1. Heart

2. Heart as a pump Two separate pumps Right heart Left heart
Blood to respiratory system
Left heart
Blood to the peripheral organs

3. Chambers Muscle composition Atrium (Primer pump) Ventricle
Atrial muscle
Ventricular muscle
Specialized muscles
Excitatory
Conductive

4. Atrial and ventricular muscles
Similar to skeletal muscles
Longer duration of contraction
Excitatory and conductive fibers
Few contractile fibrils
Contract freely
Automatic rhythmical electrical discharge
Conduction of action potential

5. Cardiac muscle Striated Arranged in a latticework
Division
Recombination
Spreading
Myosin and actin filaments

6. Cardiac muscle Syncytium
Muscle cells connected to each other via intercalated discs
Gap junctions (free diffusion of ions)
Action potential
Many cells act as one large unit

7. Two different syncytium
Atrial syncytium
Ventricular syncytium
Separation of atria from ventricle
Fibrous tissue surrounding atrioventricular (A-V) valvular openings
Prevents atrial action potential from traveling to ventricle
Allows contraction of atria ahead of ventricles

8. Ventricular action potential
150 mV
Plateau (15 times longer contraction)

9. Cause of plateau and longer action potential
Fast Na channels
Slow Ca channels (Na-Ca channels)
Longer flow of Na and Ca ions (prolonged deolarization)
Decreased K permeability after the onset of action potential
Prevents flow of K out of the cells

10. Ventricular Muscle Action Potential
Ca++ Channels
Open More
K+ Channels
Open
K+ Channels
Open More
Slow Ca++
Channels Open 1 2 3 4
phase
+20
-20
Membrane Potential
(mV)
-40
-60
-80
Fast Na+
Channels Open
-100 1 2 3 4
phase 0- Fast Na+ channels open then slow Ca++ channels
phase 1- K+ channels open
phase 2- Ca++ channels open more
phase 3- K+ channels open more
phase 4- Resting membrane potential
Seconds
Copyright © 2006 by Elsevier, Inc.

11. Velocity of signal conduction
0.3 to 0.5 mSec
Purkinje fibers
Refractory period
Absolute refractory period
0.25 to 0.3 sec in ventricular muscle
0.15 sec in atrial muscle
Relative refractory period
0.05 sec
Cause premature contraction

12. Excitation-contraction coupling
Specific mechanism
Large influx of Ca from extracellular fluid via T-tubules (critical for generating stronger contraction)
Poorly developed SR
Larger T-tubules
Mucopolysaccharides (negatively charged molecule) inside of the T-tubules
Ca ion storage

13. Cardiac cycle
Between the beginning of one heartbeat to the beginning of next heartbeat
Initiated by spontaneous generation of action potential
Sinus node
Action potential to atrium
Action potential to ventricles via A-V bundle
Delayed by 0.1 sec

14. Diastole Systole period of relaxation Blood fills the heart
Contraction

15. Cardiac Cycle (cont’d)
Figure 9-5; Guyton & Hall

16. Electrocardiogram and cardiac cycle
Five waves (P, Q, R, S, and T)
Electrical voltages generated by the heart
P-wave
Spread of depolarization through atria (contraction of atria)
Q, R, and S waves
Depolarization of ventricle
T wave
Repolarization of ventricle

17. Pressure changes in atria
Atria as primer pumps
80 % of blood flows directly through atria into the ventricle
20 % by contraction of atria
Pressure changes in atria
a-wave (contraction)
c-wave (bulging of A-V valves due to ventricular contraction)
v-wave (filling of atria while A-V valve is closed)

18. Ventricles as pump Systole Isovolumetric contraction Ejection
Rapid rise in ventricular pressure
A-V valve closure
Contraction without emptying of ventricle
Ejection
Opening of semilunar valve (aortic and plumonary)
Rapid (first 1/3, 70% emptying)
Slow (last 2/3, 30 % emptying)

19. Cardiac Cycle (cont’d)
Figure 9-5; Guyton & Hall

20. Diastole Dramatic fall of ventricular pressure after ejection
Closure of semilunar valves
Isovolumic relaxation
Opening of A-V valves
Rapid filling of ventricles (first 1/3 of diastole)

21. Cardiac Cycle (cont’d)
Figure 9-5; Guyton & Hall

22. Stroke volume End-diastolic volume Stroke volume/ejection fractionml
Stroke volume/ejection fraction
70 ml
End-systolic volume
40 to 50 ml
Increased end-diastolic volume and decreased end-systolic volume
Greater stroke volume

23. Cardiac output
Stroke volume X # heartbeat (per minute)

24. Function of valves Tricuspid and mitral valves
Prevent backflow of blood from ventricle to atria
Open and close passively
Changes in pressure
Chordae tendinea
Connection between vanes of valve and papillary muscle
Prevent valves from bulging too far during ventricular contraction

25. Aortic pressure curve Opening of aortic valves
Ventricular pressure
Stretching of aortic wall
120 mm Hg pressure
Continuous blood flow
Closure of aortic valves
Decrease in aortic pressure
80 mm Hg pressure

26. Work output
Two forms
Volume-pressure work (external work, major proportion)
Moving blood from low pressure (vein) to high pressure (artery)
Kinetic energy of blood flow
Acceleration of velocity to ejection speed through valves

27. Volume-pressure diagram
Four stages associated with cardiac cycle
Period of filling
End-systolic to end-diastolic volume
Isovolumetric contraction
Valve closure
Ejection
Isovolumetric relaxation

28. Pre- and afterload Preload A
Left Ventricular Volume
Left Ventricular Pressure A 3 4 1 2
Increased
preload
Preload
Degree of muscle tension when contraction beigns
End-diastolic pressure
Ventricle is filled
Abnormal
Alteration in pressure of ventricular filling

29. Afterload B Tension which the muscle exerts its contractile force
Corresponds to systolic pressure
Abnormal
Arterial pressure (ventricle must contract against)
Left Ventricular Volume
Left Ventricular Pressure B
Increased
afterload 3 4 2 1

30. Regulation of heart pumping
Intrinsic regulation
Changes in volume of blood flowing to the heart
Autonomic nervous system

31. Intrinsic regulation Frank-Starling mechanism
Adaptation of the heart in response to increasing flow of blood from veins
Venous return
Greater the stretch of heart muscle during filling, greater the force of contraction
Greater the volume of blood being pumped
Stretching of right atrium

32. Ventricular function curves
Stroke output curve
Relationship between atrial pressure and ventricular output

33. Ventricular function curves
Ventricular volume output curve
Relationship between two ventricles
Overall relationship
Filling of ventricle by increased atrial pressure
Increased ventricular volume and strength of pressure

35. Role of autonomic nervous system
Sympathetic nerves
Increases heart rate (70/min to /min)
Increases contraction force
Increases amount of blood being pumped out
Increases ejection pressure
Increase in maximum cardiac output by 2 to 3 X
Addition to Frank-Starling mechanism
Decreases heart rate (30 %) if inhibited
Sympathetic stimulation causes pumping to be maintained at 30 % above the level without stimulation

36. Parasympathetic nerves (Vagus nerves)
Innervates atrium
Strong stimulation can stop heartbeat for a few seconds
Heart “escapes” and beats 20-40/min as long as being stimulated
Decreases the strength of heart muscle contraction (20-30 %)
Decreases ventricular pumping by 50 % or more

37. Effects on cardiac function curve
Right atrial pressure
Controls cardiac output
Sympathetic stimulation
Increased cardiac output
Parasympathetic stimulation
Decreased cardiac output
Caused by:
Changes in heart rate
Changes in contractile strength of heart muscle

38. Role of ions Excess potassium (2 to 3 x above normal) Calcium Dilation
Flaccid heart (soft/flabby)
Decreased heart rate
Block conduction of cardiac impulses from atria to ventricle
Decreased resting membrane potential
Calcium
Spastic contraction if excess
Flaccid when deficient

39. Rhythmic excitation of heart
Components
Sinus node (sinoatrial/S-A)
Internodal pathway
Atrioventricular node (A-V node)
A-V Bundle
Bundle branches of Purkinje nerves

40. Rhythmic excitation of heart
Special system
Generation of rhythmical electrical impulses
Sinus node
Rapid conduction of impulses
Internodal pathway
A-V bundle
Left and right bundle branches of Purkinje nerve
Spread impulse throughout the ventricle
Impulse delayed by A-V node

41. Sinus node Specialized cardiac muscle
Absent of contractile muscle filament
Smaller size (3 to 5 mm) compared to surrounding atrial muscle (10-15 mm)
Capable of self-excitation
Controls the rate of beat
Entire heart
Pacemaker
Leaky membrane to Ca and Na ions
Cause of self-excitation

42. Higher resting membrane potential (-55 to -60 mV)
Higher Na ion concentrations
Generation of action potential
Slow Na channels
Rapid opening and closing of Na-Ca channels
Opening of K channel
Hyperpolarization of membrane to bring membrane potential to -55 to -60 mV

43. Membrane Potential (mV)
Rhythmical Discharge of Sinus Nodal Fiber
Slow Ca++
Channels Open
Sinus Nodal
Fiber
Ventricular
Muscle fiber
K+ Channels
Open more
+20
Threshold
-20
-40
Membrane Potential (mV) }
-60
“Resting Potential”
-80
Na+ Leak
-100 1 2 3 4
Seconds

44. Internodal pathways Action potential from S-A node
Spread throughout atrium and reach A-V node
Specialized fiber to increase speed of conduction (0.3 m/sec to 1 m/sec)
Three pathway
Anterior
Middle
Posterior
Anterior interatrial band
Transmit impulse from atria to the left atrium

45. A-V node Delayed conduction Caused by reduced number of gap junction
Greater resistance to conduction of ions
Emptying of atria before ventricular contraction

46. Internodal pathways
Initial conduction delay from S-A node to internodal pathway (0.03 sec)
About 0.1 sec (0.09 sec) delay from the time action potential arrives via internodal pathway
Another 0.04 sec delay in the penetration portion of A-V bundle
Total delay from S-A node to A-V bundle (0.16 sec)

47. Ventricular Purkinje system
Purkinje fibers
A-V node through A-V bundle into the ventricle
Very large fiber
Rapid conduction of action potential
Instantaneous transmission of action potential throughout the ventricle
High level of permeability by gap junction
Very few myofibrils

48. Left and right branches
Action potential
One-way conduction
Atria to ventricle
Arrhythmia prevention
Prevention of re-entry
Fibrous barrier between atria and ventricle
Insulator
Left and right branches

49. Main Arrival Times
S-A Node sec
A-V Node sec A-V Bundle sec Ventricular
Septum sec

50. Control of excitation Sinus node
Faster discharge rate compared to A-V node or Purkinje fibers
Pacemaker
Ectopic pacemaker (other parts of heart)
Shift from sinus node to A-V node or Purkinje fibers
Excessive excitability
Blockage of transmission
Delayed initiation of impulse (Stoke-Adams syndrome)

51. Control of rhythmicity
Parasympathetic nerves (Vagus)
Release of acetylcholine when stimulated
Increased permeability/leakage of K (hyperpolarization)
Decreased resting potential to -65 to -70 mV
Decrease rate of rhythm by S-A node
Decrease excitability of A-V junctional fibers

52. Sympathetic stimulation
Releases norepinephrine
Increased Na and Ca permeability
Increased resting membrane potential
Acceleration of self-excitation
Increased rate of sinus nodal discharge
Increased rate of conduction and level of excitability
Increased force of atrial and ventriclular contraction