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extra 4 (m) > Cardiac - Chest pain, arrhythmias, palpitations > Flashcards

Cardiac - Chest pain, arrhythmias, palpitations Flashcards

1
Q

What makes up ‘Acute Coronary Syndrome’?

A
  1. STEMI = complete blockage of an artery
  2. NSTEMI = partial blockage of an artery
  3. Unstable angina = chest pain at rest due to narrowing of coronary artery
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2
Q

What is the common underlying pathology shared between the 3 ACS conditions?

A

Plaque rupture
Thrombosis
Inflammation

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3
Q

What do platelets release that cause vasoconstriction?

A

Thromboxane A2

Serotonin

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4
Q

What are the main risk factors for ACS?

A 
Smoking
Hypertension
Hyperlipidaemia
Diabetes mellitus
Obesity
Family history of IHD (MI in first degree relative <55 years) 
Cocaine use
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5
Q

How does ACS present?

A 
Sudden onset of crushing central chest pain/tightness
Pain radiates to back, jaw, left arm
Acute dyspnoea
Nausea and vomiting
Sweating
Palpitations
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6
Q

How can you distinguish between ACS and stable angina?

A

ACS is unresponsive to GTN spray

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7
Q

What would the ECG look like in a STEMI?

A

Tall tented T waves in hyper-acute
ST elevation OR new-onset LBBB (broad QRS complexes)
Inverted T waves if ECG done days later (shows ischaemia)
Q waves remain for months

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8
Q

How do you differentiate between an MI and unstable angina?

A

Troponin levels

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9
Q

What ECG changes can be seen in an NSTEMI?

A

ST depression
T wave inversion
(might be normal)

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10
Q

At what hours post-pain onset do troponin levels rise?

A

The levels increase 3-12 hours from pain onset
They peak at 24-48 hours
Return to baseline 5-14 days

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11
Q

What does ST elevation in leads II, III, aVF indicate?

A

Inferior MI in the right coronary artery

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12
Q

What does ST depression in leads V1-4 indicate?

A

Posterior MI in the posterior descending artery

V1-4 are anterior leads so think of it as an upside down ST elevation in the posterior side of the heart

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13
Q

What does ST elevation in leads V7 to V9 indicate?

A

Posterior MI in the posterior descending artery

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14
Q

What does a new LBBB indicate?

A

STEMI

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15
Q

What ECG changes would be seen in a blockage of the circumflex coronary artery?

A

Acute postero-lateral MI

Posterior infarct

  • ST depression in V1-4
  • Dominant R waves (= upside down Q waves)

Lateral infarct - ST elevation in V6

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16
Q

What does an anterior STEMI result from?

A

Occlusion of the LAD (left anterior descending artery)

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17
Q

What ECG changes are seen in an anterior STEMI?

A

ST segment elevation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).

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18
Q

What is troponin?

A

Protein involved in cardiac and skeletal muscle contraction

When myocardial cells are damaged, troponins are released into the blood

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19
Q

Which troponins are most specific to the heart?

A

Troponins I and T

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20
Q

Aside from MIs what can cause a rise in troponin?

A

Other causes of myocardial damage:

  • Myocarditis
  • Pericarditis
  • Ventricular strain

Non-cardiac aetiology:

  • Masive PE causing right ventricular strain
  • Subarachnoid haemorrhage
  • Burns
  • Sepsis
  • Renal failure
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21
Q

What is the acute management of an MI?

A

MONAC

Morphine 5-10mg (given with metoclopramide)
Oxygen 15L/min
Nitrates - GTN spray
Aspirin/Clopidogrel 300mg loading dose

If STEMI, refer to cardiologist for PCI

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22
Q

Who should a primary PCI be offered to?

A

All patients presenting within 12 hours of symptom-onset with a STEMI who either are at or can be transferred to a primary PCI centre within 120min of first medical contact

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23
Q

If PCI is unavailable or it has been >12 hours since symptom-onset, what should be done for patients with a STEMI?

A 
Thrombolysis (-plase) 
Start fondaparinaux (factor 10a inhibitor) or LMWH
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24
Q

What advice should be given to patients post-MI?

A

Returning to work - 2-3 months
Driving - do not drive for 1 week if successful angioplasty, or 4 weeks if unsuccessful/no angioplasty, notify insurance
Sex - avoid for few weeks, return when able to walk without discomfort

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25
Q

What are the linings of the aorta?

A

Intima
Media
Adventitia

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26
Q

What happens in an aortic dissection?

A

Tear in the intima of the aortic lining, which allows blood to enter the aortic wall
A haematoma forms which separates the intima from the adventitia
A false lumen is created which extends in either direction
As the dissection extends it may damage the aortic valve or prevent circulation to the aortic branch vessels, leading to major ischaemic target organ complications

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27
Q

What are the different types of aortic dissection?

A

Type A (70%) = ascending aorta

Type B (30%) = descending aorta

28
Q

What causes death in type A/type B aortic dissection?

A

Type A - death caused by cardiac tamponade due to sudden severe aortic valve incompetence and interrupted flow to coronary arteries

Type B - death caused by malperfusion of visceral organs or lower limbs

29
Q

What are the main risk factors for aortic dissection?

A

Hypertension = most common
Smoking
Hypercholesterolaemia
Bicuspid aortic valve

Inherited conditions:

  • Marfan’s
  • Ehlers-Danlos
30
Q

How does aortic dissection present?

A

Sudden onset of sharp/tearing chest pain
Chest (type A) or back (type B)
Syncope in 10%

31
Q

What signs might be found on examination of aortic dissection?

A

Aortic regurgitation murmur
Asymmetrical/absent peripheral pulses
Neurological deficit
Type A - hypotension; type B - hypertension

32
Q

What provides a definitive diagnosis of aortic dissection?

A

CT angiogram

33
Q

What changes would be seen on a CXR in aortic dissection?

A

Widened mediastinum
‘Double knuckle’ aorta
Tracheal deviation to the right
Separation of wall of a calcified aorta

34
Q

What is the acute management of an aortic dissection?

A 
Oxygen 15L/min NRBM
IV access
Cross match for 6-10 units of blood
IV beta blockers eg. labetalol (calcium-channel blockers in contraindicated) - aim is to keep systolic BP 100-110
IV morphine + metoclopramide

Escalate to cardiology and ICU

35
Q

What is the surgical management of a Type A aortic dissection?

A
  • Ascending aorta is reconstructed with a vascular graft
  • Arch must be repaired if: primary dissection extends to beyond the aortic arch or if arch is aneurysmal
  • Aortic root repair if: aorta is dilated or if aortic valve incompetent
  • Coronary artery bypass if coronary circulation is impaired
36
Q

How are Type B aortic dissections managed?

A

Medically
Aggressive blood pressure control with nitroprusside and/or beta blocker

Surgery considered if:

  • Dissection is compromising blood flow
  • Aorta is severely dilated or there is risk of rupture
  • Hypertension cannot be controlled with medication
37
Q

What is Beck’s triad of cardiac tamponade?

A

Falling BP
Rising JVP
Muffled heart sounds

38
Q

What are some causes of pericarditis?

A

MI
Viral - coxsackie, EBV, CMV, rubella, mumps, HIV
Bacterial - TB, pneumonia, rheumatic fever
Metabolic - uraemia, hypothyroidism

39
Q

How does pericarditis present?

A

Sharp, central retrosternal chest pain that is worse on lying flat and relieved by sitting forwards
Low grade fever
Dysphagia - if there is large pericardial effusion it can push on the oesophagus

40
Q

What is heard on auscultation in pericarditis?

A

Pericardial friction rub that obscures both heart sounds

41
Q

What is Dressler’s syndrome?

A

Autoimmune pericarditis (with/without effusion) 2-14 weeks after 3% of MIs

42
Q

What ECG changes are seen in pericarditis?

A

Concave (saddle-shaped) ST segment elevation present in all chest leads
PR depression = atrial inflammation

43
Q

How do you treat pericarditis?

A

NSAIDs + PPI for 1-2 weeks
Cochicine 500mcg BD for 3 months to reduce risk of recurrence
Definitive treatment depends on cause

44
Q

What must urgently be done in cardiac tamponade?

A

Pericardiocentesis - needle drainage under US guidance

45
Q

What ECG changes are seen in AF?

A

Absent P waves

Irregularly irregular narrow QRS complexes

46
Q

What blood tests are appropriate to do in AF?

A

U&Es (K+)
Cardiac enzymes
TFTs
FBC

47
Q

What is seen on an ECG in atrial flutter?

A

Sawtooth pattern

48
Q

How do you manage acute AF in a patient that is haemodynamically unstable?

A

If there are signs of shock, syncope, acute heart failure, ischaemia, etc:
Electrical DC cardioversion under sedation

If that is unsuccessful:
IV flecainide 50-150mg or IV amiodarone 300mg then 900mg over 24h

49
Q

How do you manage AF that started > 48hours a go in a patient that is haemodynamically stable?

A

Rate control with: IV metoprolol 5mg or a rate-limiting calcium channel blocker (diltiazem/verapamil)

Start LMWH for 3 weeks before rhythm control

50
Q

What defines a narrow complex tachycardia?

A

ECG shows a rate >100bpm and QRS complex duration <120ms (3 small squares)

51
Q

How do you manage a supraventricular tachycardia if the patient is haemodynamically stable?

A

Vagal manoeuvres:

  • Carotid sinus massage for 15 sec
  • Valsalva manoeuvre - when patient is supine get them to blow plunger out of syringe

IV adenosine:

  • IV adenosine 6mg + saline flush
  • If unsuccessful repeat with 12mg then 12mg
52
Q

What side effects do you need to warn the patient about with adenosine?

A

Transient chest tightness
Dyspnoea
Headache
Flushing

53
Q

When is adenosine contraindicated?

A

Asthma
2nd/3rd degree heart block
Sinoatrial disease e.g. Wolff-Parkinson-White syndrome

54
Q

What is ventricular tachycardia?

A

Broad complex tachycardia originating from a ventricular ectopic focus

55
Q

What drug overdose can cause broad-complex tachycardias?

A

Tricyclic antidepressant overdose

56
Q

What electrolyte abnormalities can cause VT?

A

Low K+
Low Mg2+
Low Ca2+

57
Q

What is Torsades de Pointes?

A

A rare form of VT
Associated with hypokalaemia and hypomagnesaemia
Associated with long QT syndrome

58
Q

How do you treat Torsades to Pointes?

A

IV magnesium sulphate 2g over 10 minutes

59
Q

What is the treatment of VT for a haemodynamically unstable patient?

A

Electrical DC cardioversion under sedation

If that is unsuccessful:
IV flecainide 50-150mg or IV amiodarone 300mg then 900mg over 24h

60
Q

What is the treatment of VT for a haemodynamically stable patient?

A

IV amiodarone 300mg over 1hr then 900mg over 23h

61
Q

What is the most commonly identified arrhythmia in cardiac arrest patients?

A

Ventricular fibrillation

62
Q

What conditions is VF most commonly associated with?

A

Coronary artery disease e.g. acute MI, IHD

63
Q

What ECG changes are seen in VF?

A

Rate up to 500bpm

No P, QRS or T waves

64
Q

How do you manage VF?

A

Call crash team

Airway

  • Head-tilt chin-lift
  • Insert airway adjunct
  • Insert LMA

Breathing
- Bag valve mask ventilation

Circulation (use ALS algorithm)

  • Start CPR 30:2 whilst attaching defibrillator
  • Defibrillate - 1 shock
  • Immediately resume to CPR for 2 min
  • Reassess rhythm
65
Q

What are the reversible causes of cardiac arrest?

A

4 Hs:

  • Hypoxia
  • Hypovolaemia
  • Hypothermia
  • Hyper/hypokalaemia

4 Ts:

  • Tension pneumothorax
  • Tamponade (cardiac)
  • Toxins
  • Thromboembolism
66
Q

Which arrhythmias are shockable and non-shockable?

A

Shockable:

  • Ventricular fibrillation
  • Pulseless ventricular tachycardia

Non-shockable:

  • Asystole
  • PEA (pulseless electrical activity)

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