PUMPING WORK OF THE HEART
Humoral and intra cardiac mechanism of heart’ regulation.
Neural mechanism of heart’ regulation.
Objectives for Students’ Independent Studies
You should prepare for the practical class using the existing textbooks and lectures. Special attention should be paid to the following:
List:
Pumping work of the heart
1. The heart:
a). Anatomo-physiologycal properties of heart
b). Function of the heart valves
c). Function of papillary muscles
d). Heart Sounds
e). Heart murmurs
f). Properties of the cardiac muscle
2. Cardiac cycle
a). Phases of the cardiac cycle
b). Aortic pressure curve:
c). Relationship of the ECG to the cardiac cycle (Timing):
d). Relationship of the Heart Sounds to Heart Pumping
3. Cardiac volumes
4. Physiological analysis of cardiac output
a). Control of cardiac output:
b). Methods for measuring cardiac output:
5. Heart sounds
Echocardiography evaluation of heart function
6. Common characteristic of echocardiography investigation of heart
a) Kinds of echocardiography
7. Echocardiography investigation of left ventricle
a) Structures of echocardiography of left ventricle
b) Determination of end-systolic, end-diastolic sizes, thickness of left ventricle wall in systole and diastole, between ventricle septum
c). Calculation of end-systolic, end-diastolic, stroke, minute volume of heart, ejection fraction
d) Indexes of left ventricles
6. Fonocardiografia.
a). Determination on echocardiogram of left ventricle heart volumes, ejection fraction, anterior-posterior size of left ventricle
b) Determination of heart structure on D-echocardiogram
Regulation of the heart pumping
1. THE HEART
The heart is a muscular organ enclosed in a fibrous sac (the pericardium).The pericardial sac contains watery fluid that acts as a lubricant as the heart moves within the sac. The wall of the heart is composed of cardiac muscle cells, termed the myocardium. The inner surface of the wall is lined by a thin layer of endothelial cell; the endothelium. The heart is actually two separate pumps; a right heart which pumps blood through the pulmonary artery into the lung, and a left heart which pumps blood through the aorta into the peripheral organ. Each of these two pumps is consists of two chambers, an atrium and a ventricle, separated by atrioventricular valve (left; mitral valve and right; tricuspid valve). Blood exists from the right ventricle through the pulmonary valve to the pulmonary trunk, and from the left ventricle through the aortic valve into the aorta.
a). Anatomo-physiologycal properties of heart:
Pulmonary and Systemic Circulation.
Blood whose oxygen content has become partially depleted and carbon dioxide content has increased as a result of tissue metabolism returns to the right atrium. This blood then enters the ventricle, which pumps it into the pulmonary trunk and pulmonary arteries. The pulmonary arteries branch to transport blood to the lungs, where gas exchange occurs between the lung capillaries and the alveoli of the lungs. Oxygen diffuses from the air to the capillary blood; while carbon dioxide diffuses in the opposite direction. The blood that returns to the left atrium by way of the pulmonary veins is therefore enriched in oxygen and partially depleted of carbon dioxide. The blood that is ejected from the right ventricle to the lungs and back to the left atrium completes one circuit: called the pulmonary circulation.
Oxygen-rich blood in the left atrium enters the left ventricle and is pumped into a very large, elastic artery; the aorta. The aorta ascends for a short distance, makes a U-turn, and then descends through the thoracic and abdominal cavities. Arterial branches from the aorta supply oxygen-rich blood to all of the organ systems and are thus part of the systemic circulation. As a result of cellular respiration, the oxygen concentration is lower and the carbon dioxide concentration is higher in the tissues than in the capillary blood. Blood that drains into the systemic veins is thus partially depleted of oxygen and increased in carbon dioxide content. These veins empty into two large veins; the superior and inferior venae cavae that return the oxygen-poor blood to the right atrium. This completes the systemic circulation; from the heart (left ventricle), through the organ systems, and back to the heart (right atrium).
Physiology of cardiac muscle.
The heart is composed of three major types of cardiac muscle.
1- The atrial muscle.
2- The ventricular muscle.
3- Specialized excitatory and conductive muscle fibers; an excitatory system of the heart that helps spread of the impulse (action potential) rapidly throughout the heart.
Physiologic anatomy of cardiac muscle
Cardiac muscle cells (myocytes) are striated as they have typical myofibrils containing thin actin and thick myosin filaments, similar to those found in skeletal muscle, which slide along each other during the process of contraction.
Unlike skeletal muscle (no gap junction), adjacent myocardial cells are joined end to end at structures called intercalated discs, which are cell membranes that have very low electrical resistance. Within the intercalated discs, there are electrical synapses or gap junctions, these gap junctions are protein channels that allow ions to flow from the cytoplasm of one cell directly into the next cell and, therefore action potentials to move with ease from one cardiac myocyte to another. That is, when one of these cells becomes excited, the action potential spreads rapidly throughout the intercalated discs and gap junctions to stimulate the neighbor cell, so the myocardium act almost as if it is a single cell; a syncytium, i.e., the cardiac muscle contracts or behaves as a single functional unit (syncytium property).
Innervation of the heart
The heart receives a rich supply of sympathetic and parasympathetic nerve fibers. The parasympathetic contained in the vagus nerves release acetylcholine which acts on the muscarinic receptors. The sympathetic postganglionic fibers release norepinephrine (noradrenaline) which acts on beta one (β1) adrenergic receptors distributed on cardiac muscle. The circulating epinephrine hormone from adrenal medulla also combines with the same receptors (β1 receptors).
Blood supply of the heart
The myocardial cells receive their blood supply through arteries that branch from the aorta, named coronary arteries.
Coronary veins drain into a single large vein, the coronary sinus, which drain into the right atrium.
b). The function of the heart valves
The atrioventricular valves (AV valves) are composed of thin membranous cusps (fibrous flaps of tissue covered with endothelium), which hangdown in the ventricular cavities during diastole. After atrial contraction and just before ventricular contraction, the AV valves begin to close and the leaflets (cusps) come together by mean of backflow of the blood in the ventricles towards the atria.
The AV valves include:
· The mitral valve; the left AV valve; bicuspid valve, which consists of two cusps (anterior and posterior), located between left atrium and left ventricle.
· The tricuspid valve; the right AV valve, which consists of three cusps, located between right atrium and right ventricle.
The function of AV valves is to prevent backflow (prevent regurgitation; leakage) of blood into the atria during ventricular contraction. Normally they allow blood to flow from the atrium to the ventricle but prevent backward flow from the ventricle to the atria. The atrioventricular valves contain and supported by papillary muscles.
The aortic and pulmonary valves each consist of three semilunar cusps that resemble pockets projecting into the lumen of aorta and pulmonary trunk. They contaio papillary muscle. During diastole the cusps of these valves become closely approximated to prevent regurgitation of blood from aorta and pulmonary arteries into the ventricles. During systole the cusps are open towards arterial wall, leaving a wide opening for ejection of blood from the ventricles. In other words, the pulmonary and aortic valves allow blood to flow into the arteries during ventricular contraction (systole) but prevent blood from moving in the opposite direction during ventricular relaxation (diastole).
*All valves close and open passively. That is, they close when a backward pressure gradient pushes blood backward, and they open when a forward pressure gradient forces blood in the forward direction.
*There are no valves at entrance of superior, inferior vena cava and pulmonary veins into the atria. What prevents the backflow of blood from the atria toward the veins is the compression of these veins by the atrial contraction. However little blood is ejected back into veins, this represents the venous pulse seen in the neck veins (jugular veins) when the atria contracting.
c). The function of papillary muscles
The AV valves (mitral and tricuspid) are supported by papillary muscles that attach to the flaps of these valves by the chordae tendineae.The papillary muscles originated from the ventricular walls and contract at the same time when the ventricular walls contract, but these muscles do not help the valves to close or open. Instead, they pull the flaps of the valves inward, toward the ventricles to prevent too much further bulging of the flaps (cusps) backward toward the atria during ventricular contraction, to prevent leakage of blood into the atria (keep the valve flaps tightly closed). In other words, contractions of papillary muscles prevent evertion of the flaps of the AV valves into the atria which could be induced by high pressure produced by contraction of the ventricles.
Figure: Mitral (two cusps) and Aortic (three cusps) valves.
d). Heart Sounds
When the stethoscope is placed on the chest wall over the heart, two sounds are normally heard during each cardiac cycle (1st & 2nd heart sounds). Heart sounds are associated with closure of the valves with their associated vibration of the flaps of the valves and the surrounding blood under the influence of the sudden pressure changes that develop across the valve. That is, heart sound does not produced by the opening of the valve because this opening is a slow developing process that makes no noise.
1-The first heart sound (S1): is caused by closure of the AV valves when ventricles contract at systole. The vibration is soft, low-pitched lub.
2-The second heart sound (S2): is caused by closure of the aortic and pulmonary valves when the ventricles relax at the beginning of diastole. The vibration is loud, high-pitched dup. It is rapid sound because these valves close rapidly and continue for only a short period i.e., rapid, short and of higher pitch dup.
3-The third heart sound (S3): is caused by rapid filling of the ventricles, by blood that flow with a rumbling motion into the almost filled ventricles; at the middle one third (1/3) of diastole i.e., it is caused by the vibrations of the ventricular walls during the period of rapid ventricular filling that follows the opening of AV valves. It is a low-pitched sound and can be heard after the S2. It is heard iormal heart; in children and in adult during exercise. It is also heard in anemia, and AV valve regurgitation.
4-The fourth heart sound (S4): it is an atrial sound when the atria contract (at late diastole). It is a vibration sound (similar to that of S3) associated with the flow of blood into the ventricle. It is not heard iormal hearts but occurs during ventricular overload as in severe anemia, Thyroitoxicosis (hyperthyroidism) or in reduced ventricular compliance and in hypertension. If present, it is heard before S1. (S4, S1, S2, S3).
e) Heart murmurs
They are abnormal sounds, can be produced by blood flowing rapidly in the usual direction but through an abnormally narrowed valve (stenosis), by blood flowing backward through a damaged, leaky valve (incompetent, regurgitant valve) or by blood flowing between the two atria or two ventricles through a small hole: ASD (atrial septal defect), VSD (ventricular septal defect).
f). Properties of the cardiac muscle
In addition, to the syncytium property, the cardiac muscle has the property of:
· Automaticity and rhythmicity (Autorhythmicity).
· Excitability and conductivity.
· Contractility
Contractility – is the ability of the cardiac muscle to contract.
The effect of various factors on contractility is called inotropism; a positive (+ve) inotropic effect means an increase in myocardial contractility, whereas a negative (-ve) inotropic effect means a decrease in myocardial contractility.
Factors that affect cardiac contractility:
a). Mechanical
b). Cardiac
c). Extra cardiac
a). Mechanical factors:
* Preload (venous return)
* Afterload
b). Cardiac factors:
* The myocardial mass.
* The heart rate.
c). Extra cardiac factors:
These factors affect the cardiac inotropic state and they include the following:
* Neural
* Physical
* Chemical
2. CARDIAC CYCLE
Functional analysis.
Period from end of one heart contraction to end of next, is called cardiac cycle. Each cycle is initiated by spontaneous generation of an action potential in the sinus node which travels rapidly through both atria and then through the A-V bundle into the ventricles.
Because of this special arrangement of the conducting system from the atria into the ventricles, there is a delay of more than 0,1 second during passage of the cardiac impulse from the atria into the ventricles. This allows the atria to contract, pumping blood into the ventricles before the strong ventricular contraction begins. Thus, the atria act as primer pumps for the ventricles, and the ventricles in turn provide the major source of power for moving blood through the body’s vascular system.
There are two phases: systole, when heart contracts and diastole, when heart dilates.
In a normal heart, cardiac activity is repeated in a regular cycle. Heart rate is about 72 beats/minute; for the atria, the cycle lasts for about 0,15 second in systole and 0,65 second in diastole. For the ventricles, the duration of each cardiac cycle lasts about 0,8 second. If the heart rate increases, the diastole decreases, which means that the heart beating very fast may not remain relaxed long enough to allow complete filling of the ventricles before the next contraction.
For the ventricles, the two major phases of the cardiac cycle are:
· The diastole; a period of ventricular relaxation in which the ventricles fill with blood and it last for about 0,5 second.
· The systole; a period of ventricular contraction and blood ejection, lasting about 0,3 second.
Diastole can be divided into:
– Period of isometric relaxation, during which ventricles begin to relax and pulmonary valves close;
– Period of rapid filling of ventricles, when AV valves open;
– Atria systole, when atria contract and pump 20-30 % blood into ventricles.
Systole is composed by:
– Period of isometric contraction, when ventricles begin to contract and AV valves are closed;
– Period of ejection: during rapid ejection 70 % empting occur and in slow ejection last 30 % empting occur;
–
Protodiastole.
b) Intra cardiac pressure
Wiggers Diagram
During period of isometric relaxation intra ventricular pressure falls. In period of rapid filling of ventricles atria pressure becomes grater than intra ventricular pressure. In atria systole pressure in right atrium rises to 4-
Systole begins. In period of isometric contraction ventricular pressure rises. In period of ejection left ventricular pressure rises to
a). Phases of the cardiac cycle:
The cardiac cycle starts by atrial systole followed by ventricular systole then by diastole of the whole heart.
Atrial systole (atria as a pump):
It is the first phase of cardiac cycle. Blood normally flows continually (passively) from the veins into the atria and about 75% of the blood in the atria flow directly into the ventricles even before the atrial contraction. Then, atrial contraction usually causes an additional 25% filling of the ventricles. So the heart can continue to operate satisfactorily under most condition without this extra 25%, yet this 25% is needed in case of exercise.
Pressure changes in the atria during cardiac cycle
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During atrial contraction; right atrial pressure raises 4 to 6 mmHg, while the left atrial pressure raises 7 to 8 mmHg. In the atrial pressure curve, there are 3 major pressure elevations called the a, c and v atrial pressure waves:
· a wave is caused by atrial contraction.
· c wave is caused by bulging of the tricuspid valve into the right atrium during ventricular contraction because of increasing pressure in the ventricles.
· v wave result from slow flow of blood into the right atrium from the veins while the AV valve are closed during ventricular contraction. So the v wave is due to atrial filling.
Figure: Atrial pressure curve.
Clinical importance of atrial waves
Venous pulsations occur only in large veins near the heart like the jugular veins in the neck (the jugular venous pulsations). The jugular venous pulse reflects changes in right atrial pressure (the central venous pressure), i.e. the pressure changes within the right atrium are communicated to the neck jugular veins. To make the jugular venous pulsations visible in the neck, the person has to be supine with his back at a slight angle to the horizontal (45 degree). In this position, the a and v waves can be seen in the jugular veins when the neck is carefully examined. When the venous pressure is raised as in heart failure disease, the jugular veins become more prominent and the pulsation can be observed in the neck.
· x-descent is caused by pulling the AV ring down during ventricular systole; drop in right atrial pressure.
· y-descent is caused by the opening of the AV valve and the escape of the blood from the atrium into the ventricle; drop in right atrial pressure.
Ventricular cardiac cycle
The ventricular cardiac cycle consists of three phases:
· Phase one: Ventricular filling.
· Phase two: Ventricular systole.
· Phase three: Isovolumic, isometric relaxation.
1. Ventricular filling
During ventricular systole, the accumulated large amounts of blood in the atria because of the closed AV valves push the AV valves open and allow blood to flow rapidly into the ventricles. During atrial contraction, an additional amount of blood flows into the ventricles represent 25% of the filling of the ventricles.
Figure: Ventricular pressure curve.
2.Ventricular systole:
Subdivided into two phases:
1). Isovolumic, isometric contraction (isovolumetric contraction). Ventricles begin to contract, pushing AV valves close, SL valves still closed, pressure in ventricles rises. Pressure in ventricles is not enough to open semilunar valves. Therefore, All Valves Are Closed
2). Ventricular ejection – second (and last) phase of ventricular contraction. Pressure in ventricles rises and forces semilunar valves open. Blood is ejected into arteries. Ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected.
Isovolumetric contraction
It is ventricular contraction but without blood ejection (no emptying) just to close the AV valves and to open semilunar valves by the rise in intraventricular pressure (from 0 to 80 mmHg in the left ventricle). It is the isovolumetric contraction, which means only the tension is increasing in the ventricular muscle without shortening of the muscle and with no change in blood volume.
Ventricular ejection
The blood ejected from the ventricles into pulmonary trunk and aorta when the ventricular pressure rises and forces the semilunar valves open.
Left ventricular pressure rises above 80 mmHg.
Right ventricular pressure rises above 8 mmHg.
Figure: Ventricular volume curve.
2. Isovolumetric relaxation:
Isovolumic, isometric relaxation; following ventricular systole, ventricular relaxation begins suddenly and ventricular pressure falls. The blood in the aorta and pulmonary trunk backflows toward the heart closing the semilunar valves. For another 0.03 to 0.06 second, the ventricular muscle continues to relax, even though the ventricular volume does not change giving rise to the period of isovolumic relaxation in which the intraventricular pressure falls rapidly back to their low diastolic levels. Meanwhile, the atria have been filling with blood. When the pressure exerted by the blood on the atrial side of AV valves exceeds that in the ventricles, AV valves forced open and the ventricular filling phase begins again for a new cycle of ventricular pumping.
b). Aortic pressure curve:
When the left ventricle contracts, the intraventricular pressure rises rapidly until the aortic valve opens. So blood immediately flows out of the ventricle into the aorta, causes the wall of this artery to stretch and the pressure rise. Then, at the end of the systole, after the left ventricle stops ejecting blood and the aortic valve closes, the elastic recoil of the arteries maintains a high pressure even during diastole (diastolic pressure = 80 mmHg).The systolic pressure inside the aorta is equal to 120 mmHg. Incisura: is caused by a short period of backward flow of blood from the ventricle immediately before closure of the valve followed then by sudden cessation of the backflow.
Figure: Aortic pressure curve.
c). Relationship of the ECG to the cardiac cycle (Timing):
The ECG (electrocardiogram) shows the P, QRS and T waves. They are electrical voltages generated by the heart and recorded by the ECG:
· P-wave is caused by atrial depolarization; this is followed by atrial contraction, which causes a slight rise in the atrial pressure curve after the P wave.
· About 0.16 second after the onset of the P wave, the QRS waves appear as a
result of electrical depolarization of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising, as shown in the figure. Therefore, the QRS complex begins slightly before the onset of ventricular systole.
· T-wave represents ventricular repolarization at which the ventricles begin to
relax. Therefore, the T wave occurs slightly before the end of ventricular contraction.
d). Relationship of the Heart Sounds to Heart Pumping
When listening to the heart with a stethoscope, one does not hear the opening of the valves because this is a relatively slow process that normally makes no noise. However, when the valves close, the cusps of the valves and the surrounding blood vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest. When the ventricles contract, one first hears a sound caused by closure of the A-V valves. The vibration is low in pitch and relatively long-lasting and is known as the first heart sound. When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap because these valves close rapidly, and the surroundings vibrate for a short period. This sound is called the second heart sound.
Cardiac volumes
During period of isometric relaxation ventricular volume does not change. During rapid filling of ventricles period blood flows rapidly into respective ventricles. In atria systole ventricle volume increases on 20-30 %. Systole begins. In period of isometric contraction there is no volume change. In period of ejection stroke volume output occur. In protodiastole blood flows into aorta and pulmonary trunk, due to momentum.
3. PHYSIOLOGICAL ANALYSIS OF CARDIAC OUTPUT
Stroke work output is the amount of blood that left ventricle pump to aorta during each cardiac cycle. Volume of blood on each ventricle at end of diastole is called end-diastolic volume and measures 120-140 ml. Volume of blood in the each ventricle at end of systole is called end systolic volume and measures 50-60 ml.
Blood volume, which heart pumps per minute called as minute blood volume. It may be calculated by multiply stroke volume to rate of heartbeat and normally equal to 4-6,5 l/min. In physical exercises it rises to 10 l/min and more.
Cardiac output is the amount of blood pumped by each ventricle per minute, expressed in liters/minute. Normally, it is about
The cardiac output (CO) is determined through multiplying the heart rate (HR) by the stroke volume (SV).
CO = HR X SV
Heart rate = the number of heart beats/minute (aveage; 72 beat/minute).
Stroke volume = the volume of blood ejected by each ventricle with each beat.
If the HR = 72 beats/min., and the SV is of 70 ml;
Cardiac output = 72 X 70 =
As the cardiovascular system is a closed system, cardiac output of the left ventricle equals to the cardiac output of the right ventricle i.e., the two sides of the heart have the same output per minute. It is also the volume of blood flowing through either the systemic or pulmonary circulation per minute. In other words, cardiac output is the quantity of blood pumped into the aorta each minute by the heart. This is also the quantity of blood that flows through the circulation.
cardiac output= arterial blood flow = pulmonary blood flow.
Cardiac output varies widely with the level of activity of the body. Therefore, the level of body metabolism, exercise, age and size of the body influence the cardiac output. For young, healthy men, the resting cardiac output averages about 5.6 liter/min., for young women, this value is 10-20% less, but it is not constant. It might be increased even up to 30 liters/min., depending on the activity of the body. Therefore, cardiac output is a variable parameter usually it is not less than 5 liter/min., at rest to supply the body with oxygen and to maintain normal BMR (basal metabolic rate). The highest cardiac output recorded is 48 liters/min., in the Roadrunners (Hyperdynamic circulation which mean the same blood volume;
a). Control of cardiac output:
The cardiac output is controlled (either increased or decreased or maintained) by the following factors.
1). Venous return (preload).
2). Heart rate (HR)
3). Myocardial contractility.
4). Cardiac compliance.
5). Afterload.
1). Venous return:
The venous return (VR) is the amount of the blood flowing from the tissues into the veins and then into the right or left atrium each minute. So in steady state, they are equal (CO = VR) because what is pumped out from the left ventricle equals to what returned to the right side of the heart. In other words, It is the quantity of blood flowing from the veins into the right atrium each minute. It represents the preload. The venous return and CO must be equal to each other.
The CO is controlled by venous return through the following mechanisms:
Frank-Starling law; the heart pumps automatically whatever amount of blood flows into the right atrium from the veins. This law states that when increased quantities of blood flow into the heart, this stretches the walls of the heart chambers. As a result of the stretch, the cardiac muscle contracts with increased force to empty the expanded chambers i.e. the extra blood that flows into the heart (VR) is automatically pumped without delay into the aorta and flows again through the circulation.
The effect of the venous return on the heart rate by mean of stretching the heart. Stretch of the SA node in the wall of the right atrium has a direct effect on the rhythmicity of the SA node itself to increase heart rate 10 – 15% .
Another factor, the stretched right atrim initiates a nervous reflex called the Bainbridge reflex, passing first to the medullary vasomotor center and then back to the heart by sympathetic nerves, to increase the heart rate. The increase in the heart rate then helps to pump the extra blood.
Decrease in Cardiac Output Caused by Decreased Venous Return.
Anything that interferes with venous return also can lead to decreased cardiac output. Some of these factors are the following:
1. Decreased blood volume.
Resulting most often from hemorrhage. Loss of blood decreases the filling of the vascular system to such a low level that there is not enough blood in the peripheral vessels to create peripheral vascular pressures high enough to push the blood back to the heart.
2. Acute venous dilation.
In case of sudden and acute vasodilatation especially the peripheral veins involved. This results most often when the sympathetic nervous system suddenly becomes inactive. For instance, fainting often results from sudden loss of sympathetic nervous system activity, which causes the peripheral vessels, (veins), to dilate markedly. This decreases the filling pressure of the vascular system because the blood volume cao longer create adequate pressure in the flaccid peripheral blood vessels. As a result, the blood “pools” in the vessels and does not return to the heart.
3. Obstruction of the large veins.
When the large veins leading into the heart become obstructed, so that the blood in the peripheral vessels cannot flow back into the heart. Consequently, the cardiac output falls markedly.
4. Decreased tissue mass, especially decreased skeletal muscle mass.
With normal aging or with prolonged periods of physical inactivity, there is usually a reduction in the size of the skeletal muscles. This, in turn, decreases the total oxygen consumption and blood flow needs of the muscles, resulting in decreases in skeletal muscle blood flow and cardiac output.
* Regardless of the cause of low cardiac output, if the cardiac output falls below that level required for adequate nutrition of the tissues, the person is said to suffer circulatory shock. This condition can be lethal within a few minutes to a few hours.
2). Control of cardiac output:
Heart rate and cardiac output:
In resting state, (the venous return is constant), changes in heart rate between 100-200 beats/min., not affect CO markedly. However, high heart rate (more than 200 beats/minute) in patient with ventricular tachycardia (VT) or supraventricular tachycardia (SVT) may affect CO to be insufficient to maintain the nutritional needs of the body because such increase in heart rate will reduces the duration of ventricular diastole and so reduce the time available for ventricular filling that will reduce the stroke volume. On the other hand, slow heart rate may also reduce CO, as in complete heart block disease (HR < 40 beats/minute).
In exercise, (the venous return is increased), cardiac output is increased to meet the body need by increasing in both heart rate and stroke volume, the increase in heart rate is through sympathetic stimulation as the exercise is a stressful situation, while the increase in stroke volume is through the increase in venous return by the action of skeletal muscles that squeezed and pumped the blood toward the heart, and through the increased myocardial contractility.
So, the heart rate is effective in increasing the CO if the venous return is increased, otherwise the stroke volume will be decreased and so the decreased CO.
Stroke Volume
Stroke volume (SV) is defined as the amount of blood pumped out by each ventricle per beat. It is about 70 ml/beat at rest but may increase to 150 ml/beat with exercise.
The stroke volume equals to the amount of blood present in the ventricle when systole starts just before the initiation of ventricular contraction. However, the ventricles don’t completely empty themselves of blood during contraction (2/3 of blood is ejected, 1/3 is left there) therefore, a more forceful contraction can produce an increase in stroke volume.
Substruction of end-systolic volume (ESV) from end-diastolic volume (EDV) produce stroke volume (SV).
SV = EDV – ESV.
EDV: the ventricular blood volume at the end of the diastole; normally EDV = 110 to 120 ml.
ESV: the ventricular blood volume at the end of the systole; normaly ESV = 40 ml.
* Strok volume = 70 to 80 ml.
Regulation of Stroke Volume
The stroke volume is regulated by three variables:
· The end-diastolic volume (EDV).
· Sympathetic nervous system input to the ventricles (myocardial contractility; strength of ventricular contraction).
· The total peripheral resistance.
The end-diastolic volume is the amount of blood in the ventricles immediately before they begin to contract (preload). The stroke volume is directly proportional to the preload; an increase in EDV results in an increase in stroke volume. This relationship is known as the Frank-Starling law. In other words, the ventricle contracts more forcefully during systole when it has been filled to a grater degree during distole.
The stroke volume is also directly proportional to the myocardial contractility which is influenced by cardiac sympathetic nerves (norepinephrine) and circulating epinephrine secreted from adrenal medulla. Thus, when the ventricles contract more forcefully as a result of sympathetic nerve stimulation or epinephrine which is independend of a change in end-diastolic ventricular volume, they pump more blood (increased stroke volume).
The total peripheral resistance which is the impedance to blood flow in the arteries (aortic impedance). The pressure in the arterial system before the ventricle contracts is, in turn, a function of the total peripheral resistance. The higher the peripheral resistance, the higher the pressure. Thus, an increased arterial pressure tends to reduce stroke volume. The total peripheral resistance thus presents an impedance to the ejection of blood from the ventricle, or an afterload imposed on the ventricle after contraction. This means that the stroke volume is inversely proportional to the total peripheral resistance; the greater the peripheral resistance, the lower the SV.
Ejection Fraction (EF%):
The proportion of the end-diastolic volume that is ejected against a given afterload depends on the strength of ventricular contraction. Normally, contraction strength is sufficient to eject 70 to 80 ml of blood out of a total end-diastolic volume of 110 to 120 ml (2/3 of blood is ejected). The ejection fraction is thus about 65%.
In other words, the ejection fraction is the ratio of stroke volume to end-diastolic volume (EDV) and it reflects the ventricular contractility, expressed as percentage, normally it averages at rest 65% (again, about 2/3 of the EDV is ejected).
Increased ventricular contractility causes an increase in ejection fraction.
EF% = SV / EDV X 100.
EF% = 80/120 X 100 = 2/3 %. (more than 55% considered as normal).
In heart failure, the EF is reduced; < 50%.
EF can be measured by Echocardiogram (Echo) that can measure the EDV, ESV and so the SV.
3). Myocardial contractility:
It is defined as the strength of contraction at any given EDV.
Myocardial contractility exerts a major influence on stroke volume and in turn on the cardiac output. It is reduced in heart failure.
It is measured by Ejection Fraction.
Myocardial contractility is affected by the following factors :
· The preload (i.e., EDV): controls the power of cardiac contractility by Frank-Starling’s law.
· Sympathetic nerve supply: The resting cardiac sympathetic tone increases the
· cardiac pumping power to 13-15 litres/minute, and maximal sympathetic stimulation (e.g. in severe muscular exercise) increases it to about 25 litres/ minute.
· The afterload (i.e., aortic impedance): An increase in the afterload
· (e.g. due to rise of the arterial blood pressure, aortic stenosis or polycythaemia) reduces the cardiac pumping power, and vice versa.
· Ventricular hypertrophy; This may normally occur in some athletes as a result of prolonged strenuous exercises, and it can increase the cardiac pumping power up to about
4). Cardiac compliance:
It is the stretchability, elasticity, it is the change in volume per unit change in pressure = ∆V/∆P, decreased compliance in which there is a myocardial stiffness, this is in disease condition which will affect cardiac output as in cases of cadiomyopathies, and pericardial effusion.
5). Afterload:
It is the resistance that oppose cardiac output, e.g., increased arterial systolic pressure (systolic hypertension), valve disease that obstruct the outflow of blood as in case of aortic stenosis disease. So increased afterload will reduce cardiac output.
On the other hand, reduced total peripheral resistance (reduced afterload) causes high cardiac output. Conditions that can decrease the total peripheral resistance and at the same time increase the cardiac output to above normal include:
Low cardiac output: (Abnormalities)
· Fainting: low cardiac output leads to ischemia of the brain; causing fall down (fainting). It is a protective mechanism to correct the brain ischemia through increasing blood supply to the brain.
· Shock: also low cardiac output that may cause hypotension, again leading to ischaemia to the brain.
b). Methods for measuring cardiac output:
In animal experiments, cardiac output can be measured using any type of flowmeter (electromagnetic, or ultrasonic flowmeter) which can be placed on the aorta or pulmonary arteries i.e., blood flow in the root of aorta can be recorded by an electromagnetic flowmeter.
In the human, CO is measured by indirect methods that do not require surgery. Two methods commonly used are:
1)The oxygen fick method
2)The indicator dilution method
Another method is by 3) Echocardiography; it consists of emitting Ultrasonic waves to the heart. Such echoes record the ventricular movements, from which both the EDV and ESV and so the SV can be calculated. The CO then can be measured by multipling the SV X HR.
ESV è contractility and afterload.
EDV è cardiac compliance and preload (venous return).
5. HEART SOUNDS
Movement of heart structures in heart contraction produces heart sounds.
First heart sound occurs at beginning of systole, mainly due to closure of AV valves.
First heart sound or “lubb” – AV valves close and surrounding fluid vibrations at systole
Second heart sound occurs at the end of systole, mainly due to closure of semi lunar valves.
Second heart sound or “dupp”
Results from closure of aortic and pulmonary semilunar valves at diastole, lasts longer
Third heart sound occurs at beginning of middle third diastole is produced by oscillation of blood back and forth between walls of ventricles initiated by inrushing blood from atria.
Fourth heart sound occurs when atria contracts.
First and second heart sounds can head by ear. Abnormal heart sounds are known as heart murmurs. Functional murmurs appear because of insufficient function of heart valves.
Auscultation of heart sounds
Use stethoscope for listen to heart sounds. Listen to I heart sound in V intercostal space through medioclavicular line and
NERVE REGULATION OF HEART ACTIVITY
1. Influence of central nervous system
General characteristic of central nervous regulation of heart activity.
Central nervous system affects regulation of blood flow and pumping activity of the heart and provides very rapid control of arterial pressure.
Cerebral cortex control heart activity to correct it depending on body needs when performing behavioral reactions. Secondary somatic sensory zone takes part in analysis of afferent information from the hart. Pre-motor cortex may correct heart activity by descendant influences through hypothalamus. Anterior hypothalamus promotes parasympathetic control of heart activity. Posterior hypothalamus realizes their effects through sympathetic nervous system.
Conditioned-reflex regulation of the heart.
The fact, that different emotions cause changes in cardiac activity, indicating the importance of the cerebral cortex in the regulation of the heart . Proof of this is that changes in rhythm and force of heart contractions. It can be observed in humans at the mere mention or recollection of the factors that cause it certain emotions.
The most convincing data on the presence of cortical regulation of the heart obtained experimentally by the method of conditioned reflexes. If any such sound , combining multiple stimulus by pressing on the eyeballs , which causes a decrease in heart rate, then it is a stimulus that causes a decrease in cardiac activity – conditioned eye- heart reflex.
Conditioned reflex’ reactions underlying the phenomena that characterize the so-called pre-start condition athletes. Before the race they observed changes in respiration, metabolism, cardiac activity of the same nature , as well as during the actual race. As skaters at the start heart rate increases by 22-35 contractions per minute.
The bark of the brain provides an adaptive response not only to the current , but also to future events. On the mechanism of conditioned reflexes signals go ahead occurrence of these events or substantial likelihood of their occurrence , can cause adjustment functions of the heart and the entire cardiovascular system in so far as this is necessary to ensure that future activities of the body.
In extremely difficult situations (action “emergency stimulus ” according to Pavlov ) possible violations and failures of higher cortical regulatory mechanisms (neurosis in Pavlov). This, along with the disorder behavioral responses (and neurotic changes in psychological status of a person) may be significant disturbance of the heart and cardiovascular system. In some cases, these disorders can be fixed by the type of pathological conditioned reflexes. It cardiac abnormalities may occur under the influence of mere conventional signals.
The activity of the heart is regulated by two centers present in the medulla oblongata.
1) Cardiac Inhibitory centre, which is connected with the vagus nerve i.e. parasympathetic nervous system: C.I.C. It is a part of the dorsal nucleus of vagus, the axons of their neurons leave the medulla as preganglionic fibers. They relay in terminal ganglia present in the heart.
2) Cardiac accelerator (activation) centre, which is connected with the sympathetic nervous system: CAC. It lies near the inhibitory center, the axon of their neurons descend in the white matter of the spinal cord and synapse in lateral horn cells (L.H.C) of upper 5 thoracic segment. Preganglionic fibers arise from L.H.C and relay in the three cervical sympathetic ganglia. Postganglionic fibers pass from these ganglia to supply the whole heart.
These two centers receive impulses from the following sites:
a). Afferent impulses from the higher centers:
1). Cerebral cortex: Cerebral cortex affects HR as in the following conditions:
Conditioned reflexes; in certain conditions; seeing, hearing or smelling lead to “ in HR e.g. seeing the examiner or hearing about the exam leads to “ HR.
Voluntary; yoga players can increase or decrease their HR voluntarily.
Emotions: Most types of emotions ( fear, anger anxiety etc) leads to “ HR. Sudden unexpected news leads to ”HR or may stop the heart.
2). Hypothalamus:
– Stimulation of anterior nuclei (which control the parasympathetic activity) leads to ” HR as in quite sleep, and severe emotions ( sudden unexpected news).
– Stimulation of posterior nuclei (which control the sympathetic activity) leads to “ HR as in mild emotions and stress, and muscular exercise.
b). Afferent impulses from the circulatory system:
1). Afferent from the venous side (Rt. Side of the heart):
Bainbridge reflex: “ venous pressure caused by “ venous return (VR) in the right atrium leads to “HR. “ VR stimulates stretch receptors present in the wall of the tight atrium. These receptors send impulses along vagus nerve to the medulla causing stimulation of CAC and inhibition of CIC. CAC sends efferent impulses through sympathetic fibers to the SAN causing “ HR.
Some authors believe that the increase in HR results from stretch of the SAN leading to “ rate of discharge from it. So, it is a local effect and not a true nervous reflex.
Significance: The increased HR pumps the excess VR to the arterial side and prevents stagnation of blood in veins.
Mc Dowel’s reflex: ” VR (or ” pressure in right atrium) as in haemorrhage leads to reflex “ HR and V.C of arterioles.
Significance: During haemorrhage the increased HR and VC help to raise ABP and maintain circulation to the vital organs (brain, heart kidneys and liver).
2). Afferent impulses from arterial side (carotid sinus and aortic arch):
Mary’s law: The HR is inversely proportional to the arterial blood pressure provided that other factors affecting HR remain constant.
“ ABP ’” HR , ” ABP ’“ HR
Mechanism: “ ABP stimulates baroreceptors present in carotid sinus and Aortic arch from which afferent impulses pass through sinus nerve and aortic nerve. These impulses cause stimulation of CIC leading to ” HR. ” ABP as in haemorrhage reduce the inhibitory impulses from the baroreceptors leading to “ HR.
Significance: These reflex buffers the excessive changes in ABP. In case of “ ABP, the decreased HR helps to ” ABP to normal. In case of ” ABP (during haemorrhage) the increased HR helps to raise the ABP again to normal.
3). Afferent from the respiratory system:
Respiratory sinus arrhythmia: During inspiration, the HR “ while during expiration the HR ”. It is commonly seen in infants:
Mechanism: During inspiration the HR increases due to:
1. The respiratory center radiates impulses to the CAC causing its stimulation.
2. Lung inflation stimulates stretch receptors in the alveoli which send impulses (through the vagus nerve) that stimulate CAC leading to “ HR.
3. Bainbridge reflex, during inspiration the VR “ (due to“ negativity of the intra-pleural pressure), this leads to “ pressure in right which causes “ in HR.
During expiration the HR decreases due to decreased activity of respiratory center, elastic recoil of the lung, and ” VR.
4) Afferent from the other parts of the body:
1. From the muscles: Alam Smirk reflex: Contraction of any voluntary muscle leads to “ HR. Muscle contraction stimulates proprioceptors in the muscles and joints These receptors send impulses which stimulate CAC ’ “ HR, to supply the active muscle with excess blood.
2. From the skin and viscera: Mild or moderate pain from the skin leads to “ HR (due to stimulation of CAC). Severe pain from the skin (e.g. massive burn) or any pain from the viscera leads to ” HR (due to stimulation of CIC).
3. From The trigger zones: Pain from the trigger zones (sensitive areas) e.g. larynx, epigastrium, pericardium and tests produces sever decrease in HR and even stop the heart. These areas are richly supplied by parasympathetic fibers.
4. From they eye: Oculo-cardiac reflex: Pressure over the eyeball produces reflex ” HR.
( II ) Physical regulation:
In hyperthermia e.g. fever, the rise in body temperature by 1OC increases the HR by 10 beats / min, due to direct stimulation of SAN and stimulation of CAC by impulses coming from the heat regulating center in the hypothalamus.
In hypothermia, the HR decreases by 10 beats / min for each 1OC decrease in body temperature.
( III ) Chemical regulation:
1- ” O2 (Hypoxia): Mild or moderate hypoxia ’ “ HR due to stimulation of CAC, both directly and indirectly (through the chemoreceptors present in carotid body and aortic body). Severe hypoxia ’ ” HR, then the heart stops due to damage of the medullary centers and SAN.
2- “ CO2 and also “ H+ ( acidosis ): causes initial ” in HR due to stimulation of CIC followed by “ in HR due to direct stimulation of CAC and paralysis of CIC.
3- Blood hormones:
a. Adrenaline: Small dose of adrenaline “ HR due to direct stimulation of SAN. Large does of adrenaline ” HR because it produces VC and “ ABP (Mary’s law).
b. Noradrenaline: Small or large dose of noradrenaline ” HR because of the generalized V.C which leads to “ ABP (Mary’s law).
c. Thyroxin: “ HR due to direct stimulation of SAN. and “ sensitivity of SAN to the circulating adrenaline. Thyroxin also “ the general metabolism of the body which leads to “ Body temperature ’ “ HR.
4- Other chemicals:
a. Chemicals “ HR:
* Sympathomimetic drugs e.g. ephedrine and amphetamine.
* Parasympatholytic drugs e.g. atropine which inhibits the vagal effect on the heart.
* Histamine ’ marked capillary VD ’ ” ABP ’ “HR ( Mary’s law).
b. Chemicals ” HR:
* Parasympathomimetic drugs e.g. acetylcholine and pilocarpine.
* Bile salts cause direct inhibition of SAN and stimulation of CIC.
* Morphine stimulates CIC.
* Toxins e.g. typhoid and diphtheria toxins.
c). Efferent innervation of heart
The heart is regulated to a large extent through the central nervous system. The heart nerve branches from the vagus nerve (from the medulla oblongata) and the sympathetic nerve fibres from the spinal cord.
The vagus nerves are cardiac inhibitory nerves. When the vagus nerve is stimulated, the activity of the heart is inhibited. The inhibitory action of the vagus nerve is brought about as follows.
a) The heart rate is slowed down
b) The conductivity of the heart bundle is reduced.
c) The force of contraction is diminished.
d) The duration of systole is diminished but that of the diastole is increased.
e) Excitability of the heart is also reduced.
The sympathetic nerves are accelerator nerves. These fibres stimulate the SA node, AV node and also the muscles of the auricles and the ventricles Stimulation of the sympathetic nerves causes
a) Increase in frequency of heart rate
b) Increase in force of contraction
c) Increases excitability and irritability of the heart
d) Increases the conductivity of the cardiac muscle and bundle of His
thermal regulation.
Nerve supply to the heart:
I. Parasympathetic innervation: (vagus nerve)
Preganglionic fibers of vagus arise from the neurons of C.I.C. They reach the heart as preganglionic fibers and relay in terminal ganglia present in the substance of the atrial muscle particularly the nodal tissues. Postganglionic fibers supply SA node, A-V node and main stem of A-V bundle (but not its branches), atrial muscle, and coronary blood vessels. Vagus nerve does not supply the ventricles, branches of A-V bundle and Purkinje fibers.
a) Specialties of vagal innervations of the heart. Right n. vagus controls mainly right atrium and SA node. Left n. vagus control AV node, His bundle and all contractile myocardium. So irritation of right nerve causes bradycardia. Effects of left nerve lead to decrease of contractility and conductibility.
b) Effects of nn. vagus on the heart activity.
Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease. It is known as negative inotropic, dromotropic, bathmotropic and chronotropic effect.
Function of vagus nerve: (Parasympathetic supply to the heart)
It inhibits all cardiac properties; contractility, rhythmicity, excitability, and conductivity.
Constriction of coronary blood vessels.
Vagus escape phenomenon: Stimulation of vagus slow HR, strong stimulation of vagus stops the heart completely. If the strong stimulus is maintained, the ventricles begin to beat by its own rhythm “Idio-ventricular rhythm” (25 – 40 / min). This phenomenon is called vagus escape. It means escape of the ventricle from the inhibitory effect of vagus. It is a proof that the vagus does not supply the ventricles.
Physiological significance of absent vagal supply to the ventricles:
In case of idio-ventricular rhythm, the ventricular rhythm is (25-40 beats/min) which is inadequate to maintain sufficient circulation. If vagus supplies the ventricle, it will further ” the rate which is not desirable.
Vagus tone: During rest vagus nerve continuously discharge inhibitory impulses to the heart to ” the high rhythm of S-A node ( from 110-120 beat / min’ 70 beat/ min), this is called “Vagus tone”.
Mechanism of vagus tone:
It is a reflex mechanism in which the stimulus is the resting A.B.P. Receptors: baroreceptors or pressure receptors present in carotid sinus and Aortic arch.
Afferents: through sinus nerve which is a branch of Glossopharyngeal nerve (IX.C) and Aortic nerve which is a branch of vagus nerve (X.C). Centre : C.I.C.
Efferent: vagus nerve which ” the high rhythm of S-A node.
Proof: Cutting of both vagi in animal result in “ in HR. ( from 70 to 120). Stimulation of the cut end of vagus ’ ” in HR.
Vagus tone “ : In man more than women, in athletes more thaon athletes, and in adult more than children.
Physiological significance of vagus tone: Vagus tone ” HR from 120 – to 70 beat / min. This ” in HR will be a reserve to be used at times of need as in muscular exercise.
II. Sympathetic supply to the heart:
It begins at C.A.C in the medulla oblongata near C.I.C. The axons of their neuron descend in the white matter of the spinal cord, and relay at L.H.C of upper 5 thoracic segment. Preganglionic fibers of L.H.C pass in sympathetic chain and ascend upwards to relay in the three cervical sympathetic ganglia (superior, middle and inferior cervical sympathetic ganglia. Postganglionic fibers pass from the ganglia to the heart where they supply all the structures of the heart including the ventricles.
Function of sympathetic supply to the heart:
1- It increases all cardiac properties; contractility, rhythmicity, excitability, and conductivity.
2- Vasodilatation of coronary vessels.
c) Sympathetic effects.
Sympathetic nerves from Th1-5 control activity of the heart and large vessels. First neuron lays in lateral horns of spinal cord. Second neuron locates in sympathetic ganglions. Sympathetic nerve system gives to the heart vasoconstrictor and vasodilator fibers. Vasoconstrictor impulses are transmitted through alfa-adrenoreceptors, which are most spread in major coronary vessels. Transmission impulses through beta-adrenergic receptors lead to dilation of small coronary vessels.
Sympathetic influence produces positive inotropic, chronotropic, dromotropic, bathmotropic effects, which is increase of strength, rate of heartbeat and stimulating excitability and conductibility also.
d) Control of heart activity by vasomotor center. Lateral portion of vasomotor center transmit excitatory signals through sympathetic fibers to heart to increase its rate and contractility. Medial portion of vasomotor center transmit inhibitory signals through parasympathetic vagal fibers to heart to decrease its rate and contractility. Neurons, which give impulses to the heart, have constant level of activity even at rest, which is characterized as nervous tone.
Characteristics of reflexes from receptors of the heart
Reflex effects on the heart. There are three categories of cardiac reflexes:
1). own, caused by irritation of receptors cardio – vascular system ;
2). extracardiac due to the activity of any other reflex zones ;
3). nonspecific which played in response to nonspecific effects ( in physiological experiments , as well as pathology).
The most important physiological reflexes are own cardio-vascular system, which often occur during stimulation of mechanoreceptors arteries due to changes in system pressure. Thus, when the pressure in the aorta and carotid sinus reflex is spovыlnennya heart rate.
A special group of their own cardiac reflexes are those that occur in response to stimulation of arterial chemo – receptor changes in oxygen tension in the blood. Under hypoxia develops reflex of tachycardia , while breathing pure oxygen – bradycardia. These reactions are characterized by extremely high sensitivity : a person increase in heart rate has been observed at low oxygen tension by only 3 % wheo signs of hypoxia in the body to detect even impossible.
RESUME: Effect of sympathetic nerve stimulation is observed after a large latent period (10 seconds or more) and lasts long after the cessation of nerve stimulation .Characteristically, while stimulation of the sympathetic and vagus nerves dominant effect on the heart vagus nerves.
The mechanism of sympathetic effects due to the influence of catecholamines , resulting increasing membrane permeability to Ca2 + is required for enhanced coupling of excitation and contraction of myocardium , and increased permeability to K + .
Catecholamines decompose more slowly than acetylcholine as their interaction with adrenoceptors of the heart is accompanied by a more prolonged effect.
Pavlov I. P. (1887 ) found nerve fibers ( reinforcing nerve) that increase heart rate without significant increased rate (positive inotropic effect).
Inotropic effect of “reinforcing” nerve is clearly visible in the registration intraventricular pressure elektromanometrom . Pronounced impact of “amplifying” nerve on myocardial contractility is manifested especially in disorders of contractility . One such extreme violations contractility is alternatsiya heart rate when one ” normal” reduction myocardium (ventricle to develop pressure that exceeds the pressure in the aorta and by the release of blood from the ventricle into the aorta ) alternates with “weak” contraction of myocardium in which the pressure in the ventricle in systole is less than the pressure in the aorta and blood ejection occurs. “Reinforcing” the nerve not only enhances the usual contraction , but also eliminates alternatsiyi , restoring inefficient reduction to normal . According to Pavlov , these fibers are specially trophic , ie, stimulating metabolism .
Complex of these data allows us to represent the influence of the nervous system on heart rate as an adjustment , that is, the heart rhythm originates in his pacemaker and neural influences accelerate or slow down the rate of spontaneous depolarization of pacemaker cells , speeding up or slowing down so heart rate.
HUMERAL REGULATION OF HEART ACTIVITY
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Adrenaline |
secreted by the adrenal medulla of adrenal gland accelerates the rate of heart beat during emergency conditions. |
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Noradrenaline |
increases the heart beat during normal condition |
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Thyroxine |
also influence heart rate. |
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Sex hormones |
a) Effects of catecholamynes are transmitted by alfa- and bita-adrenoreceptors.
Adrenalin and noradrenalin stimulate heat activity and cause positive regulatory effects:
– Positive inotropic effect – increasing strength of heart contractions;
– Positive chrono-tropic effect – increasing heartbeat rate;
– Positive dromo-tropic effect – increasing heart conductibility;
– Positive bathmo-tropic effect – increasing excitability of heart muscle.
Nor-epinephrine increases permeability of cardiac fiber membrane to Na+ and Ca2+.
b) Effects of acetylcholin leads to increase of K+ permeability through cell membrane in conductive system, which leads to hyper-polarisation and cause such effects to the heart activity:
– Negative inotropic effect – decreasing strength of heart contractions;
– Negative chrono-tropic effect – decreasing heartbeat rate;
-Negative dromo-tropic effect – decreasing heart conductibility;
– Negative bathmo-tropic effect – decreasing excitability of heart muscle.
c) Effects of ions:
(Effects of Ca2+ – ions)
-Ca2+ causes spastic contraction of heart. Decreasing Ca2+ causes cardiac flaccidity.
Excessive concentration of K+ causes decreasing heart rate. Impulse’ transmission through AV bundle is blocked. If K+ level was previously decreased, increasing Concentration of K+ capable normalize cardiac rhythm. Na+ competes Ca2+ in contractile process. So increasing Na+ may depress cardiac contraction.
d) Effects of thyroid hormones.
Thyroid hormones increase transmission process in ribosome and nucleus of cells. Intracellular enzymes are stimulated due to increasing protein synthesis. Also increases glucose absorption and uptake of glucose by cells, increases glycolisis and gluconeogenesis. In blood plasma increases contents of free fatty acids. All these effects of thyroid hormones lead to increase activity of mitochondria in heart cells and ATP formation in it. So, both activity of heart muscle and conduction of impulses are stimulated.
e) Effects of adrenocortical hormones.
Aldosterone causes increasing Na+ and Cl– in blood and decreases K+. This is actually for producing action potential in the heart. Cortisol stimulates gluconeogenesis and increase blood glucose level. Amino acids blood level and free fatty acids concentration in blood increases also. Utilization of free fatty acids for energy increases. These mechanisms actual in stress reaction. So heart activity is stimulated.
f) Hormones of islets of Langerhans effects.
Insulin promotes facilitated diffusion of glucose into cells by activation glucokinase that phosphorilates glucose and traps it in the cell, promotes glucose utilization, causes active transport of amino acids into cells, promote translation of mRNA in ribosome to form new proteins. Also insulin promotes glucose utilization in cardiac muscle, because of utilization fatty acids for energy. Clucagone stimulate gluconeogenesis, mobilizes fatty acids from adipose tissue, promotes utilization free fatty acids foe energy and promotes gluconeogenesis from glycerol. So both hormones can increase strength of heartbeat.
g) Endocrine function of heart. Myocardium, especially in heart auricles capable to secretion of regulatory substances as atria Na-ureic peptide, which increases loss of Na+ in increase of systemic pressure, or digitalis-like substances, which can stimulate heart activity.
Effect on the activity of isolated frog hearts of adrenaline, acetylcholine, potassium and calcium ions
In a state of anesthesia, destroy the frog brain, fix it on a table preparuvalnomu belly side up. Riven chest, cut the pericardium.
Scheme of frog dissection thoracic cavity
Under the left aortic arch take two ligatures, under the right – one. Right hand should be tied. On the left arc from ligatures, located more nearlyto the heart, make a loop without tightening of it.
Preparation of isolated heart of frog by Straub
Between the ligatures cut the wall of the aorta and insert cannula with Ringer’s solution into the ventricular cavity during systole and fix it. Heart with cannula fix in tripod.
Alternately investigate the effect on the isolated heart of adrenaline, acetylcholine, potassium and calcium.
Eye-cardiac reflex in humans
On the subject determined by cardioscope heart rate. Then it Close your eyes first and second fingers to press on the eyeballs for 20 s. It should not have any pain. Simultaneously with the start rate for 40-60 seconds (10 seconds for each separately). If the frequency changes were observed, repeat the test, increasing the force pressing on the eyeballs.
Monitoring of respiratory arrhythmia in humans
With cardioscope determine the heart rate during deep inspiration and expiration. The examination should be repeated.
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Mathematical analysis of heart rate
Mathematical analysis of heart rate after a ten- transmitting stay lying down on the couch. To assess the balance of the autonomic nervous system used spectral analysis of heart rate , statistical analysis methods of heart rate and cardiointervalography on how R.M.Bayevskoho (1984). A survey carried out by registering ECG standard lead II at a speed of belt
Before the examination of the surface electrodes applied to the electrolytic paste.
Get the following indicators:
A) statistics :
1.
2. R-Rmax, ms – longest RR intervals in the survey ;
3. RRNN, ms – average length of RR intervals. The indicator reflects the outcome of regulatory effects on sinus rhythm sympathetic and parasympathetic nervous system;
4. SDNN, ms – standard deviation of normal RR intervals (RRNN). The deviation of the integral index indicates the predominance sympaymchnyh or parasympathetic influences on heart activity .
B ) Results of spectral analysis of heart rate .
1. TP ms2 – the total power spectrum reflects the total activity of the autonomic nervous system influence on heart rate ;
2. HF, ms2 – high-frequency oscillations of heart rate in the range of 0.15 – 0.4 Hz;
3. LF, ms2 – Low-frequency oscillations of heart rate in the range of 0.04 – 0.15 Hz;
4. VLF, ms2 – fluctuations in heart rate in the range of very low frequencies – 0.003 – 0.04 Hz;
5. LF / HF, conv. units. – Sympathetic- parasympathetic index indicates Spividnoshennya sympathetic and parasympathetic influences on heart rate ;
6. % VLF – the percentage of very low frequency oscillations in the total power spectrum;
7. % LF – low frequency fluctuations in the percentage of total power spectrum;
8. % HF- percent high frequency oscillations in the total power spectrum
C) Performance cardiointervalography on how R.M.Bayevskoho :
2. Fashion (Mo ) – a range of values (R-R) intervals, which are often encountered with;
3. SC – standard deviation duration of R-R intervals, c2 ;
4. The amplitude mode ( AMO) – number kardiointervaliv , which correspond to a range of fashion ,%;
5. Scale variation (RR ) – the difference between the maximum and the minimum duration of RR intervals, s;
6. Autonomic balance index ( CPI ) – shows the relationship between sympathetic i parasympathetic part of the autonomic nervous system is determined in arbitrary units ;
7. Capital adequacy regulation processes ( PAPR ) – Displays cpivvidnoshennya between the activity of the sympathetic part of the autonomic nervous system i level of functioning sinus node is determined in arbitrary units ;
8. Vegetation index rate (ODA) – describes the balance pivni autonomous regulation circuit is determined in arbitrary units ;
9. Stress index ( IN ) – reflects the degree of centralization of heart rate is determined in arbitrary units .
Based on the data set classes rytmohram classification EA March, A. Rubin (1997), according to which emit four classes:
In 1 class rytmohram are those which are characterized by well-defined wavelength in the range of high, low and very low frequencies. This modulating sympathetic – parasympathetic influences predominate over humoral- metabolic and cerebral ergotropic influences. The largest contribution to the regulation of cardiac rhythm carries parasympathetic nervous system ;
Up to 2 rytmohramy class are those in which heart rate variability reflects the predominance of waves in the low frequency range of the high and reinforced due to the influence of sympathetic modulation of heart rate ;
Grade 3 rytmohram heart rate variability characterized by a significant decrease in wave power in the spectrum of high and low frequency environment of increasing the power of waves in the range of very low frequencies. This option rytmohramy indicates a transition in the regulation of heart rate with autonomous level on humoral- metabolic.
Grade 4 is characterized by a stable rhythm in the absence of the wave structure.
MECHANISMS OF HEART AUTO REGULATION
a). Intracellular metabolic changes
In cardiomyocytes intracellular metabolism characterized by cycles of metabolic processes associated with cardiac activity. So the fastest decay of energy-rich compounds – ATP and glycogen – is at the time of systole and corresponds electrocardiogram QRS complex . Resynthesis and recovery of these substances is in diastole . In addition , there is increased protein synthesis, to rebuild structures damaged during systole and restoring ionic balance. Cardiomyocytes can, depending on the activity, selectively adsorb with blood and accumulate in the cytoplasm of substances that maintain and regulate their bioenergy.
Greater rate of metabolism or less blood flow causes decreasing O2 supply and other nutrients
Therefore rate of formation vasodilator substances (CO2, lactic acid, adenosine, histamine, K+ and H+) rises. When decreasing both blood flow and oxygen supply smooth muscle in precapillary sphincter dilate, and blood flow increases. Moderate increasing temperature increases contractile strength of heart. Prolonged increase of temperature exhausts metabolic system of heart and causes cardiac weakness. Anoxia increases heart rate. Moderate increase CO2 stimulates heart rate. Greater increase CO2 decreases heart rate.
Intrinsic regulation is performed in response changes of blood volume, flowing into the heart.
It is known as Frank Starling low. Within physiological limits heart pumps all blood that comes to it without allowing excessive damming of blood in veins. Cardiac contraction is directly proportional to initial length of its fibers. In end-diastolic volume over 180 ml excessive stretching heart fibers occurs and strength of next cardiac contraction decreases.
Anrep’s low. Increase of blood flow in aorta and so coronary arteries leads to excessive stretching surrounding myocardial cells.
According to Frank Starling low cardiac contraction is directly proportional to initial length of its fibers. So increase of coronary blood flow leads to stimulation heartbeat.
d) Boudichi phenomenon.
In evaluation heart beat rate increase of every next heart contraction is observed. It caused by rising of Ca2+ influx into myocardial cells without perfect outflow, because of shortening of cardio cycle duration.
b). Mechanisms of intercellular regulation of the heart
In cardiac muscle intercellular regulation is associated with the presence of intercalated discs – Nexus providing the necessary transport of substances , compounds myofibrils , transfer of excitation from cell to cell.
This arrangement allows the myocardium to respond to stimulation as syntsytiyu . Intercellular regulation also includes the interaction of cardiomyocytes from connective tissue cells that make up the stroma of the heart muscle . Along with mechanical support, connective tissue cells is the source of funds cardiomyocytes macromolecular organic compounds.
c). Role of cardiac Nexus in the regulation of heart
The basis of cell-cell interactions are kreatorni (creatura – create ) relationships. The essence of these relationships is that between cells is a continuous exchange of macromolecules , the regulatory function of the genetic apparatus of cells, the intensity of protein synthesis and cell differentiation . Kreatornyy relationship is between contractile and connective tissue cells of the myocardium. It provides normal contractile function of the myocardium.
Violation of cell-cell interactions leads to asynchronous excitation of myocardial cells and the appearance of cardiac arrhythmias.
By intercellular interactions and relationships include cardiomyocytes of connective tissue cells of the myocardium. The latter is not simply a mechanical supporting structure. They supply to the contractile cells of the myocardium number of complex macromolecular products necessary to maintain the structure and function of contractile cells. This type of cell-cell interactions known kreatornyh links ( GI Kosytskyy .
d). Reflex regulation of heart activity from heart receptors.
Location of receptors in the heart.
Heart muscle contains, both chemical and stretch receptors in coronary vessels, all heart cameras and pericardium. Stretch receptors are irritated by changing blood pressure in heart cameras and vessels. Chemo sensitive cells, which are stimulated by decrease O2, increase of CO2, H+ and biological active substances also, are called as chemoreceptors.
When atria pressure increase due to increasing blood volume, atria stretched.
Signals pass to afferent arterioles in kidneys to cause vasodilatation and glomerullar capillary pressure, thereby increasing glomerullar filtration. Signals also pass to hypothalamus to decrease antidiuretic hormone secretion and so fluid reabsorbtion. It causes decreasing both blood volume and arterial pressure to normal.
Other reflex reaction is known as atria and pulmonary artery reflex. When atria pressure increase due to increasing blood volume, atria stretched. Low-pressure receptors, similar to baroreceptors, in atria and pulmonary arteries stretched and stimulated. Signals pass to vasomotor center and inhibit vasculomotor area. Arterial pressure decreases to normal.
Reflex reactions from receptors of pericardium, endocardium and coronary vessels lead to stimulatio. vagus.
It leads to parasympathetic stimulation of the heart.
Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease. It is known as negative inotropic, dromotropic, bathmotropic and chronotropic effect.
Reflexes from extracardial receptors.
1). Baroreceptor reflexes.
Increasing arterial pressure stretched and stimulated baroreceptors in carotid sinus and aortic arc. Signals pass through glossopharyngeal and vagal nerve to tractus solitarius in medulla. Secondary signals from tractus solitarius inhibit vasoconstrictor center and excite vagal center. Peripheral vasodilatation and decrease both heart rate and contractility occur. Arterial pressure decreases to normal. When arterial pressure decreases, whole process occurs, causing.
2). Irritation of visceroreceptors results in stimulation of vagal nuclei, which cause decreasing blood pressure and heartbeat.
Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease. It is known as negative inotropic, dromotropic, bathmotropic and chronotropic effect. This mechanism is important for doctor in performing diagnostic procedures, when probes from apparatuses are attached into visceral organs. This may cause excessive irritation of visceral receptors.
3). Regulation of heart activity during physical exercises.
Motor areas of cerebral cortex are activated to cause exercise most of reticular activating system is also activated. Increase stimulation of vasoconstrictor and cardio acceleratory areas of vasomotor center leads to increasing arterial pressure. Contraction of skeletal muscles during exercises cause compression of blood vessels. It leads to translocation blood from peripheral vessels into heart. Cardiac output increases, because of rising arterial pressure.
Irritation of thrigeminal nerve, otherwise leads to excitation vagal nucleus through interneuronal connection. So, parasympathetic effects develop.
4). Atria and pulmonary artery reflex.
When arterial pressure increases due to increasing blood volume, atria stretched. Low-pressure receptors, similar to baroreceptors, in atria and pulmonary arteries stretched and stimulated. Signals pass to vasomotor center and inhibit vasculomotor area. Arterial pressure decreases to normal.
Excessive stretching of lung tissue causes excitation of n. vagus. It leads to parasympathetic stimulation of the heart. Parasympathetic stimulation causes decrease in heart rate and contractility, causing blood flow to decrease.
5). Danini-Ashner’s reflex
Measure initial pulse rate in sitting body position in the examinee. Than perform slight pressure to the one eye-boll by finger through 20 s. Continue calculation pulse rate during irritation. In conclusion explain the difference, which was revealed.
e). The cardiac system is self-regulating.
It is nearly impossible to consciously increase or decrease contraction rate due to its involuntary operation. The large number of influential factors affecting cardiac performance combine in a complex manner, thus providing the ability to adapt quickly and efficiently to the needs of the body. This is accomplished by two pathways. The intrinsic pathway represents the alterations occurring within the myocardial cells which do or do not depend on a change in the initial myocardial fiber length. The extrinsic pathway occurs primarily through neural and humoral adaptations. These discrete interrelated biological interactions indicate that regulating any certain physiological control pathway is not easy.
Key words and phrases: endocrine regulation, catecholamynes, alpha- and bita-adrenoreceptors, adrenalin, noradrenalin, inotropic effect, chrono-tropic effect, dromo-tropic effect, bathmo-tropic, excitability of heart muscle, effects of thyroid hormones, effects of adrenocortical hormones, insulin, glucagone, incretory function of heart, atria Na-ureic peptide, decreasing O2 supply, increase CO2, metabolic effects, Frank Starling effect.
Central nervous regulation of heart activity, regulation of blood flow, pumping activity of the heart, control of arterial pressure, cerebral cortex control heart activity, behavioral reactions, somatic sensory zone, premotor cortex, heart activity, hypothalamus, parasympathetic control of heart activity, sympathetic nervous system, efferent innervations of the heart, vagal innervations of the heart, inotropic, dromotropic, bathmotropic, chronotropic effect, reflexes from extracardial receptors and baroreceptor reflexes.
