Heart failure is a common condition that results in impaired pumping of the heart. It can be caused by structural or functional issues in the heart. There are over 5 million patients with heart failure in the US, with 500,000 new cases diagnosed each year. The two main types are systolic heart failure, characterized by reduced pumping ability, and diastolic heart failure, characterized by stiffening of the heart muscle. Treatment involves medications such as ACE inhibitors, beta blockers, diuretics, and device-based therapies like biventricular pacing for certain patients. Ongoing research is exploring new drugs and approaches for the treatment of heart failure.
This document discusses drugs used for congestive heart failure (CHF). It defines heart failure and lists its common causes. It then describes the classes of drugs used to relieve CHF symptoms and improve cardiac function, such as diuretics, vasodilators, ACE inhibitors, and beta-blockers. It provides details on cardiac glycosides like digoxin, including its pharmacology, mechanisms of action, effects, interactions, and precautions. Finally, it briefly discusses other drugs used in CHF treatment like phosphodiesterase inhibitors amrinone and milrinone, and the inotropic drug dobutamine.
The file gives the information of Cardiac Failure. Etiology of cardiac failure, types, stages of cardiac failure. It also covers the multisystem effects of cardiac failure, classification of drugs acting on cardiac failure.
This document provides an overview of recent advances in the pharmacotherapy of congestive cardiac failure (CCF). It discusses the definition, epidemiology, classification, etiology and pathophysiology of heart failure. It then examines the signs and symptoms and management approaches, including both non-pharmacological and pharmacological measures. The pharmacological section focuses on the mechanisms of action of common drug classes used to treat CCF, such as diuretics, ACE inhibitors, beta-blockers, aldosterone antagonists, and inotropic drugs.
This document discusses acute decompensated heart failure (ADHF), including:
1. ADHF is characterized by rapidly developing symptoms of new or worsening chronic heart failure requiring hospitalization. It carries a high risk of rehospitalization and mortality.
2. Causes of ADHF include non-adherence to medications, acute myocardial ischemia, arrhythmias, infections, and other cardiovascular disorders.
3. Management involves aggressive diuresis, treatment of underlying causes, optimization of disease-modifying medications, and consideration of inotropes or mechanical circulatory support for severe cases.
4. Biomarkers like BNP are useful for diagnosis, assessing severity, and guiding therapy, while
Congestive heart failure (CHF) is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by systolic or diastolic dysfunction. Common symptoms include fatigue, weight gain, cough, and shortness of breath. Treatment includes drugs that increase cardiac contractility, reduce fluid retention, block the renin-angiotensin system, dilate blood vessels, and reduce heart rate. New drugs like ivabradine and sacubitril/valsartan may also help lower hospitalization rates.
Congestive heart failure is the progressive inability of the heart to supply adequate blood flow. It is accompanied by fluid retention and is a leading cause of mortality. Drug treatments for congestive heart failure include ACE inhibitors, beta blockers, diuretics, and digoxin to reduce workload on the heart and manage symptoms. The main goals of treatment are to decrease preload and afterload on the heart and improve contractility through use of medications that target the renin-angiotensin-aldosterone system, sympathetic nervous system, and sodium and water retention.
This document discusses the pharmacological treatment of congestive heart failure. It begins by defining heart failure as the heart's inability to pump blood efficiently, resulting in inadequate oxygen delivery. The main pathophysiological changes in heart failure are then described, including increased preload and afterload, sympathetic activation, and salt and water retention. The document outlines the pharmacological targets in treatment as preload, afterload, contractility, and remodeling. Specific drugs are then discussed in detail, including digoxin for increasing contractility, diuretics and vasodilators for reducing preload and afterload, and beta-blockers for prolonging survival. Dobutamine and dopamine are also mentioned as inotropic agents for acute decompensated
Heart failure is a common condition that results in impaired pumping of the heart. It can be caused by structural or functional issues in the heart. There are over 5 million patients with heart failure in the US, with 500,000 new cases diagnosed each year. The two main types are systolic heart failure, characterized by reduced pumping ability, and diastolic heart failure, characterized by stiffening of the heart muscle. Treatment involves medications such as ACE inhibitors, beta blockers, diuretics, and device-based therapies like biventricular pacing for certain patients. Ongoing research is exploring new drugs and approaches for the treatment of heart failure.
This document discusses drugs used for congestive heart failure (CHF). It defines heart failure and lists its common causes. It then describes the classes of drugs used to relieve CHF symptoms and improve cardiac function, such as diuretics, vasodilators, ACE inhibitors, and beta-blockers. It provides details on cardiac glycosides like digoxin, including its pharmacology, mechanisms of action, effects, interactions, and precautions. Finally, it briefly discusses other drugs used in CHF treatment like phosphodiesterase inhibitors amrinone and milrinone, and the inotropic drug dobutamine.
The file gives the information of Cardiac Failure. Etiology of cardiac failure, types, stages of cardiac failure. It also covers the multisystem effects of cardiac failure, classification of drugs acting on cardiac failure.
This document provides an overview of recent advances in the pharmacotherapy of congestive cardiac failure (CCF). It discusses the definition, epidemiology, classification, etiology and pathophysiology of heart failure. It then examines the signs and symptoms and management approaches, including both non-pharmacological and pharmacological measures. The pharmacological section focuses on the mechanisms of action of common drug classes used to treat CCF, such as diuretics, ACE inhibitors, beta-blockers, aldosterone antagonists, and inotropic drugs.
This document discusses acute decompensated heart failure (ADHF), including:
1. ADHF is characterized by rapidly developing symptoms of new or worsening chronic heart failure requiring hospitalization. It carries a high risk of rehospitalization and mortality.
2. Causes of ADHF include non-adherence to medications, acute myocardial ischemia, arrhythmias, infections, and other cardiovascular disorders.
3. Management involves aggressive diuresis, treatment of underlying causes, optimization of disease-modifying medications, and consideration of inotropes or mechanical circulatory support for severe cases.
4. Biomarkers like BNP are useful for diagnosis, assessing severity, and guiding therapy, while
Congestive heart failure (CHF) is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by systolic or diastolic dysfunction. Common symptoms include fatigue, weight gain, cough, and shortness of breath. Treatment includes drugs that increase cardiac contractility, reduce fluid retention, block the renin-angiotensin system, dilate blood vessels, and reduce heart rate. New drugs like ivabradine and sacubitril/valsartan may also help lower hospitalization rates.
Congestive heart failure is the progressive inability of the heart to supply adequate blood flow. It is accompanied by fluid retention and is a leading cause of mortality. Drug treatments for congestive heart failure include ACE inhibitors, beta blockers, diuretics, and digoxin to reduce workload on the heart and manage symptoms. The main goals of treatment are to decrease preload and afterload on the heart and improve contractility through use of medications that target the renin-angiotensin-aldosterone system, sympathetic nervous system, and sodium and water retention.
This document discusses the pharmacological treatment of congestive heart failure. It begins by defining heart failure as the heart's inability to pump blood efficiently, resulting in inadequate oxygen delivery. The main pathophysiological changes in heart failure are then described, including increased preload and afterload, sympathetic activation, and salt and water retention. The document outlines the pharmacological targets in treatment as preload, afterload, contractility, and remodeling. Specific drugs are then discussed in detail, including digoxin for increasing contractility, diuretics and vasodilators for reducing preload and afterload, and beta-blockers for prolonging survival. Dobutamine and dopamine are also mentioned as inotropic agents for acute decompensated
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. There are two main types: systolic, where the heart's pumping action is weakened, and diastolic, where the heart stiffens and does not relax properly. Compensatory responses like hypertrophy can initially help but eventually worsen the heart's function. Severity is classified from mild limitations to symptoms at rest. Common drugs used are diuretics, ACE inhibitors, beta-blockers, and cardiac glycosides like digoxin which increase contractility by altering ion transport.
This document summarizes the properties and uses of drugs with cardiac inotropic effects for treating heart failure. It discusses how these drugs increase the force of cardiac contraction without proportionally increasing oxygen consumption. The document outlines the mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects of digitalis glycosides, which are commonly used inotropic drugs that work by inhibiting the sodium-potassium ATPase pump. Digitalis glycosides are used to treat both congestive heart failure and cardiac arrhythmias.
This document discusses various classes of antihypertensive agents used to treat hypertension. It defines hypertension and describes the renin-angiotensin-aldosterone system which is important in regulating blood pressure. Common classes of antihypertensive agents discussed include diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha blockers, and central sympatholytics. Lifestyle modifications including weight loss, exercise, diet changes, and avoiding tobacco are also recommended for managing hypertension.
This document discusses the pharmacological management of heart failure. It describes the major drug groups used including diuretics, ACE inhibitors, beta blockers, aldosterone receptor antagonists, and vasodilators. It explains the mechanisms of action of these drugs, such as how diuretics reduce preload and edema, ACE inhibitors reduce afterload, and beta blockers attenuate the effects of sympathetic activation. The document also discusses the treatment of acute heart failure with drugs like furosemide, morphine, and nitroglycerin to reduce preload and afterload.
Pharmacological management of heart failureNaser Tadvi
Heart failure is caused by decreased cardiac output and increased sympathetic discharge. Drugs used to treat heart failure include diuretics to reduce preload, ACE inhibitors to reduce afterload, beta blockers to attenuate sympathetic activation, and digitalis for its inotropic effects. Newer drugs target vasodilation and myosin activation to further increase cardiac efficiency while reducing energy demands. Combination therapy following an assessment of cardiac function and volume status provides the best approach for management of heart failure.
This presentation deals with the use of various drugs in the treatment of heart failure such as Digoxin, ace inhibitors, beta bloockers, calcium channel blockers
1) Chronic HF is a progressive syndrome that impairs the heart's ability to pump blood effectively. It can be caused by structural or functional changes to the heart and has two main types: HFrEF with reduced ejection fraction and HFpEF with preserved ejection fraction.
2) Risk factors include age, with risk doubling each decade, and prior conditions like hypertension, diabetes and myocardial infarction. Five-year mortality is around 50% and sudden cardiac death causes 40% of HF deaths.
3) Treatment involves managing symptoms, slowing disease progression, and preventing hospitalizations through lifestyle changes, medications, and devices. Diuretics, ACE inhibitors, beta-blockers, and aldosterone antagon
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has a high mortality rate. The most common cause is coronary artery disease. When the heart does not contract well, blood backs up in the lungs and periphery. Chronic activation of compensatory mechanisms like the sympathetic nervous system contributes to cardiac remodeling over time.
Right heart failure causes issues like leg swelling and liver enlargement due to blood backing up. Left heart failure can cause pulmonary edema. Treatment focuses on reducing symptoms, slowing disease progression, and improving survival through drugs that target the renin-angiotensin-aldosterone system, beta-blockers, diuretics, and vasodilators. Dentists
This document discusses drugs used to treat congestive heart failure. It describes several classes of drugs and their mechanisms of action. The main drug classes discussed are: ACE inhibitors, ARBs, beta-blockers, diuretics, direct vasodilators, inotropic agents like cardiac glycosides and beta-agonists, and aldosterone antagonists. The goal of treatment is to increase cardiac output, relieve symptoms, slow disease progression, and improve survival by reducing preload and afterload on the heart.
The document provides information on the pharmacotherapy of heart failure, including:
- Heart failure results from the heart's inability to pump sufficient blood due to problems with structure or function.
- It discusses the causes, pathophysiology, classification, clinical manifestations, diagnosis, and treatment of heart failure.
- Treatment involves managing symptoms, improving cardiac function, and slowing disease progression through medications, lifestyle changes, and procedures. The goal is to improve quality of life and survival.
Cardiac glycosides like digoxin are used to treat heart failure. They work by inhibiting the sodium-potassium pump in cardiac cells, increasing intracellular calcium levels and improving cardiac contractility. Digoxin has a narrow therapeutic window, so monitoring drug levels is important to avoid toxic effects like arrhythmias. It can interact with many other drugs through changes in absorption, electrolyte levels, or transporter protein activity. Careful management of digoxin therapy is needed in patients with kidney dysfunction or other conditions affecting its metabolism and clearance.
Cardiac glycosides like digoxin are used to treat heart failure and cardiac arrhythmias. They work by inhibiting sodium-potassium ATPase, increasing intracellular calcium levels, and enhancing cardiac contractility. Common side effects include nausea, arrhythmias, and toxicity at high levels. While they were once a standard treatment, newer heart failure drugs like ACE inhibitors, ARBs, beta blockers, and diuretics are now preferred due to their better safety profiles. Digitalis remains an option when symptoms are not adequately controlled by other treatments.
Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by anything that reduces the heart's ability to fill or contract properly. Common causes include hypertension, heart attacks, alcohol/drug use, and rapid heart rhythms. Symptoms include fatigue, shortness of breath, swelling, and coughing. Treatment focuses on improving cardiac contractility, reducing preload and afterload stresses on the heart, and managing fluid retention through diuretics and other medications.
A 69-year-old man with a history of congestive heart failure, diabetes, hypertension, and coronary artery disease is prescribed digoxin for symptomatic relief of worsening heart failure despite maximal medical therapy. Digoxin increases cardiac output in failing hearts by increasing stroke volume. It decreases sympathetic tone and increases vagal activity. Side effects include arrhythmias, nausea, and toxicity at high levels.
Angina pectoris is chest pain due to ischemia of the heart muscle. It is usually felt as a tightness or pressure in the middle of the chest that may spread to the neck, jaw, or arm. There are three main types - stable angina brought on by exertion, unstable angina that occurs at rest, and Prinzmetal or variant angina caused by coronary artery spasm. Treatment involves medications to relieve symptoms like nitrates, beta blockers, calcium channel blockers, and newer drugs that open potassium channels or have a cytoprotective effect. Combination therapy with two or more classes is often used for better management of angina.
Heart failure is caused by conditions that weaken the heart muscle such as coronary artery disease and hypertension. The body compensates through mechanisms like the renin-angiotensin system which cause fluid retention, edema, and increased cardiac workload worsening the failure. Treatment goals include reducing preload and afterload through diuretics and vasodilators, improving oxygenation, and increasing contractility. Medications target neurohormonal activation through ACE inhibitors, ARBs, beta-blockers and aldosterone blockade. For severe cases, devices like ICDs, CRT, LVADs and transplantation are used. Lifestyle changes and treating the underlying cause are also important.
Heart failure is caused by conditions that weaken the heart muscle such as coronary artery disease and hypertension. The body compensates through mechanisms like the renin-angiotensin system which cause fluid retention, edema, and increased cardiac workload leading to more heart failure. Treatment goals include reducing preload and afterload through diuretics and vasodilators, improving oxygenation, and increasing cardiac function. Medications target these goals including ACE inhibitors, beta-blockers, diuretics, and devices like pacemakers may also be used. Lifestyle changes and treating the underlying cause are important parts of management.
The document discusses congestive heart failure (CHF), including its pathophysiology, recent advances in management, and therapeutic approaches. It describes how CHF results from the heart's inability to pump enough blood to meet the body's needs. Over time, compensatory mechanisms like increased neurohormonal activity can damage the heart further. Treatment aims to alleviate symptoms, improve quality of life, and decrease mortality through a combination of lifestyle changes, medications, and devices.
Drugs Used in Heart Failure
Drugs without positive inotropic effects used in Heart Failure:
Diuretics
ACE/ARB & Related agents
Vasodilators
β-Adrenergic Blockers
Others
Drugs with positive inotropic effects used in Heart Failure:
Digitalis
Other positive inotropic drugs:
Bipyridines
Beta-Adrenergic agonists
Investigational positive inotropic drugs: Istaroxime, Levosimanden, Omecamtiv mecarbil
This document discusses cardiovascular drugs and diseases. It describes the functional components and structure of the heart. The main diseases covered are hypertension, congestive heart failure, coronary artery disease, myocardial infarction, and cardiac arrhythmias. For each disease, the document discusses the pathophysiology and drugs used to treat it. These include diuretics, beta blockers, calcium channel blockers, ACE inhibitors, and other classes of antihypertensive and cardiac drugs.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
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Similar to HEART FAILURE: CONGESTIVE CARDIAC FAILURE
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. There are two main types: systolic, where the heart's pumping action is weakened, and diastolic, where the heart stiffens and does not relax properly. Compensatory responses like hypertrophy can initially help but eventually worsen the heart's function. Severity is classified from mild limitations to symptoms at rest. Common drugs used are diuretics, ACE inhibitors, beta-blockers, and cardiac glycosides like digoxin which increase contractility by altering ion transport.
This document summarizes the properties and uses of drugs with cardiac inotropic effects for treating heart failure. It discusses how these drugs increase the force of cardiac contraction without proportionally increasing oxygen consumption. The document outlines the mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects of digitalis glycosides, which are commonly used inotropic drugs that work by inhibiting the sodium-potassium ATPase pump. Digitalis glycosides are used to treat both congestive heart failure and cardiac arrhythmias.
This document discusses various classes of antihypertensive agents used to treat hypertension. It defines hypertension and describes the renin-angiotensin-aldosterone system which is important in regulating blood pressure. Common classes of antihypertensive agents discussed include diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha blockers, and central sympatholytics. Lifestyle modifications including weight loss, exercise, diet changes, and avoiding tobacco are also recommended for managing hypertension.
This document discusses the pharmacological management of heart failure. It describes the major drug groups used including diuretics, ACE inhibitors, beta blockers, aldosterone receptor antagonists, and vasodilators. It explains the mechanisms of action of these drugs, such as how diuretics reduce preload and edema, ACE inhibitors reduce afterload, and beta blockers attenuate the effects of sympathetic activation. The document also discusses the treatment of acute heart failure with drugs like furosemide, morphine, and nitroglycerin to reduce preload and afterload.
Pharmacological management of heart failureNaser Tadvi
Heart failure is caused by decreased cardiac output and increased sympathetic discharge. Drugs used to treat heart failure include diuretics to reduce preload, ACE inhibitors to reduce afterload, beta blockers to attenuate sympathetic activation, and digitalis for its inotropic effects. Newer drugs target vasodilation and myosin activation to further increase cardiac efficiency while reducing energy demands. Combination therapy following an assessment of cardiac function and volume status provides the best approach for management of heart failure.
This presentation deals with the use of various drugs in the treatment of heart failure such as Digoxin, ace inhibitors, beta bloockers, calcium channel blockers
1) Chronic HF is a progressive syndrome that impairs the heart's ability to pump blood effectively. It can be caused by structural or functional changes to the heart and has two main types: HFrEF with reduced ejection fraction and HFpEF with preserved ejection fraction.
2) Risk factors include age, with risk doubling each decade, and prior conditions like hypertension, diabetes and myocardial infarction. Five-year mortality is around 50% and sudden cardiac death causes 40% of HF deaths.
3) Treatment involves managing symptoms, slowing disease progression, and preventing hospitalizations through lifestyle changes, medications, and devices. Diuretics, ACE inhibitors, beta-blockers, and aldosterone antagon
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has a high mortality rate. The most common cause is coronary artery disease. When the heart does not contract well, blood backs up in the lungs and periphery. Chronic activation of compensatory mechanisms like the sympathetic nervous system contributes to cardiac remodeling over time.
Right heart failure causes issues like leg swelling and liver enlargement due to blood backing up. Left heart failure can cause pulmonary edema. Treatment focuses on reducing symptoms, slowing disease progression, and improving survival through drugs that target the renin-angiotensin-aldosterone system, beta-blockers, diuretics, and vasodilators. Dentists
This document discusses drugs used to treat congestive heart failure. It describes several classes of drugs and their mechanisms of action. The main drug classes discussed are: ACE inhibitors, ARBs, beta-blockers, diuretics, direct vasodilators, inotropic agents like cardiac glycosides and beta-agonists, and aldosterone antagonists. The goal of treatment is to increase cardiac output, relieve symptoms, slow disease progression, and improve survival by reducing preload and afterload on the heart.
The document provides information on the pharmacotherapy of heart failure, including:
- Heart failure results from the heart's inability to pump sufficient blood due to problems with structure or function.
- It discusses the causes, pathophysiology, classification, clinical manifestations, diagnosis, and treatment of heart failure.
- Treatment involves managing symptoms, improving cardiac function, and slowing disease progression through medications, lifestyle changes, and procedures. The goal is to improve quality of life and survival.
Cardiac glycosides like digoxin are used to treat heart failure. They work by inhibiting the sodium-potassium pump in cardiac cells, increasing intracellular calcium levels and improving cardiac contractility. Digoxin has a narrow therapeutic window, so monitoring drug levels is important to avoid toxic effects like arrhythmias. It can interact with many other drugs through changes in absorption, electrolyte levels, or transporter protein activity. Careful management of digoxin therapy is needed in patients with kidney dysfunction or other conditions affecting its metabolism and clearance.
Cardiac glycosides like digoxin are used to treat heart failure and cardiac arrhythmias. They work by inhibiting sodium-potassium ATPase, increasing intracellular calcium levels, and enhancing cardiac contractility. Common side effects include nausea, arrhythmias, and toxicity at high levels. While they were once a standard treatment, newer heart failure drugs like ACE inhibitors, ARBs, beta blockers, and diuretics are now preferred due to their better safety profiles. Digitalis remains an option when symptoms are not adequately controlled by other treatments.
Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by anything that reduces the heart's ability to fill or contract properly. Common causes include hypertension, heart attacks, alcohol/drug use, and rapid heart rhythms. Symptoms include fatigue, shortness of breath, swelling, and coughing. Treatment focuses on improving cardiac contractility, reducing preload and afterload stresses on the heart, and managing fluid retention through diuretics and other medications.
A 69-year-old man with a history of congestive heart failure, diabetes, hypertension, and coronary artery disease is prescribed digoxin for symptomatic relief of worsening heart failure despite maximal medical therapy. Digoxin increases cardiac output in failing hearts by increasing stroke volume. It decreases sympathetic tone and increases vagal activity. Side effects include arrhythmias, nausea, and toxicity at high levels.
Angina pectoris is chest pain due to ischemia of the heart muscle. It is usually felt as a tightness or pressure in the middle of the chest that may spread to the neck, jaw, or arm. There are three main types - stable angina brought on by exertion, unstable angina that occurs at rest, and Prinzmetal or variant angina caused by coronary artery spasm. Treatment involves medications to relieve symptoms like nitrates, beta blockers, calcium channel blockers, and newer drugs that open potassium channels or have a cytoprotective effect. Combination therapy with two or more classes is often used for better management of angina.
Heart failure is caused by conditions that weaken the heart muscle such as coronary artery disease and hypertension. The body compensates through mechanisms like the renin-angiotensin system which cause fluid retention, edema, and increased cardiac workload worsening the failure. Treatment goals include reducing preload and afterload through diuretics and vasodilators, improving oxygenation, and increasing contractility. Medications target neurohormonal activation through ACE inhibitors, ARBs, beta-blockers and aldosterone blockade. For severe cases, devices like ICDs, CRT, LVADs and transplantation are used. Lifestyle changes and treating the underlying cause are also important.
Heart failure is caused by conditions that weaken the heart muscle such as coronary artery disease and hypertension. The body compensates through mechanisms like the renin-angiotensin system which cause fluid retention, edema, and increased cardiac workload leading to more heart failure. Treatment goals include reducing preload and afterload through diuretics and vasodilators, improving oxygenation, and increasing cardiac function. Medications target these goals including ACE inhibitors, beta-blockers, diuretics, and devices like pacemakers may also be used. Lifestyle changes and treating the underlying cause are important parts of management.
The document discusses congestive heart failure (CHF), including its pathophysiology, recent advances in management, and therapeutic approaches. It describes how CHF results from the heart's inability to pump enough blood to meet the body's needs. Over time, compensatory mechanisms like increased neurohormonal activity can damage the heart further. Treatment aims to alleviate symptoms, improve quality of life, and decrease mortality through a combination of lifestyle changes, medications, and devices.
Drugs Used in Heart Failure
Drugs without positive inotropic effects used in Heart Failure:
Diuretics
ACE/ARB & Related agents
Vasodilators
β-Adrenergic Blockers
Others
Drugs with positive inotropic effects used in Heart Failure:
Digitalis
Other positive inotropic drugs:
Bipyridines
Beta-Adrenergic agonists
Investigational positive inotropic drugs: Istaroxime, Levosimanden, Omecamtiv mecarbil
This document discusses cardiovascular drugs and diseases. It describes the functional components and structure of the heart. The main diseases covered are hypertension, congestive heart failure, coronary artery disease, myocardial infarction, and cardiac arrhythmias. For each disease, the document discusses the pathophysiology and drugs used to treat it. These include diuretics, beta blockers, calcium channel blockers, ACE inhibitors, and other classes of antihypertensive and cardiac drugs.
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- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
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DECLARATION OF HELSINKI - History and principlesanaghabharat01
This SlideShare presentation provides a comprehensive overview of the Declaration of Helsinki, a foundational document outlining ethical guidelines for conducting medical research involving human subjects.
2. Introduction to Heart Failure
• Heart unable to provide adequate perfusion
of peripheral organs to meet their metabolic
requirements
• Characterized by:
1. Reduction in cardiac output
2. Increased TPR
• Progressing to congestive heart failure (CHF) is
accompanied by peripheral and pulmonary
edema.
3. Recent Advances Vs Reality
• Major advances in recent years in
management of patients with CHF
• In 2000 an estimated 4.7 million people in the
United States had HF
• The median survival after initial diagnosis is
1.7 years for men and 3.2 years for women.
• Sudden cardiac death is common in patients
with heart failure, contributing to 50% of all
287,000 deaths in the United States last year
4. Acute Vs Chronic HF
• In a patient with acute heart failure, the
short-term aim is stabilization by providing
symptomatic treatment through intravenous
interventions.
• Management of chronic heart failure is
multifaceted, with the long-term aims of:
• relieving symptoms
• improving hemodynamics
• improving quality of life and
• decrease mortality.
5. Cardiac Vs Noncardiac targets
• Conventional belief that the primary
defect in HF is in the heart
• Reality is that HF involves many other
processes and organs
• Research has shown that therapy
directed at noncardiac targets are more
valuable than cardiac targets
6. Compensation in HF
• Heart failure is usually accompanied by an
increase in:
1. Sympathetic nervous system (SNS)
2. Chronic up-regulation of the renin-
angiotensin-aldosterone system (RAAS)
and effects of aldosterone on heart,
vessels, and kidneys.
• CHF should be viewed as a complex,
interrelated sequence of events involving
hemodynamic, and neurohormonal events.
7. Compensation contd..
• In a failing heart, the loss of contractile function leads
to a decline in CO and a decrease in arterial BP.
• Baroreceptors sense the hemodynamic changes and
initiate countermeasures to maintain support of the
circulatory system.
• Activation of the SNS serves as a compensatory
mechanism in response to the earlier
• This helps maintain adequate cardiac output by:
1. Increasing myocardial contractility and heart rate (β1-
adrenergic receptors)
2. Increasing vasomotor tone (α1-adrenergic receptors)
to maintain systemic blood pressure
8. Consequences of hyperadrenergic
state
• Over the long term, this hyperadrenergic state
leads to irreversible myocyte damage, cell death, and
fibrosis.
• In addition, the augmentation in peripheral vasomotor
tone increases LV afterload
• This places an added stress upon the left ventricle
and an increase in myocardial O2 demand
(ventricular remodeling).
• The frequency and severity of cardiac arrhythmias
are enhanced in the failing heart
11. Therapeutic Overview
Problem
• Reduced force of contraction
• Decreased cardiac output
• Increased total peripheral resistance
• Inadequate organ perfusion
• Development of edema
• Decreased exercise tolerance
• Ischemic heart disease
• Sudden death
• Ventricular remodeling and decreased function
12. Goals and drug therapy
Goals
• Alleviation of symptoms, improve quality of life
• Arrest ventricular remodeling
• Prevent sudden death
Nondrug therapy
• Reduce cardiac work; rest, weight loss, low Na+ diet
Drug therapy
• Chronic heart failure
• ACE-I, β-blockers, ARB, aldosterone antagonists, digoxin, diuretics
• Acute heart failure
• Intravenous diuretics, inotropic agents, PDE inhibitors, vasodilator
13. Signs and symptoms
• Tachycardia
• Decreased exercise tolerance & SOB
• Peripheral and pulmonary edema
• Cardiomegaly
16. Renin angiotensin system
• Baroreceptor mediated activation of the SNS
leads to an increase in renin release and
formation of angiotensin II
• Angiotensin II acts through AT1 and AT2
receptors (most of its actions occur through
AT1 receptors)
• This causes vasoconstriction and stimulates
aldosterone production
• RAS remains the most important target of
chronic CHF therapy
19. Advantages
• Improves symptoms significantly
• Improves exercise tolerance
• Slows progression of the disease
• Prolong survival in established cases
20. ADR
• What are the ADR of ACEIs?
• Cough (why?)
• Postural hypotention (why?)
• Hyperkalemia (possible Drug
interactions?)
• Contraindicated in pregnant women (1st
trimester)
• Rare: angioedema
22. Inotropes
• Increase force of contraction
• All increase intracellular cardiac Ca++
concentration
• Eg:
• Digitalis (cardiac glycoside)
• Dobutamine (β-adrenergic agonist)
• Amrinone (PDE inhibitor)
23. Cardiac glycosides
• Digitalis
• Sourced from foxglove plant
• 1785, Dr. William Withering’s
monograph on digitalis
• Has a profound effect on the cardiac
contractility
24.
25. Pck
• Two drugs (digoxin, digitoxin)
• Well absorbed orally
• 10% of population have bacteria in the gut,
which inactivate digoxin, needing an
increased dose in such
• Beware of using antibiotics in such patients
• Digoxin has a very narrow ther. Margin
26. Pck
• Taken orally
• Enters CNS (so what?)
• Renal clearance proportional to CC
• To be used with extreme caution in
patients suffering from renal
impairment
27. MOA
• Regulation of cytosolic Ca metabolism:
• Reversibly combine with sodium-potassium
ATPase of the cardiac cell membrane
• Results in inhibition of pump activity
• This leads to in intracellular Na conc.
• This favors Ca ions in the cell
• Ca levels result in increased systolic force of
contraction
30. Additional MOA
• Force of contraction resembles to that of the
normal heart
• Improved circulation leads to reduced
sympathetic activity
• This reduces PVR
• All this leads to reduction in HR
• Vagal tone is enhanced
• Finally myocardial O2 demand is reduced
31. Electrophysiological effects on the
heart
Direct Indirect (increased vagal tone)
SA Node No effect at therapeutic dose No effect at therapeutic dose
Atrial muscle High dose increases rate of
spontaneous depolarization
High dose decreases rate of
spontaneous depolarization
AV node Increased refractory period Decreased conduction velocity
Decreased conduction velocity Increased refractory period
His-Purkinje
system
Increased refractory period Increased refractory period
Decreased conduction velocity Decreased conduction velocity
High dose increases triggered
activity
None
Toxic doses enhance pacemaker
32. Uses
• Severe LV systolic dysfunction
• Only after initiation of diuretics and
vasodialtor therapy
• Management of patients with chronic atrial
fibrillation
• Cannot arrest the progression of pathological
changes causing heart failure, and does not
prolong life in patients with CHF
33. ADR
• Digitalis toxicity is one among most
commonest encountered (why?)
• Therapeutic concentration- 0.5-1.5 ng/ml
• Often the first step is discontinuation of Rx
• Digoxin levels must be monitored closely
34. Signs of digoxin toxicity
• CNS: Malaise, confusion, depression,
vertigo, vision (abnormalities in color
vision)
• GI: Anorexia, nausea, intestinal
cramping, diarrhea
• Cardiovascular: Palpitations, syncope,
arrhythmias, bradycardia, AV node
block, tachycardia
35. Factors increasing the possibility of
digoxin toxicity
• Pharmacological and toxic effects are greater
in hypokalemic patients.
• K+-depleting diuretics are a major
contributing factor to digoxin toxicity.
36. Management
Arrhythmias may be converted to normal
sinus rhythm by K+. when the plasma K+
conc. is low or within the normal range.
When the plasma K+ conc. is high,
antiarrhythmic drugs, such as lidocaine,
procainamide, or propranolol, can be used.
Severe toxicity treated with Digibind, an anti-
digoxin antibody.
37. • A 96-year-old AAF was admitted from a nursing home with
complaints of abdominal pain, N/V, dizziness, confusion and
double vision for 5 days. She was discharged from the
hospital just 4 days ago. Digoxin was started during that
previous hospitalization for control of tachycardia in atrial
fibrillation. One day prior to discharge, digoxin level was 1.8
mg/mL and digoxin dose was decreased to 125 mcg PO Q
48 hr.
PMH
Hypertension, atrial fibrillation, coronary artery disease,
stroke, congestive heart failure.
Medications
Metoprolol, Digoxin, ASA, lisinopril, Lasix, Coumadin,
Nexium
What could it be???
38. Dopamine
• Dopamine acts at a variety of
receptors (dose dependant)
• Rapid elimination- can only be
administered as a continuous infusion
39. Dobutamine
• Stimulates beta-adrenergic receptors and
produces a positive inotropic response
• Unlike the vasoconstriction seen with high
doses of dopamine, dobutamine produces
a mild vasodilatation
41. PDE inhibitors
• Inamrinone (amrinone) and Milrinone
(bipyridines)
• Acts by inhibiting the enzyme Phosphodiesterase
• Thus lead to increase of intracellular
concentrations of cAMP
• cAMP is responsible for the conversion of inactive
protein kinase to active form
• Protein kinases are responsible for
phosphorylation of Ca channels
• Thus causing increased Ca entry into the cell.
42. MOA
• Increase myocardial contractility by
increasing the Ca influx during AP
• Also have vasodilating effect
• Selective for PDE isoenzyme-3 (found
in cardiac and smooth muscle)
43. Current status
• Both are orally active
• Only available in parenteral forms
• Limited efficacy
• Clinical trials- increased mortality (oral)
• Still new drugs are under trial
44. ADR
• Inamrinone: nausea, vomiting,
arrhythmias, thrombocytopenia and liver
enzyme changes
• Withdrawn in some countries
• Milrinone: arrhythmias, less likely to
cause other ADR
45. (BNP)-Niseritide
• Brain (B-type) natriuretic peptide (BNP) is
secreted constitutively by ventricular
myocytes in response to stretch
• BNP binds to receptors in the vasculature,
kidney, and other organs, producing potent
vasodilation with rapid onset and offset of
action by increasing levels of cGMP
• Niseritide is recombinant human BNP
approved for treatment of acute
decompensated CHF.
46. BNP contd..
• It reduces systemic and pulmonary
vascular resistances, causing an
indirect increase in cardiac output and
diuresis.
• Effective in HF because cause
reduction in preload and afterload
• ADR- hypotension
47. Beta blockers
• Overwhelming evidence to support the use of
β-blockers in CHF, however
• Mechanism involved remain unclear
• Part of their beneficial effects may derive from
slowing of heart rate and decrease
myocardial O2consumption.
• This would lessen the frequency of ischemic
events and potential for development of a
lethal arrhythmia.
48. Beta blockers
• Suggested mechanisms also include reduced
remodeling
• β-Blockers may be beneficial through
resensitization of the down-regulated
receptor, improving myocardial contractility.
• Recent studies with bisoprolol, carvedilol and
metoprolol showed a reduction in mortality in
patients with these drugs
• CI in unstable cases
49. Management of Chronic HF
(combination of drugs)
• Limit physical activity
• Reduce weight
• Reduce water intake
• Control HT
• Na restriction
• Diuretics
• ACE-Is
• Digitalis (ther. margin, DI with quinidine)
• Beta blockers
• Vasodilators
50. Management of acute HF
• Diuretics
• Vasodilators
• Inotropic drugs
• Life support
• Treating cause (surgery to correct
valvular disorders)
