Cardiac oxygen supply is compromised during the night in hypertensive patients

The enhanced heart rate and blood pressure soon after awaking increases cardiac oxygen demand, and has been associated with the high incidence of acute myocardial infarction in the morning. The behavior of cardiac oxygen supply is unknown. We hypothesized that oxygen supply decreases in the morning and to that purpose investigated cardiac oxygen demand and oxygen supply at night and after awaking. We compared hypertensive to normotensive subjects and furthermore assessed whether pressures measured non-invasively and intra-arterially give similar results. Aortic pressure was reconstructed from 24-h intra-brachial and simultaneously obtained non-invasive finger pressure in 14 hypertensives and 8 normotensives. Supply was assessed by Diastolic Time Fraction (DTF, ratio of diastolic and heart period), demand by Rate-Pressure Product (RPP, systolic pressure times heart rate, HR) and supply/demand ratio by Adia/Asys, with Adia and Asys diastolic and systolic areas under the aortic pressure curve. Hypertensives had lower supply by DTF and higher demand by RPP than normotensives during the night. DTF decreased and RPP increased in both groups after awaking. The DTF of hypertensives decreased less becoming similar to the DTF of normotensives in the morning; the RPP remained higher. Adia/Asys followed the pattern of DTF. Findings from invasively and non-invasively determined pressure were similar. The cardiac oxygen supply/demand ratio in hypertensive patients is lower than in normotensives at night. With a smaller night-day differences, the hypertensives’ risk for cardiovascular events may be more evenly spread over the 24 h. This information can be obtained noninvasively

Forearm arterial pressure-volume relationships in man

Pressure-volume (p-V) relationships of a segment of the forearm circulation have been measured in nine male healthy subjects. Forearm volume was measured using electrical impedance plethysmography, arterial transmural pressure by subtracting mean arterial pressure measured contralaterally in a finger from the pressure in a cuff placed over the sensing electrodes of the plethysmograph. A special two-phase measurement waveform was designed with which cuff pressure was first increased step wise to a suprasystolic level and held at that level for 120 s, then ramped down to zero pressure in another 300 s. The step phase inflation allowed us to estimate the parameters of the interstitial liquids and total blood compartments. The total blood compartment amounted to 6.2 ml per 100 ml of tissue. The ramp phase deflation allowed us to discriminate between a first phase in which only the arteries refilled and a second phase in which the veins also distended. An arctangent function was fitted to the first phase arterial p-V relationship, describing it in model form. Total arterial volume per 100 ml of tissue amounted to 3.8 ml at physiological pressures, total arterial compliance of the forearm per centimetre length to 19.5 microliter kPa-1 cm-1 (2.6 microliter mmHg-1 cm-1) at physiological pressures, and to 340 microliter kPa-1 cm-1 (45 microliter mmHg-1 cm-1) maximum compliance at the lower, inflection point pressures. These values are in general agreement with the literature. Pulse wave velocity cannot be computed reliably from these data

Models of brachial to finger pulse wave distortion and pressure decrement

Objective: To model the pulse wave distortion and pressure decrement occurring between brachial and finger arteries. Distortion reversion and decrement correction were also our aims. Methods: Brachial artery pressure was recorded intra-arterially and finger pressure was recorded non-invasively by the Finapres technique in 53 adult human subjects. Mean pressure was subtracted from each pressure waveform and Fourier analysis applied to the pulsations. A distortion model was estimated for each subject and averaged over the group. The average inverse model was applied to the full finger pressure waveform. The pressure decrement was modelled by multiple regression on finger systolic and diastolic levels. Results: Waveform distortion could be described by a general, frequency dependent model having a resonance at 7.3 Hz. The general inverse model has an anti-resonance at this frequency. It converts finger to brachial pulsations thereby reducing average waveform distortion from 9.7 (s.d. 3.2) mmHg per sample for the finger pulse to 3.7 (1.7) mmHg for the converted pulse. Systolic and diastolic level differences between finger and brachial arterial pressures changed from -4 (15) and -8 (11) to +8 (14) and +8 (12) mmHg, respectively, after inverse modelling, with pulse pressures correct on average. The pressure decrement model reduced both the mean and the standard deviation of systolic and diastolic level differences to 0 (13) and 0 (8) mmHg. Diastolic differences were thus reduced most. Conclusion: Brachial to finger pulse wave distortion due to wave reflection in arteries is almost identical in all subjects and can be modelled by a single resonance. The pressure decrement due to flow in arteries is greatest for high pulse pressures superimposed on low means

Finapres tracking of systolic pressure and baroreflex sensitivity improved by waveform filtering

Objective. Arterial pressure waveforms distort between brachial and finger arteries, causing differences mainly in systolic pressure. Distortion, reportedly, can be removed by applying a waveform filter to the finger pressure. Design. We analysed the data from two studies that detected discrepancies in systolic tracking between Finapres and brachial pressures. The first set comprised waveforms of seven volunteers during incremental bicycle exercise to exhaustion and the second set comprised waveforms of eight volunteers during increasing phenylephrine infusion. Methods. We applied the filter and compared 1 min averaged unfiltered and waveform-filtered finger and brachial pressures. Results. During exercise, finger systolic pressure overestimated brachial increasingly, from 7 (SD 10) mmHg at rest to 27 (17) mmHg at maximal exertion. Differences were reduced by waveform filtering from 3 (SD 9) mmHg at rest to 1 (SD 15) mmHg at maximal exertion. During phenylephrine infusion finger systolic pressure overestimated brachial pressure, but the magnitude of the overestimate decreased from 14(SD 15) mmHg at baseline to -1 (SD 16) mmHg at maximal rate. After waveform filtering over-estimation was an almost constant 6 (SD 11) mmHg. Median baroreflex sensitivities from brachial, unfiltered and waveform-filtered finger pressure were 5.8, 7.5 and 5.3 ms/mmHg and correlation increased after filtering. The results indicate improved systolic pressure tracking after waveform filtering. Conclusions. Finger pressure distortion follows a general pattern correctable by waveform filtering. Waveform filtering allows a 'brachial' view to be obtained from Finapres data