Acute Coronary Syndrome Flashcards
Give the full definition of a type 1 MI
Raised troponin >99th centile + 1 of the following
a) Sx of MI
b) New ECG changes/pathalogical Q waves
c) ECHO showing loss of viable myocardium/wall motion abnormality
d) Identification of a coronary thrombus by angiography or autopsy.
There are 5 types of MI. Which ones are clinically relevant? Define them
Type 1 - Acute atherosclerotic plaque disruption with raised troponin.
Type 2 - Myacardial demand > suppy with raised troponon and !without atherothrombus.
Which types of MI are iatrogenic? Define them
Type 4 - Raised troponin secondary to PCI in the tx of MI, with troponon 5x upper limit
Type 5 - Raised Troponin secondary to CABG with troponin 10x upper limit
Which type of MI is typically diagnosed on autopsy? Define it
Type 3 - Diagnosis on autopsy with evidence of symptoms and ECG findings but bloods not sent => no troponin levels
Define the 5 types of MI
Type 1 - Acute atherosclerotic plaque disruption with raised troponin
Type 2 - Myacardial demand > suppy with raised troponon and !without atherothrombus
Type 3 - Diagnosis on autopsy with evidence of symptoms and ECG findings but bloods not sent
Type 4 - Raised troponin secondary to PCI in the tx of MI, with troponon 5x upper limit
Type 5 - Raised Troponin secondary to CABG with troponin 10x upper limit
List the symptoms of an acute MI
1) Chest pain - Acute sudden onset central crushing chest pain radiating to the jaw, neck, or left arm +/- angina =>worse on exertion/unstable angina
2) Palpitations
3) Syncope/presyncope
4) Nausea/diaphoresis
5) SOB (at rest or on exertion)
6) Symptoms of heart failure (leg swelling, dyspnea, orthopnoea, PND, sacral oedema)
You are conducting a cardiac examination on a patient suffering from an acute MI. What can you expect to hear on auscultation?
Mitral regurgitation
Gallop rhythm (HF)
You are conducting a cardiac examination on a patient suffering from an acute MI. Go through the examination stating what you are looking for in this context.
General inspection: Ashen colour, dyspnoeic
Closer inspection: Tar stains, Xanthomata, Peripheral cyanosis, Central cyanosis, Hypotension, Tachycardia, tachypnoea, scars, subcutaneous devices
Palpation: Raised JVP, Heave, Peripheral oedema, Pulmonary oedema, sacral oedema
Auscultation: Mitral regurgitation, Gallop rhythm (S3)
When examining a patient who just had an acute MI, you note a gallop rhythm. what does that indicate? What is the likely underlying diagnosis in this scenario?
S3 - It indicates rapid ventricular filling consistent with HF secondary to an acute MI
Give 5 RF for ACS
1) Prior hx or fam hx of ACS (especially in a 1st degree relative <55 males, <65 females
2) Environmental - smoking, drinking alcohol
3) Hypertension
4) Hypercholestrolaemia/ dyslipidaemia
5) Obesity
6) Diabetes
You would like to conduct an ECG on a patient suspected of suffering from an acute MI. What findings are you looking for in general?
a) ST elevation in 2 contiguous leads or new LBBB
b) ST depression or T wave changes
c) Arrhythmia
What are the Cardiac biomarkers? (3)
Troponin, CKMB, Myoglobin
What does CKMB stand for?
What is it primarily used for?
How does its levels compare to troponin?
Creatine Kinase myoglobin
Primarily used for detecting re-infarction.
It rises and falls faster than troponin
You are conducting a CXR on a patient that presenting with signs and symptoms of an acute MI. You note alveolar oedema. How does that appear on the CXR?
Perihilar/bat wing opacification
You perform a CXR on a patient that presenting with signs and symptoms of an acute MI. You note Kerley B-lines. What does that indicate?
Interstitial oedema
How is pleural effusion noted on CXR?
Fluid in the horizontal fissure
Blunting of the costophrenic
Meniscus-shaped line
white out
What are the expected findings of HF on CXR?
ABCDE
Alveolar oedema (Perihilar/bat wing opacification)
kerley B-lines (interstitial oedema)
Cardiomegaly (>50% thoracic cavity)
Dilation of upper lobe vessels
pleural Effusions (blunting, fluid in fissure, meniscus)
What CXR finding supports the diagnosis of an aortic dissection instead of MI?
widened mediastinum
Name the 2 types of echo and which one is more invasive?
What findings are you looking for when conducting an ECHO for a patient with MI
TTE ECHO looking for a
1) Atrial/ventricular size (LA enlargement, LV hypertrophy),
2) RV systolic pressure (RHF)
3) presence of valvular disease e.g. papillary rupture causing acute mitral regurgitation (rule out),
4) Atrial and ventricular filling,
5) Pericardial disease (dressler)
TOE needed for identifying left atrial thrombus. (also rule out vegetations in IE)
What murmur may occur after an MI? Describe the murmur. How is it confirmed on ECHO (2)?
What arrhythmia is common post-MI? What findings on ECG would support this?
A patient presents post-MI with bradycardia, what is the most likely ECG finding?
Mitral regurgitation (Pansystolic murmur radiating to the axilla) typically secondary to papillary rupture seen on ECHO and backflow of blood from LV to LA
Atrial fibrillation: irregularly irregular rhythm with absent P waves
Bonus points: Heart block as well!
Inverted T waves are associated with what chronic cardiac condition?
Cardiomyopathy
What imaging would you use when conducting investigations for MI (all)? Explain your reasoning (what youre looking for)
What specifically on these investigations would be consistent with MI?
CXR checking for widened mediastinum to rule out aortic dissection as well as findings of HF (ABCDE). nothing specific for MI
TTE ECHO looking for a
1) Atrial/ventricular size (LA enlargement, LV hypertrophy),
2) RV systolic pressure (RHF)
3) presence of valvular disease e.g. papillary rupture causing acute mitral regurgitation (rule out),
4) Atrial and ventricular filling,
5) Pericardial disease (dressler)
TOE needed for identifying left atrial thrombus. (also rule out vegetations in IE)
Specific for MI (papillary rupture causing mitral regurg and dressler)
The typical modality for taking an CXR is?
When assessing for cardiomegaly which modality is used?
PA normally
PA for cardiomegaly
Give the full list of investigations you would like to conduct on a patient presenting with an acute MI. Try to explain what youre looking for
Bedside:
ABG - assess for Type 1 resp failure, Electrolytes, lactic acid
ECG:
a) ST elevation in 2 contiguous leads
b) ST depression or T wave changes
c) Arrhythmia (e.g Atrial fibrillation)
Bloods:
1) FBC, CRP: raised WCC and CRP may indicate infection or Dressler’s syndrome; Low Hb => anaemia => Type 2 MI; !!! check for reduced platelets as a possible contraindication to thrombolysis.
2) Raised cardiac biomarkers: Troponin, CKMB, myoglobin. Troponin repeated every 6 hours
3) Fasting lipids/lipid profile (RF)
4) HbA1c (RF)
5) Calculate Well’s score and use d-dimer to exclude PE
Imaging:
CXR checking for widened mediastinum to rule out aortic dissection as well as findings of HF (ABCDE)
TTE ECHO looking for a Atrial/ventricular size (LA enlargement, LV hypertrophy), presence of valvular disease, pericardial disease and RV systolic pressure.
TOE needed for identifying left atrial thrombus and rule out vegetation (IE)
What is Dressler’s syndrome?
When does this typically occur?
Type of Pericarditis which occurs weeks/months post-MI
For each of the following, answer the questions:
STEMI:
NSTEMI:
Unstable Angina:
Which present with chest pain?
What ECG changes are consistent with the dx?
Which of these are likely to have raised troponin?
STEMI: Yes for Chest pain and troponin rise, ST elevation or new LBBB.
NSTEMI: Yes for chest pain and troponin rise. ST depression and/or T-wave inversion
Unstable Angina: Yes for chest pain, no raise in troponin, ECg may be normal or have non-specific changes
Using an ECG, how will you determine the location of the insult in an MI?
Tell me each type of MI with their respective leads and most likely vessel affected
+ Anterolateral: I, aVL, V1-V6 -> Proximal LAD
What type of MI is most associated with posterior MIs?
How will you determine if there is a posterior MI?
Inferior MIs (thats why we dont use GTN in inferior MIs) due to having shared blood supply (RCA)
Reciprocal changes in the anterior leads V1-V3 looking for ST depression, Tall R waves, and upright T waves (rather than inverted).
Alternatively performing additional posterior leads V7-V9
Where are leads V7-V9 put?
Same level as V6 (5th ICS, MAL) but V7 in posterior axillary line, V8 in midscapular line, V9 paraspinal line
Where are the electrodes of a 12-lead ECG placed?
12-lead ECG:
10 electrodes required to produce 12-lead ECG
4 Electrodes on all 4 limbs (RA, LL, LA, RL), 6 Electrodes on precordium (V1–6)
Monitors 12 leads (V1–6), (I, II, III) and (aVR, aVF, aVL)
Allows interpretation of specific areas of the heart
Inferior (II, III, aVF) Lateral (I, aVL, V5, V6) Anterior (V1–4)
12-lead Precordial lead placement
V1: 4th intercostal space (ICS), RIGHT margin of the sternum
V2: 4th ICS along the LEFT margin of the sternum
V4: 5th ICS, mid-clavicular line
V3: midway between V2 and V4
V5: 5th ICS, anterior axillary line (same level as V4)
V6: 5th ICS, mid-axillary line (same level as V4)
Which types of MIs should GTN be avoided?
Inferior MI
Posterior MI
What is the possible consequence of giving GTN to an inferior MI
An inferior MI is associated with posterior MIs due to the shared blood supply of the RCA
GTN and other nitrates are venodilators => reduce preload by causing blood to pool in peripheral veins and hence !!! can lead to a significant drop in CO. Compounded with the right ventricle infarction, it may lead to hypotension and reduced perfusion
How is Primary coronary intervention performed?
Radial or femoral artery access followed by placing the stent delivery system -> stent expands as balloon inflates -> Catheter removed, stent implanted.
What is the definitive management of a STEMI. Include timings
STEMI
+ Revascularisation via:
a) PCI within 90 minutes in PCI hospital or 120 minutes within non-PCI hospital
b)Thrombolysis/Fibrinolysis => Alteplase within 12 hours
Can a PCI be given after 120 minutes?
under the discretion of cardiology whereby thrombolysis has already been performed and there is still ischaemia 90 minutes later
A patient presenting with a STEMI 4 hours after onset of symptoms received thrombolysis therapy. Can they still receive PCI?
Yes, under certain conditions such as haemodynamic instability, ongoing ischaemia, and continued ST elevation 90 minutes after thrombolysis.
If a patient shows ongoing ischemia and ST elevation 90minutes after thrombolysis, PCI is then performed. How long after can you perform this PCI?
Up to 24 hours from presentation
Give your full management plan for an acute MI. Include for STEMI and NSTEMI.
First call for help and perform ABCDE as appropriate. Must include 2x wide bore cannulas etc.
+MONA-BASH:
IV Morphine/Cyclomorph
Oxygen 100% non-rebreather
Nitrate (GTN)
ACEi
Beta Blocker
Antiplatelet (Aspirin/Clopidogrel 300mg)
Statin
Heparin (STEMI - Unfractionated, NSTEMI - LMWH)
STEMI
+ Revascularisation via:
a) PCI within 90 minutes in PCI hospital or 120 minutes within non-PCI hospital
b) Thrombolysis/Fibrinolysis => Alteplase within 12 hours (but >120 mins) with continuous ECG monitoring to assess need for PCI
NSTEMI
Take serial data from ECG
Troponin repeat in 6 hours
Appropriate discharge planning taking into account comorbidities
What type of drug is spironolactone? When is it given in the context of MI management?
Aldosterone (mineralocorticoid receptor) antagonist
It is added to therapy for patients with LV dysfunction or HF symptoms
What are patients discharged with post-STEMI
DAPT: Aspirin 75mg + Clopidogrel 75mg.
Beta blockers
Statins
Nitroglycerine (as needed)
If LV dysfunction/HF - Spironolactone
What does the cardiac rehabilitation program entail?
physical recovery, lifestyle modifications (smoking, alcohol, exercise), and emotional support
What is your long term management for a patient post-MI?
Discharged drugs:
DAPT: Aspirin 75mg + Clopidogrel 75mg. Now clopidogrel lifelong, aspirin 6mo.
Beta blockers
Statins
Nitroglycerine (as needed)
If HF - Spironolactone
MDT approach:
Cardiac rehabilitation program which includes Physical recovery, emotional support, patient education and lifestyle changes:
Smoking cessation -quit.ie, education, NRT, drugs Bupropion, Varenicline
Diet modification and weight management - dietitian referral
Exercise -physiotherapist
Alcohol control <14U, education, support groups (AAA), disulfiram
Regular followups with healthcare providers to monitor ECG, adjust medications, blood tests and manage risk factors
psychological support
The short term prognosis of an NSTEMI is better than STEMI however in the long term theyre the same. What tool is used to predict future thrombotic events for patients with unstable angina and NSTEMI?
TIMI - Thrombolysis in MI predicts outcomes for future thrombotic events
What is your differential diagnosis for a patient with a clear history of an MI?
Cardiac: STEMI/NSTEMI, Unstable angina, Aortic dissection, pericarditis, Acute HF
Resp: LRTI, COPD exacerbation, PE, Pneumothorax
GI: Oesophagitis
MSK: Costochondritis
List 5 complications of an MI
NSTEMI > STEMI
Arrhythmia -> Polymorphic VT or A.fib, VF -> Sudden cardiac death
Heart block
HF
Papillary muscle rupture -> Mitral regurgitation
Ventricular aneurysm/ventricular septal defect
Dressler’s syndrome (Pericarditis post-MI)
Mitral regurgitation post-MI is due to….?
Papillary muscle rupture
How often should Troponin be checked in the case of MI?
every 6 hours regardless if STEMI or NSTEMI
What is the most common life-threatening arrhythmia that may arise from an MI? be specific. When is it most likely to occur?
Polymorphic Ventricular tachycardia typically would occur within 48-72 hours post-MI
What dose of aspirin is used in acute MI?
How about clopigodrel?
How about ticagrelor
300mg for aspirin
600mg clopidogrel
180mg for ticagrelor
What type of Heparin is given in acute MI?
Unfractionated heparin in NSTEMI
LMWH in STEMI
