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1) Pulmonary arterial hypertension (PAH) is defined as a mean pulmonary artery pressure over 25 mmHg at rest as determined by right heart catheterization along with a pulmonary vascular resistance over 3 Wood units. 2) The diagnosis of PAH requires excluding other causes of pulmonary hypertension such as left heart disease, lung disease, chronic thromboembolic pulmonary hypertension, and other rare diseases. 3) PAH results from an imbalance of vasoactive and growth factors causing remodeling of the pulmonary arteries which increases pulmonary vascular resistance and mean pulmonary artery pressure over time. 4) Treatment involves general measures to avoid worsening along with medical therapies targeting vasoactive pathways and newer PAH specific drug classes, with lung transplantation as a
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This document provides an overview of pulmonary hypertension (PH), including its definition, classification, pathophysiology, diagnostic workup, and treatment. PH is defined as a mean pulmonary arterial pressure over 25 mmHg at rest. It is classified into 5 groups, with Group 1 being pulmonary arterial hypertension. The pathophysiology involves vasoconstriction, endothelial dysfunction, and vascular remodeling. Diagnosis involves echocardiogram, right heart catheterization, and ruling out other causes. Treatment includes diuretics, anticoagulants, oxygen, and PAH-specific therapies, with the goal of improving functional status and survival.
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The document discusses pulmonary hypertension and the pulmonary circulation. It provides details on:
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This document provides information on pulmonary hypertension (PH), including its definition, classification, pathogenesis, diagnosis, and treatment. It begins with defining PH as a mean pulmonary arterial pressure greater than 25 mmHg at rest based on right heart catheterization. PH is classified into 5 groups. The pathogenesis and pathology of each group is described. Diagnostic workup includes labs, imaging like CXR, echocardiogram and right heart catheterization. Treatment involves general measures, diuretics, anticoagulants, oxygen, and PAH-specific therapies like endothelin receptor antagonists, phosphodiesterase inhibitors, prostanoids, and calcium channel blockers in some cases. Prognostic factors and goals of treatment are also discussed.
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This document provides an overview of pulmonary hypertension (PH), including its definition, grading system, clinical presentation, diagnostic workup and tests, assessment of severity and risk, pathophysiology, treatment and management, especially in ICU settings. PH is defined as a mean pulmonary arterial pressure greater than 20 mm Hg at rest or 30 mm Hg with exercise, often leading to progressive right ventricular failure. It is classified into 5 groups by the WHO based on pathophysiology and treatment. The diagnostic workup involves blood tests, imaging like echocardiogram, right heart catheterization, and tests like PFTs and CT scans. Treatment focuses on pulmonary vasodilators, diuretics, oxygen therapy, and possibly mechanical circulatory support
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The document provides information on pulmonary hypertension and pulmonary circulation. It discusses:
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3) Clinical definitions of pulmonary hypertension, pulmonary arterial hypertension, and evaluation tools like echocardiogram, CT, right heart catheterization.
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- The pathophysiology involves sustained vasoconstriction, vascular remodeling, in situ thrombosis, and increased arterial stiffness. Genetic factors like BMPR2 mutations also contribute to PAH development.
- Clinical features range from mild breathlessness to signs of right heart failure. Diagnostic tests include echocardiography, CT scans, V/Q scans, right heart catheterization and lab tests.
- Treatment involves oxygen therapy, diure
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1) Pulmonary hypertension is defined as a systolic pulmonary artery pressure >35mmHg or mean pulmonary artery pressure >25mmHg and is classified into 5 groups. Group 1 includes pulmonary arterial hypertension which can be idiopathic or associated with other conditions.
2) Pulmonary hypertension results from an imbalance between vasoconstrictors like endothelin-1 and vasodilators like nitric oxide leading to vascular remodeling and increased pulmonary pressures. Acute pulmonary hypertension in the ICU is often caused by conditions like pulmonary embolism, lung disease, heart disease or sepsis.
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1) Pulmonary hypertension is defined as a mean pulmonary artery pressure over 25 mmHg at rest. It is classified into 5 types including pulmonary arterial hypertension and pulmonary hypertension due to lung or heart disease.
2) Treatment involves general measures like oxygen therapy and prevention of infection/embolism. Calcium channel blockers and PAH-targeted drugs may be used.
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Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
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Pulmonary hypertension is abnormal elevation of pulmonary artery pressure that can be caused by several factors. It occurs when the arteries in the lungs become narrowed, blocking blood flow and overworking the heart. There are five groups of pulmonary hypertension distinguished by their causes, which include left heart disease, lung diseases that cause hypoxia, chronic thromboembolic pulmonary hypertension, rare diseases with unclear causes, and pulmonary arterial hypertension. The latter involves thickening of pulmonary arteries and is the most severe form, sometimes caused by genetic mutations. Symptoms include shortness of breath and right heart failure over time if left untreated.
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1. Pulmonary hypertension (PH) is defined as a mean pulmonary arterial pressure ≥ 25 mmHg at rest as assessed by right heart catheterization.
2. PH can be classified as pre-capillary or post-capillary based on pulmonary wedge pressure and pulmonary vascular resistance.
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Pulmonary hypertension (PH) is defined as a mean pulmonary artery pressure ≥25 mmHg at rest. It is characterized by elevated pulmonary pressures and secondary right ventricular failure. PH can be caused by genetic mutations, pulmonary arterial hypertension (PAH) second hits like congenital heart disease or HIV, or pulmonary venous hypertension second hits like COPD or heart failure. Symptoms include dyspnea, chest pain, syncope, and edema. Diagnostic testing includes echocardiogram, right heart catheterization, and blood tests. Treatment involves diuretics, oxygen, anticoagulation, and advanced therapies for PAH like vasodilators or lung transplantation.
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1) Pulmonary arterial hypertension (PAH) is defined as elevated pulmonary artery pressures leading to right heart failure and death. PAH can occur due to various causes in children including congenital heart defects.
2) A pulmonary hypertensive crisis is a life-threatening acute worsening of PAH where pulmonary vascular resistance exceeds systemic pressures, overwhelming the right ventricle. Prompt treatment is needed to prevent right heart failure.
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Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
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Pulmonary hypertension is abnormal elevation of pulmonary artery pressure that can be caused by several factors. It occurs when the arteries in the lungs become narrowed, blocking blood flow and overworking the heart. There are five groups of pulmonary hypertension distinguished by their causes, which include left heart disease, lung diseases that cause hypoxia, chronic thromboembolic pulmonary hypertension, rare diseases with unclear causes, and pulmonary arterial hypertension. The latter involves thickening of pulmonary arteries and is the most severe form, sometimes caused by genetic mutations. Symptoms include shortness of breath and right heart failure over time if left untreated.
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1. Pulmonary hypertension (PH) is defined as a mean pulmonary arterial pressure ≥ 25 mmHg at rest as assessed by right heart catheterization.
2. PH can be classified as pre-capillary or post-capillary based on pulmonary wedge pressure and pulmonary vascular resistance.
3. Treatment for PH targets three main pathways - nitric oxide-soluble guanylate cyclase-cGMP pathway, endothelin-1 pathway, and prostacyclin pathway. Medications include phosphodiesterase type 5 inhibitors, endothelin receptor antagonists, prostacyclin analogs, and riociguat.
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Pulmonary hypertension (PH) is defined as a mean pulmonary artery pressure ≥25 mmHg at rest. It is characterized by elevated pulmonary pressures and secondary right ventricular failure. PH can be caused by genetic mutations, pulmonary arterial hypertension (PAH) second hits like congenital heart disease or HIV, or pulmonary venous hypertension second hits like COPD or heart failure. Symptoms include dyspnea, chest pain, syncope, and edema. Diagnostic testing includes echocardiogram, right heart catheterization, and blood tests. Treatment involves diuretics, oxygen, anticoagulation, and advanced therapies for PAH like vasodilators or lung transplantation.
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- Diagnostic evaluation involves routine labs, biomarkers like BNP and NT-proBNP, EKG, chest x-ray, echocardiogram, and cardiac catheterization if indicated.
- Treatment focuses on ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists, and other vasodilators as first-line therapies to improve survival. Additional
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3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
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1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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- 1. PULMONARY ARTERIAL HYPERTENSION: CURRENT CONCEPTS Presented By: Moderator: Dr. Arshia Bhardwaj Dr. Kamal Singh
- 3. Definition PH – a mean pulmonary artery pressure at supine and at rest >/= 20 mmhg ; normal mPAP – 8 to 20 mmhg ( previously 25 mm hg ) PAH is defined as MPAP > /=20 mmhg at rest and Pulmonary vascular resistance > /=3 woods unit.
- 7. Pulmonary Arterial Hypertension The diagnosis of PAH requires RHC to demonstrate mPAP >/= 20 mmhg at rest and a PVR >/= 3 wood units. Additional criteria to exclude the remaining categories of PH: • PCWP </= 15 mmhg ( exclude left heart diseases i.e. group 2 PH ) • Chronic lung diseases and other causes of hypoxemia are mild or absent ( i.e. group 3 PH ) • Venous thromboembolic disease and pulmonary artery obstructions are absent ( exclude group 4 PH ) • Certain miscellaneous disorders are absent , including systemic disorders ( eg. Sarcoidosis , chronic renal insufficiency ), hematological disorders ( eg. Myeloproliferative diseases and chronic hemolytic anemia ) and metabolic disorder ( eg. Glycogen storage disorder ) ( exclude group 5 )
- 8. Pathogenesis • Ohm’s Law ( P = Flow x resistance ) • The pulmonary circulation is normally a HIGH flow and LOW resistance LOW pressure system • mPAP = ( right ventricle cardiac output x pulmonary vascular resistance ) + pulmonary alveolar occlusion pressure • PVR – occlusive vasculopathy , decrease in cross sectional area of pulmonary vascular bed, hypoxic vasoconstriction • Flow through pulmonary vasculature –CHD ,liver cirrhosis , anemia • Pulmonary venous pressure – Mitral valve disease , Left ventricular systolic or diastolic dysfunction , constrictive pericarditis , restrictive cardiomyopathy or pulmonary venous obstruction
- 12. Cellular Mediators • Imbalance Of Vasoactive Mediators NO* , Prostacyclin , VIP • Increase In Vasoconstrictive Mediators Thromboxane , 5-HT , Endothelin-1* • Increased Expression Of Growth Factors • Increased Cytokines And Inflammation
- 14. 1. Idiopathic and heritable BMPR type 2 , ALK-1 , 5-HTT ,Endoglin , SMAD-9, Caveolin 1 , KCNK-3 , EIF2AK4 2. Drugs and toxins Appetite suppressants , Rapeseed oil, Benfluorex , Dasatinib , amphetamines , cocaine , Interferon 3. Connective tissue disorders Systemic sclerosis , RA , MCTD , SLE 4. HIV gp-120 – stimulates endothelin-1 Tat – BMPR-2 Nef – plexiform lesions 5.Congenital heart diseases Septal defects , eisenmenger syndrome 6. Portopulmonary hypertension Imbalance in vasoconstrictor and vasodilators , inflammation , thromboembolism , hyperdynamic circulation 7. Schistosomiasis Presinusoidal PHTN Portosystemic collaterals eggs in pulmonary circulationgranulomatous pulmonary endarteritis 8.Vasoreactivity to CCB Functional Capillary surface area 9.Pulmonary veno-occlusive disease Genetic , autoimmune , drugs , OCPS 10. Persistent pulmonary HTN of newborn Underdevelopment , maldevelopment , maladaptation
- 15. Clinical Features • Dyspnea • Fatigue • Exertional chest pain • Exertional syncope • Edema • Abdominal pain and swelling • Raised JVP – prominent ‘ v ‘ wave TR • Parasternal heave , wide splitting of Second heart sound , Pansystolic murmur
- 19. Echocardiography • Tricuspid regurgitant jet velocity • RV size , wall thickness and function • Contribution of left heart disease
- 28. Treatment
- 29. General Measures – Avoid pregnancy • Contraception imperative • Maternal mortality 30% – Immunizations for respiratory illnesses Influenza & pneumonia vaccinations – Minimize valsalva maneuvers — increase risk of syncope • Cough, constipation, heavy lifting, etc
- 30. Classes of Therapy • MEDICAL • Diuretics • Anti coagulants (IPAH) • Digoxin • Oxygen • PAH specific therapy • SURGICAL THERAPY • Atrial septostomy • Lung transplantation
- 31. Calcium Channel Blockers • Use only when demonstrated vasoreactivity in RHC (about 10% or less of patients) • Diltiazem or nifedipine preferred. • Titrate up to maximum tolerated dose. • Systemic hypotension may prohibit use • Only 50% of patients maintain response to CCB.
- 38. Prognosis • Without Therapy 1 year survival – 85% 2 year – 68% 3 year- 57% 7 year – 49%
- 39. • REVEAL PAH SCORE 0-7 = Low risk ,90-100% one year survival 8 = Average risk ,90-95% 9= Moderately high risk 85-90% 10-11= High risk 70-85% 12-22=Very high risk <70 percent Other scores :The french pulmonary hypertension registry
- 41. Thank you