Acute Coronary Syndrome Flashcards

1
Q

What is ACS?

A

Acute Coronary Syndrome

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2
Q

What are the symptoms of ACS?

A

Chest pain.
SOB.

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3
Q

How does stable angina differ from unstable angina?

A

In stable angina, the chest pain should go away with rest.

In unstable angina, the chest pain will not go away without rest and continues for over 20minutes.

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4
Q

True or False: Angina is associated with elevated Troponin levels.

A

False - Troponin is an indication of cardiac tissue death which doesn’t occur in Angina.

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5
Q

True or False: Angina can not be seen on a 12-Lead ECG

A

True - There are no significant ECG changes seen in Angina.

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6
Q

What is a Myocardial Infaction (MI)?

A

An MI is irreversible isceamia of the cardiac tissue caused by lack of oxygen.

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7
Q

Describe how atherosclerosis can manifest into an MI if left untreated.

A

1) The coronary arteries are susceptible to the build up of Atheroma (fatty plaques).
2) In the early stages of atheroma build up the plaque begins to occlude the coronary artery (Stable Angina).
3) As the plaque hardens, it becomes harder for the artery to compesate when needed (Unstable angina).
4) If the hardened plaque breaks off, platelets surrounding the inside of vessel begin to create a thrombus (clot). If blood can flow around this thrombus then it would present as an NSTEMI - perfusion is inadequate but not completely blocked.
5) Further build of the thrombus leads to a completely occluded artery which is called a STEMI.

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8
Q

Which of the following conditions are associated with elevated Troponin?
Stable Angina
Unstable Angina
Non-ST Elevated MI
ST Elevated MI

A

NSTEMI + STEMI

Troponin is a protein that indicates cardiac tissue death, so it is only present when there is a lack of oxygen to the cardiac tissue causing ischaemia.

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9
Q

What is the difference between a NSTEMI and a STEMI?

A

An NSTEMI is a partially occluded coronary artery, there is still ischaemia but not bad enough to cause ST elevation on the ECG.
A STEMI is a full occlusion of the coronary artery, this results in significant ischaemia and ST elevation on the ECG.

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10
Q

What is the difference between a thrombus and an embolus?

A

A thrombus is a static clot.
If a part of that clot breaks off into the circulatory system it is called an embolus.

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11
Q

How is cardiac output calculated?

A

CO = SV x HR

Cardiac output = Stroke Volume x Heart Rate.

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12
Q

What is meant by stroke volume?

A

Stroke volume is the amount of blood ejected from the left ventricle into the aorta with each contraction of the heart.

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13
Q

Describe the physiology behind chest pain in ACS.

A

Increased oxygen demand caused by the plaque/thrombus forces the heart muscle to shift to anearobic respiration.

Byproducts of anaerobic respiration are lactate and hyrdogen.

The build up lactate triggers to nociceptors which send a signal of pain to the brain.

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14
Q

Describe the three components that make up or affect stroke volume.

A

Preload - How much blood fills the left ventricle.

Afterload - The pressure within the aorta that the left ventricle has to push against to eject the blood.

Contractility - The strength of the left ventricle squeezing.

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15
Q

With regards to contractility, what is Frank-Starlings law?

A

The force of contraction is proportional to the initial muscle fibre length.

i.e. the weaker the muscle the weaker the contractility.

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16
Q

Betty suffered some central stabbing chest pain that came on during her weekly jazzercise class at 9am.
She felt sick at the time and went home to rest, thinking to mention it at her GP nurse appointment later that afternoon.

At the appointment she still has the chest pain, complaining that her left arm is also quite painful, but not as bad as her chest which has become an aching pain.

Complete a full assessment of Betty’s pain using SOCRATES.

A

SOCRATES

Site: Central chest pain
Onset: Initially during exercise, but on-going at rest.
Characteristics: Stabbing and aching.
Radiation: Left Arm.
Associated Symptoms: Nausea
Timing: Several hours
Exacerbating or relieving factors: Nil
Severity: Moderate to high pain.

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17
Q

Billy has attended his GP for a health check-up after suffering some bouts of chest pain while working on his farm.
He explains that the pain normally subsides after a few minutes rest.

His observations are unremarkable apart from a slightly elevated BP (140/85).
He takes no regular medications.
He is a non-smoker.
He drinks 2-3 cans of lager each evening.
His bloods taken at his initial appointment last week show a Troponin level of 3.
His 12-Lead ECG shows no significant changes.

Based on the information above, which condition do you suspect Billy might have and why?

A

Billy likely has stable angina due to the chest pain symptoms going away after resting.
The insignificant ECG and low Troponin levels rule out any myocardial infarction.

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18
Q

A patient in the Emergency Department is identified as having ST elevation on their 12-lead ECG.
Should the patient be given supplemental oxygen?

A

No - current evidence shows that giving oxygen is contra-indicated during MI.

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19
Q

Identify 3 elements of a nursing assessment that should be completed on a patient with chest pain.

A

Baseline observations (NEWS2)
12-Lead ECG
Pain assessment (SOCRATES)
Bloods - Troponin

Past Medical History (PMH)
Patient Risk Factors
Assess family history

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20
Q

Multiple or “serial” troponins must be taken in the assessment of a patient with chest pain. Why?

A

A patient might have on-going cardiac issues or previous MI. Taking a second Troponin a few hours after the first one allows us to see if and how fast the troponin is increasing.

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21
Q

A GRACE Score divides patient into high risk (>3%) and low risk (<3%) of what?

A

Low or high risk of 6 month mortality and risk of further cardiovascular event.

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22
Q

Identify 3 elements included on a GRACE Score risk assessment.

A

Age
HR
Systolic BP
Creatinine levels
Cardiac arrest?
ST Elevation/depression
Abnormal cardiac enzymes (Troponin)
KILLIP Class (CHD, Rales or JVD, pulmonory oedema, cardiogenic shock)

23
Q

What does GTN stand for?

A

Glyceryl Trinitrate

24
Q

What is pharmacodynamics?

A

Pharmacodynamics is what the medication does to the body.

25
Q

What is pharmacokinetics?

A

Pharmacokinetics is what the body does to the drug.

i.e. how is it metabolised or excreted?

26
Q

What are the 3 pharmacodynamic effects of GTN?

A

1) Venodilation of coronary veins.

2) Vasodilation of coronary arteries.

3) Vasodilation of larger arteries outside of the heart.

27
Q

Pharmacodynamics:
GTN causes venodilation of the coronary veins, how does this aid in the reduction of chest pain?

A

Venodilation of the coronary veins reduces the amount of blood returning to the heart.
This in turn reduces cardiac preload.
Reducing workload.

28
Q

Pharmacodynamics:
GTN causes vasodilation of the coronary arteries, how does this lead to less chest pain?

A

Dilating the coronary arteries it allows more blood flow to get around the thrombus and increases perfusion to the heart muscle.

More blood flow = more oxygen = less anerobic respiration = less lactate = less chest pain.

29
Q

Pharmacodynamics:
GTN causes vasodilation of large arteries outside of the heart, how does this reduce chest pain?

A

Dialting the larger vessels outside of the heart reduces the afterload.
This reduces the workload of the heart.

Less workload = Lower oxygen requirement = less anerobic respiration = less lactate = less chest pain.

30
Q

What are some of the adverse effects of GTN Spray?

A

Reduced BP
Nausea
Dizziness

31
Q

Pharmacokinetics:
Why is GTN given via a sublingual spray?

A

GTN is almost completely absorbed in the first pass metabolism in the liver giving no therapeutic effect to the patient.
Absorbtion through the mucuous membrane allows the GTN to enter the bloodstream quickly, being useful before being metabolised in the liver.al

32
Q

Pharmacokinetics:
Why is it safe to give GTN every 5 minutes?

A

GTN has a very short half-life of 4 minutes.
This means that the circulating amount is reduced by half every 4 minutes, making it safe to top up and administer every 5 minutes.

33
Q

Gerald has central chest pain, raised Troponins and ST Elevation on a 12-Lead ECG.
What condition do they have? and WHY?!

A

ST-Elevated Myocardial Infarction (STEMI).

The raised troponins indicate that there is some cardiac tissue death, confirming that this is a MI of some sort.
The changes to his ECG indicate that the electrical conduction of the heart is taking some time to get through the dead tissue. The ST-elevation therefore makes this a STEMI.

34
Q

Karen has chest pain, raised troponins and no ECG changes.
What is likely to be going on?

A

NSTEMI.

Raised troponins indicate cardiac tissue death = MI.
No ECG changes indicate that there is some perfusion, though not much if tissue is dying.

35
Q

Penny has a GRACE score of 5%. Identify one investigation and one possible treatment she may be given.

A

Penny will be offered an angiogram which will identify the extent of the blockage of her coronary arteries. This can be immediately followed by a PCI if it is determined that the thrombus should be removed there and then.

36
Q

In the event of a suspected ACS event, which medication should be given as a first line treatment? And Why?

A

Aspirin, 300mg, chewed.

Aspirin is an anti-platelet medication, it is given to reduce the risk of a thrombus forming during an ACS event.
It is chewed in order to break the medication down so that the therapeutic effect is accelerated.

37
Q

Fondaparinux should be considered as part of the early management of NSTEMI.
In which circumstances might it be contra-indicated?

A

For patients with a high risk of bleeding, or for those who will be going for immediate angiograph.

38
Q

What 4 points should be included in the early management of NSTEMI or unstable angina?

A

1) Consider anti-platelet.
2) Consider fondaparinux unless contraindicated.
3) Assess risk of future cardiac events (GRACE).
4) Offer coronary angiograph +/- PCI/CABG

39
Q

PCI and CABG are treatments for coronary artery issues, why might one be given instead of the other?

A

PCI should be considered for a single blocked vessel.
CABG should be considered for multiple blocked vessels.

40
Q

Pharmacodynamics:
How does aspirin inhibit the formation of clots?

A

Aspirin is a COX-1 inhibitor. Cox-1 is responsible for activating the thromboxane pathway.
In normal circumstances, the thromboxane pathway releases receptors (GP11b/111a) that attach to fibrin, as they all clump together this creates a clot.

41
Q

Pharmacodynamics:
How does Clopidogrel inhibit the formation of clots?

A

Clopidogrel is an ADP receptor blocker.
ADP receptors send a signal to other platelets to activate them as part of the clotting cascade. Blocking this signal inhibits the formation of clots.

42
Q

Pharmacokinetics:

Why is Aspirin 300mg chewed?

A

Aspirin needs a first pass metabolism to enter the bloodstream and be effective. Chewing the aspirin helps to break it down quickly, increasing it’s bioavailability when metabolised in the liver.

43
Q

When is aspirin contraindicated?

A

Patient’s with asthma or high bleeding risk.

44
Q

Why is heparin or fondaparinux given subcutaneously?

A

SC has around 80% bioavailability, meaning it acts a lot faster than oral.

45
Q

Identify 2 contraindications to heparin.

A

Nephrotic Syndrome
Protein urea.
Liver failure.
Renal failure.

46
Q

What two medications are usually used in Dual anti-platelet therapy (DAPT)?

A

Aspirin and Clopidogrel.

Because aspirin prevents clots binding to fibrin and clopidogrel prevents the activation signal being sent to other platelets.

47
Q

Triple therapy is a common anti-coagulation option, what does it consist of?

A

Dual anti-platelet therapy (Aspirin and Clopidogrel)

AND

DOAC (Direct Oral Anti-coagulant) e.g. apixaban.

48
Q

Ramipril is a type of what medication?

A

ACE inhibitor

49
Q

How do ACE inhibitors reduce blood pressure?

A

They inhibit the conversion of angiotensin 1 to 2, this leads to increased vasoldilation which reduces preload. This reduces cardiac workload and output.

They reduce the release of Anti-diuretic hormone, allowing fluid to be excreted more easily.

Reduces sodium and fluid reabsorption.

50
Q

Bisoprolol is an example of what type of medication?

A

Beta blocker

51
Q

What are the two types of beta blocker and how do they differ?

A

Selective: Works only on beta 1 receptors (in the heart).

Non-selective: Works on beta 1 and 2 receptors (heart and lungs).

52
Q

What are the pharmacodynamics of beta blockers?

A

Noradrenaline normally binds to the beta 1 and 2 receptors which increases the rate and force of contractions.
Beta blockers are antagonist so they block those receptors.

Blocking the receptors reduces the rate and contractility of the contractions.

53
Q

What conditions are beta blockers used for?

A

Angina, heart failure, AF, anxiety and secondary prevention following an ACS event.

54
Q

What does atorvastatin do and why is it used in ACS management?

A

Atorvastatin reduces further build of Low density lipids, which reduces the build up of atheroma which reduces further risk of cardiac event.