Introduction
Patients presenting with chest pain, along with other symptoms suggestive of acute coronary syndromes, are increasing by the day, not only in Australia but also globally (Cullen, 2010). Indeed, according to Vermeer & Bajorek (2008), acute coronary syndromes (ACS) are increasingly becoming a major health challenge in Australia, accounting for about 25,000 mortalities and 156,000 infirmary admissions annually. Yet, not all patients presenting with chest pains have a final diagnosis for ACS, with statistics indicating between 75% and 85% of patients evaluated in Australia ultimately do not exhibit a final diagnosis of ACS (Cullen, 2010). These statistics provide compelling evidence on the need for health institutions to develop guidelines aimed at identifying patients at risk of ACS, and, more importantly, the need to continuously update them with current evidence-based knowledge to assist clinicians select the best management strategies for a typical presentation (Kumar & Cannon, 2009).
This paper aims to provide a critique to the chest pain management guidelines in use in acute clinical settings at my current hospital. In particular, the critique will first review relevant literature to explore whether existing guidelines are based on the latest literature, then rationalize how the guidelines need to be reformulated, based on current literature, to respond to presenting demands with regard to rapid risk assessment for ST-elevation acute coronary syndrome and the therapeutic management of chest pain caused by ACS.
Brief Overview of the Policy
This particular policy, last reviewed in 2010 and expected to be reviewed again in 2013, concerns itself with how to assess patients presenting with ischemic chest pain in acute ward settings, and the therapeutic management of the condition depending on severity or intensity. As is the case with other policies aimed at undertaking risk assessment for ACS, this policy comes with a flow chart demonstrating the steps to be followed in the therapeutic management of ischemic chest pain, the protocols of managing this type of pain, and a set of guidelines to ensure successful risk assessment and management of ischemic chest pain. The presented flow chart, along with the prescribed guidelines and modalities of therapeutic management, will be critiqued against current literature in the rationalization section of this paper.
Review of Current Literature
Vermeer & Bajorek (2008) observe that “…ACS encompasses a number of cardiovascular presentations which differ by the extent and duration of coronary occlusion, and include unstable angina, non-STEMI, and STEMI” (p. 591). The Scottish Intercollegiate Guidelines Network (SIGN) notes that all these conditions projects “…a common aetiology in the formation of thrombus on an inflamed and complicated atheromatous plaque” (SIGN, 2007, p. 1).
A systematic review of three articles (Siebens et al, 2007; Aroney et al, 2008; Marshall, 2011) demonstrated that the clinical presentation of ACS is most often acute chest pain and/or discomfort. Ryan & Reeder (2011) note that the primary objective of chest pain management guidelines in any hospital setting, therefore, is to aid in precisely determining the cause of the chest discomfort and/or pain, and swiftly commencing the appropriate therapy. According to SIGN (2007), many treatments, especially for ST elevation acute coronary syndrome, are time dependent, implying that clinical assessment of patients presenting with acute chest pain must be rapid, methodical and evidence-based so as to improve outcomes.
A meta-analytic review of several studies (SIGN, 2007; Werf et al, 2008; ARC/NZRC, 2011) interested in rapid risk assessment for the likelihood of ST-elevation ACS came up with almost similar baseline factors which must be considered together in the assessment of STEMI, and which include: the nature of the symptoms presenting; advancing age; history of ischemic heart disease; sexual orientation, and; the quantifiable number of traditional cardiovascular risk factors present. High risk attributes presented by patients with suspected ACS include: worsening angina; protracted or sustained pain (>20 minutes); radiation of the pain to the neck, lower jaw, or left arm; pulmonary oedema; autonomic nervous system activation (pallor, sweating); dyspnoea; irregularities of the pulse; hypotension, and; arrhythmias (SIGN, 2007; Werf et al, 2008; Marshall 2011; ICSI, 2010).
Available literature in risk assessment of patients with suspected ACS (SIGN, 2007; Marshall, 2011; Werf et al, 2008) is in agreement that such individuals require a comprehensive clinical assessment and the accurate recording of a 12 lead electrocardiogram (ECG). As observed by Werf et al (2008), “…additional recordings of lead V7-V8 or V4R are helpful to make the diagnosis in selected cases (true posterior infarction or right ventricular infarction, respectively)” (p. 2914). It is fundamentally important that ECG monitoring be initiated as soon as possible in acute care settings to detect life-threatening conditions such as arrhythmias.
Werf et al (2008) and Marshall (2011) note that blood sampling for serum markers of necrosis should be regularly done in the acute stage, but clinicians and nurses should not wait for the results to commence reperfusion treatment. However, new evidence as demonstrated by Werf et al (2008) reveals that many of these patients will show a characteristic elevation of biomarkers of myocardial necrosis and advance to Q-wave myocardial infarction.
In the therapeutic management of chest pain caused by ACS, which is the second component of this analysis, Werf et al (2008), notes that “…relief of pain is of paramount importance, not only for humane reasons but also because the pain is associated with sympathetic activation, which causes vasoconstriction and increases the workload of the heart” (p. 2914). Current practice, according to these authors, demands the administration of opiods such as morphine at intervals of 5-15 minutes until the pain fully subsides. In such context, 4-8 mg of morphine should be administered to the patient at the first instance, with additional doses of 2mg at the stated intervals until the pain is fully relieved (Werf et al, 2008;). Current evidence underlines the importance of avoiding intramuscular injections in such patients.
As expected with any administration of opiods, side effects – including nausea, vomiting, sedation, hypotension with bradycardia, dizziness, and respiratory depression – may present (Werf et al, 2008). In the light of this, current practice encourages the administration of an antiemetic (e.g. palonosetron, metoclopramide 5-10 mg intravenous) simultaneously with the opiods. Atropine (0.5-1 mg intravenous, up to a total dose of 2 mg) should be administered in the event that hypotension and bradycardia present. Oxygen (2-4 L/min) should be administered, either by mask or nasal drops, to patients who are either exhibiting symptoms of respiratory depression (e.g., breathlessness) or are exhibiting typical features of heart failure or shock. A systematic analysis of three articles (Werf et al, 2008; Marshall, 2011; Mount et al, 2008) demonstrate that non-steroidal anti-inflammatory drugs (NSAIDS) should never be administered for acute chest pain relief, in large part because of possible prothrombotic effects.
Critique & Rationalization
Based on the literature reviewed, it can be argued that the protocols and procedures contained in the hospital’s policy on the management of patients presenting with acute chest pain are current. However, there arises a need to improve some of the components based on new evidence that has been synthesized from the review.
To begin with, the policy takes cognizance of the fact that acute care settings must always have evidence-based guidelines for the rapid and consistent management of patients presenting with ischemic chest pain. This fact is corroborated by SIGN (2007) and Marshall (2011), who argue that management of such pain is critically time-dependent and, as such, clinical assessment of patients must always be rapid, methodical and evidence-based. As noted in the review of current literature (Werf et al, 2008), the policy also stresses the need to urgently respond to ischemic chest pain to assuage pain and curtail the risk of myocardial damage.
The critiqued article is consistent with current literature in terms of ECG monitoring and pain observation and assessment. However, it fails to take into account the procedure for blood sampling for serum markers of necrosis, which is needed in acute care settings. In the context of the 12 lead ECG monitoring, the policy fails to underline the importance of undertaking additional recordings of lead V7-V8 or V4R if proper diagnosis in selected cases is to be made (Werf et al, 2008). The policy also fails to incorporate high risk attributes presented by patients with suspected ACS to make the task of early risk stratification much easier and accurate. The most important attributes, according to Goyal et al (2008), include sustained pain (>20 minutes); radiation of the pain to the neck, lower jaw, or left arm, and worsening angina.
The policy is largely consistent with current literature in terms of the therapeutic management of chest pain caused by ACS. However, instead of administering oxygen (6L mask/2L nasal prongs) as a general practice for these patients, current literature encourage clinicians to use non-invasive monitoring of blood oxygen saturation to evaluate the need for oxygen administration or, in severe cases, ventilator support (Werf et al, 2008; Brieger et al, 2009). To keep in line with current practice, the revised policy should include a component detailing that non-steroidal anti-inflammatory drugs should not be administered as a remedy for relieving chest pain caused by ACS because of possible prothrombotic effects.
Conclusion
This review has brought important insights into the fore about the management of patients presenting with chest pain. A critique of the hospital’s policy against current literature demonstrates that the hospital’s guidelines on the management of ischemic chest pain in acute clinical settings are satisfactory, particularly in the development of comprehensive evidence-based guidelines for the rapid and consistent management of patients presenting with ischemic chest pain, development of procedures for rapid risk assessment, and in the therapeutic management of chest pain occasioned by ACS. However, some components of the critiqued policy need improvement, and new components need to be included to make it more comprehensive. For example, the 12 lead ECG monitoring need to be improved to include additional recordings of lead V7-V8 or V4R to facilitate proper diagnosis. In equal measure, the policy needs to incorporate the procedure for blood sampling for serum markers of necrosis, particularly in the light of the fact that this policy is used in clinical care settings. In addition to explicitly outlining the high risk attributes presented by patients with suspected ACS to make the task of early risk stratification much more easier and accurate, the policy also needs to encourage use of non-invasive monitoring of blood oxygen saturation to evaluate the need for oxygen administration rather than administering oxygen to all patients as a general practice.
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