1) The document discusses the rhythmicity and automaticity of the heart, which refers to the heart's ability to beat regularly and generate impulses without external stimuli. 2) It originates from within the heart itself (myogenic, not neurogenic) and several factors can influence the heart rate such as the autonomic nervous system, temperature, drugs, blood gases, and inorganic ions. 3) The sinoatrial node acts as the pacemaker for the heart and has membrane properties that allow it to spontaneously depolarize, initiating the heartbeat via an action potential involving sodium, calcium, and potassium ion fluxes.

1. PresentationTOPIC
RYTHEMECITYANDAUTOMATECITYOFHEART
Presented By:
1) Romeen Yasmeen
2) Safi Ullah
3) Rooh Niaz
Submitted To : Ms. Naila Gul

2. Presenter #01
ROMEEN YASMEEN

4. DEF.
• Rhythmicity is the ability of heart to beat regularly
• Automaticity is the ability of heart to generate impulses without
external stimuli
• Autorhythmicity is the ability of cardiac ms to generate impulses
without external stimuli at regular rate

5. •Origin
• Myogenic not neurogenic.
• The nerves control the rate but do not initiate the beat
Evidences:
a) Local anesthetics
e.g. cocaine block the nerve but not stop the
heart

6. B) Transplanted heart
(No nerve supply) continues to beat.
C) heart of human fetus start to beat before development of nerves

7. • Nature:
• Most cardiac fibers have the ability of self excitation especially nodal and conducting
fibers
• SAN has the greatest rhythm, so it is called "pace maker of the
heart

8. MECHANISM OF AUTORHYTHMICITY OF SAN:
•RMP of SAN is low about -55mv to -60 mv.
•This is due to natural leakiness to Na ions
Action Potential (AP):
1. Prepotential or pacemaker
potential (phase 4)
2. Upstroke (phase 0)
3. Repolarization (phase 3)

9. It is a gradual rise of membrane potential from the resting level of -55
mv to the firing level or the threshold voltage of -40 mv
Mechanism:
1. Na influx through funny (slow) Na
channels
2. Ca influx through T (=transient) -type Ca
channel
3. Decreased K+ efflux
It occurs during diastole, so it is also called the diastolic
depolarization (DD)

10. Importance of Pacemaker potential:
1. It is the cause of Rhythmicity.
2. The rate of slope of the prepotential determines the heart
rate. The more rapid is the slope, the more will be the heart
rate.

11. 2. UPSTROKE (PHASE 0):
Mechanism:
• Inward Ca++ current through L (long lasting )
Ca++ channels
•From membrane potential (– 40 m.v) to (+ 10 m.v)

12. 3. Repolarization (phase 3):
Mechanism:
• increase K+ efflux
•From membrane potential (+10 m.v) to (-60 m.v)

13. Presenter #02
Safi ullah

14. -60
-40
-
20
-
10
0
+10
Phase 0
Phase 3
Na+
ca++
mv
R.M.P
Na+
m
Na+
Na+
Na+Na+
Na+
h
K+
ca++
K+
K+K+
ca++ca++
K+K+K+
Depolarization
Phase 4
(only in
pacemaker cells
Repolarization
ca++
ca++ca++
ca++
ca++ca++ca++

15. FACTORS AFFECTING
RHYTHMICITY

16. FACTORS AFFECTING RHYTHMICITY
• CHRONOTROPISM MEANS AN INFLUENCE ON THE HEART RATE
• +VE CHRONOTROPIC → ↑ HEART RATE
• -VE CHRONOTROPIC → ↓ HEART RATE
Dra abdelaziz Hussein, Mansoura Faculty of Medicine
Factor
s
Nervous
Factors
sympat
hetic
Parasy
mpath
etic
Physical
Warming
and
cooling
Chemical
Drug
s
Gases Ions
Toxin
s

18. AUTONOMIC N. SYSTEM
SYMPATHETIC STIMULATION:
• HAS A +VE CHRONOTROPIC EFFECT
Figure 14-17: Modulation of heart rate by the nervous system
•Release noradrenalin → increases fiber membrane
permeability to Na+ & Ca++→ rapid slope of
Prepotential → threshold is reached rapidly →
increase Rhythmicity

19. AUTONOMIC N. SYSTEM
PARASYMPATHETIC STIMULATION:
• HAS A -VE CHRONOTROPIC EFFECT
Figure 14-17: Modulation of heart rate by the nervous system
•Acetylcholine released at the vagal endings
→increase the permeability of fiber membrane to
K+ → rapid K+ efflux → hyperpolarization→
decrease Rhythmicity

20. PHYSICAL FACTORS
WARMING:
• MODERATE WARMING : INCREASES RHYTHMICITY DUE TO;
a)↓permeability of the membrane to K+ ions during the
pacemaker potential, i.e. rapid slope of prepotential
b)↑speed of ionic fluxes across the membrane during the
action potential
•Excessive warming (45 ) denatures the intracellular
proteins and produces cardiac damage
•Moderate cooling decreases Rhythmicity
•Excessive cooling stop Rhythmicity

21. CHEMICAL FACTORS
1. DRUGS AND
HORMONES:•Catecholamines have +ve chronotropic effect.
•Cholinergic drugs (as methacholine) have –ve
chronotropic effect
•Thyroxine has a +ve chronotropic effect as it
stimulates the metabolism of the SAN.
•Digitalis depresses nodal tissue. It increases K+
efflux → hyperpolarization

22. CHEMICAL FACTORS
2. BLOOD GASES:
•O2 lack (hypoxia):
•Mild hypoxia increases rhythmicity
•Severe hypoxia decreases and stop rhythmicity
•Hypercapnia: has a -ve chronotropic effect
through acidemia
•H ion concentration :
•Acidosis decreases rhythmicity
•Alkalosis increases rhythmicity
•Severe acidosis and alkalosis decreases
rhythmicity .

23. CHEMICAL FACTORS
3. INORGANIC IONS :
•K ions :
• mild hyperkalemia have -ve chronotropic effect.
(because excess K in ECF decreases K efflux during
repolarization)
•Mild hypokalemia has opposite effect
•Ca ions:
• Mild increase of Ca++ (hypercalcemia) decreases
rhythmicity by activating K+ channels →
hyperpolarization → so longer time is needed to
reach threshold potential.
•Mild hypocalemia has the opposite

24. CHEMICAL FACTORS
3. INORGANIC IONS :
•K ions :
• mild hyperkalemia have -ve chronotropic effect.
(because excess K in ECF decreases K efflux during
repolarization)
•Mild hypokalemia has opposite effect
•Ca ions:
• Mild increase of Ca++ (hypercalcemia) decreases
rhythmicity by activating K+ channels →
hyperpolarization → so longer time is needed to
reach threshold potential.
•Mild hypocalemia has the opposite

25. TOXINS
•Typhoid or diphtheria toxins have a –ve
chronotropic effect, due to direct inhibitory action
on nodal tissues

26. Presenter #03
Rooh niaz