This document discusses the pathophysiology of heart failure. It begins by describing the essential functions of the heart in providing adequate blood supply and receiving blood returning from tissues. Heart failure occurs when the heart can no longer meet the metabolic demands of tissues despite normal or increased blood return. The key mechanisms involved in heart failure development include disorders of preload, contractility, and afterload. Chronic neurohormonal abnormalities also contribute to the progression of heart failure over time.
This document summarizes the pathophysiology of heart failure (HF). It discusses how HF results from abnormalities in cardiac structure/function that limit oxygen delivery to tissues, despite normal filling pressures. The progression of HF is driven by neurohumoral activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, which initially help compensate but eventually exacerbate cardiac remodeling and dysfunction. The document outlines the effects of various neurohormones involved in HF, including their normal and maladaptive roles in the progression of disease. Management of HF focuses on interrupting the harmful effects of long-term neurohumoral activation.
Congestive heart failure for ResidentsRap Cuaresma
The document discusses concepts related to heart failure including homeostasis, compensation, overcompensation, and remodeling. It describes how compensatory mechanisms initially help the heart function but can eventually lead to progression of heart failure if compensation is taken too far. The document outlines various compensatory mechanisms involving things like the autonomic nervous system, hormones, contractility, preload, and afterload. It also discusses different types of heart failure including diastolic, systolic, and those with reduced or preserved ejection fraction. Complexities in diagnosing and classifying heart failure are noted.
The document discusses congestive heart failure and its treatment with drugs. It provides details on the pathophysiology and classification of heart failure, clinical manifestations such as pulmonary edema and edema, and compensatory mechanisms. It then summarizes the mechanisms and effects of cardiac glycosides like digoxin, including their positive inotropic effects, effects on electrical conduction, and use in reducing symptoms and improving cardiac function in heart failure.
1. The document provides an overview of heart failure, including the physiology of the circulatory system, cardiac cycle, cardiac output, and pathophysiology of heart failure.
2. It describes the compensatory mechanisms in acute heart failure and the progression to chronic heart failure if not compensated, including fluid retention leading to edema.
3. The different types of heart failure are outlined, including systolic vs diastolic, left vs right sided, low vs high output, and the symptoms and causes of pulmonary and peripheral edema.
Heart failure is a clinical syndrome where the heart cannot pump enough blood to meet the body's needs. It can result from structural or functional problems with the heart ventricles. Common symptoms include shortness of breath, fatigue, and fluid retention. The prevalence of heart failure increases with age. It is classified based on ejection fraction and can have various causes like ischemic heart disease, hypertension, or cardiomyopathy. Multiple compensatory mechanisms are activated in response but ultimately lead to cardiac remodeling and further deterioration over time if left untreated. Management involves treating the underlying condition, reducing symptoms, and preventing further progression. Prognosis depends on severity of symptoms, with more severe cases having higher mortality rates.
This document provides information on congestive cardiac failure (CCF), including its definition, pathophysiology, clinical features, investigations, and management. CCF occurs when the heart muscle is weakened and cannot maintain adequate cardiac output. The pathophysiology involves changes in preload, afterload, and contractility that decrease cardiac output. Compensatory mechanisms initially help but later worsen symptoms. Clinically, CCF presents with dyspnea, edema, elevated JVP, hepatomegaly, and other signs. Investigations include BNP, ECG, echocardiogram. Management focuses on treating the underlying cause, reducing preload/afterload, and improving contractility. Diuretics, ACE inhibitors, beta
This document defines heart failure and discusses its key characteristics. It describes how heart failure occurs when the heart is unable to pump enough blood to meet the body's needs due to problems like abnormal heart muscle function or excessive loads on the heart. The document outlines the pathophysiology and progression of heart failure, including ventricular dilation and hypertrophy as compensatory mechanisms that ultimately fail. It also covers the clinical features, diagnostic tests, medical management, and nursing care considerations for patients with heart failure.
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 the pathophysiology of heart failure (HF). It discusses how HF results from abnormalities in cardiac structure/function that limit oxygen delivery to tissues, despite normal filling pressures. The progression of HF is driven by neurohumoral activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, which initially help compensate but eventually exacerbate cardiac remodeling and dysfunction. The document outlines the effects of various neurohormones involved in HF, including their normal and maladaptive roles in the progression of disease. Management of HF focuses on interrupting the harmful effects of long-term neurohumoral activation.
Congestive heart failure for ResidentsRap Cuaresma
The document discusses concepts related to heart failure including homeostasis, compensation, overcompensation, and remodeling. It describes how compensatory mechanisms initially help the heart function but can eventually lead to progression of heart failure if compensation is taken too far. The document outlines various compensatory mechanisms involving things like the autonomic nervous system, hormones, contractility, preload, and afterload. It also discusses different types of heart failure including diastolic, systolic, and those with reduced or preserved ejection fraction. Complexities in diagnosing and classifying heart failure are noted.
The document discusses congestive heart failure and its treatment with drugs. It provides details on the pathophysiology and classification of heart failure, clinical manifestations such as pulmonary edema and edema, and compensatory mechanisms. It then summarizes the mechanisms and effects of cardiac glycosides like digoxin, including their positive inotropic effects, effects on electrical conduction, and use in reducing symptoms and improving cardiac function in heart failure.
1. The document provides an overview of heart failure, including the physiology of the circulatory system, cardiac cycle, cardiac output, and pathophysiology of heart failure.
2. It describes the compensatory mechanisms in acute heart failure and the progression to chronic heart failure if not compensated, including fluid retention leading to edema.
3. The different types of heart failure are outlined, including systolic vs diastolic, left vs right sided, low vs high output, and the symptoms and causes of pulmonary and peripheral edema.
Heart failure is a clinical syndrome where the heart cannot pump enough blood to meet the body's needs. It can result from structural or functional problems with the heart ventricles. Common symptoms include shortness of breath, fatigue, and fluid retention. The prevalence of heart failure increases with age. It is classified based on ejection fraction and can have various causes like ischemic heart disease, hypertension, or cardiomyopathy. Multiple compensatory mechanisms are activated in response but ultimately lead to cardiac remodeling and further deterioration over time if left untreated. Management involves treating the underlying condition, reducing symptoms, and preventing further progression. Prognosis depends on severity of symptoms, with more severe cases having higher mortality rates.
This document provides information on congestive cardiac failure (CCF), including its definition, pathophysiology, clinical features, investigations, and management. CCF occurs when the heart muscle is weakened and cannot maintain adequate cardiac output. The pathophysiology involves changes in preload, afterload, and contractility that decrease cardiac output. Compensatory mechanisms initially help but later worsen symptoms. Clinically, CCF presents with dyspnea, edema, elevated JVP, hepatomegaly, and other signs. Investigations include BNP, ECG, echocardiogram. Management focuses on treating the underlying cause, reducing preload/afterload, and improving contractility. Diuretics, ACE inhibitors, beta
This document defines heart failure and discusses its key characteristics. It describes how heart failure occurs when the heart is unable to pump enough blood to meet the body's needs due to problems like abnormal heart muscle function or excessive loads on the heart. The document outlines the pathophysiology and progression of heart failure, including ventricular dilation and hypertrophy as compensatory mechanisms that ultimately fail. It also covers the clinical features, diagnostic tests, medical management, and nursing care considerations for patients with heart failure.
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.
Heart failure is a common and serious condition where the heart muscle is unable to pump sufficiently. It can have multiple causes and the prevalence increases significantly with age. Prognosis remains poor with high mortality rates. Diagnosis involves evaluating symptoms, signs, and testing like echocardiogram. Management focuses on general measures like diet, exercise, and reducing risk factors as well as specific treatments targeting the underlying cause and physiology of heart failure.
1. Heart failure affects 1.5-2% of the global population and is characterized by the heart's inability to pump an adequate amount of blood to meet the body's needs.
2. Common causes include coronary heart disease, hypertension, cardiomyopathies, and arrhythmias.
3. Heart failure progresses through stages from no limitation of physical activity to severe limitations where any physical activity causes deterioration of health. Treatment aims to reduce preload and afterload on the heart.
Heart failure is a clinical syndrome that results from any structural or functional impairment of the ventricle that reduces its ability to fill with or eject blood. It impacts over 5 million Americans with high costs of care. The key aspects are reduced cardiac output, ejection fraction, preload and afterload. Compensatory mechanisms initially help but eventually fail, leading to fluid overload and decompensation. Diagnosis involves history, exam, echocardiogram and blood tests. Treatment depends on symptoms and stages from risk factor modification to drug therapy and devices.
This document provides an overview of congestive cardiac failure/heart failure. It begins with definitions and terminology. It then discusses the epidemiology, etiology, risk factors, pathogenesis, complications, signs and symptoms, diagnosis, and management of heart failure. For pathogenesis, it describes the normal cardiac function and compensatory mechanisms in heart failure, including tachycardia, fluid retention, vasoconstriction, and ventricular hypertrophy. It also discusses the neurohormonal model of heart failure and factors that can precipitate or exacerbate the condition. The document provides a comprehensive review of heart failure.
This document discusses heart failure, including its definition, causes, types, and compensatory mechanisms. Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by intrinsic pump failure, an increased workload on the heart, or impaired filling of the cardiac chambers. The types of heart failure include acute or chronic, right-sided or left-sided, and forward or backward failure. When the heart begins to fail, compensatory mechanisms such as cardiac hypertrophy, dilation, and increased heart rate attempt to maintain adequate blood circulation.
A Global Problem
HIGHLY LETHAL 5 yr Survival rate “50%”
More M.I. cases now survive More Incidence of CHF due to damaged myocardium
Better options than before now available to treat CHF
Heart failure occurs when the heart cannot pump enough blood to meet the body's needs. It can be caused by problems with either the left or right side of the heart. Common causes include heart disease and hypertension. Symptoms depend on whether the left or right side is affected. The left side controls blood flow to the lungs, so left heart failure causes shortness of breath and coughing up blood. The right side controls blood returning from the body, so right heart failure causes fatigue, leg swelling and liver/kidney congestion. Over time the heart tries to compensate through enlargement but eventually decompensates leading to further symptoms.
Heart failure is a clinical syndrome that develops when –
The heart can not maintain adequate output
or
Can do so only at the expense of elevated ventricular filling pressure
Heart failure is a common condition where the heart is unable to pump enough blood to meet the body's needs. It can result from structural or functional disorders of the heart. The document provides details on the definition, causes, risk factors, pathophysiology, symptoms, diagnostic evaluation, classification systems, and treatment of heart failure. It emphasizes the importance of controlling risk factors, using medications such as ACE inhibitors and diuretics to manage symptoms, and making lifestyle changes like following a low-sodium diet and exercising regularly.
This document provides information on congestive heart failure (CHF), including its definition, pathophysiology, signs and symptoms, causes, precipitating factors, evaluation, monitoring, and management. CHF can be caused by conditions that weaken the heart muscle such as heart attacks or cardiomyopathy. It occurs when the heart cannot pump sufficiently due to problems with its electrical or mechanical function. Management involves treating underlying causes, reducing preload and afterload on the heart, and increasing cardiac contractility and output with medications, oxygen, and potentially devices like intra-aortic balloon pumps.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's demands. It can affect the left side, right side, or both sides of the heart. Common causes include heart attacks, arrhythmias, and conditions that increase the heart's workload. Symptoms include breathlessness, leg swelling, and fatigue. Diagnosis involves physical exam, chest x-ray, and blood tests to check for elevated natriuretic peptides. Treatment focuses on reducing fluid overload with diuretics, blocking the renin-angiotensin system, and managing arrhythmias. For some patients, devices or transplantation may be needed.
Heart failure is an imprecise term used to describe the state that developes when the heart cannot maintain an adequate cardiac output or can do so only at the expense of and elevated filling pressure.
OR
Heart failure is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. Congestive Heart Failure describes a condition where the heart muscle is weakened and cannot pump as strongly as before.
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.
The document provides an overview of heart failure, including its etiology, pathophysiology, diagnosis, and treatment. It discusses the incidence and prevalence of heart failure, common causes, compensatory mechanisms in the body, assessment methods, and current treatment approaches such as medications, device therapies, and lifestyle modifications. The goal is to educate medical practitioners on managing the complex clinical syndrome of heart failure.
Congestive Cardiac Failure presentation and diagnosisShah Abbas
This document provides an overview of congestive heart failure (CHF), including its definition, causes, pathophysiology, clinical manifestations, diagnostic evaluation, and management. CHF is defined as a clinical syndrome where the heart cannot pump enough blood to meet the body's needs. It is most commonly caused by conditions that overload or damage the heart such as hypertension, heart attacks, and cardiomyopathy. Clinically, it presents with symptoms of fluid backup like dyspnea, edema, and fatigue. Diagnostic tests include chest x-rays, EKGs, blood tests like BNP, and echocardiography. Treatment focuses on managing symptoms, addressing the underlying cause, and preventing complications through medications, lifestyle changes, and potentially devices
This document discusses congestive heart failure (CHF). It defines CHF as when the heart cannot produce enough cardiac output to meet the body's needs without compensatory mechanisms. The pathophysiology of CHF involves factors that increase preload and afterload on the heart as well as myocardial dysfunction. Common causes include volume overload, pressure overload, and myocardial issues. Clinical features include symptoms ranging from exertion to at rest based on severity. Treatment involves reducing preload and afterload, increasing contractility, and treating underlying causes. Digitalis is discussed as a positive inotropic agent to increase contractility.
Cardiac failure refers to the heart's inability to pump enough blood to meet metabolic demands. It can be classified in several ways, including based on severity, the side of heart involved, cardiac output level, duration, and type of function affected. Compensated heart failure involves mechanisms that return cardiac output to normal levels, while decompensated failure results in fluid retention and pulmonary or peripheral edema as compensatory mechanisms fail. Ejection fraction is normally over 50% and remains relatively normal in diastolic heart failure.
Heart failure occurs when the heart muscle is unable to pump enough blood to meet the body's needs. It can be caused by conditions that weaken the heart muscle or impair its ability to fill or contract properly. Common symptoms include shortness of breath, fatigue, and swelling in the legs or ankles. Diagnosis involves physical exam, medical history, lab tests, echocardiogram and chest x-ray to evaluate the structure and function of the heart. Treatment focuses on managing symptoms and addressing the underlying cause through lifestyle changes, medications and devices.
Heart failure is defined as a structural or functional impairment of the heart that prevents it from maintaining an adequate blood supply to meet the body's needs. It can be caused by conditions that overload or damage the heart such as hypertension, heart attacks, and cardiomyopathy. Heart failure is classified as acute or chronic and as forward or backward based on its location and symptoms. While compensatory mechanisms initially help the heart function, long term they cause further damage and worsening of heart failure over time. Diagnosis involves tests like echocardiograms, EKGs and blood tests, and treatment focuses on diuretics, ACE inhibitors and beta blockers to manage symptoms and slow progression of the disease.
Here are the answers to your questions:
1. A muscular fiber is also called a muscle cell. It contains myofibrils which are bundles of actin and myosin filaments. A sarcomere is the basic contractile unit along the myofibril, defined as the region between two Z-lines.
2. Muscle fiber shortening occurs via the sliding filament model. During muscle contraction, the heads of myosin cross-bridge with and pull on the actin filaments, drawing the Z-lines closer together and shortening the sarcomere. Many sarcomeres shortening leads to shortening of the entire muscle fiber.
3. The Starling's law states that the greater
Ppt cvs phsiology a small review for anaesthetistdrriyas03
The document discusses the cardiovascular system and heart function. It describes the heart as a pump that circulates blood through vessels to distribute essential substances and remove waste. The cardiovascular system transports 5 liters of blood per minute through a network of arteries, veins, and capillaries. Precise regulation of the cardiovascular system is achieved through neural, hormonal, and local control mechanisms.
Heart failure is a common and serious condition where the heart muscle is unable to pump sufficiently. It can have multiple causes and the prevalence increases significantly with age. Prognosis remains poor with high mortality rates. Diagnosis involves evaluating symptoms, signs, and testing like echocardiogram. Management focuses on general measures like diet, exercise, and reducing risk factors as well as specific treatments targeting the underlying cause and physiology of heart failure.
1. Heart failure affects 1.5-2% of the global population and is characterized by the heart's inability to pump an adequate amount of blood to meet the body's needs.
2. Common causes include coronary heart disease, hypertension, cardiomyopathies, and arrhythmias.
3. Heart failure progresses through stages from no limitation of physical activity to severe limitations where any physical activity causes deterioration of health. Treatment aims to reduce preload and afterload on the heart.
Heart failure is a clinical syndrome that results from any structural or functional impairment of the ventricle that reduces its ability to fill with or eject blood. It impacts over 5 million Americans with high costs of care. The key aspects are reduced cardiac output, ejection fraction, preload and afterload. Compensatory mechanisms initially help but eventually fail, leading to fluid overload and decompensation. Diagnosis involves history, exam, echocardiogram and blood tests. Treatment depends on symptoms and stages from risk factor modification to drug therapy and devices.
This document provides an overview of congestive cardiac failure/heart failure. It begins with definitions and terminology. It then discusses the epidemiology, etiology, risk factors, pathogenesis, complications, signs and symptoms, diagnosis, and management of heart failure. For pathogenesis, it describes the normal cardiac function and compensatory mechanisms in heart failure, including tachycardia, fluid retention, vasoconstriction, and ventricular hypertrophy. It also discusses the neurohormonal model of heart failure and factors that can precipitate or exacerbate the condition. The document provides a comprehensive review of heart failure.
This document discusses heart failure, including its definition, causes, types, and compensatory mechanisms. Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by intrinsic pump failure, an increased workload on the heart, or impaired filling of the cardiac chambers. The types of heart failure include acute or chronic, right-sided or left-sided, and forward or backward failure. When the heart begins to fail, compensatory mechanisms such as cardiac hypertrophy, dilation, and increased heart rate attempt to maintain adequate blood circulation.
A Global Problem
HIGHLY LETHAL 5 yr Survival rate “50%”
More M.I. cases now survive More Incidence of CHF due to damaged myocardium
Better options than before now available to treat CHF
Heart failure occurs when the heart cannot pump enough blood to meet the body's needs. It can be caused by problems with either the left or right side of the heart. Common causes include heart disease and hypertension. Symptoms depend on whether the left or right side is affected. The left side controls blood flow to the lungs, so left heart failure causes shortness of breath and coughing up blood. The right side controls blood returning from the body, so right heart failure causes fatigue, leg swelling and liver/kidney congestion. Over time the heart tries to compensate through enlargement but eventually decompensates leading to further symptoms.
Heart failure is a clinical syndrome that develops when –
The heart can not maintain adequate output
or
Can do so only at the expense of elevated ventricular filling pressure
Heart failure is a common condition where the heart is unable to pump enough blood to meet the body's needs. It can result from structural or functional disorders of the heart. The document provides details on the definition, causes, risk factors, pathophysiology, symptoms, diagnostic evaluation, classification systems, and treatment of heart failure. It emphasizes the importance of controlling risk factors, using medications such as ACE inhibitors and diuretics to manage symptoms, and making lifestyle changes like following a low-sodium diet and exercising regularly.
This document provides information on congestive heart failure (CHF), including its definition, pathophysiology, signs and symptoms, causes, precipitating factors, evaluation, monitoring, and management. CHF can be caused by conditions that weaken the heart muscle such as heart attacks or cardiomyopathy. It occurs when the heart cannot pump sufficiently due to problems with its electrical or mechanical function. Management involves treating underlying causes, reducing preload and afterload on the heart, and increasing cardiac contractility and output with medications, oxygen, and potentially devices like intra-aortic balloon pumps.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's demands. It can affect the left side, right side, or both sides of the heart. Common causes include heart attacks, arrhythmias, and conditions that increase the heart's workload. Symptoms include breathlessness, leg swelling, and fatigue. Diagnosis involves physical exam, chest x-ray, and blood tests to check for elevated natriuretic peptides. Treatment focuses on reducing fluid overload with diuretics, blocking the renin-angiotensin system, and managing arrhythmias. For some patients, devices or transplantation may be needed.
Heart failure is an imprecise term used to describe the state that developes when the heart cannot maintain an adequate cardiac output or can do so only at the expense of and elevated filling pressure.
OR
Heart failure is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. Congestive Heart Failure describes a condition where the heart muscle is weakened and cannot pump as strongly as before.
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.
The document provides an overview of heart failure, including its etiology, pathophysiology, diagnosis, and treatment. It discusses the incidence and prevalence of heart failure, common causes, compensatory mechanisms in the body, assessment methods, and current treatment approaches such as medications, device therapies, and lifestyle modifications. The goal is to educate medical practitioners on managing the complex clinical syndrome of heart failure.
Congestive Cardiac Failure presentation and diagnosisShah Abbas
This document provides an overview of congestive heart failure (CHF), including its definition, causes, pathophysiology, clinical manifestations, diagnostic evaluation, and management. CHF is defined as a clinical syndrome where the heart cannot pump enough blood to meet the body's needs. It is most commonly caused by conditions that overload or damage the heart such as hypertension, heart attacks, and cardiomyopathy. Clinically, it presents with symptoms of fluid backup like dyspnea, edema, and fatigue. Diagnostic tests include chest x-rays, EKGs, blood tests like BNP, and echocardiography. Treatment focuses on managing symptoms, addressing the underlying cause, and preventing complications through medications, lifestyle changes, and potentially devices
This document discusses congestive heart failure (CHF). It defines CHF as when the heart cannot produce enough cardiac output to meet the body's needs without compensatory mechanisms. The pathophysiology of CHF involves factors that increase preload and afterload on the heart as well as myocardial dysfunction. Common causes include volume overload, pressure overload, and myocardial issues. Clinical features include symptoms ranging from exertion to at rest based on severity. Treatment involves reducing preload and afterload, increasing contractility, and treating underlying causes. Digitalis is discussed as a positive inotropic agent to increase contractility.
Cardiac failure refers to the heart's inability to pump enough blood to meet metabolic demands. It can be classified in several ways, including based on severity, the side of heart involved, cardiac output level, duration, and type of function affected. Compensated heart failure involves mechanisms that return cardiac output to normal levels, while decompensated failure results in fluid retention and pulmonary or peripheral edema as compensatory mechanisms fail. Ejection fraction is normally over 50% and remains relatively normal in diastolic heart failure.
Heart failure occurs when the heart muscle is unable to pump enough blood to meet the body's needs. It can be caused by conditions that weaken the heart muscle or impair its ability to fill or contract properly. Common symptoms include shortness of breath, fatigue, and swelling in the legs or ankles. Diagnosis involves physical exam, medical history, lab tests, echocardiogram and chest x-ray to evaluate the structure and function of the heart. Treatment focuses on managing symptoms and addressing the underlying cause through lifestyle changes, medications and devices.
Heart failure is defined as a structural or functional impairment of the heart that prevents it from maintaining an adequate blood supply to meet the body's needs. It can be caused by conditions that overload or damage the heart such as hypertension, heart attacks, and cardiomyopathy. Heart failure is classified as acute or chronic and as forward or backward based on its location and symptoms. While compensatory mechanisms initially help the heart function, long term they cause further damage and worsening of heart failure over time. Diagnosis involves tests like echocardiograms, EKGs and blood tests, and treatment focuses on diuretics, ACE inhibitors and beta blockers to manage symptoms and slow progression of the disease.
Here are the answers to your questions:
1. A muscular fiber is also called a muscle cell. It contains myofibrils which are bundles of actin and myosin filaments. A sarcomere is the basic contractile unit along the myofibril, defined as the region between two Z-lines.
2. Muscle fiber shortening occurs via the sliding filament model. During muscle contraction, the heads of myosin cross-bridge with and pull on the actin filaments, drawing the Z-lines closer together and shortening the sarcomere. Many sarcomeres shortening leads to shortening of the entire muscle fiber.
3. The Starling's law states that the greater
Ppt cvs phsiology a small review for anaesthetistdrriyas03
The document discusses the cardiovascular system and heart function. It describes the heart as a pump that circulates blood through vessels to distribute essential substances and remove waste. The cardiovascular system transports 5 liters of blood per minute through a network of arteries, veins, and capillaries. Precise regulation of the cardiovascular system is achieved through neural, hormonal, and local control mechanisms.
Heart failure is a condition where the heart muscle is unable to pump enough blood to meet the body's needs. The heart muscle may weaken over time due to conditions like coronary artery disease or hypertension. Symptoms of heart failure include fatigue, shortness of breath, and swelling in the legs, ankles or feet.
Heart failure is a common condition that places a significant burden on healthcare systems. Specialist heart failure nurses play a key role in managing patients with acute heart failure in the hospital and after discharge through activities like identifying patients, developing care plans, educating patients, and providing early follow-up. Research shows that nurse-led interventions can substantially reduce hospital admissions and healthcare costs while improving patients' quality of life. The document describes a project that found delivering intravenous diuretics to patients in their homes or other community settings can safely and effectively avoid hospital admissions and provide better experiences for patients and caregivers compared to inpatient treatment.
Human heart anatomy and physiology Part -1Ritu Sharma
The heart is the pump responsible for maintaining adequate circulation of oxygenated blood around the vascular network of the body. It is a four-chamber pump, with the right side receiving deoxygenated blood from the body at low presure and pumping it to the lungs (the pulmonary circulation) and the left side receiving oxygenated blood from the lungs and pumping it at high pressure around the body (the systemic circulation).
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
Congestive heart failure occurs when the heart muscle is weakened and cannot pump blood effectively, causing fluid to back up into organs and tissues. Symptoms include shortness of breath, fatigue, swelling of the legs and feet. Causes include hypertension, heart attack, and heart muscle damage. Treatment involves medications like ACE inhibitors, beta blockers, diuretics to reduce symptoms and fluid buildup as well as lifestyle changes including reduced salt and fluid intake, exercise, and weight management. Patients should monitor for changes in symptoms and see a doctor promptly if symptoms worsen or new ones emerge.
This document summarizes guidelines from the 2017 ACC/AHA/HFSA Focused Update for the management of heart failure. It discusses the initial evaluation of heart failure patients including the use of biomarkers for prevention, diagnosis and prognosis. It also reviews pharmacological treatments for stage C heart failure with reduced or preserved ejection fraction. Additionally, it examines important comorbidities seen in heart failure patients such as anemia, hypertension, and sleep disordered breathing.
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The document summarizes key aspects of the cardiovascular system. It describes the heart as a hollow muscular organ with four chambers and two pumps. It also discusses the layers surrounding the heart, including the pericardium, as well as the heart's valves and conduction system which stimulate contraction. Finally, it briefly outlines factors that determine cardiac output such as preload, afterload and contractility.
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 provides an overview of the pathophysiology of heart failure. It discusses the essential functions of the heart in maintaining adequate blood supply and receiving returning blood from tissues. When the heart can no longer meet the metabolic demands of tissues, heart failure occurs. This can be due to disorders of preload, contractility, afterload, or the heart's electrical and mechanical functions. Compensatory mechanisms initially help but eventually maladapt. Neurohormonal changes further exacerbate heart failure over time. The document details causes and mechanisms of both systolic and diastolic heart failure.
The PATH program is a multi-year U.S. initiative focused on global health that works in over 50 countries. It aims to save lives and ensure self-sufficiency by providing vaccines, preventative treatments, and training for healthcare workers. The goal is to cut deaths from HIV/AIDS, tuberculosis, and malaria in half by 2020.
The PATH program aims to help homeless individuals and families in Los Angeles County access stable housing and supportive services to achieve long-term stability. It provides short-term rental assistance and case management to quickly rehouse homeless people and connect them to resources to address challenges like lack of income, untreated mental illness or substance abuse issues. The goal is to transition participants into permanent housing within a few months through this intensive temporary support and help acquiring job skills or public benefits.
The PATH program aims to improve global health and development through partnerships that accelerate innovation. It brings together experts from government, academia, non-profit, and industry to address major health challenges. The goal is to develop affordable, accessible tools like vaccines, drugs, diagnostics and devices that can have the greatest impact on improving lives in developing countries.
This document discusses the pathophysiology of heart failure. It begins by describing changes in myocardial contractility and the pressure-volume loop. Neurohumoral mechanisms are activated in heart failure as compensatory responses but become maladaptive over time, involving the sympathetic nervous system, renin-angiotensin-aldosterone system, and other factors. Left ventricular remodeling further worsens the heart's mechanical function and efficiency. Both systolic and diastolic dysfunctions can occur and are characterized by different structural and functional features.
This document summarizes key concepts in cardiovascular physiology including:
1. Determinants of cardiac output which are stroke volume and heart rate. Stroke volume is determined by preload, afterload, and contractility as described by Frank-Starling law of the heart.
2. Control of arterial blood pressure involves immediate control by baroreceptors and chemoreceptors, intermediate control by the renin-angiotensin-aldosterone system and atrial natriuretic peptide, and long-term control through sodium and water retention in the kidneys.
3. Coronary physiology includes characteristics of coronary blood flow such as intermittent flow, autoregulation to maintain flow, and metabolic and
This document discusses the cardiovascular system and types of shock. It begins by describing the five classes of blood vessels - arteries, arterioles, capillaries, venules, and veins. It then covers the structure of blood vessel walls and differences between arteries and veins. The document discusses blood pressure, circulation, and how blood flow is regulated. It defines shock and describes the four main types: hypovolemic, cardiogenic, anaphylactic, and septic shock. For each type, it explains the causes, stages, and pathophysiology.
Anatomy, physiology & patophysiology of the cardiovascularCarlos Galiano
This document provides an overview of the anatomy, physiology, and pathophysiology of the cardiovascular system as it relates to anesthesia. It discusses the structure and function of the heart and coronary circulation. It then covers topics such as cardiac cycle, hemodynamics, effects of the autonomic nervous system, and cardiovascular disorders including heart failure, hypertension, ischemic heart disease, and cardiac tamponade. For each topic, it provides details on pathophysiology and considerations for anesthesia management.
This document provides an overview of shock and its pathophysiology. It defines shock as a clinical syndrome resulting from inadequate tissue perfusion due to alterations in circulation. The stages of shock are described as compensatory, progressive, and irreversible. Compensatory mechanisms aimed at maintaining homeostasis in response to shock are discussed for various body systems. Nursing interventions for shock focus on treating its underlying cause, restoring circulating volume and hemodynamics through fluid resuscitation and vasoactive drugs, and minimizing oxygen consumption.
The document summarizes key aspects of cardiac physiology, including:
- The functions of the heart in generating blood pressure, routing blood flow, ensuring one-way flow, and regulating blood supply.
- The cardiac cycle and its phases of isovolumic contraction, ejection, isovolumic relaxation, and diastole.
- Factors that affect cardiac output including venous return, heart rate, contractility, and peripheral resistance.
- Key reflexes that regulate cardiac function such as the baroreceptor, chemoreceptor, and Bezold-Jarisch reflexes.
Heart failure is a clinical syndrome where the heart is unable to pump enough blood to meet the body's needs. It can result from any structural or functional cardiac disorder that impairs the ventricle's ability to fill with or eject blood. Some key signs and symptoms include breathlessness, ankle swelling, and fatigue. Over time, compensatory mechanisms like neurohormonal activation and ventricular remodeling can further worsen the condition by increasing preload and afterload on the heart. Common etiologies of heart failure include systolic dysfunction from conditions like heart attacks or cardiomyopathy, as well as diastolic dysfunction from issues with ventricular relaxation.
Shock is a severe pathophysiological insult associated with mitochondrial and cellular energetic failure due to reduced oxygen and nutrient delivery or ineffective utilization. It can occur with or without hypotension. The main types of shock are hypovolemic, cardiogenic, obstructive, distributive, septic, neurogenic, anaphylactic, and endocrine shock. Organ system consequences include effects on the CNS, CVS, respiratory system, kidneys, GI tract, liver, hematological system, and immune system. Pulmonary embolism can cause shock by increasing pulmonary vascular resistance and right ventricular afterload, potentially leading to right heart failure.
Peripheral resistance depends on factors like the diameter of blood vessels and viscosity of blood. Total peripheral resistance is the resistance of the entire circulation and is measured in peripheral resistance units. Blood pressure is the lateral pressure exerted by blood on vessel walls and includes systolic, diastolic, pulse and mean pressures. The body tightly regulates blood pressure through mechanisms like baroreceptor reflexes, chemoreceptor reflexes, and the renin-angiotensin system which act over different time periods to maintain homeostasis.
Cardiovascular physiology. Cardiac enzymes and their effects in the body system. Cardiac output and effects increasing and decreasing it. Calculations if Ejected fraction and other cardiac parameters.
Blood vessels transport blood throughout the body. There are three main types: arteries, which carry blood away from the heart; capillaries, where nutrients and wastes are exchanged; and veins, which carry blood back to the heart. Blood flow is regulated through pressure, resistance, and the actions of the cardiovascular system to ensure adequate circulation throughout the body. Neural and hormonal mechanisms precisely control blood pressure and flow through reflexes and the release of substances like epinephrine and norepinephrine.
The document discusses the circulatory system's response to exercise. The primary purpose is to deliver adequate oxygen and remove waste from tissues. During heavy exercise, oxygen demand can increase 15-25 times resting levels. To meet this, cardiac output and blood flow to active muscles increase through two mechanisms: 1) increased heart rate and stroke volume leading to higher cardiac output, and 2) redistribution of blood flow from inactive organs to working muscles. Proper circulatory function is critical for exercise and maintaining homeostasis.
The document provides an overview of the cardiovascular system, including the anatomy and physiology of the heart and blood vessels. It discusses the chambers of the heart, valves, coronary circulation, conduction system, and nerve supply. It also covers measurements of various pressures like mean arterial pressure, central venous pressure, and pulmonary artery pressure. Other topics include cardiac output, stroke volume, contractility, and the determinants of cardiac performance. Graphs of the cardiac cycle and Wigger's diagram are presented showing the mechanical events in systole and diastole.
Cardiovascular physiology for anesthesiamarwa Mahrous
This document discusses cardiovascular physiology including the structure and function of the heart, regulation of the cardiovascular system, blood flow through the pulmonary and systemic circulations, factors that influence cardiac output and stroke volume, and regulation of the systemic vasculature. Key points include:
- The cardiovascular system consists of the heart, blood vessels, and mechanisms that regulate blood circulation and pressure.
- Cardiac output is determined by stroke volume and heart rate. Stroke volume depends on preload, afterload, and contractility.
- The pulmonary circulation has low pressure and resistance while the systemic circulation has higher pressure and resistance.
- Autonomic nervous system and chemical factors regulate heart rate and contractility. Venous return and vascular
Heart as a pump, heart failure & its treatmentChirantan MD
The document discusses normal cardiac physiology and heart failure. It describes how cardiac function depends on preload, afterload, heart rate, and ionotropic state. It then discusses the pathophysiology of systolic heart failure, including activation of neurohormonal systems and changes at the molecular level in contractile proteins and calcium homeostasis. Compensatory mechanisms in heart failure and the progression to decompensated heart failure are also summarized.
The document summarizes cardiac physiology, including:
1. The cardiac cycle involves repetitive contraction (systole) and relaxation (diastole) of the heart chambers. Blood moves through the circulatory system based on pressure differences.
2. Key factors that influence cardiac output are preload, contractility, and afterload. Cardiac output is calculated as stroke volume multiplied by heart rate.
3. The autonomic nervous system and electrolytes like sodium, potassium, and calcium play important roles in regulating heart rate and contractility. The conduction system allows for coordinated contraction of the heart chambers.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
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ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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1. PATHOPHYSIOLOGY OF
HEART FAILURE
Prof. J. Hanacek
Technical co-operation: L. Šurinová
2. Notes to heart physiology
• Essential functions of the heart
• to cover metabolic needs of body tissue
(oxygen, substrates) by adequate blood supply
• to receive all blood comming back from the tissue
to the heart
• Essential conditions for fulfilling these functions
• normal structure and functions of the heart
• adequate filling of the heart by blood
3. Essential functions of the heart are secured
by integration of electrical and mechanical
functions of the heart
Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)
- changes of the heart rate
- changes of stroke volume
• Control of HR:
- autonomic nervous system
- hormonal(humoral) control
• Control of SV: - preload
- contractility
- afterload
4. Adaptive mechanisms of the heart
to increased load
• Frank - Starling mechanism
• Ventricular hypertrophy
– increased mass of contractile elements → ↑strength
of contraction
• Increased sympathetic adrenergic activity
– increased HR, increased contractility
• Incresed activity of R–A–A system
6. Preload
Stretching the myocardial fibers during diastole by increasing end-
diastolic volume → ↑ force of contraction during systole = Starling
´s law
preload = diastolic muscle sarcomere length leading to increased
tension in muscle before its contraction (Fig.2,3)
- venous return to the heart is important → end-diastolic
volume is influenced
- stretching of the sarcomere maximises the number
of actin-myosin bridges responsible for development of force
- optimal sarcomere length ∼ 2.2 µ m
7.
8. Myocardial contractility
Contractility of myocardium
Changes in ability of myocardium to develop the force
by contraction that occur independently on the
changes in myocardial fibre length
Mechanisms involved in changes of contractility
• ↑ amount of created cross-bridges in the sarcomere
by ↑ of [ Ca ++] i concentration
- catecholamines → ↑[ Ca++] i→ ↑ contractility
- inotropic drugs → ↑[ Ca++] i→ ↑ contractility
↑ contractility → shifting the entire ventricular function
curve upward and to the left
↓ contractility → shiffting the entire ventricular function
curve (hypoxia, acidosis) downward and to the right
9. The pressure – volume loop
• It is the relation between ventricular volume and pressure
• This loop provides a convenient framework for understanding
the response of individual left ventricular contractions
to alterations in preload, afterload, and contractility
• It is composed of 4 phases:
- filling of the ventricle
- isovolumic contraction of ventricle
- isotonic contraction of ventricle(ejection of blood)
- isovolumic relaxation of ventricle
11. Afterload
It is expressed as tension which must be developed in the wall
of ventricles during systole to open the semilunar valves and
eject blood to aorta/pulmunary artery
Laplace law:
intraventricular pressure x radius of ventricle
wall tension = --------------------------------------------------------
2 x ventricular wall thickness
↑ afterload: due to - elevation of arterial resistance
- ↑ ventricular size
- myocardial hypotrophy
↓ afterload: due to - ↓ arterial resistance
- myocardial hypertrophy
- ↓ ventricular size
12. Heart failure
Definition
It is the pathophysiological process in which
the heart as a pump is unable to meet
the metabolic requirements of the tissue for
oxygen and substrates despite the venous
return to heart is either normal or increased
13. Explanation of the terms
• Myocardial failure = abnormalities reside in the myocardium and lead
to inability of myocardium to fulfilling its function
• Circulatory failure = any abnormality of the circulation
responsible for the inadequacy in body tissue
perfusion, e.g. decreased blood volume, changes
of vascular tone, heart functiones disorders
• Congestive heart failure = clinical syndrome which is developed
due to accumulation of the blood in front
of the left or right parts of the heart
14. General pathomechanisms involved in heart
failure development
Cardiac mechanical dysfunction can develop as
a consequence in preload, contractility and afterload
disorders
Disorders of preload
↑↑ preload → length of sarcomere is more than optimal →
→ ↓ strength of contraction
↓↓ preload → length of sarcomere is well below the optimal →
→ ↓ strength of contraction
15.
16. Important: failing ventricle requires higher end-diastolic volume
to achieve the same improvement of CO that normal
ventricle achieves with lower ventricular volumes
Disorders of contractility
In the most forms of heart failure the contractility of myocardium
is decreased (ischemia, hypoxia, acidosis, inflammation, toxins,
metabolic disorders... )
Disorders of afterload due to:
• fluid retention in the body
• ↑ arterial resistance
• valvular heart diseases ( stenosis )
17.
18. Characteristic features of systolic dysfunction
(systolic failure)
• ventricular dilatation
• reducing ventricular contractility (either generalized
or localized)
• diminished ejection fraction (i.e., that fraction of end-diastolic
blood volume ejected from the ventricle during each systolic
contraction – les then 45%)
• in failing hearts, the LV end-diastolic volume (or pressure)
may increse as the stroke volume (or CO) decreases
19. Characteristic features of diastolic dysfunctions
(diastolic failure)
• ventricular cavity size is normal or small
• myocardial contractility is normal or hyperdynamic
• ejection fraction is normal (>50%) or supranormal
• ventricle is usually hypertrophied
• ventricle is filling slowly in early diastole (during the period
of passive filling)
• end-diastolic ventricular pressure is increased
21. B. MYOCARDIAL DAMAGE
1. Primary
a) cardiomyopathy
b) myocarditis
c) toxicity (e.g. alcohol)
d) metabolic abnormalities (e.g. hyperthyreoidism)
2. Secondary
a) oxygen deprivation (e.g. coronary heart disease)
b) inflammation (e.g. increased metabolic demands)
c) chronic obstructive lung disease
22. C. ALTERED CARDIAC RHYTHM
1. ventricular flutter and fibrilation
2. extreme tachycardias
3. extreme bradycardias
23. Pathomechanisms involved in heart failure
A. Pathomechanisms involved in myocardial failure
• Damage of cardiomyocytes → ↓ contractility,
↑ ↓ compliance
Consequences:
• defect in ATP production and utilisation
• changes in contractile proteins
• uncoupling of excitation – contraction process
• ↓ number of cardiomyocytes
• impairment of relaxation of cardiomyocytes with decrease
compliance of myocardium
• impaired of sympato-adrenal system (SAS) → ↓ number of
β 1-adrenergic receptors on the surface of cardiomycytes
24.
25. 2. Changes of neurohumoral control of the heart
function
• Physiology: • SNS → ↑ contractility
↑ HR
↑ activity of physiologic pacemakers
Mechanism: • ↑ sympathetic activity →↑ cAMP →
→↑[ Ca ++] i → ↑ contractility
• ↑ sympathetic activity → ↓ influence
of parasympathetic system on the heart
• Pathophysiology: normal neurohumoral control is
changed and creation of pathologic
neurohumoral mechanisms are present
26.
27. Chronic heart failure (CHF) is characterized by an imbalance of
neurohumoral adaptive mechanisms with a net results of excessive
vasoconstriction and salt and water retention
Catecholamines : - concentration in blood :
- norepinephrin – 2-3x higher at the rest than in healthy subjects
- circulating norepinephrin is increased much more
during equal load in patients suffering from CHF than
in healthy subject
- ↓ number of beta 1 – adrenergic receptors →
→ ↓ sensitivity of cardiomyocytes to catecholamines →
→ ↓ contractility
System rennin – angiotensin – aldosteron
heart failure →↓ CO →↓ kidney perfusion → stim. Of RAA
system
28. Important:
Catecholamines and system RAA = compensatory mechanisms
↑ heart function and arterial BP
The role of angiotensin II in development of heart
failure
• vasoconstriction ( in resistant vesels)
• retention of Na →↑ blood volume
• ↑ releasing of arginin – vasopresin peptide (AVP )
from neurohypophysis
29. • facilitation of norepinephrine releasing from
sympathetic nerve endings
• ↑ sensitivity of vessel wall to norepinephrine
• mitogenic effect on smooth muscles in vessels and
on cardiomyocytes → hypertrophy
• constriction of vas efferens ( in glomerulus )
• ↑ sensation of thirst
• ↑ secretion of aldosteron from adrenal gland
• mesangial conctraction → ↓ glomerular filtration rate
30.
31. Pathophysiology of diastolic heart failure
• systolic heart failure = failure of ejecting function of the heart
• diastolic heart failure = failure of filling the ventricles,
↑ resistance to filling of ventricles
Diastolic failure is a widely recognized clinical entity
But, which of the cardiac cycle is real diastole ?
32.
33. Definition of diastolic heart failure
It is pathophysiological process characterized by symptoms and
signs of congestive heart failure, which is caused by increased
filling resistance of ventricles and increased intraventricular
diastolic pressure
Primary diastolic heart failure
- no signs and symptoms of systolic dysfunction is present
- ! up to 40% of patients suffering from heart failure!
Secondary diastolic heart failure
- diastolic dysfunction is the consequence of primary
systolic dysfunction
34. Main causes and pathomechanisms of diastolic
heart failure
1. structural disorders →↑passive chamber stiffness
• intramyocardial
– e.g. myocardial fibrosis, amyloidosis, hypertrophy,
myocardial ischemia...
b) extramyocardial – e.g. constrictive pericarditis
2. functional disorders → ↓ relaxation of chambers e. g. myocardial
ischemia, advanced hypertrophy of ventricles,
failing myocardium, asynchrony in heart
functions
35. Causes and mechanism participating on impaired
ventricular relaxation
a) physiological changes in chamber relaxation due to:
– prolonged ventricular contraction
Relaxation of ventricles is not impaired !
b) pathological changes in chamber relaxation due to:
Impaired relaxation process
• delayed relaxation (retarded)
• incomplete (slowed) relaxation
36.
37.
38. • Consequences of impaired ventricular relaxation
- filling of ventricles is more dependent on diastasis
and on the systole of atrias than in healthy subjects
Symptoms and signs:
• exercise intolerance = early sign of diastolic failure
• ↓ coronary blood flow during diastole
• Causes and mechanisms involved in development
of ventricular stiffness
• ventricular compliance = passive property of ventricle
Source of compliance: cardiomyocytes and other heart
tissue to stretching
39. ↓ Ventricular compliance is caused by structural abnormalities
localized in myocardium and in extramyocardial tissue
a) Intramyocardial causes : myocardial fibrosis, hypertrophy of
ventricular wall,restrictive cardiomyopathy
b. Extramyocardial causes : constrictive pericarditis
The role of myocardial remodelling in genesis of
heart failure
• adaptive remodelling of the heart
• pathologic remodelling of the heart
40. Main causes and mechanisms involved in
pathological remodelation of the heart
1.Increased amount and size of myocytes = hypertrophy
Due to: - ↑ volume and/or pressure load
(excentric, concentric hypertrophy)
- hormonal stimulation of cardiomyocytes by
norepinephrine, angiotenzine II
2. Increased % of non-myocytic cells in myocardium
and their influence on structure and function of heart
a. endothelial cells – endothelins : mitogenic ability →
→ stimulation growth of smooth muscle cells of vessels, fibroblasts
b. fibroblasts - ↑ production of kolagens
41.
42. Symptoms and signs of heart failure
• forward failure:
symptoms result from inability of the heart to pump enough
blood to the periphery (from left heart), or to the lungs (from
the right heart)
a) forward failure of left heart:- muscle weakness, fatigue,
dyspepsia, oliguria....
• general mechanism: tissue hypoperfusion
b) forward failure of right heart: - hypoperfusion of the
lungs → disorders of gas
exchange
- decreased blood supply
to the left heart
43. 2. backward failure:
– symptoms result from inability of the heart to accept
the blood comming from periphery and from lungs
• backward failure of left heart:
– increased pulmonary capillary pressure → dyspnoea
and tachypnoea, pulmonary edema (cardiac asthma) →
→ arterial hypoxemia and hypercapnia....
b. backward failure of right heart:
– increased pressure in systemic venous system →
→ peripheral edemas, hepatomegaly, ascites →↑nocturnal diuresis....