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PATHOPHYSIOLOGY OF PULMONARY HYPERTENSION Presenter : Dr. Saurav

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Moderator : Dr D. Choudhury Presenter : Dr. Saurav

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Pulmonary circulation

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Pulmonary circulation Low pressure , low resistance system thin wall( high compliance) minimal resting tone short vessels

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Control of pulmonary circulation Two types : active & passive Active process : Local tissue product Alveolar gas concentration Neural influence Humoral effect

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Local tissue products The pulmonary vascular endothelium synthesizes, metabolizes, and converts a multitude of vasoactive mediators and plays a central role in the regulation of PVR. However, the main effecter site of pulmonary vascular tone is the pulmonary vascular smooth muscle cell . Local tissue molecules involved : Nitric oxide, endothelin, prostaglandin, Thromboxane and leukotriene

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Local tissue products NO : predominant endogenous vasodilatory discovered as endothelial-derived relaxant factor by Moncada and Palmer NOS exists in two forms: constitutive (cNOS) and inducible (iNOS cNOS enzyme is also stimulated by numerous molecules in the blood (e.g., acetylcholine, bradykinin) iNOS is usually only produced as a result of inflammatory mediators

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Endothelin-1 pulmonary vasoconstrictor two distinct G protein-coupled receptors (ETA and ETB). ETA receptors induce vasoconstriction and cellular proliferation ETB receptors promote pulmonary vasodilation and apoptosis inhibition

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Eicosanoids elaborated by the pulmonary vascular endothelium’ Prostaglandin I2 (PGI2 or epoprostenol) causes vasodilation thromboxane A2 and leukotriene B4 are elaborated under pathologic conditions and are involved in the pathophysiology of pulmonary artery hypertension

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Alveolar Gases “Hypoxic Pulmonary Vasoconstriction" an was first described nearly 60 years ago by Von Euler and Liljestrand. serves as an adaptive mechanism for diverting blood flow away from poorly ventilated to better ventilated regions of the lung and thereby improving V?A/ ratios.[49] The oxygen tension at the HPV stimulus site (PsO2 ) is a function of both PAO2 and mixed venous O2 pressure (Pv¯O2 ).[

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numerous theories were developed to explain the mechanism of HPV : In 1992, Xuan proposed that NO has a pivotal role in modulating PVR. mechanism involving the smooth muscle mitochondrial electron transport chain as the HPV sensor smooth muscle microsomal reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxido-reductase or sarcolemmal NADPH oxidase is the sensing mechanism

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Clinical effects of HPV can be classified under three basic mechanisms in humans. life at high altitude increases Ppa? increases perfusion of the apices of the lung . hypoventilation , atelectasis, or nitrogen ventilation of any region of the lung causes a diversion of blood flow away from the hypoxic to the nonhypoxic lung. in patients with C O A D, asthma, pneumonia, or mitral stenosis but not bronchospasm, administration of pulmonary vasodilator drugs causes a decrease in PaO2 and PVR and an increase in right-to-left transpulmonary shunting.[

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Neural Influences on Pulmonary Vascular Tone Sympathetic fibers cause pulmonary vasoconstriction through a1 –receptors and vasodilation through a2 -receptors and ß2 –receptors. acetylcholine through muscarinic (M3 ) receptor causes vasodilation. NANC nerves cause pulmonary vasodilation through NO-mediated systems by using vasoactive intestinal peptide as the neurotransmitter

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Humoral Influences on Pulmonary Vascular Tone Endogenous exogenous catecholamines have a predominant a1 (vasoconstrictor) effect. histamine binds directly to H1 receptors on endothelium, NO-mediated vasodilation occurs whereas Serotonin (5-hydroxytryptamine [5-HT]) is a potent vasoconstrictor peptides circulate and cause either pulmonary vasodilation (e.g., substance P, bradykinin, and vasopressin [a systemic vasoconstrictor]) or vasoconstriction (e.g., neurokinin A and angiotensin). Adenosine is a pulmonary vasodilator in normal subjects, whereas adenosine triphosphate (ATP) has a variable "normalizing effect," depending on baseline pulmonary vascular tone

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Passive Processes Cardiac Output and Lung Volume

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Effect of cardiac output

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Effect of lung volume

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Definition of PH It is defined as a mean pulmonary artery pressure >25mmHG at rest and 30mmHG with exercise.(www.mater.ie/pha-ireland/html/what.htm ) Systolic pressure in the pulmonary rises above 30mm Hg ( 4.0 kpa)( wylie 5th ) Systolic or mean pulmonary arterial pressure increases more than 30 mmhg and 20 mmhg respectively . ( API text book of medicine 6th )

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Grading of PH Pulmonary Artery Pressures another view: Systolic Pressures: (ECHOs show Systolic Pressure.) Mild PH: 40-55 mm hgModerate: 55-75 mm hgSevere: above 75 mm hg Mean Pulmonary Pressures: Mild PH: 26-35 mm hgModerate: 36-45 mm hgSevere: above 45 mm hg 15 is considered a normal mean pulmonary artery pressure and anything over 25 is considered PH. ----------------------------------------------------------------- www.clevelandareaph.com/Lungs_and_alveoli )

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Classification of PH according to the WHO 1998 . Pulmonary Arterial Hypertension:Primary Pulmonary HypertensionSporadicFamilial Pulmonary Arterial Hypertension Related to :Collagen Vascular DiseaseCongenital Systemic to Pulmonary ShuntsPortal HypertensionHIV infectionDrugs/ toxins

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Classification of PH according to the WHO 1998 Pulmonary Arterial Hypertension Anorexigens (aminorex,fenfluramine,dexfenfluramine)Definite toxic Rapeseed oilVery likely:Amphetamines, L-tryptophanPossible:meta-amphetamins, cocaine, chemotherapeutic agentsPersistent Pulmonary Hypertension of the newbornOthers

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Classification of PH according to the WHO 1998 Pulmonary Venous HypertensionLeft sided atrial or Ventricular Heart diseaseLeft sidedValvular heart diseasePulmonary veno occlusive diseasePulmonary capillary HemiangiomatosisOthers

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Classification of PH according to the WHO 1998 Pulmonary Hypertension associated with disorders of the Respiratory System and/ or hypoxaemia:Chronic obstructive lung diseaseInterstital lung diseaseSleep disordered breathingAlveolar Hypoventilation disordersChronic exposure to high altitude Neonatal lung diseaseAlveolar capillary dysplasiaOthers

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Classification of PH according to the WHO 1998 Pulmonary Hypertension caused by chronic thrombotic and /or embolic diseaseThromboembolic obstruction of Proximal Pulmonary arteriesObstruction of distal; pulmonary arteries Pulmonary embolism:Thrombus, tumour, ova, parasites, foreign materialInsitu thrombusSickle cell disease

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Classification of PH according to the WHO 1998 Pulmonary Hypertension associated with miscellaneous disease: Inflammatory SchistosomiasisSarcoidosisOthers Extrinsic compression of the central pulmonaryveins Fibrosing mediastinitisAdernopathy/Tumours

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New York Heart Association Classification I. PH patients in this category have no symptoms during ordinary physical activity, their hearts function normally. II. Although these patients are comfortable at rest, ordinary physical activity is somewhat limited by undue breathlessness, chest pain, fatigue, or near fainting.III. These PH patients usually have no symptoms at rest, but their physical activity is greatly limited by breathlessness, chest pain, fatigue, or near fainting while doing routine things. IV. These PH patients are often breathless and tired even while resting and can't do any physical activity without symptoms. They show signs of right-heart failure. Under the WHO system anyone who is prone to fainting goes into this class

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Pulmonary arterial hypertension (PAH) has a multifactorial pathobiology. Vasoconstriction, remodeling of the pulmonary vessel wall, and thrombosis contribute to increased pulmonary vascular resistance in PAH. Recent genetic and pathophysiologic studies have emphasized the relevance of several mediators in this condition, including prostacyclin, nitric oxide, ET-1, angiopoietin-1, serotonin, cytokines, chemokines, and members of the transforming-growth-factor-beta superfamily. Disordered proteolysis of the extracellular matrix is also evident in PAH

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Pathobiology Pathobiologic processes that result in PAH: inhibition of the voltage-regulated potassium channel producing vasoconstriction of the pulmonary artery smooth-muscle cells, reduced expression of nitric oxide syntheses in the endothelium of the pulmonary arterial bed increased expression of endothelin and basic fibroblast growth factor thrombin deposition related to a procoagulant state.

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Vascular Remodeling Chronic hypoxia induces: Neomuscularization of previously nonmuscularized pulmonary arterioles Medial hypertrophy of small muscular pulmonary arteries. ( advance stage of PAH) Intimal thickening by longitudinally oriented smooth muscle cells with abundant extracellular deposition of collagen and elastin (intimal fibroelastosis). (COPD n smokers may nt be associated with PH)

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Mechanisms for Vascular Remodeling impaired endothelial-dependent vasodilatation and expression of endothelial nitric oxide synthase (eNOS) is reduced Excretion of prostacyclin metabolites is decreased in COPD patients with pulmonary hypertension Pulmonary vascular expression of endothelin-1 is increased

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Mechanisms for Vascular Remodeling important role for serotonin (5-HT) and its transporter (5-HTT) in the vascular smooth muscle hyperplasia of pulmonary hypertension Increased CD8 lymphocytes were detected in the adventitia of small muscular arteries of mild COPD patients and smokers and correlated with intimal thickening and endothelial dysfunction

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Pulmonary hypertension in idiopathic pulmonary fibrosis. Vascular intimal fibrosis with luminal obliteration (arrow) in a region involved by interstitial fibrosis and chronic inflammation. Courtesy of Dr. Rubin Tuder, Johns Hopkins University.

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Role of BMP mutations in PAH

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Pleiotropic effects of the BMPs

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Conditions Associated with Pulmonary Hypertension Collagen Vascular Disease commonly with the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal involvement, sclerodactyly, and telangiectasia) and in scleroderma , and less frequently in systemic lupus erythematosus , Sjögrens syndrome dermatomyositis, polymyositis , and rheumatoid arthritis . coexistent interstitial pulmonary fibrosis Bosentan, treprostinil, and epoprostenol have been effective in clinical trials

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CONGENITAL L TO R SHUNTS common for large post-tricuspid cardiac shunts (e.g., ventricular septal defect, patent ductus arteriosus) although less common, may also occur in pre-tricuspid shunts (e.g., atrial septal defect, anomalous pulmonary venous drainage). Eisenmenger complex = VSD +PH +R?L Eisenmenger syndrome = any vascular connection at atrial, ventricular or aortopulmoanary level +PH + R?L

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PORTAL HYPERTENSION Patients with advanced cirrhosis can have the combined features of a high-output cardiac state in association with the features of pulmonary hypertension and RV failure. favorable response to epoprostenol

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PULMONARY VENOUS HYPERTENSION occurs as a result of increased resistance to pulmonary venous drainage associated with diastolic dysfunction of the left ventricle; diseases affecting the pericardium or mitral or aortic valves; or rare entities such as cor triatriatum, left atrial myxoma, extrinsic compression of the central pulmonary veins from fibrosing mediastinitis, and pulmonary venoocclusive disease.

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PULMONARY VENOUS HYPERTENSION Pulmonary venous hypertension affects the pulmonary veins and venules, producing arterialization of the external elastic lamina, medial hypertrophy, and focal eccentric intimal fibrosis. Microcirculatory lesions include capillary congestion, focal alveolar edema, and dilatation of the interstitial lymphatics.

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LEFT VENTRICULAR DIASTOLIC DYSFUNCTION It can occur with or without LV systolic failure. The most common causes are hypertensive heart disease; coronary artery disease; or impaired LV compliance related to age, diabetes, and hypoxemia. Symptoms of orthopnea and paroxysmal nocturnal dyspnea are prominent. Many patients improve considerably if LV end-diastolic pressure is lowered.

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MITRAL VALVE DISEASE These patients often have superimposed pulmonary vasoconstriction resulting in marked elevations in pulmonary artery pressures. At cardiac catheterization a pressure gradient between the pulmonary capillary wedge pressure and LV end-diastolic pressure is diagnostic of mitral stenosis

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CHRONIC OBSTRUCTIVE LUNG DISEASE hypoxic pulmonary vasoconstriction, acidemia, hypercapnia, the mechanical effects of high lung volume on pulmonary vessels, the loss of small vessels in the vascular bed, and regions of emphysematous lung destruction. only effective therapy is supplemental oxygen

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INTERSTITIAL LUNG DISEASE associated with obliteration of the pulmonary vascular bed by lung destruction and fibrosis in addition to, hypoxemia and pulmonary vasculopathy

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SLEEP-DISORDERED BREATHING The incidence of PAH <20% and is generally mild. treatments directed towards the sleep apnea are often effective in reducing pulmonary arterial pressure.

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Chronic thromboembolic phenomenon Patients appropriately treated for acute pulmonary thromboembolism with intravenous heparin and chronic oral warfarin therapy rarely develop chronic pulmonary hypertension. However, there is a subset of patients with impaired fibrinolytic resolution of the thromboembolism, which leads to organization and incomplete recanalization and chronic obstruction of the pulmonary vascular bed Pulmonary thromboendarterectomy is an established surgical treatment

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persistent pulmonary hypertension or reversal to fetal circulation Risk factors include : prematurity, infection, acidosis, hypothermia, hypercarbia or hypoxaemia and congenital heart disease. Treatment may include: supplemental oxygen, ET intubation and mechanical ventilation inhalation of nitric oxide extracorporeal membrane oxygenation (ECMO) and Rx ppt factor

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Clinical Presentation Typical symptoms include: Shortness of breath (Dyspnoea) with no obvious cause following exertion or at rest. Excessive fatigue Dizziness especially on climbing stairs or standing up Fainting (Syncope), weakness upon physical exertion Chest pain especially during physical activity Palpations Swollen legs and ankles Cough Haemoptysis

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As the Right heart continues to fail-symptom severity increases Worsening Fatigue Marked ankle oedema Throbbing sensation felt in the neck Ascites Orthnopea PND The liver may become tender Cyanosis Clubbing

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Conventional treatment CCB (nifedipine, 240 mg/d, or amlodipine, 20 mg/d) Endothelin Receptor Antagonists(bosentan Phosphodiesterase-5 Inhibitors(Sildenafil) Prostacyclins(Epoprostenol, Treprostinil) Lung Transplantation

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Thank You

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