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Regulation of heart pumping (2018)
1. Dr. Amin Jan
Assistant Professor (Physiology)
NwSM, Peshawar Pakistan
Regulation of heart pumping…
2. At rest, heart pumps only 4-6 L of blood each minute
During strenuous exercise, heart may be required to
pump four to seven times this amount
Factors regulating cardiac output:
1. Intrinsic cardiac regulation of pumping in response to
changes in volume of blood flowing into the heart and
2. Control of heart rate and strength of heart pumping by
the autonomic nervous system
3. Potassium and calcium ions in the ECF
4. Temperature
5. Increasing the arterial pressure load
4. Under most conditions, cardiac output is normally
determined almost entirely by venous return
All the local tissue venous blood flows combine and return
to the right atrium, which the heart, in turn, automatically
pumps into the arteries to flow around the circuit again
This intrinsic ability of the heart to adapt to increasing
volumes of inflowing blood is called the Frank-Starling
mechanism of the heart
5. Frank-Starling mechanism means that the greater the heart
muscle is stretched during filling, the greater is the force of
contraction and the greater the quantity of blood pumped
into the aorta
OR
Within physiological limits,
the heart pumps all the
blood that returns to it by
way of the veins
6. Explanation …
When an extra amount of blood
flows into the ventricles, the
cardiac muscle is stretched to a
greater length, which in turn
causes the muscle to contract
with increased force because
the actin and myosin filaments are brought to a more
nearly optimal degree of overlap for force generation
Therefore, the ventricle, because of its ↑sed pumping,
automatically pumps the extra blood into the arteries
7. Still another factor increasing heart pumping when its
volume is increased, is the stretch of the right atrial
wall which directly ↑ses the HR by 10-20%, hence,
also ↑se the cardiac output
9. The pumping effectiveness of the heart is also controlled
by the sympathetic and parasympathetic (vagus) nerves,
which abundantly supply the heart
10. For given levels of atrial pressure,
• Cardiac output can be ↑sed
more than 100% by sympathetic
stimulation
• By contrast, the output can be
↓sed to almost zero by vagal
(parasympathetic) stimulation
12. Strong sympathetic stimulation can ↑se the heart rate from the
normal rate of 70 bpm up to 180-200 and, rarely, even 250 bpm
Sympathetic stimulation also ↑ses force of heart contraction to
as much as double the normal, thereby ↑sing the Stroke volume
Thus, sympathetic stimulation often can ↑se the maximum
cardiac output as much as twofold to threefold, in addition to
the increased output caused by the Frank-Starling mechanism
13. Conversely, inhibition of the sympathetic nerves to the heart
can ↓se cardiac pumping to a moderate extent
Under normal conditions, sympathetic nerve fibers to heart
discharge continuously at a slow rate that maintains pumping
at about 30% above that with no sympathetic stimulation
Hence, when the activity of the sympathetic nervous system
is depressed below normal, both the heart rate and strength
of ventricular muscle contraction decrease, thereby ↓sing
the level of cardiac pumping as much as 30 % below normal
15. Strong stimulation of parasympathetic nerve fibers in the vagus
nerves to the heart can stop the heartbeat for A FEW SECONDS,
but then the heart usually “escapes” & beats at a rate of 20-40
beats/min as long as the parasympathetic stimulation continues
In addition, strong vagal stimulation
can ↓se the strength of heart muscle contraction by 20 to 30 %
16. Vagal fibers are distributed mainly to the atria and not much to
the ventricles, where the power contraction of the heart occurs
That’s why vagal stimulation mainly ↓se the heart rate rather
than to ↓sing the strength of heart contraction greatly
Yet,
the great ↓se in heart rate combined with a slight ↓se in heart
contraction strength can ↓se ventricular pumping 50% or more
18. At any given right atrial pressure, the cardiac output
increases during increased sympathetic stimulation and
decreases during increased parasympathetic stimulation
These changes in output caused by ANS stimulation
result both from changes in heart rate and from
changes in contractile strength of the heart
21. Potassium ions have a marked effect on membrane
potentials, and calcium ions play an especially important
role in activating the muscle contractile process
Hence, it is to be expected that the concentrations of
each of these two ions in the extracellular fluids also
have important effects on cardiac pumping
22. Effect of Potassium Ions…
Excess potassium in the ECF causes the heart to become dilated
and flaccid and also slows the heart rate
Large quantities of K-ions also can block conduction of cardiac
impulse from the atria to the ventricles through the A-V bundle
Elevation of K-ions concentration to only two to three times the
normal value i.e.; 8-12 mEq/L can cause severe weakness of the
heart, abnormal rhythm, and death
23. These effects result partially from the fact that a high K-ions
concentration in the ECF ↓ses the RMP in the cardiac muscle
fibers, that is, high ECF K-concentration partially depolarizes the
cell membrane, causing membrane potential to be less negative
As the membrane potential decreases,
the intensity of the action potential also decreases, which
makes contraction of the heart progressively weaker
24. Effect of Calcium Ions…
Excess Ca-ions cause effects almost exactly opposite to those of
K-ions, causing the heart to move toward spastic contraction
Conversely, deficiency of Ca-ions causes cardiac weakness,
similar to the effect of high K-ions
25. Effect of temperature on heart function…
↑sed body temperature (e.g.; fever)
greatly ↑ses the HR, some-times to double the normal rate
↓sed temperature greatly ↓ses HR, which may fall to as low as
a few beats per minute
Presumably heat ↑ses the permeability of the cardiac muscle
membrane to ions that control HR, resulting in acceleration of
the self-excitation process
26. Contractile strength of the heart often is enhanced
temporarily by a moderate ↑se in temperature, e.g;
during body exercise, but prolonged elevation of
temperature exhausts the metabolic systems of the
heart and eventually causes weakness
Therefore, optimal function of the heart depends greatly
on proper control of body temperature by the temperature
control mechanisms
