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Phase 4 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Describe hypertrophic obstructive cardiomyopathy (HoCM)

A

AD disorder

clinical features
- asymptomatic
- exertional dyspnoea
- syncope
- angina
- jerky pulse

  • ejection systolic murmur
    > louder on Valsalva, quieter on squatting
  • sudden cardiac death is mainly caused by ventricular arrhythmias (males > females)
  • can happen at rest or exercising
  • S4 heart sound
  • associated with Freidreich’s ataxia and Wolff Parkinson White

Echo
- systolic anterior movement (SAM) of anterior leaflet of mitral valve - mitral regurgitation
- asymmetric septal hypertrophy

ECG
- Non-specific ST segment and T wave abnormalities, progressive T wave inversion
- Deep Q waves

treatment
> ICD
> amiodarone (prevention)

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2
Q

Name scores used to determine risk of stroke in AF

A

CHA2DS2VASc
> CHF
> Hypertension
> Age >75 (2)
> Diabetes
> Stroke / TIA / VTE (2)
> Vascular disease
> Age 65-74
> Female

If >=2 in females or >=1 males, consider anticoagulation

prescribe DOAC even if single episode of paroxysmal AF

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3
Q

Describe the management of SVT

A

Regular narrow complex tachycardia

Acute management

vagal manoeuvres:
> Valsalva manoeuvre
> carotid sinus massage

intravenous adenosine
> rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
> contraindicated in asthmatics - verapamil is a preferable option

DC electrical cardioversion

Prevention of episodes
beta-blockers
radio-frequency ablation

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4
Q

Describe Eisenmenger’s syndrome

A

Reversal of a left-to-right shunt in a cogenital heart defect due to pulmonary hypertension

Uncorrected left-to-right results in remodelling of the pulmonary microvasculature leading to pulmonary hypertension

associated with
- ventricular septal defect
- atrial septal defect
- patent ductus arteriosus

Features
- original murmur may disappear
- cyanosis
- clubbing
- right ventricular failure
- haemoptysis, embolism

CXR: cardiomegaly and pulmonary engorgement

Management: heart-lung transplant

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5
Q

describe the murmur associated with a VSD

A

Blowing pansystolic murmur

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6
Q

Describe the causes of infective endocarditis

A

IVDU (typically causing tricuspid lesion)
- staph aureus (most common)
> tricuspid regurgitation: pansystolic murmur heard loudest over left lower sternal edge, louder during inspiration

Post-valvular surgery (first 2 months post-surgery)
- staphylococcus epidermis (coagulase negative staph or CoNS)

Streptococcus bovis is associated with colon cancer

Streptococcus viridans is the most common cause in developing countries (streptococcus mitis, streptococcus sanguinis) - mouth and dental plaques, caused by poor dental hygiene or following dental procedures

Non-infective
- Systemic lupus erythematosus (Libman-Sacks)
- Malignancy: marantic endocarditis

Culture negative causes:
- prior antibiotics
- Coxiella burnetii
- HACEK: Haemophilus, actinobacillus, cardiobacterium, eikenella, kingella

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7
Q

Describe the management of NSTEMI

A

Aspirin + ticagrelor + fondaparinux
> give unfractionated heparin if patient is undergoing PCI

Clopidogrel instead of ticagrelor if patient at high risk of bleeding

Consider PCI
> coronary angiography within 72h if GRACE score >3%

Nitrates can be given if no hypotension present

Cannot drive for 4 weeks post-MI

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8
Q

describe the initial management of ACS

A
  • Aspirin 300mg
  • Oxygen if sats <94
  • Morphine if severe pain
  • Nitrates if not hypotensive
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9
Q

Describe the management of a STEMI

A

Coronary reperfusion therapy

  • Percutaneous coronary intervention (PCI)

> If presentation is within 12h of onset of symptoms and PCI can be delivered within 120 minutes
dual antiplatelet i.e. aspirin and one of the options below

> if patient not on anticoagulant: prasugrel
if patient on anticoagulant: clopidogrel

> Offer unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor + dual antiplatelet therapy if undergoing primary PCI with radial access

  • Fibrinolysis if primary PCI cannot be given within 120 mins
    > alteplase + fondaparinux
    > repeat ECG in 60-90 mins and transfer for urgent PCI if ST elevation has not resolved
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10
Q

describe Brugada syndrome

A

Sodium channelopathy causing a high incidence of sudden death in patients with structurally normal hearts

Features
- ECG abnormality
> coved ST elevation in >1 of V1-V3 followed by a negative t wave

  • and one of the following criteria:
  • documented VF
  • polymorphic VT
  • family history of sudden cardiac death <45 yrs old
  • coved type ECGs in family members
  • syncope
  • nocturnal agonal respiration
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11
Q

describe mitral stenosis

A

main cause is rheumatic fever

features
- dyspnoea
- haemoptysis
- mid-late diastolic murmur
- loud S1
- opening snap (indicates mitral valve leaflets are still mobile)
- low volume pulse

CXR - left atrial enlargement

management
- if associated with AF, anticoagulate with warfarin / DOAC
- asymptomatic: monitor
- symptomatic: percutaneous mitral balloon valvotomy

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12
Q

which medication used in the treatment of angina can be associated with tolerance?

A

isosorbide mononitrate

may need changes in dosing regimes

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13
Q

list coronary arteries responsible for MI and the leads they are associated with

A

anteroseptal
> V1-V4
> LAD

inferior
> II, III, aVF
> RCA

anterolateral
> V1-6, aVL
> proximal LAD

lateral
> I, aVL +/- V5, V6
> left circumflex

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14
Q

describe the ECG features in posterior MI

A

ECG features
- tall R waves in V1 and V2
- confirmed by ST elevation and Q waves in posterior leads

affected vessel: left circumflex, right coronary

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15
Q

what kind of infarct can cause bradycardia or arrythmias?

A

right coronary infarct as this supplies AV node

> leads II, III and aVF

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16
Q

describe the management of acute heart failure

A
  • oxygen aiming for 94-98%
  • IV furosemide
  • nitrates if concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease
    > contraindication - hypotension
  • If still hypoxic: CPAP
  • if hypotensive
    > dobutamine
    > norepinephrine
    > mechanical circulatory assistance: intra-aortic balloon counterpulsation, ventricular assist devices
  • regular medications for heart failure like beta-blockers or ACEi should be continued unless shock, <50 bpm, 2nd or 3rd degree heart block
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17
Q

describe arrhythmogenic right ventricular dysplasia (ARVD)

A

AD inherited cardiac disorder that is the second most common cause of sudden cardiac death after HOCM

pathophysiology - right ventricular myocardium is replaced by fatty and fibrofatty tissue

features
- palpitations
- syncope during exertion
- family history of sudden cardiac death in relative <40 years old

ECG findings
> epsilon wave: small positive deflection at the end of QRS
> T wave inversion in leads V1-3

Echocardiogram
> enlarged hypokinetic right ventricle with a thin free wall

management
- sotalol as antiarrhythmic
- catheter ablation to prevent VT
- implantable cardioverter defibrillator (ICD)

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18
Q

describe Naxos disease

A

AR variant of ARVD

triad of ARVD, palmoplantar keratosis and woolly hair

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19
Q

describe aortic stenosis and its management

A

clinical features of symptomatic disease (worse on exertion)
- chest pain
- dyspnoea
- syncope
- heart failure

  • murmur: ejection systolic murmur radiating to carotids
    > fixed splitting of heart sounds

features of severe aortic stenosis
- collapsing pulse
- thrill during systole
- narrow pulse pressure
- S4
- left ventricular hypertrophy or failure

causes
- degenerative calcification
- bicuspid aortic valve
> click heard start of systole
- post-rheumatic disease
- subvalvular: HOCM
- William’s syndrome: supravalvular aortic stenosis

investigations
- echocardiogram: assess pressure gradient and surface area of valve
> elevated aortic pressure gradient, reduced valve area, reduced left ventricular ejection fraction, LVH

management
- asymptomatic: observe
> consider surgery if valvular pressure gradient >40 mmHg and LVSD

  • symptomatic: valve replacement
    > surgical AVR if young
    » TAVI (transcatheter aortic valve replacement) if high risk
    » balloon valvuloplasty in children or adults not fit for valve replacement

nitrates are contraindicated, give furosemide for symptomatic relief

20
Q

Describe ventricular septal defect and its management

A

most common cause of congenital heart disease

aetiology
- associated with chromosomal disorders e.g. Down’s syndrome, Edward’s syndrome, Patau syndrome, cri-du-chat syndrome
- congenital infections
- acquired causes e.g. post-MI

Post-natal presentation
- failure to thrive
- features of HF
> hepatomegaly
> tachypnoea
> tachycardia
> pallor

murmur: pan-systolic murmur heard at the lower left sternal border
> louder in small defects

Management
- small VSDs often close spontaneously - monitor

  • large VSDs:
    > medication for HF e.g. diuretics
    > pulmonary artery banding
    > surgical closure: transvenous catheter closure, open heart surgery

Complications
- aortic regurgitation
- infective endocarditis
- Eisenmenger’s syndrome
- right heart failure
- pulmonary hypertension

21
Q

list complications following MI

A
  • left ventricular free wall rupture
    > within 48h
    > chest pain, muffled heart sounds
    > widespread ST elevation
  • left ventricular aneurysm
    > S3, S4 heart sounds
    > persistent ST elevation
    > gradual onset pulmonary oedema
  • ventricular septal defect
    > pansystolic murmur
    > acute pulmonary oedema
  • mitral valve prolapse
    > 2-7 days post-MI
    > sudden pulmonary oedema
    > sinus tachycardia
    > prominent murmur
  • Dressler’s syndrome
  • heart failure
  • re-infarction
  • death
22
Q

describe an atrial septal defect (ASD)

A

asymptomatic in childhood

only progress to give symptoms if they remain untreated to adulthood

murmur: mid-systolic, crescendo-descrescendo murmur heard loudest at upper left sternal border
> murmur radiates to the back
> fixed S2 splitting

if left-to-right shunt exists, paradoxical embolisation can occur
> Stroke in young patients with DVT (embolus bypasses lungs)

management:
> small: monitor
> large: catheter-based closure / open heart surgery

complications: stroke, pulmonary hypertension, right-heart failure, Eisenmenger syndrome

23
Q

Describe the management of chronic heart failure

A

First-line for all patients:
- ACEi + beta-blocker
> start one drug at a time

Second-line
- aldosterone antagonist aka mineralocorticoid receptor antagonist e.g. spironolactone, eplerenone

  • SGLT2i

Third-line
- ivabradine
- sacubitril valsartan (ARNI)
- hydralazine + nitrate
- digoxin
- cardiac resynchronisation therapy (CRT)

offer annual influenza vaccine + one-off pneumococcal vaccine
> those with asplenia, splenic dysfunction of CKD need a booster every 5 years

24
Q

describe ECG changes associated with mitral stenosis

A

P mitrale
- left atrial hypertrophy/strain e.g. in mitral stenosis
- broad, notched (bifid) P waves
> most pronounced in lead II

25
Q

describe acute mitral regurgitation

A

More common infero-posterior infarction

causes: ischaemia or rupture of papillary muscle

features
- Acute hypotension
- pulmonary oedema
- early-to-mid systolic murmur

management
- vasodilator therapy
- emergency surgical repair.

26
Q

describe
- left ventricular aneurysm

  • left ventricular free wall rupture
A

left ventricular aneurysm

  • ischaemic damage weakens myocardium resulting in aneurysm formation
  • ECG: persistent ST elevation and left ventricular failure
  • thrombus may form within aneurysm increasing risk of stroke
  • management: anticoagulation

left ventricular free wall rupture

  • occurs around 1-2 weeks after MI
  • presents with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
  • management: urgent pericardiocentesis and thoracotomy
27
Q

describe a patent ductus arteriosus

A

acyanotic congenital heart defect
> connection between pulmonary trunk and descending aorta

murmur
- normal S1 with a CONTINUOUS crescendo-decrescendo “MACHINERY” murmur that continues during S2
- BELOW left clavicle

risk factors: maternal rubella infection, prematurity

features
- shortness of breath
- difficulty feeding
- poor weight gain
- LRTIs
- bounding collapsing pulses
- large pulse pressure

diagnosis: echocardiogram shows left-to-right shunt, hypertrophy

complications: pulmonary hypertension, right ventricular hypertrophy, left ventricular hypertrophy

management
- give neonate indomethacin (or ibuprofen) if echo shows PDA 1 week postnatally: inhibits prostaglandin synthesis
- monitor until 1 year with echos
- after 1 year: transcatheter or surgical closure (earlier if symptomatic)

28
Q

describe Tetralogy of Fallot

A

4 coexisting pathologies lead to right-left shunt
- ventricular septal defect (VSD)
- overriding aorta
- pulmonary valve stenosis
- right ventricular hypertrophy

> severity of right ventricular outflow tract obstruction (pulmonary stenosis) determines degree of cyanosis and clinical severity

risk factors: rubella, diabetic older mother, DiGeorge syndrome

murmur due to pulmonary stenosis: ejection systolic murmur loudest at pulmonary area (upper left sternal area)

diagnosis: echocardiogram
> CXR: boot-shaped heart

features
- cyanosis
- clubbing
- poor feeding
- ejection systolic murmur
- tet spells: cyanotic episode precipitated by waking, physical exertion or crying

management
- total surgical repair by open heart surgery

29
Q

describe coarctation of the aorta

A

congenital narrowing of descending aorta

associations
- turner’s syndrome
- bicuspid aortic valve
- berry aneurysms
- neurofibromatosis

features
- infancy: duct-dependent CHD
> may present with sudden collapse as ductus arteriosus closes
> tachypnoea, increased WOB
> weak femoral pulses
> poor feeding, grey and floppy baby
> underdevelopment of left arm (reduced flow to subclavian artery) and legs
> swollen extremities

  • adult:
    > hypertension
    > left ventricular heave (left ventricular hypertrophy)
    > radio-femoral delay
  • murmur: ejection systolic murmur, radiates to back

management
- critical coarctation: prostaglandin E1 (alprostadil) to keep ductus arteriosus open while awaiting surgery
> surgery will ligate ductus arteriosus and correct coarctation

  • mild: asymptomatic until adulthood may not require surgical input
30
Q

describe congenital pulmonary valve stenosis

A

associations
- tetralogy of fallot
- william syndrome
- noonan syndrome
- congenital rubella syndrome

features
- fatigue on exertion
- shortness of breath
- dizziness, fainting
- murmur: ejection systolic murmur heard loudest at pulmonary area (second intercostal space, left sternal border)
- palpable thrill in pulmonary area
- right ventricular heave due to right ventricular hypertrophy
- raised JVP

diagnosis: echocardiogram

management
- mild: monitor
- symptomatic or more significant stenosis: balloon valvuloplasty via venous catheter; open heart surgery

31
Q

describe Ebstein’s anomaly

A

congenital condition where tricuspid valve is lower in right side of heart leading to bigger right atrium and smaller right ventricle

associated with
> right-to-left shunt across atria via ASD leading to cyanosis
> Wolff-Parkinson-White syndrome

presentation
- heart failure
- gallop rhythm (addition of S3 and S4)
- cyanosis
- SOB, tachypnoea
- poor feeding
- collapse or cardiac arrest

diagnosis - echocardiogram

management
- treat arrhythmias and heart failure
- definitive is surgical correction

32
Q

describe transposition of the great arteries

A

attachments of aorta and pulmonary trunk are swapped
> right ventricle pumps blood into aorta and left ventricle pumps blood into pulmonary vessels

associated with: VSD, coarctation of aorta, pulmonary stenosis

diagnosis
> loud single S2, no murmur, no respiratory distress
> antenatal US
> if undetected during pregnancy, presents with cyanosis soon after birth

management
- prostaglandin infusion - maintain ductus arteriosus
- balloon septostomy to create an atrial septal defect
- open heart surgery: arterial switch - definitive management

33
Q

describe Wellen’s syndrome

A

ECG pattern caused by high-grade stenosis in left anterior descending coronary artery

features
- may or may not be pain free
- cardiac enzymes may be normal/minimally elevated.

ECG features
- biphasic or deep T wave inversion in V2-3
- minimal ST elevation
- no Q waves

34
Q

describe aortic regurgitation

A

causes
- chronic due to valve disease
> rheumatic fever
> calcific valve disease
> connective tissue diseases e.g. RA

  • chronic due to aortic root disease
    > bicuspid aortic valve
    > spondyloarthropathy e.g. ankylosing spondylitis
    > hypertension
    > syphilis
    > Marfan’s, Ehlers-Danlos
  • acute due to valve disease: infective endocarditis
  • acute due to aortic root disease: aortic dissection

features
- early diastolic murmur
- collapsing pulse, bisferiens pulse
- wide pulse pressure
- Quincke’s sign - nailbed pulsation
- De Musset’s sign - head bobbing
- mid-diastolic Austin-Flint murmur in severe AR

investigation - echocardiography

management
- surgery (TAVI) - if symptomatic with severe AR or asymptomatic with severe AR and LVSD

35
Q

state the first-line investigation for stable chest pain of suspected coronary aetiology

A

CT angiography

36
Q

list acyanotic and cyanotic congenital heart conditions

A

acyanotic
- ventricular septal defect (VSD)
- atrial septal defect (ASD)
- patent ductus arteriosus (PDA)
- coarctation of the aorta
- aortic valve stenosis

cyanotic
- tetralogy of Fallot (more common overall)
- transposition of the great arteries (TGA) (more common lesion presenting at birth)
- tricuspid atresia

37
Q

describe an atrioventricular septal defect (AVSD)

A

defect associated with trisomy 21

features
- poor feeding
- breathlessness
- poor weight gain
- puffiness
- tachycardia

murmur: systolic murmur heard loudest at upper left sternal edge

management - surgical repair

38
Q

describe an innocent murmur

A

aka physiological / functional murmurs

common in children, do not require treatment unless causing symptoms

features
- systolic
- short, soft and often vibratory/musical or “buzzing”
- best heard at left upper sternal border (pulmonary area)
- varies with posture
- no thrill
- localised with no radiation
- no added sounds e.g. clicks

venous hum: continuous blowing noise heard just below clavicles

Still’s murmur: low pitched sound heard at lower left sternal edge

39
Q

describe the different types of MI

A
  • Type I: primary coronary event
  • Type II: ischaemia due to increased oxygen demand / decreased supply
  • Type III: sudden cardiac death
  • Type IV: related to PCI (4a) or stent thrombosis (4b)
  • Type V: related to CABG
40
Q

Describe the clinical features and treatment of cardiac tamponade

A

clinical features

  • Beck’s triad: elevated venous pressure (CVP), reduced arterial pressure, reduced heart sounds
  • Pulsus paradoxus
  • electrical alternans on ECG > different heights of consecutive QRS complexes

May occur with as little as 100ml blood

Definitive management
> emergency thoracotomy
> if they still have a cardiac output, this should occur in theatre with clam shell approach
> If there is a significant delay, consider a pericardiocentesis

41
Q

describe constrictive pericarditis

A

caused by any cause of pericarditis, particularly TB

features
- dyspnoea
- right heart failure: elevated JVP, ascites, oedema, hepatomegaly
- pericardial knock: loud S3
- Kussmaul’s sign is positive: JVP rising on inspiration
- pulsus paradoxus is absent, unlike cardiac tamponade

CXR - pericardial calcification

42
Q

Describe normal ECG variants in an athlete

A
  • first degree heart block
  • sinus Bradycardia
  • Mobitz type 1 (Wenckebach) phenomenon
  • junctional rhythm
43
Q

Describe the classical features of aortic dissection and its management

A

Tearing retrosternal chest pain radiating to back

Difference in BP between left and right arms

tear in ascending aorta may be indicated by new aortic murmur e.g. aortic regurgitation

risk factor: pectus excavatum

investigations
- CXR: widened mediastinum
- ECG: widespread ST depression with normal troponin

  • CT aortic angiogram (first-line if haemodynamically stable): false lumen
    > CT CAP if unavailable

> transoesophageal echo (TOE) in clinically unstable patients

Management

type A - ascending aorta - control BP (IV labetalol) + surgery (aortic root replacement)

type B - descending aorta - control BP(IV labetalol)

44
Q

Describe the guidelines for statin treatment

A

QRISK score over 10%
> atorvastatin first-line 20mg
> Simvastatin if atorvastatin can’t be tolerated

QRISK under 10%
Dietary measures

monitoring
> LFTs at baseline, 3 months and 12 months

45
Q

List adverse effects of amiodarone and describe monitoring requirements

A
  • thyroid dysfunction: both hypothyroidism and hyper-thyroidism

> in amiodarone-induced hypothyroidism, amiodarone can be continued with levothyroxine

  • corneal deposits
  • pulmonary fibrosis/pneumonitis
  • liver fibrosis/hepatitis
  • peripheral neuropathy, myopathy
    photosensitivity
  • ‘slate-grey’ appearance
  • thrombophlebitis and injection site reactions
  • bradycardia
  • lengthens QTc interval

Monitor LFTs, TFTs every 6 months

46
Q

describe the management of angina pectoris

A

All patients should receive aspirin and a statin
> clopidogrel if previous stroke / PAD

Sublingual GTN to abort angina attacks

  • first-line: beta-blocker e.g. atenolol
    > OR rate-limiting calcium channel blocker (verapamil, diltiazem)

> > if using in combination with a beta-blocker use a longer-acting dihydropyridine CCB e.g. amlodipine, MR nifedipine

If poor response increase to maximum tolerated dose

If unsuccessful consider addition of
- Long-acting nitrate e.g. isosorbide mononitrate
- Ivabradine
- Nicorandil
- Ranolazine

Phase 4 (14 decks)

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