5. Cause ventricular contraction (the left and right bundle branches cause left and right ventricular contraction respectively)

act

branch

act

branch

Due to the sharp increase in ventricular wall tension, compression of small blood vessels between muscle fibers can significantly reduce CBF, and CBF in the deep myocardium can stop or even reverse flow during isovolumic contraction.

As aortic pressure increases, coronary artery pressure also increases, and CBF increases.

CBF decreases again

Myocardial compression of the coronary arteries is weakened or relieved, coronary blood flow resistance is reduced, CBF rises rapidly, reaches a peak in early diastole, and then gradually decreases

Prolonged isovolumetric systole/shortened isovolumetric diastole

Increased peripheral resistance/decreased arterial diastolic blood pressure

increased heart rate

Systemic vasoconstriction. The coronary arteries are mainly affected by the vasodilatory effect of metabolic substances, so the coronary arteries do not shrink, and the blood volume of the coronary arteries is redistributed.

Acts on alpha receptors to contract vascular smooth muscle

Acts on β2 receptors to relax vascular smooth muscle

The affinity for α-receptors is stronger than that for β-receptors, and the sympathetic vasoconstrictor fibers are excited, mainly causing the vasoconstrictor effect.

Innervates almost all blood vessels (distribution: skin > skeletal muscles. Internal organs > coronary arteries. cerebral blood vessels)

Among blood vessels at all levels, arterioles are the densest

vasoconstriction

Acts on M receptors in vascular smooth muscle membranes

Skeletal muscles of cats and dogs are dually innervated by sympathetic vasoconstrictor fibers and sympathetic vasodilator fibers.

Cause skeletal muscle vasodilation and increase skeletal muscle blood flow

Acts on M receptors in vascular smooth muscle membranes

A few organs (meninges, salivary glands, gastrointestinal exocrine glands and vascular smooth muscles of the external genitalia) are dually innervated by it and sympathetic vasoconstrictor nerves

Causes relaxation of the blood vessels controlled and increased blood flow

ACh can activate N-type cholinergic receptors on the membrane of postganglionic neurons

Axons form the cardiac plexus, which innervates all parts of the heart, including the sinoatrial node, the atrioventricular junction, the atrioventricular bundle, the atrial myocardium and the ventricular myocardium.

mechanism

Influence

Medulla oblongata is the basic center for regulating cardiovascular activity

inhibit nerves

mechanism

Influence

Note

The RVLM in the rostral ventrolateral region of the medulla is an important site for generating and maintaining tonic activity of cardiac sympathetic nerves and sympathetic vasoconstrictors.

thoracolumbar section

sacral segment

It is controlled by the activity of the high-level cardiovascular center and is the final efferent pathway for central regulation of cardiovascular activity.

It can complete some primitive cardiovascular reflexes and maintain a certain blood vessel tone, but its adjustment ability is low and imperfect.

mainly

effect

The afferent nerve fibers of the carotid sinus baroreceptors form the sinus nerve and join the glossopharyngeal nerve

Afferent nerve fibers from aortic arch baroreceptors travel within the vagal trunk

Entering the nucleus of the solitary tract of the medulla oblongata

start

Secondary

Pulling force↑

blood pressure↓→traction force↓

No effect (blocked impulse conduction)

Myocardial contraction, blood pressure ↑, heart rate ↓

Myocardial diastole, blood pressure↓

No effect on long-term regulation of arterial blood pressure

Resting: mean arterial pressure is 100mmHg

In patients with hypertension, baroreceptors reset the balance point

lie in

Stimulate

Afferent activity ascends through the sinus nerve and vagus nerve to the respiratory center of the nucleus of the solitary tract in the medulla oblongata

Breathing deepens and accelerates, and the sympathetic vasoconstrictor nerves are excited reflexively

It can also stimulate the vagus nerve itself, but it is not as obvious as the sympathetic nerve excitement.

Maintain relative stability of the internal environment

Located within the walls of the atria, ventricles, and large blood vessels of the pulmonary circulation

Feel two kinds of stimulation

blood volume↑→atrial pressure↑→stimulates atrial volume receptors

Endogenous or exogenous chemicals (bradykinin, H, O, adenosine) stimulate ventricular receptors (sympathetic endings in the ventricular wall)

Quickly and briefly regulate blood pressure

In severe cases, maintain blood supply to the heart and brain

Slowly regulate blood pressure over time

Juxtaglomerular cells secrete renin → hydrolyze angiotensinogen → form angiotensin I

Constrict the arterioles throughout the body and increase blood pressure

Constrict the veins and increase the amount of blood returned to the heart

Constrict blood vessels, blood pressure ↑. Heart rate ↑

Acts on some neurons in the central nervous system, reducing the sensitivity of the central nervous system to baroreceptive reflexes and strengthening central sympathetic vasoconstrictor tension.

Promotes the release of vasopressin and oxytocin from the neurohypophysis

Enhance adrenotropin release

In the center, it produces or enhances thirst and causes drinking behavior

Sodium and water reabsorption↑, blood volume↑

Accelerate heart rate and enhance cardiac contractility

vasoconstriction

Small dose → β2 receptor-based

Large doses → α receptors are also stimulated

Accelerate heart rate (not as effective as blood vessels, overall heart rate ↓), enhance cardiac contractility

blood vessels constrict, blood pressure rises

In appropriate amounts, it binds to V2 receptors in the renal distal convoluted tubules and collecting ducts.

In excess, it binds to the V1 receptor of vascular smooth muscle

Generally, when VP is secreted normally, it only exerts an antidiuretic effect. When the body experiences a severe decrease in extracellular fluid (Dehydration, massive blood loss) will increase secretion and increase blood pressure.

Activation of guanylyl cyclase→cGMP↑→calcium efflux↑→vasodilation

Inhibits smooth muscle cell proliferation

Inhibit platelet adhesion and aggregation

Relax blood vessels and inhibit platelet aggregation

Ca2-dependent potassium channel opening → vascular smooth muscle hyperpolarization → vasodilation

vasoconstrictor

Composed of endothelial cells (EC) and subendothelial layer

Forming a permeable barrier, liquids, gases and macromolecules on both sides of the pipe wall can selectively pass through this barrier

As the inner lining of blood vessels, it provides a smooth surface for blood flow

It has endocrine function and can synthesize and secrete a variety of biologically active substances.

Composed of vascular smooth muscle VSMC, elastic fibers and collagen fibers

Contraction and relaxation of vascular smooth muscle regulate blood flow to organs and tissues

Elastic fibers allow arteries to expand or contract

It is a layer of loose connective tissue containing elastic fibers, collagen fibers and various cells.

During ventricular systole, the ventricle ejects blood, part of which flows into the periphery, and part of which is stored in the aorta. The aorta wall expands (the kinetic energy of the blood is converted into the elastic potential energy of the artery), and blood pressure ↓

During ventricular diastole, the arterial wall retracts (the elastic potential energy of the artery is converted into the kinetic energy of the blood), the vascular blood flow is replenished (equivalent to the ejection not stopping), and the blood pressure ↑

1. Make intermittent ejection of blood from the ventricles become continuous blood flow in the blood vessels 2. Slow down changes in arterial pressure

greatest resistance

Control blood flow by adjusting blood flow resistance by adjusting the diameter of blood vessels

The venules contract, the posterior resistance increases, and the anterior-posterior resistance ratio↓→capillary blood pressure↑→tissue fluid production↑

Holds 60-70% (64%) of health

When it is open, blood in the arterioles can enter the venules directly without passing through the capillaries.

However, because the arterial blood enters the venules through the anastomotic branches and does not exchange substances with tissue cells, tissue hypoxia may occur.

Produced by friction between flowing blood and blood vessel walls and molecules within the blood

Blood viscosity is determined by hematocrit, blood flow rate, blood vessel caliber, and temperature

The main influencing factor is the radius of blood vessels

As the blood flows, blood pressure continues to drop, The greater the vascular resistance, the greater the decline

physiological

pathology

Arterial blood volume = ventricular ejection volume - return blood volume

Arterial blood volume = residual systolic blood – return blood volume

That is the difference between systolic blood pressure and diastolic blood pressure (SP-DP)

The person being tested is usually in a sitting or supine position, with the midpoint of the upper arm at the same level as the heart.

The measurer locates the brachial artery by palpation (touching the arterial pulse), and wraps the sphygmomanometer cuff around the subject's upper arm with appropriate tightness, with the lower edge of the cuff located 2 to 3 cm above the elbow crease.

The membranous body of the stethoscope is placed in the cubital fossa, at the pulse point of the brachial artery on the medial side of the biceps tendon.

Inflate and pressurize the air bag of the cuff. When the applied pressure is higher than the systolic pressure, the blood flow of the brachial artery is completely blocked, the brachial artery pulse disappears, and no sound can be heard on the stethoscope.

Arterial blood volume↑→systolic blood pressure↑↑

Systolic residual blood↑

Aortic pressure↑→Vascular arterial pressure difference↑ →Blood flow velocity↑→Heart return volume↑

End-diastolic arterial residual blood-/↑→Diastolic blood pressure-/↑

Cardiac cycle↓→diastole↓

Ventricular filling↓→Ejection volume↓

Diastolic residual blood↑

Systolic arterial blood volume-/↑→systolic blood pressure-/↑

diastole

systole

Pulse pressure↓

大动脉硬化

小动脉硬化

During systole, unable to contract → the ventricles eject blood into the blood vessels The inflow of blood vessels to the periphery is reduced, and the vascular blood↑

During diastole, it is impossible to relax → vascular blood flows to the periphery, vascular blood↓

Pulse pressure↑

During systole, the ejection blood vessels dilate, part of the blood is stored in the blood vessels, and the blood flow↓

During diastole, blood vessels elastically recoil, stored blood is released, and blood flow↑

Pulse pressure ↓ (result of elastic receptacle)

Systole, no vascular blood storage, blood flow↑

During diastole, there is no elastic recoil of blood vessels to release blood, and blood flow↓

Pulse pressure↑

steeper

If the ejection velocity is slow, the cardiac output is small, and the resistance encountered by ejection is large, the slope and amplitude of the ascending branch will be small.

Front section (steeper)

Falling medium wave

Back section (flatter)

Reflects the size of peripheral resistance

Surgery is 5-10cmH2O

Depends on the relationship between the heart's ejection capacity and the amount of blood returned to the heart by the veins

right atrial congestion

Reflects the volume of venous blood return to the heart

Can reflect the functional status of the heart

As a detection indicator for fluid replenishment

Mainly based on blood recovery amount ↑

Venous pressure↓

Rhythmic contraction of peripheral blood vessels → functions as a pump → flow rate ↑ → blood return volume ↑

Obstruction of venous blood flow (edema) → blood volume returned to the heart ↓

Ejection↓

Intravenous blood storage and return to the heart↑→blood volume returned to the heart↑

Lying down

suddenly changed to upright

Return blood to the right atrium↓

Directly leads to venous pressure↓

Peripheral vascular-atrial blood pressure difference↑→reflux↑

The expansion of the atria and thorax is limited, and at first the expansion effect is dominant. After that, it is mainly due to the increase in venous pressure caused by the amount of blood returned to the heart.

Central venous pressure↑

Ventricular pumping effect↑

The number of true capillaries is large and the contact area is large

True capillaries are tortuous and blood flow is slow

Thin tube wall and high permeability

The blood-flowing capillaries are the transitional part of the posterior arterioles, and their wall smooth muscles gradually reduce and disappear.

Part of the blood quickly enters the veins through this passage to ensure the amount of blood returned from the veins to the heart.

Often in a closed state, it is helpful to conserve body heat

When the ambient temperature rises, the arteriovenous anastomosis branches open, increasing blood flow to the skin and conducive to heat dissipation.

In septic or toxic shock, arteriovenous short circuits and direct access pathways are widely opened. Although the patient is in shock, his skin is warm, which is called "warm shock"

Anterior resistance↑→It is difficult for blood to enter capillaries→Capillary pressure↓

Post-resistance↑→It is difficult for blood to leave capillaries→Capillary pressure↑

At the arterioles, blood flow resistance is greatest and blood pressure drops most significantly.

Determines the opening and closing of microcirculation

Under resting conditions, only 20% to 35% of capillaries in skeletal muscle tissue are open at the same time.

When tissue metabolic activity increases, more capillaries will open, increasing the exchange area between blood and tissue, shortening the exchange distance, and increasing microcirculatory blood flow to meet the metabolic needs of the tissue.

维持组织液生成与回流平衡

Hydrostatic pressure → compresses plasma flow Colloidal osmotic pressure →absorb plasma

Systemic venous return is blocked, venous blood pressure↑, capillary blood pressure↑, resulting in an increase in effective filtration pressure

Pulmonary circulation obstruction, venous blood pressure ↑, capillary blood pressure ↑, leading to an increase in effective filtration pressure

Entering capillary blood↑→capillary blood pressure↑, resulting in an increase in effective filtration pressure

Seen in infections, burns, allergies

plasma protein extravasation

Malnutrition. Chronic diseases of liver and kidneys

Plasma colloid osmotic pressure↓

That is, the ventricle contracts, but the ventricular volume does not change, and Pv rises sharply.

Changes in ventricular blood volume＜Volume changes→Indoor pressure caused by blood ejection↓＜Indoor pressure caused by volume reduction↑→Indoor pressure↑

In the early stage, the ventricle ejects a lot of blood into the aorta and the blood flow rate is fast. At the same time, the ventricular volume shrinks rapidly. Pv and PA↑, the former has a larger amplitude.

Changes in ventricular blood volume>Volume changes→Indoor pressure caused by blood ejection↓>Indoor pressure caused by volume reduction↑→Indoor pressure↓

In the later stage, the strength of ventricular contraction weakens, the ejection velocity slows down, and Pv and PA decrease. When Pv is just less than PA, due to the large kinetic energy of the blood, the reversible pressure gradient can still continue to eject blood, and finally the ventricular area reaches the minimum.

That is, ventricular diastole, but ventricular volume does not change, and Pv drops sharply.

In the early stage, ventricular diastole, Pv↓, creates a pressure difference, suction occurs, and atrial blood flows into the ventricle rapidly. The ventricular volume expands rapidly (mainly)

Changes in ventricular blood volume>Volume changes→Indoor pressure caused by increased blood↑>Indoor pressure caused by increased volume↓→Indoor pressure↑

volume change

Blood volume changes

End of rapid ejection period (the faster the ejection, the greater the pressure)

Fast filling period end

Isovolumic contraction phase (pressure caused by ventricular contraction↑)

Isovolumic diastole (pressure caused by ventricular diastole↓)

The end of the rapid ejection period (when it is connected to the ventricle and close to the ventricular pressure)

End of isovolumic contraction (no ventricular ejection, and blood flow continues to supply the periphery, arterial blood ↓)

before ejection

Before filling

Pressure gradient and blood flow inertia

Early suction caused by ventricular-atrial pressure difference

late atrial contraction squeezing effect

Receive and store blood from venous return

Fills the ventricles, accounting for 25% of ventricular filling

ascending branch

descending branch

ascending branch

descending branch

ascending branch

descending branch

Determine valve function, heart rate, heart rhythm

Cause

Features

auscultation site

significance

Cause

Features

auscultation site

significance

Cause

Features

significance

significance

cause

develop

Performance

cause

develop

Performance

cause

develop

Performance

cause

develop

Performance

心率代偿性↑(一定范围内)→增加心输出量

Systolic blood pressure↑

The preferred index for clinical evaluation of most left ventricular systolic functions

In the compensatory phase of heart failure, the ventricles enlarge to compensate for the stroke volume (the stroke volume changes less, ventricular end diastole ↑)

Resting = 70ml × 75 times/min = 5~6L

Exercise=70ml×(160-180) times/minute=25~30L

In patients with hypertension, the arterial blood pressure increases. In order to overcome the increased ejection resistance, the myocardium must increase its contractile strength to keep the stroke volume constant, so the cardiac work volume will increase.

mechanism

reserves

mechanism

reserves

Increase heart rate without changing stroke volume

Resting: 60-100 times/min During exercise: 160-180 times/min

Under normal circumstances, cardiac output is increased mainly through increased heart rate and enhanced ventricular contraction.

When the body needs it, it first uses the heart rate reserve to increase cardiac output.

The load encountered by the myocardium before contraction (end-diastole)

heterologous autoregulation (law of the heart)

end diastolic volume = filling volume The amount of blood remaining in the ventricle after ejection

venous blood return volume (i.e. ventricular filling)

remaining health

The load encountered by the myocardium when it contracts, i.e. the arterial blood pressure (resistance to ejection of blood)

heterometric regulation

Isometric adjustment

Determines the speed at which the ventricles contract and the time it takes for the ventricular muscles to reach maximum tension.

Refers to an intrinsic characteristic of the myocardium that does not depend on preload or afterload, but can change the degree, speed, tension and other mechanical activities of the myocardium.

isometric autoregulation

the main factor of influence

The rate of each step in the cross-bridge cycle

Cytoplasmic Ca2 concentration during excitement (exogenous Ca2)

Troponin affinity for Ca2

form

significance

The cardiac cycle is prolonged → the filling volume reaches the limit, the filling volume does not increase with the extension of diastole, and the heart rate decreases → stroke volume↓

Heart rate ↑ (does not affect stroke volume)

Shortening of cardiac cycle→filling volume↓→stroke volume↓

The heart rate of newborns is faster, and as they age, the heart rate gradually slows down

The heart rate of adult women is slightly faster than that of men

People who often perform physical labor. People who do sports usually have a slow heart rate within a certain range. An accelerated heart rate can increase cardiac output.

Adr. Norepinephrine. Thyroid hormone ↑, increased heart rate

The heart rate is ↑ when the sympathetic nerve is excited, and the heart rate is ↓ when the vagus nerve is excited.

For every 1°C increase, the heart rate increases by 12 to 18 beats/min.

Excitatory, conductive, contractile

No self-discipline

Excitable, conductive and self-disciplined

No shrinkage

-90mv

starting power

resistance

The difference in ion concentration and Balance of transmembrane potential difference

Depolarization/Issue 0

Early stage of repolarization/Phase 1

Platform period/2nd period

End of repolarization/stage 3

Resting phase/Phase 4

There are fewer Ik1 channels → The resting potential is less negative → Normal potential: -80mV

Ito has more channels

Presence of acetylcholine-sensitive potassium current IK-ACh

Ik1 has fewer channels

When depolarization reaches the quenching potential level, an action potential can erupt.

mechanism

Influencing factors

Ik is activated, K flows out, and repolarization occurs

Outward current weakens

Increased inward current

Influencing factors

However, the maximum negative electrode potential of P cells is about -65mV, which cannot reach the threshold potential of fast sodium channels, and fast sodium channels are in an inactivated state.

Under the action of ACh, the maximum repolarization potential increases → automatic depolarization time course↑

the difference

When the 3rd stage repolarization reaches about -50mV

The duration of automatic depolarization determines the duration of action potential

less rhythmic than P cells

The ability to generate action potentials

Effective refractory period ERP

Relative refractory period RRP

Supernormal SNP

Note

Effective refractory period (ERP) reflects the depolarizing ability of the membrane (change in gNa) Action potential duration (APD) mainly reflects the repolarization speed of the membrane (change in gK)

The longer the time, the less exciting it is

distance

speed

Determines the presence or absence of excitability

factor

Adjacent cardiomyocytes are connected by intercalary disks, and there are many gap junctions in the sarcolemma at the intercalated disks, forming hydrophilic channels that communicate between adjacent cells, allowing action potentials to be transmitted from one cardiomyocyte to another. to another adjacent cardiomyocyte, thereby achieving excitation conduction between cells

Purkinje fibers conduct the fastest

ventricular muscle fiber conduction

The slowest speed is at the room-room junction

cell diameter

intercellular linkage

degree of cell differentiation

Phase 0 depolarization speed and amplitude

Excitability of areas adjacent to unexcited cells

sinus rhythm

potential pacemaker

ectopic pacemaker

It has high self-discipline. Before the self-regulatory tissue automatically depolarizes to the threshold potential level, the sinoatrial node impulse has been transmitted, which directly depolarizes it to the threshold potential level to produce AP.

After the sinoatrial node impulse or external driving stimulus stops, the autonomic tissue cannot immediately express its inherent rhythm, and it takes a period of time to gradually restore its autonomic nature (ventricular asystole occurs)

4-stage automatic depolarization speed

maximum repolarization potential level

threshold potential level

mechanism

Influencing factors

excitability versus contractility

conductivity versus contractility

The terminal pool of cardiomyocytes is underdeveloped and stores less Ca2. The Ca2 required for excitation-contraction coupling mainly comes from extracellular fluid.