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Semestral report from pathophysiology Authors, date of presentation, patient´s initials Present disease patient has noticed edemas of lower extremities , in time course of last 2 wks last 2-3 nights he had dyspnoe at night, no chest pain, no palpitations dry non productive cough – 2 wks he is tired, and does not tolerate physical activity - no other complaints History 7 yrs has problems with heart, and arrhytimias 2 months ex smoker, quite due to progressive dyspnoea Drugs: Isoptin ( for arrhythmias) - Cynt ( for hypertension) - Warfarin( as anticoagulant) Physical examination Patient is breathless during examination Breathing sounds are normal, right lower segment attenuated Heart action irregular, rate:100/min, P frequens, irregullaris et inaequalis BP:125/75 mm Hg, heart sounds are dull, holosystolic murmor at the apex with the propagation to left axilla intensity 2/6 Physical examination Hepatojugular reflux Abdomen above the chest niveau, v.s. ascites Liver exceeds right costal arc + 4 cm Legs: symetric edemas, both sides to the femoral level, no signs of dep venous thrombosis, arterial pulsations are present Lab tests + other exams ↑liver damage markers, ALT, AST, coagulation: Quick test 28,2% Chest X ray: right side basal shadow, v.s. fuidothorax, left costophrenical angle – small level of fluid, lungs – no infiltrative changes Heart SONO: mitral regurgitation EDV LV 67mm, EF 23%, all heart chambers dilated, with decreased systolic function and hypokinesis of all walls Lab tests + other exams Lung functions test: mild restriction EKG: atrial fibrilation, 110/min, horizontal axis deviation, TZ V4,V5, voltage criteria for LV hypertrophy with signs of LV obverload, no fresh ischemic changes Based on the symptoms, signs and other tests we conclude that our patient does complain with heart failure Categorization of symptoms and signs dyspnoe, paroxysmal nocturnal dyspnoe, night cough dull chest percussion, attenuated breathing sounds, X ray proved fluidothorax symptoms and signs of respiratory dysfunction which are caused by left heart failure, with pulmonary congestion and other consequences of pulmonary congestion however patient is ex smoker, it means some of the sympotms of signs in this case may be influenced by the fact patient had been smoking before Categorization of symptoms and signs peripheral edema, anasarca, ascites increased filling of jugular veins, hepatojugulary reflux hepatomegaly these heart is not able to eject the blood to the pulmonary artery we can clearly see congestion of peripheral venous system with edema, ascites ... Mechanisms responsible for the onset of symptoms and signs Muscle weakness and fatigue These are most common, however nonspecific symptoms of heart failure, bc the heart is not able to keep the perfusion for the peripheral organs which are enough for their metabolic demands – including muscles, thats why the patiens is weak and tired after performimg physical exercise • Dyspnoe – subjective feeling of air lack Pathomechanisms a)- increased distension of capillaries and venules in lungs - increased amount of fluids in pericapillary space - stimulation of J-receptors - stimulation of RAR in airways - increased afferent input to CNS dyspnoe + increased work of respiratory muscles bc of decreased lung compliance b) Lung congestion disorders of gas exchange hypoxemia Stimulation of perif. chemorecept. increased respir. drive overoad for muscles Decrease of ventilation Hypoxia of muscles overoad for muscles increased aff. drive to CNY dyspnoea Paroxysmal nocturnal dyspnoe – acute attack of dyspnoe during night rest Pathomechanism horizontal position when lying in bed, increased venous return, increased flow in pulmonary circulation – pulmonary edema – sudden decrease of the left ventricle function due to decrease of sympathetic activity and dominance of parasympathetic Anasarca + edemas Edema is defined as an accumulation of body fluids with inadequate distribution of lfuids in interstitial space Generalized edemas are caused by heart failure , renal failure, or problems with liver In our patient we suppose cardial background for edema creation Liver is also affected by congestive hypoxia so it may contribute to decrease production of albumine Same time the break down of aldosteron is reduced by hypoxic liver cells increasing retention of Na and water Postcapillary portal hypertension enhances onset of ascites bc of impaired Starling balance Pathomechanisms left heart failure reduction of effective arterial volume activation of SNS decreased renal perfusion activation of RAA NA + water retention Pathomechanisms right heart failure increase of hydrostatic pressure in abdomen, legs Starling balance shift more filtration than resorbtion accumulation of fluids in tissues failure of lymphatic outflow Conclusion Set your conclusions What was your intention to demonstrate and whether you did it