Reflexes

Question 1

Oculocardiac Reflex (Ashner’s Reflex, trigeminovagal reflex)

Answer 1

Definied clinical as a decrease in heart rate by 10% following pressure to the globe or traction of the ocular muscles

Anatomy: afferent limb - trigeminal (ciliary ganglion to ophthalmic division of trigeminal nerve to gasserian ganglion to the main trigeminal sensory nucleus)
efferent limb - vagus nerve (afferents synapse with visceral motor nucleus of vagus nerve located in the reticular formation and efferents travel to the heart and decrease output from the sinoatrial node)

Triggering stimuli - triggered by traction on the extraocular muscles (medial rectus), direct pressure on the globe, ocular manipulation, ocular pain

Results: sinus bradycardia, junctional rhythm, ectopic beats, atrioventricular block, ventricular tachycardia, and asystole

Question 2

Hering-Breuer inflation reflex

Answer 2

a reflex triggered to prevent the over-inflation of the lung. Pulmonary stretch receptors present on the wall of bronchi and bronchioles of the airways and respond to excessive stretching of the lung during large inspirations

Once activated, they send action potentials through large myelinated fibers of the vagus nerve to the inspiratory area in the medulla and apneustic center of the pons. IN response, the inspiratory area is inhibited directly and the apneustic center is inhibited from activating the inspiratory area. This inhibits inspiration, allowing expiration to occur

Question 3

Hering-Breuer deflation reflex

Answer 3

serves to shorten exhalation when the lung is deflated. It is initiated either by stimulation of stretch receptors or stimulation of proprioceptors activated by lung deflation. Like the inflation reflex, impulses from these receptors travel afferently via the vagus, the afferents terminate on inspiratory centers

Question 4

Bainbridge reflex

Answer 4

an increase in heart rate in response to increased central venous pressure. Its role is to match cardiac output with venous return to the heart. It is mediated by stretch receptors in the left and right atria sending signals via vagal nerve fibers (afferent limb), integration in the medulla, and ultimately inhibition of vagal outflow and stimulation of sympathetic outflow to the heart

Question 5

Bezold-Jarisch reflex

Answer 5

This reflex produces bradycardia, vasodilation, and apnea.

Toxins as well as various mechanical stressors are sensed by the walls of the cardiac chambers in the same way pain is sensed by the skin - through unmyelinated C-fibres. the afferents travel up the vagus nerve to synapse somewhere in the medulla, presumably in the nucleus of the solitary tract, exerting a cardiodepressant effect. Efferent vagal and sympathetic responses both vasodilate the peripheral circulation and slow the heart rate, producing hypotension and decreased cardiac output.

Stimulus: multiple and heterogenous stimuli, including
- mechanical: pressure and strecht (inotropy preload and afterload)
- chemical: veratrum alkaloids, ATP, capsaicin, snake venom, and various other venoms

Sensors: heterogeneous sensors distributed in all cardiac chambers

Afferent nerves: unmyelinated C-fibres of the vagus

Processor: nucleus of the solitary tract, likely involving serotonergic transmission

Efferent nerves: sympathetic fibers to the heart and peripheral smooth muscle, vagus nerve (via the cardiac ganglion)

Effector: SA node, AV node, peripheral vascular smooth muscle

Effects: hypotension (vasodilation) and bradycardia

Question 6

Branham’s reflex

Answer 6

(perhaps can be thought of as an exaggerated Bezold-Jarisch reflex)

Associated with rapid closure of a PDA: results in an acute increase in mean blood pressure from volume overload in the presence of a closed ductus, which in turn stimulates the baroreceptors, leading to a reflex bradycardia