1. Physiological properties of the Physiological properties of the heart heart

2. Location of the heart in the thorax

3. Anatomical structure of the heart

4. Points of auscultation of the heart

5. Circulation scheme of the venous and arterial blood

6. Functional properties of the heart E\ C F J Excitability Automatism Conductibility Refractoriness Contractility

7. Automaticm: ability to initiate an electrical impulse Automaticm: ability to initiate an electrical impulse Conductiblity: ability to transmit an electrical impulse from one cell to another Conductiblity: ability to transmit an electrical impulse from one cell to another Excitability: ability to respond to an electrical impulse Excitability: ability to respond to an electrical impulse Refractoriness: cardiac muscle can not be exited during the whole period of systole and early part of diastole. This period prevents waves summation and tetanus Refractoriness: cardiac muscle can not be exited during the whole period of systole and early part of diastole. This period prevents waves summation and tetanus Contractility: Contractility is the ability of the cardiac muscle to contract. In this way flowing of blood is provided. Contractility: Contractility is the ability of the cardiac muscle to contract. In this way flowing of blood is provided. Functional properties of the heart

8. Electrophysiological properties of myocadial contractile cells The level of the resting potential in contractile cardiomyocytes is within -90 - 95 mV and it is stable. Resting potential of myocardial contractile cells arises due to diffusion of K-ions from the cell and entrance of Cl-ions to cardiomyocytes, but in contrast to the phase cross-lined muscles chloric permeability of their membrane is more small than potassium and plays a minor role in the formation of the resting potential of contractile cardiomyocytes.

9. Phases of action potential 0 – depolarization 1 – beginning of rapid repolarization 2 – slowly repolarization or plateau 3 – ending rapid repolarization 4 – rest period.

10. Action Potential

11. The Action Potential in Skeletal and Cardiac Muscle

12. + + + ++ - - - - -- + Membrane Phase 0 - rapid opening of Na +-channels avalanche entrance Na + into the cell, phase 1 - reduce of permeability to Na +, while increasing it for K + and Cl-, phase 2 - entrance of Ca2 + through the slow Ca2 + channels, that leads to long-term repolarization, phase 3 - the gradual closure of Ca2 + channels, while opening Ca-excitable K + channels, which leads to K + out of the cell, phase 4 - is a restoration of initial concentration of ions in the cell and outside.

13. Electrophysiological properties of atypical cells In the cells of the conduction system resting potential is absent, instead present phase of slow spontaneous diastolic depolarization, which is due to enter through the membrane of cardiomyocytes Ca2 + ions, leading to accumulation in the cell of positively charged ions. Upon reaching by membrane potential critical point of the depolarization (about -60 mV), action potential spontaneously arises and spread by conduction system, and thence to the contractile myocardium.

14. Scheme of the action potential of atypical cardiomyocytes 0 - фаза швидкої деполяризації; 1 - швидка початкова реполяризація; 2 - повільна реполяризація (плато); 3 - швидка кінцева реполяризація; 4 – фаза спонтанної діастолічної деполяризації.

15. + + + ++ - - - - - - + Membrane Phase 0 - rapid opening of Na +-channels and Na + entry into the cell; Phase 1 - reduce of permeability to Na +, with a simultaneous increase of it for K + and Cl-, phase 2 - Ca2 + enters the cell through slow Ca2 + channels Phase 3 - the gradual closure of Ca2 + channels, while opening Ca-excitable K + channels, which leads to K + out of the cell, phase 4 – phase of slow spontaneous diastolic depolarization, which is due entrance through the membrane of cardiomyocytes Ca2 + and Na +.

16. Ionic bases of transmembrane potentials The RMP is attributed mainly to the equilibrium potential of potassium. The RMP is affected more by potassium than by any other ion. Cardiac tissues may be classified as: slow fiber fast fiber

17. Scheme of the conduction system of the heart 1 – sine-atrial node ; 2 - atrial bundle of Bachmann ; 3 - interstitial conducting paths ( Bachmann’, Venkebah’, Torel’ ); 4 atrioventricular node ; 5 – Hiss bundle; 6 - right bundle of Hiss bundle; 7 - anterior branch of the left bundle of Hiss bundle; 8 - posterior branch of the left bundle Hiss bundle; 9 - bundle of Kent ; 10 - James’ bundle ; 11 - Maheym’ bundle.

18. Automatism of heart - the ability of cells of the heart conducting system to produce independently bioelectric impulses, that cause its excitement. Structures of conducting system have different degrees of automaticity. It is established the so-called gradient of automaticity. It manifests itself in a reduced ability to automatism of different structures of the conducting system according to their distance from the sine-atrial node. Thus, if the sine-atrial node number of action potentials riches the level of 60-90 imp / min, and in the cells of Hys node - 30-40 imp / min, so in the fibers of Purkin'ye – less than 20 imp / min. Gradient of automaticity caused by different spontaneous permeability cell membrane of conduction system to Ca2 +. Based on the fact, that the sine- atrial node imposes its rhythm to the departments of conduction system, that lying lower, it is called pacemaker or pacemakers of first order. Pacemaker of second order is atrio-ventricular node. Pacemaker third order – it is Hys node and its ramifications.

19. Automaticity SA-node – 60-90 /min SA-node – 60-90 /min AV – node – 40-60 /min AV – node – 40-60 /min Hiss bungle – 30-40 /min Hiss bungle – 30-40 /min Purkinje fibers - <20 /min Purkinje fibers - <20 /min

20. The assimilation of rate Under normal circumstances, the automaticity of all sections of the conduction system is suppressed by sine-atrial node, which enforces its own rhythm. That is why all parts of the conduction system begin to work at the same pace although they have their own rhythm. The phenomenon in which the structure with slow pace of generating of action potentials assimilate more frequent rhythm from other parts of the conducting system called the assimilation of rate.

21. Setting of the artificialpacemakers Setting of the artificial pacemakers

22. The spread of excitation in the atria and AV node The spread of excitation in the atria The excitement that arose in Sino- atrial node, is conductesthrouht the atria at a speed of 0,8-1,0 m / s. At first depolarization covers the right atrium, and then – left atrium. Time of coverage by excitation of both atria – 0,1 sec. The spread of excitation in the atria The excitement that arose in Sino- atrial node, is conductesthrouht the atria at a speed of 0,8-1,0 m / s. At first depolarization covers the right atrium, and then – left atrium. Time of coverage by excitation of both atria – 0,1 sec. Conduction of excitation in the atrioventricular node With the transfer of excitation from the atria to the ventricles its delay in atrio -ventricular node is observed. It is associated with features of geometrical structure of node and the specifics development electrical potential in it. This is due to the low density of Na + channels. This delay is important for sequential excitation and contraction of atria and then the ventricles. The speed of excitation spread through atrio-ventricular node is about 0,02 m / s. Conduction of excitation in the atrioventricular node With the transfer of excitation from the atria to the ventricles its delay in atrio -ventricular node is observed. It is associated with features of geometrical structure of node and the specifics development electrical potential in it. This is due to the low density of Na + channels. This delay is important for sequential excitation and contraction of atria and then the ventricles. The speed of excitation spread through atrio-ventricular node is about 0,02 m / s.

23. is 1-1,5 m / s. The process of ventricular depolarization begins at the middle third of the interventricular septum and extends to the top and side walls of the right and left ventricle. Basal parts of the ventricles and the upper third of the interventricular septum are depolyaryzate at last. The speed of the excitation throught the His-node and the Purkinje fibers is 1-1,5 m / s. The process of ventricular depolarization begins at the middle third of the interventricular septum and extends to the top and side walls of the right and left ventricle. Basal parts of the ventricles and the upper third of the interventricular septum are depolyaryzate at last. Next delay of excitation - in the place of contact of Purkinje fibers with contractile myocytes. It is the result of summation of action potentials, which contributes to the synchronization of myocardium’ excitation. The speed of excitation conduction within ventricles averages 0,3-0,9 m / s. Next delay of excitation - in the place of contact of Purkinje fibers with contractile myocytes. It is the result of summation of action potentials, which contributes to the synchronization of myocardium’ excitation. The speed of excitation conduction within ventricles averages 0,3-0,9 m / s. The spread of excitation in the ventricles

24. Conduction of excitation in the heart

26. Conduction velocity: 0.03 m/sec internodal pathway to AV node 0.09 m/sec AV node itself 0.04 m/sec penetrating AV bundle Total delay in the AV nodal and AV bundle system = 0.13 m/sec + 0.03 m/sec from SA to AV node = 0.16 m/sec

27. Cause of slow conduction in the transitional, nodal, and penetrating AV bundle fibers: 1) Their sizes are considerably smaller than 1) Their sizes are considerably smaller than the sizes of the normal atrial muscle fibers. the sizes of the normal atrial muscle fibers. 2) All these fibers have RMP that are much 2) All these fibers have RMP that are much less negative than the normal RMP of other less negative than the normal RMP of other cardiac muscle. cardiac muscle. 3) Few gap junctions connect the successive 3) Few gap junctions connect the successive muscle cells in the pathway. muscle cells in the pathway.

28. Conduction on the Heart The sino-atrial node in humans is in the shape of a crescent and is about 15 mm long and 5 mm wide. The S-A nodal cells are self-excitatory, pacemaker cells. They generate an action potential at the rate of about 70 per minute. From the sinus node, activation propagates throughout the atria, but can not propagate directly across the boundary between atria and ventricles.

29. Excitation reaches the Bundle of His Velocity of conduction =3-4 m/sec Velocity of conduction =3-4 m/sec Increased magnitude of the AP; Increased magnitude of the AP; increased velocity of phase 0 depolarization; increased velocity of phase 0 depolarization; increased duration of the AP increased duration of the AP Excitation transmitted to the RBB and LBB and fascicles then to the ventricular muscle Excitation transmitted to the RBB and LBB and fascicles then to the ventricular muscle

30. Even more distally the bundles ramify into Purkinje fibers (named after Jan Evangelista Purkinje (Czech; 1787-1869)) that diverge to the inner sides of the ventricular walls. Propagation along the conduction system takes place at a relatively high speed once it is within the ventricular region, but prior to this (through the AV node) the velocity is extremely slow.

31. Propagation from the AV node to the ventricles is provided by a specialized conduction system. Proximally, this system is composed of a common bundle, called the bundle of His (after German physician Wilhelm His, Jr., 1863-1934). More distally, it separates into two bundle branches propagating along each side of the septum, constituting the right and left bundle branches. (The left bundle subsequently divides into an anterior and posterior branch.)

32. SA NODE PACEMAKER BECAUSE 1) Highest frequency of discharge 1) Highest frequency of discharge Other cells with low frequency of discharge. Other cells with low frequency of discharge. Called latent or potential pacemakers; abnormal Called latent or potential pacemakers; abnormal or ectopic pacemakers or ectopic pacemakers Become pacemaker when: Become pacemaker when: Develop rhythmical discharge rate that is more Develop rhythmical discharge rate that is more rapid than SA node rapid than SA node Develop excessive excitability Develop excessive excitability Blockage of transmission of the impulses from the Blockage of transmission of the impulses from the SA node to other parts of the heart SA node to other parts of the heart 2) Of overdrive suppression The greater rhythmicity of the SA node forces the other automatic cells to fire off at a faster rate than their natural discharge rate. This causes depression of their rhythmicity. SA node rhythmical discharge rate = 70-80/min AV node = 40-60/min P fibers = 15-40/min

33. Normal Impulse Conduction Sino-atrial node AV node Bundle of His Bundle Branches Purkinje fibers

34. CONDUCTIVITY spread of excitation Excitation – originates from the SA node Excitation – originates from the SA node Conduction velocity in atrial muscle = 0.3 to 0.5 m/sec Conduction velocity in atrial muscle = 0.3 to 0.5 m/sec Conduction is faster in the interatrial Conduction is faster in the interatrial bundles (presence of specialized conduction fibers) bundles (presence of specialized conduction fibers) 0.03 m/sec internodal pathway to AV node 0.09 m/sec AV node itself 0.04 m/sec penetrating AV bundle Total delay in the AV nodal and AV bundle system = 0.13 m/sec + 0.03 m/sec from SA to AV node = 0.16 m/sec

35. Cause of slow conduction in the transitional, nodal, and penetrating AV bundle fibers: 1) Their sizes are considerably smaller than 1) Their sizes are considerably smaller than the sizes of the normal atrial muscle fibers. the sizes of the normal atrial muscle fibers. 2) All these fibers have RMP that are much 2) All these fibers have RMP that are much less negative than the normal RMP of other less negative than the normal RMP of other cardiac muscle. cardiac muscle. 3) Few gap junctions connect the successive 3) Few gap junctions connect the successive muscle cells in the pathway. muscle cells in the pathway.

36. Excitation reaches the Bundle of His Velocity of conduction =3-4 m/sec Velocity of conduction =3-4 m/sec Increased magnitude of the AP; Increased magnitude of the AP; increased velocity of phase 0 depolarization; increased velocity of phase 0 depolarization; increased duration of the AP increased duration of the AP Excitation transmitted to the RBB and LBB and fascicles then to the ventricular muscle Excitation transmitted to the RBB and LBB and fascicles then to the ventricular muscleNote: AP AP of endocardial cells lasts longer than that of epicardial cells, so that depolarization proceeds from endo- to epicardial surface but repolarization repolarization travels from epicardial to endocardial surface.

37. Excitability - the ability of heart to excitation (or move to a state of physiological activity). The excitability is typical for cells of the conducting system of the heart and contractile myocardium. Changes of heart’ excitability during excitation The excitability of the heart muscle during excitation changes. If you compare the action potential with excitability, it showes that during the 0, 1 and 2 phases cell completely nonexcitable or refractory. This is so- called the absolute refractory period, when the cell is not able to respond to the stimulus of any strength (is caused by inactivation of Na +- channels). During phase 3 relative refractory period take place. During this period underthreshold irritation can cause excitement. That is, in this period there is a recovery of excitability.

38. Correlation between active potential, contraction, excitability of heart cells Correlation between active potential, contraction, excitability of heart cells 0 – rapid depolarization 1 – rapid initial repolarization 2 – slow repolarization (plateau) 3 – rapid ending repolarisation 4 – absolute refractivity; 5 – relative refractivity; 6 – period of increaseexcitability; 7 - exaltation

39. A series of successive actions in myocardial cells, starting with the trigger of contraction - the action potential of the membrane with the following intracellular processes, followed by shortening of myofibrils, called the coupling of excitation and contraction. The structural basis for coupling of excitation and contraction of cardiomyocytes is T-system, that consists transverse and longitudinal T-tubules and sarcoplasmic reticulum cisterns which stored Ca2 +. Mechanism of myocardium contraction

40. Under the influence of the action potential, Ca2 + from extracellular space and from the cisterns of the sarcoplasmic reticulum entering the myoplazma, where under its influence protein troponin (which pushes back tropomyosin from actin active sites) konformes. Therefore between actin and myosin bridges are formed. Thus, splitting of ATP takes place in this period and its energy is used for sliding of actin filaments. The more calcium ions from the troponin contacted, the more actomyosine bridges formed and the greater the force of muscle contraction.

41. The relaxation of cardiomyocytes occurs as a result of repolarization of the membrane. It is based on the fact that the impact of repolarization removes Ca2 + from the contractile proteins. After that Ca2 + captures by pumps of cysternes of sarcoplasmic reticulum. Ca2 + is also displayed in the interstitial liquid due the pump work of cell membranes. The main process, that determines the relaxation of cardiomyocytes – the removal of calcium ions from the sarcoplasma, resulting in decreasisng of Ca2 + concentration in it. Thus, complexes of Ca2 + with troponin C break, tropomyosin shiftes according to actin filaments and closes their active centers – contraction is terminated. Mechanism of relaxation of the heart muscle

42. Differences Between Skeletal and Cardiac Muscle Physiology Action Potential Action Potential –Cardiac: Action potentials conducted from cell to cell. –Skeletal, action potential conducted along length of single fiber Rate of Action Potential Propagation Rate of Action Potential Propagation –Slow in cardiac muscle because of gap junctions and small diameter of fibers. –Faster in skeletal muscle due to larger diameter fibers. Calcium release Calcium release –Calcium-induced calcium release (CICR) in cardiac  Movement of extracellular Ca 2+ through plasma membrane and T tubules into sarcoplasm stimulates release of Ca 2+ from sarcoplasmic reticulum –Action potential in T-tubule stimulates Ca ++ release from sarco- plasmic reticulum

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