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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 vagi 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 the superior and inferior vena cavae increase. This results is 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 the superior and inferior vena cavae 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 vena 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 vena 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) 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 manuever, 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: http://en.wikipedia.org/wiki/Bainbridge_reflex

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 natiuretic peptide is increased, which also promoted dieresis.
According to Costanzo 3rd Ed. pg 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

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 increase volume or pressure on the atrial/stretch mechanoreceptors.

 

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