What are the effects of vasovagal (vagal nerve) stimulation on the heart?

Effects of Vagal Nerve Stimulation on the Heart

Vagal nerve stimulation primarily causes bradycardia (decreased heart rate), reduced cardiac output, and decreased blood pressure through inhibition of sympathetic activity and enhancement of parasympathetic effects on the cardiovascular system. 1

Physiological Mechanisms

Direct Cardiac Effects

• Heart Rate: Vagal stimulation causes significant bradycardia through activation of myelinated B-fibers that innervate the heart 1
• Atrioventricular (AV) Conduction: Vagal activation impedes AV nodal conduction by affecting L-type calcium channels, which can lead to various degrees of heart block 1
• Cardiac Output: Decreases due to reduced heart rate and altered ventricular filling time 1
• Blood Pressure: Both systolic and diastolic blood pressure decrease due to reduced cardiac output and peripheral vasodilation 1, 2

Neurophysiological Pathway

• Vagal stimulation activates muscarinic receptors via acetylcholine release 3
• This activation counteracts beta-adrenergic stimulation, creating a balance between sympathetic and parasympathetic systems 1
• In preclinical studies, vagal stimulation that reduced heart rate by 5-10% showed significant cardioprotective effects 1

Clinical Manifestations

Vasovagal Response

• Characterized by inappropriate cardiac slowing (bradycardia) and arteriolar dilation 2
• Results from sudden augmentation of efferent vagal activity and reduction of sympathetic tone 2
• Can lead to decreased cerebral perfusion and syncope in severe cases 4
• Symptoms include fatigue, altered coordination, and potential fainting 4

Therapeutic Applications

Heart Failure Treatment

• Vagal nerve stimulation has shown promise in animal models of heart failure:
  • Improved left ventricular function 1
  • Reduced end-diastolic pressure 1
  • Increased survival rates (86% vs 50% in control groups) 1
  • Prevention of ventricular fibrillation 1

Arrhythmia Management

• Vagal maneuvers are used clinically to terminate supraventricular tachycardias 1
• In atrial fibrillation, vagal stimulation can help control ventricular rate 1

Clinical Considerations

Potential Adverse Effects

• Excessive vagal stimulation can cause:
  • Severe bradycardia
  • Heart blocks of varying degrees
  • Hypotension leading to syncope 1
  • Reduced cerebral blood flow 4

Counteracting Vagal Effects

• Atropine acts as an antimuscarinic agent that blocks the effects of vagal stimulation 3
• Atropine abolishes vagal cardiac slowing and prevents or reverses bradycardia 3
• Stellate ganglia stimulation can counteract vagal effects by increasing heart rate and blood pressure 5

Therapeutic Implications

• Understanding vagal effects is crucial for managing vasovagal syncope 1
• In refractory vasovagal syncope, selective atrial vagal denervation has shown promise 6
• Non-invasive vagus nerve stimulation has applications in treating certain headache disorders, with parameters carefully controlled to avoid excessive cardiac effects 7

Key Points for Clinical Practice

• Vagal stimulation produces predictable cardiac effects including bradycardia and hypotension
• The intensity of these effects depends on stimulation parameters (frequency, amplitude, duration)
• Both central (hypothalamic) and peripheral (cardiac) pathways can trigger vagal responses 2
• Therapeutic applications must carefully balance potential benefits against risks of excessive vagal activation
• Monitoring heart rate and blood pressure is essential when applying vagal stimulation therapeutically