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Julia PCP2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Name 8 risk factors for the development of IHD.

A
  • Increasing age
  • Family Hx
  • Obesity
  • Sedentary lifestyle
  • Smoking
  • Hypercholesterolaemia
  • Hypertension
  • Diabetes
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2
Q

What is the WHO definition of an AMI?

A

At least 2 of the following 3 features:

  • Symptoms of myocardial ischaemia
  • Elevation of cardiac markers (troponin or CK)
  • Typical ECG pattern involving the development of Q waves, ST segment changes or T wave changes
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3
Q

What are the reperfusion options in AMI and how soon should they be implimented?

A

Options: percutaneous intervention or fibrinolysis

Should be performed within 90 minutes of symptom onset

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4
Q

When is fibrinolysis preferred over PCI for treatment of AMI?

A
  • Early presentation
  • Invasive strategy not an option
  • There will be a delay to invasive option
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5
Q

What are the adjunctive therapies in AMI?

A

Oxygen, IV morphine, aspirin, IV heparin/clexane, IV GTN, additional antiplatelets if applicable

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6
Q

What are the benefits of starting a beta-blocker after AMI?

A
  • Reduced rates of recurrent MI
  • Reduced angina
  • Reduced arrhythmias
  • Improved LV function
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7
Q

What are contraindications to starting a beta blocker after AMI?

A

Hypotension, bradycardia, second- or third-degree heart block, severe asthma

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8
Q

In CCF following an AMI, what changes might you see on a chest X-ray?

A

Cardiomegaly, Kerley B lines, pleural effusions

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9
Q

What are cholesterol targets post-AMI?

A

Total cholesterol

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10
Q

What is the post-hospital management following a STEMI?

A
  • Review at 1 month; then 6 monthly
  • Repeat ECHO at 6 months
  • Stress testing at 1 year
  • Cholesterol profile, renal & liver function tests, CK, FBE 6 monthly
  • Regular review of lifestyle changes
  • Regular review of medication chart & compliance
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11
Q

What is the most common clinical presentation of a tachyarrhythmia?

A

Palpitations

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12
Q

What is the most common clinical presentation of a bradyarrhythmia?

A

Syncope/presyncope

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13
Q

Name 1 vital investigation in palpitations and 5 others you may consider.

A
  1. ECG

Others: Holter monitor, Event recorder, Loop recorder, Echocardiogram, Electrophysiology study, Stress testing

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14
Q

What is the usual management of premature ventricular/atrial complexes in an otherwise healthy patient?

A
  1. Reassurance
  2. Cut down caffeine
  3. Occasionally requires beta blockers or calcium channel blockers if very frequent & symptomatic
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15
Q

What is the usual management of AF?

A
  1. Rule out precipitant (eg/ hyperthyroidism, infection)
  2. Look for a cause (eg/ cardiomyopathy)
  3. Decide whether to rate control or rhythm control
  4. Evaluate the risk of stroke & how best to manage it (CHADS2)
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16
Q

Which 3 medications might be used in AF to maintain sinus rhythm (rhythm control)?

A

Sotalol, flecainide, amiodarone

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17
Q

Which 3 medications might be used to control rate in AF?

A

Beta blockers, calcium channel blockers, digoxin

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18
Q

What location does an ablation procedure target in AF?

A

Pulmonary veins (4)

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19
Q

A majority of SVTs involve which part of the cardiac conduction system?

A

AV node

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20
Q

What are 3 possible acute treatments of SVT?

A
  1. Vagal manoeuvres
  2. IV adenosine (induces transient AV block)
  3. IV verapamil
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21
Q

What are the long-term options for treatment of SVT?

A
  1. No treatment
  2. Beta blockers or calcium channel blockers - ‘pill in the pocket’ approach
  3. Catheter ablation (>95% success rate)
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22
Q

42 year-old male who has occasional palpitations - sudden onset, at rest, regular, last 5-10 minutes, resolve spontaneously & suddenly. Presents with a further episode of palpitations lasting >1 hour. What is the likely arrhythmia causing his palpitations?

A

Supra-ventricular tachycardia

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23
Q

What is the acute management for a patient presenting with VT?

A

If unstable -> DC cardioversion

If stable, can try amiodarone before DC cardioversion

Always investigate & treat the cause

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24
Q

What are the ‘red flag’ features of palpitations?

A
  • Past history of cardiac disease
  • Evidence of cardiac disease on baseline tests
  • Family history of sudden cardiac death
  • Severe symptoms
  • High risk work environment
  • High level sporting activities
  • Before/during pregnancy
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25
Q

What is the definition of syncope?

A

Transient LOC that is self-limiting. Onset is relatively rapid, leads to a fall. Recovery is complete, rapid & spontaneous.

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26
Q

What are some indications for a PPM?

A
  • Symptomatic sinus bradycardia
  • Sinus pauses >2s (day) or 2.5s (night)
  • Symptomatic 2nd or 3rd degree AV block
  • Intermittent 3rd degree AV block
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27
Q

What is the usual management of sick sinus syndrome?

A
  1. Insert PPM

2. Once PPM inserted, you can use AV nodal blocking agents to control tachycardias

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28
Q

What is a normal PR interval?

A
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29
Q

What does a bifid P wave suggest?

A

‘P mitrale’ - a sign of mitral stenosis

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30
Q

What does a peaked P wave suggest?

A

‘P pulmonale’ - a sign of lung disease

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31
Q

What is the Wenkebach phenomenon?

A

Progressive lengthening of the PR interval until a P wave is non-conducted (2nd degree heart block, Mobitz type I)

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32
Q

What is a normal QRS width?

A
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33
Q

What is a pathological Q wave?

A

A marker of electrical silence which implies established full thickness death of the myocardium (scar)

  • must be >25% the height of the corresponding R wave
  • must be present in more than 1 contiguous lead
34
Q

What are some causes of left axis deviation?

A

Left anterior hemiblock, ischaemic heart disease, cardiomyopathy, hypertension, WPW syndrome

35
Q

What are some causes of right axis deviation?

A

(normal in children & tall thin adults)

RV volume/pressure overload, COPD, PE, WPW syndrome

36
Q

What are some causes of extreme right axis deviation?

A

Lead transposition, VT, emphysema, hyperkalaemia, paced rhythm

37
Q

In which leads are the T waves normally inverted?

A

V1 (sometimes V2), III, aVR

38
Q

What does a biphasic T wave represent?

A

Critical LAD stenosis

39
Q

What does an inverted T wave represent?

A

Ischaemia

40
Q

From where to where is the QT interval measured?

A

From the start of the QRS complex to the end of the T wave

41
Q

What are the common causes of long QT?

A

Drugs (amiodarone, sotalol, azithromycin, amitriptyline, clozapine), electrolyte imbalance (hypokalaemia, hypomagnesaemia), MI

42
Q

What does echocardiography show?

A
  • Chamber size & function (EF)
  • Wall thickness
  • Cardiac structure
  • Valve morphology
  • Doppler -> flow velocities
43
Q

What is rheumatic fever?

A

A type II hypersensitivity reaction to grp A beta haemolytic Strep

44
Q

What are the clinical features of rheumatic fever?

A
  • Fever
  • Arthritis
  • Rash (erythema marginatum)
  • Subcutaneous nodules
  • Murmur
  • Sydenham’s chorea
45
Q

How is rheumatic fever diagnosed?

A

Based on Jones criteria

46
Q

What is the management of rheumatic fever?

A

Antibiotics + NSAIDs

47
Q

In mitral regurgitation, when should you aim to operate?

A

BEFORE symptoms - on echo criteria (symptoms coincide with severe disease with irreversible changes in the LV)

48
Q

In aortic stenosis, when should you aim to operate?

A

When the stenosis becomes symptomatic - the LVH will regress after surgery

49
Q

Which 2 valve pathologies can result in pulmonary hypertension?

A

Mitral regurgitation & mitral stenosis

50
Q

What are the 3 causes of aortic stenosis?

A
  • Congenital (AS 0.33% or bicuspid aortic valve 1-2%)
  • Rheumatic fever
  • Calcific - COMMON
51
Q

What is the pathophysiology of aortic stenosis?

A

Aortic stenosis creates a much greater pressure gradient across the valve that the LV must push to overcome, leading to left ventricular hypertrophy

52
Q

What are the 3 main symptoms of aortic stenosis?

A

SOB on exertion, chest pain on exertion, syncope (only appear when stenosis is severe)

53
Q

What are some physical signs of aortic stenosis (besides the murmur)?

A
  • Slow upstroke carotid pulse with a plateau
  • Heaving apex beat
  • Thrill over upper R sternal edge
54
Q

What murmur might be heard in aortic stenosis?

A

Ejection systolic ‘crescendo-decrescendo’ murmur best heard over the upper R sternal edge (with radiation to the carotids)

55
Q

What echocardiography criteria signify severe aortic stenosis?

A
  • Gradient >50mm

- Aortic valve area

56
Q

What are the treatment options for severe aortic stenosis?

A
  • Open aortic valve replacement

- Transcatheter aortic valve implant (TAVI)

57
Q

What are some cases of aortic regurgitation?

A
  • Aortic leaflet damage (endocarditis, rheumatic fever)

- Aortic root dilation (Marfan’s syndrome, aortic dissection, collagen vascular disorders, syphilis)

58
Q

What are the symptoms of aortic regurgitation?

A

NONE - until LV decompensates & person develops heart failure (SOB)

59
Q

What are some signs of aortic regurgitation (besides the murmur)?

A
  • Collapsing pulse - fast up & down stroke

- Wide pulse pressure

60
Q

What is the murmur heard in aortic regurgitation?

A

Early diastolic murmur, best heard at the upper left sternal edge

61
Q

What is the management for aortic regurgitation?

A
  • Echo every 6-12 months for severe AS

- Aortic valve replacement (when LV decompensates)

62
Q

What are the causes of mitral regurgitation?

A
  • Myxomatous degeneration
  • Ruptured chordae tendinae
  • Infective endocarditis
  • Myocardial infarct (ruptured papillary muscle)
  • Rheumatic fever
  • Collagen vascular disease
  • Cardiomyopathy
63
Q

What are the symptoms of mitral regurgitation?

A

NONE - until the LV decompensates & symptoms of heart failure occur (SOB)

64
Q

What is the murmur heard in mitral regurgitation?

A

Pansystolic murmur best heard over the apex beat during expiration

65
Q

What is the management for mitral regurgitation?

A
  • Follow-up echo 6-12 monthly for severe MR

- LV decompensation or pulmonary hypertension are triggers for valve replacement or repair

66
Q

What is the commonest valve lesion caused by rheumatic fever?

A

Mitral stenosis

67
Q

What is the major cause of mitral stenosis?

A

Rheumatic fever (esp. in women)

68
Q

What are the symptoms of mitral stenosis?

A

SOB, oedema, pulmonary disease

69
Q

What are some signs of mitral stenosis (besides the murmur)?

A
  • Mitral facies (flushing)

- Tapping apex beat - correlates with loud S1

70
Q

What murmur is heard with mitral stenosis?

A

-Rumbling diastolic murmur with opening ‘snap’

71
Q

What are the heart changes observed over time in mitral stenosis?

A
  • Atrial dilatation
  • Atrial fibrillation
  • Thrombo-embolism
  • Pulmonary congestion & oedema
  • Pulmonary hypertension
  • Right heart failure
72
Q

What are the principles of management for mitral stenosis?

A
  • Regular echo
  • Anticoagulation if AF
  • Treat AF
  • Diuretics
  • Mitral valve intervention
73
Q

What are the interventions for mitral stenosis?

A
  • Mitral valvotomy - open or closed
  • Balloon valvuloplasty
  • Mitral valve replacement
74
Q

What are the features of cardiogenic syncope?

A
  • No prodrome
  • Complete & rapid recovery
  • Sudden with acute onset
  • May be exertion related
75
Q

What are some features of a LOC that suggest epilepsy?

A
  • Urine or faecal incontinence
  • Auras
  • Post-ictal phase
76
Q

In an otherwise healthy individual, at what level should you treat blood pressure?

A

SBP >180mmHg
DBP >110mmHg
SBP >160mmHg and DBP

77
Q

When the individual has associated risk factors, at what level should you treat high blood pressure?

A

SBP >140mmHg
DBP >90mmHg
Or high CV risk

78
Q

What constitutes critical limb ischaemia?

A
  • Ischaemic rest pain
  • Ulcers
  • Gangrene
79
Q

What is the white cell trapping hypothesis of chronic venous insufficiency?

A
  • WBCs are larger & less deformable than RBCs
  • When perfusion pressure is reduced by venous hypertension, WBC plug capillaries & RBC build up behind
  • WBC activation occurs
  • Endothelial adhesion by WBC releases proteolytic enzymes & ROS causing endothelial & tissue damage
80
Q

What is the fibrin cuff hypothesis of chronic venous disease?

A
  • Increased venous pressure if directly transmitted to capillaries resulting in capillary elongation & increased endothelial permeability
  • Larger molecules such as fibrinogen become deposited into tissues -> fibrin
  • Accumulation of fibrin acts as a barrier to oxygen -> tissue hypoxia -> ulceration
81
Q

What does the CEAP classification of venous disease encompass?

A 
C = clinical
E = etiology
A = anatomy 
P = pathophysiology

Julia PCP2 (21 decks)

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