Causes of syncope

Such reductions in blood pressure could result from reduced venous return and cardiac filling or from reduced baroreflex capacity to induce peripheral vasoconstriction. In the context of exercise, the typical primary effect is obstructed systemic venous return due to elevation of intrathoracic pressure. This pressure increase can be induced voluntarily by forced expiration against a closed glottis and is known as the Valsalva manoeuvre (Fig. 10.1). It occurs naturally during any activity that involves thoracic muscle activation and breath holding, such as carrying heavy suitcases, weight lifting or straining on the lavatory.

Figure 10.1 Effects on blood pressurfilling or from reduced baroreflex capacity to induce peripherale and heart rate of 10 s forced expiration against a resistance of 44 mHg, in a young, healthy adult. During the Valsalva manoeuvre, reduced venous return is compensated by increased sympathetic vasoconstriction and tachycardia, which together restore mean blood pressure near to the pre-test value. The fact that this restoration is not complete until near the end of the manoeuvre reflects the slow time course of vascular smooth muscle contraction following sympathetic activation. This is mirrored by the relative bradycardia that occurs over the 10 s after cessation of the manoeuvre and reflects the bradycardic baroreflex response to elevated peripheral resistance.

In normal, healthy individuals, the arterial baroreflex responses to reduced stroke volume (increased peripheral resistance and tachycardia) are usually fast and large enough to maintain blood pressure at a level that allows adequate cerebral perfusion. Several factors can, however, reduce the effectiveness of these compensations so that consciousness is impaired. Reduced blood volume will reduce the efficiency of cardiac filling and so exaggerate the fall in stroke volume. Increased venous compliance will lead to greater pooling of blood in dependent veins, with less efficient mobilization of this for any given degree of sympathetic vasoconstrictor activation. Finally, any blood-borne influences that cause cerebral vasoconstriction will reduce cerebral perfusion further at any given blood pressure.

All of these additional factors may be associated with athletic performance of specific types. In competitions that involve weight divisions, many performers restrict their fluid intake dramatically in order to make weight, with resulting depletion of plasma volume. Intense, long-term dynamic training has been reported to cause increases in compliance of the large veins, predisposing these athletes to increased venous pooling and to hypotension and fainting during rapid postural change, even in the absence of a Valsalva manoeuvre (Hernandez & Franke 2004). Finally, the elevation of plasma adrenaline (epinephrine) and noradrenaline (norepinephrine) due to the generalized sympathetic discharge associated with central command is enhanced by the additional sympathetic activation due to the stress of competition. Although the cerebral vasculature itself receives only a sparse sympathetic innervation, these circulating catecholamines exert a moderate vasoconstrictor effect on the cerebral precapillary resistance vessels and so reduce brain perfusion at any given level of pressure gradient. An example of Valsalva-induced syncope in a competitive athlete appears in the Case history below.

Comment

Weight lifting, along with many other forms of static and resistive exercises involving the upper body, necessarily causes a very substantial increase in intrathoracic pressure. This is equivalent to a Valsalva manoeuvre and consequently reduces venous return, stroke volume and blood pressure.

In Joe’s case, several interactive factors were probably involved in the Valsalva manoeuvre during competition producing such a severe fall in blood pressure that he lost consciousness. First, his restricted fluid intake prior to competition would have lowered his plasma volume and reduced the amount of blood that could be mobilized from his dependent veins during sympathetic venoconstriction. Second, the stress of competition leads to elevated circulating catecholamines, which will exert some constrictor effect on the cerebral arterioles. Third, most weight lifters hyperventilate immediately before a lift. This produces hypocapnia, which lowers the cerebral interstitial proton concentration. Protons constitute the single most powerful metabolic dilator influence on the cerebral arterioles, so hypocapnia causes significant cerebral vasoconstriction.

Dependence on evaporative cooling

As discussed in Chapter 9 (p. 106), the internal heat generated by even intense prolonged exercise produces only moderate hyperthermia, so long as there is effective evaporative cooling by sweat. By definition, therefore, anything that interferes with heat loss is likely to result in excessive elevation of body temperature. If this rises to more than 41° C (106° F) then central nervous function begins to be impaired, with permanent brain damage or death occurring at only slightly higher temperatures.

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