valve disease Flashcards
valve and conditioms?
Aetiology:
Valvar:
Congenital valvar stenosis
Bicuspid Aortic valve
Degenerative calcification
Rheumatic inflammatory valvulitis
Supravalvar
Aortic coarctation
Subvalvar
Hypertrophic cardiomyopathy
compensated disease
decompensated disease
compensated disease - good lv function - few ymptoms, valve signs
decompensated disease - poor LV function - more symptoms, pressue/volume overload signs
types of bicuspid valve conditions?
aortic coarctation
Coarctation of the aorta, or aortic coarctation, is a congenital condition whereby the aorta narrows in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts.
HOCM?
Hypertrophic cardiomyopathy ("HCM") is a primary disease of the myocardium (the muscle of the heart) in which a portion of the myocardium is hypertrophied (thickened) without any obvious cause.[1][2][3][4][5][6] It is perhaps best known as a leading cause of sudden cardiac death in young athletes.[7] The occurrence of hypertrophic cardiomyopathy is a significant cause of sudden unexpected cardiac death in any age group and as a cause of disabling cardiac symptoms. Younger people are likely to have a more severe form of hypertrophic cardiomyopathy.[citation needed]
HCM is frequently asymptomatic until sudden cardiac death, and for this reason some suggest routinely screening certain populations for this disease.[8]
A cardiomyopathy is a disease that affects the muscle of the heart. With HCM, the sarcomeres (contractile elements) in the heart increase in size, which results in the thickening of the heart muscle. In addition, the normal alignment of muscle cells is disrupted, a phenomenon known as myocardial disarray. HCM also causes disruptions of the electrical functions of the heart. HCM is most commonly due to a mutation in one of 9 sarcomeric genes that results in a mutated protein in the sarcomere, the primary component of the myocyte (the muscle cell of the heart).aortic stenosis symptoms?
Symptoms:
Asymptomatic (good LV function/valve area >1cm2)
Angina (can occur with normal coronary arteries)
SOBOE (AF can exacerbate)
Syncope/dizzy spells
Emboli
Sudden cardiac death
Infective endocarditis
Signs:
Ejection systolic murmur (left sternal edge; radiating across the precordium to the carotids or the back)
Soft S2
Non-displaced/forceful apex beat
If decompensated displaced apex beat (LV enlargement) and pulmonary congestion/raised JVP.
Treatment:
Echo monitoring:
Valve
LV
Aortic root
Control BP (avoid extra cardiac afterload)
Early surgery (AVR ± CABG) if symptoms and/or LV dysfunction develop.
aortic regurgitation?
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle.[1] Aortic insufficiency can be due to abnormalities of either the aortic valve or the aortic root (the beginning of the aorta).
Aetiology:
Similar to aortic stenosis
Aortic root disease:
hypertension
Connective Tissue Diseases (e.g. Marfan’s syndrome)
Type A aortic dissection
Signs:
Wide pulse pressure/ collapsing pulse
Early diastolic murmur (longer with more severe regurgitation) Listen at end expiration
Displaced apex beat (dilated left ventricle)
Austin Flint murmur
De Musset’s sign
Quincke’s pulse
austin flint murmur?
In cardiology, an Austin Flint murmur is a low-pitched rumbling heart murmur which is best heard at the cardiac apex.[1] It can be a mid-diastolic[2] or presystolic murmur[3] It is associated with severe aortic regurgitation, although the role of this sign in clinical practice has been questioned.[4]
de mussets sign?
de Musset’s sign is a condition in which there is rhythmic nodding or bobbing of the head in synchrony with the beating of the heart, in general as a result of aortic insufficiency caused by aortic regurgitation due to aortic valve deficiency. The condition was named after the French poet Alfred de Musset.
Quincke’s pulse?
`Quincke’s pulse alternate blanching and flushing of the nail bed due to pulsation of subpapillary arteriolar and venous plexuses; seen in aortic insufficiency and other conditions and occasionally in normal persons.
mitral vlavue split into?
A1.P1/A2,p2/A3,p3
valve anatomy?
Mitral regurgitation?
Aetiology:
Mitral leaflets:
Rheumatic heart disease
Infective endocarditis
Connective tissue disease
Mitral annulus:
Degenerative calcification
‘Functional‘ dilatation – due to LV architecture distortion
Papillary muscles/chordae
Ischaemia/Infarction
Symptoms:
Acute:
sudden onset dyspnoea
Recent history of chest pain (usually > 24hours ago)
Systolic murmur (maybe quiet)
Chronic:
SOBOE/fatigue
Palpitations (associated AF)
CVA (embolic)
Signs:
Pan-systolic murmur. Loudest at the apex; radiating to the axilla.
Displaced apex beat
Irregular pulse
If decompensated:
Basal crackles
RV heave
Raised JVP
Treatment:
Vasodilators
Mitral valve repair
- quadrangular resection, annuloplasty
- goal in >80% of patients
Mitral valve replacement
- with preservation of subvalvar cords
secondary mitral regurge?
mitral stenosis?
Aetiology:
Valvar
Rheumatic (commonest)
Prosthetic valve (mechanical)
Inflow obstruction
Left atrial myxoma
Symptoms:
SOBOE/fatigue
Haemoptysis
Systemic emboli
Palpitations
Dysphagia
Signs:
Mitral facies
‘tapping’ apex beat, non-displaced
Mid-diastolic murmur (± opening snap) – longer in more severe disease.
Decompensated:
Bi-basal crackles on chest auscultation
RV heave
Raised JVP
Should not affect LV function
Treatment:
Early anticoagulation
Digoxin, verapamil, diuretics
Balloon valvotomy
- young patients without MR
- non-calcified valves
Mitral valve replacement
- with preservation of subvalvar cords
