Blood Pressure Regulation Mechanisms
To maintain a steady flow of blood from the heart to the extremities is essential for correct organ function. Moreover, making sure that a person standing up from a lying down position gets adequate blood flow to the brain requires precise cooperation of the heart, blood vessels, and kidneys, all of these with the supervision of the brain. The most crucial of regulation mechanisms of cardiovascular dynamics, are the ones that maintain blood pressure, mainly cardiac output, blood volume and peripheral resistance.
Regulation mechanisms can affect pressure both in the short-term and long-term. Short-term mechanisms usually involve a change in sympathetic and parasympathetic activity, changing cardiac output and peripheral resistance. Long-term regulation involves renal regulation of blood volume via the renin-angiotensin and aldosterone mechanisms.
When arterial blood pressure rises, it stretches baroreceptors, neural receptors located in the carotid sinuses (dilations in the internal carotid arteries, which provide the major blood supply to the brain), in the aortic arch, and in the walls of nearly every large artery of the neck and thorax. When stretched, baroreceptors send a rapid stream of impulses to the brain that provoke increased activity of parasympathetic nerves and decreased sympathetic activity. This leads to a reduction of heart rate, which induces less cardiac output, and relaxation of vascular smooth muscle, that causes an increased arterial diameter. These promote the lowering of blood pressure.
On the other hand, for falling blood pressure, the baroreceptors are inhibited and send fewer impulses to the brain, causing a decrease in parasympathetic activity and an increase in sympathetic activity. The increased activity of sympathetic nerves acts on three fronts. The first one is the increase heart rate and contractility that cause and higher cardiac output and therefore higher blood pressure. The second is the increased constriction of vascular smooth muscle and decreases arterial diameter to increase peripheral resistance and blood pressure. The third is the effect of the sympathetic activity on adrenal glands. More commonly if a period of stress occurs, the adrenal gland releases norepinephrine and epinephrine to the bloodstream, hormones that enhance the sympathetic response. Norepinephrine has a vasoconstrictive action, while epinephrine promotes generalized vasoconstriction (except in skeletal and cardiac muscle) and increases heart rate and contractility. This effect is slower-acting and a bit more prolonged than the direct nervous control.
There are more hormone control mechanisms for short-term effects on blood pressure. For example, Atrial natriuretic peptide (ANP) produced by the atria of the heart, causes generalized vasoconstriction. It also inhibits aldosterone and renin secretion, and decreases sodium and water reabsorption in the kidneys, leading to a drop in blood volume. Angiotensin, generated by renin, and involved in long-term regulation mechanisms, also stimulates intense vasoconstriction, promoting a rapid rise in systemic blood pressure.
Results and Discussion
The first and overall objective was to see how well Pulse transit time would relate to Blood Pressure. First impressions (fig.) were that PTT variations weren't very predictable, and usually not following any trend with systolic blood pressure:
Linear correlation was then calculated to assess how well a linear equation would fit the data. Furthermore, PTT was transformed according to an adaptation of the Moens-Kortweg equation describing a quadratic relationship between PTT and BP and new linear correlations were calculated.
Correlations are generally low, being either positive or negative. Extreme values of correlation improved with the quadratic transformation, however, variability is still very high, and average correlation still very low.
As PTT showed such unpredictable variability, a discussion was raised about the validity of its measurement. It has been showed that PEP estimation through impedance can result in errors of 9-12 milliseconds and with PTT measures in a 40-50 ms range, its measurement based on PAT with PEP compensation may introduce too much uncertainty. Furthermore, with Moens-Kortweg based models, it is estimated that a change of about 10 mmHg in blood pressure should inflict a change in PTT of about 8-16 ms (depending on PTT starting value), so there might be the need for very accurate measurement techniques here.
Pulse arrival time was expected to provide better correlation results and they were significantly improved. Applying PAT on the quadratic approximation provided an even superior outcome:
The next step was to separate each run consisting of exercise followed by a recovery period. Typical results:
Separating exercise and recovery periods produced improved correlation results for some runs, but accompanied by weaker results for other runs in the same patient. It's observed a high inter and intra-subject variability of the trends of variation of systolic BP with PAT.
The same study was carried out for the variation of heart rate with PAT. With separation of exercise and recovery runs there is always an observable trend of hysteresis:
Here, there is a clear 3 phase phenomenon:
first part of recovery,
second part of recovery with almost constant HR.
Most patients also seem to have a different phase into 1 minute of exercise where changes are mostly in PAT and PEP;
The first phase of recovery is where HR returns to a lower state, and is mostly HR dependent;
The final phase of recovery is dominated by PAT and PEP changes only.
It is very clear for the recovery period the fast action of HR decrease and the delayed PAT/PEP increase.
only –probably a different regulation mechanism dominates here, with a delayed effect.
could be changes in peripheral resistance with consequence in Aorta pressure that influences PEP.
Conclusions And Future Work
Pulse transit time had unpredictable changes in this study, and even with a big measurement error margin, it is not hard to deduce that it may not be the best way to get a blood pressure measurement for short physical exercises, or calibrating a system. Since, theoretically, the vasoconstriction that usually accompanies exercise should increase the pulse wave velocity (decrease in pulse transit time), we could explain a constant PTT with the incidence of a higher peripheral resistance that would slow down the arrival of blood at the extremities. This shouldn't affect the occurrence of higher blood pressure. Nevertheless, we shouldn't disregard PTT completely for future applications as we still believe it can be an important marker, e.g., for assessing peripheral resistance, useful for evaluating hemodynamic/cardiovascular status.
On the other hand, Pulse arrival time changed clearly for the exercise runs (dominated mostly by changes in Pre ejection period), had good correlations with systolic blood pressure, but their variations didn't always fit, with the possibility of one of them remaining constant while the other does not. There is also a lot of unpredictability of this occurrence even for different runs on the same patient. Therefore, we could not describe a precise and direct relationship of PAT with SBP.
Analyzing Heart Rate changes provided an interesting insight into cardiovascular dynamics. We can clearly discriminate differences in time of the variations in Heart Rate and PAT with a similar pattern occurring very frequently. We conclude that changes in PAT/PEP occur during much longer periods, especially during recovery, and compensation of HR effects strengthens this difference. With this in mind, we can distinguish the moments where the possible cardiovascular regulation mechanisms are affecting or ceasing to affect HR or PAT/PEP, e.g., increase of Heart Rate due to sympathetic activity; changes in circulatory resistance that can have an effect on Aorta pressure that can influence PEP. For that reason, there's the possibility that the identification of the incidence of regulation mechanisms may lead to a comprehensive evaluation of the cardiovascular or hemodynamic status of a subject.
Future work. Validate hypothesis using datasets, relate to cardiovascular models.