Cardiogenic Shock due to Acute MI with Preserved Ejection Fraction !

In these days humming of Heart failure with preserved EF peaked in the skies, but once we know from our primitive studies from medical school which Cardiogenic shock is the advanced form of severely LV/RV dysfunction ,  but there are some causes which having  the EF preserved of LV disorder . 

from our primitive studies we know which the following causes are those causes of CS which may have preserved the EF , Although , In inferior and Posterior wall MI , not only one ventricle involves , here we have both ventricular disorder which prompt PCI and IABP rescued the patient : 

For Further Readings Please Click Here 

Acute causes:

Cardiac tamponade – both right and left ventricular systolic function are preserved

Acute severe valvular regurgitation – both right and left ventricular systolic function are preserved

Mitral regurgitation

Aortic regurgitation

Primary tricuspid regurgitation

Acute massive pulmonary embolism – normal left ventricular ejection fraction, reduced right ventricular ejection fraction

Acute right ventricular infarction – normal left ventricular ejection fraction, reduced right ventricular ejection fraction

But what about Left Ventricular Infarction ?





*“In light of the complex pathophysiology of CS, it is not surprising that in many cases, severe impairment of contractility does not lead to shock, and conversely, LV ejection fraction (LVEF) may be only moderately depressed in CS.In fact, the mean LVEF in the SHOCK (Should we emergently revascularize Occluded coronaries for Cardiogenic shocK) trial was ~30%, and the distribution of LVEF in SHOCK overlaps with that in many post-MI trials in patients with reduced LVEF with or without heart failure  were generally ambulatory outpatients.

Although LVEF in SHOCK was usually measured while patients were on inotropic and/or balloon support, similar

values in shock and in the subacute/chronic phases of MI indicate that the magnitude of myocardial insult that causes CS need not be profound. LVEF is similar in the acute phase

of CS and 2 weeks later, when functional status is quite different, as discussed below. Furthermore, some patients

present with CS despite preservation of LVEF in the absence of severe mitral regurgitation.

Among patients in shock, however, LVEF remains a prognostic indicator.

Approximately half of all CS patients have small or normal LV size, which represents failure of the adaptive mechanism of acute dilation to maintain stroke volume in the early phase of MI. Progressive LV dilation (remodeling) in the chronic phase can be maladaptive. Serial echocardiography has dem- onstrated a small increase in LV end-diastolic volume in 2-week survivors of CS (15-mL change in median LVend-diastolic volume). Contractile function can be assessed with echocardiography or LV angiography. In addition, the indwelling PA catheter allows ongoing evaluation of CO in response to changes in therapy and volume status. Diastolic function is more difficult to assess. It is likely that abnormalities of ventricular relaxation and compliance contribute to CS in some, if not all, cases.”

* Cardiogenic Shock: Current Concepts and Improving Outcomes
 Harmony R. Reynolds and Judith S. doi: 10.1161/CIRCULATIONAHA.106.613596 2008;117:686-697Circulation.