Cardiology Flashcards

1
Q

Commonest cardiomyopathy

A

Dilated

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2
Q

What is the pathophysiology behind dilated cardiomypathy?

A

Systolic dysfunction

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3
Q

Why/When do you hear third heart sound S3?

A

Filling of the ventricle

Dilated cardiomyopathy, mitral regurg, constrictive pericarditis,

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4
Q

Why/when do you hear S4?

A

Caused by atrial contraction against a stiff ventricle (coincides with p wave)

e.g. in Ao stenosis, HOCM, HTN

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5
Q

What causes S1?

A

Closure of mitral/tricuspid valve

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6
Q

What causes S2?

A

Closure of Ao/pulmonary valves

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7
Q

How does ANP work?

A

released in response to increased blood volume / HTN

Causes vasodilation:

  • natriuretic, i.e. promotes excretion of sodium
  • lowers BP
  • antagonises actions of angiotensin II, aldosterone
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8
Q

What is associated with variability in intensity of S1?

A

Complete heart block

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9
Q

What is associated with loud S1

A

Mitral stenosis

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10
Q

Describe mitral regurg heart sounds

A

Quiet S1
Widely split s2
S3

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11
Q

most common cause Infective endocarditis?

A

Staph aureus

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12
Q

what is the commonest cause of infective endocarditis in prosthetic valve (in first two months post surgery)? + indwelling lines

A

Staph epidermidis / coagulase negative staph

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13
Q

give ECG changes in digoxin toxicity?

A
bradycardia or AV block
a short QT interval
a prolonged PR interval
ST depression
inverted T waves
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14
Q

What ECG changes are pericarditis associated with?

A

ST elevation

PR depression

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15
Q

Chest pain following MI 6 weeks. What is the likely cause

A

Dressler’s - autoimmune pericarditis

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16
Q

What type of pulse seen in hypertrophic cardiomypathy?

A

Jerky pulse

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17
Q

Causes of left axis deviation?

A

left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway (GOES RIGHT TO LEFT)
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people

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18
Q

Causes of right axis devation?

A
right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome* - left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people

N.b. WPW usually LAD - if Q asks

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19
Q

What is cardiac axis? What is normal?

A

The axis of the ECG is the major direction of the overall electrical activity of the heart

+90 to -30

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20
Q

What is the mechanism of amiodarone?

A

K+ channel blocker inhibiting repolarisation and prolonging action potential

[also blocks other channels -

(class III antiarhythmic)

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21
Q

Why are loading doses used with amiodarone?

A

Long half life

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22
Q

What is the mechanism of class 1 antiarrhythmics? Give the types/ examples for each

A

Sodium channel blockers (prevent influx of sodium into myocytes –> slower depolarisation [decreasing the slope in phase 0])

1a: procainamide
1b: lidocaine
1c: flecainide

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23
Q

What is the mechanism of class II antiarhythmics?

A

beta-blockers (e.g. metoprolol or propranolol)

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24
Q

What is the mechanism of class III antiarhythmics? How do they affect ECGs?

A

K+ channel blockers inhibiting repolarisation and prolonging action potential

Wider/longer QRS and long QT (potential for other arrhythmias)

E.g. amiodarone

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25
Q

What is the mechanism of class III antiarhythmics?

A

Calcium channel blockers - prevents influx of calcium into cell

also used in lowering BP (prevents smooth muscle contraction in vessels)

e.g. verapamil + diltiazem

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26
Q

Where should you ideally give amiodarone?

A

via a central line - due to extravasation

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27
Q

What causes a widely split S2?

A

Pulmonary stenosis
RBBB
Deep inspiration
severe mitral regurg

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28
Q

What causes a loud S2

A

Pulmonary and/or systemic HTN

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29
Q

Cause of soft S2

A

Aortic stenosis

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30
Q

Causes of a fixed split S2

A

ASD

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31
Q

What is the ECG finding in brugada syndrome?

A

Convex ST elevation V1-3 with T wave inversion (TWI)

Partial RBBB

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32
Q

What is the pathophysiology of brugada syndrome?

A

Inherited A.D. - sodium channel gene mutation

Predisposes to ventricular tachcyardias

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33
Q

What ECG changes seen in pericarditis?

A
PR depression
ST elevation (saddle)
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34
Q

What is peri-arrest tachycardia? what is the NICE guideline for treatment?

A

Unstable: shock (hypotension, pallor, sweating, confusion etc); syncope; myocardial ischaemia; heart failure [e.g. raised JVP, crackles etc]

NICE simplified into 1 unified algorithm –> give up to 3 Synchronised DC shocks

Treatment following this is if the QRS is broad or narrow + whether irregular or regular

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35
Q

What is the treatment for broad complex tachycardias?

A

Regular:
Treat as ventricular tachcyardia (unless previously confirmed SVT with BBB) –> load amiodarone following by 24hour infusion

Irregular:
either AF with BBB
AF with ventricular pre-excitation
Or torsades de pointes

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36
Q

What is the treatment for narrow complex tachycardias?

A

Regular:
Vagal manouevres –> IV adenosine
If unsuccessful - consider atrial flutter + control rate

Irregular (probable AF)

  • If onset <48hrs - electrical or chemical cardioversion
  • beta blockade >48hours
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37
Q

Unprovoked PE length of treatment?

A

6 months

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38
Q

Provoked PE treatment length

A

3 months

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39
Q

What condition is associated with Inherited long QT syndrome AND sensorineural deafness?

A

Jarvell-Lange-nielson syndrome

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40
Q

Congenital causes of long QT syndrome

A

Jervell-Lange-Nielsen syndrome (assoc with sensorineural deafness)

Romano-Ward syndrome (no deafness)

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41
Q

Drug causes of long QT syndrme

A
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron
42
Q

electrolyte imbalance causes of long QT

A

Hypocalcaemia
Hypokalaemia
Hypomagnasaemia

43
Q

target INR for mechanical valves?

A

Aortic - 3.0

Mitral - 3.5

44
Q

Medications to give for prosthetic valves?

A

bioprosthetic: aspirin
mechanical: warfarin + aspirin

45
Q

What infective endocarditis bacteria is associated with patients with colon cancer?

A

Streptococcus bovis

46
Q

what infective endocarditis bacteria is associated with

A

Strep viridans (mitis + sanguinis)

47
Q

Angina Management

A

All patients: lifetyle changes, adpirin + statin, sublinguial GTN spray

First line: beta blocker OR CCB (use rate limiting - e.g. verapamil)

If poor response: increase to maximum dose

If still symptomatic: add beta blocker or CCB
If cannot tolerate addition - long acting nitrate (e.g. ISMN)

If still symptomatic: PCI or CABG

48
Q

Contraindications for beta blockers

A

Peripheral vascular diseases
Diabetes mellitus
Chronic obstructive pulmonary disease (COPD)
Asthma

49
Q

Mechanism of action of digoxin

A

K+/Na+ ATPase inhibitor. Na+ rises in myocytes/intracellular –> calcium influx –> increased contractility of heart –> improved CO

50
Q

Problem with flecainide as an antiarrhythmic

A

Pro-arrhythmic

51
Q

Indications for a temporary pacemaker

A

symptomatic/haemodynamically unstable bradycardia, not responding to atropine
post-ANTERIOR MI: type 2 or complete heart block*
trifascicular block prior to surgery

52
Q

When are JVP cannon waves seen

A

In states where the atria + ventricle contraction is not coordinated:
e.g. ventricular tachcyardia, complete heart block, atrial flutter

53
Q

Hypertension management:

Poorly controlled hypertension, already taking an ACE inhibitor, calcium channel blocker and a standard-dose thiazide diuretic. K+ > 4.5mmol/l. What should be added next?

A

alpha or beta blocker

54
Q

Poorly controlled hypertension, already taking an ACE inhibitor, calcium channel blocker and a standard-dose thiazide diuretic. K+ < 4.5mmol/l. What should be added next?

A

Add spironolactone

55
Q

What drug to avoid in HOCM?

A

ACE-i’s, nitrates, inotropes

ACE inhibitors can reduce afterload which may worsen the LVOT gradient (LVOT obstruction in HOCM)

56
Q

Treatment for HOCM?

A

ABCDE:

Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
57
Q

How to calculate ventricular ejection fraction?

A

(Stroke volume / end diastolic LV volume) x 100

58
Q

How to calculate stroke volume?

A

end diastolic LV volume - end systolic LV volume

59
Q

Causes of prolonged PR interval

A
idiopathic
ischaemic heart disease
digoxin toxicity
hypokalaemia*
rheumatic fever
aortic root pathology e.g. abscess secondary to endocarditis
Lyme disease
sarcoidosis
myotonic dystrophy
60
Q

What is ebstein’s anomaly?

What valve defect is seen?

What arrhythmia is it associated with?

A

congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle

Tricuspid regurg

WPW (/SVT)

61
Q

How do you decide the appropriate treatment for primary pulmonary hypertension?

A

Acute vasodilator testing -

shows if patients have a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide

62
Q

What is the treatment for primary pulmonayr HTN if patient shows a positive response to vasodilator testing?

A

(Minority of patients)

Oral CCB’s

63
Q

What is the treatment for primary pulmonayr HTN if patient shows a negative response to vasodilator testing?

A

(Most patients)

  1. Prostacyclin analogues (e.g. iloprost)
  2. endothelin receptor antagonists (e.g. bosentan)
  3. Phosphodiesterase inhibitors (e.g. sildenafil)
64
Q

Long QT drugs

A
THE MASCOTS:
• Terfenadine
• Haloperidol
• Erythromycin
• Methadone
• Amiodarone
• Sotalol
• Chloroquine
• Ondansetron
• TCAs
• SSRIs
65
Q

MoA fondaparinux

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

66
Q

What organism is associated with IE in colorectal cancer?

A

Strep bovis

67
Q

Commonest cause IE?

A

Staph aureus

68
Q

Cause of IE in patients prosthetic valve <2 months?

A

Staph epidermidis

69
Q

What are the anticoagulation strategies for CHA2DS2-VASc scores?

A

0 No treatment

1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)

2 or more Offer anticoagulation

70
Q

What is seen on histology in rheumatic heart disease?

A

Aschoff bodies (granulomatous nodules)

71
Q

What CV drugs cause glucose intolerance?

A

Thiazides + loop diuretics

Beta blockers

72
Q

Example of thiazide like diuretic?

A

Indapamide

73
Q

Common side effect of ticagrelor?

A

Dyspnoea

74
Q

What type of drug is dipyridamole? MoA?

A

Antiplatelet

inhibition of platelet cAMP-phosphodiesterase

75
Q

Following ACS what is the antiplatelet management plan?

A
Aspirin lifelong (clopi if CI'ed)
AND 12 months ticagrelor
76
Q

Ticagrelor MoA

A

Antiplatelet

Same as clopi: P2Y12 inhibitor

77
Q

TIA/Stroke antiplatelet plan?

A

Clopidogrel lifelong

OR if CI’ed Aspirin + dipirydamole lifelong

78
Q

What drug causes closure of PDA? What keeps it open?

A

NSAID/ibuprofen or indomethacin (closes)

Opens: PG’s

79
Q

Prior to starting antihypertensives what should you do?

A

confirm a diagnosis of HTN with ABPM/HBPM

80
Q

What is double duct sign?

A

dilatation of the pancreatic duct and common bile ducts seen on CT suggestive of cholangiocarcinoma or pancreatic cancer

81
Q

EXAM Q: what is the treatment for paroxysmal AF (if patient has no structural heart disease)?

A

Flecainide

However, if haemodynamic instability –> DC cardioversion

82
Q

In pulseless VT in ALS algorithm what should you give if no response to 300mg amiodarone?

A

150mg amiodarone

83
Q

EXAM Q: if patient has fast AF but also has asthma and heart failure with reduced what should you use to control rate?

A

Digoxin

CANT USE b blocker as asthma and can’t use rate limiting CCBs (diltiazem or verapamil) as heart failure (remember rate limiting CCBs cause worsening of heart failure as negatively inotropic)

84
Q

Drugs contraindicated in heart failure

A

CCBs rate limiting - not verapamil

85
Q

What CCB is safe to use in HF with reduced ejection fraction

A

Amlodipine

86
Q

Example of endothelin-1 receptor antagonist

A

-sentan

E.g, bosentan, ambrisentan

87
Q

In pulmonary hypertension what drugs should be used if positive response to vasodilating testing and if negative?

A

Positive: oral CCB

Negative:

  1. endothelin 1 antagonist eg bosentan, ambrisentan
  2. Iloprost (PG analogue)
  3. phosphodiesterase inhibitors: sildenafil
88
Q

In infective endocarditis, what ECG sign makes you worried of aortic root abscess?

A

Prolonged PR

Requires surgery

89
Q

What complete heart block should you not insert pacemaker?

A

If followed by INFERIOR MI (as usually resolves)

90
Q

Most specific finding in acute pericarditis

A

PR depression

91
Q

What drug makes clopidogrel less effective?

A

Omeprazole

92
Q

Complete heart block following MI, what artery?

A

RCA

93
Q

Commonest causes of Aortic stenosis <65 and >65?

A

<65 bicuspid ao valve

> 65 calcification

94
Q

Bisferiens pulse?

A

Mixed aortic valve disease

95
Q

What drug should not be prescribed in VT and why?

A

Verapamil/CCB

Precipitates VF

class IV antiarrhythmic which only acts on nodal tissue and significantly increase the risk of ventricular fibrillation.

96
Q

Definitive treatment for Mitral stenosis

A

Percutaneous mitral commissurotomy

97
Q

If patient with CHF is on ace-i and beta blocker but is deteriorating what should you add next to improve prognosis?

A

Spironolactone

98
Q

Is psoriasis a risk factor for CVD?

A

Yes

99
Q

Trio of treatments recommended whilst awaiting PCI?

A

Aspirin
Clopidogrel
Prasugrel

100
Q

MOA of presugrel

A

Irreversibly blocks P2Y12 at ADP receptors

same as clopidogrel