Left heart failure is the type of heart failure that comes to mind when someone starts talking about heart failure. Specifically, it is left ventricular systolic dysfunction that comes to mind, and diastolic dysfunction is a distant second. I will talk some about LV heart failure due to valvular dysfunction and LVOT obstruction, but it should be its own section. Just like the right ventricle, I am hoping to simplify left ventricular heart failure to its base hemodynamics so that the management is easier to understand. If this blog post looks similar to the right ventricular lecture series, it should. The hemodynamic concepts do not change, just some of the details.
One note, heart failure with systolic dysfunction is often referred to as heart failure with reduced ejection fraction (HFrEF), and diastolic dysfunction is often referred to as heart failure with preserved EF (HFpEF). I think this is very helpful and use it most of the time, but there are patients with both systolic and diastolic dysfunction and they cannot have reduced and preserved EF at the same time. To make it more clear in this blog I will be using diastolic and systolic dysfunction.
Breaking down cardiac output in terms of the left heart.
I broke down cardiac output for left and right heart failure before. But, as a refresher, here is the stepwise breakdown for cardiac output (Figure 1).
Figure 1: Cardiac Output Breakdown
This means that heart failure can occur from dysfunction of 4 different primary sources.
1. Heart Rate
2. Preload
3. Contractility
4. Afterload
Heart rate issues can definitely lead to LV dysfunction and cardiogenic shock, but it is not unique to LV hemodynamics, as it would affect the RV as well, and so it will be left out of this breakdown.
This leaves the 3 main categories for left heart failure: preload, contractility, and afterload. Each one of these can be increased or decreased when talking about deviations from normal, but these deviations are not all consistent with heart failure. The heart failure/cardiogenic shock profile refers to too much preload, and usually not enough contractility, and too much afterload which all lead to decreased cardiac output. In the typical shock differentiation table, it actually uses surrogate pressures to differentiate cardiogenic shock (Figure 2).
Figure 2: Shock Hemodynamics
1. Preload
Definition: the stretch of the cardiomyocytes at the end of diastole. It is often referred to as ventricular filling or the volume in the left ventricle at the end of diastole (LVEDV).
The definition of preload is significantly different from the way that preload is typically talked about clinically. Clinically preload is synonymous with intravascular volume. When someone says they have too much preload, they usually mean they are volume overloaded. While preload is related to ventricular filling with volume, it does not always mean hypervolemia.
Actual preload is usually described by using a weight on a spring. If you put weight on a spring it will stretch, and when you let it go it will spring back with force. The further you pull it back the greater the force generated to return to baseline. You can however overstretch a spring and then it loses its ability to generate the force needed to return to baseline. The metal wires get stretched and lose their spring, the same thing happens with cardiomyocytes where the actin-myosin bridge is lost (Figure 3).
Figure 3: Preload and Starling Curve with Springs and Weights
Figure 4 shows the actin/myosin connection where there is increased force when the muscle is lengthened, but all that force is lost when it is stretched beyond the actin/myosin connection (D).
Figure 4: Actin/Myosin Bridges and Muscle Force
The left ventricle is big and thick and designed to pump blood against a much higher pressure than what the right ventricle has to push against. This means the LV is designed to handle increases in afterload. Being big and thick, it does not stretch well and so it does not handle increases in volume well. Figure 5 shows the LV having to work much harder in response to increased volume compared to the RV. The RV is thin and stretchy and responds well to increases in volume when not dysfunctional.
Figure 5: LV vs RV work increase in response to increased volume (1)
Disease Physiology:
Increased Preload:
When there is too much preload, it overstretches the cardiomyocytes and will move the patient to the descending limb of the Starling curve (Figure 3). This causes a decrease in stroke volume and therefore a decrease in cardiac output. The decrease in forward flow leads to a backup of blood into the left atrium and pulmonary veins. This backup of blood increases hydrostatic pressure and causes pulmonary edema. The backup also causes increased volume in the venous system which leads to hepatic and renal congestion, jugular venous distention, and lower extremity edema.
I have heard arguments that a normal LV does not have a descending limb on the Starling Curve. While I would agree that a functioning LV can compensate significantly longer than a dysfunctional LV, the LV does have a descending limb and should not be given more volume than necessary.
Decreased Preload:
Diastolic Dysfunction:
As with most concepts, there is always an outlier that complicates the picture. If we look at preload as the stretch on the cardiomyocytes then diastolic dysfunction actually has decreased preload. Diastolic dysfunction is due to two mechanisms; 1. Hypertrophy 2. Decreased lusitropy. Think about the springs being replaced with much stiffer springs so it is much more difficult to stretch them to the needed length. If they cannot stretch they will not let volume into the LV and therefore it backs up into the left atria, pulmonary veins, lungs, and venous system.
1. LV Hypertrophy (LVH): This is usually due to long-standing hypertension where the heart continues to pump against high pressure which requires more work, and the muscle hypertrophies to compensate. When LVH is seen on echo, there is some degree of diastolic dysfunction.
2. Decreased Lusitropy: Lusitropy is discussed in a previous post, but it is the active relaxation of the heart during diastole. Since it requires ATP, ischemia or supply/demand mismatches cause the heart to not relax which decreases filling/stretch and decreased preload.
Volume vs Pressure Problem:
Systolic and diastolic dysfunction both have preload problems, and systolic dysfunction can have decreased lusitropy and ventricular stiffness and the lines can blur, but the end result is that they both will have increased pressure in the LV, which transmits to the left atria and causes pulmonary edema, venous congestion and signs of decompensated heart failure.
If you only look at the hemodynamic profile of cardiogenic shock, which shows increased left atrial pressure/pulmonary capillary wedge pressure (LAP/PCWP), it will appear that systolic and diastolic dysfunction are the same disease process, when the are significantly different.
Systolic dysfunction has decreased contractility and the volume increases in the LV itself and increases the pressure in the LV which then increases the pressure in the left atria. Treatment, therefore, is focused on removing the volume to improve contractility.
Diastolic dysfunction cannot relax and has higher pressures for the same volumes and so there are high pressures in the left atrium but it is not a volume problem in the LV, it is a pressure problem. The end result is the same as systolic dysfunction, since the fluid cannot go into the LV due to poor relaxation it builds up in the LA, pulmonary veins, and venous system. Treatment should be focused on relaxing the heart and reducing the pressure in the LV, not the volume.
Figure 6: Pressure-Volume Loop of the Left Ventricle
The main difference is where the intravascular fluid backup starts.
Systolic failure can't squeeze it out and diastolic failure can't let it in.
Understanding preload makes a big difference in managing critically ill patients, not just cardiac patients. By understanding the hemodynamics and pressure vs. volume problems, patient-centered management can be done which makes a huge impact on outcomes. It can help in knowing when to stop fluid resuscitation in septic shock. It can help with knowing when to diurese post septic shock patients and when it’s better to try to improve lusitropy in a cardiac patient instead of diuresing.
The second section of this part will talk about measuring preload, which is also a big topic and I hope this series will help bring a better understanding to treating people using a hemodynamic approach.
Blog posts to come:
Left Ventricular Heart Failure Series:
Part 1a: Introducing Preload
Part 1b: Measuring Preload
Part 2: 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
References:
Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11(5):811-822. doi:10.1513/AnnalsATS.201312-446FR
Klabunde R 2015. Cardiac Preload. https://www.cvphysiology.com/Cardiac%20Function/CF007. accessed 10/10/21
Klabunde R 2017. Ventricular Diastolic Dysfunction. https://www.cvphysiology.com/Heart%20Failure/HF006. accessed 10/10/21