HEART PHYSIOLOGY RHYTHMICAL EXCITATION OF HEART

By Dr. Mudassar Ali Roomi (M.B;B.S, M.PHIL.)

CONDUCTION SYSTEM OF HEART

SA node Internodal pathways AV node AV bundle of His Right and left bundle branches Purkinje fibers

Conduction System of the Heart

SA node: sinoatrial node. The pacemaker.
Specialized cardiac muscle cells. Generate spontaneous action potentials (autorhythmic tissue). Action potentials pass to atrial muscle cells and to the AV node Action potentials conducted more slowly here than in any other part of system. Ensures ventricles receive signal to contract after atria have contracted

AV node: atrioventricular node.

AV bundle: passes through hole in cardiac C.T. skeleton to reach interventricular septum Right and left bundle branches: extend beneath endocardium to apices of right and left ventricles Purkinje fibers:
Large diameter cardiac muscle cells with few myofibrils. Many gap junctions. Conduct action potential to ventricular muscle cells (myocardium) very rapidly

SA nodal action potential

Resting membrane potential of the SA nodal fiber is -55 to -60 mvolts. The cause of this lesser negativity is that the cell membranes of the sinus fibers are naturally leaky to Na+ and Ca++ ions and entry of these ions neutralize much of the intracellular negativity.
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SA NODAL AND VENTRICULAR MUSCLE ACTION POTENTIALUS NODAL FIBER

Sinus Nodal Fiber Slow Ca++ Channels Open

+20

K+ Channels Open more

Threshold

Ventricular Muscle fiber

Membrane Potential (mV)

0 -20 -40 -60 -80 -100 0

Na+ Leak

2 Seconds

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SA nodal action potential

At -55 mvolts, the fast Na+ channels become inactivated. Therefore, only the slow sodiumcalcium channels can open and cause the depolarization. As a result, the SA nodal action potential is slower to develop than the that of the ventricular muscle. Therefore, the inherent leakiness of the sinusnodal fibers to Na+ and Ca++ ions causes their selfexcitation.******* The slowly drifting resting membrane potential which reaches to threshold by itself is also called as pre-potential or pacemaker potential. The early part of the prepotential is because of June 4, 2012

SA nodal action potential

Note: There is no phase 1 and 2 in the action potential of SA nodal fibers.

THE MECHANISM OF PRE POTENTIAL SLOPE:

SA Nodal fibers membrane is naturally more leaky to sodium and calcium As soon as the membrane potential reaches to the Resting value, the membrane becomes immediately less permeable to potassium. This allows the negativity of membrane potential to decrease towards the threshold of excitation The last of portion of pre potential is due to activation of (transient) T Type of slow calcium sodium channels. At -40 mV there is opening of L- type of calcium sodium channels.
L = Transient Type T= Lasting type

WHAT DETERMINES THE HEART RATE?

Slope of pre potential determines the heart rate. More steep- increased heart rate. Less steep- decreased heart rate. On sympathetic stimulation, there is increase in heart rate. Norepinephrine released from sympathetic fibers, increases the permeability of SA nodal fibers membrane to sodium and calcium. On vagal stimulation there is slowing of heart rate. There is release of acetylcholine which acts on SA nodal fibers to increase its permeability for potassium. Which causes hyperpolarization and less steep of prepotential.

Rate of impulse generation in heart:

SA NODE: 70-80/min AV NODE: 40-60/min AV BUNDLE,BRANCHES & VENTRICLES: 1540/min SA NODEPACEMAKER OTHERS ECTOPIC FOCI

AV Node, and Delay of Impulse Conduction from the Atria to the Ventricles
Location of the A-V node: in the posterior wall of the right atrium immediately behind the tricuspid valve there is a delay of 0.09 second in the A-V node A delay of another 0.04 second occurs mainly in A-V bundle Thus, the total delay in the A-V nodal and A-V bundle system is about 0.13 second.

AV Node, and Delay of Impulse Conduction from the Atria to the Ventricles
Cause of the Slow Conduction: caused mainly by diminished numbers of gap junctions b/w successive cells in the conducting pathways Importance of AV nodal delay: this delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins One-Way Conduction Through the A-V Bundle?

Rapid Transmission in the Ventricular Purkinje System

They are very large fibers, even larger than the normal ventricular muscle fibers and they transmit action potentials at a velocity of 1.5 to 4.0 m/sec, a velocity about 6 times that in the usual ventricular muscle and 150 times that in some of the A-V nodal fibers. Cause of rapid transmission: The rapid transmission of action potentials by Purkinje fibers is believed to be caused by a very high level of permeability of the gap junctions at the intercalated discs between the successive cells that make up the Purkinje fibers. FUNCTION: rapid transmission in Purkinje fibers is responsible for synchronous contraction of ventricular muscle.

SUMMARY OF SPREAD OF THE CARDIAC IMPULSE THROUGH THE HERAT

Conduction velocities of heart tissues: ATRIAL MUSCLE= 0.3m/sec INTERNODAL PATHWAYS= 1m/sec AV NODE: slowest 0.050.1m/sec AV BUNDLE & BRANCHES/PURKINJE SYSTEM: Maximum velocity= 1.54m/sec VENTRICULAR MUSCLE= 0.5m/sec

ECTOPIC PACEMAKER OF HEART

Normal pacemaker of heart? Ectopic pacemaker? Causes of ectopic pacemaker of heart? 1. Excessive excitability of some part of the heart other than SA node 2. Heart blocks Stokes adams syndrome? Mechanism of stokes adams syndrome ???

Effect Of Sympathetic And Parasympathetic Stimulation On Heart???

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Sympathetic Effects on Heart

Releases norepinephrine at sympathetic ending Causes increased sinus node discharge with HR upto180-200 (+ve chronotropic effect) Norepinephrine increases the permeability of SA nodal fibers to sodium and calcium which increases the slope of the prepotential. Increases rate of conduction of impulse (+ve dromotropic effect) Increases force of contraction in atria and ventricles (+ve inotropic effect) Increased excitability of heart (+ve bathmotropic effect)

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Parasympathetic Effects on Heart

Parasympathetic (vagal) nerves, which release acetylcholine at their endings, innervate SA node and A-V junctional fibers proximal to A-V node. Mechanism: Causes hyperpolarization because of increased K+ permeability in response to acetylcholine. This causes decreased transmission of impulses (-ve dromotropic effect) may be temporarily stopping heart rate. Decreased heart rate by decreasing the frequency of impulse generation (-ve chronotropic effect) Minimal decrease of force of contraction. decreased excitability of heart (-ve bathmotropic effect)
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