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MRCP > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Commonest site for atrial myxomas?

A

Left atrium (75%)

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2
Q

Symptoms of atrial myxomas?

A

Systemic – SOB, fatigue, WL, pyrexia of unknown origin
Emboli
Mitral valve obstruction
AF

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3
Q

Type of murmur with atrial myxomas?

A

Mid-diastolic murmur

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4
Q

What would you see on echo in atrial myxomas?

A

pedunculated heterogenous mass typically attached to the fossa ovalis region of the interatrial septum

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5
Q

Management of atrial myxomas?

A

Untreated, may result in thrombus + embolism

Surgery

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6
Q

ECG signs in PE?

A

Sinus tachy
a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’ (<20%)
RBBB and right axis deviation

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7
Q

What features in the pulmonary embolic rule-out criteria (PERC)?

A 
Age >50
HR >100
SpO2 <95%
Prev DVT/PE
Recent surgery/trauma
Haemoptysis
Unilateral leg swelling
Oestrogen use

If all are absent, then probability of PE <2%

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8
Q

Well’s score for PE?

A

Clinical signs and symptoms of DVT: 3
Alt Dx is less likely: 3
HR > 100: 1.5
Immobilisation >3d or surgery in the prev 4wks: 1.5
Prev DVT/PE: 1.5
Haemoptysis: 1
Malignancy (on Tx, Tx in the last 6 months, or palliative): 1

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9
Q

Use of results of well’s score?

A

PE likely - more than 4 points
PE unlikely - 4 points or less

> 4: immediate CTPA, if there will be a delay give DOAC
If CTPA negative, consider need for doppler

Less than or =4: d-dimer, if there will be a delay give DOAC

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10
Q

When would you use a V/Q scan > CTPA?

A

In renal impairment (no contrast given)

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11
Q

What is the most common type of congenital heart defect seen in adults?

A

Atrial septal defects

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12
Q

What is the most common type of ASD? What condition is this type associated with? What ECG changes might occur?

A

Ostium secundum (70%)
Associated with Holt-Oram syndrome (tri-phalangeal thumbs)
RBBB with RAD

Remember:
First most common
Second(um) ostium
Tri(phalangeal thumbs)

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13
Q

What is the OTHER of ASD (less common)? What condition is this type associated with? What ECG changes might occur?

A

Ostium primum
Presents earlier
Associated with abnormal AV valves
Found in 20% of patients with Downs Syndrome
ECG: RBBB with LAD, prolonged PR interval

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14
Q

What are the features on examination of ASD?

A

Ejection systolic murmur (occurs because of the flow through the pulmonary valve)
Fixed splitting S2 (because of more blood in R ventricle causing delayed closure of the pulmonary valve)

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15
Q 
DVLA guidance:
Cath ablation
Pacemaker + angioplasty
CABG + ACS + ICD prophylaxis
Heart Tx
ICD for ventricular arrhythmia
Group 2 ban?
Aortic aneurysm
Angina + HTN with SE
A 
DVLA guidance:
Cath ablation - 2 days
Pacemaker + angioplasty - 1wk
CABG + ACS + ICD prophylaxis - 4wks
Heart Tx - 6wks
ICD for ventricular arrhythmia - 6m
Group 2 ban? - For HTN >180/100
Aortic aneurysm >6cm - inform DVLA
AA >6.5cm - ban
Angina + HTN with SE - stop if angina occurs at rest or HTN with unacceptable SEs
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16
Q

RFs for IE?

A 
Strongest = prev IE
Rheumatic valve disease
Prosthetic valves
Congenital heart defects
IVDU (typically tricuspid lesion)
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17
Q

Causative organism for IE?

A

In LICs = strep viridans
Most © is now staph aureus
If patients have indwelling lines/following valve surgery, most © staph epidermidis (if <2 months since op)
If culture negative, consider Coxiella burnetti
Strep bovis (assoc with colorectal cancer)
Non-infective – SLE, malignancy

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18
Q

Vascular + immunological phenomena for IE?

A

Vasc: emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae/purpura
Imm: glomerulonephritis, osler’s nodes, roth spots

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19
Q

Treatment of IE?

A

Blind therapy
o Own valve – amoxicillin
o If prosthetic – vancomycin + rifampicin + gentamicin
Staph
o Own – flucloxacillin
o Prosthetic – flucloxacillin + rifampicin + gentamicin
Strep viridans
o Benzylpenicillin (if caused by less sensitive strep, add low-dose gentamicin)

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20
Q

Indications for surgery in IE?

A

Severe valvular incompetence
Aortic abscess (lengthening PR interval)
Infections resistant to abx/fungal infections
Cardiac failure refractory to standard medical treatment
Recurrent emboli after antibiotic therapy

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21
Q

Poor prognostic factors in IE?

A

Staph aureus (30% mortality)
Prosthetic valve
Culture negative endocarditis
Low complement levels

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22
Q

Who should receive prophylaxis for IE?

A

Any episode of infection in people at risk of IE should be investigated and treated promptly to reduce risk of endocarditis developing
If at risk of IE and already receiving an abx because they are undergoing GI/GU procedure, they should be given an antibiotic that covers organisms that cause IE

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23
Q

Drug causes of long QT?

A

STOMACHS EA

  • Amiodarone, sotalol
  • TCA, SSRIs
  • Methadone
  • Chloroquine
  • Terfenadine
  • Erythromycin
  • Haloperidol
  • Ondansetron
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24
Q

Causes of long QT (other than drugs)?

A
  • Low Ca/K/Mg
  • Acute MI, myocarditis
  • Hypothermia
  • SAH
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25
Q

Different between Long QT1-3?

A

Long QT1 – assoc with exertional syncope, often swimming
Long QT2 – assoc with syncope following emotional stress, exercise, auditory stimuli
Long QT3 – often occur at night/rest

More deadly as they go down

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26
Q

Management of Long QT?

A

Avoid drugs which prolong QT/other precipitants
B-blockers (not sotalol)
Implantable cardioverter defib in high risk cases

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27
Q

Normal QT for M/F? And risk of QT?

A

Normal = <430ms in M and <450ms in F

May lead to vent tachy -> torsades de points -> collapse/death

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28
Q

What are the possible complications following an MI?

A 
Tachyarrythmias – VF/VT
Cardiac arrest following VF
Cardiogenic shock
Chronic heart failure
Bradyarrythmias - AV block
Pericarditis
Left ventricular aneurysm
Left ventricular free wall rupture
VSD
Acute mitral regurgitation
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29
Q

What is Dressler’s syndrome?

A

2-3 weeks post-MI
Type of pericarditis
AI reaction against antigenic proteins which form as the myocardium recovers following an MI
Develop fever, pleuritic pain, pericardial effusion and raised ESR
Tx NSAIDS

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30
Q

What may occur in a left vent aneurysm following MI? What are the ECG changes?

A

persistent ST elevation + LVF, thrombus may form in aneurysm so need anticoagulating

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31
Q

What occurs in left vent free wall rupture?

A

Occurs 1-2wks after MI, acute HF secondary to cardiac tamponade (Tx urgent pericardiocentesis + thoracotomy)

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32
Q

What symptoms/management of a VSD following MI

A

occurs in first week, acute HF with pan-systolic murmur, Ix = echo ,Tx = surgical

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33
Q

What occurs in acute mitral regurg following MI? What type of murmur and how to treat?

A

due to ischaemia or rupture of papillary muscles. Acute hypotension + pulm oedema occur, early-to-mid systolic murmur, Tx = vasodilator therapy/surgical repair

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34
Q

What are the symptoms of malignant HTN and who is it more common in?

A

More common in younger pts, blacks
Develops rapidly, HTN (>200/130)
Symptoms: headaches +/- visual disturbances, bilateral retinal haemorrhages + exudates, protein/haematuria, chest pain/SOB, can lead to cerebral oedema and encephalopathy

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35
Q

Management of malignant HTN?

A

Reduce diastolic no lower than 100 within 12-24hrs
Bed rest
Atenolol
If severe/encephalopathic: IV sodium nitroprusside (vasodilator)/labetolol

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36
Q

What are the RFs for AF?

A
  • Hypertension
  • Coronary artery disease
  • Valvular heart disease
  • Sepsis/viral illness
  • Alcohol
  • PE
  • Thyrotoxicosis
  • MI/IHD
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37
Q

Rate control for AF?

A

Favourable factors: >65, ischaemic heart disease
Beta-blockers or rate-limiting Ca channel blockers (diltiazem)
If this fails, combine two of: B-blocker, diltiazem or digoxin (preferred in the elderly/those with co-existing heart failure)
Digoxin as a monotherapy is only acceptable in sedentary patients

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38
Q

Rhythm control for AF?

A

Favourable factors: <65, symptomatic, first presentation, lone AF or secondary to corrected precipitates (alcohol), congestive cardiac failure
1. Do Echo
2. Pre-treat for at least 4 weeks with sotalol/amiodarone if really high risk of failure (e.g. previous failure/previous recurrence)
If new onset, consider cardioversion (need anticoagulation for 4/52 first – then to continue for 4/52 afterwards)
Drug cardioversion: IV amiodarone or PO/IV flecainide (not if structural heart defect)
Electrical cardioversion: synchronise to R wave

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39
Q

Drugs used to maintain sinus rhythm after AF cardioversion?

A

B-blockers, dronedarone (class 3 anti-arrhythmic), amiodarone (BAD to go back into AF)

Use amidarone for all 3 steps - preTx if at high risk of recurrent, to chemically anticardiovert and for maintenance

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40
Q

CHA2DS2VASC score and resulting actions?

A

Look up
1 – consider anticoagulation if male
≥2 – offer anticoagulation: NOAC / Warfarin (INR 2-3)
>3 – high risk of bleeding

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41
Q

CI to warfarin in AF?

A
  • Bleeding tendency
  • Low platelets
  • Consistently high BP
  • Compliance or monitoring issues
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42
Q

ORBIT score and resulting actions?

A

Haemoglobin level +2
History of bleeding +2

Age >74 +1
GFR <60 +1
Tx with antiplatelets +1

0-2 – low risk
3 – medium
4-7 – high risk

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43
Q

Indications for temporary pacemaker?

A

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

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44
Q

Management of bradycardia?

A

If asymptomatic and rate >40bpm, no treatment
Treat cause (drugs, hypothyroidism)
If rate <40bpm or patient is symptomatic, give atropine

If no response, can either:
• More atropine
• Initiate transcutaneous pacing (similar to a defibrillators but smaller shocks)
• Isoprenaline infusion (similar to adrenaline)

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45
Q

Adverse features in bradycardia?

A

Shock, syncope, MI, HF

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46
Q

What is MOA of nicorandil? And SEs?

A

Potassium channel activator
SEs: can cause ulceration from mouth -> anus
Headache, flushing

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47
Q

Which two medications should not be prescribed together for risk of complete heart block?

A

Verapamil and B-blockers

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48
Q

Management of stable angina?

A

1) Lifestyle changes
2) Medication

ASPIRIN
STATIN
GTN SPRAY

B-blocker/CCB or both

  • If CCB used alone – use RL
  • If used in combination, use nifedipine/amlodipine

If only on one of the above, consider - long-acting nitrate, ivabradine, ranolazine or nicorandil
If taking B-blocker and CCB – add third drug and list for PCI/CABG

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49
Q

Where does BNP come from?

A

secreted by left ventricle in response to excessive stretching of myocytes

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50
Q

Effects of BNP?

A

Aim to lower BP to put less strain on the heart. Has 4 effects:
Vasodilator
Diuretic (water excretion) + natriuretic (Na excretion)
Suppresses the SNS
Inhibition of the RAAS system

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51
Q

What can BNP be used for?

A

Excluding HF if <100
Marker of prognosis in chronic HF
Guiding treatment in chronic HF

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52
Q

What causes high BNP?

A

Increased strain on the heart, so:

General ageing
Any cause of LV dysfunction - hypertrophy, ischaemia
Or generalised CCF

Problems with excretion:
CKD (reduced excretion)
Liver cirrhosis

Also DM

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53
Q

What causes low BNP?

A

Medications that reduce your blood pressure:
ACEi, ARBs, diuretics, B-blockers

Also obesity

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54
Q

In which patients should you avoid the use of RL CCB?

A

Patient with HF as inotropic effects of CCB decrease the force + speed of contraction
Also in patients with bradycardia

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55
Q

Management of SVT?

A 
Vagal manoeuvres 
IV adenosine, 6mg then 12mg, then 18mg
Verapamil – give in asthmatics (adenosine CI)
DC shock if compromised
Prevention: B-blockers/ablation
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56
Q

In which co-morbidity should adenosine be avoided in?

A

Asthmatics due to possible bronchospasm

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57
Q

Effect of adenosine?

A

causes transient heart block in the AV node

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58
Q

What enhances and blocks the effect of adenosine?

A

DEAR

dipyridamole enhances, aminophylline reduces

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59
Q

SEs of ACEi?

A

cough - due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics

ACE:
Angioedema
Cough
Elevated K

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60
Q

CI for starting ACEi?

A

Think of the SEs
Pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
AORTIC STENOSIS - may result in hypotension
hereditary of idiopathic angioedema
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L

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61
Q

End-organ damage in HTN?

A
  • Eyes: Retinopathy
  • Cardiac: LVH
  • Kidney: Proteinuria
  • Neuro: Headache, Nausea, Vomiting
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62
Q

Stage 1 HTN and Mx?

A 
Clinic: >140/90
Home: >135/85
Tx if <80 years old AND any of the following*:
• Target organ damage
• Established CVS disease
• Renal disease
• Diabetes
• 10 year cardiovascular risk of 10%+ (QRISK2 score)

TERD10

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63
Q

Stage 2 HTN?

A

Treat all if:
Clinic: >160/100
Home: >150/95

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64
Q

Target BP if >80? Target if DM?

A

> 80: 150/90

DM: 130/90

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65
Q

What is an ‘a’ wave on JVP and why might it be enlarged?

A

= normal, atrial contraction
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in AF as weak contraction

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66
Q

What is a cannon ‘a’ wave on JVP?

A 
= caused by atrial contractions against a closed tricuspid valve
Seen in:
complete heart block
ventricular tachycardia/ectopics
Nodal rhythm
Single chamber ventricular pacing
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67
Q

What does the ‘c’ wave represent in JVP?

A

closure of tricuspid valve

not normally visible

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68
Q

What is the ‘v’ wave in JVP and when might it be enlarged?

A

due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation

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69
Q

MOA of dipyridamole?

A

inhibits phosphodiesterase

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70
Q

ST elevation in V1-V4?

A

Anteroseptal, LAD

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71
Q

ST elevation in II, III, aVF?

A

Inferior, right coronary

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72
Q

ST elevation in V4-6, I, aVL?

A

Anterolateral, LAD or left circumflex

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73
Q

ST elevation in I, aVL +/- V5-6?

A

Left circumflex

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74
Q

Tall R waves in V1-2?

A

Usually left circumflex, also R coronary

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75
Q

Which medication should NOT be used in VT?

A

Verapamil - vasodilator: risk of causing significant hypotension, ventricular fibrillation and cardiac arrest

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76
Q

How to treat VT?

A

amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

If drugs fail: ICD

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77
Q

Poor prognostic factors in HOCM?

A 
syncope
FH of sudden death
young age at presentation
non-sustained VT on 24 or 48-hour Holter monitoring
abnormal BP changes on exercise
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78
Q

Inheritance and pathophysiology of HOCM?

A

Caused by mutation in the gene encoding B-myosin heavy chain protein or myosin-binding protein C
Left ventricular hypertrophy -> decreased cardiac output
50% are genetic – autosomal dominant inheritance, may be spontaneous

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79
Q

Presentation of HOCM and signs? Murmur and what makes it louder/quieter? JVP?

A

May present at any age
Sudden death (© d/t vent arrhythmias)
Angina, exertional dyspnoea, palpitations, syncope (typically following exercise), CCF

Large ‘a’ wave
Harsh ejection systolic murmur
- Increased on Valsava manoeuvre and decreases on squatting

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80
Q

ECG changes in HOCM?

A

LVH, non-spec ST/T wave abnormalities, deep Q waves, AF on occasions

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81
Q

Echo changes in HOCM?

A

MR SAM ASH
Mitral regurg (MR)
Systolic anterior motion (SAM) of the anterior MV leaflet
Asymmetrical hypertrophy (ASH)

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82
Q

HOCM management?

A 
Amiodarone – for arrythmias
B-blockers or verapamil for symptoms – aim to reduce ventricular contractility
Cardioverter defib
Dual chamber pacemaker
Endocarditis prophylaxis
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83
Q

What drugs to avoid in HOCM?

A

nitrates/ACEi

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84
Q

What conditions in HOCM associated with?

A

Friedreich’s ataxia, WPW syndrome

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85
Q

Why does amiodarone need a bolus dose?

A

Because it has a long half-life

Drugs with a long half-life are eliminated from the body slowly and only need a low maintenance dose to maintain appropriate therapeutic concentrations. However, this means that in the absence of a higher initial dose, it would take a long time for these drugs to reach a steady-state concentration

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86
Q

What is the MOA of amiodarone?

A

blocking potassium channels

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87
Q

How/what do you monitor patients taking amiodarone?

A

TFT, LFT, U&E, CXR prior to treatment

TFT, LFT every 6 months

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88
Q

SEs of amiodarone?

A

LEG PANIC

Live fibrosis/hepatitis
Extremities - peripheral neuropathy
Gynaecomastia

Pulmonary fibrosis/pneumonitis/photosensitivity
Abnormal thyroid: both hypo and hyperthyroidism
Nausea and vomiting
Injection site reactions/thrombophlebitis
Corneal deposits

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89
Q

MOA of aspirin?

A

Blocks COX1 and 2
Inhibits the production of thromboxane A2 -> decreased platelet aggregation

Also prostaglandins (NSAID effect)

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90
Q

MOA of clopidogrel?

A

Antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

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91
Q

MOA of abciximab, eptifibatide, tirofiban?

A

Glycoprotein 2b/3a receptor antagonists

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92
Q

Drugs in each class of anti-arryhthmics?

A

Look at chart

93
Q

Management of torsades de pointes?

A

IV Mg Sulphate

94
Q

Warfarin guidelines for INR?

A

MAJOR BLEED
stop warfarin, give FFP OR PCC, , IV Vit K 5 mg

MINOR BLEED
INR >8 …..stop warfarin, IV Vit K 1-3 mg, repeat dose if INR still high (>8), restart when INR <5
INR 5-8….stop warfarin, IV Vit K 1-3 mg, restart when INR <5

NO BLEED
INR >8 …..stop warfarin, oral Vit K 5 mg, repeat dose if INR still high (>8), restart when INR <5
INR 5-8….WITHHOLD 1 or 2 doses, reduce subsequent maintainance doses

95
Q

In which common scenarios should you give antiplatelets/anitcoag together/as monotherapies?

A

Stable CVD + VTE/AF - Anticoag monotherapy
Post ACS/PCI - 6m triple therapy - 6m dual therapy
VTE on Antiplatelet - calculate HAS BLED score, if low risk of bleeding -> dual therapy, if high anticoagulant monotherapy

96
Q

Stages of NYHA?

A

NYHA Class I
no symptoms
no limitation

NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in symptoms

NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity (buttoning shirt) results in symptoms

NYHA Class IV
severe symptoms
unable to carry out any physical activity and symptoms present at rest

97
Q

What may cause a cholesterol emboli?

A

Commonly secondary to vascular surgery or angiography

98
Q

Features of cholesterol emboli?

A

eosinophilia
purpura
renal failure
livedo reticularis

99
Q

CXR signs for HF?

A 
Alveolar oedema (bat wings)
Kerley B lines (interstitial oedema)
Cardiomegaly
Dilated prominent upper lobe vessels
Pleural Effusion
100
Q

Investigations for stable angina?

A

1st line – CT coronary angiography
2nd line – non-invasive functional imaging (MPS, stress echo, MR perfusion)
3rd line – Invasive coronary angiography

101
Q

Where does the catheter go when measuring pulmonary capillary wedge pressure and what area of the heart does the measurement equate to?

A

Inserted into the pulmonary artery. The pressure measured is similar to that of the left atrium (normally 6-12 mmHg)

102
Q

What is pulmonary arterial HTN defined as?

A

resting mean arterial pressure >25 mmHg

103
Q

What are the symptoms and signs on examination of pulmonary arterial HTN?

A

Progressive exertional dyspnoea
May be exertional chest pain, exertional syncope and peripheral oedema
Cyanosis
Right ventricular heave, loud P2 (hypertension, all the pressure from the blood in the lungs slams the valve shut), raised JVP with prominent ‘a’ waves, tricuspid regurgitation

104
Q

What is the inheritance pattern of pulmonary arterial HTN?

105
Q

How to investigate pulmonary arterial HTN?

A

To confirm - cardiac catheterisation to measure pressure difference
Acute vasodilator testing
o Administer IV vasodilators: epoprostenol or inhaled nitric oxide
o If significant fall, then positive test

106
Q

Management of pulmonary arterial HTN?

A

Positive result (minority): Oral CCB
Negative result (majority)
- Prostacyclin analogues: Treprostinil, iloprost
- Endothelin receptor antagonists: Bosentan, ambrisentan
- phosphodiesterase inhibitors: sildenafil
If symptoms progress, should be considered for a heart-lung transplant

107
Q

Examples of thiazide-like diuretics?

A

chlortalidone or indapamide

108
Q

Causes of ST depression?

A 
SIADH: mnemonic
syndrome X
ischaemia
secondary to Abnormal QRS (LVH, LBBB, RBBB)
digoxin
hypokalaemia
109
Q

What are the features and management of syndrome X?

A

angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography
Mx: nitrates may be useful

110
Q

Causes of acute pericarditis?

A

Infection
MI
Drugs

111
Q

Presentation of acute pericarditis and findings on auscultation?

A

Central chest pain
• Worse on inspiration and lying flat, relieved by sitting forward
Auscultation – pericardial rub (scratchy sound) at L sternal edge
Fever, cough, SOB may occur

112
Q

Investigations in pericarditis?

A

ECG – may be normal, may show widespread saddle-shaped ST elevation + PR DEPRESSION (most specific marker)
Viral serology/blood cultures/autoantibodies/fungal precipitins
For pericardial effusion – CXR may show cardiomegaly and may need an Echo

113
Q

Management of pericarditis?

A

Analgesia, treat cause

Consider combination of NSAIDs and colchicine, then steroids if relapse/unresolved

114
Q

Causes of pericardial effusion?

A

Same as pericarditis

Infection, MI, drugs

115
Q

Presentation of pericardial effusion?

A

Dyspnoea
Raised JVP
Bronchial breathing at L base
Look for signs of cardiac tamponade

116
Q

Management of pericardial effusion?

A

Treat the cause

Pericardiocentesis may be diagnostic/therapeutic

117
Q

Cause of constrictive pericarditis?

A

Often unknown or after any pericarditis

Can be caused by TB

118
Q

Presentation of constrictive pericarditis?

A

Mainly of R heart failure with increased JVP (Kussmaul’s sign – JVP rising paradoxically with inspiration), ascited, oedema, hepatomegaly
Loud S3

119
Q

Investigations in constrictive pericarditis?

A

CXR – small heart +/- pericardial calcification

Echo – cardiac catheterisation

120
Q

What is Beck’s triad and when is it seen?

A

falling BP, rising JVP, muffled heart sounds

Seen in cardiac tamponade

121
Q

What causes cardiac tamponade?

A

Any pericarditis, aortic dissection, warfarin, post-cardiac biopsy

122
Q

Presentation of cardiac tamponade? JVP?

A

Increased HR and JVP X – (Kussmaul’s sign RARE – rise of JVP on inspiration)
TAMponade = TAMpaX (no Y)
Pulsus paradoxus (abnormally large drop in stroke volume + systolic BP during inspiration)
Diagnosis – Beck’s triad (hypotension, rising JVP, muffled heart sounds)

123
Q

Investigations in cardiac tamponade?

A

CXR – big globular heart
ECG – electrical alternans, low-voltage QRS alternating with normal
Echo – diagnostic: echo-free zone (>2cm or >1cm if acute) around heart +/- diastolic collapse of R atrium + ventricle

124
Q

Management of cardiac tamponade?

A

Urgent drainage

125
Q

What is Dressler’s syndrome?

A

tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs

126
Q

What are the causes of myocarditis?

A

Idiopathic (~50%)
Viral – coxsackie, HIV
Bacterial, Lyme disease, Protozoa
AI, drugs (doxorubicin)

127
Q

ECG and blood results in myocarditis?

A

ECG – ST elevation or depression, T wave inversion, atrial arrhythmias
Raised Troponin I + T (in the absence of MI) confirms Dx
Raised inflammatory markers + BNP

128
Q

Management of myocarditis?

A

Supportive

Treat the underlying cause

129
Q

What is the MOA of Ivabradine?

A

Inhibits I’f’ (funny) ion channel which is ++ expressed in the SA node

130
Q

What are the SE of Ivabradine?

A

Visual effects, luminous phenomena (halo effects)
Headache
Bradycardia + heart block

131
Q

Hypokalaemia ECG findings?

A 
U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT

In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

132
Q

Associations with aortic dissection?

A
  • HTN – most impt
  • Trauma
  • Bicuspid aortic valve
  • Marfan’s, Ehlers-Danlos
  • Turner’s + Noonan’s syndrome
  • Pregnancy
  • Syphilis
133
Q

Symptoms of aortic dissection?

A 
o	Chest pain (“tearing”)
o	Aortic regurgitation
o	Myocardial ischaemia
o	HTN
o	Syncope
o	Neurological symptoms (d/t involvement of the spinal arteries and carotid artery)
o	Pulse deficit + BP variation >20mmHg
Typical = man in 60s with HTN and sudden onset chest pain
134
Q

Management of aortic dissections?

A

ASS and BooBs
Type A - systolic management and surgery, 2/3 of cases
Type B - beta blockers and bed rest

135
Q

Complication of aortic dissections?

A

Think about the dissection flowing back and affecting the heart

Hpertension – poor prognosis, may be d/t cardiac tamponade/MI
Aortic regurgitation

Cardiac tamponade
Occlusion of the aortic branches with resulting damaged to supplied organs (renal, iliac, spinal, coronary)

136
Q

What are the main reasons for inaccurate BP measurements?

A

wrong cuff size - too small: overestimation of BP, too large: underestimation of BP
the arm should be horizontal at the level of the heart
Lowering of the arm below heart level: overestimation of BP, above heart level: underestimation of BP
posture: the sitting position is considered standard
arm support: if the arm is unsupported this may raise the diastolic blood pressure (as the arm is performing isometric exercise)

137
Q

MOA of fondaparinux?

A

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

138
Q

What class of drugs are bivalirudin and dabigitran in?

A

Direct thrombin inhibitors

139
Q

What type of drug is indomethacin and what is the MOA?

A

NSAIDs

inhibit COX which prevents the production of prostaglandin E2

140
Q

When are NSAIDs given to children?

A

To close the PDA within 1-2 weeks of life

141
Q

When does the ductus arteriosus usually close?

A

Following the first few breaths

142
Q

Howto keep the duct open if needed due to another structural heart abnormality?

A

prostaglandin E1

143
Q

What are the high risk groups for pre-eclampsia and what should you give them from when?

A

hypertensive disease during prev preg
CKD
AI disorders such as SLE/APS
T1/2 DM

Give aspirin 75mg from 12wks til birth

144
Q

What are the normal variations in BP during pregnancy?

A

BP usually falls in the first trimester (particularly the diastolic), and continues to fall until 20-24 weeks
Then BP usually increases to pre-pregnancy levels by term

145
Q

How to define HTN in pregnancy?

A

systolic > 140 or diastolic > 90

or increase above booking readings of > 30 systolic or > 15 diastolic

146
Q

Dx criteria for pre-eclampsia?

A

Pregnancy-induced HTN in association with proteinuria (> 0.3g / 24 hours)

Oedema may occur but is now less commonly used as a criteria

Occurs in around 5% of pregnancies

147
Q

Dx of gestational HTN?

A

HTN occurring after 20 wks (if <20wks = pre-existing HTN)

No proteinuria, no oedema

Occurs in around 5-7% of pregnancies

Resolves following birth (typically after one month). Women with PIH are at increased risk of future pre-eclampsia or HTN later in life

148
Q

Which coronary artery supplies the AV node?

A

R coronary artery

149
Q

What might you hear on auscultation in complete heart block and what might the JVP look like?

A

variable intensity of S1

cannon waves in neck

150
Q

Rare adverse effects of thiazides?

A

thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

Designed to TRAP you

151
Q

Who is more at risk of developing SEs from statin?

A

Thin old diabetic lady

152
Q

Statin CIs?

A

Macrolides, preg
Avoid if Hx intracerebral haemorrhage

(Macropodes cause increased exposure to statins)

153
Q

SEs of statins?

A 
Myopathy
Liver impairment (check LFTs at baseline, 3m and 12m – stop if ALT/AST remain 3x upper limit)
154
Q

What is the gold standard investigation for providing structural images of the heart?

A

Cardiac MRI

155
Q

What is the gold standard investigation for investigating for ischaemic heart disease?

A

Cardiac CT

156
Q

Reasons to stop an exercise tolerance test?

A

exhaustion / patient request
‘severe’, ‘limiting’ chest pain
attainment of maximum predicted heart rate (220 - age)
arrhythmia develops

The 23 rule
3 mm ST depression, 2 mm ST elevation, SBP more than 230 mmHg , SBP falling more than 20mmHg, HR falling more than 20%

157
Q

Length of time that trop may be raised?

A

(T and I) – usual increase (from 3hrs, peak at 24-48hrs) then decrease (over 5-14 days)

158
Q

How to manage ACS with ST elevation?

A

• If presenting within 12 hours, PCI – Primary angioplasty (if patient can be transferred and given PCI within 120 mins), if not offer tissue plasminogen activator (tenecteplase/alteplase), if no ECG resolution after 60-90m, transfer for PCI
• If presenting over 12 hours, consider coronary angiography, then maybe PCI – always put in ‘drug-eluting’ stents now
• Add antiplatelet agent (dual antiplatelet therapy - additional to aspirin) e.g. Ticagrelor or prasugrel for 12 months, if taking an oral anticoag, add clopidogrel
Then add anti-thrombin agent e.g. heparin

159
Q

How to manage ACS without ST elevation?

A
  • Anti-thrombolytic fondaparinux (inhibits factor 10a) if low bleeding risk and no angiography planned immediately, otherwise consider unfractionated heparin
  • Add a second antiplatelet drug
  • If not at high risk of bleeding: give Ticagrelor (or prasugrel)
  • If at low risk of bleeding (or if taking an oral anticoag): give clopidogrel
  • Ticagrelor – preferred second antiplatelet, given to all patients and continued for 12 months
  • Coronary angiography – consider within 72 hours of first admission to hospital who have a poor predicted 6 month mortality (>3%) – GRACE score/haemodynamically stable
160
Q

Drugs that can cause HTN?

A 
steroids
monoamine oxidase inhibitors (phenelzine)
the combined oral contraceptive pill
NSAIDs
leflunomide
161
Q

Which marker rises first in MIs?

162
Q

What is the use of CK-MB in MIs?

A

useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)

163
Q

What are two types of strep viridans?

A

Streptococcus sanguinis

Streptococcus mitis/oralis

164
Q

What does the S3 represent?

A

A S3 heart sound is produced during passive left ventricular filling when blood strikes a compliant LV
May be normal, may be a sign of early LVF (e.g. dilated cardiomyopathy), constrictive pericarditis and mitral regurgitation

165
Q

What does the S4 represent?

A

A S4 heart sound occurs during active LV filling when atrial contraction forces blood into a noncompliant LV

= sound of the blood being forced into a stiff/small ventricle

May be heard in aortic stenosis, HOCM, hypertension, and it is rarely a normal finding

166
Q

In which conditions do you see pulses paradoxus?

A

severe asthma, cardiac tamponade

167
Q

In which condition do you see Pulsus alternans?

A

regular alternation of the force of the arterial pulse

LVF

168
Q

In which condition do you see Bisferiens pulse?

A

‘double pulse’ - two systolic peaks

mixed aortic valve disease

169
Q

In which condition do you see a jerky pulse?

A

HOCM

a rapid upstroke due to the vigorous contraction of the hypertrophic left ventricle

170
Q

Reasons to implant a ICD?

A 
long QT syndrome
HOCM
previous cardiac arrest due to VT/VF
previous MI with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35%
Brugada syndrome
171
Q

What are the ECG changes in WPW?

A

short PR interval, upsloping wide QRS (delta wave), ST-T changes

172
Q

What is the management of WPW?

A

Require electrophysiology and ablation of accessory pathway

Medical Tx – amiodarone/flecainide/sotalol

173
Q

Which treatment has not been shown to improve mortality in patients with chronic heart failure?

A

Loop diuretics

174
Q

Investigations in aortic dissection?

A

CXR – widened mediastinum
CT CAP – gold standard
TOE – gives an indication of site and extent, more suitable for unstable patients

175
Q

Which medication is most likely to improve long-term prognosis in angina?

176
Q

What is given to prevent episodes of SVT?

A

B-blockers

Ablation

177
Q

Following stent insertion for MI what is the most important factor in preventing stent thrombosis?

A

Anti-platelet therapy

178
Q

What is the histological finding in the heart of a patient with rheumatic heart disease?

A

Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

Also Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus)

179
Q 
Where are the following found:
Councilman bodies
Mallory bodies
Call-Exner bodies
Schiller-Duval bodies
A

Councilman bodies -> hepatitis C, yellow fever
Mallory bodies -> alcoholism (hepatocytes)
Call-Exner bodies-> granulosa cell tumour
Schiller-Duval bodies -> yolk-sac tumour

180
Q

Poor prognostic factors in HOCM?

A
  • Syncope
  • FH of sudden death
  • Young age at presentation
  • Non-sustained vent tachycardia on 24 or 48hr Holter monitoring
  • Abnormal BP changes on exercise
  • Increased septal wall thickness
181
Q

Components of thick filament of muscle?

182
Q

Components of the thin filament of muscle?

A

All have a T

Actin, Tropomycin, Troponin

183
Q

Which type of CHB following MI is not an indication for pacing?

A

Inferior MI

184
Q

What is sick sinus syndrome and how is it treated?

A

A group of abnormal heart rhythms thought to be from sinus node dysfunction
Causes bradycardia +/- arrest, sinoatrial block or SVT alternating with bradycardia or asystole (tachy-brady syndrome)
May need pacing if symptomatic

185
Q

Different types of S2?

loud/soft/fixed split/reversed split/widely split

A

loud: hypertension
soft: AS
fixed split: ASD
reversed split: LBBB (going backwards)
widely split: RBBB

186
Q

What is the Second most common cause of sudden cardiac death in the young and how is it inherited?

A

Arrhythmogenic Right Ventricular Cardiomyopathy

AD with variable expression

187
Q

What is the pathophysiology of Arrhythmogenic Right Ventricular Cardiomyopathy?

A

The R vent myocardium is replaced by fatty and fibrofatty tissue

188
Q

What are the investigations for Arrhythmogenic Right Ventricular Cardiomyopathy?

A

ECG – abnormalities (T-wave inversion) in V1-3
- Epsilon wave found in 50% (extra notch after QRS)
Echo – subtle, may be enlarged, hypokinetic R ventricle with a thin free wall
MRI – shows fibrofatty tissue

189
Q

What is the management of Arrhythmogenic Right Ventricular Cardiomyopathy?

A

Sotalol
Catheter ablation to prevent VT
ICD

190
Q

What is the name of the condition characterised by the triad of ARVC, palmoplatar keratosis + woolly hair

A

Naxos disease

191
Q

What are the investigations and results in dilated cardiomyopathy?

A

Plasma BNP – secreted by the ventricle in heart failure
CXR – ‘balloon appearance’ of the heart, pulmonary oedema
ECG – tachycardia, non-specific T wave changes
Echo – globally dilated hypokinetic heart and low ejection fraction, look for MR, TR

192
Q

Management of dilated cardiomyopathy?

A

Bed rest, diuretics, digoxin, ACEi, anticoagulation, biventricular pacing, ICDs, cardiac transplantation

193
Q

Hypothermia ECG changes?

A 
Jesus, Its Bloody Freezing QT
J waves
Irregular rhythm (atrial/ventricular arrhythmias)
Bradycardia 
First degree heart block
QT interval long
194
Q

What might you see on ECG and echo in Takotsubo’s cardiomyopathy?

A

ECG: ST-elevation

apical ballooning appearance - octopus pot

195
Q

Main SE of ticagrelor?

A

Dyspnoea (d/t impaired clearance of adenosine)

196
Q

What would you feel on palpation of the chest with LVH or RVH?

A

RVH: left parasternal heave
LVH: displacement of the apex

197
Q

What causes a widened pulse pressure?

A

A less compliant aorta (this tends to occur with advancing age)
Increased stroke volume in the heart

Exercise
Aortic regurg
Stiffness of the great arteries

198
Q

Features of severe AS?

A 
narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
LVH or failure
199
Q

When to measure levels in suspected digoxin toxicity?

A

Measure levels within 8-12hrs of last dose

200
Q

Features of digoxin toxicity?

A

Arrhythmias – AV block (e.g. complete heart block), resulting bradycardia
Anorexia, N&V
Confusion, esp in the elderly
Vision problems – yellowed, blurred, photophobia

201
Q

Main precipitating factor of digoxin toxicity?

A

Hypokalaemia

202
Q

ECG changes in digoxin toxicity?

A

ST depression + T wave inversion in V5-6

Bradycardia

203
Q

Management of digoxin toxicity?

A

Conservative for mild toxicity – short discontinuation + oral potassium
Serious toxicity:
First-line treatment – Digibind
IV magnesium (this protects the myocardium)

204
Q

BP definition of postural HTN?

205
Q

Potential medical management of orthostatic HTN?

A

Fludrocortisone

Alpha-receptor agonists (midodrine)

206
Q

What is the difference between UA and NSTEMI?

207
Q

Three criteria for angina?

A

Criteria for angina (cardiac chest pain):

1) Characteristic chest pain
2) Worse on exercise
3) Better after 5mins rest/GTN

208
Q

Management of cardiac failure?

209
Q

Management of HTN?

210
Q

What is Ebstein’s anomaly and what may it be caused by?

A

Congenital heart defect
May be caused by exposure to lithium in-utero
Triscuspid valve lower than normal creating a big atria

211
Q

Associations with epstein’s anomaly?

A

Associated with PFO + ASD – 80% of cases, and WPW

212
Q

Features of Ebstein’s anomaly?

A

Cyanosis
Prominent ‘a’ wave
Hepatomegaly
Tricuspid regurg – pansystolic murmur, worse on inspiration

213
Q

Investigations in Ebstein’s anomaly?

A

RBBB -> widely split S1 + S2
May be delta wave – WPW
Echo for diagnosis

214
Q

What is Brugada syndrome, what is the cause and what is the inheritance?

A

Rare inherited cause of sudden cardiac death
Autosomal dominant inheritance – sodium or calcium channelopathy
20-40% caused by mutation in the SCN5A gene which encodes the myocardial Na ion channel

215
Q

What are the ECG findings in Brugada’s syndrome?

A

RBBB

J point elevation with persistent ST elevation in V1-V3

216
Q

Management of Brugada’s syndrome?

A

In the asymptomatic, no clear treatment plan

Those at high risk of sudden cardiac death may need implantable cardioverter defibrillator (ICD)

217
Q

What condition would you think of if there is an absent limb pulse?

A

Takayasu’s arteritis

218
Q

What medication can you use in PAD if surgery is not appropriate?

A

naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life

219
Q

Management of PE with haemodynamic instability?

A

Massive PE + hypotension -> thrombolyse

Can consider IVC filters in recurrent

220
Q

Where do trop T, C and I bind to?

A

Trop T - binds Tropomyosin
Trop C - binds Calcium ions
Trop I - binds actIn

221
Q

What s Liddle’s syndrome and how is it treated?

A

Liddle’s syndrome is a rare AD condition that is one of the inherited forms of hypertension. Also have hypokalaemic alkalosis. It is thought to be caused by disordered sodium channels in the distal tubules leading to increased reabsorption of sodium.

Conventional antiHTNs are not effective. Treatment is with K sparing diuretics like amiloride.

222
Q

Management of atrial flutter?

A

is similar to that of atrial fibrillation although medication may be less effective
atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

223
Q

MOA and SEs of atropine?

A

Atropine is an antagonist of the muscarinic acetylcholine receptor
SE: tachycardia, mydriasis (dilation of pupil)

224
Q

Associations with LBBB?

A

MI
the Sgarbossa criteria can help with this - please see the link for more details
HTN
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

225
Q

Target INR for mechanical heart valve, VTE and AF?

A

Mechanical - depends on valve type and location
VTE + AF - 2.5
If second VTE - 3.5

226
Q

What is multifocal atrial tachycardia and what is the management?

A

Multifocal atrial tachycardia (MAT) may be defined as a irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease, for example COPD.

Mx = RL CCB
Ablation/digoxin don’t work

227
Q

How to remember the ECG changes in Brugada compared to arrhythmogenic right ventricular cardiomyopathy?

A

arrhythmogenic has both a T and an E in, Brugada doesn’t

Therefore arrh -> T wave inversion in V1-V3, Epsilon wave
Brugada -> ST elevation in V1-V3

228
Q

Most common causes of aortic stenosis?

A

younger patients < 65 years: bicuspid aortic valve

older patients > 65 years: calcification

MRCP (14 decks)

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