CARDIOGENIC SHOCK

cardiogenic shock with brief explanation useful for both ug/pg students

1. CARDIOGENIC SHOCK DR.MAHI 18 / 1 /20 1 9

2. Definition:- Shock may be defined as complex acute systemic circulatory failure associated with hypo perfusion of tissues, which is incompatible with life if untreated and persisting for more than a short time.

3. CLASSIFICATION HYPOVOLAEMIC CARDIOGENIC SEPTIC ANAPHYLACTIC NEUROGENIC

4. CARDIOGENIC SHOCK — BACKGROUND

5. Definition of Cardiogenic Shock State of inadequate tissue perfusion due to cardiac dysfunction or a state of end-organ hypo-perfusion due to cardiac failure Mortality rate for Cardiogenic Shock 50% - 80% Incidence of Cardiogenic Shock 5% - 8% Cardiogenic shock is the leading cause of death for patients hospitalized with acute MI CARDIOGENIC SHOCK

6.  Persistent (>30 minutes) hypotension with systolic arterial pressure <90mm Hg  Reduction in cardiac index <2.2 litres/min/m 2  Presence of elevated left ventricle filling pressure (PCWP>18 mm Hg)  Signs and symptoms of end organ hypoperfusion (restlessness,confusion,cold cyanotic extremeties,oliguria<30ml/hr )

7. Acute myocardial infarction and cardiogenic shock The most common cause of cardiogenic shock is extensive acute myocardial infarction Patients with previous impairment of ventricular function may also experience shock with the occurrence of a small infarction The cardiovascular system fails to maintain sufficient perfusion resulting in inadequate cellular metabolism and eventually cell death The consequence is irreversible cell damage

8. Timeframe for development of cardiogenic shock Median time frame for development of cardiogenic shock is 12 hours into AMI 39.6% develop cardiogenic shock within 6 hours 63.2% develop cardiogenic shock within 24 hours The majority of patients develop shock after arrival to the hospital

9. The pathophysiology of cardiogenic shock Myocardial injury causes systolic and diastolic dysfunction A decrease in cardiac output leads to a decrease in systemic and coronary perfusion This reduction in systemic and coronary perfusion worsens ischemia and causes cell death in the infarct border zone and the remote zone of myocardium

10. Pathophysiology of CS

11.  Acute MI LV Systolic failure RV infraction Papillary muscle rupture(1%) Acute VSD(1-3%) Free wall rapture(1-6%)

12. Causes of Cardiogenic Shock Predominant LV Failure 74.5% Acute Severe MR 8.3% VSD 4.6% RV Shock 3.4% T amponade/ruptur e 1.7% Other 7.5%

13. Predisposing Factors for Cardiogenic Shock Age Sysolic blood pressure Heart rate Killip class Diabetes Anterior infarction Previous infarction Peripheral vascular disease Reduced ejection fraction Large infarctions Cardiac power

14. SIGNS AND SYMPTOMS

15. Increased respiratory rate Decrease heart rate Decrease urine output

16. decreased level of consciousness That because we have decrease in the pressure that cause decrease oxygenation that means our brain non getting O2 so your brain will breaks down Decrease pressure Decrease perfusion or O2 What about our brain ?

17. How to identify Cardiogenic Shock History Physical Exam EKG Chest xray Echocardiogram Swan- Ganz Catheter

18. D i a g no s i s

19.  G/E- decreased conscious level,confusion,cyanosis,diaphoresis, pale,cool pheripheries  Tachycardia or bradycardia  Tachypnoea  Systolic BP<90mm Hg with narrow pulse pressure  Elevated JVP

20. PATIENT PRESENTATION cyanotic and have cool skin and mottled extremities Peripheral pulses are rapid and faint and may be irregular if arrhythmias are present Jugular venous distention and crackles in the lungs are usually (but not always) present Patients show signs of hypoperfusion , such as altered mental status and decreased urine output

21.  AUSCULTATION - Precordium : Apex -dyskinetic in anterior MI /LV aneurysm -hyperdynamic in VSR and MR -absent in tamponade Thrill / murmur : ventricular septal rupture/MR S3 gallop when LA pressure is high Systolic murmur- louder upon valsalva and prompt standing ( HOCM) Chest : Bilateral crackles

22. EKG If STEMI, degree and severity of EKG should agree with severity of clinical condition If ST elevations in precordial leads -> likely anterior MI -> LV pump failure is likely cause If inferior STEMI -> need marked ST elevations with reciprocal ST depressions on EKG. Check RV leads. If no reciprocal changes or RV infarct, think mechanical problems such as papillary muscle rupture Normal EKG (especially with arrhythmias): think myocarditis

23. ECHOCARDIOGRAM Overall and regional systolic function Mechanical causes of shock Papillary muscle rupture Acute VSD Free wall rupture Degree of mitral regurgitation Right ventricular infarction Other causes of shock ( tamponade , PE, valvular stenosis )

24. SWAN GANZ CATHETER

25. Therapy/Treatment ACC Guidelines Vasopressors and Inotropes Diuretics Cardiac Catheterization Intra-aortic balloon pumps (IABPs) Left Ventricular Assist Devices (LVADs)

26. VASOPRESSORS AND INOTROPES Goal: optimize perfusion while minimizing toxicity Low output syndrome without shock : start with an inotrope such as dobutamine Low output syndrome with shock : start with dopamine or norepinephrine VASOPRESSORS:- INCREASE SVR INOTROPES:- INCREASE CO

27. Vasopressors and Inotropes

28. VASOPRESSORS AND INOTROPES Dobutamine : B1 and B2, inotropic but also causes peripheral vasodilation Good for non-hypotensive cardiogenic shock INC CO & MYOCARDIAL CONTRACTILITY DOC FOR CHF WITH CAD Start with 5 ug /kg/min, don’t go higher than 20 ug /kg/min

29. DRUGS Dopamine : inotrope and vasopressor in hypotensive cardiogenic shock Up to 3 ug /kg/min – vasodilation and increase blood flow to tissue beds, but no good evidence for “renal-dose dopamine” D1 RECEPTOR Start at 5 ug /kg/min up to 1O ug /kg/min. Good inotropic and chronotropic INC HR & BP (B1) Mild peripheral vasoconstriction beyond 10 ug /kg/min (A1)

30. Vasopressors and Inotropes Norepinephrine : primarily vasoconstrictor, mild inotrope(A1 & B1) Increases SBP/DBP and pulse pressure. Increases coronary flow Start 0.01 to 3 ug /kg/min Good for severe shock with profound hypotension Epinephrine : B1/2 effects at low doses, A1 effects at higher doses Increases coronary blood flow (increases time in diastole) Prolonged exposure -> myocyte damage

31. vasopressors and inotropes Milrinone : phosphodiesterase inhibitor, decreases rate of intracellcular cAMP degradation -> increases cytosolic calcium Increases cardiac contractility at expense of increase myocardial oxygen consumption More vasodilation than dobutamine

32. Vasopressors and Inotropes Can be combined with dobutamine to increases inotropy Start bolus 25 ug /kg (if pt is not hypotensive) over 10-20 min then 0.25-0.75 ug /kg/min

33. Vasopressors and Inotropes Vasopressin : causes vasoconstriction, glyconeogenesis , platelet aggregation and ACTH release Neutral or depressant effect on cardiac output Increases vascular sensitivity to norepinephrine Good for norepinephrine -resistant shock

34. DIURETICS Mainstay of therapy to treat pulmonary edema and augment urine output No good data regarding optimal diuretic protocol or whether diuretics improve outcome in renal failure Lower doses of lasix are needed to maintain urine output when continuous infusions are used Start at 5 mg/hr, can increase up to 20 mg/hr

35. Cardiac Catheterization in Cardiogenic Shock ACC Guidelines: emergent coronary revascularization is the standard of care for CS due to pump failure (acute MI and shock).

36.  INTRA –AORTIC BALLOON PUMP( IABP )  PERCUTANEOUS VENTRICULAR ASSIST DEVICES ( p VAD )  EXTRACORPOREAL MEMBRANE OXYGENATION( ECMO )

37. Diastole Inflation Systole Intra-Aortic Balloon Counterpulsation Standby Counterpulsation Arterial Pressure SMH #619 2008 Deflation Inflation

38. Intra-Aortic Balloon Counter pulsation Reduces afterload and augments diastolic perfusion pressure Beneficial effects occur without increase in oxygen demand No improvement in blood flow distal to critical coronary stenosis No improvement in survival when used alone May be essential support mechanism to allow for definitive therapy

39. Percutaneous Tandem Heart Complete support Trans- septal puncture Need good RV function Impella Complete support Easy to insert Also need good RV function Left ventricular assist devices

40. Left Ventricular Assist Devices (LVADs)

41. IMPELLA

42. To prevent

43. Have a healthy heart Thanks to all of you for your attention