The document discusses the rhythmicity and pacemaker potential of the heart. It defines rhythmicity as the heart's ability to beat rhythmically due to action potentials it generates autonomously. The sinoatrial node is identified as the primary pacemaker of the heart due to its highest rate of discharge. Pacemaker cells in the sinoatrial node have an unstable membrane potential that allows them to slowly depolarize from -60mV to the threshold of -40mV, generating the pacemaker potential which initiates the cardiac action potential. Autonomic nerves also help regulate heart rate, with the sympathetic nervous system increasing rate and the parasympathetic nervous system decreasing it.

1. DR.MAGDI AWAD SASI
CVS PHYSIOLOGY
HEAD OF BIOLOGY SCIENCES
LIMU----BENGHAZI
MAGDI AWAD SASI1

2. Learning Objectives
MAGDI AWAD SASI2
 Define the rhythamicity and account for its myogenic origin.
 List the possible pacemakers tissues of the cardiac muscle.
 Illustrate the pacemaker potential and ionic basis of it.
 Discuss the factors affecting rhythamicity
 Describe the autonomic supply of the heart & its function

3. Circulation Reviewed
Heart – "four chambered"
Right atrium & ventricle
Pulmonary circuit
Left atrium & ventricle
Systemic circuit
Blood Vessels – "closed circulation"
Arteries –from heart
Capillaries– cell exchange
Veins – to heart

4. The Anatomy of the Heart
The Heart Wall and Cardiac Muscle Tissue
Figure 12-4(c)

5. The Anatomy of the Heart
Cardiac Muscle Cells
Shorter than skeletal muscle fibers
Have single nucleus
Have striations (sarcomere organization)
Depend on aerobic metabolism
Connected by intercalated discs
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings

6. CARDIAC MUSCLE
 ATRIAL MUSCLE
 VENTRICULAR MUSCLE
 SPECIALISES EXCITATORY &CONDUCTIVE
MUSCLE FIBERS

7. Heart function as syncytium
MAGDI AWAD SASI7
 The cardiac syncytium is a network of
cardiomyocytes connected to each other by
intercalated discs that enable the rapid
transmission of electrical impulses through the
network, enabling the syncytium to act in a
coordinated contraction of the myocardium.

8. Functional properties of the heart
• F
EXCITABILITY
AUTOMATICITY
CONDUCTIVITY
RHYTHAMICITY
CONTRACTILITY

9. N.B.
-conductivity is measured by P-R interval in the ECG
and
a-c interval in jugular venous pulse wave.

10.  Heart beats rhythmically as result of action potentials it
generates by itself.
 Two specialized types of cardiac muscle cells
A. Contractile cells
 99% of cardiac muscle cells
 Do mechanical work of pumping
 Normally do not initiate own action potentials
B. Autorhythmic cells
-- Do not contract
 Initiate and conduct action potentials responsible for contraction.
C. CONDUCTIVE TISSUE

11. Sherwood’s Human Physiology 9-11 (9-8 6th Edition)
Specialized Conduction System
► Sinoatrial (SA)
node.
► _Pacemaker___
_ MYOGENIC
► Cells exhibit
autorhythmicity.

12. The pacemaker of the heart:
= The SA- node.
♥ Contains the P- cells, which are probably the actual
pacemaker cells.
♥ Has the fastest rhythm (rate of discharge) of all parts of
the heart, 90 impulses/min.
♥ Has spontaneous (w/out stimulation) depolarization,
up to firing level.

13. The pacemaker potential
♥ The pacemaker cells are characterized by having an
unstable membrane potential.
♥ Its RMP is ( -60 mV).
♥ This is the basis for automaticity

14. Myocardial Auto-rhythmic Cells
If-channel Causes Mem. Pot. Instability
 Autorhythmic cells have different
membrane channel: If - channel
 If channels let K+ & Na+ through at -60mV
 Na+ influx > K+ efflux
 Slow depolarization to threshold
allow
current
(= I ) to flow
f = “funny”:
researchers didn’t
understand initially

15. “Pacemaker potential” starts at ~ -60mV, slowly drifts
to threshold
AP

16. Channels involved in APs of Cardiac
Autorhythmic Cells
 Slow depolarization due to If channels
 As cell slowly depolarizes: If -channels close & Ca2+
channels start opening
 At threshold: lots of Ca2+ channels open  AP to +
20mV
 Repolarization due to efflux of K+

17. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
 Characteristics of Pacemaker Cells
A. Unstable membrane potential
“Bottoms out” at -60mV
“Drifts upward” to -40mV, forming a
pacemaker potential
B. Myogenic
The upward “drift” allows the membrane to
reach threshold potential (-40mV) by itself

18. Pacemaker Prepotential:
♥ Due to gradual state of depolarization:
■ Steady  in K+ permeability
( K+ efflux), leading to
 intracellular negativity.
■ Causing spontaneous leakage
of membrane to Na+ w/out
stimulation.
 (-60 mV to -55 mV).
■ Which causes op of voltage
gated transient Ca2+ channels,
leading to some Ca2+ influx.
 (-40 mV).
?
-6

19. Pacemaker Action potential (AP) (continued)
♥ Pacemaker Repolarization:
 Opening of VG K+ channels.
 K+ diffuses outward (efflux), … (so +vity will go out of cell).
♥ Pacemaker Hyperpolarization:
■ Excessive K+ effllux,
(This will lead to hardship of K+ efflux in 2nd depolarization).
 Ectopic pacemaker:
 Pacemaker other than SA node:
 If APs from SA node are prevented from reaching these areas, these cells
will generate pacemaker potentials.
-6

20. Automaticity
Hiss bungle – 30-40 /min
SA-node – 60-90 /min
AV – node – 40-60 /min
Purkinje fibers - <20 /min

21. SA NODE PACEMAKER BECAUSE
1) Highest frequency of discharge
 Other cells with low frequency of
discharge Called latent or potential
pacemakers; abnormal
or ectopic pacemakers.
 Become pacemaker when:
Develop rhythmical discharge rate that is
more Rapid than SA node.
 Develop excessive excitability
2) Of overdrive suppression
The greater rhythmicity of
the SA node forces the
other automatic cells to fire
off at a faster rate than
their natural discharge
rate. This causes
depression of their
rhythmicity.
SA node rhythmical
discharge rate = 70-80/min
AV node = 40-60/min
P fibers = 15-40/min

22. What are the Factors affecting
rhythmicity?
1. Nervous factors :
A. Vagal stimulation
Increase K+ efflux. Decrease Ca++ influx
B. Sympathetic stimulation
Decrease K+ efflux. Increase Ca++ influx
2. Effect of temperature
A- moderate warming ->increase HR
B- Excessive warming and cooling decrease HR

24. MAGDI AWAD SASI24
 3. Effect of drugs:
I-Digitalis—decrease HR act like Ach.
II-Hormones as thyroxin and catecholamines
increase HR
III-Cholinergic drugs  decrease HR.
 4. Effect of pH :
 Alkalosis → increase HR
 Acidosis → decrease HR
 (Alkalaemia or acidaemia) producing cardiac
arrhythmias
 5. Blood gases :
Sever O2 lack or CO2 excess → decrease HR
.

25. 6. Effect of
extracellular ions
• Na+:-
Excess Na+ ions depress
the cardiac activity
(membrane
hyperpolarization)
•-Low Na+ ions, slow the
diastolic depolarization of
SA node and
•reduces rhythmicity.
-60
-70
Excess K+ or
•Decrease K+ → increase
•the slope of the prepotentials →
increase rhythmicity.
K+

26. •Excess Ca++ strengthen the myocardial contractility,
•favoring systole  leads to stoppage of the heart in systole
•Ca++ rigor).
-Low Ca++ → increase rhythmicity
Ca++:-

27. Autonomic Neurotransmitters
Modulate Heart Rate
 The speed at which pacemaker cells depolarize
determines the rate at which the heart contracts
 The interval between action potentials can be
altered by changing the permeability of the
autorhythmic cells to different ions
Increase Na + and Ca +2 permeability speeds up
depolarization and heart rate
Decrease Ca +2 permeability or increase K + permeability
slow depolarization and slows heart rate

28. Extrinsic Innervation of the Heart
 Vital centers of medulla
1. Cardiac Center
 Cardioaccelerator center
 Activates sympathetic neurons that
increase HR
 Cardioinhibitory center
 Activates parasympathetic neurons
that decrease HR
 Cardiac center receives input from
higher centers (hypotha-lamus),
monitoring blood pressure and dissolved
gas concentrations

29. THE AUTONOMIC NERVOUS SYSTEM’S AFFECT ON THE PACEMAKER CELLS
Increase Ca++ influx
Decrease K+ efflux
Slows entry of Ca++
Increases efflux of K+

30. Nerve Supply to Heart
Even though the has it own pacemaker it is still
innervated by SNS & PNS:
 Sympathetic nerves - ↑ heart rate
Lower cervical & upper thoracic spinal cord
Efferent fibers travel to cervical ganglia, cardiac nerves
arise from the cervical ganglia and innervate the
ventricular myocardium thus
↑ the force of contraction.
can raise heart rate to 230 bpm

31. Autonomic Neurotransmitters
Modulate Heart Rate
The Catecholamines: norepinephrine and epinephrine
increases ion flow through If and Ca+2 channels
 More rapid cation entry speeds up the rate of the pacemaker
depolarization
 Β1-adrenergic receptors are on autorhythmic cells
 cAMP second messenger system causes If channels to remain
open longer

32. Sympathetic Activity Summary:
increased chronotropic effects
heart rate
increased dromotropic effects
conduction of APs
increased inotropic effects
contractility

33. Autonomic Neurotransmitters
Modulate Heart Rate
 Parasympathetic neurotransmitter
(Acetylcholine) slows heart rate
Ach activates muscarinic cholinergic
receptors that
 Increase K+ permeability and
 Decrease Ca+2 permeability

34. Nerve Supply to the Heart
 Parasympathetic nerves - ↓ heart rate
 Pathway is through
 right vagal nerve innervates the electrical center of the
heart called the SA node (sinoatrial);
 vagal tone – normally slows heart rate to
70 - 80 bpm. Without vagas n. influence the heart would
have a resting heart rate of about 100 bpm.
Vagus N. (CN X);

35. References
35
 Human physiology by Lauralee Sherwood, 7th
edition
 Text book physiology by Guyton &Hall,12th edition
 Text book of physiology by Linda .s contanzo,third
edition