chest pain Flashcards

1
Q

when should troponin be repeated ?

A

6-12 hours

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2
Q

STEMI criteria

A

2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years

1.5 mm ST elevation in V2-3 in women

1 mm ST elevation in other leads

new LBBB (LBBB should be considered new unless there is evidence otherwise)

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3
Q

61-year-old gentleman has presented to A+E with severe chest pain.

ddx?

A

Cardiac causes: Acute coronary syndrome, pericarditis,

Respiratory causes: Pulmonary Embolism, Pneumothorax, Pneumonia

MSK

Gastrointestinal system: Oesophagitis, Pancreatitis, Cholecystitis, Boerhaave’s perforation of the Oesophagus, Peptic Ulcer Disease

Vascular causes: Aortic dissection,

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4
Q

What investigations are you going to do for this patient?

A

YOU MISSED OUT ON ECHO

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5
Q

management of NSTEMI ?

A

MONABASH§:

M) Morphine for analgesia ( can be given as Diamorphine IV). You should also give anti-emetics at this point.
O) Oxygen. High flow should be given in the acute setting.
N) Nitrates – this can be in the form of sub-lingual nitrates such as GTN spray, or if the patient has on going symptoms of chest pain a GTN Infusion can be started.
A) Anti-platelets. The patient should initially be given a stat dose of 300mg aspirin and which is then continued indefinitely. Clopidogrel should also be given at this dose initially.
B) Beta-Blockers should be started on presentation. Mild LVF is not an absolute contraindication to beta-blocker therapy. Beta-blockers reduce HR and BP, reducing myocardial O2 requirement and thus angina.
A) ACE-Inhibitors. Early introduction of an ACE-I has significant prognostic benefits in STEMIs, however there is less evidence in NSTEMI. However it is still recommended. The HOPE and EUROPA Trials suggest ACE-Is provide benefit in patients with Coronary Artery Disease.
S) Statins – high dose statins (Atorvastatin 80mg OD) have been shown to reduce mortality and recurrent MI in the acute setting. They have a role in clot stabilisation.
H) Heparin. This prevents coronary thrombus. Different hospitals will use different types of Low Molecular Weight Heparin. For example – Fondaparinux.

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6
Q

what to do when patient stable

NSTEMI risk assessment ?

A

in general current evidence supports early angiography and revascularisation in patients who present with either high-risk features, or patients with low risk features who have on going symptoms. Even in those patients who are low risk and settle with medical management, early angiography and revascularisation is still the recommended

Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors:
age

heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

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7
Q

Which patients with NSTEMI/unstable angina should have coronary angiography

A

immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk

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8
Q

Percutaneous coronary intervention for patients with NSTEMI/unstable angina

Further drug therapy

A

unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not

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9
Q

other risk factors ?

A

Poor LV systolic function
Previous CABG/PCI (in last 6/12)
Patients with other co-morbidities
Patients with high-risk features of NSTEMI/UA

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10
Q

Once a STEMI has been confirmed the first step is

A

discussed immediately with the on-call Cardiology Team / or my senior

percutaneous coronary intervention
should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
drug-eluting stents are now used.

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f the patient’s ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI

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11
Q

patients undergoing PCI with radial access:

A

unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus

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12
Q

common complications post Myocardial Infarction?

A

Cardiac arrest
= patients developing

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Cardiogenic shock

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease
This is difficult to treat.

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Chronic heart failure

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Bradyarrhythmias

Atrioventricular block is more common following inferior myocardial infarctions.

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Pericarditis

Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.

Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

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Left ventricular aneurysm

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

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Left ventricular free wall rupture

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Ventricular septal defect

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Acute mitral regurgitation

More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.

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Re-infarction.

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13
Q

What do you know about Dressler’s Syndrome?

A

autoimmune pericarditis, it occurs 2-10 weeks post myocardial infarction.

widespread diffuse saddle-shaped ST elevation across multiple leads. An echocardiogram may show pericardial effusion. The management of this condition is with non-steroidal anti-inflammatory medication. If there is a significant effusion it can be aspirated.

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