Acute coronary syndrome Flashcards
Main cause of acute coronary syndrome
Atheromatous plaque rupture
Other pathologies of acute coronary syndorome
- Coronary dissection (tear in tunica media)
- Coronary spasm
Assess for acute coronary syndrome
ECG and then measure troponin
NSTEMI ECG could be…
ST depression
Inverted T waves
Normal
How to meet diagnosis of acute MI?
Increase and/or decrease in cardiac biomarker preferably cardiac troponin
+ 1 of following:
Symptoms of ischaemia
New ST/T wave changes or left bundle branch block
Imaging evidence of wall abnormality (echocardiogram)
Angiography detects thrombus
Type 1 MI
Atheromatous plaque rupture, ulceration, fissure, erosion or dissection = thrombus decreasing myocardial blood flow/embolism and then necrosis
Type 2 MI
Other than coronary plaque creates instability between demand and supply of myocardial oxygen
Type 2 MI examples
Coronary artery spasm Coronary endothelial dysfunction Tachyarrhthmias/Bradyarryhthmias Anaemia Respiratory failure Hypotension Severe Hypertension
Assessment of suspected acute coronary syndrome
History: cardiac sounding? Radiation to neck/left arm/jaw? Relieved with GTN (glyceral trinitrate spray, vasodilator) How long/getting worse?
Risk factors present? (eg diabetes, smoker, high cholesterol, family history)
Examination MI
BP if systolic <90 = cardiogenic shock Tachy/Bradycardia (2:1 heart block/complete) JVP - distended (high pressure) Heart murmur Cool peripheries?
Inferior ECG leads
Lead 2
Lead 3
aVf
(right coronary artery)
Anteroseptal ECG leads
V1
V2
V3
V4
(left anterior descending)
Lateral ECG leads
Lead 1
aVL
(high lateral)
V5
V6
(left circumflex artery)
Anterior leads
V1-V6
left anterior descending
What leads affected if left coronary artery affected?
V1-V6 + aVL
What does ST elevation imply?
Sudden occlusion
or long term marker of LV aneurysm
What does ST depression imply?
under supply of blood, not sudden full occlusion
If in anterior leads (V1-V6) can be due to posterior STEMI
T wave inversion means
Under supply of blood, not sudden occlusion
ECG development STEMI
Hyperacute T waves (tombstone)
ST elevation
T wave inversion
Pathological Q waves
What do you need to do if see ST elevation?
Directly to Cath lab for emergency percutaneous coronary intervention (radial or femoral artery entrance)
NSTEMI presentation ECG
Can be normal
ST depression
Inverted T waves
Blood tests NSTEMI
Haemoglobin (rule out anaemia as considering antiplatelets)
Renal function (angiogram contrasts can induce nephropathy)
Cholesterol
HBA1C (diabetes)
Troponin
When is troponin raised?
Raised within 3 hours of damage
Peaks at 24-48 hours
Remains elevated 2+ weeks
Other investigations to do
Chest X-ray
Rule out pulmonary oedema
If widened mediastinum = aortic dissection maybe
Echocardiogram views
Apical 2 chamber view : LAD and RCA
Apical 4 chamber view: LAD, RCA and LCA
What do we use echocardiogram for?
LV function (normal or impaired)
Wall motion
Valvular disease (mitral regurg)
Complications from MI eg VSD
Management STEMI
Aspirin (300mg) P2Y12 inhibitor Morphine (ease pain) + antisickness drug (metoclopramide) Nitrate (vasodilator) Oxygen Direct transfer cath lab
Management NSTEMI
Antiplatelets (aspirin/clopidogrel - P2Y12 inhibitors)
Anti-ischaemics (beta blockers, GTN infusion)
Statins
ACE inhibitors
NSTEMI when to go to cath lab urgent (for percutaneous coronary intervention)
If chest pain persists with dynamic ECG changes
If develop arrhythmias
What is invasive coronary angiogram?
X-ray Local anaesthetic (to access radial or femoral artery) Wire occluded vessel Predilate narrowed section with balloon Stent with metal scaffold
Why do we use coronary angiogram?
Establishes type of lesion and location
Management following stent insertion
Life style change (low fat/salt, exercise)
Antiplatelets (DUAL) then aspirin for life
Statin reduce cholesterol <4mmol/L
LDL <2mmol/L
ACE inhibitor BP <140/80`
