Systemic vascular resistance is not a realiable measure of left ventriclar afterload. In this study, noradrenaline actually decreased left ventricular wall stress even though SVR increased. Higher heart rate and contractility leads to a smaller LV, lower wall stress. #emimcc #cccsky #cardiosky
Systemic vascular resistance: an unreliable index of left ventricular afterload. | Circulation
Systemic vascular resistance (SVR) is a frequently used clinical index of left ventricular
afterload. However, SVR may not adequately assess left ventricular afterload (i.e.,
ventricular internal fibe...
www.ahajournals.org
June 26, 2026 at 10:42 PM
Systemic vascular resistance is not a realiable measure of left ventriclar afterload. In this study, noradrenaline actually decreased left ventricular wall stress even though SVR increased. Higher heart rate and contractility leads to a smaller LV, lower wall stress. #emimcc #cccsky #cardiosky
Preload vs afterload 🫀
#cardiology
@lameliav.bsky.social
@liisasiil.bsky.social
@laurengroner.bsky.social
@stefantigges.bsky.social
#cardiology
@lameliav.bsky.social
@liisasiil.bsky.social
@laurengroner.bsky.social
@stefantigges.bsky.social
March 7, 2025 at 3:46 PM
Any LV, good or bad, will see SV and EF drop if afterload is increased in isolation. Healthy hearts will preserve EF when afterload is increased by increasing contractility through inotropy.
November 30, 2024 at 12:37 PM
Any LV, good or bad, will see SV and EF drop if afterload is increased in isolation. Healthy hearts will preserve EF when afterload is increased by increasing contractility through inotropy.
I remember a young pt with HLH 2/2 connective tissue dz
we treated the HLH & everything was getting better but the EF dropped from ~45 to ~35
her EF fell b/c the HLH-induced vasodilation had been afterload-reducing her
falling EF reflected systemic recovery
eventually she fully recovered #EMIMCC
we treated the HLH & everything was getting better but the EF dropped from ~45 to ~35
her EF fell b/c the HLH-induced vasodilation had been afterload-reducing her
falling EF reflected systemic recovery
eventually she fully recovered #EMIMCC
January 7, 2025 at 12:17 PM
I remember a young pt with HLH 2/2 connective tissue dz
we treated the HLH & everything was getting better but the EF dropped from ~45 to ~35
her EF fell b/c the HLH-induced vasodilation had been afterload-reducing her
falling EF reflected systemic recovery
eventually she fully recovered #EMIMCC
we treated the HLH & everything was getting better but the EF dropped from ~45 to ~35
her EF fell b/c the HLH-induced vasodilation had been afterload-reducing her
falling EF reflected systemic recovery
eventually she fully recovered #EMIMCC
Really nice article on TAPSE/TRVmax as a potential prognostic marker
From the team at Nepean ICU, led by Emma Bowcock
annalsofintensivecare.springeropen.com/articles/10....
From the team at Nepean ICU, led by Emma Bowcock
annalsofintensivecare.springeropen.com/articles/10....
The value of right ventricular to pulmonary arterial coupling in the critically ill: a National Echocardiography Database of Australia (NEDA) substudy - Annals of Intensive Care
Background Right ventricular (RV) function is tightly coupled to afterload, yet echocardiographic indices of RV function are frequently assessed in isolation. Normalizing RV function for afterload (RV...
annalsofintensivecare.springeropen.com
February 6, 2025 at 10:55 AM
Really nice article on TAPSE/TRVmax as a potential prognostic marker
From the team at Nepean ICU, led by Emma Bowcock
annalsofintensivecare.springeropen.com/articles/10....
From the team at Nepean ICU, led by Emma Bowcock
annalsofintensivecare.springeropen.com/articles/10....
Which explains why, at very low preload, EF decreases. High EF («hyperdynamic» heart) is a sign of high inotropy and/or low afterload, not low preload. #emimcc #pocus
ICU Hemodynamics:
The eternally debated question:
Assuming patient is fluid-tolerant, can #POCUS help us make the distinction between low preload (where we should reach out for fluids) and low afterload (where we should reach out for vasopressors)?
The eternally debated question:
Assuming patient is fluid-tolerant, can #POCUS help us make the distinction between low preload (where we should reach out for fluids) and low afterload (where we should reach out for vasopressors)?
April 5, 2025 at 8:48 PM
Reupping this old post, we tend to only consider the vasomotor part of peripheral resistance/afterload but it is so much more, blood rheology is complex and viscosity is important! #emimcc #cardiosky
Aside from hematocrit, temperature and glucose levels are major determinants of blood viscosity, and therefore SVR (and thus after load). Increasing temperature from 36.5-39.5 decreases viscosity by 10% #FOAMcc #FOAMed #fluidsaredrugs https://www.ncbi.nlm.nih.gov/pubmed/11368464
Blood viscosity and blood pressure: role of temperature and hyperglycemia - PubMed
We planned a study to research the relations among blood pressure (BP), viscosity, and temperature in healthy subjects and among BP, viscosity, and glucose in diabetics. With simple random sampling method, 53 healthy and 29 diabetes mellitus (DM) type II subjects were selected. Parameters were deter …
www.ncbi.nlm.nih.gov
December 4, 2024 at 8:34 PM
Reupping this old post, we tend to only consider the vasomotor part of peripheral resistance/afterload but it is so much more, blood rheology is complex and viscosity is important! #emimcc #cardiosky
ICU Hemodynamics:
The eternally debated question:
Assuming patient is fluid-tolerant, can #POCUS help us make the distinction between low preload (where we should reach out for fluids) and low afterload (where we should reach out for vasopressors)?
The eternally debated question:
Assuming patient is fluid-tolerant, can #POCUS help us make the distinction between low preload (where we should reach out for fluids) and low afterload (where we should reach out for vasopressors)?
April 4, 2025 at 5:02 PM
ICU Hemodynamics:
The eternally debated question:
Assuming patient is fluid-tolerant, can #POCUS help us make the distinction between low preload (where we should reach out for fluids) and low afterload (where we should reach out for vasopressors)?
The eternally debated question:
Assuming patient is fluid-tolerant, can #POCUS help us make the distinction between low preload (where we should reach out for fluids) and low afterload (where we should reach out for vasopressors)?
It’s unphysiological to increase afterload in isolation without matching inotropy/chronotropy. EF is a marker of ventriculoarterial coupling. Vasopressin lead to uncoupling, dobutamine recoupled the LV and arterial system. 2/
November 30, 2024 at 9:57 AM
It’s unphysiological to increase afterload in isolation without matching inotropy/chronotropy. EF is a marker of ventriculoarterial coupling. Vasopressin lead to uncoupling, dobutamine recoupled the LV and arterial system. 2/
Afterload reduction in the right patient is one of the most satisfying medical interventions imo. Potentially life saving and often staves off intubation.
Furosemide often *is* the answer, though 😉
Furosemide often *is* the answer, though 😉
All heart failure is NOT the same; and diuretics are NOT always the answer ‼️
In the very wise words of Dr. Frederik Verbrugge - "Elevated cardiac filling pressures and fluid overload are both important, yet grossly different features of acute decompensated heart failure."
#emimcc
In the very wise words of Dr. Frederik Verbrugge - "Elevated cardiac filling pressures and fluid overload are both important, yet grossly different features of acute decompensated heart failure."
#emimcc
January 9, 2025 at 1:37 PM
Afterload reduction in the right patient is one of the most satisfying medical interventions imo. Potentially life saving and often staves off intubation.
Furosemide often *is* the answer, though 😉
Furosemide often *is* the answer, though 😉
I would argue tho that we don’t pay enough attention to afterload reduction in heart failure exacerbation in these patients, so a good point to keep in mind.
April 17, 2026 at 5:42 PM
I would argue tho that we don’t pay enough attention to afterload reduction in heart failure exacerbation in these patients, so a good point to keep in mind.
Great point. The non-ventilated capillaries will be the ones who are most constricted and contributing most to RV afterload.
December 1, 2024 at 10:37 PM
Great point. The non-ventilated capillaries will be the ones who are most constricted and contributing most to RV afterload.
#Cardiosky. Being both pre-and afterload dependent, myocardial stroke work is not a contractility measure. As GLS do not correlate with SV, Strain pressure loops do not measure stroke work.
June 9, 2025 at 7:09 PM
#Cardiosky. Being both pre-and afterload dependent, myocardial stroke work is not a contractility measure. As GLS do not correlate with SV, Strain pressure loops do not measure stroke work.
PS - sometimes pressors (NE, vaso, phenyl) don't increase BP because:
- they increase afterload
- heart can't tolerate afterload so CO *decreases*
- MAP = (CO)(SVR) is *unchanged*
so failure of a pressor to increase MAP may suggest that it's squashing the CO & not helping the patient
🧵#5/5
- they increase afterload
- heart can't tolerate afterload so CO *decreases*
- MAP = (CO)(SVR) is *unchanged*
so failure of a pressor to increase MAP may suggest that it's squashing the CO & not helping the patient
🧵#5/5
a despicable me character talking on a phone with the words ok that 's not helping below him
ALT: a despicable me character talking on a phone with the words ok that 's not helping below him
media.tenor.com
January 24, 2025 at 3:02 PM
PS - sometimes pressors (NE, vaso, phenyl) don't increase BP because:
- they increase afterload
- heart can't tolerate afterload so CO *decreases*
- MAP = (CO)(SVR) is *unchanged*
so failure of a pressor to increase MAP may suggest that it's squashing the CO & not helping the patient
🧵#5/5
- they increase afterload
- heart can't tolerate afterload so CO *decreases*
- MAP = (CO)(SVR) is *unchanged*
so failure of a pressor to increase MAP may suggest that it's squashing the CO & not helping the patient
🧵#5/5
Randomly pondering the extent to which sepsis is understood as an inappropriately low afterload state vs a capillary leak syndrome
Obvs it is both….
Obvs it is both….
December 18, 2025 at 2:03 PM
Randomly pondering the extent to which sepsis is understood as an inappropriately low afterload state vs a capillary leak syndrome
Obvs it is both….
Obvs it is both….
I don't envy the central bankers tasked with managing money supply through the effects of tariffs, which simultaneously raise prices and reduce output.
For medical folks, this is like managing afterload with superimposed septic + cardiogenic shock. Each problem suggests an opposite strategy.
For medical folks, this is like managing afterload with superimposed septic + cardiogenic shock. Each problem suggests an opposite strategy.
Scary stagflation expectations in today's UMichigan print
March 14, 2025 at 2:33 PM
I don't envy the central bankers tasked with managing money supply through the effects of tariffs, which simultaneously raise prices and reduce output.
For medical folks, this is like managing afterload with superimposed septic + cardiogenic shock. Each problem suggests an opposite strategy.
For medical folks, this is like managing afterload with superimposed septic + cardiogenic shock. Each problem suggests an opposite strategy.
Great points, I really see IABP as a mechanical afterload reductor (great effect in dilated LVs and especially in dynamic mitral regurgitations), the benefit in increased DAP is more theoretical than real I think
September 10, 2026 at 7:42 PM
Great points, I really see IABP as a mechanical afterload reductor (great effect in dilated LVs and especially in dynamic mitral regurgitations), the benefit in increased DAP is more theoretical than real I think
Yes, which is why a preserved SV in the face of increased afterload is a good pragmatic indicator of a healthy heart. We see that all the time in OR.
November 30, 2024 at 12:54 PM
Yes, which is why a preserved SV in the face of increased afterload is a good pragmatic indicator of a healthy heart. We see that all the time in OR.
So here goes my first "#skytorial" on one of our studies. Looking forward to your feedback and the discussions (1/n):
Interested in how the RV adapts to preload and afterload changes?
rdcu.be/d0AT7
Interested in how the RV adapts to preload and afterload changes?
rdcu.be/d0AT7
Mechanisms maintaining right ventricular contractility-to-pulmonary arterial elastance ratio in VA ECMO: a retrospective animal data analysis of RV–PA coupling | Journal of Intensive Care
rdcu.be
November 18, 2024 at 3:25 PM
So here goes my first "#skytorial" on one of our studies. Looking forward to your feedback and the discussions (1/n):
Interested in how the RV adapts to preload and afterload changes?
rdcu.be/d0AT7
Interested in how the RV adapts to preload and afterload changes?
rdcu.be/d0AT7
Definitely, and the afterload sensitivity of the LV (wall thickness, cavity size, EF).
Easy study to do🤔
Easy study to do🤔
November 27, 2024 at 4:09 PM
Definitely, and the afterload sensitivity of the LV (wall thickness, cavity size, EF).
Easy study to do🤔
Easy study to do🤔
📝Editorial perspective: Is less sedation always better in the CICU?
Deep sedation may offer physiologic benefits in selected cardiac patients, including afterload reduction & arrhythmia control. Maybe the question is: Who needs deeper sedation, and when?
🔗 bit.ly/4dHsKJs
Deep sedation may offer physiologic benefits in selected cardiac patients, including afterload reduction & arrhythmia control. Maybe the question is: Who needs deeper sedation, and when?
🔗 bit.ly/4dHsKJs
September 22, 2026 at 6:37 PM
📝Editorial perspective: Is less sedation always better in the CICU?
Deep sedation may offer physiologic benefits in selected cardiac patients, including afterload reduction & arrhythmia control. Maybe the question is: Who needs deeper sedation, and when?
🔗 bit.ly/4dHsKJs
Deep sedation may offer physiologic benefits in selected cardiac patients, including afterload reduction & arrhythmia control. Maybe the question is: Who needs deeper sedation, and when?
🔗 bit.ly/4dHsKJs
Correct - putting patients on Vasopressin without controlling the effect on SV is a crime - I have seen patient deteriorate very fast. But on the other hand, patients with "healthy" hearts, handle increased afterload without SV drop, so in some ways you have uncovered an issue - NE masks a lot
November 30, 2024 at 11:18 AM
Correct - putting patients on Vasopressin without controlling the effect on SV is a crime - I have seen patient deteriorate very fast. But on the other hand, patients with "healthy" hearts, handle increased afterload without SV drop, so in some ways you have uncovered an issue - NE masks a lot