Cardiogenic Shock : Where do we stand?

1. Cardiogenic Shock : Where do we stand? Dr. Prasant Kr. Sahoo Consultant Cardiologist Kalinga Hospital Bhubaneswar

2. Structural mechanisms for cardiogenic shock The key factor to cardiogenic shock is the amount of LV damaged

3. Ventricular damage and Heart Failure • 25% LV affected : Heart failure manifested • >40% ventricle affected: Cardiogenic Shock

4. Aetiology of Cardiogenic Shock ( SHOCK registry)

5. Defining Cardiogenic Shock • Clinical Criteria • Haemodynamic Criteria

6. Diastolic Heart Failure • Impaired ventricular relaxation • Decrease in passive ventricular distensibility • Decrease in cardiac output is due to inadequate ventricullar filling & not impaired systolic contraction • Ventricular hypertrophy, myocardial ischaemia with stunned myocardium, mechanical ventilation • Present in 40-50% of newly diagnosed cases of heart failure

7. Hemodynamic Alterations • The earliest sign of ventricular dysfunction is increase in cardiac filling pressures • The next stage is marked by a decrease in stroke volume & increase in heart rate • The final stage is characterized by decrease in cardiac output

8. Cardiogenic Shock:Clinical Criteria • Decreased peripheral perfusion# cold clammy skin # cyanosis # altered mental status # diminished urination ( <30ml/hr.) • Signs of Heart failure

9. Cardiogenic Shock :Haemodynamic criteria • SBP <80mmHg (less than 90mmHg if on inotropic agents / IABP) • Cardiac Index < 2.2L/min/m2 • PCWP >18 mmHg

10. Killip Classification( Am. Jl. Card,1967;20,457)

11. Diagnostic studies in Cardiogenic Shock • ECG • Chest Xray • Echocardiogram • Haemodynamic monitoring • Oxygen Saturation • BNP

12. B-Natriuretic Peptide • Released by ventricular myocardium in response to ventricular volume & pressure overload • Plasma BNP >100pico/ml can be used as evidence of heart failure • Plasma BNP levels show direct correlation with severity of heart failure • Plasma BNP may be useful in monitoring clinical course of heart failure

13. ECG in Cardiogenic shock :How helpful ? • Infarct : type; location; old/fresh • Arrhythmias • Aneurysm • Pericardial Effusion

14. What to expect on CXR in pulmonary oedema ?

15. Acute Pulm. Oedema vs ARDS

16. Predicting Lt. atrial pressure from CXR • Pre oedema# upperlobe diversion / Kerley lines : 12-15 mmHg • Interstitial oedema# peribronchial cuffing : 15-20mmHg # hilar blurring : 19-24 mmHg • Alveolar blurring# bat’s wing shadowing : >25mmHg

17. Haemodynamic assesment • CVP line : unreliable, increase is only seen in later stages of right heart failure # poor reflection of LV function # limiting factors in lung disease # pulmonary embolism # RVMI • Swan Ganz catheter for PA pressures / PCWP : ideal

18. How useful is an Echo in Cardiogenic Shock ? • LV function (EF is normal in diastolic heart failure & reduced in systolic heart failure) • End diastolic volume will distinguish diastolic from systolic heart failure • Ventricular Septal rupture • Degree of Mitral Regurgitation • Tamponade • Assesment of RV function • Aortic Dissection

19. Echo in Right Heart Failure • Increase in right ventricular chamber size • Segmental wall motion abnormalities on the right • Paradoxical motion of IVS

20. Anterior wall MI

21. Mitral Regurgitation following MI

22. LV Aneurysm following MI

23. VSD following Acute MI

24. RVMI complicating IWMI

25. Management of Acute Pulmonary Oedema ( cardiac) • Posture & Oxygen • Loop diuretics • Nitrates • Opiods • ? Low dose Dopamine • Dobutamine • CPAP / Mechanical Ventilation

26. Management – Left-sided (systolic) Heart Failure High PCWP/Low CO/High BP • Nitroglycerine/Nitroprusside • Vasodilation reduce afterload & increase CO • NTG – tolerance in 16-24 hrs • Frusemide only if PCWP >20

27. Drugs in acute pulmonary oedema • Furosemide: 40-60mg initially, incremental doses 80-160mg. till diuresis • Nitroglycerine : 1-10mg/hr,titrate to achieve >30mmHg fall/ 30% fall / 105mmHg ( whichever is least) • Morphine: 3-5mg. Repeat at 15 mins. interval to total dose 15mg.

28. Management – Left-sided (systolic) Heart Failure High PCWP/Low CO/Normal BP • Ionodilators –Dobutamine/Milrinone • Dobutamine increases O2 consumption • Frusemide if PCWP >20 inspite of NTG & Dobutamine

29. Role of Dobutamine as initial choice • May be deleterious as initial choice (furthur vasodilation in hypotensive patients) • Initial choice if SBP is approx. 90mmHg • Beneficial if excessive vasoconstriction present & elevated afterload • ? Combination with Dopamine

30. Role of Phosphodiesterase inhibitors (Ionodilators ) • Inotropic and vasodilator action • Pts. Without adequate MAP may not tolerate these drugs • Little change in HR & BP • Predispose to ventricular arrhythmias

31. Milrinone : Tips for use • No evidence regarding efficacy beyond 48 hrs. • Dose: 50ug/kg bolus over 10 mins.followed by 0.375-0.750ug/kg/min • Contraindications: Acute MI;Tight AS;HOCM • Combination therapy: # with Dobutamine if BP is stable # with high dose Dopamine if BP is low

32. Management – Left-sided (systolic) Heart Failure High PCWP/Low CO/Low BP • Dopamine/Noradrenaline to increase MAP 60 mmHg • Dopamine action is unpredictable & can cause tachyarrhythmias • Dobutamine • IABP in post CABG/angioplasty

33. Inotropes in management of shock : Dosages

34. Use of Noradrenaline • If pt. is hypotensive even on large doses of Dopamine (>20ug/kg/min) • Caution # not for prolonged use # precipitation of tachycardia/ arrhythmias

35. Dopamine : dose related effects • Low doses (<4ug/kg/min): renal vasodilator • Intermediate doses ( 4-6 ug/kg/min) : enhances myocardial contractility • High doses ( >10ug/kg/min): vasoconstriction

36. Choice of Ionotrope in Cardiogenic Shock • SBP<70mmHg + clinical shock : Norepinephrine or Dopamine • SBP 70-100mmHg+clinical shock: Dopamine & then add Norepinephrine • SBP 70-100mmHg ;no clinical shock: Dobutamine • ? Role of combination therapy

37. Management – Right (diastolic) Heart Failure • Incidence not known, may be associated with systolic heart failure • PCWP <15 – fluids till PCWP 20 • If RVEDV <140ml/m2 – fluids • PCWP>15, RVEDV 140–Dobutamine • AV dissociation – sequential AV pacing

38. Fluid challenge in MI • No pulmonary oedema on CXR# Ant. MI : 250ml # Inferior MI : 400mlSwan Ganz if no improvement • Based on PCWP# <18 mmHg : fluids # >18mmHg : Inotropes

39. Management of Cardiogenic shock • Establishment of diagnosis • Intubation, Ventilation, oxygen supplementation • Swan Ganz catheterisation # PCWP<18 : fluids # PCWP>18 : inotropes • Intra Aortic Balloon Pump (IABP) • PTCA/CABG

40. Inotropes in HF : How they work?

41. Dopamine is beneficial as initial therapy of hypotensive patients in cardiogenic shock

42. How long to use Dopamine as initial agent? • Gradually uptitrate till SBP 90-100mmHg • If BP maintained with intermediate doses : think of adding Dobutamine • If high doses required: add Noradrenaline

43. Dobutamine:How it differs from Dopamine • No renal vasodilation • Stronger beta2 effect ( arteriolar vasodilation)

44. Can dobutamine be the initial choice of therapy?

45. Device therapy for Cardiogenic Shock: A last resort ?

46. Use of IABP in Cardiogenic shock • Temporary haemodynamic stability • Bridge to revascularisation • Hospital survival rates (IABP use, without revascularisation):5-20

47. IABP : basic mechanism of action

48. Advantages of IABP in Cardiogenic shock • Increases CO by approx. 25% • Reduces heart rate • Enhances coronary perfusion • Reduces LV filling pressure • Prevents reocclusion of open artery

49. Is there a role of early revascularisation in Cardiogenic shock ?

50. Cardiogenic Shock : Medical Trt. Vs Revascularisation ( SHOCK registry)