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CARDIOLOGY > ANGINA AND ACUTE CORONARY SYNDROME > Flashcards

ANGINA AND ACUTE CORONARY SYNDROME Flashcards

1
Q

What is angina?

A

pain (or constricting discomfort) in the chest, neck, shoulders, jaw, or arms caused by an insufficient blood supply to the myocardium.

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2
Q

What causes angina?

A

Mostly caused by coronary artery disease

Less commonly - valvular disease, hypertrophic obstructive cardiomyopathy, hypertensive heart disease

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3
Q

What is coronary artery disease?

A

When atherosclerotic plaques form in coronary arteries which causes a progressive narrowing of the lumen

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4
Q

What is stable angina?

A

pain that occurs predictably with physical or emotional exertion and lasts no longer than 10 minutes. It should be relived within minutes of rest or with the use of medication (e.g. GTN spray).

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5
Q

How long dose angina last?

A

Stable angina lasts no more than 10 minutes (usually less than this!)

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6
Q

What is unstable angina?

A

new onset angina or abrupt deterioration in previously stable angina, often occurring at rest

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7
Q

Why is stable angina on painful on exertion?

A

On exertion, there is an increased oxygen demand within cardiomyocytes. However, the narrowing of coronary vessels means blood flow cannot be increased to meet this demand. This results in pain

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8
Q

Whats the epidemiology of angina?

A

3% of men and 1.8% of women experience angina
Incidence is rising

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9
Q

Whats the most common single cause of death in the UK?

A

Coronary heart disease (in 2019 it caused 13% of male and 8% of female deaths)

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10
Q

What are complications of angina?

A

Stroke
MI
Unstable angina
Sudden cardiac death

Others - reduced quality of life, anxiety and depression

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11
Q

Whats the prognosis of angina?

A

With appropriate lifestyle modification and medical intervention, more than half of people with angina can expect to be symptom free within 1 year. However, some people may experience recurrence or worsening of symptoms due to progression of coronary artery disease

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12
Q

How does typical angina present?

A

Presents with all 3 of the following…
Precipitated by physical exertion.
Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms.
Relieved by rest or glyceryl trinitrate (GTN) within about 5 minutes.

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13
Q

How does atypical angina present?

A

Atypical angina presents with two of the following…
Precipitated by physical exertion.
Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms.
Relieved by rest or glyceryl trinitrate (GTN) within about 5 minutes.

In addition, atypical symptoms include gastrointestinal discomfort, and/or breathlessness, and/or nausea.

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14
Q

What are the 2 types of coronary artery disease?

A

Obstructive - stenosis in >50% of the left main coronary artery or >70% stenosis of 1 or more major coronary artery
Non-obstructive - <50% of the vessel lumen blocked

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15
Q

outline the process of atherosclerosis?

A

Endothelial dysfunction - endothelial injury causes local inflammatory response. Leads to accumulation of LDL which become oxidised by local waste products creating ROS
Plaque formation - endothelial cells attract monocytes to phagocytosis the LDLs -> Foam cells and fatty streak
Plaque rupture - continued inflammation triggers smooth muscle cell migration which forms a fibrous cap. Together with the fatty streaks this develops into an atheroma. The top of the atheroma forms a hard plaque which may rupture, exposing a collagen-rich cap where platelets can aggregate on to form a thrombus. Alternatively the thrombus may break loose, embolising to infarct a distant vessel

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16
Q

What features are suggestive of non-anginal chest pain?

A

Continuous or very prolonged pain, and/or
Unrelated to activity, and/or
Bought on by breathing, and/or
Associated with dizziness, palpitations, paraesthesia

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17
Q

What features make chest pain concerning?

A

Chest pain lasts > 10 minutes
Chest pain not relieved by two doses of GTN taken 5 minutes apart
Significant worsening/deterioration in angina (e.g. increased frequency, severity or occurring at rest)

(These features may be suggestive of ACS and patients need immediate medical attention)

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18
Q

How is the severity of angina graded?

A

According to the Canadian cardiovascular society

Grade I: angina with strenuous activity
Grade II: angina with moderate activity (e.g. slight limitation if normal activities performed rapidly).
Grade III: angina with mild exertion (e.g. difficulty climbing one flight of stairs at normal pace).
Grade IV: angina at rest

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19
Q

What is a rapid access chest pain clinic?

A

In the UK, patients with new-onset exertional chest pain suspected to be angina should have access to a rapid access chest pain clinic (RACPC). These clinics provide patients with early access to specialist cardiology assessment including diagnostic testing. It aims to identify new CAD and prevent a major cardiac event by offering earlier intervention.

GPs refer people to the clinic if their symptoms may be related to their heart.

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20
Q

Where should you refer patients with suspected angina?

A

If new angina suspected then rapid access chest pain clinic
If patients with established CAD and are already known to cardiology services - cardiology clinic

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21
Q

How should you investigate a pt with suspected angina?

A

Physical examination
Resting 12-lead ECG ASAP after presentation (dont rule out stable angina on the basis of a normal ECG)
Bloods - FBC, U&Es (needed before starting drugs), LFTs (needed before starting statins), lipid profile, HbA1c, TFTs
Diagnostic testing - CT coronary angiography - gold standard!

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22
Q

What are the 4 principles for managing angina?

A

Refer to cardiology
Advise them about diagnosis, management and when to call an ambulance
Medical treatment
procedures or surgical intervention

(RAMP)

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23
Q

What ECG changes may indicate previous MI?

A

Pathological Q waves
Left bundle branch block
ST segment and T wave abnormalities

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24
Q

How should you manage a pt with suspected stable angina whilst awaiting specialist referral?

A

Provide the pt with sublingual glyceryl trinitrate to use for the relief of symptoms
Consider prescribing aspirin until the diagnosis is confirmed

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25
Q

How should you inform a pt with stable angina on managing chest pain?

A

Stop what they are doing and rest.
Use their glyceryl trinitrate spray or tablets as instructed.
Take a second dose after 5 minutes if the pain has not eased.
Call 999 for an ambulance if the pain has not eased 5 minutes after the second dose, or earlier if the pain is intensifying or the person is unwell.

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26
Q

What is the pre-test probability of CAD?

A

the probability of presence of CAD in patient. It helps guide what further testing is required, if any, to determine the presence of CAD
Pretest probability for CAD can be estimated from the patient’s age, sex, and chest pain symptoms

Pre-test probability >15%: non-invasive functional testing recommended
Pre-test probability 5-15%: consider further testing based on basic investigations and risk factors.

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27
Q

What diagnostic testing can be done to diagnose CAD?

A

CT coronary angiography
Stress echocardiography
Coronary angiography

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28
Q

When should you offer anatomical non-invasive diagnostic testing for CAD e.g. CT coronary angiography?

A

If low clinical likelihood of CAD or no history of CAD

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29
Q

When should you offer non-invasive function testing for CAD e.g. stress echocardiography??

A

If high clinical likelihood of CAD, revascularisation therapy is likely needed or if established CAD already

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30
Q

When should you offer invasive coronary angiography for CAD e.g. coronary angiography?

A

If high clinical likelihood of CAD and symptoms unresponsive to medical therapy
Typical angina at low activity level and high risk of cardiac event
LV dysfunction on ECHO suspected secondary to CAD

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31
Q

What is functional testing for CAD?

A

Functional tests are used to diagnose obstructive CAD by the detection of myocardial ischaemia when the heart is put under stress
Examples include dobutamine stress echocardiography, stress cardiac MRI, SPECT, exercise ECG

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32
Q

What does acute coronary syndrome cover?

A

STEMI
NSTEMI
Unstable angina

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33
Q

What are the 2 main issues with the atherosclerosis in walls of coronary arteries?

A
  1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
  2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.
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34
Q

How does acute coronary syndrome present?

A

Chest pain - central/left sided, may radiate to jaw or left arm, heavy or constricting
Dyspnoea
Sweating
Nausea and vomiting

Pulse, bp, temp, o2 sats are often normal/only mildly altered
Pt may appear pale and clammy

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35
Q

What are the two most important investigations when assessing a patient with chest pain?

A

ECG
Cardiac markers e.g. troponin

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36
Q

Which leads will you see ECG changes in when the left anterior descending artery is blocked?

A

V1-V4 (anterior)

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37
Q

Which leads will you see ECG changes in when the left circumflex artery is blocked?

A

I, V5-V6, aVL (lateral)

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38
Q

Which leads will you see ECG changes in when the right coronary artery is blocked?

A

II, III, aVF (inferior)

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39
Q

Whats the mnemonic for treatment of acute coronary syndrome?

A

MONA
Morphine if in severe pain (may be associated with adverse outcomes so not given routinely anymore(
Oxygen if sats <94%
Nitrates (sublingual or IV)
Aspirin 300mg

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40
Q

When should you give oxygen in ACS?

A

If sats <94%

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41
Q

How do you manage a STEMI?

A

MONA
Second antiplatelet drug - clopidogrel, praugrel or ticagrelor
Assess eligibility for coronary reperfusion therapy and if possible give PCI within 120 minutes

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42
Q

How do you manage an NSTEMI?

A

MONA
If high risk or clinically unstable then perform a coronary angiography. Lower risk pt may have a coronary angiogram at a later date

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43
Q

What is secondary prevention?

A

Patients who’ve had an ACS require lifelong drug therapy to help reduce the risk of a further event. Standard therapy comprises the following as a minimum:
aspirin
a second antiplatelet if appropriate (e.g. clopidogrel/ticagrelor)
a beta-blocker
an ACE inhibitor
a statin

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44
Q

What is the GRACE score?

A

A scoring system to estimate 6 month mortality for pt with acute coronary syndrome

It takes into account age, HR, systolic BP< creatinine, cardiac arrest at admission, ST segment deviation, abnormal cardiac enzymes, killing class

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45
Q

What are poor prognostic factors for acute coronary syndrome?

A

Older age
development/history of heart failure
peripheral vascular disease
reduced systolic blood pressure
Killip class
initial serum creatinine concentration
elevated initial cardiac markers
cardiac arrest on admission
ST segment deviation

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46
Q

What is a Killip class?

A

A system used to stratify risk post myocardial infarction

Class 1 - no clinical signs of HF - 6% 30 day mortality
Class 2 - lung crackles, S3 - 17% 30 day mortality
Class 3 - frank pulmonary oedema - 38% 30 day mortality
Class 4 - cardiogenic shock - 81% 30 day mortality

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47
Q

Which group of people should you be cautious about giving nitrates to and why?

A

Those with hypotension as it can worsen it

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48
Q

Whats the ECG criteria for a STEMI?

A

Clinical symptoms generally of 20 minutes or more, consistent with ACD with >20 minutes of ECG features in 2 or more leads of:
2.5 mm ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB

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49
Q

What are the 2 types of coronary reperfusion therapy?

A

Percutaneous coronary intervention
Fibrinolysis

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50
Q

When should you offer PCI for a STEMI?

A

If presentation is within 12 hours of onset of symptoms and if PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given. But if pt presents after 12 hours and still have evidence of ongoing ischaemia then consider PCI still

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51
Q

When should fibrinolysis be offered for a confirmed STEMI?

A

should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given

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52
Q

What further medications should be given before./during a PCI?

A

Dual antiplatelet therapy prior to PCI - if pt not taking an oral anticoagulant then give prasugrel, if they are taking an oral anticoagulant then offer clopidogrel

If undergoing PCI with radial access - give unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor

If undergoing PCI with femoral access - give bivalirudin with bailout GPI

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53
Q

Which mode of access is now preferred for PCI?

A

Radial access

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54
Q

What drugs should be given before/during fibrinolysis for STEMI?

A

Give an antithrombin at the same time
Following the procedure give ticagrelor

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55
Q

What should you do if a pt has persistent MI following fibrinolysis?

A

Consider giving PCI

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56
Q

How should you manage an NSTEMI?

A

Give 300mg aspirin
Give fondaparinux if no immediate PCI is planned
Estimate 6 month mortality i.e. GRACE score

If low risk then conservative management with ticagrelor
If high risk then offer PCU immediately if unstable, otherwise within 72 hours. Give prasugrel or ticagrelor, give unfractionated heparin

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57
Q

What stents are best for PCI?

A

Drug-eluting stents (coated with a slow release medication to help prevent thrombosis)

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58
Q

What should be given for thrombolysis of an MI?

A

Tissue plasminogen activator
Tenecteplase or alteplase

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59
Q

How should you monitor a pt after thrombolysis?

A

ECG after 90 minutes to check there is a >50% resolution in ST elevation
If not then PCI is needed!

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60
Q

What is secondary prevention?

A

Stop smoking and avoid passive smoking
Cardio protective diet
Physical activity and avoid sedentary behaviour
Weight loss if overweight
Minimal alcohol consumption
Cardiac rehabilitation programme participation (normally initiated in hospital before discharge)
Continue precibing meds

Meds - dual antiplatelet, ACEi, beta blocker, statin

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61
Q

Outline the rules of driving after an MI?

A

For a car or motorcycle licence holder, following an MI the person does not need to inform the DVLA. However, driving should stop for a time (the length depends on factors such as type of MI and treatments). The person should check with their insurer that they are still covered for driving.
For a bus, coach or lorry licence holder, following an MI the person must stop driving for a set period and inform the DVLA using form VOCH1. Advise people that they can be fined if they continue to drive and do not inform the DVLA, and be prosecuted if involved in an accident.

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62
Q

When can resumption of sexual activity occur after an MI?

A

Sexual activity can be resumed when comfortable to do so, usually about four weeks after an MI.
Sexual activity presents no greater risk of triggering a subsequent MI in a person than if they had never had an M

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63
Q

How should you manage pt who have had an acute MI and who have symptoms/signs of HF and left ventricular systolic dysfunction?

A

With an aldosterone antagonist e.g. eplerenone
(Preferably give after ACEi therapy)

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64
Q

Outline ECG changes seen in an acute MI?

A

hyperacute T waves are often the first sign of MI but often only persists for a few minutes
ST elevation may then develop
the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
pathological Q waves develop after several hours to days. This change usually persists indefinitely

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65
Q

Which MI causes ST depression on a 12-lead ECG?

A

A posterior MI

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66
Q

What are the complications of an MI?

A

Cardiac arrest
Cardiogenic shock
Chronic HF
Tachyarrhythmias
Bradyarrhythmias
Pericarditis
Left ventricular aneurysm
Left ventricular free wall rupture
Ventricular septal defect
Acute mitral regurgitation

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67
Q

Whats the most common cause of death following an MI?

A

Cardiac arrest

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68
Q

Why do MI patients commonly go into cardiac arrest?

A

This most commonly occurs due to patients developing ventricular fibrillation

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69
Q

Why may MI patients develop cardiogenic shock?

A

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock

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70
Q

What arrhythmias are most likely following an MI?

A

Ventricualr tachyarrythmias e.g. Ventricular fibrillation and ventricular tachycardia
Bradyarrhythmias - atrioventricular block is more common following inferior MI

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71
Q

What proportion of patients will get pericarditis following a transmural MI?

A

10% of pt

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72
Q

When is pericarditis most common following an MI?

A

In the first 48 hours

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73
Q

What is Dressler syndrome?

A

Postmyocardial infarction syndrome - a form of secondary pericarditis

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74
Q

When does dressler syndrome typically occur following an MI?

A

2-6 weeks after

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75
Q

Whats the pathophysiology of dressler syndrome?

A

thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers.

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76
Q

How is dressler syndrome characterised?

A

Low grade fever, pleuritic pain, pericardial effusion and a raised ESR
Pericardial rub on auscultation

Rarely it can cause pericardial tamponade

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77
Q

How do you treat dressler syndrome?

A

NSAIDs
In more severe cases steroids may be needed and they may need pericardiocentesis to remove fluid from around the heart

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78
Q

Why does left ventricular aneurysm occur following an MI?

A

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

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79
Q

What features are associated with left ventricular aneurysm?

A

persistent ST elevation and left ventricular failure

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80
Q

Why are pt with left ventricular aneurysm anticoagulated?

A

Thrombus may form within the aneurysm increasing the risk of stroke

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81
Q

Following an MI, when is left ventricular free wall rupture most likely to occur?

A

1-2 weeks after MI

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82
Q

What proportion of pt will get left ventricular free wall rupture following an MI?

A

3% of pt

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83
Q

How do pt present with left ventricular free wall rupture?

A

Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)

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84
Q

How is left ventricular free wall rupture managed?

A

Urgent pericardiocentesis and thoracotomy are required.

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85
Q

Following an MI, when is ventricular septal defect most likely to occur?

A

In the first week following an MI

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86
Q

How common is ventricular septal defect following an MI?

A

Seen in 1-2% of pt

87
Q

What are the features of ventricular septal defect?

A

acute heart failure associated with a pan-systolic murmur

88
Q

How do you diagnose a ventricular septal defect?

A

Using an echocardiogram

89
Q

How do you manage a ventricualr septal defect?

A

Urgent surgery

90
Q

Which type of MI is acute mitral regurgitation most common with?

A

Infero-posterior infarction

91
Q

What causes acute mitral regurgitation following an MI?

A

Ischaemia or rupture of papillary muscle

92
Q

How does acute mitral regurgitation present?

A

Patients usually present with severe decompensated heart failure
dyspnea as pulmonary oedema can occur
Acute hypotension
Early-to-mid systolic murmur
symptoms of shock, including weakness, dizziness, and altered mental status

93
Q

How is acute mitral regurgitation managed?

A

Patients are treated with vasodilator therapy but often require emergency surgical repair

94
Q

How is immediate symptomatic relief achieved with angina?

A

GTN spray
(Take it then repeat after 5 minutes, if there is still pain 5 minutes after the repeat dose call an ambulance)

95
Q

How do you achieve long term symptomatic relief for stable angina?

A

Either a beta blocker or calcium channel blocker

96
Q

Whats the moa of beta blockers for managing angina?

A

They act on beta 1 adrenergic receptors on the heart which decreases sympathetic drive of the heart and slows the heart rate. This reduces the oxygen demand of the heart
They also improve mortality in patients with an MI

97
Q

Whats the moa of calcium channel blockers for managing angina?

A

Drug blocks calcium ion channels which reduces the amount of calcium entering cells of the heart = reduces HR and cardiac contractility

98
Q

What is PCI?

A

putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent.

99
Q

What is a CABG?

A

Coronary Artery Bypass Graft surgery
This involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis.

100
Q

What are major side efefcts of GTN?

A

Headache
Dizziness due to hypotension
Tachycardia

101
Q

Which calcium channel blockers should not be used alongside beta blockers and why?

A

Non-dihydropyridine calcium channel blockers, such as verapamil or diltiazem, are contraindicated with beta-blockers due to the risk of atrioventricular block (i.e. heart block)

102
Q

What is triple vessel disease?

A

stenosis of ≥ 50% in all three main epicardial coronary arteries

103
Q

What does the right coronary artery supply?

A

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

104
Q

What does the circumflex artery supply?

A

Left atrium
Posterior aspect of left ventricle

105
Q

What does the left anterior descending artery supply?

A

Anterior aspect of left ventricle
Anterior aspect of septum

106
Q

How is acute coronary syndrome diagnosed?

A

If there is ST elevation or new left bundle branch block the diagnosis is STEMI.

If there is no ST elevation then perform troponin blood tests:
If there are raised troponin levels and other ECG changes the diagnosis is NSTEMI
If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain

107
Q

What is a silent MI?

A

An MI without the chest discomfort or other symptoms

108
Q

Who is a silent MI most common in?

A

Diabetics
Due to hyperglycaemia damage autonomic nerve - reduced pain sensation

109
Q

What ECG changes are diagnostic for NSTEMI?

A

ST segment depression in a region
Deep T Wave Inversion
Pathological Q Waves (suggesting a deep infarct – a late sign)

110
Q

What can cause raised troponin?

A

Troponin - “troops’
A CAMP

ACS
CKD
Aortic dissection
Myocarditis
PE
Sepsis

111
Q

When should you do serial troponin for ACS?

A

At baseline and 12 hours after onset of symptoms

112
Q

How can you remember the complications of an MI?

A

DREAD

Death
Rupture of heart septum or papillary muscles
Enema - HF
Arrhythmia and aneurysm
Dressers syndrome

113
Q

What is a type 1 MI?

A

Traditional MI due to an acute coronary event e.g. plaque rupture or dissection

114
Q

What is a type 2 MI?

A

Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

115
Q

What is a type 3 MI?

A

Sudden unexpected cardiac death or cardiac arrest suggestive of an ischaemic event

116
Q

What is a type 4 MI?

A

MI associated with PCI / coronary stent

(Type 5 is when its associated with cardiac surgery e.g. CABG)

117
Q

Whats the definition of an MI?

A

Death of myocardial tissue secondary to prolonged and severe ischaemia.

For diagnosis it requires the detection of troponin rise and at least one of the following - symptoms of ischaemia, new ST-segment-T wave changes or new LBBB, development of pathological Q waves, imaging evidence of new loss of vbiarbla myocardium, identification of an intracoroary thrombus by angiography

118
Q

Whats the difference between myocardial infarction and myocardial injury?

A

Myocardial infarction: myocardial necrosis, seen as a rise in troponin, with evidence of acute myocardial ischaemia
Myocardial injury: myocardial necrosis, seen as a rise in troponin, without evidence of acute myocardial ischaemia

119
Q

What are examples of myocardial injury?

A

Myocarditis
Damage following cardioversion/ablation
Cytokine-mediated injury

120
Q

What can cause ST elevation?

A

Acute MI
Pericarditis/myocarditis
Normal variant
Takotsubo cardiomyopathy
Prinzmetal angina
Subarachnoid haemorrhage
Coronary Vasospasm
Ventricular aneurysm

121
Q

What can cause ST depression?

A

Acute MI
Reciprocal changes to ST elevation
Electrolyte disturbances
Digoxin effect
Bundle branch blocks

122
Q

What is fixed vs dynamic T wave inversion?

A

T wave inversion may be fixed, which is usually associated with a previous ischaemic event and associates with Q waves. Alternatively, T wave inversion may be dynamic, which is associated with acute myocardial ischaemia.

123
Q

What does it mean by ‘during a STEMI there are usually reciprocal changes on the ECG’?

A

This refers to ST depression in the leads opposite those with ST elevation.

Anterolateral STEMI: inferior ST depression (II, III, aVF)
Lateral STEMI: inferior ST depression (II, III, aVF)
Inferior STEMI: lateral ST depression (aVL, I)
Posterior STEMI: anterior ST depression (V1-V3)

124
Q

Outline the ECG changes during the natural evolution of a STEMI?

A

Minutes to hours: hyperacute T-waves
0-12 hours: ST-elevation
1-12 hours: Q-wave development
Days: T-wave inversion
Weeks: T-wave normalisation and persistent Q-waves

125
Q

What are the 3 types of cardiac enzymes that are used to assess myocardial necrosis?

A

Troponins (T or I)
Creatine kinase (CK, specifically CK-MB)
Myoglobin

126
Q

Whats the negative predictive value for exclusion of acute MI with troponin?

A

> 95% which increases to almost 100% with a second troponin at 3 hours

127
Q

When can trop be measured for an MI?

A

Within 4 hours of patient presentation

128
Q

What can cause troponin elevation?

A

Tachyarrythmias
Heart failure
Hypertensive emergencies
Critical illness (e.g. sepsis, burns)
Myocarditis
Cardiomyopathy (e.g. Takotsubo)
Structural heart disease (e.g. aortic stenosis)
Pulmonary embolism
Renal dysfunction
Coronary spasm
Acute neurological event

129
Q

What are chest pain differential diagnoses?

A

Angina
ACS
Aortic dissection
Pericarditis
PE
Pneumothorax
Pneumonia
Oesophagitis
Oesophageal spasm
PUD
Costochondritis
Rib fracture
Herpes zoster
Depression/anxiety

130
Q

How do you manage a pt with NSTEMI or unstable angina?

A

Aspirin
Initial antithrombin therapy - fondaparinux

Use GRACE to predict 6 month mortality and risk of CV events:
Low risk - conservative management, ticagrelor with aspirin and consider angiography
High risk - immediate angiography and PCI, aspirin and ticagrelor, unfractionated heparin if having PCI

131
Q

What is coronary micro vascular disease?

A

Aka cardiac syndrome X
It’s present in 30% of patients with angina and is associated with increased morbidity and mortality
Affects the tiny arteries in the heart muscle
More common in women, particularly around the time of menopause

132
Q

What are pericardial arteries?

A

Coronary arteries

133
Q

What determines the coronary dominance?

A

The artery that supplies the posterior third of the interventricular septum – the posterior descending artery

If the posterior descending artery is supplied by the RCA, then the coronary circulation can be classified as “right-dominant.”
If the posterior descending artery is supplied by the CX, a branch of the left artery, then the coronary circulation can be classified as “left-dominant.”
If the posterior descending artery is supplied by both the RCA and the CX, then the coronary circulation can be classified as “co-dominant.”

134
Q

What proportion of the general population are right coornary dominant?

A

70%
20% codominant and 10% left dominant

135
Q

Whats the transfusion threshold for patients with ACS?

A

80g/L
(Anaemia can worsen ischaemia so important to provide immediate relief)

136
Q

What are common ECG changes on posterior MI?

A

Horizontal ST depression in V1-V3 (seeing it backwards!)
Tall, broad R waves (>30ms) in V2-3
Upright T waves
Dominant R wave (R/S ratio > 1) in V2
ST elevation ib leads V7-V9

137
Q

What calcium channel blockers should be used for managing angina?

A

if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used
if used in combination with a beta-blocker then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine) - non-dihydropyridines are contraindicated

138
Q

If there is poor response to initial treatment of angina with beta blockers and calcium Channel blockers what should you do?

A

Increase meds to max tolerated dose
if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa
if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil, ranolazine
if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG

139
Q

How can you advise a pt to minimise the development of nitrate tolerance?

A

NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate

involves taking the morning dose as normal, then taking the second dose in the early afternoon. This allows a sufficiently long nitrate-free period and helps reduce tolerance

140
Q

What are examples of non-dihydropyridine CCB?

A

Verapamil and diltiazem

141
Q

What are examples of dihydropyridine CCB?

A

amlodipine, felodipine, isradipine, nicardipine, nifedipine, and nisoldipine

142
Q

non-dihydropyridine vs dihydropyridine CCB?

A

The dihydropyridines are more vascular selective and the non-dihydropyridines are more myocardial selective and tend to reduce the heart rate

143
Q

What is Prinzmetal angina?

A

Aka vasospastic angina

It develops when a coronary artery supplying blood and oxygen to your heart goes into spasm and suddenly narrows. People experiencing vasospastic angina do not typically have episodes of angina during exercise.

chest discomfort or pain at rest with transient electrocardiographic changes in the ST segment, and with a prompt response to nitrates.

144
Q

How can you distinguish between unstable angina and NSTEMI?

A

to perform serial high-sensitivity troponin tests and to observe for any rise or fall in troponin level. Elevation in troponin level points towards an NSTEMI as this confirms the diagnosis of an infarction

145
Q

Whats the difference between STEMI and NSTEMI?

A

STEMI results from complete and prolonged occlusion of an epicardial coronary blood vessel
NSTEMI usually results from severe coronary artery narrowing, transient occlusion, or microembolization of thrombus and/or atheromatous material.

146
Q

What are some performance indicators for MI?

A

‘Call-to-needle’ - the interval between the call for professional help and the initiation of thrombolytic therapy (aim is <60 minutes)
‘Door-to-needle’ - the interval between arrival at hopsital and the initiation of thrombolytic therapy (should be <20 minutes)

147
Q

How can call-to-needle time be improved?

A

Pre-hopsital thrombolysis

148
Q

What is the cardiac rehabilitation programme?

A

An individualised programme consisting of exercise sessions, information and education sessions, emotional support and wellbeing, optimisation of pharmacotherapy, psychological training and rehabilitation, evaluation and reduction of coronary disease risk factors, lifestyle modification, patient education
It gives you and you family information, support and advice, reduces your risk of having another heart event or being readmitted to hopsital, gives you a chance to meet other people going through similar experiences to you. Helps understand your condition, recover from surgery/procedure, makes lifestyle changes to improve heart health, reduces the risk of further heart problems, psychological aspects of living with a heart condition

Mostly runs 2 sessions a week, 2 hours for 10-12 weeks
May take place in a hopsital or community setting

149
Q

When should you offer cardiac rehabilitation programme

A

immediately after acute phase of MI

150
Q

Which type of MI has the least favourable prognosis?

A

Anterior

151
Q

Whats the prognosis for an MI?

A

30 day mortality 13% for STEMI in 2003 and 8% in 2011. Today at least 7/10 survive (British heart foundation)

152
Q

Outline the timeline of complications for MI?

A

Hours - potentially life threatening ventricular arrhythmias
24 hours - Bradyarrhythmias and cardiogenic shock
Days - mitral regurgitation, papillary muscle rupture, ventricular septal rupture, rupture of left ventricualr free wall
>2 weeks - dressler syndrome
Any time - life threatening arrhythmias, AF, acute heart failure

153
Q

What causes Bradyarrhythmias following an MI?

A

sinus node dysfunction, high degree AV block or bundle branch blocks

154
Q

What causes mitral regurgitation following an MI?

A

Ischaemic papillary muscles

155
Q

What causes papillary muscle rupture following an MI?

A

Necrosis

156
Q

Which MIs are most likely to result in ventricular septal rupture?

A

Transmural MI anterior infarctions

157
Q

Why causes life threatening arrhythmias following an MI?

A

Remodelling of the myocardium

158
Q

What causes acute heart failure following an MI?

A

It can occur within hours due to ‘stunning’ of the myocardium, an arrhythmia or by an extensive volume of infarction.
It can happen in the days following MI due to rupture of papillary muscle + valvular incompetence, or by ventricular rupture causing ventricular septal defect.
It can also occur anytime later due to acute decompensation of chronic HF and in those with left ventricular systolic dysfunction

159
Q

What is myocardial stunning?

A

Aka transient post-ischemic myocardial dysfunction
A state of mechanical cardiac dysfunction that can occur in a portion of myocardium without necrosis after a brief interruption in perfusion, despite the timely restoration of normal coronary blood flow.

160
Q

Outline the aetiology of an MI?

A

Occlusion of a coronary artery which can be caused by atheromatous plaque rupture with subsequent thrombi expansion, vasospasm, and emboli (secondary to AF, vegetations, prosthetics or paroxysmal emboli)

161
Q

Whats the pathophysiology of an MI?

A

Occlusion of a coronary artery which disrupts the blood supply to a region in the myocardium -> ischaemia -> myocytes become rapidly dysfunctional -> when ischaemia persists this can cause myocyte death

162
Q

How long does ischaemia have to occur for damage to myocytes to become irreversible?

A

30 minutes

163
Q

What are infarction patterns?

A

Subendocardial
Transmural

164
Q

What is subendocardial infarction?

A

Myocyte necrosis involving the subendocardium(inner cardiac wall)
NSTEMI

165
Q

What is transmural infarction?

A

My coyote necrosis involving the entire wall thickness
STEMI

166
Q

For each of the following describe which ECG leads you will see changes in and which artery is involved…
1. Inferior
2. Lateral
3. Anterior
5. Posterior

A
  1. II, III, aVF - RCA
  2. I, aVL, V5, V6 - LCx
  3. V3, V4 - LAD
  4. Tall R waves V2-3 and ST depression in V1-V4 - LCX and RCA
167
Q

What are the gross features and light microscopy features of the heart 0-30 minutes after an MI?

A

None
None

168
Q

What are the gross features and light microscopy features of the heart 30 mins-4 hours after an MI?

A

None
On LM you may see wavy fibres at the border

169
Q

What are wavy myocardial fibres?

A

Waving of the fibres caused by increased hydrostatic pressure of interstitial oedema which squeezes and stretched neighbouring fibres
Associated with focal oedema and is a characteristic sign of acute MI

170
Q

What are the gross features and light microscopy features of the heart 4-12 hours after an MI?

A

Occasional dark mottling
LM - early coagulative necrosis, oedema, haemorrhage

171
Q

What are the gross features and light microscopy features of the heart 12-24 hours after an MI?

A

Dark mottling
LM - continued coagulative necrosis, pyknotic nuclei, contraction band necrosis at margins and neutrophil influx

172
Q

What are the gross features and light microscopy features of the heart 1-3 days after an MI?

A

Mottling with the yellow-tan centre of infarct
LM - coagulative necrosis with absent nuclei and striations, interstitial neutrophilic infiltrate

173
Q

What are the gross features and light microscopy features of the heart 3-7 days after an MI?

A

Central yellow-tan softening with hyperemia at borders
LM - myofibres begin to disintegrate, dying neutrophils, macrophages

174
Q

What are the gross features and light microscopy features of the heart 7-10 days after an MI?

A

Maximally yellow-tan and soft depressed red-tan margins
LM - phagocytes and marginal granulation tissue

175
Q

What are the gross features and light microscopy features of the heart 10-14 days after an MI?

A

Red-grey depressed infarct borders
LM - well formed granulation tissue with neovasculiarsation and collagen deposit

176
Q

What are the gross features and light microscopy features of the heart 2-8 weeks after an MI?

A

Grey-white scar, progressive from the border towards the centre of the infarct
LM - increased collagen deposition

177
Q

What are the gross features and light microscopy features of the heart >2 months after an MI?

A

Scarring complete
LM - dense collagenous scar

178
Q

When does troponin T start to rise? How long does it stay elevates for?

A

3-4 hours after injury
Can stay elevated for up to 2 weeks

179
Q

Why is CK-MB not a specific marker for MI?

A

As skeletal muscle can also release it

180
Q

Whats the best marker for re-infarction?

A

CK-MB due to its early clearance (rises 3-6 hours and returns to normal by 24-36 hours)

181
Q

What is CK-MB?

A

Creating kinase myocardial band (one of the 3 isoenzymes of CK that’s primarily found in heart muscle)

182
Q

What are contraindications of beta blockers?

A

Asthma
Carcinogenic shock
Hypotension
Bradycardia
Phaeochromocytoma
Prinzmetals anina
Second and third degree AV block
Severe PAD
Sick sinus syndrome
Uncontrolled HF

183
Q

Whats the moa of nitrates in angina?

A

Either converted to NO or directly releases NO -> NO activates granulate cyclase which converts GTP to cGMP in vascular smooth muscle. CGMP is an endogenous vasodilator of vascular smooth muscle = promotes relaxation and increased blood flow in veins, arteries and cardiac tissue (mainly in veins!)
It increases blood flow to the myocardium and reduces cardiac preload and afterload, decreasing myocardial wall stress and ameliorating anginal symptoms

184
Q

What are contraindications of nitrates?

A

Aortic stenosis/mitral stenosis
Cardiac tamponade
Constrictive pericarditis
Hypertrophic cardiomyopathy
Hypotension
Hypovolaemia
Marked anaemia
Raised intracranial pressure
Toxic pulmonary oedema

185
Q

Why do nitrates cause headaches?

A

Due to vasodilation of cerebral arteries

186
Q

When are CCB indicated for angina and why?

A

When pt is unresponsive or has contraindications to beta blockers or nitrates
This is because CCB dont provide a mortality benefit

187
Q

Whats the moa of aspirin?

A

Inhibitor of thromboxane A2 synthesis which is a prominent promote of platelet activation

188
Q

What are example of P2Y12 receptor inhibitors and how do they work?

A

Clopidogrel and ticagrelor
Prevents ADP from binding to P2Y12 receptor which usually further activates platelets

189
Q

Whats the moa of heparin?

A

Binds to anti-thrombin to inhibit its effects
Also binds to factor Xa

190
Q

Whats the moa of fibrinolytics?

A

activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin.

191
Q

Why do ACEi provide a mortality benefit?

A

As they prevent ventricular cardiac remodelling and they reduce the rate of HF

192
Q

What are the types of nitrates for angina?

A

Glyceryl trinitrate - short acting, sublingual
Isosorbide mononitrate - long acting
Isosorbide dinitrate - long acting

193
Q

When should you use short and long-acting nitrates?

A

Short-acting, sublingual glyceryl trinitrate (GTN) should be offered for immediate relief of an episode of angina, or before activities that are likely to precipitate angina.
Long-acting oral nitrates should be used regularly to decrease the frequency and severity of anginal symptoms

194
Q

What are indications for nitrates?

A

Angina/MI
HF
Hypertension
Anal fissure

195
Q

What are SE of nitrates?

A

Headaches
Cutaneous flushing
Dizziness
Tachycardia
Tolerance

Due to vasodilation

196
Q

What are contraindications of nitrates?

A

Hypotension
Hypovolaemia
Severe anaemia
Cardiomyopathy
Anyone on other vasodilators e.g. ED meds/PDE5 inhibitors or alcohol. Anyone taking arginine supplementation

197
Q

Why is arginine supplementation a contraindication for nitrates?

A

As arginine is a biological precursor of nitric oxide so taking both can augment nitrates effects and potentially cause excessive venodilation with hypotension

198
Q

Who is Prinzmetal’s angina most common in?

A

Japanese people
higher in people aged 40-70 years and tends to decrease after the age of 70 years.

199
Q

How do you treat vasospastic angina?

A

Managing lifestyle factors is important in prevention. Smoking, alcohol, and high levels of anxiety have a significant role in coronary spasm.
Calcium channel blockers
Nitrates

200
Q

Why should you avoid beta blockers in vasospastic angina?

A

It can aggravate coronary artery spasm

201
Q

How does vasospastic angina present?

A

Variable from brief unnoticed episodes to severe prolonged angina. Rapid response to nitrates
This variant occurs at rest, usually lasting for between 5 and 30 minutes. Most episodes occur between midnight and early morning.
Lower exercise tolerance in the morning

202
Q

What can precipitate vasospastic angina?

A

Physical or mental stress.
Magnesium deficiency.
Alcohol consumption.
Hyperventilation.
The Valsalva manoeuvre.
Pharmacological agents such as cocaine.
Sympathomimetic agents - eg, adrenaline (epinephrine), noradrenaline (norepinephrine).
Beta-blockers.
Parasympathomimetic agents - eg, methacholine, pilocarpine.
Ergot alkaloids - eg, ergotamine.

203
Q

How is vasospastic angina diagnosed?

A

FBC, renal function, electrolytes, fasting blood glucose and lipid levels.
Cardiac enzymes and troponins to assess for acute coronary syndrome
ECG: transient ST-segment elevation corresponding to the distribution of the affected coronary artery during attacks is characteristic
Ambulatory ECG monitoring may be required because episodes of coronary artery vasospasm are often brief and ECG findings are often normal between attacks.
Coronary angiography is the gold standard for the diagnosis of variant angina

204
Q

What should you use to diagnose ACS if the pt has a contraindication to contrast?

A

Myocardial perfusion scan - use a small amount of radioactive substance to create images which show blood flow to the heart muscle

205
Q

What are examination findings in patients with ventricular septal defect post-MI?

A

Harsh, loud pansystolic murmur along the left sternal border
Palpable parasternal thrill
Low output cardiac failure features

206
Q

What is a widowmaker heart attack?

A

An MI where there is an 100% blockage in the proximal LAD

207
Q

What is crescendo angina?

A

Unstable angina just a different name

208
Q

Why are inferior MIs most likely to cause arrhythmias?

A

Inferior myocardial infarctions are typically due to occlusion of the right coronary artery. The right coronary artery supplies the AV node so a right coronary infarct can cause arrhythmias including sinus bradycardia and atrioventricular block.
(Although rbbb is more likely to be caused by an occlusion of the left anterior descending artery)

209
Q

What is nocturnal angina?

A

angina that occurs at night, during sleep.

Symptoms are commonest in the early hours of the morning when coronary artery tone is maximal i.e. coronary artery myocardium is in its most contracted state due to the body’s natural circadian rhythm - HR low, BP low, increase in parasympathetic nervous system activity = muscles in walls of cornary arteries contact resulting in a reduction in blood flow to the heart muscle

The patient often has critical coronary artery disease -

210
Q

Whats the main problem of PCI?

A

Restenosis of the artery

211
Q

CABG vs PCI?

A

For pt who both techniques are appropriate choose PCI even though chances of restensois are better. This is because the procedure is less invasive, lower chance of death during operation and much faster/easier recovery

212
Q

Which coronary aretry supplies the posterior wall of the heart?

A

Posterior descending artery

213
Q

What can be used instead of a beta blocker in managing symptomatic stable angina?

A

Long acting nutrarte
Ivabradine
Nicorandil
Ranolazine

CARDIOLOGY (19 decks)

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