Lysander W. J. Bogert

Non-invasive pulsatile arterial pressure and stroke volume changes from the human finger.

In this paper we review recent developments in the methodology of non‐invasive finger arterial pressure measurement and the information about arterial flow that can be obtained from it. Continuous measurement of finger pressure based on the volume‐clamp method was introduced in the early 1980s both for research purposes and for clinical medicine. Finger pressure tracks intra‐arterial pressure but the pressure waves may differ systematically both in shape and magnitude. Such bias can, at least partly, be circumvented by reconstruction of brachial pressure from finger pressure by using a general inverse anti‐resonance model correcting for the difference in pressure waveforms and an individual forearm cuff calibration. The Modelflow method as implemented in the Finometer computes an aortic flow waveform from peripheral arterial pressure by simulating a non‐linear three‐element model of the aortic input impedance. The methodology tracks fast changes in stroke volume (SV) during various experimental protocols including postural stress and exercise. If absolute values are required, calibration against a gold standard is needed. Otherwise, Modelflow‐measured SV is expressed as change from control with the same precision in tracking. Beat‐to‐beat information on arterial flow offers important and clinically relevant information on the circulation beyond what can be detected by arterial pressure.

Pulse contour cardiac output derived from non-invasive arterial pressure in cardiovascular disease

Pulse contour methods determine cardiac output semi‐invasively using standard arterial access. This study assessed whether cardiac output can be determined non‐invasively by replacing the intra‐arterial pressure input with a non‐invasive finger arterial pressure input in two methods, Nexfin CO‐trek® and Modelflow®, in 25 awake patients after coronary artery bypass surgery. Pulmonary artery thermodilution cardiac output served as a reference. In the supine position, the mean (SD) differences between thermodilution cardiac output and Nexfin CO‐trek were 0.22 (0.77) and 0.44 (0.81) l.min−1, for intra‐arterial and non‐invasive pressures, respectively. For Modelflow, these differences were 0.70 (1.08) and 1.80 (1.59) l.min−1, respectively. Similarly, in the sitting position, differences between thermodilution cardiac output and Nexfin CO‐trek were 0.16 (0.78) and 0.34 (0.83), for intra‐arterial and non‐invasive arterial pressure, respectively. For Modelflow, these differences were 0.58 (1.11) and 1.52 (1.54) l.min−1, respectively. Thus, Nexfin CO‐trek readings were not different from thermodilution cardiac output, for both invasive and non‐invasive inputs. However, Modelflow readings differed greatly from thermodilution when using non‐invasive arterial pressure input.

Active standing reduces wave reflection in the presence of increased peripheral resistance in young and old healthy individuals.

Objective Pressure wave reflections are age-dependent and generally assumed to increase with increasing peripheral resistance. We sought to determine the effect of standing on wave reflection in healthy older and younger individuals and the influence of increased peripheral resistance. Methods During supine rest and active standing, continuous finger arterial blood pressure was measured. Data obtained in the supine period and after 1 and 5 min standing were analysed. Aortic pressure and flow, calculated from finger pressure, were used to derive forward and backward pressure waves, reflection magnitude (ratio of backward and forward pressure waves), augmentation index, and peripheral resistance. Results Fifteen healthy older (aged 53 ± 7 years) and 15 healthy younger (aged 29 ± 5 years) individuals were included. In both groups, upon standing, stroke volume, cardiac output and pulse pressure decreased with an increase in heart rate and in diastolic pressure. In the older group peripheral resistance increased from 1.3 ± 0.4 to 1.5 ± 0.4 and 1.5 ± 0.4 for supine, 1 and 5 min standing, whereas reflection magnitude decreased from 0.67 ± 0.1 to 0.61 ± 0.1 and 0.61 ± 0.1, and augmentation index from 33 ± 11 to 23 ± 12 and 25 ± 11. In the younger group peripheral resistance increased from 0.9 ± 0.2 to 1.1 ± 0.2 and 1.1 ± 0.2, whereas reflection magnitude decreased from 0.55 ± 0.05 to 0.48 ± 0.05 and 0.49 ± 0.05 and augmentation index from 18 ± 11 to 1 ± 18 and 4 ± 19. Conclusion With standing, haemodynamic variables change similarly in older and younger individuals. The opposite changes in reflection magnitude and peripheral resistance suggest that reflection and pressure augmentation are not solely dependent on peripheral resistance.

Reconstruction of brachial pressure from finger arterial pressure during orthostasis

Introduction In patients with recurrent syncope, monitoring of intra-arterial pressure during orthostatic stress testing is recommended because of the potentially sudden and rapid development of hypotension. Replacing brachial arterial pressure (BAP) by the non-invasively obtained finger arterial pressure (FinAP) has advantages because catheterization in itself may provoke a syncope. Objective To investigate whether reconstruction of the brachial pressure curve (ReBAP) from FinAP can account for systolic and diastolic offset in the recorded pressure on the transition from a supine to an upright position and during maintained postural stress. Methods In nine healthy young subjects BAP and FinAP were recorded in the supine position, during 8 min of standing and during 20 min of 70° passive head-up tilt (HUT70) whereafter three of the subjects fainted within 20 min of HUT. The FinAP signal was modeled off-line into a reconstructed brachial pressure curve. Results For FinAP but not for ReBAP, systolic (P < 0.05) and diastolic (P < 0.001) bias increased in the transition from the supine to the HUT position. Bias for the systolic pressure in the supine position and after 7.5 and 20 min of HUT were 2, 7 and 11 mmHg for FinAP but only 0, −2 and 1 mmHg for ReBAP (P < 0.05 for HUT). For the diastolic pressure these values were −2, 5 and 8 mmHg for FinAP and 4, 5 and 6 for ReBAP (P < 0.01 for supine). Conclusions Brachial pressure reconstruction from the finger arterial pressure waveform accounts for the bias from the supine to the upright position, eliminates the bias for the systolic but not for diastolic finger pressure and reduces the trend in diastolic bias with increased tilt duration.

Effects of aging on the cerebrovascular orthostatic response

When healthy subjects stand up, it is associated with a reduction in cerebral blood velocity and oxygenation although cerebral autoregulation would be considered to prevent a decrease in cerebral perfusion. Aging is associated with a higher incidence of falls, and in the elderly falls may occur particularly during the adaptation to postural change. This study evaluated the cerebrovascular adaptation to postural change in 15 healthy younger (YNG) vs. 15 older (OLD) subjects by recordings of the near-infrared spectroscopy-determined cerebral oxygenation (cO₂Hb) and the transcranial Doppler-determined mean middle cerebral artery blood velocity (MCA V(mean)). In OLD (59 (52-65) years) vs. YNG (29 (27-33) years), the initial postural decline in mean arterial pressure (-52 ± 3% vs. -67 ± 3%), cO₂Hb (-3.4 ± 2.5 μmoll(-1) vs. -5.3 ± 1.7 μmoll(-1)) and MCA V(mean) (-16 ± 4% vs. -29 ± 3%) was smaller. The decline in MCA V(mean) was related to the reduction in MAP. During prolonged orthostatic stress, the decline in MCA V(mean)and cO(2)Hb in OLD remained smaller. We conclude that with healthy aging the postural reduction in cerebral perfusion becomes less prominent.

Abnormal haemodynamic postural response in patients with chronic heart failure

The objective was to evaluate in treated heart failure (HF) patients whether multidrug therapy interferes with the cardiovascular autonomic response to postural stress.