If you conduct fMRI experiments then you'll have at least a basic understanding of the cascade of events that we term neurovascular coupling. When the neuronal firing rate increases in a patch of brain tissue, there is a transient, local increase of the cerebral blood flow (CBF). The oxygen utilization remains about the same, however. This produces a mismatch in the rate of oxygen delivered compared to the rate of oxygen consumption. The CBF goes up a lot while the oxygenation usage increases only slightly. Hence, there is a decrease in the concentration of deoxygenated hemoglobin in the veins draining the neural tissue region, in turn reducing the degree of paramagnetism of these veins that yields a signal increase in a T2*-weighted image. The essential point is that it's blood delivery - changes in CBF - that provides the main impetus for BOLD contrast.
How is blood pressure related to CBF?
The average CBF in a normal adult brain is typically maintained at around 50 ml of blood per 100 g of brain tissue per minute (50 ml/100g/min). The average number, while useful, represents considerable spatial and temporal heterogeneity across the brain. The typical CBF in gray matter is approximately double that in white matter, and there is significant variation across each tissue type arising from tight metabolic coupling. (See Note 1.)
At the local level, blood delivery to tissue is controlled by smooth muscles on the walls of arterioles and capillaries. The degree of vessel dilation, relative to that vessel's maximum possible dilation, is called its tone - the vascular tone. There are mechanisms to expand or constrict the smooth muscles, changing the local blood flow in order to maintain the tight local coupling of CBF to metabolic demand while protecting the vasculature and the tissue against damage that might arise with systemic changes in the blood supply from non-neural mechanisms. The totality of these processes is referred to as cerebral autoregulation. More on the non-neural factors later.
This is all very well, but there is something important missing from this picture. We have neglected to consider so far that the force of blood pumped out of the heart creates a pressure gradient across the arteries and the veins, with the tissue providing a resistance in between. It's this pressure gradient that causes the blood to flow. In fact, simple electrical circuits are a convenient model here. For those of you more familiar with electron flow than blood flow, we can think of the CBF as an analog of electrical current, the pressure difference as a voltage and, naturally enough, the tissue's resistance to flow mimics an electrical resistance. Thus we get:
CBF = CPP / CVR
where CPP is the cerebral perfusion pressure, the net pressure gradient - the driving force - that generates perfusion of brain tissue, and CVR is the cerebrovascular resistance. The CVR is the sum total of all mechanisms exerting control over the vascular tone at a particular location. It isn't easily estimated without detailed knowledge of the processes that might be active. The neurovascular coupling pathways contribute to CVR, for example.
The CPP is more easily estimated. It is defined as the difference between the mean arterial blood pressure (MABP) and either the venous or intracranial pressure (ICP), whichever is lower. A typical ICP is 7-12 mmHg above the ambient (local atmospheric) pressure that is assumed to be 0 mmHg. In other words, the brain is under a small positive pressure that pushes against the skull. We also see that because MABP is quite a lot higher than ICP, there is a very close relationship between CBF, which is our parameter of relevance to BOLD contrast, and the MABP. Under normotensive conditions we can use MABP as a rough estimate of CPP, to give:
CBF ~ MABP/CVR
We have essentially averaged over the cardiac cycle here, and reduced the control of the CBF to one global (systemic) parameter - the MABP - that is regulated locally via CVR. So now we need a convenient way to assess the MABP.
Before we do that, though, let's first get familiar with the blood pressure nomenclature you've almost certainly encountered when you go to see your doctor. "One fifteen over seventy five" is not, in fact, a cricket score. Here are some quotes from the Wikipedia entry on blood pressure:
"Blood pressure (BP) is the pressure of circulating blood on the walls of blood vessels. When used without further specification, "blood pressure" usually refers to the pressure in large arteries of the systemic circulation. Blood pressure is usually expressed in terms of the systolic pressure (maximum during one heart beat) over diastolic pressure (minimum in between two heart beats) and is measured in millimeters of mercury (mmHg), above the surrounding atmospheric pressure (considered to be zero for convenience).
For each heartbeat, blood pressure varies between systolic and diastolic pressures. Systolic pressure is peak pressure in the arteries, which occurs near the end of the cardiac cycle when the (cardiac) ventricles are contracting. Diastolic pressure is minimum pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are filled (filling would be better) with blood. An example of normal measured values for a resting, healthy adult human is 120 mmHg systolic and 80 mmHg diastolic (written as 120/80 mmHg, and spoken as "one-twenty over eighty")."
With an understanding of the maximum (systolic) and minimum (diastolic) BP values in our kitbag we can go back to the idea of a mean arterial BP. The MABP is the temporal average blood pressure over the cardiac cycle. For normal resting heart rate, a convenient estimate of MABP can be derived from the systolic (SP) and diastolic pressures (DP) as:
MABP ~ DP + (SP - DP)/3 .
The MABP is considered to be the perfusion pressure experienced by organs throughout the body, including the brain. The difference, SP - DP, is termed the pulse pressure and is one of the parameters susceptible to change in certain disease conditions and aging. From Wikipedia again:
"Pulse pressure is determined by the interaction of the stroke volume of the heart, the compliance (ability to expand) of the arterial system—largely attributable to the aorta and large elastic arteries—and the resistance to flow in the arterial tree. By expanding under pressure, the aorta absorbs some of the force of the blood surge from the heart during a heartbeat. In this way, the pulse pressure is reduced from what it would be if the aorta were not compliant. The loss of arterial compliance that occurs with aging explains the elevated pulse pressures found in elderly patients."
What's the concern for fMRI?
Reconsider the relation CBF ~ MABP/CVR. Brain tissues have regional control over CVR to ensure the CBF satisfies local metabolic demands on the one hand, while on the other hand autoregulatory processes assure no local over pressure that might lead to hemorrhage. Small moment to moment changes in MABP can be accommodated by the autoregulatory processes to ensure the CBF is maintained at the rate required by local energy considerations. But how much variation in MABP can the autoregulatory compensating mechanisms handle? And what happens if MABP is abnormally high or low for a prolonged period of time, as might be the case with some disease states? Any systematic differences in MABP between groups, between conditions or over time might drive alterations in CBF, and consequently BOLD, that are interpreted as having a neural basis when they are actually caused by systemic blood pressure effects. Thus, we can recast our question of concern as: "When does MABP vary, and by how much?" This should give us a good starting point for assessing the potential contribution of BP variation to an fMRI study.
Let's take a look at "normal autoregulation." From Wikipedia again:
"Under normal circumstances a MAP between 60 to 160 mmHg and ICP about 10 mmHg (CPP of 50-150 mmHg) sufficient blood flow can be maintained with autoregulation. Although the classic 'autoregulation curve' suggests that CBF is fully stable between these blood pressure values (known also as the limits of autoregulation), CBF may vary as much as 10% below and above its average within this range.
Outside of the limits of autoregulation, raising MAP raises CPP and raising ICP lowers it (this is one reason that increasing ICP in traumatic brain injury is potentially deadly). In trauma some recommend CPP not go below 70 mmHg. Recommendations in children is at least 60 mmHg.
Within the autoregulatory range, as CPP falls there is, within seconds, vasodilatation of the cerebral resistance vessels, a fall in cerebrovascular resistance and a rise in cerebral blood volume (CBV), and therefore CBF will return to baseline value within seconds (see as ref. Aaslid, Lindegaard, Sorteberg, and Nornes 1989: http://stroke.ahajournals.org/cgi/reprint/20/1/45.pdf). These adaptations to rapid changes in blood pressure (in contrast with changes that occur over periods of hours or days) are known as dynamic cerebral autoregulation."
Variations of as much as 10% from non-neural factors are going to compete handily with BOLD signal changes produced by neurovascular coupling. In normal, healthy volunteers we are primarily concerned about the dynamics of autoregulation in response to acute changes in MABP, and responses "within seconds" sound like the time scale for fMRI experiments.
The potential for BP variation to confound BOLD signal changes to a stimulus was nicely demonstrated by Wang et al. They induced transient hypertension and hypotension in rats with pharmaceuticals and investigated the relationship between forepaw stimulation and BP, finding:
"During transient hypertension, irrespective of forepaw stimulation, BP increases (i.e., >10 mm Hg) produced a transient increase in the blood oxygen level-dependent (BOLD) intensity resulting in a significant numbers of voxels correlating to the BP time courses (P < 0.05), and the number of these voxels increased as BP increased, becoming substantial at BP > 30 mm Hg. The activation patterns with BP increases and stimulation overlapped spatially resulting in an enhanced cerebral activation to simultaneous forepaw stimulation (P < 0.05). BP decreases (>10 mm Hg) produced corresponding decreases in BOLD intensity, causing significant numbers of voxels correlating to the BP decreases (P < 0.005), and these numbers increased as BP decreased (P < 0.001)."
A study by Lui et al. in cocaine-dependent human subjects found that dobutamine infusion raised MABP but produced only localized BOLD signal changes in anterior cingulate that correlated with the BP rise. However, their study didn't employ a task, leaving open the possibility of interactions between tasks and BP changes.
What about humans not on drugs? Lots of perfectly normal, everyday things affect our BP. There are circadian changes, with greater BP in the morning and evening and lowest BP during sleep. Blood pressure and CBF change during and immediately after exercise, as demonstrated by Macintosh et al. and Smith et al.
Abnormal BP is also of concern for patients with likely impairment of cerebral autoregulation, including traumatic brain injury (TBI), hypertension, hypotension (including major blood loss, perhaps including very recent blood donation) and neurodegenerative conditions. For example, Alzheimer’s patients studied with transcranial Doppler ultrasound exhibited a low frequency variability in BP suggestive of impaired homeostasis.
The broad range of situations in which BP may change, and the strong relationship between MABP and CBF, suggests that caution is warranted. It is conceivable that variations in BP could be as consequential as respiration rate (more specifically, arterial CO2 concentration) or caffeine consumption in causing BOLD signal instability across groups of otherwise similar people, or across time for individuals. And, of course, BP fluctuations could be especially important in tasks where changes in BP might be strongly correlated with certain classes of stimuli.
Using BP data in fMRI experiments
Taking a blood pressure measurement before or after a scan may be informative but it's also insufficient. Baseline BP (before MRI) was found by Lu, Yezhuvath & Xiao to offer only a small normalizing effect on visual-evoked BOLD signals when tested across two conditions, whereas other physiological parameters had considerably more explanatory power.
Gianaros et al. observed a correlation between MABP and BOLD activity in several brain regions of participants conducting a stressful Stroop task, with BP measured once for each block of sixteen 90-second task blocks. In a later study with BP measured in the scanner once a minute, the same task produced a correlation between stressor-evoked MABP reactivity and amygdala activation.
If one has a time series of BP data then one can consider "de-noising" methods, such as regressing BP from the signal. Murphy et al. used partially inflated pressure cuffs (more on this below) to record BP once per heart beat. The BP explained 3-14% of the variance in global BOLD signal, which is about the same as is generally explained by more common physiological recordings. For example, Golestani et al. recently showed that cardiac and respiratory variability measures plus expired CO2 accounted for 5-24% of BOLD signal variability, depending on the subject. What's most notable in Murphy's BP study is the optimal lag, which was less than the repetition rate (TR) of 3 seconds. They suggest that the influence of BP on BOLD signal should be near instantaneous if it reflects CBF fluctuations subject to cerebral autoregulation.
How is BP measured non-invasively?
The familiar blood pressure measurement is performed on the brachial artery of your upper arm and uses a device called a sphygmomanometer. A what? My thoughts exactly. This is the only time I'll ever use the term since I can't pronounce it. (And if you insist on using unpronounceable medical terms to sound intelligent, in return I shall insist that you refer to MRI as zeugmatography, so there.) In Note 2, below, you'll find an explanation of how BP is measured in your doctor's office using the device with the unnecessarily fancy name. We don't need to get into its details because the standard method gives a single BP value whereas for fMRI - sorry, functional zeugmatographic - experiments we want a method that can give continuous, simultaneous BP sampling of the subject inside the scanner. At a minimum we want one BP value per heart beat.
There are commercial devices that will measure BP inside an MRI but they don't satisfy our criterion of a sample per heart beat. These devices use similar principles as the fancy word method, except that electronic circuits replace the human listening for the blood sounds in your arm. They are referred to as oscillometric BP measures. The requirement to inflate a cuff and monitor its release means that these methods take tens of seconds to get a single measurement. It is also uncomfortable and likely distracting for fMRI applications.
It turns out to be quite difficult to perform continuous non-invasive blood pressure monitoring (NIBP) at all, let alone on a subject in an MRI scanner. Discomfort, motion sensitivity and highly accurate placement of sensors relative to arteries all contribute to a general lack of robustness for many applications. There have been several attempts, however, and we can loosely divide the approaches into three groups: volume clamps (also known as vascular unloading methods), pulse wave velocity recordings, and pulse decomposition analysis. I'll review all three in a bit of detail because it could be instructive for labs attempting custom solutions, and provide guidance on what to look for if ever you go shopping for a commercial device.
Volume clamp: A volume clamp, such as the commercially available Portapres device from Finapres Medical Systems, comprises an optical source and a sensor attached to a finger, like a standard pulse oximeter except that the device also includes a small cuff which changes the pressure applied to the finger. With conventional pulse oximetry we measure the blood volume in the tissue from heartbeat to heartbeat. In the volume clamp method a small pressure is applied to the finger via the cuff, essentially clamping the arterial blood at a constant volume. Now, as the pressure wave arrives from the heart, the finger's arteries regulate their local pressure to maintain constant blood flow and avoid rupturing. Yup, local autoregulation again! A sensor recording the pressure in the cuff now reports changes in the beat to beat blood pressure of the finger, as shown in the figure below. The volume clamp is a relative measure and requires calibration to get absolute BP, but the bigger issue, apparently, is the extreme motion sensitivity.
|Fig. 4 from Peters et al. 2014: https://doi.org/10.1016/j.irbm.2014.07.002. The principle of the volume clamp method is based on a combination of standard pulse oximetry (photoplethysmography) with a pressure cuff on a finger. With the cuff uninflated the pulse oximeter reports the beat to beat blood volume (left side). With the cuff inflated the blood volume is clamped, eliminating the signal in the pulse oximeter (right side, lower trace). However, a manometer recording pressure in the cuff now reports changing blood pressure in the finger (right side, upper trace).|
Pulse wave velocity: The second class of NIBP monitors involve measuring the time taken for the systolic pressure wave to travel from the left ventricle of the heart to other locations in the body. Every time the heart contracts, ejecting blood into the aorta, it produces a pressure wave that propagates throughout the entire arterial system. (Note that the pressure wave travels faster than the blood flow. You might think of it like a sound pressure wave being carried in the wind. Sound travels faster than the air is moving.) The time taken for the pressure wave to travel to a point is called the pulse transit time (PTT). The pulse wave velocity (PWV) may then be determined using two BP sensors placed a known (arterial) distance d apart, as PWV = d/PTT. The PTT, hence PWV, depends upon systemic blood pressure via characteristics of the vascular system: the elasticity and thickness of the arterial walls, the end-diastolic arterial diameter, and blood density. As we have already seen, as systemic BP increases there are autoregulatory processes to ensure increases in arterial diameter and compliance (the reciprocal of elasticity) to maintain constant blood flow to organs and avoid hyperperfusion. Thus, an increased systemic BP produces decreased PTT and increased PWV.
All that sounds rather complicated. And if you look up articles on PWV you will find that it is. But we don't need to get that deeply involved in elasticity and whatnot, because a relative BP measure will suffice. We want a plot of changes in BP over time rather than absolute quantification, as would be important in a medical scenario. For our purposes, then, all we need is two sensors a different arterial distance from the heart, and to determine the difference in the arrival times of the pressure waves. For fixed sensor placement, any changes in BP will modulate the difference in arrival times for the pressure pulse and give us our time course. Consider the setup illustrated in this figure from Murphy, Birn & Bandettini:
In their setup, one pressure cuff is placed on a bicep at the same level as the heart, while a second cuff is placed on a thigh a distance D away. Optical sensors could be used instead of pressure cuffs, but these still produce one BP estimate per heart beat. In a custom device built specifically for MRI compatibility, one optical sensor was placed directly over the aortic valve on the sternum and the second over a carotid artery. In my lab we're tinkering with PTT approaches right now, trying to determine if we can get robust signals out of the same pressure pads we use for monitoring chest motion. Early tests are encouraging, but we're not yet ready to spend money on all the parts we'd need let alone put it into routine use! As soon as there's something definitive to say, count on a blog post on it.
Pulse decomposition analysis: The PWV methods use two sensors to measure differential arrival times of the same pressure wave. With pulse decomposition analysis (PDA) it's the reverse. The goal is to use a single sensor and measure differential timing information from two (or more) reflected pressure waves. Let's jump right in and look at the anatomical origins of these reflected waves, then we can look at the analysis and methodological limitations. Here's a schematic of the main pressure wave, labeled P1, and two reflected waves, P2 and P3, that are produced at the levels of the renal and iliac arteries, respectively:
|Figure 1 from Baruch et al. 2011. The main arterial tree is depicted on the right. It shows the initial pressure wave, #1, created by blood ejected from the heart, descending from the aortic arch. This wave also travels down the brachial artery, where it is depicted arriving at the radial artery as signal P1. The main pressure wave reflects at the juncture of the thoracic and abdominal aorta, at the level of the renal arteries, and also at the juncture of the abdominal aorta and the common iliac arteries, producing reflected signals P2 and P3 that travel back up and are eventually detected in the radial artery at times T12 and T13, respectively.|
The sensor is on a finger, at the distal end of the radial artery. The signal sensed at the finger is depicted on the left of the figure above. The sensor detects the main pressure wave, P1, after a relatively short, direct journey down the arteries of the arm. Reflected waves P2 and P3 have traveled farther: down to the level of the renal and iliac arteries, respectively, before traveling back up through the arterial tree, over into the radial artery and down to the finger, where they are detected. There are other reflected waves - reflections of reflections - but these are much weaker and we don't need to worry about them. Reflected pulse P2 arrives at time T12, typically 70-140 ms later than P1, while reflected pulse P3 arrives at time T13, 180-400 ms later.
The amplitude and timing of the primary and reflected pulses are then fed into the PDA model. How does the model estimate BP? According to a validation study performed by the method's inventors:
"The first reflection site is the juncture between thoracic and abdominal aorta, which is marked by a significant decrease in diameter and a significant change in elasticity. The reflection coefficient of this juncture is highly sensitive to blood pressure changes because of the pressure-dependent expansion of the diameter of the thoracic artery relative to that of the abdominal artery. The second (reflection) site arises from the juncture between abdominal aorta and the common iliac arteries. The renal site reflects the pressure pulse because the juncture of the aortic arteries there features significant changes in arterial diameter and wall elasticity."The specific algorithm used in PDA is proprietary, but they do tell us the key parameters in a product manual. The amplitude ratio P2/P1 is used to track beat-to-beat systolic pressure:
"The physiological model here is that the reflection coefficient of the P2 reflection site is highly pressure dependent. The reason is due to the difference between the Young’s modulus of the thoracic aorta (the “softest” artery of the body) and the abdominal aorta. With increasing systolic pressure the thoracic aorta dilates more than abdominal aorta, resulting in an increasing diameter mismatch between the two aortic sections. Decreasing pressure has the opposite effect, as is easily demonstrated by performing the valsalva maneuver."Then, the differential delay T13 between the arrival of P1 and reflected signal P3 is used to track changes in pulse pressure:
"The physiological model is that, since both pulses travel at different pressure amplitudes, they also travel at different pulse propagation velocities. As the differential pressure between them changes, so will their relative arrival time because their individual pulse propagation velocities change, causing them to accelerate or decelerate relative to each other."Recall that pulse pressure is defined as (SP - DP), so now we can easily compute diastolic pressure from the pulse pressure and systolic pressure.
Continuous NIBP in the MRI scanner
So, three broad approaches. Which one do we use for routine fMRI? This is where reality bites, I'm afraid. Gray et al. modified their Portapres volume clamp to work in their 3 T scanner. So far, however, I've not found any details on the modifications they made. Murphy et al. and Myllylä et al. both used pulse wave velocity, with pressure cuffs and optical sensors, respectively, but both are also custom setups. Finally, Whittaker et al. (ISMRM abstract #0309, 2016) recently tested the pulse decomposition analysis method used in the commercial CareTaker device, obtained through BIOPAC, Inc.
I don't know about you, but as an MRI person I have a particular affinity for anything that echoes. The PDA approach is just so damned elegant. Even the nomenclature - T12, T13, P1, P2, etc. - sounds reassuringly familiar. Except that we have a problem. The previous re-seller, BIOPAC, no longer offers the product. I did a bit of online sleuthing and it looks like CareTaker have gone on to bigger and better things. That is, they got FDA clearance, have given their product's packaging a cuddly facelift and are all set to sell thousands of devices for medical use. The small fMRI research market is probably not on their radar any longer. (I don't blame them. And I wish them continued good luck!) Perhaps we can still get CareTaker devices for research purposes. Other than the packaging it looks to be the same essential device as BIOPAC was re-selling. It may cost a lot more now, given FDA approval, and you may have to go through a medical equipment supply company to get one, but these are issues I've not broached yet.
The commercial Portapres device isn't compatible with MRI. You'd need to customize it. Pulse wave velocity might be easier to do in principle, but there's no recommended routine cuff-based method yet, and getting two cuffs on a subject, one on a thigh, may not be easy to do. For PWV with optical sensors we have two obstacles. Firstly, they were a custom development in a Finnish lab. Secondly, one optical sensor needs to be placed directly over the aorta, introducing huge privacy issues even if it works really well.
Given that commercial solutions are not yet guaranteed to work for us, I'm exploring custom approaches to PWV (strictly, PTT) as I mentioned above. We're testing pulse oximeter positions and we're testing pressure sensors. We already tried comparing pulse oximetry on a finger to a single pressure sensor on a femoral artery. The signals for both looked pretty good, except that there is no lag in the optical signal whereas the pressure signal has sufficiently long lag to render the time difference minuscule. And reversing the sensor placement isn't an option. We're now trying to devise robust configurations of two of the same types of sensor, to keep the lags consistent. In the mean time, if anyone purchases a new CareTaker device direct from the company, please let me know how much you paid for it and whether it's working well in your scanner. The Portapres device is still an option, of course, but I am concerned about motion sensitivity as well as overall sensitivity. Tasks that require the use of hands for response essentially rule out pulse oximetry, while my 17 C scanner suite can make it difficult to get good pulse oximetry from many subjects.
There is tantalizing evidence and good theoretical reasons to think that a non-invasive blood pressure measurement would be informative and complimentary to the information available in the heart and respiration rates, and expired CO2. However, at the moment the equipment to do NIBP inside the MRI scanner needs more development and testing. I encourage those labs pursuing BP measurements to get more information out in public as soon as reasonably possible. If we can reach consensus on a methodology then we can figure out how to buy/build the solution and start on the path of routine NIBP measurement.
Next up in this series: Low frequency oscillations. What are they, and how do they relate to BP?
Many thanks to Molly Bright and Dan Handwerker for sending me several references and helping me understand the limitations of current NIBP methods.
1. It is generally assumed that the CMRO2 - the metabolic rate of oxygen utilization - is very tightly coupled to local metabolic demand. For the purposes of this post I am going to assume that CBF is also tightly coupled to metabolism. Perhaps the coupling isn't quite as tight between CBF and metabolic demand as CMRO2 and metabolic demand; this is a detail we don't need to worry about here. It is quite clear from PET and other studies that we can use blood delivery as a good proxy for cellular activity, loosely defined, on a timescale of seconds to tens of minutes.
2. Measuring blood pressure with a cuff:
(Extracted from the Wikipedia page on the sphygmomanometer.)
A sphygmomanometer, also known as a blood pressure meter, blood pressure monitor, or blood pressure gauge, is a device used to measure blood pressure, composed of an inflatable cuff to collapse and then release the artery under the cuff in a controlled manner, and a mercury or mechanical manometer to measure the pressure. It is always used in conjunction with a means to determine at what pressure blood flow is just starting, and at what pressure it is unimpeded. Manual sphygmomanometers are used in conjunction with a stethoscope.
The cuff is normally placed smoothly and snugly around an upper arm, at roughly the same vertical height as the heart while the subject is seated with the arm supported. It is important that the cuff size is correct: undersized cuffs record too high a pressure, oversized cuffs may yield too low a pressure. Usually three or four cuff sizes should be available to allow measurements in arms of different size.
A stethoscope is generally required. Manual meters are used by trained practitioners. Listening with the stethoscope to the brachial artery at the antecubital area of the elbow, the examiner slowly releases the pressure in the cuff. As the pressure in the cuffs falls, a "whooshing" or pounding sound is heard (see Korotkoff sounds) when blood flow first starts again in the artery. The pressure at which this sound began is noted and recorded as the systolic blood pressure. The cuff pressure is further released until the sound can no longer be heard. This is recorded as the diastolic blood pressure.
Digital meters employ oscillometric measurements and electronic calculations. They may use manual or automatic inflation, but both types are electronic, easy to operate without training, and can be used in noisy environments. They measure systolic and diastolic pressures by oscillometric detection, employing either deformable membranes that are measured using differential capacitance, or differential piezoresistance, and they include a microprocessor.
Digital instruments use a cuff which may be placed, according to the instrument, around the upper arm, wrist, or a finger, in all cases elevated to the same height as the heart. They inflate the cuff and gradually reduce the pressure in the same way as a manual meter, and measure blood pressures by the oscillometric method. They accurately measure mean blood pressure and pulse rate, while systolic and diastolic pressures are obtained less accurately than with manual meters, and calibration is also a concern.