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EXAM > Cardio 7.5 > Flashcards

Cardio 7.5 Flashcards

1
Q

MoA of loop diuretics?

A

Inhibit the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of loop of Henle, reducing the absorption of NaCl
(2 variants of NKCC - they act on NKCC2, more prevalent in the kidneys)

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2
Q

Indications for loop diuretics?

Adverse effects?

A
  • heart failure: acute IV, chronic PO
  • resistant HTN, esp in pts with renal impairment
  • hypotension
  • hyponatraemia
  • hypokalaemia
  • hypochloraemic alkalosis
  • hypocalcaemia
  • ototoxicity
  • renal impairment (dehydration + direct toxic effect)
  • gout
  • hyperglycaemia (less common than with thiazides)
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3
Q

Associations with aortic dissection?

A
  • trauma
  • HTN
  • bicuspid aortic valve
  • pregnancy
  • syphilis
  • collagens: Marfans, Ehlers-Danlos
  • Turners & Noonans syndromes
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4
Q

Features of aortic dissection?
Stanford classifcation?
DeBakey classification?

A
  • chest pain: severe, radiates through to back & ‘tearing’ in nature
  • aortic regurgitation
  • HTN
  • involvement from specific arteries e.g. coronary -> angina, spinal -> paraplegia, distal aorta -> limb ischaemia

Stanford:
type A = ascending, 2/3
type B = descending distal to left subclavian, 1/3

DeBakey:
type I - originates in ascending aorta, propagates to at least the aortic arch & possibly beyond it distally
type II - originates in & is confined to ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally

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5
Q

Causes of a paroxysmal SVT?

A
  • sudden onset narrow complex tachycardia - typically an AVNRT: AV normal re-entry tachycardia
  • other causes include AVRT & junctional tachycardias
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6
Q

Acute Rx of SVT?

A
  • vagal manoeuvres
  • IV adenosine 6 -> 12 -> 12mg (C/I in Asthma - consider verapamil instead)
  • electrical cardioversion
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7
Q

Prevention of SVT?

A
  • beta-blockers

- radio-frequency ablation

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8
Q

Causes of LQTS/Torsades de Pointes

A
  • Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
  • TCAs, antipsychotics
  • amiodarone, sotalol, class 1a antiarrhythmics
  • chloroquine
  • terfenadine
  • erythromycin
  • hypothermia
  • myocarditis
  • SAH
  • hypocalcaemia, hypokalaemia, hypomagnesaemia
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9
Q

Rx of Torsades de pointes/LQTS?

A

IV magnesium sulphate

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10
Q

Causes of LBBB?

A
  • IHD
  • HTN
  • aortic stenosis
  • cardiomyopathy
  • rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
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11
Q

Non-pulsatile JVP

A

superior vena cava obstruction

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12
Q

Kussmaul’s sign: paradoxical rise in JVP during inspiration

A

constrictive pericarditis

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13
Q

What does A wave show in the JVP waveform?
Absent in?
Large if?

A

Atrial contraction

  • absent in AF
  • large if atrial person: TS, PS, pulm HTN
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14
Q

Cannon ‘a’ waves

A
  • caused by atrial contractions against a closed tricuspid valve
  • e.g. complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing
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15
Q

What does ‘c’ wave show in JVP?

A

Closure of tricuspid valve

- not normally visible

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16
Q

What does ‘V’ wave show in JVP?

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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17
Q

What does ‘X’ descent show in JVP?

A

Fall in atrial pressure during ventricular systole

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18
Q

What does ‘Y’ descent show in JVP?

A

Opening of the tricuspid valve

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19
Q

Drug Rx of Angina:

  • what should everyone receive in the absence of C/I?
  • what should be used to abort angina attacks?
  • what is 1st line?
  • 2nd line?
  • if monothoerapy inadequate & can’t tolerate dual Rx?
  • if on dual Rx and still Sx?
A
  • aspirin + statin
  • GTN sublingual prn
    Nb always increase to max tolerated dose before stepping up treatment
  • 1st line = beta-blocker or rate-limiting calcium-channel blocker e.g. verapamil/diltiazem
  • 2nd line, combo required of beta-blocker + long-acting dihydropyridine calcium-channel blocker e.g. MR nifedipine
  • increase to max tolerated dose

If monoRx inadequate or can’t tolerate dual then consider adding one of:

  • long-acting nitrate
  • ivabradine
  • nicorandil or
  • ranolazine

If Sx on dual Rx then:
- only add a 3rd drug whilst a pt is waiting assessment for PCI or CABG

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20
Q

Nitrates in angina - tolerance

A
  • many pts develop tolerance & experience reduced efficacy
  • take 2nd dose of ISMN after 8h instead of 12 in pts who develop tolerance, as it allows blood-nitrate levels to fall for 4h & maintains effectiveness
  • not seen in pts who take MR ISMN
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21
Q

Ivabradine (used in angina)

  • what is the MoA?
  • what are the adverse effects?
A
  • acts on If (funny) ion current which is highly expressed in the SAN, reducing cardiac pacemaker activity therefore reduces the heart rate
  • visual effects esp luminous phenomena are common
  • headache
  • bradycardia due to oA
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22
Q

5 ECG features of hypokalaemia?

- they begin when K+ falls below 2.7

A
  • prolonged PR interval
  • long QT
  • ST depression
  • small/absent/inverted T waves
  • U waves
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23
Q

What is pre-eclampsia?

When is it seen?

A

Pregnancy-induced hypertension + proteinuria (>0.3g/24h) +/- oedema
- after 20 weeks gestation

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24
Q

What does pre-eclampsia predispose to?

A
  • fetal: prematurity, IUGR
  • eclampsia
  • haemorrhage: placental abruption, intra-abdo, intra-cerebral
  • cardiac failure
  • multi-organ failure
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25
Q

What are moderate & high RFs for pre-eclampsia?

A

Moderate:

  • 1st pregnancy
  • age 40+
  • pregnancy interval > 10years
  • BMI 35+ at 1st visit
  • FHx pre-eclampsia
  • multiple pregnancy

High RFs:

  • hypertensive disease in previous pregnancy
  • CKD
  • T1DM/T2DM
  • chronic HTN
  • AI disease e.g. SLE, antiphospholipid syndrome
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26
Q

LQTS = whatare the features ass with each type?

A

LQT1 - exertional syncope, often swimming
LQT2 - syncope following emotional stress, exercise or auditory stimuli
LQT3 - events often occur at night or at rest
Otherwise: may be picked up on routine ech or family screening; ass with sudden cardiac death

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27
Q

Management of LQTS?

A
  • avoid drugs/precipitants e.g. strenuous exercise
  • beta-blockers (NOT sotalol)
  • implantable cardioverter defibrillator in high risk cases
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28
Q

MoA of statins?

A

inhibit HMG-CoA reductase - the rate-limiting enzyme in hepatic cholesterol synthesis
- therefore decreases intrinsic cholesterol synthesis

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29
Q

Statin-induced myopathy is more commnon with which statins?

What are the RFs for myopathy with statins?

A

More common with LIPOphilic statins e.g. simvastatin/atorvastatin, than relatively hydrophilic ones e.g. rosuvastatin, pravastatin, fluvastatin
- inc age, female sex, low BMI, multisystem disease e.g. DM

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30
Q

Adverse effects of statins?

when to discontinue?

A
  1. Myopathy: myalgia, myositis, rhabdomyolysis & aSx raised CK
  2. Liver impairment - check LFTs at baseline, 3m & 12m
    - discontinue if serum transaminase conc rise and persist at 3X ULN
  3. May increase risk of ICH in pts who’ve prev had a stroke therefore avoid if Hx of intracerebral hameorrhage - not seen in 1ry prevention
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31
Q

Who should receive a statin?

A

1ry atorvastatin 20mg ON
- anyone with 10yr qrisk 10%+
- assess all T2DM with qrisk
- all T1DM Dx at least 10 yrs OR aged 40 OR established nephropathy
2ry atorvastatin 80mg ON
- all with established CVD: stroke, TIA, IHD, PVD

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32
Q

Types of Ventricular tachycardia?

Rx of VT?

A

VT = broad-complex tachycardia from a ventricular ectopic focus. Has potential to precipitate VF

  1. Monomorphic VT - most commonly caused by MI
  2. Polymorphic VT - subtype of which is Torsades (precipitated by prolonged QT)

Adverse signs e.g. chest pain, heart failure, shock -> Immediate cardioversion

No adverse signs -> drug therapy
If drug therapy fails -> electrical cardioversion may be needed with synchronised DC shocks
e.g. EPS: electrophsyiological study or ICD (esp if significantly impaired LV function)

Drugs:
Amiodarone through central line
Lidocaine (caution in severe LV impairment)
Procainamide

Verapamil is contra-indicated - may precipitate VF

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33
Q

Which 4 drugs improve mortality in heart failure?

A
  1. ACE-I
  2. beta-blockers
  3. spironolactone
  4. hydralazine with nitrates
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34
Q 
Heart failure drug Rx:
Cons?
1st line?
2nd line?
If Sx persist?
What are the criteria for ivabradine?
A

Cons: rmr annual flu jab & one-off pneumococcal
Diuretics for fluid overload/Sx Rx

1st: ACE-I + beta-blocker (bisoprolol/carvedilol/nebivolol)
2nd: aldosterone antagonist OR A2RB OR hydralazine+nitrate

If Sx persis then consider cardiac resynchronisation therapy or digoxin or ivabradine
Ivabradine: must be on suitable Rx, HR > 75 and LV EF < 35%
Digoxin may improve Sx due to inotropic properties and is strongly indicated if coexistent AF. But doesn’t improve mortality

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35
Q

MoA of Sacubitril (neprilysin inhibitor) in heart failure?
It has een shown to reduce mortality, hospitalisations & improve Sx combined with an A2RB (vs enalapril) in heart failure Rx with reduced EF

A

Prevents degradation of natriuretic peptides e.g. ANP, BNP

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36
Q

Upregulation of RAAS system in heart failure

A

RAAS & sympathetic activation & vasopressin

  • -> sodum & water retention
  • -> increased ventricular preload & afterload & elevated wall stress –> BNP production –> promotes natriuresis & vasodilation
  • -> atrial stress –> ANP
  • -> ANP & BNP are inactivated by a membrane-bound endopeptidase Neprilysin (found in tissues but v high conc in kidneys)
  1. Exogenous natriuretic peptides e.g. Nesiritide recombinant human BNP showed promise & relieved dsome dyspnoea but without improving outcomes
  2. Inhibit natriuretic peptide breakdown: e.g. Sacubitril a neprilysin inhibitor - reduces mortality, hospitalisations & improves Sx when given with Valsartan vs enalapril in Rx of heart failure with reduced EF
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37
Q

Commonest clinical signs with PE?

A

Tachypnoea RR > 16 96%
Crackles 58%
Tachycardia HR > 100 44%
Fever temp > 37.8 43%

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38
Q

Suspected PE: Hx, Ex & CXR…

2-level PE Wells score?

A

3 signs & Sx of DVT: minimum of UL leg swelling & pain wilth palpation of deep veins
3 alternative Dx less likely than PE
1.5 HR > 100
1.5 immobilisation >3days or surgery in past 4wks
1.5 prev DVT/PE
1 haemoptysis
1 malignancy on Rx or Rx in last 6m or palliative

> 4 points PE likely -> CTPA

<5 points PE unlikely -> D-dimer

V/Q scan if allergy to contrast media or renal impairment

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39
Q

ECG in PE?

A
  • sinus tachycardia commonest
  • RBBB & R axis deviation associated
  • S1Q3T3: large S in lead I, large Q in lead III, inverted T in lead III
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40
Q

CTPA in PE?

V/Q scan in PE?

What is the gold standard?

A

CTPA:
- peripheral emboli affecting subsegmental arteries may be missed

V/Q scan:
- if normal virtually excludes PE but not v specific - other causes inc old PEs, AV malformations, vasculitis, prev RT. COPD gives matched defects

Gold standard = pulmonary angiography
- significant complication rate vs other Ix

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41
Q 
Arterial supply of the heart:
left aortic sinus?
right aortic sinus?
left coronary artery?
right coronary artery?

Venous drainage??

A 
L aortic sinus -> LCA
R aortic sinus -> RCA
LCA -> LAD &amp; circumflex
RCA -> posterior descending
RCA supplies SAN in 60% &amp; AVN in 90%
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42
Q

What is HOCM?

Commonest gene defects?

A
  • autosomal dominant disorder of muscle tissue caused by defects in genes encoding contractile proteins
  • most common defects involve mutation in gene encoding beta-myosin heavy chain protein or myosin protein C
  • septal hypertrophy causes LV outflow obstruction
  • prevalence 1/500
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43
Q

Features & associations of HOCM?

A
  • often aSx
  • dyspnoea, angina, syncope
  • sudden death (ventricular arrhythmia), arrhythmias, heart failure
  • JERKY pulse, large ‘A’ waves, double apex beat
  • ESM: increases with valsalva manoeuvre & decreases on squatting

Ass:

  • Friedreichs ataxia
  • WPW syndrome
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44
Q

Echo features in HOCM?

ECG?

A

Echo:
MR: mitral regurgitation
SAM: systolic anterior motion of anterior mitral valve leaflet
ASH: asymmetric hypertrophy

ECG:

  • LV hypertrophy
  • progressive T wave inversion
  • deep Q waves
  • AF sometimes seen
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45
Q

Which cardiac ion channel is most likely affected in Torsades de points?

A

Potassium channel:

  • they lengthen cardiac re-polarisation mostly by blocking specific cardiac K channels
  • the potent blocking of them & excessive lengthening of cardiac re-polarisation -> membrane oscillations (early after-depolarisation) due to Ca2+/Na re-entry
  • Early after-depolarisation, when propagated, may trigger torsade de pointes
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46
Q

DVLA notification/off driving?

  • HTN
  • angioplasty
  • CABG
  • ACS
  • angina
  • pacemaker insertion
  • ICD
  • successful catheter ablation
  • aortic aneurysm 6cm+
  • heart Tx
  • heart failure
A

HTN -> no need to notify unless unacceptable side-effects, group 2 can’t drive if BP consistently > 180/100
elective angioplasty -> 1 week off
CABG -> 4 weeks off
ACS -> 4 weeks off; 1 week if successful angio
angina -> cannot drive if Sx at rest/wheel
pacemaker insertion -> 1 week off
ICD -> off driving 1month if prophylactic; off driving 6months if for sustained ventricular arrhythmia; no more driving if group 2 driver
successful catheter ablation for arrhythmia -> 2 days off
aortic aneurysm 6cm+ -> notify dvla, needs annual R/v, if 6.5cm+ no more driving
heart Tx -> dvla don’t need to be notified
heart failure -> group 1 don’t need to notify unless incapacitating Sx, but Sx heart failure means no group 2 license regardless of Sx - if becomes aSx can regain license only if EF>40%

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47
Q

Clinical features of Sx aortic stenosis?

Features of Severe aortic stenosis?

A
  • chest pain
  • dyspnoea
  • syncope

Severe:

  • narrow pulse pressure
  • slow rising pulse
  • delayed ESM
  • soft/absent S2
  • S4
  • thrill
  • long murmur
  • LV hypertrophy or failure
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48
Q

Causes of aortic stenosis?

Rx?

A
  • degenerative calcification commonest > 65yrs
  • bicuspid aortic valve commonest < 65yrs
  • WIlliam’s syndrome: supravalvular
  • HOCM: subvalvular
  • post-rheumatic disease

aSx -> observe
aSx with valvular gradient > 40mmHg & features of LV systolic dysfunction -> consider surgery
Sx -> valve replacement
Balloon valvuloplasty limited to pts with critical aortic stenosis who aren’t fit for valve replacement

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49
Q

Causes of a prolonged PR interval (1st degree heart block)?

A
  • idiopathic
  • IHD
  • hypokalaemia
  • digoxin toxicity
  • rheumatic fever
  • aortic root pathology e.g. abscess 2ry to endocarditis
  • Lyme disease
  • sarcoidosis
  • myotonic dystrophy
  • athletes
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50
Q

Cause of short PR interval?

A

WPW syndrome

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51
Q

Features of acute pericarditis?

A
  • chest pan: may be pleuritic, often relieved sitting forwards
  • non-productive cough, dyspnoea, flu-like Sx
  • tachypnoea, tachycardia
  • pericardial rub
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52
Q

ECG changes in acute pericarditis - most specific?

A

Most specific = PR depression

can also see widespread saddle-shaped ST elevation

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53
Q

Causes of acute pericarditis?

A
  • viral e.g. Coxsackie
  • TB
  • trauma
  • uraemia (Fibrinous)
  • post-MI, Dressler’s syndrome
  • CT disease
  • hypothyroidism
  • malignancy
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54
Q

2ry prevention of MI:
Cons?
Medical?

A

Cons:

  • mediterranean diet. Don’t recommend omega-3 or oily fish. Switch butter/cheese to plant-based oils
  • exercise: 20-30mins/day
  • sexual activity can resume 4wks after uncomplicated MI (sex doesn’t increase likelihood of MI; can use sildenafil from 6months, as long as not on nitrates/nicorandil)

Med:

  • dual antiplatelet therapy - 12months clopidogrel after NSTEMI, aspirin+clopidogrel 12months if STEMI
  • ACE-I
  • beta-blocker
  • statin
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55
Q

2ry prevention of MI - when to give aldosterone antagonists?

A

Acute MI + Sx/signs of heart failure & LV systolic dysfunction -> start aldosterone antagonist licensed for post-MI Rx e.g. Eplerenone within 3-14days of MI, preferable after ACE-I Rx

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56
Q 
Xanthomata:
palmar?
eruptive?
tendon/tuberous/xanthelasma?
Rx?
A

Palmar xanthoma:
- remnant hyperlipidaemia
- may less commonly be seen in familial hypercholesterolaemia
Eruptive:
- due to high triglyceride levels, present as multiple red/yellow vesicles on extensor surfaces
- familial hypertriglyceridaemia
- lipoprotein lipase deficiency
Tendon xanthoma, tuberous xanthoma, xanthelasma:
- familial hypercholesterolaemia
- remnant hyperlipidaemia

Rx options:

  • surgical excision
  • topical trichloroacetic acid
  • laser therapy
  • electrodesiccation
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57
Q

MoA of Atropine?
Use?
Physiological effects?

A
  • antagonist of muscarinic acetylcholine receptor
  • Rx of organophosphate poisoning
  • mydriasis + tachycardia
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58
Q

Which type of valves/people are affected with infective endocarditis? (biggest RF is prev episode)

A
  • previously normal valves 50%, acute
  • rheumatic heart disease 30%
  • prosthetic valves
  • congenital heart defects
  • IVDUs (typically tricuspid)
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59
Q

Culture negative causes of infective endocarditis?

A
  • prior Abx therapy
  • Coxiella burnetii
  • Bartonella
  • Brucella
  • HACEK: haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
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60
Q

Commonest cause of infective endocarditis?

  • in developing countries?
  • in IVDUs/acute presentation?
  • indwelling lines/prosthetic valve surgery (after 2m the spectrum returns to normal)
  • colorectal cancer?
  • non-infective?
  • malignancy?
A

Commonest cause = staph aureus

  • in developing countries = streptococcus viridans e.g. mitis/sanguinis = common in mouth/poor dental
  • in IVDUs/acute presentation = staph aureus
  • indwelling lines/prosthetic valve surgery (after 2m the spectrum returns to normal) = coag-negative staph e.g. staph epidermidis
  • colorectal cancer = strep bovis
  • non-infective = SLE (Libman-Sacks)
  • malignancy = marantic endocarditis
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61
Q

ECG features in hypothermia?

A
  • bradycardia
  • J wave: small hump at end of QRS
  • 1st degree block/ prolonged PR interval
  • long QT interval
  • atrial & ventricular arrhythmias
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62
Q

Features of aortic regurgitation?

What is the Austin-Flint murmur?

A
  • early diastolic murmur
  • collapsing pulse
  • wide pulse pressure
  • mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
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63
Q

Causes of aortic regurgitation:
valve disease?
aortic root disease?

A

Valve:

  • rheumatic fever
  • infective endocarditis
  • CT disease e.g. RA/SLE
  • bicuspid aortic valve

Aortic:

  • aortic dissection
  • spondylarthropathies e.g. ank spond
  • hypertension
  • syphilis
  • Marfan’s, Ehler-Danlos
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64
Q

CHA2DS2VaSc score for AF anticoagulation?

A 
Congestive heart failure 1
Hypertension 1
Age 75+ 2
Age 65-74 1
Diabetes 1
Stroke/TIA 2
Vascular disease: IHD/PVD 1
Sex female 1

If score 1 in males then consider anticoag
If 2+ in females, offer anticoag

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65
Q

HASBLED bleeding risk assessment?

A 
Hypertension uncontrolled sBP > 160 = 1
Abnormal renal function: dialysis/Cr>200 = 1
Abnormal liver function (cirrhosis, bilirubin >2xULN, ALT/AST/ALP>3xULN) = 1
Stroke history = 1
Bleeding history/tendency = 1
Labile INRs (unstable/high, time in therapeutic range<60%) = 1
Elderly >65yrs = 1
Drugs that predispose to bleeding = 1
Alcohol use (>8drinks/wk) = 1

Score 3+ indicates high risk bleeding
- intracranial haemorrhage, hospitalisation, Hb decrease >2, transfusion

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66
Q

What is pulsus paradoxus?

When is it seen?

A
  • > 10mmHg fall in sBP during inspiration -> faint/absent pulse in inspiration
  • severe asthma, cardiac tamponade
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67
Q

When can a collapsing pulse be seen?

A
  • aortic regurgitation
  • patent ductus arteriosus
  • hyperkinetic: anaemia, thyrotoxic, fever, exercise, pregnancy
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68
Q

What is pulsus alternans?

when is it seen?

A

Regular alternation of the force of the arterial pulse

- severe LVF

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69
Q

What is bisferiens pulse?

when is it seen?

A

‘double pulse’ - 2 systolic peaks

- mixed aortic valve disease

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70
Q

When is a jerky pulse seen?

A

HOCM

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71
Q

Which women are at high risk of developing pre-eclampsia?

What should they take?

A

Aspirin 75mg OD from 12 weeks

  • hypertensive disease during previous pregnancies
  • CKD
  • autoimmune disorders e.g. SLE/antiphospholipid syndrome
  • T1DM/T2DM
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72
Q

What happens to BP in normal pregnancy?

How to define hypertension in pregnancy?

A
  • BP normally falls in 1st trimester (esp diastolic), & continues to fall until 20-24wks
  • then it usually increases to pre=pregnancy levels by term

sBP > 140 or dBP > 90
or an increase above booking readings of >30 sBP or >15 dBP

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73
Q

ECG features with digoxin?

A
  • down-sloping ST depression (reverse tick)
  • flattened/inverted T waves
  • short QT interval
  • arrthymias e.g. AV block, bradycardia
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74
Q

Clopidogrel is a thienopyridine - what is the mechanism of action & other examples?

A
  • antagonist of the P2Y12 ADP receptor, inhibiting platelet activation
  • prasugrel, ticagrelor, ticlopidine
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75
Q

When is clopidogrel indicated?

What makes clopidogrel less effective?

A

1st line after ischaemic stroke, pts with peripheral arterial disease, and used for 12months with aspirin after ACS

  • PPIs may make clopidogrel less effective
  • lansoprazole should be ok

N.b. 12months dual anti platelets after placement of a drug-eluting stent v important - delay any elective surgery

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76
Q

HTN Rx?

BP targets?

A
  1. <55yrs ACE-I
    55+ or Afro-C calcium-channel blocker
  2. ACE-I + Calcium channel blocker
  3. add a thiazide-like diuretic e.g. CHLORTHALIDONE/INDAPAMIDE

If clinic BP >140/90 after step 3 = resistant hypertension -> step 4 or expert advice

  1. consider further diuretic Rx
    K < 4.5 add spironolactone 25
    K > 4.5 add higher-dose thiazide-like diuretic Rx
    If further diuretic not tolerate or C/I or ineffective, consider alpha/beta-blocker

Specialist referral if failure to respond to step 4 measures

Age<80yrs:
clinic 140>90 abpm 135/85
Age>80yrs:
clinic 150/90 abpm 145/85

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77
Q

Cons measures &

when to treat HTN?

A

LOW SALT <6g/day ideally 3g/day
- reduce caffeine, stop smoking, less etoh, exercise, lose weight, balanced diet etc

stage 1 HTN: treat if <80yrs AND target organ damage/established CVD/renal disease/ DM /10yr Qrisk 20%+

stage 2 HTN: offer drug Rx regardless of age

if <40yrs consider specialst referral to exclude 2ry causes

Lifestyle advice for hypertension?

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78
Q

Classification of hypertension:
stage 1?
stage 2?
severe?

A
  1. clinic 140/90 or abpm/home 135/85
  2. clinic 160/100 or abpm/home 150/95
    severe: clinic sBP>180 or dBP>110
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79
Q

How do direct renin inhibitors work in hypertension?

A

e.g. Aliskiren/Rasilez
- inhibits renin, blocking conversion of angiotensinogen -> angiotensin I
- initial trials suggest reduces BP similar to ACE-I/A2RB
- diarrhoea seen
-

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80
Q

What is Eisenmenger’s syndrome?

What is it associated with?

What are 5 features?

What is the Rx?

A
  • reversal of left-to-right shunt in a congenital heart defect due to pulmonary hypertension

Ass with: VSD, ASD, PDA

  1. original murmur may disappear
  2. cyanosis
  3. clubbing
  4. RV failure e.g. raised JVP, loud P2, large a waves
  5. haemoptysis, embolism

Rx = heart-lung Tx

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81
Q

What is Wellens’ syndrome?

A

ECG manifestation of critical proximal left anterior descending artery stenosis in pts with unstable angina
- symmetrical, often deep >2mm T wave inversions in the anterior precordial leads

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82
Q 
Coronary territories:
anteroseptal
inferior
anterolateral
lateral
posterior
A

anteroseptal V1-4 LAD
inferior II, III, aVF R coronary
anterolateral V4-6, I, aVL LAD/left circumflex
lateral I, aVL +/- V5,6 Left circumflex
posterior tall R waves V1-2, usually left circumflex, also right coronary

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83
Q

Poor prognostic factors in infective endocarditis?

A
  • staph aureus
  • prosthetic valve, esp if early/acquired during surgery
  • culture negative endocarditis
  • low complement levels

Mortality:
staph 30%
bowel organisms 15%
strep 5%

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84
Q

5 indications for surgery in infective endocarditis?

A
  1. severe valvular incompetence
  2. aortic abscess (often indicated by prolonged PR interval)
  3. infections resistant to Abx/fungal infections
  4. cardiac failure refractory to standard medical Rx
  5. recurrent emboli after Abx Rx
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85
Q

Infective endocarditis suggested Abx therapy when BLIND for:
native valve?
native valve if pen allergic/MRSA/severe sepsis?

if prosthetic valve?

A

Native: amoxicillin +/- gentamicin
or vancomycin + gentamicin

Prosthetic: vancomycin + rifampicin + gentamicin

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86
Q

Infective endocarditis suggested Abx therapy when staphylococcus native valve endocarditis?

A

Flucloxacillin
or
vancomycin + rifampicin

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87
Q

Infective endocarditis suggested Abx therapy when staphylococcus prosthetic valve endocarditis?

A

flucloxacillin + rifampicin + gentamicin
or
vancomycin + rifampicin + gentamicin

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88
Q

Infective endocarditis suggested Abx therapy when caused by fully-sensitive streptococci e.g. viridins?

A

Benzylpenicillin
or
vancomycin + gentamicin

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89
Q

Infective endocarditis suggested Abx therapy when caused by less sensitive streptococci e.g. viridins?

A

benzylpenicillin + gentamicin
or
vancomycin + gentamicin

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90
Q

When does rheumatic fever develop? how to Dx?

How to get evidence of recent strep infection?

A
  • develops following an immunological reaction to recent (2-6wks ago) strep pyogenes infection

Dx = evidence of recent strep infection +
2 major or
1 major + 2minor criteria

Evidence:

  1. raised/rising streptococci Ab
  2. positive throat swab
  3. positive rapid group A streptococcal Ag test
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91
Q

Major/minor criteria for rheumatic fever?
Major = JONES
Minor = FAPR

Commonest valve affected?

A 
Joint involvement: polyarthritis
O = heart = myo/carditis/valvulitis (regurg murmur)
Nodules subcutaneous
Erythema marginatum
Sydenham's chorea

Fever
Arthralgia (as long as arthritis not a major criteria)
Prolonged PR interval
Raised ESR/CRP

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92
Q

Cardiac histology of rheumatic fever?

A
  1. Aschoff bodies: granuloma with giant cells

2. Anitschkow cells: enlarged macrophages with ovoid, wavy, rod-like nucleus

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93
Q

Aschoff bodies (granuloma with giant cells) & Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus) on histology?

A

rheumatic heart disease

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94
Q

Councilman bodies on histology?

A

hepatitis C

yellow fever

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95
Q

Mallory bodies on histology?

A

alcoholism (hepatocytes)

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96
Q

Call-Exner bodies on histology?

A

granulosa cell tumour

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97
Q

Schiller-Duval bodies on histology?

A

yolk-sac tumour

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98
Q

Causes of ST elevation on ecg?

A 
MI
pericarditis/myocarditis
normal variant - high tae-off
LV aneurysm
Prinzmetal's angina (coronary artery spasm)
Takotsubo cardiomyopathy
rare: SAH
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99
Q

What are the 2 main things the management of bradycardia depends on?

A
  1. identifying adverse signs that may indicate haemodynamic compromise
  2. identifying potential risk of asystole
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100
Q

What are adverse signs that indicate haemodynamic compromise & hence need for Rx with bradycardia?

1st line Rx?
If it fails or potential risk of asystole?

A
  • shock: hypotension sbP <90, pallor, sweating, cold, clammy extremities, confusion, impaired consciousness
  • syncope
  • myocardial ischaemia
  • heart failure

ATROPINE
TRANSVENOUS PACING

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101
Q

4 factors that indicate a potential risk of asystole with bradycardia and hence need for Rx with transvenous pacing?

What 3 interventions can be used if there is a delay in transvenous pacing?

A
  1. recent systole
  2. ventricular pause > 3seconds
  3. Mobitz type II AV block
  4. complete heart block with broad complex QRS
  • Atropine max 3mg
  • transcutaneous pacing
  • isoprenaline/adrenaline infusion titrated to response
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102
Q

NSTEMI Rx?

What should be given if not high risk of bleeding?

What should be given to pts who have an intermediate/higher risk of adverse cardiovascular events i.e. 6month mortality>3%, OR will be having angiography within 96h of hospital admission

A
  • Aspirin 300mg STAT
  • Clopidogrel 300mg 12 months
  • Nitrates/Morphine to relieve chest pain if required
  • O2 if required
  • ANTITHROMBIN Rx if not high risk of bleeding e.g. Fondaparinux -> if having angio in next 24h or Cr>265 then give unfractionated heparin

IV GLYCOPROTEIN IIb/IIIa receptor antagonists e.g. EPTIFIBATIDE/TIROFIBAN

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103
Q

With NSTEMI Rx:
What should be given to pts who have an intermediate/higher risk of adverse cardiovascular events i.e. 6month mortality>3%, OR will be having angiography within 96h of hospital admission

A

IV GLYCOPROTEIN IIb/IIIa receptor antagonists e.g. EPTIFIBATIDE/TIROFIBAN

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104
Q

Mechanism of action of e.g. EPTIFIBATIDE/TIROFIBAN

A

IV GLYCOPROTEIN IIb/IIIa receptor antagonists

- given with NSTEMI if having angio within 96h of hospital admission or higher risk of adverse cardiovascular events

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105
Q

When to consider coronary angiography in NSTEMI?

A

Within 96h of first admission to hospital in pts who have a predicted 6month mortality >3%
- also asap in pts who are clinically unstable

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106
Q

MoA of aspirin?

A

antiplatelet - inhibits production of thromboxane A2

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107
Q

MoA of clopidogrel?

A

antiplatelet - inhibits ADP binding to its platelet receptor

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108
Q

MoA of enoxaparin & fondaparinux?

A

activates antithrombin III -> potentiates inhibition of coagulation factors Xa

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109
Q

MoA of bivalirudin?

A

reversible direct thrombin inhibitor

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110
Q

MoA of abciximab/eptifibatide/tirofiban?

A

glycoprotein IIb/IIIa receptor antagonists

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111
Q

Management if major bleeding when on warfarin?

A

stop warfarin
IV vitamin K 5mg
prothrombin complex conc - FFP if not available

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112
Q

Management if minor bleeding when on warfarin, with INR>8?

A

stop warfarin
IV vitamin K 1-3mg
repeat dose vitamin K if INR still too high after 24h
restart warfarin when INR<5.0

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113
Q

Management if no bleeding when on warfarin, with INR>8?

A

stop warfarin
give vitamin K 1-5mg PO (using IV prep orally)
repeat dose vitamin K if INR still too high after 24h
restart when INR<5

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114
Q

Management if minor bleeding when on warfarin, with INR 5-8?

A

stop warfarin
IV vitamin K 1-3mg
restart when INR<5

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115
Q

Management if no bleeding when on warfarin, with INR 5-8?

A

withhold 1-2doses of warfarin

reduce subsequent maintenance dose

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116
Q

What causes S1 1st heart sound?
when is it soft?
when is it loud?

A
  • closure of mitral & tricuspid valves
  • soft if long PR or mitral regurgitation
  • loud in mitral stenosis
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117
Q

What causes S2 2nd heart sound?
when is it soft?
when does it split?

A
  • closure of aortic & pulmonary valves
  • soft in aortic stenosis
  • splitting during inspiration is normal
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118
Q

What leads to S3 3rd heart sound?

What are the causes?

A
  • diastolic filling of the ventricle
  • normal if <30yrs
  • LV failure e.g. dilated cardiomyopathy
  • constrictive pericarditis (pericardial knock)
  • mitral regurgitation
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119
Q

What leads to S4 4th heart sound?

What are the causes?

A
  • caused by atrial contraction against a stiff ventricle
  • aortic stenosis
  • HOCM
  • hypertension
  • in HOCM a double apical impulse may be felt as a result of a palpable S4
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120
Q

PE Rx?

Massive PE/compromise Rx?

A

PE -> LMWH/fondaparinux
Massive PE -> unfractionated heparin when considering thrombolysis

  • warfarin within 24h for 3 months at least - extended time if unprovoked
  • lmwh 6months if active cancer
  • cont lmwh/fondaparinux at least 5 days or until INR>2 for 24h
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121
Q

Pt with recurrent VTE disease despite maximal Rx or e.g. whilst on maximal Rx dose - what should be considered?

A

IVC filter

  • if recurrent proximal DVT/PE despite adequate anticoag Rx ONLY after considering alternative rx e.g.:
  • switching to LMWH
  • increasing target INR to 3-4 for long term high-intensity oral anticoagulant Rx
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122
Q

What is most common underlying mechanism causing prolongation of QT segment?

A
  • blockage/loss of function of K+ channels (overload of myocardial cells with K+ during ventricular repolarisation)
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123
Q

What is WPW syndrome?

What are the associations?

A
  • congenital accessory conducting pathway between atria & ventricles leading to a AV re-entry tachycardia
  • as the accessory pathway doesn’t slow conduction, AF can degenerate rapidly to VF
  • HOCM
  • mitral valve prolapse
  • Ebstein’s anomaly
  • thyrotoxicosis
  • secundum ASD
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124
Q

Possible ECG features of WPW syndrome?

A
  • short PR interval
  • wide QRS complexes with a slurred upstroke - ‘delta wave’
  • LAD if right-sided (commonest)
  • RAD if left-sided accessory pathway

Type A = left-sided pathway: dominant R wave in V1
Type B: no dominant R wave in V1
Type C: delta waves are upright in leads V1-2 but negative in leads V5-6

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125
Q

Management of WPW syndrome?

A

Definitive = radiofrequency ablation of the accessory pathway

medical:
- sotalol (AVOID IF AF - prolonging the refractory period at the AVN may increase the rate of transmission through the accessory pathway -> VT -> VF)
- amiodarone
- flecainide

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126
Q

Major disadvantage of biological/bioprosthetic valves?

What sort of anticoagulation is needed?

A
  • structural deterioration & calcification over time (i.e. higher failure rate)
  • most older pts receive a bioprosthetic valve
  • long-term anticoag usually not needed
  • warfarin 3months depending on pt factors
  • low-dose aspirin long-term
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127
Q

Major advantage & disadvantage of mechanical heart valves?

A
  • low failure rate
  • increased risk of thrombosis
  • target INR aortic valve 3.0
  • target INR mitral valve 3.5
  • only given Aspirin as well if an additional indication e.g. IHD
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128
Q

What are the features of Takayasu’s arteritis?

Association?

Rx?

A
  • large vessel vasculitis
  • typically causes occlusion of the aorta, more common in females & Asians
  • systemic features of vasculitis e.g. malaise, headache
  • unequal BP in ULs, absent limb pulse
  • carotid bruit
  • intermittent claudication
  • aortic regurgitation 20% eg early diastolic murmur

Ass with renal artery stenosis

Rx = steroids

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129
Q

What are the most important parameters to monitor whilst giving a pt is receiving IV magnesium?

A

reflexes & resp rate

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130
Q 
What is eclampsia?
When is magnesium given?
how is it given?
what should be monitored?
how long to continue Rx?
A

= development of seizures in ass with pre-eclampsia
(after 20wks gestation, pregnancy-induced hypertension, proteinuria)

  • Nb fluid restriction is important too
  • magnesium sulphate to prevent & Rx seizures
  • give when a decision to deliver has been made
  • IV 4g bolus over 5-10mins then infusion of 1g/hr
  • monitor urine output, reflexes, RR & O2 sats during Rx
  • Rx should continue for 24h after last seizure or delivery (40% of seizures occur postpartum)
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131
Q

Features of cardiac tamponade?

A 
Sx = dyspnoea
Ex =
- tachycardia, hypotension
- pulsus paradoxus
- raised JVP with absent Y descent (limited RV filling)
- muffled heart sounds
ECG = electrical alternans
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132
Q 
Differences between cardiac tamponade &amp; constrictive pericarditis?
JVP
pulsus paradoxus
Kussmaul's sign
characteristic CXR
A

cardiac tamponade:

  • JVP absent Y descent
  • pulsus paradoxus +
  • Kussmaul’s rare

Constrictive pericarditis:

  • JVP X + Y present
  • NO pp
  • Kussmaul’s sign +
  • CXR pericardial calcification
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133
Q

Poor prognostic factors in HOCM?

A
  • genetic mutation in trop T
  • young age at presentation
  • syncope
  • FHx of sudden death
  • non-sustained ventricular tachycardia on 24/48h Holter monitoring
  • abnormal BP change (low) on exercise
  • increased septal wall thickness/ventricular wall thickness>30mm
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134
Q

Adverse signs with a tachycardia that makes a person unstable i.e. peri-arrest?

Rx?

A
  • shock: sBP<90, pallor, sweating, sold, clammy, confused, impaired GCS
  • syncope
  • myocardial ischaemia
  • heart failure
  • > electrical cardioversion i.e. DC SHOCK
  • > then Rx depends if it is narrow/broad and if rhythm is regular/irregular
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135
Q

Regular broad-complex tachycardia Rx?

A
  • assume ventricular tachycardia (unless previously confirmed SVT with bbb)
  • > AMIODARONE loading dose then 24h infusion
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136
Q

Irregular broad-complex tachycardia Rx?

A

AF with BBB -> treat as narrow complex tachycardia

Polymorphic VT -> IV MAGNESIUM

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137
Q

Regular narrow complex tachycardia Rx?

A

vagal manoeuvres -> IV adenosine

- if unsuccessful consider Dx of A flutter & rate control

138
Q

Irregular narrow complex tachycardia Rx?

A

probable AF

  • if onset <48h consider electrical/chemical cardioversion
  • rate control e.g. beta-blocker/digoxin & anticoagulation
139
Q

Features of atrial myxoma?

  • site
  • systemic
  • ecg
  • murmur
  • echo
A
  • 75% left atrium, more common in females
  • dyspnoea, fatigue, weight loss, fever, clubbing, emboli
  • AF
  • mid-diastolic murmur, ‘tumour plop’
  • echo: pedunculated heterogeneous mass typically attached to fossa ovals region of the intertribal septum
140
Q

What is a well-documented complication of coronary angiography? seen more commonly in arteriopaths, AAAs
What are the features?

A

Cholesterol embolisation - emboli may break off causing renal disease

  • purpura
  • livedo reticularis
  • eosinophilia
  • renal failure
141
Q

Chest pain referral

  • current or in the last 12h with abnormal ecg?
  • 12-72h ago
  • > 72h ago
A

current -> emergency admission
12-72h ago -> same-day assessment hospital referral
>72h ago -> full assessment with ecg & troponin

142
Q

How do NICE define anginal pain?

A
  1. constricting discomfort in the front of the chest, or in neck/shoulders/jaw/arms
  2. precipitated by physical exertion
  3. relieved by rest/GTN in about 5mins

all 3 = typical angina
2 = atypical angina
1/none = non-anginal chest pain

143
Q

For patients in whom stable angina cannot be excluded by clinical assessment alone NICE what Ix are recommended by NICE?
What are the options for non-invasive functional imaging?

(e.g. Sx consistent with typical/atypical angina OR ECG changes)

A

1st line = CT coronary angiography
2nd line = non-invasive functional imaging looking for reversible myocardial ischaemia
3rd line = invasive coronary angiography

Non-invasive:

  • myocardial perfusion scintigraphy (MPS) with SPECT
  • stress echo
  • first-pass contrast-enhanced magnetic resonance MR perfusion
  • MR imaging for stress-induced wall motion abnormalities
144
Q

How does amiodarone work?

What factors limit it’s use?

A
  • class III antiarrythmic used in Rx of atrial, nodal, ventricular tachycardias
  • main MoA = blocking K+ channels which inhibits repolarisation -> prolongs action potential
  • also has some class I effect
  • long half-life 20-100days
  • ideally give into central veins (thrombophlebitis)
  • pro arrhythmic effect (lengthening of QT interval)
  • drug interactions (e.g. decreases metabolism of warfarin)
  • numerous adverse effects
145
Q

Monitoring of patients on amiodarone?

Adverse effects of amiodarone use?

A
  • TFTs, LFTs, U&Es, CXR prior to Rx
  • TFT & LFT every 6months
  • thyroid dysfunction
  • corneal deposits
  • pulmonary fibrosis/pneumonitis
  • liver fibrosis/hepatitis
  • peripheral neuropathy, myopathy
  • photosensitivity
  • slate-grey appearance
  • thrombophlebitis & injection site reactions
  • bradycardia
146
Q

ACE-I:
MoA?
uses?

A
  • inhibit conversion of angiotensin I to angiotensin II
  • 1st line HTN in <55yrs, less effective in Afro-C
  • heart failure
  • diabetic nephropathy
  • role in 2ry prevention of IHD
147
Q

ACE-I:
side-effects?
cautions & C/I?

A
  • cough 15%, upto a year after starting (inc bradykinin)
  • angioedema, upto a year after starting
  • hyperkalaemia
  • 1st dose hypotension, more common in those taking diuretics

Cautions/C/I:

  • pregnancy & breastfeeding - AVOID
  • renovascular disease - significant impairment if unDx BL renal artery stenosis
  • aortic stenosis - may result in hypotension
  • high-dose diuretic Rx (>80mg furosemide/day) significantly increases risk of hypotension
  • hereditary idiopathic angioedema
148
Q

What 2 main problems does IHD lead to i.e. the gradual buildup of fatty plaques within coronary artery walls?

What are un/modifiable RFs?

A
  1. Gradual narrowing
    - less blood -> less O2 reaching myocardium at times of increased demand
    - > angina
  2. Risk of sudden plaque rupture
    - fatty plaques which have built up in the endothelium may rupture -> sudden occlusion of the artery -> can result in no blood/O2 reaching an area of myocardium

Modifiable:
- smoking, T2DM, HTN, hypercholesterolaemia, obesity
Unmodifiable:
- increasing age, male sex, FHx

149
Q

Pathophysiology of IHD?
what triggers endothelial dysfunction?
what changes does this lead to of the endothelium?
what infiltrates the endothelium?
how are monocytes/macrophages involved?
how is the fibrous capsule of the fatty plaque formed?

A
  • endothelial dysfunction triggered by e.g. smoking, HTN, hyperglycaemia
  • > pro-inflammatory, pro-oxidant, proliferative changes to endothelium & reduced NO bioavialability
  • > fatty infiltration of sub endothelial space by LDL particles
  • > monocytes migrate from blood -> differentiate into macrophages
  • > which phagocytose oxidised LDL -> slowly turning into large ‘foam cells’ -> these macrophages die which can further propagate the inflammatory process
  • > smooth muscle proliferation & migration from the tunica media -> intimate -> results in formation of a fibrous capsule covering the fatty plaque
150
Q

2 complications of atherosclerosis i.e. plaque formation?

A
  1. Plaque forms a physical blockage in the coronary artery lumen -> can cause reduced blood flow & O2 to the myocardium - esp at times of increased demand -> angina
  2. plaque may rupture -> potentially causing a complete occlusion of the coronary artery -> may result in a MI
151
Q

Why is deep & widespread ST depression on an ecg ass with v high mortality?

A

it signifies severe ischaemia usually of LAD or left main stem

152
Q

STEMI Rx?

A
  • morphine, nitrates +/- O2
  • aspirin
  • clopidogrel
  • re-open/revascularise: 1ry PCI - balloon angioplasty & stent via catheter
153
Q

Revascularisation in an NSTEMI?

A
  • risk stratification e.g. GRACE to decide further Rx
  • if high-risk or unstable, then coronary angio performed during admission
  • lower risk can have it at a later date
154
Q

2ry prevention following ACS?

A
  • dual antiplatelet therapy (DAT)
  • ACE-I
  • beta-blocker
  • statin
155
Q

PCI Rx in a STEMI?

A
  • 1ry PCI tio pts who present within 12h of onset of Sx, IF it can be delivered within 120mins
  • otherwise fibrinolysis if >120mins
  • if ecg 90mins after fibrinolysis fails to show resolution of ST elevation then they would need transfer for PCI
156
Q 
Anaphylaxis drug Rx:
adrenaline/hydrocortisone/chlorphenamine??
<6m
6m-6yrs
6-12yrs
>12yrs
A

<6m: adrenaline 150mcg hydrocortisone 25mg chlorphenamine 250mcg/kg

6m-6yrs: adrenaline 150mcg hydrocortisone 50mg chlorphenamine 2.5mg

6-12yrs: adrenaline 300mcg hydrocortisone 100mg chlorphenamine 5mg

> 12yrs: adrenaline 500mcg hydrocortisone 200mg chlorphenamine 10mg

157
Q

Serum levels than can be taken to establish true anaphylaxis?

A

Serum tryptase

- elevated upto 12h post acute episode

158
Q

MoA of A2RBs?
Uses?
Side-effects?

A
  • block effects of angiotensin II at the At1 receptor
  • can be used where ACE-I not tolerated, evidence base that they reduce progression of renal disease in diabetic nephropathy, & losartan reduces CVD & IHD mortality in HTN
  • caution in renovascular disease
  • hypotension & hyperkalaemia
159
Q

Antiplatelet Rx 1st & 2nd line for NSTEMI?

A

lifelong aspirin & clopidogrel/ticagrelor for 12months

lifelong clopidogrel if aspirin C/I

160
Q

Antiplatelet Rx 1st & 2nd line for STEMI?

A

Lifelong aspirin + clopidogrel/ticagrelor: 1m if no/bare stent, 12m if drug-eluting stent
- lifelong clopidogrel if aspirin C/I

161
Q

Antiplatelet Rx 1st & 2nd line for TIA/Stroke?

A

Lifelong clopidogrel

- if C/I then lifelong aspirin + lifelong dypiradamole

162
Q

Antiplatelet Rx 1st & 2nd line for peripheral arterial disease?

A

Lifelong clopidogrel

- is C/I then 2nd line is lifelong aspirin

163
Q

Complications of aortic dissection?

A

Backward tear:

  • aortic incompetence/regurgitation
  • MI - inferior pattern often seen due to R coronary involvement

Forward tear:

  • unequal arm pulses & BP
  • stroke
  • renal failure
164
Q

What is arrhythmogenic right ventricular cardiomyopathy?
Pathophysiology?
Presentation?

A
  • inherited CVD which may present with syncope/sudden cardiac death - 2nd commonest cause of sudden cardiac death
  • autosomal dominant with variable expression
  • RV myocardium replaced by fatty & fibrous tissue
  • 50% have mutation of 1 of several genes which encode components of DESMOSOME
  • palpitations
  • syncope
  • sudden cardiac death
165
Q

Ix of ARVDysplasia/Cardiomyopathy?

  • ecg
  • echo
  • MRI
A

ECG - abnormalities in V1-3, typically T wave inversion
- epsilon wave 50% (terminal notch in QRS complex)
Echo - subtle early on, may show enlarged hyPOkinetic RV with a THIN free wall
- MRI useful to show fibrofatty tissue

166
Q

What is Naxos disease?

A

autosomal recessive variant of ARVC/D - traid of:

  1. ARVC
  2. palmoplantar keratosis
  3. woolly hair
167
Q

what is 1st degree heart block?

A

PR interval >0.2 seconds

168
Q

what is 2nd degree heart block Mobitz type I?

A

wenckeback phenomenon

progressive prolongation of PR interval until a dropped beat

169
Q

what is 2nd degree heart block Mobitz type II?

A

regular PR interval but often P wave is not followed by a QRS interval

170
Q

what is 3rd degree/complete heart block?

A

no association between p waves & qrs complexes

171
Q

Features of ASDs?

A
  • most likley congenital heart defect to be found in adulthood
  • 50% mortality at 50yrs
  • ESM, fixed splitting of S2
  • embolism may pass from venous system to left side of heart causing a stroke
172
Q

Difference between ostium secundum & ostium primum ASDs?

A

secundum 70%

  • ass with Holt-Oram syndrome (tri-phalangeal thumbs)
  • ECG: RBBB with RAD

Primum

  • presents EARLIER than secundum defects
  • ass with abnormal AV valves
  • ECG: RBBB with LAD, prolonged PR interval
173
Q

What is atrial flutter?
ecg?
Rx?

A
  • SVT characterised by a succession of rapid atrial depolarisation waves
  • sawtooth
  • underlying atrial rate is often ~300/min therefore the ventricular/HR is dependent on the degree of AV block (e.g. 2:1 block is 150bpm)
  • flutter waves may be visible following carotid sinus massage/adenosine

Rx similar to AF but may be less effective

  • more sensitive to cardioversion so lower energy levels may be used
  • radiofrequency ablation of tricuspid valve isthmus curative for most pts
174
Q

What is paroxysmal AF?

A

recurrent episodes of AF that terminate spontaneously

- last <7d, usually <24h

175
Q

What is persistent AF?

A

recurrent episodes of AF that is not self-terminating - usually last >7days

176
Q

What is permanent AF?

A

continuous AF that cannot be cardioverted or if attempts to do so are inappropriate
- Rx goals therefore rate control & anticoag as appropriate

177
Q

What is first detected episode of AF?

A

first detected episode (irrespective of whether it is symptomatic or self-terminating)

178
Q

Sx & signs of AF

Ix?

A
  • palpitations, dyspnoea, chest pain
  • irreg irreg pulse

ECG: ventricular ectopics, sinus arrhythmia etc can also give irreg pulse

179
Q

Rate-control AF medical strategies?

A

beta-blocker or
rate-limiting calcium channel blocker e.g. diltiazem is 1st line

If monotherapy isn’t adequate, combo therapy with 2 of:

  • beta blocker
  • diltiazem
  • digoxin
180
Q

When to consider rhythm control in AF i.e. cardiovert?

A
  • 1st onset AF
  • coexistent heart failure
  • obvious reversible cause

If onset of AF < 48h offer rate/RHYTHM control
(if >48h, start rate control)

181
Q

AF onset <48h how to manage?

A

If AF <48 h then HEPARINISE & risk stratify for long-term anticoag
Rx = Cardioversion
- electrical DC
- pharm - AMIODARONE if structural heart disease, if not, then FLECAINIDE/amiodarone

  • after electrical cardioversion if AF confirmed <48h then further anticoagulation is unnecessary
182
Q

AF onset >48h how to manage cardioversion:
i.e. how long should pts be anticoagulated first?
when can the be cardioverted immediately?
what to do if high risk of cardioversion failure?
duration of anticoagulation after electrical cardioversion?

A
  • should be anticoagulated for at least 3 weeks before cardioversion
  • OR can offer a TOE to exclude a left atrial appendage LAA thrombus - if excluded then can heparinse & cardiovert immediately (electrically)

If high risk of cardioversion failure e.g. previous failure/recurrence, then at least 4 weeks AMIODARONE/SOTALOL before electrical cardioversion

  • after electrical cardioversion, anticoagulate at least 4 weeks -> then decide further individual basis
183
Q

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation?

A

amiodarone
flecainide
others less common: quinidine, dofetilide, ibutilide, propafenone

184
Q

Agents used to control rate in patients with atrial fibrillation?

A

beta-blockers
calcium-channel blockers - rate-limiting
digoxin (not first line but preferred if coexistent heart failure)

185
Q

Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation?

A

sotalol
amiodarone
flecainide

186
Q

Factors favouring rate control in AF?

A

> 65yrs

Hx of IHD

187
Q

Factors favouring rhythm control in AF?

A 
<65yrs
Symptomatic
1st presentation
Lone AF or AF 2ry to a precipitant e.g. etoh
Congestive heart failure
188
Q

Patients with AF who develop a stroke/TIA…. what should be given and when for anticoag?

A

(Warfarin) is antocoag of choice - aspirin/dypiradmole only if needed for other comorbidities
- in acute stroke & haemorrhage excluded, can start anticoag AFTER 2 wks - LONGER if imaging shows a v large cerebral infarction

189
Q

Causes of a raised BNP (hormone produced mainly by LV myocardium in response to strain)?

A

heart failure
myocardial ischaemia
valvular disease
CKD (reduced excretion)

(ACE-I, A2RBs & diuretics reduce BNP levels)

190
Q

What are the 3 effects of BNP?

A
  1. vasodilator
  2. diuretic & natriuretic
  3. suppresses both sympathetic tone & RAAS
191
Q 
Clinical uses of BNP?
Dx
Rx
Prognosis
Screening
A

Dx: pts with acute dyspnoea - if low <100 then heart failure unlikely therefore helpful to rule it out
Rx: effective Rx in chronic heart failure lowers BNP levels (i.e. monitoring is helpful)
Prognosis: initial evidence suggests BNP is useful marker of prognosis in chronic heart failure
Screening: for cardiac dysfunction - NOT recomended for population screening

192
Q

Side-effects of beta-blockers?
Contra-indications?
Indications?

A
  • bronchospasm, cold peripheries
  • fatigue, sleep disturbances

C/I in:

  • uncontrolled heart failure
  • asthma
  • sick sinus syndrome
  • concurrent verapamil -> severe bradycardia -> block

Indications:

  • angina, post-MI, heart failure, AF, (HTN)
  • migraine prophylaxis, thyrotoxicosis, anxiety
193
Q

Bicuspid aortic valve - what is it ass with?

what are the complications?

A
  • usually aSx in childhood, occurs in 1-2% population
    Ass:
  • Left dominant coronary circulation (posterior descending artery arises from Circumflex instead of RCA)
  • Turner’s syndrome
  • 5% also have coarctation of aorta

Comp:

  • aortic stenosis/regurgitation
  • high risk aortic dissection & aneurysm of ascending aorta
194
Q

In a broad complex tachycardia, what features are suggestive of VT rather than SVT with aberrant conduction??
FAQ PILL

A 
Fusion/capture beats
AV disocciation
QRS>160ms
Positive QRS concordance in chest leads
IHD Hx
LAD, marked
Lack of response to adenosine/carotid sinus massage
195
Q

What is Brugada syndrome?
Pathophysiology?
ECG changes?
Rx?

A

inherited CVD which may present with sudden cardiac death - autosomal dominant, more common in Asians

  • large number of variants
  • 20-40% caused by mutation in the SCN5A gene which encodes myocardial sodium ion channel protein

ECG:

  • convex ST elevation >2mm in >1 of V1-3 followed by a negative T wave
  • partial RBBB
  • changes may be more apparent following fleainide

Rx = implantable cardioverted-defibrillator

196
Q

What is Buerger’s disease?

What are the features?

A

= thromboangitis obliterans
- small & medium vessel vasculitis stongly ass with smoking

  • extremity ischaemia: intermittent claudication, ischaemic ulcers
  • superficial thrombophlebitis
  • Raynaud’s phenomenon
197
Q

Cardiac enzymes - which is the first to rise?
Which is useful to look for re-infarction as it returns to normal after 2-3days (trop T remains elevated upto 10days)
When does Trop T peak?

A

Myoglobin first to rise
CK-MB useful to look for re-infarction
Trop T peaks at 12-24h

198
Q

Normal oxygen sat of blood in LA/LV/Aorta?
And in RA/RV/PA?

What is abnormal in ASD?

in VSD?

in PDA?

in VSD with Eisenmenger’s?

in PDA with Eisenmenger’s?

in ASD with Eisenmenger’s?

A

100% in left circulation
70% in right-sided circulation

ASD: pulmonary circ is 85%

VSD: RA normal 70%, RV & PA is 85%

PDA: PA 85%

VSD + E: RA, RV & PA normal 70% but LV & aorta 85%

PDA+E: aorta 85%

ASD+E: left side all 85%

199
Q

Ways of classifying cardiomyopathies?

A

1ry - predominately involve the heart
2ry - pathological myocardial involvement as part of a generalised systemic disorder
Genetic (HOCM, ARVD)
Mixed (e.g. genetic predisposition triggered by 2ry process)
Aquired (peripartum, Takotsubo)

200
Q 
Causes of 2ry cardiomyopathy? (involves dilated/restrictive)
infective
infiltrative
storage
toxicity
inflammtory/granulomatous
endocrine
neuromuscular
nutritional deficiencies
autoimmune
A

infective - Coxsackie B, Chagas disease
infiltrative - amyloid
storage - haemochromatosis
toxicity - doxorubicin, etoh
inflammtory/granulomatous - sarcoid
endocrine - DM, thyrotoxicosis, acromegaly
neuromuscular - Friedreich’s ataxia, Duchenne-Becker, muscular dystrophy, myotonic
nutritional deficiencies - Beri-Beri (thiamine)
autoimmune - SLE

201
Q

Acquired peripartum cardiomyopathy - when does it develop? RFs?

A
  • last month of pregnancy & 5months post-partum

- more common in older women, greater parity & multiple gestations

202
Q

Acquired Takotsubo cardiomyopathy - cause? Sx?
Rx?
What is seen?

A
  • stress induced eg bereavement
  • chest pain & features of heart failure
  • supportive Rx
  • transient, apical ballooning of myocardium
203
Q

Classic causes of dilated cardiomyopathy? ABCD

A

Alcohol
Beri beri (wet)
Coxsackie B virus
Doxorubicin

204
Q

Classic causes of restrictive cardiomyopathy?

A

Amyloid (commonest in UK)
post-RT
Loefller’s endocarditic (fibrosis in eosinophilic myocarditis)

  • also haemochromatosis, sarcoid, scleroderma
205
Q

Echo findings in HOCM?

mr sam ash

A

MR
Systolic Anterior Motion of the anterior mitral valve
Asymmetic Septal Hypertrophy

206
Q

ECG abnormalities in ARVD?

A
  • usually T1-3 abnormal
  • T wave inversion
  • epsilon wave in 50% - terminal notch in QRS complex
207
Q

What is CPVT: catecholaminergic polymorphic ventricular tachycardia?
pathophysiology?

A
  • inherited cardiac disease ass with sudden cardiac death
  • autosomal dominant, 1:10,000 prevalence
  • commonest cause is a defect in the RYR2: ryanodine receptor, found in myocardial sarcoplasmic reticulum
208
Q

Features & Rx of CPVT: catecholaminergic polymorphic ventricular tachycardia ?

A
  • exercise/emotion induced polymorphic ventricular tachycardia -> syncope
  • sudden cardiac death
  • Sx generally develop before age 20

Rx = beta-blockers, ICD

209
Q

3 examples of centrally active antihypertensives?

A

Methyldopa - used in HTN Rx in pregnancy

Moxonidine - used in essential HTN Rx when conventional drugs failed to control BP

Clonidine - antihypertensive effect mediated throug alpha-2 stimulation in vasomotor centre

210
Q

What are the 2 types of Cardiac CT, sueful for assessing suspected IHD?

A

Calcium score: known to be a correlation between amount of atherosclerotic plaque calcium and the risk of future ischaemic events
Contrast-enhanced CT: allows visualisation of coronary artery lumen

If combined, they have a v high NPV for IHD

211
Q

What is now the gold standard for providing structural images of the heart?
When is it useful?

A

CMR: Cardiac MRI

  • useful when assessing congenital heart disease, determining RV & LV mass, and differentiating forms of cardiomyopathy
  • can also assess myocardia perfusion with gadolinium
  • limited data on extent of coronary artery disease
212
Q

Examples of nuclear cardiac imaging radiotracers extracted by normal myocardium?

A
  • thallium
  • technetium (99mTc) sestamibi - complex used in MIBI & cardiac SPECT scans
  • FDG: fluorodeoxyglucose - used in PET scans (1rily research atm)
213
Q

Nuclear cardiac SPECT imaging - what is the role?

A
  • to assess myocardial perfusion & myocardial viability
  • 2 sets of images acquired, at rest then at stress e.g. exercise of adenosine/dypridamole
  • comparing the two helps to identify areas of ischaemia that are reversible or fixed
214
Q

What is cardiac MUGA scanning? what is it for?

A

Multi-Gated Acquisition Scan = radionuclide angiography

  • IV radionuclide technetium-99m injected
  • pt placed under a gamma camera
  • can be performed as a stress test
  • can accurately measure LV ejection fraction
  • typically used before & after cardiotoxic drugs are used
215
Q

What are the 3 indications for a temporary pacemaker?

A
  1. symptomatic/haemodynamically unstable bradycardia, NOT responding to atropine
  2. post-ANTERIOR MI: type 2 or complete heart block (post-inferior MI complete block is common and can be managed conservatively is aSx & haem stable) - obserev for 7 days before considering permanent pacing
  3. Trifascicular block prior to surgery
216
Q

MoA of Nicorandil?

A

K+ channel activator

217
Q

A transient uncommon complication of a coronary angiogram 2ry to irritation of the myocardium by the catheter?

A

Ventricular tachycardia

- pull back catheter immediately to restore normal sinus rhythm

218
Q

What is a patent foramen ovale?

Rx in pts who’va had a stroke?

A

persistent patency of a congenital opening/foramen ovale in the interatrial septum, which normally closes after birth

  • present in 20%
  • may allow embolus to pass from R->L side causing a stroke i.e. paradoxical embolus - consider if stroke in <50yrs
  • get decompression Sx related to diving, cold sensation in limb, limb pain
  • atrial septal aneurysm is a RF for PFO & when combined, increases risk of CVA. other RFs are congenital heart conditions, FHx or PMHx migraine
  • ass between migraine & PFO (closure can improve migraine Sx)
  • Rx if stroke is controversial, inc: antiplatelet, anticoagulant, PFO closure
219
Q

What is coarctation of the aorta?
What are the associations?
What are the features?

A
  • congenital narrowing of descending aorta, commoner in Males
  • Ass inc: Turner’s, bicuspid aortic valve, berry aneurysms, neurofibromatosis

Features:

  • infancy heart failure
  • adult hypertension
  • radio-femoral delay
  • apical click in aortic valve
  • mid-systolic murmur, maximal over the back
  • notching of the inferior border of ribs (collateral vessels) is NOT seen in young childers
220
Q

MoA of warfarin?

Side-effects?

A

oral anticoagulant that inhibits reduction of vitamin K to its active hydroquinone form -> acts as a cofactpr in carboxylation of clotting factord II, VII, IX, X & protein C (i.e. vit K anatagonist)

  • bleeding
  • teratogenic (but can be used if breast-feeding)
  • skin necrosis (temporary procoagulant state when initiated because protein C synthesis is reduced which can lead to thrombosis & skin necrosis)
  • purple toes
221
Q

Factors that potentiate wafarin?

A
  • liver disease
  • p450 enzyme inhibitors e.g. amiodarone, ciprofloxacin
  • cranberry juuice
  • drugs which displace warfarin from plasma albumin e.g. NSAIDs
  • drugs which inhibit platelet functino e.g. NSAIDs
222
Q

Indications for warfarin & INR targets?

A 
AF target 2.5
VTE target 2.5
recurrent VTE target 3.5
aortic mechanical valve 3.0
mitral mechanical valve 3.5
223
Q

What is pulmonary arterial hypertension?

Presentation?

A

resting mean PA pressure 25+mmHg

  • more common in females, typically presents age 30-50
  • 10% inherited autosomal dominant
  • pulm HTN can develop 2ry to chronic lung disease e.g. COPD but PAH is Dx in absence of this - HIV, cocaine, anorexigens etc inc the risk
224
Q

Features (Sx & signs) of pulmonary arterial HTN?

A
  • progressive exertional dyspnoea classically
  • exertional syncope, exertional chest pain, peripheral oedema
  • cyanosis
  • raised JVP with prominent a waves
  • RV heave
  • loud P2
  • tricuspid regurgitation
225
Q

Rx of 1ry pulmonary arterial hypertension?
what test do you do first?
Rx if +ve response?
Rx if -ve response?

A
  • > Rx underlying conditions e.g. with anticoagulants/oxygen
  • > ACUTE VASODILATOR testing helps decide appropriate Rx strategy - it aims to decide which pts show a significant fall in PA pressure after vasodilators e.g. IV epoprostenol/INH nitric oxide

+ve respone (minority)
= PO calcium channel blockers

  • ve response (majority):
  • prostacycline analogues: treprostinil, iloprost
  • endothelin receptor antagonists: bosentan
  • phosphodiesterase inhibitors: sildenafil

Pts with progressive Sx should be considered for a heart-lung Tx

226
Q

What is the mainstay Rx for 1ry pulmonary arterial HTN?

A

Prostacyclins

227
Q

Commonest cause of death as a complication of MI?

A

VF -> cardiac arrest

- ALS protocol with defib

228
Q

Complication post-MI if a large part of the ventricular myocardium is damaged in the infarction and the ejection fraction is severely affected? Rx?

A 
Cardiogenic shock
(can also be due to a mechanical complication e.g. LV free wall rupture)
- inotropic suppor &amp;/or intra-aortic balloon pump
229
Q

Complication post-MI if pt survives the acute phase of a large part of ventricular myocardium damage what can develop?

A

Chronic heart failure

  • loop diuretic
  • drugs that improve mortality
230
Q

Bradyarrhythmia that is more common after an inferior MI?

A

AV block

231
Q

Common 10% complication in the first 48h after a transmural MI?

A

Pericarditis

- may have effusion on echo

232
Q

Complication 2-6wks post-MI of fever, pleurisy, pericardial effusion & rasied ESR?
mechanism?
Rx?

A

Dressler’s syndrome (inc pericarditis)

  • autoimmune reaction against antigenic proteins formed as the myocardium recovers
  • Rx nsaids
233
Q

Complication post-MI where ischaemic damage sustained may weaken the myocardium ass with persistent ST elevation & LV failure - what is the cause?

A

LV aneurysm

  • thrombus can form within -> inc the risk of stroke
  • therefore, pts are anti coagulated
234
Q

Complication 1-2wks post-MI seen in 3%, presenting with features of acute heart failure 2ry to cardiac tamponade e.g. raised JVP, pulses paradoxus, diminished heart sounds?
Rx?

A

LV free wall rupture

- urgent pericardiocentesis & thoracotomy

235
Q

Complication-post MI seen in 1st week of 1-2% with features of acute heart failure ass with a pan-systolic murmur?

A

VSD/rupture of the inter ventricular septum

  • Dx echo (& exclude acute MR)
  • urgent surgical correction
236
Q

Complication post-MI - more common with infer-posterior infarction with an early-to-mid diastolic murmur?
cause?
Rx?

A

Acute MR

  • may be due to ischaemia of rupture of the papillary muscle
  • Rx vasodilator therapy but often require emergency surgical repair
237
Q

Causes of a loud S2?

A

HTN (systemic loud A2 or pumonary loud P2)
hyper dynamic states
ASD without pulmonary hypertension

238
Q

Cause of a soft S2?

A

aortic stenosis

239
Q

Cause of a fixed split S2?

A

ASD

240
Q

Causes of a widely split S2?

A

deep inspiration
RBBB
pulmonary stenosis
severe MR

241
Q

Causes of a reversed (paradoxical) split S2 (P2 before A2)?

A 
LBBB
severe aortic stenosis
RV pacing
WPW type B (causes early P2)
PDA
242
Q

What is the best predictor of mortality post-STEMI before discharge?

A

Above average exercise capacity

243
Q

Indications for ETT: exercise tolerance testing ECG?

What is the max predicted & target HR?

A
  • risk stratifying pts after MI
  • assessing exercise otlerance
  • risk stratifying pts with HOCM
  • assessing pts with suspected angina

Sensitivity 80% specificity 70% for IHD

Max predicted HR = 220 - Age
Target HR = at least 85% max predicted to allow reasonable interpretation of a test as low-risk or negative

244
Q

C/I to ExerciseTT/ecg?

When to stop?

A
  • MI < 7days ago
  • unstable angina
  • uncontrolled HTN sBP>180 or hypotension sBP < 90
  • aortic stenosis
  • LBBB

Stop if:

  • ‘severe’, ‘limiting’ chest pain
  • > 3mm ST depression
  • > 2mm ST elevation, stop also if rapid + pain
  • sBP > 230
  • sBP falling >20
  • attainment of max pred HR
  • HR falling >20% of starting rate
  • arrhythmia develops
245
Q

In the absence of C/I, what Rx should all be given in a STEMI?

A 
aspirin
clopidogrel/ticagrelor (improved outcome but slightly higher risk bleeding)/prasogrel = P2Y12-R antagonist
unfractionated heparin (lmwh if C/I)
246
Q

Thrombolysis in STEMI

A
  • if no access to 1ry PCI
  • tPA: tissue plasminogen activator has mortality benefits over streptokinase
  • tenecteplase is easier to administer and not inferior to alteplase with a similar adverse effect profile
247
Q

When to do an ECG after thrombolysis of a STEMI to assess whether there has been a >50% resolution in the ST elevation ?

A

90mins

  • if no adequate resolution -> rescue PCI
  • if adequate then PCI still beneficial
248
Q

Rx of hyperglycaemia in ACS?

A
  • dose-adjusted IV insulin infusion with regular monitoring of levels to BG <11.0
  • intensive insulin Rx NOT recommended routinely (DIGAMI)
249
Q

How to Dx infective endocarditis by modified Duke criteria?

A
  • path criteria +
    or 2major
    or 1major 3minor
    or 5minor
250
Q

What are pathological criteria for infective endocarditis?

A
  • positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery
  • i.e. valve tissue, vegetations, embolic fragments or intracardiac abscess content
251
Q

What are the major criteria in Dx infective endocarditis? (culture & endocardial)

A

Positive blood cultures:

  1. 2 +ve BC of typical organise e.g. strep viridans/HACEK group
  2. persistent bacteraemia from 2 +ve bCs >12h apart OR 3 +ve BCs where pathogen is less specific e.g. staph aureus/epidermidis
  3. +ve serology for Coxiella burnetii/Bartonella/Chlamydia psittaci
  4. +ve molecular assays for specific gene targets

Evidence of endocardial involvement:

  1. new valvular regurgitation
  2. +ve echo: oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves
252
Q

Minor criteria for Dx of infective endocarditis?

A
  • predisposing heart condition / IVDU
  • microbio evidence that doesn’t meet major criteria
  • fever >38
  • vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae, purpura
  • immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
253
Q

Features suggestive of restrictive cardiomyopathy rather than constrictive pericarditis?

A
  • prominent apical pulse
  • heart may be enlarged on CXR
  • absence of pericardial calcification on CXR
  • ECG abnormalities e.g. BBB, Q waves
254
Q

Signs on exam of tricuspid regurgitation?

A
  • giant V waves in JVP
  • left parasternal heave
  • pan-systolic murmur
  • pulsatile hepatomegaly
255
Q

Causes of tricuspid regurgitation?

A
  • RV dilatation
  • pulm HTN e.g. copd
  • rheumatic heart disease
  • infective endocarditis esp IVDU
  • Ebstein’s anomaly
  • carcinoid syndrome
256
Q

What is multifocal atrial tachycardia?

What is the management?

A

MAT: irregular cardiac rhythm caused by at least 3 different sites in the atria - can show morphologically at distinctive P waves
- more common in elderly with chronic lung disease e.g. COPD

Rx

  • correct hypoxia & electrolyte disturbances
  • rate-limiting calcium-channel blocker e.g. verapamil often 1st line
  • cardioversion & digoxin NOT useful
257
Q

What is the Valsalva manoeuvre?

What are the stages?

A

= forced expiration against a closed glottis -> increased intrathoracic pressure

  1. increased intracthoracic pressure
  2. increase in venous & RA pressure reduces venous return
  3. thus reduced preload & fall in cardiac output (Frank-Starling)
  4. when the pressure is released -> further slight fall in cardiac output due to increased aortic volume
  5. return of normal cardiac output
258
Q

What is a dilated cardiomyopathy?

Features>

A

Where a dilated heart leads to systolic +/- diastolic dysfunction

  • all 4 chambers affected but LV > RV
  • in the absence of congenital, valvular or ischaemic heart disease

Features inc: arrhythmias, emboli & mitral regurgitation

259
Q

Causes of dilated cardiomyopathy?

A
  • ETOH (may improve with thiamine)
  • postpartum
  • HTN

Also:

  • inherited (often people have a genetic predisposition, majority autosomal dominant)
  • infections e.g. Coxsackie B, HIV, diphtheria, parasitic
  • endocrine ege hyperthyroid
  • infiltrative eg haemochromatosis, sarcoid
  • neuromuscular eg Duchenne
  • nutritional eg Kwashiorkor, pellagra, thiamineselenium deficiency
  • drugs eg Doxorubicin
260
Q

MoA of thiazide diuretics?

A
  • inhibit sodium reabsorption at the DCT by blocking Na/Cl symporter -> more Na reaching the collecting ducts means potassium is lost
261
Q

Common & rare adverse effects of thiazide diuretics?

A
  • dehydration
  • postural hypotension
  • hyponatraemia, hypokalaemia, hypercalcaemia
  • gout
  • impaired glucose tolerance
  • impotence

Rare:
- thrombocytopenia, agranulocytosis, photosensitivity rash, pancreatitis

262
Q

What finding on auscultation would most strongly indicate dyspnoea 2ry to isolated LV failure?

A

S3 gallop rhythm - one of the most specific & early signs

263
Q

ECG:
- convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
- partial RBBB
- changes may be more apparent following flecainide
What is the Dx?

A

Brugada syndrome

264
Q

Prinzmetal angina (coronary artery spasm) treatment?

A

dihydropyridine calcium channel blocker

265
Q

What is PCI: percutaneous coronary intervention?
What happens after stent insertion?
What are the types of stent?

A
  • technique to restore myocardial perfusion in IHD in both stable angina & ACS
  • stents implanted in 95%
  • migration & proliferation of smooth muscle cells & fibroblasts occur to the treated segment
  • stent struts eventually become covered by endothelium (until thi shappens there is an increased risk of platelet aggregation leading to thrombosis)

BMS: bare-metal stent
DES: drug-eluting stent, coated with paclitaxel/rapamycin, which inhibit local tissue growth (reducing restenosis rates) but the stent thrombosis rates are increased as the process of stent endothelisation is slowed

  • > Aspirin lifelong
  • > length of clopidogrel Rx depends on type of stent, reason for insertion & consultant preference
266
Q

2 main complications of PCI?

A

Stent thrombosis - due to platelet aggregation

  • 1-2%, most commonly in the 1st month
  • usually presents with acute MI

Restenosis - due to XS tissue proliferation around stent

  • 5-20%, most commonly in first 3-6months
  • usually presents with recurrence of angina Sx
  • RFs inc DM, renal impairment & stents in venous bypass grafts
267
Q

Paroxysmal AF successfully treated with DC cardioversion 1 week ago, now on warfarin. A post-cardioversion Echo shows no structural abnormalities. How long to continue warfarin?

A 
4 weeks (at least) after successful cardioversion
- if structural abnormalities or AF likely to recur, then longer recommended
268
Q

MoA of hydralazine?

C/I?

A
  • increases cGMP leading to smooth muscle relaxation to a greater extent in arterioles than veins
    (‘older’ antihypertensive)

C/I in SLE & IHD

269
Q

Adverse effects of hydralazine?

A
  • tachycardia, palpitations, flushing
  • headache, fluid retention
  • drug-induced lupus
270
Q

What is the single most important risk factor for stent thrombosis after PCI?

A

Premature withdrawal anti platelet therapy

271
Q

Managing 2ry prevention of stable CVD with an indication for an anticoagulant?

A

anticoagulant mono therapy without anti platelet (generally, if there is a bleeding risk)

272
Q

Managing post-ACS/PCI with an indication for an anticoagulant?

A
  • stronger indication for antiplatelet Rx
  • DAT + anticoagulant for 4wks-6months after the event, then 1 anti platelet + 1 anticoagulant to complete 12months
  • but varies
273
Q

VTE when on anti platelets?

A

Calculate HASBLED - if intermediate/high-risk bleeding then consider withholding anti platelets for duration of anticoagulant Rx

274
Q

The use of beta-blockers in treating hypertension has declined sharply in the past five years. Why has this occurred?

A

Less likely to prevent stroke & potential impairment of glucose tolerance

275
Q

4 ECG changes that are considered normal variants in an athlete?

A

sinus bradycardia
junctional rhythm
1st degree heart block
Wenckebach phenomenon

276
Q

What is malignant hypertension?

What are the features?

A
  • severe HTN >200/130
  • occurs in both essential & 2ry types
  • fibrinoid necrosis of BVs -> retinal haemorrhages, exudates, proteinurial haematuria due to renal damage (benign nephrosclerosis)
  • can lead to cerebral oedema -> encephalopathy

Classically: severe headaches, nausea/vomiting, visual disturbance
Also: chest pain & dyspnoea
- papilloedema
- severe: encephalopathy e.g. seizures

277
Q

Management of malignant hypertension?

A
  • reduce diastolic no lower than 100mmHg within 12-25h
  • bed rest

Most Pts oral therapy e.g. Atenolol
If severe/encephalopathic: IV sodium nitroprusside/labetalol

278
Q

A 28F comes in with palpitations, no PMHx
HR 160 irregular
BP 123/65 mmHg
SpO2 97% (RA)
Chest clear
ECG: irregular broad complex monomorphic tachycardia with a stable axis
What is the most appropriate Rx?

A

IRREGULAR broad complex tachycardia (without features to suggest VT) therefore most likely to be SVT/AF with LBBB/aberrant conduction e.g. WPW

therefore most appropriate Rx = Amiodarone

(haemodynamically stable)
(diltiazem, bisoprolol, adenosine would enhance the aberrant pathway -> VF)

279
Q

What class of drugs can cause a hypertensive crisis (that may be used e,g, in an emergency setting, that may interact with vasopressors used to treat hypotension)?

A

monoamine oxidase inhibitors e.g. phenelzine

280
Q

Fillip class system for risk stratification post-MI with 30day mortality risk?

A

I no clinical signs of heart failure 6%
II lung crackles, S3 17%
III frank pulmonary oedema 38%
IV cardiogenic shock 81%

281
Q

Poor prognostic factors in ACS?

A 
age
development/Hx of heart failure
peripheral vascular disease
reduced sBP
Fillip class
initial serum creatinine conc
elevated initial cardiac markers
cardiac arrest on admission
ST segment deviation
282
Q

HOCM Rx?

abcde

A 
Amiodarone
Beta-blockers or verapamil for Sx
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis
283
Q

Drugs to avoid in HOCM?

A

ACE-I
Nitrates
Inotropes
- drugs that reduce preload decrease chamber size and worsen Sx & signs
- vasodilators increase outflow tract gradient and cause a reflex tachycardia that further worsens ventricular diastolic function
- inotropic drugs worsen outflow tract obstruction, don’t relieve the high end-diastolic pressure, and may induce arrhythmias

284
Q

What is the single most important test to confirm the Dx of pulmonary hypertension?

A

Cardiac catheterisation

- to measure right heart pressures

285
Q

Features of mitral valve prolapse?

A
  • atypical chest pain or palpitations
  • mid-systolic click (later if pt squatting)
  • late systolic murmur (longer if pt standing)
  • complications: MR, arrhythmias inc long QT, embolism, sudden death
286
Q

Associations of mitral valve prolapse?

A
  • 5-10% population, usually idiopathic
  • congenital: PDA, ASD, cardiomyopathy, Turner’s, Marfan’s, Fragile X, osteogenesis imperfecta, pseudoxanthoma elasticum, WPW, LQTS, Ehlers-Danlos, PCKD
287
Q

What is the aim of endothelia receptor antagonist therapy in pulmonary arterial hypertension?

A

To reduce pulmonary vascular resistance -> reduce strain on the right ventricle (i.e. RV systolic pressure)

288
Q

What are the key Ix tests used to identify patients likely to benefit from cardiac resynchronisation therapy in heart failure?
What features make them good candidates for CRT/biventricular pacing?

A
  • TTE: LV EF <35%, asynchronous contraction of LV & RV
  • ECG: LBBB/QRS>120ms
  • biventricular pacing improves quality of life & exercise tolerance by ensuring the ventricles contract at the same time due to asynchronous stimulation (LBBB causing asynchronous activation) via the conduction system
289
Q

What are the 4 features of cholesterol embolisation?

A
  • purpura
  • livedo reticularis
  • eosinophilia
  • renal failure
290
Q

MoA of Dypyradimole?

A
  • antiplatelet
  • inhibits phosphodiesterase -> elevating platelet cAMP -> reduces intracellular calcium levels
  • also reduces cellular uptake of adenosine (i.e. increases the effects) & inhibits thromboxane synthase
291
Q

Causes of LAD: left axis deviation?

A 
left anterior hemlock
LBBB
WPW syndrome - R-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people
292
Q

Causes of RAD: right axis deviation?

A 
RV hypertrophy
left posterior hemiblock
chronic lung disease -> for pulmonate
PE
ostium secundum ASD
WPW syndrome Left sided accessory pathway
normal in infant < 1yr old
minor RAD in tall people
293
Q

Causes of myocarditis?

A
  • Coxsackie, HIV
  • diphtheria, clostridia
  • Lyme disease
  • Chagas’ disease, toxoplasmosis
  • autoimmune
  • doxorubicin
  • usually young pt with acute Hx: chest pain, SOB
294
Q

VSD: ventricular septal defect

- features?

A
  • classically pan systolic murmur which is louder in smaller defects
  • commonest cause of congenital heart disease, that close spontaneously in 50%
  • congenital ass with chromosomal disorders e.g. Downs, Edwards, Patau
    non-congenital eg post-MI
295
Q

Complications of VSD?

A
  • aortic regurgitation (due to a poorly supported right coronary cusp -> cusp prolapse)
  • infective endocarditis
  • Eisenmenger’s complex
  • right heart failure
  • pulmonary hypertension (pregnancy contraindicated in pulm HTN)
296
Q

Features of severe pre-eclampsia?

A
  • HTN > 170/110 & proteinuria ++/+++
  • headache, visual disturbance, papilloedema
  • RUQ/epigastric pain
  • hyperreflexia
  • platelet count <100, abnormal liver enzymes or HELLP syndrome
297
Q

What are the physiological changes in exercise:
BP?
cardiac output?

A
  • systolic increases, diastolic decreases -> increased pulse pressure
  • in healthy young people the increase in MABP is only slight
  • increase in cardiac output can be 3-5X
  • HR increase unto 3x
  • stroke volume increase unto 1.5X
  • due to venous constriction, vasodilation & increased myocardial contractibility, as well as from the maintenance of right atrial pressure by an increase in venous return
298
Q

Causes of mitral stenosis?

A

RHEUMATIC FEVER

rarer: mucopolysaccharidoses, carcinoid, endocardial fibroelastosis

299
Q

Features of mitral stenosis?

Features if severe?

A
  • low volume pulse, atrial fibrillation
  • loud S1, opening snap
  • mid-late diastolic murmur (best heard in expiration)
  • length of murmur increases
  • opening snap becomes closer to S2
300
Q

CXR & Echo in mitral stenosis?

A

CXR: left atrial enlargement
Echo: ‘tight’ mitral stenosis implies a X-sectional area of <1cm squared (normal is 4-6)

301
Q

What is the intervention of choice in severe mitral stenosis?

A

percutaneous mitral commissurotomy

  • only if unsuccessful/contra-indicated is surgical valve replacement indicated
302
Q

Contra-indications of percutaneous mitral commissurotomy/valvotomy?

A
  • mitral valve area >1.5
  • left atrial thrombus on echo
  • > mild MR
  • severe valve calcification
  • severe concomitant aortic valve disease
  • severe combined mixed tricuspid valve disease
  • concomitant coronary artery disease req bypass surgery
303
Q

Indications for an implantable cardiac defibrillator?

A
  • LQTS
  • HOCM
  • previous cardiac arrest due to VT/VF
  • previous MI with non-sustained VT on 24h monitoring, inducing VT on electrophysiology testing & EF <35%
  • Brugada syndrome
304
Q

Causes of palpitations?

What are the 1st line Ix?

A
  • stress, arrhythmias, inc awareness of normal heart beat/extrasystoles
  • 12lead ecg
  • FBC, U&Es, TFTs
305
Q

NYHA heart failure classification?

A

I no Sx, no limitation
II mild Sx, slight limitation eg ordinary activity results in Sx
III moderate Sx, marked limitation of activity
IV severe Sx, often at rest limiting any activity

306
Q

What Ix can accurately measure LV EF?

Typically done before and after cardiotoxic drugs a usedre

A

MUGA scan - radionuclide angiography

307
Q

What is the first cardiac enzyme to rise after an MI?

A

myoglobin

308
Q

50y.o. man in ED with palpitations, no chest pain, long Hx of etoh abuse, looks malnourished.
ECG: irregular tachycardia 165bpm with a QRS duration 155ms
K+ 2.1
No signs of chock/heart failure/syncope

Next step in management?

A

IV magnesium 2g

(irregular tachycardia with broad QRS complex can be either polymorphic VT/pre-excited AF/AF with BBB.
- etoh, hypokalaemia make torsades most likely)

309
Q

What are the 2ry causes of hypertension?

A

1ry hyperaldosteronism = commonest

Renal:
- glomerulonephritis, pyelonephritis, APKD, renal artery stenosis

Endocrine:
- phaeochromocytoma, Cushing’s, Liddle’s, CAH/11-beta hydroxylase deficiency, acromegaly

Drug:
- steroids, MAO-Is, COCP, NSAIDs, leflunomide

Other:
- pregnancy, coarctation of aorta

310
Q

Gold standard Ix for aortic dissection?

A

CT aortic angiogram

311
Q

Causes of an ejection systolic murmur?

A 
aortic stenosis
pulmonary stenosis
HOCM
ASD
Fallot's
312
Q

Causes of a pansystolic murmur?

A

MR/TR (high pitched & blowing)

VSD (‘harsh’)

313
Q

Causes of a late systolic murmur?

A

mitral valve prolapse

coarctation of aorta

314
Q

Causes of a early diastolic murmur?

A 
aortic regurg (high pitched &amp; blowing)
Graham-Steel murmur of pulmonary regurg also high pitched &amp; blowing
315
Q

Causes of a mid-late diastolic murmur?

A 
mitral stenosis (rumbling)
Austin-Flint murmur (severe AR, also rumbling)
316
Q

Cause of a continuous machine-like murmur?

A

PDA

317
Q

Causes of ST depression on ecg?

A
  • 2ry to abnormal QRS: LVH, LBBB, RBBB
  • ischaemia
  • digoxin
  • hypokalaemia
  • syndrome X
318
Q

Commonest cause of drug-induced angioedema?

A

ACE-I

319
Q

Common side effect of ticagrelor?

A

Dyspnoea/breathlessness 15%

- triggered by adenosine (as ticagrelor inhibits its clearance)

320
Q

Nicotinic acid is used in treatment of hyperlipidaemia, although its use is limited by side-effects

  • what are the adverse effects
  • what are the uses in hyperlipidaemia?
A
  • lowers cholesterol & tirglyceride conc
  • raises HDL levels
  • flushing
  • impaired glucose tolerance
  • myositis
321
Q

Which non-invasive Ix provides the most accurate assessment of whether a pt has coronary artery disease?

A

Contrast enhanced cardiac CT

322
Q

What does troponin T bind to?

A

Tropomyosin which regulates actin - it associates with actin in muscle fibres and regulates muscle contraction by regulating the binding of myosin

323
Q

24y.o. female develops transient slurred speech following a flight from Aus -> UK.
CT head & ECG normal
What test is most likely to reveal the underlying cause?

A

TOEcho - paradoxical embolus from a PFO

324
Q

ECG - abnormalities in V1-3, typically T wave inversion
- epsilon wave 50% (terminal notch in QRS complex)

What is the Dx?

A

Arrhythmogenic RV cardiomyopathy

325
Q

What is currently the most common causes of viral myocarditis??

A

parvovirus b19

HHV-6

326
Q

Pre-test probability calculation for coronary artery disease for low-risk but cardiac sounding chest pain, what to do if it is:
<30%
30-60%
>60%?

A

<30% CT calcium scoring
30-60% myocardial perfusion scintigraphy
>60% invasive coronary angiography

327
Q

What is the treatment of choice to permanently restore sinus rhythm in atrial flutter?

A

Radiofrequency ablation of tricuspid valve isthmus

328
Q

How long is it best to monitor a patient for after successful treatment for anaphylaxis?

A

8 hours
- biphasic reactions (Sx recurrence after apparent resolution) occur in 1-20% of anaphylaxis episodes, and typically ~8h after the 1st reaction, although can occur upto 72h later

329
Q

What are the features of complete heart block?

A
  • syncope, heart failure
  • regular bradycardia 30-50bpm
  • wide pulse pressure
  • JVP cannon A waves
  • variable intensity of S1
330
Q

How to measure pulmonary capillary wedge pressure PCWP?

What chamber does it roughly equate to?

A
  • balloon tipped Swan-Ganz catheter inserted into pulmonary artery
  • pressure is similar to left atrium 6-12mmHg normal
  • helps determine whether pulmonary oedema is cardiogenic or not
331
Q

Which organisms contribute to the highest rate of mortality in infective endocarditis?

A

staphylococci mortality 30%

332
Q

Venous drainage of the heart: where does the coronary sinus drain into?

A

right atrium

333
Q

What is the Ix for choice for pregnant patients with a suspected DVT?

A

compression duplex US

334
Q

What is the Ix for choice for pregnant patients with a suspected PE?

A

(ECG & CXR for all)

  • compression duplex US if there are also Sx/signs of a DVT - if confirms DVT, further Ix not necessary
  • decision of V/Q or CTPA is after d/w pt & radiologist
335
Q

Risk of CTPA & V/Q scan in pregnancy?

A

CTPA: increases lifetime risk of maternal breast cancer (pregnancy makes breast tissue particularly sensitive)
V/Q scan: slightly increased risk of childhood cancer vs ctpa

336
Q

MoA of adenosine?

A
  • causes transient heart block in the AV node
  • agonist of the A1 receptor -> inhibits adenylyl cyclase -> reducing cAMP -> hyperpolarisation by increased outward K efflus
  • v short half life of 8-10seconds
337
Q

What enhances the effects of adenosine?

What reduces the effects of adenosine?

A

Enhanced by Dipyradimole

Blocked by theophyllines

338
Q

What are the adverse effects of adenosine?

A
  • chest pain
  • bronchospasm
  • can enhance conduction down accessory pathways -> increased ventricular rate e.g. WPW
339
Q

Most important factor predicting outcome post-STEMI is i.e. strongest ass with sudden death?

A

Presents of new systolic heart failure
i.e. low LV ejection fraction
large amount of myocardial damage

340
Q

What is Ebstein’s anomaly?

A

congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle

341
Q

Best Ix when you suspect a paradoxical embolisation e.g. from a PDA or ASD?

A

TOE

EXAM (21 decks)

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