Vasoconstriction is the narrowing (constriction) of blood vessels. When blood vessels constrict, the flow of blood is restricted or slowed.
Vasoconstriction may be slight or severe. It may result from disease, medication, or psychological conditions. Medications that cause vasoconstriction include:
antihistamines and decongestants
cough/cold combinations pseudoephedrine caffeine
"Psychological Effects of Combat"
The Physiology of Close Combat
An understanding of the stress of close combat begins with an understanding of the physiological response to close-range interpersonal aggression. The traditional view of combat stress is most often associated with combat fatigue and Post-Traumatic Stress Disorder, which are actually manifestations that occur after, and as a result of, combat stress. Bruce Siddle has defined combat stress as the perception of an imminent threat of serious personal injury or death, or the stress of being tasked with the responsibility to protect another party from imminent serious injury or death, under conditions where response time is minimal.
The debilitating effects of combat stress have been recognized for centuries. Phenomenon such as tunnel vision, auditory exclusion, the loss of fine and complex motor control, irrational behavior, and the inability to think clearly have all been observed as byproducts of combat stress. Even though these phenomena have been observed and documented for hundreds of years, very little research has been conducted to understand why combat stress deteriorates performance.
The key characteristic which distinguishes combat stress is the activation of the SNS. The SNS is activated when the brain perceives a threat to survival, resulting in a immediate discharge of stress hormones. This "mass discharge" is designed to prepare the body for fight-or-flight. The response is characterized by increasing arterial pressure and blood flow to large muscle mass (resulting in increased strength capabilities and enhanced gross motor skills--such as running from or charging into an opponent), vasoconstriction of minor blood vessels at the end of appendages (which serves to reduce bleeding from wounds), pupil dilation, cessation of digestive processes, and muscle tremors. Figure 2(below) presents a schematic representation of the effects of hormone induced heart rate increase resulting from SNS activation.
The activation of the SNS is automatic and virtually uncontrollable. It is a reflex triggered by the perception of a threat. Once initiated, the SNS will dominate all voluntary and involuntary systems until the perceived threat has been eliminated or escaped, performance deteriorates, or the parasympathetic nervous system activates to reestablish homeostasis.
The degree of SNS activation centers around the level of perceived threat. For example, low-level SNS activation may result from the anticipation of combat. This is especially common with police officers or soldiers minutes before they make a tactical assault into a potential deadly force environment. Under these conditions combatants will generally experience increases in heart rates and respiration, muscle tremors, and a sense of anxiety.
In contrast, high-level SNS activation occurs when combatants are confronted with an unanticipated deadly force threat and the time to respond is minimal. Under these conditions the extreme effects of the SNS will cause catastrophic failure of the visual, cognitive, and motor control systems. Although there are endless variables that may trigger the SNS, there are six key variables that have an immediate impact of the level of SNS activation. These are the degree of malevolent, human intent behind the threat; the perceived level of threat, ranging from risk of injury to the potential for death; the time available to response; the level of confidence in personal skills and training; the level of experience in dealing with the specific threat; and the degree of physical fatigue that is combined with the anxiety.