This document discusses heart failure, including its causes, symptoms, and effects on the left and right sides of the heart. Heart failure can result from systolic or diastolic dysfunction and weakens the heart's ability to pump blood efficiently. Common symptoms of left heart failure include dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Right heart failure usually results from left heart failure and causes systemic venous congestion. The document also discusses several types of congenital heart defects such as atrial septal defects, ventricular septal defects, and tetralogy of Fallot.
The document summarizes the development of the heart from its initial formation as a heart tube through the development of its chambers, valves, and conducting system. Key stages include the fusion of the bilateral heart tubes, formation of the atria, bulbus cordis and ventricles, separation of the aorta and pulmonary trunk, development of the valves and septa that divide the chambers, and incorporation of veins and changes to the exterior shape. Potential congenital anomalies are also briefly outlined.
This document discusses the pathophysiology of heart failure. It describes how heart failure can result from abnormalities in systolic or diastolic cardiac function. In heart failure with reduced ejection fraction (HFrEF), the left ventricle contracts poorly and cannot adequately pump blood. In heart failure with preserved ejection fraction (HFpEF), left ventricular filling is impaired. Both types result in inadequate blood flow and organ congestion. The document discusses neurohormonal changes, organ dysfunction, and other compensatory mechanisms involved in heart failure.
Cardiac action potentials arise from the coordinated movement of ions through membrane channels in cardiac cells. The cardiac action potential has 5 phases: rapid upstroke (phase 0) due to sodium influx, early rapid repolarization (phase 1) mediated by potassium currents, plateau phase (phase 2) maintained by calcium and potassium currents, final rapid repolarization (phase 3) due to potassium currents, and resting phase (phase 4) where the cell prepares for the next action potential. Precisely regulated ion channel function underlies the generation and propagation of action potentials and ensures normal cardiac rhythm.
The document discusses the enteric nervous system and gastrointestinal motility. It notes that the myenteric plexus controls gastrointestinal motility through peristalsis. Peristalsis is present even without input from the extrinsic nervous system. The extrinsic nervous system can only modify, not initiate, activity of the enteric nervous system.
Be the first to comment
Anatomy And Physiology of Human Heart
1. ANATOMY OF THE HEART By: Dr Mohammed Faez
2. The Heart The heart is a chambered muscular organ that pumps blood received from the veins into the arteries, thereby maintaining the flow of blood through the entire circulatory system.
3. The Heart • The heart is surrounded by membrane called Pericardium.
4. The Pericardium • The pericardium is a fibroserous sac that encloses the heart and the roots of the great vessels. • The pericardium lies within the middle mediastinum.
5. The Pericardium
6. The Pericardium • Its function is to restrict excessive movements of the heart as a whole and to serve as a lubricated container in which the different parts of the heart can contract.
Hemoglobin C and hemoglobin SC are abnormal hemoglobins caused by point mutations in the HBB gene. Hemoglobin C causes mild sickling of red blood cells, while hemoglobin SC is a compound heterozygote with both hemoglobin C and S mutations, resulting in less crystallization and occlusion than each individually. Symptoms of hemoglobin C disease include anemia, enlarged spleen, and fatigue, while hemoglobin SC causes similar but milder symptoms like anemia and pain crises. Both conditions are inherited and often diagnosed via newborn screening tests.
Cardiac failure, also known as heart failure, is a disorder where the heart loses its ability to pump blood efficiently. It occurs when the heart's output is inadequate to supply oxygen to the body. There are two main types: diastolic dysfunction, where the heart cannot fill with enough blood, and systolic dysfunction, where it cannot pump with enough force. Treatment depends on the severity and includes drugs like ACE inhibitors, ARBs, diuretics, vasodilators, and inotropic agents.
The document summarizes cardiac embryology and fetal circulation. It discusses how the heart develops from mesoderm and the formation of the heart tube. It describes how the heart tube loops to form the primitive chambers and how the chambers further develop into the four-chambered heart. It also explains the changes in circulation from fetal to post-natal, such as how the ductus arteriosus and foramen ovale normally close after birth.
The document summarizes the development of the heart from its initial formation as a heart tube through the development of its chambers, valves, and conducting system. Key stages include the fusion of the bilateral heart tubes, formation of the atria, bulbus cordis and ventricles, separation of the aorta and pulmonary trunk, development of the valves and septa that divide the chambers, and incorporation of veins and changes to the exterior shape. Potential congenital anomalies are also briefly outlined.
This document discusses the pathophysiology of heart failure. It describes how heart failure can result from abnormalities in systolic or diastolic cardiac function. In heart failure with reduced ejection fraction (HFrEF), the left ventricle contracts poorly and cannot adequately pump blood. In heart failure with preserved ejection fraction (HFpEF), left ventricular filling is impaired. Both types result in inadequate blood flow and organ congestion. The document discusses neurohormonal changes, organ dysfunction, and other compensatory mechanisms involved in heart failure.
Cardiac action potentials arise from the coordinated movement of ions through membrane channels in cardiac cells. The cardiac action potential has 5 phases: rapid upstroke (phase 0) due to sodium influx, early rapid repolarization (phase 1) mediated by potassium currents, plateau phase (phase 2) maintained by calcium and potassium currents, final rapid repolarization (phase 3) due to potassium currents, and resting phase (phase 4) where the cell prepares for the next action potential. Precisely regulated ion channel function underlies the generation and propagation of action potentials and ensures normal cardiac rhythm.
The document discusses the enteric nervous system and gastrointestinal motility. It notes that the myenteric plexus controls gastrointestinal motility through peristalsis. Peristalsis is present even without input from the extrinsic nervous system. The extrinsic nervous system can only modify, not initiate, activity of the enteric nervous system.
Be the first to comment
Anatomy And Physiology of Human Heart
1. ANATOMY OF THE HEART By: Dr Mohammed Faez
2. The Heart The heart is a chambered muscular organ that pumps blood received from the veins into the arteries, thereby maintaining the flow of blood through the entire circulatory system.
3. The Heart • The heart is surrounded by membrane called Pericardium.
4. The Pericardium • The pericardium is a fibroserous sac that encloses the heart and the roots of the great vessels. • The pericardium lies within the middle mediastinum.
5. The Pericardium
6. The Pericardium • Its function is to restrict excessive movements of the heart as a whole and to serve as a lubricated container in which the different parts of the heart can contract.
Hemoglobin C and hemoglobin SC are abnormal hemoglobins caused by point mutations in the HBB gene. Hemoglobin C causes mild sickling of red blood cells, while hemoglobin SC is a compound heterozygote with both hemoglobin C and S mutations, resulting in less crystallization and occlusion than each individually. Symptoms of hemoglobin C disease include anemia, enlarged spleen, and fatigue, while hemoglobin SC causes similar but milder symptoms like anemia and pain crises. Both conditions are inherited and often diagnosed via newborn screening tests.
Cardiac failure, also known as heart failure, is a disorder where the heart loses its ability to pump blood efficiently. It occurs when the heart's output is inadequate to supply oxygen to the body. There are two main types: diastolic dysfunction, where the heart cannot fill with enough blood, and systolic dysfunction, where it cannot pump with enough force. Treatment depends on the severity and includes drugs like ACE inhibitors, ARBs, diuretics, vasodilators, and inotropic agents.
The document summarizes cardiac embryology and fetal circulation. It discusses how the heart develops from mesoderm and the formation of the heart tube. It describes how the heart tube loops to form the primitive chambers and how the chambers further develop into the four-chambered heart. It also explains the changes in circulation from fetal to post-natal, such as how the ductus arteriosus and foramen ovale normally close after birth.
Arrhythmia - Pathophysiology and Treatment (Pharmacotherapy) Abdullah Bilal
Cardiac arrhythmias occur when the heart beats with an irregular rhythm. There are two main types - bradycardia, which is a slow heart rate below 60 bpm, and tachycardia, which is a fast heart rate over 100 bpm. Arrhythmias can be caused by coronary artery disease, electrolyte imbalances, heart muscle changes after injury or surgery. Symptoms include palpitations, dizziness, chest pain, fainting. Treatment depends on the type of arrhythmia but may include sodium channel blockers, beta blockers, drugs that prolong the action potential, calcium channel blockers, or other drugs like adenosine or magnesium.
The Renin-Angiotensin Aldosterone System (RAAS) is the most potent vasoconstrictor system in the body. It was discovered in the 1930s-1940s through experiments involving renal artery clamping and purification of renin. The key components of the conventional circulating RAAS include renin from the kidneys, angiotensinogen from the liver, angiotensin I and II produced via enzymatic cascades, and aldosterone from the adrenal cortex. Angiotensin II is the primary effector peptide and causes vasoconstriction, hypertension, atherosclerosis, and other effects by activating AT1 receptors. Local tissue RAAS also exist and influence organ function.
The document provides an overview of the anatomy and physiology of the cardiovascular system. It describes the location and layers of the heart, the four chambers of the heart, the heart valves, the conduction system, the cardiac cycle, and circulation through the systemic and pulmonary circuits. It also discusses monitoring of the heart through tools like electrocardiograms, imaging like MRI and x-rays, stress testing, and pacemakers.
This document provides an overview of heart embryology. It describes how the heart develops from two endothelial heart tubes that fuse to form sections including the atria, ventricles, and bulbus cordis. The document outlines the formation of the interatrial septum from the septum primum and secundum, as well as the absorption of the sinus venosus into the right atrium. It also discusses the development of the interventricular septum from the bulbar ridges and proliferation of tissue from the atrioventricular cushions. Common congenital heart anomalies are mentioned including defects of the atrial and ventricular septa.
The document provides an overview of renal physiology and the structure and function of the kidney and nephron. It describes the kidney as a bean-shaped organ that filters blood to produce urine and removes wastes. The nephron is the functional unit of the kidney, consisting of a glomerulus and tubules (proximal convoluted tubule, loop of Henle, distal convoluted tubule and collecting duct) that work together to regulate water and electrolyte levels via selective reabsorption and secretion processes along different portions of the tubule. The loop of Henle plays a key role in concentrating urine by establishing an osmotic gradient in the kidney medulla.
The cardiac structure includes the heart walls and chambers. Cardiac hypertrophy is an increase in heart size and weight due to mechanical overload. It can be concentric from pressure overload or eccentric from volume overload. Heart failure occurs when the heart cannot pump adequately to meet metabolic demands. It can be due to systolic or diastolic dysfunction. Right heart failure causes venous congestion while left heart failure causes pulmonary congestion.
This document discusses heart failure, including its definition, causes, types, and compensatory mechanisms. Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by intrinsic pump failure, an increased workload on the heart, or impaired filling of the cardiac chambers. The types of heart failure include acute or chronic, right-sided or left-sided, and forward or backward failure. When the heart begins to fail, compensatory mechanisms such as cardiac hypertrophy, dilation, and increased heart rate attempt to maintain adequate blood circulation.
The heart has two pumps - the right heart pumps deoxygenated blood to the lungs and the left heart pumps oxygenated blood from the lungs to the rest of the body. Blood flows through the heart via the pulmonary and systemic circuits. The heart has four chambers separated by septa - the right and left atria receive blood returning to the heart while the right and left ventricles pump blood out of the heart. Heart valves prevent backflow of blood - atrioventricular valves between atria and ventricles and semilunar valves at the exits of the ventricles. Cardiac muscle has an extended action potential and refractory period compared to skeletal muscle to coordinate the pumping of the heart.
The document discusses acyanotic heart disease, which refers to congenital heart defects present at birth that do not cause cyanosis. Common types include atrial septal defect, ventricular septal defect, and patent ductus arteriosus. These defects cause diminished pulmonary blood flow due to left-to-right shunting. Symptoms may not be present initially but can develop over months or years and include dyspnea, fatigue, and heart failure. Diagnosis involves physical exam, chest x-ray, ECG, and echocardiogram. Treatment depends on the severity but may involve surgery to correct the structural abnormality, with earlier intervention reducing long-term risks from conditions like pulmonary hypertension.
The white matter of the cerebrum contains three main types of nerve fibers: commissural fibers, association fibers, and projection fibers. Commissural fibers such as the corpus callosum connect the two cerebral hemispheres. Association fibers like the superior longitudinal bundle connect different regions within the same hemisphere. Projection fibers including those in the internal capsule connect the cerebral cortex to lower brain centers. The internal capsule specifically contains fibers that project to and from the cortex and plays an important role in motor function. Damage to the internal capsule can thus cause contralateral hemiplegia.
CONGESTIVE HEART FAILURE - DRUGS WITHOUT POSITIVE IONOTROPYBobby Prashanth
Congestive heart failure is a condition where the heart cannot supply enough blood to meet the body's needs. It is characterized by reduced cardiac output and increased peripheral resistance, progressing to edema. Treatment goals include alleviating symptoms, preventing remodeling and sudden death. Non-drug therapies include rest, weight loss, and a low sodium diet. Drug therapies target the renin-angiotensin system with ACE inhibitors and ARBs, reduce preload and edema with diuretics, and improve function with beta-blockers. While diuretics do not directly affect contractility, they reduce preload and edema. ACE inhibitors, ARBs, and vasodilators also improve pumping efficiency through various mechanisms.
This document discusses congenital heart defects, specifically patent ductus arteriosus (PDA). It provides that PDA is one of the most common congenital heart defects, occurring in 1 in 2,500-5,000 infants and affecting females twice as often as males. PDA is caused by factors like prematurity, prostaglandin E, and other congenital defects. Clinical manifestations of PDA include respiratory distress, heart failure, low immune system, and frequent respiratory infections. The document lists nursing diagnoses related to PDA such as decreased cardiac output, impaired gas exchange, and risk for infection.
This document discusses inotropic agents, which are drugs that affect the strength of contraction of the heart muscle. It describes positive inotropes that increase contraction and negative inotropes that decrease contraction. The choice of inotrope depends on its pharmacological effects and the specific cardiovascular condition. Positive inotropes discussed include calcium, calcium sensitizers like levosimendan, catecholamines, cardiac glycosides, and others. Negative inotropes include beta blockers, calcium channel blockers, and antiarrhythmics. The mechanisms and effects of various catecholamines like dopamine, dobutamine, epinephrine, and dopexamine are also outlined.
The superior vena cava receives deoxygenated blood from the upper body and delivers it to the right atrium. It is formed by the merging of the brachiocephalic veins and descends through the thoracic region into the right atrium. Its tributaries include the brachiocephalic veins, azygos vein, and intercostal veins. Obstruction of the superior vena cava can result in the development of collateral pathways through the azygos vein or between tributaries of the superior and inferior vena cavae.
The document discusses coronary circulation and coronary artery disease. It begins by describing the anatomy of the coronary blood vessels and the blood supply to the heart. It then discusses characteristics of coronary blood flow such as autoregulation and factors that regulate it like metabolites and nervous control. Measurement techniques for coronary blood flow are also outlined. The document concludes by describing coronary artery disease conditions like angina and myocardial infarction as well as treatments.
The document provides an overview of kidney anatomy and physiology. It discusses:
1. The basic functions and structures of the kidney, including filtration, homeostasis, and hormone production.
2. The anatomy of the kidney, including locations of the cortex, medulla, renal pyramids and other structures.
3. The nephron as the functional unit of the kidney, describing its role in filtration, reabsorption, secretion and other processes.
4. Key physiological concepts like the countercurrent multiplier mechanism and regulation of electrolytes and acid-base balance.
The brain is the most vital organ that requires constant blood supply to function. It has high metabolic needs but maintains constant circulation irrespective of activity. Blood flows to the brain through arteries and drains through veins and sinuses. The blood brain barrier selectively regulates substance permeability and protects the brain microenvironment. Cerebral blood flow is tightly regulated by factors like blood pressure, carbon dioxide levels, oxygen levels and intracranial pressure to maintain homeostasis.
The document discusses the pancreas and insulin. It notes that the endocrine function of the pancreas is performed by clusters of cells called islets of Langerhans, which contain four main cell types that secrete different hormones. It focuses on insulin, describing its source in beta cells, chemistry, levels in plasma, synthesis, metabolism, actions in regulating carbohydrate, protein and fat metabolism, and how its secretion is regulated primarily by blood glucose levels.
Congenital heart disease refers to abnormalities of the heart present from birth that arise during embryonic development. The abnormalities fall into two categories: shunts, which are abnormal connections that allow blood to flow between chambers in the wrong direction, and obstructions, which are narrowings that block blood flow. Shunts can cause cyanosis if deoxygenated blood enters the systemic circulation from the right side of the heart. Over time, increased blood flow or pressure from shunts can lead to pulmonary hypertension and structural changes that are irreversible. Common types of congenital heart defects include atrial and ventricular septal defects, patent ductus arteriosus, tetralogy of Fallot, and transposition of the great
Arrhythmia - Pathophysiology and Treatment (Pharmacotherapy) Abdullah Bilal
Cardiac arrhythmias occur when the heart beats with an irregular rhythm. There are two main types - bradycardia, which is a slow heart rate below 60 bpm, and tachycardia, which is a fast heart rate over 100 bpm. Arrhythmias can be caused by coronary artery disease, electrolyte imbalances, heart muscle changes after injury or surgery. Symptoms include palpitations, dizziness, chest pain, fainting. Treatment depends on the type of arrhythmia but may include sodium channel blockers, beta blockers, drugs that prolong the action potential, calcium channel blockers, or other drugs like adenosine or magnesium.
The Renin-Angiotensin Aldosterone System (RAAS) is the most potent vasoconstrictor system in the body. It was discovered in the 1930s-1940s through experiments involving renal artery clamping and purification of renin. The key components of the conventional circulating RAAS include renin from the kidneys, angiotensinogen from the liver, angiotensin I and II produced via enzymatic cascades, and aldosterone from the adrenal cortex. Angiotensin II is the primary effector peptide and causes vasoconstriction, hypertension, atherosclerosis, and other effects by activating AT1 receptors. Local tissue RAAS also exist and influence organ function.
The document provides an overview of the anatomy and physiology of the cardiovascular system. It describes the location and layers of the heart, the four chambers of the heart, the heart valves, the conduction system, the cardiac cycle, and circulation through the systemic and pulmonary circuits. It also discusses monitoring of the heart through tools like electrocardiograms, imaging like MRI and x-rays, stress testing, and pacemakers.
This document provides an overview of heart embryology. It describes how the heart develops from two endothelial heart tubes that fuse to form sections including the atria, ventricles, and bulbus cordis. The document outlines the formation of the interatrial septum from the septum primum and secundum, as well as the absorption of the sinus venosus into the right atrium. It also discusses the development of the interventricular septum from the bulbar ridges and proliferation of tissue from the atrioventricular cushions. Common congenital heart anomalies are mentioned including defects of the atrial and ventricular septa.
The document provides an overview of renal physiology and the structure and function of the kidney and nephron. It describes the kidney as a bean-shaped organ that filters blood to produce urine and removes wastes. The nephron is the functional unit of the kidney, consisting of a glomerulus and tubules (proximal convoluted tubule, loop of Henle, distal convoluted tubule and collecting duct) that work together to regulate water and electrolyte levels via selective reabsorption and secretion processes along different portions of the tubule. The loop of Henle plays a key role in concentrating urine by establishing an osmotic gradient in the kidney medulla.
The cardiac structure includes the heart walls and chambers. Cardiac hypertrophy is an increase in heart size and weight due to mechanical overload. It can be concentric from pressure overload or eccentric from volume overload. Heart failure occurs when the heart cannot pump adequately to meet metabolic demands. It can be due to systolic or diastolic dysfunction. Right heart failure causes venous congestion while left heart failure causes pulmonary congestion.
This document discusses heart failure, including its definition, causes, types, and compensatory mechanisms. Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by intrinsic pump failure, an increased workload on the heart, or impaired filling of the cardiac chambers. The types of heart failure include acute or chronic, right-sided or left-sided, and forward or backward failure. When the heart begins to fail, compensatory mechanisms such as cardiac hypertrophy, dilation, and increased heart rate attempt to maintain adequate blood circulation.
The heart has two pumps - the right heart pumps deoxygenated blood to the lungs and the left heart pumps oxygenated blood from the lungs to the rest of the body. Blood flows through the heart via the pulmonary and systemic circuits. The heart has four chambers separated by septa - the right and left atria receive blood returning to the heart while the right and left ventricles pump blood out of the heart. Heart valves prevent backflow of blood - atrioventricular valves between atria and ventricles and semilunar valves at the exits of the ventricles. Cardiac muscle has an extended action potential and refractory period compared to skeletal muscle to coordinate the pumping of the heart.
The document discusses acyanotic heart disease, which refers to congenital heart defects present at birth that do not cause cyanosis. Common types include atrial septal defect, ventricular septal defect, and patent ductus arteriosus. These defects cause diminished pulmonary blood flow due to left-to-right shunting. Symptoms may not be present initially but can develop over months or years and include dyspnea, fatigue, and heart failure. Diagnosis involves physical exam, chest x-ray, ECG, and echocardiogram. Treatment depends on the severity but may involve surgery to correct the structural abnormality, with earlier intervention reducing long-term risks from conditions like pulmonary hypertension.
The white matter of the cerebrum contains three main types of nerve fibers: commissural fibers, association fibers, and projection fibers. Commissural fibers such as the corpus callosum connect the two cerebral hemispheres. Association fibers like the superior longitudinal bundle connect different regions within the same hemisphere. Projection fibers including those in the internal capsule connect the cerebral cortex to lower brain centers. The internal capsule specifically contains fibers that project to and from the cortex and plays an important role in motor function. Damage to the internal capsule can thus cause contralateral hemiplegia.
CONGESTIVE HEART FAILURE - DRUGS WITHOUT POSITIVE IONOTROPYBobby Prashanth
Congestive heart failure is a condition where the heart cannot supply enough blood to meet the body's needs. It is characterized by reduced cardiac output and increased peripheral resistance, progressing to edema. Treatment goals include alleviating symptoms, preventing remodeling and sudden death. Non-drug therapies include rest, weight loss, and a low sodium diet. Drug therapies target the renin-angiotensin system with ACE inhibitors and ARBs, reduce preload and edema with diuretics, and improve function with beta-blockers. While diuretics do not directly affect contractility, they reduce preload and edema. ACE inhibitors, ARBs, and vasodilators also improve pumping efficiency through various mechanisms.
This document discusses congenital heart defects, specifically patent ductus arteriosus (PDA). It provides that PDA is one of the most common congenital heart defects, occurring in 1 in 2,500-5,000 infants and affecting females twice as often as males. PDA is caused by factors like prematurity, prostaglandin E, and other congenital defects. Clinical manifestations of PDA include respiratory distress, heart failure, low immune system, and frequent respiratory infections. The document lists nursing diagnoses related to PDA such as decreased cardiac output, impaired gas exchange, and risk for infection.
This document discusses inotropic agents, which are drugs that affect the strength of contraction of the heart muscle. It describes positive inotropes that increase contraction and negative inotropes that decrease contraction. The choice of inotrope depends on its pharmacological effects and the specific cardiovascular condition. Positive inotropes discussed include calcium, calcium sensitizers like levosimendan, catecholamines, cardiac glycosides, and others. Negative inotropes include beta blockers, calcium channel blockers, and antiarrhythmics. The mechanisms and effects of various catecholamines like dopamine, dobutamine, epinephrine, and dopexamine are also outlined.
The superior vena cava receives deoxygenated blood from the upper body and delivers it to the right atrium. It is formed by the merging of the brachiocephalic veins and descends through the thoracic region into the right atrium. Its tributaries include the brachiocephalic veins, azygos vein, and intercostal veins. Obstruction of the superior vena cava can result in the development of collateral pathways through the azygos vein or between tributaries of the superior and inferior vena cavae.
The document discusses coronary circulation and coronary artery disease. It begins by describing the anatomy of the coronary blood vessels and the blood supply to the heart. It then discusses characteristics of coronary blood flow such as autoregulation and factors that regulate it like metabolites and nervous control. Measurement techniques for coronary blood flow are also outlined. The document concludes by describing coronary artery disease conditions like angina and myocardial infarction as well as treatments.
The document provides an overview of kidney anatomy and physiology. It discusses:
1. The basic functions and structures of the kidney, including filtration, homeostasis, and hormone production.
2. The anatomy of the kidney, including locations of the cortex, medulla, renal pyramids and other structures.
3. The nephron as the functional unit of the kidney, describing its role in filtration, reabsorption, secretion and other processes.
4. Key physiological concepts like the countercurrent multiplier mechanism and regulation of electrolytes and acid-base balance.
The brain is the most vital organ that requires constant blood supply to function. It has high metabolic needs but maintains constant circulation irrespective of activity. Blood flows to the brain through arteries and drains through veins and sinuses. The blood brain barrier selectively regulates substance permeability and protects the brain microenvironment. Cerebral blood flow is tightly regulated by factors like blood pressure, carbon dioxide levels, oxygen levels and intracranial pressure to maintain homeostasis.
The document discusses the pancreas and insulin. It notes that the endocrine function of the pancreas is performed by clusters of cells called islets of Langerhans, which contain four main cell types that secrete different hormones. It focuses on insulin, describing its source in beta cells, chemistry, levels in plasma, synthesis, metabolism, actions in regulating carbohydrate, protein and fat metabolism, and how its secretion is regulated primarily by blood glucose levels.
Congenital heart disease refers to abnormalities of the heart present from birth that arise during embryonic development. The abnormalities fall into two categories: shunts, which are abnormal connections that allow blood to flow between chambers in the wrong direction, and obstructions, which are narrowings that block blood flow. Shunts can cause cyanosis if deoxygenated blood enters the systemic circulation from the right side of the heart. Over time, increased blood flow or pressure from shunts can lead to pulmonary hypertension and structural changes that are irreversible. Common types of congenital heart defects include atrial and ventricular septal defects, patent ductus arteriosus, tetralogy of Fallot, and transposition of the great
The document discusses the anatomy and function of the heart. It describes the four chambers of the heart, including the left and right ventricles that pump blood to the lungs and body. It also discusses the causes and features of heart failure, which can occur when the heart is unable to pump sufficiently due to conditions that weaken it over time. Common causes include hypertension, heart attacks, and cardiac diseases. Features involve congestion in the lungs and other organs from blood backing up.
This document discusses aortic valve disorders such as stenosis and regurgitation. It begins by reviewing the anatomy of the aortic valve and the cardiac cycle. Aortic stenosis is defined as a narrowing of the aortic valve that obstructs blood flow from the left ventricle. Causes include bicuspid valves and age-related calcification. Pathogenesis involves hypertrophy of the left ventricle and reduced coronary blood flow. Symptoms are related to reduced cardiac output. Aortic regurgitation occurs when the aortic valve is incompetent and allows backflow during diastole. Causes may be congenital or from conditions like rheumatic heart disease. Chronic regurgitation can lead to left ventricular
This document discusses cardiac disorders related to heart sounds and cardiac output. It begins by explaining the four heart sounds (S1-S4) and what events cause each one. It then discusses cardiac output and how it is calculated. Various cardiac disorders are described like murmurs, valvular issues, and septal defects. Valvular stenosis, prolapse, and regurgitation are explained in detail. The document compares normal heart sounds to sounds in different disorders. In summary, it provides an overview of heart sounds, cardiac output, and how various heart conditions affect these systems and can be detected by listening to heart sounds.
There are two main types of congenital heart failures in children - cyanotic and non-cyanotic. Some common types include ventricular septal defects, atrial septal defects, patent ductus arteriosus, tetralogy of Fallot, transposition of the great arteries, and hypoplastic left heart syndrome. Many of these defects can be repaired through surgical procedures like closing holes or reconstructing heart structures. Without treatment, congenital heart failures can lead to complications like heart failure, pulmonary hypertension, or developmental delays.
This document discusses different types of valvular heart disease. It begins by explaining that valvular heart disease is characterized by damage or defects to the heart's valves, which normally ensure proper blood flow. Stenotic valves become narrowed and prevent full opening, while incompetent valves do not close completely and allow blood to leak back. Over time, the heart compensates by enlarging and thickening, losing efficiency.
The document then examines specific valve diseases in more detail, outlining their causes, effects on heart function, symptoms, diagnostic tests, and treatment options. Diseases covered include mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, tricuspid regurgitation
This document provides an overview of heart failure, including its pathophysiology, types, clinical presentation, investigations, and management. Heart failure occurs when the heart cannot pump enough blood to meet the body's needs and can develop due to conditions that weaken the heart such as heart attacks or high blood pressure. Symptoms depend on whether the left side, right side, or both sides of the heart are affected. Management involves treating the underlying cause, reducing symptoms through medications, lifestyle changes, and addressing complications.
Aortic stenosis is a narrowing of the aortic valve caused by calcification or damage to the valve leaflets. It commonly occurs from age-related calcification after age 70 or in younger patients with congenital bicuspid aortic valves. Symptoms include chest pain, shortness of breath, and fainting from reduced blood flow. As the valve narrows further, the left ventricle must work harder to pump blood through, causing hypertrophy that can lead to heart failure if untreated. Surgical valve replacement is the only effective treatment for severe, symptomatic aortic stenosis.
The document discusses various types of heart valve disorders including stenosis, regurgitation, and prolapse. It describes the causes, effects, symptoms, and treatments for different valve conditions affecting the mitral, aortic, tricuspid, and pulmonary valves. Surgical interventions for valve disorders include valvuloplasty procedures to repair valves as well as valve replacement using mechanical or biological prosthetics.
This document discusses congestive heart failure (CHF), including its causes, pathophysiology, and effects on the left and right sides of the heart. CHF is caused by conditions that weaken the heart muscle, such as heart attacks, high blood pressure, and heart valve diseases. When the left ventricle fails to pump properly, blood backs up in the lungs leading to pulmonary edema and congestion. When the right ventricle fails, blood backs up in the liver, abdomen, and legs causing swelling. Common symptoms include shortness of breath, fatigue, swelling, and coughing. Treatment involves medications, lifestyle changes, and sometimes surgery.
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
This document discusses various acyanotic congenital heart diseases. It begins by classifying congenital heart disease into cyanotic and acyanotic categories. It then further divides acyanotic congenital heart disease into those with a left-to-right shunt or increased pulmonary blood flow, such as atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA), and those without a shunt such as coarctation of the aorta. The document then goes on to describe the pathophysiology, clinical features, investigations and management of ASD, VSD, and PDA in more detail. It also briefly discusses Eisenmenger syndrome.
Congenital heart defects are abnormalities in the structure of the heart that are present at birth. They affect approximately 9 in 1000 births and can cause obstructed or abnormal blood flow. Common types include septal defects, where the walls separating the left and right sides of the heart have holes, and obstructive defects, where arteries or valves are blocked. Congenital heart defects range from mild to complex and may require medication, surgery, or both for treatment depending on severity. Their causes are usually a combination of genetic and environmental factors.
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.
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.
1. Heart valve disease occurs when the heart valves do not function properly, either becoming narrowed (stenosis) or allowing backward leakage (regurgitation).
2. The four heart valves (mitral, aortic, tricuspid, pulmonary) ensure one-way blood flow through the heart and prevent backflow.
3. Common causes of valve disease include rheumatic fever, congenital defects, infections, and aging. Symptoms depend on the severity and valve affected but can include fatigue, shortness of breath, chest pain, and heart failure.
Congenital heart disease (CHD) refers to structural heart defects present at birth. Diagnosis involves history, physical exam, chest X-ray, ECG, and echocardiogram. Most CHDs can be corrected with surgery if done in a timely manner. Echocardiography can identify and determine severity of specific lesions. Pediatricians must also identify any associated conditions that could impact outcomes.
This document discusses several non-neoplastic and neoplastic disorders of white blood cells. It describes leukopenia, neutropenia, agranulocytosis, and reactive leukocytosis as non-neoplastic disorders. It then summarizes several types of lymphoid neoplasms including acute lymphoblastic leukemia/lymphoma, chronic lymphocytic leukemia/small lymphocytic lymphoma, and follicular lymphoma. Key features such as pathogenesis, clinical presentation, and distinguishing characteristics are highlighted for each condition.
The document discusses several types of blood disorders that can cause anemia or other issues. It describes red blood cell disorders like iron deficiency anemia, thalassemia, sickle cell anemia and glucose-6-phosphate dehydrogenase deficiency that can lead to hemolytic anemia. It also discusses anemia of chronic disease/inflammation and megaloblastic anemias caused by vitamin B12 or folate deficiencies that result in diminished red blood cell production. Malaria is summarized as a parasitic infection that can cause hemolytic anemia.
This document summarizes various disorders of blood vessel hyperreactivity and tumors. It describes Raynaud phenomenon which results in vasoconstriction of arteries and arterioles. It also discusses myocardial vessel vasospasm which can lead to Prinzmetal angina or myocardial infarction. Varicose veins, thrombophlebitis, and superior/inferior vena cava syndromes are also outlined. Finally, it provides details on various benign and malignant vascular tumors including hemangiomas, lymphangiomas, and Kaposi sarcoma.
This document summarizes the structure and function of blood vessels. It discusses how blood vessels are composed of smooth muscle cells and extracellular matrix lined with endothelial cells. It describes the differences between arteries, veins, capillaries and how their structures relate to their functions. It also discusses vascular diseases like atherosclerosis, aneurysms, hypertension and vasculitis at a high level.
Cardiomyopathies are diseases of the heart muscle that can be primary or secondary. The main types are dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. Dilated cardiomyopathy is characterized by cardiac dilation and contractile dysfunction. Causes include genetic factors, myocarditis, toxins like alcohol, and peripartum cardiomyopathy. Hypertrophic cardiomyopathy causes thickening of the heart walls and impaired diastolic filling. It is usually genetic and causes sarcomere protein mutations. Restrictive cardiomyopathy decreases ventricular compliance and impairs filling. Causes include amyloidosis, endomyocardial fibrosis, and Loeffler endomyocarditis. Myocarditis involves infectious or inflammatory processes targeting
This document discusses various types of arrhythmias and heart conditions including their causes, characteristics, and clinical presentations. It covers topics such as:
- Arrhythmias which can be initiated anywhere in the heart's conduction system and may present as tachycardia, bradycardia, or other irregular rhythms.
- Hypertension can lead to hypertensive heart disease over time due to increased pressure on the heart.
- Valvular heart diseases like rheumatic heart disease and degenerative valve diseases can cause stenosis or insufficiency of the heart valves.
- Infective endocarditis is a bacterial infection of the heart valves that forms vegetations and can cause embol
Ischemic heart disease (IHD) is caused by reduced blood flow to the heart muscle and usually results from plaque buildup in the coronary arteries. This leads to not enough oxygen reaching the heart muscle. The main manifestations of IHD include angina pectoris (chest pain), myocardial infarction (heart attack), and sudden cardiac death. A heart attack occurs when a plaque ruptures and causes a blood clot that completely blocks blood flow, causing heart cell death. Reperfusion through procedures like angioplasty can limit damage but also cause additional injury. Complications from a heart attack include heart failure, arrhythmias, and cardiac rupture.
This document discusses heart failure, including its causes, symptoms, and effects on the left and right sides of the heart. Heart failure can result from systolic or diastolic dysfunction and weakens the heart's ability to pump blood efficiently. Common symptoms of left heart failure include dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Right heart failure usually results from left heart failure and causes systemic venous congestion. The document also reviews several types of congenital heart defects such as atrial septal defects, ventricular septal defects, and tetralogy of Fallot.
The document discusses the endocrine functions of the thyroid gland, parathyroid glands, and their roles in calcium and bone homeostasis. Specifically, it describes how thyroid hormones are synthesized and regulated, their effects on growth, metabolism and other body systems. It also explains how parathyroid hormone regulates blood calcium levels by acting on bone, kidneys and intestines. The importance of maintaining normal calcium levels and balancing bone formation and resorption is emphasized.
This document discusses various drugs used to treat bacterial, viral, fungal and parasitic infections. It describes the mechanisms of antibacterial drugs including inhibiting cell wall synthesis, protein synthesis and DNA/RNA function. Specific drug classes are outlined for each mechanism such as penicillins, cephalosporins and aminoglycosides. The document also discusses antiviral drugs used to treat HIV including different classes that act on reverse transcriptase and protease. Finally, it briefly outlines antifungal, antiparasitic and anthelmintic drugs used to treat various infections.
This document discusses several classes of respiratory drugs including antitussives, decongestants, antihistamines, mucolytics and expectorants, bronchodilators, and anti-inflammatory drugs. It describes the mechanisms of action, indications for use, routes of administration, and potential adverse effects of drugs from each class. The classes covered include cough suppressants, nasal decongestants, antihistamines, mucus-thinning and cough-loosening drugs, beta-agonists, xanthines, anticholinergics, glucocorticoids, and cromones.
This document discusses pancreatic hormones and their role in diabetes mellitus. It describes how the pancreas functions as both an exocrine and endocrine gland, secreting digestive enzymes and hormones like insulin and glucagon. Problems with insulin production cause diabetes mellitus, characterized by high blood glucose. The document outlines the roles of insulin and glucagon in regulating blood glucose levels, compares type 1 and type 2 diabetes, and discusses treatment approaches like insulin therapy, oral medications, diet/exercise, and new therapies.
The document summarizes the major endocrine glands and their hormones. It describes the hypothalamus and pituitary gland which secretes six important peptide hormones. It also discusses the thyroid gland which produces thyroxine and triiodothyronine, regulating cellular metabolism. The parathyroid glands contain four glands which secrete parathyroid hormone regulating calcium levels. The pancreas has endocrine functions secreting insulin and glucagon to regulate blood sugar. The adrenal glands are composed of an outer cortex secreting glucocorticoids and mineralocorticoids, and an inner medulla secreting epinephrine and norepinephrine. The gonads are the testes and ovaries which produce sex
The document discusses key aspects of systematic reviews that should be addressed to minimize bias, including clearly specifying inclusion/exclusion criteria, conducting comprehensive searches to identify most relevant studies, and accounting for quality of reviewed studies. It emphasizes the importance of transparently reporting how trials were selected and quality assessed to strengthen the evidence provided by the systematic review.
This document discusses key criteria for evaluating the quality of evidence from randomized trials:
1) Groups must be comparable, which randomization aims to ensure by distributing participants evenly across groups through chance alone. Randomization can be computer-generated or through processes like coin tossing.
2) Allocation must be concealed so researchers are unaware which group a participant will be in to prevent bias. This is usually done through sealed envelopes or an off-site registry.
3) Follow-up must be complete or near-complete to prevent bias from non-random dropout patterns between groups. Less than 15% total dropout is ideal, with concerns rising above 20% where groups differ substantially.
This document discusses adrenocorticosteroids and their roles and effects in the body. It focuses on glucocorticoids like cortisol which regulate glucose, stress response, and inflammation. Glucocorticoids work by entering cells and activating receptors that travel to DNA to inhibit inflammatory genes. The document also discusses mineralocorticoids like aldosterone which regulate sodium and fluid balance. Therapeutic uses of glucocorticoids include replacement therapy for adrenal insufficiency and treatment of inflammatory/autoimmune conditions. Side effects include adrenal suppression and Cushing's syndrome.
This document discusses the roles and functions of androgens and estrogens in the male and female body. It describes how androgens and estrogens contribute to sexual development and function, their clinical uses, and potential side effects of hormone therapy. The summary also outlines the menstrual cycle and the roles of various hormones like FSH, LH, estrogen, and progesterone in regulating the female reproductive cycle.
This document discusses several classes of respiratory drugs including antitussives, decongestants, antihistamines, mucolytics and expectorants, bronchodilators, and anti-inflammatory drugs. It describes the mechanisms of action, indications for use, routes of administration, and potential adverse effects of drugs from each class. The classes covered include cough suppressants, nasal decongestants, antihistamines, mucus-thinning and cough-loosening drugs, beta-agonists, xanthines, anticholinergics, glucocorticoids, and cromones.
The document summarizes the major endocrine glands and their hormones. It describes the hypothalamus and pituitary gland which secretes six important peptide hormones. It also discusses the thyroid gland which produces thyroxine and triiodothyronine, regulating cellular metabolism. The parathyroid glands contain four glands which secrete parathyroid hormone to regulate calcium levels. The pancreas has endocrine functions secreting insulin and glucagon to regulate blood sugar. The adrenal glands are composed of an outer cortex secreting glucocorticoids and mineralocorticoids, and an inner medulla secreting epinephrine and norepinephrine. The gonads are the testes and ovaries which se
This document discusses key criteria for evaluating the quality of evidence from randomized trials:
1) Groups must be comparable, which randomization aims to ensure by distributing participants evenly across groups through chance alone. Randomization can be computer-generated or through processes like coin tossing.
2) Allocation must be concealed so researchers are unaware which group a participant will be in to prevent bias. This is usually done through sealed envelopes or an off-site registry.
3) Follow-up must be complete or near-complete, with less than 15-20% loss to follow-up to avoid bias from non-random dropout patterns between groups. Loss to follow-up threatens validity the more participants are lost.
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central19various
Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central Clinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa CentralClinic ^%[+27633867063*Abortion Pills For Sale In Tembisa Central
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
Hiranandani Hospital in Powai, Mumbai, is a premier healthcare institution that has been serving the community with exceptional medical care since its establishment. As a part of the renowned Hiranandani Group, the hospital is committed to delivering world-class healthcare services across a wide range of specialties, including kidney transplantation. With its state-of-the-art facilities, advanced medical technology, and a team of highly skilled healthcare professionals, Hiranandani Hospital has earned a reputation as a trusted name in the healthcare industry. The hospital's patient-centric approach, coupled with its focus on innovation and excellence, ensures that patients receive the highest standard of care in a compassionate and supportive environment.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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!
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
One health condition that is becoming more common day by day is diabetes.
According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
2. Failure of the pump. In the most common situation, the
cardiac muscle contracts weakly and the chambers
cannot empty properly—so-called “systolic dysfunction.”
In some cases, the muscle cannot relax sufficiently to
permit ventricular filling, resulting in diastolic dysfunction.
Obstruction to flow. Lesions that prevent valve opening
(e.g., calcific aortic valve stenosis) or cause increased
ventricular chamber pressures (e.g., systemic
hypertension or aortic coarctation) can overwork the
myocardium, which has to pump against the obstruction.
3. Regurgitant flow. Valve pathology that allows
backward flow of blood results in increased
volume workload and may overwhelm the
pumping capacity of the affected chambers.
Shunted flow. Defects (congenital or
acquired) that divert blood inappropriately
from one chamber to another, or from one
vessel to another, lead to pressure and
volume overloads.
4. Disorders of cardiac conduction.
Uncoordinated cardiac impulses or blocked
conduction pathways can cause arrhythmias
that slow contractions or prevent effective
pumping altogether.
Rupture of the heart or major vessel. Loss of
circulatory continuity (e.g., a gunshot wound
through the thoracic aorta) may lead to
massive blood loss, hypotensive shock, and
death.
5. Heart failure, often referred to as congestive heart
failure (CHF), is the common end point for many
forms of cardiac disease and typically is a
progressive condition with a poor prognosis.
Heart failure may result from systolic or diastolic
dysfunction.
Systolic dysfunction results from inadequate
myocardial contractile function, usually as a
consequence of ischemic heart disease or
hypertension.
Diastolic dysfunction refers to an inability of the
heart to adequately relax and fill, which may be a
consequence of massive left ventricular
hypertrophy, myocardial fibrosis, amyloid
deposition, or constrictive pericarditis.
6. When, the failing heart can no longer
efficiently pump blood, there is an increase in
end-diastolic ventricular volumes, increased
end-diastolic pressures, and elevated venous
pressures. Thus, inadequate cardiac output—
called forward failure—is almost always
accompanied by increased congestion of the
venous circulation—that is, backward failure.
7. Heart failure can affect predominantly the left or
the right side of the heart or may involve both
sides.
The most common causes of left-sided cardiac
failure are ischemic heart disease (IHD), systemic
hypertension, mitral or aortic valve disease, and
primary diseases of the myocardium (e.g.,
amyloidosis).
The morphologic and clinical effects of left-sided
CHF stem from diminished systemic perfusion
and elevated back-pressures within the
pulmonary circulation.
8. Dyspnea (shortness of breath) on exertion is usually
the earliest and most significant symptom of left-sided
heart failure; cough is also common as a consequence
of fluid transudation into air spaces.
As failure progresses, patients experience dyspnea
when recumbent (orthopnea); this occurs because the
supine position increases venous return from the
lower extremities and also elevates the diaphragm.
Orthopnea typically is relieved by sitting or standing,
so patients usually sleep in a semi-seated position.
Paroxysmal nocturnal dyspnea is a particularly
dramatic form of breathlessness, awakening patients
from sleep with extreme dyspnea bordering on
feelings of suffocation.
9. Other manifestations of left ventricular failure
include an enlarged heart (cardiomegaly),
tachycardia, a third heart sound (S3), and fine
ráles at the lung bases, caused by the
opening of edematous pulmonary alveoli.
Subsequent chronic dilation of the left atrium
can cause atrial fibrillation, manifested by an
“irregularly irregular” heartbeat.
10. Right-sided heart failure is
usually the consequence of
left-sided heart failure, since
any pressure increase in the
pulmonary circulation
inevitably produces an
increased burden on the right
side of the heart.
Isolated right-sided heart
failure is infrequent and
typically occurs in patients
with one of a variety of
disorders affecting the lungs;
hence it is often referred to as
cor pulmonale.
11. The common feature of these disorders is
pulmonary hypertension, which results in
hypertrophy and dilation of the right side of
the heart. In cor pulmonale, myocardial
hypertrophy and dilation generally are
confined to the right ventricle and atrium,
although bulging of the ventricular septum
to the left can reduce cardiac output by
causing outflow tract obstruction.
12. Unlike left-sided heart failure, pure right-sided
heart failure typically is not associated with
respiratory symptoms.
Instead, the clinical manifestations are related to
systemic and portal venous congestion and
include hepatic and splenic enlargement,
peripheral edema, pleural effusion, and ascites.
Venous congestion and hypoxia of the kidneys
and brain due to right-sided heart failure can
produce deficits comparable to those caused by
the hypoperfusion of left-sided heart failure.
13. Congenital heart diseases are abnormalities of the
heart or great vessels that are present at birth.
Pathogenesis
Congenital heart disease most commonly arises from
faulty embryogenesis during gestational weeks 3
through 8, when major cardiovascular structures
develop.
Thecause is unknown in almost 90% of cases. Of the
accepted etiologic factors, environmental exposures,
including congenital rubella infection, teratogens,
and maternal diabetes, and genetic factors are best
characterized.
14. The various structural anomalies in
congenital heart disease can be assigned to
three major groups based on their
hemodynamic and clinical consequences:
(1) Malformations causing a left-to-right shunt;
(2) Malformations causing a right-to-left shunt
(cyanotic congenital heart diseases); and
(3) Malformations causing obstruction.
15. A shunt is an abnormal
communication between
chambers or blood vessels.
Depending on pressure
relationships, shunts permit
the flow of blood from the
left to the right side of the
heart (or vice versa).
With right-to-left shunt, a
dusky blueness of the skin
(cyanosis) results because
the pulmonary circulation is
bypassed and poorly
oxygenated blood collected
from the venous system
enters the systemic arterial
circulation.
16. By contrast, left-to-right shunts increase
blood flow into the pulmonary circulation and
are not associated with cyanosis.
However, they expose the low-pressure, low-
resistance pulmonary circulation to high
pressures and increased volumes; these
alterations lead to adaptive changes that
increase lung vascular resistance to protect
the pulmonary bed, resulting in right
ventricular hypertrophy and—eventually
rightsided— failure.
With time, increased pulmonary resistance
also can cause shunt reversal (right to left)
and late-onset cyanosis.
17.
18. Some congenital anomalies obstruct vascular
flow by narrowing the chambers, valves, or
major blood vessels.
A malformation characterized by complete
obstruction is called an atresia.
The altered hemodynamics of congenital
heart disease usually lead to chamber dilation
or wall hypertrophy. However, some defects
result in a reduced muscle mass or chamber
size; this is called hypoplasia if it occurs
before birth and atrophy if it develops
postnatally.
19. Disorders associated
with Left-to-right
shunts are the most
common types of
congenital cardiac
malformations.
They include atrial
septal defects (ASDs),
ventricular septal
defects (VSDs), and
patent ductus arteriosus
(PDA).
20. ASDs typically increase only right ventricular
and pulmonary outflow volumes, while VSDs
and PDAs cause both increased pulmonary
blood flow and pressure.
However, as discussed earlier, prolonged left-
to-right shunting may eventually give rise to
pulmonary hypertension and right-to-left
shunting of unoxygenated blood into the
systemic circulation, a change marked by the
appearance of cyanosis (Eisenmenger
syndrome).
21. During normal cardiac development, patency is
maintained between the right and left atria by a
series of fenestrations (ostium primum and ostium
secundum) that eventually become the foramen
ovale.
This arrangement allows oxygenated blood from the
maternal circulation to flow from the right to the left
atrium, thereby sustaining fetal development.
At later stages of intrauterine development, tissue
flaps (septum primum and septum secundum) grow
to occlude the foramen ovale, and in 80% of cases,
the higher left-sided pressures in the heart that occur
at birth permanently fuse the septa against the
foramen ovale.
22. In the remaining 20% of cases, a patent
foramen ovale results; although the flap is of
adequate size to cover the foramen, the
unsealed septa can allow transient right-to-
left blood flow, such as with a Valsalva
maneuver during sneezing or straining during
bowel movements.
Although this typically has little significance,
it occasionally manifests as paradoxical
embolism, defined as venous emboli (e.g.,
from deep leg veins) that enter the systemic
arterial circulation via a foramen ovale defect.
23. In contrast to patent foramen ovale, an ASD is
an abnormal fixed opening in the atrial
septum that allows unrestricted blood flow
between the atrial chambers.
A majority (90%) of ASDs are so-called
“ostium secundum” defects in which growth
of the septum secundum is insufficient to
occlude the second ostium.
24. ASDs usually are asymptomatic until
adulthood. Although VSDs are more common,
many close spontaneously.
ASDs initially cause left-to-right shunts, due
to lower pressures in the pulmonary
circulation and the right side of the heart.
Over time, however, chronic volume and
pressure overloads can cause pulmonary
hypertension.
25. Defects in the ventricular septum allow left-
to-right shunting and constitute the most
common congenital cardiac anomaly at birth.
The ventricular septum normally is formed by
a muscular ridge that grows upward from the
heart apex fusing with a thinner membranous
partition that grows downward from the
endocardial cushions.
Most VSDs close spontaneously in childhood,
but only 20% to 30% of VSDs occur in
isolation; the remainder are associated with
other cardiac malformations.
26. Small VSDs may be asymptomatic; half of
those in the muscular portion of the septum
close spontaneously during infancy or
childhood.
Larger defects, however, result in chronic
left-to-right shunting, often complicated by
pulmonary hypertension and CHF.
Small- or medium-sized defects in the right
ventricle cause endothelial damage and
increase the risk for infective endocarditis.
27. The ductus arteriosus arises from the left
pulmonary artery and joins the aorta just distal to
the origin of the left subclavian artery.
During intrauterine life, it permits blood to flow
from the pulmonary artery to the aorta,
bypassing the unoxygenated lungs.
Within 1 to 2 days of birth in healthy term
infants, the ductus constricts and closes; these
changes occur in response to increased arterial
oxygenation, decreased pulmonary vascular
resistance, and declining local levels of
prostaglandin E2
28.
29. Complete obliteration occurs within the first
few months of extrauterine life, leaving only a
strand of residual fibrous tissue known as the
ligamentum arteriosum.
Ductal closure can be delayed (or even
absent) in infants with hypoxia (related to
respiratory distress or heart disease).
30. PDAs are high-pressure left-to-right shunts
that produce harsh, “machinery-like”
murmurs. A small PDA generally causes no
symptoms, although larger defects eventually
can lead to Eisenmenger syndrome with
cyanosis and congestive heart failure.
High-pressure shunts also predispose
patients to developing infective endocarditis.
31. While isolated PDAs should be closed as early
in life as is feasible, preservation of ductal
patency (by administering prostaglandin E)
can be lifesaving when a PDA is the only
means to sustain systemic or pulmonary
blood flow (e.g., in infants with aortic or
pulmonic atresia).
32. shunts are distinguished by early cyanosis. This
occurs because poorly oxygenated blood from
the right side of the heart flows directly into the
arterial circulation.
Two of the most important conditions associated
with cyanotic congenital heart disease are
tetralogy of Fallot and transposition of the great
vessels.
Clinical consequences of severe, systemic
cyanosis include clubbing of the tips of the
fingers and toes (hypertrophic osteoarthropathy),
polycythemia, and paradoxical embolization.
33.
34.
35. Tetralogy of Fallot is the most common
cause of cyanotic congenital heart
disease.
The four cardinal features are:
• VSD
• Right ventricular outflow tract
obstruction (subpulmonic stenosis)
• Overriding of the VSD by the aorta
• Right ventricular hypertrophy
All of the features of tetralogy of Fallot
result from anterosuperior displacement
of the infundibular septum leading to
abnormal septation between the
pulmonary trunk and the aortic root.
36. The hemodynamic consequences of tetralogy of
Fallot are right-to-left shunting, decreased
pulmonary blood flow, and increased aortic
volumes.
The clinical severity largely depends on the
degree of the pulmonary outflow obstruction.
Moreover, as the child grows and the heart
increases in size, the pulmonic orifice does not
expand proportionately, leading to progressive
worsening of the stenosis.
hypertrophic osteoarthropathy and polycythemia
(due to hypoxia) with attendant hyperviscosity;
right-to-left shunting also increases the risk for
infective endocarditis and systemic embolization.
37. The embryologic defect
is an abnormal
formation of the truncal
and aortopulmonary
septa so that the aorta
arises from the right
ventricle and the
pulmonary artery
emanates from the left
ventricle
38. There is marked right ventricular
hypertrophy, since that chamber functions as
the systemic ventricle; the left ventricle is
hypoplastic, since it pumps only to the low-
resistance pulmonary circulation.
Some newborns with transposition of the
great arteries have a patent foramen ovale or
PDA that allows oxygenated blood to reach
the aorta, but these tend to close; such
infants typically require emergent surgical
intervention within the first few days of life.
39. The dominant manifestation is cyanosis, with the
prognosis depending on the magnitude of
shunting, the degree of tissue hypoxia, and the
ability of the right ventricle to maintain systemic
pressures.
Without surgery (even with stable shunting), most
patients with uncorrected transposition of the
great arteries die within the first months of life.
However, improved surgical techniques now
permit definitive repair, and such patients often
survive into adulthood.
40. Relatively common examples of congenital
obstructions are pulmonic valve stenosis,
aortic valve stenosis or atresia, and
coarctation of the aorta.
41. Coarctation (narrowing, or constriction) of the
aorta is a common form of obstructive congenital
heart disease.
Males are affected twice as often as females,
although females with Turner syndrome
frequently have coarctation. There are two classic
forms:
• An “infantile” preductal form featuring
hypoplasia of the aortic arch proximal to a PDA
• An “adult” postductal form consisting of a
discrete ridgelike infolding of the aorta, adjacent
to the ligamentum arteriosum
42.
43. Clinical manifestations depend on the severity
of the narrowing and the patency of the
ductus arteriosus.
Preductal coarctation with a PDA usually
presents early in life, classically as cyanosis
localized to the lower half of the body;
without intervention, most affected infants
die in the neonatal period.
44. Postductal coarctation without a PDA usually
is asymptomatic, and the disease may remain
unrecognized well into adult life. Classically,
there is upper-extremity hypertension paired
with weak pulses and relative hypotension in
the lower extremities, associated with
symptoms of claudication and coldness.
Exuberant collateral circulation “around” the
coarctation often develops through markedly
enlarged intercostal and internal mammary
arteries; expansion of the flow through these
vessels can lead to radiographically visible
“notching” of the ribs.
45.
46. In most cases, significant coarctations are
associated with systolic murmurs and
occasionally palpable thrills.
Balloon dilation and stent placement or surgical
resection with end-to-end anastomosis (or
replacement of the affected aortic segment by a
prosthetic graft) yields excellent results.