LiDCO : Technology - LiDCO™ plus Hemodynamic Monitor Technology

Step 1 - Arterial Pressure Transformation into a Volume Time Waveform

An accurate way of determining the change in blood volume in the arterial tree from maximum dilatation to minimum dilatation would allow an estimate of the volume of blood flowing out of the arterial tree during a period slightly longer than diastole. Since the whole period of the cardiac cycle usually bears a (near) fixed relation to diastole simple scaling up would give the stroke volume. The relationship between the capacity of the arterial side of the circulation and the intravascular pressure can be expressed as the compliance: pressure change per unit volume change. All would be relatively simple if this was constant. However, arterial compliance has been shown to change as arterial pressure changes. A stiffening of the vasculature occurs as pressure and volume increase such that, at higher pressures, a given increase in pressure expands the arterial tree by a smaller volume. Nevertheless, the form of this curvilinear relationship (approximately exponential), though differing in its scaling, appears to be very similar in different subjects. Using a lookup table the pressure waveform can be used as the basis for calculating a continuous curve describing the general form of the arterial volume changes with every cardiac cycle for which arterial blood pressure is available.

Step 2 - Deriving Nominal Stroke Volume and the Heartbeat Duration

In order to obtain cardiac output (volume per unit time) we require stroke volume (or at least a value proportional to it ie nominal stroke volume) and also the duration of the cardiac cycle to calculate flow. The autocorrelation technique gives us both.

Nominal Stroke Volume: First of all the software subtracts the mean value of the derived arterial blood volume record, giving a description of how much the arterial blood volume changes around it. This is periodic like a sine wave but with different shaped areas above and below zero. The figure below shows how the method works by first using a pure sine wave and subjecting it to the procedure. We firstly obtain an estimate of the mean deviation from zero by multiplying all values of the waveform by themselves. This gives positive waves for both the positive and negative parts of the original sine wave - effectively a double waveform. The mean of the values of the new (double) waveform is otherwise known as the mean square. The square root of this value is a constant proportion of the amplitude of the original waveform known as the root mean square, or RMS value. It is approximately 0.7 of the amplitude. The original sine wave and the squared (double) waveform are shown for three cycles.

Estimation of the Heart Beat Duration: The precise period of the cycle can be obtained by moving one version of the volume waveform successively, step by step, relative to another. Cross multiplication and addition of the answers now gives values, which are both positive and negative. The sum for a given displacement (often referred to as a tau shift) becomes less, and with maximum opposition of the two versions of the record a negative mean square difference is obtained. This is not quite as large as the positive version originally obtained because of the asymmetrical nature of the waveform. The sum of the two magnitudes (maximum reinforcement at tau 0 and maximum opposition at some intermediate point in the cycle - not precisely half way) gives a shifted times unshifted value very close to the same squared value for zero tau shift.

Continuation of the step by step movement of one version of the waveform relative to the other eventually causes positive reinforcement again, when the moving waveform arrives one cycle further along relative to the other. This process does not give a very close value to the mean square volume: the two versions tend to vary sufficiently once they are one cycle shifted relative to each other. However, the second positive peak in the autocorrelogram occurs at a tau shift, which represents the duration of the cardiac cycle.

Step 3 - Nominal Stroke Volume & Calibration

With an estimate of the square of the volume draining from the arteries as they shrink from their maximum to their minimum size we have a volume linearly related to the stroke volume ie the nominal stroke volume. With the period of the heartbeat defined precisely by the interval to the first peak in the autocorrelogram we can therefore calculate a value linearly related to the cardiac output following calibration with an indicator dilution system.

The nominal stroke volume and cardiac output are initially uncalibrated. They are converted to calibrated data ie 'true stroke volume/cardiac output' by multiplying the nominal stroke volume by a calibration factor (patient specific correction factor [CF].) The patient specific CF is determined by inputting the cardiac output derived from an independent method of deriving cardiac output ie LiDCO™ System.

Ventricular Preload and Fluid Responsiveness

Assessing the vascular fluid volume status of ventilated patients and their likely response to additional fluid administration is vitally important in the management of critically ill patients. Most patients will require some degree of fluid resuscitation and subsequent fluid maintenance. There is a clear requirement for a non or minimally invasive method of accurately assessing fluid status.

Adequate fluid volume is important because of the observation that the degree to which the ventricle is filled before contraction is itself the main determinant of the volume of blood ejected. In other words the heart performs more efficiently when appropriately filled. The term preload refers to maximum stretch on the heart's muscle fibres at the end of diastolic filling. The degree of stretch is determined by the volume of blood contained in the ventricle at that time. The greater the volume of blood in the ventricles, the greater the stretch of the myocardial muscle fibres. Increased stretch results in a greater contraction and therefore an increased stroke volume is ejected to the body tissues. This relationship between ventricular end-diastolic filling volume and stroke volume is known as Starling's Law of the Heart. This states that the energy of contraction of the muscle is proportional to the pre contraction length of the muscle fibre.

A very common requirement in surgery and critical care patients is the need to rapidly increase the blood flow and hence oxygen delivery to the body. Given Starling's Law of the Heart the most commonly used intervention is to increase blood flow through the infusion of fluids. Unfortunately, this intervention itself is not without risks that include: volume overload, lung odema and acidosis from excess chloride ion administration. There are considerable differences in each patient's response to additional volume. Therefore there is a requirement for a hemodynamic parameter(s) that would predict the likely response to increased fluid volume and then to carefully monitor the actual stroke volume response as fluids are infused.

Unfortunately a convenient real time means of measuring the myocardial muscle fibre length/stretch response of the ventricle is not, at present, available for most critical care patients. The most common method used involves the use of a pulmonary artery catheter based measurement system. Parameters measured have included pulmonary artery occlusion pressure, and right or left ventricular end-diastolic volume. These measurements are by necessity restricted to a small number of critical care patients as the procedure requires the insertion of a catheter into the pulmonary artery. Furthermore these measurements have been reported as having variable success in fulfilling the requirements of estimating preload, ventricular volumes and subsequent response of the stroke volume to a fluid challenge.

Arterial pressure waveform derived parameters as indicators of preload status and response to volume infusion

Mechanical ventilation induces cyclical changes in ventricular stroke volume. Stroke volume is altered by the transient increase of intrathoracic pressure, after load and lung volume that occurs on inspiration. These collectively decrease the right ventricular filling volume and the stroke volume that is ejected into the pulmonary artery. Following a phase lag of two to three heart beats, representing the time taken for the blood to transit from the pulmonary circulation back to the left heart, this reduced ejection volume in turn leads to diminished filling of, and stroke volume from, the left ventricle. This variation in stroke volume also results in a cyclical fluctuation of arterial blood pressure (Systolic Pressure Variation SPV and Pulse Pressure Variation PPV.) The importance of these continuous measurements are that the magnitude of the respiratory changes in left ventricular stroke volume, or arterial pressure changes, should be proportional to the degree of ventricular preload dependence. In other words the patient will show greater cyclical changes in these parameters when the ventricle is operating on the steep, rather than flat portion of the Starling curve. These parameters can therefore provide an indication of the patient's preload status and likely response to the administration of further volume. By superimposing the "Blood Pressure Waveform" window onto the Trend, Graph or Chart screens of the LiDCO™plus, a continuous measure of stroke volume variation (SVV) and the other volume status indicators of systolic pressure and pulse pressure variation are displayed.

Systolic Pressure Variation (SPV) is the difference between the maximum and minimum values of systolic arterial pressure recorded over a single respiratory cycle.

Pulse Pressure Variation (PPV%) is measured over a single respiratory cycle and defined as the maximal pulse pressure (systolic - diastolic pressure) less the minimal pulse pressure divided by the average of these two pressures.

Stroke Volume Variation (SVV%) is measured over a single respiratory cycle and defined as the maximal stroke volume less the minimal stroke volume divided by the average of these two stroke volumes.

Contraindications for use of the PulseCO™ Autocorrelation Algorithm

The performance of the software may be compromised in the following patient groups:

Analysis of the respiratory changes in the preload parameters of: SPV, PPV% and SVV% is compromised in patients with cardiac arrythmias

PulseCO™ System Autocorrelation Algorithm

Ventricular Preload and Fluid Responsiveness

Arterial pressure waveform derived parameters as indicators of preload status and response to volume infusion

Contraindications for use of the PulseCO™ Autocorrelation Algorithm