Acute Coronary Syndrome Flashcards
Describe the major risk factors for ACS?
Age, male gender, family history of MI @ age <55.
Smoking, hypertension, diabetes, hyperlipidaemia, obesity.
Describe the typical symptoms of a patient coming in with ACS?
Describe the potential signs?
Acute central crushing chest pain lasting >20mins.
Pain may radiate to neck and down left arm.
May be associated with nausea, sweatiness, palpitations.
Distress (impending doom), pallor, tacy/bradycardia, hypo/hypertension.
What is ACS?
A spectrum of ischaemic heart disease including:
ST elevation MI (STEMI) highest mortality.
Non ST elevation MI
Unstable Angina. Lowest short term mortality but suggestive of very severe atherosclerosis so poor long term prognosis.
What is a STEMI?
A myocardial infarction ischaemia of the heart with an ST elevation on the ECG. >1mm elevation in limb leads or >2mm elevation in chest leads, in 2 consecutive leads at least
Prognosis of STEMI is worse and urgent treatment/referral to PCI team is needed.
STEMI is caused by a complete occlusion of a major coronary aa and cause a full thickness (transmural) infarct.
What is unstable angina?
Angina which presents with no particular pattern e.g not just exertion but at rest.
May start occurring more frequently (crescendo).
Or Lasting longer with greater intensity.
How can you clinically diagnose myocardial infarction?
Troponin rise with one or more of the following:
- Symptoms of ischaemia aka chest pain
- ECG changes
- Imaging evidence of regional wall defect (Echo showing abnormal pumping)
- Identification of intracoronary thrombus on angiography
Textbook definition in reality if someone presents with chest pain and ecg changes treat as MI don’t wait for troponin level.
Describe the role of anti platelet agents in ACS?
To reduce platelets sticking to atheromas and subsequently forming thrombi. Therefore reduces future risk of MI.
Example: Low dose aspirin and clopidogrel
What is a NSTEMI?
A complete occlusion of a minor coronary aa resulting in a partial thickness infarct.
No ST elevation on ECG
Describe the management of NSTEMI and the order in which you would initiate treatment in NSTEMI?
BROMANCE
In terms of order of management:
- Analgesia (morphine, GTN, also antiemetic - 10mg metochlopromide)
- Oxygen (only if sats <94)
- Aspirin and Clopidogrel loading dose 300mg
- Fondaparinux 2.5mg dose
Next 24hrs start:
- Beta blocker (bisoprolol) for life
- Ramipril
- Statin
Consider inpatient elective PCI dependent on GRACE score.
If the patient is in pain despite analgesia then this is an indication for PCI and you should discuss with the Catheter Lab.
Which regions of the heart are MI’s most likely to effect, what are the corresponding ECG leads and coronary aa?
V1, V2: Septal MI: Left ant descending/ Rt coronary aa
V2, V3, V4: Anterior MI: Left ant descending
V5, V6, Lead I + AVL: Lateral MI: Circumflex
Lead II + III + AVF: Inferior wall MI: Right coronary aa (can be any)
V2-V6: Massive anterolateral MI: Lt main stem coronary aa
V1-V4: Antero-septal MI: LAD
Note ECG leads only correspond to areas in STEMIs
What is the role of thrombolysis in ACS, when is it indicated/contraindicated?
Fibrinolytic agents breakdown thromboses by the activation of plasminogen into plasmin.
Indications:
- Recommended in STEMI where PCI is not available within 90mins.
- Post. infarct new onset left bundle branch block.
Contraindications:
Suspected bleeding/high risk bleeding/recent bleed (haemorrhagic stroke)
Allergy
Pregnancy
Severe hypertension
When is emergency PCI indicated?
What do you give post procedure?
In STEMI’s ideally in 1st 90mins.
In NSTEMI for pts with on going pain despite appropriate analgesia.
Rescue PCI in patients who have had thrombolysis but have failed to reperfuse, has had further ischaemia or further MI.
> Clopidogrel and abciximab post procedure
Describe the pathological cause underpinning ACS?
IHD caused by atherosclerosis.
- Atheromatous plaque formation.
- Platelet aggregation and adhesion.
- Localised thrombosis.
- Distal thromboembolism completely or partially occlusion a coronary aa.
Causes of thrombus formation (Virchow’s triad)
Blood flow (turbulent) Vessel walls (atherosclerosis) Blood components (hypercoagulability)
Describe the potential short and long complication of ACS?
Short:
VT/ VF: Cardiac arrest
Cardiac failure: low ejection fraction causing cardiogenic shock/ acute pulmonary oedema
Ventricular septal defect: systolic murm
Ruptured chordae tendinae: systolic murm
Haemopericardium (from ventricle rupture): cardiogenic shock
Pericarditis
Long: Dressler's syndrome: Ventricular aneurysm: persistent ST elevation and LH failure Reinfarct Chronic heart failure Arrthymias: AF or heart block
Describe the different arrhythmias that can arise following ACS?
Ventricular tachycardia or fibrillation:
Common following reperfusion. Presents with palpitations, chest pain, syncope, hypotension and pulmonary oedema.
Atrial Fibrilation: irregularly irregular heart beat. Often assymptomatic.
Bradyarrhythmias: often in posterior MIs involving the AV node.
Heart block: may occur during MI especially of inferior wall (rt coronary aa occlusion)
Describe the following short term complications: thromboembolism, ventricular septal defect, ruptured chordae tendinae and haemopericardium?
Thromboembolism:
a mural thrombus may form on the inflamed endocardium over the infarcted area and may embolise in distal organs.
Ventricular septal defect:
Intercardiac rupture through the septum causing a left right shunt leading to severe left ventricular failure.
Ruptured chordae tendinae:
Leads to mitral valve incompetence and severe regurgitation.
Haemopericardium:
Results from rupture of the ventricular wall (2-10 days after MI). Blood burst through the wall filling the pericardium. This causes a sudden rise in interpericardial pressure preventing filling of the heart, leading to rapid death from obstructive shock.
What are the long term complications of ACS?
Cardiac failure
Dressler’s syndrome
Ventricular aneurysm
Future MI
Describe cardiac failure following ACS?
Cardiac failure
LVF:
Cardiac death/ischaemia = tissue remodelling less efficient.
Presentation: Cardiomegaly (displaced apex beat). Tachycardia Exertional dysopnea, paroxysmal nocturnal dysopnea, fatigue. Crackles at the base of the lung. Pulmonary oedema.
May notice extra heart sounds and mitral regurgitation.
Rt sides heart failure often develops from lt sided heart failure:
Rt sided cardiomegaly Raised JVP Peripheral oedema Tachycardia Functional tricuspid regurgitation
What is Dressler’s syndrome?
Immune mediated pericarditis.
Rare, develops 2-10 months post infarct.
Presents as:
Sharp central chest pain radiating to neck and shoulders.
Exacerbated by movement, respiration and lying flat.
Relieved by sitting forward.
Sometimes pleural effusion which may compress bronchi causing dysopnea.
O/e:
Can hear pericardial friction rub (leaning forward 4th intercostal space sternal edge)
There may also be fever, leucocytosis and or lymphocytosis.
Treat with high dose aspirin/ NSAIDs
Describe ventricular aneurysm formation?
Gradual distension of the infarcted ventricular wall which has been replaced by an inelastic fibrous scar.
If this aneurysm ruptures it will cause haemopericardium and cardiac tamponade.
What is meant by cardiac rehabilitation?
It is a programme which encourages positive lifestyle changes and exercise post cardiac event (action heart) and should be offered to all patients following a cardiac event. Included in the cardiac rehabilitation should be secondary prevention medication.
How long after ACS can a patient drive a car/lorry?
Driving may resume 1 week after successful coronary angioplasty.
If there has been no PCI then patient can resume driving after 4 weeks if there is no other disqualifying reason.
For lorries the patient must notify the DVLA and there license will be revoked, it can be reissued after 6 weeks.
What are the secondary prevention drugs which should be started following ACS?
ACE inhibitor (Ramipril)
Aspirin 75mg od (loading dose 300mg) for life
Clopidogrel 75mg od (loading dose 300mg) one year
Beta blocker, titrate to BP (Atenolol)
Atorvastatin 80mg
Describe the ECG changes in an evolving STEMI?
- Hyperacute T waves (tented)
- ST elevation
- Q wave (downward deflection after the p wave) and T wave inversion
- ST elevation normalises (days after - Q wave and T wave inversion still present)
- T wave inversion may go back to normal (weeks after), pathological Q waves will remain.
Define significant ST elevation?
1mm/square or more in at least two consecutive limb leads.
2mm/squares or more in at least two consecutive chest leads.
New onset LBBB- considered a STEMI because you cant interpret the rest of the trace
When would you suspect a posterior MI
Deep ST depression in V1 V2 and V3
Check by putting leads on the patients back
What investigations would you do in a patient with suspected MI
FBC, U+E, trops (0+6h)
12 lead ECG
Glucose, lipids
CXR
If diagnosis still in doubt can do an echo
Describe the timescale of a raised troponin
Becomes raised at 4-8h
Reaches its maximum around 24h
Takes around 10 days to return to normal
