HUMORAL AND INTRACARDIAC MECHANISM OF HEART’ REGULATION. NEURAL MECHANISM OF HEART’ REGULATION.
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.
( I ) Nervous regulation:
The heart rate is regulated by two center present in the medulla oblongata: Cardiac.Activation.Center which is connected with the sympathetic nervous system and Cardiac.Inhibition.Center which is connected with the vagus nerve i.e. parasympathetic nervous system. The two centers receive impulses from the following sites:
(1) Afferent impulses from the higher centers:
A) 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.
(B) 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.
(2) Afferent impulses from the circulatory system:
(A) Afferent from the venous side (Rt. Side of the heart):
1. 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.
2. 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).
(B) 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.
Innervation of the heart
The activity of the heart is regulated by two centers present in the medulla oblongata.
1) Cardiac Inhibitory centre: 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 centre: 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.
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.
Function of vagus nerve: (Parasympathetic supply to the heart)
1) It inhibits all cardiac properties; contractility, rhythmicity, excitability, and conductivity.
2) 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.
Cardiac Output (COP)
During rest and exercise
Cardiac Output (COP); in the volume of blood pumped by each ventricle per minute. It equals 5-
Stroke volume (S.V); in the volume of blood pumped by each ventricle per beat. It equals the difference between end diastolic volume (EDV) and end systolic volume (ESV). COP = SV X HR.
End diastolic volume (EDV); is the volume of blood in the ventricle at the end of diastole, it is about 130 ml.
End systolic volume (ESV); in the volume of blood in the ventricle at the end of systole, it is about 60 ml.
So, SV = EDV – ESV = 130 – 60 = 70 ml
Cardiac index (C.I): in the volume of blood pumped by each ventricle per min per square meter surface area i.e. COP/ body surface area. It equals
Ejection fraction (EF): in the % ratio of the SV to the EDV.
EF = X 100, Normally it is about 65%. It is increased when the ventricular contractility and decreased when the ventricular contractility ( as in heart failure).
Factors affecting cardiac output (COP)
(I) Venous return , VR (or preload):
Under normal condition the VR and the COP are identical. When the VR (e.g. during muscular exercise) the COP. When the VR (e.g. during haemorrhage), COP to the same extent.
Factors affecting VR:
1) Pressure gradient: Pressure in the peripheral venules:
2) Respiratory movements:
A) During inspiration VR :
During normal inspiration: The intra-thoracic pressure becomes more negative (–6 mm Hg) while the intra-abdominal pressure becomes positive (due to descend of diaphragm). These two factors VR.
In forced inspiration: the intra-thoracic pressure becomes more negative (–30 mm Hg), this leads to marked in VR.
B) During expiration VR :
During normal expiration: The intra-thoracic pressure becomes less negative (–3 mm Hg), So, the VR is lesser than during inspiration.
In forced expiration: the intra-thoracic pressure becomes positive (+ 50 mmHg). This leads to stagnation of blood in the extra-thoracic veins. So, the VR markedly.
3) Muscle contraction and muscle tone:
During contraction the veins and capillaries are compressed between the muscle fibers, and so the venous blood is squeezed towards the heart leading to VR and COP. During relaxation blood does not return back because the veins contain valves which allow blood to pass only towards the heart.
Continuous contraction and relaxation of the muscle pump blood towards the heart and against gravity. So, voluntary muscles act as a “peripheral hearts”. In absence of muscle contraction, VR is helped by muscle tone.
4) Diameter of blood vessels:
a) Diameter of arterioles: If arterioles are dilated, the blood flows easily from arteries to veins increasing the VR e.g. during muscular exercise. If the arterioles are constricted the VR .
b) Diameter of capillaries: Normally about 10% only of the capillaries are opened and the other 90% are closed, this is known as capillary tone. If the capillaries are widely dilated, they will accommodate the whole blood volume. So, VR and COP are markedly decreased, ABP also leading to shock and death may occur as in sever burn.
c) Diameter of veins: Venous tone ( slight constriction ) prevents full distension of the veins with blood and, so helps to maintain VR. Loss of venous tone causes stagnation of most of the blood in the veins leading to VR and COP.
5) Arterial pulsation:
In most cases, veins run parallel to the arteries. Arterial pulsation are mechanically conducted to the veins. This helps to drive blood towards the heart owing to the presence of valves in the veins.
6) Valves of veins:
Veins of the lower limbs contain valves which are very important because they allow blood to pass only in one direction i.e towards the heart.
They divide the column of blood into segments which prevent distension of the vein by the blood. If these valves are destroyed, this leads to “varicose veins” where the veins become tortuous and filled with blood.
7) Gravity:
In the recumbent position, gravity has no effect on VR. In the erect position gravity VR from parts above the level of the heart (head and neck), and VR from parts below the level of the heart (lower limbs and abdomen).
8) Blood volume:
blood volume leads to VR and COP as during muscular exercise. The increased blood volume during exercise results from contraction of the blood reservoirs (spleen and liver). blood volume leads to VR and COP as during haemorrhage.
9) Atrial systole:
Atrial systole helps VR because it evacuates 30% of the blood into the ventricles. VR replace the evacuated blood.
10) Ventricular systole:
It forms a force from behind. It causes increase pressure in the arteries, then in capillaries and lastly in veins, thus helping VR.
(II) Arterial blood pressure (after load):
When the ABP increases suddenly, the heart is unable to pump all the blood against this high resistance. Residual blood remains in the heart is added to the next diastolic volume. The next diastolic volume , so the strength of ventricular contraction (Starling’s law) to overcome this high resistance. So, the heart adjust itself to overcome this high ABP, and so, COP remains constant.
When the elevated blood pressure is maintained, the work of the heart is increased to overcome this high resistance. This leads to ventricular hypertrophy, then heart failure where the heart is enable to pump the whole blood, so COP .
(III) Heart rate:
Changes in HR with constant VR:
1) Physiological variations of HR (50 – 100 beat / min): has no effect on COP. COP = HR x SV = 70 beats /min x 70 ml /beat = 5 liter/min.
o If HR (e.g. 100 beats / min) the diastolic periods will decrease leading to decrease SV (50 ml/beat). COP = HR x SV = 100 x 50 = 5 liter/min.
o If HR (e.g. 50 beats/min) the diastolic periods will increase leading to increase SV (100 ml/beat). COP = HR x SV = 50 x 100 = 5 liter/min.
2) Physiological (excessive) variations of HR:
o Excessive in HR (as in paroxysmal tachycardia 200/min). In this case the diastolic period is too short leading to marked in SV and in COP.
COP = HR x SV = 200 x 20 = 4000 ml/min.
o Excessive in HR (as in heart block, 25–40 beat 200/min). In this case the diastolic period becomes more prolonged and more filling occurs but up to a certain limit, after which stagnation of blood occurs outside the heart . COP = HR x SV = 30 x 120 = 3600 ml/min.
Changes in HR with change in VR (e.g. during M. exercise):
During muscular exercise both the HR and the VR (hence the SV) are increased leading to marked in COP. COP = HR x SV = 200 x 200 = 40.000 ml/min.
(IV) Strength of ventricular contraction:
SV and COP are directly proportional to the strength of the ventricular contraction. The strength of ventricular contraction is affected by:
a) Diastolic volume: Within limit, diastolic volume leads to ventricular contraction (Starling’s law).
b) Coronary blood supply: Decrease coronary blood supply leads to strength of ventricular contraction and in COP. If coronary arteries are suddenly closed (coronary thrombosis) death will occur.
Regulation Of COP:
The Cop is regulated to meet the body needs under different condition. This occurs by:
I) Intrinsic system (auto-regulation):
The heart is an automatic pump which is normally capable of pumping whatever the amount of blood that flows into the atrium ( even without HR ).
§ Iormal persons up to 15 liters / min ( i.e. 3 times COP).
§ In athletes up to 20 liters / min ( i.e. 4 times the COP).
Auto regulation controls the COP by adjusting the SV only and includes:
A) Heterometric auto-regulation: (Starling’s law)
VR end diastolic volume (EDV) of the ventricle initial length of the muscle fibers (hetero-metric) according to Starting’s law the strength of ventricular contraction SV to pump the excess VR.
SV = EDV (markedly ) – ESV (normal or slightly )
Heterometric auto-regulation is observed when a person lie down, a relatively large volume of blood shifts from the Veins of the lower limbs to the heart. The EDV and SV are increased for few heats then returns back to normal.
B) Homeo-metric auto-regulation:
If the increase in VR persists, the end diastolic volume (EDV) returns to normal within few seconds. Then the excess VR is pumped by the strong ventricular contraction which causes in the end systolic volume (ESV). So, the SV remains elevated.
SV = EDV (normal) – ESV (decreased).
The increase in the strength of ventricular contraction without change in the EDV (homeo-metric) is due to:
1. The in diastolic volume in the hetero-metric state improves the condition of the cardiac muscle ( ATP, Ca++, viscosity) which extend to the next homeo-metric state.
2. Release of myocardial catecholamine.
II) Extrinsic regulation:
The extrinsic ( Nervous and chemical) regulation controls the COP by adjusting both SV and HR.
A) Nervous regulation:
· Sympathetic stimulation COP by:
1. HR.
2. Strength of ventricular contraction. This leads to ESV and SV.
3. Rapid relaxation of the ventricles which acts as a suction force leading to ventricular filling i.e. EDV.
4. V.C which decreases the capacity of the circulatory system mean circulatory pressure (MCP) pressure gradient VR.
· Parasympathetic stimulation decreases the COP because it decreases the HR.
B) Chemical regulation:
· Chemical COP:
1. Catecholamines (adrenaline, noradrenaline and isoprenaline) and Sympathomimetic drugs (ephedrine, amphetamine); they COP because they HR and SV.
2. Thyroxin; HR (discussed before) and VR (because of the peripheral VD) SVCOP.
3. Xanthene derivatives (caffeine and theophylline) force of contraction SV COP.
4. Digitalis force of contraction SV COP.
· Chemicals COP:
5. Acetylcholine and other parasympathomimetic drugs ( methacholine, pilocarpine ) HR COP.
6. Quinidine and procainamide force of contraction SV COP.
7. O2, CO2, H+ force of contraction SV COP.
Regulation of COP
Work of the heart
during rest and exercise
The work done by the cardiac muscle is composed of two parts:
1) Pumping blood against resistance (potential work):
It represents the major part of the work of the heart. It is used to pump the blood (COP) form the ventricles to the peripheral arteries against the resistance of ABP. So, it depends on two factors; COP and ABP.
Potential work = COP x mean ABP
§ Work of the left ventricle: = 5 L x 100 mm Hg x 13.6 (density of mercury) = 6800 gm. Meter / min = 6.8 Kg. Meter / min.
§ Work of the Rt. ventricle:
oThe COP of the Rt. ventricle = COP of the left ventricle.
oThe mean pulmonary BP ( 17 mm Hg ) = 1/6 the mean arterial BP (
oSo, the work of the Rt. ventricle = 1/6 the work of the left ventricle.
§ Work of the whole heart:
= Work of left ventricle + work of Rt. ventricle.
= 6.8 + 1/6 x 6.8 = About 8 Kg. Meter / min = 480 Kg. Meter/ hour.
2) Giving velocity to the ejected blood (kinetic work):
oDuring rest the kinetic work represent about 2% of the total work of the heart ( 0.14 Kg. met / min). so, it is usually neglected.
oDuring muscular exercise it increases markedly ( up to 20% of the total work ) due to increase in the blood velocity.
Mechanical Efficiency of the heart
during rest and exercise
The energy used by the heart is partially transformed into mechanical work and the other part is liberated as heat. So, ME of the heart is the percentage ratio of the work done to the total energy expenditure.
ME of the heart equals 20 % during rest, 30% during muscular exercise, 40% in athletes during exercise and 3 % in heart failure.
ME of the heart can be increased either by:
a) Increasing the work done OR.
b) Decreasing the energy expenditure.
Since the work of the heart = COP x BP. So, the work of the heart ( and consequently the ME ) can be increased either by:
I) Loading reflex, caused by VR ( preload ):
o VR COP work of the heart ME.
oAlso, VR HR ( Bainbridge reflex ) and sympathetic stimulation O2 consumption energy expenditure.
So, the net result is a mild in ME. This means that the heart can increase its work ( to pump the excess VR ) but with much O2 consumption.
II) Unloading reflex, caused by BP ( after load ):
o ABP work of the heart M.E.
oAlso, ABP HR (Mary’s law) and vagus stimulation O2 consumption energy expenditure.
So, the net result is a marked in ME. This means that the heart can its work to overcome the high peripheral resistance (ABP) without increase in O2 consumption or energy expenditure (i.e. economically).
Cardiac reserve
The cardiac reserve is the difference between the cardiac work done during rest and that done during sever muscular exercise. The heart can its work during severe muscular exercise by about 10 times or more. The work of the heart increases during muscular exercise due to:
1. COP.
2. Arterial BP.
3. Velocity of blood flow ( the work by about 20%).
Mechanism of cardiac reserve:
The heart can perform an extra work by the following 3 mechanisms:
1) HR reserve; by acceleration:
HR from 70 beat/min 200 beat / min ( i.e. 3 times) so, the COP 3 times ( provided that the VR is adequate ) so, the work of the heart 3 times.
2) SV reserve; by dilatation ( EDV) and also by ESV:
§ SV from 70 cc /beat 200 cc / beat ( i.e.3 times ). So, the COP 3 times and also the work of the heart 3 times. SV increases due to:
§ Dilatation of the ventricle ( EDV ) which is due to VR. This leads to strength of ventricular contraction ( Starling’s law) SV.
§ Sympathetic stimulation which increases more the strength of ventricular contraction ESV SV.
COP = HR ( 3 times) x SV ( 3 times) = 9 times.
3) Hypertrophy of the cardiac muscle:
Hypertrophy is the increase in the size of the cardiac muscle which occurs very slowly as a result of prolonged strain on the heart as in:
§ Physiological hypertrophy which occurs in athletes of weight lifting and long distance runners.
§ Pathological hypertrophy which occurs in patients with hypertension, aortic stenosis or aortic regurgitation.
– Hypertrophy the strength of ventricular contraction ESV SV.
– Also, hypertrophy is accompanied by dilatation and EDV contraction (Starling’s law) SV.
Limits of the cardiac reserve:
The cardiac reserve mechanisms have certain limits, beyond which the work decreases. These limits are:
1) Excessive acceleration (above 200 beat / min), shortens the diastolic period diastolic filling SVCOP.
2) Excessive dilatation, leads to strength of the ventricular contraction because the limit of Starlings law is exceeded, so SV and COP.
3) Excessive hypertrophy causes insufficient blood supply to the hypertrophied cardiac muscle (relative ischaemia). So, the strength of the contraction leading to SV and COP.
Adaptation to methodical instruction questions:
1. Humoral regulation
a) Effects of catecholamines are transmitted by alpha- and beta-adrenal receptors.
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 acetylcholine leads to increase of K+ permeability through cell membrane in conductive system, which leads to hyper-polarization 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:
-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.
2. Mechanisms of heart auto regulation
a) 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.
b) 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.
c) 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.
3. 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.
4. Efferent innervations of the heart.
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.
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.
5. Reflex regulation of heart activity from heart receptors.
a) 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.
b) 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.
c) 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.
6. Reflexes from extracardial receptors.
a) 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.
b) 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.
c) 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.
d) 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.
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.
Multiple Choice.
Choose the correct answer/statement:
A. Ca2+
B. H+
C. Cl-
D. HCO3–
2. In examinee monitoring of heartbeat was performed. There was revealed heart rate increasing during inspiration and decreasing one during expiration. What is the cause of this phenomenon?
A. Changing of venous return
B. Changing of CO2 level in blood
C. Changing of O2 level in blood
D. Changing of intracranial pressure
E. Changing of excitement in frontal cortex
3. In experimental animal solution of ions was given in heart perfusion. At result heart becomes dilated, heart rate decreases, impulse transmission through AV-bundle was blocked, heart’s rhythm becomes abnormal. Solution of what ions was given?
A. K+
B.Ca2+
C. Mg2+
D. Na+
E. Cl–
4. In experimental animal artificial peripheral nerves, which give innervations to heart were stimulated. Increasing heart rate, force of cardiac contraction was developed. What nerves were stimulated?
A. Sympathetic nerves
B. Right vagal nerve
C. Left vagal nerve
D. Diaphragm nerve
E. Celiac plexus
5. After performing physical exercise in 34-aged man pulse rate was estimated. What possible data was obtained?
A. 56 heart beat /min
B. 60 heart beat /min
C. 75 heart beat /min
D. 80 heart beat /min
E. 120 heart beat /min
Real-life situations to be solved:
1. In patient, who recovers after shoulder fracture, during deep sleep decreasing heart beat rate was observed every time. What is the reason of bradycardia?
2. During performing bronchoscopy probe of apparatus is given into breathing pathway. When performing this procedure decreasing heart beat rate was observed suddenly. What is the reason of bradycardia?
3 In patient, who suffers from pulmonary pathology, inspiration follows by decrease of heart beat rate. What reflex mechanism may cause it?
4. Monitoring of heart activity reveals increasing rate of heartbeat in every inspiration.
What reflex mechanism may cause it?
