Why does Dilated Cardiomyopathy decreast Left ventricle peak systolic pressure?

[NeedToStudy]

Since in Dilated Cardiomyopathy the heart has trouble pumping blood, doesn't it follow that the the left ventricle systolic pressure should be increased?

---

Members don't see this ad.

 

[seminoma]

Just speculation since we haven't had cardio yet, but decreased contraction --> decreased venous return --> decreased preload --> decreased pressure.

 

[Anonymous1991]

Preload isn't the only thing you're concerned about here. Sure, pre-load is elevated, but in a dilated cardiomyopathy the ventricle has dilated and stretched beyond the optimal sarcomere length-tension relationship. In other words, you've "over stretched" the ventricle and reduced the contractility of the ventricle.

 

[Instatewaiter]

Since in Dilated Cardiomyopathy the heart has trouble pumping blood, doesn't it follow that the the left ventricle systolic pressure should be increased?

There are a few ways to think about this:
Systolic pressure is a function of the compliance of the blood vessels and the stroke volume the heart pumps out. The more blood you pump out, the higher the BP would be (with a given blood vessel compliance). In dilated cardiomyopathy, the stroke volume drops because of reduced contractility. Therefore the systolic blood pressure drops as well.

The figure above from the other poster is not applicable. First it is not in-vivo and second tends to be related to skeletal not cardiac muscle. In cardiac myocytes there is much debate over whether or not there is even a posibility of being overstretched. Most cardiologists do not think this happens (ie the downward slope on the end of the Starling curve). Furthermore, the dilation of the ventricle is not from being overstetched; it is the result of ventricular remodeling. In dilated cardiomyopathy, the contractility decreases and THEN the ventricle remodels in response. It is not from elevation in filling pressures (aka preload).

This is further demonstrated when you diurese someone and change the fillingpressure/preload. The preload or stretch of the heart (the LVEDP or wedge pressure, or LA pressure) is related to volume. If you diurese someone and drop that LVEDP (so that the myocytes are not "overstreched") you do not see the blood pressure change.

 

[Instatewaiter]

Since in Dilated Cardiomyopathy the heart has trouble pumping blood, doesn't it follow that the the left ventricle systolic pressure should be increased?

Also I think you are thinking of the left ventricular end diastolic pressure- which would be increased.

 

[Phloston]

Agree with instatewaiter that LVEDP would be increased because ESV would be greater.

EF would be decreased since systolic dysfunction is most characteristic. For Step 2, it's really HY that you use ACEi or ARB to decrease afterload in systolic dysfunction. That means the LV can't generate the pressure it needs to counteract otherwise normal afterload. That, in combination with PCWP being increased since the heart is failing to pump, peak systolic pressure is likely decreased.

Basically if your strength of contraction is lesser, you'll get reduced volume ejected per unit time and systolic pressure would be lower.

 

[Jabbed]

Preload isn't the only thing you're concerned about here. Sure, pre-load is elevated, but in a dilated cardiomyopathy the ventricle has dilated and stretched beyond the optimal sarcomere length-tension relationship. In other words, you've "over stretched" the ventricle and reduced the contractility of the ventricle.

View attachment 187219

I'm 80% sure that this figure only applies to skeletal muscle and not cardiac muscle.

 

[mcloaf]

I'm 80% sure that this figure only applies to skeletal muscle and not cardiac muscle.

Why?

 

[xffan624]

I'm 80% sure that this figure only applies to skeletal muscle and not cardiac muscle.

I've seen that applied to cardiac muscle as well. From my first year slides.

 

[Jabbed]

Why?

Something about how the greater stiffness of cardiac muscle prevents the sarcomeres from being stretched beyond a few microns within physiological limits. I'm not sure if there's any increase in length in the actual sarcomeres in DCM; isn't the dilation a result of eccentric hypertrophy?

 

[Macaroon_Berry]

Preload isn't the only thing you're concerned about here. Sure, pre-load is elevated, but in a dilated cardiomyopathy the ventricle has dilated and stretched beyond the optimal sarcomere length-tension relationship. In other words, you've "over stretched" the ventricle and reduced the contractility of the ventricle.

View attachment 187219

This is correct. It was in the Kaplan Cardiology Physio chapter, and they explained it this way as well. Remember the relationship between preload, which causes passive tension, and active tension. When you over stretch the cardiac muscle, which is striated like skeletal muse so it also has sarcomeres as well, you're stretching the sarcomere length. When you stretch to the optimal length during diastole (increase preload) the myosin cross bridges are going to contract optimally, hence giving you active tension. If you increase the preload too much, you over stretch the muscle length (this is what happens in dilated cardiomyopathy), the sarcomeres are over stretched so the actin and myosin heads can't even come in contact with each other and contract, so it would be decrease the peak systolic pressure. So: peak systolic pressure = at optimal muscle length. If you stretch the muscle too much or too little (increased or decreased preload), you would have a lower systolic pressure.

 

[pathologyDO]

Something about how the greater stiffness of cardiac muscle prevents the sarcomeres from being stretched beyond a few microns within physiological limits. I'm not sure if there's any increase in length in the actual sarcomeres in DCM; isn't the dilation a result of eccentric hypertrophy?

Nah, the reason you get decreased contractility is because sarcomeres are stretched beyond their optimum length. According to Robbins you do get some scarring which may affect contractility as well but the main thing is that cardiac m. is striated and has sarcomeres just like skeletal m., and thus stretching the heart too much leads to inefficient myosin-actin crossbridging for contraction (just like skeletal m.). Since heart contractility is decreased, so is the left ventricular systolic pressure.

Maybe you're thinking of hypertrophic cardiomyopathy rather than dilated ?

 

[Macaroon_Berry]

Something about how the greater stiffness of cardiac muscle prevents the sarcomeres from being stretched beyond a few microns within physiological limits. I'm not sure if there's any increase in length in the actual sarcomeres in DCM; isn't the dilation a result of eccentric hypertrophy?

The dilation is not a result of eccentric hypertrophy - it's the other way around. When you increase end diastolic volume, you increase the chamber size and to compensate for this dilation you get eccentric hypertrophy where sarcomeres are laid down end to end (as opposed to parallel as in concentric hypertrophy). So the eccentric hypertrophy is a result of the dilation.