PubMed Health⌕ Search

Biomedical subjects

J N Amoore

Publications and source records attributed to J N Amoore.

At least 19 recordsLinked to original sources
PubMed2000

A simulation study of the consistency of oscillometric blood pressure measurements with and without artefacts.

BACKGROUND: Oscillometric pressure is measured by analysing, in relation to the cuff pressure, low-amplitude cuff-pressure pulsations generated by each arterial pulse. The cuff pressure is sampled at the pulse rate, introducing measurement variations, which are compounded by artefactual pulses. OBJECTIVE: To study the consistency of measurements with and without artefacts using simulated waveforms. METHODS: The Propaq Smartcuf (with and without electrocardiographic synchronization), the Welch Allyn 52 000 (before and after its software had been upgraded), the Critikon DINAMAP 8100 and Compact TS and the Criticare 507 NJC were evaluated. Each monitor recorded 15 determinations at 120/80 (93) mmHg without and with either low-frequency or high-frequency artefacts generated by the Bio-Tek BP-Pump simulator. Consistency of measurements was defined as SD of less than 2 mmHg for at least two of the systolic, diastolic and mean arterial pressures with all less than 3 mmHg. RESULTS: All monitors except the Critikon 8100 satisfied the consistency criteria without artefacts with most SD less than 1 mmHg. Several satisfied the criteria with a severe low-frequency artefact (all recorded SD were less than 6 mmHg). None satisfied the criteria with a severe high-frequency artefact. High systolic blood pressures were typically recorded with a severe tremor artefact, though the Criticare device, which measures during cuff inflation, recorded lower systolic blood pressures. The Propaq device with electrocardiographic synchronization had the lowest variability, with synchronization increasing determination time. CONCLUSION: Oscillometric monitors are more sensitive to a high-frequency artefact than they are to a low-frequency artefact. Signal-processing techniques can improve consistency of measurements. Simulators can evaluate a monitor's consistency with and without artefacts.

Blood Pressure Determination↗
PubMed2000

Can simulators evaluate systematic differences between oscillometric non-invasive blood-pressure monitors?

BACKGROUND: Oscillometric non-invasive blood-pressure (NIBP) monitors estimate the arterial pressure using model-specific signal processing and algorithms. Hence each model's accuracy must be clinically evaluated. Simulators may assist the evaluation, but their ability to do so has not been verified. OBJECTIVE: To investigate whether simulators can detect systematic differences between NIBP monitors. METHODS: We tested whether a simulator can distinguish between the two different algorithms available in a particular monitor, detect calibration errors and detect systematic differences between monitors that are observed clinically. RESULTS: Simulator evaluation correctly detected 1.8 and 4.2 mmHg systolic and diastolic differences between the two Nellcor N-3100 algorithms (with specified 2 and 5 mmHg differences) but found no difference between their mean arterial pressures (as expected from the specification). Simulator evaluations detected calibration adjustments at 80/50, 120/80 and 200/150 mmHg. Simulator and clinical comparisons of two devices of the same type recording slightly different blood pressures were in close agreement, but simulator and clinical comparisons of three different models (Propaq, Critikon DINAMAP and Datex Cardiocap) were not consistently in agreement. The simulators generated oscillometric pulse shapes different from physiological recordings. CONCLUSION: The results suggest that, although simulators can reveal systematic differences between devices of the same model, they cannot be used to detect systematic differences between different NIBP models. This could be at least partly because the oscillometric pulses generated by the simulators are dissimilar to physiologically recorded pulses.

Algorithms↗
PubMed1997

Evaluation of the Critikon 8100 and Spacelabs 90207 non-invasive blood pressure monitors using a test simulator.

The Critikon Dinamap 8100 and the Spacelabs 90207 ambulatory non-invasive blood pressure (NIBP) monitors were evaluated using a test simulator using an evaluation protocol which covered a wide range of simulated pressures (with five determinations at each of six steps from 60/30 to 200/150 mm Hg), pulse rates (from 40 to 200 bpm), artefact levels (simulated motion and tremor artefact) and pulse strengths (down to 10% of the nominal strength). Determinations were made at 5 min intervals. The average and standard deviation of the five measurements at each condition were calculated. The Spacelabs recorded pressures with a greater consistency than the Dinamap which showed a higher standard deviation under all the conditions. The relatively high standard deviation of the recordings made by the Dinamap could explain the non-systematic errors found in some evaluations. Both instruments recorded pressures within 5 mm Hg of the target over the range of pressures and pulse rates, and coped well under conditions of severe artefact and weak pulsations, either by signalling inability to record or by recording satisfactorily.

Bias↗
PubMed1994

Venous collapse and the respiratory variability in systemic venous return.

OBJECTIVE: Venous collapse limits systemic venous return, but its effects on beat to beat respiratory venous return variations are less well known. The aim of this study was to investigate the effects of venous collapse on respiratory variations in venous return. METHODS: A model of venous collapse which included both an increase in haemodynamic resistance to flow and an increase in vessel compliance was incorporated in a previously described cardiovascular model. Respiration was simulated by 5 mm Hg swings of intrathoracic pressure (PTH) at different mean pressures such that the abdominal vena cava and jugular vein were either fully collapsed (mean PTH -11 mm Hg), in the transition zone between collapse and distension (mean PTH -6 mm Hg), or fully distended (mean PTH 9 mm Hg). The mean and standard deviations over each respiratory cycle of the venous return volume (flow integral over heart cycle) and the abdominal vena caval volume were recorded. RESULTS: Different venous return volume variabilities in the three operating zones of the vena cava were identified: (1) reduced variability in the collapsed zone associated with the increased haemodynamic resistance [venous return 93(SD 6) ml, abdominal vena caval volume 30(3) ml. absolute right atrial pressure -6.3(1.1) mm Hg]; (2) increased variability in the transition zone [venous return 86(24) ml, abdominal vena caval volume 81(15) ml, right atrial pressure -2.2(0.8) mm Hg]; (3) low variability in the distended zone [venous return 42(11) ml, abdominal vena caval volume 120(2) ml, right atrial pressure 10.1(1.1) mm Hg]. The greater the change in compliance with collapse the greater the increase in flow variability in the transition zone; with no change in compliance there was no increased flow variability in the transition zone. CONCLUSIONS: The results suggest that venous collapse increases the respiratory variations in venous return in the transition zone. As venous return variations contribute to arterial pressure variations, the collapsible nature of the great veins may influence respiratory variations in systemic arterial pressure.

Blood Circulation↗
PubMed1994

Buffering of respiratory variations in venous return by right ventricle: a theoretical analysis.

The role of the right ventricle (RV) in buffering systemic venous return, thereby dampening respiratory-induced variations, left ventricular (LV) stroke volume, and systemic arterial pressure variations was examined using a computer model of the cardiovascular system. Respiration was simulated by cyclical variations in intrathoracic and abdominal pressures (cycle time 5 heartbeats), causing a 43-ml fluctuation in venous return per heartbeat (mean 71 ml) compared with fluctuations of 19 ml in RV stroke volume, 6 ml in pulmonary venous flow, and only 3 ml in LV stroke volume. On a percentage basis, the RV provided 56% of the total buffering of systemic venous return, the lungs another 30%, whereas the LV only 7%. A 10-fold increase in RV diastolic compliance increased the RV stroke volume variations from 26 to 57% of the venous return variations; a 10-fold increase in RV elastance increased them from 24 to 60%, whereas decreasing pulmonary arterial pressure from 28 to 10 mmHg increased them from 28 to 56%. The results also suggest that an underrecognized function of the RV is to buffer systemic venous return and thereby keep LV stroke volume relatively constant.

Cardiovascular Physiological Phenomena↗
PubMed1993

Measurement of forces applied during the clinical cementation of dental crowns.

Uncertainty exists about the forces applied by dentists during dental crown cementation. A measuring system was developed based around a commercially available miniature (3.8 mm high and 12.7 mm diameter) load cell. The load cell was mounted in a finger stall and the applied force measured. Experimental results suggest that dentists typically apply a force to metal crowns of about 60 N for a few seconds, followed by the application of a steady force of about 20 to 30 N. Lower forces are applied to porcelain crowns.

Crowns↗
PubMed1993

Noninvasive blood pressure measurements with single and twin-hose systems--do mixtures matter?

Noninvasive blood pressure monitors which use twin- and single-hose cuffs complicate the movement of patients between bed spaces with different cuff-hose systems. We assessed, using a commercially available noninvasive blood pressure monitor function analyser, the use of single-hose cuffs coupled via a Y-piece adaptor to the twin-hose of noninvasive monitors designed for use with twin-hose cuffs. Assessments were made at three simulated pressures (200/150 mmHg, 120/80 mmHg, and 60/30 mmHg) and at normal and weak arterial pulsations. The use of a single-hose cuff attached with the Y-piece adaptor did not adversely affect the performance of the monitors.

Blood Pressure Monitors↗
PubMed1992

Theoretical analysis of the relationship between the ratio of ventricular systolic elastance to diastolic stiffness and stroke volume.

The maintenance of adequate blood circulation requires a sufficient ventricular contractility; in addition, to eject blood, the ventricles must first receive a sufficient volume, requiring a low diastolic stiffness. A simplified cardiovascular model was used to derive formulae for stroke volume (SV) as a function of atrial pressure and the ratio of ventricular end-systolic elastance to end-diastolic stiffness. A more complex cardiovascular model was used to assess the ability of the expressions to predict stroke volume under various steady-state conditions. The predicted SV correlated linearly with the model SV over a wide range of diastolic stiffnesses and systolic elastance. The formulae predict that with fixed right atrial pressure the SV is proportional to the ratio of end-systolic elastance to end-diastolic stiffness (GR) for the right ventricle, but relatively insensitive to the ratio (GL) for the left ventricle provided that GL is greater than GR. Model simulations confirmed this. When the right atrial pressure was not fixed increases in GR with fixed GL reduced the right atrial pressure with little change in SV. Similarly, varying GL with fixed GR produced little change in SV. The ratios highlight the importance of diastole to cardiac function.

Diastole↗
PubMed1992

Computer simulation of the effects of ventricular interdependence on indices of left ventricular systolic function.

The influence of ventricular interdependence on cardiovascular function has been convincingly demonstrated. In the intact cardiovascular system ventricular interdependence is always present, and thus measures of cardiac function include the contribution of ventricular interdependence (VI). A cardiovascular system model is presented and used to discuss how VI affects selected indices of left ventricular (LV) systolic function. Indices of LV function studied were the ejection fraction, stroke work, peak time derivative of ventricular pressure (dP/dT) and the LV end-systolic pressure-volume relationship. The effects of right ventricular (RV) volume through systolic VI on these indices are conveniently studied by comparing the model responses to pulmonary artery (PA) and vena caval (VC) occlusions; both PA and VC occlusion reduce LV volume, but the RV volume is increased by PA but reduced by VC occlusions. Through systolic VI the increase in RV volume with PA occlusion shifted the LV end-systolic pressure-volume relationship to the left and thus affected measures of LV maximum elastance. The LV ejection fraction, peak dP/dT and stroke work were all augmented by the increase in RV volume associated with the PA occlusion. Experimental studies comparing the responses to PA and VC occlusions are in broad agreement with the results described here. Systolic VI also shifted the cardiac function curve, a global measure of cardiac function, to the left. The results thus suggest that commonly used indices of LV systolic function are dependent on RV function and do not solely reflect LV function.

Cardiac Volume↗
PubMed1989

A system for cardiac and respiratory gating of a magnetic resonance imager.

A cardiac and respiratory gating system is described which minimises MRI distortion by using a commercially available pneumatic capsule for respiration sensing, and by isolating the ECG and respiration detector circuitry with a fibre-optic link. Operator use is facilitated by displaying, on the ECG trace, the time during the cardiac cycle when images are acquired, and by displaying the respiratory signal. The system is presently in use with a MD 800 MRI system (M&D Technology Ltd, Aberdeen) operating at 0.08 tesla.

Heart↗
PubMed1989

Model studies of the contribution of ventricular interdependence to the transient changes in ventricular function with respiratory efforts.

The effects of variations in intrathoracic pressure on left ventricular function were studied using a mathematical model of the circulation. The variations in intrathoracic pressure directly affect the left ventricular afterload, and indirectly alter left ventricular filling by changing the right ventricular volume. The decrease in intrathoracic pressure with sustained inspiratory efforts increased the left ventricular afterload and thus reduced the left ventricular stroke volume. Secondary to the reduction in stroke volume, the left ventricular end systolic and end diastolic volumes increased. Decreasing intrathoracic pressure also increased the systemic venous return, thereby increasing right ventricular volume. The model predicted that an enlarged right ventricular volume would, through diastolic ventricular interdependence, immediately reduce the left ventricular end diastolic volume (which in turn reduced the left ventricular stroke volume), while through systolic ventricular interdependence it would increase left ventricular stroke volume and reduce left ventricular end systolic volume. An increased right ventricular volume would also increase right ventricular stroke volume and after a delay of a few heart beats raise left ventricular end diastolic and stroke volumes. The net effect of respiratory variations in intrathoracic pressure on left ventricular function would be a combination of these effects. Thus on sustained inspiration the left ventricular stroke volume initially decreased (left ventricular afterload and diastolic interdependence secondary to the increase in right ventricular volume partly counteracted by the effects of systolic interdependence), followed by an increase as the increased venous return reached the left ventricle. The model indicated that the response to a forced expiratory effort was not simply the opposite of the inspiratory response, since the increase in intrathoracic pressure during a forced expiration is accompanied by increases in abdominal pressure. On sustained expiration the left ventricular stroke volume initially increased, with no significant initial change in end diastolic volume. The cardiovascular response to respiration is complex, and model studies can help to isolate and identify the various components involved.

Computer Simulation↗
PubMed1988

Respiration and the ECG: a study using body surface potential maps.

Body surface potential maps and an eccentric spheres model of the heart were used to investigate some of the factors that cause the surface ECG to change with respiration. Although the pattern of the surface maps shifted inferiorly with inspiration, the pattern itself did not change significantly, even with deep respiratory movements. However, the temporal ECGs at specific electrodes changed dramatically. The model simulations show that the contribution to the change in amplitude of the surface potential due to lung conductivity and ventricular volume changes is small. It is suggested that the major cause of the surface potential changes with inspiration is due to the change in heart position.

Adult↗
PubMed1988

The effect of variations of ventricular volume on the electrocardiogram. A comparison of two model simulations.

Two previously published models of the electrocardiogram are compared and evaluated to determine the causes and nature of the relationship between variations in ventricular volumes and surface potential. Both models included a relatively high conductivity spherical heart in a spherical torso, but in one the source was a single dipole, while in the other the source was a double-layer spherical cap. Volume conductor effects (that is the change in electrical conductivity of the torso associated with ventricular volume changes) caused a decrease in surface potential with increase in ventricular volume. Changes in position of the heart and of the strength of the activation wavefront with increases in volume may explain the increase in surface potential with ventricular volume observed in experimental studies.

Cardiac Volume↗
PubMed1987

Non-invasive assessment of lower limb ischaemia by blood velocity wave-form analysis.

Clinical examination combined with angiography is conventionally used to assess lower limb arterial disease. The shape of the blood velocity wave form in the common femoral artery varies with the extent of proximal arterial disease, suggesting that wave-form analysis may provide additional haemodynamic information of potential value in surgical decision-making. This paper studies the use of two methods of wave-form analysis, pulsatility index and Laplace transform analysis, to assess lower limb arterial disease. The blood velocity wave form was measured non-invasively at the common femoral artery using a locally developed mean frequency processor and a commercial 9.5 MHz bidirectional Doppler ultrasound unit. Wave forms from 70 limbs (35 patients) with suspected atherosclerotic arterial disease and from 20 normal limbs with no history or signs of disease were studied. Both methods of wave-form analysis provided a statistically significant separation between patients with severe and moderate disease as assessed angiographically (P less than 0.001). These results suggest that significant aorto-iliac disease can be virtually excluded by a normal common femoral wave form. Furthermore, wave-form analysis may have an important role in the follow-up of patients after bypass grafting or iliac angioplasty and in the detection of presymptomatic aorto-iliac disease.

Adult↗
PubMed1987

Ventricular interdependence and the transient response of the left ventricle to inspiration: a model study.

A mathematical model of the circulation was developed and used to study the transient variations in ventricular volumes with inspiration. The contributions of increased left ventricular afterload, ventricular interdependence, and reduced pulmonary venous flow to the initial decrease in left ventricular stroke volume were examined. Heart rate was kept constant. Right ventricular end diastolic volume increased rapidly, but transiently, with inspiration. Ventricular interdependence affected left ventricular function; it increased the magnitude of the decrease in left ventricular stroke volume, reduced the corresponding increase in end systolic volume, and appeared to be responsible for an initial decrease in end diastolic volume. Despite a 10% pooling of blood in the pulmonary circulation the decrease in pulmonary venous flow was small. It is suggested that the decrease in left ventricular stroke volume is caused both by the reduced intrathoracic pressure, which increases the afterload on the left ventricle, and by the increase in the diastolic elastance of the left ventricle caused by the increase in right ventricular volume (ventricular interdependence). The increased afterload reduces the effective ejection pressure, decreases the stroke volume, and increases the end systolic volume. The increase in left ventricular diastolic elastance, secondary to the increase in right ventricular volume, further reduces the stroke volume by increasing the left ventricular diastolic pressure at a given volume and thus decreases the end diastolic volume.

Blood Pressure↗