Cardiology - Acute Coronary Syndromes Flashcards

1
Q

What is atherosclerosis?

A

A combination of atheroma formation (fatty deposits in the artery walls) and sclerosis (stiffening of the blood vessel walls).

Atherosclerosis affects the medium and large arteries, caused by chronic inflammation and activation of the immune system to cause the deposition of lipids in the artery wall, followed by the development of fibrous atheromatous plaques.

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2
Q

Outline the three main consequences atherosclerotic plaques cause.

A
  • stiffening: causes hypertension and strain on the heart as it tries to pump blood against extra resistance.
  • stenosis: leads to reduced blood flow (e.g. precipitating angina)
  • plaque rupture: creates a thrombus that can block a distal vessel and cause ischaemia (e.g. acute coronary syndromes)
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3
Q

Give the risk factors for cardiovascular disease.

A
  • increasing age
  • family history
  • male sex
  • hypercholesterolaemia
  • smoking
  • alcohol consumption
  • poor diet
  • lack of exercise
  • obesity
  • poor sleep
  • stress
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4
Q

Give some medical co-morbidities that increase the risk of cardiovascular disease.

A
  • diabetes
  • hypertension
  • chronic kidney disease
  • rheumatoid arthritis
  • atypical antipyschotic medications
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5
Q

What lifestyle changes can be introduced to control cardiovascular disease?

A
  • address diet, exercise and obesity
  • smoking cessation
  • reduce alcohol consumption
  • optimise treatment of co-morbidities
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6
Q

The NICE guidelines (February 2023) on cardiovascular disease recommend which dietary changes?

A
  • total fat <30% of total calories
  • reduced sugar intake
  • 5 a day of fruit and vegetables
  • 2 a week of fish
  • 4 a week of legumes, seeds and nuts
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7
Q

The NICE guidelines (February 2023) on cardiovascular disease recommend what level of physical activity?

A
  • aerobic activity for 150 minutes (moderate intensity) or 75 minutes (vigorous intensity) per week
  • strength training activities at least 2 days per week
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8
Q

What is meant by

a) primary prevention of cardiovascular disease?

b) secondary prevention of cardiovascular disease?

A

a) prevention for patients that have never had a diagnosis of CVD

b) prevention for patients after a diagnosis of angina, myocardial infarction, TIA, stroke or peripheral arterial disease.

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9
Q

What are the end results of atherosclerosis?

A

See image

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10
Q

Describe the primary prevention of cardiovascular disease.

A

Medication for primary prevention based upon QRISK3 score.

NICE guidelines (February, 2023) recommend that if QRISK3 > 10%, patients are offered atorvastatin 20mg OD.

Atorvastatin 20mg OD also offered as primary prevention in all patients with CKD, and patients with T1DM over 40yrs.

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11
Q

Describe the secondary prevention of cardiovascular disease.

A

4A’s mnemonic:

  • antiplatelet medication (e.g. clopidogrel)
  • atorvastatin 80mg OD
  • atenolol (titrated to maximum tolerated dose)
  • ACEi (ramipril)
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12
Q

What is familial hypercholesterolaemia?

A

An autosomal dominant genetic condition causing elevated cholesterol levels.

Important features to remember:
- family history of premature cardiovascular disease
- very high cholesterol (>7.5mmol/L)
- tendon xanthomata

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13
Q

What is the management of familial hypercholesterolaemia?

A
  • specialist referral for genetic testing
  • statin therapy
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14
Q

Outline the pathophysiology of the acute coronary syndromes.

A

Result of a thrombus from an atherosclerotic plaque blocking a coronary artery, reducing oxygenated blood supply to the myocardium.

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15
Q

The right coronary artery (RCA) curves around the right side and under the heart, supplying the:

A
  • right atrium
  • right ventricle
  • inferior aspect of left ventricle
  • posterior septal area
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16
Q

The circumflex artery curves around the top, left and back of the heart, suppling the:

A
  • left atrium
  • posterior aspect of the left ventricle
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17
Q

The left anterior descending (LAD) travels down the middle of the heart, supplying the:

A
  • anterior aspect of the left ventricle
  • anterior aspect of the septum
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18
Q

What are the types of acute coronary syndrome?

A
  • unstable angina
  • ST elevation myocardial infarction (STEMI)
  • non-ST elevation myocardial infarction (NSTEMI)
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19
Q

Give the defining characteristics of a STEMI.

A
  • cardiac chest pain
  • ECG with ST segment elevation, or new LBBB
  • hs-Tnl raised (>100ng/L)
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20
Q

Give the defining characteristics of an NSTEMI.

A
  • cardiac chest pain
  • ECG with ST segment depression, T wave inversion, or normal
  • hs-Tnl raised (>100ng/L)
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21
Q

Give the defining features of unstable angina.

A
  • cardiac chest pain
  • ECG with ST segment depression, T wave inversion, or normal
  • hs-Tnl within normal reference range
22
Q

What are the symptoms of the acute coronary syndromes?

A
  • central, crushing chest pain*
  • nausea and vomiting
  • sweating and clamminess
  • feeling of impending doom
  • shortness of breath
  • palpitations
  • pain radiating to jaw or arms

Symptoms should continue at rest for more than 20 minutes; if they settle with rest consider angina.

*Note diabetic patients may not experience typical chest pain during ACS; referred to as silent MI.

23
Q

The following ECG is consistent with a diagnosis of which ACS?

Give the artery and area of the heart that has been affected.

A

ST segment elevation seen in limb leads I, aVL and V3-V6.

This is an anterolateral STEMI, with the left coronary artery affected.

24
Q

The following ECG is consistent with a diagnosis of which ACS?

Give the artery and area of the heart that has been affected.

A

ST segment elevation seen in limb leads V1-V4.

This is an anterior STEMI, with the LAD affected.

25
Q

The following ECG is consistent with a diagnosis of which ACS?

Give the artery and area of the heart that has been affected.

A

ST segment elevation seen in limb leads I, aVL and V5-V6.

This is a lateral STEMI, with the circumflex artery affected.gm

26
Q

The following ECG is consistent with a diagnosis of which ACS?

Give the artery and area of the heart that has been affected.

A

ST segment elevation seen in limb leads II, III and aVF.

This is an inferior STEMI, with the right coronary artery affected.

27
Q

Which protein is raised, and diagnostic, in myocardial infarction?

A

Troponin (Tnl) levels rise 3-4 hours after myocardial damage, and can remain elevated for up 2 weeks.

In order to achieve a quick diagnosis, hs-Tnl is taken on admission and again at 1 hour. The second hs-Tnl level is useful to assess whether the elevation is static, rising (recent event) or falling (older event)

28
Q

Give the hs-Tnl levels that suggest a high likelihood of myocardial infarction in

a) males

b) females

A

a) hs-Tnl > 34ng/L

b) hs-Tnl > 16ng/L

Note levels five-fold above the upper limit have a very high predictive value for myocardial infarction (>90%); elevations up to three times the upper limit have limited predictive value (50-60%).

29
Q

Besides myocardial infarction, list some other causes of raised hs-Tnl.

A
  • severe sepsis
  • malignancy
  • stroke
  • aortic dissection
  • pulmonary embolism
30
Q

Give some conditions that may mimic NSTEMI on ECG.

A

Previously established ECG changes from:
- old myocardial infarction
- LV hypertrophy
- digoxin effect

31
Q

Give some conditions that may mimic STEMI on ECG.

A
  • pericarditis (wide-spread ST elevation)
  • early repolarisation (leads V1-V2)
32
Q

How should suspected ACS be investigated?

A
  • physical examination
  • ECG
  • hs-Tnl (cardiac necrosis)
  • FBC (raised platelets)
  • U&Es (prior to ACEi and other meds)
  • LFTs (prior to statins)
  • lipid profile (risk factors)
  • TFTs (hyperthyroidism may mimic sx)
  • HbA1c and fasting glucose (diabetes)
  • CXR (investigate other causes of chest pain)
  • echocardiogram (after event to assess functional damage)
  • CT coronary angiogram (assess for coronary artery disease)
33
Q

How should STEMI be acute managed?

A
  1. IV access
  2. Pain relief (morphine, anti-emetics)
  3. Oxygenation (only if hypoxic, SpO2 >94%)
  4. Aspirin (300mg loading dose)
  5. Anti-platelet therapy (prasugrel, clopidogrel or ticagrelor)

Primary PCI if available within 2 hours of thrombolysis possible; thrombolysis if PCI not available within 2 hours.

34
Q

What is percutaneous coronary intervention (PCI)?

A

Implant of a catheter into the patient’s brachial or femoral artery, feeding it to the coronary arteries under xray guidance and injecting contrast to identify the area of blockage.

A balloon can then be inflated to widen the vessel, with a stent placed to keep the artery patent.

35
Q

What are the principles of thrombolysis in the management of STEMI?

A

Thrombolysis involves injecting a fibrinolytic medication to dissolve clots. Examples include streptokinase, alteplase and tenecteplase.

36
Q

How should NSTEMI be acute managed?

A

BATMAN:

  1. Beta-blockers
  2. Aspirin (300mg loading dose)
  3. Ticagrelor (180mg loading dose)
  4. Morphine (titrated to control pain)
  5. Anticoagulant (fondaparinux)
  6. Nitrates (e.g. GTN) to relieve coronary artery spasm

Oxygenation ONLY if hypoxaemic, aim SpO2 > 94%.

37
Q

Which scoring system can be used to assess for PCI in ACS management?

A

GRACE score gives 6-month risk of death or repeat MI after having an ACS.

If GRACE score ≥ 5%, the patient should be considered for early PCI to treat underlying coronary artery disease.

https://www.mdcalc.com/calc/1099/grace-acs-risk-mortality-calculator

38
Q

What are the complications of myocardial infarction?

A

DREAD

  1. Death
  2. Rupture of the heart septum or papillary muscles
  3. Edema (heart failure)
  4. Arrhythmia or Aneurysm
  5. Dressler’s syndrome
39
Q

What is Dressler’s syndrome?

A

A localised immune response occurring 2-3 weeks after MI, causing pericarditis.

It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade.

A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

Management is with NSAIDs and steroids. Pericardiocentesis may be required if large pericardial effusion.

40
Q

Outline the secondary prevention medical management of ACS.

A

Medical management (6 As):
1. Aspirin (75mg OD)
2. Another antiplatelet (clopidogrel or ticagrelor) for up to 12 months
3. Atorvastatin (80mg OD)
4. ACE inhibitors (e.g. ramipril, titrated as tolerated)
5. Atenolol (titrated as high as tolerated)
6. Aldosterone antagonist (if clinical heart failure)

41
Q

Outline the secondary prevention lifestyle advice of ACS.

A
  • smoking cessation
  • reduce alcohol consumption
  • Mediterranean diet
  • cardiac rehabilitation
  • optimise treatment for other medical conditions (e.g. diabetes, hypertension)
42
Q

What is stable angina?

A

Chest discomfort provoked by effort or emotion, however relieved by rest.

Radiated symptoms are more rare, but may take the form of throat tightness or arm heaviness rather than ACS radiated symptoms.

NOTE angina is unlikely if the pain is continuous or very prolonged, unrelated to activity, brought on by breathing or associated with other symptoms such as dizziness or dysphagia.

43
Q

What are the causes of stable angina?

A
  • coronary artery disease (most common)
  • aortic stenosis
  • hypertensive heart disease
  • hypertrophic cardiomyopathy
44
Q

What are the risk factors for angina?

A
  • smoking history
  • hypertension
  • hyperlipidaemia
  • diabetes mellitus
  • previous CV disease
45
Q

How should stable angina symptoms be initially investigated?

A
  • FBC
  • biochemical screen including HbA1c
  • full lipid profile
  • resting 12-lead ECG (provides information on rhythm, presence of heart block, previous MI, myocardial hypertrophy etc; cannot be used to diagnose or exclude angina)
46
Q

How should stable angina symptoms be definitively investigated if:

a) likelihood of CAD > 60%

b) likelihood of CAD 30-60%

c) likelihood of CAD 10-29%

A

a) invasive coronary angiography

b) functional imaging (e.g. stress MRI, echocardiogram)

c) CT calcium scoring - if score 1-400 perform stress MRI; if score >400 perform invasive coronary angiography.

47
Q

How should stable angina be treated?

A
  • aspirin 75mg OD
  • atorvastatin 80mg OD
  • GTN spray
  • beta-blocker or calcium channel blocker
48
Q

How should you advise a patient to take their GTN spray with stable angina?

A

Their GTN spray is used required. It causes vasodilation and helps relieves the symptoms.

Take GTN, then repeat after 5 minutes. If there is still pain 5 minutes after the repeat dose – call an ambulance.

49
Q

Give some non-cardiac causes of chest pain.

A
  • costochondritis
  • gastro-oesophageal reflux
  • pulmonary embolism
  • pneumonia
  • pneumothorax
  • psychosomatic pain
50
Q

What is cardiac rehabilitation?

A

An individualised programme, composed of exercise sessions and education sessions, that aim to improve recovery from recent cardiac events and reduce the risk of further heart problems.

https://www.bhf.org.uk/informationsupport/support/practical-support/cardiac-rehabilitation