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Cardiology 2 Flashcards

1
Q

Pre-existing HTN in pregnancy?

A
  1. A history of hypertension before pregnancy or an elevated blood pressure > 140/90 mmHg before 20 weeks gestation
  2. No proteinuria, no oedema
  3. Occurs in 3-5% of pregnancies and is more common in older women
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2
Q

Pregnancy-induced HTN mushkies (aka Gestational HTN?

A
  1. Hypertension (as defined above) occurring in the second half of pregnancy (i.e. after 20 weeks)
  2. No proteinuria, no oedema
  3. Occurs in around 5-7% of pregnancies
  4. Resolves following birth (typically after one month). Women with PIH are at increased risk of future pre-eclampsia or hypertension later in life
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3
Q

Pre-eclampsia mushkies?

A
  1. Pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours)
  2. Oedema may occur but is now less commonly used as a criteria
  3. Occurs in around 5% of pregnancies
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4
Q

Classification of AF?

A
  1. First detected episode (irrespective of whether it is symptomatic or self terminating)
  2. Recurrent episodes = when a patient has 2 or more episodes
    a. Paroxysmal AF = terminates spontaneously, episodes last <7 days, typically <24 hours
    b. Persistent AF = not self terminating, usually last >7 days
  3. Permanent AF = continuous AF which can not be cardioverted –> rate control and anticoagulation
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5
Q

Wellen’s syndrome?

A
  1. ECG manifestation of critical proximal LAD coronary artery stenosis in pts with unstable angina
  2. Characterised by symmetrical, often deep (>2mm) T wave inversions in the anterior precordial leads
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6
Q

Reversal of rivaroxaban or apixaban?

A

Andexanet alfa

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7
Q

What is pulsus alternans?

A
  1. Seen in LVF
  2. When the upstroke of the pulse alternates between strong and weak, indicated systolic dysfunction and is seen in pts with HF
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8
Q

Pulsus paradoxus?

A
  1. Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
  2. Severe asthma, cardiac tamponade
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9
Q

Slow-rising pulse causes?

A
  1. AS

Slow upstroke

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10
Q

Collapsing pulse causes?

A
  1. AR
  2. PDA
  3. Hyperkinetic states = Anaemia, Thyrotoxicosis, Fever, Pregnancy

Forceful rapid upstroke AND descent

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11
Q

Bisferiens pulse causes?

A
  1. Mixed aortic valve disease

2. ‘Double pulse’ due to 2 sharp upstrokes due to systole

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12
Q

Jerky pulse cause?

A
  1. HOCM

2. Rapid forceful upstroke

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13
Q

What percentage of VSDs close spontaneously?

A

50%

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14
Q

Causes of VSDs?

A
  1. Congenital = Downs, Edwards, Pataus, Cri-du-Chat
  2. Congenital infections
  3. Acquired = post-MI
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15
Q

When may VSDs be detected in utero?

A

During the routine 20 week scan

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16
Q

Post-natal presentations of VSDs?

A
  1. Failure to thrive
  2. Features of HF = hepatomegaly, tachypnoea, tachycardia, pallor
  3. Pan-systolic murmur which is louder in smaller defects
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17
Q

Management of VSDs?

A
  1. Small VSDs which are asymptomatic often close spontaneously are simply require monitoring
  2. Moderate to large VSDs usually result in a degree of heart failure in the first few months
    a. nutritional support
    b. medication for heart failure e.g. diuretics
    c. surgical closure of the defect
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18
Q

Complications of VSDs?

A
  1. AR (poorly supported right coronary cusp resulting in cusp prolapse)
  2. IE
  3. Eisenmenger’s
  4. RHF
  5. Pulm HTN
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19
Q

Why is pregnancy c/i in pulmonary hypertension?

A

Carries a 30-50% risk of mortality

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20
Q

Poor prognostic factors for HOCM?

A
  1. Syncope
  2. Family history of sudden death
  3. Young age at presentation
  4. Non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring
  5. Abnormal blood pressure changes on exercise
  6. Increased septal wall thickness
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21
Q

Is risk of falls alone a sufficient reason to withhold anticoagulation?

A
  1. No
  2. A patient with a 5% annual stroke risk (CHADS 2-3) would need to fall approximately 295 times per year for the benefits of anticoagulation to be out-weighed by the risk of fall-related intracranial haemorrhage
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22
Q

AF + valvular heart disease is an absolute indication for?

A

Anticoagulation

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23
Q

What is eclampsia?

A

Development of seizures in association with pre-eclampia

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24
Q

Pre-eclampsia?

A
  1. Condition seen after 20 weeks gestation
  2. Pregnancy-induced hypertension
  3. Proteinuria
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25
Q

What is used to prevent seizures in pts with severe pre-eclampsia and treat seizures once they develop?

A

Magnesium sulphate

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26
Q

Mag sulphate dose for eclampsia?

A
  1. IV bolus of 4g over 5-10 minutes

2. Followed by infusion of 1g/hour

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27
Q

What should be monitored whilst pt on mag sulph for severe pre-eclampsia/eclampsia?

A
  1. Urine output
  2. Reflexes
  3. Respiratory rate
  4. Oxygen saturation
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28
Q

Complication of mag sulph for eclampsia?

A

Respiratory depression

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29
Q

Mx of respiratory depression secondary to magnesium su;phate?

A

Calcium gluconate

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30
Q

How long should mag sulph continue after delivery in severe pre-eclampsia?

A

For 24 hours after last seizure or delivery (around 40% seizures occur post-partum)

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31
Q

Severe pre-eclampsia/eclampsia fluid management?

A

Fluid restriction

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32
Q

Statin MOA?

A

Inhibits action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis

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33
Q

Statin adverse effects?

A
  1. Myopathy
  2. Liver impairment
  3. Increased risk of intracerebral haemorrhage in pts who have had a stroke
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34
Q

Statin C/i?

A
  1. Macrolides

2. Pregnancy

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35
Q

Statin LFT monitoring?

A
  1. Baseline, 3m, 12 months
  2. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3x the upper limit of the reference range
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36
Q

Statin indications?

A
  1. Established CVD (stroke, TIA, IHD, PAD)
  2. 10 year cardiovascular risk >10%
  3. T1DM diagnosed >10 years ago OR aged >4- OR have established nephropathy
  4. CKD eGFR <60ml/min
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37
Q

Why are statins taken at night?

A

When majority of cholesterol synthesis takes place

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38
Q

Atorvastatin primary prevention?

A

20mg

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39
Q

Atorvastatin secondary prevention?

A

80mh

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40
Q

When do you increase atorvastatin 20mg?

A

If non-HDL has not reduced for >=40%, consider uptitrating to 80mg

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41
Q

What is WPW syndrome?

A

Congenital accessory conducting pathway between the atria and ventricles leading to AVRT - as the accessory pathway does not slow conduction, AF can degenerate rapidly to VF

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42
Q

WPW ECG features?

A
  1. Short PR interval
  2. Wide QRS complexes with slurred upstroke - delta wave
  3. LAD if right sided accessory pathway
  4. RAD if left sided accessory patway
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43
Q

Type A WPW?

A
  1. Left sided pathway

2. Dominant R wave in V1

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44
Q

Type B WPW?

A
  1. Right sided pathway

2. No dominant R wave in V1

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45
Q

WPW associations?

A

HEMAT

  1. HOCM
  2. Ebstein’s anomaly
  3. Mitral valve prolapse
  4. Secundum ASD
  5. Thyrotoxicosis
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46
Q

WPW management?

A
  1. Definitive = RFA of accessory pathway

2. Medical = sotalol, amiodarone, fleicanide

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47
Q

Type C WPW?

A

Delta waves are upright in leads V1-V4 but negative in V5-V6

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48
Q

When should sotalol be avoided in WPW?

A

If coexistent AF - prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

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49
Q

How is PCWP measured?

A

Using a balloon-tipped Swan-Ganz catheter which is inserted into the pulmonary artery

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50
Q

What is PCWP indicative of?

A

LA pressure, normally 6-12mmHg

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51
Q

Main use of PCWP?

A

Whether pulmonary oedema is caused by either HF or ARDS

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52
Q

Atropine MOA?

A

Muscarinic AChR antagonist

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53
Q

Atropine use?

A
  1. Organophosphate poisoning

2. Bradycardia

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54
Q

Physiological effects of atropine?

A
  1. Tachycardia

2. Mydriasis

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55
Q

Biggest RF for post-PCI stent thrombosis?

A

Withdrawal of antiplatelets

56
Q

PCI stent MOA?

A
  1. Following stent insertion, migration and proliferation of smooth muscle cells and fibroblasts occur to the treated segment
  2. The stent struts eventually become covered by endothelium
  3. Until this happens there is an increased risk of platelet aggregation leading to thrombosis
57
Q

2 main complications of PCI stent?

A
  1. Stent Thrombosis = due to platelet aggregation, occurs in 1-2% of patients, most commonly in first month, usually presents with acute MI
  2. Stent Restenosis = due to excessive tissue proliferation around the stent, occurs in 5-20% of patients, most common in the first 3-6 months, usually presents with recurrence of angina symptoms
58
Q

RFs for stent restenosis?

A
  1. DM
  2. Renal impairment
  3. Stents in venous bypass grafts
59
Q

Types of stents?

A
  1. Bare metal stents (BMS)

2. Drug-eluting stents (DES)

60
Q

What is a drug-eluting stent?

A
  1. Coated with paclitaxel or rapamycin which inhibit local tissue growth
  2. Whilst this reduces restenosis rates, the stent thrombosis rates are increased as the process of stent endothelialisation is slowed
61
Q

Antiplatelet therapy following stent insertion?

A
  1. Aspirin indefinitely

2. Clopidogrel length depends on type of stent, reason for insertion, and consultant preference

62
Q

Complete heart block following an MI lesion?

A

Right coronary artery

63
Q

Severe mitral stenosis management?

A

Percutaneous mitral commissurotomy

64
Q

Causes of mitral stenosis?

A
  1. Rheumatic fever
  2. Mucopolysaccharidoses
  3. Carcinoid syndrome
  4. Endocardial fibroelastosis
65
Q

Mitral stenosis CXR?

A

LA enlargement

66
Q

Mitral stenosis Echo?

A
  1. Cross sectional ares <1sq cm

2. (Usually cross-sectional area 4-6cm)

67
Q

Amiodarone effect on QT interval?

A

Lengthens QT interval

68
Q

Most common cause of secondary hypertension?

A

Primary hyperaldosteronism incl. Conn’s

69
Q

Classification of secondary hypertension?

A
  1. Renal
  2. Endocrine
  3. Drugs
  4. Other
70
Q

Renal causes of hypertension?

A
  1. GN
  2. PN
  3. ADPKD
  4. RAS
71
Q

Endocrine causes of hypertension?

A
  1. Primary hyperaldosteronism (most common)
  2. Cushing’s syndrome
  3. Liddle’s syndrome
  4. CAH (11-beta hydroxylase activity)
  5. Acromegaly
72
Q

Drug causes of hypertension?

A
  1. Steroids
  2. MOAi
  3. COCP
  4. NSAIDs
  5. Leflunomide
73
Q

‘Other’ causes of hypertension?

A
  1. Pregnancy

2. Coarctation of the aorta

74
Q

Cardiac tamponade presentation?

A

Beck’s triad

  1. Falling BP
  2. Rising JVP
  3. Muffled heart sounds
75
Q

Mx of cardiac tamponade?

A

Urgent pericardiocentesis

76
Q

How long should DAPT be present post insertion of DES?

A

12 months, very important

77
Q

Within how many hours should PCI be offered to NSTEMI pts?

A

Within 72 hours

78
Q

Tirofiban MOA?

A

GpIIb/IIIa inhibitor

79
Q

GpIIb/IIIa inhibitor examples?

A
  1. Abciximab
  2. Eptifibatide
  3. Tirofiban
80
Q

Aortic dissection pathophysiology?

A

Tear in the tunica intima of the wall of the aorta

81
Q

Aortic dissection RFs?

A
  1. HTN
  2. Trauma
  3. Bicuspid aortic valve
  4. Collagen = MS, EDS
  5. Congenital = Turners, Noonans
  6. Pregnancy
  7. Syphilis
82
Q

Cause of short PR interval?

83
Q

Causes of a prolonged PR interval?

A
  1. Idiopathic
  2. IHD
  3. Infection = rheumatic fever, aortic root abscess due to endocarditis, lyme disease
  4. Inflammatory = sarcoidosis
  5. Drugs = digoxin
  6. Electrolytes = hypokalaemia
  7. Neuro = myotonic dystrophy
  8. Athletes
84
Q

Causes of LBBB?

A
  1. IHD
  2. HTN
  3. AS
  4. CM
  5. Rare = Idiopathic fibrosis, digoxin toxicity, hyperkalaemia
85
Q

Diagnosing MI in pts with existing LBBB?

A

Sgarbossa criteria

86
Q

Aortic dissection on CXR?

A

Separation of the intimal calcification from the outer aortic soft tissue by border by 10mm

87
Q

Ix for Aortic dissection?

A

CT chest with contrast

88
Q

Pts on warfarin undergoing emergency surgery?

A

Give four-factor prothrombin complex concentrate 25-50 units/kg

89
Q

Pts on warfarin undergoing surgery in 6-8 hours?

A

5mg Vitamin K IV

90
Q

Bicuspid aortic valve associations?

A
  1. Turner’s syndrome
  2. Left dominant coronary circulation (the posterior descending artery arises from the circumflex instead of the right coronary artery)
  3. Coarctation of the aorta
91
Q

Complications of bicuspid aortic valve?

A
  1. Stenosis/regurgitation

2. Higher risk for aortic dissection and aneurysm formation of the ascending aorta

92
Q

Suspected DVT in pregnancy Ix?

A

Compression duplex ultrasound

93
Q

Suspected PE in pregnancy Ix?

A
  1. ECG and CXR
  2. Compression duplex ultrasound
  3. V/Q or CTPA should be taken at a local level after discussion with the pt and radiologist
94
Q

CTPA pregnancy risk?

A

Increases lifetime risk of maternal breast cancer by 13.6%

95
Q

V/Q scanning pregnancy risk?

A

Increased risk of childhood cancer compared with CTPA

96
Q

D-dimer used for PE in pregnancy?

97
Q

Bisferiens pulse?

A

Mixed aortic valve disease

98
Q

Statins and pregnancy?

A

Should be avoided in pregnancy and also 3 months before attempting pregnancy

99
Q

Most common gene mutation for Brugada syndrome?

A

Mutations in the SCN5A gene (encode myocardial sodium ion channel protein)

100
Q

CPVT (catecholaminergic polymorphic ventricular tachycardia) mutation?

101
Q

Romano-Ward syndrome genes?

A
  1. KCNQ1

2. KCNH2

102
Q

ARVC gene?

103
Q

What is Brugada syndrome?

A

A form of inherited cardiovascular disease which may present with sudden cardiac death

104
Q

Brugada inheritance?

A
  1. AD
  2. 1:5000-10,000
  3. Asians
105
Q

Brugada syndrome ECG changes?

A
  1. Convex ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave
  2. Partial RBBB
  3. ECG changes may be more apparent following the administration of fleicanide or ajmaline (the investigation of choice in suspected cases of Brugada)
106
Q

Brugada syndrome management?

107
Q

PFO present in what percentage of population?

108
Q

Wilson’s disease associated with what cardiomyopathy?

A

Restrictive cardiomyopathy

109
Q

MAT?

A

Multifocal atrial tachycardia

110
Q

What is Multifocal atrial tachycardia?

A

Irregular cardiac rhythm caused by at least 3 different sites in the atria, which may be demonstrated by morphologically distinctive p waves

111
Q

MAT is more common in what pts?

A

Elderly pts with chronic lung disease e.g. COPD

112
Q

Mx of MAT?

A
  1. Correction of hypoxia and electrolyte disturbances
  2. Rate-limiting CCBs are often first line
  3. Cardioversion and digoxin are not useful in the management of MAT
113
Q

Ix of aortic dissection?

A
  1. CXR = widened mediastinum
  2. CT Angio of chest = false lumen
  3. TOE = usntable pts too risky to take to CT
114
Q

Mx of aortic dissection?

A
  1. Type A = surgical management, but blood pressure should be controlled to a target systolic 100-120 whilst awaiting intervention
  2. Type B = conservative management, bed rest, reduce blood pressure with IV labetalol to prevent progression
115
Q

Complications of aortic dissection?

A
  1. Backward tear = aortic incompetence/regurgitation, MI (inferior pattern due to right coronary involvement)
  2. Forward Tear = unequal arm pulses and BP, stroke, renal failure
116
Q

Management of xanthelasma?

A
  1. Surgical excision
  2. Topical trichloroacetic acid
  3. Laser therapy
  4. Electrodissection
117
Q

Causes of ST elevation?

A
  1. MI
  2. Myocarditis/pericarditis
  3. Normal variant ‘high take-off’
  4. LV aneurysm
  5. Prinzmetal’s angina
  6. Takotsubo’s cardiomyopathy
  7. Rare = SAH
118
Q

AR causes?

A
  1. Valve = Rheumatic, IE, CTD (e.g. RA/SLE), bicuspid

2. Aortic root = Dissection, Ank Spond, HTN, Syphilis, MS + EDS

119
Q

LAD causes?

A
  1. Left anterior hemiblock
  2. LBBB
  3. Inferior MI
  4. WPW right sided
  5. Hyperkalaemia
  6. Congenital = ostium primum ASD, tricuspid atresia
  7. Minor LAD in obese people
120
Q

Tachycardia with rate of 150/min?

A

Atrial flutter

121
Q

What is atrial flutter?

A

A form of SVT characterised by a succession of rapid atrial depolarisation waves

122
Q

Atrial flutter ECG?

A
  1. Sawtooth
  2. As underlying atrial rate is around 300/min the ventricular rate is dependent upon the degree of AV block
  3. Flutter waves may be visible following carotid sinus massage or adenosine
123
Q

Atrial flutter management?

A
  1. Similar to AF though medication may be less effective
  2. More sensitive to cardioversion, so less energy may be used
  3. RFA of tricuspid valve isthmus is curative for most patients
124
Q

What system used to stratify risk post-MI?

A

Killip class

125
Q

Killip classes?

A

Class = Features = 30 day mortality

  1. I = no clinical signs of HF –> 6%
  2. II = lung crackles, S3 = 17%
  3. III = Frank pulmonary oedema = 38%
  4. IV = Cardiogenic shock = 81%
126
Q

Is WPW an indication for ICD?

127
Q

ICD indications?

A
  1. LQTS
  2. HOCM
  3. Prev. cardiac arrest due to VT/VF
  4. Previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35%
  5. Brugada syndrome
128
Q

Pre-eclampsia complications?

A
  1. Fetal = prematurity, IUGR
  2. Eclampsia
  3. Haemorrhage = placental abruption, intra-abdominal, intra-cerebral
  4. Cardiac Failure
  5. Multi-organ failure
129
Q

Features of severe pre-eclampsia?

A
  1. HTN >170/110
  2. Proteinuria ++/+++
  3. Headache
  4. Visual disturbance
  5. Papilloedema
  6. RUQ/epigastric pain
  7. Hyperreflexia
  8. Ply count <100, abnormal liver enzymes or HELLP
130
Q

Prinzmetal angina treatment?

A

Dihydropyridine receptor calcium channel blocker e.g. Felodipine

131
Q

Infective endocarditis diagnosis?

A

Modified Duke Criteria

  1. Pathological criteria positive OR
  2. 2 major criteria OR
  3. 1 major and 3 minor criteria OR
  4. 5 minor criteria
132
Q

IE Pathological criteria?

A

Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)

133
Q

IE major criteria?

A
  1. Positive Blood Cultures

2. Evidence of endocardial involvement = positive echo or new valvular regurgitation

134
Q

IE minor criteria?

A
  1. Predisposing heart condition or IVDU
  2. Microbiological evidence that doesnt meet major criteria
  3. Fever > 38
  4. Vascular phenomena
  5. Immunological phenomena
135
Q

Most common cause of VT clinically?

A

Hypokalaemia, followed by hypomagnesaemia

136
Q

Causes of ST depression?

A
  1. Secondary to abnormal QRS (LVH, LBBB, RBBB)
  2. Ischaemia
  3. Digoxin
  4. Hypokalaemia
  5. Syndrome X

MRCP Part 1 (4 decks)

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