LV Function

Ah, the left ventricle. The sole focus of every freshly minted third year medical student who, when referencing the patients HFrEF, astutely includes the most recently calculated ejection fraction in parenthesis after their abbreviated diagnosis. The following content will give you a basic idea of how to quantitatively and qualitatively assess left ventricular performance in systole and diastole. Ischemic cardiomyopathy will briefly be mentioned but a more in-depth look at coronary distribution and how to assess for regional wall motion abnormalities will be saved for the "CABG and Revascularization" section of this #FOAMed.

Table of Contents

LV Size and Associated Hypertrophies

Left ventricular size can be quantified using echocardiographic measurements, most of which are beyond the scope utility for the critical care echocardiographer making assessments of acute rather than chronic pathology. This section will focus on the big picture rather than the nitty gritty (don't worry, there is plenty of time for that in other sections). There are two gross ways that the left ventricle can increase in mass: concentric and eccentric hypertrophy. Below is a brief description of each.

Concentric Hypertrophy

Eccentric Hypertrophy

Measuring LV Function

There are a number of different methods to quantify left ventricular function, each with their benefits as well as their limitations. Many experienced echocardiographers will forgo most or all of these methods in favor of a visual estimation of function, which can be tempting particularly in a time-sensitive situation. Studies from the perioperative-space support that anesthesiologists even with minimal training in TEE can adequately "ballpark" left ventricular function when shown basic images from a rescue echo, however they lacked a significant amount of precision compared to quantitative measurements made by experienced echocardiographers (1; Comparison of visual estimation and quantitative measurement of left ventricular ejection fraction in untrained perioperative echocardiographers). For these reasons, if time allows, I recommend making at least one or two quantitative measurements of LV function to obtain a more precise analysis and to calibrate your own eye for making visual estimations in the future.

1. Raksamani, K., Noirit, A. & Chaikittisilpa, N. Comparison of visual estimation and quantitative measurement of left ventricular ejection fraction in untrained perioperative echocardiographers. BMC Anesthesiol 23, 106 (2023) 

Fractional Shortening

Fractional Area Change

Simpson's Method of Discs

LV dP/dt

MAPSE

Mitral  Annular Tissue Velocity (S')

Stroke Volume Calculation

Left Ventricular Diastology

While the focus is typically on left ventricular systolic function, diastology characterizes the ability for the heart to relax. This is affected by active ventricular relaxation, the compliance of the left ventricle, and external forces (ie. the pericardium). Traditionally this was measured by left heart catheterization, however creative use of tissue doppler and pulse wave doppler measurements have allowed echocardiography to supplant this more invasive method of assessment.

**Note: this section will assume comfort with both tissue doppler and pulse wave doppler - I recommend reviewing both of these as needed**

Because diastolic function can be complicated to assess and even more challenging to know how to apply one's assessment perioperatively, it has earned more than its fair share of eye-rolls along with criticisms such as "diastology is for nerds."  Despite this, it remains an important component of a patient's myocardial function (diastolic function is often the sign of ischemic heart disease), helpful for estimating left atrial pressures, and an increasingly appreciated risk factor for perioperative outcomes (https://pubmed.ncbi.nlm.nih.gov/27077638/, https://pubmed.ncbi.nlm.nih.gov/16835254/). The following will cover the basics of assessing diastolic dysfunction as well as some clinically applicable scenarios. For a greater understanding of diastolic function, I recommend reviewing one of the resources listed here.

Normal Distology

Diastole is made up of four phases:

1. Isovolumetric relaxation

2. Rapid filling

3. Diastasis

4. Atrial contraction

Isovolumetric relaxation occurs after the aortic valve has closed but before the mitral valve has opened. This is an active process during which the pressure in the left ventricle drops dramatically. When the pressure in the LV decreases below that of the left atrium, the mitral valve will open and rapid filling will occur due to the pressure gradient between the two chambers. As the left ventricle fills, the pressure inside will rise until it has equilibrated with the pressure in the left atrium, resulting in diastasis, so named because there is no flow across the mitral valve during this time. Finally, assuming a sinus rhythm, the left atrium will contract and blood will again flow into the left ventricle.

Normal Mitral Inflow Pattern

I planned to leave this for the "mitral valve" section of this website, but this is truly a prerequisite for understanding diastolic dysfunction so I will cover it briefly here.

Recall from above that during normal diastole, there are two periods during which blood flows from the left atrium to the left ventricle. If we place our pulse wave gate just below the tips of the mitral valve leaflets in diastole, we can see these two periods represented by two waves moving away from the baseline. *Note: these are easiest to assess if the echo's ECG leads have been connected to the patient such that the ECG is displayed on the echo display*

The first of these two waves is called the E wave. It represents blood that flows across the mitral valve in early diastole as a result of the active ventricular "sucking" that creates a relatively low pressure in the LV cavity.

The second of these two waves is called the A wave, so named because it represents blood flow across the mitral valve as a result of atrial contraction.

Typically, the E and A waves are similarly sized, such that the E/A ratio is ~1. Young athletic individuals have been reported to have E/A ratios of much larger than 1 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628709/) however most of these patients don't make their way to the ICU so we won't overcomplicate things with that for now.

Grades of Diastolic Dysfunction

In my opinion, diastolic dysfunction and its assessment by echocardiography are best understood starting with an explanation of its physiology.

Grade 1: Impaired relaxation

As the name implies, the ability of the left ventricle to relax during early diastole is impaired. This results in an increase in isovolumetric relaxation time, and a decrease in the velocity of the blood "sucked" into the ventricle in early diastole. This results in a lower peak of the E wave than normal, and an E/A ratio of much less than 1. Left atrial pressure (LAP) is still normal in this phase.

Grade 2: Pseudonormal

The second stage of diastolic dysfunction is characterized by a rise in LAP. This rise in pressure will overcome the poor relaxation of the left ventricle such that when the mitral valve opens during rapid filling phase of diastole, the pressure gradient is increased again and the E wave appears normal. There are other signs of diastolic dysfunction that can be detected but those will be covered below.

Grade 3: Restrictive Pattern

This final stage results from a continuation in the rise of LAP. As LAP goes up and up, the isovolumetric relaxation of diastole will shorten and peak E wave velocities will rise even further. The ventricle is so stiff and the diastolic pressure so high that little blood flows from the left atrium into the left ventricle during atrial contraction. This will decrease the size of the A wave so that the E/A ratio is significantly elevated, often >2.

Assessment by Echocardiography

The following should be taken with a large grain of salt, since the validation of diastolic indices comes from the world of spontaneously breathing outpatients and transthoracic echo. The perioperative setting in particular is made difficult by rapidly changing loading conditions that can affect mitral inflow patterns. With that in mind, there are a few commonly accepted algorithms for assessment of diastolic dysfunction that I will share below.

Again, I will link this section on tissue doppler imaging (TDI), as it is heavily used in assessment of LV diastolic function. There are two locations that it is commonly measured: the lateral annulus of the mitral valve, and the septal annulus. Just as there is an E and an A wave during the rapid filling and atrial contraction stages of diastole, there is corresponding waves that can be measured with TDI. As the ventricle fills, the annulus of the mitral valve will move "upwards" towards the base of the heart resulting in positive deflections above the baseline when measured with TDI. The wave during rapid filling is called the e', and the wave during atrial contraction a'.

The ratio between the peak of the E wave (measuring the velocity of blood flow) and the peak of the e' wave (measuring velocity of tissue motion) is at the core of diastolic assessment by echo. This is referred to as the E/e' ratio. A normal ventricle will generate a large sucking force during diastole, and LAP is typically low. Thus its peak E velocity is low and its peak e' velocity high, resulting in a low E/e' ratio. A stiff ventricle has poor sucking force and high LAP, thus is E velocity is very high and its e' velocity  low, resulting in a high E'e' ratio. This understanding of how the E/e' ratio reflects diastolic performance is critical to understanding diastology as a whole. If it doesn't make sense, read this paragraph a handful of additional times slowly and if it still doesn't make sense ask an experienced echocardiographer to explain it to you before moving on.

The first set of algorithms comes from the American Society of Echocardiography. These are not directly intended for perioperative use or for TEE (they include left atrial volumetric measurements which are near impossible to make with TEE) but I include it here for sake of completeness, and since these algorithms actually did come up during my CCEeEXAM. If you are looking only for the highest of the yields however, I suggest you scroll down further.

More can be found in their freely accessible, published 2016 guide: https://www.asecho.org/wp-content/uploads/2019/03/Left-Ventricular-Diastolic-Function-Summary-Doc.-to-Publish.pdf

For a simplified, perioperative or ICU-based approach:

Swaminathan et al. recognized the problems inherent to perioperative diastolic assessment by TEE with the full ASE guidelines. Instead, they proposed a dramatically simplified algorithm that performed well in both ability to categorize patients as well as risk-stratify with regards to incidence of major adverse cardiac events in the retrospective population of on-pump CABG patients in which their algorithm was tested (https://pubmed.ncbi.nlm.nih.gov/21492828/).

This approach uses only the peak e' velocity from the lateral mitral annulus and the calculated E/e' ratio.

Limitations

The above algorithms will reliably reflect diastolic dysfunction in most patients, however they are far from perfect and it is worth mentioning their limitations in certain patient populations. In general, since they assume sinus rhythm and rely on measurements of mitral inflow and mitral annular tissue velocities, patients with arrhythmias such as atrial fibrillation or mitral valve disease will require alternate means of evaluating diastolic function. This includes patients with significant mitral annular calicification (MAC), mitral stenosis, and mitral regurg. The precise additional methods by which diastolic function can be assessed in these patients is beyond the scope of this humble website; for that I recommend reviewing the 2016 ASE guidelines. A few additional CTICU-relevant examples will be included below:

Sinus Tachycardia

Sinus tach can lead to fusion of the mitral inflow E and A waves, making assessment by traditional means challenging. It will also have higher E velocities, since the heart has less time to fill a similar stroke volume, thus raising the E/e' ratio. Other parameters not discussed in great detail here such as isovolumetric relaxation time or pulmonary vein S/D ratio will appear like worse diastolic function than actually present.

Heart Transplantation

Heart transplant recipients have a couple of unique diastolic parameters. First, their donor hearts are denervated and thus are typically in a mildly tachycardic sinus rhythm (often ~100-110 bpm). Second, atrial function may be altered by a typical biatrial anastamosis. Third, the biatrial technique can lead to the presence of two SA nodes, one from the donor and one from the recipient, leading to altered atrial function and beat-to-beat variability in mitral inflow velocities. This can also affect pulmonary venous doppler indicies (lower S wave due to competing recepient atrial contraction). All of this leads to restrictive filling patterns as measured by echo despite the abscense of diastolic dysfunction in the donor. This is most noticeable immediately following transplant and can resolve with time.

Estimating Left Atrial Pressure (LAP)

As pulmonary arter catheters (PACs) have largely gone out of fashion in non-cardiac intensive care units, echocardiography has emerged as a reliable way to non-invasively estimate left atrial pressure or LV filling pressures. Of all the measurements and indices available, the E/e' ratio is the tool most commonly used to estimate LAP. This make some sense intuitively - a working ventricle will generate a larger sucking force (higher e') and, with a lower LAP (lower E) will have a low E/e' ratio. A stiff ventricle will generate less suction (low e') and high LAP will lead to higher E velocities and a higher E/e' ratio. The following cutoffs are recommended by the ASE for TTE using averaged e' values (between septal and lateral measurements).

For TTE: 

E/e' < 8 correlates with a normal LAP

E/e' >15 correlates with a high LAP

Just like other sensitive measurements that assess filling pressures (looking at you, CVP..) the E/e' ratio performs best at the extremes. Values in between 8 and 15 require more detailed assessments to determine if LAP is high or not.

For TEE, and in patients on mechanical ventilation, things are a bit murkier. There is a 2015 study in cardiac surgical patients which found a "moderate" correlation between E/e' and measured wedge pressures >18 using an E/e' cuttoff of 10 (sensitivity 71%, specificity 60%). This study also used exclusively lateral e' values which typically have better doppler alignment on TTE than their septal counterparts.

This correlation isn't strong enough for me to recommend making strict diagnostic interpretations of LAP only based on E/e' ratios, at least in complex ICU patients undergoing TEE, but I do think it is worth understanding as another tool that can be used in making generalized hemodynamic assessments.