Cardiac Physiology

Ikhlas M. Jenie
 Contents
 Cardiac muscle
 Cardiac cycle
 Function of valves
 Cardiac sounds
 Regulation of heart function
 Contents (cont.)
 Rhythmical excitation
 Conduction of cardiac impulse
 Regulation of excitation and conduction
 Introduction

Factors needed for proper circulation

1.A rhythmically beating heart to generate the
necessary pressure.
2.A proper condition of the blood vessels.
3.An adequate amount of circulating blood.
4.A mechanism for ensuring unidirectional flow -- >
valves
 HEART
 Heart is a part of cardiovascular system
 Main function : to pump blood -- > to circulate
along vessels -- > circulation system
 To transport
 Water
HOMEOSTASIS
 Oxygen
 Nutrition
 Metabolic
products
 Hormones
 Drugs
 HEART
 Lies in mediastinum
 2/3 -- > left side from midline
 Sternum at front
 Columna vertebralis at back
 Lungs besides
 Diaphragm at bottom
 HEART
 Contain : 4 chambers
2 atria (R atrium & L atrium)
 2 ventricles (R ventricle & L ventricle)
 Length 12 cm, wide 6 cm, weight 300 gr

 Position : cone
 Apex at bottom -- > L ventricle
 Basis on top -- > L atrium
 HEART
 Endocardium
 Endothelial cells
 Myocardium
 Cardiac muscle
 Specialized excitation & conduction system

 Epicardium
 Pericardium serosa pars viseralis
 Pericardium
 Serous pericardium
 Viseralis -- > epicardium
Pericardial space
 Parietalis

 Fibrous pericardium -- > to prevents

cardiac overstretching
 At bottom : attach the heart to diaphragm
 At top : continuous with blood vessels
 Besides : contacts with pleura parietal
 Cardiac muscle
 Muscle fibers
 Myofibrils
 Myofilaments
 Actin
 Myosin
 Cardiac Muscle
 Atrial muscle
 Ventricular muscle
 Specialized excitatory and conductive
muscle fibers
 Cardiac Muscle
 Atrial muscle
 Ventricular muscle
 Specialized excitatory and conductive
muscle fibers
 Cardiac Muscle
 Latticework arrangement
 Striated : actin & myosin filaments
 Intercalated disc : gap junction -- >
syncytium
 Atrialsyncytium
 Ventricular syncytium
Action Potentials in Cardiac Muscle
 Resting value = -85 mV
 Peak = +20 mV
 So, the AP = 105 mV
 Plateau 0.2 sec.
 Abrupt repolarization
Action Potentials in Cardiac Muscle
in the Ventricle
Action Potentials in Cardiac Muscle
 Fast sodium channels -- > AP
 Calcium-sodium channels -- > Plateau
 Decreased permeability of potassium ion
immediately after the onset of AP and
during calcium influx -- > Plateau
 Velocity of Conduction of AP
 In cardiac muscle = 0.3-0.5 m/sec.
 In Purkinje fibers = 4 m/sec
Refractory Period of Cardiac Muscle
 Interval of time during which a normal
cardiac impulse cannot re-excite cardiac
muscle = 0.25-0.3 sec. in ventricle

Duration of
plateau

 In atrium = 0.15 sec.

 Relative Refractory Period of
Cardiac Muscle
 Cardiac muscle is more difficult than
normal to excite but can be excited by
very strong stimulus = 0.05 sec.
 Excitation-Contraction Coupling
 How AP causes muscle contraction

Calcium ions
 Excitation-Contraction Coupling
 Source of Calcium ions in cardiac muscle
 Sarcoplasmic tubules
T tubules depends on calcium
concentration in the
extracellular
space
 Duration of contraction
 Atrial muscle = 0.2 second
 Ventricular muscle = 0.3 sec
 Cardiac Cycle
 The cardiac events that occur from the
beginning of one heartbeat to the
beginning of the next heartbeat
 AP in the sinus node

 Atrial impulse -- > atrial contraction 1/6 sec. earlier

AV delay Primer pump

 Ventricular impulse -- > ventricle contraction
 Cardiac Cycle
 Diastole : period of relaxation

Blood fills the heart

 Systole : period of contraction

Relationship of ECG to Cardiac Cycle
 P wave -- > spread of atrial depolarization
 QRS wave -- > ventricular depolarization
 T wave -- > ventricular repolarization
 Atrium as a Primer Pump
 Blood flows to the atrium
 Continuously from great veins into the atria
 Blood flows to the ventricle
 80% before the atrium contracts
 20% forced by atrial contraction
 Filling of the Ventricle
 Ventricular systole -- > AV valve closes --
> blood accumulate in atrium
 Ventricular diastole -- > ventricular
pressure drops -- > AV valve opens -- >
rapid filling of the ventricle
 Ventricular Diastole
 First third of diastole -- > rapid filling of
the ventricle
 Middle third of diastole -- > continuous
blood flow
from atrium
 Last third of diastole -- > atrial contraction
 Ventricular Systole
 Isovolumic (isometric) contraction
 Ejection
 Isovolumic (isometric) relaxation
 Ventricular Systole
 Isovolumic (isometric) contraction
 Ejection
 Isovolumic (isometric) relaxation
 Ventricular Systole
 Isovolumic (isometric) contraction
 Ejection
 Isovolumic (isometric) relaxation
Isovolumic (isometric) contraction
 Tension in the ventricular muscle increases
--> ventricular pressure begins to rise

 AV valve closes, semilunar valve still not

opens

 Ventricular pressure continue to rise

Isovolumic (isometric) contraction
 Tension in the ventricular muscle increases
--> ventricular pressure begins to rise

 AV valve closes, semilunar valve still not

opens

 Ventricular pressure continue to rise

Duration = 0.02 – 0.03 sec.
 Ejection
 Ventricular pressure
> 80 mmHg (left ventricle)
> 8 mmHg (right ventricle)

 Semilunar valve opens

 Blood begins to pour out of ventricle

 Ejection
 RAPID EJECTION
 70% of blood is emptied in the first third of
period of ejection
 SLOW EJECTION
 30% of blood is emptied in the next two third
of period of ejection
 Ejection
 RAPID EJECTION
 70% of blood is emptied in the first third of
period of ejection
 SLOW EJECTION
 30% of blood is emptied in the next two third
of period of ejection
Isovolumic (isometric) relaxation
 Ventricular relaxation begins suddenly -- >
intraventricular pressure decreases rapidly
 Elevated pressure in the distended aorta
and pulmonary artery -- > pushes blood
back to the ventricles -- > closes
semilunar valves
 Ventricular muscle continue to relax

Duration = 0.03 – 0.06 sec.

 End-diastolic volume (EDV)
 Stroke volume (SV)
 End-systolic volume (ESV)
 Ejection fraction (EF)
 End-diastolic volume (EDV)
 Normal filling of ventricle = 110-120 ml
 Stroke volume (SV)
 Ejection volume = 70 ml
 End-systolic volume (ESV)
 Remaining volume after ejection = 40-50 ml
 Ejection fraction (EF)
 SV = 60%
EDV
 End-diastolic volume (EDV)
 Normal filling of ventricle = 110-120 ml
 Stroke volume (SV)
 Ejection volume = 70 ml
 End-systolic volume (ESV)
 Remaining volume after ejection = 40-50 ml
 Ejection fraction (EF)
 SV = 60%
EDV
 End-diastolic volume (EDV)
 Normal filling of ventricle = 110-120 ml
 Stroke volume (SV)
 Ejection volume = 70 ml
 End-systolic volume (ESV)
 Remaining volume after ejection = 40-50 ml
 Ejection fraction (EF)
 SV = 60%
EDV
 End-diastolic volume (EDV)
 Normal filling of ventricle = 110-120 ml
 Stroke volume (SV)
 Ejection volume = 70 ml
 End-systolic volume (ESV)
 Remaining volume after ejection = 40-50 ml
 Ejection fraction (EF)
 SV = 60%
EDV
 Heart Valves
 AV valves
 Tricuspid valve
 Mitral valve

 Semilunar valves
 Aorticvalve
 Semilunar valve
 Function of valves
 AV valve -- > prevent backflow of blood
from ventricle to atrium
during ….
 Semilunar valve -- > prevent backflow of
blood from great
arteries (aorta &
pulmonary artery)
to ventricle during …
 Function of valves
 Heart valves close and open passively
 Backward pressure gradient pushes blood
backward -- > valve closes
 AV valves are thin -- > request almost no backflow
 Semilunar valves are heavier -- > rapid backflow

 Forward pressure gradient forces blood

forward -- > valve opens
AV valves
 Thinner -- > softer
backward gradient pressure
 Supported by chordae
tendinae
Semilunar valves
 Heavier -- > greater
backward gradient
pressure -- > rapid closure
 Smaller openings -- >
greater blood velocity
 Subjected to much greater
mechanical abrasion
 Supported by pliable
fibrous tissue
 Function of valves
 Papillary muscle
 It attaches to the AV valves by chordae
tendineae
 It contracts when ventricle contracts
 Its function : prevent AV valves to bulge too
far backward toward atrium during systole
 Heart Sounds
 Produced when cardiac valves close
 “lub dub, lub dub, …”
 First heart sound
 Longer but lower pitch
 Closure of A-V valve
 Sistolic sound

 Second heart sound

 Shorter duration, sharper, and higher pitch
 Closure of semilunar valves
 Diastolic sound
 Heart Sound
 Third heart sound -- > Protodiastolic gallop
 Fourth heart sound -- > Presistolic galloop
Summation Gallop

Bunyi jantung ketiga dan keempat -- >

gallop sumasi
 Heart Sound
1. Mitral component (M1)
Tricuspid component (T1)
2. Aortic component (A2)
Pulmonary component (P2)
3. Physiologic
Pathologic
4. Pathologic
Origin
Mitral valve closure
Tricuspid valve closure
Aortic valve closure
Pulmonary valve closure
Rapid LV filling
Ventricular wall vibrations
Enhanced atrial systole
 Regulation of Heart Pumping
 Intrinsic -- > Frank-Starling mechanism
 Extrinsic -- > Autonomic nervous system
 Frank-Starling Mechanism
 Intrinsic ability of the heart to adapt to
increasing volumes of inflowing blood

 The greater the heart muscle is stretched

during filling, the greater is the force of
contraction and the greater the quantity of
blood pumped into the aorta
 Frank-Starling Mechanism
 The amount of blood pumped by the heart
each minute is determined almost entirely
by the rate of blood flow into the heart
from the veins (venous return)

 Thus, within physiologic limits, the heart

pumps all the blood that returns to it by
the way of the veins
 Frank-Starling Mechanism
 Metabolism of each peripheral tissue

 Local blood flow

 Venous return

 Stroke volume
Ventricular Volume Output Curves
 Autonomic Nervous System
Control to the Heart
 Sympathetic nervous system : increases
output of the heart
 Parasympathetic nervous system (vagal) :
decreases output of the heart
 Autonomic Nervous System
Control to the Heart
 Sympathetic nervous system : increases
output of the heart
 Parasympathetic nervous system (vagal) :
decreases output of the heart
Cardiac Sympathetic and
Parasympathetic Nerves
 Sympathetic Activity to The Heart

 Normal condition -- > Sympathetic tone to

the heart
 Sympathetic stimulation :
 Heart rate
Output of the heart
 Cardiac contraction

 Inhibition of sympathetic activity :

 Heart rate Output of the heart
 Cardiac contraction
30%
Parasympathetic Activity to the Heart
 Distribution of cardiac vagal nerves -- >
mainly to atrium, not much to ventricle
 Vagal stimulation :
 Great decrease in heart rate
 Slight decrease in heart contraction

Decrease ventricular pumping

50%
Effect of Sympathetic or Parasympathetic
Stimulation on the Output of the Heart
 Effect of Potassium Ions

 Excess potassium (K+):

 Weakness of the heart
 Abnormal rhythm
 The heart dilates & becomes flaccid
 Heart rate slows
 A-V block
 Effect of Calcium Ions
 Excess :
 Cardiac spastic contraction
 Deficient :
 Cardiac flaccidity
 Effect of Temperature
 Increased temperature :
 Fever -- > Heart rate -- > cardiac weakness
 Decreased temperature :
 Hypothermia -- > Heart rate
Increasing the Arterial Pressure Load
(up to a Limit) does not Decrease
Output of the Heart
 Specialized Excitatory and
Conductive System of the Heart
 Sinus node (sinoatrial or S-A node)
 Generation normal rhythmical impulse
 Internodal pathways
 Conduct impulse from sinus node to A-V node
 A-V node
 Impulse form atrium is delayed before passing to
ventricle
 A-V bundle
 Conducts impluse from atrium to ventricle
 L & R bundle branches of Purkinje fibers
 Conduct cardiac impulse to all parts of ventricle
 Specialized Excitatory and
Conductive System of the Heart
 Sinus Node
 Small, flattened, ellipsoid
 3 mm wide, 15 mm long, 1 mm thick
 Located in superior posterolateral wall of
right atrium
 Belowand lateral to the opening of superior
vena cava
 Has no contractile filaments
 Connects directly with atrial muscle fibers
 Sinus Nodal Rhythmicity
 Resting membrane potential (RMP) = -55
to -60 mv < -- cell membrane is leaky to
sodium and calcium ions
 Fast sodium channels close (inactivated)
 Sodium influx -- > membrane potential
gradually rises -- > to reach threshold =
40 mv -- > slow sodium-calcium channels
open -- > slower action potential
 Sinus Nodal Rhythmicity
 After 100-150 msec. after its opening,
sodium-calcium channels close –
furthermore, potassium ion channels open
-- > efflux of potassium ion -- >
repolarization
 Channels of potassium ion open quite long
-- > prolonged efflux of positive ions ->
hyperpolarization
Rhythmical Discharge of
a Sinus Nodal Fiber
 Internodal pathways
 Connect directly with atrial muscle -- >
action potential from sinus node travels to
atrial muscle and A-V node
 Velocity of conduction AP in atrial muscle =
0.3 m/sec.
 Velocity of conduction AP in small bands of
atrial fibers = 1 m/sec.
 Anteriorinteratrial band -- > passes through
anterior walls of right atrium to left atrium
 Internodal pathways
 Small bands curve through corresponding
atrial walls and terminate in A-V node
 Anterior internodal pathways
 Middle internodal pathways
 Posterior internodal pathways

 Velocity of conduction of AP is fast, like as

in anterior interatrial band ( 1 m/sec.)
 A-V Node
 Location : posterior wall of RA behind
tricuspid valve
 Event : conductive delay
 Cause : diminished gap junction
 Reason : to allow time for atrium to empty
its blood into ventricle before ventricular
contraction
 Intervals of Time
 Sinus node – A-V node = 0.03 sec.
 Delay in A-V node = 0.09 sec.
 Penetrating A-V bundle = 0.04 sec.
(before initial bundle
branches)

Total = 0.16 secs.

Organization of A-V Node
Prevention of Cardiac Impulse Re-
entry from Ventricle to Atrium
1. One-way Conduction through A-V Bundle
 SPECIAL characteristics of A-V bundle :
inability of AP to travel backward from
ventricle to atrium
2. Atrioventricular fibrous tissue
 INSULATOR
 Purkinje System
 From A-V node to ventricle through A-V
bundle
 Very large fibers
 Velocity of AP transmission = 1.5 - 4
m/sec.
 High level of permeability of gap junction
 L & R Bundle Branches
 Distal portion of A-V bundle -- > passes downward
ventricular septum for 5-15 mm -- > toward apex
of the heart
 It divides into L & R bundle branches
 Lie beneath endocardium on two respective sides of
ventricular septum
 Spreads downward toward the apex
 Dividing into smaller branches
 Course sideways around ventricular chambers
 Penetrate about 1/3 the way into mucle mass
 Finally become continues with cardiac muscle fibers
 Then back toward base of the heart
 Transmission Cardiac Impulse in
Ventricular Muscle
 Velocity = 0.3-0.5 m/sec.
 Double spiral, with fibrous septa between
spiraling layers -- > angulate from
endocardial to epicardial
 Duration = 0.03 sec.
 Intervals of Time
 From
 Bundle branches-Purkinje fibers = 0.03 sec.
 Purkinje fibers-ventricular muscle = 0.03 sec.
Total = 0.03 + 0.03 = 0.06 sec
 Total Interval Time
 Sinus node – A-V node = 0.03 sec.
 Delay in A-V node = 0.09 sec.
 Penetrating A-V bundle = 0.04 sec.
 Bundle branches-Purkinje fibers = 0.03 sec.
 Purkinje fibers-ventricular muscle= 0.03 sec.
_____________________________________
 TOTAL = 0.22 sec.
Transmission of Cardiac Impulse
to the Heart
 Control of Excitation &
Conduction in the Heart
 Intrinsic rhythmical rate
 Sinus node : 70-80x/min.Pacemaker
 A-V node : 40-60 x/min.
 Purkinje fibers : 15-40 x/min.
 Ectopic pacemaker
 Develop a rhythmical discharge rate > sinus
node
 A-V node
 Purkinje fibers
 Atrial muscle
 Ventricular muscle
 Can cause
 Abnormal sequence of cardiac contraction
 Debility of heart pumping
 Ectopic pacemaker
 Caused by:
 Transmission blockage

 A-V block

 Stoke-Adams syndrome
 Control of Heart Rhythmicity &
Impulse Conduction
 Parasympathetic nerve (vagus)
 Mainly innervates : SA node & A-V node
 Lesser extent : atrial muscle
 Little to : ventricular muscle
 Sympathetic nerve
 To all parts of the heart
 Strong representation to ventricular muscle
 Parasympathetic (vagal)
Stimulation
 Parasympathetic (vagal) Stimulation -- >
ACETYLCHOLINE (Ach)
 Decreases rate of sinus node rhythm
 Decreases excitability of A-V junctional fibers
-- > slowing transmission to ventricle
 Parasympathetic (vagal)
Stimulation
 Weak - moderate stimulation
 decrease rate of heart pumping (half)
 Strong stimulation
 stop sinus node
 block A-V node ventricle stop pumping
15-20”

ventricular escape
(15-40x/min)
 Parasympathetic (vagal)
Stimulation
 Mechanism
 Ach -- > increases permeability of potassium
ions -- > efflux of K+ -- > increases negativity
inside cardiac cell -- > hyperpolarization -- >
less excitable
 In sinus node
 RMPis more negative -- > -65 to -75 mV -- >
much longer time to reach threshold potential
 Parasympathetic (vagal)
Stimulation
 Mechanism (contd..)
 In A-V node
 more difficult to be excited

 Safety factor is decreased

moderate large decrease

delays conduction blocks conduction

 Sympathetic Stimulation
 To cause :
1. Increases rate of sinus nodal discharge
2. Increases rate of conduction and excitability
in all parts
3. Increases of contraction

 Increases activity of heart

 Sympathetic Stimulation
 Mechanism :
 Sympathetic stimulation

 Norepinephrine (NE)

1. Sinus node
2. A-V node & A-V bundle
3. Cardiac muscle
 Sympathetic Stimulation
1. Sinus node
 Sodium-calcium permeability increases -- > RMP is more positive -- >
sinus node is more excitable -- > HR increases
2. A-V node & A-V bundle
 Sodium-calcium permeability increases -- > conduction time decreases
3. Cardiac muscle
 Calcium concentration intracellular increases -- > contraction increases

 Maximal stimulation
 HR increases 3x
 Cardiac contraction increases 2x