Angina Flashcards

1
Q

What causes angina

A

Narrowing of the coronary arteries reduces blood flow to the myocardium

During times of high demand such as exercise, there is insufficient supply of blood to meet demand

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2
Q

What is stable angina

A

Angina is stable when symptoms are always relieved by rest or GTN

Unstable when symptoms come on randomly whilst at rest considered ACS

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3
Q

IX for stable angina

A

CT coronary angiography - involves injecting contrast and taking CT images timed with the heart beat to highlight any narrowing

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4
Q

General management of stable angina(RAMP)

A

Refer to cardio(urgently if unstable)

Advise about diagnosis, management and when to call ambulance

Medical treatment

Procedural or surgical interventions

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5
Q

Immediate symptomatic relief of stable angina

A

GTN spray –> vasodilation

Take GTN, then repeat after 5 mins. If there is still pain 5 mins after the repeat dose –> ambulance

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6
Q

Long term symptomatic relief of stable angina

A

Beta blocker(bisoprolol 5mg OD)

Ca2+ blocker(amlodipine 5mg OD)

Other options not first line:

Long acting nitrates(isosorbide mononitrate)
Ivabradine
Nicorandil
Ranolazine

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7
Q

Secondary prevention of stable angina

A

Aspirin(75mg OD)
Atorvastatin 80mg OD
ACE inhibitor

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8
Q

Surgical interventions for angina

A

PCI with coronary angioplasty(dilating the blood vessel with a balloon and/or inserting a stent)

CABG(severe stenosis)

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9
Q

What does PCI involve

A

Involves catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast

Any areas of stenosis are highlighted on xray images which can be treated with balloon dilatation followed by insertion of a stent

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10
Q

What does coronary artery bypass graft(CABG) involve

A

Opening the chest along the sternum(midline sternotomy scar)

Taking a graft vein from the patient’s leg(usually great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis

Recovery is slower and complication rate is higher than PCI

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11
Q

What is ACS usually due to

A

Thrombus from an atherosclerotic plaque blocking a coronary artery

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12
Q

What are the three types of ACS

A

Unstable angina
STEMI
NSTEMI

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13
Q

What does the left coronary artery become

A

Circumflex and LAD

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14
Q

What does the right coronary artery supply

A

Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area

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15
Q

What does circumflex artery supply

A

Left atrium

Posterior aspect of left ventricle

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16
Q

What does LAD supply

A

Anterior aspect of left ventricle

Anterior aspect of septum

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17
Q

Diagnosis of ACS

A

ECG

  • ST elevation or new left bundle branch block –> STEMI
  • Raised troponin + other ECG changes(ST depression, T wave inversion, pathological Q waves)–> NSTEMI
  • Normal tropi levels and no ECG changes –> unstable angina or MSK pain
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18
Q

Symptoms of ACS

A
Nausea and vomiting 
Sweating and clamminess 
Feeling of impending doom 
SOB 
Palpitations 
Pain radiating to jaw or arms
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19
Q

What does silent MI refer to

A

Diabetic patients may not experience typical chest pain during ACS

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20
Q

What do pathological Q waves indicate

A

Suggest a deep infarct - a late sign –> NSTEMI

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21
Q

Heart area and ECG leads - left coronary artery

A

Anterolateral

I, aVL, v3-6

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22
Q

Heart area and ECG leads - LAD

A

Anterior

V1-4

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23
Q

Heart area and ECG leads - circumflex

A

Lateral

I, aVL, V5-6

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24
Q

Heart area and ECG leads - Right coronary artery

A

Inferior

II, III, aVF

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25
Q

What are troponins

A

proteins in cardiac muscle
Diagnosis of ACS usually requires serial troponins
Rise in troponin is consistent with myocardial ischaemia as proteins are released from ischaemic muscle

26
Q

Alternative causes of raised tropi

A
Chronic renal failure 
Sepsis 
Myocarditis 
Aortic dissection 
PE
27
Q

Acute STEMI treatment

A
Primary PCI(if available within 2 hrs) 
Thrombolysis(if PCI not available within 2 hrs)
28
Q

What does thromobolysis involve

A

Injecting a fibrinolytic medication(alteplase) to dissolve clots

Significant risk of bleeding

29
Q

Acute NSTEMI treatment BATMAN

A
Beta blockers 
Aspirin 300mg 
Ticagrelor 
Morphine 
Anticoagulant(fondaparinux) 
Nitrates 

Oxygen only if stats below 95%

30
Q

Scoring system to assess for PCI in NSTEMI

A

GRACE score - gives 6 month risk of death or repeat MI after nstemi

If medium or high risk, they are considered for early PCI

31
Q

Complications of MI (DREAD)

A
Death 
Rupture of heart septum or papillary muscles 
Edema(heart failure) 
Arrhythmia and Aneurysm
Dressler's syndrome
32
Q

What is dressler’s syndrome

A

Post-MI syndrome

Occurs around 2-3 weeks after an MI

33
Q

What causes dressler’s syndrome post-MI

A

localised immune response which causes pericarditis

34
Q

How does dressler’s syndrome present

A

Pleuritic chest pain
Low grade fever
Pericardial rub and auscultation

35
Q

Diagnosis of dressler’s syndrome

A

ECG(global ST elevation and T wave inversion)
Echocardiogram
Raised inflammatory markers(CRP and ESR)

36
Q

Management of dressler’s syndrome

A

NSAIDs(Aspirin/ibuprofen)
Steroids(predisolone) in more severe cases
Paricardiocentesis

37
Q

Secondary prevention medical management of ACS - 6 A’s

A

Aspirin 75mg OD
Atiplatelet(clopidogrel or ticagrelor for up to 12 months)
Atorvastatin 80 mg OD
ACE inhibitors(ramipril)
Atenolol
Aldosterone antagonist for those with clinical heart failure(eplerenone)

38
Q

Secondary prevention lifestyle measures - ACS

A
Smoking cessation 
Reduce alcohol consumption 
Mediterranean diet 
Cardiac rehab 
Optimise management of other co-morbidities(Diabetes and hypertension)
39
Q

Triggers of acute left ventricular failure

A

Iatrogenic(agressive IV fluids in frail elderly patient)
Sepsis
MI
Arrhythmias

40
Q

Presentation of acute LVF

A

Rapid onset SOB
Exacerbated by lying flat and improves on sitting up
Type 1 resp failure
Cough(frothy white/pink sputum)

41
Q

Examination findings in acute LVF

A
Increased resp rate 
Reduced O2 sats 
Tachycardia 
3rd heart sound 
Bilateral basal crackles 
Hypotension in severe cases
42
Q

What is BNP

A

Is a hormone that is released from the heart ventricles when myocardium is stretched beyond normal range

43
Q

What is the action of BNP

A

To relax the smooth muscle in blood vessels to reduce systemic vascular resistance making it easier for heart to pump blood through the system

BNP also acts on kidneys as a diuretic

44
Q

Other causes of raised BNP besides heart failure

A
Tachycardia 
Sepsis 
PE 
Renal impairment 
COPD
45
Q

What is the main measure of left ventricular function

A

Ejection fraction(percentage of blood in the left ventricle that is pumped out with each ventricular contraction)

Fraction above 50% is considered normal

46
Q

CXR findings in LVF

A
Cardiomegaly(defined as cardiothoracic ratio?0.5) 
Upper lobe diversion 
Bilateral pleural effusions 
Fluid in interlobar fissures 
Fluid in septal lines(kerley lines)
47
Q

Management of acute LVF(Pour SOD)

A

Pour away(stop) IV fluids
Sit up
Oxygen(if < 95%)
Diuretics

48
Q

Other management options in severe acute pulmonary oedema or cardiogenic shock

A

IV opiates(act as vasodilators)
Non-invasive ventilation(NIV)
Continuous positive airway pressure(CPAP)
Inotropes(noradrenalin)

49
Q

Which type of MIs are more likely to result in AV block

A

Inferior MI

50
Q

What can cause a left ventricular aneurysm following an MI

A

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation.

51
Q

What is a left ventricular aneurysm typically associated with

A

Persistent ST elevation and left ventricular failure

Thrombus may form within aneurysm requiring anticoagulation

52
Q

How might patients with left ventricular free wall rupture present

A

Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

53
Q

Which type of MIs more commonly cause acute mitral regurgitation

A

More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle.

54
Q

Features of acute mitral regurgitation following an MI

A

Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.

55
Q

Criteria for stable angina

A

chest pain is described as sharp (rather than constricting)
chest pain may be precipitated by physical exertion
chest pain is relieved by GTN spray within 5 minutes

56
Q

When should oxygen be given for ACS

A

do not routinely give oxygen, only give if sats < 94%

57
Q

Immediate management of suspected ACS

A

GTN
Aspirin 300mg
Oxygen if required
ECG asap

58
Q

Definition of atypical angina

A

NICE define anginal pain as the following:

  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in about 5 minutes

patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina

59
Q

1st line ix for patients in whom stable angina cannot be excluded by clinical assessment alone

A

CT coronary angiography

60
Q

Which features make atypical ACS presentation more likely

A

Being elderly, diabetic or female