Heart rate

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. • Central nervous system stimulants such as substituted amphetamines increase heart rate. • Central nervous system depressants or sedatives decrease the heart rate (apart from some particularly strange ones with equally strange effects, such as ketamine which can cause – amongst many other things – stimulant-like effects such as tachycardia). 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. This section discusses target heart rates for healthy persons, which would be inappropriately high for most persons with coronary artery disease. Influences from the central nervous system Cardiovascular centres The heart rate is rhythmically generated by the sinoatrial node. It is also influenced by central factors through sympathetic and parasympathetic nerves. 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. Both sympathetic and parasympathetic stimuli flow through the paired cardiac plexus near the base of the heart. The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the cardiac nerves. This shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increased heartrate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. 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. Doing simple deep and slow breathing exercises with one's eyes closed can also significantly reduce this anxiety and HR. In a study conducted on 8 female and male student actors ages 18 to 25, their reaction to an unforeseen occurrence (the cause of stress) during a performance was observed in terms of heart rate. In the data collected, there was a noticeable trend between the location of actors (onstage and offstage) and their elevation in heart rate in response to stress; the actors present offstage reacted to the stressor immediately, demonstrated by their immediate elevation in heart rate the minute the unexpected event occurred, but the actors present onstage at the time of the stressor reacted in the following 5 minute period (demonstrated by their increasingly elevated heart rate). This trend regarding stress and heart rate is supported by previous studies; negative emotion/stimulus has a prolonged effect on heart rate in individuals who are directly impacted. In regard to the characters present onstage, a reduced startle response has been associated with a passive defense, and the diminished initial heart rate response has been predicted to have a greater tendency to dissociation. Current evidence suggests that heart rate variability can be used as an accurate measure of psychological stress and may be used for an objective measurement of psychological stress. Factors decreasing heart rate The heart rate can be slowed by altered sodium and potassium levels, hypoxia, acidosis, alkalosis, and hypothermia. The relationship between electrolytes and HR is complex, but maintaining electrolyte balance is critical to the normal wave of depolarization. Of the two ions, potassium has the greater clinical significance. Initially, both hyponatremia (low sodium levels) and hypernatremia (high sodium levels) may lead to tachycardia. Severely high hypernatremia may lead to fibrillation, which may cause cardiac output to cease. Severe hyponatremia leads to both bradycardia and other arrhythmias. Hypokalemia (low potassium levels) also leads to arrhythmias, whereas hyperkalemia (high potassium levels) causes the heart to become weak and flaccid, and ultimately to fail. ==In different circumstances==

Heart rate is not a stable value and it increases or decreases in response to the body's need in a way to maintain an equilibrium (basal metabolic rate) between requirement and delivery of oxygen and nutrients. The normal SA node firing rate is affected by autonomic nervous system activity: sympathetic stimulation increases and parasympathetic stimulation decreases the firing rate. Resting heart rate Normal pulse rates at rest, in beats per minute (BPM): The basal or resting heart rate (HRrest) is defined as the heart rate when a person is awake, in a neutrally temperate environment, and has not been subject to any recent exertion or stimulation, such as stress or surprise. The normal resting heart rate is based on the at-rest firing rate of the heart's sinoatrial node, where the faster pacemaker cells driving the self-generated rhythmic firing and responsible for the heart's autorhythmicity are located. In one 1993 study, 98% of cardiologists suggested that as a desirable target range, 50 to 90 beats per minute is more appropriate than 60 to 100. The available evidence indicates that the normal range for resting heart rate is 50–90 beats per minute (bpm). Resting heart rate is often correlated with mortality. In the Copenhagen City Heart Study a heart rate of 65 bpm rather than 80 bpm was associated with 4.6 years longer life expectancy in men and 3.6 years in women. without severe problems through exercise stress. In general it is loosely estimated as 220 minus one's age. The maximum heart rate decreases with aging regardless of fitness, gender or diet. which is comparable to the heart rate of a mouse. For general purposes, a number of formulas are used to estimate HRmax. However, these predictive formulas have been criticized as inaccurate because they only produce generalized population-averages and may deviate significantly from the actual value. (See § Limitations.) Haskell & Fox (1970) Notwithstanding later research, the most widely cited formula for HRmax is still: :HRmax = 220 − age Although attributed to various sources, it is widely thought to have been devised in 1970 by Dr. William Haskell and Dr. Samuel Fox. Compared to the age-specific average HRmax, the Haskell and Fox formula overestimates HRmax in young adults, agrees with it at age 40, and underestimates HRmax in older adults. Limitations Maximum heart rates vary significantly between individuals. Measurement via a maximal test is preferable whenever possible, By percent, Fox–Haskell-based The THR can be calculated as a range of 65–85% intensity, with intensity defined simply as percentage of HRmax. Example for someone with a HRmax of 180 (age 40, estimating HRmax As 220 − age): : 65% Intensity: (220 − (age = 40)) × 0.65 → 117 bpm : 85% Intensity: (220 − (age = 40)) × 0.85 → 154 bpm Karvonen method The Karvonen method gauges exercise intensity as the percentage of heart rate reserve. It is named after Karvonen, author of the initial 1957 study. Karvonen's study used only six subjects, and Karvonen did not connect his recommendations to VO2 data, but later studies identified a connection. The percentage of heart rate reserve is strongly correlated with the percentage of VO2 max and the percentage of VO2 in reserve, but the correlation is not perfect. As formulas: : % intensity = (THR - HRrest) / (HRmax − HRrest) : THR = ((HRmax − HRrest) × % intensity) + HRrest Equivalently, : % intensity = (THR - HRrest) / HRreserve : THR = (HRreserve × % intensity) + HRrest Example for someone with a HRmax of 180 and a HRrest of 70 (and therefore a HRreserve of 110): : 50% Intensity: ((180 − 70) × 0.50) + 70 = 125 bpm : 85% Intensity: ((180 − 70) × 0.85) + 70 = 163 bpm Zoladz method An alternative to the Karvonen method is the Zoladz method, which is used to test an athlete's capabilities at specific heart rates. These are not intended to be used as exercise zones, although they are often used as such. The Zoladz test zones are derived by subtracting values from HRmax: : THR = HRmax − Adjuster ± 5 bpm :: Zone 1 Adjuster = 50 bpm :: Zone 2 Adjuster = 40 bpm :: Zone 3 Adjuster = 30 bpm :: Zone 4 Adjuster = 20 bpm :: Zone 5 Adjuster = 10 bpm Example for someone with a HRmax of 180: : Zone 1 (easy exercise): 180 − 50 ± 5 → 125 − 135 bpm : Zone 4 (tough exercise): 180 − 20 ± 5 → 155 − 165 bpm Heart rate recovery Heart rate recovery (HRR) is the reduction in heart rate at peak exercise and the rate as measured after a cool-down period of fixed duration. Heart rates assessed during treadmill stress test that do not drop by more than 12 bpm one minute after stopping exercise (if cool-down period after exercise) or by more than 18 bpm one minute after stopping exercise (if no cool-down period and supine position as soon as possible) are associated with an increased risk of death. People with an abnormal HRR defined as a decrease of 42 beats per minutes or less at two minutes post-exercise had a mortality rate 2.5 times greater than patients with a normal recovery. Heart rate prediction Heart rate prediction using machine learning has gained significant attention in health monitoring and sports performance research. Namazi et.al., 2025 study evaluated various models including Long Short-Term Memory (LSTM), Physics-Informed Neural Networks (PINNs), and 1D Convolutional Neural Networks (1D CNNs), using physiological data such as heart rate (HR), breathing rate (BR), and RR intervals collected from wearable sensors during sports activities. The study introduced a hybrid approach combining Singular Spectrum Analysis (SSA) with these models to enhance predictive performance. Among the tested models, the SSA-LSTM method yielded the lowest prediction error, particularly when multivariate inputs (HR + BR + RR) were used. These findings support the use of AI-driven, multivariate prediction models for real-time cardiovascular monitoring in athletic and healthcare settings. Development , the human heart begins beating at 70 to 80 beats per minute and accelerates linearly for the first month of beating. The human heart beats more than 2.8 billion times in an average lifetime. The heartbeat of a human embryo begins at approximately 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy in the medical community. The electrical depolarizations that trigger cardiac myocytes to contract arise spontaneously within the myocyte itself. The heartbeat is initiated in the pacemaker regions and spreads to the rest of the heart through a conduction pathway. Pacemaker cells develop in the primitive atrium and the sinus venosus to form the sinoatrial node and the atrioventricular node respectively. Conductive cells develop the bundle of His and carry the depolarization into the lower heart. The human heart begins beating at a rate near the mother's, about 75–80 beats per minute (bpm). The embryonic heart rate then accelerates linearly for the first month of beating, peaking at 165–185 bpm during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 bpm per day, or about 10 bpm every three days, an increase of 100 bpm in the first month. After peaking at about 9.2 weeks after the LMP, it decelerates to about 150 bpm (+/-25 bpm) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 bpm) bpm at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is: \mathrm{Age\ in\ days} =\ \mathrm{EHR} (0.3)+6 ==Clinical significance==

Manual measurement Heart rate is measured by finding the pulse of the heart. This pulse rate can be found at any point on the body where the artery's pulsation is transmitted to the surface by pressuring it with the index and middle fingers; often it is compressed against an underlying structure like bone. The thumb should not be used for measuring another person's heart rate, as its strong pulse may interfere with the correct perception of the target pulse. The radial artery is the easiest to use to check the heart rate. However, in emergency situations the most reliable arteries to measure heart rate are carotid arteries. This is important mainly in patients with atrial fibrillation, in whom heart beats are irregular and stroke volume is largely different from one beat to another. In those beats following a shorter diastolic interval left ventricle does not fill properly, stroke volume is lower and pulse wave is not strong enough to be detected by palpation on a distal artery like the radial artery. It can be detected, however, by doppler. Possible points for measuring the heart rate are: • The ventral aspect of the wrist on the side of the thumb (radial artery). • The ulnar artery. • The inside of the elbow, or under the biceps muscle (brachial artery). • The groin (femoral artery). • Behind the medial malleolus on the feet (posterior tibial artery). • Middle of dorsum of the foot (dorsalis pedis). • Behind the knee (popliteal artery). • Over the abdomen (abdominal aorta). • The chest (apex of the heart), which can be felt with one's hand or fingers. It is also possible to auscultate the heart using a stethoscope. • In the neck, lateral of the larynx (carotid artery) • The temple (superficial temporal artery). • The lateral edge of the mandible (facial artery). • The side of the head near the ear (posterior auricular artery). Electronic measurement , heart rate can be measured by ultrasonography, such as in this embryo (at bottom left in the sac) of 6 weeks with a heart rate of approximately 90 per minute. A more precise method of determining heart rate involves the use of an electrocardiograph, or ECG (also abbreviated EKG). An ECG generates a pattern based on electrical activity of the heart, which closely follows heart function. Continuous ECG monitoring is routinely done in many clinical settings, especially in critical care medicine. On the ECG, instantaneous heart rate is calculated using the R wave-to-R wave (RR) interval and multiplying/dividing in order to derive heart rate in heartbeats/min. Multiple methods exist: • HR = 1000 · 60/(RR interval in milliseconds) • HR = 60/(RR interval in seconds) • HR = 300/number of "large" squares between successive R waves. • HR = 1,500 number of large blocks Heart rate monitors allow measurements to be taken continuously and can be used during exercise when manual measurement would be difficult or impossible (such as when the hands are being used). Various commercial heart rate monitors are also available. Some monitors, used during sport, consist of a chest strap with electrodes. The signal is transmitted to a wrist receiver for display. Alternative methods of measurement include seismocardiography. Optical measurements Pulse oximetry of the finger and laser Doppler imaging of the eye fundus are often used in the clinics. Those techniques can assess the heart rate by measuring the delay between pulses. Tachycardia Tachycardia is a resting heart rate more than 100 beats per minute. This number can vary as smaller people and children have faster heart rates than average adults. Physiological conditions where tachycardia occurs: • Pregnancy • Emotional conditions such as anxiety or stress. • Exercise Pathological conditions where tachycardia occurs: • Sepsis • Fever • Anemia • Hypoxia • Hyperthyroidism • Hypersecretion of catecholamines • Cardiomyopathy • Valvular heart diseases • Acute Radiation Syndrome • Dehydration • Metabolic myopathies (At rest, tachycardia is commonly seen in fatty acid oxidation disorders. An inappropriate rapid heart rate response to exercise is seen in muscle glycogenoses and mitochondrial myopathies, where the tachycardia is faster than would be expected during exercise). Bradycardia Bradycardia was defined as a heart rate less than 60 beats per minute when textbooks asserted that the normal range for heart rates was 60–100 bpm. The normal range has since been revised in textbooks to 50–90 bpm for a human at total rest. Setting a lower threshold for bradycardia prevents misclassification of fit individuals as having a pathologic heart rate. The normal heart rate number can vary as children and adolescents tend to have faster heart rates than average adults. Bradycardia may be associated with medical conditions such as hypothyroidism, heart disease, or inflammatory disease. At rest, although tachycardia is more commonly seen in fatty acid oxidation disorders, more rarely acute bradycardia can occur. Trained athletes tend to have slow resting heart rates, and resting bradycardia in athletes should not be considered abnormal if the individual has no symptoms associated with it. For example, Miguel Indurain, a Spanish cyclist and five time Tour de France winner, had a resting heart rate of 28 beats per minute, one of the lowest ever recorded in a healthy human. Daniel Green achieved the world record for the slowest heartbeat in a healthy human with a heart rate of just 26 bpm in 2014. Arrhythmia Arrhythmias are abnormalities of the heart rate and rhythm (sometimes felt as palpitations). They can be divided into two broad categories: fast and slow heart rates. Some cause few or minimal symptoms. Others produce more serious symptoms of lightheadedness, dizziness and fainting. Hypertension Elevated heart rate is a powerful predictor of morbidity and mortality in patients with hypertension. Atherosclerosis and dysautonomia are major contributors to the pathogenesis. Faster heart rate may accompany increased production of inflammation molecules and increased production of reactive oxygen species in cardiovascular system, in addition to increased mechanical stress to the heart. There is a correlation between increased resting rate and cardiovascular risk. This is not seen to be "using an allotment of heart beats" but rather an increased risk to the system from the increased rate. Other studies have shown that a high resting heart rate is associated with an increase in cardiovascular and all-cause mortality in the general population and in patients with chronic diseases. A faster resting heart rate is associated with shorter life expectancy and is considered a strong risk factor for heart disease and heart failure, independent of level of physical fitness. Specifically, a resting heart rate above 65 beats per minute has been shown to have a strong independent effect on premature mortality; every 10 beats per minute increase in resting heart rate has been shown to be associated with a 10–20% increase in risk of death. In one study, men with no evidence of heart disease and a resting heart rate of more than 90 beats per minute had a five times higher risk of sudden cardiac death. Heart rate has many advantages as a clinical parameter: It is inexpensive and quick to measure and is easily understandable. Although the accepted limits of heart rate are between 60 and 100 beats per minute, this was based for convenience on the scale of the squares on electrocardiogram paper; a better definition of normal sinus heart rate may be between 50 and 90 beats per minute. Diet has also been found to be beneficial in lowering resting heart rate: In studies of resting heart rate and risk of death and cardiac complications on patients with type 2 diabetes, legumes were found to lower resting heart rate. This is thought to occur because in addition to the direct beneficial effects of legumes, they also displace animal proteins in the diet, which are higher in saturated fat and cholesterol. A very slow heart rate (bradycardia) may be associated with heart block. It may also arise from autonomous nervous system impairment. ==See also==