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.

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 Yorkshire-Landrace swine, waveform intensity analysis demonstrated that AIC(start) was followed by a positive intensity wave (0.3 × 10(5) ± 0.3 × 10(5) W (m(2) s(2))(-1)). Timing analysis of LV and aortic pressure waveform showed that AIC(start) was 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 Yorkshire-Landrace 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(start) is useful in the determination of the isovolumic contraction period, a well-known marker to quantify cardiac dysfunction.

Coronary-aortic interaction during ventricular isovolumic contraction.

In earlier work, we suggested that the start of the isovolumic contraction period could be detected in arterial pressure waveforms as the start of a temporary pre-systolic pressure perturbation (AIC(start), start of the Arterially detected Isovolumic Contraction), and proposed the retrograde coronary blood volume flow in combination with a backwards traveling pressure wave as its most likely origin. In this study, we tested this hypothesis by means of a coronary artery occlusion protocol. In six Yorkshire × Landrace swine, we simultaneously occluded the left anterior descending (LAD) and left circumflex (LCx) artery for 5 s followed by a 20-s reperfusion period and repeated this sequence at least two more times. A similar procedure was used to occlude only the right coronary artery (RCA) and finally all three main coronary arteries simultaneously. None of the occlusion protocols caused a decrease in the arterial pressure perturbation in the aorta during occlusion (P > 0.20) nor an increase during reactive hyperemia (P > 0.22), despite a higher deceleration of coronary blood volume flow (P = 0.03) or increased coronary conductance (P = 0.04) during hyperemia. These results show that the pre-systolic aortic pressure perturbation does not originate from the coronary arteries.

Norovirus on swabs taken from hands illustrate route of transmission: a case study.

Recently, environmental swabs from kitchen and bathroom surfaces have been described as an additional tool for the detection of norovirus in outbreak settings. This article describes an outbreak investigation in response to the reporting of gastroenteritis in three unrelated groups of 6, 12, and 13 adults approximately 30 h after having meals in the same restaurant. Fecal samples were collected from 13 patients and six food handlers, and environmental swabs were taken from the soap dispenser, working bench, doorknobs of cupboards, and the grip of a knife in the kitchen and in bathrooms as well as from the hands of each of three employees on the day of inspection. Clinical and environmental samples were analyzed separately in time and location for the presence of norovirus by real-time reverse transcription PCR. Structured interviews revealed that all staff members had suffered from gastroenteritis, one after the other. Norovirus RNA (GGI.6) was detected in 17 of 19 fecal samples as well as in 4 environmental samples, including a swab sample from the hands of a staff member who was preparing ready-to-eat food. Sequences obtained from clinical and environmental samples showed an identity of 100% (235 nucleotides). To our knowledge, this is the first case study to directly demonstrate the presence of norovirus RNA on a food handler's hands in an outbreak setting. This finding provides direct evidence for the feasibility of transmission of norovirus by a food handler to food. Education of food handlers on the infectivity of norovirus and updating of hygienic codes are strongly recommended.