Slide cardiogenic shock(diagnosis, causes and management) - .pptx

The slide for cardiogenic shock

1. CARDIOGENIC SHOCK

2. OUTLINE Introduction Pathophysiology Clinical features Investigations Management

3. Introduction Cardiogenic shock is an acute state of decreased cardiac output resulting in inadequate tissue perfusion despite adequate circulating volume Tintinalli’s Emergency Medicine 8 th Edition

4. Introduction Leading cause of in-hospital death in patients with acute myocardial infarction Incidence True incidence is unknown (die before arrival/escape estimates) 4% to 8% of patients with STEMI (incidence is declining with increased use of PCI) 2.5% of patients with NSTEMI Mortality ~50% (half of it within 48 hrs after presentation) Tintinalli’s Emergency Medicine 8 th Edition

5. Pathophysiology Cardiogenic shock is primarily pump failure Reduced cardiac output SBP drops Causing limited vital organs perfusion Reduced systemic vascular resistance DBP drops Coronary artery hypoperfusion  c ycle of worsening MI and pump dysfunction and eventual decompensation SIRS occurs after AMI and in CS Due to complement activation & release of systemic inflammatory mediators (cytokines , nitric oxide synthase)  depresses pump fx , dilates peripheral vasculature, increases risk of death Tintinalli’s Emergency Medicine 8 th Edition

6. Pathophysiology Cardiogenic Shock: Current Concepts and Improving Outcomes, Reynolds& Hochman , 2008 , AHA

7. Causes

8. Clinical features History SOB/ chest pain (difficult to obtain hx from severely ill patients) Existing IHD (from record/family/personnel) Exclude other causes of shock Sepsis, massive PE, haemorrhage Hx on risk factors Preexisting valvular disease, diabetic Tintinalli’s Emergency Medicine 8 th Edition

9. Clinical features Examination General: pale/cyanotic, cool skin, mottled skin Diaphoresis --- activation of sympathetic nervous system Altered mental state --- cerebral hypoperfusion Reduced urine output (<20cc/hour) --- renal hypoperfusion Peripheral edema --- preexisting heart failure Vital signs: Hypotension: SBP < 90 mmHg, not improved with fluid administration --- Not always; can be higher with preexisting HPT Pulse pressure < 20 mmHg -- If systemic resistance not dropped Tachycardia, tachypnea Lungs: crepitation (pulmonary edema) CVS: Raised JVP New murmur -- mechanical complication due to AMI, eg acute MR, acute Ventral septal defect Cardiac index of < 1.8 L/min/m2 without support or 2.2 L/min/m2 with support Tintinalli’s and MOH CPG Management of heart failure 2015

10. Investigations Blood Cardiac biomarkers FBC: anemia Lactate ( hypoperfusion ) Electrolytes RP / LFT (end organ dysfunction) ECG Ischemia/STEMI, rhythm, electrolytes abnormality, RV involvement (higher risk) CXR Pulmonary edema, cardiomegaly Bedside echocardiography Tintinalli’s Emergency Medicine 8 th Edition

11. Investigations – cont ’ Bedside echocardiography: IVC: volume status Pericardial effusion / cardiac tamponade Cardiac rupture (visible clot in pericardium) Estimation of EF and contractility Mitral valve morphology and motion Evaluation of chamber size: RV/LV Tintinalli’s Emergency Medicine 8 th Edition * Continuous cardiac monitoring from the beginning

12. Important considerations: Ventricular Function: Echocardiography can determine LV function and mechanical causes of cardiogenic shock If preserved LV systolic function, other causes of shock such as sepsis and intravascular volume depletion should be considered. Intra Vascular Volume Status: An absolute or relative reduction in left ventricular filling pressures may be present. This may be due to excessive diuretic or vasodilator therapy, concomitant GI bleed or RV infarction. In the absence of signs of LV failure, fluid challenge with normal saline should be administered (usual recommended volume : 200 – 500mls). Invasive haemodynamic monitoring would be useful to guide fluid therapy. Arrhythmias: Should be identified and appropriate treatment such as cardioversion or pacing instituted. Resistant arrhythmias would require additional anti- arrhythymic drug therapy. MOH CPG Mx of heart failure 2015

13. MANAGEMENT Most important intervention for ischemic related cardiogenic shock is emergent revascularization ED stabilization is temporizing measure while arranging for definitive therapy Tintinalli’s Emergency Medicine 8 th edition

14. MANAGEMENT Triage – Red zone Responsiveness Airway Breathing Supplemental oxygen, correct hypoxemia Mechanical ventilation if in respiratory failure Circulation IV access, correct hypovolemia Without pulmonary congestion: Fluid boluses 250cc- 500cc crystalloid for an RV infarction with hypotension With pulmonary congestion: vasopressors and inotropes

15. Dobutamine Increase cardiac contractility Used if SBP >90 mmHg without signs of overt shock/ organ dysfunction Has vasodilatory potential, thus avoid if SBP < 90 mmHg Usually vasoconstrictor is used in addition Dopamine Increase cardiac work by increasing heart rate & increase LVEDP (beta agonist) Norepinephrine More effect on peripheral vasoconstriction Has antithrombotic effect , preferred in SBP < 70 mmHg Epinephrine a/w increased systemic acidosis, tachycardia, dysrhythmia Phenylephrine Pure vasoconstrictor & alpha1 agonist Contraindicated –increased cardiac afterload without augmenting cardiac contractility

16. MANAGEMENT According to CPG Management of Heart Failure 2015: Treatment for cardiogenic shock or near shock ( hypoperfusion with adequate blood pressure) includes:- Inotropic support: High dose dopamine and/or noradrenaline. If blood pressure is adequate in the setting of near shock, dobutamine may be used. Mechanical device support: Intra-aortic balloon pump or LV assist device. Identifying correctable causes: MI -- prompt revascularization by PCI, apart from ventilatory support and IABP. mechanical complications -- Urgent surgery is beneficial but carries a high mortality. *rapidly correct rhythm disturbances, electrolyte abnormalities, acid base alterations

17. MANAGEMENT Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute severe HF, irrespective of time delay from MI onset   Patients with cardiogenic shock or severe heart failure initially seen at a non–PCI-capable hospital should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time delay from MI onset 2013 ACCF/AHA Guideline Mx of STEMI Early revascularization is a mainstay in the treatment of cardiogenic shock (improved 6-month mortality and 13% absolute mortality reduction at 6 years) 2014 AHA/ACC Guideline Mx of Non STE ACS

18. References Tintinallis ’ Emergency Medicine 8 th Edition Malaysian CPG on Management of Heart Failure, 2015 AHA/ACC Guideline Mx of Non STE ACS, 2014 ACCF/AHA Guideline Mx of STEMI, 2013 Cardiogenic Shock: Current Concepts and Improving Outcomes, Reynolds& Hochman , 2008 , Circulation: AHA Journal

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