Key facts:
Authors: Jamila Aliyu Dikko, Natalie Acors and Peter Glennon
Top Tip: Put an IV cannula in ASAP, cardiac arrest is possible
Key Differential Diagnoses
- Stable angina
- Pulmonary embolus
- Aortic dissection
- Pericarditis
- Other (diagnose non-serious causes, eg GI, 'musculoskeletal', with care)
Key Investigations
- ECG within 10 mins of arrival
- Cardiac Troponin I/T > 6h from onset pain (± 12h if negative, and still suspicious of cardiac pain)
- FBC, U+E, LFT, Bone, Glucose, Clotting, CRP
- CXR (to exclude other diagnoses)
- TIMI SCORE (for NSTEMI/UA): [Ref] (TIMI 0 = 5% event rate; 6/7 = 40%; TIMI ≥3 = revascularisation?)
Key Treatment
- OXYGEN high flow, if hypoxic
- IV (DIA)MORPHINE 2.5-10 mg + IV METOCLOPRAMIDE 10 mg, if pain severe
- PO ASPIRIN 300 mg stat; then 75 mg od
- PO CLOPIDOGREL 300 mg stat (NSTEMI/unstable angina), 600 mg stat (STEMI); then 75 mg od (1 year); OR PO TICAGRELOR 180 mg stat, then 90 mg bd (1 year)
- (NSTEMI/UA) SC ENOXAPARIN 1 mg/kg bd; OR SC FONDAPARINUX 2.5 mg od (if no angiography within 24 hrs)
- (STEMI) Primary percutaneous intervention (PCI) or Thrombolysis (if <12h); IV ALTEPLASE 10-15 mg (see BNF) or IV TENECTEPLASE 30-50 mg
Key Management Decision
- (STEMI) PCI or Thrombolysis (both <12h)
Background
The initial ECG can be normal in ACS. Cardiac arrest is possible as soon as the diagnosis of ACS is suspected
The approach to a patient with ischaemic sounding chest pain
- The initial aim is to ensure that ST elevation MI (STEMI) is promptly diagnosed because this will require emergency reperfusion with primary PCI or thrombolysis
- Therefore everyone with chest pain should have an ECG as soon as possible, ideally at the same time as the history and IV access are being obtained
- Even if the initial ECG does NOT show ST elevation, ECGs should be repeated at intervals if the patient has ongoing or recurrent chest pain
- Patients giving a history of cardiac-sounding chest pain at rest without ST elevation on the ECG, may have non-ST elevation MI (NSTEMI). This diagnosis rests on finding an elevated cardiac troponin level, implying heart muscle damage not sufficient to produce ST elevation. Cardiac troponins take at least 4 hours to rise after myocardial damage, and are detectable in most cases at 6 hours. In some cases the rise is not detectable until 12 hours
- Some emergency departments have bedside triple cardiac marker assays (eg Troponin I, CKMB, Myoglobin) which increase sensitivity at the expense of specificity. This can be used as a 'rule out' at 6 hours to enable early discharge of patients with an non-ischaemic sounding history, who do not have any other high risk features (diabetes, known coronary disease, ST depression on ECG; eg TIMI 0) and whose pain has settled
- If in doubt, observe, with the patient in an easily visible area, and an IV cannula in situ
Introduction
- Chest pain is common. It is a difficult symptom because the possible causes range from the trivial to the life-threatening
- ACS is one of the most common reasons for acute medical admission
- ACS is not a diagnosis. It is a syndrome, which is a collective term for the three conditions discussed and a specific diagnosis should be confirmed once all relevant information has been collected
- The three conditions are; unstable angina, NSTEMI and STEMI. The latter two terms are also not complete diagnoses. Which part of the heart is ischaemic? Ie is it a Inferior or Anterior NSTEMI?
- ACS can also present as sudden death. In MI, atypical presentations (pain in arms or mouth/neck pain, no pain ('silent'), and collapse) are well recognised, especially in the elderly, patients with diabetes, and pre-menopausal women
- ACS usually occurs when an acute thrombus forms in an atherosclerotic coronary artery. Spontaneous thrombolysis then occurs in 2/3rds
- The ECG is the most important investigation and should be done with 10 mins of presentation. BUT. In ACS it may be normal, initially (20%). The initial diagnosis of acute coronary syndrome should be based on the history. Ie, if history is good (especially in an at-risk patient), do not send them home, and treat them .. ie,
- Put a venflon in, start ACS protocol (aspirin, clopidogrel and enoxaparin/fondaparinux) make sure the patient is an observed area, and do a Troponin T at 12h, then decide. Start insulin sliding scale if patient has diabetes mellitus or raised blood glucose (BM)
- So .. HISTORY HISTORY HISTORY. STEMI or NSTEMI can evolve as you observe patient. And there are other causes of ST changes and raised Troponin. If in doubt, observe (in a visible area) and do serial ECGs, and Trop Ts, if diagnosis unclear
- If you are unsure, ask a senior to see them NOW, not in 12h
- 10% in-hospital mortality, 30% overall. 50% of deaths occur in first 2 hrs, most out of hospital. 30% of patients with unstable angina, have an MI in 3 mths. Time is myocardium [Ref]
Definition
- An acute coronary syndrome includes unstable angina, NSTEMI and STEMI
Epidemiology
- IHD is the most common cause of death in UK
- 240,000 people experience AMI (5/1000) in England and Wales per annum
Pathology
- Atheroma: plaque rupture, thrombosis, inflammation
- Rarely: coronary spasm, embolism (rare), vasculitis, dissection (aortic)
Patterns of ECG
- Inferior, = II, III and AVF
- Lateral = I, AVL, V5-6
- Septal = V1-2
- Anterior = V2-5
- Anteroseptal = V1-4
- Anterolateral = V3-6, I + aVL
- Extensive anterior / anterolateral = V1-6, I + aVL
- Posterior, V1
[Ref]
Risk factors
Non-modifiable
- Age
- Sex (male)
- Race
- Family history of premature IHD (most important single factor)
- Premature menopause
Modifiable
- BP
- Cholesterol
- DM
- Smoking
- Alcohol (J shaped curve)
- Obesity (probably, though unclear whether risk factor independent of BP and cholesterol: [Ref]
)
Note: in young people, consider vasculitis, cocaine, congenital abnormalities, increased O2 requirements (eg acute hyperthyroidism) or decreased O2 delivery (eg severe anaemia)
Symptoms
- Chest pain (left, radiating to arms, neck, face); often described as crushing, 'like a tight band'
No te: intensity and description of pain no guide to extent of ACS; pleuritic or positional pain, or chest tenderness, makes ACS less likely
[Ref] - Sweating, nausea and vomiting (favour infarction)
- Sometimes, SOB and palpitations
Note: atypical presentations (above) well recognised
Key questions
- "When did the chest pain start?"
- "Do you (or your family) have any previous history of angina or heart attacks?"
Signs
- Frequently normal
- Sometimes, low grade pyrexia
- Or, of heart failure (SOB), cardiogenic shock (pale, cold and clammy skin) , arrthymia etc
8 reasons why ACS is harder to manage than you would think
1. Causes of chest pain range from trivial (musculoskeletal) to very serious (MI, dissection). Consider the extremely broad differential diagnosis of patients with chest pain
2. Support workers will ask you to assess ECGs with no knowledge of the patient. Don't. Go and see them
3. Its all in the history and you may not have taken many. The history contains many clues which can help identify the cause of the pain. But. Beware over-reliance on words. Ie do not rely on the history alone to classify the chest pain eg MI pain is not always 'crushing' (and anyway, what is 'crushing' for one patient is 'heavy' for another); and pleuritic pain is not always worse on coughing
4. Examination is frequently normal
5. Risk factors can help to prioritise and guide investigations. BUT, risk factors have their limitations ie 75% of patients with an MI have no history of IHD. And patients with many risk factors can have an URTI
6. Investigations have their limitations. Eg, there are other causes of a raised troponin (pericarditis and renal failure). You don't know if ST depression or LBBB is new or not. Conversely ECG can be normal. CXR is usually normal
7. It is easy to be falsely reassured if initial cardiac investigations (ECG, enzymes) are normal (or 'normal for them') – further tests are often needed to confirm that the pain is not cardiac in origin. Ie it is the progression of tests that leads to a diagnosis
8. It is hard to involve seniors at 4am. Nonetheless, if you are not sure, that is what is required
Investigation
A -ve Troponin T at 12h has a useful negative predictive value. A +ve one needs interpretation
Blood
- FBC, CRP
- U+E, LFTs, Bone, Glucose, Clotting
- Troponin I (taken at 6 hrs after the onset of pain; starts to rise at 3-6 hrs); this is less reliable than the Troponin T; ie should only be used to send a patient home when the likelihood of IHD is low
- Troponin T (taken at 12 hrs after the onset of pain; starts to rise at 3-6 hrs; peaks at 12-24 hrs, lasts 2 weeks)
- Trop T is a highly sensitive and specific marker of heart muscle damage (of whatever cause, not just IHD). And the troponin test has been (by and large) a useful addition to the management of ACS, as:
- In a low risk patient, a negative Trop T at 12 hrs excludes an MI at 12 hrs. Not at 24 hrs. This negative predictive have made it a useful 'going-home test'
- BUT, it must always be interpreted in the clinical context. A negative Troponin means the patient is unlikely to be high risk today, but it does not rule out underlying serious coronary disease
- Troponins can be raised in several other (common in the ED) conditions eg pericarditis, PE and renal failure. In renal failure, it carries a poor prognosis, independent of presence of IHD
-
So. Be careful not to start worshipping the 'Troponin God'. Use the test with knowledge
Other
ECG. This should be done with 10 mins of presentation
- Unstable angina. ST-segment depression, ST-segment elevation, or T-wave inversion may occur during unstable angina but are transient. Of cardiac markers, CPK is not elevated but troponin I or T may be slightly increased. Unstable angina is clinically unstable and often a prelude to MI (30% in 3 mths) or arrhythmias or, less commonly, to sudden death
- Non-ST-segment elevation MI (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in blood; troponin I or T will be elevated) without acute ST-segment elevation or Q waves. ECG changes such as ST-segment depression, T-wave inversion, or both may be present
- ST-segment elevation MI (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by GTN; or showing new left bundle branch block. Q waves may be present. Pathological Q waves may remain as the hallmark of previous infarction. Troponins are elevated
- Thrombolysis is indicated, in STEMI, if there is ST elevation >1mm in 2 or more limb leads, >2mm in 2 or more consecutive chest leads, posterior infarction or new LBBB
- In STEMI, there is often reciprocal change (eg ST depression) in the 'reciprocal' (ie opposite) leads - eg in lateral leads in an inferior STEMI. See ECG below. This helps to distinguish it from pericarditis, where those reciprocal changes do not occur
-
Note: in ACS, 20% normal ECG initially
CXR (this is done to exclude other diagnoses eg dissection, pneumothorax)
- Do not do, if XR dept far from resuscitation, or CCU
- Do not delay Rx, whilst waiting for CXR
Cardiac magnetic resonance (CMR): can be useful to exclude or detect ACS, assess function and detect scar tissue
Inferior NSTEMI
ST depression in II, III and aVF, with hyperacute ST changes in V2
Inferior STEMI
Inferior STEMI: ST elevation in II, III and aVF; Q-wave formation in III and aVF; reciprocal ST depression and T wave inversion in aVL
- 40-50% of all MIs
- More favourable prognosis than anterior MI (in-hospital mortality only 2-9%), however certain factors indicate a worse outcome:
- <40% of patients with an inferior STEMI will have a concomitant right ventricular infarction. These patients may develop severe hypotension in response to nitrates and generally have a worse prognosis.
- <20% of patients with inferior STEMI will develop significant bradycardia due to second- or third-degree AV block. These patients have an increased in-hospital mortality (>20%)
- Inferior STEMI may also be associated with posterior infarction, which confers a worse prognosis due to increased area of myocardium at risk
- The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right coronary artery (RCA)
-
Less commonly (<20%), the culprit vessel is a dominant left circumflex artery (LCx)
Anterior STEMI
ST elevation in V2-6, I and aVL; Reciprocal ST depression in III and AVF
- Approx 50% of MIs
- Anterior STEMI results from occlusion of the left anterior descending artery (LAD)
- Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly due to larger infarct size
- Characterised by ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL)
-
With reciprocal ST depression in the inferior leads (mainly III and aVF)
Key Investigations
- ECG
- Troponins
- Diagnosis is based on 2/3 of history, ECG and cardiac enzymes [Ref]
Differential Diagnoses
- Stable angina
- Pulmonary embolus
- Aortic dissection
- Pericarditis (if myocardium involved, troponin can rise - ie myopericarditis)
- Myocarditis
- Diagnose non-serious causes (eg GI or 'musculoskeletal') with care. What is musculoskeletal anyway? Are youn sure its not a junk diagnosis)
Treatment
PCI or Thrombolysis have maximal effect if started early
Treatment - NSTEMI/UA (first line)
Drugs
- IV (DIA)MORPHINE 2.5-10 mg IV + IV METOCLOPRAMIDE 10 mg, if pain severe
Note: though there is some evidence that opiates can cause harm in ACS
[Ref] - PO ASPIRIN 300 mg stat, then 75 mg od
- PO CLOPIDOGREL 300 mg stat, then 75 mg of for 1 year (use only CLOPIDOGREL if ASPIRIN allergy). OR PO TICAGRELOR 180 mg stat, then 90 mg bd (1 year)
Note: give higher dosages even if on one/both drugs already - SC ENOXAPARIN 1 mg/kg bd; OR SC FONDAPARINUX 2.5 mg od (if no angiography within 24 hrs)
Note: some junior doctors wait for a registrar review, if it can be quick (eg do you want to give 3 anticoagulant drugs, in a frail older patient, if this is NOT an ACS?); don't give ENOXAPARIN, if on WARFARIN - SL GTN 1-2 tabs; consider IV GTN infusion 10-200 mcg/min (start high, if systolic BP >100 mmHg) if pain does not improve/recurrent
Procedures
- IV line (cardiac arrest possible at any time, especially in 1st 24h)
- OXYGEN, high flow, if hypoxic
[Ref]
Treatment - STEMI (first line)
Drugs
- IV (DIA)MORPHINE 2.5-10 mg IV + IV METOCLOPRAMIDE 10 mg, if pain severe
Note: though there is some evidence that opiates can cause harm in ACS
[Ref] - PO ASPIRIN 300 mg stat, then 75 mg od
- PO CLOPIDOGREL 600 mg stat, then 75 mg of for 1 year (use only CLOPIDOGREL if ASPIRIN allergy)
Note: give higher dosages even if on one/both drugs already - Either, IV ALTEPLASE (rt-pA) 10-15 mg (see BNF) or TENECTEPLASE 30-50 mg over 10 secs, if indication below; if <12h; f no contraindication (also below) and unless having PCI
Note: thrombolysis reduces mortality by 2-3%; rt-PA has greater risk of CVA (mainly haemorrhagic) to streptokinase but lower risk of major bleed and reinfarction - Or, Primary percutaneous intervention (PCI); if local policy, and <12h
- SL GTN 1-2 tabs; consider IV GTN infusion 10-200 mcg/min (start high, if systolic BP >100 mmHg) if pain does not improve/recurrent
Note: Give PO PRASUGREL (60 mg stat then 10 mg od)+ PO ASPIRIN if undergoing PCI and 1. Immediate PCI needed, or 2. Stent thrombosis occurs during treatment with clopidogrel, or 3. Patient has diabetes
Procedures
- IV (cardiac arrest possible at any time, esp in 1st 24h)
-
OXYGEN, high flow, if sats <94% or <88% if known COPD (N.B high-flow O2 may increase infarct size and risk of mortality): [Ref]
Benefit of thrombolysis and PCI
- Most benefit of thrombolysis occurs in first 6h. In one meta-analysis of the 9 randomised trials with more than 1000 patients, there was a 3.5% reduction in mortality in first 1 hr, 2.5% in next 2-3 hrs and 1.9% in 3-6 hrs
- This gives an NNT of 15 in first hr; and 27 in next 2-3 hrs: [Ref] .
- The advantage of PCI over thromolysis is unclear. There is some evidence that pre-hospital thrombolysis has the most effect on mortality. PCI may be 'better' unless thrombolysis can be done in first 3 hrs
- So, why does neither technique have a huge effect on mortality? Perhaps because in 2/3rds of cases, there is spontaneous thrombolysis of the clot. Also the 'before hospital' mortality is high (50%) and some in-hospital ones (eg bad LVF) have a poor prognosis. Ie, the 'good ones' get better and the 'bad ones' die whatever you do
Prescribing issues
- Round up dose of ENOXAPARIN (calculated in mg/kg) to available dose (20, 40, 60, 80 + 100 mg)
Thrombolysis: indications, contraindications
Indications
- ST elevation >1mm in 2 or more limb leads
- >2mm in 2 or more consecutive chest leads
- New LBBB
- Posterior infarction
Contraindications
- Cardiac
- Suspected aortic dissection
- Prolonged cardiopulmonary resuscitation (>5 mins)
- Neurological
- Previous stroke
- Known intracranial neoplasm
- Recent head trauma
- Other intracranial pathology
- Severe hypertension (BP>180/110mmHg)
- Gastro/surgery
- Acute peptic ulcer
- Acute internal bleeding
- Recent (less than 1 month) internal bleeding
- Recent (less than 1 month) major surgery
- Haematological
- Known bleeding diasthesis
-
Other: advanced CRF/CLF; current use of anticoagulants?
Key management decision
-
(STEMI) PCI or Thrombolysis
Admit?
- Always
Bed plan
-
CCU, or straight to cardiac catheter laboratory
Referrals
Medical
- Cardiology
Other
- Cardiac rehabilitation nurse
The Rest
If the patient is sent home early, and IHD is suspected, make sure they are seen in a rapid access chest pain clinic within 2 weeks
Maxim
- "If you send someone home with chest pain, and you get it wrong, you may be going with them"
ACS protocol, 4h targets, and 'send em home' medicine
- There is a down side of a target and protocol driven 'send em all home' mentality. Targets, by and large, have led to major clinical gain. But there is collateral damage - and that may be your relative next time. Acute coronary syndrome is a good example
- An ACS protocol, ironically, is not always- the best way of managing the ACS syndrome, and certainly not 'chest pain?cause'. But such protocols have become synonymous with the latter. They are usually too restrictive, and inhibit lateral thought. Also, the 'triple (anticoagulant) whammy' of aspirin, clopidogrel and heparin is not a benign treatment. Is it a good idea to slam a frail elderly patient with other risk factors for bleeding (eg CRF) on it, if they do not have IHD?
- For example, they have led to the (false) belief that a myocardial infarction can only be diagnosed 12 hrs after the onset of pain, is partly driven by the need to exclude the diagnosis of MI, so the patient can be sent home ASAP, to make the target; rather than to include the diagnosis, and treat accordingly. Hence ..
- You CAN measure Trop I, or Trop T BEFORE 6 hrs and 12 hrs respectively (ie against protocol), as the enzymes might be rising. This might stimulate you to repeat the ECG, that might show that the ST elevation, which was only 1 mm an hour ago, is now 2 mm - and thus indicating the need for thrombolysis or PCI. So, the window of opportunity can be missed, by over devotion to 'Trop T dogma' ('Trop T will not be done till 12 hrs' etc); and 2. 'send them home' medicine (eg 'if Trop T normal, patient can go home'). Bosses happy
- But what is the diagnosis? After all, a hospital is where we make diagnoses, and make people better. So, when managing chest pain and ?ACS, its best not to follow dogma too rigidly, and involve seniors early
Complications
- Heart failure
- Cardiogenic shock
- Arrthymia (VF risk higher in posterio-inferior MI, younger patients, smokers, bradycardia, low BP, extensive ST elevation and hypokalaemia)
[Ref] - Pericarditis
- CVA (mural thrombus, especially if AF)
- Later: VSD, MR (papillary muscle rupture), LV aneursym; reinfarction 2.6% will reinfarct in 1 yr; 31% in 10 yrs
Follow-up
- Cardiac rehabilitation nurse
Risk stratification
- There are a variety of risk stratification scores developed for patients with atypical presentations and equivocal/initially normal ECGs. None are full-proof. If in doubt, admit, put venflon in, observe in appropriate place, measure Trop I (6 hrs) or Trop T (12 hrs), and repeat ECGs; and ask senior to see
- A popular risk stratification score patients with a diagnosis of 'Chest Pain ?ACS' (?NSTEMI/?UA); ie initially normal Trop T, ECG etc) is the TIMI score: [Ref] . The higher the score, the higher the risk of IHD, and further inpatient investigation, and/or cardiac review, may be warranted. The risk of serious event (all cause death, myocardial infarction, or urgent myocardial revascularisation) according to the number of points:
- 0-1 point: 5%
- 2 points: 8%
- 3 points: 13%
- 4 points: 20%
- 5 points: 26%
- 6-7 points: 41%
Note: GRACE risk score also useful (app available)
Prognosis
- 10% in-hospital mortality, 30% overall. 50% of deaths occur in first 2 hrs, most out of hospital
- 30% of patients with unstable angina, have an MI in 3 mths
- In one large 2007 study (see references), mortality at 30 days was significantly higher among patients with diabetes than without diabetes, with UA/NSTEMI (2.1% vs 1.1%) and STEMI (8.5% vs 5.4%). But, by 1 year, patients with diabetes presenting with UA/NSTEMI had a risk of death that approached patients without diabetes presenting with STEMI (7.2% vs 8.1%). Mortality is 5% per year thereafter
- Poorer prognosis: age, female, diabetes, hospitals that admit few MIs, previous IHD, other risk factors (eg smoking, BP), anterior MI, STEMI, more ECG changes, cardiogenic shock, heart failure and arrthymias
- Better: opposite of above eg inferior MI
- Anterior infarcts tend to be larger and result in a worse prognosis than inferoposterior infarcts. They are usually due to left coronary artery obstruction, especially in the anterior descending artery; inferoposterior infarcts reflect right coronary or dominant left circumflex artery obstruction
2° Prevention + Health promotion
- Refer to cardiac rehabilitation programme
- Stop smoking
- Control DM, BP
- Take ACEi, betablocker, HMG CoA reductase inhibitor ('Statin') and aspirin, clopidogrel/ ticagrelor
- Continue clopidogrel/ticagrelor for 12 months and aspirin life long unless there are contraindications
- If LVEF ≤35% +DM/heart failure: eplerenone
- PRN GTN tablets/spray
Patient information
Don't forget
- ACS is not a diagnosis
- Put a venflon in ASAP
- ECG may be normal initially (20%)
- HISTORY HISTORY HISTORY. STEMI or NSTEMI can evolve as you observe patient. And there are other causes of ST changes and raised Troponin. So observe and do serial ECGs, and Trop Ts, if diagnosis unclear
- PCI or thrombolysis improves mortality in STEMI by 2-3%; with an NNT of 15-30 depending on how quickly it is done
- Involve seniors early
Red flags
- Heart failure
- Cardiogenic shock
- Extensive changes on ECG
