The role of the emergency department in the management of patients with atypical chest pain

The role of the emergency department in the management of patients with atypical chest pain

Michael Bryant

Michael Bryant FACEM Staff Specialist Emergency Department Ballarat Base Hospital

Address for correspondence: Dr Michael Bryant Emergency Department Ballarat Base Hospital Sturt Street Ballarat VIC 3550

Abstract There is often an inconsistent approach

to the management of patients with chest pain which is not due to myocardial infarction. The stratification of risk groups, utility of diagnostic tests and current practice in the USA are discussed. Recommendations for a change in our current practice are: 1. Patients with unstable angina, acute

myocardial infarction and those with a high suspicion of acute myocardial infarction should be admitted to hospital.

2. Those patients with atypical chest pain should be considered for early exercise testing in or from the emergency department.

3. In the absence of the facility for exercise testing in or from the emergency department, patients with atypical chest pain should be admitted to hospital.

Introduction With the advent of thrombolysis, attention

has been concentrated on making the diagnosis of acute myocardial infarction (AMI), resulting in suboptimal management of non-infarct chest pain. It is the author's observation that the management of patients with non-infarct pain has changed. Formerly, the approach to patients with atypical chest pain involved admission, investigation and exclusion of ischaemic heart disease, whereas current management seems to focus on a limited screening of patients in the emergency department (ED) to detect AMI. Commonly, investigations are used which are unable to do this in less than 24 hours. Such an approach may consist of only two sets of ECGs and cardiac enzymes six hours apart. The patient is often discharged with the potential diagnosis of unstable angina being overlooked. The reasons for the change in practice include limitations on resources such as bed availability and overt or covert pressures from Coronary Care Unit (CCU) staff to admit only patients with AMI. The inconsistency of the approach to patients with atypical chest pain may deny those patients with unstable angina or myocardial infarction an adequate standard of care.

The literature is reviewed to determine the natural history of patients who present to the ED with chest pain and to make recommend-ahons for the management of such patients.

Background Patients who present to the ED with atypical

chest pain are a difficult group to manage. Atypical chest pain may be defined as remotely consistent with but not classical of AMI: 'atypical pain in an atypical location'' that is otherwise unexplained-. Often the symptoms do not fit any obvious clinical pattern and are not

Emergency Medicine 1996 • Vol 8 171

Michael Bryant

clearly cardiac, respiratory, gastrointestinal or musculoskeletal. In contrast to patients with classical, ischaemic chest pain and underlying coronary artery disease who are admitted, patients with atypical chest pain are more likely to be sent home. Parients who are discharged home with an AMI tend to be younger, have atypical symptoms and are less likely to have a previous history of ischaemic heart disease or ECG evidence of ischaemia or AMP"*. The short-term mortality has been shown to be higher in patients discharged home with a missed AMI when compared with those admitted (26% die within 72 hours compared with 12%)-\

Discharging patients with an AMI Several prospective studies have been

performed looking at adverse events that occur after presentation to an ED with chest pain''*^ (Table 1). In these studies, follow up information was available about all patients who attended. For some of those who were discharged, however, the follow up consisted of only a phone call. The mortality rate was therefore able to be determined for all patients enrolled, but the rate of AMI was less certain. Discharged patients were thought to have had an AMI rate of 2.7-5.7% and the mortality rate was found to be 0.7-3.8%3-5.

Fifty one percent of patients who have an adverse event after presentation to the ED with chest pain (AMI, arrhythmias, death, stroke) do so within 48 hours'. Of those that die out of hospital with witnessed symptoms, 37% have consulted a medical practitioner in the days or weeks prior to the event*. This outcome contrasts with an older study that found if all patients with chest pain were admitted to a e c u for three days and subsequently were discharged home with a diagnosis of

'chest pain ?cause' no deaths occurred within 12 months^.

Not all patients who are discharged with an AMI have an atypical history*. The ECG is misread in 23-39%. There is recognised ischaemia in 26-35% (angina at rest, an ischaemic ECG). Fifty one percent have no diagnosis made.

The ECG The large number of ECGs that are misread in

patients discharged with an AMI provides strong support for having ECG machines with diagnostic capability in the ED. In addition to misreading of ECGs, the ECG is an insensitive test for detecting AMI.

Of patients with AMIs proven on postmortem, 39% had a normal ECG or only nonspecific ECG changes on an ECG performed prior to death". The initial ECG was ischaemic or indicative of infarction in only 36-60% of patients subsequently shown to have had an AMI. Conversely, 13-55% of pahents had a normal or non-specific Initial ECG'"".

Classification of patients by clinical and ECG findings

Historical factors may provide help in grading the relative risk of AMI if the initial ECG is normal or non-specific. These include age greater than 60, male gender, quality and radiation of pain and prior history of ischaemic heart disease'. Too much emphasis may be placed on epidemiological risk factors such as family history, age, gender, smoking, diabetes, cholesterol and hypertension, which are predictive of a patient's lifetime risk of AMI and not enough on hard data that may be useful for the current presentation. Indicators with genuine predictive power for AMI include past history, physical signs such as crepitations'' and diaphoresis'^ and ECG changes'^

Table 1. Adverse events

Study group

Lee et al̂

Villanueva et aP

McCarthy et al'

in patients presenting w i th chest

No. in study

3,077

265

5,773

pain

No. sent home

1,283

105

who are sent home f rom the ED

Complications at home

AMI or died Died AMI Died CVA Life threatening arrhytlimia AMI Died Arrested (resuscitated) VF (1 resuscitated) APO

35 9 6 4 3 1

20 2 1

2 1

Complications in hospital

35

1

1,030

172 Emergency Medicine 1996 • Vol f

The role of the emergency department in the management of patients with atypical chest pam

The presence of reproducible chest wall pain on palpation does not exclude AMI. In one study, two of 17 patients with reproducible chest wall pain on palpation were found to have suffered an AMI'*.

Indicators that pain may be of non-cardiac origin include breathlessness, gradually increasing and then decreasing palpitarions, numbness and tingling, dizziness, tiredness, anxiety and tense feelings^.

Despite the insensitivity of the ECG, by using it in conjunction with the clinical findings it is possible to stratify pahents according to their risk of developing AMI. A prospective trial of 7,157 patients with chest pain who attended the ED demonstrated that it is possible to stratify patients using history, examination and the initial ECG'"" (Figure 1). These groups Include obvious AMI, strong suspicion of AMI, vague suspicion of AMI (atypical chest pain) and no suspicion of AMI. Although the risk of developing an AMI for patients with unstable angina is the same as others In the strong suspicion group it is discussed separately to emphasise its importance. Natural history according to patient group 1. Obvious AMI

Only four percent of all patients with chest pain have typical symptoms with ST-segment elevation". These patients have an 80-88% probability of having AMI as some will show resolution of their ECG changes without treatment'". In this group the rate of AMI is

Figure 1 . Stratification of patients with chest pain

OBVIOUS AMI

• Typical symptoms with ST elevation

STRONG SUSPICION OF AMI • Typical symptoms without ST-T segment

elevation • Atypical symptoms with ST-T segment

changes • Sudden development of CCF • Unstable angina

VAGUE SUSPICION OF AMI

• Difficulties in interpretation of symptoms and no signs of acute ischaemia on ECG

NO SUSPICION OF AMI

• No suspicion of coronary artery disease • Stable angina

From Karlson et aV^

higher In those with no past cardiac history compared with those with a history of coronary disease'".

Recent research has focused on reducing the mortality of AMI by using thrombolyhc therapy. ISIS II demonstrated that the mortality five weeks post-AMI was reduced from 13.2% using placebo to 8.0% using streptokinase and aspirin-". Using aspirin alone was associated with a mortality rate of 9.4% compared with 9.2% when streptokinase was used alone. The GUSTO trial showed a 6.9% rate of death or disabling stroke at 30 days when accelerated tissue plasminogen activator was used. This compared with a rate of 7.8% for streptokinase^'. The apparent difference in mortality and morbidity rates between thrombolytic agents is the subject of some controversy"^^'. Whichever agent is used, the earlier that thrombolysis is commenced the lower the morbidity and mortality. The In-hospital mortality has been shown to be 1.2% if thrombolysis is commenced within 70 minutes from onset of pam compared with 8.7% if it is commenced more than 70 minutes from the onset of pain^'. The benefit In mortality reduction with aspirin is less time dependent than the use of thrombolytics. Thus, similar benefit is observed if aspirin is used up to 24 hours from onset of paln^". Unlike thrombolysis there are no eligibility criteria that need to be fulfilled prior to using aspirin. It should be used in all patients unless a contraindication exists. The role of early angioplasty versus thrombolysis is currently under Investigation. Some investigators have found no difference in myocardial salvage^' or vessel patency and mortality^^ but others have found improved left ventricular function^' and a reduced rate of non-fatal reinfarction or death with angioplasty^*"". The number of pahents receiving early angioplasty is expected to Increase in Australia in the near future^'. 2. Strong suspicion of AMI

Twenty percent of patients with chest pain fall into this group, which includes those patients with t^'pical symptoms, without ST segment elevation, atypical symptoms with ST-T segment changes, sudden development of CCF and unstable angina". Overall, patients in this group have a 20-30% probability of having an AMI'". Much present practice is to admit patients suspected of having or developing an AMI to a e c u bed for monitoring. There is a trend, however, to use the ED to exclude AMI in patients having prolonged, ischaemic-soundlng chest pain. This approach is hazardous as it can


Michael Bryant

result in the failure to recognise or diagnose patients with unstable angina with its associated risks of AMI and death. 2a. Unstable angina

Unstable angina is defined as new onset angina (less than eight weeks) that is severe or frequent (three times per day), increased frequency, severity or duration of angina, or angina at rest'̂ -̂ -̂ . This group may be subclassified into subacute and acute on the basis of the presence or absence of episodes within the preceding 48 hours'^.

Untreated unstable angina has a 17.1% risk of AMI or death in three months^^ Intensive medical therapy reduces this to 5.0% risk of AMI and 1.5% risk of death''\ Heparin and aspirin reduce the risk of AMI or death by 75% in the first five days^\ Within six days of commencing treatment with intravenous heparin the risk of AMI can be reduced to 0.8% compared with 3% for aspirin alone^. There is, however, no difference in the number of ischaemic episodes when comparing aspirin with a combination of heparin and aspirin^^.

3. Vague suspicion of AMI

Thirty five percent of patients with chest pain fall into this group'". As many as 25% of patients subsequently proven to have an AMI present with atypical symptoms and signs. Fifty percent of these patients have non-diagnostic ECGs"*. This group includes patients with difficulties in interpretation of symptoms (atypical chest pain) and no signs of acute ischaemia on ECG. Patients in this group have a 10% probability of developing an AMP". 4. No suspicion of AMI

Forty one percent of patients fall into this group'". This group is characterised by symptoms consistent with no suspicion of coronary artery disease.

5. Stable angina

These patients have a one to five percent probability of developing an AMI'". Use in the Australasian emergency department

The natural history of patients in each of these groups is widely varied, demanding different approaches to management. The management of the patient with obvious AMI or strong suspicion of AMI (groups 1 and 2) involves admission and consideration of thrombolysis or angioplasty according to the time of onset of symptoms, evidence of AMI, hospital practice and availability of resources.

For patients in groups 3 and 4, that is with vague suspicion of AMI and no suspicion of

AMI, the problem is one of identifying patients in whom coronary artery disease is the cause of their symptoms. Patients in these groups with ECG abnormalities are promptly admitted from the ED. Patients without ECG abnormalities may undergo further investigation in the ED to detect AMI. This contrasts with the situation in the USA where 'Rule out MI' (chest pain, possibly cardiac with no other obvious cause) constitutes up to 70% of CCU admissions'"*.

In Australia, patients who undergo further testing in the ED include those with: 1. Patients with prolonged (at least 20 minutes

duration), ischaemic-sounding pain who fit into group 2 (strong suspicion group). These patients are diagnosed as having unstable angina if investigation does not detect AMP".

2. Patients with a history consistent with unstable angina. These patients have the same risk of developing AMI as those with prolonged, ischaemic-sounding pain.

3. Patients with atypical pain, possibly cardiac, in whom the diagnosis may be AMI, unstable angina or other. Patients in the first two categories clearly

require admission. Often, however, these patients are investigated using serial ECGs and enzymes to detect AMI, in an approach that is more suitable for patients in category' 3. The usefulness of cardiac enzymes

There is no gold standard test for the detection of AMI. The WHO has defined criteria for the diagnosis of AMI as evolving or diagnostic ECG, and/or diagnostic ECG and abnormal enzymes, and/or prolonged cardiac pain and abnormal cardiac enzymes*. The most common currently used enzyme tests for making the diagnosis of AMI are CK and CK-MB. Tests currently undergoing evaluation for use in the early diagnosis of AMI include myoglobin, troponin T, troponin I, CK-MBl and CK-MB2. Studies evaluating newer enzyme tests diagnose AMI according to WHO criteria. Exceptions include two studies that used echocardiography to detect the development of new wall motion abnormalities"" "'l 1. CKandCK-MB

Myocardial CK is composed of 85% CK-MM and 15% CK-MB"'. Table 2 describes the detection rate of AMI over time using CK and CK-MB in a number of studies. CK is elevated on presentation in 39%-55% of patients with AMI"-*^. CK-MB mass assays may detect AMI within two to six hours of infarction whereas activity assays may require four to eight hours^^. CK-MB is elevated on presentation in 33%-60%

174 Emergency Medicine 1996 • Vol 8


of patients with AMP' •̂ . hi the largest study, CK-MB activity assays detected 77% of AMIs within 12 hours and 96% at 24 hours (in this study 5% of AMIs were diagnosed on CK or LDH alone)^". Hourly measures of CK-MB activity for three hours (resulting in four specimens for analysis) using an upward trend as an indicator of AMI may increase the sensitivity to 92% with a specificity of 96%'. Another problem with cardiac enzyme testing is that CK-MB may be elevated with skeletal muscle injury and its percentage of the total CK may not help to differentiate skeletal from myocardial injury^''".

2. CK-MBj and CK-MBz

CK-MB2 is the only subform of CK-MB to be found in myocardium. CK-MB2 subform assay has a sensitivity of 95.7% and specificity of 93.9% at six hours from symptom onset for the diagnosis of AMI*. This test is currently under investigation.

3. Myoglobin

Myoglobin levels rise within one hour of myocardial cell death and peak at four to six hours. Up to 62% of patients with AMI have an elevated myoglobin level at presentation"^'. Absolute values, trends and doubling of myoglobin levels have been used to detect AMI. The sensitivity in different reports varies from 91% at one hour from presentation, 100% at 1.5 hours", 37% at two hours and 87% at six hours from symptom onset if a doubling of myoglobin levels is used^. Myoglobin has a false positive rate of up to 24%. False posifives may be excluded by using CK-MB for verification. Most recently, it has been used in combination with carbonic anhydrase III to improve its specificity'\

4. Troponin T

Troponin is a structurally bound protein found in striated muscle cells. It is not normally found in blood. Troponin T has a 64% sensirivity for detection of AMI at presentation'"' rising to 100% within 10 hours of symptom onset. AMI can confidently be excluded if analysis is performed between 10 to 120 hours of symptom onseP". Troponin T is a more sensitive indicator of myocardial injury than CK-MB and can be used to predict the development of AMI in pafients with unstable angina (if elevated, the pafient has a 30% risk of AMI in the next two to 10 days)'^

5. Troponin I

Troponin I is found only in myocardial striated muscle. It is as sensitive as CK-MB in detecting AMI and is more specific than CK-MB in detecting AMP^-'*. Levels do not increase with skeletal muscle injury.

Inability to exclude AMI or ischaemic heart disease

None of the biochemical tests appropriate for the investigation of chest pain are able to exclude AMI without prolonged, serial testing. In addition, they do not exclude coronary artery disease or unstable angina (further research is being undertaken with troponin T). Relying on these tests to exclude AMI in less than 24 hours may result in the discharge of patients with AMIs and unstable angina.

Other tests Strategies have developed in the USA

resulting in the 'Chest Pain ED' for the management of patients in low risk groups. One strategy consists of prolonged observation of low

Table 2. Detection of AMI using CK and CK-MB

Study group Number of Number patients with an analysed AMI

Bakker et al"'̂ 290 153

Detection rate of AMI from time of presentation

Presentation 3 hours 6 hours 12 hours 24 hours

CK 61 (40%) CK-MB activity 53 (35%) CK-MB mass 92 (60%)

Gibleretal^' 59

Hedges et al"^ 773 731

21

51 48

CK-MB mass

CK 28 (55%) CK-MB 16(33%)

19(90%) 21 (100%)

Lee et a l " 422

Lee star" 1,460

102 CK41(39%)

431 See text 331 (77%) 415(96%)


Michael Bryant

risk patients in a holding ward on telemetry for up to 72 hours. There is a 4% AMI pick up rate during observation and a 1% AMI rate after discharge home'''. Another strategy involves treadmill testing in or from the ED using strict selection criteria'^'. Different approaches to treadmill testing include (Table 3): 1. Serial enzymes and ECGs for nine hours

followed by two dimensional echocardiography and a graded exercise test before being considered fit for discharge if the results are negative'''*^. One patient suffered an AMI three days after discharge. This patient was one of 782 patients with a negative or non-diagnostic exercise test.

2. Exercise testing of low risk patients (no known coronary artery disease with histories varying from typical to atypical) with a negative ECG (13% had a positive test)*l One patient had an AMI discovered during follow up in hospital after the exercise test.

Recommendations A misread ECG accounts for up to 39% of

patients discharged home with an AMI. The high morbidity and mortality associated with missing the diagnosis of AMI in an often unpredictable environment with staff of varying levels of seniority requires that serious consideration should be given to making the use

of computerised, diagnostic ECG machines mandatory in the ED.

e c u admissions are being reduced in the USA by screening patients in the Chest Pain ED. Reductions in the time taken to screen patients in the Chest Pain ED are being achieved by the performance of an early exercise test. In Victoria, most EDs are unable to access early exercise testing, therefore patients with atypical or prolonged chest pain should be admitted for the treatment of possible unstable angina and exclusion of AMI using traditional tests (ECG and cardiac enzymes). Not all of these patients need to be managed in the CCU. It may be appropriate to manage those patients in whom the diagnosis is unclear, in a general ward bed, using the initial ECG as a predictive tool for the development of complications. Patients with abnormal ECGs have a higher incidence of interventions, life-threatening complications and death'^ than those patients with a normal ECG who are admitted to hospital and who are subsequently diagnosed as having AMI""'"'^' (Table 4).

AH patients with a clear diagnosis of unstable angina should be treated with intravenous heparin and aspirin because of the demonstrated reduction in the AMI rate-'" '̂̂ . All patients with chest pain of possible cardiac origin, unless contraindicated, should be commenced on

Table 3. Results of treadmill testing in the ED

Study Number Results Positive Intermediate Negative

Tsakonis et al̂ ° 28 5 10 13

Lewis at al"̂ 93 12 12 59

Outcomes

All OK at 6 month follow up

1 had an AMI

Gibleretal'5 791 9 782 negative or nondiagnostic 1 AMI 3 days later 5 deaths within 1 month (noncardiac)

Table 4. Compl icat ion

Study

Brush et aV^ Prospective

Rouan et al ' Prospective

Zaienski et al'̂ ^

Retrospective

rates and the ini t ia l ECG in patients presenting w i th chest pain

Number of patients

469 with suspected AMI AMI rate Complications in those

896 with AMI Mortality rate

211 with ?AMI/unstable angina Complications Mortality rate

Negative initial ECG

167 25(15%)

1 (4%)

94 6 (6%)

115

0 0

Positive initial ECG

302 171 (57%) 42 (24%)

802 98(12%)

96

14(14.6%) 8 (8.3%)


The role of the emergency department m the management of patients with atypical chest pain

aspirin because of its substantial benefits and minimal risks if the pain is subsquently proven to be of cardiac origin.

Patients with recurrent or persistent pain in the ED or general ward after admission should be admitted to CCU. They have a 2.4 times greater incidence of AMI, a two to three times increased incidence of intervention and a 3.8 times risk of life threatening complications'*.

Conclusion Screening processes for ED patients with chest

pain, utilising two sets of ECGs and enzymes over a six hour period, followed by discharge and later follow-up, has not been clinically evaluated but has many theoretical risks. None of the currently available tests used in the ED has a 100% sensitivity for the detection of an AMI within six hours. Indeed, even at 12 hours the detection rate of AMls is only up to 76% using

CK and CK-MB. Patients with atypical chest pain require serial ECGs and CK-MBs over 24 hours to detect 96% of AMIs. Newer tests may reduce this time to 10 hours.

Patients with unstable angina, AMI and those with a strong suspicion of AMI should be admitted to hospital. Those patients with atypical chest pain should be considered for early exercise testing in or from the ED. In the absence of this facility these patients should be admitted.

Consideration should be given to the admission of low risk patients to stepdown units as this has been shown to be a safe strategy for those patients subsequently determined to have had AMI"-32-5o-5i M«^ .̂ These patients could possibily be admitted to a general ward bed if exercise testing is unavailable as they have a low morbidity given a normal initial ECG and enzyme assay (Figure 2).

Figure 2. Best management of patients with chest pain

CHEST PAIN

Recognised unstable angina

Obvious AMI or strong suspicion of AMI

(24% of all patients)

Vague or no suspicion of AMI (76% of all patients)

(1-10% probability of AMI)

Coronary Care Unit _AMI

AMI not detected

^ ' Early exercise

testing available

' r Admit to telemetry or general ward bed

Negative Positive

I Discharge with early follow up

Admit

Emergency Medicine I99b • Vol 8 177

Michael t

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55.

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(Accepted: 16 April 1996)


The role of the emergency department in the management of patients with atypical chest pain

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