Initiation of ventricular contraction as reflected in the aortic pressure waveform

Prior to aortic valve opening, aortic pressure is perturbed by ventricular contraction. The onset of this pressure perturbation coincides with the onset of the left ventricular (LV) isovolumic contraction, and hence will be referred to as the start of the arterially detected isovolumic contraction (AIC start). In the present study we test the hypothesis that the pressure perturbation indeed has a cardiac origin. In ten YorkshireLandrace swine, waveform intensity analysis demonstrated that AIC startwas followed by a positive intensity wave (0.3×10 5 0.3×10 5W (m 2s 2) 1). Timing analysis of LV and aortic pressure waveform showed that AIC startwas preceded by a LV pressure perturbation (3.8 1.8 ms, p < 0.001). These novel cardiac timing and aortic wave intensity findings reveal the cardiac origin of the pressure perturbation. In 15 YorkshireLandrace swine, myocardial motion analysis showed a significantly higher rate of segment shortening during the first part of the LV pressure perturbation. Therefore, both the LV and aortic pressure perturbation are most likely caused by the early phase of myocardial contraction, which also causes mitral valve closure. Consequently, AIC startis useful in the determination of the isovolumic contraction period, a well-known marker to quantify cardiac dysfunction

A novel approach to assess hemorrhagic shock severity using the arterially determined left ventricular isovolumic contraction period

Recently, the ventilatory variation in pre-ejection period (ΔPEP) was found to be useful in the prediction of fluid-responsiveness of patients in shock. In the present study we investigated the behavior of the ventilation-induced variations in the systolic timing intervals in response to a graded hemorrhage protocol. The timing intervals studied included the ventilatory variation in ventricular electromechanical delay (ΔEMD), isovolumic contraction period (determined from the arterial pressure waveform, ΔAIC), pulse travel time (ΔPTT), and ΔPEP. ΔAIC and ΔPEP were evaluated in the aorta and carotid artery (annotated by subscripts Ao and CA) and were compared with the responses of pulse pressure variation (ΔPPAo) and stroke volume variation (ΔSV). The graded hemorrhage protocol, followed by resuscitation using norepinephrine and autologous blood transfusion, was performed in eight anesthetized Yorkshire X Landrace swine. ΔAICAo, ΔAICCA, ΔPEPAo, ΔPEPCA, ΔPPAo, ΔPPCA, and ΔSV showed significant increases during the graded hemorrhage and significant decreases during the subsequent resuscitation. ΔAICAo, ΔAICCA, ΔPEPAo, and ΔPEPCA all correlated well with ΔPPAo and ΔSV (all r ≥ 0.8, all P < 0.001). ΔEMD and ΔPTT did not significantly change throughout the protocol. In contrast with ΔPEPAo, which was significantly higher than ΔPEPCA (P < 0.01), ΔAICAo was not different from ΔAICCA. In conclusion, ventilation-induced preload variation principally affects the arterially determined isovolumic contraction period (AIC). Moreover, ΔAIC can be determined solely from the arterial pressure waveform, whereas ΔPEP also requires ECG measurement. Importantly, ΔAIC determined from either the carotid or aortic pressure waveform are interchangeable, suggesting that, in contrast with ΔPEP, ΔAIC may be site independent

Hand exoskeleton structure for interacting with virtual objects

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