= > Line! te batit} 4 W)() Ms) Veda bole Syrcfrome — 16 @ graye oftrcasse | and earholescal condbione bated) on ; Usulen WLS: | Conponenfs of MS 5 ) ahdowssal (rrsccral) obesity [bist] 2) euparresl Gee toteranc (58-2) 3 Ar (AH) 4u aed 4) Lpprdomea 4) Haan dyndome 6) hs cenun ard feMoeepe) [ged ] 4 at Aepactores §) prottacrs atferocebeooci iyenegdpen eoyex.s) g )) mniveollba nse nenia Loatkss2b fucnenfropia] 4o) Lbep apria, (‘ensae be ue) Mhincel pictian (ns/)- cemplatnye Aepench on Me pocenee i 4, bacpancidyudy . a aed itt LZ oe component ‘nouede: \porionbe feadache(oue of herendonsro Thy week ns, and sale et adn } 3 dyspnea with bible Seal pefiy si naewtesanhles . as wh sp ayug PO hat s) chest pasn (‘les to coronarg. aefo descate ) 6) Long of the ck, macedhion , Ye. shen the bile any Yip onder appetite (fe to acu liremé) 8) fs ae ody werght with ablonairal Lele tiseue epesiten Altouuctneu ney 9 dey mosh Hah _ - a Wy p80 apy eee | pelyeria (due te 6-5) & Tihs Scanned with CamScannerLC 2 ; nee W atk bon todo Hvecl Tee and mato Peeguint hincat marifaietins af HS are Hype 2 Me Snare, imp unparred glucose tolerant CF Pragnashies The aan erties al Decasfene & abdominal oleic fo bet] Ths type of eipese fitsae dp cities cxeily one Teeth ad ‘recpaber reat ae ty eabeulatieg He ratio ef the Beirounfernce of thar hype a anid OES in wenn alice tes au aldonteel de deemintd apenunpeccece ofthe Waist coment )- relent, rte tatonpalaeh A Bee mens ucfer of more Cheat LC "y fre 2 utecate esas? $8 bey wight Madwach ae — A bree ce sn Hb festng, fiance eae thew bErmetft [5b-bfp-eranene ~ Jamu tede eee ele le. — tofal hides Grcter tan ESrmelf, — tevgly jects grater Yow EL nunl/. fare. a io wontl (4 624-660 usesgh ) be of op ucla tent /: (« Adipese ~ menpabecr; geapehint butte echpese col Lrishyectudes [Preiglece rad] Chekectorel [ba esters1] _festing [fe stg J Meibigee, lesepasie glycemia Lge mg] Chutcesuet i Scanned with CamScannerCappo tenepy uu guserauiu Aine, 4d filet of lypaliphy wud dieefon Ct ‘ Myveerdinl b to fe (nH) A an tneeiese mnyerersel msde Pes / ln most cases hak compence daracter ettof os develapit IK an increase x te Laol on my Candin of ere or aseticr (vextuee a atv.) [pre ee Came of MA): 1) mercesed eel [opsq nosy Vi , ) 4 meals or [wetnef 9 rw) pel 3) Jape the MH (¢ cnisng for unknown wcacms) Sleleton the expansion of ene e? mer ehaibers of he hes ttt Lh easel sarin deo Fe "eonigintteny titly i Lheewermn LK Sore ne Caf Catt PU edt (Lenegenee. ~ Ug wheat on cuorense th Hhe 7 tictelion)) and tn asotlar Bait SeAVe a5 ons ofthe signs of docem unsetion and @ fang fececage tn ney oe eae cencfoa ile ng ae . uset,pacreraleenyeh aggre ALES Oh ey | genic dileltion) (Sj ete led itt Talussesr | Sibhetion reasons fincrente prbtead (Loropense Aletchin| aru ef lerleat((myogene — 3) beet), mycerdite ) Miya ? yy ce, 6 o Tncunse protead + taal sahane” GEES: slap mint cacortai bsetoaph. Yaractertzed ty an increase Lt “ZS wero Spat Uhislenng. of ts wall (mcleal Ugur, tetnfecfats) ake umicing, tasaffviney ofthe triewspid we) Jncreese afler-loed': aeblead ij wdc (uth develep ment of eovecwtane Yrosesylun cree ete plesurthinl hyper beep h sharactorzed by tuchourng wells w fiouk off ¢ Patt he ed of FALE (ce ohoss, mdb ch, A, eb pestinfection centiecelsi5) Scanned with CamScanner/ oft rancrioular Myprtooply axe dilatation Causes: AH, heart disceses, cerdiosedecoris Clitucak hes ftaus: 4 ‘ons opis io ta fach arse of iad VEY Me be sa Semefiines without any complaints 2 % exanunation : displeceneut ft flict ate ete Lf ee ) aed down (with delatetion) il on pobpetioa uc Jobe hugh, wastant upd ile, wth re hapustrophy tiled spd, Tota, ae ee Fuss, peputepebaft 4 Me ea in dln tee prmnarhon f th Float ype RVS, npwanaxu eneroamreenoit peceun cerwenra ST 0 1, I, aVL, V4-6) ake configuration ofthe fre aopraxnnas koHgurypautiet cepatta (pite.4) On ‘aoko prep phe = 7. Ha penrrénot paxiaan Eu snes of Yee | feast in ppueie ion ° ae A owt wh at ipperourendl ve pa : ot of he of w 5 Pueynox 4. Pentrenorpayita cepaua B nepeateraaneil npoexusst Gosbnoro c aop- ian Taam H aakpyrstenue eBoro KOIITYPA, rpeUsty~ aa (peaso paapa: oe ee “c ipuesy en Mb - OaLeHMe CTEHO a 3CIIK se : ae Macca NOK HOTT TDK > S6um. vecpanclou offi DK y syne >1 3,9 eoutly Lv Peli. LV ingceailial mats en men 43S en bo west Sly: " Scanned with CamScannerVIL Arterial pressure (AP). Systolve AD is tesliel VIN, Rentgenological ewamination, 1. Dilating of the eft ventricle 2.Dilating ofthe ascevuling it of the sw IX. Blectrocantiogram. Sigs of hypertiaply ele centtel, Echocardiografic signs af stenosis of the aurtn ostium, — Thickening of eusps of the natal valve — Decrease of degice of disclosing athe asta valve = Thickening ofthe lel ventricle wall Augmentation ofthe lel ventricle sits Diagnostic criteria of tenos 1 Vabval (deed signs = Systolic murmu othe 3 Systolic tremor feakening of the 2nd tone on the = Change of valves on echocardiogram 2. Leftventrical sige: = Strengthened apes beat. = Dilating of relative dullness of the heat o the lel = Augmentation of the lefl ventricle aeconding to roentgenoscopy, cechocardivgraphics. Syndrome of hypertrophy of the Fel ventricle 3. Signs depenent on drop of curiae outlier Undue fatigusbility — Headaches, giddinesses. — Sense of faintness. — Allow systolic pressure. AH w e pumery udep en, nenense, 1H Meo a steht UC semrOMtaTOLOGY AND DIKGNOSTICS (OF ARTERIAL HYPERTENSIONS the norta ostium CG. 1 hanall ‘Arterial hypertension (AN) is a sable rising of arterial prosure (AP) — systlio fiom above or equal to 140 mma Hg and-or diastolic up othe evel from above or equal 0 90 men Hg on the dat not less than double measuring on Korolkov's method on to or more consecutive visits of the patient with interval ne less than | week ‘Types of arterial hypertensions 1. Essential, initial 2, Symptomatic, secondary. Brym e 140 fy, mullened 1 dn wnets teccty. [nahin] JZ Cui polr OPT MMMAMUN Coney Tebege Atecet ed LUM vesbeaf] i as jer een ak What are 4h vomad AP nunserg 2 Essential (nitil) AN — chronically proceeding disease of unknown etiology“! #694 with the ancestral predisposition, arising owing to interaction of genctical factors and environmental factors, characterized by stable rising of AP on the absence of organic lesion of the organs and systems regulating i ‘Symptomatic (recondary) AN is rising of arterial pressure, etiologically connested with the definite, as a rule, clinically well determined diseases of the ‘organs and systems participating in the regulation of arterial pressure, The classification of AP levels (mm Hg) in shown inthe table 10. ‘Table 10 — Classification of arterial pressure levels (mm Ha) ‘Caries ofthe AF Tae | Opium AF = Ito Sra — <0 atghity $0 Rernal AP Ta wa Categories of SAP sole AP_—| Dasani AF Tigao AP rae tay hte ‘Hypertension ofthe Tat degree of gravity 120-139, 0-99 HEE SD Tope facta dogs tareny [toot we ME Typertnion of the Jl degres Of gi > 1a > 110 leslie syste ype S10 0 i Note. 1 Ifthe levels systolic and diastolic AP correspond to different categories, ‘on the level of AP the given person is referred toa higher category. 2. In isolated systolic hypertension itis also possible to distngwish 3 degrees ‘of gravity due to on the level of systolic AP. 3. The given classification of levels of AP is applicable only to persons who do not receive antihypertensive preparations Factors determining the forceit at arterial hypertension 75: a0] A. Risk factors of cndiovascue discs which shouldbe eocsidere a assesamcat of ak "evel ofthe systolic and diastolic BP (AH of at, 2d and Sad degrees of envy) Men older than 55 yar oi Women older tan years old — Smoking —Dynlipidenia General Choesterin more han 6S moU. = ndivatings om tho pesecty of canvasculatdscase ia the family hystory (atthe age of younger tan 38 years oll for men o younger tan 63 yours ol fr women) “rates es han 102 om re han sn for wom) in (high love B. Lesion of ogans-targets. at Scanned with CamScanner_— Hypertrophy of the left ventricle (lectrocanbiyprapliy,cohsandiography). Ultrason signs of thickening of theartery wall te aibuoncheroli plague. A slight rise of serum ereatinine (119-184 neal), — Microalbuminuria (30-300 mg/h. — Plasma levels of glucose on empty stom ‘Plasma levels of glucose after meal move thaw 1A) C.Clinieal conditions associated with arterial hypeitews — Vascular diseases of the baum scheme ml, hemonhagic insult, transient infringement ofthe cerebral ‘= Heart diseases; myvcardial coronary arteries, stagnant heart failure "— Kidney diseases: diabetic nep = Diseases of the peripheral vessel ofthe inferior extremities, = Severe retinopathy: hemonlages of extnate of vtina, papilledema. —Diahetes mellitus ‘The lable risk of complication development ; opathy, renal flue, (eics — obliterating atherosclerosis of ‘Table — Risk of complication development Fak Ga ec [AT Ta dee | Al Sa ds [A PI a] ise sem ais aes [3b 12h ee ee ear | Fn more Fak Tino 3s ‘ed high | high | th— vey Comnianl Saas aa = way a ve] (Causes of arterial hypertension 1. Family reispositon. 2 Risk focors = Superfluous consumption of salt (adequate quantity is 3.58). ‘—nsufficient consumption of ealcium and magnesium with meal and water — Smoking. — Use of alcobol. —Hypodianin on tol end economic eniton. —Foybocmolona! suesfl stan in combination with cance, Types of symptomatic arterial hypertension Tea TRenulpavachymatos develope in glomsrulonepits, pylonepsl ‘congenital anomalies and other kidney diseases. me : Seneca develops i bramoscuar dyopaia of renal atten, sonspocc sonora, eronlotonis Renopiel ree ‘| 2. Endocrine — at pheochromocytoma, Cushing’s diseasesyndrome, inital tnyperedsteronism (Conn’s syndrome), hyperthyroidism, aeromega) 7 Hlemodinamie —~ at the coarctation of aorta, atherosclerosis of aorta, failure of the aortal valve, complete AV-blockage- i, «F Neurogenie at oxpani lesion ofthe brain — tumour, bruises, rues. 5, Exogenous — taking medicinal preparations, products with tryptophan. Lesion of organ-targets at arterial hypertension Heart lesion Coypertonic heer!) Tigpentonie heat is a. complex of the anatomical, biochemical and physiological changes forming inthe myocardium in AH development from oe Psinieg of the disease when these changes are not evident, up t0 the final stage resulting heat failure. 7 ‘I is characterized by the left ventricle myocardium hypertrophy with the subsequent development of heart failure, eardiae rhythm impairments, ‘atherosclerotic lesion of coronary arteries . hidheys — eryperonic nephropathy» («primarily contracted kidney»). fected retinal vessels: spastic srcture of arterioles and azteries; retinal ‘epoplexies; exudate in the retin, ‘inpalmments of the Brain: acute (ischemic and bemorthagic insult, wansitional ischemie attack), chronic (hypertonic diseirelatory encephalopetty). Clinic of arterial hypertension Complaints: corset of the disease — general malaise, sleeplessness, pains, beavy. headache, difficulty in concentration at work, pain in the beat area, sensation of Pittston inthe head, sweating, tremor, buzz in the ears, bead noises, ashing of ‘cGront sights» before eyes. nts ter — breathlessness on physical exertion, swollen legs. Gencral examination: hyperemia of face skin, visible pulsation of the bead and neck vessels Mapex Beat: positive, wide, displaced to the let, strengthened, resistant, quite ofien domed. “Ronders of absolute and relative heart dullness are displaced to the left ‘dimension of heart diameter is enlarged, dimension of diameter of vascular bundle is enlarged, calarged aortal configuration. iduscultation of the heart: weakening of Ist tone on apex, aortic accent of the 2nd tone, systolic murmur on heart apex. ‘Changes of eyeground central retinal artery osclusion, dilated veins of retina; large and fine hemorrhages, exwuates; edema of papillas of optic nerves, fedema of retina, subitaneous loss of vision, 'ACG: signs of hypertrophy of the lef ventricle and the lef atrium, Roensgenogran of the chest: elongation and protrusion of the 4th arche of the lef cantour of the heart (typertophy’ of the lett ventricle); aortal configuration; ‘donation and protrusion of tho Ist arch of the Itt contour (dilatation of aorta. s Scanned with CamScannerase pu Me 4 GES a sorates ‘Porson, / as oa f.estion Vv Otorenne cn qfoakere 1 “pect SYMPTOMATOLOGY AND DIAGNOSTICS OF MITRAL AND AORTAL VALVULAR DISEASES Cibepea. - cusp 0 Heart disease ~ 8 proof pathological change ofthe heart structure dive ‘nin vessels, bgeaking ts function Z Mlopox ecpata — ctomoe maronoruscave meee erpoceme cepaim Tin alas fonon) vu stern coevaon, iptiene ee teens = pagucceceh vio lati SS oh pepeck ey net htaie = are congenstal or acgurred anomaties v2 defer marinas of DD V1 of fear J hebs edo mn dele mamad pn ete ay Be Pir ws ion: ‘ it ‘aa wf ‘| Ye ves cle Ve ‘pte from Hheeah), vio lave | fe, Lrheacardal aud ent Aaamedly Henues, bite) pie | lke ran] te decelpmenel of hvead fash (Tira deed defn\ » Mecrl defects (nba arts) atreen pe, cpecedesbobe® ! - a Gaaser) X deca? (4nayry) Classification of heart diseases mt 1 fla conan no 1 On occurence terms: 1 Ppereseum 1 Congenital defects 2 Lipapetennive nopox 2 The acquired defects, JL, No xapaxrepy nopwxemia kiauanon cepatin u onthe fh ae eae ; 1 Stenoss of epertizes 2 Heweraotiocrs etasanon 2 Iawuitensy of valves 3 Cowra noroe 3 Combined delet stenosis and insufficiensy). Ms Mopokon cep. nopoxt. I Tio kenimecry topewentuae i On quantity of wtlected valves: a ene = 1 Oanorcmmsninde (upoerss 1, { Smslesalivier(mple, camtiadl)” Comp icaled 2 Mitroxtataunie (asruinpancnansss © 240s; 2 Multealsuie(ombnedy ‘ Coppen ta thy A Mea Detect yh dgt 4 tei's OGD -eelatie yoclapuses linia symdromes in heart discuss racine capo pm opin cepa Syndrome of valuta dees, ———— 3 Syndrome of peliclogicl process which couad the development of Laie: mremnneeat neeces aeepecepeoee keatl ia af mpsroct cx spoon sain » Cand yen ice nspos oopaienun tetamaua spy cwnromen) Syndrome of defeat ofthe valve (group of symptoms) is ew seals snow) 1 Naa le aympns change oF tea oe, ana sos. EMRE ron wars: athe cat's purringy 2, Hempampie (kocwenuste) csi jopeaae Mme bas ee arene ee emo oman ciate one noes Fe re ° : . ‘Tepwnnoaorns nopowos cepana ‘Terminology of hea diseases vi pone Ps 1 Insufficiency of he valve ice -oaaee 2 Aperture stenosis 3. Hopor ¢ epeaGaasaiaten ne roeraroanoerit sath prevalence of sl 5 Detet th 4 Defect with prev cof stenosis, 4 Bete withou secant eaten of stesso ise Howeui:1yypa uoporon wirrpa.nu ‘The nomenclature of defects of the mitrale valve ocr SIEIpaTSHOF® IBERIR Insulficteney of ths wvsale valve Fhe mitral shee jr Scanned with CamScanner(irale defect with prevalence of senosts of tbe let amovenmnctlar spree, ral dict without ssuate prealnse of male insulins or —Mirrpasaunait nopon © npeoGcamamen cTeMow e800) ATPASE syaapuoro orpeperit SP Mirpacuitsh nopor Gen Serkoro npeoérastner WarTpAsnINOR ET ‘romoerit 1 WiTPLTBHOTO CTEHOE _Lebaloyy of hat dees () hake thumate pore (pordabl «feavss ) 4) Infections endocarditis 4 aad i . - 3) Sysfenue Aiseases of comectong fisgue fost ae fe @ tea bel eal ; 7 gens disease 2 agra splatedive and ik tare pda, tgs Hheroscloro us [ermal igs Weaning Sate ro Lex bees] -% Gprasthe 2 ie fe dexcose re age Sanesed ee ay a when delete syntror (Chars a exc aurbecler au. attTabhe on Bet Lf plateth, au encleteligtdny of vais of beh Uys 4H wane waerion “aud as vaselh.vadrec ae de bmaged, ) ease fh he (ty baie) [ér2:08] sin ply Shona. don't offen A Lyoorthm ofthe charactouste of four iscace ; to disencte mutshur = a—~1— bones aus an lata On [eibe4 } pees ol depdeion lata tron[tales lap] Add,tional crgns t ae vy, ebiugal Peet te mest expreesedl ard chitec tous thm of hank, puke, consftien of Bangs aud cbhers 7 ten ture (y (TS of dood necear ches thee. Foe Use (utteacerogrent Zin. Scanned with CamScanner| ale seead MM Hepoaas ag / jue hath Tren, Mey ugereus (rom ofotprenbsten) conditions, on wfach the cord ovoy catwipardmert- yr, ereaote 7 Sieh dyn fe provide ta adequate deat War 4 partnt cm secre new, ts patho 10 on mens let Ye Hala, Cai eRe ~ ogni INSUFFICIENCY. ‘compalithents as a result of over flow of st \uouis quanlity oF Blood to PERE pagina ce — teat cong tafe ent ama open sl Pi Tie syndrome of cca icin 2S ts cr rue vole of evulating Hood (omsuonerhis, -sasi ore ate Sh ay © po Boal) a sion fe volumes of) ae i Tose the ably to proves = ‘4, Decrease in filling the ventricles with blood (Giastolic insufficiency): Quumex adequate blood supply of organs and tssves.— (lapeitP, escent pete Mtupertophic cardiomyopathy), cardiosleross, amyloidosis stent ‘Variants of circulatory insufficiency, deoggied (fake) ‘ens eens sie neue esis i atute 1 Hast oe, ee Wi te Fes a ‘mitral stenosis, tachyarrythmi eect hi ee — ee ea é Us de ' Classification of heart failure us ‘efi 2. Vase fil eZ when arteual vessels Cos hertone . on fei 3 Caras ae Uy Ooms in whch) ceri oe ord of ome id) exliagee [> ingttnt of en of Ia ee 2 bof BERS erate beat Se imgabment of Sng i a mains ote draaonacoong Be Cio a Ea 1° moral seactons directed he muses ie ; oi * ave anadapie, a te pi FF ordi to localisation of «pathological process: Delta k * toeemnem sch oneimly 7 ; ing At ce Toft-side (left ventricular, lft atrial). chrome. Etiology of heart failure —Right- side (right ventricular, right atrial) ie 1. Cardiovascular reason: THR Ge lenght sided, congestive, biventrcua) Tiypstoosen VED ; a digease 3. Heart diseases, a ‘Acute heart falhure —rather fst, quite often sudden development of ear ‘4 Cardiomyopathies end myocarites. tw hTUE RRS es such a degree of tanifeston that leads to number of ae © Signns failure end represents a direct threat othe patent = ie | E.Chronie drunkenness } oes 7. Gonstitve snd exalt pecans t Mrpcute let ventricular (lf abil) insufficiency a ; T‘Aeute sight ventricular (sight atrial insufficiency. eet eae i ‘ — Total insufficiency. 1 Eo gaane of respiration with the pulmonary hypertension, | Dinan ts eee ee areal 3. Diffuse diseases of connecting tise, | cute left ventricular insufficiency — it quickly, at times suienly Biman namin |, et eed oa a Ss & Radial berapy on the ares of mediastinum. hasgrherougget nsing bod eigen in he plenary Cirvulation, cardiac asthma and an 5. Deficiency of selenium and aviteminosiss. | alveplr hypostass ofthe unas - & Cardiotoxie ection of medicinal preprations SEE aiclar nufistney Pathogeny of heart fallare : 1, Myocardial infarction, stenocardia, The basic mechanisms: 2. Arterial hypertension. Se Mpament ofthe myocar (xiary myosanilinuicensy): 3, Diffuse myocar. Manne po Cpe ot mn ety wat Amana ul. Se rload (petfoadibg incl = a systolic overlond of Wr 5. Mitral stenosis (fatal insfficieney, conperdu.nue © 2.Resistance posi ar seund other) LS So compact area beter ss stun enon funnel E Metantium djttptis(alcbol,thyotosio and astery stenosis, aorta Cours sens 5, Cantioaslerosis (atherosslerosis, postmyecardal and others) Scanned with CamScannerCercle of bleed ciceuloxion | rpabecdrasersh 8. Excessively physical activities. 9. Transfusion of great volumes of liquid. 10. Acute decrease of urine output. Acute right ventricular insufficiency Acute right ventricular insufficiency — is sharply occurred manifested dysfunction of the right ventricle (atrium) of the heart, cat ‘blood in the venous part of systemic cieulaton. SaaS yall, ‘Acute right ventricular insufficiency aetiology ‘Acute pulmonary hypertension (acute pulmonary hea) — Severe thromboembolia of the pulmonary artery branches. Persistent attack of bronchial asthma or an asthmatic condition —Pneumothorax, especially valvular. — An extensive pneumonia. TL The acute overload ofthe right ventricle in volume: — Myocardial infarction with the rupture of the ventricular septum and sharply occurred blood shunting the from left othe right. — Infectious endocarditis of the tricuspid valve with acute tricuspid insufficiency development (Classification of chronic heart failure (N.D. Strazhesko and V. H. Vasilenko, 1935) Bop [st stage of chronic heart failure (CHF) {The initial, aten, blood circulation insufficiency, swith syrmpioms appearing only on Physical aciit. PROnCKuACE d — Ind stage of CHF. A mani 7 fong term blood circulation insufficiency, Coreg ten haemodynamics impaimient (cong in ‘and systemic cirelation The period 4. Haemodyamics impairments only in_one er systemic circulation, pian The period B.'Vivid haemodynamics impairments involving the whole of ‘the cardiovascular sytem. 5rd stage CHE. Fi with severe impeient of haemodynamics, (Gm scinoele ngs in sche of rset (Classification of chronic heart fallure (NYHA, 1964) 1g zp snmmomaic Qyslinetion of the lft venice ofthe hewt, without reslitetion of physical activity 2. FC — mild chronie heart failure. Patients with heart diseases causing a slight ao of physi ach In everyday ie theres papation, weakness, syne, ound ee rekige deprce of vont hear failure. Patients with an expressed . jon of physical activity. Palpitation, weakness, dyspnea ure caused Aol tt 20h Of at ere menion, pecan “ewcbeay ef yy 4. FC —severe CHF. Patients has complaints at rest om Matos ‘The 6-minutes test of walking “Within 6 minutes a patient can pass in a convenient rate the following distances: OFC —551 mand more. 1 FC — 426-550 m. = 2EC — 300-425 m. —3FC — 150-300 m, —4FC —less than 150m, Pulmonary hypertens Pulmonary hypertension is a pathological syndrome charecterized by BP rise in the pulmonary arteries, - ‘Forms of the pulmonary hypertension according to localization of disturbance blood-flow in the pulmonary circulation: 1, Artery-arteriol form (precapillary). 2. Capillary form. 3. Venuile-venous (posteapillary) form. 4, Arteriovenous form. 5. Obscure forms. Pulmonary beart Pulmonary heart — is hypertrophy and/or dilatation of the right ventricle of the heart, oWing to hypertension in the pulmonary circulation, caused by lungs diseases, deformation and impairments of chest motility or lesion of pulmonary vessels. Etiology of the pulmonary heart 1. Diseases primarily affecting airways and lung parenchyma. 2, Diseases primarily affecting the chest and causing its deformation and motility restriction. 3. Diseases primarily affecting pulmonary vessels. ‘Types of the pulmonary heart Accordine to the rates of development: A ncute — arises within several minutes to several o'clock ((romboernbotia of the pulmonary artery branches, valval pheumothorax, asthmatic condition, te). “T'Subacute — arises within several weeks to several months (recurrent cembolia of fine pulmonary artery branches, alveolites, ete). — Chronic — it is formed within years, decades (COPD, bronchial asthma, kyphoscoliosis, Bekhterev's disease, ts.). egy, ler ninco: Compensated — there are no signs of heart failure, —Decompensated — there are signs of heart failure Scanned with CamScannerL Si-nole curate ie decpher EC G - To eek 2 TOMS — kame J question 4 iboocpib hetersciapit3 y rows ak disease of cron wbeulan theme Pie Xe iw Clinical Me Oe feet, of heart arrhythmias (bradycardia, tachycardia, sinus arrhythmia, atrial locks, atrioventricular blocks, ventricular blocks). 2 Hour anchy thie. ~ d's veleke of heoat sly eet: jai a 2) emtial 4 fousto® Yaesu ferctin ls dite op fone cars ee Greitelion — (aeacrageruc) Control questions. th ethene 1. The basic variants of impairments of function of heart automatism. 2. Blectrocardiogram signs of sinus tachycardia and its diagnostic value. bya 3, Electrocardiogram signs of sinus bradycardia and its diagnostic value. “tatsecers(a. 2.R neimer-r 4 Electrocardiogram - signs of sinus arthythmia and its diagnostic value. (ge fuwie) 01-8158 ini!) 5-Electrocardiogram - signs of atrial blocks. QE ee: 6. Electrocardiogram - signs of atrioventricular block: vabsetine dy HSA Fisge, Vian §4os. spuratd a Sis 7. Electrocardiogram - signs of bundle branch blocks. Wha mada sg pe ~iede Literature 1. Nemtsov, L.M. General propedeutics of internal dideases: Lecture course / L.M, Nemtsov. ~ Bure6cx: BMY, 2006. — 175c. 2. Romankov, L.V. Theses of lectures on propedeutics of internal diseases / L.V. Romankov. ~ Tomens, YO «MY», 2012. ~ 156c. Internal diseases propedeutics. / V.T. Ivashkin., A.V. Okhlobystin, ~ M.: 3. Ivashkin, V.T. GEOTAR-Media, 2006, 4. PpeGenes, A.JI. Tponeaentuka suytpenux Goneauelt: YueGuux, / A.JI. TpeGenes. ~ Mx Meauuitta, 2001. 5. Myxut, H.A.. Mponexeatixa suyrpennix Gonesweli. / H.A. Myxit, B.C. Moucees. - “uy 2002. automatism ['Lymatiem] — ability b gencrarte chediewl unpulie Bd LTH RH _ eepartment ts function ofthe huert 4 reasen epprsrance onrhsbhnaie. ; 4) nometopce. when oreblins weth excitation onpalses Occurs in Stieus, pole eee ae (heG cutcule stuus node tee 3) feterotepe, —" + Momotopic arrnychma 4 typraserctoo] forbes Caokgcersti en ab Py Sitth bradycantie. regtigoeralied Kymep Hake ROWE Soy” . SS (psuclaenie) sel bier co vote affer the My i , HOE pod fe ae pee? 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Exbrasysbel, Pa asia cxectahen oad contraction ef the part Tea = — 2 MMewotopre ~ arise fom a neuyle focus of ex ecbemeel Pees Ma fey Prglpre — arise Joew diffeaet antes gheneitiaet feektonns] |” trol questions. . me asystolod PEtshiarite lig ye. pant 2, Electrocardiogram sof Sint extrayy stole, “26hF7 Saunas peel outs a 3. Hlectrocardiogram - signs of atrial extrs ep. Yeptav ewerioudee . Electrocardiogram - signs of atrioventricular extra sfepraventrbinb] “5. Electrocardiogram - s ns of ventricular extrasystole, , . a 6, Eleetrocardiogram - signs of paroxysmal tachycardias. /panee mol] Pause fpo:2) 7. Electrocardiogram - signs of fibrillation of atriums Petite fi E5211) cupnreey yagpar Pukrvdog ed, , of 2) iacep ben eumuties — WSemhlYS Sour dead n] revel eowpees [ereng) a roncpailtelte baie Literature seen Lonpartele “|. Nemtsov, 1..t. General propedeuties of internal dideases: HoLknte { jcmisev: Sucther name] —BireGen: BIMY. 2006. - 175e, ps ea 2, Romankoy. 1 ar pee ie Vow yo 1. Classification of e: Theses of lectures an propedcutics oF internal diseases / 1-V. Romankor Ws MY'».2012, 150. He MajfebazICT] 3, washkin. VI. Internal diseases prupedeutis, » V1. nunhhun. A.V, Okblobystin, —-M te catted, GEOTAR-Media, 2000, 4 TpeGeuen, AL Nponexemusa ony ypenmnn Goneameiis YueGune, / A Mecunuma, 2001 S Maxim HA. Mponexeuraxa euyrpenmnnx Soaeaen. HLA. Myxia, B.C. 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