PATENT DUCTUS ARTERIOSUS

PATENT DUCTUS ARTERIOSUS

PDA is a heart problem that is frequently noted in the first few weeks or months after birth. It is characterized by the persistence of a normal fetal connection between the aorta and the pulmonary artery which allows oxygen-rich (red) blood that should go to the body to recirculate through the lungs.

All babies are born with this connection between the aorta and the pulmonary artery. While your baby was developing in the uterus, it was not necessary for blood to circulate through the lungs because oxygen was provided through the placenta. During pregnancy, a connection was necessary to allow oxygen-rich (red) blood to bypass your baby’s lungs and proceed into the body. This normal connection that all babies have is called a ductus arteriosus.

At birth, the placenta is removed when the umbilical cord is cut. Your baby’s lungs must now provide oxygen to his or her body. As your baby takes the first breath, the blood vessels in the lungs open up, and blood begins to flow through them to pick up oxygen. At this point, the ductus arteriosus is not needed to bypass the lungs. Under normal circumstances, within the first few days after birth, the ductus arteriosus closes and blood no longer passes through it.

Illustration of the anatomy of a heart with a patent ductus arteriosus
Click Image to Enlarge
In some babies, however, the ductus arteriosus remains open (patent) and the condition now becomes known as patent ductus arteriosus (PDA). The opening between the aorta and the pulmonary artery allows oxygen-rich (red) blood to recirculate into the lungs.

Patent ductus arteriosus occurs twice as often in girls as in boys.

CAUSES OF PDA
A PDA is almost always present at birth. In some children, the PDA does not close. Although exact reasons why this happens in some patients and not in others are not known, the most common association for a PDA is prematurity.

PDA can also occur in combination with other heart defects.

WHY IS PDA A CONCERN
When the ductus arteriosus stays open, oxygen-rich (red) blood passes from the aorta to the pulmonary artery, mixing with the oxygen-poor (blue) blood already flowing to the lungs. The blood vessels in the lungs have to handle a larger amount of blood than normal. How well the lung vessels are able to adapt to the extra blood flow depends on how big the PDA is and how much blood is able to pass through it from the aorta.

Extra blood causes higher pressure in the blood vessels in the lungs. The larger the volume of blood that goes to the lungs at high pressure, the more the lungs have to cope with this extra blood at high pressure.

Children may have difficulty breathing because of this extra blood flow to the lungs at high pressure. They may remain on the ventilator for a longer period of time if they are premature. The support from the ventilator also may be high, due to this extra blood flow to the lungs.

Rarely, untreated PDA may lead to long-term lung damage. This is uncommon, however, since most children will have been treated for their PDA before the lungs get damaged.

Often, the PDA may be “silent,” that is, causing no symptoms. This is especially true in older patients (beyond the first few months of life) with small PDAs.

SYMPTOMS
The size of the connection between the aorta and the pulmonary artery will affect the type of symptoms noted, the severity of symptoms, and the age at which they first occur. The larger the opening, the greater the amount of blood that passes through that overloads the lungs.

A child with a small patent ductus arteriosus might not have any symptoms, and your child’s doctor may have only noted the defect by hearing a heart murmur. Other infants with a larger PDA may exhibit different symptoms. The following are the most common symptoms of PDA. However, each child may experience symptoms differently. Symptoms may include

Fatigue

Sweating

Rapid breathing

Heavy breathing

Congested breathing

Disinterest in feeding, or tiring while feeding

Poor weight gain

The symptoms of a PDA may resemble other medical conditions or heart problems. Always consult your child’s doctor for a diagnosis.

DIAGNOSIS
Your child’s doctor may have heard a heart murmur during a physical examination, and referred your child to a pediatric cardiologist for a diagnosis. In this case, a heart murmur is a noise caused by the turbulence of blood flowing through the PDA.

A pediatric cardiologist specializes in the diagnosis and medical management of congenital heart defects, as well as heart problems that may develop later in childhood. The cardiologist will perform a physical examination, listening to the heart and lungs, and make other observations that help in the diagnosis. The location within the chest where the murmur is heard best, as well as the loudness and quality of the murmur (such as, harsh or blowing) will give the cardiologist an initial idea of which heart problem your child may have. Diagnostic testing for congenital heart disease varies by the child’s age, clinical condition, and institutional preferences. Some tests that may be recommended include the following

:Chest X-ray.

A diagnostic test that uses invisible X-ray beams to produce images of internal tissues, bones, and organs onto film. With a PDA, the heart may be enlarged due to larger amounts of blood flow recirculating through the lungs back to the heart. Also, there may be changes that take place in the lungs due to extra blood flow that can be seen on an X-ray.

Electrocardiogram (ECG or EKG). A test that records the electrical activity of the heart, shows abnormal rhythms (arrhythmias or dysrhythmias), and detects heart muscle stress.

Echocardiogram (echo). A procedure that evaluates the structure and function of the heart by using sound waves recorded on an electronic sensor that produce a moving picture of the heart and heart valves. An echo can show the pattern of blood flow through the PDA, and determine how large the opening is, as well as how much blood is passing through it. An echo is the most common way that a PDA is diagnosed.

Cardiac catheterization. A cardiac catheterization is an invasive procedure that gives very detailed information about the structures inside the heart. Under sedation, a small, thin, flexible tube (catheter) is inserted into a blood vessel in the groin, and guided to the inside of the heart. Blood pressure and oxygen measurements are taken in the four chambers of the heart, as well as the pulmonary artery and aorta. Contrast dye is also injected to more clearly visualize the structures inside the heart. The cardiac catheterization procedure may also be an option for treatment. During the procedure, the child is sedated and a small, thin, flexible tube (catheter) is inserted into a blood vessel in the groin and guided to the inside of the heart. Once the catheter is in the heart, the cardiologist will pass a special device, either a coil or a PDA occluder (depending on the size of the PDA). This device will close the PDA and therefore stop the blood flow through the PDA.

TREATMENT OF PDA

A small patent ductus arteriosus may close spontaneously as your child grows. A PDA that causes symptoms will require medical management, and possibly even surgical repair. Your child’s cardiologist will check periodically to see whether the PDA is closing on its own. If a PDA does not close on its own, it will be repaired to prevent lung problems that will develop from long-time exposure to extra blood flow. Treatment may include:

Medical management. In premature infants, an intravenous (IV) medication called indomethacin may help close a patent ductus arteriosus. Indomethacin is related to aspirin and ibuprofen and works by stimulating the muscles inside the PDA to constrict, thereby closing the connection. Your child’s doctor can answer any further questions you may have about this treatment. As previously mentioned, some children will have no symptoms, and require no medications. However, others may need to take medications to help the heart and lungs work better. Medications may be prescribed, such as diuretics. Diuretics help the kidneys remove excess fluid from the body. This may be necessary because the body’s water balance can be affected when the heart is not working as efficiently as it could. Your doctor may also ask you to restrict the amount of fluid your child takes in.

Adequate nutrition. Most infants with PDA eat and grow normally, but premature infants or those infants with a large PDA may become tired when feeding, and are not able to eat enough to gain weight. Options that can be used to ensure your baby will have adequate nutrition include the following:

High-calorie formula or breast milk. Special nutritional supplements may be added to formula or pumped breast milk that increase the number of calories in each ounce, thereby allowing your baby to drink less and still consume enough calories to grow properly.

Supplemental tube feedings. Feedings given through a small, flexible tube that passes through the nose, down the esophagus, and into the stomach, can either supplement or take the place of bottle-feedings. Infants who can drink part of their bottle, but not all, may be fed the remainder through the feeding tube. Infants who are too tired to bottle-feed may receive their formula or breast milk through the feeding tube alone.

PDA repair or closure. The majority of children and some infants with PDA are candidates for repair in the cardiac cath lab. The goal is to repair the PDA before the lungs become diseased from too much blood flow and pressure and to restore an efficient pattern of blood flow. Surgical repair is also indicated if one of the previously mentioned conservative treatments have not been successful. Repair is usually indicated in infants younger than 6 months of age who have large defects that are causing symptoms, such as poor weight gain and rapid breathing. For infants who do not exhibit symptoms, the repair may often be delayed until after 6 to 12 months of age. Your child’s cardiologist will recommend when the repair should be performed. Transcatheter coil closure of the PDA is frequently performed first if possible because it is minimally invasive. Children need to be at least 5 kg to be considered for transcatheter closure. Thus, premature infants, because of their small size, are not candidates for this procedure, and require surgical closure of the PDA. Your child’s PDA may be repaired surgically in the operating room. The surgical repair, also called PDA ligation, is performed under general anesthesia. The procedure involves closing the open PDA with stitches or clips in order to prevent the surplus blood from entering your child’s lungs.

POSTPROCEDURE  CARE  FOR  YOUR  CHILD :
Cath lab repair or closure procedure. When the procedure is complete, the catheter(s) will be withdrawn. Several gauze pads and a large piece of medical tape will be placed on the site where the catheter was inserted to prevent bleeding. In some cases, a small, flat weight or sandbag may be used to help keep pressure on the catheterization site and decrease the chance of bleeding. If blood vessels in the leg were used, your child will be told to keep the leg straight for a few hours after the procedure to minimize the chance of bleeding at the catheterization site. Your child will be taken to a unit in the hospital where he or she will be monitored by nursing staff for several hours after the test. The length of time it takes for your child to wake up after the procedure will depend on the type of medicine given to your child for relaxation prior to the test, and also on your child’s reaction to the medication. After the procedure, your child’s nurse will monitor the pulses and skin temperature in the leg or arm that was used for the procedure. Your child may be able to go home after a specified period of time, providing he or she does not need further treatment or monitoring. You will receive written instructions regarding care of the catheterization site, bathing, activity restrictions, and any new medications your child may need to take at home.

Surgical repair. Some children who undergo PDA ligation may need to spend some time in the intensive care unit after surgery. Others may return to a regular hospital room. Your child will be kept as comfortable as possible with medications which relieve pain or anxiety. The staff will also be asking for your input as to how best to soothe and comfort your child. You will also learn how to care for your child at home before your child is discharged. The staff will give you instructions regarding medications, activity limitations, and follow-up appointments before your child is discharged. Most children will only need to stay in the hospital for a few days after the operation.

HOME CARE
Most infants and older children feel comfortable when they go home. Pain medications, such as acetaminophen or ibuprofen, may be recommended to keep your child comfortable. Your child’s doctor will discuss pain control before your child is discharged from the hospital.

Often, infants who fed poorly prior to surgery have more energy after the recuperation period, and begin to eat better and gain weight faster.

After surgery, older children usually have a fair tolerance for activity. Within a few weeks, your child should be fully recovered and able to participate in normal activity.

You will receive additional instructions from your child’s doctors and the hospital staff.

PHYSIOTHERAPY INPHYSIOTHERAPY IN PRE- AND POSTOPERATIVE PERIOD

Physiotherapy in the pre- and postoperative period is indicated in pediatric cardiac surgery in order to reduce the risk of pulmonary complications (retention of secretions, atelectasis and pneumonia)  as well as to treat such complications as it contributes to the appropriate ventilation and successful extubation .

In the preoperative, physiotherapy uses techniques of clearance, reexpansion, abdominal support and guidance on the importance and objectives of physiotherapy intervention for parents or escorts, or patients able to understand such guidance . The techniques used by postoperative physiotherapy include vibration in the chest wall, percussion , compression , manual hyperinflation , reexpansion maneuver , positioning  postural drainage , cough stimulation , aspiration, breathing exercises , mobilization  and AEF (acceleration of expiratory flow)  .

There are few current studies on the role of physiotherapy in the postoperative of pediatric cardiac surgery , especially those that approach the effectiveness of physiotherapy in the preoperative to prevent pulmonary complications after heart surgery.

The study obtained statistically significant difference regarding the presence of pulmonary complications (pneumonia and atelectasis), being more frequent in the group undergoing physiotherapy only postoperatively. Moreover, when the presence of pulmonary complications was associated with other complications regarding the time of hospital stay, such as sepsis, pneumothorax, pleural effusion and others, the group that received physiotherapy before and after surgery showed a lower risk of developing such complications. These findings demonstrate the importance of preventive action of physiotherapy preoperatively.

 The respiratory parameters (expiratory tidal volume, resistance and lung compliance) were measured 15 minutes before treatment and after 30 minutes, and lasting for 60 minutes after the intervention in case there was no need for clinical intervention.

According to Kavanagh , the treatment for atelectasis consists of physiotherapy, deep breathing, incentive spirometry. However, sometimes, atelectasis is difficult to reverse and it is necessary association with another method, as in the case report from Silva et al. , in which a child with congenital heart disease underwent heart surgery and developed this pulmonary complication after extubation in the postoperative period and the reversal of this presentation was achieved after the association of respiratory physiotherapy with inhalation of hypertonic saline solution with NaCl at 6%.

Chest radiographs and four physiotherapy sessions lasting 20 minutes were performed daily in this study, using maneuvers of pulmonary reexpansion and bronchial hygiene, bronchial postural drainage and tracheal aspiration. Immediately before and after physiotherapy inhalation of hypertonic saline solution with NaCl at 6% was associated. The authors found that this association was shown to be effective in this case .

Breathing exercises are indicated in cases of atelectasis due to thoracic or upper abdominal surgery, because they improve the respiratory efficiency, increase the diameter of the airways, which helps to dislodge secretions, preventing alveolar collapse, and facilitating the expansion of the lung and peripheral airways clerance .

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ATRIOVENTRICULAR SEPTAL DEFECT

INTRODUCTION

Atrioventricular-Septal-Defect-Picture
Atrioventricular-Septal-Defect-Picture

Congenital heart diseases affect about 8 to 10 children per 1000 live births and it is estimated the occurrence of 28,846 new cases per year in Brazil, where, on average, 23,077 surgical procedures are needed per year .

The most common congenital heart diseases in the study of Miyague et al. were acyanotic anomalies such as ventricular septal defect (30.5%), atrial septal defect (19.1%), patent ductus arteriosus (17% ), pulmonary valve stenosis (11.3%) and aortic coarctation (6.3%), while the most common cyanotic anomalies were tetralogy of Fallot (6.9%), transposition of great vessels (4.1%), tricuspid atresia (2.3%) and total anomalous pulmonary veins drainage (2%).

Children with congenital heart disease often develop changes in respiratory mechanics . In addition, heart surgery associated with cardiopulmonary bypass (CPB) also leads to a number of respiratory complications . Thus, physiotherapy in pre- and postoperative period have as main objectives the pulmonary reexpansion, airway clearance and guidance for those responsible concerning prevention of these complications .

This review aimed to update knowledge regarding the role of physiotherapy in the preoperative and postoperative pediatric cardiac surgery in the prevention of pulmonary complications.

An atrioventricular septal defect (pronounced EY-tree-oh-ven-TRIC-u-lar SEP-tal DEE-fekt) or AVSD is a heart defect affecting the valves between the heart’s upper and lower chambers and the walls between the chambers.

DEFINATION
An atrioventricular septal defect (AVSD) is a heart defect in which there are holes between the chambers of the right and left sides of the heart, and the valves that control the flow of blood between these chambers may not be formed correctly. This condition is also called atrioventricular canal (AV canal) defect or endocardial cushion defect. In AVSD, blood flows where it normally should not go. The blood may also have a lower than normal amount of oxygen, and extra blood can flow to the lungs. This extra blood being pumped into the lungs forces the heart and lungs to work hard and may lead to congestive heart failure.

There are two general types of AVSD that can occur, depending on which structures are not formed correctly:

COMPLETE AVSD

Complete-AV-Canal-Defect-Patient-Zeyd-Bastas1
Complete-AV-Canal-Defect

A complete AVSD occurs when there is a large hole in the center of the heart which allows blood to flow between all four chambers of the heart. This hole occurs where the septa (walls) separating the two top chambers (atria) and two bottom chambers (ventricles) normally meet. There is also one common atrioventricular valve in the center of the heart instead of two separate valves – the tricuspid valve on the right side of the heart and the mitral valve on the left side of the heart. This common valve often has leaflets (flaps) that may not be formed correctly or do not close tightly. A complete AVSD arises during pregnancy when the common valve fails to separate into the two distinct valves (tricuspid and mitral valves) and when the septa (walls) that split the upper and lower chambers of the heart do not grow all the way to meet in the center of the heart.

PATRIAL OR INCOMPLETE AVSD
A partial or incomplete AVSD occurs when the heart has some, but not all of the defects of a complete AVSD. There is usually a hole in the atrial wall or in the ventricular wall near the center of the heart. A partial AVSD usually has both mitral and tricuspid valves, but one of the valves (usually mitral) may not close completely, allowing blood to leak backward from the left ventricle into the left atrium.

OCCURENCE
The Centers for Disease Control and Prevention (CDC) estimates that about 2,000 babies (1 in 2,120 babies) are born with AVSD every year in the United States.

CAUSES AND RISK FACTORS
The causes of congenital heart defects, such as AVSD, among most babies are unknown. Some babies have heart defects because of changes in their genes or chromosomes. In particular, AVSD is common in babies with Down syndrome, a genetic condition that involves an extra chromosome 21 (also called trisomy 21). Congenital heart defects are also thought to be caused by the combination of genes and other risk factors, such as things the mother comes in contact with in her environment, what she eats or drinks, or certain medications she uses during pregnancy.

DIAGNOSIS
AVSD may be diagnosed during pregnancy or soon after the baby is born.

DURING PREGNANCY
During pregnancy, there are screening tests (also called prenatal tests) to check for birth defects and other conditions. AVSD may be diagnosed during pregnancy with an ultrasound test (which creates pictures of the baby using sound waves), but whether or not the defect can be seen with the ultrasound test depends on the size or type (partial or complete) of the AVSD. The healthcare provider can request a fetal echocardiogram to confirm the diagnosis if AVSD is suspected. A fetal echocardiogram is an ultrasound of the baby’s heart which shows more detail than the routine prenatal ultrasound test. The fetal echocardiogram can show problems with the structure of the heart and how well the heart is working.

AFTER BABY IS BORN
During a physical exam of an infant, a complete AVSD may be suspected. Using a stethoscope, a doctor will often hear a heart murmur (an abnormal “whooshing” sound caused by blood flowing through the abnormal hole). However, not all heart murmurs are present at birth. Babies with a complete AVSD usually do show signs of problems within the first few weeks after birth. When symptoms do occur, they may include

  • Breathing problems
  • Pounding heart
  • Weak pulse
  • Ashen or bluish skin color
  • Poor feeding, slow weight gain
  • Tiring easily
  • Swelling of the legs or belly
  • For partial AVSDs, if the holes between the chambers of the heart are not large, the signs and
  • symptoms may not occur in the newborn or infancy periods. In these cases, people with a partial
  • AVSD might not be diagnosed for years.

Symptoms which might indicate that a child’s complete AVSD or partial AVSD is getting worse include

Arrhythmia, an abnormal heart rhythm. An arrhythmia can cause the heart to beat too fast, too slow, or erratically. When the heart does not beat properly, it can’t pump blood effectively.
Congestive heart failure, when the heart cannot pump enough blood and oxygen to meet the needs of the body.
Pulmonary hypertension, a type of high blood pressure that affects the arteries in the lungs and the right side of the heart.
The healthcare provider can request one or more tests to confirm the diagnosis of AVSD. The most common test is an echocardiogram. This is an ultrasound of the heart that can show problems with the structure of the heart, like holes between the chambers of the right and left side of the heart, and any irregular blood flow. An electrocardiogram (EKG), which measures the electrical activity of the heart, chest x-rays, and other medical tests may also be used to make the diagnosis. Because many babies with Down syndrome have an AVSD, all infants with Down syndrome should have an echocardiogram to look for an AVSD or other heart defects.

TREATMENT
All AVSDs, both partial and complete types, usually require surgery. During surgery, any holes in the chambers are closed using patches. If the mitral valve does not close completely, it is repaired or replaced. For a complete AVSD, the common valve is separated into two distinct valves – one on the right side and one on the left side.

The age at which surgery is done depends on the child’s health and the specific structure of the AVSD. If possible, surgery should be done before there is permanent damage to the lungs from too much blood being pumped to the lungs. Medication may be used to treat congestive heart failure, but it is only a short term measure until the infant is strong enough for surgery.

Infants who have surgical repairs for AVSD are not cured; they might have lifelong complications. The most common of these complications is a leaky mitral valve. This is when the mitral valve does not close all the way so that it allows blood to flow backwards through the valve. A leaky mitral valve can cause the heart to work harder to get enough blood to the rest of the body; a leaky mitral valve might have to be surgically repaired. A child or adult with an AVSD will need regular follow-up visits with a cardiologist (a heart doctor) to monitor his or her progress, avoid complications, and check for other health conditions that might develop as the child gets older. With proper treatment, most babies with AVSD grow up to lead healthy, productive lives.

PULMONARY COMPLICATIONS IN PEDIATRIC CARDIAC SURGERY

Pulmonary complications of postoperative pediatric cardiac surgery observed : atelectasis, pneumonia, pleural effusion, pneumothorax, chylothorax, pulmonary hypertension, pulmonary hemorrhage and diaphragmatic paralysis, whereas the first two aforementioned complications are the more common ones.

Atelectasis, defined as collapse of a certain region of the lung parenchyma . is the most common complication in the postoperative period of cardiac surgery , by worsening oxygenation, decreasing pulmonary compliance, leading to inhibition of cough and pulmonary clearance and may lead to respiratory failure and increase pulmonary vascular resistance.

Heart surgeries associated with CPB have as adverse effect the increased capillary permeability that causes edema, which results in decreased lung compliance and gas exchange , in addition to lead to airway obstruction, atelectasis, decreased functional residual capacity and, therefore, hypoxemia .

Stayer et al. assessed the changes in resistance and dynamic pulmonary compliance in 106 children aged less than one year, with congenital heart disease who underwent cardiac surgery with CPB. These variables were measured on two occasions: before the surgical incision with ten minutes of mechanical ventilation and after disconnection of CPB and sternal closure. The authors found that newborns and patients with increased pulmonary blood flow presented preoperatively decreased lung compliance and increased respiratory resistance, whereas after surgery the latter parameter has improved. On the other hand, the infants with normal pulmonary blood flow in the preoperative had decreased lung compliance and developed in the postoperative deterioration of dynamic compliance, however, the pulmonary resistance was not affected. This study showed that heart surgery can alter the respiratory mechanics in newborns and infants.

Among the most common causes of death it can be highlighted the low cardiac output syndrome (48%), followed by lung infections (11%).

Pneumonia is one of the frequent causes of nosocomial infection in the postoperative period of heart surgery and is considered a major cause of morbidity and mortality in this population . .

PHYSIOTHERAPYPHYSIOTHERAPY IN PRE- AND POSTOPERATIVE PERIOD

Physiotherapy in the pre- and postoperative period is indicated in pediatric cardiac surgery in order to reduce the risk of pulmonary complications (retention of secretions, atelectasis and pneumonia)  as well as to treat such complications as it contributes to the appropriate ventilation and successful extubation .

In the preoperative, physiotherapy uses techniques of clearance, reexpansion, abdominal support and guidance on the importance and objectives of physiotherapy intervention for parents or escorts, or patients able to understand such guidance . The techniques used by postoperative physiotherapy include vibration in the chest wall, percussion , compression , manual hyperinflation , reexpansion maneuver , positioning. postural drainage , cough stimulation , aspiration , breathing exercises , mobilization and AEF (acceleration of expiratory flow) .

There are few current studies on the role of physiotherapy in the postoperative of pediatric cardiac surgery , especially those that approach the effectiveness of physiotherapy in the preoperative to prevent pulmonary complications after heart surgery.

Felcar et al. performed a study with 141 children with congenital heart disease, aged varying between one day old to six years, randomly divided into two groups, whereas one of them received physiotherapy in the pre- and postoperative and the other only postoperatively. The study obtained statistically significant difference regarding the presence of pulmonary complications (pneumonia and atelectasis), being more frequent in the group undergoing physiotherapy only postoperatively. Moreover, when the presence of pulmonary complications was associated with other complications regarding the time of hospital stay, such as sepsis, pneumothorax, pleural effusion and others, the group that received physiotherapy before and after surgery showed a lower risk of developing such complications. These findings demonstrate the importance of preventive action of physiotherapy preoperatively.

According to Kavanagh , the treatment for atelectasis consists of physiotherapy, deep breathing, incentive spirometry. However, sometimes, atelectasis is difficult to reverse and it is necessary association with another method, as in the case report from Silva et al. [16], in which a child with congenital heart disease underwent heart surgery and developed this pulmonary complication after extubation in the postoperative period and the reversal of this presentation was achieved after the association of respiratory physiotherapy with inhalation of hypertonic saline solution with NaCl at 6%.

Chest radiographs and four physiotherapy sessions lasting 20 minutes were performed daily in this study, using maneuvers of pulmonary reexpansion and bronchial hygiene, bronchial postural drainage and tracheal aspiration. Immediately before and after physiotherapy inhalation of hypertonic saline solution with NaCl at 6% was associated. The authors found that this association was shown to be effective in this case .

Breathing exercises are indicated in cases of atelectasis due to thoracic or upper abdominal surgery, because they improve the respiratory efficiency, increase the diameter of the airways, which helps to dislodge secretions, preventing alveolar collapse, and facilitating the expansion of the lung and peripheral airways clerance .

Campos et al. analyzed the effect of increased expiratory flow (IEF) in heart rate, respiratory rate and oxygen saturation in 48 children diagnosed with pneumonia. The variables were assessed before physiotherapy, in the first and fifth minutes after physiotherapy. The authors found a statistically significant increase in oxygen saturation and statistically significant reduction in cardiac and respiratory rate after intervention with IEF and concluded that this physiotherapeutic technique for bronchial hygiene is effective in improving lung function.

FINAL CONSIDERATIONS

The occurrence of pulmonary complications in the postoperative of heart surgery is quite common, and the atelectasis and pneumonia are highlighted among them. Since the frequency of heart surgery in children with congenital heart disease is high, it is important to make use of effective means to prevent, reduce or treat such complications.

Physiotherapy included in the multidisciplinary team contributes significantly to the better prognosis of pediatric patients undergoing heart surgery, as it prevents and treats pulmonary complications by means of specific techniques such as vibration, percussion, compression, manual hyperinflation, reexpansion maneuver, positioning, postural drainage, cough stimulation, aspiration, breathing exercises, IEF and mobilization.

It was observed the effectiveness of physiotherapy in reducing the risk and/or treating pulmonary complications caused by surgical procedure in children with congenital heart disease. Thus, more research is needed to assess the physiotherapy in the pre- and postoperative of pediatric cardiac surgery, by comparing the different techniques used by the physiotherapist in order to minimize the frequent postoperative pulmonary complications.

VENTRICULAR SEPTAL DEFECT

ventricular septal defect (VSD), a hole in the heart, is a common heart defect that’s present at birth (congenital). The hole (defect) occurs in the wall (septum) that separates the heart’s lower chambers (ventricles) and allows blood to pass from the left to the right side of the heart. The oxygen-rich blood then gets pumped back to the lungs instead of out to the body, causing the heart to work harder.

A small ventricular septal defect may cause no problems, and many small VSDs close on their own. Medium or larger VSDs may need surgical repair early in life to prevent complications.

 

VENTRICULAR SEPTAL DEFECT
VENTRICULAR SEPTAL DEFECT

SYMPTOMS
Signs and symptoms of serious heart defects often appear during the first few days, weeks or months of a child’s life.

Ventricular septal defect (VSD) symptoms in a baby may include:

  • Poor eating, failure to thrive
  • Fast breathing or breathlessness
  • Easy tiring

Doctor may not notice signs of a ventricular septal defect at birth. If the defect is small, symptoms may not appear until later in childhood — if at all. Signs and symptoms vary depending on the size of the hole and other associated heart defects.

Doctor may first suspect a heart defect during a regular checkup if he or she hears a murmur while listening to your baby’s heart with a stethoscope. Sometimes VSDs can be detected by ultrasound before the baby is born.

Sometimes a VSD isn’t detected until a person reaches adulthood. Symptoms and signs can include shortness of breath or a heart murmur doctor hears when listening to your heart with a stethoscope.

Call doctor if your baby or child:

Tires easily when eating or playing
Is not gaining weight
Becomes breathless when eating or crying
Breathes rapidly or is short of breath

Call doctor if you develop:

Shortness of breath when you exert yourself or when you lie down
Rapid or irregular heartbeat
Fatigue or weakness

CAUSES
Congenital heart defects arise from problems early in the heart’s development, but there’s often no clear cause. Genetics and environmental factors may play a role. VSDs can occur alone or with other congenital heart defects.

During fetal development, a ventricular septal defect occurs when the muscular wall separating the heart into left and right sides (septum) fails to form fully between the lower chambers of the heart (ventricles).

Normally, the right side of the heart pumps blood to the lungs to get oxygen; the left side pumps the oxygen-rich blood to the rest of the body. A VSD allows oxygenated blood to mix with deoxygenated blood, causing the heart to work harder to provide enough oxygen to the body’s tissues.

VSDs may be various sizes, and they can be present in several locations in the wall between the ventricles. There may be one or more VSD.

It’s also possible to acquire a VSD later in life, usually after a heart attack or as a complication following certain heart procedures.

RISK FACTORSRISK FACTORS
Ventricular septal defects may run in families and sometimes may occur with other genetic problems, such as Down syndrome. If you already have a child with a heart defect, a genetic counselor can discuss the risk of your next child having one.

COMPLICATION
A small ventricular septal defect may never cause any problems. Medium or large defects can cause a range of disabilities — from mild to life-threatening. Treatment can prevent many complications.
Heart failure. In a heart with a medium or large VSD, the heart needs to work harder to pump enough blood to the body. Because of this, heart failure can develop if medium to large VSDs aren’t treated.
Pulmonary hypertension. Increased blood flow to the lungs due to the VSD causes high blood pressure in the lung arteries (pulmonary hypertension), which can permanently damage them. This complication can cause reversal of blood flow through the hole (Eisenmenger syndrome).
Endocarditis. This heart infection is an uncommon complication.
Other heart problems. These include abnormal heart rhythms and valve problems.

PREVENTION
In most cases, you can’t do anything to prevent having a baby with a ventricular septal defect. However, it’s important to do everything possible to have a healthy pregnancy. Here are the basics:

Get early prenatal care, even before you’re pregnant. Talk to your doctor before you get pregnant about your health and discuss any lifestyle changes that your doctor may recommend for a healthy pregnancy. Also, be sure you talk to your doctor about any medications you’re taking.
Eat a balanced diet. Include a vitamin supplement that contains folic acid. Also, limit caffeine.
Exercise regularly. Work with your doctor to develop an exercise plan that’s right for you.
Avoid risks. These include harmful substances such as alcohol, tobacco and illegal drugs.
Avoid infections. Be sure you’re up to date on all of your vaccinations before becoming pregnant. Certain types of infections can be harmful to a developing fetus.
Keep diabetes under control. If you have diabetes, work with your doctor to be sure it’s well-controlled before getting pregnant.

If you have a family history of heart defects or other genetic disorders, consider talking with a genetic counselor before getting pregnant.

ATRIAL SEPTAL DEFECT

OVERVIEW

An atrial septal defect (ASD) is a hole in the wall between the two upper chambers of your heart (atria). The condition is present at birth (congenital).

Small defects may never cause a problem and may be found incidentally. It’s also possible that small atrial septal defects may close on their own during infancy or early childhood.

Large and long-standing atrial septal defects can damage your heart and lungs. An adult who has had an undetected atrial septal defect for decades may have a shortened life span from heart failure or high blood pressure that affects the arteries in the lungs (pulmonary hypertension). Surgery may be necessary to repair atrial septal defects to prevent complications.

SYMPTOMS
Many babies born with atrial septal defects don’t have associated signs or symptoms. In adults, signs or symptoms may begin around age 30, but in some cases signs and symptoms may not occur until decades later.

Atrial septal defect signs and symptoms may include:

Shortness of breath, especially when exercising
Fatigue
Swelling of legs, feet or abdomen
Heart palpitations or skipped beats
Stroke
Heart murmur, a whooshing sound that can be heard through a stethoscope

Shortness of breath
Tiring easily, especially after activity
Swelling of legs, feet or abdomen
Heart palpitations or skipped beats
These could be signs or symptoms of heart failure or another complication of congenital heart disease.

CAUSES
How the heart normally works

The heart is divided into four hollow chambers, two on the right and two on the left. To pump blood throughout the body, the heart uses its left and right sides for different tasks.

The right side of the heart moves blood to the lungs through vessels called pulmonary arteries. In the lungs, blood picks up oxygen then returns to the heart’s left side through the pulmonary veins. The left side of the heart then pumps the blood through the aorta and out to the rest of the body.

DEVELOPMENT OF HEART DEFECT
Doctors know that heart defects present at birth (congenital) arise from errors early in the heart’s development, but there’s often no clear cause. Genetics and environmental factors may play a role.
ATRIAL SEPTUM DEFECT
The heart is divided into four hollow chambers, two on the right and two on the left. To pump blood throughout the body, the heart uses its left and right sides for different tasks.

The right side of the heart moves blood to the lungs through vessels called pulmonary arteries. In the lungs, blood picks up oxygen then returns to the heart’s left side through the pulmonary veins. The left side of the heart then pumps the blood through the aorta and out to the rest of the body.

DEELOPMENT OF ASD
Doctors know that heart defects present at birth (congenital) arise from errors early in the heart’s development, but there’s often no clear cause. Genetics and environmental factors may play a role.

HEART WORKS WITH ASD
An atrial septal defect (ASD) allows freshly oxygenated blood to flow from the left upper chamber of the heart (left atrium) into the right upper chamber of the heart (right atrium). There, it mixes with deoxygenated blood and is pumped to the lungs, even though it’s already refreshed with oxygen.

If the atrial septal defect is large, this extra blood volume can overfill the lungs and overwork the right side of the heart. If not treated, the right side of the heart eventually enlarges and weakens. If this process continues, the blood pressure in your lungs may increase as well, leading to pulmonary hypertension.

TYPES OF ASD
SECUNDUM– This is the most common type of ASD, and occurs in the middle of the wall between the atria (atrial septum).
PRIMUM– This defect occurs in the lower part of the atrial septum, and may occur with other congenital heart problems.
SINUS VENOSUS- This rare defect usually occurs in the upper part of the atrial septum.
CORONARY SINUS- In this rare defect, part of the wall between the coronary sinus — which is part of the vein system of the heart — and the left atrium is missing.

RISK FACTORS
It’s not known why atrial septal defects occur, but congenital heart defects appear to run in families and sometimes occur with other genetic problems, such as Down syndrome. If you have a heart defect, or you have a child with a heart defect, a genetic counselor can estimate the odds that any future children will have one.

Some conditions that you have or that occur during pregnancy may increase your risk of having a baby with a heart defect, including:

  • RUBELLA INFECTION – bcoming infected with rubella (German measles) during the first few months of your pregnancy can increase the risk of fetal heart defects.
  • Drug, tobacco or alcohol use, or exposure to certain substances. Use of certain medications, tobacco, alcohol or drugs, such as cocaine, during pregnancy can harm the developing fetus.
  • Diabetes or lupus. If you have diabetes or lupus, you may be more likely to have a baby with a heart defect.
  • Obesity. Being extremely overweight (obese) may play a role in increasing the risk of having a baby with a birth defect.
  • Phenylketonuria (PKU). If you have PKU and aren’t following your PKU meal plan, you may be more likely to have a baby with a heart defect.
  • COMPLICATIONS
    A small atrial septal defect may never cause any problems. Small atrial septal defects often close during infancy.

Larger defects can cause serious problems, including:

  • Right-sided heart failure
  • Heart rhythm abnormalities (arrhythmias)
  • Increased risk of a stroke
  • Shortened life span
  • Less common serious complications may include:
  • Pulmonary hypertension. If a large atrial septal defect goes untreated, increased blood flow to your lungs increases the blood pressure in the lung arteries (pulmonary hypertension).

Eisenmenger syndrome. Pulmonary hypertension can cause permanent lung damage. This complication, called Eisenmenger syndrome, usually develops over many years and occurs uncommonly in people with large atrial septal defects.
Treatment can prevent or help manage many of these complications.

ATRIAL SEPTAL DEFECT ATRIAL SEPTAL DEFECT AND PREGNANCY
Most women with an atrial septal defect can tolerate pregnancy without any problems. However, having a larger defect or having complications such as heart failure, arrhythmias or pulmonary hypertension can increase your risk of complications during pregnancy. Doctors strongly advise women with Eisenmenger syndrome not to become pregnant because it can endanger their lives.

The risk of congenital heart disease is higher for children of parents with congenital heart disease, whether in the father or the mother. Anyone with a congenital heart defect, repaired or not, who is considering starting a family should carefully discuss it beforehand with a doctor. Some medications may need to be stopped or adjusted before you become pregnant because they can cause serious problems for a developing fetus.

PREVENTION
In most cases, atrial septal defects can’t be prevented. If you’re planning to become pregnant, schedule a preconception visit with your health care provider. This visit should include:

Getting tested for immunity to rubella. If you’re not immune, ask your doctor about getting vaccinated.
Going over your current health conditions and medications. You’ll need to carefully monitor certain health problems during pregnancy. Doctor may also recommend adjusting or stopping certain medications before you become pregnant.
Reviewing your family medical history. If you have a family history of heart defects or other genetic disorders, consider talking with a genetic counselor to determine what the risk might be before getting pregnant.

CARDIOMYOPATHY

INTRODUCTION

Cardiomyopathy is a disease of the heart muscle that makes it harder for your heart to pump blood to the rest of your body. Cardiomyopathy can lead to heart failure.

The main types of cardiomyopathy include dilated, hypertrophic and restrictive cardiomyopathy. Treatment — which might include medications, surgically implanted devices or, in severe cases, a heart transplant — depends on which type of cardiomyopathy you have and how serious it is.

SYMPTOMS
There might be no signs or symptoms in the early stages of cardiomyopathy. But as the condition advances, signs and symptoms usually appear, including:

Breathlessness with exertion or even at rest
Swelling of the legs, ankles and feet
Bloating of the abdomen due to fluid buildup
Cough while lying down
Fatigue
Heartbeats that feel rapid, pounding or fluttering
Chest discomfort or pressure
Dizziness, lightheadedness and fainting

Signs and symptoms tend to get worse unless treated. In some people, the condition worsens quickly; in others, it might not worsen for a long time.

CAUSES
Often the cause of the cardiomyopathy is unknown. In some people, however, it’s the result of another condition (acquired) or passed on from a parent (inherited).

Contributing factors for acquired cardiomyopathy include:

  • Long-term high blood pressure
  • Heart tissue damage from a heart attack
  • Chronic rapid heart rate
  • Heart valve problems
  • Metabolic disorders, such as obesity, thyroid disease or diabetes
  • Nutritional deficiencies of essential vitamins or minerals, such as thiamin (vitamin B-1)
  • Pregnancy complications
  • Drinking too much alcohol over many years
  • Use of cocaine, amphetamines or anabolic steroids
  • Use of some chemotherapy drugs and radiation to treat cancer
  • Certain infections, especially those that inflame the heart
  • Iron buildup in your heart muscle (hemochromatosis)
  • A condition that causes inflammation and can cause lumps of cells to grow in the heart and other organs (sarcoidosis)
  • A disorder that causes the buildup of abnormal proteins (amyloidosis)
    Connective tissue disorders

Illustration showing dilated cardiomyopathy
Dilated cardiomyopathy

Illustration showing hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy

TYPES OF CARDIOMYOPATHY

TYPES CARDIOMYOPATHY
TYPES OF CARDIOMYOPATHY

DILATED CARDIOMYOPATHY– In this type of cardiomyopathy, the pumping ability of your heart’s main pumping chamber — the left ventricle — becomes enlarged (dilated) and can’t effectively pump blood out of the heart.

Although this type can affect people of all ages, it occurs most often in middle-aged people and is more likely to affect men. The most common cause is coronary artery disease or heart attack.

HYPERTROPHIC CARDIOMYOPATHY – This type involves abnormal thickening of your heart muscle, particularly affecting the muscle of your heart’s main pumping chamber (left ventricle). The thickened heart muscle can make it harder for the heart to work properly.

Hypertrophic cardiomyopathy can develop at any age, but the condition tends to be more severe if it becomes apparent during childhood. Most affected people have a family history of the disease, and some genetic mutations have been linked to hypertrophic cardiomyopathy.

RESTRICTIVE CARDIOMYOPATHY- In this type, the heart muscle becomes rigid and less elastic, so it can’t expand and fill with blood between heartbeats. This least common type of cardiomyopathy can occur at any age, but it most often affects older people.

Restrictive cardiomyopathy can occur for no known reason (idiopathic), or it can by caused by a disease elsewhere in the body that affects the heart, such as when iron builds up in the heart muscle (hemochromatosis).

ARRHYTHMOGENIC RIGHT VENTRICULAR  DYSPLASIA- In this rare type of cardiomyopathy, the muscle in the lower right heart chamber (right ventricle) is replaced by scar tissue, which can lead to heart rhythm problems. It’s often caused by genetic mutations.

Unclassified cardiomyopathy. Other types of cardiomyopathy fall into this category.

RISK FACTORS

There are a number of factors that can increase your risk of cardiomyopathy, including:

  • Family history of cardiomyopathy, heart failure and sudden cardiac arrest
  • Long-term high blood pressure
  • Conditions that affect the heart, including a past heart attack, coronary artery disease or an
  • infection in the heart (ischemic cardiomyopathy)
  • Obesity, which makes the heart work harder
  • Long-term alcohol abuse
  • Illicit drug use, such as cocaine, amphetamines and anabolic steroids
  • Certain chemotherapy drugs and radiation therapy for cancer
  • Certain diseases, such as diabetes, an under- or overactive thyroid gland, or a disorder that causes the body to store excess iron (hemochromatosis)
  • Other conditions that affect the heart, such as a disorder that causes the buildup of abnormal proteins (amyloidosis), a disease that causes inflammation and can cause lumps of cells to grow in the heart and other organs (sarcoidosis), or connective tissue disorders

COMPLICATIONS

Cardiomyopathy can lead to other heart conditions, including:

Heart failure. Your heart can’t pump enough blood to meet your body’s needs. Untreated, heart failure can be life-threatening.
Blood clots. Because your heart can’t pump effectively, blood clots might form in your heart. If clots enter your bloodstream, they can block the blood flow to other organs, including your heart and brain.
Valve problems. Because cardiomyopathy causes the heart to enlarge, the heart valves might not close properly. This can lead to a backward flow of blood.
Cardiac arrest and sudden death. Cardiomyopathy can lead to abnormal heart rhythms. These abnormal heart rhythms can result in fainting or, in some cases, sudden death if your heart stops beating effectively.

PREVENTIONPREVENTION

In many cases, you can’t prevent cardiomyopathy. Let your doctor know if you have a family history of the condition.

You can help reduce your chance of cardiomyopathy and other types of heart disease by living a heart-healthy lifestyle and making lifestyle choices such as:

  • Avoiding the use of alcohol or cocaine
  • Controlling high blood pressure, high cholesterol and diabetes
  • Eating a healthy diet
  • Getting regular exercise
  • Getting enough sleep
  • Reducing your stress

ACYANOTIC CONGENITAL HEART DISEASE

Acyanotic heart defects are congenital cardiac malformations that affect the atrial or ventricular walls, heart valves, or large blood vessels. Common causes include genetic defects (e.g., trisomies), maternal infections (e.g., rubella), or maternal consumption of drugs or alcohol during pregnancy. Acyanotic heart defects are characterized pathophysiologically by a left-to-right shunt, which causes pulmonary hypertension and right heart hypertrophy.

The symptoms depend on the extent of the malformation and the resulting impairment of cardiac function. Infants may be asymptomatic or present with exercise intolerance, failure to thrive, and symptoms of heart failure. Characteristic heart murmurs are important clues for establishing the diagnosis, which is typically confirmed by visualizing the defect on echocardiography.

A chest x-ray, MRI, or cardiac catheterization may also be required to determine the indications for surgery and plan the procedure. Acyanotic heart defects requiring treatment are repaired via catheter procedures or surgery. Supportive medical therapy is needed in cases of heart failure (e.g., diuretics, inotropic agents) or if surgery cannot be performed (e.g., prostaglandin). Common complications include arrhythmias, embolisms, and infective endocarditis, especially if treatment is delayed.

Overview of acyanotic congenital heart defects

  • General clinical features
  • Normal skin tone
  • Exercise intolerance
  • Fatigue
  • Exertional tachycardia, pallor, and diaphoresis (sweating)
  • Exertional dyspnea, tachypnea
  • Recurrent bronchopulmonary infections
  • Failure to thrive
  • Heart failure in larger defects
  • Tachycardia
  • Right-sided heart failure
  • Hepatic venous congestion with hepatomegaly
  • Peripheral edema is rarely seen in infants.
  • Left-sided heart failure
  • Tachypnea, pulmonary edema
  • Low cardiac output: BP, pallor, sweating, cool extremities, poor growth, syncope
    Differential cyanosis: cyanosis in the lower extremities when the Eisenmenger reaction occurs

ATRIAL SEPTAL DEFECT (ASD)

atrial septal defect
                  atrial septal defect

EPIDEMIOLOGY
Prevalence: ~ 2/1000 live births

ETIOLOGY
Down syndrome
Fetal alchohol syndrome
Holt-Oram syndrome

PATHOPHYSIOLOGY
Impaired growth or excessive resorption of the atrial septa in utero leads to atrial septal defects.
Ostium primum atrial septal defect (ASD I): (~ 15–20%)
Ostium secundum atrial septal defect (ASD II): (~ 70%)
Typically a low-pressure, low-volume, minor left-to-right shunt ? patients are asymptomatic
In larger defects, the shunt may lead to: right heart failure, supraventricular arrhythmias, pulmonary hypertension, cor pulmonale, and/or the Eisenmenger reaction

  • CLINICAL FINDINGS
    Depend on defect size and shunt volume
    Small defects: usually asymptomatic
    Large defects
  • Palpitations
  • ASDs typically manifest with advancing age.
  • Auscultation
  • Systolic ejection murmur over the left second ICS sternal border
  • Widely split second heart sound (S2) over the left second ICS, which is fixed (does not change with respiration ), normal S1
  • Soft mid-diastolic murmur over the lower left sternal border

DIAGNOSTICS
Echocardiography (confirmatory test): to visualize the defect, its extent, and shunt volume
ECG: vertical or right axis, P pulmonale, right bundle branch block (complete or incomplete), signs of right heart hypertrophy, PR prolongation
Chest x-ray: enlarged right atrium, ventricle, and pulmonary arch; increased pulmonary vasculature

TREATMENT
In childhood, spontaneous closure may occur.
Patch repair
Indicated in symptomatic children with significant left-to-right shunt
Surgical or via percutaneous transcatheter procedure

COMPLICATION
Paradoxical embolism risk of stroke

VENTRICULAR SEPTAL DEFECT (VSD)

ventricular septal defect
ventricular septal defect

EPIDEMIOLOGY
The most common congenital heart defect (4/1000 live births)
Occurs as an isolated heart defect or in combination with others

ETIOLOGY
Genetic syndromes: Down syndrome, Edward syndrome, Patau syndrome
Fetal alcohol syndrome
Intrauterine infection (e.g., TORCH)

PATHOPHYSIOLOGY
Localization: most commonly in the membranous part of the ventricular septum (pars membranacea)
Defect in ventricular septum  left-to-right shunt with the following consequences:
LV volume overload  left ventricular hypertrophy
Excessive pulmonary blood flow  increased pulmonary artery pressures  pulmonary hypertension and right-sided heart hypertrophy
Decreased cardiac output
Possibly an Eisenmenger reaction in late stage of disease due to irreversible pulmonary hypertension

CLINICAL FINDING
Small defects: usually asymptomatic
Medium-sized or large defects
Lead to cardiac failure in the first 2–3 months of life

Palpation: Hyperdynamic precordium may be detected in hemodynamically relevant defects.
Auscultatory findings
Harsh holosystolic murmur over the left lower sternal border; typically louder in small defects
Mid-diastolic murmur over cardiac apex
Systolic thrill
Loud pulmonic S2 (if pulmonary hypertension develops)

DIAGNOSIS
Doppler echocardiography: confirms diagnosis; evaluation of defect size and shunt volume; exclusion of other anomalies
ECG: signs of right heart hypertrophy
Chest x-ray
Enhanced pulmonary vascular markings
Left atrial and ventricular enlargement
In later stages, enlarged right ventricle and pulmonary artery (due to elevated PVR)

TREATMENT
Small VSDs: rarely require surgical interventions small to moderate defects often heal spontaneously; follow-up echocardiography recommended
Symptomatic and large VSDs
Surgical (patch) repair in children < 1 year of age with signs of pulmonary hypertension and older children who did not improve with medical therapy
Closure of a VSD results in a decrease in right ventricular and left atrial pressures and an increase in left ventricular pressure when compared to pre-treatment values
Heart-lung transplant or lung transplant with concurrent VSD repair if Eisenmenger’s reaction has occurred

  • COMPLICATIONS
  • Arrhythmias
  • Right heart failure
  • Eisenmenger’s reaction
  • Infective endocarditis
  • Aortic regurgitation

CONGENITAL PATENT DUCTUS ARTERIOSUS (PDA)

patent ductus arteriosus
  patent ductus arteriosus

GLOSSARY
While still in the mother’s womb, a baby does not need their lungs to supply oxygen because they receive oxygen from their mother. Since a baby’s lungs do not provide oxygen, there is no need for the heart to pump blood to the lungs. The ductus arteriosus is a blood vessel that is present in all babies while still in the womb, and it allows blood to bypass the lungs.

When the baby is born and the umbilical cord is cut, their lungs need to supply oxygen to their body. Their lungs expand, their blood vessels relax to accept more blood flow, and the ductus arteriosus usually closes within the first hours of life. Sometimes, the ductus arteriosus does not close on its own. This is known as a patent (“open”) ductus arteriosus. While this condition is seen more often in premature babies, it may also appear in full-term infants.

SYMPTOMS OF PATENT DUCTUS ARTERIOSUS
The symptoms of a patent ductus arteriosus depend on the size of the ductus and how much blood flow it carries. After birth, if a ductus arteriosus is present, blood will flow from the aorta (the main artery in the body) into the pulmonary artery. This extra blood flow into the lungs can overload the lungs and put more burden on the heart to pump this extra blood. Some babies may need more support from a ventilator and have symptoms of congestive heart failure.

A newborn with a patent ductus arteriosus may have:

  • Fast breathing
  • A hard time breathing
  • More respiratory infections
  • Tire more easily
  • Poor growth
    However, if the patent ductus arteriosus is not large, it may cause no symptoms and your doctor may not find it until they do further evaluation of a heart murmur.
    Even if there are no symptoms, the turbulent flow of blood through the patent ductus arteriosus puts a person at a higher risk for a serious infection, known as endocarditis.

DIAGNOSIS
Because of turbulent blood flow, a patent ductus arteriosus causes a distinct sounding heart murmur that is heard on physical exam.

The murmur, along with symptoms of heart failure in a premature infant, most often lead to the diagnosis of patent ductus arteriosus. A chest X-ray will show an enlarged heart and evidence of a large amount of blood flow to the lungs. An echocardiogram is done to confirm the diagnosis. doctor can see the size of the ductus arteriosus and also find out if the heart chambers have become enlarged due to the extra blood flow.

In older children, though, their chest X-ray is typically normal. An echocardiogram will show the flow of blood through the patent ductus arteriosus and is typically done to confirm the diagnosis.

In a newborn, the patent ductus arteriosus still has the chance to close on its own. Doctor may allow more time for the patent ductus arteriosus to close on its own if their heart failure is under control. If a newborn’s symptoms are severe or it is unlikely to close on its own, medical or surgical treatment is needed.

Medicines work best for newborns. They may receive medicine, such as indomethacin or ibuprofen, to constrict the muscle in the wall of the patent ductus arteriosus and help it close. These drugs do have side effects, so not all babies can receive them.

SURGERY
A small incision is made between the ribs on the left side.
The ductus arteriosus is tied and cut.
The risk of complications with any of these treatments is low, determined mostly by how ill the child is prior to treatment.

PDA IS GOOD OR NOT
Yes. Some babies have heart defects that require the patent ductus arteriosus to remain open for them to survive.

In some heart defects, such as pulmonary atresia (an underdeveloped or blocked pulmonary valve), the patent ductus arteriosus supplies the only adequate source of blood flow to the lungs so that oxygen can be delivered to the blood. In these patients, the ductus arteriosus supplies blood to the lungs from the aorta.

COARCTACTION OF AORTA

coarctation of the aorta11
coarctation of the aorta

Coarctation (ko-ahrk-TAY-shun) of the aorta — or aortic coarctation — is a narrowing of the aorta, the large blood vessel that branches off your heart and delivers oxygen-rich blood to body. When this occurs, your heart must pump harder to force blood through the narrowed part of your aorta.
Coarctation of the aorta is generally present at birth (congenital). The condition can range from mild to severe, and might not be detected until adulthood, depending on how much the aorta is narrowed.
Coarctation of the aorta often occurs along with other heart defects. While treatment is usually successful, the condition requires careful lifelong follow-up.

SYMPTOMS
Coarctation of the aorta symptoms depend on the severity of the condition. Most people don’t have symptoms. Children with serious aortic narrowing may show signs and symptoms earlier in life, but mild cases with no symptoms might not be diagnosed until adulthood. People may also have signs or symptoms of other heart defects that they have along with coarctation of the aorta.

  • Babies with severe coarctation of the aorta may begin having signs and symptoms shortly after birth. These include:
  • Pale skin
  • Irritability
  • Heavy sweating
  • Difficulty breathing
  • Difficulty feeding
  • Left untreated, aortic coarctation in babies might lead to heart failure or death.

Older children and adults with coarctation of the aorta often don’t have symptoms because their narrowing may be less severe. If you have signs or symptoms that appear after infancy, you most commonly will have high blood pressure (hypertension) measured in your arms. However, your blood pressure is likely to be lower in your legs.

  • SIGNS AND SYMPTOMS
  • High blood pressure
  • Headache
  • Muscle weakness
  • Leg cramps or cold feet
  • Nosebleeds
  • Chest pain

Seek medical help if child has the following signs or symptoms:

  • Severe chest pain
  • Fainting
  • Sudden shortness of breath
  • Unexplained high blood pressure
  • While experiencing these signs or symptoms doesn’t necessarily mean that you have a serious problem, it’s best to get checked out quickly. Early detection and treatment might help save your life.

CAUSES

Rarely, coarctation of the aorta develops later in life. Traumatic injury might lead to coarctation of the aorta. Rarely, severe hardening of the arteries (atherosclerosis) or a condition causing inflamed arteries (Takayasu’s arteritis) can narrow the aorta, leading to aortic coarctation.

Coarctation of the aorta usually occurs beyond the blood vessels that branch off to your upper body and before the blood vessels that lead to your lower body. This can often lead to high blood pressure in your arms but low blood pressure in your legs and ankles.

With coarctation of the aorta, the lower left heart chamber (left ventricle) of your heart works harder to pump blood through the narrowed aorta, and blood pressure increases in the left ventricle. This may cause the wall of the left ventricle to thicken (hypertrophy).

Prevention

Coarctation of the aorta can’t be prevented, because it’s usually present at birth (congenital). However, if you or your child has a condition that increases the risk of aortic coarctation, such as Turner syndrome, bicuspid aortic valve or another heart defect, or a family history of congenital heart disease, early detection can help. Discuss the risk of aortic coarctation with your doctor.

CYANOTIC CONGENITAL HEART DISEASE

CYANOTIC CONGENITAL HEART DISEASE

CYANOTIC CONGENITAL HEART DISEASE
                                   CYANOTIC CONGENITAL HEART DISEASE

Cyanotic congenital heart disease (CCHD) is a condition present at birth. CYANOTIC CONGENITAL HEART DISEASE causes low levels of oxygen in the blood. A common symptom is a bluish tint to the skin, called cyanosis.

Several birth defects can cause this type of heart disease, including:

issues with the heart valves, which are the flaps in the heart that make sure the blood flows through in the right direction
an interruption in the aorta, which is the largest artery in the body
abnormalities in the large blood vessels leading to or from the heart
In many cases, if only one defect is present, there’s no cyanosis. Often more than one defect is present in CCHD.

Doctors use imaging tests to confirm the presence of defects that lead to CCHD. These include chest X-rays and echocardiograms. Medication can help relieve symptoms of cyanosis. Ultimately, most infants need to have surgery to correct the defects causing the disease. The success of the surgery depends on the severity of the defects.

RISK FACTOR FOR CONGENITAL CYANOTIC HEART DISEASE
In many cases, an infant will be born with this disease in association with a genetic factor. An infant is more at risk for CCHD when there’s a family history of congenital heart diseases. Certain genetic syndromes can be accompanied by defects that cause CCHD. These include:

Down syndrome
Turner syndrome
Marfan’s syndrome
Noonan syndrome
In some instances, outside factors can cause this disease. If a pregnant woman is exposed to toxic chemicals or certain drugs, her infant may have a higher risk of developing heart defects. Infections during pregnancy are also a factor. Poorly controlled gestational diabetes can also lead to a higher risk of the infant developing CCHD.

Defects that cause cyanotic congenital heart disease
Many physical defects in the heart can cause CCHD. Some infants may be born with several defects. Common causes can include:

CLASSIFICATION OF CHD
Classification of CHD. Cyanotic Heart Disease. Acyanotic Heart Disease. Decreased pulmonary flow: Tetralogy of Fallot. Tricuspid atresia. Other univentricular heart with pulmonary stenosis. Increased pulmonary flow: Transposition of great arteries. Total anomalous pulmonary venous return. Left – Right shunt lesions: Ventricular septal defect. Atrial Septal Defect. Atrio-ventricular Septal Defect. Patent Ductus Arteriosus. Obstructive lesions: Aortic stenosis. Pulmonary valve stenosis. Coarctation of Aorta.

TETRALOGY OF FALLOT (TOF)

TETRALOGY OF FALLOT
TETRALOGY OF FALLOT

TOF is the most common cause of CCHD. It’s a combination of four different defects. TOF includes:

A hole between the right and left ventricles of the heart
A narrow pulmonary valve
A thickening of the right ventricle muscles
A misplaced aortic valve
The defects lead to blood with and without oxygen getting mixed together and pumped throughout the body.

TRANSPOSITION OF GRAET ARTERIES (TGA)
In infants with TGA, the pulmonary and aortic valves have switched positions with their arteries. This results in low-oxygen blood getting pumped out to the rest of the body through the aorta. This blood should actually go to the lungs through the pulmonary artery.

TRICUSPID ATRESIA
In this type of defect, the tricuspid heart valve has developed abnormally or is missing entirely. This causes disruption to the normal flow of blood. Low-oxygen blood is pumped out to the body as a result.

TOTAL ANOMOLUS PULMONARY VENOUS CONNECTION (TAPVC)
TAPVC occurs when veins that bring high-oxygen blood from the lungs to the heart are connected to the right atrium. The veins should be connected to the left atrium. This defect may also be accompanied by a blockage in these veins between the lungs and the heart.

SYMPTOMS
The classic symptom of CCHD is cyanosis, or the blue coloring of the skin. This often occurs in the lips, toes, or fingers. Another common symptom is difficulty breathing, especially after physical activity.

Some children also experience spells during which their oxygen levels are very low. As a result, they get anxious, exhibit blue skin, and may hyperventilate.

Other symptoms of CCHD depend on the exact physical defect:

SYMPTOMS OF TOF
Low birth weight
Cyanosis
Poor feeding
Clubbed, or rounded, large fingers
Delayed growth
Rapid breathing

SYMPTOMS OF TGA
Rapid heartbeat
Rapid breathing
Slow weight gain
Heavy sweating

SYMPTOMS OF TRICUSPID ATRESIA
Cyanosis
Tiredness
Shortness of breath
Difficulty feeding
Heavy sweating
Slow growth
Chronic respiratory infections

SYMPTOMS TAPVC WITHOUT A BLOCKAGE
Shortness of breath
Chronic respiratory infections
Slow growth
TAPVC WITH BLOCKAGE
Cyanosis
Rapid heartbeat
Rapid breathing
Breathing difficulty, becoming very severe with time

DIAGNOSIS
Symptoms such as cyanosis, rapid heartbeat, and abnormal heart sounds can lead your child’s doctor to suspect heart defects are present. The observation of symptoms isn’t enough to make a diagnosis, though. To understand which defects are present, your child’s doctor will use tests to confirm a diagnosis.

A chest X-ray can show the outline of the heart and the location of several of the arteries and veins. To get another image of the heart, your child’s doctor may order an echocardiogram. This is an ultrasound of the heart. This test gives more details than an X-ray image.

A cardiac catheterization is a more invasive test that’s often needed to investigate the interior of the heart. This test involves moving a small tube, or a catheter, into the heart from the groin or the arm.

TRETMENT OF CYANOTIC CONGENITAL HEART DISEASETRETMENT OF CYANOTIC CONGENITAL HEART DISEASE
Treatment for CCHD may or may not be necessary depending on the severity of symptoms. In many cases, surgery to correct the physical defects in the heart is eventually necessary.

When the defect is very dangerous, the surgery may need to be performed soon after birth. In other instances, the surgery can be delayed until the child is older. Sometimes, more than one surgery is needed.

If surgery is delayed, a child may be given medications to treat the disease. Medications can help:

Eliminate extra fluids from the body
Get the heart pumping better
Keep blood vessels open
Regulate abnormal heart rhythms

OUTLOOK FOR CYANOTIC CONGENITAL HEART DISEASE
The outlook for children with CCHD varies based on the severity of the underlying defects. In mild cases, the child may be able to live a normal lifestyle with minimal medications or other treatments.

More severe cases will need surgery. Your child’s doctor will work with you toward the best treatment for your child. They can discuss your child’s particular outlook with you and if any further procedures are needed.

CONGESTIVE HEART FAILURE

DEFINATION

Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently.

Heart failure does not mean the heart has stopped working. Rather, it means that the heart’s pumping power is weaker than normal. With heart failure, blood moves through the heart and body at a slower rate, and pressure in the heart increases. As a result, the heart cannot pump enough oxygen and nutrients to meet the body’s needs. The chambers of the heart may respond by stretching to hold more blood to pump through the body or by becoming stiff and thickened. This helps to keep the blood moving, but the heart muscle walls may eventually weaken and become unable to pump as efficiently. As a result, the kidneys may respond by causing the body to retain fluid (water) and salt. If fluid builds up in the arms, legs, ankles, feet, lungs, or other organs, the body becomes congested, and congestive heart failure is the term used to describe the condition.

ANATOMY
You have four heart chambers. The upper half of your heart has two atria, and the lower half of your heart has two ventricles. The ventricles pump blood to your body’s organs and tissues, and the atria receive blood from your body as it circulates back from the rest of your body.

CHF develops when your ventricles can’t pump enough blood volume to the body. Eventually, blood and other fluids can back up inside your:

Lungs
Abdomen
Liver
Lower body
CHF can be life-threatening. If you suspect you or someone near you has CHF, seek immediate medical treatment.

TYPES OF CHF
Results of these tests help doctors determine the cause of your signs and symptoms and develop a program to treat your heart. To determine the most appropriate treatment for your condition, doctors may classify heart failure using two systems:

New York Heart Association classification. This symptom-based scale classifies heart failure in four categories. In Class I heart failure, you don’t have any symptoms. In Class II heart failure, you can perform everyday activities without difficulty but become winded or fatigued when you exert yourself. With Class III, you’ll have trouble completing everyday activities, and Class IV is the most severe, and you’re short of breath even at rest.

American College of Cardiology/American Heart Association guidelines. This stage-based classification system uses letters A to D. The system includes a category for people who are at risk of developing heart failure.

For example, a person who has several risk factors for heart failure but no signs or symptoms of heart failure is Stage A. A person who has heart disease but no signs or symptoms of heart failure is Stage B. Someone who has heart disease and is experiencing or has experienced signs or symptoms of heart failure is Stage C. A person with advanced heart failure requiring specialized treatments is Stage D.

Doctors use this classification system to identify your risk factors and begin early, more aggressive treatment to help prevent or delay heart failure.

These scoring systems are not independent of each other. Your doctor often will use them together to help decide your most appropriate treatment options. Ask your doctor about your score if you’re interested in determining the severity of your heart failure. Your doctor can help you interpret your score and plan your treatment based on your condition.

CAUSES OF CHF

RISK FACTORS
                                                    RISK FACTORS       CHF may result from other health conditions that directly affect your cardiovascular system. This is why it’s important to get annual checkups to lower your risk for heart health problems, including high blood pressure (hypertension), coronary artery disease, and valve conditions
  • HYPERTENSION
    When your blood pressure is higher than normal, it may lead to CHF. Hypertension has many different causes. Among them is the narrowing of your arteries, which makes it harder for your blood to flow through them.
  • CORONARY ARTERY DISEASE
    Cholesterol and other types of fatty substances can block the coronary arteries, which are the small arteries that supply blood to the heart. This causes the arteries to become narrow. Narrower coronary arteries restrict your blood flow and can lead to damage in your arteries.
  • VALVE CONDITIONS
    Heart valves regulate blood flow through your heart by opening and closing to let blood in and out of the chambers. Valves that don’t open and close correctly may force your ventricles to work harder to pump blood. This can be a result of a heart infection or defect.
  • OTHER CONDITIONS
    While heart-related diseases can lead to CHF, there are other seemingly unrelated conditions that may increase your risk, too. These include diabetes, thyroid disease, and obesity. Severe infections and allergic reactions may also contribute to CHF.

SYMPTOMS OF CHF

symptoms of chd
                                                     symptoms of CHD

In the early stages of CHF, you most likely won’t notice any changes in your health. If your condition progresses, you’ll experience gradual changes in your body.

  • Symptoms you may notice first Symptoms that indicate your condition has worsened
  • Symptoms that indicate a severe heart condition
  • fatigue
  • irregular heartbeat
  • chest pain that radiates through the upper body
  • swelling in your ankles, feet, and legs
  • a cough that develops from congested lungs
  • rapid breathing
  • weight gain
  • wheezing skin that appears blue, which is due to lack of oxygen in your lungs
  • increased need to urinate, especially at night
  • shortness of breath, which may indicate pulmonary edema
  • fainting
  • Chest pain that radiates through the upper body can also be a sign of a heart attack. If you experience this or any other symptoms that may point to a severe heart condition, seek immediate medical attention.

SYMPTOMS OF HEART FAILURE IN CHILDREEN 
It can be difficult to recognize heart failure in infants and young children. Symptoms may include:

  • Poor feeding
  • Excessive sweating
  • Difficulty breathing
  • These symptoms can easily be misunderstood as colic or a respiratory infection. Poor growth and low blood pressure can also be signs of heart failure in children. In some cases, you may be able to feel a resting baby’s rapid heart rate through the chest wall.

DIAGNOSIS OF CHD

X- RAYS
X- RAYS

After reporting symptoms to doctor, they may refer you to a heart specialist, or cardiologist.

Cardiologist will perform a physical exam, which will involve listening to your heart with a stethoscope to detect abnormal heart rhythms. To confirm an initial diagnosis, cardiologist might order certain diagnostic tests to examine your heart’s valves, blood vessels, and chambers.

There are a variety of tests used to diagnose heart conditions. Because these tests measure different things, doctor may recommend a few to get a full picture of your current condition.

  • ELECTROCARDIOGRAM
    An electrocardiogram (EKG or ECG) records heart’s rhythm. Abnormalities in your heart’s rhythm, such as a rapid heartbeat or irregular rhythm, could suggest that the walls of your heart’s chamber are thicker than normal. That could be a warning sign for a heart attack.
  • ECHOCARDIOGRAM
    An echocardiogram uses sound waves to record the heart’s structure and motion. The test can determine if you already have poor blood flow, muscle damage, or a heart muscle that doesn’t contract normally.
  • MRI
    An MRI takes pictures of your heart. With both still and moving pictures, this allows doctor to see if there’s damage to you heart.
  • STRESS TEST
    Stress tests show how well your heart performs under different levels of stress. Making your heart work harder makes it easier for doctor to diagnose problems.
  • BLOOD TEST
    Blood tests can check for abnormal blood cells and infections. They can also check the level of BNP, a hormone that rises with heart failure.
  • CARDIAC CATHETERISATION
    Cardiac catheterization can show blockages of the coronary arteries. Doctor will insert a small tube into blood vessel and thread it from your upper thigh (groin area), arm, or wrist.
  • CORONARY ANGIOGRAM. In this test, a thin, flexible tube (catheter) is inserted into a blood vessel at your groin or in your arm and guided through the aorta into your coronary arteries. A dye injected through the catheter makes the arteries supplying your heart visible on an X-ray, helping doctors spot blockages.

Myocardial biopsy. In this test, your doctor inserts a small, flexible biopsy cord into a vein in your neck or groin, and small pieces of the heart muscle are taken. This test may be performed to diagnose certain types of heart muscle diseases that cause heart failure.

MEDICATIONS
Doctors usually treat heart failure with a combination of medications. Depending on your symptoms, you might take one or more medications, including:

ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITOR- These drugs help people with systolic heart failure live longer and feel better. ACE inhibitors are a type of vasodilator, a drug that widens blood vessels to lower blood pressure, improve blood flow and decrease the workload on the heart. Examples include enalapril (Vasotec), lisinopril (Zestril) and captopril (Capoten).

ANGIOTENSIN 2 RECEPTOR BLOCKER –These drugs, which include losartan (Cozaar) and valsartan (Diovan), have many of the same benefits as ACE inhibitors. They may be an alternative for people who can’t tolerate ACE inhibitors.

BETA BLOCKERS- This class of drugs not only slows your heart rate and reduces blood pressure but also limits or reverses some of the damage to your heart if you have systolic heart failure. Examples include carvedilol (Coreg), metoprolol (Lopressor) and bisoprolol (Zebeta).

These medicines reduce the risk of some abnormal heart rhythms and lessen your chance of dying unexpectedly. Beta blockers may reduce signs and symptoms of heart failure, improve heart function, and help you live longer.

DIURETICS- Often called water pills, diuretics make you urinate more frequently and keep fluid from collecting in your body. Diuretics, such as furosemide (Lasix), also decrease fluid in your lungs so you can breathe more easily.

Because diuretics make your body lose potassium and magnesium, Doctor may also prescribe supplements of these minerals. If you’re taking a diuretic, Doctor will likely monitor levels of potassium and magnesium in your blood through regular blood tests.

ALDOSTERON ANTAGONIST- These drugs include spironolactone (Aldactone) and eplerenone (Inspra). These are potassium-sparing diuretics, which also have additional properties that may help people with severe systolic heart failure live longer.

Unlike some other diuretics, spironolactone and eplerenone can raise the level of potassium in your blood to dangerous levels, so talk to your doctor if increased potassium is a concern, and learn if you need to modify your intake of food that’s high in potassium.

INOTROPES- These are intravenous medications used in people with severe heart failure in the hospital to improve heart pumping function and maintain blood pressure.

DIGOXIN (Lanoxin) – This drug, also referred to as digitalis, increases the strength of your heart muscle contractions. It also tends to slow the heartbeat. Digoxin reduces heart failure symptoms in systolic heart failure. It may be more likely to be given to someone with a heart rhythm problem, such as atrial fibrillation.

You may need to take two or more medications to treat heart failure. Your doctor may prescribe other heart medications as well — such as nitrates for chest pain, a statin to lower cholesterol or blood-thinning medications to help prevent blood clots — along with heart failure medications. Your doctor may need to adjust your doses frequently, especially when you’ve just started a new medication or when your condition is worsening.

You may be hospitalized if you have a flare-up of heart failure symptoms. While in the hospital, you may receive additional medications to help your heart pump better and relieve your symptoms. You may also receive supplemental oxygen through a mask or small tubes placed in your nose. If you have severe heart failure, you may need to use supplemental oxygen long term.

SURGERY AND MEDICAL DEVICE
In some cases, doctors recommend surgery to treat the underlying problem that led to heart failure. Some treatments being studied and used in certain people include:

CORONARY BYPASS SURGERY- If severely blocked arteries are contributing to your heart failure, doctor may recommend coronary artery bypass surgery. In this procedure, blood vessels from your leg, arm or chest bypass a blocked artery in your heart to allow blood to flow through your heart more freely.

HEART VALVE REPAIR OR REPLACEMENT. If a faulty heart valve causes your heart failure, your doctor may recommend repairing or replacing the valve. The surgeon can modify the original valve to eliminate backward blood flow. Surgeons can also repair the valve by reconnecting valve leaflets or by removing excess valve tissue so that the leaflets can close tightly. Sometimes repairing the valve includes tightening or replacing the ring around the valve (annuloplasty).

Valve replacement is done when valve repair isn’t possible. In valve replacement surgery, the damaged valve is replaced by an artificial (prosthetic) valve.

Certain types of heart valve repair or replacement can now be done without open heart surgery, using either minimally invasive surgery or cardiac catheterization techniques.

IMPLANTABLE CARDIOVERTER DEFIBRILLATOR (ICDs)-

 

ICD
                  ICD

An ICD is a device similar to a pacemaker. It’s implanted under the skin in your chest with wires leading through your veins and into your heart.

The ICD monitors the heart rhythm. If the heart starts beating at a dangerous rhythm, or if your heart stops, the ICD tries to pace your heart or shock it back into normal rhythm. An ICD can also function as a pacemaker and speed your heart up if it is going too slow.

SYNCHRONISATION

CARDIAC RESYNCRHRONISATION THERAPY(CRT)- or biventricular pacing. A biventricular pacemaker sends timed electrical impulses to both of the heart’s lower chambers (the left and right ventricles) so that they pump in a more efficient, coordinated manner.

Many people with heart failure have problems with their heart’s electrical system that cause their already-weak heart muscle to beat in an uncoordinated fashion. This inefficient muscle contraction may cause heart failure to worsen. Often a biventricular pacemaker is combined with an ICD for people with heart failure.

VENTRICULAR ASSIST DEVICE (VADs)- A VAD, also known as a mechanical circulatory support device, is an implantable mechanical pump that helps pump blood from the lower chambers of your heart (the ventricles) to the rest of your body. A VAD is implanted into the abdomen or chest and attached to a weakened heart to help it pump blood to the rest of your body.

Doctors first used heart pumps to help keep heart transplant candidates alive while they waited for a donor heart. VADs may also be used as an alternative to transplantation. Implanted heart pumps can enhance the quality of life of some people with severe heart failure who aren’t eligible for or able to undergo heart transplantation or are waiting for a new heart.

HEART TRANSPLANT. Some people have such severe heart failure that surgery or medications don’t help. They may need to have their diseased heart replaced with a healthy donor heart.

Heart transplants can improve the survival and quality of life of some people with severe heart failure. However, candidates for transplantation often have to wait a long time before a suitable donor heart is found. Some transplant candidates improve during this waiting period through drug treatment or device therapy and can be removed from the transplant waiting list.A heart transplant isn’t the right treatment for everyone.

PALLIATIVE CARE AND END OF-LIFE CARE
Doctor may recommend including palliative care in your treatment plan. Palliative care is specialized medical care that focuses on easing your symptoms and improving your quality of life. Anyone who has a serious or life-threatening illness can benefit from palliative care, either to treat symptoms of the disease, such as pain or shortness of breath, or to ease the side effects of treatment, such as fatigue or nausea.

It’s possible that your heart failure may worsen to the point where medications are no longer working and a heart transplant or device isn’t an option. If this occurs, you may need to enter hospice care. Hospice care provides a special course of treatment to terminally ill people.

HOSPICE CARE ows family and friends — with the aid of nurses, social workers and trained volunteers — to care for and comfort a loved one at home or in hospice residences. Hospice care provides emotional, psychological, social and spiritual support for people who are ill and those closest to them.

Although most people under hospice care remain in their own homes, the program is available anywhere — including nursing homes and assisted living centers. For people who stay in a hospital, specialists in end-of-life care can provide comfort, compassionate care and dignity.

If you have an implantable cardioverter-defibrillator (ICD), one important consideration to discuss with your family and doctors is turning off the defibrillator so that it can’t deliver shocks to make your heart continue beating.

LIFE STYLE AND HOME REMEDIES

Making lifestyle changes can often help relieve signs and symptoms of heart failure and prevent the disease from worsening. These changes may be among the most important and beneficial you can make. Lifestyle changes your doctor may recommend include:
Stop smoking. Smoking damages your blood vessels, raises blood pressure, reduces the amount of oxygen in your blood and makes your heart beat faster.If you smoke, ask your doctor to recommend a program to help you quit. You can’t be considered for a heart transplant if you continue to smoke. Avoid secondhand smoke, too.
Discuss weight monitoring with your doctor. Discuss with doctor how often you should weigh yourself. Ask doctor how much weight gain you should notify him or her about. Weight gain may mean that you’re retaining fluids and need a change in your treatment plan.
Check your legs, ankles and feet for swelling daily. Check for any changes in swelling in your legs, ankles or feet daily. Check with your doctor if the swelling worsens.
Eat a healthy diet. Aim to eat a diet that includes fruits and vegetables, whole grains, fat-free or low-fat dairy products, and lean proteins.
Restrict sodium in diet. Too much sodium contributes to water retention, which makes your heart work harder and causes shortness of breath and swollen legs, ankles and feet.
Check with doctor for the sodium restriction recommended for you. Keep in mind that salt is already added to prepared foods, and be careful when using salt substitutes.
Maintain a healthy weight. If you’re overweight, your dietitian will help you work toward your ideal weight. Even losing a small amount of weight can help.
Consider getting vaccinations. If you have heart failure, you may want to get influenza and pneumonia vaccinations.
Limit saturated or ‘trans’ fats in your diet. In addition to avoiding high-sodium foods, limit the amount of saturated fat and trans fat — also called trans-fatty acids — in your diet. These potentially harmful dietary fats increase your risk of heart disease.
Limit alcohol and fluids. Doctor may recommend that you don’t drink alcohol if you have heart failure, since it can interact with your medication, weaken your heart muscle and increase your risk of abnormal heart rhythms.
If you have severe heart failure, doctor may also suggest you limit the amount of fluids you drink.

Reduce stress. When you’re anxious or upset, your heart beats faster, you breathe more heavily and your blood pressure often goes up. This can make heart failure worse, since your heart is already having trouble meeting the body’s demands.

Find ways to reduce stress in your life. To give your heart a rest, try napping or putting your feet up when possible. Spend time with friends and family to be social and help keep stress at bay.

Sleep easy. If you’re having shortness of breath, especially at night, sleep with your head propped up using a pillow or a wedge. If you snore or have had other sleep problems, make sure you get tested for sleep apnea.

CARDIAC ARREST

CARDIAC ARREST

Cardiac-Arrest

Cardiac arrest is a serious heart condition. The word arrest means to stop or bring to a halt. In cardiac arrest, the heart ceases to beat. It’s also known as sudden cardiac death.

Your heartbeat is controlled by electrical impulses. When these impulses change pattern, the heartbeat becomes irregular. This is also known as an arrhythmia. Some arrhythmias are slow, others are rapid. Cardiac arrest occurs when the rhythm of the heart stops.

Cardiac arrest is an extremely serious health issue. The Institute of Medicine reports that every year, more than half a million people experience cardiac arrest in the United States. The condition can cause death or disability. If someone is experiencing symptoms of cardiac arrest, seek emergency health assistance immediately. It can be fatal. Immediate response and treatment can save a life.

CLASSIFICATION
Clinicians classify cardiac arrest into “shockable” versus “non–shockable”, as determined by the ECG rhythm. This refers to whether a particular class of cardiac dysrhythmia is treatable using defibrillation. The two “shockable” rhythms are ventricular fibrillation and pulseless ventricular tachycardia while the two “non–shockable” rhythms are asystole and pulseless electrical activity.

CAUSES OF CARDIAC ARREST
A number of factors can cause sudden cardiac arrest. Two of the most common are ventricular and atrial fibrillation.

VENTRICULAR FIBRILLATION
Your heart has four chambers. The two lower chambers are the ventricles. In ventricular fibrillation, these chambers quiver out of control. This causes the heart’s rhythm to change dramatically. The ventricles begin to pump inefficiently, which severely decreases the amount of blood pumped through the body. In some cases, the circulation of blood stops completely. This may lead to sudden cardiac death.

The most frequent cause of cardiac arrest is ventricular fibrillation.

ATRIAL FIBRILATION
The heart can also stop beating efficiently after an arrhythmia in the upper chambers. These chambers are known as the atria.

Atrial fibrillation begins when the sinoatrial (SA) node doesn’t send out the correct electrical impulses. Your SA node is located in the right atrium. It regulates how quickly the heart pumps blood. When the electrical impulse goes into atrial fibrillation, the ventricles can’t pump blood out to the body efficiently.

RISK FOR CARDIAC ARREST

Certain heart conditions and health factors can increase your risk of cardiac arrest.

CORONARY ARTERY DISEASE
This type of heart disease begins in the coronary arteries. These arteries supply the heart muscle itself. When they become blocked, your heart does not receive blood. It may stop working properly.

LARGE HEART
Having an abnormally large heart places you at increased risk for cardiac arrest. A large heart may not beat correctly. The muscle may also be more prone to damage.

IRREGULAR HEART BEAT
Valve disease can make heart valves leaky or narrower. This means blood circulating through the heart either overloads the chambers with blood or does not fill them to capacity. The chambers may become weakened or enlarged.

CONGENITAL HEART DISEASE
Some people are born with heart damage. This is known as a congenital heart problem. Sudden cardiac arrest may occur in children who were born with a serious heart problem.

ELECTRICAL IMPULSE PROBLEMS
Problems with your heart’s electrical system can increase your risk of sudden cardiac death. These problems are known as primary heart rhythm abnormalities.

Other risk factors for cardiac arrest include:

  • Smoking
  • Sedentary lifestyle
  • High blood pressure
  • Obesity
  • Family history of heart disease
  • History of a previous heart attack
  • Age over 45 for men, or over 55 for women
  • Male gender
  • Substance abuse
  • Low potassium or magnesium

SIGNS AND SYMPTOMS
Early symptoms of cardiac arrest are often warning signs. Getting treatment before your heart stops could save your life.

If you are in cardiac arrest, you may:

  • Become dizzy
  • Be short of breath
  • Feel fatigued or weak
  • Vomit
  • Experience heart palpitations                                                                                                                                          Immediate EMERGENCY care is needed if someone are with experiences these symptoms
  • Chest pain
  • No pulse
  • Not breathing or difficulty breathing
  • Loss of consciousness
  • Collapse
  • Cardiac arrest may not have symptoms before it occurs. If you do have symptoms that persist, seek prompt medical care.

DIAGNOSIS

difference-between-Heart-attack-and-Cardiac-arrest
difference-between-Heart-attack-and-Cardiac-arrest

During a cardiac event that causes your heart to stop beating efficiently, it’s vital to seek medical attention immediately. Medical treatment will focus on getting blood flowing back to your body. Doctor will most likely perform a test called an electrocardiogram to identify the type of abnormal rhythm your heart is experiencing. To treat the condition, doctor will likely use a defibrillator to shock your heart. An electric shock can often return the heart to a normal rhythm.

Other tests can also be used after you have experienced a cardiac event:

Blood tests can be used to look for signs of a heart attack. They can also measure potassium and magnesium levels.
Chest X-ray can look for other signs of disease in the heart.

TREATING THE CARDIAC ARREST

defibrillator
Defibrillator

Cardiopulmonary resuscitation (CPR) is one form of emergency treatment for cardiac arrest. Defibrillation is another. These treatments get your heart beating again once it has stopped.

Medication can lower high blood pressure and cholesterol.
Surgery can repair damaged blood vessels or heart valves. It can also bypass or remove blockages in the arteries.
Exercise may improve cardiovascular fitness.
Dietary changes can help you lower cholesterol.

LONG TERM OUTLOOK OF CARDIAC ARREST
Cardiac arrest can be fatal. However, prompt treatment increases your odds of survival. Treatment is most effective within a few minutes of the arrest.

If you have experienced cardiac arrest, it’s important to understand the cause. Your long-term outlook will depend on the reason you experienced cardiac arrest. Your doctor can talk to you about treatment options to help protect your heart and prevent cardiac arrest from happening again.

PHYSICAL REHABILITATION OF CARDIOVASCULAR DISEASE

INDICATIONS
Cardiac rehabilitation should be offered to all cardiac patients who would benefit. CR is mainly prescribed to patients with ischemic heart disease, with myocardial infarction, after coronary angioplasty, after coronaro-aortic by-pass graft surgery and to patients with chronic heart failure. CR begins as soon as possible in intensive care units, only if the patient is in stable medical condition. Intensity of rehabilitation depends on patient´s condition and complications in acute phase of disease.

Cardiac rehabilitation typically comprises of four phases. The term phase is used to describe the varying time frames following a cardiac event. The secondary prevention component of CR requires delivery of exercise training, education and counseling, risk factor intervention and follow up.

Appropriate referral pathways should be set up so appropriate patients can be identified and invited to attend. Referrals should be invited by cardiologist/physician, cardiothoracic surgeon, cardiac team, cardic rehab co-ordinator, G.P., CCU nurses or members of the MDT. All referrals should include the following;

Patients name, age, address and contact number
Type of cardiac event and date of event
Cardiac history, complications and meds
Reason for referral
Referring persons name and contact number, date of request
Clinically relevant information – results of exercise stress test, echo, fasting lipid profile and fasting glucose profile

PHASES OF CARDIAC REHABILATION

PHASE 1 : IN HOSPITAL PATIENT PERIOD
2-5 days

Member of Cardiac Rehab team (CRT) should visit the patient to;

Give support and information to them and their families re: heart disease
Assist the patient to identify personal CV risk factors
Discuss lifestyle modifications of personal risk factors and help provide an individual plan to support these lifestyle changes
Gain support from family members to assist the patient in maintaining the necessary progress
Plan a personal discharge activity programme and encourage the patient to adhere to this and commence daily walks
Inform patients regarding phase II and phase III programs if available and encourage their attendance
At this stage emphasis is on counteracting the negative effects of a cardiac event not promoting training adaptations . Activity levels should be progressed using a staged approach which should be based on the patient’s medical condition. Patient should be closely monitored for any signs of cardiac decompensation.

Educational sessions should be commenced providing information re:

  • The cardiac event
  • Psychological reactions to the event
  • Cardiac pain/symptom management
  • Correction of cardiac misconceptions
  • The use of educational materials such as the heart manual and leaflets from the Irish Heart Foundation should be considered.

PHASE II: POST DISCHARGE PERIOD
GOALS :

Reinforce cardiac risk factor modification
Provide education and support to patient and family
Promote continuing adherence to lifestyle recommendations.

PHASE III: CARDIAC REHABILITATION AND SECONDARY PREVENTION
Structured exercise training with continual educational and psychological support and advice on risk factors
Should take a menu based approach and be individually tailored.
Exercise class will consist of warm up, exercise class, cool down – may also include resistance training with active recovery stations where appropriate.

Patient shouldn’t exercise if they are generally unwell, symptomatic or clinically unstable on arrival;

  • Fever/acute systemic illness
  • Unresolved/unstable angina
  • Resting BP systolic >200mmHg and diastolic > 110mmHg
  • Significant drop in BP
  • Symptomatic hypotension
  • Resting/uncontrolled tachycardia (>100bpm)
  • Uncontrolled atrial or ventricular arrhythmias
  • New/recurrent symptoms of breathlessness, lethargy, palpitations, dizziness
  • Unstable heart failure
  • Unstable/uncontrolled diabetes

NEED TO CONSIDER THE FOLLOWING ;

Local written policy clearly displayed for the management of emergency situations
Rapid access to emergency team in hospital or via ambulance
Regular checking and maintenance of all equipment
Drinking water and glucose supplements available as required
Access to and from venue, emergency exits, toilets and changing areas, lighting, surface and room space checked to ensure they’re appropriate
Enough space for patient traffic and safe placement of equipment
Adequate temperature and ventilation

MEDIAL COLLATERAL LIGAMENT INJURY

INTRODUCTION-
Your medial collateral ligament (MCL) is the knee ligament on the medial (inner) side of your knee connecting the medial femoral condyle and the medial tibial condyle. It is one of four major knee ligaments that help to stabilise the knee joint. It is a flat band of tough fibrous connective tissue composed of long, stringy collagen molecules.

The main function of the MCL is to resist valgus force, which occurs if the tibia/foot is forced outwards in relation to the knee.

ANATOMY OF MCL
ANATOMY OF MCL

CAUSES OF MCL INJURY
The MCL is injured when the (valgus) force is too great for the ligament to resist and the ligament is overstretched. This can occur through a sharp change in direction, twisting the knee whilst the foot is fixed, landing wrong from a jump, or the most common a blunt force hit to the knee, such as in football tackle. The incident usually needs to happen at speed. Muscle weakness or incoordination predispose you to a ligament sprain or tear.

SEVERITY OF MCL INJURY
The severity and symptoms of a knee ligament sprain depend on the degree of stretching or tearing of the knee ligament. You may notice an audible snap or tearing sound at the time of your ligment injury.

In a mild Grade I MCL sprain, the knee ligament has a slight stretch, but they don’t actually tear. Although the knee joint may not hurt or swell very much, a mild ligament sprain can increase the risk of a repeat injury.

With a moderate Grade II MCL sprain, the knee ligament tears partially. Knee swelling and bruising are common, and use of the knee joint is usually painful and difficult. You may have some complaints of instability or a feeling of the knee giving way.

With a severe Grade III MCL sprain, the ligament tears completely, causing swelling and sometimes bleeding under the skin. As a result, the joint is unstable and can be difficult to bear weight. You may have a feeling of the knee giving way. Often there will be no pain or severe pain that subsides quickly following a grade 3 tear as all of the pain fibres are torn at the time of injury. With these more severe tears, other structures are at risk of injury including the meniscus and/or ACL.

DIAGNOSIS

On examination, your physiotherapist will look for signs of ligament injury. There will be tenderness over the ligament site, possible swelling and pain with stress tests. MRI may also be used to diagnose a knee ligament injury and look at other surrounding structures for combination injuries.

RECOVERY TIME
Treatment of an MCL injury varies depending on its severity and whether there are other combination injuries.

medial-collateral-ligament-grading-injury
medial-collateral-ligament-grading-injury

Grade I sprains usually heal within a few weeks. Maximal ligament strength will occur after six weeks when the collagen fibres have matured. Resting from painful activity, icing the injury, and some anti-inflammatory medications are useful. Physiotherapy will help to hasten the healing process via electrical modalities, massage, strengthening and joint exercises to guide the direction that the ligament fibres heal. This helps to prevent a future tear.

When a Grade II sprain occurs, use of a weight-bearing brace or some supportive taping is common in early treatment. This helps to ease the pain and avoid stretching of the healing ligament. After a grade II injury, you can usually return to activity once the joint is stable and you are no longer having pain. This may take up to six weeks. Physiotherapy helps to hasten the healing process via electrical modalities, massage, strengthening and joint exercises to guide the direction that the ligament fibres heal. This helps to prevent a future tear and quickly return you to your pre-injury status.

When a Grade III injury occurs, you usually wear a hinged knee brace, locked into extension, and use crutches for 1-2 weeks to protect the injury from weight-bearing stresses. As pain resolves the brace can be unlocked to allow movement as tolerated. The aim is to allow for ligament healing and gradually return to normal activities. These injuries are most successfully treated via physiotherapy and may not return to their full level of activity for 3 to 4 months. All Grade III injuries should be rehabilitated under the guidance of your physiotherapist and knee specialist.

PHYSIOTHERAPYPHYSIOTHERAPY TREATMENT
Depending on the grade of injury you can start to feel better within days to just a few weeks of the injury. Your physiotherapy treatment will aim to:

1.Reduce pain and inflammation.
2.Normalise joint range of motion.
3.Strengthen your knee: esp quadriceps (esp VMO) and hamstrings.
4.Strengthen your lower limb: calves, hip and pelvis muscles.
5.Improve patellofemoral (knee cap) alignment
6.Normalise your muscle lengths
7.Improve your proprioception, agility and balance
8.Improve your technique and function eg walking, running, squatting, hopping and landing.
9.Guide return to sport activities and exercises
10.Minimise your chance of re-injury.

AIMS OF REHABILITATION-
The following examples are for information purposes only. We recommend seeking professional advice before attempting any rehabilitation. The aim of rehabilitation is to reduce pain and swelling, restore full mobility, improve strength and stability before a gradual return to full training.

GRADE 1 MCL INJURY
For a grade 1 MCL injury there may be mild tenderness on the inside of the knee over the ligament and usually no swelling. The rehabilitation guidelines for a mild medial ligament sprain can be split into 4 phases:

Phase 1: immediately following injury

Duration 1 week. Aims to reduce swelling if there is any, ensure the knee can be straightened fully and bent to more than 90 degrees and begin pain free strengthening exercises.

Rest from activities that cause pain. As pain allows, aim to walk normally without support or pain. Apply cold therapy and a compression support to limit any swelling. Apply ice for 15 minutes every 2 hours for the first day. The frequency can be gradually reduced to 3 times a day over the next few days. Do not apply ice directly to the skin as it may burn.

Sports massage techniques can usually be applied from day 2, specifically to the ligament. Ultrasound can also be applied to the ligament area. Maintain aerobic fitness with cycling. Apply cold therapy after each strengthening and stretching session.

Pain free stretching exercises for quadriceps and hamstring muscles as well as flexion and extension mobility exercises. Static strengthening exercises can begin as soon as pain allows. Isometric quadriceps exercises, calf raises with both legs and resistance band exercises for the hamstrings, hip abductors and hip extension but not for adduction as this will stress the medial ligament.

Phase 2: after 1 week
Duration 1 week. Aims – Eliminate any swelling completely, regain full range of movement, continue with strengthening exercises and return to slow jogging.

Rest from painful activities, however the athlete may be able to jog slowly as long as it is not painful. Apply cold therapy following exercise or rehabilitation exercises. Continue with stretching and strengthening exercises from phase 1.

Introduce dynamic strengthening exercises such as knee extension, knee flexion, half squats, step ups, single leg calf raise, bridging and leg press are suitable exercises if pain allows.

Cross friction massage to the ligament can be performed on alternate days. Maintain aerobic fitness with cycling, stepping machine and gentle jogging but no sudden changes of direction.

Phase 3: after 2 weeks
Duration 2 weeks. Aims to maintain full range of motion, equal strength of both legs, return to running and some sports specific training.

Continue to apply cold therapy after training sessions. Continue with sports massage techniques every 3 days. Continue with stretching exercises.

Build on dynamic strengthening exercises such as leg extension and leg curls exercises as well as squats to horizontal and lunges. Increase the intensity, weight lifted and number of repetitions. Aim for between 10 and 20 reps. Increase until the strength is equal in both legs.

In addition to straight running, start to include sideways and backwards running, agility drills and plyometric exercises. Increase speed to sprinting and changing direction drills.

Phase 4: after 4 weeks
Duration 3 to 6 weeks. Aims to return to full sports specific training and competition.

Sports massage for surrounding muscles on as weekly basis. Continue with strength training as above but start to include hopping and bounding exercises. The athlete should now be ready to gradually return to full sports specific training and then competition.

A knee support or a strapping / taping techniques may provide extra support on return to full training, however do not become reliant on this. It will weaken the joint. Use initially for confidence building.

GRADE 2 OR 3 SPRAIN-
For a grade 2+ and particularly 3 sprain it is important that the ends of the ligament are protected and left to heal without continually being disrupted. The rehabilitation guidelines for a grade 2+ or 3 medial ligament sprain (more severe) can be split into 4 phases:

Phase 1: immediately following injury

Duration 4 weeks. Aims to control swelling, maintain ability to straighten the leg bend the knee to more than 90 degrees, begin strengthening exercises.

Rest from all painful activities. Use crutches if necessary, non weight bearing to start with, then partial weight bearing from week 2 and by end of week 4 aim to be walking normally.

Wear a hinged or stabilised knee brace to protect the medial ligament. Apply cold therapy and compression. Apply ice / cold therapy for 15 minutes every 2 hours for the first 2 days and gradually reduce the frequency to 3 times a day over the next week. Pain free stretches for the hamstrings, quads, groin and calf muscles in particular. Mobility exercises should be done in the knee brace.

Sports massage (gentle cross frictions) may be possible from day 2 but allow a week for more severe injuries. As pain allows, static quads and hamstring exercises, double leg calf raises, hip abduction and extension. Knee extension mobility should only be to 30 degrees though. Maintain aerobic fitness on stationary cycle as soon as pain allows.

Phase 2: Following week 4
Duration 2 weeks. Aims to eliminate swelling, full weight bearing on the injured knee, full range of motion, injured leg almost as strong as the good one.

Continue with cold therapy and compression to eliminate swelling following exercises. Remove the knee brace at this stage. A simple stablized knee support is more suitable at this stage to apply compression to the knee. A therapist will continue with ultrasound and massage.

Range of motion exercises should continue along with isometric quadriceps exercises. Mini squats, lunges, double leg press, hamstring curls, step ups, bridges, hip abduction, hip extension and single leg calf raises can begin or be continued. It may be possible to begin to swim (not breaststroke!) or use stepper for aerobic fitness.

Phase 3: after week 6
Duration 4 weeks. Aims to regain full range of motion, strength, return to light jogging and by week 10 from injury, return to sports specific exercises.

Continue with cold therapy following training sessions. Wear a brace or support as required. Sports massage techniques to the ligament 2 to 3 times a weeks. Strengthening exercises as above increasing intensity and moving double leg exercises to single.

After week 6, no sooner, begin to run if comfortable, no sudden changes of direction though.

After week 8 begin to run sideways and backwards so by week 10 the athlete is able to begin to change direction at speed. For footballers, kicking may now be possible.

When confident enough plyometric drills, hopping, box jumps and agility drills can begin.

Phase 4: after week 10
Duration 2 to 4 weeks. Aims to return to full sports specific training and competition without a brace for support, full strength and mobility.

Gradually bring into training more and more sports specific drills, changing direction and plyometric, hopping and bounding exercises. Normal sports specific training can begin.

KNEE LIGAMENT SURGERY
Most MCL injuries resolve well with conservative management, however, surgery may be considered if there is significant ligament disruption eg Grade III. Surgery may also be required if the are significant combination injuries involving the ACL and/or meniscus. In these cases a knee specialist will guide the need for surgery.

Risks of surgery include infection, persistent instability and pain, stiffness, and difficulty returning to your previous level of activity. The good news is that better than 90% of patients have no complications post-surgery.

POST SURGICAL REHABILITATION
Post-operative knee rehabilitation is one of the most important aspects of knee surgery. The most successful and quickest outcomes result from the guidance and supervision of an experienced sports physiotherapist.

Your physiotherapy rehabilitation following knee surgery focuses on restoring full knee motion, strength, power and endurance. You’ll also require balance, proprioception and agility retraining that is individualised towards your specific sporting or functional needs.

As mentioned earlier your sports physiotherapist is an expert in this field. We suggest you contact them for the best advice in your circumstances.

Your physiotherapist will guide your return to sport. It is highly variable and depends upon on your specific knee ligament injury and the demands of your demands of your sports.

PRVENTION OF RECURRENCE
A knee strengthening, agility and proprioceptive training program is the best way to reduce your chance of a knee ligament sprain. Premature return to high-risk activities such as sport are best discussed with your physiotherapist or surgeon.