Electrical Properties of the Heart PHYSIOLOGY

Dr. Barbon

OUTLINE ❏ To prevent pulling of blood

in any part of the body
I. Pulmonary vs Systemic Circulation COMPLIANCE:
a. Cardiac Output
❏ refers to the distensibility/
b. Compliance
c. Systemic/ Pulmonary Arterial elasticity of blood vessels
Blood ❏ Pulmonary>Systemic
d. Systemic/ Pulmonary Venous SYSTEMIC PULMONARY
Blood
II. Poiseulle’s Equation
III. Cardiac Valves ARTERY Oxygenated Deoxygenated
IV. Cardiac Tissues
a. Contractile Tissue/Cardiac VEIN Deoxygenated Oxygenated
Muscles
b. Conducting Tissue
V. Length- Tension Relationship
II. Poiseulle’s Equation
between Skeletal and Cardiac Muscle
VI. Physiologic Properties of the Heart Poiseuille- Hagen Equation
a. Excitability ❏ concerned with volume flow
b. Rhythmicity ❏ derived from Ohm’s law
c. Conductivity
d. Contractility
❏ Volume flow/ Cardiac Output=
e. Relaxation Pressure/ Resistance
VII. Cardiac Muscle Hypertrophy ❏ Resistance = (8) (length) (viscosity) /
(pi)(r^4)
❏ Pressure= Blood Flow x Resistance
I. Pulmonary vs Systemic Circulation
PULMONARY CIRCULATION
● Concerns with blood passing through
the pulmonary system or the lungs
● Low resistance
● Low pressure

❏ Pulmonary and Systemic Circulation

SYSTEMIC CIRCULATION
affected by Length and radius
● Concerns with blood passing through
❏ shorter length→ lesser
the other organs
resistance and lesser pressure
● High resistance
❏ Longer length → higher
● High pressure
resistance, higher pressure
CARDIAC OUTPUT/ VOLUME FLOW
❏ Amount of blood pumped out
a given time
❏ Pulmonary= Systemic

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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon
III. CARDIAC VALVES
Valves that separate atrium from the
ventricles; Av valves
Mitral Valve
❏ Normal Size= 4-6 square
centimeters
❏ Chorda tendinae: prevents blood
flow
❏ Attachment of papillary
muscles
❏ Papillary muscles
❏ Prevent aversion or
movement of valves
toward the atrium
❏ Will allow blood from the atrium
to enter the ventricle
❏ veins--atrium→
ventricle→ arteries
❏ No back flow
Tricuspid Valve
Valves that separate ventricle from major
vesicles ( only on arterial side);
pulmonary and aortic semilunar valve
Semilunar Valve
❏ Opening is much smaller than
AV
❏ No chorda tendinae becaue they
are much stronger compared to
the AV valves
❏ AV is softer that is why
there is a need fot chorda
tendinae that will help
prevent aversion of Av
from the opposite side
❏ Normal size: 3-4 square
centimeters
There is no valve that separates major
veins from atrium
→ blood can enter more
freely
CLOSURE OF VALVES
❏ S1:
❏ Closure of AV
❏ First heart sound
❏ S2
❏ Closure of semilunar valve
❏ Second heart sound
OTHER DIFFERENCES BETWEEN AV
VALVE AND SEMILUNAR VALVE
AV valve:
❏ Thin and filmy
❏ Soft closure
❏ Bigger opening
❏ Lesser pressure
❏ Lesser velocity
❏ Slower ejection
❏ Lesser abrasion
❏ “Lub”
❏ s1= low pitch
SEMILUNAR valve:
❏ Strong but pliable
❏ Snap when it closes
❏ smaller opening
❏ Greater pressure
❏ Greater velocity
❏ Rapid ejection
❏ Prone to abrasion
❏ “Dub” or “Dup”
❏ S2- high pitched
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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

PERICARDIAL SAC Pathway of Impulse:

= prevents overstretching/ SA node
overdistension of cardiac muscles  Located at the
junction of superior
= maintians maximum stretch of the vena cava and right
cardiac muscle atrium
Internodal tracts
APEX OF THE HEART  transmits impulses from
SA node to AV node
 Apex beat of the heart= Point of
Maximal Impulse AV node
 5th intercostal space= midclavicular  located posteriorly on the
line right side of interatrial
IV. CARDIAC TISSUES septum
● Contractile tissues (non-automatic  Three zones:
cells)= CARDIAC MUSCLES a. ATRIONODAL
○ Atria and ventricular muscles = most proximal zone
○ Cells cannot generate own = transitional zone
AP and are specialized between right atrium
mainly for contraction and AV node
○ Its presence allows the heart b. NODAL ZONE
to contract even though you = middle
cut the autonomic innervation c. NODAL HIS ZONE
of the cardiac muscle = most distal
● Conducting tissues (automatic cells) = connects with
○ For transmission of impulses bundle of His
○ Cannot separate from the Purkinje System/ ventricular
contractile tissues; attached conduction system
firmly to contractile tissues of  Bundle of His
the heart = located at
○ Cells are capable of interventricular
spontaneously generating its septum
own action potential = forms right and left
independent of extrinsic bundle branches
nervous stimulation  Purkinje fibers
= present mostly at
the apex of the heart

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon
CARDIAC MUSCLES/ NON-
AUTOMATIC CELLS
❏ Striated; actin and myosin arranged
in sarcomeres
❏ less/ moderately developed SR and
transverse tubules
❏ Has its own conducting tissues
❏ Contains troponin in the thin
filaments
❏ DPHR and RYR
❏ Calcium ions enter cytoplasm from
SR and ECF(plasma)
❏ Aalso uses calcium from ECF
besides SR
❏ Involuntary (through autonomics)
❏ Sympa- excites
❏ Parasympha- inhibits
❏ Can contract without nerve
stimulatin; action potentials originate
in pacemaker cells of heart
❏ Heart does not undergo atropy, only
hypertropy
❏ Ap duration = 200-300 ms
❏ Longer ARP(ERP)
❏ Includes latent + contraction
period
❏ No tetanus ( no temporal summation)
❏ Longer ARP
❏ No fatigue
❏ Aerobic
❏ No summation
❏ T-tubules on the Z line
❏ Electrical Coupling- calcium-
induced release of Calcium 2+
❏ Phosphorylated phospholamban
❏ Greater Mitochondria
❏ Greater Connective Tissue
❏ Greater increase in tension when
stretched
❏ Lesser connections between the T-
tubules and SR
❏ Not directly connected
❏ DPHR separated from RYR
❏ Electrochemical coupling
❏ Premature Ventricular Contractions
❏ Happens only on relaxation
period of the heart (diastole)
❏ ABNORMAL SYSTOLE =
happens in diastole
❏ Abnormal contraction is
never higher than the
previous normal contractions
❏ Because Heart works
as a functional
syncitium
❏ Why is heart set to be
a functional
syncitium?
❏ Boundaries
offers no
resistance to
impulse flow
PHYSIOLOGIC ANATOMY OF
CARDIAC MUSCLE
Cardiac Muscle as Syncitium
 Intercalated disks
 Cell membranes that separate
individual cardiac muscle
cells from one another
 Cell membranes fuse to form
permeable “ communicating”
junctions called gap junctions
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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

 Allow rapid diffusion ❏ Can generate own action

of ions potentials
 From functional point of view, ❏ Electrical change moving
 Ions move with ease in the towards critical firing level/
ICF along the longitudinal threshold potential→
axes of the cardiac muscle depolarization→ creation of
fibers so that action potentials action potential→ Normal
travel easily from one cardiac negativity achieved through
muscle cell to the next, past repolarization
the intercalated discs ❏ Characteristing of
 Cardiac muscle is a syncitium of conducting tissues
many heat muscle cells in which the ❏ Stretch reflex/ myotatic
cardiac cells are so interconnected ❏ Blood entering the
that when one cell becomes excited, heart→ activation of
the action potential rapidly spreads cardiac muscle
to all of them B. RHYTHMICITY
 Two syncitiums: ❏ Chronotropic
 ATRIAL: walls of two atria C. CONDUCTIVITY
 VENTRICULAR: walls of ❏ Thromotropic
two ventricles D. CONTRACTILITY
❏ Inotropic
V. LENGTH-TENSION E. RELAXATION
RELATIONSHIP BETWEEN ❏ Lucitropic
SKELETAL AND CARDIAC MUSCLE
● Greater total tension in cardiac
Electrical properties:
muscles
a. Excitability (Bathmotropy)
● Cardiac muscles does not undergo
b. Automaticity and Rhythmicity
overstretching (Chronotropy)
c. Conductivity (Dromotropy) 2.
VI. PHYSIOLOGIC PROPERTIES OF Mechanical properties:
THE HEART a. Contractibility (Inotropy): during
SYSTOLE
A. EXCITABILITY b. Distensibility (Lusitopy): during
❏ Bathmotropic DIASTOLE
❏ Even without autonomic
nerves, heart can still
function normally

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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

.
1. EXCITABILITY
ACTION POTENTIALS IN THE
AUTOMATIC FIBERS
● Even wiithout stimulation, they
create their own action potential

● Phase 4: hypopolarizing change;

NON-STEADY
○ Electrical change allowing
the automatic cells to reach
threshold level: CARDIAC
PREPOTENTIAL/ SLOW
DIASTOLIC
DEPOLARIZING CHANGE
■ Happens during
diastole
■ Allows cells to be
depolarized
● Cardiac automatic fibers: uses
Calcium during depolarization;
greater amount of sodium ions going
in:
○ Fast sodium channels are Phase 4 – slow rise in membrane potential and
is unstable. The slow rise in membrane potential
inactivated
is called the pre-potential or slow diastolic
● -40mV : to reach threshold
depolarization. There is more Na leak channels,
● Automatic cells of the heart has membrane potential increases
greater of amount sodium ions Phase 0 – Depolarization. Somewhat inclined,
leaking. depolarization occurs slowly
○ Non steady= continuous Phase 1,2,3 –Repolarization. Inclined, occurs
action of sodium potassium slowly, there is hyperpolarization like in the
pump skeletal muscle  The increase in sodium
leakage and a decrease in the membrane
permeability to potassium will account for the
automaticity of the SA node.

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

NON- AUTOMATIC FIBERS ACTION

POTENTIAL

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon
● Phase 0:
○ Deolarization, straight
line
○ Occurs rapidly due to
opening of fast voltage-
gated Na channels Na
influx then reaches the
threshold voltage of -
60mV resulting to
depolarization  Phase 2: plateau
○ When the membrane
potential reaches -20mV,
it will open up slow, long
lasting voltage-gated
calcium channels
Calcium influx
○ Main factor in
depolarization: Na influx
● Peak of the spike
○ Na channesl close, K
channels open, calcium
channels still open
● Phase 4 : steady RMP
○ In skeletal muscles and
neurons, steady activity
of sodium-potassium
pump  Phase 3: rapid return to normal
○ Rapid repolarization (non
automatic)
■ Utilization of fast ● Phase 4 : steady RMP (-90)
voltage gated
sodium channels
● Phase 1, 2,3
○ Depolarization period in
automatic fibers
○ Phase 1 in non-automatic
fibers:
■ initial period of
repolarization;
■ opening of slow
voltage-gated
potassium
channels that will
allow potassium
influx
■ Minimal change
in electrical
activity
■ Amount of K+
that goes out is
equal to the
amount of calcium
++ that goes in
■ later on, there is
closing of calcium
channels
= leaving only K+
channels open that
will bring about
the final phase of
repolarization
negativity; potassium influx,
final phase of repolarization
○ In skeletal muscles and
neurons, steady activity is
because of sodium-
potassium pump
○ Increase membrane
permeability to potassium
is responsible for -90 mv
RMP
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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

○ Rapid
repolarization (non
automatic)
■ Utilization
of fast
voltage
gated
■ sodium
channels
Phase 0: attributed
to sodium influx
NO Hyperpolarization
■ Although
the K+
channels can
remain open for
a long time,
because of the
plateau, it is
open for a long
period of time
PERIOD OF
REFRACTORINESS

Absolute Refractory Period

○ Involves latent,
contraction, and initial part
of relaxation phase
Automatic Fibers are stimulated first
before Non-automatic fibers
= it is less negative
Normal pace maker: SA NODE

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon
 In Absolute or Effective Refractory
Period (ARP), no amount of
stimulus intensity will be able to re-
excite the membrane of that cell. It
covers the whole of depolarization
until 1/3 of the repolarization phase.
At phase 0, it is absolute refractory
because all the voltage gated sodium
channels are open and it is not able
to re-open the already open sodium
channels. In phases 1 and 2, the Na
channels are already close but it is
still absolute refractory because Na
channels are voltage gated and they
only open at a certain voltage or
membrane potential near the critical
firing level of about -60mv more so
if the membrane potential is at its
resting level. It is far from the CFL.
 In Relative Refractory Period
(RRP), its level is near the critical
firing level and resting level, the
membrane becomes more excitable
so that a stronger than threshold
stimulus can be able to open up the
voltage gated sodium channels and
elicit a second action potential.
 The importance of prolonged
duration of refractoriness is for the
ventricles to be filled with blood
resulting to a more effective
pumping action, no fatigue, no
tetanic contractions. One cannot
elicit successive action potentials or
contractions without tetanic or
sustained contractions in the cardiac
muscle = allow more time for
ventricular filling. The musculature
of the ventricle is thick so when it
contracts, it compresses the coronary
arteries. The coronary arteries supply
blood and oxygen to the cardiac
muscle thus when it is compressed,
there is poor perfusion of cardiac
muscle and less oxygen supply, this
happens if there is tetanic
contractions but in the cardiac
muscle, there are no tetanic
contractions. There is longer period
of relaxation, when the ventriclesare
relaxed, there will be better perfusion
of the cardiac muscle.
 As the membrane potential reaches
the relative refractory period as well
as the RMP, if there is stimulus later
in the RRP, that will open up more
and more voltage gated Na channels
so that its depolarization increases its
amplitude, same thing happens in the
SA node.
TUIZA, Lejanni D.| CMED-1| 2018-2019
 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

2. RHYTHMICITY potential more negative (due

to potassium channels) →
● Chronotrophic
longer interval
● Normal rhythm
○ Because of activity of
Why is excessive increase in heart rate can
automatic fibers
cause death?
○ Decrease / prolong interval in
Rapid heart rate→ no filling → no
generation of of action
output of blood coming from the heart→ no
potential
perfusion of organ systems
■ LESSER
INTERVAL: faster
heart rate →
Medulla Oblongata
TACHYCARDIA
= lower portion of brain stem
= sympathetic
= contains cranial number 10 (vagus nerve)
= Beta 1
= vagus nerve
= will make
- exerts parasympathetic effect on
membrane potential less
the heart; mostly present in the atrial region
negative
(almost none in the ventricle);
= source of
-most are attached to conducting
sympathetic nerves: stellate
tissues (SA and AV node)
ganglion→ render membrane
❏ parasympathetic mostly affects
potetial less negative (-55)-->
acetylcholine-regulated potassium
hypolarize→ more
channels
excitable→ activation of
❏ Decrease heart rate→ affects
automatic fibers→ faster
potassium conductance regulated by
generation of action potential
acetylcholine (N2)→ Inhibit release
of norepinephrine to counteract
■ LONGER:
effects of sympathetics→ decrease
Slower heart rate→
heart rate
BRADYCHARDIA
=parasympathetic
❏ activation of adenyl cyclase→ no
production of cAMP→ no/decrease
Sodium (for
norepinephrine→ decrease of
contractile tissues) and
activity of symphatetics
calcium channels (for
automatic fibers, SA node
❏ When resting, parasympathetic is
)increase→ acts on M2→
more active
hyperpolarize→ -70 mV→
rendering the membrane

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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

● Under normal condition, - from the atrium to the ventricle

cardiac activity is inhibited AV Block- problem in left vagus; longer
by the parasympathetic time in transmitting impulses from the
● Excessive stimulation→ atrium to the ventricle
cardiac arrest

PARASYMPATHETIC
Vagal= connected to the conducting fibers
● Originates in the medulla (nucleus
of atrial side
ambiguus)
Right vagus= controls SA
● Most of the vagal fibers are located
- Greater activity, greater slowing of
near the SAN and AVN
the heart rate
● Affects Ach regulated K+ channels
Left vagus= controls AV node
● Stimulates muscarinic (M2)receptors
- Greater activity, longer interval in
activation of the action potential

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

● Inhibits release of NE(sympathetic

nerves)
● Inhibits activity of the adenylate
cyclase inhibiting production of
cytosolic AMP→ (-) NE
● Predominantly affects cardiac
activity
● Excessive stimulation leads to the
cessation of cardiac activity
● Usually exerting a negative effect
on the cardiac activity

SYMPATHETIC
● Originates in the stellate/ middle
cervical g.
● Distributed to the various cardiac
tissues
● Activates Na+ and Ca2++ channels
● Stimuates B1 receptors
● Could increase HR up to 200-250/
min
● Promotes release of neuropeptide y
(NPY) phospholambdan and troponin-I
● Inhibits releases of Ach ● ACTIVATES A kinase adapter
● Increases cytosolic cAMP→
phosphorylation of some proteins by
PK-A
● PK-A phosphorylates

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

WHY IS THE SN THE HUMAN

CARDIAC PACEMAKER?
● Highest generation of action
potential coming from SN
SAN 70-100
AV 40-60
= if AV is the one that is
controlling, patient has bradycardia (AV
NODAL RHYTHM/ JUNCTIONAL
RHYTHM)
HIS BUNDLE 40
PURKINJE -15-20
SINOATRIAL NODE
Two principle cell types
● Round cells
○ The true pacemaker
● Slender elongated cells
○ Conduct impulses to the
internodal tract
3.CONDUCTIVITY
SINOATRIAL NODE CONDUCTION
○ Posterior
 SA NODE→ALL FIBERS OF ○ Right atrium
ATRIAL MUSCLES THROUGH ● WENCHEBACK
INTERNODAL TRACTS ○ Inter-atrial septum
(BACHMANN, THOREL,  SA node is the pacemaker of the heart
WENCHEBACK)--> ALL and initiates the spread of action
CONVERGING INTO THE AV potentials throughout the atria.
(fibers present are mostly connective  The ends of the sinus nodal fibers
tissue not capable of conducting spread action potentials to the atria
impulses therefore, utilizing AV through:
nodes) i. Directly with
● BACHMANN surrounding atrial
○ Left atrium muscle fibers
(slowest)
● THOREL

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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon
ii. ii. Anterior
Intraarterial band
iii. iii. Internodal
Pathways – anterior
middle or posterior
● It is only the AV node that is
capable of transmitting impulses
coming from the SA node in the
atrium to the ventricle
● Atrium contracts ahead of the
ventricle
AV NODE CONDUCTION
IMPORTANCE OF AV NODAL DELAY
❏ Inactivity of the SAN and AVN for
about 5-20 seconds leads to
spontaneous activation of other
pacemaker cells→ “ ventricular
escape”
❏ Essential so that atrium will contract
first before the ventricle
❏ Diameter of fibers in purkinje fibers
are very small→ greater resistance in
impulse flow
❏ Diameter of AV node→ lesser
resistance
❏ Intraventricular septum- part of
ventricle that is first stimulated
❏ Left side first
❏ Straighter branch of bundle
of his= faster
❏ AV node = slowest
❏ Theoretically, conductance
speed of AV is just as equal
as of the SV
❏ PURKINJE FIBERS= fastest
❏ Diameter is small
The spread of cardiac impulse from atria into
the ventricles is delayed (PHYSIOLOGIC
DELAY)
– to allow time for the atria to empty their blood
into the ventricles before ventricular contraction
begins. (ventricular filling)
• A special pathway, the anterior interatrial
myocardial band (Bachmann’s Bundle),
conducts the SA node directly to the left atrium
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 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

. • The wave of excitation ultimately reaches the

AV node, which is normally the sole entry route
of the cardiac impulse to the ventricles.

Regions of AV node:
1. Atrial-nodal (AN)
= transitional cells
=contains pacemaker cells
2. Nodal (N)
= consisting of round P cells
=Contains pacemaker cells
=responsible for delay
3. Nodal-His (NH)
= transitional cells , contains pacemaker cells

4. CONTRACTILITY

● Diad arrangement of SR and T-

tubules
● SR not much developed
○ Can use calcium from ECF
● Maintains amount of calcium in the
cytosol= activity of sodium-
potassium exchange pump
(countertransport)
● Na-K inhibitor
○ Enhance force of cardiac
contraction
○ Blocks sodium-potasium
atpase
○ Calcium remains inside
○ Lidoxin

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

TUIZA, Lejanni D.| CMED-1| 2018-2019

 Electrical Properties of the Heart PHYSIOLOGY
Dr. Barbon

5. RELAXATION

VII. CARDIAC MUSCLE HYPERTROPY

Major factor affecting coronary perfusion is
CHRONIC PRESSURE OVERLOAD myocardial
❏ AFTERLOAD
❏ Concentric ventricular hypertropy What period of cardiac activity is there
❏ Usually affects the left ventricle greater perfusion of the cardiac tissues?
❏ Thickening of the ventricular wall
due to an increased workload = DIASTOLE
(increased TPR aortic pressure
[afterload])

CARDIAC VOLUME OVERLOAD

❏ dilated (eccetric) ventricular
hypertropy

TUIZA, Lejanni D.| CMED-1| 2018-2019