This document summarizes a seminar on aortic regurgitation presented by Dr. Sachin Sondhi at IGMC Shimla on 13/08/2018. It discusses the causes and pathology of aortic regurgitation, including degenerative aortic dilation and diseases like Marfan syndrome. The pathophysiology of compensated and decompensated aortic regurgitation is explained. Physical exam findings like murmurs, pulse characteristics, and signs of heart failure are outlined. Symptoms may be initially absent but later include angina, dyspnea, and heart failure.
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
Echo assessment of lv systolic function and swmaFuad Farooq
This document discusses various techniques for assessing left ventricular systolic function using echocardiography, including:
- Visual assessment of endocardial motion and wall thickening to evaluate global and regional function
- Quantitative measures like fractional shortening, ejection fraction, and volumes
- Tissue Doppler imaging of mitral annular velocities
- Tissue tracking and strain imaging to evaluate timing and extent of myocardial contraction
- Wall motion scoring to characterize regional abnormalities
This document discusses atrioventricular septal defects (AVSDs), including their embryogenesis, classification, clinical features, imaging, and management. It describes the spectrum of AVSDs from partial to complete. Partial AVSDs involve a primum atrial septal defect with a cleft in the mitral valve. Complete AVSDs have a large ventricular septal defect with a common atrioventricular valve. Imaging like echocardiography is important for evaluating the anatomy and determining appropriate treatment, which ranges from observation to surgical repair.
This document discusses ECG patterns in congenital heart disease. It begins by outlining the significance of ECG in diagnosing congenital heart defects. It then provides an overview of normal ECG changes in children and how they evolve over time as hemodynamics change. Next, it describes how ECG can help identify situs and ventricular position. It then discusses the characteristic ECG patterns seen in common acyanotic defects like atrial septal defects and ventricular septal defects. It also covers cyanotic defects like transposition of the great arteries. The document provides detailed information on ECG features, associated conditions, complications and evolution over time for many different congenital heart defects.
This document discusses techniques for localizing the site of origin of ventricular tachycardia based on electrocardiogram characteristics. It describes that right ventricular outflow tract tachycardias typically present with left bundle branch block morphology while left ventricular sites may present with either right or left bundle branch block depending on exit site. Specific leads are discussed that can provide clues about anterior vs posterior, septal vs free wall origin within the outflow tracts. Other areas like fascicles, papillary muscles and mitral/tricuspid annuli are also summarized.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
This document outlines the integrated echocardiographic approach for assessing left ventricular diastolic function. It describes the four phases of diastole and how pulsed-wave, tissue, and color Doppler can be used to evaluate parameters like mitral inflow velocities, pulmonary vein flow, tissue velocities, and isovolumic relaxation time. By integrating measurements of left atrial size, ventricular filling velocities, annular velocities, and other Doppler data, diastolic dysfunction can be detected and graded.
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
Echo assessment of lv systolic function and swmaFuad Farooq
This document discusses various techniques for assessing left ventricular systolic function using echocardiography, including:
- Visual assessment of endocardial motion and wall thickening to evaluate global and regional function
- Quantitative measures like fractional shortening, ejection fraction, and volumes
- Tissue Doppler imaging of mitral annular velocities
- Tissue tracking and strain imaging to evaluate timing and extent of myocardial contraction
- Wall motion scoring to characterize regional abnormalities
This document discusses atrioventricular septal defects (AVSDs), including their embryogenesis, classification, clinical features, imaging, and management. It describes the spectrum of AVSDs from partial to complete. Partial AVSDs involve a primum atrial septal defect with a cleft in the mitral valve. Complete AVSDs have a large ventricular septal defect with a common atrioventricular valve. Imaging like echocardiography is important for evaluating the anatomy and determining appropriate treatment, which ranges from observation to surgical repair.
This document discusses ECG patterns in congenital heart disease. It begins by outlining the significance of ECG in diagnosing congenital heart defects. It then provides an overview of normal ECG changes in children and how they evolve over time as hemodynamics change. Next, it describes how ECG can help identify situs and ventricular position. It then discusses the characteristic ECG patterns seen in common acyanotic defects like atrial septal defects and ventricular septal defects. It also covers cyanotic defects like transposition of the great arteries. The document provides detailed information on ECG features, associated conditions, complications and evolution over time for many different congenital heart defects.
This document discusses techniques for localizing the site of origin of ventricular tachycardia based on electrocardiogram characteristics. It describes that right ventricular outflow tract tachycardias typically present with left bundle branch block morphology while left ventricular sites may present with either right or left bundle branch block depending on exit site. Specific leads are discussed that can provide clues about anterior vs posterior, septal vs free wall origin within the outflow tracts. Other areas like fascicles, papillary muscles and mitral/tricuspid annuli are also summarized.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
This document outlines the integrated echocardiographic approach for assessing left ventricular diastolic function. It describes the four phases of diastole and how pulsed-wave, tissue, and color Doppler can be used to evaluate parameters like mitral inflow velocities, pulmonary vein flow, tissue velocities, and isovolumic relaxation time. By integrating measurements of left atrial size, ventricular filling velocities, annular velocities, and other Doppler data, diastolic dysfunction can be detected and graded.
This document discusses left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). It defines LVH as an increase in left ventricle mass due to increased wall thickness or cavity size. There are two types of LVH - systolic overload from conditions like hypertension which compromise the left ventricle during systole, and diastolic overload from things like valvular diseases which compromise it during diastole. The document outlines ECG criteria for diagnosing LVH including Sokolov-Lyon and Cornell voltage criteria. It also discusses RVH manifestations on ECG like right axis deviation, tall R waves in right precordial leads, and an S1S2S3 pattern.
This document discusses the echocardiographic assessment of diastolic dysfunction. It outlines key parameters used to evaluate diastolic function including mitral inflow patterns, tissue Doppler imaging of mitral annular velocities, and pulmonary venous flow. Normal values for these parameters are provided. Guidelines for grading diastolic dysfunction according to the 2016 ASE/EACVI guidelines are presented. Special considerations for evaluating diastolic function in conditions like HCM, mitral stenosis, mitral regurgitation, and atrial fibrillation are also reviewed. Novel indices using speckle tracking echocardiography to assess diastolic function are mentioned.
M-mode echocardiography uses ultrasound to evaluate cardiac structures through motion over time. It can be used to assess morphology, movement, velocity and timing of valves and walls. Specific measurements are made of amplitudes, slopes, and time intervals which provide information on cardiac function. M-mode views of the mitral valve, aortic valve and left ventricle allow evaluation of values, wall motion, and calculation of ejection fraction, fractional shortening and left ventricular mass. Abnormal findings provide clues to conditions like valve disease, hypertrophy and ischemia.
Echocardiographic Evaluation of LV Diastolic FunctionJunhao Koh
The document discusses methods for evaluating left ventricular diastolic function using echocardiography. It describes the four phases of diastole, parameters used to assess diastolic function including mitral inflow patterns, mitral annular tissue Doppler, pulmonary vein flow, left atrial size and the Tei index. Grades of diastolic dysfunction and approaches from ASE/EAE and Mayo Clinic are summarized. Continuous wave Doppler of aortic regurgitation is also presented as a noninvasive method to evaluate left ventricular relaxation.
Hepatic veins - The Doppler interrogation Praveen Nagula
Doppler interrogation of the hepatic veins can provide information about underlying cardiovascular disorders by assessing changes in hepatic venous flow patterns related to cardiac cycle, respiration, and right heart pressures and function. Abnormal flow patterns seen on hepatic vein Doppler include increased systolic and diastolic waveforms with inspiration in constrictive pericarditis, prominent diastolic reversals with inspiration in restrictive cardiomyopathy, an enlarged and prolonged A wave in conditions with elevated right ventricular filling pressures, blunting of the S wave in right ventricular systolic dysfunction, and loss of the A wave with atrial fibrillation or arrhythmias causing atrioventricular dissociation.
1. The document discusses the management of single ventricle physiology, which involves connecting the systemic and pulmonary circulations in parallel rather than series due to the inability to establish two independent functioning ventricles.
2. The management involves initial palliation through procedures such as the bidirectional Glenn shunt or pulmonary artery banding, followed by definitive palliation with a Fontan operation around 3 years of age to connect the systemic venous return directly to the pulmonary arteries without an interposing ventricle.
3. The Fontan operation has evolved over time from atrio-pulmonary connections to total cavopulmonary connections using intra-atrial tunnels or extracardiac conduits to more efficiently direct superior vena c
This document provides an overview of echocardiography in pericardial diseases. It begins with an introduction to pericardial anatomy and pathophysiology. It then discusses various pericardial diseases that can be evaluated by echocardiography, including acute pericarditis, recurrent pericarditis, pericardial effusions, cardiac tamponade, and constrictive pericarditis. For each condition, it describes the echocardiographic findings and techniques used to evaluate the condition. It emphasizes that echocardiography is usually the initial imaging test of choice but that CT or CMR may be needed in some complex cases.
The document discusses guidelines for assessing diastolic dysfunction according to the ASE/EACVI 2016 guidelines. It defines diastolic dysfunction and describes the stages from grade I to grade IV. For each grade, it discusses the pathophysiology and key echocardiographic findings including mitral inflow patterns, tissue Doppler measurements, pulmonary vein flow, and left atrial size. The guidelines simplify the assessment of diastolic function into four grades based on parameters of left ventricular relaxation, left atrial pressure, mitral E/A ratio, E/e' ratio, pulmonary vein flow, and left atrial size.
This document provides an overview of segmental analysis for congenital heart disease. It discusses the key segments that are analyzed which include thoraco-abdominal situs, pulmonary situs, atrial situs, ventricular situs and looping, connections between segments (venous, atrioventricular, ventriculoarterial), and abnormalities that can occur in each segment. The document emphasizes evaluating each segment in a systematic, sequential manner to identify abnormalities.
Echo Differentiation of Restrictive Cardiomyopathy and Constrictive PericarditisJunhao Koh
1. The document compares and contrasts constrictive cardiomyopathy (CP) and restrictive cardiomyopathy (RCMP), discussing their definitions, etiologies, pathophysiology, and echocardiographic findings.
2. Key differences include CP presenting with thickened pericardium while RCMP presents with stiff myocardium. CP shows ventricular interdependence and respiratory variation on echo, while RCMP shows restrictive physiology from diastolic dysfunction.
3. Optimizing the echo exam is important for evaluating CP, including adjusting the respirometer waveform, Doppler sweep speed, and positions like upright to increase respiratory variation. Hepatic vein and SVC Doppler also help differentiate the conditions.
Echocardiographic evaluation of Aortic stenosisAswin Rm
This document discusses the echocardiographic evaluation of aortic stenosis. It describes assessing the anatomy and severity of AS through 2D and Doppler imaging. Key measurements include peak jet velocity, mean transvalvular pressure gradient, and aortic valve area calculated by the continuity equation. Grading of severity is based on an integrative approach using these Doppler and anatomical measurements. Causes, appearances, and complications of various types of AS are also reviewed.
Systolic anterior motion of mitral valve - SAMgagsol
This document summarizes the hospital course of an 80-year-old female admitted with weakness and nausea. Key findings include:
- Hypertrophic cardiomyopathy with systolic anterior motion (SAM) of the mitral valve was seen on echocardiogram.
- She developed respiratory acidosis and was intubated. Atrial fibrillation was also found.
- She was treated with antibiotics for possible sepsis, amiodarone for atrial fibrillation, and beta blockers were increased to control heart rate.
- SAM occurs in HCM and involves anterior movement of the mitral valve during systole, which can be exacerbated by factors like decreased preload. It is an
This document discusses ECG findings in various congenital heart diseases:
1) Acyanotic CHDs like atrial septal defect (ASD) show findings of right or left ventricular hypertrophy depending on shunt direction, while ventricular septal defect (VSD) shows signs of left or bi-ventricular overload.
2) Cyanotic CHDs like transposition of the great arteries (TGA) show right axis deviation and ventricular hypertrophy initially, evolving to match pulmonary blood flow. Tricuspid atresia typically shows left axis deviation and ventricular hypertrophy.
3) Algorithms are provided to systematically analyze ECG patterns and identify the underlying CHD based on chamber
A 73-year-old male presented with dizziness for 1 year and chest pain for 2 days. His ECG showed left bundle branch block (LBBB) and first-degree atrioventricular block, consistent with possible trifascicular block. Trifascicular block must be confirmed with bundle of His electrogram. The patient has abnormal conduction through one or more divisions of the intraventricular conduction system distal to the bundle of His, presenting as LBBB and first-degree AV block. This suggests involvement of the left and right bundles as well as the AV node, consistent with trifascicular block.
Dr. Sumedh S Ramteke's seminar discussed the jugular venous pulse (JVP) and how to assess it at the bedside. Key points included:
- The JVP reflects right atrial pressure and can be used to estimate central venous pressure.
- Waves include a, x, c, x', v, and y and indicate pressures in the right atrium and ventricle over the cardiac cycle.
- Abnormalities in different waves provide clues about underlying conditions like tricuspid regurgitation, constrictive pericarditis, and right heart failure.
- The JVP changes in characteristic ways with different arrhythmias and conduction defects. Assessment of the
This document provides an overview of echocardiographic assessment of mitral regurgitation. It describes the anatomy of the mitral valve including the leaflets, annulus, chordae, and papillary muscles. It discusses Carpentier's functional classification system for describing the mechanism of mitral valve dysfunction. Methods for assessing severity are covered, including color flow imaging, continuous wave Doppler, vena contracta width, proximal isovelocity surface area, and volumetric assessment. Key points are made about evaluating jet direction, duration, and velocity in context of blood pressure. The importance of assessing left ventricular and left atrial size and function is also highlighted.
The aortic valve has three cusps that open and close to regulate blood flow from the heart to the aorta. Aortic stenosis occurs when the valve opening narrows due to calcium buildup on the cusps. In the elderly, aortic stenosis is usually caused by age-related degeneration and calcification of the valve. Symptoms include chest pain, shortness of breath, and fainting. Diagnosis involves echocardiogram, Doppler ultrasound and cardiac catheterization. Treatment options include medications, balloon valvuloplasty, open-heart surgery to replace the valve, and newer transcatheter aortic valve replacement procedures for high-risk elderly patients.
The document discusses electrocardiogram (ECG) patterns associated with cardiac chamber enlargement, specifically right atrial enlargement (RAE) and left atrial enlargement (LAE). RAE is suggested by a tall, peaked P wave in leads II, III, AVF and a positive P wave in V1. LAE results in prolongation of the left atrial component of the P wave, increased posterior deviation of the left atrial vector, and left axis deviation of the P wave. The diagnostic accuracy of ECG findings for chamber enlargement is limited but can provide clues when correlated with imaging studies.
Echocardiographic screening for rheumatic heart diseaseRamachandra Barik
RHD affects ≈20 million people worldwide
highest in developing countries
significant morbidity and mortality
Subclinical detection adds to of secondary prophylaxis
echocardiographic definitions evolving
In 2012, the WHF published evidence-based
guidelines for the echocardiographic diagnosis of RHD
but these criteria have not yet been applied
1. Aortic regurgitation occurs when blood leaks backwards from the aorta into the left ventricle during diastole due to failure of the aortic valve leaflets to coapt properly.
2. It can be acute, caused by things like infective endocarditis or aortic dissection, or chronic, caused by conditions like bicuspid aortic valve or hypertension.
3. Chronic AR is often well-tolerated for years as the left ventricle dilates and hypertrophies to accommodate the increased volume, but acute AR can rapidly lead to heart failure and shock if not emergently treated.
Aortic regurgitation is a condition where the aortic valve leaks, causing blood to flow back into the left ventricle from the aorta during diastole. It can be chronic or acute, with chronic causes including rheumatic heart disease, infections, and connective tissue disorders. Symptoms are usually mild at first and include palpitations and fatigue, but can progress to cardiac failure. Signs include a high-volume pulse, elevated systolic blood pressure with low diastolic pressure, a diastolic murmur heard at the heart base, and signs of left ventricular volume overload. Echocardiography can confirm the diagnosis and severity. Treatment involves managing heart failure symptoms medically, but severe
This document discusses left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). It defines LVH as an increase in left ventricle mass due to increased wall thickness or cavity size. There are two types of LVH - systolic overload from conditions like hypertension which compromise the left ventricle during systole, and diastolic overload from things like valvular diseases which compromise it during diastole. The document outlines ECG criteria for diagnosing LVH including Sokolov-Lyon and Cornell voltage criteria. It also discusses RVH manifestations on ECG like right axis deviation, tall R waves in right precordial leads, and an S1S2S3 pattern.
This document discusses the echocardiographic assessment of diastolic dysfunction. It outlines key parameters used to evaluate diastolic function including mitral inflow patterns, tissue Doppler imaging of mitral annular velocities, and pulmonary venous flow. Normal values for these parameters are provided. Guidelines for grading diastolic dysfunction according to the 2016 ASE/EACVI guidelines are presented. Special considerations for evaluating diastolic function in conditions like HCM, mitral stenosis, mitral regurgitation, and atrial fibrillation are also reviewed. Novel indices using speckle tracking echocardiography to assess diastolic function are mentioned.
M-mode echocardiography uses ultrasound to evaluate cardiac structures through motion over time. It can be used to assess morphology, movement, velocity and timing of valves and walls. Specific measurements are made of amplitudes, slopes, and time intervals which provide information on cardiac function. M-mode views of the mitral valve, aortic valve and left ventricle allow evaluation of values, wall motion, and calculation of ejection fraction, fractional shortening and left ventricular mass. Abnormal findings provide clues to conditions like valve disease, hypertrophy and ischemia.
Echocardiographic Evaluation of LV Diastolic FunctionJunhao Koh
The document discusses methods for evaluating left ventricular diastolic function using echocardiography. It describes the four phases of diastole, parameters used to assess diastolic function including mitral inflow patterns, mitral annular tissue Doppler, pulmonary vein flow, left atrial size and the Tei index. Grades of diastolic dysfunction and approaches from ASE/EAE and Mayo Clinic are summarized. Continuous wave Doppler of aortic regurgitation is also presented as a noninvasive method to evaluate left ventricular relaxation.
Hepatic veins - The Doppler interrogation Praveen Nagula
Doppler interrogation of the hepatic veins can provide information about underlying cardiovascular disorders by assessing changes in hepatic venous flow patterns related to cardiac cycle, respiration, and right heart pressures and function. Abnormal flow patterns seen on hepatic vein Doppler include increased systolic and diastolic waveforms with inspiration in constrictive pericarditis, prominent diastolic reversals with inspiration in restrictive cardiomyopathy, an enlarged and prolonged A wave in conditions with elevated right ventricular filling pressures, blunting of the S wave in right ventricular systolic dysfunction, and loss of the A wave with atrial fibrillation or arrhythmias causing atrioventricular dissociation.
1. The document discusses the management of single ventricle physiology, which involves connecting the systemic and pulmonary circulations in parallel rather than series due to the inability to establish two independent functioning ventricles.
2. The management involves initial palliation through procedures such as the bidirectional Glenn shunt or pulmonary artery banding, followed by definitive palliation with a Fontan operation around 3 years of age to connect the systemic venous return directly to the pulmonary arteries without an interposing ventricle.
3. The Fontan operation has evolved over time from atrio-pulmonary connections to total cavopulmonary connections using intra-atrial tunnels or extracardiac conduits to more efficiently direct superior vena c
This document provides an overview of echocardiography in pericardial diseases. It begins with an introduction to pericardial anatomy and pathophysiology. It then discusses various pericardial diseases that can be evaluated by echocardiography, including acute pericarditis, recurrent pericarditis, pericardial effusions, cardiac tamponade, and constrictive pericarditis. For each condition, it describes the echocardiographic findings and techniques used to evaluate the condition. It emphasizes that echocardiography is usually the initial imaging test of choice but that CT or CMR may be needed in some complex cases.
The document discusses guidelines for assessing diastolic dysfunction according to the ASE/EACVI 2016 guidelines. It defines diastolic dysfunction and describes the stages from grade I to grade IV. For each grade, it discusses the pathophysiology and key echocardiographic findings including mitral inflow patterns, tissue Doppler measurements, pulmonary vein flow, and left atrial size. The guidelines simplify the assessment of diastolic function into four grades based on parameters of left ventricular relaxation, left atrial pressure, mitral E/A ratio, E/e' ratio, pulmonary vein flow, and left atrial size.
This document provides an overview of segmental analysis for congenital heart disease. It discusses the key segments that are analyzed which include thoraco-abdominal situs, pulmonary situs, atrial situs, ventricular situs and looping, connections between segments (venous, atrioventricular, ventriculoarterial), and abnormalities that can occur in each segment. The document emphasizes evaluating each segment in a systematic, sequential manner to identify abnormalities.
Echo Differentiation of Restrictive Cardiomyopathy and Constrictive PericarditisJunhao Koh
1. The document compares and contrasts constrictive cardiomyopathy (CP) and restrictive cardiomyopathy (RCMP), discussing their definitions, etiologies, pathophysiology, and echocardiographic findings.
2. Key differences include CP presenting with thickened pericardium while RCMP presents with stiff myocardium. CP shows ventricular interdependence and respiratory variation on echo, while RCMP shows restrictive physiology from diastolic dysfunction.
3. Optimizing the echo exam is important for evaluating CP, including adjusting the respirometer waveform, Doppler sweep speed, and positions like upright to increase respiratory variation. Hepatic vein and SVC Doppler also help differentiate the conditions.
Echocardiographic evaluation of Aortic stenosisAswin Rm
This document discusses the echocardiographic evaluation of aortic stenosis. It describes assessing the anatomy and severity of AS through 2D and Doppler imaging. Key measurements include peak jet velocity, mean transvalvular pressure gradient, and aortic valve area calculated by the continuity equation. Grading of severity is based on an integrative approach using these Doppler and anatomical measurements. Causes, appearances, and complications of various types of AS are also reviewed.
Systolic anterior motion of mitral valve - SAMgagsol
This document summarizes the hospital course of an 80-year-old female admitted with weakness and nausea. Key findings include:
- Hypertrophic cardiomyopathy with systolic anterior motion (SAM) of the mitral valve was seen on echocardiogram.
- She developed respiratory acidosis and was intubated. Atrial fibrillation was also found.
- She was treated with antibiotics for possible sepsis, amiodarone for atrial fibrillation, and beta blockers were increased to control heart rate.
- SAM occurs in HCM and involves anterior movement of the mitral valve during systole, which can be exacerbated by factors like decreased preload. It is an
This document discusses ECG findings in various congenital heart diseases:
1) Acyanotic CHDs like atrial septal defect (ASD) show findings of right or left ventricular hypertrophy depending on shunt direction, while ventricular septal defect (VSD) shows signs of left or bi-ventricular overload.
2) Cyanotic CHDs like transposition of the great arteries (TGA) show right axis deviation and ventricular hypertrophy initially, evolving to match pulmonary blood flow. Tricuspid atresia typically shows left axis deviation and ventricular hypertrophy.
3) Algorithms are provided to systematically analyze ECG patterns and identify the underlying CHD based on chamber
A 73-year-old male presented with dizziness for 1 year and chest pain for 2 days. His ECG showed left bundle branch block (LBBB) and first-degree atrioventricular block, consistent with possible trifascicular block. Trifascicular block must be confirmed with bundle of His electrogram. The patient has abnormal conduction through one or more divisions of the intraventricular conduction system distal to the bundle of His, presenting as LBBB and first-degree AV block. This suggests involvement of the left and right bundles as well as the AV node, consistent with trifascicular block.
Dr. Sumedh S Ramteke's seminar discussed the jugular venous pulse (JVP) and how to assess it at the bedside. Key points included:
- The JVP reflects right atrial pressure and can be used to estimate central venous pressure.
- Waves include a, x, c, x', v, and y and indicate pressures in the right atrium and ventricle over the cardiac cycle.
- Abnormalities in different waves provide clues about underlying conditions like tricuspid regurgitation, constrictive pericarditis, and right heart failure.
- The JVP changes in characteristic ways with different arrhythmias and conduction defects. Assessment of the
This document provides an overview of echocardiographic assessment of mitral regurgitation. It describes the anatomy of the mitral valve including the leaflets, annulus, chordae, and papillary muscles. It discusses Carpentier's functional classification system for describing the mechanism of mitral valve dysfunction. Methods for assessing severity are covered, including color flow imaging, continuous wave Doppler, vena contracta width, proximal isovelocity surface area, and volumetric assessment. Key points are made about evaluating jet direction, duration, and velocity in context of blood pressure. The importance of assessing left ventricular and left atrial size and function is also highlighted.
The aortic valve has three cusps that open and close to regulate blood flow from the heart to the aorta. Aortic stenosis occurs when the valve opening narrows due to calcium buildup on the cusps. In the elderly, aortic stenosis is usually caused by age-related degeneration and calcification of the valve. Symptoms include chest pain, shortness of breath, and fainting. Diagnosis involves echocardiogram, Doppler ultrasound and cardiac catheterization. Treatment options include medications, balloon valvuloplasty, open-heart surgery to replace the valve, and newer transcatheter aortic valve replacement procedures for high-risk elderly patients.
The document discusses electrocardiogram (ECG) patterns associated with cardiac chamber enlargement, specifically right atrial enlargement (RAE) and left atrial enlargement (LAE). RAE is suggested by a tall, peaked P wave in leads II, III, AVF and a positive P wave in V1. LAE results in prolongation of the left atrial component of the P wave, increased posterior deviation of the left atrial vector, and left axis deviation of the P wave. The diagnostic accuracy of ECG findings for chamber enlargement is limited but can provide clues when correlated with imaging studies.
Echocardiographic screening for rheumatic heart diseaseRamachandra Barik
RHD affects ≈20 million people worldwide
highest in developing countries
significant morbidity and mortality
Subclinical detection adds to of secondary prophylaxis
echocardiographic definitions evolving
In 2012, the WHF published evidence-based
guidelines for the echocardiographic diagnosis of RHD
but these criteria have not yet been applied
1. Aortic regurgitation occurs when blood leaks backwards from the aorta into the left ventricle during diastole due to failure of the aortic valve leaflets to coapt properly.
2. It can be acute, caused by things like infective endocarditis or aortic dissection, or chronic, caused by conditions like bicuspid aortic valve or hypertension.
3. Chronic AR is often well-tolerated for years as the left ventricle dilates and hypertrophies to accommodate the increased volume, but acute AR can rapidly lead to heart failure and shock if not emergently treated.
Aortic regurgitation is a condition where the aortic valve leaks, causing blood to flow back into the left ventricle from the aorta during diastole. It can be chronic or acute, with chronic causes including rheumatic heart disease, infections, and connective tissue disorders. Symptoms are usually mild at first and include palpitations and fatigue, but can progress to cardiac failure. Signs include a high-volume pulse, elevated systolic blood pressure with low diastolic pressure, a diastolic murmur heard at the heart base, and signs of left ventricular volume overload. Echocardiography can confirm the diagnosis and severity. Treatment involves managing heart failure symptoms medically, but severe
AR, or aortic regurgitation, occurs when the aortic valve does not close properly, allowing blood to flow backward into the left ventricle. It can be caused by damage to the aortic valve leaflets or distortion/dilation of the aortic root. In developed countries, the most common causes are aortic root dilation or a congenital bicuspid aortic valve. AR is more common in men than women. Symptomatic patients or asymptomatic patients with reduced ejection fraction or increased left ventricular dimensions require surgical treatment such as aortic valve replacement. The prognosis depends on symptoms and left ventricular function, with asymptomatic patients having normal ejection fraction having an excellent long-term prognosis.
This document discusses aortic valve stenosis, including its anatomy, function, causes, pathophysiology, classification, signs and symptoms, diagnostic evaluation, and treatment options. Key points include:
- Aortic stenosis is caused by calcification and stiffening of the aortic valve leaflets, restricting their opening and increasing the pressure gradient between the left ventricle and aorta.
- It can be congenital due to a bicuspid aortic valve or acquired from degeneration, rheumatic fever, or radiation exposure.
- Symptoms include angina, syncope, and dyspnea as the left ventricle hypertrophies and diastolic function declines in response to the increased
Aortic regurgitation occurs when the aortic valve does not close properly, allowing blood to flow back into the left ventricle. It can be caused by conditions that damage the aortic valve such as rheumatic fever or a congenital heart defect. Symptoms may include breathlessness, fatigue, and chest pain. Diagnosis is made through echocardiogram which can assess the severity. Treatment depends on severity but may involve lifestyle changes, medications, or aortic valve replacement surgery if symptoms worsen or damage to the heart progresses. Prognosis depends on severity and treatment, with severe untreated cases having a high risk of heart failure or sudden cardiac death.
Aortic stenosis is a narrowing of the aortic valve that obstructs blood flow from the left ventricle to the aorta. It is most commonly caused by calcification and fibrosis of the aortic valve. Symptoms include dyspnea, exertional dizziness, and exertional angina as the left ventricle has to work harder to maintain adequate cardiac output against the increased resistance. On examination, the carotid pulse is weak and delayed while auscultation reveals a crescendo-decrescendo systolic murmur best heard at the right upper sternal border that radiates to the carotid arteries. Management involves prompt aortic valve replacement for symptomatic severe aortic stenosis.
This document discusses left-to-right shunts, which involve recirculation of oxygenated blood back to the lungs. Common examples include atrial and ventricular septal defects as well as patent ductus arteriosus. The magnitude of shunting is determined by pulmonary and systemic vascular resistances, which change in the perinatal period. Large shunts can cause heart failure due to increased pulmonary blood flow and pressure overload on the left side of the heart. Medical management includes diuretics to reduce preload and afterload-reducing agents. Some smaller shunts may close spontaneously over time as pulmonary pressures decrease.
This document discusses pericardial diseases and various conditions that affect the pericardium. It begins by describing normal pericardial fluid volume and ventricular interdependence under normal conditions. It then discusses the history of using ultrasound to image the pericardium. Various pathological conditions are covered, including increased pericardial thickness in constrictive pericarditis, how intrapericardial pressure changes with fluid volume and pericardial stiffness, and signs of cardiac tamponade seen on echocardiogram like right atrial and ventricular collapse and IVC plethora. Finally, it describes the presentation of effusive-constrictive pericarditis.
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
NATURAL HISTORY, HEMODYNAMICS AND SURGICAL MANAGEMENT OF AORTIC STENOSIS.pptxShivani Rao
1) Natural history, hemodynamics, and surgical management of aortic stenosis is discussed. Aortic stenosis results from various etiologies and causes a reduction in aortic valve area, increasing pressure gradients and left ventricular hypertrophy.
2) Symptoms of aortic stenosis include angina, syncope and heart failure. Surgical aortic valve replacement is recommended for severe symptomatic stenosis to improve survival. Asymptomatic patients with severe stenosis may also benefit from early surgery, particularly if the stenosis is very severe or rapidly progressing.
3) Hemodynamic parameters like aortic jet velocity and mean pressure gradient determined by echocardiography are used to classify the severity of aortic stenosis and guide
This document discusses various types of valvular heart disease, including stenosis (narrowing of the valves), regurgitation (backward flow of blood through valves), aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency. It describes the causes, pathophysiology, clinical manifestations, diagnosis, and treatment of each condition. Valvular diseases are generally asymptomatic for years initially but can progress to cause heart failure if left untreated. Diagnosis is typically via echocardiogram and treatment involves lifestyle changes, medications, or valve repair/replacement surgery depending on severity.
Cardiac tamponade is a life-threatening condition caused by fluid accumulation in the pericardium that compresses the heart. Echocardiography is important for diagnosing tamponade and guiding treatment. Key echocardiographic signs include chamber collapse, increased ventricular interdependence seen on Doppler imaging, and inferior vena cava plethora. Echocardiography can also guide pericardiocentesis procedures to drain fluid from the pericardium. It is a useful non-invasive tool for both diagnosing and managing cardiac tamponade.
This document provides information on congestive cardiac failure (CCF), including its definition, pathophysiology, clinical features, investigations, and management. CCF occurs when the heart muscle is weakened and cannot maintain adequate cardiac output. The pathophysiology involves changes in preload, afterload, and contractility that decrease cardiac output. Compensatory mechanisms initially help but later worsen symptoms. Clinically, CCF presents with dyspnea, edema, elevated JVP, hepatomegaly, and other signs. Investigations include BNP, ECG, echocardiogram. Management focuses on treating the underlying cause, reducing preload/afterload, and improving contractility. Diuretics, ACE inhibitors, beta
The document discusses various types of valvular heart disease, including aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. It provides details on the causes, symptoms, physical exam findings, diagnostic tests and treatments for each condition. For aortic stenosis, the case describes a 67-year-old male with symptoms of dyspnea and chest pain, who is found to have a systolic thrill and murmur, indicating severe aortic valve stenosis. Diagnostic tests and treatments are outlined for each valvular disease.
Aortic stenosis is a narrowing of the aortic valve that obstructs blood flow from the left ventricle to the aorta. It can be congenital due to conditions like bicuspid aortic valve, or acquired through rheumatic heart disease, atherosclerosis or idiopathic hypertrophic subaortic stenosis. Over time, the obstruction causes the left ventricle to hypertrophy to maintain cardiac output, which can lead to heart failure. Symptoms include chest pain, syncope and dyspnea that worsen with exertion. Examination may reveal murmurs, decreased pulses and elevated blood pressure. Echocardiography can diagnose the severity of stenosis. Treatment involves managing symptoms, avoiding
1) Aortic regurgitation occurs when the aortic valve fails to close properly during diastole, allowing blood to flow back into the left ventricle from the aorta.
2) Chronic aortic regurgitation can increase left ventricular volume and pressure, potentially leading to heart failure. Symptoms may include dyspnea, orthopnea, and leg swelling.
3) Evaluation involves auscultating a characteristic decrescendo diastolic murmur and measuring widened pulse pressure. Echocardiography can quantify the regurgitant volume and assess left ventricular size and function.
4) Treatment depends on severity and chronicity. Mild cases may require monitoring but severe or symptomatic
Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, occurring in approximately 1 in 3,000 live births. It involves four abnormalities - a ventricular septal defect, right ventricular outflow tract obstruction, right ventricular hypertrophy, and overriding of the aorta. Without surgical repair, only 10% of patients survive beyond 20 years of age. Clinical manifestations include cyanosis, clubbing of the fingers and toes, and hypoxic spells in infants. Diagnosis is made through echocardiography, chest x-ray, and cardiac catheterization. Treatment involves palliative shunt procedures for infants or complete repair surgery to close the ventricular septal defect and widen the right ventricular
Similar to Pathophysiology of aortic regurgitation and management (20)
Surgical procedures for congenital heart diseases basicsSachin Sondhi
This document discusses surgical procedures for several congenital heart diseases, including modified Blalock-Taussig shunt (BT) vs classical BT, repair of tetralogy of Fallot (TOF), palliative procedures for TOF, indications and timing for complete TOF repair, repair of TOF with small pulmonary arteries using BT shunt, long term survival after TOF repair, Ebstein's anomaly indications and procedures, D-transposition of great arteries with ventricular septal defect and pulmonary stenosis repair, and Rastelli procedure details. Key details provided include success rates, complications risks, and considerations for various procedures.
Primary Pulmonary HTN Seminar on 19/11/2018
The seminar covered topics related to pulmonary hypertension (PH) including definitions, epidemiology, challenges in diagnosis and treatment, anatomy, pathobiology, genetics, and clinical presentation. PH is defined as a mean pulmonary arterial pressure of >25 mmHg and can be caused by various underlying disorders. Delayed diagnosis and treatment are common problems. The diagnosis requires right heart catheterization, though this test is underutilized. Guidelines for treatment are not always followed consistently.
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This document summarizes a seminar on aortic regurgitation presented by Dr. Sachin Sondhi at IGMC Shimla on 13/08/2018. It discusses the causes and pathology of aortic regurgitation, including degenerative aortic dilation and diseases affecting the aortic valve and root. The pathophysiology and hemodynamic changes in compensated and decompensated aortic regurgitation are explained. Symptoms, physical exam findings, murmurs and natural history are outlined. Indications for surgery include symptomatic patients or asymptomatic patients with reduced ejection fraction or severe left ventricular dilation. Vasodilator therapy may help preserve left ventricular function in some cases.
This document provides information on familial hypercholesterolemia (FH), including its definition, diagnostic criteria, clinical features, screening recommendations, and treatment. FH is a common genetic disorder characterized by elevated LDL cholesterol levels and a high risk of premature coronary heart disease. The majority of FH cases are caused by mutations in the LDLR gene. Diagnosis is based on clinical criteria including family and personal history of early heart disease as well as elevated LDL levels. Screening involves targeted screening of those with a family history as well as cascade screening of relatives. Treatment focuses on aggressively lowering LDL levels through lifestyle changes and cholesterol-lowering medications to reduce heart disease risk.
1. The seminar discussed coronary blood flow and myocardial oxygen consumption. Key determinants include heart rate, systolic pressure, and left ventricular contractility.
2. Myocardial oxygen extraction is near maximal at rest, so increases in demand are met by proportional increases in coronary flow and oxygen delivery.
3. Fractional flow reserve measures the ratio of distal coronary pressure to aortic pressure during maximal hyperemia. An FFR below 0.75 is associated with ischemia while above 0.80 is usually not.
This document summarizes the mechanisms of cardiac arrhythmias. It describes normal cardiac electrophysiology and the five phases of the cardiac action potential. It then discusses mechanisms that can disrupt normal rhythms, including altered automaticity, triggered activity due to afterdepolarizations, and reentry due to conduction blocks or barriers that allow circuits to form. Key features that help distinguish automatic from triggered from reentrant arrhythmias are described.
- Two strategies are used to manage patients with unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI): an early invasive strategy involving prompt coronary angiography and revascularization, or a conservative strategy using medical therapy and invasive procedures only for recurrent ischemia.
- A meta-analysis of 8 randomized controlled trials found that an early invasive strategy significantly reduced the composite of death, myocardial infarction, and rehospitalization for acute coronary syndrome compared to conservative care at 6 months follow-up in patients presenting with UA, but not in those with NSTEMI alone.
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A 24-year-old female presented with abnormal body movements and was found to have hypocalcemia. Laboratory workup showed low serum calcium, high phosphorus, and normal parathyroid hormone. She was diagnosed with hypoparathyroidism and treated with calcium supplementation, resulting in symptom improvement. The cause was determined to be idiopathic hypoparathyroidism.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
- 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
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
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.
3. • Degenerative aortic dilation,
• cystic medial necrosis of the aorta (either isolated or associated with
classic Marfan syndrome),
• aortic dilation related to bicuspid valves
• aortic dissection,
• osteogenesis imperfecta,
• syphilitic aortitis,
• ankylosing spondylitis,
• Behçet syndrome,
• psoriatic arthritis, arthritis associated with ulcerative colitis, relapsing
polychondritis,
• reactive arthritis, giant cell arteritis, and systemic hypertension, as well
as exposure to some appetite-suppressant drugs.
4. PATHOPHYSIOLOGY
1. Volume overload in LV EDV Increases Increase in chamber compliance (no increase
in EDP)
2. Increase in total SV, Forward stroke volume is maintained
3. New sarcomere (series) produces ecc. Hypertrophy
4. Although LV preload increases, LV preload at sarcomere level remains normal, Hence LV preload reserve
is maintained.
5. Augmented LV chamber volume increases wall stress and afterload, which causes concenteric hypertrophy
(AR is condition of both pressure and volume overload)
6. This produces compensated phase
7. Results in maintenance of EF, Forward stroke volume, normal diastolic pressure
8. Hemodynamic compensation lasts for decade
9. Balance between excessive afterload and combination of preload reserve and compensatory hypertrophy
cannot be maintained indefinitely.
10. Any further increase in afterload at this point decreases systolic ejection performance.
11. Symptoms of dyspnea or fatigue develop at this stage of transition.
12. Depressed LV function initially is potentially reversible process related to afterload mismatch and complete
reversal after AVR.
13. With time severe LV enlargement and remodeling and depressed function may predominate over
excessive loading as principal mechanism for declining function, at this stage AVR will not help in
regaining LV function.
5.
6.
7. • In compensated AR, sufficient wall thickening has occurred that the
ratio of ventricular wall thickness to cavity radius remains normal.
Under these conditions, end-diastolic wall stress is maintained at or
returns to normal levels.
• As AR persists and increases in severity over time, however, wall
thickening fails to keep pace with the hemodynamic load, and end-
systolic wall stress rises. At this point, the afterload mismatch results in
a decline in systolic function, and the ejection fraction falls
8. A, Normal conditions. B, The hemodynamic changes that occur in
severe acute AR. Although total stroke volume is increased, forward
stroke volume is reduced. LV end-diastolic pressure (LVEDP) rises
dramatically.
9. Hemodynamic changes occurring in chronic compensated aortic regurgitation are
shown. Eccentric hypertrophy produces increased end-diastolic volume (EDV), which
permits an increase in total, as well as forward, stroke volume. The volume overload is
accommodated, and LV filling pressure is normalized. Ventricular emptying and end-
systolic volume (ESV) remain normal.
10.
11. • In more severe cases of AR, the regurgitant flow may exceed 20 liters/min,
so the total LV output at rest approaches 25 liters/min, a level that can be
achieved acutely only by a trained endurance runner during maximal
exercise. Thus the adaptive response to gradually increasing, chronic AR
permits the ventricle to function as an effective high-compliance pump,
handling a large stroke volume, often with little increase in filling pressure.
• During exercise, peripheral vascular resistance declines and, with an increase
in heart rate, diastole shortens and the regurgitation per beat decreases,
facilitating an increment in effective (forward) cardiac output without
substantial increases in end-diastolic volume and pressure. The ejection
fraction and related ejection phase indices are often within normal limits,
both at rest and during exercise, even though myocardial function, as
reflected in the slope of the end-systolic pressure-volume relationship, is
depressed.
12. D, In chronic decompensated AR, impaired LV emptying produces an increase
in end-systolic volume and a fall in ejection fraction (EF), total stroke volume,
and forward stroke volume. Further cardiac dilation and re-elevation of LV
filling pressure occur. E, Immediately after valve replacement, preload estimated
by EDV decreases, as does filling pressure. ESV also is decreased, but to a lesser
extent. The result is an initial fall in EF. Despite these changes, elimination of
regurgitation leads to an increase in forward stroke volume, and with time
ejection fraction
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27. SYMPTOMS
• In chronic severe AR, the left ventricle gradually enlarges while the patient remains
asymptomatic for decades.
• Palpititions on lying down
• Forcefull pulsations in neck vessels
• Angina – 1. atherosclerosis 2. increased demand due to increase in mass 3. Low
coronary perfusion due to low diastolic pressure 4. osteal atherosclerotic narrowing in
luteal AR
• Nocturnal Angina - nocturnal angina may be troublesome and often is accompanied
by diaphoresis, which occurs when the heart rate slows and arterial diastolic pressure
falls to extremely low levels, attacks are frequently associated nightmares, dyspnea,
forceful heart skin flushing and profuse sweating.
• Symptoms of HF may be insidious dyspnea may occur for short periods of time or
may present before number of years before more severe symptoms of orthopnea or
PND develops.
28. Physical signs
• BP – Presence of completely normal BP excludes severe AR (SEV. AR – DBP around
40-50mm Hg)
• Heart Rate. Tachycardia shortens the time for diastolic reflux and thus may increase the
diastolic blood pressure in aortic regurgitation. Conversely, bradycardia will accentuate
the decrease in diastolic blood pressure because of the increased duration of aortic
regurgitation.
• Leg Blood Pressure. The normal increase in systolic blood pressure found in arteries
distal to the proximal aorta is exaggerated in aortic regurgitation. In severe aortic
incompetence, systolic pressure in the popliteal artery is much higher than in the
brachial artery (Hill's sign). A difference in systolic blood pressure between the arms and
the legs of greater than 40 to 50 mmHg typically is seen in major degrees of aortic
regurgitation.
29. Collapsing pulse in AR
1. Increased upstroke
due to increased
volume of ejection.
2. Downstroke -
Sudden fall in DBP
due regurgitation.
3. Due to rapid
emptying of arterial
system because of
aortic run off).
4. Aortic run off is
because of reflex
vasodilataion due to
over activation
baroreceptors (LOW
SVR).
30. Low cardiac output or heart failure may attenuate these signs. Arterial vasoconstriction occurs as stroke volume
falls. An increased heart rate in congestive heart failure (CHF) may also play a role in blunting the signs of aortic
regurgitation.
32. • S1 – Normal to soft (increase PR, decreased LV contractility, increased
LVEDP premature closure of MV), sometimes appears loud due to
fusion of ejection click
• S2 – Intensity is variable ( A2 soft in valvular and loud in aortic root
disease), splitt is narrow or single in severe AR (A2 moves to P2 due to
prolonged ejection time)
• S3 – In severe AR,
• An S3 often initiates an Austin Flint rumble when present
• S4 – In severe AR
33.
34. • Prominent murmur on right side – aortic aneurysm, sinus of
valsalva aneurysm, aortic dissection
• Sea gull or cooing dove murmer – loud musical quality due to
eversion or perforation of aortic cusp ( IE, Syphilis, trauma, ARF)
• When mitral stenosis coexists with AR, the obstruction to inflow
to left ventricular filling may attenuate the full expression of the
aortic regurgitation on clinical examination.
35. • Systolic Murmur. A systolic ejection murmur is common in moderate to severe aortic
regurgitation. It results from an abnormally large stroke volume that is ejected with
rapid force often across an anatomically deformed aortic valve into an enlarged
proximal aorta.
• Practical Point: A loud systolic murmur in a patient with severe aortic regurgitation
does not necessarily imply coexisting aortic stenosis. Typically, this systolic murmur is
short and peaks before the second half of systole if there is no aortic valve obstruction
(Figs. 15-5, 15-6B, C, 15-7A). However, with a very large ejected stroke volume the
systolic murmur lengthens in proportion to the increase in left ventricular ejection
time. Thickened aortic valve leaflets with minimal reduction in area of the aortic
orifice in the absence of a systolic left ventricular-aortic gradient may accentuate the
intensity and duration of the systolic murmur
36. • . In such instances, the systolic ejection murmur may be both loud
and long without true aortic stenosis being present. Severe aortic
regurgitation without stenosis rarely may be associated with a
grade 4/6 systolic murmur and an accompanying thrill. In these
difficult cases, the focus should be on any nonauscultatory signs of
aortic regurgitation, the blood pressure, and the quality of the
carotid pulse to assess the possibility of associated aortic stenosis.
Ifthe diastolic blood pressure is low,the pulse volume is full and
bounding, and there is evidence of peripheral vasodilation, aortic
stenosis can usually be readily excluded.
37. Austin Flint Murmur.
AFM is a low-pitched, rumbling apical diastolic murmur
that sounds exactly like the murmur of mitral stenosis
The mechanism for the genesis of the AFM has been
the focus of many investigators. Its presence generally
indicates a large diastolic leak with a regurgitant
fraction of over 50%.
38. • The mechanism appears to be related to an incomplete opening of the anterior leaflet of the mitral
valve during diastole as a result of the impact of the regurgitant stream of blood into the left
ventricular cavity.
• This premature closure of the mitral valve in mid-late diastole prevents left atrial contraction from
reopening the valve, and therefore, the presystolic component of the AFM is absent
• Other postulated mechanisms for the AFM include "relative or functional
mitral stenosis" (small left atrium, large left ventricle), diastolic mitral
regurgitation, fluttering or. vibration of the anterior leaflet of the mitral
valve resulting from the aortic diastolic jet, and selective transmission of low
to medium frequency vibrations of the aortic regurgitation murmur to the
apex. None of these phenomena adequately explain the AFM.
41. Asymptomatic Severe AR
AUTHOR PATIENTS AND
FOLLOW UP
PROGRESSION
TO
SYMPTOMS/LV
DYSFUNCTION/
DEATH
PROGRESSION
TO
ASYNPTOMATIC
LV dysfunction
BONOW ET AL 104 –
8YEARS
3.8%/YEAR 0.5%/year
TORNOS 101 –
4.6 YEARS
3%/YEAR 1.3%/YEAR
BORER 104 –
7.3 YEARS
6.2%/YEAR 0.9%/YEAR
AVERAGE 6.4 4.3%/YEAR 1.3%/YEAR
SUDDEN DEATH
0.19%/YEAR
BONOW ET AL – ESD IS SINGLE MOST IMPORTANT PREDICTOR ( ESD>50 HAS 19%
LIKLEHOOD OF PER YEAR DEATH/SYMPTOMS AND LV DYSFUNCTION. THOSE WITH
ESD BETWEEN 40-50 HAD 6% LIKEHOOD. THOSE WITH <40 HAD NO LIKLEHOOD
42.
43. ASYMPTOMATIC SEVERE AR WITH
LV DYSFUNCTION
SYMPTOMATIC SEVERE AR
PROGRESSION TO SYMPTOMS
25%/YEAR
>66% BECOME SYMPTOMATIC IN
2-3 YEARS
MORTALITY 10%/YEAR
HF 20%/YEAR
44. VASODILATOR THERAPY IN AR
• No specific therapy to prevent disease progression in chronic AR is currently
available. Uncertainty remains about whether patients with chronic AR and
evidence of significant volume overload (increased end-diastolic dimension or
volume) should be considered for vasodilator therapy to alter the natural
history of chronic LV volume overload.Short-term studies spanning 6 months
to 2 years have demonstrated beneficial hemodynamic effects of oral
hydralazine, nifedipine, felodipine, and ACE inhibitors.
• One concern about the use of any agent that appears to preserve the ejection
fraction is that it may mask progressive myocardial dysfunction; thus, when
the ejection fraction falls or becomes abnormal, myocardial dysfunction may
have progressed to such a degree that successful valve replacement may no
longer improve the ejection fraction.
45. randomly assigned 143 asymptomatic patients with isolated, severe aortic regurgitation and
normal left ventricular systolic function to receive either nifedipine (20 mg twice daily, 69
patients) or digoxin (0.25 mg daily, 74 patients).
Results
By actuarial analysis, we determined that after six years a mean (±SD) of 34 ±6 percent of the
patients in the digoxin group had undergone valve replacement, as compared with only 15 ±3
percent of those in the nifedipine group (P<0.001).
46.
47.
48. Determinants of outcome after valve
replacement
• Preoperative EF is most important
• Degree of Preoperative symptoms with same
degree of LV dysfunction
• Duration of preoperative symptoms
• EF <50%, LV DYSFUNCTION >18 MONTHS, ESD
> 55 MM, POOR EXERCISE TIME AND HIGHER
NYHA CLASS.
49. Indications of operation
• Because of their excellent prognosis in the short and
medium term, operative correction should be deferred in
patients with chronic severe AR who are asymptomatic,
exhibit good exercise tolerance, and have an ejection
fraction greater than 50% without severe LV dilation (i.e.,
end-systolic diameter 50 mm or less) or progressive LV
dilation on serial echocardiograms
50. • In the absence of obvious contraindications or
serious comorbidity, surgical treatment is advisable
for symptomatic patients with severe AR and for
asymptomatic patients with either an ejection
fraction of 50% or less or severe LV dilation (end-
systolic diameter >50 mm).
51.
52. • Asymptomatic patients with severe AR but normal LV
function have an excellent prognosis and do not require
prophylactic operation. On average, less than 6% of
patients/year require operation because of the development
of symptoms or of LV dysfunction
53. • Even after successful correction of AR,
patients with severe LV dysfunction may have
persistent cardiomegaly and depressed LV
function. Such patients often exhibit
persistent histologic changes in the left
ventricle, including massive fiber hypertrophy
and increased interstitial fibrous tissue.
Therefore it is highly desirable to operate on
patients before irreversible LV changes have
occurred.
54. • The indications for surgery for patients with severe AR secondary
to aortic sinus or ascending aortic disease are similar to those for
patients with primary valvular disease.
• However, progressive expansion of the aortic sinuses and/or
ascending aorta to a diameter greater than 55 mm with any degree
of regurgitation in patients with a bicuspid valve (or other
connective tissue disorder) also is an indication for repair of the
aortic sinuses or replacement of the ascending aorta.1
55. • This threshold is decreased to 50 mm in patients with risk factors
for dissection (family history of aortic dissection or rate of increase
in diameter of ≥0.5 cm/year). In addition, in patients with
indications for AVR as noted previously, concomitant surgery on
the aortic sinuses or ascending aorta is indicated if the amount of
aortic dilation is greater than 45 mm.