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YEAR 4 - ACC > Cardiovascular 1 - cardiac emergencies > Flashcards

Cardiovascular 1 - cardiac emergencies Flashcards

1
Q

What makes up ‘Acute Coronary Syndrome’? Describe the difference in their pathophysiology.

A

Unstable angina
- Partial occlusion of coronary vessel -> decreased blood supply -> ischaemic symptoms

NSTEMI

  • Partial occlusion of a coronary artery
  • Affects the inner layer of the heart (subendocardial infarction)

STEMI

  • Complete occlusion of a coronary artery
  • Affects full thickness of the myocardium (transmural infarction)
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2
Q

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

A
  1. Plaque rupture
  2. Thrombosis
  3. 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 an MI typically 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 features are seen on an ECG of a STEMI?

A
  • Tall tented T waves in hyper-acute
  • ST elevation OR new-onset LBBB (broad QRS complexes)
  • ST elevation must be seen in two contiguous leads with reciprocal ST depressions
  • 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 so always compare to previous ECGs)

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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 is a LBBB and what does a new LBBB on an ECG indicate? What are the ECG signs of a LBBB?

A

Indicates a STEMI

LBBB = Cardiac conduction alteration in which there is delay or obstruction of impulses sent through the left bundle branch pathway, leading to delayed left ventricle contraction

ECG signs include:

  • QRS duration ≥ 120 ms
  • a rS or QS complex in lead V1
  • a notched (M-shaped) R wave in V6
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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:

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

What is the pharmacological management of an MI?

A

MONAT

Morphine 5-10mg (given with metoclopramide)
Oxygen 15L/min
Nitrates - GTN spray 2 sprays
Aspirin 300mg PO - then taken 75mg OD lifelong
Ticagrelor 180mg PO - then taken 90mg BD for 12 months

LMWH for NSTEMI or STEMI that is not candidate for primary 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
  1. Tear in the intima of the aortic lining, which allows blood to enter the aortic wall
  2. A haematoma forms which separates the intima from the adventitia
  3. A false lumen is created which extends in either direction
  4. 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 + arch of aorta

Type B (30%) = descending aorta

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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

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29
Q

What are the main risk factors for aortic dissection?

A 
Hypertension = most common
Smoking
Hypercholesterolaemia
Bicuspid aortic valve
Cocaine/amphetamine use 
Inherited conditions:
- Marfan's
- Ehlers-Danlos
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30
Q

How does aortic dissection present?

A

Sudden onset of sharp/tearing chest pain

  • Chest (type A)
  • Back between scapulas (type B)

Depending on how far the dissection extends:

  • Syncope in 10%
  • Bowel/limb ischaemia
  • Renal failure
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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

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32
Q

What provides a definitive diagnosis of aortic dissection?

A

CT angiogram

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33
Q

What changes may 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

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34
Q

What is the acute initial 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
Cardiac monitoring

Escalate to cardiology and ICU

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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
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36
Q

How are Type B aortic dissections managed?

A

Medically
Aggressive blood pressure control with labetolol

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
Rheumatic disease - SLE, RA, sarcoidosis
Metabolic - uraemia due to renal failure, 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 defines a narrow complex tachycardia? What tachycardias are classed as narrow complex?

A

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

Examples:

  • SVT
  • AF
46
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 lying down get them to blow the plunger out of syringe

IV adenosine:

  • IV adenosine 6mg + saline flush
  • If unsuccessful repeat with 12mg then 12mg
47
Q

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

A

Transient chest tightness
Dyspnoea
Headache
Flushing

48
Q

When is adenosine contraindicated?

A

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

49
Q

What causes a broad complex tachycardia?

A

Ventricular tachycardia

50
Q

What drug overdose can cause broad-complex tachycardias?

A

Tricyclic antidepressant overdose

51
Q

What electrolyte abnormalities can cause VT?

A

Low K+
Low Mg2+
Low Ca2+

52
Q

What is Torsades de Pointes? What is it associated with?

A

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

53
Q

How do you treat Torsades de Pointes?

A

IV magnesium sulphate 2g over 10 minutes

54
Q

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

A

Amiodarone 300mg IV over 20-60 min

Then amiodarone 900mg IV over 24 hours

55
Q

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

A

Ventricular fibrillation

56
Q

What conditions is VF most commonly associated with?

A

Coronary artery disease e.g. acute MI, IHD

57
Q

What ECG changes are seen in VF?

A

Rate up to 500bpm

No P, QRS or T waves

58
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
59
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
60
Q

Which arrhythmias are shockable and non-shockable?

A

Shockable:

  • Ventricular fibrillation
  • Pulseless ventricular tachycardia

Non-shockable:

  • Asystole
  • PEA (pulseless electrical activity)
61
Q

What can be given in a cardiac arrest whilst CPR is being done and when is it given?

A
  • Give adrenaline 1:10,000 1ml every 3-5minutes

- Give amiodarone after 3 shocks

62
Q

Who is most likely to suffer a silent MI?

A

Diabetics - polyneuropathy

63
Q

What is seen on an ECG in first degree heart block?

A

PR interval > 200ms (this indicates prolonged conduction of electrical activity through the AV node)

64
Q

Does first degree heart block require management?

A

No, it is benign and does not need treating

65
Q

What is seen on an ECG in Mobitz Type 1 heart block?

A

Progressive lengthening of the PR interval, which results in a P wave that fails to conduct a QRS

66
Q

What can cause heart block?

A

Myocardial infarction - especially inferior or anterior

Drugs: calcium-channel blockers, beta-blockers, digoxin, amiodarone

High vagal tone e.g. in athletes

Cardiac surgery

Inflammatory conditions - Myocarditis, SLE, rheumatic heart disease

67
Q

What is seen on an ECG in Mobitz Type 2 heart block?

A

There are intermittent non-conducted P waves caused by a conduction system failure, especially at the His-Purkinje system

PR interval remains constant

68
Q

How does complete heart block present?

A

Syncope

69
Q

What is seen on an ECG in complete heart block?

A

Severe bradycardia

Dissociation between the P waves and the QRS complexes

70
Q

What is the definitive management for both Mobitz Type II and complete heart block?

A

Permanent pacemaker

71
Q

What are the different classifications of AF?

A
  • Acute - <48 hours
  • Paroxysmal - < 7 days and is intermittent
  • Persistent - >7 days but is amenable to cardioversion
  • Permanent - >7 days and is not amenable to cardioversion
72
Q

What constitutes fast AF?

A

HR > 100bpm

73
Q

What are some non-cardiac causes of AF?

A
  • Dehydration
  • Endocrine causes - hyperthyrodism
  • Infective causes - sepsis
  • Pulmonary causes - pneumonia, PE
  • Environmental toxins - alcohol abuse
  • Electrolyte disturbances - hypokalaemia, hypomagnesaemia
74
Q

What are signs that a patient with a tachycardia is unstable?

A

Shock - end organ hypoperfusion
Syncope - brain hypoperfusion
Chest pain - myocardial ischaemia
Pulmonary oedema - heart failure

(2 S, 2H - shock, syncope, heart attack, heart failure)

75
Q

What is the management of an unstable patient with tachycardia?

A

Synchronised DC shock (with sedation if conscious) for up to 3 attempts

If that fails, seek expert help and:

  1. Amiodarone 300mg IV over 10-20 min
  2. Repeat shock
  3. Then amiodarone 900mg over 24 hours
76
Q

What is the rate/rhythm treatment for AF if no reversible causes are found?

A

Rate control

  • Beta-blocker - bisoprolol
  • Non-dihydropyridine calcium-channel blocker - diltiazem or verapamil
  • Digoxin – especially for patients who are hypotensive or have co-existent heart failure; avoid in young patients as in increases cardiac mortality

Rhythm control

  • Only used in young patients or those with disabling symptoms
  • Flecainide - Na+ channel blocker
  • Amiodarone (only given to older, sedentary patients)
  • Sotalol - beta-blocker with additional K+ channel blocker action
77
Q

What must be considered before starting a patient on anticoagulation?

A

Thromboembolic risk

Bleeding risk

78
Q

How do you calculate thromboembolic risk?

A 
CHADS2VASc2 Score
	• Congestive cardiac failure - 1
	• Hypertension - 1 
	• Age > 75 - 2
	• Diabetes - 1 
	• Stroke or TIA - 2
	• Vascular disease - 1
	• Age 65-74 - 1
	• Female - 1
Males who score 1+ points or females who score 2+ points should be anticoagulated
79
Q

How do you calculate bleeding risk?

A 
HASBLED Score
	• Hypertension - 1
	• Abnormal renal or liver function - 2 if both present 
	• Stroke - 1 
	• Major bleed (previous) - 1
	• Labile INR - 1
	• Elderly > 65 - 1
	• Drugs/alcohol use - 2 if both
80
Q

What options are available for anticoagulation in AF? What are the pros and cons

A

DOACs - apixaban, rivaroxaban, dabigatran

  • Do not require monitoring
  • Less bleeding risks than warfarin
  • 12 hour half-life so if patient misses dose, they are not covered

Warfarin

  • Requires cover with LMWH for 5 days when initiating treatment because warfarin is initially pro-thrombotic
  • Requires regular INR monitoring and it can be affected by many drugs/food
  • 40 hour half-life so anticoagulant effect lasts days

LMWH

  • Daily treatment dose injections
  • Rare option in those who cannot tolerate oral treatment
81
Q

What treatment can be offered for patients with AF who do not have uncontrolled symptoms and have an identifiable locus in their left atrium?

A

Atrial ablation

82
Q

What effect does digoxin have on the heart?

A

It inhibits the sodium potassium adenosine triphosphatase ([Na+/K+ ATPase) ion pump in the myocardium and also has parasympathetic effects on the AV node

It is thereforenegatively chronotropic and positively ionotropic(i.e. slows heart rate but increases contractility).

83
Q

What is the immediate management of bradycardia in a patient with adverse features (i.e. shock, syncope, heart failure, MI)?

A
  1. Atropine 500mcg IV
  2. If unsatisfactory response:
    - Atropine 500mcg IV again
    OR
    - Transcutaneous pacing
    OR
    - Adrenaline 2-10mcg/min IV
  3. Arrange transvenous pacing
84
Q

What is the delta change in troponin levels?

A

Delta troponin is the percent difference between two troponin results taken in the same patient within a 3 - 8 hour time period
If it is greater than 20%, this is consistent with an MI

85
Q

What investigations should be done in all post-ACS patients?

A

Echocardiogram - check LV function
Lipid profile
HbA1c

86
Q

What are the DVLA regulations regarding ACS?

A

Stop driving for 4 weeks if no PCI/unsuccessful PCI
OR
Stop driving for 1 week if successful PCI
In both cases, the DVLA does not need to be informed

HGV drivers must inform the DVLA and stop driving for 6 weeks then meet with doctor to see if fit

87
Q

What are the 5 types of MI?

A
  1. Spontaneous MI due to plaque rupture
  2. Low oxygen/hypoperfusion due to increased oxygen demand (fibrillation/tachycardia) or decreased supply (septic shock, anaemia)
  3. Sudden unexpected cardiac death
  4. Associated with PCI or stent thrombosis
  5. Associated with cardiac surgery
88
Q

What is the long-term management after a STEMI?

A 
Aspirin
Clopidogrel/ticagrelor
Beta-blockers
ACE inhibitor
Statins

YEAR 4 - ACC (11 decks)

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