Page 96 - Clinical Pearls in Cardiology
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84  Clinical Pearls in Cardiology


              Contd...
                   Mobile and thick valve cusps Immobile and calcified cusps
                   Thin individuals       Individuals with thick chest
                                          walls
                                          Individuals with barrel-
                                          shaped chest
                                          Pericardial effusion

                     Conditions like atrial fibrillation and atrioventricular
                   dissociation (complete heart block, ventricular tachy-
                   cardia, etc.) are associated with varying intensity of the
                   first heart sound (Table 2).
                3.  What do you know about the split of second heart
                   sound?
                   The two components of second heart sound or S2 are the
                   A2 and P2. For A2 and P2 to be heard as separate sounds,
                   there should be an interval of at least 30 milliseconds
                   between them. There are two factors responsible for
                   the delayed timing of P2 and both these factors are
                   dependent on respiration. (Ref: Congenital Heart
                   Disease, Perloff. Saunders; 2012)
                   1.  Prolonged pulmonary “hangout” interval: The
                      distensibility of the proximal aorta is less and the
                      arterial wall resistance is high. Hence, the recoil force
                      and the pressure generated within the proximal aorta
                      at the end of left ventricular ejection is very high. This
                      leads to the immediate closure of aortic valve at the
                      end of left ventricular systole producing A2. But the
                      pulmonary artery is highly distensible and the
                      resistance is relatively less. Hence there is less recoil,
                      and the pressure build up within the pulmonary
                      artery at the end of right ventricular ejection is less.
                      So the closure of the pulmonary valve, which is
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