Physiological structure of the heart
The left ventricular myocardium is two to four times thicker than the right ventricular wall, because it must pump blood at a higher pressure to overcome the great resistance of the systemic circulation.
Functional structure of the heart
The heart is a hollow muscle, weighing about 300g, divided into 4 chambers: 2 atria and 2 ventricles. The right atrium and left atrium, thin wall, receive venous blood, bring to the ventricle, The right and left ventricles, thick-walled, pump blood into the arteries at high pressure. The two atria are separated by the atrial septum and the two ventricles are separated by the ascending ventricular septum.
The thickness of the heart walls in the chambers varies according to their function. The left ventricular myocardium is two to four times thicker than the right ventricular wall because it must pump blood at a higher pressure to overcome the great resistance of the systemic circulation.
The energy needed for the movement of blood comes from the heart muscle wall.
Functional structure of the heart valve system
The direction of blood flow is determined by the presence of heart valves. The heart valves are thin, flexible, connective tissue surrounded by the endocardium.
Atrioventricular valve: the space between the atrium and ventricle, the left has a mitral valve, the right has a tricuspid valve. It allows blood to flow in one direction from the atria to the ventricles. The muscular columns are attached to the atrioventricular valves by ligaments. The muscle column contracts when the ventricle contracts, it does not help the valve close, but it pulls the valve stem toward the ventricle, preventing the protrusion of the leaflets into the atrium during ventricular contraction. If a ligament is torn or if one of the muscle columns is damaged, blood can back up into the atria when the ventricles contract, sometimes causing severe cardiac dysfunction.
Semilunar valve: between the left ventricle and the aorta, there is the aortic valve, the pulmonary valve between the right ventricle and the pulmonary artery. It helps blood flow one way from the ventricles to the arteries.
All valves open and close passively, opening and closing depending on the pressure difference across the valve. For example, when atrial pressure exceeds ventricular pressure, the atrioventricular valve opens, and blood flows from the atria to the ventricles; Conversely, when ventricular pressure is greater than atrial pressure, the valve closes, preventing blood from flowing backwards from the ventricle to the atrium (Figure).
Figure: Myocardium and the Mitral Valve System.
Functional structure of the myocardium
The heart is made up of three types of the myocardium: atrial, ventricular, and specific excitatory and conduction fibres. The atrial and ventricular muscles contract like striated muscles, but the other types are weaker, but they are rhythmic and conduct impulses quickly in the heart.
Cardiac muscle cells are intermediate between skeletal and smooth muscle cells. These are small, striated, branched cells with only one nucleus. Unlike skeletal muscle, cardiac muscle cells have bridges, connected to each other into a solid block, with cell membranes that blend together. The myocardium fibres are syncytial, acting as a single unit in response to stimuli, propagating electrical potentials between the myocardium fibers rapidly across the junctions. The transmission of electrical potential from the atria to the ventricles is conducted through a special pathway called the atrioventricular junction.
Cardiac muscle fibers contain many mitochondria and blood vessels, consistent with the aerobic activity of the heart. The main component of cardiomyocytes are myofibrillar, which contain thick (myosin) and thin (actin, tropomyosin, troponin) filaments, whose contraction causes contraction of the entire myocardium. . Around the muscle fibers there is an endoplasmic reticulum (reticulum sarcoplasmic) where calcium is stored.
Thus, the main function of the myocardium is to contract itself, and they also respond in the same way in the case of disease: they either hypertrophy in overload or they necrosis to fibrous tissues in other cases.
Functional structure of the conduction system
Consists of delicate cells capable of pacemaker for the whole heart, they form the conduction system, conduct electrical potentials through the heart muscle. This conduction system ensures synchronized contraction of the cardiac chambers, including:
The sinoatrial node: also called the Keith-Flack node, is located in the atrial muscle, where the superior vena cava empties into the right atrium. The sinoatrial node generates pulses of about 80 l-100l/min, is the pacemaker node for the heart, receiving the control of sympathetic and parasympathetic fibers (X wire).
Atrioventricular node: also known as the Aschoff-Tawara node, located posteriorly to the right of the atrial septum, next to the coronary sinus foramen. Pulses 40-60l/min, controlled by sympathetic and X-wire.
Bundle of His: goes from the atrioventricular node to the interventricular septum, runs below the endocardium to the right side of the septum about 1cm, also known as the atrioventricular junction, conducts electrical potentials between the atria and ventricles, and then divides into right and left branches.
The right branch continues down to the right side of the interventricular septum, dividing into small branches running between the right ventricular myocardium called Purkinje fibres. The left branch passes through the interventricular septum, divides a thin, anterior branch and a thick posterior branch, and then also divides into Purkinje fibres to reach the left ventricular endocardium. Atrioventricular junction, bifurcation or Purkinje fibres very slow pulse rate 20-40 l/min, receiving only sympathetic fibres.
Functional structure of the nervous system
The heart is controlled by the autonomic nervous system.
The right X cord innervates the sinus node and the left X cord innervates the atrioventricular node. Parasympathetic fibers go to the atrial muscle but not to the ventricle.
The sympathetic cord reaches the base of the heart via a great vessel, then divides into the myocardium, usually following the coronary artery.
The sympathetic nervous system secretes Norepinephrine, increases sinus node frequency, increases conduction velocity, and increases contractile force. of these two systems are opposite, but have a regulating effect to ensure cardiac activity.
Physiological properties of the myocardium
Excitement is the ability to generate action potentials that cause myocardial contraction.
The heart is composed of two types of muscle cells:
The cells that generate and conduct impulses are the sinus node, the atrioventricular node, and the Purkinje network.
The cells that respond to these impulses by contraction are the atrial and ventricular muscle cells.
These properties make the heart automatic. This is a feature not found in skeletal muscle.
The electrical activity in the heart leads to contraction. Therefore, disturbances of electrical activity will lead to arrhythmias with mild to severe clinical manifestations.
Phases of myocardial potential action:
At rest, both myocardium fibers, like other living cells, are polarized, that is, there is a potential difference between the inside and outside of the cell membrane. The negative internal voltage compared to the outside is measured from -70mV to -90mV, sometimes up to -90mV to -100mV is a special type of conductive fiber such as a Purkinje fiber, called resting membrane potential. source from the difference in concentration of 3 main ions, Na+, Ca+ and mainly K+. The concentration of K+ in cardiomyocytes is very large, 30 times higher than the concentration of K+ outside the cells.
The resting myocardial membrane potential is relatively permeable to K+, and K+ tends to diffuse outward along the concentration scale. Anions (A-) in the cell do not diffuse out with K+. The lack of cations makes the electric potential in the membrane negative relative to the outside. The action potentials of cardiac muscle cells include the following phases:
Phase 0-1: upon stimulation, the cell membrane is depolarized, the membrane permeability changes, the membrane increases permeability to Na+, the Na+ channel opens rapidly and Na+ penetrates into the cell, the intracellular potential The membrane drops rapidly to 0mV and becomes +20mV positive. The action potential draws a nearly vertical line, called the rapid depolarization phase, corresponding to the R wave of the electrocardiogram (ECG).
Phase 2: plateau phase of the action potential, membrane permeability to potassium ions decreases, while permeability to sodium-calcium increases, Ca++ channels are slowly opened in cell membranes and substrate-generating reticulum, These ions enter the cytoplasm, some Na+ also enter, and the action potential appears as a plateau (plateau).
Phase 3: rapid repolarization again, membrane permeability to Ca+ decreases, K+ channels open, membrane increases permeability again to K+, K+ escapes out of the cell more, making the potential in the membrane more negative .
Phase 4: polarization, at the beginning of this phase, Na+ is transported out and K+ enters the cell by the Na+K+ATPase pump, in the presence of Mg++. The membrane potential returned to its initial value (Figure 3).
In atrial and ventricular myocytes, without spontaneous activity, phase 4 will persist, until some stimulus from neighbouring cells, the membrane potential will gradually approach a threshold and initiate action potentials with the above phases.
But in a particular type of cell of the conduction system, it will not passively wait for external stimuli, but even in the resting state, will also seek to depolarize itself. In phase 4, there is a gradual decrease in membrane permeability to K+, increased permeability to Na+ increases the potential across the membrane, the potential in the membrane gradually decreases, bringing the curve closer to the isoelectric line: that is, slow diastolic depolarization, characteristic of autonomic cells. This property makes them able to emit rhythmic pulses on their own at a certain frequency. That's why people call the heart automatic. This feature is completely independent of the nervous system, even if all nerve branches are removed as in a heart transplant, the heart still beats automatically.
This phase is fastest in the sinus node, followed by the atrioventricular node, and slowest in the Purkinje fibers, exhibiting individual impulse generation in each of these particular cell types.
Figure: Potential action of ventricular muscle fibres.
Because of the syncytial of the myocardium, the heart operates on an all-or-nothing basis. Stimulation of a certain atrial muscle fiber induces an electrical action through the atrial muscle mass, similar to that of the atrial muscle. If the atrioventricular junction is working properly, the potential will be transferred from the atria to the ventricles. When the stimulus is strong enough to bring the voltage in the membrane to the threshold, the myocardium will contract immediately to its maximum. Below that threshold. The heart muscle does not respond, nor does the heart contract any stronger.
The effect of the autonomic nervous system on rhythm cells:
The parasympathetic system prolongs the action potential duration, making the resting membrane potential more negative, thereby reducing cell excitability. Acetylcholine increases the permeability of the myocardium to K+ thereby prolonging the slow diastolic depolarization.
The above reasons reduce the rate of heartbeat cells, causing bradycardia.
In contrast, the sympathetic system reduces cell excitability and accelerates slow diastolic depolarization, thereby increasing heart rate.
Cyclic inertness of the myocardium
At different phases of the action potential, the myocardium responds differently to an external stimulus.
In phases 1 and 2, the muscle fibers are already depolarized and therefore do not respond to any stimulus, which is the absolute refractory period (0.25-0.3s in the ventricular muscle). It prevents the heart from being disturbed by an external stimulus. This is an extremely necessary protective mechanism, helping the heart muscle not to contract like skeletal muscle, a contraction of the heart will lead to circulatory arrest and death.
In phase 3, when the intramembrane potential increases to -50mV, the myocardium begins to respond to stimuli, albeit weakly, which is a period of relative refractory (0.05 s in the ventricular muscle). Towards the end of phase 3, the myocardium enters the hyper normal phase, which means that it responds very readily to even small stimuli. This period is very short (figure 4).
The refractory periods of the atrial myocardium are shorter than those of the ventricles, so the contraction rate of the atria is faster than that of the ventricles. Understanding the refractory periods of the myocardium is very helpful in understanding and treating rhythm disturbances.
Figure: Cardiac muscle action potentials and refractory periods.
Conduction of the myocardium
This property is present in all types of the myocardium. The action potential propagates along the muscle fiber forming a wave of depolarization. This wave is comparable to the wave we observe when we throw a stone into the water.
Impulse conduction velocity varies in regions of the heart. In the physiological state, the impulse from the sinus node enters the atrial muscle with a moderate velocity, 0.8-1m/s. Conduction slows down from 0.03-0.05 m/s from the atria through the AV node, the action potentials are very slow at the AV node, due to the inclusion of very small diameter fibers. After that, the velocity increases in the His bundle (0.8-2m/s) and reaches very high in the Purkinje lattice: 5m/s. It eventually slows down as it enters the ventricular muscle fibers, with a velocity of 0.3-0.5 m/s.
Figure: Conduction system and action potentials at each site in the heart.
Thus, impulse conduction from the sinus node takes 0.15s to initiate depolarization of the ventricles (Figure 5)
Calculate the rhythm of the heart muscle
Rhythmicity is the ability of the next to produce a pulse that causes the heart to contract in a regular rhythm. Normal impulses arise from the sinus node with an average frequency of 80 l/min. Next, the first two atria depolarize the right atrium before the left, and simultaneously extend to the atrioventricular node in internodal bundles. Conduction in the atrioventricular node is slowed down to give the atria time to finish contracting. This delay can be shortened by sympathetic stimulation and prolonged by the X cord.
The impulse continues along the two branches of the bundle of His into the Purkinje fibers with great velocity so that the ventricular muscle fibers are depolarized within 0.08-0.1s (time of the QRS wave on the ECG). The apex is depolarized in front of the base of the heart, so it contracts before the fundus, helping to pump blood from the snout to the base and into the arteries.
The sinus node generates impulses with the highest frequency, also known as the pacemaker node of the heart, it always plays the main role of master rhythm for the entire heart. Neurotransmitters, or hormones, can increase or slow the heart rate from the sinus node. For example, in a person at rest, parasympathetic acetylcholine causes the heart rate to beat about 75 times per minute.
In pathological cases, the atrioventricular node or atrial, ventricular muscle can also be pacing, taking over the role of the sinus node, taking over the position of commanding the heartbeat and is called the ectopic focus. , triggers include caffeine, nicotine, electrolyte imbalances, hypoxia, and side effects of medications, such as digitalis.
Thus, the appearance of peripheral foci causes the heart rate to slow down and sometimes the blood will not be enough for the brain. In such patients, when necessary, a normal heart rate can be maintained with an artificial pacemaker. In addition, there are on-demand pacemakers, not only for the normal functioning of the heart, but also to help the heart adapt by increasing the frequency during exercise or stress.
Electrocardiogram (Electrocardiogram me: ECG)
Summary of electrocardiogram
When the heart is working, an electrical current occurs in the heart muscle fibres. These currents can be recorded from electrodes placed on the skin. Thus, the electrocardiogram represents the electrical activity of the heart and can indicate the state of the heart, the frequency, nature and generation of heartbeats, the spread and effectiveness of arousals, and any disturbances. disturbances are possible.
To obtain an electrical current in the heart, electrodes of an electrocardiogram are placed on the body. Depending on the electrode placement, different leads are obtained in order to study the normal and pathological currents in the most beneficial way (Figure).
Depending on how the electrode is connected, we will have 12 leads:
Bipolar leads of the limbs: D1, D2, D3.
Enhanced limb unipolar leads: aVR, aVL, AVF.
Precordial leads V1, V2, V3, V4, V5, V6.
The electrocardiogram (electrocardiogram) consists of 5 consecutive waves with 6 consecutive letters named P, Q, R, S, T. The three waves Q, R, and S combine to form a QRS complex. . Waves above the isoelectric line are positive, waves below the isoelectric line are negative.
The atrial depolarization wave. Amplitude < 0.25mV, time < 0.1s.
Atrial repolarization is not seen on the ECG because it is mixed in the next wave.
Shows ventricular depolarization. Time 0.08s.
Q wave amplitude (0.3mV, time 0.03s.
R wave amplitude can be up to 2mV.
The S wave is similar to the Q wave.
Shows repolarization of the ventricles. Amplitude < 0.5mV, time 0.2s. Although depolarization and repolarization are opposite phenomena, the T wave is often as positive as the R wave. This suggests that the formation of arousal and its propagation is accomplished in different ways.
Is the conduction time of impulses from the atria to the ventricles, time <0.2s
Depending on heart rate, time 0.35s to 0.4s with heart rate 75 beats/min. It is the time of ventricular activity (Figure)
Figure: How to attach electrodes on the skin to record the electrocardiogram.
The electrocardiographic axis is a vector describing the depolarization of the heart, the average depolarization vector QRS shows close to the anatomical axis of the heart when arousal is propagated normally. This vector is therefore called the mean electrical axis of the heart denoted ÂQRS .
In 1913 Einthoven recorded potential differences (HSDTs) in the leads when electrodes were attached at different locations on the body. He derived the rule: the potential difference is proportional to Cos a which is the angle formed by the heart axis and the junction between the two electrodes. When the line connecting the two electrodes is parallel to the heart axis, the potential difference is greatest, the further away from the heart axis, the lower the potential difference, and when perpendicular to the heart axis, the potential difference is zero.
The length of the vector represents the potential. The triangle sides are the connecting line between the 2 electrodes of leads D1, D2, D3. Drawing the projection of the electrocardiogram vector on the sides of the triangle, we obtain different values on the sides. That is the potential difference between D1, D2, D3.
D2 is nearly parallel to the heart axis, so the potential difference is the largest, followed by D3 and finally, D1 is nearly perpendicular to the heart axis, so the potential difference is the smallest because it has the largest angle a.
Thus, potential changes in the leads also indicate the state of the probed region.
Figure: Conduction of impulses through the heart shown on an electrocardiogram.
Amplitude (mV) and duration (ms) of the waves on the electrocardiogram.
Electrocardiogram & Electrolytes
Changes in serum K+ or Ca++ concentrations often lead to changes in myocardial excitability and disturbances in the ECG.
When K+ > 6.5mmol/l, T waves are high and pointed, QT prolongation, severe cases can lead to sinus arrest.
When K+ < 2.5 mmol/l, ST is below the isoelectric line, T is biphasic and a U wave may appear following the T wave.
When Ca++ > 2.75mmol/l, the QT interval and ST segment are shortened.
When Ca++ < 2.25 mmol/l, the QT interval is prolonged.
Heart beats rhythmically, steadily, about 3000 million times for human life. This sequence of operations can be broken down into separate repetitive cycles. The time interval from the beginning of one heart sound to the beginning of another is called a cardiac cycle. During each cardiac cycle, the pressure changes in the atria and ventricles, causing them to contract and relax, blood will move from the high-pressure area to the low-pressure area. Figure 8 shows the relationship between the electrocardiogram, mechanical phenomena (contraction and dilation), and changes in inertia in atrial, ventricular, ventricular volume, and aortic pressure throughout the cycle. heart period. The pressure in this figure is in the left ventricle, while the right ventricle pressure is much lower because the right ventricular wall is thinner but the ejection volume is the same. In a normal cardiac cycle, the two atria contract while the two ventricles relax, and vice versa.
Stages of the cardiac cycle
The cardiac cycle includes the contraction phase (systole) and relaxation phase (diastole) of the atria and of the ventricles. A cardiac cycle can be divided into three main phases:
Fill the chamber:
Occurs during diastole. At this time, the ventricular muscle is completely relaxed, the intraventricular pressure decreases, the atrial pressure exceeds the ventricular pressure because the blood from the veins continuously pours into the atrial inertia. This pressure difference causes the atrioventricular valve to open and blood from the atria to the ventricles called the phase of the rapid ventricular filling (80% of the blood in the atria flows into the ventricles). At the end of this period, the atria contract (atrial depolarization: P waves on the electrocardiogram) and expel the remaining 20% of the blood volume, to initiate ventricular contraction. Atrial contraction is not absolutely necessary for adequate blood flow at a normal heart rate.
At the end of diastole, there is about 130 mL of blood in each ventricle, called the end-diastolic volume (EDV), which is important for assessing cardiac function. During the ventricular filling phase, there is a pressure differential across the semilunar valve, the aortic pressure being greater than the left ventricular pressure, acting on the valves, causing them to remain closed during this period. This prevents blood from flowing back from the arteries to the heart.
The ventricles contract:
Immediately after atrial contraction, impulses from the sinus node cross the atrioventricular node and arrive at ventricular depolarization, presenting a QRS complex on the electrocardiogram. The ventricles begin to contract, resulting in an increase in intraventricular pressure. When the ventricular pressure is greater than the atrial pressure, the atrioventricular valve closes. In about 0.05 seconds, the ventricular chamber is a closed chamber because the atrioventricular valve and the bird's nest valve are closed, the myocardial length does not change, the ventricular volume does not increase, so it is also called isovolumetric contraction. . As the ventricles continue to contract, the pressure in the heart's chambers rises very rapidly, exceeding the pressure in the arteries. At this point, the aortic valve opens, and blood is pumped into the artery, the volume of blood ejected each time the heart beats is about 70ml, called the ventricular ejection phase, lasting 0.25s, until the ventricles begin. stretch.
The volume of blood remaining in the left ventricle after ventricular systole 60 mL is called the end-systolic volume (ESV).
When the ventricles begin to dilate, the four chambers of the heart are all in diastole. Repolarization of the ventricular muscle shows T waves on the electrocardiogram. At this time, the ventricular pressure decreases after the appearance of the T wave, and gradually lower than the aortic pressure, the aortic valve closes, blood tends to pool into the semilunar valve. Blood hits the closed leaflets, creating a raised wave on the aortic pressure curve. The closure of the aortic valve creates a short interval in which the ventricular volume remains unchanged because all four valves are closed. This stage is called dilatation. The ventricles continue to dilate, and the internal pressure decreases rapidly, leading to lower atrial pressure, the atrioventricular valve opening, and the beginning of the ventricular filling phase (Figure 8).
Figure: Relationship between electrocardiogram, electrocardiogram, left ventricular volume and barogram.
Combination of systolic and diastolic
With a heart rate of 75l/min, each cardiac cycle lasts 0.8s:
During the first 0.4 seconds of the cardiac cycle, which is the dilated phase of the heart, all four chambers of the heart are in diastole. First, all the valves close, then the atrioventricular valve opens and blood begins to pour into the ventricles.
In the next 0.1s, the atria contract and the atrioventricular valve open, but the ventricles remain dilated, and the semilunar valve is closed.
For the remaining 0.3 seconds, the atria dilate and the ventricles contract. First, all valves are closed (isovolumic contraction), then the semilunar valve opens, which is the ventricular ejection phase.
During tachycardia, the diastolic period is much shorter than the systole.
The ventricles do not pump all the blood every time the heartbeats, the remaining amount of blood is about 60ml, which is the ESV as mentioned above. When the heart contracts strongly, the ESV can be as low as 10-30ml, on the other hand, when a large amount of blood enters the ventricles when the heart is dilated, the EDV can be up to 200-250ml (normally about 130ml) in a normal heart. The increase in the end-diastolic volume, together with the decrease in the end-systolic volume, causes the ejection volume to now double to normal. Thus, ESV decreases when cardiac contractility increases or external resistance decreases, and conversely, ESV increases when the heart contracts poorly or peripheral resistance increases, which causes cardiac dysfunction.
External manifestations of the cardiac cycle
The contracting ventricles not only eject blood into the aorta but also create a pressure wave that moves along the aortic wall at a velocity of 5 m/s, which reaches the radial pulse within 0.1 s after being ejected into the aorta. . The intensity of the arterial pulse depends mainly on the systolic ejection volume. When the ejection volume is weak, as in blood loss or heart failure, the pulse is weak; after an exercise, the pulse is stronger.
In the past, to listen to the heart sound, the doctor placed his ear on the patient's chest, then people used a wooden stethoscope, which is still used today to listen to the fetal heart. Currently using a conventional stethoscope (Stéthoscope). Heart sounds can also be heard with a barogram and recorded on paper tape, for the purpose of visualizing heart sound activity.
Classically, the first and second heart sounds are heard as "poum-tac" as a heartbeat. The symbols are T1 and T2.
T1 due to the closure of the atrioventricular valve, plus the vortex of blood hitting the myocardium, produces a long, clear apical low-pitched sound, shortly after ventricular systole.
T2 is closed by a semilunar valve, high and short, clearly heard at the base of the heart, early in diastole
There are also T3 sounds consistent with rapid ventricular filling, and T4 sounds due to atrial contraction, but these two sounds cannot be heard with a conventional stethoscope.
In humans at rest, the time between T2 and T1 is twice as long as the time between T1 and T2, so there is a pause between two hours. When the heart rate is rapid, this pause is shortened.
Clinically, auscultation can detect abnormal heart sounds in valvular disease.
The most important function of the cardiovascular system is to ensure an adequate cardiac output into the pulmonary and systemic circulation. All cells receive oxygen delivered by the blood every minute to maintain health and life. When the cells are active, as in exercise, they need more oxygen from the blood, while at rest, the cells' demands decrease and the work of the heart decreases.
Cardiac output (LLT) is the amount of blood that the heart pumps into the arteries per minute in each ventricle.
Cardiac Flow (ml/min) = Heart rate (beats/min) * Systolic ejection volume (ml/beat)
At rest, in a normal person with a heart rate of 72 beats/min and a systolic ejection volume of 70 mL, the cardiac output would be approximately 5000 mL/min, which is equivalent to the amount of blood in the body (5-6 liters) of a single person. adult male. Thus, the volume of whole blood passing through the two circulations takes about 1 minute.
Measure cardiac flow
There are many methods of measuring Cardiac Flow, the following are two commonly used methods:
Measure by FICK method:
This principle is based on the oxygen consumption per minute (V02) equal to the amount of oxygen that the blood takes in through the lungs per minute. With Fick's formula:
VO2 = Q (CaO2 - CvO2)
Q is cardiac output.
The oxygen concentration in the pulmonary artery is Cv02 and the oxygen concentration in the pulmonary vein is Ca02, the concentration of oxygen consumption per minute at rest is about 250 ml/min.
The 0xy consumption (V02) is calculated by measuring the volume and concentration of 0xy in exhaled air per unit time.
Ca02 is measured from a brachial or radial artery blood sample.
Cv02, also known as mixed venous blood, is taken from a catheter (catheter) inserted into the pulmonary artery.
Measure by heat dilution method:
This method requires Cardiac Catheterization and modern equipment to record the heat dilution curve.
The principle of the method: the physiological saline indicator has a temperature close to zero (ice is melting) and the volume is measured first. Insert the catheter through the peripheral vein into the pulmonary artery. The top of the tube has a device that records heat changes called a heat sensor. A cold saline solution is injected rapidly into the right atrium, and the change in temperature over time from baseline pulmonary blood temperature is recorded. From the area included in the thermal dilution and baseline, the cardiac output is rapidly calculated.
Regulates cardiac flow
A person at rest, the heart pumps about 4-6 liters/minute, as the body's oxygen demand increases or decreases, the cardiac output changes accordingly. Factors that increase systolic ejection volume or heart rate both increase cardiac output. For example, during light exercise, ejection volume may increase by 100 ml/beat and heart rate by 100 beats/min, resulting in a cardiac output of 10 l/min. During intense (but not maximal) exercise, the heart rate can reach 150 beats/min and the ejection volume is 130ml/beat, at which point the cardiac output is up to 19.5 liters/min.
Heart rate variability is important in the acute regulation of cardiac output and blood pressure. The factors that play the most important role in regulating heart rate are the autonomic nervous system and adrenal medullary hormones.
Vegetative nervous system:
The cardiovascular center in the medulla receives impulses from sensory receptors in the periphery and from higher centers such as the limbic system and the cerebral cortex. From here, the response impulse is transmitted along the sympathetic and parasympathetic nerves of the autonomic nervous system that innervate the heart.
The proprioceptor controls the movements, for example, when an athlete is about to run, the posture of the limbs and muscles will act on the proprioceptors, increasing impulses transmitted to the cardiovascular centre, increasing the heart rate. heartbeat.
Chemoreceptors pick up on chemical changes in the blood.
Baroreceptors receive changes in pressure in the great arteries and veins, the main sites of which are usually the aortic arch and carotid sinus. These reflexes are important in the regulation of blood pressure as well as heart rate.
Sympathetic fibres from the medulla oblongata travel to the spine, from the thoracic spinal cord, and from the cardiac sympathetic fibres innervate the sinus node, the atrioventricular node, and most of the heart muscle. Norepinephrine, a chemical mediator of the sympathetic system, is released, which binds to a receptor on the myocardium, increasing the rate of the spontaneous depolarization of the sinoatrial node cells, so that the threshold of the incoming potential is faster, causes an increase in heart rate, and at the same time increases the contractility of the heart, due to the increase of Ca2+ into cells through slow calcium channels.
Parasympathetic nerve to the heart via the right and left X nerves, innervating the sinoatrial node, the atrioventricular node and the atrial muscle, the release of acetylcholine reduces the rate of spontaneous depolarization, increases the polarity of the sinus node cells. atrial fibrillation, the time to threshold is slower and the heart rate decreases.
In the resting state, both sympathetic and parasympathetic activity on the heart, if the heart loses nerve control such as surgery or medication, the heart rate will increase up to 100 times/min; Under normal conditions, the heart beats about 70 beats/min, indicating that the parasympathetic system is dominant in the regulation of sinus node activity.
Although increased heart rate is a factor that increases cardiac output, the maximum limit for impulse conduction through the sinus node is about 250 beats/min, when tachycardia is above 170 beats/min, cardiac output will begin to decrease. , due to the shortened ventricular filling time during diastole. This means that as blood return to the ventricles decreases (decreased EDV), the systolic ejection volume also decreases.
Several chemical factors influence myocardial physiology and heart rate. In hypoxia, acidosis and alkalosis both decrease cardiac activity. However, the following two factors have a major impact on the heart:
Hormones: Epinephrine and norepinephrine from the adrenal medulla increase the pumping power of the heart, and have the same effect on the heart as norepinephrine from the sympathetic nervous system, increasing both heart rate and contractility. Thyroid hormone also causes an increase in heart rate.
Ion: concentration of 3 cations K+, Ca2 + and Na+ has a great impact on cardiac function. An increase in K+ or a decrease in blood Na+ reduces heart rate and contractility.
Reflex depressurization: when the pressure increases in the aortic arch and carotid sinus, received by the baroreceptors, impulses are transmitted along with the Cyon Luwig and Hering cords to the medulla oblongata, reducing sympathetic stimulation and increasing stimulation. The X-wire causes the heart to beat slowly and blood pressure to drop.
Cardiac reflex (Bainbridge reflex): when the blood returns to the heart a lot, the root of the vena cava entering the right atrium is stretched, increasing the pressure here, the baroreceptors will transmit impulses along the sensory fibers going in the X wire to Cardiovascular center in the medulla oblongata, impulses transmitted by sympathetic nerves increase heart rate and contractility, and resolve blood stasis in the right atrium.
There are also other reflexes that affect cardiac activity:
Eye-cardiac reflex: pressing firmly on the two eyeballs stimulates the end of the V cord, the impulse to the medulla stimulates the X cord, making the heart beat slowly.
Goltz reflex: if hit hard on the epigastrium can cause cardiac arrest. This reflex from the positive plexus follows the visceral cord to the medulla oblongata, strongly stimulating the X cord. Therefore, during surgery, a strong tug of the abdominal organs can cause cardiac arrest.
Sudden strong stimulation of the nasopharynx, such as strangulation, hanging, ether anesthesia can also cause cardiac arrest.
Age, gender, physical condition, and body temperature also affect heart rate. The younger the child, the faster and slower the heart rate slows down to the normal adult heart rate.
In exercisers, there is a slow heart rate of less than 60 beats/min, which is advantageous in providing enough energy during prolonged exercise.
An increase in body temperature, such as a fever, increases the heart rate. Conversely, hypothermia reduces heart rate and contractility. Currently, for heart surgery, people use hypothermia, in this way the body temperature decreases, the metabolic rate and the oxygen demand of the tissues are reduced, which is convenient for surgery.
Systolic ejection volume:
As shown in the cardiac cycle, the systolic ejection volume will be the end-diastolic volume minus the end-systolic volume. There are three important factors that regulate systolic ejection volume in different situations and ensure that the right and left ventricles pump the same amount of blood: (1) preload: the dilation of the heart before contraction (2). ) contractility: contractility of each ventricular muscle fiber (3) afterload : pressure that must be overcome before ventricular ejection begins.
Preload is the end-diastolic filling volume (EDV), the larger the EDV, within a certain limit, the greater the contractility. This is known as the Frank-Starling law of the heart after two physiologists, Otto Frank and Ernest Starling. This is the intrinsic ability to adjust ejection volume to accommodate changes in venous return.
Diastolic time and venous pressure are two factors that determine EDV. As blood flow to the heart increases, the ejection volume increases. During tachycardia, diastolic time shortens, ventricular filling decreases, and the ventricle contracts before it is filled, so ejection volume decreases, in this case called preload reduction. The Frank-Starling law has the primary purpose of keeping the systolic ejection volumes of the two ventricles simultaneously equal, in order to avoid, in the pulmonary circulation, any stasis (pulmonary edema) or unhelpful pumping, which may result lead to death.
There are extrinsic factors affecting contractility without changes in end-diastolic volume. Substances that increase contractility are called positive inotropic agents and reduce contractures are called negative inotropic agents.
Positive inotropic agents include sympathomimetic hormones, intracellular Ca2+ enhancers, and drugs such as Digitalis. These factors promote the entry of Ca2+ during the electrical activity of the heart. Negative inotropic agents include sympathomimetic inhibitors, hypoxia, acidosis, and increased K+ in the extracellular fluid.
Cardiac ejection begins when right ventricular pressure is higher than pulmonary trunk pressure (about 20 mmHg) and left ventricular pressure exceeds aortic pressure (about 80 mmHg). At this point, the semicircular valve opens and the pressure that must be overcome before the valve opens is called afterload. When afterload increases, such as when blood pressure is increased or the arteries are narrowed by atherosclerosis, systolic ejection volume is reduced and more blood remains in the ventricles at the end of systole.