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Nick Tehrani, MD
Definition
<90 mmHg
<2.2 li/min.m2
>15 mmHg
Mortality
Respiratory Distress
28% 65%
Age > 65 Female gender Large infarction Anterior infarction Prior infarction DM Prior HTN
Pathophysiology of Shock
Effect of Hypotension
Flow in normal coronary: Regulated by microvascular resistance Coronary flow may be preserved at AO pressures as low as 50 mm Hg In coronary vessel with critical stenosis: Vasodilator reserve of microvascular bed is exhausted Decrease in AO pressure => Coronary hypoperfusion
Pathophysiology of Shock
Effect of Hypotension (continued)
Normal heart extracts 65% of the O2 present in the blood Little room for augmentation of O2 extraction
Pathophysiology of Shock
Effect of:
LVEDP (mm Hg)
Elevated LVEDP
on coronary flow
Pathophysiology of Shock
Hypotension + LVEDP and critical stenosis Myocardial Hypoperfusion LV dysfunction Systemic lactic acidosis Impairment of non-ischemic myocardium worsening hypotension.
Schematic
LVEDP elevation Hypotension Decreased coronary perfusion Ischemia Further myocardial dysfunction Neurohormonal activation Vasoconstriction Endorgan hypoperfusion
Figure out the volume status, Swan if in doubt Air way Judicious afterload reduction Maintain AV synchrony Dont tolerate Afib Dual chamber pacing if A-V block present Correct Acid-Base disturbances Maintain BP ( IABP and/or Pressors).
LV O2 consumption
Williams, et.al., Circulation 1982
Thus balloon pumping increased flow to a bed fed by the critical stenosis, or collateral vessels
IABP in Acute MI
JACC 1985
IABP in Acute MI
Pre-thrombolytic era No Lytics, ASA, or Lopressor 20 patients with Acute MI and extensive myocardium at risk per baseline Thalium were Randomized. Pt.s in Shock were excluded
Std Rx
+
IABP Plus IV NTG
IABP in Acute MI
Patients had repeat Thalium scan on Day-4 No differences were observed between the two groups regarding:
-Thalium defect score comparing days 1 and 4 -The ejection fraction comparing days 1 and 4
=>
Rates of Reperfusion Lower, and Rates of Reocclusion Higher Than in non-shock pts Possible Reason: Diffusion of thrombolytic agent into the thrombus may be PRESSURE DEPENDENT.
Most thrombolytic trials specifically excluded patients in cardiogenic shock The only large placebo-controlled thrombolytic study specifically examining Pts. presenting with shock was GISSI-1 Streptokinase
=> No Benefit
Kovack, et. al., JACC 1997 Stomel, et. al., Chest 1994
TT
The younger pts., twice as likely to get TT => Selection Bias TT PPTCA PPTCA IABP IABP
TACTICS
ST elevation MI patients, presenting within 12 hours of Sx, and Cardiogenic shock 57 Patients were randomized
TACTICS
The primary endpoint of 6 month mortality was not statistically significant, P=0.3
IABP Pressors
SHOCK Trial
Whether EARLY REVASCULARIZATION improves survival among patients with cardiogenic shock?
SHOCK Trial
302 Pts. with ST elevation (or new LBBB) and cardiogenic shock
Within 36 hrs. of MI onset Within 12 hrs. of Shock onset
63% 52.4%
Revasc. Med Rx
Diff.=9% P=0.11
Diff.=13% P=0.027
Diff.=14% P<0.02
47%
30 days mortality
P=0.02 CI<1.0
P=0.002 CI<1.0
P<0.02 CI<1.0
IIb/IIIa
Antagonist
41.7%
25%
Stent Placement
35.7%
52.3%
Retrospective subgroup analysis from the PURSUIT trial Hassade, et.al., JACC, 2000 Randomization to eptifibatide did not affect the incidence of shock Patients randomized to eptifibatide who developed shock had a significantly reduced incidence of death at 30 days A possible mechanism of benefit is relief of microvascular obstruction
PTCA+Reopro N=18
70 60 50 40 30 20 10 0
On Univariate analysis:
Absence of Stent use: HR 2.39, 95% CI 1.22 to 4.67, p = 0.01
East
Absence of Abciximab use: HR 1.95, 95% CI 1.03 to 3.71, p = 0.04 Stent Only PTCA+ PTCA Reopro Only
Stent+ Reopro
Abciximab +Stenting
10% Absolute mortality reduction 1 additional life saved for each 10 patients treated.
No Reopro
With Reopro
Speculation:
Greater use of Abxicimab, and Stents in the SHOCK Trial may well have resulted in a positive primary endpoint. The age cutoff of 75 may or may not have retained its significance vis--vis increased mortality.