In this presentation, Dr Vivek Baliga, Consultant Internal Medicine, discusses a common problem in medical practice that often confuses many - diastolic heart failure. Now a misnomer, it is referred to as heart failure with preserved ejection fraction. For patient articles - http://heartsense.in/author/dr-vivek-baliga-b/ . LinkedIn - https://www.linkedin.com/in/dr-vivek-baliga-7b59b0125
Diastolic heart failure occurs when the ventricles become stiff and cannot relax fully during diastole. This prevents full ventricular filling and blood backs up in the organs. Around half of heart failure patients have diastolic heart failure. Diagnosis relies on echocardiogram showing diastolic dysfunction. Treatment focuses on controlling hypertension, volume overload, and other causes through medications like ACE inhibitors, diuretics and beta blockers.
Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.
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
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.
ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
Brugada Syndrome is characterized by ST elevation in leads V1-V3, structurally normal hearts, and a risk of life-threatening ventricular arrhythmias. It is caused by mutations in the SCN5A gene which codes for cardiac sodium channels. It is more prevalent in Southeast Asian populations and clinical manifestations often first occur in the third to fourth decade of life. Diagnosis requires a characteristic ECG pattern that can be enhanced by sodium channel blockers. An ICD is the first-line treatment for preventing sudden cardiac death from ventricular arrhythmias in symptomatic patients.
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
Diagnosis and management of acute heart failureAlaa Ateya
Acute heart failure (AHF) can be defined as new or worsening symptoms of heart failure requiring urgent medical care or hospitalization. Common triggers include non-adherence to medications or diet, infections, or worsening of underlying comorbidities like hypertension. This leads to worsening congestion through mechanisms like neurohormonal activation and myocardial injury. Around half of AHF patients have preserved ejection fraction. Ongoing myocardial damage, worsening kidney function, and elevated filling pressures all contribute to poor outcomes of AHF patients.
Diastolic heart failure occurs when the ventricles become stiff and cannot relax fully during diastole. This prevents full ventricular filling and blood backs up in the organs. Around half of heart failure patients have diastolic heart failure. Diagnosis relies on echocardiogram showing diastolic dysfunction. Treatment focuses on controlling hypertension, volume overload, and other causes through medications like ACE inhibitors, diuretics and beta blockers.
Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.
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
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.
ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
Brugada Syndrome is characterized by ST elevation in leads V1-V3, structurally normal hearts, and a risk of life-threatening ventricular arrhythmias. It is caused by mutations in the SCN5A gene which codes for cardiac sodium channels. It is more prevalent in Southeast Asian populations and clinical manifestations often first occur in the third to fourth decade of life. Diagnosis requires a characteristic ECG pattern that can be enhanced by sodium channel blockers. An ICD is the first-line treatment for preventing sudden cardiac death from ventricular arrhythmias in symptomatic patients.
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
Diagnosis and management of acute heart failureAlaa Ateya
Acute heart failure (AHF) can be defined as new or worsening symptoms of heart failure requiring urgent medical care or hospitalization. Common triggers include non-adherence to medications or diet, infections, or worsening of underlying comorbidities like hypertension. This leads to worsening congestion through mechanisms like neurohormonal activation and myocardial injury. Around half of AHF patients have preserved ejection fraction. Ongoing myocardial damage, worsening kidney function, and elevated filling pressures all contribute to poor outcomes of AHF patients.
This document discusses various types of cardiomyopathies:
- Dilated cardiomyopathy is caused by an unknown etiology and results in left ventricular dilatation and systolic dysfunction. It is a common cause of heart failure.
- Hypertrophic cardiomyopathy involves abnormal thickening of the heart muscle and can lead to outflow obstruction. It is a common cause of sudden death in young athletes.
- Restrictive cardiomyopathy causes stiff ventricles and impaired ventricular filling due to disorders like amyloidosis. It presents with symptoms of right and left heart failure.
- Other rare types discussed include arrhythmogenic right ventricular dysplasia and obliterative cardiomyopathy. Diagnosis involves imaging and endomyocardial biopsy
This document provides information on heart failure, including:
1. It defines heart failure as the inability of the heart to pump an adequate amount of blood to meet the body's needs.
2. It describes compensatory mechanisms the body uses in response to heart failure like increasing sympathetic activity and activating the renin-angiotensin system.
3. It discusses treatments for heart failure like diuretics, ACE inhibitors, beta-blockers, and cardiac glycosides which aim to reduce workload on the heart and improve contractility.
This document provides an overview of cardiac resynchronization therapy (CRT). It discusses how conduction delays can lead to electromechanical dyssynchrony and impair the heart's function. CRT aims to improve this synchrony and thereby improve systolic and diastolic function. The document outlines different types of dyssynchrony and methods to assess it, including echocardiography. Current guidelines recommend CRT for symptomatic heart failure patients with low ejection fraction and wide QRS duration. The implantation procedure involves placing right atrial/ventricular leads and a left ventricular lead via the coronary sinus.
Diagnosis, management, workup in a case of Takayasu's arteritis. Definition, synonyms, history, epidimiology, pathophysiology, etiology of Takayasu's arteritis.
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left ventricle not caused by ischemic or valvular heart disease. The document discusses the epidemiology, etiology, pathology, genetics, clinical features, diagnosis, and management of idiopathic dilated cardiomyopathy. Key points include:
- The annual incidence is 5-8 per 100,000 people with increased risk in males, blacks, and those with hypertension or chronic beta-agonist use.
- Causes include genetic mutations, viral infections, autoimmune diseases, and drugs. Pathology shows dilatation, myocyte hypertrophy and death, and extracellular matrix remodeling.
- Diagnosis involves ECG
This document discusses the classification and management of ventricular arrhythmias. It is divided into sections on classification by clinical presentation, electrocardiography, disease entity. Management of VT in structurally abnormal hearts is discussed, including those related to coronary artery disease, dilated cardiomyopathy, bundle branch reentrant tachycardia, arrhythmogenic right ventricular dysplasia, and other conditions. Clinical presentation, mechanisms, diagnostic testing, and treatment options are summarized for each condition.
Pulmonary Hypertension, Current Guidelines and Future Directions of Therapy.Bassel Ericsoussi, MD
The document discusses the classification, pathophysiology, diagnosis, and treatment of pulmonary hypertension. It is classified by the WHO into 5 groups based on underlying mechanisms. The pathophysiology involves vasoconstriction, remodeling of the pulmonary arteries, and thrombosis. Diagnosis requires right heart catheterization showing elevated pulmonary artery pressure. Prognostic factors include functional status and hemodynamics. Treatment involves basic supportive care as well as vasodilator medications, including prostanoids, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and nitric oxide. Combination therapy may provide added benefits.
The document provides information on inferior wall myocardial infarction (MI), including:
1. Definitions, epidemiology, etiology, clinical features, diagnosis, treatment and complications of inferior wall MI are discussed. Worldwide over 7 million people experience STEMIs or NSTEMIs annually.
2. Diagnosis involves ECG, cardiac imaging, cardiac biomarkers like troponin and CK-MB. Reperfusion therapy within 6 hours includes PCI or thrombolysis. General treatment measures include aspirin, clopidogrel, anticoagulants, analgesics, beta-blockers, nitrates and oxygen.
3. The history of pioneers in cardiology and development of techniques like echocardi
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
1. Atrial fibrillation (AF) is a common arrhythmia where abnormal electrical signals in the atria cause an irregular heartbeat.
2. AF increases the risk of stroke by 5 times and is associated with increased mortality, hospitalization, and decreased quality of life.
3. Management involves rate or rhythm control as well as anticoagulation to prevent stroke, with treatment depending on factors like symptoms, age, and stroke risk level.
This document provides an overview of atrial fibrillation (AF), including its pathogenesis, types, diagnosis, and management. Some key points:
- AF is the most common cardiac arrhythmia, affecting around 6% of those over 65. It increases the risk of stroke.
- It occurs when the normal sinus rhythm is overridden by disorganized electrical impulses, usually originating in the lungs.
- Types include paroxysmal, persistent, and permanent. Symptoms range from none to palpitations, dyspnea, chest pain, and neurological issues.
- Diagnosis is made via ECG showing irregular rhythm without P waves. Workup evaluates for underlying causes and stroke risk factors.
Atrial fibrillation and atrial flutter are types of arrhythmia where the heart beats irregularly. Atrial fibrillation occurs when rapid, irregular electrical signals cause the heart's upper chambers (atria) to beat very fast and irregularly. Atrial flutter is similar but the heart beats fast in a regular pattern. These conditions are diagnosed through electrocardiograms which detect abnormal heart rhythms. Holter monitors and event recorders can also detect arrhythmias over longer periods of time when symptoms occur. Complications include stroke and heart failure, so treatment focuses on rate or rhythm control and preventing clots.
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
This document provides an overview of heart failure, including definitions, epidemiology, etiology, signs and symptoms, diagnosis, and treatment. Heart failure is defined as a condition where the heart loses its ability to pump sufficient blood to the body. It may involve the left ventricle, right ventricle, or both, and can be acute or chronic. Common causes include coronary artery disease, defective heart valves, arrhythmias, cardiomyopathy, and hypertension. Diagnosis involves echocardiogram, BNP levels, and chest x-rays. Treatment includes lifestyle changes, medications to reduce preload and afterload, increase contractility, and eliminate fluid, as well as surgical procedures like angioplasty, bypass, or
This document discusses supraventricular tachycardias (SVT). It defines different types of SVT including paroxysmal SVT, which is common in emergency rooms. Quality of life is often poor for those with paroxysmal SVT. The document discusses mechanisms of SVT including reentry circuits, enhanced automaticity, and triggered activity. It provides details on differentiating AV nodal reentrant tachycardia from AV reentrant tachycardia using electrocardiogram findings. Treatment options discussed include carotid sinus massage, adenosine, and catheter ablation.
This document discusses the management of atrial fibrillation. It provides information on the causes, consequences, classification, and epidemiology of AF. It describes the acute management of AF including assessing hemodynamic status, starting anticoagulation, and deciding between rate and rhythm control strategies. Methods for rhythm control include electrical cardioversion and pharmacological cardioversion with drugs like amiodarone, ibutilide, flecainide, and propafenone. Rate control strategies use drugs like digoxin, beta blockers, calcium channel blockers, and amiodarone. The document also discusses anticoagulation for thromboembolism prevention and newer oral anticoagulants.
- Cardiac tumors are rare, with most cardiac masses representing thrombi or vegetations. Primary cardiac tumors are more often benign, with myxoma being the most common benign tumor found in the left atrium attached to the fossa ovalis. In children, rhabdomyomas and fibromas are the most typical primary benign tumors. Secondary cardiac tumors are more prevalent, spreading from other primary cancers. Noninvasive diagnosis relies on tumor location, age, imaging characteristics, and histology likelihood.
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It has many potential causes, but is often due to problems with the heart muscle itself or valves. Treatment focuses on managing symptoms with diuretics, and slowing progression with ACE inhibitors, beta-blockers, and aldosterone antagonists. Other therapies aim to improve heart function or treat underlying causes. Prognosis depends on severity but ranges from 5-50% annual mortality.
This document defines and describes heart failure, its causes, forms, and pathophysiology. Heart failure is defined as the inability of the heart to pump enough blood to meet the body's needs. It is most often caused by impaired contractility from conditions like ischemic heart disease or cardiomyopathy. Heart failure can present as systolic or diastolic dysfunction and can affect the left or right ventricle. The body undergoes adaptive and maladaptive changes like neurohormonal activation to try to maintain cardiac output as heart function declines.
This document discusses congestive heart failure in infants and children. It begins with background on the main causes of heart failure in children, which are often congenital heart disease and cardiomyopathy rather than issues like coronary artery disease that commonly cause heart failure in adults. The document then covers topics like the pathophysiology and classifications of heart failure in children, as well as diagnostic workup, management, and treatment approaches. Physical exam findings and classifications like Ross and NYHA scores are also outlined to help evaluate heart failure severity in pediatric patients.
This document discusses various types of cardiomyopathies:
- Dilated cardiomyopathy is caused by an unknown etiology and results in left ventricular dilatation and systolic dysfunction. It is a common cause of heart failure.
- Hypertrophic cardiomyopathy involves abnormal thickening of the heart muscle and can lead to outflow obstruction. It is a common cause of sudden death in young athletes.
- Restrictive cardiomyopathy causes stiff ventricles and impaired ventricular filling due to disorders like amyloidosis. It presents with symptoms of right and left heart failure.
- Other rare types discussed include arrhythmogenic right ventricular dysplasia and obliterative cardiomyopathy. Diagnosis involves imaging and endomyocardial biopsy
This document provides information on heart failure, including:
1. It defines heart failure as the inability of the heart to pump an adequate amount of blood to meet the body's needs.
2. It describes compensatory mechanisms the body uses in response to heart failure like increasing sympathetic activity and activating the renin-angiotensin system.
3. It discusses treatments for heart failure like diuretics, ACE inhibitors, beta-blockers, and cardiac glycosides which aim to reduce workload on the heart and improve contractility.
This document provides an overview of cardiac resynchronization therapy (CRT). It discusses how conduction delays can lead to electromechanical dyssynchrony and impair the heart's function. CRT aims to improve this synchrony and thereby improve systolic and diastolic function. The document outlines different types of dyssynchrony and methods to assess it, including echocardiography. Current guidelines recommend CRT for symptomatic heart failure patients with low ejection fraction and wide QRS duration. The implantation procedure involves placing right atrial/ventricular leads and a left ventricular lead via the coronary sinus.
Diagnosis, management, workup in a case of Takayasu's arteritis. Definition, synonyms, history, epidimiology, pathophysiology, etiology of Takayasu's arteritis.
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left ventricle not caused by ischemic or valvular heart disease. The document discusses the epidemiology, etiology, pathology, genetics, clinical features, diagnosis, and management of idiopathic dilated cardiomyopathy. Key points include:
- The annual incidence is 5-8 per 100,000 people with increased risk in males, blacks, and those with hypertension or chronic beta-agonist use.
- Causes include genetic mutations, viral infections, autoimmune diseases, and drugs. Pathology shows dilatation, myocyte hypertrophy and death, and extracellular matrix remodeling.
- Diagnosis involves ECG
This document discusses the classification and management of ventricular arrhythmias. It is divided into sections on classification by clinical presentation, electrocardiography, disease entity. Management of VT in structurally abnormal hearts is discussed, including those related to coronary artery disease, dilated cardiomyopathy, bundle branch reentrant tachycardia, arrhythmogenic right ventricular dysplasia, and other conditions. Clinical presentation, mechanisms, diagnostic testing, and treatment options are summarized for each condition.
Pulmonary Hypertension, Current Guidelines and Future Directions of Therapy.Bassel Ericsoussi, MD
The document discusses the classification, pathophysiology, diagnosis, and treatment of pulmonary hypertension. It is classified by the WHO into 5 groups based on underlying mechanisms. The pathophysiology involves vasoconstriction, remodeling of the pulmonary arteries, and thrombosis. Diagnosis requires right heart catheterization showing elevated pulmonary artery pressure. Prognostic factors include functional status and hemodynamics. Treatment involves basic supportive care as well as vasodilator medications, including prostanoids, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and nitric oxide. Combination therapy may provide added benefits.
The document provides information on inferior wall myocardial infarction (MI), including:
1. Definitions, epidemiology, etiology, clinical features, diagnosis, treatment and complications of inferior wall MI are discussed. Worldwide over 7 million people experience STEMIs or NSTEMIs annually.
2. Diagnosis involves ECG, cardiac imaging, cardiac biomarkers like troponin and CK-MB. Reperfusion therapy within 6 hours includes PCI or thrombolysis. General treatment measures include aspirin, clopidogrel, anticoagulants, analgesics, beta-blockers, nitrates and oxygen.
3. The history of pioneers in cardiology and development of techniques like echocardi
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
1. Atrial fibrillation (AF) is a common arrhythmia where abnormal electrical signals in the atria cause an irregular heartbeat.
2. AF increases the risk of stroke by 5 times and is associated with increased mortality, hospitalization, and decreased quality of life.
3. Management involves rate or rhythm control as well as anticoagulation to prevent stroke, with treatment depending on factors like symptoms, age, and stroke risk level.
This document provides an overview of atrial fibrillation (AF), including its pathogenesis, types, diagnosis, and management. Some key points:
- AF is the most common cardiac arrhythmia, affecting around 6% of those over 65. It increases the risk of stroke.
- It occurs when the normal sinus rhythm is overridden by disorganized electrical impulses, usually originating in the lungs.
- Types include paroxysmal, persistent, and permanent. Symptoms range from none to palpitations, dyspnea, chest pain, and neurological issues.
- Diagnosis is made via ECG showing irregular rhythm without P waves. Workup evaluates for underlying causes and stroke risk factors.
Atrial fibrillation and atrial flutter are types of arrhythmia where the heart beats irregularly. Atrial fibrillation occurs when rapid, irregular electrical signals cause the heart's upper chambers (atria) to beat very fast and irregularly. Atrial flutter is similar but the heart beats fast in a regular pattern. These conditions are diagnosed through electrocardiograms which detect abnormal heart rhythms. Holter monitors and event recorders can also detect arrhythmias over longer periods of time when symptoms occur. Complications include stroke and heart failure, so treatment focuses on rate or rhythm control and preventing clots.
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
This document provides an overview of heart failure, including definitions, epidemiology, etiology, signs and symptoms, diagnosis, and treatment. Heart failure is defined as a condition where the heart loses its ability to pump sufficient blood to the body. It may involve the left ventricle, right ventricle, or both, and can be acute or chronic. Common causes include coronary artery disease, defective heart valves, arrhythmias, cardiomyopathy, and hypertension. Diagnosis involves echocardiogram, BNP levels, and chest x-rays. Treatment includes lifestyle changes, medications to reduce preload and afterload, increase contractility, and eliminate fluid, as well as surgical procedures like angioplasty, bypass, or
This document discusses supraventricular tachycardias (SVT). It defines different types of SVT including paroxysmal SVT, which is common in emergency rooms. Quality of life is often poor for those with paroxysmal SVT. The document discusses mechanisms of SVT including reentry circuits, enhanced automaticity, and triggered activity. It provides details on differentiating AV nodal reentrant tachycardia from AV reentrant tachycardia using electrocardiogram findings. Treatment options discussed include carotid sinus massage, adenosine, and catheter ablation.
This document discusses the management of atrial fibrillation. It provides information on the causes, consequences, classification, and epidemiology of AF. It describes the acute management of AF including assessing hemodynamic status, starting anticoagulation, and deciding between rate and rhythm control strategies. Methods for rhythm control include electrical cardioversion and pharmacological cardioversion with drugs like amiodarone, ibutilide, flecainide, and propafenone. Rate control strategies use drugs like digoxin, beta blockers, calcium channel blockers, and amiodarone. The document also discusses anticoagulation for thromboembolism prevention and newer oral anticoagulants.
- Cardiac tumors are rare, with most cardiac masses representing thrombi or vegetations. Primary cardiac tumors are more often benign, with myxoma being the most common benign tumor found in the left atrium attached to the fossa ovalis. In children, rhabdomyomas and fibromas are the most typical primary benign tumors. Secondary cardiac tumors are more prevalent, spreading from other primary cancers. Noninvasive diagnosis relies on tumor location, age, imaging characteristics, and histology likelihood.
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It has many potential causes, but is often due to problems with the heart muscle itself or valves. Treatment focuses on managing symptoms with diuretics, and slowing progression with ACE inhibitors, beta-blockers, and aldosterone antagonists. Other therapies aim to improve heart function or treat underlying causes. Prognosis depends on severity but ranges from 5-50% annual mortality.
This document defines and describes heart failure, its causes, forms, and pathophysiology. Heart failure is defined as the inability of the heart to pump enough blood to meet the body's needs. It is most often caused by impaired contractility from conditions like ischemic heart disease or cardiomyopathy. Heart failure can present as systolic or diastolic dysfunction and can affect the left or right ventricle. The body undergoes adaptive and maladaptive changes like neurohormonal activation to try to maintain cardiac output as heart function declines.
This document discusses congestive heart failure in infants and children. It begins with background on the main causes of heart failure in children, which are often congenital heart disease and cardiomyopathy rather than issues like coronary artery disease that commonly cause heart failure in adults. The document then covers topics like the pathophysiology and classifications of heart failure in children, as well as diagnostic workup, management, and treatment approaches. Physical exam findings and classifications like Ross and NYHA scores are also outlined to help evaluate heart failure severity in pediatric patients.
This document discusses heart failure, including its pathophysiology, types, and causes. Heart failure occurs when the heart cannot maintain adequate output or can only do so at the expense of elevated ventricular pressures. It may result from systolic or diastolic dysfunction. Types include left, right, and bi-ventricular failure. Acute pulmonary edema is treated with oxygen, nitrates, and diuretics. Chronic heart failure is managed with drugs like diuretics, ACE inhibitors, ARBs, and beta-blockers to improve outcomes.
Diastolic heart failure occurs when the ventricles become stiff and cannot relax fully during diastole. This prevents full ventricular filling and blood backs up in the organs. Around half of heart failure patients have diastolic heart failure. Diagnosis relies on echocardiogram showing diastolic dysfunction. Treatment focuses on controlling hypertension, volume overload, and other causes through medications like ACE inhibitors, diuretics and beta blockers.
This document provides an overview of heart failure, including its definition, pathophysiology, types, causes, symptoms, diagnosis, prognosis, and treatment options. It discusses systolic and diastolic heart failure, highlighting key differences. Medical treatments that improve survival in systolic heart failure are reviewed, including ACE inhibitors, beta blockers, spironolactone/eplerenone, hydralazine/nitrates, and ARBs. The roles of diuretics, neurohormonal activation, and beta blockers are explained. Carvedilol is positioned as superior to metoprolol based on direct comparison trials.
Cardiovascular breakdown (HF) or Congestive Heart Failure (CHF) is a physiologic state wherein the heart can't siphon sufficient blood to meet the body's metabolic requirements following any underlying or useful weakness of ventricular filling or discharge of blood.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can result from conditions that weaken the heart muscle such as coronary artery disease or hypertension.
The document defines heart failure and describes its prevalence increasing with age and being higher in males than females aged 40-75. Symptoms of left ventricular failure include breathing difficulties, cough, and leg swelling while right ventricular failure symptoms include abdominal swelling and pain.
Signs include elevated jugular venous pressure, lung crackles, edema, hepatomegaly, and murmurs. Precipitating factors include infection, medications, thyroid issues, and arrhythmias. Diagnostic tests include chest x-ray, echocardiogram
This document discusses syncope, fatigue, and peripheral edema. It defines syncope as a brief loss of consciousness and describes results from the Framingham Heart Study showing increased incidence with age. Common causes of syncope include vasovagal attacks and cardiac arrhythmias. Fatigue is a feeling of tiredness that can have physical or mental causes and may be a symptom of cardiovascular disease. Peripheral edema is swelling caused by fluid in tissues and can occur in heart failure, cirrhosis, and nephrotic syndrome due to changes in capillary dynamics and sodium retention.
Cardiomyopathy is a disease of the heart muscle that can cause mechanical and electrical dysfunction. It has many causes including genetic disorders, infections, and metabolic issues.
The prognosis for cardiomyopathy is generally poor if left undiagnosed until advanced stages. Diagnostic tools include echocardiography, chest x-rays, and cardiac catheterization.
Dilated cardiomyopathy is the most common type and is characterized by the enlargement of heart chambers and thinning of the walls. It can lead to heart failure if not properly managed with medications like ACE inhibitors, beta blockers, diuretics, and devices like defibrillators if needed. The prognosis is poor with 50% of patients dying within
The Advanced Cardiovascular Life Support (ACLS) algorithm is a systematic, evidence-based approach designed to guide healthcare providers in the urgent treatment of: Cardiac arrest. Arrhythmias. Stroke. Other life-threatening cardiovascular emergencies.
Heart failure, also known as cardiac decompensation or cardiac insufficiency, occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by conditions that impair the heart muscle's ability to contract effectively or limit ventricular filling. Symptoms vary depending on whether the left or right ventricle is primarily affected and include dyspnea, fatigue, edema and others. Diagnostic tests may include echocardiography, ECG, chest x-ray and BNP level. Treatment focuses on managing symptoms, slowing disease progression, and preventing hospitalizations through lifestyle changes and medication.
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.
Heart failure is defined as the heart's inability to pump enough blood to meet the body's needs. It can be caused by conditions that impair the heart muscle or overload it. Heart failure is classified based on location (right, left, or both ventricles), timing (acute or chronic), and pumping ability (systolic or diastolic). Signs and symptoms include dyspnea, fatigue, fluid retention, and reduced exercise tolerance. Treatment involves lifestyle changes, medications to relieve symptoms and improve pumping ability, and treating the underlying cause.
Congestive heart failure (CHF) results from any structural or functional cardiac disorder that impairs the ventricle's ability to fill with or eject blood. It is diagnosed based on history, physical exam, chest x-ray, EKG, and echocardiogram. Treatment focuses on restoring normal cardiopulmonary physiology by using ACE inhibitors, beta-blockers, diuretics, and addressing pulmonary complications. Management involves evaluating the patient's stage of CHF and functional classification to determine appropriate pharmacotherapy and monitoring according to guidelines from the American Heart Association.
This document provides an overview of heart failure, including its causes, pathophysiology, clinical presentation, diagnosis and management. Heart failure occurs when the heart cannot pump enough blood to meet the body's needs. It may be due to conditions that weaken the heart muscle such as coronary artery disease. Symptoms depend on whether the left, right or both ventricles are affected and include shortness of breath, fatigue, swelling and fluid retention. Treatment focuses on managing symptoms, improving cardiac function and preventing future damage through medications, lifestyle changes and device therapies.
This document provides an overview of heart failure, including its causes, pathophysiology, clinical presentation, diagnosis and management. Heart failure occurs when the heart cannot pump enough blood to meet the body's needs. It may be due to conditions that weaken the heart muscle such as coronary artery disease. Symptoms depend on whether the left, right or both ventricles are affected and include shortness of breath, fatigue, swelling and fluid retention. Treatment focuses on managing symptoms, improving cardiac function and preventing future damage through medications, lifestyle changes and device-based therapies.
This document provides an overview of heart failure, including its pathophysiology, types, clinical presentation, investigations, and management. Heart failure occurs when the heart cannot pump enough blood to meet the body's needs and can develop due to conditions that weaken the heart such as heart attacks or high blood pressure. Symptoms depend on whether the left side, right side, or both sides of the heart are affected. Management involves treating the underlying cause, reducing symptoms through medications, lifestyle changes, and addressing complications.
This document summarizes several common heart disorders:
- Coronary heart disease is caused by plaque buildup in the coronary arteries, reducing blood flow to the heart. Atherosclerosis is a similar condition where plaques develop inside arterial walls.
- Chest pain called angina occurs due to insufficient blood supply to the heart. Arrhythmias happen when the heart's electrical system malfunctions, causing irregular heartbeats.
- Congestive heart failure occurs when the heart cannot pump enough blood to meet the body's needs. Other disorders discussed include stroke, myocardial infarction, hypotension, hypertension, rheumatic heart disease, and congenital heart disease. Risk factors and treatments are also outlined.
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2. Contents:
Definition
Pathophysiology of diastolic heart failure
Causes of diastolic heart failure
Diagnosis.
Management.
Nonpharmacological .
Pharmacologic.
Future therapies in diastolic heart failure.
3. Definition:
Heart failure is most commonly associated with impaired LV
systolic function.
However, as many as 30-40% of all patients with typical
symptoms of congestive heart failure, have a normal or slightly
reduced ejection fraction.
In these patients, diastolic dysfunction is implicated as a major
contributor, if not the primary cause of congestive heart
failure.
The syndrome of clinical heart failure with normal left
ventricular systolic function in the absence of cardiac valvular
lesions is often referred to as diastolic heart failure (DHF).
4. Epidemiology of Congestive Heart Failure:
Approximately 5 million people in the U.S. have CHF.
Over 550,000 patients are diagnosed with CHF for the first
time each year.
Primary reason for 12-15 million office visits and 6.5 million
hospital days each year
The incidence of CHF approaches 10 per 1000 population over
age 65.
Rate of hospitalization is similar to that associated with systolic
heart failure
Fewer published data on diastolic heart failure than systolic
heart failure
5. Epidemiology of Diastolic Heart Failure:
About one third of all patients with congestive heart
failure have diastolic heart failure
Prevalence is highest in patients older than 75 years
old
Mortality rate is about 5-8 % annually as compared to
10-15% among patients with systolic heart failure
Mortality rate is directly related to age and the
presence/absence of coronary disease.
6. LV Diastolic function
The assessment of left ventricular (LV) diastolic function should
be an integral part of a routine examination, particularly in
patients presenting with dyspnea or heart failure.
About half of patients with new diagnoses of heart failure have
normal or near normal global ejection fractions (EFs).
European Study Group on Diastolic Heart Failure. How to diagnose diastolic heart failure. Eur Heart J. 1998; 19: 990–1003.
7. LV Diastolic function
These patients are diagnosed with “diastolic heart
failure” or “heart failure with preserved EF.”
The assessment of LV diastolic function and filling
pressures is of paramount clinical importance to
distinguish this syndrome from other diseases such as
pulmonary disease resulting in dyspnea, to assess
prognosis, and to identify underlying cardiac disease
and its best treatment.
European Study Group on Diastolic Heart Failure. How to diagnose diastolic heart failure. Eur Heart J. 1998; 19: 990–1003.
8. The features of Diastole
Normal diastolic function is dependent on
compliance, distensibility and relaxation properties of
the ventricles.
Examining the pressure volume loops provide data
regarding diastolic function.
First of all a detailed examination of the diastolic
phase of the cardiac cycle is in order.
Vasan RS, Levy D. Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation. 2000; 101: 2118–
2121.
9. The features of Diastole
Diastole extends from closure of the aortic
valve to the closure of the mitral valve. It is
composed of four phases
Isovolumetric relaxation
Early filling
Diastasis
Atrial systole
Vasan RS, Levy D. Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation. 2000; 101: 2118–
2121.
10. The features of Diastole
The normal pressure volume loop showing the different phases of
the cardiac cycle
Vasan RS, Levy D. Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation. 2000; 101: 2118–
2121.
11. Characteristics of Systolic vs Diastolic Heart
failure
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
12. Pathophysiology of Diastolic Heart Failure
The patho-physiology of diastolic heart failure is characterized
by a low cardiac output that results typically from a ventricle
that has thick walls but a small cavity (increased left
ventricular mass/volume ratio).
When the left ventricle is stiff, it relaxes slowly in early diastole
and offers greater resistance to filling in late diastole, so the
diastolic pressures are elevated.
The low cardiac output manifests as fatigue, while the higher
end diastolic pressure is transmitted backwards through the
valve- less pulmonary veins to the pulmonary capillaries,
resulting in exertional dyspnea.
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
13. Pathophysiology of Diastolic Heart Failure
These patho-physiological abnormalities trigger
neurohormonal activation as happens in systolic
heart failure.
Symptoms may be unmasked by exercise because,
unlike normal people, patients with diastolic heart
failure are unable to augment their stroke volume by
increasing their left ventricular end diastolic volume
(Frank-Starling mechanism).
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
14. Pathophysiology of Diastolic Heart Failure
These patients often have an exaggerated response of
systolic blood pressure to exercise.
Mechanisms contributing to abnormal left ventricular
diastolic properties include stiff large arteries,
hypertension, myocardial ischemia, diabetes, and
intrinsic myocardial changes with or without
associated hypertrophy
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
15. Pathophysiology of diastolic heart failure
Abnormal relaxation and
increased stiffness are
associated with diastolic
filling abnormalities and
normal exercise tolerance
in the early phase of
diastolic dysfunction.
When the disease
progresses, pulmonary
pressures increase
abnormally during exercise
with reduced exercise
tolerance.
When filling pressures
increases further, left
atrial pressure and size
increase and exercise
tolerance falls with clinical
signs of congestive heart
failure (CHF).
16. What Causes It?
The most common cause of diastolic heart failure is the natural
effect of aging on the heart. As you age, your heart muscle
tends to stiffen, which can prevent your heart from filling with
blood properly, leading to diastolic heart failure.
But there are many health problems that can impair your left
ventricle's ability to fill properly with blood during diastole.
17. Causes Of Diastolic Heart Failure
Cause What is it? How it causes heart failure
Coronary artery
disease (CAD)
Blockage of the arteries that supply
blood to the heart
Low blood flow to the heart muscle (ischemia)
can prevent the heart from relaxing and filling
with blood.
High blood pressure Elevated pressure in your arteries Heart muscle can thicken the wall of the heart
(hypertrophy) in an effort to pump
against high blood pressure. Thickened heart
muscle limits the heart's ability to relax and fill
with blood.
Aortic stenosis Narrowed opening of the aortic
valve
The left ventricle thickens, limiting its ability to
fill.
Hypertrophic
cardiomyopathy
Inherited abnormality of heart
muscle resulting in very thick walls
of the left ventricle
Thick heart muscle prevents blood from filling
the left ventricle.
Pericardial disease Abnormality of the sac that
surrounds the heart (pericardium)
Fluid in the pericardial space (pericardial
tamponade) or a thickened pericardium
(pericardial constriction) can limit the heart's
ability to fill.
18. Causes of Diastolic Congestive Heart
Failure
Myocardial
Impaired relaxation
Epicardial or microvascular ischemia
Myocyte hypertrophy
Cardiomyopathies
Aging
Hypothyroidism
Increased passive stiffness
Diffuse fibrosis
Post-infarct scarring
Myocyte hypertrophy
Infiltrative (eg, amyloidosis, hemochromatosis, Fabry’s disease)
Brad G. Angeja, William Grossman. Evaluation and Management of Diastolic Heart Failure. Circulation. 2003;107:659–663
19. Causes of Diastolic Congestive Heart
Failure
Endocardial
Fibroelastosis
Mitral or tricuspid stenosis
Epicardial / Pericardial
Pericardial constriction
Pericardial tamponade
Coronary microcirculation
Capillary compression
Venous engorgement
Other
Volume overload of the contralateral ventricle
Extrinsic compression by tumor
Brad G. Angeja, William Grossman. Evaluation and Management of Diastolic Heart Failure. Circulation. 2003;107:659–663
21. Factors that Exacerbate Diastolic Heart Failure:
Uncontrolled hypertension
Atrial Fibrillation
Non-compliance with or inappropriate discontinuation of
medications for heart failure
Myocardial ischemia
Anemia
Renal insufficiency
Use of NSAIDS or thiazolidinediones
Dietary indiscretion with overindulgence in salty foods
22. Characteristics of Diastolic Heart Failure:
Low stroke volume
Reduced cardiac output despite a normal ejection fraction
Limited exercise tolerance as a result of elevated left
ventricular diastolic and pulmonary venous pressure ->
reduction in lung compliance -> increase in the work of
breathing
24. Diagnosis
The signs and symptoms of heart failure are nonspecific (dyspnea, exercise
intolerance, fatigue, weakness) and often can be attributed to other
conditions, such as pulmonary disease, anemia, hypothyroidism,
depression, and obesity.
Furthermore, it is difficult to distinguish diastolic from systolic heart failure
based on physical findings or symptoms.
Systolic heart failure is defined as a left ventricular ejection fraction of less
than 45 percent, but diagnostic criteria for diastolic dysfunction are still
controversial.
Cardiac catheterization remains the gold standard for demonstrating
impaired relaxation and filling, because it provides direct measurement of
ventricular diastolic pressure. However, the balance of benefit, harm, and
cost argue against its routine use in diagnosing diastolic dysfunction.
25. Diagnosis of Diastolic Heart Failure
The diagnosis of diastolic heart failure requires three
conditions to be simultaneously satisfied:
1), Presence of signs and symptoms of heart failure;
2), Presence of normal or only slightly reduced LV ejection
fraction (EF. 50%) a;
3) Presence of increased diastolic pressure or impaired filling
caused by delayed iso-volumic relaxation or elevated stiffness.
Patients with shortness of breath on exertion, pulmonary
rales, or gallop sound but with near normal systolic function
are usually diagnosed with DHF.
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
26. Non-invasive assessment of diastolic function
Several non-invasive techniques have been used for assessing
diastolic function in patients with coronary, valvular or
myocardial heart disease.
The most commonly used methods are 2D- and Doppler-
echocardiography, Doppler-tissue imaging, radionuclide
ventriculography, MR myocardial tagging and MR imaging.
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
27. Echocardiography
M-mode echocardiography has been used to assess the dimensional
changes and its first derivates during diastolic filling.
The presence of LV myocardial fibers oriented in the longitudinal direction
and located in the trabecular, subendocardial, and papillary muscle regions
has led to an increasing interest in echocardiographic assessment of the LV
long axis function.
As displacement of the atrioventricular plane towards the apex is a direct
reflection of longitudinal fiber contraction, its measurement by M mode
echocardiography provides additional information regarding global and
regional systolic and diastolic function.
Henein and Gibson states, delayed onset of lengthening can effectively
suppress early diastolic trans-mitral flow, even though the minor axis
increases and mitral cusps separate normally
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
28. During the last 2 decades Doppler-echocardiography has emerged as an
important clinical tool providing reliable and useful data on diastolic
performance. Three different approaches are routinely used in the
assessment of diastolic dysfunction: measurement of trans-mitral and
pulmonary venous flow as well as intra-ventricular filling patterns (Doppler
flow propagation).
The trans-mitral velocity pattern remains the starting point of
echocardiographic assessment of LV diastolic function; since it is easy to
acquire and can rapidly categorize patients with normal or abnormal
diastolic function by E/A ratio (early to late filling velocity).
In healthy young individuals, most diastolic filling occurs in early diastole so
that the E/A ratio is > 1.
When relaxation is impaired, early diastolic filling decreases progressively
and a vigorous compensatory atrial contraction (‘atrial kick’) occurs.
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
Echocardiography
29. Patterns of Left Ventricular Diastolic Filling as Shown by
Standard Doppler Echocardiography
30. The results in a reversed E / A ratio, increased deceleration time, and increased iso-
volumic relaxation time.
With disease progression LV compliance becomes reduced and filling pressures
begin to increase leading to compensatory augmentation of left atrial pressure with
increase in early filling despite impaired relaxation, so that filling pattern looks
relatively normal (‘pseudo-normalization’ pattern = E/A > 1).
Finally, in patients with severe decrease in LV compliance, left atrial pressure is
markedly elevated and compensates with vigorous early diastolic filling for impaired
relax-ation.
This ‘restrictive’ filling pattern (E/A > 1) is consistent with an abnormal rise in LV
pressure and an abrupt deceleration of flow with little additional filling during mid-
diastole and atrial contraction.
In extreme cases the LV pressure rise overshoots left atrial pressure so that diastolic
mitral regurgitation in mid diastole may be seen.
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
Echocardiography
31. Color Doppler M-mode provides a unique window into the fluid dynamics
of flow across the mitral valve. The speed of propagation is enhanced with
rapid relaxation and LV suction.
Clinical and experimental studies have demonstrated that the inverse
correlation to t is relatively independent of left atrial pressure.
Doppler tissue imaging yields information on intramyocardial velocity,
providing a unique insight into LV mechanics during iso-volumic contraction
and relaxation.
In normal persons the mitral annular motion is almost a mirror image of
the trans-mitral flow pattern, but in patients with pseudo normal or
restrictive filling pattern, annular motion is abnormally low, implying that it
is relatively independent of preload.
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
Echocardiography
32. It has been shown that relaxation velocities in the myocardium
are inversely correlated with t, so that a non-invasively
calculation of the time constant of relaxation seems to be
possible.
Through the integrated use of Doppler echocardiography and
Doppler tissue imaging, it is possible to obtain a fairly precise
picture of LV diastolic function.
However, atrial fibrillation or frequent ectopic beats are the
major limitation of these techniques. To overcome this
problem, averaging of several heart cycles with similar RR
intervals has been proposed.
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
Echocardiography
33. Magnetic resonance imaging
This technique has been shown to be of considerable use in the
morphologic assessment of the heart, but functional assessment can also
be obtained.
However, their clinical relevance remains to be demonstrated.
Additional information may be gained from newer techniques such as
magnetic resonance myocardial tagging, which allows the labeling of
specific myocardial regions.
From these tags the rotational and translational motion of the left ventricle
can be determined which is characterized by a systolic wringing motion
followed by a rapid diastolic untwisting.
This untwisting motion is directly related to relaxation and may be used as
a measure of the rate and completeness of relaxation as well as an
estimate of early diastolic filling
L. Mandinov et al. Diastolic heart failure. Cardiovascular Research 45 (2000) 813–825
35. Series of MR images in a control patient with normal LV function
(temporal resolution 35 ms).
The MR pictures show horizontal and vertical lines (myocardial tags)
which are superimposed on the conventional MR image.
From the movement of the grid crossing points the contraction and
relaxation behavior of the left ventricle can be determined. During
isovolumic contraction there is a counter-clockwise rotation at the
apex followed by systolic shortening.
During isovolumic relaxation there is a clockwise rotation
(‘untwisting’) which is followed by diastolic lengthening.
This systolic–diastolic contraction–relaxation behavior is altered in
patients with diastolic dysfunction with prolongation of diastolic
back-rotation.
Magnetic resonance imaging
L. Mandinov et al. Diastolic heart failure. Cardiovascular Research 45 (2000) 813–825
36. Radionuclide angiography
This technique may be used to study the rapid filling phase of diastole, the
duration of the isovolumic relaxation phase, the relative contribution of
rapid filling to total diastolic filling, and the relation between regional
nonuniformity of left ventricular function and global filling properties.
However, radionuclide angiography does not permit assessment of the left
atrial–left ventricular pressure gradient or the simultaneous evaluation of
changes in left ventricular pressure and volume during relaxation and
filling.
Therefore, complete clinical interpret tation of ‘abnormal’ left ventricular
filling indexes, or changes in these indexes after interventions, is not
possible.
Despite the inherent limitations of noninvasive assessment of left
ventricular diastolic function, radionuclide evaluation of left ventricular
filling may provide clinically useful insights.
L. Mandinov et al. Diastolic heart failure. Cardiovascular Research 45 (2000) 813–825
37. Invasive assessment of diastolic function
Cardiac catheterization with simultaneous pressure
and volume measurements is the ‘gold’ standard for
assessing LV diastolic function.
Prerequisites are high-fidelity pressure recordings
with simultaneous angio- or echocardiography or the
use of the conductance technique.
The rate of LV relaxation, rate and timing of diastolic
filling as well as myocardial and chamber stiffness can
be determined
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
38. Diagnostic criteria for diastolic heart failure
Signs or symptoms of congestive heart failure
Exertional dyspnoea [eventually objective evidence by reduced peak exercise oxygen
consumption (<25 ml . kg"1 . min"1)], orthopnea, gallop sounds, lung crepitations,
pulmonary oedema.
and
Normal or mildly reduced left ventricular systolic function:
LVEF§45% and LVEDIDI<3·2 cm . m"2 or LVEDVI<102 ml . m"2
And
Evidence of abnormal left ventricular relaxation, filling, diastolic distensibility and
diastolic stiffness:
Slow isovolumic left ventricular relaxation:
LVdP/dtmin<1100 mmHg . s"1
and/or IVRT<30y>92 ms, IVRT30–50y>100 ms, IVRT>50y>105 ms
and/or ô>48 ms
How to diagnose diastolic heart failure. European Heart Journal (1998) 19, 990–1003
39. Diagnostic criteria for diastolic heart failure
and/or slow early left ventricular filling:
PFR<160 ml . s"1 . m"2
and/or PFR<30y<2·0 EDV . s"1, PFR30–50y<1·8 EDV . s"1, PFR>50y<1·6 EDV . s"1
and/or E/A<50y<1·0 and DT<50y>220 ms, E/A>50y<0·5 and DT>50y>280 ms
and/or S/D<50y>1·5, S/D>50y>2·5
and/or reduced left ventricular diastolic distensibility:
LVEDP>16 mmHg or mean PCW>12 mmHg
and/or PV A Flow >35 cm . s"1
and/or PV A t>MV A t+30 ms
and/or A/H>0·20
and/or increased left ventricular chamber or muscle stiffness:
b>0·27
and/or b*>16
How to diagnose diastolic heart failure. European Heart Journal (1998) 19, 990–1003
40. Proposed diagnostic algorithm for diastolic
heart failure
B, constant of left ventricular chamber stiffness; BNP, Btype natriuretic peptide; E’, mitral annulus early diastolic velocity as evaluated by
tissue Doppler; E, transmitral early diastolic velocity; EF, ejection fraction; LVEDP, left ventricular end-diastolic pressure; LVEDVI, left
ventricular end-diastolic volume index; mPCWP, mean pulmonary capillary wedge pressure; NT-proBNP, N-terminal pro-brain natriuretic
peptide; RVSP, right ventricle systolic pressure. This figure is adapted with permission from [30] and from Wachter R, Edelman F.
Diagnosis of heart failure with preserved ejection fraction. Heart Failure Clinics 2014; 10:399-406.
41. HOW TO DIAGNOSE HFpEF
Walter J. Paulus, Carsten Tschöpe, et al,.How to diagnose diastolic heart failure: a consensus statement on the diagnosis.European Heart Journal Oct 2007, 28
(20) 2539-2550; DOI: 10.1093/eurheartj/ehm037.
43. How to exclude HFpEF
Diagnostic flow chart on ‘How to exclude HFNEF’ in a patient presenting with breathlessness and no signs of
fluid overload. S, TD shortening velocity.
44. NONPHARMACOLOGIC INTERVENTIONS
Lifestyle modifications are recommended to reduce
the risk of all forms of cardiovascular disease.
Measures include weight loss, smoking cessation,
dietary changes, and exercise.
Identification and treatment of comorbid conditions,
such as high blood pressure, diabetes, and
hypercholesterolemia, are important in reducing the
risk of subsequent heart failure.
45. PHARMACOLOGIC
There has been little to no progress made in identifying evidence-
based, effective, and specific treatments for patients with DHF.
Drug classes, which have been shown to improve outcomes in
patients with SHF, have proved ineffective in reducing mortality in
DHF.
This may be because of the pathophysiological heterogeneity
underlying DHF, incomplete understanding of DHF, heterogeneity of
patients included in clinical trials with variable inclusion criteria, or
contribution to DHF by extracardiac conditions.
Several drugs have been studied for the treatment of DHF:
angiotensin II receptor blockers, angiotensin-converting enzyme
inhibitors, aldosterone antagonists, b-blockers, digoxin, and
sildenafil.
Alina Nicoara, Mandisa Jones-Haywood.Diastolic heart failure: diagnosis and therapy. Curr Opin Anesthesiol 2016, 29:61–67.
46. Therapeutic approach to diastolic heart failure.
Heart rate
control is
paramount
in patients
with atrial
fibrillation.
ACE,
angiotensi
n
converting
enzyme.
47. Management of diastolic heart failure
An ideal treatment strategy for patients with diastolic dysfunction
has not been devised, and medical therapy of diastolic dysfunction is
often empirical and lacks clear-cut pathophysiologic concepts.
Nevertheless four treatment goals have been advocated for the
therapy of diastolic dysfunction:
Reduction of central blood volume (diuretics)
Improvement of LV relaxation (calcium channel block ers or ACE
inhibitors).
Regression of LV hypertrophy (decrease in wall thickness and
removal of excess collagen by ACE inhibitors, AT-2 antagonists or
spironolactone).
Maintenance of atrial contraction and control of heartrate (beta-
blockers, antiarrhythmica).
Fahad Aziza, Luqman-Arafath TK, et al. Diastolic Heart Failure: A Concise Review. J Clin Med Res • 2013;5(5):327-334
48.
49. Management of diastolic heart failure
Mineralocorticoid antagonists have been investigated for the
treatment of DHF based on the participation of the renin–
angiotensin–aldosterone system in the pathogenesis of DHF.
In the recent TOPCAT trial, the effects of spironolactone have
been studied in patients with DHF.
The primary outcome was a composite of death from
cardiovascular causes, aborted cardiac arrest, or
hospitalization for management of heart failure.
Alina Nicoara, Mandisa Jones-Haywood.Diastolic heart failure: diagnosis and therapy. Curr Opin Anesthesiol 2016, 29:61–67.
50. Management of diastolic heart failure
The results showed that spironolactone did not reduce the
incidence of the primary composite endpoint.
It has also been hypothesized that a reduction in heart rate
and therefore prolongation in diastolic filling time would result
in more favorable LV filling and better coronary perfusion and
would therefore mitigate DHF symptoms.
The effect of heart rate reduction on exercise capacity has
been studied in patients with DHF.
Alina Nicoara, Mandisa Jones-Haywood.Diastolic heart failure: diagnosis and therapy. Curr Opin Anesthesiol 2016, 29:61–67.
51. Ivabradine, an If inhibitor of the sinoatrial pacemaker, devoid of effects on cardiac
contractility has been compared with placebo in a recent randomized, crossover
study.
When compared with placebo, ivabradine significantly worsened the change in
peak VO2 in the DHF cohort and significantly reduced submaximal exercise
capacity as determined by the oxygen uptake efficiency slope.
Exercise training has been shown to improve cardiorespiratory fitness in patients
with SHF. In a recent meta-analysis of randomized clinical trials that evaluated the
efficacy of exercise training in patients with DHF, exercise training in patients with
DHF was associated with an improvement in cardiorespiratory fitness and quality
of life even if there were no significant changes in LV systolic or diastolic function.
Management of diastolic heart failure
Alina Nicoara, Mandisa Jones-Haywood.Diastolic heart failure: diagnosis and therapy. Curr Opin Anesthesiol 2016, 29:61–67.
52. A prospective randomized, multicenter study is underway with the objective
of optimizing exercise training in prevention and treatment of DHF study
(OptimEx-CLIN) and defining the optimal dose of exercise training the DHF.
A promising approach is targeting the treatment to a specific DHF phenotype.
In this vein, serelaxin, a recombinant form of human relaxin-2, has been
studied comparatively in patients with DHF and patients with SHF in the
RELAXin-Acute Heart Failure (RELAX-AHF) trial.
Serelaxin was well tolerated and effective in early dyspnea relief and in
improving multiple outcomes including 180-day mortality irrespective of LVEF.
Management of diastolic heart failure
Alina Nicoara, Mandisa Jones-Haywood.Diastolic heart failure: diagnosis and therapy. Curr Opin Anesthesiol 2016, 29:61–67.