heart rate heart rate heart rate (or pulse 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 can vary according to the body's physical needs, including the need to absorb oxygen and excrete carbon dioxide, but 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 and among these factors. it is usually equal or close to the pulse measured at any peripheral point. the american heart association states the normal resting adult human heart rate is 60-100 bpm. tachycardia is a high heart rate, defined as above 100 bpm at rest. bradycardia is a low heart rate, defined as below 60 bpm at rest. when a human sleeps, a heartbeat with rates around 40–50 bpm is common and is considered normal. when the heart is not beating in a regular pattern, this is referred to as an arrhythmia. abnormalities of heart rate sometimes indicate disease. physiology the human heart 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. as water and blood are incompressible fluids, one of the physiological ways to deliver more blood to an organ is to increase heart rate. normal resting heart rates range from 60 to 100 bpm. 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. 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). 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. 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. norepinephrine binds to the beta–1 receptor. high blood pressure medications are used to block these receptors and so reduce the heart rate. autonomic innervation of the heart – cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in the medulla oblongata of the brain. they innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus (parasympathetic) nerves that slow cardiac activity. parasympathetic stimulation originates from the cardioinhibitory region of the brain 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. effects of parasympathetic and sympathetic stimulation on normal sinus rhythm – the wave of depolarization in a normal sinus rhythm shows a stable resting hr. following parasympathetic stimulation, hr slows. following sympathetic stimulation, hr increases. input to the cardiovascular centres 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. 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. 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. 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. the limbic system can also significantly impact hr related to emotional state. during periods of stress, it is not unusual to identify higher than normal hrs, often accompanied by a surge in the stress hormone cortisol. individuals experiencing extreme anxiety may manifest panic attacks with symptoms that resemble those of heart attacks. these events are typically transient and treatable. meditation techniques have been developed to ease anxiety and have been shown to lower hr effectively. doing simple deep and slow breathing exercises with one's eyes closed can also significantly reduce this anxiety and hr. factors influencing heart rate table 1: major factors increasing heart rate and force of contraction factor effect cardioaccelerator nerves release of norepinephrine proprioreceptors increased rates of firing during exercise chemoreceptors decreased levels of o2; increased levels of h+, co2, and lactic acid baroreceptors decreased rates of firing, indicating falling blood volume/pressure limbic system anticipation of physical exercise or strong emotions catecholamines increased epinephrine and norepinephrine thyroid hormones increased t3 and t4 calcium increased ca2+ potassium decreased k+ sodium decreased na+ body temperature increased body temperature nicotine and caffeine stimulants, increasing heart rate table 2: factors decreasing heart rate and force of contraction factor effect cardioinhibitor nerves (vagus) release of acetylcholine proprioreceptors decreased rates of firing following exercise chemoreceptors increased levels of o2; decreased levels of h+ and co2 baroreceptors increased rates of firing, indicating higher blood volume/pressure limbic system anticipation of relaxation catecholamines decreased epinephrine and norepinephrine thyroid hormones decreased t3 and t4 calcium decreased ca2+ potassium increased k+ sodium increased na+ body temperature decrease in body temperature using a combination of autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control over the heart rate, but other factors can impact on this. these include hormones, notably epinephrine, norepinephrine, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and ph balance. epinephrine and norepinephrine the catecholamines, epinephrine and norepinephrine, secreted by the adrenal medulla form one component of the extended fight-or-flight mechanism. the other component is sympathetic stimulation. epinephrine and norepinephrine have similar effects: binding to the beta-1 adrenergic receptors, and opening sodium and calcium ion chemical- or ligand-gated channels. the rate of depolarization is increased by this additional influx of positively charged ions, so the threshold is reached more quickly and the period of repolarization is shortened. however, massive releases of these hormones coupled with sympathetic stimulation may actually lead to arrhythmias. there is no parasympathetic stimulation to the adrenal medulla. thyroid hormones in general, increased levels of the thyroid hormones (thyroxine(t4) and triiodothyronine (t3)), increase the heart rate; excessive levels can trigger tachycardia. the impact of thyroid hormones is typically of a much longer duration than that of the catecholamines. the physiologically active form of triiodothyronine, has been shown to directly enter cardiomyocytes and alter activity at the level of the genome. it also impacts the beta-adrenergic response similar to epinephrine and norepinephrine. calcium calcium ion levels have a great impact on heart rate and myocardial contractility: increased calcium levels cause an increase in both. high levels of calcium ions result in hypercalcemia and excessive levels can induce cardiac arrest. drugs known as calcium channel blockers slow hr by binding to these channels and blocking or slowing the inward movement of calcium ions. caffeine and nicotine caffeine and nicotine are both stimulants of the nervous system and of the cardiac centres causing an increased heart rate. caffeine works by increasing the rates of depolarization at the sa node, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses to the heart. effects of stress both surprise and stress induce physiological response: elevate heart rate substantially. 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