1. DIRECTOR, CARDIAC CATHETERIZATION
SHOCK
CARL L. TOMMASO, MD
DIRECTOR, CARDIAC CATHETERIZATION
SKOKIE HOSPITAL, NSUHS

2. CARDIOLOGISTS FREQUENTLY CALLED TO EVALUATE PATIENTS IN”SHOCK”

3. CARDIOLOGISTS FREQUENTLY CALLED TO EVALUATE PATIENTS IN”SHOCK”
REVIEW:
ISSUES SURROUNDING “NON-CARDIOGENIC SHOCK”
ETIOLOGY AND CURRENT TREATMENT OF SHOCK DUE TO STEMI

4. SHOCK IS DIAGNOSED BASED ON CLINICAL, HEMODYNAMIC, AND BIOCHEMICAL FINDINGS

5. Systemic arterial hypotension is usually present, .
SHOCK IS DIAGNOSED BASED ON CLINICAL, HEMODYNAMIC, AND BIOCHEMICAL FINDINGS
Systemic arterial hypotension is usually present, .

6. SHOCK IS DIAGNOSED BASED ON CLINICAL, HEMODYNAMIC, AND BIOCHEMICAL FINDINGS
Systemic arterial hypotension is usually present,
Clinical signs of tissue hypoperfusion,
CUTANEOUS (skin that is cold and clammy, vasoconstricted and cyanoticsis,
RENAL (urine output of <0.5 ml per kilogram of body weight per hour), and
neurologic (altered mental state, obtundation, disorientation, confusion .

7. SHOCK IS DIAGNOSED BASED ON CLINICAL, HEMODYNAMIC, AND BIOCHEMICAL FINDINGS
3. Elevated lactate levels, indicating abnormal cellular oxygen metabolism

8. SHOCK MECHANISMS
Four pathophysiological mechanisms which are not mutually exclusive:
Hypovolemia

9. SHOCK MECHANISMS
Four pathophysiological mechanisms which are not mutually exclusive:
Hypovolemia
Cardiogenic factors

10. SHOCK MECHANISMS
Four pathophysiological mechanisms which are not mutually exclusive:
Hypovolemia
Cardiogenic factors
Obstruction to cardiac filling

11. SHOCK MECHANISMS
Four pathophysiological mechanisms which are not mutually exclusive:
Hypovolemia
Cardiogenic factors
Obstruction to cardiac filling
Distributive factors

12. SHOCK MECHANISMS
Four pathophysiological mechanisms which are not mutually exclusive:
Hypovolemia (from internal or external fluid loss),
Cardiogenic factors (valvular, myocardial, arhythmia)
Obstruction to cardiac filling (PE, tamponade, pneumothorax)
Distributive factors (sepsis, anaphylaxis)

13. SHOCK FREQUENCY
Vincent J, De Backer D. N Engl J Med 2013;369:

14. SHOCK DIAGNOSIS CARDIAC OUTPUT CVP DISTRIBUTIVE ↑↑ HYPOVOLEMIC ↓
CARDIOGENIC ↑
OBSTRUCTIVE

15. SHOCK
Hypovolemia, Cardiogenic and Obstructive are characterized by low cardiac output, inadequate oxygen transport.
Distributive shock, decreased systemic vascular resistance and altered oxygen extraction. cardiac output is high,
Multiple mechanisms: ie pancreatitis; hypovolemia, sepsis and myocardial depression

16. SHOCK TREATMENT Correction of etiology Ventilatory support
Fluid rescusitation
Vasoactive
Norepinephrine
Inotropic
Dobutamine
Mechanical support
IABP
ECMO

17. CS FREQUENCY

18. CARDIOGENIC SHOCK
Reynolds H R , and Hochman J S Circulation 2008;117:

19. Reynolds H R , and Hochman J S Circulation 2008;117:686-697

20. Hochman JS et al. N Engl J Med 1999;341:625-634.

21. Hochman JS et al. N Engl J Med 1999;341:625-634.

22. Hochman JS et al. N Engl J Med 1999;341:625-634.

23. Hochman JS et al. N Engl J Med 1999;341:625-634.

24. At 30 days there was no significant overall benefit
Conclusions:
In pts with myocardial infarction who had cardiogenic shock due to left ventricular dysfunction.
At 30 days there was no significant overall benefit
of early revascularization
2. Early revascularization resulted in lower
mortality from all causes at six months.
3. Recommend that early revascularization be strongly
considered for patients with acute myocardial infarction
complicated by cardiogenic shock.
Hochman JS et al. N Engl J Med 1999;341:

25. IABP-SHOCK II .
Thiele H et al. N Engl J Med 2012;367:

26. IABP-SHOCK II .
Thiele H et al. N Engl J Med 2012;367:

27. IABP-SHOCK II .
Thiele H et al. N Engl J Med 2012;367:

28. Impella v IABP in CS
26 pts .
Seyfarth et alJ Am Coll Cardiol. 2008;52(19):

29. HYPOTHERMIA FOR CARDIAC ARREST.
The Hypothermia after Cardiac Arrest Study GroupN Engl J Med 2002; 346:

30. HYPOTHERMIA FOR CARDIAC ARREST.
The Hypothermia after Cardiac Arrest Study GroupN Engl J Med 2002; 346:

31. MECHANICAL COMPLICATIONS OF MI
Papillary muscle rupture/dysfunction
Ventricular septal defect
Right ventricular infarction
Free wall rupture
Dysrhythmias
Unknown as to current frequency-perception is that less frequent; probably for same reason as decrease CS .

32. MECHANICAL COMPLICATIONS OF MI
TREATMENT
PAPILLARY MUSCLE RUPTURE
PCI
HEMODYNAMIC SUPPORT
MVR
PAPILLARY MUSCLE DYSFUNCTION
RV INFARCTION
VOLUME ADMISTRATION
VENTRICULAR SEPTAL RUPTURE
SEPTAL OCCLUDER
DYSRHYTHMIAS
MORE AMIODARONE

33. I THANK THE SCAI FOR THE OPPORTUNITY TO SPEAK
I THANK THE AUDIENCE FOR YOUR ATTENTION
ENJOY THE RODEO