BackgroundPulse pressure, the ambulatory arterial stiffness index (AASI), and the symmetric AASI are established predictors of adverse cardiovascular outcomes. However, little is known about their relationship to cerebral autoregulation. This study evaluated whether these markers of vascular properties relate to the lower limit of cerebral autoregulation (LLA).Methods and ResultsThe LLA was determined during cardiac surgery with transcranial Doppler ultrasonography in 181 patients. All other variables were calculated from continuous intraoperative readings obtained before cardiopulmonary bypass. The LLA varied directly with the AASI (β=3.12 per 0.1 change in AASI, P<0.001) and to a lesser extent the symmetric AASI (β=2.02 per 0.1 change in symmetric AASI, P≤0.022), while peripheral pulse pressure was not significantly related (β=0.0, P>0.99). Logistic regression revealed that the likelihood of LLA being >65 mm Hg increased by 50% (95% confidence interval, 11%–102%, P=0.008) for every 0.1 increase in the AASI. The AASI was able to predict a LLA above certain thresholds (area under the curve receiver operating characteristic for AASI predicting an LLA >65 mm Hg: 0.60; 95% confidence interval, 0.51%–0.68%, P=0.043). Incorporating additional variables improved the model's predictive ability (area under the curve for AASI predicting a LLA >65 mm Hg: 0.75; 95% confidence interval, 0.68–0.82, P=0.036).ConclusionsThese data indicate that the LLA is related to the mechanical properties of the vasculature as represented by the AASI. The AASI can be used to predict LLA threshold levels during cardiac surgery. It is now possible to link elevations in the LLA with an increased AASI as determined from readily accessible intraoperative variables.

The left ventricular ejection time is routinely measured from a peripheral arterial waveform. However, the arterial waveform undergoes constant transformation as the pulse wave propagates along the arterial tree. Our goal was to determine if the left ventricular ejection time measured peripherally in the arterial tree accurately reflected the ejection time measured through the aortic valve. Moreover, we examined/accessed the modulating influence of hemodynamics on ejection time measurements. Continuous wave Doppler waveform images through the aortic valve and the simultaneously obtained radial artery pressure waveforms were analyzed to determine central and peripheral ejection times, respectively. The peripheral ejection time was significantly longer than the simultaneously measured central ejection time (174.5±25.2 ms vs. 120.7±14.4 ms; P<0.0001; 17.4±8.7% increase). Moreover, the ejection time prolongation was accentuated at lower blood pressures, lower heart rate and lower pulse wave velocity. The time difference between centrally and peripherally measured ejection times likely reflects intrinsic vascular characteristics. Moreover, given that the ejection time also depends on blood pressure, heart rate and pulse wave velocity, peripherally measured ejection times might need to be adjusted to account for changes in these variables.

The effect of blood pressure on pulse wave velocity (PWV) is well established. However, PWV variability with acute hemodynamic changes has not been examined in the clinical setting. The aim of the present study is to investigate the effect of hemodynamic changes on PWV in patients who undergo cardiothoracic surgery. Using data from 25 patients, we determined blood pressure (BP), heart rate (HR), and the left ventricular outflow tract (LVOT) velocity-time integral. By superimposing the radial arterial waveform on the continuous wave Doppler waveform of the LVOT, obtained by transesophageal echo, we were able to determine pulse transit time and to calculate PWV, stroke volume (SV), cardiac output (CO), and systemic vascular resistance (SVR). Increases in BP, HR, and SVR were associated with higher values for PWV. In contrast increases in SV were associated with decreases in PWV. Changes in CO were not significantly associated with PWV.

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Background: The effects of position and exercise on pulse wave distribution across a healthy, compliant arterial tree are not fully understood. We studied the effects of exercise and position on the pattern of pulse arrival times (PATs) in healthy volunteers. Moreover, we compared the pulse arrival time ratios to the respective distance ratios between different locations.Methods: Thirteen young healthy volunteers were studied, using an electrocardiogram and plethysmograph to simultaneously record pulse wave arrival at the ear lobe, index finger and big toe. We compared the differences in PAT between each location at rest and post-exercise in the supine, sitting, and standing position. We also compared the PAT ratio (toe/ear, toe/finger, and finger/ear) to the corresponding pulse path distance ratios.Results: PAT was shortest at the ear then finger and longest at the toe regardless of position or exercise status. PATs were shorter post-exercise compared to rest. When transitioning from a standing to sitting or supine position, PAT to the ear decreased, while the PAT to the toe increased, and PAT to the finger didn't significantly change. PAT ratios were significantly smaller than predicted by the path distance ratios regardless of position or exercise status.Conclusions: Exercise makes PATs shorter. Standing position decrease PAT to the toe and increase to the ear. We conclude that PAT and PAT ratio represent the arterial vascular tree properties as surely as pulse transit time and pulse wave velocity.

Background: Constant blood flow despite changes in blood pressure, a phenomenon called autoregulation, has been demonstrated for various organ systems. We hypothesized that by changing hydrostatic pressures in peripheral arteries, we can establish these limits of autoregulation in peripheral arteries based on local pulse wave velocity (PWV).Methods: Electrocardiogram and plethysmograph waveforms were recorded at the left and right index fingers in 18 healthy volunteers. Each subject changed their left arm position, keeping the right arm stationary. Pulse arrival times (PAT) at both fingers were measured and used to calculate PWV. We calculated ΔPAT (ΔPWV), the differences between the left and right PATs (PWVs), and compared them to the respective calculated blood pressure at the left index fingertip to derive the limits of autoregulation.Results: ΔPAT decreased and ΔPWV increased exponentially at low blood pressures in the fingertip up to a blood pressure of 70 mmHg, after which changes in ΔPAT and ΔPWV were minimal. The empirically chosen 20 mmHg window (75–95 mmHg) was confirmed to be within the autoregulatory limit (slope = 0.097, p = 0.56). ΔPAT and ΔPWV within a 20 mmHg moving window were not significantly different from the respective data points within the control 75–95 mmHg window when the pressure at the fingertip was between 56 and 110 mmHg for ΔPAT and between 57 and 112 mmHg for ΔPWV.Conclusions: Changes in hydrostatic pressure due to changes in arm position significantly affect peripheral arterial stiffness as assessed by ΔPAT and ΔPWV, allowing us to estimate peripheral autoregulation limits based on PWV.

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Both pheochromocytoma and amniotic fluid embolism (AFE) are important causes of maternal mortality. We present a case of a 29-year-old woman who developed cardiac arrest after Caesarean section, complicated by both pheochromocytoma crisis and AFE. After resuscitation, the patient developed multiple organ dysfunction, rhabdomyolysis and disseminated intravascular coagulation (DIC). After institution of multidisciplinary interventions (including the use of an intra-aortic balloon pump, extracorporeal membrane oxygenation, continuous hemodiafiltration, and neuroprotective therapeutic hypothermia) the patient made a full recovery without any apparent neurological deficit.