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Click on any of the headings and subheadings to rapidly navigate to the relevant section of the guidemap
CK-MB fraction CK-MB isoforms- unstable angina - likelihood of significant CAD
- unstable angina - factors increasing short term risk of death or AMI
- high risk ACS patient
- moderate risk ACS patient
- low risk ACS patient
- extremely low risk ACS patient
- 5-level approach to risk stratification of ACS patients
- HER protocol from the University of Cincinatti College of Medicine
- table summarising a 5-level approach to risk stratification
| Introduction |
- an ECG still remains the most specific diagnostic tool in evaluating the ED patient with chest pain => however, the initial ECG may be negative/non-diagnostic in > 40% of AMI cases
- the perfect cardiac marker test, with a 100% early sensitivity + 100% specificity in diagnosing an AMI, does not exist => different cardiac marker tests are used in varying combinations
- an ED physician must have knowledge about i) the sensitivity and specificity of each cardiac marker test, ii) the pattern of release of each cardiac marker into the bloodstream, iii) the time-period when each cardiac marker will still be detectable in the serum and iv) which combination of cardiac marker tests are readily available in his institution => so that he can develop a rational approach to selectively using the available cardiac marker tests
- this guidemap is divided into two parts - the first part provides some basic background information on cardiac markers, while the second part (medical decision-making) deals with the risk stratification of chest pain patients in an ED setting
| Total creatine kinase (CK) |
- remains the most commonly utilized cardiac enzyme test
- the serum CK includes enzymes released from a variety of sources, particularly skeletal muscle
- three different iso-enzymes of CK exist = CK-MM, CK-MB, CK-BB
- skeletal muscle consists mainly of CK-MM (99%) and CK-MB (1%)
- cardiac muscle normally contributes CK to the blood stream in the following proportions - 80% CK-MM and 20% CK-MB
- CK-BB is found primarily in the brain and contributes very little to the serum TCK level
- most of the serum CK is derived from skeletal muscle and the serum level reflects the total body muscle mass
- the serum CK increases within 4 - 6 hours of an AMI, peaks at 12 - 24 hours after an AMI and remains detectable for 48 - 72 hours
- small females with a small total body muscle mass may have low serum CK levels, which may not rise above the threhold value after an AMI => reason for always ordering the more specific CK-MB test in all patients with a suspected AMI
- using the ratio of CK-MB/CK as an index helps to detect cases of AMI where the CK may not rise above the threshold laboratory value for CK, but where small elevations in CK-MB will cause an increased CK-MB/CK index
- the CK (when used in isolation) is of limited value, because of the very high incidence of false-positive CK results
- there are many cardiac and non-cardiac conditions that cause an elevated serum CK
Cardiac causes
| - cardiac contusion | - defibrillation |
| - pericarditis | - myocardial infarction |
| - cardiac surgery | - myocardial ischemia |
| - cardiac catherization | - myocarditis
|
| - acute agitated psychosis | - acromegalic myopathy |
| - alcoholic myopathy | - amyotrophic lateral sclerosis |
| - brain infarction | - chronic renal disease |
| - convulsions | - delirium tremens |
| - dermatomyositis | - diabetes mellitus |
| - Duchenne's muscular dystrophy | - electrocution |
| - familial hypokalemic periodic paralysis | - hyperthermia |
| - hypothyroidism | - intramuscular injections |
| - malignancies and sepsis | - malignant hyperthermia |
| - myositis | - pulmonary infarction |
| - renal trauma/infarction | - Reye's syndrome |
| - rhabdomyolysis | - shock |
| - surgical procedures | - thoracic outlet syndrome |
| - trauma | - trichinella infections |
| - vigorous physical exertion
|
| CK - MB fraction |
- previously measured electrophoretically and expressed as CK activity (* time-consuming test)
- now measured by immunoassay and expressed as CK-MB mass (* a more rapid and more more sensitive test than the CK-MB activity test)
- serum CK-MB mainly comes from myocardial tissue, but a small amount comes from other tissues (small intestine, tongue, diaphragm, uterus and prostrate)
- an elevated serum CK-MB is usually highly specific for an AMI, although rare false-positives exist (mainly from skeletal muscle release and renal failure)
- a single CK-MB may be positive within hours (2 - 6 hours) after an AMI, but serial CK-MB measurements are usually required to reach 100% sensitivity for AMI
- the sensitivity at 4 hours is < 50%, but the sensitivity should reach ~ 100% for AMI 10 - 12 hours after the onset of the chest pain (* an AMI cannot be ruled-out before ~ 9 - 10 hours after the onset of symptoms; longer if the patient has ongoing chest pain)
- the CK-MB enzyme is cleared from the blood stream within 48 - 72 hours and the test will be normal if an AMI patient presents to the ED a few days days after the AMI; other causes of a false negative test include testing too early (< 6 hours) and testing too late (> 36 hours) after the onset of an AMI
- serial CK-MB testing is used by some cardiologists to determine the size of an infarct and the success of reperfusion following thrombolytic therapy (serum levels double in two hours)
- the CK-MB/CK index ratio is useful in detecting an AMI when the total CK is not elevated (small females with small total body mass); the CK-MB/CK index increases the specificity of the test
- a falsely-low CK-MB/CK index can occur in a patient having an AMI if the CK is markedly elevated secondary to associated skeletal muscle injury (even though the total CK-MB mass may be elevated from the release of CK-MB from both cardiac and skeletal muscle => the ratio is low because of the disproportionately large release of CK-MM from damaged skeletal muscle)
Causes of a false-positive
CK-MB
| - pericarditis | - cardioversion with multiple shocks |
| - prolonged tachyarrhythmia | - skeletal muscle trauma |
| - myositis, muscular dystrophies | - Reye's syndrome |
| - hypothyroidism | - alcoholism |
| - peri-partum period | - acute cholecystitis |
| - malignancy (prostrate, breast) | - drugs (aspirin, tranquilizers) |
| - collagen diseases (SLE) | - Rocky Mtn spotted fever |
| - extreme physical activity | - hyperthermia |
| - electrical/thermal burns | - rhabdomyolysis
|
| CK-MB isoforms |
- only one isoform (CK-MB2) is present in cardiac muscle
- CK-MB2 is converted to CK-MB1 in the serum and the normal serum CK-MB2/CK-MB1 ratio (about 1.0) is increased in patients with an AMI
- isoforms may be detectable 1 - 2 hours earlier than CK-MB and may also peak earlier (4 - 6 hours) than CK-MB
- the isoform test may reach > 95% sensitivity ~ 6 hours after the onset of chest pain and result in earlier exclusion of an AMI than is presently possible with CK-MB testing ( > 95 % sensitivity only after ~ 8 - 10 hours)
- however, the isoform test requires specialized equipment and is technically difficult to perform; consequently, the test is not available at all institutions
- using the CB-MB isoform test as the standard cardiac marker test results in a major increased expense and only decreases the AMI-exclusion threshold from ~ 8 hours (CK-MB) to ~ 6 hours (CK-MB isoforms)
| Myoglobin |
- arguably the most sensitive early marker of myocardial injury
- first appears in the serum within 1 - 2 hours and peaks at 4 - 6 hours; returns to baseline in 6 - 12 hours
- greatest utility is in detecting evidence of an AMI within a few hours of onset of the chest pain => ? allows for more efficient risk stratification => ? a patient with a positive serum myoglobin at the time of ED presentation should be admitted to a CCU and treated appropriately with anti-ACS therapy
- however, the test has a very low specificity (elevated levels found in many conditions eg. exhaustive exercise, trauma, rhabdomyolysis, surgery, shock, renal failure) with many false positive test results
(* it is advisable to confirm positive serum myoglobin results with more specific cardiac marker testing [eg. serum troponin] in low risk patients prior to commencing with anti-ACS therapy)
- there is a lack of an universally accepted myoglobin reference standard, and a lack of standardization between different assays => the cardiac specificity of the test is increased if it is used in conjunction with a skeletal muscle specific marker (eg. carbonic anhydrase III) or by calculating the change in serum myoglobin over 1 - 2 hours
- some investigators believe that a negative myoglobin at 4 hours effectively rules-out an AMI in low risk patients, thereby enabling earlier functional stress testing and earlier potential discharge from a chest pain unit
(* other physicians think that the myoglobin test is not really 100% sensitive and that only a negative serum CK-MB or serum troponin test at ~ 8 - 10 hours can exclude an AMI)
- serum myoglobin levels may correlate with infarct size
- as an indicator of reperfusion, serum myoglobin is probably at least as good as serum CK-MB and serum troponin and it peaks earlier
| Cardiac troponins |
- troponins are regulatory proteins in cardiac muscle that modulate the interaction between actin and myosin, functioning as a "calcium switch"
- two forms – cardiac troponin T (cTnT) and cardiac troponin I (cTnI)
(* cTnT testing is only available from one vendor, while cTnI testing is available from many vendors and the test may be more highly specific with less false positives)
- the rise in serum level of cTnT parallels the rise in serum level of cTnI after myocardial injury, and both tests parallel the rise in serum CK-MB levels in a patient with an AMI; with a similar sensitivity at 4 - 6 hours (~ 50%) and at 12 hours (> 95%) for an AMI
(* troponin testing may be more sensitive because troponin is found only in cardiac tissue and ambient serum levels are extremely low in healthy individuals, while the serum CK-MB has to exceed a broad reference range before it is regarded as positive - small rises due to minor cardiac damage may be "invisible" to standard testing procedures)
- the serum troponin levels remain elevated for 10 - 14 days and cTnT/cTnI testing is useful for detecting an AMI if the patient presents to the ED many days after an episode of chest pain (wide diagnostic window)
- a repeat qualitative serum troponin test cannot be used to detect a recurrent AMI/ACI a few days after admission for an episode of chest pain - if the initial serum troponin test was positive => serial quantitative serum troponin levels need to be measured
(* a single positive qualitative serum troponin at the time of ED presentation is not necessarily clinically useful in diagnosing an acute AMI if a chest pain patient presents to the ED with acute chest pain - if the patient also has had one-or-more episodes of chest pain > few days prior to the ED visit => the positive serum troponin could be related to the previous episode of chest pain => it is better to follow serial serum myoglobin and/or CK-MB values to determine whether the most recent episode of chest pain could be due to an AMI)
- a false-positive serum cTnT test may very rarely occur in a wide range of traumatic, inflammatory and congenital myopathies and in chronic renal failure
- a false positive serum cTnI test occurs even more rarely - near-zero incidence - in skeletal muscle disorders and renal failure and occurs mainly in other conditions causing myocardial damage eg. myocarditis, cardiac contusion, recent cardiac surgery or catheterization
(* all serum cardiac enzyme markers may be positive in rhabdomyolysis - however, the serum cTnI is usually only slightly elevated, despite signficant elevations in both the CK and CK-MB)
- a positive serum troponin test may occur in a patient with unstable angina and probably reflects a micro-infarct (infarctlet) not detectable by CK-MB testing
- a positive serum troponin test in a patient with a history suggestive of cardiac ischemia (and who has a non-diagnostic ECG and a normal CK-MB level) defines a subset of high-risk acute coronary syndrome (ACS) patients = Acute cardiac insult (ACI)
- an elevated serum troponin has been found to be an independent predictor of 30 day mortality in patients with non-Q wave infarctions and ACI, and a positive serum troponin test helps in risk stratification and ED triage => an ACS patient with a positive serum troponin test should definitely be admitted to the CCU for aggressive ACS therapy eg. anti-thrombotic agents +/- anti-platelet agents +/- early cardiac catheterization
- the increased risk of adverse cardiac events in troponin-positive patients may also directly correlate with the degree of increase of the serum troponin
- repeat serum troponin testing should be performed if the serum troponin at presentation is negative => repeat at 4 hours and again at 8 hours => ? whether early detection of increased serum troponin may allow for earlier institution of advanced ACS therapies in these "extra" (CK-MB-negative) patients identified by serum troponin testing
(* serum troponin testing may also produce a cost benefit if future studies suggest that only troponin positive patients benefit from aggressive ACS therapy)
| Emerging cardiac markers |
- cardiac markers that may detect cardiac ischemia before infarction develops (glycogen phosphorylase-BB isoenzyme, glutathione peroxidase activity), or which detect platelet activation and thrombus formation (P selectin, thrombus precursor protein) are being evaluated, but none of these cardiac marker tests have entered mainstream clinical practice
| Medical decision-making in an ED setting |
- when a patient presents to the ED with acute chest pain of < 3 - 6 hours duration, the initial objectives are to stabilize the patient, stratify risk, and determine treatment
- initial triage decisions in a patient with acute chest pain of < 3 - 6 hours duration (or other symptoms compatible with ACS) are primarily based on the clinical history and the ECG, and cardiac markers have little utility in the decision-making process
- the first decision that has to be made when risk stratifying a possible acute coronary syndrome (ACS) patient is to define that subgroup of patients, who definitely have an AMI or unstable angina based on the interpretation of an immediate ECG, and to then triage those patients to the CCU after initiating appropriate therapy in the ED
- a patient with chest pain, who has an initial ECG showing pathological ST elevations (> 1mm in two-or-more leads) or a new LBBB, is at high risk of having an AMI (and adverse cardiac complications) and the patient should be admitted to the CCU following the initiation of thrombolytic therapy in the ED (or PCTA in the cath lab)
(* cardiac markers probably have no real decision-making utility in this situation - a positive serum troponin test could be secondary to recent micro-infarctlets, or it could be due to the present AMI if there was a significant time-delay before ED presentation=> the decision of whether to use thrombolytic therapy is not necessarily influenced by the existence of a positive serum troponin test)
- a patient with chest pain, who has an initial ECG showing ST depression (> 1 mm in two or more leads - not known to be old) and/or markedly symmetrical T wave inversion in multiple leads (not known to be old), has a significant probability of having an ACS and should therefore be admitted to the CCU
(* none of the cardiac markers are sensitive/specific enough to definitely exclude an AMI before ~ 8 - 10 hours, and frequent serial sampling during the first 8 hours has no real clinical utility if the patient is going to be admitted to the CCU and treated aggressively for cardiac ischemia)
- all the other ? ACS patients should be risk stratified into high, moderate or low risk groups and triaged accordingly
- there are many sophisticated algorithmic risk stratification protocols - Goldman computer-based protocol, ACI - TIPI protocol, AHCPR clinical practice guideline protocol - but these protocols have not been widely accepted in clinical practice, and many physicians continue to base their triage decisions on medicolegal concerns, rather than using these risk-stratification protocols
- the major disadvantage of simply triaging chest pain patients on the basis of an ED physician's personal "gestalt" is that there is a marked variation in triage decision-making results between "risk-tolerant" and "risk-averse" physicians, and the establishment of a more rational triage decision-making process (suitable for all triaging physicians) may not only minimize the inadvertent discharge of AMI patients, but also minimize the unnecessary utilization of expensive hospital resources for low risk chest pain patients
- one possible approach could be to provide all ED physicians with chest pain triage pocket cards based on the ACC/AHA Guidelines for the Management of Patients with Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction
- the one pocket card is based on an assessment of the likelihood of ACS, and the second pocket card is based on an assessment of the short-term risk of death or non-fatal AMI in patients with ACS
| Likelihood that initial evaluation findings represent ACS |
| Feature | High likelihood
(Any of these symptoms) |
Intermediate likelihood
(Absence of high likelihood features and presence of any of these features) |
Low likelihood
(Absence of high and intermediate likelihood features but may have some of these features) |
| History | Chest/left arm pain or discomfort as chief symptom,
reproducing prior documented CAD
Known history of CAD/AMI |
Chest/left arm pain as chief symptom
Age > 70 year Male sex Diabetes |
Probable ischemic symptoms without any intermediate
likelihood characteristics
Recent cocaine use |
| Examination | Transient MR
Hypotension Diaphoresis Pulmonary edema or rales |
PVD | Chest discomfort reproduced by palpation |
| ECG | New (or presumably new) transient ST deviation (<0.5mm) or T wave inversion (>.02mm) with symptoms | Fixed Q waves
Abnormal ST segments or T waves not documented as new |
T wave flattening or inversion in leads with
dominant R waves
Normal ECG |
| Cardiac markers | Elevated troponin or CK-MB levels | Normal | Normal |
| Short-term risk of death or non-fatal AMI in patients with ACS |
| Feature | High-risk prognosis
(At least one of these symptoms) |
Intermediate-risk prognosis
(Absence of high-risk features and presence of any one of these symptoms) |
Low-risk prognosis
(Absence of high-risk or intermediate-risk features but may have some of these features) |
| History | Accelerating tempo of ischemic symptoms during preceding 48 hours | Prior AMI, PVD, CVD, or CABG | |
| Character of pain | Ongoing rest pain > 20 minutes | Rest pain > 20 minutes, now resolved, with moderate
or high likelihood of ACS
Rest pain < 20 minutes or relieved by sl NTG |
New onset angina without prolonged rest pain but with moderate or high likelihood of ACS |
| Clinical findings | Pulmonary edema most likely caused by ischemia
New or worsening MR murmur, S3 or new-worsening rales Unstable vital signs Age > 75 years |
Age > 70 years | |
| ECG | Rest angina with transient ST-segment changes
(>0.05mv)
Bundle branch block - new or presumed new Sustained ventricular tachycardia |
T wave inversion > 0.2mv
Pathologic Q waves |
Normal or unchanged ECG during episode of chest discomfort |
| Cardiac markers | Elevated troponin or CK-MB levels | Slightly elevated troponin (eg. TnT >0.01 but < 0.1 ng/ml) | Normal |
- however, many emergency physicians may have difficulty utilizing these risk designation tables to risk stratify patients in 'real-life' situations, and they may seek a simpler approach that is easier to use in an ED setting
- I think that the easiest approach is to simply divide chest pain patients into four ACS subgroups - high risk, moderate risk, low risk and extremely low risk (based on age + gender +/- multiplicity of coronary risk factors) - and to triage high risk patients to the CCU, moderate and low risk patients to a chest pain center (or chest pain observation unit) and to discharge extremely low risk patients
High risk ACS patients - who should be admitted to a CCU
1) a patient with chest pain, who has an initial ECG showing pathological ST elevations (> 1mm in two-or-more leads) or a new LBBB
2) a patient with chest pain, who has an initial ECG showing ST depression (> 1 mm in two or more leads - not known to be old) and/or markedly symmetrical T wave inversion in multiple leads (not known to be old)
3) a chest pain patient with hemodynamic instability, history of loss of consciousness, pulmonary edema, bilateral rales above the bases, S3 or new mitral regurgitation or echocardiographic evidence of left ventricular dysfunction
4) a chest pain patient with dynamic ST segment changes on serial ECG or continuous ST-segment trend monitoring
5) a patient with a history of known coronary artery disease (angina or previous AMI or previous angioplasty or previous CABG) + normal/unchanged ECG + typical anginal-type chest pain - especially if the pain is worse than previous angina or the same as a previous AMI, or if the anginal pain persists despite NTG therapy
6) a moderate-high clinical risk patient + normal initial ECG + positive serum troponin test at the time of ED presentation
7) a high clinical risk patient + normal physical examination + normal ECG + typical chest pain
- some physicians would only admit patients in group 7) to a CCU if they had additional risk factors - certain clinical factors and/or ECG abnormalities that significantly increased their risk of short-term adverse cardiac events eg. active, ongoing ischemic chest pain not responsive to sl NTG (IV nitrate use may be a surrogate marker for active, ongoing ischemic chest pain), systolic blood pressure < 100 mmHg, bilateral rales above the bases and malignant arryhthmias on arrival => in other words, patients with new onset angina could be admitted to a CPOU and may only need to admitted to a CCU if they had ongoing chest pain or additional risk factors
Moderate risk ACS patients - who should be admitted to a CPOU
1) a patient with a history of known coronary artery disease + normal/unchanged ECG + chest pain that is atypical and not suggestive of angina
2) a patient with chest pain + an ECG showing non-specific ST depressions of 0.05 - 1 mm, or T wave inversion > 1mm in leads with dominant R waves
3) a low clinical risk patient + normal initial ECG + positive serum troponin test
(* Bayesian analysis suggests that there is a high incidence of false positive early cardiac marker test results in a chest pain patient, who has a low pre-test clinical probability of having ischemic chest pain => further testing will be required to determine whether the initially positive cardiac marker test is truly indicative of ACS - it may be safer to admit the patient to the CCU if further testing cannot be promptly accomplished in the ED or chest pain observation unit)
4) a moderate-high clinical risk patient + normal physical examination + normal ECG + atypical chest pain
- this is a "broad" category and includes patients with atypical anginal pain (chest pain that lasts longer than 5 inutes but is atypical in character and location, patients with prolonged chest pain that waxes-and-wanes, patients with varying combinations of jaw and/or neck and/or shoulder and/or arm pain) and patients with a multiplicity of coronary risk factors, who have non-anginal chest pain
5) a patient with known stable effort angina, who develops rest angina that resolves spontaneously (or promptly following sl NTG use)
Low risk ACS patients - who can be admitted to a short-stay CPOU or sent home
1) a sub-group of low "clinical risk of severe CAD" patients + atypical chest pain
Extremely low risk ACS patients - who can be sent home
- a chest pain patient, who has a low pre-test probability of CAD + normal ECG, and who clearly has benign non-cardiac chest pain (chest pain or pressure that lasts less than 5 minutes, recurrent chest pain that is fleeting in nature, chest pain that is definitely pleuritic or musculoskeletal in nature) is an extremely low risk ACS patient => the patient can be discharged from the ED without any need to perform serial cardiac marker testing (or any other ACS-exclusionary testing) if there is no other reason to pursue alternative non-ACS diagnoses
- frequent serial sampling of cardiac markers (using an accelerated serial testing program) should be utilized for chest pain patients admitted to a chest pain center (CPOU)
- the National Academy of Clinical Biochemistry (NACB) has prepared recommendations on the use of cardiac markers - they recommend an accelerated protocol using an "early" marker that is reliably increased in the blood within 6 hours of the onset of ACS symptoms and a "definitive" marker that is reliably increased in the blood within 6 - 9 hours of the onset of ACS symptoms
- one suggested cardiac marker testing protocol recommends measuring serum myoglobin at 1 and 3 hours after ED arrival and serum troponin at 6 hours and 9 hours after ED arrival => patient is then transferred to the CCU if there are any positive ECG changes, positive cardiac markers or clinical deterioration
- a serum myoglobin-based protocol has the theoretical advantage of ratcheting-down the time it takes to "rule-out" an AMI
- an alternative approach is to only use a "definitive" cardiac marker protocol - measurement of the serum troponin at presentation, and 4 and 8 hours after presentation => this approach is simple, cost-effective and highly accurate in predicting the risk of adverse cardiac events
(* conservative physicians may want to extend the testing period to 12 hours to ensure ~ 100% sensitivity for an AMI)
- although it may be feasible to exclude an AMI in low-moderate risk patients using these accelerated serial cardiac marker protocols, further diagnostic evaluation and disposition still remains controversial
- a patient with a low pre-test clinical probability of ACS, who has a normal ECG + negative serum troponin ~ 8 hours after the onset of the chest pain, has an extremely low probability of any short-term adverse cardiac event; and many investigators feel that the low-risk patient can be safely discharged from the ED, and that any further cardiac workup can be performed on an outpatient basis
- however, some physicians think that simply excluding an AMI by cardiac marker testing does not definitely exclude significant underlying CAD in intermediate risk patients, and they think that further diagnostic evaluation is necessary prior to hospital discharge
- consequently, many chest pain centers utilize pre-discharge graded exercise ECG stress testing (or pre-discharge stress echocardiography, or pre-discharge stress nuclear perfusion imaging) as part of their standard chest pain protocol if the serial cardiac marker tests remain negative
(* some chest pain centers perform early treadmill exercise stress testing in low-risk patients if the first serum troponin measured at 3 hours after ED arrival is negative, and they do not perform serial cardiac marker testing - while other chest pain centers think that treadmill exercise testing is really only useful in patients with an intermediate probability of CAD and that it is not useful in patients with a low probability of CAD because it does not significantly change the post-test probability of severe CAD)
- a patient with negative serial troponins + negative stress testing is definitely at very low risk of having a short-term adverse cardiac event => the patient can be safely discharged and any necessary further testing can be performed as an outpatient
- some chest pain centers use up-front nuclear perfusion imaging studies and promptly discharge the patient if the study is negative - without performing serial cardiac marker testing
(* a major advantage of up-front nuclear imaging is that it may allow for the earlier detection of ACS within a few hours of ED arrival, and a negative nuclear scan often excludes ACS in low risk patients)
- other investigators use up-front electron beam computerised tomographic scanning to look for coronary calcifications, and discharge the patient if the scan is negative - without performing serial cardiac marker testing
(* this diagnostic modality is very new and further research is required to determine its place in the armamentarium of ACS-exclusionary testing)
- further studies are also needed to determine whether combined approaches
(cardiac markers + imaging studies) will allow for a better combination
of quality of care + efficiency of care
- a good overall approach may be to use the 5-level approach to
risk stratification of ACS patients as proposed by the Medical College
of Virginia
Level 1 = ECG criteria of ST-segment elevation AMI requiring
thrombolytic therapy
Level 2 = High probability of unstable angina and potential
non-Q wave AMI - manifested by transient ST-segment elevation, ST-segment
depression, T wave inversion, or known CAD + typical symtoms
Level 3 = High probability of unstable angina, but low probability
of AMI - manifested by typical symptoms lasting longer than 30 minutes,
a non-diagnostic ECG and no prior history of CAD
Level 4 = Low-to-moderate probability of unstable angina - manifested
by less than 30 minutes of typical symptoms or prolonged atypical symptoms,
a non-diagnostic ECG and no history of CAD
Level 5 = Non-cardiac chest pain
- note that the protocol suggests using immediate nuclear imaging in the ED for level 4 patients and discharge if the test is negative, and that the protocol does not recommend serial enzyme testing or stress testing prior to discharge
(* some physicians think that immediate nuclear imaging can only exclude
ACS if the sestamimbi is injected during the rest pain or within ~2 hours
of rest pain; and that a resting nuclear imaging does not otherwise exclude
ACS => they feel that stress testing is required prior to discharge)
- an aternative approach is to follow the "Heart ER" strategy
- the HER protocol from the University of Cincinnati College of Medicine
- the HER protocol is designed for low-to-moderate risk patients with chest pain who are admitted to a chest pain center; and excludes patients with acute ST segment elevation, ST segment depression > 1 mm, a history of CAD, or patients with hemodynamic instability or unstable angina
- note that a rest nuclear SPECT imaging is recommended if the patient is having pain at the time of ED arrival
- if the patient is not having chest pain at the time of ED arrival => serial cardiac marker testing is done at 0, 3 and 6 hours
- a graded exercise stress ECG test is performed prior to discharge if the serial cardiac marker tests are negative
(* a rest SPECT nuclear imaging study can be used if the patient has contra-indications to, or cannot, exercise; a stress echocardiogram can be used instead of nuclear imaging depending on institutional preferences, local test availability, local expertise and cost considerations)
- if sestamimbi nuclear imaging
is not available, one could triage patients according to this summarised
table, which is a combination of my 4-level approach and the Medical
College of Virginia's 5-level approach
| Triage of ED chest pain patients using a 5-level approach |
| Category | Criteria | Disposition |
| Level 1
Definite
|
|
CCU |
| Level 2
Definite
|
|
CCU |
| Level 3
Probable
|
|
CCU or CPOU |
| Level 4
Possible
|
|
CPOU |
| Level 5
ACS
|
|
Discharge/admit |
*Clinical pearls
Unstable angina is a clinical diagnosis and negative cardiac markers should not influence medical decision-making re: admission of chest pain patients with suspected cardiac ischemia events to a CCU
- retrospective studies show that the diagnosis of unstable angina is only made in ~ 40% of unstable angina patients at the time of ED presentation - based on the initial clinical history and/or ECG => the other 60% of unstable angina patients are diagnosed by the presence of recurring/worsening chest pain during the chest pain observation period (~ 20%) or during pre-discharge functional stress testing (~ 40%) => ? whether up-front nuclear imaging (or up-front echocardiography) may increase the early detection rate and result in earlier therapy and better outcomes
| Appendix |
| Common serum markers used to detect AMI |
| Marker | Initial elevation
after AMI |
Mean time to peak
elevation after AMI |
Time to return to baseline after AMI |
| Myoglobin | 1 - 4 h | 6 h | 18 - 24 h |
| CK-MB | 3 - 12 h | 10 - 24 h | 48 - 72 h |
| MB-isoforms | 1 - 6 h | 4 - 12 h | 38 h |
| cTnI | 3 - 12 h | 10 - 24 h | 5 - 10 days |
| cTnT | 3 - 12 h | 12 - 24 h | 5 - 14 days |
| Suggested testing schedule for cardiac markers |
| Marker | < 6 h | 6 - 12 h | 12 - 24 h | 24 - 48 h | > 48 h |
| Myoglobin | +++ | + | - | - | - |
| Troponin I | + | ++ | +++ | +++ | +++ |
| Troponin T | + | ++ | +++ | +++ | +++ |
| CK-MB | + | ++ | +++ | - | - |
| MB- isoforms | ++ | +++ | + | - | - |
- physicians should use careful judgement in interpreting cardiac marker results when working in hospitals using ‘standardized’ cardiac marker ordering protocols, which are not based on the duration of chest pain prior to ED arrival
Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.