Heart Rate Monitor Frequency

[Imke]

Aheart rate monitor (HRM) is a personal monitoring device that allows one to measure/display heart rate in real time or record the heart rate for later study. It is largely used to gather heart rate data while performing various types of physical exercise. Measuring electrical heart information is referred to as electrocardiography (ECG or EKG).

Medical heart rate monitoring used in hospitals is usually wired and usually multiple sensors are used. Portable medical units are referred to as a Holter monitor. Consumer heart rate monitors are designed for everyday use and do not use wires to connect.

Early models consisted of a monitoring box with a set of electrode leads which attached to the chest. The first wireless EKG heart rate monitor was invented in 1977 by Polar Electro as a training aid for the Finnish National Cross Country Ski team. As "intensity training" became a popular concept in athletic circles in the mid-80s, retail sales of wireless personal heart monitors started in 1983.[1]

Modern heart rate monitors commonly use one of two different methods to record heart signals (electrical and optical). Both types of signals can provide the same basic heart rate data, using fully automated algorithms to measure heart rate, such as the Pan-Tompkins algorithm.[2]

The electrical monitors consist of two elements: a monitor/transmitter, which is worn on a chest strap, and a receiver. When a heartbeat is detected, a radio signal is transmitted, which the receiver uses to display/determine the current heart rate. This signal can be a simple radio pulse or a unique coded signal from the chest strap (such as Bluetooth, ANT, or other low-power radio links). Newer technology prevents one user's receiver from using signals from other nearby transmitters (known as cross-talk interference) or eavesdropping. Note, the older Polar 5.1 kHz radio transmission technology is usable underwater. Both Bluetooth and Ant+ use the 2.4 GHz radio band, which cannot send signals underwater.

More recent devices use optics to measure heart rate by shining light from an LED through the skin and measuring how it scatters off blood vessels. In addition to measuring the heart rate, some devices using this technology are able to measure blood oxygen saturation (SpO2). Some recent optical sensors can also transmit data as mentioned above.

Newer devices such as cell phones or watches can be used to display and/or collect the information. Some devices can simultaneously monitor heart rate, oxygen saturation, and other parameters. These may include sensors such as accelerometers, gyroscopes, and GPS to detect speed, location and distance.[3] In recent years, it has been common for smartwatches to include heart rate monitors, which has greatly increased popularity.[4] Some smartwatches, smart bands and cell phones often use PPG sensors.[5]

The newer, wrist based heart rate monitors have achieved almost identical levels of accuracy as their chest strap counterparts with independent tests showing up to 95% accuracy, but sometimes more than 30% error can persist for several minutes.[9] Optical devices can be less accurate when used during vigorous activity,[10] or when used underwater.

Currently, heart rate variability is less available on optical devices.[11] Apple introduced HRV data collection to the Apple Watch devices in 2018.[12] Fitbit started offering HRV monitoring on their devices starting from the Fitbit Sense, released in 2020.[13]

Heart rate is the frequency of the heartbeat measured by the number of contractions of the heart per minute (beats per minute, or bpm). The heart rate varies according to the body's physical needs, including the need to absorb oxygen and excrete carbon dioxide. It is also modulated by numerous factors, including (but not limited to) genetics, physical fitness, stress or psychological status, diet, drugs, hormonal status, environment, and disease/illness, as well as the interaction between these factors.[1] It is usually equal or close to the pulse rate measured at any peripheral point.[2]

While heart rhythm is regulated entirely by the sinoatrial node under normal conditions, heart rate is regulated by sympathetic and parasympathetic input to the sinoatrial node. The accelerans nerve provides sympathetic input to the heart by releasing norepinephrine onto the cells of the sinoatrial node (SA node), and the vagus nerve provides parasympathetic input to the heart by releasing acetylcholine onto sinoatrial node cells. Therefore, stimulation of the accelerans nerve increases heart rate, while stimulation of the vagus nerve decreases it.[6]

As water and blood are incompressible fluids, one of the physiological ways to deliver more blood to an organ is to increase heart rate.[5] Normal resting heart rates range from 60 to 100 bpm.[7][8][9][10] Bradycardia is defined as a resting heart rate below 60 bpm. However, heart rates from 50 to 60 bpm are common among healthy people and do not necessarily require special attention.[3] Tachycardia is defined as a resting heart rate above 100 bpm, though persistent rest rates between 80 and 100 bpm, mainly if they are present during sleep, may be signs of hyperthyroidism or anemia (see below).[5]

There are many ways in which the heart rate speeds up or slows down. Most involve stimulant-like endorphins and hormones being released in the brain, some of which are those that are 'forced'/'enticed' out by the ingestion and processing of drugs such as cocaine or atropine.[11][12][13]

The heart rate is rhythmically generated by the sinoatrial node. It is also influenced by central factors through sympathetic and parasympathetic nerves.[15] Nervous influence over the heart rate is centralized within the two paired cardiovascular centres of the medulla oblongata. The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm.[16]

Parasympathetic stimulation originates from the cardioinhibitory region of the brain[17] with impulses traveling via the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of both the atria and ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization, which extends repolarization and increases the time before the next spontaneous depolarization occurs. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR. This is similar to an individual driving a car with one foot on the brake pedal. To speed up, one need merely remove one's foot from the brake and let the engine increase speed. In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately 100 bpm. Any increases beyond this rate would require sympathetic stimulation.[16]

The cardiovascular centre receive input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system which normally enable the precise regulation of heart function, via cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. The cardiovascular centres monitor these increased rates of firing, suppressing parasympathetic stimulation or increasing sympathetic stimulation as needed in order to increase blood flow.[16]

Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.[16]

There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The opposite is also true.[16]

Increased metabolic byproducts associated with increased activity, such as carbon dioxide, hydrogen ions, and lactic acid, plus falling oxygen levels, are detected by a suite of chemoreceptors innervated by the glossopharyngeal and vagus nerves. These chemoreceptors provide feedback to the cardiovascular centers about the need for increased or decreased blood flow, based on the relative levels of these substances.[16]

3a8082e126