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Finals > Cardiology Finals > Flashcards

Cardiology Finals Flashcards

1
Q

Which are the lateral ECG leads?

A

I, aVL, V5, V6

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2
Q

Which artery supplies the lateral aspect of the heart?

A

Left circumflex artery

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3
Q

Which are the septal ECG leads?

A

V1

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4
Q

What is the pattern of conduction through the heart?

A
  1. Sinoatrial node
  2. Atria
  3. AV node
  4. Depolarisation through bundle of His
  5. Purkinje fibres (left and right bundle branches)
  6. Right bundle branch depolarises the RV and left bundle branch depolarises the LV
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5
Q

What is the p wave on an ECG?

A

Atrial depolarisation

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6
Q

What is the PR interval on an ECG?

A

Conduction through AVN to the ventricles

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7
Q

What is the QRS complex on an ECG?

A

Ventricular depolarisation

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8
Q

What is the T wave on an ECG?

A

Ventricular depolarisation

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9
Q

How do you interpret an ECG?

A
  1. Patient details
  2. Rate
  3. Rhythm
  4. Axis
  5. Parameters e.g. P, PR, QRS, ST, cQT T
  6. Morphology e.g. broad/narrow/BBB
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10
Q

How long is a normal PR interval?

A

0.12-0.2 seconds

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11
Q

What does a prolonged PR interval suggest?

A

AV block

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12
Q

Where does Mobitz type 1 occur?

A

AV node

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13
Q

Where does Mobitz type 2 occur?

A

Bundle of His or Purkinje fibres

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14
Q

Where does third degree heart block happen?

A

After AV node

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15
Q

What defines broad and narrow complex QRS?

A

Narrow <0.12 seconds
Broad >0.12 seconds

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16
Q

How much must the ST be elevated to be significant?

A

> 1mm in limb leads
2mm in chest leads

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17
Q

What causes inverted T waves?

A

Ischaemia
BBB
PE
LVH
Hypertrophic cardiomyopathy
General illness

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18
Q

What is the triad for stable angina?

A
  1. Constricting chest pain may radiate to jaw/arms
  2. Relieved by rest and GTN
  3. Precipitated by physical exertion
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19
Q

What is the gold standard investigation for stable angina?

A

CT coronary angina

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20
Q

What are second line investigations for stable angina?

A

Myocardial perfusion scan
Stress echocardiogram
MR imaging

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21
Q

What are the side effects of GTN?

A

Headache
Dizziness
DUe to vasodilation

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22
Q

What are the preventative medications for stable angina?

A
  1. BB
  2. CCB (should be long acting dihydropyridine e.g. MR nifedipine)
  3. Isosorbide mononitrate
  4. Ivabradine
  5. Nicorandil
  6. Ranolazine
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23
Q

What is secondary prevention in CVD?

A

Aspirin 75mg
Atorvastatin 80mg
ACE inhibitor
Atenolol (or other BB e.g. bisoprolol)

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24
Q

How do you reduce the risk of tolerance in nitrates?

A

Asymmetric dosing

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25
Q

What are the different types of MI?

A
  1. ACS type MI
  2. Can’t cope MI
  3. Dead by MI
  4. Caused by us MI
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26
Q

Who is at higher risk of having a silent MI?

A

Diabetics

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27
Q

How to differentiate between a NSTEMI and unstable angina?

A

Troponin raised in NSTEMI but not in unstable angina
Both may have the same ECG findings e.g. T wave inversion, ST depression

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28
Q

What are the complications of ACS?

A

D eath
R upturn of septum/papillary muscles/LV free wall
E dema (HF)
A rrhythmia e.g. VT, VF and LV aneurysm
D reseller’s syndrome (2-3 weeks after)

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29
Q

What is the initial management of ACS?

A

M oprhine IV
O oxygen if <94%
N itrates IV/GTN (CI if hypotensive)
A spirit 300mg

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30
Q

What is secondary prevention post ACS?

A

Aspirin 75mg
Another antiplatelet for 12 months e.g. clopidogrel, ticagrelor, prasugrel
Atorvastatin 80mg
ACE inhibitor
Atenolol (or other BB e.g. bisoprolol)
Aldosterone antagonist for those with HF e.g. eplerenone or spironolactone

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31
Q

What is the management of an NSTEMI?

A

B ased on GRACE score. If >3% then PCI within 72 hours
A spirit 300mg
T icargrelor 180mg (clopidogrel if high bleeding risk or prasugrel if angiography)
M oprhine IV
A antithrombin with fondaparinux (if immediate angiography then unfractionated heparin)
N itrate GTN

Oxygen if <94%

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32
Q

Why should you be cautious with ACE inhibitor + aldosterone antagonist?

A

Both cause hyperkalaemia

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33
Q

What is the management of a STEMI?

A

If < 2 hours: PCI. Give aspirin and prasugrel (or clopidogrel if already taking an anticoagulant). Angioplasty and stent
If <4.5 hours: thrombectomy and thrombolysis
If <12 hours: thombolysis with antifibinolytic e.g. alteplase. Give ticagrelor after

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34
Q

What are the most common causes of pericarditis?

A

Idiopathic
Infective: most commonly viral e.g. TB, HIV, coxsackie, EBV

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35
Q

What makes the pain better in pericarditis?

A

Sitting forward

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36
Q

What can be heard on auscultation with pericarditis?

A

Pericardial friction rub (scratching)

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37
Q

What is a sign of constrictive pericarditis?

A

JVP rises with inspiration (Kussmaul’s sign)

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38
Q

Which blood tests are raised in pericarditis?

A

WCC, CRP, ESR, troponin in 30%

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39
Q

What are the ECG changes in pericarditis?

A

PR depression (most specific)
Widespread saddle shaped ST elevation

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40
Q

What is the management of pericarditis

A

NSAIDs
Colchicine taken for 3 months to reduce risk of recurrence

41
Q

What is pulsus paradoxus?

A

An exaggerated fall in blood pressure during inspiration by greater than 10 mm Hg

42
Q

What is a sign of cardiac tamponade?

A

Pulsus paradoxus

43
Q

What is cardiac output?

A

The volume of blood ejected by the heart per minute

44
Q

What is stroke volume?

A

Volume of blood ejected during each beat

45
Q

What are the causes of acute LV failure?

A

Often the result of decompensated HF:
Iatrogenic e.g. aggressive IV fluids
MI
Arrhythmias
Sepsis
Hypertensive emergency

46
Q

How does acute LV failure cause pulmonary oedema?

A

LV cannot efficiently move blood out of the heart so there is backlog in the LA, pulmonary veins and lungs
These start to leak fluid due to the increased pressure and cannot reabsorb excess fluid from surrounding tissues
Pulmonary oedema = when the lung tissue and alveoli are filled with interstitial fluid interfering with normal gas exchange

47
Q

What are the signs on auscultation of acute LV failure?

A

3rd heart sound
Bibasal crackles

48
Q

What are the signs of R sided heart failure?

A
  1. Raised JVP
  2. Peripheral oedema
  3. Hepatomegaly
49
Q

What are the signs of pulmonary oedema on CXR?

A

A lveolar oedema
B Kerley B lines (interstitial oedema)
C ardiomegaly
D ilated upper lobe vessels
E ffusions

50
Q

What is the initial management of acute LV failure?

A
  1. S it them up (gravity helps to clear upper areas of fluid)
  2. Oxygen if <94%
  3. D iuretics

Stop IV fluids

51
Q

What is the role of brain natriuretic peptide?

A

Hormone released by the ventricles in response to myocardium being stretched too much
BNP relaxes the smooth muscles in blood vessels to reduce the systemic vascular resistance so that it is easier for the heart to pump
Also acts on the kidneys as a diuretic to promote water excretion and therefore decrease circulating volume
If -ve, rules out HF. Also raised in COPD, diabetes, sepsis, renal impairment, tachycardia

52
Q

What is the management of acute lV failure when it does not respond to initial measures?

A

IV opiates e.g. morphine (vasodilator)
IV nitrates (vasodilator)
Inotropes e.g. dobutamine which increases CO and MAP by increasing contractility
Vasopressors e.g. noradrenaline (vasoconstriction)
NIV (CPAP)
Invasive ventilation (intubation and sedation)

53
Q

What is the ejection fraction?

A

The % of blood in the LV that is squeezed out with each contraction
Normal = >50% (when HFpEF, due to diastolic dysfunction where the problem is with the LV filling during diastole)

54
Q

What are the causes of chronic HF?

A

IHD
Valvular heart disease (commonly AS)
HTN
Arrhythmias
Cardiomyopathy

55
Q

What are classical symptoms of HF?

A

Orthopnoea: breathlessness when lying flat
Paroxysmal nocturnal dyspnoea: waking at night gasping
Cough with white/pink frothy sputum

56
Q

Why does PND happen in HF?

A
  1. Fluid settles across a larger SA
  2. Respiratory centre in the brain less responsive in sleep so lower RR and effort
  3. Less circulating adrenaline during sleep so myocardium more relaxed and reduced CO
57
Q

What is the medical management of HF?

A

A CE inhibitor
B eta-blocker
A ldosterone antagonist (if not controlled with A + B and reduced EF)
L oop diuretic

Titrate A + B to maximum tolerated

58
Q

What is a specific blood test for chronic HF?

A

N-terminal pro-B type natriuretic peptide

59
Q

What is additional management for HF?

A

Annual flu and COVID vaccinations
One off pneumococcal vaccination
Cardiac rehabilitation

60
Q

What are specialist medical managements for HF?

A

SGLT2 inhibitor e.g. dapagliflozin
Sacubitril with valsartan
Ivabrdadine
Hydralazine with nitrate
Digoxin if AF
Cardiac resynchronisation

61
Q

What is the referral cut off for NTproBNP in HF?

A

400-2000 = echo and seen within 6 weeks
>2000 = echo and seen within 2 weeks

62
Q

What is the referral cut off for BNP in HF?

A

100-400 = echo and seen within 6 weeks
>400 = echo and seen within 2 weeks

63
Q

What is the NY Heart Association classification?

A

I = no limitation on activity
II = comfortable at rest but symptomatic with ordinary activities
III = comfortable at rest but symptomatic with any activity
IV = symptomatic at rest

64
Q

What type of tachycardia is supraventricular tachycardia?

A

Narrow complex QRS <0.12 seconds

65
Q

What are the types of SVT?

A
  1. AV nodal re-entry tachycardia (AVNRT): where the re-entry point is back through the AV node
  2. AV re-entry tachycardia: where the re-entry point is an accessory pathway e.g. WPW syndrome
  3. Atrial tachycardia: where the signal originates in the atria somewhere other than the SAN node (not re-entry)
66
Q

How do you distinguish between SVT and sinus tachycardia?

A

SVT sudden onset
SVT has a very regular pattern without variability
Sinus tachycardia usually has an explanation e.g. fever, pain

67
Q

What is the initial management of SVT?

A
  1. Vagal manouevres e.g. valsalva (increasing intrathoracic pressure by blowing into empty syringe for 10-15 seconds) or carotid sinus massage (stimulates baroreceptors). This stimulates the parasympathetic nervous system
  2. Adenosine IV (6mg then 12mg then 18mg). Slows cardiac connection primarily through AV node
  3. Verapamil or BB
  4. Synchronised direct current cardioversion (if life threatening features). Must be synchronised as shocking during a T wave can cause VF
68
Q

What is the medical management to prevent episodes of SVT?

A

BB
Radiofrequency ablation

69
Q

What is adenosine CI in?

A

Asthma
HF
Heart block
Severe hypotension

70
Q

What blood tests are raised in myocarditis?

A

Inflammatory markers
Cardiac enzymes
BNP

71
Q

What are the ECG changes in myocarditis?

A

ST segment elevation
T wave inversion

72
Q

What is a late complication of myocarditis?

A

Dilated cardiomyopathy
Heart failure

73
Q
A
74
Q

Give four risk factors for IHD.

A

Smoking
Diabetes
Hypercholesterolaemia
HTN
Family history
Increasing age
Obesity
Sedentary lifestyle

75
Q

Which cardiac enzymes commonly rise following cardiac damage?

A

Troponin
CK-MB
CK
AST
LDH

76
Q

Can you drive after an MI?

A

Not for 4 weeks.
Do not need to inform DVLA.

77
Q

What are possible triggers of angina?

A

Cold/windy weather
Emotion
Lying down
Vivid dreams.

78
Q

What is the mechanism of action of aspirin?

A

COX1 (cycloxygenase) inhibitor

79
Q

Do loop diuretics cause hypo or hyperkalaemia?

A

Hypokalaemia

80
Q

What is the method of action of furosemide?

A

Inhibits the Na-K-2Cl cotransporter is the ascending limb of the loop of Henle, diminishing the osmotic gradient for water reabsorption

81
Q

What does using dogixin in HF show as on an ECG?

A

Reverse tick pattern
ST depression
T wave inversion in V5-V6

82
Q

What are signs of hypertensive retinopathy on fundoscopy?

A

Silver/copper wiring
Cotton wool spots
Papilloedema
Flame haemorrhage
A-V nipping.

83
Q

What are the complications of essential HTN?

A

Heart failure
IHD
Stroke
CKD
Hypertensive retinopathy
Aneurysmal disease
Peripheral vascular disease.

84
Q

What is the mechanism of action of simvastatin?

A

Inhibits HMG-CoA reductase which is the rate limiting step in cholesterol synthesis.

85
Q

What are the signs of hypercholesterolaemia on examination?

A

Xanthelasma
Tendon xanthoma
Corneal arcus

86
Q

What are the common causes of AF?

A

Pneumonia
MI
PE
Hyperthyroidism
Alcohol excess
HF
Endocarditis

87
Q

What are the complications of AF?

A

HF
Stroke
TIA
Systemic emboli
Falls

88
Q

Why is urine dipped in infective endocarditis?

A

Microscopic haematuria

89
Q

What are the boat-shaped retinal haemorrhages with a pale centre on fundcoscopy in IE?

A

Roth spots

90
Q

What criteria is used to make a diagnosis of IE?

A

Duke criteria

91
Q

What are signs of aortic regurgitation?

A

Early diastolic murmur
Collapsing pulse
Wide pulse pressure
Displaced apex beat.

92
Q

Which patients are at increased risk of IE?

A

IV drug users
Prosthetic valves
PDA
VSD
Coarctation
Mitral valve disease
Aortic valve disease e.g. bicuspid

93
Q

How does a posterior MI present?

A
94
Q

Which vessel is implicated for posterior MI?

A

RCA or circumflex

95
Q

How does a posterior STEMI show on an ECG?

A

V1-V3 ST depression
Tall R waves
AvR reciprocal ST elevation

Do posterior leads V7-V9 on the back

96
Q

What BP is needed for nitrates?

A

SBP > 90

97
Q

When is clopidogrel given instead of ticagrelor in NSTEMI?

A

Already on an anticoagulant

98
Q

What are four medications used in chronic heart failure to improve outcomes?

A

BB
ACE-i
Aldosterone antagonist
SGLT2 inhibitors

Loop diuretics are purely symptomatic relief

99
Q
A

Finals (11 decks)

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