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ECP: INTRODUCTION
ECP: THE CONCEPT
More than 40 years ago, Kantrowitz and Kantrowitz first described
the principle of "phase shift diastolic augmentation". Several groups
of physicians related this principle to the oxygen consumption difference
between flow work and pressure work by the heart (Birtwell et al. 1976).
Harken developed direct counterpulsation techniques at Harvard in
the late 1950's (Harken 1976). A femoral cutdown and external pulse
actuation was used to withdraw and return blood to the arterial system
(Birtwell et al. 1970). In the early 1960's, animal studies demonstrated
the potential efficacy of counterpulsation as a treatment following
coronary occlusion (Jacobey 1971).
The concept of counterpulsation is based on the response of the left
ventricle to reduced arterial pressure during the systolic period. A
number of investigators have demonstrated good correlation between oxygen
consumption of the left ventricle and pressure time (Birtwell et al.
1976). Additional studies concluded a correlation with maximal cardiac
oxygen consumption under constant cardiac contractility and ventricular
volume (Langou et al. 1977).
Studies of the hemodynamic effects of counterpulsation reveal several
factors that give this therapy the potential to assist patients with
low cardiac output syndromes (Birtwell et al. 1976):
In 1996 the effect of external counterpulsation treatment on exercise
hemodynamics and myocardial stress perfusion in 27 patients was studied.
81% of patients improved their exercise tolerance after treatment. Post
treatment, maximal exercise heart rate and blood pressure, while demonstrating
a linear relation with exercise duration, did not increase significantly
despite the increased exercise duration. This suggests that the increase
in exercise duration after treatment is due to both improved myocardial
perfusion and altered exercise hemodynamics. External counterpulsation
appears to exert a "training effect", decreasing peripheral vascular
resistance and the heart rate response to exercise (Lawson et al. 1996).
Hemodynamics - When the rapidly increasing pressure within the
left ventricle, caused by contraction of the myocardium, exceeds the
pressure within the aorta, the aortic valve opens and the ventricle
ejects its volume of blood. Both cardiac work and myocardial oxygen
consumption relate directly to the aortic pressure which the left ventricle
must overcome during ejection. Rapid ejection of blood from the left
ventricle causes the elastic walls of the aorta to expand to handle
the blood volume and creates a peak systolic pressure. The aortic valve
will close when the left ventricular pressure is less than the aortic
pressure. If the heart muscle is deprived of oxygen for even a few minutes,
its pumping ability diminishes and injury to the heart muscle may result.
As a protective mechanism, the heart has its own ability to regulate
blood flow by autoregulation. Autoregulation allows the heart to increase
its blood flow through enlargement of blood vessels, or decrease its
blood flow by constriction of blood vessels. However, the heart can
only increase its blood flow by autoregulation to a certain point. Once
this point is reached, the heart requires mechanical assistance to increase
the supply of oxygenated blood.
External counterpulsation (ECP) provides assistance to the heart and
other muscle/tissue by "diastolic augmentation". Diastolic augmentation
is the elevation of blood pressure during diastole. ECP produces diastolic
augmentation during diastole by sequentially inflating cuffs positioned
on the patient's calves, thighs and buttocks. Counterpulsation produces
an increase in pressure within the aorta, which increases perfusion
both within the heart and systemically. As a result, external counterpulsation
may be beneficial in several ways. Myocardial and other muscle/tissue
perfusion may be increased by the augmented diastolic pressure. Cardiac
efficiency may be improved by counterpulsation due to the pressure drop
during systole. Peripheral perfusion may also be enhanced by the rise
in mean systemic perfusion pressure. Near the end of diastole, before
the ventricles contract in systole, ECP deflates the cuffs causing a
reduction in intra-aortic volume and pressure. This can reduce the afterload
or resistance to pumping blood out of the ventricles. Because approximately
80-90% of the oxygen required by the heart is used during contraction
to pump blood out of the ventricles, counterpulsation may also be effective
in reducing the heart's oxygen requirement.
Arterial System Effect - The pressure pulse applied to the patient's
torso by ECP drives blood from the arterial system back into the aorta
and arteries of the upper body. The propagated pressure front causes
an increase in aortic pressure, the "augmented diastolic pressure" often
exceeding the normal peak systolic value. Relaxation of the air cuff
pressure pulse during cardiac systole lowers the resistance to blood
flow in the patient's buttocks and legs, reducing the back pressure
on the heart as it ejects its bolus of blood. The combination of increased
coronary flow and reduction of cardiac work (afterload) by counterpulsation
improves cardiac function.
Venous System Effect - During counterpulsation, cardiac preload
is not significantly increased by positive pulsatile pressure to the
venous system of the lower extremities. Blood in the venous bed is quickly
displaced into the low pressure, high volume venous pool. Retrograde
flow is prevented by both the low central venous pressure and valves
in the major peripheral veins when the pressure is released. This means
venous pressure remains near normal.
ECP Evolves
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