Signal Processing

The transmission of a clear signal from the impedance electrodes and precise measurement of the impedance changes by the technology are essential for the acquisition of accurate data. The impedance change/time (dZ/dt) signal (Figure 1) is converted into a 3-D view (Figure 2) which plots the impedance change in relation to the time, frequency, and power of the signal (Wigner Distribution).

From this unique 3-D waveform, important cardiac event landmarks are precisely identified and exact measurement of ventricular ejection time and other intervals are attained. The accurate calculations of hemodynamic parameters are, therefore, based on actual cardiac cycle event landmarks rather than averaged, estimated, or predicted landmarks. (Figure 3)

Continuous, noninvasive monitoring of hemodynamic status and thoracic fluid volume enables the clinician to quickly obtain data to differentiate various cardiopulmonary pathologies, institute interventions in a timely fashion, rapidly assess the patients response to therapy, and adjust therapies accordingly

Parameters

Data Output

Cardiac Output

Stroke volume x heart rate normal values 4-8 l/min., volume of blood pumped by the heart per minute, global measurement of cardiac function Evaluation and management of alterations in cardiac output are based on identifying and correcting (when possible) the specific derangements which have caused a change in cardiac output. For example, a decrease in cardiac output may occur as a result of intravascular volume depletion, myocardial dysfunction or abnormally high vascular resistance. Increased cardiac output may result from sepsis, anaphylaxis, or SIRS.

Cardiac Index

Cardiac output/ body surface area (m2), normal value 2.5-4.0 l/min/m2, cardiac output normalized for body size.

Stroke Volume

Stroke volume is evaluated with respect to its determinants: preload, afterload and contractility. The normal value is 60 to 120 ml/beats.

Therapeutic interventions intended to improve a low or sub optimal stroke volume and cardiac output are directed by the identified cause(s) of the altered stroke volume and cardiac output.

Patients with low stroke volume due to inadequate preload typically also have a normal to high Zo and require administration of intravascular fluids. Prior to fluid infusion, the response may be judged
by placing a patient supine or lifting their legs to administer a physiologic fluid bolus by increasing venous return. An increase in stroke volume related to this maneuver helps to verify the need for increased intravascular volume. The therapeutic effect of bolus fluid administration or resuscitation can be rapidly assessed by the continuous monitoring of stroke volume and cardiac output.

Decreased stroke volume due solely to increased systemic vascular resistance is uncommon except for patients with systemic hypertension or significant hypothermia. Arterial vasoconstriction is usually compensatory in nature to maintain perfusion when stroke volume and cardiac output are decreased due to inadequate preload or poor contractility. Correction of the cause of compensatory vasoconstriction should result in decreased SVR and improved stroke volume. Likewise, warming of hypothermic patients results in normalization of SVR. Management of systemic hypertension is complex and beyond the scope of this booklet, however, monitoring the administration of intravenous vasodilators and the effectiveness of outpatient therapy can easily be accomplished using the noninvasive parameters.

Low stroke volume due to reduced myocardial contractility associated with a normal to low Zo and altered contractility parameters is discussed in the next section.

Left Ventricular Contractility

Impedance cardiography measurements and calculations provide continuous assessment of the effectiveness and efficiency of left ventricular contractility as well as the evaluation of the response to interventions which impact contractility.

Pre-Ejection period (PEP)

Pre-Ejection period Duration of time for isovolumetric contraction. Normal values 0.05-0.12 seconds. Measured from Q wave of QRS complex to the opening of the aortic valve (B Point of dZ/dt). Reflects left ventricular contractile ability, lengthens with ventricular dysfunction. It is a measured impedance parameter, is the length of time from ventricular depolarization to the end of isovolumetric contraction. The PEP is measured from the Q wave of the ECG to the B point on the impedance signal. Diseased and dysfunctional ventricles require a longer period of time to increase the intraventricular pressure to overcome the ascending aortic pressure and open the aortic valve, increasing the PEP time. Other causes of longer PEP include disorders and drugs which raise systemic vascular resistance and intravascular volume overload which may over-distend the ventricles and impair myofibril shortening. Interventions to enhance contractility or reduce left ventricular end-diastolic volume should result in a shorter PEP.

Ventricular ejection time VET 

Duration of time required during systole for ejection of blood into the aorta, normal value 0.25-0.35 seconds. Measured from the opening of the aortic valve (B Point of dZ/dt) to the closing of the aortic valve (X point of dZ/dt). Reflects left ventricular contractile ability, shortens with ventricular dysfunction. Precise measurement required for stroke volume calculation. It is useful to assess inotropic activity. Left ventricular dysfunction is associated with a shortened VET due to the lengthening of PEP and a decrease in the rate and duration of myofibril contraction (shortening). Reduced stoke volume may also shorten the VET due to decreased left ventricular end diastolic volume.

PEP/VET Ratio

Ratio of systolic time intervals, pre-ejection period to ventricular ejection time, normal value 0.2-.0.4 seconds, increased ratio associated with left ventricular dysfunction due to increased time required for isovolumetric contraction.

Combining these systolic time intervals by calculating the ratio of PEP to VET (PEP/VET) eliminates the effect of heart rate and has utility as an index of left ventricular function and a monitor of therapeutic response. Left ventricular dysfunction lengthens PEP and decreases the VET therefore an increasing PEP/VET ratio is associated with impaired ventricular contractility. Positive inotropic agents shorten the PEP, have a small effect on VET and yield a decrease in PEP/VET. An intravascular fluid challenge and secondary increase in stroke volume lengthens the VET and also reduces the PEP/VET value

dZ/dt

Change of impedance over time, Normal value 0.8-2.5 Ohms / second. Measurement of left ventricular contractility useful to titrate inotropic agents and evaluate left ventricular function. Value measured from dZ/dt peek of ventricular ejection. time maximum left ventricular contractile force and blood flow velocity in the ascending aorta. A value of less then 0.3 signifies an inadequate impedance signaand waveform are generated from the velocity and quantity of blood flow from the left ventricle. A decrease in the dZ/dt value and a dampened waveform are caused by reduced contractile force and less rapid blood flow from the left ventricle. Ischemic injury from coronary artery disease, cardiomyopathies, cardiac valve disease, and certain inflammatory mediators such as myocardial depressant factor, decrease myocardial contractility and are denoted by a low dZ/dt Negative inotropic agents have a similar effect, although often desirable. Interventions directed toward improving myocardial contractility, for example administration of positive inotropic medications, increase the force and velocity of blood flow from the left ventricle into the aorta. The enhanced contractility is reflected by an increase in the dZ/dt value. Changes in the dZ/dt waveform may be subtle and difficult to discern in some instances.

A poor dZ/dt waveform and value less than 0.3 ohms/second, coupled with a low Zo (<14 ohms) is typically an indicator of poor signal quality which may be related to significant left ventricular dysfunction and considerable intercellular, interstitial or alveolar edema. The accuracy of the impedance stroke volume and cardiac output in this situation may be limited due to the small change in impedance during systole relative to the very low baseline impedance. However, stroke volume and cardiac output trending capabilities are intact and a diagnosis of low cardiac output with elevated intrathoracic fluid volume can be made.

The acceleration index (ACI)

(d2z/dt2) / Zo, normal value 2-5 Ohms/sec2 Sensitive measure of left ventricular contractility minimally affected by preload and afterload. Useful for assessing ventricular function, screening for coronary artery disease and, triturating inotropic agents. It is a direct reflection of the velocity or acceleration of blood flow in the ascending aorta and thus is an indicator of inotropic property of the myocardium. ACI is useful to evaluate the myocardial contractility because it is minimally affected by preload and afterload. Enhanced left ventricular contractility is associated with a rise in the ACI and decreased contractility causes the ACI to decrease.

Monitoring the ACI in conjunction with cardiac output during titration of positive inotropic agents provides information to maximize cardiac performance within the limits of the patient’s myocardial status. For example, patients with coronary artery disease tend to have lower baseline ACI and less of an increase during exercise or stress testing than those with normal coronary arteries (Koerner, Feng).

Thoracic Fluid Volume Status

Measured by Zo in Ohms, normal values men 18-30; women 25-35; infants 30-45. Reflects total thoracic fluids (extravascular and intravascular), primarily influenced by interstitial and alveolar fluid. Base impedance decreases with increased fluid accumulation and greater conductivity in the chest. Reliable indicator of pulmonary edema, and hypovolemia. One of the components of the stroke volume equation.
As described above, the Zo is the base thoracic impedance. It primarily reflects total blood volume, intercellular, interstitial, and alveolar fluid status. Intravascular volume depletion, hypervolemia, increases the Zo since there is less conductive fluid in the thorax. Aggressive diuretic therapy, hemorrhage, and dehydration are clinical examples which raise the Zo. An increase in air in the thorax due to pneumothorax will also increase the Zo because air is much less conductive of electrical flow than fluid.

Low base impedance is caused by increased blood volume and extravascular fluids in the thorax. Hypervolemia, hemodilution, and conditions which increase fluid leakage into the interstitial spaces, and pulmonary edema facilitate electrical conduction through the thorax and therefore lower the Zo. Pulmonary interstitial and alveolar edema are associated with Zo of less than 18 ohms and 14 ohms, respectively, in congestive heart failure patients. (Milzman, Milzman) A low Zo coupled with low cardiac output and contractility parameters, aids differential diagnosis of heart failure from similar symptoms of other pathologic origins.

B point

Point on dZ/dt waveform which is clearly distinguished by the SEEMEDX signal extraction technology processing (time, power, frequency distribution), defines the opening of the aortic valve and beginning of the ventricular ejection time (VET) , necessary to accurately calculate stroke volume.

C point

Used to measure dZ/dt max, point on dZ/dt waveform which clearly distinguished by the IQ signal processing (power, frequency distribution), defines the peak ejection which is point of maximum left ventricular contraction and blood flow velocity in the ascending aorta. Precise measurement is necessary to calculate stroke volume accurately.

X point

Point on dZ/dt waveform, which is clearly distinguished by the SEEMEDX signal processing (time, power. frequency distribution), defines the closing of the aortic valve and the end of ventricular ejection time (VET) and ventricular . systole, necessary to accurately calculate stroke volume.

Central Venous pressure

Average blood pressure of venous! System typically measured in the superior vena cava, normal value 0..4 mm Hg, reflects right ventricular end-diastolic pressure and right ventricular preload.

Thoracic length(L)

Distance between sensing thoracic impedance electrodes, from the base of the neck (just above the clavicles) to a point lateral from the lower tip of the sternum (just above the xyphoid process). Distance is measured with calipers and entered into the SEEMEDX monitor. Important measurement in the stroke volume calculation

Left cardiac work index LCWI

(MAP-PAOP) x CI x 0.0144, normal value 3-5 kg-min/m2 reflection of left ventricular work and myocardial oxygen demand. Blood pressure, entered into the monitor, and the default PAOP are used to calculate LCWI.

0hm

Unit of electrical resistance, unit of measurement for impedance.

PAOP

Pulmonary artery occlusion pressure. Also referred to as pulmonary artery wedge pressure, normal value 6-12 mmHg. Indirect reflection of left ventricular end-diastolic pressure obtained from a pulmonary artery catheter. Default value in SEEMEDX monitor used in left cardiac work index equation.

Stroke volume

Normal value 60-120 ml/beat

Volume of blood ejected into the aorta with each ventricular contraction. When calculated by measuring thoracic ascending aortic flow via impedance cardiography, requires precise measurement of VET; L, Zo, and dZ/dt max.

Systemic vascular resistance

SVR (MAP-CVP) / CO x 80, normal value 800-1200 Dyne.sec/cm5. Measurement of left ventricular afterload or the force, which the left ventricle must overcome with each contraction to eject blood into the ascending aorta.

Thoracic length

(L) Distance between sensing thoracic impedance electrodes, from the base of the neck (just above the clavicles) to a point lateral from the lower tip of the sternum (just above the xyphoid process). Distance is measured with calipers and entered into the SEEMEDX monitor. Important measurement in the stroke volume calculation.