CPPS 302 Effect of afterload and contractility on stroke volume

Define afterload

Defined as the ventricular wall tension (stress) developed during ventricular ejection (systole)

• the resistance or pressure the heart’s ventricles must overcome to eject blood into the body’s arteries during contraction

What determines the magnitude of ventricular wall tension (afterload)?

The resistance, impedance, or pressure that the ventricle must overcome before blood can be ejected

• ↑ Resistance/pressure → ↑ afterload

• The ventricle must generate greater pressure to eject blood

What is the major component of afterload for the left ventricle?

Aortic blood pressure, particularly aortic diastolic pressure, which the left ventricle must overcome to open the aortic valve and begin ejecting blood

How can ventricular wall stress (afterload) be estimated using LaPlace’s Law

σ = (p)(r) / 2h

• σ = ventricular wall stress

• p = intraventricular pressure

• r = ventricular chamber radius

• h = ventricular wall thickness

Acccording to LaPlace’s law, how do changes in pressure, ventricular radius, and wall thickness affect wall stress (afterload)?

• ↑ Pressure → ↑ wall stress (e.g. hypertension)

• ↑ Ventricular radius → ↑ wall stress (increased preload)

• ↑ Wall thickness → ↓ Wall stress (e.g., left ventricular hypertrophy)

Why does ventricular hypertrophy (thickening of wall thickness) develop as an adaptive mechainism to increased afterload?

↑ Afterload → ↑ wall stress → ↑ wall thickness (hypertrophy) → ↓ Wall stress

• Common causes: hypertension and aortic stenosis (thickening of aorta)

How does left ventricular dysfunction in heart failure lead to increased preload

Decreased contractile funciton causes inadequate ventricular emptying

• ↓ contractile function → ↑ LVESV (more blood remains after systole)

• Remaining blood + incoming venous return leads to ↑ EDV (secondary increase in prelaod)

Analogy: imagine a weak water pump that cannot empty completely for every pump, water left behind would ocmbine with incoming water during the next cycle, causing the pump to become increasingly full

Why does the Frank-Starling mechanism fail to adequetly compensate in heart failure, potentially leading to cardiomegaly

Because the heart has decreased contractile function, increasing preload produces an insufficient increase in stroke volume

• ↑ preload cannot adequately compensate for ↓ contractility

• Blood accumulates in the ventricle, contributing to enlargment of the heart

Analogy: adding more water to a weak pump doesn’t fix its inability to pump effectively. iNstead, water continues accumulating causing the chamber to stretch and enlarge over time

How does increased afterload affect the Frank-Starling curve?

Increased afterload shifts the Frank-starling curve downward and to the right

• with the same preload → ↓ SV

• To maintain the same SV → greater filling pressure(LVEDP) is needed

Like pushing an empty cart vs a full cart, you need greater pressure / effort to move the cart at the same speed

Why does increased afterload shift the Frank-Starling curve downward and to the right

Because the ventricle must generate greater pressure to overcome the increased afterload before ejecting blood

This makes ventricular ejection more difficult, reducing SV at a given preload

What is the relaitonship between afterload and the velocity of ventircular muscle fibre shortening

They have an inverse relationship

↑ Afterload → ↓ Velocity of fibre shortening → ↓ SV

Analogy: lifting a light vs heavy dumbell, lighter dumbell has less resistance → easier and faster for the muscle to shorten vs a heavier dumbell

Why does increased afterload decrease stroke volume

Increased afterload makes ventricular ejection more difficult, decreasing the velocity of muscle fibre shortening and resulting in less blood being ejected per contraction

What is Vmax in cardiology, and where is it located on the force-velocty relationship curve

Vmax is the maximum velocity of muscle fibre shortening when afterload is 0

It is represented by the Y intercept of the force-velocity curve

Why is Vmax considered an extrapolated value, and what does it indicate?

Vmax is extrapolated because shortening velocity cannot be directly measured under a true zero-load condition in this model

What does the x intercept represent on the force - velocity relationship curve

The maximum force the heart can generate at a given prelod, when muscle shortening velocity reaches zero

How does increasing preload affect the force-velocity relationship at a constant inotropic state?

Increasing preload (a→c):

• ↑ maximum force generated (X-intercept shifts right)

• Vmax remains unchanged (same Y intercept

• Intrinsic myocardial contractility remains unchanged

How does increased afterload affect the ventricular pressure-volume loop?

Increased afterload produces a taller and narrower PV loop

• ↑ ventricular pressure (greater pressure needed for ejection)

• ↑ ESV (more blood remains due to inadequate ventricular emptying)

• ↑ EDV (secondary increase in preload, LEFT over ESV + venours return)

• ↓ SV (less blood is pumped out because increased aortic pressure makes ventricular ejection more difficult)

Why does increased afterload cause ESV to increase and SV to decrease?

Increased afterload (e.g., ↑ aortic pressure) requires the ventricle to generate greater pressure to open the aortic valve

• ↑ afterload → ↓ velocity of ventricular ejection → ↓ SV

• ↑ ESV because more blood remans after systole due to inadequate ventricular emptying against the increased aortic pressure

Why does increased afterload cause a secondary increase in preload (EDV)?

↑ Afterload → ↑ ESV (more blood remains after systole becuase the ventricle cannot eject as much blood against the increased aortic pressure)

During the next diastole, the leftover blood combines with incoming venous return

↑ ESV + venous return → ↑ EDV (preload)

Why does SV decrease despite the secondary increase in EDV caused by increased afterload

Because the increase in ESV is greater than the increase in EDV (SV = EDV - ESV)

• ↑ ESV = more blood remains due to inadequate ventricular emptying against increased afterload.

• ↑ EDV = leftover blood combines with incoming venous return

• Since SV = EDV - ESV, the difference becomes smaller, resulting in ↓ SV

What is myocardial contractility (inotropic state)

The intrinsic ability of cardiac myocytes to generate force during contraciton, determined by cellular mechanisms regulating actin-myosin interactions

• Independent of changes in preload and afterload

  • ↑ Contractility → ↑ SV → ↑ Cardiac output

What distinguishes increased myocardial contractility from increased force due to preload

• ↑ PRELOAD: ↑ myocyte stretching → ↑ developed force, without changing intrinsic contractility

• ↑ Contractility: ↑ intrinsic force-generating ability of myocytes, independent of changes in preload or afterload

How does inadequate systolic emptying lead to increased ventricular end diaastolic pressure

↓ Systolic emptying → ↑ ESV (more blood remains after systole) → ↑ EDV (leftover blood + venous return) → ↑ EDP

How does ventricular compliance affect EDP when EDV increases

Hypertrophic heart: ↓ compliance (stiffer walls) → small ↑ EDV causes a large ↑ EDP because the ventricle resists stretching

Dilated heart: ↑ compliance (easier to stretch) → smaller ↑ EDV causes a smaller ↑ EDP because the ventricel accommodates more blood with less pressure increase

How does increased myocardial contractility affect the Frank-Starling curve

Increased contractility shifts the Frank-Starling curve upward

• At a given preload (EDV/EDP) → ↑ SV

• At a given SV → lower preload (EDV/EDP) is required

• Example: Epinephrine (Positive inotropic effect)

How can Frank-Starling curves be used to approximate ventricular contracitlty

Compare stroke volume at the same preload

• higher SV: greater contractility

• Lower SV: reduced contractility

How does heart failure affect the Frank-Starling relationship between preload and SV?

Decreased contractility shits the Frank-Starling curve downward

• at a given SV → higher EDV/EDP is required (because the weakened heart cannot eject blood as effectively, so it requires greater ventricular filling and stretching to achieve the same SV)

• ↑ preload produces only a small ↑ SV, especially in advanced heart failure

• The Frank-Starling mechanism cannot adequately compensate for impaired contractility

Why can a small increase in EDV cause a large increase in EDP in concentric ventricular hypertrophy?

Concentric hypertrophy increases ventricular wall thickness and reduces ventricular compliance.

• ↓ Compliance → Greater resistance to ventricular filling.

  • Small ↑ EDV → Large ↑ EDP compared with a normal heart

What is cardiac index (CI), and how does is it calculated

Cardiac index measures cardiac output relative to body surface area and is used to evalute overall cardiac performance

• CI = CO/ BSA

  • CO = cardiac output

  • BSA = Body surface area

What is ejection fraction (EF), and how is it calculated?

Ejection fraction is the percentage of end diastolic volume (EDV) ejected from the ventricle during each systolic contraction

EF = (SV / EDV) x 100%

• Normal EF is usually greater than 55%

How do changes in myocardial contractility and afterload affect ejection fraction (EF)?

↑ contractility → ↑ EF (the ventricle ejects more blood, increasing SV relative to EDV)

↑ afterload →↓ EF (increased aortic pressure makes ventricular ejection more difficult, decreasing SV relative to EDV)

What is peak + dP/dT during isovolumic contraction, and what does it indicate?

The fastest rate wt which pressure increases inside the ventricle during isovolumic contraction (Δpressure/Δtime).

• ↑ CONTRACTILE FORCE → steeper pressure slope → ↑ peak +dP/dT

• Usually occurs just before the opening of the semiluminar valves

In the peak +dP/dT what is the relationship between slope and contraction

Stronger contraction = steeper the slope

Why is peak +dP/dT nota true independent indicator of myocardial contractility?

Because peak +dP/dT influenced by several factors

• Myocardial contractility

• Preload and afterload (loading conditions)

• Heart rate (Treppe/Bowditch effect)

Therefore, changes in +dP/dT do not necessarily reflect changes in intrinsic contractility alone

Where does the highest +dP/dT usually occur

Moments BEFORE the opening of the semilunar valves

What is the Treppe (staircase) phenomenon or Bowditch effect?

The Treppe (Bowditch) effect occurs when an increase in heart rate causes the heart to contract more strongly with each successive beat

• ↑ HR → ↑ Intracellular Ca²⁺ → ↑ Myocardial contractility

How does increased heart rate lead to increased myocardial contractility according to the Bowditch effect?

• ↑ Heart Rate → less time for Na/K pump to restore ionic concentrations

• ↑ Intracellular Na accumulation → ↓ Na+/Ca exchanger-mediated Ca removal

• ↑ Intracellular Ca → More Ca binds to troponin C → ↑ actin-myosin interaction → ↑ force contraction → ↑ Myocardial contractility

What are the functions of the Na/K ATPase and Na/Ca exchanger in cardiac myocytes

Na/K ATPase: Pumps 3 Na out and 2 K in, maintaining ionic gradients

Na//Ca exchanger: Normally moves 3 Na in and 1 Ca out, helping remove intracellular calcium

What is the end-systolic pressure-volume relationship (ESPVR), and what does its slope indicate

A ESPVR describes the relationship between ventricular pressure and volume at the end of a systole

• Its slope is an indicator of myocardial contractility

• Steeper slope = greater contractility

• Flatter slope = reduced contractility

How does increased myocardial contractility affect the ESPVR and ventricular pressure-volume loop

Increased contractility shifts the ESPVR upward and to the left, with a steeper slope

• ↑ force of contraction (ventricle ejects more blood effectively)

• ↓ ESV (less blood remains after systole because more blood is ejected)

• ↑ SV (more blood is pumped out because ESV decreases while EDV remains unchaged).

What is Vmax, and why is it considered an indicator of myocardial contractility

Vmax is the theoretical maximum velocity of cardiac muscle shortening when afterload is zero

• It reflects the intrinsic contractile ability of cardiac muslce

• It cannot be measured directly and must be extrapolated from the force velocity curve

How does increased myocardial contractility affect the force-velocity curve

Increased contractility shifts the force-velocity curve upward and to the right

• ↑ Vmax (muscle fibres can shorten faster)

• ↑ Maximum foce (muscle fibres can generate greater tension)

Vmax C > B > A

How does increasing preload differ form increasing contractility on the force velocity curve

• ↑ Preload: ↑ Maximum force, but Vmax remains unchanged

• ↑ Contractility: ↑ Maximum force AND ↑ Vma