Here is Part I of our journey to to help YOU better understand PV loops and make them a little less daunting. Couldn't have done this without ⭐ @TJUHospital resident @jayamj94, and edits from @PSullivan000. Stay tuned for Part 2!
Part 1: The Basics
What is a pressure-volume (PV) loop?
A PV loop is a visual representation of the LV pressure (on the y-axis) and LV volume (on the x-axis) throughout a single cardiac cycle. (Great resource: cvphysiology.com/Cardiac%20Func…)
In addition to “typical” hemodynamics and volume measures, PV loops provide unique insights into ventricular function including the quantification of ventricular contractility, compliance, energetics, and dyssynchrony (slide from @BurkhoffMd's TEACH session; more on this to come)
Plotting LV pressure versus LV volume throughout a cardiac cycle forms a loop that can be divided into four phases (a-d). Phases a and d encompass diastole while phases b and c encompass systole.
The left side of the loop is the LV end systolic volume and the right side is the LV end diastolic volume. The width of the loop (LVESV - LVEDV) is the stroke volume (SV). The area in the loop is the stroke work: the work the LV does during ejection.
Let's break down the phases:
Phase a:
- The mitral valve opens (bottom left) when the LV pressure is lower than the LA pressure.
- The mitral valve closes at the end.
- As the ventricle fills, the LV volume correspondingly increases along with a slight increase in LV pressure (EDPVR)
The LV pressure versus volume curve during this phase is called the end-diastolic pressure-volume relationship (EDPVR). This EDPVR curve is generated by plotting multiple PV loops during a preload or afterload change and connecting their end diastolic points.
The slope of the EDPVR is an indicator of ventricular compliance. A more compliant ventricle will have lower pressures at higher volumes than a less compliant ventricle
The more complaint the ventricle the shallower the slope, whereas a stiff ventricle will have a steeper slope.
Phase b:
- Starts with the closing of the mitral valve (bottom right) and ends with the opening of the aortic valve when the LV pressure exceeds the aortic diastolic pressure.
- This isovolumetric contraction initiates systole in the cardiac cycle.
The LV contracts during this phase, however, does not involve a change in volume (i.e iso-volumetric), there is only a change in pressure. This “squeezing” and subsequent pressure change causes the aortic valve to open and blood to be ejected in the next phase.
Phase c:
- Begins with the opening of the aortic valve (top right)
- Ends with the closing of the aortic valve (top left) when the LV pressure drops below the the aortic systolic pressure.
- This is when LV ejection occurs (i.e. when ejection murmurs are heard; between S1 and S2)
During LV ejection, the LV volume decreases [1] and LV pressure increases [2] until it reaches peak LV systolic pressure.
As the LV relaxes (blood is fully ejected), the aortic valve closes and pressure drops. The LV end systolic pressure that can be generated at a given inotropic state at a given LV end systolic volume is defined as the end-systolic pressure-volume relationship (ESPVR).
The ESPVR curve can be generated by occluding the IVC (gold standard) or having a patient Valsalva, thus decreasing preload. As the preload drops, the PV loop shifts down and to the left. Decrease in preload decreases end systolic pressure and SV, causing a narrowing of the loop.
The curve created by plotting multiple PV loops during a preload or afterload change, connecting their end systolic points, is called the end-systolic pressure-volume relationship (ESPVR). The ESPVR slope is an indicator of contractility (⬆️ slope = more contractile ventricle).
Phase d:
- Begins with closing of the aortic valve (top left) and ends with opening of the mitral valve when the LA pressure exceeds the LV pressure.
- This phase represents isovolumetric relaxation (start of diastole), or relaxation of the LV without change in LV volume.
We hope this intro to PV loops helps create a firm foundation for a more advanced understanding of hemodynamics and the cardiac cycle.
Stay tuned for Part II (and beyond) to learn about afterload/preload, ventricular dysfunction, valvular disorders and much more!
I'm fully down the rabbit hole tonight - thinking about ventricular-arterial interactions in HF (HFrEF vs HFpEF). A quick thread (based off this 2012 JACC paper from Barry Borlaug and colleagues @MayoClinicCV)...
- Changes in BP & SV with Δ in ventricular loading are predictable based on ventricular-arterial coupling.
- BP ⬇️ while the SV ⬆️ with vasodilation; the extent of Δ is dictated by slope and intercept of the end-systolic pressure volume relationship: end-systolic elastance (Ees)
While elevated arterial afterload (Ea) is common to both forms of HF, the 2 entities differ dramatically in the “active” stiffness (contractility) developed by the heart at end systole, or Ees.
Part II of the Basics of PV loops: preload, coupling, afterload, ventricular dysfunction, and valvular disorders.
Big thanks to the team who helped put this together: @jayamj94 & @PSullivan000, with guest editor @RyanTedfordMD.
If you missed Part I, check it out ⬇️
- Preload is the stretching of cardiac myocytes prior to contraction (related to sarcomere length); it's measurable surrogate: ventricular end-diastolic pressure/volume.
- Δ in preload affect SV (width of PV loop), by the Frank-Starling mechanism. As preload ⬆️, SV (EDV-ESV) ⬆️.
When venous return to the heart is increased, the end-diastolic pressure and volume of the ventricles are increased, which stretches the sarcomeres, increasing their preload. In contrast, hypovolemia (i.e. hemorrhage) leads to less filling and shorter sarcomeres (reduced preload)
Patient admitted for a COPD exacerbation. You see the patient in the ED an hour after admission and look at tele and see this…what do you do next?
You examine the patient and realize they have cold extremities. Are you concerned about the patient?
You perform a bedside echo and see this… 1. What do we see here that confirmed the diagnosis from tele 2. What do we do next?
(Please answer in comments) twitter.com/i/web/status/1…
Q: Why do we use a stethoscope?
A: For many reasons, and here’s one of them that I will argue is undervalued. And is still at the heart (hint hint) of some ongoing research…
First described by Potain in 1880, the gallop rhythm refers to the presence and cadence of abnormal diastolic cardiac sounds, namely S3 and S4.
In 1989, Stevenson and Perloff described the previously unestablished relationship between physical exam signs, increased ventricular filling pressures, and decreased cardiac output in chronic HF patients. Stevenson et al. JAMA. 1989. jamanetwork.com/journals/jama/…
I actually stumbled across this while reading about something else (tweetorial pending, cc @DoctorVig), but I digress.
First, although this was a small study (69 patients), it elegantly used univariate/multivariate analysis to predict mortality. (I'm a big fan of regression)
If you look at the strong individual predictors - conduction delay, PCWP, vent. arrhythmia, RA pressure, Afib, EF%, S3, and LVEDP - only one of these metrics is free to measure. The rest require tests; with some being quite invasive.
1/ A few weeks ago while on service, I couldn't for the life of me remember the RCT evidence behind the use of beta-blockers in acute MI
According to the 2013 ACC/AHA STEMI guidelines it is a Class I recommendation (Level of Evidence: A) to start BB acutely, or within a few days
2/ Also, those with moderate or severe LV failure should receive beta-blocker therapy (Class I, Level of Evidence: B)
Furthermore the 2014 NSTEMI guidelines recommend starting BB within 24 hrs...
3/ ...assuming no signs of 1) HF, 2) low output state, 3) increased risk of cardiogenic shock, 4) other contraindications: PR interval >0.24 sec, any heart block without a pacemaker, active asthma, or reactive airway disease (Class I, Level of Evidence: A)