Clinical Use of Impedance Cardiography for Hemodynamic Assessment of Early Cardiovascular Disease and Management of Hypertension

Abstract

This article is for clinicians considering impedance cardiography (ICG) for secondary prevention. ICG is an inexpensive noninvasive technology that can be used to assess hemodynamic function of the central cardiovascular system. Diverse abnormalities of ventricular function, systolic and diastolic, can be detected by ICG. Additional data pertaining to decompensation can be obtained by taking ICG readings with the patient performing postural change, from upright to supine, to quantify the compensatory response. Vascular load consists of resistive and pulsatile loads. Systemic vascular resistance can provide a measure of resistive load. Pulsatile load has two components: arterial stiffness and wave reflection. ICG can be used to calculate arterial compliance and detect aortic wave reflection. For stage 1 hypertension, a significant issue is whether a treating clinician should add pharmacotherapy to lifestyle modification. Adults who have multiple cardiovascular risk factors with stage 1 hypertension have early cardiovascular disease. ICG can be used to identify the functional abnormalities associated with the cardiovascular disease. For the management of hypertension, ICG can be used to calculate the underlying hemodynamic parameters of cardiac index and systemic vascular resistance associated with a patient’s blood pressure. There can be wide ranges for cardiac index and systemic vascular resistance, with many patients having low cardiac index with high systemic vascular resistance or vice versa. These hemodynamic data can be used to customize pharmacotherapy. Drug titration can be guided by patient response to treatment using the initial hemodynamic data as a baseline for comparison to subsequent measurements from serial office visits.

Appendix

1.1 Background

The resistance to flow of an oscillating electrical current is known as impedance (also called electrical bioimpedance when studying a body segment). Impedance plethysmography is a method of recording changes in impedance in a body segment such as an arm or leg [57]. The placement of electrodes defines the body segment being studied. The outer electrodes apply a very tiny electrical current, oscillating in the radio frequency range, to create an electrical field. The inner electrodes record the impedance. Changes in fluid volume and flow vary inversely with the impedance of the body segment, because an increase in electrically-conductive fluid lowers the impedance of the body segment.

Impedance plethysmography which focuses on the body segment of the thorax is called impedance cardiography. The first commercially available impedance cardiograph was introduced in the late 1960s as a noninvasive and unobtrusive method of measuring systolic time intervals and cardiac output in astronauts [58]. The technique was based on measuring certain landmarks on the ICG waveform and performing calculations to obtain stroke volume relying heavily upon empirical validation. Since astronauts are very fit, the formula for stroke volume was based on a “normal” ICG waveform.

1.2 Fundamentals of Impedance Cardiography

An electric field within the thorax is created by applying oscillating, high-frequency, low-amplitude current (which the patient does not feel) from a constant-current source via a set of outer electrodes (see Leads 1 and 4 in Fig. 

Fig. 3

Electrode configuration. Electric current is applied to Leads 1 and 4. Voltage is measured by Leads 2 and 3

3). Blood is an electrically conductive saline solution with less conductive cells (such as erythrocytes) floating in it. With each heartbeat, blood movement in the thorax is the major source of impedance change. Contributing factors are changes in volume and velocity of the blood. These pulsatile changes are measured as voltage differences between a set of inner sensing electrodes (see Leads 2 and 3 in Fig. 3). Using Ohm’s Law, the impedance signal (called Z) is obtained by dividing the measured voltage by the constant applied electrical current.

The real-time impedance signal, which resembles an aortic pressure pulse wave [59], is differentiated to yield the dZ/dt signal, which represents the rate of change in thoracic impedance. To facilitate intuitive interpretation, the signal is inverted so that a decrease in impedance appears as a rise in the displayed waveform. On this ICG waveform, aortic valve opening is synchronous with the B point, and aortic valve closing is synchronous with the X point, often occurring at the nadir of the ICG waveform (see Fig. 2). The B point is the incisura of the ascending limb of the systolic wave. The time interval from the B point to the X point is ventricular ejection time. The B point determines the position of the horizontal line which is the baseline of the ICG waveform. The systolic wave is defined as the portion of the ICG waveform, during systole, which is above the baseline. The vertical distance from the baseline to the highest point on the systolic wave is [dZ/dt]max, measured in ohms per second.

In systole, the major source of the impedance change is blood movement in the aorta. The height of the systolic wave, [dZ/dt]max, correlates with left ventricular systolic function [60,61,62]. An ICG parameter, called systolic amplitude, is defined as the ratio of [dZ/dt]max divided by the average impedance of the thorax, Z₀ (ohm). Systolic amplitude is a normalized parameter with the same normal range for males and females. While at rest in a recumbent position, a heart with normal systolic function has a systolic amplitude value ≥ 0.03 (ohm/s/ohm).

With normal diastolic function, blood movement in the thorax is not rapid enough to cause a pronounced wave above the baseline in the diastolic segment of the ICG waveform. When filling pressure is elevated, the accelerated rate of filling causes a prominent diastolic wave on the ICG waveform during early diastole. In heart failure, the size of the diastolic wave, which often is synchronous to the third heart sound, may even exceed the size of the systolic wave [13].

The Frank-Starling relation states that, within limits, the force of ventricular contraction is affected by the end-diastolic length of the fibers (the average sarcomere length) comprising the muscular wall, which is closely related to the end-diastolic volume [63]. In a normal heart, the contractile force increases as muscle length increases. An increase in end-diastolic volume causes the muscle to stretch and results in a greater contractile force. This fundamental property of cardiac muscle is represented by an ascending Frank-Starling curve. As the heart fails, the left ventricle delivers a progressively smaller stroke volume from a normal or even elevated end-diastolic volume until a tip** point is reached where an increase in end-diastolic volume causes no change in contractile force. This is the onset of decompensation.

Aortic wave reflection increases afterload and, therefore, results in forward flow deceleration. On the ICG waveform, this causes a widening of the systolic wave. This first appears when the patient is upright because of the additional increase in afterload due to gravitational pooling of blood in lower extrathoracic compartments.

1.3 Impedance Cardiography Test Procedure

For the ICG test for cardiovascular function, the electrodes are applied while the patient is upright. A total of 6 spot-type electrodes are used for acquiring the ICG signal. One electrode, Lead 2, is placed at the base of the right side of the patient’s neck at or near its intersection with the frontal plane (see Fig. 3). A second electrode, Lead 1, is placed on the right side of the neck with its center being 5 cm (cm) directly above the center of the Lead 2 electrode. (For obese patients, Lead 1 electrode should be placed at least 7 cm above the Lead 2 electrode, because the extra spacing is needed to properly protect against the possibility of the skin folding between the Lead 1 and Lead 2 electrodes which would cause the leads to be too close.) Two electrodes, connected by a common leadwire to become Lead 3, are placed on opposite sides of the lower thorax on the mid-axillary line at the level of the sternal xiphoid process. And the last two electrodes, connected by a common leadwire to become Lead 4, are placed with their centers being 5 cm directly below the centers of the Lead 3 electrodes. (For obese patients, Lead 4 electrodes should be placed at least 7 cm below the Lead 3 electrodes, because the extra spacing is needed to properly protect against the possibility of the skin folding between the Lead 3 and Lead 4 electrodes which would cause the leads to be too close.)

Just prior to capturing the ICG signal, the patient should be instructed to breathe normally, remain stationary, and not speak or cough. Immediately following the capturing of the ICG signal for 5 heartbeats in the upright position, the patient is then moved to the supine position. After 30 s, the patient is again instructed to breathe normally, remain stationary, and not speak or cough. Immediately following the capturing of the ICG signal for 5 heartbeats in the supine position, the electrodes are removed from the patient.

The captured real-time impedance signal is digitized and differentiated to produce the ICG waveform which is then ensemble averaged by superimposing the 5 captured heartbeats using the R wave of the electrocardiogram as a trigger. This results in a single ICG waveform representing a single average heartbeat.

1.4 Impedance Cardiography Data Interpretation

For analytical purposes, the ICG waveform is viewed as having systolic and diastolic segments (see Fig. 2). The systolic segment is between the B point and X point. The diastolic segment occurs after the X point. An abnormal ICG waveform during systole would indicate systolic dysfunction, and a prominent wave above the baseline during diastole would indicate diastolic dysfunction.

A heart with normal function produces ICG waveforms with an easily recognizable pattern consisting of: (1) a triangular shaped systolic wave with a value of systolic amplitude ≥ 0.03 (ohm/s/ohm) during systole and no prominent wave during diastole while supine (see bottom left frame of Fig. 1); and (2) an increase in systolic amplitude with postural change from upright to supine. Since only a heart with normal function can produce this “normal” pattern, it would follow that any functional cardiovascular disorder would cause a deviation from this normal pattern. Therefore, a comparison of the ICG waveforms, while upright and supine, to the normal pattern provides a novel method of detecting cardiovascular disease. The ICG data indicate ventricular dysfunction if there is an abnormal systolic segment of the ICG waveform, there is a prominent wave in the diastolic segment of the ICG waveform, or there is not an increase in systolic amplitude from upright to supine. An abnormal systolic segment of the ICG waveform is defined as a non-triangular systolic wave, while upright or supine, or a supine systolic amplitude < 0.03 (ohm/s/ohm).

With a patient in the supine position, hemodynamic abnormalities are defined as cardiac index < 2.5 (L/min/m²), cardiac index > 4.7, systemic vascular resistance > 1500 (dyne s/cm⁵), or systemic vascular resistance < 770 (see Table 1). The thoracic fluid level is indicated by the fluid index, defined as the nominal vertical distance between leads 2 and 3 (in centimeters and adjusted for gender and body habitus) divided by Z₀ (ohm). The criterion for hypervolemia is fluid index > 1.3 (cm/ohm). Arterial compliance index is defined as supine systolic amplitude divided by supine pulse pressure. An arterial compliance index < 0.1 (ohm/s/ohm/mmHg) indicates central arterial stiffness. Fluid index and arterial compliance index are normalized parameters for both males and females.

For assessing the compensatory response to postural change, the criterion for normal ventricular function is upright systolic amplitude less than supine systolic amplitude. Decompensation is defined as upright systolic amplitude ≥ supine systolic amplitude and is considered a form of ventricular dysfunction.

For assessing aortic wave reflection, the shape of the upright systolic wave is analyzed. With normal heart function, there is a slight rounding of the upright systolic wave peak, due to the higher afterload, with the descending limb of the upright systolic wave being more convex than the descending limb of the supine systolic wave (see left frames of Fig. 1). An upright systolic wave with a pronounced widening or flattening is considered an indication of possible augmented aortic wave reflection (top right frame of Fig. 1).

1.5 ICG Standards

There are no established standards for ICG. The type and placement of electrodes are not the same for all manufacturers. All manufacturers use an electrical current with very low amplitude and high frequency, but the specific values are not the same. Manufacturers used empirical validation to make adjustments to signal processing techniques and formulas for calculating parameters, particularly stroke volume. Most of the variations in electrode placement are minor, but there are some which are clinically significant because it affects the measurement of the average impedance of the thorax, Z₀, which is used to calculate stroke volume and systolic amplitude.

Some parameters are given different names by various manufacturers. For example, systolic amplitude is called velocity index and ejection phase contractility index by others. The systolic wave is called E wave or C wave by others. The diastolic wave is called O wave by others. For thoracic fluid level, others use thoracic fluid content, defined as the reciprocal of Z₀, which trends the same as fluid index. For thoracic fluid content there are different normal ranges for males and females, whereas fluid index is a normalized parameter with the same normal range for males and females. For vascular resistance, others use systemic vascular resistance index which trends the same as systemic vascular resistance but is defined as systemic vascular resistance multiplied by body surface area.

1.6 Limitations

For cardiovascular disease, ICG can be used to detect the presence of functional abnormalities, but ICG does not identify the causes of the abnormalities. With ventricular abnormalities, ICG alone is not sufficient for a diagnosis, because some ICG abnormalities can have various underlying mechanisms. For example, a pronounced diastolic wave could be caused by elevated filling pressure or aortic regurgitation. For ventricular dysfunction, other modalities, such as echocardiography should be used for diagnosis. Vascular load abnormalities should be diagnosed using other tests including pulse wave analysis and ankle–brachial index. After a diagnosis has been made, serial ICG tests can be used to assess patient response to treatment.