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MEDICINE NEW > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Who is eligable for AAA screening?

A

Ultrasound offered to men over 65

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2
Q

What is the differential for aortic stenosis?

A

HCM- gets louder on Valsalva (more preload- whereas AS gets quieter) and HCM gets quieter with squatting (afterload)

VSD
Aortic sclerosis- normal pulse (not slow rising) doesn’t radiate to carotids
Aortic flow

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3
Q

Which bacteria is responsible for rheumatic fever?

A

Streptococcus pyogenes

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4
Q

Name two conditions associated with aortic stenosis

A

Angiodysplasia (cause of GI bleeds in the elderly)

Coarctation with bicuspid aortic valve (check BP + radioradial delay)

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5
Q

On examination you have detected an ejection systolic murmur, what further investigations would you like to do:

A

ECG- looking for LVH voltage criteria
(S wave depth in V1 + R wave height in V5 or V6 >35mm)
CXR: calcified aortic valve
Echocardiogram (severe is LVOT gradient >50mmHg and valve area less than 1cm3 area)

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6
Q

Three main symptoms of aortic stenosis:

A
  1. Chest pain
  2. Exertional dyspnoea
  3. Syncope
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7
Q

What is P mitrale and the causes?

A

A bifid P wave

In isolation- mitral stenosis and volume overload slowing emptying
With LVH- hypertension, aortic stenosis, HCM

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8
Q

What is the Duke’s criteria:

A

2M; or 1M + 2m; or 5m

M:
2 +ve blood cultures (or persistently +ve when taken at varied times)
Echo- abscess, dihiscence, vegetation, new regurgitation

m:
Atypical organism on blood cultures; suggestive echo; pyrexia; embolic phenomena; high CRP or ESR; prosthetic valve/IVDU

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9
Q

Common causes of infective endocarditis:

A 
Staph aureus (commonest)
Strep viridians

Staph epidermidis; enterococci; diptherioids; HACEK (G -ve)

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

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10
Q

If someone with infective endocarditis has an abscess at their aortic root, what ECG signs may be present?

A

PR prolongation > complete AV block

The AV node in the right atrium is closely approximated to the aortic root

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11
Q

Causes of Aortic Regurgitation:

A

Valvular:
Acute- endocarditis (no collapsing pulse)
Chronic- rheumatic fever, rheumatoid arthritis

Aortic root
Acute- dissection, trauma
Chronic- dilatation (Marfan’s, HTN)
Aortitis (syphilis, ankylosing spondylitis, vasculitis)

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12
Q

Eponymous signs of aortic regurgitation:

A

Quincke’s sign: capillary pulsations
De Musset’s sign: head nodding with each heartbeat
Corrigan’s sign: carotid pulsation
Duroziez’s sign: compress femoral artery 2cm proximal to stethoscope = systolic murmur
Traube’s sign: ‘pistol shot’ sound over femoral arteries

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13
Q

Difference between Austin Flint murmur and diastolic murmur of aortic regurgitation?

A

Early descending diastolic murmur = AR murmur

Mid diastolic crescendo murmur = Austin Flint (heard in severe AR)

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14
Q

Causes of aortic regurgitation:

Tension, been Conned, too much Rheum In it

A

Hypertension

Connective tissue: Marfans, Ehlers Danlos, osteogenesis imperfecta
Congenital: bicuspid valve

Rheum: seronegative arthritidies (ank spond, Reiter’s, psoriatic), rheumatoid arthritis, Takayasu’s

Infective: syphilis, rheumatic fever (strep pyogenes sequelae)

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15
Q

How is aortic regurgitation managed medically and definitively?

A

ACEi or ARBs to reduce afterload (systemic HTN)
Regular echo check ups- enlarging heart, LVEF, degree of AR

Surgery:
In chronic cases, replace the valve when:
Dyspnoeic + NYHA >2
Or ECG T wave inversion + EF <50% + pulse pressure >100mmHg

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16
Q

Commonest cause of mitral stenosis:

A

Rheumatic fever (commonest)

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17
Q

How small does the area of the mitral orifice have to be before a patient becomes symptomatic in mitral stenosis?

A

<2cm squared

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18
Q

If you hear a pansystolic murmur heard loudest at the apex, what investigations might you want?

A

ECG: AF + P mitrale (due to an enlarged heart)
CXR: pulmonary oedema, enlarged heart chambers (splaying of carina)
Echocardiogram + Doppler

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19
Q

What criteria is used to diagnose rheumatic fever?

A

Duckett Jones diagnostic criteria (Recent strep infection and 2M or 1M + 2m):

M:
Chorea, erythema marginatum, SC nodules, polyarthritis, carditis

m:
Pyrexia, arthralgia, PMH rheumatic fever,
Raised ESR, raised WCC, prolonged PR interval on ECG

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20
Q

If you wanted to prove a recent Group A beta haemolytic strep infection to diagnose rheumatic fever, what tests could you do?

A

Positive throat culture (normally -ve)
Rapid streptococcal antigen test +ve
Elevated streptococcal antibody titre (ASO or DNAse B titre)
Recent scarlet fever

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21
Q

Management of rheumatic fever:

A

Penicillin V

High dose aspirin- carditis/arthritis

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22
Q

A lateral thoracotomy scar may indicate which cardiac interventional procedure has occurred?

A

Mitral valvotomy- for mitral regurgitation

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23
Q

Why might a patient with mitral stenosis get a hoarse voice or dysphagia?

A

Enlarged LA atrium compressing the recurrent laryngeal nerve or the oesophagus

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24
Q

Causes of mitral regurgitation according to the valve leaflets, valve annulus (fibrous ring containing valves) + cordae pupillae

A

Valve leaflets:
Acute- endocarditis
Chronic- connective tissue disease (Marfan’s, Ehlers Danlos), myxomatous valves (stretchy valves), rheumatic fever

Valve annulus:
Chronic: calcification or LV dilatation stretching it, congenital ASD

Chordal papillae:
Acute- rupture ie MI
Chronic- fibrosis, amyloid

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25
Q

Tricuspid regurgitation causes:

A

Commonest- LVF + pulmonary hypertension (functional)

Endocarditis,
rheumatic fever,
carcinoid syndrome,
congenital (ASD, Ebstein’s, downward displacement of tricuspid valve)

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26
Q

What could a midline sternotomy scar indicate?

A

CABG- check radial artery + calves for saphenous vein harvesting
Aortic valve replacement- opening click in systole, ejection systolic murmur
Mitral valve replacement- closing click over S1, opening click in diastole

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27
Q

Potential interventions which would result in a lateral thoracotomy scar?

A

Mitral valve replacement
Mitral valve valvotomy
Coarctation repair/ BT shunt
Lung pathology- pneumonectomy, lobectomy

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28
Q

Which valve problems can be treated with a valvuloplasty?

A

Mitral or pulmonary stenosis- where valves are pliable, non-calcified and non-regurgitant.
Balloon catheter is inserted and inflated

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29
Q

Potential complications of valves:

A

Thrombosis (despite Warfarin)
Bleeding (because of Warfarin)
Haemolysis (RBCs against the valve)

Infective endocarditis
Early- S. epidermidis from skin. Late- S. viridians from blood
Prosthetic dysfunction- LVF

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30
Q

Under what circumstances might an ICD be given prior to anyone having a cardiac arrest (primary prevention)

A

MI > 4 weeks ago
+ LVEF < 35% + Non-sustained VT + positive EP study
Or
+ LVEF < 35% + broad QRS complexes

OR
Familial condition with risk of SCD (Brugada, HCM etc)

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31
Q

4 T’s that cause constrictive pericardiris

A 
Any cause of acute pericarditis
TB: cervical lymphadenopathy
Trauma: sternotomy scar
Tumour, radioTherapy: thoracotomy scar
connective Tissue disease: RA hands, SLE signs

Infection: viral (EBV, HIV, Coxsackie), bacterial, fungal

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32
Q

Dressler’s syndrome?

A

Occurs 2-10 weeks after an MI, heart surgery or pacemaker insertion.
Thought that myocardial injury stimulates formation of autoantibodies against heart muscle.

PC: Recurrent fever + chest pain ± serositis (pleural/pericardial rub)
Rx: NSAIDs, aspirin, steroids

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33
Q

Viruses that may cause acute pericarditis?

A 
Coxsackie (can cause hand foot + mouth)
Flu
Ebstein Barr virus 
Mumps
Varicella
HIV
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34
Q

Which drugs may cause acute pericarditis?

A

Antiarrhythmic (procainamide)
BP (hydralazine)
Cromolyn sodium (anti-asthma)

Isoniazid

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35
Q

In a patient with suspected constrictive pericarditis what signs might CXR uncover?

A

Calcified pericardium

Small heart

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36
Q

Difference between STEMI and NSTEMI in pathophysiology?

A

STEMI- clot of artery at site of a ruptured plaque

NSTEMI- clot of a ruptured plaque embolizes downstream to block a small artery

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37
Q

Following suspected ACS, how is GRACE score cut off used?

A

> 3% mortality risk at 6 months = need intervention

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38
Q

What things cause a rise in troponin bar an MI?

A

PE, severe sepsis, heart failure, tachy/brady arrhythmias, extreme exertion, renal failure

Gives a 5 x upper limit of normal

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39
Q

How does anticoagulation management differ according to acute or chronic AF?

A

CHADS2Vasc score is only used for chronic AF, if a patient has a score of 0 but wants to be DC-cardioverted then you should anticoagulate

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40
Q

How does Sotolol affect the ECG if given for AF?

A

Widens the QT interval, increasing risk of torsades de pointes

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41
Q

If someone has had AF for more than 48 hours and needs to be electively cardioverted, how long should you aim to anticoagulate for before doing so.

A

3 weeks

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42
Q

When is ivabradine used?

A

Patients with congestive heart failure who have tried beta blockers but can’t slow heart rate down:

Affects funny current in sinus node

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43
Q

Which patients get dysynchrony and how is it treated?

A

In patients with BBB, one ventricle contracts after the other due to slowed conduction leading to heart failure, so by pacing one ventricle early with a cardiac resynchronisation device.

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44
Q

What are the two ways ICD’s can help abort dysrhythmias?

A
  1. Shocking the heart

2. Overpacing a tachycardia at 220bpm to make the heart depolarisation become refractory so it can take over pacing.

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45
Q

What are the 5 classes of anti-arrhythmic drugs?

A 
1- Na+ channel blockers (flecainide)
2- beta blockers
3- K+ channel blockers (amiodarone)
4- Ca++ channel blockers
5- Variable (digoxin)
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46
Q

What are the driving rules for angina and angioplasty?

A

Angina- no driving if Sx with rest or emotion

Angioplasty- stop driving for 1 week

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47
Q

What vision do patients require to allow for driving?

A

6/9 in the good eye

6/12 in the bad eye

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48
Q

Signs of an atrial septal defect in adults aged 40-60?

A

As LV compliance reduces with age the L to R shunt is augmented.

Pulmonary ejection systolic murmur
Fixed S2 split
Pulmonary hypertension (tricuspid regurgitation)

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49
Q

Causes of ventral septal defects?

A

Congenital or Post MI

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50
Q

Signs of VSD:

A

Pansystolic murmur, loudest at T area

Systolic thrill± parasternal heave

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51
Q

What is Eisenmenger’s syndrome?

A

A L to R shunt reverses as pulmonary hypertension causes increased R-sided pressures.
Results in cyanosis and heart failure

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52
Q

Where does coarctation of the aorta most commonly occur and what sign does this result in?

A

Distal to the L subclavian artery = radiofemoral delay

Arteries leaving the aortic arch in order:
Brachiocephalic A (splits into R subclavian and common carotid a)
L common carotid
L subclavian

Alphabetical!

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53
Q

4 features of Tetralogy of Fallot:

A

Overriding aorta
RVH
Pulmonary stenosis
VSD

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54
Q

Causes of acute pericarditis:

A 
Vascular- MI
Infection- viruses (coxsackie, flue, epstein barr, varicella),
  bacteria, fungi
Trauma, surgery
Autoimmune- Dressler's syndrome, RA, SLE, sarcoid
Metabolic- hypothyroidism, uraemia
Idiopathic
Neoplasm- malignancy
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55
Q

Management of pericarditis:

A
  1. Ibuprofen

2. Colchicine (before steroids or immunosuppressants)

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56
Q

What are the complications of acute pericarditis:

A

Any cause of pericarditis may result in:
Pericardial effusion
Cardiac tamponade
Chronic fibrosis + constrictive pericarditis (rigid pericardium)

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57
Q

ECG has low-voltage QRS complexes, they recently were admitted with viral pericarditis, what is the likely cause?

A

Pericardial effusion- attenuates electrical signals

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58
Q

Differences between constrictive pericarditis and cardiac tamponade:

A

Constrictive pericarditis- heart encased in rigid pericardium
RHF, pericardial knock, prominant x descent on JVP
CXR- small heart

Cardiac tamponade- pericardial fluid raises chamber pressures
Falling BP
CXR- big globular heart

Both have:
Kussmaul’s sign (JVP rising with inspiration)
muffled heart sounds
Pulsus paradoxus (BP drops by 10mmHg on inspiration, can’t get enough blood to L side of heart when low lung pressure is compared to high chamber pressures)

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59
Q

How is acute myocarditis diagnosed?

A

Absence of MI, despite ECG changes and raised troponin I or T

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60
Q

Associations with dilated cardiomyopathy:

A

V: high BP
I: viral
M: Alcohol, haemochromatosis, thyrotoxicosis

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61
Q

Signs of HCM:

A

Jerky pulse
Prominant a wave in JVP
Systolic thrill at T area
Ejection systolic murmur

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62
Q

How does empirical Rx for infective endocarditis differ if the valve is native of prosthetic?

A

Native:
penicillin + vancomycin (inhibits peptidoglycan synthesis)

Prosthetic:
Vancomycin + gentamicin + rifampicin
(Same if staph is cause)

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63
Q

Which bacteria make up the HACEK organisims accounting for 3% of endocarditis?

A

Gram -ve, treated with amoxicillin + gentamicin

Haemophilus
Actinobaillus
Cardiobacterium
Eikenella
Kingella
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64
Q

What are the signs of infective endocarditis and their pathological explanation:

A 
Immune complex deposition: 
haematuria + glomerulonephritis
Roth spots- fundi
Splinter haemorrhages
Osler's nodes (OWW! Painful pulps)

Embolic phenomena:
Abscesses
Janeway lesions (way!! High 5!! Painless palmar!!)

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65
Q

Tests for infective endocarditis:

A 
FBC, CRP, ESR, U+E, Mg, LFT
Urinanalysis (blood ++)
CXR- cardiomegaly
ECG- AV block (aortic root abscess)
Echo- transthoracic if vegetations if >2mm, transoesophageal more sensitive for visualising mitral valve
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66
Q

Causes of tricuspid regurgitation:

A

T- tension in the pulmonary system > RV dilation
R-rheumatic fever
I- IE (IVDU)
C- carcinoid syndrome + congenital

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67
Q

What is Ebstein’s abnormality?

A

Downwards displacement of the tricuspid valve, small RV

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68
Q

Patient has a pansystolic murmur, loudest on inspiration, heard best at the L lower sternal border. Differential?

A

Tricuspid regurgitation
Other signs: giant v waves in JVP, RV heave, pulsatile hepatomegaly,

Pulmonary stenosis (should be louder higher up chest) or ASD- may get a split P2

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69
Q

Early diastolic murmur, loudest with inspiration, differential:

A

Tricuspid stenosis- opening snap

Pulmonary regurgitation- decrescendo

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70
Q

What is the Graham Steele murmur?

A

Decrescendo murmur in early diastole

Pulmonary regurgitation
Mitral stenosis
Pulmonary hypertension

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71
Q

Heart defects associated with:

Down’s syndrome
Turner’s syndrome
Marfan’s syndrome

A

Downs- ASD, VSD, mitral regurgitation
Turner’s- Coarctation of aorta (webbed neck)
Marfan’s- mitral valve prolapse, AR, aortic dissection (midsystolic click)

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72
Q

Management of Aortic stenosis:

A

Symptomatic or
Asymptomatic + peak gradient >50mmHg or valve area <1cm3

Open valve replacement
Transcatheter AV implantation (TAVI) or valvuloplasty

Valves:
Metallic (anticoagulation needed, long lasting)
Porcine valves (less durable)
Cadaveric

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73
Q

What causes aortic sclerosis and how is it distinguished from aortic stenosis?

A

Age- related degeneration of the valve

No carotid radiation or pulse changes (character + volume), S2 normal

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74
Q

What is the Austin Flint murmur and what causes it?

A

Mid-diastolic low pitching murmur heard at the apex

Sign of severe AR where backwards flow from aorta causes vibration against the mitral valve leaflet

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75
Q

Indications for aortic valve replacement in aortic regurgitation?

A

Increasing symptoms
Enlarging heart- LVH
T wave inversion in lateral leads

76
Q

Causes of aortic regurgitation?

A

Ao- aortic dissection (acute)
R- rheumatic fever, reiter’s syndrome, rheumatoid arthritis
T- Takayasu arteritis
I- infective endocarditis
C- connective tissue disorders (Marfan’s, Ehler’s Danlos)

77
Q

Which valve abnormality causes a malar flush?

A

Mitral stenosis

78
Q

What is a tapping apex beat associated with and why does it occur?

A

Mitral stenosis

Left atrial hypertrophy pushes heart apex towards chest wall

79
Q

An opening snap with S1 is assoicated with?

A

Mitral stenosis, as high volume of blood flowing through when it snaps shut

80
Q

Indications for mitral valve balloon valvotomy

A

Symptomatic

Or asymptomatic +
Moderate to severe stenosis ( < 1cm^2/m2 body surface area)
Pulmonary hypertension

Not calcified pliable valves

81
Q

Management of mitral stenosis:

A

Medical:
AF common- rate control + anticoagulate
Diuretics- reduce pulmonary venous congestion

Surgical:
Balloon valvotomy
Open valve replacement (only if abnormal mitral valve shape or atrial thrombus likely to be dislodged)

82
Q

Causes of mitral regurgitation?

A 
Mitral valve prolapse
Infective endocarditis
Tendon rupture of tendinae chordinae (or papillary muscle)
Rheumatic fever
Annular calcification (elderly)
LV dilatation (functional)

Connective tissue

83
Q

What kind of imaging is needed for mitral regurgitation?

A

Trans-oesophageal echo + Doppler

  • TTE doesn’t visualise the mitral valve well
  • can assess severity and suitability for repair (over replacement)
  • doppler assess size of regurgitant jet
84
Q

Associations of mitral valve prolapse:

A

Mid-systolic click ± late systolic murmur

Marfan’s, osteogenesis imperfecta (blue sclera)
Turner’s syndrome, cardiomyopathy

85
Q

What is rheumatic fever:

A

In 2% of the population, pharyngeal infection with b-haemolytic streptococci triggers rheumatic fever 2-4 weeks later when am antibody to the carbohydrate bacterial wall cross causes antigen mimicry with valve tissue

86
Q

In rheumatic fever what provides evidence of Group B a haemolytic strep infection?

A

Throat culture (usually -ve 2-4 weeks post sore throat)
Rapid strep antigen test +ve
Rising strep antibody titre (ASO or DNAse B titre)
Recent scarlet fever (strawberry tongue, macular truncal rash)

87
Q

Major + minor criteria of rheumatic fever:

Jones criteria requires evidence of strep infection (antigen, ASO titre, scarlet fever, throat culture) +2M or 1M + 2m

A

M: CASES
Carditis- CCF, cardiomegaly, murmurs,
Arthritis- flitting polyarthritis of big joints
Subcutaneous nodules
Erythema marginatum- geographical raised red edges
Syndenham’s chorea- semi purposeful movements, unusual behaviour

m:
Fever, high ESR/CRP, PMH rheumatic fever
Arthralgia or long PR interval (as long as these two aren’t the major criterion)

88
Q

Management:

A

Conservative: bed rest until CRP normal

Medical:  
Aspirin- carditis ± steroids
Benzylpenicillin
Constrict joint movement- severe arthritis
Diazepam- chorea
89
Q

Which valve is most damaged by rheumatic fever on average?

A

Mitral valves

90
Q

What prophylaxis is given for rheumatic fever?

A

Penicillin V
Given if carditis + persistent valve disease is present until age of 40

If no carditis- 10 years worth
If no carditis or valve problems- 5 years until age 21 years

91
Q

What are the cut offs for determining BP treatment?

A

Clinic reading is high = then ambulatory BP monitoring

> 135/85 mmHg + under 80 + comorbidity or risk

Comorbidity:organ damage, CVS disease, renal disease, diabetes
QRISK >20%

> 150/95:
All patients

92
Q

Lifestyle advice for hypertensive patients:

A

Diet: under 6g/day- ideally 3g/day
Balanced diet, rich in fruit and veg

Drink: less caffeine, less alcohol

Quit smoking, exercise more

93
Q

Drug management of hypertension:

A

ACEi or calcium channel blocker

A+C
A+C+D (indapamide not bendrofluthiazide)

+ aldosterone antagonist, alpha blocker, more thiazide (if K+ high)

94
Q

SEs of dihydropyridine calcium channel blockers:

A

Nifedipine- ankle oedema, gum hyperplasia, flushes

Amlodipine- ankle oedema, tiredness, nausea

95
Q

When is oral therapy recommended vs IV therapy for malignant hypertension?

A

Oral therapy normally unless CCF or encephalopathy

Avoid sudden drops in BP (cerebral hypoperfusion, autoregulation is poor)

96
Q

Patient has headache + seizures, BP is 210/120.

Aim of management?

A

Malignant hypertension encephalopathy

Intra-arterial line for monitoring
Get BP down to 110mmHg diastolic
Furosemide IV
Labetalol IV

97
Q 
BP targets for:
A. Over 80s
B. Under 80s
C. Diabetic patients
D. Proteinuric patients >1g/day
A 
Clinic BP targets:
A. 150/90
B. 140/80
C. 130/80
D. 125/75
98
Q

What is the pathological hallomark of malignant hypertension?

A

Vascular damage characterised as fibrinoid necrosis- fibrin like tissue in matrix

99
Q

Signs ot look for in malignant hypertension?

A

Systolic BP >200
Diastolic BP >110

Fundi: papilloedema, bilateral retinal (flame) haemorrhages, exudates

100
Q

Secondary causes of hypertension:

A

Renal:
V Renal artery stenosis- atherosclerosis, fibromuscular dysplasia
I- chronic pyelonephritis
T- polycystic kidneys
A- glomerulonephritidies, systemic sclerosis, PAN

Endocrine:
More salt + water retention- hyperaldoesteronism (Conn’s)
Very high cortisol mimics mineralocorticoid (Cushing’s)
Phaeochromocytoma, acromegaly, hyperparathyroidism

Coarctation of aorta
Drugs: steroids, the pill, MAOi

101
Q

How can secondary causes of hypertension be examined for?

A

Cushingoid appearance- Cushing’s
Signs of renal disease- AV fistula, RRT (glomerulonephritis)
Radiofemoral delay or weak pulses (coarctation)
Renal bruit- stenosis
Palpable kidneys- polycystic kidney

102
Q

Tests for hypertension:

A

U+Es (cushing’s, conn’s),
Ca++ (hyperparathyroidism)
Glucose + cholesterol (risk stratify)

ECG- LVH, past MI
Urinanalysis- glomerulonephritidies

Special tests: 
urinary metanephrines (phaeo)
24 hours cortisol (Cushing's)
Renal USS/ arteriography (RA stenosis)
Renin aldosterone levels (hyperaldosteronism)
103
Q

4 commonest causes of CKD:

A
  1. Diabetes
  2. Glomerulonephritidies (IgA commonest)
  3. Unknown
  4. Hypertension or renovascular disease
  5. Pyelonephritis
104
Q

4 stages of hypertensive retinopathy:

A
  1. Silver wiring
  2. AV nipping
  3. Flame haemorrhages + cotton wool spots
  4. Papilloedema
105
Q

Management of chronic heart failure?

A

Conservative:
stop smoking, reduce salt intake, optimise weight + nutrition, flu vaccine yearly, pneumococcal vaccine

Medical:
Treat cause (arrhythmia, valve issues)
Treat exacerbating factors (anaemia, thyroid disease)
Avoid exacerbating factors
(NSAIDs- fluid retention, verapamil- negative inotropic effect)

  1. ACEi AND B blocker
    (carvedilol, bisoprolol, nibivolol)
  2. Spironolactone or hydralazine + nitrate or ARB (SHARDI)
  3. Cardiac resynchronisation, digoxin, ivabradine (needs HR >75 and LVEF >35%)

± Furosemide for fluid overload

106
Q

Rx for chronic intractable heart failure:

Eg unresponsive oedema

A
  1. Symptoms:
    Switch furosemide to bumetanide
    + Metolazone thiazide (SE: profound drop in K+)
    Opiates or IV nitrates
  2. Bed rest, fluid + Na restrict
    Daily weights
  3. TED stockings + DVT prophylaxis
107
Q

What is the New York Heart Classification categories:

A
  1. Heart disease present, no undue dyspnoea ordinarily
  2. Comfortable at rest, dyspnoea on ordinary activities
  3. Less than ordinary activities causes dyspnoea, which is limiting
  4. Dyspnoea present at rest, all activity causes discomfort
108
Q

What is the difference between ANP and BNP?

A

ANP is secreted from the atria
BNP is secreted from the ventricle- related to the pressure in LV
Used to discriminate between causes of SOB
>100 is heart failure
Higher the BNP = the higher the mortality risk

109
Q

What causes systolic vs diastolic heart failure?

A

Systolic: LVEF < 50%
MI, IHD, cardiomyopathy

Diastolic: LVEF >50%, inability to relax
Restrictive cardiomyopathy, cardiac tamponade, constrictive pericarditis, hypertension

110
Q

Which symptoms occur in R-sided HF that do not occur in L-sided heart failure?

A

Peripheral oedema, ascites, facial engorgement
Pulsation in neck + face (tricuspid regurgitation)
Nausea + anorexia
Epistaxis

111
Q

Which symptoms occur in L sided heart failure, than may not occur in R sided HF (unless both sides involved)?

A

Dyspnoea, paroxysmal nocturnal dyspnoea, orthopnoea
Wheeze, nocturnal cough ± pink frothy sputum
Cold peripheries, weight loss, muscle wasting

112
Q

Drugs which improve mortality in heart failure:

A

ACEi
B-blockers
Spironolactone
Hydralazine* + nitrate

*causes drug induced lupus- antihistone Abs

113
Q

3 categories of low output heart failure:

A

Pump failure- systolic or diastolic (IHD, MI, cardiomyopathy etc)

Excessive preload- mitral regurgitation, fluid overload (NSAIDs)

Excessive afterload- aortic stenosis, hypertension

114
Q

Causes of high output heart failure:

A

Output is unable to meet metabolic demands

Anaemia
Pregnancy
Wet beriberi (thiamine deficiency)
Hyperthyroidism
Paget's
AV malformation
115
Q

Tests for suspected heart failure?

A

FBC, U+Es, BNP
CXR: alveolar oedema, B lines, cardiomegaly, dilated upper lobe vessels, pleural effusion
ECG- ?cause
Echocardiogram

In essence if BNP + ECG abnormal > echo is warranted

116
Q

What findings occur on a CXR in L-sided heart failure?

A

Alveolar shadowing- diffuse interstitial or alveolar bat wing shadowing

Kerley B lines- interlobular septal oedema

Cardiomegaly- cardiothoracic ratio >0.5

Diverted upper lobe vessels

Pleural effusions

117
Q

Framingham criteria of heart failure:

2M or 1M + 2m:

A

M:
Paroxysmal nocturnal dyspnoea

Neck vein distension
Crepitations
S3 gallop
Hepatojugular reflux (rise in JVP 3-4cm = RVF)

Acute pulmonary oedema
Cardiomegaly
Increased central venous pressure
Weight loss of 4.5kg in 5 days of treatment

m:
Bilateral ankle oedema, nocturnal cough, dyspnoea on ordinary exertion
Hepatomegaly, pleural effusion, tachycardia,
1/3rd decrease in vital capacity from max recorded

118
Q

Indications for permanent pacemaker

A

Mobitz type II AV block (random dropped beats- higher risk)
Complete AV block
Symptomatic bradycardia
Heart failure (3rd line, cardiac resynchronisation)
Drug resistant tachyarrhythmias (SVT, VT)

119
Q

Common triggers of AF:

A 
HF, IHD, post MI (22%)
PE, pneumonia, low K+ or Mg+
Mitral valve disease
Hyperthyroidism, caffeine, alcohol
'Lone' = no cause identified
120
Q

Tests for if a patient is found to have an irregularly irregular pulse:

A

U+Es (low K+ or Mg+), TFTs, cardiac enzymes

ECG: no P waves, irregular QRS
Echo: L atrial enlargement, mitral valve disease etc

121
Q

How do you decide whether to cardiovert an unstable patient with AF if they have not been anti-coagulated?

A

If onset in < 48 hours: U+Es and cardiovert

If onset in > 48 hours:

  1. rate control with verapamil or b-blockers
  2. transoesophageal echo to check thrombus free
  3. give LMWH and then can cardiovert
122
Q

Patient has has palpitations for the last 12 hours, they have chest pain and BP is 90mmHg. ECG shows fast AF.
Four steps of management?

A
  1. As under 48 hours, cardiovert:
    GA or IV sedation then 200J, 360J, 360J
    IV amiodarone as an alternative
  2. Treat associated causes- MI or pneumonia
  3. Rate control- Verapamil or bisoprolol
  4. LMWH and calculate CHADsVasc score
123
Q

Chronic AF management:

A

Anticoagulate according to CHADsVas score

Rhythm control: 
elective cardioversion (anticoagulate for 3 weeks)
or flecainide for normal heart, amiodarone if structural disease

Rate control:

  1. B blocker or Ca+ channel blocker
    • Digoxin or amiodarone
124
Q

Which factors favour rhythm control over rate control:

A

Symptoms or CCF
Younger <65 years
First presentation of lone AF or secondary to a precipitant (U+Es)

125
Q

Summarise the management strategies of new onset AF depending on stability of the patient:

A

<48 hours + unstable: DC cardiovert
<48 hours + stable: rate control, anticoagulate*, TOE> cardiovert

> 48 hours + unstable: rate control, TOE, establish anticoagulation > cardiovert
48 hours + stable: as above, but wait 3 weeks for anticoagulation

126
Q

What is the pill in the pocket strategy for paroxysmal AF?

A

Can take sotolol or flecainide when AF comes on

Only suitable if no LV dysfunction or IHD or valve disease
Have systolic BP >100mmHg, HR >70

Ensure anticoagulation

127
Q

CHADsVasc score?

A 
CCF
Hypertension >140/80
Age- 65 (1), 75 (2)
Diabetes
Sex- female (1)
Vasc- Stroke, TIA, VTE (2)

Score above 1 if male, or 2 if female warrants anticoagulation

128
Q

HASBLED score:

A 
Hypertension >160mmHg
Abnormal renal (1) or liver function (1)
Stroke
Bleeding propensity
Labile INR
Elderly >65
Drugs (NSAIDs, antiplatelets) + alcohol
129
Q

What causes a broad complex tachycardia:

A
  1. Arrhythmia originating outside the normal conduction system
  2. Abnormalities in the His-Purkinje system (BBB + SVT)
  3. SVT conducted anterograde over a accessory pathway
130
Q

When is synchronised and unsynchronised cardioversion warranted in broad complex tachycardias?

A

VF or pulseless VT: unsynchronised DC cardioversion (200J-360J if biphasic)

Stable VT: IV amiodarone
DC cardioversion as 2nd line or if deterioration

131
Q

DRABC Rx for a stable broad complex tachycardia

A 
A- oxygen
B- ABG (if evidence of pulmonary oedema, sepsis, low GCS)
C- U+Es, cardiac enzymes, Ca+, Mg+
      Amiodarone IV
      MgSO4 if torsade de pointes
132
Q

What is Brugada syndrome?

A

An autosomal dominant condition which predisposes patients to sudden cardiac death from ventricular arrythmias due to sodium channellopathies.

It is diagnosed by characteristic ECG changes

133
Q

In broad complex tachycardias, how are SVT + BBB differentiated from VT?

A

VT is more associated with:
PMH of IHD
Lack of response to adenosine

ECG changes- positive QRS concordance in chest leads, left axis deviation, complete AV block

134
Q

Differential diagnosis of narrow complex tachycardia:

A

Sinus tachycardia
Supraventricular tachycardia- AVRT or AVNRT
Atrial tachycardia

Atrial flutter
Atrial fibrillation
Multifocal atrial tachycardia- abnormal P waves
Junctional tachycardia- may not see P waves

135
Q

CI to adenosine (used in stable narrow complex tachycardia):

A

Asthma
2nd/3rd degree heart block
Smaller doses in transplanted hearts

Antagonised by theophylline, potentiated by dipyridamole

136
Q

How does treatment of narrow complex tachycardia differ once type is identified:

A

Stable > vagal manoeuvres > adenosine 6g, 12g, 12g

SVT: 2nd verapamil IV or b blocker IV

Atrial flutter: treat as AF

Multifocal atrial tachycardia: COPD associated, Rx hypoxia, verapamil

Junctional tachycardia: b blocker or amiodarone or radiofrequency ablation

137
Q

ECG changes of wolff parkinson white syndrome?

A

Delta upstroke
Short PR
Wide QRS
ST- T wave changes

138
Q

What are U waves associated with:

A

Hypokalaemia

139
Q

Things to look for in a patient with bradycardia:

A

Drug chart (b blocker, digoxin)
Sick sinus syndrome- need to look for tachybrady syndrome
Hypothyroidism

Rx: if under 40bpm is atropine IV

140
Q

Difference between atropine and adenosine?

A

Adenosine- s for stop SVTs
Slows conductance in AV node, adenosine R inhibits adenylyl cyclase, reducing cAMP, increasing K+ influx via rectifier K+ channels and hyperpolarising the cell

Atropine- p for picks up the HR
Competitive mACh R antagonist, inhibiting parasympathetic input

141
Q

A patient has an MI and develops 2nd degree heart block, what changes need to be made to their drug chart?

A

Increase rate of AV block:

B blockers
Calcium channel blockers

142
Q

In ectopic ventricular beats (pre-mature ventricular contractios) after an MI when would you investigate or treat further?

A

An isolated ectopic is fine.
Non-Sustained Ventricular Tachycardia: at least 3 in a row with HR >100bpm

NSVT within 48 hours of MI = no problem
NSVT after 48 hours of MI = needs further investigation

143
Q

Who warrants an implantable cardiac defibrillator post MI?

A

VT + EF <35%

144
Q

What is Dressler’s syndrome?

A

Autoimmune reaction to myocardial infarction
PC: pericarditis, pleural effusions, fever, anaemia, high ESR
1-3 weeks post MI

Rx: NSAIDs + steroids if severe

145
Q

Indications for a CABG:

A

For survival improvement:
Left main stem disease
Triple vessel disease (involving some of LAD)

For symptom improvement:
Refractory angina
Unstable angina
Unsuccessful angioplasty attempt

146
Q

CABG vs percutaneous coronary intervention

A

CABG- better resolution of angina, increased risk of stroke

PCI- reduced morbidity of operation + recovery time

147
Q

Which veins may be used for coronary artery bypass grafts?

A

Long saphenous vein

Internal mammary vein (look under pec margin)

148
Q

Post CABG management:

A 
Conservative: 
Exercise- walk, cycle, swim, jog
Drive at 1 month
Reduce smoking + lipid intake
Return to work at 3 months

Medical:
Aspirin 75mg
Anti-anginal drugs if angina

Interventional:
Angioplasty if angina reoccurrence is possible

149
Q

What ECG changes may constitute a STEMI?

A

ST elevation >2mm in chest leads or 1mm in limb leads
New onset LBBB
Posterior MI: horizontal ST depression + upright T waves in V1-3

150
Q

Medications to start post STEMI once PCI has been given?

A

ACEi within 24 hours
b blocker
Clopidogrel 300mg then 75mg

Warfarin if large MI + risk of mural thrombus
Aspirin 75mg
Statin

151
Q

Immediate Treatment of NSTEMI:

A

Anticoagulation:
Fondaparinux if no PCI in next 24 hours, otherwise LMWH

High risk* GRACE score:
Antiplatelet
GPIIb/IIIa antagonist Tirofiban if PCI in next 96hr
Clopidogrel after

Low risk:
Clopidogrel if risk >1.5%/year

*high risk if persistent chest pain, ST depression, troponin up, diabetes aka NSTEMI

152
Q

Difference between NSTEMI and unstable angina?

A

+ Troponin

also typically ST changes with unstable angina tend to be transient, whereas change with NSTEMI are more persistent

153
Q

A troponin level needs to be taken how many hours after an MI to exclude STEMI or NSTEMI?

A

6 hours, if normal and ECG normal at this point, very unlikely to be an MI

154
Q

In a patient presenting with angina, what rare causes may be considered as a differential?

A

Tachyarrhythmias, HCM, aortic stenosis
Arteritis
Anaemia

155
Q

Any differences in management of angina compared to post MI medical management?

A

No clopidogrel in angina

  1. Add nitrates- GTN spray (SE: headaches, hypotension)
  2. K+ channel activator (nicorandil)
  3. Ivabradine if can’t take b-blocker or Ca channel blocker
156
Q

Patient gets cardiac chest pain at rest, no normal cardiac risk factors. What could be the cause + Rx?

A

Prinzmetal angina: coronary artery spasm
ECG changes of ST elevation resolve with pain

Rx: Ca channel blockers ± long acting nitrates
Avoid aspirin + b blockers, may increase vasospasm

157
Q

How should those with stable chest pain be investigated?

A

Determine the likelihood of coronary artery disease, based on age, gender, risk factors and symptoms

Sx- typical anginal pain:

  1. Constricting chest pain
  2. Onsets with exercise
  3. Relieved by rest or GTN within ~5 minutes

High risk: smoking diabetic with hyperlipidaemia

IHx according to calculated risk:
10-29% CT coronary artery calcification score

30-60% Functional:
Myocardial perfusion scan
Stress echo
MR perfusion with contrast

60-90% Angiography
>90%. Treat as coronary heart disease

158
Q

What alterations to U+Es do thiazides cause?

A

Low K+ and low Mg+
HIGH Ca+ (t-HIGH-azides)
High urate- erk GOUT

159
Q

How do nitrates and hydralazine act differently?

A

Nitrates (and a-blockers) dilate veins and large arteries = lower preload

Hydralazine dilates the resistance vessels, aka arterioles = lowers afterload + systemic BP

160
Q

At least how many hours post dose should you check Digoxin levels?

A

6 hours

161
Q

What does Digoxin toxicity cause?

A

Confusion
Nausea + anorexia
Yellow vision
Any arrhythmia

162
Q

How do statins work?

A

Statins inhibit the enzyme HMG-CoA reductase to prevent cholesterol recycling, more has to be made de novo, reducing levels as LDL receptor expression by the liver increases.

Most effective at night when cholesterol metabolism happens most.

163
Q

SEs of statins:

A

Muscle aches
Abdo discomfort
LFTs- only act if ALT 3x baseline
Myositis, rarely rhabdomyolysis

164
Q

Cautions + CIs for ACE inhibitors:

A

PC: high K+, low Na+, hypotension, hypovolaemia

PMH: pregnancy, LVOT, severe COPD/cor pulmonale
Renal artery stenosis
Less advisable where patients have CKD + may be at risk of AKI

165
Q

ACEi side effects:

A

Dry cough
Low BP- best to take at night first time
Taste disturbance
Renal impairment

Check U+Es before and after starting.

166
Q

Describe coronary angiography:

A

Insert a small tube from a vein or radial/femoral artery to access the heart.

Measure pressures, look at cardiac anatomy, biopsies, put valve in.

Before: NBM for 6hrs before, blood tests

Risks: 
Bleeding
Reaction to contrast
Angina + arrhythmias
Infection

Alternative: CT angiography can rule out CAD well

167
Q

What is exercise testing for cardiac ischaemia:

A

ECG + BP monitoring whilst on a treadmill with increasing difficulty, look for ST changes (down sloping ST depression)

Used to confirm suspected diagnosis of IHD or assessment of exercise-induced arrhythmias

CI: severe aortic stenosis, uncontrolled HTN/ HF/ arrhythmia, acute myocarditis or pericarditis, acute aortic dissection/ PE

Hard to interpret: musculoskeletal exercise limitations, pacemaker patients, LBBB or AV block already

Stop the test if: 
chest pain, dyspnoea, cyanosis, pallor
Feeling faint or exhausted
ST elevation in leads
Arrhythmia
Development of AV block or LBBB
90% max heart rate achieved
168
Q

Where do you place chest leads in ECG:

A

V1-2: 4th intercostal space, sternal edges
V4: 5th intercostal space, mix clavicular
V3: between them
V5: same horizontal plane of V4 but anterior axillary
V6: same plane but mid axillary

Ride (RA) your (LA) green (LL) bike (RL)

169
Q

How is an incomplete bundle block different from a complete block on ECG?

A

Incomplete = less than 0.12secs

170
Q

What causes RBBB on ECGs?

A

Normal variant
PE
Cor pulmonale

171
Q

What causes LBBB on ECGs?

A

IHD
Hypertension
Cardiomyopathy
Idiopathic fibrosis

172
Q

How does LVH look on ECG compared to RVH?

A

LVH:
(S in V1) + (R in V6) > 35mm
Or (R in V6) > 25mm

173
Q

Which leads show ST elevation with the different types of MI and which arteries are affected?

A

II, III, aVF = inferior (R coronary)
V1-4 = anteroseptal (left anterior descending)
V4-6, aVL = anterolateral (LAD ± circumflex)
Tall R, ST depression in V1-2 = posterior (circumflex)

174
Q

What kind of ECG rhythm has regular normal QRS complexes, but no P wave?

A

Nodal rhythms (AVN rather than sinus node)

175
Q

How does the deflection in Leads I, II and III demonstrate axis deviation and what degrees are associated with each?

A

L axis- leaving: I up, II down, III down (-30 to -90)
However if I is up, III down and II isoelectric (0- -30) = physiological

R axis- reaching: I down, II up, III up (90- 180)

Extreme axis- v odd: I down, II down, III down (-90 - 180)

176
Q

What features can be discerned on an ECG from the shape or absence of P waves?

A

Absent: AF, AV nodal rhythm, sinoatrial block
Mitrale (bifid): delayed conduction- LA hypertrophy
Pulmonale: peaked P waves- RA hypertrophy (can occur in low K+) >2.5mm, seen in leads II, III, aVF

NB these P wave changes may only be visible in a couple of leads

177
Q

Normal range for PR interval:

A

0.12-0.2s (3-5 squares)

Short- accessory pathway
Long- AV block

178
Q

What features make up a normal Q wave?

A

< 2 squares deep
< 1 square wide
Seen in V5-6, aVL (as heart normally depolarises left to right)

If Q waves not meeting these criteria, may occur within a few hours of MI

179
Q

Which drugs cause prolongation of the QT interval?

A 
STOP hEARt
Sotolol
Tricyclics
Over the counter antihistamines
Phenothiazines (typicals)
(Hypo K+, Ca+, Mg+)
Erythromycin
Amiodarone
(Romano-Ward 
Temp low)
180
Q

How is corrected QT interval calculated?

A

QTc= QT/ square root (RR)

Corrected for RR

181
Q

What are Romano Ward and Jervell + Lange Nielsen syndrome associated with and how do they differ?

A

Both due to K+ channelopathy
Long QT syndrome, increasing risk of VT, VF, torsades

Romano-Ward autosomal D
JLN- autosomal R, get congenital sensorineural hearing loss also

182
Q

What is the J wave on an ECG and what is it associated with?

A

Hypothermia, subarachnoid haemorrhage + hypercalcaemia

Positive deflection at end of QRS (QRS-ST junction)

183
Q

In a patient with LBBB, how does the axis deviation indicate whether it is the anterior or posterior fascicle that is blocked?

A

L anterior hemiblock= left axis deviation
L posterior hemiblock = right axis devation

Anterior fascicle conducts to the upper anterior regions, whereas the posterior fascicle conducts inferior + posterior
With the fascicle blocked, the eventual depolarisation of these areas happens later and requires a large wave of depolarisation, hence as the L anterior gets depolarised late = left axis deviation
As the bottom of the heart gets depolarised late = right axis deviation

184
Q

Aside from polycystic kidney disease what are the other risk factors for a Berry aneurysm?

A

Ehlers- Danlos
Marfan’s
Neurofibromatosis

Smoking
Hypertension

185
Q

Name some non-genetic causes of dilated hypertrophic cardiomyopathy:

A

HAMS:
Haemochromotosis
Alcohol
Sarcoid

(Duchenne + muscular dystrophy)

MEDICINE NEW (22 decks)

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