Mitral regurgitation is caused by abnormalities of the mitral valve leaflets, chordae tendineae, or annulus that prevent complete coaptation of the leaflets during systole. The main causes include degenerative diseases like mitral valve prolapse or rheumatic heart disease. Severe mitral regurgitation can lead to left atrial and ventricular dilation and dysfunction over time if left untreated. Echocardiography is the main imaging modality used to assess severity based on regurgitant jet area and velocity. Surgery is recommended for symptomatic patients or asymptomatic patients with severe regurgitation and abnormal ventricular size or function. Mitral valve repair is preferred over replacement when possible due to better long-
This document discusses aortic stenosis and aortic regurgitation. It defines aortic stenosis as a narrowing of the aortic valve opening, with common causes being a bicuspid aortic valve, calcification, or rheumatic heart disease. Symptoms include angina, syncope, and dyspnea. Diagnosis involves echocardiography. Treatment options are balloon valvuloplasty or valve replacement. Aortic regurgitation is defined as retrograde blood flow through the aortic valve during diastole. Common causes are rheumatic fever, hypertension, or a bicuspid valve. Symptoms progress from palpitations to dyspnea. Physical exam may reveal a wide pulse pressure.
This document discusses different types of valvular heart disease including stenosis, regurgitation, and functional regurgitation. It provides details on specific valve diseases like mitral stenosis, mitral regurgitation, aortic stenosis, and aortic regurgitation. For each condition, it outlines the causes, pathophysiology or effects, which depend on the degree and duration of the disease. Long term effects can include hypertrophy and failure of the left or right ventricle leading to pulmonary congestion, edema, and heart failure.
This document provides information on restrictive cardiomyopathy (RCM), including its definition, classification, etiology, symptoms, diagnosis, and treatment. Some key points:
- RCM is characterized by diastolic dysfunction with a stiffened myocardium that impairs ventricular filling. It is usually not associated with ventricular dilation or hypertrophy.
- Causes include infiltrative diseases of the myocardium (e.g. amyloidosis, sarcoidosis), endomyocardial fibrosis, and genetic/familial factors.
- Symptoms are related to reduced cardiac output and include dyspnea, fatigue, arrhythmias. Diagnosis involves echocardiogram, cardiac catheterization and MRI to evaluate
This document discusses cardiac tamponade, which occurs when fluid rapidly accumulates in the pericardial sac, putting pressure on the heart and reducing cardiac function. Key points include:
- Pericardial effusion puts pressure on the heart, causing symptoms like chest pain and shortness of breath.
- Cardiac tamponade occurs when a rapid accumulation of fluid in the pericardial sac severely compresses the heart.
- Echocardiography is useful for diagnosing tamponade by showing findings like pericardial effusion, right ventricular collapse, and reduced respiratory variation in blood flow velocities.
- Tamponade is a medical emergency treated initially with medications and peric
This document discusses aortic stenosis, including its causes, symptoms, diagnosis, and treatment. It notes that aortic stenosis can be valvular, subvalvular, or supravalvular and can be caused by rheumatic fever, congenital defects, or age-related calcification. Common symptoms include chest pain, shortness of breath, fatigue, and murmurs. Diagnosis involves echocardiogram, EKG, chest X-ray and cardiac catheterization. Treatment options range from medication to manage symptoms, balloon valvuloplasty, or aortic valve replacement surgery.
Mitral stenosis is usually caused by rheumatic fever, which causes fusion and thickening of the mitral valve, restricting its opening. This restricts blood flow from the left atrium to the left ventricle, causing left atrial pressure to rise and lead to pulmonary congestion and breathlessness. The elevated left atrial pressure also raises pulmonary pressures over time, causing pulmonary hypertension, right heart strain, and eventual right heart failure if left untreated. Diagnosis is made through echocardiogram and symptoms include dyspnea, fatigue, chest pain, cough, and palpitations from potential atrial fibrillation. Treatment involves antibiotics to prevent future rheumatic fever, diuretics, and potentially mitral
Mitral regurgitation is caused by abnormalities of the mitral valve leaflets, chordae tendineae, or annulus that prevent complete coaptation of the leaflets during systole. The main causes include degenerative diseases like mitral valve prolapse or rheumatic heart disease. Severe mitral regurgitation can lead to left atrial and ventricular dilation and dysfunction over time if left untreated. Echocardiography is the main imaging modality used to assess severity based on regurgitant jet area and velocity. Surgery is recommended for symptomatic patients or asymptomatic patients with severe regurgitation and abnormal ventricular size or function. Mitral valve repair is preferred over replacement when possible due to better long-
This document discusses aortic stenosis and aortic regurgitation. It defines aortic stenosis as a narrowing of the aortic valve opening, with common causes being a bicuspid aortic valve, calcification, or rheumatic heart disease. Symptoms include angina, syncope, and dyspnea. Diagnosis involves echocardiography. Treatment options are balloon valvuloplasty or valve replacement. Aortic regurgitation is defined as retrograde blood flow through the aortic valve during diastole. Common causes are rheumatic fever, hypertension, or a bicuspid valve. Symptoms progress from palpitations to dyspnea. Physical exam may reveal a wide pulse pressure.
This document discusses different types of valvular heart disease including stenosis, regurgitation, and functional regurgitation. It provides details on specific valve diseases like mitral stenosis, mitral regurgitation, aortic stenosis, and aortic regurgitation. For each condition, it outlines the causes, pathophysiology or effects, which depend on the degree and duration of the disease. Long term effects can include hypertrophy and failure of the left or right ventricle leading to pulmonary congestion, edema, and heart failure.
This document provides information on restrictive cardiomyopathy (RCM), including its definition, classification, etiology, symptoms, diagnosis, and treatment. Some key points:
- RCM is characterized by diastolic dysfunction with a stiffened myocardium that impairs ventricular filling. It is usually not associated with ventricular dilation or hypertrophy.
- Causes include infiltrative diseases of the myocardium (e.g. amyloidosis, sarcoidosis), endomyocardial fibrosis, and genetic/familial factors.
- Symptoms are related to reduced cardiac output and include dyspnea, fatigue, arrhythmias. Diagnosis involves echocardiogram, cardiac catheterization and MRI to evaluate
This document discusses cardiac tamponade, which occurs when fluid rapidly accumulates in the pericardial sac, putting pressure on the heart and reducing cardiac function. Key points include:
- Pericardial effusion puts pressure on the heart, causing symptoms like chest pain and shortness of breath.
- Cardiac tamponade occurs when a rapid accumulation of fluid in the pericardial sac severely compresses the heart.
- Echocardiography is useful for diagnosing tamponade by showing findings like pericardial effusion, right ventricular collapse, and reduced respiratory variation in blood flow velocities.
- Tamponade is a medical emergency treated initially with medications and peric
This document discusses aortic stenosis, including its causes, symptoms, diagnosis, and treatment. It notes that aortic stenosis can be valvular, subvalvular, or supravalvular and can be caused by rheumatic fever, congenital defects, or age-related calcification. Common symptoms include chest pain, shortness of breath, fatigue, and murmurs. Diagnosis involves echocardiogram, EKG, chest X-ray and cardiac catheterization. Treatment options range from medication to manage symptoms, balloon valvuloplasty, or aortic valve replacement surgery.
Mitral stenosis is usually caused by rheumatic fever, which causes fusion and thickening of the mitral valve, restricting its opening. This restricts blood flow from the left atrium to the left ventricle, causing left atrial pressure to rise and lead to pulmonary congestion and breathlessness. The elevated left atrial pressure also raises pulmonary pressures over time, causing pulmonary hypertension, right heart strain, and eventual right heart failure if left untreated. Diagnosis is made through echocardiogram and symptoms include dyspnea, fatigue, chest pain, cough, and palpitations from potential atrial fibrillation. Treatment involves antibiotics to prevent future rheumatic fever, diuretics, and potentially mitral
The document outlines mitral regurgitation (MR), including its definition, causes, progression, signs and symptoms, and diagnostic tests. MR occurs when the mitral valve does not close properly, allowing blood to flow back into the left atrium. It begins as an acute condition but can progress to chronic compensated and decompensated phases. In acute and decompensated phases, symptoms include heart failure signs. Chronic compensated MR often presents without symptoms. Diagnosis involves physical exam, echocardiogram, and other cardiac tests.
mitral regurgitation american guidlines 2014Basem Enany
This document discusses mitral regurgitation (MR), including its etiology, clinical manifestations, physical exam findings, diagnostic testing, and management according to American Heart Association guidelines. The most common cause of primary MR in developed countries is mitral valve prolapse. Secondary MR is usually caused by ischemic heart disease, left ventricular dysfunction, or hypertrophic cardiomyopathy. Diagnosis involves echocardiography to determine the severity and mechanism of MR. Management is generally medical for mild MR but may involve surgery for severe primary MR.
Pathophysiology of aortic regurgitation and managementSachin Sondhi
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.
The mitral valve lies between the left atrium and left ventricle. Mitral stenosis is usually caused by rheumatic fever which causes scarring of the mitral valve leaflets and commissures. In early mitral stenosis, the leaflets can open but have restricted motion. Over time, the leaflets become thickened and rigid, reducing valve opening. This causes symptoms like dyspnea and pulmonary hypertension. On examination, findings may include an irregular pulse from atrial fibrillation, elevated jugular venous pressure, accentuated S1, and a diastolic murmur. Severe mitral stenosis can lead to right heart failure and complications like hemoptysis.
Mitral valve prolapse (MVP) is a common condition where the mitral valve leaflets bulge into the left atrium during systole. While often asymptomatic, it can increase the risk of arrhythmias, endocarditis, stroke, and mitral regurgitation. The classic findings are a mid-to-late systolic click and murmur. Treatment involves monitoring for complications and addressing symptoms like with beta-blockers. For severe mitral regurgitation, early surgical repair is recommended to prevent left ventricular dysfunction.
ECG- Atrial Fibrillation, CXR-P/A view-Cardiomegaly,
Echocardiogram-severe mitral stenosis with severe MR with
moderate pulmonary hypertension. Patient underwent MVR and
she is doing well.
Left ventricular outflow tract obstructions are stenotic lesions in the left ventricular outflow tract that obstruct blood flow. They impose increased pressure load on the left ventricle and can lead to ventricular hypertrophy and failure if left untreated. Clinical manifestations include acute hemodynamic deterioration, shock, and end organ injury in newborns. Long term, patients are at risk for shortness of breath, chest pain, and fainting. Treatment involves surgical intervention such as balloon valvuloplasty or valve replacement to restore blood flow. All patients with LVOTO are at lifetime risk for infective endocarditis.
The document provides information on aortic valve disease including anatomy, etiology, and pathophysiology. It describes the key components of the aortic root including the aortic annulus, cusps, sinuses, and sinotubular junction. The three main causes of aortic stenosis are discussed as congenital bicuspid valve with calcification, calcification of a normal trileaflet valve, and rheumatic disease. The pathophysiology of aortic stenosis involves left ventricular pressure overload leading to hypertrophy and eventually decreased ejection fraction if severe stenosis is not corrected.
Restrictive cardiomyopathy is characterized by stiff ventricles that do not fill properly, though systolic function is usually preserved initially. It can be caused by infiltrative diseases, fibrosis, or other processes that restrict ventricular filling. On echocardiogram, restrictive cardiomyopathy shows impaired ventricular filling and enlarged atria, while cardiac catheterization reveals elevated diastolic pressures and a distinctive "square root sign" pressure tracing. Treatment focuses on managing symptoms and underlying causes if identifiable, though prognosis is often poor without transplantation.
The document discusses diseases of the aorta, including congenital anomalies, aortic aneurysms, and aortic dissections. It describes the structure and function of the aorta and risk factors for diseases like smoking and hypertension. Symptoms, investigations, and treatments are outlined for different aortic conditions such as thoracic and abdominal aortic aneurysms. Surgical and endovascular repair options are discussed for larger aneurysms at higher risk of rupture.
The document discusses aortic regurgitation, including its anatomy, etiology, pathophysiology, epidemiology, clinical manifestations, diagnosis, and management. Key points include:
- Aortic regurgitation occurs when the aortic valve fails to close properly, allowing blood to flow back into the left ventricle during diastole.
- Causes include conditions like infective endocarditis, bicuspid aortic valve, hypertension, and Marfan syndrome.
- In acute severe cases, a rapid increase in left ventricular preload can cause pulmonary edema and cardiogenic shock. Chronic cases involve left ventricular dilation and hypertrophy to compensate for the increased preload over time.
- Physical exam may
This document discusses the use of echocardiography in evaluating various types of cardiomyopathies. It provides echocardiographic features of dilated cardiomyopathy including dilated chambers, normal wall thickness, and complications like mitral regurgitation. Hypertrophic cardiomyopathy features include unexplained hypertrophy, diastolic dysfunction, and left ventricular outflow tract obstruction. Restrictive cardiomyopathies show hypertrophy, enlarged atria, restricted filling, and elevated pressures. Left ventricular non-compaction and arrhythmogenic right ventricular cardiomyopathy also have distinct echocardiographic characteristics described.
This document summarizes electrocardiogram (ECG) findings related to myocardial infarction (MI). It describes the ECG changes that occur in the hyperacute, evolved, and chronic phases of MI. These include ST segment elevation, T wave changes, Q wave development, and other abnormalities. It also discusses ECG patterns related to injury of specific coronary artery territories and criteria for diagnosing MI when a left bundle branch block is present.
Constrictive pericarditis is caused by scarring and thickening of the pericardium, restricting cardiac filling. It is diagnosed using echocardiography which shows septal bounce, exaggerated mitral inflow, and hepatic vein reversal. While similar to restrictive cardiomyopathy, constrictive pericarditis shows increased ventricular interaction and respiratory effects on cardiac physiology. Surgical pericardiectomy is usually required for treatment but is high risk, with post-op complications common. Long-term survival depends on the underlying cause of constriction.
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.
This document discusses different types of valvular heart disease. It begins by explaining that valvular heart disease is characterized by damage or defects to the heart's valves, which normally ensure proper blood flow. Stenotic valves become narrowed and prevent full opening, while incompetent valves do not close completely and allow blood to leak back. Over time, the heart compensates by enlarging and thickening, losing efficiency.
The document then examines specific valve diseases in more detail, outlining their causes, effects on heart function, symptoms, diagnostic tests, and treatment options. Diseases covered include mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, tricuspid regurgitation
The document summarizes mitral regurgitation (MR), including its anatomy, causes, clinical presentation, diagnosis, and management. The main causes of MR include mitral valve prolapse, rheumatic heart disease, infective endocarditis, cardiomyopathy, and ischemic heart disease. Physical exam may reveal an apical holosystolic murmur radiating to the axilla. Echocardiography can quantify the degree of MR and assess left ventricular function. Treatment depends on severity of symptoms and left ventricular function.
The document discusses various types of heart valve disorders including stenosis, regurgitation, and prolapse of the mitral, aortic, tricuspid, and pulmonary valves. It describes the causes, effects, symptoms, treatments including medications, valvuloplasty, and valve replacement surgery for each type of valve disorder. Nursing diagnoses and interventions are also provided focusing on monitoring cardiac function and output, managing fluid volume and electrolytes, conserving energy, and educating the patient.
This document discusses various valvular heart diseases including global burden, aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. Key points include: rheumatic heart disease is a leading cause in developing countries while age-related calcific disease is most common in developed nations; surgical options depend on severity and include valve repair/replacement; complications can include atrial fibrillation, pulmonary hypertension, and systemic embolism. Medical management focuses on symptom control through medications and lifestyle changes while surgery aims to correct valvular abnormalities.
A short update on aortic regurgitation drmohitmathur
Aortic regurgitation can be caused by primary valve disease or primary aortic root disease. In the initial stages, increased blood flow to the left ventricle maintains cardiac output but causes increased pressure over time. Eventually, the left ventricle's function deteriorates as blood flows backward, leading to further enlargement and heart failure if untreated. Surgical replacement of the aortic valve is often needed to treat severe chronic aortic regurgitation before left ventricular dysfunction progresses. Homoeopathic treatment may help prevent immune-mediated valve damage in some cases.
Valvular Heart Disease-Fifth year students-27-7-22 . Samir Rafla.pptxSamirRafla1
This document provides an overview of mitral stenosis, including its etiology, pathophysiology, symptoms, physical exam findings, diagnostic testing, and management. Key points include:
- Mitral stenosis is usually caused by rheumatic fever and leads to thickening and fusion of the mitral valve leaflets.
- It causes elevated left atrial pressure and pulmonary hypertension over time.
- Symptoms include dyspnea and hemoptysis due to pulmonary congestion. Physical exam may reveal a diastolic murmur and opening snap.
- Echocardiogram can assess the severity of stenosis while ECG often shows left atrial enlargement. Treatment involves managing pulmonary congestion, rate control for
The document outlines mitral regurgitation (MR), including its definition, causes, progression, signs and symptoms, and diagnostic tests. MR occurs when the mitral valve does not close properly, allowing blood to flow back into the left atrium. It begins as an acute condition but can progress to chronic compensated and decompensated phases. In acute and decompensated phases, symptoms include heart failure signs. Chronic compensated MR often presents without symptoms. Diagnosis involves physical exam, echocardiogram, and other cardiac tests.
mitral regurgitation american guidlines 2014Basem Enany
This document discusses mitral regurgitation (MR), including its etiology, clinical manifestations, physical exam findings, diagnostic testing, and management according to American Heart Association guidelines. The most common cause of primary MR in developed countries is mitral valve prolapse. Secondary MR is usually caused by ischemic heart disease, left ventricular dysfunction, or hypertrophic cardiomyopathy. Diagnosis involves echocardiography to determine the severity and mechanism of MR. Management is generally medical for mild MR but may involve surgery for severe primary MR.
Pathophysiology of aortic regurgitation and managementSachin Sondhi
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.
The mitral valve lies between the left atrium and left ventricle. Mitral stenosis is usually caused by rheumatic fever which causes scarring of the mitral valve leaflets and commissures. In early mitral stenosis, the leaflets can open but have restricted motion. Over time, the leaflets become thickened and rigid, reducing valve opening. This causes symptoms like dyspnea and pulmonary hypertension. On examination, findings may include an irregular pulse from atrial fibrillation, elevated jugular venous pressure, accentuated S1, and a diastolic murmur. Severe mitral stenosis can lead to right heart failure and complications like hemoptysis.
Mitral valve prolapse (MVP) is a common condition where the mitral valve leaflets bulge into the left atrium during systole. While often asymptomatic, it can increase the risk of arrhythmias, endocarditis, stroke, and mitral regurgitation. The classic findings are a mid-to-late systolic click and murmur. Treatment involves monitoring for complications and addressing symptoms like with beta-blockers. For severe mitral regurgitation, early surgical repair is recommended to prevent left ventricular dysfunction.
ECG- Atrial Fibrillation, CXR-P/A view-Cardiomegaly,
Echocardiogram-severe mitral stenosis with severe MR with
moderate pulmonary hypertension. Patient underwent MVR and
she is doing well.
Left ventricular outflow tract obstructions are stenotic lesions in the left ventricular outflow tract that obstruct blood flow. They impose increased pressure load on the left ventricle and can lead to ventricular hypertrophy and failure if left untreated. Clinical manifestations include acute hemodynamic deterioration, shock, and end organ injury in newborns. Long term, patients are at risk for shortness of breath, chest pain, and fainting. Treatment involves surgical intervention such as balloon valvuloplasty or valve replacement to restore blood flow. All patients with LVOTO are at lifetime risk for infective endocarditis.
The document provides information on aortic valve disease including anatomy, etiology, and pathophysiology. It describes the key components of the aortic root including the aortic annulus, cusps, sinuses, and sinotubular junction. The three main causes of aortic stenosis are discussed as congenital bicuspid valve with calcification, calcification of a normal trileaflet valve, and rheumatic disease. The pathophysiology of aortic stenosis involves left ventricular pressure overload leading to hypertrophy and eventually decreased ejection fraction if severe stenosis is not corrected.
Restrictive cardiomyopathy is characterized by stiff ventricles that do not fill properly, though systolic function is usually preserved initially. It can be caused by infiltrative diseases, fibrosis, or other processes that restrict ventricular filling. On echocardiogram, restrictive cardiomyopathy shows impaired ventricular filling and enlarged atria, while cardiac catheterization reveals elevated diastolic pressures and a distinctive "square root sign" pressure tracing. Treatment focuses on managing symptoms and underlying causes if identifiable, though prognosis is often poor without transplantation.
The document discusses diseases of the aorta, including congenital anomalies, aortic aneurysms, and aortic dissections. It describes the structure and function of the aorta and risk factors for diseases like smoking and hypertension. Symptoms, investigations, and treatments are outlined for different aortic conditions such as thoracic and abdominal aortic aneurysms. Surgical and endovascular repair options are discussed for larger aneurysms at higher risk of rupture.
The document discusses aortic regurgitation, including its anatomy, etiology, pathophysiology, epidemiology, clinical manifestations, diagnosis, and management. Key points include:
- Aortic regurgitation occurs when the aortic valve fails to close properly, allowing blood to flow back into the left ventricle during diastole.
- Causes include conditions like infective endocarditis, bicuspid aortic valve, hypertension, and Marfan syndrome.
- In acute severe cases, a rapid increase in left ventricular preload can cause pulmonary edema and cardiogenic shock. Chronic cases involve left ventricular dilation and hypertrophy to compensate for the increased preload over time.
- Physical exam may
This document discusses the use of echocardiography in evaluating various types of cardiomyopathies. It provides echocardiographic features of dilated cardiomyopathy including dilated chambers, normal wall thickness, and complications like mitral regurgitation. Hypertrophic cardiomyopathy features include unexplained hypertrophy, diastolic dysfunction, and left ventricular outflow tract obstruction. Restrictive cardiomyopathies show hypertrophy, enlarged atria, restricted filling, and elevated pressures. Left ventricular non-compaction and arrhythmogenic right ventricular cardiomyopathy also have distinct echocardiographic characteristics described.
This document summarizes electrocardiogram (ECG) findings related to myocardial infarction (MI). It describes the ECG changes that occur in the hyperacute, evolved, and chronic phases of MI. These include ST segment elevation, T wave changes, Q wave development, and other abnormalities. It also discusses ECG patterns related to injury of specific coronary artery territories and criteria for diagnosing MI when a left bundle branch block is present.
Constrictive pericarditis is caused by scarring and thickening of the pericardium, restricting cardiac filling. It is diagnosed using echocardiography which shows septal bounce, exaggerated mitral inflow, and hepatic vein reversal. While similar to restrictive cardiomyopathy, constrictive pericarditis shows increased ventricular interaction and respiratory effects on cardiac physiology. Surgical pericardiectomy is usually required for treatment but is high risk, with post-op complications common. Long-term survival depends on the underlying cause of constriction.
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.
This document discusses different types of valvular heart disease. It begins by explaining that valvular heart disease is characterized by damage or defects to the heart's valves, which normally ensure proper blood flow. Stenotic valves become narrowed and prevent full opening, while incompetent valves do not close completely and allow blood to leak back. Over time, the heart compensates by enlarging and thickening, losing efficiency.
The document then examines specific valve diseases in more detail, outlining their causes, effects on heart function, symptoms, diagnostic tests, and treatment options. Diseases covered include mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, tricuspid regurgitation
The document summarizes mitral regurgitation (MR), including its anatomy, causes, clinical presentation, diagnosis, and management. The main causes of MR include mitral valve prolapse, rheumatic heart disease, infective endocarditis, cardiomyopathy, and ischemic heart disease. Physical exam may reveal an apical holosystolic murmur radiating to the axilla. Echocardiography can quantify the degree of MR and assess left ventricular function. Treatment depends on severity of symptoms and left ventricular function.
The document discusses various types of heart valve disorders including stenosis, regurgitation, and prolapse of the mitral, aortic, tricuspid, and pulmonary valves. It describes the causes, effects, symptoms, treatments including medications, valvuloplasty, and valve replacement surgery for each type of valve disorder. Nursing diagnoses and interventions are also provided focusing on monitoring cardiac function and output, managing fluid volume and electrolytes, conserving energy, and educating the patient.
This document discusses various valvular heart diseases including global burden, aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. Key points include: rheumatic heart disease is a leading cause in developing countries while age-related calcific disease is most common in developed nations; surgical options depend on severity and include valve repair/replacement; complications can include atrial fibrillation, pulmonary hypertension, and systemic embolism. Medical management focuses on symptom control through medications and lifestyle changes while surgery aims to correct valvular abnormalities.
A short update on aortic regurgitation drmohitmathur
Aortic regurgitation can be caused by primary valve disease or primary aortic root disease. In the initial stages, increased blood flow to the left ventricle maintains cardiac output but causes increased pressure over time. Eventually, the left ventricle's function deteriorates as blood flows backward, leading to further enlargement and heart failure if untreated. Surgical replacement of the aortic valve is often needed to treat severe chronic aortic regurgitation before left ventricular dysfunction progresses. Homoeopathic treatment may help prevent immune-mediated valve damage in some cases.
Valvular Heart Disease-Fifth year students-27-7-22 . Samir Rafla.pptxSamirRafla1
This document provides an overview of mitral stenosis, including its etiology, pathophysiology, symptoms, physical exam findings, diagnostic testing, and management. Key points include:
- Mitral stenosis is usually caused by rheumatic fever and leads to thickening and fusion of the mitral valve leaflets.
- It causes elevated left atrial pressure and pulmonary hypertension over time.
- Symptoms include dyspnea and hemoptysis due to pulmonary congestion. Physical exam may reveal a diastolic murmur and opening snap.
- Echocardiogram can assess the severity of stenosis while ECG often shows left atrial enlargement. Treatment involves managing pulmonary congestion, rate control for
This document provides information on valvular heart disease, focusing on mitral stenosis and mitral regurgitation. It discusses the etiology, pathophysiology, symptoms, physical exam findings, diagnostic testing, and treatment recommendations for each condition. Mitral stenosis is typically caused by rheumatic fever and leads to pulmonary hypertension from elevated left atrial pressures. Mitral regurgitation can result from several causes including rheumatic heart disease, papillary muscle dysfunction, and mitral valve prolapse. Physical exam findings help distinguish the murmurs associated with each condition. Echocardiography is important for diagnosis and determining treatment approach.
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 the chronic sequelae of rheumatic fever, including various types of valvular heart disease and myocarditis. It provides details on the pathogenesis, clinical presentation, investigations and management of mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, tricuspid stenosis and tricuspid regurgitation. Echocardiography and Doppler ultrasound are important diagnostic tools, and treatment involves medical management as well as surgical interventions like valvuloplasty or valve replacement depending on the severity of disease.
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.
The document discusses mitral stenosis and mitral regurgitation. For mitral stenosis, rheumatic heart disease is the leading cause and results in thickening and fusion of the mitral valve leaflets. This narrowing of the valve orifice leads to elevated left atrial pressures and pulmonary hypertension. Symptoms include dyspnea and palpitations. Mitral regurgitation can be acute or chronic, and has various etiologies such as rheumatic heart disease. Chronic mitral regurgitation results in left ventricular and left atrial enlargement, while acute mitral regurgitation can cause pulmonary edema due to a sudden rise in left atrial pressures. Echocardiography is important for evaluating
1. Mitral stenosis is most commonly caused by rheumatic fever and results in thickening and calcification of the mitral valve, reducing the valve orifice area and obstructing blood flow from the left atrium to ventricle.
2. The pathophysiology involves elevated left atrial pressure, pulmonary hypertension, and reduced cardiac output. Symptoms range from easy fatigability to pulmonary edema.
3. Physical exam findings include an opening snap, rumbling diastolic murmur, and signs of right heart failure in severe cases. Severity is graded based on orifice area, pulmonary artery pressure, and NYHA functional
Valvular heart disease accounts for 10-20% of cardiac surgery procedures in the US. The document discusses the causes, symptoms, diagnosis and treatment of two common types: mitral stenosis and mitral regurgitation. Mitral stenosis is usually caused by rheumatic fever and results in obstruction of blood flow from the left atrium to ventricle. Symptoms range from mild shortness of breath to pulmonary edema. Diagnosis involves echocardiography and treatment may involve medications, balloon valvuloplasty or valve replacement surgery. Mitral regurgitation occurs when the mitral valve does not close properly, allowing blood to flow back into the left atrium. It can be acute or chronic, with symptoms
Acquired valvular heart diseases with x ray findingsairwave12
This document discusses the role of chest x-rays in identifying various acquired valvular heart diseases. It describes the typical x-ray findings for several conditions: aortic stenosis shows left ventricular hypertrophy and post-stenotic aortic dilation; aortic regurgitation shows an enlarged left ventricle and aorta; mitral stenosis appears as an enlarged left atrium and pulmonary findings like cephalization; mitral regurgitation has markedly enlarged left atrium and ventricle; pulmonary stenosis presents with enlarged pulmonary arteries; tricuspid valve diseases can cause right atrial bulge. The document provides details on causes, pathophysiology and x-ray signs for each condition.
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
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
Rheumatic fever can cause inflammation of the heart valves, known as rheumatic heart disease. Repeated attacks can lead to scarring of the valves over time, most commonly affecting the mitral and aortic valves. The main manifestations include mitral stenosis, mitral insufficiency, aortic insufficiency, and tricuspid valve disease. Symptoms vary depending on the severity of valve involvement and complications such as heart failure or pulmonary hypertension. Treatment involves medications to prevent future rheumatic fever attacks as well as surgical interventions like valve repair or replacement for severe cases.
This document discusses valvular heart diseases. It describes how valves can become narrowed (stenosis) or fail to close adequately (regurgitation). The main causes of valve disease are discussed for both regurgitation and stenosis. Doppler echocardiography is highlighted as the most useful technique for assessing valvular function but may detect minor abnormalities. Regular review is important for patients with valve disease to monitor progression. Specific valve diseases like mitral stenosis, mitral regurgitation, and aortic stenosis are then described in more detail including causes, pathophysiology, symptoms, signs, and management.
This document discusses the etiology, pathophysiology, symptoms, physical exam findings, and electrocardiogram characteristics of mitral stenosis. The main causes are rheumatic heart disease in the majority of cases, and to a lesser extent infective endocarditis, mitral annular calcification, and congenital malformations. Pathophysiologically, mitral stenosis causes elevated left atrial pressure and pulmonary hypertension. Common symptoms include dyspnea, hemoptysis, thromboembolism, and right-sided heart failure. The physical exam may reveal mitral facies, elevated jugular venous pressure, an opening snap, and a decrescendo diastolic murmur.
Disorders of the heart valves commonly result from infective endocarditis, rheumatic fever, ischemia, trauma, or congenital defects. The two major types are stenosis, where the valve opening narrows, and regurgitation, where the valve does not close properly. Aortic stenosis causes the left ventricle to work harder and hypertrophy. Mitral stenosis obstructs blood flow from the left atrium to the left ventricle. Aortic and mitral regurgitation cause the heart to pump blood twice per cycle, leading to dilation and failure over time. Imaging like echocardiography is used to diagnose valve disorders while treatment involves managing symptoms medically or replacing defective valves surgically.
Chronic constrictive pericarditis is a condition where the pericardium thickens and scar tissue forms, restricting the heart's ability to fill with blood. It results from various causes like infections, radiation, surgery, or idiopathic. On examination, elevated jugular venous pressure and hepatomegaly are seen. Imaging shows thickened pericardium. Catheterization demonstrates equal pressures in the heart chambers. Definitive treatment is surgical removal of the pericardium (pericardiectomy), which improves symptoms in most patients.
Chronic constrictive pericarditis is a condition where the pericardium thickens and scar tissue forms, restricting the heart's ability to fill with blood. It results from various causes like infections, surgery, radiation, or autoimmune disorders. On examination, elevated jugular venous pressure and equalization of cardiac filling pressures are seen. Imaging like echocardiograms and CT scans show thickened pericardium. Definitive treatment is surgical removal of the pericardium (pericardiectomy), which improves symptoms in most patients.
This document discusses heart failure, including its classification, pathophysiology, clinical manifestations, investigations, and clinical syndromes. It describes how heart failure occurs when the heart is overloaded or the heart muscle is disordered. It discusses the neuroendocrine and cellular changes that occur in heart failure and how this impacts fluid retention, circulatory pressures, and organ function. Specifically, it outlines the features of left heart failure including common causes, symptoms of pulmonary congestion, physical exam findings, investigations such as echocardiography and natriuretic peptide levels, and how to differentiate it from other conditions like pulmonary disease.
This document summarizes heart failure, including its classification, pathophysiology, clinical manifestations, investigations, and management. Heart failure means the heart cannot pump sufficient blood for the body's needs. It can affect the left side, right side, or both sides of the heart. Management involves correcting underlying causes, reducing demands on the heart through diet and exercise, and pharmacological therapy including diuretics, ACE inhibitors, and other drugs to modify neuroendocrine and renal responses. The goals of treatment are to alleviate symptoms and improve prognosis.
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2. INTRODUCTION
Mitral regurgitation (MR), mitral insufficiency or
mitral incompetence is a disorder of the heart
in which the mitral valve does not close
properly when the heart pumps out blood. It
is the abnormal leaking of blood from the left
ventricle, through the mitral valve, and into
the left atrium, when the left ventricle
contracts, i.e. there is regurgitation of blood
back into the left atrium.MR is the most
common form of valvular heart disease.
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13.
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15. A dysfunction of any of these portions of the mitral
valve apparatus can cause mitral regurgitation.
The most common cause of mitral regurgitation
is mitral valve prolapse (MVP), which in turn is
caused by myxomatous
degeneration(pathological weakening of
connective tissue).
Myxomatous degeneration of the mitral valve is
more common in females, and is more common
in advancing age. This causes a stretching out of
the leaflets of the valve and the chordae
Tendineae. The elongation of the valve leaflets
and the chordae tendineae prevent the valve
leaflets from fully coapting when the valve is
closed, causing the valve leaflets to prolapse into
the left atrium, thereby causing mitral
Regurgitation.
16. Ischemic heart disease causes mitral
regurgitation by the combination of ischemic
dysfunction of the papillary muscles, and the
dilatation of the left ventricle that is present
in ischemic heart disease, with the
subsequent displacement of the papillary
muscles and the dilatation of the mitral valve
annulus.
Rheumatic fever and Marfan's syndrome (also
called Marfan's syndrome is a genetic
disorder of the connective tissue; People with
Marfan's tend to be unusually tall, with long
limbs and long, thin fingers). are other typical
causes of mitral regurgitation.
17. Secondary mitral regurgitation is due to the
dilatation of the left ventricle, causing stretching
of the mitral valve annulus and displacement of
the papillary muscles. This dilatation of the left
ventricle can be due to any cause of dilated
cardiomyopathy, including aortic insufficiency,
nonischemic dilated cardiomyopathy and
Noncompaction Cardiomyopathy. It is also called
functional mitral regurgitation, because the
papillary muscles, chordae, and valve leaflets are
usually normal.
Acute mitral regurgitation is most often caused by
endocarditis, mainly S. aureus. Papillary muscle
rupture or dysfunction, including mitral valve
prolapse, are also common causes in acute cases
18. PATHOPHYSIOLOGY
The pathophysiology of mitral regurgitation
can be broken into three phases of the
disease process:
acute phase
the chronic compensated phase
the chronic decompensated phase
19. ACUTE PHASE
Acute mitral regurgitation (as may occur due to the
sudden rupture of a chorda tendinea or papillary
muscle) causes a sudden volume overload of both the
left atrium and the left ventricle. The left ventricle
develops volume overload because with every
contraction it now has to pump out not only the
volume of blood that goes into the aorta (the forward
cardiac output or forward stroke volume), but also
the blood that regurgitates into the left atrium (the
regurgitant volume). The combination of the forward
stroke volume and the regurgitant volume is known
as the total stroke volume of the left ventricle.
20. In the acute setting, the stroke volume of the left
ventricle is increased (increased ejection
fraction), this happens because of more complete
emptying of heart. However, as it progresses the
LV volume increases and the contractile function
deteriorates and thus leading to dysfunctional LV
and a decrease in ejection fraction. The increase
in stroke volume is explained by the Frank–
Starling mechanism, in which increased
ventricular pre-load stretches the myocardium
such that contractions are more forceful.
The regurgitant volume causes a volume overload
and a pressure overload of the left atrium. The
increased pressures in the left atrium inhibit
drainage of blood from the lungs via the
pulmonary veins. This causes pulmonary
congestion.
21. CHRONIC PHASE
Compensated:
If the mitral regurgitation develops slowly over months to
years or if the acute phase can be managed with medical
therapy, the individual will enter the chronic compensated
phase of the disease. In this phase, the left ventricle
develops eccentric hypertrophy in order to better manage
the larger than normal stroke volume. The eccentric
hypertrophy and the increased diastolic volume combine to
increase the stroke volume (to levels well above normal) so
that the forward stroke volume (forward cardiac output)
approaches the normal levels.
22. In the left atrium, the volume overload causes
enlargement of the chamber of the left
atrium, allowing the filling pressure in the left
atrium to decrease. This improves the
drainage from the pulmonary veins, and signs
and symptoms of pulmonary congestion will
decrease.
These changes in the left ventricle and left
atrium improve the low forward cardiac
output state and the pulmonary congestion
that occur in the acute phase of the disease.
Individuals in the chronic compensated phase
may be asymptomatic and have normal
exercise tolerances.
23. CHRONIC PHASE
Decompensated:
An individual may be in the compensated
phase of mitral regurgitation for years, but
will eventually develop left ventricular
dysfunction, the hallmark for the chronic
decompensated phase of mitral regurgitation.
It is currently unclear what causes an
individual to enter the decompensated phase
of this disease. However, the decompensated
phase is characterized by calcium overload
within the cardiac myocyte.
24. In this phase, the ventricular myocardium is no
longer able to contract adequately to
compensate for the volume overload of mitral
regurgitation, and the stroke volume of the
left ventricle will decrease. The decreased
stroke volume causes a decreased forward
cardiac output and an increase in the endsystolic
volume. The increased end-systolic
volume translates to increased filling
pressures of the left ventricle and increased
pulmonary venous congestion. The individual
may again have symptoms of congestive
heart failure.
25. The left ventricle begins to dilate during this
phase. This causes a dilatation of the mitral valve
annulus, which may worsen the degree of mitral
regurgitation. The dilated left ventricle causes an
increase in the wall stress of the cardiac chamber
as well.
While the ejection fraction is less in the chronic
decompensated phase than in the acute phase or
the chronic compensated phase of mitral
regurgitation, it may still be in the normal range
(i.e.: > 50 percent), and may not decrease until
late in the disease course. A decreased ejection
fraction in an individual with mitral regurgitation
and no other cardiac abnormality should alert the
physician that the disease may be in its
decompensated phase.
26. SYMPTOMS AND SIGNS
The symptoms associated with mitral regurgitation
are dependent on which phase of the disease
process the individual is in. Individuals with acute
mitral regurgitation will have the signs and
symptoms of decompensated congestive heart
failure (i.e. shortness of breath, pulmonary
edema, orthopnea, and paroxysmal nocturnal
dyspnea), as well as symptoms suggestive of a
low cardiac output state (i.e. decreased exercise
tolerance). Palpitations are also common.
Cardiovascular collapse with shock (cardiogenic
shock) may be seen in individuals with acute
mitral regurgitation due to papillary muscle
rupture or rupture of a chorda tendinae.
27. Individuals with chronic compensated mitral
regurgitation may be asymptomatic, with a
normal exercise tolerance and no evidence of
heart failure. These individuals may be
sensitive to small shifts in their intravascular
volume status, and are prone to develop
volume overload (congestive heart failure).
28. CLINICAL S/S
Findings on clinical examination depend on the
severity and duration of mitral regurgitation. The
mitral component of the first heart sound is
usually soft and with a laterally displaced apex.
beat, often with heave. The first heart sound is
followed by a high-pitched holosystolic murmur
at the apex, radiating to the back or clavicular
area.
The loudness of the murmur
does not correlate well with the severity of
regurgitation. It may be followed by a loud,
palpable P2, heard best when lying on the left
side. A third heart sound is commonly heard.
Commonly, atrial fibrillation is found.
29. CHEST X-RAY
1. The chest x-ray in individuals with chronic
mitral regurgitation is characterized by
enlargement of the left atrium and the left ventricle.
2. The pulmonary vascular markings
are typically normal, since pulmonary venous
pressures are usually not significantly
elevated.
30. ECHOCARDIOGRAPHY
The echocardiogram is commonly used to
confirm the diagnosis of mitral regurgitation.
Color Doppler flow on the transthoracic
echocardiogram (TTE) will reveal a jet of
blood flowing from the left ventricle into the
left atrium during ventricular systole.
Also detect a dilated left atrium and ventricle
and decreased left ventricular function.
31. ELECTROCARDIOGRAPHY
P mitrale is broad, notched P waves in several
or many leads with a prominent late negative
component to the P wave in lead V1, and may
be seen in mitral regurgitation, but also in
mitral stenosis.
32. TREATMENT
The treatment of mitral regurgitation depends on
the acuteness of the disease and whether there
are associated signs of hemodynamic
compromise.
In acute mitral regurgitation secondary to a
mechanical defect in the heart (i.e.: rupture of a
papillary muscle or chordae tendineae), the
treatment of choice is urgent mitral valve
REPLACEMENT.
33. MEDICAL TREATMENT
If the individual with acute mitral regurgitation
is normotensive, vasodilators may be of use
to decrease the afterload . The vasodilator most
commonly used is nitroprusside.
Individuals with chronic mitral regurgitation
can be treated with vasodilators as well to
decrease afterload. In the chronic state, the
most commonly used agents are ACE
inhibitors and hydralazine. Studies have
shown that the use of ACE inhibitors and
hydralazine can delay surgical treatment of
mitral regurgitation.
34. SURGICAL TREATMENT
There are two surgical options for the
treatment of mitral regurgitation: mitral valve
replacement and mitral valve repair.
35. INTRODUCTION
Rheumatic heart disease is the commonest cause of
MR .
It usually coexists with MS and aortic valve disease ,
particularly AR .
36. PATHOPHYSIOLOGY
Due to incompetent MV , during LV contraction , a
proportion of left ventricular blood regurgitates into
LA producing pansystolic murmur at mitral area.
There is rising of left atrial and pulmonary venous
pressure and in late stages pulmonary arterial
pressure.
During diastole there is inflow of extra blood back into
left ventricle producing mid diastolic flow murmur.
38. CLINICAL FEATURES
SYMPTOMS : palpitation
Dyspnea
SIGNS :
Normal bp, good volume pulse, ankle edema , enlarged
tender lever , basal crepitations in the lungs
CVS SIGNS : hyperdynamic apex beat, systolic thrill,
pansystolic murmur , loud P2, S3, mid diastolic flow
murmur.
39. INVESTIGATIONS
Electrocardiogram – normal in mild cases, in severe
cases LVH , LAH, biventricular hypertrophy are seen
in later stages.
Chest x-ray – in mild cases it may be normal. In
advanced cases there is cardiomegaly . Mitralisation of
left cardiac border . Enlarged LA may be seen as
double density between two bronchi causing incease
in carinal angle
40. INVESTIGATIONS
2D ECHO – 2D echo assesses severety of mitral
incompetence and rules out other causes of MR, e.g.
MVP, ruptured chordae tendineae , primary CMP and
IE.
CARDIAC CATHETARISATION AND LEFT
VENTRICULAR CINE ANGIOGRAPHY – it is done to
assess MR , and in elderly patients coronary
angiography is done to rule out CAD before valve
surgery.
43. MEDICAL MANAGEMENT
Rheumatic fever prophylexis
Infective endocarditis prophylexis
Treatment of heart failure
Treatment of AF
Anticoagulation in presence of left atrial clot.
44. SURGICAL MANAGEMENT
Valve replacement or repair- acute MR needs
emergency valve repair or replacement.
If due to IHD patient may need coronary
revascularization.
46. Q- how do you judge severity of
MR ?
Systolic thrill plus pan systolic murmur over mitral
area
Presence of S3 and mid diastolic flow murmur over
mitral area.
Degree of LVH as seen clinically and on ECG and chest
x-ray.
47. Q- What is the D/D of pansystolic
murmur of MR ?
TR
VSD
PAPILLARY MUSCLE DYSFUNCTION
MITRAL VAVE PROLAPSE : 1. most common cause of
isolated MR.
2. Myxomatous degeneration of mitral leaflets
3. posterior leaflet commonly involved , aneriore leaflet
rarely
4. common in young females
5. mid or late – systolic click followed by late high pitched
systolic murmur which decreases with sitting posture.