Congenital heart disease is the most common birth defect, affecting 0.8% of newborns. The document outlines the prevalence, etiology, evaluation, specific lesions, pathophysiology, clinical manifestations, diagnosis, management, and prognosis of various congenital heart defects. Key defects discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, tetralogy of Fallot, and transposition of the great arteries. Physical exam findings, diagnostic tools, treatment options, and complications are described for each condition.
The document discusses several congenital heart diseases including ventricular septal defects (VSD), atrial septal defects (ASD), patent ductus arteriosus (PDA), pulmonary stenosis, aortic stenosis, and coarctation of the aorta. It describes the pathophysiology, clinical presentation, investigations, and management of each condition. Cyanotic heart diseases are defined as those involving a right-to-left or left-to-right shunt leading to low oxygen saturation. The document provides classification, epidemiology, etiology and detailed information about specific lesions causing cyanosis.
This document provides an overview of congenital heart disease (CHD) and anesthesia considerations for CHD. It begins with definitions and classifications of CHD, including acyanotic and cyanotic defects. Specific conditions discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, aortic stenosis, and coarctation of the aorta. For each condition, the document outlines etiology, pathophysiology, clinical presentation, diagnosis, and treatment considerations.
The document discusses atrial septal defect (ASD), including its embryology, types, pathophysiology, natural history, evaluation, and management. ASD is a congenital heart defect characterized by an opening in the interatrial septum that causes blood to flow from the left atrium to the right atrium. The size and location of the defect determines symptoms and treatment, which may include medical management, interventional closure, or surgical repair.
The document discusses congenital heart diseases, which occur in approximately 1% of live births. It describes several types of congenital heart defects including atrial septal defect (ASD), ventricular septal defect (VSD), atrioventricular canal defect, and patent ductus arteriosus - all of which involve increased pulmonary blood flow. It also discusses obstructive defects like aortic stenosis and pulmonary stenosis. The document provides details on the pathophysiology, clinical manifestations, diagnosis, and treatment of these various congenital heart conditions.
- The patient is a 36-year-old male who presented with palpitations and breathlessness on exertion. Echocardiogram revealed an atrial septal defect (ASD) of the sinus venosus type with anomalous pulmonary venous drainage and moderate pulmonary hypertension.
- Sinus venosus ASDs account for 10% of ASDs and involve a defect between the superior vena cava and right atrium, often associated with anomalous pulmonary vein drainage.
- Surgical repair is the treatment of choice, involving use of a patch to redirect pulmonary vein flow to the left atrium while closing the interatrial communication.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs including secundum, ostium primum, sinus venosus, and coronary sinus defects. ASDs are usually diagnosed through echocardiography which can determine the size and location of the defect. Small, asymptomatic ASDs may not require treatment, but larger defects with evidence of right heart strain often warrant closure either through open heart surgery or a nonsurgical approach using an implantable device delivered through catheters. Both methods effectively close the defect to prevent long-term complications like heart failure and pulmonary hypertension.
Congenital heart disease is the most common birth defect, affecting 0.8% of newborns. The document outlines the prevalence, etiology, evaluation, specific lesions, pathophysiology, clinical manifestations, diagnosis, management, and prognosis of various congenital heart defects. Key defects discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, tetralogy of Fallot, and transposition of the great arteries. Physical exam findings, diagnostic tools, treatment options, and complications are described for each condition.
The document discusses several congenital heart diseases including ventricular septal defects (VSD), atrial septal defects (ASD), patent ductus arteriosus (PDA), pulmonary stenosis, aortic stenosis, and coarctation of the aorta. It describes the pathophysiology, clinical presentation, investigations, and management of each condition. Cyanotic heart diseases are defined as those involving a right-to-left or left-to-right shunt leading to low oxygen saturation. The document provides classification, epidemiology, etiology and detailed information about specific lesions causing cyanosis.
This document provides an overview of congenital heart disease (CHD) and anesthesia considerations for CHD. It begins with definitions and classifications of CHD, including acyanotic and cyanotic defects. Specific conditions discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, aortic stenosis, and coarctation of the aorta. For each condition, the document outlines etiology, pathophysiology, clinical presentation, diagnosis, and treatment considerations.
The document discusses atrial septal defect (ASD), including its embryology, types, pathophysiology, natural history, evaluation, and management. ASD is a congenital heart defect characterized by an opening in the interatrial septum that causes blood to flow from the left atrium to the right atrium. The size and location of the defect determines symptoms and treatment, which may include medical management, interventional closure, or surgical repair.
The document discusses congenital heart diseases, which occur in approximately 1% of live births. It describes several types of congenital heart defects including atrial septal defect (ASD), ventricular septal defect (VSD), atrioventricular canal defect, and patent ductus arteriosus - all of which involve increased pulmonary blood flow. It also discusses obstructive defects like aortic stenosis and pulmonary stenosis. The document provides details on the pathophysiology, clinical manifestations, diagnosis, and treatment of these various congenital heart conditions.
- The patient is a 36-year-old male who presented with palpitations and breathlessness on exertion. Echocardiogram revealed an atrial septal defect (ASD) of the sinus venosus type with anomalous pulmonary venous drainage and moderate pulmonary hypertension.
- Sinus venosus ASDs account for 10% of ASDs and involve a defect between the superior vena cava and right atrium, often associated with anomalous pulmonary vein drainage.
- Surgical repair is the treatment of choice, involving use of a patch to redirect pulmonary vein flow to the left atrium while closing the interatrial communication.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs including secundum, ostium primum, sinus venosus, and coronary sinus defects. ASDs are usually diagnosed through echocardiography which can determine the size and location of the defect. Small, asymptomatic ASDs may not require treatment, but larger defects with evidence of right heart strain often warrant closure either through open heart surgery or a nonsurgical approach using an implantable device delivered through catheters. Both methods effectively close the defect to prevent long-term complications like heart failure and pulmonary hypertension.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs. Secundum ASDs, which occur in the fossa ovalis, account for 75% of cases. ASDs are usually diagnosed with echocardiography. Small, asymptomatic ASDs may not require treatment, but larger defects can cause heart failure and pulmonary hypertension if left untreated. Larger ASDs are often closed either surgically or non-surgically using devices delivered through catheters. Both methods are generally effective though surgery carries risks of complications.
This document provides information on atrial septal defects (ASD), including:
- ASD is the second most common congenital heart defect, accounting for 15-20% of cases. It involves a deficiency in the atrial septum.
- Types of ASD include ostium secundum (70% of cases), ostium primum, and sinus venosus defects.
- ASD causes a left-to-right shunt that can lead to enlargement of the right atrium and ventricle over time if left unrepaired. Closure is generally recommended for symptomatic patients or those with evidence of pulmonary hypertension.
- Diagnosis involves echocardiogram,
Congenital heart disease (CHD) is a common birth defect with an incidence of 8 per 1000 live births. The causes are often unknown but can be genetic or environmental. Common defects include ventricular septal defects (25-30% of cases), atrial septal defects (6-8%), and patent ductus arteriosus (6-8%). Symptoms depend on the type and severity of defect. Diagnosis involves history, physical exam, imaging like echocardiogram. Treatment may include medications or surgery depending on the defect. Untreated defects can lead to complications like heart failure, pulmonary hypertension. Prognosis is generally good after surgical repair of defects.
1. An atrial septal defect is an opening in the septum between the left and right atria, allowing blood to shunt from the left to the right side of the heart.
2. It is one of the most common congenital heart defects found in adults.
3. Symptoms range from none in small defects to fatigue and shortness of breath from right heart strain in large defects that cause significant shunting of blood from the left to the right atrium.
This document provides an overview of pediatric cardiology, including evaluating cardiovascular diseases, examining the heart, diagnostic tests, fetal circulation, congenital heart diseases, and notes on specific conditions like ventricular septal defect. Key points include how history, examination and tests are used to evaluate heart diseases, the major criteria that suggest a heart condition may be present, how fetal circulation differs from postnatal circulation, classifications of congenital heart diseases, prevalence and risk factors, and details on ventricular septal defect as the most common congenital heart disease in infants and children.
The document discusses cardiovascular disorders in children, including congenital heart diseases like ventricular septal defect (VSD). It provides details on the anatomy and physiology of the cardiovascular system in children, changes after birth, and diagnostic techniques for congenital heart diseases such as echocardiography and catheterization. VSD is described as a hole in the septum between the right and left ventricles allowing left-to-right shunting, which can cause congestive heart failure or pulmonary hypertension.
1. Ventricular septal defect (VSD) is a common congenital heart defect where there is an opening in the wall separating the left and right ventricles of the heart, allowing blood to pass between them.
2. VSDs are classified based on size (large, moderate, small) and location (perimembranous, muscular, inlet, outlet). Large VSDs require surgical intervention while small ones often close spontaneously.
3. Clinical manifestations include heart murmur, fatigue, rapid breathing, and signs of congestive heart failure. Diagnosis is made through echocardiogram, chest x-ray, and ECG. Treatment depends on severity but may involve surgery to
This document summarizes various acyanotic congenital heart diseases. It describes the pathophysiology, clinical features, diagnosis, and treatment of conditions including atrial septal defect, ventricular septal defect, patent ductus arteriosus, patent foramen ovale, pulmonary valve stenosis, and aortic valve stenosis. Common causes are genetic defects, maternal infections, or drug/alcohol use during pregnancy. These conditions are characterized by left-to-right shunts, which can cause pulmonary hypertension and right heart hypertrophy if significant in size.
Adult Congenital Heart Disease can affect over 1 million adults in the US. Common conditions include Atrial Septal Defects, Ventricular Septal Defects, Patent Ductus Arteriosus, Bicuspid Aortic Valve, Coarctation of the Aorta, Tetralogy of Fallot, and Transposition of the Great Arteries. Clinical presentation and treatment depends on the specific condition and degree of severity. Long term monitoring is important for complications. Pregnancy can also pose additional risks for some congenital heart conditions.
1. The document provides an outline and overview of congenital heart disease for anesthesia students.
2. It discusses the prevalence, etiology, evaluation, and management of various congenital heart lesions including acyanotic lesions like ASD, VSD, PDA, and obstructive lesions as well as cyanotic lesions with decreased and increased pulmonary blood flow.
3. The document describes the pathophysiology, clinical manifestations, diagnosis, and treatment of each lesion in detail.
Truncus arteriosus is a congenital heart defect where there is a single arterial trunk exiting the heart, giving rise to the pulmonary artery, aorta, and coronary arteries. This occurs when normal septation of the embryonic bulbar trunk fails to occur. Blood from the two ventricles mixes in the common trunk, resulting in decreased oxygen levels. Surgical repair is needed to separate pulmonary and systemic blood flow and close the ventricular septal defect. Without repair, complications like congestive heart failure and pulmonary hypertension can develop.
This document provides an overview of congenital heart disease, including prevalence, circulatory adjustments at birth, hemodynamic classifications, and descriptions of specific conditions like atrial septal defect (ASD) and ventricular septal defect (VSD). It notes that congenital heart defects affect 6-8 per 1000 live births and can range widely in severity. Diagnosis typically occurs by 1 week or 1 month of age. After birth, clamping of the umbilical cord and expansion of the lungs cause pressure changes and closure of passages between circulations. Conditions are classified as acyanotic or cyanotic depending on oxygen saturation levels. ASD and VSD are both described in detail including typical clinical features, imaging findings, and management
This document provides information on congenital heart disease (CHD), including epidemiology, classification, diagnosis, and treatment. It discusses several specific types of CHD such as atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), coarctation of the aorta, tetralogy of Fallot, transposition of the great arteries, tricuspid atresia, truncus arteriosus, and hypoplastic left heart syndrome. It describes the clinical presentation, investigations, and management approaches for each condition.
This document provides information on congenital heart disease, including definitions, classifications, and details on specific conditions. It defines congenital heart disease and notes its prevalence of about 1% of live births. It classifies heart defects into left-to-right shunt lesions, right to left shunt lesions, and obstructive lesions. Details are given on specific conditions including atrial septal defect, ventricular septal defect, and patent ductus arteriosus. For each, the document describes hemodynamics, clinical findings, diagnosis, and treatment. Echocardiography is highlighted as the primary diagnostic tool for congenital heart disease.
Congenital heart disease, by dr Shaymaa Fayad, El Nasr Hospital Port saidmohamed osama hussein
1. Blood from the placenta travels through the umbilical vein to the fetus's heart, bypassing the lungs via the foramen ovale. It then circulates through the aorta to the body.
2. The ductus arteriosus shunts blood away from the lungs, which are not used for gas exchange in utero.
3. At birth, closure of the ductus arteriosus and foramen ovale, along with an increase in pulmonary blood flow, directs blood through the lungs for the first time.
This document provides information on various types of acyanotic congenital heart defects, including their anatomy, physiology, clinical features, diagnosis, treatment and prognosis. It discusses atrial septal defects (ASD), ventricular septal defects (VSD), and patent ductus arteriosus (PDA). ASDs are classified based on their location. VSDs account for one-quarter of all congenital heart defects and result in left-to-right shunting. PDA causes left-to-right shunting between the aorta and pulmonary artery. Surgical or catheterization closure is often recommended for larger defects.
The lecture is for medical student. It is from Dr RUSINGIZA Emmanuel, MD, senior lecture at UR( UNIVERSITY OF RWANDA) .
It will help to understand heart diseases in newborn, infants and children.
Congenital Heart Disease is present in approximately 0.8% of children. It is commonly divided into cyanotic and noncyanotic categories based on the direction of blood flow. Tetralogy of Fallot is the most common cyanotic congenital heart defect, characterized by four anatomical abnormalities that result in deoxygenated blood mixing with oxygenated blood. Clinical features include progressive cyanosis after infancy and hypoxic spells in young children. Surgical repair is usually required. Atrial septal defect is a common noncyanotic defect where a hole exists between the upper chambers of the heart. It often causes no symptoms and may close on its own, but larger defects require closure to prevent lung and heart damage.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs. Secundum ASDs, which occur in the fossa ovalis, account for 75% of cases. ASDs are usually diagnosed with echocardiography. Small, asymptomatic ASDs may not require treatment, but larger defects can cause heart failure and pulmonary hypertension if left untreated. Larger ASDs are often closed either surgically or non-surgically using devices delivered through catheters. Both methods are generally effective though surgery carries risks of complications.
This document provides information on atrial septal defects (ASD), including:
- ASD is the second most common congenital heart defect, accounting for 15-20% of cases. It involves a deficiency in the atrial septum.
- Types of ASD include ostium secundum (70% of cases), ostium primum, and sinus venosus defects.
- ASD causes a left-to-right shunt that can lead to enlargement of the right atrium and ventricle over time if left unrepaired. Closure is generally recommended for symptomatic patients or those with evidence of pulmonary hypertension.
- Diagnosis involves echocardiogram,
Congenital heart disease (CHD) is a common birth defect with an incidence of 8 per 1000 live births. The causes are often unknown but can be genetic or environmental. Common defects include ventricular septal defects (25-30% of cases), atrial septal defects (6-8%), and patent ductus arteriosus (6-8%). Symptoms depend on the type and severity of defect. Diagnosis involves history, physical exam, imaging like echocardiogram. Treatment may include medications or surgery depending on the defect. Untreated defects can lead to complications like heart failure, pulmonary hypertension. Prognosis is generally good after surgical repair of defects.
1. An atrial septal defect is an opening in the septum between the left and right atria, allowing blood to shunt from the left to the right side of the heart.
2. It is one of the most common congenital heart defects found in adults.
3. Symptoms range from none in small defects to fatigue and shortness of breath from right heart strain in large defects that cause significant shunting of blood from the left to the right atrium.
This document provides an overview of pediatric cardiology, including evaluating cardiovascular diseases, examining the heart, diagnostic tests, fetal circulation, congenital heart diseases, and notes on specific conditions like ventricular septal defect. Key points include how history, examination and tests are used to evaluate heart diseases, the major criteria that suggest a heart condition may be present, how fetal circulation differs from postnatal circulation, classifications of congenital heart diseases, prevalence and risk factors, and details on ventricular septal defect as the most common congenital heart disease in infants and children.
The document discusses cardiovascular disorders in children, including congenital heart diseases like ventricular septal defect (VSD). It provides details on the anatomy and physiology of the cardiovascular system in children, changes after birth, and diagnostic techniques for congenital heart diseases such as echocardiography and catheterization. VSD is described as a hole in the septum between the right and left ventricles allowing left-to-right shunting, which can cause congestive heart failure or pulmonary hypertension.
1. Ventricular septal defect (VSD) is a common congenital heart defect where there is an opening in the wall separating the left and right ventricles of the heart, allowing blood to pass between them.
2. VSDs are classified based on size (large, moderate, small) and location (perimembranous, muscular, inlet, outlet). Large VSDs require surgical intervention while small ones often close spontaneously.
3. Clinical manifestations include heart murmur, fatigue, rapid breathing, and signs of congestive heart failure. Diagnosis is made through echocardiogram, chest x-ray, and ECG. Treatment depends on severity but may involve surgery to
This document summarizes various acyanotic congenital heart diseases. It describes the pathophysiology, clinical features, diagnosis, and treatment of conditions including atrial septal defect, ventricular septal defect, patent ductus arteriosus, patent foramen ovale, pulmonary valve stenosis, and aortic valve stenosis. Common causes are genetic defects, maternal infections, or drug/alcohol use during pregnancy. These conditions are characterized by left-to-right shunts, which can cause pulmonary hypertension and right heart hypertrophy if significant in size.
Adult Congenital Heart Disease can affect over 1 million adults in the US. Common conditions include Atrial Septal Defects, Ventricular Septal Defects, Patent Ductus Arteriosus, Bicuspid Aortic Valve, Coarctation of the Aorta, Tetralogy of Fallot, and Transposition of the Great Arteries. Clinical presentation and treatment depends on the specific condition and degree of severity. Long term monitoring is important for complications. Pregnancy can also pose additional risks for some congenital heart conditions.
1. The document provides an outline and overview of congenital heart disease for anesthesia students.
2. It discusses the prevalence, etiology, evaluation, and management of various congenital heart lesions including acyanotic lesions like ASD, VSD, PDA, and obstructive lesions as well as cyanotic lesions with decreased and increased pulmonary blood flow.
3. The document describes the pathophysiology, clinical manifestations, diagnosis, and treatment of each lesion in detail.
Truncus arteriosus is a congenital heart defect where there is a single arterial trunk exiting the heart, giving rise to the pulmonary artery, aorta, and coronary arteries. This occurs when normal septation of the embryonic bulbar trunk fails to occur. Blood from the two ventricles mixes in the common trunk, resulting in decreased oxygen levels. Surgical repair is needed to separate pulmonary and systemic blood flow and close the ventricular septal defect. Without repair, complications like congestive heart failure and pulmonary hypertension can develop.
This document provides an overview of congenital heart disease, including prevalence, circulatory adjustments at birth, hemodynamic classifications, and descriptions of specific conditions like atrial septal defect (ASD) and ventricular septal defect (VSD). It notes that congenital heart defects affect 6-8 per 1000 live births and can range widely in severity. Diagnosis typically occurs by 1 week or 1 month of age. After birth, clamping of the umbilical cord and expansion of the lungs cause pressure changes and closure of passages between circulations. Conditions are classified as acyanotic or cyanotic depending on oxygen saturation levels. ASD and VSD are both described in detail including typical clinical features, imaging findings, and management
This document provides information on congenital heart disease (CHD), including epidemiology, classification, diagnosis, and treatment. It discusses several specific types of CHD such as atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), coarctation of the aorta, tetralogy of Fallot, transposition of the great arteries, tricuspid atresia, truncus arteriosus, and hypoplastic left heart syndrome. It describes the clinical presentation, investigations, and management approaches for each condition.
This document provides information on congenital heart disease, including definitions, classifications, and details on specific conditions. It defines congenital heart disease and notes its prevalence of about 1% of live births. It classifies heart defects into left-to-right shunt lesions, right to left shunt lesions, and obstructive lesions. Details are given on specific conditions including atrial septal defect, ventricular septal defect, and patent ductus arteriosus. For each, the document describes hemodynamics, clinical findings, diagnosis, and treatment. Echocardiography is highlighted as the primary diagnostic tool for congenital heart disease.
Congenital heart disease, by dr Shaymaa Fayad, El Nasr Hospital Port saidmohamed osama hussein
1. Blood from the placenta travels through the umbilical vein to the fetus's heart, bypassing the lungs via the foramen ovale. It then circulates through the aorta to the body.
2. The ductus arteriosus shunts blood away from the lungs, which are not used for gas exchange in utero.
3. At birth, closure of the ductus arteriosus and foramen ovale, along with an increase in pulmonary blood flow, directs blood through the lungs for the first time.
This document provides information on various types of acyanotic congenital heart defects, including their anatomy, physiology, clinical features, diagnosis, treatment and prognosis. It discusses atrial septal defects (ASD), ventricular septal defects (VSD), and patent ductus arteriosus (PDA). ASDs are classified based on their location. VSDs account for one-quarter of all congenital heart defects and result in left-to-right shunting. PDA causes left-to-right shunting between the aorta and pulmonary artery. Surgical or catheterization closure is often recommended for larger defects.
The lecture is for medical student. It is from Dr RUSINGIZA Emmanuel, MD, senior lecture at UR( UNIVERSITY OF RWANDA) .
It will help to understand heart diseases in newborn, infants and children.
Congenital Heart Disease is present in approximately 0.8% of children. It is commonly divided into cyanotic and noncyanotic categories based on the direction of blood flow. Tetralogy of Fallot is the most common cyanotic congenital heart defect, characterized by four anatomical abnormalities that result in deoxygenated blood mixing with oxygenated blood. Clinical features include progressive cyanosis after infancy and hypoxic spells in young children. Surgical repair is usually required. Atrial septal defect is a common noncyanotic defect where a hole exists between the upper chambers of the heart. It often causes no symptoms and may close on its own, but larger defects require closure to prevent lung and heart damage.
Similar to 4.CONGENITAL HEART DISEASE(CHD).pdf uiy (20)
The document discusses the acute metabolic complications of diabetes mellitus, diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). It describes the pathogenesis, clinical presentation, diagnostic evaluation and treatment of DKA and HHS. The treatment involves fluid resuscitation, insulin therapy to lower blood glucose levels, potassium supplementation and bicarbonate therapy is not recommended for DKA. Infection is a common precipitating factor for these conditions.
The document discusses amniotic fluid disorders including polyhydramnios and oligohydraminos. Polyhydramnios is an excess of amniotic fluid and can be caused by fetal abnormalities, diabetes, or premature rupture of membranes. Oligohydraminos is a deficiency of amniotic fluid that can result from fetal abnormalities, premature rupture of membranes, or umbilical cord compression. Both conditions require assessment, carry risks of complications, and may be managed through monitoring or induction of labor.
VEDANTA AIR AMBULANCE SERVICES IN REWA AT A COST-EFFECTIVE PRICE.pdfVedanta A
Air Ambulance Services In Rewa works in close coordination with ground-based emergency services, including local Emergency Medical Services, fire departments, and law enforcement agencies.
More@: https://tinyurl.com/2shrryhx
More@: https://tinyurl.com/5n8h3wp8
The facial nerve, also known as cranial nerve VII, is one of the 12 cranial nerves originating from the brain. It's a mixed nerve, meaning it contains both sensory and motor fibres, and it plays a crucial role in controlling various facial muscles, as well as conveying sensory information from the taste buds on the anterior two-thirds of the tongue.
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A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
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This particular slides consist of- what is Pneumothorax,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is a summary of Pneumothorax:
Pneumothorax, also known as a collapsed lung, is a condition that occurs when air leaks into the space between the lung and chest wall. This air buildup puts pressure on the lung, preventing it from expanding fully when you breathe. A pneumothorax can cause a complete or partial collapse of the lung.
CHAPTER 1 SEMESTER V COMMUNICATION TECHNIQUES FOR CHILDREN.pdfSachin Sharma
Here are some key objectives of communication with children:
Build Trust and Security:
Establish a safe and supportive environment where children feel comfortable expressing themselves.
Encourage Expression:
Enable children to articulate their thoughts, feelings, and experiences.
Promote Emotional Understanding:
Help children identify and understand their own emotions and the emotions of others.
Enhance Listening Skills:
Develop children’s ability to listen attentively and respond appropriately.
Foster Positive Relationships:
Strengthen the bond between children and caregivers, peers, and other adults.
Support Learning and Development:
Aid cognitive and language development through engaging and meaningful conversations.
Teach Social Skills:
Encourage polite, respectful, and empathetic interactions with others.
Resolve Conflicts:
Provide tools and guidance for children to handle disagreements constructively.
Encourage Independence:
Support children in making decisions and solving problems on their own.
Provide Reassurance and Comfort:
Offer comfort and understanding during times of distress or uncertainty.
Reinforce Positive Behavior:
Acknowledge and encourage positive actions and behaviors.
Guide and Educate:
Offer clear instructions and explanations to help children understand expectations and learn new concepts.
By focusing on these objectives, communication with children can be both effective and nurturing, supporting their overall growth and well-being.
At Malayali Kerala Spa Ajman, Full Service includes individualized care for every client. We specifically design each massage session for the individual needs of the client. Our therapists are always willing to adjust the treatments based on the client's instruction and feedback. This guarantees that every client receives the treatment they expect.
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NURSING MANAGEMENT OF PATIENT WITH EMPHYSEMA .PPTblessyjannu21
Prepared by Prof. BLESSY THOMAS, VICE PRINCIPAL, FNCON, SPN.
Emphysema is a disease condition of respiratory system.
Emphysema is an abnormal permanent enlargement of the air spaces distal to terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.
Emphysema of lung is defined as hyper inflation of the lung ais spaces due to obstruction of non respiratory bronchioles as due to loss of elasticity of alveoli.
It is a type of chronic obstructive
pulmonary disease.
It is a progressive disease of lungs.
TEST BANK FOR Health Assessment in Nursing 7th Edition by Weber Chapters 1 - ...rightmanforbloodline
TEST BANK FOR Health Assessment in Nursing 7th Edition by Weber Chapters 1 - 34.
TEST BANK FOR Health Assessment in Nursing 7th Edition by Weber Chapters 1 - 34.
TEST BANK FOR Health Assessment in Nursing 7th Edition by Weber Chapters 1 - 34.
2. Congenital Heart Disease (CHD)
Epidemiology of CHD
Incidence - 8/1000 live births
- 3-4/100 still born
- 2/100 premature infants excluding PDA
-10-25/100 abortuses
• Most congenital defects are well tolerated during
• Most congenital defects are well tolerated during
fetal life.
Etiology - Unknown in most cases
- Genetic factors - single gene defect
- Chromosomal abnormality(Trisomy 21, 13,
and 18 and Turner syndrome )
- Environmental factors
3. CHD…
Relative Frequency of Congenital Heart Lesions
Lesions
Lesions % of all Lesions
% of all Lesions
-
- Ventricular
Ventricular septal
septal defect
defect 25
25-
-30
30
-
- Atrial
Atrial septal
septal defect (
defect (Secundum
Secundum)
) 6
6-
-8
8
-
- Patent ductus arteriosus
Patent ductus arteriosus 6
6-
-8
8
-
- Coarctation of aorta
Coarctation of aorta 5
5-
-7
7
-
- Tetralogy of Fallot
Tetralogy of Fallot 5
5-
-7
7
-
- Pulomnary Valve Sterosis
Pulomnary Valve Sterosis 5
5-
-7
7
-
- Aortic Valve Stenosis
Aortic Valve Stenosis 4
4-
-7
7
-
- d
d-
-Transposition of great arteries
Transposition of great arteries 3
3-
-5
5
-
- Hypoplastic left ventricle
Hypoplastic left ventricle 1
1-
-3
3
4. CHD…
Relative Frequency …
Lesions
Lesions % of all Lesions
% of all Lesions
-
- Hypoplastic right ventricle
Hypoplastic right ventricle 1
1-
-3
3
-
- Truncus arteriosus
Truncus arteriosus 1
1-
-2
2
-
- Total anomalous PVR
Total anomalous PVR 1
1-
-2
2
-
- Tricuspid atresia
Tricuspid atresia 1
1-
-2
2
-
- Single ventricle
Single ventricle 1
1-
-2
2
-
- Double
Double-
-outlet right ventricle
outlet right ventricle 1
1-
-2
2
-
- Others
Others 5
5-
-10
10
5. CHD …
Clues for Evaluation of an Infant with suspected CHD
1. On History and Physical Examination
-color
• Acyanotic
• Cyanotic
• Cyanotic
2. Chest roentgenogram -
Pulmonary blood flow
• Normal
• Increased/Plethora
• Decreased/Oligemia
7. I. Acyanotic Congenital Heart Diseases
1. Left to Right Shunt Lesions
1.1 Atrial Septal Defect
Defect occur in any portion of the atrium
- Ostium secundum (at fossa ovalis)-the most
common form
common form
- Ostium primum (lower atrial septum)
- Sinus venosus (upper atrial septum)
Pathophysiology
Left to right shunt
- Transatrial in OS & SV
- Transatrial & transventricular in OP
8.
9. PATHOPHYSIOLOGY.
The degree of left-to-right shunting is dependent on
the size of the defect
size of the defect,
the relative compliance of the right and left ventricles
compliance of the right and left ventricles, and
the relative vascular resistance in the pulmonary and systemic
resistance in the pulmonary and systemic
circulations
circulations.
.
In large defects, a considerable shunt of oxygenated
large defects, a considerable shunt of oxygenated
blood flows from the left to the right atrium
blood flows from the left to the right atrium.
blood flows from the left to the right atrium
blood flows from the left to the right atrium.
This blood is added to the usual venous return to the right
added to the usual venous return to the right
atrium
atrium and is pumped by the right ventricle to the lungs.
With large defects, the ratio of pulmonary to systemic blood flow (Qp :
Qs) is usually between 2 : 1 and 4 : 1.
The paucity of symptoms in infants with ASDs is related to the structure
structure
of the right ventricle in early life
of the right ventricle in early life when its muscular wall is thick and
less compliant, thus limiting the left-to-right shunt.
10. As the infant becomes older and pulmonary vascular
resistance drops, the right ventricular wall becomes
thinner and the left-to-right shunt across the ASD
increases.
The large blood flow through the right side of the heart
results in enlargement of the right atrium and ventricle
enlargement of the right atrium and ventricle
and dilatation of the pulmonary artery
dilatation of the pulmonary artery.
The left atrium may be enlarged
left atrium may be enlarged, the left ventricle and aorta
normal in size.
normal in size.
Despite the large pulmonary blood flow, pulmonary arterial
pressure is usually normal
because of the absence of a high
absence of a high-
-pressure
pressure
communication between the pulmonary and systemic
communication between the pulmonary and systemic
circulations.
circulations.
Pulmonary vascular resistance remains
Pulmonary vascular resistance remains low throughout
low throughout
childhood
childhood, although it may begin to increase in adulthood
increase in adulthood
and may eventually result in reversal of the shunt and
reversal of the shunt and
clinical cyanosis.
clinical cyanosis.
11. Acyanotic CHD…
Clinical Manifestations
Most are asymptomatic
Right ventricular lift
Wide & fixed split of 2nd heart sound
Systolic ejection murmur
Systolic ejection murmur( increased flow across the
right ventricular outflow tract into the pulmonary artery, not by
low-pressure flow across the ASD)
Mid-diastolic murmur at tricuspid area
Holosystolic murmur at mitral area in OP
12. Acyanotic CHD…
Diagnosis
Clinical
CXR - Right. V & A enlargement
- Large pulm. artery
- ↑ed pulm. vascularity
ECG - volume overload,
- right axis deviation
- minor right ventricular conduction delay
Echocardiography
Catheterization
Catheterization
Prognosis - Well tolerated
Complications –
pulm. Hypertension,
Eismenger syndrome(reversal of the shunt and clinical
cyanosis)
Treatment
Surgery
- For all symptomatic ASD
- Asymptomatic patients with shunt ratio > 2:1
19. Acyanotic CHD…
1.2 Ventricular Septal Defect
The most common cardiac malformation
Defect occur in any portion of the septum
- Membranous-majority
- Muscular – mid portion or apical region of the
ventricular septum
– Single or
– Single or
–Swiss-cheese defect(multiple)
-supracristal- less common
Pathophysiology
Lt to Rt shunt
Restrictive if defect is small (0.5cm2)
Non-restrictive - large defect (> 1cm2)
- Right and left vent. Pressure equalized
20.
21. PATHOPHYSIOLOGY.
• The physical size of the VSD is a major, but not the only
determinant of the size of the left-to-right shunt.
• The level of pulmonary vascular resistance in relation to systemic
vascular resistance also determines the shunt's magnitude.
• When a small communication is present (usually <0.5 cm2), the
VSD is called restrictive and right ventricular pressure is normal.
• The higher pressure in the left ventricle drives the shunt left to
right; the size of the defect limits the magnitude of the shunt.
• In large nonrestrictive VSDs (usually >1.0 cm2), right and left
ventricular pressure is equalized.
• In these defects, the direction of shunting and shunt magnitude
shunting and shunt magnitude
are determined by the ratio of pulmonary to systemic vascular
pulmonary to systemic vascular
resistance
resistance
22. • After birth in patients with a large VSD, pulmonary vascular
resistance may remain higher than normal, and thus the size of
the left-to-right shunt may initially be limited.
• As pulmonary vascular resistance continues to fall in the 1st few
weeks after birth because of normal involution of the media of
small pulmonary arterioles
small pulmonary arterioles, the size of the left-to-right shunt
increases.
• Eventually, a large left-to-right shunt develops, and clinical
symptoms become apparent.
• In most cases during early infancy, pulmonary vascular resistance
is only slightly elevated, and the major contribution to pulmonary
is only slightly elevated, and the major contribution to pulmonary
hypertension is the extremely large pulmonary blood flow.
• In some infants with a large VSD pulmonary arteriolar medial
thickness never decreases.
• With continued exposure of the pulmonary vascular bed to high
systolic pressure and high flow, pulmonary vascular obstructive
disease develops.
23. • When the ratio of pulmonary to systemic resistance
approaches 1 : 1, the shunt becomes bidirectional,
the signs of heart failure abate, and the patient
becomes cyanotic (
becomes cyanotic (Eisenmenger
Eisenmenger physiology
physiology, ).
• The magnitude of intracardiac shunts is usually
described by the Qp : Qs ratio.
• If the left-to-right shunt is small (Qp : Qs <1.75 : 1),
the cardiac chambers are not appreciably enlarged
and the pulmonary vascular bed is probably normal.
the cardiac chambers are not appreciably enlarged
and the pulmonary vascular bed is probably normal.
• If the shunt is large (Qp : Qs >2 : 1), left atrial and
ventricular volume overload occurs, as does right
ventricular and pulmonary arterial hypertension.
• The main pulmonary artery, left atrium, and left
ventricle are enlarged
24. Acyanotic CHD…
Clinical Manifestation
Small defects with trivial Lt to Rt Shunt
- Most common
- Asymptomatic
- Loud, harsh holosystolic M at LLSB
Large defects
- Excessive pulmonary blood flow
- Pulmonary hypertension
shunt reversal ( Eisenmenger physiology)
shunt reversal ( Eisenmenger physiology)
- Dyspnea, feeding difficulties, poor growth,
perspiration, recurrent plum. infection, heart failure
- Less harsh but more blowing holosystolic murmur
- Accentuated 2nd heart sound:
Accentuated 2nd heart sound:-
- The pulmonic component of the
2nd heart sound may be ↑ed as a result of pulmonary HTN
result of pulmonary HTN
- Mid-diastolic apical M when Qp: Qs shunt ratio > 2:1
.why??? b/c of increased blood flow across the mitral
valve
25. Acyanotic CHD…
Diagnosis
- Clinical
- CXR - Cardiomegaly
- Plethoric lung (Pulmonary vascular markings
are increased)
-frank pulmonary edema, including pleural
effusions, may be present.
- ECG( biventricular hypertrophy; P waves may be
- ECG( biventricular hypertrophy; P waves may be
notched or peaked)
- Echocardiography
Prognosis
- 30-50% small defects close by 2 yr of age
- Rarely moderate to large defects close
26. Acyanotic CHD…
Complications
- Infective endocarditis
- Recurrent lung infection
- Heart failure
- Pulmonary HTN
- Acquired pulmonary stenosis
aortic valve regurgitation
-- aortic valve regurgitation
Treatment
- Small defects - reassurance
- Prophylaxis against I
- Large defects - medical treatment (control of CHF,
promoting normal growth
prevent IE, prevent dev’t of p. HTN)
- Surgical repair between 6-12m
27.
28.
29.
30. Patent Ductus Arteriosus
• During fetal life, most of the pulmonary arterial blood is shunted
through the ductus arteriosus into the aorta .
• Functional closure of the ductus normally occurs soon after birth,
but if the ductus remains patent when pulmonary vascular
resistance falls, aortic blood is shunted into the pulmonary artery.
• The aortic end of the ductus is just distal to the origin of the left
subclavian artery, and the ductus enters the pulmonary artery at
subclavian artery, and the ductus enters the pulmonary artery at
its bifurcation.
• Female patients with PDA outnumber males 2 : 1. PDA is also
associated with maternal rubella infection during early
pregnancy.
• It is a common problem in premature infants, where it can cause
severe hemodynamic derangements and several major sequelae .
31. • When a term infant is found to have a PDA, the wall of the
ductus is deficient in both the mucoid endothelial layer
mucoid endothelial layer and
the muscular media.
muscular media.
• In a premature infant, the PDA usually has a normal
structure; patency is the result of hypoxia and immaturity.
Thus, a PDA persisting beyond the 1st few weeks of life in a
term infant rarely closes spontaneously or with
pharmacologic intervention, whereas if early pharmacologic
pharmacologic intervention, whereas if early pharmacologic
or surgical intervention is not required in a premature infant,
spontaneous closure occurs in most instances.
• A PDA is seen in 10% of patients with other congenital heart
lesions and often plays a critical role in providing pulmonary
blood flow when the right ventricular outflow tract is
the right ventricular outflow tract is
stenotic
stenotic or
or atretic
atretic or in providing systemic blood flow in the
presence of aortic
presence of aortic coarctation
coarctation or interruption
or interruption.
.
32. PATHOPHYSIOLOGY.
• As a result of the higher aortic pressure, blood shunts left to right
higher aortic pressure, blood shunts left to right
through the ductus
through the ductus, from the aorta to the pulmonary artery.
• The extent of the shunt depends on the size of the ductus and on
the ratio of pulmonary to systemic vascular resistance.
• In extreme cases, 70% of the left ventricular output may be
shunted through the ductus to the pulmonary circulation.
• If the PDA is small, pressure within the pulmonary artery, the right
• If the PDA is small, pressure within the pulmonary artery, the right
ventricle, and the right atrium is normal.
• If the PDA is large pulmonary artery pressure may be elevated to
systemic levels during both systole and diastole.
• Patients with a large PDA are at extremely high risk for the
development of pulmonary vascular disease if left unoperated.
• Pulse pressure is wide because of runoff of blood into the
pulmonary artery during diastole.
33. Acyanotic CHD…
1.3 Patent Ductus Arteriosus
Functional closure of the ductus normally occurs
soon after birth,
but if the ductus remains patent when pulmonary vascular
resistance falls, aortic blood is shunted into the pulmonary
artery.
Aortic end of the ductus distal to the
Aortic end of the ductus distal to the
origin of left subclavian artery and the other end
at bifurcation of pulmonary artery.
Male to female ratio 1:2
Pathology – Deficiency of:-
mucoid endothelial layer &
muscular media in term infant.
34. Acyanotic CHD…
Pathophysiology
Lt to Rt shunt - size
- ratio of pulm. to systemic resistance
Reversal of shunt
Clinical Manifestation
Asymptomatic in small ductus
Asymptomatic in small ductus
- Large
Wide pulse pressure
Bounding pulse
Continuous or machinery
machinery
M at 2nd Left ICS
35. Acyanotic CHD…
Diagnosis
- Clinical
- Chest X-ray
- ECG
- Echocardiography
Prognosis
- Small PDA - normal life
- Large PDA - CHF
Complications
Complications
- Infective Endocarditis/Endarteritis
- CHF
- Embolization (Pulmonary or systemic)
- Pulmonary HTN (Eisenmenger syndrome)
Treatment - Medical
- Surgical closure
40. Acyanotic CHD…
Clinical Manifestation
- Mild to moderate - asymptomatic
- Critical pulmonic stenosis
When severe pulmonic stenosis occurs in a neonate,
markedly decreased right ventricular compliance
markedly decreased right ventricular compliance
may lead to cyanosis due to right-to-left shunting through a
patent foramen ovale
- Systolic ejection murmur
- Heart failure in neonates & infants
- Rarely cyanosis
41. Acyanotic CHD…
Diagnosis
- Clinical
- CXR - Rt vent. hypertrophy
- reduced pulm. blood flow
- ECG
- Echocardiography
- Echocardiography
Prognosis - good in mild to moderate
Complications - CHF in severe Ps
- rarely IE
Treatment - vavular PS - ballon valvoplasty
- surgery
42.
43. Acyanotic CHD…
2.2 Aortic Stenosis
- Valvular - the commonest ; the leaflets
are thickened and the commissures are fused to
are thickened and the commissures are fused to
varying degrees.
- Supra valvular - the least common
- Subvalvular (subaortic)
44. Acyanotic CHD…
Clinical Manifestation
Mild stenosis
- Normal pulse & apical impulse
- Systolic ejection M (audible maximally at the
right upper sternal border and radiates to the neck and the
left midsternal border)
- Normal to enlarged heart size
- Normal to enlarged heart size
Critical stenosis
- Left ventricular failure
- pulm. edema, cardiomegaly
- Weak peripheral pulses
- Weak systolic M
- Paradoxical split 2nd heart sound
45. Acyanotic CHD…
Diagnosis
- Clinical
- CXR
- ECG
- Echocardiography
- Echocardiography
- Graded exercise testing
Prognosis is good for mild to moderate
Treatment
- Balloon valvoplasty
- Surgical
46.
47.
48.
49. Acyanotic CHD…
2.3 Coarctation of the Aorta
• Occur at any site from the arch of aorta
arch of aorta to iliac bifurcation
• 98% juxta ductal (just distal to the left
distal to the left subclavian
subclavian artery
artery)
-Less often, restriction occurs just proximal to the left
subclavian artery
Pathogenesis
• In utero arch hypoplasia
Rt heart output passes through the ductus
most commonly seen between the left subclavian artery and the
insertion of the ductus arteriosus (type A),
followed in frequency by those between the left subclavian and
left carotid arteries (type B).
50.
51. Acyanotic CHD…
Clinical Manifestation
Hypertension → mechanical obstruc on
→ renal(neurohumoral)
Differential cyanosis → pink upper extr.
→ cyanosed lower extr.
→ cyanosed lower extr.
Classic signs
- Disparity in pulse & BP in arms & legs
- Radio-femoral delay
- Systolic M at LMSB & inter-scapular area
52. Acyanotic CHD…
Diagnosis
- Clinical
- CXR - cardiomegaly & pulm. congestion
- Notching of ribs
( 3rd-8th ribs due to erosion by the large collateral arteries
large collateral arteries)
“3”sign
( 3 -8 ribs due to erosion by the large collateral arteries
large collateral arteries)
,the “3”sign
- ECG- RV(neonates & young infants),LV(older children)
hypertrophy
- Echocardiography
53. Prognosis – Untreated cases succumb by 20-40 years
Complications - CVA
- I/E
- Aneurysms(intracranial)
Treatment
Treatment
- Medical - IV PGE1 in neonatal age(to reopen
the ductus and re-establish adequate lower extremity
blood flow)
Patients with an interrupted aortic arch can be
supported with prostaglandin to keep the
ductus patent before surgical repair
- Surgery
54.
55.
56.
57. Acyanotic CHD…
3. Pulmonary Vascular Disease (Eismenger
syndrome)
- Occur in shunt lesions
VSD - mainly
ASD
ASD
PDA
- Reversal of shunt due to pulm. HTN
due to pulm. HTN
→ Cyanosis
59. II. Cyanotic Congenital Heart Disease
1. Cyanotic lesions with decreased pulmonary
blood flow
1.1 Tetralogy of Fallot
Consists: 1. Rt ventricular outflow obst.(PS)
Consists: 1. Rt ventricular outflow obst.(PS)
2. Ventricular septal defect(VSD)
3. Dextroposition
Dextroposition of the aorta with over ride of
the ventricular septum
ventricular septum
4. RV hypertrophy
60.
61.
62. Cyanotic CHD…
Pathophysiology
- Outflow obstruction
- Hypertrophy of sub pulmonic muscle
sub pulmonic muscle
- Normal or small pulmonary valve annulus
- Rarely pulmonary atresia
- Rarely pulmonary atresia
- VSD - Non-restrictive, located just below
aortic valve
-
- Aortic arch is right side
Aortic arch is right side in 20%
- Right ventricular output shunts to the
Right ventricular output shunts to the aorta
aorta
63. Cyanotic CHD…
Clinical Manifestation
- Rarely pink TOF - in the absence of obstruction
absence of obstruction
- Cyanosis
- Clubbing
- Squatting position in walking children
- Squatting position in walking children
- Paroxysmal hyper cyanotic attacks
occur during 1st 2 years
- Systolic ejection M
- Delayed growth & development
Delayed growth & development
- Single
Single 2nd heart sound
2nd heart sound
64. Cyanotic CHD…
Diagnosis
CXR - Narrow base & uplifted apex
- A
A boot or wooden shoe
boot or wooden shoe
(“coeur en sabot”)
- decreased pulm. vascularity
- Right side aortic arch in 20%
- Right side aortic arch in 20%
ECG
Echocardiography
Complication
- Cerebral thrombosis - in < 2 years
- Brain abscess
- Infective endocarditis
- Polycythemia
- CHF in pink TOF
65. COMPLICATIONS.
• Before correction, patients with the tetralogy of Fallot are
susceptible to several serious complications.
• Fortunately, most children undergo palliation or, more often,
complete repair in infancy, and these complications are rare.
• Cerebral thromboses, usually occurring in the cerebral veins or
dural sinuses and occasionally in the cerebral arteries, are
common in the presence of extreme polycythemia and
extreme polycythemia and
common in the presence of extreme polycythemia and
extreme polycythemia and
dehydration
dehydration.
• Thromboses occur most often in patients younger than 2 yr.
• These patients may have iron deficiency anemia, frequently
with hemoglobin and hematocrit levels in the normal range (but
too low for cyanotic heart disease).
• Therapy consists of adequate hydration and supportive measures.
• Phlebotomy and volume replacement with albumin or saline are
indicated in extremely polycythemic patients who are
symptomatic.
66. •
• Brain abscess
Brain abscess is less common than cerebral vascular
events and extremely rare when most patients are
repaired at young ages.
• Patients with a brain abscess are usually older than 2 yr.
• The onset of the illness is often insidious and consists of
low-grade fever or a gradual change in behavior, or both.
• Some patients have an acute onset of symptoms that
may develop after a recent history of headache, nausea,
recent history of headache, nausea,
and vomiting.
and vomiting.
may develop after a recent history of headache, nausea,
recent history of headache, nausea,
and vomiting.
and vomiting.
• Seizures may occur; localized neurologic signs depend on
the site and size of the abscess and the presence of
increased intracranial pressure.
• CT or MRI confirms the diagnosis.
• Antibiotic therapy may help keep the infection localized,
but surgical drainage of the abscess is usually necessary .
67. • Bacterial endocarditis may occur in the right
ventricular infundibulum or on the pulmonic, aortic, or,
rarely, tricuspid valves.
• Endocarditis may complicate palliative shunts or, in
patients with corrective surgery, any residual pulmonic
stenosis or VSD.
• Antibiotic prophylaxis is essential before and after dental
and certain surgical procedures associated with a high
incidence of bacteremia.
• Heart failure is not a usual feature in patients with the
• Heart failure is not a usual feature in patients with the
tetralogy of Fallot.
• It may occur in a young infant with “pink” or acyanotic
tetralogy of Fallot.
• As the degree of pulmonary obstruction worsens with
age, the symptoms of heart failure resolve and eventually
the patient experiences cyanosis, often by 6–12 mo of
age.
• These patients are at increased risk for hypercyanotic
spells at this time.
68. Cyanotic CHD…
Treatment
Severe outflow obstruction
- Medical Px - PGE1 infusion
- Prevent dehydration
- Partial exchange transfusion
- Partial exchange transfusion
- Oral propranolol for tet spells
- Surgery - Blalock Taussig
- Total correction
69.
70.
71.
72.
73. Cyanotic CHD…
1.2 Pulmonary Atresia
- With VSD - Extreme form of TOF
- Without VSD - No egress of blood from Rt vent.
- Shunt through foramen
foramen ovale
ovale to Lt atrium
to Lt atrium
Left ventricle
Left ventricle
systemic circulation
Aorta
pulmonic circulation
Hypoplastic right ventricle (PDA)
74.
75. Cyanotic CHD…
Clinical Manifestation
As the ductus arteriosus closes in the 1st
hours/days of life,infants with pulmonary atresia
and an intact ventricular septum become markedly
cyanotic.
Untreated, most patients die within the 1st
most patients die within the 1st wk
wk of
of
life.
life.
life.
life.
-severe cyanosis and respiratory distress.
-The 2nd heart sound is
2nd heart sound is single and loud.
-Often, no murmurs are audible,
but sometimes a systolic or continuous murmur
can be heard secondary to ductal blood flow
77. Cyanotic CHD…
1.3 Tricuspid atresia
- No outlet from Right atrium to Left vent.
- Systemic venous return
Rt atrium
Lt atrium
Left ventricule
systemic Pulmonic
(VSD, PDA)
81. Cyanotic CHD…
1.4 Ebstein Anomaly of the tricuspid valve
- Down ward displacement of the tricuspid valve
Down ward displacement of the tricuspid valve
- Right ventricle with two parts
- atrialized
- normal ventricular myocardium
- Abnormal tricuspid valve
- Huge Rt atrium
- Tricuspid regurgitation
- Compromised Rt ventricular function
Compromised Rt ventricular function
82.
83.
84. Cyanotic CHD…
Clinical Manifestations
- Easly fatiguability
- Cyanosis
- Dysrhythmia
- Rt to Lt shunt through formen ovale
- Holosystolic M at tricuspid area
- Heart failure
Diagnosis
Diagnosis
- CXR - box shaped heart
- ECG - Right BBB
- Superior axis deviation
Treatment
- PGE1
- Surgery
85.
86.
87. Cyanotic CHD…
2.Cyanotic CHD With increased pulmonary blood
flow
2.1 Transposition of GA
a. D -TGA (uncorrected)
- Systemic venous return to Rt atrium Normal
- Pulmonary venous return to Lt atrium
- Aorta arises from Right ventricle
- Pulm. artery arises from Lt vent. Pathology
88. Cyanotic CHD…
*Systemic & Pulmonary Circulations Consists of
two parallel circuits
*Survival is with associated
Survival is with associated –
patent foramen
patent foramen ovale
ovale
patent foramen
patent foramen ovale
ovale
VSD or
VSD or
PDA
PDA
Clinical Manifestations
- Tachypnea & cyanosis at birth
- Rarely congestive heart failure
89.
90.
91. Cyanotic CHD…
b. L. TGA (corrected transposition)
Systemic VR to normally positioned Rt atrium
Through bicuspid (Mitral) valve
Right sided left ventricle
Pulmo. artery pulm. venous return
Pulmo. artery pulm. venous return
Normally positioned Lt atrium
Through tricuspid valve
Left sided Right ventricle Aorta
92. Cyanotic CHD…
Discordant atrio-ventricular relation
the right atrium connected to the left ventricle
the left atrium to the right ventricle
-ventricular inversion
ventricular inversion
Transposition of great arteries
Transposition of great arteries
Transposition of great arteries
Transposition of great arteries
aorta arising from the right ventricle and
the pulmonary artery from the left
93. Clinical Manifestation
• Depends on associated malformation
-If pulmonary outflow is unobstructed, the clinical
signs are similar to those of an isolated VSD.
-If the TGA is associated with pulmonary stenosis
and a VSD, the clinical signs are similar to those of
and a VSD, the clinical signs are similar to those of
tetralogy of
tetralogy of Fallot
Fallot.
.
95. Cyanotic CHD…
2.2 Truncus arteriosus
- a single arterial trunk (truncus arteriosus) arises from
arises from
the heart
the heart and supplies the systemic, pulmonary, and
systemic, pulmonary, and
coronary circulations.
coronary circulations.
Clinical Manifestation
- Cyanosis
- CHF at 2-3rd m
- Systolic ejection m
Treatment - surgery
102. 2.5 Hypoplastic Left Heart Syndrome
- Under development of Lt Side of the heart
Lt Side of the heart
- Atretic aortic or mitral orifice
aortic or mitral orifice
- Non functional
Non functional Lt ventricle
- Hypoplasia of ascending aorta
Right ventricle supplies both pulm. & systemic
supplies both pulm. & systemic
circulation
circulation
circulation
circulation
