CPPS 302 Afterload and Contractility

Flashcards defining key cardiovascular terms related to afterload, contractility, and their effects on stroke volume, including relevant laws and physiological phenomena.

Afterload

The ventricular wall tension (stress) developed during ventricular ejection (systole), or the load against which the heart must counteract (diastolic pressure) before blood can be ejected out.

Which area of the heart contains the highest pressure that isovolumic contraction must overcome at the beginning of systole?

the aorta

Laplace's Law related to Afterload

Estimates ventricular wall stress (σ) as proportional to (p • r) / 2h, where p is intra-ventricular pressure, r is ventricular radius, and h is ventricular wall thickness.

Impact of Increased Ventricular Wall Thickness on Afterload

Reduces wall stress (σ) and therefore reduces afterload.

Ventricular Hypertrophy as an adaptive mechanism

A chronic increase in afterload can lead to increased ventricular hypertrophy in order to offset the increase in wall stress caused by an increased afterload; typically caused by aortic stenosis or hypertension

Effect of Increased Afterload on Muscle Fiber Shortening

Decreases the velocity of fiber shortening during contraction, resulting in a decrease in stroke volume and force of contraction.

Vmax (Maximum Velocity)

An extrapolated value for the maximum velocity that can be achieved by a muscle fiber in the absence of any load, serving as an indicator for the inotropic condition of a contractile muscle.

Impact of Increased Afterload on Pressure-Volume Loops

Results in a small elevation of EDV, a much larger elevation of ESV, decreased ejection velocity, and a decrease in stroke volume (SV) overall, as the ventricle must generate higher pressure to open the aortic valve.

Contractility (Inotropic State)

The contractile capability or force development of the heart, independent of preload and afterload (sarcomere length); a true indicator of inotropic influence related to intrinsic cellular mechanisms regulating actin-myosin interaction.

Cardiac Index (CI)

Cardiac output (CO) divided by body surface area (BSA); an increase in contractility will increase cardiac output, therefore generating a higher CI.

Ejection Fraction (EF)

The fraction of end-diastolic volume ejected from the ventricle during each systolic contraction (EF = SV / EDV); normal EF is usually greater than 55%

Treppe phenomenon (Bowditch effect)

A series of successively stronger contractions observed when muscle fibers receive closely spaced stimuli (twitch summation, e.g., due to increased heart rate), leading to increased Ca++ accumulation in the cytosol and enhanced myocardial contractility.

End-Systolic Pressure-Volume Relationship (ESPVR)

The true indicator of contractility at a given inotropic state; any increase in inotropy (contractility) shifts the ESPVR upwards to the left with a steeper slope.

Why does congestive heart failure lead to a decrease in stroke volume?

Because congestive heart failure is often induced by increased afterload, and the left ventricular dysfunction leads to an increase in LVESV, resulting in a secondary increase in preload and a decrease in the velocity of muscle fiber shortening. All together, this leads to a decrease in stroke volume

If both EDV and ESV are increasing when afterload increases, why would stroke volume still be decreasing?

because the increase in ESV is larger than the increase in EDV

How does increased contractility cause a greater change in stroke volume compared to a normal heart at a given preload?

A heart with a higher contractility will result in a lower EDP/EDV and a higher stroke volume, predicted by the Frank-Starling law

Why does an increase in preload in a failing heart have little change on stroke volume?

In a failing heart, increased preload does not significantly improve stroke volume because the heart is already operating on a flattened portion of the Frank-Starling curve, where further stretching does not enhance stroke volume. This is a direct consequence of low ventricular compliance in something like a concentric hypertrophic heart

Cardiac Index (CI)

measures overall cardiac performance, defined as cardiac output (CO) divided by body surface area (BSA)

Why is cardiac index an indirect measurement of contractility?

Since increased contractility increases SV (or CO) at a given preload, it will also generate a higher cardiac index

Ejection Fraction (EF)

the fraction of end-diastolic volume ejected from the ventricle during each systolic contraction; defined as SV/EDV; normally the ejection fraction is over 55%

During isovolumic contraction, if a steeper slope is observed indicating a faster rate of pressure development, what does that say about the heart’s physiology?

In between the mitral valve closing and the semilunar valve opening, a higher force of contraction is generated indicating increased contractility due to the Treppe phenomenon/Bowditch effect

In the Treppe phenomenon/Bowditch effect, what is the stimulus that leads to increased contractility?

a higher heart rate

What channels are influenced, and how are they influenced, when the heart’s rate increases?

The Na+-K+-ATPase has less time to restore ionic concentrations, leading to more Na+ in the cytosolic space.

This inhibits the Na+-Ca2+ exchanger, as well as this exchanger having less time to remove Ca2+ from the cytosolic space, leading to more Ca2+ in the cytosolic space.

increased [Ca2+] leads to higher myocardial contractility because Ca2+ doesn’t detach from Troponin C (TnC) and cross-bridge cycling continues, leading to twitch summation

What are the two true indicators of contractility?

The end-systolic pressure-volume relationship (LVESPVR) and changes to Vmax

How does increased contractility effect the LVESPVR?

The slope of LVESPVR becomes steeper, this drastically decreases ESV, decreases EDV, and increases venous return, which increases stroke volume as well as the ejection fraction

Why is Vmax an indicator of contractility?

Because with increased inotropy, Vmax also increases, a regular increase in preload doesn’t have any effect on Vmax, so if Vmax changes you know that contractility must be changing too

Does an increased contractility imply increased tension development? Why?

Yes, this can be observed using Vmax as an indicator, increased contractility increases tension development because higher nervous stimulation results in greater Ca2+ availability and stronger coupling of actin and myosin.