1. Atrial systole
Before the atria begin to contract, the heart is in full diastole, the pressure in the atrium and
the ventricular valve is open; Venous blood flows through the atrium into the ventricles, the
atria and ventricles are gradually filled, and the internal pressure gradually increases;
However, the intraventricular pressure is much lower than the aortic pressure, the semilunar
valve is closed, and the ventricular cavity is not connected to the aortic cavity. When the atria
begin to contract, the volume shrinks, and the internal pressure increases, blood is squeezed
into the ventricles, which fill up to 30% and contract as primary pumps. Atrial contractions last
for 0.1 seconds and then enter diastole, at which point the ventricles begin to contract.
2. Ventricular systole (isovolumetric systole, rapid ejection, slowed ejection)
Stage 1: Isochoric systole
After atrial diastosis, the ventricles begin to contract, the intraventricular pressure is sharply ↑ and
exceeds the intraatrial pressure, which is less than the aortic pressure (left ventricular pressure ↑
nearly 80mmHg), the atrioventricular valve is closed (the valve is still closed), and the
intraventricular blood volume remains unchanged, that is, the ventricular volume or the length of
the ventricular muscle fibers remains unchanged, which is called isovolumetric systole.
Characteristics: Ventricular volume is constant,
and intraventricular pressure increases rapidly
and dramatically for 0.05 seconds. Stage 2:
Rapid ejection phase
The ventricles continue to contract, the pressure rises sharply, and exceeds the aortic pressure
(80 mmHg > the left ventricle, 8 mmHg > the right ventricle), the semilunar valve opens, (the
atrioventricular valve is still closed), blood rushes into the aorta (70% of the ejection volume),
and the ventricular volume is rapidly ↓ called the rapid ejection phase. During this phase, the
ventricular volume shrinks markedly and then continues to rise intraventricular for 0.1 seconds.
Peculi
arity:
(1)
Intraventricular pressure and aortic pressure were the highest at the end of rapid ejection
(2) The amount of blood injected into the aorta from the ventricles is large (about 2/3 of the total
ejection volume) and (3) the flow rate is fast and takes little time (1/3 of the ≈systole).
Stage 3: Slowing down the ejection phase
As the volume of blood in the ventricles decreases and the contractility of the ventricular
muscles decreases, the intraventricular pressure begins to drop and the ejection rate slows
down (ejection energy = kinetic energy of the blood, which accounts for 30% of the ejection
volume), which is called the slowing ejection phase.
Features: (1) Time (2/3 of ≈ systole), low ejection volume; (2) The ventricular volume is further reduced
to the minimum of the ejection phase and lasts for 0.15s. (3) Due to peripheral blood
The resistance of the canal, the kinetic energy of the blood in the aorta is transformed into pressure
energy, so that the arterial pressure is slightly > the intraventricular pressure
3. Ventricular diastolic phase (isovolumetric diastole, rapid filling, slowing filling)
Stage 1: Isovolumetric diastole
When the ventricles begin to relax, intraventricular pressure drops rapidly (intraventricular pressure =
arterial pressure) and the aerial valve closes; The ventricles continue to relax, and the intraventricular
pressure drops rapidly (below actively
pulse pressure, higher than intraatrial pressure), the half-moon valve and atrioventricular valve are still
closed, the ventricular volume remains unchanged, and the blood does not flow, weighed
It is isovolumetric diastole.
Features: (1) The ventricular volume remains unchanged, and the internal pressure
decreases rapidly and sharply, lasting for 0.06s~0.08s. (2) The atrioventricular valve
and atrioventricular valve are closed, and (3) the atrioventricular valve closes to
produce a second heart sound
Stage 2: Rapid Filling Period
At the end of isovolumetric diastole, the intraventricular pressure ↓, when the pressure is lower
than the intraatrial pressure, the atrioventricular valve opens, the ventricles continue to diastolic
the intraventricular pressure↓, and a large amount of blood flows rapidly into the ventricles in the
atrium and large V, which is called the rapid filling phase. It takes 0.11 seconds and flows about
2/3 of the total blood into the ventricles.
Features: Lowest room pressure at the end of the fast filling period.
Stage 3: Slowing down the filling phase
As the ventricles are filled with blood, the pressure difference between the ventricles and the atria
and the greater V decreases, the intraventricular pressure rises, and the blood in the atrium flows
more slowly into the ventricles (the first half of the blood flows into the ventricles through the atrium;
The second half is the squeezing of blood into the ventricles during atrial systole. ) is called the
slowing down of the filling phase. Lasts 0.22s.
The ventricular volume then expands further and then enters another cycle of atrial contraction. In
general, blood fills the ventricles mainly by intraventricular pressure during palpation
Reduces the resulting suction effect.
1. Primary pumping function of the atrium:
(1) Diastole: blood flows directly into the ventricles from the large veins through the atrium
(2) Atrial contraction: The pressure in the atrium increases, and the atrioventricular valve is open,
and the atria further squeezes the blood into the ventricle
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(3) Atrial diastole: The intraatrial pressure drops back and the ventricles begin to contract
2. The process of ejection and filling of the left ventricle
(1) Ventricular systole: A. Isovolumetric systole: after atrial diastosis, the ventricle begins to
contract, the intraventricular pressure rises and exceeds the
intraatrial pressure, less than the aortic pressure, the semilunar
valve and the atrioventricular valve are closed, the ventricular
muscle contracts, and the intraventricular pressure rises sharply,
but the ventricular volume remains unchanged, and the
intraventricular blood volume remains unchanged. It is
characterized by a constant ventricular volume and a rapid and
substantial increase in intraventricular pressure for 0.05 seconds.
B. Rapid ejection phase: the ventricles continue to contract, the pressure rises
sharply, and exceeds the aortic pressure, the semilunar valve
opens, and blood rushes into the aorta. It is characterized by
ventricular injection into the aorta with approximately 2/3 of the
total ejection volume, rapid flow rate, marked reduction of
ventricular volume, and continued increase in intraventricular
pressure for 0.1 seconds.
C. Slowing down the ejection phase: As the intraventricular blood volume
decreases and the ventricular muscle contractility weakens, the
intraventricular pressure begins to drop and the ejection rate
slows down, which is called the slowed ejection phase.
VENTRICULAR VOLUME IS FURTHER REDUCED TO THE MINIMUM
OF THE EJECTION PHASE FOR 0.15S. Intraventricular and aortic
pressures decrease from peaks.
(2) Ventricular diastole: A. Isovolumetric diastole: When the ventricle begins to relax, the
ventricular pressure drops rapidly, lower than the aortic pressure,
higher than the atrial pressure, the semilunar valve and the
atrioventricular valve are closed, and the ventricular volume
does not change, which is called isovolic diastole. It is
characterized by a constant ventricular volume and a rapid and
substantial decrease in ventricular pressure for 0.06 to 0.08
seconds.
B. Ventricular filling phase: a. Rapid filling phase: the ventricles continue to relax,
when the pressure is lower than the atrial pressure,
the atrioventricular valve opens, the ventricular
volume increases, and a large amount of blood in the
atrium flows rapidly into the ventricle, which is called
the rapid filling phase, which accounts for 0.11S, and
the amount of blood flowing into the ventricles is
about 2/3 of the total blood volume.
b. Slowing the filling phase: The ventricular volume increases
significantly, the pressure rises, and the blood in
the atria flows more slowly into the ventricles,
called the slowing filling phase, which lasts for
0.22 seconds, and the ventricular volume is
further expanded, followed by atrial contraction
into another cardiac cycle.
c. Atrial systole: intraatrial pressure rises, and blood in the atrium
squeezes into the ventricles.
Left ventricular pumping mechanism: contraction and relaxation of the ventricles are the
underlying cause of the pressure gradient between the atria and ventricles and between the
ventricles and the aorta; The pressure gradient is the main driving force for the opening and
closing of the valve and the flow of blood between the corresponding chambers, while the
opening and closing of the valve guarantees the unidirectional flow of blood.
Heart sounds: are sounds produced by vibrations caused by the closure of heart valves and the
impact of blood against the walls of the ventricles.
Cardiogram: A graph obtained when mechanical vibrations are converted into electrical signals.
First heart sound: occurs at the beginning of systole and is a sign that the ventricles have begun to
contract, also known as a contraction. "Pounce", the sound is low and lasts for a long time.
Significance: It mainly reflects the contractility of myocardium and the function of the
atrioventricular valve.
Second heart sound: occurs at the beginning of diastolic and is a sign that the ventricles begin to
relax, also known as diastolic sounds. "Tong", the sound is high, the duration is short.
Significance: It mainly reflects the level of arterial blood pressure and the function of the
semilunar valve.
Evaluation of cardiac pumping function:
(1) Stroke volume: the amount of blood ejected from one ventricle
of the heart every beat. The amount of blood ejected from
one ventricle in one heartbeat is called stroke volume, or
stroke volume for short. Stroke volume, which is equal to
ventricular end-diastolic volume minus end-systolic volume, is
the most basic measure of the heart's pumping function.
(2) Output per minute: refers to the amount of blood ejaculated from one
ventricle per minute, also known as cardiac output. Cardiac output is equal to
stroke volume vs
The product of heart rate. Minute output = stroke volume ×
heart rate = 5~6L/min
(3) Ejection fraction: the percentage of output per body in the volume of
the end-diastolic phase. The stroke volume as a percentage of ventricular end-
diastolic volume is called
is the ejection fraction.
Significance:
(1) End-diastolic volume is related to cardiac contractility (because it is
positively correlated with the initial length of myocardium)
(2) Cardiac contraction ↑→ stroke volume ↑→ ejection fraction ↑
15
(3) Ventricular enlargement, decreased cardiac function (stroke volume can
be unchanged), → end-diastolic volume ↑→ ejection fraction↓
(4) Cardiac index: In the case of resting and fasting, the
cardiac output per unit body surface area of the
animal is called the cardiac index. Meaning: To
evaluate the cardiac function of different
individuals
(5) The amount of work done by the
heart: the work done by the
ventricles for each contraction is
called the work of each stroke. Stroke
work = stroke volume * (mean
arterial pressure - mean atrial
pressure) per cent of work =
stroke work * heart rate
The right ventricle does only 1/6 the work of the left ventricle
With the same stroke volume, the strength of myocardial contraction and the amount of work will
increase as the arterial blood pressure increases.
Regulation of cardiac pumping function (factors affecting cardiac output):
(1) Preload (heterometric self-adjustment)
The load that the myocardium encounters before contraction is called the preload of the
myocardium. It can be expressed as the degree of filling (volume) of blood at the end of ventricular
diastole. It reflects the ventricular muscle
The initial length before contraction.
Within a certain range, venous return ↑→ ventricular filling ↑→ initial length of myocardial fibers ↑→
myocardial contractility ↑→ stroke volume and cardiac output ↑
The change in myocardial contraction strength caused by the change of the initial length of the
myocardial cell itself is called heterometric autoregulation.
Significance: Capable of fine adjustment of stroke volume
(2) Isometric self-regulation = myocardial contractility
Refers to the ability to affect stroke volume by changes in the intensity and speed of myocardial
contractile activity without relying on changes in pre- and postload (ejection fraction
number). This mechanism of regulating
stroke volume is also known as isometric
autoregulation. Significance: It can have a
strong regulatory effect on continuous,
drastic cyclic changes.
(3) Afterload (influence of peripheral resistance)
It refers to the load that the myocardium encounters when it contracts, and is called the afterload of
the myocardium. Ventricular afterload refers to arterial blood pressure, so it is also called stress load.
The increase of aortic blood pressure→ the increase of cardiac ejection resistance, the
decrease of stroke volume→ the increase of end-diastolic volume→ the increase of
cardiac contraction→ the return of normal stroke blood volume, the contraction and
relaxation of blood vessels are regulated by the body's nerves and body fluids, so that
they are compatible with the metabolic level of the tissue.
Conclusion: Cardiac output is always adapted to the metabolic level of the body.
(4) Heart rate
Heart rate ×stroke volume = minute output
Within a certain range (40~150 beats/min), heart rate ↑ → output per distraction ↑
>150 beats/minute→ shortened cardiac cycle (especially during the diastolic period→), filling volume
↓→ stroke volume ↓→ output per distraction ↓
<40 beats per minute→ prolonged cardiac cycle (especially during the diastolic period), → filling
capacity is at its limit and the heart rate is too slow→ output per distraction↓
Cardiac output depends on stroke volume and heart rate.
1. Regulation of stroke volume: Under the condition that the heart rate remains unchanged, the
stroke volume is affected by the preload of the myocardium (the initial length of the muscle) and the
contraction ability of the muscle itself
Effect of afterload.
(1) Myocardial preload: the load on the ventricle before contraction. It is usually expressed in
terms of end-diastolic volume or ventricular filling volume.
Ventricular end-diastolic volume = venous return flow + remaining blood volume
after ventricular ejection
The greater the amount of venous blood in the heart, the longer the volume of
ventricular end-diastolic and the initial length of myocardium, the stronger the
myocardial contractility, and the greater the beating work.
Factors affecting venous return to the heart: Ventricular diastolic time:
inversely proportional to heart rate
Venous return velocity: depends on the difference
between the peripheral venous pressure and the
atria and ventricles.
(2) Contractility of myocardium: refers to an intrinsic characteristic of myocardium that can
change its mechanical activity without relying on the front and rear loads.
Factors affecting myocardial contractility: a. Autonomic nerves (sympathetic,
parasympathetic)
b. Multiple humoral factors (catecholamines)
16
c. Cytoplasmic Ca2+ concentration during excitation
d. Activity of ATPase
The way in which stroke volume is regulated by altering myocardial contractility is called isometric
automodulation, and this change is independent of the initial length of the myocardium before
contraction.
Heterometric autoregulation: A change in the contractility of myocardium caused by a change in
the length of the myocardial cell itself is called heterometric autoregulation.
Significance: Through the self-regulation of heterolengthy, the heart can pump out the increased
blood return to the heart in time, so as not to cause excessive blood flow to be retained in the heart
chambers, so as to maintain the venous blood volume to the heart
and cardiac output.
(3) The effect of afterload on stroke volume
Afterload – arterial blood pressure (relative to ventricles)
The peak intratricular pressure during isovolumetric systole increases with increased afterload,
the ejection phase shortens, the degree and speed of ventricular muscle shortening decreases,
and the stroke volume temporarily decreases the heart
The remaining blood volume in the ventricle increases, and if the return blood volume
remains unchanged, the volume of the end-diastolic phase increases, and the stroke
volume returns to normal through the self-regulating mechanism.
(4) Venous return
2. Regulation of heart rate
3. Cardiac reserve: the ability of cardiac output to increase according to the metabolic needs of the
body, which is called pumping function reserve or cardiac reserve.
3. Bioelectric phenomena of cardiomyocytes
(1) Physiological characteristics of myocardium - excitability, autorhythmia, conduction,
contraction
1. Excitability: Cardiomyocytes have the ability to respond to stimuli, that is, they are excitatory.
Cardiomyocytes, like other excitable cells, are also excited
After that, the excitability also has to go through various periods of change before returning
to normal.
(1) Effective (absolute) refractory period
(2) Relative refractory period
(3) Abnormal period
Characteristics of excitability: the effective refractory period is particularly long, and tonic
contraction does not occur. The length of the effective refractory period depends mainly on
period 2 (plateau period)
(2) Factors
influencing
excitability (Fig.) (1)
Resting potential
level
RP↑→ Stimulation threshold at a
distance from the threshold
potential→ →Excitability ↓ RP↓→
Stimulation threshold near the
threshold potential→
→Excitability↑ (2) Threshold
potential level
Move up → RP far from the threshold
potential→ need stimulation
threshold ↑→ excitability ↓ move
down→ RP near the threshold
potential → need stimulation
threshold ↓→ excitability ↑ (3) The
state of sodium channel
The Na+ channel is available in three states: active, inactivated, and standby:
2. Autorhythmicity: The characteristic that tissues and cells can automatically produce
rhythmic excitation without external stimuli is called autorhythmicity, referred to as automaticity.
Origin: The special conduction system in the heart (except for the nodal area of the atrioventricular
node), its automaticity Size: Sinus node P cells > atrioventricular junction> atrioventricular bundle>
Purkinje's fibers and other automaticities of the heart originate from a specific part of the heart, that
is, the pacemaker (pacemaker), also known as the autocenter. Higher vertebrates are the sinus
node. The pacemaker of fish and amphibians is located in the venous sinuses.
(1) Potential characteristics of autonomic cells
(2) Factors affecting self-discipline
(1) the speed of
automatic
diastolic
depolarization,
and (2) the
maximum
diastolic potential
level
(3) Threshold potential level (not the main influencing factor)
17
Normal pacemaker: The rhythm of the entire mammalian heart is controlled by the activity of the sinus
node, which is the dominant pacemaker for the entire heart, known as the normal pacemaker
Potential pacemaker: The autonomic tissues of other parts other than the sinus node do not exhibit
their own autorhythmicity, but only play an excitatory conduction role, which is called a potential
pacemaker.
and (3) the relationship between myocardial automaticity and heart rhythm
Autonomic cells vary in autonomic cell automaticity by site---------- sinus node-----------
atrioventricular node, Pode's fiber (90-100 beats/minute) (40-60 beats/minute) (20-40
beats/minute)
Control of potential pacemakers in the sinus node: those with a high rhythm control those with a low
rhythm. Because the one with a high rhythm has a preemptive occupation (preemptive access to the
threshold potential
Mechanisms that produce AP) and overdrive inhibition (preemptively
repressive "passive" rhythmic excitation in low-paced people).
Autonomic tissue or autonomic cell: A tissue or cell that is
autonomous
The rhythmicity of the autonomic tissues in the heart of higher animals is uneven. Sinus
node P cells> atrioventricular junction> atrioventricular bundles> Purkinje's fibers, etc
Inhomogeneous excitatory conduction velocity in the heart: (1) The slowest conduction site is
the atrioventricular node—atrioventricular delay
Physiological significance: The atrioventricles do not contract at the
same time, and the ventricular contraction follows the completion of
the atrial contraction
(2) The site of the fastest conduction is the Purkinje fibers (cells) in
the ventricle
Physiological significance: to ensure that the ventricular muscle is
almost completely synchronized to contract, resulting in a better
ejection effect.
Sinus rhythm (sinus rhythm): Normal heart rhythm is caused by impulses from the sinus node,
the highest point of automaticity, so it is called sinus rhythm. The sinus node is called the origin of
the heart beat or the starting point of the heart beat.
Ectopic rhythm (ectopic rhythm): Autonomic cells other than the sinus node replace the sinus node
and dominate the heart rhythm.
Safety factor: When normal pacemaker activity is impaired, it can still keep the heart beating at a
lower frequency as a backup pacemaker
Potential risk factors: arrhythmias can occur when automaticity is elevated and extends beyond the
sinus node.
Factors that determine and affect automaticity: (1) the speed of 4-stage automatic
depolarization; (2) The distance between the maximum diastolic potential and the threshold potential
level
Cardiomyocytes are as excitatory as nerve fibers and skeletal muscle cells. After ventricular myocytes
are excited, they experience an effective refractory period, a relative refractory period, and an ultra
period
normal periods, followed by a return to normal.
Effective refractory period: 0-stage depolarization to 3-stage repolarization to -60mV. Myocardium: 250-
300 ms, skeletal muscle: 1-3 ms
Absolute refractory period: 0-stage depolarization to 3-stage repolarization to -55mV.
Features: The effective refractory period is particularly long
Relative refractory period: -60mV to -80mV
Extraordinary: -80mV returns to -90mV
3. Conductivity: The property that the action potential generated by cardiomyocyte excitation can
propagate along the cell membrane.
1) Conduction principle:
Local current
The intercalary disc (gap connection) is a low-resistance region, and local currents can easily pass
through a special conduction system
Cardiomyocytes form a functional syncytial body that ensures that the left and right atria or ventricles
can excite and contract simultaneously
(2) Conduction characteristics:
1) Pu's fiber is the fastest → and rapid → in the room, and the synchronous contraction is facilitated
by ejection
2) The slowest atrioventricular junction→ atrioventricular delay→ facilitating the evacuation of the
atrium and filling the atrium
The atrioventricular junction is the only passage for excitation to enter the ventricles from the atrium,
and the action potential conduction velocity in the junction area is relatively slow, so that the
excitement is delayed here for a period of time before being centripetal
Ventricular transmission is called atrioventricular delay
(4) Factors affecting myocardial conductivity
1) The diameter of the cell: the diameter
is coarse→ the intracellular resistance is
small→ conduction velocity is fast, the
diameter is small→ the intracellular
resistance is large→ conduction velocity
is slow
2) The speed and magnitude of phase 0 depolarization
18
3) Excitability of adjacent membranes
4) Cell-to-cell connections
Conduction type: local current + leap disk (gap connection)
Cardiomyocytes form a functional syncytial body that ensures that the left and right atria or
ventricles can excite and contract simultaneously.
Atrioventricular delay: The atrioventricular junction is the only passage for excitation to enter the
ventricles from the atrium, and the action potential conduction velocity in the junction is extremely
slow, so that the excitement is delayed here for a period of time
It spreads to the ventricles intermittently. (The conduction of excitation at the AV junction is significantly
slowed, a phenomenon called AV delay.)
[The only conduction pathway between the atrium and the ventricle under normal
conditions in the atrioventricular junction area, in which the nodal cells are only 3 μm in
diameter and have many branches,
The conduction velocity is extremely slow, creating a 0.1S delay
in the conduction of impulses within the heart, known as
atrioventricular delay. Sympathetic stimulation of the heart
shortens atrioventricular delay, and stimulation of the vagus
nerve prolongs atrioventricular delay.
The physiological significance of atrioventricular delay: the ventricles do not begin to
contract until after the atrial contraction is completed, without the phenomenon of overlapping
atrioventricular contractions. The characteristics of the excitatory transmission pathway and the
inconsistency of conduction velocity in the heart are of great significance to ensure that all parts
of the heart carry out contraction activities in an orderly and coordinated manner.
When stimulated, electrical excitation is generated on the membrane, and then the myocardial fibers
are shortened by excitation-contractile coupling.
Characteristics of excitatory propagation in the heart: (1) The conduction velocity of various
cardiomyocytes is different, and the impulse can spread throughout the left and right atria or left and right
ventricles in a short period of time, producing "full"
or "none" contraction;
(2) There is atrioventricular delay, so as to ensure the order and coordination of
atria and ventricles, which is conducive to blood filling and ejection.
4. Contractile
The contractility of cardiomyocytes has the following characteristics:(1) It is significantly
dependent on the concentration of Ca2+ in the extracellular fluid
(2) synchronous
contraction ("total" or
"none" contraction) and
(3) no tonic contraction
occurs
(4) Pre-period contraction and compensatory intermittent
Premature contraction: an additional (artificial or pathological) suprathreshold stimulus after the
effective refractory period of the myocardium and before the next rhythmic excitation is
transmitted
An additional excitation and contraction, since it occurs before the normal contraction produced by the
next sinoatrial node excitation, is called preterm contraction.
Compensatory pauses: A long period of diastolic after a
premature contraction is often followed by a period called
compensatory pause. Fourth, the characteristics of myocardial
action potential
(1) Types and characteristics of cardiomyocytes
(1) Common cardiomyocytes (also known as contractile
cells and working cells) include atrial myocytes and
ventricular myocytes. Characteristics: Rich in myofibrils,
excitability, conductivity and contraction
Sexuality, which does not have an autonomous rhythm, is the driving force of the heart's pumping
activity.
(2) Specially differentiated cardiomyocytes (autonomic cells) include P cells and Purkinje
cells.
Characteristics: Lack of contractile ability, with the ability to produce autorhythmic excitation,
called autonomic cells. It forms the cardiac conduction system and completes the conduction
function of excitation. According to the rate of phase 0 depolarization and the presence or
absence of stage 4 autodepolarization of AP in various cardiomyocytes, myocardium is
divided into:
(1) Fast-response autonomic cells:
The depolarization rate is fast in phase 0 and there is automatic depolarization in phase 4
(2) Fast-reacting non-autonomic cells:
Rapid depolarization rate
in phase 0 and no
automatic depolarization
in phase 4 (3) Slow-
reacting autonomic cells:
The depolarization rate is slow in phase 0 and there is automatic depolarization in stage 4
(4) Slow-reacting non-autonomic cells:
The depolarization rate is slow in phase 0 and there is no automatic depolarization in phase 4
(2) Cardiac conduction system
19
The cardiac conduction system includes the sinus node, atrial conduction tissue, atrioventricular
node,
Atrioventricular tracts and their branches, as well as ventricular conduction tissues.
(1) P cells - oval, smaller than ordinary cells, mainly found in the sinus node, are the cells in
the sinus node that produce autorhythmic excitation, so they are called pacemakers.
(2) Purkinje cells – the largest in diameter and widely present in all cardiac conduction systems
except those of the sinus node and the atrioventricular node.
(3) Transmembrane potential and formation mechanism of ordinary cardiomyocytes
1. The resting potential of cardiomyocytes - the equilibrium potential formed by the movement of K+ across the membrane, the
intramembranous potential is lower than that outside the membrane
(1) Amplitude: -90 mV in the ventricular myomesa
(2) Mechanism: The equilibrium potential formed by the movement of K+ across the membrane
Conditions: (1) There is a concentration difference between the two sides of the membrane
(2) Membrane permeability is selective: K+/Na+=100/1
Results: The K+ concentration gradient diffused from the inside of the membrane to the outside
of the membrane to reach the equilibrium potential of K+
The resting potential and formation of cardiomyocytes are basically similar to
those of nerve cells and skeletal muscle cells, and it is also the transmembrane equilibrium potential of K+
generated by the flow of K+ from the cell to the outside of the cell membrane. The resting potential of cardiomyocytes
is -90mV.
2. Action potential of cardiomyocytes - In the process of cardiomyocyte depolarization, the
ion channels that play a major role are fast sodium channels (Na+
inward ion current) and slow calcium channels (Ca2+ inward ion
current); Slow sodium channels, fast potassium, and slow potassium
channels also play a role in cardiomyocyte depolarization and
repolarization.
The action potential of cardiomyocytes is different from that of nerve cells and
skeletal muscle cells: the repolarization process is complex; Long duration (300-400 ms);
Asymmetry of the ascending and descending branches of the action potential.
(1) The process of action potential
The whole action potential change process can be divided into 5 stages, of which phase 0 is the
depolarization and reverse polarization process, and l~4 phase belongs to the repolarization process.
Depolarization process (phase 0): Also known as the depolarization phase, membrane depolarization, Ap
ascending branch
Under the influence of the excitatory impulse from the sinus node, the
intramembranous potential of ventricular myocytes rises to a critical level, that
is, the threshold potential (about -70mV) level, which causes the opening
(activation) of the fast sodium channel, and the extramembranous Na+ flows
rapidly inward along the concentration difference and the potential difference,
forming an inward current of fast sodium, which causes the intramembranous
potential to rise sharply, from -90 mV at rest to +30 mV, and the potential
changes by 120 mV in l~2ms, constituting the rising branch of the action
potential. Fast sodium channel, which can be specifically blocked by tetrodotine
venom (TTX).
Repolarization process: Phase 1 - At the beginning of rapid repolarization, the membrane potential
rapidly decreases from +30 mV to about 0 mV, forming repolarization phase 1
At this point, the fast sodium channel is closed, but there is a brief K+ outflow.
Stage 2 – plateau phase (main feature), also known as slow repolarization. The
membrane potential decreases slowly, and the membrane potential is stable around
the 0 mV level for 100~150 ms. It is mainly composed of the opening of slow calcium
channels, the influx of Ca2+ (with a small amount of Na+) and the dynamic
equilibrium of ionic currents formed by K+ efflux. Initially, the Ca2+ inward ion current
is dominant, and the K+ outward ion current gradually increases over time, resulting in
the membrane potential slowly becoming negative.
Stage 3—Terminal rapid repolarization. After the plateau phase, the
repolarization of the membrane is accelerated because the Ca2+ channel has
been inactivated, but the K+ efflux increases with time
The membrane potential is rapidly repolarized until the repolarization
process is completed.
Resting phase (stage 4): The membrane potential is stable at the Rp level. Also known as
the convalescence period. The membrane potential of ventricular myocytes is stable at the resting
potential level. The action potential changes too
During the recovery period, the various ions entering and exiting the membrane
along the concentration gradient must rely on the active transport mechanism of
the membrane to restore the normal ion concentration gradient inside and outside
the cell before excitation, so as to prepare the conditions for re-excitation. The
active transport of Na+ and K+ relies on the Na+-K+ pump; The active transport of
Ca2+ is carried out by the Na+-Ca2+ exchange mechanism coupled with the influx
phase of Na+ along the concentration gradient. In stage 4, the increase of [Na+]
and [Ca2+] in the membrane and the increase of [K+] in the membrane → activate
the ion pump→ pump out Na+ and Ca2+, pump in K+→ restore normal ion
distribution
Mechanism of myocardial action potential generation: Phase 0 Formation of depolarization—
Na+
1-2ms
20
Phase 1 – K+ outflow (early stage of rapid repolarization), formation of peak
potential, inactivation of Na+ channels, and decrease of potential by rapid
K+ outflow.
10ms
Stage 2 – K+ outflow and Ca2+ inflow are in equilibrium. The K+ channel recovers
slowly, and the Ca2+ channel is activated when the membrane is
depolarized up to -40 mV. Ca2+ slow inflow and K+ outflow reach equilibrium, so
that the membrane potential is maintained at about 0mV for a long time.
100-150ms
Stage 3 — K+ efflux (Ik regenerative repolarization). The Ca2+ channel is inactivated, the
Ca2+ influx is stopped, and the permeability of the membrane to K+ is restored
and increased
High, K+ rapid outflow formation.
Stage 4 – Ion recovery (Na+-K+ pump and Na+-Ca2+ exchange). After
phase 3, the K+ efflux stops, the K+-Na+-ATP pump on the membrane is
active, the Na+ is pumped out, and the K+ is pumped in, and the Ca2+ is
transported out through the Na+-Ca2+ exchanger, so that the ion
distribution inside and outside the cell membrane and the membrane
potential return to the resting potential level.
(4) Bioelectric phenomena of specially differentiated cardiomyocytes
Autonomic cells begin automatics depolarization as soon as the end of phase 3 repolarization
of the action potential reaches its maximum, and when the depolarization reaches the threshold
potential level, it causes excitation again (out
Current action potential) stage 4 is also called diastole.
1. Transmembrane potential and characteristics of Purkinje cells (fast-reacting autonomic
cells).
1) Formation mechanism
I.. The waveform, amplitude, and formation mechanism of the 0, l, 2, and 3 phases of the action
potential of Purkinje cells are the same as those of ventricular myocytes, but for a longer duration;
Phase 4 membrane potential undergoes a slow, automatic depolarization process known as diastolic
auto-depolarization.
II.. The membrane potential at the beginning of phase 4 of autonomic cell repolarization, known as the
delta maximum diastolic potential or maximum repolarization potential, is approximately the maximum
repolarization potential of Purkinje cells
90 mV﹣ 。
III.. The cause of automatic depolarization during diastolic (i.e., phase 4): caused by an increasing
Na+-dominated inward ion current (If) + decreasing outward K+ current. Inward Na+ flow is a
leakage (or background) ionic current, which is independent of the fast Na+ channel, and is a small
amount of Na+ that continuously "leaks" from the outside of the membrane through the gap between
the channels into the membrane; The Na+ and K+ channels are activated at a stage 3 repolarization
potential of approximately -60 mV and increase in their openness (i.e., time adherence) as the stage 3
repolarization process progresses
ion channels).
2) Features
(1) The depolarization rate of phase 0 is fast and the amplitude is large
(2) The auto-depolarization rate of stage 4 is slower than that of sinus node cells, so the automaticity
is low
2. Transmembrane potential and characteristics of sinus node P cells (slow-reacting
autonomic cells).
I.. The maximum repolarization potential of Sinus node P cells is around -50~-60mV, and the stage 4 is
automatically depolarized, which is formed by a constant inward Ca2+ ion current.
II. When diastolic automatic depolarization reaches a threshold potential of -40mV, the calcium channel is
activated, Ca2+ influx, resulting in phase 0 depolarization; Subsequently, calcium channels are gradually
inactivated, and Ca2+ is influxed
Decreases accordingly, while potassium channels begin to activate, and K+ efflux gradually increases,
resulting in repolarization potentials at stages 1, 2, and 3 of the action potential.
☆ Features: There is no obvious distinction between repolarization phase 1 and phase 2, only a
smooth transition to stage 3.
1) Depolarization: -70 mV up to 0 mV
Mechanism: When the membrane potential is automatically depolarized from the maximum
repolarization potential to the threshold potential level, the calcium ion channel on the
membrane is activated, causing the slow influx and depolarization of calcium ions. The
amplitude is small
Phase 0: Ca2+ influx →→ activated slow calcium channels (Ica-L type) when phase 4 autodepolarization
reaches threshold potential
Stage 3: Progressive inactivation of calcium channels (Ica-L type) + activation of potassium
channels (IKs→ Ca2+ influx ↓+ K+ decreasing efflux (due to inactivation of potassium channels K+
decreasing efflux)
Stage 4: K+ decreasing efflux + Na+ ascending influx (If) + Ca2+ influx (Ica-T type calcium channel
activation) → slow auto-depolarization
Ion current phenomena with "self" initiation→ "self" development→ "self" termination
Characteristics of Sinus node P cell potential: (1) The action potential is only 0, 3, and 4
(2) Phase 0 is initiated by the activation of Ca2+ channels and the influx of Ca2+
21
(3) A small amount of Ca2+ influx in phase 4 causes automatic
depolarization, bursting out of the next action potential, and
the cycle repeats.
(4) The peak value of depolarization phase 0 is small, the depolarization speed is slow,
about 10V/S, and the depolarization of phase 0 is only about 0mv.
Sinus node cell action potential formation: Slow phase 0 depolarization caused by Ca2+ influx
occurs when the action potential of sinus node cells (-70) is less than the resting potential of
ventricular myocytes (-90), which corresponds to the threshold potential (-70) level of the latter,
which is one of the conditions for automatic depolarization of the sinus node.
When phase 4 autodepolarization reaches the threshold potential level (approximately -40 mV, i.e., the
slow calcium L-type channel on the membrane is activated. Ca2+ is slowly inflowing, resulting in phase 0
depolarization.
Subsequently, the Ca2+ channel is inactivated, the K+ is
outflowed, and the membrane potential is repolarized,
reaching the maximum repolarization potential, entering phase
4) Sinus node P cell potential formation mechanism: Phase 0 is
initiated by the activation of the Ca2+ channel and the influx of
Ca2+
Stage 3 is the result of a combination of Ca2+ influx and K+ efflux.
Phase 4 is when the inward current (Na+, Ca2+) exceeds the outward current
(K+), resulting in the automatic depolarization of phase 4 and the eruption of
the next movement
As an electric potential, it will be repeated on Tuesday.
Summary (action potential of autonomic cells)
1. Compared with ordinary cardiomyocytes, phase 4 of the action potential of autonomic cells is not
stable at the resting level and is automatically depolarized.
2. Autonomic cells are divided into fast-reacting cells and slow-reacting cells.
3. The 4-phase depolarization of fast-response autonomic cells is mainly a combination of Na+ inward
flow (If) that increases over time and K+ outward flow (IK) that decays over time.
The depolarization and repolarization processes are the same as those of ordinary cardiomyocytes.
4. Phase 4 depolarization of slow-reactive autonomic cells is mainly attenuated by K+ outward
current (Ik) and Na+ inward flow (If) and meridian T that increase over time
The combined effect of Ca2+ inward flow of Ca2+ channels.
5. Phase 0 depolarization of slow-reactive autonomic cells is caused by the activation of L-type slow
Ca2+ ion channels (as in normal cardiomyocytes) and the influx of slow Ca2+
Outcome. Therefore, the depolarization amplitude of phase 0 of slow-
reacting autonomic cells is low and slow. Repolarization is still caused by
increased K+ outflow. 5. The waveform of a normal ECG and its
physiological significance
ECG: A waveform in which a guide electrode is placed in a certain part of the body and the electrical
changes in the center of the heart (the combined ECG vector of each cell) are recorded throughout
the cardiac cycle.
P wave: AP ≈
atrial muscle
QRS: stage 0 of
≈ ventricular
myocardial AP
S-T segment: Stage 2 ≈ ventricular myocardial AP
T waves: ≈ the repolarization process of ventricular myocardial AP, the T waves are wide due to the
different sequences.
Electrocardiogram (ECG): It is a potential curve of the cardiac activity traced on the body
surface, reflecting the origin of cardiac excitation and the process of excitation spreading to the
atria and ventricles—not directly related to the mechanical activity of the heart.
These include: P-waves, QRS complexes, and T-waves, sometimes followed by a smaller U-wave.
P wave: reflects the process of depolarization of the left and right atrium, indicating that the atria are
about to enter systole. Normal P waves last 0.08-0.11 seconds.
QRS complex: reflects the potential
changes in the depolarization
process of the left and right
ventricles. Q wave:
ventricular septal
depolarization
R-wave: depolarization of the left and right ventricular walls
S wave: The ventricles are completely depolarized
The time occupied by the QRS complex represents the
time it takes for ventricular muscle excitation to
propagate.
T wave: a wave of lower amplitude and longer
duration after the QRS complex, which reflects the
repolarization process after excitation of both
ventricles. The repolarization process is
slower than the depolarization process, so it
takes a long time.
P-Q interval: the time period from the onset of the P
wave to the onset of the QRS complex, representing the
time from the onset of atrial to the ventricle of
excitation, i.e., the time from the onset of atrial
depolarization to the onset of ventricular depolarization.
Indicates atrioventricular conduction time.
22
A significantly prolonged P-Q interval indicates atrioventricular node
or atrioventricular bundle block, which is clinically important.
Q-T interval: refers to the time period from the beginning of the QRS complex to the end of the T wave,
representing the time at which the ventricles begin to excitatory depolarization to full repolarization. Its
length is closely related to heart rate, and the faster the heart rate, the shorter the interval. Ventricular
excitation depolarization and repolarization time.
ST segment: Refers to the line segment from the end of the QRS complex to the beginning of the T
wave. ST segments on a normal ECG should be flush with baseline. The ST segment represents that all
parts of the ventricle have been depolarized (a plateau of action potential) and there is no potential
difference between the parts, so it should be on the isopotential line.
6. Heart sounds
Heart sound – the sound produced by the heart during the pumping process due to the vibration of
valves, arterial walls, heart muscle, etc.
During the cardiac cycle, it is caused by factors such as myocardial contraction, valve opening and
closing, blood acceleration and deceleration of the cardiovascular wall, and the formation of
vortices
mechanical vibrations, which can be transmitted to the chest wall through surrounding tissues; If you
place a stethoscope in certain parts of your chest wall, you can hear sounds, called heart sounds.
First heart sound S1: Occurs at the onset of cardiac contractions, is low and long, and is mainly
caused by contraction of the ventricular muscle, closure of the atrioventricular valve, and the onset
of ejection
Vibration of the arterial wall. It occurs during cardiac contractions, lasts for a long time, and is low-
pitched, mainly reflecting the contractility of the myocardium and the function of the atrioventricular
valve.
Second heart sound S2: Occurs at the beginning of the diastolic phase, is high and short, and is
caused by sudden closure of the half-moon valve, blood impingement on the valve, and deceleration
of blood in the aorta
caused by vibrations. It occurs during the diastolic phase, which is short in duration and high in pitch,
mainly reflecting the level of arterial blood pressure and the function of the semilunar valve.
7. The main factors affecting arterial blood pressure
1. Structure of blood vessels:
(1) Elastic receptacle blood vessels: refers to the aorta, the main trunk of the pulmonary artery
and the largest branches from which they emanate.
Features: Thick pipe wall, thick nozzle, rich in elastic fibers, obvious expandability and elasticity
Function: (1) It can buffer high pressure during cardiac ejection and assist ejection during diastole; (2)
Buffer blood pressure
(2) Allocation of blood vessels—middle arteries
Characteristics: The membrane has more smooth muscle, the tube wall is elastic, and its contraction
and relaxation can regulate the blood flow distributed to all parts and organs of the body.
(4) Resistance vessels—arterioles and arterioles
Characteristics: The diameter of the tube is thin, the resistance to blood flow is large, the wall of
the tube is rich in smooth muscle, and the smooth muscle maintains a certain tension, which is the
main source of peripheral resistance. Counterpoint
Pulse blood pressure maintenance plays an important role.
(5) Exchange blood vessels—true capillaries
Features: The tube wall is composed of a single layer of endothelial cells, with only a layer of basal
membrane outside, which has the greatest permeability, and is the main place for material exchange
between blood and tissues.
(6) Volume vascular-venous system
Characteristics: large number of venous vessels, thick caliber, thin wall, easy to expand, large
capacity, play a role in blood storage.
(7) Short-circuited blood vessels—anastomotic branches of arterioles and venules
Characteristics: It is mainly distributed in the skin of fingers, toes, pinna, etc., and mainly participates
in the collective body temperature regulation.
(8) Capillary posterior resistance vessels—venules
(9)
Characteristic
s of
precapillary
sphincter:
not
innervated
2. Blood flow and blood flow velocity
Blood flow: that is, volumetric velocity, is the amount of blood flowing through a certain section of a
blood vessel per unit of time, called blood flow, and the unit is ml/min.
Blood flow velocity: refers to the linear velocity of blood flowing in the blood vessels, that is, the
distance that a particle advances in the blood vessels per unit of time, which is proportional to the
blood flow and blood
The cross-sectional area of the tube is inversely proportional.
The capillaries have the largest cross-sectional area and the smallest blood flow velocity; The aorta
has the smallest cross-sectional area and the largest blood flow velocity.
Resistance to blood flow: Derived from the frictional resistance between the components of the
blood flow (i.e., the viscosity of the blood) as it flows, and the friction between the blood and the
wall of the tube, which is affected by the caliber and length of the blood vessel.
3. Blood pressure: refers to the lateral pressure of intravascular blood flow on the blood vessel wall
per unit area. What is commonly referred to as blood pressure refers to the blood pressure in the
arteries at some of the sites that are routinely examined. High blood pressure
23
Low is expressed as a numerical value above or below atmospheric pressure (KPa).
Causes of blood pressure: (1) blood filling blood vessels - premise; (2) Peripheral
resistance – sufficient conditions; (3) arterial elastic buffering-maintenance; (4) Cardiac
ejection - necessary conditions: Arterial blood pressure changes periodically during a cardiac
cycle.
Causes of arterial blood pressure: (1) blood filling (2) cardiac ejection (3) peripheral resistance
(4) elastic receptacles of the aortic and aortic walls (a. intermittent ventricular ejection into
continuous blood in the arteries; b. reduction of the magnitude of changes in arterial blood
pressure during the cardiac cycle).
Arterial blood pressure changes: a. Arterial blood pressure changes periodically (cardiac ejection is
intermittent).
b. The further the blood flows, the lower the blood pressure (energy is constantly
consumed during blood flow P arteries> P capillaries> P veins
(1) Systolic blood pressure: the highest value of arterial blood pressure during cardiac contraction,
reflecting cardiac contraction; Arterial pressure rises to its highest value during ventricular
contraction - a reflection of the heart's contractility
(2) Diastolic blood pressure: the lowest value of arterial blood pressure during diastolic period,
reflecting peripheral resistance; When the ventricles relax when the blood pressure drops to
its lowest value, it is called diastolic blood pressure- extra-reflected
Weekly resistance
(3) Pulse pressure: the difference
between systolic blood pressure and
diastolic blood pressure - reflecting the
elastic average arterial pressure of the
arterial wall = diastolic blood pressure + 1/3
pulse pressure
☆ Factors influencing arterial blood pressure:
(1) Cardiac stroke volume: mainly affects systolic blood pressure
Assuming other factors are constant, the systolic blood pressure is
significantly increased due to an increase in stroke volume and an increase
in ejection volume, as well as diastolic blood pressure
Increase, pulse pressure increases.
Stroke volume ↑---→ systolic blood pressure ↑↑ diastolic blood pressure ↑ pulse pressure
Stroke volume ↑---→ systolic blood pressure ↓↓ Diastolic blood pressure ↓ Pulse
pressure ↑
(2) Heart rate: When the heart rate increases, the cardiac output increases, causing the systolic
blood pressure to rise; The ejection interval is shortened, and diastolic blood flows from the aorta to
the periphery
decreased, diastolic blood pressure increased markedly; The pulse pressure decreases in
comparison between the two phases.
Heart rate ↑ ---→ systolic blood pressure ↑ diastolic blood pressure ↑ pulse pressure ↓
(3) Peripheral resistance: When the increase of peripheral resistance caused by the increase of
tension in small blood vessels, the blood outflow is blocked, and the blood pressure will generally
increase; But systolic blood pressure
High, the obstruction of outflow blood is not as obvious as in diastole, so diastolic blood
pressure will rise more significantly than systolic blood pressure, and pulse pressure will
decrease.
There is a positive correlation between blood pressure and peripheral resistance
Resistance vasoconstriction → rise in peripheral resistance → increase in blood pressure
(diastolic blood pressure)
(4) The elastic receptacle effect of the aorta and the aorta: under normal circumstances,
the elasticity of the aortic box and the aortic artery have obvious buffering effect, so
the pulse pressure is far from the fluctuation amplitude of the intraventricular pressure
of the fish, and also the pulse pressure of the small arteriole. When collagen fibers in
blood vessels gradually replace elastic fibers and smooth muscle, elasticity decreases,
which is called arteriosclerosis. At this point, systolic blood pressure will rise, diastolic
blood pressure will decrease, and pulse pressure will increase significantly.
The elasticity of the walls of the arterial system is an important factor in the creation of
diastolic blood pressure
The elasticity of the tube wall is good, and the blood vessels dilate when they are contracted,
which eases the rise in blood pressure
During relaxation, the blood vessels retract, which eases the drop in blood pressure
The high or low pulse pressure
can reflect the elasticity of the
arterial wall to a certain
extent---→ systolic blood
pressure ↓ diastolic blood
pressure ↑ pulse pressure ↓
elastic ---→ systolic blood
pressure ↑ diastolic blood
pressure ↓ pulse pressure ↑
(5) Ratio of circulating blood volume to vascular volume of the circulatory system: arteries
will be caused when blood loss leads to a decrease in circulating blood volume or an increase in
vascular volume caused by a certain factor
Blood pressure drops, especially systolic blood pressure.
Circulating blood volume ↑ ---→ systolic blood pressure ↑ diastolic blood pressure ↑ pulse
pressure ↑
A sudden decrease in the amount of blood circulating (massive blood loss) and a sudden
increase in the volume of blood vessels can cause a rapid drop in blood pressure
(6) The viscosity of blood
Affects blood pressure by peripheral resistance that affects blood flow
24
The main factors that affect blood pressure are: the contractility of the heart and the
peripheral resistance of blood flow.
Arterial pulse: As the heart periodically contracts and relaxes, the aortic wall expands and
retracts as the aortic wall expands and retracts, and this pulse propagates along the arterial
wall in the form of an elastic pressure wave to the arterial terminal. This pulsation of the
arterial wall is called an arterial pulse. i.e. pulse.
The arterial pulse can not only directly reflect the rhythm of the heart rate and the cardiac cycle,
but also pass the speed, amplitude, hardness, and frequency of the pulse to a certain extent
Sex reflects the functional status of the entire circulatory system—checking the arterial pulse is
clinically important.
8. Central venous pressure, venous return blood volume and its influencing factors
Venous blood pressure: (1) Peripheral venous pressure: The blood pressure in the veins of
various organs is called peripheral venous pressure.
(2) Central venous pressure: The blood pressure in the right atrium and large veins in
the chest is called central venous pressure.
The level depends on the heart's ability to eject blood and the rate at
which venous blood returns.
The level of central venous pressure depends on the correlation
between the cardiac ejection capacity and venous return. It can be
used clinically to guide infusion. Low central venous pressure indicates
obstruction of venous return and insufficient blood volume; A
progressive increase in central venous pressure suggests rapid infusion
or cardiac ejection insufficiency.
The important role of the venous system is to carry blood back to the right atrium.
☆ The factors affecting the amount
of venous
return to the
heart are:(1)
the average
filling
pressure of
the systemic
circulation,
and (2) the
contractile
strength of
the heart
(3) Position change: lying > upright
(4) Squeezing of skeletal muscle—muscle pump
(5) Breathing exercise - (suction of chest negative pressure)
Venous pulse: fluctuations in the arterial pulse during the cardiac cycle disappear completely by the
time it reaches the capillaries, so there is no pulsation in the peripheral veins. However, it occurs
when the right atrial contraction is active
The pressure change can be reversed to the large veins close to the heart,
resulting in venous pulsations, called venous pulses.
When venous return is blocked, varicose veins and phlebitis can easily occur.
9. The composition and function of microcirculation
Microcirculation: blood circulation between arterioles and venules. It is a place where
substances are exchanged between blood and tissue fluid. Under
normal circumstances, the blood volume of microcirculation is
appropriate to the metabolic level of tissues and organs, ensuring
the blood perfusion of various tissues and organs and regulating the
blood volume back to the heart. If the microcirculation is disturbed, it
will directly affect the physiological function of the organs.
The seven components of microcirculation:(1) Arterioles – their constriction and relaxation
control blood flow to blood vessels
(2) Posterior arterioles - are direct extensions of arterioles, have the ability to
contract, and supply blood to one to several true capillaries
(3) Precapillary sphincter - its contraction state determines the blood flow into the
true capillary, and is very sensitive to the regulation of humoral factors
(4) True
capillari
es, (5)
Hemoca
pillaries,
(6)
Arteriov
enous
anasto
motic
branche
s
(7) Venules - play the role of exchanging blood vessels
There are three channels of microcirculation: (1) direct and shortcut pathway: arterioles-posterior
arterioles-capillaries-venules
Features: Only a small amount of material is exchanged, so that a
part of the blood flow is quickly returned to the heart through
microcirculation, maintaining blood flow
of the relative stability. More in skeletal muscle.
(2) Circuitous access: arterioles-posterior arterioles-true capillary network-
venules
Features: The true capillaries are intertwined into a network, the
blood flow is slow, and the tube wall is thin and permeable. This
pathway
It is the main place for blood to exchange substances, so it is also called the
nutrient pathway.
(4) Arteriovenous access: arteriole-arteriovenous anastomotic branch-venule
Characteristics: Thick blood vessel walls. It is mostly distributed in the skin,
palms, soles of the feet and auricles, and its caliber changes are related to
body temperature. End of this path
25
It has no substance exchange function, so it is also called a non-nutritive
pathway.
Question: Why are the circuitous pathways alternately open?
Answer: Norepinephrine, vasopressin, and serotonin in the blood more constantly stimulate the
posterior arterioles and precapillary sphincter, causing smooth muscle tension and causing
capillary closure. The suspension of blood flow causes the accumulation of cellular metabolites
such as CO2, H+, adenosine, ATP, K+, and histamine, causing vascular smooth muscle relaxation
and resuming perfusion.
10. The formation of tissue fluid and its influencing factors
Interstitial fluid exists in the interstitial space of tissues and cells, and is the medium of
exchange between blood and tissue cells, of which 1% can flow freely, and the rest is gelatinous
and cannot flow freely, so it will not flow to the lower parts of the body due to gravity.
The various ionic components in the interstitial fluid are the same as those in plasma, and various
plasma proteins are also present in the interstitial fluid, but their concentrations are significantly lower
than those in plasma.
Interstitial fluid is formed by the filtration of plasma through the capillary walls as blood flows
through the capillaries. As a result, plasma is filtered out of the arterial end by the blood vessel wall
to form tissue
The fluid, at the venous end, is reabsorbed back into the bloodstream, completing the material
exchange between the blood and the tissue fluid in one out and one in.
1. Generation of interstitial fluid
Effective rate overpressure = (capillary blood pressure + interstitial fluid colloidal osmotic
pressure (motility) - (plasma colloidal osmotic pressure + tissue hydrostatic pressure
(resistance).
Positive: Plasma filtrate — interstitial fluid
Negative: The interstitial fluid is re-absorbed into the bloodstream, completing the material exchange
(90% recovery)
Interstitial fluid is formed by the filtration of plasma through the capillary walls as blood flows through
the capillaries.
Therefore, the plasma is filtered out by the blood vessel wall at the arterial end to form interstitial
fluid, and at the venous end, it is reabsorbed back into the bloodstream
Exchange of substances between tissue fluids.
Factors influencing the formation of interstitial fluid: The generation and confluence of
interstitial fluid can maintain a state of dynamic equilibrium, which is an important factor to
maintain the relative stability of plasma and interstitial fluid content
(abnormalities: dehydration or edema)
(1) Capillary blood pressure
(2) Plasma colloidal osmolality
(3) Permeability of capillary walls
(4) Lymphatic reflux
2. Lymph - Under normal circumstances, about 90% of the interstitial fluid flows back into the blood at
the capillary venous end, and the remaining 10% remains in the interstitial space and enters the
capillary lymphatic vessels.
Becomes lymphatic fluid.
Physiological significance of lymphatic reflux: (1) Maintain circulating blood volume and regulate
the fluid balance between blood and tissue fluid
(2) Protein molecules in the tissue fluid are recovered
(3) It plays an important role in the absorption of nutrients, especially fat, and is
the main absorption route after fat digestion
(4) Play the role of defense and barrier of lymph nodes. Lymph nodes can
remove foreign bodies (such as red blood cells and bacteria) from the reflux lymph fluid and
affect lymph production: increased capillary blood pressure, decreased plasma colloidal
osmotic pressure, increased protein concentration in tissue fluid, and increased permeability
of capillary walls can all cause increased lymphatic production.
11. Cardiac sympathetic nerve and cardiac vagus nerve regulation of the heart and blood
vessels
Under different physiological circumstances, the metabolic level of the ancestors of each organ is
different, and the need for blood flow is also different. The body can be affected by nervous system
and humoral factors
Regulates the activity of the heart and some blood vessels, so as to meet the needs of various organs
and tissues for blood flow in different situations, and coordinate the distribution of blood volume
between various organs.
(1) Neuromodulation - cardiovascular innervation
Somatic motor nerves and autonomic nerves: (1) Somatic motor nerves, nerves that innervate
somatic movements
Governed by the consciousness of the brain; Its cell body is found
in the brain and spinal cord, and only one neuron is needed to
travel nerve impulses from the brain to the effector.
(2) The nerves innervating the internal organs—autonomic nerves, or
autonomic nerves
26
to a certain extent not under the control of consciousness; The
soma is partly found in the brain and spinal cord, and partly in
the autonomic ganglia of the peripheral nervous system, where
nerve impulses need to be replaced from the brain to the
effector. Among them, the preganglion is called the
preganglionic neuron, and the postganglionic neuron is called
the postganglionic neuron.
Release of preganglionic fiber terminals of autonomic nerves: Ach
Postganglionic fibers—Vice: distal release of Ach; Delivery: More NE is released, and a few are Ach
1. Innervation of the heart:
Effect: Faster, stronger heartbeat Positive chronological effect—increased
heart rate
Cardiac sympathetic nerve of the sympathetic nervous system Positive
transmutation - conduction acceleration
Positive variable force effect – increased contraction
Double domination Preganglionic fibers (Ach-N receptors) Postganglionic fibers (NE-β1
receptors)
Negative temporal effect
Cardiac vagus of the parasympathetic nervous system Negative metaconduction
(dominant)
Effects: Slowing, weakening of the heartbeat Negative temporal effect
(1) Sympathetic nerve: norepinephrine released from the terminals binds to the β1 receptors
of the myocardium, resulting in an increase in the heart rate, an increase in the conduction of
the atrioventricular junction, and an increase in the contractility of the atrial and ventricular
muscles. These are called positive variable temporal action, positive variable conduction,
positive variable force action. Stimulates the sympathetic nerves and facilitates ventricular
diastolic filling.
(2) Cardiac vagus nerve: the terminal releases ACH to bind to the heart M receptor, resulting in a
slowdown of the heart rate; decreased atrial muscle contractility; shortened atrial muscle refractory
period; Atrioventricular conduction
slowing down; That is, it is called negative time change, change conduction, and change force.
(3) Peptidrergic neurons: There are a variety of peptide neuroreleasing neuropeptides Y,
vasoactive intestinal peptides, calcitonin gene-related peptides, opioids, etc., which are often
compared with others
Transmitters coexist in a single nerve cell. It is mainly involved in the regulation of myocardial and
coronary artery activity. The myocardial contraction is strengthened and the coronary arteries are
dilated.
Sympathetic excitation, increased cardiac activity; The vagus nerve is excited, and cardiac activity
is suppressed; Under normal conditions, both have an effect on the heart, and the vagus nerve
Dominance prevails.
Vagus tension: A condition in which the vagus nerve has a regular and long-lasting effect on
the heart, limiting the speed and intensity of heart activity to a certain level, is called vagus
tension.
Long-term exercise increases vagus tension and slows the heart rate.
Cardiac
sympathetic
nerves
Sources: Preganglionic
neurons (thoracic
spinal cord T1-T5), postganglionic neurons (intraganglia)
Domination: The whole heart
Functions: (1) Increased heart rate - positive time; (2) Conduction acceleration -
positive variable conduction; (3) Contraction strengthening—positive variable force
MECHANISM: NA or NE released from the postganglionic terminal of the cardiac sympathetic nerve,
which binds to β 1 receptors on the membrane of cardiomyocytes, is primarily promoted by increasing the
intracellular second messenger cAMP
The opening of the Ca2+ channel, the increase of inward current, the acceleration of phase 4
depolarization of Sinus node P cells, and the high automaticity, which is a positive chronotropic
effect. The influx of Ca2+ in phase 0 of atrioventricular node slow response cellsis accelerated, and impulse
conduction is rapid; These changes increase the heart rate. The Ca2+ channels of the sarcoplasmic membrane and sarcoplasmic reticulum were more open, the
concentration of Ca2+ in the sarcoplasmincreased, and the cardiac contractility increased. At the same time, the Ca2+ pump on the sarcoplasmic
network is activated, the reuptake is enhanced, the Na+-Ca2+ exchange is stimulated, and the
diastolic is rapid and powerful, which is a positive force change, promoting ejection and blood
filling of the heart. The cardiotonic effect of norepinephrine can be specifically blocked by
propranolol (propranolol).
Vagal nerve
S
o
u
r
c
e: Preganglionic neurons (dorsal vagus nucleus, suspicious
nucleus), postganglionic neurons (postganglionic nerve fiber
myelin sheath) innervation: the whole heart (less ventricles)
Transmitter: Acetylcholine (Ach)
Effects: (1) Slow heart rate - negative time change; (2) Conduction slowing-negative
conduction; (3) Contraction slows down—negative variable force
Mechanism: Vagus nerve excitation, postganglionic fiber terminal release acetylcholine (Ach), binding to
M2-type cholinergic receptors on the myocardial cell membrane, increasing the probability of K+ channel
opening through the second messenger cGMP, reducing cAMP in cells, reducing the probability of Ca2+
channel opening, reducing the resting potential level and reducing excitability; The resting potential level of
P cells in the sinus node decreases, the outward current IK decay is slowed, and the heart rate is slowed;
The repolarization process is accelerated, Ca2+ influx is reduced, the AV node conduction is slow, and the
myocardium is retracted
27
Weak curtailment. In short, there are negative time changes, negative changes conduction, and
negative force change effects. The vagus nerve is strongly stimulated, and even cardiomyocytes
can be automatically depolarized
Temporary loss of force. The inhibitory effect of acetylcholine on cardiac activity can be specifically
blocked by atropine (belladonna).
2. Innervation of blood vessels:
(1) There are two
receptors on the blood
vessels of the
vasoconstrictor nerve (=
sympathetic constriction
N) β and α.
Vasoconstriction
(NA)+ β receptors Vasodilation
However, the ability to bind to α receptors is greater than that of β receptors, so it mainly exhibits a
contractile effect.
Most blood vessels in the body are innervated only by sympathetic nerves, and the sympathetic
nerves are constantly emitting low-frequency impulses, called sympathetic constriction atotonia.
Sympathetic nervous tension
When sex decreases, vasodilation
(2) Vasodilator nerve
a. Sympathetic vasomotor nerve: innervates skeletal muscle arterioles. Structurally sympathetic,
but its terminals secrete Ach, which is only when the animal is in emotional tension
, the impulse is released, the blood vessels are dilated, and the blood flow increases.
B. Parasympathetic vasomotor nerve: A few blood vessels are also innervated by the
parasympathetic vasomotor nerve. The transmitter Ach released from the terminal binds to the M
receptors of the blood vessels, causing blood
28
Tube diastole.
c. Dorsal root diastolic cardiovascular nerve of the spinal cord: the peripheral branches of sensory
nerves can cause local vasodilation through axonal reflexes.
(NE-a) shrink
Vasoconstriction nerve fibers (sympathetic) (Ach-N).
(NE-b) Diastolic
Sympathetic vasomotor nerve—(Ach-M).
Parasympathetic vasomotor nerve—(Ach-M).
Vasodilated nerve fibers Dorsal root vasomotor nerve of the spinal cord—
cutaneous blood vessels
Vasoactive intestinal peptide neurons (VIPs)—sweat glands
Characteristics of the action of vasoconstrictor nerve fibers: (1) Tension
activity: In a quiet state, sympathetic constrictor nerve fibers are often
emitted
1-3 low-frequency
impulses per
second,
dimensional
The tension that holds most blood vessels is called sympathetic vasotension.
(2) Uneven distribution: skin> skeletal muscle> visceral>
coronary blood vessels, cerebrovascular >
At the same site, arterioles > common arteries> veins >
capillary sphincter
(3) Vasoactive intestinal peptide
The parasympathetic neurons innervating the sweat glands not only secrete ACH to cause gland
secretion, but also release vasoactive intestinal peptides to cause vasodilation, increasing local
tissue blood flow. (1) Neuromodulation - cardiovascular center
1. The medullary cardiovascular center is the basic cardiovascular center.
A. Centers that regulate the activity of the heart
Central place Efferent
nerves
Effect
Cardiovag
al Center
(Cardiovag
al Center)
Reticular
node of
the brain
frame
Vagal nerve
Heart activity
is weakened
and blood
pressure
Cardiac
sympathetic
center (CPR)
Reticular
node of
the brain
frame
Cardiac
sympatheti
c nerves
Heart activity
is intensified,
and blood
pressure rises
B. Centers that regulate vascular activity
Central place Effect
Vascular
constric
Extend the
ventrolateral part
The heart rate increases, blood vessels constrict, and
blood pressure rises
Vascular
vasodila
Extend the
ventrolateral part
Inhibition of the activity of the sympathetic center leads
to a decrease in sympathetic contractional vascular nerve
(1) The medullary cardiovascular center is the basic cardiovascular center, which includes at least
four parts:
(1) (Cardiac sympathetic) vasoconstriction area: causes normal tension activity of cardiac
sympathetic and sympathetic constriction nerves.
(2) Vasodilation area: When excited, it can inhibit the activity of central neurons in the constriction
of the vasoconstrictor, resulting in reduced sympathetic constrictor nerve tension and vasodilation.
(3) Afferent nerve relay station: receives the information from the carotid sinus, aortic arch and
cardiac receptors, and sends out the information through the glossopharyngeal nerve and vagus
nerve
Neurons that reach the medulla oblongata and other parts of the center.
(4) Cardiac inhibition area: located in the dorsal nucleus and suspicious nucleus of the vagus nerve
in the brain, which is the cell body of the vagus neuron.
(2) Cardiovascular center above the brain: The function of the brainstem, brain, and cerebellum
located above the brain is to coordinate and integrate more complexly.
Fish hearts are also subject to dual innervation and are often under intense vagus tone inhibition.
Cardiovascular center: the site where neurons that regulate cardiovascular activity are concentrated
Bulbar cardiovascular center: The sympathetic nerve center, the vagal nerve center, and the
sympathetic constriction vascular center innervating vascular smooth muscle are all located in the
medulla oblongata. 、
29
Vascular constriction area, vasodilation area, afferent nerve alternation station,
cardiac inhibition area
Cerebellum—stimulates certain parts of the cerebellum, such as the
parietal nucleus
High cardiovascular center Hypothalamic-visceral functional integration (body
temperature, food intake, water balance, mood).
Limbic system — emotional agitation
12. Stress and chemoreceptor reflex regulation of cardiovascular activity
Cardiovascular reflexes: 1. Carotid sinus and aortic arch baroreceptor reflex -
decompression reflex: the baroreceptor is located on the adventitia of the
carotid sinus and aortic arch, and its afferent nerves join the glossopharyngeal
nerve and vagus nerve respectively. In rabbits (fish will fish) it is a single
bundle called the decompression nerve. When blood pressure rises, the
afferent impulse to the baroreceptors increases, and reflexively causes the
heart rate to slow down, cardiac output to decrease, peripheral vascular
resistance to the blood vessels, and blood pressure to drop.
2. Carotid body and main artery chemoreceptor reflex: when Pco2 ↑ Po2 ↓ [H+] ↑ in the
blood can stimulate the chemoreceptor, reflexivity
Causes deepening, acceleration of breathing, and increased blood pressure.
Reflex regulation of cardiovascular activity: (1) carotid sinus and aortic arch baroreceptor
reflexes
(2) Carotid sinus and aortic body chemoreceptor reflexes
and (3) cardiovascular reflexes induced by cardiopulmonary receptors
and (4) cardiovascular reflexes induced by somatic receptors and visceral
receptors
Baroreceptors: There are abundant sensory nerve endings under the adventitia of the
carotid sinus and aortic arch vessel walls, which mainly feel the stretch stimulation of the
blood vessel wall due to changes in blood pressure, and are often called baroreceptors.
Chemoreceptors: IN THE CAROTID AND AORTIC BODIES, OR IN SPECIFIC AREAS OF THE MEDULLA
OBLONGATA, THERE ARE CHEMICALS THAT ARE SENSITIVE TO CHANGES IN THE PARTIAL PRESSURE OF CO2, PH, ANDO2 IN THE
BLOOD
Receptors.
1. Carotid sinus and aortic arch baroreceptor reflexes
Carotid sinuses Sinus nervesGlossopharyngeal nerves
Increased blood pressure Bulbar cardiovascular center
Aortic arch The aortic nerve is the vagus nerve
Blood pressure drops
Vagal nerve
Cardiac sympathetic nerves
Rabbit – decompression nerves
Decompression reflex: The reflex activity that causes blood pressure to decrease due to impulses
from carotid sinus and aortic arch baroreceptors is called the decompression reflex.
In the usual quiet state, the animal's arterial blood pressure is already above the baroreceptor
sensory threshold. Therefore, it is caused by carotid sinus and aortic arch baroreceptors
Reflex activity, which causes a decrease in blood pressure, occurs not only when blood pressure rises,
but is often present.
The receptors of the arteries have a degree of adaptability.
The aortic arch baroreceptor afferent fibers in rabbits form a bundle of their own and accompany the
vagus nerve, called the decompression nerve.
Blood pressure increases, baroreceptor afferent impulses increase, reflexivity causes a slowing of
heart rate, decreased cardiac output, decreased peripheral vascular resistance, and a decrease in
blood pressure.
Since persistent hypertension will reduce the frequency of afferent impulses to the baroreceptors, this
phenomenon is called receptor adaptation.
Blood
pressure
Baroreceptors
C
a
r
o
ti
d
sinuses
Aortic
arch
Sinus
Nerve (+)
Decompressi
on Nerve (+)
delay
pith
C
ardiac vagus
(+) Cardiac
sympathetic
(-)
Sympathetic
constrictor
nerve (-)
Slowed
heartbeat
Vasodilation
Blood pressure
