2. Heart Rate and Its Regulation-1
2. Heart Rate and Its Regulation-1
REGULATION
HEART RATE
Definition: The heart rate is the number of times the
heart beats per minute.
Basic heart rate is set by the intrinsic conduction
system of the heart particularly the SA node.
This rate is modified by the autonomic nervous system.
Sympathetic stimulation increases the rate
(chronotropy) and force (inotropy) of contraction of
the heart.
Parasympathetic stimulation slows the heart.
The heart is under tonic inhibition from the vagus nerve
which predominates over the excitation from the
sympathetic nerve.
Both systems work in a reciprocal relationship; an
increase in sympathetic stimulation is accompanied by a
decrease in vagal inhibition and vice versa.
THE CARDIAC CENTER
The sympathetic and parasympathetic discharge to
the heart is under the control of groups of neurons in
the medulla called the cardiac center. These include:
The cardio inhibitory area located in the dorsal
nucleus of the vagus and the nucleus ambiguous sends
parasympathetic nerves via the vagus to the heart,
The cardio accelerator area projects to sympathetic
neurons in the T1 – T5 levels of the spinal cord. These
preganglionic neurons synapse with ganglionic neurons
in the upper thoracic sympathetic trunk (chain) from
where postganglionic fibres are sent to the heart
The sensory area located in the nucleus tractus
solitarius (NTS)
The heart exhibits a vagal tone. Cutting the vagus
increases the HR from 70 – 75/min to 100 – 120/min.
REGULATION OF HEART RATE
Factors that affect heart rate are:
HIGHER CENTERS: Centers in the cerebral
cortex (limbic cortex) via the hypothalamus
stimulate the cardiac center and affect heart
rate. Specific factors include: excitement,
anger, fear and sexual arousal increase HR.
Depression and grief can decrease HR.
RESPIRATORY CENTERS: During inspiration
respiratory centers in medulla radiate
impulses to cardiac center causing an
increase in HR. During expiration HR falls.
This phenomenon is known as sinus
arrythmia.
CHEMORECEPTORS: Stimulation of
chemoreceptors(aortic and carotid bodies) by rise in
pCO2 and hydrogen ion concentration not only feeds
back impulses to respiratory centers in medulla but also
exerts influence on vasomotor and cardiac center. This
results in peripheral vasoconstriction and bradycardia.
Hypoxia however causes hyperpnea and increased
secretion of catecholamines from adrenal glands
resulting in tachycardia.
BARORECEPTORS: When stimulated the baroreceptors
send their impulses via the vagus and glossopharyngeal
nerves to the nucleus tractus solitarius which sends
inhibitory impulses to the cardio accelerator area and
vaso constrictor nerves but excites vagal innervation to
the heart. This results in a slowing of heart rate,
vasodilation and fall in blood pressure.
ATRIAL RECEPTORS: Stimulation of type B atrial
stretch receptors leads to an increase in heart rate.
Type B atrial stretch receptors discharge in late
diastole at peak of atrial filling. The type A receptors
discharge during atrial systole . Rapid infusion of blood
or saline sometimes increases heart rate if it was
initially low. This is known as the Bainbridge reflex. It is
mediated by atrial stretch receptors via the vagus
(vagal inhibition and sympathetic facilitation). It is
abolished by vagotomy. The reflex competes with
baroreceptor mediated decrease in heart rate produced
by volume expansion.