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

CARDIOLOGISTS FREQUENTLY CALLED TO EVALUATE PATIENTS IN”SHOCK”

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

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

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

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 .

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

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

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

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

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

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)

SHOCK FREQUENCY Vincent J, De Backer D. N Engl J Med 2013;369:1726-1734.

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

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

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

CS FREQUENCY

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

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

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

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

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

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

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;341:625-634.

IABP-SHOCK II . Thiele H et al. N Engl J Med 2012;367:1287-1296.

IABP-SHOCK II . Thiele H et al. N Engl J Med 2012;367:1287-1296.

IABP-SHOCK II . Thiele H et al. N Engl J Med 2012;367:1287-1296.

Impella v IABP in CS 26 pts . Seyfarth et alJ Am Coll Cardiol. 2008;52(19):1584-1588.

HYPOTHERMIA FOR CARDIAC ARREST . The Hypothermia after Cardiac Arrest Study GroupN Engl J Med 2002; 346:549-556

HYPOTHERMIA FOR CARDIAC ARREST . The Hypothermia after Cardiac Arrest Study GroupN Engl J Med 2002; 346:549-556

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 .

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

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