Types of Heart Activity (Autoregulation of heart)

Homometric and Heteromeric regulation of heart

1. SEMEY MEDICAL UNIVERSITY TOIPC- Types of Heart Activity Self-Regulation SUBMITTED BY – Hitesh Kumar Godra GROUP No - 249 SUBMITTED TO – Tokesheva Gulmira Manarbekovna SMU 2018 SWS

2. PLAN Introduction-Regulation of heart activity Heterometric Autoregulation Frank–Starling law Homeometric Autoregulation Bowditch effect Anrep effect Conclusion

3. REGULATION OF THE CARDIAC ACTIVITY

4. Regulation of the Heart Intrinsic regulation : Results from normal functional characteristics, not on neural or hormonal regulation Frank-Starling’s law of the heart Bowditch´s stairs Anrep effect Extrinsic regulation : Involves neural and hormonal control Parasympathetic stimulation Supplied by vagus nerve, decreases heart rate, acetylcholine secreted Sympathetic stimulation Supplied by cardiac nerves, increases heart rate and force of contraction, epinephrine and norepinephrine released

5. Autoregulation Autoregulation  is a process within many biological systems, resulting from an internal adaptive mechanism that works to adjust (or mitigate) that system's response to stimuli. While most systems of the body show some degree of autoregulation , it is most clearly observed in the  kidney , the  heart , and the  brain .  Perfusion  of these organs is essential for life, and through autoregulation the body can divert blood (and thus,  oxygen ) where it is most needed.

6. CARDIAC OUTPUT = STROKE VOLUME x HEART RATE Autoregulation (Frank-Starling “Law of the Heart”) Contractility Sympathetic Nervous System Parasympathetic Nervous System

7. Intracardiac regulation - AUTOREGULATION Heterometric autoregulation – FRANK-STARLING LAW:„the energy of contraction is proportional to the initial length of the cardiac muscle fiber – to the end diastolic volume“ Relation between muscle fiber length and tension. Diastolic filling = end diastolic volume As the diastolic filling increases, the forces of contraction of the ventricles is increased. Principle of this law is in ultrastructure of the cardiac muscle.

8. The Frank–Starling law of the heart (also known as Starling's law and the Frank–Starling mechanism) represents the relationship between stroke volume and end diastolic volume.The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length,without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.

9. CARDIAC FUNCTION CURVE STROKE VOLUME DIASTOLIC FILLING Cardiac Output = Stroke Volume x Heart Rate Constant If: Then:  CO reflects SV Right Atrial Pressure (RAP) reflects Diastolic Filling

10. CARDIAC FUNCTION CURVE

11. Cardiac function curve  In diagrams illustrating the  Frank–Starling law of the heart , the y-axis often describes the  stroke volume ,  stroke work , or  cardiac output . The x-axis often describes  end-diastolic volume ,  right atrial pressure , or  pulmonary capillary wedge pressure . The three curves illustrate that shifts along the same line indicate a change in  preload , while shifts from one line to another indicate a change in  afterload  or  contractility . A blood volume increase would cause a shift along the line to the right, which increases left ventricular end diastolic volume (x axis), and therefore also increases stroke volume (y axis)

12. CARDIAC FUNCTION CURVE CARDIAC OUTPUT (L/min) RAP mmHg 15- 10- 5- -4 +4 +8 THE FRANK- STARLING “LAW OF THE HEART” Increased Contractility

13. Physiological roles of the FS law: 1/ maintaining the equal COs of RV and LV 2/ compensation of the law of Laplace „pressure evoked by wall of a cavity is reciprocal to its diameter“ or: the distending pressure in a distensible hollow object is equal to the tension in the wall (T) divided by the radius 3/ regulation of the COs during venous return changes

14. Homeometric regulation – „Bowditch´s stairs“ Homeometric autoregulation , in the context of the  circulatory system , is the heart's ability to increase  contractility  and restore  stroke volume  when  afterload  increases.  Homeometric autoregulation occurs  independently of cardiomyocyte fiber length,  via the Bowditch and Anrep effects.

15. Bowditch effect The  Bowditch effect  is an autoregulation method by which myocardial tension increases with an increase in heart rate. Also known as the Treppe phenomenon, Treppe effect or staircase effect. It was first observed by  Henry Pickering Bowditch  in 1871.

16. One of the explanations is the inability of the  Na + /K + - ATPase  to keep up with influx of sodium at higher heart rates. When a higher heart rate occurs, for example due to adrenergic stimulation, the L Type Calcium channel has increased activity. The 3Na + /Ca ++  exchanger (which allows 3 Na +  to flow down its gradient in exchange for 1 Ca ++  ion to flow out of the cell) works to decrease the levels of intracellular calcium. As the heart rate becomes more robust and the length of diastole decreases, the Na + /K + - ATPase , which removes the Na +  brought into the cell by the Na + /Ca ++  exchanger, does not keep up with the rate of Na +  influx. This leads to a less efficient Na + /Ca ++  exchange since the gradient is decreasing for sodium and the driving force behind calcium transport is actually the concentration gradient of sodium, therefore Ca ++  builds up within the cell. This results in an accumulation of calcium in the myocardial cell via the  sodium calcium exchanger  and leads to a greater state of inotropism , a mechanism which is also seen with cardiac glycosides.

17. Anrep effect The Anrep effect is an autoregulation method in which myocardial contractility increases with afterload . It was experimentally determined that increasing afterload caused a proportional linear increase in ventricular inotropy . The Anrep effect is named after Russian physiologist Gleb von Anrep , who described it in 1912.

18. Anrep effect This effect is found in denervated heart preparations, such as the Starling Preparation, and as such, represents an intrinsic autoregulation mechanism Functionally, the Anrep effect allows the heart to compensate for an increased end-systolic volume present and the decreased stroke volume that occurs when aortic blood pressure increases. Without the Anrep effect, an increase in aortic blood pressure would create a decrease in stroke volume that would compromise circulation to peripheral and visceral tissues.

19. Anrep effect Sustained myocardial stretch activates tension dependent Na+/H+ exchangers, bringing Na+ ions into the sarcolemma . This increase in Na+ in the sarcolemma reduces the Na+ gradient exploited by sodium-calcium exchanger (NCX) and stops them from working effectively. Ca2+ ions accumulate inside the sarcolemma as a result and are uptaken by sarco /endoplasmic reticulum Ca2+- ATPase (SERCA) pumps. Calcium induced calcium release (CICR) from the sarcoplasmic reticulum is increased upon stimulation of the cardiac myocyte by an action potential. This leads to an increase in the force of contraction of the cardiac muscle to try and increase stroke volume and cardiac output to maintain tissue perfusion.

20. On the other hand, it is presumed that the Anrep effect may be a spurious effect resulting from the recovery of the myocardium from a transient ischemia arising from the abrupt increase in blood pressure. Physiological role : better emptying of the ventricles during tachycardia Optimal and critical frequency.

21. Conclusion control of certain phenomena by factors inherent in a situation; specifically, (1) maintenance by an organ or tissue of  aconstant  blood flow despite changes in arterial pressure, and (2) adjustment of blood flow through an organ in  accorda-ncewith  its metabolic needs. heterometric   autoregulation  those intrinsic mechanisms controlling the strength of ventricular contractions that  depe-ndon  the length of myocardial fibers at the end of diastole.

22. Conclusion homeometric   autoregulation  those intrinsic mechanisms controlling the strength of ventricular contractions that  areindependent  of the length of myocardial fibers at the end of diastole.

23. REFERENCE Books: K Sembulingam Essentials of Medical Physiology Six Edition Websites: https://en.wikipedia.org/wiki/regulationofheartrate/.com Slideshare – regulation of heart