Pulmonary hypertension
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This document provides an overview of pulmonary hypertension (PH), including its anatomy, physiology, classification, pathobiology, clinical features, diagnosis, treatment, and management. PH is defined as an elevation in pulmonary arterial pressure. It is classified into 5 groups depending on its underlying cause. The pathobiology involves vasoconstriction, vascular remodeling, and right ventricular afterload increase. Clinical features are nonspecific and overlap with other cardiopulmonary conditions. Diagnosis involves tests like echocardiogram, right heart catheterization, and imaging. Treatment includes prostanoids, endothelin receptor antagonists, and nitric oxide pathway medications. Management may involve lung or heart/lung transplantation.
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Restrictive cardiomyopathy
This document provides information on restrictive cardiomyopathy (RCM), including its definition, classification, etiology, symptoms, diagnosis, and treatment. Some key points:
- RCM is characterized by diastolic dysfunction with a stiffened myocardium that impairs ventricular filling. It is usually not associated with ventricular dilation or hypertrophy.
- Causes include infiltrative diseases of the myocardium (e.g. amyloidosis, sarcoidosis), endomyocardial fibrosis, and genetic/familial factors.
- Symptoms are related to reduced cardiac output and include dyspnea, fatigue, arrhythmias. Diagnosis involves echocardiogram, cardiac catheterization and MRI to evaluate
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Restrictive cardiomyopathy
Restrictive cardiomyopathy is characterized by stiff ventricles that do not fill properly, though systolic function is usually preserved initially. It can be caused by infiltrative diseases, fibrosis, or other processes that restrict ventricular filling. On echocardiogram, restrictive cardiomyopathy shows impaired ventricular filling and enlarged atria, while cardiac catheterization reveals elevated diastolic pressures and a distinctive "square root sign" pressure tracing. Treatment focuses on managing symptoms and underlying causes if identifiable, though prognosis is often poor without transplantation.
Constrictive pericarditis
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
Pulmonary Hypertension, Current Guidelines and Future Directions of Therapy.
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.
Pulmonary hypertension
Pulmonary hypertension is defined as a mean pulmonary arterial pressure of at least 25 mm Hg. It can be caused by various conditions and is classified accordingly. Idiopathic pulmonary hypertension has no known cause. It presents with dyspnea and right heart failure. Diagnosis involves right heart catheterization showing elevated pulmonary pressures. Treatment includes diuretics, vasodilators like calcium channel blockers, endothelin receptor antagonists, phosphodiesterase inhibitors, prostanoids, and sometimes atrial septostomy or lung transplantation for severe cases refractory to medical therapy. Prognosis depends on factors like functional status, hemodynamics, and response to treatment.
Pulmonary Hypertension Basics 2021
1) Pulmonary hypertension (PH) is defined as elevated pulmonary artery pressure, while pulmonary arterial hypertension (PAH) is a subtype caused by constriction and remodeling of small pulmonary arteries.
2) PAH is a progressive disease that involves proliferation of cells in the pulmonary arteries leading to increased pulmonary vascular resistance and right heart failure if left untreated.
3) The document reviews classification of PH, diagnostic testing and evaluation algorithms, goals of treatment, and approved therapies for PAH.
Pulmonary hypertension
Pulmonary hypertension is a condition defined by abnormally high blood pressure in the lungs. It occurs when pressure in the pulmonary arteries is greater than normal. The document discusses the causes of pulmonary hypertension, including primary pulmonary hypertension which has no identifiable cause as well as secondary causes like lung diseases. Common signs and symptoms include shortness of breath, dizziness, and swelling in the legs. The condition is diagnosed through tests like chest X-rays, echocardiograms, and pulmonary function tests. Treatment focuses on reducing fluid retention, improving heart function, and vasodilation through medications. In severe cases, lung or heart-lung transplants may be required.
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This document provides information on restrictive cardiomyopathy (RCM), including its definition, classification, etiology, symptoms, diagnosis, and treatment. Some key points:
- RCM is characterized by diastolic dysfunction with a stiffened myocardium that impairs ventricular filling. It is usually not associated with ventricular dilation or hypertrophy.
- Causes include infiltrative diseases of the myocardium (e.g. amyloidosis, sarcoidosis), endomyocardial fibrosis, and genetic/familial factors.
- Symptoms are related to reduced cardiac output and include dyspnea, fatigue, arrhythmias. Diagnosis involves echocardiogram, cardiac catheterization and MRI to evaluate
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Heart failure is a clinical syndrome that results from any structural or functional impairment of the ventricle that reduces its ability to fill with or eject blood. It impacts over 5 million Americans with high costs of care. The key aspects are reduced cardiac output, ejection fraction, preload and afterload. Compensatory mechanisms initially help but eventually fail, leading to fluid overload and decompensation. Diagnosis involves history, exam, echocardiogram and blood tests. Treatment depends on symptoms and stages from risk factor modification to drug therapy and devices.
Restrictive cardiomyopathy
Restrictive cardiomyopathy is characterized by stiff ventricles that do not fill properly, though systolic function is usually preserved initially. It can be caused by infiltrative diseases, fibrosis, or other processes that restrict ventricular filling. On echocardiogram, restrictive cardiomyopathy shows impaired ventricular filling and enlarged atria, while cardiac catheterization reveals elevated diastolic pressures and a distinctive "square root sign" pressure tracing. Treatment focuses on managing symptoms and underlying causes if identifiable, though prognosis is often poor without transplantation.
Constrictive pericarditis
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
Pulmonary Hypertension, Current Guidelines and Future Directions of Therapy.
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.
Pulmonary hypertension
Pulmonary hypertension is defined as a mean pulmonary arterial pressure of at least 25 mm Hg. It can be caused by various conditions and is classified accordingly. Idiopathic pulmonary hypertension has no known cause. It presents with dyspnea and right heart failure. Diagnosis involves right heart catheterization showing elevated pulmonary pressures. Treatment includes diuretics, vasodilators like calcium channel blockers, endothelin receptor antagonists, phosphodiesterase inhibitors, prostanoids, and sometimes atrial septostomy or lung transplantation for severe cases refractory to medical therapy. Prognosis depends on factors like functional status, hemodynamics, and response to treatment.
Pulmonary Hypertension Basics 2021
1) Pulmonary hypertension (PH) is defined as elevated pulmonary artery pressure, while pulmonary arterial hypertension (PAH) is a subtype caused by constriction and remodeling of small pulmonary arteries.
2) PAH is a progressive disease that involves proliferation of cells in the pulmonary arteries leading to increased pulmonary vascular resistance and right heart failure if left untreated.
3) The document reviews classification of PH, diagnostic testing and evaluation algorithms, goals of treatment, and approved therapies for PAH.
Pulmonary hypertension
Pulmonary hypertension is a condition defined by abnormally high blood pressure in the lungs. It occurs when pressure in the pulmonary arteries is greater than normal. The document discusses the causes of pulmonary hypertension, including primary pulmonary hypertension which has no identifiable cause as well as secondary causes like lung diseases. Common signs and symptoms include shortness of breath, dizziness, and swelling in the legs. The condition is diagnosed through tests like chest X-rays, echocardiograms, and pulmonary function tests. Treatment focuses on reducing fluid retention, improving heart function, and vasodilation through medications. In severe cases, lung or heart-lung transplants may be required.
Mitral stenosis
Mitral stenosis is usually caused by rheumatic fever, which causes fusion and thickening of the mitral valve, restricting its opening. This restricts blood flow from the left atrium to the left ventricle, causing left atrial pressure to rise and lead to pulmonary congestion and breathlessness. The elevated left atrial pressure also raises pulmonary pressures over time, causing pulmonary hypertension, right heart strain, and eventual right heart failure if left untreated. Diagnosis is made through echocardiogram and symptoms include dyspnea, fatigue, chest pain, cough, and palpitations from potential atrial fibrillation. Treatment involves antibiotics to prevent future rheumatic fever, diuretics, and potentially mitral
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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
Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by structural or functional abnormalities of the heart. Common causes include coronary artery disease and hypertension. Symptoms vary depending on whether the left or right side of the heart is predominantly affected, but may include shortness of breath, fatigue, and fluid retention. Diagnosis involves blood tests, electrocardiogram, chest x-ray, and echocardiogram. Treatment focuses on managing symptoms, treating underlying causes, and medications like diuretics, ACE inhibitors, and beta-blockers. Prognosis depends on severity and can include complications like arrhythmias, kidney impairment, and cachexia.
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This document discusses ECG findings in various congenital heart diseases:
1) Acyanotic CHDs like atrial septal defect (ASD) show findings of right or left ventricular hypertrophy depending on shunt direction, while ventricular septal defect (VSD) shows signs of left or bi-ventricular overload.
2) Cyanotic CHDs like transposition of the great arteries (TGA) show right axis deviation and ventricular hypertrophy initially, evolving to match pulmonary blood flow. Tricuspid atresia typically shows left axis deviation and ventricular hypertrophy.
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This document provides an overview of cardiogenic shock, including its definition, pathophysiology, etiology, clinical presentation, diagnosis, and management. Cardiogenic shock is defined as inadequate tissue perfusion due to the heart's inability to pump an adequate amount of blood, despite adequate intravascular volume. It results from a severe reduction in cardiac output and stroke volume. The most common cause is severe left ventricular dysfunction following acute myocardial infarction, though right ventricular failure can also cause cardiogenic shock. Management involves general support measures, pharmacological therapy including inotropes and vasopressors, hemodynamic management, mechanical support such as IABP, and early reperfusion when possible. Early invasive management and avoidance of excessive fluids for right
Pulmonary hypertension
The pulmonary vascular circuit has low resistance and carries 70ml of blood normally. Blood flow is normally higher in the lung bases than apices due to gravity. The pulmonary arteries have a small diameter of 3mm or less in the upper intercostal spaces. Pulmonary hypertension is defined as a sustained elevation of pulmonary arterial pressure over 25mmHg at rest or 30mmHg during exercise, with normal pulmonary capillary wedge pressure and left ventricular end-diastolic pressure. Signs on chest X-ray include enlarged pulmonary arteries, loss of peripheral vessel markings, and enlargement of the right side of the heart in advanced disease.
Pulmonary arterial hypertension in congenital heart disease
This document discusses pulmonary arterial hypertension (PAH) in congenital heart disease (CHD). It begins with an overview of normal pulmonary circulation and its development from embryology through adulthood. It then covers the pathophysiology, definition, and classification of PAH. Specific topics discussed in more detail include PAH in single ventricle physiology, Eisenmenger syndrome, and PAH associated with decreased pulmonary blood flow. The natural history, clinical features, complications, signs and symptoms, physical exam findings, diagnostic workup, and ECG patterns of PAH in CHD are also summarized.
Diagnosis and management of acute heart failure
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.
Pulmonary thromboembolism
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Ventricular tachycardia
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.
PULMONARY HYPERTENSION
The document discusses pulmonary hypertension and the pulmonary circulation. It covers:
1) The anatomy of the pulmonary circulation including the pulmonary arterial and bronchial circulations.
2) The physiology of the low pressure pulmonary system and how blood flow is regulated.
3) The classifications, causes, signs and symptoms, and imaging manifestations of various types of pulmonary hypertension including pulmonary arterial hypertension, pulmonary hypertension due to lung/hypoxic diseases, chronic thromboembolic pulmonary hypertension, and pulmonary hypertension related to left heart disease.
4) The pathophysiology and histopathological changes seen in different forms of pulmonary hypertension.
Aortic regurgitation
1. Aortic regurgitation can be caused by diseases of the aortic root or valve such as aortopathy, calcific aortic stenosis, or bicuspid aortic valve.
2. In chronic aortic regurgitation, the left ventricle undergoes eccentric hypertrophy and maintains preload reserve to initially compensate for the volume overload. Over time, increased afterload can lead to decompensation.
3. Acute severe aortic regurgitation into a non-hypertrophied left ventricle results in a marked rise in left ventricular pressures and pulmonary edema due to the inability to increase stroke volume.
Cor pulmonale - october'18
Cor pulmonale is right ventricular heart failure caused by lung disease that leads to pulmonary hypertension. The most common cause is chronic obstructive pulmonary disease. It can be acute or chronic. Treatment focuses on managing the underlying lung condition, treating pulmonary hypertension with medications, diuretics for volume overload, anticoagulation for those at high risk of clots, and oxygen therapy. Prognosis depends on the specific lung disease, with cor pulmonale due to conditions like COPD generally having a poorer long term outlook.
AVNRT
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Cardiac tamponade
Cardiac tamponade is a serious medical condition caused by fluid accumulating in the pericardial sac surrounding the heart, putting pressure on the heart and preventing it from filling properly. Symptoms include chest pain, difficulty breathing, and low blood pressure. Diagnosis involves echocardiogram, electrocardiogram, chest x-ray or CT scan. Treatment is pericardiocentesis to drain the fluid via needle, with careful monitoring of vital signs.
Brady arryhthmias
Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.
Constrictive pericarditis
- Constrictive pericarditis results from scarring and loss of elasticity of the pericardial sac, typically due to chronic inflammation and sometimes calcification. This causes the pericardium to thicken and lose its ability to expand and contract normally.
- The inelastic pericardium prevents normal filling of the heart chambers, especially in mid to late diastole. Inspiration does not decrease pressure in the left ventricle as it normally would due to the thickened pericardium isolating the heart.
- Diagnosis involves physical exam findings like elevated JVP, hepatomegaly, and Kussmaul's sign combined with echocardiography findings like sept
Management of VENTRICULAR TACHYCARDIA (VT)
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.
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HOCM)
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by excessive thickening of the heart muscle. It was initially described in the 1950s and causes significant morbidity and mortality due to heart failure, arrhythmias, and sudden cardiac death. The pathophysiology involves left ventricular outflow tract obstruction, diastolic dysfunction, myocardial ischemia, and mitral regurgitation. Treatment involves medications, septal reduction procedures like myectomy or alcohol ablation, and implantable cardioverter-defibrillators in high-risk patients. Prognosis depends on symptom severity and risk factors for sudden cardiac death.
Pulmonary hypertension Pathophysiology and diagnosis [Autosaved].pptx
Pulmonary hypertension can be diagnosed through a combination of tests:
1. Echocardiography can detect enlarged right ventricle and elevated pulmonary artery pressure.
2. CT scans examine the lungs for signs of blood vessel enlargement or clotting.
3. Right heart catheterization precisely measures pulmonary artery pressure and is the definitive diagnostic test.
The document discusses the pathophysiology of pulmonary hypertension including endothelial dysfunction, smooth muscle cell proliferation, and imbalances in the nitric oxide and prostacyclin pathways. A variety of tests are used to diagnose pulmonary hypertension by examining the heart, lungs, and blood vessels.
Pulmonary hypertension
This document summarizes pulmonary hypertension and its management. It discusses the pulmonary circulation and pressures, types and classification of pulmonary hypertension, pathogenesis involving various molecular pathways, clinical diagnosis using echocardiography, right heart catheterization, and treatment goals and strategies. The main treatment approaches discussed are calcium channel blockers, prostanoids, endothelin receptor antagonists, phosphodiesterase inhibitors, and soluble guanylate cyclase stimulators. The goals of treatment are to palliate symptoms, improve exercise tolerance and right ventricular function, and strive to improve survival rates.
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Heart Failure
Heart failure is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by structural or functional abnormalities of the heart. Common causes include coronary artery disease and hypertension. Symptoms vary depending on whether the left or right side of the heart is predominantly affected, but may include shortness of breath, fatigue, and fluid retention. Diagnosis involves blood tests, electrocardiogram, chest x-ray, and echocardiogram. Treatment focuses on managing symptoms, treating underlying causes, and medications like diuretics, ACE inhibitors, and beta-blockers. Prognosis depends on severity and can include complications like arrhythmias, kidney impairment, and cachexia.
Ecg in congenital heart disease
This document discusses ECG findings in various congenital heart diseases:
1) Acyanotic CHDs like atrial septal defect (ASD) show findings of right or left ventricular hypertrophy depending on shunt direction, while ventricular septal defect (VSD) shows signs of left or bi-ventricular overload.
2) Cyanotic CHDs like transposition of the great arteries (TGA) show right axis deviation and ventricular hypertrophy initially, evolving to match pulmonary blood flow. Tricuspid atresia typically shows left axis deviation and ventricular hypertrophy.
3) Algorithms are provided to systematically analyze ECG patterns and identify the underlying CHD based on chamber
Cardiogenic shock
This document provides an overview of cardiogenic shock, including its definition, pathophysiology, etiology, clinical presentation, diagnosis, and management. Cardiogenic shock is defined as inadequate tissue perfusion due to the heart's inability to pump an adequate amount of blood, despite adequate intravascular volume. It results from a severe reduction in cardiac output and stroke volume. The most common cause is severe left ventricular dysfunction following acute myocardial infarction, though right ventricular failure can also cause cardiogenic shock. Management involves general support measures, pharmacological therapy including inotropes and vasopressors, hemodynamic management, mechanical support such as IABP, and early reperfusion when possible. Early invasive management and avoidance of excessive fluids for right
Pulmonary hypertension
The pulmonary vascular circuit has low resistance and carries 70ml of blood normally. Blood flow is normally higher in the lung bases than apices due to gravity. The pulmonary arteries have a small diameter of 3mm or less in the upper intercostal spaces. Pulmonary hypertension is defined as a sustained elevation of pulmonary arterial pressure over 25mmHg at rest or 30mmHg during exercise, with normal pulmonary capillary wedge pressure and left ventricular end-diastolic pressure. Signs on chest X-ray include enlarged pulmonary arteries, loss of peripheral vessel markings, and enlargement of the right side of the heart in advanced disease.
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This document discusses pulmonary arterial hypertension (PAH) in congenital heart disease (CHD). It begins with an overview of normal pulmonary circulation and its development from embryology through adulthood. It then covers the pathophysiology, definition, and classification of PAH. Specific topics discussed in more detail include PAH in single ventricle physiology, Eisenmenger syndrome, and PAH associated with decreased pulmonary blood flow. The natural history, clinical features, complications, signs and symptoms, physical exam findings, diagnostic workup, and ECG patterns of PAH in CHD are also summarized.
Diagnosis and management of acute heart failure
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.
Pulmonary thromboembolism
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Ventricular tachycardia
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.
PULMONARY HYPERTENSION
The document discusses pulmonary hypertension and the pulmonary circulation. It covers:
1) The anatomy of the pulmonary circulation including the pulmonary arterial and bronchial circulations.
2) The physiology of the low pressure pulmonary system and how blood flow is regulated.
3) The classifications, causes, signs and symptoms, and imaging manifestations of various types of pulmonary hypertension including pulmonary arterial hypertension, pulmonary hypertension due to lung/hypoxic diseases, chronic thromboembolic pulmonary hypertension, and pulmonary hypertension related to left heart disease.
4) The pathophysiology and histopathological changes seen in different forms of pulmonary hypertension.
Aortic regurgitation
1. Aortic regurgitation can be caused by diseases of the aortic root or valve such as aortopathy, calcific aortic stenosis, or bicuspid aortic valve.
2. In chronic aortic regurgitation, the left ventricle undergoes eccentric hypertrophy and maintains preload reserve to initially compensate for the volume overload. Over time, increased afterload can lead to decompensation.
3. Acute severe aortic regurgitation into a non-hypertrophied left ventricle results in a marked rise in left ventricular pressures and pulmonary edema due to the inability to increase stroke volume.
Cor pulmonale - october'18
Cor pulmonale is right ventricular heart failure caused by lung disease that leads to pulmonary hypertension. The most common cause is chronic obstructive pulmonary disease. It can be acute or chronic. Treatment focuses on managing the underlying lung condition, treating pulmonary hypertension with medications, diuretics for volume overload, anticoagulation for those at high risk of clots, and oxygen therapy. Prognosis depends on the specific lung disease, with cor pulmonale due to conditions like COPD generally having a poorer long term outlook.
AVNRT
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Cardiac tamponade
Cardiac tamponade is a serious medical condition caused by fluid accumulating in the pericardial sac surrounding the heart, putting pressure on the heart and preventing it from filling properly. Symptoms include chest pain, difficulty breathing, and low blood pressure. Diagnosis involves echocardiogram, electrocardiogram, chest x-ray or CT scan. Treatment is pericardiocentesis to drain the fluid via needle, with careful monitoring of vital signs.
Brady arryhthmias
Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.
Constrictive pericarditis
- Constrictive pericarditis results from scarring and loss of elasticity of the pericardial sac, typically due to chronic inflammation and sometimes calcification. This causes the pericardium to thicken and lose its ability to expand and contract normally.
- The inelastic pericardium prevents normal filling of the heart chambers, especially in mid to late diastole. Inspiration does not decrease pressure in the left ventricle as it normally would due to the thickened pericardium isolating the heart.
- Diagnosis involves physical exam findings like elevated JVP, hepatomegaly, and Kussmaul's sign combined with echocardiography findings like sept
Management of VENTRICULAR TACHYCARDIA (VT)
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.
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HOCM)
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by excessive thickening of the heart muscle. It was initially described in the 1950s and causes significant morbidity and mortality due to heart failure, arrhythmias, and sudden cardiac death. The pathophysiology involves left ventricular outflow tract obstruction, diastolic dysfunction, myocardial ischemia, and mitral regurgitation. Treatment involves medications, septal reduction procedures like myectomy or alcohol ablation, and implantable cardioverter-defibrillators in high-risk patients. Prognosis depends on symptom severity and risk factors for sudden cardiac death.
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Similar to Pulmonary hypertension
Pulmonary hypertension Pathophysiology and diagnosis [Autosaved].pptx
Pulmonary hypertension can be diagnosed through a combination of tests:
1. Echocardiography can detect enlarged right ventricle and elevated pulmonary artery pressure.
2. CT scans examine the lungs for signs of blood vessel enlargement or clotting.
3. Right heart catheterization precisely measures pulmonary artery pressure and is the definitive diagnostic test.
The document discusses the pathophysiology of pulmonary hypertension including endothelial dysfunction, smooth muscle cell proliferation, and imbalances in the nitric oxide and prostacyclin pathways. A variety of tests are used to diagnose pulmonary hypertension by examining the heart, lungs, and blood vessels.
Pulmonary hypertension
This document summarizes pulmonary hypertension and its management. It discusses the pulmonary circulation and pressures, types and classification of pulmonary hypertension, pathogenesis involving various molecular pathways, clinical diagnosis using echocardiography, right heart catheterization, and treatment goals and strategies. The main treatment approaches discussed are calcium channel blockers, prostanoids, endothelin receptor antagonists, phosphodiesterase inhibitors, and soluble guanylate cyclase stimulators. The goals of treatment are to palliate symptoms, improve exercise tolerance and right ventricular function, and strive to improve survival rates.
Evaluation and Management of pulmonary artery hypertension - dr sandeep mohan...
Dr. Mohanan outlines the evaluation and management of pulmonary arterial hypertension (PAH). The diagnostic workup includes clinical exams, echocardiography, pulmonary function tests, CT scans, ventilation-perfusion scans, and right heart catheterization. Prognostic testing includes the 6-minute walk test and cardiopulmonary exercise testing. Management involves pharmacological treatments, surgical options, and follow-up monitoring. The document provides details on interpreting various diagnostic tests and determining prognosis in PAH patients.
Pulmonary hypertension.pdf
Pulmonary hypertension (PH) is a disease involving remodeling of the pulmonary vasculature that increases pulmonary artery pressure and resistance. The main causes are left heart or lung disease, or it can occur as a complication of pulmonary embolism. Pulmonary arterial hypertension (PAH) is a distinct PH subtype characterized by vascular cell abnormalities and symptoms of dyspnea and chest pain. Untreated PH has a high mortality due to right heart failure. Diagnosis involves evaluating signs/symptoms, imaging, and right heart catheterization to measure pressures.
New ulmonary arterial hypertension in rheumatic diseases
This document summarizes a presentation on pulmonary artery hypertension (PAH) in rheumatic diseases. It begins with a case presentation of a patient diagnosed with limited systemic sclerosis and PAH who was treated with various medications. It then provides background on PAH classification and the pathophysiology of PAH in connective tissue diseases. Specifically, it discusses the prevalence of PAH in different rheumatic diseases like systemic sclerosis, the mechanisms involved in pathogenesis, and differences in phenotypes between SSc-PAH and non-SSc PAH. Treatment approaches are also summarized.
Cardiology and Hematology Ppt
This document discusses oxygenation and its effects on the cardiovascular and hematologic systems. It covers topics such as ventilation, respiration, circulation, and case studies involving patient assessments. Key areas of focus include the anatomy and physiology of the heart and blood vessels, diagnostic tests, common cardiovascular conditions like heart disease, heart failure, hypertension, and peripheral vascular disease. Nursing interventions are provided for treating related symptoms and managing patient care.
Pah management
This document summarizes key information about pulmonary hypertension (PH) management including: median survival rates; clinical presentation; diagnostic testing including echocardiogram, right heart catheterization, and biomarkers; risk assessment; and therapy. Median survival is 2.8 years for adults and 10 months for pediatric patients with PH. Clinical presentation includes symptoms of exertional shortness of breath, fatigue, and right ventricular failure. Diagnostic testing is aimed at confirming the diagnosis, assessing severity, and identifying the cause of PH. Risk assessment evaluates factors like functional capacity, right ventricular function, and complications to determine low, intermediate, or high risk status. Therapy involves general measures, PH-specific drug therapy, and interventional procedures in advanced cases.
Uk pulm arterhypert
Pulmonary arterial hypertension (PAH) is characterized by elevated pulmonary arterial resistance leading to right heart failure. PAH can be idiopathic, familial due to genetic mutations, or associated with other conditions. Symptoms include breathlessness, but are nonspecific, often leading to underdiagnosis. Diagnosis requires right heart catheterization to measure blood pressure and rule out other causes. Recent treatment advances have improved prognosis, but lung transplantation remains an option for severe cases.
Pulmonary hypertension with cardiac shunt determination
Pulmonary hypertension (PH) can be caused by cardiac shunts. The document discusses PH, including definitions, pathogenesis, classification, diagnosis, and cardiac shunt determination. It provides details on evaluating PH associated with cardiac shunts, such as estimating shunt size using oxygen saturation measurements from different chambers (oximetric method) during cardiac catheterization. The oximetric method involves obtaining blood samples from various locations to measure oxygen content and identify significant step-ups indicating the direction and location of shunts.
Human: Thank you for the summary. Can you provide a more concise summary in 2 sentences or less?
A Case of Idiopathic Pulmonary Hypertension
The document describes a case of a 35-year-old female admitted with complaints of breathlessness, swelling of the legs, and abdominal distension. On examination, she had elevated jugular venous pressure, enlarged liver, edema, and signs of right heart failure. Tests showed pulmonary hypertension, right ventricular dilatation, and cardiomegaly. She was diagnosed with severe pulmonary hypertension of unknown cause.
Pulmonary Hypertension.pptx
This ppt is prepared from content of braunwald, and some latest international journals. In account it make more clear concept about pulmonary hypertension.
it also contain latest ESC 2022 guidelines of pulmonary hypertension.
Presentation1.pptx
This document summarizes recent updates in understanding and treating scleroderma pulmonary hypertension. It discusses advances in defining and classifying PH in scleroderma patients based on recent guidelines. It covers updates in understanding the pathogenesis of scleroderma-associated PAH (SSc-PAH), including the vasculopathy, right ventricle involvement, and inflammation. It also summarizes risk stratification strategies and updated screening methods using tests like echocardiograms, pulmonary function tests, and blood biomarkers. Finally, it discusses current medical therapy approaches for SSc-PAH focusing on drugs targeting the nitric oxide pathway, endothelin receptors, and prostacyclins, as well as an emerging role for immunosuppression.
Diagnosis & Classification of Pulmonary Hypertension
Pulmonary hypertension is classified into 5 categories based on the underlying pathophysiology: (1) pulmonary arterial hypertension, (2) pulmonary hypertension due to left heart disease, (3) pulmonary hypertension due to lung diseases/hypoxemia, (4) chronic thromboembolic pulmonary hypertension, and (5) miscellaneous. Echocardiography, chest imaging, pulmonary function tests, and right heart catheterization are used in evaluating and diagnosing pulmonary hypertension.
Pheochromocytoma Causing Acute Pulmonary Edema in Association with Cardiogeni...
1) The document reports on a case study of a 48-year-old male patient who presented with acute pulmonary edema and cardiogenic shock that was ultimately diagnosed as being caused by a pheochromocytoma (rare catecholamine-secreting tumor).
2) Treatment for the patient's acute heart failure, pulmonary edema, and developing shock involved intravenous medications as well as surgery to remove the adrenal tumor once stabilized.
3) Pheochromocytomas can cause acute cardiomyopathy and heart and lung issues through secretion of high levels of catecholamines, which have direct damaging effects and can cause coronary spasms, increased oxygen demand, and pulmonary edema through various mechanisms. Early diagnosis and treatment are important
Pulmonary hypertension
The document provides information on pulmonary hypertension and pulmonary circulation. It discusses:
1) The pulmonary circulation begins at the right ventricle and ends at the left atrium, transporting the entire cardiac output to the lungs. It has low resistance and high compliance.
2) Pulmonary artery pressures are normally lower than systemic pressures, with mean pulmonary artery pressure around 10-12 mmHg.
3) Pulmonary vascular resistance is low due to a balance of vasodilator and vasoconstrictor prostaglandins. Resistance primarily occurs in small arteries and arterioles.
4) Pulmonary hypertension is defined as a mean pulmonary artery pressure over 25 mmHg at rest. Its causes
Pul hypertension
The document discusses pulmonary hypertension and the pulmonary circulation. It provides details on:
1) The anatomy and physiology of the pulmonary circulation and how it differs from the systemic circulation with lower pressures and resistance.
2) The pathophysiology of pulmonary hypertension including abnormalities in the endothelium, smooth muscle cells, and vascular remodeling in different types.
3) Clinical definitions of pulmonary hypertension, pulmonary arterial hypertension, and evaluation tools like echocardiogram, CT, right heart catheterization.
4) Treatment involves vasodilators, diuretics, calcium channel blockers and general measures depending on the severity and type of pulmonary hypertension.
10 Take-home messages of the 2022 ESC/ERS Guidelines for the diagnosis and ...
Hemodynamic classification of pulmonary hypertension
Three categories of PH:
pre-capillary (Pre-PH),
combined pre-and-post capillary (Cpc-PH),
and isolated post-capillary (Ipc-PH).unexplained dyspnea or signs/symptoms suggesting PH .3 different drug classes
Nitric Oxide Pathway( PDE-5is and sGCs ).PAH (without cardiopulmonary comorbidities and non-vasoresponders
Endothelin Pathway( ERA )
Prostacyclin Pathway( PCA & PRA )Comprehensive risk assessment in PAH
Pulmonary hypertension and anesthesia
Pulmonary hypertension is defined as a mean pulmonary artery pressure greater than 25 mmHg. It is classified based on whether the elevation in pressure is pre-capillary or post-capillary. The pathogenesis involves various changes in the pulmonary vasculature that lead to increased pulmonary vascular resistance. Diagnosis involves symptoms, physical exam findings, imaging like echocardiogram, and right heart catheterization. Treatment aims to improve hemodynamics and symptoms through pulmonary vasodilators and diuretics. Anesthetic management of pulmonary hypertension patients requires optimizing preload, afterload, and contractility while avoiding triggers of pulmonary hypertension. Close monitoring is important both intraoperatively and postoperatively.
Pulmonary hypertension 27 06-19
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure of ≥20 mmHg. PH is classified into 5 groups. Group 1 is pulmonary arterial hypertension, Group 2 is PH due to left heart disease, Group 3 is PH due to lung diseases/hypoxemia, Group 4 is chronic thromboembolic PH, and Group 5 is PH with unclear multifactorial mechanisms. The pathophysiology of PH involves vasoconstriction, vascular remodeling, and thrombosis in small pulmonary vessels. Clinical evaluation includes patient history, physical exam, ECG, echocardiogram, right heart catheterization, and treatment of underlying conditions.
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Pulmonary hypertension
- 1. PULMONARY HYPERTENSION MENTOR: DR. MANOJ SHRESTHA ,MD(IOM), MD CARDIOLOGY(PAK) PRESENTED BY : BHUPENDRA BAJGAIN (INTERN CARDIOMEDICINE)
- 2. PULMONARY HYPERTENSION spectrum of disease involving pulmonary vasculature and defined as an elevation in pulmonary arterial pressure( MPAP >22mmhg or pulm. systolic pressure >36 mmHg)
- 3. ANATOMY AND PHYSIOLOGY: 1. mean pulmonary arterial pressure (MPAP) 2. pulmonary capillary wedge pressure (PCWP) 3.transpulmonary gradient (MPAP-PCWP)
- 4. CLASSIFICATION 1. GROUP 1-PULMONARY ARTERIAL HYPERTENSION 2. GROUP 2- PULMONARY HTN A/W LEFT HEART DISEASE 3. GROUP 3- PUL. HTN A/W LUNG DISEASE 4. GROUP 4- PH A/W CTED 5. GROUP 5- OTHER CONDITIONS: SARCOIDOSIS, SICKLE CELL DISEASE,SCHISTOSOMIASIS
- 5. PATHOBIOLOGY VASOCONSTRICTION, VASCULAR PROLIFERATION,THROMBOSIS,INFLAMMATION VASCULAR REMODELLING DECREASED COMPLIANCE OF PULMONARY VASCULATURE INCREASED RIGHT VENTRICULAR AFTERLOAD/ TOTAL PULMONARY VASCULAR RESISTANCE INCREASED MEAN PULMONARY ARTERIAL PRESSURE & DECREASED CO COMPENSATORY TACHYCARDIA DECREASED FILLING TIME AND DECREASED PRELOAD In advanced stage, PAP decreases
- 6. MOLECULAR DETERMINANTS OF PATHOGENESIS OF PAH: ALTERATIONS IN REGULATORS OF PROLIFERATION ALTERATIONS IN INFLAMMATORY MEDIATORS ALTERATIONS IN VASCULAR TONE HYPOXIA INDUCED REMODELLING ALTERATIONS IN TGF-B SIGNALING PATHWAYS
- 7. Clinical features: NONSPECIFIC,INSIDIOUS AND OVERLAP WITH ASTHMA ,OTHER LUNG DISEASES&CARDIAC DISEASES symptoms: dyspnea, excercise intolerance fatigue chest pain pre syncope, syncope lower extremety swelling signs evidence of rt ventricular failure: i.e. eleveated JVP,lower extremity edema,ascites,hepatomegaly,pulsa tile live auscultatory; prominent S2 with loud P2, right sided S3 or S4, holosystolic tricuspid regurgitant murmur clubbing, sclerodactyly, telangiectasia, CLD stigmata
- 8. DIAGNOSIS 1. ECHOCARDIOGRAM WITH BUBBLE STUDY:IMPORTANT INITIAL SCREENING TEST, Estimate PASP, assess RV charecteristics 2. LABORATORIES- CBC, BUN, S. Cr, LFT, BNP, HIV SEROLOGY TSH, ANA 3.ELECTROCARDIOGRAPHY: Signs of rt heart enlargement
- 9. 4. RIGHT HEART CATHETERISATION(RHC): RHC WITH PULM VASODILATATION TEST 5. CARDIOPULMONARY EXCERCISE TEST(CPET): 6. PULMONARY FUNCTION TEST: spirometry and lung volumes DLCO ABG 6MW Nocturnal oxymetry 6.CHEST RADIOGRAPH: CENTRAL PULMONARY ARTERIES ENLARGEMENT,VASCULAR PRUNING AND CARDIOMEGALY
- 10. 7. HRCT CHEST ENLARGED PULMONARY ARTERIES, PERIPHERAL PRUNNING OF SMALL VESSELS, ENLARGED RIGHT VENTRICLE AND RT ATRIUM VENOUS CONGESTION INCLUDING CENTRILOBULAR GROUNDGLASS INFILTRATE AND THICKENED SEPTAL LINES 8. V/Q LUNG SCAN: 9. CT PULMONARY ANGIOGRAPHY:
- 12. PHARMACOLOGIC TREATMENT OF PAH 1. PROSTANOIDS 2. ENDOTHELIN RECEPTOR ANTAGONISTS 3. NITRIC OXIDE PATHWAY 4. COMBINATION THERAPY 5. PDE5 INHIBITORS 6. SOLUBLE GUANYLATE CYCLASE STIMULATOR
- 15. SURGICAL MANAGEMENT LUNG TRANSPLANTATION OR HEART/LUNG TRANSPLANTATION ATRIAL SEPTOSTOMY SEPTAL DEFECT CLOSURE
- 16. REFERENCES Harrisons principle of internal medicine 20th edition The Washington manual of medical therapeutics 35th edition
- 17. THANK YOU