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Cardiovascular > Heart Valve Disease > Flashcards

Heart Valve Disease Flashcards

1
Q

Aetiology of Aortic stenosis

A
  • Vast majority due to ‘Degenerative’ calcific stenosis with tricuspid valve intervention in eight decade (elderly: 65+ 45% population)
  • Bicuspid valves are a cause of earlier degeneration (5-6th decade)
  • Less common causes include rheumatic disease (accompanied by mitral valve disease, 30-60), radiotherapy (fibrosis), congenital stenosis, William’s syndrome (supravalvular AS)
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2
Q

Pathophysiology of AS

A

-Progressive restriction of leaflets leads to Valvular obstruction resulting in:
=Hypertrophy and then fibrosis of the left ventricle due to pressure overload
=Inability to augment cardiac output

  • Initial insult to endothelium of A valve
  • Lipid and inflammatory cell infiltration (analogous to atherosclerosis)
  • Fibrosis and calcification (progressive once established)

-Aortic stenosis causes ventricular pressure overload eventually leading to left ventricular dysfunction if untreated

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3
Q

Symptoms of AS

A
  • In general symptoms don’t appear until stenosis is severe
  • Angina, often in the absence of obstructive coronary disease (ventricle hypertrophy= oxygen demand supply)
  • Exertional syncope (diverted blood to muscles and vasodilatation requires increase in CO, cardiac decompensation)
  • Dyspnoea (left atrium and pulmonary veins increase= heart failure)

=CHEST PAIN, SYNCOPE, BREATHLESSNESS

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4
Q

Clinical signs AS

A
  • Ejection systolic murmur (crescendo decrescendo)
  • Quiet/ absent second heart sound (ejection of blood more prolonged when worsening, movement reduced so not closing with as much energy)
  • Radiation to carotids
  • Slow-rising pulse (restricted outflow= prolonged ejection and low volume)
  • Forceful but not displaced (volume overloaded) apex beat (hypertrophy so pressure overloaded)

Severe:
=Narrow pulse pressure, slow rising pulse, delayed ESM, soft/absent S2, S4, thrill, duration of murmur, LVH

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5
Q

Treatment of AS

A

-AS needs treatment when it is severe and:
=Patient has symptoms
OR
=LV function is deteriorating
-Medical treatment is not effective (mechanical problem): diuretics for HF
-Surgical aortic valve replacement (bioprosthetic can deteriorate/ mechanical)
=If asymptomatic but valvular gradient >40mmHg and features of LVSD consider surgery
-TAVI (trans-catheter valve implants) for those not eligible/ high risk- balloon expandable, durability? Balloon valvuloplasty in children with no aortic valve calcification
-Assessment of symptoms and left ventricular function is critical to follow-up of patients with AS

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6
Q

Prognosis of AS

A
  • Prognosis of aortic stenosis even when severe is good when asymptomatic
  • Once symptoms appear prognosis dramatically worsens
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7
Q

Long-term care of AS

A
  • Valve replacement improves symptoms in the vast majority of patients and returns them to a near-normal life expectancy although has some risks
  • The goal of management is to intervene before irreversible myocardial damage without exposing asymptomatic patients to risks of AVR too early
  • Timely surgical or trans-catheter treatment of AS can return prognosis to near-normal
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8
Q

Risks of valve replacement AS

A
  • Operative: death (~1-3%) , Stroke, PPM (pacemaker)
  • Long-term: Endocarditis (~0.5%/ year), Thrombo-embolism, Bleeding with anticoagulation (mechanical AVR), valve degeneration bioprosthetic)
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9
Q

Investigations of AS

A
  • ECG= large complexes, strain pattern (T wave inversion in 5 and 6)= left ventricular hypertrophy
  • Echo= leaflets thickened and calcified, hypertrophied LV
  • Doppler= speed of blow flow across valve= faster velocity
  • Transthoracic Echo= trace valve
  • CT= heavy calcification, volume of calcium
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10
Q

Aetiology and pathophysiology of Primary MR

A

-Primary= related the valve itself between left atrium and ventricle, anterior and posterior leaflets)
=Degenerative (most common, includes myxomatous disease and mitral valve prolapse)
=Rheumatic heart disease (with MS)
=Infective endocarditis (leaflet perforation or caudal rupture)
=Acute myocardial infarction (papillary muscle rupture, rare, urgent surgery)

RF: female, lower BMI, age, renal dysfunction, prior MI, collagen

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11
Q

Aetiology and pathophysiology of Secondary MR

A

-Secondary= caused by dysfunction of the surrounding structure
=Left ventricular dysfunction/ cardiomyopathy (distortion of the sub-valvular apparatus)

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12
Q

Symptoms of MR

A
  • Usually asymptomatic (left atrium compliance increases, LV dilatation for volume overload)
  • Dyspnoea – mainly on exertion (heart failure)
  • Orthopnoea / paroxysmal nocturnal dyspnoea
  • Fatigue
  • Palpitations (if the patient goes into AF)
  • Swelling of ankles/ pitting oedema
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13
Q

Clinical signs of MR

A
  • May find an irregular pulse (AF)
  • Blood pressure and pulse pressure are usually normal
  • Hyperdynamic displaced apex beat laterally
  • Pansystolic murmur – heard loudest at the apex, usually radiating to the axilla (depending on anterior or posterior leaflet affected), blowing, S1 quiet widely split S2
  • Signs of congestive heart failure may be present (elevated JVP, lung crepitations, pitting edema in lower limbs)
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14
Q

Investigations of MR

A

-Echocardiogram (single most useful test)
=Useful to diagnose MR, assess cause and severity of MR
=Also useful to assess LV size/function and assess for pulmonary hypertension
=Transthoracic echo is suitable for most cases
=Transoesophageal echo may be needed for patients with severe MR being considered for intervention

-ECG
=May see atrial fibrillation or a broad notched p wave

-Chest X-ray
=May see cardiomegaly and/or signs of congestive heart failure

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15
Q

Treatment of severe chronic primary MR

A

-Ongoing medical therapy with close follow-up (HF and AF)
-Mitral valve repair/replacement
-Transcatheter mitral valve intervention (Mitraclip)
=May be considered in patients with high surgical risk

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16
Q

Follow up of MR patients

A

-Asymptomatic patients with moderate MR and normal LV function
=Outpatient review every year with transthoracic echo every 1-2 years

-Asymptomatic patients with severe MR and normal LV function
=Outpatient review and transthoracic echo every 6 months

17
Q

Indications for mitral valve surgery in severe MR

A

-Symptoms + LV Ejection Fraction > 30%
-Asymptomatic + any of the following:
=LV Ejection Fraction < 60%
=Dilated LV (i.e. LV end-systolic diameter > 45 mm)
=New onset AF
=Pulmonary hypertension (pulmonary artery systolic pressure > 50 mmHg)

-Mitral valve repair where possible preferred over replacement

18
Q

Treatment of secondary/functional MR

A

-Medical treatment of underlying cardiomyopathy
=E.g. Diuretics, ACE-inhibitors, beta-blockers, spironolactone

  • Cardiac resynchronization therapy device may help
  • Some emerging evidence for transcatheter mitral valve intervention
19
Q

What is AR?

A

-Aortic valve- 3 cusps, LV outflow tract and ascending aorta
-AR occurs due to either dysfunction of AV cusps or dilatation of the aortic root/ascending aorta or both mechanisms
=allows reflux back into LV chamber in ventricular diastole (inadequate closure)
-More common in men than women (Marfan syndrome)
-Stenosis and regurgitation can happen at same time

20
Q

Aetiology of Primary valve disease (AR)

A

VALVE
- Rheumatic fever (most common in developing) (1)
-Calcific valve disease
-Connective tissue (RA, SLE)
-Bicuspid aortic valves
-Prosthetic
-Acute: endocarditis (2)

AORTIC ROOT
- Bicuspid aortic valve (congenital= most common developed)
- Myxomatous prolapse
- Trauma
- Collagen vascular disease (3): Marfan, Ehler-Danlos
-Syphilis, hyternsion, spondylo arthropathy, aortic dissection

21
Q

Aetiology of aortic root abnormalities

A

-Dilatation (stretching annulus where attached so cannot close), disease of aortic root/ ascending aorta

  • Systemic hypertension
  • Marfan syndrome/ EDS!
  • Aortitis
  • Trauma/ dissecting aneurysm
  • Idiopathic or senile aortic dilatation
  • Spondylarthropathies
22
Q

Pathophysiology of AR

A

-Backward flow of blood from aorta into LV (diastolic)

=Rapid fall of aortic pressure during diastole
==Increased pulse pressure

=Increased LV volume and pressure
==Increased LA pressure - Increased pulmonary venous pressure - Pulmonary oedema
==Increased SV (Frank-Starling Mechanism) - Peak systolic pressure increased as increased SV ejected into aorta - increased pulse pressure
==Increased diastolic wall-tension produces eccentric hypertrophy

23
Q

Symptoms AR

A

-Patients may be asymptomatic, especially in chronic AR
-Dyspnoea
=Initially on exertion
=Paroxysmal nocturnal dyspnoea (LV decompensates)
=Orthopnoea
-Palpitations
-Peripheral oedema (HF)
-Light-headedness, syncope (v low diastolic pressure)
-Angina

24
Q

Clinical signs AR

A

-Pulse
=Tachycardia
=Large volume, collapsing (Water-hammer),
=Wide pulse pressure (large difference in systolic and diastolic pressure 50mmHg)!, Corrigan sign (carotid artery)

-Displaced Apex (dilated LV)

-Early diastolic murmur
=Best heard along left sternal border @ 3rd/4th ICS with patient sitting leaning forward on peak expiration, increased with handgrip
=Collapsing, wide pulse pressure, Austin-Flint severe AR

  • Features of hyperdynamic circulation (large difference in pressure)- e.g deMusset’s (constant head bobbing movement), Quincke’s pulses (blushing and blanching nail bed), Duroziez’s sign (diastolic bruit at femoral artery), Traube’s (pistol shot), etc
  • Clinical features of HF- JVP, Bibasal crackles, hepatomegaly, peripheral oedema
25
Q

Investigations AR

A 
-Blood tests
=To investigate for endocarditis
-CXR
=Cardiomegaly
-ECG
=Sinus tachycardia
=LVH
-Echocardiography!!!!
=Confirms diagnosis, identifies cause of regurgitation and assesses for severity
26
Q

Treatment of AR

A
  • Management of AR depends on the presentation
  • Patients with Mild-Moderate AR are followed up regularly with serial echocardiography

-Surgical treatment- for severe AR/ asymptomatic but LVSD
=Aortic Valve replacement- Tissue vs mechanical valve
=+/- Aortic root/ascending aorta surgery

-Medical management
=For heart failure
==Diuretics, salt restriction
==Vasodilators
=Control of arrhythmia- betablockers/Digoxin, anticoagulation
=Treatment of Endocarditis- Antibiotics
27
Q

Prognosis and long-term care AR

A
  • Patients diagnosed with AR should be regularly followed up in cardiology clinic and surgical valve intervention planned if patients become symptomatic or develop LV dysfunction as assessed by echocardiography
  • Patients with acute severe AR are usually haemodynamically unstable and require urgent surgery compared to patients with chronic AR which is well tolerated over decades
  • All patients who undergo AV surgery are followed up in cardiology clinics
  • All patients who have mechanical aortic valve replacement remain on lifelong Warfarin
28
Q

Describe the Water hammer pulse

A
  • Collapsing
  • Rapid, abrupt and forceful upstroke and descent
  • Hyperdynamic circulation
  • Low filling resistance in blood vessels into which the LV pumps blood
29
Q

Causes of Mitral stenosis

A

-Rheumatic fever!!!
-Degenerative disease
-Congenital

30
Q

Presentation of Mitral stenosis

A

-Progressive symptoms of breathlessness (increased atrial pressure= pulmonary venous hypertension)
-Haemoptysis (pink frothy)
-Malar flush
-AF
-Fatigue
-Sequelae of thromboembolism (AF)

Mid-late diastolic murmur, best heard in expiration, loud S1, opening snap, low volume pulse

31
Q

Investigation of MS

A

-CXR: left atrial enlargement
-ECHO: stenosis

32
Q

Management of MS

A

-Percutaneous mitral valve commissurotomy/ balloon valvotomy
-Mitral valve repair or replacement
-Medical therapy for heart failure and AF (warfarin)

33
Q

Causes of tricuspid regurgitation

A

-Right ventricular infarction
-Pulmonary hypertension e.g. COPD
-Rheumatic heart disease
-Infective endocarditis (especially intravenous drug users)
-Ebstein’s anomaly
-Carcinoid syndrome

34
Q

Signs of tricuspid regurgitation

A

-Pan-systolic murmur
-Prominent/giant V waves in JVP
-Pulsatile hepatomegaly
-Left parasternal heave

Cardiovascular (52 decks)

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