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Transient asystole: aetiology and treatment by paramedics

02 March 2012
Volume 4 · Issue 3

Abstract

Transient asystole is seen relatively rarely by paramedics. It is often mistaken for syncope or seizures, which means that paramedics may miss an opportunity to help with a swift diagnosis and therefore help reduce morbidity and mortality (Deakin et al, 2010). This article explores the aetiology of transient asystole along with its pathophysiology and analyses how some prescription drugs may contribute to the onset of transient asystole. It will look at treatment options that are available to paramedics including atropine, and establish if this is the optimal treatment for the condition.

Asystole is the total cessation of any electrical activity in the heart (Walthall, 2008). It results in the myocardium not contracting (Tortora and Derrickson, 2009), leading to a lack of circulating oxygenated blood being supplied to the brain, causing irreversible brain damage and death (Ballinger and Patchett, 2007).

Transient asystole differs from terminal asystole in that it is not a total failure of electrical activity (Bashian and Wazni, 2009). The period of asystole is brief or temporary, and ends when another pacemaker site initiates an escape beat or rhythm (Winters, 2009). Without this, ventricular standstill and death would follow (Walthall, 2008). Some specific cells of the heart have the ability to generate their own impulse, albeit at a slower rate (see next section), when the rate initiated by the sinoatrial (SA) node is too slow or impaired (Rolls et al, 2007).

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