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Cardiology Flashcards

1
Q

Indications for aortic valve replacement?

A

Symptomatic patient: with transvalvular pressure gradient >40mmHg

Asymptomatic patient: Moderate or severe AS undergoing a CABG

OR Severe AS with LVSD, abnormal BP response to exercise on exercise tolerance test, episodes of VT or valve area <1cm2

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2
Q

How is aortic stenosis managed?

A

MDT approach, patient education on symptoms of severe AS.

Treat acute episodes of heart failure.

Medical: beta-blockers

Surgical options: mechanical aortic valve, tissue aortic valve, TAVI (trans-aortic valve intervention) if not fit for cardiac surgery

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3
Q

What investigations would you do on a patient with suspected aortic stenosis?

A

ECG: rhythm, LVH, ischaemic heart disease

CXR: cardiomegaly, pulmonary oedema, calcific valve

TTE: to look for aortic valve area (severe <1cm2) and mean pressure gradient across the valve (severe = >40 mmHg), LV size and function

Coronary angiogram: in case CABG needed at the same time as valve replacement

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4
Q

Causes of aortic stenosis?

A

Common: calcific degeneration and bicuspid valve (younger pt).

Uncommon: rheumatic heart disease and congenital heart disease.

Rare: IE, alkaptonuria, Paget’s disease

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5
Q

How do you know that the murmur is that of aortic stenosis and not pulmonary stenosis?

A

The site of the murmur would be different (heart loudest over pulmonary area).

There would likely be a right ventricular heave.

A younger patient is more likely to have pulmonary stenosis.

Pulmonary stenosis is louder on inspiration, whereas AS is louder on expiration.

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6
Q

Differential diagnosis for aortic stenosis?

A

Aortic sclerosis (will not radiate to carotids)
HOCM (accentuates with vasalva)
Pulmonary stenosis
Supravalvular aortic stenosis
Mitral regurgitation

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7
Q

Clinical signs of aortic stenosis?

A

Low volume, slow-rising pulse.
Conjunctival pallor.
Heaving apex beat and thrill over aortic area.
Harsh ESM (crescendo-decrescendo) heard loudest over aortic area in expiration. Radiates to the carotids. May be loudest over apex (Gallavardin phenomenon).

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8
Q

Signs of severe AS on clinical examination?

A

Low volume, slow-rising pulse.
Narrow pulse pressure.
Parasternal heave and thrill over aortic area.
Late peaking ESM.
Soft S2 (due to poorly mobile, stenotic valve).
Reversed split of 2nd heart sound.
4th heart sound.
Clinical signs of heart failure on examination.

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9
Q

What clinical features suggest a significant gradient against the aortic valve in AS?

A

Quiet 2nd heart sound.
Long duration of the mumur.
Low volume pulses.

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10
Q

Possible complications of prosthetic heart valves?

A

IE (early and late)
VTE
Complications of anticoagulation
Anaemia (haemolysis / bleeding)
Valve failure (dehiscence, leaking, calcification, stiffening of leaflets)

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11
Q

Differential diagnosis for a midline sternotomy scar without leg scars from vein harvesting?

A

CABG + LIMA graft.
Valve repair / replacement.
Cardiac surgery for structural heart defects.

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12
Q

Clinical signs of mitral regurgitation?

A

May have lateral / midline sternotomy scar.

Pulses: AF, small volume

Displaced apex beat with thrill

Pansystolic murmur loudest at the apex, radiating to the axilla. Loudest in expiration. Wide splitting of A2 P2.

May have other murmurs / aortic metallic valve (metallic 2nd heart sound)

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13
Q

Signs of severity of MR?

A

Presence of AF (late sign).

LV failure.

NOT murmur intensity!

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14
Q

Causes of mitral regurgitation?

A

Acute: IE, chordae tendineae rupture

Chronic: MVP, rheumatic heart disease, connective tissue disease, post-MI fibrosis, amyloid, calcification, functional MR (ischaemic / dilated cardiomyopathy)

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15
Q

Investigations for suspected MR?

A

Bedside: ECG (look for p-mitrale, AF and signs of previous infarction)

Bloods: FBC, inflam markers, blood cultures

Imaging: CXR (cardiomegaly, CCF signs), TTE (to look at severity + cause)

Special: 24h tape

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16
Q

Management of MR?

A

Medical:
Anticoagulation for AF.
Diuretic, beta-blocker, ACEi’s.

Percutaneous:
Mitra-clip/MTEER for palliation in inoperative cases of MVP.

Surgical:
Valve repair (preferable) with annuloplasty ring or replacement.
Aim to operate when symptomatic, prior to severe LV dysfunction / dilatation.

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17
Q

Differential diagnosis for mitral regurgitation?

A

Calcified AS produces murmur at apex that mimics MR (Gallavardin phenomenon)

Tricuspid regurgitation

VSD

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18
Q

Symptoms of HOCM?

A

LVF including breathlessness
Syncope
Chest pain
AF
Sudden death

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19
Q

Signs of HOCM on examination?

A

Jerky pulse character
May have AF
Large A waves in JVP or normal JVP
May have ICD in situ

On auscultation:
Dynamic ESM radiating to apex (dynamic = severity of murmur changes with posture). Loud/normal S1, S4, signs of LVF.

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20
Q

Sudden cardiac death risk factors in HOCM?

A

FH of sudden death
PMH of arrhythmic cardiac arrest
Episode of sustained or NSVT
Abnormal BP response to exercise
LVH >30 mm wall thickness
Unexplained syncope

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21
Q

Investigations for suspected HOCM?

A

ECG: LVH, lateral t-wave inversion, p-mitrale and deep septal q-waves.

Echo: to diagnose hypertrophy and assess severity of LVOTO.

Holter monitor: to monitor for ventricular arrhythmias.

Exercise tolerance test: to assess for BP response to exercise.

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22
Q

Management of HOCM?

A

Asymptomatic: avoidance of strenuous exercise, dehydration and vasodilators.

Symptomatic:
Beta-blockers, pacemaker, alcohol septal ablation, surgical myomectomy.

Rhythm disturbance / high risk of SCD: ICD.

Refractory despite above: cardiac transplant.

NB importance of genetic counselling of 1st degree relatives - autosomal dominant condition.

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23
Q

Clinical signs of restrictive cardiomyopathy / constrictive pericarditis?

A

Extracardiac signs which may indicate a secondary restrictive cardiomyopathy.

Raised JVP, pitting oedema, ascites, hepatomegaly.

Usually present with signs and symptoms of HF in the setting of good LV systolic function.

Echo shows atrial enlargement.

May have other signs of right-sided HF: raised JVP, dominant Y-descent, pulsus paradoxus, pericardial knock.

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24
Q

Causes of constrictive pericarditis?

A

Viral / bacterial pericarditis
Post-surgery (CABG)
Post-TB
Radiation (e.g., for lymphoma)

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25
Q

Causes of restrictive cardiomyopathy?

A

Endomyocardial fibrosis
Loffler’s syndrome (eosinophilic infiltration of myocardium)
Sarcoidosis
Scleroderma
Haemochromatosis
Amyloidosis

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26
Q

How to differentiate between restrictive cardiomyopathy and constrictive pericarditis on further imaging?

A

CXR: shows pericardial calcification in the case of constriction.

Echo: may show bright white pericardium in pericardial disease.

Cardiac MRI: to look for restrictive cardiomyopathy.

Cardiac CT: to look for both restrictive / constrictive pathology.

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27
Q

Why do you need to follow up with right or left heart catheterisation if any suspicion of restrictive cardiomyopathy or constrictive pericarditis?

A

Need to measure invasive haemodynamics.

The presence of ventricular interdependence: a fluctuating LV/RV pressure during respiration is highly diagnostic for constrictive disease.

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28
Q

Implantable cardiac device types?

A

PPMs (single RA, RV or both RA + RV).

Implantable cardiac defibrillators.

Cardiac resynchronisation therapy devices (biventricular PPMs).

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29
Q

How are the function of pacemakers coded for?

A

First letter: chamber paced (A = atria, V = ventricle, D = dual)

Second letter: chamber sensed

Third letter: response to sensed event (inhibited / dual)

Fourth letter: rate response (adapts to changes in physical activity)

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30
Q

Complications of implantable cardiac devices?

A

Pneumothorax related to venous access.
Cardiac perforation.
Pocket haematomas.
Displacement of pacemaker.
Retained stitch.
Infection requiring system explant.

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31
Q

Clinical signs of a VSD?

A

Thrill at lower left sternal edge.
Systolic murmur localised at the LLSE.
No audible A2.
Loudness does not correlate with size.
If Eisenmenger’s develops, the murmur often disappears as the gradient diminishes.

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32
Q

Clinical signs of a PDA?

A

Collapsing pulse
Thrill 2nd left interspace
Thrusting apex beat
Continuous machinery murmur below L clavicle in systole

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32
Q

Signs of pulmonary hypertension on examination?

A

Loud P2
RV heave

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32
Q

Associated heart lesions with a VSD?

A

Aortic regurgitation
PDA
Tetralogy of Fallot
Coarctation of aorta

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33
Q

Causes of a VSD?

A

Congenital: Turner’s, Downs’, William’s, Noonan’s syndromes

Acquired: traumatic, post-operative, post-MI

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34
Q

Management of a VSD?

A

Surgical: pericardial patch
Percutaneous: Amplatzer device

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35
Q

What are the components of Fallot’s tetralogy?

A

VSD
Overriding aorta
Pulmonary stenosis
RVH

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36
Q

Management of coarctation of the aorta?

A

Percutaneous: EVAR
Surgical: Dacron patch aortoplasty
Long-term antihypertensives
Long-term follow up with MR aortogram

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37
Q

Causes of an absent radial pulse?

A

Acute: embolism, aortic dissection, trauma

Chronic: coarctation of aorta, atherosclerosis, Takayasu’s arteritis, the presence of a LVAD

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38
Q

Investigations for a VSD?

A

ECG: conduction defects (BBB)

CXR: increased pulmonary perfusion (‘pulmonary plethora’)

TTE/TOE: site, size, shunt calculation and associated lesions

Cardiac catheterisation: for consideration of closure

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39
Q

Investigations for palpitations?

A

Bedside: ECG, obs, history

Bloods: electrolytes, thyroid function, 24h metanephrines (urine)

Imaging: echo - structural heart disease

Special: 24h Holter monitor, EP studies

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40
Q

What would you do in the case of an exercise-induced rhythm disturbance history?

A

Treadmill test.
If worried about something like Brugada syndrome, would consider a fleicainide challenge test.

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41
Q

Cardiac differential diagnoses for palpitations?

A

AF / atrial flutter
WPW syndrome
Multifocal atrial tachycardia
Tachy-brady syndrome / sick sinus syndrome
Ventricular tachyarrhythmia

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42
Q

Clinical findings of mixed aortic valve disease?

A

Slow-rising pulse (AS) and narrow pulse pressure (AS).

Heaving apex beat, non-displaced (AS).

ESM heard loudest in aortic region with radiation to carotids (AS).

Early diastolic murmur heard at aortic region (AR).

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43
Q

What is an Austin-Flint murmur?

A

Occurs in mixed aortic valve disease or severe AR.

It is a rumbling diastolic murmur heard loudest at LLSE.

It is caused by the regurgitant jet coming through the aortic valve in AR, and hitting the anterior mitral valve leaflet.

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44
Q

What is the predominant lesion in mixed aortic valve disease (usually)?

A

Usually the predominant lesion in mixed aortic valve disease is STENOSIS with a degree of regurgitation. As the valve stiffens, it does not close properly, and you get a leak.

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45
Q

Treatment of mixed aortic valve disease?

A

Dependent on the patient’s symptoms, and the predominant valve disease type.

If asymptomatic, treat medically:
Manage co-morbidities such as IHD and HTN.
Beta-blockers to help with symptoms.
ACEi and ARB to those with LV pathology.
Diuretics if signs of overload.

If symptomatic, the valve should be replaced:
Surgical replacement = gold standard.
Balloon valvuloplasty as temporising measure if unwell / cardiogenic shock.
TAVI if not fit for open heart surgery.

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46
Q

Causes of aortic regurgitation?

A

Aortic regurgitation can be caused by valvular pathology OR pathology of the aortic root.

Rheumatic HD
CTDs: Marfan’s, EDS
Hypertension
SLE
Osteogenesis imperfecta
Myxomatous disease

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47
Q

Signs of aortic regurgitation?

A

Collapsing pulse (wide pulse pressure)

Eponymous signs attributable to wide pulse pressure:
De Musset’s sign (head bobbing)
Quincke’s sign (capillary nailbed pulsations)
Muller’s sign (uvular pulsation)

Early diastolic murmur / Austin-Flint murmur
Displaced apex beat

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48
Q

Known complications of Ehlers-Danlos syndrome?

A

Most common are joint issues due to hypermobility, leading to joint deformity.

Cardiovascular: mitral valve prolapse, mitral regurgitation, aortic regurgitation, conduction abnormalities.

Vascular subtype: increased propensity to haemorrhage (ICH or GI).

Glaucoma / retinal issues.

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49
Q

Inheritance and implications of Marfan’s syndrome?

A

Autosomal dominant condition.
Affects the fibrillin gene and collagen generation.

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50
Q

What condition could be a differential for Marfan’s syndrome?

A

Homocystinuria, although this is not typically associated with aortic root dilatation.

I would like to assess mental status.

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51
Q

Cardiac features of Marfan’s?

A

Aortic dissection
Aortic dilatation
Aortic regurgitation
Mitral valve prolapse

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52
Q

Management of Marfan’s syndrome?

A

MDT approach, usually managed as outpatient unless warning signs of aortic dissection / decompensated valvular heart disease.

Patient education on warning signs, avoid contact sport.

Genetic counselling.

Referral to ophthalmology for screening / annual follow up.

Referral to cardiology: FU of aortic root. Life long beta-blockers to reduce risk of aortic root dilatation, and consider ARB to slow rate.

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53
Q

What are the indications for aortic root replacement in Marfan’s?

A

Aortic root diameter >50mm.

Aortic root diameter 45-50mm AND family history of aortic dissection / rapid dilatation.

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54
Q

Clinical signs on examination in a patient with Marfan’s?

A

Increased arm span to height ratio.

Marfanoid facies: retrognathia, down-slanting palebral fissure, endophthalmos, prominent supra-orbital ridges.

Eyes: ectopia lentis, blue sclerae

Mouth: high-arched palate

Chest: pectus excavatum / carinatum

Scars: midline sternotomy, lateral thoracotomy, pacemaker, scar running from anterior to posterior chest (dissection repair)

Spine: kyphoscoliosis

Feet: pes planus

Hands: arachnodactyly, Steinberg sign (distal phalanx of thumb extends beyond ulnar border of hand when folded across palm)

Hypermobile joints

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55
Q

Please list the ideal INR ranges for a metallic valve replacement: aortic, mitral and mitral ball + cage valve.

A

Aortic: 2 - 3
Mitral: 2.5 - 3.5
Mitral ball + cage: 3 - 4

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56
Q

Signs seen in patients with coarctation of the aorta?

A

Lower body underdeveloped in comparison to upper body

Signs of previous surgical repair

Stigmata of endocarditis

Radio-radial delay (if coarctation proximal to subclavian)

Radio-femoral delay + volume deficit

Differing BP from UL to LL

Co-existing syndromes, i.e., Turner’s

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57
Q

Auscultation findings in coarctation of aorta?

A

Normal / loud S1

Systolic murmur loudest over thoracic spine (length of murmur corresponds to severity of coarctation)

Can also get ESM of aortic stenosis (stenosed aortic valve)

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58
Q

Symptoms of coarctation of the aorta?

A

LVF

Uncontrolled HTN (epistaxis, headaches)

Endarteritis (infection of aorta), often presenting with pyrexia of unknown origin

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59
Q

Non-cardiac associations of coarctation of aorta?

A

Turner’s syndrome
Berry aneurysm
Neurofibromatosis type 1
Marfan’s syndrome

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60
Q

Management of coarctation of aorta?

A

Medical: antihypertensives

Surgical: repair is indicated if the peak pressure difference is >30 mmHg or asymptomatic patient with HTN or LVH

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61
Q

Signs on examination for a patient with an atrial septal defect?

A

Soft ESM loudest at pulmonary area

Fixed splitting of S2

Can get functional TR

Signs of pulmonary HTN (loud P2)

Right heart failure signs

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62
Q

Signs on examination for a patient with VSD?

A

Pansystolic murmur with ejection character

Loudness of murmur inversely proportional to size of VSD, loud pansystolic murmur of small VSD = ‘maladie de roger’

Signs of right heart failure

Eisenmenger’s syndrome: L to R shunt causes worsening pulmonary HTN and reversal to R to L shunt causing cyanotic heart disease

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63
Q

What are the defects present in Tetralogy of Fallot?

A

‘PROV’

Pulmonary stenosis
Right ventricular hypertrophy
Overriding aorta
VSD

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64
Q

Late complications of Tetralogy of Fallot?

A

Pulmonary regurgitation
Residual VSD
Arrhythmias
Aortic regurgitation
Aortic root dilatation

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65
Q

Which factors would necessitate the need for surgery in aortic regurgitation?

A

Acute severe symptomatic AR requires emergency surgery

Symptomatic patients with severe AR, regardless of LV function

Patients with severe AR undergoing cardiac surgery for another reason

Asymptomatic patients with severe AR

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66
Q

What is an Austin-Flint murmur?

A

Low-pitched, rumbling mid-diastolic murmur

A sign of severe AR

Occurs due to the fluttering of the mitral valve leaflet caused by the severe regurgitant jet of AR

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67
Q

Clinical findings of aortic regurgitation on examination?

A

General: dyspnoea

Peripheral: collapsing pulse, wide pulse pressure

Chest: displaced and hyperdynamic apex beaet, high-pitched early diastolic murmur (heard best in fixed expiration at LLSE)

Eponymous signs:
- Corrigan’s sign: ‘dancing carotid’
- DeMusset’s sign: head nodding
- Quincke’s sign: pulsation at nail bed
- Traube’s sign: pistol-shot femorals

Austin-Flint murmur

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68
Q

What signs can be found in severe aortic regurgitation?

A

Widened pulse pressure

Soft S2

Short end-diastolic murmur

S3 sound

Evidence of LV failure

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69
Q

Causes of aortic regurgitation?

A

Acute: IE, aortic dissection

Chronic: bicuspid valve (congenital), aortic root dilatation, prior IE, rheumatic fever, iatrogenic (following TAVI / balloon dilation)

CTD: RA, ank spondylitis, SLE, Ehlers-Danlos, osteogenesis imperfecta, Marfan’s syndrome

Syphilitic aortitis (rare)

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70
Q

Management of aortic regurgitation?

A

Medical:
- regular follow up and echo
- diuretics for HF
- ACEi / ARB / CCBs (vasodilators)
- Marfan’s - beta-blockers slow aortic root dilatation and reduce risk of complications

Surgical:
- AV replacement +/- CABG
- TAVI if AVR is too high risk

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71
Q

How often should patients with Marfan’s syndrome have aortic screening?

A

Yearly with an echo to monitor the proximal aorta / aortic root.

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72
Q

List some manifestations of Marfan’s syndrome.

A

High-arched palate
Tall
Arachnodactyly
Ectopia lentis (upward lens dislocation)
Arm span > height
Dural ectasia
Pectus excavatum
Joint laxity
Scoliosis
Pes planus

(Ghent criteria)

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73
Q

Examination features in a patient with an LVAD?

A

Patient does not have a pulse or recordable BP

HeartMate machine at the bedside

Battery pack with backup pack worn

Percutaneous lead exit site (RIF)

‘Polyphonic’ heart sounds to auscultation

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74
Q

Complications of LVADs?

A

Bleeding events

Thrombosis (ischaemic stroke + pump thrombosis)

Infections

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75
Q

Indications for a ventricular assist device?

A

Short-term use: recovery from MI or cardiac surgery

Long-term use: advanced heart failure

Can be used as a bridge to transplantation

76
Q

Signs to be expected in significant pulmonary stenosis?

A

Large A waves (due to delayed RA emptying)

RV heave due to pulmonary hypertension

Ejection systolic murmur at LSE due to functional tricuspid regurgitation

Widely-split second heart sound with quiet pulmonary component

77
Q

Investigations for pulmonary stenosis?

A

ECG

Echo:
- to quantify severity of PS
- to determine its aetiology (valvular, supra or subvalvular)
- to determine whether there are any other co-existing cardiac lesions or septal defects

78
Q

Inheritance pattern of Noonan’s syndrome?

A

Autosomal dominant inheritance

Variable expression

79
Q

Differences in radiation of the murmur between aortic and pulmonary stenosis?

A

AS would radiate to the carotids

AS would be accentuated by expiration (not inspiration, as PS is)

80
Q

Differential diagnosis for ESM?

A

Aortic stenosis
Pulmonary stenosis
VSD
LVOTO (HCM)

81
Q

Symptoms of severe pulmonary stenosis?

A

SOB on exertion
Effort intolerance
Signs of R sided heart failure
Syncope / presyncope

PS is associated with RVH, and AS is associated with LVH

82
Q

Features to be expected in a patient with Noonan’s syndrome?

A

Cardiac:
- pulmonary stenosis
- HCM
- septal defects

Face: proptosis, wide-set eyes, ptosis, strabismus, micrognathia, webbed neck

MSK: wide carrying angle of arms, short stature, widely spaced nipples

Cognitive: mild intellectual disabilities and developmental delay

83
Q

Features to be expected in pulmonary stenosis?

A

Loud ESM, maximal in pulmonary area

Accentuated by inspiration

Radiates to left infraclavicular region

Can be supra, intra or subvalvular (due to RVOT obstruction)

84
Q

What heart lesions are coarctation of the aorta most commonly associated with?

A

Bicuspid aortic valve (50-80%)
VSD
PDA

(Non-cardiac associations include Berry aneurysms and Turner’s syndrome)

85
Q

How does coarctation of the aorta usually present?

A

In infants as severe heart failure OR
In adolescence / adulthood as unexplained hypertension.

Variable presentation is due to the degree of narrowing that is present, and the formation of collateral arterial supply.

86
Q

Management options for coarctation of the aorta?

A

Balloon angioplasty

Endovascular stent placement

Surgery (resection and end-to-end anastomosis)

87
Q

Investigations to request in suspected coarctation of the aorta?

A

ECG: LVH

CXR: symmetrical rib notching (occurs due to collaterals through posterial intercostal arteries), and ‘figure 3 sign’ (dilatation of L subclavian artery, coarctation and post-stenotic dilatation)

Other imaging: echo with colour doppler to look for VSD / shunt, CT aortogram and MRA

88
Q

Signs and symptoms to be expected in coarctation of the aorta?

A

Headaches, epistaxis, leg claudication (due to reduced blood flow to the lower body extremities)

Visible collateral blood vessels

Weak femoral pulses with right-sided radial or brachial-femoral delay

On auscultation:
- systolic ejection click
- continuous murmur or bruits heard over scapula, anterior axillary areas and left sternal edge
- short mid-systolic murmur (from coarctation itself) - most loud under L scapula

Turners syndrome: webbing of the neck / wide carrying angle

89
Q

How is infective endocarditis diagnosed?

A

Based on the Duke criteria.

Must have either:
- 2 major criteria
- 1 major + 3 minor criteria
- 5 minor criteria

90
Q

Investigations in suspected IE?

A

Blood cultures (3 sets at different sites) prior to abx unless severely septic.

TTE: to establish endocardial involvement.

TOE: if suspected prosthetic valve endocarditis or aortic root abscess.

Regular U+Es for renal function monitoring.

ECG every 2 days to monitor PR interval (lengthening PR suggests aortic root abscess formation, early surgery indicated here).

Early cardiology review.

Pregnancy test if female.

91
Q

Management of infective endocarditis?

A

Discuss with local microbiology team and look at local trust guidelines for IE treatment.

Usually penicillin + gentamicin.

Prosthetic valve endocarditis will require IV abx for at least 6 weeks + probably valvular replacement.

92
Q

Complications of IE?

A

Direct tissue destruction: valvular failure / heart block.

Septic emboli: lung, brain, splenic abscesses.

Renal failure: systemic sepsis / immune complex glomerulonephritis.

93
Q

Indications for surgical intervention in infective endocarditis?

A

Uncontrolled infection

Haemodynamic instability

Heart block due to aortic root abscess

94
Q

Signs associated with infective endocarditis?

A

Infection-related: fever, murmur, heart failure, hepatosplenomegaly

Immune-complex formation related: Roth spots, Osler nodes, glomerulonephritis

Embolic phenomena related: conjunctival haemorrhages, Janeway lesions, splinter haemorrhages

95
Q

Complications of valve surgery?

A

Valvular failure

Valve thrombosis

Acute valvular dehiscence

Post-op endocarditis or subacute IE

Embolic phenomena (CVA / TIA)

Haemolysis (metal valve)

Bleeding (if warfarinised)

96
Q

Management options for mitral stenosis?

A

Options depend on whether the patient is symptomatic and how stenosed the valve is.

Options include:
- Observation only
- Percutaneous balloon mitral valvuloplasty (PBMV)
- Surgical repair / replacement

97
Q

Causes of mitral stenosis?

A

Most common = rheumatic fever (90%)

Rarer: congenital, degenerative, non-valvular (LA myxoma, IE with large thrombus)

98
Q

Signs of severe mitral stenosis?

A

AF
Pulmonary hypertension
Signs of CCF
Short gap between S2 and opening snap

99
Q

Auscultation findings in mitral stenosis?

A

Mid-diastolic murmur (best heard with bell, with pt in lateral decubitus position in held expiration)

100
Q

Signs of pulmonary hypertension?

A

Raised JVP with CV waves
Functional tricuspid regurgitation
Loud P2

101
Q

What is a Graham-Steele murmur?

A

Pulmonary regurgitation due to raised pulmonary pressures from mitral stenosis.

102
Q

Treatment of AS?

A

If >75 = TAVI
If <75 = surgical aortic valve replacement unless surgeons dont agree

Main contraindications to TAVI
1. PVD
2. Malignant features of annulus (wont sit correctly)
3. CAD

Main contraindications for surgical aortic valve
1. RT to chest
2. Prev sternotomy
3. CLD
4. PHTN
5. Poor LV

Untreated, severe AS has a 50% 1 year mortality

103
Q

How do you classify AS severity?

A

Character of murmur
Slow rising pulse
Cardiac decompensation
LVH (S1+R6 >35mm (7 large squares), LBBB, AF
Echo - peak gradient >64mmHg, or mean gradient >40mmHg; best measure is ratio of valve velocity vs. LVOT velocity (dimensionless index)

104
Q

Clinical signs of aortic stenosis?

A

Slow rising pulse
Narrow pulse pressure
Right ventricular failure - v waves, loud P2, basal creps
Soft A2
Loud P2
Late peaking of a long systolic murmur
S4 (Tenesee)
Gallavardin phenomenon - all over pre-cordium but importantly not radiating to axilla

105
Q

What forms the workup for a TAVI?

A

Routine bloods
PFTs if smoker
ECG gated cardiac CT
Angiogram if CT doesnt show coronary arteries well enough

106
Q

Complications of a TAVI?

A

Arrhythmias (1st degree HB)
Vascular haematomas
Stroke / MI / annular rupture

107
Q

Indications for mitral valve repair / replacement?

A

When indicated and feasible, repair is the preferred treatment

Indications for surgery:
Symptoms + severe MR on echo
Severe MR on echo + AF, LV diastolic or systolic dysfunction (all of these predict worst POST-OP outcomes, and so trigger early surgery in asymptomatic patients)
Acute MR post MI

108
Q

What are the clinical signs of severe MR?

A

Soft S1
S3/S4
Displaced heaving apex
Precordial thrill
Widely split S2 (earlier emptying of LV as some goes out of aorta, some goes into LA)
PHTN
AF

109
Q

What are the causes of mitral valve prolapse?

A

Primary (Inherited) - myxomatous degeneration
Seconday: Marfan’s, Ehler-Danlos, Pseudoxanthoma elasticum, osteogenesis imperfecta, PKD, SLE

110
Q

What causes reverse splitting of S2?

A

LBBB
HOCM
Severe AS
WPW
PDA
MR

111
Q

What is your differential for an ESM?

A

AS
Aortic sclerosis
HOCM
PS

Pan-systolic
1. MR (AS NEVER radiates to axilla)
2. VSD

112
Q

What medications must you AVOID in aortic stenosis?

A

Vasodilators (increase gradient across the valve) - ACEi, nitrates, sildenafil

113
Q

What are the causes of pulmonary stenosis?

A

Congenital
Noonans, Turner’s, Down syndrome
Rubella

114
Q

Cardiac manifestations of Marfan’s syndrome?

A

Aortic root dilation
Aortic dissection
Aortic regurgitaiton
Mitral valve prolapse

115
Q

Non-cardiac manifestations of Marfan’s syndrome?

A

Arachnodactyly
Hypermobile joints
Kertoconus and upward lens dislocation
Blue sclera
Heterochromia of irides
Iridodonesis (asymetric iris) - prev lens dislocation + repair
High arched palate
Pneumothorax
Spontaneous intracranial hypotension
Dural ectasia
Pes planus

116
Q

What is Steinberg and Walker sign?

A

Marfan syndrome.

Steinberg: When patient makes a fist enclosing thumb - thumb sticks out

Walker: 1st and 5th digit of one hand overlap over wrist of the other hand

117
Q

How do you manage aortic regurg in patients with Marfan’s syndrome?

A

Lifelong beta-blockade
Monitoring of aorta with echocardiography
Replace aortic root before diameter >45mm if FHx, 50 otherwise, or if rate of expansion is >3mm/year

118
Q

What are the signs of a failing aortic valve?

A

Blurred S2
Absence of silence in diastole

119
Q

What are the causes for clubbing?

A

Cardiac
1. Cyanotic heart disease
2. Atrial myxoma
3. Infective Endocarditis

Resp
1. Suppurative lung disease
2. Lung fibrosis
3. Lung cancer
4. Asbestos
5. Mesothelioma
6. Lung abscess

GI
1. IBD
2. Liver cirrhosis
3. HCC
4. Coeliac

Endocrine
1. Thyroid acropachy

Congenital

POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M-protein plasmacytoma, Skin changes

120
Q

What is Noonan’s syndrome?

A

Autosomal Dominant with multiple implicated genes including SHP2

Short stature
Webbed neck
Cubitus Valgus
Widely spaced nipples
Mild facial changes
Proptosis
Ptosis
Strabismus
Pectus excavatum
Learning difficulties
Impaired coagulation
Congenital heart disease - PS (most common), VSD, ASD, HOCM.

121
Q

What are the cardiac manifestations of Noonan’s syndrome?

A

PS is most common

Also VSD, ASD and HOCM

122
Q

What are the cardiac manifestations of Turner syndrome?

A

Bicuspid aortic valve
Dilation and dissection of aortic root

123
Q

What are the causes for PS?

A

Valvular
Congenital
Rheumatic
Noonan’s

Supra-valvular
Wiliams Syndrome

Subvalvular
Fallot’s

124
Q

What do you know about Turner syndrome?

A

45XO

Phenotype
Short stature
Webbed neck
Wide spaced nipples
Primary amenorrhoea
Cardiac defects including bicuspid aortic valve, aortic root dilation, and dissection
Multiple pigmented naevi
Short 4th metacarpal
Horseshoe kidney

125
Q

What are causes of VSD’s?

A

Congenital
Maternal alcohol
Aneuploidy syndromes (Down, Edward, Patau)

Acquired
Ischaemic, iatrogenic (septal puncture)

126
Q

What are the complications of a VSD?

A

IE
PHTN
Aortic regurg if peri-membranous
Arrythmias
Shunt reversal

127
Q

What is Holt-Oram syndrome?

A

AD
ASD + tri-phalangeal thumbs

128
Q

What are the clinical signs of an ASD?

A

Fixed split S2
Ejection systolic murmur (increased flow across pulmonic valve)
PHTN

129
Q

What are the complications of an ASD?

A

Arrythmias
PHTN
Eisenmenger’s
Paradoxical embolism
IE
Recurrent pneumonias

130
Q

What are the causes for ASD’s?

A

Ostium secondum (PFO, Holt-Oram)
Ostium primum (present earlier and involve mitral and tricuspids)
Sinus venosus (SVC junction) associated with anomalous pulmonary venous drainage

131
Q

What are the clinical signs of a PDA?

A

Severe - collapsing pulse
Can lead to cyanotic heart disease
Precordial thrill under left clavicle
Continuous machine like murmur with systolic accentuation
To differentiate it from PS, listen at the back - the murmur will be present here - PS will not

132
Q

Clinical signs of mitral stenosis?

A

Malar Flush
AF
Tapping apex (palpable S1)
Left parasternal heave if PHTN
Opening snap in diastole folllowed by mid-diastolic murmur heard best at apex. The more severe the stenosis, the closer the opening snap is to S2, and the longer the murmur

133
Q

Causes of mitral stenosis?

A

Congenital (rare)
Rheumatic heart disease
Valvular endocarditis
Senile degeneration

134
Q

What is the treatment for mitral stenosis?

A

If AF, anticoagulate and rate control
Mitral valvuloplasty
Surgery - valvotomy

135
Q

In a case of PHTN and suspected Eisenmenger’s, what shunts do you know of, and how would you identify them?

A

PDA - reverse splitting
VSD - Single S2
ASD - fixed split S2

136
Q

What are the possible indications for a posterolateral thoracotomy incision?

A

Pneumonectomy/lobectomy
Aortic surgery (Coarctation/dissection)
Blalock Tausig shunt (connects subclavian to pulmonary arteries and is associated with a weak ipsilateral radial pulse)

137
Q

What are causes of cyanotic heart disease?

A

ToF
Transposition of great vessels
Pulmonary atresia/stenosis
Tricuspid atresia
Ebstein’s (atrialisation of the right ventricle due to low inserting TV leaflets)
Eisenmengers (reversal of left to right shunt)

138
Q

Complications of ToF surgery?

A

PR in adolescence following surgery of ToF - needs valve replacement

139
Q

What are causes of restrictive cardiomyopathy?

A

Primary:
Lofflers
Endomyocardial fibrosis

Secondary (infiltrative):
Amyloidosis
Sarcoidosis
Haemachromatosis
Radiation

140
Q

What is constrictive pericarditis?

A

Chronic pericarditis leads to calcification of the pericardium leading to diastolic failure

141
Q

How do you manage AF?

A

Emergency: DC

Elective

Rate control (preferred)
Bisoprolol
CCB’s
Digoxin (if in heart failure)

Medical rhythm Control
Amiodarone (esp in heart failure)
Flecainide

DC
If <48 hours = heparinise and DC
If >48 hours = anticoagulate for 4 weeks +/- amiodarone if high risk of failure

142
Q

When is rhythm control preferred over rate control in AF?

A

If onset is <48 hours
If cause is reversible
If there is cardiac failure primarily due to AF
Atrial flutter amenable to ablation

143
Q

What is the ORBIT score?

A

Assess bleeding risk (CRAB!)

Clopidogrel or Aspirin (antiplatelet)
Renal impairment
Age >74
Bleeding history, Hb <130

144
Q

What are the principle management of chronic heart failure?

A

ACEi and BB
Aldosterone antagonist
SGLT-2 inhibitor
AF?: Digoxin; EF <35% despite optimising ACEi/ARB?: Sabucatril/valsrtan; African American?: Hydralazine; broad QRS? CRT
One off pneumococcal and annual influenza vaccines

145
Q

What are the medical treatments available for angina?

A

Aspirin, Statin, GTN
Rate control:
1. BB or CCB (rate limiting non-dihydropiridine eg verapamil or diltiazem)
2. BB + CCB (longer acting dihydropiridine eg amlodipine nifedipine)
3. Add third drug only if referred for PCI/CABG. These include nitrates (vasodilator and reduces pre-load), nicorandil (vasodilator), ivabradine (blocks funny channel at SAN), ranolazine (relaxes tension in muscle walls reducing oxygen demand)

146
Q

What are the indications for cardiac pacing?

A

Symptomatic sinus node disease
Mobitz II (asymptomatic)
Mobitz I (symptomatic)
Complete heart block
Persistent AV block post-MI

147
Q

What is CRT, and what are the indications?

A

Goal is to re-coordinate biventricular contraction (Leads in LV, RV, and sometimes RA). Can be connected to an AICD and pacemaker

148
Q

What are the indications for an ICD?

A

Post MI:
LVEF <30% + broad QRS
LVEF + NSVT + EP positive

Familial:
LQTS, Brugada, HCM
Cardiac arrest due to VT/VF

149
Q

What are the diagnostic criteria for IE?

A

Duke’s.
x 2 major criteria
x 1 major + 3 minor criteria
x 5 minor criteria

Major
1. Blood culture positive for typical microorganism (staph aureus, enterococcus, viridans)
2. Echo showing valvular vegetation

Minor
1. Predisposing cardiac lesion
2. IV drug use
3. Temperature >38
4. Embolic phenomena
5. Immunologic phenomena (eg glomerulonephritis)
6. Positive blood culture not meeting above criteria

150
Q

What are the risk factors for IE?

A

IVDU/Haemodialysis
Prosthesis
Structural heart/valvular disease
Rheumatic heart disease
Diabetes/CKD

151
Q

What are the signs of SUBACUTE IE?

A

Fingers, feet, eyes, kidneys

Clubbing
Petechia and splinter haemorrhages
Janeway lesions (palmar/plantar)
Osler nodes (distal finger painful)
Roth spots
Glomerulonephritis

152
Q

What are the causes of aortic regurgitaiton?

A

Acute
- Dissection
- Infective endocarditis

Chronic valve problem
- Bicuspid aortic valve
- Rheumatic heart disease
- Calcified valves
- CTD’s
- Paget’s

Chronic root problem
- Bicuspid aortic valve
- HTN
- Marfan
- Ehlers Danlos syndrome
- Ank Spond

153
Q

What are the renal complications of infective endocarditis?

A

Glomerulonephritis
Haematuria
Acute interstitial nephritis
Eosinophiluria

154
Q

What are the criteria for valve replacement in aortic regurgitation

A

Symptomatic dyspnoea and reduced excercise tolerance AND/OR
- Wide pulse pressure
- ECG changes (on ETT)
- LV enlargement >5.5cm in systole or EF <50%

155
Q

What is the prognosis in AR?

A

Asymptomatic with EF>50% - 1% mortality at 5 years

Symptomatic and (wide pulse pressure + ECG exertional changes + LV enlargement) = 65% mortality at 3 years

156
Q

How do you manage AR?

A

Medically
Rate control
Diuresis
ACEi

Symptomatic
Intervention:
- TAVI
- Valve replacement

157
Q

What murmurs might you hear with mixed aortic valve disease?

A

Ejection systolic murmur heard loudest in aortic region

Early diastolic murmur heard loudest at aortic region / LSE

May also hear Austin-Flint murmur with mixed aortic valve disease. Heard loudest at LLSE. This is due to the regurgitant jet in AR coming through the aortic valve and hitting the anterior mitral valve leaflet.

158
Q

How would you treat asymptomatic aortic stenosis?

A

Very dependent on the patient’s symptoms.

If asymptomatic, treat medically focusing on cardiovascular co-morbidities.
- beta blockers
- ACEi / ARB for those with LV pathology such as LVH
- Diuretics if signs of fluid overload

159
Q

What is generally the predominant lesion in mixed aortic valve disease?

A

Aortic stenosis with a degree of regurgitation. As the valve stiffens, it does not close properly and you get a leak.

160
Q

Causes of aortic stenosis?

A

Degenerative calcification
Bicuspid aortic valve (in younger pt)

Rheumatic fever
Fabry’s disease
SLE
Paget’s disease

161
Q

Acute and chronic causes of aortic regurgitation?

A

Caused either by valve pathology or aortic root pathology.

Acute causes: IE, trauma, aortic dissection

Chronic causes: rheumatic fever (dev countries), Marfan’s, SLE, Ehlers-Danlos, hypertension, myxomatous disease, ankylosing spondylitis.

162
Q

When would you use exercise testing in aortic stenosis?

A

Done to establish symptoms, particularly in patients that are asymptomatic but with severe disease.

Impt to look for ‘low-flow’ aortic stenosis, where the LV is impaired - the aortic valve looks severely stenosed visually, but when assessed with gradients, the gradients aren’t particularly elevated.

In this situation, a stress echo with exercise or dobutamine will differentiate between low-flow and true aortic stenosis. If low-flow is present, the valve area will get larger with increased contractility. In true stenosis, the valve area changes very little with increased cardiac output.

163
Q

What could be used as an alternative to stress echo for investigating low-flow vs true aortic stenosis?

A

Cardiac CT. Has become more popular when looking at low-flow gradients, as the degree of calcification is often related to the degree of aortic stenosis.

164
Q

Why is TAVI usually not suitable in AR?

A

Percutaneous aortic valve replacement (TAVI) is usually not suitable in AR due to aortic root dilatation.

Can use balloon valvuloplasty, but this is associated with many risks and usually only done when patients are v unwell with cardiogenic shock. Usually for AR, surgical valve replacement is 1st line.

165
Q

With mitral valve disease, what are the indications for anticoagulation?

A

If the patient has signs of atrial fibrillation

If they have had previous emboli

With mitral stenosis, additional indications for anticoagulation include a history of thromboembolic disease and LA thrombus

166
Q

How would you diagnose IE?

A

Use Duke’s criteria, of which there are 2 major and 5 minor.

Patients either need both of the 2 maj criteria, or 1 maj and 3 minor, or all 5 of the minor criteria.

Major:
1. Positive echo findings with vegetation on valve
2. Specific bacteria found on 2 separate blood cultures: staph aureus, strep viridans, HACEK group

Minor:
1. Temp over 38
2. Other positive blood cultures
3. Different echo findings consistent with IE
4. Septic emboli
5. Immunological phenomena: Janeway lesions / Osler nodes

167
Q

Name some secondary causes of mitral regurgitation.

A

Secondary causes of MR tend to affect the valve architecture.

Cardiomyopathy and IHD are the most common causes of this.

168
Q

Causes of mitral stenosis?

A

Rheumatic HD
Calcification
Fabry’s disease
RA
SLE
Carcinoid
Whipple’s disease

169
Q

Why is the L apex typically displaced in mitral regurgitation?

A

Due to dilatation of the LV and volume overload.

170
Q

What is the significance of ‘p-mitrale’ on ECG?

A

Seen in mitral stenosis, the LA tends to become hypertrophied, which is seen on ECG as an enlarged p wave with a notch.

171
Q

Management of mitral regurgitation?

A

Split into severe asymptomatic and severe symptomatic.

Anyone with severe disease and symptoms - refer for surgery.

Asymptomatic patients with severe disease:
- FU every 6-12 months
- If ejection fraction drops below 50%, refer for surgery

172
Q

Management of mitral stenosis?

A

Surgery is indicated in symptomatic patients with severe lesions.

In asymptomatic patients with severe disease:
- Follow up every 6-12 months
- Look for elevation in pulmonary pressure. If rises above 50mmHg, refer for surgery despite symptoms

173
Q

Features of pulmonary hypertension in severe mitral stenosis?

A

Functional tricuspid regurgitation
Raised JVP with CV waves
Systolic murmur loudest on inspiration

If right ventricular dysfunction - the patient may have ascites, hepatomegaly and peripheral oedema

174
Q

What is the long-term management of patients with metallic valves?

A

Want to perform serial echocardiograms to assess the function of the valve.

Will need anticoagulation with monitoring of INR in a range that is appropriate for the type of valve that they have. Warfarinised, not DOAC.

175
Q

What are some possible reasons for mitral valve replacement?

A

Mitral stenosis - but unlikely if the patient is in sinus rhythm and has no signs of pulmonary HTN.

Mitral regurgitation and IE.

176
Q

Significance of a new systolic murmur in a patient with a mitral valve replacement?

A

Concern is that the patient has developed valve incompetence with the replaced mitral valve.

Could assess this with an echo - which would also give info on whether there are any other lesions that could be causing the new murmur, such as aortic stenosis or TR.

177
Q

How would you differentiate between AS and TR clinically?

A

Tricuspid regurgitation would have V waves in the JVP.

The murmurs have different characters: AS is an ESM, whereas TR is a pansystolic murmur.

They are heard at different sites on the chest.

178
Q

If a patient has two midline sternotomy scars with no evidence of bypass grafting, what would you be thinking?

A

The patient may have had a valve re-do surgery, or have had 2 valves replaced.

179
Q

How does the treatment differ in a young person vs older person with mitral regurgitation?

A

Consider the role of repair in place of replacement in the first instance, and offer this as a surgical option.

180
Q

If you hear a widely split second heart sound that varies with respiration, what will you be thinking?

A

Tricuspid regurgitation - if varies with respiration.

With an ASD, you wouldn’t expect the S2 split to vary with respiration, it will be fixed. This is because in an ASD, there is communication between the right and left atria, and that means you get equalisation of pressures. This means there is no change in the pressures with inspiration.

181
Q

What is Eisenmenger’s syndrome?

A

Shunt reversal in the context of irreversible pulmonary HTN, which leads to central cyanosis.

182
Q

What are the possible causes of pulmonary valve disease?

A

Congenital and acquired causes.

Rubella
Down’s syndrome
Turner’s syndrome
Noonan’s syndrome

183
Q

What is the relevance of the JVP?

A

The JVP is a visible reflection of pressures in the right atrium.
Abnormalities in the right heart pressure can be seen in the JVP.
For example, in PHTN you would see a raised JVP.

184
Q

What are the indications for mitral valve replacement?

A

If the patient is symptomatic, and there are features of pulmonary HTN or fluid overload.

If the patient is symptomatic but they have a declining ejection fraction or signs of increasing LV dilatation.

Acute MR following an MI.

185
Q

What would you be looking for on echo for a patient with suspected mitral regurgitation?

A
  • Evidence of MR on doppler flow
  • Evidence of left atrial dilatation
  • Looking at the angle of the regurgitant jet to see if there is any mitral valve prolapse
186
Q

What are the triggers for surgery in asymptomatic mitral regurgitation?

A
  • LVEF <60%
  • LV end systolic dimension of >45mm
  • atrial fibrillation
  • systolic pulmonary pressure >50mmHg
187
Q

What are some causes of secondary mitral regurgitation?

A

Secondary MR is where the valve leaflets and chordae are structurally normal, but mitral regurgitation results from an imbalance between closing and tethering forces on the valve secondary to altering forces in left ventricular geometry.

Most common cause of this = ischaemic or dilated cardiomyopathies.

188
Q

Duke’s criteria for IE?

BE TIMER

A

‘BE TIMER’

Major criteria:
- Blood culture positive >2x 12h apart
- Echo evidence of endocardial involvement

Minor criteria:
- Temp >38
- Immunological phenomena (Osler’s, Roth’s)
- Microbiological evidence (positive BC not meeting maj criteria)
- Embolic phenomenon (arterial emboli, septic emboli, conjunctival haemorrhage)
- Risk factors for IE: congenital heart condition, IVDU

PACES flashcards (9 decks)

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