Explore the heart's fascinating properties: contractility, heart rate regulation, conduction velocity, and cell excitability. Delve into the mechanics of cardiac muscle and the Frank-Starling law, unraveling the interplay between stroke volume and end-diastolic volume.
Discover volume-pressure r...
Cardiac output, contractility, volumes, failure
Four main properties of the heart are discussed in physiology:
1. inotropy (ino → force) = contractility of the ventricular myocardium (can be regulated!)
2. chronotropy (chronos → time) = heart frequency (can be regulated!)
3. dromotropy (dromo → run) = conduction velocity across the AV-node (can be regulated, and will
determine the delay between atrial and ventricular activation / contraction)
4. bathmotropy (bathmos → step, like in
threshold) = cell excitability (can be regulated!)
Here, we shall discuss the contractility (inotropy).
Like skeletal muscle, the cardiac myocytes have a
“preferential length”, i.e. a length at which the
superposition of actin and myosin filament is optimal,
and the fiber is sufficiently long to avoid intracellular
overcrowding and steric hindrance.
• If the sarcomere is too short, there’s going to be
myosin-actin interference, which will reduce the
ability to produce force.
• If the sarcomere is too wide, actin and myosin
don’t interact with each other, and this will
reduce the ability to produce force.
The Frank-Starling law states describes the relationship between the stroke volume SV
and the end-diastolic volume EDV. It states that the stroke volume (of the left ventricle) will
increase in response to an increase of the left ventricular volume (before contraction, EDV), when all the
factors remain constant, due to the myocytes’ stretch that causes a more forceful systolic contraction.
Volume-pressure relations
So, a three length-force – in this case a volume-pressure – relations can be depicted, like in skeletal
muscle:
• a passive volume-pressure relation: enlarging the volume of the ventricle produces an
increasing pressure, simply due to the passive resistance and elasticity of the wall;
• a purely active volume-pressure relation: changing the volume, the fiber length changes,
and the force (and pressure) produced by the ventricular muscle increases, up to a certain length,
while it decreases beyond that length; - Starling force
• a compound volume-pressure curve that depicts the pressure the ventricle produces when
contracting at different volumes; this is the sum of the two previous curves (the “passive” and
the “purely active” one) and represents the maximum pressure that we can observe in the
ventricle for each possible value of ventricular volume – the compound curve.
The active curve is also called a “Starling” curve. Differently with respect to normal skeletal muscle
(i.e. not the heart), several distinct Starling curves can be drawn for different states (contractility) of the
heart muscle, as the contractility can be affected by any mechanism that modifies calcium movements
and levels, or by drugs that affect the actin-myosin interaction. (ESP)
The “passive” curve can be defined as the “preload” curve, as it represents the situation before the
ventricle contracts: at this time, the volume of the ventricle (end-diastolic volume, EDV) is determined
by the pressure that fills the ventricle (central venous pressure, CVP) + the volume contributed by atrial contraction;
thus, the EDV is a function of CVP and “preload” will also indicate the load that impinges on the heart
from upstream, “before”; the pressure (EDP) will be the value that corresponds to such volume on the
preload curve.
The compound curve can be defined as the “afterload” curve, as it represents the maximum
pressure (load) that the heart can face, at any value of volume; this curve determines the arterial pressure
that the ventricle can produce (downstream, “after”).
53 Body At Work II
, Enrico Tiepolo
Two important observations need to be done on this:
- we shall never observe a pair of values (volume-pressure) (developed tension) that lies outside
the area comprised between the “passive” (preload) and the compound (afterload) curves,
because the ventricle cannot produce less pressure than is generated elastically by the imposed
volume and cannot produce more pressure than can be generated by the passive elastic tension
plus the maximal active contractile force;
- ejection of blood will necessarily stop when the volume (end systolic volume, ESV) reaches
the volume that corresponds to arterial systolic pressure in the compound curve (ASP = ESP,
ejection of blood stops).
The heart at rest doesn’t operate in the range in which it produces maximal force (has maximal
contractility). If we fill the heart a bit more, it will operate better.
The contractility (inotropy) of the heart depends on:
1. Its preload, meaning how stretched the heart is before starting the contraction (its EDV).
2. The level of sympathetic stimulation to which the heart is subject to.
In the striated muscles the stimulation doesn’t change the amount of calcium released from the
ECM into the muscle cell: an AP triggers the release of Ca2+ from the ER. The contraction
force can be increased by increasing the number of APs in a second.
In the heart it works differently. The amount of calcium that enters from outside
actually regulates the contraction of force of the muscle cell. If you increase the
amount of calcium that enters in each contraction, during the successive contractions calcium
will accumulate inside the muscle cell (because it cannot be completely depleted) and inside its
ER and therefore the contractility of the muscle cells increases.
When the heart is stimulated by the sympathetic system à &-receptors are activated à Gs protein à
Adenylyl cyclase à cAMP à PKA à phospholamban is phosphorylated and its ability to inhibit SERCA
is reduced à SERCA is more activated à more Ca2+ is stored in the ER.
Two things must be kept in mind: Ca2+ is dangerous for the cells, therefore I want to fill the ER and
not accumulate Ca2+ in the cytoplasm, otherwise it would cause apoptosis of the cell; finally, we must
remember that by increasing the contractility of the heart we are reducing its efficiency, as
it will consume more O2 (like a car that goes at 90 Km/h or at 120 Km/h. The car that goes at 120
Km/h will get to destination faster, but will consume more gas).
54 Body At Work II
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