Baroreceptors in aortic arch and carotid sinus affect HR
Increase in BP
--> Increase vagal tone/decrease sympathetic tone
--> Decrease HR and contractility
... an increase in HR caused by an infusion of saline
Increased volume
--> Increased venous return to RA
--> Stimulation of atrial receptor
--> Increased HR
By similar mechanisms,
During inspiration
--> Increase venous return to RA
--> Increased HR
When blood volume is high (low HR),
--> Bainbridge reflex > Baroreceptor reflex
When blood volume is low (high HR),
--> Baroreceptor reflex > Bainbridge reflex
Moderate lung inflation may increase HR
[BL8:p95]
Stimulation of peripheral chemoreceptor
--> Stimulation of medullary vagal centre (primary effect)
--> Decreased HR
But,
Stimulation of peripheral chemoreceptor
--> Increased respiratory activity
--> Hypocapnia and increased lung stretch
Both leads to increased HR (secondary effect)
When pulmonary hyperventilation is not prevented
--> Primary and secondary effect tend to cancel out
--> Minimal effect on HR
But if patient is ventilated, cessation of ventilation causes immediate bradycardia because of primary effect and lack of secondary effect
Rhythmic changes in heart rate --> Almost entirely due to oscillations in vagal tone.
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Reviewed | 20050816 |