HEART PHYSIOLOGY

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

Assistant Professor Physiology

April 18, 2014

3-Contractility (cont..)
Cardiac function curve
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.

April 18, 2014

3-Contractility (cont..)
Cardiac function curve
ventricular function curves is a way of expressing the FrankStarling 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.
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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

April 18, 2014

6-RERACTORY PERIOD of cardiac muscle

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)**
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6-RERACTORY PERIOD of cardiac muscle (cont..)

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).
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Heart muscle cannot be tetanized!!!

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

TETANIZATION SEEN IN SKELETAL MUSCLE

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Action Potentials in Cardiac ventricular Muscle

April 18, 2014

Ventricular Muscle Action Potential

++ K+ Channels Ca Channels K+ Channels Open More Open Open More

Slow Ca++ Channels Open

+20

1 2

Membrane Potential (mV)

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

Fast Na+ Channels Open 4 0 3

phase 0- Fast Na+ channels open then slow Ca++ channels phase 1- K+ channels open Seconds phase 2- Ca++ channels open more phase 3- K+ channels open more phase membrane potential April418,Resting 2014
Copyright 2006 by Elsevier, Inc.

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Action Potential (along with ionic basis) in the ventricular Muscle

Phase 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.

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. The RMP of the SA nodal fibers is not stable. It drifts slowly to the threshold value. April 18, 2014

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IMPORTANCE OF PRE-POTENTIAL
The unstable RMP of SA nodal fibers is called as PACEMAKER POTENTIAL or PRE-POTENTIAL. the inherent leakiness of the sinusnodal fibers to Na+ and Ca++ ions causes their self-excitation.*** Therefore, pre-potential is responsible for the automaticity of the SA nodal fibers.

THE MECHANISM OF PRE POTENTIAL SLOPE:

The early portion of the RMP is due to natural leakiness of the membrane to sodium (funny current) The last of portion of pre-potential is due to activation of (transient) T -Type of calcium channels.

SA nodal action potential

At -55 mvolts, the fast Na+ channels become inactivated. So these channels are not important in the depolarization of the SA nodal fibers. Therefore, only the slow sodiumcalcium channels (L-type) can open and cause depolarization. As a result, the SA nodal action potential is slower to develop than the that of the ventricular muscle.

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SA nodal action potential (cont)

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

Rhythmical Discharge of Sinus Nodal Fiber

Sinus Nodal Fiber Slow Ca++ Channels Open Ventricular Muscle fiber

+20

K+ Channels Open more

Threshold

Membrane Potential (mV)

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

Na+ Leak

2 Seconds

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WHAT DETERMINES THE HEART RATE?

Slope of pre potential determines the heart rate. More Steeper the slope- increased heart rate.** Less steeper the slope- 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.

Effects of Sympathetic stimulation on Heart

Nor-epinephrine is released at sympathetic nerve endings Norepinephrine increases the permeability of SA nodal fibers to sodium and calcium which increases the slope of the pre-potential. It causes increased sinus node discharge with increase Heart Rate (+ve chronotropic effect) Increases force of contraction in atria and ventricles (+ve inotropic effect) It also Increases rate of conduction of impulse (+ve dromotropic 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 node. Mechanism: Causes hyperpolarization because of increased K+ permeability in response to acetylcholine. This causes Decreased heart rate by decreasing the frequency of impulse generation (-ve chronotropic effect) Minimal decrease of force of contraction (-ve inotropic effects) decreased transmission of impulses (ve dromotropic effect). It may temporarily stop the heart. decreased excitability of heart (-ve bathmotropic effect).

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