LV Systolic Function

See TTE exam LV for basic info.

LV dysfunction may be from primary cardiac disease or secondary to sepsis.
Standard echo does not measure contractility. Echo measurements of systolic function are dependent on preload, afterload and HR which should be kept in mind. For example a poor LV will often perform better with IPPV as preload and afterload are reduced.
Echo methods for measuring contractility include velocity of circumferential fibre shortening and LV wall stress relationship, mean and maximum acceleration of aortic blood flow, LV external power, maximal elastance and speckle tracking but are beyond the scope of this teaching (until such time as they come into general usage).
Dp/dt is predictive of the need for inotropes in cardiac surgery but it correlates well with fractional shortening which is simpler to measure. It can be useful with significant AR and MR which make EF inaccurate in measuring systolic function.
It is of course more important to see what the heart is actually doing, rather than what its intrinsic (load independent) contractility is, when clinical interventions are being planned.
Predicting EF accurately from eyeballing requires significant experience but there is evidence that eyeballing the LV and classifying it a normal, moderately impaired or severely impaired can be done with limited training.

LV failure

Decompensated - dilated cardiomyopathy, IHD, valve disease (AR, AS, MR). Dilated, thin walled LV with severe pulmonary hypertension.

Acute - AMI (extended or complicated eg acute regurg), sepsis, AR, myocarditis, contusion, drugs, dynamic LVOT obstruction. Normal sized LV, RWMAs if AMI, global dysfunction otherwise, moderately raised PA pressure.

Cardiogenic shock is caused by AMI more than 90% of the time. The mortality is 50-60%.
Tei index is relatively independent of HR and BP, is not based on geometric assumptions and is a better prognostic indicator for death than EF in dilated cardiomyopathy.

While most causes of cardiogenic shock are caused by AMI, in critical care the commonest cause is sepsis. In Sepsis, myocardial depression (LV and RV) is present in up to 60% in the 1st 3 days.

VSR accounts for 4% of cardiogenic shock after AMI. Causes L to R shunt. Often seen at a thinned dyskinetic area +/- a pseudoaneurysm (a pseudoaneurysm is an incomplete rupture sealed with thrombus and pericardium).
The Vmax of the shunt reflects the LV pressure gradient and if LV pressure is assumed to be equal to systolic pressure, RV systolic pressure can be calculated.

Papillary muscle rupture and acute MR = 7%. Associated with inferior MI involving the postero-medial papillary muscle. Causes eccentric MR with normal LA size.

Myocarditis - autoimmune, infection, drugs, hypersensitivity. Often prodrome of flu-like illness. Can cause global or regional dysfunction. LV usually not dilated and may have wall thickening.

Stress cardiomyopathy. Results from emotional stress and causes apical ballooning. Coronary arteries are normal. Presents acutely and is reversible.

Aortic regurgitation. Acute AR usually caused by endocarditis or aortic dissection. Acute AR can be distinguished from chronic by the PHT. If acute the LV has not had time to adapt to the increased volume so SV falls and pressure rises. The CW doppler trace reflects how quickly the aortic and LVEDP pressures equilibrate in diastole. Because the LVEDP increases rapidly with each AR jet the deceleration time of the CW doppler trace is short (PHT <200 ms). Fluttering or premature closure of the anterior MV leaflet may also be seen.

AS and MS can present acutely in times of increased demand occurs (pregnancy, thyrotoxicosis, tachyarrhythmias).