Human Heart – Diagram and Anatomy of the Heart

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Continued From Above…
pulmonary arteries and veins, and the vena cava. The inferior tip of the heart, known as the apex, rests just superior to the diaphragm. The base of the heart is located along the body’s midline with the apex pointing toward the left side. Because the heart points to the left, about 2/3 of the heart’s mass is found on the left side of the body and the other 1/3 is on the right.

Anatomy of the Heart

Pericardium

The heart sits within a fluid-filled cavity called the pericardial cavity. The walls and lining of the pericardial cavity are a special membrane known as the pericardium. Pericardium is a type of serous membrane that produces serous fluid to lubricate the heart and prevent friction between the ever beating heart and its surrounding organs. Besides lubrication, the pericardium serves to hold the heart in position and maintain a hollow space for the heart to expand into when it is full. The pericardium has 2 layers—a visceral layer that covers the outside of the heart and a parietal layer that forms a sac around the outside of the pericardial cavity.

Structure of the Heart Wall

The heart wall is made of 3 layers: epicardium, myocardium and endocardium.

• Epicardium. The epicardium is the outermost layer of the heart wall and is just another name for the visceral layer of the pericardium. Thus, the epicardium is a thin layer of serous membrane that helps to lubricate and protect the outside of the heart. Below the epicardium is the second, thicker layer of the heart wall: the myocardium.
• Myocardium. The myocardium is the muscular middle layer of the heart wall that contains the cardiac muscle tissue. Myocardium makes up the majority of the thickness and mass of the heart wall and is the part of the heart responsible for pumping blood. Below the myocardium is the thin endocardium layer.
• Endocardium. Endocardium is the simple squamous endothelium layer that lines the inside of the heart. The endocardium is very smooth and is responsible for keeping blood from sticking to the inside of the heart and forming potentially deadly blood clots.

The thickness of the heart wall varies in different parts of the heart. The atria of the heart have a very thin myocardium because they do not need to pump blood very far—only to the nearby ventricles. The ventricles, on the other hand, have a very thick myocardium to pump blood to the lungs or throughout the entire body. The right side of the heart has less myocardium in its walls than the left side because the left side has to pump blood through the entire body while the right side only has to pump to the lungs.

Chambers of the Heart

The heart contains 4 chambers: the right atrium, left atrium, right ventricle, and left ventricle. The atria are smaller than the ventricles and have thinner, less muscular walls than the ventricles. The atria act as receiving chambers for blood, so they are connected to the veins that carry blood to the heart. The ventricles are the larger, stronger pumping chambers that send blood out of the heart. The ventricles are connected to the arteries that carry blood away from the heart.

The chambers on the right side of the heart are smaller and have less myocardium in their heart wall when compared to the left side of the heart. This difference in size between the sides of the heart is related to their functions and the size of the 2 circulatory loops. The right side of the heart maintains pulmonary circulation to the nearby lungs while the left side of the heart pumps blood all the way to the extremities of the body in the systemic circulatory loop.

Valves of the Heart

The heart functions by pumping blood both to the lungs and to the systems of the body. To prevent blood from flowing backwards or “regurgitating” back into the heart, a system of one-way valves are present in the heart. The heart valves can be broken down into two types: atrioventricular and semilunar valves.

• Atrioventricular valves. The atrioventricular (AV) valves are located in the middle of the heart between the atria and ventricles and only allow blood to flow from the atria into the ventricles. The AV valve on the right side of the heart is called the tricuspid valve because it is made of three cusps (flaps) that separate to allow blood to pass through and connect to block regurgitation of blood. The AV valve on the left side of the heart is called the mitral valve or the bicuspid valve because it has two cusps. The AV valves are attached on the ventricular side to tough strings called chordae tendineae. The chordae tendineae pull on the AV valves to keep them from folding backwards and allowing blood to regurgitate past them. During the contraction of the ventricles, the AV valves look like domed parachutes with the chordae tendineae acting as the ropes holding the parachutes taut.
• Semilunar valves. The semilunar valves, so named for the crescent moon shape of their cusps, are located between the ventricles and the arteries that carry blood away from the heart. The semilunar valve on the right side of the heart is the pulmonary valve, so named because it prevents the backflow of blood from the pulmonary trunk into the right ventricle. The semilunar valve on the left side of the heart is the aortic valve, named for the fact that it prevents the aorta from regurgitating blood back into the left ventricle. The semilunar valves are smaller than the AV valves and do not have chordae tendineae to hold them in place. Instead, the cusps of the semilunar valves are cup shaped to catch regurgitating blood and use the blood’s pressure to snap shut.

Conduction System of the Heart

The heart is able to both set its own rhythm and to conduct the signals necessary to maintain and coordinate this rhythm throughout its structures. About 1% of the cardiac muscle cells in the heart are responsible for forming the conduction system that sets the pace for the rest of the cardiac muscle cells.

The conduction system starts with the pacemaker of the heart—a small bundle of cells known as the sinoatrial (SA) node. The SA node is located in the wall of the right atrium inferior to the superior vena cava. The SA node is responsible for setting the pace of the heart as a whole and directly signals the atria to contract. The signal from the SA node is picked up by another mass of conductive tissue known as the atrioventricular (AV) node.

The AV node is located in the right atrium in the inferior portion of the interatrial septum. The AV node picks up the signal sent by the SA node and transmits it through the atrioventricular (AV) bundle. The AV bundle is a strand of conductive tissue that runs through the interatrial septum and into the interventricular septum. The AV bundle splits into left and right branches in the interventricular septum and continues running through the septum until they reach the apex of the heart. Branching off from the left and right bundle branches are many Purkinje fibers that carry the signal to the walls of the ventricles, stimulating the cardiac muscle cells to contract in a coordinated manner to efficiently pump blood out of the heart.

Physiology of the Heart

Coronary Systole and Diastole

At any given time the chambers of the heart may found in one of two states:

• Systole. During systole, cardiac muscle tissue is contracting to push blood out of the chamber.
• Diastole. During diastole, the cardiac muscle cells relax to allow the chamber to fill with blood. Blood pressure increases in the major arteries during ventricular systole and decreases during ventricular diastole. This leads to the 2 numbers associated with blood pressure—systolic blood pressure is the higher number and diastolic blood pressure is the lower number. For example, a blood pressure of 120/80 describes the systolic pressure (120) and the diastolic pressure (80).

The Cardiac Cycle

The cardiac cycle includes all of the events that take place during one heartbeat. There are 3 phases to the cardiac cycle: atrial systole, ventricular systole, and relaxation.

• Atrial systole: During the atrial systole phase of the cardiac cycle, the atria contract and push blood into the ventricles. To facilitate this filling, the AV valves stay open and the semilunar valves stay closed to keep arterial blood from re-entering the heart. The atria are much smaller than the ventricles, so they only fill about 25% of the ventricles during this phase. The ventricles remain in diastole during this phase.
• Ventricular systole: During ventricular systole, the ventricles contract to push blood into the aorta and pulmonary trunk. The pressure of the ventricles forces the semilunar valves to open and the AV valves to close. This arrangement of valves allows for blood flow from the ventricles into the arteries. The cardiac muscles of the atria repolarize and enter the state of diastole during this phase.
• Relaxation phase: During the relaxation phase, all 4 chambers of the heart are in diastole as blood pours into the heart from the veins. The ventricles fill to about 75% capacity during this phase and will be completely filled only after the atria enter systole. The cardiac muscle cells of the ventricles repolarize during this phase to prepare for the next round of depolarization and contraction. During this phase, the AV valves open to allow blood to flow freely into the ventricles while the semilunar valves close to prevent the regurgitation of blood from the great arteries into the ventricles.

Blood Flow through the Heart

Deoxygenated blood returning from the body first enters the heart from the superior and inferior vena cava. The blood enters the right atrium and is pumped through the tricuspid valve into the right ventricle. From the right ventricle, the blood is pumped through the pulmonary semilunar valve into the pulmonary trunk.

The pulmonary trunk carries blood to the lungs where it releases carbon dioxide and absorbs oxygen. The blood in the lungs returns to the heart through the pulmonary veins. From the pulmonary veins, blood enters the heart again in the left atrium.

The left atrium contracts to pump blood through the bicuspid (mitral) valve into the left ventricle. The left ventricle pumps blood through the aortic semilunar valve into the aorta. From the aorta, blood enters into systemic circulation throughout the body tissues until it returns to the heart via the vena cava and the cycle repeats.

The Electrocardiogram

The electrocardiogram (also known as an EKG or ECG) is a non-invasive device that measures and monitors the electrical activity of the heart through the skin. The EKG produces a distinctive waveform in response to the electrical changes taking place within the heart.

The first part of the wave, called the P wave, is a small increase in voltage of about 0. 1 mV that corresponds to the depolarization of the atria during atrial systole. The next part of the EKG wave is the QRS complex which features a small drop in voltage (Q) a large voltage peak (R) and another small drop in voltage (S). The QRS complex corresponds to the depolarization of the ventricles during ventricular systole. The atria also repolarize during the QRS complex, but have almost no effect on the EKG because they are so much smaller than the ventricles.

The final part of the EKG wave is the T wave, a small peak that follows the QRS complex. The T wave represents the ventricular repolarization during the relaxation phase of the cardiac cycle. Variations in the waveform and distance between the waves of the EKG can be used clinically to diagnose the effects of heart attacks, congenital heart problems, and electrolyte imbalances.

Heart Sounds

The sounds of a normal heartbeat are known as “lubb” and “dupp” and are caused by blood pushing on the valves of the heart. The “lubb” sound comes first in the heartbeat and is the longer of the two heart sounds. The “lubb” sound is produced by the closing of the AV valves at the beginning of ventricular systole. The shorter, sharper “dupp” sound is similarly caused by the closing of the semilunar valves at the end of ventricular systole. During a normal heartbeat, these sounds repeat in a regular pattern of lubb-dupp-pause. Any additional sounds such as liquid rushing or gurgling indicate a structure problem in the heart. The most likely causes of these extraneous sounds are defects in the atrial or ventricular septum or leakage in the valves.

Cardiac Output

Cardiac output (CO) is the volume of blood being pumped by the heart in one minute. The equation used to find cardiac output is: CO = Stroke Volume x Heart Rate

Stroke volume is the amount of blood pumped into the aorta during each ventricular systole, usually measured in milliliters. Heart rate is the number of heartbeats per minute. The average heart can push around 5 to 5.5 liters per minute at rest.

Heart Health Problems

Heart disease is very common, disrupting the normal function of this important organ and often causing death. Visit our Diseases and Conditions section to learn more about common cardiovascular diseases and how we can prevent them. For information about your personal hereditary risks of a variety of conditions involving the heart (such as those arising from hemochromatosis or G6PDD, to name two very common hereditary disorders), learn more about DNA health testing.

Patent Ductus Arteriosus (PDA) | American Heart Association

What is it?

An unclosed hole in the aorta.

Before a baby is born, the fetus’s blood does not need to go to the lungs to get oxygenated. The ductus arteriosus is a hole that allows the blood to skip the circulation to the lungs. However, when the baby is born, the blood must receive oxygen in the lungs and this hole is supposed to close. If the ductus arteriosus is still open (or patent) the blood may skip this necessary step of circulation. The open hole is called the patent ductus arteriosus.

More information for parents of children with PDA

What causes it?

The ductus arteriosus is a normal fetal artery connecting the main body artery (aorta) and the main lung artery (pulmonary artery). The ductus allows blood to detour away from the lungs before birth.

Every baby is born with a ductus arteriosus. After birth, the opening is no longer needed and it usually narrows and closes within the first few days.

Sometimes, the ductus doesn’t close after birth. Failure of the ductus to close is common in premature infants but rare in full-term babies. In most children, the cause of PDA isn’t known. Some children can have other heart defects along with the PDA.

How does it affect the heart?

Normally the heart’s left side only pumps blood to the body, and the right side only pumps blood to the lungs. In a child with PDA, extra blood gets pumped from the body artery (aorta) into the lung (pulmonary) arteries. If the PDA is large, the extra blood being pumped into the lung arteries makes the heart and lungs work harder and the lungs can become congested.

How does the PDA affect my child?

If the PDA is small, it won’t cause symptoms because the heart and lungs don’t have to work harder. The only abnormal finding may be a distinctive type of murmur (noise heard with a stethoscope).

If the PDA is large, the child may breathe faster and harder than normal. Infants may have trouble feeding and growing at a normal rate. Symptoms may not occur until several weeks after birth. High pressure may occur in the blood vessels in the lungs because more blood than normal is being pumped there. Over time this may cause permanent damage to the lung blood vessels.

What can be done about the PDA?

If the PDA (ductus) is small, it doesn’t make the heart and lungs work harder. Surgery and other treatments may not be needed. Small PDAs often close on their own within the first few months of life.

Most children can have the PDA closed by inserting catheters (long thin tubes) into the blood vessels in the leg to reach the heart and the PDA, and a coil or other device can be inserted through the catheters into the PDA like a plug. The figure below on the left shows one example of how a catheterization is used to close the ductus. If surgery is needed, an incision is made in the left side of the chest, between the ribs. The ductus is closed by tying it with suture (thread-like material) or by permanently placing a small metal clip around the ductus to squeeze it closed. If there’s no other heart defect, this restores the child’s circulation to normal. In premature newborn babies, medicine can often help the ductus close. After the first few weeks of life, medicine won’t work as well to close the ductus and surgery may be required.

What activities can my child do?

If the PDA is small, or if it has been closed with catheterization or surgery, your child may not need any special precautions regarding physical activity and may be able to participate in normal activities without increased risk.

As far as follow up in the future, depending on the type of PDA closure, your child’s pediatric cardiologist may examine it periodically to look for uncommon problems. The long-term outlook is excellent, and usually no medicines and no additional surgery or catheterization are needed.

Congenital Heart Defect ID sheet

More information for adults with PDA

What causes it?

The ductus arteriosus is a normal fetal artery connecting the main body artery (aorta) and the main lung artery (pulmonary artery). The ductus allows blood to detour away from the lungs before birth.

Every baby is born with a ductus arteriosus. After birth, the opening is no longer needed and it usually narrows and closes within the first few days of life.

Sometimes the ductus doesn’t close after birth. Failure of the ductus to close is common in premature infants but rare in full-term babies, and the cause is usually not known. Some patients can have other heart defects along with the PDA.

How does it affect the heart?

Normally the heart’s left side only pumps blood to the body, and the right side only pumps blood to the lungs. In a person with PDA, extra blood gets pumped from the body artery (aorta) into the lung (pulmonary) arteries. If the PDA is large, the extra blood being pumped into the lung arteries makes the heart and lungs work harder and the lungs can become congested.

How does the PDA affect me?

If the PDA is small, it won’t cause symptoms or problems because the blood flow and pressure in the heart and lungs aren’t changed appreciably from normal. The only abnormal finding may be a distinctive type of murmur (noise heard with a stethoscope), sometimes called a “machinery” murmur.

If the PDA is large, breathlessness may be due to reduced heart function or problems related to high pressures in the lungs. High pressure may occur in the lung vessels because more blood than normal is being pumped there. Over time this may cause permanent damage to the lung blood vessels (pulmonary hypertension).

What if the defect is still present? Should it be repaired in adulthood?

If the PDA is small, it doesn’t have to be closed because it doesn’t make the heart and lungs work harder.

Patients with a moderate- or large-sized PDA may develop problems related to the increased blood flow to the lungs. These patients may have improvement if the PDA is closed. Closing the PDA can now usually be performed by catheter coil placement or other device insertion to plug the abnormal communication (referred to as interventional or therapeutic catheterization(PDF).)

Surgery may be the best treatment option for some patients. The surgeon doesn’t have to open the heart to fix the PDA. An incision is made in the left side of the chest, between the ribs. The PDA is closed by tying it with suture (thread-like material) or by permanently placing a small metal clip around the PDA to squeeze it closed. Occasionally in the adult, a surgical patch is used. If there’s no other heart defect, this restores the circulation to normal.

If I still have a PDA, what activities can I do?

If the PDA is small, or if the PDA has been closed with catheterization or surgery, you may not need any special restrictions and may be able to participate in normal activities without increased risk.

Patients with moderate or large PDAs and patients with pulmonary hypertension may need to restrict activity. They should discuss this with their cardiologist.

Ongoing Care

What will I need in the future?

Depending on the type of PDA closure, your cardiologist may examine it periodically to look for uncommon problems. The long-term outlook is excellent, and usually no medicines and no additional surgery or catheterization are needed.

Medical Follow-up

Patients with a small PDA need periodic follow-up with a cardiologist. Patients with a PDA that’s been successfully closed rarely require long-term cardiology follow-up unless there’s additional cardiac disease. Only rarely will they need to take medicine after surgical or device closure. Your cardiologist can monitor you with noninvasive tests if needed.

Activity Restrictions

Most patients with a small unrepaired PDA or a repaired PDA don’t need any special precautions and can participate in normal activities without increased risk. After surgery or catheter closure, your cardiologist may advise some limitations on your physical activity for a short time even if there’s no pulmonary hypertension.

Exercise restriction is recommended for patients with pulmonary hypertension related to PDA.

Endocarditis Prevention

Endocarditis prophylaxis is generally not needed more than six months after PDA device closure. However, endocarditis prophylaxis is recommended for PDA patients with a history of endocarditis, for those with prosthetic valve material and for unrepaired PDA with associated pulmonary hypertension and cyanosis. See the section on endocarditis for more information.

Pregnancy

Unless there’s pulmonary hypertension or signs of heart failure, pregnancy is low risk in patients with PDA.

Will You Need More Surgery?

Once a PDA has been closed, it’s unlikely that more surgery will be needed. Rarely, a patient may have a residual hole. Whether it will need to be closed depends on its size.

Congenital heart defects and critical CHDs

What are congenital heart defects?

Congenital means present at birth. Congenital heart defects (also called CHDs) are heart conditions that a baby is born with. These conditions can affect the heart’s shape or how it works or both. CHDs can be mild or serious.

CHDs are the most common types of birth defects. Birth defects are structural changes present at birth that can affect almost any part of the body. They may affect how the body looks, works or both. Birth defects can cause problems in overall health, how the body develops or how the body works. 

Critical congenital heart defects (also called critical CHDs or critical congenital heart disease) are the most serious congenital heart defects. Babies with critical CHDs need surgery or other treatment within the first year of life. Without treatment, critical CHDs can cause serious health problems and death. 

Nearly 1 in 100 babies (about 1 percent or 40,000 babies) is born with a heart defect in the United States each year. About 1 in 4 babies born with a heart defect (about 25 percent) has a critical CHD. Some heart defects don’t need treatment or can be treated easily. But others, like some critical CHDs, may need surgeries over several years.

How can heart defects affect your baby?

Heart defects can affect different parts of your baby’s heart, including:

• Heart chambers. The heart has four chambers. The two upper chambers (also called atria) receive blood. The two lower chambers (also called ventricles) pump blood out of the heart to other parts of the body.
• Septum. This is a wall that separates the right and left sides of the heart. There is a wall between the two atria, and a wall between the two ventricles.
• Heart valves. These valves open and close to control blood flow through the heart. They help blood move in the right direction as it’s pumped to other parts of the body.
• Arteries and veins near the heart. Arteries are blood vessels that carry blood away from the heart to the body. The aorta is the main artery that carries blood away from the heart to the rest of the body. Veins are blood vessels that carry blood from the body to the heart.

Heart defects can affect blood flow, causing your baby’s blood to:

• Slow down
• Go in the wrong direction or to the wrong place
• Be blocked
• Not have enough oxygen to carry throughout the body

Some of these blood flow problems can cause fluid buildup in the lungs (also called lung congestion or pulmonary edema). Fluid in the lungs can make it harder for your baby to breathe. Babies with serious heart defects may develop heart failure (also called congestive heart failure). This is when the heart can’t pump blood as well as it should.

What are examples of critical CHDs?

Critical CHDs include:

Coarctation of the aorta (also called COA). In this condition, part of the aorta is too narrow. This can reduce or block the flow of blood to the body. The heart muscles need to work harder to get blood out of the heart. This extra stress on the heart can weaken the heart muscle and cause other heart problems. Babies with COA are treated with surgery or a procedure called balloon angioplasty. In this procedure, a provider uses a catheter (a thin, flexible tube) with a tiny balloon that he expands to stretch open the aorta. He may put in a stent, which is a small mesh-covered tube used to keep the blood vessel open. Many children with COA need to take medicine to lower their blood pressure. Blood pressure is the force of blood against the walls of the arteries. 

Dextro-Transposition of the Great Arteries (also called d-TGA). Babies with this condition have the positions of two important arteries switched. This means the blood that’s pumped to the body may not have enough oxygen. Babies with d-TGA need heart surgery soon after birth to help get oxygen-rich blood from the heart to the rest of the body. They may need medicines to make their heart pump better, lower their blood pressure, help the body get rid of extra fluid or slow down the heart if it’s beating too fast. If the heart is beating too slowly, they may need a pacemaker. A pacemaker is a small device placed under the skin in the chest to help control the heartbeat.

Interrupted aortic arch (also called IAA). In this condition, a part of the aorta is missing. This means that the heart can’t send blood through the aorta to the rest of the body. Babies with IAA need surgery soon after birth to repair the aorta.

Pulmonary atresia (also called PA). In this condition, the heart’s pulmonary valve doesn’t form properly or at all. The pulmonary valve controls blood flow from the right ventricle of the heart to the lungs. If a baby has PA, blood can’t flow from the heart to the lungs to pick up oxygen for the body. Babies with PA usually need medicine to improve blood flow until they can be treated with cardiac catheterization or surgery. During cardiac catheterization, your baby’s provider moves a catheter into a blood vessel and guides it to his heart. Then he can use a tiny balloon to expand the valve. Or he may put in a stent to keep a blood vessel open. But most babies with PA need surgery soon after birth to widen or replace the pulmonary valve. 

Single ventricle defects. In this group of conditions, a baby’s heart has one ventricle that works well enough to pump blood instead of two ventricles. Single ventricle defects include:

• Ebstein anomaly. In this condition, the heart’s tricuspid valve (the valve between the two right chambers of the heart) doesn’t work properly. This means blood can leak back into the wrong part of the heart. Babies with this condition may need surgery to repair or replace the tricuspid valve. They also may need medicines to control their heart rate, improve blood flow or treat any signs of heart failure.  
• Hypoplastic left heart syndrome (also called HLHS). In this condition, the left side of the heart doesn’t form correctly, and the heart can’t pump blood to the body properly. A baby with HLHS needs several different types of surgery starting soon after birth to help increase blood flow to her body. Some babies also need medicines to make their heart muscle stronger, lower their blood pressure or help the body get rid of extra fluid. If the condition is very severe or if surgeries weaken the heart, the baby may need a heart transplant. A heart transplant is surgery in which a damaged heart is removed and replaced with a healthy heart from another person.
• Tricuspid atresia. In this condition, the heart’s tricuspid valve (the valve between the two right chambers of the heart) isn’t formed. This means that blood can’t flow correctly through the heart or to the rest of the body. Babies with tricuspid atresia may need one or more surgeries starting soon after birth to increase blood flow to the lungs and bypass (go around) the part of the heart that’s not working properly. Some babies need medicines to make the heart muscle stronger, lower their blood pressure, or help the body get rid of extra fluid.
• Double-outlet right ventricle (also called DORV). In this condition, the aorta connects to the heart’s right ventricle instead of the left ventricle. There’s also a hole between the two ventricles. This means that the blood being pumped to the body may not have enough oxygen. Babies with DORV need surgery to repair the heart.

Tetralogy of Fallot (also called TOF). Babies with this condition have a combination of four heart defects that limits oxygen in blood that’s pumped to the body. Babies with TOF need heart surgery soon after birth to improve blood flow to the lungs and the rest of the body.  

Total anomalous pulmonary venous return (also called TAPVR). In this condition, the veins that take blood from the lungs to the heart don’t connect to the heart the right way, so the body doesn’t get enough oxygen. Babies with this condition need surgery so that blood can flow better through the heart.

Truncus arteriosus (also called common truncus). Babies with this condition have only one artery that leaves the heart instead of two arteries. They also have only one valve that controls the blood that leaves the heart instead of two valves. This means that blood with oxygen mixes with blood that doesn’t have oxygen. So too much blood goes to the lungs, and the heart has to work harder to pump blood to the rest of the body. Babies with this condition need surgery to repair the heart and blood vessels. Some babies may need medicines to make the heart muscle stronger, lower their blood pressure or help the body get rid of extra fluid.

As they grow older, most babies with critical CHDs need regular checkups with a pediatric cardiologist to check the heart and look for any other health problems.

What are common congenital heart defects and how are they treated?

Common CHDs include: 

Patent ductus arteriosus (also called PDA). This condition happens in the connection (called the ductus arteriosus) between two major blood vessels leading from the heart: the pulmonary artery and the aorta. The ductus arteriosus is open when a baby is in the womb. If it doesn’t close properly after birth, blood that doesn’t have enough oxygen can flow in the wrong direction. This can weaken the heart muscle and lead to heart failure. Sometimes a PDA may close on its own. But some babies need medicine, procedures with catheters or heart surgery.

Septal defects. These conditions leave a hole in the septum. This can cause blood to go in the wrong direction or to the wrong place, or it can cause extra blood to be pumped to the lungs. Types of septal defects include:

• Atrial septal defect (also called ASD). This is when the hole is in the wall that separates the right and left atria.
• Ventricular septal defect (also called VSD). This is when the hole is in the wall that separates the right and left ventricles. VSDs are the most common type of heart defect.
• Atrioventricular septal defect (AVSD). This is when there are holes between the chambers of the right and left side of the heart, and the valves between these chambers may not form correctly. 

Some small septal defects close on their own. Heart surgery or procedures with catheters can fix larger septal defects. Babies with AVSD usually need heart surgery.

What causes congenital heart defects?

Heart defects can begin to develop in the first 6 weeks of pregnancy when the heart is forming, often before you know you’re pregnant. We’re not sure what causes most congenital heart defects, but these things may play a role: 

Changes in genes or chromosomes

Some babies have heart defects because of changes in their chromosomes or genes. Chromosomes are the structures that hold genes. Genes are part of your body’s cells that store instructions for the way your body grows and works. Genes are passed from parents to children. Certain gene changes (also called mutations) are linked to heart defects. At least 15 in 100 (15 percent) of CHDs are linked to genetic or chromosomal conditions. For example, about half of babies with Down syndrome have heart defects.

If you, your partner or one of your other children has a congenital heart defect, your next baby may be more likely to have one, too. So you may want to meet with a genetic counselor. This is a person who is trained to help you understand genes, birth defects and other medical conditions that run in families, and how they can affect your health and your baby’s health.

Health conditions in mom

Having one of these conditions may increase your risk of having a baby with a CHD:

• Lupus (also called systemic lupus erythematosus or SLE). Lupus is an autoimmune disease. This is a health condition that happen when antibodies (cells in the body that fight off infections) attack healthy tissue by mistake. Lupus can damage the joints, skin, kidneys, heart, lungs and other body parts.
• Maternal phenylketonuria (also called PKU). PKU is a condition in which your body can’t break down an amino acid called phenylalanine. Amnio acids help build protein in your body. Without treatment, phenylalanine builds up in the blood and causes health problems. Most pregnant women with PKU can have healthy babies if they follow a special mean plan that’s low in phenylalanine.
• Obesity (being very overweight). If you’re obese, you have an excess amount of body fat, and your body mass index (BMI) is 30 or higher. To find out your BMI, go to www.cdc.gov/bmi.
• Preexisting diabetes (also called type 1 or type 2 diabetes). This is a medical condition in which your body has too much sugar (called glucose) in your blood. Preexisting means you had diabetes before you got pregnant. Diabetes can damage organs in your body, including blood vessels, nerves, eyes and kidneys.
• Rubella (also called German measles). This is an infection that causes mild flu-like symptoms and rash on the skin. Having rubella during pregnancy may increase your baby’s risk for a CHD.

Medicines you take

Taking certain medicines may increase your baby’s risk of having a CHD. Tell your provider about any medicine you take before you try to get pregnant. This includes prescription medicines, over-the counter medicine, herbal products and supplements. 

If the medicine you take may be harmful to your baby, you may be able to change to one that’s safer. But some medicines may be critical to your own health, even if they may affect your baby. You and your provider can weigh the benefits and risks of medicine you take to give you the healthiest possible pregnancy. Don’t start or stop taking any prescription medicine before, during or after pregnancy without talking to your health care provider first. Starting, stopping or changing medicines may cause serious health problems for you or your baby. 

These are examples of medicines that may increase your baby’s risk of having a CHD:

• ACE inhibitors. These medicines are used to treat high blood pressure and other conditions. High blood pressure is when the force of blood against the walls of the blood vessels is too high. It can stress your heart and cause problems during pregnancy.
• Isotretinoin. This medicine is used to treat acne.
• Lithium. This medicine is used to treat depression. Depression (also called depressive disorder, major depression and clinical depression) is a medical condition that causes feelings of sadness and a loss of interest in things you like to do. It can affect how you feel, think and act and can interfere with your daily life. It needs treatment to get better.
• Statins. These medicines are used to treat high cholesterol. Cholesterol is a substance in your blood. Too much cholesterol can increase your risk of heart disease.
• Thalidomide. This medicine is used to treat certain skin conditions, infections, certain types of cancer and complications from HIV (stands for human immunodeficiency virus). HIV attacks the body’s immune system and is the virus that causes AIDS. In a healthy person, the immune system protects the body from infections, cancers and some diseases.

Conditions in your everyday life (lifestyle and environment)

Some things in your life and environment (where and how you live) may increase your chances of having a baby with a CHD. These include:

• Drinking alcohol during pregnancy. If you’re pregnant, trying to get pregnant or think you may be pregnant, don’t drink alcohol.
• Smoking before or during pregnancy. Women who smoke anytime during the month before pregnancy or during the first 3 months of pregnancy are more likely to have a baby with a CHD than women who don’t smoke.

If you smoke or drink alcohol, ask your health care provider about getting help to quit.

How do you know if your baby has a congenital heart defect?

If your health care provider doesn’t find a severe congenital heart defect in your baby during pregnancy, it’s usually diagnosed soon after birth or during the first few months of life. Less severe heart defects may not be found until children are older.

During pregnancy

Your provider may use a test called fetal echocardiogram (also called fetal echo) to check your baby’s heart. This test uses ultrasound to make a picture of your baby’s heart while still in the uterus (womb). You can have this test at about 18 to 24 weeks of pregnancy.

You may need a fetal echocardiogram if:

• Your provider finds a possible problem, like an abnormal heart rhythm in your baby, during an ultrasound.
• Your baby has a genetic or chromosomal condition, like Down syndrome, that may be linked to CHDs.
• You have a family history of heart problems. This means that you, your partner or someone in your families has heart problems.
• You have a health condition, like diabetes, that may play a role in CHDs.
• You’re taking a medicine that can increase the risk of your baby having a CHD.

After birth

Your baby is tested for critical CHDs as part of newborn screening before she leaves the hospital after birth. Newborn screening checks for serious but rare and mostly treatable conditions. It includes blood, hearing and heart screening. All states require newborn screening, and all states except California require screening for critical CHDs. California requires that providers offer screening for critical CHDs. 

Babies are screened for critical CHDs with a simple test called pulse oximetry (also called pulse ox). This test checks the amount of oxygen in your baby’s blood. Low levels of oxygen can be a sign of a heart defect. Pulse oximetry uses a pulse oximeter machine with sensors that are placed on your baby’s skin. The test is painless and only takes a few minutes. Pulse oximetry can find many but not all critical CHDs. Your baby’s provider also may find a heart defect by doing a physical exam. 

If tests find that your baby has a critical CHD, she can get early care and treatment to prevent more serious health problems. Your baby’s provider can refer your baby to a pediatric cardiologist for treatment. This is a doctor who treats babies and children with heart conditions. 

What are signs and symptoms of congenital heart defects?

Signs of a condition are things someone else can see or know about you, like you have a rash or you’re coughing. Some CHDs have no signs, so you may not know that your baby has a CHD until he’s older. 

Signs of heart defects include:

• A heart murmur. This is a blowing, whooshing or rasping sound heard during a heartbeat. It’s caused by rough blood flow through the heart valves or near the heart.   Your baby’s provider may hear a murmur when she checks your baby’s heartbeat using a stethoscope.
• A pounding heart
• A weak pulse
• Gray or blue color of the skin, lips or fingernails
• Sleepiness while feeding or being very sleepy at other times
• Swollen belly or legs or puffiness around the eyes
• Trouble breathing or fast breathing. Breathing problems while feeding can lead to slow weight gain.

If your baby has any of these signs, call his provider right away. Your baby’s provider may use these tests to check for heart defects:

• Physical exam. Your baby’s provider listens to your baby’s heart and lungs with a stethoscope and looks for other signs of a heart defect.
• Echocardiogram (also called an echo or cardiac ultrasound). This is an ultrasound of the heart. Your baby’s provider can see the heart beating and check the heart’s valves and other parts.
• Electrocardiogram (also called EKG or ECG). This test records the heart’s electrical activity. It shows how fast the heart is beating and if its rhythm is steady or not. It also shows the size and position of the heart’s chambers.
• Chest X-ray. This test makes pictures of your baby’s chest and organs, like the heart and lungs. It can show if the heart is enlarged. It also can show if the lungs have extra blood or other fluid in them. An enlarged heart or extra fluid in the lungs can be signs of heart failure.
• Pulse oximetry
• Cardiac catheterization

Last reviewed: June, 2019

Anomalous Pulmonary Venous Return | CS Mott Children’s Hospital

What is an anomalous pulmonary venous return?

Anomalous pulmonary venous return (APVR) is a rare heart defect that occurs when the pulmonary veins fail to form normally while the baby is in the mother’s womb. It comprises <1% of all congenital heart defects. The cause of the problem is not known. In the normal heart, there are four pulmonary veins that bring red blood back from the lungs to the heart’s left upper chamber (the left atrium). Two of the veins bring red blood from the right lung and two bring red blood from the left lung. In a baby with anomalous pulmonary venous return, one or more of the pulmonary veins returns to the right atrium instead of the left atrium. If all the pulmonary veins are affected, the diagnosis is total anomalous pulmonary venous return (TAPVR). When a child has anomalous pulmonary veins, the abnormal veins take one of three possible pathways. The most common is the “supra-cardiac type”   with the pulmonary veins (1) returning to the superior vena cava (2) via a bridging vein (3). Next most common is the “intra-cardiac type” with the pulmonary veins (1)returning directly to the right atrium (2) via a tube-like structure called the coronary sinus (3). Least common is the “infra-cardiac type” with the pulmonary veins (1) returning below the heart via the inferior vena cava (2). Sometimes, there is a mixed pattern with the veins returning to more than one abnormal site. In all types, when all four pulmonary veins are affected, there is also a hole, called an atrial septal defect (ASD), in the wall that separates the heart’s upper chambers. While APVR can be the only heart problem, it co-occurs with many complex heart defects.

How does this problem affect my child’s health?

The timing and degree of symptoms depend on the number of veins affected and whether there are any sites along the veins that are narrow blocking blood flow. When a child has anomalous pulmonary veins, red blood re-enters the venous system, that is, it goes right back to where it came from instead of flowing to the left heart where it can be pumped out to the body. As a result, there is too much blood flow to the lungs, and if all the veins are affected, there is no direct path for red blood to reach the body. In this case, the only way for any blood to reach the left heart is to flow from the right atrium across the atrial septal defect to the left atrium. In partial anomalous venous return (PAPVR), if only one vein is affected, there are usually no symptoms. If two veins from the same side are affected, symptoms of shortness of breath with exertion and low stamina may occur during childhood. The symptoms are usually mild and may not ever occur. However, during the adult years, too much blood flow to the lungs can lead to a serious problem called pulmonary artery hypertension. It is for this reason, that careful assessment by a specialist is needed to determine if surgery should be done. TAPVR is a serious problem that needs surgical repair soon after the diagnosis is made. While most babies with TAPVR have no symptoms at birth, about 50% develop symptoms during the first month of life, and almost all have symptoms by one year of age. Symptoms include congestive heart failure (rapid breathing, clammy sweating, low energy, irritability, poor feeding, and poor growth), and cyanosis, a bluish color of the lips and nailbeds that can be quite mild. Blockage of the veins can occur at any of the three abnormal sites and results in severe breathing problems. A small atrial septal defect results in early and severe symptoms as well.

How is this problem diagnosed?

Prenatal diagnosis: Anomalous pulmonary venous return can be diagnosed before birth by a fetal echocardiogram or heart ultrasound as early as 18 weeks into the pregnancy. This test is done when there is a family history of congenital heart disease or when a question is raised during a routine prenatal ultrasound. Symptoms: In most cases symptoms of congestive heart failure and/or cyanosis alerts parents or health care providers that the child may have a heart problem. These symptoms are most often noted during the first days or weeks of life. Cyanosis refers to a bluish color of the baby’s lips and nailbeds and occurs when blood oxygen levels are low. Symptoms of congestive heart failure in infants include rapid breathing, clammy sweating, poor feeding, and poor growth. Physical findings: Most babies with anomalous pulmonary venous return are born at term and are a normal weight and length (since before birth the baby’s oxygen comes from the mother). After birth, the baby’s lips and fingernails may look blue. A heart murmur is almost always heard. If congestive heart failure is present, the heart rate and breathing rate will be increased. Medical tests: The suspected diagnosis is confirmed by an echocardiogram. Sometimes, a heart catheterization is needed to determine the extent of the problem and/or to help the doctors plan the surgery. An oxygen saturation test is used to measure the blood oxygen levels. Other tests include an electrocardiogram and chest x-ray.

How is the problem treated?

TAPVR is a serious heart defect and left untreated, most children would not survive the first year of life. Treatment consists of a heart operation to re-route all of the pulmonary venous return to the left atrium. The ASD is also closed with a patch. The timing of surgery depends, in part, on whether or not obstruction is present. If it is, surgery is done on an urgent basis, otherwise, surgery is usually done early, within the first six months of life. Indications for surgical repair of PAPVR include excessive blood flow to the lungs as evidenced by symptoms and/or the results of heart tests done. What are the long-term health issues for these children? Long-term results are excellent for most children after following repair of APVR. Possible complications after surgery include obstruction at the site of the repair, development of pulmonary artery hypertension, and later (during adulthood), abnormal heart rhythms such as atrial flutter and sick sinus syndrome. SBE prophylaxis: An increased risk for subacute bacterial endocarditis (SBE) following repair of APVR may be present. This is an infection of the heart caused by bacteria in the blood stream. Children with heart defects are more prone to this problem because of the altered flow of blood through the heart. It can occur after dental work or medical procedures on the GI or respiratory tract because these procedures almost always result in some bacteria entering the blood. SBE can usually be prevented by taking an antibiotic before these procedures. If the surgery result is good, SBE may not be needed. Exercise guidelines: An individual exercise program is best planned with the doctor so that all factors can be included. In general, children with APVR (without other heart problems) do not have any exercise restrictions.

References

Geva T, Van Praagh S. Anomalies of the pulmonary veins. In Allen H, Gutgesell Clark E, Driscoll D, eds. Moss and Adams’ Heart Disease in Infants, Children, and Adolescent. Philadelphia, PA: Lippincott, Williams & Wilkins, 2001; 736-772. Lupinetti FM, Kulik TJ, Beekman RN, Crowley DC, Bove EL. Correction of total anomalous pulmonary venous connection in infancy. J Thor Cardiovasc Surg 1993; 106:880-885. Reitz BA & Yuh DD. Cyanotic defects. In Congenital Cardiac Surgery, Reitz BA & Yuh DD, eds. New York NY: McGraw-Hill,2002, 148-152. Reviewed September, 2012

Coronavirus: Images reveal how COVID-19 ‘destroys’ the lungs | World News

Researchers in the US have used virtual reality (VR) for the first time to reveal how coronavirus attacks the lungs and kills people.

Such is the ferocity with which coronavirus can target the lungs, even otherwise healthy people can fall seriously ill – and could die.

The images, from George Washington University Hospital in Washington DC paint a stark picture of the potential impact of the COVID-19 disease, which can be so serious that even patients who survive may be left with lifelong breathing difficulties.

In these images, which were recreated from the university’s first COVID-19 patient in mid-March, the green areas show where the virus has damaged tissue in the lungs.

Image:
The infection causes the lungs to become inflamed. Pic: George Washington University Hospital

“There is such a stark contrast between the virus-infected abnormal lung and the more healthy, adjacent lung tissue,” explains Dr Keith Mortman, chief of thoracic surgery at GWHU.

“The damage that we’re seeing is not isolated to any one part of the lung.

“This is severe damage to both lungs diffusely.”

Such damage could come in the form of an illness such as pneumonia or acute respiratory distress syndrome (ARDS), which stops oxygen from reaching vital organs.

Normally oxygen would enter down the windpipe and head into the lungs, filling up air sacs that then enter red blood cells, which in turn circulate around the heart and the body.

ARDS would stop the oxygen before it gets to the lungs, starting a domino effect for the rest of the body.

Image:
The damage can stop oxygen getting to vital organs. Pic: George Washington University Hospital

GHWU has been using its so-called Surgical Theater VR technology since 2016 – it has previously been used for surgical planning and to educate patients.

The COVID-19 patient – a man in his late 50s – had mild symptoms (fever, cough, shortness of breath) to start with, but his condition deteriorated and he needed to be hospitalised and placed on a ventilator.

When his condition escalated further, he was transferred to GWUH for more intensive treatment called ECMO, which stands for extracorporeal membrane oxygeneration.

It sees blood removed from the body, infused with oxygen, and then returned to the body.

Image:
The patient is a man in his 50s who initially had mild symptoms. Pic: George Washington University Hospital

Speaking on GWHU’s coronavirus podcast, Dr Mortman said the damage shown in the images suggests COVID-19 could have long-lasting effects on its most critical victims.

He said: “It starts off as a viral infection, but you can see that it becomes severe inflammation in the lung, and when it does not subside it becomes scarring, creating long term damage.

“It could really impact somebody’s ability to breathe in the long term.”

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Your guide to self-isolating

Dr Mortman said that while the majority of people who get infected will recover well from minor symptoms or have no symptoms whatsoever, around 20% will develop more severe problems.

Hospital admission, intensive care treatment and ventilation could all follow.

“People who so far have not been heeding the warning of public health professionals can see these images and the destruction that’s being caused in the lungs, and why these patient’s lungs are failing to the point of needing a mechanical ventilator,” he said.

“Hopefully the public can see these images and start to understand why this situation is so serious and how this virus really is not discriminating among various people.”

Heart Lung Machine – an overview

Cardiopulmonary Bypass

The concept of cardiopulmonary bypass (CPB), commonly known as the heart–lung machine, became a reality in the early 1950s when it was used in a succession of patients to correct congenital cardiac problems such as atrial septal defect, the failure of the completion of the formation of a partition between the left atrium and the right atrium. CPB is a form of extracorporeal circulation, meaning circulation outside of the body. Substituting a machine for the heart and lungs to pump the blood and provide gas exchange allowed surgeons to stop the heart and stop ventilation so as to have an opportunity to open the heart and work on its interior, correcting and reconstructing congenital defects. As CPB began to evolve and improve in the first decade of its use, pioneering medical centers and surgical teams began to use it for acquired cardiac problems, such as valve surgery, in addition to correcting congenital defects. By the 1960s, valve replacement surgery became a reality, and at the beginning of the CABG era in the early 1970s, CPB was used as well.

With the ability of the surgeon to stop the heart and work on its interior during this era, the potential to apply lessons learned in peripheral vascular surgery to the coronary arteries became real. The coronary arteries course over the surface of the heart (epicardial) and are visible and palpable. The use of the principles of peripheral aterial bypass to the coronary arteries was applied in the early days of CABG, and with CPB and cardioplegia, the surgeon was now able to work in a still, bloodless field, using familiar techniques in this new setting.

The heart and lungs provide gas exchange and perfusion of more than 37 trillion living cells. The idea of designing a machine that could take over the function of the heart and lungs was conceptualized in 1813 by Le Gallois; however, the first attempts to actually apply the concept occurred in the early 1950s (Groom and Fitzgerald, 2017). The first successful use of cardiopulmonary bypass was in 1953 by a surgeon, John H Gibbon Jr., and his team at Jefferson Hospital in Philadelphia, Pennsylvania (Stammers, 1997). Gibbon used his heart–lung machine to “perfuse the patient” allowing her heart to be stopped while he and his team opened her right atrium and sutured closed her atrial septal defect. The early years following that landmark case were not so promising. Five subsequent procedures at Jefferson Hospital where cardiopulmonary bypass was used by Gibbon were not successful as all five patients did not survive, and he abandoned the use of the heart–lung machine. At least seventeen other cases were performed in the early 1950s using some form of extracorporeal circulation, and only Dr. Gibbon’s patient survived. Nonetheless, his one successful case served to inspire others, including John Kirklin at The Mayo Clinic, C. Walton Lillihei at the University of Minnesota, and Denis Melrose at Hammersmith Hospital in London, to press with their research and application the heart–lung machine with CPB techniques that were crude compared to today’s standards. (Fig. 15).

Fig. 15. The Mark-Clowes heart–lung machine with a membrane oxygenator in use at Maine Medical Center in 1959. Sixteen units of donor blood were needed to prime this heart-lung circuit.

With permission from Archives of Maine Medical Center.

The accomplishments of these early pioneers in cardiac surgery have been described as being “one of the boldest and most successful feats of man’s mind.” (Eloesser, 1970).

Since the 1950s, CPB has steadily improved in terms of survival and reduction in complications such as hemorrhage, stroke, and kidney injury. CPB techniques are used for temporary or longer-term support, known as extracorporeal membrane oxygenation (ECMO).

CPB has been designed as an integrated system that provides nutritive solutions with an appropriate hemodynamic driving force to maintain whole-body homeostasis, protecting the patient from ischemic injury. Over the last three decades options for the use of CPB for coronary artery revascularization have been developed such as percutaneous interventions (angioplasty and stenting), and by surgical procedures not utilizing CPB, collectively called off-pump CABG surgery (OPCAB) and procedures using hybrid miniaturized circuits to support the circulation during grafting.

The benefit of CPB was validated in a randomized clinical trial, the Randomized Off-pump or On BYpass (ROOBY) trial, involving 2203 elective or urgent coronary artery bypass grafting (CABG) patients randomized to either off- or on-pump surgery is a testament to the efficacy and safety of CPB as currently practiced. At one year, the on-pump group had significantly better composite outcomes (death, myocardial infarction, or repeat revascularization) than the off-pump group (9.9% vs. 7.4%; P = 0.04). The overall rate of graft patency was lower in the off-pump group than in the on-pump group as well (82.6% vs. 87.8%; P < 0.01).

The ROOBY Trial and other trials demonstrated that off-pump CABG yielded no advantage in clinical outcomes and cost over on-pump CABG (Shroyer et al., 2009). A metaanalysis which included 12 randomized clinical trials reported a 38% increased rate of early revascularization with off-pump surgery (Takagi et al., 2013). Moller and colleagues published a systematic review including over 15,000 subjects that reported no clinical benefit in mortality, stroke, or myocardial infarction or increased survival benefit of OPCAB (Møller et al., 2012).

A cardiovascular perfusionist is a specialized healthcare professional who operates the heart–lung machine during cardiac surgery and other surgeries that require cardiopulmonary bypass to manage the patient’s circulatory physiology (Fig. 16). After a patient’s circulation is accessed thru large cannulae (tubing providing connection to the CPB circuit) in the right atrium in the ascending aorta, the perfusionist, under the direction of the heart surgeon, has the ultimate aim of providing satisfactory gas exchange and metabolic needs at the cellular level (Galletti and Brecher, 1962). CPB is being used to provide perfusion for about 1.4 million patients each year around the globe. It has become evident that efforts should be directed toward measuring the adequacy of perfusion at the cellular level and at the end organ level is where we should be focusing our attention as we try to improve patient support with CPB (Ranucci et al., 2005; Demers et al., 2000; de Somer et al., 2011).

Fig. 16. S-5 Heart-lung machine (LivaNova, Houston, TX). The cardiovascular perfusionist operating the pump is seated at the lower left.

With permission from RC Groom, CCP, Director of Cardiopulmonary Perfusion, Maine Medical Center, Portland Maine, USA.

The principal component of the Heart–lung machine includes pumps, reservoirs, tubing, and filters. The CPB circuit consists of a number of components for gas exchange, temperature regulation, filtration, monitoring, and safety mechanisms. Fig. 17 is a diagram of the various components of the CPB circuit (Kim et al., 2013).

Fig. 17. Diagram of a cardiopulmonary bypass circuit. (A) Centrifugal pump, (B) reservoir and oxygenator, (C) solution, (E) heart–lung machine, (F) cardioplegia heat exchanger, (G) manometer for the cardioplegia system, (H) del Nido cardioplegia solution.

Reprinted with Permission J Extra Corp Technol 2014 46(4): 317–323.

Blood drains by gravity or with the use of gentle suction into the oxygenators venous reservoir labeled (B). (A) represents the arterial pump that pumps the blood from the venous reservoir (B) and delivers blood to the membrane oxygenator which is attached to the lower part of the venous reservoir. Once oxygen, carbon dioxide, and heat exchange have occurred the blood is directed thru an arterial blood filter (C). A purge line to the upper most part of the filter and serves for the removal any microemboli that may have been introduced into the blood during its passage through the circuit. The oxygenated blood is introduced back into the patient’s circulatory system through a cannulae (a large tube connected to the circuit) placed in the ascending aorta. The line attached to intravenous bags labeled (D) provides a method for priming the CPB circuit with electrolyte fluid or a port for adding blood during bypass. Four roller pumps labeled (E) in the diagram are auxiliary pumps. The one on the far left is used to pump cardioplegia solution with a mixture of blood and additives, labeled (H), used to arrest the heart. This solution is cooled with a separate heat-exchanger labeled (F).

90,000 Lungs, heart and kidneys: what COVID-19 patients will suffer from

Coronavirus leads to serious complications in a person who has undergone a new infection, scientists say. So, according to British researchers, COVID-19 can cause pneumonia, from which the patient will have to be treated for up to 15 years. Meanwhile, cardiologists say that any patient can develop heart disease as a result of COVID-19 disease, and neurologists warn of irreversible kidney damage as a result of infection.

“It will take 15 years to recover”

Lungs in patients who have undergone coronavirus COVID-19, even after recovery, may remain damaged – their treatment will take up to 15 years. This is evidenced by a study by the British Faculty of Intensive Care Medicine (FICM), reports The Sunday Times.

The staff of the institution recorded that many of those infected with the coronavirus who were admitted to the intensive care unit developed acute respiratory distress syndrome (ARDS) – an inflammation of the lungs that prevents the supply of vital organs with sufficient oxygen.

In Wuhan, where the outbreak was recorded, 17% of all COVID-19 infected people who were examined between January 1 and 20 developed ARDS, according to the US National Center for Biotechnology. At the same time, another study, published in the scientific journal The Lancet, claims that 29% of patients seen from mid-December to early January in Wuhan developed ARDS.

FCIM explained that the mucous membranes of the lungs of these infected people were inflamed from the coronavirus – as a result, fluid from the nearby blood vessels seeped into the air sacs of the lungs, thereby making it difficult to breathe.

Those who have this problem may “take up to 15 years for their lungs to heal.”

Now the mortality rate from this syndrome is 30-40%, said the deputy director of the University of California at San Francisco for intensive care medicine Michael Matthew. “There is no specific treatment for ARDS. You can only use a ventilator for a long time to give patients the opportunity to recover, but this is not done. Survivors with ARDS are limited in physical activity and have poor physical condition associated with severe muscle wasting and weakness, ”he explained to The Sunday Times.

At the same time, older people are most susceptible to ARDS due to weaker immunity, according to a study by the American Medical Association.

“The heart may be affected”

The Faculty of Intensive Care Medicine warns that the coronavirus can leave other organs damaged as well. “The heart can be affected, ranging from inflammation (myocarditis) to heart failure,” the study said.

One in five coronavirus patients in Wuhan had heart damage, according to a study published in the scientific journal JAMA Cardiology.

At the same time, not all those infected had chronic heart disease. “We are seeing cases where people who do not have chronic heart disease are injured. You can imagine if the heart already has problems with work. Such a patient does not have the opportunity to cope with such a problem, ”said the deputy director for preventive cardiology at the School of Medicine. Johns Hopkins Erin Michos on Radio Science.

According to South Korean cardiologist Kim In Chol, there are three main ways coronavirus can damage the heart, reports The Korea Herald.At the first, the patient has a low level of oxygen in the blood or hypoxia. As a result, the capacity of the lungs to exchange carbon dioxide for oxygen is compressed, which injures the heart muscle. Second, a vital organ can be damaged by an extreme immune response called a cytokine storm that attacks healthy tissue – including the heart.

According to the latest version, the coronavirus can directly affect the heart muscle by binding to the membrane protein ACE2 in heart cells.

It is noted that the infection can aggravate existing cardiovascular disease or cause new heart problems in healthy patients, which they will then struggle with throughout their lives.

So, COVID-19 can cause rupture of atherosclerotic plaques in the coronary arteries, followed by a heart attack, as well as lead to atrial fibrillation and, in general, deterioration of the heart, according to a study by the European Society of Cardiology.

“It is likely that even in the absence of prior heart disease, the heart muscle may be affected by coronavirus disease.In general, damage to the heart muscle can occur in any patient with or without heart failure, but the risk is higher in those already suffering from the disease, ”said Dr. Mohammad Majid, assistant professor of cardiology at the McGovern School of Medicine at the University of Texas.

“Acute kidney injury”

As mentioned earlier, the coronavirus enters the body by binding to a type of receptor called ACE2 – they are found not only in the cells of the heart and lungs, but also in the kidneys.This could damage the organ, George Thomas, a nephrologist at the Cleveland Clinic at the Glickman Clinic’s Institute of Urology and Kidney, told The Independent. Also, the kidneys can be injured due to a lack of oxygen or blood clots from the virus, Dr. Holly Kramer, president of the National Kidney Foundation, told NBC News.

When researchers in Wuhan performed an autopsy on people who died from COVID-19, they found that nine of the 26 who died had kidney damage – meanwhile, seven patients had traces of coronavirus in this organ.The research report was published in the medical journal Kidney International.

“This raises a very clear suspicion that at least some of the acute kidney injury we are seeing is due to a direct viral kidney injury that is different from what was seen during the 2002 coronavirus outbreak.”

– Paul Palevsky, a nephrologist at the University of Pittsburgh School of Medicine, told NBC News.

Meanwhile, the World Health Organization says there is little scientific evidence of the negative effects of COVID-19 on the kidneys.Nonetheless, James Cherry, professor of pediatrics at the David Geffen School of Medicine at the University of California, Los Angeles, said that kidney damage is still associated with coronavirus infection, but indirectly. “When you have pneumonia, you have less oxygen circulating, and this can damage your kidneys,” he explained in a conversation with the medical portal Healthline.

90,000 Pulmonary fibrosis: causes, symptoms, treatment of the disease | Diffuse, interstitial, linear, focal, idiopathic pulmonary fibrosis

Fibrosis is a diagnosis indicating scarring, while pulmonary fibrosis is scarring of the lungs.In patients with such a diagnosis, the elastic properties and extensibility of the lung tissue are reduced, the passage of oxygen through the walls of the alveoli is difficult. The disease is extremely difficult to treat and can lead to irreversible consequences. Pathology is found in most cases in people over 60 years old.

Symptoms of fibrosis

Among the pronounced symptoms of pulmonary fibrosis:

• shortness of breath, which worsens after exercise,
• attacks of dry cough,
• persistent chest pain,
• wheezing,
• discoloration of lips and limbs,
• increase in phalanges,
• weight loss,
• fatigue and general weakness.

Other diseases of the respiratory system also have similar symptoms, so if unpleasant signals appear, it is best to consult a doctor immediately. An accurately diagnosed diagnosis will help in a short time to make the most correct decision about the treatment regimen and start implementing it.

Causes of the disease

Pathology can be caused by various reasons:

• hereditary predisposition,
• inflammatory processes in the lungs,
• infectious diseases,
• negative impact of the environment,
• work in hazardous production,
• exposure to radiation therapy,
• chronic autoimmune diseases,
• complication of lung diseases,
• treatment with various drugs.

Bad habits, such as smoking, can also cause dangerous pathology. However, there are cases of the development of the disease without the presence of any pronounced cause. Each individual patient must undergo a full examination to identify the factors that influenced the onset of the pathology, this will help to choose the right treatment that will significantly improve the condition.

Types of disease

There are two main types of pulmonary fibrosis:

• idiopathic pulmonary fibrosis, when the cause of the disease cannot be determined,
• interstitial fibrosis when the cause is clearly established.

In addition, the form of the disease can be unilateral and bilateral, focal, when a small separate area of ​​the organ is affected, and total.

Diagnostic Methods

In order to diagnose the disease, the pulmonologist will prescribe to the patient:

• general blood test,
• X-ray examination,
• CT and MRI lungs,
• tissue biopsy,
• breathing tests.

What are the complications?

If the symptoms of pulmonary fibrosis are left unattended, serious consequences and complications are possible:

• respiratory failure,
• pulmonary hypertension,
• chronic cor pulmonale,
• secondary infections.

Methods of prevention

In order to keep your lungs healthy, it is important to follow important rules:

• use personal protective equipment when working in hazardous industries,
• give up bad habits,
• timely treat lung diseases and other infectious diseases,
• to monitor the state of the respiratory system while undergoing various diagnostic and treatment methods, as well as taking certain medications.

Fibrosis treatment

Treatment of the disease is prescribed by a professional specialist, taking into account the results of the examination and the characteristics of the course of the disease in the patient. There are a number of drugs that help prevent the addition of various infections, the development of inflammation. Treatment of fibrosis is supported by therapeutic breathing exercises and the complete elimination of provoking factors. With the total form of the disease, surgical intervention is recommended.

In the early stages of the disease, therapy is used to reduce scar formation.You can consult with a pulmonologist and make an appointment by calling our clinic or through the form on the website.

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Radiology

Radiological research methods, over a short historical period of their development and use in medicine, have become one of the leading methods of scientific and clinical research. Through the use of radiography, fluoroscopy, fluorography, computed tomography, the doctor is able to observe the functioning of many organs and body systems in normal and pathological conditions without invasive intervention.This feature makes X-ray methods one of the most important in the diagnosis of diseases. With the help of X-ray diagnostics, timely recognition of various diseases, including the most frequent and formidable ones – traumatic injuries, inflammation, neoplasms, is ensured. The subject of the study of radiology, as a science, is the entire organism as a whole, and therefore this science and the methods used by it can be considered universal.

In all types of X-ray examinations, a beam of X-rays is directed to the examined part of the body.The radiation that has passed through the patient’s body hits a film or digital receiver, which transmits the resulting image to a computer screen. The image on the film becomes visible after photo processing.

X-ray examination is based on the special property of X-rays to penetrate dense opaque media and be absorbed by them to an unequal extent, depending on their chemical composition and physical properties. As a result, a flat image of internal organs is obtained on a photosensitive screen that senses X-rays that have passed through a part of the human body.Different organs and tissues give shadows of unequal intensity on the screen, which makes it possible to distinguish them from each other. For example, against the background of the lungs transparent for X-rays, you can examine the heart (set the size, position), determine the inflammatory areas in the lungs. Direct X-ray examination is especially successfully used in the diagnosis of the integrity of the bones of the skeleton, since the bone tissue absorbs X-rays to the greatest extent and contrasts very well against the background of the rest of the tissues of the human body.

When performing an X-ray examination, an image of the translucent part of the body is usually first obtained on a light-sensitive screen ( fluoroscopy ). In this case, the doctor has the ability to position the person relative to the radiation source in such a way that the image of the examined organ is the most informative from the diagnostic point of view. Then the image is fixed on a light-sensitive material ( X-ray ) for further decoding and documentation of the study.

At fluoroscopy, intense shadows on the screen correspond to dense organs and tissues, lighter shadows refer to less dense formations containing gas, i.e. the image is positive. On radiographs, the image is negative, i.e. the ratio of darkening and enlightenment is the opposite. Since in fluoroscopy and radiography, shadow images are opposite to each other by their nature, in everyday practice, in order to avoid misunderstandings that may arise when interpreting negative and positive images, any radiological picture is always described on the basis of positive (i.e.that is, those taking place with scopic transmission) relations. For example, a metallic foreign body in the lungs causes the appearance of a completely bright area in the image, which, when described, is designated as an intense shadow …

Our medical center has a modern digital X-ray machine AXIOM Iconos R200 manufactured by Siemens, which provides the entire spectrum of X-ray diagnostics from head to foot, incl. in bedridden patients, including fluoroscopy, radiography and tomography, both on film and in digital form.During the research, the visual and voice contact of the radiologist with the patient is constantly maintained.

The device includes a patient’s rotary table with a variable inclination from -17 ° to + 90 ° with a radiator mounted above the table on a motorized stand, 40 cm. electro-optical converter, X-ray generator with digital control Polydoros (65 kW), remote control. The complex is equipped with a powerful digital FLUOROSPOT COMPACT system, which provides very high image quality and low radiation exposure, as well as a film-free technology for real-time patient research with post-processing and the ability to archive 1024×1024 images to a hard disk and CDs (up to 360 images.on 1 disk).

The digital system allows, in addition to conventional X-ray studies with digital archiving of images, to perform peripheral angiography (including subtraction), tomography, there are programs to reduce radiation exposure by 90%, the ability to transfer images over computer networks in DICOM format and obtain high-quality hard copies X-ray images on a laser or thermal film camera.

Research in progress:

• Fluorography (X-ray of the lungs and other organs of the chest).The study is indispensable for the diagnosis of pathologies of the lungs and heart. It is a highly informative, affordable and safe method.
• Radiography of bone structures, including the structures of the skull, as well as the structures of the spine with functional studies of its sections, which allows detecting deformations, displacements, fractures, and masses.
• X-ray examination of organs of the chest (lungs, heart) and gastrointestinal tract (esophagus, stomach, duodenum 12), including those with normal and double contrast.
• Irrigoscopy – contrast fluoroscopic examination of the large intestine by the method of retrograde filling, including under conditions of double contrast.
• Hysterosalpingography (HSG) contrast radiographic examination of the woman’s reproductive system to identify obstruction of the fallopian tubes, as one of the causes of infertility.

Recording and preparation for complex examinations (X-ray of the stomach, urography, irrigoscopy, etc.)must be discussed with an X-ray laboratory assistant as these studies take considerable time.

Rules for conducting X-ray examinations,
established by the Ministry of Health and federal laws of Russia

Research on children .

• Strictly as directed by a doctor.
• Mandatory in the presence of adults.
• Required documents: Birth certificate of the child OR passport of one of the parents, where the child is registered .
• When conducting research, infants and young children require the presence of 2 adults (for fixing an infant (movable) child on the table of the apparatus)

FLG (fluorography) – passport is required.

Additional documents. In accordance with the legislation of Russia (Rules for the provision of paid medical services by medical organizations dated 04.10.2012 No. 1006), when concluding a contract for the provision of medical services, the contract must contain the customer’s (patient’s) data: full name, passport data, address of residence.Thus, to conclude a contract for the provision of medical services, the patient must provide his passport data

Perfusion lung scintigraphy

Lung perfusion scintigraphy is a study of pulmonary blood flow using special radiopharmaceuticals (RP), which are distributed in the lungs in proportion to pulmonary blood flow. In those places where the blood flow is most intense – the accumulation is higher, where it is reduced – the accumulation is lower, up to a complete absence.

Preparation for lung scintigraphy: no preparation required.

Benefits:

• Sensitive method for detecting thromboembolism of the branches of the pulmonary artery, both large and small
• Imaging in combination with low-dose CT to assess structural changes in the lungs
• Evaluation of the study results is carried out in accordance with the modified PIOPED II criteria, based on the recommendations of the European Radiological Societies
• Each report is prepared by two doctors of the department (“double reading” method), if necessary, with the involvement of the staff of the Department of Radiation Diagnostics and Therapy of the leading medical university of Russia – RNMU named after N.I.N.I. Pirogov and issued on the day of research

Indications for lung scintigraphy:

• Thromboembolism of the branches of the pulmonary artery (PE).
• Determination of the degree of invasive growth of lung tumors.
• Quality control of treatment.

Contraindications: pregnancy, with caution when breastfeeding.

Restrictions:

• Patients with severe pulmonary arterial hypertension.
• Patients with severe pneumosclerotic changes in the lung tissue.

Features of the study: the study is short-term, takes from 10 to 15 minutes, is carried out immediately after the introduction of the radiopharmaceutical. The conclusion is issued on the day of the study.

Used radiopharmaceuticals (RFP):
Macrotech, 99mTc: Macroaggregates of human serum albumin (MAA) labeled with 99m-Technetium (99mTc-MAA).Introduced intravenously. The method is based on temporary embolization of the arteriolar-capillary bed of the lungs (approximately one ten-thousandth of its volume, which in no way can lead to a clinically significant impairment of pulmonary perfusion). In case of vascular occlusion (PE), MAA does not penetrate into the capillary network of the affected areas of the lung and these areas are visualized on scintigrams as perfusion defects.

Patients, coming to the study, must have extracts from medical records or an outpatient card, X-ray results and conclusions (if any) CT, MRI.

Normal perfusion lung scintigraphy in the anterior, two lateral and posterior projections: is normal, the image obtained when recording in the anterior, posterior and lateral projections corresponds in its shape and position to the radiological picture of the lung. The boundaries of the pulmonary fields are well visualized, the distribution of the drug in the lungs is uniform, there are no zones of hypofixation.

Microscopic picture of the myocardium, liver and lung tissue in chronic heart failure and its dynamics when using medicinal substances

ZAMOTAEVA M.N., Sul’din A. M., Erastova M. V., Inchina V. I., Konorev V. V., Kuznetsov Yu. V.

MICROSCOPIC PICTURE OF MYOCARDIAL, LIVER AND PULMONARY TISSUE IN CHRONIC HEART FAILURE AND ITS DYNAMICS WHEN USING DRUG SUBSTANCES Abstract. This article is devoted to the study of the microscopic picture of the myocardium, liver and lung tissue in chronic heart failure in the experiment and its dynamics with the introduction of medicinal compounds in order to correct the disorders that occur under the influence of oxidative stress.High cardioprotective activity of Ambiol and effective correction of disorders in the lungs and liver in 3-hydroxypyridine acetylcysteinate have been demonstrated.

Keywords: chronic heart failure, experimental model, antioxidants, cytoprotectors.

ZAMOTAEVA M. N., SULDIN A. M., ERASTOVA M. V., INTCHINA V. I., KONOREV V. V., KUZNETSOV YU. V.

MICROSCOPIC PATTERN OF MYOCARDIUM, HEPATIC AND PULMONARY TISSUE IN CHRONIC HEART FAILURE AND ITS DYNAMICS WHEN USING MEDICAL SUBSTANCES Abstract.This article presents a study of the microscopic picture of myocardium, hepatic and pulmonary tissue in chronic heart failure in experiment and the dynamic changes with introducing medication in order to correct disorders arising under the influence of oxidative stress. High cardioprotective activity of ambiol and effective correction of lung and liver disorders in 3-oxypyridine acetylcysteine ​​were convincingly demonstrated.

Keywords: chronic heart failure, experimental model of CHF, antioxidants, cytoprotectors.

Introduction. In 2018, the Global Burden of Disease study for Russia and the CIS countries ended, covering statistical data from 1980 to 2016, which once again showed that diseases of the heart and blood vessels still rank first in terms of their importance, both in medical and and in social aspects [1]. Chronic heart failure (CHF), being a disappointing result of the cardiovascular continuum, significantly reduces the quality of human life and reduces the overall life expectancy of the country’s population, with a prevalence in the Russian population of about 7% [2].

At the same time, despite the achievements of medicine in the field of cardiology and cardiac surgery, the introduction of such groups of drugs as antagonists into treatment protocols

RAAS and highly selective beta-blockers acting on the main links in the pathogenesis of cardiovascular diseases, a poor prognosis in CHF remains. This requires us to search for new ways to solve this problem.

When considering the pathogenesis of CHF, we come to the conclusion that, along with the activation of neurohormones and a decrease in the systolic function of the left ventricle, the most common process that damages both the heart and other organs is lipid peroxidation (LPO), mediated by immuno-inflammatory reactions with increased expression of pro-inflammatory cytokines , as well as imbalance between free radicals and the activity of antioxidant enzymes, leading to oxidative stress (OS) [3; four].

Disturbances in CHF caused by damage and remodeling of the myocardium lead to structural and functional changes and decreased functions in all organs and tissues of the body. In the pathogenesis of CHF, hemodynamic and ischemic mechanisms of damage to the liver and lungs are closely intertwined. Ischemia provokes LPO activation. All this leads to the formation of ischemic hepatitis, congestive hepatopathy, the end of which, in the later stages of CHF, is cardiac fibrosis and cirrhosis of the liver [5; 6].Similar mechanisms lead to lung damage [7].

Thus, the search and study of compounds that affect these processes is justified and, in the future, will give us another group of drugs that have a protective effect not only on the heart, but also on other “target organs” that can improve the prognosis and quality of life of patients with CHF.

Materials and methods.The experiments were carried out on 48 non-linear white rats, which were kept in accordance with standard vivarium conditions. The animals were divided into 6 groups, 8 rats each: 1st – intact; 2nd – control, in animals of which a model of chronic myocardial damage was formed by the introduction of epinephrine hydrochloride at a dose of 1 mg / kg and oxytocin at a dose of 5 U / kg three times, intraperitoneally with an interval of 48 hours; in the 3rd group, for the purpose of correction, Mexidol was administered at a dose of 25 mg / kg; in the 4th – 3-hydroxypyridine acetylcysteinate at a dose of 25 mg / kg; in the 5th group, the correction was carried out with Ambiol at a dose of 17 mg / kg.At the end of the formation of the model, the compounds were injected daily intraperitoneally for 10 days. Then, a study of the macro- and microscopic state of the target organs of animals (heart, lungs and liver) was carried out: their appearance, the percentage of organ weight to body weight or relative weight was characterized, using a Mikmed-6 microscope and the ToupView program, morphometry of micropreparations stained hematoxylin and eosin. Statistical processing of the material was carried out

on a personal computer with the statistical software package “Excel”.Using the Student’s t-test, the reliability of the difference in arithmetic means was calculated at a significance level of 5%.

Results and discussion. The relative heart weight of the animals of the 1st group was 0.4 ± 0.01% of the body weight. Macroscopic picture: the color of the heart is normal, the epicardium is brilliant. In group 2, there is a significant increase in the relative heart mass by 23% (p <0.05), the surface of the heart is dull. Microscopically, areas of necrosis were revealed, on which shrinkage and deformation of nuclei, a decrease in their size, hyperchromia, displacement of nuclei to the periphery of cells are visible, thus, the nuclei of cells underwent karyopyknosis.The cytoplasm is more oxyphilic. The destruction of cells and fibers of cardiomyocytes is expressed, areas of their compensatory hypertrophy are found. There are pronounced interstitial and pericellular edema, diffuse cellular infiltration, and replacement of individual parts of the myocardium with connective tissue are observed. Expressed plethora and dystonia of the vessels in the stroma, especially in the microcirculatory unit, there is a marginal standing of leukocytes, there are hemorrhages between the muscle fibers.

In the 3rd group of rats, the relative heart mass decreased by 7% in relation to the control.On macroscopic examination, the epicardium is dull. The microscopic picture is close to intact animals: cell nuclei and cytoplasm are slightly changed, destroyed cardiomyocytes practically did not occur, the microvasculature was without pathological changes, hemorrhages were absent, but the severity of interstitial edema and cellular tissue infiltration continued.

In the 4th study group, there was a significant decrease in the relative heart mass of animals by 35% (pk <0.05) in relation to the control.Macroscopically, the epicardium of the heart is brilliant. The histological picture: the cardiomyocytes are structurally similar to those in intact animals, there are no hemorrhages, interstitial edema persists, but its severity is much less than in the previous group, there is insignificant cellular infiltration.

In the 5th batch of animals, when compared with the control, it was noted that the relative heart mass significantly decreased by 30% (pk <0.05).On macroscopic examination, the epicardium is brilliant. Microscopic picture: the cellular structure is normal, there are no hemorrhages, interstitial edema is not pronounced, there is no cellular infiltration.

According to the results of morphometry in the control group of animals, there were 39 ± 7 large nuclei and 84 ± 12.2 small nuclei in the fields of view, 0.6 ± 0.5 cell clusters (replacement connective tissue). Correction with Mexidol reduced the number of large nuclei

by 31%, and the number of small nuclei increased by 15.3% in relation to the control, the number of cell clusters did not change.Correction of 3-hydroxypyridine with acetyl cesteinate led to an increase in the number of large nuclei by 15% and a decrease in the number of small nuclei by 24% in relation to the control, the number of cell clusters is 67% less than in the control. Against the background of the use of ambiol, the number of large nuclei increased by 64% in comparison with the 2nd group of animals, and the number of small nuclei decreased by 43% compared to the control, no accumulations of cellular elements were found.

In intact animals, the relative lung mass was 0.5 ± 0.2% of the total body weight.On a macroscopic examination, the lung tissue is pink, airiness is normal, the visceral pleura shines in the light. In animals of the 2nd series, an increase in the relative mass of the lungs by 92% was noted. Macroscopic examination: the color of the lungs is reddish, the size is increased, in some animals, when cut, foamy sputum is pronounced. Histological characteristics: the transverse size of alveocytes is increased, there are visible areas of increased oxyphilicity of the cytoplasm. In the lung tissue, there are focal atelectasis and distelectasis, the phenomenon of acute alveolar emphysema, pronounced diffuse cellular infiltration, edema of the interstitial and alveolar tissue, full-blooded vessels with single intraalveolar hemorrhages are noticeable.

The relative weight of the lungs of animals from the 3rd group decreased by 26% compared to the control. Macroscopically, the visceral pleura is dull, airiness is normal. Histologically, single foci of distelectasis are revealed, oxyphilic coloration of the cytoplasm of cells is noted, the intensity of interstitial edema is reduced in relation to the control, a decrease in cellular infiltration and the disappearance of alveolar edema, and the absence of hemorrhages.

The relative weight of the lungs of rats from the 4th series decreased in comparison with the control by 28%.On examination, the airiness of the lung tissue is normal, the visceral pleura reflects light. Microscopic picture: the cellular structure of the alveoli is not disturbed, there are no cellular infiltration, tissue edema and hemorrhages. In animals of the 5th group, a decrease in the relative mass of the lungs in relation to the control by 27% was noted, the macro- and microscopic characteristics converge with those in the previous series of animals.

In animals of the 1st group, the relative weight of the liver is 3.2 ± 0.2% of the total body weight.Macroscopically, the color of the liver is red-brown; it is covered with a shiny visceral peritoneum. The relative liver mass in rats of the 2nd series significantly increased by 46% (p <0.05). On macroscopic examination, the surface of the liver is cloudy, the color is pale brown. Microscopic characteristic: lobular structure is expressed

is unsatisfactory, the cytoplasm of hepatocytes is granular, the cells are prone to hydropic dystrophy, interstitial edema is expressed, there are areas of cellular tissue infiltration, the central vein is full-blooded and dilated, central necrosis is observed in the liver lobules, and there are also areas of liver tissue with linear necrosis.

The relative liver weight of the animals of the 3rd series decreased by 11.5% significantly compared to the control. Macroscopically, the color of the organ is red-brown, the visceral peritoneum is unclear. Microscopic picture: the granularity of the cytoplasm of the cells is preserved, the interstitial edema of the tissue is less pronounced than in the previous series, the cellular infiltration is preserved, the central veins are full-blooded. There are no hepatocytes with hydropic dystrophy, and areas of necrotic liver tissue.

When compared with the control in animals of the 4th series, a significant decrease in the relative weight of the liver by 26% (pk <0.05) was revealed. On examination, the color of the liver is red-brown, the surface is shiny, the edges are even. Microscopic picture: the lobular structure of the tissue is well expressed, the cytoplasm is not granular, there are no signs of hydropic dystrophy and destruction of hepatocytes, the central veins of the lobules are less dilated, there is no interstitial edema, there are isolated areas of cellular infiltration.

In the 5th group of the studied animals, the decrease in the relative mass of the liver in relation to the control group was 13%. Macroscopic examination: liver tissue is red-brown, the surface is dull. The results of microscopic examination are similar to the results of the 3rd series of rats.

Conclusions. In this study, Mexidol at a dose of 25 mg / kg, Ambiol at a dose of 17 mg / kg and 3-hydroxypyridine acetylcysteinate at a dose of 25 mg / kg significantly improve the state of the organs under investigation according to microscopic examination.Possessing an inhibitory effect on LPO processes and the development of OS, these substances effectively protect the heart and “target organs” from damage and the development of congestive plethora in them.

These compounds have unequal cytoprotective effect. Thus, Ambiol at a daily dose of 17 mg / kg showed the greatest cardioprotective ability, compared with 3-hydroxypyridine acetylcysteinate and mexidol, slowing down remodeling of the heart ultrastructure.

According to the experimental data, 3-hydroxypyridine acetylcysteinate in a daily dose of 25 mg / kg, in relation to mexidol and ambiol, has a more pronounced hepato- and pulmoprotective effect, reducing congestion in these organs.

Mexidol at a daily dose of 25 mg / kg, having a cytoprotective effect on the studied tissues, compared to other compounds, was less effective in CHF.

REFERENCES

1. Starodubov V. I. The burden of disease in Russia from 1980 to 2016: a systematic analysis for the Global Burden of Disease Study 2016 // Lancet. – 2018. – Vol. 392 (10153). – P. 1138-1146.

2. Garganeyeva AA, Bauer VA, Borel KN Pandemic of the XXI century: chronic heart failure is a burden of modern society.Epidemiological aspects (literature review) // Siberian medical journal. – 2013. – No. 29 (3). – S. 8-12.

3. Okovityy SV, Sukhanov DS Antihypoxants in modern clinical practice // Clinical medicine. – 2012. – No. 90 (9). – S. 63-68.

4. Frolova EB, Yaushev MF Modern understanding of chronic heart failure // Bulletin of modern clinical medicine.- 2013. – No. 2. -S. 87-93.

5. Storozhakov GI, Ettinger OA Liver damage in chronic heart failure // Heart failure. – 2005. – No. 1. – S. 28-32.

6. Bhogal R. H., Curbishley S. M., Weston C. J. Reactive oxygen species mediate human hepatocyte injuri during hypoxia | reoxygenation // Liver Transpl. – 2010. – Vol. 6. -P. 1303-1313.

7.Zhilyaeva Yu. A., Mikhin VP State of the parameters of blood lipid peroxidation and elastic properties of the vascular wall in patients with coronary heart disease during therapy with generic statins // Kursk scientific and practical bulletin “Man and his health”. – 2013. – No. 4. – S. 66-72.

90,000 Drowning – types, signs, first aid

How long does a person live if he loses the ability to breathe? Brain cells remain viable under hypoxic conditions for no more than 5-6 minutes.Although drowning in cold water, this time may increase. In any case, assistance to the victim should be provided even before the arrival of the medical team. In this situation, the matter is decided by minutes. This is why it is so important to know how to help.

Not all people, however, are ready to answer the question, let alone show in practice how to act correctly in case of drowning. And this is very sad. For some reason, many believe that only employees of specialized services should have such skills, while an ordinary person far from medicine does not need to know this.But life sometimes puts people in difficult situations. It is very scary to see a loved one die and not know how to help him.

What is drowning? This is a life-threatening condition characterized by the inability to breathe as a result of a person getting into water or other liquid. This often fills the airways with water, although this is not strictly necessary. Death from respiratory failure can occur even if the lungs remain “dry.” By this sign, by the way, different types of drowning are distinguished.

Classification by mechanism leading to death.

Types of drowning and their characteristics:

– True Drowning. It is called so because in this case water (or other liquid) enters the lungs. The pathological processes underlying true drowning differ depending on whether the drowning has occurred in fresh or salt water.

In the first case, water quickly penetrates from the alveoli into the vascular bed, thinning the blood and destroying red blood cells.

Salt water, on the contrary, promotes the release of plasma from the vessels, which is accompanied by thickening of the blood, as well as the development of pulmonary edema.

– Asphyxia drowning. In this case, water does not enter the lungs, since the glottis closes, protecting the respiratory tract from the penetration of fluid into them. However, breathing still becomes impossible, because with laryngospasm, air is also not allowed through. A person dies from suffocation.

– Syncopal drowning. The main cause of death is reflex cardiac arrest.At the same time, the lungs remain “dry”. A similar situation is possible when drowning in very cold water.

Classification by the color of the victim’s skin.

Types of drowning by skin color:

– White asphyxia. As the name suggests, it is characterized by a pronounced pallor of the skin. Occurs if the airways are not flooded with liquid. This type is most typical for the syncope mechanism of drowning, when death occurs as a result of the cessation of cardiac activity.

– Blue asphyxia. It occurs when the victim makes a breathing movement, as a result of which the lungs are filled with water. The skin becomes cyanotic due to severe hypoxia. Death occurs due to respiratory failure. Cardiac arrest occurs after the cessation of breathing.

Appearance of the victim.

Different types of drowning have certain differences in clinical manifestations. If the victim was conscious at the time of immersion in the water, the scenario for the development of events looks something like this.A person tries to escape by swallowing water. Breathing becomes impossible, the body experiences hypoxia, as a result of which a characteristic bluish color of the skin appears. Expansion of the veins of the neck is often observed. Pink foam comes out of the mouth. If a person is removed from the water at the stage of agony, breathing and cardiac activity can still be preserved.

If drowning was preceded by depression of the functions of the central nervous system (intoxication, poisoning, intoxication), laryngospasm often occurs.The lungs are not filled with water, but death also occurs as a result of asphyxiation. The skin becomes bluish.

Syncope drowning occurs against the background of severe fright or cold shock. The cessation of cardiac activity comes to the fore in pathogenesis. The skin is pale, there is no discharge of fluid and foam from the victim’s nose and mouth, which is characteristic of other types of drowning. White asphyxia is most favorable for resuscitation, the time of clinical death with it can be significantly lengthened.

Basic principles of drowning rescue.

The types of drowning are varied and require different approaches to care, but the general principles in all cases remain the same. All events include 2 stages:

– Removing the victim from the water.

– Assistance ashore.

How to save a drowning person correctly? No matter how different types of drowning may differ from each other, first aid for drowning should begin with ensuring the safety of the rescuer himself.A drowning person (if he is still conscious) can behave extremely inadequately. That is why, when pulling the victim out of the water, you should be careful. Otherwise, the rescuer risks himself being in the role of a drowning man.

If the person is close enough to the shore, you can try to reach him with a stick, use a rope or other device to pull him out. If the victim is too far away, you will have to swim to get to him. The main thing in this situation is not to forget about the danger, because the victim can drown his savior.Therefore, you need to act quickly and unceremoniously. It is best to swim up to the drowning person from behind and wrap one hand around his neck, you can grab his hair (this is even safer), and then pull him out onto land as soon as possible.

Remember: don’t need to get into the water if you don’t swim well!

Types of drowning, first aid for drowning. Activities ashore

There are different types of drowning, and their symptoms are discussed above. This knowledge must be taken into account when providing assistance to the victim.

– Everything is extremely simple, if the person taken out of the water is conscious. The main actions will be aimed at warming him and calming him down.

– If a person is unconscious, the first thing to do is to remove water from the respiratory tract. With white asphyxia, this does not need to be done, you can immediately proceed to resuscitation.

– In the case of the blue type of drowning, first we cleanse the mouth and nose of algae, sand, etc. Then we press on the root of the tongue, thereby determining the presence of a gag reflex.Preservation of the latter means that the victim is alive, so the first priority will be to remove water from the lungs and stomach. To do this, turn the victim onto his stomach, turn his head to one side, induce vomiting in him several times, press on the chest. Then we repeat these actions every 5-10 minutes, until water stops coming out of the mouth and nose. It is necessary to monitor breathing and pulse, be ready to perform resuscitation.

– If the gag reflex is absent, an urgent need to check the existence of life support functions of the body.Most likely, they will not be. Therefore, you should not spend a lot of time (no more than 1-2 minutes) to remove water from the lungs, but start resuscitation as soon as possible.

Features of resuscitation in case of drowning

The above were different approaches to providing assistance to the victim. There are different types of drowning, it is not surprising that the measures, they require different ones. However, cardiopulmonary resuscitation is always performed according to a specific plan, which is not influenced by the causes that led to clinical death.

What is included in the complex of measures for revitalization?

– Restoration of airway patency.

– Artificial respiration.

– Indirect cardiac massage.

No matter how different types of drowning may differ, first aid always begins with cleansing the mouth and nose of sand, algae, vomit, etc. Then water is removed from the lungs. To this end, the victim should be turned face down and laid with his stomach on his knee. The head will thus be lower than the body.Now you can press on the chest, stimulating the fluid out of the lungs. If a small child is being helped, he can be thrown over his shoulder, head down, or even taken by the legs and turned over, thereby creating more favorable conditions for water to drain from the lungs.

Next, we move on to performing the triple reception of Safar. The victim should be laid on a hard surface, his head tilted back, the lower jaw should be pushed forward with fingers and, pressing on the chin, the mouth should be opened.Now you can start artificial respiration. Pressing our lips tightly to the victim’s mouth, we exhale. The criterion for effectiveness will be the lift of the chest. After two exhalations, we begin an indirect heart massage. Place the base of the right hand on the lower third of the sternum, place the left hand over the right. We begin to perform chest compressions, making sure that the arms remain straight, do not bend at the elbows. The expiration to compression ratio should be 2 to 30 (2 expirations, 30 compressions), regardless of whether one or two rescuers are performing resuscitation.