The Bainbridge reflex (aka, atrial reflex) occurs when the heart rate increases in response to a rise in

atrial pressure. This is a compensatory mechanism since increased right atrial pressures frequently result
from elevated left heart pressures from decreased cardiac output. Elevating the heart rate should
increase the cardiac output.

The Bainbridge reflex acts in opposition to the carotid baroreceptor reflex which increases heart rate
when the stretch is decreased in states of hypotension or hypovolemia.

Sinus arrhythmia may be explained by the Bainbridge reflex, as venous return increases during
inhalation causing a brief increase in heart rate.

The Bainbridge Reflex

A scientist by the name of Francis Arthur Bainbridge reported this reflex in 1915 when he was
experimenting on dogs. Bainbridge found that infusing blood or saline into the animal increased heart
rate. This phenomenon occurred even if arterial blood pressure did not increase. He further observed
that heart rate increased when venous pressure rose high enough to distend the right atrium, but
denervation of the vagus nerve to the heart eliminated these effects.

The Bainbridge reflex, also called the atrial reflex, is an increase in heart rate due to an increase in
central venous pressure. Increased blood volume is detected by stretch receptors located in both atria
at the venoatrial junctions.

Control of Heart Rate

The Bainbridge reflex and the baroreceptor reflex act antagonistically to control heart rate. The
baroreceptor reflex acts to decrease heart rate when BP rises. When blood volume is increased, the
Bainbridge reflex is dominant; when blood volume is decreased, the baroreceptor reflex is dominant.
The Bainbridge reflex is seen in dogs, but experiment has shown that it is not as significant in primates.
There is evidence, however, that the Bainbridge reflex does occur in humans, as in after delivery of an
infant when a large volume (up to 800 mL) of uteroplacental blood is put back into the mother's
circulation, resulting in tachycardia.

Venous Return

As venous return increases, the pressure in both superior and inferior vena cava increase. This results in
an increase in the pressure of the right atrium, which stimulates the atrial stretch receptors. These
receptors in turn signal the medullary control centers to decrease parasympathetic tone via the vagus
nerve to the heart, leading to increased heart rate, also known as tachycardia.

Increasing the heart rate serves to decrease the pressure in both superior and inferior vena cava by
drawing more blood out of the right atrium. This results in a decrease in atrial pressure, which serves to
bring in more blood from the venae cavae (superior vena cava and inferior vena cava are collectively
called the venae cavae), resulting in a decrease in the venous pressure of the great veins. This continues
until right atrial blood pressure returns to normal levels, upon which the heart rate decreases to its
original level.

Atrial Stretch Receptors

In the right atrium, the stretch receptors occur at the junction of the venae cavae In the left atrium, the
junction is at the pulmonary veins. Increasing stretch of the receptors stimulates both an increase in
heart rate and a decrease in vasopressin (a.k.a. anti-diuretic hormone - ADH) secretion from posterior
pituitary. This decrease in vasopressin secretion results in an increase in the volume of urine excreted,
serving to lower BP. In addition, stretching of atrial receptors increases secretion of atrial natriuretic
peptide (ANP), which promotes increased water and sodium excretion through the urine.

Respiratory Sinus Arrhythmia

Bainbridge Reflex is involved in Respiratory Sinus Arrhythmia. During inhalation intrathoracic pressure
decreases. It triggers increased venous return which is registered by stretch receptors, which via
Bainbridge Reflex increases the heart rate momentarily during inspiration. This is not to be confused
with a Valsalva maneuver, in which high intrathoracic pressure generated by a deep breath and bearing
down stimulates the vagus nerve and leads to a slowing of the heart rate, or bradycardia.

Reference textbooks excepts

Miller 7th ed.p.409

The Bainbridge reflex is elicited by stretch receptors located in the right atrial wall and the cavoatrial
junction. An increase in right-sided filling pressure sends vagal afferent signals to the cardiovascular
center in the medulla. Theses afferent signals inhibit parasympathetic activity, thereby increasing heart
rate. Acceleration of the heart rate also results from a direct effect on the SA node by stretching the
atrium. The changes in heart rate are dependent on the underlying heart rate before stimulation.
Nagelhout (Nurse Anesthesia) 4th ed.p.480

The Bainbridge reflex is elicited as a result of an increased volume of blood in the heart, which causes
sympathetic nervous system stimulation. Stretch receptors are located in the right atrium, junction of
the vena cava, and pulmonary veins. The Sinoatrial node is involved in this process and can increase
heart rate by 10% to 15%. This reflex helps to prevent sequestration of blood in veins, atria, and
pulmonary circulation. Antidiuretic hormone secretion from the posterior pituitary gland is decreased,
resulting in decreased circulating volume. Atrial natriuretic peptide is increased, which also promoted
dieresis.

Costanzo 3rd ed.p.163

According to Costanzo 3rd ed.p. 163 information from the low-pressure atrial receptors travels in the
vagus nerve to the nucleus solitaries (as does information from the high-pressure arterial receptors
involved in the baroreceptor reflex). The difference lies in the response of the medullary cardiovascular
centers to the low- and high-pressure receptors. Whereas an increase in pressure at the arterial high-
pressure receptors produce a decrease in heart rate (trying to lower the arterial pressure back to
normal), an increase in pressure at the venous low-pressure receptors produce and increase in heart
rate (Bainbridge reflex). The lo-pressure atrial receptors, sensing that blood volume is too high, direct an
increase in heart rate and, thus, an increase in cardiac output; the increase in cardiac output leads to
increased renal perfusion and increased sodium and water excretion.

Barash 6th ed.p.221

High-pressure sensitive receptors in the LV and low-pressure responsive elements in the atria and RV
consist of stretch-induced mechanoreceptors that respond to pressure or volume changes. These
receptors activate myelinated vagal afferent fibers that project to the nucleus solitarius and increase
sympathetic nerve activity to the SA node but not to the ventricles, thereby increasing heart rate but not
contractility. Distention of these mechanoreceptors also increases renal excretion of free water by
inhibition of antidiuretic hormone secretion from the posterior lobe of the pituitary gland. It appears
highly likely that the Bainbridge reflex may be mediated by distention of these mechanoreceptors.
Second, a diffuse receptor network is distributed throughout the cardiac chambers that projects via
unmyelinated vagal afferent neurons to the nucleus tractus solitarius. These receptors behave like the
carotid and aortic mechanoreceptors and produce a vasodepressor response consisting of vagus
activation concomitant with a simultaneous increase in venous capacitance.

Conclusion
In looking through all the text the consensus to me is that the Bainbridge reflex is only when you see an
increased heart rate from increased volume or pressure on the atrial/stretch mechanoreceptors.

Bainbridge reflex, also called atrial reflex, acceleration of the heart rate resulting from increased blood
pressure in, or increased distension of, the large systemic veins and the right upper chamber of the
heart. This reflex, first described by the British physiologist Francis Arthur Bainbridge in 1915, prevents
the pooling of blood in the venous system.

Special pressure sensors called baroreceptors (or venoatrial stretch receptors) located in the right
atrium of the heart detect increases in the volume and pressure of blood returned to the heart. These
receptors transmit information along the vagus nerve (10th cranial nerve) to the central nervous system.
This response results in the activation of sympathetic nerve pathways that serve to increase the strength
of contraction of the heart muscle and to increase heart rate (tachycardia). The Bainbridge reflex can be
blocked by atropine, is diminished or absent when the initial heart rate is high, and can be abolished by
cutting the vagus nerves.