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physiology blood circulation
The mind map of physiology of blood circulation includes the circulatory system, the definition of blood circulation, the main functions of blood circulation, the pumping function of the heart, the electrophysiology and physiological characteristics of the heart, let’s take a look!
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blood circulation
circulatory system
relatively closed piping system
Regulated by nerve and humoral factors
Main components
Cardiovascular system (main role)
Composition of the heart, blood vessels and the blood present in the heart chambers and blood vessels
Blood vessels are divided into arteries, capillaries and veins
Lymphatic system (auxiliary role)
Composition, lymphatic vessels and lymphoid organs
process
Peripheral lymphatic vessels collect part of the tissue fluid to form lymph. The lymph flows centripetally along the lymphatic vessels and merges into the venous blood.
definition of blood circulation
The beating of the heart drives blood circulation within the cardiovascular system
Main functions of blood circulation
Complete material transport in the body, transport nutrients and O2 required for cell metabolism, and transport metabolic waste and CO2 to the excretory organs
Transport hormones and bioactive substances
The maintenance of relatively stable physical and chemical properties of the body's internal environment and the realization of the blood's defensive and immune functions also depend on target cells.
heart pumping function
definition
The driving effect of the heart's rhythmic contraction and relaxation on the blood is called the heart's pumping function or blood pumping function
cardiac cycle
A cycle of mechanical activity composed of one contraction and relaxation of the heart is called the cardiac cycle
The length of the cardiac cycle is inversely related to heart rate
heart pumping process
atrial systole
It is actually the end diastole of the previous cycle
When the atria contract, both intraatrial pressure and intraventricular pressure increase slightly.
0.1 S, 10-30% blood further fills the ventricles; active rapid filling period
ventricular systole
isovolumetric contraction phase
Intraventricular pressure increases; volume remains unchanged; ventricle becomes a closed cavity; 0.05S;
If aortic pressure increases or myocardial contractility weakens, the isovolumic contraction period is prolonged
rapid ejection period
The intraventricular pressure reaches the maximum; the volume decreases significantly; the atrioventricular valve closes and the semilunar valve opens; blood is ejected from the ventricle to the aorta; the flow rate is fast; the ejection volume accounts for 2/3 of the total blood volume; 0.1S;
slow down ejection phase
The ejection volume accounts for 1/3 of the total blood volume; 0.15S
In the middle and late stages of the rapid ejection period, and even during the entire slowed ejection period, the intraventricular pressure is already lower than the aortic pressure.
ventricular diastole
isovolumetric diastole
0.06 – 0.08 S, ventricular closed chamber
The ventricular muscles continue to relax and the intraventricular pressure decreases
ventricular filling phase
rapid filling period
The intraventricular pressure is lower than the intraatrial pressure and intravenous pressure; the volume increases significantly; the atrioventricular valve opens and the semilunar valve closes; blood flows into the ventricle from the large veins and atria; the flow rate is fast; the ventricular filling volume accounts for 2/3 of the total filling volume ;0.11S.
slow down filling phase
0.22S, a small amount of blood flows from the atrium into the ventricle.
atrial systole
The role of the atria in the heart's pumping of blood
primary pumping action of the atria
Its main function is to receive and store blood returning from the veins
Primary pump action facilitates cardiac ejection and venous return
Changes in intraatrial pressure during the cardiac cycle
Three smaller forward waves appear
a wave
Atrial contraction increases Blood flow into the ventricles decreases
c wave
Increased ventricular contraction and decreased ventricular ejection
v wave
Venous return increases, blood flow into the ventricles decreases
Cardiac output and cardiac pumping reserve
cardiac output
Stroke volume: the amount of blood ejected from one ventricle in one heart beat
Ejection fraction: the ratio of stroke volume to ventricular end-diastolic volume, generally 55%-65% in healthy adults
Output per minute (cardiac output or cardiac output): The total amount of blood ejected by one ventricle per minute, equal to the product of stroke volume and heart rate
Cardiac index: (The cardiac output of a person at rest is the same as the basal metabolic rate, which is not proportional to the weight, but to the body surface area) The cardiac output calculated per unit body surface area is called the cardiac index, resting and fasting The heart index measured under normal circumstances is called the resting heart index, which can be used as an evaluation index to compare the heart function of individuals with different body shapes.
heart work capacity
Stroke work: the work done by one ventricular contraction, stroke work = stroke volume * ejection pressure kinetic energy
Work per minute: the work done by the ventricles per minute, = stroke work * heart rate Under normal circumstances, the work of the right ventricle is only 1/6 of that of the left ventricle (the mean pressure of the pulmonary artery is 1/6 of the mean pressure of the aorta).
heart pumping reserve
Cardiac Reserve: The ability of cardiac output to increase in response to the body's metabolic needs. The maximum amount of blood that the heart can eject per minute is called the maximum output (more than 35 liters), which reflects the health of the heart. The size of the cardiac reserve is mainly determined by the reserves of stroke volume and heart rate.
Stroke volume reserve: Stroke volume is the difference between ventricular end-diastolic volume and end-systolic volume.
Contraction period reserve (mainly)
Achieved by enhancing myocardial contractility and improving ejection fraction
diastolic reserve
Heart rate reserve: The resting heart rate of a normal healthy adult is 60-100 beats/min. If the stroke volume remains unchanged and the heart rate is accelerated within a certain range, when the heart rate reaches 160 to 180 beats/min, the cardiac output can increase to 2 to 2.5 times the resting level, which is called the heart rate reserve. However, if the heart rate is too fast (more than 180 beats/min), the diastolic period is too short and the ventricular filling is insufficient, which can lead to reduced stroke volume and cardiac output.
Factors affecting cardiac output
front load
Preload can make skeletal muscles at a certain initial length before contraction. The initial length of ventricular muscle depends on the blood filling volume at the end of ventricular diastole. In other words, the volume at the end of ventricular diastole is equivalent to the preload of the ventricle.
Factors affecting preload (ventricular end-diastolic filling blood volume = venous return blood volume, remaining blood volume)
venous blood return volume
ventricular filling time
The heart rate is accelerated, the ventricular diastole and filling time are shortened, the filling volume is reduced, and the stroke volume is reduced. Sympathetic nerve excitement also accelerates diastole and shortens isovolumetric diastole, which to a certain extent compensates for the adverse effects of diastole shortening on ventricular filling.
If the ventricular filling time is continued to be prolonged after the ventricles are fully filled, the venous blood return volume cannot be further increased.
venous return velocity
When ventricular filling remains unchanged, the venous return velocity is fast, the ventricular filling volume is large, and the stroke volume increases.
ventricular diastolic function
It is related to the falling rate of elevated Ca2 in myocardial cells at the end of systole. The faster the falling rate, the faster the diastolic rate and the greater the volume of venous return to the heart.
ventricular compliance
When ventricular compliance is high, the amount of blood that can be tolerated increases at the same ventricular filling pressure.
intrapericardial pressure
Increased teeth in the pericardium hinder heart filling and reduce stroke volume
The amount of blood remaining in the ventricle after ejection
The volume of venous return to the heart remains unchanged: an increase in the remaining ventricular blood volume will lead to an increase in filling volume, an increase in filling pressure, and a subsequent increase in stroke volume.
When the residual blood volume of the ventricle increases, the ventricular pressure during diastole increases, and the volume of venous blood return to the heart decreases, but the total filling volume does not necessarily increase.
Abnormal myocardial autoregulation: regulation of changes in myocardial contractility by changing the initial length of the myocardium
Heart function curve and heart law
The filling pressure is 5-15mmHg, which is the rising branch of the curve. 12-15mmHg is the optimal ventricular preload. Under normal circumstances, the left ventricular filling pressure is about 5-6mmHg, which is far lower than its optimal preload. This indicates that the ventricle has a large initial length reserve, which can be achieved by increasing the end-diastolic ventricular length. Pressure or volume increases cardiac output.
When the filling pressure is 15-20mmHg, the curve gradually becomes flat, indicating that changes in preload within this range have little effect on pump function.
The filling pressure is >20 mmHg, the curve is flat or slightly decreased, and there is no obvious descending branch (except pathology).
Anti-overextension properties of normal ventricular myocardium
The heart has less stretchability, mainly due to the presence of connexins within the sarcomere.
After the initial length reaches a certain level, it is no longer parallel to the indoor pressure.
Significance: Finely adjust the stroke volume to balance the ventricular ejection and venous return blood volume, thereby maintaining the ventricular end-diastolic volume and pressure within the normal range (such as changes in body position, sudden increase in arterial blood pressure, etc.)
Afterload of myocardial contraction: The load or resistance that a muscle encounters when it begins to contract. It does not increase the initial length of the muscle, but it hinders the shortening of the muscle. Isometric contraction. Arterial pressure is afterload
When aortic pressure increases, the isovolumic contraction period is prolonged, and the ejection period is shortened accordingly. At the same time, the speed and amplitude of myocardial contraction are reduced, the ejection rate is slowed, and the stroke volume is reduced. If the arterial pressure continues to increase, pathological changes such as myocardial hypertrophy will occur due to long-term strengthening of ventricular contraction activity, leading to a decrease in pumping function.
myocardial contractility
Definition: The intrinsic characteristics of myocardium that can change its mechanical activity independently of preload and afterload (external factors that affect heart pumping).
Isometric self-regulation: In an intact ventricle, the enhanced myocardial contractility can shift the cardiac function curve to the upper left, that is, under the same preload condition, the stroke power increases and the heart's pumping function is significantly enhanced. This regulation of the heart's pumping function by changing the contractility of the myocardium is called isometric regulation
Influencing factors
The ratio of activated cross-bridges to the maximum cross-bridges: Any factor that can increase the degree of increase in cytoplasmic Ca2 after excitement and the affinity of troponin for Ca2 can increase the ratio of activated cross-bridges and enhance muscle contraction ability. For example, catecholamines increase cytoplasmic Ca2, and calcium sensitizers (such as theophylline) can increase the affinity of troponin for Ca2.
The activity of myosin head ATPase, thyroid hormone enhances the activity of myosin, and the expression of myosin molecular subtypes changes
Heart rate: Normal adult: 60-100 beats/minute.
Heart rate changes greatly with age, gender and different physiological states
Within a certain range, increased heart rate can increase cardiac output
Overall, heart rate is regulated by neural and humoral factors
Heart rate increases when sympathetic nerves are strengthened
Heart rate slows when vagus nerve increases
Cardiac function evaluation
Categories include cardiac ejection function evaluation and cardiac diastolic function evaluation
Evaluating cardiac function from changes in ventricular pressure
Assessment of cardiac ejection function
dP/dtmax is often used to compare cardiac contractility in different functional states.
Ventricular diastolic function evaluation
Ventricular pressure and diastolic pressure change rate curve can be used as an indicator of cardiac diastolic function
-dP/dtmax can be used to compare cardiac diastolic function in different functional states
Evaluating cardiac function from changes in ventricular volume
Ventricular systolic function assessment
Clinically, LVEF (left ventricular ejection fraction) is the preferred index to evaluate left ventricular contractility in most patients. In addition, both the rate of volume change and the rate of diameter change can be used to reflect changes in ventricular contractility.
Ventricular diastolic function evaluation
Left cardiac catheterization is the gold standard for assessing ventricular diastolic capacity
Evaluation of cardiac function from changes in ventricular pressure and volume
Measurement of cardiac work capacity
heart work
External work is the mechanical work done by the contraction of the ventricle to generate and maintain a certain pressure and promote blood flow.
Internal energy is the energy consumed during cardiac activity to complete the active transport of ions across the membrane, generate excitement and contraction, generate and maintain heart wall tension, and overcome the viscous resistance within the myocardial tissue.
Stroke work
The external work done by the ejection of blood during one ventricular contraction mainly manifests as raising a certain volume of blood to a certain pressure level to increase the potential energy of the blood, and making a certain volume of blood have a certain blood flow energy.
Every share of work
The work done by the ventricle to contract and eject blood per minute, that is, the stroke work multiplied by the heart rate
The output of the left and right ventricles is basically the same, but the amount of work done is different
Application of ventricular pressure-volume loop to evaluate cardiac function
Cardiac catheterization to plot ventricular pressure_time curves
Echocardiography plots ventricular volume_time curve
The pressure and volume corresponding to each time point are plotted as the ventricular pressure_volume loop.
Changes in the ring can reflect changes in preload and afterload End-systolic curve reflects ventricular contractility
heart sounds
Cause: mechanical vibration That is, the contraction and relaxation of the myocardium, the opening and closing of the heart valves, the changes in blood flow velocity, the turbulence caused by the impact of the blood flow on the ventricular wall and the aortic wall, can all be transmitted to the chest wall through the surrounding tissues, and the corresponding sounds can be heard in certain parts with a stethoscope. sound, heart sound
Heart sounds occur at some special periods of the cardiac cycle. Usually, the first and second heart sounds can be heard by auscultation. Some young people and healthy children can hear the third heart sound.
The first heart sound: It marks the beginning of ventricular systole; it is characterized by low pitch and long duration; it is clear at the apex beat (mid-clavicular line of the fifth left intercostal space) Second heart sound: It marks the beginning of ventricular diastole; it is characterized by high frequency and relatively short duration; it is clear in the second intercostal space on the right and left sides of the sternum (i.e. auscultation of the aortic valve and pulmonic valve) Third heart sound: a low-frequency, low-amplitude sound that occurs at the end of the rapid ventricular filling period. It is the result of ventricular wall vibration due to the sudden stretching of the ventricular wall and papillary muscles and the sudden decrease in filling blood flow velocity. The fourth heart sound: also known as atrial sound, appears in the late stage of ventricular diastole. It is a group of vibrations related to atrial contraction that occur before ventricular systole. Normal atrial contraction generally does not make a sound, and is more common in pathological conditions. (Abnormally forceful atrial contractions, reduced left ventricular compliance)
Electrophysiology and physiological properties of the heart
Characteristics of action potential of cardiomyocytes compared with nerves and skeletal muscles
Long duration and complex shape
The action potential of each part of the cardiomyocyte and the various ion currents that form this point are quite different due to different cells, but the common characteristics are basically similar.
Each period of the action potential involves more than two ion currents.
The generation of an action potential includes two processes: passive and active ion transfer.
Cardiomyocytes (according to histological and electrophysiological characteristics)
working cells
Category: Atrial myocardium and ventricular myocardium
Has a stable resting potential and mainly performs contraction function
autonomous cells
Sinoatrial node cells and Purkinje cells
Most have no stable resting potential
Participates in forming a special conduction system in the heart, which can automatically generate rhythmic excitement
Cardiomyocytes (according to the speed of action potential depolarization)
fast response cells
Atrial myocardium, ventricular myocardium, Purkinje cells
Action potential characteristics: large depolarization speed and amplitude, fast excitation conduction speed, slow repolarization process and can be divided into several phases
slow responding cells
sinoatrial node cells and atrioventricular node cells
Action potential characteristics: small depolarization speed and amplitude, slow excitation conduction speed, slow repolarization process without clear phase difference
Fast-responding cells and slow-responding cells can transform under certain experimental conditions or pathological conditions.
Physiological characteristics of myocardium (based on the bioelectrical activity of myocardial cell membrane)
Excitability
conductivity
self-discipline
Contractibility
Transmembrane potential of cardiomyocytes and its formation mechanism
Inward current (depolarization); Outward current (repolarization or hyperpolarization)
resting potential
Normal value: The resting potential of myocardial working muscle cells is stable, -90~-80mV-90mV Production mechanism: (1) K+ outflow, through the inward rectifying potassium channel (Ik1 channel) as the main component (2) Sodium inward background current (Na -inward background current) and pump current. The inflow of Na partially offsets the potential difference formed by the outflow of K
The size of the resting potential mainly depends on the K concentration difference between the intracellular fluid and the extracellular fluid and the permeability of the membrane to K. The equilibrium potential formed by the diffusion of K to the outside of the membrane is the main source of the resting potential.
Ventricular myocyte action potential consists of five periods of depolarization and repolarization.
Phase 0: (rapid depolarization period), phase 0 is short, only takes up 1-2 milliseconds, Na channel is a fast channel, rapid activation and inactivation, phase 0 depolarization mainly contains sodium inward current (similar to depolarization Forming positive feedback), the T-type calcium current is another ion current in phase 0 depolarization.
Phase 1: In the early stage of rapid repolarization, the spike potential is generated by the rapid change of membrane potential in phase 0 and phase 1. The instantaneous outward current is the main transmembrane current that causes the rapid repolarization of ventricular myocytes in phase 1. Its main ion component is K , there are obvious species differences; there is also chlorine current in phase 1. Under normal circumstances, the strength of this chloride ion is small, and its effect in phase 1 is weak and short-lived. However, under the action of catecholamines (or when sympathetic nerves are excited), the role of chloride ions cannot be ignored.
Phase 2: Plateau phase (the negative pole is slow, accounting for 100-150 milliseconds, which is the main reason for the long action potential and is unique to the action potential of cardiomyocytes.) Inward current: ICa-L is the main depolarizing current in this period. Calcium channels are relatively slow, called slow channels; there is also slowly inactivated INa, and there is also Na-Ca2 exchange current. Outward current: The inward rectification characteristic of the inward rectifier potassium current (Ik1) is an important reason for the long duration of the plateau period. The early delayed rectifier potassium current (Ik gradually increases with time) mainly resists L-type calcium ion influx. In the late stages, it becomes the dominant ionic current in membrane repolarization. In addition, the pump current is also a continuously active outward current
Inward rectification, a phenomenon in which the permeability of the channel to K is reduced due to depolarization of the membrane
Phase 3: The end of rapid repolarization, lasting 100-150 milliseconds, is the main part of repolarization (until it returns to the resting potential level) The main ion flow is the outward current: Ik. The delayed rectification K channel continues to strengthen, Ik1. The inward rectification K channel accelerates the terminal repolarization. Sodium pump current, INa-Ca are involved, 3rd phase repolarization
Phases 0 to 3 are called action potential duration, and the ventricular muscle action potential duration is 200-300 milliseconds.
Phase 4: Complete repolarization phase (quiet phase), the distribution of ions inside and outside the cell is restored, and normal excitability is maintained. Na -K pump (external) completes the external transport of Na and the internal transport of K Na -Ca2 exchange (inward) - 3 sodium enters the sac and Ca2 is pumped out, na is pumped out by the sodium pump, Ca2 can also be pumped out by the calcium pump
In summary, the action potential process includes passive ion transfer and active ion transfer. Active transfer maintains an unequal distribution of ions across the cell membrane, ie maintaining the normal excitability of the cell. The absolute amount of ion transfer is small and will not cause huge changes in the internal environment.
Atrial myocyte action potential
Atrial myocytes are fast-response cells, with a smaller negative potential than ventricular myocytes, and their action potentials are morphologically similar to ventricular myocytes.
The It0 channel of the atrial muscle is well developed, resulting in the plateau phase not being apparent and the distinction between phase 2.3 and phase 2.3 not obvious.
Repolarization is faster and the action potential is shorter, 150-200 milliseconds
Atrial myocytes have acetylcholine-sensitive potassium currents that can hyperpolarize, resulting in shortened action potentials
There are many types of potassium channels, and they are regulated by neurotransmitters. During atrial fibrillation, various ion currents change, which is called electrical remodeling.