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Cardio > Acute coronary syndromes > Flashcards

Acute coronary syndromes Flashcards

1
Q

Cardiac chest pain generally presents due to 1 of 4 causes

What are these?

A

New exertional angina - most common

Unstable angina

Acute MI

Sudden cardiac death

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2
Q

What is the difference between stable and unstable angina?

A

Stable angina only occurs on exertion - when myocardial demand for oxygen increases past supply

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3
Q

What are the key symptoms/signs of stable angina?

A

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)

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4
Q

What aspect of WIrchow’s triad causes angina?

A

Changes of vessel wall

Angina causes by atherosclerotic plaque in coronary arteries

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5
Q

How big does a plaque need to be to cause stable angina?

A

Obstructive plaque

Occludes >70% of the lumen

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6
Q

How big does a plaque need to be to risk acute coronary syndromes?

A

It is not the plaques size that really matters (although it has to be&raquo_space;70% occlusion)

ACS’s caused by spontaneous plaque rupture & local thrombosis with occlusion

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7
Q

Plaque rupture causes the formation of ___________

A

Atherothrombosis

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8
Q

What is included in ‘Acute coronary syndromes’?

A

Unstable angina

NSTEMI - Non ST segment elevation MI

STEMI - ST segment elevation MI

Sudden cardiac death

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9
Q

What is the basic difference between symptoms of stable angina and of ACS?

A

ACS will give symptoms at rest whereas stable angina is only on exertion

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10
Q

What are the risk factors for coronary artery disease?

A

Age, gender, family/genetics, creed (the usual)

Previous angina, other cardiac events & interventions

Smoking
Diabetes 
Hyperlipidaemia 
Hypertension 
Lifestyle
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11
Q

Describe the typical presentation of Unstable angina pectoris (UAP)

A

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”

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12
Q

Describe the typical presentation for NSTEMI

A

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”

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13
Q

How would you examine someone with suspected UAP or NSTEMI?

A

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
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14
Q

What piece of kit is needed to diagnose NSTEMI (or STEMI)?

A

ECG

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15
Q

What features on an ECG would you look for, for UAP and NSTEMI, on an ECG?

A

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)
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16
Q

Why must you take ‘serial ECGs’?

A

To detect late changes

This is essential in differentiation UAP & NSTEMI (and in general diagnosis)

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17
Q

How often are ACS symptoms ‘Atypical’?

A

Atypical symptoms are relatively common

Atypical symptoms more common in:

  • Women
  • Elderly
  • Diabetics
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18
Q

What are the typical atypical symptoms for UAP & NSTEMI?

A

Breathlessness alone +/- signs of heart failure

Nausea & vomiting +/- other autonomic symptoms

Epigastric pain +/- indigestion

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19
Q

Why would you take bloods of someone presenting with cardiac pain?

What biomarkers would be looked for?

A

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
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20
Q

If someone presents with cardiac chest pain and all the symptoms of ACS

Why can you not make a diagnosis entirely from their bloods?

A

Elevated troponin (cTn) can be caused by may different things, not just ACS & atherothrombosis

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21
Q

What is cardiac troponin?

A

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)

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22
Q

Why can’t you measure the cTn levels in someones blood immediately after they present with ACS?

A

cTn blood levels take a while to rise after acute ischaemia

They have a characteristic rise & fall of blood levels

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23
Q

Contrast the levels of elevation of cTn in the blood after different ACSs

A

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

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24
Q

Aside from cTn, what other molecules’ levels in the blood can be measured to help identify & diagnose acute MI?

A

Myoglobin

CK-MB

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25
Q

What is the acronym for the immediate treatment of UAP & NSTEMI?

A

ABCDE then MONA

26
Q

What does MONA represent?

A

Morphine (or diamorphine)
Oxygen
Nitroglycerine (GTN spray or tablet)
Aspirin 300mg orally (crush/chew)

27
Q

What is included in the long term therapy for UAP & NSTEMI?

A

Anti-platelet therapy

Anti-thrombotic therapy

‘other medical therapy’

Coronary revascularisation

28
Q

Summarise anti-platelet therapy for UAP & NSTEMI patients

A

All ACS patients:

Aspirin + ADP receptor blocker (Clopidogrel, Prasugrel or Ticagrelor)

This is usually continued for 1 year following ACS event

29
Q

Aspirin & ADP receptor blockers are given together to patients after an episode of ACS

What doses n shite do you give?

A

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
30
Q

Antithrombotic therapy = what drug?

A

HEPARIN

various types

31
Q

Summarise anti-thrombotic therapy for ACS patients

A

IV unfractioned Heparin (UFH)

or

Sub cutaneous Low molecular weight Heparin (LMWH)

or

Fondaparinux s/c

32
Q

Which is better out of UFH & LMWH?

A

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

33
Q

Asid from anti-platelet and anti-thrombotic therapy, what other agents can be given to ACS patients?

A

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

34
Q

Who should receive coronary revascularisation?

A

High risk patients with UAP/NSTEMI

Clear evidence that these patients benefit from surgery as well as medical therapy

35
Q

What are the different methods of interventional treatment of UAP or NSTEMI?

A

Coronary angiography & revasculariastion by Percutaneous intervention (PCI)

Coronary Artery Bypass Graft (CABG)

36
Q

What is the Seldinger technique?

A

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

37
Q

Describe how an coronary angiography is carried out once the catheter is inserted.

A

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

38
Q

What happens in a CABG?

A

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

39
Q

Summarise the overall hospital treatment route for a patient who presents in hospital with UAP/NSTEMI

A

Hospital stay of 2-7 days

Some receive only medical therapy
Some receive medical therapy & angiography
Some receive medical therapy, angiography and revascularisation.

40
Q

What causes STEMI?

A

Atherothrombosis - plaque rupture

When the rupture leads to occlusion of the coronary lumen & thus infarction of the distal myocardium (ie everything it usually supplies)

41
Q

Generally, the further up the coronary artery that the thrombus is, the ______

A

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

42
Q

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?

A

Left ventricle

Less damage to the LV results in better survival

43
Q

What are the ways to open an infarcted coronary artery?

A

Fibrinolysis or Primary PCI

44
Q

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?

A

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

45
Q

Which is better for STEMI treatment, Primary PCI or fibrinolytic therapy?

A

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

46
Q

If PCI is better than Fibrinolytic therapy, when would it be necessary?

A

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)

47
Q

List the best to worst treatments for STEMI by mortality rate

A

PCI

Prehospital fibrinolytic therapy (thrombolysis)

In-hospital fibrinolytic therapy (thrombolysis)

48
Q

What is the risk with fibrinolytic therapy for STEMI? (or any thrombolysis)

A

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
49
Q

Summarise when PCI is best for STEMI admitted patients

A

Door-balloon <90 mins

> 3 h symptom onset

Cardiogenic shock, HF

High bleeding risk

Diagnosis uncertain - e.g coronary dissection

50
Q

Summarise when fibrinolytic therapy is suitable for a patient admitted with STEMI

A

Door-balloon >90 mins

(D-B) –(D-N) > 1-2hrs

<3 h symptom onset

51
Q

Summarise the preventative treatment strategy for STEMI

A

General measures - smoking, diet etc

Co-morbidities - BP, glycaemic control for Diabetes

Medicine:

  • Aspirin & clopidogrel - for 1 year
  • Beta blockers
  • Statins
  • ACE inhibitors
52
Q

What is the goal HR for a patient with ACS, using Beta blockers?

A

< 60 bpm

53
Q

What is the goal for treatment of STEMI using Statins?

A

Reduce LDL-c to < 3.2 mmol/L

Reduce Total-c to 5 mmol/L

54
Q

When are ACE inhibitors prescribed to patients who had STEMI?

A

Always prescribed, if Left ventricular dysfunction

Usually, but not always prescribed, if normal function

Ramipril 5mg BiD or equivalent.

55
Q

What is the in-patient investigation for STEMI?

A

Echo cardiogram

Provides information that allows determination of prognosis n risk n shit

56
Q

What do you look for on an echo of someone with STEMI?

A

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)

57
Q

What are the most important determinants of MI survival?

A

Age

Left ventricular ejection fraction

58
Q

What is the survival rate for sudden cardiac death?

A

Only 2% of patients resuscitated & survive

59
Q

What happens to the electrical activity of the heart in sudden cardiac death?

A

Irregular, ineffectual ventricular fibrillating activity caused by multiple, uncoordinated wavelets of electrical activity.

60
Q

Ventricular fibrillation is one of types/causes of sudden cardiac death

What do you do if someone has VF arrest?

A

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

61
Q

How does the chance of survival of SCD through resuscitation change over time?

A

Chance of success reduced by 7-10% each minute

For best chance, resuscitation must be started in the first 3-4 minutes

Cardio (41 decks)

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