2nd lecture-on-heart-physio-dr-roomi

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BY

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

HEART PHYSIOLOGY

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• Frank-Starling mechanism of the heart cotraction: greater the heart muscle is stretched during diastolic filling (more initial or end diastolic length), the greater is the force of contraction and the greater is the quantity of blood pumped into the aorta (within Physiologic limits).

• Frank starling Law is applied to each individual skeletal muscle fiber but on heart as a whole.

3-CONTRACTILITY (CONT..)

Cardiac function curve

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• ventricular function curves is a way of expressing the Frank-Starling mechanism of the heart.

• Greater the venous return greater will be cardiac output.***

• MECHANISM: (as actin myosin move apart by stretching to an optimum length contract more powerfully.

3-CONTRACTILITY (CONT..)

Cardiac function curve

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4-EXCITABILITY- BATHMOTROPY

• Excitability is the property to respond to stimuli.

• Stimuli: nervous, chemical, mechanical, electrical.

• This property enables the heart muscles to respond to artificial pacemaker.***

• The nerves, drugs, ions and ischemia affect the excitability of cardiac muscles.

• +ve bathmotropic effect: epinephrine, nor-epinephrine, sympathetic stimulation, caffeine, theophylline

• -ve bathmotropic effect: acetylcholine, parasympathetic stimulation.

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5- ALL OR NONE LAW (CARDIAC MUSCLE)

• Heart muscle contracts to its maximum or not at all in response to a threshold stimulus.

• Obeyed by heart muscle as a whole because heart is a functional syncitium. ***

• skeletal muscle fibers show it individually

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DEFINITION: it is the interval during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle. (0.25-0.30 sec)

• Absolute refractory period: It is the period during which already excited cardiac muscle does not respond to a second stimulus. (0.25 sec)**

• Relative refractory period: It is the period during which already excited cardiac muscle gives response to a powerful excitatory stimulus. (0.05 sec)**

6-RERACTORY PERIOD OF CARDIAC MUSCLE

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• The normal refractory period of the ventricle is almost equal to the duration of plateau phase of 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).

6-RERACTORY PERIOD OF CARDIAC MUSCLE (CONT..)

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• It is due to plateau in action potential of cardiac muscle because plateau increases the refractory period.

HEART MUSCLE CANNOT BE TETANIZED!!!

TETANIZATION SEEN IN SKELETAL MUSCLE

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ACTION POTENTIALS IN CARDIAC VENTRICULAR MUSCLE

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Ventricular Muscle Action Potential

-100

-80

-40

-60

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0

-20

2 3 40 1

Mem

bra

ne

Pot

enti

al(m

V)

Seconds

Fast Na+

Channels Open

Slow Ca++

Channels Open

0

1

2

3

4

phase

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.

ACTION POTENTIAL (ALONG WITH IONIC BASIS) IN THE VENTRICULAR MUSCLEPhase 0: Initial upswing of action potential.

o fast Na+ Channels open

Phase 1: The potential may repolarize slightly before starting the plateau phase.

o fast voltage gated Na+ Channels are inactivated.

o Outward Rectifier K+ Channels open transiently, causing slight repolarization.

o Membrane potential remains near zero.

Phase 2: Plateau Phase :This stage is responsible for prolonging the cardiac action potential, making it longer than a nerve action potential.

Oslow Na+/Ca+2 Channels open, to keep the cells depolarized.

Phase 3: Repolarization

o Ca+2 Channels close.

o Delayed Rectifier K+ Channels open to effect normal repolarization.

Phase 4 : resting membrane potential.

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• 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.

SA NODAL ACTION POTENTIAL

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-100

-80

-40

-60

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0

-20

2 3 40 1

Seconds

Mem

bran

e P

oten

tial

(m

V)

Threshold

Sinus Nodal Fiber

Na+ Leak

Slow Ca++

Channels Open

K+ ChannelsOpen more

Ventricular Muscle fiber

}

“Resting Potential”

Rhythmical Discharge of Sinus Nodal Fiber

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• At -55 mvolts, the fast Na+ channels become “inactivated”.

• Therefore, only the slow sodium-calcium channels can open and cause the action potential.

• 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 self-excitation.*******

SA NODAL ACTION POTENTIAL

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.

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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 pre-potential.• 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.(- inotropic effect)• decreased excitability of heart (-ve bathmotropic effect)