The Vagus Nerves

The autonomic nervous system.

The sympathetic nervous system prepares the body for fight or flight situations, increases heart rate and strength of heart beat, dilates coronary arteries, constricts peripheral arteries, relaxes bronchial smooth muscles, and controls body temperature.

The parasympathetic nervous system promotes rest and digestion, slows breathing and heart rate, stimulates digestion and secretion of digestive enzymes, opens sphincters, constricts pupils, and regulates body temperature.

The cell bodies of the preganglionic neurons are located in the grey matter of the spinal cord or brain stem.

The cell bodies of the postganglionic neurons are located in the autonomic ganglia.

The right vagus nerve courses posteriorly to the right subclavian artery and enters the thorax by passing anterior to the right subclavian artery. It then descends posterior to the right brachiocephalic vein and enters the posterior mediastinum. The left vagus nerve passes anterior to the aortic arch and descends in the posterior mediastinum, between the left common carotid artery and the left subclavian artery.

The left recurrent laryngeal nerve loops around the arch of the aorta and ascends in the tracheoesophageal groove, posterior to the ligamentum arteriosum. Its close proximity to the aorta makes it susceptible to injury or compression, leading to vocal cord dysfunction and hoarseness.

The sympathetic trunks are paired structures that lie on either side of the vertebral column. They extend from the base of the skull to the coccyx. Each trunk consists of a series of ganglia connected by nerve fibers.

The sympathetic trunks play a crucial role in the fight-or-flight response by activating various physiological responses. They innervate smooth muscles, glands, and blood vessels, controlling functions such as vasoconstriction, pupil dilation, and increased heart rate.

Horner's syndrome is characterized by a triad of symptoms, including ptosis (drooping of the upper eyelid), miosis (constriction of the pupil), and anhidrosis (decreased sweating) on the affected side of the face.

Ectopic pacemaker activity, Delayed after-depolarisations, Circus re-entry, Heart block

They inhibit action potential propagation and reduce the rate of cardiac depolarisation during phase 0

To reduce mortality following MI and to prevent recurrence of tachycardias provoked by increased sympathetic activity

The Vaughan Williams classification is a system used to categorize anti-dysrhythmic drugs based on their mechanism of action and electrophysiological effects.

'Use-dependent' block refers to the ability of certain anti-dysrhythmic drugs to preferentially block ion channels in rapidly depolarizing or frequently firing cells.

Class IV anti-dysrhythmic drugs work by blocking calcium channels in cardiac cells, thereby reducing the influx of calcium ions and slowing down the rate of electrical conduction. They are primarily used to treat supraventricular dysrhythmias, such as atrial fibrillation and atrial flutter.

Class 4 drugs, such as verapamil and diltiazem, block cardiac voltage-gated L-type calcium channels. This results in the slowing of conduction through the SA and AV nodes, where the conduction of the action potential relies on slow calcium currents. These drugs also shorten the plateau of the cardiac action potential and reduce the force of contraction of the heart.

The main drug in Class 4 is verapamil, which is used to prevent recurrence of supraventricular tachycardias (SVTs) and to reduce the ventricular rate in patients with atrial fibrillation (provided they do not have Wolff-Parkinson-White syndrome). However, Class 4 drugs are ineffective and dangerous in ventricular dysrhythmias. Diltiazem, another Class 4 drug, is similar to verapamil but has more effect on smooth muscle calcium channels and has less bradycardia.

Adenosine, which is produced endogenously, acts on the A1 receptor and hyperpolarizes cardiac conducting tissue, slowing the heart rate. It decreases pacemaker activity and is used to terminate supraventricular tachycardias (SVTs).

Digoxin, a cardiac glycoside derived from the foxglove plant, increases vagal efferent activity to the heart, reducing sinoatrial firing rate (decreasing heart rate) and conduction velocity of electrical impulses through the atrioventricular node. Toxic concentrations of digoxin can disturb sinus rhythm. It is used in the treatment of certain cardiac conditions, but caution must be taken to avoid toxic concentrations.

Shortening diastole, increased ventricular end diastolic pressure, reduced diastolic arterial pressure

Atherosclerosis, thrombosis, coronary spasms

Severe and crushing chest pain, often retrosternal or on the left side of chest, can radiate to left arm, neck, jaw, and back, brought on by exertion, cold or excitement

Stable angina is predictable chest pain that occurs during exertion and is caused by a fixed narrowing of the coronary arteries. Unstable angina, on the other hand, occurs at rest or with less exertion than stable angina and is associated with a thrombus around a ruptured atheromatous plaque without complete occlusion of the vessel.

Variant (Prinzmetal) angina is a less common type of angina that is caused by coronary artery spasm. The exact cause of the spasm is not completely understood, but it is sometimes associated with atherosclerosis.

The main treatments for angina to reduce chest pain symptoms include beta-blockers, nitrates, calcium channel antagonists, nirocandil, ivabradine, and ranolazine.

Verapamil and diltiazem have a vasodilator effect mainly on resistance vessels, which reduces afterload. They also dilate coronary vessels, which is important in variant angina. In terms of clinical uses in angina, the choice of CCB depends on comorbidity and drug interactions. Amlodipine or lercanidipine are safe in patients with heart failure and can be used instead of a Beta-Blocker in Prinzmetal angina or alongside beta-blockers in most angina. However, diltiazem or verapamil should not be used in patients with heart failure, bradycardia, AV block, or in the presence of a Beta-Blocker.

The side effects of CCBs include headache, constipation, and ankle edema. Other clinical uses of CCBs include their role as antidysrhythmics, mainly verapamil, which slows ventricular rate in rapid atrial fibrillation and prevents recurrence of supraventricular tachycardia (SVT). CCBs also have an effect on hypertension, mainly amlodipine or lercanidpine.

Nicorandil combines activation of potassium K+ATP channels with nitrovasodilator actions. It causes hyperpolarization of vascular smooth muscle, acting as both an arterial and venous dilator. However, it can cause headaches, flushing, and dizziness. Nicorandil is used for patients who remain symptomatic despite optimal management with other drugs.

Ivabradine inhibits funny “f”-type channels in the heart, reducing cardiac pacemaker activity and heart rate. Ranolazine is a unique anti-anginal drug used as a last resort.