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Angina + ACS Flashcards

1
Q

What are the branches of the left main coronary artery and what part of the heart do they supply?

A

Circumflex= left atrium and ventricle

Left anterior descending= anterior and inferolateral part of LV and septum

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2
Q

What parts of the heart does the right coronary artery supply?

A 
RA 
RV
Inferior LV
Branch to SAN
Septum

I.e. dominant vessel in 85% of people

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3
Q

What is the primary cause of angina? Why does exertion or emotional stress precipitate angina?

A

Narrowing or occlusion of 1 (+) major coronary arteries by atheroma

They cause an imbalance between myocardial O2 demand and supply which results in ischaemia that causes the pain associated with angina

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4
Q

Why is angina associated with ST-depression?

A

Dysfunction between O2 demand and supply leads to cellular acidosis and lactate production due to changes to anaerobic respiration which leads to ST depression

ST depression is associate with ischaemia rather than infarction

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5
Q

What pathologies can cause angina and why?

A

Aortic stenosis
-unable to maintain adequate coronary perfusion

Hypertrophic cardiomyopathy
-increased O2 demand due to increased thickness of myocardium

Severe anaemia
-decreased O2 capacity

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6
Q

What is the pathology behind angina developing into MI?

A

Atherosclerotic plaque ruptures to induce an acute thrombosis and cause complete occlusion of a coronary artery

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7
Q

Ischaemic heart disease can be associated with different clinical outcomes/conditions. What are examples of manifestations?

A

Angina

Myocardial infarction

Sudden death

Cardiac failure due to damage experienced from previous MI

Arrhythmias (atrial fibrillation or ventricular arrhythmias)

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8
Q

What are the differentials for chest pain outside of ACS?

A

Musculoskeletal pain

Thoracic/cervical root pain (can radiate into arms)

Peptic ulcer disease

GORD

PE

Aortic coarctation

Aortic dissection

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9
Q

A patient presents with squeezing feeling in chest and their chest feels heavy. They also say they have pain behind their breastbone. Is this cardiac or non-cardiac?

A

Cardiac

Pain behind breast bone= retrosternal discomfort

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10
Q

A patient comes with sharp stabbing chest pain which is aggravated by respiration or movement. Is this cardiac or non-cardiac?

A

Non-cardiac

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11
Q

A patient presents with pain across the mid-thorax and they say it is moving to their arms, neck and jaw. Is this cardiac or non-cardiac?

A

Cardiac

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12
Q

A patient presents with pain in left sub-mammary area or hemithorax. Is this cardiac or non-cardiac pain?

A

Non- cardiac

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13
Q

If someone was experiencing cardiac pain, when would you expect it to be exacerbated and relieved? Why?

A

During exercise
Excitement or stress

Associate with increased HR or BP

Relief:

  • rest
  • Nitrates (GTN)
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14
Q

If someone was experiencing non-cardiac chest pain, when would you expect it to be exacerbated and relieved? Why?

A 
After exercise 
With specific movements i.e. Moving arms 
Possible localised tenderness 
Pain at rest 
Cold weather 
After meals

Relief:

  • analgesics
  • antacids
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15
Q

What clinical signs or co-morbidities would you expect to find in someone suspected of angina/IHD?

A

Hyerlipidaemia= look for arcus, xanthomas or tendons

Hypertension

Peripheral vascular disease= reduced or absent pulses

Diabetes (neuropathy or retinopathy or peripheral vascular disease)

Anaemia

Murmurs

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16
Q

What are the features of unstable angina?

A

New onset= w/i 4 weeks

Progressively worse i.e. increased freuquency/severity =crescendo angina

Prolonged cardiac pain w/o evidence of mi= >15-20 mins despite rest and GTN

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17
Q

How can patients with refractory unstable angina be managed? What needs to be done in-order to select patients for this form of management?

A

Early coronary angiography to revascularise

Patients been to have been stabilised by initial therapy
Troponin needs to be measure to determine if myocardium damaged
Stress-testing done

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18
Q

How can you differentiate between ischaemia and infarction on an ECG?

A 
Ischaemia= ST depression 
Infarction= ST elevation, T inversion and Q wave formation (T + Q waves changes occur later)
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19
Q

Changes in leads II/III/aVF indicate indicate ischaemia or infarction in which part of the heart? Which arteries are likely to be affected?

A

Inferior= part of heart supplied by R coronary or distal circumflex artery

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20
Q

Changes in leads V4-6 and aVL indicate ischaemia or infarction in which part of the heart? Which arteries are likely to be implicated?

A

NOTE: tend to be leads which ST segment change can be seen
Anterolateral part of heart

Arteries= LAD

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21
Q

What blood tests are important to do with IHD?

A

FBC= look for presence of anaemia
Lipids= hyperlipidaemia
HbA1c= need to exclude diabetes
Thyroid function

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22
Q

Why is it important to assess thyroid function in patients with IHD?

A

Thyroxine (T4)= increases resting HR and LV contractility
T3= decreased SVR by acting on arteriolar SM

Hyperthyroidism= increase T4= increased HR and LV contractility i.e. increased strain on heart

Hypothyroidism= decreased T4= decreased HR and LV

23
Q

What is the 1st line investigation of stable chest pain? What is the alternative if this therapy is not appropriate?

A

CT coronary angiogram (non-invasive)

Functional/stress test

  • stress= treadmill/bike/adenosine
  • assess= ECG/SPECT (asses myocardium perfusion)/ Echo (assess LV function)
24
Q

What is the role of a pressure wire used during coronary angiography?

A

Assess the pressure across the stenosis artery which is important when considering re-perfusion

25
What are the typical ECG changes in an acute MI?
ST elevation (occurs within few minutes) Q wave i.e. if >40mm wide or 2mm deep= associated with current or previous MI EG= full thickness damage to myocardium I.e can persist after MI T wave inversion i.e. Normally follows ST elevation becoming less marked
26
How would you diagnose an acute STEMI?
History - chest pain >30mins - dyspnoea - nausea + vomiting - sweating - collapse ECG - ST- elevation present w/i minutes - Pathological Q waves and T inversion come later Blood tests; -troponin T or I
27
What can be done as part of secondary prevention following MI?
Smoking cessation Manage hyperlipidaemia Hypertension Dietary modifications Control of diabetes Physical activity
28
What are the 2 main aims of angina therapy?
Increase O2 supply Decreased O2 demand
29
What therapy methods can be used to increases the O2 supply to the myocardium?
- beta-blockers= increase length of diastole which increases the length of time which blood flows through coronary vessels and increases cardiac perfusion - Nitrates or Ca2+ anatagonists= decrease the coronary tone= increases BF - Nitrates= decrease LV diastolic pressure= decreased myocardial tension meaning increased perfusion of innermost layers of myocardium - Stenting/ballooning/CA bypass= all act to revascularise
30
What therapy methods are used to decrease O2 demand of myocardium?
Beta-blocker= decrease HR and contractility Nitrates= decrease wall tension
31
What are the 3 main functions of beta blockers in the context of angina? What is an example of beta-blocker used in angina?
Increase length of diastole to increase cardiac perfusion Decrease HR Decrease contractility Atenolol, bisoprolol, metoprolol
32
What are the 2 main functions of nitrates in treating angina? What is an example of a nitrate use for angina?
Decrease coronary tone= increased BF Decreased LV diastolic pressure= decreased wall tension leads to increased perfusion of innermost myocardium GTN spray
33
What are the 5 different types of drugs you might expect someone who suffers from angina to be on?
Antiplatelets - lifelong aspirin OR clopidogrel (P2Y12 inhibitor) if intolerant - aspirin + P2Y12 inhibitor for high risk patients Short acting nitrate (GTN spray) -symptomatic relief or prophalytic Beta blockers -atenolol/ bisoprolol/ metoprolol Long-acting nitrates -decrease reliance on GTN Potassium channel opener(Nicorandil) /If channel blocker (Ivabradine) -delays repolarisation
34
Do NSTEMI patients need to go to the cath lab immediately? Why?
No | Lack of ST elevation indicates that there is not complete occlusion so will manage in CCU with medication
35
How are patients suffering from N-STEMI treated medically? What is the aim of this treatment?
Aims to maximise cardioprotection to prevent further events from occuring SAABA High dose statin - 80mg atorvostatin - ask as prevention for further incident - decreased inflammation in coronary arteries Antiplatelet (dua-antiplatelet) - Asparin= 1 week - Clopidogrel= for 1 year ACEi/ARB -when patient has LV dysfunction, hypertension or diabetes Beta-blocker - reduce myocardial oxygen demand - target HR= 50-60 - bisoprolol Anticoagulant (only until discharge) -Fondaparinux/Epixaban/Rivoroxiban
36
What are the 2 procedures involved in revascularisation? What are the indications for each procedure?
CABG (coronary artery bypass graft) - L main stem disease - triple vessel disease - angina unresponsive to drugs - unsuccessful PCI PCI (angioplasty + stenting) - persistent symptoms - STEMI or high risk N-STEMI (haemodynamically unstable)
37
What are the key investigations for acute coronary syndrome?
ECG Obs to check for haemodynamics Bloods= FBC and troponin Call cardiology
38
The acute management for ACS can be remembered by the acronym MONAC. Using this, what are the 5 main forms of intermediate management for ACS?
``` Morphine Oxygen (only if <94%) Nitrates= GTN spray Aspirin= 300mg loading dose Clopidogrel ``` I.e. dual platelet therapy
39
What is the long term/ secondary prevention for ACS? (Acronym= SAAB(A))
Statins (high dose) Antiplatelets (dual)= Aspirin (life long) + Clopidogrel/Prasugrel ACEi Beta-blockers NOTE: Possible anticoagualent whilst in hospital (standard treatment)-> only until discharge
40
What is the pathogenesis of atherosclerosis and how can this result in development of ACS?
- inflammatory stimuli causes damage and increased permeability of muscular artery endothelium - lipids accumulate under tunica intima and form fatty streak - stimulates inflammatory cells (macrophages) to accumulate= become foam cells - SM proliferation and CT synthesis leas to production of collagenous fibrous cap - artery becomes occluded= decrease blood flow and vessels unable to compensate for change in BF demand
41
What are signs that artherosclerosis causing angina is progressing?
Increasing incapacitated by chest pain Unable to climb stairs More medication required
42
What is the difference between stable angina and unstable angina?
``` Stable= symptoms relieved by rest or GTN Unstable= symptoms come on randomly at rest and are not relieved by GTN ```
43
Why is an echo required as part of investigations for N-STEMI?
Need to assess LV function -decreased LV function (<35% EF) increases the risk of VF and VT Patient might need ICD if LV function does not improve 6 weeks following N-STEMI
44
What are the 3 most common acute complications which can occur post MI? What are the other possible complications?
1. Rupture of myocardium-> leads to blood pooling in the pericardial sac-> TAMPONADE i.e. need to do an echo following MI 2. Pupillary muscle rupture-> MR due to muscles not able to close valve leaflets-> increases pressure in LA which leads to increased back pressure into pulmonary circ -> Pulmonary oedema 3. VSD-> necrosis of septum leads to rupture of tissue Others: - Cardiogenic shock - LVF - Bradyarrhythmias - Tachyarrhythmias - RVF - Pericarditis - Systemic embolism -> PE - Late malignant ventricular arrhythmias - Dressler’s syndrome= immune response due to damage to heart tissue or pericardial sac - LV aneurysm
45
Why do bradyarrhythmias occur as a complication of MI?
Inferior MIs can lead to damage to nodal tissue -can lead to AV blocks of varying degrees RCA associated MIs can lead to ischaemic damage to SAN which leads to AVN becoming pacemaker which present as bradycardia
46
Why are MI patients at risk for tachyarrhythmias?
MI associated with fall in potassium, hypoxia and acidosis= all risk factors for tachyarrhythmias
47
Why is there an increased risk of systemic embolism following MI?
Mural thrombus can form which can lead to emboli forming
48
What kind of murmur can occur post-MI and what causes this form of murmur in context of an MI?
Pan-systolic murmur Mitral regurgitation -damage/dysfunction of papillary muscles leads to valve leaflets not closing properly= regurg Ventricular septal defect= due to necrosis of septal tissue leading to rupture and apparent VSD
49
What is an indication that a STEMI has completed? In what time frame does this usually occur? How is this patient then treated?
Development of Q waves >12hrs Treat as NSTEMI Possible indications for PCI or stenting if symptoms don’t improve Finish with late presenting STEMI
50
What vessel can be used as an alternative for saphenous vein in CABG? Which coronary artery is it grafted for?
Left internal mammary artery (LIMA) | Used for LAD (v rare procedure)
51
Why does a patient need to be fluid off-loaded before having a PCI?
The contrast injection can cause a fluid shift which leads to pulmonary oedema -patients need to be assessed for HF before PCI
52
Why is MI pain referred to left side?
T1-5 is associated with detecting pain from the heart The neuronal cell bodies of nerves associated with detecting pain from arm are also found at this level Therefore the CNS cannot discern if pain is coming from heart or from dermatome associated with T1-5
53
How would you differentiate between the 3 forms of ACS?
1st= Is there ST elevation: - Yes= must be STEMI - No= must be NSTEMI or unstable angina 2nd= If no ST elevation then do blood test for troponins: - Yes= must be NSTEMI rather than unstable angina -> will also see ST depression on ECG - No= Unstable angina or other cause of CP
54
Why would you need to do an echo post-MI?
- Assess to see the function of cardiac muscle-> stunned or dead tissue which might result in decreased ventricular function - Assess for cardiac tamponade which might have occured if myocardium had ruptured - Assess the state of the valves to see if MR has occured (likely due to ischaemic damage or rupture of papillary muscles)

Cardiology (15 decks)

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