Physical examination

The physical examination is generally not helpful in diagnosing ACSs when compared with the value of historical data and ECG findings, except when it points to an alternate process. On the other hand, clinicians must not be lulled into a sense of security by chest pain that is partially or fully reproduced by palpation, because 11% may have infarction or UAP [26]. Pope and colleagues [2] found the pulse rate to be lower in patients who had a final diagnosis of ACSs versus those who had a final diagnosis of non-ACS (P — .02), but this difference was not considered clinically significant.

Pulse rate observation in isolation appeared to be generally not helpful in ACSs identification. First, the patient's pulse rate could be slowed by the presence of P-blockers as part of a prior treatment regime, coincident vagal stimulation from ACSs (eg, reflex bradycardia and vasode-pressor effects associated with inferoposterior wall AMI), or diagnostic/therapeutic procedures in the ED (eg, phlebotomy, intravenous access). Second, the patient's pulse may be increased by adrenergic excess from just having to come to the ED and everything that accompanies such a visit, in addition to the adrenergic excess (eg, tachycardia and increased peripheral vascular resistance) associated with possible ongoing ACSs.

In a large series of patients in the ED who had suspected ACS, median first and highest systolic blood pressures (SBPs) were higher in patients who had a final diagnosis of ACSs [2]. This finding suggests that the adrenergic excess associated with ACSs might be greater than that associated with non-ACS diagnoses. However, to use this hypothesis as a predictive factor, clinicians must have some idea of their patient's baseline blood pressure, which is not the case in most ED evaluations. Thus, the usefulness of this observation may be limited.

In the same series [2], in addition to the effect of adrenergic release during acute ischemia, the higher initial and highest pulse pressures found in patients who had a final diagnosis of ACSs may also reflect the lower compliance of the ische-mic left ventricle. Of relevance to those who are candidates for thrombolytic therapy, excess pulse blood pressure (the extent to which a patient's pulse pressure exceeded 40 mmHg for patients who had an SBP of more than 120 mmHg) places these patients at increased risk for thrombolysis-related intracranial hemorrhage [29].

Pope and colleagues [3] found that median first, median highest, and median lowest SBPs of patients who had AMI and were subsequently classified as Killip class 4 (cardiogenic shock) were above the threshold of this classification (SBP <90 mmHg) for these three blood pressure observations. This finding suggests that the adrenergic excess associated with ACSs may be greater than that associated with non-ACS diagnoses. Although the number of such patients in this analysis was small, it did suggest that patients who have ACSs can present with apparently normal blood pressures and can go on to develop cardiogenic shock.

Abnormal vital signs and certain combinations of these have been shown to be critical observations in clinical outcome prediction. The reported probability of infarction decreases with a normal respiratory rate [38] and increases with diaphoresis [15], but other signs mainly help identify high-risk patients who have infarction [56]. In the predictive instrument for AMI mortality proposed by Selker and colleagues [36], blood pressure, pulse, and their interaction figured prominently in three of the six clinical variables used to develop the prediction instrument.

Finally, rales (of any degree), but not S3 gallops, have been more frequently seen in patients who have a final diagnosis of ACSs [2]. This finding is not surprising, as several clinical syndromes of pump failure can complicate ACSs. The investigators'

failure to find association between an S3 gallop rhythm and ACSs at final diagnosis is surprising, but it may have to do with a failure to document this finding consistently in the medical record on the part of the physicians in the EDs at study sites.

Standard 12-lead ECG

A complete summary of evidence related to the diagnostic usefulness of the standard ECG was recently published [20,57], and this background will not be repeated in this article. However, the National Heart Attack Alert Program (NHAAP) Working Group on ''Evaluation of Technologies for Identifying Acute Cardiac Syndrome'' [57] found that most studies evaluate the accuracy of the technologies and only a few evaluate the clinical impact of routine use. Furthermore, the group concluded that although the standard ECG is a safe, readily available, and inexpensive technology with a high sensitivity for AMI, it is not highly sensitive or specific for ACSs. However, the ECG findings remain an integral, if not the most important, part of the evaluation of patients who have chest pain, and the Working Group recommended that they remain the standard of care for evaluating patients who have chest pain in the ED.

The ECG provides essential information when the diagnosis is not obvious by symptoms alone [58], despite one study noting that the results of the ECG infrequently changed triage decision based on initial clinical impressions [59]. The generally dominant weights given to ECG variables in mathematic models for predicting ACSs substantiate this impression [6,7,10,15,16]. Moreover, the initial ECG is increasingly important in intrahospital triage because of its value in predicting complications of AMI [60-62].

The fundamental limitations in the standard ECG include:

• Single brief sample

• Lack of perfect detection

• Confounding baseline patterns

• Interpretation

• Clinical context

• Imperfect sensitivity and specificity

First, it is a single brief sample of the whole picture of the changing supply-and-demand characteristics of unstable ischemic syndromes. If a patient who has UAP is temporarily pain-free when the ECG is obtained, the resulting tracing may poorly represent the patient's ischemic myocardium.

Second, 12-lead ECG is limited by its lack of perfect detection [63]. Small areas of ischemia or infarction may not be detected; conventional leads do not examine satisfactorily the right ventricle [64] or posterior basal or lateral walls (eg, AMIs in the distribution of the circumflex artery) [65,66].

Third, some ECG baseline patterns make interpretation difficult or impossible, including prior Q waves, early repolarization variant, left ventricular hypertrophy, bundle branch block, and dysrhythmias [67]. Lee and colleagues [9] demonstrated that when the current ECG shows ischemic findings, availability of a prior comparison ECG improved triage.

Fourth, ECG waveforms are frequently difficult to interpret, causing disagreement among readers—so-called ''missed ischemia.'' In a study of patients who had AMI and were sent home, ECGs tended to show ischemia or infarction not known to be old, with 23% of the missed diagnoses owing to misread ECGs [8]. Jayes and colleagues [53] compared ED physician readings of ECGs with formal interpretations by expert electrocar-diographers, and calculated sensitivities of 0.59 and 0.64 and specificities of 0.86 and 0.83 for ST-segment and T-wave abnormalities, respectively. McCarthy and colleagues [18] and a review of litigation in missed AMI cases [68] emphasized this factor of incorrect ECG interpretation. In the largest study to date of ACSs in the ED, Pope and colleagues [3] found that although the rate of missed diagnoses of ACSs (2.1% AMI, 2.3% UAP) was low, there was a small but important incidence of failure by the ED clinician to detect ST-segment elevations of 1 to 2 mm in the ECGs of patients who had MI (11%). Correct ECG interpretation by ED physicians is doubly important today because of the need to use interventions such as thrombolytic agents and percutaneous coronary intervention appropriately in ACSs.

Fifth, the implications of the ECG findings must be interpreted in their clinical context, a process performed intuitively by clinicians and formally stated in Bayesian analysis. When symptoms alone strongly suggest ischemia, a normal or minimally abnormal ECG will not substantially decrease the probability of ischemia. Conversely, when the presentation is inconsistent with acute ischemia, an abnormal ECG (unless diagnostic abnormalities are present) will only modestly increase the likelihood of ischemia. Bayes' rule tells us that the ECG will have the greatest impact when symptoms are equivocal [69].

Finally, the ECG suffers from imperfect sensitivity and specificity for ACS. When interpreted according to liberal criteria for MI (ie, ECGs that show any of the following as positive for AMI: nonspecific ST-segment or T-wave changes abnormal but not diagnostic of ischemia; ischemia, strain, or infarction, but changes known to be old; ischemia or strain not known to be old; and probable AMI), the ECG operates with high (but not perfect) sensitivity (99%) for AMI, at the cost of low specificity (23%; positive predictive value 21%; negative predictive value 99%). Conversely, when interpreted according to stringent criteria for AMI (only ECGs that show probable AMI), sensitivity (61%) drops and specificity equals 95% (positive predictive value 73%; negative predictive value 92%) [20].

Despite its usefulness, the ECG is insufficiently sensitive to make the diagnosis of ACSs consistently. The ECG should not be relied on to make the diagnosis but rather should be included with history and physical examination characteristics to identify patients who appear to have a high risk for ACSs (ie, a supplement to, rather than a substitute for, physician judgment). In rule-out AMI patients, a negative ECG carries an improved short-term prognosis [60,70-73]. Providing the interpreter with old tracings would intuitively seem to be of value because baseline abnormalities make current evaluation difficult. However, Rubenstein and Greenfield [74], in a study of 236 patients presenting to EDs with the complaint of chest pain, found that only a small proportion might have benefited from having a previous baseline ECG available (5% might have avoided unnecessary admission). Furthermore, there was no patient for whom a baseline ECG would have aided in avoiding an inappropriate discharge. ECG sampling should be periodic, not just static. The pitfalls of not ordering ECGs in younger, atypical patients, and of misinterpretation should be anticipated. Finally, clinicians should not be reluctant to obtain a second opinion—by fax transmission if necessary—for difficult tracings.

ST-segment and T-wave abnormalities

ST-segment and T-wave abnormalities are the sine quo non of ECG diagnosis of ACSs. Numerous studies [63,73,75] have found that 65% to 85% of CCU patients who have ST-

segment elevation alone will have had an infarction. Other investigators found that if Q waves and ST-segment elevation were present, 82% to 94% actually sustained AMI [63]. However, it must be remembered that ST-segment elevation can occur in the absence of ischemia (ie, ''early repolarization'' variant, pericarditis, left ventricular hypertrophy, and previous infarction even in the absence of a ventricular aneurysm) [76]. Conversely, Pope and colleagues [2] showed that a large percentage of patients who have ACS (20% AMI, 37% UAP) can present with initial normal ECGs.

In their study of patients in the ED who had suspected ACS, Pope and colleagues [2] found that ST-segment elevation of either 1 to 2 mm or more than 2 mm was more frequently associated with a final diagnosis of ACSs (9% ACS versus 7% non-ACS; 5% ACS versus 1% non-ACS, respectively; P = .001). A full 30% of patients who have ST-segment elevation of 1 mm or greater had a final diagnosis of AMI. In addition, in a study of missed diagnosis of ACSs in the ED, Pope and colleagues [2] found a small but important incidence of failure by the ED clinician to detect ST-segment elevations of 1 to 2 mm in the ECGs of patients who had AMI (11%). This incidence represents an important and potentially preventable contribution to the failure to admit such patients.

ST-segment depression usually indicates suben-docardial ischemia. If these abnormalities are new, persistent, and marked, the likelihood of AMI increases. About 50% to 67% of admitted patients who have new or presumed new isolated ST-segment depression have infarctions [64,75]; even more patients have probable ischemia. Pope and colleagues [2] found that all degrees of ST-segment depression (0.5, 1, 1-2, and >2 mm) were more commonly associated with a final diagnosis of ACSs (12% ACS versus 7% non-ACS; 8% ACS versus 3% non-ACS; 2% ACS versus 0% non-ACS, respectively; P = .001). A full 19% of patients who had ST-segment depression of at least 0.5 mm or greater had a final diagnosis of AMI. Quantitative ST-segment depression and cardiac Troponin T status have been found to be complementary in assessing risk among ACS patients [77]. ST-seg-ment depression may also occur in nonischemic settings, including patients who are hyperventilating, those taking digitalis, those who have hypokale-mia, and those who have left ventricular strain (without voltage criteria) [76].

Inverted T waves may reflect acute ischemia. One study showed that isolated T-wave inversion occurred in 10% of CCU admissions, of whom 22% had AMI [78]. T-wave changes may reflect prior myocardial damage or left ventricular strain [76]. The study by Pope and colleagues [2] found that certain T-wave patterns (inverted 1-5 mm, inverted R 5 mm, or elevated) were more frequently associated with a final diagnosis of ACS (32% ACS versus 17% non-ACS; 1% ACS versus 0% non-ACS; 4% ACS versus 1% non-ACS, respectively; P — .001). Flattened T waves did not have the same association with an ACS final diagnosis (18% ACS versus 20% non-ACS; P — .001). Furthermore, 39% of patients who had inverted T waves of at least 1 mm or greater had a final diagnosis of AMI.

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