2nd Lecture on Heart Physiology by Dr. Roomi

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April 18, 2012 1

BY

DR. MUDASSAR ALI ROOMI (MBBS, M.PHIL)


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1-Automaticity and rhythmicity(autorhythmicity):

2:Conductivity

3-Contractility:

4-Excitability

5- All or none Law

6-Reractory period

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Frank-Starling mechanism of the heartcotraction: greater the heart muscle isstretched during diastolic filling (more initial

or end diastolic length), the greater is the forceof contraction and the greater is the quantity ofblood pumped into the aorta(withinPhysiologic limits).

Frank starling Law is applied to eachindividual skeletal muscle fiber but on heart asa whole.

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Excitability is the property to respond to stimuli.

Stimuli: nervous, chemical, mechanical, electrical.

This property enables the heart muscles to respondto artificial pacemaker.***

The Nerves, drugs, ions and ischemia affect the

excitability of cardiac muscles.

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Each fiber contracts to its maximum or not atall in response to a threshold stimulus.

Obeyed by each skeletal muscle fiber

individually but by heart muscle as a wholebecause heart is a functional syncitium. ***

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DEFINITION: it is the interval during which anormal cardiac impulse cannot re-excite analready excited area of cardiac muscle. (0.30-0.35

sec) Absolute refractory period: It is the period

during which already excited cardiac muscle doesnot respond to a second stimulus. (0.25-0.30 sec)**

Relative refractory period: It is the period duringwhich already excited cardiac muscle givesresponse to a powerful excitatory stimulus. (0.05

sec)**April 18, 2012 8


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The normal refractory period of the ventricle isalmost equal to the duration of plateau phaseof action potential. ****

The refractory period of atrial muscle (0.15 sec)is much shorter than that of the ventricles (0.25

to 0.30 sec).

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During relative refractoryperiod earlyprematurecontraction may occur

if heart is stimulated bya strong stimulus.

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It is due to plateau inaction potential ofcardiac muscle

because plateauincreases therefractory period.

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TETANIZATION SEEN INSKELETAL MUSCLE


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Ventricular Muscle Action Potential

-100

-80

-40

-60

+20

0

-20

2 3 40 1

MembranePotential

(mV

)

Seconds

Fast Na+

Channels Open

Slow Ca++

Channels Open

0

1

2

3

4

K+ Channels

Open

phase 0- Fast Na+ channels open then slow Ca++ channelsphase 1- K+ channels openphase 2- Ca++ channels open morephase 3- K+ channels open morephase 4- Resting membrane potential

K+ Channels

Open More

Ca++ Channels

Open More

Copyright 2006 by Elsevier, Inc.April 18, 2012 13


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Resting membranepotential of the SAnodal fiber is -55 to -60mvolts.

The cause of this lessernegativity is that thecell membranes of thesinus fibers are

naturally leaky to Na+and Ca++ ions andentry of these ionsneutralize much of theintracellular negativity.

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-100

-80

-40

-60

+20

0

-20

2 3 40 1

Seconds

Mem

branePotential(mV)

Threshold

Sinus Nodal

Fiber

Na+

Leak

Slow Ca++Channels Open

K+ Channels

Open more

Ventricular

Muscle fiber

Rhythmical Discharge of Sinus Nodal Fiber

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At -55 mvolts, the fast Na+channels becomeinactivated.

Therefore, only the slowsodium-calcium channelscan open and cause theaction potential.

As a result, the SA nodal

action potential is slower todevelop than the that of theventricular muscle.

Therefore, the inherentleakiness of the sinusnodal

fibers to Na+ and Ca++ ionscauses their self

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2nd Lecture on Heart Physiology by Dr. Roomi

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