11 thoughts on “A Question”

  1. Nice article, thanks.I *used* to have the time to read articles, but all that seems to have been taken over by my day job and the need for sleep.

  2. Any intracerebral bleed can cause ECG changes, subarachnoids are especially likely to do this. The change can range from non-specific ST and T wave changes through to those that look just like an MI. The mechanism is said to be the massive outpouring of catecholamines that accompany a bleed that then cause coronary vasospasm. The changes often resolve completely

  3. Yep, it's the catecholamines all the way. Patients are totally drained for weeks after a SAH; nil catecholamines left to deal with everyday demands.

  4. It doesn't come much simpler than that.(As in, trying to simplify the language used erases the meaning from the question)

  5. I've included the relevant text from a review article in AnaesthesiaH.B. Lim and M Smith

    Systemic complications after head injury: a clinical review

    Anaesthesia, 2007 62 ;474-482

    I'm not sure about the copyright / fair usage so you may or may not want to post the whole excerpt, but you may want to include the link to the article (pay per view I'm afraid)

    http://www.blackwell-synergy.com/doi/full/10.1111/j.1365-2044.2007.04998.x

    Cardiac abnormalities after subarachnoid haemorrhage are well characterised and include global myocardial dysfunction and electrocardiographic (ECG) changes [7]. Regional wall motion abnormalities are particularly prevalent and related to catecholamine-induced myocardial injury [8]. Cardiovascular abnormalities also occur after severe TBI but the pathophysiology of these changes is less well understood. However, as with subarachnoid haemorrhage, the massive catecholamine release associated with severe TBI is believed to be implicated [9, 10], with the degree of catecholamine release directly related to the severity of the brain injury [9].

    ECG changes after TBI may occur in the absence of an acute coronary event [11, 12] and are related to the degree of intracranial hypertension [13]. Prolongation of the QT interval, ST segment abnormalities, flat or inverted T waves, U waves, peaked T waves, Q waves and widened QRS complexes have all been described [13, 14]. Prolonged QTc syndrome is particularly associated with the presence of traumatic subarachnoid haemorrhage and the degree of QTc prolongation corresponds to the severity of the head injury [15]. ECG changes evolve over several days after injury and most are transient, resolving within 2 weeks, although prolonged QT interval and U waves may be permanent [14]. Prolonged QTc syndrome may predispose to ventricular arrhythmias [15].

    The sympathetic hyperactivity associated with severe TBI causes direct injury to the myocardium [16]. Catecholamine-induced vasoconstriction is intense, leading to hypertension and tachycardia and a secondary increase in myocardial oxygen demand. However, because catecholamines also induce coronary vasoconstriction, there is no simultaneous increase in myocardial oxygen delivery and subendocardial ischaemia may occur, resulting in impairment of ventricular function. The catecholamine surge may also cause direct injury to the myocardium and subendocardial haemorrhage is present in up to 50% of patients who die from their head injury [17]. In a study of fatal head injury, 15.7% of patients developed global systolic dysfunction and regional wall motion abnormalities [18]. Left ventricular dysfunction is particularly common and may be reversible [19]. ECG abnormalities, particularly symmetrical T wave inversion or prolonged QTc, are risk factors for left ventricular systolic dysfunction [20].

    The initial catecholamine response after TBI results in a hyperdynamic circulation usually characterised by tachycardia and hypertension, although a marked sinus bradycardia, due to a baroreceptor reflex, is also classically described (the Cushing response). Raised intracranial pressure (ICP) causes depression of sympathetic activity because of disruption of brainstem autonomic pathways by a variety of causes including direct injury, cerebral swelling and diffuse axonal injury [21]. Conventional teaching suggests that isolated head injury does not result in hypotension in adults and, whilst this wisdom reinforces the importance of identifying and treating active bleeding, there is evidence to support a neurogenic aetiology of hypotension in some cases. In one study neurogenic hypotension occurred in 13% of patients with isolated head injury and was associated with a higher mortality than haemorrhagic hypotension [22]. Neurogenic hypotension may result from disruption of brainstem centres for haemodynamic control and is often associated with diffuse axonal injury [23].

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