Part 1:
*Defining Ventri...
Metadata
- Author: @Thind888 on Twitter
- Full Title: Part 1:
*Defining Ventri... - Category: #tweets
- URL: https://twitter.com/Thind888/status/1277393232167649280
Highlights
- Part 1:
Defining ventricular preload
The conceptual definition of preload is quite straightforward: end-diastolic myocardial load/stretch. At the microscopic level, it's the sarcomere length we are interested in, which would increase with higher end-diastolic load (preload)
1/ (View Tweet) - 2/
The importance of preload is in effecting the Frank-Starling mechanism: increase in ventricular performance with ⬆️ preload. The basis of F-S relationship is primarily the sarcomere Force-Length relation.
At sarcomere length of ~2.3 μm, actin-myosin interaction is optimized.
(View Tweet) - 3/
Any further increase in sarcomere length does not improve ventricular performance (flat part of F-S curve).
So when we give fluids, what we're really trying to achieve is an ⬆️in the average sarcomere length.The clinical definition of preload is much more controversial! ([View Tweet](https://twitter.com/Thind888/status/1277393309489672192)) - 4/
For LV, the two most commonly used measures are LVEDV and LVEDP
Before we compare these, let's model the ventricle as a fluid-filled perfectly spherical balloon (obviously an approximation). If we fill the balloon with more fluid, it's size (LVEDV) and pressure (LVEDP) will⬆️ (View Tweet) - 6/
Pitfalls with LVEDV
(i) For a given LVEDV, the wall stretch (and LVEDP) would vary depending on the physical characteristics of the ventricle. E.g. 110cc is a normal adult LVEDV but would generate enormous LVEDP in kids!
Another example is eccentric hypertrophy (in DCM). (View Tweet) - 7/ As new sarcomeres are added in series, the unstressed volume of LV ⬆️. So the same LVEDV would generate ⬇️LVEDP compared to normal hearts.
(ii) Secondly, LVEDV disregards unstressed volume. E.g. in our model, balloon A has some volume (LVEDV) but its pressure (LVEDP) is zero!
(View Tweet) - 8/
Pitfalls of LVEDP
In my mind, LVEDP is a much more robust measure of LV preload and circumvents the pitfalls of LVEDV. However, a few considerations:
(i) It's the transmural LVEDP that matters (more on this later)
(ii) A given LVEDP doesn't fully describe wall stress (View Tweet) - 9/ Why? Enter LaPlace's law! {T=PR/2w}
For a given LVEDP, the amount of wall tension is dependent on the curvature of the sphere. If curvature is low (bigger sphere), same pressure causes higher wall tension.
Here's an excellent tweetorial on this -
https://t.co/uv5SVlkcC1 (View Tweet) - 10/ Wall stress/tension provides the complete description of ventricular preload. Wall tension is the orthogonal stress on the LV wall that would be proportional to average sarcomere length.
LaPlace's law states that:
Tension (T) = (Pressure x radius) / 2.width (LV thickness)
(View Tweet) - 11/
Summary:
For a stressed LV, preload is a function of LVEDP, LVEDV and LV thickness (w)
Mathematically, volume is the cube root of radius, so the influence of LVEDP > LVEDV.
Also, a thick LV (⬆️w) (e.g. HTN), would result in a lower wall stress for a given LVEDP/LVEDV. (View Tweet) - 12/ Special scenario: RV
Here's the kicker with RV preload: normal human RV operates at or below its unstressed volume! (PMID: 27613549).
Volume loading a normal RV initially does not invoke the F-S mechanism as its wall stress (preload) is zero! (RVEDV < unstressed volume)
(View Tweet) - 13/ Of course, a volume overloaded RV would operate via the F-S curve.
This under-appreciated fact has critical implications:
(i) (Transmural) RA pressure is normally zero.
(ii) Hence, in an unstressed RV, a CVP reading > zero reflects pericardial pressure (more on this later). (View Tweet) - Here's a beautiful commentary unifying wall stress to explain both preload and afterload: PMID: 11824209
Submitting for peer-review with the Heart Failure community!
@FH_Verbrugge @VerwerftJan @TheWrightHeart @CharlieJainMD @yreddyhf @RyanTedfordMD @OKiamanesh @SunitChaudhryMD (View Tweet) - Addendum:
https://t.co/WR9nlYensm (View Tweet)
Part 1:
*Defining Ventri...
Metadata
- Author: @Thind888 on Twitter
- Full Title: Part 1:
*Defining Ventri... - Category: #tweets
- URL: https://twitter.com/Thind888/status/1277393232167649280
Highlights
- Part 1:
Defining ventricular preload
The conceptual definition of preload is quite straightforward: end-diastolic myocardial load/stretch. At the microscopic level, it's the sarcomere length we are interested in, which would increase with higher end-diastolic load (preload)
1/ (View Tweet) - 2/
The importance of preload is in effecting the Frank-Starling mechanism: increase in ventricular performance with ⬆️ preload. The basis of F-S relationship is primarily the sarcomere Force-Length relation.
At sarcomere length of ~2.3 μm, actin-myosin interaction is optimized.
(View Tweet) - 3/
Any further increase in sarcomere length does not improve ventricular performance (flat part of F-S curve).
So when we give fluids, what we're really trying to achieve is an ⬆️in the average sarcomere length.The clinical definition of preload is much more controversial! ([View Tweet](https://twitter.com/Thind888/status/1277393309489672192)) - 4/
For LV, the two most commonly used measures are LVEDV and LVEDP
Before we compare these, let's model the ventricle as a fluid-filled perfectly spherical balloon (obviously an approximation). If we fill the balloon with more fluid, it's size (LVEDV) and pressure (LVEDP) will⬆️ (View Tweet) - 6/
Pitfalls with LVEDV
(i) For a given LVEDV, the wall stretch (and LVEDP) would vary depending on the physical characteristics of the ventricle. E.g. 110cc is a normal adult LVEDV but would generate enormous LVEDP in kids!
Another example is eccentric hypertrophy (in DCM). (View Tweet) - 7/ As new sarcomeres are added in series, the unstressed volume of LV ⬆️. So the same LVEDV would generate ⬇️LVEDP compared to normal hearts.
(ii) Secondly, LVEDV disregards unstressed volume. E.g. in our model, balloon A has some volume (LVEDV) but its pressure (LVEDP) is zero!
(View Tweet) - 8/
Pitfalls of LVEDP
In my mind, LVEDP is a much more robust measure of LV preload and circumvents the pitfalls of LVEDV. However, a few considerations:
(i) It's the transmural LVEDP that matters (more on this later)
(ii) A given LVEDP doesn't fully describe wall stress (View Tweet) - 9/ Why? Enter LaPlace's law! {T=PR/2w}
For a given LVEDP, the amount of wall tension is dependent on the curvature of the sphere. If curvature is low (bigger sphere), same pressure causes higher wall tension.
Here's an excellent tweetorial on this -
https://t.co/uv5SVlkcC1 (View Tweet) - 10/ Wall stress/tension provides the complete description of ventricular preload. Wall tension is the orthogonal stress on the LV wall that would be proportional to average sarcomere length.
LaPlace's law states that:
Tension (T) = (Pressure x radius) / 2.width (LV thickness)
(View Tweet) - 11/
Summary:
For a stressed LV, preload is a function of LVEDP, LVEDV and LV thickness (w)
Mathematically, volume is the cube root of radius, so the influence of LVEDP > LVEDV.
Also, a thick LV (⬆️w) (e.g. HTN), would result in a lower wall stress for a given LVEDP/LVEDV. (View Tweet) - 12/ Special scenario: RV
Here's the kicker with RV preload: normal human RV operates at or below its unstressed volume! (PMID: 27613549).
Volume loading a normal RV initially does not invoke the F-S mechanism as its wall stress (preload) is zero! (RVEDV < unstressed volume)
(View Tweet) - 13/ Of course, a volume overloaded RV would operate via the F-S curve.
This under-appreciated fact has critical implications:
(i) (Transmural) RA pressure is normally zero.
(ii) Hence, in an unstressed RV, a CVP reading > zero reflects pericardial pressure (more on this later). (View Tweet) - Here's a beautiful commentary unifying wall stress to explain both preload and afterload: PMID: 11824209
Submitting for peer-review with the Heart Failure community!
@FH_Verbrugge @VerwerftJan @TheWrightHeart @CharlieJainMD @yreddyhf @RyanTedfordMD @OKiamanesh @SunitChaudhryMD (View Tweet)