1. The document discusses drug trials for acute decompensated heart failure and their results. Many trials tested drugs like nesiritide, milrinone, tezosentan, levosimendan, tolvaptan, and rolofylline but did not show clinical benefit.
2. It proposes classifying patients based on their clinical profile into those with volume overload, reduced cardiac output, or a combination, to help determine optimal treatment which may include diuretics, vasodilators, inotropes, or renal preservation agents.
3. The management of acute heart failure is divided into initial, in-hospital, and discharge phases, with goals like establishing diagnoses, treating precip
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
Heart failure Update as per, 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the
Management of Heart Failure and 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
This document discusses atrial fibrillation (AF), the most common cardiac arrhythmia. It provides background on AF including its history, classification, epidemiology, etiology, pathophysiology, clinical features, diagnosis and electrocardiographic characteristics. Key points discussed are that AF results from triggers in the pulmonary veins initiating reentry circuits in the atria, and that it begets itself over time through electrical and structural remodeling of the atria. Management involves identifying and treating underlying causes, rate control, and anticoagulation to prevent thromboembolism.
Atrial flutter is an abnormal heart rhythm where the atria beat too fast, usually between 240-340 beats per minute. It often occurs in patients with underlying heart conditions that cause enlargement or damage to the atria, such as rheumatic heart disease, congenital heart disease, or COPD. Common symptoms include palpitations, chest discomfort, and fatigue. Treatment options include medications to slow the heart rate or restore normal rhythm, cardioversion, catheter ablation, or implanting a pacemaker.
This document provides an overview of atrial fibrillation (AF), including its pathogenesis, types, diagnosis, and management. Some key points:
- AF is the most common cardiac arrhythmia, affecting around 6% of those over 65. It increases the risk of stroke.
- It occurs when the normal sinus rhythm is overridden by disorganized electrical impulses, usually originating in the lungs.
- Types include paroxysmal, persistent, and permanent. Symptoms range from none to palpitations, dyspnea, chest pain, and neurological issues.
- Diagnosis is made via ECG showing irregular rhythm without P waves. Workup evaluates for underlying causes and stroke risk factors.
Sinus tachycardia is characterized by a heart rate over 100 beats per minute originating from the sinus node. It can be a normal response to exercise or stress or indicate underlying conditions like heart failure. Symptoms may occur if the heart rate is very fast or the patient has heart disease. Treatment involves addressing the underlying cause and reducing stress or anxiety.
Cardiomyopathy slideshare Dilated cardiomyopathy Hypertrophic cardiomyopathy ...Adarsh SA
Cardiomyopathy is a disease of the heart muscle that makes it harder for the heart to pump blood. There are several types classified by structural and functional abnormalities. The main types are dilated, hypertrophic, restrictive, and arrhythmogenic right ventricular cardiomyopathy. Dilated cardiomyopathy is the most common type and causes the heart chambers to enlarge and the heart muscle to thin and weaken over time, reducing its ability to pump blood. Management involves identifying underlying causes, treating heart failure symptoms, and controlling arrhythmias.
A brief synopsis of acute decompensated heart failureDr Emad efat
This document provides an overview of acute decompensated heart failure (ADHF). It defines ADHF as a clinical syndrome characterized by the development of respiratory distress due to rapidly accumulated fluid in the lungs. The document categorizes heart failure based on systolic vs diastolic function, left vs right sided, acute vs chronic onset, and NYHA functional classification. Common symptoms, physical exam findings, causes, risk factors, differential diagnoses, and initial investigations are described. Imaging findings on chest x-ray indicative of different stages of heart failure are also summarized.
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
Heart failure Update as per, 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the
Management of Heart Failure and 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
This document discusses atrial fibrillation (AF), the most common cardiac arrhythmia. It provides background on AF including its history, classification, epidemiology, etiology, pathophysiology, clinical features, diagnosis and electrocardiographic characteristics. Key points discussed are that AF results from triggers in the pulmonary veins initiating reentry circuits in the atria, and that it begets itself over time through electrical and structural remodeling of the atria. Management involves identifying and treating underlying causes, rate control, and anticoagulation to prevent thromboembolism.
Atrial flutter is an abnormal heart rhythm where the atria beat too fast, usually between 240-340 beats per minute. It often occurs in patients with underlying heart conditions that cause enlargement or damage to the atria, such as rheumatic heart disease, congenital heart disease, or COPD. Common symptoms include palpitations, chest discomfort, and fatigue. Treatment options include medications to slow the heart rate or restore normal rhythm, cardioversion, catheter ablation, or implanting a pacemaker.
This document provides an overview of atrial fibrillation (AF), including its pathogenesis, types, diagnosis, and management. Some key points:
- AF is the most common cardiac arrhythmia, affecting around 6% of those over 65. It increases the risk of stroke.
- It occurs when the normal sinus rhythm is overridden by disorganized electrical impulses, usually originating in the lungs.
- Types include paroxysmal, persistent, and permanent. Symptoms range from none to palpitations, dyspnea, chest pain, and neurological issues.
- Diagnosis is made via ECG showing irregular rhythm without P waves. Workup evaluates for underlying causes and stroke risk factors.
Sinus tachycardia is characterized by a heart rate over 100 beats per minute originating from the sinus node. It can be a normal response to exercise or stress or indicate underlying conditions like heart failure. Symptoms may occur if the heart rate is very fast or the patient has heart disease. Treatment involves addressing the underlying cause and reducing stress or anxiety.
Cardiomyopathy slideshare Dilated cardiomyopathy Hypertrophic cardiomyopathy ...Adarsh SA
Cardiomyopathy is a disease of the heart muscle that makes it harder for the heart to pump blood. There are several types classified by structural and functional abnormalities. The main types are dilated, hypertrophic, restrictive, and arrhythmogenic right ventricular cardiomyopathy. Dilated cardiomyopathy is the most common type and causes the heart chambers to enlarge and the heart muscle to thin and weaken over time, reducing its ability to pump blood. Management involves identifying underlying causes, treating heart failure symptoms, and controlling arrhythmias.
A brief synopsis of acute decompensated heart failureDr Emad efat
This document provides an overview of acute decompensated heart failure (ADHF). It defines ADHF as a clinical syndrome characterized by the development of respiratory distress due to rapidly accumulated fluid in the lungs. The document categorizes heart failure based on systolic vs diastolic function, left vs right sided, acute vs chronic onset, and NYHA functional classification. Common symptoms, physical exam findings, causes, risk factors, differential diagnoses, and initial investigations are described. Imaging findings on chest x-ray indicative of different stages of heart failure are also summarized.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It results from conditions that damage or weaken the heart muscle such as hypertension, heart attack, or cardiomyopathy. Symptoms include dyspnea, fatigue, swelling, and weakness. Diagnosis involves chest x-rays, ECGs, and echocardiograms. Treatment focuses on managing symptoms with diuretics, ACE inhibitors, beta blockers, and addressing the underlying heart condition if possible through surgery or lifestyle changes.
This document discusses the classification and management of ventricular arrhythmias. It is divided into sections on classification by clinical presentation, electrocardiography, disease entity. Management of VT in structurally abnormal hearts is discussed, including those related to coronary artery disease, dilated cardiomyopathy, bundle branch reentrant tachycardia, arrhythmogenic right ventricular dysplasia, and other conditions. Clinical presentation, mechanisms, diagnostic testing, and treatment options are summarized for each condition.
This document presents the case of a 22-year-old male who presented with symptoms of easy fatigability, abdominal discomfort, lower extremity edema, and breathlessness on exertion. Physical examination revealed cachexia, elevated jugular venous pressure, pitting edema, hepatomegaly, and elevated heart rate and respiratory rate. Initial testing suggested right heart failure and differentials included constrictive pericarditis, restrictive cardiomyopathy, and dilated cardiomyopathy. Further testing including echocardiogram, cardiac catheterization, and CT scan established a diagnosis of constrictive pericarditis based on findings of pericardial thickening and equalization of diastolic pressures between the right and left ventricles
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
The document outlines a presentation on hypertension and hypertensive disorders for allied health workers. It begins with an introduction and outline covering hypertension and hypertensive disorders of pregnancy. The outline discusses risk factors and diagnosis of hypertension, as well as management of hypertensive crisis. Guidelines for diagnosing and treating hypertension from sources like the 2020 Philippine CPG are also summarized.
Cardiac resynchronization therapy (CRT) and implantable cardioverter defibrillators (ICDs) can help optimize heart failure management. CRT improves symptoms, reduces hospitalizations, and increases survival in patients with reduced ejection fraction, left bundle branch block, and wide QRS duration. ICDs prevent sudden cardiac death in high-risk patients with prior heart failure, low ejection fraction, or history of dangerous arrhythmias. New devices use adaptive and multi-point pacing to better resynchronize the left ventricle. Device therapy improves outcomes when guided by clinical evidence and used in appropriate heart failure patients.
Constrictive pericarditis is caused by scarring and thickening of the pericardium, restricting cardiac filling. It is diagnosed using echocardiography which shows septal bounce, exaggerated mitral inflow, and hepatic vein reversal. While similar to restrictive cardiomyopathy, constrictive pericarditis shows increased ventricular interaction and respiratory effects on cardiac physiology. Surgical pericardiectomy is usually required for treatment but is high risk, with post-op complications common. Long-term survival depends on the underlying cause of constriction.
Pulmonary Hypertension, Current Guidelines and Future Directions of Therapy.Bassel Ericsoussi, MD
The document discusses the classification, pathophysiology, diagnosis, and treatment of pulmonary hypertension. It is classified by the WHO into 5 groups based on underlying mechanisms. The pathophysiology involves vasoconstriction, remodeling of the pulmonary arteries, and thrombosis. Diagnosis requires right heart catheterization showing elevated pulmonary artery pressure. Prognostic factors include functional status and hemodynamics. Treatment involves basic supportive care as well as vasodilator medications, including prostanoids, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and nitric oxide. Combination therapy may provide added benefits.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves correcting underlying factors, lifestyle modifications, and maximizing medications like loop diuretics, ACE inhibitors, beta blockers, and aldosterone antagonists.
This document discusses the management of atrial fibrillation. It provides information on the causes, consequences, classification, and epidemiology of AF. It describes the acute management of AF including assessing hemodynamic status, starting anticoagulation, and deciding between rate and rhythm control strategies. Methods for rhythm control include electrical cardioversion and pharmacological cardioversion with drugs like amiodarone, ibutilide, flecainide, and propafenone. Rate control strategies use drugs like digoxin, beta blockers, calcium channel blockers, and amiodarone. The document also discusses anticoagulation for thromboembolism prevention and newer oral anticoagulants.
Diagnosis and management of acute heart failureAlaa Ateya
Acute heart failure (AHF) can be defined as new or worsening symptoms of heart failure requiring urgent medical care or hospitalization. Common triggers include non-adherence to medications or diet, infections, or worsening of underlying comorbidities like hypertension. This leads to worsening congestion through mechanisms like neurohormonal activation and myocardial injury. Around half of AHF patients have preserved ejection fraction. Ongoing myocardial damage, worsening kidney function, and elevated filling pressures all contribute to poor outcomes of AHF patients.
Dr Vivek Baliga - Diastolic heart failure - A complete overviewDr Vivek Baliga
In this presentation, Dr Vivek Baliga, Consultant Internal Medicine, discusses a common problem in medical practice that often confuses many - diastolic heart failure. Now a misnomer, it is referred to as heart failure with preserved ejection fraction. For patient articles - http://heartsense.in/author/dr-vivek-baliga-b/ . LinkedIn - https://www.linkedin.com/in/dr-vivek-baliga-7b59b0125
Takotsubo cardiomyopathy (TC), also known as "broken heart syndrome", is an acute cardiac syndrome that presents similarly to acute coronary syndrome (ACS) but is caused by transient left ventricular dysfunction rather than coronary artery blockages. It often occurs in post-menopausal women in response to severe emotional or physical stress and is characterized by abnormal ventriculograms showing apical ballooning of the left ventricle. While difficult to distinguish from ACS initially, differentiating the two is important to avoid unnecessary thrombolysis in TC patients. The pathophysiology of TC involves excess catecholamine release and microvascular dysfunction resulting in reversible myocardial stunning.
This document provides guidance on preparing patients for cardiac catheterization. Key steps include obtaining informed consent, taking a thorough medical history, performing a physical exam and lab tests, choosing an appropriate contrast dye, pre-medicating high-risk patients, and ensuring equipment is functioning properly. Proper pre-cath preparation can help reduce risks like contrast-induced kidney injury or allergic reactions to dye.
This document discusses the clinical approach to evaluating patients presenting with palpitations. It defines palpitations and describes the physiology and common causes. Cardiac causes account for 43% of cases, while psychiatric conditions cause 31%. The document outlines the diagnostic evaluation including history, physical exam, ECG and ambulatory monitoring. It provides guidance on when to refer to cardiology or admit to the hospital. The management focuses on reassurance, lifestyle changes, treating underlying conditions, anxiolytics, beta-blockers, antiarrhythmics or cardioversion depending on the severity and nature of the arrhythmia.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
Congestive cardiac failure is a progressive condition caused by impaired cardiac pumping, often due to hypertension, coronary artery disease, or heart valve problems. It results in fluid overload and decreased tissue perfusion as the heart cannot generate enough oxygen to meet the body's demands. When fluid accumulates in the lungs, it causes pulmonary edema and respiratory issues. Signs and symptoms include fluid overload, shortness of breath, edema, and elevated jugular vein distension. Diagnosis involves examination, chest X-ray, EKG, echocardiogram, and blood tests. Treatment includes eliminating causes, reducing heart workload, optimizing medications, and preventing exacerbations. Surgical options are CABG, heart surgery, or transplant in severe
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can develop when the heart muscle is damaged, such as from a myocardial infarction. There are two main types - left heart failure which causes blood to back up in the lungs, and right heart failure where blood backs up in the body. Symptoms depend on whether it is left or right heart failure, and include shortness of breath, fatigue, swelling, and coughing. Treatment focuses on reducing cardiac workload, increasing blood oxygen levels, and limiting fluid buildup through medications, oxygen therapy, and monitoring for arrhythmias.
The preoperative evaluation consists of gathering patient information and formulating an anesthetic plan to reduce perioperative risks. Inadequate planning and errors in preparation are common causes of anesthetic complications. The evaluation includes reviewing medical history and test results, performing a physical exam, consulting specialists, and optimizing the patient's medical condition prior to elective surgery. The goal is to ensure the patient is in the best possible state before undergoing anesthesia and procedures.
This document provides information on interscalene brachial plexus blocks, including indications, contraindications, anatomy, techniques, complications, and references. It describes Winnie's anterior approach using landmarks to identify the interscalene groove for injection, as well as a posterior approach. Areas of blockade, continuous techniques, and use of nerve stimulation are also summarized. Supraclavicular blockade as an alternative is outlined with similar details.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It results from conditions that damage or weaken the heart muscle such as hypertension, heart attack, or cardiomyopathy. Symptoms include dyspnea, fatigue, swelling, and weakness. Diagnosis involves chest x-rays, ECGs, and echocardiograms. Treatment focuses on managing symptoms with diuretics, ACE inhibitors, beta blockers, and addressing the underlying heart condition if possible through surgery or lifestyle changes.
This document discusses the classification and management of ventricular arrhythmias. It is divided into sections on classification by clinical presentation, electrocardiography, disease entity. Management of VT in structurally abnormal hearts is discussed, including those related to coronary artery disease, dilated cardiomyopathy, bundle branch reentrant tachycardia, arrhythmogenic right ventricular dysplasia, and other conditions. Clinical presentation, mechanisms, diagnostic testing, and treatment options are summarized for each condition.
This document presents the case of a 22-year-old male who presented with symptoms of easy fatigability, abdominal discomfort, lower extremity edema, and breathlessness on exertion. Physical examination revealed cachexia, elevated jugular venous pressure, pitting edema, hepatomegaly, and elevated heart rate and respiratory rate. Initial testing suggested right heart failure and differentials included constrictive pericarditis, restrictive cardiomyopathy, and dilated cardiomyopathy. Further testing including echocardiogram, cardiac catheterization, and CT scan established a diagnosis of constrictive pericarditis based on findings of pericardial thickening and equalization of diastolic pressures between the right and left ventricles
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
The document outlines a presentation on hypertension and hypertensive disorders for allied health workers. It begins with an introduction and outline covering hypertension and hypertensive disorders of pregnancy. The outline discusses risk factors and diagnosis of hypertension, as well as management of hypertensive crisis. Guidelines for diagnosing and treating hypertension from sources like the 2020 Philippine CPG are also summarized.
Cardiac resynchronization therapy (CRT) and implantable cardioverter defibrillators (ICDs) can help optimize heart failure management. CRT improves symptoms, reduces hospitalizations, and increases survival in patients with reduced ejection fraction, left bundle branch block, and wide QRS duration. ICDs prevent sudden cardiac death in high-risk patients with prior heart failure, low ejection fraction, or history of dangerous arrhythmias. New devices use adaptive and multi-point pacing to better resynchronize the left ventricle. Device therapy improves outcomes when guided by clinical evidence and used in appropriate heart failure patients.
Constrictive pericarditis is caused by scarring and thickening of the pericardium, restricting cardiac filling. It is diagnosed using echocardiography which shows septal bounce, exaggerated mitral inflow, and hepatic vein reversal. While similar to restrictive cardiomyopathy, constrictive pericarditis shows increased ventricular interaction and respiratory effects on cardiac physiology. Surgical pericardiectomy is usually required for treatment but is high risk, with post-op complications common. Long-term survival depends on the underlying cause of constriction.
Pulmonary Hypertension, Current Guidelines and Future Directions of Therapy.Bassel Ericsoussi, MD
The document discusses the classification, pathophysiology, diagnosis, and treatment of pulmonary hypertension. It is classified by the WHO into 5 groups based on underlying mechanisms. The pathophysiology involves vasoconstriction, remodeling of the pulmonary arteries, and thrombosis. Diagnosis requires right heart catheterization showing elevated pulmonary artery pressure. Prognostic factors include functional status and hemodynamics. Treatment involves basic supportive care as well as vasodilator medications, including prostanoids, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and nitric oxide. Combination therapy may provide added benefits.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves correcting underlying factors, lifestyle modifications, and maximizing medications like loop diuretics, ACE inhibitors, beta blockers, and aldosterone antagonists.
This document discusses the management of atrial fibrillation. It provides information on the causes, consequences, classification, and epidemiology of AF. It describes the acute management of AF including assessing hemodynamic status, starting anticoagulation, and deciding between rate and rhythm control strategies. Methods for rhythm control include electrical cardioversion and pharmacological cardioversion with drugs like amiodarone, ibutilide, flecainide, and propafenone. Rate control strategies use drugs like digoxin, beta blockers, calcium channel blockers, and amiodarone. The document also discusses anticoagulation for thromboembolism prevention and newer oral anticoagulants.
Diagnosis and management of acute heart failureAlaa Ateya
Acute heart failure (AHF) can be defined as new or worsening symptoms of heart failure requiring urgent medical care or hospitalization. Common triggers include non-adherence to medications or diet, infections, or worsening of underlying comorbidities like hypertension. This leads to worsening congestion through mechanisms like neurohormonal activation and myocardial injury. Around half of AHF patients have preserved ejection fraction. Ongoing myocardial damage, worsening kidney function, and elevated filling pressures all contribute to poor outcomes of AHF patients.
Dr Vivek Baliga - Diastolic heart failure - A complete overviewDr Vivek Baliga
In this presentation, Dr Vivek Baliga, Consultant Internal Medicine, discusses a common problem in medical practice that often confuses many - diastolic heart failure. Now a misnomer, it is referred to as heart failure with preserved ejection fraction. For patient articles - http://heartsense.in/author/dr-vivek-baliga-b/ . LinkedIn - https://www.linkedin.com/in/dr-vivek-baliga-7b59b0125
Takotsubo cardiomyopathy (TC), also known as "broken heart syndrome", is an acute cardiac syndrome that presents similarly to acute coronary syndrome (ACS) but is caused by transient left ventricular dysfunction rather than coronary artery blockages. It often occurs in post-menopausal women in response to severe emotional or physical stress and is characterized by abnormal ventriculograms showing apical ballooning of the left ventricle. While difficult to distinguish from ACS initially, differentiating the two is important to avoid unnecessary thrombolysis in TC patients. The pathophysiology of TC involves excess catecholamine release and microvascular dysfunction resulting in reversible myocardial stunning.
This document provides guidance on preparing patients for cardiac catheterization. Key steps include obtaining informed consent, taking a thorough medical history, performing a physical exam and lab tests, choosing an appropriate contrast dye, pre-medicating high-risk patients, and ensuring equipment is functioning properly. Proper pre-cath preparation can help reduce risks like contrast-induced kidney injury or allergic reactions to dye.
This document discusses the clinical approach to evaluating patients presenting with palpitations. It defines palpitations and describes the physiology and common causes. Cardiac causes account for 43% of cases, while psychiatric conditions cause 31%. The document outlines the diagnostic evaluation including history, physical exam, ECG and ambulatory monitoring. It provides guidance on when to refer to cardiology or admit to the hospital. The management focuses on reassurance, lifestyle changes, treating underlying conditions, anxiolytics, beta-blockers, antiarrhythmics or cardioversion depending on the severity and nature of the arrhythmia.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
Congestive cardiac failure is a progressive condition caused by impaired cardiac pumping, often due to hypertension, coronary artery disease, or heart valve problems. It results in fluid overload and decreased tissue perfusion as the heart cannot generate enough oxygen to meet the body's demands. When fluid accumulates in the lungs, it causes pulmonary edema and respiratory issues. Signs and symptoms include fluid overload, shortness of breath, edema, and elevated jugular vein distension. Diagnosis involves examination, chest X-ray, EKG, echocardiogram, and blood tests. Treatment includes eliminating causes, reducing heart workload, optimizing medications, and preventing exacerbations. Surgical options are CABG, heart surgery, or transplant in severe
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can develop when the heart muscle is damaged, such as from a myocardial infarction. There are two main types - left heart failure which causes blood to back up in the lungs, and right heart failure where blood backs up in the body. Symptoms depend on whether it is left or right heart failure, and include shortness of breath, fatigue, swelling, and coughing. Treatment focuses on reducing cardiac workload, increasing blood oxygen levels, and limiting fluid buildup through medications, oxygen therapy, and monitoring for arrhythmias.
The preoperative evaluation consists of gathering patient information and formulating an anesthetic plan to reduce perioperative risks. Inadequate planning and errors in preparation are common causes of anesthetic complications. The evaluation includes reviewing medical history and test results, performing a physical exam, consulting specialists, and optimizing the patient's medical condition prior to elective surgery. The goal is to ensure the patient is in the best possible state before undergoing anesthesia and procedures.
This document provides information on interscalene brachial plexus blocks, including indications, contraindications, anatomy, techniques, complications, and references. It describes Winnie's anterior approach using landmarks to identify the interscalene groove for injection, as well as a posterior approach. Areas of blockade, continuous techniques, and use of nerve stimulation are also summarized. Supraclavicular blockade as an alternative is outlined with similar details.
Damage Control Laparotomy - an evidence based approachYasser Abbas
Dr. Yasser Abbas outlines the concept of damage control surgery, which involves temporarily controlling bleeding and contamination through techniques like packing and temporary abdominal closure, to allow time for resuscitation before definitive repair. Damage control is indicated for patients who are hemodynamically unstable, coagulopathic, acidotic, or hypothermic and involves three phases - initial surgery to control bleeding, ICU resuscitation to correct physiological derangements, and a second surgery for definitive repair once stabilized. The goal of damage control is to prevent the "lethal triad" of acidosis, coagulopathy, and hypothermia in order to improve survival rates.
The document discusses liver function tests and the clinical significance of various enzymes and biomarkers. It is divided into several sections that cover: the functions of the liver; classification of liver function tests into groups that indicate hepatocellular damage or cholestasis; specific enzymes such as ALT, AST, ALP, GGT and their levels in different liver conditions or diseases; clinical cases and how to interpret abnormal enzyme profiles and biomarkers.
1. Hypothyroidism is a clinical syndrome where the thyroid gland fails to produce sufficient thyroid hormones.
2. It can be primary, meaning it is caused by problems with the thyroid gland itself, or central/secondary, caused by problems with the pituitary gland or hypothalamus.
3. Symptoms affect many body systems and include fatigue, weight gain, dry skin, constipation, muscle weakness, decreased heart rate, impaired cognition and more.
This document discusses a case of hyperthyroidism in a 39-year-old female presenting with nervousness, anxiety, palpitations, diarrhea, and weight loss. On examination, she had a heart rate of 110 bpm, tremor, increased reflexes, and an enlarged thyroid. Laboratory tests found high free T3 and T4, low TSH, and positive thyroid stimulating immunoglobulins, consistent with a diagnosis of Graves' disease. Graves' disease is an autoimmune disorder causing hyperthyroidism through thyroid stimulating antibodies. If left untreated, hyperthyroidism can progress to a thyroid storm, a life-threatening condition of severe hypermetabolism.
1. sudakshina an approach to thyroid swelling finalArkaprovo Roy
The document provides information on the anatomy and function of the thyroid gland. It discusses the gross anatomy including coverings, blood supply from arteries like the superior thyroid artery, and venous drainage. It also describes the nerve supply including parasympathetic fibers from the vagus and recurrent laryngeal nerves and sympathetic fibers from cervical ganglia. The lymphatic drainage is to prelaryngeal, jugulodigastric and pretracheal lymph nodes. Key aspects of surgical anatomy are highlighted regarding ligating arteries and removing the gland with its true capsule. The function of producing T3, T4, and calcitonin hormones is summarized. Normal and abnormal thyroid hormone levels are provided to define euthyroidism, hyperthy
The thyroid gland sits in front of the trachea. It synthesizes the hormones T3 and T4 through a process involving absorption of iodine from the diet, trapping of iodide in thyroid follicular cells, organification of iodide by binding it to tyrosine residues on thyroglobulin, coupling of iodotyrosines to form the hormones, and release of T3 and T4 into circulation in response to TSH. Thyroid imaging using radiopharmaceuticals like Tc-99m pertechnetate, I-123, or I-131 allows evaluation of thyroid anatomy and function through visualization and quantification of radiotracer uptake.
Hyperthyroidism, Reference: Hyperthyroid, Harrison's Principles of Internal Medicine, Soheil Elahi, Islamic Azad University of Medicine- International Branch (IAUM-int)
The document provides an outline on the physiology and causes of hyperthyroidism, also known as thyrotoxicosis. It discusses the thyroid gland, thyroid hormone synthesis and regulation, clinical features of Graves' disease and toxic multinodular goiter, diagnosis of hyperthyroidism, and management approaches including antithyroid drugs, radioactive iodine therapy, surgery, and novel minimally invasive therapies. It also covers thyroid storm as a life-threatening emergency characterized by abrupt release of thyroid hormones.
The document discusses liver function tests and bilirubin metabolism. It describes that liver function tests are useful for diagnosing and monitoring liver diseases. A battery of tests are needed since the liver has diverse functions including excretion, metabolism, protein and plasma synthesis, and storage. Specific tests mentioned include liver enzymes, albumin, prothrombin time, tumor markers, bilirubin, and dye excretion tests. The types of jaundice - hemolytic, obstructive, and hepatic - are distinguished based on conjugated and unconjugated bilirubin levels as well as other factors. Various inborn errors affecting bilirubin metabolism are also outlined.
This document provides an overview of pancreatitis and pancreatic pseudocysts. It defines acute and chronic pancreatitis, describes the pathogenesis involving premature activation of pancreatic enzymes, and lists common causes like gallstones. Signs and symptoms include abdominal pain while complications involve local issues like pseudocysts or systemic problems. Diagnosis involves blood tests, imaging, and assessing severity with tools like BISAP score. Management focuses on supportive care, treating underlying causes, and draining complications surgically or minimally invasively. Pseudocysts are pancreatic fluid collections that often resolve on their own but sometimes require intervention.
This document provides an overview of hypothyroidism, including its definition, effects on different organ systems, types, causes, investigations, and treatment. Some key points are:
- Hypothyroidism is a deficiency in thyroid hormone secretion, occurring in 2-15% of the population more commonly in women. Risk increases with age.
- It affects the cardiovascular, respiratory, renal, central nervous, neuromuscular, gastrointestinal, and hematological systems, causing decreased metabolism.
- Types include primary, central, and congenital hypothyroidism. Causes include iodine deficiency, autoimmune disease, surgery, radiation, and certain drugs.
- Investigations include thyroid function tests and antibodies
The document discusses diseases of the pancreas, including congenital anomalies, endocrine and exocrine pancreatic diseases, acute and chronic pancreatitis, and pancreatic tumors. It provides details on the causes, pathophysiology, clinical presentation, diagnosis, and treatment of each condition. Key points include the role of gallstones and alcohol as common causes of acute pancreatitis, the use of CT and lab tests to diagnose and determine severity, and supportive care along with surgical or endoscopic interventions for severe cases.
The document discusses the history and development of the internet over the past 50 years, from its origins as a US military program called ARPANET to the commercialization of the world wide web in the 1990s. It led to an explosion of new technologies and services over the following decades that have transformed how people live and work through greater connectivity and access to information.
Surgery
This document discusses damage control surgery (DCS), which is an abbreviated laparotomy designed to prioritize physiological recovery over anatomical reconstruction for seriously injured patients. It has four phases: pre-hospital resuscitation (Phase 0), abbreviated laparotomy to control bleeding and contamination (Phase I), intensive care to restore physiology (Phase II), and definitive repair once stabilized (Phase III). The goals of DCS are to restore physiology first before completing anatomical reconstruction, in order to improve survival outcomes for major trauma patients.
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
The document provides guidance on principles of trauma care. It discusses the primary and secondary surveys that should be conducted to assess and treat trauma patients. The primary survey involves assessing the patient's airway, breathing, circulation, disability, and exposure to identify life-threatening injuries. This includes steps like ensuring an open airway, checking for adequate breathing, feeling for pulses, and conducting a brief neurological exam. The secondary survey involves a more thorough head-to-toe examination to identify and treat all injuries, as well as taking a medical history. Trauma scoring systems are also described to help determine if a patient requires transfer to a higher level trauma center.
Acute Decompensated Heart Failure : What is New ?drucsamal
Prof. U. C. SAMAL is an expert in cardiology who has held leadership positions in several cardiological societies. The document discusses the management of acute decompensated heart failure and summarizes recent changes to guidelines. It provides an overview of pharmacological interventions for acute heart failure such as diuretics, vasodilators, and inotropes. Non-invasive ventilation and risk stratification scores are also mentioned. The document emphasizes the importance of both short-term stabilization and long-term management through multi-disciplinary programs to prevent readmissions.
Heart failure is a clinical syndrome characterized by symptoms such as breathlessness and fatigue caused by structural or functional abnormalities of the heart. It is a leading cause of hospitalization in people over 65. Up to 50% of heart failure patients die within 5 years of diagnosis.
The document discusses classifications of heart failure based on ejection fraction and functional capacity. It provides guidelines on the management of acute heart failure, including treatments to reduce congestion and increase perfusion. Chronic heart failure treatment focuses on reducing mortality and hospitalizations through optimized medical therapy including ACE inhibitors, beta-blockers, MRAs, and newer drugs like sacubitril/valsartan. Device therapies like ICDs and CRT are recommended for
A comprehensive approach to Atrial Fibrillation. Everything you need to know about Atrial fibrillation. Including recent 2014 AHA guidelines of management.
This document discusses heart failure with preserved ejection fraction (HFpEF). It begins by defining HFpEF and noting that approximately half of heart failure patients have normal or near-normal ejection fractions. The document then reviews various classification systems for HF, diagnostic criteria, echocardiographic assessment of HFpEF, risk factors, and challenges in diagnosing and treating HFpEF. It concludes by discussing current and potential future treatment approaches for HFpEF, including drugs targeting comorbid conditions that are common in HFpEF patients.
Acute and chronic heart failure (ESC guidline)Mohammad Uddin
This document summarizes guidelines from the 2016 European Society of Cardiology for the diagnosis and treatment of acute and chronic heart failure. It defines heart failure and the different types based on left ventricular ejection fraction. It describes symptoms and signs of heart failure, recommended tests for initial assessment and diagnosis, and algorithms for diagnosis. It provides guidance on treatments recommended for all symptomatic patients with reduced ejection fraction heart failure, as well as selected patients. The document concludes with practical guidance on the use of ACE inhibitors, beta blockers, and mineralocorticoid receptor antagonists in heart failure patients.
The document discusses heart failure, including its definition, stages, causes, symptoms, and treatment guidelines. It provides an overview of epidemiology and costs of heart failure. Guidelines from ACC/AHA classify heart failure into stages A through D based on risk or presence of symptoms. Treatment involves managing risk factors, addressing neurohormonal activation, and following medication protocols tailored to each stage.
This document provides an overview of heart failure (HF), including definitions, epidemiology, pathophysiology, diagnosis, and treatment. Some key points:
- HF is a clinical syndrome where cardiac output is insufficient to meet the body's demands. It can be acute or chronic, and involve systolic or diastolic dysfunction.
- Risk factors include hypertension, coronary artery disease, and drugs like doxorubicin. Incidence increases with age.
- Diagnosis involves history, physical exam, BNP, echocardiogram, and other tests. BNP is useful to differentiate cardiac from pulmonary causes of dyspnea.
- Treatment depends on stage and includes ACE inhibitors, beta blockers,
The document provides information on the diagnosis and management of heart failure with preserved ejection fraction (HFpEF) according to ESC guidelines. It notes that HFpEF has a different epidemiological profile than heart failure with reduced ejection fraction (HFrEF), with older, female, obese, and hypertensive patients who are less likely to have coronary heart disease. The diagnosis of HFpEF is more difficult than HFrEF as other potential causes must be ruled out first. No treatments have convincingly reduced morbidity and mortality for HFpEF, though diuretics are used to control symptoms and treatment of comorbidities is important. The guidelines recommend controlling blood pressure and provide limited guidance for HFpEF management in
This document discusses various types of supraventricular tachycardias (SVTs), including their causes, mechanisms, diagnosis, and treatment. It covers atrial fibrillation, atrial flutter, atrial tachycardia, and AV nodal reentrant tachycardia. For each type, it discusses epidemiology, mechanisms, classification, evaluation with tests like ECG and echocardiogram, anticoagulation measures, and treatment options like medications, cardioversion, and catheter ablation. Rate control is emphasized as usually preferable to rhythm control for atrial fibrillation.
The document summarizes guidelines for the treatment of heart failure. Key points include:
- The 2022 guidelines recommend the use of sacubitril/valsartan (ARNi) as initial treatment for HFrEF, and suggest SGLT2 inhibitors may also be used as initial treatment.
- For HFpEF, SGLT2 inhibitors are recommended based on evidence that empagliflozin reduces hospitalizations. Other medications like ARNi, MRAs, and BB may also be considered but require further study.
- Treatment focuses on guideline-directed medical therapy including ACEi/ARB, BB, MRAs, and diuretics, with addition of other drugs like SGLT2
Heart Failure(HFrEF) management- an Overview Ashok Dutta
This document provides an overview of heart failure management. It defines heart failure and describes its types and classifications. Symptoms include dyspnea and fatigue while signs include circulatory congestion or hypoperfusion. Treatment involves establishing a diagnosis, determining risk factors and severity, and taking a multidisciplinary approach. The main treatment goals are reducing mortality and morbidity by modifying risks, preventing disease progression, and improving quality of life. Guideline directed medical therapy includes diuretics, ACE inhibitors, beta blockers, MRAs, ARNIs, and SGLT2 inhibitors. Device therapies like ICDs and CRT can be used, and management depends on the ACC/AHA stages of heart failure.
This document provides an overview of a case of a 70-year-old African American female presenting with acute respiratory distress and signs of a non-ST elevated myocardial infarction (NSTEMI). It discusses her medical history of cardiovascular risk factors and presents her vital signs, physical exam findings, laboratory and imaging results supporting the diagnosis of NSTEMI. The document then outlines her pharmacological management including antiplatelet therapy, anticoagulation, beta-blockers, ACE inhibitors and statins as well as her appropriate treatment options going forward.
anesthesia in patient a patient with IHD posted for lap cholecystectomy. pres...Swastika Swaro
1) The document discusses anaesthetic management for laparoscopic cholecystectomy in patients with coronary artery disease (CAD), outlining how to provide safe anaesthesia for non-cardiac surgery in these high-risk patients.
2) Patients with CAD have increased perioperative cardiac risk due to exaggerated hemodynamic responses to stimuli. Careful preoperative risk stratification is important to identify risk factors and determine if preoperative intervention is needed.
3) Intraoperatively, the goals are to maintain a normal heart rate and blood pressure, adequate oxygen delivery, and minimize hemodynamic stress responses through careful use of anesthetic agents and techniques. Close monitoring is important to detect and treat any cardiac complications promptly.
Low dose dopamine increases GFR and RBF. The DAD-HF trial investigated 60 patients randomized to low dose furosemide (continuous infusion 0.5 mg/kg/day) with or without low dose dopamine (2 μg/kg/min). Dopamine preserved renal function compared to furosemide alone in patients with acute decompensated heart failure. There were no significant differences found in a trial comparing high vs low dose furosemide or bolus vs continuous infusion on renal function or symptoms. Novel agents targeting fluid overload, renal function, contractility, and vasomotion may provide new therapeutic options for acute heart failure.
Prof. U. C. SAMAL provides an overview of acute decompensated heart failure and what is new in the field. He discusses similarities and differences between acute myocardial infarction and acute heart failure syndromes. Mortality rates are high for both conditions, though clinical benefits of interventions are greater for acute MI based on published clinical trials. The document then discusses definitions and classifications of acute heart failure syndromes, as well as guidelines for diagnosis and treatment from ESC and ACC/AHA. Biomarkers that can help with diagnosis, prognosis, and guiding therapy are also summarized.
This document discusses systemic hypertension, including:
- Definitions of different classifications of hypertension according to WHO and AHA guidelines.
- Differences between hypertensive emergencies and urgencies.
- Common causes and clinical presentations of secondary hypertension.
- Recommended treatment approaches for various hypertensive crises and emergencies, including targets for blood pressure reduction.
- Drugs commonly used to lower blood pressure such as labetalol, nicardipine, nitroglycerin, and sodium nitroprusside.
This document summarizes several studies on the use of ACE inhibitors and angiotensin receptor blockers (ARBs) in treating heart failure and reducing cardiovascular risk. The HOPE trial showed that the ACE inhibitor ramipril reduced cardiovascular events in high-risk patients. The CHARM trial found that the ARB candesartan reduced cardiovascular outcomes in heart failure patients, both alone and in combination with ACE inhibitors. The ONTARGET trial aimed to compare the ARB telmisartan to ramipril, and their combination, to determine if telmisartan was non-inferior to ramipril and if their combination provided additional benefit.
This document provides an overview of congestive heart failure in adults. It begins with definitions and epidemiology, describing CHF as the heart's inability to pump enough blood due to structural or functional abnormalities. Main causes include reduced ejection fraction, volume overload, and pressure overload. Signs and symptoms include fatigue, shortness of breath, and leg swelling. The document then covers diagnosis, investigations such as BNP levels, classifications like NYHA staging, pathophysiology, types, manifestations, and management with medications like diuretics, ACE inhibitors, beta-blockers, and treatment of underlying conditions. It concludes with contraindicated medications in pregnancy or CHF.
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
This document discusses the stages, phenotypes, and treatment of heart failure. It describes:
1) The stages of heart failure from A to D, with stages C and D involving structural changes and previous or current symptoms where drug therapies are routinely used.
2) The phenotypes of heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) along with their respective treatment goals.
3) The pharmacological management of stage C HFrEF which involves the routine use of diuretics, ACE inhibitors, beta blockers, and aldosterone antagonists to control symptoms, improve quality of life, and reduce mortality and hospitalizations.
Similar to Acute Decompensated Heart Failure : What is New ? (20)
Should functional mr be fixed in heart failuredrucsamal
This document discusses functional mitral regurgitation (FMR) in heart failure patients. It presents evidence that even mild FMR results in poor survival outcomes, and that FMR is not just a late marker but also a cause of worse prognosis. Surgical mitral repair using a small, complete, rigid ring to reduce the mitral annulus has been shown to improve survival, ventricular remodeling, and functional status compared to no repair or incomplete repairs that do not fully correct FMR. Ongoing studies are exploring newer percutaneous approaches to treating FMR, but surgical repair remains the standard treatment when anatomically feasible to fully correct FMR.
Aortic Valve Stenosis with low EF : TAVR versus Replacementdrucsamal
1) Patients with low ejection fraction (EF < 50%) and severe aortic stenosis who undergo transcatheter aortic valve replacement (TAVI) have similar mortality at 1 year compared to those with higher EF, despite being higher risk.
2) TAVI is associated with significant improvements in EF, symptoms, and quality of life over 1 year in patients with very low EF (≤30%). However, mortality remains higher compared to those with EF >30%.
3) Both TAVI and surgical aortic valve replacement (SAVR) are associated with improvements in EF at 3 months in propensity matched populations with low EF. Short term outcomes are similar, but TAVI is associated with more pacemakers
When is less more minimally invasive surgery in low efdrucsamal
The document discusses treatment options for patients with reduced ejection fraction and secondary mitral regurgitation, including the use of minimally invasive mitral valve surgery which can be considered for elderly patients or those with comorbidities. It presents a case study of a 69-year-old male with severe secondary mitral regurgitation who underwent a minimally invasive mitral valve repair which eliminated his mitral regurgitation and improved his symptoms and ejection fraction. Long-term data on isolated mitral valve surgery in patients with reduced ejection fraction shows improvement in mitral regurgitation and functional status with no difference in survival between repair and replacement
The document discusses when to consider tricuspid valve repair. Tricuspid regurgitation is associated with poor prognosis, especially when secondary to left-sided heart lesions, cardiomyopathy, pulmonary hypertension, or in the setting of LVAD placement or heart transplantation. Tricuspid valve repair is indicated for severe, symptomatic primary tricuspid regurgitation, and may also be considered for significant functional regurgitation concurrent with mitral valve surgery, after isolated mitral valve surgery if regurgitation is severe, or when placing a continuous-flow LVAD. Prophylactic tricuspid annuloplasty during heart transplantation reduces the severity of post-operative regurgitation and is associated with improved long-term survival
Cad and low ef does viability assessment matterdrucsamal
This document discusses the value of viability studies in patients with coronary artery disease (CAD) and low ejection fraction (EF). It summarizes several studies on the topic and discusses their limitations. A key trial was the STICH trial, which found no significant difference in outcomes between revascularization and medical therapy alone, challenging the belief that revascularization benefits those with viable myocardium. The document concludes that while viability concepts are biologically plausible, recent trials create confusion and there is no consensus on how to apply viability testing in practice.
This document discusses the conundrum of managing mitral regurgitation (MR) in patients with heart failure. It highlights the importance of using multimodality imaging to:
1) Assess the severity of MR at rest and with exercise to determine risk and need for intervention.
2) Evaluate left ventricular function, dyssynchrony, viability and ischemia to determine indications for cardiac resynchronization therapy or revascularization.
3) Assess left ventricular remodeling and mitral valve deformation to predict risk of recurrent MR after repair and determine the best repair/replacement option.
Imaging provides essential information to optimize treatment strategies for MR in heart failure.
The complex patient vad transplant exchange or hospicedrucsamal
This document discusses the case of a 76-year-old man presenting with heart failure symptoms and recurrent cough syncope. Testing revealed cardiac amyloidosis due to a TTR gene mutation. For patients with TTR amyloidosis, treatment options include organ transplantation, TTR stabilizers in clinical trials, or enrollment in hospice. Given his age and comorbidities, the man's options included a left ventricular assist device, extended criteria transplant, or a clinical trial for TTR amyloidosis treatment. He was ultimately listed and transplanted, and has since recovered well.
The complex patient vad transplant exchange or hospicedrucsamal
This document discusses the case of a 76-year-old man presenting with heart failure symptoms and recurrent cough syncope. Testing revealed cardiac amyloidosis due to a TTR gene mutation. For patients with TTR amyloidosis, treatment options include organ transplantation, TTR stabilizers in clinical trials, or enrollment in hospice. Given his age and comorbidities, the man's options included a left ventricular assist device, extended criteria transplant, or a clinical trial for TTR amyloidosis treatment. He was ultimately listed and transplanted within a month, and has since recovered well.
Surgical director heart transplant and mechanical assist device programdrucsamal
The document discusses a 55-year-old female patient with a history of rheumatic valve disease and multiple prior heart surgeries who was admitted with recurrent heart failure and an ejection fraction below 10%, outlining her medical history and current status, treatment options, and clinical course including optimization, a redo aortic valve replacement and implantation of a HeartMate II left ventricular assist device.
The complex patient vad ransplant vad exchange or hospicedrucsamal
L.B. is a 62-year-old man with a long history of coronary artery disease and heart failure who has undergone multiple coronary bypass surgeries. He now has an ejection fraction of 25% and intractable ventricular tachycardia despite medical management. Due to the risks of ablation, the team is considering options like hospice care, cardiac transplantation, VAD implantation, or VAD exchange to treat his advanced heart failure. A cardiac catheterization revealed multiple occluded arteries and stenoses. Given his medical history and surgical history, the team must determine the best treatment approach for his condition.
This document discusses the management of mitral regurgitation (MR) in heart failure patients. It explores the differences between primary and functional (secondary) MR, and notes that correcting primary MR may improve outcomes but the benefits are less clear for functional MR which is primarily a ventricular problem. The document reviews potential management options for MR in heart failure including optimal medical therapy, cardiac resynchronization therapy, surgery, and percutaneous techniques such as the MitraClip system. It presents evidence from studies on the acute effects of CRT and the impact of CRT on functional MR severity. It also discusses guidelines on indications for mitral valve surgery in chronic secondary MR and barriers to surgery.
Whom to refer for mitral valve repair and whom notdrucsamal
This document discusses the treatment of mitral regurgitation in patients with heart failure. It describes the mechanisms of functional and ischemic mitral regurgitation. While medical therapy can improve symptoms and survival, cardiac resynchronization therapy may also help reduce mitral regurgitation severity and improve outcomes. Surgery to repair the mitral valve is an option but the risk of recurrence of mitral regurgitation is high, especially with more advanced left ventricular remodeling. Randomized trials are still needed to determine whether surgical correction provides clear benefits over medical therapy alone in high-risk patients. Percutaneous mitral valve repair may be a lower risk option for inoperable patients to reduce symptoms.
Devices and intervention in heart failure.drucsamal
- The document discusses the speaker's receipt of honoraria and research support from numerous pharmaceutical and device companies.
- It summarizes several journal articles and studies related to left ventricular remodeling post-myocardial infarction, baroreflex activation therapy for heart failure, and the effects of bi-ventricular pacing on left ventricular ejection fraction and end-systolic volume.
- Key findings from the PACE trial are highlighted showing improvements in left ventricular ejection fraction and end-systolic volume up to 2 years with bi-ventricular pacing compared to right ventricular pacing alone.
European Journal of Heart Failure's year in Cardiologydrucsamal
This document contains information about Prof. Fausto J. Pinto who is the Head of Cardiology at University Hospital Sta Maria-HPV and University of Lisbon in Portugal. It discloses that he has received consultancy fees and lecture fees from various pharmaceutical companies. It also contains several figures and images from various medical studies and publications related to cardiology.
This document lists the collaborations and conflicts of interest for speakers Thomas F. Lüscher and Marco Metra. It notes that they have received research grants, educational grants, and honoraria from numerous pharmaceutical companies. The rest of the document discusses the European Heart Journal, including new associate editors, submission rates and acceptance rates, impact factors, and plans to launch new open access and supplement journals.
This document summarizes a presentation on cardiology topics including acute and advanced heart failure. It discusses trends in heart failure hospitalizations and mortality. It describes different hemodynamic profiles in acute heart failure patients and their corresponding treatments. It also discusses topics like iron deficiency in heart failure, sleep disordered breathing, and a study showing sleep disordered breathing is common in acute heart failure and predicts mortality.
This document discusses the importance of prevention in treating cardiovascular disease. It outlines stages of heart failure progression from asymptomatic left ventricular dysfunction to refractory heart failure. Clinical trials show benefits of treating hypertension and post-MI left ventricular dysfunction to prevent heart failure. Treatment with ACE inhibitors reduces mortality and morbidity from heart failure. Prevention of risk factors is emphasized as the best strategy to avoid full-blown heart disease.
Can we afford heart failure management in the futuredrucsamal
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This document discusses statistics related to heart failure. It summarizes data on outcomes for hospitalized heart failure patients compared to chronic heart failure patients. Hospitalized patients generally have worse outcomes, with high 1-year mortality rates around 25-27%. Chronic heart failure patients have lower but still significant 1-year mortality rates of around 5-6%. The document also reviews real-world data showing high readmission rates after hospitalization for heart failure. It concludes that while treatments for chronic heart failure with reduced ejection fraction have improved outcomes over decades, more efforts are still needed to improve care and outcomes for hospitalized patients and those with preserved ejection fraction.
The heart failure association global awareness programme.drucsamal
The Global Heart Failure Awareness Programme aims to make the prevention and management of heart failure a global health priority. It is led by the Heart Failure Association of the European Society of Cardiology and supported by educational grants. The programme's objectives are to build a common global approach to raising awareness of heart failure among targeted audiences and to call for heart failure to be a health priority in every country. It plans to achieve this through developing educational content, building advocacy coalitions, and implementing initiatives at the national and local levels between 2015 and 2017.
Gemma Wean- Nutritional solution for Artemiasmuskaan0008
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GEMMA Wean is available in 0.1mm, 0.2mm and 0.3mm. There is also a 0.5mm micro-pellet, GEMMA Wean Diamond, which covers the early nursery stage from post-weaning to pre-growing.
The facial nerve, also known as cranial nerve VII, is one of the 12 cranial nerves originating from the brain. It's a mixed nerve, meaning it contains both sensory and motor fibres, and it plays a crucial role in controlling various facial muscles, as well as conveying sensory information from the taste buds on the anterior two-thirds of the tongue.
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This particular slides consist of- what is hypertension,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is summary of hypertension -
Hypertension, also known as high blood pressure, is a serious medical condition that occurs when blood pressure in the body's arteries is consistently too high. Blood pressure is the force of blood pushing against the walls of blood vessels as the heart pumps it. Hypertension can increase the risk of heart disease, brain disease, kidney disease, and premature death.
At Apollo Hospital, Lucknow, U.P., we provide specialized care for children experiencing dehydration and other symptoms. We also offer NICU & PICU Ambulance Facility Services. Consult our expert today for the best pediatric emergency care.
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Acute Decompensated Heart Failure : What is New ?
1. Prof. U. C. SAMAL
MD, FICC, FACC, FIACM, FIAE, FISE, FISC, FAPVS
Ex-HOD Medicine & Prof. Cardiology
Patna Medical College, Patna, Bihar
Past President, Indian College of Cardiology
Permanent & Chief Trustee, ICC-HFFI
National Executive Member, Cardiological Society of India
President, CSI Bihar
Acute Decompensated Heart Failure :
What Is New ?
2. Drug failures in acute heart failure
Trial name Drug tested Patients enrolled
VMAC Nesiritide Decompensated CHF
Excluded SBP < 90 mmHg, Mean SBP > 124 mmHg
No LVEF cut point
OPTIME Milrinone Decompensated systolic heart failure,
not requiring inotropes
Excluded SBP < 80 mmHg, Mean SBP = 120 mmHg
Mean LVEF = 23%
VERITAS Tezosentan Acute heart failure
Two out of four-↑BNP, pulmonary oedema, CXR
congestion,
LVEF < 40%, Mean LVEF = 20% in VERITAS I and
28% in VERITAS II
Mean SBP = 131 in VERITAS I and 132 in VERITAS II
SURVIVE Levosimendan Acute decompensated HF requiring inotropes
LVEF < 30%, Mean LVEF = 24$
Mean SBP-116 mmHg
3. Trial name Drug tested Patients enrolled
REVIVE -2 Levosimendan Acute decompensated HF
Symptomatic despite i.v. diuretic
LVEF < 35%, Excluded SBP > 90 mmHg
EVEREST Tolvaptan Hospitalized for decompensated CHF
LVEF ≤ 40%, Excluded SBP < 120 mmHg
Mean LVEF = 27.5%, Mean SBP= 120 mmHg
PROTECT I
and II
Rolofylline Acute heart failure, Impaired renal function
↑BNP
ASCEND-HF Nesiritide Acute decompensated heart failure
Drug failures in acute heart failure
4. Some new therapeutic agents for acute heart
failure and their potential targets
Agent For patients with these
clinical features
Diuretics, vasopressin
antagonists,
adenosine antagonists
Patients with signs of fluid
overload, high BNP
Vasodilators Normal to high SBP, high BNP
Inotropes Low SBP, signs of
Hypoperfusion
Renal preservation agents Renal dysfunction
Myocardial protection agents CAD, or ongoing ischaemia
5. Proposed classification for patients who present with acute
heart failure syndromes
ACCF/AHA
stage
Explanation of stage
Worsening chronic
HF (75%)
Stage C C: structural heart disease with
prior or current symptoms of HF
Advanced HF (5%) Stage D D: refractory HF requiring
specialized interventions
De novo HF (20%) Stage B most
common, but also
Stage A
Also neither A
nor B
B: structural heart disease but
without signs or symptoms of HF
A: at high risk for HF but without
structural heart disease or
symptoms of HF
6. Phases of acute heart failure syndromes management
PHASES
PHASES GOALS AVAILABLE TOOLS
Initial or
emergency
department
phase of
management
Treat life threatening
conditions
Establish the diagnosis
Determine the clinical
profile
Identify and treat
precipitant
Disposition
Examples: STEMI - reperfusion therapy
History, physical exam, EKG, X-ray,
natriuretic peptide level
BP, HR, signs (e.g. pulmonary oedema),
ECG, X-ray,
laboratory analysis, echocardiography
History, physical exam, X-ray, ECG,
laboratory analysis
No universally accepted risk-stratification
method
Frontiers in Cardiovascular Medicine EHJ 2010:31;784-793
7. Phases of acute heart failure syndromes management
PHASES
PHASES GOALS AVAILABLE TOOLS
IN – HOSPITAL
PHASE
Monitoring and
reassessment
Assess right and left
ventricular pressures
Assess and treat (in the
right patient) other cardiac
and non-cardiac conditions
Assess for myocardial
viability
Signs/symptoms, HR, SBP, ECG,
orthostatic changes, body weight,
laboratory analysis (BUN/Cr,
electrolytes), potentially BNP
SBP (orthostatic changes, valsalva
manoeuvre), echocardiography, BNP/NT-
proBNP, PA catheter
Echo-Doppler, cardiac catheterization,
electrophysiology testing
MRI, stress testing, echocardiography,
radionuclear studies
Frontiers in Cardiovascular Medicine EHJ 2010:31;784-793
8. Phases of acute heart failure syndromes management
PHASES
PHASES GOALS AVAILABLE TOOLS
DISCHARGE
PHASE
Assess functional capacity
Re-evaluate exacerbating
factors (e.g. non-
adherance, infection,
anaemia, arrhythmias,
hypertension) and treat
accordingly
Optimize pharmacological
therapy
Establish post-discharge
planning
6 min walk test
Examples: physical therapy, education for
diet control and medication, evaluation for
sleep apnoea
ACCF/AHA and ESC guidelines
Discharge instructions including body
weight monitoring, smoking cessation,
medication adherance, follow-up
Frontiers in Cardiovascular Medicine EHJ 2010:31;784-793
9. Frontiers in Cardiovascular Medicine EHJ 2010:31;784-793
ESC divides pts. Into six clinical profiles
1.Worsening or decompensated chronic HF
2.Pulmonary Oedema
3.Hypertensive HF
4.Cardiogenic shock
5.Isolated right HF
6.ACS and HF with the explicit acknowledgement
that there is overlap between groups
The ACCF/AHA divides patients based on
presenting clinical profile into three main
groups:
(i) volume overload, manifested by pulmonary
and/or systemic congestion, usually due to
increases in blood pressure (BP),
(ii) severely reduced cardiac output often with
hypotension, and
(iii) combined volume overload and cardiogenic
shock
ESC Guidelines
10. Initial Therapeutic Management
Target Therapeutic example Mechanism of action Side effects
Alleviate
congestion
IV furosemide Water and sodium
excretion
Electrolyte abnormalities
Reduce
elevated LV
filling
pressures
IV nitrates Direct relaxation of
vascular smooth muscle
cells through various
mechanisms
Hypotension, decreased
coronary perfusion
pressure
Poor cardiac
performance
Inotropes Activate camp or calcium
sensitization resulting in
improved contractility; also
powerful vasodilators: in
effect, inodilators
Hypotension,
arrhythmias, myocardial
damage, association with
increased morbid events
Tachycardia
and increased
systemic blood
pressure (i.e. in
cases of
excessive
sympathetic
tone
Beta-blockers: IV esmolol
may be used when HF is
related to AF with RVR
and/or severe hypertension
Blockade of beta-1 and
beta-2 receptors
Bradycardia,hypotension,
negative inotropy;
however given short half-
life of esmolol, these side
effects should be short
lived
Frontiers in Cardiovascular Medicine EHJ 2010:31;784-793
11. Short- and long-term novel therapies for AHF syndromes
Short term Long term Both
Levosimendan [LIDO, CASINO, SURVIVE]
Nesiritide[ROSE, DOSE-AHF]
Relaxin [RELAX-AHF]
Myosin Activators Omecamtiv Mecarbil
[ATOMIC-AHF]
RyR2 stabilizers/ rycals
Cinaciguat (UIT)
Adenosine regulating agents
Stresscopin
Istaroxime [HORIZON-HF]
Ularitide [TRUE-AHF, SIRIUS II, URGENT]
Urocrotins [UNICORN]
Hypertonic Saline
Ultrafiltration [RAPID-CHF, UNLOAD]
IABP
EECP [PEECH]
CAFA
IMT
Direct renin
Inhibitors (DRI)
[ASTRONAUT]
Macronutrients
Micronutrients
CRT/AICD
Adenosine Antagonists
[PROTECT, REACH UP rolofylline]
Vasopressin Antagonists
[EVEREST, TACTICS-HF]
Digoxin [DIG]
CD-NP
Frontiers in Cardiovascular Medicine EHJ 2010:31;784-793 modified 2013
12. Clinical RELEVANCE of promising novel biomarkers(AHFS)
Biomarker Diagnosis Prognosis Therapy guidance Cardiac
Production
NT-proBNP and
BNP
++++ ++++ ++ Solely
Serum Sodium ++ ++ ++ No
Serum Creatinine ++ ++ ++ No
MR-proANP +++ ++++ Likely similar to NT-
ProBNP/BNP
Solely
sST2 + ++++ ? Not Exclusively
Hs troponin-I
[EFFECT]
+ ++++ ? Solely
MR-proADM - ++++ ? No
Cystatin C - ++++ ? No
NGAL - ++++ ? No
GDF-15 - +++ ? Not Exclusively
β- Trace protein - +++ ? No
Gal-3 - +++ ? Not exclusively
CRP - ++ ? No
TNF-α - ++ ? No
IL-6 - ++ ? No
PTX3 - ++ ? Unknown
MPO - ++ ? Not exclusively
ET-1 - ++ ? Not exclusively
Copeptin - ++ ? No
PCT ++ ++ ++ No
12
Clinical Chemistry 58:1 127–138 (2012)
14. Summary of the main utility biomarkers in AHFS
Biomarkers Diagnosis & pathophysiology Adverse prognosis
PCT [serum] Cut off 0.05ng/ml 0.05 -0.5ng/ml local infection
0.5-2ng/ml systemic infection
2-10ng/ml SIRS – sepsis
>10ng/ml sepsis
NGAL [serum and
urine]
Cut off 150ng/ml serum, 130ng/ml urine
Cardiorenal syndrome
>100ng/ml
Copeptin [serum] Median 3.7pmol/l
AHF vascular alterations
>54.2pmol/l
MR-proADM [SERUM] AHF vascular alterations >2.15nmol/l
ADMA AHF oxidative stress
15. Modes of presentation of ADHF
Clinical status Heart
rate
SBP
mmHg
Cl L /
min /m3
Pulmonary
capillary
wedge
pressure
mmHg
Conges
tion
killip/for
rester
Diuresis Hypope
rfusion
End organ
hypoperfusion
I acute
decompensated
congestive heart
failure
+ / - Low
normal /
high
Low
normal /
high
Mild elevation K II / F II + +/- _
II Acute heart failure
with hypertension/
hypertensive crisis
Usually
elevated
High +/- >18 K II-IV/ F
II / III
+/- +/- + WITH CNS
symptoms
III Acute heart
failure with
pulmonary edema
+ Low
normal
Low Elevated K III / F II + +/- -
IVa Cardiogenic
shocka/low-output
syndrome
+ Low
normal
Low, <2.2 >16 K III-IV/ F
I-III
Low + +
IVb Severe
cardiogenic shock
>90 <90 <1.8 >18 K IV / F IV Very low ++ +
V High-output
failure
+ +/- + +/- K II / F I-II + - -
VI Right-sided acute
heart failure
Usually
low
Low Low Low F I +/- +/-, acute
onset
+/-
16. Patient presenting with dyspnea
Differential diagnosis
cardiac -- Consider acute
coronary syndrome
Physical exam, chest x-ray,
ECG, BNP level
Treatment option for HF with SBP
<90mmHg or shock –diuretics,
inotropes, vasodilators and /or
nesiritide to follow
BNP <100pg/ml BNP 100-500pg/ml BNP >500pg/ml
HF very unlikely [2%] Clinical suspicion of
HF or past h/o HF
HF very likely [95%]
HF highly probable [90%]
Differential diagnosis
noncardiac -- consider
COPD, pulmonary
embolism, asthma,
pneumonia, sepsis
Treatment option for HF with SBP >
90mmHg -- diuretics with nesritide
esp. with CKD & pulmonary
congestion may consider adding
vasodilators if hypertensive may
consdider adding inotropes for poor
perfusion
Treatment option --
•Diuretics as required
•Consider nesritide if any of the
following - Scr>1.5mg/dl, CrCl
<60ml/min, BUN >10mg/dl,
pulmonary congestion or for border
line hemodynamic instability
17. Comprehensive Assessment
Potential targets Method of assessment
Congestion JVP, Body wt, peripheral edema
LV function, valvular ds, wall
motion abnormalities, aneurysm
ECHO Doppler, MRI, Nuclear
imaging
Ischaemia Pharmacological or exercise
testing with imaging
CAD Cardiac catheterization and
angiography
Ventricular dyssnchrony [wide
QRS]
Electrocardiogram
Viable but dysfunctional
myocardium
Low dose dobutamine ECHO, MRI
18. Myocardium Coronary
arteries
Electrical
system
Valves
•Surgery
•Procedural
•Statins
•Per EDC
guidelines
Pericardium
LV
dysfunction
•ACE-I or ARB
•Beta blockers
•Aldosterone
antagonist
•Hydral / ISDN
•Digoxin
•Macronutrients
•Micronutrients
•Metabolic
modulators
CAD
•Anti platelet
•Statins
•Revascularization
•Other ESC
guideline
recommended
therapy for
secondary
prevention
Sudden cardiac
death
•ICD
•B- blockers
•Aldesterione
antagonist
Ventriculasr
dysschrony
•CRT +/- ICD
Atrial fibrillation
•Rate control – digoxin – b-
blocker, non dihydropyridine ca
channel blockers
•Warfarin
•Rhythm control
•MAZE procedure
Congestion – [ salt restriction, diuretics, ultrafiltarion, vasopressin antagonists]
Hypertension [ACE I or ARB, diuretics, other per ESC guidelines
Enhance adherence [education, disease management, performance improvement system
Cardiac reconstruction
[five overacting thematic targets – myocardium, coronary arteries, electrical system, pericardium, valves]
20. AHFS : NOT VERIFIED
Similarities and differences between acute MI & AHFS in
hospitalization in the US
Incidence 1 million per year 1 million per year
Mortality
Pre hospitalization
In hospital
After discharge [ 60-90 d]
High
3-4%
2%
?
3-4%
10%
Myocardial injury Yes Likely
Pathophysiological target Clearly defined
[coronary thrombosis]
Uncertain
Clinical benefits of
interventions in published
clinical trial
Beneficial Minimal / no benefit or
deleterious compared with
placebo
ACC / AHA recommendation LEVEL A NONE
Circulation
Circulation
Special report
Acute Heart Failure Syndrome
21. Omecamtiv Mecarbil (OM) is a
Novel Selective Cardiac Myosin
Activator
Malik FL, et al. Science 2011; 331:1439-43
Teerlink JR, et al. Lancet 201; 378:667-75; Cleland JGF, et al. Lancet
2011; 378:676-83
22.
23.
24. Acute Heart Failure Syndrome(s)
• Acute heart failure (AHF) is defined as a rapid
onset or change in the signs and symptoms of
HF, resulting in the need for urgent therapy.
• Symptoms are primarily the result of severe
pulmonarycongestion due to elevated left
ventricular (LV) filling pressures(with or without
low cardiac output).
• AHFS can occur in patientswith preserved or
reduced ejection fraction (EF).
• Concurrentcardiovascular conditions such as
coronary heart disease (CHD),hypertension,
valvular heart disease, atrial arrhythmias, and/or
noncardiac conditions (including renal
dysfunction, diabetes,anemia) are often present
and may precipitate or contributeto the
pathophysiology of this syndrome
25. EBM in AHFS?
• The first randomizedplacebo-controlled
AHFS trials were published as late as
2002.
Cuffe MS, et al. for the Outcomes of a Prospective Trial of Intravenous Milrinone forExacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Effects of short-term,
intravenous milrinone on acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002; 287: 1541–1547.
PublicationCommittee forthe VMAC Investigators. Intravenous nesiritide vs nitroglycerin fortreatment of decompensated congestive heart failure: a randomized controlled trial.
JAMA. 2002; 287: 1531–1540
• None of the placebo-controlled AHFS
studies conducted to datehas shown
either a consistent improvement of in-
hospital orpostdischarge survival or a
26. AHFS – Goals of treatment
• † Emergency treatment phase
• Improve symptoms
• Restore oxygenation
• Improve organ perfusion and haemodynamics
• Limit cardiac/renal damage
• Minimize ICU length of stay
• † In-hospital management phase
• Stabilize patient and optimize treatment strategy
• Initiate appropriate (life-saving) pharmacological therapy
• Consider device therapy in appropriate patients
• Minimize hospital length of stay
• † Discharge planning phase
• Plan follow-up strategy
• Educate and initiate appropriate lifestyle adjustments
• Provide adequate secondary prophylaxis
• Prevent early readmission
• Improve quality of life and survival
27. AHFS: which appropriate targets
of therapy ?
• Traditionally, reduction in pulmonary
capillary wedge pressure (PCWP)and/or
increase in cardiac output.
• However, other therapeutictargets may
include blood pressure control, myocardial
protection,neurohormonal modulation, and
preservation of renal function.
29. Patient Selection and Treatment
Congestion at Rest
YesNo
Warm & Dry
PCWP normal
CI normal
(compensated)
Cold & Wet
PCWP elevated
CI decreased
Cold & Dry
PCWP low/normal
CI decreased
Vasodilators
Nitroprusside
Nitroglycerin
Inotropic Drugs
Dobutamine
Milrinone
Calcium Sensitizers
Normal
SVR
High
SVR
Low
Perfusion
at Rest
No
Yes
Warm & Wet
PCWP elevated
CI normal
Natriuretic
Peptide
Nesiritide
or
Stevenson LW. Eur J Heart Fail. 1999;1:251.
30. Adverse Drug Effects
• Non-Potassium-Sparing Diuretics
Intravenous loop diuretics may improve symptoms and fluid loss
initially but also may contribute to renal function decline.This may
be related not only to intravascular volume depletionbut also to
further neurohormonal activation resulting in avasomotor
nephropathy.
• Intravenous loop diuretics may be associated with worse
outcomes in AHFS patients.
• Inotropic Therapy
Intravenous inotropes increase myocardial oxygen consumption,
causing myocardial damage in the setting of hibernating
myocardium. Use of inotropes has consistently been associated
with increasedmortality.
• Vasodilators
Excessive vasodilatation in AHFS may lead to blood pressure
decrease, potentially exacerbating myocardial ischemia and renal
hypoperfusion.
31. AHFS: which appropriate targets
of therapy ?
Perspectives
• Managing fluids,
• Preserving renal function
32. • Loop diuretics are an essential component of therapy for patients with acute decompensated
heart failure, but there are few prospective data to guide their use.
• In a prospective, double-blind, randomized trial, we assigned 308 patients with ADHF to
receive furosemide administered intravenously by means of either a bolus every 12 hours or
continuous infusion and at either a low dose (equivalent to the patient’s previous oral dose) or
a high dose (2.5 times the previous oral dose).
• Among patients with ADHF, there were no significant differences in patients’ global
assessment of symptoms or in the change in renal function when diuretic therapy was
administered by bolus as compared with continuous infusion or at a high dose as compared
with a low dose.
Furosemide
33. • The study tests the hypothesis that in patients admitted with acutely decompensated heart failure (ADHF),
achievement of adequate body hydration status with intensive medical therapy, modulated by combined
bioelectrical vectorial impedance analysis (BIVA) and B-type natriuretic peptide (BNP) measurement, may contribute
to optimize the timing of patient’s discharge and to improve clinical outcomes.
• 300 ADHF pts underwent serial BIVA and BNP measurement. Therapy was titrated to reach a BNP value of 250
pg/ml, whenever possible.
• Our study confirms the hypothesis that combined BNP/BIVA sequential measurementshelp to achieve adequate fluid
balance status in patients with ADHF and can be used to drive a ‘‘tailored therapy,’’ allowing clinicians to identify
high-risk patients and possibly to reduce the incidence of complications secondary to fluid management strategies.
35. • Small studies have indicated that adenosine A1
receptor antagonists enhance diuresis and may
improve renal function in patients with chronic heart
failure or AHF.
• 2,033 AHF pts, volume overload, eCrCl 20 - 80
ml/min, and elevated BNP randomized (2:1) within 24
h of hospital presentation to rolofylline 30 mg/day or
intravenous placebo for up to 3 days.
• In this large, phase III clinical trial, the adenosine A1
receptor antagonist rolofylline did not prevent
persistent worsening renal function in AHF patients
with volume overload and renal dysfunction.
Rolofylline
36. •Effects of rolofylline on endpoints in relation to baseline renal function.
•The secondary morbidity/mortality endpoint, the risk of death or cardiovascular or renal rehospitalization through
day 60, was lower in the rolofylline group compared with the placebo group only in patients with a baseline eCrCl 30
ml/min (hazard ratio: 0.64; 95% CI: 0.43 to 0.95), but not in the other subgroups
Rolofylline
38. • Istaroxime is a novel intravenous agent with inotropic and lusitropic properties related to inhibition of Na/K
adenosine triphosphatase (ATPase) and stimulation of sarcoplasmic reticulum calcium ATPase.
• 120 AHF pts and reduced systolic function. Three sequential cohorts of 40 patients each were randomized 3:1
istaroxime:placebo to a continuous 6-h infusion. The first cohort received 0.5 g/kg/min, the second 1.0 g/kg/min, and
the third 1.5 g/kg/min istaroxime or placebo.
• In patients hospitalized with HF, istaroxime improved PCWP and possibly diastolic function. In contrast to available
inotropes, istaroxime increased SBP and decreased HR.
Istaroxime
39. •Urocortins are a recently discovered group of peptide hormones of the corticotropin releasing factor
family. They bind with a strong affinity to the CRH-R2 receptor, which is highly expressed in the
myocardium and in the vascular endothelium.
•Urocortins exhibit potent inotropic and lusitropic effects on rat and sheep hearts and activates a group of
myocyte protective pathways collectively known as ‘reperfusion injury salvage kinase’.
•In healthy humans show that brief intravenous infusions of urocortin 2 in healthy humans induce
pronounced dose-related increases in cardiac output, heart rate, and left ventricular ejection fraction while
decreasing systemic vascular resistance; similar effects were seen in HF patients.
Urocortins
41. • Nesiritide is approved in the United States for early relief of dyspnea in patients with acute heart failure.
Previous meta-analyses have raised questions regarding renal toxicity and the mortality associated with
this agent.
• We randomly assigned 7141 patients
• Coprimary end points were the change in dyspnea at 6 and 24 hours, and the composite end point of
rehospitalization for heart failure or death within 30 days.
• Nesiritide was not associated with an increase or a decrease in the rate of death and rehospitalization
and had a small, nonsignificant effect on dyspnea when used in combination with other therapies.
• It was not associated with a worsening of renal function, but it was associated with an increase in rates
of hypotension. On the basis of these results, nesiritide cannot be recommended for routine use in the
broad population of patients with acute heart failure.
Nesiritide
42. These molecules have been engineered to combine the beneficial aspects of different natriuretic peptides
into a single molecule while minimizing potentially negative actions.
CD-NP is a combination of C-type natriuretic peptide (CNP) and Dendroapsis NP
(DNP).
Although lacking natriuretic effects, CNP is a more selective venodilator than BNP, thus reducing the risk of
significant hypotension. On the other side, DNP possesses significant natriuretic activity, at the expense of
possible hypotensive effects.
The chimeric peptide CD-NP combines the favourable natriuretic effects of DNP with the venodilatory profile
of CNP, reducing the risk for harmful side effects.
Preliminary studies in AHFS patients are ongoing.
Chimeric natriuretic peptides
43. • Cinaciguat (BAY 58-2667) is a soluble guanylate cyclase (sGC, second messenger that internalizes the message
carried by intercellular messengers such as peptide hormones and NO) activator that is being developed as a first-
in-class treatment for acute decompensated heart failure (ADHF). It acts independently of the sGC ligand nitric
oxide.
• Cardioprotective effects in animal models, and pilot clinical studies found that it was well tolerated, unloaded the
heart and increased cardiac output.
• This placebo-controlled, randomized, double-blind, multicenter, international phase IIb study investigated the safety
and efficacy of intravenous cinaciguat (per-protocol) as add-on to standard therapy in 139 patients with ADHF
(NYHA functional class III and IV; pulmonary capillary wedge pressure [PCWP] ≥ 18 mmHg).
• Cinaciguat rapidly and significantly reduced PCWP and PVR and increased cardiac output in patients with ADHF,
without impairing cardiac or renal function. Hypotension occurred in some patients; further dose titration studies
are therefore required to establish the optimal dosing strategy for this promising new therapy.
Cinaciguat
44. Adenosine regulating agents
•This new class of drugs, whose prototype is represented by acadesine, has been developed to mimic the
protective effects of adenosine during ischaemia.
•Acadesine exerts its pharmacological actions by increasing adenosine bioavailability and by activating
50adenosine monophosphate (AMP) signalling cascade via its metabolite 5-aminoimidazole-4-carboxamide
riboside (ZMP).
•The first mechanism leads to multiple anti-ischaemic effects (maintenance of endothelial function and
vasodilation, inhibition of platelet aggregation and neutrophil activation), whereas the latter ameliorates
glucose uptake and free fatty acid oxidation thus increasing ATP synthesis. Importantly, acadesine exerts
its actions only in areas undergoing net ATP catabolism (such as ischaemic tissues) thereby avoiding
potentially harmful peripheral vasodilator effects.
Acadesine
45. First identified as a pregnancy hormone with powerful vascular effects, relaxin is
currently under investigation for its systemic and renal vasodilatory actions.
In AHFS patients with high SBP, data from a Phase II trial have demonstrated an
improvement in dyspnoea with a single dose.
A Phase III clinical trial is currently underway.
Relaxin
46. In-Hospital Management Phase
• This phase begins once the patient is stabilized
and dyspneais improved.
• Because a significant number of patients
continueto have signs and symptoms of HF, the
goals of this phase arecontinued hemodynamic
and symptomatic improvement while preventing
myocardial and renal injury.
• Patients who are not treated withACE inhibitors,
angiotensin receptor blockers, ß-blockers,or
aldosterone antagonists should receive these
therapies, asrecommended by recent guidelines
48. Discharge-Planning Phase
• Despite the clinical evidence supporting the use of
implantablecardiac defibrillators and cardiac
resynchronization therapyin patients with chronic
HF and systolic dysfunction, theirrole in AHFS
patients is not clear.
• The available data suggest that a significant number
of AHFSpatients are not being evaluated for
potential beneficial surgicalprocedures that include
myocardial revascularization, LV reconstruction,
mitral valve surgery, or cardiac transplantation.
49. AHFS where are we? Where are we going?
• AHFS is a complex condition with substantial morbidity and
mortalityand enormous utilization of health resources and cost.
• Thereare numerous challenges in caring for this population.
• UniformAHFS classification is currently lacking, and management
strategiesvary markedly.
• There is a general consensus that to reduce mortality,morbidity, and
the economic burden of AHFS, systematic researchefforts on clinical
application and translation of promisingbasic science results are
needed.
• Pathophysiologically basedinterventions (eg, cardiorenal syndrome)
may be particularlyappealing.
• A special focus should be on choice of appropriatemanagement
strategies, including minimizing the use of drugswith adverse
effects and development and validation of knownprognostic markers
to guide AHFS interventions.
50. …of note, every large published clinical trial conducted in patients with
AHFs has been negative in terms of efficacy, safety, or both.
…However, most international multicenter clinical trials completed to
date were conducted on fairly undifferentiated populations of patients
with AHFs.
….homogeneous pathophysiological disease states within the
heterogeneity of aHFs is of paramount importance to clinical trial design
and aHFs therapy.
… Future trials conducted in aHFs must abandon the ‘one-sizefits- all’
approach in favor of an approach that takes into account the varied and
distinct pathophysiologies of aHFs.
51. Milton Packer 2008 JCF
• … Yet, despite substantial advances in our understanding and
management of heart failure, we have had
• few successes and many failures.
• Nearly 1,000 new drugs and devices have been developed for
the treatment of heart failure duringthe past 20 years, but only
9 have received regulatory approval and are being used in the
clinical setting.
• Most of our efforts to correct fluid retention, stimulate the
inotropic state of the heart, and modulate neurohormonal
systems have not predictably improved the condition of
patients with HF…
53. rhBNP
D
R I
M
K
R
G
S
S
S
S
G
L
G
F
C
C
S S
G
SGQVM
K V L
R
R
H
KPS
Effects of Nesiritide
Venous, arterial, coronary
VASODILATION
CARDIAC
INDEX
Preload
Afterload
PCWP
Dyspnea
HEMODYNAMIC
CARDIAC
No increase in HR
Not proarrhythmic
Aldosterone
Endothelin
Norepinephrine
SYMPATHETIC AND
NEUROHORMONAL SYSTEMS
Fluid volume
Preload
Diuretic
usage
NATRIURESIS
DIURESIS
RENAL
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70. (1) Symptom relief.
(2) Measures of congestion relief (i.e. improvement in
clinical signs).
(3) Index hospitalization data (e.g. length of stay).
(4) Prevention of end-organ damage (heart and
kidney).
(5) Post-discharge: death and rehospitalization data.
Federal Drug Administration (FDA) Study Group as a general
guide for choosing the components of the endpoints to be
included when testing different types of drugs in different patient
subgroups, although not all of them would be necessary in a
single trial
Position Statement European Journal of Heart Failure (2011)
71.
72.
73. Simplified schematic of guanylyl cyclase (GC) pathways, which have cyclic guanosine monophosphate (cGMP) as their second messenger. Nitric
oxide is produced by endothelial cells and activates soluble GC in the target cell. ANP and BNP stimulate GC-A (also called NP receptor A), while
CNP stimulates GC-B (also called NP receptor B). DNP is a GC-agonist first discovered in snake venom. CD-NP is a chimeric peptide composed of
the ring structure and amino terminus of CNP and the carboxyterminus of DNP; it activates both GC-A and GC-B. Natriuretic peptides also bind to
the non-GC-linked natriuretic peptide C receptor, the biological significance of which beyond NP clearance is currently unclear. Cyclic GMP
modulates cGMP-dependent protein kinase G, cGMP-regulated PDEs, and cGMP-regulated cation channels. The cGMP signal is terminated by
PDEs that hydrolyze cGMP to GMP, or by extrusion into the extracellular space. The NPs are degraded by a variety of peptidases. Cyclic GMP
signaling can be enhanced by (1) the use of NO mimetics such as nitrovasodilators, (2) direct sGC stimulators, (3) exogenous NPs, (4) inhibiting
NP degrading enzymes, and (5) inhibiting the activity of cGMP-hydrolyzing PDEs. ANP, atrial natriuretic peptide; BNP, B-type natriuretic peptide;
cGMP, cyclic guanosine monophosphate; GMP, guanosine monophosphate; GC, guanylyl cyclase; DNP, Dendroaspis natriuretic peptide; DPP4,
dipeptidyl peptidase IV; NEP, neutral endopeptidase; NO, nitric oxide; PDE, phosphodiesterase; PKG, protein kinase G; RA, natriuretic peptide
receptor A; sGC, soluble guanylate cyclase.
74. Schematic illustrating three different forms of soluble guanylate cyclase and their respective responsiveness to nitrovasodilators, heme-dependent
sGC stimulators (e.g., BAY 41-2272), and heme-independent sGC activators (e.g., cinaciguat [also known as BAY 58-2667]). Nitric oxide (NO) and
nitrovasodilators only stimulate sGC when it, contains the heme moiety with a ferrous iron (Fe2+
); furthermore, NO and nitrovasodilators have cGMP-
independent actions. BAY 41-2272 also activates only the NO-sensitive sGC but without the cGMP-independent actions of NO and nitrovasodilators.
Cinaciguat activates heme-free sGC, which is insensitive to NO, and also inhibits its degradation. The question marks indicate that little is known
about the transition between the different forms, their prevalence in health and disease, and their potential restoration to the reduced, NO-sensitive
form. cGMP, cyclic guanosine monophosphate; Fe, iron; sGC, soluble guanylate cyclase.
(From Boerrigter G, Burnett JC Jr. Soluble guanylate cyclase: not a dull enzyme. Circulation 2009;119(21):2752-2754.)
75. Mechanism of action of novel contractility-enhancing medications. Levosimendan enhances contractility by increasing responsiveness of
myofilaments to calcium. The cardiac myosin activator CK 1827-452 stimulates myosin adenosine triphosphatase (ATPase), thereby increasing force
generation. Istaroxime inhibits activity of plasma membrane sodium-potassium ATPase and increases the activity of sarcoplasmic/endoplasmic
reticulum calcium ATPase (SERCA). ADP, adenosine diphosphate; ATP, adenosine triphosphate; I-1, protein phosphatase inhibitor-1; P, phosphate;
PLB, phospholamban; PP1, protein phosphatase; RyR2, ryanodine receptor; TnC, troponin C; TnI, troponin I; TnT, troponin T.
(Modified from Tavares M, Rezlan E, Vostroknoutova I, et al. New pharmacologic therapies for acute heart failure. Crit Care Med 2008; 36[Suppl]:S112-
S120.)
76. Forrester Hemodynamic Subsets
Subset Description
I: Warm and dry (normal)
PCWP 15–18 mmHg and CI
>2.2 L/min/m2
II: Warm and wet (congestion)
PCWP >18 mmHg and CI >2.2
L/min/m2
III: Cold and dry (hypoperfusion)
PCWP 15–18 mmHg and CI
<2.2 L/min/m2
IV: Cold and wet (congestion and
hypoperfusion)
PCWP >18 mmHg and CI <2.2
L/min/m2
77. Treatment Goals for ADHF
•Improve symptoms, especially congestion and low-output sympt.
•Restore normal oxygenation
•Optimize volume status
•Identify etiology
•Identify and address precipitating factors
•Optimize chronic oral therapy
•Minimize side effects
•Identify patients who might benefit from revascularization
•Identify patients who might benefit from device therapy
•Identify risk of thromboembolism and need for anticoagulation
•Educate patients concerning medications and self-management of
heart failure
•Consider and, where possible, initiate a disease-mgt. program
78. Subset I: Warm and Dry
• Therapy is the optimization of oral medications
Pharmacotherapy for ADHF
Subset II: Warm and Wet
• Patient has hypervolemia
• IV diuretics and plus or minus vasodilators, nesiritide
79. Subset III: Cold and Dry
• Patient has hypoperfusion
• Therapy:
oIf PCWP <15 mmHg, IV fluids until PCWP 15–18
mmHg
oIf PCWP ≥15 mmHg and MAP <50 mmHg, IV
dobutamine
oIf PCWP ≥15 mmHg, MAP ≥50 mmHg and
compelling indication for inotrope, IV inotrope
oIF PCWP ≥15 mmHg, MAP ≥50 mmHg and no
compelling indication for inotrope, IV vasodilator
Pharmacotherapy for ADHF
80. Subset IV: Cold and Wet
• Patient has hypoperfusion and hypervolemia
• Therapy:
oIV diuretics
oIf MAP <50 mmHg, IV dobutamine
oIf MAP ≥50 mmHg and compelling indication for
inotrope, IV inotrope
oIf MAP ≥50 mmHg and no compelling indication for
inotrope, IV vasodilator
Pharmacotherapy for ADHF
81. Discharge Criteria for Patients With ADHF
•Treat exacerbating factors (i.e., discontinuation of contraindicated
medications)
•Patient is at a "dry" weight
•Oral medication regimen stable for 24 hours
•Patient and family education completed, including clear discharge
instructions
•Left ventricular ejection fraction documented
•Smoking cessation counseling initiated
•Follow-up clinic visit scheduled, 7 to 10 days out
•Optimal pharmacologic therapy achieved or intolerance
documented
•Plans for postdischarge management
82. Ideal properties for an acute heart failure
syndromes therapy
• Improve signs and symptoms (e.g. dyspnoea)
• Improve haemodynamics without adversely effecting heart rate
and blood pressure
• Improve the neurohumoral profile
• Do not cause myocardial and/or kidney damage
• Be effective in the context of current evidence-based therapy
such as ACE-I and beta-blockers
• Demonstrate efficacy in both the acute and chronic setting
• Be affordable
• Reduce both in-hospital and post-discharge morbidity and
mortality.
84. Medicine and dietary non compliance :
Cardiac causes
•Ischemia
•Arrhythmia
•Uncontrolled hypertension
Noncardiac causes
•Infection (pneumonia with or without hypoxia)
•Exacerbation of comorbidity (chronic obstructive
pulmonary disease)
•Pulmonary embolus
Toxins (nonsteroidal anti-inflammatory drugs)
Volume overload
85. Istaroxime: Na/K-ATPase
Inhibitor
Change in left ventricular dP/dtmax comparing istaroxime (PST-
2744) to dobutamine in 5 dogs with chronic ischemic heart
failure. No difference was found between PST-2744 and 5
μg/kg/min dobutamine. Both significantly increased dP/dtmax (p
< 0.05). Reproduced with permission.J Am Coll Cardiol. 2006;48(12):2397-2409.
86. Responses of Natriuretic Peptides, ET-1, and Cortisol
Mean 95% confidence interval of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), cortisol,
endothelin-1 (ET-1), and N-terminal pro-brain natriuretic peptide (NT-proBNP) during and after 4-h infusions
(shaded in gray) of placebo (open circles) or urocortin (Ucn2) (solid circles). *p < 0.05 and **p < 0.01 indicate
significant time-by-treatment interaction in the specific time phase.
Chan et al. JACC: Heart Failure Vol. 1,
87. Responses of Ucn-2, PRA, AngII, Aldosterone, and
Ucn-1
Mean 95% confidence interval of plasma aldosterone, angiotensin-II (AngII), plasma renin activity (PRA), urocortin-2
(Ucn2), and urocortin-1 (Ucn1) during and after 4-h infusions (shaded in gray) of placebo (open circles) or Ucn2 (solid
circles). yp < 0.001 indicates significant time-by-treatment interaction in the specific time phase.
Chan et al. JACC: Heart Failure Vol. 1,
88. Pulmonary Pressures, Cardiac Output, and
Calculated
Total Peripheral Resistance Responses
Right heart catheter parameters (mean SEM) during and after 4-h
infusions (shaded in gray) of placebo (open circles) or urocortin-2 (solid
circles). *p < 0.05 and yp < 0.001 indicate significant time-by-treatment
interaction in the specific time phase. cTPR ¼ calculated total peripheralChan et al. JACC: Heart Failure Vol. 1,
89. Congestion at rest
Low
perfustion
at rest
No Yes
Warm &
dry PCWP
normal CI
normal
Warm &
wet PCWP
elevatedCI
normal
Cold & dry
PCWP
low /
normal CI
decreased
Cold & wet PCWP
elevated CI decreased
Normal SVR High SVR
Natriuretic
Peptides
Nesiritide
Or
Vasodilators
Nitroprusside
Nitroglycerine
No
Yes
Inotropic Drugs
Dobutamine
Milrinone
Calcium Sensitizers
Editor's Notes
In HF patients with reduced LVEF and CI, ascending doses of JNJ-39588146 were associated with progressive increases in CI and reductions in SVR without significant effects on PCWP, HR, or SBP