29 - Cardiovascular Disease 2 Flashcards
Left-sided heart failure
Kidneys - pre-renal azotemia, salt and fluid retention
Brain - irritability, decreased attention, stupor -> coma
Clinical presentation of left heart failure
Pulm congestion and oedema Heart failure cells Dyspnea Orthopnea PND Blood tinged sputum Cyanosis Elevatory pulmonary WEDGE pressure
Right sided heart failure - aetiology
Aetiology - left failure cor pulmonare
Right sided heart failure - symptoms and signs
Liver and spleen
Kidneys
Pleura/pericardium
Peripheral tissues
Opening problems of valves
Stenosis
Closing problems of valves
Regurgitation / incompetence / insufficiency
Aortic stenosis
Calcification of a deformed valve
Senile
Rheumatic
Mitral stenosis
Rheumatic heart disease
Rheumatic heart diseases is related to Strep A infection
Can cause pancarditis (whole heart) or…
either endo, myo or pericarditis
Pathology of acute valvular problems
Inflammation Aschoff bodies Anitaschkow cells Pancarditis Vegetations on chordae tendinae at leaflet jxn
Pathology of chronic valvular problems
Thickened valves
Commisural fusion
Thick, short, chordae tendinae
Mitral annular calcification
Calcification of the mitral skeleton
Usually no dysfunction
Regurgitation usually but stenosis possible
F»M
Causes of aortic regurgitations
Rheumatic
Infectious
Aortic dilations - syphilis, rheumatoid arthritis, marfan
Causes of mitral regurgitations
Mitral valve prolapse (MVP) Infectious Fen-Phen Papillary muscles, chordae tendinae Calcification of mitral ring
Mitral valve prolapse - what is it, incidence
Myxomatous (connective tissue) degeneration of the mitral valve
Associated with connective tissue disorders
Floppy valve
3% incidence F»M
Easily seen on echocardiagram
Mitral valve prolapse - clinical features
Usually asymptomatic Mid-systolic click Holosystolic murmur if regurg. present Occasional chest pain, dyspnea 97% are cool 3% have infective endocarditis, mitral insuffiency, arrythmias, sudden death
Congenital heart defects e.g.s
Faulty embryogenesis (week 3 - 8)
Usually mono-morphic i.e single lesion
May not be evident until later life
Overall incidence of 1% of births
L->R shunts
No cyanosis
Pulmonary hypertension
Significant pulmonary hypertension is irreversible
All conditions have ‘D’s’ in their name
R->L shunts
Cyanosis
Venous emboli become systemic = paradoxical
All conditions have ‘T’s’ in their name
Obstructions can occur where in congenital heart disease
Aorta
Pulm. art.
ASD - features
Not patent foramen ovale
Usually asymptomatic until adult
90% are secundum
VSD - features
Most common CHD defect
Only 30% are isolated
Often with tetralogy of fallot
90% involve the membranous system
But, if muscular system, = ‘swiss-cheese’ septum
Small ones close spontaneously
Large ones progress to pulm. hypertension
PDA - features
Patent ductus arteriosus
90% isolated
Associated with VSD, coarctation of aorta, pulm/aortic stenosis
Either shunt is possible as pulm hypertension approaches systemic pressure
Closing defect in early life may be life saving
Keeping it open with prostaglandin E may be life-saving
Murmur = continous harsh, machine-like
Why would prostaglandin E be life-saving in PDA?
Transposition of great vessels could have occurred in which case you need deoxy and oxy blood to mix or death would occur.
