Physiological properties of the heart

1. Physiological properties of theheart

2. Location of the heart in the thorax Circulation scheme of the venous and arterial blood

3. Anatomical structure of the heart Points of auscultation of the heart

4. Functional properties of the heart • Automaticm: ability to initiate an electrical impulse • Conductiblity: ability to transmit an electrical impulse from one cell to another • 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 • Contractility: Contractility is the ability of the cardiac muscle to contract. In this way flowing of blood is provided.

5. Electrophysiological properties of myocadial contractile cells The level of the resting potential in contractile cardiomyocytes is within -90 - 95 mV and it is stable. Restingpotential 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 potassiumand plays a minor role in the formation of the resting potential of contractile cardiomyocytes.

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

7. Action Potential

8. The Action Potential in Skeletal and Cardiac Muscle

9. Ionic bases oftransmembrane potentials • The RMP is attributed mainly to theequilibrium potential of potassium. The RMPis affected more by potassium than by anyother ion. • Cardiac tissues maybe classified as: • slow fiber • fast fiber

10. 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 - Hys node;6 - right bundle of Hys node;7 - anterior branch of the left bundle of Hys node;8 - posterior branch of the left bundle Hys node;9 - bundle of Kent ;10 - James’ bundle ;11 - Maheym’ bundle.

11. 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.

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

13. 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.

14. Setting of the artificialpacemakers

15. Thespreadofexcitationintheatriaand AV node • The spread of excitation in the atriaThe 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 nodeWith 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.

16. Thespreadofexcitationintheventricles • 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 Purkinjefibers 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.

17. Conduction of excitation in the heart

18. 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 andventricles.

19. 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.

20. 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.)

21. SA NODE PACEMAKER BECAUSE 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 • 1) Highest frequency of discharge • Other cells with low frequency of discharge. • Called latent or potential pacemakers; abnormal • or ectopic pacemakers • Become pacemaker when: • Develop rhythmical discharge rate that is more • rapid than SA node • Develop excessive excitability • Blockage of transmission of the impulses from the • SA node to other parts of the heart

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

23. CONDUCTIVITYspread of excitation • Excitation – originates from the SA node • Conduction velocity in atrial muscle = 0.3 to 0.5 m/sec • Conduction is faster in the interatrial • 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

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

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

26. 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 excitationThe 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.

27. 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

28. Mechanism of myocardium contraction 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 +.

29. Mechanism of myocardium contraction 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.

30. Mechanism of relaxation of the heart muscle 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.

31. Differences Between Skeletal and Cardiac Muscle Physiology Action Potential Cardiac: Action potentials conducted from cell to cell. Skeletal, action potential conducted along length of single fiber 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-induced calcium release (CICR) in cardiac Movement of extracellular Ca2+ through plasma membrane and T tubules into sarcoplasm stimulates release of Ca2+ from sarcoplasmic reticulum Action potential in T-tubule stimulates Ca++ release from sarco-plasmic reticulum

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