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Cardiovascular Complications during Acute SCI

Disrupted sympathetic innervation and unopposed parasympathetic activity after cervical or high-thoracic SCI leads to cardiovascular abnormalities, which includes profound changes in arterial BP and HR. Complications that arise can be short-term (acute), long-term (chronic) or both. During the acute phase of SCI, patients typically present with neurogenic shock, which refers to a condition that is characterized by the simultaneous presence of bradycardia and arterial hypotension without any other determined etiology. Together these conditions are recognized as an acute complication occurring following SCI (Furlan & Fehlings, 2008; Krassioukov, 2009; Popa et al. 2010).

Bradycardia is defined as a HR of less than 60 beats per minute (bpm). Arterial hypotension is defined as a systolic BP below 90 mmHg and a diastolic BP of less than 60 mmHg (Popa et al. 2010; Wecht et al. 2013). Lower basal HR and low resting blood pressure are both regarded as a consequence of reduced SNS activity in the initial stages following SCI (Teasell et al. 1996). Orthostatic hypotension (OH) or intolerance following SCI is commonly seen in patients with high SCI, especially early after injury (Sampson et al. 2000). OH occurs when there is a significant decrease in BP during postural changes, and may be symptomatic or asymptomatic (Illman et al. 2000). More specifically, OH is characterized by a decrease in systolic BP of 20 mmHg or more or a reduction in diastolic pressure of 10 mmHg or more on assuming an upright posture from a supine position (Claydon et al. 2006). Postural hypotension for injuries above the thoracic SNS output is related to the absence of reflex vasoconstriction and pooling of blood in extremities due to reduced SNS efferent activity in response to sudden postural changes (Teasell et al. 1996).

In addition, acute SCI patients may also experience autonomic dysreflexia (AD), a condition characterized by transient episodes of hypertension and imbalanced reflex sympathetic discharge in response to stimulation below the level of injury. During AD, systolic BP reaches up to 300 mmHg and is accompanied by symptoms such as headache, slow HR and upper body flushing. This reaction is graded, as opposed to all-or-none, and is seen in SCI patients with lesions above level T6, with rare occurrences in injuries below this level (Karlsson, 2006; Krassioukov et al. 2003). ADis recognized as a cardiovascular complication characteristic of chronic SCI but has been observed in some cases to occur earlier (Krassioukov, 2009; Krassioukov et al. 2003; Silver, 2000). The following three sections evaluate incidence of neurogenic shock, OH and AD during acute SCI.