Anatomy and physiology of the cardiac system The electrocardiogram a, curves and interpretation of the first and second heart sounds. Generation of action potential within the myocardium ,the gap junctions and how they propagate electrical pilese from sinoatrial mode and ectopoic heartbeat.

1. CVS
L. S LUMBUKA

2.  Weight of the heart 300g
 Work: 75/min, 10000
beats /day
 35 million beats /year, 2.5
billion beats/life
 70ml/beat, 7200 l/day
The work of the heart in one life is equivalent to
lifting 30 tons to the Mount Everest
The busy and hard working heart!

3. INTRODUCTION
 The parts of the heart normally beat in orderly sequence: Contraction of
the atria (atrial systole) is followed by contraction of the ventricles
(ventricular systole), and during diastole all four chambers are relaxed.
 The cardiac electric activity that triggers heartbeat originates in a
specialized cardiac conduction system and spreads via this system to all
parts of the myocardium.
 The structures that make up the conduction system are the sinoatrial node
(SA node), the internodal atrial pathways, the atrioventricular node (AV
node), the bundle of His and its branches, and the Purkinje system.

4. Functional Anatomy of the Heart
Intrinsic Conduction System
 Consists of “pacemaker” cells
and conduction pathways
 Coordinate the contraction
of the atria and ventricles

5.  The SA node is the normal cardiac pacemaker,
with its rate of discharge determining the rate
at which the heart beats.
 It discharges most rapidly, with depolarization
spreading from it to the other regions before
they discharge spontaneously.
 The other parts of the conduction system under
abnormal conditions, are capable of
spontaneous discharge.

6. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
 Characteristics of Pacemaker Cells
 Smaller than contractile cells
 Don’t contain many myofibrils
 No organized sarcomere structure
 do not contribute to the contractile force of the
heart
normal contractile
myocardial cell
conduction myofibers
SA node cell
AV node cells

7. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
 Characteristics of Pacemaker Cells
 Unstable membrane potential
 “bottoms out” at -60mV
 “drifts upward” to -40mV, forming a pacemaker potential
 Myogenic
 The upward “drift” allows the membrane to reach threshold potential (-40mV) by itself
 This is due to
1. Slow leakage of K+ out & faster leakage Na+ in
 Causes slow depolarization
 Occurs through If channels (f=funny) that open at negative membrane potentials and start closing
as membrane approaches threshold potential
2. Ca2+ channels opening as membrane approaches threshold
 At threshold additional Ca2+ ion channels open causing more rapid depolarization
 These deactivate shortly after and
3. Slow K+ channels open as membrane depolarizes causing an
efflux of K+ and a repolarization of membrane

8. The SA node cell
 Maximal repolarization
(diastole) potential, –
70mv
 Low amplitude and long
duration of phase 0.
 not so sharp as ventricle
cell and Purkinje cell.
 No phase 1 and 2
 Comparatively fast
spontaneous
depolarization at phase 4
8
A, Cardiac ventricular cell
B, Sinoatrial node cell

9. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
 Characteristics of Pacemaker Cells

10. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
 Altering Activity of Pacemaker Cells
 Sympathetic activity
 NE and E increase If channel activity
 Binds to β1 adrenergic receptors which activate cAMP and increase If channel
open time
 Causes more rapid pacemaker potential and faster rate of action potentials
Sympathetic Activity Summary:
increased chronotropic effects
heart rate
increased dromotropic effects
conduction of APs
increased inotropic effects
contractility

11. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
 Altering Activity of Pacemaker Cells
 Parasympathetic activity
 ACh binds to muscarinic receptors
 Increases K+ permeability and decreases Ca2+ permeability = hyperpolarizing
the membrane
 Longer time to threshold = slower rate of action potentials
Parasympathetic Activity
Summary:
decreased chronotropic effects
heart rate
decreased dromotropic effects
 conduction of APs
decreased inotropic effects
 contractility

12. Automaticity (Autorhythmicity)
 Some tissues or cells have the ability to
produce spontaneous rhythmic excitation
without external stimulus.
 Different intrinsic rhythm of rhythmic
cells
 Purkinje fiber, 15 – 40 /min
 Atrioventricular node 40 – 60 /min
 Sinoatrial node 90 – 100 /min
 normal pacemaker
 latent pacemaker
 ectopic pacemaker
12

13. Myocardial Physiology
Contractile Cells
 Special aspects
 Intercalated discs
 Highly convoluted and interdigitated
junctions
 Joint adjacent cells with
 Desmosomes & fascia adherens
 Allow for synticial activity
 With gap junctions
 More mitochondria than skeletal muscle
 Less sarcoplasmic reticulum
 Ca2+ also influxes from ECF reducing
storage need
 Larger t-tubules
 Internally branching
 Myocardial contractions are graded!

14. Myocardial Physiology
Contractile Cells
 Special aspects
 The action potential of a contractile cell
 Ca2+ plays a major role again
 Action potential is longer in duration than a “normal” action potential
due to Ca2+ entry
 Phases
4 – resting membrane potential @ -90mV
0 – depolarization
 Due to gap junctions or conduction fiber action
 Voltage gated Na+ channels open… close at 20mV
1 – temporary repolarization
 Open K+ channels allow some K+ to leave the cell
2 – plateau phase
 Voltage gated Ca2+ channels are fully open (started during initial
depolarization)
3 – repolarization
 Ca2+ channels close and K+ permeability increases as slower
activated K+ channels open, causing a quick repolarization
 What is the significance of the plateau phase?

15. 15
t (msec)
-90
0
+20
0 300
0
1
2
3
4
Phase 0: rapid
depolarization, 1-2ms
Phase 1: early rapid
repoarization, 10 ms
Phase 2: plateau, slow
repolarization, the
potential is around 0
mv. 100 – 150ms
Phase 3, late rapid
repolarization. 100 –
150 ms
Phase 4 resting potentials
General description
Resting potential: -90mv
Action Potential

16. Ion Channels in Ventricular Muscle 16
Ventricular
muscle
membrane
potential
(mV)
-50
0
200 msec
Inactivating K channels (ITO)
“Rapid” K channels (IKr)
“Slow” K channels (IKs)
IK1
Voltage-gated
Na Channels
“Ultra-rapid” K channels (IKur)
Voltage-gated
Ca Channels

17. Myocardial Physiology
Contractile Cells
 Plateau phase prevents summation due to the elongated refractory
period
 No summation capacity = no tetanus
 Which would be fatal

18. 18
+25
Time (msec)
0 0.1 0.2 0.3
-125
-100
-75
-50
-25
0
0
4
1
2
3
Transmembrane
Potential RRP
ARP
 Absolute Refractory Period – regardless of the strength of a
stimulus, the cell cannot be depolarized.
 Relative Refractory Period – stronger than normal stimulus can
induce depolarization.
(1) Refractory Period

19. Refractory Period
 Absolute Refractory Period (ARC): Cardiac
muscle cell completely insensitive to further
stimulation
 Relative Refractory Period (RRC): Cell
exhibits reduced sensitivity to additional
stimulation
19

20. Myocardial Physiology
Contractile Cells
 Initiation
 Action potential via pacemaker cells to
conduction fibers
 Excitation-Contraction Coupling
1. Starts with CICR (Ca2+ induced Ca2+
release)
 AP spreads along sarcolemma
 T-tubules contain voltage gated L-type Ca2+
channels which open upon depolarization
 Ca2+ entrance into myocardial cell and
opens RyR (ryanodine receptors) Ca2+
release channels
 Release of Ca2+ from SR causes a Ca2+
“spark”
 Multiple sparks form a Ca2+ signal
Spark Gif

21. Myocardial Physiology
Contractile Cells
 Excitation-Contraction Coupling cont…
2. Ca2+ signal (Ca2+ from SR and ECF) binds to troponin to initiate
myosin head attachment to actin
 Contraction
 Same as skeletal muscle, but…
 Strength of contraction varies
 Sarcomeres are not “all or none” as it is in skeletal muscle
 The response is graded!
 Low levels of cytosolic Ca2+ will not activate as many myosin/actin
interactions and the opposite is true
 Length tension relationships exist
 Strongest contraction generated
when stretched between 80 &
100% of maximum (physiological
range)
 What causes stretching?
 The filling of chambers
with blood

22. Myocardial Physiology
Contractile Cells
 Relaxation
 Ca2+ is transported back into the SR
and
 Ca2+ is transported out of the cell by
a facilitated Na+/Ca2+ exchanger
(NCX)
 As ICF Ca2+ levels drop, interactions
between myosin/actin are stopped
 Sarcomere lengthens

23. 23
Conducting System of Heart

24. Flow of Cardiac Electrical Activity
(Action Potentials)
24
SA node Pacing (sets heart rate)
Atrial Muscle 0.4m/s
AV node 0.02 m/s Delay
Purkinje System 4m/s Rapid, uniform spread
Ventricular
Muscle
1m/s

25. characteristics of conduction in heart
 Delay in transmission at the A-V node (150 –200 ms) – sequence of the atrial
and ventricular contraction – physiological importance
 Rapid transmission of impulses in the Purkinje system – synchronize
contraction of entire ventricles – physiological importance
25

26. Effect of autonomic nerve activity on the heart
Region affected Sympathetic Nerve Parasympathetic Nerve
SA node Increased rate of diastole
depolarization ; increased
cardiac rate
Decreased rate of diastole
depolarization ; Decreased
cardiac rate
AV node Increase conduction rate Decreased conduction rate
Atrial muscle Increase strength of
contraction
Decreased strength of
contraction
Ventricular
muscle
Increased strength of
contraction
No significant effect

27. The ECG
 Can record a reflection of cardiac electrical activity on the skin-
EKG
 The magnitude and polarity of the signal depends on
 what the heart is doing electrically
 depolarizing
 repolarizing
 whatever
 the position and orientation of the recording electrodes
27

28. 28
The Normal Electrocardiogram (ECG)
Concept: The record of potential fluctuations of
myocardial fibers at the surface of the body

29. Uses of the ECG
 Heart Rate
 Conduction in the heart
 Cardiac arrhythmia
 Direction of the cardiac vector
 Damage to the heart muscle
 Provides NO information about pumping or
mechanical events in the heart.
29

30. The Heart as a Pump
 I Cardiac Cycle
 The period from the end of one heart
contraction to the end of the next

31. 2 The Phases of the Cardiac Cycle
(1)Period of isometric (isovolumetric
or isovolumic) contraction
Events: ventricular contraction
ventricular pressure rise 
atrioventricular valve close 
the ventricular pressure increase sharply
Period: 0.05 sec
Importance: enable the ventricular pressure to rise from 0 to
the level of aortic pressure (after-load)

32. (2) Period of ejection
Events: ventricular contraction continuously
 the ventricular pressure rise above the arterial pressure
 semilumar valves open
  blood pours out of the ventriclesRapid ejection period
(0.10s, 60% of the stroke volume)
 Reduced ejection period (0.15s, 40% of the stroke
volume)

33. (3) Period of isometric (isovolumic) relaxation
Events:
ventricular muscle relax
 the ventricular pressure fall
 lower than the aortic pressure
 aortic valve close
the ventricular pressure fall sharplyPeriod: 0.06-
0.08 s
Importance: Enable the ventricular pressure fall to
the level near the atrial pressure

34. (4) Period of filling of the ventricles
Events: Ventricular muscle relax continuously
 the ventricular pressure is equal or lower than the atrial pressure
 atrioventricular valve open
 blood accumulated in the atria rushes
into the ventricular chambers quickly from
the atrium to the ventricle. Period of rapid
filling. (0.11s, amount of filling, 2/3)
Period of reduced filling (0.22s, little blood
fills into the ventricle)

35. (5) Atrial systole
 Significance, 30% of the filling
 Be of major importance in determining the final cardiac
output during high output states or in the failing heart

37. LEFT VENTRICULAR PRESSURE/VOLUME P/V LOOP
LEFT
VENTRICULAR
PRESSURE
(mmHg)
LEFT VENTRICULAR VOLUME (ml)
A B
C
D
E
F
100 150
50
0
120
40
80

38. region produced by the functioning of
the heart.
S1- first sound
Atrioventricular valves and surrounding fluid vibrations as valves
close at beginning of ventricular systole
S2- second sound
closure of aortic and pulmonary semilunar valves
at beginning of ventricular diastole
S3- third sound
vibrations of the ventricular walls when suddenly
distended by the rush of blood from the atria
Heart Sounds

39. II Cardiac Output
 Stroke Volume – The volume pumped by the heart with
each beat,
 = end diastole volume – end systole volume, about 70 ml
 Ejection Fraction – Stroke volume accounts for the
percentage of the end diastolic volume,
 = stroke volume / end diastole volume X 100%, normal range,
55-65%

40. II Cardiac Output
 3. Minute Volume, or Cardiac Output – the volume of the blood pumped by one
ventricle in one minute
 = stroke volume X heart rate.
 It varies with sex, age, and exercise
 4. Cardiac Index, the cardiac output per square meter of body surface area.
 the normalized data for different size individuals,
 the normal range is about 3.0 – 3.5 L/min/m2