Title Pharmacological therapies for acute cardiogenic shock Title (croatian) Farmakološko liječenje u akutnom kardiogenom šoku Author Marija Radić Mentor Boško Skorić (mentor)Committee member Boško Skorić (predsjednik povjerenstva)Committee member Davor Miličić (član povjerenstva)Committee member Martina Lovrić Benčić (član povjerenstva)Granter University of Zagreb Defense date and country 2021-07-16, Croatia Scientific / art field, BIOMEDICINE AND HEALTHCARE Scientific / art field, BIOMEDICINE AND HEALTHCARE Abstract Cardiogenic shock (CS) is a life threatening condition, a state of end-organ hypoperfusion, caused by cardiac failure leading to low cardiac output and inability of cardiovascular system to provide adequate flow of oxygen-rich blood to body-extremities and vital organs. This is a clinical syndrome characterized by a systemic hypotension <90 mmHg, and signs of tissue hypoperfusion,
usually as a sequela of an acute myocardial infarction. Cardiogenic shock can also arise from nonischemic causes, like myocarditis, endocarditis and pericardial tamponade. The incidence of cardiogenic shock is in decline, which reflects increased use of coronary reperfusion strategies for MI, including primary percutaneous coronary intervention (PCI) and fibrinolytic therapy which by limiting the infarct size also reduces the risk of shock development. Initial medical treatment includes IVFs, inotropes and vasopressors. Inotropes are divided into subgroups, according to their mechanism of action we distinguish beta-agonists, phosphodiesterase III inhibitors and Ca2+ sensitizers. Inotropes act on heart contractility, vasopressors increase vasoconstriction, consequently causing increase in mean arterial pressure (MAP) and Ca2+ sensitizers, among other pharmacological agents, are used to increase sensitivity of myocardiocytes on intracellular Ca2+ level. Pathophysiology of CS is not fully understood, it is a vicious cycle: when it is caused by infarction, ischemia leads to myocardial dysfunction which causes left ventricular systolic and diastolic dysfunction manifested with elevated left ventricular end diastolic pressure (LVEDP), decreased cardiac output and decreased coronary perfusion. Systemic hypoperfusion causes compensatory vasoconstriction and tachycardia which increases myocardial oxygen demand and subsequently worsens myocardial ischemia. This self-perpetuating cycle leads to progressive myocardial dysfunction and finally to the multi-organ failure unless it is interrupted by an adequate therapy. CS is an emergency condition requiring rapid diagnosis with prompt initiation of supportive pharmacological therapy, etiologic treatment and careful patient monitoring are of a vital importance. The goal of medical management is to restore heart function and tissue perfusion and with the aim of prevention end-organ damage.
Abstract (croatian) Kardiogeni šok (KŠ) je po život opasno stanje koje karakterizira nedostatna perfuzija ciljnih organa nastala kao posljedica preniskog minutnog volumena, odnosno nesposobnosti srca da održi potreban protok krvi u tijelu. To je klinički sindrom karakteriziran sustavnom hipotenzijom <90 mmHg i znakovima tkivne hipoperfuzije. Najčešće nastaje kao posljedica akutnog infarkta miokarda. KŠ može biti uzrokovan i neishemijskom bolešću srca, kao posljedica bolesti srčanih zalistaka,
miokarditisa, endokarditisa ili tamponade. Učestalost KŠ je u padu, što se objašnjava povećanom upotrebom koronarne reperfuzije u liječenju infarkta miokarda, uključujući perkutanu koronarnu intervenciju i fibrinolitičku terapiju koje smanjuju područje infarkta, time smanjujući rizik nastanka šoka. Temeljni principi farmakološkog liječenja KŠ uključuju intravensku tekućinu, odnosno održavanje adekvatnog volumena, inotrope i vazopresore. Inotropi su prema načinu djelovanja podijeljeni u tri skupine: beta-agoniste, inhibitore fosfodiesteraze tipa 3 i Ca2+ senzitizere. Inotropi pojačavaju kontraktilnost miokarda time povećavajući udarni i minutno volumen, vazopresori uzrokujući vazokonstrikciju dovode do porasta sustavnog arterijskog tlaka. Patofiziologija kardiogenog šoka nije u potpusti objašnjena – ona predstavlja circulus vitiosus: kada je KŠ uzrokovan infarktom, ishemija miokarda uzrokuje dijastoličku i sistoličku disfunkciju lijeve klijetke, što ima za posljedicu povišeni end-dijastolički tlak lijeve klijetke, smanjeni minutni volumen i dodatno smanjenu koronarnu perfuziju čime se perpetuira ishemijom uzrokovana disfunkcija miokarda. Sistemska hipoperfuzija uzrokuje aktiviranje kompenzatornih mehanizama, dovodeći do vazokonstrickije i tahikardije koje povećavaju potrebe mikoarda za kisikom. Posljedica svega je daljnje pogoršanje ishemije i disfunkcije srca, hipoperfuzije organa, te ukoliko se odgovarajućim liječenjem ne postigne poboljšanje hemodinamskog stanja bolesnika, krajnji rezulatat je zatajivanje ciljnih organa i smrt bolesnika. KŠ je zbog navedenog hitno stanje koje zahtijeva brzu dijagnozu i suportivnu farmakološku terapiju. Cilj liječenja je popraviti funkciju srca i time poboljšati perfuziju tkiva kako bi se spriječilo zatajivanje organa.
Keywords
cardiogenic shock
pharmacological therapy
myocardial infarction
Keywords (croatian)
kardiogeni šok
farmakološka terapija
infarkt miokarda
Language english URN:NBN urn:nbn:hr:105:563021 Study programme Title: Medicine (in English language) Type of resource Text File origin Born digital Access conditions Open access Terms of use Created on 2021-12-21 12:21:20
