Pathophysiology of Pulmonary and Visceral Circulation

1. Pathophysiologyof Pulmonary and Visceral Circulation Tatár M.

2. Pulmonary circulation

3. Anatomy • arteries > 1 mm: thin wall, media consists mainly from elastin and collagen fibres • arteries 0.1- 1 mm: muscular layer represents 5% of external diameter • arteriols<0.1 mm: mainly elastic tissue; connections with capillary system, postcapillaryvenules and bronchial arteries (aroundtheneck of terminalbronchioles) • venules: communication with bronchial circulation • veins: media rich of muscle cells – active contraction • bronchopulmonal anastomosis: 2/3 of bronchialblood flows to left atrium

4. Hemodynamics • high flow with low resistance; enormous blood volume changes without marked pressure changes • pulmonary blood flow depends on respiratory movements and activity of left ventricle • marked effect of left atrium pressure • inspiration improves blood flow into thoracic cavity, expiration improves pulmonary blood flow • main goal of the regulation of pulmonary circulation is to maintaine optimal gas exchange - ventilation is regulated mainly centrally - pulmonary perfusion locally: humoral substances and respiratory gases • mean pressure in pulmonary artery – 12-16 mmHg; in pulmonary veins – 6-10 mmHg

6. Pulmonary thromboembolic disease

7. Mechanisms • block of pulmonaryartery (P.A.) flowwithembolus • alwaysassociatedwithdilation of bronchialcirculation • hemorrhagicinfarctionisrelativelyuncommon (bronchialarterysupply) • classification: a) acuteminor b) acutemassive c) subacutemassive d) chronicthromboembolichypertension

8. Effects on the lungs • smallemboli – no detectableeffect • symptomatology: dyspnea, chestpain • lunginfarction – syptomsarisingfromthecombination of disturbedlungfunction and toxiceffect of feverwithtachycardia and tachypnea Hypoxemiawithnormo- or hypocapnia: - overperfusion of unembolisedlung - ventilation of deadspace - hyperventilation(anxiety)

9. Effects on the heart and circulation • normalcardiac output evenwhenembolusaffectspulm. function • obstruction of 50% of pulm. circulationiscompromisingrightventricle • sudden and severe obstruction – acuterightventriclefailure(hypotension, dizzeness, syncope), couldprogress to obstructiveshock • subacutemassiveobstructionduringweeks – timeforsomehypertrophy of rightventricle – P.A. pressure 60-90 mm Hg • chronicthromboembolicpulmonaryhypertension– generalizedintimal and medialhypertrophy – chronicrightheartfailure

10. Pulmonary hypertension (PH)

11. Causes 1. Idiopathic (primary) PH - arteriopathyofunknownetiology - allbranches of P.A.: medialhypertrophy, fibrinoidnecrosis, narrowing of lumen 2. Heartdiseases a)  P.A. bloodflow (left-to-rightshunt) b)  pulmonaryvenouspressure (leftheartfailure) 3. Respiratorysystemdisorders (frequently COPD) - alveolarhypoxia(functionalobstruction) a) smoothmusclecontraction in P.A. through a directeffect on intracellularcalcium level b) reduction in NO production - musclehypertrophy in themedia(fixedmorphologicalobstruction) - lossofcapillarybedin areasof severe emphysema

12. Ischemia of the organs in peritoneal cavaty

13. Characteristics of splanchnic circulation • richcollateralsupplyin thisteritory – occlusions a. mesentericainf. result in comparativelylittledisturbances in bloodsupply • portalvenoussystemis of largecapacity and canpool a considerableproportion of bloodvolume • musclevascularplexus in intestinalwallhas more collateralcirculationthanmucosalplexus – in certaintypes of ischemiamucosa has selectivelyundergonecompletenecrosis

17. Physiology of intestinal circulation • autoregulation: - constantflowwithpressuresbetween 80-160 mmHg to keephydrostaticpressure - precapillaryarterioles in villouscirculationare responsible • postprandialhyperemia • intestinalcounter-currentexchangerforoxygenisinvolvedduringhypotension ischemia of apical part of villoussystem

20. Mesenteric ischemia • occlusive (embolisation, massivevenoustrombosis): - rare in comparisonwithnon-occlusiveform - transmuralinfarction - loss of circulatingvolume; peritonitis • non-occlusive and relative: - common in criticallyillpatients - cardiacfailure, hypovolemicshock, sepsis

22. Mesenteric circulation • GIT: - barrieragainstverynoxiousintraluminalenvironment - nutrientsprovideoptimalconditionsforthegrow of microorganisms and helmints • mucosalcirculation: - essentialto sustainebalancebetweenagressiveintraluminal toxins and barriercomponents - compensatoryadjustments in capillarysurficearea and oxygenextraction

25. Ischemic injury to intestinal mucosa • Hypoxia: • critical level of bloodflow intracellularenergystores • amplification of apicalvillousischemiawithcounter-currentexchange of O2 • intracellularaccumulation of hypoxantine

27. Ischemic Injury to Intestinal Mucosa 2. Postischemicreperfusion: • freeoxygenradicals • activation of residentneutrophils – anothersource of reactiveoxygenmetabolites • promotion of conversion of xantinedehydrogenase to xantineoxidaseviaproteolysis • proteases (pancreas, granulocytes)

31. Systemic Mediators of Splanchnic Origin • ischemicbowelreleasestoxicagentswhich, in turn, affectthecardiovascularsystem and lead to development of shock and multiple organ failure • bacterialtranslocation (bacterialleavetheintestinallumen): role of macrophages, ischemicchanges of intestinalarchitecture • endotoxins: Tr and Leu aggregation, abnormaltissueperfusion,  capillarypermeability

32. Syndromes related to splanchnic ischemic injury • stressulceration: acutenon-occlusiveischemicerosions • ischemichepatitis: centrilobularhepatocellularnecrosis • ischemicpancreatitis: due to circulatorydisorderswithoutotherpredisposingfactors • acuteintestinalischemia: severe abdominalpain and intenseperistalticactivity • focalischemia of thesmallintestine: edema, cellinfiltrationintothemucosafollowed by fibrousstricture • ischemiccolitis: damage of mucosal and muscularlayersreplaced by scar and stricture • chronicintestinalischemia (intestinalangina): painoccuring in relation to meals; inability to producepostprandialhyperemia

33. Ischemic gut as the „motor“ of multiorgan failure • alterations in gutadynamicileus, „thirdspace“, hypermetabolism, loss of barrierfunction - uppergutiscolonised by pharyngealmicroflora - aspirationpneumonia = invasion of gastricflora • source of endogenousvasodilators in hemorrhage, cardiacfailure, sepsis - damage of mucosalbarrierbacterialtranslocation toxinsintothecirculation