Links to articles on the site dealing with the "heart rate" topic.
According to the "American Heart Association" (AHA) the normal HR for an adult at rest is between 60-100 bpm. When the heart rate is too fast, therefore above 100 bpm at rest, it is called tachycardia. Conversely, if it is too slow, or less than 60 bpm at rest, it is called bradycardia. During sleep, a slow heartbeat with rates of 40-50 bpm is commonly considered normal. talks about arrhythmia Heart rate abnormalities can be (but not necessarily) true symptoms of disease.
(always in correspondence with the sinoatrial node). The "accelerating nerve" (accelerance nerve) is responsible for the sympathetic action, releasing norepinephrine (noradrenaline) on the cells of the sinoatrial node; the vagus nerve, on the other hand, provides parasympathetic entry by releasing acetylcholine in the same site. Therefore, stimulation of the accelerance nerve increases the heart rate, while stimulation of the vagus nerve decreases it.Increasing heart rate, while maintaining constant blood volume, increases peripheral blood flow and oxygenation. Normal resting heart rates range from 60 to 100 bpm. Bradycardia is defined as a resting rate below 60 bpm However, rates of 50 to 60 bpm are quite common even among healthy people and do not necessarily require special medical attention. Tachycardia, on the other hand, is defined as a resting heart rate above 100 bpm, although persistent rates between 80-100 bpm, especially during sleep, can be a symptom of hyperthyroidism or anemia.
- Exogenous central nervous system stimulants such as "substituted amphetamines" increase heart rate
- Central nervous system antidepressants or sedatives reduce heart rate (aside from some such as ketamine, which can cause stimulant effects such as tachycardia, among other things)
There are many reasons and mechanisms why the heart rate speeds up or slows down. Most require stimulants such as endorphins and hormones released in the brain, many of which are drug induced.
Note: The next section will discuss "target" heart rates for healthy people and are inadequate for most people with coronary artery disease.
Influence of the central nervous system (CNS)
Cardiovascular Centers
Heart rate is generated rhythmically by the sinoatrial node and is also influenced by central factors via the sympathetic and parasympathetic nerves. The nervous influence on CF is centralized within the two cardio-circulatory centers of the medulla oblongata. Cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardio-accelerating nerves, while cardio-inhibitory centers decrease cardiac activity via parasympathetic stimulation as a component of the vagus nerve. During rest, both centers provide light stimulation to the heart, contributing to autonomous tone, similar to what happens in the toning of skeletal muscles. Normally, vagal stimulation predominates; if unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm.
Both sympathetic and parasympathetic stimuli flow through the associated cardiac plexus near the base of the heart. The cardioaccelerator center also arrives with additional fibers, forming the cardiac nerves via the sympathetic ganglia (the cervical ganglia plus the upper thoracic ganglia T1-T4) at both the SA and AV nodes, as well as additional fibers for the two atria and two ventricles. The ventricles are more richly innervated by sympathetic fibers than by parasympathetic fibers. Sympathetic stimulation causes the neurotransmitter norepinephrine (also known as norepinephrine) to be released at the neuromuscular junction of the cardiac nerves. This shortens the repolarization period, thereby accelerating the rate of depolarization and contraction, which results in an increase in the heart rate. Opens chemical channels or ligands of sodium and calcium, allowing for an influx of positively charged ions.
Norepinephrine binds to the beta-1 receptor. Not surprisingly, high blood pressure medications are used to block these receptors by reducing heart rate.
Parasympathetic stimulation comes from the cardioinhibitory region, with impulses traveling through the vagus nerve (cranial nerve X). The vagus nerve sends branches to both the SA and AV nodes, and to portions of the atria and ventricles. Parasympathetic stimulation releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction. ACh slows HR by opening dependent chemical or ligand channels of potassium ions to slow the rate of spontaneous depolarization, which prolongs repolarization and increases the time before the next spontaneous depolarization occurs. Without any nerve stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm Since rest rates are considerably lower, it becomes apparent that parasympathetic stimulation normally slows the heart rate.
To be clear, this process is similar to an individual driving a car while accelerating but keeping one foot on the brake pedal. To gain speed, simply remove the foot from the brake and let the engine gain normal speed. In the case of the heart, reducing parasympathetic stimulation would decrease ACh release, which would allow HR to increase to about 100 bpm Any increase beyond this rate requires sympathetic stimulation.
Stimulation of the cardiovascular centers
The cardiovascular centers are stimulated by a series of visceral receptors by means of impulses that travel through the visceral sensory fibers within the vagus nerve and sympathetic nerves through the cardiac plexus. Among these receptors we recognize various proprioceptors, baroreceptors and chemoreceptors, as well as various stimuli. of the limbic system which normally allow a precise regulation of cardiac function, through cardiac reflexes. The increase in physical activity results in an increase in stimulation rates (firing) by the various proprioceptors located in the muscles, in the joint capsules and in the tendons. Cardiovascular centers monitor these increased rates of stimulation, either by suppressing parasympathetic activity or by increasing the sympathetic stimulation needed to increase blood flow.
Similarly, baroreceptors are elastic receptors located in the aortic sinus, carotid bodies, venous cavities, and other places, including the pulmonary vessels and the right side of the heart itself. Firing rates from baroreceptors are a function of blood pressure, level of physical activity and relative blood distribution. The heart centers control the firing of the baroreceptors to maintain cardiac homeostasis, a mechanism called the "baroreceptor reflex". cardiac stimulation decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and elongation decrease, the frequency of baroreceptor stimulation decreases and cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.
A similar reflex, called atrial reflex (Bainbridge reflex), is associated with varying rates of blood flow to the atria. An increase in venous return lengthens the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their pace of stimulation and stretch due to the increase in blood pressure, the heart center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The reverse also occurs.
The increase in metabolic by-products associated with increased activity, such as carbon dioxide (CO2), hydrogen ions and lactic acid, and the reduction in oxygen levels, are detected by a series of chemoreceptors innervated by the glossopharyngeal and nerves. vagal: These chemoreceptors provide feedback to the cardiovascular centers on the need to increase or decrease blood flow, based on the relative levels of these substances.
The limbic system can also have a significant impact on heart rate related to emotional state. During times of stress, it is not uncommon to identify a higher-than-normal HR, often accompanied by a surge in cortisol (the stress hormone). Individuals with severe anxiety may experience panic attacks with symptoms similar to those of heart attacks. These events are generally transient and treatable. Meditation techniques and deep breathing exercises with closed eyes are commonly used to relieve anxiety and have been shown to effectively lower HR.
Factors affecting heart rate
Main factors that increase heart rate and force of contraction
Factors that reduce heart rate and force of contraction
By combining autorhythmicity and innervation, the cardiovascular center is able to provide relatively precise control over the heart rate; however, there are many other factors that can have a significant impact. These include:
- Hormones, especially epinephrine (adrenaline), norepinephrine and thyroid hormones
- Various ions including calcium, potassium and sodium
- Body temperature
- Hypoxia
- PH balance.
Epinephrine and norepinephrine
The "fight-or-flight" mechanism is determined by catecholamines, adrenaline and noradrenaline - secreted by the adrenal medulla - and by sympathetic stimulation. Epinephrine and norepinephrine have similar effects: they bind to beta-1 adrenergic receptors and open sodium and calcium dependent ion or ligand channels. The rate of depolarization is increased by this additional influx of positively charged ions, and hence the threshold is reached more rapidly, shortening the repolarization period However, massive releases of these hormones, coupled with sympathetic stimulation, can actually induce arrhythmia.The adrenal medulla is not subject to parasympathetic stimulation.
Thyroid hormones
In general, increased levels of thyroid hormones - thyroxine (T4) and triiodothyronine (T3) - increase heart rate; excessive levels can trigger tachycardia. The impact of thyroid hormones is longer lasting than that of catecholamines. The physiologically active form of triiodothyronine has been shown to enter cardiomyocytes directly and alter activity at the genome level. It also has an impact on the beta adrenergic response in a manner similar to epinephrine and norepinephrine.
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Ionic levels of calcium have a great impact on heart rate and contractility: the increase in this ion causes an increase in both. High levels of calcium ions cause hypercalcemia and, if excessive, can induce cardiac arrest. Drugs known as blockers of the heart. Calcium channels slow HR by binding to these channels and blocking or slowing the inward migration of calcium ions.
Caffeine and nicotine
Caffeine and nicotine are both stimulants of the nervous system and heart centers that cause an increase in heart rate. Caffeine works by increasing the rates of depolarization in the SA node, while nicotine stimulates the activity of sympathetic neurons that transmit impulses to the heart.
Effects of stress
Both fear and stress induce an elevation in heart rate. In a study conducted on 8 actors of both sexes and aged between 18 and 25 years, the reaction (HR) to an unexpected event (stressor) during a performance was measured; of these, half were on stage and the other half behind the scenes. Offstage actors reacted immediately by increasing HR and reducing it quickly, while those on stage reacted over the next 5 minutes but HR slowly decreased (so-called passive defense A stressor therefore has a more delayed but prolonged effect on heart rate in individuals not directly affected.
Factors that reduce heart rate
Heart rate can be slowed by altered sodium and potassium levels, hypoxia, acidosis, alkalosis, and hypothermia. The relationship between electrolytes and CF is complex. What is certain is that maintaining electrolyte balance is essential for the normal wave of depolarization. Of the two ions, potassium has the greatest clinical significance. Initially, both hyponatremia (low sodium levels) and hypernatremia (high sodium levels) can lead to tachycardia. Severe hypernatremia can lead to fibrillation. Severe hyponatremia leads to both bradycardia and other arrhythmias. Hypokalaemia (low potassium levels) leads to arrhythmias, while hyperkalaemia (high potassium levels) causes the heart to become weak, flaccid and stop.
For energy production, the heart muscle relies solely on aerobic metabolism. Hypoxia - an insufficient supply of oxygen - leads to a decrease in HR, as the metabolic reactions that fuel the heart's contraction are limited.
Acidosis is a condition in which there are excess hydrogen ions in the blood, expressing a low pH value. Alkalosis is a condition in which very few hydrogen ions are present and the patient's blood has a high pH. Normal pH should remain in the 7.35-7.45 range, so a lower number than this range represents acidosis and a higher number represents alkalosis. Enzymes, being regulators or catalysts of virtually all biochemical reactions , are sensitive to pH and remain affected by it.These variations and the consequent slight physical variations of the active site on the enzyme reduce the rate of formation of the enzyme-substrate complex, subsequently decreasing the rate of many enzymatic reactions, which can have complex effects on CF. "enzyme.
The last variable is body temperature. A high body temperature is called hyperthermia, while too low a temperature is called hypothermia. A slight hyperthermia results in an increase in HR and force of contraction. Hypothermia slows the speed and strength of heart contractions. The slowing of the heart is one component of the much more complex blood shift, which diverts blood to essential organs as divers (especially freedivers) gain depth. Submarine. If sufficiently cooled, the heart can stop beating, a technique that can be used during open heart surgery. In this case, the patient's blood is normally diverted to an artificial "heart-lung" machine to maintain the "blood supply and gas exchange of the body until surgery is completed and sinus rhythm restored. Excessive hyperthermia and hypothermia both result in death."
. The normal trigger rate of the SA node is affected by autonomic nervous system activity: sympathetic stimulation increases and parasympathetic stimulation decreases the firing rate. Different measurements can be used to describe heart rate:Normal heart rates at rest, in beats per minute (bpm):
Basal or resting heart rate (HRrest) is defined as the heart rate of a person who is awake, placed in a neutral environment and not subject to recent exertion or stimulation, such as stress or fear. The normal range is 60-100 beats per minute. HR at rest is often related to mortality. For example, all-cause mortality increases by 1.22 (hazard ratio) when heart rate exceeds 90 bpm. mortality of patients with myocardial infarction increases from 15% to 41% if the heart rate exceeds 90 bpm. The ECG of 46,229 individuals with low risk of cardiovascular disease revealed that 96% had a resting heart rate between 48 and 98 beats per minute. Finally, 98% of cardiologists believe the "60 to 100" range is too high, and a vast majority of them agree that 50 to 90 bpm would be more appropriate. The normal resting heart rate is based on the resting activation rate of the sinoatrial node of the heart, where the fast pacemaker cells are located that drive the self-generated rhythmic firing responsible for the autrihythmicity of the heart. For endurance athletes a elite level, it is not unusual to have a resting heart rate below 50 bpm.
(HRmax) is the highest heart rate an individual can achieve without experiencing serious problems during exercise and generally decreases with age. Since HRmax varies from individual to individual, the most accurate way to measure it is through a test, in which a person is subjected to controlled physiological stress (usually from a treadmill) while being monitored with ECG. Exercise intensity is periodically increased until desired changes in heart function are observed, at which point the subject is directed to stop.The typical duration ranges from ten to twenty minutes.
Newbies are advised to perform this test only in the presence of medical personnel, due to the associated risks. However, a rough estimate can be made using a formula. However, these predictive systems are inaccurate because they focus exclusively on age. It is known that there is a "limited correlation between maximum heart rate and" age. "
. The thumb should not be used to measure another person's heart rate, as excessive pressure may interfere with the correct perception of the pulse.The radial artery is the easiest to use. However, in emergency situations the most reliable arteries for measuring heart rate are the carotids. displaced blood is largely different from one beat to another.
The possible points for measuring heart rate are:
- Ventral wrist on the thumb side (radial artery)
- Ulnar artery
- Neck (carotid arteries)
- Inside the elbow or below the biceps muscle (brachial artery)
- Groin (femoral artery)
- Posterior to the medial malleolus on the feet (posterior tibial artery)
- Center of the dorsum of the foot (dorsalis pedis)
- Behind the knee (popliteal artery)
- Above the abdomen (abdominal aorta)
- Chest (apex of the heart), which can be felt with the hand or fingers. It is also possible to auscultate the heart using a stethoscope
- Temples (superficial temporal artery)
- Lateral border of the mandible (facial artery)
- Side of the head near the ear (posterior auricular artery).
Correlation with risk of cardiovascular mortality
Various investigations indicate that an elevated resting heart rate is a risk factor for mortality in homeothermic mammals, particularly cardiovascular mortality in humans. Faster CF may accompany increased production of inflammatory molecules and reactive oxygen species production in the cardiovascular system, as well as increased mechanical stress on the heart. There is therefore a correlation between the increase in resting frequency and cardiovascular risk.
An international study by Australians of patients with cardiovascular disease showed that heart rate is a key indicator for heart attack risk. The study, published in "The Lancet" (September 2008), observed 11,000 people in 33 countries who were treated for heart problems. Those patients whose heart rate was above 70 bpm had a significantly higher incidence of heart attacks, hospital admissions, and the need for surgery. Higher HR is thought to be correlated with an increase in heart attacks and about a + 46% of hospitalizations fatal and non-fatal events.
Other studies have shown that "high resting HR is associated with increased cardiovascular and all-cause mortality in the general population and in patients with chronic disease. Faster resting heart rate is associated with shorter life expectancy and it is considered a strong risk factor for heart disease and heart failure, regardless of physical fitness level. In particular, a resting heart rate above 65 beats per minute has been shown to have a strong independent effect on premature mortality; a 10 beats per minute increase in resting heart rate has been shown to be associated with a 10-20% increased risk of death. In another study, men with no evidence of heart disease and a resting heart rate of more than 90 beats per minute had a five times greater risk of sudden cardiac death. Similarly, another study found that men with a resting heart rate of over 90 beats per minute had an almost double increased risk of cardiovascular disease mortality; in women it was associated with a triple increase.
Given the data, heart rate should be considered in evaluating cardiovascular risk, even in apparently healthy individuals. Heart rate has many advantages as a clinical parameter; in particular, it is cheap and quick to measure, and is easily understood. Although accepted heart rate limits are between 60 and 100 beats per minute, a better definition of normal includes a range of 50 to 90 beats per minute.
Exercise, diet, lifestyle and drug remedies can be very helpful in reducing resting heart rate. In the various studies on the correlation to the risk of death and cardiac complications in patients with type 2 diabetes, the consumption of legumes has been shown to be useful in "lowering the heart rate at rest. This is thought to happen thanks to direct but also indirect beneficial effects. , such as reducing cholesterol and saturated fat.
Too slow heart rate (bradycardia), which can result from impaired autonomic nervous system, can be associated with cardiac arrest.
