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MRCP Cardio > Cardio > Flashcards

Cardio Flashcards

1
Q

Mitral stenosis causes (4)

A

rheumatic fever, mucopolysaccharidoses, carcinoid and endocardial fibroelastosis

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2
Q

What is mitral stenosis

A

blood flow across the mitral valve from the left atrium to the left ventricle. This leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart

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3
Q

Features of mitral stenosis (8)

A
  • dyspnoea
    ↑ left atrial pressure → pulmonary venous hypertension
  • haemoptysis
    due to pulmonary pressures and vascular congestion
    may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins
  • mid-late diastolic murmur (best heard in expiration)
  • loud S1
  • opening snap
    indicates mitral valve leaflets are still mobile
  • low volume pulse
  • malar flush
  • atrial fibrillation
    secondary to ↑ left atrial pressure → left atrial enlargement
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4
Q

Features of severe mitral stenosis (2)

A
  • length of murmur increases
  • opening snap becomes closer to S2
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5
Q

Echo changes of mitral stenosis

A

the normal cross-sectional area of the mitral valve is 4-6 sq cm. A ‘tight’ mitral stenosis implies a cross-sectional area of < 1 sq cm

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6
Q

What is pre-eclampsia?

A
  • condition seen after 20 weeks gestation
  • pregnancy-induced hypertension
  • proteinuria
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7
Q

What is eclampsia?

A
  • seizures
  • condition seen after 20 weeks gestation
  • pregnancy-induced hypertension
  • proteinuria
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8
Q

Magnesium in pre-eclampsia

A

should be given once a decision to deliver has been made
in eclampsia an IV bolus of 4g over 5-10 minutes should be given followed by an infusion of 1g / hour
urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment
respiratory depression can occur: calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression
treatment should continue for 24 hours after last seizure or delivery (around 40% of seizures occur post-partum)

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9
Q

What is Ebstein’s anomaly?

A

congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle. It is sometimes referred to as ‘atrialisation’ of the right ventricle. May be caused by exposure to lithium in-utero.

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10
Q

What is associated with Ebstein’s anomaly?

A
  • patent foramen ovale (PFO) or atrial septal defect (ASD) is seen in at least 80% of patients, resulting in a shunt between the right and left atria
  • Wolff-Parkinson White syndrome
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11
Q

Clinical features of Ebstein’s anomaly (5)

A
  • cyanosis
  • prominent ‘a’ wave in the distended jugular venous pulse,
  • hepatomegaly
  • tricuspid regurgitation
    pansystolic murmur, worse on inspiration
  • right bundle branch block → widely split S1 and S2
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12
Q

Risk factors for infective endocarditis

A
  • The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis.
    previously normal valves (50%, typically acute presentation)
  • the mitral valve is most commonly affected
    rheumatic valve disease (30%)
  • prosthetic valves
    congenital heart defects
    intravenous drug users (IVDUs)
    e.g. typically causing tricuspid lesion)
    others: recent piercings
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13
Q

Most common cause of IE in normal and IVDU

A

Staphylococcus aureus

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14
Q

Most common cause of IE with poor dental hygeine

A

historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries
technically Streptococcus viridans is a pseudotaxonomic term, referring to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are Streptococcus mitis and Streptococcus sanguinis
they are both commonly found in the mouth and in particular dental plaque

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15
Q

Culture -ve causes of IE (5)

A
  • prior antibiotic therapy
  • Coxiella burnetii
  • Bartonella
  • Brucella
  • HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
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16
Q

ECG changes in hypothermia (5)

A
  • bradycardia
  • ‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
  • first degree heart block
  • long QT interval
  • atrial and ventricular arrhythmias
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17
Q

What is Eisenmenger’s syndrome?

A

reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

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18
Q

What is associated with Eisenmenger’s syndrome? (3)

A
  • ventricular septal defect
  • atrial septal defect
  • patent ductus arteriosus
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19
Q

Features of Eisenmenger’s syndrome

A
  • original murmur may disappear
  • cyanosis
  • clubbing
  • right ventricular failure
  • haemoptysis, embolism
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20
Q

Management of Eisenmenger’s syndrome

A

heart-lung transplantation

21
Q

ECG changes post STEMI

A

ST segments gradually return towards normal over two weeks while Q waves persist and T waves flatten or become inverted

22
Q

Cardiac tamponade features (3)

A

Beck’s triad
- hypotension
- raised JVP
- muffled heart sounds

23
Q

What is Wolff-Parkinson-White syndrome?

A

caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.

24
Q

ECG features of WPW (4)

A
  • short PR interval
  • wide QRS complexes with a slurred upstroke - ‘delta wave’
  • left axis deviation if right-sided accessory pathway
    in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation
  • right axis deviation if left-sided accessory pathway
25
Q

Associations of WPW (5)

A
  • HOCM
  • mitral valve prolapse
  • Ebstein’s anomaly
  • thyrotoxicosis
  • secundum ASD
26
Q

Effects of BNP (3)

A
  • vasodilator
  • diuretic and natriuretic
  • suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
27
Q

Where is BNP produced?

A

left ventricular myocardium in response to strain

28
Q

Features of severe AS (8)

A
  • narrow pulse pressure
  • slow rising pulse
  • delayed ESM
  • soft/absent S2
  • S4
  • thrill
  • duration of murmur
  • left ventricular hypertrophy or failure
29
Q

Causes of AS (5)

A
  • degenerative calcification (most common cause in older patients > 65 years)
  • bicuspid aortic valve (most common cause in younger patients < 65 years)
  • William’s syndrome (supravalvular aortic stenosis)
  • post-rheumatic disease
  • subvalvular: HOCM
30
Q

Features suggesting VT rather than SVT with aberrant conduction (7)

A
  • AV dissociation
  • fusion or capture beats
  • positive QRS concordance in chest leads
  • marked left axis deviation
  • history of IHD
  • lack of response to adenosine or carotid sinus massage
  • QRS > 160 ms
31
Q

What causes Pulsus parodoxus (2)

A

Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or
absent pulse in inspiration
* Severe asthma, cardiac tamponade

32
Q

Causes of slow rising/ plateau pulse (1)

A

Aortic stenosis

33
Q

Causes of collapsing pulse (3)

A
  • Aortic regurgitation
  • Patent ductus arteriosus
  • Hyperkinetic (anemia, thyrotoxic, fever, exercise/pregnancy)
34
Q

Causes of pulsus alternans (1)

A

Regular alternation of the force of the arterial pulse
* Severe LVF

35
Q

Causes of bisferiens pulse (1)

A

‘Double pulse’ - two systolic peaks
* Mixed aortic valve disease

36
Q

Causes of Jerky pulse (1)

A

HOCM

37
Q

Causes of S1 heart sound (2)

A

Closure of mitral and tricuspid valve

38
Q

Causes of soft S1 (2)

A
  • Long PR
    -Mitral regurg
39
Q

Causes of loud S1 (1)

A

Mitral stenosis

40
Q

Causes of variable intensity S1 (1)

A

complete heart block

41
Q

Cause of S2 heart sound

A

caused by the closure of the aortic valve (A2) closely followed by that of the pulmonary valve
(P2)

42
Q

Cause of loud S2 (3)

A
  • Hypertension: systemic (loud A2) or pulmonary (loud P2)
  • Hyperdynamic states
  • Atrial septal defect without pulmonary hypertension
43
Q

Causes of soft S2 (1)

A

Aortic stenosis

44
Q

Causes of fixed split S2 (1)

A

Atrial septal defect

45
Q

Causes of widely split S2 (4)

A
  • Deep inspiration
  • RBBB
  • Pulmonary stenosis
  • Severe mitral regurgitation
46
Q

Causes of reversed split S2 (5)

A
  • LBBB
  • Severe aortic stenosis
  • Right ventricular pacing
  • WPW type B (causes early P2)
  • Patent ductus arteriosus
47
Q

Causes of S3

A

Caused by diastolic filling of the ventricle

  • Considered normal if < 30 years old (may persist in women up to 50 years old)
  • Heard in left ventricular failure, constrictive pericarditis
  • Gallop rhythm (S3) is an early sign of LVF
48
Q

Causes of S4

A
  • may be heard in aortic stenosis, HOCM, hypertension
  • caused by atrial contraction against a stiff ventricle
  • in HOCM a double apical impulse may be felt as a result of a palpable S4

MRCP Cardio (1 decks)

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