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Functi on of Heart as a Pump Lecture 41 Dr. Khaled Ibrahim.

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Presentation on theme: "Functi on of Heart as a Pump Lecture 41 Dr. Khaled Ibrahim."— Presentation transcript:

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2 Functi on of Heart as a Pump Lecture 41 Dr. Khaled Ibrahim

3 By the end of this session, the student should be able to: 1)Illustrate and discuss the action potential of contractile cardiac fibers. 2)Describe the excitability changes during cardiac action potential. 3)Describe excitation-contraction coupling of the cardiac muscle. 4)Describe the intrinsic regulation of the cardiac pumping. 5)Describe the effect of various extrinsic factors on cardiac pumping (nervous, physical and chemical). By the end of this session, the student should be able to: 1)Illustrate and discuss the action potential of contractile cardiac fibers. 2)Describe the excitability changes during cardiac action potential. 3)Describe excitation-contraction coupling of the cardiac muscle. 4)Describe the intrinsic regulation of the cardiac pumping. 5)Describe the effect of various extrinsic factors on cardiac pumping (nervous, physical and chemical).  Guyton & Hall Textbook of Physiology - 12 th ed. P. 103-104 & 110-112.

4 CONTRACTILITY Definition:  It is the ability of the cardiac muscle to convert the stored chemical energy of fuel (ATP) into mechanical energy or work.  In case of cardiac muscle, contractility is manifested by: pumping & circulation of blood (cardiac contraction gives the blood its velocity).

5 Ionic basis of action potential of cardiac muscle (contractile muscle fibers):

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9 Q? Why does the action potential of cardiac muscle have a plateau, while that of skeletal muscle does not? 1- A moderate quantity of Ca 2+ diffuses to the inside of cardiac muscle fiber during the action potential and for a prolonged time. The plateau occurs during this prolonged influx of Ca 2+. But very little amount of Ca 2+ diffuses in skeletal muscle 2- Immediately after the onset of action potential, the permeability of cardiac muscle for K + decreases 5 folds. It is believed that this is due to excess Ca 2+ influx. The  permeability to K + ----->  K + efflux which prevents rapid repolarization -----> plateau. This effect that does not occur in skeletal muscle

10 Relation between the mechanical response (contraction) and Electrical response (action potential)  Contraction (systole) starts just after depolarization and reaches its maximum by the end of the plateau.  Relaxation (diastole) starts with the rapid phase of repolarization.  Repolarization is complete by the end of the first half of diastole

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12 Excitability changes during the action potential Following the application of a threshold stimulus, excitability passes by the following phases 1- Absolute refractory period (ARP)  During this period, the excitability of the cardiac muscle is completely lost.  No other stimulus, whatever its strength can excite the cardiac muscle.  It coincides (corresponds) with: the phase of rapid depolarization and the repolarization till the end of plateau (= during systole of cardiac muscle).  Significance: Due to this long ARP, tetanus cannot be produced in cardiac muscle. Tetanization of cardiac muscle is fatal because the heart as a pump must contract and relax to fill with blood.

13 N.B.: ARP in skeletal muscle is very short and equals only the latent period, so tetanus can occur to increase the tension of the muscle to move or carry objects

14 2- Relative refractory period (RRP)  During this period, the excitability gradually recovers until it reaches the normal value.  A stronger stimulus applied during the RRP would produce a weaker systole.  This period coincides with the rapid repolarization (= the first half of diastole).  Significance: This is the phase where extrasystole occurs

15 3- Supernormal phase (SNP)  During this phase, the excitability rises above the normal.  A weaker stimulus is needed to excite the cardiac muscle, and a stronger contraction is produced.  It coincides with the second half of diastole. (= after the end of action potential).  Significance: Physiologically: Stimuli adjusted to occur during the SNP of the preceding cycles, would produce systoles of increasing strength. This is called the “staircase phenomenon” or “treppe phenomenon”.

16  Excitation-contraction coupling in the myocardial muscle fibers:  It is the mechanism by which the action potential causes the myofibrils of the muscle to contract. Mechanism:

17  Rules controlling contractility : 1-All or non rule: * When a cardiac muscle unit is stimulated by an adequate stimulus (minimal or threshold), it responds maximally giving maximal contraction But when it is stimulated by an inadequate stimulus, it does not respond at all. * This is due to its syncytial nature. The two atria form a syncytium while the two ventricles form another syncytium. Impulses travel from the atrial to the ventricular syncytium only through the AV bundle. = intrinsic regulation of the cardiac pumping

18 2- Staircase phenomenon or Treppe phenomenon: * If the cardiac muscle is stimulated by successive maximal stimuli, the 1 st few contractions show gradual  in magnitude which is represented graphically as a staircase. After that, the strength of contraction becomes stable at its normal level. * Mechanism: 1)The first stimulus produces thermal (warming of the muscle), chemical (  activity of the muscle enzymes) & ionic changes (  Ca 2+ inside the muscle) which improve the physiological state of the cardiac muscle (i.e., better physiological conditions). 2)The second stimulus fall in the supernormal phase of excitability.

19 Question: Does the staircase phenomenon contradicts the All or none rule? No. Because For the all or none rule to be applied, all physiological conditions should remain constant. Question: Does the staircase phenomenon contradicts the All or none rule? No. Because For the all or none rule to be applied, all physiological conditions should remain constant.

20 3- Starling's low of the heart:  It was studied by Starling in the isolated denervated heart.  It states that: WITHIN CERTAIN LIMIT, THE GREATER THE INITIAL LENGTH OF THE CARDIAC MUSCLE FIBER, THE GREATER THE FORCE OF MYOCARDIAL CONTRACTION.  The initial length of cardiac muscle fiber is determined by the degree of diastolic filling i.e. End Diastolic Volume (EDV) (It is the volume of the blood in the ventricles at the end of diastole).  According to starling's law: excess venous return (amount of blood returning to the atria from the peripheral veins) e.g. during muscular exercise --->  the initial length of muscle fibers (EDV) ---->  the force of ventricular contraction.

21  Significance: This prevents stagnation of blood in venous side. WHILE, Overstretching of the muscle fibers, e.g., heart failure causes marked  contractility.  Normally, the pericardium allows optimal increase in diastolic volume and prevents overstretching.  Mechanism of Starling's law: It is myogenic in nature through  the overlappement between thin & thick filaments.

22 Inotropism Definition: an effect on myocardial contractility. A +ve Inotropic effect is that which  myocardial contractility. A -ve Inotropic effect is that which  myocardial contracility. A +ve Inotropic effect is that which  myocardial contractility. A -ve Inotropic effect is that which  myocardial contracility.

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