PHONOCARDIOGRAPHY 



725 



in the volume of right heart fiiUng from the two sources. 

 If tliis is the case, then murmur intensity of the 

 audible murmurs on the thorax would be expected 

 not to change. There is, however, an alternate expla- 

 nation for the relatively unvarying systolic duration. 

 In the normal, it appears that stroke volume can be 

 increased by an increased systemic \enous return with 

 consequent lengthening of systole. With atrial septal 

 defect the stroke volume is greater than normal. In 

 this circumstance the same volume of increased venous 

 return results in a smaller percentage increment in 

 stroke volume which may not appreciably affect the 

 din-ation of mechanical systole. In this circumstance, 

 whereas the dtn-ation of systole is invariant the right 

 heart inflow and outflow are increased and one would 

 expect an increase in miu-mur intensity. Our own 

 experience indicates that there may be either no 

 change in murmur intensity or an increase with 

 inspiration, but the exact hemodynamic circum- 

 stances in which each obtains is not clear. Further 

 investigation is warranted. 



When murmurs arise otit oi communications where 

 the shunt is right-to-left, the alterations in pressure 

 and flow produced by inspiration, if it has any eff~ect 

 at all, can be expected to cause an increase in the 

 intensity of the murmur. Also one would not expect 

 the problem of the balance of effects with regard to 

 atrial septal defects. 



When the \'alsalva maneuver is employed in the 

 manner described above, changes in the intensity of 

 shunt murmius will also be noted. Following release 

 of the forced expiration there is an appreciable delay 

 in the return of left heart flow so that for left-to-right 

 shunts there is a delay in the return of murmur 

 intensity. For murmurs due to right-to-left shunts 

 one expects an immediate return of murmur intensity. 



Effect of Pharmacological Agents on Murmurs 



Since murmiu' intensity is based on flow one can 

 employ, in addition to respiration, certain pharmaco- 

 logical agents to change temporarily the flow and 

 thereby elucidate valuable information. 



This discussion will be concerned primarily with 

 the hemodynamic principles in\olved, and no dis- 

 cussion of the specific agents or means of adminis- 

 tration will be attempted. Reference should be made 

 to original publications (3, ig, 21, 94, 99, 100). 



Consider first the effect of changing arteriolar re- 

 sistance to flow on systolic murmurs of valvular origin. 

 If the murmur originates at the semilunar \'alve, de- 

 creasing vascular resistance will cause a faster runofF 



of blood and tend to decrease the great vessel pressure. 

 This will result in an increased gradient of pressure 

 and if the ventricle is able to meet the demand, an 

 increased volume ejected. In this circumstance one 

 would expect an increased intensity of the murmur. 

 On the other hand if resistance is increased, there will 

 be a tendency for the gradient and flow to be reduced 

 transiently with a decrease in murmur intensity. If 

 the murmur originates at the atrioventricular valve 

 then one can expect changing arteriolar resistance to 

 produce just the opposite effect. It should be re- 

 membered here, in the case of atrio\entricular valve 

 insufficiency, that the ventricle is ejecting blood both 

 forward into the great vessel and backward into the 

 atrium. The percentage of the total amount moved 

 that goes in each direction is a function of the re- 

 sistance to flow in that direction. Therefore, when the 

 resistance to flow forward in the direction of the great 

 vessel is increased, the relative backflow into the 

 atrium is increased, with a consequent increase in 

 murmur intensity. Conversely, a decrease in forward 

 resistance increases the flow in this direction and, by 

 decreasing the relative backward flow, decreases 

 murmur intensity. This phenomenon put forward 

 first with respect to the efl'ects on pressure (12), 

 but equally eff"ective on murmur production, has been 

 found of value in the recognition and assessment of 

 mitral insufficiency. 



A very similar situation exists with diastolic miu'- 

 murs arising out of insufficiency of the semilunar 

 valve. Here the great vessel flow di\ides itself between 

 forward flow into the smaller vessels and back flow 

 into the \entricle on the basis of the relative resistance 

 offered to each pathway. If the small vessel resistance 

 is increased then the relative backward flow will in- 

 crease with a consequent increase in murmur in- 

 tensity. A decrease in vascular resistance will increase 

 the relative forward flow and decrease murmiu- in- 

 tensity. Since forward flow across the atrio\entricular 

 valve in atrioventricular stenosis is determined by the 

 gradient of pressure across the valve, changes in 

 vascular resistance affecting great vessel flow and ven- 

 tricular performance will not directly affect this 

 murmur. Alterations produced can be \ariable de- 

 pending in large part on the nature of the \entricular 

 response; in particular, the eff'ect on the ventricular 

 diastolic pressure. 



In all of the abo\'e considerations attention must be 

 directed not only at the primary effect of changes in 

 \'ascular resistance but also at secondary or com- 

 pensatory effects. In some situations these will affect 

 murmur intensity in the same direction as the primary 



