Aortic Regurgitation

Aortic Regurgitation

·        Causes:

o   Intrinsic valvular disease:

§  Acute lesions: Rheumatic fever, infective endocarditis (have high index of suspicion), traumatic rupture, aortic dissection (may also have dissected coronary arteries ® MI)

§  Chronic lesions: Congenital lesions, rheumatic heart disease, arteritis, aortic aneurysm, collagen diseases, ankylosing spondylitis and Reiter‟s Syndrome (may be secondary to aortitis)

o   Aortic disease: degenerative aortic dilatation, syphilitic aortitis, Ankylosing Spondylitis, rheumatoid arthritis, Marfan‟s syndrome

·        Key features:

o   LV hypertrophy

o   Large aorta

o   ­Stroke volume

o   Wide pulse pressure eg 140/50 (­systolic due to extra work of the heart, ¯diastolic due to back flow)

·        Symptoms:

o   Acute: dyspnoea – often paroxysmal, orthopnea, pink frothy sputum. Chest pain, sudden death, etc. If sub-acute, possibly embolisation

o   Chronic: Symptoms unrelated to severity. Either awareness of ­force of contraction (palpitations) or LV disease/failure

·        Signs:

o   Pulses: prominent pulsations in the neck (Corrigan‟s Sign), throbbing peripheral pulses, prominent apex beat over a wide area

o   Auscultation: high-pitched, blowing diastolic murmur beginning immediately after S2. The more severe the longer it lasts. Systolic flow murmur

·        Pathogenesis:

o  Acute: ­LV blood volume ® ­left atrial and pulmonary pressure ® oedema. ­Pressure inside a non-compliant pericardium ® ­RH pressures. ¯Myocardial flow due to ¯aortic diastolic pressure and constricted pericardium ® ischaemia, further dysfunction, etc

o  Chronic/Gradual: ® eccentric hypertrophy with low filling pressure. ­Stroke volume ® ­systolic pressure ® baroreceptor reflex ® peripheral vasodilation ® further widening of the pulse pressure. Copes with tachycardia better than stenosis: ¯proportion of cycle in diastole ® ¯proportion of blood flowing back into the ventricle. However, ­peripheral resistance (eg cold, iso-tonic exercise, sympathetic nervous stimulation) ® ­pressure load on the heart

·        Complications:

o  LV failure + myocardial fibrosis (secondary to hypertrophy, ischaemia, etc) late in the progression

o  Infective endocarditis

o  Conduction defects less common

o  No pulmonary oedema unless LV hypertrophy

·        Differential diagnosis:

o  Pulmonary regurgitation + pulmonary hypertension

o  Other causes of rapid run-off: patent ductus, arterio-venous fistula