Acute coronary syndromes Flashcards
Cardiac chest pain generally presents due to 1 of 4 causes
What are these?
New exertional angina - most common
Unstable angina
Acute MI
Sudden cardiac death
What is the difference between stable and unstable angina?
Stable angina only occurs on exertion - when myocardial demand for oxygen increases past supply
What are the key symptoms/signs of stable angina?
Central chest tightness - often with radiation to neck and/or arms
Aggravated by exertion or stress
Relief by stopping activity & rapid improvement with sublingual nitrate (GTN spray)
What aspect of WIrchow’s triad causes angina?
Changes of vessel wall
Angina causes by atherosclerotic plaque in coronary arteries
How big does a plaque need to be to cause stable angina?
Obstructive plaque
Occludes >70% of the lumen
How big does a plaque need to be to risk acute coronary syndromes?
It is not the plaques size that really matters (although it has to be»_space;70% occlusion)
ACS’s caused by spontaneous plaque rupture & local thrombosis with occlusion
Plaque rupture causes the formation of ___________
Atherothrombosis
What is included in ‘Acute coronary syndromes’?
Unstable angina
NSTEMI - Non ST segment elevation MI
STEMI - ST segment elevation MI
Sudden cardiac death
What is the basic difference between symptoms of stable angina and of ACS?
ACS will give symptoms at rest whereas stable angina is only on exertion
What are the risk factors for coronary artery disease?
Age, gender, family/genetics, creed (the usual)
Previous angina, other cardiac events & interventions
Smoking Diabetes Hyperlipidaemia Hypertension Lifestyle
Describe the typical presentation of Unstable angina pectoris (UAP)
UAP, angina on effort, but of progressive, increasing frequency & severity
Often provoked by less exertion and/or then at rest
“It started when I was walking up the stairs so I sat down but the pain just kept on getting worse”
Describe the typical presentation for NSTEMI
Myocardial ischaemic symptoms occurring at rest
“I was sitting watching eastenders and all of a sudden i had a really tight pain on my chest”
How would you examine someone with suspected UAP or NSTEMI?
Might look like shite but also might look fine
Not really any specific signs/features to find
Check:
- HR & BP
- Auscultate for murmurs & crackles in chest
What piece of kit is needed to diagnose NSTEMI (or STEMI)?
ECG
What features on an ECG would you look for, for UAP and NSTEMI, on an ECG?
You would look at:
ST segment:
- ST depression?
- Transient ST elevation?
- T wave inversion?
If the patient’s pain has gone:
- Is the ECG normal? = UAP (generally)
- Is the ECG abnormal? = NSTEMI (generally)
Why must you take ‘serial ECGs’?
To detect late changes
This is essential in differentiation UAP & NSTEMI (and in general diagnosis)
How often are ACS symptoms ‘Atypical’?
Atypical symptoms are relatively common
Atypical symptoms more common in:
- Women
- Elderly
- Diabetics
What are the typical atypical symptoms for UAP & NSTEMI?
Breathlessness alone +/- signs of heart failure
Nausea & vomiting +/- other autonomic symptoms
Epigastric pain +/- indigestion
Why would you take bloods of someone presenting with cardiac pain?
What biomarkers would be looked for?
Cardiac biomarkers are useful in diagnosing UAP & NSTEMI
Cardiac troponin (cTn) I & T
Useful for:
- Diagnosis
- Risk stratification
- High cTn indicates risk of adverse events
If someone presents with cardiac chest pain and all the symptoms of ACS
Why can you not make a diagnosis entirely from their bloods?
Elevated troponin (cTn) can be caused by may different things, not just ACS & atherothrombosis
What is cardiac troponin?
cTn - the contractile apparatus of myocytes thin (actin) filaments
Cardiac troponin is unique and is only detectable in the blood if myocyte intergrity is compromised (this makes their levels elevate)
Why can’t you measure the cTn levels in someones blood immediately after they present with ACS?
cTn blood levels take a while to rise after acute ischaemia
They have a characteristic rise & fall of blood levels
Contrast the levels of elevation of cTn in the blood after different ACSs
Acute MI - massive (largest) increase in cTn levels
UAP - smaller increase in cTn levels
As UAP causes a smaller elevation, there is a AMI reference limit, so if cTn levels rise above it, they know it is AMI
Aside from cTn, what other molecules’ levels in the blood can be measured to help identify & diagnose acute MI?
Myoglobin
CK-MB
What is the acronym for the immediate treatment of UAP & NSTEMI?
ABCDE then MONA
What does MONA represent?
Morphine (or diamorphine)
Oxygen
Nitroglycerine (GTN spray or tablet)
Aspirin 300mg orally (crush/chew)
What is included in the long term therapy for UAP & NSTEMI?
Anti-platelet therapy
Anti-thrombotic therapy
‘other medical therapy’
Coronary revascularisation
Summarise anti-platelet therapy for UAP & NSTEMI patients
All ACS patients:
Aspirin + ADP receptor blocker (Clopidogrel, Prasugrel or Ticagrelor)
This is usually continued for 1 year following ACS event
Aspirin & ADP receptor blockers are given together to patients after an episode of ACS
What doses n shite do you give?
Aspirin 75-150mg* daily
ADP receptor blocker:
- Clopidogrel - Bolus 300mg & 75mg daily
- Prasugrel - Bolus 60mg & 10mg daily
- Ticagrelor - Bolus 180mg & 90mg BD daily
- from other lectures but not 100% sure
Antithrombotic therapy = what drug?
HEPARIN
various types
Summarise anti-thrombotic therapy for ACS patients
IV unfractioned Heparin (UFH)
or
Sub cutaneous Low molecular weight Heparin (LMWH)
or
Fondaparinux s/c
Which is better out of UFH & LMWH?
Low molecular weight Heparin (LMWH) seems to have more benefits:
- Improved clinical outcome
- Easier to administer s/c rather than IV
- No need to monitor
However, even LMWH is being replaced by specific anti-thrombotic Fondaparinux
^also s/c
Asid from anti-platelet and anti-thrombotic therapy, what other agents can be given to ACS patients?
Beta-blockers:
- To reduce HR (50-60 bpm target)
- Should be used, but only in absence of contraindications
Statins:
- Blood thinners (anti-coagulatants)
- Reduce risk of both acute & chronic events in future
ACE inhibitors:
- always if left ventricular dysfunction nut not if normal function
Who should receive coronary revascularisation?
High risk patients with UAP/NSTEMI
Clear evidence that these patients benefit from surgery as well as medical therapy
What are the different methods of interventional treatment of UAP or NSTEMI?
Coronary angiography & revasculariastion by Percutaneous intervention (PCI)
Coronary Artery Bypass Graft (CABG)
What is the Seldinger technique?
Technique of catheterisation of an artery such as the Femoral artery. Used in PCI.
1) Needle stuck in artery
2) Guide wire passed through needle
3) Needle withdrawn
4) Catheter introduced over guide wire
Describe how an coronary angiography is carried out once the catheter is inserted.
Guide wire passed through the plaque in the coronary artery
Double-lumen catheter with ballon slid through plaque and expanded, temporarily dilating the plaque bit
Balloon catheter with stent is moved into the recently dilated area of the plaque & expanded - stretching out the stent
Catheter and guide wire removed & stent remains
What happens in a CABG?
Bypass created from the aorta or one of it’s immediate branches (ie subclavian) to the coronary arteries
Connects the oxygenated supply to the systemic circulation to the coronary
Summarise the overall hospital treatment route for a patient who presents in hospital with UAP/NSTEMI
Hospital stay of 2-7 days
Some receive only medical therapy
Some receive medical therapy & angiography
Some receive medical therapy, angiography and revascularisation.
What causes STEMI?
Atherothrombosis - plaque rupture
When the rupture leads to occlusion of the coronary lumen & thus infarction of the distal myocardium (ie everything it usually supplies)
Generally, the further up the coronary artery that the thrombus is, the ______
The more proximal the thrombus, the worse it is - as a greater area is infarcted
However, distal blockages can be bad if they are in key structures & can cause stuff like rupturing of the papillary muscle etc
In STEMI, the level of necrosis of the infarcted tissue is time dependent. The earlier the vessel can be opened, the more of the heart can be salvaged, and the better the prognosis.
Less damage to which ventricle, in particular, indicates better survival?
Left ventricle
Less damage to the LV results in better survival
What are the ways to open an infarcted coronary artery?
Fibrinolysis or Primary PCI
The Critical time dependent period after infarction of the myocardium is the goal time to reperfuse the patient after the MI
How long is this period, and why is it important?
2 & a half hours after MI
If reperfusion carried out in this time period, then there is a minimum of around 80% reduction in mortality and the myocardium can be salvaged
PCI most effective when carried out within 120-150 minutes of onset
Which is better for STEMI treatment, Primary PCI or fibrinolytic therapy?
Primary PCI
Reduction in ‘all cause’ & cardiac mortality, recurrent MI & reduced risk of heamorrhagic stroke
PCI is most effective if delivered within 120-150 minutes of patients call for help
If PCI is better than Fibrinolytic therapy, when would it be necessary?
Alternative to PCI if unable to perform (eg if ‘door to balloon’ time is longer than 90 mins)
Aim to begin within 90 minutes of call for help, or 30 minutes of entering hospital, although, pre-hospital start of treatment has a much lower overall mortality rate (15-20% less)
List the best to worst treatments for STEMI by mortality rate
PCI
Prehospital fibrinolytic therapy (thrombolysis)
In-hospital fibrinolytic therapy (thrombolysis)
What is the risk with fibrinolytic therapy for STEMI? (or any thrombolysis)
Bleeding & intra-cranial haemorrhage
High risk in patients:
- Age >75
- Female
- Previous stroke
- Low bodyweight
- SBP > 160 mmHg (hypertensive)
- INR > 4
- Chronic kidney disease & elevated creatinine
Summarise when PCI is best for STEMI admitted patients
Door-balloon <90 mins
> 3 h symptom onset
Cardiogenic shock, HF
High bleeding risk
Diagnosis uncertain - e.g coronary dissection
Summarise when fibrinolytic therapy is suitable for a patient admitted with STEMI
Door-balloon >90 mins
(D-B) –(D-N) > 1-2hrs
<3 h symptom onset
Summarise the preventative treatment strategy for STEMI
General measures - smoking, diet etc
Co-morbidities - BP, glycaemic control for Diabetes
Medicine:
- Aspirin & clopidogrel - for 1 year
- Beta blockers
- Statins
- ACE inhibitors
What is the goal HR for a patient with ACS, using Beta blockers?
< 60 bpm
What is the goal for treatment of STEMI using Statins?
Reduce LDL-c to < 3.2 mmol/L
Reduce Total-c to 5 mmol/L
When are ACE inhibitors prescribed to patients who had STEMI?
Always prescribed, if Left ventricular dysfunction
Usually, but not always prescribed, if normal function
Ramipril 5mg BiD or equivalent.
What is the in-patient investigation for STEMI?
Echo cardiogram
Provides information that allows determination of prognosis n risk n shit
What do you look for on an echo of someone with STEMI?
Size of the abnormality of wall contraction, and whether it is akinetic or hypokinetic
Overall contractility
Presence & degree of Mitral regurgitations - (inferiors)
Presence of mural thrombus - (antero-apical MI’s)
What are the most important determinants of MI survival?
Age
Left ventricular ejection fraction
What is the survival rate for sudden cardiac death?
Only 2% of patients resuscitated & survive
What happens to the electrical activity of the heart in sudden cardiac death?
Irregular, ineffectual ventricular fibrillating activity caused by multiple, uncoordinated wavelets of electrical activity.
Ventricular fibrillation is one of types/causes of sudden cardiac death
What do you do if someone has VF arrest?
Defibrillation is the only effective treatment for VF arrest
However, VF arrest quickly deteriorates into ‘asystole’ - Flatline
It is much more difficult to restore cardiac output oncer the heart has flatlined
How does the chance of survival of SCD through resuscitation change over time?
Chance of success reduced by 7-10% each minute
For best chance, resuscitation must be started in the first 3-4 minutes
