The Heart

Functional structure of cardiac

muscle
• The basic structural unit is the sarcomere.
• Tight and gab junctions.
– the gab junctions act as a low resistance bridges that
allow spread of excitation wave between cardiac cells
– The tight juctions exert mechanical connection between
cardiac muscle fibers.
• It contains actin and myosin with striations
of dark A-bands and light I- bands.
• each transverse tubule is surrounded by
cisternae of sarcoplasmic reticulum.
• Most of the energy of the heart is derived
from aerobic oxidation
The cardiac muscle differs from
skeletal muscle in:

 being not dependent on central nervous

system.
 having no neuromuscular junctions.
 acting as a single unit or functional
syncitium.
Functional division:
• Nodal or pacemaker tissue
– It is the tissue that is able to initiate nerve impulse
in an automatic and regular manner, examples :
SAN (sinoatrial node) and AVN (atrio-ventricular
node).
• Junctional (Conductive tissue) : this
system conducts nerve impulse from site of
initiation to all parts of the heart as fast as
possible.
• Contractile (muscular) tissue : It is the
issue that is able to contract and act as a
pump.
Properties of cardiac muscle
 Autorhythmicity
 Conductivity
 Excitability
 Contractility
Autorhythmicity

 It is the ability of autorhythmic cells

present in the heart to generate nerve
impulses in regular and independent
manner.
 Autorhythmic cells
◦ SAN Its rhythm is 100 impulse / minute
◦ AVN.: Its rhythm is 50 imulse/ minute
◦ Purkinje fibers: Its rhythm is 25 impulse /
minute
Autorhythmic cells
 have unstable resting membrane potential
 at – 60 mv resting level, there is
spontaneous depolarization due to
decrease in K+ and increase in Na+ and
Ca+ permeability
 SAN is the pacemaker of the heart
 because it discharge nerve impulses at
the highest rhythm about 100 impulse /
minute.
Factors affecting Autorhythmicity
 Sympathetic stimulation increases
autorhythmicity by decreasing membrane
permeability to K+
 Parasympathetic stimulation decreases
automaticity due to increase in K+
permeability
 Increase in body temperature by 1o C
increases heart rate by 20 bpm
 Mechanical stretch of right atrium stimulates
SAN
 Catecholamines also stimulate SAN.
• Chrotropic effect:
– It is the increase of rate of discharge of SAN
and hence increase heart rate.
• Positive chronotropic effect : Increase of
HR
– Examples
• Sympathetic stimulation
• Catecholamines (adrenaline and noradrenaline)
• Negative chronotropic effect: Decrease of
HR
– Examples
• Parasympathetic (vagal) stimulation
• Acetylcholine.
Conductivity:

 It is the ability of the heart to conduct

nerve impulses from the site of initiation
to all parts of the ventricles through a
specialized conductive system as fast as
possible.
Importance of AVN
• It acts as one way conduction of nerve
impulse from atrium to ventricle
• It delays the nerve impulse for about 0.1
second to allow atrial excitation to be
completed before the start of ventricular
excitation
• AVN also has a long absolute refractory
period to protect the ventricle from high
atrial rhythms
• AVN act as a latent pacemakerin case of
damage of SAN
 The highest conductive velocity
occurs in Purkinje fibers while the
highest rate of discharge occurs in
SAN
Excitability
 It is the ability of cardiac muscle to
respond to stimulation by producing action
potential.
 Two types of electrical responses.
◦ Fast response is recorded from fast response
fibers or contractile fibers
◦ slow response recorded from slow response
fibers or autorhythmic cells.
 Slow Response
• It is the action potential recorded from SAN
or AVN. It is formed from the following
phases:
– Prepotential : it is the unstable resting membrane
potential of the slow fibers.
• The membrane potential changes from -60 mv to the
firing level of – 45 mv.
• is due to decrease potassium efflux and increase
sodium and calcium influx.
– Depolarization of action potential occurs by
calcium influx
– Repolarization occurs by potassium efflux.
 Fast response
• It is the action potential recorded from
contractile cells.It is formed of the following
phases :
– Phase 4 : resting state -90 mv.
– Phase 0 : fast depolarization from -90 mv to + 30
mv it is due to sodium influx through fast volt-
sensitive sodium channels.
– Phase 1 : rapid small repolarization : It is due to
potassium efflux.
– Phase 2 : Plateau : It is a plateau phase and is due
to both calcium influx and potassium efflux.
– Phase 3 : rapid repolarization : It is due to
potassium efflux.
 50. During which phase
of the ventricular action
potential is the
membrane potential
closest to the K+
equilibrium potential?

 (A) Phase 0
 (B) Phase 1
 (C) Phase 2
 (D) Phase 3
 (E) Phase 4
 During which phase
of the ventricular
action potential is
the conductance to
Ca2+ highest?
 (A) Phase 0
 (B) Phase 1
 (C) Phase 2
 (D) Phase 3
 (E) Phase 4
 Which phase of the
ventricular action
potential coincides
with diastole?
 (A) Phase 0
 (B) Phase 1
 (C) Phase 2
 (D) Phase 3
 (E) Phase 4
Contractility
 It is the intrinsic ability of cardiac muscle
to generate force at a constant length.
 Excitation contraction coupling
◦ depolarization of cardiac muscle cells will lead
to opening of volt sensitive calcium channels in
the sarcolemma causing calcium influx.
◦ The increased intracellular calcium will activate
another calcium sensitive calcium channels in
the cisternae of sarcoplasmic reticulum
◦ release of calcium from sarcoplasmic reticulum
to the cytoplasm
Contractility
 Excitation contraction coupling
◦ increase intracellular calcium will bind troponin
c
◦ this will cause binding of actin to myosin with
sliding of actinover myosin.
◦ shortening of sarcomeres and so muscle
contraction
◦ Relaxation of cardiac muscle occurs by
decreasing cytosolic calcium
◦ pumping calcium to extracellular fluid or to
cisternae of sarcoplasmic reticulumby active
mechanism.
Ion movements during the contraction of cardiac muscle. ATPase = adenosine
triphosphatase
Factors affecting cardiac muscle
contractility
 Intrinsic:
◦ Preload
◦ Afterload
◦ Heart Rate
 Extrinsic
◦ Nervous
 Sympathetic
 Parasympathetic
◦ Humoral
 Hormones
 Chemixcals and drugs
Intrinsic regulation of Contractility
 Preload
◦ Its effect is determined by Starling law
◦ It is a direct relationship within limit . So
◦ Increase VR (venous return) will cause stretch
of the muscle of ventricle and this leads to
increase preload so force of contraction
increases.
◦ If the ventricle is overstretched, force of
contraction will decrease.
Intrinsic regulation of Contractility
 Afterload
◦ it is defined as the load imposed on the muscle
during contraction or the force against which
the heart pumps blood
◦ The high arterial blood pressure and aortic
stenosis are examples of afterloads.
◦ Increase afterload is inversely proportional to
the velocity of shortening.
 Effect of heart rate on contraction
◦ Increase HR increases force of contraction
Extrinsic regulation of Contractility
 Nervous factors
◦ Sympathetic stimulation has a positive inotropic
effect by increasing availability of calcium
◦ Parasympathetic stimulation has negative inotropic
effect by decreasing calcium but this effect is
exerted only on the atria
 Humoral factors
◦ Catecholamines have a positive inotropic
◦ Calcium may stop the heart in systole
◦ potassium stops the heart in diastole.
◦ Digitalis has a positive inotropic effect by
increasing calcium inside the cardiac cells.
◦ Calcium channel blockers (nefidipine) : has a
negative inotropic effect
Pharmacology Box
Use of Digitalis
Digitalis, or its clinically useful preparations (digoxin and
digitoxin) has been described in medical literature for over 200
years. It was originally derived from the foxglove plant.
(Digitalis purpurea is the name of the common foxglove.)
Correct administration can strengthen contractions through
digitalis inhibitory effects on the Na, K ATPase, resulting in
greater amounts of Ca2+ release and subsequent changes in
contraction forces.
Digitalis can also have an electrical effect in decreasing AV
nodal conduction
velocity and thus altering AV transmission to the ventricles.
Choose the ONE best answer.
IV.1 A 65-year-old man with a history of
hypertension is prescribed a Ca2-channel
blocker to help reduce his blood pressure. What
is the likely effect of this drug on the ventricular
myocardium?

A. It would have no effect.

B. It would increase contractility.
C. It would increase heart rate.
D. Phase 2 would be reduced.
E. Phase 1 would be prolonged.
The physiologic function of the
relatively slow conduction through the
atrioventricular (AV) node is to allow
sufficient time for

(A) runoff of blood from the aorta to the

arteries
(B) venous return to the atria
(C) filling of the ventricles
(D) contraction of the ventricles
(E) repolarization of the
ventricles