Venous Pooling in the Standing Postition
Upon standing up blood pools in the lower body. This causes a decrease in the amount of blood returning to the heart, and therefore the heart does not fill with enough blood.

Among all the creatures of God we were blessed with the erect standing and walking positions, however our veins take a large burden for that erect postion. For example, imagine you are walking with your dog.

You are walking on your 2 feet and your dog is walking on 4 feet. As the blood is being pumped out of the left side of your heart it supplies the blood to your brain, upper body, and then it travels via your arteries down to your legs and feet to supply the muscles with oxygen and blood flow. This blood also has to return back against gravity through the veins to your heart. It now has to travel all the way from your feet back to the right side of your heart not aided by any pump other than the pumping effects of your leg muscles around your leg veins. To help your veins sustain that blood returning to the right side of your heart, your veins are equiped with numerous one-way valves that allow the blood to go only one direction towards your heart and away from the ground (against gravity).

Even with 95 mmHg pressure in the veins, if a person is not moving his muscles to help the blood to be pumped back to the heart it will cause the veins to become enlarged and saggy.

This pressure is enough to push the blood back to the heart. If the person does not move around (like an old lady who sits most of the time in a chair), the veins in her legs will become congested. Some of the water in the blood will ooze out causing swelling in the legs. This excess of fluid from the tissues in the legs (edema) is luckily also handled by the body (especially in young people) by a system called lymphatics. This is another system that takes care of the excess fluid which went outside the vessels and returned them back to the veins. Even then the system can become overtaxed and the fluid (edema) persists in the leg.

When the veins get saggy and the one way valves which direct the blood back to the heart become pushed far apart, this leads to the valves themselves becoming incompetent which aggrivates the situation even further. So, if the blood collects a lot in the veins, so that the blood returning back to the heart is less, this will effect the filling of the heart. It can eventually lead to low blood pressure, the person will feel dizzy and weak and may faint.

Normal Veins

The amount of blood ejected by the each heartbeat is reduced.
To make up for the fact that each heart beat is now delivering less blood to the brain, the heart starts to beat faster. If each heart beat was delivering 2 ounces of blood (60 ml), and the heart was beating at 60 beats per minute, then the body was receiving 120 ounces of blood each minute (2 ounces x 60 ml = 120 ounces). Now if each heartbeat is delivering only 1 ounce, the heart has to beat at 120 beats per minute, to sustain the same amount of blood flow to the body.

How did the heart know that it has to beat fast?
There are special sensors in the walls of the major arteries leaving the heart known as baroreceptors, they are strategically located in the aortic arch and carotid arteries leading to the brain. In addition there are low pressure sensors in the walls of the heart called mechanoreceptors.

• The receptors sense the decrease in blood pressure, and activate the sympathetic nerves.
• The sympathetic nerves act on the sinus node so the heart can beat faster and also make blood vessels constrict (vasoconstriction).
• The receptors are like relaying little stations that broadcast to the central nervous system. This whole mechanism acts to reverse the decline in blood pressure and maintain cerebral perfusion.

Conversely, when the subject is recumbent, the sensory activity of cardiac mechanoreceptors increases, and reflexes sympathetic inhibition and parasympathetic activation cause vasodilatation and bradycardia.

So what happens in the patient with neurocardiogenic syncope?
The compensatory response to the patient's assuming an upright posture is interrupted after several minutes and replaced by a paradoxical withdrawal of sympathetic activity and an increase in parasympathetic (vagal) activity. Characteristically, the resulting reduction in blood pressure is severe, sympathetic activity is inhibited, plasma norepinephrine levels do not increase, and the heart rate decreases.

What makes this interruption happen?
The nuclei and groups of neurons in the medulla that trigger parasympathetic activity (the nucleus ambiguous and the dorsal motor nucleus of the Vagus Nerve) and those that control sympathetic activity (the Rostral Ventromedial and Ventrolateral Medulla) are modulated by sensory input from arterial baroreceptors and cardiac mechanoreceptors.

The prevailing hypothesis is that the excessive activation of the cardiac mechanoreceptors by mechanical or chemical factors during a period of sympathetic excitation and the possible hypersensitivity of these nerve endings are the underlying mechanisms of neurocardiogenic syncope. The circumstances that lead to syncope and the response to medications favor that hypothesis.