Heart rate

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Heart rate, or heart pulse, is the speed of the heartbeat measured by the number of heartbeats per unit of time — typically beats per minute (bpm). The heart rate can vary according to the body's physical needs, including the need to absorb oxygen and excrete carbon dioxide. Activities that can provoke change include physical exercise, sleep, anxiety, stress, illness, ingesting, and drugs.

The normal resting adult human heart rate ranges from 60–100 bpm.[1] Bradycardia is a slow heart rate, defined as below 60 bpm. Tachycardia is a fast heart rate, defined as above 100 bpm at rest.[2] When the heart is not beating in a regular pattern, this is referred to as an arrhythmia. These abnormalities of heart rate sometimes indicate disease.[3]

Physiology[edit]

Normal heart sounds as heard with a stethoscope

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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, 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.[4]

Due to individuals having a constant blood volume, one of the physiological ways to deliver more oxygen to an organ is to increase heart rate to permit blood to pass by the organ more often.[3] Normal resting heart rates range from 60–100 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 80–100 bpm, mainly if they are present during sleep, may be signs of hyperthyroidism or anemia (see below).[3]

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, many of which are those that are 'forced'/'enticed' out by the ingestion and processing of drugs.

This section discusses target heart rates for healthy persons and are inappropriately high for most persons with coronary artery disease.[5]


Factors influencing heart rate[edit]

Table 1: Major factors increasing heart rate and force of contraction[6]
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[6]
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 Decreased 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 epinephrine, norepinephrine, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance (Table 1 and Table 2).[6]

Epinephrine and norepinephrine[edit]

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.[6]

Thyroid hormones[edit]

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.[clarification needed] It also impacts the beta adrenergic response similar to epinephrine and norepinephrine.[6]

Calcium[edit]

Calcium ion levels greatly impact on heartrate and contractility; increased 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.[6]

Caffeine and nicotine[edit]

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.[6] Both stimulants are legal and unregulated, and are known to be addictive.[6]

Factors decreasing heart rate[edit]

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 CO 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.[6]

Heart muscle relies exclusively on aerobic metabolism for energy. Hypoxia (an insufficient supply of oxygen) leads to decreasing HRs, since metabolic reactions fueling heart contraction are restricted.[6]

Acidosis is a condition in which excess hydrogen ions are present, and the patient’s blood expresses a low pH value. Alkalosis is a condition in which there are too few hydrogen ions, and the patient’s blood has an elevated pH. Normal blood pH falls in the range of 7.35–7.45, so a number lower than this range represents acidosis and a higher number represents alkalosis. Enzymes, being the regulators or catalysts of virtually all biochemical reactions - are sensitive to pH and will change shape slightly with values outside their normal range. These variations in pH and accompanying slight physical changes to the active site on the enzyme decrease the rate of formation of the enzyme-substrate complex, subsequently decreasing the rate of many enzymatic reactions, which can have complex effects on HR. Severe changes in pH will lead to denaturation of the enzyme.[6]

The last variable is body temperature. Elevated body temperature is called hyperthermia, and suppressed body temperature is called hypothermia. Slight hyperthermia results in increasing HR and strength of contraction. Hypothermia slows the rate and strength of heart contractions. This distinct slowing of the heart is one component of the larger diving reflex that diverts blood to essential organs while submerged. If sufficiently chilled, the heart will stop beating, a technique that may be employed during open heart surgery. In this case, the patient’s blood is normally diverted to an artificial heart-lung machine to maintain the body’s blood supply and gas exchange until the surgery is complete, and sinus rhythm can be restored. Excessive hyperthermia and hypothermia will both result in death, as enzymes drive the body systems to cease normal function, beginning with the central nervous system.[6]

Heart rates in different circumstances[edit]

Resting heart rate[edit]

The basal or resting heart rate (HRrest) is measured while the subject is relaxed but awake, in a neutrally temperate environment, and not having recently exerted himself or herself nor having been subject to a stress or even a surprise (for example the simple noise of a doorbell can augment the heart rate and blood pressure). The typical resting heart rate in adults is 60–80 beats per minute (bpm). For endurance athletes at the elite level, it is not unusual to have a resting heart rate between 33 and 50.[citation needed] This is the firing rate of the heart sinoatrial node (SAN), where the faster heart pacemaker cells driving the self-generated rhythmic firing and responsible for the cardiac muscle automaticity[7] are located.

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 SAN firing rate is affected by autonomic nervous system activity: sympathetic stimulation increases and parasympathetic stimulation decreases the firing rate.[8]

Target heart rate[edit]

For healthy persons, the Target Heart Rate or Training Heart Rate (THR) is a desired range of heart rate reached during aerobic exercise which enables one's heart and lungs to receive the most benefit from a workout. This theoretical range varies based mostly on age; however, a person's physical condition, sex, and previous training also are used in the calculation. Below are two ways to calculate one's THR. In each of these methods, there is an element called "intensity" which is expressed as a percentage. The THR can be calculated as a range of 65–85% intensity. However, it is crucial to derive an accurate HRmax to ensure these calculations are meaningful (see "Maximum heart rate" section above).

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 → 153 bpm
Karvonen method

The Karvonen method factors in resting heart rate (HRrest) to calculate target heart rate (THR), using a range of 50–85% intensity:[9]

THR = ((HRmax − HRrest) × % intensity) + HRrest

Example for someone with a HRmax of 180 and a HRrest of 70:

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 derives exercise zones 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

Maximum heart rate[edit]

The maximum heart rate (HRmax) is the highest heart rate an individual can achieve without severe problems through exercise stress,[10][11] and generally decreases with age. Since HRmax varies by individual, the most accurate way of measuring any single person's HRmax is via a cardiac stress test. In this test, a person is subjected to controlled physiologic stress (generally by treadmill) while being monitored by an ECG. The intensity of exercise is periodically increased until certain changes in heart function are detected on the ECG monitor, at which point the subject is directed to stop. Typical duration of the test ranges ten to twenty minutes.

Adults who are beginning a new exercise regimen are often advised to perform this test only in the presence of medical staff due to risks associated with high heart rates. For general purposes, a formula is often employed to estimate a person's maximum heart rate. However, these predictive formulas have been criticized as inaccurate because they generalized population-averages and usually focus on a person's age. It is well-established that there is a "poor relationship between maximal heart rate and age" and large standard deviations around predicted heart rates.[12] (see Limitations of Estimation Formulas).

The various formulae provide slightly different numbers for the maximum heart rates by age.

A number of formulas are used to estimate HRmax

Tanaka, Monahan, & Seals

From Tanaka, Monahan, & Seals (2001):

  • HRmax = 208 − (0.7 × age)  [13]

Their meta-analysis (of 351 prior studies involving 492 groups and 18,712 subjects) and laboratory study (of 514 healthy subjects) concluded that, using this equation, HRmax was very strongly correlated to age (r = −0.90). The regression equation that was obtained in the laboratory-based study (209 − 0.7 x age), was virtually identical to that of the meta-study. The results showed HRmax to be independent of gender and independent of wide variations in habitual physical activity levels. This study found a standard deviation of ~10 beats per minute for individuals of any age, meaning the HRmax formula given has an accuracy of ±20 beats per minute. [13]

In 2007, researchers at the Oakland University analyzed maximum heart rates of 132 individuals recorded yearly over 25 years, and produced a linear equation very similar to the Tanaka formula, HRmax = 206.9 − (0.67 × age), and a nonlinear equation, HRmax = 191.5 − (0.007 × age2). The linear equation had a confidence interval of ±5–8 bpm and the nonlinear equation had a tighter range of ±2–5 bpm. Also a third nonlinear equation was produced: HRmax = 163 + (1.16 × age) − (0.018 × age2).[14]

Haskell and Fox
Fox and Haskell formula; widely used.

Notwithstanding the research of Tanaka, Monahan, & Seals, the most widely cited formula for HRmax (which contains no reference to any standard deviation) 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.[15] Inquiry into the history of this formula reveals that it was not developed from original research, but resulted from observation based on data from approximately 11 references consisting of published research or unpublished scientific compilations.[16] It gained widespread use through being used by Polar Electro in its heart rate monitors,[15] which Dr. Haskell has "laughed about",[15] as the formula "was never supposed to be an absolute guide to rule people's training."[15]

While it is the most common (and easy to remember and calculate), this particular formula is not considered by reputable health and fitness professionals to be a good predictor of HRmax. Despite the widespread publication of this formula, research spanning two decades reveals its large inherent error, Sxy = 7–11 bpm. Consequently, the estimation calculated by   HRmax = 220 − age   has neither the accuracy nor the scientific merit for use in exercise physiology and related fields.[16]

Robergs and Landwehr

A 2002 study[16] of 43 different formulas for HRmax (including that of Haskell and Fox – see above) published in the Journal of Exercise Psychology concluded that:

  1. no "acceptable" formula currently existed, (they used the term "acceptable" to mean acceptable for both prediction of VO2, and prescription of exercise training HR ranges)
  2. the least objectionable formula was:
HRmax = 205.8 − (0.685 × age)
This had a standard deviation that, although large (6.4 bpm), was considered acceptable for prescribing exercise training HR ranges.
Gulati (for women)

Research conducted at Northwestern University by Martha Gulati, et al., in 2010[17] suggested a maximum heart rate formula for women:

HRmax = 206 − (0.88 × age)
Gellish

A 2008 study from Lund, Sweden gives reference values (obtained during bicycle ergometry) for men:

HRmax = 203.7 / ( 1 + exp( 0.033 × (age − 104.3) ) )  [18]

and for women:

HRmax = 190.2 / ( 1 + exp( 0.0453 × (age − 107.5) ) )  [19]
Other formulae
  • HRmax = 206.3 − (0.711 × age)
(Often attributed to "Londeree and Moeschberger from the University of Missouri")
  • HRmax = 217 − (0.85 × age)
(Often attributed to "Miller et al. from Indiana University")

Limitations of Estimation Formulas[edit]

Maximum heart rates vary significantly between individuals.[15] Even within a single elite sports team, such as Olympic rowers in their 20s, maximum heart rates have been reported as varying from 160 to 220.[15] Such a variation would equate to a 60 or 90 year age gap in the linear equations above, and would seem to indicate the extreme variation about these average figures.

Figures are generally considered averages, and depend greatly on individual physiology and fitness. For example an endurance runner's rates will typically be lower due to the increased size of the heart required to support the exercise, while a sprinter's rates will be higher due to the improved response time and short duration. While each may have predicted heart rates of 180 (= 220 − age), these two people could have actual HRmax 20 beats apart (e.g., 170-190).

Further, note that individuals of the same age, the same training, in the same sport, on the same team, can have actual HRmax 60 bpm apart (160–220):[15] the range is extremely broad, and some say "The heart rate is probably the least important variable in comparing athletes."[15]

Heart rate reserve[edit]

Heart rate reserve (HRreserve) is the difference between a person's measured or predicted maximum heart rate and resting heart rate. Some methods of measurement of exercise intensity measure percentage of heart rate reserve. Additionally, as a person increases their cardiovascular fitness, their HRrest will drop, thus the heart rate reserve will increase. Percentage of HRreserve is equivalent to percentage of VO2 reserve.[20]

HRreserve = HRmax − HRrest

This is often used to gauge exercise intensity (first used in 1957 by Karvonen).[21]

Karvonen's study findings have been questioned, due to the following:

  • The study did not use VO2 data to develop the equation.
  • Only six subjects were used, and the correlation between the percentages of HRreserve and VO2 max was not statistically significant.[22]

Heart rate recovery[edit]

Heart rate recovery (HRrecovery) is the reduction in heart rate at peak exercise and the rate as measured after a cool-down period of fixed duration.[23] A greater reduction in heart rate after exercise during the reference period is associated with a higher level of cardiac fitness.[24]

Heart rates that do not drop by more than 12 bpm one minute after stopping exercise are associated with an increased risk of death.[23] Investigators of the Lipid Research Clinics Prevalence Study, which included 5,000 subjects, found that patients with an abnormal HRrecovery (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.[24] Another study by Nishime et al. and featuring 9,454 patients followed for a median period of 5.2 years found a four-fold increase in mortality in subjects with an abnormal HRrecovery (≤12 bpm reduction one minute after the cessation of exercise).[24] Shetler et al. studied 2,193 patients for thirteen years and found that a HRrecovery of ≤22 bpm after one minute "best identified high-risk patients".[24] They also found that while HRrecovery had significant prognostic value it had no diagnostic value.[24]

Training regimes sometimes use HRrecovery as a guide of progress and to spot problems such as overheating or dehydration.[25][better source needed] After even short periods of hard exercise it can take a long time (about 30 minutes) for the heart rate to drop to rested levels.[citation needed]

Development[edit]

At 21 days after conception, 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 3.5 billion times in an average lifetime.

The human embryon heart begins beating 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 inititated 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 (EHR) 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.[26]

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

There is no difference in male and female heart rates before birth.[27]

Clinical significance[edit]

Measurement[edit]

Wrist heart rate monitor

Manual measurement[edit]

Heart rate monitor with a wrist receiver

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. (A good area is on the neck, under the corner of the jaw.) 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 doesn't 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.[28][29]

Possible points for measuring the heart rate are:

  1. The ventral aspect of the wrist on the side of the thumb (radial artery).
  2. The ulnar artery.
  3. The neck (carotid artery).
  4. The inside of the elbow, or under the biceps muscle (brachial artery).
  5. The groin (femoral artery).
  6. Behind the medial malleolus on the feet (posterior tibial artery).
  7. Middle of dorsum of the foot (dorsalis pedis).
  8. Behind the knee (popliteal artery).
  9. Over the abdomen (abdominal aorta).
  10. 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.
  11. The temple (superficial temporal artery).
  12. The lateral edge of the mandible (facial artery).
  13. The side of the head near the ear (posterior auricular artery).
ECG-RRinterval

Electronic measurement[edit]

In obstetrics, 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 = 1,500/(RR interval in millimeters)
  • HR = 60/(RR interval in seconds)
  • HR = 300/number of "large" squares between successive R waves.

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 pulse oximetry and seismocardiography.[30]

Tachycardia[edit]

Main article: 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 condition when tachycardia occurs are

  1. Exercise
  2. Pregnancy
  3. Emotional conditions such as anxiety or stress.

Pathological conditions when tachycardia occurs are:

  1. Sepsis
  2. Fever
  3. Anemia
  4. Hypoxia
  5. Hyperthyroidism
  6. Hypersecretion of catecholamines
  7. Cardiomyopathy
  8. Valvular heart diseases
  9. Acute Radiation Syndrome

Bradycardia[edit]

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.

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,[citation needed] one of the lowest ever recorded in a healthy human. Martin Brady achieved the world record for the slowest heartbeat in a healthy human with a heart rate of just 27 bpm in 2005 (a record that still stands).[31]

Arrhythmia[edit]

Main article: Cardiac dysrhythmia

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.

Correlation with cardiovascular mortality risk[edit]

A number of investigations indicate that faster resting heart rate has emerged as a new risk factor for mortality in homeothermic mammals, particularly cardiovascular mortality in human beings. 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.[32]

An Australian-led international study of patients with cardiovascular disease has shown that heart beat rate is a key indicator for the risk of heart attack. The study, published in The Lancet (September 2008) studied 11,000 people, across 33 countries, who were being treated for heart problems. Those patients whose heart rate was above 70 beats per minute had significantly higher incidence of heart attacks, hospital admissions and the need for surgery. University of Sydney professor of cardiology Ben Freedman from Sydney's Concord hospital, said "If you have a high heart rate there was an increase in heart attack, there was about a 46 percent increase in hospitalizations for non-fatal or fatal heart attack."[33]

Standard textbooks of physiology and medicine mention that heart rate (HR) is readily calculated from the ECG as follows:

HR = 1,500/RR interval in millimeters, HR = 60/RR interval in seconds, or HR = 300/number of large squares between successive R waves. In each case, the authors are actually referring to instantaneous HR, which is the number of times the heart would beat if successive RR intervals were constant. However, because the above formula is almost always mentioned, students determine HR this way without looking at the ECG any further.

Very low heart rate (bradycardia) may be associated with heart block. It may also arise from autonomous nervous system impairment - this in turn is correlated with criminal tendencies.[34]

Bibliography[edit]

References[edit]

This article incorporates text from the CC-BY book: OpenStax College, Anatomy & Physiology. OpenStax CNX. 30 jul 2014..

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