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MRCP Combined > Cardio > Flashcards

Cardio Flashcards

1
Q

What occurs to blood pressure during exercise?

A

Systolic increases, diastolic decreases - leads to increased pulse pressure

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2
Q

Why does cardiac output increase during exercise?

A

Venous constriction, increased venous return, increased myocardial contractibility

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3
Q

Why does systemic vascular resistance fall during exercise?

A

Vasodilation in skeletal muscles

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4
Q

What are the stages of Valsalva maneouvre?

A
  1. Increased intra-thoracic pressure
  2. Resultant increases in venous and right atrial pressures reduces venous return
  3. Reduced preload leads to a fall in cardiac output (Frank Starling mechanism)
  4. When the pressure is released there is a further slight fall in cardiac output due to increased aortic volume
  5. Return of normal cardiac output
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5
Q

In what conditions are S1 and S2 soft?

A

S1: soft in MS
S2: soft in AS

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6
Q

When is S3 normal

A

<30 years or women <50 years

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7
Q

What is a pathological cause of S3?

A

Left ventricular failure
MR
Constrictive pericarditis

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8
Q

What causes S4?

A

Atrial contraction against a stiff ventricle

AS, HOCM, Hypertension

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9
Q

What does the left coronary artery turn into?

A

LAD and circumflex

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10
Q

What does the right coronary artery turn into?

A

Posterior descending

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11
Q

Which artery supplies the SA node in 60% and AV node in 90%?

A

Right coronary

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12
Q

What is bicuspid aortic valve associated with?

A

Left dominant coronary circulation, where the posterior descending artery arises from the circumflex instead of the right coronary

+ Turner’s syndrome, coarctation of the aorta

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13
Q

Which cardiac abnormality is most common in Down’s syndrome?

A

AVSD

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14
Q

What murmur is heard in ASD?

A

Ejection systolic, louder on inspiration, fixed split S2

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15
Q

What is ASD associated with?

A

Ebstein’s anomaly, foetal alcohol syndrome

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16
Q

What is Ebstein’s anomaly?

A

Tricuspid leaflet dysplasia, apical displacement of the tricuspid annulus, abnormalities of RA and RV

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17
Q

What are the signs of tricuspid regurgitation?

A

Pansystolic murmur
Prominent V waves in JVP
Pulsatile hepatomegaly
Left parasternal heave

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18
Q

What is a risk factor for Ebstein’s anomaly?

A

Exposure to lithium in utero

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19
Q

What is Ebstein’s anomaly associated with?

A

PFO/ASD

WPW

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20
Q

What are the signs of Ebstein’s anomaly?

A 
Cyanosis
Prominent a wave in JVP
Hepatomegaly
TR
RBBB --> widely split S1 and S2
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21
Q

What type of coarctation of the aorta is more common in adults?

A

Postductal (distal to the ductus arteriosus) which occurs after the left subclavian artery branches from the aorta

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22
Q

What are the signs of coarctation of the aorta?

A

Infancy - heart failure
Adults - HTN

Radiofemoral delay
Midsystolic murmur, maximal over back
Apical click
Notching of inferior border of ribs

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23
Q

Which cardiac enzyme is the first to rise in cardiac damage?

A

Myoglobin

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24
Q

What is the first line investigation in stable cardiac chest pain?

A

CT coronary angiography

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25
Q

What 3 other imaging modalities are 2nd line in investigating stable cardiac chest pain, looking for reversible myocardial ischaemia?

A

MPS with SPECT
Stress echo
MR perfusion

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26
Q

What is the 3rd line investigation in stable cardiac chest pain?

A

Invasive coronary angiography

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27
Q

What are the indications for exercise tolerance tests?

A

Assessing patients with suspected angina

Risk stratifying post MI/HOCM

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28
Q

When is exercise tolerance contraindicated?

A 
MI<7 days
Unstable angina
Systolic BP>180bpm or <90bpm
AS
LBBB
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29
Q

What artery supplies the lateral aspect of the heart and which leads does this correspond to?

A

Circumflex

V5, V6, I

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30
Q

What artery supplies the anterior of the heart and which leads does this correspond to?

A

LAD

V1-V4

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31
Q

Which artery supplies the inferior aspect of the heart and which leads does this correspond to?

A

Right coronary

II, III, aVF

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32
Q

What is the ECG criteria for STEMI?

A

ECG changes in 2 or more contiguous leads and persist for >20 minutes:

V2-V3:
Women: 1.5mm STE
Men>40: 2mm STE
Men<40: 2.5mm STE

All other leads:
1mm STE
New LBBB

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33
Q

What is the management of blood glucose in T2DM post MI?

A

IV insulin

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34
Q

What is the general management of STEMI?

A

300mg aspirin
Oxygen if SpO2 <94%
Morphine/nitrates
PCI within 120 minutes OR fibrinolysis

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35
Q

What medications are given prior/during PCI?

A

Prasugrel

Radial access: Unfractionated heparin + bailout GPIIb/IIIa inhibitor

Femoral access: bivalirudin + bailout GPI

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36
Q

What medications are given prior/during fibrinolysis?

A

Antithrombin

Ticagrelor post procedure

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37
Q

What measures are taken if patient is high bleeding risk?

A

If having PCI: swap prasugrel to ticagrelor

If being thrombolysed: swap ticagrelor for clopidogrel

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38
Q

What type of stent is used in PCI?

A

Drug eluting to reduce the risk of restenosis

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39
Q

What type of access if preferred in PCI?

A

Radial

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40
Q

In the PCI pathway, if a patient is already taking anticoagulation, what changes are made to the drugs?

A

Aspirin 300mg as normal

Instead of prasugrel, give clopidogrel

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41
Q

What other procedure are performed during PCI?

A

Thrombus aspiration

Complete revascularisation

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42
Q

What is the general management of NSTEMI?

A

Aspirin 300mg

Estimate 6 month mortality:
Low risk - ticagrelor, fondaparinux
High risk - PCI

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43
Q

Why are nitrates avoided in RV infarct?

A

Reduces preload

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44
Q

How is 6 month mortality estimated in NSTEMI?

A

GRACE

Uses age, HR, BP, cardiac (Killip class), renal function, cardiac arrest of presentation, ECG findings, trop levels

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45
Q

What are 5 differentials for ST elevation?

A 
Pericarditis/myocarditis
Normal variant - high take off
Left ventricular aneurysm
Prinzmetal's angina
Takotsubo cardiomyopathy
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46
Q

What is the general management of angina?

A

Aspirin
Statin
SL GTN spray PRN

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47
Q

What is the first line treatment of angina?

A

BB or CCB

If CCB monotherapy - rate limiting e.g. verapamil/diltiazem

Increase to max tolerated dose

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48
Q

What is the second line treatment of angina?

A

BB and CCB

CCB must be dihydropyridine e.g. nifedipine, if combining with BB

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49
Q

What is the third line treatment of angina?

A

Long acting nitrate
Ivabradine
Nicorandil
Ranolazine

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50
Q

What is the treatment of Prinzmetal’s angina?

A

Dihydropyridine CCB

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51
Q

What is the most common cause of arrest in MI?

A

VF

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52
Q

What 2 types of pericarditis occur post MI?

A

Post 48h

Post 2-6w (Dressler’s syndrome, autoimmune)

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53
Q

What are the signs of LV aneurysm?

A

Persistent STE and LV failure

No chest pain

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54
Q

How does LV free wall rupture present?

A

Acute heart failure secondary to cardiac tamponade

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55
Q

Which 2 post MI complications present with acute heart failure and pansystolic murmur?

A

Acute MR

VSD

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56
Q

Which type of infarction is acute MR more common with?

A

Infero-posterior infarction

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57
Q

What is the most common cause of secondary hypertension?

A

Primary hyperaldosteronism

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58
Q

Which drugs cause secondary hypertension?

A 
Steroids
MAOs
COCP
NSAIDs
Leflunomide
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59
Q

Define PAH.

A

Resting mean pulmonary artery pressure >25mmHg

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60
Q

What are the features of pulmonary hypertension?

A

Progressive exertional dyspnoea

Exertional syncope, chest pain, peripheral oedema

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61
Q

What are the signs of pulmonary hypertension?

A

RV heave
Loud P2
Raised JVP with prominent a waves
TR

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62
Q

What is the management of PAH?

A

Acute vasodilator testing (administration of IV epoprostenol/inhaled NO)

+ve (minority): PO CCB
-ve (majority): prostacyclin analogues (iloprost), endothelin receptor antagonists (bosentan), PDE inhibitors (sildenafil)

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63
Q

What are the 8 reversible causes of cardiac arrest?

A

Hypoxia
Hypovolaemia
HyperK, hypoK, hypoBM, hypoCa
Hypothermia

Thrombosis
Tension pneumo
Tamponade
Toxins

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64
Q

What is the first line treatment of heart failure?

A

ACEI and BB

One drug started at a time

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65
Q

Which beta blockers are licensed for use in heart failure?

A

Bisoprolol
Carvedilol
Nebivolol

66
Q

What is the 2nd line treatment of heart failure?

A

Aldosterone antagonist

67
Q

What is the 3rd line treatment of heart failure?

A 
Ivabradine
Sacubitril-valsartan
Digoxin
Hydralazine + nitrate
Cardiac resynchronisation therapy
68
Q

What is the mechanism of sacubitril valsartan?

A

Prevents degradation of natriuretic peptides such as BNP and ANP

69
Q

Why is digoxin used in heart failure if it has no affect on mortality?

A

May improve symptoms due to inotropic properties

70
Q

What are the indications for CRT?

A

Wide QRS/LBBB

Ejection fraction<35%

71
Q

What are 6 causes of increased BNP, except LV failure?

A 
Tachycardia
Hypoxaemia
Sepsis
COPD
Diabetes
Cirrhosis
72
Q

What are 6 causes of decreased BNP?

A

Obesity
Diuretics
ACEI, BB, AA, ARB

73
Q

What valvular abnormality is seen in William’s syndrome?

A

Supravalvular aortic stenosis

74
Q

What are the 2 causes of aortic stenosis?

A

<65: bicuspid valve

>65: calcification

75
Q

What are the features of severe AS?

A 
Narrow pulse pressure
Slow rising pulse
Delayed ESM
Soft S2
S4
Thrill
LV failure
76
Q

When is aortic valve replacement indicate?

A

Symptomatic
Valvular gradient >40
LVSD

77
Q

What are the signs of mitral stenosis?

A 
Mid-late diastolic murmur, loudest in expiration
Loud S1, opening snap
Low volume pulse
Malar flush
AF
78
Q

What is the management of mitral stenosis?

A

Severe: percutaneous mitral commissurotomy –> mitral valve replacement

If unsuitable for open surgery - transcatheter mitral valve replacement

79
Q

What is the treatment of mitral regurgitation?

80
Q

What drugs are used in pharmacological cardioversion in AF?

A 
Amiodarone
Flecainide (if no structural heart disease)
81
Q

To what is electrical cardioversion synchronised to in AF?

A

The R wave

82
Q

What happens if shock is delivered during T wave during AF?

A

This is ventricular repolarisation

Can trigger T on T phenomenon which leads to VF

83
Q

In non emergency situations, how long duration of anticoagulation is needed before electrical cardioversion for AF?

84
Q

Why is conservative management recommended in complete heart block following inferior MI?

A

Ischaemic AV conduction block

Tends to resolve upon successful revascularisation of the infarcted AV nodal tissue

85
Q

What is the management of 2nd degree/complete heart block following anterior MI?

A

Temporary pacing wire

May also be a bridging measure to insert PPM

86
Q

What are the indications for a temporary pacemaker?

A

Symptomatic/heamodynamically unstable bradycardia, not responding to atropine
Post anterior MI
Trifascicular block prior to surgery

87
Q

In what condition is variable intensity of S1 seen?

A

Complete heart block

88
Q

When are 3 successive shocks prior to CPR indicated?

A

Witnessed cardiac arrest whilst on monitor

89
Q

What are the ECG changes of hypokalaemia?

A 
U waves
Small/inverted T waves
Prolonged PR interval
ST depression
Long QT
90
Q

What are the ECG changes of hypothermia?

A

Bradycardia
J waves
First deg heart block
Long QT

91
Q

What is the name of the condition where there is a congenital accessory conducting pathway between the atria and ventricles leading to AVRT?

A

Wolff-Parkinson White syndrome

92
Q

In WPW, Why can AF degenerate rapidly to VF?

A

The accessory pathway does not slow conduction

93
Q

What are the ECG features of WPW?

A

Short PR
Wide QRS with slurred upstroke (delta wave)

Type B: LAD, no dominant R wave in V1

Type A: RAD, dominant R wave in V1

94
Q

What is type A and B WPW?

A

Type A: left sided accessory pathway

Type B: right sided accessory pathway

95
Q

What are 5 associations of WPW?

A 
HOCM
MV prolapse
Ebstein's anomaly
Thyrotoxicosis
Secundum ASD
96
Q

What is the treatment of WPW?

A

Amiodarone/flecainide
Sotalol if not AF
Radiofrequency ablation of accessory pathway

97
Q

What is the atrial rate in atrial flutter?

98
Q

What is the treatment of atrial flutter?

A

Similar to AF

Medications less effective, cardioversion more effective - lower energy levels

Radiofrequency ablation of the tricuspid valve isthmus

99
Q

What is the mechanism of action of nicorandil?

A

Potassium channel activator

Activates guanylyl cyclase with increases cGMP –> vasodilation

100
Q

What are 3 side effects of nicorandil?

A

Headache, flushing, ulceration

101
Q

How does atropine treat bradycardia?

A

Inhibits vagal tone by modulating the SA node

102
Q

What is the mechanism of action of amiodarone?

A

Blocks K channels - inhibits repolarisation and prolongs the AP
Also blocks Na channels

103
Q

Name 6 side effects of amiodarone

A 
Thyroid dysfunction
Corneal deposits
Pulm/liver fibrosis
Slate grey appearance
Prolonged QT
Bradycardia
104
Q

How do ADP receptor inhibitors, such as clopidogrel and ticagrelor work?

A

Inhibition of P2Y12 receptor which reduces platelet aggregation

ADP is one of the main platelet activation factors

105
Q

Why does ticagrelor cause dyspnoea?

A

Impaired clearance of adenosine

106
Q

How does dipyridamole work?

A

Inhibits phosphodiesterase, which elevates platelet cAMP which reduces intracellular calcium

107
Q

How does adenosine work?

A

Blocks AV node - agonist of A1 receptor in AV node which inhibits adenylyl cyclase –> reducing cAMP –> hyperpolarization by increased K efflux

108
Q

What are the ECG signs of digoxin toxicity?

A

Downsloping ST depression
Flattened/inverted T waves
Short QT
AV block/bradycardia

109
Q

What is the mechanism of action of statins?

A

Inhibits HMG-CoA reductase which is the rate limiting enzyme in hepatic cholesterol synthesis

110
Q

What are the risk factors for myopathy in patients who take statins?

A 
Female
Older age
Low BMI
Diabetes
Lipophilic statins
111
Q

What are the indications for statins?

A

Q risk >10%
Established CV disease
T1DM: diagnosed >10 years, aged >40, or established nephropathy

112
Q

Why are statins taken at night?

A

This is when the majority of cholesterol synthesis takes place

113
Q

What is the pathophysiology of Takotsubo cardiomyopathy?

A

Apical ballooning like octopus pot due to severe hypokinesis of mid and apical segments, preservation of basal segments

114
Q

What are the genetics of HCOM?

A

Mutation in gene encoding beta-myosin heavy chain protein or myosin binding protein C

115
Q

What is the pathophysiology of HCOM?

A

LV hypertrophy –> decreased compliance –> decreased cardiac output

Mainly diastolic dysfunction

Myofibrillar hypertrophy + disarray and fibrosis of myocytes

116
Q

What are the signs of HCOM?

A

Jerky pulse
Large a waves of JVP
Double apex beat
ESM, increases with Valsalva and decreases on squatting

117
Q

What is seen on echo and ECG in HCOM?

A

Echo: asymmetric septal hypertrophy with systolic anterior movement of anterior leaflet of mitral valve

ECG: LV hypertrophy, progressive TWI, deep Q waves

118
Q

What are 5 poor prognostic features of HCOM?

A 
Syncope
FH SCD
Young age at presentation
Increased septal wall thickness >30mm
Abnormal BP change on exercise
119
Q

What is the management of HCOM?

A

ABCDE

Amiodarone
Betablockers/verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis
120
Q

Which drugs should be avoided in HCOM?

A

Nitrates
ACEIs
Inotropes

121
Q

Why are nitrates avoided in heart failure?

A

Vasodilation reduces preload

122
Q

What are the causes of restrictive cardiomyopathy?

A 
Amyloid
Haemochromatosis
Loffler's syndrome
Sarcoid
Scleroderma
123
Q

How can restrictive cardiomyopathy be differentiated from constrictive pericarditis?

A

Prominent apical pulse
No pericardial calcification
Enlarged heart
Bundle branch block and Q waves

124
Q

What is the inheritance of arrhythmogenic right ventricular cardiomyopathy?

A

Autosomal dominant

125
Q

What are the ECG changes of arrhythmogenic right ventricular cardiomyopathy?

A

TWI V1-V3

Epsilon wave in 50% (terminal notch in QRS)

126
Q

What is the treatment of ARVC?

A

Sotalol
Catheter ablation to prevent VT
ICD

127
Q

What is the triad of Naxos disease?

A

ARVC (AR variant)
Palmoplantar keratosis
Woolly hair

128
Q

What is the pathophysiology of LQTS?

A

Defects in alpha subunit of slow delayed rectifier K channel

129
Q

What are the congenital causes of LQTS?

A

Jervell-Lange Nielsen (deafness)

Romano-Ward (no deafness)

130
Q

What are the acquired causes of LQTS?

A

Drugs: amiodarone, sotalol, SSRIs, TCAs, chloroquine, macrolides, ondansetron, methadone

Low K, Ca, Mg

131
Q

What is the management of LQTS?

132
Q

What is the genetics of Brugada syndrome?

A

Autosomal dominant

SCN5A gene - encodes myocardial sodium ion channel

133
Q

What are the ECG changes of Brugada syndrome?

A

Convex ST elevation >2mm in >V1-V3, followed by TWI

Partial RBBB

Changes more apparent following administration of flecainide or ajmaline

134
Q

Name 6 causes of pericarditis

A 
Coxsackie virus
TB
Uraemia
Dressler's
CTD
Malignancy
135
Q

What are the ECG changes of pericarditis?

A

Diffuse saddle shaped ST elevation

PR depression

136
Q

What is the pathophysiology of rheumatic fever?

A

Strep pyogenes infection (cell wall includes M protein which is highly antigenic)

Activation of innate immune system leading to antigen presentation to T cells

Molecular mimicry (form of T2 hypersensitivity)

Antibodies against M protein cross-react with myosin

137
Q

What are the major criteria of rheumatic fever?

A 
Erythema marginatum
Sydenham's chorea
Polyarthritis
Carditis/valvulitis
SC nodules
138
Q

What is the treatment of rheumatic fever?

A

PO penicillin V

139
Q

Which cause of infective endocarditis is linked to dental work?

A

Strep viridans (includes strep mitis, strep sanguinis)

140
Q

Infective endocarditis caused by staph epidermis is most common in what scenario?

A

Indwelling lines

Prosthetic valve surgery

141
Q

Strep bovis/gallolyticus endocarditis is associated with what?

A

Colorectal Ca

142
Q

Name 4 culture negative causes of endocarditis.

A

Coxiella burnetti
Bartonella
Brucella
HACEK

143
Q

What are 4 poor prognostic features of IE?

A

S.aureus
Prosthetic valve
Culture -ve
Low complement

144
Q

What is the treatment of IE of prosthetic valves?

A

Rifampicin + gentamicin + fluclox/vancomycin

145
Q

What is Eisenmenger’s syndrome?

A

The reversal of left to right shunt in congenital heart defect due to pulmonary hypertension

146
Q

What are the signs of Eisenmenger’s syndrome?

A 
Original murmur may disappear
Cyanosis
Clubbing
RV failure
Loud S2
Large a waves in JVP
147
Q

What is the function of BNP?

A

Vasodilator
Diuretic, natriuretic
Suppresses sympathetic tone and RAAS

148
Q

Name 2 causes of reduced BNP

A

ACEIs/ARBs

Digoxin

149
Q

Which scan measures LVEF accurately and is used before and after use of cardiotoxic drugs?

A

Multi-gated acquisition scan (MUGA)

150
Q

What can SPECT imaging do?

A

Assess myocardial perfusion and viability

151
Q

What are the 2 methods of assessing IHD in cardiac CT?

A

Calcium score

Contrast enhanced - visualisation of coronary artery lumen

152
Q

What is a risk factor for multi-focal atrial tachycardia?

A

Chronic lung disease

153
Q

What are the pathways in AVNRT?

A

Slow (alpha) with short refractory period

Fast (beta) with long refractory period

154
Q

What is the management of AVNRT?

A

Vagal maneouvres
IV adenosine 6 –> 12 –> 12
Cardioversion

155
Q

What is the treatment of AVNRT in asthmatics?

A

Substitute adenosine for verapamil

156
Q

Which features suggest VT rather than SVT with aberrant conduction?

A 
QRS>160
Capture and fusion beats
AV dissociation
Marked LAD
History of IHD
Lack of response to adenosine/carotid sinus massage
Positive QRS concordance in chest leads
157
Q

What is the treatment of sustained (>30s) VT?

A

Shock etc: synchronised DC cardioversion

Amiodarone, lidocaine

158
Q

What are the causes of polymorphic VT?

A

If prolonged QT: TDP

If bidirectional: digoxin toxicity

159
Q

What is the pathophysiology of VT caused by digoxin toxicity?

A

Triggered activity - due to early or late after-depolarisations

160
Q

What is the pathophysiology of monomorphic VT?

A

Re-entry

Abnormal automaticity

161
Q

What is the treatment of TDP?

A

IV magnesium sulphate

MRCP Combined (58 decks)

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