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Year 1 HLB > Acute Coronary Syndrome and Sudden Death > Flashcards

Acute Coronary Syndrome and Sudden Death Flashcards

1
Q

What is the most likley pathology underlying all acute cornary syndrones?

A
  • coronary thrombosis
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2
Q

In coronary thrombosis what is the name of the cap that covers the plaque, and what can happen in coronary thrombosis?

A
  • fibrous cap covering collagen and lipids becomes vulnerable
  • fibrous cap ruptrues releasing collagen and lipids
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3
Q

If the fibrous cap on an atherosclerosis plaque ruptures, what can happen?

A
  • lipids and collagen are released
  • platelets come into contact with collagen
  • platelet clotting factors are activated and a blood clot forms
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4
Q

Once the platelet have been activated and a blood clot forms, what can happen next?

A
  • blood clot can cause a complete occlusion
  • blood clot can cause a partial occlusion
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5
Q

What can happen if the coronary artery has a partial or complete block?

A
  • partial = unstable angina
  • complete = major ST elevation MI
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6
Q

When diagnosing a patient with acute coronary syndrome, what pain do they generally present with?

A
  • usual cardiac pain
  • occurs at rest
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7
Q

When diagnosing a patient with acute coronary syndrome, what happens to their colour and sweat?

A
  • appear pale
  • sweaty
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8
Q

When diagnosing a patient with acute coronary syndrome, can commonly be seen in an ECG?

A
  • can be normal
  • ST elevation (major MI)
  • ST depression
  • T wave inversion
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9
Q

In angina and myocardial infaction what would you see in troponin levels?

A
  • angina = normal levels
  • MI = high levels
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10
Q

Is creatine kinase (CK) an effective measure for a myocardial infraction?

A
  • generally no as present in all muscles
  • CK-MB is specific to cardiac muscle
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11
Q

When is troponin not effective in a myocardial infarction?

A
  • if a patient has more than one MI
  • troponin stays in the blood for up to 6 days
  • CK-MB can distinguish between new and old MI
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12
Q

There are 3 types of coronary syndrome. what are they?

A

1 - unstable angina

2 - Non-ST elevation MI (NSTEMI)

3 - ST elevation MI (STEMI)

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13
Q

Unstable angina is one of the 3 acute coronary syndromes, what would happen to a patients:

1 - chest pain

2 - ECG

3 - troponin levels

A

1 - chest pain = increased cardiac chest pain (occurs at rest)

2 - ECG = could be normal or abnormal

3 - troponin levels = normal levels

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14
Q

Non-ST elevation is one of the 3 acute coronary syndromes, what would happen to a patients:

1 - chest pain

2 - ECG

3 - troponin levels

A

1 - chest pain = cardiac chest pain

2 - ECG = may be normal or abnormal

3 - troponin levels = increased levels

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15
Q

ST elevation MI is one of the 3 acute coronary syndromes, what would happen to a patients:

1 - chest pain

2 - ECG

3 - troponin levels

A

1 - chest pain = cardiac chest pain

2 - ECG = ST elevation

3 - troponin levels = elevated levels

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16
Q

Of the 3 acute coronary syndromes, unstable angina, Non-ST elevation MI (NSTEMI) and ST elevation MI (STEMI), which is the most serious, where 1 is the most serious and 3 is the least serious?

A

1 - ST elevation MI (STEMI)

2 - Non-ST elevation MI (NSTEMI)

3 - Unstable angina

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17
Q

Which leads on the ECG signal demonstrate the anterior aspect of the heart?

A
  • V1-V4
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18
Q

When managing acute coronary syndrome patients what is the first drugs they are given as anticoagulants and anti-platelets?

A
  • anticoagulants = low molecular weight heparin (factors 2,7,9,10,11,12)
  • anti-platelets = asprin (COX-1 inhibition)
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19
Q

In additon to anti-coagulants and anti platelets, what other drug might be given acutely to aleviate symptoms?

A
  • glyceryl trinitrate
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20
Q

What are the 3 signs of severity in a patient with acute coronary syndrome?

A
  • severity of pain
  • ECG changes
  • troponin levels
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21
Q

In a patient with acute coronary syndrome, and who is experiencing an MI with ST elevation, what is now one of the most common treatments to treat patients?

A
  • Percutaneous coronary intervention service clinic
  • catheter inserted with wire
  • balloon inflated and stent is implanted
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22
Q

If an artery is occulded in an acute MI, how long before the tissue begins to die and what is the total time heart muscle can be saved surrounding the MI?

A
  • 15 minutes before tissue becomes necrotic
  • can still save the cardiac tissue up to 12 hours after MI
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23
Q

In patients with acute MI, what treatment has changed medicine and has reduced mortality?

A
  • percutaneous coronary intervention (stenting)
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24
Q

Percutaneous coronary intervention (PCI) has improved outcomes and mortality in patients with acute coronary MI. If they can be transferred to a PCI service within what time, that should always be the case?

A
  • <2 hours
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25
Q

What is primary prevention in medicine?

A
  • stopping patients from having condition in the first place
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26
Q

What is secondary prevention in medicine?

A
  • stop patients have a re-occurance or original problem
27
Q

In secondary prevention patients with acute coronary syndrome are given a mixture of different medications. They all have their initial effects, but also have a secondary effect that is beneficial to the patient. Dual anti-platelet medication (aspirin and clopidogral), which is able to prevent stent thrombosis. But what else can it help with?

A
  • beneficial even in patients with no stent
  • given up to 1 year
28
Q

In secondary prevention patients with acute coronary syndrome are given a mixture of different medications. They all have their initial effects, but also have a secondary effect that is beneficial to the patient. ACE inhibitors (Ramipril), is able to prevent adverse LV remodelling. But what else can it help with?

A
  • reduces further coronary events
29
Q

In secondary prevention patients with acute coronary syndrome are given a mixture of different medications. They all have their initial effects, but also have a secondary effect that is beneficial to the patient. Beta blockers are given to prevent recurrent ischaemia and arrhythmias. But what else can it help with?

A
  • improve prognosis in patients with LV function
30
Q

In secondary prevention patients with acute coronary syndrome are given a mixture of different medications. They all have their initial effects, but also have a secondary effect that is beneficial to the patient. Statins are given to prevent artheroma progression. But what else can it help with?

A
  • reduce vascular inflammation
  • reduce risk of coronary events
31
Q

What is sudden cardiac death?

A
  • unexpted death due to cardiac causes
  • occur over a short term (<1 hour from onset)
32
Q

What is the main cause of sudden cardiac death?

A
  • severe ventricular arrhymias
  • no organisation or co-ordination on ECG
  • can kill patients in 15 minutes
33
Q

What are some of the commenest causes of sudden cardiac death?

A
  • ischaemic heart disease = acute MI and large LV scar due to MI
  • cardiomyopathies = hypertophic, dilated and right ventricular
34
Q

How many people die each year in the UK from ischaemic heart disease?

A
  • 60,000
  • 50% of which die suddenly
35
Q

Are men or women more likley to die from ischaemic heart disease?

A
  • males
  • 3:1 (male:women)
36
Q

What is the average age people die from ischaemic heart disease?

A

between 45-75 years old

37
Q

What is hypertrophic cardiomyopathy?

A
  • heart thickens, mainly in the septum
38
Q

What does autosomal dominant mean?

A
  • mutation occurs on a non sex chromosome
  • only one gene is needed to cause the mutation
39
Q

What is the main cause of hypertrophic cardiomyopathy?

A
  • autosomanl dominant inheritance of mitated gene
40
Q

What is the main cause of sudden cardiac death in young people aged <30 years?

A
  • gentic hypertrophic cardiomyopathy
41
Q

In hypertrophic cardiomyopathy what can the increase in septum size do to the blood flow out of the heart?

A
  • impede LV outflow
42
Q

In hypertrophic cardiomyopathy what can the increase in septum size do to the mitral valve?

A
  • cause mitral regurgitation
  • can cause heart murmours
43
Q

In hypertrophic cardiomyopathy what causes cardiac pain?

A
  • increased cardiac muslce requires more O2
  • lack of O2 causes pain
44
Q

In hypertrophic cardiomyopathy what causes breathlessness?

A
  • the heart becomes stiff and increases pressure backwards
  • increased pressure enters lungs causing breathlessness
45
Q

In hypertrophic cardiomyopathy the increase in heart size can increase so much it causes reduced blood to the brain causing black outs. What is this called?

A
  • syncope (blackout in cardiology)
46
Q

Are ECGs able to detect hypertrophic cardiomyopathy, and if so generally why are they detected?

A
  • yes abnormal ECG
  • normally detected during a screening for something
47
Q

In hypertrophic cardiomyopathy what patterns can be seen on their ECGs?

A
  • QRS complexes are large and overlap
48
Q

In patients who have had a MI that has caused a scar. What can this do to the electrical pathway in the heart?

A
  • can cause a short circuit
49
Q

In patients who have had a MI that has caused a scar, it can cause arrhymias due to a short circuit of the electrical pathway. What can this do to the heart rate and the most likley arrhymia that may occur?

A
  • increased heart rate
  • ventricular tachycardia
50
Q

What is the normal route of re-entry?

A
  • there will be 2 routes, one fast and one slow
  • these routes will surround a section of heart tissue
51
Q

The fast pathway generally reaches the end of the fibre, but also enters the slower pathway whilst the slower conduction is still travelling down the slower pathway. What happens to the electrical signal where the fast and slow pathways meet?

A
  • they cancel each other out
  • heart continues to pump normally
52
Q

Although re-entry can be harmless and cause no major problems, what can an ectopic beat at the perfect do to the fast and slow pathways?

A
  • ectopic beat or scar can block the fast pathway
  • the slow pathway moves through the fast pathway as it is no longer refractory
  • this causes re-entry
53
Q

Why is re-entry important?

A
  • it is responsible for most cardiac rhythm abnormalities
54
Q

What is the Vaughan Williams drug classifications?

A
  • classes drugs based on their electrophysical properties
55
Q

In the Vaughan Williams drug classification for arrhymias which drugs are classed as class II drugs?

A
  • beta blockers (bisoprolol)
56
Q

In the Vaughan Williams drug classification for arrhymias which drugs are classed as class IV drugs?

A
  • Ca2+ channel blockers
  • Verapamil
57
Q

Do drugs that are used for arrhymias improve mortality?

A
  • no
  • they suppress the arrhymias
58
Q

What is the main problem with arrhymia drugs?

A
  • they can cause arrhymias
59
Q

What is syncope?

A
  • transient loss of consciousness
  • due to cerebral hypo-perfusion
60
Q

Does syncope occur slow or quickly?

A
  • rapid onset
  • short duration
  • spontaneous complete recovery
61
Q

In patients with syncope, how can you tell if it is a normal faint or something more serious?

A
  • normal faints occur with >10 seconds of warning
  • syncope is almost instant
62
Q

In patients with syncope, would you expect this to occur during activity with breathlessness?

A
  • normal faints do not occur with exercise
  • normal faints do not cause breathlessness
63
Q

If a patient has syncope with known cardiac disease and they hurt themselves during the fall, is it likley to be a normal faint?

A
  • no
  • people with cardiac disease arrhymias more likely to be serious
  • signifcant injury as no warning

Year 1 HLB (25 decks)

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