AL-Iraqia university/ College of Medicine Lect.

5
Dr.Mahasen Mohammed CVS Physiology
The heart rate
Objectives:
1. Define heart rate.
2. Summarize the factors that regulate heart rate.
3. Describe how a change in preload, afterload, and myocardial contractility will
affect cardiac performance.

The heart rate refers to the ventricular rate of beating per min. It can be determined
by counting the arterial radial pulse, the heart sounds (using the stethoscope) or the
number of cycles in an ECG record /minute. Normally, it averages 72 beats/minute
(range 60-100 beats/minute) in young adult males during rest. Heart rate higher than
100 beats/minute is called tachycardia and a rate lower than 60 beats/minute is called
bradycardia. Mechanisms that affect the cardiac rate are said to have a chronotropic
effect (chrono = time). Those that increase cardiac rate have a positive (+ve)
chronotropic effect β agonists (Salbutamol;Ventolin)); those that decrease the rate have
a negative (-ve) chronotropic effect (B blockers (Propranolol; Inderal).
The heart rate is basically determined by the strength of the vagal tone, and is normally
subjected to many physiological variations such as:
 It is about 120 beats/minute in newly born infants (due to absence of the vagal
tone) then it decreases to about 72 beats/minute at the age of 20 years.
 It is more in females than in males (due to less vagal tone in females).
 It is slowest in athletes (due to a stronger vagal tone than in sedentary persons).
 It sometimes shows diurnal variations (being lowest in the early morning).
Regulation of the heart
rate:
The heart rate is
regulated (SA node
discharge) by the
following factors:

 Neural.
 Chemical.
 SA node activity.

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Nervous regulation of the heart rate:
The heart receives both sympathetic and parasympathetic (vagal) nerves. Functions of
the cardiac sympathetic nerves(+ve chronotropic effect,+ve inotropic effect,+ve
dormotropic) Functions of the cardiac parasympathetic nerves When activated they
lead to depression of all cardiac properties.

The heart rate is nervously regulated through the cardiovascular centers which control
the sympathetic and parasympathetic discharge to the heart. The activity of these centers
is affected by:

A- Higher centers.
B- Reflexes.

Higher centers:
(1) The cerebral cortex. Cortical influence on heart rate is evident in emotions (the heart
rate is altered on seeing, hearing or thinking of a certain event).
(2) The hypothalamus and limbic system. These structures (with the cortex) are
concerned with emotional reactions. Most emotions are associated with tachycardia and
vasoconstriction which increases the arterial blood pressure (ABP), (e.g. before starting
a race, or examination) but some are associated with bradycardia and vasodilation which
decreases the ABP (e.g. when hearing shocking news).
(3) The respiratory center. Respiratory sinus arrhythmia; this term refers to the increase
of the heart rate during inspiration and to the decrease of heart rate during expiration
that occurs normally in young subjects and children. The tachycardia that occurs during
inspiration is due to; 1-excitation of the vasoconstrictor center (VCC) by the inspiratory
center, 2- and Bainbridge reflex which is initiated during inspiration by rise of the right
atrial pressure as a result of increase of the venous return.

Reflexes:
Bainbridge reflex (atrial stretch reflex) is an increase in heart rate due to an increase
in central venous pressure. Increased blood volume is detected by stretch receptors
(Cardiac Receptors) located in both atria at the venoatrial junctions.
An increase in the right atrial pressure or increased distention of the right atrium leads
to heart acceleration. Impulses are discharged mostly from atrial receptors via afferent
nerve fibers to the medullary VCC leading to reflex increase increased sympathetic
activity to the sinoatrial node (SAN) , increasing the heart rate with no fall in
parasympathetic activity.

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Baroreceptor reflex
This reflex is initiated by stretch receptors, which are located in the carotid sinus and
aortic arch. They are stimulated when stretched; signals from the carotid arteries are
transmitted through the glossopharyngeal nerves while signals from the arch of aorta
are transmitted through the vagus nerves into; the cardiovascular centers.
The baroreceptor signals inhibit the vasoconstrictor center and excite the vagal center
(CIC) resulting in vasodilation, decreased heart rate. In other words, a rise in arterial
blood pressure produces reflex decrease in heart rate whereas a fall in arterial blood
pressure produces reflex increase in heart rate.

The carotid sinus reflex

An external pressure on the carotid sinus area (is a dilated area at the base of the internal
carotid artery just superior to the bifurcation of the internal carotid and external carotid
at the level of the superior border of thyroid cartilage behind the angle of the mandible)
produces reflex slowing of the heart rate and peripheral vasodilation. The applied
external pressure stimulate the baroreceptors in the carotid sinus which leads to reflex
increase in the vagal tone to the heart (bradycardia) and decrease in the sympathetic
vasoconstrictor tone (vasodilation). On the same basis, an attack of paroxysmal atrial
(but not ventricular) tachycardia can be terminated by initiating a carotid sinus reflex,
through external massaging of the carotid sinus. A strong blow on the carotid sinus area
could lead to complete cardiac arrest. Some individuals pathologically have an abnormal
hypersensitivity of the carotid sinus. Thus, mild pressure on the carotid sinus area e.g.
during shaving or by a tight collar, produces bradycardia and generalized vasodilation,
which may markedly decrease the cardiac output and arterial blood pressure resulting
in brain ischemia and fainting. Such cases can be treated by anticholinergic drugs
(Atropine) to block the vagal discharge to the heart.

Chemical regulation of the heart rate:

A- Effect of changes in blood gases.
 Hypoxia.
 Hypercapnia and acidosis.
Hypoxia:
Moderate hypoxia (O2 lack) increases the heart rate by 3 mechanisms:
 Direct mechanism (by stimulating the SA node pacemaker cells).
 Central mechanism (by inhibiting the CIC).
 Reflex mechanism (by stimulating the VCC through exciting the peripheral
chemoreceptors in the carotid and aortic bodies.
On the other hand, severe hypoxia causes reduction of the heart rate due to inhibition of
the SA node activity and paralysis of the medullary cardiovascular centers.

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Hypercapnia and acidosis:
A moderate hypercapnia (CO2 excess) and acidosis (increased H+ ion concentration)
increase the heart rate by the following mechanisms:
 Inhibition of the CIC.
 Stimulation of the VCC through exciting the peripheral chemoreceptors.
 Stimulation of the VCC through exciting the central chemoreceptors.
On the other hand, severe hypercapnia or acidosis decreases the heart rate due to
inhibition of SA node activity and paralysis of medullary cardiovascular centers.

B- Effects of hormones, drugs and chemicals:

 Adrenaline; Small doses increase the heart rate by a direct action on the beta one
(B1) receptors in the SA node.
 Thyroxine: This increases the heart rate by direct stimulation of the SA node and
increasing its sensitivity to catecholamines.
 Atropine: This accelerates the heart by blocking parasympathetic activity.
 Histamine: This is a potent vasodilator (VD) substance which leads to marked
drop of the ABP, resulting in heart acceleration.
 Bile salts: inhibit SA node activity & stimulate the CIC leading to bradycardia.
 Autonomic drugs: Sympathomimetic drugs (amphetamine) cause tachycardia
while parasympathomimetic drugs (acetylcholine) cause bradycardia.

SA node activity:
Factors that directly affect the SA node activity:
 Body temperature; (physical factors) An increase of the body temperature by 1
°C increases the heart rate by 10-20 beats/minute and vice versa.
 Mechanical factors; Right atrial distension may directly excite the SA node
leading to tachycardia.
 Chemical factors; The SA node is directly excited by mild hypoxia,
Catecholamines, thyroxine, while it is directly inhibited by severe hypoxia and
hypercapnia, bile salts, and cholinergic drugs.
 Thyroid hormones (T3, T4) again have direct action on SA node. Increases in the
level of circulating thyroid hormones increases the rate at which SA node beats
e.g., in case of Thyroitoxicosis disease, there is an increase in heart rate, (resting
tachycardia; HR > 100 beats/minute).