Myocardial infarction

March 2018 | by EMauthor


The 'universal' definition of myocardial infarction = rise in cardiac biomarkers plus any one of the following:


symptoms of ischaemia

ischaemic ECG changes

acute abnormality on noninvasive imaging

thrombus on angiography


The clinical classification of MI:


Type 1: Spontaneous MI related to ischaemia due to a primary coronary event such as plaqueerosion and/or rupture, fissuring, or dissection.

Type 2: MI secondary to ischaemia due to increased oxygen demand or decreased oxygen supply (e.g. coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension).

STEMI — the thrombus completely occludes the lumen of the artery resulting in progressive necrosis of myocardium. The ECG shows acute ST-segment elevation.

Non-ST segment elevation myocardial infarction (NSTEMI) — the volume of thrombus is insufficient to occlude the artery or does so only temporarily. There is some myocardial necrosis, evidenced by a rise in cardiac biomarkers and often non-specific ECG abnormalities (e.g. ST-segment depression or T-wave inversion).


Clinical features


In the textbooks there is central chest tightness or heaviness. It may radiate to one or both arms, the neck, jaw or teeth. Don't get too obsessed with this presentation--it is becoming increasingly clear that atypical presentations are often overlooked. Also remember from above that 'symptoms of ischaemia' is one of only four features required to define an MI along with positive biomarkers. Atypical presentations include


Sudden shortness of breath which can manifest in the extreme as acute left ventricular failure

Pain in the arms, jaw, back, epigastrium or abdomen

Indigestion, even if relieved by antacids

Profound fatigue and weakness

Syncope or collapse

Acute confusion in the elderly


Focused physical examination, including vital signs, general state of the patient, chest and heart examination and state of peripheral perfusion. This will more often than not be normal in acute MI.


Investigations


Chest radiograph is useful in ruling out other causes of symptoms and examining the mediastinal width especially if intending to give Fondaparinux

Main basic description of ECG changes (best explained hands-on)

oST segment elevation with reciprocal ST segment depression = STEMI

oTall wide T wave (hyper-acute T wave, may become a STEMI)

oNew onset left bundle branch block (STEMI equivalent)

oPathological Q waves (more than 1/3 depth of the R wave and more than 0.04 seconds or one small square wide)

o(Deep) T wave inversion

oLoss of progression of R wave in the chest leads

oTall wide R wave with ST depression in lead V1 and V2 (posterior MI)

Localisation of the ECG changes will determine the area of the infarcts

oAntero-septal: V1 through to V3

oAnterior: V1 through to V4

oAntero-lateral: V4 through to V6, I and aVL

oLateral: I and aVL

oInferior: II, III, and aVF

oInfero-lateral: II, III, aVF, V5 and V6

Will need serial ECGs

If you have an interest in echocardiography then by all means scan, preferably with the assistance of a consultant or interested colleague, but obviously don't rule anything out based on a bedside scan.

We use a highly-sensitive cardiac troponin T assay in the trust which rises within hours (see the section on ROACS) which will usually have been drawn from the patient at triage. You only have to wait the result if it will change your management. Examples of when you do not have to wait for troponin result:

oThe symptoms are suggestive of at least unstable angina in any case

oThe sample has been drawn within about 2 hours of the patient's symptoms


Initial treatment of NSTEMI


If SaO2 <90% or breathless, low flow O2

Cardiac monitor

After screening for contraindications, give aspirin 300 mg and clopidogrel 300 mg

oIf CXR normal and ongoing pain give fondaparinux 2.5 mg.

Morphine 2.5–10mg IV + metoclopramide 10mg IV

Pain can be controlled by GTN infusion (50 mg in 50 mL saline 0-10 mL per hour)

We usually hold beta blockers until the patient is admitted

Discuss with cardiology registrar in the CTC if

oIncreasing GTN requirements

oOngoing dynamic ECG changes

oOther concerns e.g. recent discharge from CTC


Initial treatment of STEMI


Cardiac monitor

Aspirin 300mg (unless already given by GP/paramedics)

Morphine 2.5–10mg IV + anti-emetic, eg metoclopramide 10mg IV

Fax ECG to PPCI hotline and discuss with cardiology SpR who will send the CNS to retrieve the patient


 Key point: remember to counsel the patient on the differential diagnosis and his / her treatment, including reporting side effects such as bleeding, which is a risk. Document that you have done this.


Targets for STEMI


NICE Guidelines


Do not use CGS or cardiogenic shock caused by suspected acute STEMI to determine whether a person is eligible for PCI

Offer coronary angiography for people with acute STEMI if:

oPresentation < 12 hours of onset of symptoms and

oPrimary PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given.


Myocardial infarction RCEM reperfusion standards:


Door to ECG 10 min

Door to Needle 30 min

Call to Needle 60 min

Aspirin given


Always remember to screen for relative contraindications before giving antiplatelets or anticoagulants, namely:


Recent head injury

Bleeding diathesis

Recent surgery

Melaena




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