How the Heart Works & Pumps Blood Through The Human Body

The heart is an amazing organ. It pumps oxygen and nutrient-rich blood throughout your body to sustain life. This fist-sized powerhouse beats (expands and contracts) 100,000 times per day, pumping five or six quarts of blood each minute, or about 2,000 gallons per day.

Your heart is a key part of your cardiovascular system, which also includes all your blood vessels that carry blood from the heart to the body and then back to the heart.

How Does Blood Travel Through the Heart?

As the heart beats, it pumps blood through a system of blood vessels, called the circulatory system. The vessels are elastic, muscular tubes that carry blood to every part of the body.

Blood is essential. In addition to carrying fresh oxygen from the lungs and nutrients to the body’s tissues, it also takes the body’s waste products, including carbon dioxide, away from the tissues. This is necessary to sustain life and promote the health of all parts of the body.

There are three main types of blood vessels:

• Arteries. They begin with the aorta, the large artery leaving the heart. Arteries carry oxygen-rich blood away from the heart to all of the body’s tissues. They branch several times, becoming smaller and smaller as they carry blood further from the heart and into organs.
• Capillaries. These are small, thin blood vessels that connect the arteries and the veins. Their thin walls allow oxygen, nutrients, carbon dioxide, and other waste products to pass to and from our organ’s cells.
• Veins. These are blood vessels that take blood back to the heart; this blood has lower oxygen content and is rich in waste products that are to be excreted or removed from the body. Veins become larger and larger as they get closer to the heart. The superior vena cava is the large vein that brings blood from the head and arms to the heart, and the inferior vena cava brings blood from the abdomen and legs into the heart.

This vast system of blood vessels — arteries, veins, and capillaries — is over 60,000 miles long. That’s long enough to go around the world more than twice!

Where Is Your Heart and What Does It Look Like?

The heart is located under the rib cage, slightly to the left of your breastbone (sternum) and between your lungs.

Looking at the outside of the heart, you can see that the heart is made of muscle. The strong muscular walls contract (squeeze), pumping blood to the rest of the body. On the surface of the heart, there are coronary arteries, which supply oxygen-rich blood to the heart muscle itself. The major blood vessels that enter the heart are the superior vena cava, the inferior vena cava, and the pulmonary veins. The pulmonary artery exits the heart and carries oxygen-poor blood to the lungs. The aorta exits and  carries oxygen-rich blood to the rest of the body.

On the inside, the heart is a four-chambered, hollow organ. It is divided into the left and right side by a muscular wall called the septum. The right and left sides of the heart are further divided into two top chambers called the atria, which receive blood from the veins, and two bottom chambers called ventricles, which pump blood into the arteries.

The atria and ventricles work together, contracting and relaxing to pump blood out of the heart. As blood leaves each chamber of the heart, it passes through a valve. There are four heart valves within the heart:

• Mitral valve
• Tricuspid valve
• Aortic valve
• Pulmonic valve

The tricuspid and mitral valves lie between the atria and ventricles. The aortic and pulmonic valves lie between the ventricles and the major blood vessels leaving the heart.

The heart valves work the same way as one-way valves in the plumbing of your home. They prevent blood from flowing in the wrong direction.

Each valve has a set of flaps, called leaflets or cusps. The mitral valve has two leaflets; the others have three. The leaflets are attached to and supported by a ring of tough, fibrous tissue called the annulus. The annulus helps to maintain the proper shape of the valve.

The leaflets of the mitral and tricuspid valves are also supported by tough, fibrous strings called chordae tendineae. These are similar to the strings supporting a parachute. They extend from the valve leaflets to small muscles, called papillary muscles, which are part of the inside walls of the ventricles.

How Does Blood Flow Through the Heart?

The right and left sides of the heart work together. The pattern described below is repeated over and over, causing blood to flow continuously to the heart, lungs, and body.

Right Side of the Heart

• Blood enters the heart through two large veins, the inferior and superior vena cava, emptying oxygen-poor blood from the body into the right atrium of the heart.
• As the atrium contracts, blood flows from your right atrium into your right ventricle through the open tricuspid valve.
• When the ventricle is full, the tricuspid valve shuts. This prevents blood from flowing backward into the atria while the ventricle contracts.
• As the ventricle contracts, blood leaves the heart through the pulmonic valve, into the pulmonary artery and to the lungs, where it is oxygenated and then returns to the left atrium through the pulmonary veins.

Left Side of the Heart

• The pulmonary veins empty oxygen-rich blood from the lungs into the left atrium of the heart.
• As the atrium contracts, blood flows from your left atrium into your left ventricle through the open mitral valve.
• When the ventricle is full, the mitral valve shuts. This prevents blood from flowing backward into the atrium while the ventricle contracts.
• As the ventricle contracts, blood leaves the heart through the aortic valve, into the aorta and to the body.

How Does Blood Flow Through Your Lungs?

Once blood travels through the pulmonic valve, it enters your lungs. This is called the pulmonary circulation. From your pulmonic valve, blood travels to the pulmonary artery to tiny capillary vessels in the lungs.

Here, oxygen travels from the tiny air sacs in the lungs, through the walls of the capillaries, into the blood. At the same time, carbon dioxide, a waste product of metabolism, passes from the blood into the air sacs. Carbon dioxide leaves the body when you exhale. Once the blood is oxygenated, it travels back to the left atrium through the pulmonary veins.

What Are the Coronary Arteries of the Heart?

Like all organs, your heart is made of tissue that requires a supply of oxygen and nutrients. Although its chambers are full of blood, the heart receives no nourishment from this blood. The heart receives its own supply of blood from a network of arteries, called the coronary arteries.

Two major coronary arteries branch off from the aorta near the point where the aorta and the left ventricle meet:

• Right coronary artery supplies the right atrium and right ventricle with blood. It branches into the posterior descending artery, which supplies the bottom portion of the left ventricle and back of the septum with blood.
• Left main coronary artery branches into the circumflex artery and the left anterior descending artery. The circumflex artery supplies blood to the left atrium, side and back of the left ventricle, and the left anterior descending artery supplies the front and bottom of the left ventricle and the front of the septum with blood.

These arteries and their branches supply all parts of the heart muscle with blood.

Coronary artery disease occurs when plaque builds up in the coronary arteries and prevents the heart from getting the enriched blood it needs. If this happens, a network of tiny blood vessels in the heart that aren’t usually open called collateral vessels may enlarge and become active. This allows blood to flow around the blocked artery to the heart muscle, protecting the heart tissue from injury.

How Does the Heart Beat?

The atria and ventricles work together, alternately contracting and relaxing to pump blood through your heart. The electrical system of the heart is the power source that makes this possible.

Your heartbeat is triggered by electrical impulses that travel down a special pathway through the heart.

• The impulse starts in a small bundle of specialized cells called the SA node (sinoatrial node), located in the right atrium. This node is known as the heart’s natural pacemaker. The electrical activity spreads through the walls of the atria and causes them to contract.
• A cluster of cells in the center of the heart between the atria and ventricles, the AV node (atrioventricular node) is like a gate that slows the electrical signal before it enters the ventricles. This delay gives the atria time to contract before the ventricles do.
• The His-Purkinje network is a pathway of fibers that sends the impulse to the muscular walls of the ventricles, causing them to contract.

At rest, a normal heart beats around 50 to 90 times a minute. Exercise, emotions, fever, and some medications can cause your heart to beat faster, sometimes to well over 100 beats per minute.

The Heart of the Matter

All of the blood in your body travels through your heart about once a minute.

Your heart is an efficient machine with a specialized set of working parts. Learn what these parts are, and how they work together, by reading below.

Parts of the Heart

Taking Sides

Your heart is divided into two sides—right and left. A thick wall of tissue called the septum separates the right and left sides.

The right side of a heart usually appears to the left in diagrams, and the left side on the right.

Chambers

The atria are your heart’s upper chambers. They collect blood as it flows into the heart.

The ventricles are your heart’s lower chambers. They pump blood from the heart to the rest of the body.

Valves

Your heart has four valves. These valves only open in one direction, to prevent blood from flowing backward. Valves control the flow of blood from the atria to the ventricles, and from the ventricles to the rest of the body. 

Your tricuspid valve controls the flow of oxygen-poor blood from the right atrium to the right ventricle. 

Your pulmonary valve controls the flow of blood from the right ventricle to the pulmonary artery, which carries blood from your heart to your lungs.

Your mitral valve controls the flow of oxygen-rich blood from the left atrium to the left ventricle.

Your aortic valve controls the flow of blood from the left ventricle to the rest of your body.

Arteries

Arteries are blood vessels that transport blood from the heart to the body. Your heart has two major arteries and several coronary arteries.

Your aorta carries oxygen-rich blood from the left ventricle of your heart to the rest of your body.

Your coronary arteries branch off from the aorta to carry oxygen-rich blood to the myocardium—the heart muscle itself.

Veins

Veins are blood vessels that carry blood from the body to the heart. Your heart has six major veins.

The superior vena cava carries oxygen-poor blood from the upper body to the right atrium.

The inferior vena cava carries oxygen-poor blood from the lower half of the body to the right atrium.

Four pulmonary veins carry oxygen-rich blood from the lungs to the left atrium.

Going with the Flow

1. Oxygen-poor blood flows into the right atrium from the vena cavae (superior and inferior vena cava).

2. Blood is pumped through the tricuspid valve from the right atrium to the right ventricle.

3. Blood is pumped through the pulmonary valve from the right ventricle to the pulmonary artery.

4. Blood flows through the pulmonary artery to the lungs.

5. Oxygenated blood flows from the lungs to the pulmonary veins.

6. Blood flows from the pulmonary veins to the left atrium.

7. Blood is pumped through the mitral valve from the left atrium to the left ventricle.

8. Blood is pumped through the aortic valve to the aorta, coronary arteries, and the rest of the body.

How your heart works

What is your heart?

Your heart is about the size of your clenched fist. It lies in the front and middle of your chest, behind and slightly to the left of your breastbone.

It is a muscle that pumps blood to all parts of your body to provide it with the oxygen and nutrients in needs to function.  

Your heart has the right and left separated by a wall. Each side has a small chamber called the atrium (pronounced ay-tree-um), which leads into a large pumping chamber called a ventricle (pronounced ven-tri-kl). There are 4 chambers:

• left atrium
• left ventricle
• right atrium
• right ventricle.

The right side of your heart

The right side of your heart collects blood on its return from the rest of your body.

The blood entering the right side of your heart is low in oxygen. This is because oxygen is removed from your blood as it circulates through your body’s organs and tissues. 

Your heart then pumps the blood to your lungs so it can receive more oxygen.

Once it has received oxygen, your blood returns directly to the left side of your heart, which then pumps it out again to all parts of your body.

The left side of your heart

The left ventricle of your heart is larger and thicker than the right ventricle. This is because it has to pump the blood further around the body, and against higher pressure, compared with the right ventricle.

To make sure your blood flows in the correct direction, valves guard the entrance and exits of your hearts chambers.

Where to get help

• Always dial triple zero (000) to call an ambulance in a medical emergency
• See your doctor
• Visit a GP after hours
• Visit healthdirect (external site) or call 1800 022 222
• Phone the Heart Foundation Helpline on 13 11 12

This information provided by

Acknowledgements
Heart Foundation

This publication is provided for education and information purposes only. It is not a substitute for professional medical care. Information about a therapy, service, product or treatment does not imply endorsement and is not intended to replace advice from your healthcare professional. Readers should note that over time currency and completeness of the information may change. All users should seek advice from a qualified healthcare professional for a diagnosis and answers to their medical questions.

Heart, How it Works

The heart pumps blood to the brain, lungs, and body. A heart that works well is needed for good health and to sustain life. To understand heart problems better, it may help to learn how a healthy heart works.

The heart muscle 

The heart muscle squeezes (contracts) to pump blood. When it relaxes, it refills with blood. To do its work, the heart muscle needs a constant supply of oxygen. Oxygen is supplied to the heart muscle by blood vessels that wrap around the surface of the heart. They include:

• The left main coronary artery. This branches into the:
  • Circumflex coronary artery. This supplies blood to the back left side of the heart.
  • Left anterior descending coronary artery. This supplies blood to the front left side of the heart.

•  The right coronary artery. This supplies blood to the bottom, right side, and back of the heart muscle.

Inside the heart

The inside of the heart is divided into right and left sides. Each side has an upper chamber and a lower chamber. The upper chamber is called the atrium. The lower chamber is called the ventricle . The right atrium fills with blood from the body while it’s relaxed. When it contracts, it pumps blood to the right ventricle. The right ventricle then pumps blood to the lungs. The blood picks up oxygen in the lungs. The left atrium then fills with oxygen-rich blood from the lungs. It pumps this blood to the left ventricle. From there, the blood is pumped to the brain, coronary arteries, and the rest of the body.

Valves control the flow. There are 4 valves in the heart. When the heart beats, valves act like 1-way doors. This keeps blood moving forward through the heart and into the body and lungs.

The cycle continues. The right side of the heart pumps oxygen-poor blood from the body to the lungs, where gets oxygen again. The left side of the heart pumps oxygen-rich blood from the lungs to the body. Once the body’s organs and tissues have removed the oxygen from the blood, the blood returns to the heart. The cycle is then repeated.

Parts of the heart 

• Superior vena cava. This carries oxygen-poor blood from the upper part of the body to the right atrium.
• Inferior vena cava. This carries oxygen-poor blood from the lower part of the body to the right atrium.
• Right atrium. This gets oxygen-poor blood from the body through the superior vena cava and the inferior vena cava and pumps the blood to the right ventricle. 
• Tricuspid valve. This lets oxygen-poor blood to flow forward from the right atrium to the right ventricle.
• Right ventricle. This pumps oxygen-poor blood through the pulmonary valve.
• Pulmonary valve. This lets oxygen-poor blood to flow forward to the pulmonary artery.
• Pulmonary artery. This carries oxygen-poor blood to the lungs to get oxygen.
• Pulmonary veins. These carry oxygen-rich blood from the lungs to the left atrium.
• Left atrium. This gets oxygen-rich blood from the lungs through the pulmonary veins and pumps the blood to the left ventricle.
• Mitral valve. This lets oxygen-rich blood to flow forward from the left atrium to the left ventricle.
• Left ventricle. This pumps oxygen-rich blood through the aortic valve.
• Aortic valve. This lets oxygen-rich blood to flow forward to the aorta.
• Aorta. This carries oxygen-rich blood to the rest of the body.

© 2000-2021 The StayWell Company, LLC. All rights reserved. This information is not intended as a substitute for professional medical care. Always follow your healthcare professional’s instructions.

The History of the Heart

The History of the Heart

A HISTORY OF THE HEART

“For the concept of a circuit of the blood
does not destroy, but rather advances traditional medicine.”  –
William Harvey, 1649

The heart has played an important role in
understanding the body since antiquity.  In the fourth century B. C., the
Greek philosopher Aristotle identified the heart as the most important organ of
the body, the first to form according to his observations of chick
embryos.   It was the seat of intelligence, motion, and sensation — a hot,
dry organ. 
Aristotle described it as a three-chambered organ that was the center of
vitality in the body.  Other organs surrounding it (e.g. brain and lungs)
simply existed to cool the heart.

In his treatise On the
Usefulness of the Parts of the Body, written in the second century A. D., Galen reaffirmed common ideas about the heart as the source of the body’s innate heat and as the organ most
closely related to the soul:  “The heart is, as it were, the hearthstone and source of the innate
heat by which the animal is governed.”  He
also observed carefully many of its unusual physical properties.  “The heart is a hard flesh, not easily injured. In hardness, tension,
general strength, and resistance to injury, the fibers of the heart far
surpass all others, for no other instrument performs such continuous, hard
work as the heart.”  He argued that the expansion and contraction of
the heart was a function of its role as an intelligent organ:   “The complexity of [the heart’s] fibers. .. was prepared by Nature
to perform a variety of functions… enlarging when it desires to attract
what is useful, clasping its contents when it is time to enjoy what has
been attracted, and contracting when it desires to expel residues.”

However, Galen was not afraid to contradict others
in matters of detailed anatomy, such as Aristotle’s claim that the heart
is the origin of the nerves.  He further argued that the heart was
secondary to the liver in its importance to the operations of the body, since it
was not the site of the production of the humors.  His ideas generally
predominated until the mid-seventeenth century.

As the scientific and philosophical writings of
Aristotle became more important in medieval Islam and Europe, physicians began
to puzzle over the discrepencies between these two ancients.  At the
beginning of the eleventh century, for example, Avicenna in his Canon of
Medicine integrated Aristotle’s ideas within his largely Galenic physiology
when he wrote:  “[The heart is the] root of all faculties and gives the faculties
of nutrition, life, apprehension, and movement to several other members. ” 
He believed that heart produced breath, the “vital power or innate
heat” within the body; it was an intelligent organ that controlled and
directed all others.  He identified the pulse as “a movement in the heart and arteries which takes the
form of alternate expansion and contraction, whereby the breath becomes
subjected to the influence of the air inspired.”  Despite Avicenna’s
recommendation to pay more attention to the heart, and the writings of the
Syrian jurist-physician Ibn al-Nafis in the thirteenth century on pulmonary
transit, most medical practitioners preferred Galen’s idea that the veins
connected the operations of the liver to the heart, which circulated vital
spirits throughout the body via the arteries.  Look at this published image
of the heart on the left.  How does it exemplify the vagueness of its
anatomy?

The Renaissance revival of anatomy made it possible
for physicians to clarify basic structures in the heart.   By this point,
they commonly agreed the heart was divided
into four parts with two ventricles and two auricles.  Wondering at the confusion over the divisions of the
heart’s chambers, Andres de Laguna wrote in 1535, “The heart has only two ventricles, a right and a left. I do not
know what is the meaning of the riddle proposed by the people who add a
third ventricle to the heart unless perhaps they intend by it those pores
which are found in the septum.”  The drawing on the right by Leonardo
da Vinci, probably from the 1490s, illustrates the typical Renaissance image of
the heart as a Galenic organ with two basic chambers dividing by the
septum.  Look closely at it.  What function would the
“pores” that Laguna mentioned have served?  Can you see them?

Leonardo, for all his ability to draw and observe the heart
with a great deal of accuracy, did not deviate significantly from Galen’s
account of it.  “The heart of itself is not the beginning of life but is a vessel
made of dense muscle vivified and nourished by an artery and a vein as are
the other muscles.   The heart is of such density that fire can scarcely damage
it.”  Yet he offered a more elaborate mechanical account of the heart,
underscoring the relationship between heat and motion.  He began to puzzle
over the actual movement of the heart, writing:

“At one and the same time, in one and the same subject, two opposite
motions cannot take place, that is, repentance and desire. Therefore, if
the right upper [auricle] and lower ventricles are one and the same, it
is necessary that the whole should cause at the same time one and the same
effect and not two effects arising from diametrically opposite purposes
as one sees in the case of the right ventricle with the lower, for whenever
the lower contracts, the upper dilates to accommodate the blood which has
been driven out of the lower ventricle.”

Look at his drawing on the left above.  How
does it differ from his earlier image of the heart?  To what extent does it
reflect his interests in physics and engineering?

By the middle of the sixteenth century, a handful
of physicians had begun to wonder about several key aspects of the traditional
heart.   Were the arteries truly separate from the veins?  Was the
heart really divided by its septum in such a way that arterial and venous fluids
were physically distinct?  Was the septum the key site of interchange
between blood and pneuma?  Both Michael Servetus and Realdo Colombo
returned to theme raised by Ibn al-Nafis:  pulmonary transit.  Andreas
Vesalius, who initially accepted the idea of the porous septum, eventually
rejected it because he found that he could not see it in repeated dissections of
cadavers.  Yet it was not until the English physician William Harvey wrote
his On the Circulation of the Blood (1628) that a viable alternative to
Galenic physiology became widely accepted.

Harvey supported the Aristotelian notion of the
heart.  He wrote in 1653:  “The heart is situated at the 4th and 5th ribs. Therefore [it is]
the principal part because [it is in] the principal place, as in the center
of a circle, the middle of the necessary body.”  He examined carefully
the function of all of its different parts and came to a reverse conclusion of
Galen and his medieval and Renaissance readers:  he believed that the heart
was actively at work when it was small, hard and contracted (systole), expelling
blood, and at rest when it was large and filled with blood (diastole). 
In 1628, he wrote:  “[T]he heart’s one role is the transmission of the
blood and its propulsion,, by means of the arteries, to the extremities
everywhere.”  Needless to say, Harvey firmly dismissed the idea of a
porous septum. 

Yet he did not challenge the metaphysical
intepretation of the heart.  The heart, as Master Nicolaus had aptly
observed in the late twelfth century, was the primary “spiritual member” of the body.  As such, it was the seat of
all emotions.  “If indeed from the heart alone rise anger or passion, fear, terror,
and sadness; if from it alone spring shame, delight, and joy, why should
I say more?” wrote Andreas de Laguna in 1535.  Harvey metaphorically
described the heart as the “king” or “sun” of the body to
underscores its cosmological significance.  Popular imagery of the heart,
such as this image to your left from the mid-seventeenth century, combined
scientific and cultural ideas.  This image, not from a medical text,
effectively conveys a detailed external anatomy of the heart while demonstrating
its cultural significance.  What do you think the message is?

By the end of seventeenth century, the anatomical knowledge of the heart was
surprisingly accurate and Harvey’s ideas were widely accepted.  The French
philosopher Rene Descartes, who was one of the first scholars to accept Harvey’s
new theory, too his ideas a step further when he argued that the heart was like
a pump or, better yet, a combustion engine.  The heart became an important
site for debating the pros and cons of mechanistic and vitalistic accounts of
the body, since it served both agendas.  

QUESTIONS:  WHAT MADE THE
HEART A SIGNIFICANT ORGAN?  WHAT MADE IT, ANATOMICALLY AND PHILOSOPHICALLY,
SO HARD TO UNDERSTAND?

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Body Home page

Some Additional Readings

Frontiers | A healthy heart is not a metronome: an integrative review of the heart’s anatomy and heart rate variability

Introduction

The Heart

The heart is about the size of a closed fist, weighs between 250 and 350 g, and beats approximately 100,000 times a day and 2.5 billion times during an average lifetime. The muscular heart consists of two atria and two ventricles. The atria are upper receiving chambers for returning venous blood. The ventricles comprise most of the heart’s volume, lie below the atria, and pump blood from the heart into the lungs and arteries. Deoxygenated blood enters the right atrium, flows into the right ventricle, and is pumped to the lungs via the pulmonary arteries, where wastes are removed and oxygen is replaced. Oxygenated blood is transported through the pulmonary veins to the left atrium and enters the left ventricle. When the left ventricle contracts, blood is ejected through the aorta to the arterial system (Marieb and Hoehn, 2013; Tortora and Derrickson, 2014).

The Cardiac Cycle

The cardiac cycle consists of systole (ventricular contraction) and diastole (ventricular relaxation). During systole, blood pressure (BP) peaks as contraction by the left ventricle ejects blood from the heart. Systolic BP is measured during this phase. During diastole, BP is lowest when the left ventricle relaxes. Diastolic BP is measured at this time.

Pacemakers

The heart contains autorhythmic cells that spontaneously generate the pacemaker potentials that initiate cardiac contractions. These cells continue to initiate heartbeats after surgeons sever all efferent cardiac nerves and remove a heart from the chest cavity for transplantation. Autorhythmic cells function as pacemakers and provide a conduction pathway for pacemaker potentials.

The sinoatrial (SA) node and atrioventricular (AV) node are the two internal pacemakers that are primarily responsible for initiating the heartbeat. The electrocardiogram (ECG) records the action of this electrical conduction system and contraction of the myocardium (Figure 1).

Figure 1. The generation of the electrocardiogram. Credit: Alila Sao Mai/Shutterstock.com.

Cardiac Conduction

In a healthy heart, the SA node initiates each cardiac cycle through spontaneous depolarization of its autorhythmic fibers. The SA node’s intrinsic firing rate of about 60–100 action potentials per minute usually prevents slower parts of the conduction system and myocardium (heart muscle) from generating competing potentials. The AV node can replace an injured or diseased SA node as pacemaker and spontaneously depolarizes 40–60 times per minute. The SA node generates an electrical impulse that travels through the atria to the AV node in about 0.03 s and causes the AV node to fire (Figure 2). The P wave of the ECG is produced as muscle cells in the atria depolarize and culminates in contraction of the atria (atrial systole).

Figure 2. The depolarization and repolarization of the heart. Credit: Alila Sao Mai/Shutterstock.com.

The signal rapidly spreads through the AV bundle reaching the top of the septum. These fibers descend down both sides of the septum as the right and left bundle branches and conduct the action potential over the ventricles about 0.2 s after the appearance of the P wave. Conduction myofibers, which extend from the bundle branches into the myocardium, depolarize contractile fibers in the ventricles (lower chambers), resulting in the QRS complex followed by the S-T segment. Ventricular contraction (ventricular systole) occurs after the onset of the QRS complex and extends into the S-T segment. The repolarization of ventricular myocardium generates the T wave about 0.4 s following the P wave. The ventricles relax (ventricular diastole) 0.6 s after the P wave begins (Tortora and Derrickson, 2014).

Regulation of the Heart

In a healthy organism, there is a dynamic relative balance between the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). PNS activity predominates at rest, resulting in an average HR of 75 beats per minute (bpm). This is significantly slower than the SA node’s intrinsic rate, which decreases with age from an average 107 bpm at 20 years to 90 bpm at 50 years (Opthof, 2000). The parasympathetic branch can slow the heart to 20 or 30 bpm or briefly stop it (Tortora and Derrickson, 2014). This illustrates the response called accentuated antagonism (Olshansky et al., 2008). Parasympathetic nerves exert their effects more rapidly (<1 s) than sympathetic nerves (>5 s; Nunan et al., 2010).

A major cardiovascular center, located in the medulla of the brainstem, integrates sensory information from proprioceptors (limb position), chemoreceptors (blood chemistry), and mechanoreceptors (also called baroreceptors) from the heart and information from the cerebral cortex and limbic system. The cardiovascular center responds to sensory and higher brain center input by adjusting heart rate via shifts in the relative balance between sympathetic and parasympathetic outflow (Shaffer and Venner, 2013).

In a healthy individual, the HR estimated at any given time represents the net effect of the neural output of the parasympathetic (vagus) nerves, which slow HR, and the sympathetic nerves, which accelerate it. At rest, both sympathetic and parasympathetic nerves are tonically active with the vagal effects dominant. Therefore, HR reflects the relative activity of the sympathetic and parasympathetic systems; with the more important question being, is the relative balance (HR) appropriate for the context the person is engaged in at any given moment? In other words, is HR higher during the daytime and when dealing with challenging tasks, and lower at night, during sleep or when not engaged in challenging duties or activities?

The most obvious effect of vagal activity is to slow or even stop the heart. The vagus nerves are the primary nerves for the parasympathetic system and innervate the intrinsic cardiac nervous system and project to the SA node, AV node, and atrial cardiac muscle. Increased efferent activity in these nerves triggers acetylcholine release and binding to muscarinic (mainly M2) receptors. This decreases the rate of spontaneous depolarization in the SA and AV nodes, slowing HR. Because there is sparse vagal innervation of the ventricles, vagal activity minimally affects ventricular contractility.

The response time of the sinus node is very short and the effect of a single efferent vagal impulse depends on the phase of the cardiac cycle at which it is received. Thus, vagal stimulation results in an immediate response that typically occurs within the cardiac cycle in which it occurs and affects only one or two heartbeats after its onset. After cessation of vagal stimulation, HR rapidly returns to its previous level. An increase in HR can also be achieved by reduced vagal activity or vagal block. Thus, sudden changes in HR (up or down) between one beat and the next are parasympathetically mediated (Hainsworth, 1995).

An increase in sympathetic activity is the principal method used to increase HR above the intrinsic level generated by the SA node. Following the onset of sympathetic stimulation, there is a delay of up to 5 s before the stimulation induces a progressive increase in HR, which reaches a steady level in 20–30 s if the stimulus is continuous (Hainsworth, 1995). The slowness of the response to sympathetic stimulation is in direct contrast to vagal stimulation, which is almost instantaneous. However, the effect on HR is longer lasting and even a short stimulus can affect HR for 5–10 s. Efferent sympathetic nerves target the SA node and AV node via the intrinsic cardiac nervous system, and the bulk of the myocardium (heart muscle). Action potentials conducted by these motor neurons trigger norepinephrine (NE) and epinephrine (E) release and binding to beta-adrenergic (β 1) receptors located on cardiac muscle fibers. This speeds up spontaneous depolarization in the SA and AV nodes, increases HR, and strengthens the contractility of the atria and ventricles. In failing hearts, the number of β 1 receptors is reduced and their cardiac muscle contraction in response to NE and E binding is weakened (Ogletree-Hughes et al., 2001).

Afferent Modulation of Cardiac and Brain Activity

The field of neurocardiology explores the anatomy and functions of the connections between the heart and brain (Davis and Natelson, 1993; Armour, 2003) and represents the intersection of neurology and cardiology. While efferent (descending) regulation of the heart by the autonomic nervous system (ANS) is well known, newer data have suggested a more complex modulation of heart function by the intrinsic cardiac nervous system (Kukanova and Mravec, 2006). These intracardiac neurons (sensory, interconnecting, afferent, and motor neurons) (Verkerk et al., 2012) can operate independently and their network is sufficiently extensive to be characterized as its own “little brain” on the mammalian heart (Armour, 2008, p. 165). The afferent (ascending) nerves play a critical role in physiological regulation and affect the heart’s rhythm. Efferent sympathetic and parasympathetic activity are integrated with the activity occurring in the heart’s intrinsic nervous system, including the afferent signals occurring from the mechanosensory and chemosensory neurons (Figure 3).

Figure 3. The neural communication pathways interacting between the heart and the brain are responsible for the generation of HRV. The intrinsic cardiac nervous system integrates information from the extrinsic nervous system and from the sensory neurites within the heart. The extrinsic cardiac ganglia located in the thoracic cavity have connections to the lungs and esophagus and are indirectly connected via the spinal cord to many other organs such as the skin and arteries. The vagus nerve (parasympathetic) primarily consists of afferent (flowing to the brain) fibers which connect to the medulla, after passing through the nodose ganglion. Credit: Institute of HeartMath.

Interestingly, the majority of fibers in the vagus nerve (approximately 85–90%) are afferents, and signals are sent to the brain via cardiovascular afferents to a greater extent than by any other major organ (Cameron, 2002). Mechanical and hormonal information is transduced into neurological impulses by sensory neurons in the heart before being processed in the intrinsic nervous system. These impulses then travel to the brain via afferent pathways in the spinal column and vagus nerve (McCraty, 2011).

Short-term regulation of BP is accomplished by a complex network of pressure-sensitive baroreceptors or mechanosensitive neurons which are located throughout the heart and in the aortic arch. Since BP regulation is a central role of the cardiovascular system, the factors that alter BP also affect fluctuations in HR. Intrinsic cardiac afferent sensory neurons (Figures 4, 5) transduce and distribute mechanical and chemical information regarding the heart (Cheng et al., 1997) to the intrinsic cardiac nervous system (Ardell et al., 1991). The afferent impulses from the mechanosensitive neurons travel via the glossopharyngeal and vagal nerves to the nucleus of the solitary tract (NST), which connects with the other regulatory centers in the medulla to modulate SNS outflow to the heart and the blood vessels. There is also some modulation of parasympathetic outflow to the heart via connections to the dorsal vagal complex. Thus, mechanosensitive neurons affect HR, vasoconstriction, venoconstriction, and cardiac contractility in order to regulate BP (Hainsworth, 1995). This input from the heart can also modulate and impact hormonal release (Randall et al., 1981).

Figure 4. Microscopic image of interconnected intrinsic cardiac ganglia in the human heart. The thin, light blue structures are multiple axons that connect the ganglia. Credit: Dr. Andrew Armour and the Institute of HeartMath.

Figure 5. This drawing shows the location and distribution of intrinsic cardiac ganglia which are interconnected and form the “heart brain.” Note how they are distributed around the orifices of the major vessels. Credit: Dr. Andrew Armour and the Institute of HeartMath.

The heart not only functions as an intricate information processing and encoding center (Armour and Kember, 2004), but is also an endocrine gland that can produce and secrete its own hormones and neurotransmitters (Cantin and Genest, 1985, 1986; Mukoyama et al., 1991; Huang et al., 1996). For instance, atrial myocytes can secrete atrial natriuretic peptide (ANP), a hormone that promotes salt and water excretion, to lower BP and produce vasodilation (Dietz, 2005). Additionally, intrinsic cardiac adrenergic cells can synthesize and secrete catecholamines such as dopamine, NE, and E (Huang et al., 1996) in addition to high concentrations of oxytocin (Gutkowska et al., 2000).

Research insights from the field of neurocardiology have confirmed that the neural interactions between the heart and brain are more complex than thought in the past. This research has shown that complex patterns of cardiovascular afferent activity occur across time scales from milliseconds to minutes (Armour and Kember, 2004). This work has also shown that the intrinsic cardiac nervous system has both short-term and long-term memory functions, which can influence HRV and afferent activity related to pressure, rhythm, and rate, as well as afferent activity associated with hormonal factors (Armour, 2003; Armour and Kember, 2004; Ardell et al., 2009).

John and Beatrice Lacey conducted heart–brain interaction studies and were the first to suggest a causal role of the heart in modulating cognitive functions such as sensory-motor and perceptual performance (Lacey, 1967; Lacey and Lacey, 1970, 1974). They suggested that cortical functions are modulated via afferent input from pressure-sensitive neurons in the heart, carotid arteries, and aortic arch (Lacey, 1967). Their research focused on activity occurring within a single cardiac cycle, and they confirmed that cardiovascular activity influences perception and cognitive performance. Research by Velden and Wölk found that cognitive performance fluctuates at a rhythm around 10 Hz. They also demonstrated that the modulation of cortical function via the heart’s influence is due to afferent inputs on the neurons in the thalamus which globally synchronizes cortical activity (Velden and Wölk, 1987; Wölk and Velden, 1989). An important aspect of their work was the finding that it is the “pattern and stability” (the rhythm) of the heart’s afferent inputs, rather than the number of neural bursts within the cardiac cycle, that are important in modulating thalamic activity, which in turn has global effects on brain function.

This growing body of research indicates that afferent information processed by this intrinsic cardiac nervous system (Armour, 1991) can influence activity in the frontocortical areas (Lane et al., 2001; McCraty et al., 2004) and motor cortex (Svensson and Thorén, 1979), affecting psychological factors such as attention level, motivation (Schandry and Montoya, 1996), perceptual sensitivity (Montoya et al., 1993), and emotional processing (Zhang et al., 1986). Intrinsic cardiac afferent neurons project to nodose and dorsal root ganglia, the brainstem (dorsal root ganglia first project to the spinal cord), the hypothalamus, thalamus, or amygdala, and then to the cerebral cortex (Kukanova and Mravec, 2006; McCraty et al., 2009).

Heartbeat Evoked Potentials

Heartbeat evoked potentials (HEPs) can be used to identify the specific pathways and influence of afferent input from the heart to the brain. HEPs are segments of electroencephalogram (EEG) that are synchronized to the heartbeat. The ECG R-wave is used as a timing source for signal averaging, resulting in waveforms known as HEPs. Changes in these evoked potentials associated with the heart’s afferent neurological input to the brain are detectable between 50 and 550 ms after each heartbeat. There is a replicable and complex distribution of HEPs across the scalp. Researchers can use the location and timing of the various components of HEP waveforms, as well as changes in their amplitudes and morphology, to track the flow and timing of cardiovascular afferent information throughout the brain (Schandry and Montoya, 1996).

MacKinnon et al. (2013) reported that HRV influences the amplitude of heartbeat evoked potentials (HEP N250s). In this specific context, self-induction of either negative or positive emotion conditions by recalling past events reduced HRV and N250 amplitude. In contrast, resonance frequency breathing (breathing at a rate that maximizes HRV amplitude) increased HRV and HRV coherence (auto-coherence and sinusoidal pattern) above baseline and increased N250 amplitude. The authors speculated that resonance frequency breathing reduces interference with afferent signal transmission from the heart to the cerebral cortex.

What Is Heart Rate Variability?

Ever since Walter Cannon introduced the concept of homeostasis in 1929, the study of physiology has been based on the principle that all cells, tissues, and organs maintain a static or constant “steady-state” condition in their internal environment. However, with the introduction of signal processing techniques that can acquire continuous time series data from physiologic processes such as heart rate, BP, and nerve activity, it has become abundantly apparent that biological processes vary in a complex and nonlinear way, even during “steady-state” conditions. These observations have led to the understanding that healthy physiologic function is a result of continuous, dynamic interactions between multiple neural, hormonal, and mechanical control systems at both local and central levels. For example, we now know that the normal resting sinus rhythm of the heart is highly irregular during steady-state conditions rather than being monotonously regular, which was the widespread notion for many years. A healthy heart is not a metronome.

With the ability to measure the ECG in 1895, and the later development of modern signal processing which first emerged in the 1960s and 1970s, the investigation of the heart’s complex rhythm rapidly exploded. The irregular behavior of the heartbeat is readily apparent when heart rate is examined on a beat-to-beat basis, but is overlooked when a mean value over time is calculated. These fluctuations in heart rate result from complex, non-linear interactions between a number of different physiological systems (Reyes Del Paso et al., 2013).

The interactions between autonomic neural activity, BP, and respiratory control systems produce short-term rhythms in HRV measurements (Hirsch and Bishop, 1981, 1996; McCraty et al., 2009) (Figure 6). The most common form for observing these changes is the heart rate tachogram, a plot of a sequence of time intervals between R waves. Efferent sympathetic and parasympathetic activity is integrated in and with the activity occurring in the heart’s intrinsic nervous system, including the afferent signals occurring from the mechanosensitive and chemosensory neurons, all of which contribute to beat-to-beat changes. HRV is thus considered a measure of neurocardiac function that reflects heart–brain interactions and ANS dynamics.

Figure 6. Display of short-term HRV activity. Credit: Institute of HeartMath.

Circadian rhythms, core body temperature, metabolism, hormones, and intrinsic rhythms generated by the heart all contribute to lower frequency rhythms [e.g., very-low-frequency (VLF) and ultra-low-frequency (ULF)] that extend below 0.04 Hz. Due to their long time periods, researchers use 24-h HRV recordings to provide comprehensive assessment of their fluctuations (Kleiger et al., 2005). In concert, these multiple influences create a dynamic physiological control system that is never truly at rest and is certainly never static. In healthy individuals, it remains responsive and resilient, primed and ready to react when needed.

How Is HRV Detected?

Clinicians use ECG or photoplethysmograph (PPG) sensors to detect the interbeat interval (IBI). While the ECG method had been considered to be more accurate than the PPG method because early software algorithms could more easily detect the sharp upward spike of the R wave than the curved peak of the blood volume pulse signal, newer algorithms have improved peak detection from the pulse wave. The ECG method should be used when recordings are contaminated by frequent abnormal beats (e.g., premature ventricular contractions), since the ECG’s morphology and timing properties allow software algorithms to discriminate normal sinus beats from ectopic beats (Mateo et al., 2011).

All HRV assessments are calculated from an IBI file. However, in some cases there can be differences in the IBI files derived from ECG and PPG data. Several studies have shown that when the recordings are taken during a resting state (sitting quietly as done in most resting baseline recordings), the IBI values between ECG and PPG are highly correlated (Giardino et al., 2002; Schafer and Vagedes, 2013). However, during ambulatory monitoring or when a person experiences a stressor strong enough to activate the sympathetic system, there can be significant differences due to changes in pulse transit time (the time it takes the BP wave to propagate from the heart to the periphery), which result from changes in the elasticity of the arteries. When arteries stiffen due to sympathetic activation, the BP wave travels faster. The accuracy of HRV measurements is primarily determined by the sampling rate of the data acquisition system. Kuusela (2013) recommends a sampling rate of 200 Hz unless overall variability among RR intervals is unusually low, as in case of heart failure. In contrast, Berntson et al. (2007) recommend a minimum sampling rate of 500–1000 Hz. However, for many applications, like HRV biofeedback (HRVB), a sampling rate of 126 Hz may be adequate.

There are many ECG configurations, with varying numbers of leads, used for ambulatory and stationary monitoring. For example, a standard three-lead ECG chest placement locates active and reference electrodes over the right and left coracoid processes, respectively, and a second active electrode over the xiphoid process (Figure 7).

Figure 7. ECG electrode placement. Credit: Truman State University Center for Applied Psychophysiology.

Why Is HRV Important?

An optimal level of variability within an organism’s key regulatory systems is critical to the inherent flexibility and adaptability or resilience that epitomizes healthy function and well-being. While too much instability is detrimental to efficient physiological functioning and energy utilization, too little variation indicates depletion or pathology.

HRV Is a Marker for Disease and Adaptability

The clinical importance of HRV was noted as far back as 1965 when it was found that fetal distress is preceded by alterations in HRV before any changes occur in heart rate itself (Hon and Lee, 1963). In the 1970s, HRV analysis was shown to predict autonomic neuropathy in diabetic patients before the onset of symptoms (Ewing et al., 1976). Low HRV has since been confirmed as a strong, independent predictor of future health problems and as a correlate of all-cause mortality (Tsuji et al., 1994; Dekker et al., 1997). Reduced HRV is also observed in patients with autonomic dysfunction, including anxiety, depression, asthma, and sudden infant death (Kazuma et al., 1997; Carney et al., 2001; Agelink et al., 2002; Giardino et al., 2004; Lehrer et al., 2004; Cohen and Benjamin, 2006).

Based on indirect evidence, reduced HRV may correlate with disease and mortality because it reflects reduced regulatory capacity, which is the ability to adaptively respond to challenges like exercise or stressors. For example, patients with low overall HRV demonstrated reduced cardiac regulatory capacity and an increased likelihood of prior myocardial infarction (MI). In this sample, a measure of cardiac autonomic balance did not predict previous MIs (Berntson et al., 2008).

Patient age may mediate the relationship between reduced HRV and regulatory capacity. HRV declines with age (Umetani et al., 1998) and aging often involves nervous system changes, like loss of neurons in the brain and spinal cord, which may degrade signal transmission (Jäncke et al., 2014) and reduce regulatory capacity.

Reduced regulatory capacity may contribute to functional gastrointestinal disorders, inflammation, and hypertension. While patients with functional gastrointestinal disorders often have reduced HRV (Gevirtz, 2013), HRVB has increased vagal tone and improved symptom ratings in these patients (Sowder et al., 2010).

The PNS may help regulate inflammatory responses via a cholinergic anti-inflammatory system (Tracey, 2007). While the experimental administration of lipopolysaccharide to healthy volunteers decreases HRV and vagal tone (Jan et al., 2009), HRVB training has reduced the symptoms produced by this intervention (Lehrer et al., 2010).

Hypertensive patients often present with reduced baroreflexes and HRV (Schroeder et al., 2003). HRVB can increase baroreflex gain, which is the amplitude of HR changes, and HRV, and decrease BP (Lehrer, 2013). Several randomized-controlled studies have documented BP reductions in hypertensive patients who received HRVB (Elliot et al., 2004; Reineke, 2008).

HRV is also an indicator of psychological resiliency and behavioral flexibility, reflecting the individual’s capacity to adapt effectively to changing social or environmental demands (Beauchaine, 2001; Berntson et al., 2008). More recently, several studies have shown an association between higher levels of resting HRV and performance on cognitive performance tasks requiring the use of executive functions (Thayer et al., 2009) and that HRV, especially HRV-coherence, can be increased in order to produce improvements in cognitive function as well as a wide range of clinical outcomes, including reduced health care costs (Lehrer et al., 2003, 2008; McCraty et al., 2003; Bedell and Kaszkin-Bettag, 2010; Alabdulgader, 2012).

HRV Analysis Methods

It was recognized as far back as 1979 that nomenclature, analytical methods, and definitions of HRV measures required standardization. Therefore, an International Task Force consisting of members from the European Society of Cardiology and the North American Society for Pacing and Electrophysiology was established. Their report was published in Task Force (1996).

HRV can be assessed with various analytical approaches, although the most commonly used are frequency domain or power spectral density (PSD) analysis and time domain analysis. In both methods, the time intervals between each successive normal QRS complex are first determined. All abnormal beats not generated by sinus node depolarizations are eliminated from the record.

Analogous to the EEG, we can use power spectral analysis to separate HRV into its component rhythms that operate within different frequency ranges (Figure 8). PSD analysis provides information of how power is distributed (the variance and amplitude of a given rhythm) as a function of frequency (the time period of a given rhythm). The main advantages of spectral analysis over the time domain measures are that it supplies both frequency and amplitude information about the specific rhythms that exist in the HRV waveform, providing a means to quantify the various oscillations over any given period in the HRV recording. The values are expressed as the PSD, which is the area under the curve (peak) in a given segment of the spectrum. The power or height of the peak at any given frequency indicates the amplitude and stability of the rhythm. The frequency reflects the period of time over which the rhythm occurs. For example, a 0.1 Hz frequency has a period of 10 s. In order to understand how power spectral analysis distinguishes the various underlying physiological mechanisms that are reflected in the heart’s rhythm, a brief review of these underlying physiological mechanisms follows.

Figure 8. This figure shows a typical HRV recording over a 15-min period during resting conditions in a healthy individual. The top trace shows the original HRV waveform. Filtering techniques were used to separate the original waveform into VLF, LF, and HF bands as shown in the lower traces. The bottom of the figure shows the power spectra (left) and the percentage of power (right) in each band. Credit: Institute of HeartMath.

Figure 8 shows a typical example of an HRV recoding from an adult human at rest. Using filtering techniques, the high-frequency (HF), low-frequency (LF), and VLF bands have been extracted from the original HRV signal and spectral power has been calculated for each band.

Sources of HRV

The Task Force report (1996) divided heart rhythm oscillations into four primary frequency bands. These included the HF, LF, VLF, and ULF bands. The Task Force report also stated that the analysis should be done on 5-min segments, although other recording periods are often used. When other recording lengths are analyzed and reported, the length of the recording should be reported since this has large effects on both HRV frequency and time domain values.

High-Frequency Band

The HF spectrum is the power in each of the 288 5-min segments (monitored during a 24-h period) in the range from 0.15 to 0.4 Hz. This band reflects parasympathetic or vagal activity and is frequently called the respiratory band because it corresponds to the HR variations related to the respiratory cycle. These HR changes are known as respiratory sinus arrhythmia (RSA). Heart rate accelerates during inspiration and slows during expiration. During inhalation, the cardiovascular center inhibits vagal outflow resulting in speeding the heart rate. Conversely, during exhalation, it restores vagal outflow resulting in slowing the heart rate via the release of acetylcholine (Eckberg and Eckberg, 1982). The magnitude of the oscillation is variable, but can usually be exaggerated by slow, deep breathing.

The modulation of vagal tone helps maintain the dynamic autonomic regulation important for cardiovascular health. Deficient vagal inhibition is implicated in increased morbidity (Thayer et al., 2010). The mechanism linking the variability of HR to respiration is complex and involves both central and reflex interactions. A large number of studies have shown that total vagal blockade essentially eliminates HF oscillations and reduces the power in the LF range (Pomeranz et al., 1985; Malliani et al., 1991).

Reduced parasympathetic (high frequency) activity has been found in a number of cardiac pathologies and in patients under stress or suffering from panic, anxiety, or worry. Lowered parasympathetic activity may primarily account for reduced HRV in aging (Umetani et al., 1998). In younger healthy individuals, it is not uncommon to see an obvious increase in the HF band at night with a decrease during the day (Lombardi et al., 1996; Otsuka et al., 1997).

Low-Frequency Band

The LF band ranges between 0.04 and 0.15 Hz. This region was previously called the “baroreceptor range” or “mid-frequency band” by many researchers, since it primarily reflects baroreceptor activity while at rest (Malliani, 1995). The vagus nerves are a major conduit though which afferent neurological signals from the heart and other visceral organs are relayed to the brain, including the baroreflex signals (De Lartique, 2014). Baroreceptors are stretch-sensitive mechanoreceptors located in the chambers of the heart and vena cavae, carotid sinuses (which contain the most sensitive mechanoreceptors), and the aortic arch (Figure 9). When BP rises, the carotid and aortic tissues are distended, resulting in increased stretch and, therefore, increased baroreceptor activation. At normal resting BPs, many baroreceptors actively report BP information and the baroreflex modulates autonomic activity.

Figure 9. Credit: Alila Sao Mai/Shutterstock.com.

Active baroreceptors generate action potentials (“spikes”) more frequently. The greater their stretch or detection of an increased rate of change, the more frequently baroreceptors fire action potentials. Baroreceptor action potentials are relayed to the NST in the medulla, which uses baroreceptor firing frequency to measure BP. Increased activation of the NST inhibits the vasomotor center and stimulates the vagal nuclei. The end-result of baroreceptor activations tuned to pressure increases is inhibition of the SNS and activation of the PNS. By coupling sympathetic inhibition with parasympathetic activation, the baroreflex maximizes BP reduction when BP is detected as too high. Sympathetic inhibition reduces peripheral resistance, while parasympathetic activation depresses HR (reflex bradycardia) and contractility. In a similar manner, sympathetic activation, along with inhibition of vagal outflow, allows the baroreflex to elevate BP. Baroreflex gain is commonly calculated as the beat-to-beat change in HR per unit of change in BP. Decreased baroreflex gain is related to impaired regulatory capacity and aging.

The existence of a cardiovascular system resonance frequency, which is caused by the delay in the feedback loops in the baroreflex system, has been long established (Vaschillo et al., 2011). Lehrer et al. have proposed that each individual’s cardiovascular system has a unique resonance frequency, which can be identified by measuring HRV while an individual breathes between 7.5 and 4.5 breaths per minute (Lehrer et al., 2013). When the cardiovascular system oscillates at this frequency, there is a distinctive high-amplitude peak in the HRV power spectrum around 0.1 Hz. Most mathematical models show that the resonance frequency of the human cardiovascular system is determined by the feedback loops between the heart and brain (deBoer et al., 1987; Baselli et al., 1994). In humans and many other mammals, the resonance frequency of the system is approximately 0.1 Hz, which is equivalent to a 10-s rhythm.

The sympathetic system does not appear to produce rhythms much above 0.1 Hz, while the parasympathetic system can be observed to affect heart rhythms down to 0.05 Hz (20-s rhythm). During periods of slow respiration rates, vagal activity can easily generate oscillations in the heart rhythms that cross over into the LF band (Ahmed et al., 1982; Tiller et al., 1996; Lehrer et al., 2003). Therefore, respiratory-related efferent vagally-mediated influences are particularly present in the LF band when respiration rates are below 8.5 breaths per minute or 7-s periods (Brown et al., 1993; Tiller et al., 1996) or when an individual sighs or takes a deep breath.

In ambulatory 24-h HRV recordings, it has been suggested that the LF band also reflects sympathetic activity and the LF/HF ratio has been controversially reported as an assessment of the balance between sympathetic and parasympathetic activity (Pagani et al., 1984, 1986). A number of researchers (Tiller et al., 1996; Eckberg, 1997; Porges, 2007; Rahman et al., 2011; Heathers, 2012) have challenged this perspective and have persuasively argued that in resting conditions, the LF band reflects baroreflex activity and not cardiac sympathetic innervation.

The perspective that the LF band reflects sympathetic activity came from observations of 24-h ambulatory recordings where there are frequent sympathetic activations primarily due to physical activity, but also due to emotional stress reactions, which can create oscillations in the heart rhythms that cross over into the lower part of the LF band. In long-term ambulatory recordings, the LF band fairly approximates sympathetic activity when increased sympathetic activity occurs (Axelrod et al., 1987). This will be discussed in more detail in the VLF section. Unfortunately, some authors have assumed that this interpretation was also true of short-term resting recordings and have confused slower breathing-related increases in LF power with sympathetic activity, when in reality it is almost entirely vagally mediated. Remember that the baroreflex is primarily vagally mediated (Keyl et al., 1985).

Porges (2007) suggests that under conditions when participants pace their breathing at 0.1 Hz (10-s rhythm or 6 breaths per minute), which is a component of many HRVB training protocols, the LF band includes the summed influence of both efferent vagal pathways (myelinated and unmyelinated, which reflects total cardiac vagal tone).

Autonomic Balance and the LF/HF Ratio

The autonomic balance hypothesis assumes that the SNS and PNS competitively regulate SA node firing, where increased SNS activity is paired with decreased PNS activity. While some orthostatic challenges can produce reciprocal changes in SNS activation and vagal withdrawal, psychological stressors can also result in independent changes in SNS or PNS activity. It is now generally accepted that both branches of the ANS can be simultaneously active (Berntson and Cacioppo, 1999). Therefore, the relationship between the SNS and PNS in generating LF power appears to be complex, non-linear, and dependent upon the experimental manipulation employed (Berntson et al., 1997; Billman, 2013).

The ratio of LF to HF power is called the LF/HF ratio. The interpretation of the LF/HF ratio is controversial due to the issues regarding the LF band described above. However, once the mechanisms are understood as well as the importance of the recording context (i.e., ambulatory vs. resting conditions and normal vs. paced breathing), the controversy is resolved. Recall that the power in the LF band can be influenced by vagal, sympathetic, and baroreflex mechanisms depending on the context, whereas HF power is produced by the efferent vagal activity due to respiratory activity. It is often assumed that a low LF/HF ratio reflects greater parasympathetic activity relative to sympathetic activity due to energy conservation and engaging in “tend-and-befriend” behaviors (Taylor, 2006). However, this ratio is often shifted due to reductions in LF power. Therefore, the LF/HR ratio should be interpreted with caution and the mean values of HF and LF power taken into consideration. In contrast, a high LF/HF ratio may indicate higher sympathetic activity relative to parasympathetic activity as can be observed when people engage in meeting a challenge that requires effort and increased SNS activation. Again, the same cautions must be taken into consideration, especially in short-term recordings.

Very-Low-Frequency Band

The VLF band is the power in the HRV power spectrum range between 0.0033 and 0.04 Hz. Although all 24-h clinical measures of HRV reflecting low HRV are linked with increased risk of adverse outcomes, the VLF band has stronger associations with all-cause mortality than the LF and HF bands (Tsuji et al., 1994, 1996; Hadase et al., 2004; Schmidt et al., 2005). Low VLF power has been shown to be associated with arrhythmic death (Bigger et al., 1992) and PTSD (Shah et al., 2013). Additionally, low power in this band has been associated with high inflammation in a number of studies (Carney et al., 2007; Lampert et al., 2008) and has been correlated with low levels of testosterone, while other biochemical markers, such as those mediated by the HPA axis (e.g., cortisol), did not (Theorell et al., 2007).

Historically, the physiological explanation and mechanisms involved in the generation of the VLF component have not been as well defined as the LF and HF components, and this region has been largely ignored. Long-term regulation mechanisms and ANS activity related to thermoregulation, the renin-angiotensin system, and other hormonal factors may contribute to this band (Akselrod et al., 1981; Cerutti et al., 1995; Claydon and Krassioukov, 2008). Recent work by Dr. Andrew Armour has shed new light on the mechanisms underlying the VLF rhythm and suggests that we may have to reconsider both the mechanisms and importance of this band.

Dr. Armour’s group has developed the technology to obtain long-term single-neuron recordings from a beating heart, and simultaneously, from extrinsic cardiac neurons (Armour, 2003). Figure 10 shows the VLF rhythm obtained from an afferent neuron located in the intrinsic cardiac nervous system in a dog heart. In this case, the VLF rhythm is generated from intrinsic sources and cannot be explained by sources such as movement. The black area in the bottom of the figure labeled “rapid ventricular pacing” shows the time period where efferent spinal neurons were stimulated. The resulting increase in efferent sympathetic activity (bottom row) clearly elevates the amplitude of the single afferent neuron’s intrinsic VLF rhythm (top row).

Figure 10. Long-term single-neuron recordings from an afferent neuron in the intrinsic cardiac nervous system in a beating dog heart. The top row shows neural activity, the second row, the actual neural recording, and the third row, the left ventricular pressure. This intrinsic rhythm has an average period of 90 s with a range between 75 and 100 s (0.013–0.01 Hz), which falls within the VLF band. Credit: Dr. Andrew Armour and the Institute of HeartMath.

This work, combined with findings by Kember et al. (2000, 2001), implies that the VLF rhythm is generated by the stimulation of afferent sensory neurons in the heart, which in turn activate various levels of the feedback and feed-forward loops in the heart’s intrinsic cardiac nervous system, as well as between the heart, the extrinsic cardiac ganglia, and spinal column. Thus, the VLF rhythm is produced by the heart itself and is an intrinsic rhythm that appears to be fundamental to health and well-being. Dr. Armour has observed that when the amplitude of the VLF rhythm at the neural level is diminished, an animal subject is in danger and will expire shortly if they proceed with the research procedures (personal communication with McCraty). Sympathetic blockade does not affect VLF power and VLF activity is seen in tetraplegics, whose SNS innervation of the heart and lungs is disrupted (Task Force, 1996; Berntson et al., 1997). These findings further support a cardiac origin of the VLF rhythm.

In healthy individuals, there is an increase in VLF power that occurs during the night and peaks before waking (Huikuri et al., 1994; Singh et al., 2003). This increase in autonomic activity may correlate with the morning cortisol peak.

In summary, experimental evidence suggests that the VLF rhythm is intrinsically generated by the heart and that the amplitude and frequency of these oscillations are modulated by efferent sympathetic activity. Normal VLF power appears to indicate healthy function, and increases in resting VLF power may reflect increased sympathetic activity. The modulation of the frequency of this rhythm due to physical activity (Bernardi et al., 1996), stress responses, and other factors that increase efferent sympathetic activation can cause it to cross over into the lower region of the LF band during ambulatory monitoring or during short-term recordings when there is a significant stressor.

Ultra-Low-Frequency Band

The ULF band falls below 0.0033 Hz (333 s or 5.6 min). Oscillations or events in the heart rhythm with a period of 5 min or greater are reflected in this band and it can only be assessed with 24-h and longer recordings (Kleiger et al., 2005). The circadian oscillation in heart rate is the primary source of the ULF power, although other very slow-acting regulatory processes, such as core body temperature regulation, metabolism, and the renin-angiotensin system likely add to the power in this band (Bonaduce et al., 1994; Task Force, 1996). Different psychiatric disorders show distinct circadian patterns in 24-h heart rates, particularly during sleep (Stampfer, 1998; Stampfer and Dimmitt, 2013).

The Task Force report (1996) stated that analysis of 24-h recordings should divide the record into 5-min segments and that HRV analysis should be performed on the individual segments prior to the calculation of mean values. This effectively filters out any oscillations with periods longer than 5 min. However, as shown in Figure 11, when spectral analysis is applied to entire 24-h records, several lower frequency rhythms are easily detected in healthy individuals. At the present time, the clinical relevance of these lower frequency rhythms is unknown, largely due to the Task Force guidelines that eliminate their presence from most analysis procedures.

Figure 11. This figure shows the power in the various frequency bands for 24-h HRV and 95% confidence intervals for each of the bands. The left side of the figure reveals a number of slower rhythms that make up the ULF band. The analysis was conducted using the healthy sample described in Umetani et al. (1998). The right side of the figure shows an analysis of the same data performed on 5-min segments as is traditionally done. Credit: Institute of HeartMath.

Time Domain Measurements of HRV

Time domain measures are the simplest to calculate and include the mean normal-to-normal (NN) intervals during the entire recording and other statistical measures such as the standard deviation between NN intervals (SDNN). However, time domain measures do not provide a means to adequately quantify autonomic dynamics or determine the rhythmic or oscillatory activity generated by the different physiological control systems. Since they are always calculated the same way, data collected by different researchers are comparable, but only if the recording lengths are exactly the same and the data are collected under the same conditions.

Time domain indices quantify the amount of variance in the IBI using statistical measures. For 24-h recordings, the three most important time domain measures are the SDNN, the SDNN index, and the RMSSD. For short-term assessments, the SDNN, RMSSD, pNN50, and HR Max – HR Min are most commonly reported.

SDNN

The SDNN is the standard deviation of the normal (NN) sinus-initiated IBI measured in milliseconds. This measure reflects the ebb and flow of all the factors that contribute to heart rate variability (HRV). In 24-h recordings, the SDNN is highly correlated with ULF and total power (Umetani et al., 1998). In short-term resting recordings, the primary source of the variation is parasympathetically-mediated RSA, especially with slow, paced breathing protocols.

SDNN values are highly correlated with the lower frequency rhythms discussed earlier (Table 1). Low age-adjusted values predict both morbidity and mortality. Classification within a higher SDNN category is associated with a higher probability of survival. For example, patients with moderate SDNN values, 50–100 ms, have a 400% lower risk of mortality than those with low values, 0–50 ms, in 24-h recordings (Kleiger et al., 1987).

Table 1. Correlations between time and frequency domain measures in 24-h recordings.

SDANN

The SDANN is the standard deviation of the average NN intervals (mean heart rate) for each of the 5-min segments during a 24-h recording. Like the SDNN, it is measured and reported in milliseconds. This index is correlated with the SDNN and is generally considered redundant.

SDNN Index

The SDNN index is the mean of the standard deviations of all the NN intervals for each 5-min segment of a 24-h HRV recording. Therefore, this measurement only estimates variability due to the factors affecting HRV within a 5-min period. It is calculated by first dividing the 24-h record into 288 5-min segments and then calculating the standard deviation of all NN intervals contained within each segment. The SDNN Index is the average of these 288 values. The SDNN index is believed to primarily measure autonomic influence on HRV. This measure tends to correlate with VLF power over a 24-h period.

RMSSD

The RMSSD is the root mean square of successive differences between normal heartbeats. This value is obtained by first calculating each successive time difference between heartbeats in milliseconds. Then, each of the values is squared and the result is averaged before the square root of the total is obtained. The RMSSD reflects the beat-to-beat variance in heart rate and is the primary time domain measure used to estimate the vagally-mediated changes reflected in HRV. While the RMSSD is correlated with HF power (Kleiger et al., 2005), the influence of respiration rate on this index is uncertain (Schipke et al., 1999; Pentillä et al., 2001). Lower RMSSD values are correlated with higher scores on a risk inventory of sudden unexplained death in epilepsy (DeGiorgio et al., 2010).

pNN50

The pNN50 is the percentage of adjacent NN intervals that differ from each other by more than 50 ms. It is correlated with the RMSSD and HF power. However, the RMSSD typically provides a better assessment of RSA (especially in older subjects) and most researchers prefer it to the pNN50 (Otzenberger et al., 1998).

HR Max – HR Min

HR Max – HR Min is the average difference between the highest and lowest HRs during each respiratory cycle. This measure is especially used for assessment in paced breathing protocols and is highly correlated with the SDNN and RMSSD.

Polyvagal Theory

As previously discussed, increased efferent activity in the vagal nerves (also called the 10th cranial nerve) slows the heart rate, yet has an opposite effect in the lungs as it increases bronchial tone. According to Porges’ (2011) polyvagal theory, the ANS must be considered a “system,” with the vagal nerves containing specialized subsystems that regulate competing adaptive responses. His theory proposes competing roles for the unmyelinated fibers in the vagus, which originate in the dorsal motor complex, and newer myelinated nerves, which originate in the nucleus ambiguus. He hypothesizes that the unmyelinated fibers are involved in regulating the “freeze response” and respond to threats through immobilization, feigning death, passive avoidance, and shutdown (the freeze response).

In Porges’ view, the evolution of the ANS was central to the development of emotional experience and affective processes central to social behavior. As human beings, we are not limited to fight, flight, or freezing behavioral responses. We can self-regulate and initiate pro-social behaviors (e.g., the tend-and-befriend response) when we encounter stressors. Porges calls this the social engagement system and the theory suggests that this system depends upon the healthy functioning of the myelinated vagus, a vagal brake, which allows for self-regulation and ability to calm ourselves and inhibit sympathetic outflow to the heart. This implies that standardized assessment of vagal tone could serve as a potential marker for one’s ability to self-regulate.

The theory suggests that the evolution and healthy function of the ANS sets the limits or boundaries for the range of one’s emotional expression, quality of communication, and ability to self-regulate emotions and behaviors. The theory describes the details of the anatomical connections from higher brain structures with the centers involved in autonomic regulation and argues that the afferent systems are an important aspect of the ANS. The theory provides insights into the adaptive nature of physiological states and suggests these states support different types or classes of behavior (Porges, 2011).

The SNS, in concert with the endocrine system, responds to threats to our safety through mobilization, fight-or-flight, and active avoidance. The SNS responds more slowly and for a longer period of time (i.e., more than a few seconds) than the vagus system. According to this theory, quality communication and pro-social behaviors can only be effectively engaged when these defensive circuits are inhibited.

Neurovisceral Integration: The Central Autonomic Network Model

Thayer and Lane (2000) outline a neurovisceral integration model that describes how a set of neural structures involved in cognitive, affective, and autonomic regulation are related to HRV and cognitive performance. In this complex systems model, the anatomical details of a central autonomic network (CAN) are described that link the NST in the brainstem with forebrain structures (including the anterior cingulate, insula, ventromedial prefrontal cortex, amygdala, and hypothalamus) through feedback and feed-forward loops. They propose that this network is an integrated system for internal system regulation by which the brain controls visceromotor, neuroendocrine, and behavioral responses that are critical for goal-directed behavior, adaptability, and health.

Thayer et al. (2012) contend that dynamic connections between the amygdala and medial prefrontal cortex, which evaluate threat and safety, help regulate HRV through their connections with the NST. They propose that vagally-mediated HRV is linked to higher-level executive functions and that HRV reflects the functional capacity of the brain structures that support working memory and emotional and physiological self-regulation. They hypothesize that vagally-mediated HRV is positively correlated with prefrontal cortical performance and the ability to inhibit unwanted memories and intrusive thoughts. In their model, when the CAN decreases prefrontal cortical activation, HR increases and HRV decreases. The prefrontal cortex can be taken “offline” when individuals perceive that they are threatened. Prolonged prefrontal cortical inactivity can lead to hypervigilance, defensiveness, and social isolation (Thayer et al., 2009).

The CAN model predicts reduced HRV and vagal activity in anxiety. Friedman (2007) argues that anxiety is associated with abnormal ANS cardiac control. HRV indices consistently show low vagal activity in patients diagnosed with anxiety disorders. This finding challenges the completeness of the sympathetic overactivation explanation of anxiety. Friedman observes that “metaphorically, investigators were searching for a ‘sticky accelerator’ while overlooking the possibility of ‘bad brakes’” (p. 186). From his perspective, anxiety disorders can involve varying degrees of sympathetic overactivation and parasympathetic underactivation.

The Psychophysiological Coherence Model

McCraty and Childre (2010) at the Institute of HeartMath also take a dynamic systems approach that focuses on increasing individuals’ self-regulatory capacity by inducing a physiological shift that is reflected in the heart’s rhythms. They theorize that rhythmic activity in living systems reflects the regulation of interconnected biological, social, and environmental networks. The coherence model also suggests that information is encoded in the dynamic patterns of physiological activity. For example, information is encoded in the time interval between action potentials and patterns in the pulsatile release of hormones. They suggest that the time intervals between heartbeats (HRV) also encode information which is communicated across multiple systems, which helps synchronize the system as whole. The afferent pathways from the heart and cardiovascular system are given more relevance in this model due the significant degree of afferent cardiovascular input to the brain and the consistent generation of dynamic patterns generated by the heart. It is their thesis that positive emotion in general, as well as self-induced positive emotions, shift the system as a whole into a more globally coherent and harmonious physiological mode associated with improved system performance, ability to self-regulate, and overall well-being.

They use the term “physiological coherence” to describe the orderly and stable rhythms generated by living systems. Physiological coherence is used broadly and includes all of the specific approaches for quantifying the various types of coherence measures, such as cross-coherence (frequency entrainment between respiration, BP, and heart rhythms), or synchronization among systems (e.g., synchronization between various EEG rhythms and the cardiac cycle), auto-coherence (stability of a single waveform such as respiration or HRV patterns), and system resonance.

“A coherent heart rhythm is defined as a relatively harmonic (sine-wave-like) signal with a very narrow, high-amplitude peak in the LF region of the HRV power spectrum with no major peaks in the VLF or HF regions. Coherence is assessed by identifying the maximum peak in the 0.04–0.26 Hz range of the HRV power spectrum, calculating the integral in a window 0.030 Hz wide, centered on the highest peak in that region, and then calculating the total power of the entire spectrum. The coherence ratio is formulated as: (Peak Power/[Total Power – Peak Power])” (14).

The Heart Rhythm Coherence Hypothesis

As discussed above, neurocardiology research has established that heart-brain interactions are remarkably complex. Patterns of baroreceptor afferent activity modulate CNS activity over time periods that range from milliseconds to minutes; that is, not only within a cardiac cycle (Armour and Kember, 2004). The intrinsic cardiac ganglia demonstrate both short- and long-term memory. This affects afferent activity rhythms produced by both mechanical variables (e.g., pressure and HR) that occur over milliseconds (single cycles) and hormonal variables that fluctuate over periods ranging from seconds to minutes (Armour, 2003; Armour and Kember, 2004; Ardell et al., 2009). McCraty proposed the heart rhythm coherence hypothesis which states that the pattern and stability of beat-to-beat heart rate activity encode information over “macroscopic time scales,” which can impact cognitive performance and emotional experience. For a more detailed discussion, see McCraty et al. (2009).

Increasing Vagal Afferent Traffic

Mechanosensitive neurons (baroreceptors) typically increase their firing rates when the rate of change in the function to which they are tuned increases. Heart rhythm coherence, which is characterized by increased beat-to-beat variability and the rate of heart rate change, increases vagal afferent traffic from the cardiovascular system to the brain. This perspective is supported by the MacKinnon et al. (2013) HEP study, discussed earlier, which showed that resonance frequency breathing increased the amount of HRV, HRV coherence, and N250 amplitude in the HEPs. The authors speculated that resonance frequency breathing may have increased vagal afferent traffic and reduced interference with its transmission through subcortical areas to the cerebral cortex.

There has been increasing interest in treating a wide range of disorders with implanted pacemaker-like devices for stimulating the vagal afferent pathways. The FDA has approved these devices for the treatment of epilepsy and depression, and they have been investigated in treating obesity, anxiety, and Alzheimer’s disease (Kosel and Schlaepfer, 2003; Groves and Brown, 2005). Neuroradiology research has established that increases in tonic vagal afferent traffic inhibit thalamic pain pathways traveling from the body to the brain at the level of the spinal cord. This finding may explain why studies have shown vagal afferent stimulation can reduce cluster and migraine headaches (Mauskop, 2005) and HRV coherence training reduces chronic pain (Berry et al., 2014).

Resonance Frequency Breathing

Lehrer et al.’s resonance frequency model proposes that the delay in the baroreflex system’s feedback loops creates each individual’s unique cardiovascular system resonance frequency (Lehrer, 2013). While their theoretical model assumes that taller individuals and men have lower resonance frequencies than women and shorter individuals due to the former’s larger blood volumes, height only accounts for 30% of the variance in resonance frequency. Breathing, rhythmic muscle tension, and emotional stimulation at a person’s resonance frequency can activate or stimulate the cardiovascular system’s resonance properties (Lehrer et al., 2009).

They suggest that when people breathe at this rate, which varies in adults from 4.5 to 6.5 breaths per minute, they “exercise” the baroreflex. They have shown that during this paced period, HR and BP oscillations are 180° out of phase, and HRV amplitude is maximized (deBoer et al., 1987; Vaschillo et al., 2002). They also suggest that this phase relationship between HR, respiration, and BP results in the most efficient gas exchange and oxygen saturation (Bernardi et al., 2001; Vaschillo et al., 2004; Yasuma and Hayano, 2004).

With practice, people can learn to breathe at their cardiovascular system’s resonance frequency. This aligns the three oscillators (baroreflex, HR, and BP) at that frequency and moves the peak frequency from the HF range (≈0.2 Hz) to the LF range (≈0.1 Hz). Breathing at the resonance frequency more than doubles the energy in the LF band (0.04–0.15 Hz). This corresponds to the Institute of HeartMath’s heart rhythm coherence, which is associated with a “narrow, high-amplitude, easily visualized peak” from 0.09 to 0.14 Hz (McCraty et al., 2009; Ginsberg et al., 2010, p. 54).

Resonance frequency breathing is typically used in the context of HRVB training. Several months of steady practice can reset the baroreflex gain so that it is sustained, even when clients are not receiving feedback (Lehrer et al., 2003; Lehrer, 2013). Increased baroreflex gain is analogous to a more sensitive thermostat, allowing the body to regulate BP and gas exchange more effectively (Lehrer, 2007).

An Integrative Perspective

There has been a paradigm shift in the medical treatment of diverse disorders like depression, epilepsy, and pain using vagal nerve stimulation (Kosel and Schlaepfer, 2003; Groves and Brown, 2005; Mauskop, 2005). Instead of exclusively targeting sympathetic activation, physicians also attempt to increase vagal tone. Behavioral interventions like HRVB and emotional self-regulation strategies represent non-invasive methods of restoring homeostasis.

HRVB exercises the baroreceptor reflex to enhance homeostatic regulation. Both the heart rhythm coherence and resonance frequency approaches to HRVB teach clients to produce auto-coherent (sinusoidal) heart rhythms with a single peak in the LF region and no significant peaks in the VLF and HF regions (McCraty and Childre, 2010; Lehrer et al., 2013). The coherence model and HEP research (MacKinnon et al., 2013) predict that increased HRV will increase vagal afferent transmission to the forebrain, activate the prefrontal cortex, and improve executive function.

Emotional self-regulation strategies (Forman et al., 2007; McCraty and Atkinson, 2012) can contribute to improved client health and performance, alone, or in combination with HRVB training. McCraty theorizes that emotional self-regulation can increase resilience and accelerate recovery from stressors. From Porges’ (2011) perspective, self-regulation through social engagement and bonding can reduce SNS activation while increasing HRV. The CAN model (Thayer et al., 2012) predicts that perception of safety will reduce the activation of the amygdala and increase the prefrontal cortex’s ability to exercise top-down control of emotional responses. Finally, from a heart rhythm coherence perspective, emotional self-regulation reduces the SNS activation and/or vagal withdrawal that increase short-term VLF power (Bernardi et al., 1996), decrease shorter-term LF power, and disrupt heart rhythm coherence.

Summary

The SA node normally generates the heartbeat, which is modulated by autonomic efferent neurons and circulating hormones. There is a dynamic balance between sympathetic and parasympathetic nervous outflows in a healthy, resilient, and responsive nervous system. HRV is generated by multiple regulatory mechanisms that operate on different time scales. Recent findings demonstrate the importance of the intrinsic cardiac nervous system and cardiac afferents in generating the heart rhythm and modulating the time interval between heartbeats. Vagally-mediated HRV appears to represent an index of self-regulatory control, such that individuals with greater resting HRV perform better on tests of executive functions.

Since the LF band primarily reflects the vagally-mediated transmission between the heart and the central nervous system in the context of short-term BP regulation, resting measurements should not be used as markers of SNS activity. Based on 24-h monitoring, ULF and VLF rhythms are more strongly associated with overall health status than HF rhythms. When age-adjusted values are low, they are also more strongly associated with future health risk and all-cause mortality.

HRVB exercises the baroreceptor reflex to enhance homeostatic regulation and restore regulatory capacity. Both the heart rhythm coherence and resonance frequency approaches to HRVB train clients to produce auto-coherent heart rhythms with a single peak in the LF region (typically around 0.1 Hz) and no significant peaks in the VLF and HF regions. Emotional self-regulation strategies can contribute to improved client health and performance, alone, or in combination with HRVB training. A coherent heart is not a metronome since its rhythms are characterized by dynamic complexity with stability over longer time scales.

Conflict of Interest Statement

Neither Dr. Fred Shaffer nor Mr. Christopher L. Zerr have any relevant affiliation or financial involvement with any organization or entity with a financial interest or financial conflict with the subject matter discussed in the manuscript. Dr. Rollin McCraty is the Chief Scientist for the Institute of HeartMath, which has generously contributed several of the graphics used in this manuscript.

Acknowledgments

The authors want to express their profound thanks to Mike Atkinson, Richard Gevirtz, Paul Lehrer, Donald Moss, and John Venner for their generous contributions to this article.

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What is Cardiovascular Disease? | American Heart Association

Cardiovascular disease can refer to a number of conditions:

Heart disease

Heart and blood vessel disease (also called heart disease) includes numerous problems, many of which are related to a process called atherosclerosis.

Atherosclerosis is a condition that develops when a substance called plaque builds up in the walls of the arteries. This buildup narrows the arteries, making it harder for blood to flow through. If a blood clot forms, it can block the blood flow. This can cause a heart attack or stroke.

Heart attack

A heart attack occurs when the blood flow to a part of the heart is blocked by a blood clot. If this clot cuts off the blood flow completely, the part of the heart muscle supplied by that artery begins to die.

Most people survive their first heart attack and return to their normal lives, enjoying many more years of productive activity. But experiencing a heart attack does mean that you need to make some changes.

The medications and lifestyle changes that your doctor recommends may vary according to how badly your heart was damaged, and to what degree of heart disease caused the heart attack.

Learn more about heart attack.

Stroke

An ischemic stroke (the most common type of stroke) occurs when a blood vessel that feeds the brain gets blocked, usually from a blood clot.

When the blood supply to a part of the brain is cut off, some brain cells will begin to die. This can result in the loss of functions controlled by that part of the brain, such as walking or talking.

A hemorrhagic stroke occurs when a blood vessel within the brain bursts. This is most often caused by uncontrolled hypertension (high blood pressure).

Some effects of stroke are permanent if too many brain cells die after being starved of oxygen. These cells are never replaced.

The good news is that sometimes brain cells don’t die during stroke — instead, the damage is temporary. Over time, as injured cells repair themselves, previously impaired function improves. (In other cases, undamaged brain cells nearby may take over for the areas of the brain that were injured.)

Either way, strength may return, speech may get better and memory may improve. This recovery process is what stroke rehabilitation is all about.

Learn more about stroke. 

Heart failure

Heart failure, sometimes called congestive heart failure, means the heart isn’t pumping blood as well as it should.
Heart failure does not mean that the heart stops beating — that’s a common misperception. Instead, the heart keeps working, but the body’s need for blood and oxygen isn’t being met.

Heart failure can get worse if left untreated. If your loved one has heart failure, it’s very important to follow the doctor’s orders.

Learn more about heart failure.

Arrhythmia

Arrhythmia refers to an abnormal heart rhythm. There are various types of arrhythmias. The heart can beat too slow, too fast or irregularly.

Bradycardia, or a heart rate that’s too slow, is when the heart rate is less than 60 beats per minute. Tachycardia, or a heart rate that’s too fast, refers to a heart rate of more than 100 beats per minute.

An arrhythmia can affect how well your heart works. With an irregular heartbeat, your heart may not be able to pump enough blood to meet your body’s needs.

Learn more about arrhythmia.

Heart valve problems

When heart valves don’t open enough to allow the blood to flow through as it should, a condition called stenosis results. When the heart valves don’t close properly and thus allow blood to leak through, it’s called regurgitation.
If the valve leaflets bulge or prolapse back into the upper chamber, it’s a condition called prolapse. Discover more about the roles your heart valves play in healthy circulation.

Learn more about heart valve disease.

Common treatments

Here are some common treatments for different types of cardiovascular disease:

Heart Valve Problems

Arrhythmia

Heart Attack

Stroke

Diagnostic tests, surgical procedures and medications

In the hospital and during the first few weeks at home, the doctor may perform several tests and procedures. These tests help the doctor determine what caused the stroke or heart attack, and how much damage was done. Some tests monitor progress to see if treatment is working.

Learn more about diagnostic tests and procedures.

Learn more about surgical procedures that may have been performed at the hospital.

Cardiac medications

The medications prescribed in the wake of a cardiac event can aid in recovery and work to prevent another stroke or heart attack.

If you’re a caregiver, make it your responsibility to help your loved one take medications as directed and on time. Educate yourself about the medications that your loved one must take. Know what those medicines do, and what their goal is.

It’s important to follow your doctor’s directions closely, so ask questions and take notes.
Learn more about cardiac medications.

90,000 The structure of the human heart and features of its work. Get your heart examined at MEDSI

The human heart is located in the chest, approximately in the center with a slight shift to the left. It is a hollow muscular organ. Outside it is surrounded by a membrane – the pericardium (pericardial sac). There is fluid between the heart and the pericardial sac, which moisturizes the heart and reduces friction during its contractions.

The heart is divided into four chambers: two right – right atrium and right ventricle, and two left – left atrium and left ventricle.Normally, the right and left halves of the heart do not communicate with each other. With congenital defects in the atrial and interventricular septa, holes may remain through which blood flows from one half of the heart to the other. The atria and ventricles are connected by holes.

At the edges of the holes are the leaflet heart valves: on the right – tricuspid, on the left – bicuspid, or mitral. The bicuspid and tricuspid valves provide blood flow in one direction – from the atria to the ventricles.There are also valves between the left ventricle and the aorta extending from it, as well as between the right ventricle and the pulmonary artery extending from it. Because of the shape of the valves, they are called crescent. Each semilunar valve consists of three leaflets that resemble pockets. The free edge of the pockets is turned into the lumen of the vessels. The semilunar valves provide blood flow in only one direction – from the ventricles to the aorta and pulmonary artery.

The work of the heart includes two phases: contraction (systole) and relaxation (diastole).The cardiac cycle consists of atrial contraction, ventricular contraction, and subsequent relaxation of the atria and ventricles. The contraction of the atria lasts 0.1 sec, the contraction of the ventricles – 0.3 sec.

• During diastole: the left atrium fills with blood, blood flows through the mitral opening into the left ventricle, during the contraction of the left ventricle, blood is pushed out through the aortic valve, enters the aorta and spreads to all organs.In the organs, oxygen is transferred to the tissues of the body for their nutrition. Further, the blood is collected through the veins into the right atrium, through the tricuspid valve it enters the right ventricle.

• During ventricular systole: venous blood is pushed into the pulmonary artery and into the vessels of the lungs. In the lungs, the blood is oxygenated, that is, it is saturated with oxygen. Oxygenated blood is collected through the pulmonary veins into the left atrium.

The rhythmic, constant alternation of the phases of systole and diastole, necessary for normal operation, is ensured by the emergence and conduction of an electrical impulse through the system of special cells – through the nodes and fibers of the cardiac conduction system. Impulses appear first in the uppermost, so-called, sinus node, which is located in the right atrium, then pass to the second, atrioventricular node, and from it – along thinner fibers (legs of the His bundle) – to the muscle of the right and left ventricles, causing contraction of all their muscles.

The heart itself, like any other organ, requires oxygen for nutrition and normal activity. It is delivered to the heart muscle through its own vessels of the heart – the coronary. These arteries are sometimes called coronary arteries.

The coronary vessels extend from the base of the aorta. They are divided into the right coronary artery and the left coronary artery. The left coronary artery, in turn, divides into the anterior interventricular and circumflex arteries. The right coronary artery supplies the walls of the right atrium and ventricle, the posterior part of the interventricular septum and the posterior wall of the left ventricle, the sinus and atrioventricular nodes.The left coronary artery supplies blood to the anterior part of the interventricular septum, the anterior and lateral walls of the left ventricle, and the left atrium.

Normal heart rate ranges from 55 to 85 bpm. Under load, the frequency increases naturally. You can determine the heart rate by the pulse.

Pulse is the vibration of the arterial wall that occurs with each contraction of the heart.

The movement of blood through the vessels depends on the pressure created by the heart at the moment of ejection of blood and the resistance of the walls of the vessels to the blood flow.The pressure in the aorta at the time of contraction of the ventricles of the heart is maximum, and is called systolic. During relaxation, a residual pressure remains in the left ventricle, which is called diastolic pressure. The blood pressure is influenced by the lumen of the blood vessels, the viscosity of the blood, and the amount of blood circulating in the vessels. As you move away from the heart, blood pressure decreases and becomes lowest in the veins. The difference between high blood pressure in the aorta and low pressure in the vena cava ensures a continuous flow of blood through the vessels.

Athlete’s heart / For a healthy lifestyle! / Articles / Center for Contemporary Cardiology

A beautiful young girl is looking at us from the photo. This is 21-year-old biathlete Alina Yakimkina. In February 2015, she died on the track of a 15-kilometer individual race, not reaching the finish line quite a bit …
Alexey Cherepanov, Sergey Grinkov, Sergey Zholtok, Konstantin Eremenko, Bruno Pezzai – this is just the beginning of a huge mournful list of young athletes who died during competition or training. “Center for Contemporary Cardiology” has already raised this topic. The famous Krasnoyarsk cardiologist Konstantin Zlodeev in an interview with the newspaper “Gorodskie Novosti” tells in detail what processes occur in the heart of an athlete during training and competition.

An athlete’s heart

“How does an athlete’s heart differ from the heart of an ordinary person? – a reader contacted us with this question in connection with her concern for the health of her son.The child spends almost all his free time in the gym. At the physical examination, the doctor said that there are some changes in the heart, but they are explained by sports loads and do not pose a danger. Is it so”?

We should start with the question: what is a “sports heart” anyway? This term includes structural and functional changes in the heart that occur during prolonged, intense physical exertion. They started talking about this issue a long time ago (the term itself was introduced at the end of the 19th century by the German doctor S.Henshen) and are actively researching it ever since.

– Sport is hard physical work, which has certain costs, – explains Konstantin Zlodeev. Konstantin, cardiologist of the highest qualification category, member of the European and All-Russian Scientific Society of Cardiology. – In addition to the heart, many organs and tissues in the body can wear out – most often joints, cartilage, spine. In humans, a “sports heart” occurs when loads that exceed submaximal.

According to the cardiologist, it is quite simple to identify the number of submaximal loads – it is calculated by age and heart rate: age must be subtracted from 220; normal under load – the pulse should not exceed 80% of the resulting value. This load does not cause structural changes in the cardiovascular system. Loads falling under this threshold are beneficial for the body. Anything more leads to changes in the heart.

“The sports heart has two phases: adaptive and maladaptive,” notes Konstantin Valentinovich . – The adaptive phase does not carry any pathological changes, it is completely reversible: if the loads stop, the state of the heart approaches the heart of an ordinary person. The changes that occur in the adaptive phase are more compensating. They do not harm, but on the contrary strengthen the heart. Long-term loads cause thickening of the walls of the heart, the so-called hypertrophy, as well as bradycardia – a decrease in the heart rate. In the first phase, they do not manifest themselves clinically – there are no complaints: the athlete feels good, calmly takes new levels of physical activity, and gives a wonderful result.Such adaptive loads are not dangerous – this is a variant of the norm that does not require any treatment.

The first phase can only be identified by additional studies – electrocardiography, ultrasound. Nevertheless, if such changes are identified, this is the first signal that you need to monitor the heart, try to adjust the training regimen, their frequency, intensity, and rest periods. If you monitor this carefully, the changes will remain at a useful level and will not progress.

– The maladaptive, second phase, is already associated with pathological changes, – continues Konstantin Zlodeev. – Treatment is needed here, the cessation of intense exertion. And then, after that, it is no longer possible to return the heart to a completely normal state. The transition to the maladaptive phase is more typical for professional sports, where the athlete, knowing what is at stake, goes to these costs. But the heart is a muscle, unlike the biceps, it cannot grow indefinitely. With exhausting, prolonged loads, the heart begins to stretch: not only the walls, but also the chambers of the heart (this is called dilatation) increase.Which can lead to heart failure, and, in extreme cases, to arrhythmic death. Arrhythmic death – clinical death, arises from pronounced hypertrophy in the myocardium, pathological foci of arrhythmia – all kinds of serious failures in the heart. Because of this, defibrillators are required at all sporting events.

According to the doctor, in order to track the transition, you need to undergo constant examinations and testing. Even if nothing bothers, the athlete should come for examination once a year.Many drugs are being produced today to help prevent the transition to the second phase. Sports medicine is very developed, but consultation with a specialist is necessary.

– When you stop intensive training, – says Konstantin Valentinovich, – the athlete quickly gains weight, and muscle tissue turns into adipose tissue. If the “sports heart” has passed into the second phase, this does not mean that you need to lie down and lie down, you just need to remove the outrageous loads and move on to dynamic, light ones: running and swimming.Even for athletes with heart failure, we still recommend moderate exercise in order to maintain their cardiovascular system.

The specialist advises to pay attention to the following signs visible to the naked eye that indicate danger: a sharp decrease in resistance to stress, shortness of breath, edema, increased heartbeat on those loads that were previously well tolerated. With increasing loads, these signs are a reason to adjust training. With these symptoms, it is imperative to seek medical attention.

Alexander Mazurov

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World Heart Day 2020

World Heart Day has been held since 2000 at the initiative of the World Heart Federation with the support of the World Health Organization (WHO). Until 2011, this event was celebrated on the last Sunday in September. Since 2011, World Heart Day has been celebrated annually on September 29th. The date was supported by UNESCO, WHO, Heart Federation and other international companies.In 2020, World Heart Day is held under the motto “Heart for Life”, the meaning of which boils down to the importance of maintaining a healthy heart for the life of any person.

The purpose of the events held on this day is to promote preventive measures to reduce mortality from heart disease, raise awareness of the population about the problems of heart disease, the correct lifestyle to prevent them, and draw people’s attention to their health as much as possible. The mission is not only to identify the problem, but also to help the population solve it.Since in the world today, cardiovascular diseases remain the leader among the causes of death.

More than 17 million people die of heart disease every year. WHO expects this number to exceed 23 million by 2030. Stroke and coronary heart disease (CHD) are the leading causes of death in patients worldwide, accounting for 31% of all deaths (according to WHO). In Russia, alas, this percentage is higher – 57%. According to the WHO, 80% of deaths from heart attacks and strokes can be prevented by controlling unhealthy diet, tobacco smoking, alcohol abuse, sleep quality and increased physical activity.

The main risk factors for the development of cardiovascular diseases are arterial hypertension, high levels of total blood cholesterol and its fractions, overweight, physical inactivity, tobacco smoking and stress. If you adhere to a healthy lifestyle, engage in simple walks, avoid smoking (including passive smoking), limit alcohol consumption, balance your diet, increase useful exercise, monitor blood pressure and improve your health, then it is quite possible to avoid strokes, heart attacks, ischemic heart disease and many heart and cardiovascular diseases.

It is necessary to follow the recommendations:

• Stop smoking.
• Limit consumption of table salt to 6 g per day. Do not keep the salt shaker on the table, try to cook food without salt, eat fresh vegetables and fruits, refuse canned or salty foods.
• Normalize body weight. Each extra kilogram is accompanied by an increase in blood pressure by 2 mm Hg. Art. It is important to normalize body weight, which is judged by the value of the body mass index, which should be less than 25.Body mass index is determined by the formula: body weight (kg) divided by height, expressed in meters and squared (m2).
• Reduce the consumption of fatty and sweet foods (cookies, sweets, chocolate, ice cream). The calorie content of the daily diet should correspond to the energy consumption of the body. The average energy requirement for women is 1500-1800 kcal per day, for men – 1800-2100 kcal per day.
• Food should be steamed, boiled or baked.When cooking, you need to use vegetable fats (olive, sunflower, corn oil). The most acceptable is the so-called “Mediterranean diet” with sea fish and an abundance of vegetables and fruits.
• Exercise daily for at least 30 minutes. It is important to exercise regularly, at least 5 days a week (walking and swimming are optimal).
• It is necessary to control the level of blood pressure. Make sure that the blood pressure is not higher than 140/90 mm Hg.Art.
• Check blood cholesterol (lipid) levels periodically. The desired total cholesterol concentration is less than 200 mg / dL (5 mmol / L), with the correct balance of its constituents.
• Check your blood glucose (blood sugar) level periodically. Fasting glucose levels in the morning should be less than 100 mg / L (5.5 mmol / L).
• Learn to control stress. Chronic lack of sleep, as well as constant psychological stress, weaken the immune system, exhaust a person, cause arrhythmias and cardiac disorders in general.

Lifestyle change activities are talked about a lot, but they are rarely performed. This is psychologically difficult. Now it is fashionable to lead a healthy lifestyle! It’s never too late to change your lifestyle and diet if your health is dear to you, because the heart is the trigger. After the onset of signs of coronary heart disease, risk factors contribute to the progression of the development of the disease, therefore, one of the stages of treatment is the correction of risk factors.

On the eve of the World Heart Day, the “Heart Days” action will also be held at the Bryansk Regional Cardiological Dispensary.Measures are aimed at reducing the growth of cardiovascular diseases, preventing their complications and reducing deaths. It is necessary to convey to the consciousness of the population what danger is fraught with pathologies of the heart and blood vessels, which are acquiring the character of an epidemic. If earlier ischemic stroke and heart attack were a disease of the elderly, today young people are at risk.

Heart block

From early childhood, we are taught to take care of the heart, because the heart is the most important organ in the human body.But, unfortunately, the modern lifestyle, unhealthy diet, stressful situations at work and at home lead to heart problems.

The list of heart diseases is long, but this article will focus on heart blockages. This disease is a partial or complete loss of the ability of any part of the myocardium (cardiac muscle layer) to conduct an electrical impulse. Violation of conduction can be transient or permanent, complete and incomplete. The blockade can occur in any part of the heart.It is customary to distinguish between blockade 1, 2 and 3 degrees.

Etiology

To heart block various disorders of the tissues of the heart muscle layer result from angina pectoris, myocardial infarction, weakness of the sinus node, myocarditis, ischemic heart disease, arterial hypertension, cardiosclerosis. Heart block is also formed during high physical exertion on the heart muscle (for example, in athletes). The danger is also the excess of the dose or the use of certain drugs (cardiac glycosides, antiarrhythmics).The occurrence of blockages may be associated with a genetic predisposition.

Symptoms

With 1st degree heart block, electrical impulses pass, but very weakly. No symptoms are observed. Blockade of the 1st degree, as a rule, is detected in the diagnosis of other cardiological diseases. If measures are not taken in time, then the 1st degree of heart block can go to the 2nd.

With blockade of the 2nd degree, some of the impulses do not enter the ventricles at all.In this case, dizziness, weakness, pain in the chest area may be observed. The pressure may be low, and the pulse may be irregular.

3rd degree heart block – these are cases when impulses are not carried out at all. The disease manifests itself in the form of general fatigue, lethargy, drowsiness, shortness of breath, nausea, vomiting, chest pain. With a 3rd degree heart block, instant death is possible. The appearance of seizures indicates the presence of the so-called Morgan-Adams-Stokes syndrome. This syndrome is very often the cause of death.

If you find at least one or more of the above symptoms, then immediately consult a doctor! Measures taken in time can save your life. Even if you feel great, you should have a regular check-up with a cardiologist on a regular basis. Since many diseases, including 1st degree heart block, can be completely asymptomatic.

Diagnostics

A conventional electrocardiogram is used to diagnose 2nd degree heart block.To detect blockade of the 1st and 3rd degree, Holter monitoring (ECG over a long period of time) and treadmill test (ECG recording during physical exertion) are used. Echocardiography may be required for a more accurate diagnosis.

All of the above diagnostic methods are used at the Cardiological Center for Diagnostics and NLS-Treatment. Our center has the latest equipment required to detect any cardiovascular disease.But, as you know, medicine does not stand still, and we try to keep up with it. The specialists of the cardiological center widely practice the modern method of diagnostics and treatment – NLS-graphy.

NLS-graphy is the last word in science. This technique makes it possible to diagnose a particular disease as accurately as possible. NLS research methods have a positive effect on the results of surgical treatment. The use of a new diagnostic method reduces or completely eliminates the X-ray exposure of the patient.

Treatment

Blockade of the 1st degree is not cured in any way. She, as a rule, indicates any concomitant cardiac disease, by curing which, you can get rid of the blockade.

It is possible to overcome the blockade of the 2nd and 3rd degree thanks to correctly selected drug treatment. It is important to remember that some medicines used in the treatment of heart disease can lead to complications if the dosage is incorrect.

The “Cardiological Center for Diagnostics and NLS Treatment” employs highly qualified specialists who, thanks to their extensive medical experience, can accurately diagnose any heart disease.Our experts will select for you a comprehensive treatment that will improve your health in a short time.

Choosing the “Cardiological center for diagnostics and NLS treatment”, you will make the right choice.

90,000 Straight to the heart. Cardiologist on the consequences of the coronavirus | HEALTH: Medicine | HEALTH

It is already known that COVID-19 hits various human organs and systems. Pneumonia is the most common complication, but far from the only one. Liver, kidneys, and heart can be affected.How the coronavirus “hits” the human “motor” in the material “AiF-Tyumen” .

Get Hit

The coronavirus causes a number of changes in the body, which also affect the cardiovascular system. Violation of blood clotting leads to the formation of microthrombi, changes in the rigidity of the vascular wall cause high blood pressure – and these are just some of the consequences of the virus. Especially seriously, covid is capable of hitting the health of people with pre-existing diseases of the heart and blood vessels.Illness can worsen a stable condition and lead to a crisis.

“There is a group of infectious diseases of the myocardium – the so-called myocarditis, the cause of which lies in viral, bacterial, fungal infections or toxins. The mechanism of damage to the heart muscle is associated with the effect of pathogenic microorganisms and their metabolic products on the heart tissue. Also, damage occurs against the background of the body’s general reaction to inflammation. With coronavirus infection, the risk of damage to the heart and the cardiovascular system as a whole is undoubtedly high, often this leads to serious consequences, especially in the presence of chronic cardiovascular and endocrine diseases, “says cardiologist, head of the department of rehabilitation treatment of Tyumen scientific center Timofey Semenikhin .

This is not to say that problems with the heart and blood vessels occur in everyone who has had covid. Cores are in the first place in the risk group. As practice shows, people with such chronic diseases as ischemic disease, arterial hypertension, with problems of the endocrine system – diabetes mellitus, overweight, the elderly often have increased thrombus formation. Patients with coronary heart disease, atherosclerotic vascular lesions may have repeated heart attacks due to microthrombosis of the coronary vessels.If a blood clot gets into the vessels of the brain, it can result in a stroke, if in the lungs – thromboembolism or pulmonary infarction, in other organs – their ischemic damage. Therefore, patients with chronic diseases need to be especially careful.

But those who did not previously know problems with blood vessels and heart, when the coronavirus ricochets, can also get hit. Therefore, according to the doctor, it is important to monitor blood pressure and pulse, especially if after an illness it is not possible to recover for a long time.If there is increased fatigue, fatigue, headaches, and during normal physical exertion, shortness of breath and pressing, compressive pains in the heart, palpitations, a feeling of “interruption”, there is no rhythm of the pulse, you should consult a specialist to understand the reasons for this condition.

In case of severe pain in the heart region lasting more than five minutes, you need to call an ambulance

“Shortness of breath, although not quite a specific syndrome for heart disease, should not be ignored.This can be a sign of damage to the cardiovascular system, along with an interruption in the pulse. And if there is pain in the region of the heart, discomfort during exertion, for example, when walking, climbing stairs, then alarm bells require immediate medical attention.

If there is (severe pressing, tearing, burning) pain in the region of the heart (lasting more than five minutes), dizziness, increased pressure, you do not need to get up through force, run somewhere. I would recommend: call an ambulance, sit in a chair or lie down, you can still take aspirin or nitroglycerin, ”the doctor notes.

Return to former life

Correct recovery from coronavirus is just as important as proper treatment. The disease can remind of itself for a long time. The sooner rehabilitation begins, the sooner you will be able to return to your usual way of life.

“After the end of the acute stage of the disease, weakness, fatigue, excitability or, conversely, drowsiness, sleep disturbances at night, memory loss, various sensations in the heart persist,” says the doctor. – Each case requires an individual approach, your analyzes and recommendations.If it is not possible to return to the previous physical and emotional state, as before the disease, the restoration of the body is required, ”said Timofey Semenikhin.

And special attention should be paid to physical activity through well-chosen exercises and training programs. Medical massage and physiotherapy will not be superfluous. Of course, a doctor should select a recovery complex.

“Since our main patients are people with diseases of the cardiovascular system, we pay great attention to recovery from coronavirus, taking into account this feature of their health,” says the cardiologist.

First tests

Against the background of news that the coronavirus causes increased blood clots, anticoagulants began to be bought in pharmacies. Some prescribe these drugs to themselves for prophylaxis. However, the desire to prevent blood clots can turn out to be no less serious problems than a heart attack or stroke.

Self-administration of anticoagulants can cause gastrointestinal bleeding

“It is absolutely impossible to take anticoagulants for prophylaxis without indications.They are appointed according to the results of tests and under the supervision of a doctor, explains Timofey Semenikhin. – There are several groups of drugs that affect blood clotting and directly on a blood clot. But before discharging them, the doctor assesses the risk of bleeding on special scales, if it is high, then you have to change tactics. Moreover, some anticoagulants require weekly monitoring of blood clotting. In addition, when prescribing these drugs, gender, age, and concomitant diseases are taken into account.Self-administration can cause gastrointestinal bleeding. As a rule, internal bleeding at an early stage is difficult to suspect, they may not particularly manifest themselves until the onset of a critical situation. ”

You need to be more careful with taking vitamins. Today, the method of preventing viral infections is vaccination; vitamins do not have a specific effect on the virus.

The cardiologist reminds that vitamins are medicines, so they should be prescribed by a doctor after examination, consultation and testing, which will show whether there is vitamin deficiency or not.Excessive intake of these drugs can lead to hypervitaminosis, and some of these substances in large quantities become toxic.

To strengthen the heart, the best “vitamin”, according to the doctor, is active rest, balanced nutrition, sleep and wakefulness, regular physical activity: walks, physiotherapy exercises, jogging, skiing and skating. Such physical education and immunity will strengthen, and will raise the mood – without any chemical additives.

Surprising facts about heart and blood

• William Park
• BBC Future

May 25 2016

Photo author, iStock

The most complex creation of the universe, undoubtedly, remains the human brain.But our heart and circulatory system are equally exciting. BBC Future has some interesting facts about them.

The heart pumps a lot of blood

Our heart is a very hardworking organ.

Within five minutes, he pumps five liters of blood. In an hour, the heart makes an average of 4200 beats and pumps 300 liters of blood.

In one year, it pumps enough blood to fill the Olympic pool – more than 2.5 million liters – and makes 38.5 million contractions to do so.

Heartbeat Affects Behavior

When we have to make a difficult decision, we often say that we made this choice with our heart.

But did you know that this expression can have a literal meaning? Heart rate affects our feelings, emotions and even intuition – from pain and empathy for another person to the suspicion that your man may be cheating on you.

Researcher Agustín Ibanez of the University of Favaloro in Buenos Aires had a unique opportunity to test this assumption when he met a man with two hearts.Carlos (the man’s name has been changed) had another heart, a mechanical one, located in the chest just below his real heart. Carlos received a heart transplant, which helped his weak heart muscles work.

Photo author, SPL

Sign up to photo,

Scientists have replaced the patient’s blood with saline, thus trying to prolong his life his perception of reality and even his mind.

Scientists have found a way to live without blood

What happens when our heart stops? Is it possible to bring a person back to life from the moment of clinical death, when all the basic vital functions – heartbeat and brain activity – have stopped?

Surgeons today have tried a radical new procedure. They replaced the patient’s blood with saline in an attempt to prolong his life.

This experimental study seems to blur the line between life and death.The patient’s body is cooled to about 10-15 C. Since the body’s metabolism has already stopped, blood is not needed in order to supply oxygen to the cells. Replacing blood with cold salt water is the best way to maintain an overall low body temperature.

We still don’t know why we have different blood types

One of the biggest mysteries of our circulatory system has remained unsolved for over a century.

We still do not fully know why people have different blood types.We know that they are determined by various molecules on the surface of red blood cells. And we realize the importance of this process, since enzymes in our body recognize red blood cells precisely thanks to these molecules.

That is why blood can only be transfused to a person of the corresponding group – enzymes cannot recognize another group.

Photo author, Science Photo Library

Pidpis to photo,

Why did nature endow us with different blood types?

But why do we have different blood types? Why didn’t nature make it so that we all have a universal set of molecules in our blood cells?

One day we will be able to live with an artificial heart… or a pig’s heart

Xenotransplantation – the use of animal tissue in the human body – dates back to at least 1682, when the Dutch surgeon Job Janssson van Meerkeren reported the successful transplantation of a fragment of a dog’s bone into the skull of a Russian soldier.

Researchers are now actively exploring the possibility of transplanting hearts from other animals, such as pigs, to humans.

Another line of research aims to grow human hearts using tissue engineering.

Some people drink blood without any benefit

Perhaps the most surprising use of blood is to consume it internally, preferably fresh, to relieve a number of medical complaints.

There are entire communities of people around the world who drink fresh human blood for medicinal purposes. Doses of the red drink are kindly provided by relatives, friends or volunteers.

Photo by Olivia Howitt

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Blood tastes differently depending on blood type, diet and amount of fluid you drink

These “medical vampires” claim that regular blood intake helps them relieve symptoms such as headaches , fatigue, stomach pain that no other treatment works for.

However, scientists believe that drinking blood is unlikely to have any benefit, and the relief it brings is actually just a placebo effect. But the fact that people are feeling better is a testament to the powerful effect the ritual of consuming human blood has on the mind.

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the original of this article in English you can visit the website

BBC Future.

What is good for your heart? (information for the population)

If you add up the length of all the capillaries in the body of an adult, you get a figure of 100 thousand kilometers! This thread can wrap our planet twice along the equator.How to keep such a large-scale system healthy? How can you help your heart to withstand daily stress so that it works “without failure” throughout its life? There are several guidelines for accomplishing this task.

1. Cardio load

The most beneficial cardiac exercise is vigorous walking. It rejuvenates blood vessels, accelerates blood circulation, and helps the heart muscle to work fully. Most centenarians walk daily, and many cover impressive distances.

Unlike running, walking does not shock the joints and does not dramatically increase the heart rate.And by combining active walking with a walk in the fresh air, you thereby get a double benefit: improving the functioning of the respiratory system and the condition of the skin.

So, 10 thousand steps is the minimum with which you are able to compensate for a sedentary lifestyle in the modern world. Whoever wants to improve health and achieve active longevity can safely double this figure.

2. Nutrition for the heart

In addition to factors beyond the control of humans (ecology, hereditary and genetic predisposition), nutrition has a significant effect on the work of the heart, which is confirmed by research.

Recommendations for water consumption are as follows: 1.5 – 2 liters per day. However, if there are signs of heart failure (edema), you should try to drink no more than 1-1.2 liters of liquid per day (including soups, jelly, etc.). You can’t drink less either, otherwise the excretion of nitrogenous metabolic products will be difficult, weakness and constipation may appear. It is necessary to limit salt intake, to avoid edema and increased blood pressure, the norm is no more than 5 g per day. Also, limit your sugar intake, give up fatty foods, exclude rich broths, fried and smoked meat, spicy foods.Periodically spend fasting days (for example, 300g of cottage cheese, 500g of apples, 400ml of kefir, 200g of boiled potatoes, use 5 meals a day).

What is good for the heart? Primarily foods rich in potassium and magnesium, omega acids and antioxidants:

• Fish . At least twice a week, fatty fish should be included in the diet – salmon, mackerel, sardine, rich in polyunsaturated fatty omega acids. the most valuable foods for the heart.
• Vegetable oils. Contains vitamin E and antioxidants. The fats of lard are useful in that they strengthen the work of the heart without contributing to the development of atherosclerosis (pork fatty meat, on the contrary, is harmful to the heart).
• Carrots. Rich source of vitamins (A, E, K), folate and potassium.
• Nuts (walnuts, hazelnuts, almonds, pine nuts, pistachios) . Helps lower cholesterol levels (unless, of course, eat them in handfuls), contain monounsaturated fats and vitamin E.Reduce the risk of heart attack by 30-50%.
• Apples . It is generally difficult to overestimate their importance. Contains vitamins and antioxidants.
• Bananas. As a source of potassium and a significant amount of magnesium, they help to reduce blood pressure and normalize the nervous system, normalize the hemoglobin content in the blood and the blood circulation process. Lemon, persimmon, pumpkin are also useful for the content of potassium, carotenes and vitamin A for the heart, which can strengthen and normalize the work of the heart muscle.
• Pomegranate is one of the most valuable fruits for strengthening and maintaining the condition of the heart and blood vessels. Its consumption prevents the development of atherosclerosis, maintains the level of blood flow and oxygenation of the heart.
• Flaxseed. Rich source of alpha-linoleic acid. Helps lower cholesterol levels.
• Garlic . It also lowers cholesterol, and also thins the blood, lowering its viscosity.
• Legumes .They are rich in protein, which is so essential for the normal functioning of the heart muscle.
• Dried fruits. And especially dried apricots. It is high in potassium and antioxidants. To strengthen and restore the cardiovascular system, it is advisable to use Amosov’s (Russian cardiologist) paste, which is a crushed mixture of nuts and dried fruits. It is also very beneficial to eat 20-30 grams of dark chocolate a day.
• Tomatoes . Helps normalize heart rate.

3. Exercise “Birch”

This exercise, lasting 2-3 minutes, can replace cardio training. What is the use of “Birch”:

• Improves blood circulation.
• Rest for the heart muscle. In this position, the heart receives both the payload and the opportunity to relax.
• Prevention of varicose veins. And this is also part of the beneficial effect on the cardiovascular system as a whole.
• Normalization of the kidneys, intestines and thyroid gland (if you press your chin to your chest and breathe evenly, calmly).The normal functioning of the whole organism as a whole and the heart, including, depends on the health of these organs.
• Deep relaxation. “Birch” helps to relieve fatigue, get rid of stress, “clear your head.” And thus help your heart.

4. Lymphatic drainage exercises

Pay attention to lymphatic drainage exercises every day!

Healthy capillaries – healthy heart. And in order to improve their work, you need to be distracted from other activities for only 1-3 minutes! For example, the Mikulin (Soviet Academician) heel kicks will take you 30-60 seconds maximum.You just need to raise the heels from a standing position 5 cm from the floor and sharply lower them down. Repeat 30-60 times. For sedentary work, it is recommended to do this exercise every 1 to 2 hours.

And the exercise “Vibration” will take you 1-3 minutes. To do this, it is enough to lie down, raise your arms and legs up and shake them arbitrarily.

5. Calm, only calm

This is the most difficult point. How to maintain balance in our time, not to succumb to the influence of negative circumstances and aggressive people? Our heart will respond in one way or another, because we are not robots.Where to start – learn to relax physically (Director of the Franklin Method Institute in Switzerland – Eric Franklin):

1.Imagine that you are standing under a waterfall. Water flows around your neck, shoulders and back. All tension is washed away.

2 Relaxing the shoulders: lift your shoulders up, and now lower them down very slowly. Raise your shoulders up again. Now let your shoulders drop downward under the gravity of the Earth, exhaling loudly with the sound “Aaa”. Repeat etc.

3.Patting Where do you feel muscle tension? There and pat. This technique helps to improve blood circulation, relax muscles.

4. Shake your arms and legs at different intensities to loosen the muscles.