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- Y6 Cardiovascular > Extra ACS notes > Flashcards

Extra ACS notes Flashcards

1
Q

What does the term ACS encompass?

A

Unstable angina

STEMI

NSTEMI

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2
Q

How do you manage an MI?

A
  1. Bedside tests -
    • ECG (stress test)
    • urine dipstick
    • sputum sample
    • ABG
  2. Bloods
    • FBC
    • cardiac enzymes
    • U&E
    • CRP
  3. Scans
    • CX (rule out aortic dissection)
    • CT angiogram
    • 24 hour tape (ECG)
    • Echocardiogram

Old infarct is shown by Q waves on ECG

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3
Q

How do you treat an MI acutely?

A
  1. Pain relief
  2. Nitrates (GNT spray)
  3. Oxygen
  4. Aspirin - stops clotting
  5. Anticoagulants
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4
Q

How do you treat an MI chronically?

A

Clopidogrel (blood thinner)

(and manage symptomatic heart failure)

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5
Q

What is the advantage and disadvantage of warfarin over other DOACS? What does INR stand for?

A

Warfarin is reverible but requires more monitoring in INR clinics.

NB: International Standardised Ratio

  • 1.0-1.5 is normal
  • low= blood not thin enough
  • high = thin blood
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6
Q

Which patients should you not give beta blockers to?

A

Asthmatics - they can precipitate bronchospasm

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7
Q

What groups of patients are more likely to develop a silent myocardial infarction?

A

Older women

Diabetics

Elderly

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8
Q

Describe the management of ACS.

A

Acronym: MONAC FP

  1. Morphine - to relieve pain and its related sympathetic activity
  2. Oxygen - only if saturation is less than 90%
  3. Nitrates - GTN sublingual - reduces myocardial oxygen demand
  4. Aspirin+ P2Y12 inhibitor - limit secondary thrombosis by inhibiting platelet activation and subsequent platelet aggregation
  5. Clopidogrel (P2Y12 inhibitor) - antiplatelet
  6. Fondaparinux - like a LMW heparin - anticoagulant
  7. PCI - percutaenous coronary intervention or CABG
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9
Q

What is the aetiology of cardiac chest pain? Why does angina change?

A

Fatty deposits called plaque build up in the coronary arteries over time(atherosclerosis). These plaques obstruct flow and may cause myocardial ischaemia, which is felt as chest pain.

Diagram: if coronary flow doesn’t keep up with increased myocardial oxygen consumption then MI occurs. Vicious cycle - MI leads to increased O2 demand and blood flow.

Arteries are able to constrict and relax in the presence of atheromateous lesions. This gives rise to changing patterns of angina e.g. cold days.

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10
Q

How do these drugs affect the triad of factors which contribute to MI? (beta blockers, Ca channel blockers, nitrates)

A

Beta blockers - reduce exercise induced heart rate and reduce myocardiac oxygen demand

Ca channel blockers (e.g.amlodipine) - decrease the peripheral resistance against which heart has to pump

Nitrates - increase coronary dilatation so increases blood flow

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11
Q

Is angina essential for a heart attack to occur?

A

You can get a coronary thrombus leading to MI before previous angina pectoris.

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12
Q

Describe the atheroma process.

A
  • There has to be damage to the vascular endothelium to begin with.
  • Plaques probably rupture and heal a few times. It is only when there is a major rupture and clot formation at the site that leads to MI.
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13
Q

What percentage of people who suffer MI die outside the hospital?

Can atherosclerosis only occur in the arteries?

True or false: vessels can dilate and constrict in the presence of a thrombus.

True or flase: patients that have a coronary thrombosis causing MI usually have angina pectoris beforehand.

A

40%

Yes - sometimes called arteriosclerosis.

True

False - only 20% have angina before MI

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14
Q

Put these into order (pathogenesis of atherosclerosis)

  • Leukocyte recruitment
  • Endothelial damage
  • Lipoprotein oxidation
  • Foam cell formation
A

Endothelial damage occurs (by whatever means e.g. metabolic stress), this allows lipoprotein to collect in the intima. As the lipoproteins are free from plasma antioxidants they will then become oxidatively modified. Next leukocytes are recruited and finally mononuclear phagocytes differentiate into macrophages and transform into lipid laden foam cells.

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15
Q

Define angina pectoris. What are some other causes?

A

Chest discomfort due to MI typically associated with coronary artery disease i.e. it is not synonymous with MI but is usually due to MI.

(NB: other causes include aortic stenosis, hypertrophic obstructive cardiomyopathy)

Cardinal symptoms of aortic stenosis: chest pain, SOB, dizziness, collapse (also low BP)

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16
Q

What are the types of angina?

A

Stable angina - occurs over several weeks without major deterioration although symptoms may vary considerably over time e.g. with exertion, stress.

Unstable angina - abruptly worsening angina or new angina at low work load

Variant (Prinzmetal) angina - spontaneous (i.e. no precipitating cause) angina with ST elevation on ECG. Intense coronary spasm at the site of an atheromatous lesion, usually occurs at night.

Syndrome X - angina with objective evidence of MI (e.g. ST depression) in the absence of evident coronary atherosclerosis or epicardial (large vessel) disease.

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17
Q

Who gets syndrome X? What is the triad?

A

Usually post menopausal females.

Triad of this syndrome: anginal chest pain, positive exercise test, angiographically normal coronary arteries.

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18
Q

What are the ECG changes in Prinzmetal’s angina? What information is key in diagosis?

A

Profound ST elevation in lead II when symptomatic which goes away as the symptoms disappear.

Usually at night (so monitor for 24hr)

History is key: patients get an intense chest pain when they go to bed which wakes them up at night

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19
Q

What is decubitus angina? Describe the aetiology.

A

Chest pain when patients lie flat in bed. This is caused by a severe obstruction in the coronary artery.

Lie down –> decreased venous pooling –> increase in myocardial work

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20
Q

What is meant by acute coronary insufficiency?

What is meant by crescendo?

A

ACI- another term for unstable angina

Crescendo - increasing frequency and severity of the chest pain.

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21
Q

What type of pain is angina?

A

Dull pain - pressure not sharp

22
Q

Name a disadvantage of GTN spray.

A
  • AS well as relaxing the coronary artries, it can also dilate the lower end of the oesophagus.
  • Therefore oesophageal spasm (brought on by eating spicy food) will also be treated by GTN.

So difficult to use GTN relief as a destinguisher of whether the chest pain is cardiac or oesophageal.

23
Q

Describe the differences between these chest pains.

  • Angina
  • MI
  • Aortic dissection
  • Pericarditis
A
  • Angina - dull pressure-like pain
  • MI - sudden, severe, sweating
  • Aortic dissection - tearing pain - abdo or back
  • Prericarditis - sharp, sudden, worse by breathing, postural (worse when lying on left side)
24
Q

What prophylactic medication should you give to a patient with valve disease who is going to attend the dentist?

A

Valve disease–>

2 sachets of Amoxyl (3g) *if not allergic to penicillin - take 30min before procedure and 6 hours after

*if allergic to penicillin then give Clindacicin

25
Q

What percentage of MI are followed by angina?

A

50%

26
Q

What does this ECG of a previous MI show?

A

There is an abnormal Q wave in leads II, III and AVF (inferior leads)

V6 and V7 also show T wave inversion

27
Q

How does ST segment depression correlate with disease severity in an exercise ECG?

A

Disease severity increases with degree of ST depression

There is also crude correlation between exercise capacity and post MI prognosis - 9% mortality if <10mins on Bruce Protocol and 2% mortality if >10mins. If you can exercise a lot then you have less severe disease after the infarct.

*Bruce Protocol is an exercise protocol

28
Q

What does this figure show?

A

Patients with MI will get ST segment depression when they exercise

However, patients with Syndrome X will also get ST depression without MI on exertion

29
Q

When should you stop the exercise stress test?

A
  1. Rapidly dropping ST segment
  2. Blood pressure drops with exercise (CO output is dropping because the disease is so severe –> VT/VF)
  3. Severe chest pain
  4. Arrhythmias (e.g. AF/ VT)
30
Q

Which of these are involved in the cause of death of cardiac myocytes following infarction?

  • Actin-myosin crosslinking
  • Lack of oxygen
  • Sodium leaking into cells
  • Cytokines
  • Cessation of Na/K ATPase pumps
  • Neurotransmitter depletion
A

Cause of death of cardiac myocytes following infarction is…

  • Lack of oxygen to cells resulting in the
  • Lack of ATP synthesis, causing
  • Na/K ATPase pumps to stop working properly. This causes
  • Sodium to leak into cells bringing water with it and then the cells swell and die.
31
Q

True or false?

Hypertrophic obstructive cardiomyopathy affects males more than females.

A

False - it is an inherited condition with equal sex incidence.

32
Q

A 25 year old patient presents with a sudden chest pain, which is made worse by movement. What is the most likely cause?

  • Pneumothorax
  • Acute myocardial infarction
  • Muscoskeletal spasm
  • Unstable angina as a result of familial hypercholesterolaemia
  • Inflammation of the pancreas
A

Muscoskeletal spasm

33
Q

What types of angina are described?

A

NB: Prinxmental angina is vasospastic angina with spontaneous ST elevation on ECG. Cardiac syndrome X has is angiographically normal but abnormal on ECG.

34
Q

What are the causes?

A
35
Q

List 4 drugs used to treat angina.What are the aims of treatment?

A
  • Beta blockers - atenolol, metorpolol, bisoprolol (start on once a day; cardioprotective)
  • Nitrates - dihydropyridines (nifedipine/amlodipine), others (diltiazem, verapamil)
  • Ca channel antagonists - GTN, long-acting nitrates (ISMN, ISDN)
  • Nicorandil
  1. To reduce morbidity and mortality
  2. To eliminate angina with minimal adverse effect allwoing the patient to return to normal activities.

Treatments which alleviate symptoms are usually different from the ones that alter prognosis - so consider this deeply.

36
Q

How do you manage angina?

A
37
Q

Broadly speaking, what are the main two reasons for angina? Give examples of each.

A
38
Q

What are the main types of calcium antagonists? How do calcium antagonists work in angina? Why should they not be used as monotherapy?

A
  1. Dihydropyridines (–> peripheral vasodilation). Not suitable for monotherapy(–>reflex tachy). Amlodipine is more vasoselective than nifedipine (because it has a less -ve inotropic effect i.e. decrease myocardial contractility)
  2. Verapamil/Diltiazem act on periphery and on the heart. These are also -ve chronotropic.
  • They cause peripheral vasodilation so reduce systemic vascular resistance and also vasodilate the coronary arteries.They are -ve inotropic.
  • Systemic vascular resistance will drop which will cause an increase in sympathetic drive which causes an increase in HR. May counterbalance the anti-anginal effect. So combine with beta-blocker.

Particularly useful in vasospastic angina.

39
Q

Which medication should you give first in angina? What dose? What HR?

A

Beta blocker - 25mg atenolol per day, aim to acheive resting HR 55-60 and/or 75% of HR that provokes ischaemia during exercise.

40
Q

What are the conraindications to beta-blockers?

A
41
Q

What are the side effects of beta blockers?

A
  • Fatigue and lethargy
  • Insomnia and nightmares
  • Worsening claudication or asthma
  • Impotence and erectile dysfunction
42
Q

When are calcium antagonists contraindicated? What are the side effects?

A

Contraindicated in:

  • Decompensated heart failure
  • Diltiazem and verapamil (act on AV node) - bradycardia, high grade AV block, sick sinus syndrome

Side effects:

  • Hypotension peripheral oedema, cardiac decompensation, constipation.
  • Headache, flushing, dizziness.
43
Q
A
44
Q

Where do nitrates act? How? Why do you ask patients to stop taking them at night?

A
  • On vascular smooth muscle. Reduces preload and dilates the coronary arteries.
  • GTN is for immediate relief or prophylaxis before exercise.
  • Long-acting nitrates - add to or instead of beta blockers or Ca antag
  • Nitrate free interval required (8-12h/day) - to prevent nitrate tolerance. So they don’t take it at night.
45
Q

When are nitrates contraindicated? What are the side effects?

A

Contraindicated in outflow tract obstruction.

Side effects:

  • headache
  • hypotension (can be life-threatening if coad with sildenafil)
  • presyncope and syncope

sildenafil (viagra) and nitrates cannot be used together.

46
Q

What is nicorandil? How does it act? Name a contraindication and side effect.

A

This is a potassium channel agonist.

It is most useful when beta blcokers and Ca antag cannot be used due to contraindications or unacceptable side-effects.

47
Q

Which treatment is most important in a patient with Prinzmental’s angina?

A

Anti-platelet - usually aspirin or sometimes clopidogrel.

48
Q

Regarding the physiological role of nitric oxide (and therefore actions of nitrates):

NO activates…

Guanylyl Cyclase generates…

CGMP activates a…

Muscle relaxation results from a dephosphorylated…

A

NO activates guanylyl cyclase which converts GTP to cGMP.

This then activates a cGMP dependent protein kinase which leads to the phosphorylation of many proteins,

which in turn results in the dephosphorylation of light chain myosin causing smooth muscle relaxation.

49
Q

True or false?

There is not an attenuation of magnitude of pharmacological effect upon repeated use of nitrates.

A

False

There is marked attenuation so you must have nitrate free times of the day.

50
Q

Describe what is meant by coronary angiogram.

A

Tueb inserted into artery at the groin and directed towards the coronary arteries.

A dye is injected and X rays of the heart and coronary arteries are taken.

51
Q

What is meant by PTCA? Which patients is it most beneficial in?

A
  • Percutaneous transluminal coronary angioplasty (PTCA)
  • There is no benefit of having angioplasty in chronic stable angina. The narrowings are only pushed into the walls (not removed). PTCA is only beneficial on long term outlook in acute MI where the coronary artery can be opened up.
  • 20-30% restenosis rates in the first 3-6 months (but now <10%- patients are put onto antiproliferative agents which reduce rate of restenosis)
  • Revascularisation etc should only be considered if medical therapy fails.

- Y6 Cardiovascular (47 decks)

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