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LV DYSFUNCTION

•  Is the LV dysfunction acute or chronic

   Is it an issue with contractility

  Is it an issue with relaxation

  Is it a valvular issue

  Is it an external issue eg pericardial effusion/ PE

LV SYSTOLIC DYSFUNCTION

When you're assessing LV systolic function,

1. examine the LV in all views before making a call.
2. look closely at the change in cavity size diastole to systole (should decrease 30-50%) 
3. look for myocardial thickening in systole (should be about 50%) and whether an abnormality is global or regional.
4. look at the EPSS (should be <5mm, >10mm closely correlates well with decreased EF)

Further, look for upstream consequences of the decreased EF:

1. Dilated LA
2. Pulmonary HT and B lines
3. Dilated RV
4. Dilated IVC
5. Ascites

These changes take longer to develop and may not be seen with acute LV systolic dysfunction. 

CAUSES to consider for global reduced LV systolic function

myocarditis: viral, post partum, autoimmune

drugs and toxins: chemotherapy, RT, drug overdose, alcoholism

endocrine: hypothyroidism

Acute LV systolic dysfunction (post partum cardiomyopathy)

ACUTE LV REGIONAL SYSTOLIC DYSFUNCTION

Regional wall motion abnormalities causing LV dysfunction is usually due to ischaemia; however, always consider conditions such as takatsubo, trauma and aortic dissection.

ISCHAEMIA

The regional wall motion abnormality (RWMA) will usually follow an arterial distribution. It is easiest to pick RWMA in the PSAx. Focus your gaze on the anechoic centre of the LV and just watch to see which walls come in to the centre and which ones do not. Once you figure out which walls, match this to an arterial territory. And then consider other areas supplied by this artery and confirm that these walls also have decreased contractility. Eg: in PSAx inferiorlateral wall has decreased contractility, in PLAx this should be decreased as well. inferolateral wall is supplied by the circumflex or the RCA: so is the RV down as well or is the lateral wall of the LV down. 

In acute ischaemia, the LV wall will still be normal thickness. 

If the RWMA does not match a vasular territory consider other causes such as myocardial dysfunction due to trauma, takatsubo, myocarditis etc

TAKATSUBO

colloquially called "broken heart syndrome" this condition typically affects middle aged females following a particularly intense life stress. The heart is said to look like ceramic vessel which the Japanese use to catch octopi. On echo: the heart will be dilated with only the basal segments of the LV contracting, while the apex balloons out. 

PLAx: Takatsubo: note base of heart at inferiolateral wall and septum contracting well, whereas the rest of the LV not contracting. This does not fit an arterial territory

CHRONIC LV SYSTOLIC DYSFUNCTION

In this case, the LV will be dilated and the walls may thin.  The LA (due to the back pressure caused by increased LV end-diastolic pressure) will dilate. The pulmonary system will slowly develop increased resistance and pulmonary HT. The RV is initially dilated. However with the development of pulmonary HT. it will start to hypertrophy. Look for RWMA, valvular dysfunction etc to determine the underlying cause. 

Chronic DCM: PLAx showing a dilated LV, EPSS >5mm, dilated RV and LA (note the normal sized aorta which looks tiny next to the RV and LA - should be 1:1:1)

LV HYPERTROPHY

LV DIASTOLIC DYSFUNCTION

Diastolic dysfunction can lead to heart failure symptoms with preserved ejection fraction. The easiest 2D feature of LV diastolic dysfunction is a dilated LA in the absence of significant mitral valve pathology (5). Diagnosis of LV diastolic dysfunction is made by looking at the mitral inflow patterns in A4C. However, this is not really a part of emergency bedside echo so I won't go into it here (6), 

LV diastolic failure can cause exertional dyspnoea without signs typical of systolic heart failure. The patient may have B lines due to pulmonary oedema (7). These patients do well with treatments such as spirolactone, AT-II inhibitors and B blockers to name a few (8). 

Back pressure caused by LV impaired relaxation will eventually cause pulmonary hypertension and features of RV pressure overload. 

Watching for LA dilatation in real time when fluid loading a hypotensive septic patient can help determine when to start inotropes. 

PLAx: LV hypertrophy and dilated LA suggesting diastolic dysfunction

PLAx: Dilated LV and severely dilated LA. However note hockey stick appearance (rheumatic MV) to anterior mitral leaflet: likely some mitral stenosis and regurgitation contributing to dilated LA (colour may help)

LV OUTFLOW TRACT OBSTRUCTION

The LVOT obstruction in LV hypertrophy typically occurs in states with decreased intravascular volume/ venous return (eg peripheral vasodilation, valsalva or dehydration) and with increased demand (eg exercise). This can occur unexpectedly in the elderly with sigmoid septum due to hypertension when they become septic or dehydrated. The most important thing to remember in patients with LVOT obstruction is to preserve intravascular volume and venous return and decrease tachycardia. Measures which increase LV squeeze like inotropes will make the obstruction worse. 

There are two main mechanisms to LVOT obstruction: 

1. LV cavity obstruction because the hypertrophic LV walls obliterate the cavity during systole

LV walls almost touching with each systole. You could imagine, it wouldn't take much to cause cavity obstruction.

2. SAM: systolic anterior motion of the mitral valve. This is where the venturi effect of systole pulls the anterior mitral leaflet towards the septum causing outflow obstruction. 

An example of SAM

Snap shot of clip above showing the AV valves open (systole) but the LV cavity is almost obliterated by the anterior mitral valve aparatus.

LVOT continuous wave doppler will give the typical dagger waveform: delayed peak and high velocities. A PG >30 is indicative of significant obstruction (9). 

Typical dagger shape and high velocities of the LVOT cw waveform suggesting cavity obstruction (from European society of cardiology (8)

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REFERENCES

1. Bahl A, Johnson S, Altwail M, Brackney A, Xiao J, Price J, Shotkin P, Chen NW. Left Ventricular Ejection Fraction Assessment by Emergency Physician-Performed Bedside Echocardiography: A Prospective Comparative Evaluation of Multiple Modalities. J Emerg Med. 2021 Dec;61(6):711-719

2. Unlüer EE, Karagöz A, Akoğlu H, Bayata S. Visual estimation of bedside echocardiographic ejection fraction by emergency physicians. West J Emerg Med. 2014 Mar;15(2):221-6.

3. Akinboboye O, Sumner J, Gopal A, King D, Shen Z, Bardfeld P, Blanz L, Brown EJ Jr. Visual estimation of ejection fraction by two-dimensional echocardiography: the learning curve. Clin Cardiol. 1995 Dec;18(12):726-9.

4. Lorell BH, Carabello BA. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. Circulation. 2000 Jul 25;102(4):470-9. doi: 10.1161/01.cir.102.4.470. PMID: 10908222.4. 

5. Lo Q, Thomas L. Echocardiographic evaluation of diastolic heart failure. Australas J Ultrasound Med. 2010;13(1):14-26.

6. Anthony C, Akintoye E, Wang T, Klein A. Echo Doppler Parameters of Diastolic Function. Curr Cardiol Rep. 2023 Apr;25(4):235-247.

7. Simonovic D, Coiro S, Deljanin-Ilic M, Kobayashi M, Carluccio E, Girerd N, Ambrosio G. Exercise-induced B-lines in heart failure with preserved ejection fraction occur along with diastolic function worsening. ESC Heart Fail. 2021 Dec;8(6):5068-5080

8. Omote K, Verbrugge FH, Borlaug BA. Heart Failure with Preserved Ejection Fraction: Mechanisms and Treatment Strategies. Annu Rev Med. 2022 Jan 27;73:321-337.

9. Bermudez Jimenez, F. How to…measure intraventricular obstruction in hypertrophic cardiomyopathy. European Society of Cardiology. Oct 2021