1. Electrical and mechanical properties of the heart [Part 1]

2. Learning Outcomes…
At the end of the lecture, students should be able to:
Relate properties of cardiac muscle with cardiac impulse and its conduction.
Explain why cardiac muscle cannot be tetanized.
Define pacemaker potential and describe mechanism of generation of cardiac impulse.
List the components of conduction system of heart and describe the pathway of conduction of impulse from Sinoatrial node to ventricular muscle.
Describe the physiologic mechanism and significance of the AV nodal delay.
List the phases of action potential of ventricular muscle fiber and relate the changes in membrane permeabilities for ions during these phases.

3. Learning Outcomes…
Explain the ectopic focus and its clinical significance. Explain the variations in shape and conduction velocities of action potential in different parts of the conduction system.
Explain the terms inotropic, chronotropic and dromotropic and bathmotropic.
Describe effects of sympathetic and parasympathetic stimulation on rate and conduction velocity of cardiac impulse.
Explain the term sinus arrhythmia and describe how is it produce and its clinical significance.

4. Properties of Cardiac Muscle
What are the actions of heart can you identify from this picture
Impulse generation
Impulse conduction
Contraction
Above actions are Regular?

5. Properties of the cardiac muscle
Four basic properties, essential for functioning of heart as the effective pump of the CVS. These are:
1. Excitability
2. Autorhythmicity
  3. Conductivity  
4. Contractility

6. Excitability self-excitable fibers
Ability to respond to a threshold stimulus by developing an action potential followed by contraction.
Origin of impulse by SA node, AV Node, ventricular muscle and purkinje fibers reveals the excitability of cardiac muscle.

7. Absolute refractory period
the excitability level is 0%.
No response of the heart muscle irrespective of any strength of stimulus
begins with depolarization till mid-repolarization
lasts for the whole period of systole and the early part of diastole. MV
ARP
-90 7

8. Relative refractory period
excitability level is more than 0 but less than 100% of the resting basal level.
Heart responds only to stronger stimuli.
short period that begins at mid-repolarization and ends shortly before complete repolarization.
lasts for a short period during diastole. MV
-90
RRP 8

9. Significance of the long refractory period
It lasts for the whole period of systole and the early part of diastole.
This means that the ventricle would not respond to any stimulus until it finishes with its systole and have some diastole.
So the long absolute refractory period protects the ventricle against tetnization if it receives multiple successive stimuli. 9

10. Autorhythmicity
Ability of the cell to generate impulse spontaneously at regular intervals i.e in a rhythmic manner
Attributed to unstable or less negative resting membrane potential of pace maker cells of the heart.
The site having highest frequency of impulse drives the whole heart and is called the pacemaker of the heart

11. Conductivity
Ability to conduct cardiac impulses from pace maker to entire heart ~ through specialized conducting system or cardiac muscle fibers itself.
Due to presence of intercalated discs contain
desmosomes to hold the cardiac cells together and
gap junctions which allow ions to pass freely from cell to cell during excitation
Specialized muscle fibers also constitute conducting system of the heart e.g. Internodal pathway, A-V node, bundles of His & purkinje fibers.

12. Contractility
Ability to convert chemical energy into mechanical energy.
Systole and diastole of the heart represents contraction and relaxation respectively.
Contraction is preceded by excitation process.

13. The pacemaker potential and mechanism of generation of cardiac impulse

14. Electrical Activity of Heart
Heart beats rhythmically as result of action potentials it generates by itself (autorhythmicity)
Two specialized types of cardiac muscle cells
Contractile cells~ ventricular muscle
99% of cardiac muscle cells
Do mechanical work of pumping
Normally do not initiate own action potentials
Autorhythmic cells~ SA Node, AV Node , Purkinje Fibers
Do not contract
Specialized for initiating and conducting action potentials responsible for contraction of working cells

15. The pacemaker potential
The pacemaker cells are characterized by having an unstable membrane potential.

16. Na+ K+ AUTOMATICITY Gradually increasing PNa -0 -60 mV THRESHOLD
RESTING

17. The pacemaker potential
Have unstable resting potentials called pacemaker potentials
Slowly depolarizes to from a basal value of ~ -60mV to a critical firing level of –45 mV (threshold for action potential).
an action potential is fired and the cycle is repeated.
membrane continues to repolarizes to below -60 mV causes hyperpolarisation.
Due natural leakiness for positive ions, membrane again reaches to basal level of -55 to -60 mv.
Same cycle is repeated again.

18. Frequency of Impulse discharge in Auto rhythmic cells

19. Conducting Tissues of the Heart
APs spread through myocardial cells through gap junctions.
Impulses cannot spread to ventricles directly because of fibrous tissue.
Conduction pathway:
SA node.
AV node.
Bundle of His.
Purkinje fibers.

20. Locations of noncontractile cells capable of autorhythmicity
Sinoatrial Node (SA node)
Specialized region in right atrial wall near opening of superior vena cava
It is 15mm long, 3mm wide, 1mm thick.
Pacemaker of the heart
It is supplied by right vagus.

21. Conducting Tissues of the Heart
INTERNODAL FIBERS
Internodal Fibers – Anterior, Middle and Posterior [Bachman, Wenchkeback, Thorel].
Atrioventricular Node (AV node)
Small bundle of specialized cardiac cells located at base of right atrium at posterior part of inter atrial septum.
It is supplied by left vagus.

22. Conducting Tissues of the Heart
Bundle of His (atrioventricular bundle)
tract of specialized cardiac cells that originate at AV Node and passes through the fibrous ring and enters interventricular septum
Divides to form right and left bundle branches which travel down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls
Purkinje fibers
Small, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium

23. Spread to Atria
Cardiac impulse originates at SA node and spread to the atria [via gap junction] – Atrial Syncytium, therefore, both atria depolarize same time.
Impulse [AP] goes simultaneously to AV-Node by Internodal pathway.
AV-Node is the only point of electrical contact between atria and ventricle [as atria and ventricle are separated by fibrous ring which is non-conductive].

24. Spread to A-V Node AV – Node
impulse after leaving SA node takes 0.03 sec to reach the AV node.
delay of 0.1 sec at AV-Node

25. Spread to AV Bundle & Ventricles
After AV delay of 0.1sec, impulse [AP] travels quickly via Right Bundle Branch and Left Bundle Branch [branches of Bundle of His] to Purkinje Fibers to the ventricles.
Both ventricle depolarize, than contract at same time.
Conduction in Purkinje Fiber is fastest
2-4 meter/sec, therefore, both ventricle depolarize quickly and at the same time.

26. one-way conduction in A-V bundle
The A-V bundle conducts impulses only in one direction, i.e. from the A-V node to the bundle branches.
prevents the reentry of impulses from the ventricles into the atria.

27. Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

28. Conduction speed in cardiac tissue
Slowest Conduction at
AV – Node
Fastest Conduction –
Purkinje Fibers 28

29. Physiologic mechanism and significance of the AV nodal delay

30. Mechanism of the AV nodal delay
Slow conduction at AV-Node?
Because there are less gap junctions.
Diameter of the fiber is small.

31. Significance of AV nodal delay
Allows atria to empty their blood into the ventricles before ventricular contraction begins.
Increases the efficiency of the pumping action of the heart

32. Phases of action potential of ventricular muscle fiber and Altered membrane permeabilities for ions during these phases. 32

33. ACTION POTENTIALS FROM DIFFERENT AREAS OF THE HEART
ATRIUM
VENTRICLE mv
-90mv mv
-90mv mv
-60mv
SA NODE
time 33

34. Phases of Action Potential
Action potential in heart varies in different parts and broadly grouped in to two;
Slow response action potential is produced by fibers of SA node, AV node, Av bundle and injured myocardium and demonstrate only three phase
Fast response action potential is generated by atrial muscle, ventricle muscle and purkinje fiber and shows 5 phases.

35. MEMBRANE POTENTIAL (mV)
PHASE
0 = Rapid Depolarization
(inward Na+ current) 1 1
Early partial repolarization 2
2 = Plateau
(inward Ca++ current)
3 = Repolarization
(outward K+ current)
MEMBRANE POTENTIAL (mV)
4 = Resting Potential 3 4
-90
TIME 35

36. Phase 0 (Rapid depolarization): It is caused by the rapid influx of Na+ into the cell.
Phase 1 (Early partial repolarization): During this phase, the permeability of the membrane to Na+ is rapidly reduced, but the membrane permeability for both Ca2+ and K+ increases. The overall effect is a small change in the membrane potential toward the resting membrane potential (repolarization).
Phase 2 (Plateau of the action potential): This coincides with an increased permeability for Ca2+. The inward movement of Ca2+ and the decreased efflux of K+ maintain the membrane potential near zero during this phase of the action potential.
Phase 3 (Rapid repolarization): due to a reduction of the inward Na+ and Ca2+ currents and a large increase in the outward K+ current.
Phase 4 (Complete repolarization): the membrane goes back to the resting level (- 90 mV). Na+-K+ pump works to drive the excess Na+ out and the excess K+ in. 36

37. MEMBRANE POTENTIAL (mV)
ACTION POTENTIALS
VENTRICULULAR
CELL
SAN 1 2 3 3 4
-50
-50
MEMBRANE POTENTIAL (mV) 4 4 4
-100
-100 37

38. Slow response Action potential
Phase 0; depolarization phase of the action potential due to opening of slow ca++-Na+ channels allow influx of positive ions
Phase 3: repolarization phase of the action potential due to inactivation of slow Ca++ Na+ channels which remains open for short period and simultaneously opening of K+ channels increasing the outward flow of K+ ions & bring the membrane potential to resting level.
Phase 4; unstable, slowly spontaneous depolarizing phase, due to influx of Na+ ions through the channel which remain open at rest, continue to depolarize membrane till it reaches to threshold level of -45 mV. Slow decline in membrane permeability for K+ ions also contribute to depolarizing potential during this phase.

39. Fast Vs Slow response Action potential
The slow response action potential differs from the action potential of the contractile myocardial cells in the following:
     
Depolarization phase is mainly due to Ca2+ influx through long-lasting (L-type) Ca2+-channels.
Depolarization phase is relatively slow to develop.   
There is no plateau phase.
Repolarization immediately follows depolarization.

40. Ectopic foci
An ectopic focus is an area in the contractile myocardium, which discharges electrical impulses.
Normally, the contractile myocardium has a stable resting membrane potential and is incapable of discharging impulses.
Under some non-physiological conditions, some myocardial cells acquire rhythmic electrical activity and act as foci that send un-timed electrical impulses or might even take over the heart and act as the pacemaker.

41. Do you see any difference between two heart
Heart A has only one pace maker generating impulse B A
Heart A is beating normally
Heart B is not beating normally
Heart B has multiple pace makers generating impulses hence incordinated action of heart

42. Clinical Significance
serve as a protective function by initiating a cardiac impulse before prolonged cardiac standstill can occur; these beats are called escape beats
the ectopic site will assume the role of pacemaker and sustain a cardiac rhythm; this is referred to as an escape rhythm
after the sinus node resumes normal function, the escape focus is suppressed

43. Variations in shape and conduction velocities of action potential in different parts of the conduction system.

45. Sympathetic nerve supply
There is a resting sympathetic tone that tends to increase the heart rate up to 120 beats/min.
This tone is weak and is masked by the strong inhibitory vagal tone that decreases the heart rate down to 75 beats/min during rest.
However, stimulation of the sympathetic cardiac nerves has a +ve chronotropic effect. The heart rate may go up to 200 beats/min.
The sympathetic chemical transmitter noradrenaline decreases the permeability of the pacemaker membrane to K+. This accelerates the depolarization of the membrane → shortens the duration of the pacemaker potential → increases the frequency of discharge of impulses from the S-A node → increases the heart rate.

46. Parasympathetic nerve supply
There is a resting inhibitory vagal tone that keeps the heart rate at its resting level of ~ 75 beats/min.
During deep quite sleep, the vagal tone increase and the heart rate decreases down to 60 beats/min.
Vagal stimulation has a –ve chronotropic effect.
The parasympathetic chemical transmitter acetyl choline increases the permeability of the pacemaker membrane to K+. This slows down the depolarization of the membrane → prolongss the duration of the pacemaker potential → deccreases the frequency of discharge of impulses from the S-A node → decreases the heart rate.

47. Cutting or blocking the vagal nerve supply to the heart (e. g
Cutting or blocking the vagal nerve supply to the heart (e.g., by atropine) leads to an increase in the heart rate up to ~ 120 beats/minute. This is the sinus rhythm boosted by the resting sympathetic tone.
If this is followed by cutting or blocking the sympathetic nerve supply to the heart (e.g., by atenolol), the heart rate decreases down to 105 beats/minute; the natural inherent sinus rhythm.
Cutting or blocking the sympathetic nerve supply to the heart with an intact vagal parasympathetic supply produces no significant change in heart rate, i.e. it remains at its resting level of ~ 75 beats/minute.

48. Physical factors
Arise in body temperature by 1 °C increases the heat rate by 20 beats/minute.
The rise in body temperature increase the heart rate by increasing the permeability of he membrane to Ca++ during the pacemaker potential and increasing the speed of ionic fluxes across the membrane during the action potential.
The only physiological condition that rises body temperature above the normal resting range is muscular exercise.

49. Self Study; Think and answer
During fever, heart rate is normally increased. At rest, which component of autonomic nervous system influences the heart more?

50. Area affected
Effect of parasympathetic stimulation
Effect of sympathetic stimulation
SA node
Decrease rate of depolarization , heart rate
Increase rate of depolarization, increase heart rate
AV node
Decrease excitability, increase AV nodal delay
Increase excitability ,decrease AV nodal delay
Ventricular conduction pathway
No effect
Increase excitability, hasten the conduction through bundle of hiss & purkinje fibers
Atrial muscle
Decrease contractility,
Increase contractility
Ventricular muscle
No effect
Adrenal medulla
Promotes secretion of epinephrine ,that augments the sympathetic nervuos system actions on heart
Veins
Increaser venous return which increases the strength of cardiac contraction through Frank-starling mechanism

51. References Text book physiology by Guyton &Hall,11th edition
Human physiology by Lauralee Sherwood, seventh edition
Ganong’s Review of Medical Physiology - 23rd edition
Essential Medical Physiology 3rd edition - L. Johnson