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Year 3: Cardiovascular > Acute coronary syndrome (Complete) > Flashcards

Acute coronary syndrome (Complete) Flashcards

1
Q

What is acute coronary syndrome?

A

Umbrella term of acute presentations of ischaemic heart disease

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2
Q

What are the 3 subtypes of ACS?

A

STEMI

NSTEMI

Unstable angina

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3
Q

What are the main clinical features of ACS?

A

Chest pain

Dyspnoea

Palpitations

Sweating

Nausea and vomitting

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4
Q

What are the main characteristics of ACS chest pain?

A

Central crushing chest pain

Radiation to jaw or arms

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5
Q

What types of patients present with atypical presentations of ACS?

A

Elderly

Diabetics

Females

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6
Q

What are atypical presentations of ACS?

A

Epigastric pain

Back pain

Pain described as burning or stabbing

Can be characterisitc of indigestion

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7
Q

What are the main investigations to consider in patients suspected of ACS?

A

Bedside:
Basic obs: Check for haemodynamic instability

ECG: Check for any changes suggestive of STEMI or NSTEMI

Bloods:
FBC: Check for thrombocytopenia which is bleeding risk and anaemia

Troponin: Elevated in STEMI and NSTEMI

Creatinine U&Es: Check for baseline kidney functions (possible AKI) and eGFR which is needed in GRACE score.

LFTs: Assess bleeding risk before anticoagulation

Blood glucose: check for risk factor and manage hyperglycaemia in diabetics

Lipid profile: check for risk factors

CRP: Rule out other causes of chest pain

Imaging:

CXR: Rule out other differentials of chest pain

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8
Q

What investigation findings are suggestive of unstable angina?

A

No troponin elevation

ECG findings:
* New ST deppresion
* New T-wave inversion (due to delays in repolarisation of inner layers of heart)
* No ECG changes

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9
Q

What investigation findings are suggestive of NSTEMI?

A

Elevated troponin

ECG changes:
* New ST-depression
* New T wave inversion
* Normal (1/3rd of patients)

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10
Q

What investigation findings are suggestive of STEMI?

A

Elevated troponin

ECG changes:
* New ST elevation
* New Left bundle branch block (LBBB)

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11
Q

What findings on ECG are suggestive of a posterior MI?

A

ST deppresion in the anterior and septal leads (V1-V4)

Peaked R waves in V1 and V2 (cell death posteriorly causes more positive depolarisation towards chest leads)

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12
Q

What ECG findings must be present to diagnose a patient with STEMI?

A

Must show ST elevation in 2 or more continguous leads and:

ST elevation > 1mm in limb leads

ST elevation >2 mm in precordial leads (chest leads)

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13
Q

What findings must be shown to diagnose a patient with NSTEMI?

A

Patient must have signs/symptoms suggestive of ACS (N.B. Diabetics and elderly may be assymptomatic)

Elevated troponin

No ST elevation on ECG

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14
Q

What is the common management for all types of ACS?

A

MONA:

Morphine (Only given for patients with severe pain)

Oxygen (if sats below 94%)

Nitrates (IV or sublingual)

Aspirin (300mg)

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15
Q

Morphine should only be given in ACS during what circumstances?

A

Patient is in severe pain

This is due to adverse outcomes associated with morphine administration

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16
Q

Administration of nitrates in management of ACS should be considered with caution in which group of patients?

A

Hypotensive patients

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17
Q

What is the management plan for patients with STEMI?

A
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18
Q

When is percutaneous intervention indicated in patients with STEMI?

A

Within 12 hours of onset of symptoms

PCI can be done within 120 minutes of medical contact.

PCI can be considered if still showing signs of ongoing ischaemia after 12 hours

19
Q

What mediation should be given before a PCI procedure in treatment of STEMI?

A

Dual antiplatelet therapy:

Aspirin

Prasugrel (or ticagrelor if bleeding risk)

20
Q

What medication is given during a PCI procedure with radial access?

A

Unfractioned heparin

Glycoprotein inhibitor (GPI): for bailout

21
Q

What medications are given during fibrinolysis (aka thrombolysis) of patient with STEMI?

A

Fibrinolytic drugs: Ateplase or tenecteplase

Parenteral anticoagulation: (e.g. Unfractioned heparin, fondaparinux, enoxaparin)

P12Y2 inhibitors: e.g.Ticagrelor (Clopidogrel if bleeding risk or on DOAC)

22
Q

What medication should be swapped in patients in need of PCI who are already on antocoagulant?

A

Swap prasugrel for clopidogrel instead

(If patient is high bleeding risk but not on anticoagulant then swap for ticagrelor instead)

23
Q

If patient still experiencing signs of ischaemia after fibrinolysis, what is next management for patient?

A

Percutaneous intervention

AKA Primary angioplasty

24
Q

What is the management plan for patient with NSTEMI/Unstable angina?

A
25
Q

What is the post MI management plan for patients?

A

Medicine:Should be started on 5 following drugs:

Aspirin 75mg (anti-platelet)

Clopidogrel 75mg or ticagrelor 90mg (second antiplatelet)

Beta-blocker (Bispropolol)

ACE-inhibitor

High dose statin (e.g. Atorvastatin 80mg)

Post MI investigations:

ECHO: All patients should have one done to check for any HF

Cardiac rehabilitation referral: All patients

Ischaemia testing: Consider for patients who havent have an angiography to check for inducible ischaemia.

26
Q

What are some complications of MI?

A

Ventricular arrhythmia

2nd, 3rd degree heart block

Recurrent ischaemia/infarction/angina

Acute mitral regurgitation

Congestive heart failure

Cardiogenic shock

Cardiac tamponade

Ventricular septal defects

Left ventricular thrombus/aneurysm

Left/right ventricular free wall rupture

Dressler’s Syndrome

Acute pericarditis

27
Q

How do ventricular arrythmias tend to present in patients with MI?

A

Tend to occur post MI, during cardiac catheterisation or during reperfusion.

Tend to be short-lived and self resolve

If they do persist however, they should be treated in accordance with advance life support protocols

28
Q

How does recuurent ischaemia/infarction/angina tend to present in patients with MI?

A

Can re-occur due to thrombosing of inserted stents. (Requires re-intervention)

New infarcts can occur in new vascular territories

Angina and chest pain can last for a while after an MI, especially in patients with NSTEMI

29
Q

Why are MI patients at risk of congestive heart failure?

A

Can occur as a consequence of impairment heart muscle function secondary to ischaemia.

Ventricular function may improve over months as heart muscle recovers

Hence why all patients require an ECHO

30
Q

Heart block most commonly occcurs in which types of MI?

A

Inferior MI

This is because RCA supplies the SA node

31
Q

How is heart block post-MI managed?

A

Observation as many resolve

Transcutaenous/venous pacing if symptomatic

Permament pacing if failure to resolve

32
Q

How does left ventricular thrombus/aneurysm present?

A

Presents mainly in patients with anterior MI (this is because myocardium is suscpetible to stress and at risk of rupture)

May present silently, cause arrythymias or embolic events (e.g. stroke, acute limb ischaemia ect).

Persistent ST-elevation and signs of left ventricular failure

33
Q

How is left ventricular aneurysm/thrombosis diagnosed?

A

ECHO

ECG may show persistent ST elevation

34
Q

How does left ventricular wall rupture present and how is it managed?

A

Rapid tamponade as blood fills into pericardial space.

Tamponade followed by cardiac arrest/death within seconds

Managed by pericardiocentesis and surgery but prognosis extremely poor

35
Q

Why can acute mitral regurgitation present in patients post MI?

A

Occurs because of papillary muscle rupture secondary to MI.

36
Q

How does acute mitral regurgitation present in patients with MI?

A

Pansystolic murmur heard best at the apex

Severe and sudden heart failure

Diagnosed on ECHO and requires surgical intervention

37
Q

What is ventricular septal defect?

A

Rupture in septum which seperates ventricles

38
Q

How does ventricular septal defect tend to present in patients post MI?

A

Tends to present within first week post MI

Anterior MI tends to cause apical and simple ruptures

Inferior MI tends to cause basal and more complex ruptures

Presents with following symptoms:

Shortness of breath
Chest pain
Heart failure
Hypotension

Harsh, loud pan-systolic murmur along the left sternal border.

Palpable parasternal thrill.

39
Q

How is ventricular septal defect post MI managed?

A

Emergency cardiac surgery

40
Q

What is Dressler’s syndrome

A

Post-infaction pericarditis

41
Q

When does Dressler’s syndrome typically present post MI?

A

2-3 week to a few months after MI (Patients that get pericarditis immediately after MI is NOT considered Dresslers syndrome)

N.B. Caused due to inflammatory response from ischaemic/necrotic tissue

42
Q

How is Dressler’s syndrome managed?

A

High dose aspirin

43
Q

What are contraindictions to fibrinloysis/thrombolysis?

A

Active internal bleeding

Recent haemorrhage, trauma or surgery (including dental extraction)

Coagulation and bleeding disorders

Intracranial neoplasm

Stroke < 3 months

Aortic dissection

Recent head injury

Severe hypertension

44
Q

What biochemical marker is useful in identifying possible re-infarct of a patient who had a recent MI?

A

Creatinin kinase MB as it has quicker clearance than troponin

Most specific for myocardium and typically rasied 3 times above upper limit.

(Troponin wont be helpful as it can be raised up to 2 weeks post MI)

Year 3: Cardiovascular (30 decks)

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