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blood circulation(1)
This is a mind map about blood circulation (1), which mainly includes an overview, the pumping function of the heart, electrical activity and physiological characteristics, etc.
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blood circulation
Overview
circulatory system
Cardiovascular System
Blood circulates in a certain direction in the cardiovascular system over and over again
Blood (transport regulation immune buffering), blood vessels (pipes), heart (pump-power)
Material transport (most basic), body fluid regulation, maintenance of homeostasis, blood defense, endocrine (atrial natriuretic peptide)
lymphatic system
heart pumping function
Cardiac cycle and heart rate
Cardiac cycle (one heartbeat) 0.8s
A contraction and relaxation of the heart constitute a cycle of mechanical activity
Atrial systole 0.1s → atrial diastole 0.3s → global diastole 0.4s
Heart rate (HR)
heart beats per minute
When normal people are quiet, 75
Sinus slowness 60; Sinus speed 100
Cardiac cycle=60s/heart rate
Heart rate mainly affects diastole Fast HR and short diastolic period are not conducive to myocardial rest and ventricular filling (tachyarrhythmia → HF)
heart pumps blood
Ventricular relaxation and contraction
Ventricular diastole-filling (atrium-ventricular)
atrioventricular valve
Ventricular contraction-ejection (ventricular-arterial)
arterial valve
Valves that open and close in one direction keep blood moving in a certain direction in the heart
basic mechanism
Ventricular contraction or relaxation - changes in intraventricular pressure - changes in the pressure gradient between intraatrial pressure and intraventricular pressure - arterial pressure - valve opening or closing - blood flow (unidirectional)
pumping process
Atrial systole 0.1s
Intraventricular pressure < aortic pressure
Atrioventricular valve opening
ventricular volumemax
Atrial contraction ejection provides 25% of ventricular blood volume The remaining 75% of ventricular blood volume actively fills during diastole
ventricular systole
Isovolumic contraction period 0.05s
Intraatrial pressure < intraventricular pressure < intraarterial pressure
Atrioventricular and semilunar valves close
Indoor pressure rise rate max, ventricular volume max, aortic pressure min
Rapid ejection period 0.1s
intraatrial pressure <ventricular pressure> intraarterial pressure
Atrioventricular valves close, arterial valves open
Indoor pressure max
The ejection volume accounts for 2/3 of the total ejection volume
Slow down the ejection period by 0.15s
Intraatrial pressure < intraventricular pressure < intraarterial pressure
Atrioventricular valves close, arterial valves open
Blood continues to flow into the artery relying on inertial counter-pressure gradient, the ejection speed slows down, and the ejection volume decreases.
The ventricular volume is min, but there is still 60 to 80 ml of blood.
The ejection volume accounts for 1/3 of the total ejection volume
ventricular diastole
Isovolumetric diastole period 0.07s
Intraatrial pressure < intraventricular pressure < intraarterial pressure
Atrioventricular and arterial valve closure
Indoor pressure reduction rate max, ventricular volume min
Rapid filling period 0.11s
Intraatrial pressure>Intraventricular pressure<Intraarterial pressure
Atrioventricular valve opens, arterial valve closes
The filling volume accounts for 2/3 of the total filling volume
Indoor pressure min
Slow down filling period 0.22s
Intraatrial pressure>Intraventricular pressure<Intraarterial pressure
Atrioventricular valve opens, arterial valve closes
ventricular volumemax
*Right ventricular pressure level is 1/6 to 1/5 that of the left ventricle
Heart sounds and phonogram
S1
Ventricles contract and atrioventricular valves close low, long
S2
The ventricles relax and the arterial valves close high, short
S3: children, teenagers S4: Pathology
Evaluation of heart pumping function
cardiac output
Stroke volume and ejection fraction
Stroke volume (stroke volume) SV
The amount of blood ejected by one ventricle during one contraction
Stroke volume 70ml = ventricular end diastolic volume – ventricular end systolic volume
Ejection fraction (EF)
Stroke volume as a percentage of ventricular end-diastolic volume 55% to 60%
Reflects ventricular pumping efficiency
Output per heart rate and cardiac index
Output per minute (cardiac output) CO
The amount of blood ejected from one ventricle per minute
Cardiac output 5L/min = stroke volume 70 × heart rate 75
Women are 10% lower than men
Not proportional to body weight, proportional to body surface area
cardiac index CI
CO/body surface area
3～3.5L/min/m2
Quiet, fasting → Resting CI: Comparing cardiac function in individuals with different body shapes
heart work capacity
Stroke work: the work done by the ventricle in one contraction
Work per minute: work done by the ventricles per minute
*The stroke volume of the left and right ventricles is equal, and the work capacity of the right ventricle is only 1/6 of the left ventricle (mean pulmonary artery pressure = 1/6 mean aortic pressure)
Heart force/heart pump function reserve
The ability of cardiac output to increase in response to the body's metabolic needs
Reflects the health of the heart and its pumping function
Depends on stroke volume, HR
stroke volume reserve
Systolic Reserve (Main)
Enhance myocardial contractility and ejection fraction
Reserve volume: 55~60ml
diastolic reserve
Increase end-diastolic volume, 15ml
Heart rate reserve: 160～180ml/mim
Factors affecting cardiac output
stroke volume
front load
Initial length of ventricular muscle ⇔ Ventricular end-diastolic volume (volume of venous return to the heart, volume of remaining blood in the ventricle after ejection)
Abnormal autoregulation
Myocardium changes the initial length of myocardial cells, causing myocardial contraction to strengthen, thereby regulating stroke volume.
Frank-Starling curve Starling's Law of Heart
Within a certain range, the ventricular end-diastolic volume (pressure) increases. The longer the initial length, the stronger the ventricular contractility, and the greater the stroke volume and stroke work.
Affects preload
venous blood return volume
Increased ventricular filling time/venous return velocity → increased venous return blood volume → increased end-diastolic volume, large ventricular compliance → increased stroke volume
The amount of blood remaining in the ventricle after ejection
afterload
Aortic blood pressure increases, stroke volume decreases, residual blood volume increases, and next stroke volume increases
Aortic pressure is in the range of 80-170mmHg, and cardiac output generally remains unchanged.
myocardial contractility/ myocardial inotropic state
The intrinsic characteristics of its mechanical activities that can be changed independently of preload (independent of initial length) and afterload
isometric autoregulation
Regulation of cardiac pumping function by changing myocardial contractility
Influencing factors
Number of activated cross-bridges
Myosin head ATPase activity
CA, cardiac drugs↑; ACh, hypoxia, acidosis, HF↓
heart rate
Within a certain range, the heart rate increases and cardiac output increases
Heart rate is too fast, stroke volume is significantly reduced, and cardiac output decreases
electrical activity and physiological properties
Cardiomyocyte classification
Function (whether phase 4 will automatically depolarize)
working cells
Atrial myocardium, ventricular myocytes
There is a stable resting potential (RP) that mainly performs contractile functions
autonomous cells
Sinoatrial node cells, Purkinje cells
Can automatically generate excitement
Depolarization speed (phase 0 ion channel type)
fast response cells
Atrial myocytes, ventricular myocytes, Purkinje cells
Depolarization speed and amplitude are large, and conduction speed is fast (triggered by fast sodium channels)
slow responding cells
sinoatrial node, atrioventricular node cells
Depolarization speed and amplitude are small, and conduction speed is slow (triggered by slow calcium channels)
working cells
RP: K equilibrium potential
AP
ventricular myocytes
Features
The ascending and descending limbs are asymmetrical and have a platform. Repolarization is slow and lasts for a long time, divided into 5 phases. Various ion channels are involved
Five issues
Phase 0 (depolarization phase): rapid inflow of Na
Voltage-dependent fast Na channel ← blockade by tetrodotoxin TTX
Stage 1 (initial stage of rapid repolarization): transient K outflow
4-AP blocking
Phase 2 (platform phase): Ca2 inflow and K outflow
Determines the length of the effective refractory period
Verapamil blocks (slow Ca channels)
Stage 3 (end of rapid repolarization)━K Outflow progressively increases
AP
Phase 4 (resting phase) - sodium pump, calcium pump
autonomous cells
Basic features: 4 phases of slow, automatic depolarization
No RP, only maximum diastolic potential (maximum repolarization potential) MDP
sinoatrial node P cells
The formation mechanism of AP
Period 0 (depolarization process)
Ca2 influx
Phase 3 (repolarization process)
Ca2 inflow↓, K outflow↑
Phase 4 (automatic depolarization process)
K outflow progressively attenuates (mainly); Na influx progressively increases, transient Ca2 influx
AP characteristics
① The stages are 0, 3, and 4, with no obvious stages 1 and 2. ②The maximum diastolic potential (-70mV) and threshold potential are both low ③Phase 0 depolarization is slow, long lasting, and small in amplitude ④The speed of automatic depolarization in phase 4 is significantly faster than that of Purkinje
Purkinje cells
Phase 0~3 same working cells Phase 4 automatic depolarization: Na inflow progressively increases (main); K outflow progressively attenuates
Phase 4 If is blocked by cesium
electrocardiogram
P wave: depolarizing contraction of the atrium
QRS complex: depolarization of ventricular contractions
T wave: ventricular diastolic repolarization (stage 3)
U wave: related to Purkinje fiber repolarization
P-R interval
P starting point→QRS complex starting point
atrioventricular conduction time
P-R segment
P end point→start point of QRS complex
Room-room junction
ST segment
plateau
Physiological properties of myocardium
Excitability
Factors that determine and influence excitability
RP or the difference between maximum diastolic potential and threshold potential
The distance between RP and threshold potential↑→stimulation threshold required to cause excitation↑→excitability↓.
The state of the ion channels used in phase 0 depolarization
Both Na channels and Ca2 channels have three alternative states of activation and inactivation.
Whether it is in a standby state determines the presence or absence of excitability The number of spare state channels determines the level of excitability
Cyclic changes in cardiomyocyte excitability
Effective refractory period ERP
Absolute refractory period ARP 0～-55
Na channels are completely inactivated Cannot generate new AP
No reaction or excitement
Local reaction period LRP -55～-60
Na channel begins to resurrect Cannot generate new AP
Reactive but not excited
Relative refractory period RRP -80～-90
Na channel partial resurrection
Suprathreshold stimulation can produce AP
be excited
Supernormal period -90
Most Na channels resurrected
Subliminal stimulation can produce a second excitation
The relationship between periodic changes in excitability and myocardial contractile activity
No tetanic contraction occurs
The effective refractory period is particularly long, corresponding to the systole and early diastole of the myocardium.
Ensure alternating contraction and relaxation, which is beneficial to cardiac ejection and ventricular filling
Premature contractions and compensatory pauses
After the effective refractory period and before the arrival of the next sinoatrial node excitement, the myocardium receives an external stimulus, which can produce a preterm excitement and cause premature contraction.
Premature excitement also has an effective refractory period. The subsequent excitement from the sinoatrial node falls within the effective refractory period of the premature excitement. Therefore, a longer period of ventricular diastole after the premature contraction is called a compensatory interval.
Autonomy (automatic rhythmicity)
The ability or characteristic of cardiomyocytes to automatically produce rhythmic excitation in the absence of external stimulation.
Factors affecting self-discipline
Phase 4 automatic depolarization speed (main): fast speed, high self-discipline, fast heart rate
Sinoatrial node 100; atrioventricular junction 50; Purkinje fibers 25
The difference between the maximum repolarization potential and the threshold potential
Normal pacemaker points of the heart and sinus rhythm
Normal pacemaker: sinoatrial node - sinus rhythm
Ectopic pacemaker - ectopic heart rhythm
How the sinoatrial node controls potential pacemakers
Be the first to occupy
The sinoatrial node is preemptively excited to generate action potentials, making it impossible for autonomous excitement at each potential pacemaker point to occur.
overdrive depression
The potential pacemaker is passively excited driven by the excitation of the sinoatrial node, and the frequency is much higher than its own automatic excitation frequency. When the external overdrive stimulus ceases, the autonomy of the potential pacemaker cannot be restored immediately, and it takes a period of time to recover its own autonomy from the suppressed state.
Purpose: To prevent the occurrence of ectopic beats
Clinically, if the pacemaker needs to be temporarily interrupted, its driving frequency needs to be gradually slowed down
conductivity
The ability of cardiomyocytes to conduct excitation
Excitatory conduction pathways in the heart and their characteristics
room delay
When sinus rhythm excitement is transmitted to the atrioventricular junction, the conduction speed slows down significantly, delaying the impulse by 0.1 s.
Purpose: to avoid overlapping of atrial and ventricular contractions
slowest
Room-room junction
fastest
Purkinje fibers: 2~4m/s (maintains synchronous contraction of the ventricles)
Factors affecting conductivity
Conduction velocity is proportional to diameter Cardiomyocyte diameter (major factor)
Purkinje's fibers have the largest diameter, the smallest resistance, and the fastest excitement conduction speed.
Phase 0 depolarization speed and amplitude
Membrane response curve: X resting membrane potential, maximum depolarization rate in Y0 phase
Phenytoin shifts the membrane reaction curve to the upper left and accelerates conduction velocity
Quinidine shifts the membrane response curve to the lower right
Excitability of membranes adjacent to unexcited areas
sodium channel status
The difference between threshold potential and RP
Contractibility
ability of muscle filaments to glide
Features
1. No tetanic contraction occurs Long effective refractory period
2. Synchronous shrinkage ("all-or-none" shrinkage) Excitement conduction speed is fast
3. Highly dependent on extracellular fluid Ca2 Underdeveloped sarcoplasmic reticulum
Influencing factors
Ca concentration
Sympathetic N and CA accelerate Ca influx and enhance myocardial contractility
Vagus nerve and ACh reduce Ca influx and reduce myocardial contractility