Properties of Myocardium Lecture - MBBS & Physiology LecturesProperties of Myocardium Lecture - MBBS & Physiology Lectures

Properties of Myocardium slideshow

  • Striations
  • Involuntary
  • Gap junctions
  • Function as syncytium
  • Excitability*
  • Refractory period*
  • Contractility*
  • Autorhythmicity*
  • Conductivity*

Properties of Myocardium


•Excitability (Bathmotropicaction)

•Auto rhythmicity

•Conductivity (Dromotropicaction)


•Contractility (Inotropic action)

•Refractory period

•Staircase / treppeeffect

•Gap junctions
•Function as syncytium
•Refractory period


•Excitabilityis the ability of acardiaccell to generate an action potential at its membrane in response to depolarization(stimulated) and to transmit an impulse along the membrane.
•Velocity of conduction
•In atrial and ventricular muscles —0.3 to 0.5 m/sec
•In purkinjefibers —4m/sec

Action Potential

•Action potential with plateau
•Atrial muscles
•Ventricular muscles
•Bundle of HIS
•Purkinje Fibers
•Action potential without plateau
•SA node
•AV node

Resting Membrane Potential

•It is the potential difference across the cell membrane at rest
•It is negative inside with respect to outside

Action Potential

•Action Potential with Plateau
•Phase 0
•Phase 1
•Phase 2
•Phase 3
•Phase 4

Action Potential with Plateau

•Five phases
•Phase 0
•Opening of voltage gated sodium channels
•Sudden influx of sodium ions
•Phase 1 (early repolarization)
•Closure of voltage gated sodium channels
•Outfluxof potassium ions under electrochemical gradient

Action Potential with Plateau

•Phase 2 (Plateau)
•Opening of voltage gated calcium channels(L-type)
•Influx of sodium and calcium ions
•Outfluxof potassium ions under electrochemical gradient
•Phase 3 (Repolarization)
•Closure of voltage gated calcium channels
•Opening of voltage gated potassium channels

•Phase 4 (Resting membrane potential)
•Stable resting membrane potential
•-85 to -90 mV
•Mainly determined by potassium ions

Properties of Myocardium

•Gap junctions
•Function as syncytium
•Refractory period

Refractory Period

•Duration of total refractory period almost the duration of action potential

•Absolutely Refractory Period
•Period during 2ndaction potential cannot be generated
•Comprises of phase 0,1,2 and about half of phase 3 (until voltage is about -50mV)
•Duration 250 to 300 msec
•Inactivation of voltage gated sodium channels
•Closure of inactivation gates

•Relative Refractory Period
•Period during 2ndaction potential can be generated but with a stronger stimulus
•From absolute refractory period to the voltage reaching resting level
•Duration 50msec
•Some voltage gated sodium channels are reset
•Potassium efflux continues

Significance of refractory period
•Heart muscle cannot be tetanized
•Long refractory period almost approaches duration of muscle twitch (~300ms)
•Determines heart rate
•About 170 to 240 per minute
•Due to refractory period of AV node (250 to 350 msec)
•Due to long refractory period, already stimulated area can not be stimulated
•Prevent reentry and arrythmias

•Long refractory period (250 msec) compared to skeletal muscle (3msec)
•During this period membrane is refractory to further stimulation until contraction is over.
•Prevents tetanization
•Gives time to heart to relax after each contract ion, prevent fatigue
•It allows time for the heart chambers to fill during diastole before next contraction
•During refractory period threshold for the stimulus is increased

Properties of Myocardium

•Gap junctions
•Function as syncytium
•Refractory period


•Definition: ability of cardiac muscle to contract in response to stimulation
•All Or None Law
•The response to a threshold stimulus is maximal. If the stimulus is below threshold there is no response provided the physiological conditions remain constant
•The cardiac muscle follows the all or none law as a whole.
•In the case of skeletal muscle, all-or-none law is applicable only to a single muscle fiber

Treppeor Stair-case Phenomenon

•When stimuli of same strength are applied at short intervals, an increase in the height of contraction is observed.
•This is due to the BENEFICIAL EFFECT -increase in the level of calcium ions.


Ability of cardiac muscle to contract
•Excitation contraction coupling
•Process by which action potential on sarcolemma reach cardiomyocytes
•Role of T tubules
•Role of calcium ions
•Role of actin and myosin filament

•Calcium induced calcium release—process whereby calcium can trigger release of further calcium from the muscle sarcoplasmic reticulum.
•DHP receptors
•Ryanodine receptors
•Decreased calcium from T tubule—strength of muscle contraction
•More developed T tubules as compare to skeletal muscle
•Diameter 5 times more
•Electronegative inside —binds ample amount of calcium
•Duration of action potential
•Atrial muscle —0.2sec
•Ventricular muscle —0.3sec

Excitation Contraction Coupling


•Cardiac output is the quantity of blood pumped into the aorta each minute by the heart. This is also the quantity of blood that flows through the circulation
•Stroke Volume Amount of blood pumped out of each ventricle per beat; also called ‘Systolic discharge
•Venous return is the quantity of blood flowing from the veins into the right atrium each minute.

Frank Starling Law

By venous return:
•Force of contraction of a muscle fiber is proportional to its initial length .It is known as Starling’s law of muscle contraction

Auto rhythmicity

•Definition: the ability of the heart to initiate its beat continuously and regularly without external stimulation
•Automaticity is the ability of certain cells of the heart to regularly depolarize without an external stimulus telling them to do so
•Myogenic (independent of nerve supply)

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