Mechanism of Bradycardia after SAB
Some people mistakenly call this reaction a Bainbridge reflex. That is not correct.
Miller’s Anesthesia 7th Ed.p.1616
The heart rate during a high neuraxial block typically decreases as a result of blockade of the cardioaccelerator fibers arising from T1 to T4. The heart rate may decrease because of a fall in right atrial filling which decreases outflow from intrinsic chronotropic stretch receptors located in the right atrium and great veins. Note - Miller does not call this a Bainbridge reflex.
Barash – Clinical Anesthesia 6th Ed.p.946
The mechanism responsible for bradycardia is not clear. Blockade of sympathetic cardioaccelerator fibers originating from T 1-4 spinal segments is often suggested as the cause. The fact that bradycardia is more common with high blocks supports this mechanism. However, significant bradycardia sometimes occurs with blocks that are seemingly too low to block cardioaccelerators. Diminished venous return has also been proposed as a cause of bradycardia during spinal anesthesia. Intracardiac stretch receptors have been shown to reflexively decrease heart rate when filling pressures fall. Note- Barash does not call this a Bainbridge reflex either.
Nagelhout - Nurse Anesthesia 4th Ed.p.1059
Blockade of the sympathetic nervous system causes arterial vasodilation, decreased SVR, venous pooling, and a reduction in venous return. These changes cause a redistribution of blood that often results in hypotension. If the block is high enough, the sympathetic nerve fibers that innervate the heart, known as the cardioaccelerators (T 1 to T 4), become anesthetized. An imbalance occurs between vagal fibers, and the heart rate often slows, further contributing to hypotension.
Note- no mentions of Bainbridge reflex. The 3rd Ed. of Nagelhout – Nurse Anesthesia does say this effect (blocking of the cardiac accelerators) results in a slowing of the heart rate that is known as the Bainbridge reflex..... but this statement is removed in the newer version (4th Ed.) and replaced with the statement “ An imbalance occurs between vagal fibers, and the heart rate often slows, further contributing to hypotension.”
Most patients do not experience a significant change in heart rate after spinal anesthesia, but in young (age < 50), healthy (ASA class 1) patients there is a higher risk of bradycardia. Beta-blocker use also increases the risk of bradycardia. The incidence of bradycardia in the non-pregnant population is about 13%. The sympathetic cardiac accelerator fibers emerge from the T1 to T4 spinal segments, and blockade of these fibers is proposed as the cause of bradycardia. Decreased venous return may also cause bradycardia, due to a fall in filling pressures. This triggers the intracardiac stretch receptors to lower the heart rate. Even though both of these mechanisms are proposed to cause bradycardia, other as yet undetermined factors may contribute to the bradycardia seen with spinal anesthesia. Even though bradycardia is usually well tolerated, asystole and second- and third-degree heart block can occur, so it is wise to be vigilant when monitoring a patient after spinal anesthesia and treat promptly and aggressively. Hypotension occurs in about 33% of the non-obstetric population.
Note - Again no mention of or calling this a Bainbridge reflex