The Cardiovascular Dizziness Connection: Role of Vestibular Autonomic Interactions in Aging and Dizziness

Introduction

Without a doubt, vestibular dysfunction can cause dizziness; however, other systems that interact with the vestibular system can also be involved. The goal of this chapter is to discuss the role of cardiovascular reflexes in contributing to dizziness.

A common symptom that often causes a patient to seek medical attention for the evaluation of dizziness is presyncope: the feeling of “lightheadedness” before fainting. Even young healthy individuals with intact vestibular systems commonly report dizziness and lightheadedness during tilt table testing. Participants generally report dizziness but not true vertigo. So why are these individuals reporting dizziness during an upright tilt?

Although the mechanism remains unclear, the assumption is that reductions in cerebral blood flow (CBF) result in symptoms associated with presyncope. In fact, recent evidence has found that both orthostatic hypotension (decreased blood pressure when standing) and cerebral hypoperfusion (reduction in brain blood flow) are related to incidents of dizziness. To understand why CBF would be reduced during upright posture requires an understanding of how blood pressure and CBF are regulated when we are standing or when we rise from a supine or seated position. To explore this connection, blood pressure regulation and regulation of brain blood flow are described in this chapter.

In addition, fascinating evolving evidence suggests that the vestibular system provides important signals that assist in the regulation of blood pressure and brain blood flow. This chapter also explores these vestibular connections in the context of their impact on the development of dizziness and vertigo.

Regulation of Blood Pressure

Regulation of blood pressure is essential to health because blood flow through all organs is dependent on adequate driving pressure. To produce that pressure, the heart pumps approximately 86,000 times/day to maintain blood flow and pressure throughout the body. Pressure at the aorta, where blood is ejected from the left ventricle, is determined by the following equation:

where MAP is the mean arterial pressure, CO is the cardiac output (total blood flow out of the heart each minute), and TPR is the total peripheral resistance of blood vessels throughout the body. Cardiac output is determined by the heart rate multiplied by the stroke volume, the amount of blood pumped in one contraction of the left ventricle. Thus to maintain adequate pressure we must maintain the stroke volume. Because the heart is a passive pump (i.e., it fills passively), the volume it ejects is based on how much blood is returned to the heart and how forcefully the heart contracts. The return of blood to the heart is determined by a number of properties, but because we are interested in the relationship to dizziness and vertigo, which are symptoms that normally occur when upright, we must consider the importance of the upright posture in cardiovascular regulation.

Humans are bipedal and, unlike quadrupeds, during upright standing, there is a significant distance between the head and the feet. This unique posture results in substantial movement of blood from the upper torso to the legs ( Fig. 15.1 ).

Sufficient cardiac output is required to maintain blood pressure (MAP; Eq. 15.1 ). Cardiac output is the product of heart rate and stroke volume, and stroke volume is determined by venous return (the amount of blood returning to the heart); therefore, assumption of the upright position results in considerable reduction in venous return. The result of this reduction in venous return is a drop in mean arterial blood pressure, which if uncompensated results in syncope (i.e., loss of consciousness). An example of this response was demonstrated in a group of elderly males and females who participated in the Maintenance of Balance, Independent Living, Intellect and Zest in the Elderly (MOBILIZE) Boston study ( Fig. 15.2 ).

Note that within 10 seconds of initiating the stand, the participants had roughly a 20-mmHg drop in mean arterial pressure (MAP). The decrease in pressure was transient, and by 30 seconds the blood pressure had returned to baseline levels. This regulation of blood pressure is essential to maintaining consciousness. Returning to Eq. (15.1) , some variables can be modified to maintain pressure. One of these variables is cardiac output, which is dependent on the stroke volume and heart rate. When humans stand upright, there is translocation of blood to the lower limbs and reduction in stroke volume. This results in a reduction in arterial pressure as seen in Fig. 15.2 . To return blood pressure to normal levels, there is a need to modify (increase) the heart rate and/or resistance, which is accomplished by the baroreflex.

Baroreflex Regulation of Blood Pressure

The baroreflex is a mechanism that regulates blood pressure in response to sudden pressure changes. The baroreflex senses pressure changes through stretch receptors located in the aortic arch and carotid arteries at the bifurcation of the common carotid artery into the external and internal carotid arteries. Stretch of these arteries is interpreted as an increase in pressure and results in increased neural firing ( Fig. 15.3 ). These neural signals result in the activation of cardiovascular control centers in the brainstem, which in turn results in changes in the heart rate and resistance. The detailed neural networks involved in the baroreflex response are well described but beyond the scope of this chapter.

Briefly, the baroreflex is able to modulate the heart rate by activating the autonomic nervous system, which directly controls the heart rate. By activating the parasympathetic system, the heart rate slows , and this effect can occur within one beat. Heart rate control under 100 beats per minute is primarily parasympathetic mediated, so the fastest response to a decrease in blood pressure is parasympathetic withdrawal , which allows the heart rate to increase immediately. The baroreflex can cause an increase not only in the heart rate by decreasing parasympathetic tone but also in the contractility of the heart by increasing sympathetic activity to the heart. However, this mechanism is more likely to predominate at higher heart rates, such as those achieved during exercise.

The other baroreflex-mediated response to blood pressure changes is to change peripheral vascular resistance. In humans, parasympathetic activity seems to have little effect on vascular resistance, unlike in many quadrupeds. In contrast, increases in sympathetic activity to the peripheral vessels result in vasoconstriction and an increase in peripheral vascular resistance.

To return to how humans respond to assuming the upright posture, Fig. 15.2 illustrates that there is a reduction in blood pressure. This is sensed by the stretch receptors, resulting in the baroreflex initiating an immediate increase in the heart rate to compensate for the decrease in stroke volume caused by blood moving into the lower limbs. As can be seen in Fig. 15.2 , there is an immediate increase in the heart rate resulting from baroreflex-mediated parasympathetic withdrawal. Despite the increase in heart rate, blood pressure continues to fall. At the same time as the heart rate increases, to maintain mean arterial blood pressure, there is a baroreflex-mediated increase in sympathetic activity to peripheral blood vessels resulting in vasoconstriction. This increase in resistance, which takes approximately 10 seconds, results in increased total peripheral resistance and thus increased MAP ( Eq. 15.1 ; MAP = CO × TPR). As can be seen in Fig. 15.2 , roughly 10 seconds after standing, blood pressure begins to rise and returns to baseline levels in approximately 25 seconds. One can also see that the heart rate begins to decrease within 20 seconds after standing, as resistance compensates for reduced stroke volume.

Returning to the discussion of what this has to do with dizziness and vertigo, without this baroreflex response to drops in pressure, humans would be unable to maintain adequate blood flow to the brain when standing, which would produce dizziness (presyncope) and even loss of consciousness. In fact, in a study of 11,429 patients, orthostatic hypotension (i.e., abnormally low blood pressure when upright) in the first minute of standing was strongly related to dizziness. Because that first minute is the period during which the baroreflex must adjust for the shift of blood into the lower limbs, these data highlight the importance of considering the baroreflex and blood pressure regulation in patients with dizziness, especially when dizziness occurs after standing.

It is well known that aging results in blunting of the baroreflex. This is thought to be the result of stiffening of large vessels, which reduces stretch during changes in blood pressure. Thus, if the same pressure decrease results in an attenuated stretch because of vessel stiffening, an inappropriately low or diminished heart rate increase would be expected. Furthermore, aging processes appear to hinder the ability of increased sympathetic outflow to effect vasoconstriction and increased resistance. Thus elderly individuals are at a greater risk for orthostatic hypotension, which produces dizziness. In addition, some blood pressure medications (e.g., alpha blockers, calcium channel blockers) dampen the ability of peripheral blood vessels to vasoconstrict, and other blood pressure medications (e.g., beta blockers) do not allow the heart to increase its rate to maintain blood pressure.

Thus far this chapter has focused on blood pressure regulation based on the assumption that orthostatic hypotension could be contributing to reductions in CBF and thus the development of dizziness. However, the picture is more complicated than this. It is necessary to understand how CBF is regulated to examine its possible role in dizziness.