CASE STUDY 1
Acute coronary syndrome
Peter Brown is a 58-year-old gentleman who has experienced an episode of crushing
central chest pain while at work. Peter works as a taxi driver and a colleague has taken
him to the Accident and Emergency Department. On admission, Peter is sweaty,
clammy, nauseated and short of breath. He is complaining of chest pain radiating to
his left arm. This is Peter’s ﬁrst presentation to hospital and he has no relevant past
medical history. Peter smokes approximately 20–30 cigarettes per day and takes
alcohol at weekends only. Peter is anxious and is concerned that his wife and children
are informed. He also states his ...view middle of the document...
Furthermore, Henderson (2010) states that in Europe
the estimated incidence of acute coronary syndrome (ACS) lies between 1 in 80 and 1
in 170 of the population. While awareness of risk factors may reduce these ﬁgures, it is
imperative that nursing staff are aware of the seriousness of ACS and the risk it poses to
life. Effective and efﬁcient assessment together with early treatment is at the heart of
An ST elevation myocardial infarction is characterized by ﬁssures or cracks in the atherosclerotic plaques of coronary arteries. As Henderson (2010) explains, plaque rupture triggers
platelet aggregation and activation of the coagulation cascade. This results in coronary
thrombosis and a resulting occlusion in the coronary artery. The size and pattern of the
myocardial infarction are dependent on the location and extent of the occlusion.
Central crushing chest pain
When assessing the patient with a probable ACS, it is imperative to undertake a good history
in relation to the patient’s chest pain and presenting symptoms. It is notable that while chest
pain is one of the main symptoms of ACS, it does not occur in 25 per cent of all cases (Naik
et al. 2007). This is particularly common among patients with diabetes who may not sense
pain due to peripheral neuropathy.
Chest pain arises due to myocardial ischaemia, and the coronary occlusion. As Woods et al.
(2010) state, chest discomfort is related to an imbalance between oxygen supply and demand.
Blood is essentially trying to ‘push’ its way past an obstruction. A myocardial infarction
results when there is prolonged ischaemia, causing irreversible damage to the heart muscle.
Part of the heart muscle is not receiving oxygenated blood due to an obstructed coronary
artery. The lack of oxygenated blood contributes to the pain felt by Peter. Furthermore, the
triggering of the inﬂammatory process, when there is myocardial injury together with the
cellular change from aerobic to anerobic metabolism, causes an increase in the production of
lactic acid. The inﬂammatory process together with the release of lactic acid causes swelling,
oedema and increased pressure on nerve endings, resulting in chest pain.
Sweaty and clammy sensation
Signiﬁcant coronary arterial occlusion will stimulate the sympathetic nervous system (SNS).
This stimulation of the SNS will signal the release of adrenaline and noradrenaline from the
adrenal medulla. Adrenaline release is rapid and will cause a tachycardia in an effort to
maintain homeostasis. The release of adrenaline and noradrenaline also causes peripheral
vasoconstriction due to their effects on alpha- and beta-adrenergic receptors (Karch 2008).
The effect of these naturally occurring catechalomines is to make the skin feel sweaty, slightly
cold and clammy. Furthermore, the release of catecholamines also heightens the state
of anxiety by increasing...