physio material ans heart cvs

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AUTONOMIC CONTROL OF HEART A normally functioning heart is innervated by para sympathetic and sympathetic fibers .Both systems simultan-eously control cardiac function. The SA node displays intrinsic automaticity ( spontaneous pacemaker activity ) at a rate of 100-110 action potentials ("beats") per minute. This intrinsic rhythm is primarily influenced by autonomic nerves , with vagal influences being dominant over sympathetic influences at rest. This " vagal tone " reduces the resting heart rate down to 60-80 beats/min. The SA node is predominantly innervated by efferent branches of the right vagus nerves, although some innervation from the left vagus is often observed. Experimental denervation of the right vagus to the heart leads to an abrupt increase in SA nodal firing rate if the resting heart rate is below 100 beats/min. A similar response is noted when a drug such as atropine is administered. This drug blocks vagal transmission at the SA node by antagonizing the muscarinic receptors that bind to acetylcholine, which is the neurotransmitter released by the vagus nerve In hyperadrenergic states, sympathetics overrides parasympathetics.Vagus nerve stimulation results in domination of parasympathetic system.

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Page 1: Physio Material ANS Heart CVS

AUTONOMIC CONTROL OF HEART

A normally functioning heart is innervated by para sympathetic and sympathetic fibers .Both systems simultan-eously control cardiac function. The SA node displays intrinsic automaticity (spontaneous pacemaker activity) at a rate of 100-110 action potentials ("beats") per minute. This intrinsic rhythm is primarily influenced by autonomic nerves, with vagal influences being dominant over sympathetic influences at rest.  This "vagal tone" reduces the resting heart rate down to 60-80 beats/min.  The SA node is predominantly innervated by efferent branches of the right vagus nerves, although some innervation from the left vagus is often observed.  Experimental denervation of the right vagus to the heart leads to an abrupt increase in SA nodal firing rate if the resting heart rate is below 100 beats/min. A similar response is noted when a drug such as atropine is administered. This drug blocks vagal transmission at the SA node by antagonizing the muscarinic receptors that bind to acetylcholine, which is the neurotransmitter released by the vagus nerveIn hyperadrenergic states, sympathetics overrides parasympathetics.Vagus nerve stimulation results in domination of parasympathetic system.

Page 2: Physio Material ANS Heart CVS

Autonomic nerves

Sympathetic nerves supply atria and ventriclesParasympathetic nerves Supply atria but ventricles are sparsely supplied

Sympathetic fibers ……………….. release norepinephrine

Parasympathetic fibers ……………… release acetylcholine

Sympathetic stimulation causes norepinephrine release from the nerve fibers in heart and simultaneously causes epinephrine and norepinephrine release from adrenal medulla into the bloodstream.

RECEPTORS IN CARDIAC TISSUE

ADRENERGIC RECEPTORS ( for epinephrine and norepinephrine )

CARDIAC MUSCLE (Atria and Ventricles)

Beta 1 and Beta 2 receptors

CORONARIES

Alpha 1 and Beta 2 receptors

CHOLINERGIC RECEPTORS (for acetylcholine)

CARDIAC MUSCLE

M2 RECEPTORS

Page 3: Physio Material ANS Heart CVS

FUNDAMENTAL PROPERTIES OF CARDIAC TISSUE

BATHMOTROPY…………… Excitability and

automaticity of SA node

DROMOTROPY ……………. Conductivity of cardiac

impulse

CHRONOTROPY………… Heart Rate

INOTROPY…………………. Contractility of cardiac

muscle

LUSITROPY ................. Relaxation of cardiac muscle

+ve increased effect

-ve decreased effect

EFFECT EFFECT

PARASYMPATHETIC SYMPATHETIC

BATHMOTROPIC - VE + VE

Page 4: Physio Material ANS Heart CVS

DROMOTROPIC - VE + VE

CHRONOTROPIC - VE + VE

INOTROPIC - VE in atria

Slightly –ve in ventricles

+ VE

LUSITROPIC -VE + VE

Beta 1 (mainly) and Beta 2 …….. +VE EFFECTS

M2 ………………………………. - VE EFFECTS