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CARDIOGEN IC SHOCK

University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras. MEDICINE 4 th year English Program Suport de curs. CARDIOGEN IC SHOCK. CARDIOGEN IC SHOCK. Defini tion Etiolog y Pathophysiology C linic al signs Monitori ng

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CARDIOGEN IC SHOCK

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  1. University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras MEDICINE 4th year English Program Suport de curs CARDIOGENIC SHOCK

  2. CARDIOGENIC SHOCK • Definition • Etiology • Pathophysiology • Clinical signs • Monitoring • Positive şi etiological diagnosis • Differential diagnosis • Principlesof treatment

  3. DEFINITION = clinicalsyndrome caused byan acute disturbance of heart function, whichresults in reduction of systemic blood pressure and tissue hypoperfusion with consecutive dysfunction of systems and organs. = systemic BP< 90mmHg or mean BP< cu 30mmHg compared with basic values IC < 2,2l/min m2 PCPB > 15mmHg

  4. ETIOLOGY • Decreased myocardial contractility • Myocardial infarction • Cardiomiopathy • Drugs,metabolic/electrolytic/acid-base disturbances, post-extracorporeal circulation • Ventricular outflow obstruction • Aortic stenosis • Hypertrofic subvalvular aortic stenosis • Ventricular filling disturbances • Mitral stenosis • Atrial myxoma • Valvular dysfunction • Acute mitral regurgitation • Acute tricuspid regurgitation • Cardiac dysrhytmias • Tachyarrhytmias • Bradyarrhytmias • Cardiac rupture • Myocardial infarction • Chest trauma

  5. PATHOPHYSIOLOGY myocardial ischemia± necrosis → LV, RV, both  • Systolic myocardial dysfunction→  contractility→ cardiac output→  Cardiac Index →  systemic BP • Diastolic myocardial dysfunction→  LV compliance→ ↑ LVTDP → ↑ retrograde pressure → ↑ PCPB → pulmonary congestion→ hypoxemia • Neuro-vegetativeresponse→↑sympatic stimulation +↑ cortisol, ADH + ↑ SRAA → peripheral vasoconstriction → oliguria + metabolic acidosis compensatoryeffects decompensatory effects viciouscircles =death spiral

  6. PATHOPHYSIOLOGY

  7. CLINICAL SIGNS • Arterial hypotension • Signs of tissue hypoperfusion • Signs of pulmonary congestion • altered mental status • Cyanosis, cold extremities, profuse sweating • Hypotension, low pulse amplitude • Tachypnea, dyspnea,pulmonary rales , turgescent jugular veins • Tachycardia, arrhythmias (brady-/tachyarrhytmias),heart murmursor overlapping heart sounds • Oliguria

  8. MONITORING • clinical signs • mental status, skin temperature and colour • SpO2 • invasive BP • ECG • CVP • other hemodynamic parameters • pulmonary artery pressure, PCPB,RVS, RVP, DC, SvO2 • echocardiography • urinary output • pH + blood gas analysis • function oforgan and systems • renal, liver,coagulation tests, electrolytes, Hb, Ht, WBC count, bllod glucose

  9. MONITORING

  10. MONITORING

  11. MONITORING

  12. MONITORING

  13. MONITORING

  14. MONITORING

  15. MONITORING • clinical signs • mental status, skin temperature and colour • SpO2 • invasive BP • ECG • CVP • other hemodynamic parameters • pulmonary artery pressure, PCPB,RVS, RVP, DC, SvO2 • echocardiography • urinary output • pH + blood gas analysis • function oforgan and systems • renal, liver,coagulation tests, electrolytes, Hb, Ht, WBC count, bllod glucose

  16. DIAGNOSIS • positivediagnosisclinical signs hemodynamic parametres • etiological diagnosisECG Hemodynamic parametersMyocardialenzymes Echocardiography others investigations

  17. DIFFERENTIAL DIAGNOSIS

  18. ABBREVIATIONS: • HR – heart rate • BP – arterial blood pressure • CO – cardiac output • CVP –central venous pressure • PAOP – pulmonary artery occlusion pressure • SVR – systemic vascular resistance • Da-v O2 – oxygen arterial-venous difference • SvO2 – mixed venous blood oxygen saturation

  19. PRINCIPLES OF TREATMENT • early and aggresive treatment – save time • Save functional myocardium improvementof the myocardial oxygen supply/demand balance • Save ischemic myocardium Myocardial reperfusion

  20. PRINCIPLES OF TREATMENT • Improvement of the myocardial oxygen supply -demand relationship • ↑ myocardial oxygen supply • Correction of hypoxemia – O2therapy,ventilatory support (CPAP, PEEP) • Correction of hypotension – volemic therapy vasoconstrictors • Improvement of cardiac output - inotropic agents •  myocardial oxygen demand • Treatment ofpain – opioids, analgesics • Treatment of cardiac dysrhythmias – cardioversion antiarrhytmic agents pacing • Othermeans of hemodynamic support • Intraaortic ballon counterpulsation • Mechanical ventricular assist devices

  21. PRINCIPLESOF TREATMENT

  22. PRINCIPLES OF TREATMENT • myocardial reperfusion • Thrombolysis • PTCA • Cardiac surgery: emergency coronary artery by-pass correction of mechanical defects cardiac transplant

  23. CONCLUSIONS • Cardiogenic shock is most frequently, the consequence of acute myocardial infarction • Mortality is high(40-80%) • The clinical picture consists of arterial hypotension, signs of tissue hypoperfusion and signs of pulmonary congestion • Invasive hemodynamic monitoring is essential for diagnosis and guidance of treatment • Early start of treatment and early myocardial reperfusion – improved chances of survival • Early PTCA - the treatment of choice.

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