Tonometric arterial pulse sensor with noise cancellation.

Arterial tonometry provides for the continuous and noninvasive recording of the arterial pressure waveform. However, tonometers are affected by motion artifact that degrades the signal. An arterial tonometer was constructed using two piezoelectric transducers centered within a solid base. In two subjects, one transducer was positioned over the radial pulse (p) and the other was positioned on the wrist not overlying the pulse (n). The presence of induced motion artifact and any noise was removed after signal digitization by noise cancellation. Besides fixed weighting, two adaptive algorithms were used for cancellation-LMS and differential steepest descent (DSD). Criteria were developed for comparison of the adaptive techniques. The best fixed weighting for noise cancellation was w=0.6. For fixed-weighting, LMS, and DSD, the mean peak-to-peak errors were 1.22+/-0.54, 1.18+/-0.30, and 1.16+/-0.23 V, respectively, and the mean point-to-point errors were 15.86+/-3.15, 11.40+/-1.96, and 10.13+/-1.25 V, respectively. Noise cancellation using a common-mode reference input substantially reduces motion artifact and other noise from the acquired tonometric arterial pulse signal. Adaptive weighting provides better cancellation than fixed weighting, likely because the mechanical gain at the transducer-skin interface is time-varying.

Measurement and monitoring of electrocardiogram belt tension in premature infants for assessment of respiratory function.

BACKGROUND: Monitoring of the electrocardiogram (ECG) in premature infants with conventional adhesive-backed electrodes can harm their sensitive skin. Use of an electrode belt prevents skin irritation, but the effect of belt pressure on respiratory function is unknown. A strain gauge sensor is described which measures applied belt tension. METHOD: The device frame was comprised of an aluminum housing and slide to minimize the device weight. Velcro tabs connected housing and slide to opposite tabs located at the electrode belt ends. The slide was connected to a leaf spring, to which were bonded two piezoresistive transducers in a half-bridge circuit configuration. The device was tested for linearity and calibrated. The effect on infant respiratory function of constant belt tension in the normal range (30 g-90 g) was determined. RESULTS: The mechanical response to a step input was second order (fn = 401 Hz, zeta = 0.08). The relationship between applied tension and output voltage was linear in the range 25-225 gm of applied tension (r2 = 0.99). Measured device sensitivity was 2.18 mV/gm tension using a 5 V bridge excitation voltage. When belt tension was increased in the normal range from 30 gm to 90 gm, there was no significant change in heart rate and most respiratory functions during monitoring. At an intermediate level of tension of 50 gm, pulmonary resistance and work of breathing significantly decreased. CONCLUSION: The mechanical and electrical design of a device for monitoring electrocardiogram electrode belt tension is described. Within the typical range of application tension, cardiovascular and respiratory function are not substantially negatively affected by electrode belt force.

Experimental evaluation of the elastic determinants of myocardial function in vivo.

Shortening of myocardial fibers occurs following force development in those fibers. The extent, speed and timing of shortening are determined by kinetics and extent of force. However, shortening is also influenced by the elastance/viscosity of the muscle tissue, because that determines the coupling between force and shortening. In the in vivo dog heart, we estimated that coupling by measuring local myocardial force and fiber shortening independently under various conditions. We determined the effect of positive and negative inotropy (by intracoronary injection of dobutamine and acetylcholine, respectively), and of dysfunctional contraction produced by local ischemia/reperfusion and BDM. Under baseline and both positive and negative intropy, most shortening occurred during systole, and dobutamine increased the proportion of total shortening in early systole from 45.8 +/- 8.5% to 74.9 +/- 9.6%. During reperfusion following ischemia, shortening in early systole was markedly reduced to 16.5 +/- 2.9; BDM caused a similar reduction to 16.5 +/- 8.1. Most of the shortening occurred during early diastole (53.0 +/- 6.8 for reperfusion, and 54.0 +/- 10.3 for BDM). These effects were all reversible. It is concluded that energetic efficiency is greatly affected by the elastic properties coupling force and shortening. Thus appropriate analysis of muscle function must take into account the changeable elastic properties of the tissue-both force and shortening, and their interaction must be considered.

Cardiac force and muscle shortening in regional ischemia: asynchronization and possible uncoupling.

Acute myocardial ischemia affects both cardiac muscle force development and shortening in the affected regions. The exact mechanisms are unclear. We investigated myocardial function during ischemia and reperfusion both experimentally and with a muscle fiber model. The model was subjected to perturbations in contractility and force activation. Results show that the cardiac muscle model reflects many of the physiological changes observed in myocardial ischemia and reperfusion. Asynchronization between force generation and muscle shortening observed during regional ischemia and reperfusion may be dependent on the extent of their uncoupling.

Effects of partial ischaemia and volume loading on myocardial efficiency and cardiac performance in dogs.

AIMS AND METHODS: To determine whether volume loading may be beneficial for the performance of ischaemic heart, myocardial ischaemia was created by partial occlusion of the left anterior descending coronary artery (LAD) to reduce the blood flow to 30 approximately 40% of basal level in 11 open chest anaesthetised dogs. Global left ventricular function as well as regional performance were studied under four different levels of volume loading, euvolemia (EUVO), hypervolemia (HYPER), normovolemia and hypovolemia. RESULTS: Left ventricular dP/dt(max) and cardiac output were decreased significantly during partial occlusion (3511.2+/-425.2 mmHg/s and 0.9+/-0.1 l/min) compared with pre-occlusion (4486.5+/-419.2 mmHg/s and 1.3+/-0.1 l/min) (P<0.05). Cardiac work was also lowered during partial occlusion (75.4+/-5.2 vs. 106.5+/-2.4 mmHgxl/min) (P<0.05). During volume loading, cardiac output and work were elevated (1.2+/-0.2 l/min and 94.0+/-5.4 mmHgxl/min) compared with EUVO (P<0.05). Local contractile dysfunction occurred in the LAD region after partial occlusion. There were no significant differences of dysfunction between any conditions of volume loading. Percentage shortening of the LAD region was decreased during partial occlusion (8.3+/-1.1 vs. 25.0+/-2.7%) and also was higher in HYPER (13.5+/-2.6%) than that in EUVO (P<0.05). Partial occlusion and different conditions of volume loading did not significantly change the force and local work in the LAD region. Myocardial O(2) consumption (MVO(2)) in LAD region was decreased during partial occlusion with different levels of volume loading (P<0.05). Local myocardial efficiency (work/MVO(2)) was increased during partial occlusion compared with pre-occlusion (941.3+/-56.2 vs. 551.0+/-65.5 gxmm/ml O(2)/min/100 g, P<0.05) and was also higher in HYPER (1208.6+/-48.4 gxmm/ml O(2)/min/100 g) than that in EUVO (P<0.05). Local systolic work was decreased during partial occlusion compared with pre-occlusion (9.5+/-1.5 vs. 14.2+/-1.3 gxmm/beat), whereas local myocardial systolic mechanical efficiency was increased (496.3+/-45.7 vs. 667.2+/-39.8 gxmm/ml O(2)/min/100 g). There were no significant changes of local systolic work and local systolic myocardial efficiency between different volume loading, although they tend to be elevated with increasing volume loading. CONCLUSION: Increase of blood volume by 15% improved the impaired global performance caused by partial occlusion of the LAD in open-chest dogs. This improvement was not accompanied by further dysfunction or increased MVO(2) of ischaemic myocardium, and therefore might be beneficial without causing further damage to the insulted myocytes.