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Human Heart: Anatomy, Function & Facts

The human heart is an organ that pumps blood throughout the body via the circulatory system, supplying oxygen and nutrients to the tissues and removing carbon dioxide and other wastes.

“The tissues of the body need a constant supply of nutrition in order to be active,” said Dr. Lawrence Phillips, a cardiologist at NYU Langone Medical Center in New York. “If [the heart] is not able to supply blood to the organs and tissues, they’ll die.”

Human heart anatomy

In humans, the heart is roughly the size of a large fist and weighs between about 10 to 12 ounces (280 to 340 grams) in men and 8 to 10 ounces (230 to 280 grams) in women, according to Henry Gray’s “Anatomy of the Human Body.” 

The physiology of the heart basically comes down to “structure, electricity and plumbing,” Phillips told Live Science.

The human heart is about the size of a fist. (Image credit: tlorna Shutterstock)

The human heart has four chambers: two upper chambers (the atria) and two lower ones (the ventricles), according to the National Institutes of Health. The right atrium and right ventricle together make up the “right heart,” and the left atrium and left ventricle make up the “left heart.” A wall of muscle called the septum separates the two sides of the heart.

A double-walled sac called the pericardium encases the heart, which serves to protect the heart and anchor it inside the chest. Between the outer layer, the parietal pericardium, and the inner layer, the serous pericardium, runs pericardial fluid, which lubricates the heart during contractions and movements of the lungs and diaphragm.

The heart’s outer wall consists of three layers. The outermost wall layer, or epicardium, is the inner wall of the pericardium.  The middle layer, or myocardium, contains the muscle that contracts. The inner layer, or endocardium, is the lining that contacts the blood.

The tricuspid valve and the mitral valve make up the atrioventricular (AV) valves, which connect the atria and the ventricles. The pulmonary semi-lunar valve separates the right ventricle from the pulmonary artery, and the aortic valve separates the left ventricle from the aorta. The heartstrings, or chordae tendinae, anchor the valves to heart muscles.

The sinoatrial node produces the electrical pulses that drive heart contractions.

Human heart function

The heart circulates blood through two pathways: the pulmonary circuit and the systemic circuit.

In the pulmonary circuit, deoxygenated blood leaves the right ventricle of the heart via the pulmonary artery and travels to the lungs, then returns as oxygenated blood to the left atrium of the heart via the pulmonary vein.

In the systemic circuit, oxygenated blood leaves the body via the left ventricle to the aorta, and from there enters the arteries and capillaries where it supplies the body’s tissues with oxygen. Deoxygenated blood returns via veins to the venae cavae, re-entering the heart’s right atrium.

Of course, the heart is also a muscle, so it needs a fresh supply of oxygen and nutrients, too, Phillips said.

The cardiovascular system circulates blood from the heart to the lungs and around the body via blood vessels. (Image credit: The BioDigital HumanTM developed by NYU School of Medicine and BioDigital Systems LLC)

“After the blood leaves the heart through the aortic valve, two sets of arteries bring oxygenated blood to feed the heart muscle,” he said. The left main coronary artery, on one side of the aorta, branches into the left anterior descending artery and the left circumflex artery. The right coronary artery branches out on the right side of the aorta.

Blockage of any of these arteries can cause a heart attack, or damage to the muscle of the heart, Phillips said. A heart attack is distinct from cardiac arrest, which is a sudden loss of heart function that usually occurs as a result of electrical disturbances of the heart rhythm. A heart attack can lead to cardiac arrest, but the latter can also be caused by other problems, he said.

The heart contains electrical “pacemaker” cells, which cause it to contract — producing a heartbeat.

“Each cell has the ability to be the ‘band leader’ and [to] have everyone follow,” Phillips said. In people with an irregular heartbeat, or atrial fibrillation, every cell tries to be the band leader, he said, which causes them to beat out of sync with one another.

A healthy heart contraction happens in five stages. In the first stage (early diastole), the heart is relaxed. Then the atrium contracts (atrial systole) to push blood into the ventricle. Next, the ventricles start contracting without changing volume. Then the ventricles continue contracting while empty. Finally, the ventricles stop contracting and relax. Then the cycle repeats. 

Valves prevent backflow, keeping the blood flowing in one direction through the heart.

Facts about the human heart

  • A human heart is roughly the size of a large fist.
  • The heart weighs between about 10 to 12 ounces (280 to 340 grams) in men and 8 to 10 ounces (230 to 280 grams) in women.
  • The heart beats about 100,000 times per day (about 3 billion beats in a lifetime).
  • An adult heart beats about 60 to 80 times per minute.
  • Newborns’ hearts beat faster than adult hearts, about 70 to 190 beats per minute.
  • The heart pumps about 6 quarts (5.7 liters) of blood throughout the body.
  • The heart is located in the center of the chest, usually pointing slightly left.

Editor’s Note: If you’d like more information on this topic, we recommend the following book:

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Additional resources

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Your Heart & Blood Vessels

The heart is located under the rib cage, to the left of the breastbone (sternum) and between the lungs. Your heart is an amazing organ. Shaped like an upside-down pear, this fist-sized powerhouse pumps five or six quarts of blood each minute to all parts of your body.

The Heart and Blood Vessels

Large red vessel (the aorta) – Large artery that carries blood from of the left ventricle to the arteries of the body.

Large blue vessel (vena cava) _(includes the superior and inferior vena cava) – _Large vein that empties blood into the right atrium of the heart.

Front View (Anterior) of the Heart

Outside View of the Back (Posterior) of the Heart

Coronary veins (in blue) take oxygen-poor (“deoxygenated”) blood that has already been “used” by muscles of the heart and returns it to the right atrium.

Circumflex artery – supplies blood to the left atrium and the side and back of the left ventricle.

Left coronary artery – divides into two branches (the circumflex artery and the left anterior descending artery).

Left anterior descending artery (LAD) – supplies blood to the front and bottom of the left ventricle and the front of the septum.

Pulmonary veins bring oxygen-rich blood back to the heart from the lungs.

Right coronary artery (RCA) – supplies blood to the right atrium, right ventricle, bottom portion of the left ventricle and back of the septum.

Inside the Heart

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 atria – top chambers, which receive blood from the veins and
  • Two ventricles – bottom chambers, 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 (also called pulmonary 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, preventing 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 valve are also supported by tough, fibrous strings called chordae tendineae. These are similar to the strings supporting a parachute. The chordae tendineae extend from the valve leaflets to small muscles, called papillary muscles, which are part of the inside walls of the ventricles.

The normal aortic valve

The normal mitral valve

How the Heart Works | Froedtert & the Medical College of Wisconsin

The heart is a muscular organ that pumps blood continuously throughout the body. It is comprised of four chambers — the right and left atrium and the right and left ventricle.

The chambers of the heart work together by alternately contracting and relaxing to pump blood throughout the heart. To accomplish this, the heart uses an electrical system to trigger a heartbeat. Essentially, the electrical system is the power source that makes all the heart’s functions possible.

Blood vessels lead in and out of the chambers, which receive and distribute blood throughout the body. The four chambers are connected by four valves — the tricuspid, pulmonic, mitral and aortic valves. These valves work like one-way doors, allowing blood to flow in only one direction.

Blood Circulation

As the heart beats, it pumps blood through a system of blood vessels called the circulatory system. The blood that these vessels carry is essential for the body to function. Blood carries oxygen and nutrients to your body’s tissues, assists in the removal of carbon dioxide and waste products and promotes the overall health of the body’s tissues. There are three main types of vessels that make up this system:

  • Arteries
  • Veins
  • Capillaries

How blood flow works

Blood enters the heart through two large veins, the inferior and superior vena cava, emptying into the right atrium. It flows from the right atrium through the tricuspid valve into the right ventricle. The right ventricle pumps blood to the pulmonic valve, and the blood flows into the pulmonary artery and to the lungs. Oxygenated blood returns from the lungs to the heart via the pulmonary vein into the left atrium. From the left atrium, blood flows through the mitral valve to the left ventricle. From the left ventricle blood leaves the heart through the aortic valve and flows into the aorta and to the body.

Coronary Arteries

The heart muscle needs its own supply of oxygen and nutrients to pump properly. Although its chambers are full of blood, the heart receives no nourishment from this blood. The heart receives its own supply of blood through a network of arteries of the body known as the coronary arteries.

Functions of right and left coronary arteries

The coronary arteries wrap around the surface of the heart. The two main coronary arteries, the right coronary artery and the left coronary artery, branch off from the aorta. The right coronary artery supplies the right atrium and right ventricle. It branches into the posterior descending artery. The left coronary artery branches into the circumflex artery and the left anterior descending artery. The left coronary artery supplies the left atrium and the left ventricle.

Narrow coronary arteries

Collateral circulation is a network of tiny blood vessels that usually remain inactive. When coronary arteries narrow to the point that blood flow to the heart is limited, collateral vessels become enlarged and active. This process allows for blood flow around the blocked artery to the heart muscle.

Anatomy and Function of the Coronary Arteries

Coronary arteries supply blood to the heart muscle. Like all other tissues in the body, the heart muscle needs oxygen-rich blood to function. Also, oxygen-depleted blood must be carried away. The coronary arteries wrap around the outside of the heart. Small branches dive into the heart muscle to bring it blood.

What are the different coronary arteries?

The 2 main coronary arteries are the left main and right coronary arteries.

  • Left main coronary artery (LMCA). The left main coronary artery supplies blood to the left side of the heart muscle (the left ventricle and left atrium). The left main coronary divides into branches:

    • The left anterior descending artery branches off the left coronary artery and supplies blood to the front of the left side of the heart.

    • The circumflex artery branches off the left coronary artery and encircles the heart muscle. This artery supplies blood to the outer side and back of the heart.

  • Right coronary artery (RCA). The right coronary artery supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes, which regulate the heart rhythm. The right coronary artery divides into smaller branches, including the right posterior descending artery and the acute marginal artery. Together with the left anterior descending artery, the right coronary artery helps supply blood to the middle or septum of the heart.

Smaller branches of the coronary arteries include: obtuse marginal (OM), septal perforator (SP), and diagonals.

Why are the coronary arteries important?

Since coronary arteries deliver blood to the heart muscle, any coronary artery disorder or disease can have serious implications by reducing the flow of oxygen and nutrients to the heart muscle. This can lead to a heart attack and possibly death. Atherosclerosis (a buildup of plaque in the inner lining of an artery causing it to narrow or become blocked) is the most common cause of heart disease.

What Side of Your Body Is Your Heart On?

What side is your heart on? It may not be the answer you’re expecting! Chest pain is an issue that understandably makes many people nervous, but knowing some basic facts about your heart and the rest of your body can help you feel more at ease and informed.

Read this guide to learn your heart location, where the heart is located in relation to other organs, what kind of chest pain may indicate a heart issue, and other potential causes of chest pain.


What Side Is Your Heart On?

Where is the heart located? While most people think their heart is located on the left side of their chest, (after all, isn’t that where you place your hand when you say the Pledge of Allegiance?) your heart location is actually close to the center of your chest, just slightly shifted to the left side. About two-thirds of your heart is on the left side of your chest, and one-third is on the right side, so it’s pretty nearly centered.

To get technical about it, your heart is located in your mediastinum (a membranous space located between the lungs), which itself is in the center of your thorax (the part of the body between your neck and abdomen).

The heart is commonly thought to be on the left side of your body since it’s this side of the heart that does most of the work. The left side is stronger and is the part of the heart that pumps oxygen-rich blood to other parts of the body, so it’s primarily this side of the heart (located slightly on the left side of your chest) that you feel beating when you put your hand on your chest, leading people to think that the entire heart is on the left side of the chest. Your heart is about the size of your fist, so if you make a fist and put it over the center of your chest, you’ll get a good idea of where your heart is located.


Where Is the Heart Located in Relation to Other Organs?

Because of its central location in your chest, your heart is close to a lot of other vital organs. Your heart is located behind your sternum and between your two lungs. The heart is located closer to the front of your chest, in front of your esophagus and spine. Below your heart is your diaphragm, stomach, and liver. The diagram below shows where the heart location in respect to other organs.


What Kinds of Chest Pain Indicate a Heart Issue?

Often when people feel chest pain, they worry they are experiencing a heart attack or other serious heart issue. While many times the chest pain is caused by something other than your heart (see the next section), you should always call your doctor, call 911, or go to the hospital if you’re concerned that you’re having a heart issue.

The classic symptom of a heart attack is pain on the left side of your chest. This pain can range from mild to severe, and many people report feeling pressure or a squeezing sensation in their chest. The pain may be steady or come and go.

Common symptoms of chest pain that is caused by heart issues include:

  • Pain that is usually worse in the morning
  • Pain that feels deep or heavy as opposed to sharp and stabbing
  • Pain that feels worse when you exert yourself

However, chest pain due to a heart issue is not only limited to pain on the left side of the chest. Pain may also occur in other areas such as on either side of the upper chest, radiating down one or both arms, and behind your ribs. The pain can also spread to your back, upper part of the stomach, shoulders, neck, and jaw.

Other common symptoms of a heart attack include:

  • Shortness of breath
  • Nausea and/or vomiting
  • Dizziness
  • Breaking out in a sweat

If you experience these symptoms, call 911 immediately, even if you’re not sure you’re having a heart attack.




What Are Other Causes of Chest Pain?

Chest pain isn’t something you should brush off, but fortunately there are many causes of chest pain besides a heart attack. In fact, the pain may not even be related to your heart at all. Below are some non-cardiac causes of chest pain.


Pain on the Left or Right Side of Your Chest

  • Tear or strain in your chest wall: Pulls, strains, or tears to the Pectoralis Major or Pectoralis Minor can also cause chest pain. The pain often increases when you touch the area or move in certain ways.
  • Pneumonia: Pneumonia is a lung infection that inflames the air sacs of one or both lungs. If you only have pneumonia in one lung, that may be the only side of the chest where you feel pain. Pneumonia is often accompanied by a fever, cough, and a general feeling of malaise.
  • Pulmonary embolism: A pulmonary embolism is when a blood clot lodges in an artery of the lung. If a PE occurs, you’ll often feel a sharp, stabbing pain on the side of your chest where that lung is located that feels worse when you take deep breaths.
  • Inflamed pancreas: If your pancreas is inflamed, you’ll often have intense pain that begins behind your rib cage and spreads to the right side of your chest. The pain is often worse when you lie down.


Pain in Your Upper Abdomen

  • Appendicitis: Appendicitis occurs when your appendix becomes inflamed. Your appendix is located in the lower right side of your abdomen, but the pain can spread to your middle and upper abdomen, especially if the infection becomes severe.
  • Gallbladder infection: If you have a gallbladder infection or gallstones, you may feel sharp, stabbing pains in your upper abdomen.
  • Liver infection: When the liver is inflamed or infected with hepatitis, it can cause pain in your upper abdomen which also spread to the right side of your chest.
  • Digestion issue: Indigestion, heartburn, or other digestive issue can cause discomfort and pain that spreads to the upper abdomen and sometimes the chest and esophagus.


Recap: What Side Is Your Heart On?

What side of the body is the heart on? The heart’s location is erroneously thought to be the left side of the chest, but your heart is actually located nearly in the center of your chest, behind your sternum and between your two lungs.

Pain on the left side of the chest is often connected with heart problems because it usually the left side of the heart that causes pain when there is a health issue. Heart problems are a serious, and sometimes fatal, health issue, and if you’re ever concerned about chest pain you’re experiencing, contact your doctor or go to the hospital immediately. However, chest pain can be caused by many issues not related to the heart, such as an issue with your lungs, liver, or digestion.

Don’t spend too much time trying to self-diagnose though. Whenever you have a health issue that worries you, make an appointment with your doctor so you can get an accurate diagnosis.


BBC Science & Nature – Human Body and Mind

System: Cardiovascular

Location: Between your lungs

Physical description: Grapefruit-sized and cone-shaped

Function: To pump oxygen-rich blood throughout your body and oxygen-poor blood to your lungs

Cardiac muscle

Your heart is an incredibly powerful organ. It works constantly without ever pausing to rest. It is made of cardiac muscle, which only exists in the heart. Unlike other types of muscle, cardiac muscle never gets tired.

Four chambers

Your heart is divided into four hollow chambers. The upper two chambers are called atria. They are joined to two lower chambers called ventricles. These are the pumps of your heart.

One-way valves between the chambers keep blood flowing through your heart in the right direction. As blood flows through a valve from one chamber into another the valve closes, preventing blood flowing backwards. As the valves snap shut, they make a thumping, ‘heart beat’ noise.

Double pump

Blood carries oxygen and many other substances around your body. Oxygen from your blood reacts with sugar in your cells to make energy. The waste product of this process, carbon dioxide, is carried away from your cells in your blood.

Your heart is a single organ, but it acts as a double pump. The first pump carries oxygen-poor blood to your lungs, where it unloads carbon dioxide and picks up oxygen. It then delivers oxygen-rich blood back to your heart. The second pump delivers oxygen-rich blood to every part of your body. Blood needing more oxygen is sent back to the heart to begin the cycle again. In one day your heart transports all your blood around your body about 1000 times.

Your right ventricle pumps blood to your lungs and your left ventricle pumps blood all around your body. The muscular walls of the left ventricle are thicker than those of the right ventricle, making it a much more powerful pump. For this reason, it is easiest to feel your heart beating on the left side of your chest.


Unlike skeletal muscle cells that need to be stimulated by nerve impulses to contract, cardiac muscle cells can contract all by themselves. However, if left to their own devices, cardiac muscle cells in different areas of your heart would beat at different rates. Muscle cells in your ventricles would beat more slowly than those in your atria. Without some kind of unifying function, your heart would be an inefficient, uncoordinated pump. So, your heart has a tiny group of cells known as the sinoatrial node that is responsible for coordinating heart beat rate across your heart. It starts each heartbeat and sets the heartbeat pace for the whole heart.

Damage to the sinoatrial node can result in a slower heart rate. When this is a problem, an operation is often performed to install an artificial pacemaker, which takes over the role of the sinoatrial node.

Heart rate

Without nervous system control, your heart would beat around 100 times per minute. However, when you are relaxed, your parasympathetic nervous system sets a resting heart beat rate of about 70 beats per minute, (resting heart rate is usually between 72-80 beats per minute in women and 64-72 beats per minute in men).

When you exercise or feel anxious your heart beats more quickly, increasing the flow of oxygenated blood to your muscles. This is triggered by your sympathetic nervous system. Your heart rate also increases in response to hormones like adrenalin.

On average, your maximum heart rate is 220 beats per minute minus your age. So a 40 year old would have a maximum heart rate of 180 beats per minute.

Oxygen supply to your heart

Although your heart is continually filled with blood, this blood doesn’t provide your heart with oxygen. The blood supply that provides oxygen and nutrients to your heart is provided by blood vessels that wrap around the outside of your heart.

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How Blood Flows Through the Heart and Lungs

The heart is a complex organ, using four chambers, four valves, and multiple blood vessels to provide blood to the body. Blood flow itself is equally complex, involving a cyclic series of steps that move blood trough the heart and to the lungs to be oxygenated, deliver it throughout the body, then bring blood back to the heart to re-start the process.

This is the key function of the cardiovascular system: consuming, transporting, and using oxygen throughout physical activity (which includes when you are at rest). Disruptions in blood flow through the heart and lungs can have serious effects.

artpartner-images / Getty Images

Blood Flow Step by Step

The heart has two upper chambers—the left and right atriums—and two larger lower chambers—the left and right ventricles. A series of valves control blood flow in and out of these chambers.

Electrical impulses, controlled by the cardiac conduction system, make the heart muscle contract and relax, creating the rate and rhythm of your heartbeat.  Here are the steps of blood flow through the heart and lungs:

  1. The blood first enters the right atrium.
  2. The blood then flows through the tricuspid valve into the right ventricle.
  3. When the heart beats, the ventricle pushes blood through the pulmonic valve into the pulmonary artery.
  4. The pulmonary artery carries blood to the lungs where it “picks up” oxygen and then leaves the lungs to return to the heart through the pulmonary vein.
  5. The blood enters the left atrium, then descends through the mitral valve into the left ventricle.
  6. The left ventricle then pumps blood through the aortic valve and into the aorta, the artery that feeds the rest of the body through a system of blood vessels.
  7. Blood returns to the heart from the body via two large blood vessels called the superior vena cava and the inferior vena cava. This blood carries little oxygen, as it is returning from the body where oxygen was used.
  8. The vena cavas pump blood into the right atrium and the cycle of oxygenation and transport begins all over again.

Arteries generally transport oxygen-rich blood. The pulmonary artery is unique: It is the only artery in the human body that carries oxygen-poor blood.

Importance of Valves

Without valves, the ventricles of the heart couldn’t develop any force or pressure. It would be like pumping up a flat tire with a huge hole in it: No matter the effort you put into pumping, the tire would never inflate.

In the case of the heart, blood would come into the chamber and just slosh through it, exiting out the valve at the bottom or upward in the wrong direction each time the ventricle tried to pump blood.

All four of the heart valves open and close at just the right times to keep the blood flowing through the heart in the right direction. Part of the sound of your heartbeat is valves closing.

Blood Flow Positive and Negative Effects

A healthy heart normally beats anywhere from 60 to 70 times per minute when you’re at rest. This rate can be higher or lower depending on your health and physical fitness; athletes generally have a lower resting heart rate, for example.

Your heart rate rises with physical activity, as your muscles consume oxygen while they work. The heart works harder to bring oxygenated blood where it is needed.

Disrupted or irregular heartbeats can affect blood flow through the heart. This can happen in multiple ways:

  • Electrical impulses that regulate your heartbeat are impacted, causing an arrythmia, or irregular heartbeat. Atrial fibrillation is a common form of this.
  • Conduction disorders, or heart blocks, affect the cardiac conduction system, which regulates how electrical impulses move through the heart. The type of block—an atrioventricular (AV) block or bundle branch block—depends on where it occurs in the conduction system.
  • Damaged or diseased valves can become ineffective or leak blood in the wrong direction.
  • A blocked blood vessel, which can happen gradually or suddenly, can disrupt blood flow, such as during a heart attack.

If you experience an irregular heartbeat or cardiac symptoms like chest pain and shortness of breath, seek medical help immediately.

Frequently Asked Questions

In what direction does blood flow through the heart?

Blood moves in two directions simultaneously. De-oxygenated blood enters the right side of the heart and is pumped towards the lungs to pick up oxygen. Then that oxygen-rich blood re-enters the heart on the left side and is pumped out to the cells of the body.

What affects your heart rate?

Physical exertion will force your heart to beat faster and raise your heart rate. Many factors can also affect your resting heart rate. These include:

  • Medications
  • How physically fit you are
  • Air temperature and humidity
  • Body position (standing, sitting, lying down)
  • Emotions (anxiety, stress)
  • Body mass

Does exercise improve blood flow?

Yes. Exercise strengthens your heart muscle so it works more efficiently and supports blood flow. Exercise also helps you maintain a healthy weight, reduces your risk of high cholesterol and high blood sugar, and improves blood vessel function, all of which will also help blood circulate effectively.

A Word From Verywell

Healthy blood flow is critical to overall health. Physical activity is one of the best ways to achieve and maintain optimal functioning of your heart and lungs.

If you have health issues, partner with your doctor on the best way to keep your heart rate and rhythm—and therefore, your blood flow—healthy. It’s one of the most important things you can do for a long life.

90,000 cardiac ultrasound and ECG: difference and indications for research

Ultrasound of the heart and ECG are functional examinations of the heart. But the essence of these methods is different. The cardiologist decides which examination the patient should undergo. Sometimes it is just an ultrasound or only an ECG. And sometimes, for a complete picture, the doctor prescribes both methods.

Ultrasound of the heart

Cardiac ultrasound or echocardiography is a method of examining the anatomy of the heart muscle. During the procedure, the diagnostician directs a special apparatus to the heart.The device transmits ultrasonic waves through the body. Our organs reflect and partially absorb waves. The ability to reflect / absorb ultrasound of different human tissues is different. The ultrasound machine receives the reflected waves and converts them into an image on the monitor.

What does ultrasound of the heart show?

  • Valve status.
  • Pathologies, for example, a tumor or a previous microinfarction.
  • Velocity of blood flow to the heart.
  • Diameter of vessels.
  • Changes in the thickness of the walls of the ventricles and atria.
  • Changes in large vessels.
  • Blood clots.
  • Is there fluid in the pericardial sac?

A professional cardiologist, based on the results of ultrasound, detects many heart diseases. The doctor makes a conclusion based on the results of the study, taking into account age, gender, lifestyle and many other factors. Therefore, during the examination, answer the doctor’s questions in detail and honestly.

Indications for ultrasound of the heart

The doctor prescribes an ultrasound of the heart according to indications:

  • weakness and dizziness;
  • fainting and recurrent headaches;
  • nausea due to high blood pressure;
  • shortness of breath;
  • swelling on the body in the late afternoon, especially on the legs;
  • persistent and recurrent pain in the chest or under the scapula;
  • heart palpitations or cardiac arrest;
  • pale or bluish skin;
  • murmurs in the region of the heart;
  • suspicion of congenital or acquired heart disease;
  • vascular pathology, for example, varicose veins or thrombophlebitis;
  • Suspected rheumatism, lupus erythematosus or scleroderma;
  • Upcoming surgery if there is a history of heart problems or if the patient is over 50 years old.

If after the usual echocardiography the doctor still has doubts, he can prescribe an ultrasound of the heart through the esophagus. Such a study gives the patient some discomfort, but gives a more accurate result.

There are no contraindications to ultrasound examination. It is safely prescribed to everyone, including children and pregnant women.


The heart is our “electric motor”. Electrical impulses are generated in a special group of cells in the atria.They make the parts of the heart contract. An ECG is a recording of the electrical activity of the heart in a curve. Electrodes are placed on your body to take an ECG reading. To increase the permeability of the electric current, the doctor-diagnostician lubricates the places under the electrodes with a special gel. The procedure itself takes several minutes. The study is usually carried out in a lying or sitting position. There are types of ECG: study under stress, daily ECG monitoring according to Holper.

What does the ECG show?

  • Violation of the rhythm of the heartbeat: brady and tachycardia, extrasystole, atrial fibrillation.
  • Myocardial ischemia.
  • Incorrect impulse conduction or blockade.

The disadvantage of an ECG is that the study will show those disorders in the work of the heart that affect its work at the time of recording. False positive results are not uncommon for ECGs. If the doctor has doubts about the reliability of the ECG, then he additionally prescribes an ultrasound of the heart.

Indications for ECG

Cardiologist prescribes an electrocardiogram according to indications:

  • heart rhythm disturbances;
  • hypertension;
  • infection, inflammation or other pathologies of the heart;
  • alcohol and smoking abuse;
  • pregnancy;
  • increased blood cholesterol level;
  • transferred tonsillitis;
  • Increased health requirements by profession for pilots, drivers, military men, athletes, etc. d.

Doctors prescribe an ECG for 80% of patients who are admitted to hospital. There are no contraindications to the study. Now you can take an electrocardiogram even outside the hospital. For example, at the pharmacy or at the gym.

Remember! If you feel the slightest discomfort or pain in the heart area, then this is a reason to consult a doctor. Take care of your heart and be healthy!

Metabolic Cardiomyopathy | Cardiology Manual

(E.G. Nesukay)


Metabolic cardiomyopathy (previously it was defined as myocardial dystrophy, myocardial dystrophy) – non-inflammatory myocardial damage of various etiologies, which is based on metabolic disorders, the process of energy generation and / or a violation of its transformation into mechanical work, leading to myocardial dystrophy and insufficiency of contractile and other functions of the heart.


Metabolic cardiomyopathy develops as a result of exposure to pathogenic factors in various diseases and conditions (Scheme 8. 1).

Among the physical factors can be considered radiation, vibration, overheating, hypothermia, hyperinsolation.

Chemical factors include drugs, toxic effects of household and industrial poisons.


In the occurrence and development of metabolic lesions of the myocardium in various diseases, a violation of the innervation, transport and utilization of energy in cardiomyocytes, that is, their energy supply, is of significant importance.

The tension of regulatory systems, myocardial function and metabolic processes in cardiomyocytes limits the reserve capacity of the heart. Prolonged hyperfunction in itself, and especially in unfavorable conditions against the background of the underlying disease, can lead to an energy deficit and impairment of adaptive changes in the myocardium.

The mechanisms of a decrease in energy production in a damaged heart include a decrease in capillary density, an increase in intercapillary distance, as well as a larger diameter of hypertrophied cardiomyocytes, which impairs oxygen diffusion and causes myocardial hypoxia. One of the mechanisms is also associated with dysfunction of mitochondria, which is caused by a reduced synthesis of oxidative enzymes due to a violation of the proliferative response, which is partially mediated by the expression of PPARα receptors, which play a key role in mitochondrial biogenesis. These receptors regulate the transcription of many enzymes and carriers (transporters) that are involved in the transport and oxidation of fatty acids. Also, the ability of the heart to restore stores of high-energy phosphates is reduced.A decrease in fatty acid oxidation causes lipid accumulation and contributes to the necrosis of damaged membranes, while the release of reactive molecules (cytochromes, oxygen radicals) leads to apoptosis. Accelerated glycolysis, caused by a violation of oxidative phosphorylation, leads to acidosis, which inhibits many of the processes involved in the contraction-relaxation process. Of the latter, the most important is the increase in the concentration of calcium in the cytosol, which initiates many vicious circles leading to myocyte necrosis.

In the progression of metabolic cardiomyopathy, the leading role is played by the enhancement of the reactions of free radical lipid peroxidation of cell membranes. Damaging membranes, hydroperoxides and free radicals reduce the activity of lipid-dependent enzymatic reactions (which include the main vital enzymes of ion transport and the mitochondrial respiratory chain), change the membrane-receptor systems of the cell with the development of a mediator imbalance, activate proteolytic and lysosomal enzymes.

Pathological anatomy

Metabolic lesions of the myocardium cover all stages of metabolic disorders of the heart muscle – from functional disorders to gross structural changes. Morphological changes occur inside myocardial cells and are not accompanied by an increase in their number. Mitochondria and the endoplasmic reticulum are the most sensitive to pathogenic effects. For degenerative changes in the myocardium, mosaic disturbance of the structure of cardiomyocytes is characteristic: in the same cell, among the swollen mitochondria with partially or completely destroyed internal septa, there may be mitochondria with a normal structure.

As a rule, the elimination of the pathogenic cause leads to a gradual normalization of the ultrastructures of the cardiomyocyte, which is due to intracellular regenerative processes. Damaged myofibrils are restored as a result of the vigorous activity of ribosomes: intracellular edema is gradually eliminated, glycogen grains appear, and the number of fatty inclusions decreases. With prolonged and intense exposure to damaging factors on the myocardium, dystrophic changes can lead to profound morphological changes, ending with the development of myocardiofibrosis.

The death of a part of the myocardium is compensated by an increase in the mass of specific structures in intact cells, hyperplasia of mitochondria, sarcoplasmic reticulum, ribosomes occurs. As a result, myocardial hypertrophy develops, which is a compensatory regenerative-hyperplastic reaction characteristic of the myocardium. Biochemical processes are often disrupted in the LV.

Clinical picture

Clinical manifestations are diverse and not specific. The initial stages can be asymptomatic; over time, a decrease in myocardial contractility can lead to severe HF.

Often, against the background of manifestations of the underlying disease, cardialgia is noted (more often in the apex of the heart (92%), less often behind the sternum (15%)), expansion of the boundaries of the heart, muffled tones, a slight systolic murmur at the apex of the heart, rhythm disturbances (mainly extrasystolic arrhythmia ).


ECG is the leading method in recognizing dystrophic changes in the myocardium, which relate mainly to the repolarization process and are manifested most often by changes in the end part of the ventricular complex: depression of the ST segment is noted, which has an ascending character to a positive T wave.The T wave can also be deformed, low amplitude, flattened, or negative.

A decrease in the voltage of the QRS complex can also be determined, especially pronounced in obesity and myxedema; in thyrotoxicosis, the amplitude of the teeth is often increased. In some cases, there may be a slowdown in intra-atrial conduction, an increase in the Q – T interval, and intraventricular conduction disorders. Of the rhythm disturbances, sinus tachycardia and extrasystolic arrhythmia are most often noted.

When formulating a diagnosis, one should first of all indicate the underlying disease or etiological factor, the nature of the course of cardiomyopathy and the main clinical manifestations (the presence of rhythm and conduction disturbances, the stage of HF).

In the differential diagnosis of metabolic cardiomyopathy, exercise and medication tests, if necessary, coronary angiography may be important.


Regardless of the damaging factor, the following provisions may be fundamental for metabolic cardiomyopathy:

  • Disorders of myocardial metabolism with timely treatment are reversible;
  • severe HF develops relatively rarely, mainly in the final stage of the disease, but the resulting HF is resistant to cardiac glycosides and the success of therapy depends entirely on the degree of restoration of disturbed metabolism in the myocardium.

Helping patients should begin with eliminating the cause of myocardial dystrophy. Quitting smoking and alcohol abuse, excluding physical and psycho-emotional overstrain is of no small importance.

Along with the treatment of the underlying disease, it is necessary to restore an adequate energy metabolism. At the forefront is the use of a complex of drugs aimed at improving the transport of oxygen in the tissue and its utilization.

Two groups of drugs can influence the metabolism in a cell: regulators of an extracellular nature (hormones, blockers and stimulants of the central and peripheral nervous system) and regulators of metabolism of an intracellular nature (enzymes and antienzymes, vitamins, cofactors, various metabolites), which have an effect on various pathways of metabolism.

In case of violation of the processes of oxidative phosphorylation, a complex of vitamins is used, including vitamins B 1 , B 2 , pantothenic and lipoic acids. Vitamins of group B affect protein, lipid, carbohydrate-energy metabolism, synthesis of amino acids, nucleotides.

Among drugs with antioxidant properties, tocopherol acetate is widely used, its combination with vitamin PP (nicotinic acid) improves the energy supply of the contractile function of the myocardium.Vitamin C is an active antioxidant that participates in redox processes.

Sufficient intake of essential amino acids into the body is of great importance for the normalization of myocardial metabolism; including methionine, leucine, alanine, valine, lysine, trionine, tryptophan, which are a plastic material for the synthesis of protein, enzymes, coenzymes. To improve their absorption, it is recommended to prescribe them in combination with anabolic steroids (methandienone, nandrolone).

With the progression of the dystrophic process, the use of potassium chloride, potassium and magnesium asparaginate inside is shown to eliminate the natural deficiency of intracellular potassium, imbalance in the balance of calcium and magnesium, which leads to the restoration of the regulation of excitability and conductivity of the myocardium, its automatism and contractility.

To activate the synthesis of proteins and nucleic acids, salts of orotic acid (potassium / magnesium orotate) are used.

The therapy should be aimed at increasing energy generation and increasing myocardial resistance to hypoxia.Recently, much attention has been paid to the role of the serotonergic system in the regulation of the stress response. A specific feature of nicotinamide is its ability to stimulate the processes of aerobic oxidation and glycogen metabolism, thereby increasing the resistance of cardiomyocytes to hypoxia.

Trimetazidine has a direct cyto- and membrane-protective effect on cardiomyocytes in hypoxic conditions.

The duration of intensive metabolic therapy in the early stages in patients with predominantly functional disorders is 2-3 weeks.With the progression of myocardial dystrophy and detection of organic lesions of the heart, the course of therapy should be repeated several times a year.


The cardiovascular system is often involved in the pathological process in diseases of the endocrine glands. Functional changes in the heart can prevail in the clinical picture, and the patient with endocrine disease becomes, in fact, a “cardiac” patient. Heart damage in endocrine diseases is mainly due to metabolic disorders caused by a lack or excess of one or another hormone in the body.

Heart disease in case of diabetes mellitus

The term “diabetic cardiomyopathy” was first proposed in 1954 to denote cardiac changes preceding coronary heart disease.


The pathogenesis of metabolic cardiomyopathy in diabetes mellitus is multifactorial, damage to the cardiovascular system is caused by complex metabolic disorders arising from absolute or relative insulin deficiency and impaired glucose tolerance.

The pathogenesis of myocardial disorders includes several main mechanisms: damage to cardiomyocytes, microcirculatory and neurovegetative disorders. The first mechanism is associated with a violation of the metabolism of cardiomyocytes, a decrease in the efficiency of energy, plastic processes and a change in ionic metabolism, as a result of which the compensatory capabilities of the cardiovascular system are reduced, the contractile function of the myocardium is impaired, and tolerance to physical exertion decreases.The second mechanism is based on microcirculatory disorders in small myocardial arteries as a local manifestation of generalized microangiopathy. The third mechanism involves damage to the autonomic nervous system as a result of the formation of neurovegetative dystrophy.

Cardiomyopathy, not caused by impaired coronary circulation, occurs in young patients with juvenile diabetes mellitus, for whom the development of severe atherosclerosis is uncharacteristic, or in older patients without concomitant coronary artery disease.

Insulin has a direct effect on the heart, which consists in increasing the supply and stimulation of the oxidation of glucose and lactate, increasing the formation of glycogen in the myocardium. The indirect effect of insulin is to reduce the content of fatty acids in the blood plasma, reducing their supply to the heart.

Insulin deficiency causes impaired glucose utilization by tissues and enhances the breakdown of lipids and proteins, also leads to pronounced changes in the composition of the internal environment of the body – hyperglycemia, hyperketonemia, hyperlipidemia with accumulation of fatty acids in the blood, dysproteinemia, metabolic acidosis, oxidative stress causes apoptosis of myocytes.These disorders are the determining factors in changes in the structure and function of the myocardium.

The pathogenesis and morphogenesis of diabetic heart disease are caused not only by the effect of hyperinsulinemia on the vascular endothelium, energy and metabolic processes in the myocardium, but are also directly related to toxic-metabolic damage to cardiomyocytes.

It is believed that the cause of the destruction of the structures of cardiomyocytes, disruption of the structure of the sarcolemma and its derivatives, changes in ionic equilibrium and a decrease in the activity of the actomyosin complex of cardiomyocytes is direct glucose toxicity.

Tissue hypoxia plays an important role in the pathogenesis of cardiomyopathy. Of great importance in the development of hypoxia is the violation of oxygen transport by the blood, the function of respiratory enzymes under the influence of pronounced acidosis. With diabetes mellitus, the need for tissues, including the myocardium, for oxygen is increased.

An important factor in the development of myocardial dystrophy is a violation of the neuroendocrine regulation of the heart, associated with the predominance of the effects of counterinsular hormones. It has been proven that patients experience an increase in the production of adrenocorticotropic and somatotropic hormones, as well as glucocorticoids, catecholamines and glucagon, which leads to the initiation of a whole group of metabolic and ultrastructural processes that cause the development of metabolic cardiomyopathy.

The pathogenesis of increased myocardial stiffness is associated with impaired calcium transport, electromechanical imbalance, accompanied by asynchronous relaxation and mechanical factors.

Pathological anatomy

Characterized by myocardial fibrosis associated with a violation of the intracellular metabolism of nitric oxide and calcium, as well as with proliferative processes caused by the action of insulin and IGF. The morphological basis of myocardial dystrophy in diabetes mellitus is microangiopathy, characterized by infiltration of mast cells and fibrinoid swelling of the walls of small vessels.Morphological examination reveals the development of apoptotic degeneration, the loss of synaptic vesicles, the appearance of large vacuoles in the cytoplasm of the cells of the sympathetic ganglia. During histochemical study, the deposits of glycoproteins are determined in the walls of the vessels. At the ultrastructural level, a thickening of the basement membrane of the vascular wall is determined. Great importance is attached to the disorganization of the muscle fibers of the hypertrophied myocardium.

Clinical picture and diagnosis

Patients with juvenile diabetes mellitus occasionally notice stabbing pain in the region of the heart.The occurrence of rest tachycardia is associated with damage to the vagus nerve and the relative predominance of the tone of the sympathetic part of the autonomic nervous system. Tachycardia is accompanied by ineffective myocardial contractions, which leads to depletion of energy resources and ultimately to a decrease in myocardial contractile function and the development of heart failure.

The size of the heart is within normal limits. Some muffling of heart sounds and systolic murmur at the apex are more often noted in patients with diabetes mellitus for more than 5 years.Further, hyperglycemia and insulin resistance are associated with an increase in LV mass and the onset of HF symptoms.

On the ECG, sinus tachycardia or bradycardia, ventricular extrasystolic arrhythmia, repolarization disorders: ST segment displacement, amplitude change, inversion, flattening, flattening or biphasic T wave, disturbance of intraventricular conduction are noted.

In echocardiography, the earliest sign of myocardial damage in diabetes mellitus is impaired diastolic function, which is noted in 27–69% of asymptomatic patients.

In the analysis of blood, the level of glucose in the blood plasma on an empty stomach> 7.0 mmol / l.


One of the main objectives of the treatment of patients with diabetic cardiomyopathy is the prevention of further progression of myocardial damage and the development of heart failure. It is important to combat risk factors: smoking, obesity, sedentary lifestyle, unbalanced diet. Lifestyle recommendations should include the rationale for an appropriate low-calorie diet for weight loss, smoking cessation, and regular exercise.

An important task is the normalization of metabolism, which includes the achievement of target levels of glucose, aglucosuria, normalization of the level of glycated hemoglobin. Regular physical activity can reduce insulin resistance, increase glucose tolerance, promote the utilization of blood glucose and free fatty acids in muscles, and have a beneficial effect on the functioning of the cardiovascular system.

Pharmacotherapy of type II diabetes mellitus is aimed at enhancing insulin secretion, reducing insulin resistance and is represented by drugs with various mechanisms of action: biguanides, sulfonylurea derivatives, glitazones, glinides, α-glucosidase inhibitors, insulin.The use of metformin improves blood glucose control in diabetic patients and reduces overall mortality by 36%.

To restore metabolic disorders in the myocardium, preparations of α-lipoic acid are prescribed, which activates mitochondrial enzymes, increases glucose oxidation, slows down gluconeogenesis and ketogenesis, as an antioxidant protects cells from the damaging effects of free radicals. Also used drugs that contribute to the correction of metabolic disorders in the myocardium: trimetazidine, trimethylhydrazinium propionate.



Dysfunction of the cardiovascular system – the appearance of a “thyrotoxic heart” is a frequent complication of thyrotoxicosis. Changes in the cardiovascular system in thyrotoxicosis (“thyrotoxic heart”) are caused by the effect of excess amounts of thyroid hormones (L-thyroxine and 3,5,3-triiodine-L-thyronine) on metabolic processes in the myocardium, hemodynamics and the sympathetic nervous system. One of the important effects of thyroid hormones is the uncoupling of oxidative phosphorylation, which leads to a decrease in the content of ATP and creatine phosphate in the heart muscle.As a result, anabolic processes are suppressed: the synthesis decreases and the breakdown of glycogen and protein increases, the content of potassium in erythrocytes and other cells decreases. Oxygen consumption by the myocardium increases, but the efficiency of its utilization in the process of biological oxidation decreases. With an excess of thyroxine, the permeability of the mitochondrial membranes is disturbed.

Under the influence of thyroid hormones there is an increase in the contractile function of the myocardium, probably due to the activation of the stimulating effect on the heart and the direct action of thyroxine on the heart muscle.Due to disturbances in energy processes and changes in the potassium-sodium pump, spontaneous depolarization in the cells of the sinus node accelerates, which causes more frequent formation of impulses in it. An excess of thyroid hormones alters the sympathetic and parasympathetic influences on the myocardium. With a high degree of thyrotoxicosis, as a result of a sharp decrease in the efficiency of biological oxidation, the predominance of protein breakdown over its synthesis, the level of energy resources and plastic processes decreases, which ultimately leads to inhibition of the contractile function of the myocardium.


The heart hyperfunction in thyrotoxicosis is based on an increase in myocardial contractility, which is due to both an increase in the activity of the sympathetic nervous system and the direct action of thyroid hormones on the myocardium. With thyrotoxicosis, abrupt changes in hemodynamics occur: the IOC increases (mainly due to an increase in heart rate), blood flow velocity and BCC. Peripheral vascular resistance in the systemic circulation decreases, and in the small circle increases.As a result, pulse pressure rises. The heart experiences diastolic overload, and the right parts of the heart also have systolic overload, the increased work of the heart occurs in an extremely unfavorable mode for it: due to changes in hemodynamics, the LV works under conditions of constant isotonic hyperfunction, and the right one – under conditions of a mixed type of hyperfunction (load volume and resistance) , however, there are no conditions for the development of compensatory myocardial hypertrophy (increased breakdown and decreased protein synthesis, reduced the amount of ATP and creatine phosphate).All this quickly leads to the development of HF.

Pathological anatomy

Histological changes in the myocardium in thyrotoxicosis are characterized by inflammation and degeneration up to the development of foci of necrosis and fibrosis. Histological changes in the myocardium are variable and nonspecific. The factors causing damage to the cardiovascular system in patients with diffuse toxic goiter, first cause dystrophic changes, and later degenerative-sclerotic.With a severe course of the disease, degenerative changes in mitochondria and their decay occur.

Clinical picture and diagnosis

Patients often complain of pain in the region of the heart, often aching, stabbing, often of angina pectoris, as well as palpitations that occur at rest, but inadequately increases with physical exertion. Patients report increased excitability, sweating, muscle weakness, hand tremors, and weight loss. A significant symptom is persistent sinus tachycardia, the severity of which corresponds to the severity of the toxic goiter.A tachysystolic form of atrial fibrillation is diagnosed in 10–20% of patients. An increase in SBP is characteristic, which is due to an increase in cardiac output. Shortness of breath is noted both during exertion and at rest. Heart failure, mainly right ventricular failure, is noted in 15-25% of cases. Symptoms of left ventricular failure are usually less pronounced because pancreatic weakness occurs very quickly.

On examination, precordial pulsation and pulsation of the arteries are noted. An increase in the sonority of heart sounds, especially the first, is determined by auscultation; systolic murmur at the apex of the heart and LA is almost always heard.

On the ECG, in addition to sinus tachycardia or atrial fibrillation, there is an increase in the amplitude of the P wave, sometimes changes in the QRS complex, a decrease in the ST segment and the voltage of the T wave.

At an early stage of the disease, echocardiography reveals moderate hypertrophy – thickening of the posterior wall, interventricular septum and an increase in LV contractile function. In the future, dilatation of the heart cavities develops, the mass of the myocardium increases, the systolic and minute volume of blood decreases, and the contractile function of the myocardium decreases.

In the blood serum, an increase in the levels of total and free thyroxine, triiodothyronine, a decrease in the level of thyroid-stimulating hormone is determined.


It is carried out in three directions: normalization of thyroid function (achievement of the euthyroid state), elimination of circulatory failure and restoration of sinus rhythm (with atrial fibrillation).

Compensation of thyrotoxicosis is achieved with the use of antithyroid drugs or surgery or radioiodine therapy.

To reduce sinus tachycardia, it is inappropriate to use cardiac glycosides, β-adrenergic receptor blockers are widely prescribed. With the tachysystolic form of atrial fibrillation, combined treatment with antiarrhythmic agents (propafenone) and β-adrenergic receptor blockers is performed, seeking to restore sinus rhythm or transfer atrial fibrillation to normosystolic form.

Treatment of HF has no specific features and must necessarily be carried out against the background of antithyroid therapy.It should be borne in mind that the sensitivity of the myocardium to digitalis glycosides may be increased.



The change in the demographic structure of society has led to an increase in the proportion of women in the older age group in the population (currently there are about 500 million women over 50 in the world, that is, in menopause).

The existence of a connection between a disorder of the heart and a change in the function of the female genital organs has been known for a long time.The disease can develop as a result of estrogen deficiency, not only during menopause, but also in young women with various gynecological diseases (uterine fibroids, endometriosis, etc.), with post-castration and premenstrual syndromes. Menopause cardiomyopathy is sometimes diagnosed in men (menopause is noted in 10–20% of males).


Menopause, not being a disease itself, leads to disruption of the endocrine balance in the body and contributes to the development of cardiovascular diseases.

In the pathogenesis of metabolic disorders, the violation of the activity of estrogens, which normally have a beneficial effect on protein and electrolyte metabolism in the myocardium and regulate sympathetic influences on the heart, is of primary importance. With pathological menopause, metabolic disorders occur in the myocardium, leading to dystrophic changes, in most cases of a reversible nature and only in some cases ending in the development of myocardiofibrosis (cardiosclerosis) (Scheme 8.2). The increase in the amount of abdominal fat and the development of abdominal obesity are associated with both physiological changes and lifestyle changes.Among the causes of abdominal obesity after menopause, one can single out a change in the energy balance – a decrease in the rate of metabolic processes along with an increase in appetite and an increase in energy intake from food against the background of an increase in the tone of the sympathetic nervous system, increased glucocorticoid stimulation and a drop in growth hormone levels. The pathogenesis of climacteric hypertension is based on hypoestrogenism, which is accompanied by an increase in the excitability of the hypothalamic-pituitary structures, a violation of the central and peripheral regulation of vascular tone.One of the mechanisms is the absence of the depressant effect of follicular hormone during menopause.

Clinical picture

The most common complaints are prolonged, almost constant pain in the region of the heart of a various nature, localized to the left of the sternum, in the apex. The pain is not triggered by physical exertion. Cardialgia does not stop after taking nitroglycerin. Characterized by a heartbeat with a normal pulse, not associated with physical activity, often appears at rest.

Patients often complain of a feeling of dissatisfaction with inhalation, the inability to inhale deeply, which is not associated with physical exertion and often occurs at rest.

Typical disorders of the autonomic nervous system: hyperemia or pale skin, sweating, hot flushes, palpitations, numbness of the extremities, chills, respiratory rhythm disturbances, polyuria, dizziness, thermoregulation disorders.

A large number of complaints are due to changes in the mental state: emotional lability, irritability, tearfulness, increased excitability, often depressed mood, fears, memory impairment.The aggravation of symptoms is associated with stress, especially emotional stress.

With pathological menopause, symptomatic hypertension often occurs. Subsequently, after the disappearance of hot flushes and other manifestations of climacteric syndrome, a neurotic state can cause the development of hypertension.

In most men with climacteric cardiomyopathy, some symptoms of pathological menopause from the genitourinary system are noted: absence or decrease (rarely increase) libido, decreased potency.Patients often complain of urinary disorders, which is usually associated with benign prostatic hyperplasia.

Vasomotor syndrome manifests itself in the form of hot flushes, that is, a sudden sensation of heat in the upper half of the body, face, neck, which is successively replaced by hyperemia and sweating. Along with the rush of blood in certain areas of the body, paresthesias periodically appear: a feeling of numbness, tingling, creeping creeps.

Menopausal cardiomyopathy may occur acutely or develop gradually.There is a mismatch between the intensity and duration of the pain syndrome and the satisfactory state of blood circulation.

An objective examination is characterized by a discrepancy between the abundance of complaints and the absence of clinical signs of coronary heart failure or heart failure.


On the ECG, the most frequent changes are ST segment depression and / or T wave inversion, which are mainly recorded in the right and middle chest leads (V 1-4 ). The T wave can be negative for a long time, then positive, and after a few days again negative without any connection with the clinical picture of the disease, against the background of a satisfactory condition of the patient.Changes in the ECG do not correspond to clinical manifestations, physical activity practically does not affect the configuration of the teeth. Sinus arrhythmia, atrial and ventricular premature beats, paroxysmal supraventricular tachycardia often occur. Occasionally, violations of atrioventricular and intraventricular conduction are recorded.

In the early stages, climacteric cardiomyopathy occurs more often in isolation and is characterized by a typical clinical picture of the disease. In later periods, the clinical picture depends on the addition of ischemic heart disease, inflammatory processes in the myocardium and other diseases, which undoubtedly aggravates the course of cardiomyopathy and worsens the prognosis.


Should be aimed at eliminating all symptoms of the disease. Lifestyle modification is important, including increased physical activity and adherence to a diet that limits saturated fat intake and increases the proportion of mono- and polyunsaturated fats and coarse fiber in the diet. To normalize the activity of the nervous system, sedatives, tranquilizers, and sometimes antidepressants are usually prescribed.

For the treatment of hypertension in postmenopausal women, it is most advisable to prescribe ACE inhibitors and diuretics, which should be neutral in relation to the parameters of carbohydrate and lipid metabolism.Postmenopausal women should be prescribed only highly selective new generation β-adrenergic receptor blockers that do not adversely affect lipid and carbohydrate metabolism.

Appointment of hormone replacement therapy is pathogenetically justified in the treatment of patients with climacteric cardiomyopathy. They use drugs containing estrogens and gestagens. Sex hormones suppress the increased activity of the hypothalamic-pituitary structures of the brain and indirectly affect the heart, normalizing the influence of the autonomic nervous system.It is possible that sex hormones weaken the increased activity of SAS and thereby normalize metabolic processes in the myocardium. Estrogens have a direct vasodilating effect on coronary vessels, and also normalize electrolyte and protein metabolism in the myocardium. Doses and total duration of treatment depend on the initial hormonal background and estrogen levels; treatment should be carried out under the supervision of an endocrinologist. It should be noted that climacteric cardiomyopathy is a self-healing disease in which hormones have only an auxiliary substitution effect, hormonal therapy should be prescribed for a long time.Treatment with hormones eliminates the painful manifestations of climacteric syndrome and after the end of age-related restructuring of the endocrine system, the disease disappears.


Generally favorable. The decrease in working capacity in most cases is temporary. The complete shutdown of patients from the usual work environment, as a rule, plays a negative role, leads to an excessive concentration of attention on painful sensations from the heart.


Metabolic disorders in the body are always reflected in the course of metabolic processes in the myocardium, often causing a violation of its function and structure.In various diseases, one or more metabolic pathways may initially be disturbed, which in the future will necessarily affect the energy supply of the heart muscle. With some metabolic disorders in the interstitial tissue of the myocardium and in the coronary vessels, pathological products of impaired metabolism of proteins, carbohydrates, minerals are deposited or excess components of normal metabolism accumulate. Such diseases include amyloidosis, glycogenosis, hemochromatosis, etc.



Amyloidosis is a systemic disease of unknown etiology, characterized by extracellular deposition in organs and tissues (mainly in the media of arteries, perivascular connective and nervous tissue, in the reticuloendothelial system, as well as in the myocardium, kidneys, liver, skin) of a special protein of β-fibrillar structure – amyloid …

Etiology and pathogenesis

Amyloidosis is a consequence of a violation of protein metabolism and can be acquired or hereditary.Hereditary amyloidosis is an autosomal dominant disorder. A number of authors associate the development of the disease with a change in the properties of tissue proteins due to autoimmune processes under the influence of an antigen-antibody complex. Dysproteinemia with the accumulation of coarsely dispersed protein fractions and abnormal proteins (paraproteins) in the blood plasma leads to the release of the latter from the tissue vessels with the formation of amyloid substances.

In recent years, a more accurate biochemical identification of proteins that make up amyloid fibrils has become possible, on the basis of which the types of amyloid have been identified, the relationship of certain types with clinical forms of amyloidosis has been determined, and precursor proteins presumably involved in protein synthesis have been studied.

There are four types of amyloidosis: primary (systemic), secondary, familial (hereditary) and senile (senile).

The most common primary type (85%) with a predominant heart lesion, in which amyloid is formed by light chains of immunoglobulin k and λ molecules (AL-type), is often associated with myeloma, is more common in men and rarely at the age of less than 30 years.

Secondary amyloidosis occurs as a result of the formation of non-immunoglobulin proteins, myofibrils contain non-immunoglobulin amyloid protein A (type AA), which often occurs in chronic inflammatory diseases – rheumatoid arthritis, tuberculosis, Crohn’s disease and familial Mediterranean fever.

Familial or hereditary amyloidosis is most often the result of the formation of a mutant prealbumin protein (transthyretin). An autosomal dominant type of inheritance has been established. The genes responsible for the synthesis of these proteins have been identified, and the nature of the gene mutations has been identified.

Senile cardiac amyloidosis, also known as SSA amyloid, is due to the formation of abnormal transthyretin in older individuals. There are two forms of age-related amyloidosis — atrial amyloidosis, which involves only the atria, and senile aortic amyloidosis, which is limited to the aorta.

Pathological anatomy

The myocardium with amyloidosis of the heart is very dense to the touch, thickened, little amenable to stretching. The volume of the heart cavities is not significantly changed or slightly increased. Amyloid is deposited in different parts of the heart, mainly in the myocardium of the atria and ventricles, the endocardium, in the valves, pericardium, often in the sinus and AV nodes, as well as in small arterial and venous vessels, including the vasa vasorum of the coronary arteries, narrowing their lumen up to full obturation.As a result, the muscle fibers of the heart are “walled up” in the masses of amyloid, which leads to atrophy of the contractile myocardium.

Clinical picture

Amyloid heart disease has no specific symptoms, develops gradually and can be asymptomatic for a long time, even if amyloid deposits are detected in the myocardium during biopsy. It should be noted that during the onset of symptoms there is a very significant infiltration of the heart with amyloid. Some patients experience pain in the region of the heart, sometimes angina pectoris, as a result of the accumulation of amyloid deposits in the coronary arteries.

In 10-15% of cases, there is orthostatic hypotension, sometimes with symptoms of syncope.

With auscultation against the background of muffled heart sounds, you can hear the systolic murmur of mitral regurgitation, with the development of HF – the protodiastolic rhythm of the gallop.

Various rhythm disturbances are often identified, which can often be the cause of sudden death. Some patients have severe bradycardia.

HF are detected in 45–56% of patients. Initially, right ventricular HF dominates with increased pressure in the jugular veins, hepatomegaly, peripheral edema, and ascites.Systolic dysfunction and congestive heart failure then occur.


Changes in the ECG are nonspecific, the most typical is the presence of bradycardia, a decrease in the amplitude of the teeth. Sometimes the presence of an abnormal Q wave and the absence of an R wave in leads V 1-3 simulate MI. The accumulation of amyloid deposits in the conducting system can cause various disorders of impulse formation and conduction – various conduction disturbances are possible, including complete heart block: atrial and ventricular arrhythmias are often detected (sick sinus syndrome, atrial fibrillation (in 30% of patients), ventricular extrasystolic arrhythmia ).

Two-dimensional echocardiography and Doppler ultrasonography are the main methods of non-invasive diagnostics. Examination reveals normal or reduced dimensions of the LV cavity with significant thickening of the myocardium and a characteristic violation of its structure with a diffuse granular luster (Fig. 8.1a, b). There is also a thickening of the interatrial septum and valve cusps, enlargement of the atria, the presence of a small or moderate pericardial effusion. Violation of LV and RV diastolic function occurs according to the restrictive type of violation of their filling.In severe cases, there are signs of varying degrees of impairment of the systolic function of both ventricles.

With fluoroscopy, a decrease in the pulsation of the heart contour is noted, the size of the heart is enlarged (cardiomegaly) and usually does not correspond to the severity of congestive heart failure.

Recent achievements include the introduction into clinical practice of the method of scintigraphy with the serum P-component labeled 123 I (SAP) to assess the distribution of amyloid in the body.The P-component is contained in a small amount (5–10%) in all types of amyloid; radioactive SAP injected into a patient with amyloidosis specifically binds to amyloid deposits and can be visualized and quantified on a series of scintigrams. The method is especially useful for monitoring the dynamics of amyloid tissue deposits during treatment.

Scintigraphy with technetium isotope 99m Tc-pyrophosphate, capable of binding to many types of amyloid, is also used for diagnosis, but this test turns out to be positive only with significant amyloid deposits in the heart, which can also be determined using echocardiography.

MRI is used to identify myocardial thickening and small size of the LV cavity in amyloidosis, which is comparable to echocardiography data.

The diagnosis of amyloidosis must be confirmed by endomyocardial biopsy. When studying tissue biopsies, it is important not only to identify amyloid, but also to conduct an immunohistochemical study to identify its type.

The diagnosis of “amyloidosis of the heart” is more often established during autopsy, since in a number of cases during life, objective reasons are not revealed that could explain the occurrence of pathological signs.


Therapy for primary amyloidosis includes cellular antiplasma therapy, which stops the production of light chains, as well as the use of alkylating agents (melphalan) and prednisolone. The beneficial effect of chemotherapy has been shown in two randomized trials. Stem cell transplantation with organ remission is promising in 50% of cases. Another approach to the treatment of cardiac amyloidosis may be the use of thalidomide with dexamethasone. Recently, lenalidomide has been shown to be effective.

Antiarrhythmic drugs are prescribed for the treatment of patients with cardiac arrhythmias. With the phenomena of complete transverse blockade and weakness of the sinus node, implantation of an artificial pacemaker is effective. Pacemakers are used to treat patients with severe, clinically pronounced conduction disorders.

HF is often refractory to drug therapy. For reducing circulatory failure, the main drugs are diuretics, which are used with caution in low doses, and vasodilators – ACE inhibitors or angiotensin II receptor blockers, although they are poorly tolerated and can cause significant hypotension or orthostatic symptoms, especially in patients with amyloid-induced dysfunction autonomic nervous system.It is not recommended to use digoxin because of its toxicity and the risk of arrhythmias, but with careful ECG monitoring, it can be used to control the rhythm in patients with atrial fibrillation.

Calcium channel blockers are ineffective in the treatment of cardiac amyloidosis. Patients may be hypersensitive to the negative inotropic effects of calcium channel blockers, and their use may lead to an increase in decompensation symptoms.

β-adrenergic receptor blockers can provoke life-threatening conduction disturbances.

With a sharp decrease in atrial contractility, indicating massive infiltration, even with sinus rhythm, the use of antiplatelet agents or anticoagulants is indicated, which is due to an increased risk of thrombus formation.

Heart transplantation is usually not performed, since relapses of amyloidosis occur in the allograft, as well as its steady progression in other organs, which reduces the life expectancy of patients.


The course of amyloidosis is progressive, the prognosis is unfavorable, although it depends on the form, timing of diagnosis and the degree of involvement of vital organs.Each of the four main types of amyloid disease has varying degrees of cardiac involvement, clinical symptoms, and prognosis. The survival rate of patients with senile amyloidosis is much higher than with primary amyloidosis – on average, respectively, 60.0 and 5.5 months from the time of diagnosis. Death (approximately 1.5–2.5 years after the first signs of heart damage appear) usually occurs due to rhythm and conduction disturbances, as well as extracardiac complications (pulmonary or systemic embolism).In patients with the involvement of the conducting system, sudden death often occurs. The lowest survival rate was noted in patients with congestive heart failure refractory to therapy (on average 6 months), a feature of which is predominantly right-heart or total type with a sharp swelling of the cervical veins and a significant increase in venous pressure, congestive liver enlargement and cavity edema (hydrothorax, hydropericardium, ascites).


Hunger and cachexia


Fasting, prolonged malnutrition, cachexia lead to disturbances in the activity of the heart, which are accompanied by a decrease in myocardial mass, usually proportionally less than a decrease in body weight due to atrophy of muscle fibers, degenerative changes in the myocardium and heart failure.

Pathological anatomy

During starvation, vacuolization of myofibrils, especially around the nuclei, changes in the chromatin of nuclei and mitochondria are observed microscopically. In advanced cases, brown atrophy and dystrophic changes in the myocardium are detected.

Clinical picture and diagnosis

The main manifestations of dysfunction of the cardiovascular system during fasting are sinus bradycardia, a decrease in IOC, a decrease in venous pressure and blood pressure (mainly systolic), which is often accompanied by dizziness, and with rapid movement from a horizontal position to a vertical one – fainting.Edema often occurs due to hypoproteinemia and an increase in BCC (but not HF).

On the ECG, deviation of the heart axis to the right, sinus bradycardia, low voltage of the teeth, sometimes changes in the T wave and QRS complex are noted, which, apparently, are caused by a violation of the metabolism of energy and electrolytes in the myocardium.

Treatment consists in restoring adequate nutrition.



Epidemiological studies indicate that obesity is associated with cardiovascular disease and premature mortality.Obesity itself leads to complex and prognostically unfavorable heart damage. The likelihood of developing LVH in individuals with normal body weight is 5.5%, and in obese individuals – 30%. According to the Framingham study, there is a highly reliable relationship between BMI, cavity dimensions and LV wall thickness.

According to modern concepts, obesity is an independent risk factor for the development of heart failure, being its cause in 11% of men and 14% of women in the United States. According to the Framingham Study, an increase in BMI for every 1 kg / m2 2 increases the risk of HF by 5% in men and by 7% in women, regardless of other risk factors.


Obesity can be an independent disease resulting from excessive consumption of high-calorie foods, or a syndrome that accompanies various diseases, and develops due to a number of neuroendocrine, social, behavioral and genetic factors. Genetic factors play an important role in the development of obesity. Research results indicate that there is a rarely identified group of genes that cause significant obesity, but more often identify genes for “susceptibility” that determine the tendency to obesity and regulate the distribution of fat mass in the body, the rate of metabolic processes and their response to physical activity and diet, control food intake. habits.More than 41 sites in the genome have been identified that are possibly associated with the development of obesity in the population.


In obesity, there is a gradual increase in the size of adipose tissue cells, leading to a change in their properties. The hormonal-metabolic shifts characteristic of obesity can directly affect the structure and mass of the myocardium. In obese patients, adipocytes of adipose tissue release a large number of biologically active substances involved in the regulation of vascular tone: angiotensin II, interleukins, prostaglandins, estrogens, IGF, TNF-α, plasminogen activator-1 inhibitor, leptin and others, which increases the risk of cardiovascular -vascular complications, while the level of adiponectin, a specific circulating protein of adipose tissue, which is involved in the regulation of lipid and glucose metabolism, decreases (Scheme 8.3). Leptin synthesized in adipose tissue, an important marker of energy balance, stimulates hypersympathicotonia, increases the level of ACTH, cortisol and aldosterone.

Changes in the functioning of the hypothalamic-pituitary system are of leading importance in the development of various forms of obesity. The endocannabinoid system, presented in the brain (hypothalamus) and peripherally in adipose tissue (adipocytes), liver, skeletal muscles and the digestive tract, through type 1 cannabinoid receptors (CB1) participates in the central and peripheral regulation of energy balance, as well as glucose metabolism and lipids, plays a role in controlling food intake and body weight.Hyperactivation of this system is associated with motivation for increased food intake and obesity and leads to disruption of the feedback mechanisms that maintain stable homeostasis.

Addition of hypertension in obesity occurs in about 60% of patients, the mechanisms of its formation are associated with the development of hormonal and metabolic abnormalities caused by the accumulation of adipose tissue. The key role among them is played by the development of insulin resistance and compensatory hyperinsulinemia, which, increasing sodium retention by the kidneys, contributes to the further growth of the BCC.Leptin, which stimulates the sympathetic nervous system, can also have a hypertensive effect. Obesity, hypertension, dyslipidemia and hyperglycemia, which are based on insulin resistance, are combined into the concept of “metabolic syndrome”.

With a high degree of obesity, a certain role of hypoxia in changes in the neuroendocrine regulation of blood circulation and in the development of myocardial dystrophy cannot be ruled out. The inclusion of a hypoxic factor in the pathogenesis of dystrophic lesions of the heart can become an essential mechanism not only for their occurrence, but also for the development of heart failure.


The heart of obese patients experiences volume overload. BCC and blood plasma volume increase in proportion to the degree of increase in body weight, which leads to an increase in LV filling and stroke volume, dilatation and an increase in LV mass. It is believed that the increase in cardiac output in obesity is physiologically associated with the satisfaction of the metabolic requirements of the increased tissue body mass. The development of cardiovascular complications in obesity is associated with the depletion of the compensatory mechanisms of the myocardium, due to an increase in the value of the BCC, which is formed in proportion to the volume of the vascular network of peripheral tissues.The increasing content of adipose tissue in the body desynchronizes the physiological relationship between the heart and the blood flow of peripheral metabolically active tissues.

Cardiac output at rest in severely obese patients reaches 10 l / min, and from ⅓ to ½ of this volume is used to provide blood flow in adipose tissue. The increased blood volume in turn increases venous return to the RV and LV, causing them to dilate, increasing wall tension. This leads to LVH, which is accompanied by a decrease in diastolic chamber compliance, leading to an increase in LV filling pressure and its expansion.

An increase in myocardial thickness reduces excessive tension of its fibers, which allows maintaining normal LV contractility, while simultaneously creating preconditions for diastolic dysfunction, which is based on a relative decrease in the number of capillaries per unit volume of muscle tissue and worsening conditions for oxygen diffusion in hypertrophied muscle fibers. As LV dilatation progresses, an increase in wall tension leads to systolic dysfunction.

Pathological anatomy

In obesity, there is an increased deposition of adipose tissue under the epicardium of both ventricles and in the superficial layers of the myocardium, which eventually leads to atrophy of muscle fibers, their replacement with adipose tissue (cor adiposum). The myocardium on the cut has a yellowish tint. The presence of diffuse muscle hypertrophy, which is the most characteristic manifestation of obesity on the part of the cardiovascular system, is revealed.

Clinical picture

In an adult, obesity is established with a BMI> 30.0 kg / m 2 .Clinically pronounced circulatory disorders develop in patients with BMI> 40.0 kg / m 2 .

Complaints of pain in the heart of a aching, stabbing character, palpitations and interruptions in the work of the heart during physical exertion. As excess body weight accumulates, progressive dyspnea gradually develops during exertion, orthopnea and paroxysmal nocturnal dyspnea occur, edema of the lower extremities appears, and an increase in the abdomen is possible in volume.

Many prospective studies have found that an increase in body weight leads to an increase in blood pressure.Patients with obesity have a high risk of IHD, which is especially aggressive and difficult.

The heart takes a “lateral” position due to the high position of the diaphragm, shifting to the left and somewhat posteriorly. Severe deafness of tones is determined by auscultation. The pulse tends to increase.

In extreme obesity, a clinical syndrome is sometimes noted, manifested by a combination of drowsiness, alveolar hypoventilation and pulmonary hypertension with pancreatic hypertrophy – Pickwick’s syndrome.


ECG usually shows sinus tachycardia, deviation of the electrical axis of the heart to the left, decreased ST segment in I – II and V 5–6 leads, flattened and negative T wave. In some patients, a low-amplitude P wave III and deep Q ІІІ . There are signs of LVH.

Echocardiography reveals LV hypertrophy and dilatation, an increase in the left atrium, and the diameter of the ascending aorta. With the help of Doppler echocardiography, signs of diastolic dysfunction are detected, and aortic regurgitation can be determined.Subsequently, there is a violation of the systolic function. Layering of the pericardial layers is possible due to the deposition of fat. EchoCG studies are often difficult due to the large thickness of the chest, narrowing of the intercostal spaces, and posterior displacement of the heart.

In the study of hemodynamic parameters, an increase in the BCC was revealed in all patients, which was accompanied by an increase in the rigidity of the LV myocardium, an increase in its filling pressure and SV. With increasing obesity, there is an increase in RV end-diastolic pressure, mean PA pressure, pulmonary capillary wedge pressure, and LV end-diastolic pressure.These changes cause the expansion of the cavities of the left atrium, RV and right atrium. As a rule, blood pressure in the pancreas is also increased.

The X-ray picture is always changed due to the high standing of the diaphragm and the accumulation of fat in the apex of the heart, which creates a picture of its apparent enlargement. The pulsation is sluggish, the tone of the heart is lowered.


Initial dystrophic changes in the myocardium in obesity are largely reversible with normalization of body weight.The first step in treatment is to correct dietary habits and increase physical activity. Specific recommendations include 30 minutes of physical activity at least 5 times a week, reducing food calories to an average of 1,500 kcal / day, reducing fat intake to 30-35% of daily energy value (with the proviso 10% for monounsaturated fatty acids, such as olive oil ), avoiding transgenic fats, increasing the consumption of foods containing fiber up to 30 g / day and avoiding liquid mono- and disaccharides.

Medicinal and surgical methods of obesity treatment are used to reduce body weight. Lipase inhibitors (peripheral agents) and anorexigenic agents (centrally acting) are prescribed.

Treatment of cardiovascular disorders in obese patients depends on the nature of the heart disease. For the treatment of hypertension, it is most advisable to prescribe ACE inhibitors and diuretics, which should be neutral in relation to the parameters of carbohydrate and lipid metabolism.Only highly selective beta-adrenergic receptor blockers of a new generation should be prescribed, which do not have a negative effect on lipid and carbohydrate metabolism.

In the presence of signs of HF, treatment is carried out in accordance with modern recommendations.



One of the forms of alcoholic heart disease, observed in 50% of people who abuse alcohol for a long time.

Alcoholic cardiomyopathy is detected in approximately ⅓ of all patients with non-ischemic cardiomyopathy, 40-50% of patients die within 3-6 years.


Ethanol and / or its metabolites are the etiological factor. The development of alcoholic cardiomyopathy can cause stress conditions, malnutrition (deficiency of proteins, vitamins), hereditary predisposition, viral infection against the background of decreased immunity, changes in the initial state of the myocardium. There is not always a clear parallelism between the amount of ethanol consumed, the duration of intoxication and the severity of heart damage.


The main metabolite of ethanol, acetaldehyde, has a direct damaging effect on the cellular and subcellular membranes of cardiomyocytes, associated with their ability to dissolve lipids and increase the fluidity of biological membranes.At a certain stage of intoxication, this can cause metabolic disorders in the myocardium and inhibition of the main pathways of energy utilization in heart cells, as a result of inhibition of the function of the respiratory chain of mitochondria, myocardial hypoxia occurs. An indirect effect occurs as a result of the influence of alcohol on various parts of the nervous system and the function of the adrenal glands.

Pathological anatomy

Long-term alcohol consumption causes fatty infiltration of the myocardium, degenerative changes in the walls of the coronary arteries and neurons located in the heart.Microscopic examination reveals the disappearance of the transverse striation of myofibrils, pycnosis of nuclei, interstitial edema, vacuole and fatty degeneration, sometimes single or multiple foci of necrosis, small areas of fibrosis.

Clinical picture

As a rule, patients stubbornly deny alcohol abuse.

A detailed clinical picture with symptoms of heart failure, persistent rhythm and conduction disturbances, thromboembolic complications, cardiomegaly are rarely detected.

The first clinical manifestation is most often rhythm disturbances without signs of congestive heart failure. The development of the disease has several stages – from functional disorders, transient heart rhythm disturbances to persistent myocardial hypertrophy with the subsequent development of heart failure.

The most frequent and typical clinical symptoms include:

  • agitation, hand tremors, fussiness, verbosity;
  • feeling of shortness of breath, cardialgia, tachycardia;
  • cold extremities;
  • sensation of heat throughout the body, flushing of the skin of the face, injection of the sclera;
  • sweating;
  • increase in blood pressure.

The initial signs of the disease are considered to be palpitations and shortness of breath during exercise. In the later stages of the disease, the patient’s condition gradually worsens.


On the ECG, characteristic changes are a shortening of the P – Q interval, lengthening of the Q – T interval in combination with a slight elevation of the ST segment and a pointed high T wave with a wide base, sinus arrhythmia, brady- or tachycardia. Often, rhythm disturbances (atrial and ventricular extrasystolic arrhythmia, atrial fibrillation) and conduction (atrioventricular and intraventricular blockade) occur after prolonged and / or single consumption of large amounts of alcohol (“festive” heart syndrome).

The absence of a definite cause of atrial fibrillation (thyrotoxicosis, rheumatic heart disease) in young men may indicate the presence of alcoholic cardiomyopathy.

Diagnosis is also made difficult by the absence of markers of alcoholic heart disease.

It is easier to diagnose alcoholic cardiomyopathy if there is a history of long-term alcohol use and clinical signs of cardiomegaly, arrhythmia, or congestive heart failure are determined in the absence of other causes that can lead to similar cardiac disorders.

An echocardiographic study reveals dilatation of the LV cavity, a decrease in its contractility, and diffuse hypoxia is possible. Doppler imaging may show signs of mitral regurgitation.


Alcohol consumption must be excluded during treatment. Complete withdrawal can stop the progression of heart damage early (usually in the first 2–6 months).

In the early stages without manifestations of HF and in the presence of cardialgia, tachycardia, hypertension and arrhythmias, β-adrenergic receptor blockers are recommended.With severe cardiomegaly, cardiac glycosides should be prescribed, however, their intake should be strictly controlled in order to prevent the cardiotoxic effect. Complex treatment includes diuretics, vitamins, anabolic hormones, potassium and magnesium salts.


With a complete refusal to drink alcohol and under the influence of treatment, the size of the heart in patients with alcoholic cardiomyopathy often decreases. The restoration of the basic functions of the myocardium and the improvement of the general condition occur very slowly, the periods of relative recovery are calculated in months and years.


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Heart tumors, myxoma – diagnostics and treatment in St. Petersburg, price

Tumors of the heart are neoplasms of different structure, arising from the tissues of the heart itself or growing into them from other organs. Neoplasms can invade the heart muscle, pericardium, affect the valves and septa of the heart.

Classification of tumors

All cardiac tumors can be divided into PRIMARY (developing from heart tissue) and SECONDARY (occurring as metastases of a primary non-cardiac malignant tumor).Primary heart tumors occur in cardiology with a frequency of up to 0.2%; secondary (metastatic) – 25-30 times more often.

Primary tumors are classified as benign (75% of all primary tumors) and malignant (25%).

Benign primary tumors:
  • myxoma (75% of all benign cardiac tumors)
  • lipoma
  • papillary fibroelastoma
  • rhabdomyoma
  • fibroma, hemangioma, teratoma and other tumors are less common
Malignant primary tumors:
  • sarcoma (angiosarcoma, leiomyosarcoma, rhabdomyosarcoma, fibrosarcoma, liposarcoma, osteosarcoma)
  • lymphoma
  • mesothelioma

Symptoms of myxoma

The clinical picture of the disease is extremely diverse and not very specific, depending on the localization of the tumor, its mobility, the presence of a “leg”, size, ability to fragmentation, the possibility of germination into the cardiac conduction system.Patients are worried about shortness of breath, chest pain, dizziness, fainting, various types of arrhythmias.

The defeat of the conducting system is manifested by a variety of rhythm and conduction disturbances (blockade, paroxysmal supraventricular and ventricular tachycardias). As a rule, this is typical for tumors growing in the thickness of the wall (fibroma, rhabdomyoma) of the heart.

The most common myxomas are a jelly-like consistency of education, localized in all chambers of the heart (more often in the left atrium – up to 75%), having a leg of various widths, which they attach to the wall of the heart chamber.

Mixomas are dangerous because:

  1. 1. Violate intracardiac hemodynamics, creating an obstacle to blood flow through the valves, causing a picture of valvular stenosis or insufficiency; the severity of complaints often depends on the position of the patient’s body.
  2. 2. Lead to embolism, causing strokes, kidney and intestinal infarctions, ischemia of the extremities. This happens due to the detachment of “pieces” of the tumor and blockage of blood flow in the affected organ outside the heart.

Diagnosis of heart tumors

Relatively rare occurrence, varied localization in the chambers of the heart, differences in structure and size make the diagnosis of neoplasms a difficult task. A number of surveys are currently in use:

  1. 1. ECG is not very informative, but, due to its availability, it is often used and allows one to suspect myocardial hypertrophy, conduction and rhythm disturbances, myocardial ischemia, etc.d.
  2. 2. Chest X-ray reveals an enlarged heart and signs of pulmonary hypertension.
  3. 3. Echocardiography (transthoracic and transesophageal) in the vast majority of cases provides enough information about education and the most optimal way to treat it.
  4. 4. MRI and MSCT of the heart is used when there is insufficient echocardiographic data.
  5. 5.Ventriculography and probing of the heart chambers are currently rarely used in the diagnosis of neoplasms.

Indications for operation

Each specific case of the disease is unique and requires an individual approach. Nevertheless, we can say for sure that the presence of myxoma in the heart cavity is an indication for its elimination by surgery, since the risk of fatal complications is very high.

Lipomas, hemangiomas often require monitoring and control over time.Most often, benign neoplasms can be removed radically, with a low probability of recurrence, which is achieved by excision of the formation with the surrounding tissues and subsequent plasty of the resulting defect. Sometimes in such patients, after removal of the formation, a violation of the anatomy of the heart valve apparatus is revealed, which requires its plastic or (less often) valve replacement.


Patient operability should be assessed if a malignant heart tumor is suspected.Most often, such patients fail to perform radical surgery; surgical treatment is combined with radiation or chemotherapy and is palliative.

All cardiac tumors carry the potential danger of deadly complications, namely: heart failure, arrhythmias, pericarditis, cardiac tamponade, systemic embolism.

Patent ductus arteriosus

Anatomically, this duct is a short vessel connecting the descending aorta with the pulmonary artery.Since it is a physiological shunt, it is necessary for the fetus to live in the womb. Immediately after the first breath, it is no longer needed, and after a few hours or days it closes on its own. If this does not happen, then the message remains, and blood continues to be shunted from the large to the pulmonary circulation.

With rare and exceptions, patent ductus arteriosus (Botallov) is perhaps the most harmless, “harmless” of all congenital heart defects. The heart, although it is enlarged, copes with the load quite easily.The pressure in the pulmonary artery system is slightly increased. Children with this defect develop and grow normally and, with the exception of a “murmur” in the heart, usually do not differ from their peers in any way. However, with a large duct, there may be signs of heart overload and clinical signs in the form of more frequent colds, shortness of breath on exertion. Then you have to do something. Here we will make a reservation that with huge ducts, 9 mm, and even more, when their diameter exceeds the size of the aorta itself – the main artery of the body, the newborns are extremely difficult in their clinical condition, progressive heart failure, a huge heart occupies almost the entire chest, displacing the lungs interfering with their normal functioning.The operation is urgent, it is performed for health reasons.

A special picture develops with persisting patent ductus arteriosus in premature infants. The situation can develop according to different scenarios. With a small diameter of the duct and a body weight of more than 2 kg, the situation is usually not an emergency, the duct has a chance of self-closing, the child copes with the load on the heart, observation is enough. But with a baby weighing less than a kilogram, in an incubator (a special medical bed for nursing newborns) and unable to breathe spontaneously, i.e.that is, constantly breathing with the help of an artificial respiration apparatus, even a duct with a diameter of 3-4 mm causes huge hemodynamic disturbances. Transportation of such babies to a cardiac surgery hospital (and to any other) is associated with a huge risk for them, and therefore often cardiac surgeons go to maternity hospitals and hospitals where babies with such extreme low body weight are nursed, and there, on the spot, an operation is performed to eliminate the duct …

After surgery, the risk of which is almost zero, children feel great, and they and their parents quickly forget the unpleasant moment in their life.The ligation of the patent ductus arteriosus is radical, i.e. a completely curing operation, and after it the person is practically healthy.

Strictly speaking, patent ductus arteriosus is not a congenital heart defect, because his heart is normal. It is assigned to this group because of its importance in fetal circulation and because of the disturbances to which it can lead to untimely closure. Old, “pre-surgical” textbooks indicate that it is possible to live with this defect only up to 35-40 years.

In recent years, thanks to the emergence of new instruments and the accumulation of experience, the patent ductus arteriosus is increasingly closed using X-ray surgical techniques. This is done not in an ordinary operating room, but in an X-ray surgery room, and you can read about the procedure and preparation of the child above, where catheterization and cardiac catheterization are described.

In this case, a special catheter with a device at the tip, which will close the duct from the lumen of the descending thoracic aorta, will be inserted into the child by puncture (puncture) of the artery in the thigh, at the very top.The procedure takes 1-1.5 hours and compares favorably with the operation, in which you still need to open the chest with a sufficiently large incision, leave a drain (a tube to remove air and fluid), which will be removed only the next day. Now, with the help of various devices (spirals, occluders), it is possible to close a duct of almost any diameter and shape. But an operation, even such, is an operation, and if it can be avoided by obtaining the same effect, then it should be done.

By the way, the operation of ligation of the patent ductus arteriosus was first performed in 1938, and this date is considered the year of birth of surgery for congenital heart defects.

Heart monitoring

The heart is the main “motor” of the human body. Therefore, the study of its work requires a high accuracy of the parameters. Holter monitoring of the heart is one of the types of research on the work of the cardiovascular system.

The heart is the main “motor” of the human body. Therefore, the study of its work requires a high accuracy of the parameters. Holter monitoring of the heart is one of the types of research on the work of the cardiovascular system.The method was founded by Norman Holter, after whom the portable research instrument is named.

What is a Holter?

Diagnostics is a long-term recording of the electroactivity of the heart. You can record data using a special device for a whole day. The holter is attached to the patient’s belt during the examination. The patient is not limited in his movements for the duration of the study – he simply wears the device around the clock on his belt.

Using the device, determine:

  • blood pressure surges;

  • pathology of vascular and heart activity;

  • cyclical changes in the work of the heart;

  • the work of the myocardium.

Holter blood pressure monitoring can be performed for about 7 days. With the help of the study, pressure drops in the blood vessels are recorded and cardiac changes are detected. Holter research gives the doctor a complete picture of the work of the heart and blood vessels.

The device registers the electrical activity of the heart. When the organ is working, a certain electric field is formed. The device reads all changes in its parameters. The method is based on the properties of electrocardiography and allows you to identify the slightest changes in the work of the cardiovascular system.

Indications for Holter examination

The main indications for diagnostics are:

  • arrhythmia attacks of unknown etiology;

  • myocardial ischemia;

  • congenital heart defects;

  • hypertension;

  • angina pectoris;

  • frequent dizziness;

  • heartache;

  • evaluation of the work of the pacemaker.

The study helps to identify the causes of recurrent or persistent heart pain. Tingling sensation can occur without physical exertion, when turning the torso or in a supine position. The device gives an accurate clinical picture of various disorders in the work of the heart.

With the help of holter, the causes of arterial hypertension and hypertension, a previous heart attack, are identified. Diagnostics shows the localization of ischemia, the daily conductance of the organ, the degree of danger of the defect, an attack of arrhythmia.It helps to identify the features of episodes of the disease, which are accompanied by pain in the heart. The daily ECG shows the reaction to various stimuli and helps to establish an accurate diagnosis.

The modern Holter system helps to identify the risk of developing a serious cardiac disease and reduces the risk of cardiac arrhythmias. The latest generation devices detect the slightest changes in the work of the heart.

Keeping a diary during examination

The diary of daily monitoring of the work of the heart helps the doctor find the best solutions to eliminate the disease.From the recorder, wires leave, which are connected to special sensors on the body. The device records the sensor signals.

At the time of the diagnosis, the patient is given a diary in which the patient writes down all the symptoms and sensations. The patient indicates the start and end times of seizures, dizziness and other unpleasant conditions. On the device at this moment, he presses the desired button. Holter ECG records all changes in heart rate.

In some cases, the doctor prescribes the implementation of moderate physical activity – you need to climb stairs or do a couple of exercises.All changes in the work of the heart are recorded by the device. Before the start of the test, the time is recorded in the diary. All changes and feelings before and after the test are entered into the form.

Contraindications and side effects

Diagnostics dictates its own rules – during the study, you cannot:

  • take a shower;

  • hitting the device;

  • expose yourself to high or low temperatures;

  • expose the device to the action of an aggressive environment;

  • subject the device to vibration;

  • overload your body with exercise;

  • take alcohol;

  • smoking;

  • abuse coffee.

As for the contraindications to the diagnosis itself, there are practically none. Monitoring is prescribed with caution during pregnancy and in case of mental disorders.

The device does not cause any discomfort or pain. The only drawback may be inconvenience during sleep.

Runner’s heart rate. What you need to know and how to use this knowledge

Running is one of the most accessible types of physical activity, with definite training results.Even if you do not set any specific sports goals for yourself, you still develop some function of your body: you improve your overall health, recover from tough competitions or workouts that were yesterday or the day before yesterday, increase the body’s endurance and burn fat, expand the aerobic capacity of the body, increase the ability to a speed that you have never run at all or could only run a very short distance. Each of the goals is achieved with the help of a certain load, well, where there is a load, there will also be a heart rate, which in a running environment is usually measured in units of “beats per minute”.

Running heart rate is a very good and objective indicator (because expressed in numbers) of the load on your body – the higher the heart rate, the higher the load, the more the body uses up energy, but also the faster you can run. This suggests a close analogy with the movement of a car – the more you press on the gas, the more fuel enters the engine, the more power is generated when it is burned, and the faster the car goes.

If you are an athlete who is actively involved in sports, if you are an amateur who regularly participates in competitions, then we have special discount cards for you that allow you to receive significant discounts on the equipment, shoes or clothing you need.

However, it should be noted that this analogy has an even deeper meaning: with different fuel supply, with different engine power output, different things happen – when you just start the car and start off, the car barely picks up speed, then – switching to second gear you accelerate even faster, after switching to third speed you can already overtake slower fellow travelers, at fourth speed, at above average rpm you have access to cruising speed on the freeway, well, fifth or sixth speed is already for that, when you need to get from point A to point B very quickly, or there is no speed limit on the highway.

It is impossible to reach a speed of 100 km / h at the first speed, just like starting from a traffic light at “fourth” is very bad for the engine of the car. Each switch has its own job. Each “speed” is for a specific application.

The same is the case with the heart rate. At first, you warm up and run very slowly – the pulse value in this case will be barely distinguishable from the state of rest. Further, you increase the speed, and the pulse also begins to gradually increase.After that, you go to your usual speed, the pulse also reaches a higher value. But, here you decide to add more, for example, you want to overtake some slower runner in a race, or you want to improve your final time, which you achieved the last time. Even more speed – even more heart rate, now – you are just a bird flying low over the asphalt or trail track at this moment. The speed is pleasant for you, everything is easy, no hard feelings. However, you decided that it would be good to accelerate harder and put more power into your “engine” – the speed increased to the maximum and you cannot run faster purely physically.The pulse is at the highest value and it seems that a little more and your heart will jump out of your chest. That’s all, the limit to your physical capabilities, your “car” cannot “go” faster in any way – the pulse is at maximum, the legs do not run, it is dark in the eyes.

An important conclusion that can be drawn from the idea that at a certain speed you can get a certain result, what at a certain heart rate, (more precisely, in a certain range), it is also possible to achieve a strictly defined training result.That is, if you need to lose weight, then you need to run in the heart rate zone in which fat is burned. You need to train endurance, pump the cardiovascular system – you run in another zone. If you want the muscles of the body to become stronger, you also run in a certain zone.

What if you start to run very slowly, barely changing from walking, and your heart rate is already very high> 180 beats?

This may mean several things:

  1. You are very overtrained and your body is not yet fully rested.You do not need to continue jogging – walk and even slowly until your heart rate returns to acceptable levels.
  2. You are in poor physical shape, most likely you are a beginner and you, to begin with, you need to regularly walk a certain number of kilometers. At first, it may not look very interesting – you probably decided to run a marathon already this fall, but the truth is, and it is true that if your heart rate when walking with a slight tension “scales” for a value of 160-180 beats, then your heart just not ready for such loads and you need to start with walking, gradually, and in very small doses, adding the transition to light running.For people who are just starting to run, the transition “walking> jogging” can be one year, after which you will be able to run at an acceptable heart rate for an hour and a half at a slow pace.
  3. You have questions about the work of the cardiovascular system and you urgently need to see a specialist doctor. Continuing training is not worth it at all and in any way – health is more expensive!
  4. Your body is severely depleted by high loads, it is extremely low in carbohydrates – fuel for running and water for cooling the body.

Special sports nutrition and drinking with isotonic drugs can compensate for the loss of carbohydrates and water.

We recommend you a detailed article about what “sports nutrition” is, why you need it and why it allows you to qualitatively replenish the expended energy and increase productivity during training or in the process of competition.

All isotonics in “Kant”

All sports nutrition in “Kant”

Why do all people have different “heart rate zones”?

The fact is that people are all different – one has a weight of 70 kg, another has 90, one is a beginner, the other is a master of sports in athletics and is included in the “ten” best results at the Moscow Marathon, one runner is only started training and his cardiovascular system is far from ideal, and the other has been training for 15 years and has already run 20 marathons.In total, there are several main factors that affect the heart rate:

  • Body weight.

    People who are overweight have a high percentage of body fat and high heart rates compared to those who have less fat. Fat is a ballast that the body needs to carry over a distance, the more it is, the more muscles have to “work”, the more the heart has to pump blood to feed them and the higher the pulse.

  • Training level.

    The higher the level of fitness, the greater the body’s ability to use the cardiovascular system to assimilate oxygen dissolved in the blood, which is pumped by the heart from the lungs to the muscles. Higher training – the heart needs less effort, pulse – lower, lower training – the heart rate is higher.

  • Smoking and drinking alcohol.

    Bad habits that affect the state of the cardiovascular system and increase the value of the pulse.

  • Air temperature.

    In case of heat, the heart, in addition to delivering oxygen-enriched blood to the muscles, also works to cool the body, performing, in fact, double work. Double work = more effort = higher heart rate.

  • Painful condition. Before, during training, immediately after. Moreover, if you have recently been ill with COVID-19.

    Intensive running lowers the immune system, and then there is the disease with its viruses and bacteria, as well as drugs.Naturally, the heart begins to work much more intensively in order to saturate the blood with the necessary elements to increase immunity, but if it is more intense, it means that the pulse value will definitely be far higher than the usual numbers.

  • Stress and tense emotional state.

    The nervous system during stress works with great tension, the pulse in a state of physical rest can go off scale for 100 beats per minute. During stress in the human body there is an increased production of the corresponding hormones (adrenaline and norepinephrine), which “accelerate” the heart.Most athletes, going to a responsible start, notice an increased heart rate even before they crossed the starting line – this is just a consequence of the action of hormones. And imagine that additional strokes from physical stress are added to the value of the pulse from emotional stress … Of course, the value of the number of beats per minute will be higher.

How to define heart rate zones?

In order to understand exactly how “heart rate zones” are defined, let’s clarify the terminology.There are concepts of heart rate – heart rate and pulse. Heart rate is the number of heartbeat cycles, a physiological indicator of the heart rate for a certain period, and “pulse” is the number of blood impulses that the heart pushed out after contraction, which created a measured oscillation of the artery walls that arose over a certain period of time.

A more accurate parameter for determining the “heart rate zones” is the heart rate, i.e. the number of heart cycles, not the pulse, which, in fact, is a consequence of the heartbeat cycles.

The heart rate value (like the pulse) is a purely individual value and depends on the temporary and permanent factors that we have given above. The pulse zones are calculated from the MHR value – the maximum value of the heart rate. MHR is the highest number of heartbeats per minute, which is achieved at the maximum capacity of the body during intense training. This is the highest number of beats per minute your heart is capable of performing at maximum load.

To calculate the MHR, you should not use mnemonic rules such as “…. (digit) – age = MHR “. Everyone’s organism is different and such an equation has no scientific explanation.

MHR is best recognized in special laboratories, where there is the necessary equipment in the form of treadmills and heart rate monitors.

For the same reason, it makes no sense to calculate heart rate zones in absolute numbers. Qualified physiologists and sports physicians claim, and we agree with them, that at present it is correct to calculate the heart rate zones, relying not on specific heart rate numbers, but on the percentage of the HRM found during the test in the laboratory.

Knowing your own indicator of the maximum heart rate, you can calculate your own, personal heart rate zones and make your training plan, which will develop certain qualities, and with which you can prepare for important starts.

A competent training plan should include training of various orientations – for “pumping” certain qualities: an increase in general physical endurance, the development of speed-strength qualities, recovery training after heavy loads and pre-competition, unloading periods.

What quality is trained in each heart rate zone?

From resting heart rate to MHR, there are different heart rate zones that correspond to workouts of varying intensity. Currently, a gradation of five pulse zones has been adopted. Training in each of the zones has its own characteristics and gives a certain result.

1. Very low intensity wellness area (white / gray).

50-60% of the MHR. This is where general physical endurance improves.Training in this zone improves overall fitness, facilitates recovery from challenging and prolonged workouts, and prepares runners for high heart rate workouts. Training in this area is the most comfortable, easy and accessible even for beginners. This zone is best suited for those who are either just starting to exercise, who are overweight, or have a low overall level of physical fitness – the base.

2. Fitness area (blue).

60-70% of the MHR.Training in this zone also helps to increase overall endurance. When exercising in this zone, the connection of fats as energy sources begins, the quality of muscle fibers increases, and the density of the network of capillaries through which oxygen is delivered to the muscles begins to increase. Training in the second zone is an essential part of the training program for every runner looking to lose weight. Training in this zone will increase the total calories burned compared to the previous zone.The condition of the cardiovascular and respiratory systems is significantly improved.

3. Aerobic zone (green)

70-80% of the MHR. Most effective endurance training area. This type of running trains the aerobic capabilities of our body, i.e. the ability to absorb oxygen and transfer it as efficiently as possible to the muscles. Training in this area stimulates the development of a large network of small capillaries. The number, elasticity and diameter of blood vessels increase, the volume of the lungs increases, the functional state of the respiratory system improves, and the heart becomes stronger.Training in this zone increases the efficiency of blood circulation in the heart and skeletal muscles. When exercising in this heart rate zone, lactic acid begins to enter the bloodstream.

4. Anaerobic zone (yellow / orange).

80-90% of the MHR. Training in this zone develops maximum performance and improves speed endurance, i.e. the ability to run quickly and for a long time. When the pulse reaches 90% of the MHR, oxygen, which is carried by the blood, begins to be insufficient for oxidative reactions, so the cells go into anoxic anaerobic mode.Fats in this zone are practically not burned, and carbohydrates stored by the body are used to obtain energy.

A by-product of metabolism in anaerobic mode is lactic acid, which begins to be secreted especially intensively. It causes an ever-increasing feeling of fatigue in the muscles, so training in the anaerobic zone will not work for a long time. In this zone, short-term high-intensity training is usually planned and performed. The result of training is an improvement in the indicator of maximum oxygen consumption, which means that the “acidification” of muscle fibers in trained runners will come later.The value of the threshold of anaerobic metabolism, at which the body ceases to utilize lactic acid, is also pushed to the larger side. Endurance is greatly improved.

5. Zone of maximum effort (red)

90-100% of the MHR. Training in this area develops maximum performance. The body learns to work at the limit of its capabilities, spending all available energy reserves, the respiratory system and the cardiovascular system work with the maximum possible efficiency, at the limit of their capabilities.Lactic acid will intensively accumulate in the blood, and after a few minutes you will not be able to continue the exercise due to total fatigue. Training in this area is typical for professional athletes in the pre-competition period. For people who want to lose weight or simply improve their health, being in the “red” zone is highly discouraged, neither in the competitive nor in the training period. If you have driven yourself into this zone, then our recommendation is to get out of it as quickly as possible.

How to control in which “heart rate zone” do you train?

This can be done in the following ways:

1. Calculation of heart rate on the carotid artery or wrist.

A method that has practically never been used anywhere, but it may come in handy if you have doubts about the accuracy of the indicators of your modern electronic gadgets that measure heart rate.

Place two fingers on the inner side of the wrist or in the carotid artery, on the neck.It is in these places that the pulse is felt in the best way. You count the number of beats in 15 seconds, the indicator is multiplied by 4. The method is inconvenient in that it cannot be used on the go and the heart rate value cannot be fixed during the entire time of your workout.

2. Use of electronic heart rate monitors.

Currently, there are several types of such devices and methods of reading heart rate values ​​with their help.

Among the many varieties of gadgets, the models with a chest mount are the most convenient and most accurate.The sensor located on the belt picks up electrical impulses from the heart during a stroke and transmits these values ​​via a Bluetooth radio channel to receiving devices, which can be a special device, a wristwatch or a smartphone with a fitness app installed.

After you receive data on your MHR and calculate the values ​​of your heart rate zones in specific numbers of heart rate, you enter these values ​​into watches, statistics systems, and also into your fitness applications.

During a training process or a competition, heart rate sensors transmit heart rate data to your watch or smartphone, and you see on the screen of your watch or smartphone in which “heart rate” zone your current heart rate is located.After training or competition, this data is saved in the statistics system and you can later analyze how accurately you performed the tasks of the training plan.

All sports watches and heart rate sensors in Kant

Key models:

Special article on the use of gadgets in running training

A detailed article on the Suunto sports watch.Overview of important “chips” and necessary functions

How do I use my heart rate zones for training?

First of all, it should be noted that each training plan is made exclusively for a specific runner, for his goals and objectives, taking into account the physical condition in which the runner is before the start of the training process, taking into account the time before the key start for which the person is preparing.

If you want to train with high quality, we recommend that you contact our partners – companies that have proven themselves in the organization of training processes:

For quality workouts you will definitely need:

  • running shoes
  • Quality Running Clothes
  • If you are going to do trail running, then running backpacks will be difficult to do without
  • belt bags will help you take everything you need for a run: phone, keys, wallet, gels, water bottle, etc.p.
  • special bottles and flasks for water. Different volume and color
  • massage balls, rollers, cylinders, fitness bands, training loops – this is what will help you during physical training and in the process of recovery after runs
  • running sunglasses
  • sports nutrition – to maintain your tone on the races and to recover after
  • bandages and tapes will help you recover better and faster or protect you from injuries

The goal of any training plan is the development, improvement of completely specific, physiological parameters, physical and mental qualities.Well, since there is a meaningful “goal”, then it is obvious that there is a certain starting point – something from which you begin your path to the goal. In order to understand what state you are in, why you “start”, what you need to train, we recommend that you undergo special testing – a treadmill test in a laboratory or a medical center, which objectively, in “numbers”, will show – in what state your body is in.

Treadmill test is a test of an athlete on a treadmill with an assessment of the functional state of his cardiovascular system, the level of BMD (maximum oxygen consumption), clarification of the MHR and TANM (the threshold of anaerobic metabolism or lactate threshold, after which the body is no longer able to process the secreted milk acid enough).Such testing allows you to detect a dangerous pathology on the part of the cardiovascular system even before the start of intensive running exercises, since it is carried out at the limit of the body’s functional capabilities.

The test results in a “digital” picture of your condition. Based on these data, your “heart rate zones” are determined, your training plan is built, which should develop what you need to develop and what is desirable.

Heart rate training tips:

  1. All runners should alternate the first four heart rate zones during their workout.The training process should include training in all zones. Keep the “red” zone for competition when you are at the top of your fitness.
  2. The warm-up should be based on the principle: “first we turn on the first gear and drive very slowly, when the engine warms up then we will strain it.” The overwhelming majority of professional trainers say that a warm-up before the workout itself is an urgent need, but it should smoothly immerse the body in an increasing load, stretching unheated muscles is traumatic.Light jogging with heart rate acceleration to the second heart rate zone so that the muscles are saturated with blood is the best prelude to a good warm-up.
  3. Recovery training after high intensity training is just as important as any workout before and should be done entirely in the green or blue heart rate zone.
  4. Recovery is just as important as stress. Lack of recovery, “more and more”, deviating from the training plan – one of the most common mistakes beginner runners make, directly leading to injuries and depressed emotional background.Recovery time – for both physical and emotional relaxation. If, after the recovery period, during training, you see that your heart rate is “off scale”, that at the usual speed your heart rate “flies” to a different heart rate zone, this is a sign that you are not well rested and you need to lower your ambitions about the intensity of training. …
  5. Interval training is just as important as long or tempo training. Beginner runners often neglect them, but they must be done.The settings in your gadgets will help you to control being in a certain heart rate zone, without going to the “maximum”.
  6. If your main task is to “lose weight”, then you need to alternate training in the fitness – “green” and aerobic – “orange” zones – №3 and №4. However, if this is not enough for you, and you want to improve your own endurance, for example – to achieve the best time on official races, then you can increase the number of anaerobic training in the “orange” zone – number 4.
  7. Perhaps one of the easiest ways to explain the difference between aerobic and anaerobic zones is to say, “If you can talk calmly while running, then this is your aerobic zone. If you run at such a speed that you cannot speak freely, then you are running in the anaerobic zone. ”

Going to training with a specific goal, run, focusing on your heart rate, trying not to go beyond a specific heart rate zone – so you can progress without injury and emotional burnout.

It’s never too late and never too early to start training with running. Running is an extremely democratic sport available at any age. Before starting any training cycle, be sure to consult a doctor, get tested and get admission to jogging.

We highly recommend buying everything related to running after a personal visit to the Kant store and consultation with our professional salesmen.

If you live in a city where there are no our stores, then this is not an obstacle to purchasing what you need.Simply, when making a purchase through our online store, please note that we have delivery by couriers and transport companies.

You can also use self-pickup if it is more convenient for you

However, if you are sure of the model, if you are sure that the specified size or size will suit you 100%, then our online store is at your service. When buying via the Internet, we offer various payment systems:

  • in cash to courier
  • by bank transfer
  • by card
  • by installments
  • with gift certificate

All details on different forms of payment

New items in Kant:

We also recommend you useful articles on “running” topics:

Upon purchase, you can apply the accumulated or welcome bonuses for the first purchase.To do this, you need to register in the new bonus program “Kant” and receive welcome bonus rubles to your account only for registration.

90,000 Drowning. First aid for drowning

Drowning – terminal condition or death due to aspiration (penetration) of fluid into the airways, reflex cardiac arrest in cold water, or spasm of the glottis, which as a result leads to a decrease or cessation of gas exchange in the lungs.

Drowning – a type of mechanical asphyxia (suffocation) as a result of water ingress into the respiratory tract.

There are the following types of drowning:

  • True (wet or primary)
  • Asphytic (“dry”)
  • Syncopal
  • Secondary drowning (“death on water”)

True Drowning

A condition involving the penetration of fluid into the lungs, occurring in about 75 to 95% of deaths on water.A characteristic long struggle for life.

Examples of true drowning are freshwater and seawater drowning.

Fresh water drowning.

Upon penetration into the lungs, fresh water is rapidly absorbed into the blood, since the concentration of salts in fresh water is much lower than in blood. This leads to a thinning of the blood, an increase in its volume and the destruction of red blood cells. Sometimes pulmonary edema develops. A large amount of stable pink foam is formed, which further disrupts gas exchange.The circulatory function is terminated as a result of impaired contractility of the ventricles of the heart.

Drowning in sea water.

Due to the fact that the concentration of dissolved substances in seawater is higher than in blood, when seawater enters the lungs, the liquid part of the blood, together with proteins, penetrates from the blood vessels into the alveoli. This leads to thickening of the blood, an increase in the concentration of potassium, sodium, calcium, magnesium and chlorine ions in it. A large amount of fluid is heated in the alveoli, which leads to their stretching up to rupture.As a rule, when drowning in sea water, pulmonary edema develops. The small amount of air that is in the alveoli contributes to whipping the liquid during respiratory movements with the formation of a persistent protein foam. Gas exchange is sharply disrupted, cardiac arrest occurs.

There are three clinical periods in true drowning:

Start period.

The victim is conscious and still able to hold his breath on repeated dives.The rescued responds inadequately to the situation (some may be depressed, others may be overly active and agitated). Skin and visible mucous membranes are cyanotic. Breathing is frequent, noisy, can be interrupted by bouts of coughing. Primary tachycardia and arterial hypertension are soon replaced by bradycardia and a subsequent decrease in blood pressure. The upper abdomen is usually swollen due to the large amount of water entering the stomach. Vomiting of swallowed water and gastric contents may occur.Acute clinical manifestations of drowning quickly disappear, orientation is restored, but weakness, headache and cough persist for several days.

Agonal period.

The victim is unconscious. Pulse and respiratory movements are saved. Heartbeats are weak, deaf. The pulse can be determined exclusively on the carotid and femoral arteries. The skin is cyanotic, cold to the touch. A frothy pink liquid is discharged from the mouth and nose.

The period of clinical death.

The appearance of the victim during this period of true drowning is the same as in agonal. The only difference is the absence of pulse and respiratory movements. On examination, the pupils are dilated, do not react to light. During this period, resuscitation measures are rarely successful.

Asphytic drowning

Occurs as a result of liquid irritation of the upper respiratory tract (without aspiration of water into the lungs, as a result of laryngospasm) and is observed in 5-20% of all drowned people.In most cases, asphytic drowning is preceded by a preliminary depression of the central nervous system, a state of alcoholic intoxication, a blow to the surface of the water. As a rule, the initial period cannot be diagnosed. In agony, there is a rare labile pulse on the main arteries. Breathing can look like “false respiratory” (with clean airways). Over time, respiration and blood circulation are suppressed and the transition to the period of clinical death, which lasts longer with asphytic drowning (4-6 minutes).With resuscitation, it is usually difficult to overcome the trismus of the masticatory muscles and laryngospasm.

Syncopal drowning

Characterized by primary reflex cardiac arrest and respiratory arrest caused by the ingress of even small amounts of water into the upper respiratory tract. With this type of drowning, the onset of clinical death is the first priority. Pulse and respiration are absent, pupils are dilated (do not react to light). The skin is pale. A similar mechanism of development has the so-called “ice shock”, or immersion syndrome, which develops as a result of reflex cardiac arrest during sudden immersion in cold water.

Secondary drowning (“death on water”)

Occurs as a result of primary arrest of blood circulation and respiration (myocardial infarction, epileptic seizure, etc.). A feature of this type of drowning is that the ingress of water into the respiratory tract occurs secondarily and unhindered (when a person is already in the period of clinical death).

Changes in the body during drowning, in particular, the timing of dying under water, depend on a number of factors: on the nature of the water (fresh, salty, chlorinated fresh water in swimming pools), on its temperature (ice, cold, warm), on the presence impurities (silt, mud, etc.)from the state of the victim’s body at the time of drowning (fatigue, agitation, alcoholic intoxication, etc.).

Time is of the utmost importance in resuscitation. The earlier the revival starts, the more chances of success. Based on this, it is advisable to start artificial respiration already on the water. For this, air is periodically blown into the mouth or nose of the victim during his transportation to the shore or to the boat. The victim is examined on the shore.If the victim did not lose consciousness or is in a state of slight fainting, then in order to eliminate the consequences of drowning, it is enough to smell the ammonia and warm the victim.

If the circulatory function is preserved (pulsation in the carotid arteries), there is no breathing, the oral cavity is freed from foreign bodies. To do this, it is cleaned with a finger wrapped in a bandage, and removable dentures are removed. Often, the victim’s mouth cannot be opened due to a spasm of the masticatory muscles. In these cases, mouth-to-nose artificial respiration is performed; if this method is ineffective, a mouth expander is used, and if it is not there, then some flat metal object is used (do not break your teeth!).As for the release of the upper respiratory tract from water and foam, it is best to use suction for these purposes. If not, the victim is placed with his stomach down on the rescuer’s thigh, bent at the knee joint. Then sharply, vigorously squeeze his chest. These manipulations are necessary in those cases of resuscitation, when it is impossible to carry out artificial ventilation of the lungs due to the closure of the airways with water or foam. This procedure must be carried out quickly and energetically. If there is no effect within a few seconds, artificial ventilation of the lungs should be started.If the skin is pale, then it is necessary to proceed directly to artificial ventilation of the lungs after cleansing the oral cavity.

The victim is laid on his back, freed from the restraining clothing, his head is thrown back, placing one hand under the neck, and the other is placed on the forehead. Then the lower jaw of the victim is pushed forward and upward so that the lower incisors are in front of the upper ones. These techniques are performed with the aim of restoring the patency of the upper respiratory tract. After that, the rescuer takes a deep breath, holds his breath a little and, pressing his lips tightly to the victim’s mouth (or nose), exhales.In this case, it is recommended to pinch the nose (when breathing mouth to mouth) or mouth (when breathing mouth to nose) of the animate with your fingers. The exhalation is carried out passively, while the airways must be open.

If, during artificial ventilation of the lungs, water is released from the victim’s respiratory tract, which impedes ventilation of the lungs, turn your head to the side and raise the opposite shoulder; in this case, the mouth of the drowned person will be below the chest and the liquid will pour out. After that, artificial ventilation of the lungs can be continued.In no case should the artificial ventilation of the lungs be stopped when the victim’s spontaneous respiratory movements appear, if his consciousness has not yet been restored or the breathing rhythm is disturbed or sharply accelerated, which indicates an incomplete restoration of respiratory function.

In the event that there is no effective blood circulation (there is no pulse in the large arteries, heart beats are not heard, blood pressure is not determined, the skin is pale or cyanotic), chest compressions are performed simultaneously with artificial ventilation.The caregiver stands to the side of the victim so that his hands are perpendicular to the surface of the drowned person’s chest. The resuscitator places one hand perpendicular to the sternum in its lower third, and places the other over the first hand, parallel to the plane of the sternum. The essence of chest compressions is a sharp compression between the sternum and the spine; while the blood from the ventricles of the heart enters the large and small circle of blood circulation. The massage should be performed in the form of sharp jerks: there is no need to strain the muscles of the arms, but one should, as it were, “dump” the weight of one’s body downward – it leads to the sternum deflection by 3-4 cm and corresponds to the contraction of the heart.In the intervals between the pushes, the hands cannot be torn off the sternum, but there should be no pressure – this period corresponds to the relaxation of the heart. The movements of the rescuer should be rhythmic with a thrust rate of about 100 per minute.

Massage is effective if the pulsation of the carotid arteries begins to be detected, the dilated pupils become narrower, and the cyanosis decreases. When these first signs of life appear, chest compressions should be continued until a heartbeat is heard.

If resuscitation is performed by one person, then it is recommended to alternate chest compressions and artificial respiration as follows: 1 blow of air is performed for 4-5 pressures on the sternum. If there are two rescuers, then one is engaged in indirect heart massage, and the other – artificial ventilation of the lungs. In this case, 1 blowing of air is alternated with 5 massage movements.

It should be borne in mind that the stomach of the victim can be filled with water, food; this makes it difficult to carry out artificial ventilation of the lungs, chest compressions, and provokes vomiting.

After removing the victim from the state of clinical death, he is warmed (wrapped in a blanket, covered with warm heating pads) and massage of the upper and lower extremities from the periphery to the center is performed.

In case of drowning, the time during which a person can be revived after being removed from the water is 3-6 minutes.

The temperature of the water is of great importance for the timing of the victim’s return to life. When drowning in ice water, when the body temperature drops, revival is possible even 30 minutes after the accident.

No matter how quickly the rescued person regains consciousness, no matter how well his condition may seem, the placement of the victim in a hospital is an indispensable condition.

Transportation is carried out on a stretcher – the victim is placed on his stomach or on his side with his head down. With the development of pulmonary edema, the position of the body on the stretcher is horizontal with the head end raised. During transportation, artificial lung ventilation is continued.

Brief sequence of actions:

  • Make sure nothing threatens you.Remove the victim from the water. (If you suspect a spinal fracture, remove the victim on a board or shield.)
  • Place the victim with his stomach on your knee, let the water drain from the respiratory tract. Ensure the patency of the upper respiratory tract. Cleanse the oral cavity from foreign objects (mucus, vomit, etc.).
  • Call (on your own or with the help of others) an ambulance.
  • Determine the presence of a pulse in the carotid arteries, the reaction of the pupils to light, spontaneous breathing.
  • If there is no pulse, breathing or pupil response to light, proceed immediately to cardiopulmonary resuscitation. Continue resuscitation until medical personnel arrive or until spontaneous breathing and heart rate are restored
  • After restoring breathing and cardiac activity, give the victim a stable lateral position.