center of the renal arterial color flow jet (and with an angle correction of <=60 degrees), a pulsed Doppler spectrum signal was monitored and recorded. Flow velocity was continuously monitored before, during, and after sequential external counterpulsation in a similar frequency to that described for the carotid flow measurement.
Measurements
Peak systolic flow velocity and flow velocity integrals were calculated at baseline, during, and immediately after the cessation of counterpulsation. At each time point five beats were measured and averaged. In addition, the peak of the newly created diastolic flow wave was measured for the augmented beats. The augmentation in flow velocity integral was calculated by subtracting the nonaugmented beat flow velocity integral from the augmented beat flow velocity integral. The percent augmentation was calculated with the following formula:
% augmentation = ([FVIAU - FVINA] x 100) / FVINA
where FVIAU is the augmented beat flow velocity integral and FVINA is the nonaugmented beat flow velocity integral.
In all patients, attempts were made to compare augmented and nonaugmented beats at a similar heart rate. This comparison could best be achieved at the termination of counterpulsation because the sudden cessation of counterpulsation did not change the heart rate.
Results
Carotid Blood Flow Velocity
With the initiation of SECP, a new diastolic wave was seen on carotid Duplex scanning in all patients (Fig. 2). This new wave persisted throughout the period of SECP and did not change in magnitude. The peak of this diastolic wave was 62% to 110% of the magnitude of the peak systolic wave (mean 75% +/- 7%). This new diastolic wave increased the flow velocity integral per beat in all patients. On the average, the mean flow velocity integral per beat increased 6.1 cm (22%), from 27 +/- 1.8 cm without SECP to 33.1 +/- 2.3 cm with SECP. This increase was statistically significant (P = 0.001). The peak systolic flow velocity increased by a mean of 4.2 cm/sec during SECP from 75.6 +/- 4.4 cm/sec to 79.8 +/- 5 cm/sec (P = 0.02), a mean increase of 6%. In the 12 patients in whom it was measured, the diameter of the carotid artery with and without SECP did not differ (10.91 mm before SECP and 10.86 mm after). No significant changes in cardiac cycle lengths occurred.
Figure 2. (click here to zoom image) Left common carotid Duplex. With SECP on (upper frame) there is prominent diastolic flow velocity wave (D) that reaches peak of 115 cm/sec (82% of peak systolic wave). Also note that systolic flow velocity wave (S) is higher during SECP. With SECP on, flow velocity integral is 49 cm. With SEPC off, flow velocity integral is 37 cm (increment by SECP of 32%).
Renal Blood Flow Velocity
With SECP, a new diastolic wave was seen on renal Duplex scanning in each patient (Fig. 3). This diastolic wave reached 45% to 115% (mean 68% +/- 10%) of the magnitude of the systolic wave during SECP. With SECP, renal artery flow velocity integral increased in each patient. The flow velocity integral per beat increased 4 cm (19%), from 21 +/- 1 cm to 25 +/- 1 cm. This increase was significant (P = 0.0001). The peak systolic flow velocity increased during SECP by 5 cm (8%), from 59 +/- 3 cm/sec to 64 +/- 4 cm/sec. This increase was also statistically significant (P = 0.006). Cardiac cycle length did not significantly change. Renal artery diameter could not be measured with accuracy.
Figure 3. (click here to zoom image) A, Right renal artery Duplex at baseline (BL) and during (SECP). Augmented diastolic flow velocity wave with SECP. Flow velocity integral (FVI) increased from 16 cm at BL to 20 cm with SECP (an increment of 25%). B, Turning SEPC off (arrow) results in cessation of diastolic augmentation.
Discussion
Although external counterpulsation has been shown to be an effective modality in the treatment of cardiovascular catastrophes, it has not as yet gained wide acceptance as a therapeutic modality. This may be because earlier equipment was cumbersome, immobile, and occasionally unreliable. A resurgence of interest in the possible uses of external counterpulsation has started in the last few years after intriguing reports that demonstrated an improvement in symptoms of angina in patients with coronary artery disease.[10, 11] Recently, our institutions cooperated in a protocol designed to evaluate the effect of SECP on patients with inoperable coronary artery disease with angina. In addition, more sophisticated and reliable units have been introduced by the industry. The system we used was portable, easy to operate, and effective. SECP was well tolerated by all patients and had no significant side effects.
Most previous reports that evaluated the effect of both intraaortic and external diastolic counterpulsation have concentrated on their effect on the intracardiac, aortic and pulmonary arterial pressure, as well as on cardiac output. It has become quite clear that counterpulsation improves cardiac output, decreases left ventricular diastolic pressure, decreases myocardial ischemia and improves left ventricular contractility.[7-9] Selective flow measurement data are available only on coronary flow. Our laboratory has reported that coronary flow augmentation during intraaortic balloon counterpulsation can be evaluated by Doppler transesophageal echocardiography.[12] We studied six patients who were clinically dependent on an intraaortic balloon pump and observed a significant increase in coronary artery flow velocity integral, with increments that ranged from 60% to 176% (mean 87%). Kern et al.[13] used intracoronary Doppler and demonstrated a significant increase in intracoronary flow during intraaortic balloon counterpulsation. To date, there are no data regarding selective flow augmentation to vital organs such as the brain or the kidneys in human beings during diastolic counterpulsation.
In patients with low cardiac output, decreased blood flow to the brain and kidneys may cause serious and sometimes permanent complications. Maintaining adequate blood flow to these organs remains a continuous challenge in the care of critically ill patients. External counterpulsation may achieve a significant increase in blood flow to vital organs. This noninvasive and well-tolerated treatment may therefore possibly support patients with decreased cerebral and renal perfusion.
Limitations
As mentioned, the diameter of the renal artery could not be reliably measured on the Duplex scan. This limitation in technique makes it impossible to measure the volume changes in renal blood flow. However, if diameter did not significantly change with SECP (we found none in the carotid artery), the velocity change with SECP reveals the order of magnitude change in flow volume. Secondly, although intraaortic balloon counterpulsation has been shown to have beneficial effects on cardiac output, decreased left ventricular end-diastolic pressure, decreased myocardial ischemia, and left ventricular contractility, these effects have not been proven for SECP. In fact, a study by Kern et al.[14] with an external counterpulsation device reported no augmentation of coronary blood flow. However they did note an increase in the diastolic pressure time/systolic pressure time index ratio, which suggested that subendocardial perfusion could be favorably altered with this technique. This finding could explain the beneficial clinical effects of SECP in patients with coronary disease.
Finally, the flow increases that we have demonstrated have been predominantly in diastole, and there is no documentation that augmentation of diastolic flow will be clinically beneficial in flow beds that receive much of their flow in systole. However, there is normally a high end-diastolic flow velocity in the renal artery,[15] indicating a low-resistance bed. In addition, in the common carotid artery, 70% to 80% of the measured flow is directed to the brain,[15] which is also a 1ow-resistance bed and has diastolic flow in this vessel.
Our study has shown that there is an immediate, sustained improvement in cerebral and renal blood flow during SECP. However, when counterpulsation is terminated, this augmentation stops. It is not known whether these statistically significant increases in cerebral and renal blood flow are of a sufficient magnitude to produce a clinical benefit. Furthermore, whether there would be a lasting benefit to intermittent counterpulsation is unknown. Specifically, further studies must be done to determine if there would be an acute or lasting improvement in the neurologic status or renal function of patients with cerebral or renal hypoperfusion who are treated with SECP.
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