Left Heart Failure: Understanding hemodynamics Part 2a: Contractility at the Physiological Level

It is time to get into LV contractility. This is obviously a big topic, so much time and effort are put into LV contractility. It is looked at as the most important component of LV hemodynamics, but I would argue that it is not. That being said, it is important to be able to evaluate a patient's contractility.

Breaking down cardiac output in terms of the left heart.

Let’s relook at the breakdown of cardiac output into its four core components (Figure 1). I have added the preload component from part 1.

Figure 1: Cardiac output breakdown

2. Contractility

Contractility can be defined according to ventricular contractility or myocardial contractility. It makes sense to use ventricular contractility as this is more useful clinically and is referred to as ventricular function.

Myocardial contractility: Defined as the contraction of the myocyte independent of preload or afterload conditions. It is dependent on the degree of binding between the actin and myosin. Beta-1 agonists and phosphodiesterase inhibitors increase the amount of available calcium which improves this interaction and increases contractility (1,2).

Ventricular function: Defined as the contraction of the ventricle at a given filling volume and systolic pressure. This is the definition we use when referring to the Frank-Starling curve. As filling volume increases it increases the stretch, or preload, and the contractility increases (Figure 2) (1,2).

Figure 2: Starling Curve

Disease physiology:

The two main physiological pathways for LV contractility dysfunction are ischemic and non-ischemic.

Ischemic cardiomyopathy: Decreased contractility of the left ventricle due to ischemic disease. This is most commonly due to coronary artery disease (CAD) where the plaques in the coronary artery cause narrowing that lead to decreased flow and a decrease in oxygen delivery to the myocardial tissue causing a non-ST elevation myocardial infarction (NSTEMI). When there is a rupture of the plaque it can cause complete occlusion and an ST elevation MI (STEMI). Decreased oxygen leads to cell death which leads to fibrosis. The LV dilates to compensate for the fibrosis and decrease in function. Ischemic cardiomyopathy will typically have a regional wall motion abnormality (RWMA) that correlates with the diseased coronary artery.

Non-ischemic cardiomyopathy: Decreased contractility of the left ventricle not related to ischemia. This encompasses a wide variety of disease processes. Common causes include viral myocarditis, auto-immune (SLE), infiltrative (amyloid), or genetic diseases. Non-ischemic cardiomyopathy usually encompasses the entire LV and presents with a global hypokinesis.

Physiologically Looking at Contractility:

Contractility can be estimated using the pressure-volume loop of the left ventricle or by directly measuring the LV pressure over time.

1. End Systolic Pressure-Volume Relationship (ESPVR):

The pressure-volume loop of the left ventricle is incredibly useful in understanding the overall function of the LV (Figure 3). The bottom curve is the filling of the left ventricle and is called the filling curve. The right side of the loop is the isovolumetric contraction when the LV contracts with both valves closed. The top of the loop is the ejection curve when the LV ejects its stroke volume, and the final side of the loop is the isovolumetric relaxation when the LV relaxes with both valves closed.

Figure 3: Left Ventricular Pressure-Volume Loop

There is a line drawn starting from the point where the volume in the LV is at zero venous return. This point has been found experimentally. The line is drawn from this point through the upper left corner of the pressure-volume loop. This line is called the end-systolic pressure-volume relationship (ESPVR). The ESPVR is the contractility of the left ventricle. This line is △P/△V which is systolic elastance. The systolic elastance is the inotropic state of the ventricle.

Figure 4: Defining ESPVR

When the LV contractility decreases with systolic heart failure the cardiac loop slides to the right and the ESPVR, or elastance, decreases (Figure 5).

Figure 5: ESPVR and decreasing LV function

2. △P/△t:

The other way to look at LV contractility is by looking at the relationship of pressure over time. This is done by measuring the LV pressure directly through a cardiac cycle. The maximum rate of rise of the pressure during isovolumetric contraction (IC) is a great measure of LV contractility (4).

Figure 6: Left Ventricular Pressure/Time Scalar

Figure 7: Measuring Contractility as △P/△t

Table 1: △P/△t values

The physiology of contractility can be difficult to visualize or work through, but it does not come to the bedside well. Clinically it can be difficult to adequately estimate LV contractility and so we have to look at LV function or performance instead. The second part of this will get into the more common clinical measurements of contractility and how they can be used to evaluate the patient.

Left Ventricular Heart Failure Series:

Part 1a: Introducing Preload

Part 1b: Measuring Preload

Part 2a: Physiological Contractility

Part 2b: Clinical Contractility

Part 3: Afterload

Part 4: Managing LV dysfunction

Other Left-Sided Heart Failure:

Part 1: Valvular disease

Part 2: LVOT obstruction/SAM

Cardiogenic Shock:

Part 1: Why a Protocol is Needed

Part 2: Cardiogenic Shock Protocols

Part 2b: Contractility at the Clinical Level

References:

1. Davidson, B.P., Giraud, G.D., 2012. Left Ventricular Function and the Systemic Arterial Vasculature: Remembering What We Have Learned. Journal of the American Society of Echocardiography 25, 891–894.. doi:10.1016/j.echo.2012.06.020

2. Solaro RJ. Regulation of Cardiac Contractility. San Rafael (CA): Morgan & Claypool Life Sciences; 2011. Available from: https://www.ncbi.nlm.nih.gov/books/NBK54078/

3. Hamlin RL, del Rio C. dP/dt(max)--a measure of 'baroinometry'. J Pharmacol Toxicol Methods. 2012;66(2):63-65. doi:10.1016/j.vascn.2012.01.001

4. Chengode S. Left ventricular global systolic function assessment by echocardiography. Ann Card Anaesth. 2016;19(Supplement):S26-S34. doi:10.4103/0971-9784.192617

5. Abuomara HZA, Hassan OM, Rashid T, Baraka M. Myocardial performance index as an echocardiographic predictor of early in-hospital heart failure during first acute anterior ST-elevation myocardial infarction. Egypt Heart J. 2018;70(2):71-75. doi:10.1016/j.ehj.2017.12.001

6. Caballero L, Kou S, Dulgheru R, et al. Echocardiographic reference ranges for normal cardiac Doppler data: results from the NORRE Study. Eur Heart J Cardiovasc Imaging. 2015;16(9):1031-1041. doi:10.1093/ehjci/jev083