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MindMap Gallery Physiology—blood circulation
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Physiology—blood circulation
This is a mind map of physiology-blood circulation, including the regulation of cardiovascular activity, vascular physiology, etc.
Edited at 2023-11-16 17:41:04
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Physiology—blood circulation
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- Outline
blood circulation
Regulation of cardiovascular activity
neuromodulation
cardiovascular innervation
innervation of heart
cardiac sympathetic nerve
postganglionic fiber
Neurotransmitters
Norepinephrine (NE)
receptor
B1 adrenergic receptor (B1 receptor)
blockers
metoprolol
positive isotropic action
Increased myocardial contractility
positive chronotropic action
increased heart rate
positive dromotropic action
conduction velocity increases
preganglionic fiber
Neurotransmitters
ACh
receptor
N1 receptor
The cardiac sympathetic nerves on both sides have different innervation of the heart
left side
Dominate
Atrioventricular junction and ventricular myocardium
effect
Myocardial contractility increases during excitement
Right
Dominate
sinoatrial node
effect
Heart rate increases when excited
cardiac vagus nerve
postganglionic fiber
Neurotransmitters
ACh
receptor
M receptor
blockers
atropine
Negative inotropic, chronotropic, and conductive effects (mainly atrial muscle)
preganglionic fiber
Neurotransmitters
ACh
receptor
N1 receptor
The innervation of the heart by the vagus nerve on both sides of the heart is different
left side
Dominate
Room-room junction
effect
Atrioventricular conduction velocity slows down during excitement
Right
Dominate
sinoatrial node
effect
heart rate slows down
Cardiosympathetic tension and cardiovagal tension
innervation of blood vessels
vasoconstrictor nerve fibers
vasodilatory nerve fibers
cardiovascular center
cardiovascular reflex
baroreflex/depressor reflex
When arterial blood pressure suddenly rises, it can reflexively cause heart rate to slow down, cardiac output to decrease, vasodilation, peripheral resistance to decrease, and blood pressure to drop.
receptor
carotid sinus, aortic arch
Features
Do not directly feel blood pressure changes, but feel the mechanical stretch stimulation of the blood vessel wall
The frequency of incoming impulses is directly proportional to the degree of expansion of the arterial wall
Carotid sinus baroreceptors are more sensitive
afferent nerve
sinus nerve, aortic nerve
reflection effect
Baroreceptor reflex function curve
Reflects the relationship between intrasinus pressure and changes in arterial blood pressure
The scope of work
60～180mmHg
set point
The intersection point where mean arterial pressure and intrasinus pressure are equal
The normal fluctuation range of blood pressure lies in the steep section of the curve
It indicates that it can sensitively regulate blood pressure and is a negative feedback
Normal mean blood pressure is in the middle of the curve
Prompts two-way regulation of blood pressure
resetting
Set point rises, keeping blood pressure relatively stable at high levels
physiological significance
Quickly adjust arterial blood pressure in a short period of time and maintain arterial blood pressure relatively constant
Acute bleeding/sudden change from supine position to upright position
Decreased carotid sinus pressure → baroreceptor reflex
chemoreceptor reflex
receptor
carotid body
aortic body
reflection process
effect
Regulating breathing, reflexively causing breathing to deepen and accelerate, and then reflexively affecting cardiovascular activity through changes in respiratory movements.
Features
Regulatory effects are exerted under conditions of hypoxia, blood loss, hypotension and acidosis
physiological significance
Raise blood pressure in emergency situations to redistribute circulating blood volume, thereby ensuring that important organs such as the heart and brain receive priority blood supply in critical situations.
brain ischemia response
condition
Acute massive hemorrhage, low arterial blood pressure, high intracranial pressure → reduced cerebral blood volume
Performance
Sympathetic vasoconstrictor tension increases significantly → arterial blood pressure increases, improving cerebral blood supply
Cardiovascular reflexes caused by cardiopulmonary receptors (volume receptors)
body fluid regulation
self-regulation
Vascular Physiology
Functional characteristics of various types of blood vessels
elastic reservoir vessel
include
aorta, pulmonary artery
Function
maintain blood flow
buffer arterial blood pressure
Systolic blood pressure should not be too high and diastolic blood pressure should not be too low
distribute blood vessels
include
From elastic reservoir vessels to branch vessels in front of arterioles
precapillary resistance vessels
include
arterioles and arterioles
precapillary sphincter
Smooth muscle surrounding the origin of true capillaries, whose contraction and relaxation control the closing and opening of subsequent capillaries
exchange blood vessels
True capillaries
postcapillary resistance vessels
venule
volumetric vessels
venous system
short circuit blood vessel
arteriovenous anastomosis
regulate body temperature
Hemodynamics
vascular compliance
venous compliance
low pressure
Geometry
high pressure
vasodilation
blood flow and velocity
blood flow
The amount of blood flowing through a certain cross section of a blood vessel per unit time
Poiseuille's law (only for laminar flow)
blood flow velocity
The linear velocity of a particle in blood moving within a blood vessel
Directly proportional to blood flow and inversely proportional to blood vessel cross-sectional area
laminar and turbulent flow
blood flow pattern
laminar flow
The flow rate is fastest at the center of the axis, and the flow rate becomes slower closer to the pipe wall.
turbulence
Reynolds number (Re)
blood resistance
The resistance encountered by blood as it flows through blood vessels
include
inside blood molecules
between blood molecules and blood vessel walls
Features
Friction with each other→energy consumption→blood pressure gradually decreases
The main site of resistance is small blood vessels (arterioles)
Factors affecting resistance
Factors affecting blood viscosity
Hematocrit
The bigger → the higher the viscosity
Shear rate of blood flow
In the case of laminar flow, the ratio of the difference in blood flow velocity between two adjacent layers to the thickness of the liquid layer
Classification
Newtonian liquid
The viscosity of a homogeneous liquid does not change with changes in shear rate
plasma
non-newtonian liquid
The viscosity of heterogeneous liquids increases with decreasing shear rate
Whole blood
axial flow
The higher the shear rate, the more obvious the laminar flow phenomenon, and the red blood cells are concentrated in the central axis of the blood flow.
blood vessel caliber
temperature
Temperature decreases and viscosity increases
Measurement
blood pressure
Arterial blood pressure and arterial pulse
arterial blood pressure
The lateral pressure of blood flowing in an artery on the arterial wall per unit area (usually referred to as aortic pressure)
forming conditions
Proper cardiovascular filling is a prerequisite
average filling pressure of circulatory system
For a short time after the heart stops ejecting blood, the blood pressure is the same everywhere in the circulatory system. The blood pressure at this time
Influencing factors
circulating blood volume
More quantity means more pressure
circulation system capacity
Small capacity and big pressure
Cardiac ejection and peripheral resistance are necessary conditions
heart ejection
peripheral resistance
Mainly refers to the resistance of arterioles and arterioles to blood flow
Elastic reservoir function of aorta and large arteries
Change intermittent ejection of ventricular blood into continuous blood flow in arteries
Buffer blood pressure changes to avoid excessive pulse pressure
Measurement
direct measurement method
indirect measurement method
normal value
Systolic pressure (SP)
The highest value of blood pressure in the aorta during a cardiac cycle = the end of the rapid ejection period
100～120mmHg
Diastolic pressure (DP)
The lowest value of intra-aortic blood pressure reached during a cardiac cycle = the end of isovolumetric contraction
60～80mmHg
Pulse pressure (PP)
The difference between systolic and diastolic blood pressure
mean arterial pressure
The average arterial blood pressure at each moment of a cardiac cycle
Approximately = diastolic blood pressure 1/3 pulse pressure
30～40mmHg
physiological significance
Promote blood flow
physiological fluctuations
Daily rhythm of arterial blood pressure
twin peaks twin valleys
2 to 3 hours in the morning, low after 8 hours in the evening
6 to 10 hours in the morning, 4 to 8 hours in the afternoon
For the control of high blood pressure, not only the daytime blood pressure should be controlled at normal levels, but the nighttime blood pressure should also be controlled at normal levels.
sports
increased systolic blood pressure
Diastolic blood pressure and mean arterial pressure were slightly increased
age and gender
After arteriosclerosis in the elderly
Systolic blood pressure gradually increases with age, diastolic blood pressure gradually decreases with age, mean arterial pressure has no significant change, and pulse pressure increases
Arterial blood pressure of both arms
Left high, right low
Hypertension and Prehypertension
Factors affecting arterial blood pressure
cardiac stroke volume
heart rate
peripheral resistance
Elastic reservoir function of aorta and large arteries
circulatory system fullness
Venous blood pressure and venous return volume
venous blood pressure
Central venous pressure (CVP)
Right atrium and intrathoracic large venous blood pressure
normal value
4～12cmH2O
Influencing factors
cardiac ejection capacity
venous blood return volume
peripheral venous pressure
Venous blood pressure of various organs
Effect of gravity on venous pressure
hydrostatic pressure
transmural pressure
venous blood return volume
=(Peripheral venous pressure-CVP)/Venous resistance
venous resistance to blood flow
Factors affecting the amount of venous blood returned to the heart
mean systemic filling pressure
The greater the filling volume, the greater the volume of blood returned to the heart by the veins
myocardial contractility
Increased myocardial contractility → more complete ejection → decreased CVP → increased venous return
Right heart failure→right atrial pressure increases→return blood volume decreases
Distended external jugular veins, liver congestion, and lower limb edema
Postural changes
skeletal muscle squeeze
Muscle pump, accelerated venous return
respiratory movements
breathing pump
When inhaling, the thoracic cavity volume increases and the negative pressure increases → the large veins and right atrium in the thoracic cavity become more dilated → promote venous return
Microcirculation
Microcirculation components and blood flow pathways
tissue fluid
Filtration and reabsorption
90% returns from the veins and 10% returns from the lymph
Factors affecting tissue fluid production
capillary blood pressure
Elevated → increased tissue fluid production
plasma colloid osmotic pressure
Decrease → decrease in albumin → increase in tissue fluid production
capillary permeability
Increase → Increase tissue fluid production
lymphatic drainage
Blocked→Increased tissue fluid production
Filariasis
heart pumping function
condition
Heart muscle cells contract, driving blood flow
Valves ensure the direction of blood flow
Heart pumping process and mechanism
cyclical activity of the heart
cardiac cycle
myocardial action potential periodic electrical activity
physical signs
ECG
cardiac cycle
A mechanical activity cycle consisting of one contraction and relaxation of the heart (atrium/ventricular)
Systole
diastole
physical signs
heart sounds
heart rate
75 beats/min→cardiac cycle: 60/75＝0.8s
Characteristics of the cardiac cycle
Diastole > Systole
Give the heart muscle a full rest
The atria and ventricles do not contract at the same time (atria first, ventricles later)
Ensure normal blood pumping function
There is a global diastole
The period when both ventricles and atria are in a state of relaxation (=atrial diastole-ventricular systole=)
Heart rate mainly affects diastole
heart pumping process
The process of ejection and filling of the ventricle (taking the left heart as an example)
period of atrial systole
Atrial contraction → intraatrial pressure increases → blood is further squeezed into the ventricle
Accounts for 25% (10-30%) of each ventricular filling volume
Time 0.1s
period of ventricular systole
Period of Isovolumic contraction
process
Ventricular contraction → rise in intraventricular pressure → intraventricular pressure > intraatrial pressure → atrioventricular valve closure
Intraventricular pressure < arterial pressure → arterial valve closure
Features
The indoor volume remains unchanged, but the indoor pressure rises sharply.
produce first heart sound
Lasts 0.03s
0.05s
period of ventricular ejection
period of rapid ejection
process
The ventricular muscle contracts strongly → the intraventricular pressure rises → the intraventricular pressure > the arterial pressure → the arterial valve opens → blood is rapidly ejected from the ventricle into the artery
Features
Large ejection volume (accounting for 2/3 of the total ejection volume)
Ventricular volume is significantly reduced and intraventricular pressure reaches a peak
Lasts 0.1s
period of reduced ejection
process
Ventricular muscle contraction weakens → Indoor pressure is slightly less than arterial pressure → Indoor blood continues to enter the artery with the strong kinetic energy of ejection → Ejection speed slows down
Features
Low ejection volume
0.15s (time taken)
Arterial pressure slightly > intraventricular pressure
period of ventricular diastole
Period of Isovolumic relaxation
process
Ventricular diastole → intraventricular pressure decrease → intraventricular pressure > intraatrial pressure, atrioventricular valve closure
Intraventricular pressure < arterial pressure → arterial valve closure
Features
The indoor volume remains unchanged and the pressure drops sharply
Both atrioventricular and arterial valves are closed
second heart sound
Lasts 0.03～0.06s
0.06～0.08s
period of ventricular filling
period of rapid filling
Ventricular myocardial relaxation → intraventricular pressure decreases (can be negative pressure) → intraventricular pressure < intraatrial pressure → atrioventricular valve opening → atrium and large vein blood quickly enters the ventricle due to ventricular suction → ventricular volume rapidly increases
Features
Account for 2/3 of the total filling volume
Indoor pressure is lowest at the end of the rapid filling period
0.11s
period of reduced filling
Ventricular myocardial relaxation → intraventricular pressure decreases → intraventricular pressure < intraatrial pressure (pressure difference decreases) → blood in the atrium and large veins continues to enter the ventricle
0.22s
The role of the atria, ventricles, and valves in the heart's pumping of blood
primary pumping action of the atria
Facilitates venous return and cardiac ejection
Most of the time is in the diastolic phase → receives and stores the blood that is constantly returning from the veins
The atrial wall is thin and the contraction force is not strong → contraction only assists in ventricular filling
Atrial contraction can further increase the ventricular end-diastolic volume = increase the initial length of ventricular myocardium before contraction → increase myocardial contractility → improve ventricular pumping function
atrial fibrillation
Unable to contract normally → Reduced passive filling during ventricular diastole → Reduced ventricular end-diastolic volume → Reduced ventricular ejection volume
The contraction and relaxation of the left ventricular muscle are the fundamental cause of changes in left ventricular intraventricular pressure and the pressure gradient between the three.
Pressure gradient—the main force driving blood flow between the three
Dynamic force of ventricular ejection during systole
Increased pressure produced by ventricular muscle contraction
blood flow inertia
Dynamics of ventricular filling during diastole
early active ventricular relaxation
late atrial contraction
Right ventricular pumping process
Pulmonary artery pressure is 1/6 of aortic pressure
The change in intraventricular pressure in the right ventricle is much smaller than the change in intraventricular pressure in the left ventricle
Changes in intraatrial pressure during the cardiac cycle
a wave
signs of atrial contraction
c wave
Ascending branch: When the ventricles contract, blood pushes the atrioventricular valves into the atria, causing a slight increase in intraatrial pressure.
Descending branch: ventricular ejection, volume decreases, valve moves downward, atrial volume expands, intra-atrial pressure decreases
v wave
ascending branch
venous return
descending branch
Atrioventricular valve opening during ventricular diastole
Heart pump function
The rhythmic contraction and relaxation of the heart drive the blood
Cardiac output and cardiac functional reserve
Stroke volume and output per minute
stroke volume/stroke volume
The amount of blood ejected by one ventricle in one contraction
= End-diastolic volume of the ventricle (end-diastolic volume, EDV) - End-systolic volume of the ventricle (end-systolic volume, ESV)
Normal adult quiet state: EDV-ESV=125-55=70ml
Basic indicator of heart pumping function
ejection fraction
Stroke volume as a percentage of ventricular end-diastolic volume
Healthy adults: 55% ~ 65%
significance
Normally, stroke volume and ventricular end-diastolic volume are compatible (compare individuals with different ventricular end-diastolic volumes)
More accurately reflects the heart’s pumping function
Ventricular dysfunction and abnormal ventricular enlargement
Stroke volume remains unchanged, ventricular end-diastolic volume increases → ejection fraction decreases
Ventricular end-diastolic volume is related to contractility (initial length)
Increased cardiac contractility → increased ejection fraction
Compare commonly used assessment indicators of cardiac function in the same individual under different conditions.
Output per minute/cardiac output (cardiac output)
The amount of blood ejected from one ventricle per unit time
Factors affecting cardiac output
stroke volume
Ventricular myocardial preload and abnormal autoregulation
Ventricular muscle preload (=ventricular end-diastolic volume)
It can be reflected by ventricular end-diastolic pressure (EDP) → ventricular end-diastolic pressure = intra-atrial pressure → intra-atrial pressure at ventricular end-diastole reflects ventricular preload
heterometric autoregulatuon
Regulation of changes in myocardial contractility by changing the initial length of the myocardium
ventricular function curve
process
The ventricular diastolic time is prolonged, the venous return velocity increases → the venous return blood volume increases → the ventricular end-diastolic volume increases → the initial length of the ventricle increases → the myocardial systolic length increases → the stroke volume increases
significance
Maintain balance between stroke volume and blood return volume
Fine adjustment for small changes in stroke volume
Anti-overextension properties of normal ventricular myocardium
Factors affecting preload (= factors affecting ventricular diastolic filling)
venous blood return volume
venous return velocity
ventricular filling time
ventricular diastolic function
Diastolic Ca fall rate
ventricular compliance
intrapericardial pressure
ventricular end-systolic blood volume
Afterload of ventricular contraction (aortic pressure)
load encountered during myocardial contraction
process
Arterial pressure rises → Peak intraventricular pressure rises during isovolumic contraction → Isovolumic contraction phase is prolonged, ejection period is shortened, ejection velocity slows down → Stroke volume decreases
Afterload increases → Stroke volume decreases → Ventricular end-diastolic volume increases → Preload increases → Alien autoregulation → Stroke volume recovers
Afterload increases beyond a certain range → Myocardial systole increases → Myocardial shortening increases → Stroke volume remains at a high level (causing myocardial hypertrophy for a long time)
Myocardial contractility
The characteristic of the myocardium that changes its own contractility independent of preload and afterload
Myocardial contractility increases → the ventricular function curve shifts upward to the left
isometric autoregulation
Under the condition of unchanged preload and postload, the cardiac stroke volume changes through changes in the mechanical activity (contraction intensity and speed) of the cardiomyocytes themselves.
Influencing factors
Number of activated cross bridges
intracellular Ca concentration
Affinity of troponin and Ca
ATPase activity
stimulate sympathetic nerves
Increased myocardial contractility
Hypoxia, acidosis
H and Ca competitively inhibit binding to troponin
acetylcholine
Inhibit Ca channel opening
heart rate
Cardiac output = Stroke volume × Heart rate
Heart rate increases within a certain range and cardiac output increases
When the heart rate is too fast (>170-180 beats/min), cardiac output decreases
When the heart rate is too slow (<40 beats/min), cardiac output decreases
ladder phenomenon
The phenomenon of increased myocardial contractility caused by increased heart rate or stimulation frequency
mechanism
It may be related to the increase in intracellular Ca concentration when the heart rate increases
Influencing factors
Nervous and humoral regulation
Increased sympathetic nervous activity → increased heart rate
Increased vagus nerve activity → slowed heart rate
Elevated adrenaline, norepinephrine, and thyroid hormones → increased heart rate
Body temperature rises faster
different individuals
age
Newborn baby
gender
Female fast
regular exercise
Heart rate is usually slow
same individual
Quiet, slow sleep
Exercise, emotional excitement
=Stroke volume×Heart rate
Adapt to the body’s metabolic level
Not suitable for individuals of different body shapes
Healthy adults: 5L/min
Basic indicator of heart pumping function
cardiac index
Cardiac output calculated per unit body surface area
=cardiac output/body surface area
normal value
3.0～3.5L/（min•m*2）
significance
Commonly used assessment indicators when comparing cardiac function among different individuals.
different body shapes
different ages
The highest is around 10 years old (4 units), and the elderly is 80 years old (2 units)
exercise intensity
Pregnancy, eating, emotional stress
heart pumping reserve
cardiac reserve
The ability of cardiac output to increase in response to the body's metabolic needs
Heart rate reserve (first to mobilize)
Heart rate is 60~100 beats/min→160~180 beats/min
Heart rate is too fast → diastole is too short → ventricular filling is insufficient → stroke volume and cardiac output are reduced
Heart failure (heart rate reserve can only be 120 to 140 beats/min)
Myocardial contractility weakens → stroke volume decreases → in order to normalize cardiac output, heart rate increases compensatory = heart rate reserve is used in resting state
Proportional to cardiac output
stroke volume reserve
=systolic reserve diastolic reserve
Increase systolic reserve (=reduced ventricular end-systolic volume→maximum 35~40ml)
Enhance myocardial contractility and ejection fraction
Increase diastolic reserve (=increased ventricular end-diastolic volume→maximum 15ml)
Increase end-diastolic volume
The normal ventricular cavity cannot be excessively expanded → the systolic reserve is much greater than the diastolic reserve
Reflects the health of the heart
Cardiac function evaluation
stroke work/stroke work
The external work done by the ejection of blood during one contraction of the ventricle
= Pressure-Volume work Blood kinetic energy = Stroke volume × Indoor pressure increase during cardiac cycle Blood kinetic energy
Approximate = pressure - volume work = stroke volume × (mean arterial pressure - left atrial arterial pressure)
Comparing cardiac pumping function under different arterial blood pressure conditions
minute work
The work done by the ventricle to contract and eject blood per minute
=Stroke power×Heart rate
Comparing cardiac pumping function under different arterial blood pressure conditions
Myocardial oxygen consumption is parallel to myocardial work, and the energy released by myocardial contraction is mainly used to maintain blood pressure.
heart sounds
The turbulence caused by the opening and closing of heart valves/changes in blood flow velocity/the impact of blood flow and blood on the ventricular wall and aortic wall causes mechanical vibration.
Record
Only the first and second heart sounds can be heard by auscultation (some teenagers can hear the third heart sound)
The phonocardiogram can record four heart sounds
Features
Electrophysiology of the heart and its physiological properties
characteristic
Electrophysiological properties
Excitability
Cells have the ability or property to generate action potentials after being stimulated
Cyclic changes in cardiomyocyte excitability
installment
Effective refractory period (ERP) (0 period depolarization-repolarization-60mv)
installment
Absolute refractory period (ARP)
No matter how strong the stimulation is, it will not cause a period of depolarization of myocardial cells.
Phase 0 depolarization-repolarization phase 3 membrane potential reaches -55mv
local reaction period
Administration of suprathreshold stimulation can cause a local response, but no period of action potential occurs
Repolarization-55mv—-60mv
reason
Sodium channels are completely inactive or have not yet returned to a standby state in which they can be activated
Features
Extremely long
Relative refractory period (RRP) (repolarization -60mv--80mv)
Suprathreshold stimulation can cause myocardial cells to generate action potentials
reason
Some sodium channels begin to resurrect into a backup state
However, the number of sodium channels activated under threshold stimulation cannot reach the threshold potential to generate an action potential.
Supra normal period (SNP) (repolarization -80--90mv)
Sub-threshold stimulation can trigger a new action potential
reason
Sodium channels basically resurrected
The membrane potential level is close to the threshold potential
Features
Long effective refractory period
significance
Prevent the myocardium from producing complete tonic contraction and ensure alternation of ventricular contraction and contraction
compensatory pause after presystole
Characteristics of newly generated action potentials in the relative refractory period and supranormal period
Stage 0 depolarization speed and amplitude are lower than normal
reason
The membrane potential level is lower than the resting potential, and the opening rate and number of sodium channels are low.
Action potential duration and refractory period are short → prone to preterm excitation
Excitation conduction speed is slow
Relationship between excitability changes and mechanical contraction during ventricular myocardial action potentials
Effective refractory period covers: systole and early diastole
Premature excitation and premature systole
After the effective refractory period of the ventricular muscle, before the next excitation of the sinoatrial node arrives, the ventricle may be excited and contracted in advance by an external stimulus.
compensatory pause
A presystole is often followed by a longer period of ventricular diastole
reason
Premenstrual excitement also has its relative refractory period. If the next sinus node excitement falls during this period, no contraction will occur.
Factors affecting cardiomyocyte excitability
Excitability measure
threshold
Low threshold → high excitability
factor
Resting potential or maximum repolarizing potential level
The larger the absolute value → the lower the excitability
threshold potential level
Ion channel properties causing phase 0 depolarization
Sodium channel/L-type calcium channel
voltage dependence and time dependence
Three functional states
Standby (resting)
activation
inactivate
self-discipline
The ability/characteristics of the myocardium to automatically generate rhythmic excitation in the absence of external stimulation
Special conduction system of the heart
pacemaker of heart
Metric: Number of spontaneous APs generated per minute
Sinus node (100 times/min)
Interventricular junction (50 times/min)
Purkinje (25 times/min)
Classification
normal pacemaker
sinoatrial node
sinus rhythm
potential pacemaker
Other autonomic tissues only function as excitatory conductors under normal circumstances and do not show their own rhythmicity.
Normal pacemaker fails to function → potential pacemaker compensation
ectopic pacemaker
The abnormal increase in autonomic rhythm of the potential pacemaker exceeds the sinoatrial node and can replace the sinoatrial node to generate propagable excitement and control cardiac activity.
The primary mechanism by which the sinoatrial node controls potential pacemakers
Be the first to occupy
When the potential pacemaker reaches the threshold potential before its own phase 4 automatic depolarization, the excitement from the sinoatrial node has activated it to generate an action potential.
overdrive
When autonomic cells are stimulated at a frequency higher than their natural frequency, they are excited at the frequency of the external stimulus.
overdrive depression
After the external overdrive stimulus is stopped, the autonomous cells cannot immediately display their inherent autonomous activities.
Features
The greater the frequency difference between the two pacing points, the stronger the suppression effect, and the longer the inactivity time after the drive is interrupted.
reason
Overdrive → the number of action potentials increases → hyperpolarization → overdrive suppression, the membrane potential still stays at the hyperpolarization level → the autonomic cells’ own phase 4 automatic depolarization is not easy to reach the potential level, and brief cardiac arrest occurs
Factors that determine and influence self-discipline
4-stage automatic depolarization speed
The faster, the higher the self-discipline
maximum repolarization potential level
The younger you are, the higher your self-discipline is.
threshold potential level
The higher you move up, the lower your self-discipline.
conductivity
Cardiomyocytes have the ability or property to conduct excitation
premise
There are gap junctions in the myocardial intercalated disk
Conduction of excitement in the heart
Special conduction system of the heart
Sinoatrial node, atrioventricular node, atrioventricular bundle, left and right bundle branches, Purkinje fibers
Excitation conducts at different speeds in various parts of the heart
way
speed
The atrioventricular node zone is the slowest
reason
Small fiber diameter
Leap disk has few gap connections
Slow-responding cells, phase 0 depolarization speed is low and amplitude is small
significance
atrip ventricular delay
Ensure that ventricular contraction occurs after atrial contraction, which is beneficial to ventricular filling and ejection
Purkinje fiber is the fastest
reason
Thick fiber
There are many gap connections in leap disks
Large fiber coverage area
significance
Make the left and right ventricles contract almost simultaneously
Features
Direct electrical transmission between cardiomyocytes
Orderly spread of excitement through special conduction system
The conduction velocity is not uniform everywhere
Special conduction system has a filtering and protective effect on rapid excitement
filter protection
The atrioventricular node area is composed of slow-reacting cells with a long refractory period → Abnormal high-frequency excitement of the atrium cannot be transmitted down
For example, if the atrial frequency is 300 beats/min, the ventricular frequency is still 150 beats/min.
Factors that determine and influence conductivity
structural factors
cardiomyocyte diameter
Bigger is faster
Large diameter → small resistance
Gap junctions between cardiomyocytes
Physiological factors (main)
Action potential phase 0 depolarization speed and amplitude
Phase 0 depolarization amplitude is large → the potential difference between excited and non-excited parts is large → the local current is strong and the spread distance is large → the excitation conduction is fast
Phase 0 depolarization is fast → the potential difference with adjacent unexcited parts is generated quickly → local current is formed quickly → excitatory conduction is fast
Membrane potential level (directly affects the rate and amplitude of phase 0 depolarization)
Reduced membrane potential → more inactivation of sodium channels → slow and low depolarization → low excitability
The membrane potential level is greater than the normal resting potential level → the sodium channel is already fully open → the maximum depolarization speed does not increase
Excitability of membranes adjacent to unexcited areas
The adjacent membrane is in the effective refractory period → cannot cause excitement
The adjacent membrane is in a relative refractory period or a supernormal period → the depolarization speed is slow and the amplitude is small → the excitatory conduction is slow
Mechanical and physiological properties
Contractility (the pumping function of the heart)
Classification
According to whether there is self-discipline (whether period 4 automatically depolarizes)
working cells
atrium, ventricular muscle
There is no self-discipline in excitement, conduction, and contraction.
autonomous cells
P cells, Purkinje fibers and other special conductive tissues of the heart
No shrinkage
According to the depolarization speed in period 0 (slow Ca or fast Na)
fast response cells
Fast Na channel is open
Ventricular myocardium, atrial myocardium, Purkinje
slow responding cells
Slow Ca channels open
sinoatrial node, nodal area
Transmembrane potential of working cells and its formation mechanism
resting potential
Formation mechanism
Ek: K is formed through the efflux of potassium channel Ik1
The driving force driving the flow of K across the membrane: Ek-Vm
Inwardly rectifying potassium channel Ik1
Features
Ungated ion channel (always open)
Openness is only affected by membrane potential
Reduced permeability (closed) due to depolarization: inward rectifying properties, open due to repolarization
mechanism
Depolarization caused by membrane stimulation → in order to restore the original resting potential → K outflow; hyperpolarization caused by membrane stimulation → in order to restore the resting potential → K influx
K outflow caused by depolarization 40mv < K influx caused by hyperpolarization 40mv
other
There is also a certain degree of permeability to Na in the resting state → the resting potential is slightly lower than the calculated potassium equilibrium potential
Na background current
pump current
-90mV: K opening → K outflow at rest
Action potential
(ventricular myocytes) fast response action potential (working cells)
Action potential duration (APD)
Phase 0 depolarization begins ~ Phase 3 repolarization is completed
Ventricular myocytes 200~300ms
various ion channels
outward current
Ito channel (instantaneous outward current)
Depolarization up to -30mv is activated
direction
Inside the membrane → Outside the membrane
Features
K transient outflow channel
inhibitor
Tetraethylamine, 4-aminopyridine
Ik channel (delayed rectifier potassium current)
Depolarization-40mv activates, repolarization-50mv inactivates
direction
Inside the membrane → Outside the membrane
Features
Activation and deactivation are extremely slow (slower than L-type Ca)
Ik1 channel (inward rectifying potassium current)
inward rectification
The phenomenon that the permeability of Ik1 channels to K is reduced due to membrane depolarization
The permeability to K is high during RP, and the permeability to K is low during depolarization → maintain low potassium permeability in the 2-plateau phase
inward current
fast channel
Depolarization up to -70mv is activated, 0mv is inactivated
direction
outside the membrane→inside the membrane
Features
Quick to activate, quick to deactivate
Positive feedback
Regenerative Na influx→rapid depolarization in phase 0
activator
Phenytoin
inhibitor
Tetrodotoxin TTX (not sensitive)
L-type Ca channels (slow channels)
Depolarization threshold potential -30～-40mv
direction
outside the membrane→inside the membrane
Features
Activation, deactivation, and resurrection are all slow
Current is greater than T type
Less permeable than fast Na channels
Not very specific
inhibitor
Mn, verapamil
T-type Ca channel
threshold potential
Depolarization reaches -50～-60mv
direction
outside the membrane→inside the membrane
Features
Fast activation, fast deactivation (transient)
Small current (tiny)
installment
Phase 0—rapid depolarization phase
Stimulation → depolarization (-90mv → 30mv) = ascending branch of action potential
Time: 1～2ms
mechanism
fast channel
T-type calcium channel (little role)
Na channel blockade → slowed down excitatory conduction
Features
Depolarization slows down
The amplitude of the ascending branch decreases
Complete block → slow reaction potential
inhibitory block
Class I antiarrhythmic drugs
Phase 1 - Early stage of rapid repolarization
Membrane potential 30mv → 0mv = descending branch of action potential
Time 10ms
mechanism
Ito channel
CL channel
Weak effect
Sympathetic nerve stimulation/catechol → enhanced effect
Phase 2-Platform Phase
0mv→-40mv
time
100～150ms
mechanism
inward ion current
L-type Ca current
Slow inactivation INa
Na-Ca exchange current
outward ion current
Ik1 channel
Ik channel
Mainly counteracts the inward current dominated by L-type Ca channels
The main current responsible for membrane repolarization
Na pump
Little effect
Inhibited→Intracellular Ca increases→Secondly causes late afterdepolarization
Factors affecting the length of the plateau period
Phase 3 - the end of rapid repolarization
-40～-90mv
mechanism
Slow Ca inactivation
Increased Ik channel permeability
Ik1 revives at -60mv →K regenerative current
Potassium current positive feedback during repolarization is unique to cardiomyocytes
INa-Ca
Na pump
Phase 4 - Complete repolarization phase/resting phase
-around 90mv
mechanism
Sodium pump enhancement
Na-Ca exchanger enhancement
3 Na are transferred into the cell and 1 Ca is transferred out of the cell
Ca pump
digitalis drugs
Inhibit Na pump → Na-Ca exchange is blocked → Ca remains in the cell in large amounts → myocardial contraction is strengthened
Features
Complex shape
long lasting
Stage 2 is the characteristic stage that is different from nerve and skeletal muscle Ap.
plateau
Effective refractory period
No tetanic contraction occurs
Asymmetry between ascending and descending limbs of action potential
Phase 4 membrane potential is stable
An action potential process, including passive ion transport and active ion transport
Transmembrane potential of autonomous cells and its formation mechanism
Sinoatrial node P cell action potential
installment
Issue 0
When phase 4 automatic depolarization reaches the threshold potential → activate L-type calcium channels (no fast Na channels)
Issue 3
L-type Ca is gradually inactivated
Ik channel open
Issue 4
Ik channel gradually deactivates and closes when repolarization reaches -50mv (mainly) - the main pacemaker current of sinoatrial node cells
progressive decay
If channel (funny)
Features
Self-initiating, self-developing, self-terminating ion flow
Inward ion current that gradually increases over time
Mainly Na (a small amount of K)
Repolarization starts to activate at -60mv, fully activates at -100mv, depolarizes to -50mv and automatically deactivates and shuts down.
blockers
cs
Not fully activated → little effect
T-type Ca channel (Ni can block)
Phase 4 automatic depolarization is activated to -50mv
Depolarize the membrane to threshold potential → trigger a new action potential
Small current, short time → little effect
Features
Maximum repolarization potential -70mv [fewer Ik1 channels], threshold potential -40mv (both higher than Purkinje cells)
Phase 0 depolarization
Small amplitude (depolarization to 0mv)
Slow speed, long journey
Lack of INa channels, small maximum repolarization potential → Na channel inactivation
Dependent on L-type Ca channels
No obvious repolarization stages 1 and 2
Lack of Ito channel
Phase 4 automatic depolarization is fast
P cells are small in size → small in membrane capacitance → fast in charging and discharging
High membrane resistance → a small amount of current can cause significant changes in potential
super cum small
Purkinje cell action potential
Features
Fast response action potential → divided into five periods: 0, 1, 2, 3, and 4
Maximum repolarization potential-90mv
4th phase automatic depolarization
The Ik channel gradually closes when the repolarization reaches -50mv.
If channel gradually activates
Voltage dependence Time dependence
If channel density is low → phase 4 depolarization is slow
Compare
Features
Maximum repolarization potential (MRP)
The potential when the autonomic cell action potential reaches the maximum polarization state at the end of the third phase of repolarization
No stable resting potential → Phase 4 automatic depolarization
Increasing over time
The basis for autonomous cells to produce autonomous excitation
Surface electrocardiogram (ECG)
Place the measuring electrode on a certain part of the body surface to record the comprehensive electrical changes of the heart.
ECG waveform is different from AP
reason
ECG is extracellular recording
ECG for multi-cell recording
Basic principles (voltage-time relationship curve)
Membrane polarization theory (galvanic couple theory)
volume conductor principle
The significance of ECG lead patterns and normal ECG waves and intervals
EKG leads
When recording an electrocardiogram from the body surface, guide the placement of the electrodes and the line connecting the electrocardiograph
Each wave
P wave
Left and right atrium depolarization
QRS wave
Left and right ventricular depolarization
Wave complex widening → ventricular conduction obstruction/ventricular hypertrophy
Increased wave group amplitude → myocardial hypertrophy
T wave
ventricular repolarization
U wave
Each interval
PR interval (PQ interval)
start
Starting point of P wave → starting point of QRS wave
reflect
atrioventricular conduction time
The time it takes for the excitement generated by the sinoatrial node to reach the ventricle via the atria, the atrioventricular junction and the atrioventricular bundle and cause the ventricles to start to excite
QT interval
start
QRS wave starting point→T wave ending point
reflect
The time from the onset of ventricular depolarization to complete repolarization
ST segment
start
End point of QRS wave→start point of T wave
reflect
action potential plateau
Neural regulation of cardiac activity
Effects of vagus nerve stimulation
reflection in electrocardiogram
slow heart rate
Prolonged PR interval
Sympathetic nervous system effects
Effects of high blood K on myocardium
Effects of low blood K on myocardium