The human heart While heart rhythm is regulated entirely by the sinoatrial node under normal conditions,<unk>  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<unk> , 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<unk> . Normal resting<unk> s range from 60 to 100 bpm. Bradycardia is defined as a resting<unk>  below 60 bpm. However,<unk> s from 50 to 60 bpm are common among healthy people and do not necessarily require special attention. Tachycardia is defined as a resting<unk>  above 100 bpm, though persistent rest<unk> s 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<unk> . * Central nervous system depressants or sedatives decrease the<unk>  (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<unk>  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<unk> s for healthy persons, which would be inappropriately high for most persons with coronary artery disease. Influences from the central nervous system Cardiovascular centres The<unk>  is rhythmically generated by the sinoatrial node. It is also influenced by central factors through sympathetic and parasympathetic nerves. Nervous influence over the<unk>  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<unk>  of depolarization and contraction, which results in an increased<unk> . 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<unk> . 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<unk>  by opening chemical- or ligand-gated potassium ion channels to slow the<unk>  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<unk> s are considerably less than this, it becomes evident that parasympathetic stimulation normally slows<unk> . 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<unk>  to increase up to approximately 100 bpm. Any increases beyond this<unk>  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<unk> . Following parasympathetic stimulation,<unk>  slows. Following sympathetic stimulation,<unk>  increases. Input to the cardiovascular centres The cardiovascular centres 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<unk> s of firing by various proprioreceptors located in muscles, joint capsules, and tendons. The cardiovascular centres monitor these increased<unk> s 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.<unk> s 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<unk>  of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the<unk>  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<unk> s 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<unk>  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<unk> . 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<unk>  related to emotional state. During periods of stress, it is not unusual to identify higher than normal<unk> s, 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<unk>  effectively. Doing simple deep and slow breathing exercises with one's eyes closed can also significantly reduce this anxiety and<unk> . Factors influencing<unk>  Using a combination of autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control over the<unk> , 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<unk>  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<unk> ; 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
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