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2. Heart Rate and Its Regulation-1

The document discusses heart rate, its definition, and regulation through the autonomic nervous system, including the roles of sympathetic and parasympathetic stimulation. It details factors affecting heart rate such as higher centers, respiratory centers, chemoreceptors, baroreceptors, atrial receptors, and the impact of exercise, sleep, temperature, hormones, and ions. Additionally, it mentions conditions like sick sinus syndrome and the effects of hypoxia and hypercapnia on heart rate.

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0% found this document useful (0 votes)
16 views9 pages

2. Heart Rate and Its Regulation-1

The document discusses heart rate, its definition, and regulation through the autonomic nervous system, including the roles of sympathetic and parasympathetic stimulation. It details factors affecting heart rate such as higher centers, respiratory centers, chemoreceptors, baroreceptors, atrial receptors, and the impact of exercise, sleep, temperature, hormones, and ions. Additionally, it mentions conditions like sick sinus syndrome and the effects of hypoxia and hypercapnia on heart rate.

Uploaded by

emmylucky545
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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HEART RATE AND ITS

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.

HYPOXIA AND HYPERCAPNIA: These have a direct


effect on cardiac center to increase heart rate.
CORONARY CHEMOREFLEX: (Bezold Jarisch Reflex)
In experimental animals injection of some drugs e.g.
serotonin, capsaicin and phenyl diguanides into
coronary artery supplying left ventricle causes apnea
followed by rapid breathing, hypotension and
bradycardia – this is known as the coronary
chemoreflex. Such a response is not observed with
drug infusion into atria or right ventricle.
EXERCISE: During anticipatory phase of exercise
vagal inhibition causes increased heart rate. As
exercise progresses sympathetic stimulation
contributes to increased heart rate.
SLEEP: During sleep HR is slowest.
PHYSICAL TRAINING: increases vagal tone lowering
the heart rate. Heart is lower in those who are
physically fit.
 TEMPERATURE: Rate of SA node discharge increases with
temperature increase.
 HORMONES: Thyroxine increases heart rate by increasing
number of and affinity of β – adrenergic receptors in the heart
thereby increasing its sensitivity to catecholamines.
Hyperthyroidism cause tachycardia that persists during sleep
while hypothyroidism results in bradycardia.
 SINUS DISORDER: (SICK SINUS SYNDROME) This occurs in
the elderly and maybe due to SA node fibrosis or
degeneration. It presents as bradycardia, sinus arrest with
pauses, paroxysmal tachycardia and other forms of
arrhythmias.
 JAUNDICE AND RAISED INTRACRANIAL PRESSURE: cause
bradycardia.
IONS
Hyperkalemia (high blood K+) lowers the resting
potential of the cardiac cells and may lead to heart
block or cardiac arrest
Hypokalemia causes life threatening arrythmias
Hypocalcemia (low blood Ca+)depresses the heart
because calcium helps initiate heart contraction
Hypercalcemia produces a tight coupling of the
excitation – contraction mechanism thus prolonging
the plateau phase of the action potential. This
increases heart irritability and spastic heart
contractions that allow the heart little rest.

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