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blood circulation
Mind map about blood circulation, the components of the circulatory system: Heart: The power (pump) that circulates blood Blood vessels: A system of tubes through which blood flows (distributes blood)
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blood circulation
introduction
The composition of the circulatory system
Heart: The power (pump) that circulates blood
Blood vessels: A system of tubes through which blood flows (distributes blood)
Function
Transport nutrients, metabolic raw materials and products
Achieve body fluid regulation
Maintain internal homeostasis
heart pumping function
Heart pumping process and mechanism
cardiac cycle
concept
Definition: A cycle of mechanical activity consisting of one contraction and relaxation of the atrium or ventricle.
Divided into systole and diastole
The cardiac cycle and heart rate have a reciprocal relationship. If the heart rate = 75 beats/min, then one cardiac cycle = 0.8s
Heart rate refers to the number of times the heart beats per minute, normal 60 to 100 beats/minute
The length of the cardiac cycle is related to the heart rate, and the two are reciprocals of each other.
The resting heart rate of an adult is 75 beats/minute, and the cardiac cycle is 0.8 seconds. Atrial systole occupies 0.1s and diastole 0.7s After the ventricular systole lasts for 0.3 seconds, it switches to ventricular diastole for 0.5 seconds (the first 0.4 seconds of ventricular diastole is the whole heart diastole)
Features
The atria contract anteriorly and the ventricles contract posteriorly.
Synchronous activity of the left and right atria or ventricles
Diastolic time > Systolic time
The global diastolic period is 0.4 seconds, which is conducive to myocardial rest and ventricular filling.
When the heart rate increases, the cardiac cycle shortens, especially the diastolic period. The working time of cardiomyocytes is relatively prolonged
heart pumping blood
heart pumping process
ventricular systole
Isovolumic contraction period (0.05s)
Process: The ventricle begins to contract, and the intraventricular pressure rises sharply → the atrioventricular valve closes (the arterial valve is still closed) → volume The product remains unchanged and blood does not flow → the ventricle continues to contract
Features
Indoor pressure rises fastest
Volume remains unchanged and blood does not flow
Rapid ejection period (0.1s)
Process: The ventricle continues to contract (intraatrial pressure <ventricular pressure>arterial pressure) → the aortic valve opens (the atrioventricular valve is still closed state) → rapid ejection of blood into the artery (accounting for 70% of ejection volume) → rapid decrease in ventricular volume
Features
At the end of the rapid ejection period, intraventricular pressure and aortic pressure are the highest
Less time spent, greater blood ejection volume
Slow down ejection period (0.15s)
Process: rapid ejection of blood into the artery → ventricular volume decreases (intraatrial pressure < intraventricular pressure > arterial pressure) → aortic valve opens, atrial valve opens The ventricular valve closes and inertia ejects blood into the artery (accounting for 30% of the ejected blood volume) → the ventricular volume continues to decrease.
Features: Slow down intraventricular pressure during ejection period < aortic pressure, rely on inertial pressure gradient to continue ejection
ventricular diastole
Isovolumic relaxation period (0.07s)
Process: The ventricle begins to relax, and the intraventricular pressure drops rapidly (atrial pressure < ventricular pressure < arterial pressure) → (intraventricular pressure = dynamic Pulse pressure) the main and pulmonary valves close, the atrioventricular valves close → the ventricles continue to relax → the intraventricular pressure drops sharply, the atrioventricular valves close ventricular valve remains closed
Features: Volume remains unchanged, blood does not flow
Rapid filling period (0.11s)
Process: At the end of isovolumetric diastole, intraventricular pressure decreases (intraatrial pressure > intraventricular pressure < arterial pressure) → atrioventricular valve opens, arterial The valve closes → the ventricle continues to relax, and the intraventricular pressure drops → the blood in the atrium and large veins quickly enters the ventricle (suction, Accounting for 2/3 of total filling) → ventricular volume rises rapidly
Slow down filling period (0.22s)
Process: ① The blood in the ventricles is filled → the pressure difference between the ventricles and the great atrium veins decreases (the speed of blood flowing into the ventricles slows down) ② Atrial systole: the atrium contracts, the atrial volume decreases → the intraatrial pressure increases → the atrioventricular valve opens (the arterial valve in a closed state) → squeeze blood into the ventricles (accounting for 25% of ventricular filling)
Features
In the first half, blood from the large veins flows into the ventricles through the atria, and in the second half, blood is squeezed into the ventricles during atrial systole.
At the end of the slowed filling phase, the ventricular volume reaches its maximum during atrial systole
atrial systole
is the end-diastolic phase of the previous round of ventricular activity
Before the atrial systole, the heart is in full diastole, the semilunar valves are closed, the atrioventricular valves are open, and the amount of blood returning to the ventricles accounts for 75% of the total ventricular filling volume.
The role of the atria in the heart's pumping of blood
primary pumping action of the atria
Ventricular filling mainly depends on the suction action of ventricular diastole
The contraction of the atrium increases the filling volume of the ventricle by 1/4 to 1/3, increases the end-diastolic volume of the ventricle, and increases the initial length of ventricular muscle contraction, thus improving the pumping function of the ventricle.
further filling of the ventricles
Reduce intraatrial pressure and facilitate venous return
Changes in intraatrial pressure during the cardiac cycle
Three smaller forward waves a, c, and v appear sequentially from the pressure curve recorded in the left atrium.
Cardiac output and heart pumping reserve
cardiac output
Stroke volume (stroke volume) and ejection fraction
Stroke volume: The amount of blood ejected from one ventricle in one heartbeat Stroke volume = ventricular end-diastolic volume - end-systolic volume (adult, quiet: 70ml)
Ejection fraction: stroke volume/ventricular end-diastolic volume=60~80/130~145ml=50~60%
significance
It is related to end-diastolic volume and cardiac contractility. The greater the ejection fraction, the less blood remains in the ventricle. It is an indicator of the heart's pumping function.
Increased cardiac contractility→increased stroke volume→increased ejection fraction
Ventricular enlargement and cardiac function decrease (stroke volume remains unchanged) → end-diastolic volume increases → ejection fraction decreases
Minute output and cardiac index
Output per minute
Definition: The amount of blood ejected from one ventricle per minute (cardiac output)
Cardiac output = stroke volume × heart rate = 70ml × 75 beats/min = 5.25L/min
Cardiac output is adapted to the body's metabolic level, and can be as high as 25~35L/min during strenuous exercise
The cardiac output of the human body at rest is directly proportional to the body surface area. Women are about 10% lower than men
heart index
Definition: Under resting conditions, cardiac output per square meter of body surface area = 3.0~3.5L/min·m2
Cardiac index = output per minute/body surface area
Meaning: To assess the cardiac function of different individuals
Reserve of heart pump function (cardiac reserve)
Concept: The ability of cardiac output to increase with the body's metabolic demands - cardiac reserve
Meaning: Reflects the health of the heart and the pumping function of the heart
The cardiac output in the resting state is 5L. During strenuous physical exertion, the cardiac output can reach 30L, which is 6 times the resting state.
mental reserve
Heart rate reserve (2-2.5 times)
stroke volume reserve
Systolic reserve (end-systolic volume reserve, increase in ejection fraction)
Diastolic reserve (ventricular end-diastolic volume reserve)
Factors affecting cardiac output (preload, afterload, contractility) Cardiac output = Stroke volume × Heart rate
Adjustment of stroke volume
front load
ventricular muscle preload
End-diastolic volume (=residual blood volume, venous return blood volume) is equivalent to preload
Preload → the muscle has a certain length (initial length)
Increased preload → increased initial myocardial length → increased myocardial contractility → increased stroke volume
Myocardial heterologous autoregulation
concept
Definition: Myocardial contractility changes with the initial length of the myocardium.
Features: small adjustment range
Meaning: Finely adjust stroke volume
Cardiac Function Curves and Heart Laws
cardiac function curve
Ventricular end-diastolic pressure or volume and Stroke volume or stroke work relationship curve
Within a certain range, preload (ventricular end-diastolic pressure) increases → stroke volume increases Excessive preload → Stroke volume no longer continues to increase
12~15mmHg is the optimal preload of the ventricle At this time, the effective overlap between thick and thin myofilaments in the sarcomere is optimal, and the myocardial contractility is strongest.
The filling pressure is between 15~20mmHg → the curve becomes flatter Changes in preload within this range have little effect on pumping function
There is no obvious descending branch of the curve subsequently (unlike skeletal muscle) Obvious descending branches only appear in severe pathological cases The reason why there is no obvious descending branch: the extracellular matrix of myocardial cells contains a large number of collagen fibers, which prevents myocardial cells from being further elongated.
Heart Law: The phenomenon that increasing ventricular end-diastolic volume within a certain range can enhance ventricular contractility
Contractility: isometric autoregulation
Concept: The myocardium can change its mechanical activity (including the intensity and speed of myocardial contraction) independent of preload and afterload. an intrinsic characteristic that regulates stroke volume
Significance: It has a powerful regulatory effect on sustained and severe cyclic changes.
Myocardial contractility increases → the cardiac function curve shifts to the upper left Myocardial contractility decreases→cardiac function curve shifts to the lower right
isometric autoregulation
The mechanism of regulating blood pumping function by changing myocardial contractility
Increase in blood pressure → decrease in stroke volume → increase in myocardial contractility → increase in stroke volume
Influencing factors: Affected by various links in the excitation-contraction coupling and myofilament sliding process
Number of activated cross-bridges: Depends on the intracytoplasmic Ca2 concentration (catecholamines) and Troponin affinity for Ca2 (calcium sensitizers such as theophylline)
ATPase activity of myosin head (increased by thyroid hormone and physical exercise)
Afterload: aortic blood pressure
Arterial blood pressure continues to rise → Long-term myocardial contraction is strengthened → Myocardial hypertrophy (pathological) → Decreased blood pumping function (hypertensive heart disease)
Regulation of heart rate [increase in heart rate (HR) → increase in cardiac output] *within a certain range*
HR>170~180 times/min (HR is too fast) Ventricular energy consumption increases, ventricular filling time decreases significantly → filling volume decreases Ventricular energy consumption increases, ventricular filling time decreases significantly → stroke volume decreases → cardiac output decreases
HR<40 times/min (HR is too slow) The diastolic period is too long → the ventricular filling reaches the limit → the stroke volume cannot be increased → the cardiac output decreases
Factors leading to an increase in HR
Increased sympathetic nervous activity
Increased adrenaline and norepinephrine in the blood
Increased thyroid hormone (hyperthyroidism)
body temperature rises
Factors leading to HR decline
Increased vagus nerve activity
Assessment of cardiac function
heart work
heart contraction work
Pressure energy (potential energy) – creates and maintains blood pressure (99%)
Kinetic energy - promote blood flow (1%)
heart work capacity
More comprehensive than simply using cardiac output to evaluate cardiac pumping function
When arterial blood pressure increases, the ventricle must strengthen contraction, increase oxygen consumption and work in order to eject the same amount of blood as before.
Stroke power = stroke volume × 1/103 × (mean arterial pressure - mean atrial pressure) × 13.6 = 83.1 (g·m) Work per minute = stroke work × heart rate × 1/103 = 6.23 (Kg·m/min) Efficiency of the heart = external work done by the heart/oxygen consumption of the heart
heart sounds
Heart sounds are produced by vortexes formed by heart contraction, valve closure, changes in blood flow velocity, and blood hitting the ventricular wall. and vibrations caused by aortic walls
Most of the time during the cardiac cycle, only the first and second heart sounds can be heard.
The first heart sound marks the beginning of ventricular contraction The second heart sound marks the onset of ventricular relaxation
Electrophysiology and physiological properties of the heart
introduction
myocardial tissue
Excitability
self-discipline
conductivity
Electrophysiological properties
Contractibility
Mechanical properties
Cardiomyocytes
Working cells: maintain the pumping function of the heart Atrial and ventricular myocytes Contractile, excitable, conductive, no self-discipline
Autonomic cells: generate and propagate excitement and control the rhythmic activity of the heart (special conduction system) Sinoatrial node P cells, Purkinje cells Excitable, conductive, self-disciplined, non-contractile
Transmembrane potential of cardiomyocytes and its formation mechanism
Working cell transmembrane potential and its formation mechanism
Resting potential (ventricular myocytes)
Amplitude: -90mV
Mechanism: K equilibrium potential (similar to skeletal muscle), [K ]i>[K ]o - the cell membrane is highly permeable to K
Action potential (ventricular myocytes) Features: Has a slow 2-stage plateau period
Features
All or none, pulsed (cannot be summed), unattenuated conduction
The repolarization process is complex, lasts for a long time, and the descending limb and ascending limb are very asymmetrical. There is a longer 2-stage plateau period
Action potential is divided into phases 0, 1, 2, 3, and 4
Depolarization: 0 period
Transmembrane potential: -90mv→ 20~ 30mv (super emission)
Opening time: only 1~2ms, 200~400V/s
Fast sodium channel: -70mv activation, lasting 1~2ms, strong specificity (only Na permeable), blocker (TTX)
Process: stimulation → depolarization → threshold potential → activation of fast sodium channels → Na influx → Na equilibrium potential (phase 0)
Early stage of rapid repolarization: 1 period
Transmembrane potential: 20~ 30mv→0mv
Development time: 10ms
K channel: can be blocked by K channel blockers (tetraethylamine, 4-aminopyridine)
Process: inactivation of fast sodium channels → a transient outward current, activation of K channels → K outflow → rapid repolarization (Phase 1)
Platform period (2nd period)
Transmembrane potential: 0mv (main characteristic of ventricular muscle)
Opening time: 100~150ms
Slow Ca2 channel: activation and deactivation are slower than Na channel; blocker (Mn2, verapamil)
Process: When depolarization reaches -40mv in phase 0, the slow Ca2 channel is activated → the K current channel is activated → Ca2 slow The inflow and K outflow are in equilibrium → slow repolarization (plateau period)
End of rapid repolarization (Phase 3)
Transmembrane potential: 0mv~-90mv
Opening time: 100~150ms
Process: slow Ca2 channel inactivation → K current channel permeability increases → K outflow gradually increases (positive feedback) → fast Rapid repolarization to resting potential level (Phase 3)
Resting period (4th period)
The membrane potential is stable at -90mv (Na -K pump, Na -Ca2 exchange and Ca2 pump)
Process: Na and Ca2 increase inside the membrane, K increases outside the membrane → activate proton pump → pump out Na and Ca2 pump, pump Enter K → restore normal ion distribution
Autonomic cell transmembrane potential and its mechanism
Overview
The ability of the myocardium to automatically produce excitement according to a certain rhythm - autodiscipline
The bioelectricity characteristic of autonomous cells is four stages of automatic depolarization. When the threshold potential is reached, a new action potential bursts out.
Can cause autonomous cells to generate automatic depolarization inward current, also called pacing current
Purkinje cell action potential
The action potential is similar to that of ventricular myocytes, but with phase 4 automatic depolarization
Phase 4: The inward current If (Na inward flow) gradually increases, and the K outward current gradually decreases (the effect of the If current is host). If current can be blocked by cesium (Cs)
Sinoatrial node cell action potential
Morphological characteristics of sinoatrial node cell AP
The absolute values of the maximum repolarization potential (-70mv) and threshold potential (-40mv) are smaller than those of Purkinje fibers
Phase 0 depolarization is slower than Purkinje fibers (7ms) and has a lower amplitude (70mv)
No repolarization phase 1 and phase 2 plateau
Phase 4 automatic depolarization is faster than Purkinje fibers
The formation mechanism of AP in sinoatrial node cells The maximum repolarization potential is -60~-65mv; the net inward current causes automatic depolarization → threshold potential (-40mv)
Phase 0: When phase 4 automatic depolarization reaches the threshold potential → activate slow Ca2 channel (L-type calcium channel) → Ca2 inflow → Phase 0 depolarization (-40~0mv)
Stage 3: Slow calcium channels are gradually inactivated, potassium channels are activated → Ca2 inflow decreases, K outflow → Stage 3 repolarization (0~-65mv)
Phase 4: Decreasing outflow of K (the most important ion basis), increasing influx of Na (If), influx of Ca2 (L type calcium channel activation) → slow depolarization (-65~-40mv)
Whether to depolarize automatically according to phase 4: autonomous cells, non-autonomous cells According to the speed of phase 0 depolarization: fast responding cells, slow responding cells
Depolarization is caused by Na→fast response cells (ventricular myocytes, Purkinje cells) Depolarization is caused by Ca2 → slow responding cells (sinoatrial node cells)
Physiological properties of cardiomyocytes Electrophysiological properties: excitability, conductivity, autonomy; mechanical properties: contractility
Excitability: the ability of cardiomyocytes to become excited in response to stimulation Metric: Threshold Strength (Threshold)
Factors affecting excitability
Resting potential (RP) level
RP moves downward → farther away from the threshold potential → the threshold for stimulation increases → the excitability decreases
RP moves upward→closer to the threshold potential→threshold for stimulation decreases→excitability increases
threshold potential level
The threshold potential shifts upward → the RP is far away from the threshold potential → the threshold for stimulation increases → the excitability decreases
The threshold potential shifts downward → RP is closer to the threshold potential → the threshold for stimulation decreases → the excitability increases
Properties of ion channels that cause phase 0 depolarization
Three functional states: activation, deactivation and standby
Whether most of the sodium channels (or calcium channels) on the cell membrane are in a standby state is a prerequisite for whether the cell is excitable.
Cyclic changes in excitability
Due to the existence of the plateau phase, the effective refractory period (ERP) is particularly long (200ms), which is equivalent to ventricular systole and early diastole (an important electrophysiological characteristic of ventricular myocytes)
A long effective refractory period can ensure that the ventricular muscle does not contract tonic, realizes the rhythmic activity of alternating contraction and relaxation, and ensures normal blood pumping function.
Premature contractions and compensatory pauses
Premature contraction: The heart receives a stimulus other than sinus rhythm and the contraction occurs before sinus rhythm contraction, which is called systolic contraction. Anterior contraction, also called premature contraction
Compensatory interval: A longer period of relaxation that occurs after a presystole is called a compensatory interval.
self-discipline Indicator: Frequency of automatic excitement per unit time
Concept: The heart can automatically produce rhythmic excitation without the influence of external factors.
The bioelectricity characteristic of autonomous cells is four stages of automatic depolarization. When the threshold potential is reached, a new action potential bursts out.
Differences in levels of automaticity within the heart: Sinoatrial node>Atrioventricular node>Purkinje's fibers 100 50 25
Whether to depolarize automatically according to phase 4: autonomous cells, non-autonomous cells According to the speed of phase 0 depolarization: fast responding cells, slow responding cells
pacemaker
Normal pacemaker and ectopic pacemaker
Normal pacemaker - sinoatrial node (sinus rhythm)
Ectopic pacemaker – a pacemaker outside the sinoatrial node (ectopic rhythm)
Causes of arrhythmia
autorhythmia
sinoatrial node rhythmic suppression
conduction block
The control mechanism of the sinoatrial node on potential pacemakers
Seize the first opportunity: The sinoatrial node is more autonomous than other potential pacemakers
Overdrive suppresses autonomic cells when subjected to higher than their natural frequencies When stimulated, it will be excited according to the frequency of external stimulation.
Factors affecting self-discipline
The distance between the maximum repolarization potential and the threshold potential
The gap between the maximum repolarization potential and the threshold potential decreases → the time for automatic depolarization to reach the threshold potential decreases → the autonomy increases
The gap between the maximum repolarization potential and the threshold potential increases → the time for automatic depolarization to reach the threshold potential increases → the autonomy decreases
4-stage automatic depolarization speed
Fast automatic depolarization → Short time to reach threshold potential → Increased self-discipline
The speed of automatic depolarization is slow → the time to reach the threshold potential is long → the autonomy is reduced
conductivity Index: action potential conduction velocity
Concept: Cardiomyocytes have the ability or characteristic to conduct excitation
Principle: local current
The part with the fastest conduction speed: Purkinje fiber, up to 4m/s The intercalated disk (gap link) structure between cardiomyocytes forms a low-resistance area, making the ventricular muscle a functional syncytium with high contraction synchrony.
Characteristics of intracardiac conduction: two fast and one slow
Atrioventricular delay: Because the conduction speed of excitement in the atrioventricular junction area is particularly slow, it takes a while for excitement to pass through here. conduction to the ventricles, this phenomenon is called atrioventricular delay Significance: Make the ventricles start to contract after the atria have completed contraction, ensuring that the atria and ventricles can relax and contract in sequence and in a coordinated manner. activities to ensure the realization of the heart’s pumping function
Factors affecting conductivity
structural factors
cell diameter Large cell diameter → small internal resistance → large local current → increased conductivity
Purkinje fiber cells: 70μm, 4m/s Sinoatrial node cells: 5-10μm, 0.05m/s Atrioventricular node cells: 0.3μm, 0.02m/s
Number and openness of intercellular gap links The number of intercellular gap links in the atrioventricular junction zone is small → the conduction velocity is slow
Differentiation Atrioventricular node cells are composed of more embryonic cells
physiological factors
Action potential phase 0 depolarization speed and amplitude
Phase 0 depolarization is fast → local current is formed quickly → conductivity is increased
Phase 0 depolarization amplitude is large → local current is strong → conductivity increases
Excitability of the myocardium adjacent to unexcited areas
The absolute value of the resting potential of the adjacent membrane increases or the threshold potential shifts upward → the excitability decreases → the time required for membrane depolarization to reach the threshold potential increases → the conductivity decreases
Contractibility
Characteristics of myocardial contraction
No complete tetanic contraction: the myocardium always maintains a rhythmic movement of alternating contraction and relaxation.
"All-or-none" contraction: ensuring that all parts of the heart work together
Ca2 dependence: [Ca2 ]o rises → Ca2 influx increases → muscle contraction increases [Ca2]o decreases→Ca2 inflow decreases→muscle contractility decreases
Calcium-induced calcium release mechanism (myocardium)—sarcolemmal depolarization activates L-type calcium channels and Ca2 influx. Ca binds to the calcium binding site of the sarcoplasmic reticulum, causing the opening of calcium release channels Conformational changes trigger calcium release (skeletal muscle) - depolarization of the sarcolemma causes voltage sensitization of L-type calcium channels The displacement of the peptide segment leads to a conformational change like a "plugging" effect, which opens the sarcoplasmic reticulum calcium release channel.
Surface electrocardiogram (ECG)
The recording method of ECG is extracellular recording, and what is recorded is the comprehensive vector change of the electrical activity of each cell in the entire heart during the cardiac cycle.
Applications of electrocardiogram: twelve leads
effect
Record the electrical activity of the normal human heart
Determine the impact of medications or electrolytes on the heart
Six limb leads Six chest leads
Three standard limb leads and three compression limb leads: 1 positive 2 negative
six chest leads
Normal electrocardiogram waveforms and their significance
P wave: atrial depolarization, 0.08~0.11s
QRS complex: ventricular depolarization (waveform is large and complex), 0.06~0.1s, under normal circumstances, atrial repolarization wave masked in QRS waves
T wave: ventricular repolarization, 0.05~0.25s
U wave: visible in some leads; currently thought to be related to ventricular repolarization
PR interval: atrioventricular conduction interval, 0.12~0.20s Fast heart rate, short PR interval; conduction block, prolonged PR interval
QT interval: the time from ventricular depolarization to repolarization Fast heart rate, shortened QT interval; slow heart rate, prolonged QT interval
ST segment
Normal: level with baseline
Abnormal: deviation from baseline (myocardial ischemia, acute myocardial infarction)
organ circulation
Regulation of cardiovascular activity
introduction
Purpose of adjustment: Adapt to the body's needs
Stabilize blood pressure
Coordinate blood supply to various organs
Adjustment method
neuromodulation
body fluid regulation
self-regulation
Long-term regulation of arterial blood pressure (renal)
neuromodulation
cardiovascular innervation
innervation of heart
cardiac sympathetic nerve
Origin: mediolateral columns T1~5 of the spinal cord
Innervation: various parts of the heart including the sinoatrial node, atrioventricular node, atrioventricular bundle, atrial myocardium and ventricular myocardium
Postganglionic fiber transmitter: norepinephrine (NE)
Physiological effects: Binds with β1 receptors on myocardial cell membrane, producing positive chronotropy, positive inotropy, and positive inotropy conduction.
Mechanism of action of cardiac sympathetic nerves
cardiac vagus nerve
Origin: Dorsal vagal nucleus and nucleus ambiguus of the medulla oblongata
Innervation: Various parts of the heart including the sinoatrial node, atrial myocardium, atrioventricular junction, atrioventricular bundle and its branches
Postganglionic fiber transmitter: acetylcholine (ACh)
Physiological effects: Binds to the M receptor on the myocardial cell membrane to produce negative chronotropy, negative inotropy, and negative inotropy conduction
Mechanism of action of cardiac vagus nerve
The role of Ca2 in the physiological functions of cardiomyocytes
systolic function
Key ions for excitation-contraction coupling Increased intracellular [Ca2]→increased myocardial contractility
The opening of L-type calcium channels on the membrane increases, and extracellular [Ca2] increases
conduction function
Action potential phase 0 depolarization Increased speed and amplitude → increased conduction velocity
Increased opening of L-type calcium channels on slow-responsive cell membranes
"Self-discipline" function
In Phase 4, the inward current increases → the pacing frequency increases → the heart rate increases
Increased opening of T-type calcium channels on the sinoatrial node cell membrane
Characteristics of cardiac neuromodulation
Innervated by dual nerves: vagus nerve; sympathetic nerve - mutual antagonism and mutual inhibition
The vagus nerve is dominant in the quiet state
There is usually a certain amount of nervous activity, and the nerve fibers continue to send low-frequency impulses. Increased sympathetic nervous activity → increased heart rate Increased vagus nerve activity → decreased heart rate
innervation of blood vessels
sympathetic vasoconstrictor nerve fibers
Overview
Almost all blood vessels are innervated by sympathetic vasoconstrictor nerves (except capillaries)
Most blood vessels in the body are only innervated by sympathetic vasoconstrictor nerves, but with different densities. Distributed most densely in skin, skeletal muscles, and internal organs; least in heart and cerebral blood vessels Among the blood vessels of the same organ, the arterioles are most densely distributed
Origin: thoracolumbar segment of spinal cord
Change point: paraganglion or prevertebral ganglion
Postpartum fiber release transmitter: norepinephrine (NE)
Receptor: alpha receptor - vasoconstriction β2 receptors – vasodilation
Features
Different blood vessels have different nerve distribution densities Skin>Skeletal muscle>Internal organs>Coronary arteries, cerebral arteries Among the blood vessels of the same organ, the arterioles are most densely distributed
There is always a continuous impulse to maintain the basic tone of blood vessels Sympathetic vasoconstrictor fiber impulse ↑ → further contraction of vascular smooth muscle Sympathetic vasoconstrictor fiber impulse↓→Vascular smooth muscle relaxation
sympathetic vasoconstrictor nerve fiber excitation
Vasoconstriction→Total peripheral resistance↑→Blood pressure↑
Vasoconstriction → Increased organ blood flow resistance → Organ blood flow↓
Pre-capillary resistance/post-capillary resistance↑→Capillary pressure↓→Tissue fluid reabsorption↑, generation↓
Volume vasoconstriction → venous return↑
vasodilatory nerve fibers Generally not involved in blood pressure regulation
Sympathetic vasodilatory nerve fibers
Neurotransmitter: acetylcholine
Receptor: M receptor
Distribution area: skeletal muscle arterioles
Effect: Vasodilation, increased skeletal muscle blood flow
parasympathetic vasodilatory nerve fibers
Neurotransmitter: acetylcholine
Receptor: M receptor
Distribution area: salivary glands, gastrointestinal glands, blood vessels of external genitalia, etc.
Effect: vasodilation, increased local blood flow
cardiovascular center Medulla Oblongata: Basic Cardiovascular Center
Definition: A site where neurons related to controlling cardiovascular activity are concentrated. Available at all levels, mainly in the medulla oblongata
Medulla oblongata: Important nuclei that regulate cardiovascular activity
The ventrolateral part of the rostral end of the medulla oblongata - the constrictor area: enhances cardiac sympathetic tone and sympathetic constrictor tone. Descending fibers arrive Spinal cord, controls sympathetic preganglionic neuron activity
The ventrolateral part of the caudal end of the medulla oblongata - the vasodilatory area: reduce the sympathetic vasoconstrictor tension
Nucleus tractus solitarius - afferent nerve relay station for baroreceptive reflex
Dorsal nucleus of the vagus nerve and nucleus ambiguus, central vagal tone
cardiovascular reflex
Carotid sinus-aortic arch baroreflex (depressor reflex) negative feedback regulation
Reflection arc composition
Baroreceptors: sensory nerve endings under the adventitia of the carotid sinus and aortic arch vessels
Instead of directly feeling the changes in blood pressure, you can feel the stretch of the blood vessel wall. The degree of expansion of the arterial wall is proportional to the frequency of incoming impulses
Afferent nerves: carotid sinus → sinus nerve → glossopharyngeal nerve Aortic arch → (decompression nerve) → vagus nerve
central-medullary nucleus of the solitary tract
Efferent nerves: cardiac vagus, cardiac sympathetic and sympathetic vasoconstrictor nerves
Effector - heart and blood vessels
Baroreceptor reflex function curve
Isolating the carotid sinus from the rest of the circulatory system while maintaining its connection with the central nervous system through the sinus nerves, artificial Change the perfusion pressure in the carotid sinus and observe the changes in systemic blood pressure
Relationship curve between intrasinus pressure and arterial blood pressure: baroreceptor reflex function curve
When mean arterial pressure = intrasinus pressure, it is the closed-loop working point of this reflex, indicating that the intrasinus pressure and mean arterial pressure are at this Balance is reached horizontally through this reflex, which is the set point of the baroreceptor reflex. At this time, the normal blood pressure range has an impact on the blood pressure. pressure regulation is the most sensitive
Physiological significance: Rapid regulation of arterial blood pressure in a short period of time does not play a major role in long-term regulation of arterial blood pressure.
Hypertensive patients: reprogramming of the baroreceptor reflex In chronic hypertensive patients or experimental hypertensive animals, the baroreflex function curve shifts to the upper right and the setting point rises, which is called the resetting of the baroreceptor reflex.
Baroreceptor reflex function curves of normal people and hypertensive patients
Carotid and aortic body chemoreceptive reflexes
Suitable stimulation: PO, decrease, PCO, increase, H increase
①PO2↓, PCO2↑, [H ]↑→Carotid body and aortic body chemoreceptors→Sinus nerves and vagus nerve→Respiratory center→Deepened and accelerated breathing (mainly) ② PO2↓, PCO2↑, [H ]↑→ Carotid body Aortic body chemoreceptors → Sinus nerve Vagus nerve → Cardiovascular center → Heart rate and cardiac output ↑, brain and cardiac blood flow ↑ Abdominal and splanchnic blood flow ↓, peripheral resistance ↑ →blood pressure↑
physiological significance
① Within the normal blood pressure range, chemoreceptors mainly regulate breathing and have no significant regulatory effect on blood pressure. The chemoreceptor reflex only works in emergency situations: ① The blood pressure is too low and the chemoreceptors are obviously hypoxic in the local area. ②Hypoxic environment, asphyxia ③Acidosis
②In emergency situations, the heart rate is accelerated, cardiac output is increased, blood pressure is increased, and blood flow to the skin and internal organs is reduced to ensure adequate blood supply to the brain and heart - relocation to relieve emergencies
cardiovascular reflexes from cardiorespiratory receptors Cardiopulmonary receptors are also called volume receptors
Receptors—atria, ventricles, and walls of large blood vessels in the pulmonary circulation
Suitable stimulation: mechanical stretch: BP↑/blood volume↑→stretch↑→receptor excitability↑ Chemical substances: prostaglandins, bradykinin, etc.
Physiological significance: ① Usually there are tense impulses, which inhibit the cardiovascular center and reduce blood pressure and renin levels. Not too high ② part will cause the heart rate to increase. Regulate circulating blood volume
process
cardiovascular reflexes induced by somatosensory receptors Stimulation of somatic afferent nerves (intensity and frequency of stimulation) → cardiovascular reflexes
Cardiovascular reflexes caused by other visceral receptors Dilation of internal organs → slowing of heart rate, peripheral vasodilation → transient blood pressure↓
Oculo-cardiac reflex and Galtz reflex Pressing the eyeballs and squeezing the abdomen → cardiovascular reflex
cerebral ischemic response Cerebral blood flow ↓ → Sympathetic vasoconstrictor tension ↑ → Peripheral vasoconstriction, arterial blood pressure ↑ → Restore blood supply to the brain
body fluid regulation
renin-angiotensin system The renin-angiotensin-aldosterone system plays an important role in the long-term regulation of arterial blood pressure
Composition of the renin-angiotensin system
Schematic diagram of the conversion process
Renin: an acidic protease synthesized and secreted by renal juxtamlomerular cells
Angiotensinogen in plasma can be converted into angiotensin I under the action of renin; and then converted into angiotensin II and III under the action of corresponding enzymes.
Biological effects of angiotensin Ⅱ (Ang Ⅱ) Angiotensin II is a highly active blood pressure substance
It can constrict the arterioles throughout the body and increase peripheral resistance; it can also constrict veins, increase the amount of blood returned to the heart, and increase cardiac output.
Causes the adrenal cortex to release aldosterone, which promotes the reabsorption of Na and water by the renal tubules.
Promote the release of norepinephrine from sympathetic nerve endings
Acting on certain parts of the brain through the ventricular wall, the nervous activity of the sympathetic vasoconstrictor center is strengthened, and the peripheral vascular resistance is increased (sympathetic excitement)
Adrenaline and norepinephrine
Catecholamines
Source: Mainly adrenal glands, minor sympathetic nerve endings Adrenal medulla secretes: ① Norepinephrine (NE): 20% ②Adrenaline (E): 80%
intravenous norepinephrine
Vasopressin (antidiuretic hormone)
process
effect
Antidiuretic effect: Acts on the V2 receptors of the renal distal convoluted tubule and collecting duct → promotes water reabsorption → urine output↓ (at physiological dose)
Constrict blood vessels: Act on V1 receptors on vascular smooth muscle →constrict blood vessels →blood pressure↑ (at large doses)
Plays an important role in maintaining a constant extracellular fluid volume and arterial blood pressure.
Vascular Physiology
introduction
Microcirculation
Capillaries - exchange of substances
venule
arterioles
Vascular wall
The blood vessel wall includes
smooth muscle
Fibrous connective tissue – collagen
elastic fiber tissue - elastin
Structurally and functionally intact endothelial cells on the inner side of the blood vessel wall
Functional characteristics of various types of blood vessels
Functional classification of blood vessels (physiological functions)
elastic reservoir vessel
Structural features
Aorta, main pulmonary artery and their largest branches
The tube wall is thick, rich in elastic fibers, and has obvious elasticity and expansibility.
Features
Buffers blood pressure fluctuations and can withstand larger blood pressure
Maintain continuous blood flow within the arterial system
Blood can pass quickly with less resistance
Pressure vessel: potential energy of heart contraction
low compliance
Compliance: Evaluates how vessel pressure changes as volume changes Aorta - low compliance, high pressure, easy pumping of blood High compliance - easy to expand, easy to store blood, not easy to pump out
elastic blood vessel wall
systolic dilation
diastolic retraction
distribute blood vessels
Structural features
The arterial duct from behind the elastic reservoir vessel to before branching into arterioles, that is, the middle artery
Features
Transport blood to various organs throughout the body
precapillary resistance vessels
Structural features
Including arterioles and arterioles, which have smaller diameters and greater resistance to blood flow
Vascular walls are rich in smooth muscle
The inner diameter is less than 0.1mm, there are few elastic fibers, smooth muscles can adjust the inner diameter, and there is more sympathetic nerve distribution
Features
Adjust blood flow resistance
Caliber is regulated by neurohumoral factors
The main part of the body that regulates organ blood flow and blood redistribution
precapillary sphincter
Structural features
The smooth muscle that surrounds the origin of true capillaries and is part of the resistance vessels
Features
Control the opening amount of capillaries within a certain period of time
exchange blood vessels
Structural features
Capillaries are small in diameter and their walls are composed of only a single layer of endothelial cells with high permeability.
Features
Blood flows through capillaries from small arteries to medium arteries (site of material exchange)
postcapillary resistance vessels
Structural features
venule
Features
Diastolic activity can affect the ratio of front and rear resistance of capillaries, thereby changing the blood pressure, blood volume and filtration function of capillaries, and affecting the distribution of body fluids inside and outside blood vessels.
volumetric vessels
Structural features
venous system
Features
Blood storage bank (60%~70%)
Great adaptability
Have venous valves
Low mean venous pressure (2mmHg)
short circuit blood vessel
Structural features
Anastomotic branches between arterioles and venules in a vascular bed
Features
related to body temperature regulation
endocrine function of blood vessels
Endocrine functions of vascular endothelial cells
The synthesized and released vasodilator substances and vasoconstrictor substances (endothelin, thromboxane A2) restrict and balance each other.
Damage to vascular endothelial cells reduces the release of vasodilator substances (nitric oxide, hydrogen sulfide, prostacyclin, etc.)
Endocrine functions of vascular smooth muscle cells
Synthesize and secrete renin and angiotensin to regulate local blood vessel tone and blood flow
Synthesis of extracellular matrix collagen, elastin and proteoglycans
Endocrine functions of other blood vessel cells
Protect, support and nourish blood vessels
secrete vasoactive substances
Hemodynamics
Overview
fluid laws
The circulatory system is a closed system
Blood flow puts pressure on blood vessels
Blood flows along the pressure gradient
pressure gradient in the cardiovascular system
Blood flows along the pressure gradient = overall flow
Pressure gradient is produced by the heart
Pressure gradient persists
systemic pressure gradient
Aortic pressure = mean arterial pressure (MAP) = 90
Vena cava pressure = central venous pressure (CVP) = 0
Systemic pressure gradient = aortic pressure - vena cava pressure = mean venous pressure - central venous pressure = 90mmHg
Pulmonary resistance < systemic resistance
pressure gradient in pulmonary circulation
Pulmonary artery pressure=15
Pulmonary venous pressure=0
Pulmonary circulation pressure gradient = pulmonary artery pressure - pulmonary venous pressure = 15mmHg
Blood flow (Q) and blood flow velocity
Blood flow (Q) refers to the amount of blood flowing through a certain blood vessel cross-section per unit time.
Blood flow resistance (R)
Blood flow resistance (R) comes from external friction (L, r) and internal friction (η), and total peripheral resistance mainly comes from arterioles
Factors affecting blood viscosity: hematocrit, blood flow shear rate, blood vessel caliber, temperature
Influencing factors
Inner diameter of blood vessels: vasoconstriction, resistance becomes larger; vasodilation, inner diameter becomes larger, resistance becomes smaller
Blood vessel length: The longer the blood vessel, the greater the resistance; the shorter the blood vessel, the smaller the resistance.
The viscosity of blood = eta, determined by the number of red blood cells and protein concentration
When the radius of the blood vessel is reduced by half, the blood flow resistance increases to 16 times its original value.
Arterioles and arterioles are the main sites that produce resistance to blood flow
blood pressure
The amount of blood flow in an organ is mainly affected by mean arterial pressure and blood vessel radius.
Changes in the caliber of arterioles and arterioles are the most important factor in regulating organ blood flow and blood redistribution between organs
The drop in blood pressure is directly proportional to the blood flow resistance. The drop in blood pressure is most significant in the arteriole segment with the greatest blood flow resistance.
arterial blood pressure and arterial pulse
arterial blood pressure
The definition of blood pressure: the lateral pressure of the blood flowing in the blood vessel on the blood vessel wall per unit area, that is, the pressure of the blood
arterial blood pressure formation
The three elements (heart, blood, and tubes) that form arterial blood pressure: sufficient blood volume, heart pumping, and certain peripheral resistance
One center and two basic points
Prerequisites
Enough blood to fill the cardiovascular system
The degree of blood filling in the circulatory system can be expressed by the average filling pressure of the circulatory system The average filling pressure of the human circulatory system is about 7mmHg
Mean filling pressure depends on the relationship between blood volume and vascular volume Increase in blood volume or decrease in vascular volume and increase in average filling volume Blood volume decreases or vascular volume increases, and average filling volume decreases
Basic factors (necessary conditions)
heart ejection
The energy produced by the contraction of the ventricular muscles is used in two ways: as kinetic energy for blood flow and as potential energy for the expansion of the aorta.
Kinetic energy - 1%, potential energy - 99%
peripheral resistance
Mainly refers to the resistance of arterioles and arterioles to blood flow
As the blood flows, the pressure gradually decreases
auxiliary factors
Aortic elastic reservoir function
effect
Buffers blood pressure fluctuations
Continuous blood flow in blood vessels
Increasing age → Decreased compliance of blood vessel wall → Decreased elastic reservoir function → Significant increase in systolic blood pressure and increased diastolic blood pressure
Arterial blood pressure measurement and normal values
normal values for arterial blood pressure
Systolic blood pressure: the blood pressure that reaches its highest value in the middle of ventricular systole (100~120mmHg)
Diastolic blood pressure: the blood pressure at the end of ventricular diastole when the arterial blood pressure reaches its lowest value (60~80mmHg)
Pulse pressure: the difference between systolic blood pressure and diastolic blood pressure, related to aortic elasticity (30~40mmHg)
Mean arterial pressure (MAP) = diastolic blood pressure 1/3 pulse pressure = 1/3 systolic blood pressure 2/3 diastolic blood pressure =Heart rate (HR)×Stroke volume (SV)×Total peripheral resistance (TRP) =100mmHg
Factors affecting mean arterial pressure: heart rate, stroke volume, peripheral resistance
Measurement of arterial blood pressure
Generally refers to the aortic pressure. Because the blood pressure drop is small, the brachial artery pressure measured on the upper arm is usually used as the aortic pressure.
Direct method: cannulation (radial artery, femoral artery, dorsalis pedis artery cannulation) Indirect method: Korotkoff sound auscultation method
Direct measurement method is mostly used in critical patients
Hypertension and Prehypertension
Diagnostic criteria for hypertension Hypertension is defined as blood pressure ≥140/90mmHg in adults at rest
In 1998, systolic blood pressure ≥140mmHg or diastolic blood pressure ≥90mmHg was considered hypertension. If it is not reached, it is prehypertension. The lower limit of normal is 90/60mmHg. Normal arterial blood pressure has gender, age and individual differences.
2017
Diagnostic criteria for hypotension
It is generally believed that adults with arterial blood pressure lower than (90/60mmHg) are hypotension/shock
Classification of clinical manifestations of hypotension
acute hypotension
The patient's blood pressure suddenly drops from normal or higher levels, and in severe cases, syncope and shock may occur.
chronic hypotension
constitutional hypotension
It is more common in women and the elderly and is generally believed to be related to genetics or physical weakness.
orthostatic hypotension
Hypotension due to postural changes
secondary hypotension
Certain diseases or medications can cause low blood pressure
Clinically, high blood pressure often causes damage to important organs such as the heart, brain, and kidneys, while hypotension may be caused by disease or damage to the body's organs. Therefore, clinical diagnosis should pay attention to the symptoms of hypotension
Factors affecting arterial blood pressure
cardiac stroke volume
Changes in stroke volume mainly affect systolic blood pressure The level of systolic blood pressure mainly reflects the stroke volume
heart rate
Changes in heart rate mainly affect diastolic blood pressure
peripheral resistance
Peripheral resistance mainly affects diastolic blood pressure The level of diastolic blood pressure mainly reflects the size of peripheral resistance.
Elastic reservoir function of aorta and large arteries
The elastic reservoir function mainly reduces the fluctuation amplitude of arterial blood pressure during the cardiac cycle.
Decreased elasticity of large arteries (simple large arteriosclerosis) → increased systolic blood pressure, decreased diastolic blood pressure, and significantly increased pulse pressure Both large arteries and small arteries are sclerotic (elderly people) → systolic blood pressure rises significantly, diastolic blood pressure rises, and pulse pressure rises
Matching of circulating blood volume and vascular system capacity
Massive blood loss → Decreased circulating blood volume → Significant drop in blood pressure (blood volume needs to be replenished)
Allergy, toxic shock → increase in blood vessel volume → decrease in blood return to the heart → decrease in blood pressure (vasoconstriction is required)
Increase in circulating blood volume or decrease in blood vessel volume → increase in blood pressure (physiological basis for blood transfusion and vasoconstrictor drugs to increase blood pressure)
arterial pulse
Overview
Definition: During each cardiac cycle, the intra-arterial pressure generates periodic waveforms, causing the arterial wall to pulsate.
Arterial pulse diagram under normal and pathological conditions
arterial pulse waveform
Ascending branch
During the rapid ejection phase of the ventricles, the blood vessel walls are dilated
If the resistance is large, the cardiac output is small, and the ejection rate is slow, the slope will be small and the amplitude will be low.
descending branch The shape of the descending branch can roughly reflect the magnitude of peripheral resistance.
Anterior segment: Late in ventricular ejection, arterial blood pressure gradually decreases
Falling medium wave: The moment when the ventricles relax and the aorta closes, the blood in the aorta moves toward Reflux in the ventricular direction, retraction of the tube wall, causing a reentry wave in the descending branch
Postpart: Ventricular diastole, arterial blood pressure continues to decrease
propagation velocity of arterial pulse waves to peripheral arteries
Arterial pulse travels along the arterial wall to peripheral blood vessels
It spreads faster than blood flow
Venous blood pressure and venous blood return volume
Overview
vein
Large diameter, thin tube wall
The presence of valves allows blood to flow in one direction
Found in peripheral veins
missing central vein
Veins are capacitive vessels
High compliance
Mainly for blood storage function
At rest, 60% of blood is stored in veins
venous blood pressure
peripheral venous pressure
Definition: Venous blood pressure of various organs or limbs
When systemic blood passes through arteries and capillaries and reaches venules, blood pressure drops to about 15~20mmHg
venous pulse
Normally, the venous pulse is not obvious
In heart failure, venous pressure increases and there is obvious venous pulse in the neck
Central venous pressure (CVP)
Definition: Blood pressure in the right atrium and large veins in the chest As the end point of systemic circulation, the right atrium has the lowest blood pressure, close to 0
Normal value: 4~12cmH2O Clinically used as an indicator to control the speed and volume of fluid replacement Low: Insufficient infusion volume Too high: too fast infusion/cardiac insufficiency
The level of central venous pressure depends on the relationship between the heart's ejection capacity and the amount of blood returned to the heart by the veins. The stronger the heart's ejection ability, the more blood that returns to the heart can be ejected into the arteries in a timely manner, and the central venous pressure will be lower. The venous return speed accelerates, the central venous pressure increases, the amount of blood returned to the heart increases, and the organ circulation increases
Systemic pressure gradient = aortic pressure (mean arterial pressure) - vena cava pressure (central venous pressure) = 90mmHg
Effect of gravity on venous pressure
When lying down: all parts of the body are at the same level as the heart, and the hydrostatic pressure is roughly the same. Gravity plays no important role in venous blood flow
When standing upright: the veins in the feet are full, and above the level of the heart, the veins in the blood vessels are The pressure is lower than when lying down, such as a collapsed vein in the neck
orthostatic hypotension When a person turns from lying down to standing upright, the veins in the lower part of the body expand due to the increased hydrostatic pressure → blood accumulates in the veins → venous return decreases → central venous pressure decreases → stroke volume and cardiac output decrease → contract pressure drop
venous blood return volume
Factors affecting venous blood return to the heart
Average filling pressure of the circulatory system (pressure in the circulatory system measured during ventricular fibrillation, 7mmHg) Mean filling pressure rises → venous return rises Mean filling pressure decreases → venous return decreases
myocardial contractility Increased cardiac contractility→increased ejection volume→increased ejection fraction→diastolic period Internal pressure decreases → suction force increases → venous return increases Decreased cardiac contractility → Decreased ejection fraction → Increased diastolic internal pressure → Central venous Increased blood pressure → decreased venous return → jugular venous distension, hepatic congestion and enlargement, and lower limb edema
Postural changes Lying position → Standing position → The lowered part of the body accommodates the rise of blood → Decreased venous return Lower limb venous return blood volume when lying >upright
① Elevate the affected limb → facilitate venous return and prevent edema ②For patients with heart failure, take a semi-recumbent position → the venous blood return to the heart of the lower limbs decreases ③Suddenly standing after squatting for a long time →blood stagnation in the lower limbs →reduced venous blood return to the heart →reduced cardiac output →Drop in blood pressure→Insufficient blood supply to the brain and retina→Temporary dizziness, fainting, and blurred vision
The squeezing action of skeletal muscles (muscle pump) When the lower limbs exercise → produce a squeezing effect on the veins → increase venous return (venous valves)
Respiration (breathing pump) During inspiration → the negative pressure in the pleural cavity increases → the venous return increases
venous resistance to blood flow
The resistance of veins to blood flow is very small, accounting for only 15% of the total resistance of the entire systemic circulation.
The amount of venous blood returned to the heart per unit time depends on peripheral venous pressure and central venous pressure pressure difference, and venous resistance to blood flow
Varicose veins
Earthworm-like appearance
Varicose veins in the lower limbs are often caused by insufficiency of the femoral saphenous vein valve. Causes reflux of superficial venous blood flow and increases venous pressure in lower limbs
It is more common in people who sit and stand for long periods of time and who are engaged in other manual labor, with an incidence rate of 10 to 15%.
Treatment methods: superficial vein high ligation and stripping, ligation and stripping, intracavitary thermal ablation and closure
Microcirculation refers to blood circulation between arterioles and venules
The composition of the microcirculation
Typical microcirculation includes arterioles, posterior arterioles, precapillary sphincter, true capillaries, blood-flowing capillaries, arteriovenous anastomotic branches, venules, etc.
Features
Capillary permeability varies in various locations
40 billion roots
Effective exchange area 1000 square meters
Regulation of microcirculatory blood flow
capillary blood pressure
Arterial end: 30~40mmHg
Venous end: 10~15mmHg
Middle section: about 25mmHg
Depends on the ratio of precapillary resistance to postcapillary resistance The larger the ratio, the smaller the capillary blood pressure.
branch
Arterioles - main gate
Precapillary sphincter-dividing gate (not controlled by sympathetic nervous system)
Venules (Posterior Portal
Precapillary resistance - arterioles, post-arterioles
Postcapillary resistance: venules
microcirculatory blood flow pathways
roundabout pathway (nutritional pathway)
Arterioles → Posterior arterioles → Precapillary sphincter → True capillaries → Venules
Features: The main place for exchange between blood and tissue fluid, open alternately, blood flow is slow, It is a place for material exchange (capillaries have thin walls and high permeability)
direct access road
Arterioles → posterior arterioles → blood capillaries → venules
Features: Blood quickly enters veins through this pathway, which is more common in skeletal muscles.
Arteriovenous short circuit
Arteriole→arteriovenous anastomotic branch→venule
Characteristics: non-nutritional pathway, involved in body temperature regulation, more in the skin (Thick blood vessel walls and intact smooth muscle) "Warm shock"
Regulation of microcirculatory blood flow
Microcirculatory blood flow is affected by local metabolic levels - autoregulation
The opening and closing of true capillaries is controlled by the precapillary sphincter. 20-30% open, contraction and relaxation alternate 5-10 times/min
Substance exchange in microcirculation
Material exchange is the basic function of microcirculation
Method: Diffusion, filtration and reabsorption, swallowing (less likely, such as plasma proteins)
Physiological characteristics of microcirculation
Low blood pressure: Capillary pressure is significantly reduced, providing power for the generation and reflux of tissue fluid
Slow blood flow: The total cross-sectional area of capillaries is large, so blood flow is slow. at the capillaries Blood and cells have sufficient time to exchange substances
Large potential blood volume: If a person's liver capillaries are all opened, they can accommodate the whole body's circulating blood volume
The perfusion volume is variable: when a certain microcirculatory functional unit is open, its blood perfusion volume increases; when it is closed, the blood flow decreases sharply.
tissue fluid medium for exchange of substances between cells and blood
production of tissue fluid
Composition of tissue fluid
Free-flowing liquid tissue accounts for 1%
Collagen fibers and hyaluronic acid are jelly-like and cannot flow freely, accounting for 99%
Generation and reflux of tissue fluid
The generation and reflux of tissue fluid is a continuous process with no obvious boundaries and is in dynamic equilibrium.
90% of the tissue fluid is reabsorbed back into the blood at the venous end, and 10% enters the lymphatic capillaries called lymph.
Effective filtration pressure: the difference between the power of filtration and the power of reabsorption Kf is the filtration coefficient =Kf【(capillary blood pressure interstitial fluid colloid osmotic pressure)-(plasma colloid osmotic pressure interstitial fluid hydrostatic pressure)】 Arterial end: (30 15)-(25 10) = 10mmHg Venous end: (12 15)-(25 10)=-8mmHg
Effective filtration pressure > 0 → interstitial fluid production (arterial end)
Effective filtration pressure <0 → tissue fluid reflux (venous end)
Factors affecting tissue fluid production
Increased capillary blood pressure → increased tissue fluid
Inflammation → dilation of arterioles (decreased anterior resistance) → increase in capillary pressure → increase in tissue fluid (local edema)
Right heart failure → Obstruction of venous return (increased posterior resistance) → Increased capillary pressure → Increased tissue fluid (edema of lower limbs)
Effective colloid osmotic pressure decreases
Kidney disease, liver disease, severe malnutrition → hypoalbuminemia → decreased plasma colloid osmotic pressure → increased tissue fluid (general edema)
Decreased lymphatic flow
Filariasis → Obstruction of lymphatic drainage → Accumulation of tissue fluid (edema)
Increased permeability of capillary walls
The permeability of the capillary wall increases → plasma proteins enter the interstitial fluid → the colloid osmotic pressure of the interstitial fluid increases, Decrease in plasma colloid osmotic pressure → increase in tissue fluid (edema) For example: burns, allergies
Lymph production and regulation
In a normal person, approximately 120ml of lymph fluid enters the blood circulation per hour in a quiet state.
100ml→thoracic catheter
20ml→right lymphatic duct
enter vein
Physiological functions of lymph production and return
Recycle protein and absorb nutrients
Remove red blood cells, bacteria, and foreign matter from tissues
Balance the production and absorption of tissue fluid