Dr. Sameh Ahmad Muhamad abdelghany provides an overview of heart failure including its causes, types, pathophysiology, risk factors, diagnosis, and treatment. Heart failure is defined as a clinical syndrome resulting from structural or functional defects in the heart that prevent it from sufficiently pumping blood to meet the body's needs. The most common causes are coronary artery disease, high blood pressure, and diabetes. Treatment involves managing underlying causes, removing precipitating factors, and utilizing medications, diet modifications, exercise, and devices as needed.
The document defines and provides average values for various lung volumes and capacities, including:
- Tidal volume is the volume of air inhaled and exhaled during normal breathing, averaging 500 ml.
- Inspiratory reserve volume is the additional air that can be inhaled beyond normal tidal breathing, averaging 3200 ml.
- Residual volume is the air that remains in the lungs after maximum exhalation, averaging 1200 ml.
- Total lung capacity is the total amount of air the lungs can hold, averaging 6000 ml.
The document discusses cardiac electrophysiology and contractility. It describes the pacemaker potential and automaticity of the sinoatrial node, which allows it to initiate action potentials without external stimulation at a rate of 100 beats per minute. It also discusses the conduction of action potentials through the heart via the atrioventricular node, bundle of His, and Purkinje fibers. Contraction is triggered by increases in intracellular calcium levels. The cardiac action potential is longer than in skeletal muscle, lasting 200-300 milliseconds, which allows time for relaxation between contractions.
This document discusses atrial septal defects (ASDs), which are holes between the left and right atria of the heart that allow blood to pass from the left to the right side. The main types of ASDs are secundum, primum, and sinus venosus defects. If left unrepaired, an ASD can cause increased blood flow to the lungs, enlargement of the right atrium, and inadequate blood flow to the body. Surgical closure or device closure are treatment options to close the defect and restore normal blood flow patterns.
The document provides an overview of the anatomy of the heart and surrounding structures. It describes the location of the heart in the chest and its internal and external structures. These include the four chambers of the heart (right and left atria and ventricles), major blood vessels (veins and arteries), surrounding membranes (pericardium), and other anatomical details.
The document summarizes fetal and neonatal physiology related to circulation and respiration. It discusses how the fetus gets oxygen from the mother's blood through the placenta via simple diffusion down a partial pressure gradient. The fetus's blood has adaptations like fetal hemoglobin that enhance oxygen delivery. As the fetus grows, its increasing oxygen needs are met through a higher uterine blood flow from the mother, more fetal blood flow to the placenta, and fetal adaptations in hemoglobin and cardiovascular structure. At birth, the fetal circulation transitions as the placenta is detached and lungs expand, allowing pulmonary circulation to increase while structures like the ductus arteriosus and foramen ovale close.
Ms. Neelam Naz worked at Unique Grammar School for over a year from April 2013 to September 2014 as a senior teacher for matriculation and commerce, and assistant financial manager. During her time at the school, she organized events and served on the discipline committee. She was awarded Teacher of the Year for 2013-2014 for producing the highest matriculation results in the school's history. Her leadership skills and dedication to her work were outstanding, and she was nominated for the position of principal before leaving to continue her studies.
The document provides an overview of the human heart, including its location in the chest, size, and main function of pumping blood throughout the body. It describes the four chambers of the heart - the two upper atria which receive blood and the two lower ventricles which pump blood out. The septum separates the left and right sides, and valves ensure blood flows in only one direction. A healthy heart makes a lub-dub sound with each beat as the valves open and close. Maintaining a healthy lifestyle through exercise, diet, and avoiding smoking can keep the heart working properly.
University Orientation Completion LetterBrandon Green
Brandon Green has been informed that he has successfully completed the University Orientation workshop and that his previous transfer coursework has been evaluated. He is encouraged to check his student website for a summary of transfer credits and progress toward his degree. Additionally, the letter provides information about scholarship opportunities to help fund his education and the potential to earn credit for work completed outside the classroom through Prior Learning Assessment if his program is eligible.
The document defines and provides average values for various lung volumes and capacities, including:
- Tidal volume is the volume of air inhaled and exhaled during normal breathing, averaging 500 ml.
- Inspiratory reserve volume is the additional air that can be inhaled beyond normal tidal breathing, averaging 3200 ml.
- Residual volume is the air that remains in the lungs after maximum exhalation, averaging 1200 ml.
- Total lung capacity is the total amount of air the lungs can hold, averaging 6000 ml.
The document discusses cardiac electrophysiology and contractility. It describes the pacemaker potential and automaticity of the sinoatrial node, which allows it to initiate action potentials without external stimulation at a rate of 100 beats per minute. It also discusses the conduction of action potentials through the heart via the atrioventricular node, bundle of His, and Purkinje fibers. Contraction is triggered by increases in intracellular calcium levels. The cardiac action potential is longer than in skeletal muscle, lasting 200-300 milliseconds, which allows time for relaxation between contractions.
This document discusses atrial septal defects (ASDs), which are holes between the left and right atria of the heart that allow blood to pass from the left to the right side. The main types of ASDs are secundum, primum, and sinus venosus defects. If left unrepaired, an ASD can cause increased blood flow to the lungs, enlargement of the right atrium, and inadequate blood flow to the body. Surgical closure or device closure are treatment options to close the defect and restore normal blood flow patterns.
The document provides an overview of the anatomy of the heart and surrounding structures. It describes the location of the heart in the chest and its internal and external structures. These include the four chambers of the heart (right and left atria and ventricles), major blood vessels (veins and arteries), surrounding membranes (pericardium), and other anatomical details.
The document summarizes fetal and neonatal physiology related to circulation and respiration. It discusses how the fetus gets oxygen from the mother's blood through the placenta via simple diffusion down a partial pressure gradient. The fetus's blood has adaptations like fetal hemoglobin that enhance oxygen delivery. As the fetus grows, its increasing oxygen needs are met through a higher uterine blood flow from the mother, more fetal blood flow to the placenta, and fetal adaptations in hemoglobin and cardiovascular structure. At birth, the fetal circulation transitions as the placenta is detached and lungs expand, allowing pulmonary circulation to increase while structures like the ductus arteriosus and foramen ovale close.
Ms. Neelam Naz worked at Unique Grammar School for over a year from April 2013 to September 2014 as a senior teacher for matriculation and commerce, and assistant financial manager. During her time at the school, she organized events and served on the discipline committee. She was awarded Teacher of the Year for 2013-2014 for producing the highest matriculation results in the school's history. Her leadership skills and dedication to her work were outstanding, and she was nominated for the position of principal before leaving to continue her studies.
The document provides an overview of the human heart, including its location in the chest, size, and main function of pumping blood throughout the body. It describes the four chambers of the heart - the two upper atria which receive blood and the two lower ventricles which pump blood out. The septum separates the left and right sides, and valves ensure blood flows in only one direction. A healthy heart makes a lub-dub sound with each beat as the valves open and close. Maintaining a healthy lifestyle through exercise, diet, and avoiding smoking can keep the heart working properly.
University Orientation Completion LetterBrandon Green
Brandon Green has been informed that he has successfully completed the University Orientation workshop and that his previous transfer coursework has been evaluated. He is encouraged to check his student website for a summary of transfer credits and progress toward his degree. Additionally, the letter provides information about scholarship opportunities to help fund his education and the potential to earn credit for work completed outside the classroom through Prior Learning Assessment if his program is eligible.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against developing mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
the 1st aortic arch – disappears (a small portion persists and forms a piece of the maxillary artery)
the 2nd aortic arch – disappears (small portions of this arch contributes to the hyoid and stapedial arteries)
the 3rd aortic arch - has the same development on the right and left side
it gives rise to the initial portion of
the internal carotid artery,
the remainder of its trunk is
formed by the cranial portion of
the dorsal aorta + primitive internal
carotid
the external carotid is deriving from
the cranial portion of the ventral aorta
the common carotid corresponds to a
portion of the ventral aorta between
exits of the third and fourth arches
The cardiovascular system includes the heart and blood vessels. The heart weighs 200-400 grams and pumps around 7,751 litres of blood daily. It is located behind the sternum and is surrounded by membranes. Blood enters and exits the heart through major vessels while valves regulate flow between chambers. The heart muscle generates electrical impulses and contractions to circulate blood throughout the body. Cardiac output is regulated intrinsically through preload and afterload as well as extrinsically through the nervous and endocrine systems.
1. The kidney concentrates urine through active transport mechanisms that create a hyperosmotic medullary interstitium and facilitate water reabsorption in the presence of ADH.
2. The loop of Henle acts as a countercurrent multiplier, trapping solutes in the medulla through sequential transport and creating an osmotic gradient.
3. Urea recycling and the countercurrent exchange function of vasa recta help maintain the high solute concentration in the medullary interstitium, allowing further water reabsorption and concentrated urine production.
The document discusses the mechanism of respiration, which involves breathing and the exchange of gases through diffusion in the alveoli. Inspiration is an active process where inhaling decreases pressure and draws air into the lungs. Expiration is passive as exhaling increases pressure and expels air. Oxygen diffuses into blood and tissues while carbon dioxide diffuses out, carried by hemoglobin, plasma, and bicarbonate ions to the lungs.
This document provides information on congenital heart disease (CHD). It discusses the epidemiology and etiology of CHD. It then describes the relative frequency of different congenital heart lesions. It provides clues for evaluating infants with suspected CHD and discusses various cyanotic and acyanotic CHD conditions like ventricular septal defects, tetralogy of Fallot, transposition of the great arteries and Ebstein's anomaly in detail including their pathophysiology, clinical manifestations, diagnosis and treatment.
This document discusses oxygen transport and delivery in the body. It covers:
1. Oxygen is transported bound to hemoglobin (97%) and dissolved in plasma (3%). Oxygen diffuses from alveoli into plasma and binds to hemoglobin in red blood cells.
2. Arterial oxygen content is determined by dissolved oxygen and oxygen bound to hemoglobin. Normal arterial content is 20 ml O2/100ml blood. Venous content is normally 15 ml O2/100ml blood.
3. Oxygen delivery depends on cardiac output and arterial oxygen content. Normal delivery is 1000 ml O2/min. Oxygen uptake by tissues is normally 250 ml O2/min.
This document provides updated guidelines and reference values for cardiac chamber quantification by echocardiography. It summarizes recommendations for measuring and evaluating left ventricular size, function, mass and regional wall motion. Reference values are given for linear dimensions, volumes and ejection fraction of the left ventricle based on a large number of normal subjects. The document also summarizes guidelines for assessing right ventricular size and function, as well as the size and function of the left and right atria, aortic root dimensions, and inferior vena cava size. Partition values are only provided for left ventricular ejection fraction and left atrial volume due to limitations of existing data.
This document provides an overview of the conduction system of the heart. It begins with the development of the primitive cardiac tube and differentiation of heart structures. It then describes the specialized conduction tissues including the sinoatrial node, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers. It discusses impulse conduction through the heart and characteristics of cardiac conduction cells. Finally, it covers conduction defects, implications for congenital heart anomalies like ASD and VSD, and considerations for cardiac surgery.
This document discusses cardiac output and its measurement. It defines cardiac output as the amount of blood ejected by each ventricle per minute, which is calculated as stroke volume multiplied by heart rate. It describes several methods to measure cardiac output, including the indicator dye dilution method, thermodilution, and measurement of inhaled inert gases. It discusses factors that can cause cardiac output to vary, such as age, sex, environmental temperature, exercise, and various pathological conditions.
The cardiac conduction system is made up of four main structures that stimulate contraction of the heart muscle in a coordinated way. The sinoatrial node acts as the pacemaker and initiates electrical impulses throughout the heart. The atrioventricular node receives impulses from the atria and slows conduction to allow for filling of the ventricles before contraction. Specialized fibers called Purkinje fibers rapidly conduct electrical signals from the atrioventricular node to trigger simultaneous contraction of the ventricles. An electrocardiogram traces the electrical activity of the heart along the body surface and is used to analyze the function of the conduction system.
The document discusses the Fick Principle, which states that cardiac output or blood flow to an organ can be calculated using the difference in concentration of a marker substance in the blood before and after it passes through the organ. Specifically:
1) Cardiac output is the volume of blood pumped by the heart per minute and can be determined using the Fick Principle by measuring the difference in oxygen concentration of arterial and venous blood from the lungs.
2) The Fick Principle involves determining the volume of the marker substance (e.g. oxygen) consumed per minute, the concentration of the marker in arterial blood, and the concentration in venous blood leaving the organ.
3) Using sample oxygen concentration values
Echocardiography made easy all thing you want to know part aAHMED ESAWY
The document discusses the history and development of chocolate over centuries. It details how cocoa beans were first used as currency by the Mayans and Aztecs before being introduced to Europe in the 16th century. The document then explains how chocolate became popularized as a drink in Europe in the 17th century and how its production and consumption expanded globally over subsequent centuries.
This document summarizes the anatomy and branches of the major arteries and veins in the human circulatory system. It describes the layers of blood vessel walls and then lists and defines the major arteries and veins. These include the pulmonary veins, vena cava, pulmonary artery, aorta, and their primary branches. The document then discusses the specific branches of the coronary, carotid, and brachial arteries in more detail.
Valvular heart disease can cause mitral regurgitation and mitral stenosis. Rheumatic fever is a common cause of valvular heart disease and results in scarring of the heart valves over multiple attacks. Mitral stenosis causes the mitral valve to narrow over time, increasing the pressure in the lungs and right side of the heart. Mitral regurgitation occurs when the mitral valve does not close properly, allowing blood to flow back into the left atrium. Both conditions can cause shortness of breath and heart failure if left untreated. Echocardiography is the primary test used to diagnose valvular heart disease and determine severity.
This document provides an overview of pulmonary circulation. It discusses:
1) The functional anatomy of the three circulations in the lungs - pulmonary, bronchial, and lymphatic.
2) The characteristic features of pulmonary circulation including its low pressure, resistance, and high capacitance.
3) The regulation of pulmonary blood flow through neural and chemical control mechanisms like hypoxia and hypercapnia.
4) How factors like gravity and exercise can impact regional pulmonary blood flow and alveolar ventilation.
This document discusses several types of cyanotic congenital heart disease:
1. Tetralogy of Fallot is the most common cyanotic heart disease, characterized by four anatomical features - ventricular septal defect, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy. It causes cyanosis due to right-to-left shunting.
2. Transposition of the great arteries involves the aorta arising from the right ventricle and pulmonary artery from the left ventricle. It requires mixing of blood between circulations to survive.
3. Truncus arteriosus is a rare condition where a single artery supplies both circulations. It is usually associated with a ventricular septal defect.
This document provides an overview of congestive heart failure in adults. It begins with definitions and epidemiology, describing CHF as the heart's inability to pump enough blood due to structural or functional abnormalities. Main causes include reduced ejection fraction, volume overload, and pressure overload. Signs and symptoms include fatigue, shortness of breath, and leg swelling. The document then covers diagnosis, investigations such as BNP levels, classifications like NYHA staging, pathophysiology, types, manifestations, and management with medications like diuretics, ACE inhibitors, beta-blockers, and treatment of underlying conditions. It concludes with contraindicated medications in pregnancy or CHF.
1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves lifestyle modifications, medications like diuretics, ACE inhibitors, beta blockers, and devices or transplantation for refractory cases.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against developing mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
the 1st aortic arch – disappears (a small portion persists and forms a piece of the maxillary artery)
the 2nd aortic arch – disappears (small portions of this arch contributes to the hyoid and stapedial arteries)
the 3rd aortic arch - has the same development on the right and left side
it gives rise to the initial portion of
the internal carotid artery,
the remainder of its trunk is
formed by the cranial portion of
the dorsal aorta + primitive internal
carotid
the external carotid is deriving from
the cranial portion of the ventral aorta
the common carotid corresponds to a
portion of the ventral aorta between
exits of the third and fourth arches
The cardiovascular system includes the heart and blood vessels. The heart weighs 200-400 grams and pumps around 7,751 litres of blood daily. It is located behind the sternum and is surrounded by membranes. Blood enters and exits the heart through major vessels while valves regulate flow between chambers. The heart muscle generates electrical impulses and contractions to circulate blood throughout the body. Cardiac output is regulated intrinsically through preload and afterload as well as extrinsically through the nervous and endocrine systems.
1. The kidney concentrates urine through active transport mechanisms that create a hyperosmotic medullary interstitium and facilitate water reabsorption in the presence of ADH.
2. The loop of Henle acts as a countercurrent multiplier, trapping solutes in the medulla through sequential transport and creating an osmotic gradient.
3. Urea recycling and the countercurrent exchange function of vasa recta help maintain the high solute concentration in the medullary interstitium, allowing further water reabsorption and concentrated urine production.
The document discusses the mechanism of respiration, which involves breathing and the exchange of gases through diffusion in the alveoli. Inspiration is an active process where inhaling decreases pressure and draws air into the lungs. Expiration is passive as exhaling increases pressure and expels air. Oxygen diffuses into blood and tissues while carbon dioxide diffuses out, carried by hemoglobin, plasma, and bicarbonate ions to the lungs.
This document provides information on congenital heart disease (CHD). It discusses the epidemiology and etiology of CHD. It then describes the relative frequency of different congenital heart lesions. It provides clues for evaluating infants with suspected CHD and discusses various cyanotic and acyanotic CHD conditions like ventricular septal defects, tetralogy of Fallot, transposition of the great arteries and Ebstein's anomaly in detail including their pathophysiology, clinical manifestations, diagnosis and treatment.
This document discusses oxygen transport and delivery in the body. It covers:
1. Oxygen is transported bound to hemoglobin (97%) and dissolved in plasma (3%). Oxygen diffuses from alveoli into plasma and binds to hemoglobin in red blood cells.
2. Arterial oxygen content is determined by dissolved oxygen and oxygen bound to hemoglobin. Normal arterial content is 20 ml O2/100ml blood. Venous content is normally 15 ml O2/100ml blood.
3. Oxygen delivery depends on cardiac output and arterial oxygen content. Normal delivery is 1000 ml O2/min. Oxygen uptake by tissues is normally 250 ml O2/min.
This document provides updated guidelines and reference values for cardiac chamber quantification by echocardiography. It summarizes recommendations for measuring and evaluating left ventricular size, function, mass and regional wall motion. Reference values are given for linear dimensions, volumes and ejection fraction of the left ventricle based on a large number of normal subjects. The document also summarizes guidelines for assessing right ventricular size and function, as well as the size and function of the left and right atria, aortic root dimensions, and inferior vena cava size. Partition values are only provided for left ventricular ejection fraction and left atrial volume due to limitations of existing data.
This document provides an overview of the conduction system of the heart. It begins with the development of the primitive cardiac tube and differentiation of heart structures. It then describes the specialized conduction tissues including the sinoatrial node, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers. It discusses impulse conduction through the heart and characteristics of cardiac conduction cells. Finally, it covers conduction defects, implications for congenital heart anomalies like ASD and VSD, and considerations for cardiac surgery.
This document discusses cardiac output and its measurement. It defines cardiac output as the amount of blood ejected by each ventricle per minute, which is calculated as stroke volume multiplied by heart rate. It describes several methods to measure cardiac output, including the indicator dye dilution method, thermodilution, and measurement of inhaled inert gases. It discusses factors that can cause cardiac output to vary, such as age, sex, environmental temperature, exercise, and various pathological conditions.
The cardiac conduction system is made up of four main structures that stimulate contraction of the heart muscle in a coordinated way. The sinoatrial node acts as the pacemaker and initiates electrical impulses throughout the heart. The atrioventricular node receives impulses from the atria and slows conduction to allow for filling of the ventricles before contraction. Specialized fibers called Purkinje fibers rapidly conduct electrical signals from the atrioventricular node to trigger simultaneous contraction of the ventricles. An electrocardiogram traces the electrical activity of the heart along the body surface and is used to analyze the function of the conduction system.
The document discusses the Fick Principle, which states that cardiac output or blood flow to an organ can be calculated using the difference in concentration of a marker substance in the blood before and after it passes through the organ. Specifically:
1) Cardiac output is the volume of blood pumped by the heart per minute and can be determined using the Fick Principle by measuring the difference in oxygen concentration of arterial and venous blood from the lungs.
2) The Fick Principle involves determining the volume of the marker substance (e.g. oxygen) consumed per minute, the concentration of the marker in arterial blood, and the concentration in venous blood leaving the organ.
3) Using sample oxygen concentration values
Echocardiography made easy all thing you want to know part aAHMED ESAWY
The document discusses the history and development of chocolate over centuries. It details how cocoa beans were first used as currency by the Mayans and Aztecs before being introduced to Europe in the 16th century. The document then explains how chocolate became popularized as a drink in Europe in the 17th century and how its production and consumption expanded globally over subsequent centuries.
This document summarizes the anatomy and branches of the major arteries and veins in the human circulatory system. It describes the layers of blood vessel walls and then lists and defines the major arteries and veins. These include the pulmonary veins, vena cava, pulmonary artery, aorta, and their primary branches. The document then discusses the specific branches of the coronary, carotid, and brachial arteries in more detail.
Valvular heart disease can cause mitral regurgitation and mitral stenosis. Rheumatic fever is a common cause of valvular heart disease and results in scarring of the heart valves over multiple attacks. Mitral stenosis causes the mitral valve to narrow over time, increasing the pressure in the lungs and right side of the heart. Mitral regurgitation occurs when the mitral valve does not close properly, allowing blood to flow back into the left atrium. Both conditions can cause shortness of breath and heart failure if left untreated. Echocardiography is the primary test used to diagnose valvular heart disease and determine severity.
This document provides an overview of pulmonary circulation. It discusses:
1) The functional anatomy of the three circulations in the lungs - pulmonary, bronchial, and lymphatic.
2) The characteristic features of pulmonary circulation including its low pressure, resistance, and high capacitance.
3) The regulation of pulmonary blood flow through neural and chemical control mechanisms like hypoxia and hypercapnia.
4) How factors like gravity and exercise can impact regional pulmonary blood flow and alveolar ventilation.
This document discusses several types of cyanotic congenital heart disease:
1. Tetralogy of Fallot is the most common cyanotic heart disease, characterized by four anatomical features - ventricular septal defect, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy. It causes cyanosis due to right-to-left shunting.
2. Transposition of the great arteries involves the aorta arising from the right ventricle and pulmonary artery from the left ventricle. It requires mixing of blood between circulations to survive.
3. Truncus arteriosus is a rare condition where a single artery supplies both circulations. It is usually associated with a ventricular septal defect.
This document provides an overview of congestive heart failure in adults. It begins with definitions and epidemiology, describing CHF as the heart's inability to pump enough blood due to structural or functional abnormalities. Main causes include reduced ejection fraction, volume overload, and pressure overload. Signs and symptoms include fatigue, shortness of breath, and leg swelling. The document then covers diagnosis, investigations such as BNP levels, classifications like NYHA staging, pathophysiology, types, manifestations, and management with medications like diuretics, ACE inhibitors, beta-blockers, and treatment of underlying conditions. It concludes with contraindicated medications in pregnancy or CHF.
1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves lifestyle modifications, medications like diuretics, ACE inhibitors, beta blockers, and devices or transplantation for refractory cases.
1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves correcting underlying factors, lifestyle modifications, and maximizing medications like loop diuretics, ACE inhibitors, beta blockers, and aldosterone antagonists.
This document provides guidelines for the pharmacological management of heart failure. It defines heart failure and classifies it based on ejection fraction into heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). For patients with HFrEF (stage C), it recommends using ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists, hydralazine/isosorbide dinitrate, and diuretics. For patients with HFpEF (stage C), evidence-based pharmacological therapies have not been identified. The document also provides dosing recommendations for common heart failure medications like loop diuretics, ACE inhibitors, and beta-blockers
This document discusses congestive heart failure and cor pulmonale. It defines heart failure as the heart's inability to pump an adequate amount of blood to meet the body's needs. Heart failure results from any structural or functional abnormalities that impair the ventricle's ability to eject or fill with blood. Cor pulmonale is right heart failure secondary to lung diseases that cause pulmonary hypertension and back up of blood into the right side of the heart. The document reviews the causes, pathophysiology, signs, symptoms, diagnostic testing, and management of both conditions.
Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It affects over 5 million Americans. The prevalence increases with age, reaching nearly 10% in those over 80. Symptoms include fatigue, shortness of breath, swelling, and more. Treatment focuses on reducing cardiac workload through diuretics, beta blockers, ACE inhibitors, and other drugs. Device therapies like CRT can also help certain patients. Lifestyle changes and strict medication adherence are important for managing the condition.
Diagnosis and treatment of Acute and Chronic Heart failureM A Hasnat
This document discusses the diagnosis and treatment of acute and chronic heart failure. It begins by defining heart failure and describing its classification based on ejection fraction, location in the heart, onset/severity, and ACC/AHA stages. It then covers the essential initial investigations, recommended additional investigations, and pharmacological and device-based treatment approaches. It concludes by discussing methods for delaying or preventing the development of heart failure and managing acute heart failure episodes.
This document provides an overview of congestive heart failure (HF), including its epidemiology, types, diagnostic tests, treatment options, and management. Some key points:
- Nearly 5 million Americans currently live with HF, with over 550,000 new cases diagnosed yearly. It costs over $30 billion annually.
- HF occurs when the heart cannot pump sufficiently due to conditions like heart attack or hypertension damaging the heart muscle.
- Diagnostic tests include echocardiograms and BNP/NT-proBNP levels. HF is classified by ejection fraction and NYHA functional class.
- Treatment involves medications like ACE inhibitors, ARBs, beta blockers, and diuretics to manage symptoms. L
Heart failure is a condition where the heart is unable to pump enough blood to meet the body's needs. It can result from any structural or functional issues impairing the ventricle's ability to eject or receive blood. Treatment involves controlling risk factors, lifestyle changes, and medications like diuretics, ACE inhibitors, beta blockers, and aldosterone antagonists. Complications include fluid retention, arrhythmias, hepatic and renal dysfunction. Refractory cases may require devices, transplantation, or palliative care.
Heart failure is a common and serious condition where the heart muscle is unable to pump sufficiently. It can have multiple causes and the prevalence increases significantly with age. Prognosis remains poor with high mortality rates. Diagnosis involves evaluating symptoms, signs, and testing like echocardiogram. Management focuses on general measures like diet, exercise, and reducing risk factors as well as specific treatments targeting the underlying cause and physiology of heart failure.
Heart failure is a clinical syndrome where the heart is unable to pump enough blood to meet the body's needs. It can be caused by conditions that reduce the heart's ability to contract or fill properly and common symptoms include dyspnea, fatigue, and edema. Upon presentation, patients exhibiting signs of congestion such as elevated jugular pressure, rales, and edema are treated with diuretics, while those with low blood pressure or organ dysfunction may require inotropic support or mechanical circulatory support.
Heart failure occurs when the heart cannot pump enough blood to meet the body's needs. Symptoms range from none in mild cases to being present at rest in severe cases. Heart failure prevalence increases with age and the most common causes are coronary artery disease and high blood pressure. Treatment involves managing symptoms with diuretics, ACE inhibitors, beta blockers, and controlling heart rate and rhythm with medications. For severe cases, surgical options like defibrillators, resynchronization therapy, transplant, or ventricular assist devices may be used.
The document provides guidelines for the management of heart failure. It discusses the epidemiology of heart failure, classifications based on ejection fraction, stages based on symptoms and disease progression, and treatment recommendations for each stage. Key points include increasing risk with age, treatments including controlling risk factors in early stages and use of diuretics, ACE inhibitors, ARBs, and beta blockers in later stages, and tailored treatment for those with heart failure and comorbidities like diabetes or hypertension.
Congestive heart failure in an orthopedic patientIgbinlade Damola
This document discusses heart failure in an orthopedic patient. It begins with definitions and classifications of heart failure, including systolic vs diastolic, left vs right sided, acute vs chronic, and low vs high output failure. It then covers the pathophysiology, risk factors, clinical manifestations, diagnosis, lab findings, and treatment of heart failure, including medication and patient counseling.
Heart failure is a clinical syndrome characterized by symptoms such as breathlessness and fatigue caused by structural or functional abnormalities of the heart. It is a leading cause of hospitalization in people over 65. Up to 50% of heart failure patients die within 5 years of diagnosis.
The document discusses classifications of heart failure based on ejection fraction and functional capacity. It provides guidelines on the management of acute heart failure, including treatments to reduce congestion and increase perfusion. Chronic heart failure treatment focuses on reducing mortality and hospitalizations through optimized medical therapy including ACE inhibitors, beta-blockers, MRAs, and newer drugs like sacubitril/valsartan. Device therapies like ICDs and CRT are recommended for
The document provides an overview of heart failure, including its etiology, pathophysiology, diagnosis, and treatment. It discusses the incidence and prevalence of heart failure, common causes, compensatory mechanisms in the body, assessment methods, and current treatment approaches such as medications, device therapies, and lifestyle modifications. The goal is to educate medical practitioners on managing the complex clinical syndrome of heart failure.
The document defines heart failure as a clinical syndrome characterized by typical symptoms such as breathlessness and swelling caused by structural or functional abnormalities of the heart. This results in reduced cardiac output and elevated pressures in the heart at rest or during stress. Heart failure is classified based on ejection fraction and other factors, and can involve either the left or right side of the heart. Long term, heart failure leads to neurohormonal activation and pathological remodeling of the heart muscle over time.
The document discusses heart failure, including its definition, stages, causes, symptoms, and treatment guidelines. It provides an overview of epidemiology and costs of heart failure. Guidelines from ACC/AHA classify heart failure into stages A through D based on risk or presence of symptoms. Treatment involves managing risk factors, addressing neurohormonal activation, and following medication protocols tailored to each stage.
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
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...Donc Test
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Study Guide Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Course Hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Answers Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Course hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Study Guide Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Ebook Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Questions Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Stuvia
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
4. 4
Introduction
Definiton:
A clinical syndrome resulting from any structural or
functional cardiac defect
The heart is unable to pump sufficiently to maintain blood
flow to meet the body's needs
5. 5
Introduction
The most common causes of heart failure are
coronary artery disease, high blood pressure, and
diabetes.
HF is diagnosed on the presence of characteristic
signs and symptoms and not on the basis of any
diagnostic tests
6. 6
Introduction
Heart failure is a common, costly, and potentially fatal
condition.
In 2015 it affected about 40 million people globally.
Overall around 2% of adults have heart failure and in those
over the age of 65, this increases to 6–10%.
In the year after diagnosis the risk of death is about 35%
after which it decreases to below 10% each year.
9. 9
Types of HF
According to cardiac output:
a. Low-Output Heart Failure
b. High-Output Heart Failure
According to anatomical side
a. Left side heart failure
b. Right side heart failure
According to onset
a. Acute heart failure
b. Chronic heart failure
14. 14
Pathophysiology of HF
Pump fails → decreased stroke volume /CO.
Compensatory mechanisms kick in to increase CO
SNS stimulation → release of epinephrine/nor-
epinephrine
o Increase HR
o Increase contractility
o Peripheral vasoconstriction (increases afterload)
Myocardial hypertrophy: walls of heart thicken to
provide more muscle mass → stronger contractions
15. 15
Pathophysiology of HF
Hormonal response:
↓ renal perfusion interpreted by juxtaglomerular
apparatus as hypovolemia. Thus: Kidneys release
renin, which stimulates conversion of antiotensin I →
angiotensin II, which causes:
o Aldosterone release → Na retention and water
retention (via ADH secretion)
o Peripheral vasoconstriction
16. 16
Pathophysiology of HF
Compensatory mechanisms may restore CO to near-
normal.
But, if excessive the compensatory mechanisms can
worsen heart failure because:
Vasoconstriction:
o ↑ the resistance against which heart has to pump (i.e.,
↑ afterload), and may therefore ↓ CO
17. 17
Pathophysiology of HF
Na and water retention:
o ↑ fluid volume, which ↑ preload. If too much
“stretch” (d/t too much fluid) → ↓ strength of
contraction and ↓ CO
Excessive tachycardia → ↓ diastolic filling time →
↓ventricular filling → ↓ SV and CO
22. 22
C/P of HF
Symptoms
Left Heart Failure:
o Dyspnea on exertion
o Dyspnea at rest
o Orthpnea
o Paroxysmal nocturnal dyspnea (PND)
o Fatigue, inability to exercise
23. 23
C/P of HF
Symptoms
Right Heart Failure:
o Swelling of feet, hands
o Abdominal distention/fullness
o Right upper quadrant pain
o Early satiety
o Weight loss (cardiac cachexia)
24. 24
C/P of HF
Signs
Left Heart Failure:
o Rales
o Pleural effusions
o Displaced apical impulse
o Tachycardia, LVS3, murmur of MR(mitral regurge)
o Narrow pulse pressure
25. 25
C/P of HF
Signs
Right Heart Failure:
o Edema of lower extremities
o Elevated JVP(jugular vein pressure)/+
HJR(hepatojugular reflux)
o RVS3, murmur of TR(tricuspid regurge)
o Hepatomegaly, RUQ(right upper quadrant) tenderness
o Ascites - Pleural effusions
27. 27
Classification of HF
New York Heart Association (NYHA)
Class I : symptoms of HF only at levels that would
limit normal individuals.
Class II : symptoms of HF with ordinary exertion
Class III : symptoms of HF on less than ordinary
exertion
Class IV : symptoms of HF at rest
28. 28
Classification of HF
American College of Cardiology and the American
Heart Association(ACC/AHA) Guidelines
Stage A : High risk of HF, without structural heart
disease or symptoms
Stage B : Heart disease with asymptomatic left
ventricular dysfunction
Stage C : Prior or current symptoms of HF
Stage D : Advanced heart disease and severely
symptomatic or refractory HF
30. 30
Investigation
I. LAB
A) Non specific
CBC(Since anemia can exacerbate heart failure)
Serum electrolytes and creatinine( before starting high
dose diuretics)
Fasting Blood glucose(To evaluate for possible diabetes
mellitus)
Thyroid function tests
Viral studies (If viral myocarditis suspected)
Others
31. 31
Investigation
I. LAB
B) Specific
BNP:
o With chronic heart failure, atrial myocytes secrete
increase amounts of atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) in response to high atrial
and ventricular filling pressures
o Promotes vasodilation, diuresis and natriuresis
o Usually is > 400 pg/mL in patients with dyspnea due to
heart failure.
34. 34
Investigation
III. Cardiac testing
ECG:
o May show specific cause of heart failure e.g Ischemic
heart disease
ECHO:
o Left ventricular ejection fraction
o Structural/valvular abnormalities
35. 35
Investigation
III. Cardiac testing
Exercise Testing
o Should be part of initial evaluation of all patients with
CHF.
Coronary arteriography
o Should be performed in patients presenting with heart
failure who have angina or significant ischemia
o Measure cardiac output, degree of left ventricular
dysfunction, and left ventricular end-diastolic pressure.
36. 36
Diagnosis of HF
HF should be suspected on the basis of clinical
presentation and radiographic findings.
It’s a clinical diagnosis. There is no diagnostic test!
Depressed ventricular EF should be confirmed with
echocardiography, or cardiac catheterization with left
ventriculography.
38. 38
Treatment
Management of Chronic heart failure:
General measures
Correct underlying cause
Remove precipitating cause
Prevention of deterioration of cardiac function
Control of congestive HF state
40. 40
Treatment
Nonpharmacologic therapy:
Exercise training:
o for stable HF patients increased exercise capacity,
decreased hospitalization rate, increased quality
of life, decreased symptoms.
Weight loss in obese patients
Dietary Na restriction
41. 41
Treatment
Nonpharmacologic therapy:
Fluid and free water restriction especially if
hyponatremic
Minimize medications known to have deleterious
effects on heart failure (negative inotrops, NSAIDs,
over-the-counter stimulants)
Oxygen
Fluid removal (dialysis, thoracentesis, paracentesis)
42. 42
Medical Treatment
Order of drug therapy
o Loop diuretics
o ACE inhibitor (or ARB if not tolerated)
o Beta blockers
o Digoxin
o Hydralazine, Nitrate
o Potassium sparing diuretics
43. 43
Medical Treatment
Diuretics
A. Loop diuretics
Furosemide, buteminide
For Fluid control, and to help relieve symptoms
B. Potassium-sparing diuretics
Spironolactone, eplerenone
Help enhance diuresis
Maintain potassium
Shown to improve survival in CHF
44. 44
Medical Treatment
ACE Inhibitor
Improve survival in patients with all severities of heart
failure.
Begin therapy low and titrate up as possible:
o Enalapril
o Captopril
o Lisinopril
If cannot tolerate, may try ARB
45. 45
Medical Treatment
Beta Blocker therapy
Certain Beta blockers (carvedilol, metoprolol,
bisoprolol) can improve overall survival in NYHA
class II to III HF, probably in class IV.
Contraindicated:
o Heart rate <60 bpm
o Symptomatic bradycardia
o Signs of peripheral hypoperfusion
o COPD, asthma
o Prolonged PR interval, 2nd or 3rd degree heart block
46. 46
Medical Treatment
Hydralazine plus Nitrates
Hydralazine + Isosorbide dinitrate
can be useful to reduce morbidity or mortality in
patients with current or prior symptomatic HF who
cannot be given an ACE inhibitor or ARB
Recommended for African Americans with NYHA
class III–IV
Decreased mortality, lower rates of hospitalization, and
improvement in quality of life.
47. 47
Medical Treatment
Digoxin
Given to patients with HF to control symptoms such as
fatigue, dyspnea, exercise intolerance
Digoxin can be used in HF patients with atrial
fibrillation to help rate control
Shown to significantly reduce hospitalization for heart
failure, but no benefit in terms of overall mortality.
48. 48
Medical Treatment
Other important medication
Statin therapy:
recommended in CHF for the secondary prevention of
cardiovascular disease.
Benefits:
o Improved LVEF(left ventricular ejection fraction)
o Reversal of ventricular remodeling
o Reduction in inflammatory markers e.g CRP
49. 49
Medical Treatment
Meds to AVOID in heart failure
NSAIDS
o Can cause worsening of pre-existing HF
Thiazolidinediones
o Cause fluid retention that can exacerbate HF
Metformin
o increased risk of potentially lactic acidosis
50. 50
Implantable Cardioverter-
Defibrillators for HF
Sustained ventricular
tachycardia is
associated with sudden
cardiac death in HF.
About one-third of
mortality in HF is due
to sudden cardiac
death.
52. 52
Acute Decompensated HF
Cardiogenic pulmonary edema is a common and
sometimes fatal cause of acute respiratory distress.
Characterized by the transudation of excess fluid into
the lungs secondary to an increase in left atrial and
subsequently pulmonary venous and pulmonary
capillary pressures.
53. 53
Acute Decompensated HF
Causes:
Acute MI
o Rupture of chordae tendinae/acute mitral valve
insufficiency
Volume Overload
o Transfusions, IV fluids
o Non-compliance with diuretics, diet (high salt intake)
Worsening valvular defect
o Aortic stenosis
55. 55
Acute Decompensated HF
Clinical manifestations:
Signs
o Tachypnea
o Tachycardia
o Hypertension/Hypotension
o Crackles on lung exam
o Increased JVD(jagular venous distension)
o S3, S4 or new murmur