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.
 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
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