1. Heart Prepared by Dr F.Nikbakht Assistant professor of Medical school

2. Cardiac muscle

3. Cardiac Muscle

5. Sinus node and the Purkinje system of the heart, showing also the A-V node, atrial internodal pathways, and ventricular bundle branches

6. Organization of the A-V node. The numbers represent the interval of time from the origin of the impulse in the sinus node. The values have been extrapolated to human beings.

7. Transmission of the cardiac impulse through the heart, showing the time of appearance (in fractions of a second after initial appearance at the sinoatrial node) in different parts of the heart.

8. Rhythmical action potentials (in millivolts) from a Purkinje fiber and from a ventricular muscle fiber, recorded by means of microelectrodes

9. Rhythmical discharge of a sinus nodal fiber. Also, the sinus nodal action potential is compared with that of a ventricular muscle fiber.

10. Force of ventricular heart muscle contraction, showing also duration of the refractory period and relative refractory period, plus the effect of premature contraction. Note that premature contractions do not cause wave summation, as occurs in skeletal muscle.

12. Regulation of Heart Rate (HR) by Autonomic Nervous System Denervated Heart Heart Rate ~100/min (Intrinsic Heart Rate) Parasympathetic Nervous System (PNS: Vagus Nerve) Could Decrease HR to Zero (Cardiac Arrest) Sympathetic Nervous System (SNS: Cardiac Nerves) Could Increase HR by 300% Normal HR (~72/min) Is dominated by PNS

13. Parasympathetic NS, Inhibits cardiac APs Sympathetic NS stimulates cardiac APs

14. Mechanism of Vagal Effects Vagal Nerve Terminals Neurotransmitter = Acetylcholine Muscarinic Receptors K ChannelsHyperpolarization Longer time to reach threshold (Slower Heart Rate)

15. Mechanism of Sympathetic Effect Sympathetic Nerve Terminals Neurotransmitter = Norepinephrine Beta-adrenergic Receptors Leak Na ChannelsFaster Rate of Spontaneous Depolarization Faster to reach threshold (Faste Heart Rate)

16. Conducting System of Heart

18. Cardiac Cycle Heart is two pumps that work together, right and left half Repetitive contraction (systole) and relaxation (diastole) of heart chambers Blood moves through circulatory system from areas of higher to lower pressure. Contraction of heart produces the pressure

19. The cardiac cycle

20. Cardiac cycle

21. Ejection Fraction Ejection Fraction = Stroke Volume/End-Diastolic Volume Ejection Fraction is a measure of cardiac contractility

22. The pressure-volume loop

24. Heart Sounds First heart sound or “lubb” Atrioventricular valves and surrounding fluid vibrations as valves close at beginning of ventricular systole Second heart sound or “dupp” Results from closure of aortic and pulmonary semilunar valves at beginning of ventricular diastole, lasts longer Third heart sound (occasional) Caused by turbulent blood flow into ventricles and detected near end of first one-third of diastole

25. SoundOrigin 1st soundClosure of mitral and tricuspid valves 2nd soundClosure of aortic and pulmonary valves 3rd soundRapid ventricular filling in early diastole 4th soundVentricular filling due to atrial contraction

26. Regulation of stroke volume & heart rate Measurement of cardiac output Regulation of heart rate neural Regulation of stroke volume Preload Afterload Neural Control of cardiac output

27. Regulation of heart rate l Sympathetic nervous system –sympathetic nerves release norepinephrine –plus circulating epinephrine from adrenal medulla –both act on ß-receptors on sinoatrial node –increases slope of the pacemaker potential –increases heart rate = tachycardia +25 0 -25 -50 -75 mV

28. Regulation of heart rate l Parasympathetic nervous system –vagus releases ACh –acts on muscarinic receptors on sinoatrial node –hyperpolarises cells and decreases slope of pacemaker potential –decreases heart rate = bradycardia +25 0 -25 -50 -75 mV

29. Regulation of stroke volume - preload Starlings Law states - the energy of contraction is proportional to the initial length of the cardiac muscle fibre Length Tension (= preload)

30. Regulation of stroke volume - preload In vivo, preload is affected by the End Diastolic Volume End Diastolic Volume Stroke Volume Increased venous return, increases EDV, and therefore increases stroke volume = self-regulation Resting EDV

31. Regulation of stroke volume - afterload Afterload is the load against which the muscle tries to contract In vivo, afterload is set by the arterial pressure against which the blood is expelled (this in turn depends on the Total Peripheral Resistance) If TPR increases, stroke volume will go down

32. Regulation of stroke volume - neural Sympathetic nervous system sympathetic nerves releasing norepinephrine plus circulating epinephrine from adrenal medulla both act on ß 1 -receptors on the myocytes increases contractility (an inotropic effect) gives stronger, but shorter contraction Parasympathetic little effect End Diastolic Volume Stroke Volume + sympathetic stimulation

33. Control of cardiac output HR increases via decrease vagal tone & increased sympathetic tone Contractility increases via increased sympathetic tone alters inotropic state & shortens systole Venous return increases via venoconstriction & skeletal/respiratory pumps maintains preload Total peripheral resistance falls due to arteriolar dilation in muscle, skin & heart reduces afterload CO increase 4-6 times HR x SV = CO