From the Guidelines
Vomiting can lead to vasovagal syncope through a complex interplay of physiological responses, ultimately resulting in a sudden drop in blood pressure and cerebral hypoperfusion, as described in the European Heart Journal guidelines on syncope management 1. The mechanism by which emesis leads to vasovagal syncope involves the stimulation of the vagus nerve, triggering an overactive parasympathetic response. This response is characterized by a sudden drop in heart rate (bradycardia) and dilation of blood vessels (vasodilation), reducing blood pressure dramatically 1. As blood pressure falls, inadequate blood flow reaches the brain, causing temporary cerebral hypoperfusion that leads to loss of consciousness. Some key factors that contribute to this process include:
- Decreased cardiac output due to venous pooling or diminished blood volume
- Impaired peripheral vascular resistance, often caused by widespread vasodilation
- Cerebral hypoperfusion resulting from abnormally high cerebral vascular resistance or low carbon dioxide tension
- Transient failure of protective mechanisms, such as cerebrovascular auto-regulation and arterial baroreceptor-induced adjustments According to the guidelines, a decrease in systolic blood pressure to 60 mmHg is associated with syncope, and as little as a 20% drop in cerebral oxygen delivery can cause loss of consciousness 1. To prevent vomiting-induced syncope, individuals should prioritize sitting or lying down at the first sign of nausea, staying hydrated, and avoiding triggers like prolonged standing or hot environments during episodes of vomiting, as these measures can help maintain blood pressure and prevent cerebral hypoperfusion 1.
From the Research
Mechanism of Emesis Leading to Vasovagal Syncope
- The exact mechanism by which emesis (vomiting) leads to vasovagal syncope is not directly stated in the provided studies 2, 3, 4, 5, 6.
- However, it can be inferred that vasovagal syncope is a complex neurologic reflex that can be triggered by various factors, including pain, fear, anxiety, or emotional upset 6.
- The studies suggest that vasovagal syncope is characterized by a transient loss of consciousness due to cerebral hypoperfusion, which can be caused by a decrease in preload, sympathetic and parasympathetic modulation, vasodilation, and cardioinhibition 5.
- Emesis may trigger vasovagal syncope by activating the vagus nerve, which can lead to a decrease in heart rate and blood pressure, resulting in cerebral hypoperfusion 6.
- The taxing of autoregulatory mechanisms, including the autonomic nervous system, adequate blood volume, and intact skeletal and respiratory muscle pumps, can also contribute to the development of vasovagal syncope 6.
Key Factors Involved in Vasovagal Syncope
- Decrease in preload 5
- Sympathetic and parasympathetic modulation 5
- Vasodilation 5
- Cardioinhibition 5
- Activation of the vagus nerve 6
- Autoregulatory mechanisms, including the autonomic nervous system, adequate blood volume, and intact skeletal and respiratory muscle pumps 6